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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







J Comput Aided Mol Des. 1999 Jan;13(1):57-68.
A computational model of the nicotinic acetylcholine binding site.

Galvez-Ruano E, Iriepa-Canalda I, Morreale A, Lipkowitz KB.

Departamento de Quimica Organica, Universidad de Alcala, Alcala de Henares, Spain.

We have derived a model of the nicotinic acetylcholine binding site. This was accomplished by using three known agonists (acetylcholine, nicotine and epibatidine) as templates around which polypeptide side chains, found to be part of the receptor cavity from published molecular biology studies, are allowed to flow freely in molecular dynamics simulations and mold themselves around these templates. The resulting supramolecular complex should thus be a complement, both in terms of steric effects as well as electronic effects, to the agonists and it should be a good estimation of the true receptor cavity structure. The shapes of those minireceptor cavities equilibrated rapidly on the simulation time scale and their structural congruence is very high, implying that a satisfactory model of the nicotinic acetylcholine binding site has been achieved. The computational methodology was internally tested against two rigid and specific antagonists (dihydro-beta-erytroidine and erysoidine), that are expected to give rise to a somewhat differently shaped binding site compared to that derived from the agonists. Using these antagonists as templates there were structural reorganizations of the initial receptor cavities leading to distinctly different cavities compared to agonists. This indicates that adequate times and temperatures were used in our computational protocols to achieve equilibrium structures for the agonists. Overall, both minireceptor geometries for agonists and antagonists are similar with the exception of one amino acid (ARG209).


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10087500&dopt=Abstract



Rev Med Liege. 2003 Jan;58(1):19-21.
[Effects of nicotine and cannabinoids on the central nervous system]

[Article in French]

Seutin V.

Departement de Sciences precliniques BP (service de Pharmacologie), Centre de Recherches en Neurobiologie Cellulaire et Moleculaire (CNCM), Universite de Liege.

We describe the molecular mechanisms of action of nicotine and delta 9-tetrahydrocannabinol, the most potent component of cannabis. Like other drugs of abuse, these compounds enhance dopamine release in a precise area of the limbic system when administered acutely. It has recently been shown that the cannabinoid receptors on which delta 9-tetrahydrocannabinol acts are also activated by endogenous ligands such as anandamide. This unconventional neurotransmitter appears to have important physiological effects in the central nervous system. Both preclinical and clinical evidence suggests that nicotine is more addictive than delta 9-tetrahydrocannabinol. However, the intimate interactions that exist between cannabinoid and opioid systems within the brain suggest that cannabinoids should not be considered as harmless drugs of abuse.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12647593&dopt=Abstract



Pflugers Arch. 1999 Mar;437(4):603-10.
Influence of substrate structure on substrate binding to the renal organic cation/H+ exchanger.

Wright SH, Wunz TM.

Department of Physiology, College of Medicine, University of Arizona, Tucson, AZ 85724, USA. shwrigh.arizona.edu

The carrier-mediated exchange of H+ for organic cations ("OC/H+ exchange") is the active step in OC secretion in renal proximal tubules. Although hydrophobicity is known to be an important criterion for binding of substrates to this transporter, the degree to which steric parameters of substrate structure influence binding to the exchanger is unclear. We examined this issue by measuring the inhibition of OC/H+ exchange produced by a group of quaternary ammonium compounds which share a common structural motif: an N1-pyridinium residue. Activity of the OC/H+ exchanger was determined by measuring transport of [14C]tetraethylammonium (TEA) in brush-border membrane vesicles (BBMV) from rabbit renal cortex. Transport was measured in the presence of a pH gradient (pHin 6.0; pHout 7.5) to maximize TEA/H+ exchange. Apparent inhibitory constants (Ki values) for each test agent were measured. The test agents included 4-phenylpyridiniums and 3-phenylpyridiniums, quinoliniums and acridiniums. The planar structure of these compounds permits a direct test of whether the presence of planar hydrophobic mass in different orientations relative to the pyridinium motif exerts a systematic effect on substrate binding to the OC/H+ exchanger. The hydrophobicity of each group of compounds was systematically varied by addition of different substituents at the quaternary nitrogen. Whereas decreases in Ki proved to be proportional to hydrophobicity, the position of the phenyl-ring substituent(s) had no effect on substrate interaction with the exchanger. The results led to the development of a preliminary quantitative structure-activity relationship (QSAR) correlating substrate hydrophobicity and substrate binding to the OC/H+ exchanger. This QSAR was used to predict the binding of 1-methyl-4-phenylpyridinium (MPP+), (+) and (-)nicotine, (+) and (-)ephedrine, quinine and quinidine to the OC/H+ exchanger. Molecular graphics representation of the 3D structures of the test agents was used to develop a working model of a hydrophobic, planar receptor surface on the OC/H+ exchanger against which substrates are suggested to interact during binding. Development of the QSAR and receptor surface model open the way to quantitative tests of the specific physical and structural determinants of substrate selectivity by the renal OC/H+ exchanger.


online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10089574&dopt=Abstract








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 an essential part of our body, just like appendix. What little 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.

Hair Million is a blend of Asian herbs that wards off hair loss and promotes hair growth. Of various approaches to hair restoration, Hair Million offers advantages including low cost compared with other methods or drugs, and safety, because it is made of safe and healthy herbs.














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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