bluuebunny/crossref_metadata_2025_split huggingface dataset:
Voltammetric Detection of Aqueous Glyphosate on a Copper and Poly(Pyrrole)‐electromodified Activated Carbon Fiber
Authors: Shrivastava Surabhi , Kumar Arun , Verma Nishith , Chen Bor‐Yann , Chang Chang‐Tang 
Published: November 2020

AbstractAqueous glyphosate (GLYP) was voltammetrically detected using a Cu‐(poly)pyrrole composite electrochemically deposited on activated carbon fiber for the first time in a single‐step method. Differential pulse voltammetry indicated good linearity (R2= 0.9902) in the response over 0.02–12 mg L−1range, with a low limit of detection (0.01 mg L−1). The sensor exhibited reproducibility for soil and fruit samples (RSD values = 2.41 and 3.87%, respectively). The response showed repeatability over 100 consecutive measurements. The response was also unaffected by the interfering substances containing the same functional groups as in GLYP and its metabolite. The method described in this study is facile.
Characterization and electrocatalytic properties of electrospun Pt‐IrO2 nanofiber catalysts for oxygen evolution reaction
Authors: Wang Zhi Ming , Liu Peng , Cao Yan Peng , Ye Feng , Xu Chao , Du Xiao Ze 
Published: November 2020

SummaryIn this study, novel Pt‐IrO2 nanofiber catalysts for oxygen evolution reaction (OER) were successfully prepared using the electrospinning method with a high‐concentration precursor solution. The composition and structure of catalysts were characterized, and the electrocatalytic performance of the nanofiber catalysts in water electrolysis was investigated from various aspects such as overpotential, charge transfer resistance, and exchange current density. Special attention was paid on the effect of Pt/Ir ratio on the electrocatalytic activity of the electrospun nanofibers. The results showed that the Pt‐IrO2 nanofiber catalysts with average fiber diameters ranging from 10 to 100 nm can be successfully obtained by the electrospinning method, and the average diameter decreased with the increase of Pt content. Since a bigger amount of IrO2 content and a thinner fiber structure are all beneficial to the electrocatalytic performance, the Pt‐IrO2 catalysts with Pt:Ir = 1:9 and Pt:Ir = 9:1 both showed better catalytic performance for OER than the commercial IrO2, which was also demonstrated by the lower charge transfer resistance and higher exchange current density. As a result, the overpotentials of Pt‐IrO2 catalysts with Pt:Ir = 1:9 and Pt:Ir = 9:1 are 50 mV and 32 mV lower than the overpotential of the commercial IrO2 at 30 mA cm−2 in 0.5 M H2SO4, respectively. The electrospun Pt‐IrO2 nanofiber catalyst with proper Pt content seems to be very promising since it can not only improve the catalytic performance and the safety of PEM electrolysis cells, but also reduce the amount of more expensive Ir in catalysts.
Effects of kiwi’s pectin methylesterase inhibitor, nanomilling and pasteurization on orange juice quality
Authors: Bazaraa Wael A. , Ammar Abdalla S. , Aqlan Abdulghani M. 
Published: November 2020

AbstractEndogenous pectin methylesterase (PME) is the enzyme responsible for phase separation and cloud loss in orange juice (OJ) manufacturing. The effect of kiwi's PME inhibitor (PMEI), nanomilling, and pasteurization on OJ quality was evaluated. The microbial quality, PME activity, OJ separation, pH, ascorbic acid content and the sensory characteristics of the juice were followed during 5 weeks storage (4°C). PMEI as freeze‐dried kiwi powder (0.3%, w/w) succeeded in inhibiting 89.3% of the OJ PME without affecting the microbial and the sensory quality. Nanomilling of OJ pulp, to prepare nano‐particles OJ (NPOJ), reduced the initial microbial load by 1.65 and 1.83 log for psychrotrophs and yeasts and molds, respectively; significantly (p < .05) inactivated 40.9% of the residual PME activity and the juice separation was significantly reduced by 48.3% (after 14 days of storage). Nanomilling exhibited no effect on OJ pH, but slight (p < .05) decrease in ascorbic acid content was noted. The combination of PMEI with NPOJ resulted in improved OJ stability with reduced separation to 36.4% of that of control. Such combination also allowed to use a lower pasteurization temperature at lower exposure time (60°C/5 min) needed to obtain new NPOJ with comparable high quality as fresh OJ and which has a shelf life of 3 weeks (4°C).
Hepatic Predictors of Mortality in Severe Acute Respiratory Syndrome Coronavirus 2: Role of Initial Aspartate Aminotransferase/Alanine Aminotransferase and Preexisting Cirrhosis
Authors: Frager Shalom Z. , Szymanski James , Schwartz Jonathan M. , Massoumi Hatef S. , Kinkhabwala Milan , Wolkoff Allan W. 
Published: November 2020

