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The Real Cause of Influenza Epidemics

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Influenza does not follow the predicted patterns for infectious diseases. In fact, there are several conundrums associated with influenza epidemics, such as:

1. Why is influenza both seasonal and ubiquitous — and where is the virus between epidemics?

2. Why are influenza epidemics so explosive?

3. Why do epidemics end so abruptly?

4. What explains the frequent coincidental timing of epidemics in countries of similar latitudes?

5. Why did epidemics in previous ages spread so rapidly, despite the lack of modern transport?

A theory gaining weight in the scientific community explains influenza epidemics as a result of a dormant disease, which become active in response to vitamin D deficiency. This theory provides answers for many of the above questions. A disease that remains dormant until vitamin D-producing sunlight exposure is reduced by a winter or rainy season would explain a widespread seasonal disease with a rapid onset and decline.

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There is compelling epidemiological evidence that indicates vitamin D deficiency is just such a “seasonal stimulus.”Recent evidence confirms that lower respiratory tract infections are more frequent, sometimes dramatically so, in those with low levels of vitamin D. Researchers have also found that 2,000 IU of vitamin D per day abolished the seasonality of influenza, and dramatically reduced its self-reported incidence.

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Faulty Gene Causes Heart Attack Death

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A faulty gene variant that can cause heart attack mortalities also potentially opens the way for improved treatment following such attacks.
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“It’s been known for some time that a defective ACE2 gene is associated with high blood pressure, but our research has also clearly linked one variant of this gene to a greater likelihood of mortality after heart attack,” said lead researcher Barry Palmer of Otago University, Christchurch.

“This is particularly in middle aged males who have acute coronary syndromes, or reduced flow of blood to the heart,” he added.

Otago scientists carried out the study over three years on a large cohort of 1,075 people (males and females) recruited from hospitals. They found, after adjusting for variables such as age, that male patients are almost twice as likely to die if they had one particular (defective) variant of the ACE2 gene.

“This is the first time ever that this variant of the ACE2 gene has been identified in terms of survivability,” said Palmer. “It will be useful in terms of other research we’re doing on tailoring heart disease treatment more accurately to the patient.”

“If we can identify those people at greater risk we may be able to do more earlier on in their treatment, and it’s easy enough to identify if someone has this variant of the gene.”

Males are more prone than females to the effects of the ACE2 gene variant which is linked to reduced survival because of their chromosomal make-up. That’s because males have only one copy in each cell of the ACE2 gene on the X chromosome and none on the Y chromosome, whereas females have two X chromosomes, according to an Otago release.

This means that if a male has a defective ACE2 gene variant there is no complementary chromosome which can compensate for that ineffective gene. Females have an alternative copy of the gene on their second X chromosome which can compensate for the defective ACE2 gene, and provide normal blood pressure to the heart.

In its normal form on the X chromosome the ACE2 gene produces an enzyme which controls blood pressure by influencing hormone levels. It is only when that gene is defective that blood pressure may increase.

The research was published in the October issue of the American Heart Journal.

You may click to see:->FAMILIAL HYPERCHOLESTEROLAEMIA Cardiovascular disease

Sources:
The Times Of India

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Ailmemts & Remedies

Corns and Calluses

 

The foot is an engineering marvel that cannot be duplicated by robotics. It is composed of 26 bones, 33 joints and around a hundred tendons, ligaments and muscles of various sizes, well oiled and sliding smoothly over each other.

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The foot is encased in thick and leathery skin that protects it from injury. Our feet take us everywhere from the time we first learn to walk till we are finally laid to rest. Yet, somehow, we tend to take our feet for granted until they malfunction, cause pain or refuse to perform as instructed.

Some orthopaedic abnormalities of the feet, like clubfoot, flat feet, congenitally dislocated hips or knock knees, are present from birth. Sometimes shoes may be purchased for conformity to fashion disregarding the requirements of the feet. They maybe ill fitting, too tight or too large. Pointed toe stilettos are notoriously guilty. The gait becomes abnormal as pressure is applied unevenly to the skin of the foot. Irregularity may also occur in old age as a result of arthritis or injury.

When pressure is exerted unevenly on the foot, the skin tends to thicken abnormally. This callused skin may remain like that or develop into a corn. This happens in areas where the skin is rubbed persistently or where the skin is under uneven pressure. Common places are the heel, the ball of the foot and the sides of the toes.

The skin over the unsightly hardened area on the foot, a callus, is dead. So there is no inflammation or pain. Eventually the callus may harden to form a corn. The corn has a central area of inflammation and is painful and tender. It is usually situated near the base of the fifth toe. If the feet are pushed into tight fitting shoes, corns will form between the toes as well. Perspiration and moisture cannot escape from this area causing the corn to become macerated and tender.

If a callus or corn is beginning to develop, the first step would be to determine if there is any source of pressure which has set off the thickening of the skin. Sometimes it may even be due to a sudden increase in the level of exercise or interest in some new sport. Once the cause has been identified it should be removed, or else the callus will exacerbate.

The foot should first be soaked in warm water with rock salt and commercially available liquid soap. After 10 minutes the affected area should be gently rubbed with a pumice stone or a foot scrubber. Some baby oil or moisturiser should then be applied. This gets rid of the corn (or callus) at an early stage.

If the callus is hard and the punctum or tip of the corn is easily visible, commercially advertised OTC (over the counter) corn plasters may be used. Most of them contain salicylic acid — a keratolytic agent that softens and breaks down hard skin. They need to be applied on a dry foot and left in place till the corn softens and falls out. They should not be used on soft corns between the toes.

Wearing loose footwear with low heels and a well-cushioned insole can also relieve the pain. Slippers should be made of soft rubber like MCR (micro cellular rubber). Acupressure slippers are also helpful.

