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7篇 您的检索式:作者名="Deepak Shukla"
    题名 作者 年代 出处 被引量
1The Importance of Heparan Sulfate in Herpesvirus Infection显示文摘Herpes simplex virus type-1 (HSV-1) is one of many pathogens that use the cell surface glycosaminoglycan heparan sulfate as a receptor. Heparan sulfate is highly expressed on the surface and extracellular matrix of virtually all cell types making it an ideal receptor. Heparan sulfate interacts with HSV-1 envelope glycoproteins gB and gC during the initial attachment step during HSV-1 entry. In addition,a modified form of heparan sulfate,known as 3-O-sulfated heparan sulfate,interacts with HSV-1 gD to induce fusion between the viral envelope and host cell membrane. The 3-O-sulfation of heparan sulfate is a rare modification which occurs during the biosynthesis of heparan sulfate that is carried out by a family of enzymes known as 3-O-sulfotransferases. Due to its involvement in multiple steps of the infection process,heparan sulfate has been a prime target for the development of agents to inhibit HSV entry. Understanding how heparan sulfate functions during HSV-1 infection may not only be critical for inhibiting infection by this virus,but it may also be crucial in the fight against many other pathogens as well.Christopher D. O'Donnell Deepak Shukla 2008Virologica Sinica2008,23,6:3
2Graft Copolymerization: A Kinetic Study显示文摘Shailesh Kumar Shukla Deepak Srivastava 2003Journal of polymer materials2003,20,:1
3Herpes Simplex Epithelial and Stromal Keratitis: An Epidemiologic Update显示文摘Asim V. Farooq Deepak Shukla 2012Survey of Ophthalmology2012,,5:1
4Chenopodium quinoa-An Indian perspective显示文摘Atul Bhargava Sudhir Shukla Deepak Ohri 2006Industrial Crops and Products2006,23,:1
5Chenopodium quinoa —An Indian perspective显示文摘Atul Bhargava Sudhir Shukla Deepak Ohri 2005Industrial Crops & Products2005,,1:1
6Hepatic endogenous defense potential of propolis after mercury intoxication显示文摘Exposure to mercuric chloride(HgCl2;5 mg kg–1 body weight;i.p.)induced oxidative stress in mice and substantially increased lipid peroxidation(LPO)and oxidized glutathione(GSSG)levels,decreased the level of reduced glu-tathione(GSH)and various antioxidant enzymes in liver and also increased the activities of liver marker enzymes in serum.Therapy with propolis extract,a resinous wax-like beehive product(200 mg kg–1 orally,after mercury administration),for 3 days inhibited LPO and the formation of GSSG and increased the level of GSH in the liver.Release of serum transaminases,alkaline phosphatase,lactate dehydrogenase and-glutamyl transpeptidase were significantly restored after propolis treatment.The activities of antioxidant enzymes,that is,superoxide dismutase,catalase,glutathione-S-transferase and glucose-6-phosphate dehydrogenase,were also concomitantly restored towards normal levels after propolis administration.These observations clearly demonstrate that propolis treatment augments antioxidant defense against mercury-induced toxicity and provide evidence that propolis has therapeutic potential as a hepatoprotective agent.Monika BHADAURIA Sangeeta SHUKLA Ramesh MATHUR Om PAGRAWAL Sadhana SHRIVASTAVA Sonia JOHRI Deepmala JOSHI Varsha SINGH Deepak MITTAL Satendra Kumar NIRALA 2008Integrative Zoology2008,3,4:0
7CCR5A32 mutation does not influence the susceptibility to HCV infection, severity of liver disease and response to therapy in patients with chronic hepatitis C显示文摘AIM: To study whether CCR5A32 mutation was associated with viral infection and severity of liver disease. METHODS: Two hundred and fifty two histologically proven, chronic HCV patients (mean age: 41±14 years; M/F: 164/88) were genotyped. PCR based genotyping of 32 bp deletion at the CCR5 locus was done. Four-hundred and eight matched healthy controls were studied to assess susceptibility to HCV infection. To assess correlation of immune gene polymorphism with severity of HCV related liver disease, patients with chronic HCV infection were divided into those with a fibrosis score of≤2 (mild) or > 2 (severe) and histological activity index (HAI) of≤5 or > 5. For correlation between CCR5A32 mutations and response to therapy, 129 patients who completed therapy were evaluated. RESULTS: The majority (89.4%) of the patients were infected with genotype 3. The frequency of homozygous CCR5A32 mutants was comparable to HCV patients as compared to the healthy controls (0.7% vs 0%, P = 0.1). Further more, the frequency of CCR5A32 mutation was comparable in patients with mild or severe liver disease. (P=NS). There was also no association observed with response to therapy and CCR5A32 mutation. CONCLUSION: CCR5A32 mutation does not have a role in disease susceptibility, severity or response to therapy in patients with chronic hepatitis C infection.Ankur Goyal PV Suneetha GT Kumar Deepak K Shukla Naveen Arora Shiv K Sarin 2006World Journal of Gastroenterology2006,12,29:0
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