Miracle-dz/UniFAR-FTUs huggingface dataset:
Plasticity plays a dominant role in regulating the phenological variations of sugar maple populations in Canada

Global changes affect the growing conditions of terrestrial ecosystems, causing a mismatch between plant phenology and local climates in Northern regions. Due to their long lifespan and irregular regeneration periods, trees cannot respond quickly enough to climate variability through long-term genetic adaptation. In this study, we explored the phenological plasticity and genetic variation among populations of bud burst in sugar maple (Acer saccharum Marsh.) seedlings from 30 Canadian provenances with contrasting climates planted in two common gardens near and at the northern limit of the species’ range. We tested the hypothesis that phenotypic plasticity and genetic variation among populations affect bud phenology. We expect that phenotypic plasticity is more important in regulating bud phenology due to the high variability in short-term weather events characterizing this part of North America. Bud development and leafing occurred in April–May, with complete bud burst lasting between 21 and 29 days. On average, bud swelling differed by 12 days between common gardens. Both factors site (common gardens) and provenance significantly affected bud burst, demonstrating phenological plasticity and genetic variation of sugar maple, respectively. A significant interaction between site and provenance was also found. Overall, the site (11.8–90.3%) contributed more than provenance (0–3.1%) to the variance in timings of bud burst, indicating a dominant role of plasticity in regulating spring phenology. Our study demonstrated the concurring effects of genetic variation and phenological plasticity of sugar maple and revealed the dominant role of the latter factor. The high plasticity observed in sugar maple has a crucial role in the phenological adaptation of maple and the survival of its local populations in a context of changing climate.
The cause–effect relation of tuberculosis on incidence of diabetes mellitus

Tuberculosis (TB) is one of the oldest human diseases and is one of the major causes of mortality and morbidity across the Globe. Mycobacterium tuberculosis (Mtb), the causal agent of TB is one of the most successful pathogens known to mankind. Malnutrition, smoking, co-infection with other pathogens like human immunodeficiency virus (HIV), or conditions like diabetes further aggravate the tuberculosis pathogenesis. The association between type 2 diabetes mellitus (DM) and tuberculosis is well known and the immune-metabolic changes during diabetes are known to cause increased susceptibility to tuberculosis. Many epidemiological studies suggest the occurrence of hyperglycemia during active TB leading to impaired glucose tolerance and insulin resistance. However, the mechanisms underlying these effects is not well understood. In this review, we have described possible causal factors like inflammation, host metabolic changes triggered by tuberculosis that could contribute to the development of insulin resistance and type 2 diabetes. We have also discussed therapeutic management of type 2 diabetes during TB, which may help in designing future strategies to cope with TB-DM cases.
Association between the lean nonalcoholic fatty liver disease and risk of incident type 2 diabetes in a healthy population of Northwest China: a retrospective cohort study with a 2-year follow-up period

Aims We aimed to explore the metabolic features of lean nonalcoholic fatty liver disease (Lean-NAFLD) and its association with the risk of incident type 2 diabetes in young and middle-aged people. Methods We conducted a retrospective cohort study of 3001 participants who were enrolled in a health check-up program from January 2018 to December 2020 in the Health Management Center of Karamay People’s Hospital. The age, sex, height, weight, body mass index (BMI), blood pressure, waist circumference (WC), fasting plasma glucose (FPG), lipid profiles, serum uric acid and alanine aminotransferase (ALT) of the subjects were collected. The cutoff point of BMI for lean nonalcoholic fatty liver disease is <25 kg/m2. A COX proportional hazard regression model was used to analyze the risk ratio of lean nonalcoholic fatty liver disease to type 2 diabetes mellitus. Results Lean NAFLD participants had many metabolic abnormalities, such as overweight and obesity with nonalcoholic fatty liver disease. Compared with lean participants without nonalcoholic fatty liver disease, the fully adjusted hazard ratio (HR) for lean participants with nonalcoholic fatty liver disease was 3.83 (95% CI 2.02-7.24, p<0.01). In the normal waist circumference group (man<90cm, woman<80 cm), compared with lean participants without NAFLD, the adjusted hazard ratios (HRs) of incident type 2 diabetes for lean participants with NAFLD and overweight or obese participants with NAFLD were 1.93 (95% CI 0.70-5.35, p>0.05) and 4.20 (95% CI 1.44-12.22, p<0.05), respectively. For excess waist circumference (man≥90 cm, woman ≥80 cm) compared with lean participants without NAFLD, the adjusted hazard ratios (HRs) of incident type 2 diabetes for lean participants with NAFLD and overweight or obese participants with NAFLD were 3.88 (95% CI 1.56-9.66, p<0.05) and 3.30 (95% CI 1.52-7.14, p<0.05), respectively. Conclusion Abdominal obesity is the strongest risk factor for type 2 diabetes in lean nonalcoholic fatty liver disease.
Cuproptosis-related genes signature and validation of differential expression and the potential targeting drugs in temporal lobe epilepsy

