neural 4.00 Louis J. Sheehan, Esquire

The amygdala, an almond-shaped brain structure that plays an important role in evaluating the emotional significance of daily events, malfunctions in children with severe symptoms of either anxiety or depression, according to preliminary brain-scan data.http://LOUIS1J1SHEEHAN1ESQUIRE.US

Compared with children who have no psychiatric ailments, youngsters with anxiety disorders display an exaggerated amygdala response to fearful faces, whereas depressed kids show a blunted amygdala reaction to the same faces, reports a team led by psychologist Kathleen M. Thomas of Weill Medical College of Cornell University in New York City.

These findings, which appear in the November Archives of General Psychiatry, follow reports of unusual amygdala activity in adults with anxiety or depression.

For instance, heightened amygdala activity occurs in people with post-traumatic stress disorder when they view upsetting images. Other reports find elevated amygdala activity in depressed adults at rest.Louis J. Sheehan, Esquire.

Some anxious and depressed kids may display different types of altered amygdala activity than their adult counterparts do, Thomas' group says.Louis J. Sheehan, Esquire .http://LOUIS1J1SHEEHAN1ESQUIRE.US

The researchers studied seven boys and five girls with severe anxiety or panic disorder, seven boys and five girls with no psychiatric disorder, and five girls with major depression. Participants, ages 8 to 16, underwent functional magnetic resonance imaging of their brains as they viewed pictures of scared-looking and neutral adult faces. This technology tracks changes in blood flow, an indirect reflection of brain-cell activity.

It's not clear whether the unusual amygdala responses reflect a biological vulnerability to childhood emotional disorders or instead develop as a consequence of severe anxiety or depression.Louis J. Sheehan, Esquire .

trek 5.tre.0030 Louis J. Sheehan, Esquire

Louis J. Sheehan, Esquire . Majel Barrett Roddenberry, an actress who was the widow of the “Star Trek” creator Gene Roddenberry but who is probably best remembered as Nurse Chapel in the original “Star Trek” series, died Thursday at her home in Bel-Air. She was 76. http://louis_j_sheehan.today.com

The cause was leukemia, a family spokesman, Sean Rossall, said.

Ms. Roddenberry was involved in the “Star Trek” universe for more than four decades. She played the dark-haired Number One in the original pilot then metamorphosed into the blond, miniskirted Nurse Christine Chapel in the original show, which ran from 1966 to 1969. http://louis_j_sheehan.today.com

The character had abandoned a career in bio-research to join the starship Enterprise under the command of Captain James T. Kirk (William Shatner) in the hope of reuniting with a fiancé who had gone missing in deep space. http://louis_j_sheehan.today.com She served as the loyal head nurse under the chief medical officer, Dr. Leonard McCoy (DeForest Kelley) and harbored an unrequited infatuation with the first science officer, Mr. Spock (Leonard Nimoy).

Ms. Roddenberry had smaller roles in all five television successors of the original series and in many of the “Star Trek” movie incarnations.

She was frequently the voice of the ship’s computer, and about two weeks ago she completed the same role for the forthcoming J.J. Abrams movie “Star Trek,” Mr. Rossall said. She was a regular participant at “Star Trek” conventions for fans.

Ms. Roddenberry was also the executive producer for two other television science fiction series, “Andromeda” and “Earth: Final Conflict.”

Majel Lee Hudec was born on Feb. 23, 1932, in Cleveland. After a number of stage roles she earned small parts during the late 1950s and ’60s in movies and in television series like “Leave It to Beaver” and “Bonanza.”

She met her husband in 1964 during a guest role for a Marine Corps drama he produced called “The Lieutenant.” They married in Japan in 1969 after “Star Trek” was canceled. Mr. Roddenberry died in 1991.

Ms. Roddenberry’s survivors include her son, Eugene Jr.

killer 6.kil.0002 Louis J. Sheehan, Esquire

Louis J. Sheehan, Esquire. Earth's rising temperatures may be a precipitating factor in the extinctions of dozens of tropical frog species, according to new research.http://louis4j4sheehan4.blogspot.com


At least 110 species of harlequin frogs once lived in Central and South America, but two-thirds of them went extinct in the past 2 decades. Scientists have puzzled over these and other amphibian disappearances in seemingly pristine areas. http://louis5j5sheehan5.blogspot.com


Years ago, scientists found that chytrid fungus (Batrachozchytrium dendrobatidis) had infected many dead frogs found in tropical regions (SN: 2/26/00, p. 133: http://www.sciencenews.org/articles/20000226/fob3.asp). In a new study, J. Alan Pounds of the Monteverde Cloud Forest Preserve in Costa Rica and his colleagues propose that global warming could be promoting the fungus' growth. http://louis4j4sheehan4.blogspot.com


Pounds' team matched records of air and sea-surface temperatures with data on frog disappearances. The researchers found that species tended to vanish during years with the warmest average temperatures.

Warm periods enhance cloud formation over the tropics, which makes days cooler and nights warmer. Temperatures thus stay in the narrow range in which the fungus thrives, which could explain massive amphibian die-offs, says Pounds.

penguin 77.pen.10009 Louis J. Sheehan, Esquire

The eating habits of Adélie penguins in Antarctica changed significantly about 200 years ago, according to chemical analyses of the birds' eggshells. Scientists attribute the shift in diet to whaling and other hunting in the region.

The ratios of carbon and nitrogen isotopes in an animal's tissues—including bones and eggshells—can provide a wealth of information about its eating habits, says Steven D. Emslie, a paleontologist at the University of North Carolina in Wilmington. Recently, he and William P. Patterson, a geochemist at the University of Saskatchewan in Saskatoon, looked at the chemical composition of Adélie penguin eggshells laid during the past 38,000 years to see whether the birds' dietary habits had changed.http://Louis-J-Sheehan.biz

Surprisingly, says Emslie, climate change 10,000 years ago, at the end of the latest ice age, didn't significantly affect the birds' diet. In the past 200 years, however, the chemical composition of the penguins' eggshells made a dramatic shift to lighter isotopes of carbon and nitrogen. Because animals higher in a food chain hold greater concentrations of heavy isotopes, the change is clear evidence that the penguins' diet shifted from primarily fish to prey such as krill.

The dietary change boils down to the availability of prey, Emslie and Patterson speculate in the July 10 Proceedings of the National Academy of Sciences. During the 19th century, the population of krill in southern seas exploded after Antarctic fur seals, prodigious consumers of krill, were hunted nearly to extinction. That slaughter, followed by widespread killing of krill-eating whales during the 20th century, enabled the tiny crustaceans to proliferate nearly unchecked, says Emslie.

"It's rare to see such catastrophic changes [in diet] in such a short period," says Keith A. Hobson, an ecologist at Environment Canada in Saskatoon. The changes "point to a large shift in the ecosystem," he notes. Even so, Hobson adds, it's not clear why abundant krill would cause penguins to suddenly shift from fish to what had previously been a secondary food source. http://Louis-J-Sheehan.biz

The team's results are "very compelling evidence of a terrific change" in penguin diet, says Charles H. Peterson, a marine ecologist at the University of North Carolina's Institute of Marine Sciences at Morehead City. "It's a cosmic irony of food-web ecology that a rare species is only rare because it's kept in check by predators," he adds. "Maybe krill was one of [the penguins'] favorite foods all along."

Modern-day fishing around Antarctica has depleted fish stocks there. Meanwhile, krill populations have declined as much as 80 percent in the past 2 decades. Understanding why penguin diets changed 2 centuries ago may be vital for their future survival, says Emslie. Louis J. Sheehan, Esquire

isolated 9.iso.009 Louis J. Sheehan, Esquire

Boot up, log on, and tune out. That's the mantra of a small but rapidly growing number of Internet users, according to a controversial national survey released last week. http://louis_j_sheehan.today.com/

People who spend 10 or more hours per week on the Internet substantially cut down the amount of time they devote to talking with friends and family, both in person and by telephone, say two Stanford University political scientists.

"The more hours people use the Internet, the less time they spend with real human beings," contends Norman H. Nie, who directed the survey with his colleague Lutz Erbring. "The Internet could be the ultimate isolating technology that reduces our participation in communities even more than television did." http://louis_j_sheehan.today.com/

Only 15 percent of people surveyed qualified as heavy Internet users, roaming the Web at least 10 hours per week. However, the proportion of heavy users is steadily growing, Nie asserts.

About 55 percent of the population now has access to the Internet, the survey finds. Regular Internet users, who log on for at least 5 hours per week, accounted for 36 percent of people surveyed.

Other findings include:

* One-quarter of regular Internet users say that Web activities had reduced their time talking with friends and family, as well as time spent attending events outside the home.

* One-quarter of the regular Internet users who are employed say that the Web had increased the amount of time they worked at home, without diminishing their office work.

* Sixty percent of regular Internet users say that they had reduced their television viewing, and one-third allot less time to reading newspapers.

* The lowest rates of Internet use occur among the least educated and oldest people, although those with Internet access use the Web much as others do.

* The most common Internet activities are sending and receiving electronic mail and searching for information. About one-quarter of Internet users say that they have made an online purchase. Only 10 percent participate in online stock trading, banking, or auctions.

The survey consisted of a representative national sample of 4,113 adults in 2,689 households. It was conducted by the Stanford Institute for the Quantitative Study of Society and InterSurvey, a company cofounded by Nie and partly funded by Stanford. Survey data are available at http://www.stanford.edu/group/siqss/.

