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Three 'super-Earths' discovered: Are the seven planets uncovered in nearby solar system capable of supporting life?

They orbit Gliese 667C, one of three stars 22 light years away in the constellation of Scorpius

Astronomers believe they have found an alien solar system packed with a record-breaking three potentially habitable worlds.

New observations of the star Gliese 667C—about one-third the mass of our sun—is home to between five and seven planets, three of which are classified as super-Earths. All three are larger than our own planet, but smaller than gas giants like Uranus and Neptune.

But what makes all the difference is that these super-Earths orbit in what is known as the “Goldilocks Zone”—the region around a star where temperatures are just right for liquid water, a key ingredients in the recipe for life, to exist.

“These planets are good candidates to have a solid surface and maybe an atmosphere like the Earth’s, not something like Jupiter,” said study co-author and University of Washington astronomer Rory Barnes in a statement this week.

What makes this finding so exciting is that for the first time, astronomers have three potentially rocky or ocean worlds orbiting the same star. And at 22 light-years away from Earth, Gliese 667C and it’s two companion stars are considered relatively close neighbors to our solar system, making them ideal candidates for future extraterrestrial searches for life.

Lock on Life?

Since Gliese 667C is so much smaller and cooler than our own sun, it’s habitable zone is much closer in, meaning the super-Earths take anywhere from 20 to 100 days to orbit. Astronomers suspect this indicates the planets are gravitationally more influenced by their parent star than Earth is by the sun.

“The close proximity of these planets in the habitable zone to the host star makes it likely they are ‘tidally locked,’ which in this case means the same hemisphere always faces the star,” Barnes said. “Fortunately, we know that this state can still support life.”

These finding were made possible thanks to years of radial velocity measurements of the starlight using some of the world’s largest observatories ; including the Keck Observatory, in Hawaii, and the European Southern Observatory’s 3.6 meter telescope and Las Campanas Observatory, both in Chile. Radial velocity measures a star’s wobble caused by the gravitational tug of orbiting planets by looking for the telltale shifts in a star’s light spectrum as the planets appear to move away and towards us. The more massive a planet, and the tighter its orbit, the higher effect it will have on its star. Since these planets were relatively small their signals were hidden in the original data and so a re-analysis and new observations helped to confirm their existence.

At least two to four other planets outside the habitable zone may exist but still need to be confirmed by further observations.

The implications of this packed planetary system on the hunt for Earth-like planets could be profound. Barnes and his team believe this discovery may indicate that low mass suns like this red dwarf—many of which populate the Milky Way—may routinely harbor multiple low-mass planets in their habitable zones. This means that there could be many more habitable planets in the Milky Way than we ever thought.

[MIKA27]

Destined to Fail? How the division of Korea led to the Korean War

If there is one issue on which historians should be able to agree, it is that the artificial division of a country usually creates more problems than it solves. The twentieth century is full of examples: Ireland in 1921, Germany after each of the two world wars, the partition of India in 1947, the creation of Israel in 1948. Korea’s division led to a war which proved as serious as any of the difficulties encountered by those nations. A unique set of internal and external factors combined to create a conflict which almost precipitated a nuclear war. President Truman wrote in despair in December 1950, ‘I’ve worked for peace for five years and six months and it looks like World War III is here.’

Fortunately, Truman was proved wrong.

The US was able to restrain itself from using the atomic bomb, and the USSR decided not to become fully involved in the war. Instead, North Korean and later Chinese troops fought a conventional war against the United Nations forces led by the US.

International losses were heavy: up to 1 million Chinese, 33,000 Americans, and 686 British soldiers were killed. However, for Korea the war was truly cataclysmic, leaving an estimated 3 million civilians (approximately a tenth of the population) and 500,000 soldiers dead (from North and South), and ending with a stalemate which has left the country divided to this day. This article will examine the division of Korea into North and South, and consider how this led to war.

A Line on a Map

The division of Korea in August 1945 was a practical response to the situation in East Asia at the end of the Second World War. The USSR had entered the war against Japan a week previously, and Soviet troops were marching south through Japanese-controlled Korea when news came of Japan’s surrender. Japan’s defeat had occurred sooner than anticipated by the US command, which did not yet have troops in Korea, so in order to prevent the USSR from seizing control of the whole country (as had recently happened in Eastern Europe), it was agreed that the Soviets and the Americans would divide Korea between them. Two US colonels were given half an hour with a map and a ruler, and decided on the 38th parallel as it gave the US control of the capital, Seoul, and was already printed on most maps of Korea.

The line cut across a thousand years of Korea’s history as a unified nation. It also ran counter to economic logic, as the resulting halves were interdependent; industry was concentrated in the north, while the south was predominantly given over to agriculture.

Most importantly, the division flew in the face of the wishes of the Korean population. Koreans had suffered under Japanese colonial rule since 1910, and by 1945 Korean nationalism was at fever pitch. Korean independence was, in fact, almost the only thing which the vast majority of Koreans agreed on. The country had yet to modernise its economy, and was effectively still a feudal society with vast areas of land concentrated in the hands of a privileged elite, many of whom had worked with the hated Japanese administration. Korean politics was therefore dominated by left-wing groups, some of which where Communist, calling for land reform and the punishment of collaborators, and by right-wing elements who hoped to maintain the status quo within an independent Korea.

An opportunity to build consensus across the political divide was lost in 1945 when the US refused to work with the Korean People’s Republic (KPR), a coalition of parties which included rightists, moderates, and Communists, all keen to provide a united front so that government could be passed into Korean hands. However, the US was determined that Korea should be prepared for independence via a long trusteeship, principally to ensure that Communism would not take root. The KPR declined to accept American authority, claiming that it was the official government, and as a result it was first ignored and then outlawed by the American Military Government. The differences between members of the KPR made it an inherently unstable organisation, but it would surely have been a good starting point from which to work toward a united self-governing Korea.

Polarisation

Korea’s political landscape was complex, and the division of the country only served to polarise the right and left further.

Spontaneous ‘People’s Committees’ sprang up across Korea, formed by communities seeking control at a local level. In the North the USSR encouraged these groups as a recruiting vehicle for the Communists. However, the US viewed left-wing activity as a threat, particularly given the presence of Communists in many People’s Committees. The American Military Government, headed by General Hodge, did not distinguish between home-grown Communism , more a product of anti-imperialism than Marxism, and Soviet-controlled Communism . People’s Committees were therefore shut down in the South and under US rule left-wing activity was heavily restricted.

Hodge knew little about Korea, and did not even have anyone in his staff who could translate Korean. As a result he depended heavily on members of the aristocratic elite who had been educated in English, an association which only deepened his suspicion of leftists. In an attempt to unify the South under a pro-American figurehead, the US arranged for the nationalist septuagenarian Syngman Rhee to return to Korea from the USA, where he had been in exile for over 30 years. This was a miscalculation. Rhee was so virulently anti-Communist that US censors had to screen his speeches to remove the most inflammatory remarks. Far from being a unifying figure, Rhee would first help to scupper negotiations for the reunification of Korea, and then, having achieved the Presidency, go on to create a right-wing police state in which political opponents were arrested in their thousands.

The Soviet-controlled North was moulded into a totalitarian state under the leadership of Kim Il Sung, a young Communist guerrilla fighter who was brought in by the USSR in October 1945. The Communist policy of land redistribution was popular, as was the fact that the North was nominally being run by a Korean, and by the late 1940s up to a quarter of the adult population were members of the North Korean Communist Party. However, the USSR’s desire to create an obedient satellite state led to the ‘re-education’ of those who did not conform politically, and many thousands of right-leaning Koreans fled to the South. Homogeneity within the Korean Communist Party was achieved by expelling members who challenged Kim’s leadership.

Thus it was that, under US and Soviet control, Korea was transformed from a single nation with political fissures running horizontally through society, into a peninsula with a vertical polarisation between North and South. This suited both the US and the USSR within the context of the Cold War, and as Adrian Buzo has written: ‘… their policies derived from the nature of their mission: they were occupying powers, not nation builders.’ The historian Richard Whelan has contrasted Korea’s situation with that of Austria, a country divided between American-British, French, and Russian zones after the Second World War, but which was able to gain independence in 1955. He writes: ‘the difference was that in Austria the dominant parties of the left and the right were moderate enough to be able to form a stable coalition. In Austria the most powerful political forces were centripetal, in Korea centrifugal.’

Peaceful Reunification?

The division of Korea had always been intended to be temporary, the plan being to form a provisional government to unify the country. The government would then govern under the trusteeship of the Soviet- US Joint Commission. This was agreed in the Moscow Accords of December 1945, but by September 1947 it was clear that the Joint Commission was unworkable. North and South were now so opposed to each other, and so tightly bound to the superpowers, that talks on a provisional government failed.

The US allowed Rhee’s Representative Democratic Council (RDC) to attend the talks, despite a previous agreement that groups who were anti-trusteeship would be excluded. The RDC was campaigning against trusteeship, and the USSR therefore refused to recognise it. The USA would not consider removing the RDC because, as a right-wing grouping, its inclusion was required to produce a provisional government that the US could accept. There were no moderate Korean political parties, and in the absence of the RDC any government would have been dominated by Communists and leftists. America’s patronage of Rhee, and support of authoritarian rightists, had ultimately prevented reunification under trusteeship: ironic given that the US had designed the scheme.

Following the breakdown of talks, the USSR suggested that both occupying powers withdraw their armies and leave the Koreans to come to some arrangement. The result would probably have been civil war resulting in a Communist victory. However, in an attempt to save the situation Truman referred the matter to the United Nations, which set up a United Nations Temporary Commission on Korea (UNTCOK) to oversee democratic elections for a fully independent Korean government. This was Korea’s final chance for peaceful reunification, but it was squandered. The USSR would not allow elections to go ahead as it feared that the 9 million Koreans in the North would be outvoted by the 16 million Koreans in the South, resulting in the formation of a pro-American government. In May 1948, UNTCOK oversaw elections in the South which gave the Presidency of the new Republic of Korea to Syngman Rhee. The North held its own elections in August 1948 which, unsurprisingly, placed Kim Il Sung at the head of the new Democratic People’s Republic of Korea (DPRK). The division of Korea was now permanent and polarisation was absolute. War was now the only way to achieve reunification.

Sabre-rattling

From their inception, the governments of both South Korea and North Korea openly advocated military reunification. Kim claimed that his government represented the whole of Korea, not simply the North, and provided support to guerrilla activity in the South.

Meanwhile, Syngman Rhee frequently alluded to an invasion, which so concerned the Americans that they restricted the amount of military aid given to South Korea. The historian Bruce Cummings has shown that border fighting took place in a series of battles across the 38th Parallel, particularly in the summer of 1949. It appears that the South was as much to blame as the North in these incidents, and may even have initiated more conflicts than the North. Both Korean leaders were committed nationalists, harnessing popular support from their commitment to unification. In January 1950 Kim told the Soviet ambassador: ‘Lately I do not sleep at night. If the matter of the liberation of the people of the southern portion of Korea and the unification of the country is drawn out, then I can lose the trust of the people of Korea.’

Superpowers

Each side was therefore keen to launch a civil war, but they were restrained by their dependence on the US and the USSR. The superpowers provided massive amounts of aid to their Korean protégés, ensuring that they retained influence in Korea. The US would not support an invasion, and without military and financial support South Korea was unable to act. Far from being a model of liberty and capitalism, this ‘tight little dictatorship run as a police state’ (US journalist A.T. Steele, writing in 1949) was racked by economic problems and internal dissent. In the North, Kim needed Stalin’s backing to launch an invasion, and initially the Soviet leader was unwilling to help, fearing that any invasion might prompt American intervention. Evidence from the Soviet archives shows that Kim lobbied Stalin from March 1949, when his invasion request was flatly turned down, through to January 1950, when Stalin began arming North Korea in preparation for the attack.

Four key factors caused Stalin to change his mind. Firstly, the USA pulled its troops out of South Korea in June 1949, leaving only 500 military advisers behind. Secondly, the USSR acquired the atomic bomb in August 1949, meaning that any attempt by the US to intervene in a civil war in Korea now carried far greater risks. Thirdly, in October 1949 Mao’s Communists emerged victorious from the Chinese civil war, a sea change in Asian politics and one which the US made no direct attempt to prevent. Fourthly, additional evidence of the US’s unwillingness to intervene militarily in Asia was provided by Secretary of State Dean Acheson’s National Press Club Speech in January 1950, in which he described a ‘defensive perimeter’ around the USA. It included Japan, the Philippines, and the Aleutians, but Korea was excluded. Stalin was prepared to support the attack, provided that Mao gave his consent to conflict on China’s doorstep. Mao had received significant help from North Korea in the civil war, some tens of thousands of Koreans having fought on the side of the Communists, and he therefore agreed to Kim’s invasion.

Widening Participation

Stalin was not the prime mover behind the outbreak of war, but rather the sponsor of Kim’s ambition to reunite his country. However, the US rightly surmised that the USSR was involved and, to Stalin and Kim’s great surprise, took action to prevent Korea from being overrun by Communists. Truman needed to ‘draw the line’ in Korea to maintain his containment policy and prevent the USSR from expanding in Asia as it had in Eastern Europe. The US was keen to legitimise its decision to support South Korea, and by the 27th June had obtained backing from the UN. (The USSR was unable to veto the resolution at the Security Council. It was boycotting the UN because China had been denied membership.) The entry of the US and UN into Korea would transform the conflict from a civil war to an international one. In September 1950 the US would take the decision to ‘roll-back’ Communist forces, with the aim of pushing them out of North Korea entirely. The decision to push up to the Yalu River, Korea’s border with China, would precipitate a massive military response from the Chinese and the start of ‘an entirely new war’ (General MacArthur, commander of UN forces).

Conclusion

The Korean War developed into a major Cold War conflict, a war which neither the Americans nor the Chinese could afford to lose.

It did not begin as such. Rather, it began as a civil war, albeit with the involvement of the USSR and China. The pressure for war came from Koreans, both north and south of the border. It was a war which seemed inevitable to many at the time, including American observers, given the desire for reunification emanating from all levels of society. The division of Korea in 1945 had ignored the nation’s long history, economic situation, and public opinion. Peaceful reunification had been ruled out by the polarisation of North and South under Soviet and American occupation, and then by the aggressive regimes supported by the superpowers. Hence by 1948 war was effectively inevitable. The timing of the war would be determined by the USSR, and the nature and scale of the fighting would ultimately be determined by US and Chinese intervention, but at heart this was a Korean war: the result of the nation’s arbitrary division.

[MIKA27]

History: St Margaret of York

Margaret Clitherow, a butcher’s wife from York, was one of only three women martyred by the Elizabethan state. Her execution in 1586 was considered gruesome, even by the standards of the time. Peter Lake and Michael Questier tell her story.

