bluuebunny/crossref_metadata_2025_split huggingface dataset:
Arsenic trioxide ameliorates experimental autoimmune encephalomyelitis in C57BL/6 mice through inducing apoptosis of CD4+ T cells
Authors: An Ke , Xue Mengjiao , Zhong Jiaying , Yu Shengnan , Qi Zhongquan , Xia Junjie 
Published: March 2020

Abstract
Background: Multiple sclerosis (MS) is an immune-mediated disease of the central nervous system characterized by severe demyelination of white matter. There is no definite cure for MS owing to its complex pathogenesis. Experimental autoimmune encephalomyelitis (EAE) is an ideal animal model for the study of MS. Arsenic trioxide (ATO) is an ancient Chinese medicine used for its therapeutic properties for several autoimmune diseases. It is also used to inhibit acute immune rejection due to its anti-inflammatory and immunosuppressive properties. However, it is unclear whether ATO has a therapeutic effect on EAE, and the underlying mechanisms have not been clearly elucidated. In this study, we attempted to explore the possibility of using ATO to ameliorate EAE in mice.Methods: ATO (0.5 mg/kg/day) was administered intraperitoneally to EAE mice 10 days post-immunization for 8 days. On day 22 post-immunization, the spinal cord, spleen, and blood were collected to analyze demyelination, inflammation, microglia activation, and proportion of CD4+ T cells. In vitro, for mechanistic studies, CD4+ T cells were sorted from the spleen of naïve C57BL/6 mice and treated with ATO and then used for apoptosis assay, JC-1 staining, transmission electron microscope, and western blotting.Results: ATO delayed the onset of EAE and alleviated the severity of EAE in mice. Treatment with ATO also attenuated demyelination, alleviated inflammation, reduced microglia activation and decreased the expression of IL-2, IFN-γ, IL-1β, IL-6, and TNF-α in EAE mice. Moreover, the number and proportion of CD4+ T cells in the spinal cord, spleen, and peripheral blood were reduced in ATO-treated EAE mice. Finally, ATO induced CD4+ T cells apoptosis through the mitochondrial pathway both in vitro and in vivo. Additionally, the administration of ATO had no adverse effect on the heart, liver, and kidney function and did not induce apoptosis in the spinal cord.Conclusions: Overall, our findings indicated that ATO plays a protective role in the initiation and progression of EAE and has the potential to be a novel drug in the treatment of MS.
Clinical and microbiological characteristics of Cryptococcus gattii isolated from 7 hospitals in China
Authors: Jin Liang , Cao Jingrong , Xue Xinying , Wu Hua , Wang Lifeng , Guo Ling , Shen Dingxia 
Published: March 2020

Abstract
Background: Infection, even outbreak, caused by Cryptococcus gattii (C. gattii ) has been reported in Canada and the United States, but there were sparsely-reported cases of C. gattii in China. Our interest in occurrence, clinical manifestation, laboratory identification and molecular characterization of Chinese C. gattii strains leads us to this research.
Results: Out of 254 clinical isolates, initially identified as Cryptococcus neoformans (C. neoformans ), eight strains were re-identified as C. gattii. Multi-locus sequence typing (MLST) showed genotype VGI accounted for the most (6 / 8), the other two strains were genotype VGII（VGIIa and VGIIb respectively）with 3 specific spectra of molecular weight about 4342, 8686, 9611 Dalton by MALDI-TOF MS. The minimal inhibitory concentrations (MICs) of Fluconazole with Yeast one was 2～4 times higher than that with ATB fungus 3 and MICs of antifungal agents against VGII strains were higher than against VGI strains. Comparative proteome analysis showed that 329 and 180 proteins were highly expressed by C. gattii VGI and VGII respectively. The enrichment of differentially expressed proteins was directed to Golgi complex.Conclusions: Infection by C. gattii in China occurred sparsely. Genotype VGI was predominant but VGII was more resistant to antifungal agents. There was significant difference in protein expression profile between isolates of VGI and VGII C. gattii.
Key words: Cryptococcus gattii, Genotype, Antifungal agents, Spectrum, differential protein
Polymorphisms in endoplasmic reticulum aminopeptidase genes are associated with cervical cancer risk in a Chinese Han population
Authors: Li Chuanyin , Li Yaheng , Yan Zhiling , Dai Shuying , Liu Shuyuan , Wang Xia , Wang Jun , Zhang Xinwen , Shi Li , Yao Yufeng 
Published: March 2020

