The process, created in the laboratory of Rick A. Wetsel, Ph.D., a professor of molecular medicine at the IMM, is described in this week’s edition of the Proceedings of the National Academy of Sciences (PNAS). Research scientist Dachun Wang, M.D., is lead author of the article, “A pure population of lung alveolar epithelial type II cells derived from human embryonic stem cells.”

“We have developed a reliable molecular procedure which facilitates, via genetic selection, the differentiation of human embryonic stem cells into an essentially pure population of lung epithelial cells,” said Wetsel, noting the procedure also can be used to create other types of highly-specialized cells.

Scientists at the IMM used the in vitro method to create lung epithelial cells known as alveolar epithelial type II. The cells were derived from a human embryonic stem cell line approved by the National Institutes of Health (NIH).

The method involves the use of protein markers under the control of cell-specific promoters to convert undifferentiated human embryonic stem cells into highly-specialized cells. The human embryonic stem cells were cultured on specially coated dishes and transfected with a lung epithelial gene regulator of a drug selection gene.

“It is a general technology for developing select cells from human embryonic stem cells,” said C. Thomas Caskey, M.D., the IMM’s chief operating officer, director and CEO-elect. “The technology has allowed us to develop a platform that could potentially be useful in the development of spinal cord cells, heart cells, nerve cells and others.”

James T. Willerson, M.D., president of the UT Health Science Center at Houston, said " I believe this is an important development by the Wetsel laboratory at the IMM. I look forward to seeing its transitional impact."

Alveolar epithelial type II cells are called “the stem cells of the lungs” because of their versatility and many important functions. They produce proteins including surfactant that inflates lungs. They also make other cells lining the inner lung. “They regulate lung fluids and oxygen levels,” Wetsel said.

The cells are part of the tiny air sacs lining the lower airways known as alveoli. Tissue thin, they transfer oxygen into the blood and remove carbon dioxide. If the walls of the hundreds of millions of alveolus in a pair of lungs could be spread out and placed side by side, they would cover the floor of a classroom.

According to Wetsel, transplantable alveolar epithelial type II cells can be explored as treatments for pulmonary genetic diseases, acquired lung disease, as well as lung trauma caused by car accidents, gunshot wounds and sports injuries. “These are the cells that can potentially be used for regenerative lung repair,” he said.

Hereditary lung disorders most likely to benefit from transplantation of alveolar epithelial type II cells include respiratory distress syndrome of the newborn, alpha-1 related emphysema and cystic fibrosis, Wetsel believes. “All three of these diseases are caused by single gene defects and therefore have been logical candidates for gene therapy,” Wetsel said.

Respiratory distress syndrome of the newborn, a condition affecting premature infants less than 37 weeks of age, may be caused by a genetic mutation triggering a surfactant shortage. Likewise, alpha-1 related emphysema, a condition affecting 100,000 Americans, results from an inherited deficiency of alpha-1 antitrypsin. Further, cystic fibrosis is the second most common childhood onset inherited disorder in the United States.

Transplantable alveolar epithelial type II cells may also one day be helpful in the treatment of other lung diseases including chronic obstructive pulmonary disease (COPD), the fourth leading cause of death in the United States, claiming the lives of 122,283 Americans in 2003, and asthma, Wetsel said.

Still years away from their use in regenerative medicine, Wetsel said the next step involves research trials with mice.

Other IMM investigators participating in the study included David L. Haviland, Ph.D., assistant professor in the Center for Immunology and Autoimmune Diseases, and Eva Zsigmond, Ph.D., assistant professor and associate director of the IMM’s Laboratory for Developmental Biology.

Funding for the study of the NIH-approved human embryonic stem cell line was provided by Houston philanthropists Clive and Nancy Runnells.

Dr. Shuming Nie, PhD, professor in the Coulter Department of Biomedical Engineering at Emory University and the Georgia Institute of Technology and director of cancer nanotechnology at Emory’s Winship Cancer Institute, highlights recent research in at the 225th National Meeting of the American Chemical Society on March 27.