On March 25th, 1586, naked but for a linen shift, Margaret Clitherow was crushed to death in the Toll Booth on the Ouse Bridge in the city of York. The sanction was known as thepeine forte et dure. She was, we are told, ‘in dying one quarter of an hour. A sharp stone, as much as a man’s fist’, was ‘put under her back’. Upon her, or rather, onto the door placed over her, were put stones ‘to the quantity of seven or eight hundred weight at the least, which, breaking her ribs, caused them to burst forth of the skin’.

Sentence had been pronounced against her in highly controversial circumstances a few days before. While Clitherow and the sheriff, Mr Fawcett, bickered in her last moments over whether she died as a martyr for Christian faith and the true (Catholic) church or as a traitor to her husband, children and country, the undersheriff, Mr Gibson, stood sobbing in the doorway. Clitherow’s was an extraordinary fate – she was one of only three women martyred by the Elizabethan state – and her execution was the product of an extraordinary confluence of circumstances. The proceedings against her had spun out of control, culminating in a show trial, which backfired against the local regime that initiated it and gained both sympathy and notoriety for Mrs Clitherow herself.

Margaret Clitherow (born c.1552) was a butcher’s wife and a relatively well connected member of York society. Her stepfather, Henry May, was a coming man. A protégé of the so-called ‘Puritan Earl’ and lord president of the council of the North, Henry Hastings, 3rd Earl of Huntingdon, May’s rapid and seemingly irresistible rise took him to the lord mayoralty of York in early 1586.

York might have been the seat of royal government in the North, but it also harboured many prominent Catholics among its governing elite. These were people whose Catholicism was often as covert as it was enduring. Many Catholics had gone along to get along, mimicking conformity to the national Church while they continued to harbour Catholic beliefs and contacts. Sometimes they slipped over the line into overt separation and then lapsed back again into some form of conformity (compliance with the 1559 Act of Uniformity) in order to avoid the toils of the law and to retain their hold on local office and influence.

Blessed release

From the 1570s a core of ‘recusants’ (refusers) emerged, people who would not attend the services of the heretical church at any price. Mrs Clitherow was one of these. Her recalcitrance was established in the face of (but also, ironically, in part enabled by) the conformity of her husband, John Clitherow, who paid the fines levied on her for her disobedience and seems to have tolerated, without enthusiasm, her periodic spells in prison. Clitherow herself appears to have regarded her confinements as a blessed release from her taxing daily round as a wife, mother and local businesswoman. She used her time in jail, among other things, to teach herself to read.

In spite of her husband’s conformity, Clitherow’s house in the Shambles became a centre of Catholic activity. It functioned as a safe house for priests who had been trained in the new seminaries on the Continent; it also served as a small Catholic school. It was a place where Mass was said and confessions were heard.

Clitherow’s refusal to go to church and her consequent periods of imprisonment ensured that her defiance was a matter of public knowledge. But in the early 1580s, as the authorities’ crackdown on Catholic separatism intensified and many of the priests she harboured were arrested, indicted for treason and hanged, drawn and quartered at the Knavesmire (the usual site of public execution in York), her non-compliance became more overt. It culminated in her making regular night-time pilgrimages to the Knavesmire itself. According to John Mush, the priest who acted as Clitherow’s confessor for the last two years of her life, here she would kneel and pray at the killing ground for as long as the nerves of her accomplices would allow her: a semi-private devotion but also an extremely bold, semi-public and provocative performance.

Mush’s subsequent account of Mrs Clitherow’s life, The Life and Death of Mistris Margaret Clitherow, on which much of this narrative is based, suggests that her existence in the butcher’s shop in the Shambles in York was not one of unmitigated serenity. He muttered darkly about the crosses she had to bear on account of her marriage. More controversial was Mush’s claim that Clitherow’s gestures of defiance, her public performances of principled Catholic recalcitrance, were directed not only at the Protestant authorities. They were aimed also at her fellow Catholics who had taken the line of least (or less) resistance and in some sense had conformed to the demands of the regime: in other words, obeying to various extents the requirements of the Act of Uniformity. Such people did not see themselves as having sold out. But that was precisely what more zealous Catholics thought that they had done. Indeed, the more extreme among them insisted that attendance at the services of the national Church constituted the heinous sin of schism. This had, for example, been a central claim in the recent mission of the two Jesuits, Edmund Campion and Robert Parsons. Campion had passed through York a few years earlier. Mrs Clitherow would not have met him because she was in prison at the time but her public defiance clearly rendered her something of a poster girl for these rigorist clergy, a standing rebuke to her less confrontational co-religionists. It did not make her popular with those quieter Catholics whose position she challenged. John Mush reports that some of them responded to her Christian admonition on this subject with the equally charitable suggestion that her confrontational stance was making matters worse by attracting the hostile attention of the authorities, while depriving her husband and children of the services of a wife and mother.

Illustration from 'A Thankfull Remembrance of God's Mercy' by George Carlton, 1627, showing the Jesuits Robert Parsons and Edmund Campion at a monstery. Parsons holds a papal licence. Campion is also show on a gallows in the background his ultimate fate. British Museum

So bitter did these clashes of opinion become that they provoked a series of rumours that Mrs Clitherow was far too close to her priestly house guests and far too disobedient to her husband to qualify as the sort of saint that her supporters said she was. Claims to heightened sanctity were met with accusations of hypocrisy, pride and corruption.

By the mid-1580s Mrs Clitherow had become a local cause célèbre. For their part, the authorities were armed with new anti-Catholic legislation passed during the 1585 Parliament and they now decided to move against her. In this they were responding both to the obvious tensions within the local Catholic community and to the activism of a minority of that group. They were also, undoubtedly, considering the recent spate of plotting against Elizabeth in favour of Mary Stuart, underwritten by Mary’s Guise relatives in France and some of the representatives of the Spanish monarchy, plotting that threatened the security of the English Protestant state.

In Margaret Clitherow’s case wider national and international issues were refracted through the micro-politics, indeed through the family politics, of York. The death of her mother and the rise of her step-father, Henry May, to the mayoralty deprived Mrs Clitherow of a major source of protection and gave the ambitious May a personal as well as an ideological motive to put her in her place. Accordingly, on March 10th, 1586 John Clitherow was suddenly summoned to appear before the Council of the North (as he thought, to answer for the fact that his wife had sent their son abroad to be educated). In fact this was a ruse to get him out of the way while his house was searched. The resident priest and the schoolmaster managed to escape but Mrs Clitherow and a large amount of liturgical paraphernalia were seized. Margaret was charged with the new capital offence of harbouring priests. Since the priest had vanished, the only witness against her was a 14-year-old boy who had been frightened into admitting that she had been harbouring seminary clergy.

The authorities decided that Mrs Clitherow should be brought to book in a show trial designed to demonstrate to the Catholics of the North the price of defying the law. It is unclear whether the ultimate aim was to kill her or frighten her into some sort of submission.

Presumably the latter was the preferred option, but the former must have been an acceptable outcome if she proved obstinate. That was precisely what she proved to be, not merely by refusing to conform but by refusing to plead to the charge against her at all.

Margaret’s refusal to be tried by jury left the authorities with no legal option but to punish her by the medieval torture of being pressed beneath weights until either she submitted with a plea or she died.

Reasons for resistance

Why exactly did Margaret Clitherow resist in this way? In public she claimed that her decision not to plead was motivated by Christian charity; she did not want her blood to be on the consciences of the jurors. It seems she anticipated (and local historical research supports this) that, if she did comply with established court procedure, some of the more conformist of York’s Catholics (exactly the ones who tended to criticise her zeal) would have been empanelled as jurors to sit in judgment on her, in the formal legal sense but in a moral sense, too. This was something she absolutely would not countenance.

Clitherow’s refusal to plead entirely turned the tables on the authorities. Seeking a trial to demonstrate the extent of local popish superstition and sedition and to illustrate the price of further defiance, the authorities got more than they bargained for. They got the trial but it was now one that could all too easily be used to demonstrate the tyranny of the regime, as it prepared to have an innocent wife and mother pressed to death, in effect without a trial at all.

This situation seems to have caused considerable consternation on the bench. The judges redoubled their efforts to get Margaret to bend before the law. She was visited in prison by some of York’s godliest Protestant clergy, at least one of whom, a Puritan, Giles Wigginton, may even have felt some sympathy for her. Members of her family tried to persuade her to bow to authority. Even her stepfather, now aware of just how bad things were beginning to look, went down on his knees, begging her to make some small gesture towards conformity, so that he could get her freed. One of the judges, John Clench, was clear in his own mind that the case against Clitherow was sufficiently weak, that if she would just agree to be tried, she would indeed get off.

But Clitherow was having none of it. It was put to her that she might be pregnant, on which grounds she might at least be reprieved. A jury of women was convened to examine her and they gave it as their opinion that she probably was with child. Still Clitherow would not capitulate beyond saying that she might be, but that it was for others to decide.

At this point Clench began to insist that they could not execute a pregnant woman. But then, if they took this course, Clitherow would have appeared to have won. Whether she was pregnant or not, some of the hard men on the Council in the North insisted that she had to die. Mush narrates a scene in which some of the more hawkish members of the council crowded in on Clench in his chamber one evening and told him in no uncertain terms that the death sentence would be carried out whether he liked it or not. Ralph Hurlestone added that, if Clitherow was pregnant, then let the sin of the child’s death be upon his own conscience. And so the affair played itself out to its grisly conclusion in the Tollbooth.

Throughout, Mrs Clitherow played the martyr with alacrity and conviction. It was a role for which she had been prepared by watching various of her priestly mentors and charges go to their deaths at the Knavesmire. At one point Mush told her that, if she continued to behave as she was doing, she should prepare herself for martyrdom. Her conduct at her trial suggests that she had taken these words to heart. She made a point of displaying a smiling insouciance in the face of the authorities and her likely fate.

True martyr or merry devil

The result was a series of contradictory verdicts on her behaviour. Some said she had become suffused with the Holy Spirit and was dying a true martyr’s death. Others claimed that her smiles showed she had been possessed by a ‘merry devil’ and that her recalcitrance represented little short of suicide. When her fate was sealed, in a last desperate attempt to spin the affair in their favour, the authorities had recourse to the tactic of circulating rumours about her. Her stepfather had even spread claims that her spiritual closeness to the priests had taken a carnal, expressly sexual form. In other words, Margaret Clitherow’s disobedience to her husband and disregard for her children had produced a literal infidelity, as the unruly wife and undutiful mother morphed into a fully fledged adulteress and *****, just as contemporary gender ideology predicted it would. This was an attempt to turn Mrs Clitherow’s indifference in the face of her imminent doom, her consummate performance of the martyr’s role, into its polar opposite. It was based on various entirely antithetical accounts of her character that had been circulating among both the Protestants and, crucially, the Catholics of York over the previous few years.

The resulting debates produced the text by John Mush. The Life and Death of Mistris Margarit Clitherow reproduces a great many of the rumours about her. It does so in order to refute them and, of course, in so doing grants us a remarkable insight into the micro-politics of York in the mid-1580s. Mush’s text was designed to confirm Clitherow as a martyr and a saint, the holiness of whose life and death established once and for all the truth of the Catholic rigorism that she had espoused from the moment of her first conversion in the mid-1570s. The account, a masterpiece in its way, was a polemical work directed not only at the regime that had put her to death but also at her less zealous Catholic neighbours, those who were failing to live up to her example and who had actively participated in the smear campaigns against her with slurs of disobedience, selfishness and sexual impurity.

In this light Clitherow emerges as a victim of a frankly intolerant regime. Yet, as we have seen, the events of early 1586 did not occur in a vacuum. It is possible to make the case that Clitherow and her friends’ separatism was political as much as religious (in that those two terms can ever really be kept apart in this period). For example, Mush’s account of Clitherow was only one of a number of manuscript works written by him in the 1580s. It has been possible to prove nearly conclusively that at least two other anonymous major polemical pieces were also penned by him between 1586 and 1588; one is a biting denunciation of the Earl of Huntingdon’s government in the North as a brutal tyranny; the other is a scathing attack on Catholics who were prepared to offer a measure of religious conformity and to claim, on that basis, that they were politically loyal to the queen and were also good Catholics. Significantly, this latter piece, which in effect called on all good Catholics to reject the authority of a heretical and persecuting regime, was completed on May 10th, 1588, only weeks before the Armada appeared in the English Channel.

In 1587 a depiction of Clitherow’s fate appeared in a tract by Richard Verstegan, a polemicist who worked for what was known as the Holy Catholic League, the union of Frenchmen, supported by Philip II of Spain, who opposed the accession to the French throne of a heretic, Henry of Navarre, in succession to the last of the Valois, Henry III. Included in the same tract was a drawing of the execution of Mary Stuart. The Elizabethan regime could hardly be blamed if and when it concluded that it had to defend itself against popish plotting, whether it was being mounted in places such as York or to fulfil the global ambitions of the Spanish monarchy.

All this serves to point to the wider stakes involved in the Clitherow case. On the one hand it is tempting to see Margaret Clitherow – as a range of earlier commentators have seen her – as a victim, not merely of the tyranny and oppression of the Elizabethan state in general and of Huntingdon’s regime in the North in particular but also, in some sense, of her own clerical minders. Some have argued that, in effect, they manipulated and exploited the natural piety of a simple and unlettered woman to vindicate their own rigorist version of a wholly recusant Catholicism and the cult of martyrdom that underwrote it. She was, after all, heavily influenced by an ardent style of Counter-Reformation piety. After her death Mush sought to enlist her example in his own ideological crusades.

But Clitherow also emerges from Mush’s narrative as someone wholly aware of the stakes, spiritual, individual and political, for which she was playing. Both the form and the timing of her death were a direct product of her own choices, choices which a whole range of people begged and bullied her to reverse but to which, alone in her prison cell and finally in the Toll Booth, she remained true. At the end, we might think of her as almost entirely the mistress of her own fate: fully aware of what her trial and death could be made to mean, convinced that her eternal salvation was at stake and that she was dying for the true faith. In so doing, she certainly believed that she was giving a much needed example to her contemporaries while sending her own soul directly to heaven; thus she shaped her end with all the determination, grace and passive aggression required of a ‘saint’ and martyr.

Yet if she died a victim of a persecuting regime she was also, as we have seen, a victim of the wider political situation of the early to mid-1580s. The significance of this horrible episode is that it enables historians, at the very least, to say something meaningful about the processes of the later English Reformation. It allows us to eavesdrop into the micro-political world of religious change in post-Reformation England. If Mush had not written this account we would have no idea about the traumatic and tension-filled world of gender and family politics that framed Margaret Clitherow’s experience of religious change in Elizabethan York. In fact, if the execution had not happened and we knew about Mrs Clitherow at all, we would probably regard her as just another rather pig-headed, if not empty-headed, recusant wife of a conforming husband. In this scenario she would be a perfect illustration of how there was a kind of continuity of Catholic-style religion in places such as York, regulated by the Protestant authorities but also superintended and controlled through the mechanisms of marriage and other types of family relationship. This, then, would be a perfect exemplar of how moderate the English Reformation was, something that many scholars have taken to be the crowning achievement of the Elizabethan Settlement.

