Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “SEROSITIS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 37 records · Page 2Linked to original sources

Reversible inhibition by lanthanum of the hydrosmotic response to serosal hypertonicity in toad urinary bladder.

In the urinary bladder of amphibia, hypertonicity of the serosal bath (SH) evokes an increase in transepithelial water permeability, the characteristics of which resemble the response to antidiuretic hormone (ADH). The ionic dependency, in particular for Ca2+, appears very similar for SH- and ADH-induced water fluxes. In the present experiments La3+ was used as a probe to study the Ca2+-dependency of the hydrosmotic response to SH in isolated urinary bladder of the toad Bufo marinus. Addition of La3+ (5 mM) on the serosal side of the membrane produced a significant and reversible increase in basal transepithelial water flux. The hydrosmotic response elicited by adding 250 mM mannitol to the serosal Ringer's solution was inhibited by 30% in the absence of serosal Ca2+. Similarly, the hydrosmotic response to SH was inhibited by 37%, 30% and 40% when 5 mM La3+ was added to the serosal medium 30 min before, concommitantly with, or 60 min after induction of SH. The inhibition of transepithelial water flux observed in the absence of serosal Ca2+ or in the presence of serosal La3+ was reversible. The results support a critical role for Ca2+ in the modulation of transepithelial water permeability in the urinary bladder of amphibia. Ca2+ presumably exerts its effects at a post-cyclic AMP step.

Animals↗

Electrogenic Cl- absorption by Amphiuma small intestine: dependence on serosal Na+ from tracer and Cl- microelectrode studies.

The Na+ requirement for active, electrogenic Cl- absorption by Amphiuma small intestine was studied by tracer techniques and double-barreled Cl- -sensitive microelectrodes. Addition of Cl- to a Cl- -free medium bathing in vitro intestinal segments produced a saturable (Km = 5.4 mM) increase in short-circuit current (ISC) which was inhibitable by 1 mM SITS. The selectivity sequence for the anion-evoked current was Cl- = Br- greater than SCN- greater than NO-3 greater than F- = I-. Current evoked by Cl- reached a maximum with increasing medium Na concentration (KM = 12.4 mM). Addition of Na+, as Na gluconate (10 mM), to mucosal and serosal Na+-free media stimulated the Cl- current and simultaneously increased the absorptive Cl- flux (JCl m----s) and net flux ( JClnet ) without changing the secretory Cl- flux ( JCls ----m). Addition of Na+ only to the serosal fluid stimulated JClm ----s much more than Na+ addition only to the mucosal fluid in paired tissues. Serosal DIDS (1 mM) blocked the stimulation. Serosal 10 mM Tris gluconate or choline gluconate failed to stimulate JClm ----s. Intracellular Cl- activity ( aiCl ) in villus epithelial cells was above electrochemical equilibrium indicating active Cl- uptake. Ouabain (1 mM) eliminated Cl- accumulation and reduced the mucosal membrane potential (psi m) over 2 to 3 hr. In contrast, SITS had no effect on Cl- accumulation and hyperpolarized the mucosal membrane. Replacement of serosal Na+ with choline eliminated Cl- accumulation while replacement of mucosal Na+ had no effect. In conclusion by two independent methods active electrogenic Cl- absorption depends on serosal rather than mucosal Na+. It is concluded that Cl- enters the cell via a primary (rheogenic) transport mechanism. At the serosal membrane the Na+ gradient most likely energizes H+ export and regulates mucosal Cl- accumulation perhaps by influencing cell pH or HCO-3 concentration.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗

Serosal invasion in TNM staging of mass-forming intrahepatic cholangiocarcinoma.

