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991.
Background
The objective of this study was to confirm provisional quantitative trait loci (QTL) for cocaine-induced locomotor activation, on chromosomes 1, 5, 6, 9, 12, 15, 16, 17, and 18, previously identified in the AXB/BXA recombinant inbred (RI) and AcB/BcA recombinant congenic (RC) strains of mice derived from A/J (A) and C57BL/6J (B6) progenitors. This was accomplished through a genetic analysis of cocaine-induced activity in an AxB6 F2 cross and a phenotypic survey across a panel of B6.A chromosome substitution strains (CSS) mice. Mice were tested for cocaine-induced activity, following administration of saline and cocaine (20 mg/kg), utilizing an open-field procedure.Results
Among AxB6 F2 mice, differences in cocaine-induced activity were associated with loci on chromosome 1 (D1Mit305), 5 (D5Mit409), 16 (D16Mit131), and 18 (D18Mit189). A survey of the CSS panel confirmed cocaine QTLs on chromosomes 5 and 15, previously identified in RI or RC strains. Overall, the regions on chromosomes 5 and 18 represent verification of QTL previously identified in both the RC and RI strains. Additionally, the B6 allele for these QTL was consistently associated with greater relative cocaine activation.Conclusions
Collectively, chromosome 5 and 18 QTL have now been replicated in multiple independent crosses derived from the A/J and C57BL/6J progenitors. The use of an in silico analysis highlighted potential candidate genes on chromosomes 5 and 18. The present results complement the targeted gene approach currently prevalent in the study of cocaine and provide a broader empirically based focus for subsequent candidate gene studies. 相似文献992.
Deep Raj Sharma Amanjit Bal R. Vijayaraghavan Kiran Dip Gill 《Toxicology and applied pharmacology》2009,240(2):208-229
Recent global events have focused attention on the potential threat of international and domestic chemical terrorism, as well as the possibility of chemical warfare proliferation. Sulphur mustard (SM) is one of the potent chemical warfare agents (CWA), which initiates a cascade of events that converge on the redox mechanisms common to brain injury. The present study was designed to examine the effects of chronic SM exposure on neurobehavioral impairments, mitochondrial oxidative stress in male Swiss Albino mice and its role in inducing apoptotic neuronal cell death. The animals were divided into four groups (control, low, medium and high dose) of 5 animals each. Exposure to SM was given percutaneously daily for 12 weeks. The results demonstrated impairment in neurobehavioral indices viz. rota rod, passive avoidance and water maze tests in a dose dependent manner. There was a significant increase in lipid peroxidation and protein carbonyl content whereas, decrease in the activity of manganese superoxide dismutase (MnSOD), glutathione reductase and glutathione peroxidase suggesting impaired antioxidant defense system. Immunoblotting of cytochrome c, Bcl-2, Bax and activation of caspase-3 suggest induction of apoptosis in a dose dependent manner. Finally, increased p53 expression suggests that it may target the mitochondrial pathway for inducing apoptosis in response to DNA damage signals. In conclusion, chronic SM exposure may have the potential to generate oxidative stress which may trigger the release of cytochrome c as well as caspase-3 activation in neurons leading to cell death by apoptosis in a dose dependent manner which may in the end be responsible for the disruption of cognitive functions in mice. 相似文献
993.
Woodall WG Delaney HD Kunitz SJ Westerberg VS Zhao H 《Alcoholism, clinical and experimental research》2007,31(6):974-987
BACKGROUND: Randomized trial evidence on the effectiveness of incarceration and treatment of first-time driving while intoxicated (DWI) offenders who are primarily American Indian has yet to be reported in the literature on DWI prevention. Further, research has confirmed the association of antisocial personality disorder (ASPD) with problems with alcohol including DWI. METHODS: A randomized clinical trial was conducted, in conjunction with 28 days of incarceration, of a treatment program incorporating motivational interviewing principles for first-time DWI offenders. The sample of 305 offenders including 52 diagnosed as ASPD by the Diagnostic Interview Schedule were assessed before assignment to conditions and at 6, 12, and 24 months after discharge. Self-reported frequency of drinking and driving as well as various measures of drinking over the preceding 90 days were available at all assessments for 244 participants. Further, DWI rearrest data for 274 participants were available for analysis. RESULTS: Participants randomized to receive the first offender incarceration and treatment program reported greater reductions in alcohol consumption from baseline levels when compared with participants who were only incarcerated. Antisocial personality disorder participants reported heavier and more frequent drinking but showed significantly greater declines in drinking from intake to posttreatment assessments. Further, the treatment resulted in larger effects relative to the control on ASPD than non-ASPD participants. CONCLUSIONS: Nonconfrontational treatment may significantly enhance outcomes for DWI offenders with ASPD when delivered in an incarcerated setting, and in the present study, such effects were found in a primarily American-Indian sample. 相似文献
994.