In the world of Margaret Clitherow, however, this is not how things were; and Mush’s account of her life describes the fractious internal politics of the post-Reformation Catholic community as it tried to respond to the regime’s demands for obedience in matters of religion. Some Catholics wanted to accept the conformist olive branch offered to them by the regime, some did not; still others were unsure what to do. But Margaret Clitherow’s fate, and indeed her subsequent identity as a saint and a martyr (she was beatified in 1929 and canonised in 1970 as one of the 40 martyrs of England and Wales) showed the dangers inherent in playing politics with people’s consciences and in redrawing the already contested line between religion and politics, between secular allegiance and religious identity: an issue that is as intractable today as it proved to be in York during the 1580s.

[MIKA27]

Beyond 100: Our genes harbor many secrets to a long and healthy life. And now scientists are beginning to uncover them.

On a crisp January morning, with snow topping the distant Aspromonte mountains and oranges ripening on the nearby trees, Giuseppe Passarino guided his silver minivan up a curving mountain road into the hinterlands of Calabria, mainland Italy’s southernmost region. As the road climbed through fruit and olive groves, Passarino, a geneticist at the University of Calabria, chatted with his colleague Maurizio Berardelli, a geriatrician. They were headed for the small village of Molochio, which had the distinction of numbering four centenarians—and four 99-year-olds—among its 2,000 inhabitants.

Soon after, they found Salvatore Caruso warming his 106-year-old bones in front of a roaring fire in his home on the outskirts of the town. Known in local dialect as “U’ Raggiuneri,” the Accountant, Caruso was calmly reading an article about the end of the world in an Italian version of a supermarket tabloid. A framed copy of his birth record, dated November 2, 1905, stood on the fireplace mantle.

Caruso told the researchers he was in good health, and his memory seemed prodigiously intact. He recalled the death of his father in 1913, when Salvatore was a schoolboy; how his mother and brother had nearly died during the great influenza pandemic of 1918-19; how he’d been dismissed from his army unit in 1925 after accidentally falling and breaking his leg in two places. When Berardelli leaned forward and asked Caruso how he had achieved his remarkable longevity, the centenarian said with an impish smile, “No Bacco, no tabacco, no Venere—No drinking, no smoking, no women.” He added that he’d eaten mostly figs and beans while growing up and hardly ever any red meat.

Passarino and Berardelli heard much the same story from 103-year-old Domenico Romeo—who described his diet as “poco, ma tutto; a little bit, but of everything”—and 104-year-old Maria Rosa Caruso, who, despite failing health, regaled her visitors with a lively version of a song about the local patron saint.

On the ride back to the laboratory in Cosenza, Berardelli remarked, “They often say they prefer to eat only fruits and vegetables.”

“They preferred fruit and vegetables,” Passarino said drily, “because that’s all they had.”

Although eating sparingly may have been less a choice than an involuntary circumstance of poverty in places like early 20th-century Calabria, decades of research have suggested that a severely restricted diet is connected to long life. Lately, however, this theory has fallen on hard scientific times. Several recent studies have undermined the link between longevity and caloric restriction.

In any case, Passarino was more interested in the centenarians themselves than in what they had eaten during their lifetimes. In a field historically marred by exaggerated claims and dubious entrepreneurs hawking unproven elixirs, scientists studying longevity have begun using powerful genomic technologies, basic molecular research, and, most important, data on small, genetically isolated communities of people to gain increased insight into the maladies of old age and how they might be avoided. In Calabria, Ecuador, Hawaii, and even in the Bronx, studies are turning up molecules and chemical pathways that may ultimately help everyone reach an advanced age in good, even vibrant, health.

The quest for genetic answers has brought international scientific attention to people like Nicolas Añazco, known as “Pajarito,” Little Bird in Spanish.

In many ways Little Bird is a typical teen. He plays computer games and soccer and has been known to sneak a glance at the pinup calendar that resides beside a framed picture of the Last Supper on the dining room wall of his family’s four-room home in the rural uplands of Ecuador’s El Oro Province. In this steep and rugged, yet oddly lush, landscape at the foot of the Andes—with a hint of Shangri-La in its exotic mix of bananas, cauliflower, and tamarillo—the young man helps his father process the sugarcane that surrounds the house.

Little Bird, 17, said he became grudgingly aware of the reason for his nickname at age six, when he looked around at his classmates: “I realized that I was going to be smaller than them.” Much smaller.

Because of a recessive mutation in a single gene, Little Bird looks like an eight-year-old and is three feet nine inches tall—much shorter than his brother Ricardo, who is a year older. The mutation causes a disease of impaired growth called Laron syndrome.

But it may also protect Little Bird from serious diseases that typically ravage humans as they age. And even in this area of geographical isolation and historical poverty, word of that has gotten around.

One afternoon Little Bird and three other Laron syndrome men from the region held court for an interview at the back of an appliance store, their feet dangling in child’s-size shoes from their chairs. Freddy Salazar, 39 years old and three feet ten inches tall, had recently had his 1997 Chevy Forsa retrofitted with elevated pedals and a raised seat so he could see through the windshield to negotiate his town’s steep hills. Victor Rivera, 23 years old and slightly taller than Salazar, was the subject of a famous photograph, shown at many scientific meetings, taken when he was four—so small that the ear of corn he was holding was a little larger than his arm. Luis Sanchez, at 43 an elder statesman among the group, threw back his head in laughter, which was joined by the others’ high-pitched voices, when someone asked if they were aware of the latest scientific reports about their condition.

“We are laughing,” he explained, “because we know we are immune to cancer and diabetes.”

That somewhat overstates the scientific results to date but reflects a growing interest among researchers to interrogate the genomes of unusually healthy or long-lived groups of people, whose isolation, geographical or cultural, makes it easier to find genetic clues to longevity, disease resistance, and good health at an advanced age.

One such scientist is Little Bird’s physician, Jaime Guevara, who was born in El Oro Province. Fascinated by the region’s “little people,” as they have been known since before their condition even had a name, he began to study them around 1987, and during a quarter century of epidemiological sleuthing he identified about a hundred people with the Laron mutation sprinkled through the hills of southern Ecuador.

Meche Romero Robles, a 40-year-old single mother, is also one of Guevara’s patients. Just over four feet tall, Robles lives with her teenage daughter, Samantha, in a cinder-block, metal-roofed home perched on a hillside in the town of Piñas. “Look at her!”

Guevara cried, giving the elder Robles an affectionate hug. “She should have diabetes. Given her body mass index, she must have diabetes. But she doesn’t.” Even to a nonmedical eye, Meche appeared obese. Like so many little people, however, she remained free of diabetes. “I realized this in 1994,” Guevara said, “but no one would believe me.”

That began to change in 2005, when Valter Longo, a cell biologist at the University of Southern California who studies aging, invited Guevara to USC to describe his research. A decade earlier Longo had begun to manipulate the genes of simple organisms like single-celled yeast, creating mutations that allowed them to live longer. The reasons for this varied. Some mutants could repair their DNA more effectively than normal cells; others demonstrated a heightened ability to minimize the damage from oxidants. Still others became better able to derail the type of DNA damage that would promote cancer in humans.

Others were studying the same processes. In 1996 Andrzej Bartke, a scientist at Southern Illinois University, tinkered with mouse genes that are involved with growth. He showed—not surprisingly—that shutting down the growth hormone pathway resulted in smaller mice. What was surprising was that they lived longer—about 40 percent longer—than normal mice.

Could similar processes be at work in humans? Could genetic anomalies protect against diseases of age? Zvi Laron, the Israeli endocrinologist who in 1966 first described the dwarfism that came to be named after him, had found dozens of people scattered through central and eastern Europe with the rare syndrome. Longo thought Guevara’s patients might represent an experiment of nature—an isolated population with a condition that linked genetics to longevity.

The Ecuadorian Laron people can be traced, researchers believe, back to the late 15th century, when Jews traveled from the Iberian Peninsula to the New World with a very specific piece of baggage: a genetic misspelling known as the E180 mutation in the growth hormone receptor gene, which produces the molecule that receives the body’s growth signals. This distinctive misspelling in the genetic code has also turned up in Israel.

“The presumption is that Sephardic Jews were desperate to leave Spain and Portugal because of the Inquisition,” says Harry Ostrer, a medical geneticist at Albert Einstein College of Medicine in New York City who has collaborated with Guevara. “They went to North Africa, the Middle East, southern Europe. Many ventured to the New World as well, but the Inquisition followed them. So it was in their interest to get out of cities like Lima and Quito, where the church maintained its strongest presence.”

They settled in small towns and villages sprinkled across 75 square miles of rural Ecuador, where until the 1980s there were few roads, no phones, and no electricity. Over the centuries the mutation lurked and spread in the population, amplified by isolation and inbreeding. “Theoretically we are all from the same family,” says Christian Asanza Reyes, an economist in Balsas, whose tall frame belies the mutation he and his wife passed on to two of their three children.

Guevara and Longo began to collaborate in 2006. Guevara had found a homogeneous group in one geographic location with a known genetic mutation that seemed to block the development of diabetes and cancer in individuals. Within the Laron group there were no cases of diabetes and only a single, nonlethal malignancy. In a control group of people the same age living in the same area, Guevara and Longo found that 5 percent developed diabetes and 20 percent died of cancer. Follow-up experiments conducted by Longo at USC showed that blood taken from the Ecuadorian patients seemed to protect human cells from laboratory-induced cancers. What was the magic ingredient in their blood?

“Nothing,” Longo says.

Nothing? In fact, it was the absence of something—a hormone known as IGF-1, or insulin-like growth factor. The blood was protective, Longo says, because it had unusually low levels of IGF-1, which plays an important role in childhood growth but has also been implicated as an accelerant of cancers and as a powerful regulator of metabolism. Could controlling the presence of one hormone in human blood postpone the diseases of old age? It’s probably not quite that simple, but the insulin–IGF-1 connection keeps popping up in longevity research.

In Calabria the hunt for hidden molecules and mechanisms that confer longevity on people like Salvatore Caruso begins in places like the Ufficio Anagrafe Stato Civile (Civil Registry Office) in the medieval village of Luzzi. The office windows here offer stunning views of snow-covered mountains to the north, but to a population geneticist the truly breathtaking sights are hidden inside the tall file cabinets ringing the room and on shelf after shelf of precious ledgers numbered by year, starting in 1866. Despite its well-earned reputation for chaos and disorganization, the Italian government, shortly after the unification of the country in 1861, ordered local officials to record the birth, marriage, and death of every citizen in each commune, or township.

Since 1994 scientists at the University of Calabria have combed through these records in every one of Calabria’s 409 comuni to compile an extraordinary survey. Coupling family histories with simple physiological measurements of frailty and the latest genomic technologies, they set out to address fundamental questions about longevity. How much of it is determined by genetics? How much by the environment? And how do these factors interact to promote longevity—or, conversely, to hasten the aging process? To answer all those questions, scientists must start with rock-solid demographic data.

“Here is the book from 1905,” explained Marco Giordano, one of Giuseppe Passarino’s young colleagues, opening a tall, green ledger. He pointed to a record, in careful cursive, of the birth of Francesco D’Amato on March 3, 1905. “He died in 2007,” Giordano noted, describing D’Amato as the central figure, or proband, of an extensive genealogical tree. “We can reconstruct the pedigrees of families from these records.”

Cross-checking the ledger entries against meticulously detailed registry cards (pink for women, white for men) going back to the 19th century, Giordano, along with researchers Alberto Montesanto and Cinzia Martino, has reconstructed extensive family trees of 202 nonagenarians and centenarians in Calabria. The records document not only siblings of people who lived to 100 but also the spouses of siblings, which has allowed Passarino’s group to do a kind of historical experiment on longevity. “We compared the ages of D’Amato’s brothers and sisters to the ages of their spouses,” Giordano explained. “So they had the same environment. They ate the same food. They used the same medicines. They came from the same culture. But they did not have the same genes.” In a 2011 paper the Calabrian researchers reported a surprising conclusion: Although the parents and siblings of people who lived to at least 90 also lived longer than the general population, a finding in line with earlier research, the genetic factors involved seemed to benefit males more than females.

The Calabrian results on gender offer yet another hint that the genetic twists and turns that confer longevity may be unusually complex. Major European studies had previously reported that women are much likelier to live to 100, outnumbering male centenarians by a ratio of four or five to one, with the implication that some of the reasons are genetic. But by teasing out details from family trees, the Calabrian researchers discovered an intriguing paradox: The genetic component of longevity appears to be stronger in males—but women may take better advantage of external factors such as diet and medical care than men do.

In the dimly lit, chilly hallway outside Passarino’s university office stand several freezers full of tubes containing centenarian blood. The DNA from this blood and other tissue samples has revealed additional information about the Calabrian group. For example, people who live into their 90s and beyond tend to possess a particular version, or allele, of a gene important to taste and digestion. This allele not only gives people a taste for bitter foods like broccoli and field greens, which are typically rich in compounds known as polyphenols that promote cellular health, but also allows cells in the intestine to extract nutrients more efficiently from food as it’s being digested.

Passarino has also found in his centenarians a revved-up version of a gene for what is called an uncoupling protein. The protein plays a central role in metabolism—the way a person consumes energy and regulates body heat—which in turn affects the rate of aging.

“We have dissected five or six pathways that most influence longevity,” says Passarino. “Most of them involve the response to stress, the metabolism of nutrients, or metabolism in general—the storage and use of energy.” His group is currently examining how environmental influences—everything from childhood diet to how long a person attends school—might modify the activity of genes in a way that either promotes or curtails longevity.

Another continent, another genetic island. It was a gray day in the Bronx, and 81-year-old Jean Sisinni paced back and forth on a gray carpet in a third-floor room on Morris Park Avenue. As she walked, Sisinni struggled to recite every other letter of the alphabet (“B, D, F, H”), while the sensor on her forehead measured activity in her prefrontal cortex, and the carpet simultaneously registered the location, path, and velocity of every step.

“You’re doing great!” said Roee Holtzer, a neuropsychologist at Albert Einstein College of Medicine who has been conducting studies of brain function and mobility in the elderly.

If this sounds like a scientific variation on the old joke about being able to walk and chew gum at the same time, go ahead and laugh. In a series of studies over the past several years Holtzer and neurologist Joe Verghese have shown that the amount of thinking people are able do in the executive, prefrontal part of the brain while they walk and talk predicts the risk of dementia, loss of mobility, and falls.

These experiments complement research at Einstein led by Nir Barzilai, an Israeli doctor with a mop of gray hair atop a youthful face who in 1998 began a study of three New York centenarians. The Einstein project has since grown to include more than 500 centenarians in and around New York City—all from central Europe and all Ashkenazi Jews, a historically isolated and culturally insular population. In this homogeneous group, research has again revealed a set of genes related to longevity, some of which have also turned up in Italy.

