Comparison of Sedative Effects of Alfaxalone-Ketamine and Alfaxalone-Midazolam Administered Intramuscularly in Chickens.

The objective of this study was to compare the sedative effects of intramuscular alfaxalone combined with either ketamine or midazolam in chickens (Gallus gallus domesticus). A prospective, randomized blinded crossover study design with a 7-day washout period was used. Nine adult layer hens received alfaxalone 15 mg/kg with ketamine 5 mg/kg IM (treatment AK) or alfaxalone 15 mg/kg with midazolam 1 mg/kg IM (treatment AM). Time to lateral recumbency, time to loss of righting reflex, induction quality, duration of loss of righting reflex, time to sternal recumbency or vigorous response to stimulation, and time to standing were recorded. Muscle tone, response to noxious stimulation, heart rate, respiratory rate, and oxygen saturation were monitored once the righting reflex was absent. Induction and recovery times were not different between treatments. Lateral recumbency was induced in 8 of 9 birds receiving AK compared to 6 of 9 birds receiving AM. Righting reflex was absent in 7 of 9 and 5 of 9 chickens administered AK and AM, respectively. Median time to loss of righting reflex for AK and AM were 5.5 (4.3-9.3) minutes and 9.1 (4.8-15.0) minutes, respectively (P = .88). Median duration of loss of righting reflex was 21.6 (16.0-36.9) minutes for AK and 21.1 (11.9-26.4) minutes for AM (P = .38). Alfaxalone-ketamine resulted in moderate excitation during induction. Further investigations are warranted to investigate the effects of alfaxalone and midazolam or ketamine at different doses.

Insulinotropic nucleobindin-2/nesfatin-1 is dynamically expressed in the haemochorial mouse and human placenta.

The placenta is the physiological bridge between mother and fetus and has life-sustaining functions during pregnancy, including metabolic regulation, fetal protection and hormone secretion. Nucleobindin-2 (NUCB2) is a calcium- and DNA-binding protein and precursor of nesfatin-1, a signalling peptide with multiple functions, including regulation of energy homeostasis and glucose transport. These are also key functions of the placenta, yet NUCB2/nesfatin-1 expression has never been comprehensively studied in this organ. In the present study, mouse placental samples from Embryonic Day (E) 7.5 to E17.5 and human chorionic villi from the first and second trimester, as well as term pregnancy, were analysed for NUCB2/nesfatin-1 expression by immunohistochemistry with an antiserum that recognised both NUCB2 and nesfatin-1. From E7.5 to E9.5, NUCB2/nesfatin-1 was expressed in the ectoplacental cone, then parietal trophoblast giant cells and early spongiotrophoblast. At E10.5-12.5, NUCB2/nesfatin-1 expression became detectable in the developing labyrinth. From E12.5 and onwards, NUCB2/nesfatin-1 was expressed in the glycogen trophoblast cells, as well as highly expressed in syncytiotrophoblast, sinusoidal trophoblast giant cells and fetal capillary endothelial cells of the labyrinth. In all trimesters of human pregnancy, NUCB2/nesfatin-1 was highly expressed in syncytiotrophoblast. In addition, there was a significant increase in NUCB2 expression in human primary trophoblast cells induced to syncytialise. Thus, the haemochorial mammalian placenta is a novel source of NUCB2/nesfatin-1 and likely a site of its action, with potential roles in glucose homeostasis and/or nutrient sensing.