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Current therapies for chronic hepatitis B (CHB) include nucleos(t)ide analogues (NAs) and interferon (IFN), but their relative efficacy as monotherapy or in combination has not been examined systematically for HBsAg loss (functional cure). Hence, we systematically reviewed the evidence for HBsAg loss in CHB patients treated with IFN, NA or the combination. We searched PubMed, EMBASE and abstracts from EASL, Asia Pacific Association for study of the Liver and American Association for the Study of Liver Disease for randomized controlled trials of CHB patients, comparing NA, IFN or the combination. The Cochrane Risk of Bias tool v2.0 and GRADE method were used. Analyses were stratified by NA genetic barrier, cirrhosis, type of combination therapy, HBeAg, treatment naivety, IFN dosage/duration and outcome duration. Sensitivity analysis was performed for selected strata, and HBsAg loss was measured at the end-of-study (EOS), end-of-treatment (EOT) or end-of-follow-up (EOF). Effects were reported as risk differences (RD) with 95% confidence intervals (CI) using a random-effects model. Forty-five studies were included, all with low risk of bias. For HBsAg loss at EOS, when comparing combination vs IFN, RD&nbsp;=&nbsp;1%, 95%CI-1%, 2%; combination vs NA, RD&nbsp;=&nbsp;5%, 95%CI 3%,7%; IFN vs NA, RD&nbsp;=&nbsp;3%, 95%CI 2%,5%. Subgroup analysis showed a significant effect of standard IFN dose vs nonstandard; IFN duration ≥48&nbsp;weeks vs 2&nbsp;years of follow-up. Similar findings were seen in HBsAg seroconversion, but only three studies reported HBsAg seroreversion. In conclusion, IFN monotherapy/combination had a small but significant increase in HBsAg loss over NA, associated with standard dose of IFN and ≥48&nbsp;weeks of therapy, although this effect faded over time. © 2020 John Wiley &amp; Sons Ltd.Always on the lookout for articles from the European Journal of Neurology, one in particular has attracted a lot of attention because the results are really fascinating. Although replication is needed, Alves and colleagues addressed a priority issue in clinical research demonstrating that Parkinson's disease (PD) was associated with an increased risk of stroke but the risk of myocardial infarction (MI) and cardiovascular mortality was not significantly increased However, a very important issue and still neglected by neuroscientists are the aspects related to sudden death in PD (SUDPAR). SUDPAR is defined as unexpected death of a PD patient without an evident cause on autopsy. This article is protected by copyright. All rights reserved.Oral squamous cell carcinoma is associated with many known risk factors including tobacco smoking, chronic alcoholism, poor oral hygiene, unhealthy dietary habits and microbial infection. Previous studies have highlighted Candida albicans host tissue infection as a risk factor in the initiation and progression of oral cancer. C. albicans invasion induces several cancerous hallmarks, such as activation of proto-oncogenes, induction of DNA damage and overexpression of inflammatory signalling pathways. However, the molecular mechanisms behind these responses remain unclear. A recently discovered fungal toxin peptide, candidalysin has been reported as an essential molecule in epithelial damage and host recognition of C. albicans infection. [https://www.selleckchem.com/products/iberdomide.html CC220] Candidalysin has a clear role in inflammasome activation and induction of cell damage. Several inflammatory molecules such as IL-6, IL-17, NLRP3 and GM-CSF have been linked to carcinogenesis. Candidalysin is encoded by the ECE1 gene, which has been linked to virulence factors of C. albicans such as adhesion, biofilm formation and filamentation properties. This review discusses the recent epidemiological burden of oral cancer and highlights the significance of the ECE1 gene and the ECE1 protein breakdown product, candidalysin in oral malignancy. The immunological and molecular mechanisms behind oral malignancy induced by inflammation and the role of the toxic fungal peptide candidalysin in oral carcinogenesis are explored. With increasing evidence associating C. albicans with oral carcinoma, identifying the possible fungal pathogenicity factors including the role of candidalysin can assist in efforts to understand the link between C. albicans infection and carcinogenesis, and pave the way for research into therapeutic potentials. This article is protected by copyright. All rights reserved.The karyotype of bone-marrow cells at the time of diagnosis is one of the most important prognostic factors in patients with myelodysplastic syndromes (MDS). In some cases, the acquisition of additional genetic aberrations (clonal evolution [CE]) associated with clinical progression may occur during the disease. We analyzed a cohort of 469 MDS patients using a combination of molecular cytogenomic methods to identify cryptic aberrations and to assess their potential role in CE. We confirmed CE in 36 (8%) patients. The analysis of bone-marrow samples with a combination of cytogenomic methods at diagnosis and after CE identified 214 chromosomal aberrations. The early genetic changes in the diagnostic samples were frequently MDS specific (17 MDS-specific/57 early changes). Most progression-related aberrations identified after CE were not MDS specific (131 non-MDS-specific/155 progression-related changes). Copy number neutral loss of heterozygosity (CN-LOH) was detected in 19% of patients. MDS-specific CN-LOH (4q, 17p) was identified in three patients, and probably pathogenic homozygous mutations were found in TET2 (4q24) and TP53 (17p13.1) genes. We observed a statistically significant difference in overall survival (OS) between the groups of patients divided according to their diagnostic cytogenomic findings, with worse OS in the group with complex karyotypes (P = .021). A combination of cytogenomic methods allowed us to detect many cryptic genomic changes and identify genes and genomic regions that may represent therapeutic targets in patients with progressive MDS. © 2020 Wiley Periodicals, Inc.BACKGROUND Intralesional 5-fluorouracil (5-FU) in combination with triamcinolone acetonide (TAC) has been recommended as a promising alternative for keloids not responding to silicone-based products, cryotherapy or intralesional corticosteroids alone. Although numerous studies support the efficacy of this regime, there is a lack of objective data. OBJECTIVES In this study, we evaluate the therapeutic effect of four courses of intralesional 5-FU in combination with TAC (31) utilizing 3D analysis (PRIMOS®pico ), ultrasound and scar scales such as the Patient and Observer Scar Assessment Scales (POSAS) and the Dermatology Life Quality Index (DLQI). METHODS Twenty-five patients with keloids were treated using 5-FU and TAC every four weeks. Objective assessments were performed and the scar scales administered at baseline, as well as during consecutive visits at one- and 12-month follow-up (FU). Routine laboratory tests were performed at baseline and at one-month FU. RESULTS 3D PRIMOS and ultrasound measurements revealed highly significant and stable reductions in height (baseline mean score 4.