[Effects of urogenital mycoplasma and chlamydial infections on male fertility].

Objective： This study aimed to assess the impact of urogenital ureaplasma urealyticum (Uu), Mycoplasma hominis (Mh), and Chlamydia trachomatis (Ct) infections on semen quality in men.Methods： In this study, 1022 males were enrolled at the Department of Reproductive Medicine, Rizhao People's Hospital, Shandong Province from October 2014 to January 2023. The participants included 393 in the infertility group, 139 in the recurrent miscarriage group, and 490 in the control group. Based on age, 852 cases were < 36 years old, and 170 cases were ≥ 36 years old. All patients underwent routine semen analysis and tests for Uu, Mh, and Ct, with results statistically analyzed for their impact on semen quality and compared among different age groups. Results: Among the 1022 patients, 344 (33.6%) were Uu-positive, 49 (4.7%) were Mh-positive, and 31 (3.0%) were Ct positive. The sperm concentration, total sperm count, forward sperm motility rate (PR), sperm motility rate (PR+NP) and normal sperm morphology rate of Uu Mh and/or Ct-positive patients were significantly lower than those of the negative group, and the overall difference between the two groups was statistically significant (P<0.05). The positive rate of Uu infection was 41.7% in the infertility group, 30.2% in the recurrent miscarriage group and 28.2% in the control group, and the overall positive rate of the three groups was statistically significant(P<0.05). The positive rate of Mh infection was 6.9% in the infertility group, 8.6% in the recurrent miscarriage group and 2.0% in the control group, and the overall positive rate of the three groups was statistically significant (P<0.001). The positive rate of Ct infection was 6.1% in the infertility group, 2.9% in the recurrent miscarriage group and 0.6% in the control group, and the overall positive rate of the three groups was statistically significant (P<0.001). The positivity rate of Uu infection was 35.8% at the age of <36 years and 22.9% at the age ≥ 36 years, and there was a statistically significant difference in the positivity rate between the two groups (P<0.05). Conclusion: The prevalence of Uu infection in the male urogenital tract is significantly higher than that of Mh and Ct, which is the main pathogen of urogenital tract infection in men. Uu, Mh and Ct infections have adverse effects on sperm concentration, total sperm count, sperm forward motility rate (PR), sperm motility rate (PR+NP) and normal sperm morphology rate, which will lead to a decrease in semen quality and affect male fertility. Genital tract infections are closely related to age, and the prevalence of Uu infection is higher in the younger age group.

Hyperuricemia induces lipid disturbances by upregulating the CXCL-13 pathway.

The molecular mechanism underlying hyperuricemia-induced lipid metabolism disorders is not clear. The purpose of the current study was to investigate the mechanism of lipid disturbances in a hyperuricemia mice model. RNA-Seq showed that differentially expressed genes (DEGs) in the fatty acid synthesis signaling pathway were mainly enriched and CXCL-13 was significantly enriched in protein-protein interaction networks. Western blotting, Q-PCR, and immunofluorescence results further showed that hyperuricemia upregulated CXCL-13 and disturbed lipid metabolism in vivo and in vitro. Furthermore, CXCL-13 alone also promoted the accumulation of lipid droplets and upregulated the expression of FAS and SREBP1, blocking AMPK signaling and activating the PKC and P38 signaling pathways. Silencing CXCL-13 reversed uric-acid-induced lipid droplet accumulation, which further downregulated FAS and SREBP1 expression, inhibited the p38 and PKC signaling, and activated AMPK signaling. In conclusion, hyperuricemia induces lipid metabolism disorders via the CXCL-13 pathway, making CXCL-13 a key regulatory factor linking hyperuricemia and lipid metabolism disorders. These results may provide novel insights for the treatment of hyperuricemia.NEW & NOTEWORTHY The underlying molecular mechanism of hyperuricemia-induced lipid metabolism disorders is still unclear. The study aimed to investigate the mechanism of lipid disturbance in hyperuricemia mice model. To our knowledge, we proposed for the first time that CXCL-13 may be a key regulator of hyperuricemia and lipid metabolism disorders. These results may provide new insights for the clinical treatment of hyperuricemia.

Neutrophil extracellular traps are associated with enhanced procoagulant activity in liver cirrhosis patients with portal vein thrombosis.

