Miracle-dz/UniFAR-FTUs huggingface dataset:
Dominate or Delete: Decentralized Competing Bandits in Serial Dictatorship

Online learning in a two-sided matching market, with demand side agents continuously competing to be matched with supply side (arms), abstracts the complex interactions under partial information on matching platforms (e.g. UpWork, TaskRabbit). We study the decentralized serial dictatorship setting, a two-sided matching market where the demand side agents have unknown and heterogeneous valuation over the supply side (arms), while the arms have known uniform preference over the demand side (agents). We design the first decentralized algorithm – UCB with Decentralized Dominant-arm Deletion (UCB-D3), for the agents, that does not require any knowledge of reward gaps or time horizon. UCB-D3 works in phases, where in each phase, agents delete dominated arms – the arms preferred by higher ranked agents, and play only from the nondominated arms according to the UCB. At the end of the phase, agents broadcast in a decentralized fashion, their estimated preferred arms through pure exploitation. We prove both, a new regret lower bound for the decentralized serial dictatorship model, and that UCB-D3 is order optimal.
Robust Footstep Planning and LQR Control for Dynamic Quadrupedal Locomotion

In this letter, we aim to improve the robustness of dynamic quadrupedal locomotion through two aspects: 1) fast model predictive foothold planning, and 2) applying LQR to projected inverse dynamic control for robust motion tracking. In our proposed planning and control framework, foothold plans are updated at 400 Hz considering the current robot state and an LQR controller generates optimal feedback gains for motion tracking. The LQR optimal gain matrix with non-zero off-diagonal elements leverages the coupling of dynamics to compensate for system underactuation. Meanwhile, the projected inverse dynamic control complements the LQR to satisfy inequality constraints. In addition to these contributions, we show robustness of our control framework to unmodeled adaptive feet. Experiments on the quadruped ANYmal demonstrate the effectiveness of the proposed method for robust dynamic locomotion given external disturbances and environmental uncertainties.
A quantitative model of a cooperative two-state equilibrium in DNA: experimental tests, insights, and predictions

Abstract Quantitative parameters for a two-state cooperative transition in duplex DNAs were finally obtained during the last 5 years. After a brief discussion of observations pertaining to the existence of the two-state equilibrium per se, the lengths, torsion, and bending elastic constants of the two states involved and the cooperativity parameter of the model are simply stated. Experimental tests of model predictions for the responses of DNA to small applied stretching, twisting, and bending stresses, and changes in temperature, ionic conditions, and sequence are described. The mechanism and significance of the large cooperativity, which enables significant DNA responses to such small perturbations, are also noted. The capacity of the model to resolve a number of long-standing and sometimes interconnected puzzles in the extant literature, including the origin of the broad pre-melting transition studied by numerous workers in the 1960s and 1970s, is demonstrated. Under certain conditions, the model predicts significant long-range attractive or repulsive interactions between hypothetical proteins with strong preferences for one or the other state that are bound to well-separated sites on the same DNA. A scenario is proposed for the activation of the ilvPG promoter on a supercoiled DNA by integration host factor.
Contribution to the knowledge of the endemic Australian genus Binburrum Pollock, 1995 (Coleoptera: Pyrochroidae: Pilipalpinae), with description of three new species

Abstract Binburrum Pollock, 1995 is a small group of fire-coloured beetles (Tenebrionoidea: Pyrochroidae: Pilipalpinae) endemic to Australia with five described species. Herein, three new species of Binburrum – B. articuno (southeastern South Australia), B. moltres (northeastern Queensland, Australia), and B. zapdos (northeastern Queensland) – are described based on comparative anatomy, highlighting the underestimated diversity of this genus. Binburrum angusticollis Pollock, 1995 is newly recorded from New South Wales, Australia. Descriptions of new species are supplemented with digital photographs and scientific illustrations of habitus and salient structures. A key for the identification of Binburrum is provided.
Structural equation modeling of mental health in gentrifying neighborhoods in Austin, Texas

