bluuebunny/crossref_metadata_2025_split huggingface dataset:
An investigation of enablers and inhibitors of crowdfunding adoption: Empirical evidence from startups in China
Authors: Yang Qin , Lee Young‐Chan 
Published: December 2018

AbstractIn recent years, crowdfunding has emerged as a new fundraising technique for startup ventures. Crowdfunding allows small businesses and startups to seek funding from a large number of private investors, the so‐called “crowdfunders.” Crowdfunding is beneficial for startup ventures by offering a variety of financial and nonfinancial benefits such as helping to solve funding difficulties, providing value‐added involvement, facilitating access to further funding, and providing publicity. In contrast, diffusion processes of new business innovations have become increasingly complicatedly and multifaceted in recent years. Potential users today are exposed to a wide range of influences that include word‐of‐mouth communications, network externalities, and social signals. Despite the advantages associated with crowdfunding, the crowdfunding industry faces slow rates of diffusion in the Chinese market because crowdfunding ventures often fail to translate into adoption behavior. This study investigates the enablers and inhibitors of crowdfunding adoption intention from the perspective of startups by employing the two‐factor theory, status quo bias theory, and innovation diffusion theory. These theories allow crowdfunding researchers and platform managers to test the relative influence of both reasons for (enablers) and reasons against (inhibitors) crowdfunding adoption in a single framework. In conclusion, considering the phenomenon of startups in China, the results of this study will fill the paucity of empirical research in the innovation resistance area, shedding light on the motivation of entrepreneurs to avoid crowdfunding as a financing course as well as providing crowdfunding managers and policymakers with strategic recommendations.
MicroRNA‐101 protects bladder of BOO from hypoxia‐induced fibrosis by attenuating TGF‐β‐smad2/3 signaling
Authors: Wang Ning , Duan Liujian , Ding Jie , Cao Qifeng , Qian Subo , Shen Haibo , Qi Jun 
Published: December 2018

AbstractBladder outlet obstruction is a common disease, which always evokes urinary bladder wall remodeling significantly. It has been suggested that bladder outlet obstruction can make the bladder progression from inflammation to fibrosis, and hypoxia may play a vital role. It has been found the expression of microRNA‐101 varied in bladder after BOO. But what role microRNA‐101 and hypoxia play in bladder is not well known. This study is to investigate the mechanism of microRNA‐101 and hypoxia in fibrosis of bladder after BOO. We found the expression of microRNA‐101 and hif‐1α increased in bladder after BOO. Hypoxia could promote the expression of extracellular matrix subtypes and microRNA‐101 in BSMCs. When microRNA‐101b was translated into BSMCs, the smad2/3 signaling pathway was found to repress. Dual luciferase reporter detected that microRNA‐101b attenuated the TGF‐β signaling pathway by inhibiting the expression of TGFβR1. Then, we conclude microRNA‐101b is induced by hypoxia and represses fibrosis of BSMCs by inhibiting the expression of TGFβR1 through TGF‐β signaling pathway, and it may be an anti‐fibrotic miRNA for therapy. © 2018 IUBMB Life, 71(1):235–243, 2019
Implications of the presence of an emergency medicine pharmacist during critical care trauma patient resuscitation
Authors: Lamkin Lynn , Lindsey Savannah , Weant Kyle , Shoff Hugh , Pinkston Christina 
Published: December 2018

PurposeThe available literature has shown that the presence of an Emergency Medicine Pharmacist (EMP) is associated with decreased time to medication procurement, a reduction in medication errors, and overall cost avoidance. However, there is limited literature that systematically evaluates the impact of EMPs in the treatment of critically ill trauma patients presenting to the emergency department (ED).MethodsThis study was a retrospective chart review evaluating 1082 adult patients presenting to the critical care area (CCA) of the ED at the University of Louisville Hospital in Louisville, Kentucky for trauma evaluation from July 2014 to December 2014. The study group consisted of patients presenting to the CCA when an EMP was present. Primary outcomes included time to administration of antibiotics, analgesia medication, sedation medication, rapid sequence intubation (RSI), and anticoagulation reversal. Secondary outcomes included time to administration of appropriate antibiotics at an appropriate dose and vaccination administration.ResultsThe presence of an EMP was associated with a statistically significant decreased median time from triage to the administration of an analgesic medication (11 minutes [interquartile range (IQR) 8‐27] vs 13 minutes [IQR 8.5‐20], P = 0.04). There was no statistically significant difference in triage time to antibiotic administration, RSI, sedation medication administration, or anticoagulation reversal. Patients in the EMP group were more likely to receive appropriate empiric antibiotics compared with the control group (80.7% vs 52.2%, P = 0.01).ConclusionThe presence of an EMP was associated with decreased time to analgesia medication administration as well as an increased likelihood of the administration of appropriate empiric antibiotics in critically ill trauma patients.
Effect of single‐nucleotide polymorphism in pri‐microRNA‐124 on poststroke motor function recovery
Authors: Chen Shangjun , Chen Yuhong , Gao Yadong , Zuo Yi , Zhou Xiaowei 
Published: December 2018

