Effect of sulfamethazine on sexual precocity and neuropeptide Y neurons within the tuberoinfundibular region of the chick brain

A hitherto ignored microvillous cell type, distinct from microvillous supporting cells and other microvillous cell types, was encountered in olfactory and respiratory epithelia of nasal turbinates of rat fetuses, near the transition between these two epithelia. The apex of the cell resembles the apices of vestibular hair cells. The cell has a cone-shaped bundle of microvilli, resembling the complex bundle of hair-cell stereocilia, accompanied by a cilium. Therefore we called this cell type the nasal hair cell. Cilium and microvilli seemed adhered. Cell numbers were very low, up to about 5 per turbinate. The cell's appearance is precocious compared to that of olfactory receptor and supporting cells. Also, while the apices of olfactory receptor and supporting cells and of ciliated respiratory cells underwent major morphological maturation during the developmental period from embryonic day 16 to day 21, the apical structures of the nasal hair cell only changed marginally from embryonic day 16, when they were first seen, through to at least embryonic day 21. The cell's location and precociously mature appearance suggests that it plays a special role in the development of nasal epithelia.     

Inhibition of reaper-induced apoptosis by interaction with inhibitor of apoptosis proteins (IAPs)

IAPs comprise a family of inhibitors of apoptosis found in viruses and animals. In vivo binding studies demonstrated that both baculovirus and Drosophila IAPs physically interact with an apoptosis-inducing protein of Drosophila, Reaper (RPR), through their baculovirus IAP repeat (BIR) region. Expression of IAPs blocked RPR-induced apoptosis and resulted in the accumulation of RPR in punctate perinuclear locations which coincided with IAP localization. When expressed alone, RPR rapidly disappeared from the cells undergoing RPR-induced apoptosis. Expression of P35, a caspase inhibitor, also blocked RPR-induced apoptosis and delayed RPR decline, but RPR remained cytoplasmic in its location. Mutational analysis of RPR demonstrated that caspases were not directly responsible for RPR disappearance. The physical interaction of IAPs with RPR provides a molecular mechanism for IAP inhibition of RPR's apoptotic activity.     

Splanchnic ischemia and bacterial translocation in the abdominal compartment syndrome

BACKGROUND AND METHODS: Major trauma or abdominal injury may lead to the development of increased intra-abdominal pressure (IAP) and the onset of the abdominal compartment syndrome. Although the effect of raised IAP on systemic and splanchnic hemodynamics have been described, the consequences of the resultant gut hypoperfusion in this setting are unknown. Bacterial translocation (BT) occurs after a period of splanchnic ischemia and may contribute to later organ failure. A rodent model was used to examine the effect of raised IAP on ileal mucosal blood flow (MBF) and BT. IAP was increased to 25 mm Hg for 60 minutes and mean arterial blood pressure was maintained with fluid. Animals were killed 24 hours later and examined for BT. RESULTS: Increased IAP resulted in a decrease of MBF to 63% of baseline despite maintaining normal mean arterial blood pressure. BT occurred principally to the mesenteric lymph nodes after 60 minutes of IAP at 25 mm Hg. CONCLUSIONS: Increased IAP leads to decreased MBF and to BT, which may contribute to later septic complications and organ failure.