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Culdocentesis is currently a widely used diagnostic technique in gynecology. Although associated with numerous theoretical risks, few complications have been documented in anecdotal reports. Rectal serosal hematoma, an unusual complication of culdocentesis, is described.
To examine steroid-induced biochemical alterations in the mast cell secretory process, rats were injected with intramuscular dexamethasone or saline for 4 days, and serosal mast cells and lung tissue were obtained from each group. Radioligand binding studies utilizing 1-[propyl-1,2-3H]dihydroalprenolol (3H-DHA) demonstrated a 23.1 +/- 0.8% increase in rat lung beta-adrenergic receptors in steroid-treated rats, but the mast cell beta-adrenergic receptors were unaffected. Neither resting mast cell cyclic adenosine 3':5'-monophosphate (cAMP) levels nor the degree of cAMP augmentation induced by isoproterenol were changed by steroid administration. Mast cells from rats treated with dexamethasone released only 48.6 +/- 8.9 and 58.8 +/- 6.0% of the beta-hexosaminidase released from saline-treated rat mast cells when sensitized with anti-dinitrophenyl (DNP) IgE and challenged with DNP-bovine serum albumin antigen or the calcium ionophore A23187, respectively. [3H]serotonin release in cells from steroid-treated rats was 41.8 +/- 7.9 and 87.6 +/- 2.6% of control release stimulated by antigen or A23187, respectively. [14C]arachidonic acid incorporation into mast cell phospholipids followed by antigen or A23187 challenge revealed that cells from dexamethasone-treated rats release 61.3 +/- 15.6% and 62.1 +/- 11.8% of labeled metabolites, respectively, compared to controls. The addition of exogenous arachidonic acid 5 min prior to antigen challenge caused a similar decrease in mediator release in cells from saline- and steroid-treated rats (36.7 +/- 6.1 and 38.4 +/- 0.9%, respectively). When arachidonic acid was added to sensitized cells after specific antigen, no significant changes in beta-hexosaminidase release were noted in either group. Chronic in vivo dexamethasone administration markedly decreases mast cell mediator release without changing resting cAMP levels. The release of arachidonic acid metabolites is reduced in steroid-treated cells, possibly through the inhibition of phospholipases. Exogenous arachidonic acid cannot overcome this inhibition, suggesting that an earlier step in phospholipid metabolism, perhaps involving phospholipase C, may be important.
Chymase, the major neutral protease of the rat serosal mast cell (RMC) secretory granule, causes RMC to release their secretory granules and to oxidatively metabolize endogenous arachidonic acid to prostaglandin D2 (PGD2). The granule markers, endogenous beta-hexosaminidase and exogenously added [3H]serotonin, were released from 2.5 X 10(5) RMC in 50 microliters in parallel and in dose-response fashion, reaching a maximum net percent release of approximately 50% with 0.5 to 1.0 units chymase (15 U/mg)/ml. With incremental concentrations of chymase, the release of granule markers occurred with a shorter lag period and in a greater maximal net percent, whereas the release of PGD2 was dose-related without a reduction in latency to detectable generation. Inhibition of the esterase activity of chymase with lima bean trypsin inhibitor decreased the subsequent mast cell response, indicating that the active site of chymase was required to initiate granule secretion and PGD2 generation. The monophasic indomethacin-resistant rise in cellular cAMP at 15 to 45 sec coincident with the onset of chymase-induced mediator release and PGD2 secretion is similar to that observed with IgE receptor-initiated coupled activation-secretion. The ability of heparin to block the activation function of chymase without inhibition of esterase activity reveals a possible physiologic regulatory mechanism for limiting the potential action of secreted chymase.
Rat serosal mast cells cultured in the presence of heat-inactivated fetal calf serum incorporated (35S) sulfate into heparin proteoglycan of approximately Mr = 750,000 after a 3-h pulse and a 2-h chase. beta-D-Xyloside (0.1 mM) treatments of cultures of rat mast cells resulted in an insignificant increase in total (35S) sulfate incorporation and the appearance of free glycosaminoglycans without a change in proteoglycan size. At higher beta-D-xyloside concentrations, total (35S)sulfate incorporation was inhibited and an increase in the relative glycosaminoglycan content was observed concomitant with a reduction in proteoglycan amount and size. As assessed by susceptibility to digestion by chondroitinase ABC, hydrolysis by nitrous acid, [3H]hexosamine content, and electrophoretic mobility, only heparin chains were polymerized onto the proteoglycan core in all cultures. In contrast, individual glycosaminoglycans which appeared only after beta-D-xyloside treatment were predominantly chondroitin sulfate rather than heparin, indicating that the beta-D-xyloside acceptor supported polymerization of chondroitin sulfate but not of heparin glycosaminoglycan. Thus, the peptide core is an important determinant for the synthesis of heparin glycosaminoglycan by rat peritoneal mast cells.
Lymphatic vessels of small intestine submucosal and serosal-muscular layers in mice and bats have been studied by electron microscopy and tridimensional reconstruction of thin serial sections. Lymphatic endothelium has a continuous appearance, it lacks fenestrations and pores and it is encircled by a thick connective tissue layer. The endothelial wall shows intraendothelial channels, quite similar to those previously described in the lacteal vessels. The author believes that the above mentioned intraendothelial channels, together with pinocytotic vesicles, play a fundamental role in the transendothelial transport of fluids, proteins and macromolecules. Moreover, intercellular specialized junctional complexes do not appear to take any part in this process.
