bluuebunny/crossref_metadata_2025_split huggingface dataset:
The temporal dynamics of structure and content in sentence comprehension: Evidence from fMRI‐constrained MEG
Authors: Matchin William , Brodbeck Christian , Hammerly Christopher , Lau Ellen 
Published: September 2018

AbstractHumans have a striking capacity to combine words into sentences that express new meanings. Previous research has identified key brain regions involved in this capacity, but little is known about the time course of activity in these regions, as hemodynamic methods such as fMRI provide little insight into temporal dynamics of neural activation. We performed an MEG experiment to elucidate the temporal dynamics of structure and content processing within four brain regions implicated by fMRI data from the same experiment: the temporo‐parietal junction (TPJ), the posterior temporal lobe (PTL), the anterior temporal lobe (ATL), and the anterior inferior frontal gyrus (IFG). The TPJ showed increased activity for both structure and content near the end of the sentence, consistent with a role in incremental interpretation of event semantics. The PTL, a region not often associated with core aspects of syntax, showed a strong early effect of structure, consistent with predictive parsing models, and both structural and semantic context effects on function words. These results provide converging evidence that the PTL plays an important role in lexicalized syntactic processing. The ATL and IFG, regions traditionally associated with syntax, showed minimal effects of sentence structure. The ATL, PTL and IFG all showed effects of semantic content: increased activation for real words relative to nonwords. Our fMRI‐guided MEG investigation therefore helps identify syntactic and semantic aspects of sentence comprehension in the brain in both spatial and temporal dimensions.
Prospective intervention opportunities regarding device ownership and the reduction of damage to handheld ruggedized devices with shift workers
Authors: Burch Reuben F. , Strawderman Lesley , Cannon Angela B. , Vander Linde Rebecca 
Published: September 2018

AbstractIndustrial equipment such as ruggedized handheld computers, scanners, and label printers used within asset tracking environments are expensive to purchase and costly to repair. For organizations that use this equipment, there is value in understanding when and why damage occurs and how much of those costs are potentially associated with the employees’ own sense of psychological ownership and organizational pride. Given the connection between psychological ownership and pride, the purpose of this study was to analyze employee surveys to determine what methods, tools, or programs could reduce repair and replacement while developing a stronger sense of ownership for ruggedized devices used in material‐handling industries by shift workers. Unstructured interviews about device repair with management from a large industrial company were utilized to create a multiple‐choice, anonymous online survey (n = 353). Of the six interventions proposed, assigning the same device to the same employee every shift appeared to have the most consistent and positive response. Destruction rates and costs should be posted for employee viewing and managers of workgroups with consistently high destruction rates should receive additional training. An incentive‐based program for employees responsible for the least amount of device damage as well as an individual‐assignment of devices to employees may be considered. Applications for this student include providing a tool with which organizations can use to gauge employee ownership of equipment as well as to identify interventions that may aid in mitigating expenses associated with industrially rugged equipment.
Lymphomagenic properties of a HIV p17 variant derived from a splenic marginal zone lymphoma occurred in a HIV‐infected patient
Authors: Caccuri Francesca , Muraro Elena , Gloghini Annunziata , Turriziani Ombretta , Riminucci Mara , Giagulli Cinzia , Mastorci Katy , Fae' Damiana Antonia , Fiorentini Simona , Caruso Antonino , Carbone Arnaldo , Dolcetti Riccardo 
Published: September 2018