OBJECTIVE: Patients with liver cirrhosis (LC) commonly exhibit hypercoagulability and tend to develop thrombosis. Neutrophil extracellular traps (NETs) are associated with a variety of thrombotic conditions, but their possible value in portal vein thrombosis (PVT) is not known. We assessed whether NETs promote thrombosis and contribute to the procoagulant state in patients with LC. METHODS: The circulating levels of NETs markers (myeloperoxidase, neutrophil elastase, citrullinated histone H3) were measured in 72 patients (median age, 55 years; 48 [66.7%] men) with LC from September 2020 to February 2021. Then they were divided into two groups: patients with or without PVT. NETs procoagulant activity was assessed based on thrombin-antithrombin complex (TAT complex) and Factor X. The levels of plasma markers were determined by ELISA. RESULTS: There were 28 patients with PVT and 44 patients without PVT. The levels of NETs markers and hypercoagulability markers in the plasma of cirrhosis patients with PVT were significantly higher than those of cirrhosis patients without PVT (p < 0.05). Additionally, the levels of the NETs markers correlated with TAT complex and Factor X (Spearman correlation rho >0.73, p < 0.0001). CONCLUSIONS: Neutrophil extracellular traps seem to enhance procoagulant activity in LC patients with PVT; thus, they may be a practical predictor of PVT as well as a rapid and easy-to-use diagnostic and treatment guide for PVT in patients with cirrhosis.

Uric acid drives intestinal barrier dysfunction through TSPO-mediated NLRP3 inflammasome activation.

BACKGROUND AND AIM: Intestinal epithelial dysfunction is the foundation of various intestinal and extra-intestinal diseases, while the effects and mechanism of uric acid on the intestinal barrier are little known. TSPO has been shown to be related to the generation of ROS and is involved in regulating inflammation, whether uric acid drives intestinal epithelial dysfunction through TSPO-mediated NLRP3 inflammasome activation is unknown. METHODS: UOX gene knockout mouse (UOX-/-) were used for models of hyperuricemia. Fluorescein isothiocyanate (FITC)-labeled dextran was used to assess in vivo intestinal permeability. Serum lipopolysaccharide (LPS) and culture supernatants IL-1ß were measured using ELISA Kit. IEC-6 exposed to different concentrations of uric acid was used for in vitro experiment. Protein content and mRNA were assessed using Western blotting and Q-PCR, respectively. Intracellular ROS was determined using flow cytometry and fluorescence microscope. Mitochondrial membrane potential was detected on an immunofluorescence. Small interfering RNA transfection was used to assess the interaction between translocator protein (TSPO) and NLRP3 inflammasome. N-acetyl-L-cysteine (NAC) was used as ROS scavenger. RESULTS: Our results showed that hyperuricemia mice were characteristic by increased intestinal permeability. Hyperuricemia upregulated TSPO, increased production of ROS and activated NLRP3 inflammasome, which resulted in lower expression of occludin and claudin-1. In vitro, we showed that soluble uric acid alone increased the expression of TSPO, depolarized mitochondrial membrane potential, increased ROS release and activated NLRP3 inflammasome, which further reduced the expression of occludin and claudin-1. Silencing TSPO suppressed NLRP3 inflammasome activation and increased expression of claudin-1 and occludin, which was accompanied by lower levels of ROS. Scavenging ROS also significantly inhibited NLRP3 inflammasome activation without change of TSPO, indicating that TSPO-mediated NLRP3 inflammasome activation was dependent on ROS. CONCLUSIONS: In conclusion, uric acid drives intestinal barrier dysfunction through TSPO-mediated NLRP3 inflammasome.

Hyperuricemia is associated with impaired intestinal permeability in mice.

Hyperuricemia is associated with many metabolic diseases. However, the underlying mechanism remains unknown. The gut microbiota has been demonstrated to play significant roles in the immunity and metabolism of the host. In the present study, we constructed a hyperuricemic mouse model to investigate whether the metabolic disorder caused by hyperuricemia is related to intestinal dysbiosis. A significantly increased intestinal permeability was detected in hyperuricemic mice. The difference in microflora between wild-type and hyperuricemic mice accompanies the translocation of gut microbiota to the extraintestinal tissues. Such a process is followed by an increase in innate immune system activation. We observed increased LPS and TNF-α levels in the hyperuricemic mice, indicating that hyperuricemic mice were in a state of low-grade systemic inflammation. In addition, hyperuricemic mice presented early injury of parenteral tissue and disordered lipid metabolism. These findings suggest that intestinal dysbiosis due to an impaired intestinal barrier may be the key cause of metabolic disorders in hyperuricemic mice. Our findings should aid in paving a new way of preventing and treating hyperuricemia and its complications.NEW & NOTEWORTHY Hyperuricemia is associated with many metabolic diseases. However, the underlying mechanism remains unknown. We constructed a hyperuricemic mouse model to explore the relationship between intestinal dysbiosis and metabolic disorder caused by hyperuricemia.