Abstract
Background: Antigen-processing machinery molecules play crucial roles in infectious diseases and cancers. Studies have shown that variants in endoplasmic reticulum aminopeptidase (ERAP) genes can influence the enzymatic activity of ERAP proteins and are associated with the risk of diseases. In the current study, we evaluated the influence of ERAP gene (ERAP1 and ERAP2) variants on susceptibility to cervical intraepithelial neoplasia (CIN) and cervical cancer.
Methods: Six single nucleotide polymorphisms (SNPs) in ERAP1 and 5 SNPs in ERAP2 were selected and genotyped in 556 CIN patients, 1072 cervical cancer patients, and 1262 healthy control individuals. Candidate SNPs were genotyped using SNaPshot assay. And the association of these SNPs with CIN and cervical cancer was analysed.
Results: The results showed that allelic and genotypic frequencies of rs26653 in ERAP1 were significantly different between cervical cancer and control groups (P=0.001 and 0.004). The allelic frequencies of rs27044 in ERAP1 and rs2287988 in ERAP2 were significantly different between control and cervical cancer groups (P=0.003 and 0.004). Inheritance model analysis showed that genotypes of rs27044, rs26618, rs26653 and rs2287988 SNPs may be associated with the risk of cervical cancer (P=0.003, 0.004, 0.001 and 0.002). Additionally, haplotype analysis results showed that the ERAP1 haplotype, rs27044C-rs30187T-rs26618T-rs26653G-rs3734016C, was associated with a lower risk of cervical cancer (P=0.001). The ERAP2 haplotypes rs2549782G- rs2548538A-rs2248374A-rs2287988G-rs1056893T (P=0.009 and 0.006) and rs2549782T-rs2548538T-rs2248374G-rs2287988A-rs1056893T (P=0.003 and 0.009) might be associated with cervical cancer and the development from CIN to cervical cancer. Conclusion: Our results indicated that rs27044, rs26618 and rs26653 in ERAP1 and rs2287988 in ERAP2 influenced susceptibility to cervical cancer.
The effect of virtual reality on motor anticipation and hand function in patients with subacute stroke: A randomised trial on movement-related potential.
Authors: Chen Ling , Chen Yi , Lo Wai Leung Ambrose 
Published: March 2020

