As far back as the 5^th century BC the Greek physician Hippocrates wrote about the use of a bitter powder extracted from willow bark that reduced fevers and eased aches and pains. Native Americans also used an infusion of willow bark for similar purposes. What was this remarkable "healing" principle within the bark that relieved disease?

Known as salicylic acid (from the Latin salix, willow tree), this pain-killing compound is widely distributed throughout plants, where it functions as a hormone. The more vegetables and fruits you consume, the more likely you are to have a physiologically significant concentration of salicylic acid in your blood.

This is why, for instance, vegans and vegetarians generally have higher levels than most grain- and meat-based consumers. [1]

The chemical acetyl-salicylic acid, commonly known as aspirin, is a synthetic form of salicylic acid, a compound which is formed when salicin, a bitter compound naturally found within plants like white willow bark, is broken down within the human body.

Salicylic acid can also be synthesized endogenously from benzoic acid, and its urinary metabolite, salicyluric acid, has been found to overlap levels in patients on low-dose aspirin regimens. Cell research indicates that salicylic acid compounds (known as salicyclates) actually compare surprisingly well to aspirin in reducing inflammatory activity.[2]

While salicylic acid is found naturally in plants as salicylates, acetyl-salicylic acid does not exist in nature, is not formed as byproduct of natural salicylate consumption,[3] and is produced only through industrial synthesis. For example, this is one method of synthesis:

Acetylsalicylic acid is prepared by reacting acetic anhydride with salicylic acid at a temperature of <90 deg C either in a solvent (e.g., acetic acid or aromatic, acyclic, or chlorinated hydrocarbons) or by the addition of catalysts such as acids or tertiary amines."[4]

Also, the chemical modification of natural salicylic acid with an acetyl group results in the acetylation of hemoglobin,[5] essentially chemically altering the natural structure-function of our red blood cells and subsequent hemodynamics. In essence, aspirin, a semi-synthetic compound, makes the blood tissue itself semi-synthetic.

Three quarters of the cotton clothes bought in Britain today are made from a genetically modified crop, according to experts, including items available in major High Street stores.

The so-called 'franken frocks' will not harm the health of the person wearing the GM cotton but many feel that the public has not been consulted about the long term implications on the environment.

Simon Ferringo, the author of a new book exposing the realities of the industry, explained that while only 12 countries grow GM they account for most of the world's production.

In India up to 90 per cent of the crop is now genetically engineered to be resistant to certain pests. In China and the US it is also GM.

"There is no breakdown of GM or non-GM cotton use in the UK, but as an importer of finished textiles from regions where cotton is mostly GM, it is assumed up to ¾ is from GM seeds," he said.

Caffeine consumption could help to ease cognitive decline and lower the risks of developing Alzheimer's disease by blocking inflammation in the brain, suggest researchers.

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Consumption of coffee could be cheap and safe way to help to speed up and improve the bowel functions of people after surgery, according to new data.

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Scientists studying a rare genetic disorder have identified a molecular pathway that may play a role in schizophrenia, according to new research in the Oct. 10 issue of The Journal of Neuroscience. The findings may one day guide researchers to new treatment options for people with schizophrenia -- a devastating disease that affects approximately 1 percent of the world's population.

Schizophrenia is characterized by a multitude of symptoms, including hallucinations, social withdrawal, and learning and memory deficits, which usually appear during late adolescence or early adulthood. Efforts to identify disease causes have been complicated by the fact that no single genetic mutation is strongly associated with the disease. By studying a rare genetic disorder that increases the risk of schizophrenia, Laurie Earls, PhD, and colleagues in the laboratory of Stanislav Zakharenko, MD, PhD, at St. Jude Children's Research Hospital identified molecular changes that affect memory and are also present in people with schizophrenia.

Approximately 30 percent of people with a genetic disorder known as 22q11 deletion syndrome develop schizophrenia, making it one of the strongest risk factors for the disease. In previous studies of mice with the 22q11 deletion, Zakharenko's group identified changes in nerve cells leading to deficits in the hippocampus -- the brain's learning and memory center -- that appear with age. In the current study, the group confirmed similar molecular changes occur in people with schizophrenia. They also zeroed in on the gene contributing to the nerve cell changes.

A new study reinforces the finding that a region of the genome involved in immune system function, called the major histocompatibility complex (MHC), is involved in the genetic susceptibility to schizophrenia.

