bluuebunny/crossref_metadata_2025_split huggingface dataset:
Connections between academic burnout, resilience, and psychological well‐being in nursing students: A longitudinal study
Authors: Ríos‐Risquez Mᵃ Isabel , García‐Izquierdo Mariano , Sabuco‐Tebar Emiliana de los Ángeles , Carrillo‐Garcia César , Solano‐Ruiz Carmen 
Published: July 2018

AbstractAimsThe aim of this study was to explore the longitudinal associations between academic burnout and resilience and psychological well‐being, and the stability of these variables in a sample of university nursing students.BackgroundNursing students frequently suffer academic burnout, which is brought on by different situations experienced during the training process and that can concern his psychological well‐being. Resilience is a personal resource that allows adverse situations to be handled in a successful way.DesignLongitudinal design.MethodsData were collected at two moments separated by 18 months (2014–2016), with 218 students at T1 and 113 at T2. At each time a questionnaire was given to them, with questions about socioeconomic demographics and three validated scales to measure academic burnout, resilience, and psychological well‐being.ResultsThe three dimensions that make up academic burnout remained steady over time, while resilience increased and psychological well‐being improved. Hierarchical regression analyses revealed the longitudinal effect of emotional exhaustion at T1 and at T2 they showed the longitudinal effect of resilience on psychological well‐being at T2. The inverse hierarchical regression analyses did not reveal significant relationships for any of the variables measured at T2 in connection with psychological well‐being measured at T1.ConclusionsEmotional exhaustion was the most relevant dimension of academic burnout when predicting psychological well‐being in the analysed sample. Moreover, resilience has an important positive effect on psychological well‐being in the analysed sample. The practical implications of the results are discussed from the perspective of academic training and some recommendations are given for future research in this field.
Trends and variations in per capita expenditure on adult intellectual disabilities health and social care across Scotland, and by urban/rural class
Authors: Okon Marian , Henderson Angela , Kinnear Deborah , Cooper Sally‐Ann 
Published: July 2018

AbstractBackgroundFollowing the global financial crisis in 2007/08, the UK implemented an austerity programme which may impact on services. Scotland comprises both densely populated urban conurbations and highly dispersed remote rural and island communities.MethodExpenditure data were extracted from Scottish Government statistics. Per capita expenditure was calculated using adjusted Scotland's 2011 census data.ResultsThere was a 3.41% decrease in real term expenditure on adult intellectual disabilities services between 2012/13 and 2014/15 (>£32 million). In 2014/15, per capita expenditure on adult intellectual disabilities health care ranged from £1,211 to £17,595; social care from £21,147 to £83,831; and combined health and social care expenditures from £37,703 to £85,929. Per capita expenditure on combined health and social care was greater in rural areas, with more on intellectual disabilities social care, though less on health care.ConclusionsScottish expenditure on adult intellectual disabilities services has not kept abreast of rising living costs. It varies considerably across the country: a postcode lottery.
Modelling cadmium‐induced cardiotoxicity using human pluripotent stem cell‐derived cardiomyocytes
Authors: Shen Jiaxi , Wang Xiaochen , Zhou Danni , Li Tongyu , Tang Ling , Gong Tingyu , Su Jun , Liang Ping 
Published: July 2018

AbstractCadmium, a highly ubiquitous toxic heavy metal, has been widely recognized as an environmental and industrial pollutant, which confers serious threats to human health. The molecular mechanisms of the cadmium‐induced cardiotoxicity (CIC) have not been studied in human cardiomyocytes at the cellular level. Here we showed that human pluripotent stem cell‐derived cardiomyocytes (hPSC‐CMs) can recapitulate the CIC at the cellular level. The cadmium‐treated hPSC‐CMs exhibited cellular phenotype including reduced cell viability, increased apoptosis, cardiac sarcomeric disorganization, elevated reactive oxygen species, altered action potential profile and cardiac arrhythmias. RNA‐sequencing analysis revealed a differential transcriptome profile and activated MAPK signalling pathway in cadmium‐treated hPSC‐CMs, and suppression of P38 MAPK but not ERK MAPK or JNK MAPK rescued CIC phenotype. We further identified that suppression of PI3K/Akt signalling pathway is sufficient to reverse the CIC phenotype, which may play an important role in CIC. Taken together, our data indicate that hPSC‐CMs can serve as a suitable model for the exploration of molecular mechanisms underlying CIC and for the discovery of CIC cardioprotective drugs.
The expression of MMP‐1 and MMP‐9 is up‐regulated by smooth muscle cells after their cross‐talk with macrophages in high glucose conditions
Authors: Macarie Razvan Daniel , Vadana Mihaela , Ciortan Letitia , Tucureanu Monica M. , Ciobanu Andrea , Vinereanu Dragos , Manduteanu Ileana , Simionescu Maya , Butoi Elena 
Published: July 2018

