Bird Flu Spreads To Several Commercial Farms In Nigeria

Authorities in Nigeria say that several commercial farms in states neighbouring Kaduna state now have H5N1 infected poultry.

Infected farms have been found in the following areas of Nigeria:

-- Kano
-- Plateau
-- Katsina
-- Bauchi
-- Abuja

Some humans with respiratory symptoms are also being tested for bird flu infection. Samples have been sent to a laboratory in Surrey, England.

The first bird flu outbreak (among poultry) is known to have started in Kaduna state on January 10th. Experts believe the virus had already been around for a while and that many other birds, and perhaps some humans, had been infected.

Patient records are being checked in the states of Kaduna, Kano and Katsina for signs of bird flu like symptoms - to check whether infection had taken place earlier. So far, nothing has been found.

Backyard poultry is very common in Nigeria, making it very hard for authorities to really gauge the scale of this outbreak. There are probably about 140 million heads of poultry in Nigeria, most of them are in the south-western part of the country. 60% of the country's poultry can be found in small backyard flocks.

The World Health Organization has expressed concern about the possible spread of bird flu to Nigeria's neighbours, where borders are porous and restrictions are difficult to enforce. Rumours are flying that the H5N1 virus strain has spread rapidly into neighbouring countries - there is no official confirmation of this, neither by national governments nor international organisations.

Written by: Christian Nordqvist
Editor: Medical News Today

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Human Brain Evolution And Eating Fish From Shoreline Environments

Forget the textbook story about tool use and language sparking the dramatic evolutionary growth of the human brain. Instead, imagine ancient hominid children chasing frogs. Not for fun, but for food.

According to Dr. Stephen Cunnane it was a rich and secure shore-based diet that fuelled and provided the essential nutrients to make our brains what they are today. Controversially, according to Dr. Cunnane our initial brain boost didn't happen by adaptation, but by exaptation, or chance.

"Anthropologists and evolutionary biologists usually point to things like the rise of language and tool making to explain the massive expansion of early hominid brains. But this is a Catch-22. Something had to start the process of brain expansion and I think it was early humans eating clams, frogs, bird eggs and fish from shoreline environments. This is what created the necessary physiological conditions for explosive brain growth," says Dr. Cunnane, a metabolic physiologist at the University of Sherbrooke in Sherbrooke, Quebec.

The evolutionary growth in hominid brain size remains a mystery and a major point of contention among anthropologists. Our brains weigh roughly twice as much as our similarly sized earliest human relative, Homo habilis two million years ago. The big question is which came first - the bigger brain or the social, linguistic and tool-making skills we associate with it?

But, Dr. Cunnane argues that most anthropologists are ignorant or dismissive of the key missing link to help answer this question: the metabolic constraints that are critical for healthy human brain development today, and for its evolution.

Human brains aren't just comparatively big, they're hungry. The average newborn's brain consumes an amazing 75-per cent of an infant's daily energy needs. According to Dr. Cunnane, to fuel this neural demand, human babies are born with a built-in energy reservoir - that cute baby fat. Human infants are the only primate babies born with excess fat. It accounts for about 14 per cent of their birth weight, similar to that of their brains.

It's this baby fat, says Dr. Cunnane, that provided the physiological winning conditions for hominids' evolutionary brain expansion. And how were hominid babies able to pack on the extra pounds? According to Cunnane their moms were dining on shoreline delicacies like clams and catfish.

"The shores gave us food security and higher nutrient density. My hypothesis is that to permit the brain to start to increase in size, the fittest early humans were those with the fattest infants," says Dr. Cunnane, author of the book Survival of the Fattest, published in 2005.

Unlike the prehistoric savannahs or forests, argues Dr. Cunnane, ancient shoreline environments provided a year-round, accessible and rich food supply. Such an environment was found in the wetlands and river and lake shorelines that dominated east Africa's prehistoric Rift Valley in which early humans evolved.

Dr. Cunnane points to the table scrap fossil evidence collected by his symposium co-organizer Dr. Kathy Stewart from the Canadian Museum of Nature, in Ottawa. Her study of fossil material excavated from numerous Homo habilis sites in eastern Africa revealed a bevy of chewed fish bones, particularly catfish.

