Miracle-dz/UniFAR-FTUs huggingface dataset:
Atomic‐Precision Repair of a Few‐Layer 2H‐MoTe2 Thin Film by Phase Transition and Recrystallization Induced by a Heterophase Interface

2D semiconductors have emerged as promising candidates for post‐silicon nanoelectronics, owing to their unique properties and atomic thickness. However, in the handling of 2D material, various forms of macroscopic damage, such as cracks, wrinkles, and scratches, etc., are usually introduced, which cause adverse effects on the material properties and device performance. Repairing such macroscopic damage is crucial for improving device performance and reliability, especially for large‐scale 2D device arrays. Here, a method is demonstrated repair damage to few‐layer 2H‐MoTe2 films with atomic precision, and its mechanism is elucidated. The repaired 2H‐MoTe2 inherits the lattice orientation of the adjacent original 2H‐MoTe2, thereby forming an atomically perfect lattice at the repaired interface. The time‐evolution experiments show that the interface between the 2H‐ and early formed 1T'‐MoTe2 plays an important role in the subsequent phase transition and recrystallization. Electrical measurements on the original MoTe2, repaired MoTe2, and cross‐interface regions show unobservable differences, indicating that the repaired MoTe2 has the same electrical quality as the original one and the interface does not introduce extra scattering centers for carrier transport. The findings provide an effective strategy for macroscopic damage repair of few‐layer 2H‐MoTe2, which paves the way for its practical application in advanced electronics and optoelectronics.
The COVID-19 Outbreak and Affected Countries Stock Markets Response

This paper evaluates the short-term impact of the coronavirus outbreak on 21 leading stock market indices in major affected countries including Japan, Korea, Singapore, the USA, Germany, Italy, and the UK etc. The consequences of infectious disease are considerable and have been directly affecting stock markets worldwide. Using an event study method, our results indicate that the stock markets in major affected countries and areas fell quickly after the virus outbreak. Countries in Asia experienced more negative abnormal returns as compared to other countries. Further panel fixed effect regressions also support the adverse effect of COVID-19 confirmed cases on stock indices abnormal returns through an effective channel by adding up investors’ pessimistic sentiment on future returns and fears of uncertainties.
Effects of fasting on isolated murine skeletal muscle contractile function during acute hypoxia

Stored muscle carbohydrate supply and energetic efficiency constrain muscle functional capacity during exercise and are influenced by common physiological variables (e.g. age, diet, and physical activity level). Whether these constraints affect overall functional capacity or the timing of muscle energetic failure during acute hypoxia is not known. We interrogated skeletal muscle contractile properties in two anatomically distinct rodent hindlimb muscles that have well characterized differences in energetic efficiency (locomotory- extensor digitorum longus (EDL) and postural- soleus muscles) following a 24 hour fasting period that resulted in substantially reduced muscle carbohydrate supply. 180 mins of acute hypoxia resulted in complete energetic failure in all muscles tested, indicated by: loss of force production, substantial reductions in total adenosine nucleotide pool intermediates, and increased adenosine nucleotide degradation product—inosine monophosphate (IMP). These changes occurred in the absence of apparent myofiber structural damage assessed histologically by both transverse section and whole mount. Fasting and the associated reduction of the available intracellular carbohydrate pool (~50% decrease in skeletal muscle) did not significantly alter the timing to muscle functional impairment or affect the overall force/work capacities of either muscle type. Fasting resulted in greater passive tension development in both muscle types, which may have implications for the design of pre-clinical studies involving optimal timing of reperfusion or administration of precision therapeutics.
NO placental inflammation

The placenta is the site at which nutrient and waste exchange between the fetus and its mother occurs. Fetal growth and development are dependent upon an efficient placenta, requiring close proximity of well-developed fetal and maternal placental circulations . In humans, the extraembryonic trophoblast cells of the blastocyst burrow deep into the endometrial lining and stroma of the uterine wall and progress as far as the maternal spiral arteries. Invasive cytotrophoblasts erode the endothelial and smooth muscle cells of these arteries and maternal blood flows into pools lined by the syncytiotrophoblasts. On the fetal side, the functional units of the placenta are the villi, that is, branching columns of syncytiotrophoblast, cytotrophoblast and mesodermal stromal cells. Branches of the umbilical vessels delve into the extraembryonic mesodermal columns, populating them with capillaries. Thus, fetal blood is separated from maternal blood by a single layer each of umbilical capillary endothelial cells (ECs), cytotrophoblasts and syncytiotrophoblasts. Impaired placental development and/or function results in fetal growth restriction (FGR) and is associated with pre-eclampsia (PE), levels are markedly increased in women with PE and FGR. Haemoglobin is also S-nitrosylated and Hb-NO in human umbilical artery is only half of that in umbilical vein, demonstrating that placentally-derived NO is transported for release in the fetus during deoxygenation. In human neonates (<4 days old) receiving oxygen support, tracheal fluid RS-NO was only 10% of normal and adding NO to the oxygen improved the situation. In PE pregnancies Hb synthesis is increased and may appear in the free form in the fetal circulation. A recent elegant study found that the Hb concentration was increased in the cord blood in FGR. In ex vivo placental perfusion studies, increasing Hb sequestered NO and increased umbilical vessel resistance. In vitro incubation of placental ECs in Hb induced a pro-inflammatory phenotype, with release of interleukin (IL)-1  , TNF-  and NK-  B (Brook et al. , 2018). Thus, free Hb will exacerbate FGR, or could even cause it. Hence, protein nitrosylation and subsequent NO release has important physiological outcomes in terms of blood flow and airway function, including in the fetus and neonate.
Contactless Real-Time Heartbeat Detection via 24 GHz Continuous-Wave Doppler Radar Using Artificial Neural Networks

