Introduction Undergraduate medical research is very important not only for scientific learning but also for career progress. However, there are barriers, especially in developing countries, that restrict undergraduate research. This study aims to evaluate the barriers experienced by medical students in conducting research at undergraduate level. Methods It was an observational, cross-sectional survey conducted with 687 clinical students of two public medical universities of Pakistan. A self-structured questionnaire consisting of seven items was administered to assess the barriers in conducting research at undergraduate level. Data was processed and analysed through SPSS v 22.0 (IBM Corp., Armonk, NY, USA). Results Lack of knowledge as a barrier was identified by 90.68% (n = 623) students. The second most common barrier identified by the students was lack of time (88.79%; n = 610), followed by lack of mentoring as the third most common barrier (85.74%; n = 572). Subgroup analysis showed that lack of knowledge, lack of mentoring, limited data base access, lack of time, and lack of finances were more crucial barriers for female gender (p < 0.05). Only lack of interest was a crucial barrier for male gender (p < 0.05). Conclusion A number of barriers need to be addressed in order to enhance students' participation in clinical research such as lack of interest, funding, and poor availability of research mentors and access to scientific databases to improve participation in clinical research. Substantial amendments in the medical undergraduate curriculum are needed.
Introduction High-sensitivity C-reactive protein (hs-CRP) has emerged to be a very useful and reliable clinical marker of primary as well as secondary cardiovascular morbidity and mortality. Elevated hs-CRP contributes to underlying atherogenesis and worsens disease prognosis. Along with their lipid-lowering properties, statins also contribute to the alleviation of micro-inflammation and reduces pro-inflammatory markers. The aim of this study is to compare the effects of rosuvastatin and atorvastatin in lowering hs-CRP levels in statin-naive patients admitted with acute coronary syndrome (ACS). Methods In this prospective, open-label randomized trial, group A was given rosuvastatin 40 mg daily and group B was given atorvastatin 20 mg daily along with standard post-ACS therapy. Lipid profile (mg/dL), hs-CRP (mg/L) and erythrocyte sedimentation rate (ESR) (mm/Hr) were recorded and measured as the baseline (before starting therapy) and then again after four weeks. The data were analyzed using SPSS for Windows version 22.0 (IBM Corp., Armonk, NY). Results With four weeks of treatment, both group A and B showed statistically significant reduction in serum hs-CRP levels (p<0.0001). In group A, there was a mean 51% decrease in hs-CRP levels, and in group B, a 35% reduction was seen. Group A showed markedly low hs-CRP levels than group B after four weeks of therapy (18.46 ± 6.35 vs. 24.67 ± 8.45) (p<0.0001). Group A showed mean 16% decrease in ESR levels as compared to 14% decrease in group B. Group A showed lower ESR levels than group B after four weeks of therapy (19.59 ± 11.83 vs. 20.52 ± 12.13) (p<0.0001). Conclusion Rosuvastatin showed a 50% decrease and atorvastatin showed a 35% reduction in serum hs-CRP levels in statin-naive ACS patients. Rosuvastatin has a more effective role in reducing micro-inflammation in ACS patients.
Despite several advancements in stroke care, disparities continue to exist with regard to sex differences in cerebrovascular disease. These sex differences are due to a combination of several factors, many of which are unique to the female sex. Some of these unique factors, such as pregnancy and menopause, are related to hormonal changes seen throughout the female life cycle. Hormonal fluctuations, which impact the protective effects of the female sex hormones, can be induced by the use of hormonal contraception. Other risk factors, although present in both sexes, have a higher prevalence in elderly females, such as atrial fibrillation leading to cardioembolic strokes. Similarly, differences in premorbid modified Rankin Scale have an impact on the differences in stroke outcome between the two sexes. Clinical research aimed toward highlighting potential causes of these disparities has shown important differences in the calibers of blood vessels in the cerebral circulation between the two sexes, whereas basic science research has shown differences in circulating endothelial progenitor cell pools between males and females, with higher levels being more protective. With the increasing awareness of these sex differences, future research is being geared toward gender-specific modes of therapy, focusing on the molecular level, as well as the individual patient.
Henoch-Schönlein purpura (HSP) is a vasculitic syndrome that commonly involves small vessels of the skin, joints, intestines, and kidney. Although skin involvement is a sine qua non for the diagnosis of HSP, renal involvement is the greatest cause of long-term morbidity and mortality. Renal involvement in HSP is identified by proteinuria and/or hematuria. This was seen in 29% of individuals under the age of 16 among the nearly 1600 previously reported cases of HSP reviewed by Austin and Balow. 1 Hypertension and renal failure are less common complications of the renal vasculitis seen in this disease. In a review of 88 cases of childhood HSP, 35 children had an acute nephritic syndrome complicating their hematuria, defined as 2 of the following: hypertension, azotemia, and oliguria. 2 Treatment of HSP is largely supportive. Corticosteroids may be of use in treating abdominal pain, 3 and their use in arthritis is controversial, but uncontrolled or retrospective trials do not support the use of glucocorticoids in HSP nephritis 4 (reviewed in Austin and Balow 1 )We report the case of 2 children with HSP who had significant hypertension resistant to treatment with b-adrenergic blocking agents and vasodilators, one of whom had no other evidence of renal disease. In one child, the hypertension responded to therapy with captopril, suggesting a renin-angiotensin-mediated mechanism for the hypertension. In both children, initiation of corticosteroid therapy resulted in prompt resolution of hypertension, permitting the discontinuation of antihypertensive medications. The hypertension recurred with tapering of the steroids, only to respond to higher doses of glucocorticoids. Case 1A previously well 4-year-11-month-old white boy was admitted to a local hospital with a 3-day history of crampy abdominal pain and a 1-day history of emesis and fever to 39°C. He had been evaluated 1 week earlier for ankle pain with erythema and possible swelling. The pain woke him at night, prevented ambulation on first rising, and improved during the day. He had no respiratory symptoms or rash. Physical examination at the referring hospital revealed him to be afebrile with a BP of 108/58 mm Hg. His abdomen had mild epigastric tenderness and moderate splenomegaly (2 cm below left costal margin). The remainder of the examination was normal. His CBC (complete blood count) was normal, but the ESR (erythrocyte sedimentation rate) was 54 mm/h. Serum electrolytes were normal; urea nitrogen was 15 mg/dL, and creatinine was 0.4 mg/dL. Urinalysis showed only trace protein (30 mg/dL) but was otherwise completely normal. An X ray of the abdomen showed only fecal impaction. Abdominal ultrasound confirmed splenomegaly (9.5 cm) but was otherwise unremarkable.Abdominal pain persisted despite oral hydration and an enema. The patient developed painful swelling of the right knee and was intolerant of oral alimentation, so he was transferred to the Children's Hospital of Buffalo. Here, physical examination showed him to have episodes of severe colicky abdominal pain...
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