AbstractPatients with diabetes mellitus have an increased risk of myocardial infarction and coronary artery disease‐related death, exhibiting highly vulnerable plaques. Many studies have highlighted the major role of macrophages (MAC) and smooth muscle cells (SMC) and the essential part of metalloproteases (MMPs) in atherosclerotic plaque vulnerability. We hypothesize that in diabetes, the interplay between MAC and SMC in high glucose conditions may modify the expression of MMPs involved in plaque vulnerability. The SMC‐MAC cross‐talk was achieved using trans‐well chambers, where human SMC were grown at the bottom and human MAC in the upper chamber in normal (NG) or high (HG) glucose concentration. After cross‐talk, the conditioned media and cells were isolated and investigated for the expression of MMPs, MCP‐1 and signalling molecules. We found that upon cross‐talk with MAC in HG, SMC exhibit: (i) augmented expression of MMP‐1 and MMP‐9; (ii) significant increase in the enzymatic activity of MMP‐9; (iii) higher levels of soluble MCP‐1 chemokine which is functionally active and involved in MMPs up‐regulation; (iv) activated PKCα signalling pathway which, together with NF‐kB are responsible for MMP‐1 and MMP‐9 up‐regulation, and (v) impaired function of collagen assembly. Taken together, our data indicate that MCP‐1 released by cell cross‐talk in diabetic conditions binds to CCR2 and triggers MMP‐1 and MMP‐9 over‐expression and activity, features that could explain the high vulnerability of atherosclerotic plaque found at diabetic patients.
Aldolase A as a prognostic factor and mediator of progression via inducing epithelial–mesenchymal transition in gastric cancer
Authors: Jiang Zhonghua , Wang Xiaohong , Li Jing , Yang Hongmei , Lin Xin 
Published: July 2018

AbstractGlycolysis is regarded as the hallmark of cancer development and progression, which involves a multistep enzymatic reaction. This study aimed to explore the clinicopathological significance and potential role of glycolytic enzyme aldolase A (ALDOA) in the carcinogenesis and progression of gastric cancer (GC). ALDOA was screened from three paired liver metastasis tissues and primary GC tissues and further explored with clinical samples and in vitro studies. The ALDOA protein level significantly correlated with a larger tumor diameter (P = .004), advanced T stage (P < .001), N stage (P < .001) and lymphovascular invasion (P = .001). Moreover, the expression of ALDOA was an independent prognostic factor for the 5‐year overall survival and disease‐free survival of patients with GC in both univariate and multivariate survival analyses (P < .05). Silencing the expression of ALDOA in GC cell lines significantly impaired cell growth, proliferation and invasion ability (P < .05). Knockdown of the expression of ALDOA reversed the epithelial–mesenchymal transition process. Mechanically, ALDOA could affect the hypoxia‐inducible factor (HIF)‐1α activity as demonstrated by the HIF‐1α response element–luciferase activity in GC cells. Collectively, this study revealed that ALDOA was a potential biomarker of GC prognosis and was important in the carcinogenesis and progression of human GC.
Kallistatin attenuates endothelial senescence by modulating Let‐7g‐mediated miR‐34a‐SIRT1‐eNOS pathway
Authors: Guo Youming , Chao Lee , Chao Julie 
Published: July 2018

