bluuebunny/crossref_metadata_2025_split huggingface dataset:
Musical Experience Offsets Age-Related Decline in Understanding Speech-in-Noise: Type of Training Does Not Matter, Working Memory Is the Key
Authors: Zhang Lei , Fu Xueying , Luo Dan , Xing Lidongsheng , Du Yi 
Published: August 2020

Objectives:
Speech comprehension under “cocktail party” scenarios deteriorates with age even in the absence of measurable hearing loss. Musical training is suggested to counteract the age-related decline in speech-in-noise (SIN) perception, yet which aspect of musical plasticity contributes to this compensation remains unclear. This study aimed to investigate the effects of musical experience and aging on SIN perception ability. We hypothesized a key mediation role of auditory working memory in ameliorating deficient SIN perception in older adults by musical training.

Design:
Forty-eight older musicians, 29 older nonmusicians, 48 young musicians, and 24 young nonmusicians all with (near) normal peripheral hearing were recruited. The SIN task was recognizing nonsense speech sentences either perceptually colocated or separated with a noise masker (energetic masking) or a two-talker speech masker (informational masking). Auditory working memory was measured by auditory digit span. Path analysis was used to examine the direct and indirect effects of musical expertise and age on SIN perception performance.

Results:
Older musicians outperformed older nonmusicians in auditory working memory and all SIN conditions (noise separation, noise colocation, speech separation, speech colocation), but such musician advantages were absent in young adults. Path analysis showed that age and musical training had opposite effects on auditory working memory, which played a significant mediation role in SIN perception. In addition, the type of musical training did not differentiate SIN perception regardless of age.

Conclusions:
These results provide evidence that musical training offsets age-related speech perception deficit at adverse listening conditions by preserving auditory working memory. Our findings highlight auditory working memory in supporting speech perception amid competing noise in older adults, and underline musical training as a means of “cognitive reserve” against declines in speech comprehension and cognition in aging populations.
Cutaneous and systemic connections in lupus
Authors: Maz Mitra P. , Michelle Kahlenberg J. 
Published: August 2020

Purpose of review
Systemic lupus erythematosus (SLE) is a systemic autoimmune disease with multiple manifestations, with a majority of SLE patients having cutaneous involvement. Despite ongoing research, the relationship between SLE and cutaneous lupus erythematosus (CLE) pathogeneses remains unknown. This review will compare advances in understanding the cause and pathogenesis of SLE and CLE.

Recent findings
Recently, mechanisms by which immune cell populations contribute to the pathogenesis of SLE and CLE have been queried. Studies have pointed to transitional B cells and B-cell activating factor (BAFF) signaling as potential drivers of SLE and CLE, with belimumab clinical data supporting these hypotheses. Ustekinumab trials and an exciting regulatory T cell (Treg) adoptive transfer in an SLE patient with cutaneous disease have suggested a role for T-cell-targeted therapies. The theory that neutrophil extracellular traps may be a source of autoantigens in SLE remains controversial, while neutrophils have been suggested as early drivers of cutaneous disease. Finally, plasmacytoid dendritic cells (pDCs) have been studied as a potential therapeutic target in SLE, and anti-blood DC antigen (anti-BDCA) antibody clinical trials have shown promise in treating cutaneous disease.

Summary
Although recent findings have contributed to understanding SLE and CLE pathogenesis, the mechanistic link between these diseases remains an area requiring further research.
Does Standard Physical Therapy Increase Quadriceps Strength in Chronically Ventilated Patients? A Pilot Study*
Authors: Supinski Gerald S. , Valentine Emily N. , Netzel Paul F. , Schroder Elizabeth A. , Wang Lin , Callahan Leigh Ann 
Published: August 2020

Objectives:
Physical therapy is standard care for mechanically ventilated patients, but there is no evidence, using nonvolitional, objective measurements, that physical therapy increases muscle strength in this population. The present study tested the hypothesis that 2 weeks of standard, conventional physical therapy provided at a ventilator weaning facility would increase quadriceps strength in mechanically ventilated patients.

Design:
Prospective observational study.

Setting:
Ventilator weaning unit.

Patients:
Patients who were transferred from an acute care hospital because of failure to wean from mechanical ventilation and who were receiving physical therapy as prescribed by facility staff.

Interventions:
None.

