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    <title>NISCAIR Online Periodicals Repository Collection: IJEB Vol.48(08) [August 2010]</title>
    <link>http://nopr.niscair.res.in/handle/123456789/9980</link>
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      <title>Effect of combined treatment of thioperamide with some antiepileptic drugs on methionine-sulfoximine induced convulsions in mice</title>
      <link>http://nopr.niscair.res.in/handle/123456789/9993</link>
      <description>Title: Effect of combined treatment of thioperamide with some antiepileptic drugs on methionine-sulfoximine induced convulsions in mice
&lt;br/&gt;
&lt;br/&gt;Authors: Vohora, Divya; Khanam, Razia; Pal, Shanthi N; Pillai, K K
&lt;br/&gt;
&lt;br/&gt;Abstract: Methionine-sulfoximine&#xD;
(MSO), a convulsant is known to &#xD;
increase&#xD;
the activity of histamine N-methyl transferase. The effect of a selective H3&#xD;
receptor agonist R- (&lt;img src='/image/spc_char/alpha.gif' border=0&gt; ) methylhistamine (RAMH) and antagonist (thioperamide,&#xD;
THP) and some &#xD;
antiepileptic&#xD;
drugs (gabapentin and sodium valproate) have been evaluated on MSO-induced&#xD;
convulsions in mice. The effect of THP was also evaluated in combination with&#xD;
these antiepileptic drugs. Sodium valproate (300 mg/kg, po) and gabapentin &#xD;
(400&#xD;
mg/kg, po) offered protection against MSO-induced convulsions as evidenced by a&#xD;
significant prolongation of latency to abnormal dorsoflexion and complete&#xD;
protection against mortality within 6 h of administration. THP (15 mg/kg, ip)&#xD;
alone and in combination with sub-effective doses of gabapentin (75 mg/kg, po)&#xD;
and sodium valproate (75 mg/kg, po) revealed no significant differences from&#xD;
the control group or either drug alone. Hence, &#xD;
the&#xD;
convulsant action of MSO does not appear to be mediated &#xD;
via&#xD;
histaminergic mechanisms.
&lt;br/&gt;
&lt;br/&gt;Page(s): 858-860</description>
      <pubDate>Thu, 29 Jul 2010 22:58:59 GMT</pubDate>
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    <item>
      <title>Genetic characterization of dengue virus serotypes causing concurrent infection in an outbreak in Ernakulam, Kerala, South India</title>
      <link>http://nopr.niscair.res.in/handle/123456789/9992</link>
      <description>Title: Genetic characterization of dengue virus serotypes causing concurrent infection in an outbreak in Ernakulam, Kerala, South India
&lt;br/&gt;
&lt;br/&gt;Authors: Anoop, M; Issac, Aneesh; Mathew, Thomas; Philip, Sairu; Kareem, Nabeel Abdul; Unnikrishnan, R; Sreekumar, E
&lt;br/&gt;
&lt;br/&gt;Abstract: Dengue fever, a&#xD;
mosquito-borne viral infection, causes significant morbidity and has become&#xD;
endemic in the Indian subcontinent. Virus strains currently circulating in many&#xD;
parts of the country are not well studied at the molecular level. In the&#xD;
present study, genetic characterization of virus strains from a dengue outbreak&#xD;
that occurred in and around a tertiary care hospital in Ernakulam, Kerala in the&#xD;
year 2008 has been reported. By reverse transcription polymerase chain reaction&#xD;
(RT-PCR), 37 out of 75 (49.3%) clinically suspected cases were positive for dengue&#xD;
viral RNA. Among these, 21 (56.8%) samples showed concurrent infection with&#xD;
multiple serotypes of the virus. Majority of the combined infections were&#xD;
caused by dengue serotype 2 and 3. Co-infections with type 1 and 2 in two&#xD;
patients, and type 1, 2 and 3 in one patient were also observed. The core-pre-Membrane&#xD;
(&lt;i style=""&gt;CprM)&lt;/i&gt; junction nucleotide sequencing&#xD;
and phylogenetic analysis revealed that the&#xD;
type 1 strains were related to the viral strains reported from Delhi-2001 and&#xD;
Gwalior-2002 dengue outbreaks, while the&#xD;
type 2 strains were related to the strains from Gwalior-2001 epidemic. Sequences&#xD;
of type 3 strains did not show clear relation to any of the previous Indian&#xD;
isolates, and in the phylogenetic analysis, they formed a distinct lineage&#xD;
within the Indian type 3 strains. This study indicates hyperendemicity of dengue&#xD;
in the region with the presence of multiple serotypes and high rates of&#xD;
co-infection, and local genomic evolution of the viral strains involved in this&#xD;
outbreak.
