Objective To investigate the correlations between plasma levels of carnitine(CT),free fat acid(FFA) and insulin resisitance in children with simple obesity.Methods Fifty-six children diagnosed with simple obesity were enrolled as study group(obesity group),36 healthy children as control group.The concentration of plasma level of insulin was measured by radioimmunoassay(RIA),CT was measured by high performance liquid chromatography(HPLC),FFA and triglyceride(TG) were measured by enzymatic-colorimetric assay.Body mass index(BMI) and waist to hip ratio(WHR) were caculated.Insulin sensitivity index (InSI) and insulin resistance index (InRI) were cacula-ted by homeostasis model assessment of insulin resistance (HOMA-IR).SPSS 13.0 software was used to analyze the data.Results The concentration of CT in plasma was (43.67?12.75) ?mol/L in obesity group,(58.31?21.25) ?mol/L in control group,respectively.There was a significant difference between 2 groups (t=2.566 P

ObjectiveTo explore the character of cognitive potential P300 in major depressive disorder ( MDD ) patients between with and without family history and compare the cognitive function between them.MethodsSixty-seven MDD patients with family history and sixty-seven MDD patients without family history were assigned to research group,sixty-seven healthy volunteers were assigned to control group,and ERP P300 detections were conducted in all subjects.Results①To compare with control group ( ( 189.33 ± 51.13 ) ms) and MDD without family history group( ( 193.55 ± 40.01 )ms),the N2 latency was prolonged more significantly in MDD with family history group ( ( 208.40 ± 33.05 ) ms ) (P ＜ 0.05 ).②Compared with control group ( ( 3.38 ± 5.52 ) μV ),the N2 amplitude was decreased more significantly in MDD without ( ( 2.47 ± 1.87 ) μV ) and with family history ( ( 2.36 ± 2.10) μV ),(P ＜ 0.05 ).ConclusionThere is an obvious cognitive function damaged in the MDD patients with and without family history and the MDD patients with family history are more serious.

Objective To investigate the effects in elasticity of anterior tibial artery in new patients with type 2 diabetes caused by medicines of reducing blood sugar. Methods One hundred patients with type 2 diabetes were involved. The patients were divided into control group(50 cases) and case group(50 cases) according the vascular complications (including macroangiopathy and microangiopathy). Maxmum of circumferential strain(CSmax) of anterior tibial artery was acquired through strain and strain rate imaging. Local blood pressure which included local systolic blood pressure(LSBP) and local diastolic blood pressure (LDBP) of anterior tibial artery was measured at the same time. Strain-blood pressure index(SBPI) of anterior tibial artery was calculated, SBPI = CSmax/[(LSBP - LDBP)/LDBP] × 100%. It took six months for each patient to take medicines of reducing blood sugar. Then SBPI of anterior tibial artery was calculated again. Parameters were compared inter- and intra-groups. Results SBPI of anterior tibial artery after therapy was higher than that before therapy in control group( P<0. 05). There was no significant difference between SBPI of anterior tibial artery before therapy and that after therapy in case group( P >0. 05). SBPI of anterior tibial artery in case group was lower than that in control whatever before and after therapy( P < 0. 05). Conclusions The protection of medicines of reducing blood sugar on elasticity of anterior tibial artery in new diabetic patients without vascular complications was better.

Animals ; Carcinoma, Neuroendocrine ; metabolism ; pathology ; physiopathology ; Carcinoma, Small Cell ; metabolism ; pathology ; physiopathology ; Cell Differentiation ; Chromogranin A ; metabolism ; Humans ; Male ; Neuroendocrine Cells ; metabolism ; pathology ; Prostatic Neoplasms ; metabolism ; pathology ; physiopathology

Objective To study the immunoregulatory effects of thalidomide on the peripheral blood T-lymphocytes of rheumatoid arthritis patients.Methods MTr was used to detect the effects of different thalidomide concentrations on the proliferation of T-cells.Flow eytometry was used to analyze T-cells early apoptosis and the T-cells subsets in different concentration of thalidomide.The mRNA expression of IL-6,IL- 10 and TNF-α was measured by RT-PCR method.Results The level of thalidomide at 500 μg/ml inhibited the proliferation of T-ceils and the CD3+CD28+ expression of T-cell subsets,but promoted the early apoptosis and the CD8+CD152+ expression of T-cell subsets.Thalidomine at any concentration could inhibit the mRNA expression of IL-6,TNF-α.However,the level of thalidomide that could promote the mRNA expression of IL- 10 was 100 μg/ml and 500 μg/ml.Conclusion Thalidomide can inhibit the proliferation of T lymphocytes and the expression of CD3+CD28+ on T-cell subsets.It can promote the early apoptosis and the CD8+CD152+ expression of T-cell subsets.Thalidomide inhibits the mRNA expression of IL-6 and TNF-α but promote the mRNA expression of IL-10.Thalidomide has immuno-regulatory effects on rheumatoid arthritis T-cells.

