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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

Neuroscience. 2003;120(1):191-205.
Pifithrin-alpha suppresses p53 and protects cochlear and vestibular hair cells from cisplatin-induced apoptosis.

Zhang M, Liu W, Ding D, Salvi R.

Center for Hearing and Deafness, Hearing Research Laboratory, 215 Parker Hall, University at Buffalo, Buffalo, NY 14214, USA.

Cisplatin, a commonly used antineoplastic agent, destroys the sensory hair cells in the cochlear and vestibular system leading to irreversible hearing loss and balance problems. Cisplatin-induced hair cell damage presumably occurs by apoptosis. Recent studies suggest that p53 may play an important role initiating cisplatin-induced apoptosis in some cell types. To determine if p53 plays a role in cisplatin-mediated hair cell loss, cochlear and utricular organotypic cultures were prepared from postnatal day 3-4 rats and treated with cisplatin or cisplatin plus pifithrin-alpha (PFT), a p53 inhibitor. Control cultures were devoid of p53 immunolabeling, caspase-1 and caspase-3 labeling and p53 protein was absent from Western blots. Cisplatin (1-10 microg/ml) caused a dose-dependent loss of hair cells in cochlear and utricular cultures, up-regulated phospho-p53 serine 15 immunolabeling, increased the expression of phospho-p53 serine 15 in Western blots from 6 to 48 h after the onset of cisplatin-treatment, and increased caspase-1 and caspase-3 labeling in cochlear and vestibular cultures. Addition of PFT (20-100 microM) to cisplatin-treated cochlear and utricular cultures resulted in a dose-dependent increase in hair cell survival; suppressed the expression of p53 in Western blots and eliminated caspase-1 and caspase-3 labeling in cultures. These results suggest that the tumor suppressor protein, p53, plays a critical role in initiating apoptosis in cochlear and vestibular hair cells. Temporary suppression of p53 with PFT provides significant protection against cisplatin-induced hair cell loss and offers the potential for reducing the ototoxic, vestibulotoxic and neurotoxic side effects of cisplatin.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12849752&dopt=Abstract [PubMed - in process]

Hear Res. 2003 May;179(1-2):43-52.
Establishment and characterization of rat progenitor hair cell lines(1).

Ozeki M, Duan L, Hamajima Y, Obritch W, Edson-Herzovi D, Lin J.

Department of Otolaryngology, University of Minnesota Medical School, University of Minnesota, 2001 Sixth Street S.E., 216 Lions Research Building, 55455, Minneapolis, MN, USA

Cochlear progenitor hair cell lines are useful for studies of cellular specification, gene expression features, and signal transduction involved in the development of hair cells. To obtain embryonic and postnatal cochlear progenitor hair cell lines, we immortalized primary cultures of sensorineural epithelial cells from otocysts on embryonic day 12 (E12) and explants of the organ of Corti tissues on postnatal day 5 (P5). Primary cultures and explants were then transduced by the E6/E7 genes of human papilloma virus type 16. Transduced cells were passed for >50 passages and partial clonal cells were isolated from the above P5 organ of Corti explants by limiting dilution. The expression of neuronal, neural, epithelial, hair cell markers, and important transcription factors were then examined in these cell clones. Clones that express the above markers were considered as being progenitor hair cells. At least two representative cell lines, one from a mixed culture of otocyst epithelial cells and the other from the organ of Corti cells, ultimately expressed hair cell markers and neuronal/neural cell markers. The former only expressed the early hair cell marker oncomodulin and myosin VIIa, whereas the latter expressed oncomodulin, calretinin, myosin VIIa and Brn 3.1. These cell lines may represent progenitor hair cells at the different stages of cochlear development.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12742237&dopt=Abstract [PubMed - in process]

Natl Toxicol Program Tech Rep Ser. 1978;113:1-107.
Bioassay of 2-Chloro-p-phenylenediamine Sulfate for Possible Carcinogenicity (C AS No. 61702-44-1).

National Toxicology Program.

