bluuebunny/crossref_metadata_2025_split huggingface dataset:
Infant and young child feeding practices in Lebanon: a cross-sectional national study
Authors: Naja Farah , Hwalla Nahla , Chokor Fatima Al Zahraa , Zgheib Rasha , Nasreddine Lara 
Published: April 2022

AbstractObjective:To assess infant and young child feeding (IYCF) practices in Lebanon and investigate their associations with socio-demographic and lifestyle factors.Design:A cross-sectional national survey was conducted in 2012–2013. In addition to a socio-demographic and lifestyle questionnaire, a 24-h dietary recall for the children was collected, with mothers as proxies. IYCF practices were assessed based on the 2021 indicators of the WHO.Setting:Lebanon.Participants:Children aged 0–23 months and their mothers (n469).Results:While the majority of infants were ever breastfed (87·6 %), the prevalence of exclusive breast-feeding (BF) in those under 6 months of age was 11·0 %. Early initiation of BF was 28 %. A greater child’s birth order, partner’s support for BF, higher parental education, maternal BF knowledge and non-smoking were associated with higher odds of meeting BF recommendations. As for complementary feeding, 92·8 % of children (6–23 months) met the minimum meal frequency indicator, 37·5 % met the minimum dietary diversity (MDD) and 34·4 % met the minimum adequate diet (MAD). The consumption of unhealthy food was observed amongst 48·9 % of children, with nearly 37 % consuming sweet beverages. Older maternal age and maternal overweight/obesity were associated with lower odds of meeting MDD and MAD, while child’s age and partner’s support for BF were associated with higher odds.Conclusions:The results documented suboptimal IYCF practices amongst Lebanese children and identified a number of factors associated with these practices. Findings from this study will help guide the development of culture-specific programmes aimed at improving IYCF practices in Lebanon.
Development and preliminary validation of a scale to assess physicians’ emotional distress intolerance in end-of-life care communication
Authors: Brondolo Elizabeth , Keating Luke , Crete Abigail , Kaur Amandeep , Randrianarivony Rina , Statman David , Schwartz Joseph E. , Basello Gina , Roth Alan R. 
Published: April 2022

AbstractContextEnd-of-life care (EOLC) communication is beneficial but underutilized, particularly in conditions with a variable course such as chronic obstructive pulmonary disease (COPD) and congestive heart failure (CHF). Physicians’ emotional distress intolerance has been identified as a barrier to EOLC communication. However, studies of emotional distress intolerance in EOLC have largely relied on anecdotal reports, qualitative data, or observational studies of physician–patient communication. A free-standing measure of multiple dimensions of distress tolerance is warranted to enable the identification of individuals experiencing distress intolerance and to facilitate the effective targeting of interventions to improve distress tolerance.ObjectivesThis study provides preliminary data on the reliability and validity of the Physician Distress Intolerance (PDI) scale. We examine potential subdimensions of emotional distress intolerance.MethodFamily medicine and internal medicine physicians completed the PDI, read vignettes describing patients with COPD or CHF, and indicated whether they initiated or delayed EOLC communication with their patients with similar conditions.ResultsExploratory and confirmatory factor analyses were performed on separate samples. Confirmatory factor analysis confirmed that a three-factor solution was superior to a two- or one-factor solution. Three subscales were created: Anticipating Negative Emotions, Intolerance of Uncertainty, and Iatrogenic Harm. The full scale and subscales had adequate internal consistency and demonstrated evidence of validity. Higher scores on the PDI, indicating greater distress intolerance, were negatively associated with initiation and positively associated with delay of EOLC communication. Subscales provided unique information.Significance of resultsThe PDI can contribute to research investigating and addressing emotional barriers to EOLC communication.
Developing and Testing an Instrument to Measure the Culture for	Psychological Empowerment in Organizations (IMPEC)
Authors: Schermuly Carsten Christoph , Koch Jan , Creon Laura Elisabeth , Drazic Ivana , Graßmann Carolin 
Published: April 2022