As they gathered more and more data, the Einstein researchers noticed that the Ashkenazi centenarians had exceptionally high levels of HDL, often called the good form of cholesterol, and that the children of these centenarians had even higher levels. This sent them off to analyze the DNA of about a hundred genes known to be involved in cholesterol metabolism. What they found was a variant, a distinct genetic subtype, of a gene known as CETP (cholesteryl ester transfer protein) that was more common in centenarians than in others.

When they investigated the centenarian version of the CETP gene, they confirmed earlier research showing that this particular variant protects against cardiovascular disease, and they have gone on to show that many people with this genetic subtype—not just centenarians but other Ashkenazi Jews and even non-Jewish residents of the Bronx—perform better on cognitive tasks like the “walking while talking” experiments. Two major pharmaceutical companies are now testing drugs that inhibit the amount of CETP, as the centenarian gene variant does.

Barzilai and his colleagues have also focused on the mitochondria of centenarians. Mitochondria are the cell’s power plants, with their own DNA, their own genes, their own genetic variants—all with key metabolic responsibilities. Barzilai and his team have identified several mitochondrial proteins, which they dubbed mitochines, associated with people who live into their 90s and 100s. One of these molecules, humanin, looks especially interesting, at least in animal experiments. Barzilai says that giving a single shot of humanin to a diabetic rat normalizes its glucose levels and essentially erases diabetic symptoms in a few hours. It also prevents arteriosclerosis and Alzheimer’s in mice prone to these diseases and somehow limits coronary damage when researchers induce heart attacks in the experimental animals.

Einstein’s large and ambitious longevity program is part of a sea change sweeping human genetics research, where the prevailing emphasis for the past 20 years has been on the search for so-called disease genes. “Everybody is looking for genes for diabetes and obesity and things like that,” says Barzilai. “I think one reason we are not finding them is because we also have protective sets of genes.” Many researchers are now focused largely on the search for those protective genes, which seem to override genes associated with disease or aging.

One of the most intriguing genes is called FOXO3. In yet another study of an isolated, homogeneous population, University of Hawaii researchers have found variants of the gene in long-lived Japanese-American men on the island of Oahu. This gene is in the same insulin–IGF-1 pathway that has popped up both in studies of yeast and worms and in the Laron population in southern Ecuador.

Protective genes are also the target of a study at the Scripps Translational Science Institute in La Jolla, California, where physician Eric Topol and colleagues are riffling through the DNA of about a thousand people they call the wellderly. These are people over the age of 80 who have no chronic diseases, such as high blood pressure, coronary artery disease, or diabetes, and have never taken prescription drugs for them. “There must be modifying genes that explain why these individuals are protected from the deleterious genes that affect the aging process,” Topol says. “The hunt is on.”

The race to find the keys to longevity has even led scientists to a place that looks increasingly important in setting every individual’s rate of aging: the womb. Researchers at Einstein now suspect that our pattern of aging may be set very early, perhaps before we’re born.

To study this hypothesis, Francine Einstein and John Greally have been examining subtle chemical markings on the DNA of stem cells recovered from the umbilical cord blood of babies born in the Bronx and comparing differences in infants who were, for their gestational age, small, normal, or large. They have found that the pattern of DNA markings in both small and large infants is significantly different compared with that of normal-size babies. These results form part of a hot new field of biology called epigenetics, which studies how environmental influences can etch chemical modifications in DNA and thus introduce lifelong changes in the activity of genes. As Barzilai explains it, “There might be influences in the uterus that affect genetic mechanisms that somehow set your rate of aging.” The fetus, in other words, may be father of the old man.

If nothing else, the plethora of new studies indicates that longevity researchers are pushing the scientific conversation to a new level. In October 2011 the Archon Genomics X Prize launched a race among research teams to sequence the DNA of a hundred centenarians (dubbing the contest “100 over 100”).

But genes alone are unlikely to explain all the secrets of longevity, and experts see a cautionary tale in recent results concerning caloric restriction. Experiments on 41 different genetic models of mice, for example, have shown that restricting food intake produces wildly contradictory outcomes. About half the mouse species lived longer, but just as many lived less time on a restricted diet than they would have on a normal diet. And last August a long-running National Institute on Aging experiment on primates concluded that monkeys kept on a restricted-calorie diet for 25 years showed no longevity advantage. Passarino made the point while driving back to his laboratory after visiting the centenarians in Molochio. “It’s not that there are good genes and bad genes,” he said. “It’s certain genes at certain times. And in the end, genes probably account for only 25 percent of longevity. It’s the environment too, but that doesn’t explain all of it either. And don’t forget chance.”

Which brought to mind Salvatore Caruso of Molochio, now 107 years old and still going strong. Because he broke his leg 88 years ago, he was unfit to serve in the Italian Army when his entire unit was recalled during World War II. “They were all sent to the Russian front,” he said, “and not a single one of them came back.” It’s another reminder that although molecules and mechanisms yet unfathomed may someday lead to drugs that help us reach a ripe and healthy old age, a little luck doesn’t hurt either.

[MIKA27]

EXILED, A STYLISH ASIAN SHOOT-'EM-UP

The true action aficionados know that the only genre better suited to rapid-fire gunplay and edge-of-your-seat showdowns than the Western is the Hong Kong crime picture.

Set in Macao in the late '90s, just before the colony's handover from Portugal to China, Exiled follows the exploits of a group of lifelong friends reunited after one is targeted for a hit that the others are assigned to execute. Agreeing not to take out their mutual buddy — only after the lot of them engage in an exhilarating apartment-set shootout that ends in a stalemate, naturally — they soon find themselves working together to pull off that quintessential One Last Job, a hit against a rival mob boss who refuses to loosen his grip on the Macao market as the Chinese gangsters set out to follow the national expansion. If this all sounds a bit complicated, it never overwhelms in practice, in part because the focus rarely strays for long from the action, which is doled out often in the form of its many standalone set pieces. The best of these involves a chance encounter between enemy factions at an all-night underground clinic, where a crooked doctor is interrupted mid-surgery by a request at gunpoint — a request, which, yes, ends in total mayhem.

I love Hong Kong crime flicks!

[MIKA27]

THE MEN WHO WERE ALMOST SUPERMAN

Superman's history with celluloid goes far beyond what eventually hit movie screens. In fact, the man in tights has been plagued with development hell so many times that a graveyard of actors can now claim that they were almost able to leap buildings in a single bound. And that's not to say that Christopher Reeve got his big break easy-squeezy, either! The truth is that almost every leading man in the 1970s was considered for the role. The same goes for the 1990s and 2000s, when the road to Krypton was littered with potholes so big that entire productions fell into them just weeks before shooting. In celebration of Man of Steel, out tomorrow, here is a handful of delectable casting choices that almost were and nearly could have been.

DUSTIN HOFFMAN

Yes, Dustin Hoffman was considered for Richard Donner's 1978 version of Superman, the strongest living being on Earth. Word has it that his name was on an approved casting list from DC Comics that was submitted to the producers. Talk didn't go far with the actor, however, who even ended up also turning down the role of villainous Lex Luthor after passing on the orphaned hero from space. Thankfully Hoffman was free to instead make Straight Time, which has become a cult favorite.

ROBERT REDFORD

Also on DC's list of approved actors was none other than Dustin's co-star in All the President's Men, Robert Redford, who was Hollywood's golden boy during that time. In fact, the actor would've been Superman if not for money demands and the lack of a finished script. That being said, many considered this a relief. As one agent remarked: "Redford would have been playing Redford playing Superman. After all, who would have believed him flying around in a blue leotard and red booties?"

BURT REYNOLDS

It's true — good ol' Burt was considered for the role, as were such screen legends as Clint Eastwood, Steve McQueen, Nick Nolte, James Caan, Jon Voight, Sam Elliot, and yes, Charles Bronson (who, as one source says it, was deemed "too earthy" for the role). Still, Reynolds is a wild choice. Smokey and the Bandit came out the same year Superman was in front of the camera, as did Semi-Tough, two of the actor's biggest hits. Even more head-scratching is the idea that Burt would have kept his moustache while wearing the tights, since it was already becoming a staple of his persona (though it did go the way of the Dodo a few years later for the romantic comedy Starting Over).

SYLVESTER STALLONE

Two years before Superman was released, Rocky catapulted Sylvester Stallone into worldwide fame. Apparently the Italian Stallion screen-tested for the role, though he was deemed "too ethnic." Other reports claim that Marlon Brando, who was paid a world record $3.7 million for two weeks of work on the picture, refused to let a rising star such as Stallone overshadow him. Either way, he would have been an interesting choice, to say the least.

BRUCE JENNER

No lie — Kim Kardashian's stepfather screen-tested for Superman. While absurd, one could see how the producers would want to cash in on the all-American gold medalist playing the adopted son of America. The truth is that Jenner's screen test was terrible. He wasn't much of an actor — a fact that was solidified a few years later when the athlete co-starred in the Village People movie, Can't Stop the Music, sporting cutoffs and a midriff-bearing shirt, which is probably as far from blue tights as you can get.

HARRISON FORD

Though his name isn't mentioned in any of the references to the casting of Donner's film, Harrison Ford let it slip in 2009 to MTV News that he believes that he was once being considered for the role. Of course this would have been before his breakout success in Star Wars, which was released three months after Christopher Reeve was announced as the star in a press conference in early 1977. True or not, it's delicious to think about a cocky pre-fedora Ford as the Man of Steel, shaggy hair and all.

NICOLAS CAGE

A decade after Christopher Reeve's franchise died out in a noble but flawed fight with the Cold War and Nuclear Man (see: Superman IV: A Quest for Peace), Tim Burton mounted a new Superman film with epic proportions, starring none other than Nicolas Cage! Of the few failed Superman productions that never saw the light of day, this is by far the most famous. In fact, Metalpocalypse producer/director Jon Schnepp recently ran a successful Kickstarter campaign to fund a documentary about the legendary film whose plug was pulled too early. Sporting a script by Kevin Smith (who's shared his own bizarre experiences on the production throughout the years) and featuring a take on "The Death of Superman" comic series, the film would have been a bonkers ride that would have included Superman in an electric suit, aliens, and a robot fighting two polar bears (!). The reason the production was cancelled is still murky, though the utter failure of Batman & Robin a year earlier in 1997 probably had something to do with it.

CHRISTIAN BALE

Two years before Batman Begins and six years after Tim Burton's failed film, Warner Bros. was in active development of a Superman vs. Batman film. Two actors met with director Wolfgang Petersen (Air Force One) for the role of the Man of Steel — one being Josh Hartnett and the other, yes, Christian Bale! Things didn't get too serious since the idea of the two characters brawling it out was a lot more tantalizing than the script. In fact, it was another script that derailed this film — that being the J.J. Abrams screenplay that had Brett Ratner attached to direct. That was the same production that saw Brendan Fraser and Jude Law screen-test for the role. Of course, that production was shelved as well when Bryan Singer was hired to deliver his not-so-great Superman Returns in 2006.

D.J. COTRONA

After the so-so reaction to Superman Returns, Warner Bros. hadn't made up their mind on what to do with Brandon Routh's version of the character, so they did what any Hollywood studio would do and pumped tons of money into a Justice League movie featuring a different big boy in blue. This flick would be helmed by Mad Max's George Miller and came quite close to actually being filmed. Peter Jackson's Weta Digital studio was making the costumes and the cast was set (including rapper Common as the Green Lantern), yet the writer's strike of '07-'08 hounded the production, along with rising production costs (some reports put the production around $300 million). Not only did Miller have those headaches to worry about, his casting choices were not too well-received either. Carrying the brunt of the scorn was actor D.J. Cotrona, most recently seen doing not so much in the G.I. Joe sequel. The poor guy was pounced on and not really given a chance to show what he could do. This quote from Jay Baruchel, who was supposed to play the villain (think about that!), paints an interesting picture of what could have been: "It would have been the neatest vision of Batman and the coolest vision of Superman you've ever seen. It would have been dark and fairly brutal and quite gory and just ***** epic." Oh really?

JOE MANGANIELLO

True Blood fans take notice — your beloved bare-chested wolf dude almost got a shot at the Kryptonian gold. In fact, if not for the steamy super-outrageous HBO series, Joe could have been the Man of Steel in Zac Snyder's new film. Ironically, the show was both the main reason he was being considered for the project and the main reason he couldn't take it on, as shooting schedules conflicted far too much. And that, ladies and gents, is how Henry Cavill ended up the new man in textured tights. He's quite good, by the way, though it's totally okay to stop and wonder what could have been.

MIKA: I really can't imagine any of the above as Superman and being able to pull it off convincingly. Even Bale as Man of Steel, no way. Batman, absolutely perfect casting for him.

The worst choice, and there are many would be a "Rain-Man" Dustin Hoffman flying to K-Mart!

By the way.... Who The "Moderated* is D.J Cotrona!?

[MIKA27]

These Astonishing Vietnam War Firefight Photos Look Like Laser Hell

When James Speed Hensinger was 22, he’d already spent nine months fighting in Vietnam, spending his nights in perpetual fear of snipers hiding in the mountains above. So come April of 1970, after fielding multiple night-time hits from a single sniper and his AK47, the 173rd Airborne Brigade — of which Hensinger was a part — decided to hit back with an arsenal of insane proportions.

With nothing but a 35mm Nikon FTN camera and a few sandbags in place of a tripod, Hensinger captured long exposure shots of the astonishing attack: rounds from 7.62mm M60 machine gun sped from both sides while an M42 Duster open turret tank shot 40mm anti-aircraft guns down the centre, all followed by high explosive shells shot from an M2 Browing .5 calibre machine gun. All this for a single, Viet Cong fighter who never stood a chance.

Describing the grim aftermath, Hensinger says:

We sent out patrols during the day, and found a blood trail one morning. Otherwise, we never found him.

With a firestorm of such epic proportions, it’s no surprise that all we have left are these astonishing and telling images of a war no one stood a chance of winning.

[MIKA27]

Watch A Guy Freak People Out By Floating In The Air On A Moving Bus

Although this prank video is an obvious attempt at force inducing viral-ity by Pepsi Max, it’s still a pretty fun watch. The magician Dynamo tricks people into thinking he can levitate by ‘magically’ following a bus around as it moves across London. Watch people freak out when they see him float.

It’s always fun to see the look on people’s faces when they see something so obviously fake and impossibly real. Many of them revert back to their childhood selves with a sort of puzzled hope dressed all over their eyes. They know it’s not real but they still want to believe.

The stunt is similar to performance artist Johan Lorbeer’s trick of floating in the air, the arm touching the bus is not actually Dynamo’s arm, it’s just a bar that’s able to support his body.

If Superman was real, he’d be in advertising, I guess.

