DreamPharm Products:
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 ||
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 ||
caffeine related research references ||
nicotine related research references
J Chromatogr B Biomed Sci Appl. 2000 Sep 15;746(2):331-8.
Liquid chromatographic method for the simultaneous determination of caffeine and fourteen caffeine metabolites in urine.
Bendriss EK, Markoglou N, Wainer IW.
Department of Oncology, McGill University, Montreal, Quebec, Canada.
An HPLC method has been developed for the separation and the determination of caffeine and its metabolites in urine samples using a one extraction-analysis run and UV detection. The compounds were extracted by liquid-liquid extraction using chloroform-isopropylalcohol (85:15, v/v). Chromatographic separation was accomplished on an ODS analytical column with a mobile phase containing 0.05% acetic acid/methylalcohol (92.5:7.5, v/v). Compounds were monitored at 280 nm. The method was validated for the determination of AFMU, 1X, 1U, 17X and 17U caffeine metabolites required to assess the metabolic activity of the enzymes subject to in vivo caffeine testing. The validated assay was applied to urine samples from ten healthy volunteers. The method was proved to be suitable to assess simultaneously the enzymatic activity of cytochrome P450 CYP1A2 and CYP2A6, as well as N-acetyltransferase and xanthine oxidase.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11076088&dopt=Abstract
Circulation. 2000 Nov 14;102(20):2541-7.
Hypoxia/reoxygenation stimulates intracellular calcium oscillations in human aortic endothelial cells.
Hu Q, Ziegelstein RC.
Department of Medicine, Division of Cardiology, Johns Hopkins Bayview Medical Center, Johns Hopkins University School of Medicine, Baltimore, MD 21224-2780, USA.
BACKGROUND: We have previously shown that hydrogen peroxide stimulates endothelial [Ca(2+)](i) oscillations. This study was performed to determine whether posthypoxic reoxygenation stimulates [Ca(2+)](i) oscillations in vascular endothelial cells. METHODS AND RESULTS: Hypoxia (glucose-free 95% N(2)/5% CO(2) bicarbonate buffer for 60 minutes) stimulated an increase in [Ca(2+)](i) from 111.9+/-7. 9 to 161.7+/-17.7 nmol/L (n=12, P:<0.01) in indo 1-loaded human aortic endothelial cells. On reoxygenation (glucose-containing 95% air/5% CO(2) bicarbonate buffer), 13 of 16 cells responded with repetitive [Ca(2+)](i) oscillations with an average amplitude of 570. 6+/-59.3 nmol/L, occurring at a mean interval of 0.28+/-0.04/min and persisting for >/=60 minutes. [Ca(2+)](i) oscillations were still observed in 4 of 7 cells studied in Ca(2+)-free buffer but did not occur when the intracellular Ca(2+) store was first depleted during hypoxia by either 1 micromol/L thapsigargin or by 10 mmol/L caffeine (n=6 for each). Reoxygenation-induced [Ca(2+)](i) oscillations were abolished by 10 micromol/L diphenyleneiodonium, an inhibitor of NAD(P)H oxidase (n=7), and by polyethylene glycol (PEG)-catalase (5000 U/mL, n=4) but were not prevented by inhibitors of xanthine oxidase (n=5), cyclooxygenase (n=4), nitric oxide synthase (n=5), the mitochondrial electron transport chain (n=4), or by PEG-superoxide dismutase (n=5). CONCLUSIONS: Posthypoxic reoxygenation stimulates repetitive [Ca(2+)](i) oscillations that are dependent on Ca(2+) release from an intracellular pool and require extracellular Ca(2+) to be maintained. These oscillations may be initiated by NAD(P)H oxidase-derived hydrogen peroxide and may play a role in signal transduction during ischemia/reperfusion in vivo.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11076830&dopt=Abstract
J Biol Chem. 2001 Feb 16;276(7):5296-302. Epub 2000 Nov 13.
The Haemophilus ducreyi cytolethal distending toxin induces cell cycle arrest and apoptosis via the DNA damage checkpoint pathways.
Cortes-Bratti X, Karlsson C, Lagergard T, Thelestam M, Frisan T.
Microbiology and Tumorbiology Center, Department of Cell and Molecular Biology, Karolinska Institutet, Stockholm S-171 77, Sweden.
The cytolethal distending toxins (CDTs) induce cell cycle arrest by a mechanism still not well characterized. We demonstrate that the effect of the Haemophilus ducreyi CDT (HdCDT) is cell type-specific: B cell lines underwent apoptosis, epithelial cells and keratinocytes arrested exclusively in G(2), whereas normal fibroblasts arrested both in G(1) and G(2). We studied normal keratinocytes and fibroblasts, which are relevant for understanding the pathogenicity of H. ducreyi. The response to HdCDT resembles the checkpoint response activated by ionizing radiation. Both responses were characterized by an early induction of the p53 gene and the cyclin-dependent kinase inhibitor p21 in fibroblasts, and activation of the chk2 kinase in epithelial cells. In the Ataxia Telangiectasia-mutated gene (ATM)-deficient lymphoblastoid cell lines, intoxication was significantly delayed compared with ATM wild type cells, and was associated with a slower kinetic of p53 stabilization, suggesting that the early response to HdCDT is ATM-dependent. Activation of ATM-dependent pathways was further confirmed by the ability of caffeine to partially override the HdCDT-mediated cell cycle arrest. Our data shed new light on the mechanism of action of this novel family of bacterial toxins, limiting the target candidates to DNA or molecules directly involved in activation of checkpoint responses.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11076947&dopt=Abstract
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.
DreamPharm Online Healthy Supplements ||
Lutein ||
Progesterone Cream ||
Natural herbal formula for hair loss problems ||