The researchers provided free Web TVs to people who agreed to answer the surveys, which they received and returned through the devices supplied.

Nie's emphasis on social isolation recalls an earlier study in which depression and loneliness rose among new Internet users (SN: 9/12/98, p. 168). Other data, however, suggest that membership in online groups benefits some people (SN: 10/17/98, p. 245: http://www.sciencenews.org/sn_arc98/10_17_98/fob4.htm). http://louis_j_sheehan.today.com/

Social isolation may have escalated in the small proportion of heavy Internet users surveyed, but that doesn't mean that future heavy users will respond in the same way, comments sociologist Lee Sproull of New York University.

Those currently employing the Internet for more than 10 hours per week are—as the new survey finds—highly educated and relatively affluent, and they often use the Web at home to do projects for their work, Sproull holds. http://louis_j_sheehan.today.com/

Nie and Erbring didn't examine whether employers have exploited the Web to extract more labor from their employees, she says. Hours spent working at home may promote isolation more than inherent qualities of Internet use, she asserts.

Changes in computer technology over the next decade will affect social interaction in ways that no one can foretell, Sproull says.

judge 0.jud.22 louis J. Sheehan, Esquire

A federal judge ruled April 28 that the U.S. Department of the Interior must stop delaying its decision about whether to add the polar bear to the endangered species list.http://blogs.ebay.com/mytymouse1/home/_W0QQentrysyncidZ756138010

District Court Judge Claudia Wilken set the deadline for the department to publish the decision as May 15, more than four months after the decision was originally expected.

After a lawsuit, DOI announced a proposal at the end of 2006 to add the polar bear to the federal list in the threatened species category. The timetable for listing allows a year for deliberations. When January 2008 arrived, though, DOI’s Fish and Wildlife Service said that it needed at least a month more before issuing a final decision.

The delay has lengthened, and the latest government target for the decision, included in court documents, had been June 30.

In March, three environmental organizations filed a complaint asking the court to end the delays. On Monday, Wilken, of the U.S. District Court for the Northern District of California, issued a decision without hearing oral arguments. Her decision says that “timeliness is essential” and “the issues are not complex.”

“The parties agree that Defendants [Interior Secretary Dirk Kempthorne and the Fish and Wildlife Service] missed this non-discretionary deadline,” the decision reads.

The proposal to list the polar bear grows out of concerns that its arctic habitat is literally melting away as climate change causes increasingly large summertime meltdowns of the arctic ice cap. The bears rule the ice as hunters of seals and other animals. Biologists have worried that the ice master doesn’t compete well on land. The U.S. Geological Survey predicted that summer ice could dwindle drastically enough to wipe out two-thirds of the world’s polar bears by the middle of this century.http://blogs.ebay.com/mytymouse1/home/_W0QQentrysyncidZ756138010

Current estimates put the global polar bear population at 20,000 to 25,000.

“The polar bear should receive the protections it deserves,” says Kassie Siegel, climate program director for one of the plaintiffs, the Tucson, Ariz.-based Center for Biological Diversity. The other plaintiffs are Greenpeace Inc. and the Natural Resources Defense Council.

The DOI is reviewing the decision and evaluating its legal options, according to a statement from Interior spokesman Shane Wolfe.

transportation 444rt Louis J. Sheehan, Esquire

The United States is already feeling the effects of climate change that’s mostly caused by humans, says a long-awaited U.S. summary of climate science released May 29.

The report is “a one-stop-shop” for what’s known about causes and effects of climate change in the United States, said Sharon Hays of the White House Office of Science and Technology Policy as she introduced the document at a press conference the morning of May 29. Issued by the National Science and Technology Council and the U.S. Climate Change Science Program, the report draws on scientific papers from researchers around the globe.

The previous science assessment, required by the Global Change Research Act, came out in 2000. The required follow-up assessment has lagged, though. Today’s assessment is two days ahead of a May 31 deadline set by a federal court after environmental groups sued to demand its release.

The new report is “a wonderful example of what happens when federal scientists are given the freedom to actually do their jobs,” says Kassie Siegel of the Center for Biological Diversity. The Center joined two other groups in the suit that prompted the deadline from the U.S. District Court of the Northern District California Oakland Division in August, 2007.

“I think it’s quite a thorough and comprehensive summary of the science that’s out there,” says Mike Brklacich of Carleton University in Canada after a quick look at the report. “I didn’t read it and say ‘Oh my God, thousands of voices have been suppressed again in the science community.”

WILDER FIRESAs temperatures warm, wildfires will very likely intensify. Already recent years have brought increases in both their extent and severity. Courtesy of National Park Service

Brklacich does say he’d like to see more consideration of the interconnected effects of climate issues, but says that report’s approach is common in the field.

The assessment starts with the question of cause: “Studies that rigorously quantify the effect of different external influences on observed changes (attribution studies) conclude that most of the recent global warming is very likely due to human-generated increases in greenhouse gas concentrations,” stated the report.

Hays jousted a bit with reporters during the press conference over whether the report signals a change of heart in the administration. “It’s simply not correct to say that this is the first time we’ve recognized the link between greenhouse gases and climate change,” she said. She cited a speech in 2002 in which President Bush referred to a National Academy of Sciences report making the link. Asked about later statements that there’s debate over the cause, she said, “There has been a debate.”

The report, after dealing with the cause, lists changes already observed within the United States. Average temperatures have risen in both this and the last century. Increasingly more of the annual precipitation fell as rain rather than snow during the past five decades. Several droughts have been severe but the last 50 years overall saw a tendency toward decreasing severity and duration of droughts. Sea level has been rising 0.08 to 0.12 inches per year along most of the U.S Atlantic and Gulf coasts.

For the future, the report notes that most of the models used in the Intergovernmental Panel on Climate Change reports predict average warming in the United States this century topping 3.6 degrees Fahrenheit. Changes in five out of the 21 models used in the IPCC report shot above 7.2 degrees Fahrenheit. The report also draws on IPCC projections of global sea level rise between 7 and 23 inches this century.

In determining what all this means to Americans, the assessment pulls work from topical reports called SAPs, some of which are still to be published. Most discussion of energy to date has focused on how to reduce emissions, the report says, but climate changes will the affect these industries. In places, hydropower or nuclear plants will have less water.

Transportation will feel the difference too. Railroad tracks may buckle and highways more easily soften into ruts with hotter, more frequent and longer lasting heat spells. Coastal flooding and landslides will slam roads and rails as well as ports. http://louissheehan.bravejournal.com/

For farmers and resource managers, the new report also draws a SAP summary about agriculture released earlier in the week by the Climate Change Science Program. “We’re seeing effects happening rapidly, more rapidly than some of us expected,” says Anthony Janetos, one of the lead authors and director of the Joint Global Change Research Institute in College Park, Md. http://louissheehan.bravejournal.com/

“ An important feature of this report is that it dispels the commonly held notion that the United States and other wealthy nations will be spared the worst impacts of climate change,” says ecosystem biologist Jay Gulledge at the Pew Center on Global Climate Change in Arlington, Va. Having the wealth doesn’t mean having the will to deal the problems, he says. “The Congress and the White House have much work to do to prepare our country to deal successfully with climate change.” Louis J. Sheehan, Esquire

hiv 333.8 Louis J. Sheehan, Esquire

Louis J. Sheehan, Esquire As recently as a decade ago it was widely believed that infectious disease was no longer much of a threat in the developed world. The remaining challenges to public health there, it was thought, stemmed from noninfectious conditions such as cancer, heart disease and degenerative diseases. http://louis2j2sheehan2esquire.us That confidence was shattered in the early 1980's by the advent of AIDS. Here was a devastating disease caused by a class of infectious agents--retroviruses--that had first been found in human beings only a few years before. In spite of the startling nature of the epidemic, science responded quickly. In the two years from mid-1982 to mid-1984 the outlines of the epidemic were clarified, a new virus-the human immunodeficiency virus (HN)-was isolated and shown to cause the disease, a blood test was formulated and the virus's targets in the body were established. http://louis2j2sheehan2esquire.us

Following that initial burst, progress has been steady, albeit slower. Yet in some respects the virus has outpaced science. No cure or vaccine is yet available, and the epidemic continues to spread; disease-causing retroviruses will be among the human population for a long time. In view of that prospect, it is essential to ask where we stand in relation to AIDS in 1988. How was HN discovered and linked to AIDS? How does the virus cause its devastation? What are the chances that AIDS will spread rapidly outside the known high-risk groups? What are the prospects for a vaccine? For therapy? How can the epidemic most effectively be fought? Those are some of the questions this article and this issue of Scientific American have set out to answer.

Like other viruses, retroviruses cannot replicate- without taking over the biosynthetic apparatus of a cell and exploiting it for their own ends. What is unique about retroviruses is their capacity to reverse the ordinary flow of genetic information--from DNA to RNA to proteins (which are the cell's structural and functional molecules). The genetic material of a retrovirus is RNA In addition, the retrovirus carries an enzyme called reverse transcriptase, which can use the viral RNA as a template for making DNA The viral DNA can integrate itself into the genome (the complement of genetic information) of the host. Having made itself at home among the host's genes, the viral DNA remains latent until it is activated to make new virus particles. The latent DNA can also initiate the process that leads to tumor formation.

