Miracle-dz/UniFAR-FTUs huggingface dataset:
Drought exerts a greater influence than growth temperature on the temperature response of leaf day respiration in wheat (Triticum aestivum)

We assessed how the temperature response of leaf day respiration (Rd) in wheat responded to contrasting water regimes and growth temperatures. In Experiment 1, well-watered and drought-stressed conditions were imposed on two genotypes; in Experiment 2, the two water regimes combined with high (HT), medium (MT) and low (LT) growth temperatures were imposed on one of the genotypes. Rd was estimated from simultaneous gas exchange and chlorophyll fluorescence measurements at six leaf temperatures (Tleaf) for each treatment, using the Yin method for non-photorespiratory conditions and the non-rectangular hyperbolic fitting method for photorespiratory conditions. The two genotypes responded similarly to growth and measurement conditions. Estimates of Rd for non-photorespiratory conditions were generally higher than those for photorespiratory conditions but their responses to Tleaf were similar. Under well-watered conditions, Rd and its sensitivity to Tleaf slightly acclimated to LT but did not acclimate to HT. Temperature sensitivities of Rd were considerably suppressed by drought, and the suppression varied among growth temperatures. Thus, it is necessary to quantify interactions between drought and growth temperature for reliably modelling Rd under climate change. Our study also demonstrated that the Kok method, a currently popular method for estimating Rd, underestimated Rd significantly and should be abandoned. Highlight Leaf day respiration (Rd) acclimated little to growth temperature, but significantly to drought by reducing its thermal sensitivity. The Kok method underestimates Rd and should no longer be used.
The cytokine receptor Fn14 regulates neuronal transcription during development and brain function in the adult

Cytokine signaling between microglia and neurons is required for synapse elimination during brain development, but the mechanisms by which neurons respond to microglia-derived cytokines remain to be fully defined. Here, we demonstrate that microglia are necessary for sensory experience-dependent synapse elimination in the dorsal lateral geniculate nucleus (dLGN) of the mouse, a process previously shown to be mediated by the microglia-derived cytokine TWEAK and its neuronal receptor Fn14. Single-nucleus RNA-sequencing in mice lacking Fn14 or TWEAK at the height of experience-dependent refinement revealed that TWEAK-Fn14 signaling coordinates robust programs of gene expression in excitatory thalamocortical neurons of the dLGN. Gene targets of TWEAK and Fn14 are enriched for regulators of synapse and chromatin remodeling, suggesting that TWEAK-Fn14 signaling coordinates neuronal transcription to promote circuit refinement and epigenomic maturation in response to experience. We further find that Fn14 expression is not restricted to the dLGN but extends to other brain regions as well, both during development and in the adult. Consistent with the expression of Fn14 outside of the visual system, Fn14 knockout mice show significant impairments in multiple tests of memory task proficiency. At baseline, loss of Fn14 does not affect macroscopic neural activity measured by electroencephalogram recordings in vivo. However, mice lacking Fn14 displayed worse seizure outcomes and were less likely to survive when seizures were pharmacologically induced. Thus, TWEAK-Fn14 signaling coordinates neuronal transcription during development and contributes to cognitive function in the adult. Taken together, these data reveal that molecular pathways associated with inflammation in the periphery can coordinate with sensory experience to shape neuronal transcription and connectivity across the lifespan. Highlights Microglia regulate sensory-dependent refinement at the retinogeniculate synapse TWEAK-Fn14 signaling induces the expression of neuronal genes involved in synaptic and chromatin remodeling Fn14 signaling is dispensable for learning but required for memory in multiple tasks Loss of Fn14 exacerbates seizure susceptibility and the severity of seizure outcomes
Constructing Functional Networks of Phosphorylation Sites Using Co-Phosphorylation