CARD8 rs2043211 polymorphism is associated with gout in a Chinese male population.

BACKGROUND &AIM: Previous studies have suggested genetic factors are involved in the development of gout. We performed a case-control study to investigate the genetic association between CARD8 rs2043211 polymorphism and gout. METHODS: A total of 396 male patients with gout and 403 age- and sex- matched healthy controls were included in this study. Genotyping was performed using TaqMan SNP Genotyping Assays. An association analysis was carried out using the χ² test. The genotype-phenotype analysis was also conducted. RESULTS: The genotype distribution of CARD8 rs2043211 polymorphism confirmed to HWE in the controls (P = 0.27). There was an obvious difference in the genotype distribution of CARD8 rs2043211 polymorphism between cases and controls (P = 0.017). In addition, there was an obvious association between CARD8 rs2043211 polymorphism and gout under the recessive comparison model (AA vs. TT/TA: OR = 0.65, 95%CI 0.47-0.88, P = 0.006). Patients carrying genotype TT of CARD8 rs2043211 polymorphism had higher triglycerides levels compared to those carrying the AA genotype (2.77±2.08 mmol/L vs. 2.07±1.15 mmol/L, P = 0.01). Patients with the TT genotype also had significantly higher systolic blood pressure compared with those with the AA genotype (142.11±21.10 mmHg vs. 135.38±14.66 mmHg, P = 0.03). Patients carrying TT genotype also had an increased risk of renal calculus compared with those carrying the AA genotype. CONCLUSION: CARD8 rs2043211 polymorphism is significantly associated with susceptibility to gout in Chinese Han males.

Mechanical Behaviors of the Origami-Inspired Horseshoe-Shaped Solar Arrays.

The importance of flexibility has been widely noticed and concerned in the design and application of space solar arrays. Inspired by origami structures, we introduce an approach to realizing stretchable and bendable solar arrays via horseshoe-shaped substrate design. The structure has the ability to combine rigid solar cells and soft substrates skillfully, which can prevent damage during deformations. The finite deformation theory is adapted to find the analytic model of the horseshoe-shaped structure via simplified beam theory. In order to solve the mechanical model, the shooting method, a numerical method to solve ordinary differential equation (ODE) is employed. Finite element analyses (FEA) are also performed to verify the developed theoretical model. The influences of the geometric parameters on deformations and forces are analyzed to achieve the optimal design of the structures. The stretching tests of horseshoe-shaped samples manufactured by three-dimensional (3D) printing are implemented, whose results shows a good agreement with those from theoretical predictions. The developed models can serve as the guidelines for the design of flexible solar arrays in spacecraft.

LINC01061 triggers inflammation and inflammasome activation in autoimmune thyroiditis via microRNA-612/BRD4 axis.

Considering the significance of LINC01061 in papillary thyroid cancer, here, we commenced to study the role of LINC01061 in autoimmune thyroid disease (AITD) and the potential mechanism. Thyroid tissues were attained from patients with AITD, and Nthy-ori 3-1 cells were induced with lipopolysaccharide (LPS), followed by measurement of LINC01061, microRNA (miR)-612, and BRD4 expression as well as their binding relation. The ectopic expression and silencing experimentations were carried out in LPS-induced Nthy-ori 3-1 cells to detect cell viability and apoptosis as well as inflammation and inflammasome. BRD4 and LINC01061 upregulation and miR-612 downregulation were observed in thyroid tissues of AITD patients and LPS-induced Nthy-ori 3-1 cells. Mechanistic analysis manifested that LINC01061 bound to miR-612 that negatively targeted BRD4. LINC01061 upregulated BRD4 to enhance cell viability, trigger inflammation and inflammasome activation but reduce apoptosis of LPS-induced Nthy-ori 3-1 cells by sponging miR-612. In conclusion, LINC01061 induced the occurrence of AITD by upregulation of miR-612-mediated BRD4 expression.