More than just filling the larder, shorelines provided essential brain boosting nutrients and minerals that launched Homo sapiens brains past their primate peers, says Dr. Cunnane, the Canada Research Chair in Brain Metabolism and Aging.

Brain development and function requires ample supplies of a particular polyunsaturated fatty acid: docosahexaenoic acid (DHA). DHA is critical to proper neuron function. Human baby fat provides both an energy source for the rapidly growing infant grey matter, and also, says Dr. Cunnane, a greater concentration of DHA per pound than at any other time in life.

Aquatic foods are also rich in iodine, a key brain nutrient. Iodine is present in much lower amounts from terrestrial food sources such as mammals and plants.

It was this combination of abundant shoreline food and the "brain selective nutrients" that sparked the growth of the human brain, he says.

"Initially there wasn't selection for a larger brain," argues Dr. Cunnane. "The genetic possibility was there, but it remained silent until it was catalyzed by this shore-based diet."

Dr. Cunnane acknowledges that for the past 20 years he's been swimming upstream when it comes to convincing anthropologists of his position, especially that initial hominid brain expansion happened by chance rather than adaptation.

But, he says, the evidence of the importance of key shoreline nutrients to brain development is still with us - painfully so. Iodine deficiency is the world's leading nutrient deficiency. It affects more than a 1.5 billion people, mostly in inland areas, and causes sub-optimal brain function. Iodine is legally required to be added to salt in more than 100 countries.

Says Dr. Cunnane: "We've created an artificial shore-based food supply in our salt."


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Oxygen Loss To Unborn Children Detected Earlier By New Sensor

Article Date: 19 Feb 2006 - 8:00am (UK)

Researchers at the University of Warwick, and the University Hospitals Coventry and Warwickshire NHS Trust, have devised a new sensor which has the power to dramatically improve the amount of early warning doctors and midwives get of a dangerous situation in the birth process when the unborn child's brain is starved of oxygen - Fetal Hypoxia.

The threat of fetal hypoxia carries dangers not only for the child but also for the woman giving birth as doctors often proceed quickly to a caesarean section if they feel there is a significant threat of fetal hypoxia. However current tests for this condition require blood samples to be taken to a lab for examination leading to delays which means doctors having to decide sometimes to proceed with a cesarean section rather than take the risk on waiting on that full analysis.

University of Warwick researcher Professor Nick Dale had been looking at the science surrounding a chemical that can be found in blood called hypoxanthine. An unborn child with more than 5 micromoles (5 millionths of a mole) of hypoxanthine per litre of their blood is at severe risk of fetal hypoxia. Professor Dale was frustrated at the lack of effective instrumentation available to detect and study this chemical and devised his own fine tuned probe to examine the chemical. On talking with colleagues in the University of Warwick's Medical School and University Hospitals Coventry and Warwickshire NHS Trust they pointed out that the probes would be of massive benefit to doctors in the delivery room.

Warwick Medical School researchers have examined the probes and say that the use of Professor Dale's probes to test for hypoxanthine would give doctors in delivery rooms almost instant data on whether the unborn child faced fetal hypoxia. This would allow doctors to take more informed decisions as to whether to proceed to a caesarean section and probably therefore reduce the number of caesareans conducted. Another advantage is that Professor Dale's test also requires much less fine tuning than current tests (the blood PH test currently used to detect fetal hypoxia problems needs to identify a shift of as little of 0.05 PH).

Professor Dale is thrilled by the medical interest in his probes and is now working through a spin-out company Sarissa Biomedical Ltd - to take the work further. Sarissa is already talking with a number of medical instrument manufacturers and aims to establish a partnership between Sarissa, a medical instrument manufacturer and venture capitalists to produce a full blown medical instrument using the new probes and then to take it to full clinical trials in hospital delivery rooms.

