Asian Science Citation Index is committed to provide an authoritative, trusted and significant information by the coverage of the most important and influential journals to meet the needs of the global scientific community.  
ASCI Database
308-Lasani Town,
Sargodha Road,
Faisalabad, Pakistan
Fax: +92-41-8815544
Contact Via Web
Suggest a Journal
Articles by T.M. Ali
Total Records ( 2 ) for T.M. Ali
  S.A. Saeed , H. Rasheed , T.M. Ali , Y. Qazi , S. Kabraji , L. Paul , R. Khan , F.A. Hussain and S. Ahmad
  This study was conducted to investigate the effects of nimesulide in platelet aggregation. It shows that nimesulide (1-100 μ M) inhibited platelets aggregation induced by adrenaline, (20-200 μ M). It also inhibed thromboxane A2 (TXA2) formation by platelets at low concentration (IC50; 1 μ M). However, much lower concentrations of nimesulide (0.01-0.1 μ M) potentiated the aggregatory response of subthreshold concentrations of adrenaline (0.2-2 μ M). Such an effect was blocked by Ca2+-channel blockers, verapamil and diltiazem (IC50: 7 and 46 μ M, respectively), nitric oxide donor, SNAP (IC50: 2 μ M) and cinchonine (10 nM) but not by genistein (up to 10 μ M). These results are indicative of the concentration-dependent dual effects of nimesulide on human platelet aggregation. The synergistic effect of low doses of nimesulide and adrenaline seems to be mediated through inhibition of multiple signaling pathways.
  S.A. Saeed , H. Rasheed , S. Kumar , T.M. Ali , M.U. Butt , R.Dhangana , A. Jafri , S. Zehra and A.H. Gilani
  This study was conducted to examine the mechanism(s) of synergistic interaction of platelet-activating factor (PAF) and arachidonic acid (AA) in platelet aggregation. We found that the synergism in platelet aggregation mediated by subthershold concentration of PAF (5-40 nM) and AA (0.1-0.2mM) was inhibited by PAF receptor blocker (WEB 2086, IC50= 0.6 μM) showing that the effect is receptor mediated. To examine the role of the downstream signaling pathways, we found that such an interaction was inhibited by calcium channel blockers, diltiazem (IC50= 15 μM) and verapamil (IC50 = 20 μM), as well as by low concentrations of phospholipase C (PLC) inhibitor (U73122; IC50 = 6 μM) and MAP kinase inhibitor, PD 98059 (IC50= 3.5 μM). Inhibitor of AA-cyclooxygenase (flurbiprofen: IC50 = 3 μM) also inhibited PAF and AA induced aggregation showing the involvement of COX pathway. On the other hand, herbimycin A, a specific inhibitor of tyrosine light chain kinase (TLCK) and SNAP, a nitric oxide (NO) donor also inhibited PAF and AA-induced aggregation with IC50 values of 15 and 1.7 μM respectively. However, the inhibitor of protein kinase C (chelerythrine; 20 μM)) had no effect on aggregation induced by PAF and AA. These data suggest that the synergism between PAF and AA in platelet aggregation involves activation of PLC, COX, MAP kinase, TLCK and NO signaling pathways.
Copyright   |   Desclaimer   |    Privacy Policy   |   Browsers   |   Accessibility