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Croft, N.

Publications and source records attributed to Croft, N..

2 recordsLinked to original sources

Juveniles exhibit lower heatwave tolerance than adults in a reef-building coral

Marine heatwaves cause widespread coral bleaching and mortality, yet thermal responses often differ between adult and juvenile corals, with the latter frequently being more tolerant. Whether the observed enhanced tolerance of juveniles reflects intrinsic physiological differences across life stages or simply reduced environmental stress due to shaded microhabitats occupied by juveniles, or a combination of both factors, remains unclear. To test whether colony size determines thermal responses and if a threshold size exists for tolerance, we exposed 89 colonies of the reef-building coral Acropora aff. digitifera to a 6-week, 32.5 C simulated marine heatwave under controlled light conditions, with cumulative stress reaching 20 C-weeks. Contrary to expectations, ~2 C-weeks less heat stress was required to trigger bleaching and mortality in coral juveniles compared to adults. Mortality divergence across colony sizes was greatest at ~10 C-weeks, when the smallest corals exceeded 80% mortality, whereas the largest colonies showed <10% mortality. A breakpoint in survival odds was apparent at 13.4 cm diameter, corresponding to the size at onset of sexual maturity in the native wild population for this species. These results indicate an ontogenetic shift in physiological heat tolerance, with larger reproductively mature colonies showing enhanced tolerance. The apparent survival advantage of juveniles in the reef frequently reported during bleaching events could be more likely due to micro-environmental buffering than intrinsic physiological tolerance. Our findings suggest that juvenile corals may be more vulnerable to climate change than previously thought, particularly as declining habitat complexity could reduce microhabitat refugia on future reefs.

ecology↗

Transcriptomic profiling reveals a pro-nociceptive role for Angiotensin II in inflammatory bowel disease

ObjectiveVisceral pain is a leading cause of morbidity in inflammatory bowel disease (IBD), contributing significantly to reduced quality of life. Currently available analgesics often lack efficacy or have intolerable side-effects, driving the need for a more complete understanding of the mechanisms causing pain. MethodsWhole transcriptome gene expression analysis was performed by bulk RNA sequencing of colonic biopsies from patients with ulcerative colitis (UC) and Crohns disease (CD) reporting abdominal pain and compared with non-inflamed control biopsies. Putative pro-nociceptive mediators were identified based on pathway analysis of differentially expressed genes in IBD tissue and single cell gene expression in colonic neurons. Pro-nociceptive activity of identified mediators was assessed in assays of sensory neuron and colonic afferent activity. ResultsRNA sequencing analysis highlighted a 7.6-fold increase in the expression of angiotensinogen transcripts, Agt, the precursor to angiotensin II (Ang II), in samples from UC patients (p = 3.2x10-8). Consistent with the marked expression of the angiotensin AT1 receptor in colonic neurons, Ang II elicited an increase in intracellular Ca2+ in capsaicin-sensitive, voltage gated sodium channel subtype NaV1.8-positive sensory neurons. Ang II also evoked action potential discharge in high-threshold colonic nociceptors. These effects were inhibited by the AT1 receptor antagonist valsartan. ConclusionFindings from our study identify AT1 receptor-mediated colonic nociceptor activation as a novel pathway of visceral nociception in IBD patients with UC. This work highlights the potential utility of angiotensin receptor blockers, such as valsartan, as treatments for pain in IBD.

neuroscience↗