A heart failure self-management program for patients of all literacy levels: A randomized, controlled trial [ISRCTN11535170]

BACKGROUND: Self-management programs for patients with heart failure can reduce hospitalizations and mortality. However, no programs have analyzed their usefulness for patients with low literacy. We compared the efficacy of a heart failure self-management program designed for patients with low literacy versus usual care. METHODS: We performed a 12-month randomized controlled trial. From November 2001 to April 2003, we enrolled participants aged 30–80, who had heart failure and took furosemide. Intervention patients received education on self-care emphasizing daily weight measurement, diuretic dose self-adjustment, and symptom recognition and response. Picture-based educational materials, a digital scale, and scheduled telephone follow-up were provided to reinforce adherence. Control patients received a generic heart failure brochure and usual care. Primary outcomes were combined hospitalization or death, and heart failure-related quality of life. RESULTS: 123 patients (64 control, 59 intervention) participated; 41% had inadequate literacy. Patients in the intervention group had a lower rate of hospitalization or death (crude incidence rate ratio (IRR) = 0.69; CI 0.4, 1.2; adjusted IRR = 0.53; CI 0.32, 0.89). This difference was larger for patients with low literacy (IRR = 0.39; CI 0.16, 0.91) than for higher literacy (IRR = 0.56; CI 0.3, 1.04), but the interaction was not statistically significant. At 12 months, more patients in the intervention group reported monitoring weights daily (79% vs. 29%, p < 0.0001). After adjusting for baseline demographic and treatment differences, we found no difference in heart failure-related quality of life at 12 months (difference = -2; CI -5, +9). CONCLUSION: A primary care-based heart failure self-management program designed for patients with low literacy reduces the risk of hospitalizations or death

p21 produces a bioactive secretome that places stressed cells under immunosurveillance

Immune cells identify and destroy damaged cells to prevent them from causing cancer or other pathologies by mechanisms that remain poorly understood. Here, we report that the cell-cycle inhibitor p21 places cells under immunosurveillance to establish a biological timer mechanism that controls cell fate. p21 activates retinoblastoma protein (Rb)-dependent transcription at select gene promoters to generate a complex bioactive secretome, termed p21-activated secretory phenotype (PASP). The PASP includes the chemokine CXCL14, which promptly attracts macrophages. These macrophages disengage if cells normalize p21 within 4 days, but if p21 induction persists, they polarize toward an M1 phenotype and lymphocytes mount a cytotoxic T cell response to eliminate target cells, including preneoplastic cells. Thus, p21 concurrently induces proliferative arrest and immunosurveillance of cells under duress

Transfer learning in a biomaterial fibrosis model identifies in vivo senescence heterogeneity and contributions to vascularization and matrix production across species and diverse pathologies

Cellular senescence is a state of permanent growth arrest that plays an important role in wound healing, tissue fibrosis, and tumor suppression. Despite senescent cells’ (SnCs) pathological role and therapeutic interest, their phenotype in vivo remains poorly defined. Here, we developed an in vivo–derived senescence signature (SenSig) using a foreign body response–driven fibrosis model in a p16-CreERT2;Ai14 reporter mouse. We identified pericytes and “cartilage-like” fibroblasts as senescent and defined cell type–specific senescence-associated secretory phenotypes (SASPs). Transfer learning and senescence scoring identified these two SnC populations along with endothelial and epithelial SnCs in new and publicly available murine and human data single-cell RNA sequencing (scRNAseq) datasets from diverse pathologies. Signaling analysis uncovered crosstalk between SnCs and myeloid cells via an IL34–CSF1R–TGFβR signaling axis, contributing to tissue balance of vascularization and matrix production. Overall, our study provides a senescence signature and a computational approach that may be broadly applied to identify SnC transcriptional profiles and SASP factors in wound healing, aging, and other pathologies.</p

Transfer learning in a biomaterial fibrosis model identifies in vivo senescence heterogeneity and contributions to vascularization and matrix production across species and diverse pathologies

