Colon cancer in aged primates - Full source: American Journal of Primatology, 1998, Vol 44, Iss 1, pp 19-27
The age-related incidence of colon cancer was surveyed from a total of 301 necropsy cases of rhesus monkeys ranging in age from 13-37 years performed at the Wisconsin Regional Primate Research Center during the past 15 years. The monkeys lived in indoor cages and were fed with monkey chow and supplemental fruits. The survey found a total of 51 malignant tumors, and among them 25 cases were colon cancer. The incidence of colon cancer increased with advancing age: 3.2% increase at 13-19 years, 9.2% increase at 20-25 years, 13.5% increase at 26-29 years, and 20.7% increase at 30-37 years. Most cancers were located in the cecum (first part of large intestine near colon). Precancerous polypous lesions were not found in all cases. However, all cases had local invasion to the muscular wall. Cancer had spread to the lymph nodes in only two cases. As in humans, colon cancer is a common outcome of aging in nonhuman primates.
Aging and the brain: A new frontier - Full source: Annals of Neurology, 1997, Vol 42, Iss 6, pp 819-828
The brain as is particularly vulnerable to age-related changes (ARCs), and senescence is by far the most powerful risk factor for neurological diseases of the elderly such as Alzheimer's disease. As we study the biology of ARCs, the concept of senescence as an unalterable result of the passage of time is beginning to change. Both individual and species differences in longevity illustrate the variable effects of time. Whereas human life expectancy has been extended by prevention and treatment of specific diseases, life span can be altered by modifying the processes producing ARCs. Models of prolonged life span including modifications of longevity genes and restricted caloric intake demonstrate the feasibility of extending longevity throughout the evolutionary development of species. Both programmed (genetic) and variable factors produce ARCs. Cell survival depends on a balance of opposing factors- cancer gene and anti-cancer gene products, cyclins, growth factors, etc.; cell death results when the balance shifts. Variable factors, including accumulation of oxygen free radicals, protein conformational changes, and secondary loss of mitochondrial (specialized cell organelle) energy production, can also result in neuronal degeneration. To prevent the increased neuronal vulnerability of senescence, ARCs must be modified. The "new frontier" in neurology is the challenge of understanding the changes of aging, both to determine their impact on disease and to prevent their consequences.
Folic acid and memory improvement - Full source: Archives of Gerontology and Geriatrics, 1997, Vol 26, Iss 1, pp 1-13
The specific role of low folic acid levels in the physiopathology of dementia is still under debate. However, a growing consensus is emerging in the literature where low folate as well as cobalamin levels in aged patients with cognitive deficits are being considered as a sign of functional problems in the absorption and utilization of vitamins, and not merely as a sign of bad eating habits. The results of a majority of investigations indicated that folate treatment was effective in lessening cognitive deficits. Results from this study demonstrated that patients treated with folic acid for 60 days showed a significant improvement on both memory and attention efficiency when compared with a placebo group.
Mechanism and prevention of Alzheimer's disease - Full source: Brain Research, 1997, Vol 776, Iss 1-2, pp 40-50
In Alzheimer's disease, neurotoxic starch-like constituents of protein called beta-amyloid peptides cause a harmful inflow of calcium ions into neurons. This increase in calcium ions is expected to trigger intracellular events that eventually cause cell dysfunction and cell death. The findings indicate a very early molecular event in the neurotoxicity of Alzheimer's disease occurs. To combat the neurotoxic effect of aggregated beta-amyloid peptides, a series of very short antagonistic peptides have been devised. Using a library of hexapeptides (protein formation) made from amino acids, these so-called "decoy" peptides were selected by their ability to complex with the tagged beta-amyloid peptide and are able to abolish the calcium inflow caused by aggregated beta-amyloid peptides, and thus prevent cell dysfunction and cell death.
Effect of GH on bone metabolism - Full source Calcified Tissue International, 1998, Vol 62, Iss 1, pp 40-46
Reduced bone mineral density (BMD) and the prevalence for osteoporosis are symptoms of growth hormone deficiency (GHD) syndrome. GH replacement therapy is now available for GH-deficient adults. This study investigated the long-term effects of GH replacement therapy on (BMD) and bone metabolism in 19 adult patients with GHD over a period of 18 months. The initially decreased IGF-I (insulin growth factor) concentrations rose significantly during 18 months of therapy to levels within the normal range. Parameters of bone formation showed a significant increase in the first 6 months of therapy, followed by a slight decrease in the next months. Markers of bone resorption also increased significantly with a peak value after 6 months and remained above baseline values after 18 months. BMD of the neck bone showed an increase after 18 months of therapy. However, the increase in BMD was significant only in the lumbar spine. It was concluded that GH replacement therapy in adult patients with GHD causes a pronounced increase in bone turnover and increases BMD of the lumbar spine and the femoral neck.