Measurements and Main Results:
We employed a novel, nonvolitional objective technique, quadriceps twitch force generation in response to femoral nerve magnetic stimulation, to assess leg strength before and after 2 weeks of conventional physical therapy. The duration and specific exercises provided to patients were also recorded. In a subset of patients, we measured muscle activation intensity using wireless electromyogram recordings. Indices of respiratory function (maximum inspiratory pressure generation and the rapid shallow breathing index) were also assessed. Patients’ responses to 2 weeks of physical therapy were poor; on average, quadriceps twitch fell by –1.02 ± 0.71 Newtons. Neither physical therapy duration nor specific forms of exercise were identified to positively impact quadriceps twitch. Electromyogram recordings indicated that during training, muscle activation was poor. Consequently, therapists spent substantial time performing exercises that elicited little muscle activation. Physical therapy did not improve respiratory function.

Conclusions:
Standard physical therapy delivered in a ventilator weaning facility failed to improve quadriceps leg strength in a majority of mechanically ventilated patients. The fact that mechanically ventilated patients fail to achieve high levels of muscle activation during physical therapy provides a potential explanation as to why physical therapy may often be ineffective. We speculate that use of novel methods which increase muscle activation during exercise may improve responses of mechanically ventilated patients to physical therapy.
Long noncoding RNA XIST knockdown suppresses the growth of colorectal cancer cells via regulating microRNA-338-3p/PAX5 axis
Authors: Li Wei , He Yingchun , Cheng Zhaoling 
Published: August 2020

Background
Colorectal cancer is one of the most common human cancers worldwide. Long noncoding RNAs (lncRNAs) and microRNAs (miRNAs) have been reported as the regulators in cancers. The purpose of this study was to reveal the functional mechanisms of lncRNA x inactive specific transcript (XIST) and miR-338-3p in colorectal cancer cells.

Methods
The transcription level and protein level of genes were assessed by quantitative real-time PCR (qRT-PCR) and western blot assay, respectively. 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT) assay and flow cytometry analysis were used to determine cell proliferation ability and apoptosis rate, respectively. In addition, cell migratory ability and invasive ability were measured using transwell assay. Besides, the interaction between miR-338-3p and XIST or paired box 5 (PAX5) was predicted by starBase or TargetScan and then verified by the dual-luciferase reporter assay.

Results
XIST and PAX5 expression were increased, and miR-338-3p expression was decreased in colorectal cancer tissues and cells. XIST knockdown significantly repressed cell proliferation, migration and invasion, and accelerated apoptosis in colorectal cancer cells. Interestingly, XIST directly downregulated miR-338-3p expression to increase PAX5 level. As expected, XIST knockdown inhibited colorectal cancer cell growth by modulating miR-338-3p expression. Furthermore, miR-338-3p suppressed cell growth via downregulation of PAX5 level in colorectal cancer cells.

Conclusion
Our results demonstrated that the downregulation of XIST inhibited cell proliferation, migration and invasion, and induced apoptosis through modulating miR-338-3p/PAX5 axis in colorectal cancer cells, providing potential target for the prevention and treatment of colorectal cancer.
Time of dissociation between microcirculation, macrocirculation, and lactate levels in a rabbit model of early endotoxemic shock
Authors: Zhang Hong , Li Lei , Wu Jun , Qu Hong-Ping , Tang Yao-Qing , Chen De-Chang 
Published: August 2020

Abstract

Background
The relationship between macrocirculation and microcirculation remains controversial. The loss of coherence between microcirculation and macrocirculation has already been found in late-stage sepsis shock. The objective of this study was to determine the earliest possible time of detecting the loss of coherence between microcirculation and macrocirculation in early-stage endotoxemic shock.

Methods
We randomized 24 female New Zealand white rabbits into two groups: endotoxemic shock group (n = 14) and control group (n = 10). Rabbits in the endotoxemic shock group were equipped with arterial and venous catheters and received an intravenous infusion of Escherichia coli lipopolysaccharide (LPS, 2 mg/kg over 10 min). Rabbits in the control group received the same dose of saline infusion. Microcirculatory perfusion parameters were assessed in the sublingual mucosa using sidestream dark-field video microscopy. Systemic hemodynamics and blood lactate levels were measured at baseline and over a 120-min period.

Results
Ninety minutes after completing LPS infusion, all animals in the endotoxemic shock group developed a hypodynamic septic condition, characterized by low cardiac output and increased systemic vascular resistance; 120 min after completing LPS infusion, the mean arterial pressure decreased by 25% (P = 0.01), confirming ongoing endotoxemic shock. However, significant decreases in sublingual microcirculatory parameters of small vessels (microvascular flow index, perfused vessel density, and proportion of small perfused vessels) were observed 30 min after completing LPS infusion (P = 0.01, for all), and threshold decreases of 30% were found 60 min after completing LPS infusion (P = 0.001, for all) in the endotoxemic shock group. Lactate levels significantly increased to more than 2 mm/L at 90 min and more than 4 mm/L at 120 min in the endotoxemic shock group (P = 0.02 and P = 0.01, respectively).