Introduction: Temporal lobe epilepsy (TLE) is the most common subtype of epilepsy in adults and is characterized by neuronal loss, gliosis, and sprouting mossy fibers in the hippocampus. But the mechanism underlying neuronal loss has not been fully elucidated. A new programmed cell death, cuproptosis, has recently been discovered; however, its role in TLE is not clear. Methods: We first investigated the copper ion concentration in the hippocampus tissue. Then, using the Sample dataset and E-MTAB-3123 dataset, we analyzed the features of 12 cuproptosis-related genes in TLEs and controls using the bioinformatics tools. Then, the expression of the key cuproptosis genes were confirmed using real-time PCR and immunohistochemical staining (IHC). Finally, the Enrichr database was used to screen the small molecules and drugs targeting key cuproptosis genes in TLE. Results: The Sample dataset displayed four differentially expressed cuproptosis-related genes (DECRGs; LIPT1, GLS, PDHA1, and CDKN2A) while the E-MTAB-3123 dataset revealed seven DECRGs (LIPT1, DLD, FDX1, GLS, PDHB, PDHA1, and DLAT). Remarkably, only LIPT1 was uniformly upregulated in both datasets. Additionally, these DECRGs are implicated in the TCA cycle and pyruvate metabolism—both crucial for cell cuproptosis—as well as various immune cell infiltrations, especially macrophages and T cells, in the TLE hippocampus. Interestingly, DECRGs were linked to most infiltrating immune cells during TLE’s acute phase, but this association considerably weakened in the latent phase. In the chronic phase, DECRGs were connected with several T-cell subclasses. Moreover, LIPT1, FDX1, DLD, and PDHB were related to TLE identification. PCR and IHC further confirmed LIPT1 and FDX1’s upregulation in TLE compared to controls. Finally, using the Enrichr database, we found that chlorzoxazone and piperlongumine inhibited cell cuproptosis by targeting LIPT1, FDX1, DLD, and PDHB. Conclusion: Our findings suggest that cuproptosis is directly related to TLE. The signature of cuproptosis-related genes presents new clues for exploring the roles of neuronal death in TLE. Furthermore, LIPT1 and FDX1 appear as potential targets of neuronal cuproptosis for controlling TLE’s seizures and progression.
Interplay between chromosomal architecture and termination of DNA replication in bacteria

