Rat lung microvascular endothelial cells (LMVEC) was cocultured with rat pulmonary arterial smooth muscle cells (PASMC), and the cultures were randomly divided into 4 groups: normal homotypic group (NH), normal coculture group (NC), lipopolysaccharide homotypic group (LH), LPS coculture group (LC). The cell cycles were analysed with flow cytometry. The results showed that after the treatment of 100ng/ml LPS for 16h, the number of cells in G 1 phase was decreased in both homotypic and coculture of LMVEC and PASMC, while that in S+G 2/M were increased. The number of cells in G 1 phase was larger in LC than LH, but the number of cells at S+G 2/M phase was less in LC than LH. Compared with normal group, the unmber of LMVEC at S phase was increased by homotypic and coculture after the treatment with LPS. It is concluded that LPS could effect the cell cycle and accelerate the cell division, and there is a complicated regulatory mechanism in cell proliferation between LMVEC and PASMC.

Objective To investigate the expression of activating receptors (NKG2D and NKp46), inhibitory receptors (NKG2A and KIR) as well as costimulatory molecules (OX40, 4-1BB and ICOS) on peripheral blood natural killer (NK) cells from patients with recurrent genital herpes (RGH). Methods Four-color immunofluorescence staining with flow cytometry was used to detect the expression of NKG2D, NKG2A, KIR and NKp46 in 44 patients with RGH and 40 normal human controls, and to detect the expression of OX40, 4-1BB and ICOS in 29 patients with RGH and 29 normal human controls. Results The proportions of NKG2D-positive and NKp46-positive NK cells significantly decreased in patients with RGH than those in the normal human controls [(93.3 ± 5.4)% vs (96.9 ± 2.5)%, (88.9 ± 8.7)% vs(93.4 ± 4.1)%, respectively, both P < 0.01]. Between the patients and controls, no significant difference was observed in the expression of NK cell inhibitory receptors, NKG2A [(41.8 ± 14.4)% vs (46.0 ± 14.7)%, P > 0.05] or KIR [(68.3 ± 19.1)% vs (69.1 ± 17.6)%, P > 0.05]. A lower expression of costimulatory molecule OX40 was noted in NK cells from patients with RGH compared with those in normal controls [(1.0 ± 1.1)% vs (1.8 ± 1.7)%, P < 0.05]. Conclusions Herpes simplex virus infection could down-regulate the expression of NK cell activating receptors and costimulatory molecules, subsequently suppress the activation of NK cells, and lead to the escape of virus-infected cells from the killing of NK cells.

The 5-enolpyruvylshikimate-3-phosphate (EPSP) synthase activity of Sclerotinia sclerotiorum is one of the multifunctional enzyme AROM activities, which catalyzes a reversible conversion of shikimate 3-phosphate (S3P) and phosphoenolpyruvate (PEP) to EPSP and inorganic phosphate, and is inhibited by the herbicide glyphosate (N-phosphonomethyl glycine). AROM protein has been purified from Sclerotinia sclerotiorum and the EPSP synthase has been analyzed. The results indicated that the optimal pH and temperature of EPSP synthase were 7.2 and 30℃ respectively. The activation energy of the heat-deactivated reaction of the enzyme was found to be 69.62 kJ/mol. Both of the substrates, S3P and PEP, were showed to inhibit the reaction rate when their concentrations exceeded 1 mmol/L and 2 mmol/L respectively. The Km of 140.98 μmol/L for PEP and 139.58 μmol/L for S3P were obtained by Dalziel equation which was a steadystate kinetic equation of the enzymatic reaction with the double substrates. The kinetic pattern of the enzyme was consistent with a sequential mechanism. Inhibition of the EPSP synthase reaction by glyphosate was competitive with respect to PEP, with the Ki 0. 32 μmol/L, and noncompetitive with regard to S3P. Activation by [ K+ ] was observed in the forward reaction. The Km (PEP) was lowered by increasing [ K+ ], while the Km (S3P) changed irregularly and the Ki (PEP) was enhanced.

Technologies for the trans-institutional sharing of scientific data were studied with the sharing of nucleic acid sequence data as the study object , such as leaving a flexible space for implementation of the unified standards in working out the criteria for data sharing , implementing regular point to point data sharing and updating in agree-ment of institutional league , and providing multiple data services according to the unified working process by giving considerations to the local demands .The significance of trans-institutional sharing of scientific data under the insti-tutional league model was summarized for the reference in constructing the scientific datasharing platform.

MicroRNAs (miRNAs) are evolutionarily conserved small noncoding RNAs of-22 nucleotides that exist in a wide variety of organisms,including animals,plants and virus.Mature miRNAs are able to control gene expression at a post-transcriptional level,either by blocking mRNA translation or inducing their degradation.Hepatitis B virus X protein (HBX) is a 17000 protein that is implicated to play a crucial role in hepatocarcinogenesis.Recently,many studies have shown that HBX is associated with miRNA regulation,and is involved in regulating fundamental biological processes of tumor in cell proliferation,differentiation and apoptosis.