Conclusions
Changes in microcirculatory perfusion precede changes in macrocirculation and lactate levels in a rabbit model of endotoxemia shock. Microcirculation, macrocirculation, and oxygen metabolism are distinct in early-stage endotoxic shock.
Prognostic significance of the hemoglobin A1c level in non-diabetic patients undergoing percutaneous coronary intervention: a meta-analysis
Authors: Li Yan , Li Xiao-Wen , Zhang Yin-Hua , Zhang Lei-Min , Wu Qing-Qing , Bai Zhao-Run , Si Jin , Zuo Xue-Bing , Shi Ning , Li Jing , Chu Xi 
Published: August 2020

Abstract

Background
The predictive value of hemoglobin A1c (HbA1c) levels in non-diabetic patients with myocardial infarction undergoing percutaneous coronary intervention (PCI) is still controversial. This study aimed to evaluate whether HbA1c levels were independently associated with adverse clinical outcomes in non-diabetic patients with coronary artery disease (CAD) who had undergone PCI by performing a meta-analysis of cohort studies.

Methods
This meta-analysis included non-diabetic patients with CAD who had undergone PCI. A systematic search for publications listed in the PubMed, Embase, and Cochrane Library databases from commencement to December 2018 was conducted. Studies evaluating the adverse clinical outcomes according to abnormal HbA1c levels in non-diabetic patients diagnosed with CAD who had undergone PCI were eligible. The primary outcomes were long-term all-cause deaths and long-term major adverse cardiac events, and the secondary outcome was short-term all-cause deaths. The meta-analysis was conducted with RevMan 5.3 and Stata software 14.0. Odds ratios (ORs) were pooled using a random or fixed-effects model, depending on the heterogeneity of the included studies. Sub-group analysis or sensitivity analysis was conducted to explore potential sources of heterogeneity, when necessary.

Results
Six prospective cohort studies involving 10,721 patients met the inclusion criteria. From the pooled analysis, abnormal HbA1c levels were associated with increased risk for long-term all-cause death (OR 1.39, 95% confidence interval [CI] 1.16–1.68, P = 0.001, I
2 = 45%). Sub-group analysis suggested that abnormal HbA1c levels between 6.0% and 6.5% predicted higher long-term major adverse cardiac event (including all-cause deaths, non-fatal myocardial infarction, target lesion revascularization, target vessel revascularization, recurrent acute myocardial infarction, heart failure requiring hospitalization, and stent thrombosis) risk (OR 2.05, 95% CI 1.46–2.87, P < 0.001, I
2 = 0). Contrarily, elevated HbA1c levels were not associated with increased risk of short-term all-cause death (OR 1.16, 95% CI 0.88–1.54, P = 0.300, I
2 = 0).

Conclusions
An abnormal HbA1c level is an independent risk factor for long-term adverse clinical events in non-diabetic patients with CAD after PCI. Strict control of HbA1c levels may improve patient survival. Further studies in different countries and prospective cohort studies with a large sample size are required to verify the association.
Association of interleukin-18 gene polymorphisms with Takayasu arteritis in a Chinese Han population
Authors: Wen Dan , Zhou Xian-Liang , Du Xin , Dong Jian-Zeng , Ma Chang-Sheng 
Published: August 2020

Abstract

Background:
Interleukin-18 (IL18) gene polymorphisms are related to many inflammatory and autoimmune diseases. However, a correlation analysis between IL18 −607C/A and −137G/C gene polymorphisms and Takayasu arteritis (TA) is lacking.

Methods:
This study enrolled 200 patients with TA as the case group and 334 region-, age-, and sex-matched healthy subjects as the control group. We genotyped alleles and genotypes at positions −607 and −137 of the IL18 gene and analyzed the distribution frequencies. Mann-Whitney U test, t test, Chi-squared test and Hardy-Weinberg equilibrium were performed.

