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Interferon research abs 1 ||
Hemoglobin research abs ||
Stem cell research abs ||
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Herpes research abs ||
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hair research abs ||
hair related research references ||
testosterone related research references ||
melanin related research references ||
nicotine related research references
J Neurosci. 2003 Jul 23;23(16):6537-45.
Critical residues of the Caenorhabditis elegans unc-2 voltage-gated calcium channel that affect behavioral and physiological properties.
Mathews EA, Garcia E, Santi CM, Mullen GP, Thacker C, Moerman DG, Snutch TP.
Biotechnology Laboratory and Department of Zoology, University of British Columbia, Vancouver, British Columbia, Canada V6T 1Z3.
The Caenorhabditis elegans unc-2 gene encodes a voltage-gated calcium channel alpha1 subunit structurally related to mammalian dihydropyridine-insensitive high-threshold channels. In the present paper we describe the characterization of seven alleles of unc-2. Using an unc-2 promoter-tagged green fluorescent protein construct, we show that unc-2 is primarily expressed in motor neurons, several subsets of sensory neurons, and the HSN and VC neurons that control egg laying. Examination of behavioral phenotypes, including defecation, thrashing, and sensitivities to aldicarb and nicotine suggests that UNC-2 acts presynaptically to mediate both cholinergic and GABAergic neurotransmission. Sequence analysis of the unc-2 alleles shows that e55, ra605, ra606, ra609, and ra610 all are predicted to prematurely terminate and greatly reduce or eliminate unc-2 function. In contrast, the ra612 and ra614 alleles are missense mutations resulting in the substitution of highly conserved residues in the C terminus and the domain IVS4-IVS5 linker, respectively. Heterologous expression of a rat brain P/Q-type channel containing the ra612 mutation shows that the glycine to arginine substitution affects a variety of channel characteristics, including the voltage dependence of activation, steady-state inactivation, as well as channel kinetics. Overall, our findings suggest that UNC-2 plays a pivotal role in mediating a number of physiological processes in the nematode and also defines a number of critical residues important for calcium channel function in vivo.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12878695&dopt=Abstract
J Neurophysiol. 2003 Jul 23 [Epub ahead of print].
Characterization of neuronal nicotinic acetylcholine receptors in the membrane of unmyelinated human C-fiber axons by in vitro studies.
Lang PM, Burgstahler R, Sippel W, Irnich D, Schlotter-Weigel B, Grafe P.
Physiology, University of Munich, Munich, Germany; Anesthesiology, University of Munich, Munich, Germany.
Application of acetylcholine to peripheral nerve terminals in the skin is a widely used test in studies of human small fiber functions. However, a detailed pharmacological profile and the subunit composition of nicotinic acetylcholine receptors in human C-fiber axons are not known. In the present study, we recorded acetylcholine-induced changes of the excitability and of the intracellular Ca(2+) concentration in C-fiber axons of isolated human nerve segments. In addition, using immunohistochemistry, an antibody of a subtype of nicotinic acetylcholine receptor was tested. Acetylcholine and agonists reduced the current necessary for the generation of action potentials in C-fibers by up to 30 %. This increase in axonal excitability was accompanied by a rise in the free intracellular Ca(2+) concentration. The following rank order of potency for agonists was found: epibatidine >> 5-Iodo-A-85380 > 1,1-dimethyl-4-phenylpiperazinium iodide > nicotine > cytisine > acetylcholine; choline had no effect. The epibatidine-induced increase in axonal excitability was blocked by mecamylamine and, less efficiently, by methyllycacontine and dihydro-beta-erythroidine. Many C-fiber axons were labeled by an antibody that recognizes the alpha5 subunit of nicotinic acetylcholine receptors. In summary, electrophysiological and immunohistochemical data indicate the functional expression of nicotinic acetylcholine receptors composed of alpha3, alpha5, and beta4 but not of alpha4/beta2 or of alpha7 subunits in the axonal membrane of unmyelinated human C-fibers. In addition, the observations suggest that the axonal membrane of C-fibers in isolated segments of human sural nerve can be used as a model for presumed cholinergic chemosensitivity of axonal terminals.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12878715&dopt=Abstract [PubMed - as supplied by publisher]
J Invest Dermatol. 2003 Aug;121(2):362-7.
Influx of calcium and chloride ions into epidermal keratinocytes regulates exocytosis of epidermal lamellar bodies and skin permeability barrier homeostasis.
Denda M, Fuziwara S, Inoue K.
Shiseido Research Center, Fukuura, Kanazawa-ku, Yokohama, Japan. mitsuhiro.dendo.shiseido.co.jp
In the nervous system, influx of calcium and chloride ions into neurons regulates the signaling system by excitation and inhibition, respectively. In this study, we demonstrated the effects of the ion influx into epidermal keratinocytes in the permeability barrier repair process of the skin after damage. Topical application of the neurotransmitters glutamate and nicotine, which activate the calcium channel in neurons, delayed the barrier repair after tape stripping. In contrast, the neurotransmitters GABA and glycine, which activate the chloride channel in neurons, accelerated barrier repair. Topical application of the calcium ionophore ionomycin delayed barrier recovery and chloride ionophore 1 accelerated barrier repair after barrier disruption by tape stripping and acetone treatment. Ionomycin increased the intracellular calcium concentration in cultured keratinocytes whereas the chloride ionophore 1 increased the intracellular chloride ion concentration. In vivo light microscopy and electron microscopy observation showed acceleration of the exocytosis of lipid-containing lamellar bodies by the chloride ionophore and delay of the exocytosis by the calcium ionophore. These results suggest that, like the nervous system, influx of calcium and chloride ions into epidermal keratinocytes through ionotropic receptors plays a crucial role in cutaneous barrier homeostasis.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12880429&dopt=Abstract [PubMed - in process]
Loss of hair changes the appearance of a person, and the identity of the person in social context to a certain extent.
Hair growth is a complex biological process, which has not yet been completely understood. A multitude of therapeutic measures, including drugs, surgery, and suppelements have been made available, and used. However, due to the diversity of the problems underlying hair loss, there is no single solution for all hair loss cases. Most of chemical drugs and hair transplantation surgeries are not free from varying degrees of undesirable side effects on health.
Hair Million is an alternative solution to hair loss problems. Albeit only anecdotally, it has demonstrated efficacy in
the improvement for age-related hair thinning and hair loss for a significant fraction of people who take it
as recommended. We do not know the mechanisms of action as to how Hair Million works to help stop hair loss, and promote hair growth. We only know by
anecdotal observations. There has been no clinical trials nor placebo controlled statistical analysis.
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.
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Lutein ||
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Natural herbal formula for hair loss problems ||