No abstract available.
Animals ; Carnitine* ; Heart* ; Myocardium* ; Rats*

BACKGROUND: Use of corticosteroid appears to increase the risk of upper gastrosintestinal side effects associated with NSAIDs. But, there is no study for the effects of these drugs to NSAID induced small intestinal damage. Therefore, we examed the effects of corticosteroid to NSAID induced enteropathy and bacterial translocation. METHODS: Rat received no drug, NSAID alone (diclofenac 80 mg/kg per os), corticosteroid alone (dexamethasone 5 mg/kg intraperitoneal, 2 times) or NSAID with corticosteroid. Amounts of food intakes, body weight, intestinal permeability, enteric aerobic bacterial counts in small and large intestine, serum biochemical profiles, and pathologic findings of ileum were measured. Cultures of the mesenteric lymph nodes, as well as liver, spleen and systemic blood were taken. RESULTS: Diclofenac or dexamethasone alone administration caused gut barrier damage, enteric bacterial overgrowth and increased bacterial translocation. The supplements with dexamethasone increased NSAID induced gut barrier damage, villous atrophy, enteric bacterial overgrowth and bacterial translocation to mesenteric lymph nodes, liver, spleen and systemic blood. Also, these increased diclofenac induced body weight loss, but not hypoproteinemia. CONCLUSION: Corticosteroid increase NSAID induced body weight loss, gut barrier dysfunction, villous atrophy, enteric bacterial overgrowth and bacterial translocation in experimental animals.
Animals ; Anti-Inflammatory Agents, Non-Steroidal ; Atrophy ; Bacterial Load ; Bacterial Translocation* ; Body Weight ; Dexamethasone ; Diclofenac ; Hypoproteinemia ; Ileum ; Intestine, Large ; Intestine, Small ; Liver ; Lymph Nodes ; Permeability ; Rats* ; Spleen

OBJECTIVE: The purpose of this study was to investigate the efficacy and tolerability of atypical antipsychotics (AAPs) with augmentation by blonanserin in schizophrenic patients. METHODS: aA total of 100 patients with schizophrenia who were partially or completely unresponsive to treatment with an AAP were recruited in this 12-week, open-label, non-comparative, multicenter study. Blonanserin was added to their existing AAP regimen, which was maintained during the study period. Efficacy was primarily evaluated using the Positive and Negative Syndrome Scale (PANSS) at baseline and at weeks 2, 4, 8, and 12. Predictors for PANSS response (≥20% reduction) were investigated. RESULTS: The PANSS total score was significantly decreased at 12 weeks of blonanserin augmentation (-21.0±18.1, F=105.849, p<0.001). Moreover, 51.0% of participants experienced a response at week 12. Premature discontinuation of blonanserin occurred in 17 patients (17.0%); 4 of these patients dropped out due to adverse events. The patients who benefited the most from blonanserin were those with severe symptoms despite a treatment with a higher dose of AAP. CONCLUSION: Blonanserin augmentation could be an effective strategy for patients with schizophrenia who were partially or completely unresponsive to treatment with an AAP.
Antipsychotic Agents* ; Humans ; Prospective Studies* ; Schizophrenia

BACKGROUND AND OBJECTIVES: The mucosal epithelium of middle ear and eustachian tube needs hydration to maintain proper amount of moisture. Recent discoveries of various types of water channel proteins (aquaporins ; AQPs) in mucous epithelium suggest that they play critical roles in the regional regulation of water balance. The purpose of this study is to assess the distribution and expression of different subtypes of AQPs in the rat eustachian tube. SUBJECTS AND METHOD: We analyzed the distribution and expression of AQP1, 2, 4, 5, and 7 using RT-PCR, Western blot, and immunohistochemistry study in the rat middle ear and eustachian tube samples. RESULTS: The expression of the mRNA of AQP1, 4, and 5 were observed in the rat eustachian tube and middle ear. The bands of AQP1, 4, and 5 were detected at 28 kDa, 31 kDa, and 26 kDa proteins in the Western blot analysis, respectively. The immunohistochemical analysis demonstrated that AQP1 was expressed in fibroblasts at subepithelial portions of the rat eustachian tube and that AQP4 was observed at the basolateral membrane of the ciliated epithelial cells. The distribution of AQP5 in rat eustachian tube was limited to the apical surface of serous gland cells, but all of the epithelial goblet cells were labeled negative. CONCLUSION: We demonstrated that there are various subtypes of AQP in rat eustachian tube and that they existed at specific cells and sites. This study may be a preliminary study to determine the possibility of relationship between AQP expression and AQP-related disease in the middle ear and eustachian tube.
Animals ; Aquaporins ; Blotting, Western ; Ear, Middle ; Epithelial Cells ; Epithelium ; Eustachian Tube* ; Fibroblasts ; Goblet Cells ; Immunohistochemistry ; Membranes ; Rats* ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger