In 2013, BSOM and UCM in Saudi Arabia entered a partnership, one that would transfer the medical school curriculum from BSOM to UCM. All components of the curriculum including courses, learning materials, instructional methods (peer instruction sessions (PI), team based learning sessions), and examinations were transferred. In fall 2014, UCM initiated its first class of medical students who matriculated into the first year of the BSOM curriculum at UCM. One year 1 course, Molecular Basis of Medicine (MBM) is comprised of molecular biology, biochemistry, metabolism, and human genetics. Our goal was to compare directly final grades of the UCM and BSOM Med 1 students in MBM. Analysis of the grading showed that 92.7% of BSOM students (n=111) passed the course, compared to 91.6% of UCM students (n=70). When broken down by sex, 96.7 % of UCM men (n=30) passed, while 93% of BSOM men (n=57) passed. UCM women (n=40) had 87.8 % pass rate, compared to 92.6 % for BSOM women (n=54).The final course averages were 80.5% +/− 10 for UCM and 84.4% +/− 8.4 for BSOM students, suggesting that there is a similar outcome in the two countries using the same material. Women achieved scores of 78.3% +/− 11 at UCM while at BSOM, they scored at 83.6% +/− 8.7. Men averaged 82.1% +/− 10 at UCM and 85.1% +/− 8.0 at BSOM. However, the two institutions exhibited distinctly different results on exams; UCM students achieved 76.7 %+/− 9 average on exams, while BSOM students scored 82.6% +/− 8.9. Furthermore, UCM men achieved 79.6% +/− 10, while the women scored 74.5% +/− 9 as compared to BSOM men scoring 83.3 %+/− 9 and 81.9% +/− 9 for BSOM women. UCM faculty greatly enhanced student learning by initiating innovative teaching techniques for their students. UCM faculty devised PI based reviews prior to exams, assessed each examination result, and using guidelines established by the Saudi government and Qassim University, made adjustments to exams. The analyzed data to date suggest that there is no major difference in the final student grades for the first iteration of MBM between BSOM and UCM. The only observed difference between BSOM and UCM student achievement is that UCM students are stronger in the active learning portion of MBM and weaker in the examination portion of MBM than BSOM Med 1 students. In order to address this potential problem, the UCM faculty and administration have revamped the premed curriculum at Qassim University/UCM. More data analyses on MBM at both UCM and BSOM in the coming years will provide additional and more quantitative results on this unique partnership. The BSOM-UCM partnership is best exemplified by the MBM course, in which a team of dedicated team of faculty and administrators implemented a complete, well-established course from a fully accredited USA medical school in a new medical school in the Kingdom of Saudi Arabia despite being separated by 8000 miles in distance.
Objective: Egypt has one of the highest incidences of intrauterine fetal growth restriction (IUGR) around the world. In the current study, we tried to explore the effect of Aflatoxin B1 toxicity as a risk factor of IUGR and to determine the role of placental apoptotic indices in the pathogenesis of IUGR and their association with maternal risk factors as residency, working and exposure to smoking.
Materials and Methods: A case-control study was done at Women Health Hospital; Assiut University, Egypt included 60 pregnant women with asymmetrical IUGR besides a control group of 40 normal pregnancies were selected. Maternal urine samples were obtained for measuring Aflatoxin B1 level by layer chromatography. Quantitative determination of human placental Bcl-2 and caspase-3 using a monoclonal antibody-based enzyme-linked immunosorbent assay kits were performed.
Results: The results showed that aflatoxin B1 positive cases in the IUGR group had significantly higher placental caspase-3 and lower placental Bcl-2 concentrations than those which were aflatoxin B1 negative (p<0.01). The levels of placental apoptotic indices were higher in working women who lived in urban areas and those exposed to cigarette smoke than non-working women who lived in rural areas and non-smokers.
Conclusions: Aflatoxin B1 may affect the fetal growth by increasing the placental apoptosis. These results may highlight the importance of aflatoxin B1 which may contribute to the complex etiology of IUGR. Placental apoptotic indices levels were significantly affected by maternal residency, working and exposure to smoking in pregnancies complicated with IUGR.
Abstract: Background: Testosterone facilitates various metabolic processes in the bones, muscles, bone marrow, brain and immune system. Testosterone deficiency may contribute to cardiovascular diseases, central obesity and metabolic dysfunction.
