Miracle-dz/UniFAR-FTUs huggingface dataset:
Research Progress and Challenges of Transient Protection for Transmission Lines in Large-Scale Wind Farms

With the continuous advancement of renewable energy grid-connected technology, wind power plays an important role in it due to its mature technology and is developing rapidly around the world (Rezaei et al., 2020; Tian et al., 2017). The safe operation of the systems will be affected by randomness, intermittency, and volatility after large-scale wind farms are connected to the grid, among which impact on relay protection is the most significant (Telukunta et al., 2017; Xi et al., 2016). There are many differences in fault characteristics after large-scale wind farms are connected to the grid compared with traditional power grids (Yang et al., 2016). These differences are mainly reflected in frequency offset, weak feed, and high harmonics, which cause problems such as incorrect operation and decreased sensitivity when traditional power frequency protection is used in largescale wind farms (Niknezhad and Sadesh, 2021; Ma et al., 2020). A large-scale wind farms system, the current waveform on the wind farm after a three-phase short-circuit, and the protection coordination scheme of the transmission line are shown in Figure 1. With the continuous rise of global energy consumption and changes in load demand (Yang et al., 2020a; Sun and Yang, 2020), the performance of relay protection is required to develop towards higher-speed operation due to the nonlinearity and fragility of electronic power equipment (Yang et al., 2020b). After a fault, rich fault information is available in high-frequency transients, and the time window required for transient protection is short (Chen et al., 2019). The rapidity of transient protection action is more in line with the requirements of modern power systems. Therefore, the study of transient protection is a current developmental trend in relay protection. The idea of relay protection based on transient is that the transmission line is protected at high speed through fault transient information. In recent years, research based on the principle of transient protection mainly includes time-domain distance protection, protection based on double-ended waveform comparison, and protection based on fault traveling waves. In this paper, the current transient protection methods for large-scale wind farms are summarized. The advantages and disadvantages of each type of method are discussed. The latest progress and challenges of transient protection for large-scale wind farms are summarized.
Decompositions of n-Partite Nonsignaling Correlation-Type Tensors With Applications

When an n-partite physical system is measured by n observers, the joint probabilities of outcomes conditioned on the observables chosen by the n parties form a nonnegative tensor, called an n-partite correlation tensor (CT). In this paper, we aim to establish some characterizations of nonsignaling and Bell locality of an n-partite CT, respectively. By placing CTs within the linear space of correlation-type tensors (CTTs), we prove that every n-partite nonsignaling CTT can be decomposed as a linear combination of all local deterministic CTs using single-value decomposition of matrices and mathematical induction. As a consequence, we prove that an n-partite CT is nonsignaling (resp. Bell local) if and only if it can be written as a quasi-convex (resp. convex) combination of the outer products of deterministic CTs, implying that an n-partite CT is nonsignaling if and only if it has a local hidden variable model governed by a quasi-probability distribution. As an application of these results, we prove that a CT is nonsignaling if and only if it can be written as a quasi-convex of two Bell local ones, revealing a close relationship between nonsignaling CTs and Bell local ones.
A Communication Coding System for Use in High Conflict Interpersonal Relationships

Conflict is a natural but uncomfortable part of all human relationships. Researchers and practitioners alike are interested in developing training and therapeutic methods for teaching couples and families healthy conflict management styles. However, the research literature offers little for practitioners in the way of specific verbal and nonverbal “skills” they can teach to their clients and patients. In this paper, we examine the work of Dr. Steven Winer, educator and practitioner in Communication, with a focus on anger management and conflict resolution in interpersonal relationships. We review the research literature on interpersonal conflict and compare it to the advice offered through Dr. Winer's workshops, which he developed through years of viewing over 4,000 videotapes of communication behavior patterns exhibited by his clients during conflict role-play sessions.
STIM and Orai Mediated Regulation of Calcium Signaling in Age-Related Diseases

