bluuebunny/crossref_metadata_2025_split huggingface dataset:
Intraoperative multispectral and hyperspectral label‐free imaging: A systematic review of in vivo clinical studies
Authors: Shapey Jonathan , Xie Yijing , Nabavi Eli , Bradford Robert , Saeed Shakeel R , Ourselin Sebastien , Vercauteren Tom 
Published: March 2019

AbstractMultispectral and hyperspectral imaging (HSI) are emerging optical imaging techniques with the potential to transform the way surgery is performed but it is not clear whether current systems are capable of delivering real‐time tissue characterization and surgical guidance. We conducted a systematic review of surgical in vivo label‐free multispectral and HSI systems that have been assessed intraoperatively in adult patients, published over a 10‐year period to May 2018. We analysed 14 studies including 8 different HSI systems. Current in‐vivo HSI systems generate an intraoperative tissue oxygenation map or enable tumour detection. Intraoperative tissue oxygenation measurements may help to predict those patients at risk of postoperative complications and in‐vivo intraoperative tissue characterization may be performed with high specificity and sensitivity. All systems utilized a line‐scanning or wavelength‐scanning method but the spectral range and number of spectral bands employed varied significantly between studies and according to the system's clinical aim. The time to acquire a hyperspectral cube dataset ranged between 5 and 30 seconds. No safety concerns were reported in any studies. A small number of studies have demonstrated the capabilities of intraoperative in‐vivo label‐free HSI but further work is needed to fully integrate it into the current surgical workflow.
Bowman‐Birk inhibitor modifies transcription of autophagy and apoptosis genes in an in vitro model of Alzheimer's disorder
Authors: Akbari Samaneh , Akrami Hassan , Mostafaei Ali , Kiani Sudabeh 
Published: March 2019

AbstractAlzheimer, a current neurodegenerative disorder has adverse effects on memory and behavior. β‐Amyloid peptide accumulations are the hallmarks of Alzheimer. Dysfunction of autophagy and apoptosis is detected in Alzheimer's disease. The effect of Bowman‐Birk inhibitor (BBI), purified from soybean, was investigated in autophagy and apoptosis in Alzheimer treatment. Treated‐PC12 cells with 1000 nM HgCl2 induced amyloid β (Aβ) accumulation. Treatment of PC12 cells with 1000 nM HgCl
2 and then 500 μg/mL BBI could decrease the expression ratio of Bax/Bcl2 and increase the expression of beclin1, Bnip3, Atg5, and autophagy‐related genes. These results indicated that BBI could inhibit Aβ accumulation by inducing autophagy, and also the neuroprotective effect was detected through decreasing apoptosis in the in vitro model of Alzheimer's disease. These results provided further evidence for the potential effectiveness of BBI in the treatment of Alzheimer's disease.
Importin‐4 functions as a driving force in human primary gastric cancer
Authors: Xu Xia , Zhang Xinchao , Xing Huaixin , Liu Zhifang , Jia Jihui , Jin Chunyuan , Zhang Yingjie 
Published: March 2019

AbstractObjectivesImportin‐4 (IPO4) is responsible for transporting histones H3 and H4 into the nucleus for chromatin assembly. But, the role of IPO4 in cancer, especially in gastric cancer (GC), has not been fully understood. We aim to determine the expression and function of IPO4 in GC.Materials and MethodsBioinformatics analysis was used to study the association of IPO4 and GC using GEO data and the Kaplan‐Meier plotter. The quantitative real‐time polymerase chain reaction and Western blot analysis were used to determine the IPO4 level in GC cells and tissues. Small interfering RNAs (siRNAs) were used to knockdown endogenous IPO4 expression in GC cells. Cell counting kit‐8 (CCK‐8), colony formation and transwell assays were used to examine the effect of IPO4 on cell proliferation and migration.ResultsIPO4 mRNA is overexpressed in GC tissues using bioinformatics analysis of three groups’ transcriptome data, and high level of IPO4 is negatively correlated with poor long‐term survival using the Kaplan‐Meier plotter analysis. Western blot analysis further shows that IPO4 protein levels are also overexpressed in GC tissues and a number of GC cell lines. Endogenous IPO4 level can be inhibited by specific siRNA effectively. Importantly, CCK‐8, colony formation, and transwell assays demonstrate that IPO4 knockdown by siRNA impairs GC cell proliferation and migration.ConclusionsOur data suggest that IPO4 contributes to GC progression and poor prognosis, and may function as a driving force in GC progression.
The potential regulatory role of miR16 to the interplay between interferon and transforming growth factor beta pathways through IRF3 and SMAD7 in hepatitis C virus infected patients
Authors: Hany Noha Mohamed , Hammouda Abd‐El‐Rahman M. A. , Nabih Enas Samir , Mohamed Sherif Moneir 
Published: March 2019