Objectives To study the impact of initial age of treatment on testicular morphology and function in male pa-tients with multiple pituitary hormone deficiency using human chorionic gonadotropin (hCG) and human menopausal gonadotro-pin (hMG). Methods Patients with multiple pituitary hormone deficiency were treated with hCG and hMG while keeping other hormone levels normal. Correlations among their testicular volume, follicle-stimulating hormone (FSH), luteinizing hormone (LH), and height, bone age were analyzed. Results After 6-month hCG and hMG treatment, the penis length of 54 male patients was significantly increased from (2.58 ± 0.69) cm to (4.19 ± 0.77) cm , and penis circumference was also increased from (3.71 ± 1.36) cm to (5.95 ± 1.26) cm;the testicular volume was increased from (1.76 ± 1.49) ml to (5.20±2.30) ml;height was increased from (147.01 ± 12.29) cm to (151.98 ± 11.52) cm and bone age was increased from (11.22 ± 2.71) years to (11.64 ± 2.72) years;the differences before and after treatment were statistically significant (all P<0.01). As the patients' age increased, their testicular volume and testosterone level increased slowly, and significant differences amongst each age group were found (P<0.05). The in-creased value of testicular volume, serum FSH and LH levels, and height growth tended to be negatively correlated to the initial age of therapy (r=-0.517~-0.334, P<0.05). Conclusions Early and proper treatment in male patients with multiple pituitary hormone deficiency using hCG and hMG improves testicular function and secondary sex characteristics.

To investigate different effects of fiscal health expenditure, household spending on health and social health expenditure on narrowing the gap between urban and rural health resource allocation. Methods: With the relevant data of China’ s medical and health through 1985-2011 years, taking methodology of the state space model to estimate the varying-time elasticity of different types of expenditures on urban and rural health resource allocation gap. Results: For narrowing the gap, household health expenditure played the leading role, fiscal health expenditure played smaller role and the social health expenditure played the supplementary role; the elastic of different health expenditure proportion was fluctuated before 2002, which became stable after 2002; it is easy to improve the “hard conditions” rather than the “soft conditions” . Conclusion: To accelerate the process of urban and rural medical security system integration, it is inevitable to establish an efficient configuration mechanism for urban and rural health expense, balanced develop urban and rural medical insurance system and scientifically guide social health investment.

Antiporters ; genetics ; Base Sequence ; Female ; Glycogen Storage Disease Type I ; diagnosis ; genetics ; Humans ; Infant ; Monosaccharide Transport Proteins ; genetics ; Mutation ; Polymerase Chain Reaction ; Sequence Analysis, DNA

Objective To evaluate the value of CT scan in diagnosis of the splenic lesions.Methods A retrospective analysis was made on the CT scans of 33 patients with surgically and pathologically proven splenic lesions,which included plain CT scan(n=33),biphasic contrast-enhanced CT scan(n=28)and contrast delay scanning(n=6).Results In 33 cases,non-neoplastic lesions were 6 cases,including tuberculosis(n=2),hematomas(n=3)and inflammatory pseudotumor associated with a cavernous hemangioma(n=1).Benign tumors were 13 cases,including cysts(n=5),hemangiomas(n=4),lymphanioma(n=1)and lymph-hemangiomas(n=3).Malignant tumors were 14 cases,including malignant lymphoma(n=8),metastases(n=4),malignant myofibroblastoma and hemangioendothelial sarcoma(n=1,respectively).Conclusion CT is of significant value in diagnosis of splenic lesions.

OBJECTIVE To investigate the effect of phosphotyrosine interaction domain containing 1 (PID1, NYGGF4) onpromotion of IR and HCC, and explore its underlying mechanisms. METHODS Lentivirus were used to mediate the knockdown of PID1 in HFD induced IR mouse model as well as ob/ob mice. Intraperitoneal glucose and insulin tolerance were performed 4 weeks after lentivirus injection. Hydrodynamics-based transfection was applied to induce the liver specific overexpression of PID1. Flow cytometry was exerted to detect the proportion and function of immune cells.qRT-PCR and Western blot were used to detect the expression of downstream pathways of PID1. Liquid chromatography-mass spectrometry (LC-MS) and co-immunoprecipitation (Co-IP) were conducted to identify proteins interacting with PID1.Chromatin immunoprecipitation(ChIP)was operated to measure the modification of H3K4me3 of PID1 promoter.RESULTS PID1 restriction improved insulin resistance,hyperglycemia and fatty liver. Conversely, hepatic knockdown of PID1 attenuated liver xenografted tumor growth. Moreover,PID1 liver-specific protooncogenes via hydrodynamics-based transfection established a primary hepatocellular carcinoma mouse model,induced an immunosuppressive environment,with the reduction of CD3+,CD4+,CD8+T cells,retarded maturation of dendritic cells(DCs),pronounced differentiation of regulatory T cells(Tregs),and recruitment of MDSC.In addition,PID1 overexpression activated prolifer-ation related genes, promoted anti-inflammatory genes, suppressed pro-inflammatory genes, induced glycolysis and lipid metabolism genes to facilitate tumorigenesis in liver. Importantly, PID1 exerted its tumor-promoting function through binding to epidermal growth factor receptor(EGFR)and activation of downstream KRAS/ERK pathway.As such,PID1 exist trimethylation of histone H3 at lysine 4(H3K4me3) modification and IR up-regulated the expression of PID1 by activation the H3K4me3 modification. CONCLUSION PID1 is a new gene that exerts both liver cancer-promoting and insulin resistance inducing function.IR accelerates liver cancer development and progression partially dependent on the activation of PID1.