Abstract Having poor mental health can be life-threatening, and problems tied to it are prevalent in communities across the United States (US). The city of Austin is one of the ten cities in the US undergoing rapid urban gentrification; however, there is insufficient empirical evidence on the impact of this process on residents’ health. Consequently, this study explored the concept of weathering and life course perspective using data of 331 residents recruited from two regions endemic with gentrification to assess the health impacts of gentrification. We used a triangulation method including univariate, bivariate correlation, and multiple linear regression implemented through the structural equation model to examine the complex pathways to three health outcomes—measured stress, self-rated mental health, and depression symptoms. Bivariate Pearson’s correlation indicated a significant positive association between gentrification score and mental health symptoms and stress. However, the direct association between gentrification and depression disappeared in the causal/path model. In support of the weathering hypothesis, this study found that stress score was directly related to the adulthood depression score. Therefore, this research builds on the accumulating evidence of environmental stress and mental health in the US’s rapidly changing physical and sociocultural environment. Hence, implementing and guaranteeing social equity of resources will improve residents’ health and reduce the cost of health care spending at both the household level and the city government level.
Exploring the role of City Networks in supporting urban resilience to COVID-19 in conflict-affected settings

Abstract Background: It is estimated that by 2050, almost 70 percent of the global population will be residing in urban areas. In recent years, cities have become central in tackling key urban challenges and have demonstrated greater flexibility in policymaking and innovation than national governments. Cities are currently more inclined to learn from each other via networks, partnerships, and pairings to develop solutions to many global challenges including pandemics such as COVID-19. Aim: To explore the role cities and city networks present in supporting urban resilience to pandemics focusing on conflict-affected settings. Methods: A desk-based literature review of academic and grey sources was conducted followed by thematic analysis. Results: Although most COVID-19 response plans have been developed and implemented by governments, the pandemic has revealed the significant potential for city networks in providing platforms for knowledge sharing and coordination of mitigation plans to address pandemic-specific interventions. We found that in conflict settings, city networks continue to play only a minor role, if any, compared to humanitarian and informal actors. Conclusion: City networks have the potential to contribute to strengthening global collaborative approaches to pandemic responses, but this has not been given sufficient investment and even less so in conflict-affected settings. It is essential for these networks to be integrated within a wider multidisciplinary and multisectoral platform that includes academics, humanitarian and informal actors.
Neuroprotective Roles of the Reverse Transsulfuration Pathway in Alzheimer’s Disease

The reverse transsulfuration pathway has emerged as a central hub that integrates the metabolism of sulfur-containing amino acids and redox homeostasis. Transsulfuration involves the transfer of sulfur from homocysteine to cysteine. Cysteine serves as the precursor for several sulfur-containing molecules, which play diverse roles in cellular processes. Recent evidence shows that disruption of the flux through the pathway has deleterious consequences. In this review article, I will discuss the actions and regulation of the reverse transsulfuration pathway and its links to other metabolic pathways, which are disrupted in Alzheimer’s disease (AD). The potential nodes of therapeutic intervention are also discussed, which may pave the way for the development of novel treatments.
Longitudinal Evolution of Bone Microarchitecture and Bone Strength in Type 2 Diabetic Postmenopausal Women With and Without History of Fragility Fractures—A 5-Year Follow-Up Study Using High Resolution Peripheral Quantitative Computed Tomography

Introduction Diabetic bone disease is characterized by an increased fracture risk which may be partly attributed to deficits in cortical bone quality such as higher cortical porosity. However, the temporal evolution of bone microarchitecture, strength, and particularly of cortical porosity in diabetic bone disease is still unknown. Here, we aimed to prospectively characterize the 5-year changes in bone microarchitecture, strength, and cortical porosity in type 2 diabetic (T2D) postmenopausal women with (DMFx) and without history of fragility fractures (DM) and to compare those to nondiabetic fracture free controls (Co) using high resolution peripheral quantitative computed tomography (HR-pQCT). Methods Thirty-two women underwent baseline HR-pQCT scanning of the ultradistal tibia and radius and a FU-scan 5 years later. Bone microarchitectural parameters, including cortical porosity, and bone strength estimates via µFEA were calculated for each timepoint and annualized. Linear regression models (adjusted for race and change in BMI) were used to compare the annualized percent changes in microarchitectural parameters between groups. Results At baseline at the tibia, DMFx subjects exhibited the highest porosity of the three groups (66.3% greater Ct.Po, 71.9% higher Ct.Po.Volume than DM subjects, p < 0.022). Longitudinally, porosity increased significantly over time in all three groups and at similar annual rates, while DMFx exhibited the greatest annual decreases in bone strength indices (compared to DM 4.7× and 6.7× greater decreases in failure load [F] and stiffness [K], p < 0.025; compared to Co 14.1× and 22.2× greater decreases in F and K, p < 0.020). Conclusion Our data suggest that despite different baseline levels in cortical porosity, T2D women with and without fractures experienced long-term porosity increases at a rate similar to non-diabetics. However, the annual loss in bone strength was greatest in T2D women with a history of a fragility fractures. This suggests a potentially non-linear course of cortical porosity development in T2D bone disease: major porosity may develop early in the course of disease, followed by a smaller steady annual increase in porosity which in turn can still have a detrimental effect on bone strength—depending on the amount of early cortical pre-damage.
The Vbeta13 T Cell Receptor Monoclonal Antibody Reduces Hyaluronan and CD68+, CD3+, and CD8+ Cell Infiltrations to Delay Diabetes in Congenic BB DRLyp/Lyp Rats

