bluuebunny/crossref_metadata_2025_split huggingface dataset:
Theoretical insights of codoping to modulate electronic structure of $$\hbox {TiO}_2$$ and $$\hbox {SrTiO}_3$$ for enhanced photocatalytic efficiency
Authors: Kumar Manish , Basera Pooja , Saini Shikha , Bhattacharya Saswata 
Published: September 2020

Abstract$$\hbox {TiO}_2$$

TiO
2

and $$\hbox {SrTiO}_3$$

SrTiO
3

are well known materials in the field of photocatalysis due to their exceptional electronic structure, high chemical stability, non-toxicity and low cost. However, owing to the wide band gap, these can be utilized only in the UV region. Thus, it’s necessary to expand their optical response in visible region by reducing their band gap through doping with metals, nonmetals or the combination of different elements, while retaining intact the photocatalytic efficiency. We report here, the codoping of a metal and a nonmetal in anatase $$\hbox {TiO}_2$$

TiO
2

and $$\hbox {SrTiO}_3$$

SrTiO
3

for efficient photocatalytic water splitting using hybrid density functional theory and ab initio atomistic thermodynamics. The latter ensures to capture the environmental effect to understand thermodynamic stability of the charged defects at a realistic condition. We have observed that the charged defects are stable in addition to neutral defects in anatase $$\hbox {TiO}_2$$

TiO
2

and the codopants act as donor as well as acceptor depending on the nature of doping (p-type or n-type). However, the most stable codopants in $$\hbox {SrTiO}_3$$

SrTiO
3

mostly act as donor. Our results reveal that despite the response in visible light region, the codoping in $$\hbox {TiO}_2$$

TiO
2

and $$\hbox {SrTiO}_3$$

SrTiO
3

cannot always enhance the photocatalytic activity due to either the formation of recombination centers or the large shift in the conduction band minimum or valence band maximum. Amongst various metal-nonmetal combinations, $$\hbox {Mn}_\text {Ti}\hbox {S}_\text {O}$$

Mn
Ti

S
O

(i.e. Mn is substituted at Ti site and S is substituted at O site), $$\hbox {S}_\text {O}$$

S
O

in anatase $$\hbox {TiO}_2$$

TiO
2

and $$\hbox {Mn}_\text {Ti}\hbox {S}_\text {O}$$

Mn
Ti

S
O

, $$\hbox {Mn}_\text {Sr}\hbox {N}_\text {O}$$

Mn
Sr

N
O

in $$\hbox {SrTiO}_3$$

SrTiO
3

are the most potent candidates to enhance the photocatalytic efficiency of anatase $$\hbox {TiO}_2$$

TiO
2

and $$\hbox {SrTiO}_3$$

SrTiO
3

under visible light irradiation.
Electrophysiological assessment of temporal envelope processing in cochlear implant users
Authors: Gransier Robin , Carlyon Robert P. , Wouters Jan 
Published: September 2020

AbstractCochlear-implant (CI) users rely on temporal envelope modulations (TEMs) to understand speech, and clinical outcomes depend on the accuracy with which these TEMs are encoded by the electrically-stimulated neural ensembles. Non-invasive EEG measures of this encoding could help clinicians identify and disable electrodes that evoke poor neural responses so as to improve CI outcomes. However, recording EEG during CI stimulation reveals huge stimulation artifacts that are up to orders of magnitude larger than the neural response. Here we used a custom-built EEG system having an exceptionally high sample rate to accurately measure the artefact, which we then removed using linear interpolation so as to reveal the neural response during continuous electrical stimulation. In ten adult CI users, we measured the 40-Hz electrically evoked auditory steady-state response (eASSR) and electrically evoked auditory change complex (eACC) to amplitude-modulated 900-pulses-per-second pulse trains, stimulated in monopolar mode (i.e. the clinical default), and at different modulation depths. We successfully measured artifact-free 40-Hz eASSRs and eACCs. Moreover, we found that the 40-Hz eASSR, in contrast to the eACC, showed substantial responses even at shallow modulation depths. We argue that the 40-Hz eASSR is a clinically feasible objective measure to assess TEM encoding in CI users.
Thyroxine binding to type III iodothyronine deiodinase
Authors: Bayse Craig A. , Marsan Eric S. , Garcia Jenna R. , Tran-Thompson Alexis T. 
Published: September 2020

