A qualitative exploration of the perspectives of international medical students residing in university hostels amid COVID-19 pandemic lockdown

BackgroundCOVID-19 pandemic has portentously frightened the existence of life all over the world. The lockdown approach was adopted as a containment strategy as the disease itself has manifested severe social, economic, and psychiatric implications. ObjectivesTo explore the perception and preparedness of international medical students residing in university hostels amid the COVID-19 pandemic lockdown. DesignA semi-structured interview guide was developed in this qualitative study design. All the interviews were audio-taped, transcribed verbatim, and then analyzed for thematic contents by standard content analysis framework. SettingInterviews were conducted in university hostels in Punjab, Pakistan. ParticipantsA total of 11 international medical students were interviewed face-to-face through the purposive sampling technique to obtain in-depth individual viewpoints. ResultsThe thematic content analysis yielded five major themes: Familiarity with COVID-19, Perceptions and attitudes towards COVID-19, Preparedness for safety against COVID-19, Barriers to lifestyle, and Psychological perspectives. A better general perception and preparedness among international medical students regarding COVID-19 was found. Good knowledge regarding the overview of COVID-19; adequate preventive approaches such as social distancing, use of masks, gloves, and sanitizers; and compliance with the lockdown measures were reported by the respondents. The pertinent issue raised by the respondents is the disturbance in normal routine due to distortion in social life and isolation that may cause psychological stress. ConclusionsThe findings from this study lighten the peoples perspectives that help the government to prepare public health strategies based on population-focused approaches. The present study demonstrates the respondents opinion on COVID-19 management by personal hygiene, social distancing, and complying with the lockdown measures. Furthermore, it demands that timely and evidence-based teaching-learning techniques should be adopted for students engagement which ensures mental health and self-motivation as well. Therefore, they can utilize their time productively which could have a long-term effect on their careers and healthcare services.

Involvement of throm box aneA2 and tyrosine kinase in the synergistic interaction of platelet activating factor and calcium ionophore A23187 in human platelet aggregation

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 subthreshold concentrations of PAF (5 nM) and A23187 (1 micrometer) was inhibited by PAF receptor blocker (WEB 2086, IC50=0.65 micrometer) and calcium channel blockers, diltiazem (IC50=13 micrometer) and verapamil (IC50=18 micrometer). Pretreatment of platelets with PAF and A23187 induced rise in intracellular calcium and this effect was also blocked by verapamil. While examining the role of the down stream signaling pathways, we found that 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 micrometer), a cyclooxygenase inhibitor (indomethacin; IC50=0.2 micrometer) and inhibitor of TLCK, herbimycin A with IC50 value of 5 micrometer. The effect was also inhibited by a specific TXA2 receptor antagonist, SQ 29548 with very low IC50 value of 0.05 micrometer. However, the inhibitors of MAP kinase, PD98059 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 thromboxane and tyrosine kinase pathways.

Molecular mechanisms involved in human platelet aggregation by synergistic interaction of platelet-activating factor and 5-hydroxytryptamine

Our recent studies have shown that co-activation of Gq and Gi proteins by 5-hydroxytryptamine (5-HT) and adrenaline show synergism in human platelet aggregation. This study was conducted to examine the mechanism(s) of synergistic interaction of 5-HT and platelet activating factor (PAF) in human platelets. We show that PAF, but not 5-HT, increased platelet aggregation in a concentration-dependent manner. However, low concentrations of 5-HT (2 microM) potentiated platelet aggregation induced by subthreshold concentration of PAF (40 nM) indicating a synergistic interaction between the two agonists and this synergism was blocked by receptor antagonists to either 5-HT or PAF. 5-HT also potentiated the effect of PAF on thromboxane A2 (TXA2) formation and phosphorylation of extracellularly regulated mitogen-activated protein kinases (ERK1/2). The synergism of 5-HT and PAF in platelet aggregation was inhibited by calcium (Ca2+) channel blockers, verapamil and diltiazem, phospholipase C (PLC) inhibitor, U73122, cyclooxygenase (COX) inhibitor, indomethacin, and MEK inhibitor, PD98059. These data suggest that synergistic effect of 5-HT and PAF on human platelet aggregation involves activation of PLC/Ca2+, COX and MAP kinase pathways.

Molecular mechanisms involved in human platelet aggregation by synergistic interaction of platelet-activating factor and 5-hydroxytryptamine

Our recent studies have shown that co-activation of Gq and Gi proteins by 5-hydroxytryptamine (5-HT) and adrenaline show synergism in human platelet aggregation. This study was conducted to examine the mechanism(s) of synergistic interaction of 5-HT and platelet activating factor (PAF) in human platelets. We show that PAF, but not 5-HT, increased platelet aggregation in a concentration-dependent manner. However, low concentrations of 5-HT (2 microM) potentiated platelet aggregation induced by subthreshold concentration of PAF (40 nM) indicating a synergistic interaction between the two agonists and this synergism was blocked by receptor antagonists to either 5-HT or PAF. 5-HT also potentiated the effect of PAF on thromboxane A2 (TXA2) formation and phosphorylation of extracellularly regulated mitogen-activated protein kinases (ERK1/2). The synergism of 5-HT and PAF in platelet aggregation was inhibited by calcium (Ca2+) channel blockers, verapamil and diltiazem, phospholipase C (PLC) inhibitor, U73122, cyclooxygenase (COX) inhibitor, indomethacin, and MEK inhibitor, PD98059. These data suggest that synergistic effect of 5-HT and PAF on human platelet aggregation involves activation of PLC/Ca2+, COX and MAP kinase pathways.