[MIKA27]

The Girl Who Turned to Bone

Unexpected discoveries in the quest to cure an extraordinary skeletal condition show how medically relevant rare diseases can be.

When Jeannie Peeper was born in 1958, there was only one thing amiss: her big toes were short and crooked. Doctors fitted her with toe braces and sent her home. Two months later, a bulbous swelling appeared on the back of Peeper’s head. Her parents didn’t know why: she hadn’t hit her head on the side of her crib; she didn’t have an infected scratch. After a few days, the swelling vanished as quickly as it had arrived.

When Peeper’s mother noticed that the baby couldn’t open her mouth as wide as her sisters and brothers, she took her to the first of various doctors, seeking an explanation for her seemingly random assortment of symptoms. Peeper was 4 when the Mayo Clinic confirmed a diagnosis: she had a disorder known as fibrodysplasia ossificans progressiva (FOP).

The name meant nothing to Peeper’s parents—unsurprising, given that it is one of the rarest diseases in the world. One in 2 million people have it.

Peeper’s diagnosis meant that, over her lifetime, she would essentially develop a second skeleton. Within a few years, she would begin to grow new bones that would stretch across her body, some fusing to her original skeleton. Bone by bone, the disease would lock her into stillness. The Mayo doctors didn’t tell Peeper’s parents that. All they did say was that Peeper would not live long.

“Basically, my parents were told there was nothing that could be done,” Peeper told me in October. “They should just take me home and enjoy their time with me, because I would probably not live to be a teenager.” We were in Oviedo, Florida, in an office with a long, narrow sign that read The International Fibrodysplasia Ossificans Progressiva Association. Peeper founded the association 25 years ago, and remains its president. She was dressed in a narrow-waisted black skirt and a black-and-white striped blouse. A large ring in the shape of a black flower encircled one of her fingers. Her hair was peach-colored.

Peeper sat in a hulking electric wheelchair tilted back at a 30-degree angle. Her arms were folded, like those of a teacher who has run out of patience. Her left hand was locked next to her right biceps. I could make out some of the bones under the skin of her left arm: long, curved, extraneous.

“It’s good to finally meet you,” she said when I walked in. Her face was almost entirely frozen; she spoke by drawing her lower lip down and out to the sides. Bones had immobilized her neck, so she had to look at me with a sidelong gaze. Her right hand, resting on her wheelchair’s joystick, contained the only free-moving joint in her body. It rose and swung toward me. We shook hands.

Peeper’s condition is extremely rare—but in that respect, she actually has a lot of company. A rare disease is defined as any condition affecting fewer than 200,000 patients in the United States. More than 7,000 such diseases exist, afflicting a total of 25 million to 30 million Americans.

The symptoms of these diseases may differ, but the people who suffer from them share many experiences. Rare diseases frequently go undiagnosed, or misdiagnosed, for years. Once people do find out that they suffer from a rare disease, many discover that medicine cannot help them. Not only is there no drug to prescribe, but in many cases, scientists have little idea of the underlying cause of the disease. And until recently, people with rare diseases had little reason to hope this would change. The medical-research establishment treated them as a lost cause, funneling resources to more-common ailments like cancer and heart disease.

In 1998, this magazine ran a story recounting the early attempts by scientists to understand fibrodysplasia ossificans progressiva.

Since then, their progress has shot forward. The advances have come thanks in part to new ways of studying cells and DNA, and in part to Jeannie Peeper.

Starting in the 1980s, Peeper built a network of people with FOP. She is now connected to more than 500 people with her condition—a sizable fraction of all the people on Earth who suffer from it. Together, members of this community did what the medical establishment could not: they bankrolled a laboratory dedicated solely to FOP and have kept its doors open for more than two decades. They have donated their blood, their DNA, and even their teeth for study.

Meanwhile, the medical establishment itself has shifted its approach to rare diseases, figuring out ways to fund research despite the inherently limited audience. Combined with Peeper’s dedication, this sea change has enabled scientists to pinpoint the genetic mutation that causes her disease and to begin developing drugs that could treat, and possibly even cure, it.

Although rare diseases are still among the worst diagnoses to receive, it would not be a stretch to say there’s never been a better time to have one.

When Peeper’s parents received their daughter’s diagnosis, they didn’t tell her. She enjoyed a kickball-and-bicycles childhood in Ypsilanti, Michigan, and only became aware of her disorder when she was 8.

“I remember vividly, because I was getting dressed for Sunday school,” she told me. She realized that she could no longer fit her left hand through her sleeve. “My left wrist had locked in a backwards position”—the result of a new bone that had grown in her arm.

Peeper’s doctors took a muscle biopsy from her left forearm. Afterward, she wore a cast for six weeks. When it came off, she couldn’t flex her elbow. A new bone had frozen the joint.

Over the next decade, as Peeper grew more bones—rigid sheets stretching across her back, her right elbow locking, her left hip freezing—she became accustomed to pain.

But, like most kids, she adapted. When she could no longer write with her left hand, she learned to use her right. When her left leg locked, she put a crutch under her arm and tipped her body forward to walk. She even learned how to drive. After graduating from high school, Peeper lived on her own in an apartment, taking classes at a local college.

When pain from a fall kept her in bed for three days, her parents, who had recently retired to Florida, begged her to move in with them. She caved, enrolling at the University of Central Florida. There she earned a bachelor’s degree in social work, interning at nursing homes and rehabilitation centers. In 1985, three weeks after graduating, Peeper tripped over a blanket in her parents’ home. “My hip hit the corner of an end table,” she said, “and that changed my life.”

Her body responded to the fall by growing another bone. She could feel her right hip freezing in place. She knew that if she couldn’t stop it, she would probably never be able to walk again. Before the fall, Peeper had been planning on getting a job as a social worker. Now she couldn’t even get dressed by herself. On top of it all, she was lonely. She assumed that, of the 6 billion–odd people in the world, she was the only one with a second skeleton.

“I don’t know how to explain it,” she told me. “I never dwelled on it—Is there someone else? Could there be someone else?—in my thinking. I thought I was the only one with this condition. That’s all I had ever known.”

Peeper asked her doctors back in Michigan about getting one of her locked hips replaced with an implant. They referred her to a National Institutes of Health physician named Michael Zasloff. Zasloff had been trained as a geneticist, and sometimes he would encounter patients with rare genetic disorders; in 1978, he met a young girl with FOP. “I’d never seen anything quite like it,” Zasloff told me. “I had no idea what it was.”

When Zasloff asked his adviser, Victor McKusick—at the time the world’s greatest clinical geneticist—what caused fibrodysplasia ossificans progressiva, McKusick told him he didn’t have a clue. So Zasloff headed to the medical library.

The first detailed report of the disease dates back to 1736. A London physician named John Freke sent a letter to the Royal Society about a patient he had just seen:

There came a Boy of a healthy Look, and about Fourteen Years old, to ask of us at the Hospital, what should be done to cure him of many large Swellings on his Back, which began about Three Years since, and have continued to grow as large on many Parts as a Penny-loaf, particularly on the Left Side.

Freke noted how superfluous bones arose from the boy’s every neck vertebra and rib: “Joining together in all Parts of his Back, as the Ramifications of Coral do, they make, as it were, a fixed bony Pair of Bodice.”

In the generations that followed, doctors recorded almost nothing more about the disease. Zasloff found only two papers from the 20th century. He was in the worst position a doctor can be in: he didn’t know how to help a young patient in pain, and he had nothing to tell her distressed parents. He decided to adopt FOP as part of his research.

As a geneticist at the National Institutes of Health, Zasloff had the greatest medical resources he could desire at his disposal. But he still struggled to get his hands on information about FOP—largely because he was hard-pressed to find anyone who had it. Zasloff took over the care of a few patients who had been referred to McKusick, and he began accepting new referrals. But many doctors didn’t even know what the disease was, let alone how to diagnose it. Over a decade, Zasloff managed to examine 18 people with FOP. That made him the world’s expert on the disease.

When Peeper visited Zasloff in 1987, he told her that a hip implant would be impossible. He had learned this lesson the hard way.

Years earlier, he’d taken a biopsy from a patient’s thigh, and the trauma had triggered the growth of a new bone. He suspected that the biopsy Peeper’s doctors had taken from her arm years earlier had caused it to freeze.

Before meeting Peeper, Zasloff had mostly treated children, whose youth and parents had buffered them from a full awareness of their fate. But in Peeper, Zasloff could sense the encroachment of profound solitude. She knew no one who could begin to understand her experience. So although Zasloff could offer her no medicine, he realized he could put her in touch with his other patients.

To Peeper, the list of 18 names Zasloff gave her was a revelation. “I thought, I need to do something to connect everyone, to let everyone know all these people are out there,” she said. Back home in Florida, she sent a letter and questionnaire to everyone on the list. Some of Zasloff’s patients had died, but 11 surviving ones wrote back: an artist and a bookkeeper, a little boy and a middle-aged woman.

Peeper responded to each letter, and she and her correspondents became friends. She began arranging to meet some of them, in order to lay eyes for the first time on someone else with her condition. “I just assumed that everybody was going to look like me,” she told me. But FOP is fickle in the positions in which it freezes people. One woman Peeper met was locked in a horizontal position and lived on a gurney. Another’s torso was angled backwards. Peeper met a girl who had lost an arm to a misdiagnosis: her doctors had thought the swelling in her left arm was a tumor. When they performed surgery, her arm began bleeding uncontrollably and they had to amputate it.

Four times a year, Peeper sent out a newsletter she called “FOP Connection.” She included questions people sent her—What to do about surgery? How do you eat when your jaw locks?—and printed answers from other readers. But her ambitions were much grander: she wanted to raise money for research that might lead to a cure. With a grand total of 12 founding members, she created the International Fibrodysplasia Ossificans Progressiva Association (IFOPA).

Peeper didn’t realize just how quixotic this goal was. FOP had never been Zasloff’s main area of research. As the director of the Human Genetics branch of the NIH, he had discovered an entirely new class of antibiotics, and in the late 1980s, he left the NIH to develop them at the Children’s Hospital of Philadelphia. His departure meant that no one—not a single scientist on Earth—was looking for the cause of FOP.

And no one was likely to. Zasloff’s powerful position in the scientific establishment had afforded him the liberty to study the disease, but for younger scientists looking to make their names, rare diseases were a big risk. FOP was just as complex as diseases that were 100,000 times more common. But with so few patients to study, the odds of failing to discover anything about it were high. When the NIH’s grant reviewers decided which projects to fund, those odds often scared them away.

For Peeper’s plan to work, she’d need someone who was prepared to risk his or her career.

One day last November, Frederick Kaplan, the Isaac and Rose Nassau Professor of Orthopedic Molecular Medicine in Orthopedic Surgery at the University of Pennsylvania, was sitting cross-legged on the floor of an exam room. Kaplan, 61, is a small, precise man. On the day I visited his clinic, he was dressed in a blue shirt, charcoal pants, and a tie covered in faces that looked like they had been drawn by children.

“How’s kindergarten?” he asked, looking up.

Above him, sitting in a chair, was a dark-haired 5-year-old from Bridgewater, New Jersey, named Joey Hollywood. His parents, Suzanne and Joe, sat in the corner of the exam room. Joey liked towering over his doctor. He smiled down at Kaplan as he kicked his legs under one arm of the chair and then slipped them under the other. “I ride the bus,” he said.

“Joey,” Kaplan said, “let’s play Simon Says.” Kaplan stood up and slapped his hands to his sides. Joey swung out of his chair and stood as well. Kaplan twisted his head to the left to look at Joey’s parents. Joey did not turn his neck. Instead, he pivoted on his feet to turn his entire body. Kaplan turned back to Joey and raised his arms to the ceiling. Joey tipped up his hands at his sides.

“He’s quite adaptive,” Joe said. “At school they were horrified to find he was using his face to turn on light switches. So they gave him a stick.”

“Can we slip that nice shirt off?,” Kaplan asked. “I’m just going to check your back.”

Joey let Suzanne draw his shirt over his head, revealing two tangerine-size mounds on his back, each faintly filigreed with veins.

Joey was born with malformed big toes, like Peeper and most other people with FOP. A few months later, a lump appeared on his back. “When I saw it,” Suzanne told me, “I said, ‘That can’t be normal.’ ”

Joey’s symptoms came and went, but not until the fall of 2011, when he was 4, did it become clear that something was seriously wrong. Bones had grown in his neck, freezing it hard as stone. The Hollywoods were referred to Kaplan, who has replaced Zasloff as the world’s leading FOP expert. A few months later, Joey’s right arm fused to his ribs, and more swellings appeared on his back.

As Joey munched on pretzels, his parents asked Kaplan about the risks of hearing loss (in young patients, ear bones sometimes fuse together), and about what had happened to Kaplan’s other patients.

“I’ve seen 700 patients with FOP around the world, and it’s clear that there’s a lot of different ways to divide patients,” Kaplan said.

One identical twin might be only mildly affected, while the other would be trapped in a wheelchair. Some patients developed a frenzy of bones as children, and then inexplicably stopped. “I’ve seen it go quiet for years and years.”

“So it’s very unpredictable,” Joe said, hopefully.

Suzanne looked over at Joey. “This is my son every day,” she said. “I don’t want to have him look back at his childhood and say, ‘My parents were always sad.’ ”

“When you’re here, we focus on FOP,” Kaplan told her. “Remember the things that are important and helpful for Joey to live as safe a life as he can.” He shrugged his shoulders. “And then forget the FOP.”

When Kaplan started out as an orthopedic surgeon in the late 1970s, he treated patients with a wide range of common bone diseases, such as osteoporosis and rickets. In the mid-1980s, however, he became interested in genetics. He suspected that for many of his patients’ treatments, a pipette of DNA would become more useful than a bone saw.

In 1988, Kaplan met Michael Zasloff. Zasloff had just left the NIH and moved to Philadelphia, but he was still hoping to find someone to take up his FOP research. He’d heard through the Penn grapevine that Kaplan had become interested in genetics, so when he spotted him at a clinic, Zasloff introduced himself and immediately asked Kaplan whether he had heard of the disease.

Kaplan did in fact have two adult patients with the condition, but it held no unique interest for him. Then Zasloff told Kaplan about an idea he was playing around with. Some scientists had recently injected a kind of protein called BMP into mice and found that the animals developed little bony marbles in response. Zasloff wondered whether extra BMP might be the secret to FOP.

He could tell Kaplan was curious. He suggested they work on the disease together.

“I don’t think you want me in your lab,” Kaplan told him. “I’m an orthopedic surgeon. I’m not a scientist.”

Zasloff persisted, asking Kaplan to join him for some upcoming appointments he had with young FOP patients, including a baby named Tiffany Linker.

“That was it,” Kaplan told me. “In an adult, you see what’s already past. When you meet a child, it’s like seeing a beautiful building, and a plane’s about to destroy it.”

