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Background: The co-occurrence of schizophrenia and type 2 diabetes mellitus (T2DM) has been well documented. Recent genome-wide association studies and meta-analyses have shown robust associations of the solute carrier family 30 member 8 (SLC30A8) gene variants with T2DM in various populations. We examined the involvement of the SLC30A8 in the susceptibility to schizophrenia in a Han Chinese population., Methods: The SLC30A8 rs13266634 gene polymorphism was genotyped in 837 chronic schizophrenic and 1109 unrelated healthy controls by using a case control design. We also assessed clinical symptoms., Results: There were no significant differences in the rs13266634 genotype (χ(2)  = 1.95, df = 2, p = 0.38) and allele (χ(2)  = 0.47, df = 1, p = 0.50) distributions between the patient and control groups. There was no association between rs13266634 and clinical symptoms., Conclusion: The SLC30A8 gene variation does not appear to contribute a genetic basis for the co-occurrence of schizophrenia and T2DM., (Copyright © 2012 John Wiley & Sons, Ltd.)

Objective: To study the destructive effects of the membrane lipid microdomain with methyl β cyclodextrin (MβCD) on the proliferation, transdifferentiation and cell cycle of type II alveolar epithelial cell (AEC II)., Methods: The membrane lipid microdomain of AEC II was destroyed by MβCD (MβCD interference group) in vitro, and then cultured with DMEM as control. Cell number was counted with hemacytometer; the proliferation rate was measured by methyl thiazolyl tetrazolium (MTT); flow cytometry was used to assay the cell cycle. The expressions of AEC II specific surfactant protein-C (SP-C) and AECI specific aquaporin 5 (AQP5) were detected by immunofluorescence and Western blotting analyses., Results: Compared with control group, cell number and the cell proliferation was decreased in MβCD interference group at 24, 48 and 72 hours after interaction [cell numbers (×10(6)/ml): 2.74±0.56 vs. 8.05±0.92, 4.45±0.68 vs. 10.52±0.81, 7.82±0.59 vs. 11.39±0.81; MTT results (A value): 0.25±0.20 vs. 0.45±0.02, 0.35±0.03 vs. 0.54±0.28, 0.48±0.04 vs. 0.59±0.05, all P<0.01]. MβCD could increase the percentage of cells in G0/G1 phases and decreased the percentage in S phases at 24 hours [G0/G1 phases: (60.06±1.65)% vs. (43.43±3.59)%; S phases: (16.20±2.17)% vs. (34.07±2.63)%, both P<0.05 ]. Incubation of AEC II with MβCD resulted in up regulation of the expression of SP-C (0.54±0.04 vs. 0.47±0.03, 0.19±0.03 vs. 0.06±0.02) and down regulation of AQP5 (0.30±0.04 vs. 0.43±0.06, 0.39±0.04 vs. 0.59±0.04) at 48 hours and 72 hours after interaction (P<0.05 or P<0.01)., Conclusion: The destruction of membrane lipid microdomain by the MβCD can inhibit proliferation and transdifferentiation of AEC II, and induce cell cycle arrest in G1 phase.

Aim: To study whether over-starvation aggravates intestinal mucosal injury and promotes bacterial and endotoxin translocation in a high-altitude hypoxic environment., Methods: Sprague-Dawley rats were exposed to hypobaric hypoxia at a simulated altitude of 7000 m for 72 h. Lanthanum nitrate was used as a tracer to detect intestinal injury. Epithelial apoptosis was observed with terminal deoxynucleotidyl transferase dUTP nick end labeling staining. Serum levels of diamino oxidase (DAO), malondialdehyde (MDA), glutamine (Gln), superoxide dismutase (SOD) and endotoxin were measured in intestinal mucosa. Bacterial translocation was detected in blood culture and intestinal homogenates. In addition, rats were given Gln intragastrically to observe its protective effect on intestinal injury., Results: Apoptotic epithelial cells, exfoliated villi and inflammatory cells in intestine were increased with edema in the lamina propria accompanying effusion of red blood cells. Lanthanum particles were found in the intercellular space and intracellular compartment. Bacterial translocation to mesenteric lymph nodes (MLN) and spleen was evident. The serum endotoxin, DAO and MDA levels were significantly higher while the serum SOD, DAO and Gln levels were lower in intestine (P < 0.05). The bacterial translocation number was lower in the high altitude hypoxic group than in the high altitude starvation group (0.47 ± 0.83 vs 2.38 ± 1.45, P < 0.05). The bacterial translocation was found in each organ, especially in MLN and spleen but not in peripheral blood. The bacterial and endotoxin translocations were both markedly improved in rats after treatment with Gln., Conclusion: High-altitude hypoxia and starvation cause severe intestinal mucosal injury and increase bacterial and endotoxin translocation, which can be treated with Gln.