Faithful transmission of the genome from one generation to the next is key to life in all cellular organisms. In the majority of bacteria, the genome is comprised of a single circular chromosome that is normally replicated from a single origin, though additional genetic information may be encoded within much smaller extrachromosomal elements called plasmids. By contrast, the genome of a eukaryote is distributed across multiple linear chromosomes, each of which is replicated from multiple origins. The genomes of archaeal species are circular, but are predominantly replicated from multiple origins. In all three cases, replication is bidirectional and terminates when converging replication fork complexes merge and ‘fuse’ as replication of the chromosomal DNA is completed. While the mechanics of replication initiation are quite well understood, exactly what happens during termination is far from clear, although studies in bacterial and eukaryotic models over recent years have started to provide some insight. Bacterial models with a circular chromosome and a single bidirectional origin offer the distinct advantage that there is normally just one fusion event between two replication fork complexes as synthesis terminates. Moreover, whereas termination of replication appears to happen in many bacteria wherever forks happen to meet, termination in some bacterial species, including the well-studied bacteria Escherichia coli and Bacillus subtilis, is more restrictive and confined to a ‘replication fork trap’ region, making termination even more tractable. This region is defined by multiple genomic terminator (ter) sites, which, if bound by specific terminator proteins, form unidirectional fork barriers. In this review we discuss a range of experimental results highlighting how the fork fusion process can trigger significant pathologies that interfere with the successful conclusion of DNA replication, how these pathologies might be resolved in bacteria without a fork trap system and how the acquisition of a fork trap might have provided an alternative and cleaner solution, thus explaining why in bacterial species that have acquired a fork trap system, this system is remarkably well maintained. Finally, we consider how eukaryotic cells can cope with a much-increased number of termination events.
Transforming growth factor-β1 and SMAD signalling pathway in the small airways of smokers and patients with COPD: potential role in driving fibrotic type-2 epithelial mesenchymal transition

Background COPD is a common disease characterized by respiratory airflow obstruction. TGF-β1 and SMAD pathway is believed to play a role in COPD pathogenesis by driving epithelial mesenchymal transition (EMT). Methods We investigated TGF-β1 signalling and pSmad2/3 and Smad7 activity in resected small airway tissue from patients with; normal lung function and a smoking history (NLFS), current smokers and ex-smokers with COPD GOLD stage 1 and 2 (COPD-CS and COPD-ES) and compared these with normal non-smoking controls (NC). Using immunohistochemistry, we measured activity for these markers in the epithelium, basal epithelium, and reticular basement membrane (RBM). Tissue was also stained for EMT markers E-cadherin, S100A4 and vimentin. Results The Staining of pSMAD2/3 was significantly increased in the epithelium, and RBM of all COPD groups compared to NC (p <0.0005). There was a less significant increase in COPD-ES basal cell numbers compared to NC (p= 0.02). SMAD7 staining showed a similar pattern (p <0.0001). All COPD group levels of TGF-β1 in the epithelium, basal cells, and RBM cells were significantly lower than NC (p <0.0001). Ratio analysis showed a disproportionate increase in SMAD7 levels compared to pSMAD2/3 in NLFS, COPD-CS and COPD-ES. pSMAD negatively correlated with small airway calibre (FEF25–75%; p= 0.03 r= -0.36). EMT markers were active in the small airway epithelium of all the pathological groups compared to patients with COPD. Conclusion Activation of the SMAD pathway via pSMAD2/3 is triggered by smoking and active in patients with mild to moderate COPD. These changes correlated to decline in lung function. Activation of the SMADs in the small airways is independent of TGF-β1, suggesting factors other than TGF-β1 are driving these pathways. These factors may have implications for small airway pathology in smokers and COPD through the process of EMT, however more mechanistic work is needed to prove these correlations.
Immune-checkpoint protein VISTA in allergic, autoimmune disease and transplant rejection

Negative checkpoint regulators (NCRs) reduce the T cell immune response against self-antigens and limit autoimmune disease development. V-domain Ig suppressor of T cell activation (VISTA), a novel immune checkpoint in the B7 family, has recently been identified as one of the NCRs. VISTA maintains T cell quiescence and peripheral tolerance. VISTA targeting has shown promising results in treating immune-related diseases, including cancer and autoimmune disease. In this review, we summarize and discuss the immunomodulatory role of VISTA, its therapeutic potential in allergic, autoimmune disease, and transplant rejection, as well as the current therapeutic antibodies, to present a new method for regulating immune responses and achieving durable tolerance for the treatment of autoimmune disease and transplantation.
Original research: longitudinal evaluation of cognitively demanding daily function using performance-based functional assessment highlights heterogeneous trajectories in cognitive and functional abilities in people with Parkinson’s disease