AbstractBackgroundThe defensive strategy against hepatitis C virus (HCV) infection depends on two antiviral pathways; interferon (IFN) and transforming growth factor β (TGFβ). We aimed at verifying the relation between TGFβ and IFN antiviral pathways in HCV infection through SMAD7 and IRF3, and whether a possible regulatory role for microRNA‐16 (miR16) on the interplay between IFN and TGFβ signaling pathways exists or not.MethodsWe evaluated miR16, IRF3 and SMAD7 expression by real‐time polymerase chain reaction in HCV infected patients and age and gender matched healthy controls.ResultsmiR16 expression was significantly higher while IRF3 and SMAD7 expression was significantly lower in HCV patients compared with healthy controls. Meanwhile, miR16 was negatively correlated to SMAD7 in HCV patients while IRF3 and SMAD7 were positively correlated.ConclusionsThe interplay between IFN and TGFβ pathways through IRF3 and SMAD7 in the context of immunity against HCV infection could be under the control of miR16.
Inhibition of lncRNA MEG3 protects renal tubular from hypoxia‐induced kidney injury in acute renal allografts by regulating miR‐181b/TNF‐α signaling pathway
Authors: Pang Xinlu , Feng Guiwen , Shang Wenjun , Liu Lei , Li Jingfeng , Feng Yonghua , Xie Hongchang , Wang Junxiang 
Published: March 2019

AbstractEarly damage to transplanted organs initiates excess inflammation that deteriorates existing injury, which is a leading cause of graft loss. Long noncoding RNAs (lncRNAs) are recently thought to play a significant role in cellular homeostasis during pathological process of kidney diseases. The aim of this study was to assess the function and mechanism of lncRNA, maternally expressed gene 3 (MEG3), on early renal allografts pathogenesis. Real‐time polymerase chain reaction (RT‐PCR) analysis found that the levels of MEG3 and miR‐181b‐5p were increased and decreased respectively in grafted kidney. The Western blot assay showed that TNF‐alpha was upregulated in the kidney and in HK‐2 cells. Administering MEG3‐specific small interfering RNA (siRNA) in mice silenced MEG3 expression and protected kidney renal allograft from injury. Bioinformatical analysis and luciferase assay indicated that MEG3 is a target of miR‐181b‐5p. MEG3 inhibition and overexpression promoted and suppressed miR‐181b‐5p levels respectively. In addition, Western blot and immunohistochemical staining suggested that decreased TNF‐alpha expression was observed in the kidney. In contrary to MEG3, miR181b overexpression attenuated hypoxia‐induced HK‐2 cell apoptosis, as well as suppressed hypoxia‐induced TNF‐alpha upregulation. In luciferase reporter assay, we confirmed that miR‐181b directly bound to the 3′‐untranslated region (3′‐UTR) of TNF‐alpha, thereby negatively regulating the TNF‐alpha expression. Our data suggested that MEG3 functions as a competing endogenous RNA for miR‐181b to regulate the TNF‐alpha expression in hypoxia‐induced kidney injury in acute renal allografts.
Plant latex thrombin‐like cysteine proteases alleviates bleeding by bypassing factor VIII in murine model
Authors: Urs Amog P. , Rudresha G. V. , Manjuprasanna V. N. , Suvilesh K. N. , Gowda M. D. Milan , Yariswamy M. , Hiremath Vilas , Ramakrishnan Chandrasekaran , Savitha M. N. , Jayachandra K. , Sharanappa P. , Vishwanath B. S. 
Published: March 2019

AbstractHemostasis is a tightly regulated process which maintains a fluid state of blood within the vasculature and provides thrombotic response upon tissue injury. Various scientific studies have implicated the role of plant latex proteases in hemostasis using in vitro experiments. However, in vivo models substantiate their role in hemostasis. Therefore, in the present study, the effect of plant latex thrombin‐like proteases (PTLPs) on hemostasis was investigated systematically using mice tail bleeding as a preclinical model. In this direction, latex protease fractions (LPFs), which showed potent thrombin‐like activity, were selected as they act directly on fibrinogen to form clot and quickly stop bleeding. Thrombin‐like activity was exhibited mainly by cysteine proteases. Calotropis gigantea,
Carica papaya, Jatropha curcas, Oxystelma esculentum,
Tabernaemontana divaricata, and
Vallaris solanacea LPFs and papain from
C.
papaya latex significantly reduced bleeding on a topical application in normal and aspirin administered mice. In addition, PTLPs accelerated the clotting of factor VIII deficient plasma, while, papain brought back the clotting time to normal levels acting like a bypassing agent. Further, papain failed to show activity in the presence of specific cysteine protease inhibitor iodoacetic acid; confirming protease role in all the activities exhibited. At the tested dose, PTLPs except
C.
gigantea did not show toxicity. Further, structural and sequence comparison between PTLPs and human thrombin revealed structural and sequence dissimilarity indicating their unique nature. The findings of the present study may open up a new avenue for considering PTLPs including papain in the treatment of bleeding wounds.
Long noncoding RNA TALNEC2 regulates myocardial ischemic injury in H9c2 cells by regulating miR‐21/PDCD4‐medited activation of Wnt/β‐catenin pathway
Authors: Hao Lin , Wang Juan , Liu Na 
Published: March 2019

