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Background and Purpose Post-operative ileus (POI) is induced by intestinal inflammation. Here, we aimed to clarify the effects of 5-HT3 receptor antagonists against POI.

Deletion of cellular isoform of prion protein (PrP(C)) increases neuronal predisposition to damage by modulating apoptosis and the negative consequences of oxidative stress. In vivo studies have demonstrated that PrP(C)-deficient mice are more prone to seizure, depression, and induction of epilepsy and experience extensive cerebral damage following ischemic challenge or viral infection. In addition, adenovirus-mediated overexpression of PrP(C) reduces brain damage in rat models of cerebral ischemia. In experimental autoimmune encephalomyelitis, PrP(C)-deficient mice reportedly have a more aggressive disease onset and less clinical improvement during the chronic phase than wild-type mice mice. In mice given oral dextran sulfate, PrP(C) has a potential protective role against inflammatory bowel disease. PrP(C)-deficient mice demonstrate significantly greater increases in blood glucose concentrations after intraperitoneal injection of glucose than wild-type mice. Further in vivo challenges to PrP gene-deficient models and conditional knockout models with siRNA and in vivo administration of PrP-ligating agents may assist in refining knowledge of the lymphoid function of PrP(C) and predicting the effects of anti-PrP treatment on the immune system. Together, these findings indicate that PrP(C) may have multiple neuroprotective and anti-inflammatory roles, which explains why this protein is so widely expressed.

This study investigated the morphological changes of lungs in F344/N rats (9-36 months old). We initially examined general and quantitative morphological changes, and then we used immunohistochemistry to detect distributional changes in collagen subtypes (types I, III, and IV) and smooth muscle cell (SMC) markers (alpha-smooth muscle actin (ASMA), gamma-smooth muscle actin (GSMA), desmin, and vimentin) in the lungs. In 24-month-old rats, alveolar ducts and alveolar sacs were enlarged, and alveoli were wider and shallower than in younger animals. In old rats (>/=27 months), terminal and respiratory bronchioles and alveolar ducts were dilated and alveoli were more extended than in 24-month-old rats. No age-related distributional changes were observed for collagen types I, III, and IV as revealed by immunohistochemistry, or elastin as revealed by resorsin fuchsin. SMCs in the extra- and intrapulmonary bronchi were immunoreactive for ASMA, GSMA, and desmin, but not for vimentin at all ages. In old rats (>/=27 months), SMCs were loosely arranged in comparison with younger animals, and stainability for GSMA and desmin was decreased. In the respiratory bronchioles and alveolar ducts, a few cells immunoreactive for ASMA and vimentin were observed in the smooth muscle aggregations of the alveolar orifice in rats younger than 12 months. In older rats (>20 months), cells immunoreactive for ASMA and vimentin were increased in septal tips. In conclusion, extension of distal airways and immunohistochemical changes of SMC markers in F344/N rat lungs were evident by approximately 24 months of age, but there was no apparent change in connective tissue morphology.

The aim of this study was to evaluate the effects of permanent tracheostomy on baseline breathing, reflex responses to lung hyperinflation (1.5 kPa) and right atrial capsaicin injection (5 micrograms/kg) before and at 3 and 5 weeks after tracheostomy in sevoflurane-anaesthetized spontaneously breathing dogs (n = 6). In all observation periods, apnoeic responses, represented by an increase in expiration time after lung inflation and right atrial capsaicin injection, were consistently observed to be a result of the Hering-Breuer inflation reflex and the pulmonary C-fibre chemoreflex. Investigation at 3 and 5 weeks after tracheostomy revealed no significant evidence of changing baseline breathing pattern or reflex responses to lung inflation and capsaicin in any ventilatory variable (inspiration time, expiration time, tidal volume, expired ventilation, and end-tidal PCO2) from levels recorded before surgery. These results indicate that permanent tracheostomy, at least up to 5 weeks, does not affect the baseline breathing pattern, the Hering-Breuer inflation reflex or the pulmonary C-fibre chemoreflex. Further, our investigation provides a useful canine model in respiratory physiology.

Corpuscular nerve endings in the nasal respiratory mucosa of the dog were investigated by immunohistochemical staining specific for protein gene product 9.5 by light and electron microscopy. In the nasal respiratory mucosa, complex corpuscular endings, which displayed bulbous, laminar and varicose expansions, were distributed on the dorsal elevated part of the nasal septum and on the dorsal nasal concha. The endings were 300-500 microm long and 100-250 microm wide. Some axons gave rise to a single ending while others branched into 2 endings. Cryostat sections revealed that the corpuscular endings were located within the nasal respiratory epithelium. On electron microscopy, immunoreactive nerve terminals that contained organelles, including mitochondria and neurofilaments, were observed within the epithelial layer near the lumen of the nasal cavity. Some terminals contacted the goblet cell. Such terminal regions were covered by the cytoplasmic process of ciliated cells and were never exposed to the lumen of the nasal cavity. These nerve endings are probably activated by pressure changes.