“We believe biomedical nanotechnology will soon produce major advances in molecular diagnostics, therapeutics, molecular biology and bioengineering,” Dr. Nie says. “Already, scientists have begun to develop functional nanoparticles that are linked to biological molecules such as peptides, proteins and DNA.”

Nanoparticles assume special properties by virtue of their miniature size that distinguish them from larger particles, including changes in color as they grow smaller and smaller. Because of their compact structure, nanoparticles emit light and can act as a fluorescent tag. This makes them highly suitable as contrast agents for magnetic resonance imaging (MRI), in positron emission tomography (PET) for molecular imaging in patients, or as fluorescent tracers in optical microscopy. Nanoparticles also have advantages over conventional dyes: they fade less quickly, they are less toxic to cells and they can be used in combination to create almost an infinite number of colors.

Although nanoparticles are similar in size to biomolecules such as proteins and DNA, human-made nanoparticles can be engineered to have specific or multiple functions. Bioconjugated quantum dots, consisting of different sized dots embedded in tiny beads made of polymer material, can be finely tuned to a myriad of different colors that can tag a multitude of different proteins or genetic sequences in a process called “multiplexing.”

By chemically binding the quantum dots to particular genes and proteins, scientists including Dr. Nie are developing molecular nanoprobes to rapidly analyze biopsy tissue from cancer patients, to monitor the effectiveness of drug therapy, as scaffolding in tissue engineering, and as “smart bombs” to deliver controlled amounts of drugs into genetically classified tumor cells.

Now a team led by McMaster University hematologist Dr. Catherine Hayward has discovered the genetic cause of Quebec Platelet Disorder (QPD). They have gone on to develop a genetic test for the condition — a major advance in diagnosing this serious and unusual bleeding problem. Their research appears in the journal Blood.

The condition is called a platelet disorder because it transforms platelets (blood cells that control bleeding) from clot formers into clot busters.

It is called QPD because careful detective work has traced all individuals with this condition back to one Quebec family. In parts of Canada, about one out of 150,000 persons have QPD and the new genetic test is expected to uncover many more.

Hayward, a professor of both the departments of medicine and pathology and molecular medicine in the Michael G. DeGroote School of Medicine, calls the discovery of the genetic cause of QPD a "milestone" in her career.

Because the genetic cause of most bleeding disorders continues to be a mystery, "it’s satisfying to know that our team tackled the genetic cause of a really fascinating genetic disorder and have an answer," she said. "And, it’s not the answer anybody expected, which makes it even more interesting."

QPD is an autosomal dominant bleeding disorder, which means a person only needs to receive the abnormal gene from one parent to inherit the disease. The research team discovered that QPD is caused by a mutation involving an extra copy of the gene PLAU, the urokinase plasminogen activator (uPA) gene that causes overproduction of an enzyme that accelerates blood clot breakdown and this turns platelets into clot busters.

This is "novel," Hayward said, "as QPD is the very first bleeding disorder attributed to having an extra copy of a gene, rather than a defective copy. QPD is also the first bleeding problem attributed to a mutation in the uPA gene."

"The types of mutation that causes some bleeding problems are mistakes that are likely to happen again, and typically, they cause a protein to become defective or deficient," said Hayward. "Now that we know the mutation, we can focus on solving why there is tremendous uPA overproduction in QPD platelets, which will give us fundamental, new insights on how the uPA gene is controlled."

The work is already having a positive impact on the lives of many people. A recent newborn of the family most impacted by the condition was able to have a test immediately to discover whether he had the condition.

"The family needed to know whether this child would need life-long monitoring, and treatments to counteract their clot busting platelets, as having a definite yes or no answer early is key to proper treatment," said Hayward.

Hayward’s group at McMaster worked with a Canadian team of investigators including Andrew Paterson at the Hospital for Sick Children in Toronto, and Georges Rivard at the University of Montreal.

Hayward and Rivard believe that the known cases they have studied over the last decade are "the tip of the iceberg" and that the true prevalence of QPD has been underestimated because, until the genetic test became available, there was no way to routinely test bleeders for this condition.

