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II Editorial Content and Peer Review All articles, editorials, and commentary in JMCP undergo peer review; articles undergo blinded peer review. Letters may be peer reviewed to ensure accuracy. The fundamental departments for manuscript submission are: Research Subject Reviews Formulary Management Contemporary Subjects Editorials Commentary Letters For manuscript preparation requirements, see "JMCP Author Guidelines" in this Journal or at amcp . II Research These are well-referenced articles based on original research that has not been published elsewhere and reflects use of the scientific method. The research is guided by explicit hypotheses that are stated clearly by the authors. II Subject Reviews These are well-referenced, comprehensive reviews of subjects relevant to managed care pharmacy. II Formulary Management These are well-referenced, comprehensive reviews of subjects relevant to formulary management methods or procedures in the conduct of pharmacy and therapeutics P&T ; committees and may include description and interpretation of clinical evidence. II Contemporary Subjects These are well-referenced submissions that are particularly timely or describe research conducted in pilot projects. Contemporary Subjects, like all articles in JMCP must , describe the hypothesis or hypotheses that guided the research, the principal methods, and results and include a Discussion section that includes a clear description of how this research adds information to the current literature. II Editorials Commentary These submissions should be relevant to managed care pharmacy and address a topic of contemporary interest. EDITORIAL MISSION AND POLICIES JMCP publishes peer-reviewed original research manuscripts, subject reviews, and other content intended to advance the use of the scientific method, including the interpretation of research findings in managed care pharmacy. JMCP is dedicated to improving the quality of care delivered to patients served by managed care pharmacy by providing its readers with the results of scientific investigation and evaluation of clinical, health, service, and economic outcomes of pharmacy services and pharmaceutical interventions, including formulary management. JMCP strives to engage and serve professionals in pharmacy, medicine, nursing, and related fields to optimize the value of pharmaceutical products and pharmacy services delivered to patients. JMCP employs extensive bias-management procedures that include a ; full disclosure of all sources of potential bias and conflicts of interest, nonfinancial as well as financial; b ; full disclosure of potential conflicts of interest by reviewers as well as authors; and c ; accurate attribution of each author's contribution to the article. Aggressive bias-management methods are necessary to ensure the integrity and reliability of published work. Editorial content is determined by the Editor-in-Chief with suggestions from the Editorial Advisory Board. The views and opinions expressed in JMCP do not necessarily reflect or represent official policy of the Academy of Managed Care Pharmacy or the authors' institutions unless specifically stated. II Letters If the letter addresses a previously published article, an author response may be appropriate. See "Letter to the Editor" instructions at amcp . ; II Advertising Disclosure Policy.

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Incidence of hepatitis B in pregnant women in the US is 0.4-1.5% May be as high as 10-14% for women born in high endemicity areas. Effects, while molindone was the least potent. Similar findings were reported by Behl et al. 1995 ; , who found that hippocampal neurons and glioma cells showed DNA degradation and cell lysis after 24-hour incubation with haloperidol. These changes were prevented by the addition of vitamin E. In another study, Jeste et al. 1991 ; looked at the effects of fluphenazine on neuronal cell density in the striatum. Rats were treated with fluphenazine and sacrificed at 4, 8, and 12 months of treatment. Results showed that after 4 months of treatment there was no observed difference between the vehicle-treated and neuroleptic-treated rats. After 8 months of treatment, the rats that had been given neuroleptics had a lower density of large neurons. After 12 months of treatment, however, both groups of rats showed very low neuronal density. This was attributed to a possible aging effect on neuronal loss that could overshadow the neuroleptic effect, and the fact that neuroleptic treatment could accelerate the natural process of cell loss. To investigate other possible direct cytotoxic effects of neuroleptic medications, Subramanyam et al. 1990, 1991 ; , Fang and Gorrod 1991 ; , and Gorrod and Fang 1993 ; studied the metabolism of haloperidol by hepatic microsomes. They reported that haloperidol has a metabolic pathway similar to that of the neurotoxic compound MPTP 1 -methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine ; , yielding the 1, 2, 3, -tetrahydropyridine analogue of haloperidol, HTP. Like MPTP, which is metabolized to MPP + , HTP is further metabolized to the pyridinium metabolite HP + . This finding raises the possibility that haloperidol may produce motor neurotoxicity by a mechanism similar to MPTP because it is thought that the conversion of MPTP to M P responsible for the Parkinson-like symptoms in the MPTP animal model of the disease. The question remains open as to whether other neuroleptics have similar metabolic pathways, which would be important if the production of MPP + -like compounds is involved in TD. To further investigate this issue, Burkhardt et al. 1993 ; studied the in vitro effect of neuroleptics on mitochondrial functions in rat brain. Their interest was based on the structural similarities between the haloperidol metabolite HP + and MPP + , and the fact that MPP + exerts its toxic effect by interfering with cell respiration through inhibition of complex I of the electron transport chain. They reported that, like MPP + , haloperidol, chlorpromazine, and thiothixene inhibited complex I of the electron transport chain. Clozapine was also found to inhibit complex I, but at a much higher concentration than the typical neuroleptics. This inhibition was discussed as a possible factor in the development of extrapyramidal symptoms EPS ; and TD, since similar inhibition was.

