First record of sea snake (Hydrophis elegans, Hydrophiinae) entrapped in marine debris.

Entanglement in derelict fishing gear and other marine debris is a major threat to the survival of large marine wildlife like cetaceans, seabirds and sea turtles. However, no previous reports of entanglement or entrapment have been recorded in sea snakes (Hydrophiinae). We report here on a sea snake (Hydrophis elegans) found with a ceramic washer encircling its body captured from the north-east coast of Queensland, Australia. The ring had constricted the body and over time caused extensive damage to the underlying tissues. A post-mortem examination showed the snake was severely emaciated as the ring restricted the passage of food to the stomach and intestine. This is the first record of mortality due to marine debris entrapment in sea snakes.

Estuarine crocodiles ride surface currents to facilitate long-distance travel.

1. The estuarine crocodile (Crocodylus porosus) is the world's largest living reptile. It predominately inhabits freshwater and estuarine habitats, but widespread geographic distribution throughout oceanic islands of the South-east Pacific suggests that individuals undertake sizeable ocean voyages. 2. Here we show that adult C. porosus adopt behavioural strategies to utilise surface water currents during long-distance travel, enabling them to move quickly and efficiently over considerable distances. 3. We used acoustic telemetry to monitor crocodile movement throughout 63 km of river, and found that when individuals engaged in a long-distance, constant direction journey (>10 km day(-1)), they would only travel when current flow direction was favourable. Depth and temperature measurements from implanted transmitters showed that they remained at the water surface during travel but would dive to the river substratum or climb out on the river bank if current flow direction became unfavourable. 4. Satellite positional fixes from tagged crocodiles engaged in ocean travel were overlaid with residual surface current (RSC) estimates. The data showed a strong correlation existed between the bearing of the RSC and that of the travelling crocodile (r(2) = 0.92, P < 0.0001). 5. The study demonstrates that C. porosus dramatically increase their travel potential by riding surface currents, providing an effective dispersal strategy for this species.

Satellite tracking reveals long distance coastal travel and homing by translocated estuarine crocodiles, Crocodylus porosus.

Crocodilians have a wide distribution, often in remote areas, are cryptic, secretive and are easily disturbed by human presence. Their capacity for large scale movements is poorly known. Here, we report the first study of post-release movement patterns in translocated adult crocodiles, and the first application of satellite telemetry to a crocodilian. Three large male Crocodylus porosus (3.1-4.5 m) were captured in northern Australia and translocated by helicopter for 56, 99 and 411 km of coastline, the last across Cape York Peninsula from the west coast to the east coast. All crocodiles spent time around their release site before returning rapidly and apparently purposefully to their capture locations. The animal that circumnavigated Cape York Peninsula to return to its capture site, travelled more than 400 km in 20 days, which is the longest homeward travel yet reported for a crocodilian. Such impressive homing ability is significant because translocation has sometimes been used to manage potentially dangerous C. porosus close to human settlement. It is clear that large male estuarine crocodiles can exhibit strong site fidelity, have remarkable navigational skills, and may move long distances following a coastline. These long journeys included impressive daily movements of 10-30 km, often consecutively.

Estrogen receptor-mediated down-regulation of corticotropin-releasing hormone gene expression is dependent on a cyclic adenosine 3',5'-monophosphate regulatory element in human placental syncytiotrophoblast cells.

Placental CRH plays a major role in the mechanisms controlling human pregnancy and parturition. Understanding how placental CRH production is regulated is therefore of importance. Previously we have shown that placental expression of CRH peptide and mRNA are inhibited by estrogens, in contrast to the stimulatory effects of estrogen on hypothalamic CRH production. Our current study found that in placental cells cotransfected with a CRH promoter construct and an estrogen receptor-alpha expression vector results in a differential regulation whereby 17beta-estradiol (E2) decreased and the putative pure estrogen antagonist, ICI 182780, increased CRH promoter activity. Sequential deletion of the CRH promoter indicated that the region between -248 and -213 bp was essential for the effect of both E2 and ICI 182780. This region contains a consensus cAMP regulatory element (CRE) that is a requirement for E2- and ICI 182780-mediated activity because the CRE motif can confer E2 inhibition on a heterologous promoter such as rabbit beta-globin. Mutation of the CRE resulted in a complete reversal of E2 and ICI 182780 regulatory effects. In summary, our results demonstrate that a consensus CRE is required for the action of estrogen receptor ligands in human placental syncytiotrophoblast cells.

Corticotropin-releasing hormone causes vasodilation in human skin via mast cell-dependent pathways.

CRH plays a central role as a mediator of the hypothalamic-pituitary-adrenal axis and stress response and is a potent vasodilator. Previously, we have shown that CRH causes a gender-specific vasodilation in human skin, although the mechanism by which CRH operates is unclear. CRH causes mast cell degranulation in rat skin. As such, histamine and other mast cell-derived factors may be indirectly responsible for the vasodilatory effects of CRH, although CRH is also known to act directly on the vasculature. CRH-induced vasodilation in human skin was examined using laser Doppler flowmetry and iontophoresis in adult females. CRH (1 nM) was administered iontophoretically to the forearm, and blood flow was measured simultaneously in the same area by laser Doppler. CRH-induced dilation of the skin microvasculature was significantly reduced in the presence of the mast cell degranulation inhibitor, sodium cromoglycate, the histamine H(1)-antagonist, promethazine, or the H(2)-antagonist, ranitidine. CRH-induced dilation was also significantly reduced in the presence of the nitric oxide synthase inhibitor, N(omega)-nitro-L-arginine methyl ester, or the cyclooxygenase inhibitor, piroxicam. These findings provide novel evidence that CRH-induced vasodilation in human skin occurs via mast cell degranulation and is principally mediated by histamine and, to a lesser extent, by prostacyclin and nitric oxide.

Estrogen represses whereas the estrogen-antagonist ICI 182780 stimulates placental CRH gene expression.

CRH and estrogens, produced by placental trophoblasts, have been suggested to play pivotal roles in the control of human parturition. Estrogen has been shown to affect hypothalamic CRH expression. Therefore, we evaluated 17 beta-estradiol (E2) in the regulation of CRH gene expression in placental cells. E2 inhibited CRH mRNA expression in a dose-dependent manner, which paralleled the decrease in CRH protein levels in culture media. A complete estrogen receptor (ER) antagonist, ICI 182780, not only blocked repression of CRH mRNA levels by E2, but up-regulated CRH mRNA and protein synthesis. An ER alpha-mixed agonist/antagonist and ER beta antagonist, 4-hydroxytamoxifen, also down-regulated CRH gene expression. Using quantitative RT-PCR, we found that placental trophoblasts express predominantly the ER alpha form of the receptor. Transient transfection assays conducted in the choriocarcinoma cell line JEG-3 demonstrated that E2 repressed CRH promoter activity, whereas the antagonist ICI 182780 up-regulated CRH promoter activity when ER alpha was cotransfected. These studies demonstrate that E2 represses placental CRH gene expression through an ER alpha-mediated mechanism. Estrogen may therefore modulate placental CRH production, influencing the rate of rise of maternal plasma CRH concentrations and potentially the length of gestation.