Abstract
Background: Impaired cognitive ability to anticipate the required control may affect functional recovery. The cortical excitability of task related motor anticipation for upper limb movement induced by virtual reality (VR) training is unknown.
Aims: To investigate the changes of motor anticipation, cortical excitability and upper limb function induced by VR training in subacute stroke survivors.
Methods: Upper limb hemiparesis resulting from the first occurrence of stroke within 1 to 6 months were recruited. Participants were randomly allocated to conventional therapy or VR intervention. Electroencephalogram (EEG) and electromyography (EMG) were simultaneously recorded during palmar grasp motion. Outcome measures of contingent negative variation (CNV) latency, mean peak amplitude, electromyography (EMG) reaction time, Upper Limb Fugl-Meyer Assessment (UL-FMA) and the Action Research Arm Test (ARAT) were recorded pre and post intervention. The EEG and EMG differences between the two groups were assessed by mixed model ANOVA (p=0.05). The differences in UL-FMA and ARAT were assessed Wilcoxon signed-rank test (p=0.05).
Results: The reduction in EMG reaction time difference, CNV latency and mean peak amplitude were significantly lower in the VR group than the control group when executing movement with the paretic hand. ARAT and UL-FMA scores were significantly higher in the VR group than the control group post intervention.
Conclusions: The findings indicated a reduction in brain computational demand during palmar grasp task. Improvements in clinical function in the VR group suggested that VR intervention may be more beneficial in improving upper limb function patients with subacute stroke. Improvement in upper limb function may be related to improvement of the neural anticipatory process.
Trial registration: Chinese Clinical Trial Registry (Registration No.: ChiCTR-IOC-15006064). Registered on 11 May 2015. Retrospectively registered. http://www.chictr.org.cn/searchprojen.aspx
Clinical validation of full genotyping CLART® HPV4S assay on SurePath and ThinPrep collected screening samples according to the International Guidelines for Human Papillomavirus Test Requirements for Cervical Screening
Authors: Ejegod Ditte Møller , Lagheden Camilla , Bhatia Ramya , Pedersen Helle , Boada Elia Alcañiz , Sundström Karin , Cortés Javier , Josë F. Xavier Bosch , Cuschieri Kate , Dillner Joakim , Bonde Jesper 
Published: March 2020

Abstract
Background

To ensure the highest quality of human papillomavirus (HPV) testing in primary cervical cancer screening, novel HPV assays must be evaluated in accordance with the international guidelines. Furthermore, HPV assay with genotyping capabilities are becoming increasingly important in triage of HPV positive women in primary HPV screening. Here we evaluate a full genotyping HPV assay intended for primary screening.

Methods

The CLART® HPV4S (CLART4S) assay is a newly developed full-genotyping assay detecting 14 oncogenic (16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 66, 68) and two non-oncogenic HPV genotypes (6, 11). It was evaluated using SurePath and ThinPrep screening samples collected from the Danish and Swedish cervical cancer screening programs, respectively. For calculation of sensitivity, 81 SurePath and 80 ThinPrep samples with confirmed ≥CIN2 were assessed. For clinical specificity analysis, 1,184 SurePath and 1,169 ThinPrep samples from women with
Geniposide, a component of Gardenia jasminoides Ellis, inhibits NF-ĸB to attenuate LPS-induced injury in intestinal epithelial cells
Authors: Cui Yizhe , Qiao Xinyue , Wang Qiuju , Wu Rui 
Published: March 2020

Abstract
Background: The nuclear factor-ĸB (NF-ĸB) transcriptional system is a major effector pathway involved in inflammatory responses. Previous studies found that a Gardenia decoction (GD) inhibited the expression of NF-κB in a lipopolysaccharide (LPS)-stimulated mouse intestinal injury model. Herein, we hypothesized that geniposide (GE), a component of Gardenia jasminoides Ellis, also exerts anti-inflammatory effects and inhibits NF-ĸB activity in LPS-induced intestinal epithelial cells (IEC-6). IEC-6 cells were stimulated with LPS, following which the effects of GE on NF-ĸB signaling in the IEC-6 cells were examined by western blotting to detect IĸB phosphorylation/degradation. The expression of NF-κB was determined by immunofluorescence assay (IFA). Enzyme-linked immunosorbent assay (ELISA) was used to detect the inhibitory effect of GE on the release of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and interleukin-1β (IL-1β) activated by LPS in IEC-6 cells. In addition, the migration ability of IEC-6 cells was observed by the scratch method. Results: These results showed that GE dose-dependently downregulated levels of the proinflammatory cytokines TNF-α, IL-6 and IL-1β that had been upregulated by LPS and suppressed the phosphorylation of IĸB and NF-ĸB induced by LPS. Our findings indicated that GE could reduce LPS-induced NF-ĸB signaling and proinﬂammatory expression in IEC-6 cells and significantly enhance the migration of IEC-6 cells. Moreover, GE inhibited the expression of NF-κB, nuclear transfer, and transcriptional activity in IEC-6 cells. Conclusion: GE could block the synthesis of inflammatory factors of IEC-6 cells by inhibiting activation of the IĸB/NF-κB signaling pathway induced by LPS.
Evolution and genetic diversity of atypical porcine pestivirus (APPV) from piglets with congenital tremor in Guangxi province, Southern China
Authors: Shi Kaichuang , Xie Shou-yu , Zhao Jing , Liu Hui-xin , Yin Yan-wen , Chen Zhenhai , Si Hong-bin , Qu Su-jie , Lu Wen-jun , Feng Shu-ping 
Published: March 2020

