bluuebunny/crossref_metadata_2025_split huggingface dataset:
The effect of GNAQ methylation on GnRH secretion in sheep hypothalamic neurons
Authors: Zhai Manjun , Zhao Zongsheng , Yang Min , Liang Yanping , Liang Huihui , Xie Yifan , Han Jilong 
Published: August 2019

AbstractKazakh sheep are seasonal estrous animals, and gonadotropin‐releasing hormone (GnRH) is the key to fertility regulation. The nutritional level has a certain regulatory effect on estrous, and vitamin B folate plays a role in DNA methylation, directly participating in the process. The goal of this study was to determine whether folate is involved in GnAQ methylation and its effect on GnRH secretion. The hypothalamic neurons of Kazakh fetal sheep were treated with folate at concentrations of 0 mg/mL, 4 mg/mL, 40 mg/mL, and 80 mg/mL. GnAQ promoter methylation, DNMT1, GnAQ expression, and GnRH secretion following treatment with different concentrations of folate were analyzed. One CpG site was methylated in the GNAQ promoter with 40 mg/mL folic acid, and no CpG methylation was found in the other groups. GnAQ expression was related to folate concentration and showed a trend of increasing first and then decreasing. The GnRH expression level in the 40 mg/mL folate group was significantly higher than in the other three groups (
P < .05). These results demonstrate that the appropriate folate concentration promoted GANQ promoter methylation, which in turn affected GnRH secretion.
Overexpressed miR‐196a accelerates osteogenic differentiation in osteoporotic mice via GNAS‐dependent Hedgehog signaling pathway
Authors: Zhong Li‐Na , Zhang Yu‐Zhu , Li Hong , Fu Hui‐Ling , Lv Cheng‐Xiu , Jia Xiu‐Juan 
Published: August 2019

AbstractOsteoporosis (OP), a common metabolic bone disease, is accompanied by reduced bone mass, bone mineral density (BMD), as well as microstructure destruction of bone. Previously, microRNA‐196a‐2 (miR‐196a‐2) and miR‐196a‐3p were reported for its involvement in BMD. Herein, this study set out to identify the functional relevance of miR‐196a in osteogenic differentiation in osteoporotic mice and explore the associated mechanism by establishing an OP mouse model. Guanine nucleotide binding protein, alpha stimulating (GNAS) was verified as a target gene of miR‐196a, which was decreased in OP mice. Furthermore, the bone marrow stromal cells (BMSCs) were then extracted from OP mice and treated with miR‐196 mimic/inhibitor or small interfering RNA against GNAS to investigate miR‐196a interaction with GNAS and the Hedgehog signaling pathway. BMSCs in OP mice transfected with miR‐196a mimic or si‐GNAS displayed the elevated expression of Smo, ALP, Runx2, and OPN, as well as bone gla protein and tartrate‐resistant acid phosphatase, elevated ALP vitality and bone formation ability as well as reduced expression of GNAS and PTCH. Taken conjointly, overexpression of miR‐196a repressed GNAS expression by activating the Hedgehog signaling pathway, thus promoting osteogenic differentiation in mice with OP.
A novel regulatory role of TRAPPC9 in L‐plastin‐mediated osteoclast actin ring formation
Authors: Hussein Nazar J. , Mbimba Thomas , Al‐Adlaan Asaad A. , Ansari Mohammad Y. , Jaber Fatima A. , McDermott Scott , Kasumov Takhar , Safadi Fayez F. 
Published: August 2019