The depleting Vβ13a T cell receptor monoclonal antibody (mAb) 17D5 prevents both induced and spontaneous autoimmune diabetes in BB rats. Here it was tested in congenic DRLyp/Lyp rats, all of which spontaneously developed diabetes. Starting at 40 days of age, rats were injected once weekly with either saline, His42 Vβ16 mAb, or 17D5 mAb and monitored for hyperglycemia. Diabetes occurred in 100% (n = 5/5) of saline-treated rats (median age, 66 days; range 55–73), and in 100% (n = 6/6) of His42-treated rats (median age, 69 days; range 59–69). Diabetes occurred in fewer (n = 8/11, 73%) 17D5-treated rats at a later age (median 76 days, range 60–92). Three (27%) of the 17D5-treated rats were killed at 101–103 days of age without diabetes (17D5 no-diabetes rats). Survival analysis demonstrated that 17D5 mAb delayed diabetes onset. Saline- and His42-treated rats had severely distorted islets with substantial loss of insulin-positive cells. These rats exhibited prominent hyaluronan (HA) staining, with the intra-islet HA+ accumulations measuring 5,000 ± 2,400 µm2 and occupying 36 ± 12% of islet area, and severe (grade 4) insulitis with abundant infiltration by CD68+, CD3+, and CD8+ cells. The 17D5 mAb-treated rats with delayed diabetes onset exhibited less severe insulitis (predominantly grade 3). In contrast, the 17D5 no-diabetes rats had mostly normal islets, with insulin+ cells representing 76 ± 3% of islet cells. In these rats, the islet HA deposits were significantly smaller than in the diabetic rats; the intra-islet HA+ areas were 1,200 ± 300 µm2 and accounted for 8 ± 1% of islet area. Also, islet-associated CD68+ and CD3+ cells occurred less frequently (on average in 60 and 3% of the islets, respectively) than in the diabetes rats (present in >95% of the islets). No CD8+ cells were detected in islets in all 17D5 no-diabetes rats. We conclude that mAb 17D5 delayed diabetes in DRLyp/Lyp rats and markedly reduced expression of HA and concomitant infiltration of CD68+, CD3+, and CD8+ cells. Our findings underscore the importance of refining immune suppression in prevention or intervention clinical trials to use mAb reagents that are directed against specific T cell receptors.
Cortisol Co-Secretion and Clinical Usefulness of ACTH Stimulation Test in Primary Aldosteronism: A Systematic Review and Biases in Epidemiological Studies