AbstractIodothyronine deiodinases (Dios) are important selenoproteins that control the concentration of the active thyroid hormone (TH) triiodothyronine through regioselective deiodination. The X-ray structure of a truncated monomer of Type III Dio (Dio3), which deiodinates TH inner rings through a selenocysteine (Sec) residue, revealed a thioredoxin-fold catalytic domain supplemented with an unstructured Ω-loop. Loop dynamics are driven by interactions of the conserved Trp207 with solvent in multi-microsecond molecular dynamics simulations of the Dio3 thioredoxin(Trx)-fold domain. Hydrogen bonding interactions of Glu200 with residues conserved across the Dio family anchor the loop’s N-terminus to the active site Ser-Cys-Thr-Sec sequence. A key long-lived loop conformation coincides with the opening of a cryptic pocket that accommodates thyroxine (T4) through an I⋯Se halogen bond to Sec170 and the amino acid group with a polar cleft. The Dio3-T4complex is stabilized by an I⋯O halogen bond between an outer ring iodine and Asp211, consistent with Dio3 selectivity for inner ring deiodination. Non-conservation of residues, such as Asp211, in other Dio types in the flexible portion of the loop sequence suggests a mechanism for regioselectivity through Dio type-specific loop conformations. Cys168 is proposed to attack the selenenyl iodide intermediate to regenerate Dio3 based upon structural comparison with related Trx-fold proteins.
Luteolin modulates SERCA2a via Sp1 upregulation to attenuate myocardial ischemia/reperfusion injury in mice
Authors: Hu Ya , Zhang Chengmeng , Zhu Hong , Wang Shuai , Zhou Yao , Zhao Jiaqi , Xia Yong , Li Dongye 
Published: September 2020

AbstractThe sarco/endoplasmic reticulum Ca2+ ATPase 2a (SERCA2a) is responsible for calcium transport during excitation–contraction coupling and is essential for maintaining myocardial systolic/diastolic function and intracellular Ca2+ levels. Therefore, it is important to investigate mechanisms whereby luteolin modulates SERCA2a expression to attenuate myocardial ischemia/reperfusion injury. C57BL/6j mice were randomly divided into eight groups. The expression and activity of SERCA2a was measured to assess interactions between the SERCA2a promoter and the Sp1 transcription factor, and the regulatory effects of luteolin. We used serum LDH release, serum cardiac troponin I level, hemodynamic data, myocardial infarction size and apoptosis-related indices to measure SERCA2a cardio-protective effects of luteolin pretreatment. Sp1 binding to SERCA2a promoter under ischemia/reperfusion conditions in the presence or absence of luteolin was analyzed by chromatin immunoprecipitation. Our experimental results indicated that during myocardial ischemia/reperfusion injury, luteolin pretreatment upregulated the expression levels of SERCA2a and Sp1. Sp1 overexpression enhanced the expression of SERCA2a at the transcriptional level. Luteolin pretreatment reversed the expression of SERCA2a through the increased expression of Sp1. Moreover, we demonstrated that luteolin pretreatment appeared to exert myocardial protective effects by upregulating the transcriptional activity of SERCA2a, via Sp1. In conclusion, during myocardial ischemia/reperfusion, Sp1 appeared to downregulate the expression of SERCA2a. Luteolin pretreatment was shown to improve SERCA2a expression via the upregulation of Sp1 to attenuate myocardial ischemia/reperfusion injury.
Changes in endothelial function during educational hospitalization and the contributor to improvement of endothelial function in type 2 diabetes mellitus
Authors: Goshima Yukiko , Okada Yosuke , Torimoto Keiichi , Fujino Yoshihisa , Tanaka Yoshiya 
Published: September 2020

AbstractOnly a few reports have examined vascular endothelial function before and after educational hospitalization and the factors that affect it in patients with type 2 diabetes mellitus (T2DM). The aim of this study was to assess vascular endothelial function before and after educational hospitalization and identify factors that affect it. In 65 patients with T2DM who underwent peripheral arterial tonometry (EndoPAT) before and after hospitalization, vascular endothelial function (reactive hyperemia index [RHI]), glucose metabolism, lipid metabolism, and blood pressure were assessed before and after hospitalization. The primary endpoint was hospitalization-induced changes in vascular endothelial function. Educational hospitalization significantly improved the natural logarithmically scaled RHI (L_RHI) from 0.555 ± 0.212 to 0.625 ± 0.245 (p = 0.012). Multivariable logistic regression analysis identified hypoglycemia during hospitalization as the single factor that significantly altered vascular endothelial function (p = 0.019). The odds of achieving normal vascular endothelial function were 0.08 times lower (95% confidence interval, 0.01–0.67) for each episode of hypoglycemia. Furthermore, multivariable analysis identified hypoglycemia during hospitalization as the single factor that worsened L_RHI. Our study showed that educational hospitalization of patients with T2DM improved vascular endothelial function, and that the development of hypoglycemic episodes had a significant negative impact on normalization of vascular endothelial function.
Distribution and relative expression of vasoactive receptors on arteries
Authors: Liu Xinhao , Luo Dan , Zhang Jie , Du Lei 
Published: September 2020