Results:
After adjusting for risk factors, the adjusted odds ratios and 95% confidence intervals at position −607C/A were 0.533, 0.391 to 0.880 (P = 0.010); 0.266, 0.586 to 1.002 (P = 0.051); and 0.122, 0.552 to 1.420 (P = 0.613) under the dominant, additive, and recessive models, respectively. For the −137G/C polymorphism, the adjusted odds ratios and 95% confidence intervals were 1.571, 1.068 to 2.311 (P = 0.022); 1.467, 1.086 to 1.980 (P = 0.012); and 1.815, 0.901 to 3.656 (P = 0.095) under the dominant, additive, and recessive models, respectively. Moreover, regardless of the model used, we found no statistical difference in distribution frequency between the active and quiescent states of TA for the −607C/A (P = 0.355, 0.631, and 0.705, respectively) and −137G/C polymorphisms (P = 0.205, 0.385, and 0.208, respectively).

Conclusions:
The IL18 −607C/A gene polymorphism may decrease the risk of TA, and thus is a protective factor, whereas −137G/C may increase the risk of TA, and thus is a risk factor. However, neither polymorphism was related to activity (active vs. quiescent) of TA.
Silencing of Long Noncoding RNA Zinc Finger Antisense 1 Protects Against Hypoxia/Reoxygenation-induced Injury in HL-1 Cells Through Targeting the miR-761/Cell Death Inducing p53 Target 1 Axis
Authors: Xiang Xiaojun , Zheng Lei , Li Xuewen 
Published: August 2020

Abstract:
Acute myocardial infarction (AMI) is a major cause of morbidity and mortality worldwide. Long noncoding RNAs have demonstrated to be associated with AMI pathogenesis. In this study, we aimed to investigate the function and mechanism of zinc finger antisense 1 (ZFAS1) on hypoxia/reoxygenation (H/R)-induced injury in HL-1 cells. The levels of ZFAS1, miR-761, and cell death–inducing p53 target 1 (CDIP1) in the serum of AMI patients and HL-1 cells were detected by quantitative real-time polymerase chain reaction or western blot. Cell viability and apoptosis were assessed by the Cell Counting Kit-8 assay and flow cytometry, respectively. Lactate dehydrogenase release, malondialdehyde content, superoxide dismutase expression, and glutathione peroxidase were evaluated using commercially corresponding assay kits. Targeted interactions among ZFAS1, miR-761, and CDIP1 were validated by dual-luciferase reporter and RNA immunoprecipitation assays. Our data indicated that ZFAS1 was upregulated and miR-761 was downregulated in the serum of patients with AMI and H/R-induced HL-1 cells. ZFAS1 silencing or miR-761 overexpression alleviated H/R-induced injury in HL-1 cells. Moreover, ZFAS1 acted as a sponge to sequester miR-761, and CDIP1 was directly targeted and inhibited by miR-761. ZFAS1 knockdown protected HL-1 cell from H/R-induced injury through miR-761, and CDIP1 mediated the alleviated effect of miR-761 overexpression on H/R-induced HL-1 cell injury. Furthermore, ZFAS1 regulated CDIP1 expression through acting as a miR-761 sponge. In addition, CDIP1 silencing protected HL-1 cell from H/R-induced injury. Our current work suggested that the knockdown of ZFAS1 protected against H/R-induced injury in HL-1 cells at least partly through the regulation of miR-761/CDIP1 axis, illuminating a novel therapeutic avenue for AMI management.
Resveratrol Stimulates the Na+–Ca2+ Exchanger on the Plasma Membrane to Reduce Cytosolic Ca2+ in Rat Aortic Smooth Muscle Cells
Authors: Yan Fuman , Lu Jun , Zhang Yunting , Li Xiao , Chan Wai-Ho , Zhao Qiannan , Kwan Hiu-Yee , Liu Haimei , Yao Xiaoqiang 
Published: August 2020