AbstractTrafficking protein particle complex 9 (TRAPPC9) is a major subunit of the TRAPPII complex. TRAPPC9 has been reported to bind nuclear factor κB kinase subunit β (IKKβ) and NF‐kB‐inducing kinase (NIK) where it plays a role in the canonical and noncanonical of nuclear factor‐κB (NF‐kB) signaling pathways, receptively. The role of TRAPPC9 in protein trafficking and cytoskeleton organization in osteoclast (OC) has not been studied yet. In this study, we examined the mRNA expression of TRAPPC9 during OC differentiation. Next, we examined the colocalization of TRAPPC9 with cathepsin‐K, known to mediate OC resorption suggesting that TRAPPC9 mediates the trafficking pathway within OC. To identify TRAPPC9 protein partners important for OC‐mediated cytoskeleton re‐organization, we conducted immunoprecipitation of TRAPPC9 in mature OCs followed by mass spectrometry analysis. Our data showed that TRAPPC9 binds various protein partners. One protein with high recovery rate is L‐plastin (LPL). LPL localizes at the podosomes and reported to play a crucial role in actin aggregation thereby actin ring formation and OC function. Although the role of LPL in OC‐mediated bone resorption has not fully reported in detail. Here, first, we confirmed the binding of LPL to TRAPPC9 and, then, we investigated the potential regulatory role of TRAPPC9 in LPL‐mediated OC cytoskeleton reorganization. We assessed the localization of TRAPPC9 and LPL in OC and found that TRAPPC9 is colocalized with LPL at the periphery of OC. Next, we determined the effect of TRAPPC9 overexpression on LPL recruitment to the actin ring using a viral system. Interestingly, our data showed that TRAPPC9 overexpression promotes the recruitment of LPL to the actin ring when compared with control cultures. In addition, we observed that TRAPPC9 overexpression reorganizes actin clusters/aggregates and regulates vinculin recruitment into the OC periphery to initiate podosome formation.
Linc‐RoR promotes proliferation, migration, and invasion via the Hippo/YAP pathway in pancreatic cancer cells
Authors: Chen Wei , Wang Huizhi , Liu Yawen , Xu Wei , Ling Chen , Li Yafang , Liu Junqiang , Chen Mengjiao , Zhang Youli , Chen Baoding , Gong Aihua , Xu Min 
Published: August 2019

AbstractLarge intergenic noncoding RNA regulator of reprogramming (Linc‐RoR) was first identified as a regulator to increase the emergence of induced pluripotent stem cells through reprogramming differentiated cells and is abnormal expression in a variety of malignant tumors. However, the function of Linc‐RoR in pancreatic cancer progression needs further clarification. The data from this study demonstrated that Linc‐RoR knockdown suppressed cell proliferative capacity and colony formation, while Linc‐RoR overexpression promoted these behaviors. In particular, Linc‐RoR overexpression promoted the level of mesenchymal markers, inhibited the expression of epithelial markers, as well as enhanced pancreatic cancer cells migration and invasion, whereas Linc‐RoR knockdown inhibited the expression of mesenchymal markers, promoted the expression of epithelial markers, as well as weakened pancreatic cancer cells migration and invasion. Further study revealed that Linc‐RoR knockdown brought about a significant fall in YAP phosphorylation and a rise in total YAP, while Linc‐RoR overexpression produced the opposite results. Specifically, Linc‐RoR promoted YAP in the cytoplasm into the nucleus. Taken together, we conjectured that Linc‐RoR promoted proliferation, migration, and invasion of pancreatic cancer cells by activating the Hippo/YAP pathway. YAP might be an underlying target of Linc‐RoR and mediate epithelial‐mesenchymal transition (EMT) in pancreatic cancer (PC); thus, Linc‐RoR might be a very meaningful biomarker for PC.
Effects of dexmedetomidine on glioma cells in the presence or absence of cisplatin
Authors: Yang Hui , Chen Yudan , Yan Hui , Wu Hao 
Published: August 2019