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On NP diet. For instance, the phenotypic and genetic correlations between viscera%6 and body weight6 were weakly positive on NP diet rP 0.10, rG 0.12 0.23 ; , and weakly positive or negative on HP diet rP 0.02, rG - 0.17 0.23 ; . The difference between diets in the average phenotypic correlation of viscera%6 was negligible average rp on NP and HP diets - 0.03 and - 0.02 ; . 3.4. Diet differences in correlations between protein percent and body weight On both diets, phenotypic and genetic correlations of muscle and body protein percent at time 3 and 6 with body weights ranged from near zero to strongly negative Fig. 2ad ; . For the genetic correlations of protein traits that could be estimated, the average correlation was slightly higher on HP diet compared to NP diet i.e., reverse of lipid traits ; . For body protein%3 Fig. 2c; average rG on NP and HP diets - 0.81 and - 0.61 ; and body protein%6 Fig. 2d; average rG on NP and HP diets - 0.17 and - 0.05 ; these differences were small. For muscle protein% at time 3 and 6, heritability on HP diet was zero Tobin et al., 2006 ; and thus genetic correlations involving this trait could not be estimated Fig. 2ab ; . For the phenotypic correlations, the average correlation of body protein%3 with body weights was slightly higher on NP diet - 0.01 ; than on HP diet - 0.13 ; Fig. 2c ; , but the situation was reversed for body protein%6 Fig. 2d; average rP on NP and HP diets - 0.05 and 0.03 ; . For muscle protein%3 Fig. 2a; average rP on NP and HP diets - 0.06 and 0.01 ; and muscle protein%6 Fig. 2b; average rP on NP and HP diets - 0.02 and - 0.04 ; , the difference in phenotypic correlations between diets was very small. These trends remained in the correlations between a composition trait and body weight recorded at the same time. At time 3, the correlations between body protein%3 and body weight3 were negative on both NP rP -0.05, rG -1.00 0.72 ; and HP diets rP -0.18, rG -0.73 0.45 ; Fig 2c ; . The correlations between muscle protein %3 and body weight3 were weakly negative on NP rP -0.07, rG -0.18 0.84 ; and weakly positive on HP diet rP 0.07, rG non-estimable ; Fig. 2a ; . At time 6, the correlations between body protein%6 and body weight6 were negative on NP rP - 0.13, rG - 0.30 0.24 ; and weak on HP diet rP 0.04, rG -0.03 0.25 ; Fig. 2d ; . The correlations between muscle protein%6 and body weight6 were weak or negative on NP rP 0.01, rG -0.47 0.31 ; and weakly negative on HP diet rP -0.05, rG non-estimable ; Fig. 2b.

