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Mucus Secretion (mucus + secretion)
Selected AbstractsTranslocation of viable Aeromonas salmonicida across the intestine of rainbow trout, Oncorhynchus mykiss (Walbaum)JOURNAL OF FISH DISEASES, Issue 5 2006F Jutfelt Abstract The pathogenic bacterium Aeromonas salmonicida is the causative agent of the destructive disease furunculosis in salmonids. Horizontal transmission in salmonids has been suggested to occur via the skin, gills and/or intestine. Previous reports are contradictory regarding the role of the intestine as a route of infection. The present study therefore investigates the possibility of bacterial translocation across intestinal epithelia using Ussing chamber technology, in vitro. Intestinal segments were exposed for 90 min to fluorescein isothiocyanate-labelled pathogenic A. salmonicida. Sampling from the serosal side of the Ussing chambers showed that bacteria were able to translocate across the intestinal epithelium in both the proximal and distal regions. Plating and subsequent colony counting showed that the bacteria were viable after translocation. During the 90 min exposure to A. salmonicida, the intestinal segments maintained high viability as measured by electrical parameters. The distal region responded to bacterial exposure by increasing the electrical resistance, indicating an increased mucus secretion. This study thus demonstrates translocation of live A. salmonicida through the intestinal epithelium of rainbow trout, suggesting that the intestine is a possible route of infection in salmonids. [source] Intrahepatic cholangiocarcinoma diagnosed preoperatively as hepatocellular carcinomaJOURNAL OF SURGICAL ONCOLOGY, Issue 2 2004Masakazu Yamamoto MD Abstract Background Some cases of mass-forming intrahepatic cholangiocarcinoma (ICC) are diagnosed as hepatocellular carcinoma (HCC) based on preoperative imaging and clinical findings. We investigated the backgrounds of such cases. Methods Sixty-seven patients with mass-forming ICC underwent surgery from 1980 to 2002. Twenty-four of these patients received a diagnosis of HCC preoperatively. We compared the group diagnosed as HCC and that diagnosed as ICC. ICC was diagnosed histopathologically in all 67 patients. Results The specific clinical findings included high rates of associated hepatitis C virus infection, high levels of serum alpha fetoprotein, lower levels of serum CA19-9, small dimension of the tumor, hypervascular staining on angiography or computed tomography, lower rates of lymph node metastasis, and high rates of HCC occurrence in the group diagnosed as HCC. None of the patients underwent extrahepatic bile duct resection and most patients did not undergo lymph node dissection in the group diagnosed as HCC. The rates of mucus secretion and the ductal expression of mucin core protein-1 (MUC1) were significantly different between the subgroups. The cumulative survival rates were significantly better in the group diagnosed as HCC than in the group diagnosed as ICC. Conclusion Patients with ICC given a preoperative diagnosis of HCC had distinct clinical features and could be treated with the same operation as HCC patients. J. Surg. Oncol. 2004;87:80,83. © 2004 Wiley-Liss, Inc. [source] The roles of prostaglandin E receptor subtypes in the cytoprotective action of prostaglandin E2 in rat stomachALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 2000H. Araki Summary Aim: To investigate the EP receptor subtype involved in the gastroprotective action of prostaglandin (PG) E2 using various EP receptor agonists in rats, and using knockout mice lacking EP1 or EP3 receptors. Methods: Male SD rats and C57BL/6 mice were used after an 18-h fast. Gastric lesions were induced by oral administration of HCl/ethanol (150 m m HCl in 60% ethanol). Rats were given various EP agonists i.v. 10 min before HCl/ethanol: PGE2, sulprostone (EP1/EP3 agonist), butaprost (EP2 agonist), 17-phenyl-,-trinorPGE2 (17-phenylPGE2: EP1 agonist), ONO-NT012 (EP3 agonist) and 11-deoxyPGE1 (EP3/EP4 agonist). In a separate study, the effect of PGE2 on HCl/ethanol lesions was examined in EP1 - and EP3 -receptor knockout mice. Results: Gastric lesions induced by HCl/ethanol were dose dependently prevented by PGE2; this effect was mimicked by sulprostone and 17-phenylPGE2 and was significantly antagonized by ONO-AE-829, an EP1 antagonist. Neither butaprost, ONO-NT012 nor 11-deoxyPGE1 exhibited any protective activity against HCl/ethanol-induced gastric lesions. PGE2 caused an inhibition of gastric motility as well as an increase of mucosal blood flow and mucus secretion, the effects being mimicked by prostanoids activating EP1 receptors, EP2/EP3/EP4 receptors and EP4 receptors, respectively. On the other hand, although HCl/ethanol caused similar damage in both wild-type mice and knockout mice lacking EP1 or EP3 receptors, the cytoprotective action of PGE2 observed in wild-type and EP3 -receptor knockout mice totally disappeared in mice lacking EP1 receptors. Conclusion: The gastric cytoprotective action of PGE2 is mediated by activation of EP1 receptors. This effect may be functionally associated with inhibition of gastric motility but not with increased mucosal blood flow or mucus secretion. [source] Species differences in bradykinin receptor-mediated responses of the airwaysAUTONOMIC & AUTACOID PHARMACOLOGY, Issue 1 2002K. M. Ellis Summary1 Bradykinin (BK) is a nine amino acid peptide (Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg) formed from the plasma precursor kininogen during inflammation and tissue injury. The actions of BK are mediated by G protein-coupled cell surface receptors, designated B1 and B2. 