Miracle-dz/UniFAR-FTUs huggingface dataset:
Practical Papercraft Models from Meshes

We present a new approach to generate papercraft models from meshes. The input mesh is approximated by a set of quadric surface proxies. Each quadric proxy is then cut and unfolded into a 2D papercraft pattern. Our method has the following advantages : First, we produce smoother papercraft models than previous methods. Second, the 2D patterns of papercraft models are easy to cut and glue. Finally, the 2D patterns of papercraft models are more meaningful due to the pre-defined cutting rules. We demonstrate this by physically assembling papercraft models from our algorithm.
Sex‐based differences in referral of heart failure patients to outpatient clinics: a scoping review

Guidelines recommend that hospitalized patients newly diagnosed with HF be referred to an outpatient HF clinic (HFC) within 2 weeks of discharge. Our study aims were (i) to assess the current literary landscape on the impact of patient sex on HFC referral and outcomes and (ii) to provide a qualitative overview of possible considerations for the impact of sex on referral patterns and HF characteristics including aetiology, symptom severity, investigations undertaken and pharmacologic therapy.
Enhanced In Vitro and In Vivo Potency of a T Cell Epitope in the Ebola Virus Glycoprotein Following Amino Acid Replacement at HLA-A*02:01 Binding Positions

Vaccine efficacy and immunity to viral infection are often measured by neutralizing antibody titers. T cells are specialized subsets of immune cells with antiviral activity, but this response is variable and difficult to track. ABSTRACT Studies on Ebola virus disease (EVD) survivors and clinical studies on Ebola virus (EBOV) vaccine candidates have pinpointed the importance of a strong antibody response in protection and survival from EBOV infection. However, little is known about the T cell responses to EBOV or EBOV vaccines. We used HLA-A*02:01 (HLA-A2) transgenic mice to study HLA-A2-specific T cell responses elicited following vaccination with EBOV glycoprotein (EBOV-GP) presented with three different systems: (i) recombinant protein (rEBOV-GP), (ii) vesicular stomatitis replication-competent recombinant virus (VSV-EBOV-GP), and (iii) modified vaccinia Ankara virus recombinant (MVA-EBOV-GP). T cells from immunized animals were analyzed using peptide pools representing the entire GP region and individual peptides. Regardless of the vaccine formulation, we identified a minimal 9mer epitope containing an HLA-A2 motif (FLDPATTS), which was confirmed through HLA-A2 binding affinity and immunization studies. Using binding prediction software, we identified substitutions surrounding position 9 (S9V, P10V, and Q11V) that predicted enhanced binding to the HLA-A2 molecule. This enhanced binding was confirmed through in vitro binding studies and enhanced potency was shown with in vivo immunization studies using the enhanced sequences and the wild-type sequence. Of note, in silico studies predicted the enhanced 9mer epitope carrying the S9V substitution as the best overall HLA-A2 epitope for the full-length EBOV-GP. These results suggest that EBOV-GP-S9V and EBOV-GP-P10V represent more potent in vivo immunogens. Identification and enhancement of EBOV-specific human HLA epitopes could lead to the development of tools and reagents to induce more robust T cell responses in human subjects. IMPORTANCE Vaccine efficacy and immunity to viral infection are often measured by neutralizing antibody titers. T cells are specialized subsets of immune cells with antiviral activity, but this response is variable and difficult to track. We showed that the HLA-A2-specific T cell response to the Ebola virus glycoprotein can be enhanced significantly by a single residue substitution designed to improve an epitope binding affinity to one of the most frequent MHC alleles in the human population. This strategy could be applied to improve T cell responses to Ebola vaccines designed to elicit antibodies and adapted to target MHC alleles of populations in regions where endemic infections, like Ebola virus disease, are still causing outbreaks with concerning pandemic potential.
M1-like tumor-associated macrophages enhance proliferation and anti-apoptotic ability of liver cancer cells via activating the NF-κB signaling pathway

