A comparative study on effectiveness of workshop education versus education via mobile learning (m-learning) in developing medical students’ knowledge and skill about cardiopulmonary resuscitation

INTRODUCTION: A variety of educational approaches are being used today to improve learning in the field of cardiopulmonary resuscitation. Therefore, the present study was conducted to compare workshop education with education via mobile learning (M-learning) in terms of their efficacy in developing medical students’ knowledge and skills about cardiopulmonary resuscitation. MATERIAL AND METHODS: The present study was quasi-experimental performed on 60 interns selected from a university of medical sciences in southwest Iran. Participants were assigned to either the workshop education group (n = 30) or the mobile learning group (n = 30). Before and after the intervention, the knowledge and skills of the participants in terms of basic and advanced cardiopulmonary resuscitation were measured by a questionnaire. The collected data were analyzed using descriptive statistics, Independent-Samples t-Test, Paired-Samples t-Test, and Chi-Square Test in SPSS software v. 22. RESULTS: Education via mobile learning caused a significant increase in the participants’ knowledge about cardiopulmonary resuscitation (p < 0.05). However, this method did not result in a significant difference in the participants’ skill scores, while the workshop education group showed a significant increase in their cardiopulmonary resuscitation skill scores (p < 0.05). CONCLUSIONS: Our results revealed that education via mobile learning was better in enhancing medical students’ knowledge about cardiopulmonary resuscitation. However, workshop education was more effective in developing practical skills in the field of cardiopulmonary resuscitation. Accordingly, educators are recommended to employ a combination of mobile learning and workshop education for achieving better results

Cerebral Ischemia/Reperfusion Injury in the Hyperthyroid Rat

Background: Hyperthyroidism as a risk factor for stroke is not conclusive. There are no definite data on the relationship between ischemic cerebrovascular injury and hyperthyroidism. This study was designed to define whether the outcomes of post-ischemic stroke injury are influenced by chronic hyperthyroidism. Methods: Two groups of hyperthyroid (HT) and control euthyroid rats of equal numbers (n=22) were included in the study. Hyperthyroidism was induced for 4 weeks by adding L-thyroxine (300 μg/kg) to drinking water. The middle cerebral artery occlusion technique was used to induce focal cerebral ischemia. Neurological disability (neurological deficit score [NDS]) was evaluated after 24 hours, and the rats were sacrificed to obtain their brain. Triphenyl Tetrazolium Chloride (TTC) staining and Evans Blue (EB) extravasation were used to quantify cerebral infarct volume and cerebrovascular integrity disruption. Data analysis was done using SPSS, version 21. Results: Thyroid hormones levels, T3 (314±7 vs. 198±3 ng/dL; P=0.001) and T4 (9.8±0.3 vs. 3.08±0.07 μg/dL; P=0.001), were significantly higher in the HT group than in the controls. Furthermore, most clinical signs seen in hyperthyroid patients were also present in the HT group. Comparison of the data on cerebral ischemia between the HT and control groups showed significant increases in the NDS (2.76±0.16 vs. 2.23±0.09; P=0.03), cerebral infarct volume (479±12 vs. 266±17 mm3; P=0.001), and EB extravasation (50.08±2.4 vs. 32.6±1.2 μg/g; P=0.001) in the former group. Conclusion: The intensified cerebral infarct size and cerebrovascular integrity disruption suggested that chronic hyperthyroidism aggravated post-stroke injury in the rats. More investigation is required to analyze the pathological mechanisms underlying the association between cerebrovascular disease and hyperthyroidism

Blockade of Central Angiotensin II AT1 Receptor Protects the Brain from Ischemia/Reperfusion Injury in Normotensive Rats

Background: Stroke is the third leading cause of invalidism and death in industrialized countries. There are conflicting reports about the effects of Angiotensin II on ischemia-reperfusion brain injuries and most data have come from chronic hypertensive rats. In this study, hypotensive and non-hypotensive doses of candesartan were used to investigate the effects of angiotensin II AT1 receptor blockade by transient focal cerebral ischemia in normotensive rats. Methods: In this experimental study, 48 male Sprague-Dawley rats were randomly divided into four groups (n=12). Sham group, the control ischemic group, and two ischemic groups received candesartan at doses of 0.1 or 0.5 mg/kg at one hour before ischemia. Transient focal cerebral ischemia was induced by 60 minutes occlusion of the middle cerebral artery, followed by 24 h reperfusion. The neurological deficit score was evaluated at the end of the reperfusion period. The total cortical and striatal infarct volumes were determined using triphenyltetrazolium chloride staining technique. Tissue swelling was calculated for the investigation of ischemic brain edema formation. Results: In comparison with the control ischemic group, AT1 receptor blockade with both doses of candesartan (0.1 or 0.5 mg/kg) significantly improved neurological deficit and lowered cortical and striatal infarct sizes. In addition, pretreatment with candesartan significantly reduced ischemia induced tissue swelling. Conclusion: Angiotensin II by stimulating AT1 receptors, participates in ischemia-reperfusion injuries and edema formation. AT1 receptor blockade with candesartan decreased ischemic brain injury and edema and improved neurological outcome