AbstractWith the extensive use of dexmedetomidine (Dex) in the surgical resection of tumours for its potent sedative and analgesic properties, its effects on various properties of tumours have received increased attention. The study described herein aimed to investigate the effects of Dex on glioma cells in the presence or absence of cisplatin (DDP). Glioma U251 and U87MG cells were treated with different doses (1‐50 nM) of Dex for 12 hours, then recultured in a Dex‐free medium. In addition, Dex was added to U251 and U87MG cells 12 hours before or simultaneously with a 12‐hour DDP treatment. Treatment with Dex increased the viability of both cell lines; this effect continued for at least 24 hours after Dex was removed. A cell invasion assay indicated that Dex inhibited cell invasion at 50 nM, but not at 10 nM. Western blot analysis showed that Dex increased the expression of phosphorylated extracellular‐signal‐regulated kinase 1/2, phosphoitide 3‐kinase and p‐AKT, but decreased ROCK protein levels at a dose of 50 nM. Intracellular Ca
2+ concentration was decreased by Dex in a dose‐dependent manner. DDP toxicity was attenuated by 10 nM Dex added either before or with DDP treatment. However, pretreatment with 50 nM Dex instead enhanced the toxicity of DDP. Single‐dose treatment with Dex did not significantly change glioma volume in nude mice, but changed the expression of Ki67 and matrix metalloproteinase‐3 in the tumour. In conclusion, this study provides evidence of the regulatory effects of Dex on proliferation, invasion and chemosensitivity of glioma cells, and outlines potential mechanisms for these effects.
Identification of the complex regulatory relationships related to gastric cancer from lncRNA‐miRNA‐mRNA network
Authors: Wang Jie , Ding Yanrui , Wu Yanyan , Wang Xiaxia 
Published: August 2019

AbstractThe oncogenesis and progression of gastric cancer are closely correlated with the complex regulatory relationships among messenger RNA (mRNA), long noncoding RNA (lncRNA), and microRNA (miRNA). After constructing the gastric cancer lncRNA‐miRNA‐mRNA regulatory network, we analyzed the network topology properties and found that lncRNA ADAMTS9‐AS2 and C20orf166‐AS1 and miRNA hsa‐mir‐204 are key nodes. Further functional enrichment analysis and survival analysis were performed on these key nodes and the RNAs interacting with them. We found that CHRM2, ANGPT2, and COL1A1 interacting with ADAMTS9‐AS2 are enriched in the PI3K‐Akt signaling pathway, and low expression of the ADAMTS9‐AS2 is closely related to the prognosis of patients. Abnormal expression of CACNA1H, FLNA, and FLNC interacting with lncRNA C20orf166‐AS1 is associated with MAPK signaling pathway in gastric cancer. In addition, the downregulated miRNA hsa‐mir‐204 promotes invasion and proliferation of gastric cancer cells by regulating the abnormal expression of mRNAs (CHRDL1 and NPTX1) and lncRNAs (ADAMTS9‐AS2, NKX2‐1‐AS1, TLR8‐AS1, and VCAN‐AS1). This study systematically analyzed the lncRNA‐miRNA‐mRNA regulatory network of gastric cancer, which not only has a new understanding of the pathogenesis of gastric cancer, but also provides new insights for the early diagnosis and treatment of gastric cancer.
MiRNA‐27a decreases ultraviolet B irradiation‐induced cell damage
Authors: Zhang YuanJing , Yang ChunJun , Yang Sen , Guo Ze 
Published: August 2019

AbstractMiRNAs were involved in the various biological process through mediating the posttranscriptional gene silencing. The abnormal expression of miRNAs is also involved in various disorders. Our previous study showed that miRNA‐27a (miR‐27a) was upregulated after ultraviolet B (UVB) irradiation. However, the function of miR‐27a in UVB‐induced cell damage is still unclear. In this study, we used the miR‐27a overexpression and knockdown lentivirus to transfect UVB irradiated HaCaT cell line and observed the influence of miR‐27a on UVB irradiated damages in cells. We found that miR‐27a removed cyclobutane pyrimidine dimers (CPDs) and decreased the cell apoptosis after UVB radiation. Further studies showed that miR‐27a directly decreased the expression and luciferase activity of target genes transactive response DNA‐binding protein (TARDBP) and apoptotic protease activating factor‐1 (APAF‐1). In conclusion, miR‐27a can inhibit CPDs, reduce the cell apoptosis and down‐regulate its target genes TARDBP and APAF‐1 induced by UVB irradiation in HaCaT cells. It is indicated that miR‐27a may serve as a target for UVB irradiation protection.
Interleukin‐1 beta induces autophagy of mouse preimplantation embryos and improves blastocyst quality
Authors: Pan Yangyang , Wang Meng , Wang Libin , Xu Gengquan , Baloch Abdul Rasheed , Kashif Jam , Fan Jiangfeng , Yu Sijiu 
Published: August 2019