Liver cancer is the second leading cause of cancer-associated death worldwide. The present study aimed to evaluate the infiltration of M1-like tumor-associated macrophages (TAMs) and explore the role of infiltration of M1-like TAMs in the proliferation and apoptosis evasion of liver cancer cells. Furthermore, the association between M1-like TAM and the efficacy of postoperative transcatheter arterial chemoembolization (TACE) for patients with liver cancer was investigated. The levels of CD68, human leukocyte antigen-DR and phosphorylated NF-κB (p-)p65 were detected by western blot analysis and immunohistochemistry. Cell cycle analysis, MTT and clonogenic assays were utilized to investigate the proliferation of liver cancer cells. It was indicated that M1-like TAM increased the p-p65/p65 ratio in liver cancer cells and promoted cell proliferation. Furthermore, JSH-23, an inhibitor that prevents p65 from entering the nucleus, decreased the proliferation of liver cancer cells in M1-like TAM-conditioned medium. In addition, M1-like TAM increased the number of liver cancer cells in the S and G2/M phases of the cell cycle and also upregulated the expression levels of cyclin-dependent kinase (CDK)1, CDK2 and cyclin D1. By contrast, M1-like TAM decreased the expression level of p21. Through these effects, the anti-apoptotic ability of liver cancer cells was enhanced. Of note, JSH-23 reversed these changes related to the cell cycle, anti-apoptotic ability and the expression levels of proteins induced by M1-like TAM in liver cancer cells. In conclusion, the infiltration of M1-like TAM in liver tissue negatively influenced the efficacy of postoperative TACE for patients with liver cancer.
Non-aura visual disturbance with high visual aura rating scale scores has stronger association with migraine chronification than typical aura

Objectives To investigate the clinical correlates of visual symptoms in patients with migraine. Method Patients with migraine that attended our headache clinics were enrolled. Headache profiles, disability, and comorbidities were acquired with structured questionnaires. A semi-structured visual phenomenon questionnaire was also used to assess the characteristics of visual symptoms, including visual aura in patients with migraine with aura and transient visual disturbance in patients with migraine without aura. Headache specialists interviewed with the participants for the ascertainment of diagnosis and verification of the questionnaires. Result Migraine with aura patients with visual aura (n = 743, female/male = 2.3, mean age: 34.7 ± 12.2 years) and migraine without aura patients with non-aura transient visual disturbance (n = 1,808, female/male = 4.4, mean age: 39.4 ± 12.6 years) were enrolled. Patients with transient visual disturbance had higher headache-related disability and more psychiatric comorbidities. Chronic migraine was more common in migraine without aura than migraine with aura patients (41.9% vs. 11.8%, OR = 5.48 [95% CI: 4.33–7.02], p < 0.001). The associations remained after adjusting confounding factors. Conclusion Presence of non-aura transient visual disturbance may suggest a higher migraine-related disability and is linked to higher risk of chronic migraine than typical migraine aura in migraine patients. Further studies are needed to elucidate the potential mechanism.
SHG techniques to investigate the surface and the bulk of aqueous solutions

Second Harmonic Generation (SHG) a nonlinear optical process sensitive to medium structure deviation from centrosymmetry has been used to investigate the bulk and the surface of an aqueous phase. Using the combination of incoherent SHG, also named Hyper Rayleigh Scattering (HRS), and interface coherent SHG, we have investigated the neat air-water interface. In this paper, we report an analysis where the experimental conditions have been investigated to have the best contrast between the surface and the volume contributions. Our data are described within a simple model allowing us to normalize the surface contribution to the volume one.
Innovations and Stepwise Evolution of CBFs/DREB1s and Their Regulatory Networks in Angiosperms.

The C-repeat binding factors/Dehydration-responsive element binding protein 1s (CBFs/DREB1s) have been identified as major regulators of cold acclimation in many angiosperm plants. However, their origin and evolutionary process associated to cold responsiveness are still lacking. By integrating multi-omics data of genomes, transcriptomes, and CBFs/DREB1s genome-wide binding profiles, we unveil the origin and evolution of CBFs/DREB1s and their regulatory network. Gene collinearity and phylogeny analyses show that CBF/DREB1 is an innovation evolved from tandem duplication (TD)-derived DREB III gene. A subsequent event of ε-whole genome duplication (ε-WGD) led to two CBF/DREB1 archetypes (Clade I and II) in ancient angiosperms. In contrast to cold-insensitivity of Clade I and their parent DREB III genes, Clade II evolved a further innovation in cold-sensitive response and was stepwise expanded in eudicots and monocots by independent duplications. In geological time, the duplication events were mainly enriched around the Cretaceous-Paleogene (K-Pg) boundary and/or in the Late Cenozoic Ice Age, when the Global Average Temperature (GAT) significantly decreased. Consequently, the duplicated CBF/DREB1 genes contributed to the rewiring of CBFs/DREB1s-regulatory network for cold tolerance. Altogether, our results highlight an origin and convergent evolution of CBFs/DREB1s and their regulatory network probably for angiosperms adaptation to global cooling. This article is protected by copyright. All rights reserved.
Effects of TAMP family on the tight junction strand network and barrier function in epithelial cells