The novel coronavirus severe acute respiratory syndrome coronavirus 2 (SARS‐CoV2) is the causative agent of coronavirus disease 2019 (COVID‐19). The presenting symptoms of this virus are variable, and there is an increasing body of literature on risk factors for mortality. The aim of this study was to evaluate the effect of initial aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels and preexisting liver disease, including cirrhosis, in a cohort of patients admitted with COVID‐19 infection at a tertiary care hospital network in the Bronx, New York. We reviewed 3,352 patients who had a positive SARS‐CoV2 nasal swab, were over 18 years of age, and had an associated inpatient admission and discharge (or death) to the Montefiore Medical Center from February 28, 2020, to May 22, 2020. Of these, 39/86 (45%) patients died when the initial ALT was >5 times the upper limit of normal (ULN); 115/230 (50%) patients died when the initial AST was >3 times the ULN. The mortality of patients without preexisting liver disease was 26.6% compared to a mortality rate of 29.5% in patients with liver disease. Subgroup analysis showed a mortality of 36.1% in the patients with cirrhosis. Cirrhosis conferred a hazard ratio for mortality of 1.67 (95% confidence interval, 1.09, 2.55; P = 0.019). The baseline Model for End‐Stage Liver Disease score was not prognostic in the cirrhosis cohort. There was no statistical difference between mortality in patients with a history of compensated or decompensated cirrhosis. The most common cause of death in the cirrhosis cohort was respiratory failure. Conclusion: COVID‐19 hepatitis may lead to poor outcomes in patients who are hospitalized for the disease. Patients with cirrhosis are at a higher risk of COVID‐19‐related mortality.
Conjunctive representation of what and when in monkey hippocampus and lateral prefrontal cortex during an associative memory task
Authors: Cruzado Nathanael A. , Tiganj Zoran , Brincat Scott L. , Miller Earl K. , Howard Marc W. 
Published: November 2020

AbstractAdaptive memory requires the organism to form associations that bridge between events separated in time. Many studies show interactions between hippocampus (HPC) and prefrontal cortex (PFC) during formation of such associations. We analyze neural recording from monkey HPC and PFC during a memory task that requires the monkey to associate stimuli separated by about a second in time. After the first stimulus was presented, large numbers of units in both HPC and PFC fired in sequence. Many units fired only when a particular stimulus was presented at a particular time in the past. These results indicate that both HPC and PFC maintain a temporal record of events that could be used to form associations across time. This temporal record of the past is a key component of the temporal coding hypothesis, a hypothesis in psychology that memory not only encodes what happened, but when it happened.
Factors affecting in‐hospital cost and mortality of patients with stroke: Evidence from a case study in a tertiary hospital in China
Authors: Liu Chuang , Luo Li , Duan Lijuan , Hou Shangyan , Zhang Baoyue , Jiang Yan 
Published: November 2020

AbstractObjectiveThe study aims to investigate the factors causing the difference of stroke patients' in‐hospital cost and study these factors on health outcome in terms of mortality.MethodsEight hundred and sixty‐two in‐patients with stroke in a tertiary hospital in China from 2017 to 2019 were included in the database. Descriptive statistics indexes were used to describe patients' in‐hospital cost and mortality. Based on Elixhauser coding algorithms, multiple linear regression and logistic regressions (LRs) were used to evaluate the impact of factors identified from univariate analysis on in‐hospital cost and mortality, respectively. In addition to LRs, a comparison study was then carried out with random forest, gradient boosting decision tree and artificial neural network.ResultsFactors affecting both cost and mortality are age, discharged day‐of‐week, length of stay, stroke subtype, other neurological disorders, renal failure, fluid and electrolyte disorders and total number of comorbidities.ConclusionWith the increase of age, the mortality rate of in‐patients (except for the juvenile) with stroke increases and the cost of hospitalization decreases. Intracerebral haemorrhage is the most devastating stroke for its highest mortality in short length of stay. Medical services should focus on these specific comorbidities.
MEG3 aggravates hypoxia/reoxygenation induced apoptosis of renal tubular epithelial cells via the miR‐129‐5p/HMGB1 axis
Authors: Mao Huihui , Huang Qiao , Liu Ying 
Published: November 2020