The measurement of human vital signs is a highly important task in a variety of environments and applications. Most notably, the electrocardiogram (ECG) is a versatile signal that could indicate various physical and psychological conditions, from signs of life to complex mental states. The measurement of the ECG relies on electrodes attached to the skin to acquire the electrical activity of the heart, which imposes certain limitations. Recently, due to the advancement of wireless technology, it has become possible to pick up heart activity in a contactless manner. Among the possible ways to wirelessly obtain information related to heart activity, methods based on mm-wave radars proved to be the most accurate in detecting the small mechanical oscillations of the human chest resulting from heartbeats. In this paper, we presented a method based on a continuous-wave Doppler radar coupled with an artificial neural network (ANN) to detect heartbeats as individual events. To keep the method computationally simple, the ANN took the raw radar signal as input, while the output was minimally processed, ensuring low latency operation (<1 s). The performance of the proposed method was evaluated with respect to an ECG reference (“ground truth”) in an experiment involving 21 healthy volunteers, who were sitting on a cushioned seat and were refrained from making excessive body movements. The results indicated that the presented approach is viable for the fast detection of individual heartbeats without heavy signal preprocessing.
Transient receptor potential channel TRPV4 mediates TGF-β1-induced differentiation of human ventricular fibroblasts.

BACKGROUND Cardiac fibroblasts (CFs) are principal extracellular matrix-producing cells. In response to injury, CFs transdifferentiate into myofibroblasts. Intracellular calcium (Ca2+) signaling, involved in fibroblast proliferation and differentiation, is activated in fibroblasts through transient receptor potential (TRP) channels, but the function of these channels has not been investigated in human ventricular CFs. Under evaluation in this study, was the role of TRP channels in the differentiation of human ventricular CFs induced by transforming the growth factor beta (TGF-β), a pro-fibrotic cytokine. METHODS Human ventricular CFs were used in this study. The differentiation of CFs into myofibroblast was induced with TGF-β and was identified by the expression of smooth muscle actin. RESULTS Results indicate that Ca2+ signaling was an essential component of ventricular CF differentiation. CFs treated with TGF-β demonstrated increased expression of a TRP channel, TRPV4, both at the mRNA and protein levels, which corresponded with CF-myofibroblast trans-differentiation, as evidenced by the upregulation of α-smooth muscle actin, a myofibroblast marker, and plasminogen activator inhibitor-1, which are fibrogenesis markers. An agonist of TRPV4 induced the conversion of CFs into myofibroblasts, whereas it's antagonist as well a Ca2+ chelating agent reduced it, indicating that the Ca2+ influx throughTRPV4 is required for CF trans-differentiation. Overall, these results demonstrate that TRPV4-mediated Ca2+ influx participates in regulating the differentiation of human ventricular CFs into myofibroblasts through the MAPK/ERK pathway. CONCLUSIONS Overall, these results demonstrate that TRPV4-mediated Ca2+ influx participates in regulating the differentiation of human ventricular CFs into myofibroblasts through the MAPK/ERK pathway.
Legionella pneumophila and Protozoan Hosts: Implications for the Control of Hospital and Potable Water Systems