Occludin, tricellulin, and marvelD3 belong to the tight junction (TJ)‐associated MARVEL protein family. Occludin and tricellulin jointly contribute to TJ strand branching point formation and epithelial barrier maintenance. However, whether marvelD3 has the same function remains unclear. Furthermore, the roles of the carboxy‐terminal cytoplasmic tail, which is conserved in occludin and tricellulin, on the regulation of TJ strand morphology have not yet been explored in epithelial cells. We established tricellulin/occludin/marveld3 triple‐gene knockout (tKO) MDCK II cells and evaluated the roles of marvelD3 in the TJ strand structure and barrier function using MDCK II cells and a mathematical model. The complexity of TJ strand networks and paracellular barrier did not change in tKO cells compared to that in tricellulin/occludin double‐gene knockout (dKO) cells. Exogenous marvelD3 expression in dKO cells did not increase the complexity of TJ strand networks and epithelial barrier tightness. The expression of the carboxy‐terminal truncation mutant of tricellulin restored the barrier function in the dKO cells, whereas occludin lacking the carboxy‐terminal cytoplasmic tail was not expressed on the plasma membrane. These data suggest that marvelD3 does not affect the morphology of TJ strands and barrier function in MDCK II cells and that the carboxy‐terminal cytoplasmic tail of tricellulin is dispensable for barrier improvement.
Delivery of human natural killer cell-derived exosomes for liver cancer therapy: an in vivo study in subcutaneous and orthotopic animal models

Abstract Exosomes are nanosized extracellular vesicles secreted by various cell types, including those of the immune system, such as natural killer (NK) cells. They play a role in intercellular communication by transporting signal molecules between the cells. Recent studies have reported that NK cell-derived exosomes (NK-exo) contain cytotoxic proteins-induced cell death. However, the characteristics and potential functions of NK-exo, especially for the liver cancer are poorly understood. In this study, we investigated the anti-tumor effects of NK-exo in the primary liver cancer, hepatocellular carcinoma (HCC), using the orthotopic and subcutaneous tumor model. We found that NK-exo expressed both typical exosomal markers (e.g. CD63, CD81, and Alix) and cytotoxic proteins (e.g. perforin, granzyme B, FasL, and TRAIL). NK-exo were selectively taken up by HCC cells (e.g. Hep3B, HepG2, and Huh 7). Interestingly, Hep3B cells induced the highest cytotoxicity compared with HepG2 and Huh7 cells, and substantially enhanced the apoptosis by NK-exo. Furthermore, we demonstrated that NK-exo inhibited the phosphorylation of serine/threonine protein kinases (e.g. AKT and ERK1/2), and enhanced the activation of specific apoptosis markers (e.g. caspase-3, -7, -8, -9, and PARP) in Hep3B cells. NK-exo also exhibit the active targeting ability and potent therapeutic effects in both orthotopic and subcutaneous HCC mouse models. Overall, these results suggest that NK-exo indicate strong anti-tumor effects in HCC, which are mediated by novel regulatory mechanisms involved in serine/threonine kinase pathway-associated cell proliferation and caspase activation pathway-associated apoptosis.
Host factors associated with either VP16 or VP16‐induced complex differentially affect HSV‐1 lytic infection

Herpes simplex virus type 1 (HSV‐1) is an important human pathogen with neurotropism. Following lytic infection in mucosal or skin epithelium, life‐long latency is established mainly in sensory neurons, which can periodically reactivate by stress, leading to recurrent disease and virus transmission. During the virus's productive infection, the tegument protein VP16, a component of HSV‐1 virion, is physically associated with two cellular factors, host cell factor‐1 (HCF‐1), and POU domain protein Oct‐1, to construct the VP16‐induced complex, which is essential to stimulate immediate early (IE)‐gene transcription as well as initiate the lytic programme. Apart from HCF‐1 and Oct‐1, VP16 also associates with a series of other host factors, making a VP16‐induced regulatory switch to either activate or inactivate virus gene transcription. In addition, VP16 has effects on distinct signalling pathways via binding to various host molecules that are essentially related to innate immune responses, RNA polymerases, molecular chaperones, and virus infection‐induced host shutoff. VP16 also functionally compensates for given host factors, such as PPAR‐γ and ß‐catenin. In this review, we provide an overview of the updated insights on the interplay between VP16 and the host factors that coordinate virus infection.
Staphylococcus lugdunensis Uses the Agr Regulatory System to Resist Killing by Host Innate Immune Effectors

