Adaptation of sea turtles to climate warming: Will phenological responses be sufficient to counteract changes in reproductive output?

Sea turtles are vulnerable to climate change since their reproductive output is influenced by incubating temperatures, with warmer temperatures causing lower hatching success and increased feminization of embryos. Their ability to cope with projected increases in ambient temperatures will depend on their capacity to adapt to shifts in climatic regimes. Here, we assessed the extent to which phenological shifts could mitigate impacts from increases in ambient temperatures (from 1.5 to 3°C in air temperatures and from 1.4 to 2.3°C in sea surface temperatures by 2100 at our sites) on four species of sea turtles, under a "middle of the road" scenario (SSP2-4.5). Sand temperatures at sea turtle nesting sites are projected to increase from 0.58 to 4.17°C by 2100 and expected shifts in nesting of 26-43 days earlier will not be sufficient to maintain current incubation temperatures at 7 (29%) of our sites, hatching success rates at 10 (42%) of our sites, with current trends in hatchling sex ratio being able to be maintained at half of the sites. We also calculated the phenological shifts that would be required (both backward for an earlier shift in nesting and forward for a later shift) to keep up with present-day incubation temperatures, hatching success rates, and sex ratios. The required shifts backward in nesting for incubation temperatures ranged from -20 to -191 days, whereas the required shifts forward ranged from +54 to +180 days. However, for half of the sites, no matter the shift the median incubation temperature will always be warmer than the 75th percentile of current ranges. Given that phenological shifts will not be able to ameliorate predicted changes in temperature, hatching success and sex ratio at most sites, turtles may need to use other adaptive responses and/or there is the need to enhance sea turtle resilience to climate warming.

No effect of short-term exposure to high-fibre diets on the gastrointestinal morphology of layer hens (Gallus gallus domesticus): body reserves are used to manage energy deficits in favour of phenotypic plasticity.

Using layer hens, Gallus gallus domesticus, we compared the digestive capabilities of birds on a low-fibre diet (LF, 8.49% neutral detergent fibre; NDF), with those fed a high-fibre diet balanced for energy and protein to match the LF diet (high fibre balanced, HFB; NDF = 15.61%) and those fed a high fibre unbalanced (HFU) diet (NDF = 16.68%). The HFU diet had the lowest apparent dry matter (DM) metabolisability at 58.14 ± 6.46%, followed by HFB, 65.87 ± 3.50 and the LF diet, 70.49 ± 7.07%. Despite significant differences between apparent DM metabolisabilities of LF and HFU diets, no morphometric changes in the gastrointestinal tract (GIT) of layer hens were observed (including crop, gizzard, proventriculus, liver, large intestine, paired caeca and small intestine). Conversely, body mass losses were recorded for animals on HFU diet, while those on the LF and HFB diets actually gained body mass over the 14-day trials. We suggest that the body mass losses seen in the animals fed HFU diets were attributed to losses in adipose tissue, but this was not quantified. Assuming body mass losses were mainly in adipose tissue, we propose that adipose may act to buffer environmental challenges like shortfalls in nutrient acquisition when dietary energy requirements are not met. Compared with smaller birds (e.g. quail), the larger body size of the layer hens may offer them a greater safety margin in terms of body energy reserves before changes in the GIT might be needed to redress energy deficits associated with hard-to-digest, high-fibre diets.

The effect of EHV-1 infection upon circulating leucocyte populations in the natural equine host.

It has been suggested that EHV-1 infection may perturb immune responsiveness in the natural equine host. The mechanism underlying this phenomenon is not clear, but disturbances of circulating leucocyte populations could contribute. In order to objectively assess the nature of the haematological changes provoked by EHV-1 infection, two groups of conventionally-maintained Welsh mountain ponies were challenge-infected intra-nasally with the Ab4 isolate of EHV-1. These groups were controlled by similarly-sized groups of non-infected ponies. All data generated was subjected to rigorous statistical analysis. Whole leucocyte count, neutrophil count, lymphocyte count, pan T cell count (RVC1 + cells-putative CD5 homologue), T cell subset count (RVC3 + cell-putative CD8 homologue), RVC2 + cells (putatively class II MHC+) and B cell count were recorded in experimental and control subjects at frequent intervals post-infection via flow cytometry. The principal abnormalities post-infection were T cell lymphopaenia, neutropaenia and the appearance of blastic cells of undetermined lineage. This study underlined the variability of EHV-1 infection in the natural, outbred equine host.

Cholesterol metabolism in distance runners.