AbstractKallistatin, a plasma protein, protects against vascular and organ injury. This study is aimed to investigate the role and mechanism of kallistatin in endothelial senescence. Kallistatin inhibited H2O2‐induced senescence in human endothelial cells, as indicated by reduced senescence‐associated‐β‐galactosidase activity, p16INK4a and plasminogen activator inhibitor‐1 expression, and elevated telomerase activity. Kallistatin blocked H2O2‐induced superoxide formation, NADPH oxidase levels and VCAM‐1, ICAM‐1, IL‐6 and miR‐34a synthesis. Kallistatin reversed H2O2‐mediated inhibition of endothelial nitric oxide synthase (eNOS), SIRT1, catalase and superoxide dismutase (SOD)‐2 expression, and kallistatin alone stimulated the synthesis of these antioxidant enzymes. Moreover, kallistatin's anti‐senescence and anti‐oxidant effects were attributed to SIRT1‐mediated eNOS pathway. Kallistatin, via interaction with tyrosine kinase, up‐regulated Let‐7g, whereas Let‐7g inhibitor abolished kallistatin's effects on miR‐34a and SIRT1/eNOS synthesis, leading to inhibition of senescence, oxidative stress and inflammation. Furthermore, lung endothelial cells isolated from endothelium‐specific kallistatin knockout mice displayed marked reduction in mouse kallistatin levels. Kallistatin deficiency in mouse endothelial cells exacerbated senescence, oxidative stress and inflammation compared to wild‐type mouse endothelial cells, and H2O2 treatment further magnified these effects. Kallistatin deficiency caused marked reduction in Let‐7g, SIRT1, eNOS, catalase and SOD‐1 mRNA levels, and elevated miR‐34a synthesis in mouse endothelial cells. These findings indicate that endogenous kallistatin through novel mechanisms protects against endothelial senescence by modulating Let‐7g‐mediated miR‐34a‐SIRT1‐eNOS pathway.
The involvement of Toll‐like receptor 9 in the pathogenesis of erosive autoimmune arthritis
Authors: Fischer Anita , Abdollahi‐Roodsaz Shahla , Böhm Christina , Niederreiter Birgit , Meyer Brigitte , Yau Anthony C. Y. , Lönnblom Erik , Joosten Leo A. B. , Koenders Marije , Lehmann Christian H. K. , Dudziak Diana , Krönke Gerhard , Holmdahl Rikard , Steiner Günter 
Published: July 2018

AbstractEndogenous nucleic acids and their receptors may be involved in the initiation of systemic autoimmune diseases including rheumatoid arthritis (RA). As the role of the DNA sensing Toll‐like receptor (TLR) 9 in RA is unclear, we aimed to investigate its involvement in the pathogenesis of autoimmune arthritis using three different experimental models of RA. The data obtained revealed involvement of TLR9 in the T cell‐dependent phase of inflammatory arthritis. In rats with pristane‐induced arthritis (PIA), TLR9 inhibition before disease onset reduced arthritis significantly and almost completely abolished bone erosion. Accordingly, serum levels of IL‐6, α‐1‐acid‐glycoprotein and rheumatoid factor were reduced. Moreover, in TLR9−/− mice, streptococcal cell wall (SCW)‐induced arthritis was reduced in the T cell‐dependent phase, whereas T cell‐independent serum‐transfer arthritis was not affected. Remarkably, while TLR7 expression did not change during in vitro osteoclastogenesis, TLR9 expression was higher in precursor cells than in mature osteoclasts and partial inhibition of osteoclastogenesis was achieved only by the TLR9 antagonist. These results demonstrate a pivotal role for TLR9 in the T cell‐dependent phases of inflammatory arthritis and additionally suggest some role during osteoclastogenesis. Hence, endogenous DNA seems to be crucially involved in the pathophysiology of inflammatory autoimmune arthritis.
Rho GTPases are involved in S1P‐enhanced glomerular endothelial cells activation with anti‐myeloperoxidase antibody positive IgG
Authors: Sun Xiao‐Jing , Chen Min , Zhao Ming‐Hui 
Published: July 2018

AbstractSphingosine‐1‐phosphate (S1P) is a crucial regulator in vascular inflammation. Our recent study found that under pathophysiological concentration in active anti‐neutrophil cytoplasmic antibody (ANCA)‐associated vasculitis (AAV), S1P participated in MPO‐ANCA‐positive IgG‐induced glomerular endothelial cell (GEnC) activation via a S1P receptor (S1PR)‐dependent way. However, the downstream signalling pathways are not fully clear yet. In this study, we demonstrated that Rho guanosine triphosphatases (GTPases) signalling pathways, RhoA and Rac1 in particular, were implicated in MPO‐ANCA‐positive IgG‐mediated GEnCs activation enhanced by pathophysiological concentration of S1P in AAV. These results provide mechanistic insights into vascular barrier dysfunction in AAV, which may facilitate the development of effective therapies.
Changes in the appendicular skeleton during metamorphosis in the axolotl salamander (Ambystoma mexicanum)
Authors: Thampi Parvathy , Liu Jinpeng , Zeng Zheng , MacLeod James N. 
Published: July 2018

