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Eur J Epidemiol. 2003;18(5):401-5.
Relation of coffee, green tea, and caffeine intake to gallstone disease in middle-aged Japanese men.

Ishizuk H, Eguchi H, Oda T, Ogawa S, Nakagawa K, Honjo S, Kono S.

Department of Preventive Medicine, Faculty of Medical Sciences, Kyushu University, Fukuoka, Japan.

A possible protective effect of coffee or caffeine intake in the formation of gallstones has been suggested in some epidemiological studies. We examined the relation of coffee, green tea, and caffeine intake to gallstone disease in middle-aged Japanese men, distinguishing known gallstones from unknown diagnosed gallstones. Study subjects were 174 cases of gallstones as determined by ultrasonography, 104 cases of postcholecystectomy, and 6889 controls of normal gallbladder in the total of 7637 men who received a health examination at four hospitals of the Self-Defense Forces (SDF). Of the 174 cases of prevalent gallstones, 50 had been aware of having gallstones. Previously diagnosed gallstones and postcholecystectomy were combined as known gallstone disease. The consumption of coffee and green tea was ascertained by a self-administered questionnaire, and caffeine intake was estimated. Statistical adjustment was done for body mass index, smoking, alcohol use, rank in the SDF, and hospital. Coffee and caffeine intake were associated each with a statistically significant increase in the prevalence odds of known gallstone disease, but unrelated to newly diagnosed gallstones. Adjusted odds ratios of known gallstone disease were 1.7 (95% confidence interval [CI] 1.1-2.8) for coffee consumption of five cups or more per day vs. no consumption and 2.2 (95% CI: 1.3-3.7) for caffeine intake of 300 mg/day or more vs. less than 100 mg/day. The consumption of green-tea showed no material association with either unknown gallstones or known gallstone disease. The findings do not support a hypothesis that coffee drinking may be protective against gallstone formation.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12889685&dopt=Abstract [PubMed - in process]

J Biol Chem. 2003 Jul 30 [Epub ahead of print].
Activation of p53 by oxidative stress involves PDGFbeta receptor-mediated ATM kinase activation.

Chen K, Albano A, Ho A, Keaney JF Jr.

Medicine Dept., Boston University School of Medicine, Boston, MA 02118.

Phosphorylation of the p53 tumor suppressor protein is a critical event in the up-regulation and activation of p53 during cellular stress. In this study, we characterized the signaling pathway linking oxidative stress to p53 through the platelet-derived growth factor b (PDGFb) receptor and the ataxia telangiectasia mutated (ATM) kinase. In response to H2O2, we observed phosphorylation of p53 specifically at serine 15, but not serine 9, 20, or 392. Phosphorylation of Ser-15 was correlated with enhanced induction and functional activation of p53 manifest as transcription of the p53 target p21CIP/WAF. We found that H2O2 induced phosphorylation of the PDGFb receptor and increased ATM kinase activity two events integral to p53 activation as either AG1433 (a PDGFb receptor inhibitor) or caffeine (ATM kinase inhibitor) inhibited Ser-15 phosphorylation. Similarly, p53 activation by H2O2 was inhibited by kinase inactive forms of the PDGFb receptor or ATM. Inhibition of ATM kinase had no effect on H2O2-induced PDGFb receptor tyrosine phosphorylation, whereas PDGFb receptor suppression with RNA interference impaired H2O2-induced ATM activation, indicating ATM lies downstream to the PDGFb receptor in this signaling cascade. Functionally, inhibition of the PDGFb receptor abrogated the inhibition of cell proliferation and promotion of apoptosis due to H2O2 treatment. Thus, these data link PDGFb receptor transactivation to H2O2-induced p53 phosphorylation and suggest a functional role for growth factor receptors in modulation of p53 function.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12890678&dopt=Abstract [PubMed - as supplied by publisher]

J Neurosci. 2003 Jul 30;23(17):6894-903.
Presynaptic calcium stores modulate afferent release in vestibular hair cells.

Lelli A, Perin P, Martini M, Ciubotaru CD, Prigioni I, Valli P, Rossi ML, Mammano F.

Venetian Institute of Molecular Medicine, via Giuseppe Orus 2, 35129 Padua, Italy.

Hair cells, the mechanoreceptors of the acoustic and vestibular system, are presynaptic to primary afferent neurons of the eighth nerve and excite neural activity by the release of glutamate. In the present work, the role played by intracellular Ca2+ stores in afferent transmission was investigated, at the presynaptic level, by monitoring changes in the intracellular Ca2+ concentration ([Ca2+]i) in vestibular hair cells, and, at the postsynaptic level, by recording from single posterior canal afferent fibers. Application of 1-10 mm caffeine to hair cells potentiated Ca2+ responses evoked by depolarization at selected Ca2+ hot spots, and also induced a graded increase in cell membrane capacitance (DeltaCm), signaling exocytosis of the transmitter. Ca2+ signals evoked by caffeine peaked in a region located approximately 10 microm from the base of the hair cell. [Ca2+]i increases, similarly localized, were observed after 500 msec depolarizations, but not with 50 msec depolarizations, suggesting the occurrence of calcium-induced calcium release (CICR) from the same stores. Both Ca2+ and DeltaCm responses were inhibited after incubation with ryanodine (40 microm) for 8-10 min. Consistent with these results, afferent transmission was potentiated by caffeine and inhibited by ryanodine both at the level of action potentials and of miniature EPSPs (mEPSPs). Neither caffeine nor ryanodine affected the shape and amplitude of mEPSPs, indicating that both drugs acted at the presynaptic level. These results strongly suggest that endogenous modulators of the CICR process will affect afferent activity elicited by mechanical stimuli in the physiological frequency range.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12890784&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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