ABSTRACT
Enterovirus D68 (EV-D68) was first isolated in 1962, and then reported infrequently. As its genetic diversity increased rapidly, the detection rate of EV-D68 has been rising worldwide in recent decade. Since EV-D68 caused the most widespread outbreak in the United States, Canada and Europe in 2014, an increasing number of studies had reported that EV-D68 was associated with severe respiratory diseases and neurological complications, even death. However, the pathogenesis of EV-D68 remains unclear. Moreover, no vaccines or specific antiviral agents are available for prevention and treatment for EV-D68 infection at present. Therefore, continued surveillance and rapid diagnosis of EV-D68 infection will be beneficial to prevent and manage the potential outbreak. This article gives an overview of the biological characteristics, clinical features, and epidemiology of EV-D68.
ABSTRACT
Objective To observe and explore the risk factors of nonalcoholic fatty liver diseas(NAFLD) complicated with hypertension in the enterprise retirees .Methods A total of 209 NAFLD patients diagnosed by ultrasound combined with questionnaire were collected in the enterprise retirees,and they were divided into the NAFLD with hypertension group(100 cases)and NAFLD without hypertension group (109 cases)after combined with physical examination results and past medical history.The relevant data of the two groups were retrospectively analyzed,and the risk factors of NAFLD complicated with hypertension disease were analyzed.Results The levels of age(t =1.69,P <0.05),body mass index(BMI)(t =0.36,P <0.05),waist circumference(t =0.64,P <0.05), total cholesterol(TC)(t =2.31,P <0.05),total bilirubin(TBS)(t =6.83,P <0.05),serum creatinine(Scr)(t =2. 20,P <0.05)in NAFLD complicated with hypertension group were higher than those in NAFLD group,and the differ-ences were statistically significant(P <0.01 or P <0.05).The logistic regression analysis showed that TC(OR =4.2)was the independent influencing factor of NAFLD with hypertension.Conclusion NAFLD is closely associated with hypertension,NAFLD can be incorporated into chronic disease management system with high blood pressure in order to improve the value of the disease in the elderly,and it is conducive to the further study of NAFLD and the management of other chronic disease.
ABSTRACT
Objective To study the neuroprotective role of TFP5 in a MPTP-induced mouse model of Parkinson's disease (PD).Methods C57BL/6 mice were used as experimental animals.Briefly, 5 consecutive days of intraperitoneal injection of 25 mg/Kg 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was applied to induce mouse PD model.The mice were randomized into 5 groups including control group,model group, scrambled TFP5 peptide (Scb) group, TFP5 group and roscovitine group.On the 7th day after the first injection of MPTP,behavior tests were performed, and then western blot method was employed to detect the expression of p25 and phosphorylated MEF2D in substantia nigra.Tyrosine hydroxylase (TH) immunohistochemical staining was performed to observe the apoptosis of dopaminergic neurons in substantia nigra pars compacta (SNpc) 28 days after the first injection of MPTP.Results MPTP increased the expression of p25 (0.48±0.10 vs 0.26±0.02, P＜0.05) and phosphorylated MEF2D (0.81±0.10 vs 0.22±0.02, P＜0.05) in substantia nigra, but decreased the number of dopaminergic neurons in SNpc (348.67±24.40 vs 463.29± 19.61, P＜0.05),resulting in motor impairment in the model mice (P＜0.05).Intraperitoneal injection of 30mg/Kg of TFP5 for 3 days effectively reduced the excessive phosphorylation of MEF2D (0.25 ± 0.12 vs 0.81 ± 0.10, P＜ 0.05) in substantia nigra, rescued dopaminergic neuron reduction of SNpc (422.92±8.41 vs 348.67±24.40, P＜0.05), and improved the motor ability of the model mice (P ＜0.05).Roscovitine exerted almost same neuroprotective role as TFP5 ,while Scb had no protective effect.Conclusion TFP5 can rescue MPTP-induced damage of dopaminergic neurons in substantia nigra, and thus improve motor impairment of model mice,which may be mediated by the inhibition of Cdk5/p25 activity.