“Poverty and its related social phenomena are the major challenges humankind faces here at the beginning of the 21st century,” Nelson Mandela said when he spoke at Johns Hopkins ten years ago, as part of the annual Milton S. Eisenhower Symposium. His subject? Capitalism, and its effect on poverty worldwide.
“The gap between the rich and the poor is widening rather than closing. We are producing enough to feed, clothe, shelter, educate and provide health care for all the people of the world. Yet, the poor are becoming poorer and more socially deprived,” Mandela said. “Those are the issues facing capitalism, not only in the United States, but throughout the world.”
Mandela went on to decry the U.S. invasion of Iraq, and to remind listeners that America and Americans are in the position to act as leaders to ensure that the spread of free-market capitalism wouldn’t only enrich the rich, but “produce results that lead to a tangibly better life for all.”
Mandela, of course, practiced what he preached better than most. Johns Hopkins Dean Katherine S. Newman has been studying the generation of South Africans who were children when apartheid ended, and who are now in their late 20s and early 30s. “For the young people I have come to know during four years of fieldwork and analysis, he has been the very essence of dignity and integrity,” Newman says. “They measure every political figure who has followed him against Mandela’s very high standard and often find them lacking. They are looking with concern now toward those who must pick up the mantle of leadership and guide what is a country of enormous promise through a period of extreme inequality and catastrophic unemployment, especially in their generation.”
Marfan syndrome is a rare genetic disorder that’s thought to have affected Abraham Lincoln, Sergei Rachmaninoff, and the Egyptian pharaoh Akhenaten. It affects everything from the heart to the lungs to the skeleton, and results in abnormally long limbs and fingers. Although the disease was first described in 1896, it wasn’t until nearly a hundred years later that the gene that caused it was identified — by Johns Hopkins geneticist Hal Dietz.
“[When] researchers first found the mutation, in 1990, it seemed to lead to a dead end. The mutation was in fibrillin-1, a protein in connective tissue, suggesting that the tissue was falling apart because its molecular rivets did not work,” a recent New York Times article about Dietz noted. “And if that was true, Dr. Dietz said, ‘there was nothing you could do to alter the course of the disease.'”
But after a decade of further study, Dietz was able to conclude that the original model was wrong; he also pioneered the use of a blood pressure drug to treat the disease.
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