AbstractBackgroundStroke is a leading cause of long‐term disability and further one of the main causes of motor impairment. The current study aimed to investigate whether miR‐124 polymorphism (rs531564) influences the motor function of patients after stroke.MethodsIn total, 56 patients with stroke‐induced motor dysfunction were enrolled. Box and block test (BBT) and Fugl‐Meyer assessment (FMA) were performed to evaluate the motor functions in all participants. Computation analysis, luciferase activity, PCR assays, and Western blot analysis were performed to reveal the molecular mechanism underlying the effect of miR‐124 polymorphism on motor functions.ResultsThe 56 participants were genotyped as CC, CG, and GG, respectively. The serum miR‐124 was significantly upregulated in the CC group than that in the GC and GG groups. According to the result of FMA or BBT, there was no obvious difference in upper and lower limb motor functions between CC and CG/GG groups 1 week after the treatment. In addition, scores of BBT and FMA exhibited apparent improvement in both groups at 1 month and 3 months after the treatment. Furthermore, improvements in the CG/GG groups were more significant as compared with those in the CC group. CDK4 was a target of miR‐124, and the effect of miR‐124 on the motor function recovery might be mediated by CDK4.ConclusionThe presence of a minor allele, G, of miR‐124 polymorphism (rs531564) reduced the expression of miRNA and upregulated the expression of CDK4, which may contribute to the effect of rs531564 on the motor function recovery in poststroke patients.
LncRNA‐MIAT regulates fibrosis in hypertrophic cardiomyopathy (HCM) by mediating the expression of miR‐29a‐3p
Authors: Zhou Jing , Zhou Yu , Wang Cong‐xia 
Published: December 2018

AbstractAimThis study aimed to investigate the molecular mechanism underlying the fibrosis in hypertrophic cardiomyopathy (HCM).MethodQuantitative real‐time polymerase chain reaction (qRT‐PCR) was performed to measure the expression of potentially relevant microRNAs (miRNAs) and long noncoding RNAs (lncRNAs) in patients with HCM suffering from fibrosis and patients with HCM free of fibrosis. In addition, the regulatory relationship between lncRNAs and miR‐29a was studied using a luciferase assay. Subsequently, area under the receiver‐operating characteristics (ROC) curve (AUC) analysis was conducted to predict the diagnostic value of myocardial infarction‐associated transcript (MIAT), miR‐29a, H19, and MEG3 in patients with HCM. Finally, the predicted regulatory relationship betwe en miR‐29a and MIAT was validated by transfecting cells with different plasmids.ResultmiR‐29a and MIAT were differently expressed between the fibrosis (+) HCM group and the fibrosis (−) HCM group, thus establishing a negative relationship between the expression of these two genes. In addition, both MIAT and miR‐29a showed the ability to accurately predict the prognosis in patients with HCM. Furthermore, the luciferase activity of wild‐type MIAT was evidently suppressed in cells transfected with miR‐29a mimics, suggesting that the expression of miR‐29a was apparently downregulated in the presence of MIAT.ConclusionThe results obtained in this study collectively indicated that the MIAT might be associated with the development of fibrosis (+) HCM via negatively regulating the expression of miR‐29a.
A long noncoding RNAs signature to improve survival prediction in endometrioid endometrial cancer
Authors: Xu Qinyang , Yang Qin , Zhou Yang , Yang Bikang , Jiang Rongzhen , Ai Zhihong , Teng Yincheng 
Published: December 2018