###

Notes for Editors:
1. This story will also available as a Video News Release from 12.15 GMT on 14th February see the Research TV web site for details: http://www.research-tv.com/

2. Sarissa's web site is http://www.sarissa-biomedical.com/

3. The research has received funding from the Mercia Fund, Midven & Wellcome Trust.

For further Information please contact:

Professor Nick Dale, University of Warwick and Sarissa Biomedical 024 76 523729 email: n.e.dale@warwick.ac.uk


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Johns Hopkins Researchers Discover Key Protein Linked To Transverse Myelitis And Multiple Sclerosis

Hopkins researchers have discovered a single molecule that is a cause of an autoimmune disease in the central nervous system, called transverse myelitis (TM), that is related to multiple sclerosis.

In a study published in the October issue of The Journal of Clinical Investigation, psychiatrist Adam Kaplin, M.D., Ph.D., an assistant professor at The Johns Hopkins University School of Medicine, and neurologist Douglas Kerr, M.D., Ph.D., also an assistant professor at Hopkins, showed that the levels of the protein, IL-6, are dramatically elevated in the spinal fluid of transverse myelitis (TM) patients.

Although the majority of TM patients suffer a single attack, 15 percent to 30 percent of patients go on to develop full-blown MS. TM evolves rapidly and without warning and usually results in permanent impairment, including weakness of the legs and arms, bowel and bladder dysfunction, pain and paralysis.

IL-6 is a chemical messenger that cells of the immune system use to communicate with one another. One of the cell types injured by high levels of IL-6 includes oligodendrocytes, which help produce the protective myelin sheath coating around nerve cells. The findings offer one possible mechanism responsible for demyelinating disorders, such as TM and MS, and may aid in the development of effective therapies against these disorders, the researchers say.

"This is the first time a single culprit has been identified as causing a CNS autoimmune disease," said Kaplin.

The researchers began investigating the protein IL-6 when they became aware that TM patients suffered from memory impairment and depression. IL-6 has been implicated in mood and concentration disorders.

"This discovery is a success story that begins with listening carefully to what patients are telling us about their suffering and then collaborating across disciplines to open up new avenues of investigation," said Kaplin.

"TM is related to other autoimmune disorders of the nervous system, including Guillain-Barré syndrome, MS and acute disseminated encephalomyelitis. This study may give us a foothold in understanding all of these disorders and how they are linked together. The benefit is, therefore, not only to those who are paralyzed by TM, but to those who have disabilities due to a variety of autoimmune disorders. We are actively using these findings to aid in developing future diagnostic, prognostic and therapeutic advancements," said Kerr, director of the Johns Hopkins Transverse Myelitis Center, the only center devoted to TM in the world.

Researchers analyzed 42 inflammatory proteins in the cerebrospinal fluid of both TM and healthy patients. They found that IL-6 was consistently elevated in TM patients' spinal fluid. Further, the level of IL-6 directly correlated with the severity of paralysis.

Using cell culture and animal studies, the researchers confirmed that elevated IL-6 levels were directly injurious to the spinal cord. They showed that spinal fluid from TM patients induced death of spinal cord cells when cultured in a dish and that IL-6, when infused in adult rats, induced paralysis. Under the microscope, tissue from IL-6-infused rats showed demyelination and injury of axons, pathology that was nearly identical to that seen in human patients with TM.

Kerr and Kaplin also deduced that the reason IL-6 elevations injure only the spinal cord and not other regions of the nervous system was because distinct regions of the nervous system have different responses to IL-6. They concluded that these different types of responses might be a part of why different autoimmune disorders of the nervous system affect distinct regions and cause distinct symptoms.

"When we started, we knew nothing about the bad players in this drama in the spinal cord of CNS autoimmune diseases - it was a classic murder mystery and we set out together to find out 'who done it'," said Kaplin. "We've answered who could have done it, and how, and where."

###

Funding for this study was provided by the National Institutes of Health.
Other investigators involved in this study, conducted solely at Hopkins, were Deepa M. Deshpande, M.S.; Erick Scott, B.S.; Chitra Krishnan, M.S.; Jessica S. Carmen, B.S.; Irina Shats, M.S.; Tara Martinez, B.S.; Jennifer Drummond, B.S.; Sonny Dike, M.D.; Mickail Pletnikov, M.D., Ph.D.; Sanjay C. Keswani, M.B.; Timothy H. Moran, Ph.D.; Carlos A. Pardo, M.D., and Peter A. Calabresi, M.D.
_____________________________
This story has been adapted from a news release issued by Johns Hopkins Medical Institutions.

