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The aim of this study was to establish a murine model of lower genital tract infection by and and evaluate differences in pathogenicity of five serotypes. BALB/c female mice were divided into seven groups (five mice in each group), including five groups infected in the lower genital tract after treatment with estradiol with U. urealyticum serotypes 4 and 8 and U. parvum serotypes 1, 3, and 6, respectively, and two control groups of untreated mice and estradiol treated mice. The presence of infection was determined on solid and liquid culture media. Tumor necrosis factor-alpha (TNF-α) expression in lower genital tract secretions was determined by PCR, and morphological and histological changes of the lower genital tract were observed. The genital secretions of all inoculated mice were positive for U. urealyticum and U. parvum on culture in both liquid and solid media. TNF-α expression at 7 and 14 days after infection was markedly increased as compared with that of the controls. Morphological changes of the external genitalia included hair loss and erosions, and histological examination revealed infiltration by inflammatory cells. The five serotypes tested were all found to be pathogenic, and the pathogenicity varied with serotype 4 showing the greatest pathogenicity. [ABSTRACT FROM AUTHOR]

A novel actinobacterium, designated KC 17012 T , was isolated from lead zinc tailings collected from Lanping, Yunnan, PR China. Comparative 16S rRNA gene sequencing showed that KC 17012 T belonged to the genus Streptomyces and was most closely related to the type strains of Streptomyces neyagawaensis (98.34%), Streptomyces panaciradicis (98.34%) and Streptomyces heilongjiangensis (98.27%). Phylogenetic tree analysis revealed strain KC 17012 T formed a distinct clade. The genome size was 8.64 Mbp with a DNA G+C content of 70.8%. Digital DNA-DNA hybridization and average nucleotide identity values between the genome sequence of strain KC 17012 T and those of S. neyagawaensis JCM 4796 T (25.3 and 81.5 %) and S. panaciradicis NBRC 109811 T (30.1 and 85.7 %) were below the thresholds of 70 and 96% for prokaryotic conspecific assignation. The strain formed long straight aerial hyphae which generated regular short rod spores with spiny surfaces. Growth occurred at 10-45 °C, pH 6-8 and with 0-9 % NaCl (w/v). Strain KC 17012 T contained ll-diaminopimelic acid and the major whole-cell hydrolysates included glucose, mannose and ribose. The menaquinones were MK-9(H 4 ), MK-9(H 6 ) and MK-9(H 8 ). The major cellular fatty acids were iso-C 15 : 0 , anteiso-C 15 : 0 , iso-C 16 : 0 and anteiso-C 17 : 0 . The polar lipid profile consisted of diphosphatidylglycerol, phosphatidylethanolamine, phosphatidylglycerol, phosphatidylinositol, phosphatidylinositol mannoside, one unidentified lipid and one unidentified phospholipid. On the basis of the results of a polyphasic taxonomic study, it is concluded that KC 17012 T represents a novel species of the genus Streptomyces , for which the name Streptomyces plumbidurans sp. nov., is proposed. The type strain is KC 17012 T (CGMCC 4.7704 T =JCM 35204 T ).

Previous studies have demonstrated that G-protein coupled receptor kinase interacting protein-1 (GIT1) and microRNAs (miRNAs) serve an important role in chondrocyte proliferation and migration. However, a limited number of studies conducted thus far have investigated the association between GIT1 and miRNAs. In the present study, putative miR‑195 binding sites in the GIT1 3'‑untranslated region were identified using common bioinformatic algorithms (miRanda, TargetScan, miRBase and miRWalk), and it was demonstrated that they may be involved in regulating GIT1 expression. Following transfection of miR‑195 mimics in chondrocytes, the expression of GIT1 was significantly reduced, whereas the expression was significantly increased following transfection with miR‑195 inhibitors. In addition, the results of the current study demonstrated that increased miR‑195 expression may downregulate chondrocyte proliferation and reduce cell migration. However, chondrocyte proliferation and migration was enhanced following suppression of miR‑195 expression. Furthermore, upon co‑transfection of miR‑195 and GIT1 expression vectors, the inhibitory effect of miR‑195 on chondrocyte proliferation and migration was attenuated. Therefore, miR‑195 may affect chondrocyte proliferation and migration via targeted regulation of GIT1 expression. The results of the current study provide novel evidence for the regulatory mechanisms of miRNAs in bone and cartilage tissues, which may facilitate further research and provide a greater understanding of different osteoarticular diseases.