2 BK has a plethora of effects in the airways including bronchoconstriction, bronchodilation, stimulation of cholinergic and sensory nerves, mucus secretion, cough and oedema resulting from promotion of microvascular leakage. These airway effects are mediated in the main by the B2 receptor subtype. 3 BK acts mainly indirectly, primarily through airway nerve activation, but also by the release of prostanoids, thromboxanes and nitric oxide (NO). 4 Airway responses to BK have been studied in detail in guinea-pigs, mice, sheep and rats. This review describes the effects of BK in these species and draws comparison with its effects in normal humans and patients with respiratory diseases. 5 Despite its many and varied effects in the airways of animals and man, the exact contribution of BK to airways disease remains unclear. [source] Hypertonic saline nasal provocation and acoustic rhinometryCLINICAL & EXPERIMENTAL ALLERGY, Issue 4 2002J. N. Baraniuk Summary Background Hypertonic saline (HTS) acts as an airway irritant in human nasal mucosa by stimulating nociceptive nerves and glandular secretion. HTS does not change vascular permeability. In asthma, HTS causes airflow obstruction. Objective To determine the effect of HTS on mucosal swelling using acoustic rhinometry (AcRh). Potential vasodilator effects were controlled by maximally constricting mucosal vessels with oxymetazoline (Oxy). Method Normal subjects had AcRh before and 30 min after either 0.05% Oxy or saline (0.9% NaCl) nasal treatments. Nasal provocations followed immediately with five step-wise incremental escalating doses of HTS administered at 6-min intervals. AcRh was performed 1, 3 and 5 min after each HTS administration, and then after blowing the nose at 5 min. The minimum cross-sectional area (Amin), volume of the anterior 6 cm of nasal cavity (V6) and incremental changes from pre-drug treatment baseline levels (,, mean ±,SEM) were calculated. Results Oxy increased Amin by 46% (, = 0.48 ± 0.07 cm2, P = 0.0001) and V6 by 53% (, = 9.9 ± 1.5 mL, P < 1 × 10,7) during the first 30 min. Saline (vehicle) treatment had no effect. The maximum HTS dose had no effect after 1 or 3 min. However, in the 4th and 5th minutes there were reductions in Amin (, = 0.07 ± 0.03 cm2, P = 0.035) and V6 (, = 1.57 ± 0.42 mL, P = 0.004) with an increase in the weight of secretions (, = 700 ± 100 mg, P < 0.05). Blowing the nose returned Amin and V6 towards baseline. Oxy had no effect on HTS-induced changes in Amin, V6, pain, rhinorrhea or weight of secretions. Conclusion HTS induced nociceptive nerve stimulation and mucus secretion, and reduced V6 and Amin. Oxy caused vasoconstriction but did not alter HTS-induced effects. HTS may stimulate neurogenic axon response-mediated glandular secretion that contributes to perceptions of nasal obstruction in normal subjects. [source] Mixed Nasal Mucus as a Model for Sinus Mucin Gene Expression StudiesTHE LARYNGOSCOPE, Issue 2 2002FRCS, Mahmoud S. Ali MSc Abstract Objective/Hypothesis It is necessary to obtain sinus mucus from the paranasal sinus cavities to study mucin gene expression occurring in the sinuses during chronic sinusitis. This requires an invasive procedure to access the sinus cavity. There are embryological as well as histological similarities between nasal and sinus epithelia; therefore, we postulated that the mucin expression in the secreted nasal and sinus mucins might be similar. Nasal mucus, which can be obtained easily, could then replace sinus mucus in these studies. Study Design Sinus and nasal mucus from six patients with chronic sinusitis were analyzed in this study. Methods High-molecular-weight glycoproteins (mucins) were isolated and purified by sequential density gradient centrifugation in caesium chloride (CsCl). Enzyme-linked immunosorbent assay was performed to identify the antigenic identity of these mucins. Results The MUC2, MUC5AC, and MUC5B mucin genes were all expressed in the nasal and sinus mucus secretions. Antigenic studies showed an inverse relationship between MUC2 and MUC5AC expression in nasal and sinus mucus secretions. The MUC5B gene was the major mucin gene expressed in sinus mucus but not in nasal mucus. Expression of MUC2 was significantly higher in sinus mucus. Expression of MUC5AC was different between nasal and sinus mucus. Conclusions Individual mucin expression in sinus and nasal mucus was markedly different. From this preliminary study, we conclude that nasal mucus is not a suitable substitute for sinus mucus in sinus mucin gene studies and that different pathological processes are taking place in nasal and sinus tissue in chronic sinusitis. [source] | ||||||||||