Severe reduction in the β‐cell number (collectively known as the β‐cell mass) contributes to the development of both type 1 and type 2 diabetes. Recent pharmacological studies have suggested that increased pancreatic β‐cell proliferation could be due to specific inhibition of adenosine kinase (ADK). However, genetic evidence for the function of pancreatic β‐cell ADK under physiological conditions or in a pathological context is still lacking. In this study, we crossed mice carrying LoxP‐flanked Adk gene with Ins2‐Cre mice to acquire pancreatic β ‐cell ADK deficiency (Ins2‐Cre ± Adk fl/fl ) mice. Our results revealed that Ins2‐Cre +/‐ Adk fl/fl mice showed improved glucose metabolism and β‐cell mass in younger mice, but showed normal activity in adult mice. Moreover, Ins2‐Cre ± Adk fl/fl mice were more resistant to streptozotocin (STZ) induced hyperglycaemia and pancreatic β‐cell damage in adult mice. In conclusion, we found that ADK negatively regulates β‐cell replication in young mice as well as under pathological conditions, such as STZ induced pancreatic β‐cell damage. Our study provided genetic evidence that specific inhibition of pancreatic β‐cell ADK has potential for anti‐diabetic therapy.

Background: Epilepsy and seizure are one of the most common serious neurological disorders, and most patients either stop having seizures or less commonly die of them. Methods: This retrospective cross-sectional study targeting adult Sudanese patients was conducted in the EEG units of the department of physiology, faculty of medicine, and the National Ribat University. Recordings were obtained from a digital EEG machine (Medtronic pl-EEG). The Statistical Package for Social Sciences (Windows version 15; SPSS) was used for statistical analysis. The study's main objective was to determine the percentage of abnormal EEGs in adult Sudanese epileptic patients who were referred to the Ribat EEG unit from March 2007 to September 2010. Results: Nine hundred and fifty patients were included in this study, abnormal EEGs was seen in 54.7%, while it was normal was in 45.3%; primary generalized seizures constituted 45.5%, while focal onset seizures were collectively observed in 43.4%, other types of epilepsy counted for 11.2%. Conclusion: This study showed that males were more affected than females, abnormal EEG was maximal in the age group16–30 years. Epileptiform seizure discharges decrease with age, generalized seizure discharges were dominated seizure.

Background: During pregnancy, maternal metabolic environment is modified by a rise in serum levels of estrogen and progesterone, pancreatic beta-cell hyperplasia and an increase in the secretion of insulin. Hyperinsulinemia leads to an increase in peripheral glucose utilization, a decline in fasting plasma glucose levels, increased tissue storage of glycogen, increased storage of fats and decreased lipolysis. The aim of our current study to investigate the changes in lipid profile, blood glucose and blood pressure throughout three trimesters in pregnant ladies. Materials and Methods: This is a hospital based, descriptive analytical cross-sectional study, performed at refer clinic of Omdurman Maternity hospital in Khartoum state. Included 150 apparently healthy pregnant ladies in the study group and 40 healthy non-pregnant ladies as a control group. Anthropometric measurements and blood pressure were measured and blood sample was obtained to analyzed lipid profile and blood glucose. Results: Data analysis showed that the mean level of triglyceride tend to change from slight increase in first trimester and significant increase in the second and third trimester. While mean level of HDL tend to change from slight decrease in the first and second trimester to significant decrease in the third trimester. Whereas there was an increase in both total cholesterol and LDL but was not significant. The mean level of fasting blood glucose was significantly raised in third trimester compared to other first and second Trimesters. Both component of blood pressure was significantly elevated in the first and third trimesters compare to second trimester. Conclusion: Normal pregnancy is associated with dyslipidemic changes due to elevated pregnancy related hormones. Increased insulin resistance leads to production of dyslipidemic changes in mother in form of elevated TG, total cholesterol, LDL and decreased HDL in serum and increased random blood glucose.