Catesbek4633

Shifts in the timing of cyclic seasonal life-history events are among the most commonly reported responses to climate change, with differences in response rates among interacting species leading to phenological mismatches. Within a species, however, males and females can also exhibit differential sensitivity to environmental cues and may, therefore, differ in their responsiveness to climate change, potentially leading to phenological mismatches between the sexes. This occurs because males differ from females in when and how energy is allocated to reproduction, resulting in marked sex-differences in life-history timing across the annual cycle. In this review, we take a Tinbergian perspective and examine sex-differences in timing of vertebrates from adaptive, ontogenetic, mechanistic, and phylogenetic viewpoints with the goal of informing and motivating more integrative research on sexually dimorphic phenologies. We argue that sexual and natural selection lead to sex-differences in life-history timing and that it and genome resources grow. We recommend that greater attention be placed on determining sex-differences in timing mechanisms and monitoring climate change responses in both sexes, and we discuss how new tools may provide key insights into sex-differences in phenology from all four Tinbergian domains.Acute megakaryoblastic leukemia of Down syndrome (DS-AMKL) is a model of clonal evolution from a preleukemic transient myeloproliferative disorder requiring both a trisomy 21 (T21) and a GATA1s mutation to a leukemia driven by additional driver mutations. We modeled the megakaryocyte differentiation defect through stepwise gene editing of GATA1s, SMC3+/-, and MPLW515K, providing 20 different T21 or disomy 21 (D21) induced pluripotent stem cell (iPSC) clones. GATA1s profoundly reshaped iPSC-derived hematopoietic architecture with gradual myeloid-to-megakaryocyte shift and megakaryocyte differentiation alteration upon addition of SMC3 and MPL mutations. Transcriptional, chromatin accessibility, and GATA1-binding data showed alteration of essential megakaryocyte differentiation genes, including NFE2 downregulation that was associated with loss of GATA1s binding and functionally involved in megakaryocyte differentiation blockage. T21 enhanced the proliferative phenotype, reproducing the cellular and molecular abnormalities of DS-AMKL. Our study provides an array of human cell-based models revealing individual contributions of different mutations to DS-AMKL differentiation blockage, a major determinant of leukemic progression.The physical properties of grain boundaries in halide perovskites, especially their atomic structure, have not been fully understood yet. We report that Σ5 [130] symmetrical tilt grain boundaries can be stabilized by rigid body translation which is moving one side of the grain parallel with respect to the adjacent grain. Such reconstruction passivates grain boundaries by removing Pb-Pb and I-I interactions that introduce shallow defect states in the band gap. Rigid body translation also stabilizes the [110] antiphase boundary as well in both CsPbI3 and CsPbBr3.The increasing prevalence of antimicrobial-resistant bacterial infections has ushered in a major global public health crisis. Judicious or restricted antimicrobial use in animal agriculture, aiming to confine the use for the treatment of infections, is the most commonly proposed solution to reduce selection pressure for resistant bacterial strains and resistance genes. However, a multifaceted solution will likely be required to make acceptable progress in reducing antimicrobial resistance, due to other common environmental conditions maintaining antimicrobial resistance and limited executionary potential as human healthcare and agriculture will continue to rely heavily on antimicrobials in the foreseeable future. Drawing parallels from systematic approaches to the management of infectious disease agents and biodiversity loss, we provide examples that a more comprehensive approach is required, targeting antimicrobial resistance in agroecosystems on multiple fronts simultaneously. We present one such framework, based on nested biological units of antimicrobial resistance, and describe established or innovative strategies targeting units. Some of the proposed strategies are already in use or ready to be implemented, while some require further research and discussion among scientists and policymakers. We envision that antimicrobial resistance mitigation strategies for animal agriculture combining multiple tools would constitute powerful ecosystem-level interventions necessary to mitigate antimicrobial resistance.Elevated hematocrit is associated with cardiovascular risk; however, the causality and mechanisms are unclear. The JAK2V617F (Jak2VF) mutation increases cardiovascular risk in myeloproliferative disorders and in clonal hematopoiesis. Jak2VF mice with elevated WBCs, platelets, and RBCs display accelerated atherosclerosis and macrophage erythrophagocytosis. To investigate whether selective erythroid Jak2VF expression promotes atherosclerosis, we developed hyperlipidemic erythropoietin receptor Cre mice that express Jak2VF in the erythroid lineage (VFEpoR mice). VFEpoR mice without elevated blood cell counts showed increased atherosclerotic plaque necrosis, erythrophagocytosis, and ferroptosis. Selective induction of erythrocytosis with low-dose erythropoietin further exacerbated atherosclerosis with prominent ferroptosis, lipid peroxidation, and endothelial damage. VFEpoR RBCs had reduced antioxidant defenses and increased lipid hydroperoxides. Phagocytosis of human or murine WT or JAK2VF RBCs by WT macrophages induced ferroptosis, which was prevented by the ferroptosis inhibitor liproxstatin-1. Liproxstatin-1 reversed increased atherosclerosis, lipid peroxidation, ferroptosis, and endothelial damage in VFEpoR mice and in Jak2VF chimeric mice simulating clonal hematopoiesis, but had no impact in controls. Erythroid lineage Jak2VF expression led to qualitative and quantitative defects in RBCs that exacerbated atherosclerosis. Phagocytosis of RBCs by plaque macrophages promoted ferroptosis, suggesting a therapeutic target for reducing RBC-mediated cardiovascular risk.The gut microbial communities of mammals provide numerous benefits to their hosts. However, given the recent development of the microbiome field, we still lack a thorough understanding of the variety of ecological and evolutionary factors that structure these communities across species. Metabarcoding is a powerful technique that allows for multiple microbial ecology questions to be investigated simultaneously. Here, we employed DNA metabarcoding techniques, predictive metagenomics, and culture-dependent techniques to inventory the gut microbial communities of several species of rodent collected from the same environment that employ different natural feeding strategies [granivorous pocket mice (Chaetodipus penicillatus); granivorous kangaroo rats (Dipodomys merriami); herbivorous woodrats (Neotoma albigula); omnivorous cactus mice (Peromyscus eremicus); and insectivorous grasshopper mice (Onychomys torridus)]. Of particular interest were shifts in gut microbial communities in rodent species with herbivorous andiversity underlying DNA metabarcoding techniques. However, these methods offer power in allowing the investigation of several questions concurrently, thus enhancing our understanding of gut microbial ecology.The transcription factor STAT1 plays a critical role in modulating the differentiation of CD4+ T cells producing IL-17 and GM-CSF, which promote the development of experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS). The protective role of STAT1 in MS and EAE has been largely attributed to its ability to limit pathogenic Th cells and promote Tregs. Using mice with selective deletion of STAT1 in T cells (STAT1CD4-Cre), we identified a potentially novel mechanism by which STAT1 regulates neuroinflammation independently of Foxp3+ Tregs. STAT1-deficient effector T cells became the target of NK cell-mediated killing, limiting their capacity to induce EAE. STAT1-deficient T cells promoted their own killing by producing more IL-2 that, in return, activated NK cells. Elimination of NK cells restored EAE susceptibility in STAT1CD4-Cre mice. Therefore, our study suggests that the STAT1 pathway can be manipulated to limit autoreactive T cells during autoimmunity directed against the CNS.