AbstractThe apoptosis of renal tubular epithelial cells (TECs) during ischemia/reperfusion (I/R) facilitates the progression of acute kidney injury (AKI). This study aimed to probe the role of long noncoding RNA maternally expressed 3 (MEG3) in I/R‐induced apoptosis of TECs. In this study, with CoCl2 and hypoxia/reoxygenation treatments, cell models were established to mimic I/R using the human kidney tubular cell line HK‐2. In HK‐2 cells, expression of MEG3 detected using quantitative real‐time polymerase chain reaction (qRT‐PCR), was significantly upregulated after CoCl2 treatment and hypoxia/reoxygenation treatment. The results of cell counting kit‐8 assay and flow cytometry suggested that knockdown of MEG3 significantly increased the viability of HK‐2 cells but inhibited its apoptosis, while overexpression of MEG3 exerted the reverse effects. Additionally, expression levels of interleukin 6 and tumor necrosis factor‐α in the medium were elevated after MEG3 was overexpressed in HK‐2 cells. Together with qRT‐PCR and Western blot analysis, a dual‐luciferase reporter gene assay was used to verify the interactions among MEG3, miR‐129‐5p, and HMGB1. The results demonstrated that in HK‐2 cells, miR‐129‐5p was a target of MEG3, and HMGB1 served as a target gene of miR‐129‐5p. Besides this, compared with the control group, the expression levels of MEG3 and HMGB1 in samples derived from AKI patients were remarkably upregulated, and the expression of miR‐129‐5p was downregulated. Therefore, taken together, we conclude that the overexpression of MEG3 induced by I/R promotes apoptosis of TECs via regulating the miR‐129‐5p/HMGB1 axis.
Insights into the regulatory role and clinical relevance of mediator subunit, MED12, in human diseases
Authors: Srivastava Srishti , Kulshreshtha Ritu 
Published: November 2020

AbstractTranscriptional dysregulation is central to many diseases including cancer. Mutation or deregulated expression of proteins involved in transcriptional machinery leads to aberrant gene expression that disturbs intricate cellular processes of division and differentiation. The subunits of the mediator complex are master regulators of stimuli‐derived transcription and are essential for transcription by RNA polymerase II. MED12 is a part of the CDK8 kinase module of the mediator complex and is essential for kinase assembly and function. Other than its function in activation of the kinase activity of CDK8 mediator, it also brings about transcription repression or activation, in response to several signalling pathways, a function that is independent of its role as a part of kinase assembly. Accumulating evidence suggests that MED12 controls complex transcription programs that are defining in cell fate determination, differentiation, and carcinogenesis. Mutations or differential expression of MED12 manifest in several human disorders and diseases. For instance, MED12 mutations are the gold standard for the diagnosis of several X‐linked intellectual disability syndromes. Further, certain MED12 mutations are categorised as driver mutations in carcinogenesis as well. This is a timely review that provides for the first time a wholesome view on the critical roles and pathways regulated by MED12, its interactions along with the implications of MED12 alterations/mutations in various cancers and nonneoplastic disorders. Based on the preclinical studies, MED12 indeed emerges as an attractive novel therapeutic target for various diseases and intellectual disorders.
GBE attenuates arsenite‐induced hepatotoxicity by regulating E2F1‐autophagy‐E2F7a pathway and restoring lysosomal activity
Authors: Chen Xiong , Wang Dapeng , Sun Baofei , Liu Chunyan , Zhu Kai , Zhang Aihua 
Published: November 2020