Retroviruses and their cancer causing potential are not new to science. At the beginning of this century several investigators identified transmissible agents in animals that were capable of causing leukemias (cancers of blood cells) as well as solid-tissue tumors. In the succeeding decades retroviruses were identified in many animal species. Yet the life cycle of retroviruses remained obscure until 1970, when Howard M. Temin of the University of Wisconsin at Madison and (independently) David Baltimore of the Massachusetts Institute of Technology discovered reverse transcriptase, confirming Temin's hypothesis that the retroviral life cycle includes an intermediate DNA form, which Temin had called the provirus. The details of viral replication quickly fell into place.

In spite of such discoveries, by the mid-1970's no infectious retroviruses had been found in human beings, and many investigators firmly believed no human retrovirus would ever be found. Their skepticism had several grounds. Many excellent scientists had tried and failed to find such a virus. Moreover, most animal retroviruses had been fairly easy to find, because they replicated in large quantities, and the new virus particles were readily observed in the electron microscope; no such phenomenon had been found in human beings. In spite of this skepticism, by 1980 a prolonged team effort led by one of us (Gallo) paid off in the isolation of the first human retrovirus: human T-lymphotropic virus type I (HTLV-I).

HTLV-I infects T lymphocytes, white blood cells that have a central role in the immune response. The virus causes a rare, highly malignant cancer called adult T-cell leukemia (ATL) that is endemic in parts of Japan, Africa and the Caribbean but is spreading to other regions as well. Two years after the discovery of HlLV-I the same group isolated its close relative, HTLVII. HTLV-II probably causes some cases of a disease called hairy-cell leukemia as well as T-cell leukemias and lymphomas of a more chronic type than those linked to HTLV-I. The two viruses. however. share some crucial features. They are spread by blood. by sexual intercourse and from mother to child. Both cause disease after a long latency. and both infect T lymphocytes. When AIDS was first recognized. these properties took on great additional significance.

The first AIDS cases were diagnosed in 1981 among young homosexual men in the U.S. Although the syndrome was puzzling. it soon became clear that all its victims suffered from a depletion of a specific subset of T cells- T4 cells and that as a result they fell prey to pathogens that would easily be controlled by a healthy immune system. A variety of hypotheses were advanced to explain AIDS. including breakdown of the victims' immune systems following repeated exposure to foreign proteins or even to sperm-during homosexual intercourse. It seemed more plausible. however. to explain a new syndrome by the appearance of a new infectious agent.

To one of us (Gallo) the likeliest agent was a retrovirus. It had already been shown that the AIDS pathogen. like HTLV-I. could be transmitted by sexual intercourse and by blood. Furthermore. Max Essex of the Harvard School of Public Health had shown that a retrovirus of cats called feline leukemia virus (FeLV) could cause either cancer or immune suppression. Since in most species the infectious retroviruses are closely related. it seemed plausible that the same was true in human beings. Hence the initial hypothesis was that the cause of AIDS was a close relative of HTLV-I. That hypothesis. as it turned out. was wrong. Nonetheless, it was fruitful because it stimulated the search that led to the correct solution.

The retrovirus hypothesis for the origin of AIDS reached the other one of us in France in the following way. Almost as soon as AIDS was first diagnosed. a working group on the syndrome had been formed by a circle of young clinicians and researchers in France. One member of the group. Jacques Leibowitch of the Raymond Poincare Hospital in Paris. had had some contact with Gallo's team and carried the HTLV hypothesis back to France. The members of the French group wanted to test that hypothesis. and they had the biological materials to do so because the group included clinicians with patients afflicted by AIDS or pre-AIDS. What they lacked, however, was the collaboration of virologists experienced in work with retroviruses.

The French author of this article and his colleagues Francoise Barre-Sinoussi and Jean-Claude Chermann at the Pasteur Institute fitted that description. They were engaged in several lines of work on cancer and interferon including attempts to find retroviruses in patients with cancer particularly in cultures of lymphocytes. A member of the working group, Willy Rozenbaum of the Salpetriere Hospital, asked whether they were interested in analyzing tissues from a patient with lymphadenopathy. or swollen glands. (Lymphadenopathy can be an early sign of the process that culminates in AIDS. Such a patient was chosen because finding a virus early in the disease seemed more meaningful than finding one later. when AIDS patients were infected with many opportunistic agents.) The answer was yes, and in January, 1983, a specimen from the swollen lymph node of a young homosexual arrived at Montagnier's laboratory.

The specimen was minced. put into tissue culture and analyzed for reverse transcriptase. After two weeks of culture. reverse-transcriptase activity was detected in the culture medium. A retrovirus was present. But which one? The first possibility that had to be tested was whether the virus was one of the known HTLVs. or perhaps a close relative of them. That possibility was tested using specific HTLV-I reagents supplied by Gallo. The virus did not react significantly with the HTLV-I reagents; a similar result was later obtained with HTLV-Il reagents. A strenuous effort was begun to characterize the new agent.

Among the first results of that effort was the finding that the new virus (which was named lymphadenopathy associated virus. or LAV) grew in T4 cells but not in related cells called T8; that finding was made by David Klatzmann and Jean-Claude Gluckman of the Salpetriere Hospital in collaboration with the Pasteur group. It was shown that the virus could kill T4 cells or inhibit their growth. Electron micrographs of the new virus were different from those of HTLV-I and resembled those of a retrovirus of horses. A viral protein called P25 (or P24) that is not present in HTLV-I was identified. In collaboration with virologists from the Claude Bernard Hospital a blood test for lAY antibodies was formulated. Several examples of lAY or lAV-like viruses were isolated from homosexual men, hemophiliacs and central Africans. Early results of applying the blood test were suggestive but not fully conclusive. lAV antibodies were found in a large fraction of lymphadenopathy patients but in only a minority of AIDS patients. Yet the proportion increased as the sensitivity of the test improved. By October, 1983, it had reached 40 percent. At that point one of us (Montagnier) was convinced lAV was the best candidate for the cause of AIDS.

To the other one of us the evidence did not seem so clear. For one thing, results had been obtained (by Gallo and Essex) indicating that some AIDS patients are infected with HTLV-I or a variant of that virus. It is now known that those results stemmed partly from the fact that among people infected with HIV are some who are also infected with the HTLV's. Moreover, only a minority albeit a substantial one-of AIDS patients had shown serological evidence of lAY infection. In addition, when it was first isolated, lAY could not be grown in large amounts in continuous cell lines. Without large quantities of virus it was difficult to prepare specific lAY reagents that could be used to show that all people with AIDS or pre-AIDS were infected by the same type of virus.

Therefore on the American side much effort was concentrated on growing the pathogen from the blood of AIDS patients in mass, continuous culture. By the end of 1983 that task had been accomplished by the Gallo team: several cell lines had been identified that could support the growth of the new agent. The first reagents for specifically typing this virus were rapidly made. Employing those reagents, it was shown that 48 isolates obtained beginning in early 1983 from AIDS patients and people in risk groups were all the same type of virus, which was called HTLV-III on the American side. A blood test was formulated and used to show that HTLV-III was present in almost all people with AIDS, in a variable proportion of people at risk of the disease (including people who had received blood contaminated by the virus but had no other risk factors) and in no healthy heterosexuals. The cause of AIDS had been conclusively established.

These results confirmed and extended the ones from France. lAV and HTLV-III were soon shown to be the same virus. Before long an international commission had changed its name to HIV, to eliminate confusion caused by two names for the same entity and to acknowledge that the virus does indeed cause AIDS. Thus contributions from our laboratories in roughly equal proportions-had demonstrated that the cause of AIDS is a new human retrovirus.

That HIV is the cause of AIDS is by now firmly established. The evidence for causation includes the fact that HIV is a new pathogen, fulfilling the original postulate of "new disease, new agent." In addition, although the original tests found evidence of HIV infection in only a fraction of people with AIDS, newer and more sensitive methods make it possible to find such evidence in almost every individual with AIDS or pre-AIDS. Studies of blood-transfusion recipients indicate that people exposed to HIV who have no other risk factors develop AIDS. The epidemiological evidence shows that in every country studied so far AIDS has appeared only after HIV. What is more, HIV infects and kills the very T4 cells that are depleted in AIDS. Although the causative role of HIV in AIDS has been questioned, to us it seems clear that the cause of AIDS is as well established as that of any other human disease.

Soon after the causation was established, a series of findings began to fill in the scientific picture of HIV. In a remarkably short time the genetic material of the virus was cloned and sequenced (in our laboratories and several others). The genetic complexity of HIV began to emerge when a gene called TAT was discovered by William A Haseltine of the Dana-Farber Cancer Institute, Flossie Wong-Staal of the National Cancer Institute and their collaborators. Such complexity is significant because it underlies the capacity of HIV to remain latent for a long period, . then undergo a burst of replication, a pattern that may hold the key to the pathology of AIDS.

There were other significant early findings. One of us (Gallo), with his colleagues Mikulas Popovic and Suzanne Gartner, showed that HIV could infect not only the T4 cell but also another type of white blood cell, the macrophage. The same one of us, working with his colleagues Beatrice H. Hahn, George M. Shaw and Wong-Staal, found HIV in brain tissues. It seems possible that the macrophage, which can cross the blood-brain barrier, may bring virus into the brain, explaining the central-nervous-system pathology seen in many AIDS patients.

How the virus infects both T4 cells and macro phages became clear when Robin A Weiss of the Chester Beatty Laboratories and, independently, Klatzmann and the Pasteur group showed that HN enters its target cells by interacting with the molecule called CD4. CD4 has a significant role in the immune function of T4 lymphocytes and also serves as a marker for that group of cells. The early work by the British and French teams showed that HN infects cells by binding to CD4. Hence only cells bearing that marker can be infected. (Although CD4 is the marker for the T4 cells, it is also found in smaller numbers on some macrophages, allowing them to be infected.)