"Diagnosis is important as drugs for other platelet problems and transfusions just don’t work for the QPD clot busting problem," said Hayward.

The research was supported funds from the Canadian Institutes of Health Research (CIHR), the Heart and Stroke Foundation of Ontario and Bayer Canada. Federal funding was also provided by Hayward’s Canada Research Chair in Molecular Hemostasis and Paterson’s Canada Research Chair on the Genetics of Complex Diseases.

The European Infliximab for Psoriasis Efficacy and Safety Study
(EXPRESS) was a placebo-controlled trial on 378 patients with moderate
to severe psoriasis, to test the efficacy and safety of the drug. The
findings, published in the 15 October issue of The Lancet, show that
80% of patients achieved at least a 75% improvement in symptoms after
ten weeks treatment with the drug, as opposed to just 3% of those
receiving a placebo.

Psoriasis is a chronic condition which results when skin cells
over-produce and accumulate on the surface of the skin, producing red,
scaly ‘plaques’ which may itch and bleed. It is thought to be genetic
in origin and is a consequence of an abnormal inflammatory response in
the skin. Around 2% of the population suffer from the disease, with
about 30% of cases considered moderate to severe, but until now
treatment options have been limited.

Infliximab blocks the activity of ‘tumour necrosis factor
alpha’ (TNF-alpha), a protein involved in inflammation, and the vast
majority of the trial subjects treated with the drug achieved
clinically-significant levels of skin clearance. Nearly 60% experienced
at least a 90% improvement in symptoms — or near-complete skin
clearance — after ten weeks, versus 1% receiving the placebo, whilst
26% achieved complete skin clearance (versus 0% receiving the placebo).
The improvements continued throughout the 50-week study.

Professor Christopher Griffiths, the University academic
leading the trial from the Dermatology Centre at Hope Hospital,
Salford, said: “These results indicate that Infliximab is a very
effective therapy among the newer biological treatments for psoriasis.
As a dermatologist, I am very encouraged by the data, which show that
patients with moderate to severe psoriasis can rapidly achieve skin
clearance and that these results can be maintained.”

Patients receiving Infliximab also experienced a good response
in nail psoriasis, which is present in 20 — 50% of psoriasis patients
and often thought of as a treatment-resistant disease. By week 24 of
the trial, those receiving the drug were experiencing a 56% average
decrease in this condition, and again this response was maintained
throughout the trial.

“Physicians’ assessments of the patients’ conditions backed up
our findings,” confirmed Professor Griffiths, “with 83% of those
receiving the drug assessed as having minimal or cleared symptoms by
week 10 of the trial as opposed to just 4% of those receiving the
placebo.”

In a study of 72 habitual coffee drinkers, the researchers found that subjects produced more adrenaline and noradrenalin and had higher blood pressure on days when they drank caffeine compared with days they abstained. The two stress hormones are vital to helping the body react quickly in times of danger or stress, but they can damage the heart over a lifetime of heightened production, said James Lane, associate research professor of psychiatry at Duke.

Lane prepared results of his study, funded by the National Heart, Lung and Blood Institute, for presentation Thursday to a meeting of the 1999 Society of Behavioral Medicine.

"Moderate caffeine consumption makes a person react like he or she is having a very stressful day," Lane said in an interview before the meeting. "If you combine the effects of real stress with the artificial boost in stress hormones that comes from caffeine, then you have compounded the effects considerably."

During the two-week study, the subjects experienced, on average, a 32 percent increase in adrenalin and a 14 percent increase in noradrenaline on days when they consumed caffeine. Their blood pressure rose an average of 3 points.

Lane's study builds on smaller ones in which he found that caffeine boosted blood pressure, heart rate and stress hormones in subjects who drank 4 to 5 cups of caffeine per day. In the current study, Lane replicated those findings and added to them by showing that subjects' blood pressures and stress hormone levels stayed elevated until bedtime, even though they last consumed caffeine between noon and 1 p.m.

Occasional surges of stress hormones temporarily raise heart rate, blood pressure and mental acuity – long enough to accomplish the task at hand. But an excess of stress hormones has been shown to compromise health in a variety of ways, from damaging blood vessels to weakening the immune system.