AbstractArterial tone is regulated by multiple ligand-receptor interactions, and its dysregulation is involved in ischemic conditions such as acute coronary spasm or syndrome. Understanding the distribution of vasoactive receptors on different arteries may help guide the development of tissue-specific vasoactive treatments against arterial dysfunction. Tissues were harvested from coronary, mesenteric, pulmonary, renal and peripheral human artery (n = 6 samples of each) and examined using a human antibody array to determine the expression of 29 vasoactive receptors and 3 endothelin ligands. Across all types of arteries, outer diameter ranged from 2.24 ± 0.63 to 3.65 ± 0.40 mm, and AVPR1A was the most abundant receptor. The expression level of AVPR1A in pulmonary artery was similar to that in renal artery, 2.2 times that in mesenteric artery, 1.9 times that in peripheral artery, and 2.2 times that in coronary artery. Endothelin-1 was expressed at significantly higher levels in pulmonary artery than peripheral artery (8.8 times), mesenteric artery (5.3 times), renal artery (7.9 times), and coronary artery (2.4 times). Expression of ADRA2B was significantly higher in coronary artery than peripheral artery. Immunohistochemistry revealed abundant ADRA2B in coronary artery, especially vessels with diameters below 50 μm, but not in myocardium. ADRA2C, in contrast, was expressed in both myocardium and blood vessels. The high expression of ADRA2B in coronary artery but not myocardium highlights the need to further characterize its function. Our results help establish the distribution and relative levels of tone-related receptors in different types of arteries, which may guide artery-specific treatments.
Association of familial history of diabetes or myocardial infarction and stroke with risk of cardiovascular diseases in four German cohorts
Authors: Mühlenbruch Kristin , Menzel Juliane , Dörr Marcus , Ittermann Till , Meisinger Christa , Peters Annette , Kluttig Alexander , Medenwald Daniel , Bergmann Manuela , Boeing Heiner , Schulze Matthias B. , Weikert Cornelia 
Published: September 2020

AbstractSince family history of diabetes is a very strong risk factor for type 2 diabetes, which is one of the most important risk factors for cardiovascular disease (CVD), it might be also useful to assess the risk for CVD. Therefore, we aimed to investigate the relationship between a familial (parents and siblings) history of diabetes and the risk of incident CVD. Data from four prospective German cohort studies were used: EPIC-Potsdam study (n = 26,054), CARLA study (n = 1,079), SHIP study (n = 3,974), and KORA study (n = 15,777). A multivariable-adjusted Cox regression was performed to estimate associations between familial histories of diabetes, myocardial infarction or stroke and the risk of CVD in each cohort; combined hazard ratios (HRMeta) were derived by conducting a meta-analysis. The history of diabetes in first-degree relatives was not related to the development of CVD (HRMeta 0.99; 95% CI 0.88–1.10). Results were similar for the single outcomes myocardial infarction (MI) (HRMeta 1.07; 95% CI 0.92–1.23) and stroke (HRMeta 1.00; 95% CI 0.86–1.16). In contrast, parental history of MI and stroke were associated with an increased CVD risk. Our study indicates that diabetes in the family might not be a relevant risk factor for the incidence of CVD. However, the study confirmed the relationship between a parental history of MI or stroke and the onset of CVD.
A modular chromosomally integrated toolkit for ectopic gene expression in Vibrio cholerae
Authors: Dalia Triana N. , Chlebek Jennifer L. , Dalia Ankur B. 
Published: September 2020