BACKGROUND/PURPOSE: The Liver Cancer Study Group of Japan established a tumor-nodule-metastasis (TNM) staging system for mass-forming intrahepatic cholangiocarcinoma, with T determined by tumor number and size and vascular or serosal invasion. Serosal invasion is not considered in the designation established by the International Union Against Cancer. METHODS: Sixty-three patients who underwent hepatic resection for mass-forming intrahepatic cholangiocarcinoma were investigated retrospectively, with the investigation including univariate and multivariate analyses of potential prognostic factors. RESULTS: By log-rank test, tumor size more than 3.0 cm, vascular invasion, lymph node metastasis, intrahepatic metastasis, and involved resection margin, but not serosal invasion, were associated significantly with poor prognosis. Even in patients with serosal invasion, the postoperative outcome was much better in those without than in those with vascular invasion. Multivariate analysis identified vascular invasion, lymph node metastasis, and an involved resection margin as independent prognostic factors. When serosal invasion was excluded from tumor staging, the 5-year survival rates became more clearly stratified: 100% in those with stage I disease, 62% in those with stage II, 25% in those with stage III, and 7% for patients with stage IV. CONCLUSIONS: Serosal invasion showed no survival impact after hepatic resection for mass-forming intrahepatic cholangiocarcinoma. When serosal invasion was omitted from the TNM staging proposed by the Liver Cancer Study Group of Japan, stratification of postoperative survival between stages was more effective.

Adult↗

Effects of a small serosal hydrostatic pressure on sodium and water transport and morphology in rabbit gall-bladder.

1. In order to investigate the mechanism of serosal pressure-induced inhibition of isosmotic fluid transport, the effect of 4.5 cm water serosal pressure on spontaneous water transfer (J(v)) in rabbit gall-bladders was measured (in the presence of a supporting soft nylon net on the mucosal side) in a modified Ussing chamber. This allowed unidirectional Na(+) fluxes ([Formula: see text] and [Formula: see text]), transepithelial potential difference and resistance (R(t)) to be measured simultaneously. The effects of the serosal pressure were also investigated by light and electron microscopy.2. During pressure application, R(t) increased due to a covering effect of the mucosal support. The serosal pressure caused a parallel decrease in J(v) and net Na(+) transport ([Formula: see text]) across the free epithelial surface of 80-85%. About 85% of the decrease in [Formula: see text] was due to a decrease in [Formula: see text].3. After inhibition of 93% of fluid absorption by serosal 10(-3)M-ouabain, pressure-induced change in J(v) was only 8% of the spontaneous fluid transport rate.4. Control Na(+) flux ratio ([Formula: see text]) was 3.5. The pressure-induced increase in steady-state [Formula: see text] of 30-35% therefore contributed little to the decrease in [Formula: see text]. Further, this increase in [Formula: see text] was completely prevented by mucosal 10(-3) M-amiloride.5. All pressure-induced effects on transport and electrical parameters were reversible.6. The light microscopical and scanning electron microscopical results showed that half of the epithelial surface was covered by the nylon net following serosal pressure application. Ruptures in the epithelium were not seen. Thin section and freeze fracture electron microscopy demonstrated continuous, well developed tight junctions both in control and experimental condition.7. It is concluded that a serosal pressure of only 4.5 cm water causes inhibition of a cellular active Na(+) and water transport with only minimal, if any, contribution from paracellular filtration. This would seem incompatible with the concept that an active ion transport mechanism localized in the basolateral cell membrane is responsible for transepithelial fluid transport. The possibility of a mechanical fluid transport mechanism via elements of a tubulo-cisternal endoplasmic reticulum is raised.

Amiloride↗

Magnitude of serosal changes predicts peritoneal recurrence of gastric cancer.

BACKGROUND: Peritoneal dissemination is the most frequent mode of recurrence in patients with gastric cancer. We tried to identify factors that predict peritoneal recurrence with high sensitivity. STUDY DESIGN: Clinical and pathologic data from 587 consecutive patients with gastric cancer were reviewed retrospectively. The stepwise Cox proportional hazards regression model was used to assess the prognostic significance of the magnitude of serosal changes. Multiple stepwise logistic regression analysis was used to determine factors associated with peritoneal recurrence in 375 patients who underwent curative resection. RESULTS: The 5-year survival rate of patients with S2 disease (greatest dimension of macroscopic serosal changes >/= 2.5 cm) was 18%, which was worse than S0 (no serosal changes) and S1 disease (macroscopic serosal changes < 2.5 cm)(p < 0.001). Patients with S0 tumors who underwent curative resection had the best 5-year survival rate. Multivariate analyses indicated that the magnitude of serosal changes was an independent prognostic factor for survival both overall and after curative resection. Logistic regression analysis showed that peritoneal recurrence was more than four times as likely with S2 than with S0 or S1 tumors. The sensitivity for predicting peritoneal recurrence was 79%; the sensitivity of cytologic examination was 38%. CONCLUSIONS: Magnitude of serosal changes is easy to measure intraoperatively and predicts peritoneal recurrence of gastric cancer with greater sensitivity than conventional peritoneal lavage cytology.