AbstractPurposeThe dysregulation of long noncoding RNAs (lncRNAs) has been reported to be correlated to carcinogenesis and cancer progression. Endometrial cancer (EC), arising from the endometrium or the inner lining of the uterus, is one of the most common gynecological malignancies. We aim to explore the prognostic value of the lncRNAs in patients with endometrioid endometrial cancer (EEC) and to identify the potential lncRNA signature for predicting survival of patients with EEC.MethodsWe performed a genome‐wide analysis of the lncRNA expression profiling in The Cancer Genome Atlas (TCGA)‐Uterine Corpus Endometrial Carcinoma database (408 EEC) to identify the prognosis related lncRNAs for the EEC. The patients with EEC were randomly divided into a training set (204 for endometrioid) and a testing set (204 for endometrioid). The lncRNA signature was identified in the training set, and then independently validated in the testing set and the complete set (training set plus testing set).ResultsWe developed a nine‐lncRNA signature‐based risk score in the patients with EEC. The risk score based on the novel lncRNAs signature was able to separate patients of training set into high‐and low‐risk groups with significantly different overall survival and progression‐free survival. These can also be successfully confirmed in the testing set and complete set.ConclusionA nine‐lncRNA expression signature was identified and validated which can predict EEC patient’s survival. These findings may have important implications in the understanding of the potential therapeutic methods for patients with EEC.
Electrospun poly‐l‐lactic acid/polyvinyl alcohol nanofibers improved insulin‐producing cell differentiation potential of human adipose‐derived mesenchymal stem cells
Authors: Ojaghi Mohammad , Soleimanifar Fatemeh , Kazemi Alireza , Ghollasi Marzieh , Soleimani Masoud , Nasoohi Nikoo , Enderami Seyed Ehsan 
Published: December 2018

AbstractCombination of adipose‐derived mesenchymal stem cells (ADSCs) and synthetic materials in terms of pancreatic tissue engineering can be considered as a treatment of diabetes. This study aimed to evaluate the differentiation of human ADSCs to pancreatic cells on poly‐l‐lactic acid/polyvinyl alcohol (PLLA/PVA) nanofibers as a three‐dimensional (3D) scaffold. Mesenchymal stem cells (MSCs) were characterized for mesenchymal surface markers by flow cytometry. Then ADSCs were seeded on 3D scaffolds and treated with pancreatic differentiation medium. Immunostaining assay showed that ADSCs were very efficiently differentiated into a relatively homogeneous population of insulin‐producing cells. Moreover, real‐time RT‐PCR results revealed that pancreas‐specific markers were highly expressed in 3D scaffolds compared with their expression in tissue culture plates and this difference in expression level was significant. In addition, insulin and C‐peptide secreted in response to varying concentrations of glucose in the 3D scaffold group was significantly higher than that in 2D culture. The results of the present study confirmed that PLLA/PVA scaffold seeded with ADSCs could be a suitable option in pancreatic tissue engineering.
Effect of Tribulus terrestris saponins on proliferation of adipose‐derived mesenchymal stem cells
Authors: Patel Apurva , Soni Anjali , Sharma Preeti 
Published: December 2018

AbstractAdipose‐derived mesenchymal stem cells (ASCs) transplantation has shown great promise for treating various diseases; however, poor viability of transplanted ASCs because of oxidative stress has limited its therapeutic efficiency. Plant saponins are recently been reported to have antioxidant activity tested in various cancer cell lines. This study was designed to investigate the protective effects of Tribulus terrestris saponins (TTS) on the proliferation of ASCs. The cytotoxic activity of hydrogen peroxide (H2O2) was determined by treating ASCs with 100, 200, 300, 400, and 500 µM H2O2 for 2 hours. ASCs were treated with 6.25, 12.5, 25, 50, and 100 µg/mL concentrations of TTS for the proliferative experiment. To check the protective effect of TTS, experiments were designed in two ways. In one set, ASCs were pretreated with different concentrations of TTS for 2 hours and then apoptosis was induced by treating them with 400 µM H2O2 for next 2 hours, while in other set, ASCs were first treated with 400 µM H2O2 for 2 hours and subsequently with different concentrations of TTS for 24 hours. The vitality and proliferation potential of cells were detected by 3‐(4,5‐Dimethylthiazol‐2‐Yl)‐2,5‐diphenyltetrazolium bromide (MTT) assay. The result of the current study shows that in response to stress‐induced by H2O2 at concentration of 400 µM, ASCs underwent growth arrest and cell viability was reduced to half while treatment with TTS before and after H2O2 exposure significantly prevents premature apoptosis. The findings suggest that saponins may act as an effective protective agent against oxidative stress–induced ASCs apoptosis.
Overexpression of Hes1 is involved in sensitization of K562 cells to Imatinib
Authors: Eskandari Sedigheh , Yazdanparast Razieh 
Published: December 2018