Role of bone morphogenetic proteins in form-deprivation myopia sclera.

PURPOSE: To clarify the role of bone morphogenetic proteins (BMP-2,-4,-5) in sclera remodeling during myopia induction and their effect on sclera fibroblasts in cell culture. METHODS: Reverse transcription and polymerase chain reaction (RT-PCR) as well as immunofluorescence were used to detect the expression of the BMPs in human and guinea pig posterior sclera. In guinea pig form-deprivation myopia (FDM) model, RT-PCR and western blotting were used to investigate changes of BMP expression in the posterior sclera. Human sclera fibroblast (HSF) was primarlly cultured and treated with various doses of BMP-2. Cell proliferation was evaluated by the MTT assay. RT-PCR and western-blot were used to determine the changes of collagen I, aggrecan, and possible activated signal pathway. Cell phenotype and activated signal pathway, especially for α-smooth muscle actin (α-SMA) and phospho-smad1/5/8 were then further investigated by cytoimmunofluorescence staining. RESULTS: Both human and guinea pig sclera express BMP-2, -4, and -5. In FDM eyes, BMP-2 and BMP-5 expression were reduced in the posterior sclera. Cell proliferation increased significantly (p<0.05) and more cells differentiated into myofibroblast when incubated with 100 ng/ml BMP-2 . The expressions of collangen I, aggrecan, and phospho-smad1/5/8 significantly increased (p<0.05 respectively) as well. CONCLUSIONS: Various BMPs were expressed in human and guinea pig sclera. In the posterior sclera, the expressions of BMP-2 and BMP-5 decreased in FDM eyes. BMP-2 might be able to promote HSF proliferation and differentiation, as well as to help extracellular matrix synthesis potentially through classical Smad pathway.

Soluble uric acid induces inflammation via TLR4/NLRP3 pathway in intestinal epithelial cells.

OBJECTIVES: Hyperuricemia is a risk for cardiovascular and metabolic diseases, but the mechanism is ambiguous. Increased intestinal permeability is correlated with metabolic syndrome risk factors. Intestinal epithelial cells play a pivotal role in maintaining intestinal permeability. Uric acid is directly eliminated into intestinal lumen, however, the mechanism and effect of uric acid on intestinal epithelial cells is poorly explored. Here we carried out an analysis to identify the effect and mechanism of uric acid on intestinal epithelial cells. MATERIALS AND METHODS: IEC-6 was exposed to different concentrations of uric acid to simulate the effect of uric acid on intestinal epithelial cells. Cell viability was determined by MTS assay. Protein content and mRNA were assessed using Western blotting and Q-PCR, respectively. Intracellular ROS was determined using flow-cytometry and fluorescence microscopy. Mitochondrial membrane potential was detected by immunofluorescence using a mitochondrial membrane potential assay kit with JC-1. Small interfering RNA transfection was used to suppress the expression of TLR4. RESULTS: We found soluble uric acid alone increased the release of ROS, depolarized the mitochondrial membrane potential, up-regulated TSPO, increased the expression of TLR4 and NLRP3, and then activated NLRP3 inflammasome and NF-κB signaling, which further resulted in lower expression of tight junction protein and exerted adverse effects on intestinal epithelial cells. Furthermore, the elevated IL-1ß could be restored by silencing of TLR4, indicating soluble uric acid induces inflammation via the TLR4/NLRP3 pathway. CONCLUSION: Soluble uric acid exerted detrimental effect on intestinal epithelial cells through the TLR4/NLRP3 pathway.

Association of Hyperuricemia With Immune Disorders and Intestinal Barrier Dysfunction.