Kaplan began by setting up a space in one of Zasloff’s labs and learning how to conduct molecular-biology experiments. Within two years, his obsession had surpassed even Zasloff’s, and he’d devoted himself entirely to the disease. His colleagues were mystified; at the time, rare diseases were still considered professional suicide. “They would say, ‘You are absolutely insane to work on this,’ ” Kaplan recalls.

Meanwhile, in Florida, Peeper was building her network. When families got an FOP diagnosis, they would find their way to her organization and talk with Peeper. She put her education in social work to good use, introducing frightened families to the logistics of life with FOP. “She gave me a lot of hope,” says Holly LaPrade, a Connecticut woman who was 16 when she first spoke to Peeper. “She told me how she went to college, how she had a degree, how she had founded this organization, and about all the people she had become friends with.”

Peeper asked Kaplan, whom she’d met through Zasloff, to become IFOPA’s medical adviser, and he traveled to Florida to attend the occasional gatherings Peeper organized for fellow patients and their families. These events were a medical boon for him, offering the rare opportunity to examine dozens of patients in a single weekend. From those exams and conversations, Kaplan began assembling a natural history of the disorder.

The group’s members gave him more than their stories and DNA: they began raising money. Nick Bogard, whose son Jud had been diagnosed with the disease at age 3, organized a golf tournament in Massachusetts that raised $30,000. That money allowed Kaplan to host the first scientific conference about FOP, in 1991. Other families hosted barbecues, ice-fishing tournaments, swim-a-thons, bingo nights. In 2012 alone, Peeper’s organization raised $520,000 for research. That’s not much compared with, say, the $1 billion that the NIH distributes each year for diabetes research. But these funds were crucial for Kaplan, who sought to escape the rare-disease trap. IFOPA’s money—as well as gifts from other private donors and an endowment accompanying Kaplan’s professorship at Penn—made it possible for him to work single-mindedly on FOP for more than two decades.

In 1992, Kaplan hired a full-time geneticist named Eileen Shore to help establish a lab for the disorder. Shore had worked on fruit-fly larvae as a graduate student, and as a post-doctoral researcher, she had studied the molecules that allow mammal cells to stick together as they develop into embryos. Kaplan didn’t mind that Shore knew almost nothing about FOP. What he wanted in a geneticist was an expertise in development: the mystery of how the body takes shape.

First, they set out to understand how the disease worked. Based on their conversations with patients, they learned that bone growth could be caused by even slight trauma to muscles. A tumble out of bed or even a quick brake at a stoplight might cause a flare-up—a swelling that may or may not lead to new bone growth. A visit to the dentist could do the trick, if the jaw was stretched too far. Even a flu shot to the biceps was enough. Some flare-ups subsided without any lasting effect, while others became nurseries for new bone.

Most people with the condition develop their first extra bone by the age of 5. Their second skeletons usually start around the spine and spread outward, traveling from the neck down. By 15, most patients have lost much of the mobility in their upper bodies.

Ninety percent of people with FOP are misdiagnosed at first, and many doctors take biopsies before they realize what they’re dealing with. “I see the scars, and I say to the parents, ‘Can you get me the biopsy?,’ ” Kaplan says. “Because it’s sitting in a closet somewhere. Those samples are like gold.”

Examining the biopsies, Kaplan, Shore, and their students worked out the microscopic path of FOP: At the start of a flare-up, immune cells invade bruised muscles. Instead of healing the damaged area, they annihilate it. A few progenitor cells then crawl into the empty space, and in some cases give rise to new bone.

“Your muscle isn’t turning to bone,” says Shore. “It’s being replaced by bone.”

Everything Shore and Kaplan observed fit nicely with Zasloff’s original theory: FOP is the result of cells that produce too much BMP.

To test that idea, Shore and Kaplan drew blood from their patients. (This procedure doesn’t trigger new bone growth, remarkably enough.) In 1996, they reported in The New England Journal of Medicine that the blood cells of people with the condition contain an abundance of a particular protein called BMP4. For the first time, scientists had found a molecular signature of the second skeleton. They hoped they had also found a path toward a cure.

Eighty percent of rare diseases are caused by a genetic mutation. For example, severe combined immunodeficiency—the “bubble boy” disease that robs children of an immune system—most commonly arises when a gene called IL2RG is altered. Normally, the gene helps signal immune cells to develop. If the signal goes quiet, children never gain a full immune system and can’t fight infections.

To treat rare diseases, scientists first look for the broken gene. Kaplan and Shore suspected that FOP was caused by a genetic mutation that led the body to make too much BMP4. In the early 1990s, they didn’t have access to today’s sophisticated genome-sequencing tools, so they began sorting slowly through the human genome’s 20,000 genes.

“Based on what we already knew about FOP, we could make an educated guess and say, ‘I think this is a likely gene,’ ” Shore told me. “And then we sequenced it and looked for mutations.”

The first candidate was, of course, the gene that produces BMP4. Shore and Kaplan sliced this gene out of cells from people with FOP, sequenced it, and compared it with a version taken from people without the condition. Unfortunately, the two versions were a perfect match.

When Kaplan’s colleagues heard the disappointing news, they offered him their sympathies. A mutation of the BMP4 gene would have been such a nice story, they said. Kaplan kept searching. If the culprit wasn’t that particular protein, he reasoned, it might be one of its known associates. By the late 1990s, scientists had discovered a few of the other genes that BMP4 depends on to get its job done—genes that are required to switch the protein on, for example, and genes that make receptors onto which it can latch.

Kaplan and Shore inspected gene after gene, year after year. But they failed to find a mutation unique to people with FOP.

Meanwhile, IFOPA set up a Web site, which attracted anxiously Googling parents, many from other countries. The group arranged for some of those families to attend its gatherings, along with foreign doctors who wanted to learn how to recognize the disorder.

When these doctors went home, they added more patients to the network. Eventually, this broadening community led Kaplan to patients who had children who also suffered from the disorder.

Studying families is one of the best ways to pinpoint a mutated gene. By comparing the DNA of parents and children, geneticists can identify certain segments that consistently accompany a disorder. Because most people with FOP never have children, Kaplan and Shore had assumed they couldn’t use this method. But then the online patient network began surfacing exceptions: a family in Bavaria, one in South Korea, one in the Amazon. All told, seven families emerged; Kaplan traveled to meet a few of them and draw their blood.

Back in Philadelphia, Shore and her colleagues examined the DNA from these samples and narrowed down the possible places where the FOP gene could be hiding. By 2005, they had tracked the gene to somewhere within a small chunk of Chromosome 2. “It was a huge step,” says Shore. “But there were still several hundred genes in that region.”

By a fortunate coincidence, scientists at the University of Rochester had just studied one of those several hundred genes. They had discovered that the gene, called ACVR1, made a receptor. The receptor grabbed BMP proteins and relayed their signal to cells. In the margin of the paper in which the scientists described ACVR1, Kaplan wrote, “This is it.”

Shore and her staff inspected the gene as it occurred in people with FOP. The same mutation appeared in precisely the same spot in every patient’s cells. Once they had double- and triple-checked their results, once they had written a paper describing the mutation, Kaplan and Shore planned a press conference. In the spring of 2006, Kaplan called Peeper to tell her something she had doubted she would live long enough to hear.

“We need you to come to Philadelphia,” he said. “We’ve found the gene.”

A rare disease is a natural experiment in human biology. A tiny alteration to a single gene can produce a radically different outcome—which, in turn, can shed light on how the body works in normal conditions. As William Harvey, the British doctor who discovered the circulation of blood in the 17th century, observed more than 350 years ago, “Nature is nowhere accustomed more openly to display her secret mysteries than in cases where she shows tracings of her workings apart from the beaten paths.”

Take Jeannie Peeper’s second skeleton: In many ways, it is profoundly normal. The new bones contain marrow. If fractured, they heal nicely. They are much like the bones of other mammals, of reptiles, of fish. In all those animals, bones develop under the control of the same network of genes—a network that, having shaped the bodies of our pre-vertebrate ancestors, is older even than bone itself.

What is not normal is when these bones form. Normally, new bones develop only in embryos. As children grow, those bones extend; when those bones break, new cells repair them. But almost no one develops entirely new bones outside the womb.

Finding the FOP mutation was a coup, but Kaplan and Shore still had no idea how it worked. They set about studying baby teeth from young patients, as well as mice they genetically altered, to observe the mutation in action. Seven years later, they had pieced together an understanding of the far-reaching effects. The ACVR1 receptor normally grabs onto BMP proteins and relays their signal into cells. But in people with FOP, the receptors become hyperactive. The signal they send is too strong, and it lasts too long.

In embryonic skeletons, the effects are subtle—for example, deformed big toes. Only later, after birth, does the mutation start to really make its presence known. One way it does this, Shore and Kaplan learned, is by hijacking the body’s normal healing process.

Say you bruise your elbow, killing off a few of your muscle cells. Your immune cells would swarm to the site to clear away the debris, followed by stem cells to regenerate the tissue. As they got to work, the two kinds of cells would converse via molecular signals.

Shore and Kaplan suspect that BMP4 is an essential part of that exchange. But in someone with FOP, the conversation is more of a screaming match. The stem cells kick into overdrive, causing the immune cells not just to clear the damage but to start killing healthy muscle cells. The immune cells, in turn, create a bizarre environment for the stem cells. Instead of behaving as if they’re in a bruise, these cells act as if they’re in an embryo. And instead of becoming muscle cells, they become bone.

In the context of FOP, new bone is a catastrophe. But in other situations, it could be a blessing. Some people are born missing a bone, for example, while others fail to regenerate new bone after a fracture. And as people get older, their skeletons become fragile; old bone disappears, while bone-generating stem cells struggle to replace what’s gone.

FOP may be an exquisitely rare bone condition, but low bone density is not: 61 percent of women and 38 percent of men older than 50 suffer from it. The more bone matter people lose, the more likely they are to end up with osteoporosis, which currently afflicts nearly one in 10 older adults in the United States alone. For decades, doctors have searched for a way to bring back some of that bone. Some methods have helped a little, and others, such as estrogen-replacement therapy, have turned out to have disastrous side effects in many women.

Giving someone a second skeleton is not a cure for osteoporosis. But if Kaplan and his colleagues can finish untangling the network of genes that ACVR1 is a part of, they could figure out how to use a highly controlled variation on FOP to regrow bones in certain scenarios. “It’s like trying to harness a chain reaction at the heart of an atom bomb,” he told me, “and turning it into something safe and controllable, like a nuclear reactor.”

This would not be the first time the study of a rare disease unearthed new treatment options for more-common afflictions. In 1959, Don Frederickson of the National Heart Institute discovered a strange disorder, now called Tangier disease, which caused tonsils to turn orange. The color resulted from a buildup of cholesterol, he found. Forty years later, scientists identified the mutated gene that causes Tangier disease and figured out how it helps shuttle cholesterol out of cells. Researchers are now trying out drugs that boost the performance of this gene as a way to lower the risk of heart disease.

Only recently, though, has medicine begun to formally recognize the value of the “secret mysteries” that rare diseases can reveal.

Kaplan’s office at the University of Pennsylvania is loaded like a well-packed shipping container. When I visited him there in November, he had to scooch through the narrow spaces between his desk and filing cabinets filled with X‑rays and medical reports.

Framed photographs of his patients covered most of the surfaces and blocked part of his narrow window.

Kaplan pointed to a picture of Tiffany Linker, the patient who, as a baby, had persuaded him to stake his career on FOP. He told me that last July, at 23, Linker had passed away. “It’s been a rough year,” he said.

When I talked with young people with the disease, though, I was struck by their optimism. In the 1980s, Peeper had to type out letters to reach a dozen other people with her condition. Today, someone recently diagnosed with FOP can hop on Facebook, pose a question—how to drink from a glass if you can no longer raise it to your mouth, for example—and get an immediate answer from one of hundreds of people with the same disease.

One frequent topic of conversation within today’s FOP community is the possibility that a cure, or at least a treatment, may not be far away. As Kaplan, Shore, and other scientists decipher the cause of the disease, some promising drugs are emerging that may be able to stop it. At the Children’s Hospital of Philadelphia, for example, researchers have been testing a drug based on a certain type of molecule that can prevent new bone from growing in FOP mice by breaking the chain of signals that command progenitor cells to turn into bone.

The search for a cure is accelerating, thanks in part to new programs designed to incentivize the study of rare diseases. A different drug option, currently being investigated by a team of scientists at Harvard Medical School, has benefited from these programs. In a broader experiment in 2007, the scientists tested more than 7,000 FDA-approved compounds on zebra-fish embryos, watching for whether any of them affected the animals’ development. One molecule caused the zebra fish to lose the bottom of its tail fin. When the scientists looked more closely at this compound, they discovered that it latched onto a few receptors, including ACVR1—the receptor that Shore and Kaplan had recently discovered was overactive in FOP patients.

The Harvard researchers wondered whether the drug could work as a treatment for FOP. They tinkered with the compound, creating a version that had a stronger preference for ACVR1 than other types of receptors. When they tested it on mice with an FOP-like condition, it quieted the signals from ACVR1 receptors, thereby stopping new bones from forming.

After publishing its results in 2008, the Harvard team failed to find a pharmaceutical company willing to invest in pushing the drug into human trials. The problem wasn’t that drugs for rare diseases can’t turn a profit. In fact, once they’re on the market, they can be quite lucrative. Insurance companies are willing to cover drugs that can cost tens of thousands of dollars a year if they eliminate even-more-costly types of care. But bringing a drug to market can be a hugely expensive gamble—one that companies weren’t willing to take for a potential treatment for a rare disease.

In 2011, the Harvard scientists found a backer: a new NIH program called Therapeutics for Rare and Neglected Diseases. This program collaborates with scientists to develop rare-disease drugs that can’t survive the harsh economics of the pharmaceutical establishment.

“They’re almost like the pharmaceutical company and we’re the scientific advisory board,” says Ken Bloch, one of the Harvard scientists. “From my perspective, it’s spectacular, because it fills that gap.” Researchers from the NIH program are currently running preclinical tests of the Harvard team’s drug on mice to make sure it doesn’t have any unexpected toxic side effects. They’re also tinkering with the drug to see whether they can create more-potent forms—all with an eye to getting it ready for clinical human trials.

If this particular drug, or any other one, gets to clinical trials, it will face another set of hurdles. A typical trial for a drug treating a common disease like diabetes might involve thousands of patients. That scale makes it possible to run statistical tests ensuring that the drug really is effective. It also allows scientists to detect side effects that might affect relatively few patients. But even if you enrolled every FOP patient in the United States, a trial would still be a fraction of the size of a conventional one.

In recent years, the FDA has responded to this bind by smoothing out the approval of drugs for rare diseases. If doctors can’t find thousands of patients to enroll in a clinical trial, they are now allowed to conduct smaller trials that meet certain guidelines.

Obtaining a detailed medical history for each subject in a smaller trial, for example, makes his or her individual response to a certain drug all the more revealing.