AbstractAutophagy is one of the basic cellular mechanism during preimplantation development of mammalian embryos, and it plays crucial role in several physiological processes. It is induced by interleukin (IL)‐1β in mammalian cells. Our present study shows that IL‐1β is important for autophagy activation in embryo development. Our in vitro culture system analysis shows effect of IL‐1β in medium on the development of mouse embryos and it was found to be concentration dependent. A preimplantation embryo culture using medium containing IL‐1β did not improve cleavage and blastocyst development rates of mouse embryos; however, blastocyst quality was significantly improved by increasing total cell number, especially in supplementary 20 ng/mL IL‐1β. Furthermore, autophagy activation mainly occurs in 2 to 4 cell embryo and blastocyst, 20 ng/mL IL‐1β into culture medium can effectively enhance levels of messenger RNA and protein of autophagy‐related‐factors in 2 to 4 cell embryos and blastocyst, while these factors reduce in VGX‐1027 (IL‐1β inhibitor) groups that also reduce the quality of blastocyst. Effects of IL‐1β on the development of embryo reduced in 20 ng/mL IL‐1β supplemented group when 5 mM 3‐methyladenine (3‐MA) was also added, which used to inhibit autophagy activation in endogenous PtdIns3Ks signal pathway. Our current results show that exogenous IL‐1β can effectively induce autophagy in mouse embryos at stages of 2 to 8 cell and blastocyst, that also help to improve the quality of blastocyst.
Association between the TOX3 rs3803662 C>T polymorphism and recurrent miscarriage in a southern Chinese population
Authors: Huang Wendong , Zhou Huazhong , Li Qisen , Pi Lei , Xu Yufen , Fu LanYan , Yang Yanfang , Lu Zhaoliang , Che Di , Gu Xiaoqiong 
Published: August 2019

AbstractBackgroundStudies have shown that some genetic polymorphisms associated with breast cancer susceptibility may also be associated with abortion. The TOX3 gene plays a key role during the onset of breast cancer, and reproductive factors such as abortion are risk factors for breast cancer. However, there is currently no study describing the relationship between the TOX3 rs3803662 C>T polymorphism and the risk of recurrent miscarriage. Therefore, we investigated whether the TOX3 rs3803662 C>T polymorphism is associated with recurrent miscarriage susceptibility in this case‐control study.MethodsWe recruited 248 recurrent miscarriage patients and 392 healthy controls from the southern Chinese population and performed genotyping using the TaqMan method.ResultsThe results showed no evidence that TOX3 rs3803662 C>T is associated with recurrent miscarriage (CT and CC: corrected OR = 1.038, 95% CI = 0.737‐1.461, P = .8321; TT and CC: adjusted OR = 0.989, 95% CI = 0.591‐1.656, P = .9659; dominant model: adjusted OR = 1.027, 95% CI = 0.742‐1.423, P = .8712; recessive model: adjusted OR = 0.969, 95% CI = 0.600‐1.566, P = .8975).ConclusionAccording to this study, the TOX3 rs3803662 C>T polymorphism may not be associated with recurrent miscarriage in the southern Chinese population. A larger multicenter study is needed to confirm the results.
Confirmatory factor analysis of the Inventory of Statements About Self‐injury in a Spanish clinical sample
Authors: Pérez Sandra , García‐Alandete Joaquín , Cañabate Montserrat , Marco Jose H. 
Published: August 2019