Protein phosphorylation is a ubiquitous regulatory mechanism that plays a central role in cellular signaling. According to recent estimates, up to 70% of human proteins can be phosphorylated. Therefore, characterization of phosphorylation dynamics is critical for understanding a broad range of biological and biochemical processes. Technologies based on mass spectrometry are rapidly advancing to meet the needs for high-throughput screening of phosphorylation. These technologies enable untargeted quantification of thousands of phosphorylation sites in a given sample. Many labs are already utilizing these technologies to comprehensively characterize signaling landscapes by examining perturbations with drugs and knockdown approaches, or by assessing diverse phenotypes in cancers, neuro-degerenational diseases, infectious diseases, and normal development. Here, we comprehensively investigate the concept of “co-phosphorylation”, defined as the correlated phosphorylation of a pair of phosphosites across various biological states. We integrate nine publicly available phospho-proteomics datasets for various diseases (including breast cancer, ovarian cancer and Alzhemier’s disease) and utilize functional data related to sequence, evolutionary histories, kinase annotations, and pathway annotations to investigate the functional relevance of co-phosphorylation. Our results across a broad range of studies consistently show that functionally associated sites tend to exhibit significant positive or negative co-phosphorylation. Specifically, we show that co-phosphorylation can be used to predict with high precision the sites that are on the same pathway or that are targeted by the same kinase. Overall, these results establish co-phosphorylation as a useful resource for analyzing phospho-proteins in a network context, which can help extend our knowledge on cellular signaling and its dysregulation.
Decreased USP2a Expression Inhibits Trophoblast Invasion and Associates With Recurrent Miscarriage

An appropriate development of the placenta consisting of trophoblast cell migration, invasion, proliferation, and apoptosis, is essential to establishing and maintaining a successful pregnancy. Ubiquitin‐specific protease 2a (USP2a) regulates the processes of metastasis in multiple tumor cells. Yet, no known research has focused on exploring the effect of USP2a on trophoblasts and its possible mechanism in the pathogenies of recurrent miscarriage (RM). In this study, we first detected the decreased mRNA levels and the protein levels of USP2a in placental villous tissue samples from the RM patients. In vitro assays verified that overexpression of USP2a promoted human trophoblast proliferation, migration, invasion, whereas knockdown of USP2a inhibited these processes. Mechanistically, USP2a activated PI3K/Akt/GSK3β signaling pathway to promote nuclear translocation of β‐catenin and further activated epithelial-mesenchymal transition (EMT) in the trophoblasts. Moreover, transforming growth factor-beta (TGF-β) up-regulated USP2a expression in trophoblasts. Interestingly, M2 macrophage secreted TGF-β induced trophoblast migration and invasion, and an anti-TGF-β antibody alleviated this effect. Collectively, this study indicated that USP2a regulated trophoblast invasion and that abnormal USP2a expression might lead to aberrant trophoblast invasion, thus contributing to RM.
Preclinical Testing of Living Tissue-Engineered Heart Valves for Pediatric Patients, Challenges and Opportunities

Introduction: Pediatric patients with cardiac congenital diseases require heart valve implants that can grow with their natural somatic increase in size. Current artificial valves perform poorly in children and cannot grow; thus, living-tissue-engineered valves capable of sustaining matrix homeostasis could overcome the current drawbacks of artificial prostheses and minimize the need for repeat surgeries. Materials and Methods: To prepare living-tissue-engineered valves, we produced completely acellular ovine pulmonary valves by perfusion. We then collected autologous adipose tissue, isolated stem cells, and differentiated them into fibroblasts and separately into endothelial cells. We seeded the fibroblasts in the cusp interstitium and onto the root adventitia and the endothelial cells inside the lumen, conditioned the living valves in dedicated pulmonary heart valve bioreactors, and pursued orthotopic implantation of autologous cell-seeded valves with 6 months follow-up. Unseeded valves served as controls. Results: Perfusion decellularization yielded acellular pulmonary valves that were stable, no degradable in vivo, cell friendly and biocompatible, had excellent hemodynamics, were not immunogenic or inflammatory, non thrombogenic, did not calcify in juvenile sheep, and served as substrates for cell repopulation. Autologous adipose-derived stem cells were easy to isolate and differentiate into fibroblasts and endothelial-like cells. Cell-seeded valves exhibited preserved viability after progressive bioreactor conditioning and functioned well in vivo for 6 months. At explantation, the implants and anastomoses were intact, and the valve root was well integrated into host tissues; valve leaflets were unchanged in size, non fibrotic, supple, and functional. Numerous cells positive for a-smooth muscle cell actin were found mostly in the sinus, base, and the fibrosa of the leaflets, and most surfaces were covered by endothelial cells, indicating a strong potential for repopulation of the scaffold. Conclusions: Tissue-engineered living valves can be generated in vitro using the approach described here. The technology is not trivial and can provide numerous challenges and opportunities, which are discussed in detail in this paper. Overall, we concluded that cell seeding did not negatively affect tissue-engineered heart valve (TEHV) performance as they exhibited as good hemodynamic performance as acellular valves in this model. Further understanding of cell fate after implantation and the timeline of repopulation of acellular scaffolds will help us evaluate the translational potential of this technology.
Gestational Diabetes Mellitus in Pregnancy Increased Erythropoietin Level Affecting Differentiation Potency of Haematopoietic Stem Cell of Umbilical Cord Blood