Approaches to the prevention and control of skin cancer - Full source: Cancer and Metastasis Reviews, 1997, Vol 16, Iss 3-4, pp 309-327
Skin dancer is the most common and the most preventable form of cancer. Nonmelanoma skin cancers are associated with cumulative exposure to ultraviolet radiation, while melanoma is associated with intense episodes of ultraviolet exposure resulting in sunburns. The risk factors are associated with the development of skin cancer include: exposure to ultraviolet radiation; genetic factors such as skin type, eye and hair color, tendency to burn and tan, and having freckles and moles; a personal or family history of skin cancer; and occupational sun exposure. Primary prevention behaviors include applying SPF 15+ sunscreen 30 minutes before exposure, reapplying SPF 15+ sunscreen every 1 1/2, to 2 hours or after swimming or sweating, dressing in protective clothing, using shade, limiting exposure during peak sun hours, and avoiding artificial sources of-ultraviolet radiation such as tanning beds. While skin cancer screenings have shown promising results, few studies have a follow-up component. Future studies should focus on developing effective strategies for making sun protective behaviors routine and determining the effectiveness of skin cancer screening.
Alcohol's effect on the blood - Full source: Clinica Chimica Acta, 1997, Vol 266, Iss 2, pp 141-147
The oxidative effect of alcohol on lipid peroxidation and antioxidant enzymes such as superoxide dismutase, glutathione peroxidase and plasma gamma-glutamyl transferase (GGT) levels of plasma of red and white blood cells was investigated in 36 healthy non-drinkers and 72 alcohol drinkers. Red blood cell lipid peroxidation of the drinkers was significantly reduced compared to that of controls. Plasma GGT level was significantly increased. Also, there was a significant correlation between serum GGT level and the amount of alcohol. There were no significant differences between all the other parameters of both groups. Reduced lipid peroxidation of red blood cells without any accompanying increase in the activities of antioxidant enzymes indicates an alteration in lipid composition of red blood cell membranes might be responsible due to the alcohol.
Diet and the prevention of cancer - Cancer and Metastasis Reviews, 1997, Vol 16, Iss 3-4, pp 357-376
Cancer ranks as the second-leading cause of death in developed countries and diet has long been suspected as playing a prominent role in its cause. As a result, a substantial amount of research has been devoted to this field of study. This study identified specific nutrients, foods, or combination of these that are causally related to the development of cancer. In the full abstract, they examined the growing body of evidence on dietary causal factors and explored the practical prospects for prevention of cancer overall.
Green tea induces cancer cell death - Journal of the National Cancer Institute, 1997, Vol 89, Iss 24, pp 1881-1886
The polyphenolic compounds present in green tea show cancer chemopreventive effects in many animal tumor models. This study investigated the effect of green tea polyphenols and the major constituent, epigallocatechin-3-gallate, on the induction of apoptosis (programmed cell death) and regulation of cell cycle in human and mouse cancer cells. Treatment of cancer cells with green tea polyphenols and its components resulted in the formation of internucleosomal DNA fragments, characteristic of apoptosis (programmed cell death). Hence, green tea may protect against cancer by causing cell cycle arrest and inducing apoptosis. It needs to be evaluated in human trials.
Adsorption of mutagens to chlorophyllin-chitosan, an insoluble form of chlorophyllin - Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis, 1997, Vol 381, Iss 2, pp 243-249
Chlorophyllin, a water soluble derivative of chlorophyll, is known to suppress the mutagenic and carcinogenic actions of compounds such as aflatoxin. This study observed that chlorophyllin can form an insoluble salt-like material when mixed with chitosan, a polyglucosamine, and that the solid chlorophyllin-chitosan can efficiently trap mutagenic compounds. The adsorbed polycyclic mutagens became purified with buffers of acidic pH. Thus the mixture of Chlorophyllin-chitosan may be expected to be useful as an intercepting agent against polycyclic mutagens and carcinogens.
Dietary fatty acids and prostate cancer - Nutrition and Cancer - an International Journal, 1997, Vol 29, Iss 2, pp 114-119
This study examined the effects of unsaturated fatty acids on human prostate cancer cell growth in nude mice. In Experiment 1, groups of 25 mice were fed 23% fat diets containing 18% corn oil, 5% linseed oil, and 18% menhaden oil. Seven days later they were injected with prostate cancer cells. The diets were continued for six weeks. There was a 30% reduction in tumor growth in the 18% menhaden oil group. The tumor phospholipid fatty acid patterns suggested that the tumor inhibitory effect of the high menhaden oil diet was due, at least in part, to a reduction of arachidonic acid available for prostaglandin biosynthesis. In Experiment 2, groups of 25 mice were injected with prostate cancer cells directly into the prostate gland and fed a high-fat linoleic acid rich, or a low-fat diet for 10 weeks. All but 7 of the 50 mice had developed large macroscopic tumor. However, the mean tumor weight in the high-fat group was twice that in the low-fat group. This shows that a stimulatory effect of dietary fatty acids on prostate cancer cell growth may work on an initial tumor cell mass.