Objective: To observe the proliferation and phenotype-switching of pulmonary arterial smooth muscle cell (PASMC) induced by hypoxia and interfered by Ad-PKGIα. And to investigate the potential regulative role of PKGIα gene in the molecule mechanism of hypoxia pulmonary vessel remodeling (HPVR)., Methods: To establish the pure PASMC cultured by tissue-sticking methods. Semi-quantitative reverse transcription and polymerase chain reaction (RT-PCR) and Western blot were used to examine the PKGIα mRNA and protein expression after PASMC were transfected by Ad-PKG. The mRNA and protein expressive change of smooth muscle alpha actin (SM-alpha-actin) determined the degree of cell phenotype-switching. The changes of PASMC proliferation were determined by flow cytometry and ³H-TdR incorporated way., Results: Ad-PKGIα could transfect into PASMC and highly express. Hypoxia down-regulated the expression of SM-alpha-actin protein (44.25 ± 5.34 in normoxia, 32.18 ± 4.19 in 12 h hypoxia condition, 21.90 ± 2.44 in 24 h hypoxia condition, P < 0.05), that could be blocked by the transfection of Ad-PKGIα. Hypoxia could push PASMC mitosis and proliferating (³H-TdR incorporated way: 7570 ± 371 in normoxia, 12,020 ± 831 in 12 h hypoxia condition, 14,924 ± 1491 in 24 h hypoxia condition, P < 0.05), that could be blocked by the transfection of Ad-PKGIα, too., Conclusions: The results suggested that PKGIα signaling pathway might play an important role in the molecule mechanism of HPVR. And PKGIα gene might be a target point of gene therapy.

A new SNP located in IGF-2 gene of Wuzhishan pig was detected while a C --> T silent mutation at position 17 of exon 8 was detected by Single-Strand Conformational Polymorphism (SSCP). The value of polymorphism information content (PIC) indicated that this locus had intermediate polymorphism information content (0.25 < PIC < 0.5). The results of the fitness of Hardy-Weinberg equilibrium was in disequilibrium (P < 0.01). SAS analysis together with the multiple comparisons between polymorphisms and growth traits showed that: the differences of carcass weight (P = 0.024), withers height (P = 0.037) and chest girth (P = 0.025) in 10-month-old generation group were very remarkable.

Objective: To investigate the effect of seawater on expression of protease-activated receptor 2 (PAR-2) in adenocarcinoma of lung cell line A549 cells, and the inflammatory injury on A549 cells induced by seawater., Methods: A549 cells were randomly divided into four groups: control group, 2 hours group, 4 hours group, 8 hours group, in which cells were treated with seawater for 2, 4 and 8 hours respectively. After seawater treatment, cells were collected for real-time quantitative reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting analysis to determine the expression of PAR-2 mRNA and its protein. Supernatant were collected for tumor necrosis factor-alpha (TNF-alpha) and interleukin-8 (IL-8) which were determined by enzyme-linked immunosorbent essay (ELISA)., Results: The expression of PAR-2 mRNA and protein of A549 cells increased in a time-dependent manner after seawater treatment, significantly so after 2 hours in all groups (both P<0.05), and peaked at 4 hours after seawater treatment (1.8-fold and 2.2-fold respectively, both P<0.01), followed by a decrease though still higher than those of control group significantly (both P<0.01). TNF-alpha and IL-8 in supernatant increased significantly after seawater treatment, peaking at 2 hours after seawater treatment [(214.35+/-20.85) ng/L, (55.86+/- 5.65) ng/L ] and then followed by a slight decrease though still significantly higher than those of control group [(25.86+/-3.85) ng/L, (6.97+/-1.77) ng/L, all P<0.01]., Conclusion: Seawater can induce significant inflammation of A549 cells and up-regulate the expression of PAR-2 on A549 cells.