Antidepressant Use During Pregnancy Appears Associated With Withdrawal Symptoms In Newborns

Article Date: 13 Feb 2006 - 0:00am (UK)

Almost one-third of 60 newborn infants whose mothers took antidepressants during pregnancy experienced neonatal abstinence syndrome, a type of withdrawal with symptoms that include high-pitched crying, tremors and disturbed sleep, according to a study in the February issue of Archives of Pediatrics & Adolescent Medicine, one of the JAMA/Archives journals.

Between one-tenth and one-fourth of women will develop depression in their lifetimes, according to background information in the article. The stress of pregnancy can worsen the condition and increase the need for medications. Selective serotonin reuptake inhibitors (SSRIs) are a commonly used class of antidepressants; they are known to cross the placenta, prompting research into their effects on infants.

Rachel Levinson-Castiel, M.D., of the Children's Medical Center of Israel, Petah Tiqwa, and colleagues examined 120 babies born between Jan. 1, 2002, and Aug. 31, 2004, at Rabin Medical Center in Israel. Sixty of the infants' mothers took SSRIs for prolonged periods of time, including during the third trimester. These infants and 60 control infants without exposure to SSRIs were assessed two hours after birth and again at regular intervals if they displayed withdrawal symptoms.

Of the 60 infants with exposure to SSRIs, 18 (30 percent) had neonatal abstinence syndrome and eight of those cases were severe. The most common symptoms were tremor, gastrointestinal problems, an abnormal increase in muscle tone (hypertonicity), sleep disturbances and high-pitched cries. None of the infants with symptoms required treatment, and none of the 60 infants without exposure to SSRIs developed the syndrome.

"The high prevalence of neonatal abstinence syndrome in infants exposed to SSRIs in utero should be brought to the attention of family physicians, psychiatrists, gynecologists, pediatricians and mothers," the authors write. "Because maternal depression during pregnancy also entails a risk to the newborn, the risk-benefit ratio of continuing SSRI treatment should be assessed." If a mother and physician decide medication is necessary, she should be prescribed the minimum dose and number of drugs that would be effective for her condition.

In addition, the authors conclude, the infants of mothers taking SSRIs should be monitored closely after birth for a minimum of 48 hours "Follow-up of exposed infants, particularly those who develop severe symptoms, is needed to assess the long-term effects of prolonged exposure to SSRIs."

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Memory Problems At Menopause: Nothing To Forget About

Women who feel that they become more forgetful as menopause approaches shouldn't just "fuhgetabout it": There may be something to their own widespread reports that they're more likely to forget things as menopause approaches, say scientists who reported results from a small study today at the annual meeting of the International Neuropsychological Society in Boston.

The team from the University of Rochester Medical Center found that the issue is not really impaired memory. Instead, the team found a link between complaints of forgetfulness and the way middle-aged, stressed women learn or "encode" new information.

"This is not what most people think of traditionally when they think of memory loss," said co-author Mark Mapstone, Ph.D., assistant professor of Neurology. "It feels like a memory problem, but the cause is different. It feels like you can't remember, but that's because you never really learned the information in the first place."

The findings come from Mapstone and Miriam Weber, Ph.D., memory experts at the University's Memory Disorders Clinic who are seeing more and more middle-aged women who say they are having problems with forgetfulness.

"We see a lot of women who are afraid they are losing their minds," said Weber, a senior instructor of Neurology, who presented the results. "A lot of women complain that their thinking or their memory isn't what it used to be. Their big fear is that it's early Alzheimer's disease."

The team found nothing to support the idea that such women are on their way to developing Alzheimer's disease, and they didn't find any problem with what most people consider "memory." But they did make a finding that helps explain why women in their 40s and 50s frequently say they're having memory problems: It's possible that their changing moods and hectic lives make it harder to keep track of everything.

The work is the latest salvo in a years-long back and forth about memory, menopause, and estrogen. Doctors long thought that hormone-replacement therapy helped protect women against cognitive decline. But three years ago, scientists announced that HRT slightly raises the risk of developing dementia. Those results came soon after other results where scientists said that HRT brings with it increased risk of breast cancer, heart disease, and stroke.

