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Studies have found that the UK has the worst outcome in western Europe. In one study the differences in the proportion of patients dead or dependent between the UK and eight other European countries were between 150 and 300 events per 1000 patients.

What underlies this variation and why is outcome so poor in the UK, asks Professor Hugh Markus at St George’s University of London?

Differences in the process of care are likely to be important, he writes. In many European countries stroke care is an integral part of neurology. In contrast, in the UK it has, until recently, been a “Cinderella” subject, often falling between neurology and general and geriatric medicine.

It is tempting to conclude that this lack of interest has led to underinvestment and a resulting poor outcome, he says. Yet the cost of care of stroke patients seems to be as high, if not higher, in the UK than in European countries with better outcomes.

He suggests several organisational and structural problems, such as poor focus on acute stroke care.

This has become even more important now that there are specific treatments for acute stroke, such as thrombolysis (giving anti-clotting drugs to patients within three hours of a stroke), he says. Effective thrombolysis services exist in many countries in Europe, North America, and Australia, where in some centres as many as 20-30% of eligible patients receiving thrombolytic therapy. Currently less than 1% receive such therapy in the UK.

These deficiencies have already been recognised in England in a 2005 National Audit Office report, he writes. The report concluded that if care was better organised, every year ВЈ20m could be saved, 550 deaths could be avoided, and 1700 patients would recover fully who would not otherwise do so. In response, England’s Department of Health National Stroke Strategy is due to publish its recommendations in autumn 2007.

A major challenge is to change the perception of stroke among both health professionals and the public, so that stroke is viewed as a condition that requires emergency action. The UK also has a severe shortage of specialists trained in acute stroke care and access to imaging technology, says Markus.

For example, in many European countries, brain scans are performed on admission in the accident and emergency department, while in the UK many units struggle to provide it within 24 hours, despite research showing that scanning patients immediately is the most cost effective strategy.

Improved early diagnosis with imaging, together with improved monitoring and treatment of physiological parameters, will improve outcome independent of administration of thrombolysis, he concludes. If we can set such acute systems in place they will also facilitate implementation of other new treatments.

“Editorial: Improving the outcome of stroke”
BMJ Volume 335 pp 359-60
bmj

Idiopathic pulmonary fibrosis (IPF) is a chronic, late-onset disease of lung parenchyma with unknown etiology. IPF has been treated with corticosteroids and immunosuppressive agents, but the prognosis and the response to treatment have remained poor, and the estimated time of survival from the diagnosis is less than 3 years. The pathogenesis and etiology of IPF are unknown, but the reports of multiple affected family members in the same family support the influence of genetic factors.

In their previous studies researchers at the University of Helsinki and the University Hospital of Helsinki observed that the prevalence of idiopathic pulmonary fibrosis distributed unevenly in Finland. The prevalence was two times higher in eastern and southern Savo (45/100 000 inhabitants) compared to the prevalence in Finland (16-18/100 000).

The researchers identified multiplex families with IPF and noticed that familial IPF patients clustered within Savo and Carelia, the same areas with the high prevalence, suggesting that they most likely share a common disease-causing allele introduced by a common ancestor.

They performed a genome-wide scan with six multiplex families. Three regions on chromosomes 3, 4, and 13 obtained NPL scores of 1.7, 1.7, and 1.6, respectively, and on chromosomes 9 and 12 possible shared haplotypes were seen. These five loci were fine mapped with 63 markers in an extended data set.

After fine mapping the researchers did not detect the linkage to the loci on chromosomes 3, 9, 12, and 13. On chromosome 4q31.1 the NPL score increased to 2.1, and one third of the affected families (8/24) shared a 110 kb haplotype, while none of the unaffected family members carried it. The susceptibility haplotype was carried in 34 % of all the genotyped families (12/35), and in 7.7 % (11/143) of 143 controls, with an odds ratio of 6.3 (p=0.0001, 95 % CI=2.3-15.9).

