Carcinoma, Renal Cell ; genetics ; metabolism ; pathology ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit ; genetics ; metabolism ; Kidney Neoplasms ; genetics ; metabolism ; pathology ; Loss of Heterozygosity ; Mutation ; Von Hippel-Lindau Tumor Suppressor Protein ; genetics ; metabolism ; von Hippel-Lindau Disease ; genetics ; metabolism ; pathology

A total of 1342 individuals underwent physical examinations according to the criteria of metabolic syndrome of International Diabetes Federation (IDF) in 2005.And 314 patients with metabolic disorders were screened for diabetes by standard meal and methods oral glucose tolerance test (OGTT).Newly diagnosed diabetics was 12 (4.1％ ) vs.17 (5.8％) respectively.No significant difference existed between two methods (P =0.332).Kendall's (τ)b =0.313,Kendall's (τ)c =0.208 and Gamma coefficient =0.580 (P =0.000).The mixed meal method was correlated with OGTT,Kappa =0.258 (P =0.000) and two methods were consistent.Diabetic screening should be stressed in the subjects with metabolic abnormalities.And the detecting efficiency of postprandial plasma glucose is similar to OGTT.

Totally 1136 individuals aged over 40 underwent health check up in March to May 2009. Fasting blood glucose, 2-h post-challenge blood glucose, glycated hemoglobin A1c ( HbA1c), total cholesterol, triglyceride, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol and serum uric acid were measured. The diagnosis of metabolic syndrome was based on the International Diabetes Federation Criteria. The results shows that total body fat, region body fat indices, blood pressure, blood glucose and serum uric acid levels increased with the age ( P < 0.01) . The prevalence rate of metabolic syndrome in this group of individuals were 15. 1% (171/1136) , and increased with age (P<0.01). The most common combination of metabolic syndrome was central obesity-hypertension-dyslipidemia (40. 9% , 70/171). Unconditional logistic regression revealed that waist-hip-ratio, body mass index and uric acid were the risk factors for metabolic syndrome.

Objective:To study of immuno-intervention with prostaglandin E2(PGE_2) on tumor necrsis factor(TNF-?),interleukin 10(IL-10),SOD and NO in rats attacked by vibrio vulnificus.Methods:27 normal rats and 27 hepatopathy rats,they were divided into Vv attacked group,ofloxacin treatment group and combined PGE_2 with ofloxacin protect group(n=9).Results:The result of cytokines detection showed that serum IL-10 and SOD level of combined PGE_2 with ofloxacin protect group was significantly higher than that of ofloxacin treatment group,however,TNF-? and NO level of PGE_2 immuno-protect group were significantly lower than those of ofloxacin treatment group(P

Objective To investigate the expression and cellular localization of cyclin-dependent kinase 5 (Cdk5) in cerebral cortex after subarachnoid hemorrhage (SAH) in rats.Methods Fifty-two male Sprague Dawley (SD) rats were randomly divided into either a sham operation group (n =12) or a SAH group (n =40).The latter was randomly redivided into 6,12,24 h,and day 2 and 3 subgroups (n =8 in each group).A rat SAH model was induced by injecting fresh blood into the prechiasmatic cistern.Western blot and immunohistochemistry were used to detect the expression of Cdk5 in rat brain cortex.Double labeling immunofluorescence staining was used to detect the cellular localization of Cdk5 protein in cerebral cortex.Neuronal nuclear antigen labeled neurons,and glial fibrillary acidic protein labeled astrocytes.Results Western blot showed that the expression of Cdk5 protein was up-regulated at 12 hours after SAH (t =3.709,P =0.001),and it reached the peak on day 1 (t =3.475,P=0.002).Immunohistochemistry showed that the proportion of Cdk5 positive cell was also increased gradually after SAH,and the changes of time course were consistent with the results of Western blot,and it reached the peak on day 1 (t =4.320,P =0.000).Double labeling immunofluorescence showed that Cdk5 was mainly expressed in the neuronal cytoplasm in the sham operation group,and Cdk5 shifted to the neuronal nuclei in the SAH group.Cdk5 was mainly colocalized between astrocytes and neurons.Conclusions SAH up-regulates the expression of Cdk5 protein in cerebral cortex.Cdk5 may be involved in early brain injury after SAH.

Objective To summarize our experience in the diagnosis and management of popliteal artery entrapment syndrome (PAES). Methods This is a retrospective study on 10 patients (13 limbs)who were admitted for symptoms of claudication and the diagnosis of popliteal entrapment was established either with angiography,computed tomographic angiography,magnetic resonance angiogram or during the operation in recent 7 years (2002-2009).All patients were treated surgically. Results The mean age at the time of presentation was (25 ±7) years old (range,17-41 years).Claudication was the most frequent presenting symptom (12 limbs).The surgical procedures consisted of simple musculotendinous dissociation in 1 limb,thrombectomy with balloon angioplasty in 1 limb,musculotendinous dissociation plus thromboendarterectomy with autogenous saphenous vein (ASV)patch angioplasty in 2 limbs,ASV graft interposition or bypass in 6 limbs and graft interposition or bypass in 3 limbs.At a median follow-up of (35 ±27) months (range,2 months-7 years),there were no intraoperative or long-term postoperative complications and all the patients were cured. Conclusions PAES is an unusual but important cause of peripheral vascular insufficiency especially in young patients.A combined approach is necessary for diagnosis.Popliteal artery release alone or with vein bypass or reconstruction is the treatment of choice.