Legionella pneumophila is an opportunistic waterborne pathogen of public health concern. It is the causative agent of Legionnaires’ disease (LD) and Pontiac fever and is ubiquitous in manufactured water systems, where protozoan hosts and complex microbial communities provide protection from disinfection procedures. This review collates the literature describing interactions between L. pneumophila and protozoan hosts in hospital and municipal potable water distribution systems. The effectiveness of currently available water disinfection protocols to control L. pneumophila and its protozoan hosts is explored. The studies identified in this systematic literature review demonstrated the failure of common disinfection procedures to achieve long term elimination of L. pneumophila and protozoan hosts from potable water. It has been demonstrated that protozoan hosts facilitate the intracellular replication and packaging of viable L. pneumophila in infectious vesicles; whereas, cyst-forming protozoans provide protection from prolonged environmental stress. Disinfection procedures and protozoan hosts also facilitate biogenesis of viable but non-culturable (VBNC) L. pneumophila which have been shown to be highly resistant to many water disinfection protocols. In conclusion, a better understanding of L. pneumophila-protozoan interactions and the structure of complex microbial biofilms is required for the improved management of L. pneumophila and the prevention of LD.
Mesencephalic astrocyte–derived neurotrophic factor is an ER-resident chaperone that protects against reductive stress in the heart

We have previously demonstrated that ischemia/reperfusion (I/R) impairs endoplasmic reticulum (ER)-based protein folding in the heart and thereby activates an unfolded protein response sensor and effector, activated transcription factor 6α (ATF6). ATF6 then induces mesencephalic astrocyte-derived neurotrophic factor (MANF), an ER-resident protein with no known structural homologs and unclear ER function. To determine MANF's function in the heart in vivo, here we developed a cardiomyocyte-specific MANF-knockdown mouse model. MANF knockdown increased cardiac damage after I/R, which was reversed by AAV9-mediated ectopic MANF expression. Mechanistically, MANF knockdown in cultured neonatal rat ventricular myocytes (NRVMs) impaired protein folding in the ER and cardiomyocyte viability during simulated I/R. However, this was not due to MANF-mediated protection from reactive oxygen species generated during reperfusion. Because I/R impairs oxygen-dependent ER protein disulfide formation and such impairment can be caused by reductive stress in the ER, we examined the effects of the reductive ER stressor DTT. MANF knockdown in NRVMs increased cell death from DTT-mediated reductive ER stress, but not from nonreductive ER stresses caused by thapsigargin-mediated ER Ca2+ depletion or tunicamycin-mediated inhibition of ER protein glycosylation. In vitro, recombinant MANF exhibited chaperone activity that depended on its conserved cysteine residues. Moreover, in cells, MANF bound to a model ER protein exhibiting improper disulfide bond formation during reductive ER stress but did not bind to this protein during nonreductive ER stress. We conclude that MANF is an ER chaperone that enhances protein folding and myocyte viability during reductive ER stress.
Development of an Analytical Model to Describe the Disperse Melting in Wave-Dispersion Screws

The progressive development of new screw concepts in single screw extrusion also makes it necessary to develop new models for the correct process description. When looking at wave-dispersion screws, the disperse melting behavior should be mentioned in particular, which has so far been less researched and modeled than the conventional melting behavior, as it occurs in standard screws. Therefore, an analytical model is presented in this paper, which considers the disperse melting under consideration of the melt and solid temperature. The basic assumption is Fourier heat conduction from the melt surrounding the particles into the particles. Furthermore, the melt temperature development by dissipation and the cooling effects were modeled analytically. Additionally, the solid bed temperature was modeled by a 2D-FDM method. By dividing the screw into several calculation sections with constant boundary conditions, it was subsequently possible to calculate the melting process over the screw length. The model developed shows comprehensible results in verification and successfully reproduces the solids content over the screw length with a mean deviation of absolute 11% in validation tests using cooling/pulling-out experiments.
Polygenic Scores to Assess Atherosclerotic Cardiovascular Disease Risk

An individual’s susceptibility to atherosclerotic cardiovascular disease is influenced by numerous clinical and lifestyle factors, motivating the multifaceted approaches currently endorsed for primary and secondary cardiovascular disease prevention. With growing knowledge of the genetic basis of atherosclerotic cardiovascular disease—in particular, coronary artery disease—and its contribution to disease pathogenesis, there is increased interest in understanding the potential clinical utility of a genetic predictor that might further refine the assessment and management of atherosclerotic cardiovascular disease risk. Rapid scientific and technological advances have enabled widespread genotyping efforts and dynamic research in the field of coronary artery disease genetic risk prediction. In this review, we describe how genomic analyses of coronary artery disease have been leveraged to create polygenic risk scores. We then discuss evaluations of the clinical utility of these scores, pertinent mechanistic insights gleaned, and practical considerations relevant to the implementation of polygenic risk scores in the health care setting.
Surgical results in older patients with lumbar spinal stenosis according to gait speed in relation to the diagnosis for sarcopenia

