Attitudes and barriers of medical students towards conducting research in a medical college

Background: It is well known that evidence-based medicine is the rule for clinical practice. This can be enhanced by conducting good research. Medical students being the future doctors should contribute significantly. But the research among the medical students is very poor with respect to presentations and publications. In view of this data the study was done to know their perception, attitude and barriers for conducting research.Methods: This was a cross sectional observational study involving three different batches of medical students by giving a semi-structured questionnaire.Results: The response among the participants to involve in research was only 30%. Among them the overall attitude and barrier score were 3.69±0.29 and 3.63±0.42 respectively with statistical significance shown between genders and not between batches. The biggest barrier was lack of previous research experience (91.67%). The most common motivational factor was self-interest (90.7%).Conclusions: If given sufficient training and facilities provided, we should be able to get more research among the medical students

Requirement of Mouse BCCIP for Neural Development and Progenitor Proliferation

Multiple DNA repair pathways are involved in the orderly development of neural systems at distinct stages. The homologous recombination (HR) pathway is required to resolve stalled replication forks and critical for the proliferation of progenitor cells during neural development. BCCIP is a BRCA2 and CDKN1A interacting protein implicated in HR and inhibition of DNA replication stress. In this study, we determined the role of BCCIP in neural development using a conditional BCCIP knock-down mouse model. BCCIP deficiency impaired embryonic and postnatal neural development, causing severe ataxia, cerebral and cerebellar defects, and microcephaly. These development defects are associated with spontaneous DNA damage and subsequent cell death in the proliferative cell populations of the neural system during embryogenesis. With in vitro neural spheroid cultures, BCCIP deficiency impaired neural progenitor's self-renewal capability, and spontaneously activated p53. These data suggest that BCCIP and its anti-replication stress functions are essential for normal neural development by maintaining an orderly proliferation of neural progenitors

Clinico pathological study of cutaneous lesions in HIV positive patients

Background: AIDS is a fatal illness caused by human immunodeficiency virus. About 90% ofthe HIV infected individuals sufferfrom one ormore skin lesions.The proportion of skincomplications and severity of several common cutaneous diseases are increased in HIV infected patients. Aim: 1. To study the histopathology of different cutaneous lesions present in HIV positive patients. 2. To correlate histopathological diagnosis with clinical diagnosis of skin lesions in HIV positive patients. Materials and Methods: Clinico pathological study of 65 skin biopsy specimens from HIVseropositive patients with cutaneous manifestations was carried out. Laboratory findings carriedout for the patients like routine haematological tests, serology test for HIV and CD4 and CD8 T cell count were noted and included in the study. Results: A total of 31 skin lesions were identified from 65patients. Specific microscopic findings were seen in all these cases. The infectious etiology was seen in 26 cases (40%), non infectious skin lesions in 23 cases (35.38%) and neoplastic lesions in 3 cases (4.61%). The spectrum of histopathological findings was correlated with clinical diagnosis. Clinico-histopathological discrepancies were observed in 5cases(7.66%). Conclusion: Cutaneous biopsy confirmed the diagnosisin many cases andin few cases it revealed clinically unsuspected diagnosis which reiterates the necessity of histopathologic investigations of cutaneous lesions in HIV/AIDS patients

Serodiagnosis of dengue using NS1 antigen, dengue IgM, dengue IgG antibody with correlation of platelet counts

Introduction: The dengue virus causes one of the most important mosquito-borne viral diseases.Annually, it affects up to 100 million people. Early laboratory diagnosis of dengue infection isimportant, as itcan allow early intervention and better prognosis. Dengue IgM antibody isdetected usually after five days of infection. NS1 antigen can be detected as early as day one.Platelet count is the only non-dengue parameter that can support the diagnosis of the dengueshock syndrome (DSS) and dengue hemorrhagic fever (DHF). This study was done to correlate the platelet count and dengue parameters detected either by rapid card test or by ELISA methods. Materials and Methods: Five hundred ninety three clinical samples suspicious of dengue were collected from April2020 to September2020. The received samples were tested by rapid methods and ELISA for dengue parameters and for platelet count by automated Becmon Coulter5partcellanalyser. Results: Out of 593 samples, 90 samples were positive by rapid tests that included NS1 antigentest, IgM and IgG dengue by immune chromatographic tests. Sixty one samples were positive bydengue IgM and dengue IgG ELISA.Samplespositivefordengue IgM antibodies orNS1antigen alone or positive for both were classified as primary dengue infection. Samples positivefor dengue IgG antibody or dengue IgG and IgM antibodies were classified as secondary dengue infections. Of the 90 cases positive by rapid card test, 62 cases were classified as primary dengueinfection and 28 cases as secondary dengue infection. Total 61 cases were positive by ELISAtests of these 35 cases were diagnosed as primary dengue and remaining 26 cases as secondary dengue infection. Conclusion: Thus the rapid tests such as NS1 antigen test, IgM and IgG dengue antibody can be used for the diagnosis in small peripheral laboratories. Thrombocytopenia was more consistent with cases positive for only IgG. Though MAC ELISA is more sensitive and specific than rapid methods, detection of NS1 antigen by immunochromatograpy test helps in early detection

Galanin protects against behavioral and neurochemical correlates of opiate reward

The mechanisms underlying responses to drugs of abuse have been widely investigated; however, less is known about pathways normally protective against the development of drug reinforcement. These pathways are also important since they may regulate individual differences in vulnerability to addiction. The neuropeptide galanin and its binding sites are expressed in brain areas important for drug reward. Previous studies have shown that centrally infused galanin attenuates morphine place preference and peripheral injection of galnon, a galanin agonist, decreases opiate withdrawal signs. The current studies in galanin knockout (GKO) mice examined the hypothesis that galanin is an endogenous negative regulator of opiate reward and identified downstream signaling pathways regulated by galanin. We show that GKO mice demonstrate increased locomotor activation following morphine administration, which is inhibited by acute administration of galnon. GKO mice also show enhanced morphine place preference, supporting the idea that galanin normally antagonizes opiate reward. In addition, morphine-induced ERK1/2 phosphorylation was increased in the VTA of both WT and GKO mice, but only the GKO mice showed increases in ERK1/2 and CREB phosphorylation in the amygdala or nucleus accumbens. Furthermore, a single systemic injection of galnon in GKO mice was sufficient to reverse some of the biochemical changes brought about by morphine administration. These data suggest that galanin normally attenuates behavioral and neurochemical effects of opiates; thus, galanin agonists may represent a new class of therapeutic targets for opiate addiction