Faecal steroid excretion, including betasitosterol excretion, whole-body cholesterol synthesis, plasma lipids, and lipoprotein concentrations and habitual diet, were determined in 14 male distance runners and 14 sedentary men. The proportion of cholesterol-derived steroids excreted as bile acids, and the quantity of betasitosterol excreted in the faeces were significantly (P less than 0.05) higher in the runners compared with the sedentary men. Faecal betasitosterol excretion and the proportion of cholesterol-derived steroids excreted as bile acids were correlated significantly in the distance runners and the sedentary men (r = 0.774, n = 28, P less than 0.001). These results suggest that greater dietary intake of plant sterols may contribute to the higher proportion of cholesterol-derived steroids excreted as bile acids in distance runners.

Fecal bile acid concentration in distance runners.

Fecal bile acid concentration, fecal characteristics, bowel habits and habitual food intake were measured in male distance runners (n = 14) and sedentary men (n = 14). Fecal bile acid concentration was significantly (p less than 0.05) lower and stool weight, frequency of defecation and daily intake of fibre, carbohydrate, and protein were significantly (p less than 0.01) higher in the runners. After adjustment for differences in dietary fibre intake, fecal bile acid concentration was no longer significantly different between the distance runners and the sedentary men, but frequency of defecation remained significantly (p less than 0.05) higher in the runners. This study has identified lower fecal bile acid concentration in distance runners, which was probably due mainly to dilution of colon contents by higher consumption of dietary fibre. These findings may be relevant to the reduced incidence of colon cancer in physically active subjects.

Plasma noncholesterol sterols in male distance runners and sedentary men.

Plasma lathosterol concentration is taken to be an index of the rate of cholesterol synthesis and plasma concentrations of plant sterols just as campesterol and betasitosterol are taken to be indeces of cholesterol absorption efficiency. These noncholesterol sterols were measured in plasma from 14 male distance runners and 10 sedentary men. Plasma lathosterol concentration was 30% lower (P less than 0.02) and plasma betasitosterol concentration was 33% higher (P less than 0.02) in the runners compared to the sedentary men. Plasma concentrations of lathosterol and plant sterols were inversely and significantly (P less than 0.05) correlated in both the runners and the sedentary men. Plasma plant sterol concentrations were correlated positively and significantly (P less than 0.01) with plasma high density lipoprotein cholesterol (HDL-C) concentrations in the runners and sedentary men combined. These findings suggest that more efficient cholesterol absorption may lead to higher plasma plant sterol concentrations and may contribute to lower cholesterol synthesis rates, reduced concentrations of plasma lathosterol and higher plasma HDL-C concentration in distance runners.

Effects of beta endorphin on specific immune responses in man.

Synthetic human beta endorphin shows a biphasic effect on the production of specific anti-herpes viral antibodies in vitro. At higher concentrations antibody production is reduced, at lower concentrations it is enhanced. In a proportion of donors whose cells do not produce specific antibody when cultured with antigen alone, the lower concentrations of beta endorphin allow antigen-driven specific antibody production to occur. Specific anti-herpes viral antibodies are also made by natural killer (NK) cell-depleted populations from the same non-producer donors. beta endorphin also exerts biphasic effects on NK, although the direction of the modulation is a mirror image of the effects on antibody production. This suggests that the immunomodulatory actions of beta endorphin on specific immune responses are mediated in part by effects on NK suppressor-inducer cells.

Differential effects of beta-endorphin fragments on human natural killing.

The endogenous opiate peptide, beta-endorphin, has two effects on human natural killing (NK). Preincubation of effector lymphocytes with between 10(-7) and 10(-11) M beta-endorphin increases NK. Preincubation with lower concentrations results in a reduction in NK. Endorphin peptides containing an unmodified N-terminal sequence, and which are known to bind only to opiate receptors, increase NK. Sequences reported to bind only to nonopiate receptors reduce NK.

Human immune responses to herpes simplex virus, varicella-zoster and cytomegalovirus in vitro.

The cell principally responsible for lymphocyte proliferation to herpes simplex virus (HSV), varicella-zoster (VZ) and cytomegalovirus (CMV) has been shown to be a T cell of helper phenotype. Lymphocytes from a proportion of proliferation-positive normal individuals produced anti-viral antibody in vitro. Although in some cases, and at some time-points, the antibody was specific for the priming virus, in others, antibodies to more than one virus were detected. Similarly, some T-cell clones proliferated specifically to the priming virus, whereas others were not specific for the virus used in the priming culture. Two clones helped the production of HSV-specific antibody, one by autologous, the other by both autologous and allogeneic non-T cells.