BACKGROUND: More than 30-40% of uric acid is excreted via the intestine, and the dysfunction of intestinal epithelium disrupts uric acid excretion. The involvement of gut microbiota in hyperuricemia has been reported in previous studies, but the changes and mechanisms of intestinal immunity in hyperuricemia are still unknown. METHODS: This study developed a urate oxidase (Uox)-knockout (Uox-/-) mouse model for hyperuricemia using CRISPR/Cas9 technology. The lipometabolism was assessed by measuring changes in biochemical indicators. Furthermore, 4-kDa fluorescein isothiocyanate-labeled dextran was used to assess gut barrier function. Also, 16S rRNA sequencing was performed to examine the changes in gut microbiota in mouse feces. RNA sequencing, Western blot, Q-PCR, ELISA, and immunohistochemical analysis were used for measuring gene transcription, the number of immune cells, and the levels of cytokines in intestinal tissues, serum, kidney, liver, pancreas, and vascellum. RESULTS: This study showed that the abundance of inflammation-related microbiota increased in hyperuricemic mice. The microbial pattern recognition-associated Toll-like receptor pathway and inflammation-associated TNF and NF-kappa B signaling pathways were significantly enriched. The increased abundance of inflammation-related microbiota resulted in immune disorders and intestinal barrier dysfunction by upregulating TLR2/4/5 and promoting the release of IL-1ß and TNF-α. The levels of epithelial tight junction proteins occludin and claudin-1 decreased. The expression of the pro-apoptotic gene Bax increased. The levels of LPS and TNF-α in systemic circulation increased in hyperuricemic mice. A positive correlation was observed between the increase in intestinal permeability and serum levels of uric acid. CONCLUSION: Hyperuricemia was characterized by dysregulated intestinal immunity, compromised intestinal barrier, and systemic inflammation. These findings might serve as a basis for future novel therapeutic interventions for hyperuricemia.

The altered gut microbiota of high-purine-induced hyperuricemia rats and its correlation with hyperuricemia.

Some studies on the hyperuricemia (HUA) have focused on intestinal bacteria. To better understand the correlation between gut microbiota and HUA, we established a HUA rat model with high-purine diet, and used 16S rRNA genes sequencing to analyze gut microbiota changes in HUA rats. To analyze the potential role played by gut microbiota in HUA, we altered the gut microbiota of HUA rats with antibiotics, and compared the degree of uric acid elevation between HUA and antibiotic-fed HUA rats (Ab+HUA). Finally, we established a recipient rat model, in which we transplanted fecal microbiota of HUA and normal rats into recipient rats. Three weeks later, we compared the uric acid content of recipient rats. As a result, the diversity and abundance of the gut microbiota had changed in HUA rats. The Ab-fed HUA rats had significantly lower uric acid content compared to the HUA rats, and gut microbiota from HUA rats increased uric acid content of recipient rats. The genera Vallitalea, Christensenella and Insolitispirillum may associate with HUA. Our findings highlight the association between gut microbiota and HUA, and the potential role played by gut microbiota in HUA. We hope that this finding will promote the isolation and culture of HUA-related bacteria and orient HUA-related studies from being correlational to mechanistic. These steps will therefore make it possible for us to treat HUA using gut microbiota as the target.

Construction of physical-crosslink chitosan/PVA double-network hydrogel with surface mineralization for bone repair.

Weak mechanical properties, lack biocompatibility and relatively bioinert are formidable obstruct in application of bone repair materials. Multifunctional composite materials have been considered as a viable solution to this problem. Here, a new double network (DN) hydrogel was constructed by physical cross-linking of medical grade poly (vinyl alcohol) (PVA) and chitosan in KOH/urea dissolution system. The obtained hydrogel demonstrated excellent tensile strength (0.24 MPa), elongation at break (286%), and high compressive strength (0.11 MPa on the strain of 60%). Our studies showed that the prepared hydrogel had excellent biocompatibility in vitro and the introduction of hydroxyapatite (HAp) by surface mineralization imparted hydrogel the ability to induce rat bone marrow stem cells (rBMSCs) differentiation. The in vivo experiments revealed that the surface mineralized double network hydrogel significantly accelerated simultaneous regeneration of bone defects in a rabbit bone defect model. All the results indicated that this hydrogel has the potential as a bone repair material.

Fabrication of hydroxyapatite/hydrophilic graphene composites and their modulation to cell behavior toward bone reconstruction engineering.