AbstractTyrosine kinase inhibitor (TKI)‐based therapy has created promising results among much chronic myeloid leukemia (CML) patients. Imatinib as a relatively specific inhibitor of Bcr‐Abl is at present one of the undisputed therapeutic agent for newlydiagnosed patients with CML. However, the occurrence of imatinib‐resistance enlightens the urgent need to identify other therapeutic agents against CML. Juglone (5‐hydroxy‐2‐methyl‐1, 4‐naphthoquinone) exerts cytotoxic effects against various human cancer cell lines. However, the mechanisms through which Juglone induces anticancer effects in CML especially in comparison with imatinib treatment remain unknown. Our results revealed that Juglone‐inhibited K562 cells growth through inducing apoptosis. Based on our Western blot analyses, Juglone significantly reduced p‐Akt levels and increased the expression level of Forkhead box O1 (FoxO1) and FoxO3a proteins. Moreover, hairy/enhancer of split‐1 (Hes1) protein, overexpressed under the influence of Juglone, is apparently involved in Juglone‐induced apoptosis among K562 cells. Conversely, treatment with imatinib attenuated Hes1 protein expression. Considering the different functional mechanism of Juglone compared with imatinib, it seems that Juglone treatment could be a useful alternative strategy for the treatment of patients with imatinib‐resistance.
Wnt signaling reprograms metabolism in dental pulp stem cells
Authors: Uribe‐Etxebarria Véronica , Agliano Alice , Unda Fernando , Ibarretxe Gaskon 
Published: December 2018

AbstractHuman dental pulp stem cells (DPSCs) can differentiate to a wide range of different cell lineages, and share some gene expression and functional similarities with pluripotent stem cells. The stemness of DPSCs can also be pharmacologically enhanced by the activation of canonical Wnt signaling. Here, we examined the metabolic profile of DPSCs during reprogramming linked to Wnt activation, by a short (48 hr) exposure to either the GSK3‐β inhibitor BIO (6‐bromoindirubin‐3´‐oxine) or human recombinant protein WNT‐3A. Both treatments largely increased glucose consumption, and induced a gene overexpression of pyruvate and mitochondrial acetyl‐coA producing enzymes, thus activating mitochondrial tricarboxylic acid cycle (TCA) metabolism in DPSCs. This ultimately led to an accumulation of reducing power and a mitochondrial hyperpolarization in DPSCs. Interestingly, Nile Red staining showed that lipid fuel reserves were being stored in Wnt‐activated DPSCs. We associate this metabolic reprogramming with an energy‐priming state allowing DPSCs to better respond to subsequent high demands of energy and biosynthesis metabolites for cellular growth. These results show that enhancement of the stemness of DPSCs by Wnt activation comes along with a profound metabolic remodeling, which is distinctly characterized by a crucial participation of mitochondrial metabolism.
Rapamycin enhances growth inhibition on urothelial carcinoma cells through LKB1 deficiency‐mediated mitochondrial dysregulation
Authors: Whang Young Mi , Kim Myeong Joo , Cho Min Ji , Yoon Hoyub , Choi Young Wook , Kim Tae‐Hyoung , Chang In Ho 
Published: December 2018

AbstractRapamycin, a mammalian target of rapamycin (mTOR) inhibitor, has significant potential for application in the treatment of urothelial carcinoma (URCa) of the bladder. Previous studies have shown that regulation of the AMP‐activated serine/threonine protein kinase (AMPK)–mTOR signaling pathway enhances apoptosis by inducing autophagy or mitophagy in bladder cancer. Alteration of liver kinase B1 (LKB1)‐AMPK signaling leads to mitochondrial dysfunction and the accumulation of autophagy‐related proteins as a result of mitophagy, resulting in enhanced cell sensitivity to drug treatments. Therefore, we hypothesized that LKB1 deficiency in URCa cells could lead to increased sensitivity to rapamycin by inducing mitochondrial defect‐mediated mitophagy. To test this, we established stable LKBI‐knockdown URCa cells and analyzed the effects of rapamycin on their growth. Rapamycin enhanced growth inhibition and apoptosis in stable LKB1‐knockdown URCa cells and in a xenograft mouse model. In spite of the stable downregulation of LKB1 expression, rapamycin induced AMPK activation in URCa cells, causing loss of the mitochondrial membrane potential, ATP depletion, and ROS accumulation, indicating an alteration of mitochondrial biogenesis. Our findings suggest that the absence of LKB1 can be targeted to induce dysregulated mitochondrial biogenesis by rapamycin treatment in the design of novel therapeutic strategies for bladder cancer.
Type I IFNs in the female reproductive tract: The first line of defense in an ever-changing battleground
Authors: Cumming Helen E , Bourke Nollaig M 
Published: December 2018