Abstract: Psychological empowerment – the experience of competence, meaning, self-determination and impact at work – has become very popular in organizational research. Meta-analytic results show many positive consequences of psychological empowerment and many different antecedents such as positive leadership, high performance practices, and work design characteristics. However, scarce research is available on how organizational culture influences psychological empowerment. We believe a missing instrument is one reason for the underdevelopment in this field. For this reason, we developed IMPEC (Instrument Measuring Psychological Empowerment Culture) for measuring specific cultural values for psychological empowerment. IMPEC was tested in four studies. In the first study ( n = 208 German employees), the reliability, factor structure, and its relationship with psychological empowerment and affective variables were analyzed. The second study had two waves ( n = 182 German employees) in which the predictive and incremental value of the IMPEC for performance-oriented variables were evaluated. In the third study, the instrument was translated into English and validated in a US sample ( n = 346). Finally, a multi-wave study was conducted in a German setting ( n = 210) to test if the IMPEC could predict critical constructs better than the empowerment climate questionnaire.
Statistical Analysis of Small Faults in Rotated Blocks of Crust Near the Húsavík‐Flatey Transform Fault, Northern Iceland
Authors: Hummel Natalie V. , Waag‐Swift Seth , Titus Sarah J. 
Published: April 2022

AbstractThe dextral Húsavík‐Flatey fault, in northern Iceland, provides a unique opportunity to observe an oceanic transform fault on land. Structural and paleomagnetic measurements from lavas and dikes on Flateyjarskagi peninsula indicate that rocks adjacent to the fault have rotated clockwise more than 100°. We examine the effect of this rotation on the orientations of small faults that developed in rocks adjacent to the transform fault. We also use patterns in small‐scale data to build on models of the style of deformation surrounding the fault. We apply statistical tools including spatial regressions to structural data to estimate the amount of distributed shearing around the transform fault, and to predict the orientations of rotated structures. Some small faults are consistent with predicted rotations, while others are consistent with the modern kinematics, suggesting that they postdate block rotation. This protracted temporal history for small faults complicates paleostress interpretations from rocks adjacent to the Húsavík‐Flatey fault. Previous studies assumed the small faults formed in their modern orientations and attributed their variability to stress variations, whereas we identify populations of faults that have likely rotated to their present‐day attitudes.
Dynamics and Predictability of Tropical Cyclone Rapid Intensification in Ensemble Simulations of Hurricane Patricia (2015)
Authors: Tao Dandan , van Leeuwen Peter Jan , Bell Michael , Ying Yue 
Published: April 2022

AbstractHurricane Patricia (2015) over the eastern Pacific was a record‐breaking tropical cyclone (TC) under a very favorable environment during its rapid intensification (RI) period, which makes it an optimal real case for studying RI dynamics and predictability. In this study, we performed ensemble Kalman filter analyses at Patricia's early development stage using both traditional observations and the Office of Naval Research Tropical Cyclone Intensity (TCI) field campaign data. It is shown that assimilating the inner‐core TCI observations produces a stronger initial vortex and significantly improves the prediction of RI. Analysis of observation sensitivity experiments shows that the deep‐layer dropsonde observations have high impact on both the primary and secondary circulations for the entire troposphere while the radar observations have the most impact on the primary circulations near aircraft flight level. A wide range of intensification scenarios are obtained through two sets of ensemble forecasts initialized with and without assimilating the TCI data prior to the RI onset. Verification of the ensemble forecasts against the TCI observations during the RI period shows that forecast errors toward later stages can originate from two different error sources at early stages of the vortex structure: One is a timing error from a delayed vortex development such that the TC evolution is the same but shifted in time; the other is due to a totally different storm such that there is no moment in time the simulated storm can obtain a correct TC structure.
Tomatidine-stimulated maturation of human embryonic stem cell-derived cardiomyocytes for modeling mitochondrial dysfunction
Authors: Kim Ye Seul , Yoon Jung Won , Kim Dasol , Choi Seunghak , Kim Hyoung Kyu , Youm Jae Boum , Han Jin , Heo Soon Chul , Hyun Sung-Ae , Seo Jung-Wook , Kim Deok-Ho , Kim Jae Ho 
Published: April 2022

