Objective To study the effect of anti-epileptic,nootropic drugs on the expression of NCAM and ERK2 in the hippocampus changes on the epileptic rats with cognitive dysfunction.Methods A total of 120Wistar rats were used.20 controls and 100 in which epilepticus with cognitive dysfunction were randomly assigned to 5 groups (n =20/group) that received daily treatments for 30 days with either (1) saline (epilepsy),(2) carbamazine (traditional anti-epileptic),(3) oxcarbazine (new anti-epileptic),(4) aniracetam (brain protective),or (5) donepezil (nootopic).Spatial learning and memory were assessed with a Morris Water Maze (MWM).Hippocampus tissue was assessed for NCAM1 and ERK-2 mRNAs by RT-PCR and proteins by immunochemistry.Results The mean escape latency of the place navigation test:EP group ((67.14 ± 7.37)s)was all higher than NS group (35.78 ± 4.84 s)and there was statistical significance (P ＜ 0.01),carbamazepine group ((81.23 ± 9.46)s) ＞ EP group((67.14 ±7.37)s) ＞ donepezi group((53.75 ±6.74) s) (P＜0.01).Immunohistochemical and RT-PCR result:carbamazepine ＜ oxcarbazepine ＜ epilepsy ＜ aniracetam ＜ donepezi group.Compared with control group,donepezil group ＞ control group (P ＜ 0.01),aniracetam group ＞ control group (P ＜ 0.05).Conclusion ERK-2 expression is decreased and NCAM 1 expression is increased in the hippocampus in the epileptic rats.Thus,both are involved in cognitive dysfunction.Carbamazepine aggravates cognitive dysfunction,whereas donepezil improves cognitive dysfunction associated with epilepsy.

AIM: To study the protective effect of puerarin on the atherosclerosis of RAW264.7-derived foam cells.METHODS: The model of foam cells was established by incubating the RAW264.7 cells with ox-LDL.The choles-terol uptake was evaluated by a DiI-ox-LDL binding assay.The ability of cholesterol efflux of the RAW264.7-derived foam cells was detected by cholesterol efflux assay.The protein levels of LC3II, P62, CD36, ABCA1, LAL and p-AMPK were determined by Western blot.RESULTS: Puerarin treatment reduced the cholesterol uptake capacity and enhanced the cho-lesterol efflux rate.The protein levels of LC3II, ABCA1 and LAL in puerarin group were higher than that in ox-LDL group, while the protein levels of P62 and CD36 were obviously decreased, and those in rapamycin treatment group had the same change as puerarin group.The protein levels of LC3II, ABCA1 and LAL were obviously decreased and the protein level of p-AMPK was increased after co-treated with 3-MA.CONCLUSION: Puerarin promotes LAL and ABCA1-mediated cho-lesterol efflux in ox-LDL-treated RAW264.7 macrophages, which might enhance autophagy through AMPK-dependent path-way for cholesterol efflux regulation, and reduce the uptake of lipids by CD36 negative regulation.

INTRODUCTIONThe present study aimed to investigate the possible associations between serum levels of visfatin, an adipokine, and atherosclerosis in patients with ischaemic cerebrovascular disease.

METHODSA total of 95 participants were recruited for this study. Group A comprised 35 individuals with no history of cerebrovascular disease (control group) and Group B comprised 60 patients with ischaemic cerebrovascular disease. Group B was further categorised into two subgroups based on the ultrasonographic findings of the common carotid artery intima‑media thickness (CCA‑IMT) - Group B1 consisted of 21 patients with no atherosclerosis (i.e. CCA‑IMT ≤ 0.9 mm) and Group B2 consisted of 39 patients with atherosclerosis (i.e. CCA‑IMT > 0.9 mm). The body mass index, fasting blood total cholesterol, triglycerides, high‑density lipoprotein cholesterol, low‑density lipoprotein cholesterol and glucose levels of each patient were measured. Serum visfatin levels were determined using enzyme‑linked immunosorbent assays. Visfatin levels were compared between groups, and stepwise logistic regression analysis was used to identify risk factors for atherosclerosis, including visfatin levels.

RESULTSThe mean serum visfatin level of the patients in Group B was higher than that in Group A (75.5 ± 77.80 ng/mL vs. 8.6 ± 4.69 ng/mL; p < 0.05) and the level was higher in patients from Group B2 than those from Group B1 (89.0 ± 80.68 ng/mL vs. 50.4 ± 72.44 ng/mL; p < 0.05). Multivariate regression analysis showed that CCA‑IMT values were not significantly associated with visfatin levels. However, logistic regression analysis showed that serum visfatin was an independent risk factor for atherosclerosis (odds ratio 37.80; p = 0.004).

CONCLUSIONSerum visfatin may be an independent risk factor for cerebral infarction, as high serum visfatin levels are positively associated with the underlying pathogenic mechanisms of ischaemic cerebrovascular disease.

Adipokines ; metabolism ; Adipose Tissue ; pathology ; Adult ; Aged ; Atherosclerosis ; blood ; complications ; Body Mass Index ; Brain Ischemia ; blood ; complications ; Carotid Intima-Media Thickness ; Case-Control Studies ; Cerebrovascular Disorders ; blood ; complications ; Enzyme-Linked Immunosorbent Assay ; Female ; Humans ; Inflammation ; Logistic Models ; Male ; Middle Aged ; Nicotinamide Phosphoribosyltransferase ; blood ; Risk Factors

To summarize the perioperative nursing experience of a child with Berry syndrome who underwent radical surgery.The key points of preoperative care include the prevention of heart failure and vigilance against ischemia and hypoxia in the lower limbs.The key points of postoperative care include maintaining stable cardiac function,preventing pulmonary hypertension crisis,ensuring safe transition during delayed chest closure,paying attention to psychological support,and emphasizing continuous care.After 54 days of careful treatment and nursing care,the child recovered well and was discharged from the hospital.The follow-up was couducted a month after discharge,and the child was good.