Tight spatiotemporal regulation of intracellular Ca2+ plays a critical role in regulating diverse cellular functions including cell survival, metabolism, and transcription. As a result, eukaryotic cells have developed a wide variety of mechanisms for controlling Ca2+ influx and efflux across the plasma membrane as well as Ca2+ release and uptake from intracellular stores. The STIM and Orai protein families comprising of STIM1, STIM2, Orai1, Orai2, and Orai3, are evolutionarily highly conserved proteins that are core components of all mammalian Ca2+ signaling systems. STIM1 and Orai1 are considered key players in the regulation of Store Operated Calcium Entry (SOCE), where release of Ca2+ from intracellular stores such as the Endoplasmic/Sarcoplasmic reticulum (ER/SR) triggers Ca2+ influx across the plasma membrane. SOCE, which has been widely characterized in non-excitable cells, plays a central role in Ca2+-dependent transcriptional regulation. In addition to their role in Ca2+ signaling, STIM1 and Orai1 have been shown to contribute to the regulation of metabolism and mitochondrial function. STIM and Orai proteins are also subject to redox modifications, which influence their activities. Considering their ubiquitous expression, there has been increasing interest in the roles of STIM and Orai proteins in excitable cells such as neurons and myocytes. While controversy remains as to the importance of SOCE in excitable cells, STIM1 and Orai1 are essential for cellular homeostasis and their disruption is linked to various diseases associated with aging such as cardiovascular disease and neurodegeneration. The recent identification of splice variants for most STIM and Orai isoforms while complicating our understanding of their function, may also provide insight into some of the current contradictions on their roles. Therefore, the goal of this review is to describe our current understanding of the molecular regulation of STIM and Orai proteins and their roles in normal physiology and diseases of aging, with a particular focus on heart disease and neurodegeneration.
The Game for Three: Salmonella–Host–Microbiota Interaction Models

Colonization of the gastrointestinal (GI) tract by enteric pathogens occurs in a context strongly determined by host-specific gut microbiota, which can significantly affect the outcome of infection. The complex gameplay between the trillions of microbes that inhabit the GI tract, the host, and the infecting pathogen defines a specific triangle of interaction; therefore, a complete model of infection should consider all of these elements. Many different infection models have been developed to explain the complexity of these interactions. This review sheds light on current knowledge, along with the strengths and limitations of in vitro and in vivo models utilized in the study of Salmonella–host–microbiome interactions. These models range from the simplest experiment simulating environmental conditions using dedicated growth media through in vitro interaction with cell lines and 3-D organoid structure, and sophisticated “gut on a chip” systems, ending in various animal models. Finally, the challenges facing this field of research and the important future directions are outlined.
Genotype-Driven Pathogenesis of Atrial Fibrillation in Hypertrophic Cardiomyopathy: The Case of Different TNNT2 Mutations

Atrial dilation and atrial fibrillation (AF) are common in Hypertrophic CardioMyopathy (HCM) patients and associated with a worsening of prognosis. The pathogenesis of atrial myopathy in HCM remains poorly investigated and no specific association with genotype has been identified. By re-analysis of our cohort of thin-filament HCM patients (Coppini et al. 2014) AF was identified in 10% of patients with sporadic mutations in the cardiac Troponin T gene (TNNT2), while AF occurrence was much higher (25–75%) in patients carrying specific “hot-spot” TNNT2 mutations. To determine the molecular basis of arrhythmia occurrence, two HCM mouse models expressing human TNNT2 variants (a “hot-spot” one, R92Q, and a “sporadic” one, E163R) were selected according to the different pathophysiological pathways previously demonstrated in ventricular tissue. Echocardiography studies showed a significant left atrial dilation in both models, but more pronounced in the R92Q. In E163R atrial trabeculae, in line with what previously observed in ventricular preparations, the energy cost of tension generation was markedly increased. However, no changes of twitch amplitude and kinetics were observed, and there was no atrial arrhythmic propensity. R92Q atrial trabeculae, instead, displayed normal ATP consumption but markedly increased myofilament calcium sensitivity, as previously observed in ventricular preparations. This was associated with reduced inotropic reserve and slower kinetics of twitch contractions and, importantly, with an increased occurrence of spontaneous beats and triggered contractions that represent an intrinsic arrhythmogenic mechanism promoting AF. The association of specific TNNT2 mutations with AF occurrence depends on the mutation-driven pathomechanism (i.e., increased atrial myofilament calcium sensitivity rather than increased myofilament tension cost) and may influence the individual response to treatment.
The Na+/H+ Exchanger 3 in the Intestines and the Proximal Tubule of the Kidney: Localization, Physiological Function, and Key Roles in Angiotensin II-Induced Hypertension

