World scientists' warning: The behavioural crisis driving ecological overshoot.

Previously, anthropogenic ecological overshoot has been identified as a fundamental cause of the myriad symptoms we see around the globe today from biodiversity loss and ocean acidification to the disturbing rise in novel entities and climate change. In the present paper, we have examined this more deeply, and explore the behavioural drivers of overshoot, providing evidence that overshoot is itself a symptom of a deeper, more subversive modern crisis of human behaviour. We work to name and frame this crisis as 'the Human Behavioural Crisis' and propose the crisis be recognised globally as a critical intervention point for tackling ecological overshoot. We demonstrate how current interventions are largely physical, resource intensive, slow-moving and focused on addressing the symptoms of ecological overshoot (such as climate change) rather than the distal cause (maladaptive behaviours). We argue that even in the best-case scenarios, symptom-level interventions are unlikely to avoid catastrophe or achieve more than ephemeral progress. We explore three drivers of the behavioural crisis in depth: economic growth; marketing; and pronatalism. These three drivers directly impact the three 'levers' of overshoot: consumption, waste and population. We demonstrate how the maladaptive behaviours of overshoot stemming from these three drivers have been catalysed and perpetuated by the intentional exploitation of previously adaptive human impulses. In the final sections of this paper, we propose an interdisciplinary emergency response to the behavioural crisis by, amongst other things, the shifting of social norms relating to reproduction, consumption and waste. We seek to highlight a critical disconnect that is an ongoing societal gulf in communication between those that know such as scientists working within limits to growth, and those members of the citizenry, largely influenced by social scientists and industry, that must act.

Exercise-induced elevations in cerebral blood velocity are greater in running compared to cycling at higher intensities.

The optimal exercise intensity and modality for maximizing cerebral blood flow (CBF) and hence potential exposure to positive, hemodynamically derived cerebral adaptations is yet to be fully determined. This study compared CBF velocity responses between running and cycling across a range of exercise intensities. Twenty-six participants (12 females; age: 26 ± 8 years) completed four exercise sessions; two mode-specific maximal oxygen consumption (VO2max ) tests, followed by (order randomized) two incremental exercise protocols (3-min stages at 35%, 50%, 65%, 80%, 95% VO2max ). Continuous measures of middle cerebral artery velocity (MCAv), oxygen consumption, end-tidal CO2 (PET CO2 ), and heart rate were obtained. Modality-specific MCAv changes were observed for the whole group (interaction effect: p = .01). Exercise-induced increases in MCAvmean during cycling followed an inverted-U pattern, peaking at 65% VO2max (Δ12 ± 7 cm/s from rest), whereas MCAvmean during running increased linearly up to 95% VO2max (change from rest: Δ12 ± 13 vs. Δ7 ± 8 cm/s for running vs. cycling at 95% VO2max ; p = .01). In contrast, both modalities had an inverted-U pattern for PET CO2 changes, although peaked at different intensities (running: 50% VO2max , Δ6 ± 2 mmHg; cycling: 65% VO2max , Δ7 ± 2 mmHg; interaction effect: p = .01). Further subgroup analysis revealed that the running-specific linear MCAvmean response was fitness dependent (Fitness*modality*intensity interaction effect: p = .04). Above 65% VO2max , fitter participants (n = 16; male > 45 mL/min/kg and female > 40 mL/min/kg) increased MCAvmean up to 95% VO2max , whereas in unfit participants (n = 7, male < mL/min/kg and female < 35 mL/min/kg) MCAvmean returned toward resting values. Findings demonstrate that modality- and fitness-specific profiles for MCAvmean are seen at exercise intensities exceeding 65% VO2max .

Scalp biopsy identifies systemic amyloidosis presenting as isolated telogen effluvium: A case report.

AL amyloidosis is a complication of B-cell dyscrasias and multiple myeloma, manifest as deposition of antibody fragments in many different organs, including the skin. We describe a rare case of this systemic disease which presented with isolated scalp alopecia. Further investigation led to the diagnosis of an occult plasma-cell dyscrasia, showing the benefit of including systemic amyloidosis in the differential diagnosis of alopecia. The biopsy finding of cutaneous amyloidosis should prompt further workup to exclude an underlying pathology.

The design and rationale of SAVE BC: The Study to Avoid CardioVascular Events in British Columbia.

Atherosclerotic cardiovascular disease (ASCVD) is highly heritable, particularly when it occurs at a young age. The screening of individuals with premature ASCVD, although often recommended, is not routinely performed. Strategies to address this gap in care are essential. We designed the Study to Avoid CardioVascular Events in British Columbia (SAVE BC) as a prospective, observational study of individuals with a new diagnosis of very premature ASCVD (defined as age ≤ 50 years in males and age ≤ 55 years in females) and their first-degree relatives (FDRs) and spouses. FDRs and spouses will undergo screening for cardiovascular (CV) risk factors and subclinical ASCVD using a structured screening algorithm. All subjects will be followed longitudinally for ≥10 years. The overall goal of SAVE BC is to evaluate the yield of a structured screening program for identifying individuals at risk of premature ASCVD. The primary objectives of SAVE BC are to identify and follow index cases with very premature ASCVD and their FDRs and to determine the diagnostic yield of a structured screening program for these individuals. We will collect data on CV risk factors, medication use, CV events, and healthcare costs in these individuals. SAVE BC will provide insight regarding approaches to identify individuals at risk for premature ASCVD with implications for prevention and treatment in this population.