What's Hot

What's Hot

April 2001

What's Hot Archive

April 27, 2001

Elevated homocysteine associated with memory impairment in older indiviudals

May's American Journal of Clinical Nutrition reported the results of a study based on information obtained from the third National Health and Nutrition Examination Survey, which was conducted from 1991 to 1994. One thousand two hundred ninety-nine men and women sixty years of age and over of different ethnic backgrounds who had no history of stroke participated in the study. Serum concentrations of nutrients including folate, cholesterol and homocysteine were measured and test subjects were given delayed recall tests consisting of series of words and of a short paragraph. The analysis of test scores showed that 75% had perfect scores on the word delayed-recall test and 17.4 had perfect scores defined by recall of six important points on the paragraph delayed-recall test, yet low scores were rare for the latter.

After adjustment for age, sex, race, years of education, income and serum creatinine, when divided into two groups consisting of highest and lowest serum folate levels, study participants who were in the high serum folate group had the greatest recall of the paragraph's main ideas, and conversely participants with low folate had lower recall. Those with low folate status and high serum homocysteine concentrations had poorer recall than those in this group with lower homocysteine. Homocysteine levels were also inversely associated with the word-delayed recall scores. Although a relationship between low folate and poor memory could exist, the researchers' analysis found associations between elevated homocysteine and poor recall that were independent of folate status, indicating that homocysteine may have a direct effect. In participants with serum homocysteine levels greater than 13.7 mmol/Liter, test scores were similarly poor regardless of their folate status.

Diagnoses such as Alzheimer's disease and stroke-induced dementia have been associated with elevated homocysteine. This study shows that elevated homocysteine is associated with memory impairment without stroke.

—D Dye

 

April 25, 2001

Dried human cells brought back to life

In researched published in the April 21 2001 issue of New Scientist Magazine, scientists at the Virginia Tech Center for Genomics in Blacksburg, Virginia reported drying kidney cells and rehydrating them eight days later to observe half of cells resume normal reproduction. The technique, developed by researcher Malcolm Potts, is based on the observation of a cyanobacterium that can dry out and survive for centuries on rock surfaces by surrounding itself with a substance called glycan that protects cell membranes by forming a coating over the cells. Potts and colleague David Helm purified glycan and combined it with human kidney cells, then dried the cells at room temperature. After eight days, 50% of the cells recovered from drying and began dividing, a remarkable feat as human cells usually die within seconds when deprived of water. Potts announced at a Society for Experimental Biology meeting held this month in Canterbury, England, "It's a breakthrough. By applying the techniques we have found in cyanobacteria, we can dry out human cells. It's very exciting."

In a New Scientist article published last year, a researcher at the University of California, San Diego reported that human cells dried for five days had been revived, but the cells had to be first genetically modified to produce trehalose, a sugar that protects cells against freezing and drying from the inside. The newest technique utilized nonmodifed normal cells.

The technique may have many possible uses such as prolonged storage of blood products and enhanced shelf life for vaccines and antibodies. The Virginia Tech researchers hope that in the future tissues and organs could be dried and revived, but they don't believe that this will be achieved by the use glycan alone. Potts stated, "In the end it's bound to require a combination of different approaches."

—D Dye

 

April 23, 2001

Anticholinergic drugs associated with increased delirium

Anticholinergic (ACH) drugs are a group of medications that act in opposition to the cholinergic effects of the autonomic nervous system. They diminish the effect of the neurotransmitter acetylcholine, a hormone that facilitates the transmission of nervous impulses. Anticholinergics include the belladonna alkaloids such as atropine, hyoscyamien and scopalamine. They are used to relieve cramping of the intestines, bladder or stomach, to treat peptic ulcer, to prevent nausea and vomiting, and to help regulate heartbeat during surgery, among other uses. Research findings concerning anticholinergic drugs as a risk factor for delirium have been conflicting.

A study published in the April 23 2001 issue of Archives of Internal Medicine sought to evaluate the association between longterm ACH use and delirium symptoms. Two hundred seventy-eight hospital patients aged sixty-five and older who had been diagnosed with delirium were followed for up to three weeks and regularly assessed for the condition. Intake of anticholinergic and other drugs was measured for each day, and change in medication in the twenty-four hours prior to assessment for delirium was computed.

Forty-seven potentially anticholinergic medications were found to have been used by the study participants. After adjustment for other factors, an increase in the severity of delirium symptoms was significantly associated with several measures of anticholinergic medication use the previous day. The diagnosis of dementia in these patients did not modify the association between anticholinergic medication intake and the severity of delirium symptoms. The finding confirms anticholinergic drugs as one cause of delirium in older patients.