AbstractDespite antiretroviral therapy, HIV+ individuals still have increased risk to develop lymphomas, including marginal zone lymphomas, suggesting that factors other than HIV‐related immunosuppression are probably acting as lymphomagenic factors in the HIV setting. The possible pathogenic involvement of HIV p17 protein variants was investigated in a particularly informative case of HIV‐related splenic marginal zone lymphoma, which was negative for oncogenic virus infections, thus allowing us to assess the possible direct contribution of these HIV‐encoded proteins to lymphomagenesis. The presence of p17 protein was analyzed by immunohistochemistry in lymphoma tissue. Recombinant p17 protein derived from the dominant sequence detected in plasma and lymphoma biopsy was characterized for B‐cell proliferation, clonogenicity in soft agar, in vitro tube formation and wound healing. Intracellular signaling was investigated by immunoblotting. HIV p17 protein was detected in reactive lymphoid follicles but not within lymphoma cells. An identical dominant variant p17 sequence, p17‐Lyrm, carrying a 117 to 118 Ala‐Ala insertion was detected in both plasma and lymphoma tissue. Recombinant p17‐Lyrm enhanced B‐cell proliferation and clonogenicity promoted the formation of capillary‐like structures and enhanced endothelial cell migration. Unlike reference p17, the p17‐Lyrm variant enhanced the activation of Akt and ERK, critical kinases in lymphomagenesis. p17‐Lyrm clonogenic activity was dependent on the activation of Akt but not of ERK1/2. These results indicated that HIV p17 variants with distinct molecular signatures and functional properties may accumulate in lymphoid tissues of HIV‐infected individuals where they may act as a local stimulus promoting the development of lymphomas.
Changes in inpatients' distribution and benefits under institution level–based quota payment for specific diseases in rural China: An interrupted time‐series analysis
Authors: Li Hao‐Miao , Chen Ying‐Chun , Gao Hong‐Xia , Zhang Yan , Su Dai , Chang Jing‐Jing , Jiang Di , Hu Xiao‐Mei , Lei Shi‐Han 
Published: September 2018

SummaryThe distribution of patients is increasingly disordered in China, which leads to the waste of medical resources, increase in inpatients' economic burden, and decrease in benefits from health insurance. Institution level–based quota payment for specific diseases represents a typical payment‐system reform mode in rural China that rationalizes the distribution of rural inpatients. The aim of this study is to evaluate the effectiveness of this mode by estimating rural inpatients' distribution among hospitals at different levels, per capita cost of hospitalization, and actual compensation ratio and then to provide suggestions to advance this mode. Interrupted time‐series analysis was applied to evaluate the effect of the reform mode in the study, and Weiyuan County, Gansu Province, was selected as our sample. Institution level–based quota payment for specific diseases in Weiyuan County has rationalized the distribution of rural inpatients and improved their benefit levels. Further research should be conducted to evaluate the appropriateness of medical services, the health outcomes of rural inpatients, and the sustainability and replicability of the policy.
Using voluntary agreements to exclude stock from waterways: An evaluation of project success and persistence
Authors: Moore Harriet Elizabeth , Rutherfurd Ian D 
Published: September 2018

Abstract

Agriculture is one of the major drivers of ecological degradation in river basins. Excluding stock (cows and sheep) from grazing riverbanks and accessing rivers is one of the most common river restoration activities. To be effective, stock exclusion must be maintained indefinitely. In Australia, and elsewhere, stock exclusion projects are most commonly implemented by establishing voluntary agreements between landholders and government agencies. This study examined the extent to which landholders in 3 catchment management authority (CMA) regions in southeast Australia maintain stock exclusion from waterways, whether vegetation on riverbanks recovered, and the effectiveness of assessment methods. It was found that nearly half of landholders continue to graze stock on the riverbank. There has been some success with improving the condition of riparian vegetation. Sites with full stock exclusion contain the pre-European abundance of juvenile trees, and sites with continued grazing contain significantly lower abundance of juvenile trees. Establishing the effectiveness of management was made more difficult by the inconsistent methods used by the different CMAs. Stock exclusion projects implemented with voluntary agreements have the potential to succeed if oversight is improved between government agencies and CMAs and between CMAs and landholders. Projects will be easier to assess if regional authorities use consistent methods of assessment. Voluntary agreements are only suitable for environmental management if projects are monitored, maintained, and assessed appropriately. Integr Environ Assess Manag 2019;15:237–247. © 2018 SETAC
Mitigating Myside Bias in Argumentation
Authors: Christensen‐Branum Lezlie , Strong Ashley , Jones Cindy D'On 
Published: September 2018

AbstractThe ubiquity of written argument in academic contexts has underscored the importance of effective argument evaluation and writing pedagogies. Teachers can improve students’ argumentation proficiency by intentionally addressing myside bias, the propensity to support arguments with which one preemptively agrees while selectively ignoring contradictory claims and evidence. In this article, the authors identify three themes detected in a review of the literature on myside bias and offer instructional implications and strategies to address myside bias in secondary and postsecondary classrooms. Such strategies that promote critical reflection and balanced argument have implications for academic achievement and critical thinking skills beyond the classroom.
Ionic cobalt but not metal particles induces ROS generation in immune cells in vitro
Authors: Chamaon Kathrin , Schönfeld Peter , Awiszus Friedemann , Bertrand Jessica , Lohmann Christoph H. 
Published: September 2018

