Miracle-dz/UniFAR-FTUs huggingface dataset:
Does a Good Firm Breed Good Organizational Citizens? The Moderating Role of Perspective Taking

Although some previous studies have examined the impact of corporate social responsibility (CSR) on employees in an organization, they have mainly focused on employees’ perceptions or attitudes rather than behaviors. However, in that employees’ behaviors are the direct outcome of the perceptions or attitudes and critically affect organizational outcomes, we need to investigate the impact of CSR on employees’ behaviors. Based on the context-attitude-behavior framework, we investigate the underlying process of the association between CSR and employees’ behavior with a moderated mediation model. Specifically, we hypothesize (1) the intermediating effect of organizational commitment (OC) in the association between CSR and organizational citizenship behavior (OCB) and (2) the contingent role of employees’ perspective taking ability (PT) in the CSR-OC link. Using three-wave survey data from 301 currently working employees in Korea, we found that OC mediates the association between CSR and OCB and that PT can positively moderate the CSR-OC link. Our findings suggest that OC (as an intermediating process) and PT (as a contingent factor) function as important underlying mechanisms to elaborately describe the CSR-OCB link.
LACK OF SYMBIONT ACCOMMODATION controls intracellular symbiont accommodation in root nodule and arbuscular mycorrhizal symbiosis in Lotus japonicus

Nitrogen-fixing rhizobia and arbuscular mycorrhizal fungi (AMF) form symbioses with plant roots and these are established by precise regulation of symbiont accommodation within host plant cells. In model legumes such as Lotus japonicus and Medicago truncatula, rhizobia enter into roots through an intracellular invasion system that depends on the formation of a root-hair infection thread (IT). While IT-mediated intracellular rhizobia invasion is thought to be the most evolutionarily derived invasion system, some studies have indicated that a basal intercellular invasion system can replace it when some nodulation-related factors are genetically modified. In addition, intracellular rhizobia accommodation is suggested to have a similar mechanism as AMF accommodation. Nevertheless, our understanding of the underlying genetic mechanisms is incomplete. Here we identify a L. japonicus nodulation-deficient mutant, with a mutation in the LACK OF SYMBIONT ACCOMMODATION (LAN) gene, in which root-hair IT formation is strongly reduced, but intercellular rhizobial invasion eventually results in functional nodule formation. LjLAN encodes a protein that is homologous to Arabidopsis MEDIATOR 2/29/32 possibly acting as a subunit of a Mediator complex, a multiprotein complex required for gene transcription. We also show that LjLAN acts in parallel with a signaling pathway including LjCYCLOPS. In addition, the lan mutation drastically reduces the colonization levels of AMF. Taken together, our data provide a new factor that has a common role in symbiont accommodation process during root nodule and AM symbiosis.
Pre-operative ultrasonographic evaluation of inferior vena cava collapsibility index and caval aorta index as new predictors for hypotension after induction of spinal anaesthesia: A prospective observational study