The sodium (Na+)/hydrogen (H+) exchanger 3 (NHE3) is one of the most important Na+/H+ antiporters in the small intestines of the gastrointestinal tract and the proximal tubules of the kidney. The roles of NHE3 in the regulation of intracellular pH and acid–base balance have been well established in cellular physiology using in vitro techniques. Localized primarily on the apical membranes in small intestines and proximal tubules, the key action of NHE3 is to facilitate the entry of luminal Na+ and the extrusion of intracellular H+ from intestinal and proximal tubule tubular epithelial cells. NHE3 is, directly and indirectly, responsible for absorbing the majority of ingested Na+ from small and large intestines and reabsorbing >50% of filtered Na+ in the proximal tubules of the kidney. However, the roles of NHE3 in the regulation of proximal tubular Na+ transport in the integrative physiological settings and its contributions to the basal blood pressure regulation and angiotensin II (Ang II)-induced hypertension have not been well studied previously due to the lack of suitable animal models. Recently, novel genetically modified mouse models with whole-body, kidney-specific, or proximal tubule-specific deletion of NHE3 have been generated by us and others to determine the critical roles and underlying mechanisms of NHE3 in maintaining basal body salt and fluid balance, blood pressure homeostasis, and the development of Ang II-induced hypertension at the whole-body, kidney, or proximal tubule levels. The objective of this invited article is to review, update, and discuss recent findings on the critical roles of intestinal and proximal tubule NHE3 in maintaining basal blood pressure homeostasis and their potential therapeutic implications in the development of angiotensin II (Ang II)-dependent hypertension.
Editorial: Coronavirus Disease (COVID-19): The Mental Health, Resilience, and Communication Resources for the Short- and Long-term Challenges Faced by Healthcare Workers

Citation: Mitchell AEP, Galli F, Keyworth C, Vegni E and Salas E (2022) Editorial: Coronavirus Disease (COVID-19): The Mental Health, Resilience, and Communication Resources for the Shortand Long-term Challenges Faced by Healthcare Workers. Front. Psychol. 13:904328. doi: 10.3389/fpsyg.2022. 904328 Editorial: Coronavirus Disease (COVID-19): The Mental Health, Resilience, and Communication Resources for the Shortand Long-term Challenges Faced by Healthcare Workers
A Non-redundant Function of MNS5: A Class I α-1, 2 Mannosidase, in the Regulation of Endoplasmic Reticulum-Associated Degradation of Misfolded Glycoproteins

Endoplasmic Reticulum-Associated Degradation (ERAD) is one of the major processes in maintaining protein homeostasis. Class I α-mannosidases MNS4 and MNS5 are involved in the degradation of misfolded variants of the heavily glycosylated proteins, playing an important role for glycan-dependent ERAD in planta. MNS4 and MNS5 reportedly have functional redundancy, meaning that only the loss of both MNS4 and MNS5 shows phenotypes. However, MNS4 is a membrane-associated protein while MNS5 is a soluble protein, and both can localize to the endoplasmic reticulum (ER). Furthermore, MNS4 and MNS5 differentially demannosylate the glycoprotein substrates. Importantly, we found that their gene expression patterns are complemented rather than overlapped. This raises the question of whether they indeed work redundantly, warranting a further investigation. Here, we conducted an exhaustive genetic screen for a suppressor of the bri1-5, a brassinosteroid (BR) receptor mutant with its receptor downregulated by ERAD, and isolated sbi3, a suppressor of bri1-5 mutant named after sbi1 (suppressor of bri1). After genetic mapping together with whole-genome re-sequencing, we identified a point mutation G343E in AT1G27520 (MNS5) in sbi3. Genetic complementation experiments confirmed that sbi3 was a loss-of-function allele of MNS5. In addition, sbi3 suppressed the dwarf phenotype of bri1-235 in the proteasome-independent ERAD pathway and bri1-9 in the proteasome-dependent ERAD pathway. Importantly, sbi3 could only affect BRI1/bri1 with kinase activities such that it restored BR-sensitivities of bri1-5, bri1-9, and bri1-235 but not null bri1. Furthermore, sbi3 was less tolerant to tunicamycin and salt than the wild-type plants. Thus, our study uncovers a non-redundant function of MNS5 in the regulation of ERAD as well as plant growth and ER stress response, highlighting a need of the traditional forward genetic approach to complement the T-DNA or CRISPR-Cas9 systems on gene functional study.
Increasing Liana Abundance and Associated Reductions in Tree Growth in Secondary Seasonally Dry Tropical Forest

