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To examine the factor structure of autism spectrum disorder (ASD) and the psychometric properties of the German Symptom Checklist for Autism Spectrum Disorders (SCL-ASD). Data were collected from 312 clinical referrals with suspected ASD (2-18 years). Confirmatory factor analyses and analyses of reliability, convergent and divergent validity were performed. A bifactor model with one general ASD factor and two specific factors (interaction-communication; restricted, repetitive behaviors) provided an adequate data fit. Internal consistencies of the SCL-ASD subscales and the total scale were > 0.70. Correlations with measures of ASD traits were higher than correlations with measures of externalizing and internalizing symptoms. The results support a factor structure consistent with DSM-5/ICD-11 criteria. The SCL-ASD has sound psychometric properties.

This article focuses on efforts to regulate live-in care in Swiss households. Based on a sociology of legitimation, the model is conceptualised as a fragile order with a need for legitimation, and expectations towards its regulation are examined. While claims to justice serve as principles of criticism, austerity-based claims legitimise the arrangement. The need for adjustment is dealt with in a way that the model remains possible. Regulation remains fragmented and the debate about costs overshadows the question of how to (re-)organise long-term care.

Chronic alcohol intoxication decreases muscle strength/function and causes mitochondrial dysfunction. Aerobic exercise training improves mitochondrial oxidative capacity and increases muscle mass and strength. Presently, the impact of chronic alcohol on aerobic exercise-induced adaptations was investigated. Female C57BL/6Hsd mice were randomly assigned to one of four groups: control sedentary (CON SED; n = 26), alcohol sedentary (ETOH SED; n = 27), control exercise (CON EX; n = 28), and alcohol exercise (ETOH EX; n = 25). Exercise mice had running wheel access for 2 h a day, 7 days a week. All mice were fed either control or an alcohol-containing liquid diet. Grip strength testing and EchoMRI were performed before and after the interventions. After 6 wk, hindlimb muscles were collected for molecular analyses. A subset of mice performed a treadmill run to fatigue (RTF), then abstained from alcohol for 2 wk and repeated the RTF. Alcohol decreased lean mass and forelimb grip strength compared with control-fed mice. Alcohol blunted the exercise-induced increase in muscle mass (plantaris and soleus), type IIa fiber percentage in the plantaris, and run time to fatigue. Mitochondrial markers (Citrate synthase activity and Complex I-IV, COXIV and Cytochrome C protein expression) were increased with exercise regardless of ETOH in the gastrocnemius but not tibialis anterior muscle. Two weeks of alcohol abstinence improved RTF time in ETOH EX but not in ETOH SED. These data suggest that alcohol impairs some exercise-induced adaptations in skeletal muscle, but not all were negatively affected, indicating that exercise may be a beneficial behavior even while consuming alcohol. NEW & NOTEWORTHY: Alcohol consumption during an aerobic exercise training period prevented training-induced increases in run to fatigue time and grip strength. Cessation of alcohol allowed for recovery of endurance performance within 2 wk. The worsened exercise performance after alcohol was unrelated to impairments in markers of mitochondrial health. Therefore, some adaptations to exercise training are impaired with alcohol use (endurance performance, muscle growth, and strength), while others remain mostly unaffected (mitochondrial health). [ABSTRACT FROM AUTHOR]

The intrinsic skeletal muscle core clock has emerged as a key feature of metabolic control and influences several aspects of muscle physiology. Acute alcohol intoxication disrupts the core molecular clock, but whether chronic consumption, like that leading to alcoholic myopathy, is also a zeitgeber for skeletal muscle remains unknown. The purpose of this work was to determine whether chronic alcohol consumption dysregulates the skeletal muscle core molecular clock and clock-controlled genes (CCGs). C57BL/6Hsd female mice (14 weeks old) were fed a control (CON) or alcohol (EtOH) containing liquid diet for 6 weeks. Gastrocnemius muscles and serum were collected from CON and EtOH mice every 4-h for 24-h. Chronic alcohol consumption disrupted genes of the core clock including suppressing the rhythmic peak of expression of Bmal1, Per1, Per2, and Cry2. Genes involved in the regulation of Bmal1 also exhibited lower rhythmic peaks including Reverb α and Myod1. The CCGs, Dbp, Lpl, Hk2, and Hadh were also suppressed by alcohol. The nuclear expression patterns of MYOD1, DBP, and REVERBα were shifted by alcohol, while no change in BMAL1 was detected. Overall, these data indicate that alcohol disrupted the skeletal muscle core clock but whether these changes in the core clock are causative or a consequence of alcoholic myopathy requires future mechanistic confirmation. [ABSTRACT FROM AUTHOR]

Depression is common among patients with breast cancer (BC) and their spouses. The diagnosis of BC often results in negative cognitive processes, such as appraisals of harm/loss, intrusive thoughts, and [...]