Gastrectomy↗

Alanine efflux across the serosal border of turtle intestine.

The exit of alanine across the serosal border of the epithelial cells of turtle intestine was measured by direct and indirect techniques. A decrease or an increase in cell Na did not affect the amino acid flux from cell to serosal solution. Cells loaded with Na and alanine did not exhibit any extrusion of alanine when their serosal membranes were exposed to an Na-free medium containing alanine. However, substantial amino acid extrusion was observed across the mucosal cell border under similar conditions. Although alanine flux across the serosal membrane appeared to be Na-independent, it showed a tendency toward saturation as cellular alanine concentration was elevated. The results are consistent with the postulate that the serosal and mucosal membranes of intestinal cells are asymmetrical with respect to amino acid transport mechanisms. The serosal membrane appears to have an Na-independent carrier-mediated mechanism responsible for alanine transport while transport across the mucosal border involves an Na-dependent process.

Alanine↗

The role of prostaglandins in the bradykinin-induced activation of serosal afferents of the rat jejunum in vitro.

1. This study was performed to elucidate the role of prostaglandins in the action of bradykinin on serosal afferent neurones supplying the rat jejunum. Extracellular recordings of multi-unit activity were made from serosal afferents in isolation, using a novel in vitro preparation. The discharge of single afferents within the multi-unit recording was monitored using waveform discrimination software. 2. All afferents tested were both mechano- and capsaicin sensitive. Application of bradykinin elicited increases in whole nerve discharge in a concentration-dependent manner. The agonist potency estimate (EC50) was 0.62 +/- 0.12 microM and is consistent with an interaction at the B2 receptor subtype. 3. The stimulatory effect of bradykinin on serosal afferents was antagonized by a specific antagonist of the B2 receptor, HOE140. In contrast, a selective B1 receptor antagonist, [des-Arg10]HOE140, had no effect. The IC50 estimate obtained for HOE140 was 1.6 nM and again consistent with an interaction at B2 receptors. 4. The response to a submaximal concentration of bradykinin (1 microM) was significantly reduced to 24.4 +/- 54.9 % of control following blockade of cyclo-oxygenase activity with naproxen (10 microM). The addition of 1 microM prostaglandin E2 (PGE2), in the presence of naproxen, had no direct effect on afferent activity, but fully restored the response to bradykinin in 15 single afferents. 5. In summary, bradykinin stimulates serosal afferents by a direct action on kinin B2 receptors that are present on serosal afferent terminals. The response to bradykinin is dependent on the presence of prostaglandins, particularly PGE2. We suggest that bradykinin has a self-sensitizing action, whereby it stimulates the release of PGE2, which in turn sensitizes the endings of serosal afferent neurones responsive to bradykinin.

Animals↗

Effects of changes in the composition of the serosal solution on the electrical properties of the toad urinary bladder epithelium.

1. The potential profile and the cellular and paracellular transepithelial resistances of the toad urinary bladder were measured, by means of micro-electrode techniques, as functions of the osmolality of the serosal solution. 2. Reductions in serosal osmolality (that increase the rate of active sodium transport) produced proportional decreases in the electrical resistances of the apical and basal-lateral cell membranes, while the changes in resistance of the paracellular pathway were more complex. The apical membrane potential increased. 3. Increases in serosal osmolality (that decrease sodium transport) produced increases in the electrical resistances of both cell membranes, and moderate reduction in the paracellular resistance. The polarity of the apical membrane potential reversed. 4. These results indicate that reductions in serosal solution osmolality stimulate sodium transport by increasing both the sodium permeability of the luminal cell membrane (thus increasing sodium entry), and the electromotive force generated at the serosal border of the cell, thus enhancing the rate of sodium pumping. Conversely, increases in osmolality reduced sodium transport by reducing both the sodium permeability of the luminal membrane and the serosal membrane electromotive force.