The critical region harbors two novel candidate genes, ELMOD2, and LOC152586 that both are poorly characterized. An in vitro translation assay with LOC152586 failed to produce any peptide suggesting it is not a protein-coding gene. mRNA expression of ELMOD2 was decreased in lung biopsies derived from IPF patients (N=6) compared to healthy controls (N=7).

ELMOD2 is potentially involved in apoptosis, phagocytosis, cell engulfment, and cell migration. It is expressed in functionally relevant tissue, in lung and in fibroblasts, and its expression is significantly decreased in IPF lung compared to healthy lung. Therefore ELMOD2 becomes a prime candidate gene for familial IPF.

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Hodgson U, Pulkkinen V, Dixon M, Peyrard-Janvid M, Rehn M, Lahermo P, Ollikainen V, Salmenkivi K, Kinnula V, Kere J, Tukiainen P, Laitinen T: ELMOD2 Is a Candidate Gene for Familial Idiopathic Pulmonary Fibrosis. Am J Hum Genet. 2006 Jul;79(1):149-54. Epub 2006 May 9

Contact: Dr. Ulla Hodgson

University of Helsinki

Even though his mother had diabetes, Joe Kessler didn’t know he was at risk. In fact, if it wasn’t for a routine check up, Joe may not have found out that he has diabetes, too.

“I was taking a physical and it was caught by accident just through the blood work. While I was glad it did, – I did not go to the doctor for that reason,” says Joe.

Since then, Joe has had to pay close attention to what he eats. Experts have known for some time that diabetes is linked to things like fatty and sugary foods. But now researchers at Ohio State University Medical Center have found a strong connection between diabetes, diet, and air pollution.

Doctor Sanjay Rajagopalan says air pollution not only affects your lungs, it also causes problems in other organs. His research team exposed mice to the same dirty air that many of us breathe every day.

“Every mouse that we exposed to high fat diet, along with exposure to inhaled particulates had marked worsening of diabetes,” says Dr. Rajagopalan.

The tests showed that air pollution caused inflammation, increased body fat and interferes with how the mice processed insulin, a hallmark of diabetes. And the effects were strongest when combined with poor diet. It’s not good news considering one in three Americans is obese, and one in six lives with poor air quality.**

“It’s interesting that the diabetic increases have been most notable in urbanized areas, where there’s been a high percentage of patients being exposed to bad air,” says Dr. Rajagopalan.

For years, Joe breathed bad air while working as a fabricator and welder. Today he’s an avid boater and doesn’t take a single breath of fresh air for granted.

There are steps you can take to protect yourself. Doctors say if you live in an area with poor air quality try to limit your exposure, especially during the worst conditions. And don’t be a couch potato, avoid fatty foods and get moderate exercise.

**Total Prevalence of Diabetes & Pre-diabetes, American Diabetes Association, retrieved January 2009 from diabetes/diabetes-statistics

**State of the Air 2008, American Lung Association, retrieved January 2009 from: lungusa

lungusa/site/c.dvLUK9O0E/b.34894/apps/s/content.asp?ct=5318243

Ohio State University Medical Center

“Our study found that greater than one in three U.S. adults had liver disease, even after excluding those with traditional risk factors such as alcoholism and viral hepatitis,” said Matthew Cave, MD, assistant professor, department of medicine, division of gastroenterology and hepatology at the University of Louisville. “Our study shows that some of these cases may be attributable to environmental pollution, even after adjusting for obesity, which is another major risk factor for liver disease.”

Using the 2003-2004 National Health and Nutrition Examination Survey (NHANES), researchers from the University of Louisville study examined chronic low-level exposure to 111 common pollutants including lead, mercury, PCBs and pesticides and their association with otherwise unexplained liver disease in adults. The specific pollutants included were detectable in 60 percent or more of the 4,500 study subjects.

Dr. Cave added that this analysis used only the ALT liver enzyme as a marker of liver injury, and cautioned that this associative study does not prove causality. However, he added that previous animal studies do suggest causality for many of these chemicals. Dr. Cave and his co-authors also plan to examine the additive effects of environmental pollutants on liver disease in children and adults with risk factors including obesity, viral hepatitis, and alcoholism in the NHANES population.