Cellular senescence is a state of permanent growth arrest that plays an important role in wound healing, tissue fibrosis, and tumor suppression. Despite senescent cells’ (SnCs) pathological role and therapeutic interest, their phenotype in vivo remains poorly defined. Here, we developed an in vivo–derived senescence signature (SenSig) using a foreign body response–driven fibrosis model in a p16-CreERT2;Ai14 reporter mouse. We identified pericytes and “cartilage-like” fibroblasts as senescent and defined cell type–specific senescence-associated secretory phenotypes (SASPs). Transfer learning and senescence scoring identified these two SnC populations along with endothelial and epithelial SnCs in new and publicly available murine and human data single-cell RNA sequencing (scRNAseq) datasets from diverse pathologies. Signaling analysis uncovered crosstalk between SnCs and myeloid cells via an IL34–CSF1R–TGFβR signaling axis, contributing to tissue balance of vascularization and matrix production. Overall, our study provides a senescence signature and a computational approach that may be broadly applied to identify SnC transcriptional profiles and SASP factors in wound healing, aging, and other pathologies.</p

Transfer learning in a biomaterial fibrosis model identifies in vivo senescence heterogeneity and contributions to vascularization and matrix production across species and diverse pathologies

Cellular senescence is a state of permanent growth arrest that plays an important role in wound healing, tissue fibrosis, and tumor suppression. Despite senescent cells’ (SnCs) pathological role and therapeutic interest, their phenotype in vivo remains poorly defined. Here, we developed an in vivo–derived senescence signature (SenSig) using a foreign body response–driven fibrosis model in a p16-CreERT2;Ai14 reporter mouse. We identified pericytes and “cartilage-like” fibroblasts as senescent and defined cell type–specific senescence-associated secretory phenotypes (SASPs). Transfer learning and senescence scoring identified these two SnC populations along with endothelial and epithelial SnCs in new and publicly available murine and human data single-cell RNA sequencing (scRNAseq) datasets from diverse pathologies. Signaling analysis uncovered crosstalk between SnCs and myeloid cells via an IL34–CSF1R–TGFβR signaling axis, contributing to tissue balance of vascularization and matrix production. Overall, our study provides a senescence signature and a computational approach that may be broadly applied to identify SnC transcriptional profiles and SASP factors in wound healing, aging, and other pathologies.</p

Transfer learning in a biomaterial fibrosis model identifies in vivo senescence heterogeneity and contributions to vascularization and matrix production across species and diverse pathologies

Cellular senescence is a state of permanent growth arrest that plays an important role in wound healing, tissue fibrosis, and tumor suppression. Despite senescent cells’ (SnCs) pathological role and therapeutic interest, their phenotype in vivo remains poorly defined. Here, we developed an in vivo–derived senescence signature (SenSig) using a foreign body response–driven fibrosis model in a p16-CreERT2;Ai14 reporter mouse. We identified pericytes and “cartilage-like” fibroblasts as senescent and defined cell type–specific senescence-associated secretory phenotypes (SASPs). Transfer learning and senescence scoring identified these two SnC populations along with endothelial and epithelial SnCs in new and publicly available murine and human data single-cell RNA sequencing (scRNAseq) datasets from diverse pathologies. Signaling analysis uncovered crosstalk between SnCs and myeloid cells via an IL34–CSF1R–TGFβR signaling axis, contributing to tissue balance of vascularization and matrix production. Overall, our study provides a senescence signature and a computational approach that may be broadly applied to identify SnC transcriptional profiles and SASP factors in wound healing, aging, and other pathologies.</p

Dissolved organic carbon transformations and microbial community response to variations in recharge waters in a shallow carbonate aquifer