AbstractObjectivesThe main aim of the present study was to confirm the two‐factor structure of the Inventory of Statements About Self‐injury‐ Part II (ISAS‐II), analyze its psychometric properties and test–retest reliability of Parts I and II of the ISAS.MethodThe sample was composed of 355 Spanish participants diagnosed with eating disorders or borderline personality disorder (mean age 27.89, standard deviation = 13.31; 315 women, 40 men). Two models proposed for the ISAS‐II were analyzed by means of confirmatory factorial analysis.ResultsA two‐factor model was confirmed, and a model with self‐care included in the intrapersonal factor was preferable. The ISAS‐II showed positive correlations with emotional dysregulation. Test–retest reliability showed statistically significant correlations at 7 months (n = 123).ConclusionThe ISAS‐II is a valid instrument to assess nonsuicidal self‐injury in Spanish populations, making it possible to assess these behaviors, which require valid and reliable measures worldwide.
Postoperative complications are main reason for noncompliance with enhanced recovery after surgery program in patients undergoing hepatectomy and pancreatectomy
Authors: Philip Justus , Fairtile Richard , Cocieru Andrei 
Published: August 2019

Background and AimEnhanced recovery after surgery (ERAS) protocols are reported to improve postoperative outcomes in patients undergoing a routine protocol and postoperative outcomes in patients undergoing hepatic and pancreatic resections at our institution.MethodsA total of 99 consecutive patients at a single institution managed with a similar ERAS protocol were divided into the “early” (50 patients) and “late” (49 patients) cohorts. Both cohorts were statistically identical in demographics and range of surgical procedures performed. Postoperative complications, readmission, reoperation rates, and length of stay were analyzed. Categorical variables were statistically compared using Fisher's exact test and continuous variables using t‐test and Mann–Whitney U‐test when appropriate.ResultsThere were 32 hepatectomies/18 pancreatectomies in the “early” cohort and 22 hepatectomies/29 pancreatectomies in the “late” cohort. The overall complication rate was 38.8%, with a 30‐day readmission rate and reoperation rate of 16.1 and 5%, respectively. There was one mortality (1%). Group‐specific overall complication rate (40 vs 38.7%, P = 0.8), readmission rate (20 vs 12.2%, P = 0.4), reoperation rate (6 vs 4%, P = 1.0), and mortality (2 vs 0%, P = 1.0) were not statistically significant between both groups.ConclusionsDespite similar rates of adherence to the established ERAS 24 protocol, there was no improvement in median length of stay (7 days) between the “early” and “late” groups. The only reason for noncompliance with the ERAS protocol was development of surgery‐related complications.
Normal range for MR elastography measured liver stiffness in children without liver disease
Authors: Sawh Mary Catherine , Newton Kimberly P. , Goyal Nidhi P. , Angeles Jorge Eduardo , Harlow Kathryn , Bross Craig , Schlein Alexandra N. , Hooker Jonathan C. , Sy Ethan Z. , Glaser Kevin J. , Yin Meng , Ehman Richard L. , Sirlin Claude B. , Schwimmer Jeffrey B. 
Published: August 2019