Animals↗

Serosal and cutaneous recordings of gastric myoelectrical activity in patients with gastroparesis.

The aims of this study were to 1) investigate gastric myoelectrical activity in patients with gastroparesis, 2) validate the cutaneous electrogastrogram (EGG) in tracking the frequency change of the gastric slow wave, and 3) investigate the effect of electrical stimulation on gastric myoelectrical activity. Gastric myoelectrical activity was recorded in 12 patients with documented gastroparesis using serosal electrodes for > 200 min in each subject. All recordings were made at least 4 days after surgery. Each session consisted of a 30-min recording in the fasting state and a 30-min recording after a test meal. The test meal (liquid or mixed) was selected according to patient's tolerance. Electrical stimulation was performed in three subjects via the serosal electrodes at a frequency of 3 cycles/min. Gastric myoelectrical activity was recorded using serosal electrodes in each session. The serosal recording showed slow waves of 2.5 to 4.0 cycles/min in all 12 subjects. Absence of spikes was noted in 11 of the 12 subjects. The simultaneous serosal and cutaneous recording of gastric myoelectrical activity showed that the frequency of the EGG was exactly the same as that of the serosal recording. Liquid meals resulted in a significant decrease in slow-wave frequency (Student's t test, P = 0.006), and the EGG accurately reflected this change. Electrical stimulation had no effect on the frequency of the gastric slow wave and did not induce spikes.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Antigen-induced release of histamine from rat tissues in vitro: dissociation in development of serosal mast cell, lung tissue, and tracheal tissue response capacity.

We examined the temporal development and the fading in Sprague Dawley rats, actively sensitized to ovalbumin (OA), of the capacity of serosal mast cells, chopped lung tissue, and occasionally chopped tracheal tissue, to respond at antigen challenge in vitro with histamine release. Response capacity of both serosal mast cells and lung tissue developed within 2-3 weeks after injection of 1 microgram OA or more together with 100 mg of alum. Maximum response capacity was observed in cells and tissue from animals injected with 10 micrograms OA, part of the response capacity then remained until 3 months after immunization. Development of serosal mast cell reactivity was occasionally dissociated from that of lung tissue. When low amounts of alum (1 or 10 mg) were employed as adjuvant, lung tissue reactivity could be induced in the virtual absence of serosal mast cell response capacity. Silica gel was less efficient than alum as an adjuvant for induction of a primary response, but 'secondary' tissue responses could be induced when silica gel was used as an adjuvant. Pretreatment of the animals with cyclophosphamide before the booster injection enhanced and prolonged the response capacity of lung tissue. Animals injected with OA together with Freund's complete adjuvant did not provide responding serosal mast cells; response capacity of lung tissue varied with immunization dose of antigen. Antigen-induced histamine release from chopped tracheal tissue did not correlate to response capacity of lung tissue. Thus, the development in the rat of response capacity with respect to antigen-induced histamine release dissociates from serosal mast cells, lung tissue, and tracheal tissue.

Adjuvants, Immunologic↗

Transport of salicylamide from intestinal lumen to serosal compartment.

This study was aimed to clarify the fate of the perfused drug and the characteristics of the serosal compartment. A portion of rat small intestine immersed in a solution regarded as the serosal compartment was perfused in situ and the permeability of drugs into the mesenteric venous blood and into the serosal solution were determined. The cumulative amounts of salicylamide (SAM) transported to the mesenteric venous blood and the serosal compartment were 19.7 and 45.8% of amount disappeared from the intestinal lumen, respectively and those of benzoic acid (BA) were 47.4 and 12.7%, respectively. The permeability of SAM into the serosal compartment was 2.8 times of that into the mesenteric venous blood, while the permeability of BA into the serosal compartment was only one fourth of that into the mesenteric venous blood.

Animals↗

Utility of serosal stamp cytology as an indicator for high-risk peritoneal metastasis in colorectal cancer surgery.

