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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







Nicotine Tob Res. 2003 Jun;5(3):357-62.
Tobacco smoke exposure and decreased serum and red blood cell folate levels: data from the Third National Health and Nutrition Examination Survey.

Mannino DM, Mulinare J, Ford ES, Schwartz J.

Air Pollution and Respiratory Health Branch, Division of Environmental Hazards and Health Effects, Centers for Disease Control and Prevention, Atlanta GA, USA. dmannindc.gov

The aim of this cross-sectional study was to determine the effects of smoke exposure on serum and red blood cell folate levels. Data collected as part of the Third National Health and Nutrition Examination Survey were analyzed. Serum and red blood cell folate levels were measured in active smokers and nonsmokers with high, moderate, and low exposure to environmental tobacco smoke. After adjusting for dietary intake of folate and other covariates, we found that both smokers and nonsmokers with high smoke exposure had lower red blood cell folate levels than did nonsmokers with low smoke exposure (-86 nmol/l [95% confidence interval, CI, -101 to -71 nmol/l] for smokers; -50 nmol/l [95% CI -69 to -31 nmol/l] for nonsmokers with high smoke exposure, compared with nonsmokers with low smoke exposure). Similarly, after adjustment of dietary intake of folate and other covariates, the log serum folate level also was decreased (-0.29 log nmol/l [95% CI -0.33 to -0.25 log nmol/l] for smokers; -0.16 log nmol/l [95% CI -0.20 to -0.12 log nmol/l] for nonsmokers with high smoke exposure, compared with nonsmokers with low smoke exposure). Tobacco smoke exposure is associated with decreased folate levels, which may be a mechanism for some of the health effects of active and passive smoking.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12791531&dopt=Abstract [PubMed - in process]



Nicotine Tob Res. 2003 Jun;5(3):369-74.
Prenatal nicotine increases testosterone levels in the fetus and female offspring.

Smith LM, Cloak CC, Poland RE, Torday J, Ross MG.

Department of Pediatrics, Harbor-UCLA Medical Center, University of California, Los Angeles, School of Medicine, USA. smitcrc.rei.edu

Epidemiological studies have shown that smoking during pregnancy markedly increases the risk for future tobacco use by adolescent female offspring. It has been hypothesized that the increased smoking risk in females is secondary to a nicotine-induced increase in fetal plasma testosterone levels that persist to adult life. To test this hypothesis, we randomized pregnant Sprague-Dawley rats to receive either saline or nicotine from Day 4 until the end of gestation. Blood samples for testosterone levels were obtained from 30- and 120-day-old offspring. In addition, blood samples for testosterone levels were obtained prior to and following a 2-day infusion of nicotine to chronically catheterized ovine fetuses. Maternal nicotine exposure resulted in increased plasma testosterone in 30-day-old female rat offspring, with no differences found in nicotine-exposed males. In addition, plasma testosterone levels increased in ovine fetuses in response to the nicotine infusion. We conclude that prenatal nicotine exposure increases plasma testosterone levels chronically in adolescent female rat offspring and acutely in both male and female ovine fetuses. Although our findings lack correlative behavioral information on the female offspring, these data are consistent with human epidemiological data suggesting that prenatal environmental influences may have marked effects on the subsequent smoking behaviors of offspring.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12791533&dopt=Abstract [PubMed - in process]



Nicotine Tob Res. 2003 Jun;5(3):375-85.
Acceptability and validity of hair collection from Latino children to assess exposure to environmental tobacco smoke.

Woodruff SI, Conway TL, Edwards CC, Hovell MF.

Graduate School of Public Health, San Diego State University, San Diego, CA 92123, USA. swoodruail.sdsu.edu

This study assessed the acceptability of collecting hair from Latino children to measure environmental tobacco smoke (ETS) exposure and examined the concurrent validity between nicotine and cotinine levels in children's hair in relation to adult reports of the children's ETS exposure. Trained Latina lay community health advisors recruited 143 Spanish-speaking Latino adult volunteers and their children. Bilingual-bicultural measurement technicians collected two types of data: (a) the adult's paper-and-pencil report about the child's past-month exposure to cigarettes in the home and car and (b) a sample of the child's hair to be analyzed for nicotine and cotinine. Of the eligible subjects, 8.5% declined to participate because of the hair collection protocol, some citing cultural beliefs. Among participants in the study, few problems arose related to hair collected, probably because of the culturally sensitive approach used during recruitment and measurement. Adults' reports of exposure, hair nicotine, and hair cotinine showed considerable variation and were skewed to the right. Average nicotine levels for these children appeared to be comparable to those reported elsewhere, whereas cotinine levels appeared to be somewhat lower. Hair nicotine was more detectable than hair cotinine and, compared with cotinine, showed a clearer linear relationship with adults' reports. However, associations between adults' reports and both biological measures were modest. Collecting hair samples in the field (i.e., participants' homes) to measure Latino children's ETS exposure is generally acceptable when appropriate methods are used. Hair nicotine may be a more valid and practical biological measure than hair cotinine. Hair sampling may be a potentially useful, noninvasive technique in ETS studies, although the modest associations of constituents in children's hair with adults' reports indicates that each measure provides different information about ETS exposure.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12791534&dopt=Abstract [PubMed - in process]








The average human scalp is covered by approximatey 100,000 hair follicles. Each hair undergoes hair cycle and normally 50-100 hairs randomly fall out a day, which is unnoticeable because lost hair is replaced by as many new hairs springing up daily. Hair loss results from the fall out of hair from the hair follicle. Alopecia or excessive, premature hair loss is the condition caused by many factors. Loss of hair itself does not pose critical health problems because biological role of human hair is relatively marginal. Hair on our scalp protects the head from mechanical shock, heat loss, and exposure to UV-light. The eyelashes and eyebrowes protect the eyes, and hair in the ear canal or the nasal passages help filter out particles and pathogens, thus protecting our internal organs. However, hair does play important social role: it is one of the major determinants of our appearance and identity in daily life. Fullness of hair also implicates or manifests physical integrity and youthfulness of the person. Losing hair could have more than just emotional impacts on individuals. The hair is a unique organ that goes through a characteristic cycle consisting of an immature phase, a growing phase called anagen, a transitional phase between the growing phase and the resting phase called catagen, and finally a resting phase called telogen in which the hair stops growing, waiting to fall out. 85-90% of hairs on our body are in anagen phase or growing phase, which lasts anywhere from two to five years. This phase is followed by a short regression phase, or catagen, which lasts 2-3 weeks. Approximately 1% of hair follicles are in catagen. Approximately 10-15% of hair follicles are in the resting phase, the telogen, which lasts about 3-5 months. Hair follicles typically goes through 10-20 asynchronous cycles during the lifetime. Persistent loss of more than 150 hairs would consist a state of hair loss, or alopecia, albeit it could be temporary.














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