Schizophrenia is among the most disabling psychiatric disorders. Approximately 80% of the risk for developing schizophrenia is heritable, but there has been slow progress in identifying genetic variation that contributes to the risk for schizophrenia.

The current paper contributes to this growing literature by identifying variants of genes that influence the function of the immune system which may contribute to the heritable risk for schizophrenia.

Two large, international, collaborating groups of scientists -- the Wellcome Trust Case Control Consortium 2 and the Irish Schizophrenia Genomics Consortium -- conducted this new study.

They first performed what is called a discovery scan, where they analyzed over 6 million genetic variants in schizophrenia patients and controls from Ireland. This allowed them to compile a list of variants that showed the strongest association signals with schizophrenia.

The speed and degree to which the pupil of the eye responds is a standard test for alertness. It has also been used to assess how sleepy or exhausted a person is. Now, research to be published in the International Journal of Bioinformatics Research and Applications suggests that measuring pupil response alone is not enough and that a person's rate of blinking should also be incorporated to obtain a more precise measure of alertness.

The work could be important in the care of people with multiple sclerosis and other conditions. It might also be automated and ultimately used to automatically monitor patients, drivers, pilots, machine operators or others.

Minoru Nakayama of the Tokyo Institute of Technology and colleagues at Aichi Medical University point out that how the pupil of the eye dilates and contracts can be a useful way to measure alertness, but tests have demonstrated that the precise response of the pupil does not correlate well with the actual degree of sleepiness before any other signs become apparent. They point out that blinking subtly affects pupil response and have now developed a new approach that combines pupillography with blinking assessment.

The approach could side-step subjective assessment by healthcare workers in clinical situations. Moreover, it could be developed into an early-warning system to reduce workplace, road and other accidents by alerting operators and drivers to their level of alertness before sleepiness impinges on their behavior.

Researchers at Western University have created a mouse model that reproduces some of the chemical changes in the brain that occur with Alzheimer's, shedding new light on this devastating disease. Marco Prado, Vania Prado and their colleagues at the Schulich School of Medicine & Dentistry's Robarts Research Institute, looked at changes related to a neurotransmitter or chemical messenger, named acetylcholine (ACh), and the kinds of memory problems associated with it.

The research is now published online by PNAS.

The researchers, including first author Amanda Martyn, created a mouse line that doesn't have enough ACh being secreted by neurons in the same brain regions affected by Alzheimer's disease. They found this neurochemical failure caused problems with spatial memory, the stored information that is needed for navigating one's environment. For instance, the memory needed to drive across town. They also found the reduction of ACh led to hyperactivity, which many patients with Alzheimer's experience.

Incredible, groundbreaking new research just published in the Journal of the Medical Association of Thailand found that the primary polyphenol in turmeric - curcumin - is able to repair and even regenerate the liver tissues in diabetic rats.

Researchers at the Srinakharinwirot University in Bangkok administered curcumin to rats afflicted with diabetes and whose livers demonstrated the characteristic pathology and destruction of tissues and microvasculature. The curcumin was able to trigger a significant reversal of the condition.

"Fascinatingly, liver microvasculature in curcumin treated group developed into regenerate and repair into healthy and normal characteristics," the research team said, in its findings. "These results optimistically demonstrated the potential use of curcumin as a novel therapeutic agent in liver pathology of diabetic rats."

Researchers at Mount Sinai School of Medicine have shown for the first time in an animal model that vitamin C actively protects against osteoporosis, a disease affecting large numbers of elderly women and men in which bones become brittle and can fracture. The findings are published in the October 8 online edition of PLoS ONE.

"This study has profound public health implications, and is well worth exploring for its therapeutic potential in people," said lead researcher Mone Zaidi, MD, Professor of Medicine (Endocrinology, Diabetes and Bone Disease, and of Structural and Chemical Biology, and Director of the Mount Sinai Bone Program.

"The medical world has known for some time that low amounts of vitamin C can cause scurvy and brittle bones, and that higher vitamin C intake is associated with higher bone mass in humans, "said Dr. Zaidi. "What this study shows is that large doses of vitamin C, when ingested orally by mice, actively stimulate bone formation to protect the skeleton. It does this by inducing osteoblasts, or premature bone cells, to differentiate into mature, mineralizing specialty cells."