In addition, even the small boost in blood pressure seen in this study – an average of 3 points during the day and evening – can have clinical significance, Lane said. A review of nine major studies of blood pressure and heart-disease risk showed that a 5-point difference in diastolic blood-pressure – the lower number used to assess health risk – was associated with at least a 34 percent increase in stroke and a 21 percent increase in the incidence of coronary heart disease

While researchers have long known that caffeine can boost stress hormones and blood pressure, Lane said most studies have been conducted in a laboratory setting under tightly controlled circumstances where a single dose of caffeine is compared to none in a short time span. Lane said his body of research is unique because it measures blood pressure, heart rate and stress hormone levels at timed intervals during normal working conditions, while subjects are exposed to a range of moods and activities.

"You can measure how caffeine affects people in the laboratory, but that doesn't tell you what effects the drug has in the real world when people are exposed to normal stressors and activities," he said.

In the current study, Lane also studied the effects of caffeine on women taking oral contraceptives, since previous research suggested that this population might be more responsive to the negative effects of caffeine. But Lane found no such effect. In fact, women taking oral contraceptives showed slightly less of a stress response to caffeine than a control group of women.

Lane's next study will measure the effects of eliminating caffeine from the diets of people with high blood pressure. The goal is to see if stopping caffeine use can be a useful therapy in reducing hypertension, along with diet, exercise and salt reduction.

The study results could lead to widespread changes in treatment for HIV patients, particularly those diagnosed at an advanced stage, experts say.

"Even in San Francisco, one of the first epicenters of HIV in the United States, we still find that many people present late in the course of their illness with an opportunistic infection," said Mitch Katz, MD, San Francisco’s director of health, who was not involved in the study. "This study shows that it is life-saving to treat those persons with antiretroviral drugs while they are still in the hospital. The results of this study will change practices throughout the world."

Some 60,000 to 70,000 newly HIV-infected individuals are identified every year in the United States, according to recently revised figures from the federal Centers for Disease Control and Prevention. A growing number of these patients, particularly minorities, youth, injection-drug users and those in poor rural areas, are being diagnosed late in the disease process when they’ve already developed life-threatening conditions, said Andrew Zolopa, MD, associate professor of infectious diseases and geographic medicine at Stanford and first author of the study. When these patients come for treatment of these complications, doctors are often reluctant to give them anti-AIDS drugs at the same time, fearing the two therapies could interfere with one another.

"A lot of people wait, thinking, ‘Let’s get the patient out of acute crisis, and then we’ll deal with the underlying HIV infection later,’" said Zolopa. "But that answer is wrong. If we’re more aggressive with HIV drugs, we can reduce AIDS-related complications and death by 50 percent. It’s a substantial clinical benefit."

The study was conducted by the AIDS Clinical Trials Group, the world’s largest clinical trial organization. Results will be published May 18 in the online journal PLoS-ONE.

William Powderly, MD, dean of medicine at the University College Dublin School of Medicine, said the study addresses one of the last, longstanding unknowns in the management of AIDS.

"Clinicians have long grappled with the question of whether or not early treatment with antiviral drugs will help people who come to the hospital with advanced infections, such as pneumonia," said Powderly, the study’s senior author. "The answer is clearly yes. Early antiviral treatment for HIV improves the clinical outcome, including the likelihood of surviving in the next few months. It probably does so by improving the immune system and therefore adds to the ability to resist these infections."

The study findings, presented in abstract form at an earlier scientific meeting, are already starting to change clinical practices. The International AIDS Society, the CDC and the British AIDS Society all have adopted guidelines that recommend that early antiretroviral treatment be considered in patients with an opportunistic infection, Zolopa noted.

The study involved 262 patients at 39 sites across the United States, from Puerto Rico to Seattle. An additional 20 patients were enrolled in a hospital in Johannesburg, South Africa. Eighty-five percent of the patients were men whose median age was 28. They were an ethnically diverse group: 37 percent were black, 36 percent Hispanic, 23 percent white and 5 percent Asian.