Abstract
Background: Atypical porcine pestivirus (APPV) was identified and associated with congenital tremor (CT) type A-II in new born piglets and has been reported in many countries around the world since 2015. In China, the first APPV infection in swine herds was reported in Guangdong province in 2016. To investigate the genetic characteristics of APPV from Guangxi province seated in Southern China, the full-length sequences of APPV strains were amplified and analyzed. Results: Tissue samples from neonatal piglets with CT from Guangxi province were detected by reverse transcription-polymerase chain reaction (RT-PCR). APPV positive samples were amplified, cloned and sequenced, and the complete genomic sequences of five APPV strains were obtained. Sequence analysis revealed that all six APPV strains from Guangxi province, including five strains from this study and one from other researchers, shared 83.3%-97.5% nucleotide identity of complete genome and 91.7%-99.1% amino acid identity of open reading frame (ORF) with one another, and shared 77.7%-97.7% nucleotide identity of complete genome and 90.6%-99.3% amino acid identity of ORF with other reference strains available in Genbank. Phylogenetic analysis indicated that the APPV strains from Guangxi province belonged to four different subgroups in the phylogenetic tree based on the complete genomic sequences, and similar topology was observed in the phylogenetic trees based on N pro , E rns and E2 gene sequences, respectively. No sign of recombination was observed for strains from Guangxi province by using Recombination Detection Program 4 (RDP4) and Simplot analysis. Evolution analysis performed on the complete genome of 58 APPV strains available in Genbank showed that APPV strains from America, Europe and Asia during 2006-2019 evolved at a mean rate of 1.37×10 -4 substitutions/site/year, and the most recent common ancestor ( tMRCA ) of them was estimated as 1700.5 years ago. Conclusions: The findings of this study indicated that there existed a high degree of genetic diversity of APPV from Guangxi province, Southern China, which provided important information on the epidemiological features and evolutionary relationships of APPV.
Hypoxia-induced lncRNA -NEAT1 sustains the growth of hepatocellular carcinoma via regulation of miR-199a-3p/UCK2: integrative bioinformatics analysis and experimental validation
Authors: Zhang Qiangnu , Cheng Qian , Xia Mengting , Huang Xiaotao , He Xiaoyan , Liao Juan 
Published: March 2020

