Objective:To identify the different subtypes of acute ischemic stroke, and estimate the frequency of various risk factors among these patients.Methods:In this retrospective, cross-sectional study, we reviewed the medical records of patients admitted with the diagnosis of acute ischemic stroke at King Fahd Hospital of the University, Al-Khobar, Saudi Arabia from March 2008 till December 2015. The demographic characteristics, subtypes of stroke, risk factors (hypertension, diabetes mellitus, hyperlipidemia, coronary artery disease, atrial fibrillation, valvular heart disease) and other relevant data were documented on pre-defined data sheets.Results:The records of 343 patients were included in the study; 64.4% were male and 35.6% were female. The mean age was 59.3+13.6 (mean+SD) years for males, and 66.8+14.9 years for females. Small vessel occlusion was the most common etiologic subtype of ischemic stroke (32.1%), followed by cardio embolic (21.9%), and large artery atherosclerosis (14.6%). The middle cerebral artery was the most commonly affected territory. Hypertension was found in 78.1%, diabetes mellitus in 62.7%, hyperlipidemia in 54.8%, and ischemic heart disease in 24.2% of patients.Conclusion:Small vessel occlusion was the most common etiology in our cohort. The onset of stroke at a relatively younger age group in the male population is of great concern and needs to be verified by further epidemiological studies. Adequate control of modifiable risk factors may help in reducing the disease burden caused by stroke.
Type 2 diabetes is a growing public health concern and accounts for approximately 90% of all the cases of diabetes. Besides insulin resistance, type 2 diabetes is characterized by a deficit in β-cell mass as a result of misfolded human islet amyloid polypeptide (h-IAPP) which forms toxic aggregates that destroy pancreatic β-cells. Heat shock proteins (HSP) play an important role in combating the unwanted self-association of unfolded proteins. We hypothesized that Hsp72 (HSPA1A) prevents h-IAPP aggregation and toxicity. In this study, we demonstrated that thermal stress significantly up-regulates the intracellular expression of Hsp72, and prevents h-IAPP toxicity against pancreatic β-cells. Moreover, Hsp72 (HSPA1A) overexpression in pancreatic β-cells ameliorates h-IAPP toxicity. To test the hypothesis that Hsp72 (HSPA1A) prevents aggregation and fibril formation, we established a novel C. elegans model that expresses the highly amyloidogenic human pro-IAPP (h-proIAPP) that is implicated in amyloid formation and β-cell toxicity. We demonstrated that h-proIAPP expression in body-wall muscles, pharynx and neurons adversely affects C. elegans development. In addition, we demonstrated that h-proIAPP forms insoluble aggregates and that the co-expression of h-Hsp72 in our h-proIAPP C. elegans model, increases h-proIAPP solubility. Furthermore, treatment of transgenic h-proIAPP C. elegans with ADAPT-232, known to induce the expression and release of Hsp72 (HSPA1A), significantly improved the growth retardation phenotype of transgenic worms. Taken together, this study identifies Hsp72 (HSPA1A) as a potential treatment to prevent β-cell mass decline in type 2 diabetic patients and establishes for the first time a novel in vivo model that can be used to select compounds that attenuate h-proIAPP aggregation and toxicity.
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