Phylogenetic and molecular characterization of coxsackievirus A24 variant isolates from a 2010 acute hemorrhagic conjunctivitis outbreak in Guangdong, China

<p>Abstract</p> <p>Background</p> <p>Acute hemorrhagic conjunctivitis is a common disease in China. As a notifiable disease, cases are registered by ophthalmologists on the AHC surveillance system. An AHC outbreak caused by CA24v was observed in Guangdong Province in 2007 by the National Disease Supervision Information Management System. Three years later, a larger outbreak occurred in Guangdong during the August-October period (2010). To characterize the outbreak and compare the genetic diversity of CA24v, which was determined to be the cause of the outbreak, the epidemiology and the molecular characterization of CA24v were analyzed in this study.</p> <p>Results</p> <p>A total of 69,635 cases were reported in the outbreak. 73.5% of index cases originated from students, children in kindergarten and factory workers, with the ≦ 9 age group at the highest risk. The male to female ratio was 1.84:1 among 0-19 years. 56 conjunctival swabs were collected to identify the causative agent from five cities with the AHC outbreak. 30 virus strains were isolated, and two of the genomes had the highest identity values (95.8%) with CA24v genomes. Four CA24v genotypes were identified by phylogenetic analysis for the VP1 and 3C regions. CA24v which caused the outbreak belonged to genotype IV. Furthermore, full nucleotide sequences for four representative isolates in 2010 and 2007 were determined and compared. 20 aa mutations, two nt insertions and one nt deletion were observed in the open reading frame, with 5'- and 3'- UTR respectively between them.</p> <p>Conclusions</p> <p>CA24v was determined to be the pathogen causing the outbreak and belongs to genotype IV. VP1 is more informative than 3C^Profor describing molecular epidemiology and we hypothesize that accumulative mutations may have promoted the outbreak.</p

Streptococcus suis Sequence Type 7 Outbreak, Sichuan, China

An outbreak of Streptococcus suis serotype 2 emerged in the summer of 2005 in Sichuan Province, and sporadic infections occurred in 4 additional provinces of China. In total, 99 S. suis strains were isolated and analyzed in this study: 88 isolates from human patients and 11 from diseased pigs. We defined 98 of 99 isolates as pulse type I by using pulsed-field gel electrophoresis analysis of SmaI-digested chromosomal DNA. Furthermore, multilocus sequence typing classified 97 of 98 members of the pulse type I in the same sequence type (ST), ST-7. Isolates of ST-7 were more toxic to peripheral blood mononuclear cells than ST-1 strains. S. suis ST-7, the causative agent, was a single-locus variant of ST-1 with increased virulence. These findings strongly suggest that ST-7 is an emerging, highly virulent S. suis clone that caused the largest S. suis outbreak ever described

Circulation of reassortant influenza A(H7N9) viruses in poultry and humans, Guangdong Province, China, 2013.

Influenza A(H7N9) virus emerged in eastern China in February 2013 and continues to circulate in this region, but its ecology is poorly understood. In April 2013, the Guangdong Provincial Center for Disease Control and Prevention (CDC) implemented environmental and human syndromic surveillance for the virus. Environmental samples from poultry markets in 21 city CDCs (n=8,942) and respiratory samples from persons with influenza-like illness or pneumonia (n=32,342) were tested; viruses isolated from 6 environmental samples and 16 patients were sequenced. Sequence analysis showed co-circulation of 4 influenza A(H7N9) virus strains that evolved by reassortment with avian influenza A(H9N2) viruses circulating in this region. In addition, an increase in human cases starting in late 2013 coincided with an increase in influenza A H7 virus isolates detected by environmental surveillance. Co-circulation of multiple avian influenza viruses that can infect humans highlights the need for increased surveillance of poultry and potential environmental sources.This study was financially supported by 12th five-year-major-projects of China’s Ministry of Public Health. Grant No: 2012zx10004-213 and by the PREDICT Surveillance Animal Human Interface Project of GVF. Grant No: Gvf: 06-09-057-02.This is the accepted version. It'll be replaced with the final pdf when it's available