BackgroundMagnetic resonance elastography (MRE) can determine the presence and stage of liver fibrosis. Data on normative MRE values, while reported in adults, are limited in children.PurposeTo determine the distribution of MRE‐measured liver stiffness in children without liver disease.Study TypeProspective, observational.PopulationEighty‐one healthy children (mean 12.6 ± 2.6 years, range 8–17 years).Field Strength/Sequence3.0T Signa HDxt, General Electric MR Scanner; 2D GRE MRE sequence.AssessmentHistory, examination, laboratory evaluation, and (MR) exams (proton density fat fraction, PDFF, and MRE) were performed. MR elastograms were analyzed manually at two reading centers and compared with each other for agreement and with published values in healthy adults and thresholds for fibrosis in adult and pediatric patients.Statistical TestsDescriptive statistics, Bland–Altman analysis, t‐test to compare hepatic stiffness values with reference standards.ResultsStiffness values obtained at both reading centers were similar, without significant bias (P = 0.362) and with excellent correlation (intraclass correlation coefficient [ICC] = 0.782). Mean hepatic stiffness value for the study population was 2.45 ± 0.35 kPa (95th percentile 3.19 kPa), which was significantly higher than reported values for healthy adult subjects (2.10 ± 0.23 kPa, P < 0.001). In all, 74–85% of subjects had stiffness measurements suggestive of no fibrosis.Data ConclusionMean liver stiffness measured with MRE in this cohort was significantly higher than that reported in healthy adults. Despite rigorous screening, some healthy children had stiffness measurements suggestive of liver fibrosis using current published thresholds. Although MRE has the potential to provide noninvasive assessment in patients with suspected hepatic disease, further refinement of this technology will help advance its use as a diagnostic tool for evidence of fibrosis in pediatric populations.Level of Evidence: 1Technical Efficacy: 5J. Magn. Reson. Imaging 2020;51:919–927.
Renal perfusion imaging by MRI
Authors: Zhang Jeff L. , Lee Vivian S. 
Published: August 2019

Renal perfusion can be quantitatively assessed by multiple magnetic resonance imaging (MRI) methods, including dynamic contrast enhanced (DCE), arterial spin labeling (ASL), and diffusion‐weighted imaging with intravoxel incoherent motion (IVIM) analysis. In this review we summarize the advances in the field of renal‐perfusion MRI over the past 5 years. The review starts with a brief introduction of relevant MRI methods, followed by a discussion of recent technical developments. In the main section of the review, we examine the clinical and preclinical applications for three disease populations: chronic kidney disease, renal transplant, and renal tumors. The DCE method has been routinely used for assessing renal tumors but not other renal diseases. As a noncontrast alternative, ASL was extensively explored in both preclinical and clinical applications and showed much promise. Protocol standardization for the methods is desperately needed, and then large‐scale clinical trials for the methods can be initiated prior to their broad clinical use.Level of Evidence: 5Technical Efficacy: Stage 2J. Magn. Reson. Imaging 2019. J. Magn. Reson. Imaging 2020;52:369–379.
Real‐life effectiveness and safety of the daclatasvir/asunaprevir combination therapy for genotype 1b chronic hepatitis C patients: An emphasis on the pretreatment NS5A resistance‐associated substitution test
Authors: Jang Eun Sun , Kim Kyung‐Ah , Kim Young Seok , Kim In Hee , Lee Byung Seok , Lee Youn Jae , Chung Woo Jin , Jeong Sook‐Hyang 
Published: August 2019

AbstractThis study aimed to investigate the real‐life effectiveness and safety of daclatasvir (DCV) and asunaprevir (ASV) combination therapy in Korean patients. We consecutively enrolled patients with genotype 1b hepatitis C virus (HCV) infection treated with at least one dose of DCV/ASV combination therapy in seven tertiary hospitals of South Korea. The sustained virologic response (SVR) rates and safety according to intention‐to‐treat (ITT) and per‐protocol (PP) analyses were evaluated. Among the 526 enrolled patients, 91% showed negative (87%) or “undetermined” (4%) resistance‐associated substitution (RAS); 9% did not undergo RAS testing. The SVR rates for ITT and PP were 89.3% and 95.0% in treatment‐naive patients and 93.2% and 95.6% in treatment‐experienced patients, respectively. In PP analysis, negative RAS was associated with higher SVR (96.3%) than with “undetermined RAS” (85.7%) or “not tested for RAS” (84.4%). Adverse events were reported in 185 (35.4%) patients, and events leading to discontinuation were observed in 4.3% of the study population. Forty‐two (8.0%) patients developed transaminase elevation (≥2 × upper normal limit), resulting in treatment discontinuation in six (1.1%) patients. DCV/ASV combination therapy showed acceptable efficacy in genotype 1b compensated HCV‐infected patients with negative pretreatment RAS. Although most adverse events were tolerable to continue antiviral treatment, adequate monitoring for transaminase elevation is warranted.