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Depression is common among doctors. However, concerns remain that doctors are unlikely to ask for help when symptoms of depression arise.

To determine rates and patterns of help-seeking for depression amongst doctors and to identify predictors of and barriers to such behaviour.

A secondary analysis was conducted on a nationwide survey of 12 252 Australian doctors. The study sample consisted of doctors who reported having ever felt seriously depressed (N=4154; 33.9% of total sample). Rates of help-seeking, professional help-seeking behaviours and self-reported barriers were explored. Logistic regression was used to examine the association between professional help-seeking and predetermined predictive factors.

60% (95% Confidence Interval (CI)58.5%-61.5%) of doctors who have ever felt seriously depressed reported some form of professional help-seeking for depression. The most common barrier to help-seeking was 'privacy/confidentiality'. Females (Odds Ratio(OR) = 1.74; 95%CI1.50-2.01; p < 0.001), locaity of depressed doctors were able to seek professional help, many were not. Major barriers to professional help-seeking, particularly concerns about confidentiality and impact on career, remain a problem. Male, overseas-trained, junior doctors, surgeons and pathologists/radiologists were less likely to seek help for depression. Targeted interventions are required to increase appropriate help-seeking for depression in doctors. This article is protected by copyright. All rights reserved.Determining the abundance of leukocyte subtypes, including lymphocyte subpopulations, not only in blood but also in lymphatic tissues, is inevitable to assess the immune status of an organism for research purposes. However, nucleated thrombocytes and erythrocytes exacerbate many hematological techniques in avian species. In order to enable a rapid discrimination of leukocyte subsets from lymphatic tissues of chicken, we adapted existing flow cytometric methods for counting leukocytes in chicken blood. We established staining and gating strategies allowing the flow cytometric characterization and enumeration of total leukocytes, thrombocytes, monocytes/macrophages, CD8α+ lymphocytes, CD4+ T cells, γδ T cells, and B cells in chicken spleen and CD8α+ lymphocytes, CD4+ T cells, γδ T cells, and B cells among intraepithelial lymphocytes in chicken cecal tonsils. For this, we prepared single-cell suspensions of spleen and isolated intraepithelial lymphocytes from cecal tonsils without density centrifugation, and performed antibody staining of cells without subsequent washing steps to prevent cell loss and falsification of obtained cell counts. © 2020 The Authors. Cytometry Part A published by Wiley Periodicals LLC on behalf of International Society for Advancement of Cytometry.Venetoclax and hypomethylating agent (HMA) combination therapy is FDA-approved for elderly or unfit acute myeloid leukemia (AML) patients unable to withstand intensive chemotherapy. The primary objective of the current study was to impart our institutional experience with the above regimen, outlining response, survival outcomes, and its determinants amongst 86 treatment- naïve and relapsed/refractory AML patients. A total of 44 treatment-naïve AML patients, median age 73.5 years, enriched with secondary, therapy related and ELN adverse risk disease (n = 27) were studied. The CR/CRi rates of 50% (22 of 44 patients) were superior to 23% in a matched AML cohort treated with HMA alone (P = .005). Response rates were similar with TP53, FLT3, NPM1 and IDH mutations (P = .31). Moreover, CEPBA mutations (P = .03) and neutropenia (P = .05) emerged as predictors of complete response. Survivalwas prolonged in patients achieving CR/CRi (17 vs 3 months without CR/CRi, P  65 years, AML with myelodysplasia, JAK2, DNMT3A, and BCOR mutations predicted complete response. Survival distinctions were based on CR/CRi (median survival 15 vs 3 months with/without CR/CRi; P  less then  .001), and TP53 mutation status (P = .04). In summary, we corroborate existing reports demonstrating superior response and prolonged survival with venetoclax and HMA in treatment -naïve and relapsed/refractory AML patients regardless of genotype. Additionally, we identify unique predictors of response to therapy which require validation.

To optimize the therapeutic strategy for cirrhotic patients manifesting hepatic encephalopathy, factors affecting the outcome of patients receiving rifaximin were evaluated.

The subjects were 95 patients receiving rifaximin. Serum ammonia levels were measured serially during rifaximin treatment. Factors associated with long-term outcomes and cumulative survival rates were evaluated.

Serum ammonia levels were decreased at 4weeks after rifaximin treatment compared to the levels at baseline even in patients receiving rifaximin as an add-on therapy with lactitol hydrate (P < 0.001) and reduction values were negatively correlated with the maximal diameter of portosystemic shunts (r = -0.275, P = 0.009). Overt encephalopathy occurred in 37 patients (38.9%) during rifaximin treatment, and the hazard function analysis identified 90days as a high-risk term for developing the first-time overt encephalopathy. selleck Thus, the long-term outcome was judged as favorable in 77 patients (81.1%) in whom overt encephalopathy was absent for at least 90days during rifaximin initiation. A multivariate analysis revealed that furosemide, especially at daily doses of ≥20mg both at baseline and during rifaximin treatment, was a significant factor associated with unfavorable outcome (P= 0.009 and P= 0.022, respectively) as well as occurrence and recurrence of overt encephalopathy (P= 0.012). Moreover, furosemide treatment significantly deteriorated the cumulative survival rate of patients receiving rifaximin (P= 0.026).

Furosemide contributed to the deteriorated outcome of patients receiving rifaximin. Consequently, rifaximin should be given before increasing the furosemide dose, and the furosemide dose should not be increased during rifaximin treatment.

Furosemide contributed to the deteriorated outcome of patients receiving rifaximin. Consequently, rifaximin should be given before increasing the furosemide dose, and the furosemide dose should not be increased during rifaximin treatment.