The Function Role of miR-181a in Chemosensitivity to Adriamycin by Targeting Bcl-2 in Low-Invasive Breast Cancer Cells

Objectives: miR-181a is involved in immunity, metabolism, tumor suppression or carcinogenesis reported by many other studies. However, its role in the development of chemosensitivity to adriamycin in low-invasive breast cancer cells remains unclear. The aim of this study is to define the function role of miR-181a in promoting the efficacy of adriamycin-based neoadjuvant chemotherapy. Methods: Cell survival analysis was detected by Cell Counting Kit-8 assay. Apoptotic cells were quantitatively detected using FITC Annexin V apoptosis Detection Kit I. Bcl-2 protein expression was measured by western blot. Luciferase reporter vector with the putative BCL-2 3' untranslated region (3'UTR) was constructed to explore whether BCL-2 was a direct target gene of miR-181a. Real-time PCR was performed to test the expression of miR-181a and Bcl-2 in the selected breast cancer tissue samples. Results: The down-regulation of miR-181a decreased adriamycin-induced apoptosis in MCF-7 cells. Transfected with miR-181a mimic in cells resulted in the decreased expression of Bcl-2. The alteration of miR-181a expression did not significantly affect the chemosensitivity to adriamycin in MCF-7 and MCF-7/ADR cells with genetic knockout of Bcl-2. miR-181a may suppress Bcl-2 expression by forming imperfect base pairing with the 3'UTR of Bcl-2 gene such that a negative relationship between miR-181a and Bcl-2 in MCF-7 and MCF-7/ADR cells is observed. Conclusions: At least in part, the detection of miR-181a may direct the clinical medication in patients with neoadjuvant chemotherapy because of miR-181a enhanced adriamycin-induced apoptosis via targeting Bcl-2

Long noncoding RNA

Abstract To gain an insight into the molecular mechanisms of cetuximab resistance in colorectal cancer, we generated a cetuximab‐resistant cell line (H508/CR) and performed RNA sequencing to identify the differential expression patterns of noncoding RNAs (ncRNAs) and mRNAs between cetuximab‐sensitive and resistant cells. A total of 278 ncRNA transcripts and 1,059 mRNA transcripts were dysregulated in the cetuximab‐resistant cells. The expression levels of nine selected long noncoding RNAs (lncRNAs) were validated using quantitative real‐time PCR. Functional analysis revealed that several groups of lncRNAs might be involved in pathways associated with cetuximab resistance. Increased glucose consumption and lactate secretion in cetuximab‐resistant cells suggested that glucose metabolism might be involved in cetuximab resistance. In addition, lncRNA LINC00973 was upregulated in the H508/CR cell line and cells transfected with a LINC00973 short interfering RNA exhibited reduced cell viability, increased apoptosis, and decreased glucose consumption and lactate secretion. Our results provide essential data regarding differentially expressed lncRNAs and mRNAs in cetuximab‐resistant cells, which may provide new potential candidates for cetuximab therapy

Ion Dynamics of Water-in-Salt Electrolyte with Organic Solvents in Nanoporous Supercapacitor Electrodes

Water-in-salt electrolytes blended with organics solvents, that is, organic solvent/water mixed electrolytes, are promising for applications in next-generation energy storage devices vitally needed for industrial electrification and decarbonization. However, the electrolyte ion diffusion behaviors within nanoporous supercapacitor electrodes are poorly understood. Here a systematic investigation into supercapacitor resistances and ion kinetics is carried out experimentally and with numerical simulations. The electrochemical results on the nanoporous electrodes reveal a nonmonotonic (decreasing, increasing, and then decreasing) trend of supercapacitor resistances with increasing solvent mobility, challenging the long-held views that supercapacitor resistances decrease with elevated mobility of organic solvent. The abnormal trend is examined by numerical molecular dynamics simulations of electrolyte ion diffusion within 0.95 nm nanochannels. The electrolyte conductivity is related to cation–anion interactions within nanochannels. We further confirm the crucial interplay of the van der Waals sizes of solvent molecules and channel width in determining electrolyte conductivity in nanoporous electrodes.</p