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Putative muscle stem cells promote <i>Xenopus</i> tail regeneration by modifying macrophage function via <i>c1qtnf3</i>

In Xenopus laevis tadpole tail regeneration, lineage-restricted tissue stem cells produce differentiated cells that form regenerated tail tissues, but the behavioral dynamics of tissue stem cells during tail regeneration remain largely unknown. We previously reported that multiple tissue stem/progenitor cells can be efficiently enriched from regeneration buds using the side population (SP) method. Here, we performed trajectory inference using single-cell RNA sequencing data of the SP fraction to construct differentiation trajectories and identify putative tissue stem cell populations that initiate differentiation pathways. We found that complement c1q tumor necrosis factor-related protein 3 ( c1qtnf3 ) is specifically expressed in putative muscle stem cells (MSC) and, using knockdown (KD; CRISPR/Cas9-based F0 crispants) experiments, demonstrated that c1qtnf3 is necessary for tail regeneration. Furthermore, we found that the impaired tail regeneration by c1qtnf3 KD was accompanied by abrogation of macrophage-like cell accumulation at the amputation site. These phenotypes were rescued by macrophage-like cell-specific forced expression of neutrophil cytosolic factor 1 , a gene related to effector molecule production in myeloid cells, suggesting that the impaired tail regeneration by c1qtnf3 KD is due to macrophage dysregulation. Our findings suggest that, in Xenopus , putative MSC modulate macrophage function via c1qtnf3 expression for successful tail regeneration.

High frequency body site translocation of nosocomial Pseudomonas aeruginosa

Abstract Pseudomonas aeruginosa is an important nosocomial pathogen which can cause serious infections across diverse anatomic locations. Infections can spread within an individual to different body sites, but the rate and directionality of this process is unknown. Here, we explore within-host diversity as well as the body site translocation dynamics using de-convoluted metagenomic P. aeruginosa reads from 256 hospital patients sampled at both respiratory and gut sites. Of the 84 patients where P. aeruginosa genomes could be recovered, there were 27 cases where the same P. aeruginosa clone was detected across multiple body sites. Using a simulation approach, we find that the majority of body site sharing is likely due to within-patient translocation of clones rather than independent acquisition from the hospital environment. Using ancestral reconstruction, we predict that most clones likely occupied a respiratory niche, and that the probable direction of clone transmission is lung-to-gut. Analysis of within-patient variation highlights strong enrichment of mutations in genes associated with antimicrobial resistance, irrespective of sample type. We report significantly more translocation than has been previously reported and highlight that lower respiratory tract infections can result in persistent gut colonisation of P. aeruginosa , a major risk factor for sepsis in vulnerable patients.

Ailanthone restrains hepatocellular carcinoma progression by inducing ferroptosis and disrupting mitochondrial homeostasis

IAA was involved in phosphorus deficiency-induced cluster roots formation in Macadamia integrifolia

How weather affects cognitive and physical outcomes in older adults

Objective To ascertain whether, in comparison to the participants’ expected abilities, the weather may cause abnormally poor cognitive or physical performance. Design Secondary analysis of a randomised controlled trial Setting Study conducted between May, 2008, and Feb, 2011 in 13 memory centres in France and Monaco Participants 1313 participants from the MAPT trial, a 5-year multicentre prevention trial, which included dementia-free individuals aged over 70 years. Participants presented subjective memory complaints, slow gait speed and/or an instrumental activity of daily living limitation. Main outcome measures Cognition was assessed using a composite cognitive Z-score (composed of digit symbol substitution test, free and cued selective reminding test, Mini-mental state, category fluency) and subjective memory complaints. Physical function was assessed using gait speed, the short physical performance battery (SPPB) and its components, and grip strength. Abnormally low scores were defined as an observed score that was lower than the individual’s expected ability by at least the minimal clinically important difference. Results Higher outdoor temperature was associated with a significantly increased risk of abnormally low gait speed or SPPB (respectively OR 1.13 95% CI (1.04, 1.22) and OR 1.15 95% CI (1.03, 1.29) for 10 degrees Celsius), but did not significantly increase the risk of abnormally low cognitive function. Conclusion Our results suggest that weather conditions should be strongly considered when assessing the physical performance of older adults in the context of clinical practice and clinical research as examination in hot weather might lead to false conclusions on the participants’ abilities.

