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Interferon research abs 1 || Hemoglobin research abs || Stem cell research abs || Nucleic acid research abs || Herpes research abs || Bronchitis research abs || Schizophrenia research abs || Tuberculosis research abs || Pneumonia research abs || Constipation research abs || Laxative research abs || hair research abs || hair related research references || testosterone related research references || melanin related research references || nicotine related research references





columbia.edu

BACKGROUND AND PURPOSE: Cigarette smoking is a risk factor for the formation and rupture of intracranial aneurysms. Few studies have examined predictors of resumption of cigarette smoking after a first episode of subarachnoid hemorrhage (SAH). METHODS: Of 620 SAH patients treated between July 1996 and November 2002, we prospectively evaluated continued cigarette use in 152 smokers alive at 3 months. Univariate and multivariate logistic regression analyses were used to identify potential demographic, social, and clinical predictors of continued cigarette use, defined as smoking > or =1 cigarette per week in the month before follow-up. RESULTS: Thirty-seven percent (56 of 152) resumed smoking after their SAH. Patients who continued smoking were younger, were more often black, had begun smoking at an earlier age, and had a higher frequency of prior alcohol or cocaine use and self-reported depression or anxiety than those who quit (all P<0.05). Smoking at < or =16 years of age (odds ratio [OR], 5.88; 95% confidence interval [CI], 2.33 to 14.29), self-reported depression (OR, 5.29; 95% CI, 2.10 to 13.35), and prior alcohol use (OR, 4.51; 95% CI, 1.45 to 14.05) independently predicted continued cigarette use. Smokers had a functional outcome similar to that of nonsmokers at 3 months but were more likely to resume alcohol consumption (OR, 3.88; 95% CI, 1.91 to 7.88). CONCLUSIONS: More than one third of prior smokers continue to use nicotine after SAH. Young age at smoking onset and a history of depression or alcohol use are risk factors for continued cigarette use. Targeted smoking cessation programs are needed to reduce the high rate of smoking resumption after SAH.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12843355&dopt=Abstract [PubMed - in process]



Clin Pharmacol Ther. 2003 Jul;74(1):69-76.
Effects of polymorphism in promoter region of human CYP2A6 gene (CYP2A6*9) on expression level of messenger ribonucleic acid and enzymatic activity in vivo and in vitro.

Yoshida R, Nakajima M, Nishimura K, Tokudome S, Kwon JT, Yokoi T.

Division of Drug Metabolism, Faculty of Pharmaceutical Sciences, Kanazawa University, Japan.

Cytochrome P450 (CYP) 2A6 catalyzes nicotine C-oxidation, leading to cotinine formation, a major metabolic pathway of nicotine in humans. There are genetic polymorphisms in the human CYP2A6 gene. Previously, we demonstrated that in vivo nicotine metabolism is impaired with the CYP2A6*4, CYP2A6*7, and CYP2A6*10 alleles in Japanese subjects and Korean subjects. An allele possessing a point mutation in the TATA box termed CYP2A6*9 (T-48G) has been reported to decrease the transcriptional activity in vitro as assessed by luciferase assay. In this study we investigated the effects of the CYP2A6*9 allele on in vivo enzymatic activity by evaluating nicotine metabolism. The mutation of T-48G was found only on the CYP2A6*1A allele but not on the CYP2A6*1B allele. Allele frequencies of CYP2A6*9 in Japanese subjects (n = 92) and Korean subjects (n = 209) were 21.3% and 22.3%, respectively. In Korean subjects the cotinine/nicotine ratios as an index of nicotine metabolism in the subjects with CYP2A6*9/CYP2A6*9 (4.3 +/- 2.4) were significantly lower than those in the subjects with CYP2A6*1A/CYP2A6*9 (7.7 +/- 5.6) and CYP2A6*1A/CYP2A6*1A (10.4 +/- 9.2) (P <.05 and P <.005, respectively). In Japanese subjects a similar result was observed, although it was not significant. Thus it is suggested that the mutation in the TATA box (CYP2A6*9 allele) caused the decreased in vivo enzymatic activity. With an in vitro study, it was shown that the expression levels of CYP2A6 messenger ribonucleic acid and coumarin 7-hydroxylase activity in human livers genotyped as CYP2A6*1/CYP2A6*9 and CYP2A6*9/CYP2A6*9 tended to be lower than those in human livers genotyped as CYP2A6*1/CYP2A6*1, although there was no significant difference because of the small number of samples. These in vitro data supported the in vivo data demonstrating that the CYP2A6*9 allele caused the decreased expression level and enzymatic activity of CYP2A6.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12844137&dopt=Abstract



