bluuebunny/crossref_metadata_2025_split huggingface dataset:
HIV testing uptake among pregnant women attending private midwife clinics: challenges of scaling up universal HIV testing at the private sectors in Indonesia
Authors: Wulandari Luh Putu Lila , Lubis Dinar S.M. , Widarini Putu , Widyanthini Desak Nyoman , Wirawan I. Made Ady , Wirawan Dewa Nyoman 
Published: May 2019

SummaryIntroductionBeing ranked seventh among countries with the highest number of new pediatric HIV infection, around 3% of new pediatric HIV infection worldwide occurs in Indonesia. UNAIDS has set a goal of elimination of mother‐to‐child HIV transmission, and private sector plays a critical role in achieving this goal. More than half of pregnant women in Indonesia seek antenatal care (ANC) services at private sectors, particularly at private midwife clinics. However, no published data is available on the rates of HIV testing uptake among pregnant women at these clinics, reflecting important gap on prevention of mother to child HIV transmission programmatic data.PurposeA longitudinal study was conducted to examine the rates of HIV testing uptake among pregnant women attending private midwife clinics in Bali and were referred to Voluntary HIV counselling and testing (VCT) clinics for a HIV test.MethodsSeventy midwives from private clinics were asked to suggest women, who were deemed to be at risk of HIV, to seek HIV testing at the nominated VCT clinics and to provide the women with a referral. Data were then analyzed to identify the percentage of women who took HIV testing at the VCT clinics among those referred by the midwives.ResultsThe midwives referred 619 women to VCT clinics. Of the referred women, only 321 (52%; 95% CI, 47.8%‐55.9%) took a HIV test at the appointed clinics. Among these who tested, three (0.9%) were HIV positive. This study identified a challenge in scaling up HIV testing coverage among women seeking ANC services at private sectors. Implications and recommendations are discussed.
β‐Elemene suppresses the proliferation of human airway granulation fibroblasts via attenuation of TGF‐β/Smad signaling pathway
Authors: Xue Cheng , Lin Xiao‐Ping , Zhang Jia‐Min , Zeng Yi‐Ming , Chen Xiao‐Yang 
Published: May 2019

AbstractBackgroundBenign airway stenosis is easily to recur as a result of hyperplastic airway granulation tissues. Our previous study proved that a Chinese drug, β‐elemene, could inhibit the proliferation of fibroblasts cultured from these tissues, which could decrease the recurrence rate of this disease.MethodsTo find out the mechanism for this effect, we first cultured normal human airway fibroblasts and human airway granulation fibroblasts with different concentrations of β‐elemene for the same time or the same dose of β‐elemene for different times to explore the dose/time‐effect relationship between the drug and these cells. Then we used gene microarray to screen out the most important pathway by which the drug influenced human airway granulation fibroblasts. At last, we assessed the condition of this pathway in human airway granulation fibroblasts and verified the effect of this drug on this pathway.Resultsβ‐Elemene inhibited the proliferation of human airway granulation fibroblasts in a dose but no time‐dependent manner and did not affect normal human airway fibroblasts. Affecting the expression of transforming growth factor β (TGF‐β)/Smad pathway may be the key mechanism for this effect. This pathway was activated in human airway granulation fibroblasts and β‐elemene inhibited it in a dose‐dependent manner. This effect was similar to the pathway inhibitor, SB431542, and exogenous TGF‐β could attenuate this effect.ConclusionThese results indicated that suppressing TGF‐β/Smad pathway was possibly the key mechanism by which β‐elemene inhibits the proliferation of human airway granulation fibroblasts. This pathway may be a promising target to treat benign airway stenosis.
Lentiviral‐mediated silencing of mast cell‐expressed membrane protein 1 promotes angiogenesis of rats with cerebral ischemic stroke
Authors: Jian Rui , Yang Min , Xu Fangyuan 
Published: May 2019