AbstractArsenic is an environmental toxicant. Its overdose can cause liver damage. Autophagy has been reported to be involved in arsenite (iAs3+) cytotoxicity and plays a dual role in cell proliferation and cell death. However, the effect and molecular regulative mechanisms of iAs3+ on autophagy in hepatocytes remains largely unknown. Here, we found that iAs3+ exposure lead to hepatotoxicity by inducing autophagosome and autolysosome accumulation. On the one hand, iAs3+ promoted autophagosome synthesis by inhibiting E2F1/mTOR pathway in L‐02 human hepatocytes. On the other, iAs3+ blocked autophagosome degradation partially via suppressing the expression of INPP5E and Rab7 as well as impairing lysosomal activity. More importantly, autophagosome and autolysosome accumulation induced by iAs3+ increased the protein level of E2F7a, which could further inhibit cell viability and induce apoptosis of L‐02 cells. The treatment of Ginkgo biloba extract (GBE) effectively reduced autophagosome and autolysosome accumulation and thus alleviated iAs3+‐induced hepatotoxicity. Moreover, GBE could also protect lysosomal activity, promote the phosphorylation level of E2F1 (Ser364 and Thr433) and Rb (Ser780) as well as suppress the protein level of E2F7a in iAs3+‐treated L‐02 cells. Taken together, our data suggested that autophagosome and autophagolysosome accumulation play a critical role for iAs3+‐induced hepatotoxicity, and GBE is a promising candidate for intervening iAs3+ induced liver damage by regulating E2F1‐autophagy‐E2F7a pathway and restoring lysosomal activity.
GDF11 restricts aberrant lipogenesis and changes in mitochondrial structure and function in human hepatocellular carcinoma cells
Authors: Hernandez Sharik , Simoni‐Nieves Arturo , Gerardo‐Ramírez Monserrat , Torres Sandra , Fucho Raquel , Gonzalez Jonathan , Castellanos‐Tapia Lyssia , Hernández‐Pando Rogelio , Tejero‐Barrera Elizabeth , Bucio Leticia , Souza Verónica , Miranda‐Labra Roxana , Fernández‐Checa José C. , Marquardt Jens U. , Gomez‐Quiroz Luis E. , García‐Ruiz Carmen , Gutiérrez‐Ruiz María C. 
Published: November 2020

AbstractGrowth differentiation factor 11 (GDF11) has been characterized as a key regulator of differentiation in cells that retain stemness features. Recently, it has been reported that GDF11 exerts tumor‐suppressive properties in hepatocellular carcinoma cells, decreasing clonogenicity, proliferation, spheroid formation, and cellular function, all associated with a decrement in stemness features, resulting in mesenchymal to epithelial transition and loss of aggressiveness. The aim of the present work was to investigate the mechanism associated with the tumor‐suppressive properties displayed by GDF11 in liver cancer cells. Hepatocellular carcinoma‐derived cell lines were exposed to GDF11 (50 ng/ml), RNA‐seq analysis in Huh7 cell line revealed that GDF11 exerted profound transcriptomic impact, which involved regulation of cholesterol metabolic process, steroid metabolic process as well as key signaling pathways, resembling endoplasmic reticulum‐related functions. Cholesterol and triglycerides determination in Huh7 and Hep3B cells treated with GDF11 exhibited a significant decrement in the content of these lipids. The mTOR signaling pathway was downregulated, and this was associated with a reduction in key proteins involved in the mevalonate pathway. In addition, real‐time metabolism assessed by Seahorse technology showed abridged glycolysis as well as glycolytic capacity, closely related to an impaired oxygen consumption rate and decrement in adenosine triphosphate production. Finally, transmission electron microscopy revealed mitochondrial abnormalities, such as cristae disarrangement, consistent with metabolic changes. Results provide evidence that GDF11 impairs cancer cell metabolism targeting lipid homeostasis, glycolysis, and mitochondria function and morphology.
PD‐L1 versus tumor mutation burden: Which is the better immunotherapy biomarker in advanced non‐small cell lung cancer?
Authors: Dong Aoran , Zhao Yiming , Li Zhihua , Hu Hai 
Published: November 2020

AbstractPD‐L1 and tumor mutation burden (TMB) are the most widely used immunotherapy biomarkers to identify populations who would attain clinical benefit, with the higher values predicting better therapeutic efficacy. This review addresses the predictive values and unresolved challenges of these two biomarkers. PD‐1 and PD‐L1 inhibitors have induced durable and effective responses in patients with advanced non‐small cell lung cancer, confirmed by multiple clinical trials and real‐world studies. Different clinical trials, involving both PD‐1/PD‐L1 inhibitors alone and combination regimens, adopted either PD‐L1 or TMB to stratify the patients, although the predictive capabilities of these two biomarkers are different. In the first‐line setting, PD‐L1 of 50% or more as a cut‐off value can help select candidates for pembrolizumab or atezolizumab monotherapy; however, these two biomarkers poorly predict the efficacy of immunotherapy combination regimens as first‐line treatments. In the second‐line setting, although patients can benefit from nivolumab regardless of PD‐L1 expression, both PD‐L1 and blood TMB can be used as biomarkers to find patients suitable for atezolizumab. Except for inaccurate predictiveness, there are many unresolved problems with regard to the two biomarkers, such as the lack of standard detection methods, and their susceptibilities to other dynamic changes. The predictive values of TMB and PD‐L1 were low in most circumstances; however, PD‐L1 expression greater than ≥ 50% can help select appropriate patients for pembrolizumab and atezolizumab, respectively, as first‐line monotherapies. Higher PD‐L1 or TMB was associated with greater efficacy for atezolizumab as a second‐line monotherapy.
Salvage living donor liver transplantation for hepatocellular carcinoma recurrence after hepatectomy: Quantitative prediction using ADV score
Authors: Hwang Shin , Song Gi‐Won , Ahn Chul‐Soo , Kim Ki‐Hun , Moon Deok‐Bog , Ha Tae‐Yong , Jung Dong‐Hwan , Park Gil‐Chun , Yoon Young‐In , Lee Sung‐Gyu 
Published: November 2020