2-Chloro-p-phenylenediamine sulfate is a salt of 2-chloro-p-phenylenediamine and sulfuric acid. It is a component of commercial hair dyes and was selected for bioassay by the National Cancer Institute because of the increased bladder cancer incidence noted among dye manufacturing workers. A bioassay for possible carcinogenicity of 2-chloro-p-phenylenediamine sulfate was conducted using Fischer 344 rats and B6C3F1 mice. 2-Chloro-p-phenylenediamine sulfate was administered in the feed, at either of two concentrations, to groups of 50 male and 50 female animals of each species. The dietary concentrations used in the chronic bioassay were 0.3 and 0.15 percent for the high and low dose rats, respectively, and 0.6 and 0.3 percent for the high and low dose mice, respectively. Compound administration was for 105 to 107 weeks in rats, 87 weeks in high dose mice, and 104 to 105 weeks in low dose mice. The only groups observed during an untreated period after dosing were the high dose mice, observed for 18 weeks after compound administration ceased. For each species, 20 animals of each sex were placed on test as controls. There were no significant positive associations between the administered dietary concentrations of 2-chloro-p-phenylenediamine sulfate and mortality for rats of either sex or male mice. There was a significant positive association between dosage and mortality for female mice; however, adequate numbers of animals in all groups survived sufficiently long to be at risk from late-developing tumors. There were no statistically significant positive associations between dietary exposure to the compound and the incidences of any tumor in rats. There was an increased incidence of transitional-cell hyperplasia of the renal pelvic epithelium in both male and female rats, and transitional-cell tumors of the urinary bladder were present in three dosed rats. These lesions indicated a possible carcinogenic effect, but are not considered as sufficient evidence of carcinogenicity. In mice, no tumors occurred in statistically significantly higher incidences in the dosed mice than in controls. Under the conditions of this bioassay there was insufficient evidence that dietary administration of 2-chloro-p-phenylenediamine sulfate was carcinogenic to Fischer 344 rats and B6C3F1 mice. Levels of Evidence of Carcinogenicity: Male Rats: Negative Female Rats: Negative Male Mice: Negative Female Mice: Negative Synonyms: 2-chloro-1,4-benzenediamine sulfate; 3-chloro-4-aminoaniline sulfate; o-chloro-p-phenylenediamine sulfate; C.I. Oxidation Base 13A; Ursol Brown 0

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12799678&dopt=Abstract [PubMed - as supplied by publisher]

Sci Total Environ. 2000 Oct 2;259(1-3):31-43.
Health assessment for mercury exposure among schoolchildren residing near a gold processing and refining plant in Apokon, Tagum, Davao del Norte, Philippines.

Akagi H, Castillo ES, Cortes-Maramba N, Francisco-Rivera AT, Timbang TD.

National Institute for Minamata Disease, Japan.

Artisanal gold-mining activities in the Philippines have proliferated since the early 1980s. Presently, environmental and health monitoring conducted by several governmental agencies is limited to the determination of total mercury only. Previous studies undertaken focused mainly on the exposure of adults and workers to mercury during mining/processing operations. However, in one area in Mindanao, mined ores are brought down and processed in the lowlands where residential communities are exposed to environmental pollutants resulting from gold processing/refining operations. The area of study is Apokon, Tagum, Davao del Norte, which has 29 gold processing and refining plants. Health complaints among schoolchildren in Apokon Elementary School were received by the Department of Health and were attributed to the mercury pollution in the environment. As part of a collaboration with the Health Department, UP-National Poisons Control and Information Service, the National Institute for Minamata Disease (NIMD), Japan, provided technical assistance in the analytical determination of mercury in biological and environmental samples. Elevated mercury concentrations were noted in some of the river systems up to 15 km from the mining areas. Environmental quality monitoring showed T-Hg sediment levels ranged from 0.553 to 66.471 microg/g dry wt. while water samples from river systems exhibited mercury levels from 72.8 to 78.4 ng/ml. Twenty-seven sediment samples from river systems near mining operations and seven water samples were also brought to the Institute for analysis. Fish samples collected showed levels ranging from 1.07 to 438.8 ng/g for total mercury and 0.71-377.18 ng/g for methylmercury. Methylmercury content in fish is predominant. All water and sediment samples collected from three sampling sites have elevated T-Hg level while three fish species have elevated T-Hg and methylmercury levels (WHO/CDC, 1994). Blood and hair samples from 162 schoolchildren aged 5-17 years were collected and analyzed at the NIMD for mercury analysis. Analytical procedures used in the NIMD for mercury testing were applied. Laboratory results showed that total mercury hair samples ranged from 0.278 to 20.393 microg/g while methylmercury hair results were from 0.191 to 18.469 microg/g. Methylmercury in hair showed levels from 45.96 to 99.81%. Total blood mercury levels ranged from 0.757 to 56.88 microg/l while Me-Hg blood levels ranged from 1.36 to 46.73 microg/l. It was determined that 10 children had elevated T-Hg blood levels while one child had high total and methylmercury levels in hair. A summary of physical examination results showed that the predominant findings include under-height, gingival discoloration, adenopathy, underweight and dermatologic abnormalities among children examined.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11032133&dopt=Abstract

Hair loss is a problem in modern soceity. Examining the factors of hair growth may shed light on how hair loss might occur. How long can hair grow before it stops growing eventually if it does? Given that the hair growth rate is quite uniform and constant, somewhere between 0.3-0.5 millimeters per day, it's believed that the length of anagen, the growth phase, differs among individuals, and this is the major determinant to the maximum hair length. For some individuals, anagen may last ten years. Of course the length of the anagen is governed by genes, and the genetic background of the individuals. Non-genetic factors such as nutritional condition, weather, seasonal changes (hair may grow a bit faster during winter), taking medications, health condition may of course influence the rate of hair growth as well as The shape of the hair, straight or curly, is dependent on the shape of the follicle. A circular or round hair follicle would generate straight hair, while the follicle with oval or elliptical shapes (in its cross-section) would produce a curly hair.

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.

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