The patients all had one or more opportunistic infection, with the most common ones being pneumocystis jirovecii pneumonia, cryptococcal meningitis and serious bacterial infections. Patients with tuberculosis were excluded from the study because it was unclear what the optimal antiviral treatment was for these patients, Zolopa said.

The patients, who were enrolled between May 2003 and August 2006, were separated into two groups: those who got antiretroviral treatment early and those for whom this treatment was delayed until their opportunistic infections had been dealt with. The patients were all offered antiretroviral drugs free of charge. The drugs for the study were supplied by Abbott Laboratories (lopinavir/ritonavir), Gilead Sciences (tenofovir and emtricitabine) and Bristol-Myers Squibb (stavudine).

The patients in the early intervention arm of the study were treated with ARVs within an average of 12 days, while those in the deferred group received the treatment within an average of 45 days after the start of treatment for the opportunistic infection. Among the patients treated early, there were 20 (14.2 percent) who died or developed another significant AIDS-related complication. That compared with 34 patients (24.1 percent) in the deferred group who died or suffered a new complication.

In addition, the patients in the early treatment group saw a much swifter recovery of their immune systems. The early group patients saw their T-cell counts, a measure of the immune cells destroyed by the AIDS virus, increase to more than 100 within four weeks. In the deferred treatment group, it took 12 weeks for the patients’ T cells to reach that same level, the researchers reported.

"I was quite impressed at how rapidly these T cells could rise in these patients," Zolopa said. "By starting ARVs early you can effectively reduce the window of vulnerability where another AIDS-related complication could develop."

Zolopa said there was no difference between the two sets of patients in their adherence to their prescribed regimens. One concern in treating patients with ARVs soon after being diagnosed with AIDS is that they might not stick to their treatments and could then develop drug resistance. But adherence did not prove to be an issue, he noted.

"Starting the therapies early didn’t scare people off," he said.

According to Zolopa, the study results probably provide some guidance for patients in developing countries, though each country would have to determine its own strategy for initiating ARVs in patients with advanced AIDS.

"These results do have important implications across the globe," he said.

Although the study did not include patients with tuberculosis, the most common AIDS-related complication among patients in sub-Saharan Africa, early ARV treatment has been shown in other, more recent studies to be of value in those patients with TB, Powderly said.

Zolopa said implementing the study findings could entail some logistical challenges, as hospitals will have to develop interdisciplinary teams, including pulmonary specialists, emergency physicians, pharmacists and others, in coordinating early treatment for these critically ill patients as they come into the system.

Other researchers in the study are Janet Andersen, ScD, and Lauren Komarow, both with Harvard School of Public Health; Ian Sanne, MD, of the South African College of Physicians; Alejandro Sanchez, MD, of the USC Keck School of Medicine; Evelyn Hogg with Social & Scientific Systems, Inc.; and Carol Suckow with the Frontier Science and Technology Research Foundation.

The study was funded by the National Institutes of Health through the Division of AIDS.

Pulmonary arterial hypertension, which is high blood pressure in the lungs, currently has only a few treatment options, but most cases lead to premature death. It is caused by a cancer-like excessive growth of cells in the wall of the lung blood vessels. It causes the lumen, the path where blood travels, to constrict putting pressure on the right ventricle of the heart which eventually leads to heart failure.

Evangelos Michelakis, his graduate student Gopinath Sutendra and a group of collaborators have found that this excessive cell growth can be reversed by targeting the mitochondria of the cell, which control metabolism of the cell and initiate cell death.

By using dichloroacetate (DCA) or Trimetazidine (TMZ), mitochondria targeted drugs, the activity of the mitochondria increases which helps induce cell death and regresses pulmonary hypertension in an animal model, says Sutendra.

Current therapies only look at dilating the constricted vessels rather than regression, so this is a very exciting advancement for the lab.

"In the pulmonary hypertension field they’re really looking for new therapies to regress the disease, it might be the wave of the future," said Sutendra. "The other thing that is really exciting is that TMZ and DCA have been used clinically in patients so it’s something that can be used right away in these patients."