Lianas are thought to be increasing and altering tree growth and ecosystem productivity in tropical forests, but less research has focused on secondary or seasonally dry tropical forest. We report on an 11-year study of tree growth and liana presence from Guanacaste, Costa Rica, where we measured the diameter growth and liana presence on more than 1,700 trees in regenerating forest of different ages. We find that the proportion of trees without lianas is decreasing and the number of trees with lianas occupying more than 10% of tree’s crowns is increasing. We also find that lianas are affecting the diameter growth of trees. The 11-year average relative growth rates of trees with lianas in more than 10% of the tree’s crown are lower than the relative growth of trees with no lianas or lianas in less than 10% of their crown. Year-to-year, tree relative growth rate is related to annual precipitation and tree diameter. However, trees that were heavily infested with lianas (i.e., with lianas in more than 50% of their crowns) had lower relative growth and a weaker precipitation-growth relationship. This work underscores the value of long-term longitudinal data in secondary forest and adds critical data on dry forest liana abundance change.
Lactate Dehydrogenase as a Potential Therapeutic Drug Target to Control Babesia bigemina

Babesia bigemina is a tick-borne apicomplexan hemoprotozoan responsible for bovine babesiosis. The current drugs used for bovine babesiosis treatment have several drawbacks, including toxicity, the lack of effectiveness to clear the parasite, and potential to develop resistance. Identifying compounds that target essential and unique parasite metabolic pathways is a rational approach toward finding alternative drug treatments. Based on the genome sequence and transcriptomics analysis, it can be inferred that anaerobic glycolysis is the dominant adenosine triphosphate (ATP) supply for Babesia, and lactate dehydrogenase (LDH) is one of the essential enzymes in this pathway. Furthermore, the Babesia LDH sequence is distinct from its bovine homologue and thus a potential chemotherapeutic target that would result in decreasing the ATP supply to the parasite but not to the host. Gossypol is a known efficient specific inhibitor of LDH in the sensu stricto B. bovis and the sensu lato B. microti, among other related parasites, but no such data are currently available in the sensu stricto B. bigemina parasites. Hereby, we show that the LDH amino acid sequence is highly conserved among sensu stricto but not in sensu lato Babesia spp. A predictive structural analysis of B. bigemina LDH showed the conservation of the key amino acids involved in the binding to gossypol compared to B. bovis. Gossypol has a significant (P < 0.0001) inhibitory effect on the in vitro growth of B. bigemina, with IC50 of 43.97 mM after 72 h of treatment. The maximum IC (IC98) was observed at 60 mM gossypol. However, a significant effect on the viability of cattle PBMC was observed when the cells were cultured with 60 mM (IC98) gossypol compared with DMSO-exposed control cells. Interestingly, B. bigemina cultured at 3% oxygen expresses significantly higher levels of LDH and is more resistant to gossypol than the parasites maintained at ambient conditions containing ~20% oxygen. Altogether, the results suggest the potential of gossypol as an effective drug against B. bigemina infection, but the risk of host toxicity at therapeutic doses should be further evaluated in in vivo studies.
Brain Tumor Infodemiology: Worldwide Online Health-Seeking Behavior Using Google Trends and Wikipedia Pageviews