Objective: To determine factors associated with quality of life (QOL) in epileptics and the variations between men and women, younger and older people., Methods: A total of 204 patients (160 younger, 49 older; 125 men, 79 women) were interviewed by the quality of life in epilepsy-31 (QOLIE-31), side effect profile (SEP), self-rating anxiety scale (SAS) and Hamilton depression scale (HAMD). Medical and socio-demographic data were acquired from patient records. Multivariate linear regressive analyses were used to determine the set of best predictors of composite QOLIE-31 score., Results: No statistical difference was revealed in QOLIE-31 overall score either between younger and older patients or between men and women. Among all patients, regressive analyses revealed that SEP (beta = - 0.395, P = 0.000) and SAS (beta = -0.152, P = 0.016) were two strong predictors of QOLIE-31 overall score. Grouped by gender, among men, epilepsy duration (beta = -0.165, P = 0.028) and seizure frequency (beta = -0.284, P = 0.001) respectively associated with QOLIE-31 overall score and "social function" score while the number of AEDs (antiepileptic drugs) substantially correlated with QOLIE-31 overall score among women (beta= -0.238, P = 0.006). Grouped by ages, seizure frequency (beta = -0.284, P = 0.000) and education level (beta = 0.203, P = 0.005) predicted QOLIE-31 "social function" score only among younger patients; among older patients, a significant association were found between the number of AEDs and QOLIE-31 overall score (beta = - 0.363, P = 0.004)., Conclusion: Side effects of AEDs and number of AEDs exert greater effect on QOL in women and older patients. And such seizure-related variables as epileptic duration and seizure frequency influence QOL only among men and younger patients.

Objective: To observe the effect of dizocilpine (MK801), a noncompetitive antagonist of N-methyl-D-aspartic acid (NMDA) receptor, on P-glycoprotein (P-gp) expression after limbic seizure, and to explore whether NMDA receptor play a role in the regulation of P-gp expression during limbic seizure., Methods: 120 Wistar rats were randomly divided into 2 equal sets. 50 rats in Set 1 underwent intraperitoneal injection of lithium chloride, scopolamine, and pilocarpine so as to cause status epilepticus (SE) for 90 min. Then diazepam was given to terminate the SE. The rats were killed 0, 3, 6, 14, and 72 h after the SE respectively. The hippocampus was isolated. Realtime fluorescent quantitative RT-PCR (qRT-PCR) was used to detect the expression of multidrug resistance gene 1a (mdr1a) and mdr1b. Immunohistochemistry was used to detect the P-gp. The rats were used as controls. Another 60 rats (Set 2) were randomly divided into 3 equal groups: control group, given with normal saline (NS) only, SE group, given with NS 20 min before administration of pilocarpine, and MK801 group, given with MK801 20 min before administration of pilocarpine. The 3 groups in Set 2 were further divided into 2 equal subgroups of 10 rats to be killed 6 or 24 h after SE., Results: The mdr1a expression in hippocampus within 72 h after seizure was much higher at each time point: the level of mdr1a expression instantly after the seizure was terminated was [5.6 (2.9) x 10(5) mRNA copies/40 ng total RNA], significantly higher than that of the controls [2.4 (1.1) x 10(5) mRNA copies/40 ng total RNA, P < 0.05], increased to the level of [7.6 (6.3) x 10(5), P < 0.01] 3 h after, and kept at such level till 72 h after. The msr1b expression transiently increased 2.2 and 2.4 times that of the controls respectively 3 h and 6 h after the seizure was terminated [(3.3 +/- 0.4) x 10(4), and (3.6 +/- 1.0) x 10(4), both P < 0.01)]. The expression level of mdr1a 6 h after the seizure was terminated of the MK801 group was (4.3 +/- 0.8) x 10(5) and the expression level of mdr1b 6 h after the seizure was terminated of the MK801 group was (2.0 +/- 0.7) x 10(4), both significantly lower than those of the SE group (both P < 0.01). The P-gp expression level 24 h after the seizure was terminated of the MK801 group was 26.6 +/- 5.0 pieces of microvessels/400 times field, significantly lower than that of the SE group (39.0 +/- 4.1, P < 0.01)., Conclusion: MK801 down-regulates the overexpression of P-gp after seizure, which indicates that NMDA receptor may be involved in the regulation of P-gp expression during seizure. Therefore, it is possible to prevent the overexpression of P-gp after seizure by inhibiting NMDA receptor's overactivation effectively.

Objective: To detect the gene mutation of a family with piebaldism., Methods: Diagnosis of a patient with piebaldism was constructed by pathology, ultrastructural examination and typical clinical-phenotype. Detection of gene mutation was carried out by PCR and DNA sequencing., Results: G 2528A substitution transition in the KIT gene was found in the proband of the family with piebaldism. This mutation resulted in S850N substitution in protein product of KIT gene. No mutation was found in 100 normal individuals and other family members., Conclusion: The mutation of S850N maybe one cause of clinical phenotype of the family with piebaldism.

Objective: To detect gene mutation in proband and his mother from a family with piebaldism., Methods: Diagnosis of a patient with piebaldism was validated by pathology, ultrastructural examination and the typical clinical manifestation. PCR and DNA sequencing were carried out to detect gene mutation of a family with piebaldism., Results: G1833A transition in the KIT gene was found in the proband of the family with piebaldism. This mutation resulted in V604I substitution in KIT gene. No mutation was found in 100 normal individuals and other family members., Conclusion: The mutation of V604I is the cause of clinical phenotype of the family with piebaldism.