Dr. Cave will present these data, Chronic Low-Level Exposure to Toxicants Linked to Liver Disease in U.S. Adults (Abstract #289), on Monday, June 1 at 8:30 a.m. CDT in S105, McCormick Place.

Source:
Aimee Frank

American Gastroenterological Association

“Einstein has become a leader in research on aging, a process relevant to every organ system and almost every disease,” said Allen M. Spiegel, M.D., the Marilyn and Stanley M. Katz Dean. “This award from the National Institute on Aging is a tribute to the outstanding research conducted by Nir Barzilai, Ana Maria Cuervo, Jan Vijg and their colleagues.”

The establishment of Einstein’s Center is based on eight years of work by the College of Medicine’s Institute for Aging Research, founded in 2002 by director Nir Barzilai, M.D., professor of medicine and of genetics and the Ingeborg and Ira Leon Rennert Professor of Aging Research. Dr. Barzilai will also be director of Einstein’s Center.

“The role of age in disease is underestimated,” explained Dr. Barzilai. “Aging is a major factor for the development of most adult onset diseases. If we are able to determine the biology of aging, then we can look for ways to protect against it and increase health span, or living disease-free even into advanced old age. Our research – in both the Institute and our new Center – is ultimately aimed at finding treatments to prevent or slow this process.”

Einstein’s Center will be run under the auspices of the Institute, enhancing the institute’s already robust research component. Currently, there are 48 Einstein investigators, 13 regional members (including a special alliance with Brown University), and 4 national members (most with active collaborations with Einstein faculty) who work on research projects launched under the Institute. This work will continue under the new Einstein Center.

Einstein’s Center will contain three research resource cores. The cores established under the Institute, are unique to the College of Medicine, and are novel in their use of technology. The Cellular and Tissue Aging Core will provide current and innovative aging-specific measurements of cellular function; the Genomics and Epigenomics of Aging Core will offer global genome and epigenome screening resources, including analysis pipelines uniquely tailored to aging research; and the Healthy Aging Physiology Core will perform sophisticated integrative metabolic studies to determine ‘healthy aging’ physiology, including metabolism, body composition and energy balance, cardiac and cognitive/functional behavior, and exercise.

Among those leading Einstein’s Center will be Ana Maria Cuervo, M.D., Ph.D., professor of developmental and molecular biology, of anatomy and structural biology, and of medicine. A recognized expert on cellular and organ aging, Dr. Cuervo will direct the Cellular and Tissue Aging Core.

“These are very exciting times for aging research,” said Dr. Cuervo. “Over the last 10 years, we have seen researchers embrace the important molecular advances and methods developed in other areas to make great strides in our understanding of aging. It is only through this transformation that the design of interventions aimed at increasing health span is now possible.”

Another Center leader will be Jan Vijg, Ph.D., professor and chair of genetics and the Lola and Saul Kramer Chair in Molecular Genetics. He has established state-of-the-art genetic cores crucial for the Institute and will lead the Genomics and Epigenomics of Aging Core, as well as the Research Development Core, which will provide seed funding for new investigators and the expansion of ongoing research.

“A deeper understanding of the genomic and epigenomic processes underlying aging will help us to increase health span,” said Dr. Vijg. “With support from Einstein leadership and cutting-edge technologies at our disposal, investigators – both at Einstein and at partner institutions – can take advantage of the latest equipment and analysis to advance work in the field.”

“Albert Einstein College of Medicine is a welcomed addition to the NIA’s Nathan Shock Centers of Excellence in the Basic Biology of Aging,” said Felipe Sierra, Ph.D., director of NIA’s Division of Aging Biology. “Nathan Shock was dedicated to characterizing normal changes versus disease-related changes in aging. Einstein’s three research cores will carry on Shock’s mission and add to our understanding of the cellular, genetic, and physiological factors that influence health and longevity.”

Dr. Barzilai will run the Healthy Aging Physiology Core. Other faculty members in the Center include Yousin Suh, Ph.D., associate professor of medicine and of genetics, who will run the seminar series for the center. Radhika Muzumdar, M.D., M.B.B.S., associate professor of pediatrics and medicine, will organize the center’s annual retreat, which will be co-chaired by the American Federation for Aging Research.