AbstractHuman embryonic stem cell-derived cardiomyocytes (hESC-CMs) have been reported to exhibit immature embryonic or fetal cardiomyocyte-like phenotypes. To enhance the maturation of hESC-CMs, we identified a natural steroidal alkaloid, tomatidine, as a new substance that stimulates the maturation of hESC-CMs. Treatment of human embryonic stem cells with tomatidine during cardiomyocyte differentiation stimulated the expression of several cardiomyocyte-specific markers and increased the density of T-tubules. Furthermore, tomatidine treatment augmented the number and size of mitochondria and enhanced the formation of mitochondrial lamellar cristae. Tomatidine treatment stimulated mitochondrial functions, including mitochondrial membrane potential, oxidative phosphorylation, and ATP production, in hESC-CMs. Tomatidine-treated hESC-CMs were more sensitive to doxorubicin-induced cardiotoxicity than the control cells. In conclusion, the present study suggests that tomatidine promotes the differentiation of stem cells to adult cardiomyocytes by accelerating mitochondrial biogenesis and maturation and that tomatidine-treated mature hESC-CMs can be used for cardiotoxicity screening and cardiac disease modeling.
Mitotic protein kinase-driven crosstalk of machineries for mitosis and metastasis
Authors: Kim Chang-Hyeon , Kim Da-Eun , Kim Dae-Hoon , Min Ga-Hong , Park Jung-Won , Kim Yeo-Bin , Sung Chang K. , Yim Hyungshin 
Published: April 2022

AbstractAccumulating evidence indicates that mitotic protein kinases are involved in metastatic migration as well as tumorigenesis. Protein kinases and cytoskeletal proteins play a role in the efficient release of metastatic cells from a tumor mass in the tumor microenvironment, in addition to playing roles in mitosis. Mitotic protein kinases, including Polo-like kinase 1 (PLK1) and Aurora kinases, have been shown to be involved in metastasis in addition to cell proliferation and tumorigenesis, depending on the phosphorylation status and cellular context. Although the genetic programs underlying mitosis and metastasis are different, the same protein kinases and cytoskeletal proteins can participate in both mitosis and cell migration/invasion, resulting in migratory tumors. Cytoskeletal remodeling supports several cellular events, including cell division, movement, and migration. Thus, understanding the contributions of cytoskeletal proteins to the processes of cell division and metastatic motility is crucial for developing efficient therapeutic tools to treat cancer metastases. Here, we identify mitotic kinases that function in cancer metastasis as well as tumorigenesis. Several mitotic kinases, namely, PLK1, Aurora kinases, Rho-associated protein kinase 1, and integrin-linked kinase, are considered in this review, as an understanding of the shared machineries between mitosis and metastasis could be helpful for developing new strategies to treat cancer.
27-hydroxycholesterol linked high cholesterol diet to lung adenocarcinoma metastasis
Authors: Li Xingkai , Chen Hengchi , Zhang Lizhen , Chen Li , Wei Wei , Gao Shugeng , Xue Qi , Li Yue , Wang Bing , Li Jiagen , Gao Yushun , Lin Yanliang 
Published: April 2022

AbstractDietary cholesterol has been implicated to promote lung cancer. Lung adenocarcinoma (LAC) is a main type of lung cancer, whereas the functional mechanism of cholesterol in LAC remained largely unknown. In the present study, we evidenced that cholesterol promoted cell proliferation and invasion of LAC in vitro as well as LAC metastasis in vivo. Cyp27A1 knockdown reduced the cholesterol-induced LAC cells proliferation and invasion. In contrast, Cyp7B1 knockdown enhanced the effect of cholesterol on LAC cells proliferation and invasion. Furthermore, Cyp27A1 deficiency remarkably reduced high cholesterol-induced LAC metastasis in vivo. Mechanism investigation demonstrated that exposure of LAC cells to 27-hydroxycholesterol induced the phosphorylation of AKT and NFκB p65, and promoted the expression of peptidylprolyl isomerase B (PPIB), especially in the coculture with THP1-derived macrophage. Meanwhile, 27-hydroxycholesterol induced the secretion of FGF2 and IL-6, which contributed to the expression of snail and vimentin. Luciferase report assay and ChIP assay confirmed that NFκB p65 controlled the transcription of PPIB. Inhibiting NFκB p65 activation reduced PPIB expression. PPIB inhibition reduced 27-hydroxycholesterol-induced expression of snail and vimentin. These results indicated that 27-hydroxycholesterol linked high cholesterol and LAC metastasis by regulating NFκB/PPIB axis and the secretion of FGF2 and IL-6.
Disrupted presynaptic nectin1-based neuronal adhesion in the entorhinal-hippocampal circuit contributes to early-life stress-induced memory deficits
Authors: Wu Chen , Gong Qian , Xu Xue , Fang Ping , Wang Chi , Yu Jing-Ying , Wang Xing-Xing , Fang San-Hua , Chen Wen-Juan , Lou Hui-Fang , Liu Yu-Hui , Wang Liang , Liu Yi-Jun , Chen Wei , Wang Xiao-Dong 
Published: April 2022