OBJECTIVE Recent studies have demonstrated that the Nlrp3 inflammasome serve as a central role in the pathogenesis of cardiovascular diseases and endothelial dysfunction occurs in association with several cardiovascular risk factors. Given the demonstrated anti-inflammatory effects of aspirin, the present study was designed to test whether aspirin diminish NLRP3 inflammasome activation and prevent endothelium injury and associated coronary artery damage during LPS. METHODS Mouse carotid arterial endothelial cells (CAECs) were cultured and treated with 0.1-3 mmol·L-1 of aspirin in response to LPS (2 μg·mL-1) stimuli. After 24 h, the Nlrp3 inflammasome complexes consist of varied proteins were analyzed by WB. NO and T-AOC in the supernatant was detected by ELISA. Intracellular reactive oxygen species (ROS) generation for 24 h was observed by DCF fluorescence. The mice were treated with aspirin (12.5 mg·kg-1 per day, 62.5 mg·kg-1 per day, 125 mg·kg-1 per day) and dexametha?sone (0.0182 mg · kg- 1 per day) for 7 d. The level of IL- 1β,IL- 18 protein was detected by ELISA. RESULTS Immunofluorescence results showed the colocalization of Nlrp3 with ASC or caspase 1 decrease in a concentration- dependent manner. Meanwhile, the expression of Nlrp3 and caspase 1 protein was decreased with the concentration of aspirin, but no changes the expression of ASC protein. Nlrp3 protein levels in CAECs were 0.33- 0.8- fold and cle- caspase 1 protein levels in CAECs were 0.48-1-fold compared to those in LPS stimulation when treated with 0.1-3 mmol·L-1 aspirin for 24 h (P<0.01). Aspirin significantly antagonized the effect of LPS on NO (1.22-1.91-fold that of LPS stimulation, P<0.01) and T-AOC expression (1.02-1.90-fold that of LPS stimulation, P<0.01). As the different concentration of aspirin treated, the generation of ROS was 0.51-1.10-fold that of LPS stimulation (P<0.01). In vivo data shown the level of IL-1β, IL-18 protein from serum are in concordance with the level of Nlrp3 inflammasome activation. CONCLUSION We conclude that aspirin has anti- inflammatory properties, protecting CAECs from LPS-induced injury by inhibition of NLRP3 inflammasome activation through ROS pathway.

Objective:To study the effects of FcγRIIb gene modified dendritic cells on liver function and rejection after orthotopic liver transplantation in rats.Methods:The recombinant lentivirus expression vector TRE-FcγRIIb containing Lewis rat FcγRIIb gene was constructed by gene cloning technique. TRE-FcγRIIb expression virus and TET-on regulatory virus were packaged and co-infected with immature dendritic cells derived from DA rat bone marrow. The expression of FcγRIIb was detected. Donor rats DA and recipient Lewis were paired according to body weight and then randomly divided into three groups. The control group (group A) did not receive any pretreatment. The Lewis rats in group B were treated with cyclosporin A on the 2nd day after liver TX. Immature dendritic cells derived from bone marrow of DA rats were injected intravenously one day before liver TX in FcγRIIb gene modified immature dendritic cells (1×10 6 cells)group (group C). Blood and liver tissue were biopsied 7 days after operation to detect liver function and pathological changes. Results:The abnormal liver function in FcγRIIb gene modified immature dendritic cells group (group C) was significantly lower than that of control group 7 days after operation ( P<0.05), and the liver pathological rejection of FcγRIIb gene modified immature dendritic cells group (group C) was significantly lower than that of control group 7 days after operation ( P<0.05). The average survival days of rats in the control group was 12.8 days; the average survival days of rats in the cyclosporin A group was 65.3 days; the average survival days of rats in the FcγRIIb gene-modified immature dendritic cell group was 58.5 days. Conclusion:FcγRIIb gene modified immature dendritic cells can ameliorate liver dysfunction and acute liver rejection after orthotopic liver transplantation.

