Frontlines

New evidence points to brain trauma as an environmental risk factor for Alzheimer disease (AD). Researchers at the University of Pennsylvania School of Medicine have shown that multiple, mild head injuries accelerate ß-amyloid plaque deposition, believed to be an etiologic factor in AD (K. Urya et al., "Repetitive mild brain trauma accelerates Aß deposition, lipid peroxidation and cognitive impairment in a transgenic mouse model of Alzheimer amyloidosis," Journal of Neuroscience, 22:446-54, Jan. 15, 2002.) Researchers anesthetized wild-type mice and transgenics (Tg2576) predisposed to develop AD-like amyloid plaques and then tapped the animals' heads once or twice. Compared to mice tapped once and wild types, transgenic animals tapped twice scored worse in water maze tests. Amyloidosis was greatly accelerated in all tapped transgenics, and isoprostanes, produced by lipid peroxidation, increased in all struck mice. John Q. Trojanowski, codirector for the University of Pennsylvania's Center for Neurodegenerative Disease Research, says, "The next steps would be to let the animals live longer after a [traumatic brain injury] to see if the process continues to be accelerated." Various therapies, he says, could be tested—antioxidants, ibuprofen, and nonsteroidal anti-inflammatories—to see if accelerated amyloidosis would decelerate. "This opens the doors to lots of neat ways to help people."

UK academics get paid peanuts in comparison with their contemporaries in North America, Europe, and Australia, according to a recent study by NATFHE—The University & College Lecturers' Union. UK academics earned £21,800 in salary and compensation, almost £30,000 less than US academicians earned and £50,000 less than that of their Canadian counterparts, according to analysis of the 1998 data. The survey includes earnings of all academic staff, including part-time workers, and calculates the value of benefits paid by governments for comparison with those paid by US universities that lack a national health system. Tom Wilson, NATFHE's head of universities, says the United Kingdom's earnings figures reflect the large number of part-time, postgraduate, and junior researchers who generally receive lower salaries than do full-time academics. While British universities traditionally pay similar wages across disciplines, these numbers are most acutely felt in the sciences where comparative salaries in industry are commonly among the highest. "It's hard to get people to consider a career in academia when they are faced with a low starting salary and pretty low lifestyle of earning," Wilson says. NATFHE estimates the UK government needs to spend £675 million to reform university pay, tackle gender discrimination, and increase staffing to meet expansion targets.

Contradicting expectation and previous work, the absence of integrins has been shown to foster tumorogenesis. (L.E. Reynolds et al., "Enhanced pathological angiogenesis in mice lacking b₃ integrin or b₃ and b₅ integrins," Nature Medicine, 8:27-34, January 2002). Blocking the action of integrins, molecules that coordinate blood vessel growth, has been regarded as a key route in developing anti-angiogenic therapies to treat cancer. In fact, Vitaxin, a monoclonal antibody to the integrin a_vb₃, is in clinical trials. Postdoctoral fellow Louise E. Reynolds, cell adhesion and disease laboratory, Imperial Cancer Research Fund, St. Thomas' Hospital, London, and her colleagues found that mice deficient in b₃ or b₃ and ß₅ integrins not only supported "tumor growth and angiogenesis," but both were enhanced in animals lacking b₃, and both b₃ and b₅ integrins. David Cheresh, professor of immunology and vascular biology at the Scripps Research Institute, says the results are not surprising. By creating integrin-deficient mice, he says, "you've eliminated an apoptotic signal ... [and] a pathway that would normally reduce the available number of endothelial cells in the tissue." Because blood vessels are made of endothelial cells, Cheresh argues, the absence of integrins could lead to the growth and spread of tumors.

The French-American Technology Development Initiative has chosen the Port of Technology, a Philadelphia-based life science business incubator, to ease the entry of French companies into the United States. "By definition, the sheer size of the US market makes it a key target for an awful lot of life sciences companies," says Carlos Kearns, vice president for public and international affairs at the University City Science Center, a research center maintained by multiple academic institutions, which established the Port. The Franco-American initiative selected the Port of Technology after surveying resources available from incubators across the country. Kearns expects that Philadelphia's active French Chamber of Commerce and French Institute for Culture and Technology at the University of Pennsylvania will help keep companies in the area. "The companies will bring a lot of intellectual capital with them, but they will be looking at trained graduates from Penn as well," he says. Four French companies plan to commission market studies this spring and relocate to Philadelphia if the market proves as promising as expected.

Using high definition thermal imaging to capture a facial reflection could obviate the polygraph and maybe aid in homeland security. When people lie, they often become startled or anxious and produce physiological effects, such as excessive blood flow in the area around the eyes. The Mayo Clinic of Rochester and Honeywell Laboratories of Minneapolis have developed a thermofacial screening that is statistically similar to a polygraph's efficacy and can be given with significantly less hassle (I. Pavlidis, et al., "Seeing through the face of deception," Nature, 415:35, Jan. 3, 2002.) The new technology rapidly analyzes facial blood flow and quantifies the results. The new thermal imaging system correctly detected lying in more than 80% of the subjects. Unlike a polygraph, this technology can be used remotely and doesn't require much manpower. Once refined, the technique could become a mainstay of airport security. "Questioners at the ticket counter won't have to rely on human instinct.... They will have a machine to help," says Ioannis Pavlidis, senior principal research scientist at Honeywell. "This [technology] works on the spot and gives the potential first-time offender less of a chance."

Harvard Medical School researchers have apparently reversed type 1 diabetes disease in the pancreas by triggering existing adult stem cells into action. (S. Ryu et al., "Reversal of established autoimmune diabetes by restoration of endogenous ß cell function," Journal of Clinical Investigation, 108[1]:63-72, July 2001; see also "The Stem Cell-Cloning Plot Thickens,"). Donor islet cells transplanted into nonobese diabetic mice along with CFA (which induces tumor necrosis factor-a and kills cells in the pancreas that attack insulin-producing islet cells) reversed autoimmunity and restored endogenous pancreatic islet function within 40 days. The procedure returned 75% of the mice to normal glycemia, a ratio that has held fast for two years. Discovering that the long-term normoglycemia correction occurred because the islets reappeared in the pancreas was a surprise. "Our findings suggest that the stem cells are already there, but the disease is not letting them function," says lead investigator Denise Faustman. "The procedure doesn't use stem cells from fetuses because the body makes them itself." The findings suggest that other autoimmune diseases could be cured if mutant cells, which attack organ function, were eliminated, and if existing adult stem cells could regrow replacement organs. The findings changed the team's plans; they had wanted to follow the initial procedure with additional transplants of healthy islet cells. Now, they want to define how the procedure eliminates disease. Says Faustman, "It was a real surprise to us that this approach was so good at getting rid of the underlying disease, and the fact [that] the organ regrew islet cells was stunning."