Coagulase-negative staphylococci (CoNS) are frequently commensal bacteria that rarely cause disease in mammals. Staphylococcus lugdunensis is an exceptional CoNS that causes disease in humans similar to virulent Staphylococcus aureus, but the factors that enhance the virulence of this bacterium remain ill defined. Here, we used random transposon insertion mutagenesis to identify the agr quorum sensing system as a regulator of hemolysins in S. lugdunensis. ABSTRACT Coagulase-negative staphylococci (CoNS) are frequently commensal bacteria that rarely cause disease in mammals. Staphylococcus lugdunensis is an exceptional CoNS that causes disease in humans similar to virulent Staphylococcus aureus, but the factors that enhance the virulence of this bacterium remain ill defined. Here, we used random transposon insertion mutagenesis to identify the agr quorum sensing system as a regulator of hemolysins in S. lugdunensis. Using RNA sequencing (RNA-seq), we revealed that agr regulates dozens of genes, including hemolytic S. lugdunensis synergistic hemolysins (SLUSH) peptides and the protease lugdulysin. A murine bacteremia model was used to show that mice infected systemically with wild-type S. lugdunensis do not show overt signs of disease despite there being high numbers of bacteria in the livers and kidneys of mice. Moreover, proliferation of the agr mutant in these organs was no different from that of the wild-type strain, leaving the role of the SLUSH peptides and the metalloprotease lugdulysin in pathogenesis still unclear. Nonetheless, the tropism of S. lugdunensis for humans led us to investigate the role of virulence factors in other ways. We show that agr-regulated effectors, but not SLUSH or lugdulysin alone, are important for S. lugdunensis survival in whole human blood. Moreover, we demonstrate that Agr contributes to survival of S. lugdunensis during encounters with murine and primary human macrophages. These findings demonstrate that, in S. lugdunensis, Agr regulates expression of virulence factors and is required for resistance to host innate antimicrobial defenses. This study therefore provides insight into strategies that this Staphylococcus species uses to cause disease.
Cross sections for production of the OH(A2Σ +→X2 Π) fluorescence by photodissociation of H2O vapour

Cross sections for production of the OH(A2 Sigma + to X2 Pi ) fluorescence in the lambda lambda 2800-3300 AA region by photodissociation of H2O were measured using primary photons in the lambda lambda 760-1336 AA wavelength region. The maximum cross section is 1.55 MB, at lambda 1238.3 AA and the minimum is 0.2 Mb at lambda 760.4 AA. Combining these results with data published by other authors, the yield for the OH(X2 Pi )+H(2S) process is found to be larger than 72% for the presently studied primary photon wavelengths in the lambda lambda 991.6-1335.7 AA region. Fluorescence in the lambda lambda 3060-3300 AA region, produced by photons at several selected wavelengths, was compared with theoretical synthetic rotational spectra of the OH(A2 Sigma +, nu '=0, J' to X2 Pi , nu "=0, J") band.
Informal care in times of a public health crisis: Objective burden, subjective burden and quality of life of caregivers in the Netherlands during the COVID‐19 pandemic