Objective To explore the effect of autophagy regulator on the injury of rat hippocampal neurons induced by oxygen-glucose deprivation (OGD).Methods Rat hippocampal neurons were cultivated in primary and subjected to OGD to simulate neuronal hypoxic ischemia injury for 2 hours or 6 hours followed by reperfusion for 12 hours with or without 3-methyladenine (3-MA, 20μmol/L) or rapamycin (0.2μmol/L). The morphology of neurons was observed with optical microscope. The expression of autophagy-related protein (LC3, P62) and apoptosis-related protein (cleaved caspase-3) were assessed by Western Blot analysis. The apoptosis of neurons was detected by flow cytometry, the release rate of lactate dehydrogenase (LDH) was calculated by automatic biochemical analyzer, and the cell activity was determined by methyl thiazolyl tetrazolium (MTT) colorimetric assay.Results Compared with the control group, the expression of LC3 Ⅱ/Ⅰ (gray value: 3.091±0.160, 3.422±0.186 vs. 0.256±0.021), cleaved caspase-3 (gray value: 0.230±0.025, 0.440±0.051 vs. 0.050±0.007), neuronal apoptotic rate, LDH release rate [(38.50±4.15)%, (59.60±5.65)% vs. (12.40±1.32)%] were increased, while the expression of P62 (gray value: 0.290±0.025,0.120±0.026 vs. 0.450±0.040), neuronal activity [(71.40±7.23)%, (42.80±4.12)% vs. (100.30±2.30)%] were decreased at 2 hours or 6 hours after OGD (allP < 0.05). When the time of OGD was 2 hours and it was combined with 3-MA, the expression of LC3 Ⅱ/Ⅰ (gray value: 2.281±0.121), the neuronal activity [(51.10±5.73)%] were decreased, while the expression of P62 and cleaved caspase-3 (gray scale: 0.410±0.037, 0.330±0.027, respectively), neuronal apoptotic rate, the injury of neurons [LDH release rate: (47.30±4.43)%] were increased (allP < 0.05). When the time of OGD was 2 hours and it was combined with rapamycin, the expression of LC3 Ⅱ/Ⅰ (gray value: 3.689±0.214), the neuronal activity [(85.30±8.56)%] were increased, while the expression of P62 and cleaved caspase-3 (gray value: 0.170±0.040, 0.090±0.096, respectively), neuronal apoptotic rate, the injury of neurons [LDH release rate: (24.30±2.14)%] were decreased (allP < 0.05). On the contrary, when the time of OGD was 6 hours and it was combined with 3-MA, the expression of LC3 Ⅱ/Ⅰ and cleaved caspase-3 (gray value: 3.021±0.178, 0.240±0.017), neuronal apoptotic rate, the injury of neurons [LDH release rate: (36.60±3.45)%] were decreased, while the expression of P62 (gray value: 0.350±0.060), the neuronal activity [(59.70±6.13)%] were increased (allP < 0.05). When the time of OGD was 6 hours and it was combined with rapamycin, the expression of LC3 Ⅱ/Ⅰ and cleaved caspase-3 (gray value: 3.923±0.201, 0.590±0.062), neuronal apoptotic rate, the injury of neurons [LDH release rate:(71.20±7.81)%] were increased, while the expression of P62 (gray value: 0.070±0.008), the neuronal activity [(27.30±2.12)%] were decreased (allP < 0.05).Conclusion The enhancement of autophagy has protective effect on neurons under the condition of mild OGD, while it can aggravate the injury of neurons induced by a long-time OGD.

Electroencephalography (EEG) is an important instrument for the evaluation of brain function, and an irreplaceable diagnostic technique for nervous system diseases. At present, China still lacks professional child-EEG talents. Therefore, it is a task of great priority to establish an effective and practical training method and foster more child-EEG physicians. As most trainees have not learned EEG before and only have limited time for learning, we divide the child-EEG training into three phases, includ-ing theory learning, practice training, and EEG reading and interpretation on the basis of the general rules in learning EEG. In the theory learning phase, basic EEG knowledge is taught comprehensively to form a solid foundation for future study. In practice training phase, the trainees acquire important skills of EEG by carrying out complete EEG monitoring, eliminating EEG artifacts, observing seizures, and read real-time EEG. In the phase of EEG reading and interpretation, the trainees learn to analyze EEG gradually by read-ing and report EEG under the guidance of the senior physician. Strict examination is arranged for each phase to evaluate study results objectively. The phased model is designed to implement a step-by-step training of child-EEG and foster the trainee's independent ability to carry out EEG inspection.

Objective To find the expression level and the role of ENST00000460164 in luminal A breast cancer.Methods The expression level of ENST00000460164 in breast cancer tissues was detected by RT-qPCR.pll3.7-ENST00000460164-shRNA and empty vector,pll3.7,were transfected into MCF-7 cells.Cell cycle was measured by flow cytometry.Western blot was used to detect the expression of P16INK4A and cyclinD1.Results ENST00000460164 was highly expressed in luminal A breast cancer tissues as compared to the adjacent non-cancer tissues.The knockdown of ENST00000460164 resulted in the G1 cell-cycle arrested,cyclin D1 downregulated and P16INK4A upregulated in MCF-7 cells.Conclusions ENST00000460164 is overexpressed in luminal A breast cancer.ENST00000460164 may control G1/S transition by regulating P16INK4A or cyclin D1 expression.

Animals ; Biological Availability ; Drug Carriers ; chemistry ; Drug Delivery Systems ; Humans ; Lactic Acid ; chemistry ; pharmacokinetics ; Nanoparticles ; Polyesters ; Polyethylene Glycols ; chemistry ; pharmacokinetics ; Polyglactin 910 ; chemistry ; pharmacokinetics ; Polyglycolic Acid ; chemistry ; pharmacokinetics ; Polymers ; chemistry ; pharmacokinetics