AbstractTotal joint replacement is one of the most successful procedures in orthopedic surgery today. However, metal implant materials undergo wear and corrosion processes. Generated particles and ions can cause a variety of cellular reactions. Cobalt‐containing alloys are used frequently in implant materials. Some studies suggest that cobalt exhibits potential cytotoxic effects, for example, via generation of reactive oxygen species (ROS). To further elucidate the effects of cobalt on human cells, we determined cell viability and cytosolic and mitochondrial superoxide formation after incubation of either ions or particles with different cells. MM‐6 and Jurkat cell lines were treated for 24, 48 and 72 h with either CoCrMo particles or cobalt ions (supplied as CoCl2). A total of 24 h exposure of both forms of cobalt did not induce cell death using terminal deoxynucleotidyl transferase (TUNEL) and trypan blue assay. Interestingly, the formation of superoxide (O2.−) is evoked mainly by ionic CoCl2 but not cobalt particles. Cobalt alloy particles are likely to even suppress O2.− formation in mitochondria in both used cell lines. Furthermore, we did not observe any effect of cobalt particles on O2.− formation in peripheral blood mononuclear cells (PBMCs) from healthy donors. We also found that the O2− formation by CoCl2 within mitochondria is a generalized effect for all cell types used, while the formation of superoxide in cytosolic compartment is cell‐type dependent. In summary, our data suggest that cobalt ions specifically induce the formation of O2.−, whereas the cobalt particles were better tolerated. © 2018 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater 107B: 1246–1253, 2019.
Sodium butyrate ameliorates lipopolysaccharide‐induced cow mammary epithelial cells from oxidative stress damage and apoptosis
Authors: Li Lin , Wang Huan‐Huan , Nie Xin‐Tian , Jiang Wan‐Ru , Zhang Yuan‐Shu 
Published: September 2018

AbstractThis study investigated the molecular mechanism by which sodium butyrate (NaB) causes oxidative stress damage induced by lipopolysaccharide (LPS) on cow mammary epithelial cells (MAC‐T). We found that NaB significantly increased the activities of antioxidant enzymes, including superoxide dismutase, glutathione peroxidase, catalase, peroxidase, and total antioxidant capacity and decreased the reactive oxygen species production in LPS‐induced MAC‐T cells. NaB attenuated protein damage and reduced apoptosis in LPS‐induced MAC‐T cells. The messenger RNA (mRNA) levels of caspase‐3, caspase‐9, and Bax decreased, while the Bcl‐2 mRNA level increased in LPS‐induced MAC‐T cells treated with NaB. Our results showed that NaB treatment increased the phosphoinositide 3‐kinase (PI3K) and phospho‐AKT (P‐AKT) protein levels, whereas it decreased the Bax, caspase‐3, and caspase‐9 protein levels in LPS‐induced MAC‐T cells. However, the increase in PI3K and P‐AKT protein levels and the decrease in Bax, caspase‐3, and caspase‐9 protein levels induced by NaB treatment were reversed when the cells were pretreated with LY294002 (PI3K inhibitor). These results indicate that NaB ameliorates LPS‐induced oxidative damage by increasing antioxidative enzyme activities and ameliorating protein damage in MAC‐T cells. In addition, NaB decreased apoptosis by inhibiting caspase‐3, caspase‐9, and Bax protein levels, and this action was mainly achieved via activation of the PI3K/AKT signaling pathways in LPS‐induced MAC‐T cells. These results provide substantial information for NaB as a chemical supplement to treat oxidative stress and its related diseases in ruminants.
MicroRNA‐140 attenuates myocardial ischemia‐reperfusion injury through suppressing mitochondria‐mediated apoptosis by targeting YES1
Authors: Yang Shuguo , Li Haide , Chen Lianghua 
Published: September 2018