The Division of Aging Biology of the National Institute on Aging supports Nathan Shock Centers of Excellence in the Basic Biology of Aging across the U.S. The other centers are in Maine (The Jackson Laboratories), Michigan (University of Michigan), Texas (University of Texas Health Sciences Center in San Antonio), and Washington (University of Washington).

The Nathan Shock Centers are named in honor of Nathan Wetherell Shock, Ph.D., who began his gerontology career in 1941. He took a two-man aging unit and built it into the internationally respected Gerontology Research Center of the National Institute on Aging, NIH. Dr. Shock was the catalyst for the emergence of aging research in the United States and overseas for nearly half a century.

Source:

Albert Einstein College of Medicine of Yeshiva University

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(JAMA. 2007;297:2241-2250)

Please see the article for additional information, including other authors, author contributions and affiliations, financial disclosures, funding and support, etc.

Contact: Michael Strecke
JAMA and Archives Journals

The initiative takes a strong ethical stand against doping, particularly as it relates to interaction, use, or prescription among ACSM members. ACSM and USADA will begin a second phase of the program to establish a national coalition with other organizations and sports governing bodies to adopt these ethical standards. A planned third phase will encourage licensing boards and other certifying organizations to include anti-doping rules.

“Integrity is among the supreme values for athletes and for those who train and treat them or sanction athletic events,” said Robert E. Sallis, M.D., FACSM, president of ACSM. “With this statement of principles, ACSM members are pledging to uphold the integrity of their practice with athletes and, in doing so, support the integrity of athletics as a whole. We consider the adoption of these principles to be a big step and we look forward to a continued and fruitful partnership with the U.S. Anti-Doping Agency.”

“In its mission, the United States Anti-Doping Agency acknowledges the importance of ensuring the health of athletes as well as preserving the well-being and integrity of sport,” said Ralph W. Hale, M.D., chair of the USADA Board of Directors. “Every athlete is responsible under the anti-doping rules for any violation involving his or her use of a prohibited substance or method and can be sanctioned accordingly. Those who advise them or assist with any unethical practices must also be held accountable. We welcome the ACSM’s commitment to ensuring that its members, the sports medicine and exercise science professionals who fulfill important roles in the care and training of athletes, adhere to the highest professional standards.”

“Up to now the emphasis has been on athletes, and often on detection and sanctions for doping rather than prevention,” said Gary I. Wadler, M.D., FACSM, an expert in doping and steroid use in sports. “Now we’re working to directly involve the professionals who work with the athletes, emphasizing their professional education and responsibilities.”

Other organizations commit to anti-doping statement

More than a dozen other organizations have endorsed a brief statement committing them to the principles of drug-free sport. In coming weeks, ACSM and USADA will invite endorsement by scores of organizations involved in medicine, sports governance and sanctioning, health, fitness and other fields.

“It’s gratifying to see so many front-line organizations sign on unequivocally to oppose doping,” said Sallis. “This underscores the importance of integrity, fair competition and medically sound practices in sport.”

The American College of Sports Medicine is the largest sports medicine and exercise science organization in the world. More than 20,000 international, national, and regional members are dedicated to advancing and integrating scientific research to provide educational and practical applications of exercise science and sports medicine.

The United States Anti-Doping Agency is responsible for the testing and results management process for athletes in the U.S. Olympic and Paralympic Movement. USADA is equally dedicated to preserving the integrity of sport through research initiatives and educational programs.

American College of Sports Medicine

A team of researchers has been using an animal model to investigate potential links between testosterone supplements and cardiovascular and renal disease. The team, comprised of Radu Iliescu, Licy L. Yanes, Julio C. Sartori-Valinotti, and Jane F. Reckelhoff, is affiliated with the University of Mississippi Medical Center’s Department of Physiology and Biophysics, Jackson, MS. Their most recent study and an overview of data from other human and animal studies is part of the upcoming conference, Sex and Gender in Cardiovascular-Renal Physiology and Pathophysiology. The meeting, sponsored by The American Physiological Society (APS; The-APS), is being held August 9-12, 2007 at the Hyatt Regency Austin on Town Lake, Austin, TX.

