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  <title>NOPR Collection:</title>
  <link rel="alternate" href="http://nopr.niscpr.res.in/handle/123456789/357" />
  <subtitle />
  <id>http://nopr.niscpr.res.in/handle/123456789/357</id>
  <updated>2026-10-12T23:35:07Z</updated>
  <dc:date>2026-10-12T23:35:07Z</dc:date>
  <entry>
    <title>Sodium Stibogluconate: Therapeutic use in the Management of Leishmaniasis</title>
    <link rel="alternate" href="http://nopr.niscpr.res.in/handle/123456789/386" />
    <author>
      <name>Roychoudhury, Jayeeta</name>
    </author>
    <author>
      <name>Ali, Nahid</name>
    </author>
    <id>http://nopr.niscpr.res.in/handle/123456789/386</id>
    <updated>2008-03-19T04:30:22Z</updated>
    <published>2008-02-01T00:00:00Z</published>
    <summary type="text">Title: Sodium Stibogluconate: Therapeutic use in the Management of Leishmaniasis
Authors: Roychoudhury, Jayeeta; Ali, Nahid
Abstract: Leishmaniasis causes significant morbidity and mortality worldwide. The disease is endemic in developing countries of tropical regions, and in recent years economic globalization and increased travel has also spread to people in developed countries. In the absence of effective vaccines and vector-control measures, the main line of defense against the disease is chemotherapy. Organic pentavalent antimonials, including sodium stibogluconate have been the first-line drug for the treatment of leishmaniasis for the last several decades, and clinical resistance to these drugs has emerged as a primary obstacle to successful treatment and control. The present review describes the structure, activity, mode of action of sodium stibogluconate and mechanism of resistance towards this drug in leishmaniasis.
Page(s): 16-22</summary>
    <dc:date>2008-02-01T00:00:00Z</dc:date>
  </entry>
  <entry>
    <title>Xenobiotic-induced Immune Alterations: Implications in Health and Disease</title>
    <link rel="alternate" href="http://nopr.niscpr.res.in/handle/123456789/385" />
    <author>
      <name>Banerjee, Basu Dev</name>
    </author>
    <author>
      <name>Chakraborti, Ayanabha</name>
    </author>
    <author>
      <name>Suke, Sanvidhan G</name>
    </author>
    <author>
      <name>Ahmed, Rafat S</name>
    </author>
    <author>
      <name>Tripathi, A K</name>
    </author>
    <id>http://nopr.niscpr.res.in/handle/123456789/385</id>
    <updated>2008-03-18T04:30:21Z</updated>
    <published>2008-02-01T00:00:00Z</published>
    <summary type="text">Title: Xenobiotic-induced Immune Alterations: Implications in Health and Disease
Authors: Banerjee, Basu Dev; Chakraborti, Ayanabha; Suke, Sanvidhan G; Ahmed, Rafat S; Tripathi, A K
Abstract: Immune function may be significantly altered following occupational, inadvertent or therapeutic exposure to chemically diverse xenobiotics. The environmental chemicals like pesticides, halogenated hydrocarbons, polychlorinated dibenzofurans, organic solvents, asbestos, silica, heavy metals etc. may interact with both cellular and humoral components of the immune system which can result in altered immune status that in turn may lead to decreased resistance to infection, certain forms of neoplasia or in some cases exacerbate allergy or autoimmunity. Recent advances in pharmacogenomics and toxicogenomics have contributed a lot to delineate the mechanism of interaction of xenobiotics with the biological system at the cellular and molecular level. However, detection of immune changes on exposure to immunotoxic agents is highly complex, especially in humans due to several confounding factors like age, sex, race gender, co- existence of disease, food habits, smoking etc. Thus, establishing a quantitative relationship between immunotoxicological data and risk assessment, following xenobiotic exposure is still a challenge. The present article reviews the immune alterations caused by exposure to variety of xenobiotics, and their implications in health and disease.
Page(s): 7-15</summary>
    <dc:date>2008-02-01T00:00:00Z</dc:date>
  </entry>
  <entry>
    <title>TRendys Meeting Report 2007</title>
    <link rel="alternate" href="http://nopr.niscpr.res.in/handle/123456789/384" />
    <author>
      <name />
    </author>
    <id>http://nopr.niscpr.res.in/handle/123456789/384</id>
    <updated>2008-03-18T04:30:19Z</updated>
    <published>2008-02-01T00:00:00Z</published>
    <summary type="text">Title: TRendys Meeting Report 2007
Page(s): 61-64</summary>
    <dc:date>2008-02-01T00:00:00Z</dc:date>
  </entry>
  <entry>
    <title>Exogenous administration of dehydroepiendrosterone attenuates loss of superoxide dismuatse activity in the brain of old rats</title>
    <link rel="alternate" href="http://nopr.niscpr.res.in/handle/123456789/383" />
    <author>
      <name>Sinha, Nupur</name>
    </author>
    <author>
      <name>Taha, Asia</name>
    </author>
    <author>
      <name>Baquer, N Z</name>
    </author>
    <author>
      <name>Sharma, Deepak</name>
    </author>
    <id>http://nopr.niscpr.res.in/handle/123456789/383</id>
    <updated>2008-03-18T04:30:19Z</updated>
    <published>2008-02-01T00:00:00Z</published>
    <summary type="text">Title: Exogenous administration of dehydroepiendrosterone attenuates loss of superoxide dismuatse activity in the brain of old rats
Authors: Sinha, Nupur; Taha, Asia; Baquer, N Z; Sharma, Deepak
Abstract: The influence of exogenously administered dehyroepiendrosterone (DHEA) on the activity of superoxide dismutase (SOD) was investigated in the mitochondrial and cytosolic fractions from cerebral cortex, cerebellum, hippocampus and medulla regions of the brains of 12- and 22-months old rats. DHEA was administered daily at the dose of 30 mg/kg/body wt, intraperitonially (i.p) in both age groups of rats for 1 month. Results showed that SOD activity was significantly higher in the mitochondrial fraction than in the cytosolic fraction, in DHEA-treated animals in both age groups. This indicated that exogenous DHEA affected mitochondrial SOD more than the cytosolic SOD. In terms of percent increase, 22 months-old animals showed significant increase in the SOD activity in both the fractions of all the four brain regions than in the 12 months old DHEA-treated animals. This showed that exogenous DHEA provided more protection to the SOD in ageing brain of older rats (22 months) than the younger (12 month) ones. The study suggests that exogenous DHEA is more beneficial at old age in terms of neuroprotection against oxidative stress-mediated brain dysfunctions and may protect age-related alterations in cognitive functions like learning and memory.
Page(s): 57-60</summary>
    <dc:date>2008-02-01T00:00:00Z</dc:date>
  </entry>
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