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Pseudozyma spp. are described as environmental yeasts but have also been identified as rare human pathogens found in immunocompromised patients. This systematic review details the clinical manifestations, diagnostic methodology, and empirical anti-fungal therapy for this rare yeast. PubMed, LILACS, Scielo, and Web of Science databases were searched for articles about Pseudozyma spp. infections from inception to June 2019. Inclusion criteria were any published studies that included patients with Pseudozyma spp. infection. Infections were identified using criteria set forth by the European Organization for Research and Treatment of Cancer, and were further classified according to clinical, laboratory, or radiologic findings, microbiologic confirmation, and response to therapy. Eleven articles were included with 15 patients. Oncological and/or hematological disorders were the most reported risk factors. Nontraditional microbiological methods correctly identified Pseudozyma spp., whereas traditional methods failed to identify fungal genus. Species were identified by sequencing, and most demonstrated a higher minimal inhibitory concentration (MIC) for fluconazole and echinocandins. MICs for itraconazole, voriconazole, and posaconazole varied by species. All isolates were susceptible to amphotericin B, which was the most used treatment. Pseudozyma spp. infections usually present with fever and are diagnosed by blood culture. Most species studied appeared to be resistant to fluconazole and echinocandin. Voriconazole, posaconazole, and amphotericin were effective in treating P. aphidis. However, more studies are needed to evaluate voriconazole and posaconazole in species other than P. aphidis. © The Author(s) 2020. Published by Oxford University Press on behalf of The International Society for Human and Animal Mycology.Importance Tobacco use is the leading cause of preventable death in the US. An estimated annual 480 000 deaths are attributable to tobacco use in adults, including from secondhand smoke. It is estimated that every day about 1600 youth aged 12 to 17 years smoke their first cigarette and that about 5.6 million adolescents alive today will die prematurely from a smoking-related illness. Although conventional cigarette use has gradually declined among children in the US since the late 1990s, tobacco use via electronic cigarettes (e-cigarettes) is quickly rising and is now more common among youth than cigarette smoking. e-Cigarette products usually contain nicotine, which is addictive, raising concerns about e-cigarette use and nicotine addiction in children. Exposure to nicotine during adolescence can harm the developing brain, which may affect brain function and cognition, attention, and mood; thus, minimizing nicotine exposure from any tobacco product in youth is important. Objective To update its 2013 recommen provide interventions, including education or brief counseling, to prevent initiation of tobacco use among school-aged children and adolescents. (B recommendation) The USPSTF concludes that the current evidence is insufficient to assess the balance of benefits and harms of primary care-feasible interventions for the cessation of tobacco use among school-aged children and adolescents. (I statement).Importance Interventions to discourage the use of tobacco products (including electronic nicotine delivery systems or e-cigarettes) among children and adolescents may help decrease tobacco-related illness and injury. Objective To update the 2013 review on primary care-relevant interventions for tobacco use prevention and cessation in children and adolescents to inform the US Preventive Services Task Force. EGFR inhibitor Data Sources The Cochrane Central Register of Controlled Trials and Cochrane Database of Systematic Reviews, MEDLINE, PsyINFO, and EMBASE (September 1, 2012, to June 25, 2019), with surveillance through February 7, 2020. Study Selection Primary care-relevant studies; randomized clinical trials and nonrandomized controlled intervention studies of children and adolescents up to age 18 years for cessation and age 25 years for prevention. Trials comparing behavioral or pharmacological interventions with no or a minimal tobacco use intervention control group (eg, usual care, attention control, wait list) were inopion at 26 weeks (n = 523; 17% [300 mg] and 6% [150 mg] vs 10% [placebo]; 24% [150 mg] vs 28% [placebo]) and 1 trial of nicotine replacement therapy at 12 months (n = 257; 8.1% vs 8.2%). One trial each (n = 2586 and n = 1645) found no beneficial intervention effect on health outcomes or on adult smoking. No trials of prevention in young adults were identified. EGFR inhibitor Few trials addressed prevention or cessation of tobacco products other than cigarettes; no trials evaluated effects of interventions on e-cigarette use. There were few trials of pharmacotherapy, and they had small sample sizes. Conclusions and Relevance Behavioral interventions may reduce the likelihood of smoking initiation in nonsmoking children and adolescents. Research is needed to identify effective behavioral interventions for adolescents who smoke cigarettes or who use other tobacco products and to understand the effectiveness of pharmacotherapy.This study aimed to evaluate the impact of quantitative baseline Aspergillus-specific immunoglobulin G (IgG) serum levels on weight changes of patients with chronic pulmonary aspergillosis (CPA) under antifungal treatment. We retrospectively reviewed data of patients diagnosed with CPA between April 2015 and March 2018 at the National Aspergillosis Centre (Manchester, UK). All patients were on continued antifungal treatment for 12 months. Data on Aspergillus-specific IgG levels, St George's quality of life (SGQoL) variables and weight at baseline, 6 months and 12 months were extracted. We defined a high serum Aspergillus-specific IgG as ≥ 200 mg/l (Group A) and low level  less then  200 mg/l (Group B). Forty-nine patients (37 male; 12 female), median age 65 years (range 29-86) were studied. Overall, 33% (n = 16) of the patients were in Group A. The baseline characteristics between the two groups were similar. The median Charlson comorbidity index was 4 (range 0-5) and 3 (range 0-9) for Group A and Group B, respectively (P = .