Clinical trials are expected to be the next step. Michelakis is currently working with a college in the United Kingdom to have patients with pulmonary hypertension take DCA.

Loyola was the first and only medical center in the Chicago area five years ago to begin evaluating the Medtronic PRESTIGE ™Artificial Cervical Disc that the FDA approved July 16, 2007. This is the only cervical disc approved by the FDA. Nockels was principal investigator for the Loyola site.

It is estimated that more than half of people ages 40 and older have cervical disc disease, characterized by degenerative changes in the upper spine. Cervical discs are located between the seven vertebrae of the neck.

“The prosthesis simulates the function of a natural cervical disc and provides patients with the ability to move their necks compared to the traditional practice of spinal fusion,” said Nockels, associate professor and vice chair, department of neurological surgery, Loyola University Chicago Stritch School of Medicine, Maywood, Ill. “As a result, patients recover more quickly and get back to work faster.

“The results of the clinical trial show that the disc is strong enough to withstand sudden movement and to support the head,” said Nockels. “Patients are able to move their head up and down, and from side to side.”

When Wheaton, Ill., resident Tom N’s neck pain was diagnosed as degenerative disc disease, the then-41-year-old businessman could barely lift a cup of coffee. He didn’t know if he could ever play golf again. But after surgery at Loyola, Tom plays golf, wrestles with his children and lifts his coffee cup and other objects with ease.

“Since the surgery, Tom no longer has neck and arm pain; no longer experiences numbness at night; and no longer has trouble sleeping,” said Nockels.

Natural discs are gel-like cushions that act as shock absorbers between each vertebrae in the spine. Herniation, resulting from disc degeneration, injury or heavy lifting, can occur when a portion of the disc is pushed out of place and presses on adjacent nerve endings.

Symptoms include pain radiating down the arm and numbness, in addition to neck pain. As a result, many people have difficulty sleeping. Discs dehydrate and shrink over time, producing areas where bone touches bone. Cervical disc disease typically increases as baby boomers age.

The new artificial disc, placed through an incision at the front of the neck, is designed to alleviate neck pain and other ailments associated with disc herniations, spinal arthritis and other spine degenerative conditions. The disc consists of a stainless-steel ball and trough that functions as a joint. It is attached to the vertebrae with screws. The components are designed to act as a pivot point, which may allow the spine to move more naturally.

Loyola was one of 20 centers nationwide evaluating the device in a study monitored by the U.S. Food and Drug Administration.

“The new device eliminates the need for transplanted human bone, which is required with spinal fusion,” said Nockels. “In addition, it permits more motion of the neck. This reduces the likelihood of stress on the surrounding vertebrae, which could lead to further degeneration in adjacent discs.

“Previously, the only approved method to help patients was to clear away the problem disc material and then fuse adjacent cervical vertebrae together with screws and a metal plate,” said Nockels. “This permanent fusion of bone eliminates normal movement and adds stress on the vertebrae above and below the fusion.

“Although anecdotal, several disc recipients in the clinical trial have been involved in serious motor vehicle accidents,” said Nockels. “One was a front-end crash; another occurred 10 weeks after the disc surgery. Some patients were subject to air bag deployment.

In spite of this, follow-up X-rays of these patients show continued normal function and no device-related problems,” Nockels reported.

Nockels noted that the artificial cervical disk is not for everyone. You have to have some ability to move, so someone with severe arthritis is not a candidate. In addition, the cervical disc disease must be only in one level of the neck, not throughout.

Nockels also is the chief of Loyola’s division of neurological spinal disorder and director of the spinal cord injury repair laboratory.

The department of neurological surgery is actively involved in research on complex neurological pathologies and its spinal cord injury repair lab is investigating novel treatments for repair of the injured spinal cord.

The ProgeNIA project will focus on Sardinia, an isolated Mediterranean island where historically there has been little immigration. As a result, most inhabitants share common ancestors and have inherited many of the same genetic traits. The interrelatedness of this population should simplify the identification of genes involved in age-related conditions, such as cardiovascular disease.