AbstractThe ability to express genes ectopically in bacteria is essential for diverse academic and industrial applications. Two major considerations when utilizing regulated promoter systems for ectopic gene expression are (1) the ability to titrate gene expression by addition of an exogenous inducer and (2) the leakiness of the promoter element in the absence of the inducer. Here, we describe a modular chromosomally integrated platform for ectopic gene expression in Vibrio cholerae. We compare the broadly used promoter elements Ptac and PBAD to versions that have an additional theophylline-responsive riboswitch (Ptac-riboswitch and PBAD-riboswitch). These constructs all exhibited unimodal titratable induction of gene expression, however, max induction varied with Ptac > PBAD > PBAD-riboswitch > Ptac-riboswitch. We also developed a sensitive reporter system to quantify promoter leakiness and show that leakiness for Ptac > Ptac-riboswitch > PBAD; while the newly developed PBAD-riboswitch exhibited no detectable leakiness. We demonstrate the utility of the tightly inducible PBAD-riboswitch construct using the dynamic activity of type IV competence pili in V. cholerae as a model system. The modular chromosomally integrated toolkit for ectopic gene expression described here should be valuable for the genetic study of V. cholerae and could be adapted for use in other species.
Identification of pathogenic missense mutations using protein stability predictors
Authors: Gerasimavicius Lukas , Liu Xin , Marsh Joseph A. 
Published: September 2020

AbstractAttempts at using protein structures to identify disease-causing mutations have been dominated by the idea that most pathogenic mutations are disruptive at a structural level. Therefore, computational stability predictors, which assess whether a mutation is likely to be stabilising or destabilising to protein structure, have been commonly used when evaluating new candidate disease variants, despite not having been developed specifically for this purpose. We therefore tested 13 different stability predictors for their ability to discriminate between pathogenic and putatively benign missense variants. We find that one method, FoldX, significantly outperforms all other predictors in the identification of disease variants. Moreover, we demonstrate that employing predicted absolute energy change scores improves performance of nearly all predictors in distinguishing pathogenic from benign variants. Importantly, however, we observe that the utility of computational stability predictors is highly heterogeneous across different proteins, and that they are all inferior to the best performing variant effect predictors for identifying pathogenic mutations. We suggest that this is largely due to alternate molecular mechanisms other than protein destabilisation underlying many pathogenic mutations. Thus, better ways of incorporating protein structural information and molecular mechanisms into computational variant effect predictors will be required for improved disease variant prioritisation.
Ruthenium (II) complex cis-[RuII(ŋ2-O2CC7H7O2)(dppm)2]PF6-hmxbato induces ROS-mediated apoptosis in lung tumor cells producing selective cytotoxicity
Authors: Costa Mônica Soares , Gonçalves Yasmim Garcia , Borges Bruna Cristina , Silva Marcelo José Barbosa , Amstalden Martin Krähenbühl , Costa Tássia Rafaella , Antunes Lusânia Maria Greggi , Rodrigues Renata Santos , Rodrigues Veridiana de Melo , de Faria Franca Eduardo , Zoia Mariana Alves Pereira , de Araújo Thaise Gonçalves , Goulart Luiz Ricardo , Von Poelhsitz Gustavo , Yoneyama Kelly Aparecida Geraldo 
Published: September 2020

AbstractRuthenium complexes have been extensively explored as potential molecules for cancer treatment. Considering our previous findings on the remarkable cytotoxic activity exhibited by the ruthenium (II) complex 3-hydroxy-4-methoxybenzoate (hmxbato)-cis-[RuII(ŋ2-O2CC7H7O2)(dppm)2]PF6 against Leishmania promastigotes and also the similar metabolic characteristics between trypanosomatids and tumor cells, the present study aimed to analyze the anticancer potential of hmxbato against lung tumor cells, as well as the partial death mechanisms involved. Hmxbato demonstrated selective cytotoxicity against A549 lung tumor cells. In addition, this complex at a concentration of 3.8 µM was able to expressively increase the generation of reactive oxygen species (ROS) in tumor cells, causing an oxidative stress that may culminate in: (1) reduction in cellular proliferation; (2) changes in cell morphology and organization patterns of the actin cytoskeleton; (3) cell arrest in the G2/M phase of the cell cycle; (4) apoptosis; (5) changes in the mitochondrial membrane potential and (6) initial DNA damage. Furthermore, we demonstrated that the induction of programmed cell death can occur by the intrinsic apoptotic pathway through the activation of caspases. It is also worth highlighting that hmxbato exhibited predominant actions on A549 tumor cells in comparison to BEAS-2B normal bronchial epithelium cells, which makes this complex an interesting candidate for the design of new drugs against lung cancer.
Marginal superiority of maize: an indicator for density tolerance under high plant density
Authors: Liu Guangzhou , Liu Wanmao , Yang Yunshan , Guo Xiaoxia , Zhang Guoqiang , Li Jian , Xie Ruizhi , Ming Bo , Wang Keru , Hou Peng , Li Shaokun 
Published: September 2020