Objective: To observe changes in liver X receptor-alpha (LXR alpha) in acute lung injury (ALI) in rats induced by lipopolysaccharide (LPS) to explore mechanism of LXR alpha in pathogenesis of ALI., Methods: Forty-eight Wistar rats were randomly divided into two groups. ALI model was reproduced by intravenous injection of LPS (5 mg/kg), and control group was injected with normal saline (2.5 ml/kg). At 1, 2, 4, 8 hours after ALI, artery blood gas analysis, lung tissue wet/dry weight (W/D) ratio, myeloperoxidase (MPO) activity, lung histopathologic changes were observed. The expressions of LXR alpha and tumor necrosis factor-alpha (TNF-alpha) mRNA were detected by reverse transcription-polymerase chain reaction (RT-PCR). TNF-alpha content was measured with enzyme linked immunosorbent assay (ELISA). LXR alpha protein in lung tissues was assessed by immunohistochemistry., Results: Compared with the control group, in ALI rats at different time points, partial pressure of oxygen in arterial blood (PaO(2)) decreased significantly, lung W/D weight ratio and MPO activity increased significantly (all P<0.05), histopathology of lung revealed signs of injury. After injury, expression of LXR alpha mRNA in lung tissue decreased markedly, and expression of TNF-alpha mRNA in lung tissue increased markedly (all P<0.05). TNF-alpha increased markedly in lung homogenate and blood serum at the same period, and TNF-alpha reached peak value at 4 hours. Immunohistochemical staining of LXR alpha showed that lung tissues of normal rats express LXR alpha significantly, however, after injury, expression of LXR alpha in lung tissue decreased markedly (all P<0.05)., Conclusion: Lung tissues of normal rats express LXR alpha. The decreased LXR alpha mRNA and protein expressions in the lung tissue of rats with ALI caused by LPS may be associated with the occurrence of ALI.

Objective: To determine the effects of nuclear factor-alpha B (NF-alpha B) on peroxisome proliferator activated receptor gamma (PPAR gamma) expression in the murine macrophage cell line Ana-1, based on the investigation of the PPAR gamma expression stimulated by lipopolysaccharide (LPS)., Methods: Ana-1 cells were divided randomly into seven groups: control group, LPS groups (cells were activated by 0.1 mg/L LPS for 1, 2, 4, 8 hours respectively), SN50 group (cells were stimulated by 50 mg/L SN50 for 4 hours) and NF-alpha B high expression plasmid transfected group. PPAR gamma and tumor necrosis factor-alpha(TNF-alpha) mRNA levels were assayed by reverse transcription-polymerase chain reaction (RT-PCR) and the TNF-alpha protein was measured by enzyme linked immunosorbent assay (ELISA) after being activated by LPS. The eukaryotic expression vector of murine NF-alpha B p65 gene was constructed and stably transfected into Ana-1 cells with DOTAP liposome . The PPAR gamma expression and NF-alpha B p65 translocation as stimulated by LPS and SN50 were assayed by Western blotting., Results: Expressions of both PPAR gamma mRNA and protein were downregulated when cells were stimulated by LPS, which were accompanied with the activity of NF-alpha B and TNF-alpha in Ana-1 cells (all P<0.05). The eukaryotic expression vectors containing murine p65 gene were successfully constructed and stably transfected into Ana-1 cells. LPS stimulation and NF-alpha B p65 gene overexpression resulting in upregulation of p65 could downregulate PPAR gamma expression in Ana-1 cells (r=-0.913, P<0.05).But downregulation of NF-alpha B by SN50 could upregulate PPAR gamma expression in the nucleus (r=-0.959, P<0.05)., Conclusion: LPS can markedly decrease the expression of PPAR gamma in Ana-1 cells, which may be related to its activity of enhancing NF-alpha B. NF-alpha B p65 gene can control PPAR gamma expression in the reverse direction in Ana-1 cells.

