BackgroundOsteoporosis, a reduction in bone mineral density, represents the most common metabolic bone disease. Postmenopausal women are particularly susceptible to osteoporosis when their production of estrogen declines. For these women, fracture is a leading cause of morbidity and mortality. This study was conducted to evaluate the protective effects of olive oil supplementation against osteoporosis in ovariectomized (OVX) rats.MethodsWe studied adult female Wistar rats aged 12-14 months, divided into three groups: sham-operated control (SHAM), ovariectomized (OVX), and ovariectomized rats supplemented with extravirgin olive oil (Olive-OVX) orally for 12 weeks; 4 weeks before ovariectomy and 8 weeks after. At the end of the experiment, blood samples were collected. Plasma levels of calcium, phosphorus, alkaline phosphatase (ALP), malondialdehyde (MDA), and nitrates were assayed. Specimens from both the tibia and the liver were processed for light microscopic examination. Histomorphometric analysis of the tibia was also performed.ResultsThe OVX-rats showed a significant decrease in plasma calcium levels, and a significant increase in plasma ALP, MDA, and nitrates levels. These changes were attenuated by olive oil supplementation in the Olive-OVX rats. Light microscopic examination of the tibia of the OVX rats revealed a significant decrease in the cortical bone thickness (CBT) and the trabecular bone thickness (TBT). In addition, there was a significant increase in the osteoclast number denoting bone resorption. In the Olive-OVX rats these parameters were markedly improved as compared to the OVX group. Examination of the liver specimens revealed mononuclear cellular infiltration in the portal areas in the OVX-rats which was not detected in the Olive-OVX rats.ConclusionsOlive oil effectively mitigated ovariectomy-induced osteoporosis in rats, and is a promising candidate for the treatment of postmenopausal osteoporosis.

It had been suggested that chronic exposure to Schistosoma mansoni prevents the onset of Th1-mediated diseases such as diabetes mellitus. The present study was carried out on four groups of mice: (1) control group, (2) group infected with S. mansoni, (3) group injected with streptozotocin to induce diabetes, and (4) group infected and then 3 months postinfection injected with streptozotocin. No differences were detected between the infected non-diabetic and infected diabetic groups regarding worm burden, tissue egg count, and oogram. At the same time, results showed a reducing effect of S. mansoni infection on the rate of glucose uptake by the diaphragm with reduction in glycogen content of soleus muscle. This an important issue since skeletal muscle is the primary site for insulin-stimulated glucose disposal. In conclusion, because of the detected depressed peripheral glucose uptake by the diaphragm, the protecting effect of helminths infection in diabetes should be reconsidered, to be able to devise therapeutic strategies for the treatment of autoimmune diseases.

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Background. Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) plays an important role in the regulation of cellular energy metabolism, and it is involved in obesity and type 2 diabetes mellitus (T2DM). Its expression is elevated in the liver of T2DM mouse models. Literature reports show that chronic β2 stimulation improved insulin sensitivity in T2DM. Objectives. We aimed to test the hypotheses that chronic β2 stimulation-induced improvement in insulin sensitivity involves changes in the expression of PGC-1α and glucose transporter 4 (GLUT4). Animals and Methods. We fed a locally inbred, 8 months old mice, a high fat diet (HFD) to induce diabetes. These mice gained weight and became insulin resistant. The β2 agonist salbutamol had a beneficial effect on both glucose tolerance and insulin sensitivity after 4 weeks. Results. Salbutamol beneficial effect persisted after 4 weeks of its discontinuation. HFD caused an up regulation of the hepatic PGC-1 α expression by 5.23 folds (P< 0.041) and salbutamol reversed this effect and caused a down regulation by 30.3 folds (P< 0.0001). PGC-1 α and GLUT4 expression in the muscle was not affected by salbutamol (P> 0.05). Conclusion. Down regulation of the liver's PGC-1 α contributes to the beneficial effect of the chronic β2 stimulation on glucose tolerance and insulin sensitivity in T2DM mice.

Purpose Majority of the assessments, appraisals and placements have been disturbed, with some being cancelled, postponed, or modified in design. New approaches for assessment should be well-thought-out. This work attempts at capturing the collective wisdom of educators in the Middle East and North Africa region (MENA), providing an understanding of the online assessment conceptual framework in the era of COVID-19 that tells the story rather than determining cause and effect, and identifying the biggest gaps that derail the digital transformation. Methods A qualitative inductive study using the grounded theory approach was implemented following a synchronous virtual online meeting, a summary of the reflections as well as experiences of medical education experts was prepared. Data for this qualitative study were collected from the meeting. The meeting was video-recorded and transcribed by the researchers. Thematic analysis was performed by three separate researcher coders. The authors then discussed together until they reached a consensus. Results Three main thematic areas were identified: 1) feasibility, 2) exam fairness/equity and 3) acceptable graduate attributes, society/community acceptance. Conclusion The COVID-19 era necessitated revisiting of our assessment strategies to cope with new changes within the available context. Rapid adaptation is required.

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Background The unbalanced gut microbiota, poorly ingested enriched fiber foods, leaky gut is connected to the progression of chronic kidney disease (CKD). The leaky gut translocates uremic toxins to the systemic circulation, promote systemic inflammation, worsen CKD. Decreasing the uremic toxins influx from the gut may decrease the progression of CKD. So, we aimed to evaluate the effect of probiotic and symbiotic supplementation on the leaky gut and their role to prevent CKD progression. Methods 48 white albino rats were randomly allocated into 6 groups: sham group; CKD rats; probiotic treated and symbiotic treated rats. Treatment started either immediately or 2 weeks after the operation for each treated group. Blood pressure, body weight changes, serum level of urea, creatinine, indoxyl sulphate and CRP were determined. Histological studies of kidney remnants and intestine and renal fibrosis index were calculated. SPSS program was used for statistics. Results Serum urea, creatinine, indoxyl sulphate, CRP, fibrosis index and blood pressure significantly increased in CKD rats. Probiotic treatment decreased serum level of urea, creatinine and CRP and fibrosis index. Symbiotic treatment decreased the serum level of urea, creatinine, indoxyl sulphate and CRP compared to CKD rats. Blood pressure and fibrosis index were decreased significantly upon symbiotic treatment. Conclusions A strong correlation between the gut microbial ecosystem and CKD has been proved. The use of probiotics and symbiotic to modulate an unhealthy gut microbiome is a promising intervention to delay CKD progression specially in early stages. Symbiotic results were better than probiotic alone.

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