Abstract
Background: The long noncoding RNA (lncRNA) nuclear paraspeckle assembly transcript 1 (NEAT1) has emerged as a novel player in hepatocellular carcinoma (HCC). Hypoxia is a common characteristic of the microenvironment of HCC. However, it remains unclear whether lncRNA-NEAT1 is induced by hypoxia in HCC, and the mechanism that underlies LncRNA-NEAT1 function is not well characterized. Methods: The expression changes of lncRNA-NEAT1 in HCC cell lines under hypoxic conditions were examined by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). The regulatory effect of HIF-1α on lncRNA-NEAT1 was confirmed with chromatin immunoprecipitation (ChIP) and luciferase reporter assays. The function of lncRNA-NEAT1 on HCC cell growth under hypoxic conditions was determined by CCK-8 assay and flow cytometry. lncRNA -NEAT1 was predicted to serve as a competing endogenous RNA (ceRNA) within microRNA (miRNA)/mRNA axes based on microarray data, public HCC-related datasets and integrative bioinformatics analysis, and the miR-199a-3p/UCK2 axis was selected and validated by qRT-PCR, western blotting, RNA immunoprecipitation, and luciferase reporter analyses. The role of miR-199a-3p/UCK2 in HCC and its functional association with lncRNA-NEAT1 were assessed both in vitro and in vivo . Results : LncRNA-NEAT1 expression was significantly induced by hypoxia in SNU-182 and HUH7 cells. HIF-1α was shown to regulate lncRNA-NEAT1 transcription. Under hypoxic conditions, lncRNA-NEAT1 maintained the growth of HCC cells and inhibited apoptosis and cell cycle arrest. LncRNA-NEAT1 was predicted to regulate a panel of HCC-associated miRNA-mRNA pairs consisting of 8 miRNAs and 13 mRNAs. Furthermore, lncRNA-NEAT1 was demonstrated to serve as a miR-199a-3p sponge that regulates UCK2 expression and to play a tumor-suppressive role in HCC, while UCK2 promotes cell growth. LncRNA-NEAT1 was shown to function as a ceRNA of miR-199a-3p/UCK2 both in HCC cells under hypoxic conditions and in an animal model. Conclusion: LncRNA-NEAT1 is a hypoxia-responsive lncRNA in HCC that sustains the growth of HCC cells by regulating HCC-associated mRNAs that interact with tumor-suppressive miRNAs. The lncRNA-NEAT1/miR-199a-3p/UCK2 pathway may contribute to the progression of HCC in a hypoxic microenvironment and therefore may represent a novel therapeutic target for HCC.
JARID1B promotes colorectal cancer proliferation and Wnt/β-catenin signaling via decreasing CDX2 level
Authors: Huang Da , Xiao Fan , Hua Fuzhou , Luo Zhenzhong , Huang Zhaoxia , Chen Sha , Cheng Xiuzhi , Zhang Xinyue , Fang Weilan , Hu Xiaoyun , Liu Fanrong 
Published: March 2020

Abstract
Background: Jumonji AT-rich interactive domain 1B(JARID1B) has been shown to be upregulated in many human cancers and plays a critical role in the development of cancers cells. Nevertheless, its functional role in colorectal cancer (CRC) progression is not fully understood. Methods: Herein, JARID1B expression levels were detected in clinical CRC samples by western blotting and qRT-PCR. DLD-1 cells with JARID1B knockdown or overexpression by stably transfected plasmids were used in vitro and in vivo study. Colony formation, 5-ethynyl-20-deoxyuridine (EdU) and Real Time Cellular Analysis(RTCA) assays were used to detect cell proliferation and growth. Transcriptome and CHIP assays were used to examine the molecular biology changes and molecular interaction in these cells. Nude mice was utilized to study the correlation of JARID1B and tumor growth in vivo. Results: Here, we first observed that JARID1B was significantly upregulated in CRC tissue compared to adjacent normal tissues. In CRC patients, JARID1B high expression was positively relation with poor overall survival. Multivariate analyses revealed that high JARID1B expression was an independent predictive marker for the poor prognosis of CRC. In addition, we found that JARID1B promoted CRC cells proliferation by Wnt/β-catenin signaling pathway. Further studies demonstrated CDX2 as a downstream target of JARID1B, and our data demonstrated that CDX2 is crucial for JARID1B -mediated Wnt/β-catenin signaling pathway. Mechanistically, we demonstrated that JARID1B regulated CDX2 expression through demethylation of H3K4me3. Conclusions: CDX2 inhibited by JARID1B-derived H3K4me3 methylation promoted cells proliferation of CRC via Wnt/β-catenin signaling pathway. Therefore, our studies provided a novel insight into the role of JARID1B in CRC cells proliferation and potential new molecular target for treating CRC.
Risk Factors for Acute Kidney Injury in Acute Pancreatitis: A 7-year Retrospective Analysis of Patients in a Large Tertiary Hospital
Authors: Yu Bingjun , He Wenhua , Lu Nonghua 
Published: March 2020