Background Longitudinal assessment of functional abilities in Parkinson’s disease (PD) is needed to determine the efficacy of cognitive interventions in providing meaningful improvements in daily life. Additionally, subtle changes in instrumental activities of daily living may precede a clinical diagnosis of dementia and could aid earlier detection of and intervention for cognitive decline. Objective The primary goal was to validate the longitudinal application of the University of California San Diego Performance-Based Skills Assessment (UPSA). An exploratory secondary goal was to determine whether UPSA may identify individuals at higher risk of cognitive decline in PD. Methods Seventy participants with PD completed the UPSA with at least one follow-up visit. Linear mixed effects modeling was used to identify associations between baseline UPSA score and cognitive composite score (CCS) over time. Descriptive analysis of four heterogeneous cognitive and functional trajectory groups and individual case examples was performed. Results Baseline UPSA score predicted CCS at each timepoint for functionally impaired and unimpaired groups (p < 0.01) but did not predict the rate change in CCS over time (p = 0.83). Participants displayed heterogenous trajectories in both UPSA and CCS during the follow-up period. Most participants maintained both cognitive and functional performance (n = 54), though some displayed cognitive and functional decline (n = 4), cognitive decline with functional maintenance (n = 4), and functional decline with cognitive maintenance (n = 8). Conclusion The UPSA is a valid measure of cognitive functional abilities over time in PD. Given the heterogeneity of functional and cognitive trajectories, this performance-based assessment did not predict cognitive decline with this relatively short follow-up. Further work is needed to understand longitudinal functional assessments in PD-associated cognitive impairment.
Axo-axonic cells in neuropsychiatric disorders: a systematic review

Imbalance between excitation and inhibition in the cerebral cortex is one of the main theories in neuropsychiatric disorder pathophysiology. Cortical inhibition is finely regulated by a variety of highly specialized GABAergic interneuron types, which are thought to organize neural network activities. Among interneurons, axo-axonic cells are unique in making synapses with the axon initial segment of pyramidal neurons. Alterations of axo-axonic cells have been proposed to be implicated in disorders including epilepsy, schizophrenia and autism spectrum disorder. However, evidence for the alteration of axo-axonic cells in disease has only been examined in narrative reviews. By performing a systematic review of studies investigating axo-axonic cells and axo-axonic communication in epilepsy, schizophrenia and autism spectrum disorder, we outline convergent findings and discrepancies in the literature. Overall, the implication of axo-axonic cells in neuropsychiatric disorders might have been overstated. Additional work is needed to assess initial, mostly indirect findings, and to unravel how defects in axo-axonic cells translates to cortical dysregulation and, in turn, to pathological states.
SDPipe: A Semi-Decentralized Framework for Heterogeneity-aware Pipeline-parallel Training

The increasing size of both deep learning models and training data necessitates the ability to scale out model training through pipeline-parallel training, which combines pipelined model parallelism and data parallelism. However, most of them assume an ideal homogeneous dedicated cluster. As for real cloud clusters, these approaches suffer from the intensive model synchronization overheads due to the dynamic environment heterogeneity. Such a huge challenge leaves the design in a dilemma: either the performance bottleneck of the central parameter server (PS) or severe performance degradation caused by stragglers for decentralized synchronization (like All-Reduce). This approach presents SDPipe, a new semi-decentralized framework to get the best of both worlds, achieving both high heterogeneity tolerance and convergence efficiency in pipeline-parallel training. To provide high performance, we decentralize the communication model synchronization, which accounts for the largest proportion of synchronization overhead. In contrast, we centralize the process of group scheduling, which is lightweight but needs a global view for better performance and convergence speed against heterogeneity. We show via a prototype implementation the significant advantage of SDPipe on performance and scalability, facing different environments.
Distributed optimization with communication constraints

