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Articles by Sheikh Arshad Saeed
Total Records ( 4 ) for Sheikh Arshad Saeed
  Sheikh Arshad Saeed , Imran Manzoor , Javeria Quadri , Shumaila Tasneem and Shabana Usman Simjee
  Evidence is growing that bioactive substances found in a variety of plant-derived foods have the potential to reduce the risk of chronic diseases, such as cardio vascular disease and cancer. These substances can be categorized as: flavonoids and allied phenolic and polyphenolic compounds, terpenoids, alkaloids and sulphur-containing compounds. Much of the evidence collated to date is derived from animal studies, in vitro experiments and ex vivo studies in humans. Work should focus on their bioavailability in humans and the quantity required for their beneficial effects.
  Sheikh Arshad Saeed , Sarah Khalid Khan , Saira Abdul Aziz Samani , Kashfa Farhat , Natasha Imtiaz Hansraj , Asthma Mushir Ahmad Khan , Ameer Zaigham Rasheed , Abdul Mueed Zafar , Muhammad Ameen Rauf and Sagheer Ahmad
  Blood plasma was found to contain endogenous inhibitor of prostaglandin (PG) synthase (EIPS) and this activity was associated with at least two plasma components, albumin and haptoglobin. Hemoglobin, a stimulant of PG biosynthesis which is bound by haptoglobin, reversed the inhibitory effect of haptoglobin and reduced the inhibition by albumin, acetylsalicylate or indomethacin. It is proposed that in physiological situations the albumin-associated EIPS mainly helps to prevent excessive PG production, whereas in tissue injury the acute phase protein haptoglobin plays a more important role. Possible clinical applications of EIPS are discussed.
  Huma Rasheed , Afshin Hasan Tirmizi , Farah Salahuddin , Nida Batool Rizvi , Mehreen Arshad , Saadia Zohra Farooq and Sheikh Arshad Saeed
  The present study was carried out to examine the mechanisms of the synergistic interaction of PAF and A23187 mediated platelet aggregation. We found that platelet aggregation mediated by subthershold concentrations of PAF (5-40 nM) and A23187 (0.5- 1 μM) was inhibited by PAF receptor blocker (WEB 2086; IC50=0.65 μM) and calcium channel blockers, verapamil (IC50=18 μM) and diltiazem (IC50=13 μM). While examining the role of the down stream signaling pathways, we found platelet aggregation induced by the co-addition of PAF and A23187 was also inhibited by low concentrations of phospholipase C (PLC) inhibitor (U73122; IC50=10 μM), a cyclooxygenase inhibitor (indomethacin; IC50=0.2 μM) and inhibitor of TLCK with IC50 value of 5 μM. The effect was also inhibited by a specific TXA2 receptor antagonist (SQ 29, 548), with very low IC50 value of 0.05 μM. However, The inhibitors of MAP kinase (PD 98059) and, protein kinase C (chelerythrine) had no effect on PAF and A23187-induced platelet aggregation. These data suggest that the synergism between PAF and A23187 in platelet aggregation involves activation of PLC/Ca2+, TLCK and COX pathways.
  Sheikh Arshad Saeed , M. Iqbal Choudhary , Kiran Fatima , Akbar Jaleel Zubairi , Imran Manzoor , Mahnaz Nuruddin Gitay and Seema Saeed
  Many of us would like to experience a healthy old age. It might now be possible to achieve this goal by protecting our immune system from the damage that accumulates with time. The story starts with the explorer, Ponce de Leon, who set forth from Spain in 1513 in search of the `Fountain of Youth`. Both before and since that time, claims have been put forth, often without the benefit of scientific testing, that certain interventions may increase lifespan or promote sustained health in old age. Age-associated reductions in circulating levels of peroxisome proliferator activated receptor α (PPARα) activators such as dehydroepiandrosterone-3β (DHEAS) may compromise normal cellular responses that involve PPARα activation, thereby hindering the essential maintenance of cellular redox balance. Excesses in reactive oxygen species can lead to the activation of nuclear factor-kappa β (NF-κB) and the downstream expression of some NF-κB controlled inflammatory genes. This imbalance in redox state appears to be intimately linked to many age-associated alterations in immune function and other ageing-related tissue damage. Supplementing aged mice with PPARα activators has proven to be helpful in re-establishing cellular redox balance, thereby promoting the reacquisition of immune competence and possibly alleviating a number of age-associated pathophysiologies. An understanding of the ageing at the molecular level offers hope for strengthening the aged immune system; thereby preventing some of the diseases commonly linked to advanced age.
 
 
 
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