Purpose: The purpose of this study was to evaluate the implication of gait speed, which is a prerequisite for the diagnosis of sarcopenia in older patients with lumbar spinal stenosis (LSS). Methods: This study was conducted in a total of 235 patients with LSS who underwent surgical treatment. The state of sarcopenia and pre-sarcopenia, including gait speed, were evaluated before and after the operation. Results: The proportion of patients with lower than at baseline levels of skeletal muscle mass index (SMI) and gait speed was 27.2% and 17.9%, respectively. Significant changes were observed in gait speed, whereas SMI showed no significant differences between the preoperative and postoperative periods. Sarcopenic patients presented lower levels of activities of daily living preoperatively than pre-sarcopenic patients. However, favorable surgical results were obtained postoperatively. Significant changes were observed in gait speed, whereas grip strength and SMI showed no significant differences between the preoperative and postoperative periods. The postoperative decrease in SMI was not significant. Conclusion: Postoperative gait speed was significantly improved, whereas muscle mass did not increase in the patients in this study. Therefore, low gait speed in patients with LSS seems to be derived from a neurologic disorder. The surgical results in low muscle mass patients without low gait speed were similar to those with low gait speed. Sarcopenia in elderly patients with locomotor disease should be evaluated using muscle mass alone without assessing physical performance.
Morphological variation associated with trophic niche expansion within a lake population of a benthic fish

Ecological theory suggests that generalist species should have traits with multiple adaptive peaks. Consequently, in heterogeneous environments such adaptive landscapes may lead to phenotypic divergence that becomes fixed in populations via reproductive isolation, thus driving speciation. However, contrary to this expectation, the process of ecological diversification in wild populations is not always associated with obvious trait divergence and reproductive isolation due to some ecological and geographic constrains. To examine the ecological conditions that promote (or inhibit) divergence is quite important to improve our understanding of the underlying mechanisms. Here we examine how the patterns of trait variation (divergence/non-divergence) are determined in relation to ecological niche expansion and gene flow using a benthic fish, Pseudogobio esocinus, in the Lake Biwa system, Japan. The fish exhibited various patterns of morphological variation in mouth parts among populations. Lake fish tended to have a smaller mouth compared with river fish and also showed remarkable individual variations within some local samples. Lake fish utilized chironomid larvae as the primary prey, as in riverine fish. But, fish with smaller and narrower mouths utilized significantly higher proportions of amphipods (a novel prey unique to the lake) as their secondary prey. Microsatellite analysis detected no genetic structuring in the Lake Biwa catchment, suggesting no reproductive separation among eco-morphologically divergent individuals. Our results exemplify population niche expansion associated with continuous eco-morphological variation without divergence, and provide insights into the role of non-discrete diversification for thriving in heterogeneous environments.
Natural Language Generation Model for Mammography Reports Simulation

Extending the size of labeled corpora of medical reports is a major step towards a successful training of machine learning algorithms. Simulating new text reports is a key solution for reports augmentation, which extends the cohort size. However, text generation in the medical domain is challenging because it needs to preserve both content and style that are typical for real reports, without risking the patients’ privacy. In this paper, we present a conditioned LSTM-RNN architecture for simulating realistic mammography reports. We evaluated the performance by analyzing the characteristics of the simulated reports and classifying them into benign and malignant classes. An average classification AUC was calculated over two distinct test sets. A qualitative analysis was also performed in which a masked radiologist classified 0.75 of the simulated reports as real reports, showing that both the style and content of the simulated reports were similar to real reports. Finally, we compared our RNN-LSTM generative model with Markov Random Fields. The RNN-LSTM provided significantly better and more stable performance than MRFs ($p< 0.01$, Wilcoxon).
The Relationship between Trauma Exposure and Psychiatric Hospitalization for Suicide Ideation or Suicide Attempt among Patients Admitted to a Military Treatment Setting

Suicide attempts and psychiatric hospitalization represent the final outcomes of a complex dynamical system of interacting factors that influence a particular individual’s likelihood of engaging in suicidal behavior, as well as their ability to seek help prior to acting upon suicidal impulses. This study examined the association between different types of lifetime trauma exposure and the likelihood of psychiatric hospitalization following a suicide attempt (SA) rather than suicidal ideation (SI) alone. Electronic medical records for 1100 U.S. military service members and their dependents admitted to a military psychiatric inpatient setting for SA or SI were reviewed for documented lifetime trauma exposure history. Findings indicated that exposure to at least one childhood trauma of any type, and childhood neglect in particular, increased the likelihood that an individual would be hospitalized for SA rather than SI. Exploratory gender-stratified analyses demonstrated that childhood neglect, childhood sexual abuse, and adulthood traumatic loss may be linked with the likelihood of being hospitalized for SA. These findings demonstrate the importance of developing more detailed and nuanced conception of factors known to be associated with suicide as their effects may depend on details of their timing and nature, as well as their interactions with other systems.