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hair related research references ||
testosterone related research references ||
melanin related research references ||
caffeine related research references ||
nicotine related research references
Cell Calcium. 2001 Feb;29(2):85-96.
Calcium homeostasis and cell death in Sol8 dystrophin-deficient cell line in culture.
Marchand E, Constantin B, Vandebrouck C, Raymond G, Cognard C.
Laboratoire des Biomembranes et Signalisation Cellulaire, UMR CNRS/Universi&tacute; de Poitiers, Poitiers, France. eric.marchanoila.fr
Abnormalities of calcium homeostasis are involved in the process of cell injuries such as Duchenne muscular dystrophy characterized by the absence of the protein dystrophin. But how the absence of dystrophin leads to cytosolic calcium overload is as yet poorly understood. This question has been addressed with skeletal muscle cells from human DMD muscles or mdx mice. Although easier to obtain than human muscles, mdx muscle cells have provided controversial data concerning the resting intracellular calcium level ([Ca2+](i)). This work describes the culture of Sol8 cell line that expresses neither dystrophin nor adhalin, a dystrophin-associated protein. The [Ca2+](i)and intracellular calcium transients induced by different stimuli (acetylcholine, caffeine and high potassium) are normal during the first days of culture. At later stages, calcium homeostasis exhibits drastic alterations with a breaking down of the calcium responses and a large [Ca2+](i)elevation. Concomitantly, Sol8 cells exhibit morphological signs of cell death like cytoplasmic shrinkage and incorporation of propidium iodide. Cell death could be significantly reduced by blocking the activity of calpains, a type of calcium-regulated proteases. These results suggest that Sol8 cell line provides an alternative model of dystrophin-deficient skeletal muscle cells for which a clear disturbance of the calcium homeostasis is observed in culture in association with calpain-dependent cell death. It is shown that transfection with a plasmid cDNA permits the forced expression of dystrophin in Sol8 myotubes as well as a correct sorting of the protein. This approach could be used to explore possible interactions between dystrophin deficiency, calcium homeostasis alteration, and dystrophic cell death. 2001 Harcourt Publishers Ltd.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11162846&dopt=Abstract
J Biol Chem. 2003 Mar 14;278(11):9309-17.
ATP activates ataxia-telangiectasia mutated (ATM) in vitro. Importance of autophosphorylation.
Kozlov S, Gueven N, Keating K, Ramsay J, Lavin MF.
The Queensland Institute of Medical Research, PO Royal Brisbane Hospital, Herston Qld 4029, Australia.
Ataxia-telangiectasia Mutated (ATM), mutated in the human disorder ataxia-telangiectasia, is rapidly activated by DNA double strand breaks. The mechanism of activation remains unresolved, and it is uncertain whether autophosphorylation contributes to activation. We describe an in vitro immunoprecipitation system demonstrating activation of ATM kinase from unirradiated extracts by preincubation with ATP. Activation is both time- and ATP concentration-dependent, other nucleotides fail to activate ATM, and DNA is not required. ATP activation is specific for ATM since it is not observed with kinase-dead ATM, it requires Mn2+, and it is inhibited by wortmannin. Exposure of activated ATM to phosphatase abrogates activity, and repeat cycles of ATP and phosphatase treatment reveal a requirement for autophosphorylation in the activation process. Phosphopeptide mapping revealed similarities between the patterns of autophosphorylation for irradiated and ATP-treated ATM. Caffeine inhibited ATM kinase activity for substrates but did not interfere with ATM autophosphorylation. ATP failed to activate either A-T and rad3-related protein (ATR) or DNA-dependent protein kinase under these conditions, supporting the specificity for ATM. These data demonstrate that ATP can specifically induce activation of ATM by a mechanism involving autophosphorylation. The relationship of this activation to DNA damage activation remains unclear but represents a useful model for understanding in vivo activation.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12645530&dopt=Abstract
Cell Calcium. 2001 Mar;29(3):149-60.
Multiple effects of caffeine on Ca2+ release and influx in human B lymphocytes.
Sei Y, Gallagher KL, Daly JW.
Department of Anesthesiology, Uniformed Services University of The Health Sciences, Bethesda, MD 20814-4799, USA. ysesuhs.mil
Caffeine has been used as a pharmacological tool to study the ryanodine receptor (RYR)-mediated Ca2+ release from caffeine-sensitive, inositol 1,4,5,-trisphosphate (IP3)-insensitive pools. In the present study, we demonstrate multiple effects of caffeine on Ca2+ homeostasis in human B lymphocytes. Although B cells express a functional RYR, which can be activated by 4-chloro-m-cresol following depletion of IP(3)-sensitive pools, caffeine does not activate RYR-mediated Ca2+ release. Instead, caffeine dose-dependently inhibited IP3 receptor (IP3R)-mediated Ca2+ release, RYR-mediated Ca2+ release and B cell receptor-initiated Ca2+ influx, while high concentrations of caffeine (> or = 25 mM) induced a Ca2+ influx. In contrast with its ability to suppress receptor-stimulated Ca2+ influx, caffeine had no significant effect on the store-operated Ca2+ (SOC) channel-dependent Ca2+ influx induced by thapsigargin. Thus, caffeine may act as an inhibitor on a single or multiple site(s) responsible for regulating the IP3R channel, RYR channel and presumably the receptor-mediated SOC channel. The present report may be the first demonstration of multiple effects of caffeine on Ca2+ mobilization in single cell type. Our results suggest the need for caution regarding use of caffeine simply as a RYR-activator to study Ca2+ homeostasis in eucaryotic cells.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11162852&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
hair loss.
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.
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