AbstractThe goal of this study was to explore the role of tumor associated long noncoding RNA expressed on chromosome 2 (TALNEC2) in protecting against myocardial ischemic injury, as well as its underlying molecular mechanism. We established a cell model of myocardial injury through treating H9c2 cells with hypoxia, and the expression level of TALNEC2 was analyzed. Further, in vitro studies investigated the functional role of TALNEC2 dysregulation in hypoxia injury by assessing cell proliferation, migration, invasion, and apoptosis. Moreover, the expression of miR‐21 was determined after dysregulation of TALNEC2, and whether TALNEC2‐regulated hypoxia injury in H9c2 cells via regulating miR‐21 expression were explored. Furthermore, the regulatory relationship between TALNEC2 and Wnt/β‐catenin pathway was also investigated. TALNEC2 was highly expressed in the serum from patients with myocardial ischemic compared with that in healthy persons. Hypoxia‐induced injury in H9c2 cells. Overexpression of TALNEC2 aggravated hypoxia injury in H9c2 cells. TALNEC2 could negative regulate the miR‐21 expression, and overexpression of TALNEC2 aggravated hypoxia injury by downregulation of miR‐21. Moreover, miR‐21 negatively regulated the PDCD4 expression, and PDCD4 was a target of miR‐21. Further studies disclosed that the overexpression of TALNEC2 further activated the Wnt/β‐catenin pathway in hypoxia‐treated H9c2 cells, implying that the Wnt/β‐catenin pathway was a downstream mechanism mediating the role of TALNEC2 in regulating hypoxia injury in H9c2 cells. These findings confirmed the key functions of TALNEC2 in regulating myocardial ischemic injury. Upregulation of TALNEC2 may aggravate hypoxia injury in H9c2 cells via regulating miR‐21/PDCD4‐medited activation of the Wnt/β‐catenin pathway. TALNEC2 may serve as a promising therapeutic target in myocardial ischemia.
A comprehensive study of CD44 rs 187115 variant and cancer risk in a central Chinese population
Authors: Chen Bifeng , Yi Can , Wang Jingdong , Wang Jieling , Zhang Jingli , Gu Xiuli , Feng Xianhong 
Published: March 2019

AbstractThe rs187115, an intronic variant of CD44 gene, has been previously reported to play a potential role in genetic susceptibility to cancer. Here, we comprehensively examined the association between CD44 rs187115 variant and cancer risk (breast cancer, cervical cancer, lung cancer, gastric cancer, liver cancer, colon cancer, and rectal cancer) in a central Chinese population. The rs187115 variant was genotyped with the polymerase chain reaction‐restriction fragment length polymorphism assay. In this study, we observed that rs187115 was associated with the risk of cervical, lung, and liver cancer, but not with the risk of breast, gastric, colon, rectal or colorectal cancer. Of note, the G allele and G allele genotypes of rs187115 conferred an increased risk of cervical, lung, and liver cancer. To improve the statistical strength, a followed meta‐analysis was conducted. The results demonstrated that rs187115 was significantly associated with cancer risk, and the significant association remained in the stratification analysis by ethnicity, genotyping method, and cancer type. Collectively, the CD44 rs187115 variant may be associated with the risk of cervical, lung, and liver cancer in the central Chinese population, and may be used as a potential biomarker for cancer predisposition in the Asian population, especially in the Chinese population.
LIMK1 depletion enhances fasudil‐dependent inhibition of urethral fibroblast proliferation and migration
Authors: Liang Ying‐Chun , Li Xiao‐Dong , Wu Yu‐Peng , Ke Zhi‐Bin , Liu Zhang‐Qi , Chen Shao‐Hao , Wei Yong , Zheng Qing‐Shui , Xue Xue‐Yi , Xu Ning 
Published: March 2019