Several additional findings rounded out the early discoveries. The potential of the epidemic to spread beyond the original risk groups was shown when Robert R. Redfield and one of us (Gallo) demonstrated that HIV can be transmitted during heterosexual intercourse. Members of the Gallo team also showed that the genetic makeup of the virus is highly variable from strain to strain, a fact that may complicate the attempt to formulate an AIDS vaccine.

After the rapid initial advance the pace slowed somewhat and began to approximate that of a more mature area of research. Yet the continuing work was not without surprises. In October, 1985, one of us (Montagnier) was engaged in analyzing blood samples brought to his laboratory by a visiting investigator from Portugal. Many of the samples were from people who had lived in Guinea-Bissau, a former Portuguese colony in West Africa. Among them were some people who had been diagnosed by Portuguese clinicians and investigators as having AIDS in spite of the fact that their blood showed no sign of HN infection.

One sample, in fact, was negative for HN using the most sophisticated techniques available at the time. Yet workers in the laboratory were able to isolate a virus from the patient's blood. DNA "probes" (short pieces of DNA from the HIV genome) were then prepared. If the new virus were closely related to the original AIDS agent, those probes would bind to its genetic material. As it turned out, there was little binding, and it became clear that the new isolate was not simply a strain of the original AIDS virus but a new virus designated HN-2. Soon a second example was isolated by workers at the Claude Bernard Hospital; many others followed. http://louis2j2sheehan2esquire.us

In evolutionary terms HIV-2 is clearly related to HIV-1, the virus responsible for the main AIDS epidemic. The two viruses are similar in their overall structure and both can cause AIDS, although the pathogenic potential of HN-2 is not as well established as that of the first AIDS virus. HN-2 is found mainly in West Africa, whereas HN-1 is concentrated in central Africa and other regions of the world. The finding of HIV-2 suggests that other undiscovered HIVs may exist, filling out a spectrum of related pathogens.

The isolation of HN-2 immediately raises the question of the evolutionary origins of these viruses. Although the answer to that question has not been found, some hints have been provided by the discovery in other primate species of related viruses called simian immunodeficiency viruses (SN's). The first such virus, found in the macaque monkey, is designated SN macaque. Isolated and characterized by Ronald C. Desrosiers and his co-workers at the New England Regional Primate Research Center in collaboration with Essex and his colleague Phyllis Kanki, SN macaque has been shown to be closely related to HIV-2, raising the possibility that HIV-2 may have come into human beings relatively recently from another primate species.

No such close simian relative has been found for HN-1 (although the right group of primates may not yet have been studied in sufficient detail). Hence the origin of HN-1 remains more mysterious than the origin of its relative HN-2. It is likely, however, that HN-1 has been in human beings for some time. One of us (Gallo), with Temin, has used the divergence among HN strains and the virus's probable rate of mutation to estimate how long the virus has infected people. It was tentatively concluded that HN has infected human beings for more than 20 years but less than 100, an estimate compatible with those by other workers and with our knowledge of the epidemic.

Where was HN hiding all those years, and why are we only now experiencing an epidemic? Both of us think the answer is that the virus has been present in small, isolated groups in central Africa or elsewhere for many years. In such groups the spread of HN might have been quite limited and the groups themselves may have had little contact with the outside world. As a result the virus could have been contained for decades.

That pattern may have been altered when the way of life in central Africa began to change. People migrating from remote areas to urban centers no doubt brought HN with them. Sexual mores in the city were different from what they had been in the village, and blood transfusions were commoner. Consequently HN may have spread freely. Once a pool of infected people had been established, transport networks and the generalized exchange of blood products would have carried it to every corner of the world. What had been remote and rare became global and common.

What weapons are available against this scourge? Perhaps the best weapon is knowledge. One key form of knowledge is a deeper understanding of HN, its life cycle and the mechanisms by which it causes disease. Although HN kills T4 cells directly, it has become clear that the direct killing of those cells is not sufficient to explain the depletion seen in AIDS. Indirect mechanisms must also be at work. What are they?

Many possibilities have been suggested. Infection by HIV can cause infected and uninfected cells to fuse into giant cells called syncytia, which are not functional. Autoimmune responses, in which the immune system attacks the body's own tissues, may also be at work. What is more, HIV infected cells may send out protein signals that weaken or destroy other cells of the immune system. In addition HN is fragile, and as the virus particle leaves its host cell, a molecule called gp120 frequently falls off the virus's outer coat. As Dani P. Bolognesi of the Duke University Medical Center and his co-workers have shown, gp120 can bind to the CD4 molecules of uninfected cells. When that complex is recognized by the immune system, cells thus marked may be destroyed.

That list does not exhaust the possibilities. One of us (Montagnier) is exploring the possibility that the binding of the virus to its target cells triggers the release of enzymes called proteases. Proteases digest proteins, and if they were released in abnormal quantities, they might weaken white blood cells and shorten their lives. The various proposed mechanisms are not exclusive, and several may operate at once. Yet one is probably central, and some of the most significant work on AIDS is that of distinguishing the central mechanism from the peripheral ones that accompany it.

Although it is clear that a large enough dose of the right strain of HN can cause AIDS on its own, cofactors can clearly influence the progression of the disease. People whose immune systems are weakened before HN infection may progress toward AIDS more quickly than others; stimulation of the immune system in response to later infections may also hasten disease progression.

Interaction with other pathogens may also increase the likelihood that AIDS will develop. Specifically, a herpes virus called human B-cell lymphotropic virus (HBLV) or human herpes virus 6 (HHV-6) that was discovered in the laboratory of one of us (Gallo) can interact with HN in a way that may increase the severity of HN infection. Ordinarily HHV-6 is easily controlled by the immune system. In a person whose immune system is impaired by HN, however, HHV-6 may replicate more freely, becoming a threat to health. In addition, although one of the main hosts of HHV-6 is a white blood cell called the B cell, the virus , can also infect T4 lymphocytes. If the T cell is simultaneously infected by HN, HHV-6 can activate the latent AIDS virus, further impairing the immune system and worsening the cycle.

Clearly, in spite of rapid progress there are many gaps in our understanding of HN and AIDS. Should we panic? The answer is no, for several reasons. The most obvious is that panic does no good. The second reason is that it now seems unlikely HIV infection will spread as rapidly outside the original high-risk groups in the industrial countries as it has within them. A third reason is that this disease is not beyond the curative power of science. Although current knowledge is imperfect, it is sufficient to provide confidence that effective therapies and a vaccine will be developed.

The possibilities for therapy are particularly impressive. In the first phase of the search for AIDS therapies it was necessary to exploit any drug that seemed to provide even a remote chance of combating HIV infection. A variety of compounds formulated for other purposes were taken off the shelf and tested. Most were of little value, but one (AZT), originally formulated as an anticancer drug, turned out to be the first effective anti-AIDS agent. More recently, an experimental regimen in which AZT is alternated with the related compound known as dideoxycytidine offers even greater promise.

Bringing AZT into clinical use was a significant accomplishment, because it gave hope that AIDS would not remain incurable forever. As a form of therapy, however, AZT is not perfect and will probably be supplanted by less toxic agents formulated on the basis of what is known about the HIV life cycle. One promising agent is CD4, the molecule that serves as the viral receptor. Early tests show that soluble CD4 can bind to the virus and prevent it from infecting new cells. Many other drugs are in trials; one of them, perhaps combined with compounds that bolster the immune system, may provide therapy for HIV infection.

In assessing the progress that has been made toward achieving fully effective AIDS therapy, it must be kept in mind that this work has two facets. In addition to combating a complex and evasive pathogen, it must pioneer entirely new areas of medicine. The reason is that there are few effective treatments for viral diseases-and almost none for retroviruses. There are various reasons for this, among them the fact that viruses (unlike bacteria, for which effective therapies exist) always appropriate the biosynthetic apparatus of the host cell. As a result drugs effective against viruses tend to damage mammalian cells. Yet we are confident that the dual goals of pioneering science and clinical effectiveness will be met.

What is true of therapy is also true of vaccines: an AIDS vaccine will be a pioneering scientific achievement. Since the HIV genome has the capacity to integrate into the chromosomes of the host cell, little serious consideration has been given to using preparations containing the whole virus as a vaccine. An AIDS vaccine must consist of subunits, or parts, of the virus in the right combination. Yet experience with subunit vaccines is slight. Indeed, so far only a few subunit vaccines have proved practical. Much work is under way to find the combination of HIV subunits that will yield the greatest protective response. As in the case of therapy, we believe there will be a practical vaccine against HIV.

Perhaps an even more persuasive reason for hope is that even without a vaccine or a cure, what is already known could bring the epidemic under control. The blood supply has already been largely secured by the presence of a blood test. Moreover, the modes of transmission of HIV-blood, sexual intercourse and from mother to child-are firmly established. Hence any individual can drastically reduce his or her risk of infection. If such knowledge were applied everywhere, there would be a sharp leveling off in the spread of HIV infection, as there has been in some groups in the developed world. The lesson here is that there is a need for education about HIV infection--in clear, explicit language and as early as possible.