Prevention of photoimmunosuppression and photocarcinogenesis by topical nicotinamide - Nutrition and Cancer - an International Journal, 1997, Vol 29, Iss 2, pp 157-162
Ultraviolet (UV) B irradiation leads to a potent immunosuppression of the capacity to reject tumors. If this immunosuppression is critical for the development of most skin tumors, then its prevention should result in prevention of photocarcinogenesis. D,L-alpha-tocopherol, tannic acid, or alpha-difluoromethylornithine has shown a correlation between the inhibition of photoimmunosuppression and prevention of photocarcinogenesis. Treatment of UV-irradiated mice with 40 mu mol of nicotinamide twice weekly starting two weeks before UV irradiation and throughout the experiment prevented this immunosuppression. UVB irradiation consisted of five weekly 30-minute exposures to banks of six FS40 Westinghouse fluorescent sunlamps. Application of nicotinamide to UV-irradiated mice reduced skin tumor incidence from 75% to 42.5%. Thus topical nicotinamide prevented the immunosuppression and skin tumor-induction created by UVB irradiation.
Dietary change as a strategy for preventing cancer - Full source: Cancer and Metastasis Reviews, 1997, Vol 16, Iss 3-4, pp 377-392
Diet and cancer hypotheses correspond to one of two conceptual approaches to 'diet': 1) focus on specific nutrients and other chemical constituents of food; and 2) emphasis on the action of whole foods or food patterns. Four types of scientific investigation are available for advancing our understanding of diet and cancer: animal experiments, human metabolic (clinical nutrition) studies, observational relationships-of various factors determining the frequency and distribution of diseases, studies, and randomized, controlled trials. Considerable attention is now being paid to the joint action of dietary factors and 'susceptibility' genes. The full abstract considers the extent to which dietary change can be considered a realistic strategy for preventing major cancers - those of the lung, breast, prostate, and colorectum.
Do nutritional supplements lower the risk of stroke or hypertension? - Full source: Epidemiology, 1998, Vol 9, Iss 1, pp 9-15
Between 1986 and 1991, 29,584 persons rook part in a randomized nutritional intervention trial in Linxian, China. The area residents had chronically low intakes of several nutrients and high rates of esophageal and gastric cardia cancer as well as stroke. Individuals were randomized to one of eight groups which received combinations of four supplements: 1) retinol and zinc (factor A); 2) riboflavin and niacin (factor B); 3) vitamin C and molybdenum (factor C); 4) and beta-carotene, alpha-tocopherol (vitamin E), and selenium (factor D). Participants who received factor D had reductions in total mortality (9%) and total cancer mortality (13%). These individuals also had the largest reduction in stroke mortality of (95%). Hypertension, however, was not less prevalent among those receiving factor D. These findings contrast with the larger reductions in stroke death and hypertension found in a parallel trial of Linxian subjects with esophageal dysplasia who received a multivitamin/mineral supplement. However, this suggests that the effects were largely derived from nutrients other than those received in the present study.
Antioxidative effect of melatonin in the brain oxidative stress induced by adriamycin - Journal of Physiology and Biochemistry, 1997, Vol 53, Iss 3, pp 301-305
A single high adriamycin (AD, an antibiotic) dose (designed to cause oxidative stress) (25 mg/kg) was administered to the rat brain. Melatonin was injected daily three days before and after oxidative stress induction. Melatonin prevented significant lipoperoxide increase in plasma, hypothalamus and brain cortex. CAT activity which was decreased in hypothalamus by AD, increased by simultaneous melatonin administration. These results, especially those concerning lipoperoxide content changes, showed a powerful antioxidative effect of melatonin at both neural and extraneural levels in rats. CAT changes in the presence of melatonin suggest that there is a relationship between a scavenger role of the pineal hormone and a high oxidative activity in the brain hypothalamy area. When these results are taken together, they also show that melatonin, besides, producing the extraneural effect, can act as a powerful antioxidative agent in organs such as the brain, very rich in lipid susceptible to oxidation in the neuronal as well as the extraneuronal tissues. - Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis, 1997, Vol 381, Iss 2, pp 243-249
Chlorophyllin, a water soluble derivative of chlorophyll, is known to suppress the mutagenic and carcinogenic actions of compounds such as aflatoxin. This study observed that chlorophyllin can form an insoluble salt-like material when mixed with chitosan, a polyglucosamine, and that the solid chlorophyllin-chitosan can efficiently trap mutagenic compounds. The adsorbed polycyclic mutagens became purified with buffers of acidic pH. Thus the mixture of Chlorophyllin-chitosan may be expected to be useful as an intercepting agent against polycyclic mutagens and carcinogens.
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