© 2016, The Author(s). In carbonate aquifers, dissolved organic carbon from the surface drives heterotrophic metabolism, generating CO2 in the subsurface. Although this has been a proposed mechanism for enhanced dissolution at the water table, respiration rates and their controlling factors have not been widely evaluated. This study investigates the composition and concentration of dissolved organic carbon (DOC) reaching the water table from different recharge pathways on a subtropical carbonate island using a combination of DOC concentration measurements, fluorescence and absorption characterisation. In addition, direct measurements of the microbial response to the differing water types were made. Interactions of rainfall with the vegetation, via throughfall and stemflow, increase the concentration of DOC. The highest DOC concentrations are associated with stemflow, overland recharge and dissolution hole waters which interact with bark lignin and exhibit strong terrestrial-derived characteristics. The groundwater samples exhibit the lowest concentrations of DOC and are comprised of refractory humic-like organic matter. The heterotrophic response seems to be controlled by the concentration of DOC in the sample. The terrestrially sourced humic-like matter in the stemflow and dissolution hole samples was highly labile, thus increasing the amount of biologically produced CO2 to drive dissolution. Based on the calculated respiration rates, microbial activity could enhance carbonate dissolution, increasing porosity generation by a maximum of 1%kyr−1 at the top of the freshwater lens

Economic and Environmental Impacts of Harmful Non-Indigenous Species in Southeast Asia

10.1371/journal.pone.0071255PLoS ONE88-POLN

Relationship Between Literacy, Knowledge, Self-Care Behaviors, and Heart Failure-Related Quality of Life Among Patients With Heart Failure

ABSTRACTBACKGROUNDWe sought to examine the relationship between literacy and heart failure-related quality of life (HFQOL), and to explore whether literacy-related differences in knowledge, self-efficacy and/or self-care behavior explained the relationship.METHODSWe recruited patients with symptomatic heart failure (HF) from four academic medical centers. Patients completed the short version of the Test of Functional Health Literacy in Adults (TOFHLA) and questions on HF-related knowledge, HF-related self-efficacy, and self-care behaviors. We assessed HFQOL with the Heart Failure Symptom Scale (HFSS) (range 0–100), with higher scores denoting better quality of life. We used bivariate (t-tests and chi-square) and multivariate linear regression analyses to estimate the associations between literacy and HF knowledge, self-efficacy, self-care behaviors, and HFQOL, controlling for demographic characteristics. Structural equation modeling was conducted to assess whether general HF knowledge, salt knowledge, self-care behaviors, and self-efficacy mediated the relationship between literacy and HFQOL.RESULTSWe enrolled 605 patients with mean age of 60.7years; 52% were male; 38% were African-American and 16% Latino; 26% had less than a high school education; and 67% had annual incomes under $25,000. Overall, 37% had low literacy (marginal or inadequate on TOFHLA). Patients with adequate literacy had higher general HF knowledge than those with low literacy (mean 6.6 vs. 5.5, adjusted difference 0.63, p < 0.01), higher self-efficacy (5.0 vs. 4.1 ,adjusted difference 0.99, p < 0.01), and higher prevalence of key self-care behaviors (p < 0.001). Those with adequate literacy had better HFQOL scores compared to those with low literacy (63.9 vs. 55.4, adjusted difference 7.20, p < 0.01), but differences in knowledge, self-efficacy, and self-care did not mediate this difference in HFQOL.CONCLUSIONLow literacy was associated with worse HFQOL and lower HF-related knowledge, self-efficacy, and self-care behaviors, but differences in knowledge, self-efficacy and self-care did not explain the relationship between low literacy and worse HFQOL

A Plan for Community Event-Based Surveillance to Reduce Ebola Transmission - Sierra Leone, 2014–2015.

Ebola virus disease (Ebola) was first detected in Sierra Leone in May 2014 and was likely introduced into the eastern part of the country from Guinea. The disease spread westward, eventually affecting Freetown, Sierra Leone's densely populated capital. By December 2014, Sierra Leone had more Ebola cases than Guinea and Liberia, the other two West African countries that have experienced widespread transmission. As the epidemic intensified through the summer and fall, an increasing number of infected persons were not being detected by the county's surveillance system until they had died. Instead of being found early in the disease course and quickly isolated, these persons remained in their communities throughout their illness, likely spreading the disease