BACKGROUND Hypotension after spinal anaesthesia is a common side effect that may be harmful. Patients’ susceptibility to intra-operative hypotension can be affected by many pre-operative factors. OBJECTIVES The current study aimed to evaluate the efficacy of both pre-operative inferior vena cava collapsibility index (IVCCI) and inferior vena cava to aorta diameter (IVC : Ao) index for predicting postspinal anaesthesia hypotension (PSAH). DESIGN Prospective observational blinded study. SETTING Operating room from June 2017 to February 2018. PATIENTS One hundred adult patients of both sexes, American Society of Anesthesiologists’ physical status 1 or 2 scheduled for elective surgery under spinal anaesthesia were included in this study. INTERVENTIONS Patients received spinal anaesthesia performed at the level of L3 to 4 or L4 to 5 intervertebral space with the patient in the sitting position then placed in the supine position immediately after neuraxial block and kept supine throughout the study period (30 min). IVCCI and IVC : Ao index were assessed pre-operatively. Baseline noninvasive blood pressure was recorded before administration of spinal anaesthesia then every minute after spinal blockade for 30 min. MAIN OUTCOME MEASURES The primary outcome was to evaluate the predictive values of both IVCCI and IVC : Ao index for detecting PSAH and the secondary outcomes were to compare the predictive values of both IVCCI and IVC : Ao index and to detect other clinical predictors for PSAH using logistic regression analysis. RESULTS Forty-five patients developed PSAH (45%). IVCCI was significantly higher in patients who developed PSAH than in patients who did not, while IVC : Ao index was significantly lower in patients who developed PSAH than in patients who did not. Hypotension after induction of spinal anaesthesia was defined as an absolute value of SBP less than 90 mmHg, a decrease in SBP more than 30% of the baseline value or an absolute value of arterial blood pressure less than 60 mmHg. Logistic regression analysis revealed that IVCCI and IVC : Ao index were good predictors of the occurrence of PSAH. Receiver operating characteristic curve analysis showed that IVC : Ao index had a sensitivity of 96%, a specificity of 88%, and an accuracy of 95% to predict PSAH at a cut-off point less than 1.2. IVCCI had a sensitivity of 84%, a specificity of 77%, and an accuracy of 84% to predict PSAH at a cut-off point more than 44.7%. CONCLUSION Pre-operative IVCCI and IVC : Ao index are good predictors of the occurrence of PSAH. However, IVC : Ao index is a more powerful predictor than IVCCI.
The Global Problem of Insufficient Sleep and Its Serious Public Health Implications

Good sleep is necessary for good physical and mental health and a good quality of life. Insufficient sleep is a pervasive and prominent problem in the modern 24-h society. A considerable body of evidence suggests that insufficient sleep causes hosts of adverse medical and mental dysfunctions. An extensive literature search was done in all the major databases for “insufficient sleep” and “public health implications” in this review. Globally, insufficient sleep is prevalent across various age groups, considered to be a public health epidemic that is often unrecognized, under-reported, and that has rather high economic costs. This paper addresses a brief overview on insufficient sleep, causes, and consequences, and how it adds to the existing burden of diseases. Insufficient sleep leads to the derailment of body systems, leading to increased incidences of cardiovascular morbidity, increased chances of diabetes mellitus, obesity, derailment of cognitive functions, vehicular accidents, and increased accidents at workplaces. The increased usage of smart phones and electronic devices is worsening the epidemic. Adolescents with insufficient sleep are likely to be overweight and may suffer from depressive symptoms. The paper concludes by emphasizing sleep quality assessments as an important early risk indicator, thereby reducing the incidence of a wide spectrum of morbidities.
Repair Schwann cell update: Adaptive reprogramming, EMT, and stemness in regenerating nerves

Schwann cells respond to nerve injury by cellular reprogramming that generates cells specialized for promoting regeneration and repair. These repair cells clear redundant myelin, attract macrophages, support survival of damaged neurons, encourage axonal growth, and guide axons back to their targets. There are interesting parallels between this response and that found in other tissues. At the cellular level, many other tissues also react to injury by cellular reprogramming, generating cells specialized to promote tissue homeostasis and repair. And at the molecular level, a common feature possessed by Schwann cells and many other cells is the injury‐induced activation of genes associated with epithelial–mesenchymal transitions and stemness, differentiation states that are linked to cellular plasticity and that help injury‐induced tissue remodeling. The number of signaling systems regulating Schwann cell plasticity is rapidly increasing. Importantly, this includes mechanisms that are crucial for the generation of functional repair Schwann cells and nerve regeneration, although they have no or a minor role elsewhere in the Schwann cell lineage. This encourages the view that selective tools can be developed to control these particular cells, amplify their repair supportive functions and prevent their deterioration. In this review, we discuss the emerging similarities between the injury response seen in nerves and in other tissues and survey the transcription factors, epigenetic mechanisms, and signaling cascades that control repair Schwann cells, with emphasis on systems that selectively regulate the Schwann cell injury response.
Preventing Substance Use in American Indian Youth: The Case for Social Support and Community Connections