—D Dye

 

April 20, 2001

Alcohol-associated breast cancer risk nullified by folic acid

Although moderate amounts of alcohol consumption have been linked with a lower risk of heart disease, the risk of breast cancer among postmenopausal women who drink even moderately is higher than for nondrinkers. According to a new analysis conducted by Mayo Clinic researchers, consumption of only 400 micrograms folic acid by postmenopausal women who drink alcohol lowers their risk of breast cancer to that of women who abstain from drinking. The study, published in the May 2001 issue of Epidemiology, examined data obtained from dietary and medical questionnaires completed by the Iowa Women's Health Study cohort, consisting of 41,836 postmenopausal women who were followed for twelve years. One thousand five hundred eighty-six women in the study developed breast cancer.

The research, led by Thomas Sellers PhD, found that women whose folic acid intake was in the lowest tenth percentile and whose alcohol use was higher than the median of four grams per day experienced a 59% increased risk of breast cancer compared to women who abstained from drinking and whose folic acid intake was above 350 micrograms per day, slightly under the US RDA. But women who consumed over four grams of alcohol per day whose folic acid acid intake was the highest experienced the same risk of breast cancer as teetotalers.

Dr Sellers commented, "Recent surveys of the U.S. population show most people do not get adequate folate. Taking a multivitamin should help individuals meet the RDA - just check the label to ensure you're getting 100 percent of the requirement . . . Alcohol is metabolized to acetaldehyde, a known carcinogen. People who have adequate folate intake, however, may have a better capacity to repair DNA damage caused by acetaldehyde. This study adds to the growing body of evidence that if you have adequate folate, you are not increasing your risk of breast cancer by drinking in moderation."

—D Dye

 

April 18, 2001

Antisense therapy looking promising for brain tumors

In research published in the April 15 2001 issue of the Journal of Clinical Oncology, researchers at Jefferson Medical College treated twelve brain cancer patients with a DNA therapy called antisense, which blocks the type-1 insulin-like growth factor receptor (IGF-1R) leading to apoptosis (programmed cell death) and immune system stimulation. Because the IGF-1 receptor sends signals for the proliferation of cells, blocking the receptor has a beneficial effect on patients with cancerous tumors. The participants in this study had anaplastic astrocytoma or glioblastoma, both lethal forms of brain cancer. The majority of the patients in the Phase I trial experienced partial shrinkage of their tumors, while in two the tumors temporarily disappeared, although most have experienced relapses since their initial treatments.

Study coauthor, Renato Baserga MD commented, "The observation is quite remarkable and very unexpected. It's a one-two punch. We knew that targeting the IGF receptor induces apoptosis, but unexpectedly, it also induced a host immune response that strengthens the killing of tumor cells."

The study involved removal of the tumor, treatment of the cells outside the body with antisense to IGF-R1 and reimplantation in the patient's abdomen for twenty-four hours to allow the antisense to kill cancer cells through apoptosis. Research team member David W Andrews MD explained, "We think that when the cells die, they release factors, perhaps small peptides, that are directly cytotoxic to the tumor and at the same time, may be immunogenic. We have evidence that over time, a T-cell cellular immune response may be generated."

Although the researchers believe that the treatment has the potential to be used for other cancers, their research has been frustrated by a lack of availability of the antisense which must be manufactured according to strict FDA standards, and the requirement of more preclinical data by the FDA.

—D Dye

 

April 16, 2001

Vitamin C low in head trauma and intracerebral hemorrhage

Animal studies have shown that the damage that occurs with stroke or head injury is in large part caused by the production of reactive oxygen species and excess free radicals, unstable molecules that react with other molecules and damage tissue. Hemorrhage causes the release of heme-iron, which participates in free radical reactions that product reactive oxygen species. These peroxidize lipids, such as those found in the brain. This peroxidation may change the permeability and fluidity of brain cell membranes, which can damage cellular function.

In the present study, which sought to examine the formation of reactive oxygen species in humans by measuring antioxidant depletion, six female and seven male head trauma patients, and one woman and fourteen men with intracerebral hemorrhage were enrolled in the study within twenty-four hours of the onset of their injury. The patients as well as forty controls were examined via CT scan of the brain to determine the extent of injury and had blood samples drawn. Plasma concentrations of vitamin C, vitamin E, coenzyme Q10 and uric acid were determined by lab analysis. All of the patients with brain injuries had significantly lower vitamin C levels compared to the controls. Vitamin C levels in the head trauma and intracerebral hemorrhage patients were were inversely correlated with the diameter of the injury. No correlations were observed between antioxidant levels and smoking status, hypertension, calorie intake, diabetes, serum cholesterol and other factors.