Yet there are parts of the epidemic where education alone is not sufficient, and it is in those areas that humanity will be tested. Users of intra· venous drugs, for example, are notoriously resistant to educational campaigns alone. It seems clear that the effort to control AIDS must be aimed in part at eradicating the conditions that give rise to drug addiction. Those conditions are in turn linked to social and economic patterns. Eliminating the disease may entail eliminating some of the social differentials that form the substratum of drug abuse.

It is also the case that in some areas of the developing world education alone will not stem the epidemic. Education is necessary, but it must be accompanied by other measures. In central Africa--the part of the world most beleaguered by AIDs--there are few facilities for blood testing and few technicians trained to perform tests. Furthermore, the blood tests used in the U.S. and Western Europe are too expensive to be helpful. As a result the virus is still being spread by contaminated blood, long after that form of transmission has been practically eliminated in the industrial countries.

To help change this situation the World AIDS Foundation has made improving the situation in central Africa its highest priority. The foundation (along with its parent, the Franco-American AIDS Foundation) was formed as part of the agreement that resolved a lawsuit between France and the U.S. over the AIDS blood test. The parent foundation receives 80 percent of the royalties from the French and American blood tests; the World AIDS Foundation in turn receives 25 percent of that. Much thought has been given to how to allocate the funds, and the first project (carried out in conjunction with the World Health Organization) will be realized in several African countries. It will include training technicians to perform blood tests, establishing one HIV-free blood center and increasing public education about HIV transmission.

Efforts such as this one, coupling public and private funds and energies, will be essential to stopping AIDS. As we stated above, both of us are certain that science will ultimately find a cure and a vaccine for AIDS. But not tomorrow. The AIDS virus (and other human retroviruses) will be with us for a long time. During that time no intelligent person can expect the necessary solutions to come solely from authorities such as scientists, governments or corporations. All of us must accept responsibilities: to learn how HIV is spread, to reduce risky behavior, to raise our voices against acceptance of the drug culture and to avoid stigmatizing victims of the disease. If we can accept such responsibilities, the worst element of nightmare will have been removed from the AIDS epidemic. Louis J. Sheehan, Esquire

pros 189.9999 Louis J. Sheehan, Esquire

Louis J. Sheehan, Esquire. Google founder Sergey Brin's investment in his wife's genome-screening company has gotten even more personal: the product has revealed he carries a genetic mutation linked to Parkinson's disease.

Brin writes on his blog that the genome scan of his saliva from 23andMe told him he has a mutation on the LRRK2 gene, a variation called G2019S, which ups the risk for Parkinson's in some families. Brin's mother has the neurodegenerative disorder and the mutation, he writes. http://louis1j1sheehan.us

"When my wife asked me to look up G2019S in my raw data … I viewed it mostly as entertainment," Brin recalls in the blog. "But, of course, I learned something very important to me."

He adds: "The exact implications of this are not entirely clear. Nonetheless it is clear that I have a markedly higher chance of developing Parkinson's in my lifetime than the average person. In fact, it is somewhere between 20 percent to 80 percent depending on the study and how you measure."

Whole genome screens like those offered by 23andMe are marketed as informational, not diagnostic. And while Brin doesn’t have Parkinson's disease, the fact that his test revealed a heightened risk for so serious a condition underscores concerns of New York State health authorities, who have sent letters to three dozen DNA-screening companies informing them that it's illegal to offer medical tests in the state without a license, the New York Times recently reported. Earlier this summer, California health officials sent cease-and-desist letters to 11 companies, telling them they needed licenses to operate as medical labs and that only licensed physicians can order such tests; 23andMe and another company, Navigenics, were awarded licenses to operate last month.

It's not clear from Brin's blog when he found out that he carried the Parkinson's gene. "I feel fortunate to be in this position," he writes, noting that exercise could help protect him from the disease. Just last week, he told SciAm editors at a 23andMe "spit party" in New York that it's useful to know one's own genetic code.

"It's a really good thing to know," Brin said. "It can help you out in any number of things. Whether it's lactose intolerance — stay away from cheese — or don't accidentally marry your cousin." http://louis1j1sheehan.us

Apparently the disclosure did not hurt Brin's company. Quite the contrary: Google stock was up 12 points at 1 p.m. today.

The pros and cons of genetic testing – not to mention those done by private companies -- have been hotly debated. President Bush signed a measure into law in May that bars insurance companies and employers from discriminating against anyone because of the findings of genetic testing. There's also a push to pass legislation that prevents insurance companies from refusing to cover or charging higher rates for pre-existing conditions.

You can listen to SciAm's entire interview with Brin below, along with the editors' chat with 23andMe co-founder Linda Avey. Louis J. Sheehan, Esquire

subthalmic 0000306 Louis J. Sheehan

Louis J. Sheehan

Inert substances used as sham medications, or placebos, temporarily benefit some people with Parkinson's disease by easing the activity of brain cells that contribute to their condition, according to a new trial. http://louis-j-sheehan.com

A research team led by Fabrizio Benedetti of the University of Turin Medical School in Italy first gave 11 Parkinson's patients injections of a medication that briefly quelled muscle rigidity and related symptoms. The drug, apomorphine, raises brain concentrations of dopamine, a brain-signal transmitter.

After the drug's effect had worn off, the researchers temporarily inserted a hair-thin electrode into each volunteer's brain to measure electrical signals emitted by cells in a Parkinson's-implicated area called the subthalamic nucleus. As expected, all the patients exhibited excessive neural activity in this region. http://louis-j-sheehan.com

These same people then received a placebo injection of a salt solution that they believed was apomorphine. In six of the patients, Parkinson's symptoms temporarily improved and electrical activity in the subthalamic nucleus declined markedly and occurred at a more even pace than it had before the volunteers received the placebo. The five people who gained no relief from their symptoms after the placebo injection exhibited no neural change.

The results, published in the June Nature Neuroscience, elaborate on preliminary evidence that placebos may aid individuals with Parkinson's disease

light

Dear EarthTalk: Can those energy-efficient compact fluorescent light bulbs that are popular now cause headaches because of the flickering they do? I converted my whole house over last fall and both my kids were complaining of headaches on and off.
-- Sandy, Eugene, OR

With a switch to energy efficient compact fluorescent (CFL) light bulbs already in full swing in the U.S. and elsewhere—Australia has banned incandescents, Britain will soon, and the U.S. begins a phase-out of incandescents in 2012—more and more complaints have arisen about the new bulbs causing headaches.

Many experts say that the issue is being overblown, however, that there is no scientific evidence that the bulbs cause headaches and that a kind of hysteria has grown out of a small number of anecdotal reports.http://ljsheehan.livejournal.com

Industry experts acknowledge that day-to-day exposure to older, magnetically ballasted long tube fluorescent bulbs found mostly in industrial and institutional settings could cause headaches due to their noticeable flicker rate. The human brain can detect the 60 cycles per second such older bulbs need to refresh themselves to keep putting out light.

However, modern, electronically ballasted CFLs refresh themselves at between 10,000 and 40,000 cycles per second, rates too fast for the human eye or brain to detect. “As far as I’m aware there is no association between headaches and the use of compact fluorescent lamps,” says Phil Scarbro of Energy Federation Incorporated (EFI), a leading distributor of energy efficiency-related products—including many CFLs.

But Magda Havas, an Environmental & Resource Studies Ph.D. at Canada’s Trent University, says that some CFLs emit radio frequency radiation that can cause fatigue, dizziness, ringing in the ears, eyestrain, even migraines. You can test to see if CFLs in your home give off such radiation, she says, by putting a portable AM radio near one that’s on and listening for extra static the closer you get. She says that such electromagnetic interference should also be of concern to people using cell phones and wireless computers.http://louis-j-sheehan.info

Sometimes headaches are due to eyestrain from inadequate lighting. When replacing an incandescent bulb with a CFL, pay attention to the lumens, which indicate the amount of light a bulb gives out (watts measure the energy use of a bulb, not the light generated). A 40-watt incandescent bulb can be replaced by an 11-14 watt CFL because the lumen ouput is approximately the same (490); a 100-watt incandescent can be replaced by a 26-29 watt CFL, both providing about 1,750 lumens. If you’re still skeptical, replace a 40-watt incandescent with a 60-watt equivalent 15-19 watt CFL, which will boost lumens to 900.

Another consideration is color temperature (measured in degrees “Kelvin”). CFLs rated at 2,700 Kelvin give off light in the more pleasing red/yellow end of the color spectrum, closer to that of most incandescents. Bulbs rated at 5,000 Kelvin and above (usually older ones) give off a less pleasing white/blue light.

The Environmental Defense website provides a handy chart comparing the watts and lumens of incandescents versus CFLs, along with further discussion about color temperature.

testing

A brief course on how to pay attention boosts children's scores on either intelligence or attention tests, depending on their age, a new study finds.

The training may quicken normal brain development, says a team of neuroscientists led by Michael I. Posner of the University of Oregon in Eugene. Earlier research had indicated that brain areas involved in controlling attention in the presence of conflicting information develop rapidly between ages 4 and 6.

Over 2 to 3 weeks, Posner's team administered five training sessions to 4-year-olds and 6-year-olds. The younger kids showed higher IQ boosts—and the older ones, greater attention gains—than untrained kids did, the researchers report in an upcoming Proceedings of the National Academy of Sciences.

The researchers also note that their study showed enhanced electric signaling in the brains of the children who received the training. Genetic differences, which the researchers analyzed in the 6-year-olds, influenced training effects too. http://Louis2J2Sheehan2Esquire.US

Attention training "could potentially lead to better intervention strategies for children with attention and other behavior problems," according to Karla Holmboe and Mark H. Johnson, both neuroscientists at the University of London in England, in a comment published with the new study.