AbstractLIM kinase 1 (LIMK1) is an important regulator of the cell cytoskeleton. This study aimed to examine the role of LIMK1 in mediating the effects of the Rho kinase (ROCK) inhibitor fasudil. In vitro cultures of urethral fibroblasts were divided into LIMK1 knockdown (LIMK1 KD) and LIMK1 control (LIMK1 NC) experimental groups. Each group was incubated with fasudil (50 μmol/L) with or without transforming growth factor β1 (10 ng/mL) for 24 hours. Wound healing and Transwell assays were performed to determine cell migration. Flow cytometry was used to determine apoptosis. LIMK1, collagen I, collagen III, phospho‐myosin light chain (p‐MLC), alpha smooth muscle actin (α‐SMA), and phospho‐Cofilin (p‐Cofilin) expression was examined by Western blot analysis. The expression of LIMK1 was further validated in human urethral scar tissues. Transwell and wound healing assays revealed that the cells of the LIMK1 KD group exhibited significantly attenuated migration, when compared with those of the LIMK1 NC group (
P < 0.05). Cell migration was also attenuated in the LIMK1 KD group treated with fasudil (
P < 0.05). Flow cytometry analysis revealed that apoptosis was higher in the LIMK1 KD group than that in LIMK1 NC group (
P < 0.05). Apoptosis was also enhanced in the LIMK1 KD group treated with fasudil (
P < 0.05). Western blot analysis demonstrated that LIMK1, collagen I, collagen III, p‐MLC, α‐SMA, and p‐Cofilin expression was significantly attenuated in both the fasudil‐treated and untreated LIMK1 KD groups (
P < 0.05). LIMK1 was positively expressed in human urethral scar tissues while it was negatively expressed in normal urethra tissues. In conclusion, loss of LIMK1 expression inhibits the Rho/ROCK pathway‐dependent proliferation and migration via downregulation of collagen I, collagen III, p‐Cofilin, and α‐SMA. LIMK1 loss can also enhance the inhibitory effects of fasudil on the proliferation and migration of urethral fibroblasts.
Genetic variants in promoter regions associated with type 2 diabetes mellitus: A large‐scale meta‐analysis and subgroup analysis
Authors: Wu Ling , Wang Chi Chiu 
Published: March 2019

AbstractBackgroundPromoter plays important roles in regulating transcription of genes. Association studies of genetic variants in promoter region with type 2 diabetes (T2D) risk have been reported, but most were limited to small number of individual genetic variants and insufficient sample sizes. In addition, the effect of study populations and demographic characteristics were often neglected.MethodsIn this study, we conducted a large‐scale meta‐analysis and subgroup analysis of T2D associated genetic variants in the promoter regions to evaluate their contribution to the susceptibility in T2D. Alleles and genotypes from cohort or case‐controlled studies were extracted for future study. Total 41 742 cases and 50 493 controls for three loci were involved in 70 articles.ResultsSeventy case‐controlled studies of three genes with 41 742 cases and 50 493 controls were included. Meta‐analysis showed only rs266729 and rs17300539 of ADIPOQ, and rs1884613, rs2144908, and rs4810424 of
HNF4A were significantly associated with T2D risk. Subgroup analysis showed that both rs266729 and rs17300539 of
ADIPOQ were associated with the risk of T2D in Caucasian population, but only rs266729 of
ADIPOQ in Asian population and rs2144908 in other population including multinational North American. For diagnostic criteria, rs266729 of ADIPOQ and rs2144908 of HNF4A were associated with T2D risk when WHO/ADA diagnostic criteria were used. For genotyping methods, both rs266729 of ADIPOQ and rs2144908 of HNF4A were associated with T2D risk when other than Taqman and Sequencing methods were used.ConclusionsT2D was significantly associated with promoter rs266729, rs17300539, rs1884613, rs2144908, and rs4810424, and the association of T2D risk were affected by study population, diagnostic criteria, and genotype methods.
Up‐regulation of circular RNA hsa_circ_0037909 promotes essential hypertension
Authors: Bao Xingjie , He Xin , Zheng Shuying , Sun Jihan , Luo Yizhe , Tan Ronghui , Zhao Jinshun , Zhong Fade , Zhang Lina 
Published: March 2019

