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    <title>DSpace Collection:</title>
    <link>http://localhost:80/xmlui/handle/123456789/14324</link>
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    <pubDate>Thu, 12 Mar 2026 04:14:24 GMT</pubDate>
    <dc:date>2026-03-12T04:14:24Z</dc:date>
    <item>
      <title>Epigallocatechin gallate inhibits corneal neovascularization in ratalkaline burn model</title>
      <link>http://localhost:80/xmlui/handle/123456789/16078</link>
      <description>Title: Epigallocatechin gallate inhibits corneal neovascularization in ratalkaline burn model
Authors: Li, Huiyan; Ye, Bei; Zhu, Lili; Wu, Lianqun
Abstract: To evaluate the effectiveness of epigallocatechin gallate (EGCG) in inhibiting corneal neovascularization in&#xD;
rat alkaline burn model. Corneal neovascularization model was induced by sodium hydroxide alkaline burn injury in SD rats. Rats were randomly divided into two groups and were given intraperitoneal injection with EGCG or PBS per day for up to 14 days respectively. Corneal inflammation and neovascularization area were assessed on days3, 7, and 14 after cauterization with digital photographs. Vascular endothelial growth factor (VEGF) and pigment epithelium derived factor (PEDF) mRNA levels were measured by reverse transcription-polymerase chain reaction (qRT-PCR). The nucleartransfactor-Κb (NF-κB) subunit P65 protein was assayed by immunohistochemistry. The differences of corneal inflammation scores between two groups were  significant. The area of CNV between two groups had no significant difference on day3 but have significant difference on days 7 and 14.The PDEF mRNA expression in EGCG group was significantly higher and the expression of VEGF mRNA was lower than those in PBS group. The results of immunohistochemistry showed from day 7, expression of NF-κB P65protein was suppressed considerably in EGCG group. This study demonstrates that EGCG inhibits corneal neovascularization in a rat model induced by alkali burn.</description>
      <pubDate>Thu, 17 May 2018 00:00:00 GMT</pubDate>
      <guid isPermaLink="false">http://localhost:80/xmlui/handle/123456789/16078</guid>
      <dc:date>2018-05-17T00:00:00Z</dc:date>
    </item>
    <item>
      <title>Aryl sulfonate based anticancer alkylating agents</title>
      <link>http://localhost:80/xmlui/handle/123456789/16077</link>
      <description>Title: Aryl sulfonate based anticancer alkylating agents
Authors: Sheikh, Hamdullah Khadim; Tanzila Arshad; Ghazala Kanwal
Abstract: This research work revolves around synthesis of antineoplastic alkylating sulfonate esters with dual alkylating&#xD;
sites for crosslinking of the DNA strands. These molecules were evaluated as potential antineoplastic cross linking alkylating agents by reaction with the nucleoside of Guanine DNA nucleobase at both ends of the synthesized molecule. Synthesis of the alkylating molecules and the crosslinking with the guanosine  nucleoside was monitored by MALDITOF mass spectroscopy. The synthesized molecule’s crosslinking or adduct forming rate with the nucleoside was compared with that of 1,4 butane disulfonate (busulfan), in form of time taken for the appearance of [M+H]+ . It was found that aryl sulfonate leaving group was causing higher rate of nucleophilic attack by the Lewis basic site of the nucleobase. Furthermore, the rate was also found to be a function of electron withdrawing or donating nature of the substituent on the aryl ring. Compound with strong electron withdrawing substituent on the para position of the ring reacted fastest. Hence, new alkylating agents were synthesized with optimized or desired reactivity.</description>
      <pubDate>Wed, 16 May 2018 00:00:00 GMT</pubDate>
      <guid isPermaLink="false">http://localhost:80/xmlui/handle/123456789/16077</guid>
      <dc:date>2018-05-16T00:00:00Z</dc:date>
    </item>
    <item>
      <title>Anticholinergic drug atropine diminishes newly formed fear memory in male rats</title>
      <link>http://localhost:80/xmlui/handle/123456789/16076</link>
      <description>Title: Anticholinergic drug atropine diminishes newly formed fear memory in male rats
Authors: Sahar Rafiq; Saara Ahmad; Fatima Ahmed; Zehra Batool; Saad Bilal Ahmed; Sadia Saleem; Fizza Naqvi; Laraib Liaquat; Asia Afzal; Saida Haider