Abstract Aims: This study explored the relationship between social support, community connections, self-esteem, and culture on misuse in American Indian youth. Methods: The study team developed a culturally-responsive 16-question survey for American Indian youth ages 12–20 living in six American Indian communities in the Great Plains Region of the United States. The study was grounded in primary socialization theory and variables were explored using regression models. Results: A total of 565 American Indian youth completed the participant survey between January 2016 and August 2017. The present study found that community connections were negatively associated with marijuana use in American Indian youth. Higher community connection scores were associated with higher social support and self-esteem scores. Conclusions: Tribally-led prevention initiatives can fill an important socio-behavioral prevention gap by facilitating social support opportunities for American Indian youth who may not have adequate support from immediate family or friends.
Protective Effects of Total Saponins of Aralia elata (Miq.) on Endothelial Cell Injury Induced by TNF-α via Modulation of the PI3K/Akt and NF-κB Signalling Pathways

Atherosclerosis is an arterial disease associated with inflammation. Hence, the discovery of novel therapeutic agents for suppressing inflammatory responses is urgent and vital for the treatment of atherosclerosis in cardiovascular diseases. The total saponins of Aralia elata (Miq.) Seem. (TAS) are the main components extracted from the Chinese traditional herb Longya Aralia chinensis L. , a folk medicine used in Asian countries for treating numerous diseases, enhancing energy and boosting immunity. However, the protective effects of TAS against inflammation-triggered vascular endothelial dysfunction, a critical early event during the course of atherosclerosis, and the potential mechanisms of this protection have been not demonstrated. Accordingly, the aim of this study was to investigate the anti-inflammatory and anti-apoptotic effects and the protective mechanisms of TAS, and show how TAS ameliorates human umbilical vein endothelial cell (HUVEC) damage caused by tumour necrosis factor-α (TNF-α). The results indicated that TAS exerted cytoprotective effects by inhibiting TNF-α-triggered HUVEC apoptosis, mitochondrial membrane potential depolarisation, and the regulation of inflammatory factors (IL-6, MCP-1, and VCAM-1) while suppressing NF-κB transcription. Furthermore, this phenomenon was related to activation of the phosphoinositide 3-kinase (PI3K)/Akt signalling pathway. Blocking the Akt pathway with LY294002, a PI3K inhibitor, reversed the cytoprotective effect of TAS against TNF-α-induced endothelial cell death. Moreover, LY294002 partially abolished the effects of TAS on the upregulation of the Bcl-2 family of proteins and the downregulation of Bax protein expression. In conclusion, the results of our study suggest that TAS suppresses the inflammation and apoptosis of HUVECs induced by TNF-α and that PI3K/Akt signalling plays a key role in promoting cell survival and anti-inflammatory reactions during this process.
Adrenomedullin Induces Cardiac Lymphangiogenesis After Myocardial Infarction and Regulates Cardiac Edema Via Connexin 43

Rationale: Cardiac lymphangiogenesis contributes to the reparative process post-myocardial infarction, but the factors and mechanisms regulating it are not well understood. Objective: To determine if epicardial-secreted factor AM (adrenomedullin; Adm=gene) improves cardiac lymphangiogenesis post-myocardial infarction via lateralization of Cx43 (connexin 43) in cardiac lymphatic vasculature. Methods and Results: Firstly, we identified sex-dependent differences in cardiac lymphatic numbers in uninjured mice using light-sheet microscopy. Using a mouse model of Admhi/hi (Adm overexpression) and permanent left anterior descending ligation to induce myocardial infarction, we investigated cardiac lymphatic structure, growth, and function in injured murine hearts. Overexpression of Adm increased lymphangiogenesis and cardiac function post-myocardial infarction while suppressing cardiac edema and correlated with changes in Cx43 localization. Lymphatic function in response to AM treatment was attenuated in mice with a lymphatic-specific Cx43 deletion. In vitro experiments in cultured human lymphatic endothelial cells identified a novel mechanism to improve gap junction coupling by pharmaceutically targeting Cx43 with verapamil. Finally, we show that connexin protein expression in cardiac lymphatics is conserved between mouse and human. Conclusions: AM is an endogenous, epicardial-derived factor that drives reparative cardiac lymphangiogenesis and function via Cx43, and this represents a new therapeutic pathway for improving myocardial edema after injury.
Vastatin (the NC1 domain of human type VIII collagen a1 chain) is linked to stromal reactivity and elevated in serum from patients with colorectal cancer

