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Lane Shelton posted an update 6 months, 4 weeks ago
Earthworms are ecological engineers that can contribute to the displacement of biological control agents such as the entomopathogenic nematodes (EPNs) and fungi (EPF). However, a previous study showed that the presence of cutaneous excreta (CEx) and feeding behavior of the earthworm species Eisenia fetida (Haplotaxida Lumbricidae) compromise the biocontrol efficacy of certain EPN species by reducing, for example, their reproductive capability. KD025 Whether this phenomenon is a general pattern for the interaction of earthworms-entomopathogens is still unknown. We hypothesized that diverse earthworm species might differentially affect EPN and EPF infectivity and reproductive capability. Here we investigated the interaction of different earthworm species (Eisenia fetida, Lumbricus terrestris, and Perionyx excavatus) (Haplotaxida) and EPN species (Steinernema feltiae, S. riojaense, and Heterorhabditis bacteriophora) (Rhabditida) or EPF species (Beauveria bassiana and Metarhizium anisopliae) (Hypocreales), in two indepamong species. Thus, E. fetida was detrimental to M. anisopliae and B. bassiana after eight days post-exposure, whereas Lumbricus terrestris resulted only detrimental to B. bassiana. In addition, most of the CEx treatments of both earthworm species decreased B. bassiana virulence and growth. However, the EPF M. anisopliae was unaffected when exposed to L. terrestris CEx, while the exposure to E. fetida CEx produced contrasting results. We conclude that earthworms and their CEx can have positive, deleterious, or neutral impacts on entomopathogens that often coinhabit soils, and that we must consider the species specificity of these interactions for mutual uses in biological control programs. Additional studies are needed to verify these interactions under natural conditions.
To investigate residential mobility among community-living adults with spinal cord injury (SCI) and the individual, health, and neighborhood factors associated with the propensity to relocate.
Retrospective analysis of data from the National SCI Model Systems (SCIMS) Database collected between 2006 and 2018 and linked with the American Community Survey 5-year estimates.
Community.
Not applicable.
People with traumatic SCI (N=4599) who participated in 2 waves of follow-up and had residential geographic identifiers at the census tract level.
Moving was a binary measure reflecting change in residential locations over a 5-year interval. Move distance distinguished nonmovers from local movers (different tracts within the same county) and long-distance movers (to different county or state). Move quality included 4 categories stayed/low poverty tract, stayed/high poverty tract, moved/low poverty tract, and moved/high poverty tract.
One in 4 people moved within a 5-year interval (n=1175). Of the movers,s for individuals with SCI and other chronic disabilities.
Although people with SCI relocated at a lower rate than has been reported in the general population, moving was a frequent occurrence postinjury. People from vulnerable groups were more likely to remain in or relocate to socioeconomically disadvantaged neighborhoods, thus increasing the risk for health disparities and poorer long-term outcomes among minorities and people from low-income households. These findings inform policy makers’ considerations of housing, health care, and employment initiatives for individuals with SCI and other chronic disabilities.Emerging evidence suggests a key contribution to non-alcoholic fatty liver disease (NAFLD) pathogenesis by Th17 cells. The pathogenic characteristics and mechanisms of hepatic Th17 cells, however, remain unknown. Here, we uncover and characterize a distinct population of inflammatory hepatic CXCR3+Th17 (ihTh17) cells sufficient to exacerbate NAFLD pathogenesis. Hepatic ihTh17 cell accrual was dependent on the liver microenvironment and CXCR3 axis activation. Mechanistically, the pathogenic potential of ihTh17 cells correlated with increased chromatin accessibility, glycolytic output, and concomitant production of IL-17A, IFNγ, and TNFα. Modulation of glycolysis using 2-DG or cell-specific PKM2 deletion was sufficient to reverse ihTh17-centric inflammatory vigor and NAFLD severity. Importantly, ihTh17 cell characteristics, CXCR3 axis activation, and hepatic expression of glycolytic genes were conserved in human NAFLD. Together, our data show that the steatotic liver microenvironment regulates Th17 cell accrual, metabolism, and competence toward an ihTh17 fate. Modulation of these pathways holds potential for development of novel therapeutic strategies for NAFLD.
Insulin resistance is a key factor in the pathogenesis of nonalcoholic fatty liver disease (NAFLD). We evaluated the importance of subcutaneous abdominal adipose tissue (SAAT) inflammation and both plasma and SAAT-derived exosomes in regulating insulin sensitivity in people with obesity and NAFLD.
Adipose tissue inflammation (macrophage and T-cell content and expression of proinflammatory cytokines), liver and whole-body insulin sensitivity (assessed using a hyperinsulinemic-euglycemic clamp and glucose tracer infusion), and 24-hour serial plasma cytokine concentrations were evaluated in 3 groups stratified by adiposity and intrahepatic triglyceride (IHTG) content (1) lean with normal IHTG content (LEAN; n= 14); (2) obese with normal IHTG content (OB-NL; n= 28); and (3) obese with NAFLD (OB-NAFLD; n= 28). The effect of plasma and SAAT-derived exosomes on insulin-stimulated Akt phosphorylation in human skeletal muscle myotubes and mouse primary hepatocytes was assessed in a subset of participants.
Proinf1 concentrations and both plasma and SAAT-derived exosomes. ClinicalTrials.gov number NCT02706262.Rank signaling enhances stemness in mouse and human mammary epithelial cells (MECs) and mediates mammary tumor initiation. Mammary tumors initiated by oncogenes or carcinogen exposure display high levels of Rank and Rank pathway inhibitors have emerged as a new strategy for breast cancer prevention and treatment. Here, we show that ectopic Rank expression in the mammary epithelia unexpectedly delays tumor onset and reduces tumor incidence in the oncogene-driven Neu and PyMT models. Mechanistically, we have found that ectopic expression of Rank or exposure to Rankl induces senescence, even in the absence of other oncogenic mutations. Rank leads to DNA damage and senescence through p16/p19. Moreover, RANK-induced senescence is essential for Rank-driven stemness, and although initially translates into delayed tumor growth, eventually promotes tumor progression and metastasis. We uncover a dual role for Rank in the mammary epithelia Rank induces senescence and stemness, delaying tumor initiation but increasing tumor aggressiveness.
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