AimsEssential hypertension (EH) is a high prevalence disease facing a public health challenge. People were little known about the genetics of diagnosing the cause of EH. Circular RNAs that have a continuous cycle of covalent closure, without affected by RNA exonuclease, and are more stable and hard to degrade may involve into the molecule regulation mechanism of EH as an important biomedical.MethodsqRT‐PCR was used to analyze circRNAs in total volume of human blood and the induced human aortic endothelial cells (HAECs) and human umbilical vein endothelial cells (HUVECs). Our case‐control study was involved with 48 pairs of case controls with sex and age (±3 years) match. We conducted t test, Pearson's χ2 test, and receiver operating characteristics (ROC) curve analysis for the corresponding analysis.ResultsThe expression level of hsa_circ_0037909 in EH patients was significantly higher than that in the healthy controls (P = 0.007), and the expression level of hsa‐miR‐637 in EH patients was significantly lower in than that in the healthy controls (P = 0.039); the same result appears in the HAECs and HUVECs. Hsa‐miR‐637 (adjusted P = 0.018), hsa_circ_0037909 (adjusted P = 0.005), HDL (adjusted P = 0.024), and serum creatinine (adjusted P = 0.014) were brought into the model which performed logistic regression analysis. The combination of two RNAs was excellent (P < 0.001) through ROC curve analysis. Hsa_circ_0037909 was significantly positively correlated with serum creatinine (P < 0.001) and low‐density lipoprotein (LDL) (P = 0.017).ConclusionsOur findings suggested that the combination of hsa_circ_0037911 and hsa‐miR‐637 may be a significant important biomarker for early diagnosis of EH. Hsa_circ_0037909 may affect serum creatinine or LDL leading to the formation of EH.
Identifying and addressing mental health providers’ perceived barriers to clinical video telehealth utilization
Authors: Perry Kristen , Gold Sari , Shearer Erika M. 
Published: March 2019

AbstractObjectiveClinical video telehealth (CVT) is an innovative modality to provide care directly to Veterans’ homes. Despite prior training initiatives, CVT remains underutilized. This project sought to better understand barriers to implementation and to compare responses of CVT utilizers versus nonutilizers.MethodMental health staff were invited to complete an online anonymous survey on their use of CVT in clinical practice.ResultsA total of 159 mental health staff completed the survey. Although the majority of the sample endorsed personal use of a video chat program, less than half reported using CVT for patient care. Among nonutilizers, lack of training was the most frequently endorsed barrier to CVT use whereas administrative burden was the most frequently endorsed barrier by utilizers.ConclusionsThis study extends existing literature by determining barriers to CVT adoption. It identifies several barriers among utilizers versus nonutilizers. Discussion includes potential guidelines for overcoming barriers to CVT utilization.
Misophonia: A scoping review of research
Authors: Potgieter Iskra , MacDonald Carol , Partridge Lucy , Cima Rilana , Sheldrake Jacqueline , Hoare Derek J. 
Published: March 2019

AbstractObjectiveTo scope the literature describing misophonia populations, management, and research opportunities.MethodLiterature searches for research studies describing patients diagnosed with misophonia, defining a patient profile, or outlining development or testing of an intervention for misophonia. A data extraction form was developed and piloted before data from each article were independently charted by two researchers. Researchers then agreed on a final data set for each article.ResultsThirty‐one records were included. The misophonia population was described in terms of onset age, triggers, reaction, coping strategies, and comorbid conditions. We identified nine outcome measures. Case studies on treatments included cognitive behavioral therapy, counterconditioning, mindfulness and acceptance, dialectical behavioral therapy, and pharmaceuticals. Future research priorities identified included clarifying the phenomenology and prevalence of misophonia, and randomized controlled trials of treatments.ConclusionMisophonia is under‐researched but there are strong foundations for future research to finalize diagnostic criteria, validate outcome measures, and trial treatments.
Melatonin‐mediated regulation of autophagy: Making sense of double‐edged sword in cancer
Authors: Mirza‐Aghazadeh‐Attari Mohammad , Mohammadzadeh Amir , Adib Ali , Darband Saber Ghazizadeh , Sadighparvar Shirin , Mihanfar Ainaz , Majidinia Maryam , Yousefi Bahman 
Published: March 2019

AbstractMuch research has been conducted to discover novel techniques to reverse the process of tumorigenesis and, cure already stablished malignancies. One well‐stablished approach has been the use of organic compounds and naturally found agents such as melatonin whose anticancer effects have been shown in multiple studies, signaling a unique opportunity regarding cancer prevention and treatment. Various agents use a variety of methods to exert their anticancer effects. Two of the most important of these methods are interfering with cell signaling pathways and changing cellular functions, such as autophagy, which is essential in maintaining cellular stability against multiple exogenous and endogenous sources of stress, and is a major tool to evade early cell death. In this study, the importance of melatonin and autophagy are discussed, and the effects of melatonin on autophagy, and its contribution in the process of tumorigenesis are then noted.