AbstractThe cell adhesion molecule nectin3 and its presynaptic partner nectin1 have been linked to early-life stress-related cognitive disorders, but how the nectin1-nectin3 system contributes to stress-induced neuronal, circuit, and cognitive abnormalities remains to be studied. Here we show that in neonatally stressed male mice, temporal order and spatial working memories, which require the medial entorhinal cortex (MEC)-CA1 pathway, as well as the structural integrity of CA1 pyramidal neurons were markedly impaired in adulthood. These cognitive and structural abnormalities in stressed mice were associated with decreased nectin levels in entorhinal and hippocampal subregions, especially reduced nectin1 level in the MEC and nectin3 level in the CA1. Postnatal suppression of nectin1 but not nectin3 level in the MEC impaired spatial memory, whereas conditional inactivation of nectin1 from MEC excitatory neurons reproduced the adverse effects of early-life stress on MEC-dependent memories and neuronal plasticity in CA1. Our data suggest that early-life stress disrupts presynaptic nectin1-mediated interneuronal adhesion in the MEC-CA1 pathway, which may in turn contribute to stress-induced synaptic and cognitive deficits.
PRMT5 critically mediates TMAO-induced inflammatory response in vascular smooth muscle cells
Authors: Liu He , Jia Kunpeng , Ren Zhengnan , Sun Jia , Pan Li-Long 
Published: April 2022

AbstractA high plasma level of the choline-derived metabolite trimethylamine N-oxide (TMAO) is closely related to the development of cardiovascular disease. However, the underlying mechanism remains unclear. In the present study, we demonstrated that a positive correlation of protein arginine methyltransferase 5 (PRMT5) expression and TMAO-induced vascular inflammation, with upregulated vascular cell adhesion molecule-1 (VCAM-1) expression in primary rat and human vascular smooth muscle cells (VSMC) in vitro. Knockdown of PRMT5 suppressed VCAM-1 expression and the adhesion of primary bone marrow-derived macrophages to TMAO-stimulated VSMC. VSMC-specific PRMT5 knockout inhibited vascular inflammation with decreased expression of VCAM-1 in mice. We further identified that PRMT5 promoted VCAM-1 expression via symmetrical demethylation of Nuclear factor-κB p65 on arginine 30 (R30). Finally, we found that TMAO markedly induced the expression of nicotinamide adenine dinucleotide phosphate oxidase 4 (Nox4) and production of reactive oxygen species, which contributed to PRMT5 expression and subsequent VCAM-1 expression. Collectively, our data provide novel evidence to establish a Nox4-PRMT5-VCAM-1 in mediating TMAO-induced VSMC inflammation. PRMT5 may be a potential target for the treatment of TMAO-induced vascular diseases.
Anti-apoptotic HAX-1 suppresses cell apoptosis by promoting c-Abl kinase-involved ROS clearance
Authors: Dong Qincai , Li Dapei , Zhao Huailong , Zhang Xun , Liu Yue , Hu Yong , Yao Yi , Zhu Lin , Wang Guang-Fei , Liu Hainan , Gao Ting , Niu Xiayang , Zheng Tong , Song Caiwei , Wang Di , Bai Yu , Jin Jing , Liu Zijing , Jin Yanwen , Li Ping , Cao Cheng , Liu Xuan 
Published: April 2022

AbstractThe anti-apoptotic protein HAX-1 has been proposed to modulate mitochondrial membrane potential, calcium signaling and actin remodeling.HAX-1mutation or deficiency results in severe congenital neutropenia (SCN), loss of lymphocytes and neurological impairments by largely unknown mechanisms. Here, we demonstrate that the activation of c-Abl kinase in response to oxidative or genotoxic stress is dependent on HAX-1 association. Cellular reactive oxygen species (ROS) accumulation is inhibited by HAX-1-dependent c-Abl activation, which greatly contributes to the antiapoptotic role of HAX-1 in stress. HAX-1 (Q190X), a loss-of-function mutant responsible for SCN, fails to bind with and activate c-Abl, leading to dysregulated cellular ROS levels, damaged mitochondrial membrane potential and eventually apoptosis. The extensive apoptosis of lymphocytes and neurons inHax-1-deficient mice could also be remarkably suppressed by c-Abl activation. These findings underline the important roles of ROS clearance in HAX-1-mediated anti-apoptosis by c-Abl kinase activation, providing new insight into the pathology and treatment of HAX-1-related hereditary disease or tumorigenesis.
Smurf2-induced degradation of SMAD2 causes inhibition of hair follicle stem cell differentiation
Authors: Lin Bojie , Huang Dan , Lin Guanyu , Miao Yong , Wang Jin , Fan Zhexiang , Hu Zhiqi 
Published: April 2022