Objective: To establish a method for the determination of furans in tea by headspace-gas chromatographic mass spectrometry. Methods: The 20% sodium chloride solution and isotope internal standards were added to the crushed and weighed tea sample. Furan, 2-methylfuran, 3-methylfuran, 2,5-dimethylfuran were separated by HP-PLOT Q capillary column and then determined by gas chromatography mass spectrometry with electron impact ionization mode. Results: In the range of 5-400 ng, good linear relationships were observed in the four furan compounds, with the correlation coefficients ranging from 0.999 2 to 0.999 6. The detection limits ranged from 0.2 to 1.9 μg/kg, the quantification limit ranged from 0.4 to 3.1 μg/kg. The recovery rates of furans ranged from 95.4% to 128.2% when spiked at 5.0, 20.0 and 100.0 μg/kg, and the relative standard deviations ranged from 0.8% to 11.3%. Eighty-one tea samples were determined, the concentration of four furan compounds was highest in black tea, followed by dark tea, oolong tea, green tea and scented tea. Conclusion Headspace-gas chromatography-mass spectrometry can reduce the matrix interference of tea, and meet the requirements in the linear range, recovery and precision, which is suitable for simultaneous determination of four furan compounds in tea.

AIM:To observe the structural basis of ocular motility abnormalities in patients with congenital fibrosis of the extraocular muscles type Ⅰ ( CFEOM Ⅰ) due to missense mutations in the developmental kinesin KIF21A using high - resolution magnetic resonance imaging ( MRI) .
METHODS: Totally 11 affected individuals reported KIF21A mutations were correlated with MRI studies demonstrating extraocular muscles ( EOMs ) size, location, contractility, and innervation. EOMs and the motor nerve in the orbits were imaged with T1 weighted in a triplanar scan using a dual-phased coils with 2. 0mm thick. Motor nerves were imaged at the brainstem using head coils and 3D-FIESTA with 0. 6-mm thick.
RESULTS: Patients with CFEOM Ⅰ exhibited different degrees of hypoplasia of oculomotor nerve, the abducens nerve and the trochlear nerve were also affected, of which 8 cases of orbital section could see the signal of abnormal nerve dominated by oculomotor nerve to lateral rectus. The both sides of six EOMS in all patients exhibited variable atrophy and abnormal bright internal signal on T1 imaging, particularly severe for the superior rectus and levator muscles.
CONCLUSION: High - resolution MRI can directly demonstrate pathology of motor nerves,affected EOMs, and ‘Pulley' hypoplasia caused by CFEOM Ⅰ due to mutations in KIF21A,and these findings suggest that the neuronal hypoplasia is the etiological factor of CFEOM.

Astragalus polysaccharide(APS), one of the main active components of Astragali Radix, plays an anti-tumor effect by regulating the inflammatory microenvironment of tumors. Exosomes are small extracellular vesicles with a diameter ranging from 50 to 200 nm and carry several biological components from parental cells such as nucleic acids and proteins. When combined with recipient cells, they play an important role in intercellular communication and immune response. In this study, exosomes released from H460 cells at the inflammatory state or with APS addition activated by Toll-like receptor 4(TLR4) were extracted by ultracentrifugation and characterized by Western blot, transmission electron microscopy, and nanoparticle tracking analysis. The exosomal proteins derived from H460 cells in the three groups were further analyzed by label-free proteomics, and 897, 800, and 911 proteins were identified in the three groups(Con, LPS, and APS groups), 88% of which belonged to the ExoCarta exosome protein database. Difference statistical analysis showed that the expression of 111 proteins was changed in the LPS group and the APS group(P<0.05). The biological information analysis of the differential proteins was carried out. The molecular functions, biological processes, and signaling pathways related to the differential proteins mainly involved viral processes, protein binding, and bacterial invasion of proteasome and epithelial cells. Key differential proteins mainly included plasminogen activator inhibitor-1, laminin α5, laminin α1, and CD44, indicating that tumor cells underwent systemic changes in different states and were reflected in exosomes in the inflammatory microenvironment. The analysis results also suggested that APS might affect the inflammatory microenvironment through the TLR4/MyD88/NF-κB signaling pathway or the regulation of the extracellular matrix. This study is conducive to a better understanding of the mechanism of tumor development in the inflammatory state and the exploration of the anti-inflammatory effect of APS at the exosome level.
Humans ; Exosomes/metabolism* ; Proteomics ; Toll-Like Receptor 4/metabolism* ; Lipopolysaccharides ; Astragalus Plant/chemistry* ; Lung Neoplasms/metabolism* ; Polysaccharides/metabolism* ; Tumor Microenvironment