AbstractMyocardial ischemia‐reperfusion (I/R) injury is thought to have its detrimental role in coronary heart disease (CHD), which is considered as the foremost cause of death all over the world. However, molecular mechanism in the progression of myocardial I/R injury is still unclear. The goal of this study was to investigate the expression and function of microRNA‐140 (miR‐140) in the process of myocardial I/R injury. The miR‐140 expression level was analyzed in the myocardium with I/R injury and control myocardium using quantitative real‐time polymerase chain reaction. Then the relation between the level of miR‐140 and YES proto‐oncogene 1 (YES1) was also investigated via luciferase reporter assay. Assessment of myocardial infarct size measurement of serum myocardial enzymes and electron microscopy analysis were used for analyzing the effect of miR‐140 on myocardial I/R injury. We also used Western blot analysis to examine the expression levels of the mitochondrial fission–related proteins, Drp1 and Fis1. miR‐140 is downregulated, and YES1 is upregulated after myocardial I/R injury. Overexpression of miR‐140 could reduce the increase related to myocardial I/R injury in infarct size and myocardial enzymes, and it also could inhibit the expression of proteins related to mitochondrial morphology and myocardial I/R‐induced mitochondrial apoptosis by targeting YES1. Taken together, these findings may provide a novel insight into the molecular mechanism of miR‐140 and YES1 in the progression of myocardial I/R injury. MiR‐140 might become a promising therapeutic target for treating myocardial I/R injury.
Protective effect of N‐(p‐amylcinnamoyl) anthranilic acid, phospholipase A2 enzyme inhibitor, and transient receptor potential melastatin‐2 channel blocker against renal ischemia–reperfusion injury
Authors: Çakır Murat , Tekin Suat , Taşlıdere Aslı , Çakan Pınar , Düzova Halil , Gül Cemile Ceren 
Published: September 2018

AbstractThe production of reactive oxygen species and inflammatory events are the underlying mechanisms of ischemia‐reperfusion injury (IRI). It was determined that transient receptor potential melastatin‐2 (TRPM2) channels and phospholipase A2 (PLA
2) enzymes were associated with inflammation and cell death. In this study, we investigated the effect of
N‐(
p‐amylcinnamoyl) anthranilic acid (ACA), a TRPM2 channel blocker, and PLA
2 enzyme inhibitor on renal IRI. A total of 36 male Sprague‐Dawley rats were divided into four groups: control, ischemia‐reperfusion (I/R), I/R + ACA 5 mg, I/R + ACA 25 mg. In I/R applied groups, the ischemia for 45 minutes and reperfusion for 24 hours were applied bilaterally to the kidneys. In the I/R group, serum levels of the blood urea nitrogen (BUN), creatinine, cystatin C (CysC), kidney injury molecule‐1 (KIM‐1), neutrophil gelatinase‐associated lipocalin (NGAL), and interleukin‐18 increased. On histopathological examination of renal tissue in the I/R group, the formation of glomerular and tubular damage was seen, and it was detected that there was an increase in the levels of malondialdehyde (MDA), caspase‐3, total oxidant status (TOS), and oxidative stress index (OSI); and there was a decrease in total antioxidant capacity (TAC) and catalase enzyme activity. ACA administration reduced serum levels of BUN, creatinine, CysC, KIM‐1, NGAL, interleukin‐18. In the renal tissue, ACA administration reduced histopathological damage, levels of caspase‐3, MDA, TOS, and OSI; and it increased the level of TAC and catalase enzyme activity. It has been shown with the histological and biochemical results in this study that ACA is protective against renal IRI.
Investigation of follicular helper T cells, as a novel player, in preeclampsia
Authors: Heydarlou Hanieh , Eghabl‐Fard Shadi , Ahmadi Majid , Aghebati‐Maleki Leili , Dolati Sanam , Movassaghpour Ali Akbar , Jadidi‐Niaragh Farhad , Danaei Shahla , Mahmoudilafout Farzaneh , Talebi Mehdi , Rahimifar Shahrzad , Yousefi Mehdi 
Published: September 2018