Abstract: Post-traumatic stress disorder (PTSD) is a condition which is triggered shortly after experiencing traumatic&#xD;
events. PTSD is complicated by the fact that people with PTSD often develop additional disorders such as phobias, addiction, depression, panic disorder and obsessive–compulsive disorder. Beta-adrenergic and cholinergic system both are involved in memory formation as well as in emotional response associated with memory. It is reported that the administration of beta-adrenergic and cholinergic antagonist results in the impairment in memory formation. Here, we examined the potential of beta-adrenergic antagonist propranolol and muscarinic cholinergic antagonist atropine for impairing the recently formed fear memory associated with PTSD. Reconsolidation is the memory process during which labile memory converts into permanent memory. In this study it is hypothesized that if recently formed fear memory is disturbed during reconsolidation phase by pharmacological intervention then it could be possible to impair wellconsolidated fear memory. Atropine and propranolol were injected in separate set of rats (n=6) just after the reactivation of fear memory. Short term memory and long term memory were monitored after 2 h and 24 h of reactivation respectively. Results of current study demonstrated that only atropine showed significant impairment of reconsolidation of newly formed fear memory whereas propranolol did not show fear memory disrupting effects. The results emphasize&#xD;
the significance of pharmacological intervention to impair reconsolidation of newly formed fear memory.</description>
      <pubDate>Tue, 15 May 2018 00:00:00 GMT</pubDate>
      <guid isPermaLink="false">http://localhost:80/xmlui/handle/123456789/16076</guid>
      <dc:date>2018-05-15T00:00:00Z</dc:date>
    </item>
    <item>
      <title>Synthesis, characterization and antihypertensive activity of 2-phenyl substituted benzimidazoles</title>
      <link>http://localhost:80/xmlui/handle/123456789/16075</link>
      <description>Title: Synthesis, characterization and antihypertensive activity of 2-phenyl substituted benzimidazoles
Authors: Khan, Muhammad Tariq; Muhammad Tahir Razi; Syed Umer Jan; Muhammad Mukhtiar; Rahman Gul; IzharUllah; Abid Hussain; Asif Mehmood Hashmi; Muhammad Taufiq Ahmad; Nisar Ahmed Shahwani; Imran Rabbani
Abstract: Hypertension is one of cardiovascular disease that is not sufficiently prevented and controlled at both hospital&#xD;
and community levels. Hypertension resulted in significant morbidity and mortality. The benz-imidazole ring is very important pharmacophore in modern drug discovery. The substituted benzimidazoles are the important for medicinal research. Researchers have reported that substituted Benzimidazoles are the structural isosteres of nucleotides, and easily allow them to interact with the different biopolymers, possess pharmacological activity especially antihypertensive activity. Angiotensin II Receptor Antagonists/Blockers (ARBs) compete with angiotensin II at the receptor site and block the contractile effect of angiotensin II in all vascular smooth muscles. Among all Angiotensin II Receptor Antagonists/Blockers (ARBs), Telmisartan, Milfasartan and many others have benzimidazole ring in their structure. In this study Angiotensin II Receptor Antagonists/Blockers (ARBs) have been prepared. Synthesized compounds were characterized by physical data and FTIR spectroscopic technique. Synthesized compounds studied were finally screened for their antihypertensive activity by tail cuff method of measurement of blood pressure by NIBP apparatus (None&#xD;
Invasive Blood Pressure) using Chart 5.0 software. The compounds synthesized were 2-(3- nitrophenyl)-1Hbenzimidazole (1a), 3-(1H benzimidazol-2-yl)aniline (1b) and 5-(1H-benzimidazol-2-yl)-2- methoxyphenol (1c). The synthesized compounds have shown antihypertensive activity by taking Losartan as lead compound.</description>
      <pubDate>Mon, 14 May 2018 00:00:00 GMT</pubDate>
      <guid isPermaLink="false">http://localhost:80/xmlui/handle/123456789/16075</guid>
      <dc:date>2018-05-14T00:00:00Z</dc:date>
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