Abstract
The primary function of the female reproductive tract (FRT) is to enable successful reproduction, yet the biologic mechanisms required to accomplish this, which include fluctuating sex hormones and tolerance of semen and a semi-allogeneic fetus, can leave this unique mucosal environment susceptible to pathogenic challenge. Consequently, the FRT has evolved specialized innate and adaptive immune responses tailored to protecting itself from infection without compromising reproductive success. A family of innate immune cytokines that has emerged as important regulators of these immune responses is the type I IFNs. Type I IFNs are typically rapidly produced in response to pathogenic stimulation and are capable of sculpting pleotropic biologic effects, including immunomodulation, antiproliferative effects, and inducing antiviral and bactericidal molecules. Here, we review what is currently known about type I IFN-mediated immunity in the FRT in human, primate, and murine models and explore their importance with respect to three highly relevant FRT infections: HIV, Zika, and Chlamydia.
Type 1 IFNs in the epithelium in the female reproductive tract. Constitutively expressed IFNɛ provides a primary barrier to prevent initial infection, whereas IFNα and IFNβ are rapidly induced to respond once pathogens are detected.
Surrogate‐assisted design of microstrip corporate feeds integrated with linear microstrip array apertures for required sidelobe levels
Authors: Koziel Slawomir , Ogurtsov Stanislav 
Published: December 2018

AbstractA systematic computer‐aided design of low‐sidelobe linear microstrip antenna arrays is proposed. It starts from identifying the corporate feed architecture which is optimal for a given excitation taper under constrains imposed on the power splits within the feed. The novelty of the approach includes utilization of a numerically efficient simulation‐based kriging model of unequal split microstrip junctions for implementation of the optimal microstrip feed, and simulation‐based tuning of the excitation taper. The tuning is carried out with surrogate‐assisted optimization which is based on the electromagnetic simulations of an integrated array circuit comprising the aperture and the feed. Additionally, in‐phase excitation of the array aperture radiators is ensured with a simulation‐based correction of the corporate feed microstrip branches. The approach is implemented iteratively to realize the nominal sidelobe level. The approach is demonstrated with design of a 12‐element H‐plane 25‐dB sidelobe level Tschebyscheff array. Experimental validation is provided.
Downregulation of tyrosine hydroxylase phenotype after AAV injection above substantia nigra: Caution in experimental models of Parkinson’s disease
Authors: Albert Katrina , Voutilainen Merja H. , Domanskyi Andrii , Piepponen T. Petteri , Ahola Sari , Tuominen Raimo K. , Richie Christopher , Harvey Brandon K. , Airavaara Mikko 
Published: December 2018

AbstractAdeno‐associated virus (AAV) vector‐mediated delivery of human α‐synuclein (α‐syn) gene in rat substantia nigra (SN) results in increased expression of α‐syn protein in the SN and striatum which can progressively degenerate dopaminergic neurons. Therefore, this model is thought to recapitulate the neurodegeneration in Parkinson's disease. Here, using AAV to deliver α‐syn above the SN in male and female rats resulted in clear expression of human α‐syn in the SN and striatum. The protein was associated with moderate behavioral deficits and some loss of tyrosine hydroxylase (TH) in the nigrostriatal areas. However, the immunohistochemistry results were highly variable and showed little to no correlation with behavior and the amount of α‐syn present. Expression of green fluorescent protein (GFP) was used as a control to monitor gene delivery and expression efficacy. AAV‐GFP resulted in a similar or greater TH loss compared to AAV‐α‐syn and therefore an additional vector that does not express a protein was tested. Vectors with double‐floxed inverse open reading frame (DIO ORF) encoding fluorescent proteins that generate RNA that is not translated also resulted in TH downregulation in the SN but showed no significant behavioral deficits. These results demonstrate that although expression of wild‐type human α‐syn can cause neurodegeneration, the variability and lack of correlation with outcome measures are drawbacks with the model. Furthermore, design and control selection should be considered carefully because of conflicting conclusions due to AAV downregulation of TH, and we recommend caution with having highly regulated TH as the only marker for the dopamine system.