Aim: to investigate the effects of testosterone deficiency on blood glucose levels, insulin sensitivity, vitamin D, Homeostatic model assessment of insulin resistance (HOMA-IR), Homeostatic model assessment for beta function (HOMA-IR) and serum lipids in rat models of andropause. Methods, 48 male rats divided into 4 equal groups (n=12/group); a) Control (C) group. b) Orchiectomy (O) group underwent bilateral removal of the testicles. c) Orchiectomy and treated (O+T) group given daily IM testosterone replacement therapy for 7 days, d) Sham and treated (Sh+T) group in which sham operated rats were given the same daily dose of T as O+T group for 7 days. Results: we found that plasma glucose concentration increased significantly (P<0.001) in O group. This increase was corrected by testosterone injection in O+T group. In (Sh+T) group, there is a significant reduction in serum glucose (P<0.001). We also found that insulin level reduced significantly (P<0.001) in O group. This reduction in insulin level was corrected by testosterone. In (Sh+T) group, insulin level increased significantly. 25-OHVD3 was reduced significantly (P<0.05) in O group and increased significantly in O+T group. HOMA-IR level decreased significantly (P<0.001) and this reduction was corrected by Testosterone. HOMA-β reduced significantly (P<0.001) and this reduction was corrected by Testosterone in O+T group. In SH group, there is a marked increase in HOMA-β. We also found insignificant differences between the four groups in serum triglycerides. However, we found very highly significant differences in total cholesterol, LDL and VLDL between C group and O group and very highly significant differences between O+T group and Sh+T group in comparison with O group. We also found significant differences in serum HDL-c in (O) group in comparison with (C) group and between O+T and Sh+T groups in comparison with O group. In conclusion, we found
significant reduction in 25-OH(VD), Testosterone, Insulin, HOMA-IR and HOMA-B and significant increase in glucose serum levels in O group and these changes were corrected by Testosterone injection in O+T group. We also found insignificant differences between the four groups in serum triglycerides. However, we found highly significant differences in total cholesterol, LDL, HDL-c and VLDL between C group and O group and very highly significant differences between O+T group and Sh+T group in comparison with O group.
Understanding the pathogenesis and the molecular mechanisms of diabetic nephropathy (DN) helps its timely detection and prevention. The current work aims tomeasure serum sestrin 2 and betatrophin levels in healthy and type diabetic (T2DM)subjects with/or without diabetic nephropathy (DN) and also to test their correlation with serum neutrophil gelatinase associated lipocalin (sNGAL); indicator of DN.
This study included 96 subjects; 20 healthy (G1) and 76 T2DM [22 normoalbuminuric (G2), 35 microalbuminuric (G3) and 19 macroalbuminuric (G4)]. Serum sestrin 2, betatrophin and NGAL were measured by their corresponding kits.
Significant low levels of serum sestrin 2 andhigh levels of serum betatrophin were found in T2DM group when compared to G1 (p = 0.002,p > 0.001, respectively) and this difference is manifested in G4 followed, in order, by G3, G2 then G1 (p= > 0.001 for both). Also, serum sestrin2 levels showed significant negative correlations with sNGAL in G1 (r = −0.497, p = 0.026), G2 (r = −0.784, p > 0.001), G3 (r = −0.894, p > 0.001) and G4 (r = −0.896, pp. > 0.001) while serum betatrophin levels showed significant positive correlations with sNGAL in G2 (r = 0.681, p > 0.001), G3 (r = 0.518, p > 0.001) and G4 (r = 0.727, p > 0.001).
Serum sestrin 2 levels decrease significantly while betatrophin levels increase significantly in T2DM patients with DN especially those with macroalbuminuria. These levels have significant effect strengths on the indicator of diabetic nephropathy; sNGAL which might indicate their valuable role in the timely detection and prevention of the development of DN.
Background: Oxidative stress, lipid profile and renal functions are well-known conventional risk factors for diabetes mellitus (DM). Metformin and gliclazide are popularly used monotherapy drugs for the treatment of DM. Aims: This study aims to assess the short-term treatment of single and dual therapy of glipizide/metformin on oxidative stress, glycemic control, serum lipid profiles and renal function in diabetic rats. Methods: DM was induced in rats with streptozotocin (STZ), then five different treatments were applied, including group I (untreated healthy control), group II (diabetic and untreated), group III (diabetic and treated with metformin), group IVI (diabetic and treated with glipizide) and group V (diabetic and treated with a combination of metformin and glipizide. Lipid peroxidation (LPO), nitric oxide (NO), total antioxidant capacity (TAC), fasting blood glucose (FBG), glycated hemoglobin (HbA1c), total cholesterol, triglycerides, high-density lipoprotein (HDL), low-density lipoprotein (LDL), creatinine and urea were measured. Results: Compared to the untreated DM group, FBG and HbA1c were significantly reduced in the DM groups (p < 0.01) treated with metformin (159.7 mg/dL & 6.7%), glipizide (184.3 mg/dL & 7.3%) and dual therapy (118 mg/dL & 5.2%), respectively. Treatment with dual therapy and metformin significantly decreased LPO and NO levels but increased TAC in diabetic rats more than glipizide compared to untreated diabetic rats. Furthermore, metformin (19.8 mg/dL, p < 0.001), glipizide (22.7 mg/dL, p < 0.001), and dual therapy (25.7 mg/dL, p < 0.001) significantly decreased urea levels in the treated rats compared to untreated DM rats (32.2 mg/dL). Both drugs and their combination exhibited a substantial effect on total cholesterol, HDL, LDL and atherogenic index. Conclusions: These results suggest that the therapeutic benefits of metformin and glipizide are complementary. Metformin exhibited superior performance in improving glycemic control and decreasing oxidative stress, while glipizide was more effective against dyslipidemia. These findings could be helpful for the treatment of future vascular patients, antilipidemic medicines and antioxidant therapy to improve the quality of life.