Knudsenmcelroy8973

Our data demonstrated that CCL14 inhibited the proliferation and invasion of colon cancer cells through suppressing the formation of M2-like TAMs.

Our data demonstrated that CCL14 inhibited the proliferation and invasion of colon cancer cells through suppressing the formation of M2-like TAMs.

To examine the prevalence and risk factors for readmission after inpatient rehabilitation in stroke survivors, in a developed multi-ethnic Southeast Asian country.

A retrospective cohort study of 1,235 stroke survivors who completed inpatient rehabilitation in a tertiary rehabilitation centre.

A total of 296 (24.0%) patients with stroke were readmitted within the first year, and 87 (7.0%) patients were readmitted 1-3 years after stroke. Significant risk factors for readmission of patients in the first year post-stroke were older age (p = 0.027), lower admission Functional Independence Measure (FIM) motor (p = 0.001) and cognition scores (p = 0.025), a Charlson Comorbidity Index (CCI) ≥1 (p < 0.001) and the presence of at least 1 medical complication during initial hospitalization (p < 0.001), while FIM gain was found to be protective (p < 0.001). Looking at readmission after 1 year post-stroke, a CCI≥1 (p < 0.001) and the presence of medical complications during initial hospitalization (p < 0.001) were risk factors for readmission, while FIM gain (p = 0.001) was protective. Common causes for readmission include recurrent stroke and falls.

There is a high readmission rate in stroke survivors, even after the first year post-stroke. Interventions, such as fall risk assessments, vaccinations, meticulous catheter care, intensified secondary risk factors interventions and continued post-discharge rehabilitation, may hold promise for reducing readmission rates.

There is a high readmission rate in stroke survivors, even after the first year post-stroke. Interventions, such as fall risk assessments, vaccinations, meticulous catheter care, intensified secondary risk factors interventions and continued post-discharge rehabilitation, may hold promise for reducing readmission rates.

Media sources have consistently described older adults as a medically vulnerable population during the COVID-19 pandemic, yet a lack of concern over their health and safety has resulted in dismissal and devaluation. SF1670 This unprecedented situation highlights ongoing societal ageism and its manifestations in public discourse. This analysis asks how national news sources performed explicit and implicit ageism during the first month of the pandemic.

Using content and critical discourse analysis methods, we analyzed 287 articles concerning older adults and COVID-19 published between March 11 and April 10, 2020, in four major U.S.-based newspapers.

Findings indicate that while ageism was rarely discussed explicitly, ageist bias was evident in implicit reporting patterns (e.g., frequent use of the term "elderly," portrayals of older adults as "vulnerable"). Infection and death rates and institutionalized care were among the most commonly reported topics, providing a limited portrait of aging during the pandemic. The older "survivor" narrative offers a positive alternative by suggesting exceptional examples of resilience and grit. However, the survivor narrative may also implicitly place blame on those unable to survive or thrive in later life.

This study provides insight for policy makers, researchers, and practitioners exploring societal perceptions of older adults and how these perceptions are disseminated and maintained by the media.