The hypothalamus-pituitary-adrenal (HPA) axis plays an important role in primary aldosteronism. Aldosterone biosynthesis is regulated not only by angiotensin II in the renin-angiotensin-aldosterone system, but also by adrenocorticotropic hormone (ACTH), one of the key components of the HPA axis. Although previous studies have reported cortisol cosecretion in primary aldosteronism, particularly aldosterone-producing adenoma (APA), the clinical relevance of such aldosterone and cortisol cosecretion from APA and hypertension or other metabolic disorders has not been fully established. Several somatic mutations including KCNJ5 and CACNA1D are known to induce autonomous production of aldosterone in APA, and the aldosterone responsiveness to ACTH may vary according to each mutation. The ACTH stimulation test has been reported to be a useful tool to distinguish the subtypes of primary aldosteronism (e.g., unilateral vs bilateral) in some studies, but it has not been commonly applied in clinical practice due to limited evidence. Given the recent advancement of imaging, omics research, and computational approach, it is important to summarize the most updated evidence to disentangle the potential impact of cortisol excess in primary aldosteronism and whether the ACTH stimulation test needs to be considered during the diagnostic process of primary aldosteronism. In this article, we conducted a systematic review of epidemiological studies about (i) cortisol cosecretion in primary aldosteronism and (ii) the ACTH stimulation test for the diagnosis of primary aldosteronism (including subtype diagnosis). Then, we discussed potential biases (e.g., confounding bias, overadjustment, information bias, selection bias, and sampling bias) in the previous studies and introduced some advanced epidemiological/statistical methods to minimize these limitations. A better understanding of biases and epidemiological perspective on this topic would allow us to produce further robust evidence and balanced discussion about the causal mechanisms involving the HPA axis and clinical usefulness of the ACTH stimulation test among patients with primary aldosteronism.
Characterization and Reactivity of Triperoxo Vanadium Complexes In Protic Solvents

ESI-MS and 51V NMR techniques have been used to detect the formation of vanadium triperoxo complexes in protic solvents. RHF/6-311++G(d,p) ab initio calculations were also carried out to address the structure and the energy requirements of vanadium peroxo species formed from vanadates and hydrogen peroxide. Such studies point to a step-by-step decomposition process involving the triperoxo vanadium complex, as highlighted by ESI-MSn experiments. The reactivity of the triperoxo compound has been examined in an alcohol/water mixture with the aim of elucidating its oxidative behavior; evidence for the formation of the HOO− anion as an active oxidant in solution has been obtained.
NMR Characterization of the Interactions Between Glycosaminoglycans and Proteins

Glycosaminoglycans (GAGs) constitute a considerable fraction of the glycoconjugates found on cellular membranes and in the extracellular matrix of virtually all mammalian tissues. The essential role of GAG-protein interactions in the regulation of physiological processes has been recognized for decades. However, the underlying molecular basis of these interactions has only emerged since 1990s. The binding specificity of GAGs is encoded in their primary structures, but ultimately depends on how their functional groups are presented to a protein in the three-dimensional space. This review focuses on the application of NMR spectroscopy on the characterization of the GAG-protein interactions. Examples of interpretation of the complex mechanism and characterization of structural motifs involved in the GAG-protein interactions are given. Selected families of GAG-binding proteins investigated using NMR are also described.
Hydrogen Storage Experiments for an Undergraduate Laboratory Course—Clean Energy: Hydrogen/Fuel Cells

Global interest in both renewable energies and reduction in emission levels has placed increasing attention on hydrogen-based fuel cells that avoid harm to the environment by releasing only water as a byproduct. Therefore, there is a critical need for education and workforce development in clean energy technologies. A new undergraduate laboratory course for students has been developed, entitled, Clean Energy: Hydrogen/Fuel Cells. If hydrogen is to be used on a large-scale basis, the storage of hydrogen becomes a crucial issue for mobility and transport applications. Fuel cell technology would be practical if hydrogen could be stored in a safe, efficient, compact, and economic manner. The experiments reported here train students to measure the hydrogen storage capacity of aqueous hydrochloric acid solution and solid magnesium hydride by measuring the consumption of hydrogen with a hydrogen fuel cell and evaluating its performance. In addition, students also gain fundamental experience handling gases and us.
Functional Studies of Novel FOXL2 Variants in Chinese Families With Blepharophimosis–Ptosis–Epicanthus Inversus Syndrome