Objective: To explore the effects of suppressors of cytokine signaling (SOCS)3 gene on expression of c-fos, c-jun mRNA and proliferation of rat pulmonary arterial smooth muscle cells(PASMCs) under hypoxia., Methods: PASMCs were co-transfected with pEFSOCS3 and pSV2neo by liposome, and then expression of SOCS3 protein was detected by immunocytochemistry. After PASMCs were exposed to normoxic and hypoxia at various time points respectively, expression of c-fos and c-jun mRNA was assessed by semi-quantitive RT-PCR. Flow cytometric DNA analysis was used to detect cell cycles., Results: Expression of SOCS3 protein was confirmed by Western blot in PASMCs transfected with SOCS3 gene. The c-fos mRNA level in control cells peaked at 2 h of hypoxia and declined at 4 h, then peaked at 8 h secondly and declined at 12 h. C-fos mRNA level in SOCS3 gene-transfected cells at 2 h and 8 h exposed to hypoxia was lower than that in control cells at the same time points respectively (P < 0.01). The c-jun mRNA level increased at 2 h after exposure of control cells to hypoxia, peaked at 6 h of hypoxia and declined to the basal levels at 12 h. C-jun mRNA level of SOCS3 gene-transfected cells at 2 h, 4 h, 6 h, 8 h under hypoxia was lower than that in controls cells at the same time points. Compared with control PASMCs, cells in transfected with SOCS3 gene at G(1)/G(0) phase increased and those at S + G(2)/M phase decreased under normoxic and hypoxia (P < 0.01)., Conclusion: Hypoxia induced expression of c-fos and c-jun genes, which might play an vital role in the early stage of PASMCs proliferation. SOCS3 protein may inhibit proliferation of PASMCs by lowering the tyrosine-phosphorylated level of STAT3 protein under hypoxia.

The properties of organic matter in steppe chernozem, steppe wind-blown soil and cultivated wind-blown soil were studied by analyzing the status of organo-mineral complex and the combined status and composition of humus. The results showed that different types and utilization patterns of soil had very different effects on the properties of soil organic matter. The amounts of total organic carbon, biomass C, heavy fraction C, extractable humus (HE) and loosely-combined humus and the humification degree were higher in steppe chernozem than in wind-blown soil. Steppe soil had higher amounts of total organic carbon, biomass C, heavy fraction C, HE and different combined humus than sunflower wind-blown soil, but humification degree had no obvious difference.

Objective: To investigate the expression levels of signal transducers and activators of transcription (STATs) in the lung tissue of hypoxic pulmonary hypertension (HPH) rat models., Methods: The Wister rat HPH models were divided into 4 groups: 1 week group (H1), 2 week group (H3), 3 week group (H3), and 4 week group (H4) (n = 12 in each group). The levels of STATsmRNA expression of the lung tissue were measured by reverse transcription-polymerase chain reaction (RT-PCR) and Northern blot. The protein expression of STATs and cellular morphologic changes were observed by immunohistochemistry and Tiger image analysis., Results: The RT-PCR showed that the levels of STAT1mRNA expression of the lung tissue in H1 1.25 +/- 0.12, H2 2.28 +/- 0.15 and H3 1.27 +/- 0.12 were significantly higher than that in the healthy control group 0.61 +/- 0.07 (P < 0.01); the levels of STAT2mRNA expression in H1 0.54 +/- 0.06, H2 1.01 +/- 0.08 and H3 1.36 +/- 0.09 were significantly higher than that in control group 0.30 +/- 0.03 (P < 0.01); the mRNA expressions of STAT3 in H1 0.74 +/- 0.11, H2 1.19 +/- 0.13 and H3 0.80 +/- 0.08 were significantly higher than that in control group 0.26 +/- 0.10 (P < 0.01); and the mRNA expressions of STAT5 in H1 0.92 +/- 0.10, H2 1.23 +/- 0.10 and H3 1.03 +/- 0.11 were significantly higher than that in control group 0.60 +/- 0.11 (P < 0.01). The Northern blot assay demonstrated that the expressions of STAT1mRNA in H1 0.49 +/- 0.10 and H3 0.67 +/- 0.07 were significantly different from that in H2 0.91 +/- 0.07 (P < 0.01); the expressions of STAT3mRNA in H1 2.10 +/- 0.21 and H3 2.58 +/- 0.17 were significantly different from that in H1 3.56 +/- 0.29 (P < 0.01); the expressions of STAT5mRNA in H1 0.99 +/- 0.10 and H3 1.45 +/- 0.12 were significantly different from that in H2 1.79 +/- 0.15 (P < 0.01). It is obvious that the mRNA expressions of STATs in the lung tissue of rat HPH models were increased in the 1st week, to the highest in the 2nd week, and decreased in the 3st week, and all higher than that of control group. The granules of STAT3 and STAT5, positively stained, were observed in the cytoplasm of pulmonary alveolar wall, intrapulmonary vascular and bronchial wall in H3. The protein expressions of STAT3 8.16 +/- 0.49 and STAT5 6.03 +/- 0.37 in H3 were markedly higher than those in H1, H4, and control group., Conclusion: The up-regulation of the STATs expression in lung tissue of HPH rat models suggested that the STATs were involved in the pathogenesis of HPH formation.