Abstract:
Resveratrol is well known to exhibit vascular relaxant and antihypertensive effects. In this study, we determined the effects of resveratrol on the modulation of cytosolic [Ca2+] level and adenosine 5′-triphosphate–induced Ca2+ release from the sarcoplasmic reticulum (SR) in rat aortic smooth muscle cells (ASMCs) and explored its underlying mechanisms. In this article, cytosolic [Ca2+] and SR [Ca2+] in ASMCs were determined by Fluo-4/acetoxymethyl and Mag-Fluo-4/acetoxymethyl respectively. Resveratrol (20, 50, and 100 µM) caused a rapid and substantial reduction in cytosolic [Ca2+] in ASMCs bathed in normal Hank's Balanced Salt Solution or Ca2+-free Hank's Balanced Salt Solution. Pretreatment with resveratrol reduced adenosine 5′-triphosphate–induced SR Ca2+ release and SR Ca2+ content. In the cells bathed in Na+-free physiological saline, which favors the reverse mode of the Na+–Ca2+ exchanger (NCX), resveratrol induced an increase in cytosolic [Ca2+] and SR [Ca2+]. However, its effect on cytosolic [Ca2+] was inhibited by the selective NCX inhibitor, SEA0400. Our findings suggest that resveratrol reduces cytosolic [Ca2+] and SR [Ca2+] in ASMCs in normal physiological saline, which might be, at least in part, mediated by the NCX.
Myocardial Infarction–associated Transcript Knockdown Inhibits Cell Proliferation, Migration, and Invasion Through miR-490-3p/Intercellular Adhesion Molecule 1 Axis in Oxidized Low-density Lipoprotein-induced Vascular Smooth Muscle Cells
Authors: Ma Haifeng , Zheng Lingling , Qin Hao , Wang Wenwen 
Published: August 2020

Abstract:
Emerging evidence has demonstrated that long noncoding RNAs are related to the pathogenesis of atherosclerosis. We aimed to investigate the roles and molecular mechanisms of myocardial infarction–associated transcript (MIAT) in the proliferation, migration, and invasion of oxidized low-density lipoprotein (ox-LDL)-induced vascular smooth muscle cells (VSMCs). Quantitative real-time polymerase chain reaction was conducted to determine the levels of MIAT, microRNA490-3p (miR-490-3p), and intercellular adhesion molecule 1 (ICAM1). Cell Counting Kit-8 assay was performed to assess cell proliferation. Transwell assay was used to evaluate cell migration and invasion. Western blot assay was performed to measure the protein levels of proliferating cell nuclear antigen, N-cadherin, matrix metalloprotein-9, and ICAM1. Dual-luciferase reporter, RNA immunoprecipitation, and RNA pull-down assays were conducted to verify the relationship between miR-490-3p and MIAT or ICAM1. MIAT was elevated in atherosclerosis patients' serum and ox-LDL–induced VSMCs. MIAT knockdown suppressed cell proliferation, migration, and invasion in ox-LDL–stimulated VSMCs. MIAT acted as a sponge of miR-490-3p, and miR-490-3p deficiency overturned the inhibition of MIAT knockdown on VSMC proliferation, migration, and invasion. ICAM1 was a direct target of miR-490-3p, and ICAM1 silencing repressed the proliferation, migration, and invasion of ox-LDL–stimulated VSMCs. Moreover, ICAM1 overexpression reversed the impacts of MIAT knockdown on ox-LDL–induced VSMC proliferation, migration, and invasion. MIAT knockdown could depress cell proliferation, migration, and invasion through miR-490-3p/ICAM1 axis in ox-LDL–induced VSMCs.
Chemokine (C-C motif) Ligand 6 Aggravates Hypoxia Reoxygenation–induced Apoptosis in H9c2 Cells Through Enhancing the Expression of Insulin-like Growth Factor 2-Antisense
Authors: Li Xiufen , Aishan Bilali , Yang Yan , Xie Yang , Lati Dilimu , Tuerxun Paerhati 
Published: August 2020

Abstract:
Chemokine (C-C motif) ligand 6 (CCL6), one of the small cytokines in the CC chemokine family, has been reported to involve in renal ischemia–reperfusion (I/R) injury. However, the role of CCL-6 in myocardial I/R injury is nonelucidated. In this study, we used in vitro H9c2 cell model to investigate the overall contributions of CCL6 to myocardial I/R injury. We found the elevated level of CCL6 from the reanalysis of data set GSE-4105 and in hypoxia–reoxygenation (H/R)-injured H9c2 cells. CCL6 silencing attenuated the cardiomyocyte apoptosis induced by H/R injury, whereas exogenous CCL6 treatment aggravated the apoptosis of H/R-injured H9c2 cells. During CCL6 administration, the expression of numerous long noncoding RNAs was differentially regulated. Quantitative RT-Polymerase chain reaction assay demonstrated that insulin-like growth factor 2 (IGF2)-Antisense (AS) had the highest induction by CCL6 addition. IGF2-AS silencing alleviated the apoptosis of H/R-injured H9c2 cells. Collectively, we have identified a potential mechanism by which high expression of CCL6 contributes to the H/R-induced apoptosis in H9c2 cells through enhancing the expression of IGF2-AS. These findings also give evidence of the feasibility of CCL6 or long noncoding RNA IGF2-AS as a potential target for modulation or therapeutic intervention in myocardial I/R injury.