AbstractMarginal superiority is a common phenomenon in crops, and is caused by the competitiveness of individual plant for resources and crop adaptability to crowded growth conditions. In this study, in order to clarify the response of marginal superiority to maize morphology and plant-density tolerance, field experiments without water and nutrition stress were conducted at Qitai Farm in Xinjiang, China, in 2013–2014 and 2016–2019. The results showed that no more than three border rows of all the cultivars had marginal superiority under high density, about 90% of all the cultivars had no more than two border row that had marginal superiority and a significant negative correlation was observed between marginal superiority and population grain yield (first border row: y = − 2.193x + 213.9, p < 0.05; second border row: y = − 2.076x + 159.2, p < 0.01). Additionally, marginal superiority was found to have a significant positive relationship with plant density (first border row: y = 6.049x + 73.76, p < 0.01; second border row: y = 1.88x + 95.41, p < 0.05) and the average leaf angle above the ear (first border row: y = 2.306x + 103.1, p < 0.01). These results indicated that the smaller the leaf angle above the ear, the weaker the marginal superiority and the higher the grain yield. It suggests that the magnitude of marginal superiority in the border rows can be an indicator for plant-density tolerance under high density. What’s more, cultivars with small leaf angle above the ear can be selected to weaken the marginal superiority and improve grain yield under high plant density. Conversely, cultivars with a large leaf angle above the ear can be selected to achieve higher individual yield in intercropping systems with no more than four rows alternated with other crops.
Sensitively switchable visible/infrared multispectral detection and imaging based on a tandem perovskite device
Authors: Liu Jiaxin , Zou Yousheng , Huang Bo , Gu Yu , Yang Yan , Han Zeyao , Zhang Yuanzhou , Xu Xiaobao , Zeng Haibo 
Published: September 2020

Sensitively switchable visible/infrared multispectral detection and imaging in single photodetector based on perovskite materials is demonstrated with Ion/Ioff ratio of ∼104, specific detectivty of 1012 Jones, mode-switch rate of 1000 Hz.
Prognostic value of aberrantly expressed methylation genes in human hepatocellular carcinoma
Authors: Zhen Limin , Ning Gang , Wu Lina , Zheng Yongyuan , Yang Fangji , Chen Tongtong , Xu Wenxiong , Liu Ying , Xie Chan , Peng Liang 
Published: September 2020

Abstract
Objectives: To identify the prognostic value of aberrantly methylated differentially expressed genes (DEGs) in hepatocellular carcinoma (HCC) and to explore the underlying mechanisms of tumorigenesis.
Methods: Gene expression profiles (GSE65372 and GSE37988) were analyzed using GEO2R to obtain aberrantly methylated DEGs. Functional enrichment analysis of screened genes was performed by the Database for Annotation, Visualization, and Integrated Discovery (DAVID). Cytoscape software was used to analyze the PPI network and to select hub genes. Transcriptional and proteinic expression data of hub genes were obtained through UALCAN and the Human Protein Reference Database. Finally, we analyzed the prognostic value of hub genes with the Kaplan–Meier Plotter and MethSurv database.
Results: In total, 24 up-hypomethylated oncogenes and 37 down-hypermethylated tumor suppressor genes (TSGs) were identified, and 8 hub genes, including 4 up-hypomethylated oncogenes (CDC5L, MERTK, RHOA and YBX1) and 4 down-hypermethylated TSGs (BCR, DFFA, SCUBE2 and TP63), were selected by PPI. Higher expression of methylated CDC5L-cg05671347, MERTK-cg08279316, RHOA-cg05657651 and YBX1-cg16306148, and lower expression of methylated BCR-cg25410636, DFFA-cg20696875, SCUBE2-cg19000089 and TP63-cg06520450, were associated with better overall survival (OS) in HCC patients. Multivariate analysis also showed they were independent prognostic factors for OS of HCC patients.
Conclusions: In summary, different expression of methylated genes above mentioned were associated with better prognosis in HCC patients. Altering the methylation status of these genes may be a therapeutic target for HCC, but it should be further evaluated in clinical studies.