Post-weaning social isolation modifies neonatal anoxia-induced changes in energy metabolism and growth of rats.

Neonatal oxygen deficiency in rats may disturb growth and long-term metabolic homeostasis. In order to facilitate metabolic evaluation, the subjects are usually housed individually. However, social isolation associated with individually housed conditions alters animal behavior, which may influence the experimental results. This study investigated the effects of social isolation on neonatal anoxia-induced changes in growth and energy metabolism. Male and female Wistar rats were exposed, on postnatal day 2 (P2), to either 25-min of anoxia or control treatment. From P27 onward, part of the subjects of each group was isolated in standard cages, and the remaining subjects were housed in groups. At P34 or P95, the subjects were fasted for 18 h, refeed for 1 h, and then perfused 30 min later. Glycemia, leptin, insulin, and morphology of the pancreas were evaluated at both ages. For subjects perfused at P95, body weight and food intake were recorded up to P90, and the brain was collected for Fos and NeuN immunohistochemistry. Results showed that male rats exposed to neonatal anoxia and social isolation exhibited increased body weight gain despite the lack of changes in food intake. In addition, social isolation (1) decreased post-fasting weight loss and post-fasting food intake and (2) increased glycemia, insulin, and leptin levels of male and female rats exposed to anoxia and control treatments, both at P35 and P95. Furthermore, although at P35, anoxia increased insulin levels of males, it decreased the area of the ß-positive cells in the pancreas of females. At P95, anoxia increased post-prandial weight loss of males, post-fasting food intake, insulin, and leptin, and decreased Fos expression in the arcuate nucleus (ARC) of males and females. Hyperphagia was associated with possible resistance to leptin and insulin, suspected by the high circulating levels of these hormones and poor neuronal activation of ARC. This study demonstrated that continuous social isolation from weaning modifies, in a differentiated way, the long-term energy metabolism and growth of male and female Wistar rats exposed to neonatal anoxia or even control treatments. Therefore, social isolation should be considered as a factor that negatively influences experimental results and the outcomes of the neonatal injury. These results should also be taken into account in clinical procedures, since the used model simulates the preterm babies' conditions and some therapeutic approaches require isolation.

High Occurrence of Chelonid Alphaherpesvirus 5 (ChHV5) in Green Sea Turtles Chelonia mydas with and without Fibropapillomatosis in Feeding Areas of the São Paulo Coast, Brazil.

Chelonid alphaherpesvirus 5 (ChHV5) has been consistently associated with fibropapillomatosis (FP), a neoplastic disease that affects sea turtles globally. The DNA of ChHV5 has been detected in cutaneous and noncutaneous tissues (e.g., lung) of green sea turtles Chelonia mydas with (FP+) and without (FP-) clinical signs of FP, indicating a persistent ChHV5 infection. Previously published and custom primer pairs were used to amplify the fragments of ChHV5 unique long (UL) partial genes (UL30 and UL18) through end-point PCR from cutaneous tumors (n = 31), nontumored skin (n = 49), and lungs (n = 26) from FP+ (n = 31) and FP- (n = 18) green sea turtles. The DNA of ChHV5 was detected in cutaneous tumors (80.6%, 25/31), nontumored skin (74.2%, 23/31 FP+; 27.8%, 5/18 FP-), and lung samples (91.7%, 11/12 FP+; 100%, 14/14 FP-). The high occurrence of ChHV5 observed in lung samples from FP- individuals was unexpected (14/14), providing the first evidence of ChHV5 DNA presence in lungs of individuals without FP. Our results also revealed high ChHV5 occurrence among the tested cohort (93.9%, 46/49) and suggested that a large proportion (83.4%, 15/18) of FP- green sea turtles had subclinical ChHV5 infections. Hence, our findings support the hypothesis that ChHV5 requires one or more possibly environmental or immune-related co-factors to induce FP.