Nine risk management lessons for practitioners.

Risk management is an essential skill for professionals and is important throughout the course of their careers. Effective risk management blends a utilitarian focus on the potential costs and benefits of particular courses of action, with a solid foundation in ethical principles. Awareness of particularly risk-laden circumstances and practical strategies can promote safer and more effective practice. This article reviews nine situations and their associated lessons, illustrated by case examples. These situations emerged from our experience as risk management consultants who have listened to and assisted many practitioners in addressing the challenges they face on a day-to-day basis. The lessons include a focus on obtaining consent, setting boundaries, flexibility, attention to clinician affect, differentiating the clinician’s own values and needs from those of the client, awareness of the limits of competence, maintaining adequate legal knowledge, keeping good records, and routine consultation. We highlight issues and approaches to consider in these types of cases that minimize risks of adverse outcomes and enhance good practice. (PsycINFO Database Record (c) 2018 APA, all rights reserved

Bioactive Seco-Lanostane-Type Triterpenoids from the Roots of <i>Leplaea mayombensis</i>

Fractionation of the ethyl acetate-soluble extract of the roots of <i>Leplaea mayombensis</i> afforded two new 3,4-seco-lanostane-type triterpenoids, leplaeric acids A and B (<b>1</b>, <b>2</b>), the new lanostane-type triterpenoid leplaeric acid C (<b>3</b>), and six known natural products (<b>5</b>–<b>10</b>). Derivatization of the main constituent, <b>1</b>, afforded the dimethyl ester <b>4</b>, the monoamide <b>11</b>, and diamide <b>12</b> for SAR studies. The structures of these compounds were established through spectroscopic methods, and a single-crystal X-ray diffraction analysis was used to confirm the relative configuration of compound <b>1</b>. These lanostane derivatives are unique since they are the first C-21-oxygenated lanostanes isolated from plant sources. Preliminary biological assays against the MDA MB 231 breast cancer cell line showed that compounds <b>1</b>, <b>2</b>, <b>4</b>, and <b>11</b> have modest cytotoxic activity. Compound <b>2</b> was the most active, with an IC₅₀ of 55 ± 7 μM. From these results, the amides (<b>11</b>, <b>12</b>) derived from triterpenoid <b>1</b> were found to be less active than the derived esters (<b>2</b>, <b>4</b>)

Association of alcohol consumption with allergic disease and asthma: a multi-centre Mendelian randomization analysis.

AIMS: To use the rs1229984 variant associated with alcohol consumption as an instrument for alcohol consumption to test the causality of the association of alcohol consumption with hay fever, asthma, allergic sensitization and serum total immunoglobulin (Ig)E. DESIGN: Observational and Mendelian randomization analyses using genetic variants as unbiased markers of exposure to estimate causal effects, subject to certain assumptions. SETTING: Europe. PARTICIPANTS: We included a total of 466 434 people aged 15-82 years from 17 population-based studies conducted from 1997 to 2015. MEASUREMENTS: The rs1229984 (ADH1B) was genotyped; alcohol consumption, hay fever and asthma were self-reported. Specific and total IgE were measured from serum samples. FINDINGS: Observational analyses showed that ever-drinking versus non-drinking, but not amount of alcohol intake, was positively associated with hay fever and inversely associated with asthma but not with allergic sensitization or serum total immunoglobulin (Ig)E. However, Mendelian randomization analyses did not suggest that the observational associations are causal. The causal odds ratio (OR) per genetically assessed unit of alcohol/week was an OR = 0.907 [95% confidence interval (CI) = 0.806, 1.019; P = 0.101] for hay fever, an OR = 0.897 (95% CI = 0.790, 1.019; P = 0.095) for asthma, an OR = 0.971 (95% CI =  0.804, 1.174; P = 0.763) for allergic sensitization and a 4.7% change (95% CI = -5.5%, 14.9%; P = 0.366) for total IgE. CONCLUSIONS: In observational analyses, ever-drinking versus not drinking was positively associated with hay fever and negatively associated with asthma. However, the Mendelian randomization results were not consistent with these associations being causal

Association of alcohol consumption with allergic disease and asthma: a multi-centre Mendelian randomization analysis.

AIMS: To use the rs1229984 variant associated with alcohol consumption as an instrument for alcohol consumption to test the causality of the association of alcohol consumption with hay fever, asthma, allergic sensitization and serum total immunoglobulin (Ig)E. DESIGN: Observational and Mendelian randomization analyses using genetic variants as unbiased markers of exposure to estimate causal effects, subject to certain assumptions. SETTING: Europe. PARTICIPANTS: We included a total of 466 434 people aged 15-82 years from 17 population-based studies conducted from 1997 to 2015. MEASUREMENTS: The rs1229984 (ADH1B) was genotyped; alcohol consumption, hay fever and asthma were self-reported. Specific and total IgE were measured from serum samples. FINDINGS: Observational analyses showed that ever-drinking versus non-drinking, but not amount of alcohol intake, was positively associated with hay fever and inversely associated with asthma but not with allergic sensitization or serum total immunoglobulin (Ig)E. However, Mendelian randomization analyses did not suggest that the observational associations are causal. The causal odds ratio (OR) per genetically assessed unit of alcohol/week was an OR = 0.907 [95% confidence interval (CI) = 0.806, 1.019; P = 0.101] for hay fever, an OR = 0.897 (95% CI = 0.790, 1.019; P = 0.095) for asthma, an OR = 0.971 (95% CI =  0.804, 1.174; P = 0.763) for allergic sensitization and a 4.7% change (95% CI = -5.5%, 14.9%; P = 0.366) for total IgE. CONCLUSIONS: In observational analyses, ever-drinking versus not drinking was positively associated with hay fever and negatively associated with asthma. However, the Mendelian randomization results were not consistent with these associations being causal