Wynnskafte7292

viours during the COVID-19 pandemic in Spain. Moreover, the SMILE-C was sensitive to detect these changes and presented good initial psychometric properties. Further follow-up studies should collect relevant data to promote healthy lifestyles in pandemic times.

This research aimed to identify what supports and what hinders job autonomy for midwives in New Zealand.

Registered midwives participated in an open-ended, online survey in 2019. Anonymised participants were asked to describe an incident when they felt they were using their professional judgement and/or initiative to make decisions and the resultant actions. The data was analysed thematically.

The participants identified that autonomy is embedded within midwifery practice in New Zealand. Self-employed midwives who provide continuity of care as Lead Maternity Carers, identified they practice autonomously 'all the time'. The relationship with women and their family, and informed decision making, motivated the midwife to advocate for the woman - regardless of the midwife's work setting. Midwifery expertise, skills, and knowledge were intrinsic to autonomy. Collegial relationships could support or hinder the midwives' autonomy while a negative hospital work culture could hinder job autonomy.

Midwives identified that autonomous practice is embedded in their day to day work. It strengthens and is strengthened by their relationships with the woman/whanau and when their body of knowledge is acknowledged by their colleagues. Job autonomy was described when midwifery decisions were challenged by health professionals in hospital settings and these challenges could be viewed as obstructing job autonomy.

The high job autonomy that New Zealand midwives enjoy is supported by their expertise, the women and colleagues that understand and respect their scope of practice. When their autonomy is hindered by institutional culture and professional differences provision of woman-centred care can suffer.

The high job autonomy that New Zealand midwives enjoy is supported by their expertise, the women and colleagues that understand and respect their scope of practice. When their autonomy is hindered by institutional culture and professional differences provision of woman-centred care can suffer.

The Top End of Australia has a high proportion of Indigenous people with a high burden of chronic cardiac and pulmonary diseases likely to contribute to pulmonary hypertension (PH). The epidemiology of PH has not been previously studied in this region.

Patients with PH were identified from the Northern Territory echocardiography database from January 2010 to December 2015 and followed to the end of 2019 or death. Pulmonary hypertension was defined as a tricuspid regurgitation velocity ≥2.75 m/s measured by Doppler echocardiography. The aetiology of PH, as categorised by published guidelines, was determined by reviewing electronic health records.

1,764 patients were identified comprising 49% males and 45% Indigenous people. The prevalence of PH was 955 per 100,000 population (with corresponding prevalence of 1,587 for Indigenous people). Hypertension, atrial fibrillation, diabetes and respiratory disease were present in 85%, 45%, 41% and 39%, respectively. Left heart disease was the leading cause for PH (58%), the majority suffering from valvular disease (predominantly rheumatic). Pulmonary arterial hypertension (PAH), respiratory disease related PH, chronic thromboembolic PH (CTEPH) and unclear multifactorial PH represented 4%, 16%, 2% and 3%, respectively. Selleckchem Berzosertib Underlying causes were not identifiable in 17% of the patients. Only 31% of potentially eligible patients were on PAH-specific therapy. At census, there was 40% mortality, with major predictors being age, ePASP and Indigenous ethnicity.

Pulmonary hypertension is prevalent in Northern Australia, with a high frequency of modifiable risk factors and other treatable conditions. Whether earlier diagnosis, interpretation and intervention improve outcomes merits further assessment.

Pulmonary hypertension is prevalent in Northern Australia, with a high frequency of modifiable risk factors and other treatable conditions. Whether earlier diagnosis, interpretation and intervention improve outcomes merits further assessment.

High-intensity interval training (HIIT) and aerobic training (AT) both improve cardiac function; however, their effects on cardiac function after myocardial infarction (MI) and the molecular mechanisms are unclear. In this study, HIIT, AT and sedentary (SED) interventions were performed for 4 weeks to compare the effects on cardiac function after MI and explore a more suitable approach for clinical application and the potential mechanisms.

Twenty-four (24) male rats were randomly divided into a control group (CON), MI-sedentary group (MI-SED), MI-aerobic training group (MI-AT), and MI-high-intensity interval training group (MI-HIIT). After 4 weeks of intervention the exercise capacity, heart rate (HR), left ventricular end-diastolic diameter (LVEDD), left ventricular end systolic diameter (LVESD), left ventricular ejection fraction (LVEF), AMP-activated protein kinase α1 (AMPKα1), cardiomyocyte morphology, and cardiac mitochondria were assessed.

After intervention 1) exercise capacity in the MI-AT (49.0mbers; the MI-HIIT group displayed swollen and vacuolated cardiac mitochondria with disrupted cristae; the MI-AT and MI-HIIT groups had significantly increased cardiac mitochondrial numbers than the MI-SED group; there was no statistical difference between the MI-AT and MI-HIIT groups.

Aerobic training and HIIT for 4 weeks had similar cardioprotection and were superior to SED intervention. Both AT and HIIT improved cardiac function and exercise capacity by upregulating AMPKα1 expression. However, 4 weeks of intervention resulted in left ventricular dilation and cardiac myocardial mitochondrial injury in the MI-HIIT group.

Aerobic training and HIIT for 4 weeks had similar cardioprotection and were superior to SED intervention. Both AT and HIIT improved cardiac function and exercise capacity by upregulating AMPKα1 expression. However, 4 weeks of intervention resulted in left ventricular dilation and cardiac myocardial mitochondrial injury in the MI-HIIT group.