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Objectives Recently, the Gram-negative bacterium Klebsiella oxytoca has been identified as an emerging pathogen. Here we report the draft genome of a 2,3-butanediol-producing strain, K. oxytoca CCTCC M207023, isolated from soil in Nanjing, China. The tetracycline-resistant phenotype and the high yield of 2,3-butanediol was demonstrated. Methods The draft genome of K. oxytoca CCTCC M207023 was determined using an Illumina NovaSeq™ 6000 next-generation DNA sequencing platform. Clean sequencing data were subsequently assembled using SOAPdenovo. Results The draft genome of K. oxytoca CCTCC M207023, comprising 5 658 144 bp and with a GC content of 56.50%, was assembled into 5262 open-reading frames (ORFs). Antimicrobial resistance genes were also annotated. Conclusions The draft genome sequence of K. oxytoca CCTCC M207023 reported here will be a reference for comparative analysis with the antimicrobial resistance mechanisms for the safety of 2,3-butanediol industrial production.

Background: In consideration of characteristics and functions, extra-cellular signal-regulated protein kinase 5 (ERK5) signaling pathway could be a new target for spinal cord injury (SCI) treatment. Our study aimed to evaluate the roles of ERK5 signaling pathway in secondary damage of SCI. Methods: We randomly divided 70 healthy Wistar rats into five groups: ten in the blank group, 15 in the sham surgery + BIX02188 (sham + B) group, 15 in the sham surgery + dimethyl sulfoxide (DMSO; sham + D) group, 15 in the SCI + BIX02188 (SCI + B) group, and 15 in the SCI + DMSO (SCI + D) group. BIX02188 is a specific inhibitor of the ERK5 signaling pathway. SCI was induced by the application of vascular clips (with the force of 30 g) to the dura on T10 level, while rats in the sham surgery group underwent only T9-T11 laminectomy. BIX02188 or DMSO was intra-thecally injected at 1, 6, and 12 h after surgery or SCI. Spinal cord samples were taken for testing at 24 h after surgery or SCI. Results: Expression of phosphorylated-ERK5 (p-ERK5) significantly increased after SCI. Application of BIX02188 indeed inhibited ERK5 signaling pathway and reduced the degree of spinal cord tissue injury, neutrophil infiltration and proinflammatory cytokine expression, nuclear factor-κB (NF-κB) activation and apoptosis (measured by TdT-mediated 2′-deoxyuridine 5′-triphosphate nickend labeling, expression of Fas-ligand, BCL2-associated X [Bax], and B-cell lymphoma-2 [Bcl-2]). Double immunofluorescence revealed activation of ERK5 in neurons and microglia after SCI. Conclusion: ERK5 signaling pathway was activated in spinal neurons and microglia, contributing to secondary injury of SCI. Moreover, inhibition of ERK5 signaling pathway could alleviate the degree of SCI, which might be related to its regulation of infiltration of inflammatory cells and release of inflammatory cytokines, expression of NF-κB and cell apoptosis. Key words: Extracellular signal-regulated protein kinase 5; Mitogen activated protein kinase; Spinal cord injury; Nuclear factor-κB; Apoptosis

Background This study aims to explore the efficacy and safety of prostaglandina E1 (PE1) for the treatment of patients with thrombo-occlusive vasculitis (TOV). Methods Electronic databases (Cochrane Library, PUBMED, EMBASE, Web of Science, Scopus, the Allied and Complementary Medicine Database, Chinese Biomedical Literature Database, and China National Knowledge Infrastructure) will be sought from onset to the March 1, 2020 without language and publication status restrictions. We will include any potential randomized controlled trials that examined the efficacy of PE1 for the treatment of patients with TOV. We will appraise study quality using Cochrane risk of bias tool, and will assess the evidence quality using Grading of Recommendations Assessment Development and Evaluation. We will use RevMan 5.3 Software for statistical analysis. Results A high-quality synthesis of present evidence of PE1 for the treatment of patients with TOV will be provided in this study. Conclusion This study will provide evidence to judge whether PE1 is an effective intervention for TOV. Systematic review registration INPLASY202040081.

Type 2 diabetes mellitus (T2DM)[1] is a type of metabolic disease caused by metabolic disorders in the endocrine system and characterized by hyperglycemia. Insufficient insulin secretion and insulin resistance are the basic pathologic characteristics of T2DM. According to the International Diabetes Federation (IDF),[2] the prevalence of diabetes among adults aged 20–79 in 2017 was 8.8% from a total population of 425 million, which will reach 629 million by 2045. Additionally, it is estimated that approximately half of all adult patients worldwide have not been diagnosed as of 2017. In 2017, approximately 4 million adults died of diabetes, and 46.1% of patients died before reaching the age of 60 years. These data show that the number of patients with diabetes is increasing at an alarming rate and have come to represent a challenge for human health. In addition, T2DM accounts for approximately 95% of the total population of diabetes, which leads to significant losses for human and economic health.[3] T2DM is a chronic disease that can cause a series of complications that can lead to death.[4] Therefore, preventing or delaying the occurrence of complications is the main purpose of treating T2DM, and the key link for those suffering from diabetes is to maintain blood glucose levels within the normal range.[5] At present, the treatment of T2DM mainly depends on lifestyle intervention[6] (such as nutrition therapy and physical activity), oral medication[7] (such as biguanides, sulfonylureas, and α-glucoside inhibitors), injected drugs[8] (such as insulin and glucagon-like peptide-1 [7–36] amide [GLP-1] agonists), surgical treatment,[9] and complementary and alternative treatment.[10] T2DM is known as a major “Xiao-Ke disease” in ancient Chinese books. And Chinese have used herbal medicines to treat the diseases for more than 1500 years. There is a growing body of research showing that herbal medicine can effectively treat T2DM.[11–13] In this study, we reviewed the therapeutic action of herbal medicine in T2DM via anti-inflammatory and anti-oxidation characteristics, regulation of blood lipid metabolism, anti-glucose effects, and other mechanisms [Figures ​[Figures11–5]. Open in a separate window Figure 1 The anti-inflammatory effect of herbal medicine in type 2 diabetes mellitus. TNF-α: tumor necrosis factor-α; TLR4-MyD88: toll-like receptor 4-myeloid differential protein-88; IL-1β: interleukin-1β; NLRP3: NACHT, LRR, and PYD domain-containing protein 3; WMW: Wu-Mei-Wan; NF-κB: nuclear transcription factor kappa B; IκBα: inhibitor of NF-κB; COX2: cyclo-oxgenase 2; IL-8: interleukin-8; IL-6: interleukin-6.

