223 research outputs found
The educational ideas of Mahatma Gandhi
An analysis of Gandhi’s ideology and educational aims and processes, emphasising the role of the mother. The central feature of education as envisaged by Gandhi is that it should be through a productive craft
Gene Dosage-Dependent Negative Regulatory Role of β-Arrestin-2 in Polymicrobial Infection-Induced Inflammation
ABSTRACT
β-arrestin-2 (β-arr2) is a scaffolding protein of the arrestin family with a wide variety of cellular functions. Recent studies have demonstrated differential roles for β-arr2 in inflammation following endotoxemia and cecal ligation and puncture (CLP) models of sepsis. Because CLP-induced inflammation involves response to fecal contents and necrotic cecum in addition to microbial challenge, in this study, we examined the role of β-arr2 in an exclusively polymicrobial infection (PMI) model. In addition, we examined the role of gene dosage of β-arr2 in polymicrobial sepsis. Our studies demonstrate that β-arr2 is a negative regulator of systemic inflammation in response to polymicrobial infection and that one allele is sufficient for this process. Our results further reveal that loss of β-arr2 leads to increased neutrophil sequestration and overt inflammation specifically in the lungs following polymicrobial infection. Consistent with this, specific NF-κB and mitogen-activated protein kinase (MAPK) signaling pathways were differentially activated in the β-arr2 knockout (KO) mice lungs compared to the wild type (WT) following PMI. Associated with enhanced inflammation in the KO mice, PMI-induced mortality was also significantly higher in KO mice than in WT mice. To understand the differential role of β-arr2 in different sepsis models, we used cell culture systems to evaluate inflammatory cytokine production following endotoxin and polymicrobial stimulation. Our results demonstrate cell-type- as well as stimulus-specific roles for β-arr2 in inflammation. Taken together, our results reveal a negative regulatory role for β-arr2 in polymicrobial infection-induced inflammation and further demonstrate that one allele of β-arr2 is sufficient to mediate most of these effects.</jats:p
Cytokine and hormonal regulation of bone marrow immune cell Wnt10b expression
This study is funded by National Center for Complementary and Integrative Health (https://nccih.nih.gov/), U.S National Institutes of Health (Grant Code: 1R01AT007695-01) awarded to LRM and NP and by National Institute of Diabetes and Digestive and Kidney Diseases (www.niddk.nih.gov/), U.S National Institutes of Health (Grant code: R01DK101050) awarded to LRM and NP. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.Peer reviewedPublisher PD
Lactobacillus reuteri 6475 increases bone density in intact females only under an inflammatory setting
Peer reviewedPublisher PD
Microbiota Reconstitution Does Not Cause Bone Loss in Germ-Free Mice
We thank Jenny Auchtung, James Collins, and Laura Schaefer for technical support. James Collins, and Laura Schaefer provided expertise in tissue collection for the animal experiments, and Jenny Auchtung provided expertise in bioinformatics and microbial community analysis. This work was supported by NIH grant NCCIH R01AT007695-05 to N.P., L.M., and R.A.B., as well as seed funding from Baylor College of Medicine to R.A.B. The authors report that they have no competing interests.Peer reviewedPublisher PD
Temporal and regional intestinal changes in permeability, tight junction, and cytokine gene expression following ovariectomy-induced estrogen deficiency
The work presented within this study was funded in part by NCCIH (R01AT007695) and NIDDK (R01DK101050Peer reviewedPublisher PD
A randomized, open-label, multicentre, phase 2/3 study to evaluate the safety and efficacy of lumiliximab in combination with fludarabine, cyclophosphamide and rituximab versus fludarabine, cyclophosphamide and rituximab alone in subjects with relapsed chronic lymphocytic leukaemia
Can Airway Abnormalities be the Elephant in the Room in Children with Congenital Heart Disease?
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