Objective: To investigate the expressions of interleukin 6 (IL-6) and Janus kinases (JAKs) in rats with hypoxia induced pulmonary hypertension (HPH)., Methods: Sixty male Wistar rats were randomized into 5 groups with 12 animals in each: a one-week hypoxic group (H(1) group), a two-week hypoxic group (H(2) group), a three-week hypoxic group (H(3) group), a four-week hypoxic group (H(4) group), a normal oxygen group (N group). The rat model of HPH was replicated in normal baric hypoxic cabin. The levels of IL-6 and JAKs mRNA were measured by using reverse transcription-polymerase chain reaction (RT-PCR); The expression of JAKs protein and cell morphologic changes were observed by immunohistochemistry., Results: (1) The levels of IL-6 mRNA in H(1) (1.67 +/- 0.09), H(2) (2.26 +/- 0.12) and H(3) (1.55 +/- 0.11) groups were significantly higher than that in N group (1.20 +/- 0.11, all P < 0.01). The levels of JAK1 mRNA in H(1) (2.11 +/- 0.09), H(2) (2.85 +/- 0.12) and H(3) (2.36 +/- 0.13) groups were significantly higher than that in N group (1.62 +/- 0.10, all P < 0.01); The levels of JAK2 mRNA in H(1) (1.41 +/- 0.07), H(2) (2.02 +/- 0.13) and H(3) (1.36 +/- 0.09) groups were significantly higher than that in N group (1.01 +/- 0.09, all P < 0.01); The levels of JAK3 mRNA in H(1) (0.86 +/- 0.11), H(2) (1.45 +/- 0.10) and H(3) (0.91 +/- 0.13) groups were significantly higher than that in N group (0.55 +/- 0.08, all P < 0.01). The levels of TYK2 mRNA in H(1) (1.36 +/- 0.10), H(2) (1.76 +/- 0.11) groups were significantly higher than that in N group (0.57 +/- 0.07, all P < 0.01). The levels of IL-6 and JAKs mRNA in H(2) group were significantly higher than those in H(1) and H(3) groups (all P < 0.01). (2) Histochemical staining of JAK1 and JAK3 in H(3) group showed yellow cytoplasm of alveolar wall cells, bronchial wall cells and small blood wall cells; The active protein contents of JAK1 (5.36 +/- 0.32) and JAK3 (4.88 +/- 0.29) were markedly increased as compared with N group (1.52 +/- 0.18, 1.22 +/- 0.09, respectively; all P < 0.01) by TIGER image analysis method., Conclusions: The levels of IL-6, JAKs mRNA and protein can increase in pulmonary tissues of rats with HPH. It suggests that IL-6/JAKs pathway may take part in the pathogenesis of HPH.