True seven day a week acute care physical therapy (PT) coverage is rare. Our facility is one of a few in Canada that has increased weekend PT coverage on medicine units to seven days of full PT staffing levels.

This article investigates the perspectives of physical therapists involved in the change with the focus on the emotional experiences of those therapists.

Thematic analysis of interview and focus group transcripts with 18 physical therapist and 2 manager participants were aligned with four themes of 1) optimism, hope and excitement; 2) frustration, guilt, and resentment; 3) fear, anxiety, uncertainty, and vulnerability; and 4) ambivalence, neutrality, and impartiality.

Although there were several perceived benefits to quality of care and work/life balance, participants' comments also reflected frustration, guilt, and resentment related to the rapid implementation of the change and the impact of altered work schedules.

Participants emphasized the need to discuss large changes with staff prior to implementation in order to prevent frustration and resentment. Cilengitide mouse Participants also felt that increased acute care PT coverage over seven days is valuable, but other allied health professions also need a proportional increase in staffing to improve hospital flow.

Participants emphasized the need to discuss large changes with staff prior to implementation in order to prevent frustration and resentment. Participants also felt that increased acute care PT coverage over seven days is valuable, but other allied health professions also need a proportional increase in staffing to improve hospital flow.

Innovative digital technology systems that support and monitor real-time medication intake are now available commercially; however, there is limited knowledge of the use of such technology in patients' homes. One such smart medication dispenser, spencer, provides alerts to patients to take their medications and allows for tracking and reporting real-time medication adherence data.

The objectives of this study were to examine the use of a smart medication dispenser as a medication adherence and self-management support tool for community dwelling adults over a 6-month period, in addition to usability, usefulness, satisfaction, and impact on caregiver support.

This prospective, observational study invited community-dwelling adults aged 45 years and older taking at least one chronic medication and their caregivers to use this smart medication dispenser for their medication administration for 6 months. Adherence was defined as a dose intake within 2 hours post scheduled time. Real-time adherence data were coI 2.11-5.98).

Smart medication adherence products such as spencer, when connected and clinically monitored, can be a useful solution for medication management and have the potential to improve caregiver burden.

Smart medication adherence products such as spencer, when connected and clinically monitored, can be a useful solution for medication management and have the potential to improve caregiver burden.