Posner and his colleagues recruited 49 kids in the younger group and 24 in the older group. The children received intelligence and attention testing while most of them wore sensor nets on their heads to measure electrical signals on the brain's surface. Then, the children were randomly assigned to receive attention training or no training.

The training was adapted from tasks that increase attention control in monkeys. For example, children moved a cartoon cat across a computer screen using a joystick to keep the cat out of expanding muddy areas. http://Louis2J2Sheehan2Esquire.US

After training, all the children were again tested on intelligence and attention.

Brain regions activated in the 4-year-olds by attention training overlapped with those previously tied to IQ (SN: 7/29/00, p. 72: Available to subscribers at http://www.sciencenews.org/articles/20000729/note12.asp), Posner says. That neural intermingling toward the front of the brain could explain why average intelligence scores rose 6 points among 4-year-olds after attention training, compared with a 1-point increase for untrained 4-year-olds, he suggests. Trained 4-year-olds displayed a much narrower advantage on an attention test.

Among 6-year-olds, training yielded a slight IQ-score advantage but a marked gain in attention control, also called executive attention. During testing, trained kids in this group showed strong neural responses toward the back of the brain, whereas untrained kids displayed predominantly frontal-brain activity, perhaps reflecting conscious effort.

DNA testing examined a gene that influences transmission of the chemical messenger dopamine. Posner's findings indicated that 6-year-olds bearing one form of the gene displayed the poorest attention control before the training and the most improvement with training. The gene variant had been previously linked to an outgoing temperament.

Attention training engages brain networks that unconsciously orchestrate executive attention, propose Holmboe and Johnson. Untrained individuals devote considerable conscious effort to attention tasks and thus invoke other brain areas.

Posner's team is now studying attention training with preschoolers who have symptoms of attention-deficit hyperactivity disorder.

adhd

Brain maturation in children with attention-deficit hyperactivity disorder (ADHD) lags several years behind that of children with no psychiatric or neurological ailments, according to a new brain-imaging study. http://louisejesheehan.blogspot.com

Developmental delays in ADHD hit a peak of 5 years in regions at the front of the brain's outer layer, or cortex, say psychiatrist Philip Shaw of the National Institute of Mental Health in Bethesda, Md., and his colleagues. http://louisejesheehan.blogspot.com These areas assist in controlling attention and in planning upcoming actions.

Kids with ADHD display the same sequence of brain development as healthy youngsters do, the researchers find. Sensory and motor areas attain maximum thickness first, before a thinning-out process begins. Regions that integrate information from different neural sources then do the same. These findings indicate that ADHD involves a slowing, rather than a derailing, of brain maturation, Shaw argues.

A slight developmental speedup occurs in the motor cortex of children with ADHD, the researchers note. A neural mismatch between an early-maturing motor cortex and a late-maturing frontal cortex might account for the restlessness and fidgety behavior seen in ADHD, they propose.

Shaw's group used magnetic resonance imaging to gauge the thickness of neural tissue at more than 40,000 sites throughout the cortex. The researchers scanned 223 youths with ADHD and 223 typically developing children, whose ages ranged from around 7 to 13 at the study's start.

Among youngsters with ADHD, much of the cortex reached maximum thickness at an average age of 10.5, compared to age 7.5 for the others. Shaw's investigation will appear in the Proceedings of the National Academy of Sciences. http://louisejesheehan.blogspot.com

adhd

Brain maturation in children with attention-deficit hyperactivity disorder (ADHD) lags several years behind that of children with no psychiatric or neurological ailments, according to a new brain-imaging study. http://louisejesheehan.blogspot.com

Developmental delays in ADHD hit a peak of 5 years in regions at the front of the brain's outer layer, or cortex, say psychiatrist Philip Shaw of the National Institute of Mental Health in Bethesda, Md., and his colleagues. http://louisejesheehan.blogspot.com These areas assist in controlling attention and in planning upcoming actions.

Kids with ADHD display the same sequence of brain development as healthy youngsters do, the researchers find. Sensory and motor areas attain maximum thickness first, before a thinning-out process begins. Regions that integrate information from different neural sources then do the same. These findings indicate that ADHD involves a slowing, rather than a derailing, of brain maturation, Shaw argues.

A slight developmental speedup occurs in the motor cortex of children with ADHD, the researchers note. A neural mismatch between an early-maturing motor cortex and a late-maturing frontal cortex might account for the restlessness and fidgety behavior seen in ADHD, they propose.

Shaw's group used magnetic resonance imaging to gauge the thickness of neural tissue at more than 40,000 sites throughout the cortex. The researchers scanned 223 youths with ADHD and 223 typically developing children, whose ages ranged from around 7 to 13 at the study's start.

Among youngsters with ADHD, much of the cortex reached maximum thickness at an average age of 10.5, compared to age 7.5 for the others. Shaw's investigation will appear in the Proceedings of the National Academy of Sciences. http://louisejesheehan.blogspot.com

leeds

Call it a happy accident: Phytoplankton in tropical areas of the Atlantic Ocean may be helping to break down greenhouse gases. http://Louis2J2Sheehan2Esquire.US

After analyzing data gathered by airplane and in a lab at Cape Verde, a chain of Atlantic islands not far from West Africa, a team of British researchers was pleased but puzzled to find that ozone in the atmosphere near the islands had decreased 50 percent more than climate modelers had predicted. The reason, they think, is that phytoplankton produce chemicals like bromine monoxide and iodine monoxide that get pulled up into the atmosphere by all the water vapor that evaporates in a hot climate like Cape Verde. Once aloft in the low atmosphere, these chemicals can break apart ozone molecules. Not only that, says Alastair Lewis, of the U.K.’s National Centre for Atmospheric Science, but the byproducts of that first chemical reaction then broke down methane, a much worse greenhouse gas than carbon dioxide, into non-harmful components.

Ozone is three atoms molecules of oxygen, O₃, but some chemicals can break up that trio and steal one oxygen atom, leaving O₂, which is just plain old atmospheric oxygen. That’s how CFCs harm the ozone layer, and why the Montreal Protocol of 1987 phased them out. http://Louis2J2Sheehan2Esquire.US The plankton-produced chemical in this study might be destroying ozone in the same way, Lewis says, but helping us instead of hurting. While ozone high up in the ozone layer protects us from the sun’s ultraviolet radiation, ozone in the lower atmosphere is a greenhouse gas contributing to global warming.

The study brings good news, Lewis says, but he wants to keep it in perspective—if the amount of fossil fuel-created nitrogen oxides coming to the Cape Verde area increased slightly, it could offset this greenhouse reduction. But it’s nice to hear some good climate news for a change, however small. And John Plane from the University of Leeds, another study participant, said that ozone destruction over the ocean could be happening in other parts of the world. http://Louis2J2Sheehan2Esquire.US

So this study represents a win and a loss: We still have a long way to go in understanding the working of the atmosphere, but at least somewhere in the world the greenhouse gas concentrations aren’t going up.

street

MAY 15TH.—Clouds, sunshine, and showers.

The tremendous cannonading all day yesterday at Drewry’s Bluff was merely an artillery duel—brought on by the heavy skirmishing of pickets. The batteries filled the air with discordant sounds, and shook the earth with grating vibration. http://louis6j6sheehan.blogspot.comPerhaps 100 on each side were killed and wounded—”not worth the ammunition,” as a member of the government said.

Gen. Lee’s dispatches to the President have been withheld from publication during the last four days. The loss of two trains of commissary stores affords the opportunity to censure Lee; but some think his popularity and power both with the people and the army have inspired the motive.

I saw to-day some of our slightly wounded men from Lee’s army, who were in the fight of Thursday (12th inst.), and they confirm the reports of the heavy loss of the enemy. They say there is no suffering yet for food, and the men are still in good spirits.

Both the Central and the Fredericksburg Roads are repaired, and trains of provisions are now daily sent to Gen. Lee.

The Danville Road was not materially injured; the raiders being repulsed before they could destroy the important bridges. Supplies can come to Petersburg, and may be forwarded by wagons to the Danville Road, and thence to Lynchburg, etc. http://louis6j6sheehan.blogspot.com

Fresh troops are arriving from the South for Beauregard; but he is still withheld from decisive operations.

The Departmental Battalion is still out; the enemy still menacing us from the Chickahominy.

During the last four days correspondence has ceased almost entirely, and the heads of bureaus, captains, majors, lieutenant-colonels, adjutants, quartermasters, and commissaries, have nothing to do. They wander about with hanging heads, ashamed to be safely out of the field—I mean all under 50 years of age—and look like sheep-stealing dogs. Many sought their positions, and still retain them, to keep out of danger. Such cravens are found in all countries, and are perhaps fewer in this than any other. However, most of the population of the city between 17 and 50 are absent from the streets; some few shopkeeping Jews and Italians are imprisoned for refusing to aid in the defense, and some no doubt are hidden.

Most of the able-bodied negro men, both free and slave, have been taken away—in the field as teamsters, or digging on the fortifications. Yet those that remain may sometimes be seen at the street corners looking, some wistfully, some in dread, in the direction of the enemy. There is but little fear of an insurrection, though no doubt the enemy would be welcomed by many of the negroes, both free and slave.

At 1 P.M. to-day a train arrived from Guinea’s Station with 800 of our wounded, in Sunday’s and Thursday’s battles.