Cerebral Ischemia-Reperfusion Injuries in Vanadyl-Treated Diabetic Rats

Background: Ischemic stroke recovery is poor in diabetic mellitus (DM). Vanadium compounds (vanadium) relieve DM signs, but their influences on cerebral ischemia/reperfusion injury (I/RI) are inconclusive. Herein, the intensity of I/RI was inspected in vanadium-treated DM rats. Methods: Rats made diabetic with a single intravenous dose of streptozocin (39 mg/kg). Normal and DM rats used water or vanadyl solution for 45 days. Under isoflurane anesthesia, right middle cerebral artery occlusion was performed for 60 minutes and 12 hours reperfusion. Ischemic rats were divided into untreated-control normal (ICN) and diabetic (ICD), vanadium-treated normal (IVTN) and diabetic (IVTD) groups (n=14 each). After neurological deficit score (NDS) test, the rats were sacrificed and their brain removed and stained with triphenyltetrazolium chloride (TTC) to measure cerebral infarct volume (CIV, mm3) or Evans blue extravasation (EBE, μg/g wet-tissue). Data analysis was performed using one-way ANOVA and Tukey’s test (SPSS software, version 21.0) and P values <0.05 were considered statistically significant. Results: Blood glucose (BG, mg/dL) was similar in ICN and IVTN, elevated in IVTD and ICD (245±6 vs. 344±2, P<0.001). The increased CIV in ICN and IVTN was similar (48±2 and 34±5), very high in ICD but lower in IVTD (249±37 vs. 110±16, P<0.001). EBE was absent in non-lesioned hemispheres, similarly increased in lesioned hemispheres of ICN and IVTN (14±1 and 13±1). EBE in IVTD was significantly lower than ICD (21±2 vs. 33±5, P=0.01). Conclusion: I/RI was moderate in normoglycemia and did not change with vanadium. Hyperglycemia robustly intensified I/RI. Vanadium ameliorated hyperglycemia and reduced I/RI. Nonetheless, more investigations are required to link the mechanisms of vanadium on DM and stroke injuries

Local Administration of L-Arginine Accelerates Wound Closure

Objective(s)The process of wound healing involves tightly integrated events including inflammation, granulation tissue formation and remodeling. Systemic administration of L arginine promotes wound healing but its global side effects are undesirable. To confine the action of L-arginine at the site of injury, we tested the effects of local administration of L arginine on the healing of excisional wound in the rat.Materials and MethodsFull thickness excisional wounds were generated on the dorsum of adult male rats. The test wounds received 200 µm or 400 µm of L-arginine on day 3 and 5 post-wounding. Normal saline was injected into the sham wounds which were otherwise treated as the test wounds. Control wounds remained unmanipulated. The wound size was monitored daily by imaging. To determine the rate of wound closure, wound images were scanned and the rate of size reduction was analyzed and quantified by ScnImage software. The repaired tissues were harvested on day 12 post-wounding. The tissue sections were prepared and stained for microscopic examination. ResultsWounds treated with L-arginine showed a significant increase in the rate of wound closure. The morphology of basal keratinocytes was altered, and the thickness of neoepidermis was markedly reduced in the wounds treated with L-arginine. Both tested dose of L-arginine were equally effective. ConclusionLocal administration of L-arginine accelerates wound closure and has profound effects on keratinocytes performance during the process of healing. Therefore, it can be potentially used for treatment of skin disorders, in particular, those characterized by hyperkeratosis

Analysis of Outcomes in Ischemic vs Nonischemic Cardiomyopathy in Patients With Atrial Fibrillation A Report From the GARFIELD-AF Registry

IMPORTANCE Congestive heart failure (CHF) is commonly associated with nonvalvular atrial fibrillation (AF), and their combination may affect treatment strategies and outcomes