The immunoproteasome regulates ILC2 responses by modulating mitochondrial capacity

Type 2 innate lymphoid cells (ILC2s) contribute to type 2 immunity but have also been associated with multiple inflammatory diseases, including airway inflammation and asthma. We report that beyond its function of degrading poly-ubiquitinylated proteins, the immunoproteasome (i-20S) is required for the proper function of ILC2s by controlling their mitochondrial capacity. We found that 90% of the catalytic β subunits of proteasomes in human ILC2s (hILC2s) are the immuno- (β5i) rather than constitutive (β5c) isoform. Specific, noncovalent, reversible inhibition of i-20S β5i (LMP7) in hILC2s induced ROS production, which inhibited aconitase, leading to altered mitochondrial function and reduced levels of ATP. Reprogramming of metabolic status by an LMP7 inhibitor impaired ILC2 activation, without significant cytotoxicity or preventing their recovery. Hence, the selective inhibition of i-20S in ILC2 cells did not kill them but reversibly depleted their ATP, preventing their activation and cytokine secretion. In mice, proteasome inhibition similarly blocked mitochondrial function and ILC2 activation, preventing airway inflammation in response to IL33 and asthma in response to house dust mites. These findings reveal a previously unappreciated linkage between proteasome blockade, central carbon metabolism, and mitochondrial function and identify a strategy to regulate immune cell metabolism in inflammatory diseases.

Cohering particles via weak electromagnetic waves for highly conductive polymer composites

Psychometric properties and validation of the Polish version of the wheelchair user’s shoulder pain index

The association between child sexual abuse and mental health in Chinese vocational high school students

Prognostic factors influencing venous patency after thrombectomy in patients with May-Thurner syndrome

Purpose To evaluate the prognostic significance of venographic findings and procedural factors for long-term venous patency after thrombectomy in patients with May-Thurner syndrome (MTS)-associated deep vein thrombosis (DVT). Materials and Methods This retrospective cohort study included 75 patients with iliofemoral DVT secondary to MTS, who underwent thrombectomy between January 2011 and April 2023. Key venographic findings—venous stenosis (≥50%), venous spur, and persistent collaterals—along with stent placement and diameter were analyzed. The primary outcome was 24-month venous patency, assessed using univariate tests, Kaplan–Meier survival analysis, and multivariate Cox proportional hazards modeling. Results At 24 months, 58 patients (77.3%) maintained venous patency, whereas 17 (22.7%) experienced reocclusion. Univariate and Kaplan–Meier analyses showed that stenosis ≥50%, venous spur, persistent collaterals, and absence of stent placement were significantly associated with reduced patency (all p  &lt; 0.05). However, in the multivariate Cox model, only venous stenosis ≥50% remained a statistically significant independent predictor of reocclusion (hazard ratio [HR]=5.04; 95% Confidence Interval: 1.28–19.82; p  = 0.021). Stent placement (HR = 1.78; p  = 0.337) and diameter ( p  = 0.349) were not independently associated with patency. Conclusion Residual venous stenosis ≥50% following thrombectomy is an independent predictor of reduced long-term patency in patients with MTS. While stent placement was associated with better outcomes in the univariate analysis, it did not independently predict patency after adjustment, likely due to treatment-related confounding factors. Effective anatomical resolution of stenosis may be more critical than stent deployment. Prospective studies are warranted to clarify the prognostic impact of venographic findings and interventional strategies.

Autism-associated <i>Scn2a</i> haploinsufficiency disrupts in vivo dendritic signaling and impairs flexible decision-making

SCN2A is a high-confidence risk gene for autism spectrum disorder. Loss-of-function mutations in Scn2a reduce dendritic excitability in neocortical pyramidal cells. However, the impact of Scn2a haploinsufficiency on dendritic signaling in vivo, particularly during behavior, is unknown. In this study, we used two-photon microscopy to image dendritic calcium transients in deep layer pyramidal cells in the mouse medial frontal cortex. Scn2a +/− mice had diminished coupling between apical and proximal dendritic compartments. Pyramidal tract neurons had abnormal event rates, while intratelencephalic neurons had compartment-specific alterations indicative of diminished dendritic integration. In a matching pennies task, Scn2a +/− mice were inflexible in the face of changing competitive pressure. Apical dendritic tuft in intratelencephalic neurons typically encoded reward and strategy, but these task-specific representations were altered in Scn2a +/− mice. Collectively, the findings demonstrate that Scn2a haploinsufficiency weakens dendritic integration in vivo and disrupts dendritic encoding of task variables during flexible decision-making.

