Objective To investigate the risk factors of aneurysmal subarachnoid hemorrhage (aneuryismal sub?arachnoid hemorrhage, aSAH) vasospasm (cerebral vasospasm, CVS) and provide the basis for the clinical prevention and treatment of CVS. Methods A retrospective analysis of clinical data was conducted on 255 cases aSAH patients receiving treatment between March 2012 and March 2014 in First Affiliated Hospital of Xinjiang Medical University Department of Neurosurgery, s treated. The clinical data included admission age, gender, ethnicity, history of hypertension, smoking his?tory, arterial tumor site, improved Fisher grading, admission Hunt-Hess grade, the dosage of Nimodipine, dehydrating agent, white blood cell count, blood glucose, blood lipids, blood calcium levels, platelet count. Univariate analysis and multivariate Logistic retrospective analysis were used to analyze the association between above-mentioned factors and the occurrence of CVS. Results A total of 73 cases developed CVS after aSAH and incidence rate of CVS was 28.6%. Uni?variate analysis showed that there were significant differences between patients with and without CVS in history of hyper? tension, smoking history, improved Fisher grade, admission Hunt-Hess grade, small doses of nimodipine, white blood cell count and blood glucose (P<0.05). The Logistic regression analysis showed that the history of hypertension, smoking history, improved Fisher grade, admission Hunt-Hess grade, a small dose of Nimodipine and white blood cell count were risk factors of CVS after aSAH (P<0.05). Conclusions the History of hypertension, smoking history, improved high Fish?er grade, high admission Hunt-Hess grade are independent risk factors of CVS after aSAH. A small dose of Nimodipine is a protective factor while increase in white blood cell count is a risk predictor, which should be controlled by enhancing clinical prevention.

Objective To identify Anaplasma species circulating among livestock and rodents from Xitianmu Mountain area in Zhejiang province , Southeastern China and to analyze variations regarding to their 16S rRNA gene.Methods Samples of spleen, liver and blood were collected to extract DNAs .The 16S rRNA gene fragments of Anaplasma species were amplified by using a nested PCR and then sequenced .Ho-mology analysis was conducted by using BLAST program .The multiple sequence alignment and phylogenetic analyses comparing with the sequences of other Anaplasma species in GenBank were conducted by using MEGA 5.0 software.Results The 16S rRNA gene fragments of Anaplasma were detected in 1 cattle, 8 goats, 5 Rattus confucianus, 1 Apodemus agrarius, 1 Berylmys bowersi and 1 squirrel out of 129 animals. The natural infection rate of Anaplasma was 13.2% in animals from Xitianmu Mountain area in Zhejiang . The alignment and phylogenetic analyses indicated that there were at least four Anaplasma species prevalent in livestock and rodents from Xitianmu Mountain area , including Anaplasma phagocytophilum, Anaplasma marginale, Anaplasma centrale and Anaplasma bovis.Moreover, there was a variant that obviously differed from Anaplasmma bovis and other Anaplasma sp.in GenBank.Conclusion The Anaplasma infection was detected among livestock and rodents from Xitianmu Mountain area in Zhejiang province .A newly discovered variant in rodents was likely to be a novel species .More close attention should be paid to Anaplasma infec-tion among human in Xitianmu Mountain area .