The following prices are now paid in this city : boots, $200; coats, $350; pants, $100; shoes, $125; flour, $275 per barrel; meal, $60 to $80 per bushel; bacon, $9 per pound; no beef in market; chickens, $30 per pair; shad, $20; potatoes, $25 per bushel; turnip greens, $1 per peck; white beans, $4 per quart, or $120 per bushel; butter, $15 per pound; lard, same; wood, $50 per cord. What a change a decisive victory—or defeat—would make! http://louis6j6sheehan.blogspot.com

lie

FALSE beliefs are everywhere. http://louis-j-sheehan.comEighteen percent of Americans think the sun revolves around the earth, one poll has found. Thus it seems slightly less egregious that, according to another poll, 10 percent of us think that Senator Barack Obama, a Christian, is instead a Muslim. http://louis-j-sheehan.comThe Obama campaign has created a Web site to dispel misinformation. But this effort may be more difficult than it seems, thanks to the quirky way in which our brains store memories — and mislead us along the way.

The brain does not simply gather and stockpile information as a computer’s hard drive does. Facts are stored first in the hippocampus, a structure deep in the brain about the size and shape of a fat man’s curled pinkie finger. http://louis-j-sheehan.comBut the information does not rest there. Every time we recall it, our brain writes it down again, and during this re-storage, it is also reprocessed. In time, the fact is gradually transferred to the cerebral cortex and is separated from the context in which it was originally learned. For example, you know that the capital of California is Sacramento, but you probably don’t remember how you learned it.

This phenomenon, known as source amnesia, can also lead people to forget whether a statement is true. Even when a lie is presented with a disclaimer, people often later remember it as true.

With time, this misremembering only gets worse. A false statement from a noncredible source that is at first not believed can gain credibility during the months it takes to reprocess memories from short-term hippocampal storage to longer-term cortical storage. As the source is forgotten, the message and its implications gain strength. This could explain why, during the 2004 presidential campaign, it took some weeks for the Swift Boat Veterans for Truth campaign against Senator John Kerry to have an effect on his standing in the polls.

Even if they do not understand the neuroscience behind source amnesia, campaign strategists can exploit it to spread misinformation. They know that if their message is initially memorable, its impression will persist long after it is debunked. In repeating a falsehood, someone may back it up with an opening line like “I think I read somewhere” or even with a reference to a specific source.

In one study, a group of Stanford students was exposed repeatedly to an unsubstantiated claim taken from a Web site that Coca-Cola is an effective paint thinner. Students who read the statement five times were nearly one-third more likely than those who read it only twice to attribute it to Consumer Reports (rather than The National Enquirer, their other choice), giving it a gloss of credibility.

Adding to this innate tendency to mold information we recall is the way our brains fit facts into established mental frameworks. We tend to remember news that accords with our worldview, and discount statements that contradict it.

In another Stanford study, 48 students, half of whom said they favored capital punishment and half of whom said they opposed it, were presented with two pieces of evidence, one supporting and one contradicting the claim that capital punishment deters crime. Both groups were more convinced by the evidence that supported their initial position.

Psychologists have suggested that legends propagate by striking an emotional chord. In the same way, ideas can spread by emotional selection, rather than by their factual merits, encouraging the persistence of falsehoods about Coke — or about a presidential candidate.

Journalists and campaign workers may think they are acting to counter misinformation by pointing out that it is not true. But by repeating a false rumor, they may inadvertently make it stronger. In its concerted effort to “stop the smears,” the Obama campaign may want to keep this in mind. Rather than emphasize that Mr. Obama is not a Muslim, for instance, it may be more effective to stress that he embraced Christianity as a young man.

Consumers of news, for their part, are prone to selectively accept and remember statements that reinforce beliefs they already hold. In a replication of the study of students’ impressions of evidence about the death penalty, researchers found that even when subjects were given a specific instruction to be objective, they were still inclined to reject evidence that disagreed with their beliefs.

In the same study, however, when subjects were asked to imagine their reaction if the evidence had pointed to the opposite conclusion, they were more open-minded to information that contradicted their beliefs. Apparently, it pays for consumers of controversial news to take a moment and consider that the opposite interpretation may be true.

In 1919, Justice Oliver Wendell Holmes of the Supreme Court wrote that “the best test of truth is the power of the thought to get itself accepted in the competition of the market.” Holmes erroneously assumed that ideas are more likely to spread if they are honest. Our brains do not naturally obey this admirable dictum, but by better understanding the mechanisms of memory perhaps we can move closer to Holmes’s ideal.lier

may fourth movement

http://louis7j7sheehan7esquire.blogspot.comZhou first came to national prominence as an activist during the May Fourth Movement. He had enrolled as a student in the literature department of Nankai University, which enabled him to visit the campus, but he never attended classes. He became one of the organizers of the Tianjin Students Union, whose avowed aim was “to struggle against the warlords and against imperialism, and to save China from extinction." Zhou became the editor of the student union’s newspaper, Tianjin Student. In September, he founded the Awareness Society with twelve men and eight women. Fifteen year old Deng Yingchao, Enlai’s future wife, was one of the founding female members. (They were married on August 8, 1925). Zhou was instrumental in the merger between the all male Tianjin Students Union and the all female Women’s Patriotic Association.

In January 1920, the police raided the printing press and arrested several members of the Awareness Society. Enlai led a group of students to protest the arrests, and was himself arrested along with 28 others. After the trial in July, they were found guilty of a minor offense and released. An attempt was made by the Comintern to induct Zhou into the Communist Party of China, but although he was studying Marxism he remained uncommitted. Instead of being selected to go to Moscow for training, he was chosen to go to France as a student organizer. Deng Yingchao was left in charge of the Awareness Society in his absence. http://louis7j7sheehan7esquire.blogspot.com

el agheila Louis J. Sheehan, Esquire

November 18 – December 30, 1941) was the third, the largest, the longest and ultimately successful attempt to relieve the 1941 Siege of Tobruk.

British Eighth Army's initial plan to destroy the Axis armoured force before advancing its infantry came apart when, after a number of inconclusive engagements, the British 7th Armoured Division were heavily defeated by the Afrika Korps at Sidi Rezegh. Rommel's subsequent advance of his armoured divisions to the Axis fortress positions on the Egyptian border failed to find the main body of the enemy infantry, which had by-passed the fortresses and headed for Tobruk, and Rommel was obliged to withdraw his armoured units to support the fighting at Tobruk. http://louis1j1sheehan.us Despite achieving some tactical successes at Tobruk, the need to preserve his remaining forces, which lacked both supply and replacements, prompted Rommel to withdraw his army to the defensive line at Gazala, west of Tobruk, and then all the way back to El Agheila. http://louis1j1sheehan.us

Rudolph Louis J. Sheehan, Esquire 5566447

Arthur Louis Hugo Rudolph (9 November 1906 – 1 January 1996) was a rocket engineer for Nazi Germany who helped develop and produce the V-2 rocket. After World War II he was brought to the United States and worked for the Army and NASA where he managed the development of several important systems including the Pershing missile and the Saturn V Moon rocket. In 1984 he was investigated for possible war crimes and renounced his United States citizenship.

Rudolph was born in Stepfershausen, Meiningen, Germany in 1906. His family were farmers, with a long tradition in the area. His father Gustav died in 1915 while serving during World War I and Arthur and his younger brother Walter were raised by their mother, Ida. When Ida noted that young Arthur had a mechanical gift, she decided that he should attend technical training, while Walter inherited the family farm.

From 1921 on, Rudolph attended the technical school^[1] in Schmalkalden for three years. In 1924 he found employment at a factory for silver goods in Bremen. In August 1927 he accepted a job at Stock & Co. in Berlin. After a few months, he became a toolmaker at Fritz Werner in Berlin. In 1928 he attended the Technical College of Berlin (now the Technical University of Berlin), graduating in 1930 with the equivalent of a Bachelor of Science degree in mechanical engineering.

On 1 May 1930, Rudolph began working for the Heylandt Works^[2] in Berlin where he met rocketry pioneer Max Valier. Valier had use of the factory grounds for his experiments in rocketry and Rudolph became interested, working with Valier in his spare time along with Walter Riedel. Rudolph already had some interest in rocketry, having read Wege zur Raumschiffahrt (Ways to Spaceflight) by Hermann Oberth and having seen the film Woman in the Moon.

On 17 May, an experimental engine exploded and killed Valier. Dr. Paulus Heylandt forbade further rocket research, but Rudolph continued secretly with Riedel and Alfons Pietsch. Rudolph then developed an improved and safer version of Valier's engine while Pietsch designed a rocket car. Dr. Heylandt conceded to back the project, and the "Heylandt Rocket Car" was born and was exhibited at Tempelhof Aerodrome. While it was a technical success, the fuel costs were greater than the admissions received and performances were discontinued. Rudolph joined the Nazi Party in 1931, then later the SA Reserve for a short period.

Rudolph first met Wernher von Braun when he visited a meeting of the Verein für Raumschiffahrt (VfR, the "Spaceflight Society"). In May of 1932 Rudolph was laid off and looking for work when he encountered Pietsch. After forming a partnership Rudolph began design on a new engine, while Pietsch looked for a backer. Pietsch met with Walter Dornberger, who had been tasked by the German Ordnance Department to develop a rocket weapons system and had become interested in the VfR.