Lysosomal acidity and cathepsin L activate eosinophils via ARG1-mediated arginine metabolism in allergic airway inflammation

Honokiol inhibits gastric cancer via tumor microenvironment modulation: a bioinformatics and single-cell analysis

Outcomes of sequential therapy for advanced upper tract urothelial cancer and bladder cancer

Interventions to improve racial and ethnic equity in critical care: A scoping review

Background Racial and ethnic disparities in the delivery and outcomes of critical care are well documented. However, interventions to mitigate these disparities are less well understood. We sought to review the current state of evidence for interventions to promote equity in critical care processes and patient outcomes. Methods Four bibliographic databases (MEDLINE/PubMed, Web of Science Core Collection, CINAHL, and Embase) and a list of core journals, conference abstracts, and clinical trial registries were queried with a pre-specified search strategy. We analyzed the content of interventions by categorizing each as single- or multi-component, extracting each intervention component during review, and grouping intervention components according to strategy to identify common approaches. Results The search strategy yielded 11,509 studies. Seven-thousand seventeen duplicate studies were removed, leaving 4,491 studies for title and abstract screening. After screening, 93 studies were included for full-text review. After full-text review by two independent reviewers, eleven studies met eligibility criteria. We identified ten distinct intervention components under five broad categories: education, communication, standardization, restructuring, and outreach. Most examined effectiveness using pre-post or other non-randomized designs. Conclusions Despite widespread recognition of disparities in critical care outcomes, few interventions have been evaluated to address disparities in the ICU. Many studies did not describe the rationale or targeted disparity mechanism for their intervention design. There is a need for randomized, controlled evaluations of interventions that target demonstrated mechanisms for disparities to promote equity in critical care.

OPEN STOMATA 1 activates SLAC1 anion channel primarily through CPK15 in ABA-induced stomatal closure in <i>Arabidopsis</i>

The Ca 2+ -independent OST1 and Ca 2+ -dependent protein kinases CPKs both activate the anion channel SLAC1 during ABA-induced stomatal closure pathway. However, the mechanism by which OST1 regulates SLAC1 activation and its relationship with CPKs remain unclear. Here, we identify that OST1 primarily activates SLAC1 in this process through CPK15. Mutation of CPK15 significantly impairs ABA-induced stomatal closure and increases drought sensitivity. OST1 interacts with CPK15 and phosphorylates it at T103, which is essential for ABA-induced stomatal closure. Moreover, CPK15 can phosphorylate eight sites in the N terminus of SLAC1 to activate its anion currents in oocytes. Expression of SLAC1 8D (a phosphomimetic form) in oocytes constitutively activates anion channel activity and effectively restores the impaired ABA-induced stomatal closure of cpk15-1 but not by SLAC1 8A (a phospho-dead form). Furthermore, activated CPK15 by OST1 and Ca 2+ enhances its activity toward SLAC1, and mutations of both OST1 and CPK15 have additive effect on ABA-induced stomatal closure, suggesting that CPK15 activates SLAC1 through both direct and indirect mechanisms. These findings demonstrate the key role of CPK15 in ABA-induced stomatal closure, revealing a connection between OST1 and CPKs in both Ca 2+ -independent and Ca 2+ -dependent pathways in ABA-induced stomatal closure.

Uni-traveling-carrier photodiode based on MoS2/GaN van der Waals heterojunction for high-speed visible-light detection

Producing unexpected emotional expressions in others reduces one’s own agency

Investigating adsorption of 5-fluorouracil and 6-mercaptopurine on icosahedral silver nanoparticles through DFT and TDDFT

Surface roughness profile separation using singular spectrum analysis

Surface roughness is a critical parameter used to describe the microscopic geometric deviations of a part, and serves as an essential indicator for assessing the quality of surface processing in various mechanical components. This study evaluates Singular Spectrum Analysis (SSA) for surface roughness profile separation, comparing its effectiveness with the ISO standard Gaussian filter. Using NIST roughness measurement data, this study investigates how SSA’s window length and grouping method affect roughness parameters. The findings indicate that with an appropriately chosen window length, the SSA technique can effectively separate roughness signals and yield roughness parameter values comparable to those obtained using the Gaussian filter, such as the arithmetical mean deviation of the assessed profile ( Ra ), the root mean square deviation of the assessed profile ( Rq ), and the kurtosis of the assessed profile ( Rku ). These findings establish SSA as a viable alternative for surface roughness profile separation, with broad applications in surface metrology.