AbstractHair follicle stem cells (HFSCs) are implicated in the formation of hair follicles and epidermis. This study aims to clarify the role of SMAD2 in regulating the differentiation of HFSCs, which is involved with Smurf2. Functional assays were carried out in human HFSCs to assess the effect of SMAD2 and Smurf2 with altered expression on growth dynamics of HFSCs. Ubiquitination of SMAD2 and its protein stability were assessed. The binding relationship between NANOG and DNMT1 was assessed. A mouse skin wound model was induced to verify the effects of Smurf2/SMAD2/NANOG/DNMT1 on wound healing. SMAD2 overexpression was observed in HFSCs during differentiation and its ectopic expression contributed to promotion of differentiation and apoptosis of HFSCs while arresting cell proliferation. Mechanistic investigations indicated that Smurf2 promoted the ubiquitination and degradation of SMAD2, thus causing downregulation of SMAD2 expression. By this mechanism, NANOG expression was reduced and the subsequent DNMT1 transcriptional expression was also diminished, leading to suppression of differentiation and apoptosis of HFSCs while stimulating cell proliferation. Moreover, in vivo data showed that Smurf2 upregulation limited epidermal wound healing in mice by inhibiting the SMAD2/NANOG/DNMT1 axis. Our work proposed a potential target regarding SMAD2 restoration in promoting HFSC differentiation and skin wound healing.
Monocyte subpopulation profiling indicates CDK6-derived cell differentiation and identifies subpopulation-specific miRNA expression sets in acute and stable coronary artery disease
Authors: Witten Anika , Martens Leonie , Schäfer Ann-Christin , Troidl Christian , Pankuweit Sabine , Vlacil Ann-Kathrin , Oberoi Raghav , Schieffer Bernhard , Grote Karsten , Stoll Monika , Markus Birgit 
Published: April 2022

AbstractCoronary artery disease (CAD) is a long-lasting inflammatory disease characterized by monocyte migration into the vessel wall leading to clinical events like myocardial infarction (MI). However, the role of monocyte subsets, especially their miRNA-driven differentiation in this scenario is still in its infancy. Here, we characterized monocyte subsets in controls and disease phenotypes of CAD and MI patients using flow cytometry and miRNA and mRNA expression profiling using RNA sequencing. We observed major differences in the miRNA profiles between the classical (CD14++CD16−) and nonclassical (CD14+CD16++) monocyte subsets irrespective of the disease phenotype suggesting the Cyclin-dependent Kinase 6 (CDK6) to be an important player in monocyte maturation. Between control and MI patients, we found a set of miRNAs to be differentially expressed in the nonclassical monocytes and targeting CCND2 (Cyclin D2) that is able to enhance myocardial repair. Interestingly, miRNAs as miR-125b playing a role in vascular calcification were differentially expressed in the classical subset in patients suffering from CAD and not MI in comparison to control samples. In conclusion, our study describes specific peculiarities of monocyte subset miRNA expression in control and diseased samples and provides basis to further functional analysis and to identify new cardiovascular disease treatment targets.
Decoding health status transitions of over 200 000 patients with traumatic brain injury from preceding injury to the injury event
Authors: Mollayeva Tatyana , Tran Andrew , Chan Vincy , Colantonio Angela , Sutton Mitchell , Escobar Michael D. 
Published: April 2022

AbstractFor centuries, the study of traumatic brain injury (TBI) has been centred on historical observation and analyses of personal, social, and environmental processes, which have been examined separately. Today, computation implementation and vast patient data repositories can enable a concurrent analysis of personal, social, and environmental processes, providing insight into changes in health status transitions over time. We applied computational and data visualization techniques to categorize decade-long health records of 235,003 patients with TBI in Canada, from preceding injury to the injury event itself. Our results highlighted that health status transition patterns in TBI emerged along with the projection of comorbidity where many disorders, social and environmental adversities preceding injury are reflected in external causes of injury and injury severity. The strongest associations between health status preceding TBI and health status at the injury event were between multiple body system pathology and advanced age-related brain pathology networks. The interwoven aspects of health status on a time continuum can influence post-injury trajectories and should be considered in TBI risk analysis to improve prevention, diagnosis, and care.