There is a large amount of research into maternal health as a health issue, but maternal health as a development issue has been less explored. This Review analyses the evidence from the past 20 years on the links between maternal health and development to examine maternal health within a development framework. We note that although existing evidence suggests that these links are strong, further research is needed to definitively substantiate how and to what extent maternal health and development affect each other. Further, we find that progress and investment in maternal health have lagged far behind estimates of what is needed to achieve the Millennium Development Goals. 相似文献
995.
A phase I clinical trial with monoclonal antibody ch806 targeting transitional state and mutant epidermal growth factor receptors 总被引:1,自引:0,他引:1
Scott AM Lee FT Tebbutt N Herbertson R Gill SS Liu Z Skrinos E Murone C Saunder TH Chappell B Papenfuss AT Poon AM Hopkins W Smyth FE MacGregor D Cher LM Jungbluth AA Ritter G Brechbiel MW Murphy R Burgess AW Hoffman EW Johns TG Old LJ 《Proceedings of the National Academy of Sciences of the United States of America》2007,104(10):4071-4076
An array of cell-surface antigens expressed by human cancers have been identified as targets for antibody-based therapies. The great majority of these antibodies do not have specificity for cancer but recognize antigens expressed on a range of normal cell types (differentiation antigens). Over the past two decades, our group has analyzed thousands of mouse monoclonal antibodies for cancer specificity and identified a battery of antibodies with limited representation on normal human cells. The most tumor-specific of these antibodies is 806, an antibody that detects a unique epitope on the epidermal growth factor receptor (EGFR) that is exposed only on overexpressed, mutant, or ligand-activated forms of the receptor in cancer. In vitro immunohistochemical specificity analysis shows little or no detectable 806 reactivity with normal tissues, even those with high levels of wild-type (wt)EGFR expression. Preclinical studies have demonstrated that 806 specifically targets a subset of EGFR expressed on tumor cells, and has significant anti-tumor effects on human tumor xenografts, primarily through abrogation of signaling pathways. The present clinical study was designed to examine the in vivo specificity of a chimeric form of mAb 806 (ch806) in a tumor targeting/biodistribution/pharmacokinetic analysis in patients with diverse tumor types. ch806 showed excellent targeting of tumor sites in all patients, no evidence of normal tissue uptake, and no significant toxicity. These in vitro and in vivo characteristics of ch806 distinguish it from all other antibodies targeting EGFR. 相似文献
996.
Proliferation of breast cancer cells is mediated by estrogen receptors (ER)-ERalpha and ERbeta. At present, contradictory observations complicate the understanding of involvement of ERbeta in breast cancer and functional definition of ERbeta as a prognostic marker. A stable expression of full length ERbeta was established in the ERalpha-positive MCF-7 breast carcinoma cell line to evaluate the role for ERbeta in maintenance of cell viability and estrogenic response, as well as proliferation, morphology and cell cycle progression. In order to verify in vivo tumourigenicity of ERbeta transfectants were transplanted into nude mice. Transfection of ERbeta in MCF-7 resulted in a marginal increase of gelsolin protein expression. Constitutive expression of ERbeta resulted in a significant 30% inhibition of cellular growth compared with transfection of the mock vector alone (p=0.043). This reduction in growth was associated a retardation of transition into S-phase of the cell cycle. The in vitro response to 17beta-estradiol was reversed in cells over-expressing ERbeta (p=0.016). However, no difference in response to the antiestrogens tamoxifen and ICI 182,780 was observed in the presence of ERbeta. Importantly, over-expression of ERbeta prevented establishment and growth of tumours as subcutaneous xenografts in immunodeficient mice in vivo. These observations support the notion that ERbeta is a tumour suppressor and is exploitable in terms of cancer prevention, improving therapeutic response or predicting disease progression. 相似文献
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