BACKGROUND/AIMS: Although peritoneal lavage cytology is widely performed during surgery for gastric cancer and the results have been reported to provide an accurate prognostic factor, its value has not been well established in colorectal cancer. In this study, we demonstrated the utility of serosal stamp cytology from the viewpoint of cell adhesion molecules. METHODOLOGY: Between 1997 and 1999, peritoneal lavage cytology and serosal stamp cytology were performed in 34 patients with resectable colorectal cancer. Epithelial cadherin (E-cadherin) was examined as an index of the progress degree of peritoneal metastasis. RESULTS: Although peritoneal lavage cytology was positive in one case, serosal stamp cytology was positive in 10 cases. E-cadherin expression was lost in all peritoneal lavage cytology and/or serosal stamp cytology positive patients. CONCLUSIONS: Our data indicate that serosal stamp cytology is more sensitive and simple than peritoneal lavage cytology. Serosal stamp cytology may be useful in identifying patients at high risk for peritoneal recurrence.

Adult↗

Serosal membranes (pleura, pericardium, peritoneum). Normal structure, development and experimental pathology.

This monograph offers a comprehensive review of the present knowledge of the structure of the serosal coverings of the pleural, pericardial, and peritoneal cavities in humans and laboratory animals. The authors provide data from their own research--with transmission and scanning electron microscopy--on the structure of the main components of the serosal membranes: mesothelial cells, underlying basal lamina, and submesothelial connective tissue layer. Two main types of mesothelial cells (flat and cubic) are distinguished and their distribution on the parietal serosal sheets and on the visceral coverings of various organs is described. The openings between mesothelial cells (stomata) and their relations with lymphatic lacunae are described thoroughly. Special reference is made to the serosal accumulations of lymphoid tissue (milky spots). The transcellular and intercellular transport to and from serosal cavities is studied by means of horseradish peroxidase tracing experiments. The prenatal and postnatal developmental studies are focused on human and rat pleura. The alterations of serosal membranes after experimental hemothorax, pneumonectomy, and peritonitis caused by Pseudomonas aeruginosa application suggest the existence of early, reversible, and late, definite periods.

Animals↗

Tumors of serosal tissue origin.

Primary serosal neoplasms demonstrate a wide spectrum of growth patterns and biologic aggressiveness. The adenomatoid tumor is uniformly benign, whereas the diffuse malignant mesothelioma pursues a downhill clinical course, rapidly leading to fatality. The cystic peritoneal mesothelioma occupies an intermediate position characterized by persistent and/or recurrent disease but without progression to death. The distinction of an epithelial mesothelioma from metastatic adenocarcinoma remains a challenging problem. In the vast majority of cases, this can be accomplished by combining routine histochemistry, immunocytochemistry, and electron microscopy. The absence of epithelial mucins and nonreactivity with antibodies to CEA strongly favor mesothelioma. Ultrastructurally observed long, thin, sinuous surface microvilli without a glycocalix, well-developed desmosomes, and abundant tonofilaments add further support for a primary serosal neoplasm. The sarcomatoid mesothelioma can easily be confused with a chest-wall sarcoma. Despite lacking ultrastructural evidence of "epithelial" differentiation, immunocytochemical studies demonstrate cytokeratin. This distinguishes the sarcomatoid mesothelioma from most soft-tissue sarcomas. There remains a small number of cases, particularly those in the "poorly differentiated" or "transitional" category, in which the distinction between mesothelioma and metastatic carcinoma remains difficult. In this situation, it is imperative that all the clinical information be closely reviewed and a diligent search for a primary site be carried out. There are many parallels between reactive and neoplastic serosal tissue. The desmoplastic/sarcomatoid mesothelioma morphologically and immunocytochemically resembles the reactive multipotential subserosal cell (MSC) of injured serosal tissue, whereas the adenomatoid tumor, cystic peritoneal mesothelioma, and epithelial mesothelioma resemble surface mesothelium. The poorly differentiated mesothelioma resembles a stage of maturation between the two extremes, and thus the term "transitional" mesothelioma is suggested. The localized fibrous tumor of the pleura is unique among all other serosal neoplasms in its failure to express cytokeratin. It more closely resembles the unspecialized connective tissue fibroblast of normal serosal tissue, and thus may be more analogous to a soft-tissue tumor than to the remaining mesothelial-derived neoplasms.

Asbestos↗

Hepatitis B virus: a possible cause of serositis in hemodialysis patients.