AbstractCerebral ischemic stroke is a devastating neurological disease with high rates of morbidity, disability, and mortality. Lentiviral‐mediated mast cell‐expressed membrane protein 1 (MCEMP1) has been shown to function in ischemic stroke. Hence, this study aims to explore the function of MCEMP1 specifically in angiogenesis, neuronal proliferation, and apoptosis in rats with cerebral ischemic stroke. Initially, stroke‐related genes were obtained through microarray‐based gene expression analysis, followed by the construction of a lentiviral vector for MCEMP1 shRNA and establishment of the middle cerebral artery occlusion model. After rats were transfected with MCEMP1 shRNA lentivirus, microvessel density (MVD), expression of MCEMP1, caspase‐3, and vascular endothelial growth factor (VEGF), and neuronal proliferation and apoptosis were measured to explore the role of MCEMP1 in cerebral ischemic stroke. MCEMP1 was found to be highly expressed in rats with cerebral ischemic stroke. Silencing of MCEMP1 led to upregulation of VEGF, while downregulation of caspase‐3, and resulted in the promotion of MVD in rats with ischemic stroke. Moreover, MCEMP1 silencing could increase Ki67 positive cells and reduce terminal deoxynucleotidyl transferase‐mediated dUTP nick‐end labeling positive cells in the marginal zone of cortical infarction in rats. Our study provides evidence that silenced MCEMP1 could enhance angiogenesis and suppress neuronal apoptosis in rats with cerebral ischemic stroke, highlighting that MCEMP1 silencing could serve as a therapeutic target for cerebral ischemic stroke treatment.
Inhibition of myeloid differentiation 1 specifically in colon with antisense oligonucleotide exacerbates dextran sodium sulfate‐induced colitis
Authors: Chen Xiaoxing , Pan Huaqin , Li Jin , Zhang Guqin , Cheng Shizhe , Zuo Na , Zhao Qiu , Peng Zhiyong 
Published: May 2019

AbstractMyeloid differentiation 1 (MD‐1), also known as lymphocyte antigen 86 (Ly86), is a soluble protein homologous to MD‐2 and forms a complex with radioprotective 105 (RP105). RP105/MD‐1 complex negatively regulates toll‐like receptor 4 (TLR4) signaling and is involved in several immune disorders. However, the precise role of MD‐1 in inflammatory bowel diseases (IBD) remains poorly understood. To further investigate the involvement of MD‐1 in IBD, we inhibited MD‐1 in colon with antisense oligonucleotide (AS‐ODN) and assessed the effect of MD‐1 inhibition on dextran sodium sulfate (DSS)‐induced colitis. We discovered that MD‐1 protein expression was remarkably decreased in both patients with ulcerative colitis and mice with DSS‐induced colitis. For the first time, we showed that oral administration of MD‐1 AS‐ODN to mice significantly suppressed the MD‐1 protein levels in colon rather than systemic tissues. Subsequently, we found that MD‐1 AS‐ODN treated mice were more susceptible to DSS‐induced colitis based on loss of body weight, colon length, histological scores, and disease activity index. MD‐1 inhibition also significantly enhanced inflammatory cytokines production such as IL‐6 and IL‐1β in colons. Finally, mice treated with MD‐1 AS‐ODN exhibited increased messenger RNA levels of TLR4 and MyD88 after DSS exposure and showed enhanced nuclear factor (NF)‐κB activation compared with the control. Taken together, specifically suppression of MD‐1 in colon tissues with AS‐ODN exacerbates DSS‐induced experimental colitis in mice, which is possibly related to activation of TLR4/NF‐κB signaling.
ELK1‐induced upregulation of lncRNA TRPM2‐AS promotes tumor progression in gastric cancer by regulating miR‐195/ HMGA1 axis
Authors: Huang Bo , Chang Cheng , Wang Bai‐lin , Li Huiwen 
Published: May 2019

AbstractLong noncoding RNAs (lncRNAs) have been confirmed to be aberrantly expressed in various diseases including tumors. Recently, a new tumor‐related lncRNA, lncRNA TRPM2 antisense RNA (TRPM2‐AS), was shown to be involved in many tumors, such as lung cancer and breast cancer. However, the expression and role of TRPM2‐AS in the development of gastric cancer (GC) have not been elucidated. In the current study, we provided evidence that the expression levels of TRPM2‐AS were increased in both GC tissues and cell lines. We also showed that overexpression of TRPM2‐AS was modulated by ELK1, a transcription factor. The results of clinical assays showed that higher expressions of TRPM2‐AS were significantly related with invasion depth, TNM stage, lymphatic metastasis, and shorter overall survival. Further clinical assays using multivariate analysis suggested that TRPM2‐AS expression was an independent prognostic factor in patients with GC. Functional experiments illustrated that depression of TRPM2‐AS suppressed proliferation, migration, and invasion in GC cells. In terms of mechanism, we found that TRPM2‐AS directly inhibited miR‐195, which targeted the 3′‐untranslated region of high‐mobility group AT‐hook 1 (HMGA1) messenger RNA. Overall, these findings revealed that ELK1‐induced overexpression of TRPM2‐AS promoted the development and progression of GC in part through miR‐195/HMGA1 signaling axis, and established its candidacy as a new cancer biomarker for GC patients.
RETRACTED: Propofol‐induced miR‐219‐5p inhibits growth and invasion of hepatocellular carcinoma through suppression of GPC3‐mediated Wnt/β‐catenin signalling activation
Authors: Gong Ting , Ning Xue , Deng Zhiya , Liu Mingyu , Zhou Beixian , Chen Xijun , Huang Shisi , Xu Yan , Chen Zhongqing , Luo Rongcheng 
Published: May 2019