Psychopharmacology (Berl). 2003 Jul 4 [Epub ahead of print].
Environmental enrichment decreases nicotine-induced hyperactivity in rats.

Green TA, Cain ME, Thompson M, Bardo MT.

Department of Psychology, University of Kentucky, 115 Kastle Hall, KY 40506, Lexington, USA.

RATIONALE. Previous research has determined that rats reared in an enriched condition (EC) are more sensitive to the effects of acute systemic amphetamine than rats raised in an impoverished condition (IC). OBJECTIVES. The present experiments examined the effect of environmental enrichment on locomotor activity following repeated injections of nicotine. Experiment 1 assessed differences in locomotor activity in EC and IC rats and experiment 2 assessed differences between EC rats and rats housed in pairs without novel objects or daily handling (social condition; SC) to determine whether enrichment causes changes beyond that of social contact alone. METHODS. In experiment 1, EC and IC rats were treated with saline, 0.2 mg/kg or 0.8 mg/kg nicotine, and locomotor activity was assessed for 60 min. Nicotine-induced activity was measured every 48 h for a total of eight sessions. All rats were challenged with 0.8 mg/kg nicotine on session 9. In experiment 2, EC and SC rats were treated with saline or 0.2 mg/kg nicotine, and locomotor activity was assessed using the same regimen as in experiment 1. RESULTS. In experiment 1, EC rats exhibited less sensitivity than IC rats to the psychostimulant effect of nicotine upon both acute and repeated administration. On the nicotine challenge session (session 9), EC rats were again less sensitive to the hyperactive effects of nicotine. In experiment 2, EC rats were also less sensitive than SC rats to nicotine-induced hyperactivity across repeated injections. CONCLUSIONS. These results suggest that environmental enrichment during development reduces the stimulant effect of nicotine.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12845407&dopt=Abstract [PubMed - as supplied by publisher]







Natural Herbal Supplement: Hair Million


Hair loss alone does not pose significant health problems. In fact, there are people who opt for baldness as an alternative hair style. However, in general, however, hair loss is not considered desirable.

The most ostensive feature that distinguishes us human from chimps and other primates is the lack of bodily hair. During evolutionary process, we have lost the majority of hair. Hair is no longer a biologically essential part of our body, just like appendix. The hair we still have on our scalp and a few other bodily parts is still regarded as significant for reasons other than biological necessity. Hair loss is naturally accompanied by aging process, although the extent of hair loss and the timing of onset vary widely among individuals. Thus, loss of hair and baldness is considered as a symbol of maturity or old age. Like winkles and other signs of aging, hair loss is not welcome by most people, because we don't welcome aging, and being perceived as an aging person. However, it is alopecia, or premature hair loss that especially concerns certain people.

While the hair loss and resulting baldness in general have not been proven to be related to underlying health problems, there are certain correlations between hair loss and health problems. For instance, premature hair loss could suggest premature aging or nutritional and hormonal imbalance, stressful life, use of drugs that cause hair loss as a side effect, skin disease, or heart disease. The balding appearance could also impart a subdued impression of integrity in bodily health and youthfulness.












DHEA is a natural hormone, and it is produced in our body by the adrenal glands. DHEA has been suggested to provide numerous potential benefits. DHEA (or dehydroepiandrosterone) is converted into androgens (male hormones) or estrogens (female hormones) in the cells. Our bodies produce decreasing amount of DHEA as we get older. various health benefits: To deter aging, improve sexual function/erectile dysfunction, treat cognitive decline, enhance athletic performance, facilitate weight loss, improve strength, prevent osteoporosis, enhance immunomodulation for rheumatic conditions, and treat depression.





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