ResearchMedical and pharmacy students’ attitudes towards physician-pharmacist collaboration in Kuwait

Objective : To assess and compare the attitudes of medical and pharmacy students towards physician - pharmacist collaboration and explore their opinions about the barriers to collaborative practice in Kuwait. Methods : A cross - sectional survey of p harmacy and medical students (n=467) was conducted in Faculties of Medicine and Pharmacy, Kuwait University. Data were collected via self - administered questionnaire from first - year pharmacy and medical students and students in the last two professional yea rs of the pharmacy and medical programs. Descriptive and comparative analyses were performed using SPSS, version 22. Statistical significance was accepted at p \u3c 0.05. Results : The response rate was 82.4%. Respondents had overall positive attitudes toward s physician - pharmacist collaboration. Pharmacy students expressed significantly more positive attitudes than medical students (p\u3c 0.001). Medical students rated th e three most significant barriers to collaboration to be: pharmacists’ separation from patien t care areas (n=100, 70.0%), lack of pharmacists’ access to patients’ medical record (n=90, 63.0%) and physicians assuming total responsibility for clinical decision - making (n=87, 60.8%). Pharmacy students’ top three perceived barriers were : lack of pharmac ists’ access to patients’ medical record (n=80, 84.2%), organizational obstacles (n=79, 83.2%), and pharmacists’ separation from patient care areas (n=77, 81.1%). Lack of interprofe ssional education was rated the fourth - largest barrier by both medical (n=7 9, 55.2%) and pharmacy (n=76, 80.0%) students. Conclusions : Medical and pharmacy students in Kuwait advocate physician - pharmacist collaborative practice, but both groups identified substantial barriers to implementation. Efforts are needed to enhance under graduate/postgraduate training in interprofessional collaboration, and to overcome barriers to physician - pharmacist collaboration to advance a team approach to patient care

Effects of Cardiac Hypertrophy, Diabetes, Aging, and Pregnancy on the Cardioprotective Effects of Postconditioning in Male and Female Rats

Background. Aging, left ventricular hypertrophy (LVH), diabetes mellitus, and pregnancy are well-recognized risk factors that increase the prevalence of cardio-ischemic events and are linked to poor clinical recovery following acute myocardial infarction. The coexistence of these risk factors with ischemic heart disease (IHD) deteriorates disease prognosis and could potentially lead to fatal arrhythmias and heart failure. The objective of this study was to investigate the vulnerability of hearts with aging, LVH, diabetes, and pregnancy to ischemic insult and their response to pacing postconditioning- (PPC-) induced heart protection. Methods. Hearts isolated from aged, spontaneously hypertensive and diabetic male and female rats and hearts from pregnant female rats (n=8 per group) were subjected to coronary occlusion followed by reperfusion using a modified Langendorff system. Hemodynamics data were computed digitally, and cardiac damage was accessed by measurements of infarct size and cardiac enzyme release. Results. There were no significant differences in the vulnerability of all hearts to ischemic insult compared to their respective controls. PPC improved cardiac hemodynamics and reduced infarct size and cardiac enzyme release in hearts isolated from aged and spontaneously hypertensive female rats and female rats with hypertrophied hearts subjected to PPC (P<0.001). Aged or hypertrophied male hearts were not protected by PPC maneuver. Moreover, the protective effects of PPC were lost in diabetic male and female hearts although retained in hearts from pregnant rats. Conclusions. We demonstrate that aging, LVH, diabetes mellitus, and pregnancy do not affect cardiac vulnerability to ischemic insult. Moreover, PPC mediates cardioprotection in a gender-specific manner in aged and spontaneously hypertensive rats. Diabetes mellitus provokes the protective effects of PPC on both genders equally. Finally, we demonstrate that PPC is a new cardioprotective maneuver in hearts from pregnant female rats

The effect of sphingosine-1-phosphate on colonic smooth muscle contractility: Modulation by TNBS-induced colitis

<div><p>Aim</p><p>Increased levels of circulating sphingosine-1-phosphate (S1P) have been reported in ulcerative colitis. The objective of this study was to examine the effect of S1P on colonic smooth muscle contractility and how is it affected by colitis.</p><p>Methods</p><p>Colonic inflammation was induced by intrarectal administration of trinitrobenzene sulfonic acid. Five days later colon segments were isolated and used for contractility experiments and immunoblotting.</p><p>Results</p><p>S1P contracted control and inflamed colon segments and the contraction was significantly greater in inflamed colon segments. S1P-induced contraction was mediated by S1PR1 and S1PR2 in control and S1PR2 in inflamed colon segments. S1PR3 did not play a significant role in S1P-induced contractions in control or inflamed colon. S1PR1, S1PR2 and S1PR3 proteins were expressed in colon segments from both groups. The expression of S1PR1 and S1PR2 was significantly enhanced in control and inflamed colon segments, respectively. S1PR3 levels however were not significantly different between the two groups. Nifedipine significantly reduced S1P-induced contraction in control but not inflamed colon segments. Thapsigargin significantly reduced S1P-induced contraction of the inflamed colon. GF 109203X and Y-27632, alone abolished S1P-induced contraction of the control but not inflamed colon segments. Combination of GF 109203X, Y-27632 and thapsigargin abolished S1P-induced contraction of inflamed colon segments.</p><p>Conclusion</p><p>S1P contracted control colon via S1PR1 and S1PR2 and inflamed colon exclusively via S1PR2. Calcium influx (control) or release (inflamed) and calcium sensitization are involved in S1P-induced contraction. Exacerbated response to S1P in colitic colon segments may explain altered colonic motility reported in patients and experimental models of inflammatory bowel disease.</p></div

The Interplay between the Renin Angiotensin System and Pacing Postconditioning Induced Cardiac Protection.