AbstractBackgroundSalvage liver transplantation is a definite treatment for recurrent hepatocellular carcinoma (HCC) after hepatectomy. ADV score is calculated by multiplying α‐fetoprotein and des‐γ‐carboxyprothrombin concentrations and tumor volume. Prognostic accuracy of ADV score was assessed in patients undergoing salvage living donor liver transplantation (LDLT) and their outcomes were compared with patients undergoing primary LDLT.MethodsThis study was a retrospective, single‐center, case‐controlled study. Outcomes were compared in 125 patients undergoing salvage LDLT from 2007 to 2018 and in 500 propensity score‐matched patients undergoing primary LDLT.ResultsIn patients undergoing salvage LDLT, median intervals between hepatectomy and tumor recurrence, between first HCC diagnosis and salvage LDLT, and between hepatectomy and salvage LDLT were 12.0, 37.2, and 29.3 months, respectively. Disease‐free survival (DFS, P = .98) and overall survival (OS, P = .44) rates did not differ significantly in patients undergoing salvage and primary LDLT. Pretransplant and explant ADV scores were significantly predictive of DFS and OS in patients undergoing salvage and primary LDLT (P < .001). DFS after prior hepatectomy (P = .52) and interval between hepatectomy and LDLT (P = .82) did not affect DFS after salvage LDLT. Milan criteria and ADV score were independently prognostic of DFS and OS following salvage LDLT, and prognosis of patients within and beyond Milan criteria could be further stratified by ADV score.ConclusionsRisk factors and posttransplant outcomes were similar in patients undergoing salvage and primary LDLT. ADV score is surrogate biomarker for posttransplant prognosis in salvage and primary LDLT recipients. Prognostic model incorporating ADV scores can help determine whether to perform salvage LDLT.
Genetic implications in quality palliative care and preventing opioid crisis in cancer‐related pain management
Authors: Sumitani Masahiko , Nishizawa Daisuke , Hozumi Jun , Ikeda Kazutaka 
Published: November 2020

AbstractThe prevalence of cancer‐related pain is 64% among patients with metastatic, advanced, or terminal cancer, 59% among patients undergoing anticancer treatment, and 33% among patients who completed curative treatment. According to the World Health Organization cancer pain relief guidelines, opioid analgesics are the mainstay analgesic therapy in addition to conventional first‐step analgesics, such as non‐steroidal anti‐inflammatory drugs and acetaminophen. The indications for strong opioids have recently been expanded to include mild‐to‐moderate pain in addition to moderate‐to‐severe pain. The U.S. Centers for Disease Control and Prevention guidelines emphasize that realistic expectations should be weighed against potential serious harm from opioids, rather than relying on the unrealized long‐term benefits of these drugs. Therefore, treatment strategies for both cancer‐related chronic or acute pain have been unfortunately deviated from opioid analgesics. The barriers hindering adequate cancer‐related pain management with opioid analgesics are related to the inadequate knowledge of opioid analgesics (e.g., effective dose, adverse effects, and likelihood of addiction or tolerance). To achieve adequate opioid availability, these barriers should be overcome in a clinically suitable manner. Genetic assessments could play an important role in overcoming challenges in opioid management. To balance the improvement in opioid availability and the prevention of opioid misuse and addiction, the following two considerations concerning opioids and genetic polymorphisms warrant attention: (A) pain severity, opioid sensitivity, and opioid tolerance; and (B) vulnerability to opioid dependence and addiction.