This strategy can only work, however, if a high percentage of patients with a rare disease are willing to join a clinical trial. And that’s where people like Peeper become invaluable. Thanks to the active global community she created, any clinical trial for an FOP drug now has hundreds of potential participants.

On one of my visits to Philadelphia, Kaplan took me to see Harry. We met in the pillared entryway of the College of Physicians of Philadelphia, a medical society founded in 1787. Kaplan was wearing a tie covered in skeletons. We descended a flight of stairs to the Mütter Museum, an eerie basement collection of medical specimens. We passed cabinets filled with conjoined twins, pieces of Albert Einstein’s brain, and a cadaver turned to soap. We walked up to a glass case, which a curator opened for us. Inside loomed a skeleton beyond imagining.

It belonged to Harry Eastlack, a man with fibrodysplasia ossificans progressiva who asked shortly before he died in 1973 that his body be donated to science. Harry stands with one leg bent back, as if preparing to kick a soccer ball, and the other hinged unnaturally forward; his arms hover in front of his body; his back and neck curve to one side, forcing his eye sockets to gaze at the floor. Before a typical skeleton goes on display, the bones have to be wired and bolted together. Eastlack’s skeleton needed almost no such help. It is a self-supporting scaffolding, its original structure overlain with thorns, plates, and strudel-like sheets.

“The first time I saw Harry, I stood here mesmerized,” Kaplan told me, shining a red laser on a ligament in Harry’s neck that had become a solid bar running from the back of his head to his shoulders. “I’m still learning from him.”

Thanks to Kaplan’s enduring fascination with her disease, Jeannie Peeper can now realistically imagine a time—perhaps even a few years from now—when people like her will take a pill that subdues their overactive bones. They might take it only after a flare-up, or they might take a daily preventative dose. In a best-case scenario, the medication could allow surgeons to work backwards, removing extra bones without the risk of triggering new ones.

At 54, with an advanced case of FOP, Peeper does not imagine that she’ll benefit from these breakthroughs. But she is optimistic that her younger friends will, and that one day, far in the future, second skeletons will exist only as medical curiosities on display. All that will remain of her reality will be Harry Eastlack, still keeping watch in Philadelphia, reminding us of the grotesque possibility stored away in our genomes.

[MIKA27]

This Is How Japan Trolls Google Street View

Google Street View trolling is not new. People around the world love pulling hijinks when they see the Google Street View apparatus rolling down the street. Folks in Japan did some truly epic trolling.

As IT Media points out, writers at Japanese humour site Daily Portal Z got the drop that the Google Street View would be making its way through Tokyo. So, a while ago, the DPZ writers showed up near Mitaka Station, all carrying masks so they could turn themselves into “human pigeons”. The result has recently appeared on Google (see for yourself here).

They even watch you even as you make your way down the street. *shudder*

This kind of stuff isn’t new for the site: Last February, PDZ did a story on wearing a pigeon mask in public. Here were the results:

[mazolaman]

Pidgeon one to Pidgeon two..."Is that guy taking a dump"?

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Pidgeon one to Pidgeon two..."Is that guy taking a dump"?

Pidgeon Two to Pidgeon One... Affirmative!

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Ford’s Wireless Brake Lights Warn Other Drivers There’s Traffic Ahead

In an attempt to improve safety and reduce the number of accidents on the world’s curviest roads, Ford has developed an experimental brake light that lets vehicles behind you know there’s slow traffic ahead, even if they can’t see your lights.

The enhanced brake lights include a wireless transmitter that sends a signal to following vehicles which activates a light on their dashboard indicating there’s slow traffic ahead. It’s less useful on straight stretches of road where you can see an upcoming traffic jam well before you have to slow down, but when visibility’s limited due to bad weather, or on twisty roads where there could be stopped traffic just around the next bend, it gives drivers ample time to ease off the accelerator instead of having to suddenly slam on the brakes.

Ford hasn’t said if or when it plans to implement the new technology in upcoming models, but it’s a step towards vehicle-to-vehicle communications which will assist in everything from improved traffic and weather reports, to new forms of anonymous road rage. Exciting times.

[MIKA27]

The Incredible Jaguar C-X75 Will Give You Goosebumps

Who knew that Jaguar could make something so incredible looking on the outside while making something that’s twice as exciting on the inside: a hybrid supercar with next-generation technology designed to affix your jaw to the floor. When automakers get together to celebrate an anniversary, they don’t muck about.

Meet the Jaguar C-X75 Concept. It’s a hybrid-supercar, which sounds a bit like the idea of getting Miranda Kerr naked only to realise she looks like your nanna underneath, but lo: the C-X75 will blind you with beautiful science.

To celebrate a big anniversary, Jaguar hand-picked some of its best engineers, along with engineers from the Williams F1 racing team (!!!) to build a car to a simple set of specifications: Jaguar wanted a car that was as fast as a Bugatti Veyron, as ecologically friendly as a Toyota Prius together with the battery life of a Holden Volt. Those are simple enough specifications to say, but actually getting it done is another story.

Miraculously, however, it now exists: an 800-bhp, track-eating monster with the looks of a Lamborghini, a 0-100mph (160km/h) speed of six seconds and a rev-range that might as well develop its own gravity field.

To achieve this legendary performance, Jaguar built a car with a 1.6-litre supercharged and turbocharged petrol engine, before bolting on two electric motors next to it, almost taking the concept of a Holden Volt to the absolute extreme. The effect is an engine that has an effective rev-range of over 10,000 RPM.

Now, of course, this is only a concept car right now, which means you probably can’t buy it unless your surname is Gates, Cook or Rinehart and have the bank balance to back it up, but Jaguar have said that this technology that makes the C-X75 so perfect can trickle down into future Jaguar cars that ordinary people can buy.

[MIKA27]

State Of Decay Refused Classification, Banned In Australia

I was surprised when it came out just 24 hours ago that Saints Row IV had been Refused Classification, but now for a double-dose of nostalgia we get to read it again! Microsoft’s State Of Decay has been officially Refused Classification by the Classification Board, effectively banning the game in Australia.

The statement came late yesterday evening that the game had been banned, and we’re now waiting on official confirmation and reasoning from the Classification Board on why it copped a banhammer to the face.

The statement that Kotaku got yesterday reads like Microsoft is considering a resubmission to the Classification Board, although we’ll have to play wait and see at this stage.

MIKA: Yet another 'Nanny State/Country" we live in here in Oz!

[MIKA27]

An Amazing Photo Of China’s Space Station Crossing The Sun

While it’s the International Space Station that tends to take all the glory, there is in fact another: China’s Tiangong-1, which went into low-Earth orbit in 2011. In this amazing pictures, you can see it silhouetted against the sun.

Captured by astrophotographer Thierry Legault on June 16 in southern France, the image shows the H-shaped object between the sunspots. In fact, Shenzou-10 spacecraft is docked to Tiangong-1 right now, and each one makes up half of the H. The entire transit across the sun took less than half a second — so Legault did an amazing job snapping the image.

[MIKA27]

We’ve Grappled With Televised Death Since The First TV Suicide In 1938

The family of a Phoenix man who committed suicide this past September has filed a lawsuit against Fox News over the live broadcast of the event. Understandably, the family says that they suffered emotional distress after the broadcast, which was seen on TV sets and computer screens all over the world.

Anchor Shepard Smith apologized immediately after airing the suicide, but a national debate about the disturbing voyeurism of televised police chases ensued.

Sadly, very little of this debate about death on television is new. Suicide on TV is something that the medium has grappled with since its inception — before many people even knew how to properly define the technology.

On June 23, 1938, Marion Perloff jumped to her death from the 11th floor of the Time and Life building in New York City. This would have been just another suicide of many that would occur that year — America was still in the throes of the Great Depression — but something made this one particularly unique. It was the first suicide ever witnessed by TV cameras.

Television was still very much in its infancy in 1938. A bare-bones receiver might set you back $US400 (about $US6400 adjusted for inflation) and even if you were an early adopter with a set, there was very little programming to watch. But engineers from RCA were busy working on improving TV technology in 1938, ramping up their efforts for what was hoped to be TV’s big coming out party at the 1939 New York World’s Fair.

NBC cameraman Ross Plaisted was testing his video and audio equipment in Rockefeller centre when he spotted the 28-year-old Ms Perloff descending from the 11th floor. He picked up the shot when she’d reached the sixth floor and followed her with his lens all the way to the ground. A parabolic microphone picked up the deathly sounds and the gathering crowd’s commotion after her leap.

The only people who saw the grisly images come flickering through were NBC engineers sitting in the third floor of the RCA Building. But despite the fact that it wasn’t broadcast, the woman’s tragic end was discussed as a dark milestone everywhere from Time magazine to radio trade publications to local newspapers throughout the US.

“Death for the first time flashed across a television screen,” Time declared. And it wouldn’t be the last. The second suicide scene ever caught by TV camera would occur just a month later and just a few blocks away. When 26-year-old John Warde stood on the 17th floor of the Gotham Hotel on 5th Avenue, the police and Warde’s family tried to coax him inside.

“SUICIDE NO. 2 TELEVISED!” read the grisly headline from the October 1938 issue of Radio-Craft magazine. Warde stood on the ledge of that 5th Avenue hotel for over 10 hours before jumping in front of a crowd of 10,000 horrified onlookers. The suicide was again not broadcast to a wide audience over the airwaves. But this time it was the lack of sunlight and a primitive distribution channel that saved early adopting New Yorkers from such a grisly sight in their homes.

Years later, moviegoers would also be spared from having to relive Warde’s demise. The 1951 film titled Fourteen Hours, which dramatises the last day of Warde’s life, ends with the disturbed young man surviving the fall. Unlike in the movies, live TV news cameras (whether they’re from the 1930s or today) can’t guarantee us a happy ending.

[MIKA27]

8 Designs That Rethink The Way We’re Buried

The way we bury our dead hasn’t changed much over the past 2000 years. But it needs to change soon, according to a group of designers, philanthropic foundations and funeral directors who sponsored a recent design competition to rethink burial traditions in the face of emerging problems with the status quo. It’s a less less macabre concept than it sounds.

In fact, there are some pretty compelling reasons to change the way we bury each other. For one thing, we’re running out of space: in cities especially, cemetery overcrowding is a major problem. More importantly, both burial and cremation are surprisingly bad for the environment, not to mention the health of the living — our dental fillings, for example, release thousands of pounds of mercury into the atmosphere when we’re cremated.

What’s holding up a revolution in the way we bury our dead? The answer is complex. Most of us are uncomfortable with talking candidly about death, and ritual is there to help to calm that anxiety. There are also legal hurdles with unconventional burials, not to mention challenges from the established commercial industry that surrounds funerals. Still, the “natural burial” movement, which seeks to make bural more eco-friendly, is gaining momentum. So are less conventional burial methods, from space-borne ashes to fireworks.

So in April, Designboom launched Design for Death, a competition that invited designers to propose new burial methods. In the end, they received 2,050 proposals and distributed over $US100,000 in prize money. A group of jurors — including architect Richard Meier, artist Ray Ceasar, and the director of the National Funeral Directors Association — voted to pick the best.

Some of them are trite, others are powerful — and most are a bit of both. After all, the ways we mourn (and the ways we take and give comfort) differ for everyone. With that in mind, some of these designers make powerful arguments for change. Check them out below.

The Infinity Burial Project by Jae Rhim Lee

“By trying to preserve dead bodies, we deny death, poison the living, and further harm the environment,” says MIT research fellow and artist, Jae Rhim Lee, the designer behind the so-called Mushroom Death Suit. The idea is simple: certain strains of mushrooms are actually able to remediate toxins. Knowing that the average body is host to 219 different chemicals — all of which seep into the soil when we decompose — Jae Rhim’s proposal would use “death suit” covered in the mushrooms to prevent the spread of toxins into the soil.

Emergence by Enzo Pascual, Pierre Rivière

Three French designers proposed this eco-casket, made from biodegradable plastics and embedded with a tree seedling, as an alternative to a traditional steel, wood, or plastic box. The beautiful thing about their design? Co2 emitted from your body’s decomposition will power a perpetually-glowing headstone on the surface. It’s a self-powered memorial.

Urn for a Ceremony by Agnes Hegedus

Hungarian designer Agnes Hegedus created this elegant little urn for a style of burial that was once more popular: the water-based cremation. Except in this case, the body isn’t cremated on the water. Rather, an urn containing your ashes floats out to sea aboard a clay pot, which is designed to sink slowly down to the ocean floor. The pots would cost only a few dollars to make.

“I Wish To Be Rain” by Studio PSK and Matter & Fact

The increasingly common practice of “cloud seeding”, which alters the intensity of natural rainfall by literally “seeding” it with particular chemicals, serves as the basis for this idea from two UK design teams. “Humans now have the ability affect, control and even cause natural phenomena, whether it is rain, an earthquake or a flood,” write the designers. “We wonder if a person could do this not just by their actions, but literally transform themselves into types of natural spectacle.” The concept would use a weather balloon to carry your ashes into the sky — releasing them high above the earth, to be “rained” back down in millions of droplets of water. Though it’s probably deeply illegal, it’s still a lovely idea.

Design for Death Living by Ancunel Steyn

“Multifunctional land is not a non-renewable resource,” argues Ancunel Steyn, the South African designer behind this proposal. “The question is, how can we reduce space required to store the dead?” Steyn proposed an urban design that would intersperse memorials with public infrastructure: from parks, to art galleries, to mixed-used commercial buildings. The memorials themselves would take up a very small, tissue box-sized space, stacked on a series of walls arranged around the site.

Family Tree by Loucas Papantoniou and Asta Sadauskaite

Two Lithuanian designers created this hexagonal design for an urn-storage system. The idea, as the title suggests, is to create a literal family tree of urns. There’s also a digital element, which could come off as smart or tacky, depending on how you feel about SMS-based memorials: “The urn vault is made of wood, with an OLED display cap,” explain the duo. “The display emits a serene, pulsing light that conveys spirituality and displays the name of the deceased with a short memorial message.”

Souvenair by Chen Jiashan

This simple design, by French artist Chen Jiashan, is half windchime and half urn. “Why should we keep the deceased ones away from our eyes?,” asks Jiashan. “The souvenair, small in size but clearly visible, can be hanged at home or in a public place. Its tiny and appeasing ‘ding’ recalls the presence of the loved one whenever some wind blows.”

[MIKA27]

IKEA designs a smarter flat-pak refugee shelter:

If there’s any company on earth with an expertise in designing things that are easy to transport and assemble, it’s Ikea. So it makes perfect sense that the Swedish furniture manufacturer would team up with the United Nations High Commissioner for Refugees—or the UNCHR for short—to redesign the temporary shelters that millions of refugees around the world call home.

The tent-based structures currently deployed by the UN are not only time-consuming to assemble, but lack insulation against the heat and cold. What’s more, the tents usually only survive for about six months, which is a huge problem since refugees often have to call these shelters home for years. So the engineers working for the Ikea Foundation came up with a simple four wall structure that’s an improvement in every way.

