Objective To investigate the etiology and risk factors of stroke in young adults from Southern Sichuan, China to provide a basis for prevention and treatment of stroke. Methods The data of 398 young patients with first-ever stroke (aged 18 to 44) admitted to department of Neurology, the Affiliated Hospital of Luzhou Medical College from 2009 to 2013 was retrospectively analyzed. Four hundred twenty-five cases of stroke (aged greater than or equal to 45) were re?cruited by stratified random sampling to analyze its causes and risk factors in the same period. Results ① Young stroke accounted for 6.09% of all hospitalized stroke patients in which 78.39% of young stroke was ischemic, 64.57%was male and 58.04% aged from 40 to 44. ② According to TOAST etiology classification group, the percentage of large-artery atherosclerosis, small-vessel, cardioembolism, other determined and undetermined reasons were 56.09%, 17.95%, 9.93%, 10.90% and 5.13% in young stroke, respectively. Compared with the elderly group, other determined and undetermined reasons were higher, and the small-vessel was lower in young stroke (P<0.05). Hypertensive cerebral hemorrhage accounted for 50%of Hemorrhage in young group, and the type of Hemorrhage between two groups was no statistically significant.(P>0.05).③ Risk factors analysis revealed that the constituent ratio of smoking (34.92%), hyper?lipidemia (31.41%), alcohol (20.10%), obesity (13.07%), rheumatic heart disease (6.03%) in youth group were higher whereas hypertension(66.12%), diabetes(20.47%)and coronary heart disease(10.82%)were lower in young stroke com?pared with the elderly group (P<0.05). Conclusion ①Large-artery atherosclerosis is the most common etiology of youth ischemic stroke. ② Hypertensive cerebral hemorrhage is the most frequent type in Hemorrhagic stroke. ③ Hyperten?sion, smoking and hyperlipidemia are the most common risk factors to stroke.

Objective:To evaluate the effect of sirtuin 3 (SIRT3) overexpression on hypoxia-reoxygenation (H/R) injury to hippocampal neurons of mice exposed to high glucose and its relationship with SOD2.Methods:The normally cultured HT22 neurons at the logarithmic phase were selected and divided into 3 groups ( n=12 each) using a random number table method: high-glucose normoxia group (HG group), high glucose+ H/R group (HHR group) and high glucose+ H/R+ SIRT3 overexpression group (HHR+ SIRT3 group). To establish high glucose model, the neurons in 3 groups were cultured in high-glucose culture medium (glucose concentration of 50 mmol/L) for 8 h. In HHR and HHR+ SIRT3 groups, the cells were exposed to glucose-free and hypoxia for 6 h and then cultured in the high-glucose normoxic environment for 24 h to establish the high glucose and HR injury model.In HHR+ SIRT3 group, the neurons were transfected with SIRT3 overexpressed lentivirus.The cell viability was recorded by the cell counting kit-8 assay, reactive oxygen species (ROS) content was detected by flow cytometry, mitochondrial malonaldehyde (MDA) content, superoxide dismutase (SOD) activity, catalase (CAT) activity and adenosine triphosphate (ATP) content were determined by colorimetry, mitochondrial membrane potential (MMP) was detected by JC-1 probe, and the expression of nuclear respiratory factor 1 (NRF1), mitochondrial transcription factor A (TFAM), SIRT3, SOD2 and acetylated SOD2 (ac-SOD2) was detected by Western blot. Results:Compared with HG group, cell viability, SOD activity, CAT activity, ATP content, MMP, NRF1 and the expression of TFAM and SIRT3 were significantly decreased, and ROS content, MDA content and ac-SOD2/SOD2 ratio were increased in group HHR and group HHR+ SIRT3 ( P<0.05). Compared with HHR group, cell viability, SOD activity, CAT activity, ATP content, MMP, NRF1 and the expression of TFAM and SIRT3 were significantly increased, and ROS content, MDA content and ac-SOD2 /SOD2 ratio were decreased in HHR+ SIRT3 group ( P<0.05). Conclusion:SIRT3 overexpression can alleviate hypoxia-reoxygenation (H/R) injury to hippocampal neurons of mice incubated in high glucose medium, and the mechanism is related to activation of SOD2 deacetylation.