Background: Eighteen out of 45 children were reported with respiratory illness during an outbreak at a temporary dormitory in a nursery school in China in 2011. To study the outbreak and to determine the risk factors for infection, an epidemiological investigation was performed.Methods: A total of 45 children under the help of the guardians and parents completed a standardized questionnaire. In addition, they were asked to supply acute and convalescent serum sample and throat swab for laboratory diagnosis. A Mycoplasma-like case based on the following clinical criteria: an illness onset after 31 May 2011, characterized by a cough, fever(>37.5°C), or at least 3 of the following symptoms: fever, sore throat, cough or expectoration, runny or stuffy nose. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP), minimal inhibitory concentrations and sequencing were performed to determine the genotype, antibiotic resistance and sequence polymorphisms of the isolated strains, respectively.Results: The paired sera revealed that 15 patients were infected with Mycoplasma pneumoniae. Epidemiology confirmed that this was a point-source outbreak, characterized by a short incubation period, a high secondary attack rate and a long period of hospitalization. PCR-RFLP analysis revealed that the 12 isolated strains of M. pneumoniae shared the same subtype P1 gene, and 23S rRNA sequence analysis showed that these strains harbored two macrolide-resistant gene related point mutations at position 2063 and 2617.Discussion: In this outbreak, the major risk factor was the distance between the first patient's bed and the beds of close contacts less than three meters. The strains isolated in this study were found to harbor two point mutations conferring macrolide resistance indicating the importance of pathogen and drug resistance surveillance systems.

Autism spectrum disorders (ASD) are heterogeneous neurodevelopmental disorders that are characterized by deficits in social interaction, verbal and nonverbal communication, and restrictive interests and repetitive behaviors. While human genetic studies have revealed marked heritability in ASD, it has been challenging to translate this genetic risk into a biological mechanism that influences brain development relevant to the disorder phenotypes. This is partly due to the complex genetic architecture of ASD, which involves de novo gene mutations, genomic abnormalities, and common genetic variants. Rather than trying to reconstitute the clinical disorder, using genetic model animals to examine specific features of core ASD pathophysiology offers unique opportunities for refining our understanding of neurodevelopmental mechanisms in ASD. A variety of ASD-relevant phenotypes can now be investigated in rodents, including stereotyped and repetitive behaviors, and deficits in social interaction and communication. In this review, we focus on several prevailing mouse models and discuss how studies have advanced our understanding of synaptic mechanisms that may underlie ASD pathophysiology. Although synaptic perturbations are not the only alterations relevant for ASD, we reason that understanding the synaptic underpinnings of ASD using mouse models may provide mechanistic insights into its etiology and lead to novel therapeutic and interventional strategies.

We report an atypical enteropathogenic Escherichia coli O127a:K63 with resistance to quinolones and third-generation cephalosporins isolated from a 2010 food poisoning outbreak involving 112 adults in China. Two resistance genes (bla(CTX-M-15), aac(6')-Ib-c) and five mutations (two in gyrA, two in parC, one in parE) coexisted in this enteropathogenic E. coli.

Two chiral sulfur compounds, tert-butyl tert-butanethiosulfinate (1) and tert-butanesulfinamide (2), with inversion of configuration, have been studied by Raman optical activity (ROA) and electronic circular dichroism combined with density functional theory calculation. With the S-S linkage in 1, the couplings between the two tertiary carbon atoms often generate large ROA signals, whereas the tertiary carbon atom itself generally makes a large contribution to ROA signals in 2 for similar vibrational modes. The conformational dependence of ROA parameters provides probing conformation around the S-S bond from a new perspective. The simultaneous use of electronic circular dichroism and ROA is warranted to extract reliable conformational information. ROA provides a suitable candidate for the stereochemical study of chiral sulfur compounds, especially its capability of sensing the conformation around the S-S bond. Chirality 00:000-000, 2012. © 2012 Wiley Periodicals, Inc.

The ability to induce apoptosis is the most important tumor-suppression function of p53. Inhibitory member of apoptosis-stimulating protein of p53 family (iASPP) is an apoptotic-specific regulator of p53. iASPP suppresses apoptosis by inhibiting the transactivation function of p53 on the promoters of proapoptotic genes; however, the mechanism whereby iASPP influences apoptosis in tumor cells with mutant or deficient p53 has not been completely defined. In this study, we investigated the role of iASPP in the p63/p73 apoptosis pathway. iASPP inhibited apoptosis independently of p53 in tumor cells, mainly by inhibiting the transcriptional activity of p63/p73 on the promoters of proapoptotic genes. Because p63 and p73 are rarely mutated in human cancers, inhibiting the expression of endogenous iASPP may provide a useful strategy for restoring the apoptotic activity of p63 and p73 in human tumors with p53 loss or mutation. These results represent a promising new strategy for the treatment of cancers with non-wild-type p53.