AbstractAxolotl salamanders (Ambystoma mexicanum) remain aquatic in their natural state, during which biomechanical forces on their diarthrodial limb joints are likely reduced relative to salamanders living on land. However, even as sexually mature adults, these amphibians can be induced to metamorphose into a weight‐bearing terrestrial stage by environmental stress or the exogenous administration of thyroxine hormone. In some respects, this aquatic to terrestrial transition of axolotl salamanders through metamorphosis may model developmental and changing biomechanical skeletal forces in mammals during the prenatal to postnatal transition at birth and in the early postnatal period. To assess differences in the appendicular skeleton as a function of metamorphosis, anatomical and gene expression parameters were compared in skeletal tissues between aquatic and terrestrial axolotls that were the same age and genetically full siblings. The length of long bones and area of cuboidal bones in the appendicular skeleton, as well as the cellularity of cartilaginous and interzone tissues of femorotibial joints were generally higher in aquatic axolotls compared with their metamorphosed terrestrial siblings. A comparison of steady‐state mRNA transcripts encoding aggrecan core protein (ACAN), type II collagen (COL2A1), and growth and differentiation factor 5 (GDF5) in femorotibial cartilaginous and interzone tissues did not reveal any significant differences between aquatic and terrestrial axolotls.
Monitoring chemotherapy‐induced alopecia with trichoscopy
Authors: Rossi Alfredo , Caterina Fortuna Maria , Caro Gemma , Cardone Michele , Garelli Valentina , Grassi Sara , Carlesimo Marta 
Published: July 2018

SummaryBackgroundChemotherapy‐induced alopecia (CIA) ranks among the psychologically most devastating effects of cancer treatment for oncological patients, with an overall incidence of 65%. Nowadays trichoscopy is largely employed in the diagnosis of alopecia, but no description of CIA trichoscopic pattern is present in literature.AimsWe want to create an organic description of CIA trichoscopic aspects.MethodsOncological patients candidate to chemotherapy drugs, afferent to our trichological outpatient were studied. Anamnesis, clinical exam, clinical global photography, pull test, trichogram, and trichoscopy were conducted at the different moments of therapeutic treatment.ResultsA definite trichoscopic pattern in the different phases of treatment was observed. After the first 3 weeks of chemotherapy rare and scattered black dots, broken hairs, flame hairs and pohl pinkus appeared. At the end of chemotherapy besides the features described above, numerous thin hair in regrowth were detected, together to rare terminal hair, scattered black dots and circle hair. Three months after chemotherapy a progressive increase of follicular units and elongation of the existing hair were visible.ConclusionsWe propose an description of CIA trichoscopic pattern and its evolution during the different phases of chemotherapy.
Real‐Time Cerebral Hemodynamic Response to Tactile Somatosensory Stimulation
Authors: Hage Benjamin , Way Emily , Barlow Steven M. , Bashford Gregory R. 
Published: July 2018

ABSTRACTBACKGROUND AND PURPOSERecent studies in rodents suggest that somatosensory stimulation could provide neuroprotection during ischemic stroke by inducing plasticity in the cortex–vasculature relationship. While functional magnetic resonance imaging (fMRI) has shown that somatosensory stimulation increases cerebral blood flow (CBF) over several seconds, subsecond changes in CBF in the basal cerebral arteries have rarely been studied due to temporal resolution limitations. This study characterized hemodynamic changes in the middle cerebral arteries (MCAs) during somatosensory stimulation with high temporal resolution (100 samples/s) using functional transcranial Doppler ultrasound (fTCD).METHODSPneumotactile somatosensory stimulation, consisting of punctate pressure pulses traversing the glabrous skin of the hand at 25 cm/s, was used to induce CBF velocity (CBFV) response curves. Changes in CBFV were measured in the bilateral MCAs using fTCD. All 12 subjects underwent three consecutive trials consisting of 20 seconds of stimulation followed by 5 minutes of rest.RESULTSSharp, bilateral increases in CBFV of about 20% (left MCA = 20.5%, right MCA = 18.8%) and sharp decreases in pulsatility index of about 8% were observed during stimulation. Left lateralization of up to 3.9% was also observed. The magnitude of the initial increase in CBFV showed significant adaptation between subsequent trials.CONCLUSIONSPneumotactile somatosensory stimulation is a potent stimulus that can evoke large, rapid hemodynamic changes, with adaptation between successive stimulus applications. Due to its high temporal resolution, fTCD is useful for identifying quickly evolving hemodynamic responses, and for correlating changes in hemodynamic parameters such as pulsatility index (PI) and CBFV.
Effects of indirect facilitation on functional diversity, dominance and niche differentiation in tropical alpine communities
Authors: Danet Alain , Anthelme Fabien , Gross Nicolas , Kéfi Sonia 
Published: July 2018