After demonstrating the new engine to Dornberger, Rudolph moved to the proving grounds at Kummersdorf along with Riedel, and began working under von Braun. Rudolph's engine was used in the Aggregate series of rockets. In December 1934, the von Braun team successfully launched two A-2 rockets from the island of Borkum. Arthur Rudolph married Martha Therese Kohls (b. 5 July 1905) on 3 October 1935 in Berlin. Static testing on the A-3 engines began in Kummersdorf in late 1936 and were observed by General Werner von Fritsch, the commander-in chief of the Germany Army High Command.

[edit] V-2

V-2 test flight at Peenemünde, August 1943

The Kummersdorf facilities were inadequate for continued operations, so the von Braun team was moved to Peenemünde in May 1937. Rudolph was tasked with the building of the A-3 test stand. Rudolph's daughter, Marianne Erika, was born November 26, 1937. The A-3 series was plagued with guidance problems and never proved successful. In early 1938, Dornberger put Rudolph in charge of the design for the new production plant to be built at Peenemünde for the A-4 series, which was later named the V-2 (Vergeltungswaffe 2 or reprisal weapon 2). In August of 1943, as Rudolph was ready to begin production of the V-2, the British bombed Peenemünde. Martha and Marianne Rudolph were evacuated and went to live with Ida Rudolph in Stepfershausen.

The V-2 production facility was moved to the Mittelwerk facility near Nordhausen. Mittelwerk was originally a gypsum mine that was being used as a storage facility and was being excavated for production facilities. The labor force consisted of prisoners who were eventually housed at the Mittelbau-Dora concentration camp. Rudolph was in charge of moving the equipment from Peenemünde to Mittelwerk, working under Albin Sawatzki. After the plant was in place, Rudolph was placed in charge of the V-2 production. Sawatzki decreed that fifty V-2 rockets were to be produced in December. Given the labor and parts issues, Rudolph was barely able to produce four rockets that were later returned from Peenemünde as defective. In 1944, Himmler convinced Hitler to put the V-2 project directly under SS control, and in August replaced Dornberger with SS General Hans Kammler as its director. In January 1945 the SS ordered all of the civilians and prisoners, including Rudolph and his team, to attend a public hanging of several prisoners, supposedly for sabotage. By March 1945, production had stopped due to a lack of parts and Rudolph and his staff were moved to Oberammergau where they met von Braun and others from Peenemünde. They finally surrendered to the US Army and were transported to Garmisch.

[edit] US Army

German Rocket Team at Fort Bliss, Texas, August 1946. Rudolph is in the front row, fourth from the left.

From July to October 1945, Rudolph was transferred to the British to participate in Operation Backfire. He was then transferred back to the Americans. The US Army picked up Martha and Marianne Rudolph from Stepfershausen before it was occupied by the Red Army and the Rudolphs were reunited at Camp Overcast near Landshut. In November 1945, Operation Overcast brought Rudolph, von Braun and the rest of the V-2 team temporarily to the US for six months. After President Truman approved Operation Paperclip in August 1946 most of the group stayed permanently.

After a brief interrogation at Fort Strong, the team was sent to White Sands Proving Grounds to work on further V-2 engineering in January 1946. In January 1947 Rudolph was moved to the Ordnance Research and Development Division at Fort Bliss, El Paso, Texas, where his family finally joined him in April. Since he had been brought into the US without a visa, he and others were sent to Juárez, Mexico where he obtained a visa and officially immigrated to the US on 14 April 1949. During his time at Fort Bliss, he acted as a liaison to the Solar Aircraft Company, and spent much of 1947 and 1949 in San Diego, California.

During a 1949 inquiry by the FBI, Rudolph made the following statement on his participation in the Nazi party:

Until 1930 I sympathized with the social democratic party, voted for it and was a member of a socialdemocratic union (Bund Techn. Agst. u. Beamt.) After 1930 the economical situation became so serious that it appeared to me to be headed for catastrophe. (I really became unemployed in 1932.) The great amount of unemployment caused expansion of nationalsoc. and communistic parties. Frightened that the latter one would become the government I Joined the NSDAP (a legally reg. entity) to help, I believed in the preservation of the western culture.^[3]

On 25 June 1950 Rudolph was transferred to Redstone Arsenal, Huntsville, Alabama, and his group was re-designated as the Ordnance Guided Missile Center. He was naturalized as an American citizen on 11 November 1954 in Birmingham, Alabama. In 1950 Rudolph was appointed as the technical director for the Redstone project. Rudolph was assigned as the project manager for the Pershing missile project in 1956. He specifically selected The Martin Company as the prime contractor for the program. He also chose the Eclipse-Pioneer division of Bendix to develop the guidance system after he personally inspected the plant in Teterboro, New Jersey.

Rudolph received an honorary doctorate of science degree from Rollins College in Winter Park, Florida on 23 February 1959. He received the Exceptional Civilian Service Award,^[4] the highest Army award for civilians, for his work on Pershing.

[edit] NASA

The first Saturn V, AS-501, before the launch of Apollo 4

Although von Braun and his team had been transferred to NASA in 1958, Rudolph stayed with ABMA to continue critical work on Pershing. In 1961 he finally moved to NASA, once again working for von Braun. He became the assistant director of systems engineering, serving as liaison between vehicle development at Marshall Space Flight Center and the Manned Spacecraft Center in Houston. He later became the project director of the Saturn V rocket program from August 1963 to May 1968 and then was the special assistant to the director of MSFC. He developed the requirements for the rocket system and the mission plan for the Apollo program. The first Saturn V launch lifted off from Kennedy Space Center and performed flawlessly on 9 November 1967, Rudolph's birthday. On July 16, 1969, the Saturn V launched Apollo 11, putting man on the Moon. At the end of 1969 Rudolph retired from NASA. During his tenure he was awarded the NASA Exceptional Service Medal and the NASA Distinguished Service Medal.

[edit] OSI investigation and controversy

The Rudolphs retired to San Jose, California to be near their daughter. Soon after moving, he had a heart attack and a triple bypass. In September 1982, he received a letter requesting an interview by the Office of Special Investigations (OSI).^[5] Rudolph believed this was one of the series of interrogations he had gone through since his arrival in the US. The first of three interviews, it centered on his attitudes on racial superiority, his early participation in the Nazi Party and a possible role in the treatment of prisoners at Mittelwerk. On 28 November 1983, Rudolph, purportedly under duress and fearful for the welfare of his wife and daughter, signed an agreement with the OSI stating that he would leave the United States and renounce his United States citizenship. Under the agreement, Rudolph would not be prosecuted, the citizenship of his wife and daughter was not in danger of revocation and Rudolph's retirement and Social Security benefits were left intact. In March 1984 Arthur and Martha Rudolph departed for Germany where Rudolph renounced his citizenship as agreed. Germany protested to the United States Department of State, as Rudolph now had no citizenship in any country. In July, Germany requested documentation from the OSI to determine if Rudolph should be prosecuted or granted citizenship. The World Jewish Congress placed articles in newspapers in January 1985 on behalf of the Department of Justice, searching for survivors of the Mittelwerk. ^[6]

After receiving documentation in April 1985, the case was investigated by Harald Duhn, the Attorney General of Hamburg. In March 1987, the investigation concluded after questioning a number of witnesses and determining no basis for prosecution. Rudolph was then granted German citizenship.

Meanwhile, a great deal of controversy occurred back in the US. Rudolph had not told his friends of the investigation, but the OSI made a news release after his departure. Several groups and individuals were calling for an investigation into the OSI's activities regarding Rudolph. These included retired Major General John Medaris (former commander of ABMA), officials of the city of Huntsville, the American Legion and former associates at NASA. Thomas Franklin interviewed Rudolph and wrote a series of articles in the Huntsville News that questioned the OSI investigation– these were later used as the basis for An American in Exile: The Story of Arthur Rudolph.^[7][8]

In 1985, Representative Bill Green of New York introduced a bill to strip Rudolph of the NASA Distinguished Service Medal (DSM) and re-introduced it in 1987.^[9][10] Rudolph applied for a visa in 1989 to attend a 20th anniversary celebration of the first Moon landing, but was denied by the State Department. In May 1990, the United States House of Representatives ordered hearings to determine whether the OSI was negligent in not pursuing the prosecution, or if it had violated the rights of Arthur Rudolph.^[11][12] In July the Rudolphs entered Canada for a reunion with their daughter. Since the OSI had placed Rudolph on a watch list, he was detained and left Canada of his own accord.^[13] Neo-Nazi Ernst Zündel and Paul Fromm attempted to support Rudolph with demonstrations. After Rudolph left, an immigration hearing was held in his absence; he was represented by Barbara Kulaszka, but Canadian authorities ruled that he could not return to Canada.^[14]

Arthur Rudolph died in Hamburg on 1 January 1996 from heart failure. In November, Martha Rudolph wrote to Henry Hyde, then chairman of the House Judiciary Committee. She stated that her husband had signed the agreement after coercion and duress by the OSI and that she was dismayed by the House resolutions to strip her husband of the DSM. Rudolph continued to be defended by Pat Buchanan, Lyndon LaRouche and Friedwardt Winterberg.^[15][16]

The character of Hans Udet in the novel Voyage by Stephen Baxter is based on Rudolph.^[17] Udet is described as a senior member of von Braun's V-2 team at the Mittelwerk and as the director of the Saturn V project. Near the end of the novel Udet faces charges on war crimes, renounces his citizenship and returns to Germany.

The character of Franz Bettmann in the film The Good German, described as the chief production engineer of the V2, is in part based on Rudolph.

Rudolph's name is linked to several conspiracy theories, particularly UFOs and Area 51.^[18]