ABSTRACT Vastatin, a fragment derived from type VIII collagen, is one of the least studied collagen-derived matrikines. Vastatin can be detected in serum but little is known regarding the relevance of serum vastatin in colorectal cancer (CRC). In this study, serum vastatin was measured (ELISA) in 67 healthy controls and 48 CRC patients prior to resection and compared to clinicopathological parameters and serum biomarkers of stromal reactivity (C3M, VICM). Impact of resection and chemotherapy were evaluated by comparing baseline values with a 3-month follow-up sample (n = 23). Serum vastatin was detectable in 114 of 115 subjects. At baseline vastatin was elevated in CRC compared to controls (P < 0.001) with a diagnostic accuracy (AUROC) of 0.865, p < 0.0001. Vastatin correlated with age in controls but not in patients with CRC; no association was seen with clinicopathological parameters. Vastatin was independently associated with C3M (stepwise linear regression coefficient 0.25, p = 0.046). Overall, no difference was seen in vastatin levels between baseline and follow-up. In conclusion, vastatin is elevated in serum from patients with CRC and correlate with interstitial matrix degradation (C3M). This indicates that vastatin is linked to stromal reactivity and suggests that vastatin has biomarker potential in CRC. The association with clinicopathological parameters and treatment effect needs further evaluation.
Circumventing senescence is associated with stem cell properties and metformin sensitivity

Most cancers arise in old individuals, which also accumulate senescent cells. Cellular senescence can be experimentally induced by expression of oncogenes or telomere shortening during serial passage in culture. In vivo, precursor lesions of several cancer types accumulate senescent cells, which are thought to represent a barrier to malignant progression and a response to the aberrant activation of growth signaling pathways by oncogenes (oncogene toxicity). Here, we sought to define gene expression changes associated with cells that bypass senescence induced by oncogenic RAS. In the context of pancreatic ductal adenocarcinoma (PDAC), oncogenic KRAS induces benign pancreatic intraepithelial neoplasias (PanINs), which exhibit features of oncogene‐induced senescence. We found that the bypass of senescence in PanINs leads to malignant PDAC cells characterized by gene signatures of epithelial‐mesenchymal transition, stem cells, and mitochondria. Stem cell properties were similarly acquired in PanIN cells treated with LPS, and in primary fibroblasts and mammary epithelial cells that bypassed Ras‐induced senescence after reduction of ERK signaling. Intriguingly, maintenance of cells that circumvented senescence and acquired stem cell properties was blocked by metformin, an inhibitor of complex I of the electron transport chain or depletion of STAT3, a protein required for mitochondrial functions and stemness. Thus, our studies link bypass of senescence in premalignant lesions to loss of differentiation, acquisition of stemness features, and increased reliance on mitochondrial functions.
Nocturnal Atrial Fibrillation Caused by Mutation in KCND2, Encoding Pore-Forming (&agr;) Subunit of the Cardiac Kv4.2 Potassium Channel