The authors write that, consistent with animal findings, the study provides evidence of oxidative stress induced antioxidant (specifically vitamin C) depletion in head trauma and intracerebral hemorrhage. They note that vitamin C forms the first line of antioxidant defense and protects lipids from peroxidation, and that the effect of vitamin C supplementation on these types of patients remains to be studied.

—D Dye

 

April 13, 2001

Ginkgo and alpha-lipoic acid reduce stroke damage

A study published in the April 2001 issue of the American Heart Association journal Stroke reported the effects of two antioxidants, ginkgo biloba and alpha-lipoic acid, given to mice in whom ischemic strokes were experimentally induced. Ginkgo and lipoic acid are known to be reduce the formation of free radicals, as well as inhibiting platelet and white blood cell activation and adhesion, and improving cerebral blood flow, all of which could be beneficial to someone suffering from a stroke. Ginkgo and lipoic acid have also been shown to protect the brain in models of ischemia, the condition of lack of blood flow to an area that occurs during stroke or heart attack.

In a randomized trial of ginkgo, sixty mice received either a low oral dose of 50 mg per kilogram body weight, a high dose of 100 mg per kilogram body weight, or a placebo for a period of seven days. On the seventh day of the study, strokes were induced in the mice, followed by return of blood flow forty-five minutes later. After twenty-four hours the mice were evaluated and the volume of the infarct, or damaged area, was determined. In the study utilizing lipoic acid, twenty-four mice were injected with 100 mg per kilogram lipoic acid, or a placebo one and a half hours before stroke was induced.

Mice receiving lipoic acid and the low dose of ginkgo had signifcantly smaller infarcted areas than the mice that received the placebo. However, 10% of the mice receiving the high dose of ginkgo experienced areas of intracerebral hemorrhage within the infarct and this group had on average had infarct volumes comparable to the controls. The mice receiving lipoic acid had higher neurologic scores in addition to smaller infarct volumes compared to the placebo group.

Ginkgo and alpha-lipoic acid may be helpful for humans at risk of thrombotic stroke. Caution might be exercised when considering taking high doses of ginkgo by someone at risk for hemorrhagic stroke.

—D Dye

 

April 9, 2001

Probiotics help prevent allergies in infants

Atopic diseases such as atopic eczema, asthma and allergic rhinitis are appearing more frequently in children in developed countries, with various theories accounting for this increase. A randomized placebo-controlled trial published in the April 7 2001 issue of the journal, The Lancet demonstrated that probiotics given to pregnant two to four weeks before delivery and to infants for six months after birth helped prevent the development of atopic eczema in this group of children. Because proper gastrointestinal flora promote antiallergenic processes, the researchers in this study sought to determine whether they would help prevent allergies in children. Beneficial microflora have an antiallergic effect by promoting T-helper-1-type immunity, generating transforming growth factor, which helps suppress T-helper-2-induced allergic inflammation, and inducing IgA production which is a part of mucosal immune defense.

One hundred fifty-nine expectant mothers with a family history of ectopic disease were recruited from a Finnish community. Participants were randomized to receive capsules containing the probiotic Lactobacillus rhamnosis or a capsules containing a placebo (microcrystalline cellulose). After delivery, breastfeeding women continued the supplements, and the children of those not breastfeeding received the supplement mixed with water. Children were examined at three, six, twelve, eighteen and twenty-four months. By twenty-four months, forty-six children were diagnosed with atopic eczema. The group receiving the probiotic supplement was found to have half the rate of atopic eczema as the placebo group.

The researchers note that a decrease in the ratio of beneficial bifidobacteria to clostridia in early life precedes the development of atopic disease. They suggest that gut microflora have unexplored immunomodulatory properties which may prove to be vital in combatting the frequency of atopic disease and possibly other immunological diseases.

—D Dye

 

April 6, 2001

Vitamin A augments interferon in human cells

Research conducted at Penn State University has revealed that the active form of vitamin A plays a role in immune response by enhancing the effect of interferon. Interferon is an immune system regulator and one of the body's defense chemicals.