Background: The in utero environment has many factors that can support cell differentiation. Cytokines, chemokines and growth factors play big roles in haematopoietic mechanisms. Some diseases like gestational diabetes mellitus (GDM) might affect the environment and haematopoietic stem cell (HSC) quality. The aim of this study is to investigate the adverse effects of GDM on umbilical cord blood (UCB) HSC in terms of differentiation potency including the UCB parameters used for banking and transplantation purposes. Methods: UCB-HSC was collected from 42 GDM and 38 normal pregnancies. UCB-HSC was isolated and further enriched using immuno-magnetic separation beads (MACS). The UCB-HSC were cultured in methylcellulose media to investigate the differentiation potency. The level of erythropoietin (EPO) and insulin in the UCB plasma was measured using enzyme linked immunoassay (ELISA) technique. Result: The UCB parameters; volume, total nucleated count (TNC) and total CD34+ cells were significantly reduced in the GDM group compared to the control group. The number of HSC progenitors' colonies were significantly reduced in the GDM group except for progenitor BFU-E, which was significantly increased (GDM = 94.19 ± 6.21, Control = 73.61 ± 2.73, p = 0.010). This data was associated with higher EPO level in GDM group. However, the insulin level in the GDM group was comparable to the Control group. Conclusion: Our results suggest that the changes in the in utero environment due to abnormalities during pregnancy such as GDM might affect the differentiation potency of UCB-HSC. These findings can be considered as an additional parameter for the inclusion and exclusion criteria for UCB banking, particularly for mothers with GDM.
Frailty Predicts Poor Prognosis of Patients After Percutaneous Coronary Intervention: A Meta-Analysis of Cohort Studies

Background: Frailty has been related to a higher risk of cardiovascular events, while the association between frailty and outcomes for patients with coronary artery disease (CAD) after percutaneous coronary intervention (PCI) remains unclear. We performed a meta-analysis of cohort studies to evaluate the above association. Methods: Cohort studies aiming to determine the potential independent association between frailty and clinical outcomes after PCI were identified by search of PubMed, Embase, and Web of Science databases from inception to February 22, 2021. A random-effects model that incorporates the possible heterogeneity among the included studies was used to combine the results. Results: Ten cohort studies with 7,449,001 patients were included. Pooled results showed that frailty was independently associated with higher incidence of all-cause mortality [adjusted risk ratio (RR) = 2.94, 95% confidence intervals (CI): 1.90–4.56, I2 = 56%, P < 0.001] and major adverse cardiovascular events [(MACEs), adjusted RR = 2.11, 95% CI: 1.32–3.66, I2 = 0%, P = 0.002]. Sensitivity analyses limited to studies including elderly patients showed consistent results (mortality: RR = 2.27, 95% CI: 1.51–3.41, I2 = 23%, P < 0.001; MACEs: RR = 2.44, 95% CI: 1.44–4.31, I2 = 0%, P = 0.001). Subgroup analyses showed that characteristics of study design, follow-up duration, or type of PCI did not seem to significantly affect the associations (P-values for subgroup analyses all >0.05). Conclusions: Frailty may be an independent risk factor of poor prognosis for patients with CAD after PCI.
Conspicuous Consumption in Emerging Markets: The Case of Starbucks in Colombia as a Global and Sustainable Brand