Background Searching the internet for information on common neurologic symptoms and diseases has been increasing in recent times. It is postulated that online search volume data could be utilized to gauge public awareness and real-world epidemiological data regarding brain tumors. Objectives The goal of this study was to describe the pattern of online search queries of keywords related to neoplasms of the central nervous system (CNS). Methods Using Google Trends, search activity from January 2004 – January 2021 was quantified using relative search volume (RSV). The average RSV for the first 3 years was compared with the final 3 years to account for percent change. Wikipedia article views from July 2007 – January 2021 were generated using Pageviews. Peaks in RSV and page views were then matched for related news. Results “Brain tumor”, “brain cancer”, “glioblastoma”, and “glioma” had the highest search volume. RSV from Google Trends and views of Wikipedia pages reflected comparable data in terms of known prevalence rankings of tumor subtypes. There were no observable trends that could correlate to the rising numbers of brain tumor cases worldwide. However, headlines of personalities being diagnosed with glioblastomas were mostly responsible for temporary increases in public interest. Conclusions Transient rises in online search volume mirror public awareness of more aggressive CNS neoplasms that have a high burden of disease. Worldwide interest in brain tumors may not necessarily correspond to clinical occurrence, but may signify an unmet gap in providing accurate online information to neuro-oncologic patients.
Hemodynamic Changes During Physiological and Pharmacological Stress Testing in Patients With Heart Failure: A Systematic Review and Meta-Analysis

Although disease etiologies differ, heart failure patients with preserved and reduced ejection fraction (HFpEF and HFrEF, respectively) both present with clinical symptoms when under stress and impaired exercise capacity. The extent to which the adaptation of heart rate (HR), stroke volume (SV), and cardiac output (CO) under stress conditions is altered can be quantified by stress testing in conjunction with imaging methods and may help to detect the diminishment in a patient’s condition early. The aim of this meta-analysis was to quantify hemodynamic changes during physiological and pharmacological stress testing in patients with HF. A systematic literature search (PROSPERO 2020:CRD42020161212) in MEDLINE was conducted to assess hemodynamic changes under dynamic and pharmacological stress testing at different stress intensities in HFpEF and HFrEF patients. Pooled mean changes were estimated using a random effects model. Altogether, 140 study arms with 7,248 exercise tests were analyzed. High-intensity dynamic stress testing represented 73% of these data (70 study arms with 5,318 exercise tests), where: HR increased by 45.69 bpm (95% CI 44.51–46.88; I2 = 98.4%), SV by 13.49 ml (95% CI 6.87–20.10; I2 = 68.5%), and CO by 3.41 L/min (95% CI 2.86–3.95; I2 = 86.3%). No significant differences between HFrEF and HFpEF groups were found. Despite the limited availability of comparative studies, these reference values can help to estimate the expected hemodynamic responses in patients with HF. No differences in chronotropic reactions, changes in SV, or CO were found between HFrEF and HFpEF. When compared to healthy individuals, exercise tolerance, as well as associated HR and CO changes under moderate-high dynamic stress, was substantially impaired in both HF groups. This may contribute to a better disease understanding, future study planning, and patient-specific predictive models. Systematic Review Registration [https://www.crd. york.ac. uk/prospero/], identifier [CRD42020161212].
Dissecting the Role of Immune Checkpoint Regulation Patterns in Tumor Microenvironment and Prognosis of Gastric Cancer

Many studies suggest that immune checkpoint molecules play a vital role in tumor progression and immune responses. However, the impact of the comprehensive regulation pattern of immune checkpoint molecules on immune responses, tumor microenvironment (TME) formation, and patient prognosis is poorly understood. In this study, we evaluated immune checkpoint regulation patterns in 1,174 gastric cancer (GC) samples based on 31 immune checkpoint genes (ICGs). Three distinct immune checkpoint regulation patterns with significant prognostic differences were ultimately identified. Moreover, GC patients were divided into two subgroups according to immune checkpoint score (ICscore). Patients with lower ICscore were characterized by a favorable prognosis and enhanced immune infiltration as well as an increased tumor mutation burden, non-recurrence, and microsatellite instability-high. Collectively, this study indicated that immune checkpoint regulation patterns were essential to forming the diversity of TME and a better understanding of that will contribute to assessing the characteristics of TME in GC, which intends to improve the development of immunotherapy.