Cell adhesion was the first step of bone reconstruction. While hydroxyapatite (HA)/graphene composites had been utilized for improving the cell adhesion and bone osteogenesis, the impact of cell adhesion and HA/graphene composites, especially HA/hydrophilic graphene (HG) composites, on internal interaction force and external surface properties remained poorly understood. Here, higher stability HA/HG composites were synthesized without extra ion introduction with in situ self-assembling method. And with XRD, FT-IR, XPS and Raman analyses, the evidences of the formation of HA and the introduction of HG was clear. TEM and SEM images showed the net-like spatial structure due to the internal interaction force between HA and HG, which provided the strain stimulation for cell adhesion. Subsequently, the external surface properties of HA/HG composites demonstrated that the roughness and hydrophilic ability of HA/HG composites could be artificially regulated by increasing the content of HG. Besides, the cell proliferation rate of HA/HG composites had been investigated. Compared to the intrinsic HA, HA/5%HG possessed the higher cell proliferation rate (264.81%) and promoted the spreading and growth of MC3T3-E1 cells. Finally, the regulation mechanism between HA/HG and cell adhesion were illuminated in detail. The excellent regular behavior of HA/HG composites for cell adhesion made them promising candidates for bone reconstruction and repairing. The present work provided the reference for the design of modifiable biomaterials and offered much inspiration for the future research of bone reconstruction engineering.

Cost-benefit analysis of enhanced recovery after hepatectomy in Chinese Han population.

BACKGROUND: Enhanced recovery after surgery (ERAS) programs have been proved effective for enhancing the clinical healing rate and reducing hospitalization cost in most countries of the world. It's a multi-model approach that designed to optimize perioperative pathway, attenuate the surgical stress response, and decrease postoperative complications. OBJECTIVE: The economic benefit from the application of ERAS to colorectal surgery has been demonstrated in China. However, such economic benefit of ERAS programs for hepatectomy hasn't been clarified yet. This study was carried out to explore the clinical efficacy and cost effectiveness of ERAS in Chinese Han population after hepatectomy. METHODS: ERAS program was implemented in our department for hepatectomy in December 2016. In total, 79 consecutive patients after hepatectomy were chosen as ERAS group (ERAS protocol) in coming half year while 121 consecutive patients after hepatectomy were chosen as Pre-ERAS group (traditional protocol) in past half year. The operation time, intraoperative blood loss, length of hospital stay (LOS), complication, readmission, and hospitalization cost of 2 groups were compared. RESULTS: The LOS of ERAS group was 5.81 ±â€Š1.79 days, significantly shorter than that of Pre-ERAS group (8.06 ±â€Š3.40 d) (P = .000). The operation time was 168.03 ±â€Š46.20 minutes for ERAS group and 175.41 ±â€Š64.64 minutes for Pre-ERAS group respectively (P = .417). The intraoperative blood loss was 166.58 ±â€Š194.13 mL (ERAS group) and 205.45 ±â€Š279.63 mL (Pre-ERAS group) (P = .293). It should be noted that the hospitalization cost of ERAS group was 51556.18 ±â€Š8926.05 Yuan (7835.05 ±â€Š1355.45 US dollars), significantly less than that of Pre-ERAS group 60554.66 ±â€Š15615.31 Yuan (9202.56 ±â€Š2371.24 US dollars) (P = .000). The application of ERAS effectively saved 8998.48 Yuan (1367.51 US dollars) for each patient. CONCLUSIONS: ERAS implementation for hepatectomy surgery is safe and feasible for Chinese Han population. It eventually enhanced the clinical healing rate. The benefits from such programs include a reduction of the LOS, complication, and readmission rates. So each patient has access to better medical service. It effectively relieved the financial burden of patients. The benefits from such programs include a reduction of the hospitalization cost, especially in medication cost. So each patient can afford the diseases.

An Intron Variant of SLC2A9 Increases the Risk for Type 2 Diabetes Mellitus Complicated with Hyperuricemia in Chinese Male Population.

