Meat Feeding Restricts Rapid Cold Hardening Response and Increases Thermal Activity Thresholds of Adult Blow Flies, Calliphora vicina (Diptera: Calliphoridae)

Virtually all temperate insects survive the winter by entering a physiological state of reduced metabolic activity termed diapause. However, there is increasing evidence that climate change is disrupting the diapause response resulting in non-diapause life stages encountering periods of winter cold. This is a significant problem for adult life stages in particular, as they must remain mobile, periodically feed, and potentially initiate reproductive development at a time when resources should be diverted to enhance stress tolerance. Here we present the first evidence of protein/meat feeding restricting rapid cold hardening (RCH) ability and increasing low temperature activity thresholds. No RCH response was noted in adult female blow flies (Calliphora vicina Robineau-Desvoidy) fed a sugar, water and liver (SWL) diet, while a strong RCH response was seen in females fed a diet of sugar and water (SW) only. The RCH response in SW flies was induced at temperatures as high as 10°C, but was strongest following 3h at 0°C. The CTmin (loss of coordinated movement) and chill coma (final appendage twitch) temperature of SWL females (-0.3 ± 0.5°C and -4.9 ± 0.5°C, respectively) was significantly higher than for SW females (-3.2 ± 0.8°C and -8.5 ± 0.6°C). We confirmed this was not directly the result of altered extracellular K+, as activity thresholds of alanine-fed adults were not significantly different from SW flies. Instead we suggest the loss of cold tolerance is more likely the result of diverting resource allocation to egg development. Between 2009 and 2013 winter air temperatures in Birmingham, UK, fell below the CTmin of SW and SWL flies on 63 and 195 days, respectively, suggesting differential exposure to chill injury depending on whether adults had access to meat or not. We conclude that disruption of diapause could significantly impact on winter survival through loss of synchrony in the timing of active feeding and reproductive development with favourable temperature conditions

Trophic macrophages in development and disease

Specialized phagocytes are found in the most primitive multicellular organisms. Their roles in homeostasis and in distinguishing self from non-self have evolved with the complexity of organisms and their immune systems. Equally important, but often overlooked, are the roles of macrophages in tissue development. As discussed in this Review, these include functions in branching morphogenesis, neuronal patterning, angiogenesis, bone morphogenesis and the generation of adipose tissue. In each case, macrophage depletion impairs the formation of the tissue and compromises its function. I argue that in several diseases, the unrestrained acquisition of these developmental macrophage functions exacerbates pathology. For example, macrophages enhance tumour progression and metastasis by affecting tumour-cell migration and invasion, as well as angiogenesis

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Ablation strategies for the management of symptomatic Brugada syndrome: A systematic review

Ablation approaches have been described for the management of symptomatic ventricular arrhythmias in patients with Brugada syndrome, but this treatment is still considered experimental. We aimed to perform a systematic review of the current evidence on the use of catheter ablation in Brugada syndrome. MEDLINE, Embase, and Scopus were searched for articles describing the use of catheter ablation for ventricular arrhythmia management in Brugada syndrome. We included 11 case series and 11 case reports including a total of 233 patients. Ablation strategies included epicardial mapping with substrate modification (n = 180; 77.3%), endocardial-only mapping with substrate modification (n = 17; 7.3%), ventricular fibrillation (VF)–triggering premature ventricular complex ablation (n = 5; 2.1%), and mixed approaches (n = 31; 13.3%). During a 2.5- to 78-month follow-up period, the success rates in preventing ventricular tachycardia or VF (VT/VF) were 96.7%, 70.6%, and 80% with epicardial, endocardial, and triggering premature ventricular complex ablation approaches, respectively. Among patients who underwent both epicardial and endocardial mapping, there was no identifiable endocardial substrate in 92.9% of cases. Elimination of type 1 Brugada-pattern electrocardiogram was attained in 98.3% and 34.8% of the epicardial and endocardial ablation groups, respectively. VT/VF occurred in 7 of 9 patients (77.8%) who had persistent or recurrent J-ST elevation and in none of the 24 patients with complete resolution during follow-up. Pharmacologic provocation augmented the abnormal area. Epicardial substrate modification appears to be more effective than endocardial-only approach in preventing VT/VF. Persistent or recurrent J-ST elevation appears to represent a marker of failure of ablation. Ablation seems to be an acceptable strategy for patients with Brugada syndrome and VT/VF