Abstract In the Netherlands, about one‐third of the adult population provides unpaid care. Providing informal caregiving can be very straining in normal times, but the impact of a public health crisis on caregivers is largely unknown. This study focuses on the question of how caregiver burden changed following the COVID‐19 pandemic, and what characteristics were related to these changes. We use self‐reported data from a sample of 965 informal caregivers from the Netherlands 3 months into the pandemic to investigate how the objective burden (i.e. hours spent on caregiving) and the subjective burden had changed, and what their care‐related quality of life (CarerQol) was. We found that on average the subjective burden had increased slightly (from 4.75 to 5.04 on a 0–10 scale). However, our analysis revealed that some caregivers were more affected than others. Most affected caregivers were women, and those with low income, better physical health, decreased psychological health, childcare responsibilities, longer duration of caregiving and those caring for someone with decreased physical and psychological health. On average, time spent on care remained the same (a median of 15 h per week), but certain groups of caregivers did experience a change, being those caring for people in an institution and for people with a better psychological health before the pandemic. Furthermore, caregivers experiencing changes in objective burden did not have the same characteristics as those experiencing changes in perceived burden and quality of life. This shows that the consequences of a public health crisis on caregivers cannot be captured by a focus on either objective or subjective burden measures or quality of life alone. Long‐term care policies aiming to support caregivers to persevere during a future crisis should target caregivers at risk of increased subjective burden and a lower CarerQol, such as women, people with a low income and people with childcare responsibilities. Such policies should consider that reducing objective burden may not necessarily lead to a reduction in subjective burden for all caregivers.
Effectiveness and Minimum Effective Dose of App-Based Mobile Health Interventions for Anxiety and Depression Symptom Reduction: Systematic Review and Meta-Analysis

Background Mobile health (mHealth) apps offer new opportunities to deliver psychological treatments for mental illness in an accessible, private format. The results of several previous systematic reviews support the use of app-based mHealth interventions for anxiety and depression symptom management. However, it remains unclear how much or how long the minimum treatment “dose” is for an mHealth intervention to be effective. Just-in-time adaptive intervention (JITAI) has been introduced in the mHealth domain to facilitate behavior changes and is positioned to guide the design of mHealth interventions with enhanced adherence and effectiveness. Objective Inspired by the JITAI framework, we conducted a systematic review and meta-analysis to evaluate the dose effectiveness of app-based mHealth interventions for anxiety and depression symptom reduction. Methods We conducted a literature search on 7 databases (ie, Ovid MEDLINE, Embase, PsycInfo, Scopus, Cochrane Library (eg, CENTRAL), ScienceDirect, and ClinicalTrials, for publications from January 2012 to April 2020. We included randomized controlled trials (RCTs) evaluating app-based mHealth interventions for anxiety and depression. The study selection and data extraction process followed the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. We estimated the pooled effect size using Hedge g and appraised study quality using the revised Cochrane risk-of-bias tool for RCTs. Results We included 15 studies involving 2627 participants for 18 app-based mHealth interventions. Participants in the intervention groups showed a significant effect on anxiety (Hedge g=–.10, 95% CI –0.14 to –0.06, I2=0%) but not on depression (Hedge g=–.08, 95% CI –0.23 to 0.07, I2=4%). Interventions of at least 7 weeks’ duration had larger effect sizes on anxiety symptom reduction. Conclusions There is inconclusive evidence for clinical use of app-based mHealth interventions for anxiety and depression at the current stage due to the small to nonsignificant effects of the interventions and study quality concerns. The recommended dose of mHealth interventions and the sustainability of intervention effectiveness remain unclear and require further investigation.
The relationship of caregiver self-efficacy to caregiver outcomes: a correlation and mediation analysis

Abstract Objectives Caregivers of individuals with Alzheimer’s disease and related dementias experience significant burden and adverse outcomes. Enhancing caregiver self-efficacy has the potential to mitigate these negative impacts, yet little is known about its relationship with other aspects of caregiving. This study examined the relationship between self-efficacy and outcomes; identified factors associated with self-efficacy; examined the mediating role of self-efficacy; and analyzed whether there were racial/ethnic differences. Methods Data from caregivers (N = 243) were collected from the Caring for the Caregiver Network study. Participants’ level of self-efficacy, depression, burden, and positive aspects of caregiving was assessed using validated measures. Results Two self-efficacy subscales predicted caregiver depression, burden, and positive aspects of caregiving. Being White, a spouse, or having a larger social network predicted lower self-efficacy for obtaining respite. Higher income and lower preparedness predicted lower self-efficacy for controlling upsetting thoughts and responding to disruptive behaviors. Self-efficacy for controlling upsetting thoughts mediated the relationship between preparedness and depression along with the relationship between preparedness and burden. Race/ethnicity did not improve model fit. Conclusion Self-efficacy plays an important role in caregiver outcomes. These findings indicate that strategies to improve caregiver self-efficacy should be an integral component of caregiver interventions.