AbstractQuestionPositive interactions between plants have well‐known effects on community species richness and biomass via micro‐environment improvements. However, the effects of indirect facilitation performed by a nurse on an associated plant community, occurring e.g., through protection against grazing, have not attracted much attention in the literature so far, in particular regarding the functional traits of the associated plant communities. Because characteristics of trait distributions can reveal selective pressures at play, they offer valuable information for the study of grazing pressure. Here, we tested the extent to which indirect facilitation affects the amount of distinct trait combinations (H1), trait dominance (H2) and niche differentiation between species (H3) of associated plant communities living under nurse plants.LocationTropical alpine peatlands, Cordillera Real, Bolivia.MethodsWe set up a grazing exclusion experiment over two dominant nurse cushion species: one providing indirect facilitation under grazing pressure and the other not. We measured three functional traits in the associated communities, which are known to vary depending on the grazing level: LDMC, leaf thickness and maximum height. We assessed the amount of distinct trait combinations by computing the volume of the phenotypic space (H1). The variation in trait dominance was quantified with kurtosis and skewness of the trait distributions (H2). The variation in niche differentiation was evaluated using mean intra‐population trait variance relative to intra‐community trait variance (H3).ResultsWe did not find a significant effect of grazing and indirect facilitation on the volume of the phenotypic space (H1). However, our study revealed a significant effect of indirect facilitation on dominance in the associated communities by maintaining the evenness of the trait distributions (maximum height and leaf thickness) in grazed compared to ungrazed plots (H2), and on niche differentiation by maintaining trait overlaps (LDMC and maximum height) between species in grazed compared to ungrazed contexts (H3).ConclusionOur results suggest that indirect facilitation promotes the co‐existence of contrasting functional strategies (H2) and species niches (H3) in associated plant communities subject to grazing. These results reflect the buffering effect of indirect facilitation on the grazing selective pressures exerted on associated plant communities living under the protection of nurses.
Gain‐of‐function variants of FtsA form diverse oligomeric structures on lipids and enhance FtsZ protofilament bundling
Authors: Schoenemann Kara M. , Krupka Marcin , Rowlett Veronica W. , Distelhorst Steven L. , Hu Bo , Margolin William 
Published: July 2018

SummaryEscherichia coli requires FtsZ, FtsA and ZipA proteins for early stages of cell division, the latter two tethering FtsZ polymers to the cytoplasmic membrane. Hypermorphic mutants of FtsA such as FtsA* (R286W) map to the FtsA self‐interaction interface and can bypass the need for ZipA. Purified FtsA forms closed minirings on lipid monolayers that antagonize bundling of FtsZ protofilaments, whereas FtsA* forms smaller oligomeric arcs that enable bundling. Here, we examined three additional FtsA*‐like mutant proteins for their ability to form oligomers on lipid monolayers and bundle FtsZ. Surprisingly, all three formed distinct structures ranging from mostly arcs (T249M), a mixture of minirings, arcs and straight filaments (Y139D) or short straight double filaments (G50E). All three could form filament sheets at higher concentrations with added ATP. Despite forming these diverse structures, all three mutant proteins acted like FtsA* to enable FtsZ protofilament bundling on lipid monolayers. Synthesis of the FtsA*‐like proteins in vivo suppressed the toxic effects of a bundling‐defective FtsZ, exacerbated effects of a hyper‐bundled FtsZ, and rescued some thermosensitive cell division alleles. Together, the data suggest that conversion of FtsA minirings into any type of non‐miniring oligomer can promote progression of cytokinesis through FtsZ bundling and other mechanisms.