“With this project we want to study aging, and in particular to identify genes involved in the development of several pathophysiological conditions typical of old age,” said David Schlessinger, Ph.D., chief of the NIA’s Laboratory of Genetics. “The Sardinian population, thanks to its genetic patrimony, can make a fundamental contribution to the understanding of human biology.”

The project, a collaborative effort of the NIA and the Italian National Research Council, officially began in November. It will be directed by Giuseppe Pilia, M.D., of L’Instituto sulle Talassemie ed Anemie Mediterranee in Cagliari, Sardinia. The investigators aim to recruit more than 4,000 men and women ages 14 and older to participate in the project. In the first phase of the project, the volunteers will undergo a series of tests. During these evaluations, investigators will be looking in detail at two traits: high arterial stiffness and positive emotions. Once volunteers who have extreme values for one or both of these two traits have been identified, investigators will seek out family members to determine if they also have these extremes. After that, investigators plan to conduct genetic analysis on individuals who share those traits to try to identify underlying genes.

These traits were selected for several reasons. Independent data from the NIA’s Baltimore Longitudinal Study of Aging identifies vascular stiffness as perhaps the most important predictor of mortality from heart disease. The ability to reduce vascular stiffness could have a major influence on reducing deaths from heart disease. In addition, it has been reported that positive emotions—joy, happiness, love, and excitement—can have profound impact on life satisfaction and health as we age. Both the physical and emotional traits are considered to have strong genetic components and have been extensively studied by NIA scientists.

Sardinia, which was first settled around 6,000 BC, is home to one of the world’s few “founder” populations. These populations, including those located in Iceland, Finland, and French-speaking Quebec, arose from small numbers of individuals. Over time, these populations grew in size without much immigration from the outside world. Because most of the society is interrelated, individuals share much of their genetic information, which makes it easier to track genetic effects through generations.

The scientists will concentrate their research efforts in Ogliastra, a region on the eastern side of the island surrounded by mountains and the Mediterranean Sea. Because of the terrain, the 300,000 residents of this region have traditionally been isolated from other islanders, making them an ideal founder population. “Sardinians speak of Ogliastra as an island within the island,” Dr. Schlessinger says.

When a particular genetic trait, such as extreme arterial stiffness, exists in founder populations it is likely that the same one or few genes are responsible for the trait in all affected individuals. Once the genes for a certain complex trait are identified within a founder population, researchers can use this information to isolate interacting genes and assess their importance in more heterogeneous populations, like those of mainland Europe or the United States.

“This study can ultimately help prevent some diseases by letting us know who has the risk factors that indicate they should change diet or exercise or otherwise change their lifestyle in a way that might save lives,” Dr. Schlessinger said.

Photos are available online at progenia/stampa2.php.

ARS chemist J. Vincent Edwards at the ARS Southern Regional Research Center in New Orleans, La., is testing specially-treated cotton fabrics that might someday be made into military uniforms and gauze pads that can stanch bleeding, prevent infections and promote healing. His fabrics can also be made into hospital sheets that are highly absorbent, smooth, soft and antibacterial, to treat or even prevent bed sores.

To impart antibacterial and blood-clotting properties, Edwards uses chitosan, a carbohydrate in shrimp shells. He has developed a technique to more uniformly distribute the chitosan in cotton fabric, compared with the chitosan-treated cotton gauze pads currently on the market. This innovation should lead to more effective cotton wound dressings and improved high-tech military clothing.

The work builds on Edwards’ previous invention of a treated cotton gauze pad that also promotes healing—even of deep and painful bed sores. Paradoxically, although the body rushes protease enzymes to such wound sites to promote healing, sending too many of them can create excess inflammation and actually prevent healing.

Edwards achieved the healing effect by treating gauze pads with negatively charged phosphoric acid, which pulls positively charged excess proteases out of a wound. His research has shown that the improved gauze dressings may also attract protein-building macrophages necessary for skin to heal.

Tissue Technologies of Richmond, Va., has the licensing rights to the ARS-patented, protease-absorbing technology and has sublicensed it to a manufacturer and marketer. The U.S. Food and Drug Administration approved the gauze bandage in 2006.