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hair related research references ||
testosterone related research references ||
melanin related research references ||
nicotine related research references
Behav Pharmacol. 2003 Jul;14(4):279-94.
Effects of drugs of abuse and signal predictability in two models of sustained attention in pigeons.
Lemmonds CA, Wenger GR.
Department of Pharmacology and Toxicology, University of Arkansas for Medical Sciences, Little Rock 72205, USA.
The acute effects of ethanol, pentobarbital, D-amphetamine and nicotine were determined in two animal models of attention. This study examined if changing the predictability of the stimulus presentation modifies drug effects under two attention tasks, in male White Carneau pigeons. The first task was a continuous-trial sustained attention task. For seven pigeons, the frequency of signal presentation was constant and predictable, once every 60 s [a fixed-interval 60 s (FI-60) signal presentation]. For seven additional pigeons, the frequency of signal presentation averaged once every 60 s, but the interval between presentations was random and variable [a variable-interval 60 s (VI-60) signal presentation]. Following ethanol (0.3-3 g/kg) and pentobarbital (0.3-13 mg/kg), decreases in p(hit) and large increases in p(false alarm) occurred at doses that did not impair response rates. Following D-amphetamine (0.03-5.6 mg/kg) and nicotine (0.03-3 mg/kg), a significant decrease in p(hit) and increase in p(miss) occurred at doses that did not impair response rates. The second task was a discrete-trial attention task, under which eight pigeons were presented a constant and predictable signal and eight were presented a random and unpredictable signal. Following ethanol (0.3-3 g/kg) and pentobarbital (0.3-13 mg/kg), drug effects on accuracy occurred at doses that suppressed responding. The schedule of signal presentation did not alter the effects of ethanol or pentobarbital. Following D-amphetamine (0.03-5.6 mg/kg) and nicotine (0.03-3 mg/kg), a significant decrease in p(hit) and increase in p(error of omission) occurred at doses that did not impair response latencies, but there were no differences between pigeons responding under the predictable (FI-60) or variable (VI-60) signal presentations. The observation of differential drug effects [e.g. p(false alarms)] on performance under the continuous-trial procedure supports the validity of the procedure for measuring drug effects on attention. However, changes in signal predictability had little effect on control or drug conditions under this continuous-trial sustained attention procedure.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12838034&dopt=Abstract [PubMed - in process]
Behav Pharmacol. 2003 Jul;14(4):323-9.
Do different mechanisms underlie two anxiogenic effects of systemic nicotine?
Tucci S, Genn RF, Marco E, File SE.
Centre for Neuroscience, GKT School of Biomedical Sciences, King's College London, UK. sonia.tucccl.ac.uk
Alpha7 nicotinic acetylcholine receptors (alpha7 nAChRs) and 5-hydroxytryptamine 1A (5-HT1A) receptors have been implicated in the anxiogenic effects of centrally administered nicotine, but the receptors that mediate the anxiogenic effects of systemic nicotine are not known. This study explored whether competitive nAChR antagonists [dihydro-beta-erythroidine (DHbetaE), 4 mg/kg, and methyllycaconitine (MLA), 5 mg/kg], and a 5-HT1A receptor antagonist (WAY 100635, 0.5 and 1 mg/kg) could block the effects of two anxiogenic doses of nicotine in the social interaction test of anxiety. The anxiogenic effect of 0.1 mg/kg nicotine, given 5 min before the test, was blocked by DHbetaE and WAY 100635, establishing roles for alpha4beta2 nAChRs and 5-HT1A receptors. None of the antagonists could block the effect of 0.45 mg/kg nicotine, given 30 min before the test, precluding firm conclusions about the mechanisms underlying this anxiogenic effect. However, there was evidence for a role of alpha7 nAChRs in mediating an endogenous anxiogenic tone, since MLA itself had an anxiolytic effect that was blocked by both doses of nicotine. Thus, both alpha7 and alpha4beta2 nAChRs might have a role in mediating the anxiogenic effects of nicotine.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12838038&dopt=Abstract [PubMed - in process]
Behav Pharmacol. 2003 Jul;14(4):343-50.
Discriminative stimulus effects of ethanol with a conditioned taste aversion procedure: lack of acetaldehyde substitution.
Quertemont E.
Universite de Liege, Departement des Sciences Cognitives, Laboratoire de Neuroscience Comportementale et de Psychopharmacologie, Liege, Belgium. equertemonlg.ac.be
Acetaldehyde has been suggested to mediate a number of the pharmacological and behavioural effects of ethanol. Recently, several studies investigated the role of acetaldehyde in the subjective effects of ethanol, but obtained conflicting results. With the discriminative taste aversion (DTA) procedure, high acetaldehyde doses were shown to substitute for the discriminative stimulus effects of ethanol. In contrast, the operant drug discrimination protocol failed to show any substitution effect of acetaldehyde. Several methodological differences between the two procedures could explain these discrepancies, and particularly the absence of an individual discrimination criterion in the DTA procedure. In the present study, the DTA procedure was adapted to introduce such a criterion. In addition, the effects of acetaldehyde were compared with those of other drugs, for which the substitution effects for ethanol are well known. Rats were trained to discriminate 1.0 g/kg ethanol from saline in a DTA protocol. When the rats met the criterion of ethanol discrimination, various doses of several drugs were tested for their ethanol stimulus substitution effects: ethanol, acetaldehyde, dizocilpine, diazepam and nicotine. The results showed a clear dose-dependent discrimination of ethanol stimulus effects. In addition, dizocilpine fully substituted for ethanol, while diazepam only partially substituted. In contrast, both acetaldehyde and nicotine failed to substitute for ethanol. These results show that acetaldehyde is not significantly involved in the subjective and discriminative stimulus effects of ethanol. Acetaldehyde up to toxic doses did not substitute for the ethanol discriminative stimulus in the DTA protocol, when non-specific effects were carefully controlled.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12838040&dopt=Abstract [PubMed - in process]
Like developmental biology of any part of our body, hair growth is a complicated process. Hence the homework for
modern science to yet unravel the process and mechanism to a completion. There exist a number of traditional and alternative therapeutic methods that include drugs, surgery, suppelements, and even snake oils that have been developed and used for those who lose hair.
No understanding, and there is no solution. Of course, none of these approaches are perfect for all hair loss problems, especially due to the heterogeneity of the causes underlying hair losses. Most of chemical drugs and hair transplantation surgeries are accompanied by undesirable side effects.
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