Conspicuous consumption symbolizes ostentatious and material consumption through the purchase of products and services with a higher economic value and that allows their consumers to excel socially. However, conspicuous consumption often does not represent social and environmental values, because their products are often not characterized by being made through sustainable processes. United Nations, through its sustainable development agenda, invited companies to be aware of the social and environmental problems of the world and to be able to generate strategies that can be sustainable over time and allow the growth of both the company and society in general. This study analyses the case of Starbucks as a global and sustainable brand, which also generates conspicuous consumption in emerging markets. In this way, we explain how this brand generates a social status in emerging markets, which allow their consumers to excel socially. On the other hand, we explain how Starbucks contributes positively to sustainability in these types of markets, generating greater well-being for both the environment and society in general. In this way, this brand manages to transmit messages with symbolic values of social status, as well as social and environmental awareness. This research allows us to see how Starbucks is able to generate conspicuous consumption in Colombia, which is the third largest exporter of coffee in the world but is also capable of generating sustainable processes that help Colombian coffee growers and the environment. This research used a quantitative methodology based on a structured questionnaire made for conspicuous consumers of the Starbucks brand in Colombia, whose data were processed through the statistical program PLS 3.2. 7. This research details the sustainable processes carried out by this brand in this developing country and the reasons why its consumption in this emerging market is considered conspicuous. For this research, family allocentrism, ethnocentrism, and patriotism are considered antecedents of conspicuous consumption, and brand image and brand loyalty are considered their results.
Detection of Anti-SARS-CoV-2-S2 IgG Is More Sensitive Than Anti-RBD IgG in Identifying Asymptomatic COVID-19 Patients

Characterizing the serologic features of asymptomatic SARS-CoV-2 infection is imperative to improve diagnostics and control of SARS-CoV-2 transmission. In this study, we evaluated the antibody profiles in 272 plasma samples collected from 59 COVID-19 patients, consisting of 18 asymptomatic patients, 33 mildly ill patients and 8 severely ill patients. We measured the IgG against five viral structural proteins, different isotypes of immunoglobulins against the Receptor Binding Domain (RBD) protein, and neutralizing antibodies. The results showed that the overall antibody response was lower in asymptomatic infections than in symptomatic infections throughout the disease course. In contrast to symptomatic patients, asymptomatic patients showed a dominant IgG-response towards the RBD protein, but not IgM and IgA. Neutralizing antibody titers had linear correlations with IgA/IgM/IgG levels against SARS-CoV-2-RBD, as well as with IgG levels against multiple SARS-CoV-2 structural proteins, especially with anti-RBD or anti-S2 IgG. In addition, the sensitivity of anti-S2-IgG is better in identifying asymptomatic infections at early time post infection compared to anti-RBD-IgG. These data suggest that asymptomatic infections elicit weaker antibody responses, and primarily induce IgG antibody responses rather than IgA or IgM antibody responses. Detection of IgG against the S2 protein could supplement nucleic acid testing to identify asymptomatic patients. This study provides an antibody detection scheme for asymptomatic infections, which may contribute to epidemic prevention and control.
Response of Mungbean (cvs. Celera II-AU and Jade-AU) and Blackgram (cv. Onyx-AU) to Transient Waterlogging

Mungbean [Vigna radiata (L.) Wilczek] and blackgram [Vigna mungo (L.) Hepper] are important crops for smallholder farmers in tropical and subtropical regions. Production of both crops is affected by unexpected and increasingly frequent extreme precipitation events, which result in transient soil waterlogging. This study aimed to compare the waterlogging tolerance of mungbean and blackgram genotypes under the varying duration of waterlogging stress at germination and seedling stages. We evaluated the responses to different durations of transient waterlogging in a sandy clay loam under temperature-controlled glasshouse conditions. Waterlogging durations were 0, 1, 2, 3, 4, 5, 6, 7, and 8 days during germination and 0, 2, 4, 8, and 16 days during the seedling stage. We used two mungbean genotypes (green testa), Celera II-AU (small-seeded), and Jade-AU (large-seeded), contrasting in seed size and hypocotyl pigmentation, and a blackgram genotype (black testa), Onyx-AU. Waterlogging reduced soil redox potential, delayed or even prevented germination, decreased seedling establishment, and affected shoot and root development. In the seedlings waterlogged (WL) at 15 days after sowing (DAS), adventitious root formation and crown nodulation varied between the genotypes, and 16 days of waterlogging substantially reduced growth but did not result in plant death. Plants in soil with waterlogging for 8–16 days followed by drainage and sampling at 39 DAS had reduced shoot and root dry mass by 60–65% in mungbean and 40% in blackgram compared with continuously drained controls, due at least in part to fewer lateral roots. Soil plant analysis development (SPAD) chlorophyll content was also reduced. Onyx-AU, a blackgram genotype, was more tolerant to transient waterlogging than Jade-AU and Celera II-AU in both growth stages. Of the two mungbean genotypes, Celera II-AU had a greater seedling establishment than Jade-AU post waterlogging imposed at sowing. In contrast, Jade-AU had more plant biomass and greater recovery growth than Celera II-AU after waterlogging and recovery during the seedling stage. Both species were delayed in emergence in response to the shorter periods of transient waterlogging at germination, and with the longer waterlogging germination and emergence failed, whereas at the seedling stage both showed adaptation by the formation of adventitious roots.
Urine Proteomics Differentiate Primary Thrombotic Antiphospholipid Syndrome From Obstetric Antiphospholipid Syndrome