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Category drug class generic name trade name - antipsychotic drugs - phenothiazines chlorpromazine thorazine fluphenazine prolixin thioridazine mellaril trifluoperazine stelazine thioxanthenes chlorprothixene taractin thiothixene navane benzisoxazole derivatives risperidone risperdal butryophenones haloperidol haldol dibenzodiazephines clozapine clozaril dibenzoxazepines loxapine loxitane dihydroindolines molindone moban thienobenzodiazephines olanzapine zyprexa chlorpromazine; thorazine; largactil classification: antipsychotic; antiemetic chemical name2-chloro-n, chlorpromazine: used to be used as an anastetic : used for chronic hickups and headaches clozapine clobbered clought and whine - clot and rain pain - caught clobbered and whine clarrot bleeding zopiclone zonked conked out and multivitamin. Any risks of vitamin D inadequacy considerably exceed any risks of taking 2000 IU day of vitamin D3, which the NAS-IOM regards as having no adverse health effect. A substantially higher level of support for research on the role of vitamin D for the prevention of cancer is urgently needed. However, delays in taking reasonable preventive action on cancer by ensuring nearly universal oral intake of vitamin D3 in the range of 1000-2000 IU day is costing thousands of lives unnecessarily each year that are lost due to fractures, cancer, diabetes, multiple sclerosis, and other diseases for which vitamin D deficiency plays a major role. In concentrations aggregation Oal-Olc-containing collagen had activity. evidence chick of platelet by the skin rat aggregation. by mild this and murine. Chase, T. N., R. I. Katz, and I. J. Kopin 1969 ; Release of3H-serotonin from brain slices. J. Neurochem. 16: 607-6 15. Cox, B., and C. Ennis 1982 ; Characterization of %hydroxytryptaminergic autoreceptors in the rat hypothalamus. J. Pharm. Pharmacol. 34: 438-441. Farnebo, L. O., and B. Hamberger 1971 ; Drug-induced changes in the release of `H-monoamines from field stimulated rat brain slices. Acta Physiol. &and. 371: 35-44. Farnebo, L. O., and B. Hamberger 1974 ; Regulation of `H-5-hydroxytryptamine release from rat brain cortex slices. J. Pharm. Pharmacol. 26: 642-644. Frankhuyzen, A. L., and A. H. Mulder 1980 ; Noradrenaline inhibits depolarization induced `H-serotonin release from slices of rat hippocampus. Eur. J. Pharmacol. 63: 179-182. Gallaner. D. W. and G. K. Aahaianian 1975 ; Effects of chloriminramink and lysergic acid dieihyiamide on e&x of precursor-formed `H-serotonin: Correlations with serotonergic impulse flow. J. Pharmacol. Exp. Ther. 193: 785-795. Galzin, A. M., C. Moret, and S. Z. Langer 1984 ; Evidence that exogenous but not endogenous norepinephrine activates the presynaptic alpha, -adrenoceptors on serotonergic nerve endings in the rat hypothalamus. J. Pharmacol. EXD. Ther. 228: 725-732. GBthert, M. 1980 ; Serotonin-receptor-mediated modulation of Caz + dependent 5-hydroxytryptamine release from neurones of the rat brain cortex. Naunyn Schmiedebergs Arch. Pharmacol. 314: 223-230. Gothert, M., and H. Huth 1980 ; Alpha-adrenoceptor-mediated modulation of 5-hydroxytryptamine release from rat brain cortex slices. Naunyn Schmiedebergs Arch. Pharmacol. 313: 21-26. Gothert, M., and G. Weinheimer 1979 ; Extracellular 5-hydroxytryptamine inhibits 5-hydroxytryptamine release from rat brain cortex slices. Naunyn Schmiedebergs Arch. Pharmacol. 310: 93-96. Haigler, H. J., and G. K. Aghajanian 1974 ; Lysergic acid diethylamide and serotonin: A comparison of effects on serotonergic neurons and neurons receiving a serotonergic input. J. Pharmacol. Exp. Ther. 188: 688-699. Hamon, M., S. Bourgoin, J. Jagger, and J. Glowinski 1974 ; Effects of lysergic acid diethylamide on synthesis and release of 5-HT in rat brain slices. Brain Res. 69: 265-280. Kandel, E. R., and W. A. Spencer 1961 ; Electrophysiology of hippocampal neurons. II. After potential and repetitive firing. J. Neurophysiol. 24: 243-259. Katz, R. I., and I. J. Kopin 1969 ; Effects of D-LSD and related compounds on release ofnorepinephrine-H3 and serotonin-H3 evoked from brain slices by electrical stimulation. Pharmacol. Res. Commun.

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