If the corn does not respond to these simple measures, it has to be surgically removed. A qualified dermatologist or surgeon can do it as an outpatient office procedure.

Newer, relatively painless techniques involve freezing the corn with liquid nitrogen or dry ice or removing it with laser technology. It is dangerous to perform “home surgery” — slicing off the corn with a knife or blade. Dangerous debilitating infections can occur due to such amateur attempts.

Diabetics need to take particular care of their corns and calluses and consult their physicians if they have a problem. They may have compromised blood supply to their feet or numbness of the nerves. This may make them insensitive to the pain making them inadvertently ignore the corn. Any self-treatment (especially salicylic corn plasters) is likely to result in dangerous infection.

Some simple rules one should follow:

• Wear proper footwear and socks

• Wash the feet well at night before going to bed

• Moisturise the feet with oil or cream once a day

• Keep the areas between the toes dry, particularly after a bath

• Treat arthritis, blisters, corns and calluses promptly

Appropriate footwear for various sports should be used. One pair of “canvas” shoes should not be used for all activities.

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Sources: The Telegraph (Kolkata, India)

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Prolonged Lack of Sleep Affects Brain

 

Brain activity differs significantly in sleep-deprived and well-rested people, according to a new study that uses the latest imaging techniques.

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The study, by Singapore-based researchers, shows that the sleep-deprived experience periods of near-normal brain function – interspersed with severe drops in attention.

“The main finding is that the brain of the sleep-deprived individual is working normally sometimes, but intermittently suffers from something akin to power failure,” said Clifford Saper of Harvard University, an expert unaffiliated with the study.

Findings of the study have been published in the latest issue of The Journal of Neuroscience .

The research team, led by Michael Chee, used functional magnetic resonance imaging (fMRI) to measure brain blood flow in people who were either kept awake all night or allowed a good night’s sleep. Researchers tested the same participants in both conditions.

During imaging, participants did a task that required visual attention. Researchers showed them large letters composed of many smaller letters. Participants were asked to identify either the large or small letters and to indicate their responses by pushing a button.

Well-rested and sleep-deprived volunteers showed a range of reaction times. Those participants with the fastest responses, both in sleep-deprived and well-rested conditions, showed similar patterns of brain activity.

However, well-rested and sleep-deprived participants with the slowest responses – also called attentional lapses – showed different patterns of brain activity.

Previous research showed that attentional lapses normally induce activity in frontal and parietal regions of the brain, command centres that may compensate for lost focus by increasing attention.

However, during attentional lapses, Chee and colleagues found reduced activity in these brain command centres in sleep-deprived compared to well-rested volunteers. This finding suggests that sleep deprivation reduces the brain’s ability to compensate for lost focus.

Sleep-deprived people also showed reduced activity in brain regions involved in visual processing during attentional lapses.

Because the brain becomes less responsive to sensory stimuli during sleep, reduced activity in these regions suggests that, during attentional lapses, the sleep-deprived brain enters a sleep-like state.

You may click to see:->Lack of sleep can be fatal

Sources: The Times Of India

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Sedentary Life ‘Speeds Up Ageing’

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Leading a sedentary lifestyle may make us genetically old before our time, a study suggests.

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...There is now another good reason for regular exercise, say researchers.

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A study of twins found those who were physically active during their leisure time appeared biologically younger than their sedentary peers.

The researchers found key pieces of DNA called telomeres shortened more quickly in inactive people. It is thought that could signify faster cellular ageing.

The King’s College London study appears in Archives of Internal Medicine.

An active lifestyle has been linked to lower rates of cardiovascular disease, type 2 diabetes and cancer.

However, the latest research suggests that inactivity not only makes people more vulnerable to disease, but may actually speed up the ageing process itself.

The King’s team studied 2,401 white twins, asking them to fill out questionnaires on their level of physical activity, and taking a blood sample from which DNA was extracted.

They particularly focused on telomeres, the repeat sequences of DNA that sit on the ends of chromosomes, protecting them from damage.

As people age, their telomeres become shorter, leaving cells more susceptible to damage and death.

Examining white blood cells from the immune system in particular, the researchers found that, on average, telomeres lost 21 component parts – called nucleotides – every year.

But men and women who were less physically active in their leisure time had shorter leukocyte telomeres compared to those who were more active.

The average telomere length in those who took the least amount of exercise – 16 minutes of physical activity a week – was 200 nucleotides shorter than those who took the most exercise – 199 minutes of physical activity a week, such as running, tennis or aerobics.

The most active people had telomeres of a length comparable to those found in inactive people who were up to 10 years’ younger, on average.

Direct comparison of twins who had different levels of physical activity produced similar results.

Impact of stress

The researchers suggest that physically inactive people may be more vulnerable to the damage caused to cells by exposure to oxygen, and to inflammation.

Stress is also thought to have an impact on telomere length, and the researchers suggest people who exercise regularly may help to reduce their stress levels.

Writing in the journal, the researchers said: “Our results show that adults who partake in regular physical activity are biologically younger than sedentary individuals.

“This conclusion provides a powerful message that could be used by clinicians to promote the potential anti-ageing effect of regular exercise.”

In an accompanying editorial, Dr Jack Guralnik, of the US National Institute on Aging, said more work was needed to show a direct relationship between ageing and physical activity.

He said: “Persons who exercise are different from sedentary persons in many ways, and although certain variables were adjusted for in this analysis, many additional factors could be responsible for the biological differences between active and sedentary persons.

“Nevertheless, this article serves as one of many pieces of evidence that telomere length might be targeted in studying ageing outcomes.”

“This conclusion provides a powerful message that could be used by clinicians to promote the potential anti-ageing effect of regular exercise”
By King’s College London researchers

Sources: BBC NEWS,29TH. JAN’08

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