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 ||
nicotine related research references
Brain Res. 2003 Mar 14;966(1):95-102.
Melatonin inhibition of nicotine-stimulated dopamine release in PC12 cells.
Schiller ED, Champney TH, Reiter CK, Dohrman DP.
Department of Human Anatomy and Medical Neurobiology, College of Medicine, Texas A&M University System Health Science Center, College Station, TX 77843-1114, USA.
Melatonin, a pineal hormone, modifies numerous physiologic processes including circadian rhythms and sleep. In specific tissues, melatonin appears to have an inverse relationship with dopamine. To examine this relationship, a pheochromocytoma cell line (PC12) was used to determine the extent of melatonin's ability to inhibit nicotine-stimulated dopamine release. Multiple experiments were conducted that examined: (1). the dose response of acute melatonin (5 min); (2). the effects of chronic melatonin (16 h pre-exposure); (3). the effects of prior nicotine or melatonin exposure (5 min) on melatonin's ability to alter dopamine release from a second 5-min nicotine exposure; and (4). the role of melatonin receptors (by pertussis toxin inhibition) on nicotine-stimulated dopamine release. In the dose response studies, melatonin inhibited nicotine-stimulated dopamine release with an ED50 of 8.6 microM. Chronic exposure to melatonin had no effect on melatonin's acute inhibition of nicotine-stimulated dopamine release. Prior nicotine or melatonin exposure had little effect on subsequent melatonin or nicotine exposure, except that the cells exposed to nicotine were not responsive to a second exposure to nicotine. Blockade of melatonin receptor function by pre-exposure to pertussis toxin (16 h) did not prevent melatonin's inhibition of nicotine-stimulated dopamine release. However, the toxin-treated cells were less inhibited by melatonin when compared to control cells suggesting a partial role for melatonin receptors. These results indicate that melatonin can acutely inhibit nicotine-stimulated dopamine release in PC12 cells. This model system allows detailed examination of melatonin's cellular actions as well as supporting a role for melatonin on neuronal dopamine release.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12646312&dopt=Abstract
Int J Eat Disord. 1999 Mar;25(2):143-50.
Predictors of bone mineral density in patients with eating disorders.
Goebel G, Schweiger U, Kruger R, Fichter MM.
Klinik Roseneck, Center for Behavioral Medicine, Prien, Germany.
OBJECTIVE: The objective of this study was to examine potential clinical predictors of bone density in patients with eating disorders. METHOD: We studied 137 women with anorexia nervosa, bulimia nervosa, or eating disorder not otherwise specified (NOS) after admission to the hospital. Clinical data of patients were collected by clinical interview and standardized questionnaires. Bone mineral density of the lumbar spine was measured by dual energy x-ray absorptiometry. RESULTS: Lumbar bone density was significantly correlated to present and past minimum weight even after correction for height and age. Other factors did not reach significance. CONCLUSION: Normalized present and past weight is the best predictor of lumbar bone density in patients with eating disorders. Factors like reduced caloric intake, binge eating, vomiting, menstrual status, and use of estrogen, laxatives, and nicotine seem to have no independent effect on bone density in this group of patients.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10065391&dopt=Abstract
J Psychopharmacol. 1998;12(4):375-9.
Nicotine-induced grooming: a possible dopaminergic and/or cholinergic mechanism.
Zarrindast MR, Sedaghati F, Borzouyeh F.
Department of Pharmacology, School of Medicine, Tehran University of Medical Sciences and Shohada Hospital, Iran.
The ability of nicotine, to induce grooming in rats was studied. Grooming was induced by i.p. injection of different doses (0.0675-0.5 mg/kg) of nicotine to rats. The effect was dose-dependent. However, the response was decreased with increasing doses of the drug from 0.25-0.5 mg/kg. Administration of the dopamine (DA) D1/D2 receptor agonist apomorphine (0.025-5 mg/kg, i.p.) also caused grooming in a dose-dependent manner. High doses of apomorphine (0.1-0.5 mg/kg, i.p.) also induced a lower degree of response. Combination of a low dose of nicotine (0.0675 mg/kg) with different doses of apomorphine did not show any interaction. However, there was an interaction between a high dose of nicotine and apomorphine. Thus, combination of a higher dose of nicotine (0.125 mg/kg) with apomorphine, reduced apomorphine-induced grooming. The muscarinic receptor antagonist atropine (5 and 10 mg/kg), peripheral nicotinic receptor antagonist hexamethonium (5 and 10 mg/kg), central nicotinic receptor antagonist mecamylamine (1 and 3 mg/kg) and D1 DA receptor antagonist SCH23390 (0.05 and 0.1 mg/kg) all decreased the response to nicotine. Atropine, mecamylamine and SCH23390 by themselves reduced spontaneous grooming. It is concluded that nicotine elicits grooming indirectly through a possible D1 dopaminergic mechanism. However, muscarinic and nicotinic cholinergic mechanism(s) may be involved.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10065912&dopt=Abstract
Beautiful, dense hair is a dream for many people.
Hair growth is a sophisticated biological process, which has not yet been understood.
A multitude of therapeutic measures, including drugs, surgery, and suppelements have been developed.
However, due to the diversity of the problems underlying hair loss, there is no single solution that
can address all hair loss cases. Another problem is that 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 cope with hair loss problems.
Anecdotally, it shows prositive results and improvement especially for age-related hair thinning and hair loss
for a large group of people who take it as suggested. Although personal experiences and anecdotal evidences
indicate that it works, we still do not understand the mechanisms of action as to how Hair Million works to
help stop hair loss, and promote hair growth. There has been no clinical trials nor placebo controlled statistical
analysis on the efficacy of Hair Million on hair loss and hair growth. R & D costs dearly, and no one would
afford to research complex herbal ingredients, which are often not patentable at all because they are
made by mother nature.
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 ||
Natural herbal formula for hair loss problems ||