After androgen ablation therapy (AAT), advanced prostate cancer (Pca) eventually progresses to castration-resistant Pca (CRPC); however, the biomarkers that are used to predict its prognosis are limited. In this study, serum samples from four patients with advanced Pca were collected at the time of the initial diagnosis and 3 months after AAT. Proteomic changes were analyzed with two-dimensional differential in-gel electrophoresis and matrix-assisted laser desorption/ionization time-of-flight mass spectrometry. Altogether, nine proteins were differentially expressed in the samples collected at diagnosis and in the samples collected after AAT. Among them, the expression of transthyretin (TTR) was 1.58-fold lower and clusterin (CLU) was 1.51-fold higher in the sera of post-AAT patients compared with those in the sera from pre-AAT patients. The significant changes in serum TTR and CLU in post-AAT patients were further confirmed by a large-scale ELISA. Immunohistochemistical staining revealed that the expression levels of TTR and CLU were significantly higher in Pca tissue than in normal and benign prostate hyperplasia tissue. The expression levels of TTR and CLU in Pca tissue were found to be associated with the grade and stage of Pca. Overall, this study indicated that TTR and CLU might be used to monitor the efficacy of AAT therapy and serve as biomarkers for the prognosis of Pca.

ABSTRACT: The authors would like to retract the article "Screening and Identification of a Renal Carcinoma Specific Peptide from a Phage Display Peptide Library". After the article was published it was revealed that the data in figure three, reported to show the Immunohistochemical staining of renal carcinoma, actually shows the results from an unrelated experiment on lung tissue due to incorrect labeling. The authors apologize to the readers, reviewers, and editors for publishing this erroneous data.

ABSTRACT BACKGROUND:Cysteinyl leukotriene 1 (CysLT(1)) receptor expression is known to be increased in the airway mucosa of asthmatics especially during exacerbations however nothing is known of its expression in chronic obstructive pulmonary disease (COPD). METHODS:We applied immunohistochemistry and in situ hybridization to endobronchial biopsies to determine inflammatory cell CysLT(1) receptor protein and mRNA expression in:(i) 15 non-smoker controls (NSC),(ii) 16 smokers with moderate/severe COPD in its stable phase (S-COPD) and (iii) 15 with COPD hospitalised for a severe exacerbation (SE-COPD). RESULTS:The total number of (CD45+) bronchial mucosal inflammatory cells and those expressing CysLT(1) receptor protein were significantly greater in SE-COPD [CysLT(1) receptor protein: median (range)= 139 (31-634)] as compared with S-COPD [32 (6-114)] or NSC [16 (4-66)](P< 0.001 for both). CysLT(1) receptor gene expression showed similar differences. A greater proportion of CD45+ cells expressed CysLT(1) receptor protein in SE-COPD [median (range)= 22%(8-81)] compared to S-COPD [10%(4-32)] P < 0.03) or NSC [7%(1-19)](P < 0.002). In SE-COPD the relative frequencies of CysLT(1) receptor expressing cells were: tryptase+ mast cells > CD68+ monocytes/macrophage > neutrophils > CD20+ B-lymphocytes = EG2+ eosinophils. Moreover, there were positive correlations between the numbers of cells expressing CysLT(1) receptor protein and the numbers of CD45+ cells (r = 0.78; P < 0.003) and tryptase+ mast cells (r = 0.62; P < 0.02). CONCLUSIONS:Bronchial mucosal CysLT(1) receptor positive inflammatory cells are present in the bronchial mucosa in COPD in greatest number in those experiencing a severe exacerbation.

We report here on the first identification of Shigella flexneri subserotype 1c in China. We also report the emergence of resistance to ciprofloxacin and third-generation cephalosporins in this subserotype 1c for the first time. Isolates of seven strains circulating in China yielded three new sequence types and seven pulsed-field gel electrophoresis patterns, thus demonstrating the existence of high genetic diversity within the isolates. Overall, the seven isolates showed reduced susceptibility to ciprofloxacin; one isolate was ciprofloxacin resistant, whilst another developed resistance to ciprofloxacin, norfloxacin, cefotaxime and ceftriaxone.

Induced pluripotent stem cells (iPSCs) have the potential to revolutionise cell therapy; however, it remains unclear whether iPSCs can be generated from human osteoarthritic chondrocytes (OCs) and subsequently induced to differentiate into chondrocytes. In the present study, we investigated the differentiation potential of OCs into iPSCs using defined transcription factors and explored the possibility of using these OC-derived iPSCs for chondrogenesis. Our study demonstrates that iPSCs can be generated from OCs and that these iPSCs are indistinguishable from human embryonic stem cells (hESCs). To promote chondrogenic differentiation, we used lentivirus to transduce iPSCs seeded in alginate matrix with transforming growth factor-β1 (TGF-β1) and then in vitro co-cultured these iPSCs with chondrocytes. Gene expression analysis showed that this combinational strategy promotes the differentiation of the established iPSCs into chondrocytes in alginate matrix. Increased expression of cartilage-related genes, including collagen II, aggrecan, and cartilage oligomeric matrix protein (COMP), and decreased gene expression of the degenerative cartilage marker, vascular endothelial growth factor (VEGF), were observed. The histological results revealed a dense sulphated extracellular matrix in the co-culture of TGF-β1-transfected iPSCs with chondrocytes in alginate matrix. Additionally, in vivo chondroinductive activity was also evaluated. Histological examination revealed that more new cartilage was formed in the co-culture of TGF-β1-transfected iPSCs with chondrocytes in alginate matrix. Taken together, our data indicate that iPSCs can be generated from OCs by defined factors and the combinational strategy results in significantly improved chondrogenesis of OC-derived iPSCs. This work adds to our understanding of potential solutions to osteoarthritic cell replacement problem.