The dysregulation of proliferation and migration of vascular smooth muscle cells (VSMCs) contributes to atherosclerosis (AS) and accumulating reports indicate the crucial role of long noncoding RNA in AS. However, the role of small nucleolar RNA host gene 12 (SNHG12) in regulating the phenotypes of VSMCs and AS remains largely unknown. Quantitative reverse-transcription polymerase chain reaction (qRT-PCR) was used to detect the expression levels of SNHG12 and miR-199a-5p in an in vivo AS model and VSMCs treated by oxidized low-density lipoprotein (ox-LDL). The proliferation ability, migration ability, and apoptosis of VSMCs were tested by cell counting kit-8, Transwell assay, and terminal deoxynucleotidyl transferase dUTP nick end labeling assay, respectively. StarBase database was used to predict the binding sites between miR-199a-5p and SNHG12. The interaction between miR-199a-5p and SNHG12 was validated by qRT-PCR, western blot, and luciferase reporter assay. Western blot was used to examine the effects of SNHG12 and miR-199a-5p on the expression of hypoxia-inducible factor 1α (HIF-1α). We found that the expression level of SNHG12 was significantly increased in the animal model and VSMCs treated by ox-LDL. Knockdown of SNHG12 suppressed the proliferation and migration abilities of VSMCs, while overexpression of SNHG12 had the opposite effects. Mechanically, we validated that miR-199a-5p was a target of SNHG12, and the target gene of miR-199a-5p, HIF-1α could be indirectly and positively regulated by SNHG12. In conclusion, SHNG12 targeting miR-199a-5p/HIF-1α contributed to the pathophysiological process of AS by regulating the phenotypes of VSMCs, and could be a potential therapy target for this disease.

// Yue-Lun Zhang 1, 2 , Jin-Qiu Yuan 1, 2 , Kai-Feng Wang 3 , Xiao-Hong Fu 1, 2 , Xiao-Ran Han 1, 2 , Diane Threapleton 1 , Zu-Yao Yang 1, 2 , Chen Mao 1, 2 , Jin-Ling Tang 1, 2 1 Division of Epidemiology, The Jockey Club School of Public Health and Primary Care, The Chinese University of Hong Kong, Hong Kong, China 2 Shenzhen Municipal Key Laboratory for Health Risk Analysis, Shenzhen Research Institute of The Chinese University of Hong Kong, Shenzhen, Guangdong Province, China 3 Division of Epidemiology, School of Public Health and Tropical Medicine, Southern Medical University, Guangzhou, Guangdong Province, China Correspondence to: Chen Mao, email: maochen@cuhk.edu.hk Jin-Ling Tang, email: jltang@cuhk.edu.hk Keywords: non-small cell lung cancer, epidermal growth factor receptor, prevalence, systematic review, meta-analysis Received: May 17, 2016 Accepted: September 25, 2016 Published: October 12, 2016 ABSTRACT Objectives: Estimate the epidermal growth factor receptor ( EGFR ) mutation prevalence in all non-small cell lung cancer (NSCLC) patients and patient subgroups. Results: A total of 456 studies were included, reporting 30,466 patients with EGFR mutation among 115,815 NSCLC patients. The overall pooled prevalence for EGFR mutations was 32.3% (95% CI 30.9% to 33.7%), ranging from 38.4% (95% CI: 36.5% to 40.3%) in China to 14.1% (95% CI: 12.7% to 15.5%) in Europe. The pooled prevalence of EGFR mutation was higher in females (females vs. males: 43.7% vs. 24.0%; OR: 2.7, 95% CI: 2.5 to 2.9), non-smokers (non-smokers vs. past or current smokers: 49.3% vs. 21.5%; OR: 3.7, 95% CI: 3.4 to 4.0), and patients with adenocarcinoma (adenocarcinoma vs. non-adenocarcinoma: 38.0% vs. 11.7%; OR: 4.1, 95% CI: 3.6 to 4.8). Materials and Methods: PubMed, EMBASE, and the Cochrane Library were searched to June 2013. Eligible studies reported EGFR mutation prevalence and the association with at least one of the following factors: gender, smoking status and histology. Random-effects models were used to pool EGFR mutation prevalence data. Conclusion: This study provides the exact prevalence of EGFR mutations in different countries and NSCLC patient subgroups.