Objective To investigate the effect of miR-129 on Alzheimer's disease using an in vitro model. Methods The hippocampal neurons of neonatal SD rats were cultured and divided into control,miR-129 mimic,miR-129 inhibitor,Aβ,Aβ+miR-129 mimic,Aβ+miR-129 inhibitor,amyloid precursor protein(APP)-siRNA transfection groups. Neurons were treated with β-amyloid(Aβ)to construct the Alzheimer's disease cell model. Gene expression was detected by RT-PCR and western blot. Cell apoptosis was determined by Hoechst/PI stai-ning. Cell viability was measured by MTT assay. The target gene of miR-129 was validated by luciferase reporter assay. Results Compared with the control group,Aβ could significantly reduce the expression of miR-129. Compared with the control group,overexpression of miR-129 in hippocampal neurons could alleviate the cytotoxicity of Aβ,which was manifested by reducing apoptosis and increasing cell viability. Inhibition of miR-129 expression further aggravated Aβ-induced apoptosis and decreased viability. In addition,the amyloid precursor protein(APP)was i-dentified as the target gene of miR-129,and interference with APP could alleviate Aβ-induced apoptosis and decrease the cytotoxicity of Aβ, which was similar to the effects of overexpression of miR-129. Conclusion miR-129 was involved in the pathogenesis of AD by regulating the expression of APP.

The alleviation of neurological function and recovery after cerebral ischemia is of critical importance. Recent studies have identified certain roles of tissue repair by neural stem cell (NSC) transplantation. Erythropoietin (EPO) may exert tissue protective function. In this study, NSCs were genetically modified to express EPO, and were tested for neurological functions. Meanwhile, bcl-2 protein expression was measured along with the discovery of potential mechanisms, in an attempt to discover novel pathways for treating brain ischemia. A total of 45 SD rats were prepared for middle cerebral artery occlusion (MCAO) model, followed by the direct injection of cerebral cortical NSCs that were modified to express EPO genes in vitro. Neurological functions, along with bcl-2 protein expression levels, were quantified by functional scores, RT-PCR and Western blotting. EPO-modified NSCs, after transplantation, significantly elevated neurological function scores of model rat. In those animals, we also found remarkably increased expression of bcl-2 in the sense of both mRNA and proteins (P < 0.05). Our study illustrated the anti-apoptotic role of EPO-modified NSCs in cerebral ischemia rats via up-regulating bcl-2 protein expression, thus decreasing the focal ischemia damage and protecting neural functions.

Objective It is to observe the significance of serum amyloid A ( SAA ) , insulin-like growth factor ( IGF-1), insulin-like growth factor binding protein -3 (IGFBP-3) and D-dimer in patients with acute cerebral infarction de -tection.Methods 87 patients with acute cerebral infarction selected as acute cerebral infarction were divided into mild group (32 cases), moderate group (18 cases) and severe group (37 cases ) according to neurological impairment score , and were also divided into small area group (29 cases), middle area group (22 cases) and large area group (36 cases) according to the maximum diameter by CT.30 healthy persons were selected as control group .The levels of D-dimer, IGF-1, IGFBP-3 and SAA were compared between acute cerebral infarction group and healthy control group , the relationship among the levels of D-dimer, IGF-1, IGFBP-3 and SAA IGF-1, neurological deficit scores and infarct area were observed in acute cerebral infarction, D-dimer, IGF-1, IGFBP-3 and SAA levels were also detected before and after treatment in patients with acute cerebral infarction .Results The levels of D-dimer and SAA in acute cerebral infarction group was significantly higher than those in control group ( P<0.01 ) , the D-dimer and SAA levels increased in acute cerebral infarction group , as the neuro-logical deficit scores and infarct area increased (P<0.01), and after treatment D -dimer and SAA levels were significantly lower than those before treatment ( P<0 .01 );while the levels of IGF-1 and IGFBP-3 were significantly lower in acute cer-ebral infarction group compared with control group (P<0.01), and the levels of IGF -1 and IGFBP-3 were significantly lower in acute cerebral infarction area as the neurological deficit scores and infarct area increased (P<0.01), after treatment the levels of IGF-1 and IGFBP-3 levels significantly increased than those before treatment (P<0.01).Conclusion The levels of D-dimer, IGF-1,IGFBP-3 and SAA involve in the development of acute cerebral infarction , it is of great signifi-cance for judging the severity of cerebral infarction and infarct size .