This thesis addresses problems of optimization to be solved collectively (distributely, we say) by groups of networked agents having limited communication and computation capabilities. The focus is on two paradigmatic problems, average consensus and coverage control. The former consists in computing the average of values which are priory known to the agents, while the latter consists in optimally deploying robotic agents in a given environment. Their solution is possible thanks to iterative algorithms which exploit the available communications among agents, described by a graph. Research has been very intense in latest years on these problems, due to strong applicative motivations: these algorithms are crucial for the design of networks of sensors, and for the coordinated motion of groups of unmanned vehicles. Namely, the ultimate goal of these algorithms is to make such artificial networks able to self-organize and perform specific tasks without a centralized supervision. In the thesis networks have been considered, which allow only communication in pairs, or limited to messages belonging to a discrete alphabet. Several novel algorithms for the solution of the above optimization problems are proposed: they are proved to lead the agents to the desired solution, and their performance is studied. The mathematical tools required for the analysis are novel, or need to be used in a non-standard way. They are drawn from very different branches of pure and applied mathematics: spectral graph theory, Markov chains, combinatorics, linear algebra, set-valued analysis, convex and discrete geometry, topology of hyper-spaces of sets.
Incorporating TOMS Ozone Measurements into the Prediction of the Washington, D.C., Winter Storm during 24–25 January 2000

Abstract In this study, a methodology is proposed for incorporating total column ozone data from the Total Ozone Mapping Spectrometer (TOMS) into the initial conditions of a mesoscale prediction model. Based on the strong correlation between vertical mean potential vorticity (MPV) and TOMS ozone (O3) that was found in middle latitudes at both 30- and 90-km resolutions, using either analyses or 24-h model forecasts, a statistical correlation model between O3 and MPV is employed for assimilating TOMS ozone in a four-dimensional variational data assimilation (4DVAR) procedure. A linear relationship between O3 and MPV is first assumed: O3 = α(MPV) + β. The constants α and β are then found by a regression method. The proposed approach of using this simple linear regression model for ozone assimilation is applied to the prediction of the 24–25 January 2000 East Coast winter storm. Three 4DVAR experiments are carried out assimilating TOMS ozone, radiosonde, or both types of observations. It is found that adjustm.
Business Performance in Automotive Vehicle Customs Business in Indonesia

Purpose: This study aims to determine Business Performance in Automotive Vehicle Customs Business in Indonesia. This study uses the RBV basis in analyzing phenomena and research findings. The population of this study is the owners of customs workshops throughout Indonesia. Method:The number of samples is determined using the Isaac table equation to obtain a total sample of 300 respondents. Data collection uses questionnaires that are distributed offline and online. Data measurement uses answers Strongly Agree, Agree, Disagree, Strongly Disagree, with a rating scale of 1 to 4. Data processing uses the SMART PLS3 application. The results of this study found that Customer Orientation, Adaptive Technology, and Marketing Capability had a positive effect on the Business Performance of custom workshops. This can be seen from the results of the discriminate validity test and the final result of Smart PLS3 data processing. Result: This study found that Customer Orientation, Adaptive Technology, and Marketing Capability positively affected the Business Performance of custom workshops. This can be seen from the results of the discriminate validity test and the final result of Smart PLS3 data processing. The findings of this study support the study that Customer Orientation towards repair shop customers, Adaptive Technology of workshops in the production of custom motorbikes, and Marketing Capability owned by custom repair shops have a good effect in the long term. This is strengthened because the custom workshop is a service industry that prioritizes the needs and desires of its customers; they work and produce based on online and offline market demands apart from the needs of company assets. The public and their customers will notice the use and application of technology in completing custom motorbikes. This is the opinion given by the custom builders that I met. They explained that in the production of custom motorcycles, we must meet the needs and wishes of customers, which will affect market demand for custom motorcycle orders that we will work on later. These results support the finding that research on custom builders will increase if we can meet the needs and desires of consumers and markets on a widespread or commercial basis.