Modified forms of interferon are used to treat autoimmune diseases such as multiple sclerosis, arthritis and chronic inflammation, and maintaining adequate vitamin A levels may enhance the effectiveness of these forms of interferon. In the research reported at the Experimental Biology 2001 conference in Orlando Florida this week, human macrophages, which are immune system cells that mediate the inflammatory response and also lead to antibody production, were stimulated in the presence of sufficient vitamin and in vitamin A deficient conditions. Vitamin A led to increased interferon activity.

Research team leader Dr. Catharine Ross, of Penn State's College of Health and Human Development, commented, "There are quite a few animal studies that show that vitamin A deficiency affects inflammation and the immune system's response. These new data from experiments with human cells suggest that vitamin A augments natural interferon's regulatory response. Less interferon may be necessary when the active form of vitamin A is adequate."

The research demonstrated as well that vitamin A can inhibit tumor necrosis factor and other immune and inflammatory mediators. "We're looking at these basic cellular processes in order to understand the mechanisms of productive immune responses and to try to find ways to control the pathologic responses. While these basic studies are not targeted at specific diseases, they do shed light on the underlying disease processes," stated Dr Ross.

—D Dye

 

April 4, 2001

Vitamin D supplements may suppress multiple sclerosis

The Experimental Biology 2001 Conference held in Orlando, Florida, was the site of a presentation this week of a paper reporting the results of a study in which 1000 iu vitamin D given to multiple sclerosis patients appeared to increase transforming growth factor beta-1, which is associated with suppression of the immune response that produces MS symptoms. Interleukin-2, which is associated with the cells that induce the disease, was also found to be lower.

Study coauthor Dr Margherita Cantorna, Assistant Professor of Nutrition at Penn State, had conducted prior research at the University of Wisconsin on mice susceptible to MS which demonstrated that vitamin D supplementation could prevent the development of the disease. Dr Cantorna and others have hypothesized that lower levels of sunlight received by individuals living at higher latitudes may be a factor in the development of the disease, possibly because of less production of vitamin D within the skin that occurs. The incidence of multiple sclerosis is almost zero at the equator, and increases in both hemispheres with higher latitudes. The current study sought to determine if the positive changes occurring in mice who received vitamin D supplements would also occur in humans. Although not in progress long enough to observe a remission in the disease's clinical symptoms, the changes in blood chemistry observed may indicate positive benefits for MS patients.

Dr Cantorna stated, "I think that if you are an MS patient, it would be best to continue to follow your personal physician's advice. On the other hand, since adequate amounts of vitamin D are difficult to get from diet and because MS patients often have to stay out of the sun, they might want to consider taking a vitamin D supplement at the current recommended daily requirement level. There are potential benefits for bone health and for the immune system as well."

—D Dye

 

April 2, 2001

Human genome project results reveal new tumor suppressor gene

The April 2001 issue of Nature Genetics published the findings of the National Human Genome Research Institute and the M.D. Anderson Cancer Center at the University of Texas of a new tumor suppressor gene that is likely to be involved in prostate, breast and other cancers. When tumor suppressor genes are inactivated, cells grow out of control and become cancer. The gene, named ST7, for "suppression of tumorigenicity (on chromosome) 7" is expressed throughout normal tissue but is frequently mutated or deleted in epithelial tumors, such as colon, ovary, breast and prostate cancers. Although thirty tumor suppressor genes have so far been identified, this is the first discovered single-handedly by a researcher, Jean Claude Zenklusen, Ph.D, utilizing the results of the human genome project.

Dr Zenklusen, who is the lead author of the study, found defects in ST7 in breast and colon cancer cells. By inserting a normal copy of the gene into tumor cells with defective ST7, the cancer cells were unable to produce tumors in mice. The gene may work by inhibiting angiogenesis, the process by which tumors grow new blood vessels which enables them to grow and metastasize. Dr Zenklusen commented, "If ST7 is involved in regulating angiogenesis, it may prove to be a target for developing drugs that would interfere with that process. Without an adequate blood supply, a tumor withers away and dies. So theoretically, if you could prevent angiogenesis, you might be able to come up with a way to kill the tumor without harming the patient."

Study coauthor Eric Green, MD PhD, Chief of the Genome Technology Branch in the National Human Genome Research Institute Division of Intramural Research stated, "Inactivating a tumor suppressor gene is like disabling the brakes on a car. Without the function of such a gene, a tumor keeps growing out of control. And just like a car without brakes, the consequences can be fatal."

—D Dye

 

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