Latest Study

The team is presenting its work entitled, “Testosterone Supplements Promote Renal Injury and Exacerbate Hypertension in Aging Spontaneously Hypertensive Rats (SHR),” in which spontaneously hypertensive rats were used as a model for genetic hypertension.

Three groups of rats were used: intact, gonadectomized (at eight months of age), and testosterone-supplemented rats. Testosterone supplements were administered chronically via pellets and rats were monitored until 13 months of age. Blood pressure was measured at the end of the experiment via indwelling arterial catheters inserted into conscious, freely moving rats. Urine was collected for two hours and urinary protein excretion was determined.

The researchers found that blood pressure was significantly higher in testosterone-supplemented male SHR as compared with intact rats, whereas castration did not alter blood pressure levels. Testosterone supplemented SHR excreted more urinary protein than intact rats, and castration reduced proteinuria (urinary protein).

The results suggest that testosterone supplementation of aging male SHR promotes renal injury and thereby exacerbates hypertension. The results also show that removal of endogenous androgens later in life (eight months) prevents the development of hypertensive renal injury without altering existing hypertension levels.

The Big Picture

The study is part of the researchers’ ongoing project to investigate the effects of testosterone-supplementation in animal models of disease that mimic the characteristics of the human male population that currently receive testosterone supplements. They are currently testing the hypotheses that the natural decrease in testosterone brought on by aging may affect the progression of pre-existing cardiovascular/renal disease.

The American Physiological Society (APS; The-APS) has been an integral part of the scientific discovery process since it was established in 1887. Physiology is the study of how molecules, cells, tissues and organs function to create health or disease.

The APS meeting is being held August 9-12, 2007 at the Hyatt Regency Austin on Town Lake, Austin, TX. Members of the media are invited to attend the sessions.

The-APS

“Today’s report shows that worryingly, complaining about health and social care services can be a difficult and complex experience. As the largest users of health and social care services, older people are going to be particularly affected.

“People who make complaints about either health or social care services are likely to already be in a vulnerable position. When older people are poorly or need care, the last thing they need is to feel like they can’t complain, have nowhere to turn, or have to jump through hoops to have their issues heard. Sometimes making a complaint can be as frustrating and upsetting as the original problem.

“In addition to this, older people who pay for their own care in private care homes don’t have access to the complaints system for social care. This inequity in the system must be addressed – around 115,000 older people are affected in this way(1).

“If care for sick people isn’t satisfactory, it’s essential that complaints are acted upon straight away – that way lessons can be learned and mistakes aren’t repeated. The complaints system for our health and social care services must be transparent, open and well promoted – and reducing the complexity of both systems is an absolute must. Ideally we would like to see one complaints system for both health and social care.”

Notes

Of residents in care homes operated by private or voluntary organisations (373,000), 31% pay all their own care costs (115,000); 59% have fees wholly or partially funded by local authorities (221,000), and 10% by the NHS (37,000). (23% of nursing home residents are funded by the NHS, who do not fund residential care residents.) Source: Care of Elderly People UK Market Survey 2007 – Twentieth Edition, Laing and Buisson, 2007

Help the Aged produces an information sheet, aimed at people who are having problems with their care home, local council, or the NHS. How to Make a Complaint, is available from helptheaged or 020 7239 1845

Help the Aged is the charity fighting to free disadvantaged older people in the UK and overseas from poverty, isolation, neglect and ageism. It campaigns to raise public awareness of the issues affecting older people and to bring about policy change. The Charity delivers a range of services: information and advice, home support and community living, including international development work. These are supported by its paid-for services and fundraising activities – which aim to increase funding in the future to respond to the growing unmet needs of disadvantaged older people. Help the Aged also funds vital research into the health issues and experiences of older people to improve the quality of later life.

Help the Aged urgently needs donations and support to help it in the increasingly challenging fight to free disadvantaged older people from poverty, isolation and neglect.

Help the Aged