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The observed variation in the body size responses of endotherms to climate change may be explained by two hypotheses: the size increases with climate variability ( the starvation resistance hypothesis ) and the size shrinks as mean temperatures rise ( the heat exchange hypothesis ). Across 82 Australian passerine species over 50 years, shrinking was associated with annual mean temperature rise exceeding 0.012°C driven by rising winter temperatures for arid and temperate zone species. We propose the warming winters hypothesis to explain this response. However, where average summer temperatures exceeded 34°C, species experiencing annual rise over 0.0116°C tended towards increasing size. Results suggest a broad-scale physiological response to changing climate, with size trends probably reflecting the relative strength of selection pressures across a climatic regime. Critically, a given amount of temperature change will have varying effects on phenotype depending on the season in which it occurs, masking the generality of size patterns associated with temperature change. Rather than phenotypic plasticity, and assuming body size is heritable, results suggest selective loss or gain of particular phenotypes could generate evolutionary change but may be difficult to detect with current warming rates.

Background: The prognostic impact of coronary microvascular dysfunction after percutaneous coronary intervention (PCI) remains unclear in patients with stable coronary artery disease. This study sought to investigate the prognostic value of microvascular function measured immediately after PCI in patients with stable coronary artery disease., Methods: We enrolled 572 patients with stable coronary artery disease who underwent PCI and elective measurement of the index of microcirculatory resistance (IMR) immediately after PCI from 8 centers in 4 countries. Impaired microvascular function was defined as IMR≥25 (high IMR). Major adverse cardiac events, including death, myocardial infarction (MI) and target vessel revascularization, were evaluated., Results: During a median follow-up duration of 4.0 years, the cumulative major adverse cardiac events rate was significantly higher in the high IMR group (n=66/148) compared with the low IMR group (n=128/424; hazard ratio [HR], 1.56; 95% CI, 1.16-2.105; P =0.001), primarily due to a higher rate of periprocedural MI (HR, 1.59; 95% CI, 1.11-2.28; P =0.004) but also due to higher rates of mortality (HR, 1.59; 95% CI, 0.76-3.35; P =0.22), spontaneous MI (HR, 2.10; 95% CI, 0.67-6.63; P =0.20) and target vessel revascularization (HR, 1.40; 95% CI, 0.77-2.54; P =0.27). Cumulative risk for death, spontaneous MI, and target vessel revascularization was higher in the high IMR group (HR, 1.55; 95% CI, 0.99-2.43; P =0.056), as was death and spontaneous MI alone (HR, 1.79; 95% CI, 0.96-3.36; P =0.065). On multivariable analysis, high IMR post-PCI was an independent predictor of major adverse cardiac events., Conclusions: IMR measured immediately after PCI predicts adverse events in patients with stable coronary artery disease.

Although the lethal consequences of extreme heat are increasingly reported in the literature, the fitness costs of exposure to sublethal high air temperatures, typically identified in the 30-40 degrees C range, are poorly understood. We examine the effect of high (> or = 35 degrees C) daily maxima on body condition of a semiarid population of White-plumed Honeyeaters, Ptilotula penicillatus, monitored between 1986 and 2012. During this 26-yr period, temperature has risen, on average, by 0.06 degrees C each year at the site, the frequency of days with thermal maxima > or = 35 degrees C has increased and rainfall has declined. Exposure to high temperatures affected body condition of White-plumed Honeyeaters, but only in low-rainfall conditions. There was no effect of a single day of exposure to temperatures > or = 35 degrees C but repeated exposure was associated with reduced body condition: 3.0% reduction in body mass per day of exposure. Rainfall in the previous 30 d ameliorated these effects, with reduced condition evident only in dry conditions. Heat-exposed males with reduced body condition were less likely to be recaptured at the start of the following spring; they presumably died. Heat-exposed females, regardless of body condition, showed lower survival than exposed males, possibly due to their smaller body mass. The higher mortality of females and smaller males exposed to temperatures > or = 35 degrees C may have contributed to the increase in mean body size of this population over 23 years. Annual survival declined across time concomitant with increasing frequency of days > or = 35 degrees C and decreasing rainfall. Our study is one of few to identify a proximate cause of climate change related mortality, and associated long-term demographic consequence. Our results have broad implications for avian communities living in arid and semiarid regions of Australia, and other mid-latitudes regions where daily maximum temperatures already approach physiological limits in regions affected by both decreased precipitation and warming.