This study provides insight for policy makers, researchers, and practitioners exploring societal perceptions of older adults and how these perceptions are disseminated and maintained by the media.The emergence of coronavirus disease-2019 (COVID-19) has caused unprecedented challenge to manage the bodies of the dead. link2 The disposal of the dead becomes a challenge as there is a shortage of coffins, and crematoriums are overwhelmed. A recent correspondence published in the Journal of Public Health highlighted the importance of performing the last rites in a time of COVID-19 pandemic. This paper argues that the bodies of those who have died because of COVID-19 should be treated with respect and dignity.Axons and dendrites are distinguished by microtubule polarity. In Drosophila, dendrites are dominated by minus-end-out microtubules, whereas axons contain plus-end-out microtubules. Local nucleation in dendrites generates microtubules in both orientations. To understand why dendritic nucleation does not disrupt polarity, we used live imaging to analyze the fate of microtubules generated at branch points. We found that they had different rates of success exiting the branch based on orientation correctly oriented minus-end-out microtubules succeeded in leaving about twice as often as incorrectly oriented microtubules. Increased success relied on other microtubules in a parallel orientation. From a candidate screen, we identified Trim9 and kinesin-5 (Klp61F) as machinery that promoted growth of new microtubules. In S2 cells, Eb1 recruited Trim9 to microtubules. Klp61F promoted microtubule growth in vitro and in vivo, and could recruit Trim9 in S2 cells. In summary, the data argue that Trim9 and kinesin-5 act together at microtubule plus ends to help polymerizing microtubules parallel to pre-existing ones resist catastrophe.About 70% of breast cancers overexpress estrogen receptor α (ERα, encoded by ESR1). Tamoxifen, a competitive inhibitor of estrogen that binds to ER, has been widely used as a treatment for ER-positive breast cancer. However, 20-30% of breast cancer is resistant to tamoxifen treatment. The mechanisms underlying tamoxifen resistance remain elusive. We found that Yes-associated protein (YAP; also known as YAP1), connective tissue growth factor (CTGF; also known as CCN2) and cysteine-rich angiogenic inducer 61 (Cyr61; also known as CCN1) are overexpressed, while ERα is downregulated in tamoxifen-resistant breast cancer. Inhibition of YAP, CTGF and Cyr61 restored ERα expression and increased sensitivity to tamoxifen. Overexpression of YAP, CTGF, and Cyr61 led to downregulation of ERα and conferred resistance to tamoxifen in ER-positive breast cancer cells. Mechanistically, CTGF and Cyr61 downregulated ERα expression at the transcriptional level by directly binding to the regulatory regions of the ERα-encoding gene, leading to increased tamoxifen resistance. Also, CTGF induced Glut3 (also known as SLC2A3) expression, leading to increased glycolysis, which enhanced cell proliferation and migration in tamoxifen-resistant cells. Together, these results demonstrate a novel role of YAP, CTGF and Cyr61 in tamoxifen resistance and provide a molecular basis for their function in tamoxifen-resistant breast cancer.Dysregulated immunity and widespread metabolic dysfunctions are the most relevant hallmarks of the passing of time over the course of adult life, and their combination at midlife is strongly related to increased vulnerability to diseases; however, the causal connection between them remains largely unclear. By combining multi-omics and functional analyses of adipose-derived stromal cells established from young (1 month) and midlife (12 months) mice, we show that an increase in expression of interferon regulatory factor 7 (IRF7) during adult life drives major metabolic changes, which include impaired mitochondrial function, altered amino acid biogenesis and reduced expression of genes involved in branched-chain amino acid (BCAA) degradation. Our results draw a new paradigm of aging as the 'sterile' activation of a cell-autonomous pathway of self-defense and identify a crucial mediator of this pathway, IRF7, as driver of metabolic dysfunction with age.In Saccharomyces cerevisiae, the selective autophagic degradation of mitochondria, termed mitophagy, is critically regulated by the adapter protein Atg32. link3 Despite our knowledge about the molecular mechanisms by which Atg32 controls mitophagy, its physiological roles in yeast survival and fitness remains less clear. Here, we demonstrate a requirement for Atg32 in promoting spermidine production during respiratory growth and heat-induced mitochondrial stress. During respiratory growth, mitophagy-deficient yeast exhibit profound heat-stress induced defects in growth and viability due to impaired biosynthesis of spermidine and its biosynthetic precursor S-adenosyl methionine. Moreover, spermidine production is crucial for the induction of cytoprotective nitric oxide (NO) during heat stress. Hence, the re-addition of spermidine to Atg32 mutant yeast is sufficient to both enhance NO production and restore respiratory growth during heat stress. Our findings uncover a previously unrecognized physiological role for yeast mitophagy in spermidine metabolism and illuminate new interconnections between mitophagy, polyamine biosynthesis and NO signaling.Upon exposure to amyloid-β oligomers (Aβ1-42), glial cells start expressing proinflammatory cytokines, despite an increase in levels of repressive microRNAs (miRNAs). Exploring the mechanism of this potential immunity of target cytokine mRNAs against repressive miRNAs in amyloid-β-exposed glial cells, we have identified differential compartmentalization of repressive miRNAs in glial cells that explains this aberrant miRNA function. In Aβ1-42-treated cells, whereas target mRNAs were found to be associated with polysomes attached to endoplasmic reticulum (ER), the miRNA ribonucleoprotein complexes (miRNPs) were found to be present predominantly with endosomes that failed to recycle to ER-attached polysomes, preventing repression of mRNA targets. Aβ1-42 oligomers, by masking Rab7a proteins on endosomal surfaces, affected Rab7a interaction with Rab-interacting lysosomal protein (RILP), restricting the lysosomal targeting and recycling of miRNPs. RNA-processing body (P-body) localization of the miRNPs was found to be enhanced in amyloid-β-treated cells as a consequence of enhanced endosomal retention of miRNPs. Interestingly, depletion of P-body components partly rescued the miRNA function in glial cells exposed to amyloid-β and restricted the excess cytokine expression. This article has an associated First Person interview with the first author of the paper.The TREX-TAP pathway is vital for mRNA export. For spliced mRNA, the TREX complex is recruited during splicing; however, for intronless mRNA, recruitment is sequence dependent. However, the export of cytoplasmic long noncoding RNA (lncRNA) is poorly characterized. We report the identification of a cytoplasmic accumulation region (CAR-N) in the intronless lncRNA, NKILA. CAR-N removal led to strong nuclear retention of NKILA, and CAR-N insertion promoted the export of cDNA transcripts. In vitro RNP purification via CAR-N, mass spectrometry, and siRNA screening revealed that SRSF1 and SRSF7 were vital to NKILA export, and identified a cluster of SRSF1/7 binding sites within a 55 nucleotide sequence in CAR-N. Significant nuclear enrichment of NKILA was observed for NKILA lacking CAR-N or the cluster of binding sites in knock-in models. Depletion of TREX-TAP pathway components resulted in strong nuclear retention of NKILA. RNA and protein immunoprecipitation verified that SRSF1/7 were bound to NKILA and interacted with UAP56 and ALYREF.