At roughly twice the size of current temporary dwellings, the new shelters are built around a simple framework of poles and connectors covered in lightweight insulated plastic panels that reflect sunlight in the day, and retain heat in the evening. And while assembly only takes about four hours, the completed shelter will last for almost three years, even in harsh conditions.

It goes without saying that electricity is a luxury that most refugee camps are lacking. So as these shelters are being tested in Ethiopia next month, Ikea and the UNCHR are looking to further advance the design with netting that not only blocks heat, but also works as a solar panel to charge a battery that can power lighting throughout the night. And since Ikea’s involved, here’s to hoping some of these shelters even come already furnished.

[MIKA27]

Ai Weiwei’s Shockingly Detailed Remake of His Life in a Chinese Prison

Six iron boxes sit where pews should be at the Church of Sant’Antonin in Venice. They’re big—5×12 feet and nearly 2.5 tons each—and hulking and sort of out of place in the context of their beautiful, peaceful surroundings. It’s not until you take a closer look that you notice something even stranger: a slight slit in the metal, leading you to the lifelike dioramas of a man inside a prison cell.

The man is Ai Weiwei, the Chinese artist known for his political activism and talent for pushing buttons. After spending 81 days in prison for alleged tax evasion in 2011, it makes sense that the prolific artist wasn’t just going to sit back and pretend it never happened. Once released, he set to work with a team of assistants and sculptors to create S.A.C.R.E.D., an installation that gives viewers a very literal look at Ai’s experience in solitary detention.

The six fiberglass dioramas depict painstakingly detailed scenes of how Ai spent his days. They’re intimate moments of him sleeping on a white cot, being interrogated by officers, being watched as he eats food and uses the bathroom. The minutiae, from the clothes hanging in his closet to the white padding on his cell walls, were reconstructed from Ai’s memory. “He was watched all the time during his detention under obsessive surveillance at a very close proximity,” says Maurizio Bortolotti, curator S.A.C.R.E.D. “Through his dioramas he upturns this situation, making us the viewers watching the guards who are in turn watching him.”

S.A.C.R.E.D. is part of Ai’s larger exhibition Disposition, a parallel event to the Venice Biennale curated by Zuecca Project Space and Lisson Gallery. The artist’s other Zuecca-curated piece includes “Straight,” a sculptural installation which showcases 150 tons of straightened steel bars Ai gathered from the 2008 Sichuan earthquake rubble.

Though both pieces are highly-personal and stem from traumatic events, Bortolotti notes that they (like much of Ai’s work) are meant to provoke viewers into thinking about the contradictions of contemporary China. “The force of this work and that of more recent works by Ai Weiwei is that he was able to move art strongly towards social engagement once again, after decades in which it was not able to do that,” Bortolotti said. “In that sense, and for some other reasons, I think S.A.C.R.E.D. is really a masterpiece.”

The exhibitions are on view at the Venice Biennale until September 15.

[MIKA27]

Behold the Space-Age Mustang That Never Was

The design brief from the Ford brass was simple: Create a compact sports car for cash-strapped 20-somethings. The result was the Mustang I, a mid-engined two-seater with an integrated roll-hoop and a visor for a windscreen. It was the birth of an icon, but it bore no resemblance to the iconic pony cars that made it to production.

In the summer of 1962, the Fairland Group — an internal team at Ford lead by legendary automotive maverick Lee Iacocca — was tasked with creating a competitor to the Chevrolet Corvair. It wanted to create something sleek, slick, and affordable, with an innovative drivetrain and the performance to match.

Designers Eugene Bordinat, John Najjar, and Philip T. Clark got to work, first crafting the design out of clay and, once approved by the board, rendering it in an aluminum skin — an exotic material for cars of the era. The body was mounted into a cutting-edge spaceframe, but to make the Mustang as rigid as possible, the seats were molded into the aluminum tub. That meant they couldn’t move, so the engineers developed a steering column and a three-pedal setup that would articulate towards the driver.

Mounted behind the passenger compartment was an import from Germany: a 1,500cc, 60-degree V4 pulled from the Ford Cardinal. Two Mustang I’s were developed, one with 89 horsepower for the street, another with 109 horsepower for track use.

When Ford unveiled the Mustang I to the throngs at the United States Grand Prix in Watkins Glen, New York in 1962, none other than Dan Gurney — famed Formula One racing driver — took the track version around the circuit. To the astonishment of the crowd (and Gurney and Ford PR) the Mustang concept was posting lap times were nearly on par with the F1 cars racing that weekend.

Over the course of two years, the Mustang I was trotted out across the U.S., but the space-age sexy coupe wasn’t long for this world. Recognizing that an aluminum-bodied, mid-engine sports car would be a hellish headache to produce at scale, Ford began development of the Mustang II concept. That would use the Falcon’s platform as its underpinnings, with a proper 4.7-liter V8 mounted up front and sending power to the rear wheels. It looks much the same today as when it finally went on sale in 1965.

The only design element that made it to production were the side-mounted scoops aft of the doors, originally intended to cool that midship engine. And on the retail version, they were there strictly for style.

http://youtu.be/t8kWWpzm2Ho

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700,000-Year-Old Horse Genome Shatters Record for Sequencing of Ancient DNA

By piecing together the genetic information locked inside a frozen, fossilized bone, scientists have deciphered the complete genome of an extinct prehistoric horse that roamed the Yukon more than 700,000 years ago. The work rewrites the evolutionary history of the horse and smashes the previous record for the oldest complete genome ever sequenced. In doing so, it redefines how far back in time scientists can travel using DNA sequences as their guide.

Every time a cowboy throws a leg over the saddle and gallops off on his horse, he’s riding on top of 4 million years of evolutionary history. But this history is mostly a mystery. We know surprisingly little about how natural selection and thousands of years of selective breeding by humans have shaped these animals on the genetic scale.

Horses were once considered a textbook example for the smooth transition of one species into another, a perfect illustration of Darwin’s theories. Ancient equine species — dog-sized animals with five toes – gradually evolved into towering, hooved thoroughbreds. Or so the story went. But with every fossil that was unearthed, a more tangled picture emerged.

Then DNA sequencing came along, allowing scientists to reconstruct how organisms change over time down to the resolution of single letters in the DNA code.

In the new study, a multinational team of scientists led by Ludovic Orlando and Eske Willerslev at the University of Copenhagen used what’s become a common approach: comparing the DNA of modern species to DNA recovered from fossil remains, in this case a fossil bone fragment found near Thistle Creek, Canada. By pushing DNA sequencing technology to its limits, they were able to rewind the evolutionary clock back further than ever before.

The previous record for oldest genome was an 80,000-year-old ancient cousin of humans whose genome was sequenced from a single finger bone found in Siberia. The Thistle Creek horse appears to be nearly ten times as old, which provided new challenges for the scientists. DNA sequencing technology is constantly improving, but the information that researchers get in the end is only as good as the DNA that they start with. And that’s where scientists like Orlando are fighting a losing battle against nature.

Recent technological advances, several developed solely for this work, allowed the horse genome wranglers to read their DNA sequences with as little as a single molecule of starting material. And beefed up computing power meant they could rebuild genomes stretching billions of bases from chunks as small as 25 individual letters. “It is a 12.2 billion-piece jigsaw puzzle,” said Mike Bunce, a paleogeneticist at Murdoch University, who was not involved in the study.

Not only was the DNA heavily degraded, the bone itself had adopted a host of microbial residents, the tiny engines of decomposition, each full of their own DNA. The team again turned to powerful computer programs to pick out which sequences belonged to the horse and which belonged to the bacteria.

The final product of all this work was a complete rough draft sequence of the Thistle Creek horse’s genome.

In order to place the Thistle Creek Horse on the evolutionary timeline, the researchers compared its genome to those of a younger extinct species, several modern domestic horses, a donkey, and a wild Asian horse. The results of this comparison, reported today in Nature, push back the origin of the Equus lineage, which includes all living horses, zebras and donkeys, to a common ancestor living 4 million years ago.

As part of their analysis, the team sequenced the genome of the Przewalski’s horse, an endangered species native to the Mongolian steppes. Their results confirm that the Przewalski’s horse is Earth’s last remaining truly wild horse population, highlighting a critical need for species conservation. Finally, along the way, the researchers assembled the first complete genome of the donkey, a creature that seems forever doomed to life in the horse’s shadow.

The team also uncovered other chemical secrets locked within the Thistle Creek bone. Using machines designed to smash proteins into their amino acid building blocks, the researchers decoded the sequence of 73 prehistoric horse proteins. Orlando says they originally looked at the proteins as a way to gauge how well the sample had been preserved, but were surprised to find so many untouched. Studying the proteins that flowed through the bloodstream of this horse provides a snapshot of molecules in action taken three quarters of a million years ago.

But the most fascinating question raised by the work is this: How damaged and scarce can ancient DNA be before scientists will be unable to weave a genome from its frayed strands?

Last year, Bunce and colleagues squashed the dreams of Jurassic Park fans when they demonstrated the frustratingly short half-life of DNA. Every 521 years or so, about half the DNA in any particular sample will break down into its chemical components. Even when buried in permafrost, Earth’s cold-storage freezer, long DNA molecules become short ones and individual DNA bases are erased forever. While this spells a huge setback for scientists aiming clone extinct species, it doesn’t rule out sequencing extinct genomes.

Bunce predicts that in the coming years, there will be a race to sequence even more degraded prehistoric genomes using less DNA.

Przewalski horses, the last remaining species of wild horse, in Khomyntal, Western Mongolia

Eddy Rubin, director of the Department of Energy’s Joint Genome Institute, predicts a shift in how researchers study these ancient species. “DNA is really a very accurate predictor of what happened,” he says, “much more so than bony structures.” Rubin suggests that a warming climate and thawing permafrost means “there may be other samples that reside in friendly environments out there that could push back what we know about the origin of species.”

That includes our own. The ability to reconstruct fossil genomes is already revolutionizing the study of human origins.

Until recently, scientists trying to retrace our evolution have focused primarily on bones uncovered in tropical environments, such as the famous Australopithecus skeleton known as Lucy. But important human relatives like Neanderthals and Denisovans lived alongside our ancestors as far north as Siberia.

This new research provides a scaffold to build upon as genome detectives push the one million year threshold. And as DNA sequencing technology marches forward, geneticists are able to reach further back in time. But the Thistle Creek horse reminds us that decoding a DNA sequence only tells part of the story. Researchers around the world continue to analyze the genetics of horses past and present using this data as their guide, perhaps one day identifying the changes that molded modern horses.

As scientists amass more and more sequencing data from less and less starting material at an ever faster pace, they promise to keep their colleagues busy figuring out what it all means for many years to come.

[MIKA27]

Pioneer’s New Soundbar Is Beautifully Simple And Wonderfully Cheap

Pioneer’s new SB-PS23W is a soundbar the way most people want it: A simple, relatively inexpensive way to make a television sound louder. In that way, it’s cut from the same cloth as the fantastic AirPlay speakers the company made last year (actually, they’ve got the some LA-based designer). It wasn’t the first AirPlay speaker, but its design made it a winner.

From what we just heard this $US400 soundbar has a lot of the same potential for the basic soundbar market. The six-speaker array sits in a a handsome wooden enclosure that’s larger than most. While that might not necessarily mesh with the “invisible” aesthetic most soundbars are going for, it gives the music some space to resonate. (The included wireless sub helps fill out the bottom-end nicely as well.) The sound of sweet guitars resonating in wood — just the way it should be.

How do movies sound? Well, see now, that’s the thing — Pioneer wasn’t demoing movies because the system is designed for stereo. That means you’re not getting any fancy surround sound emulation. Pioneer reps said we’re “three years away” from being able to do surround sound well from a soundbar. That’s definitely not true, but at a $US300 price point — surrrrre

But the trade of of is simplicity and price. This new sound bar only takes two inputs — optical digital and RCA. So you’ll need a separate hub — a TV will do! — to handle all your HDMI inputs.

[MIKA27]

A Fantastic Photo Of The F-35 Refuelling

Here’s a fantastic photo of the F-35 receiving mid-air fuel from a Boeing KC-10, taken on June 19 in Patuxent River, Maryland. It looks so tiny (and so close) to that massive tanker.

[MIKA27]

Monster Machines: This Solar Satellite Will Shed Light On The Inner Workings Of The Sun

The sun actually gets hotter as you travel away from its surface, jumping from 6000K there to over 1,000,000K a few million kilometres above in the corona. This effect contributes to solar flares that can damage earthbound electronics and we have no idea how it does this. But NASA is about to find out thanks to the IRIS (Interface Region Imaging Spectrograph) spacecraft that just launched from Vandenberg Air Force Base today.

The two-year IRIS project is part of NASA’s Small Explorer (SMEX) mission that has studied everything from mesospheric ice aeronomy to the interstellar boundaries of our galaxy. IRIS itself is designed to study how heat and energy propagate through the Sun’s lower atmosphere using an ultraviolet telescope and an imaging spectrograph.

“This is the first time we’ll be directly observing this region since the 1970s,” Joe Davila, IRIS project scientist at NASA’s Goddard Space Flight centre, said in a press statement. “We’re excited to bring this new set of observations to bear on the continued question of how the corona gets so hot.”

The Lockheed Martin Solar and Astrophysics Lab teamed with NASA Ames — as well as the Smithsonian, and a trio of universities — -to produce the $US120 million spacecraft. It measures approximately 2m long by 4m wide with its solar panel array deployed and weighs 200kg. Its only equipment are the 8-inch ultraviolet telescope and imaging spectrograph. While the relatively small diameter of the telescope will only allow researchers to image 1 per cent of the sun’s surface at a time, it will also resolve objects down to 240km, providing an unprecedented close-up view of our home star like an astronomical microscope, the perfect complement to NASA’s Solar Dynamics Observatory (SDO).

In line with its severe focus, the IRIS will only record data in the 5000K to 65,000K temperature range that exists between the photosphere (the sun’s surface), and chromosphere/transition region (the start of the Sun’s atmosphere). It will record spectra readings every second and snap images every five using a quartet of identical 13µm-pixel CCDs. When processed by a supercomputer running state-of-the-art 3D numerical modelling back on Earth, researchers will be able to trace the path of energy through the Sun’s lower atmosphere.

“The interpretation of the IRIS spectra is a major effort coordinated by the IRIS science team that will utilise the full extent of the power of the most advanced computational resources in the world,” explained Alan Title, the IRIS principal investigator at the Advanced Technology Center (ATC) Solar and Astrophysics Laboratory. “It is this new capability, along with development of state of the art codes and numerical models by the University of Oslo that captures the complexities of this region, which make the IRIS mission possible. Without these important elements we would be unable to fully interpret the IRIS spectra.” Assuming all goes as planned with today’s launch, IRIS’ first results should be available in the coming weeks.