AbstractPropofol is one of the most extensively used intravenous anaesthetic agents, which has been found to improve the surgical intervention outcome of several types of cancer, including hepatocellular carcinoma (HCC). Additionally, in vitro and in vivo experiments have also indicated that propofol affects the biological behaviour of HCC. However, the underlying mechanisms of the surgical resection of HCC with propofol have not been fully understood. In the present study, we aimed to investigate the underlying mechanism of propofol inhibition of the growth and invasion of HCC cells. Our results showed that treatment with propofol suppressed the proliferation, invasion and migration of HCC in vitro. The subcutaneous xenograft tumour and orthotopic xenograft tumour experiments in nude mice showed that propofol significantly decreased tumour volumes, growth rates and the liver orthotopic xenograft tumour in vivo. Furthermore, the underlying mechanism investigations of the suppressive effects of propofol on HCC cells revealed that propofol treatment upregulated the expression levels of the candidate tumour suppressor miR‐219‐5p. Silencing of propofol‐induced miR‐219‐5p using anti‐miR‐219‐5p abrogated the inhibitory effects on the proliferation, migration and invasion of HCC cells exerted by propofol treatment. Additionally, we demonstrated that propofol reversed the epithelial‐mesenchymal transition of Huh7 and SMMC7721 cells via miR‐219‐5p induction. The molecular mechanism behind these findings is that propofol‐induced miR‐219‐5p inhibits HCC cell progression by targeting glypican‐3 and subsequently results in the inhibition of Wnt/β‐catenin signalling. Taken together, our study provides new insights into the advantages of the surgical intervention of HCC with propofol anaesthetization.
Upregulation of IGF‐IIRα intensifies doxorubicin‐induced cardiac damage
Authors: Pandey Sudhir , Kuo Wei‐Wen , Ho Tsung‐Jung , Yeh Yu‐Lan , Shen Chia‐Yao , Chen Ray‐Jade , Chang Ruey‐Lin , Pai Pei‐Ying , Padma V. Vijaya , Huang Chih‐Yang , Huang Chih‐Yang 
Published: May 2019

AbstractCardiotoxicity by doxorubicin hampers its therapeutic potential as an anticancer drug, but mechanisms leading to cardiotoxicity remain contentious. Through this study, the functional contribution of insulin‐like growth factor receptor type II α (IGF‐IIRα) which is a novel stress‐inducible protein was explored in doxorubicin‐induced cardiac stress. Employing both in vitro H9c2 cells and in vivo transgenic rat models (SD‐TG [IGF‐IIRα]) overexpressing IGF‐IIRα specifically in heart, we found that IGF‐IIRα leads to cardiac structural abnormalities and functional perturbations that were severely aggravated by doxorubicin‐induced cardiac stress. Overexpression of IGF‐IIRα leads to cumulative elevation of stress associated cardiac hypertrophy and apoptosis factors. There was a significant reduction of survival associated proteins p‐Akt and estrogen receptor β/α, and abnormal elevation of cardiac hypertrophy markers such as atrial natriuretic peptide, cardiac troponin‐I, and apoptosis‐inducing agents such as p53, Bax, and cytochrome C, respectively. IGF‐IIRα also altered the expressions of AT1R, ERK1/2, and p38 proteins. Besides, IGF‐IIRα also increased the reactive oxygen species production in H9c2 cells which were markedly aggravated by doxorubicin treatment. Together, we showed that IGF‐IIRα is a novel stress‐induced protein that perturbed cardiac homeostasis and cumulatively exacerbated the doxorubicin‐induced cardiac injury that perturbed heart functions and ensuing cardiomyopathy.
An integrative bioinformatics pipeline to demonstrate the alteration of the interaction between the ALDH2*2 allele with NAD+ and Disulfiram
Authors: J Christy Priyadharshini , D Thirumal Kumar , P Sneha , R Siva , W Charles Emmanuel Jebaraj , C George Priya Doss , Zayed Hatem 
Published: May 2019