The blepharophimosis–ptosis–epicanthus inversus syndrome (BPES) is a rare autosomal dominant disease mainly caused by FOXL2 variants. This genetic disorder is usually characterized by eyelid malformation and ovarian dysfunction. However, no reliable genotype/phenotype correlations have been established considering the ovarian phenotype. Here, we detected 15 FOXL2 variants including nine novel ones from 7 families and 8 sporadic cases, which expanded the spectrum of FOXL2 variants and identified a potential clinical cause. Functional studies, with respect to the effect of FOXL2 on the StAR promoter, showed that non-sense variants that lead to protein truncation before the polyalanine tract and missense variants [c.307C > T; p.(Arg103Cys), c.311A > C; p.(His104Pro), c.320G > A; p.(Ser107Asn), and c.335T > A; p.(Phe112Tyr)] within the central portion of the FOXL2 forkhead domain significantly affect its suppressor activity. Such changes may explain the mechanism underlying a more severe phenotype, more likely to result in BPES type I. Furthermore, the missenses variants c.307C > T; p.(Arg103Cys), c.311A > C; p.(His104Pro), and c.320G > A; p.(Ser107Asn) were not able to transactivate OSR2, which is consistent with the eyelid malformation in these patients. The results from our cohort have expanded the spectrum of FOXL2 variants and have provided insights into genotype/phenotype correlations.
Absence of Pannexin 1 Stabilizes Hippocampal Excitability After Intracerebral Treatment With Aβ (1-42) and Prevents LTP Deficits in Middle-Aged Mice

Beta-amyloid protein [Aβ(1-42)] plays an important role in the disease progress and pathophysiology of Alzheimer's disease (AD). Membrane properties and neuronal excitability are altered in the hippocampus of transgenic AD mouse models that overexpress amyloid precursor protein. Although gap junction hemichannels have been implicated in the early pathogenesis of AD, to what extent Pannexin channels contribute to Aβ(1-42)-mediated brain changes is not yet known. In this study we, therefore, investigated the involvement of Pannexin1 (Panx1) channels in Aβ-mediated changes of neuronal membrane properties and long-term potentiation (LTP) in an animal model of AD. We conducted whole-cell patch-clamp recordings in CA1 pyramidal neurons 1 week after intracerebroventricular treatments of adult wildtype (wt) and Panx1 knockout (Panx1-ko) mice with either oligomeric Aβ(1-42), or control peptide. Panx1-ko hippocampi treated with control peptide exhibited increased neuronal excitability compared to wt. In addition, action potential (AP) firing frequency was higher in control Panx1-ko slices compared to wt. Aβ-treatment reduced AP firing frequency in both cohorts. But in Aβ-treated wt mice, spike frequency adaptation was significantly enhanced, when compared to control wt and to Aβ-treated Panx1-ko mice. Assessment of hippocampal LTP revealed deficits in Aβ-treated wt compared to control wt. By contrast, Panx1-ko exhibited LTP that was equivalent to LTP in control ko hippocampi. Taken together, our data show that in the absence of Pannexin1, hippocampi are more resistant to the debilitating effects of oligomeric Aβ. Both Aβ-mediated impairments in spike frequency adaptation and in LTP that occur in wt animals, are ameliorated in Panx1-ko mice. These results suggest that Panx1 contributes to early changes in hippocampal neuronal and synaptic function that are triggered by oligomeric Aβ.
C21orf91 Regulates Oligodendroglial Precursor Cell Fate—A Switch in the Glial Lineage?

Neuropathological diseases of the central nervous system (CNS) are frequently associated with impaired differentiation of the oligodendroglial cell lineage and subsequent alterations in white matter structure and dynamics. Down syndrome (DS), or trisomy 21, is the most common genetic cause for cognitive impairments and intellectual disability (ID) and is associated with a reduction in the number of neurons and oligodendrocytes, as well as with hypomyelination and astrogliosis. Recent studies mainly focused on neuronal development in DS and underestimated the role of glial cells as pathogenic players. This also relates to C21ORF91, a protein considered a key modulator of aberrant CNS development in DS. We investigated the role of C21orf91 ortholog in terms of oligodendrogenesis and myelination using database information as well as through cultured primary oligodendroglial precursor cells (OPCs). Upon modulation of C21orf91 gene expression, we found this factor to be important for accurate oligodendroglial differentiation, influencing their capacity to mature and to myelinate axons. Interestingly, C21orf91 overexpression initiates a cell population coexpressing astroglial- and oligodendroglial markers indicating that elevated C21orf91 expression levels induce a gliogenic shift towards the astrocytic lineage reflecting non-equilibrated glial cell populations in DS brains.