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Lutein-20||Herbs for headache, fever, and migraine ||
Milk thistle||Saw palmetto||
Triple B Super Vision||Garlic, Ginger, and Grapeseed Extract||
Ginseng and Ginkgo||Hair Million||
DHEA||Coenzyme Q10||
Sleep Aid herbal formula - natural sleep aid||Herbal Breath - herbs for bad breath problems.||
Weight loss herbal formula||Ginkgo biloba||
Colon cleansing, Laxative for constipation relief, laxative, and colon cleansing||ViaVita, Lecithin for healthy liver
Interferon research abs 1 ||
Hemoglobin 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 ||
caffeine related research references ||
nicotine related research references
Br J Clin Pharmacol. 2000 Oct;50(4):311-4.
In vitro evaluation of potential in vivo probes for human flavin-containing monooxygenase (FMO): metabolism of benzydamine and caffeine by FMO and P450 isoforms.
Lang DH, Rettie AE.
Department of Medicinal Chemistry, University of Washington, Seattle, WA 98195, USA.
AIMS To determine the FMO and P450 isoform selectivity for metabolism of benzydamine and caffeine, two potential in vivo probes for human FMO. METHODS Metabolic incubations were conducted at physiological pH using substrate concentrations of 0.01-10 mM with either recombinant human FMOs, P450s or human liver microsomes serving as the enzyme source. Products of caffeine and benzydamine metabolism were analysed by reversed-phase h.p.l.c. with u.v. and fluorescence detection. RESULTS CYP1A2, but none of the human FMOs, catalysed metabolism of caffeine. In contrast, benzydamine was a substrate for human FMO1, FMO3, FMO4 and FMO5. Apparent Km values for benzydamine N-oxygenation were 60 +/- 8 microM, 80 +/- 8 microM, > 3 mM and > 2 mM, for FMO1, FMO3, FMO4 and FMO5, respectively. The corresponding Vmax values were 46 +/- 2 min-1, 36 +/- 2 min-1, < 75 min-1 and < 1 min-1. Small quantities of benzydamine N-oxide were also formed by CYPs 1A1, 1A2, 2C19, 2D6 and 3A4. CONCLUSIONS: FMO1 and FMO3 catalyse benzydamine N-oxygenation with the highest efficiency. However, it is likely that the metabolic capacity of hepatic FMO3 is a much greater contributor to plasma levels of the N-oxide metabolite in vivo than is extrahepatic FMO1. Therefore, benzydamine, but not caffeine, is a potential in vivo probe for human FMO3.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11012553&dopt=Abstract
J Sleep Res. 2000 Sep;9(3):269-72.
Does caffeine confound relationships among adrenergic tone, blood pressure and sleep apnoea?
Bardwell WA, Ziegler MG, Ancoli-Israel S, Berry CC, Nelesen RA, Durning A, Dimsdale JE.
Department of Psychiatry, University of California at San Diego, La Jolla, California 92093-0804, USA. wabardwelcsd.edu
The purpose of this study was to determine whether caffeine consumption confounds the relationship among adrenergic tone, as measured by urinary norepinephrine (NE), blood pressure (BP) and obstructive sleep apnoea (OSA). Data were analysed using correlation and regression analysis, analysis of covariance and t-tests. Subjects included normotensives and hypertensives with and without OSA: 38 men, 23 women, aged 30-60 y; 100-150% of ideal body weight; without other major illness. Patients were studied using polysomnography, caffeine consumption was assessed, 24-h urinary NE levels were examined and ambulatory BP was recorded. Patients with OSA (N=27) reported significantly greater caffeine consumption than those without OSA (N=34) (295 vs. 103 mg, P=0.010), but caffeine was not significantly correlated with their ambulatory BP. In contrast, NE excretion correlated with caffeine consumption (r=0.24, P=0.041), apnoea severity (r=0.65, P < 0.001) and BP (r=0.34, P < 0.005). Significant OSA-NE and BP-NE relationships remained even after controlling for caffeine consumption. Patients with OSA consumed nearly three times the amount of caffeine as patients without OSA. While caffeine partially explains the increased adrenergic tone in patients with OSA and the relationship between BP and NE, it does not appear to contribute significantly to the relationship between OSA and elevated BP.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11012866&dopt=Abstract
Cell Calcium. 2000 Jun;27(6):329-38.
NO-induced modulation of calcium-oscillations in pulmonary vascular smooth muscle.
Pauvert O, Marthan R, Savineau J.
Laboratoire de Physiologie Cellulaire Respiratoire (INSERM E9937), Universite Bordeaux 2, Bordeaux Cedex, France.
The effect of the nitric oxide (NO) donor sodium nitroprusside (SNP) on both [Ca(2+)](i)and mechanical activity was studied in the rat isolated pulmonary artery (RPA). In freshly isolated myocytes loaded with 1 microM indo-lacetoxymethyl ester for 30 min, short (40-60 s) application of ATP (100 microM) or ET-1 (0.1 microM) induced 3-6 cyclic rises in [Ca(2+)](i)(Ca-oscillations) of decreasing amplitude. Preincubation of cells with SNP (10-250 microM) for 10 min had no effect on the resting [Ca(2+)](i)value, but progressively abolished the oscillations. A similar effect was obtained with 8-bromo-cGMP (100-500 microM). SNP (0.001-100 microM) concentration-dependently relaxed ATP (10 mM, n = 4) and ET-1 (0.1 microM, n = 4)-precontracted RPA. 1H-[1,2,4]oxadiazolol [4,3,-a]quinoxalin-1-one (ODQ, 10 microM), a potent inhibitor of the cytosolic guanylyl cyclase, fully reversed the effect of SNP on ATP-induced [Ca(2+)](i)oscillations as well as on ATP-precontracted RPA. In contrast, N-[2-(methylamino)ethyl]-5-isoquinolinesulfonamide (H8, 10 microM), a potent inhibitor of cGMP-dependent protein kinase (PKG), did not alter the effect of SNP. Caffeine (5 mM) induced only one transient [Ca(2+)](i)-increase (n = 24), the amplitude of which was altered neither by SNP nor by 8-bromo-cGMP. Our results show that the relaxing effect of NO in RPA is related, at least in part, to its action on the Ca-signalling pathway. NO interacts with inositol trisphosphate pathway without interacting with the ryanodine-sensitive receptor. Finally, the effect of NO involves an increase in cGMP but appears independent of activation of PKG. 2000 Harcourt Publishers Ltd.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11013463&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.
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 ||
Progesterone Cream ||
Natural herbal formula for hair loss problems ||