Abstract
Background Acute kidney injury (AKI) is a serious complication of acute pancreatitis (AP) and causes a high risk of mortality. The aim of this study was to investigate the risk factors for AKI in patients in the early phase of AP.Methods In this retrospective observational study, 1655 AP patients were divided into an AKI and a non-AKI group. Age, sex, BMI, APACHE II score, smoking history, hypertriglyceridaemia (HTG), alcohol abuse, biliary disease, organ failure, pancreatic necrosis and necrosis debridement were collected from the hospital record database.Results 1036 males (62.6%) and 619 females (37.4%) were enrolled in this study. 1255 and 430 AP patients were included in the non-AKI and AKI groups, respectively. The mean age was 45.90±11.73 years. Hospital and intensive care unit (ICU) lengths of stay were 18.13±43.26 and 31.53±72.47 days, respectively. The incidence of organ failure and pancreatic necrosis were 25.0% and 32.2%, respectively. The morbidity of percutaneous catheter drainage (PCD) and operative necrosectomy (ON) was 10.9%, and the mortality among AP patients was 6.3%. HTG was identified as a risk factor for AKI in AP (P=0.001). The incidence of organ failure (P=0.001), pancreatic necrosis (P=0.001) and necrosis debridement were greater in the AKI group than those in the non-AKI group.Conclusions HTG is an independent risk factor for AKI in AP. AP patients with AKI have adverse outcomes such as high rates of organ failure, pancreatic necrosis, and necrosis debridement and longer hospital and ICU lengths of stay.
The five primary prostaglandins stimulate contractions and phasic activity of the urinary bladder urothelium, lamina propria and detrusor
Authors: Stromberga Zane , Chess-Williams Russ , Moro Christian 
Published: March 2020

Abstract
Background: Inflammation is often associated with several bladder dysfunctions, including overactive bladder (OAB) and interstitial cystitis/bladder pain syndrome (IC/PBS). As such, inflammation of the bladder and the actions of inflammatory mediators may contribute to the development of the urinary symptoms. This study assessed the actions of PGE 2 , PGF 2 , PGD 2 , TXA 2 , and PGI 2 on the urinary bladder urothelium with lamina propria (U&LP), as well as the detrusor smooth muscle.Methods: Studies were carried out using isolated tissue baths, where strips porcine bladder U&LP or detrusor were exposed to varying concentrations of prostaglandin agonists (1 µM and 10 µM).Results: All assessed prostaglandin agonists contracted both the U&LP and detrusor smooth muscle, with the rank order of contractile response effectiveness as: PGE 2 > PGF 2α > TXA 2 > PGD 2 > PGI 2 . In U&LP, treatment with PGE 2 (10 µM) increased tonic contractions by 1.36 ± 0.09 g (n = 42, p < 0.001) and phasic contractions by 40.4 ± 9.6% (n = 42, p < 0.001). In response to PGF 2α (10 µM), U&LP tonic contractions increased by 0.79 ± 0.06 g (n = 14, p < 0.001) and phasic activity by 13.3% ± 5.3% (n = 15, p < 0.05). In detrusor preparations, PGE 2 (10 µM) increased tonic contractions by 1.32 ± 0.13 g (n = 38, p < 0.001) and PGF 2α (10 µM) by 0.97 ± 0.14 g (n = 12, p < 0.001). Only 34% (n = 48) of all detrusor preparations exhibited spontaneous activity prior to the addition of any agonist at a frequency of 2.03 ± 0.12 cpm. In preparations that did not exhibit initial phasic activity, all of the prostaglandin agonists were capable of commencing phasic activity.Conclusions: The urinary bladder U&LP and detrusor respond to a variety of prostaglandin agonists, with their activation resulting in direct contractions, as well as increases to spontaneous contractile activity. This study presents the prostaglandin receptor system as a potential therapeutic target for lower urinary tract dysfunction.