An epidemiologic survey in a maintenance hemodialysis population of 300 patients was undertaken to relate the appearance of acute serositis (pericarditis, pleuritis or ascites) to HBsAg antigenemia. A significant number of incidents of serositis occurred in patients acutely or chronically infected with hepatitis B surface antigen (HBsAg) suggesting an etiologic role for the virus in the serositis of uremia. In 2 patients with both end-stage renal disease and chronic HBsAg antigenemia, immunofluorescent studies of serosal tissues showed fluorescent clusters interpreted to be HBs antigen-antibody complexes. It is concluded that an immunologic response to viremia may be one of the causes of serositis in uremia.

Adult↗

Circulating immune complexes: possible toxins responsible for serositis (pericarditis, pleuritis, and peritonitis) in renal failure.

In 71 patients (41 men, 30 women) with advanced renal failure maintained on hemodialysis (HD), continuous ambulatory peritoneal dialysis (CAPD), or within 8 weeks after the commencement of dialysis therapy (ED), studies were performed searching for evidence of serositis and the blood levels of circulating immune complexes (CIC), measured by the polyethylene glycol precipitation method. Mean CIC levels were elevated in these patients compared to the 58 healthy subjects (mean +/- SEM 725 +/- 40, and 260 +/- 34 micrograms/ml, respectively). Serositides were significantly more prevalent in ED patients compared to both remaining groups, and tended to occur less frequently in CAPD than in HD patients. CIC levels were significantly lower in CAPD than in ED patients. The levels of CIC were significantly higher in patients with serositis compared to those without evidence of serosal inflammation (mean +/- SEM 868 +/- 71 and 677 +/- 53 micrograms/ml, respectively). In addition, immune complex-like materials were found in all of 4 effusate samples and in 10 of 27 peritoneal dialysates. It is suggested that immune complexes may be the 'uremic toxins' responsible for the serositis of renal failure, and may be secreted into serous effusions. Immune complex-like material can be removed in peritoneal dialysate, which may contribute to the lower CIC levels and lower incidence of serositis in the CAPD patients.

Adult↗

Increased CA 125 serum levels in patients with advanced acute leukemia with serosal involvement.

BACKGROUND: CA 125 is a tumor marker used for the diagnosis and monitoring of ovarian carcinoma. This marker also has been found to be increased in patients with serosal effusion derived from nonneoplastic inflammatory disease and in a few instances of advanced non-Hodgkin lymphoma with serosal involvement. METHODS: CA 125 levels were tested in the serum of 15 patients with acute myeloblastic leukemia (AML) at the time of diagnosis and in 3 patients with advanced leukemia with serosal involvement. In two patients with elevated serum CA 125 levels, a CA 125 assay was performed on leukemic cells and on the supernatant fluid of short term liquid culture. RESULTS: Increased serum CA 125 was found in the three patients with acute leukemia with extramedullary localization and serosal effusion, whereas it was normal in 15 AML patients tested at the time of diagnosis. CA 125 was not detectable in leukemic cell extracts nor in the supernatant fluid of primary cultures. CONCLUSIONS: These results indicate that leukemic cells were unable to produce CA 125 and suggest that its elevation in the serum is likely due to a serosal inflammatory reaction caused by the leukemic infiltration.

Adult↗

Serosal imprint cytology in colonic cancer: a simple staging technique.

Accurate staging of colonic cancer is essential in defining the rational use of adjuvant treatments. Recent studies have shown that prognostic accuracy can be significantly improved by recognition of primary tumour extension to the free serosal surface. This study compares the technical results of serosal imprint cytology with the results of histology in assessing serosal involvement. When analysed in terms of the modified Dukes' staging the results of cytology imprints taken from the peritoneum overlying the colonic primary were positive for tumour cells in 4/13 Dukes' B, 7/14 Dukes' C, and 5/9 metastatic cancers. Imprint cytology was positive in 6/7 Dukes' B and C cases with histological serosal invasion and was suspicious in the remaining case. However, a further 5/20 cases without identified invasion on routine histology also had positive cytology. Imprint cytology is an adjunct to routine histology which is easily performed and allows more precise staging of serosal involvement in Dukes' B and C colonic cancers. Final evaluation of this technique requires long-term follow-up of patients.

Colon↗