When it comes to memory, a study in 2003 of more than 800 women found no evidence that memory problems occur as part of menopause. But neuropsychologists like Weber and Mapstone continue to see a steady stream of patients reporting memory problems as they approach menopause, mixing in with more typical older patients with problems like Alzheimer's disease.

So Weber and Mapstone put 24 women who complained of memory problems through a battery of tests that tested several cognitive skills, not just traditional memory, where a piece of information is stored away and then retrieved later.

Like the 2003 study, Weber and Mapstone found no evidence that women approaching menopause suffer from strictly memory problems any more than anyone else - of the 24 women tested, they found only one who had any type of impaired memory, where a person flat out forgets things she once knew or remembered.

Looking more closely, however, they did find that the women who complained more about problems with forgetfulness had a harder time learning or "encoding" new information, which can masquerade as a problem with memory. While the team found a clear correlation between the level of the women's complaints and their ability to learn new information, Weber and Mapstone point out that none of the women actually had an impaired ability to learn new information. They say a larger, more thorough study, involving hundreds of women and a broad array of cognitive tests before and during menopause, is needed to understand the link more fully.

Mapstone and Weber liken the problem of encoding new information to a situation where a doctor tells a patient that something serious may be wrong and gives a lot of detail. Afterwards, the person gets home and can hardly remember what the doctor said. It's not that the person necessarily forgot what was said; it's more likely that they never really heard the doctor the first time, because they were so anxious and worried.

The same may be true of women approaching menopause, many of whom live a life filled with stress and worry. Indeed, Weber and Mapstone found that most of the women in their study had some sort of mood distress, including symptoms of depression or anxiety.

"When people spread their attention thin, it's difficult to encode new information. When they're worried or anxious about being late for work, or the problems of an aging parent - that sort of stress can rob your attentional resources and impact your ability to encode information properly," said Mapstone, who said similar difficulty taking in new information is typical of nearly any man or woman who is anxious or depressed.

Weber said the study points out the importance for women who are feeling anxious or depressed to seek treatment, a step that should ease any cognitive difficulties.

"What characterizes these women is that they're being pulled in a lot of different directions. Many work - they have careers, aging parents, children. Then they're going through this dramatic hormonal change," Weber said.

"This will resonate for most women," said Weber. "There really is something going on. And perhaps knowing that their perceived problems with memory do not suggest early dementia might alleviate their concerns and actually improve their functioning - it's one less thing to worry about."

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Contact: Tom Rickey



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Long-lived Worms Yield Aging Insight

Genetic analysis could contribute to understanding of human longevity
Betterhumans Staff



Comparison of long-lived engineered worms with unaltered counterparts has revealed new insight into the genetics of aging.

The long-lived worms—Caenorhabditis elegans—have a mutated form of the gene daf-2.

A principal regulator of the worms' lifespan, the gene was first reported as critical to aging in 1993. Worms lacking a fully functional version live about twice as long as normal counterparts.

Researchers at the BC Cancer Agency's Genome Sciences Centre in Vancouver, British Columbia and the University of Missouri-Columbia have now learned more about the genetics underlying the extended lifespan, insight that could contribute to the understanding of human aging.

"Many processes involved in nematode aging may have fundamental and analogous roles in humans," says study leader Angela Brooks-Wilson of the BC Cancer Agency. "The human orthologs of some gene family members identified in this study have been associated with human age-related diseases."

Expression of longevity

For their study, Brooks-Wilson and colleagues prepared special libraries of genetic information. The libraries, called SAGE for "serial analysis of gene expression," provide a measurement of differences in gene expression.

They found that during early and middle age, the long-lived worms had reduced expression in genes linked with metabolic processes. The difference became less pronounced with increasing age.

"We speculate that the apparent metabolic repression in early and mid-life adults contributes substantially to the observed longevity of daf-2," says Julius Halaschek-Wiener of the BC Cancer Agency, the study's first author.

The researchers also found an increase in stress-response factors in aging adult worms, which supports current theories that protection against cellular stress is associated with greater longevity.

The study is reported in the journal Genome Research (read abstract).

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