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    <dc:date>2026-05-08T17:46:28Z</dc:date>
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  <item rdf:about="http://localhost:80/xmlui/handle/123456789/362">
    <title>A Comparative Cross-Platform Meta-Analysis to Identify Potential Biomarker Genes Common to Endometriosis and Recurrent Pregnancy Loss</title>
    <link>http://localhost:80/xmlui/handle/123456789/362</link>
    <description>Title: A Comparative Cross-Platform Meta-Analysis to Identify Potential Biomarker Genes Common to Endometriosis and Recurrent Pregnancy Loss
Authors: Guha, Pokhraj
Abstract: Endometriosis is characterized by unwanted growth of endometrial tissue in different locations of the female reproductive tract. It may lead to recurrent pregnancy loss, which is one of the worst curses for the reproductive age group of human populations around the world. Thus, there is an urgent need for unveiling any common source of origin of both these diseases and connections, if any. Herein, we aimed to identify common potential biomarker genes of these two diseases via in silico approach using meta-analysis of microarray data. Datasets were selected for the study based on certain exclusion criteria. Those datasets were subjected to comparative meta-analyses for the identification of differentially expressed genes (DEGs), that are common to both diagnoses. The DEGs were then subjected to protein-protein networking and subsequent functional enrichment analyses for unveiling their role/function in connecting two diseases. From the analyses, 120 DEGs are reported to be significant out of which four genes have been found to be prominent. These include the CTNNB1, HNRNPAB, SNRPF and TWIST2 genes. The significantly enriched pathways based on the above-mentioned genes are mainly centered on signaling and developmental events. These findings could significantly elucidate the underlying molecular events in endometriosis-based recurrent miscarriages.</description>
    <dc:date>2021-04-01T00:00:00Z</dc:date>
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  <item rdf:about="http://localhost:80/xmlui/handle/123456789/361">
    <title>A brief review on cigarette induced cellular damage</title>
    <link>http://localhost:80/xmlui/handle/123456789/361</link>
    <description>Title: A brief review on cigarette induced cellular damage
Authors: Guha, Pokhraj
Abstract: Cigarette smoking has become one of the most common addictions in context to the present scenario of tobacco consumption. Comprising of nearly 7000 chemicals, cigarette smoke have both free radicals and oxidizing agents in both smoke tar and gas phase, both of which can cause oxidative stress in human health. Long time smoking causes decreased serum immunoglobulin level but increased level of auto– antibodies. During chronic oxidative stress resulting from cigarette smoking, cells secrete mucus and increased viscosity of mucus in airways makes it susceptible to bacterial infection. Furthermore, chronic exposure of lungs to tobacco smoke causes unfolded protein response, ER stress and altered ceramide metabolism. Apart from the above mentioned facts, Cigarette smoking can also cause senescence resulting in abnormal wound healing that exaggerates pathogenesis of COPD. Although there are several management therapies available for COPD management, but the permanent cellular damages due to smoking are irreparable and results in disease exaggeration and suffering.</description>
    <dc:date>2020-12-30T00:00:00Z</dc:date>
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  <item rdf:about="http://localhost:80/xmlui/handle/123456789/360">
    <title>Arecoline plays dual role on adrenal function and glucose-glycogen homeostasis under thermal stress in mice</title>
    <link>http://localhost:80/xmlui/handle/123456789/360</link>
    <description>Title: Arecoline plays dual role on adrenal function and glucose-glycogen homeostasis under thermal stress in mice
Authors: Sarkar, Hari Prasad
Abstract: Arecoline has biomedical importance, but it has untoward side effects on endocrine functions. The aim is to investigate its role on adrenal activity under thermal stress by ultrastructural and hormonal parameters in mice. Cold (4 °C) or heat (37 °C) stress, or arecoline (10 mg/kg body wt), each for 7 days in cold or heat stress stimulated adrenocortical activity ultrastructurally with an elevation of corticosterone level. Adrenomedullary activity was suppressed in cold stress with depletion of catecholamine levels. In heat stress, adrenomedullary activity was stimulated ultrastructurally with an elevation of catecholamine levels. Arecoline treatment alone, or in cold or heat stress suppressed adrenomedullary activity, judged by ultrastructural and hormonal parameters. Arecoline treatment caused hypoglycemia with an elevation of glycogen level, but cold or heat stress, or arecoline treatment in thermal stress caused hyperglycemia, with a fall in glycogen profile. Thus, arecoline in thermal stress plays a dual role on adrenal function and glucose-glycogen homeostasis in mice.</description>
    <dc:date>2020-07-01T00:00:00Z</dc:date>
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