&lt;br/&gt;
&lt;br/&gt;Page(s): 849-857</description>
      <pubDate>Thu, 29 Jul 2010 22:58:59 GMT</pubDate>
    </item>
    <item>
      <title>Antioxidant activity of carotenoid lutein &lt;i&gt;in vitro&lt;/i&gt; and &lt;i&gt;in vivo&lt;/i&gt;</title>
      <link>http://nopr.niscair.res.in/handle/123456789/9991</link>
      <description>Title: Antioxidant activity of carotenoid lutein &lt;i&gt;in vitro&lt;/i&gt; and &lt;i&gt;in vivo&lt;/i&gt;
&lt;br/&gt;
&lt;br/&gt;Authors: Sindhu, Edakkadath R; Preethi, Korengath C; Kuttan, Ramadasan
&lt;br/&gt;
&lt;br/&gt;Abstract: Carotenoid lutein was evaluated for its antioxidant potential both &lt;i style=""&gt;in vitro&lt;/i&gt; and &lt;i style=""&gt;in vivo&lt;/i&gt;. Lutein was&#xD;
found to scavenge superoxide radicals, hydroxyl radicals and inhibited &lt;i style=""&gt;in vitro&lt;/i&gt; lipid peroxidation.&#xD;
Concentrations needed for 50 % inhibition (IC&lt;sub&gt;50&lt;/sub&gt;) were 21, 1.75 and 2.2 &lt;img src='/image/spc_char/micro.gif' border=0&gt; g/mL respectively. It scavenged&#xD;
2,2-diphenyl-1-picryl hydrazyl (IC&lt;sub&gt;50&lt;/sub&gt; 35 &lt;img src='/image/spc_char/micro.gif' border=0&gt; g/mL) and&#xD;
nitric oxide radicals (IC&lt;sub&gt;50 &lt;/sub&gt;3.8 &lt;img src='/image/spc_char/micro.gif' border=0&gt; g/mL) while 2,2-azobis-3-ethylbenzthiozoline-6-sulfonic acid&#xD;
radicals were inhibited at higher concentration. Ferric reducing power (50%) of&#xD;
lutein was found to be equal 0.3μmols/mL&#xD;
of FeSO&lt;sub&gt;4&lt;/sub&gt;.7H&lt;sub&gt;2&lt;/sub&gt;O. Its oral administration inhibited&#xD;
superoxide generation in macrophages &lt;i style=""&gt;in&#xD;
vivo&lt;/i&gt; by 34.18, 64.32 and 70.22 % at doses of 50, 100 and 250 mg/kg body&#xD;
weight. The oral administration of lutein in mice for 1 month significantly&#xD;
increased the activity of catalase, superoxide dismutase, glutathione reductase&#xD;
and glutathione in blood and liver while the activity of glutathione peroxidase&#xD;
and glutathione-S-transferase were found to be increased in the liver tissue.&#xD;
Implication of these results in terms of its role in reducing degenerative&#xD;
diseases is discussed.
&lt;br/&gt;
&lt;br/&gt;Page(s): 843-848</description>
      <pubDate>Thu, 29 Jul 2010 22:58:59 GMT</pubDate>
    </item>
    <item>
      <title>Effect of &lt;i&gt;Aloe vera&lt;/i&gt; gel extract on antioxidant enzymes and azoxymethane-induced oxidative stress in rats</title>
      <link>http://nopr.niscair.res.in/handle/123456789/9990</link>
      <description>Title: Effect of &lt;i&gt;Aloe vera&lt;/i&gt; gel extract on antioxidant enzymes and azoxymethane-induced oxidative stress in rats
&lt;br/&gt;
&lt;br/&gt;Authors: Anilakumar, K R; Sudarshanakrishna, K R; Chandramohan, G; Ilaiyaraja, N; Khanum, Farhath; Bawa, A S
&lt;br/&gt;
&lt;br/&gt;Abstract: The&#xD;
present work was undertaken with a view to study the&#xD;
effect of oral feeding of 2% &lt;i&gt;Aloe vera&lt;/i&gt; gel extract (AGE) for 30 days on&#xD;
azoxymethane (AOM)-induced oxidative stress in rats. It was observed that AOM&#xD;
administration resulted in a significant increase in malondialdehyde and&#xD;
conjugated dienes, with reduction in hepatic glutathione (GSH), vitamin A and&#xD;
uric acid contents. AOM-induced reduction in hepatic GSH and uric acid was&#xD;
brought back to normal by AGE. There was a significant raise in hepatic catalase,&#xD;
superoxide dismutase and glucose-6-phosphate dehydrogenase (G-6-PD) activities as&#xD;
a result of feeding of the extract. Ingestion of the extract effected reduction&#xD;
in AOM-induced colonic GSH-peroxidase, G-6- PD and glutathione S-transferase&#xD;
and femur bone marrow micronuclei formation. Hence, it is suggested that &lt;i&gt;Aloe&#xD;
vera&lt;/i&gt; gel extract possess the ability to reduce AOM- induced oxidative&#xD;
stress and toxicity in liver.
&lt;br/&gt;
&lt;br/&gt;Page(s): 837-842</description>
      <pubDate>Thu, 29 Jul 2010 22:58:59 GMT</pubDate>
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