Antiphospholipid syndrome (APS) is a multisystem disorder characterized by thrombosis and/or recurrent fetal loss. This clinical phenotype heterogeneity may result in differences in response to treatment and prognosis. In this study, we aimed to identify primary thrombotic APS (TAPS) from primary obstetric APS (OAPS) using urine proteomics as a non-invasive method. Only patients with primary APS were enrolled in this study from 2016 to 2018 at a single clinical center in Shanghai. Urine samples from 15 patients with TAPS, 9 patients with OAPS, and 15 healthy controls (HCs) were collected and analyzed using isobaric tags for relative and absolute quantification (iTRAQ) labeling combined with liquid chromatography-tandem mass spectrometry analysis to identify differentially expressed proteins. Cluster analysis of urine proteomics identified differentiated proteins among the TAPS, OAPS, and HC groups. Urinary proteins were enriched in cytokine and cytokine receptor pathways. Representative secreted cytokines screened out (fold change >1.20, or <0.83, p<0.05) in these differentiated proteins were measured by enzyme-linked immunosorbent assay in a validation cohort. The results showed that the levels of C-X-C motif chemokine ligand 12 (CXCL12) were higher in the urine of patients with TAPS than in those with OAPS (p=0.035), while the levels of platelet-derived growth factor subunit B (PDGFB) were lower in patients with TAPS than in those with OAPS (p=0.041). In addition, correlation analysis showed that CXCL12 levels were positively correlated with immunoglobulin G anti-β2-glycoprotein I antibody (r=0.617, p=0.016). Our results demonstrated that urinary CXCL12 and PDGFB might serve as potential non-invasive markers to differentiate primary TAPS from primary OAPS.
Quantifying the Impact of Phenoconversion on Medications With Actionable Pharmacogenomic Guideline Recommendations in an Acute Aged Persons Mental Health Setting

Introduction: Polypharmacy and genetic variants that strongly influence medication response (pharmacogenomics, PGx) are two well-described risk factors for adverse drug reactions. Complexities arise in interpreting PGx results in the presence of co-administered medications that can cause cytochrome P450 enzyme phenoconversion. Aim: To quantify phenoconversion in a cohort of acute aged persons mental health patients and evaluate its impact on the reporting of medications with actionable PGx guideline recommendations (APRs). Methods: Acute aged persons mental health patients (N = 137) with PGx and medication data at admission and discharge were selected to describe phenoconversion frequencies for CYP2D6, CYP2C19 and CYP2C9 enzymes. The expected impact of phenoconversion was then assessed on the reporting of medications with APRs. Results: Post-phenoconversion, the predicted frequency at admission and discharge increased for CYP2D6 intermediate metabolisers (IMs) by 11.7 and 16.1%, respectively. Similarly, for CYP2C19 IMs, the predicted frequency at admission and discharge increased by 13.1 and 11.7%, respectively. Nineteen medications with APRs were prescribed 120 times at admission, of which 50 (42%) had APRs pre-phenoconversion, increasing to 60 prescriptions (50%) post-phenoconversion. At discharge, 18 medications with APRs were prescribed 122 times, of which 48 (39%) had APRs pre-phenoconversion, increasing to 57 prescriptions (47%) post-phenoconversion. Discussion: Aged persons mental health patients are commonly prescribed medications with APRs, but interpretation of these recommendations must consider the effects of phenoconversion. Adopting a collaborative care model between prescribers and clinical pharmacists should be considered to address phenoconversion and ensure the potential benefits of PGx are maximised.