Thursday, November 30, 2006

Adenosine, Caffeine and Sleep

Coffee keeps me awake but how? Researchers at the University of Texas Southwestern Medical Center at Dallas may have found out the reason. In the Biocompare article, Overworked Brains Release Adenosine To Slow Cells, Trigger Sleep, UT Southwestern Researchers Find, a biochemcial explanation may be at hand. When the brain is hard at work a substance known as adenosine is released. Adenosine is a nucleoside; an essential biochemical found in DNA and in an essential energy conferring compound known as adenosine triposphate. Adenosine is also used in other bodily functions.

Caffeine has the capacity to block adenosine and its sleep inducing effects. The implications for insomnia and other sleep disorders is promising although there may be much more to these problems than adenosine. As the article states: "Coffee and tea are blocking the link between the prolonged neural activity of waking and increased levels of adenosine in cells, which is why they prevent us from getting drowsy."

Preventing Cancer with Onions and Garlic

Onions and Garlic May Prevent Cancers Study Shows Eating Lots of the Pungent Herbs May Keep Certain Types of Cancer at Bay indicates that research results support the claim that consuming lots of these or other alliums may lower the risk for all sorts of cancers with the exception of breast and prostate cancers.

Results appeared in the American Journal of Clinical Nutrition.

Tuesday, November 21, 2006

Antioxident Pain Killers

An Ohio State University news release 'ANTIOXIDANTS: NEW KID ON THE BLOCK FOR PAIN RELIEF?' details research findings indicating that currently used pain killers such as morphine may eventually be replaced by antioxident-based pain killers.

Antioxidents neutralize free radicals; substances that can cause damage to cells. Free radicals are an inevitable by-product of metabolic activity and are therefore found in all organisms. In healthy individuals the body's natural protective mechanisms keep harmful effects of free radicals in check. However, when their effects overwhelm bodily defenses, disease or cancer can result.

An additional effect of free radicals may be chronic pain. There is experimental evidence that mice and other rodents have experienced pain relief because of antioxidents. The reason is likely linked to a capacity of antioxidents to break down free radicals.

Sunday, November 19, 2006

Fighting Cancer with "Smart Drugs"

Treatments associated with cancer can have some very unpleasant side effects. Chemotherapy and radiation treatement can kill cancer cells but at the expense of much collateral damage to normal cells. Researchers at Massachusetts General Hospital Cancer Center are trying to remedy this problem with an approach that targets molecules of cancer cells, found in lung and other thoracic cancers, which enable their proliferation. An article called 'The New Strategy: ‘Smart Drugs’ for Specific Lung Cancers' details the specifics.

In addition to eliminating some side effects, the "smart drugs" that are directed at molecular targets of cancer cells, have the potential to be more effective at fighting the cancer itself. One such molecular target is known as epidermal growth factor receptor (EGFR). This protein's function involves the regulation of the growth of cells. It is found on the surface of cancer cells and receives extra-cellular signals. The disruption of normal cellular regulatory functions is frequently associated with cancer. A strategy that entails the inhibition of EGFR offers the possibility of halting the growth of cancer cells.

Iressa is a drug that is utilized in this EGFR inhibition strategy. The drug has had limited beneficial effects for some patients with lung cancer. These tend to be mostly women who have never smoked. The article notes that there is a particular mutation that has significance with regard to patient responsiveness to Iressa. This mutation, affecting the EGFR receptor, made patients having the mutation, better able to benefit from Iressa.

Friday, November 10, 2006

Moles and Skin Cancer

'Why don’t all moles progress to melanoma?' is the questioned posed and answered by this study referred to by the linked news release.

The news release cites the fact that moles are found on everyone but are generally only a cosmetic nuisance. Sometimes though, abnormal cell division leads to cancer. According to the article one in 65 Americans contracts skin cancer during their lifetime. But what triggers skin cancer also known as melanoma?

Mutations, that are cancer causing, exist in nine out of ten moles according to the article and three out of ten melanomas start in a mole. Yet it has been apparent that something inhibits the development of cancer in moles. The inhibiting mechanism is associated with a cellular organelle known as the endoplasmic reticulum of which there are two types: the rough endoplasmic reticulum and the smooth endoplasmic reticulum.

Like all mechanisms cellular mechanisms can malfunction. Amino acid chains in an endoplasmic reticulum, which are folded to specific functional shapes by other proteins known as chaperones, can at times accumulate too quickly and overload the system. This in turn can be lethal to the cell containing the ER.

The article reveals that in response the ER is able to send out signals initiating what is known as the UPR or unfolded protein response. If this works protein production can be adjusted so that the backlog is eliminated. If this fails the ER can initiate a process known as apoptosis which results in cellular suicide.

Researchers have found that the ER can sense oncogene activity and respond with a strategy that prevents malignant cell transformation. The strategy involves stopping the cell cycle thus preventing cell division. The cells live but do not proliferate.

Together with apoptosis this cellular defense mechanism helps ensure that moles do not become melanomas. In most cases the strategy is successful.

Balancing Two Proteins in Skin Cancer

An article is found online in Science Daily entitled 'Signal Protein Shows Promise For Blocking Tumor Promoters In Skin Cells.' It refers to two proteins involved in signaling pathways which control cellular differentiation and growth. The relationship between the two proteins offers potential new treatment for skin cancer.

According to the article a protein named Srcasm has a functional relationship to another protein known as Src. Their numerical relationship appears to be an inversely related one. High quantities of Src seem to be accompanied by low levels of Srcasm. When levels of Srcasm are elevated the amount of Src decreases. Src kinases are a family of enzymes that can promote tumor formation. In most skin cancers and other carcinomas, like colon and breast cancer, levels of Src are found to be elevated while levels of Srcasm are low. Research indicates that Srcasm can reduce levels of Src kinases in cells.

A contemplated strategy to treat skin cancer entails utilizing an adenovirus as a carrier of a gene, that when introduced into skin cells, can code for the protein Srcasm. The next research step involves an attempt to determine if Srcasm can reverse skin tumor formation.