AbstractAlcohol use disorder (AUD) is a multifactorial psychiatric behavior disorder. Disulfiram is the first approved drug by the Food and Drug Administration for alcohol‐dependent patients, which targets the ALDH2 enzyme. Several genes are known to be involved in alcohol metabolism; mutations in any of these genes are known to be associated with AUD. The E504K mutation in the ALDH2 of the precursor protein or the E487K of the mature protein (E504K/E487K; ALDH2*2 allele) is carried by approximately 8% of the world population. In this study, we aimed to test the known inactive allele ALDH2*2, to validate the use of our extensive computational pipeline (in silico tools, molecular modeling, and molecular docking) for testing the interaction between the ALDH2*2 allele, NAD+, and Disulfiram. In silico predictions showed that the E504K variant of ALDH2 to be pathogenic and destabilizing with the maximum number of prediction in silico tools. Consequently, we studied the effect of this mutation mainly on the interaction between NAD+‐E504K and Disulfiram‐E504K complexes using molecular docking technique, and molecular dynamics (MD) analysis. From the molecular docking analysis with NAD+, we observed that the interaction affinity of the NAD+ decreases with the impact of E504K variant. On the other hand, the drug Disulfiram showed similar interaction in both the native and mutant ALDH2 proteins. Further, the comprehensive MD analysis predicted that the E504K destabilizes the protein and influences the NAD+ and Disulfiram interactions. Our findings reveal that the interaction of NAD+ to the protein is disturbed by the E504K/E487K variant whereas the drug Disulfiram has a similar effect as both native ALDH2 and ALDH2 bearing E504K/E487K variant. This study provides a platform to understand the effect of E504K/E487K on the molecular interaction with NAD+ and Disulfiram.
miR‐148‐3p and miR‐152‐3p synergistically regulate prostate cancer progression via repressing KLF4
Authors: Feng Feng , Liu Hui , Chen Aiping , Xia Qinghua , Zhao Yong , Jin Xunbo , Huang Jianjun 
Published: May 2019

AbstractBackgroundmiR‐148‐3p and miR‐152‐3p as the tumor suppressors have been reported in various cancer types. Our study is aimed to discuss the synergistic effect of miR‐148‐3p and miR‐152‐3p in prostate cancer (PCa).MethodsBioinformatics algorithm and luciferase reporter assays were used to verify whether miR‐148‐3p and 152‐3p could bind with the 3′‐untranslated region (3′‐UTR) of Kruppel‐like factor 4 (KLF4). PCa cell growth in vivo was analyzed using the mouse xenograft tumor model.ResultsmiR‐148‐3p and miR‐152‐3p were reduced in PCa tumor tissues. Moreover, the protein expression of KLF4 was increased in PCa tissues. The 3′‐UTR of KLF4 contained the conserved binding sites with miR‐148‐3p and miR‐152‐3p. The mimics or inhibitors of miR‐148‐3p and/or miR‐152‐3p could downregulated or upregulated KLF4 expression, respectively. miR‐148‐3p and miR‐152‐3p‐induced PCa cell growth inhibition were observed both in vivo and in vitro. KLF4 overexpression had the ability to neutralize the antitumor effect of miR‐148‐3p/152‐3p in vivo and in vitro.ConclusionmiR‐148‐3p/152‐3p family could serve as tumor suppressors in PCa via repressing KLF4.
Retracted: Long noncoding RNA LINC00052 inhibits colorectal cancer metastasis by sponging microRNA‐574‐5p to modulate CALCOCO1 expression
Authors: Yu Gangfeng , Xiong Dongmei , Liu Zhengshu , Li Yongguo , Chen Ke , Tang Hua 
Published: May 2019

AbstractThe dysregulation of long‐chain noncoding ribonucleic acid (lncRNA) is a common phenomenon in many human cancers. Some studies on the biological function of long intergenic non‐protein‐coding RNA 52 (LINC00052) in cancer indicate that this gene can act as either oncogene or tumor suppressor in some kinds of cancers, such as breast cancer, gastric cancer, liver cancer, and lung cancer. However, the biological function of LINC00052 in colorectal cancer (CRC) has not been studied. Quantitative reverse‐transcription polymerase chain reaction (qRT‐PCR) and Western blot (WB) techniques were applied to detect the expression levels of LINC00052, miR‐574‐5p, and calcium‐binding and coiled‐coil domain 1 (CALCOCO1) in CRC cells and tissues. We authenticated the biological function of LINC00052 and miR‐574‐5p in CRC, and find some target genes for LINC00052 and miR‐574‐5p via bioinformatics methods. Dual‐luciferase reporter gene assay was performed to identify the interaction between LINC00052 and miR‐574‐5p or CALCOCO1 and miR‐574‐5p. The results demonstrated that LINC00052 was downregulated in CRC tissues compared with their adjacent tissues. And LINC00052 could suppress CRC cells metastasis both in vivo and in vitro. Beyond that, miR‐574‐5p was upregulated in CRC tissues, and as an oncogene, it accelerated CRC cell migration and invasion. More importantly, the results of our research demonstrated that LINC00052 could regulate the expression of CALCOCO1 via sponging miR‐574‐5p in CRC. Overall, our study illuminated the lncRNA‐miRNA functional networks in CRC, and these results might provide a new research direction for the diagnosis and treatment of CRC.
LXRα‐mediated downregulation of EGFR suppress colorectal cancer cell proliferation
Authors: Liang Xiaolong , Cao Yi , Xiang Song , Xiang Zheng 
Published: May 2019

