A co-created multimethod evaluation of recovery education in Ireland.

Background: This paper aims to explore the impact of recovery education on recovery knowledge, attitudes and the quality of life of students undertaking recovery education, contributing to the evidence base in relation to the impact of recovery education. It also explores the experiences of all stakeholders involved in the co-facilitation, delivery and participation in recovery education.

Setting And Participants: This study evaluates the experiences of stakeholders involved in the co-facilitation, delivery and participation in recovery education across four recovery colleges in Ireland.

Congenital Unilateral Renal Aplasia in a Cynomolgus Monkey () With Investigation Into Potential Pathogenesis.

We describe and characterize unilateral renal aplasia in a cynomolgus monkey () from a chronic toxicology study adding to the limited histopathology reports of congenital renal anomalies in macaques. In the current case, the affected kidney was macroscopically small and characterized microscopically by a thin cortex with an underdeveloped medulla and an absent papilla. The remnant medulla lacked a corticomedullary junction and contained only a few irregular collecting duct-like structures.

Metastasis is regulated via microRNA-200/ZEB1 axis control of tumour cell PD-L1 expression and intratumoral immunosuppression.

Immunosuppression of tumour-infiltrating lymphocytes (TIL) is a common feature of advanced cancer, but its biological basis has remained obscure. We demonstrate here a molecular link between epithelial-to-mesenchymal transition (EMT) and CD8(+) TIL immunosuppression, two key drivers of cancer progression. We show that microRNA-200 (miR-200), a cell-autonomous suppressor of EMT and metastasis, targets PD-L1.

BRAF inhibitors suppress apoptosis through off-target inhibition of JNK signaling.

Vemurafenib and dabrafenib selectively inhibit the v-Raf murine sarcoma viral oncogene homolog B1 (BRAF) kinase, resulting in high response rates and increased survival in melanoma. Approximately 22% of individuals treated with vemurafenib develop cutaneous squamous cell carcinoma (cSCC) during therapy. The prevailing explanation for this is drug-induced paradoxical ERK activation, resulting in hyperproliferation.

Sorafenib suppresses JNK-dependent apoptosis through inhibition of ZAK.

Sorafenib is U.S. Food and Drug Adminstration-approved for the treatment of renal cell carcinoma and hepatocellular carcinoma and has been combined with numerous other targeted therapies and chemotherapies in the treatment of many cancers.

Synergistic effect of IL-6 and IL-4 in driving fate revision of natural Foxp3+ regulatory T cells.

Expression of forkhead transcription factor Foxp3 defines a distinct lineage of naturally arising regulatory T cells (nTregs) that is segregated from effector CD4(+) T cells during early development in the thymus. It remains elusive whether nTregs can convert into effector cells by turning off their Foxp3 expression and, if so, whether Th17 is a default alternative fate choice. In this report we provide compelling evidence showing that effector T cell-polarizing cytokines IL-6 and IL-4 can act synergistically to induce marked downregulation and inactivation of Foxp3 gene expression in mouse nTregs, and consequently the loss of suppressor phenotype and functions.

The immune system provides a strong response to even a low exposure to virus.

How influenza virus dose affects the size of the immune response has not been clearly documented. Mice were challenged with three doses of influenza virus spanning a 100-fold range. Increasing the viral input dose increased the degree of weight loss observed, the clinical score and eventual mortality.

Cutting edge: regulation of CD8+ T cell effector population size.

Naive CD8(+) T cells are activated on encounter with Ag presented on dendritic cells and proliferate rapidly. To investigate the regulation of naive CD8(+) T cells proliferation, we adoptively transferred TCR-transgenic CD8(+) T cells into intact mice together with Ag-pulsed dendritic cells. Regardless of the number of cells initially transferred, the expansion of activated Ag-specific CD8(+) T cells was limited to a ceiling of effector cells.

C-terminal deletions of the Escherichia coli RecA protein. Characterization of in vivo and in vitro effects.

A set of C-terminal deletion mutants of the RecA protein of Escherichia coli, progressively removing 6, 13, 17, and 25 amino acid residues, has been generated, expressed, and purified. In vivo, the deletion of 13 to 17 C-terminal residues results in increased sensitivity to mitomycin C. In vitro, the deletions enhance binding to duplex DNA as previously observed.

RecA Protein from the extremely radioresistant bacterium Deinococcus radiodurans: expression, purification, and characterization.

The RecA protein of Deinococcus radiodurans (RecA(Dr)) is essential for the extreme radiation resistance of this organism. The RecA(Dr) protein has been cloned and expressed in Escherichia coli and purified from this host. In some respects, the RecA(Dr) protein and the E.