BACKGROUND: The aim of this study was to explore the associations of haplotypes of the glucose transporter 9 (SLC2A9) genes with type 2 diabetes mellitus (T2DM) complicated with hyperuricemia (HUA). METHODS: Overall, 608 Chinese males, enrolled from the Affiliated Hospital of Medical College of Qingdao University in 2009-2012, were genotyped. The subjects included 167 withT2DM (average age of onset (58.07±11.82 yr), 198 with HUA subjects (average age of onset (39.20±9.73) yr), 115 with T2DM complicated with HUA (average age of onset (51.24±10.09) yr), and 128 control subjects (average age (41.92±10.01) yr). Patients genotypes of the SNPs; including rs734553 was determined by PCR method. Each genotype was regressed assuming the co-dominant, dominant and the recessive models of inheritance with covariates of duration of total glucose, uric acid, urea nitrogen, triglyceride, cholesterol, and creatinine levels. RESULTS: Chi-square test revealed that rs734553polymorphism was both significantly associated with HUA as well as T2DM complicated HUA, but not with pure T2DM. After adjustment for age and gender, analysis showed that people with C allele had higher risk of HUA and T2DM complicated HUA than those without C allele. And none of the subjects had the homozygous genotype for SLC2A9 (CC). CONCLUSION: The SLC2A9 mutation increases the risk for T2DM complicated HUA in Chinese population, which suggested that intron variants between two relatively conserved exons could also be associated with diseases. In patients of T2DM complicated with HUA, the diagnosis and detection of SLC2A9 gene variants should be caused enough attention.

The characteristics of expansins in wheat coleoptiles and their responses to water stress.

As the key regulators of cell wall extension during plant growth, expansins play an important role in regulating the development and response of plants to adverse environment. The characteristics of expansins in wheat coleoptiles and their responses to water stress were studied. Expansin proteins were extracted from wheat coleoptiles by the methods of Hepes or SDS. The activities of expansins were measured with an improved extensometer and the amount of expansins was measured by immunoblot analysis with the expansin antibody. The results showed that in coleoptiles, the extension of native cell walls depended on acidic pH, and the expansins were found to be located at cell walls by location analysis. Expansins from wheat coleoptiles could induce cell wall extension both of cucumber hypocotyls and coleoptiles, and vice versa, albeit with differences noted in extension activity. The changes in activity and abundance of expansins in wheat coleoptiles in response to water stress suggest that expansins may play a significant role in the tolerance of wheat plants to water stress.

Association of an Exon SNP of SLC2A9 Gene with Hyperuricemia Complicated with Type 2 Diabetes Mellitus in the Chinese Male Han Population.

Several recent genome-wide association studies and following studies have identified that genetic variants of SLC2A9 are associated with hyperuricemia (HUA) and diabetes mellitus (DM). Here, we set to investigate whether the exon 9 of SLC2A9 gene variations is associated with HUA complicated with Type 2 DM (T2DM) in the Chinese male Han population. The present study was designed to study rs2280205 polymorphism in exon 9 of SLC2A9 in 232 Chinese male subjects. Rs2280205 locus was genotyped in 52 T2DM subjects, 65 HUA subjects, 55 subjects with HUA complicated with T2DM, as well as 60 control subjects in this study. DNA from peripheral blood was purified and amplified by polymerase chain reaction (PCR). The PCR products were then digested by restriction enzyme MSPI, and part of PCR products was sequenced and analyzed. There was no significant difference in the levels of cholesterol, creatinine, and urea nitrogen between the Control Group and the HUA group. There was also no significant difference in levels of cholesterol between the DM group and Control Group. No significant difference in cholesterol and uric acid was observed between the HUA group and the HUA accompanied with DM group (P > 0.05). However, there was no statistical significance in the genotype frequency in these groups (P > 0.01). Results of the present study suggest that the exon 9 of SLC2A9 gene 109C/T polymorphism is not associated with HUA and diabetes in population living in the coastal area of Shandong province, China.

Study on the diversity of Bacteroides and Clostridium in patients with primary gout.

To analyze the diversity of both Bacteroides and Clostridium in patients with primary gout and the difference from that of normal individuals. And to investigate the relationship between the primary gout and the intestinal flora. Fecal samples of 90 cases with the primary gout and 94 cases normal comparison group were selected, together with the cases that match the filter criteria. The DNA is extracted from the feces. 16S rRNA specific primers of both Bacteroides and Clostridium were adopted for the PCR amplification. The molecular fingerprints of Bacteroides and Clostridium in both the primary gout group and the normal control group were obtained through DGGE and subjected for further analysis on both the diversity and the similarity. Compared with normal individuals, the number of bands and Shannon-Weaver (H') of Bacteroides in patients with primary gout was not reduced, but significantly decreased in Clostridium. Furthermore, the intra-group and inter-group similarity of both Bacteroides and Clostridium were lower. The primary gout has caused the structural change of both Bacteroides and Clostridium, inducing the low similarity, especially for Clostridium. It has statistic significance. The gut predominant flora may play an important role in the development of primary gout.