Background: Paroxysmal atrial fibrillation (AF) can be caused by gain-of-function mutations in genes, encoding the cardiac potassium channel subunits KCNJ2, KCNE1, and KCNH2 that mediate the repolarizing potassium currents Ik1, Iks, and Ikr, respectively. Methods: Linkage analysis, whole-exome sequencing, and Xenopus oocyte electrophysiology studies were used in this study. Results: Through genetic studies, we showed that autosomal dominant early-onset nocturnal paroxysmal AF is caused by p.S447R mutation in KCND2, encoding the pore-forming (&agr;) subunit of the Kv4.2 cardiac potassium channel. Kv4.2, along with Kv4.3, contributes to the cardiac fast transient outward K+ current, Ito. Ito underlies the early phase of repolarization in the cardiac action potential, thereby setting the initial potential of the plateau phase and governing its duration and amplitude. In Xenopus oocytes, the mutation increased the channel’s inactivation time constant and affected its regulation: p.S447 resides in a protein kinase C (PKC) phosphorylation site, which normally allows attenuation of Kv4.2 membrane expression. The mutant Kv4.2 exhibited impaired response to PKC; hence, Kv4.2 membrane expression was augmented, enhancing potassium currents. Coexpression of mutant and wild-type channels (recapitulating heterozygosity in affected individuals) showed results similar to the mutant channel alone. Finally, in a hybrid channel composed of Kv4.3 and Kv4.2, simulating the mature endogenous heterotetrameric channel underlying Ito, the p.S447R Kv4.2 mutation exerted a gain-of-function effect on Kv4.3. Conclusions: The mutation alters Kv4.2’s kinetic properties, impairs its inhibitory regulation, and exerts gain-of-function effect on both Kv4.2 homotetramers and Kv4.2-Kv4.3 heterotetramers. These effects presumably increase the repolarizing potassium current Ito, thereby abbreviating action potential duration, creating arrhythmogenic substrate for nocturnal AF. Interestingly, Kv4.2 expression was previously shown to demonstrate circadian variation, with peak expression at daytime in murine hearts (human nighttime), with possible relevance to the nocturnal onset of paroxysmal AF symptoms in our patients. The atrial-specific phenotype suggests that targeting Kv4.2 might be effective in the treatment of nocturnal paroxysmal AF, avoiding adverse ventricular effects.
HCN4 knockdown in dorsal hippocampus promotes anxiety‐like behavior in mice

Hyperpolarization‐activated and cyclic nucleotide‐gated (HCN) channels mediate the Ih current in the murine hippocampus. Disruption of the Ih current by knockout of HCN1, HCN2 or tetratricopeptide repeat‐containing Rab8b‐interacting protein has been shown to affect physiological processes such as synaptic integration and maintenance of resting membrane potentials as well as several behaviors in mice, including depressive‐like and anxiety‐like behaviors. However, the potential involvement of the HCN4 isoform in these processes is unknown. Here, we assessed the contribution of the HCN4 isoform to neuronal processing and hippocampus‐based behaviors in mice. We show that HCN4 is expressed in various regions of the hippocampus, with distinct expression patterns that partially overlapped with other HCN isoforms. For behavioral analysis, we specifically modulated HCN4 expression by injecting recombinant adeno‐associated viral (rAAV) vectors mediating expression of short hairpin RNA against hcn4 (shHcn4) into the dorsal hippocampus of mice. HCN4 knockdown produced no effect on contextual fear conditioning or spatial memory. However, a pronounced anxiogenic effect was evident in mice treated with shHcn4 compared to control littermates. Our findings suggest that HCN4 specifically contributes to anxiety‐like behaviors in mice.
Changes in Fingerprints Depending on Physiological Factors

The aim of the study was to determine the effect of gender, body mass index, and time on the width of friction ridge impressions in fingerprints and the content of sweat and sebum forming the print. The research showed that the friction ridge impressions of women are significantly wider than those of men, and this tendency persists throughout the existence of the print. The differences may result from the anatomical structure of the skin, as well as from the use of protective products such as creams, which are used more often by women. The width of friction ridge impression is similar in underweight and overweight people, but greater than in those with normal body weight, and the amount of sweat and sebum increases with body weight. The passage of time significantly reduces both the width of the friction ridge impression and the content of sweat and sebum secretions in the print.