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Milk thistle||Saw palmetto||
Triple B Super Vision||Garlic, Ginger, and Grapeseed Extract||
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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
Addict Biol. 1996;1(3):237-54.
Are tobacco and alcohol use related to Alzheimer's disease? A critical assessment of the evidence and its implications.
Tyas S.
Department of Epidemiology and Biostatistics, The University of Western Ontario, Canada.
Elucidation of the association of tobacco and alcohol use with Alzheimer's disease (AD) may advance etiological hypotheses and provide a theoretical basis for treatment. There is currently no cure or effective treatment for AD, and no cause has been established. Pharmacological evidence supports a plausible biological mechanism for the involvement of tobacco use: nicotine compensates for some of the cholinergic deficits observed in AD. Epidemiological evidence, however, is inconsistent, although recent meta-analyses also support a protective effect. Although smoking per se is certainly not advocated, further investigation of a potential protective effect of nicotine on AD is warranted. Pharmacological studies implicate alcohol use as a possible risk factor for AD; the epidemiological studies are again inconclusive. Alcohol consumption is associated with daily smoking and smokers are, in turn, more likely to consume alcohol. Since tobacco use may decrease the risk of developing AD and alcohol use may increase it, it is important to consider these two substances together: the effect of one may negate the other. This literature review critically evaluates the evidence for an association of tobacco and alcohol use with AD and identifies key issues for further research.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12893463&dopt=Abstract [PubMed - in process]
Nature. 1999 Apr 29;398(6730):805-10.
Reduced antinociception in mice lacking neuronal nicotinic receptor subunits.
Marubio LM, del Mar Arroyo-Jimenez M, Cordero-Erausquin M, Lena C, Le Novere N, de Kerchove d'Exaerde A, Huchet M, Damaj MI, Changeux JP.
CNRS UA D1284-Neurobiologie Moleculaire, Institut Pasteur, Paris, France.
Nicotine exerts antinociceptive effects by interacting with one or more of the subtypes of nicotinic acetylcholine receptors (nAChRs) that are present throughout the neuronal pathways that respond to pain. To identify the particular subunits involved in this process, we generated mice lacking the alpha4 subunit of the neuronal nAChR by homologous recombination techniques and studied these together with previously generated mutant mice lacking the beta2 nAChR subunit. Here we show that the homozygous alpha4-/- mice no longer express high-affinity [3H]nicotine and [3H]epibatidine binding sites throughout the brain. In addition, both types of mutant mice display a reduced antinociceptive effect of nicotine on the hot-plate test and diminished sensitivity to nicotine in the tail-flick test. Patch-clamp recordings further reveal that raphe magnus and thalamic neurons no longer respond to nicotine. The alpha4 nAChR subunit, possibly associated with the beta2 nAChR subunit, is therefore crucial for nicotine-elicited antinociception.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10235262&dopt=Abstract
Am J Physiol Regul Integr Comp Physiol. 2003 Jul 31 [Epub ahead of print].
The intrinsic cardiac nervous system in tachycardia induced heart failure.
Arora RC, Cardinal R, Smith FM, Ardell JL, Dell'Italia LJ, Armour JA.
Department of Anatomy and Neurobiology, Dalhousie University, Halifax, Nova Scotia, Canada.
Objective: To test the hypothesis that early stage heart failure differentially affects the intrinsic cardiac nervous system's capacity to regulate cardiac function. Methods: Following 2 wks of rapid ventricular pacing, in 9 anesthetized canines, cardiac and right atrial neuronal function were evaluated in situ in response to enhanced cardiac sensory inputs, stimulation of extracardiac autonomic efferent neuronal inputs and close coronary arterial administration of neurochemicals that included nicotine. Right atrial neuronal intracellular electrophysiological properties were then evaluated in vitro in response to synaptic activation and nicotine. Intrinsic cardiac nicotine sensitive neuronally induced cardiac responses were also evaluated in 8 sham-operated, unpaced animals. Results: Two weeks of rapid ventricular pacing reduced the cardiac index by 54%. Intrinsic cardiac neurons of paced hearts maintained their cardiac mechano- and chemo-sensory transduction properties in vivo. They also responded normally to sympathetic and parasympathetic preganglionic efferent neuronal inputs, as well as to locally administered alpha- or beta-adrenergic agonists or angiotensin II. The dose of nicotine needed to modify intrinsic cardiac neurons was 50 times greater in failure compared to normal preparations. That dose failed to alter monitored cardiovascular indices in failing preparations. Phasic and accommodating neurons identified in vitro displayed altered intracellular membrane properties compared to control, including decreased membrane resistance, indicative of reduced excitability. Conclusions: Early stage heart failure differentially affects the intrinsic cardiac nervous system's capacity to regulate cardiodynamics. While maintaining its capacity to transduce cardiac mechano- and chemosensory inputs, as well as inputs from extracardiac autonomic efferent neurons, intrinsic cardiac nicotine sensitive local circuit neurons differentially remodel such that their capacity to influence cardiodynamics becomes obtunded.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12893651&dopt=Abstract [PubMed - as supplied by publisher]
Vitamins, amino acids, oils for topical application, and prescription medications...
There are a number of approaches to hair loss problems.
Hair Million is an herbal alternative. It is a formula made of traditional, edible herbs
and has been anecdotally demonstrated the efficacy to ward off hair loss
problems.
There is no singular medical or alternative cure for hair loss since the
biology of hair growth is a highly complicated phenomenon.
It is unknown how Hair Million stops hair loss,
and promotes hair restoration.
The advantages of Hair Million over other approaches are, firstly, Hair Million is comparatively inexpensive,
and secondly, it is made only of traditionally used safe and healthy herbs that promote hair growth
according to Chinese pharmacopoeia. In addition, Hair Million is cardiotonic, meaning that Hair Million consists of herbs
that strengthens your heart, according to Chinese medicine. There is an interesting research paper which correlates baldness
to heart diseases: people with alopecia or hair loss
problems are significantly more likely to develop heart attacks.
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 ||
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Natural herbal formula for hair loss problems ||