Accumulating evidence suggests a cardioprotective role of pacing postconditioning (PPC) maneuvers in animal models and more recently in humans. The procedure however remains to be optimized and its interaction with physiological systems remains to be further explored. The renin angiotensin system (RAS) plays a dual role in ischemia/reperfusion (I/R) injury. The interaction between RAS and PPC induced cardiac protection is however not clearly understood. We have recently demonstrated that angiotensin (1-7) via Mas receptor played a significant role in PPC mediated cardiac protection against I/R injury.The objective of this study was to investigate the role of angiotensin converting enzyme (ACE)-chymase-angiotensin II (Ang II)-angiotensin receptor 1 (AT1) axes of RAS in PPC mediated cardiac protection.Isolated rat hearts were subjected to I/R (control) or PPC in the presence or absence of Ang II, chymostatin (inhibitor of locally produced Ang II), ACE blocker (captopril) or AT1 antagonist (irbesartan). Hemodynamics data was computed digitally and infarct size was determined histologically using TTC staining and biochemically by measuring creatine kinase (CK) and lactate dehydrogenase levels.Cardiac hemodynamics were significantly (P<0.001) improved and infarct size and cardiac enzymes were significantly (P<0.001) reduced in hearts subjected to PPC relative to hearts subjected to I/R injury. Exogenous administration of Ang II did not affect I/R injury or PPC mediated protection. Nonetheless inhibition of endogenously synthesized Ang II protected against I/R induced cardiac damage yet did not block or augment the protective effects of PPC. The administration of AT1 antagonist did not alleviate I/R induced damage. Interestingly it abrogated PPC induced cardiac protection in isolated rat hearts. Finally, PPC induced protection and blockade of locally produced Ang II involved enhanced activation of ERK1/2 and Akt components of the reperfusion injury salvage kinase (RISK) pathway.This study demonstrate a novel role of endogenously produced Ang II in mediating I/R injury and highlights the significance of AT1 signaling in PPC mediated cardiac protection in isolated rodents hearts ex vivo. The interaction between Ang II-AT1 and PPC appears to involve alterations in the activation state of ERK1/2 and Akt components of the RISK pathway

Effect of S1P on KCl-induced contractions in control and colitic colon segments.

<p>After equilibration colonic segments from control rats were contracted twice with KCl (80m M) and washed immediately after reaching a peak contraction. Then colonic segments were incubated with BSA (40 μM) or S1P (10 or 40 μM) and allowed to reach a maximal response (A). Traces of S1P (40μM) induced contraction in control and colitic colon segments are shown in (B), arrows indicate S1P addition. Mean S1P (40μM) induced contraction in control and colitic colon segments is shown in (C). Data is mean ± SEM of S1P induced contraction expressed relative to the second KCl-induced contraction, * P < 0.05.</p

The Role of calcium and calcium sensitization pathways in S1P induced contraction in control and colitic colon.

<p>Colonic segments from control (n = 3–6) and colitic (n = 3–7) rats were equilibrated in Krebs solution for 30 min and contracted twice with KCL with consecutive washes after the maximal contraction was reached. Tissues were then preincubated with L-type calcium channel blocker (nifedipine, 1μM) or SERCA antagonist (thapsigargin, 10μM) (A) or with PKC antagonist (GF 102903x, 1μM), ROCK inhibitor (Y-27632, 10μM) or inhibitor cocktails (B) for 30 min before the addition of S1P (40μM). Data is mean ± SEM of S1P induced contraction expressed relative to the second KCl-induced contraction, * P < 0.05 versus S1P induced contraction in corresponding group.</p

Proposed mechanism of S1P induced contraction in control and colitic colon.

<p>In control colon S1P activates S1PR1 and S1PR2 and induce contractions that are dependent on calcium influx via L-type calcium channels, calcium release from the sarcoplasmic reticulum and calcium sensitization pathways including PKC and Rho kinase (A). In colitic colon however S1P induces larger contractions via S1PR2 that are independent of calcium influx through L-type calcium channels yet it involves intracellular calcium release and calcium sensitization pathways (B). The contribution of these pathways however appears to be different in control and inflamed colon segments. Whereas the blockade of a single pathway completely abolishes the response to S1P in control segments, S1P induced contractions appear to be salvaged by other pathways in inflamed colon segments. Eradication of S1P induced contraction in inflamed colon require simultaneous blockade of intracellular calcium release (SERCA) and calcium sensitization pathways (PKC and Rho kinase).</p

Characterization of ulcerative colitis.

<p>(A) Colon weight to length ratio in control and colitic rats. (B) Representative eosin and hematoxylin stained colon sections from control and TNBS-treated rats. Data is mean ± SEM, *P < 0.05.</p

The Role of S1PR in S1P induced contraction in control and colitic colon.

<p>Colonic segments from control (A) and colitic (B) rats were equilibrated in Krebs solution for 30 min and contracted twice with KCL (80mM) with consecutive washes after the maximal contraction was reached. Tissues were then preincubated with S1PR1 agonist (SEW2871, 1μM) S1PR1 antagonist (W146, 10μM), S1PR2 antagonist (JTE-013, 1μM) or with S1PR3 antagonist (CAY-10444, 10μM) for 30 min before the addition of S1P (40μM). Data is mean ± SEM of S1P induced contraction is expressed relative to the second KCl-induced contraction, * P < 0.05 relative to S1P induced contraction.</p