AbstractPreeclampsia (PE) is characterized by hypertension and proteinuria. It occurs in an around 3% to 5% of all pregnancies worldwide. The fetus is kind of semiallograft to the maternal host; immune system components encounter fetal antigens and develop adverse immune responses. Recently, it has been observed that the immune system plays an important role in PE. In the current study, we have tried to investigate the role of follicular helper T (Tfh) cells in the pathogenesis of PE. Blood samples of 49 PE women and 50 healthy controls were collected. Peripheral blood mononuclear cells were isolated, cells were cultured, and then RNA was extracted. Autoantibody and secretory cytokine levels were analyzed by ELISA. Tfh frequency and transcription levels of the related molecules and cytokine were assessed by flow cytometry and real‐time PCR, respectively. The frequency of circulating Tfh cell in PE women was significantly higher compared with the healthy pregnant woman (Tfh cells with CD4+ICOS
+,
P = 0.0064 and Tfh cells with CD4
+CXCR5
+,
P = 0.029). Moreover, mRNA expression levels of CXCR5, BCL6, IL‐21, and IL‐6 (
P = 0.0006,
P = 0.008,
P = 0.0063, and
P = 0.027, respectively) were upregulated in PE patients. Furthermore, IL‐6 (
P = 0.0014) and IL‐21 (
P = 0.0059) levels in both group were assayed and the results showed increased in patient group. We also measured autoantibody levels including antiphospholipid antibodies (
P = 0.0001), anticardiolipin antibodies (
P = 0.0004), anti‐TPO (
P = 0.0008), anti‐TG (
P = 0.001) in circulation of PE group, which were higher than the control group. This study provided insights into the involvement of Tfh cells in etiology and pathogenesis of PE, probably by developing autoantibodies.
Hydrogen gas reduces chronic intermittent hypoxia‐induced hypertension by inhibiting sympathetic nerve activity and increasing vasodilator responses via the antioxidation
Authors: Guan Peng , Lin Xiao‐Meng , Yang Sheng‐Chang , Guo Ya‐Jing , Li Wen‐Ya , Zhao Ya‐Shuo , Yu Fu‐Yang , Sun Zhi‐Min , An Ji‐Ren , Ji En‐Sheng 
Published: September 2018

AbstractMolecular hydrogen is reported to be used medically to ameliorate various systemic pathological conditions. This study aimed to investigate the effect of hydrogen (H2) gas on hypertension induced by intermittent hypoxia in rats. The adult rats were exposed to chronic intermittent hypoxia (CIH) 8 hours/day for 5 weeks and/or H
2 gas 2 hours/day. We found that the systolic and diastolic blood pressure (BP) increased significantly in rats exposed to intermittent hypoxia, both of which were markedly attenuated after H treatment. Furthermore, intermittent hypoxia exposure elevated renal sympathetic nerve activity, consistent with plasma norepinephrine. Additionally, H
2 gas significantly improved CIH‐induced abnormal vascular relaxation. Nevertheless, inhalation of H
2 gas alone did not cause such changes. Moreover, H
2 gas‐treated rats exposed to CIH showed a significant reduction in 8‐hydroxy‐2 deoxyguanosine content and increases in superoxide dismutase activity, indicating improved oxidative stress. Taken together, these results indicate that H
2 gas has significant effects on the reduction of BP without any side effects. Mechanistically, inhibition of sympathetic activity and reduction of systemic vascular resistance may participate in this process via the antioxidant activity of H
2.
Simulated microgravity reduces intracellular‐free calcium concentration by inhibiting calcium channels in primary mouse osteoblasts
Authors: Sun Zhongyang , Li Ying , Zhou Hua , Cai Min , Liu Jing , Gao Shanshan , Yang Junsheng , Tong Liangcheng , Wang Jianling , Zhou Sheng , Hu Zebing , Wang Yixuan , Wang Ke , Zhang Lijun , Wang Han , Zhang Lianchang , Shi Fei , Cao Xinsheng , Zhang Shu , Ji Yongzhang , Zhao Jianning 
Published: September 2018

AbstractCalcium homeostasis in osteoblasts plays fundamental roles in the physiology and pathology of bone tissue. Various types of mechanical stimuli promote osteogenesis and increase bone formation elicit increases in intracellular‐free calcium concentration in osteoblasts. However, whether microgravity, a condition of mechanical unloading, exerts an influence on intracellular‐free calcium concentration in osteoblasts or what mechanisms may underlie such an effect are unclear. Herein, we show that simulated microgravity reduces intracellular‐free calcium concentration in primary mouse osteoblasts. In addition, simulated microgravity substantially suppresses the activities of L‐type voltage‐sensitive calcium channels, which selectively allow calcium to cross the plasma membrane from the extracellular space. Moreover, the functional expression of ryanodine receptors and inositol 1,4,5‐trisphosphate receptors, which mediate the release of calcium from intracellular storage, decreased under simulated microgravity conditions. These results suggest that simulated microgravity substantially reduces intracellular‐free calcium concentration through inhibition of calcium channels in primary mouse osteoblasts. Our study may provide a novel mechanism for microgravity‐induced detrimental effects in osteoblasts, offering a new avenue to further investigate bone loss induced by mechanical unloading.