Objective:]To investigate the role of Arpin protein in bone repair by mediating migration of host bone marrow mesenchymal stem cells (BMSCs) to the bone defect area after transplantation of tissue engineering bone (TEB).Methods:Immunofluorescence was used to observe the expression and relative localization of Arpin and Arp2/3 proteins in BMSCs. Lentiviruses that ware designed to interfere with Arpin expression were constructed to transfect BMSCs for knockdown Arpin expression. Knockdown efficiency was verified by real-time quantitative reverse transcription PCR ( qRT-PCR) and Western blot. According to different levels of Arpin protein expression, experiments were divided into empty vector control group and an Arpin expression inhibition group in vitro and in vivo. In vitro experiments: the cell migration model was established with a migration chamber, then the cells from both groups were seeded on the up chamber, and the number of migrated cells were detected by fluorescence microscopy. Cells from both groups were seeded on six-well plates. Model of wound healing experiment was established and wound healing ratio was examined by microscopy. In vivo experiments: 8-week-old C57BL/6 mice were selected and assigned to empty vector control group and Arpin expression inhibition group according to the random number table, with 6 rats per group. Diaphysis of 2 mm and periosteum in the middle femur were excised to make a large segment of bone defects. Then, TEB was transplanted into the defect area and fixed.Green fluorescein-labeled BMSCs (1 million cells per mouse) from empty vector control group and Arpin expression inhibition group were injected through the tail vein. Number of BMSCs homing to the bone defect area was detected by immunofluorescence staining at day 2 and 7 after operation. At 4 weeks after operation, the femur was taken for a Micro-CT scan to analyze bone mass density(BMD), bone volume density (BV/TV), trabecular spacing (Tb.Sp) and trabecular thickness (Tb.Th). Then, the specimens were stained with pathological HE and MASSON staining to observe the quality of bone formation. Results:Mouse BMSCs expressed Arpin protein, which was located at the cell edge relative to Arp2/3. After transfection of lentivirus, BMSCs expressed green fluorescent protein, and the expression of Arpin gene and protein in Arpin expression inhibition group were decreased compared to empty vector control group ( P<0. 01). BMSCs migration was enhanced in Arpin expression inhibition group compared to empty vector control group [(76.6±6.6) vs. (105.7±6.5)] ( P<0. 01). Wound healing was accelerated in Arpin expression inhibition group compared to empty vector control group [(43.8±0.19)% vs. (62.6±3.2)%]( P<0.01). At day 2 after operation, immunofluorescence results showed no significant difference in cell migration between the two groups and almost no labeled cells migrated. At day 7 after operation, more cells migrated to the transplanted area in Arpin expression inhibition group compared to empty vector control group [(5.7±1.5) vs. (11.3±1.5)] ( P<0.01). At 4 weeks after operation, Micro-CT results showed that Arpin expression inhibition group had better bone formation quality than empty vector control group [BMD: (172.7±6.0)mg/cm 3vs. (140.0±6.0)mg/cm 3, BV/TV: (28.8±1.3)% vs. (23.4±0.9)%, Tb.Sp: (0.33±0.01)μm vs. (0.28±0.01)μm, Tb.Th: (0.11±0.01)μm vs.(0.15±0. 01)μm]( P<0.05). Pathological staining showed there were more new bone tissue in Arpin expression inhibition group ( P<0.01). Conclusion:Silencing Arpin protein expression promotes BMSCs to migrate to the bone defect area and improves bone repair effect.

Iron is an essential element for living organisms that plays critical roles in the process of bacterial growth and metabolism. However, it remains to be elucidated whether piuB encoding iron-uptake factor is involved in iron uptake and pathogenicity of Xanthomonas axonopodis pv. glycines (Xag). To investigate the function of piuB, we firstly generated a piuB deletion mutant (ΔpiuB) by homologous recombination. Compared with the wild-type, the piuB mutant exhibited significantly reduced growth and virulence in host soybean. The mutant displayed markedly increased siderophore secretory volume, and its sensitivity to Fe³⁺, Cu²⁺, Zn²⁺ and Mn²⁺ was significantly enhanced. Additionally, the H₂O₂ resistance, exopolysaccharide yield, biofilm formation, and cell mobility of ΔpiuB were significantly diminished compared to that of the wild-type. The addition of exogenous Fe³⁺ cannot effectively restore the above characteristics of ΔpiuB. However, expressing piuB in trans rescued the properties lost by ΔpiuB to the levels in the wild-type. Taken together, our results demonstrated that PiuB is a potential factor for Xag to assimilate Fe³⁺, and is necessary for Xag to be pathogenic in host soybean.
Iron ; Glycine max ; Virulence ; Xanthomonas axonopodis/genetics* ; Hydrogen Peroxide