AbstractLiver X receptors (LXRs) are members of the nuclear receptor family, including the LXRα (NR1H3) and LXRβ (NR1H2) subtypes, which are related to the metabolism of glucose and cholesterol and possess anti‐inflammatory functions. Mounting evidence has linked LXRs to the inhibition of cell proliferation in a variety of cancers. We revealed a differential distribution for NR1H3, but not for NR1H2, in colorectal cancer and adjacent normal tissues. We found that NR1H3 enhanced the inhibitory action of GW3965, an agonist of LXRs, on the proliferation of colorectal cancer cells. Upregulation of NR1H3 enhanced the inhibition of cell proliferation by GW3965 while silencing of NR1H3 attenuated the inhibitory effect of GW3965 on cell proliferation. Bioinformatic prediction and luciferase assays showed that NR1H3 was able to inhibit the activity of the epidermal growth factor receptor (EGFR) promoter. Moreover, we demonstrated that activation of NR1H3 inhibited the growth of transplanted tumors in an animal experiment, with the inhibition accompanied by downregulation of EGFR. Our findings suggest that NR1H3 controls cell proliferation by affecting EGFR promoter activity. The high expression of EGFR was due to the downregulation of NR1H3 which is a novel molecular mechanism in the development of colorectal cancer.
Experimental study of influence of composition on radiopacity of fiber post materials
Authors: Erik Ayşe Aydoğmuş , Erik Cevat Emre , Yıldırım Derya 
Published: May 2019

AbstractThis experimental study aims to evaluate the radiopacity of various fiber post materials and to determine the effects of material composition as analyzed by energy‐dispersive X‐ray spectrophotometry (EDS; EDAX Team Software; EDAX, Inc., Mahwah, NJ) on radiopacity. Five specimens of seven fiber post materials with 2‐mm thickness were prepared and digital radiographs were taken with an aluminum stepwedge (SW) and 2‐mm‐thick tooth slice. The mean gray values (MGVs) of specimens were measured using the histogram function of a computer graphics program (Adobe Photoshop CS6; Adobe System, Inc., San Jose, CA). The MGVs of fiber post materials were compared with an aluminum SW and dentin of equal thickness. The fiber post specimens were examined by scanning electron microscopy and EDS analysis performed for the elementary analysis of material composition. The MGVs of fiber posts ranged between 83.67 ± 3.64 and 57.80 ± 7.08 pixels. Materials were sorted in descending order of MGV as follows: Reforpost, Carbopost, D.T. Light‐Post, Easypost, Glassix Radiopaque, Dentolic Glass Fiber Post, and RelyX Fiber Post. All fiber posts demonstrated significantly higher radiopacity values than 2‐mm‐thick aluminum (p < .05). EDS analysis results indicated that the evaluated fiber posts included various elements for radiopacity in different ratios. All tested fiber post materials showed radiopacity values above the minimum recommendations of the International Organization for Standardization. EDS analysis results indicated that each manufacturer used different compositions of elements like zirconium, barium, titanium, and iron for achieving radiopacity in materials.
Colonoscopy technologies for diagnostics and drug delivery
Authors: Ahmed Rajib , Santhirakumar Krieshshanthan , Butt Haider , Yetisen Ali K. 
Published: May 2019

AbstractWith a global increase of colorectal cancer, inflammatory bowel disease and other colon‐related illnesses, advanced technologies are needed for imaging of the colon and localized drug delivery. Optical colonoscopy is the gold standard for imaging of the colon. However, existing colonoscopy approaches have a high adenoma misdiagnosis rate, which can be lethal for patients. This article reviews the emergence of virtual colonoscopy, dye‐based chromoendoscopy, electronic chromoendoscopy and capsule endoscopy in diagnosis. Flexible spectral imaging colour enhancement, the use of second‐generation capsule endoscopy and i‐scan were described. Moreover, a drug delivery system using capsule endoscopy was discussed. Finally, this review includes market analyses of commercial products, clinical trials and future prospects of colonoscopy devices.