Alzheimer's disease (AD) is a progressive neurodegenerative disorder and is the most common form of dementia among the aging population. Although the incidence of the disease continues to increase, no cure has been developed. Effective treatment is restricted not only due to the lack of curative medicine, but also due to limited understanding of the underlying mechanisms and the difficulties in accurately diagnosing AD in its earliest stages prior to clinical symptoms. Micro (mi) RNAs (miR) have gained increasing attention in the investigation of neurodegenerative diseases. Previous reports have demonstrated that deregulation of miR‑146a‑5p is associated with the pathogenesis of human AD. In the present study, the coding region of primary (pri)‑miR‑146a in patients with AD was scanned and the rare C allele of rs2910164 was found to be associated with AD. Using reverse transcription quantitative polymerase chain reaction, it was demonstrated that site variation reduced the expression of mature miR‑146a‑5p. Notably, a reduction in the expression of miR‑146a‑5p led to less efficient inhibition of target genes, including Toll‑like receptor (TLR)2, which is important in the pathogenesis of AD. Biological function investigations in RAW264.7 cells indicated that, compared with the G allele, the rare C allele upregulated the expression of tumor necrosis factor‑α following stimulation with β‑amyloid. These findings suggested that one common polymorphism in pri‑miR‑146a may contribute to the genetic predisposition to AD by disrupting the production of miR‑146a‑5p and affecting the expression and function of TLR2.

目的:探讨奥扎格雷联合阿司匹林治疗进展性脑梗死的效果.方法:选择进展性脑梗死病人60例,随机分为治疗组(30例)及对照组(30例),两组在常规治疗的基础上,治疗组应用奥扎格雷联合阿司匹林治疗,对照组单用阿司匹林治疗,2周后观察神经功能缺损的变化.结果:治疗组总有效率为86.7％,对照组总有效率为73.3％,两组比较有显著性差异(P＜0.01).结论:奥扎格雷联合阿司匹林治疗进展性脑梗死疗效明显,无明显不良反应.

Parkinson disease (PD) is a common neurodegenerative disease. Most people with PD are idiopathic, with no specific known cause. Recently, several studies have indicated small proportion of PD cases may result from a mutation in some specific genes. However, the involved pathways of these genes and the co-expression patterns of associated pathways still remain unclear. Here, we aimed to systematically investigate PD related pathways by using microarray dataset GSE7621 from the public database library of gene expression omnibus and gene set enrichment analysis on the datasets. Furthermore, candidate transcription factors were also explored by distant regulatory elements software. As a result, 11 up-regulated pathways (such as glycosaminoglycan degradation) and 24 down-regulated pathways (such as ErbB signaling pathway and Long-term depression) were identified as PD related. Most of them were classified into the maps of human diseases, organismal system, and metabolism with no previous reports. Finally, we constructed co-expression networks of related pathways with the significant core genes and transcription factors, such as OCT and HNF3. All of these may be helpful to better understand the molecular mechanisms of human PD in genome wide.

Objective To observe the effect of trimetazidine on coronary heart disease combined with arrhythmia. Methods Eighty-one patients were randomly divided into treatment group(n = 42) and control group(n = 39). Patients in the control group received routine therapy and patients in the treatment group took trimetazidine orally 20 mg three times per day on the basis of routine therapy. Resting electrocardiogram(ECG),Holter,blood routine,urine routine,liver function and renal function were detected before and after treatment. Changes of resting ECG and Holter were used to evaluate the curative effect. Present symptoms and the results of laboratory examinations were used to evaluate the adverse reactions. Results Compared with the control group,the ischemic ST-T of ECG improved signifi cantly and the numbers of arrhythmia decreased signifi cantly in the treatment group(P 0.05). There was no difference in the adverse reactions between two groups. Conclusion Trimetazidine may be used effectively and safely in patients with coronary heart disease complicating arrhythmia.