Although rat liver epithelial cell (RLEC) lines have been developed by a number of laboratories, the identity of the clonogenic nonparenchymal progenitors is unknown. To provide insight into the derivation of RLEC, we immunoisolated serosal liver mesothelial cells (LMC) and bile duct epithelial cells and attempted to propagate each epithelial cell population using culture conditions routinely employed to establish RLEC lines. Briefly, the selective reactivity of LMC with two bile duct cell surface markers, OC.2 and BD.2, was exploited to develop an immunocytochemical technique to isolate LMC. Livers were collagenase dissociated, the mesothelial capsule was "peeled" and digested with pronase to destroy contaminating hepatocytes, and rare biliary ductal epithelial cells were immunodepleted using OC.2. LMC were subsequently isolated by selective binding to magnetic beads adsorbed with BD.2 and cultured in supplemented Waymouths 752/1 media containing 10% fetal calf serum. Proliferating BD.2+ LMC rapidly formed epithelial-like monolayers that could be continuously subcultured after trypsinization. In contrast, attempts to establish cell lines from purified OC.2+ bile duct epithelial cells were unsuccessful. Results from reverse transcriptase polymerase chain reaction analysis confirmed that LMC expressed Wilms' tumor transcripts, a lineage marker for mesodermally-derived cells. In summary, our findings clearly demonstrate that LMC can be continuously propagated using culture conditions routinely employed to establish RLEC lines, an observation that supports the contention that some RLEC lines may be derived from LMC.
Argyrophilic nucleolar organizer regions (AgNORs) were determined in 38 pleural and peritoneal effusions from patients with malignant solid tumors. The results were correlated with the cytologic diagnosis and flow cytometric DNA analysis to determine the diagnostic potential of this technique. Cytologically, 13 effusions were benign, 23 malignant and 2 indeterminate (5.2%). The mean AgNOR counts for benign, malignant and indeterminate specimens were 2.99, 3.94 and 3.50, respectively. Low AgNOR counts (< 4.0) were obtained in 12 (90.9%) of the 13 benign, 16 (60.0%) of the 23 malignant and 1 of the indeterminate effusions. High AgNOR counts (> 4.0) were noted in 1 (9.1%) of the benign, 7 (35.0%) of the malignant and 1 (5.0%) of the indeterminate specimens. There was no statistically significant difference between the AgNOR count in benign and malignant effusions (P = .48). All 10 benign effusions analyzed with flow cytometry were DNA diploid. Seven (35.0%) of the 20 cytologically malignant effusions were DNA aneuploid, and 13 (70.0%) were DNA diploid. Proliferative activity was low (< 7.0%) in 23 cases and high (> 7.0%) in 7 (6 malignant and 1 benign). There was no statistical correlation between the AgNOR count and DNA ploidy (P = .11) or proliferative activity (P = .23). We conclude that the AgNOR method lacks sensitivity as a diagnostic tool for serosal cavity effusions.
A nineteen-year-old woman whose Hodgkin's disease had relapsed experienced acral erythema in association with a asymptomatic pericardial friction rub following autologous bone marrow transplantation. An echocardiogram revealed a large pericardial and right pleural effusion. Since blood cultures gave negative results, renal function was normal, and the patient had neither neutropenia nor elevated temperature, an infectious cause was deemed unlikely and invasive procedures were not performed. These effusions resolved spontaneously. We propose that this patient's acral erythema and associated pericardial and pleural inflammation represent cutaneous and serosal toxic reactions to high-dosage chemotherapy that occur with the onset of leukocyte recovery. If so, acral erythema may signal the beginning of a toxic drug reaction. The appearance of erythema associated with lymphocyte recovery is due to immune hypersensitivity secondary to immaturity of the reconstituting immune system. Thus, we recommend that patients with acral erythema be examined for pleuropericarditis, especially if they experience chest pain.
Mast cells and macrophages coexist in the human arterial intima where oxidation of low density lipoproteins (LDL) also takes place during atherosclerosis. To investigate whether mast cells play a role in macrophage-mediated oxidation of LDL, a model system was designed in which mast cells and macrophages were cocultured in incubation medium containing LDL. Stimulation of rat serosal mast cells to induce exocytosis of their cytoplasmic granules was found to inhibit macrophage-mediated oxidation of LDL. The inhibitory effect depended on the ability of mast cell-derived histamine, released from the exocytosed granules into the medium, to bind the copper ions necessary for propagation of the macrophage-initiated oxidation of LDL. In addition to binding free copper ions, the mast cell-derived histamine was also capable of inhibiting oxidation of LDL propagated by copper ions bound to the apolipoprotein B component of the LDL particle. The results indicate that mast cells may prevent cell-mediated oxidation of LDL and imply a potentially preventive role for the mast cell in atherosclerosis.
The proliferative activity of cancer cells, as indicated by numbers of argyrophilic nucleolar organizer regions (AgNORs), at five sites along the invasive margin of the tumor was assessed for 65 patients with histologically proven and curatively operated gastric adenocarcinoma that had invaded the serosa. The mean number of AgNORs in cells at the invasive margin of the tumor was 4.6. Patients with high AgNOR scores (AgNOR score > or = 4.6, n = 34) had a significantly elevated frequency of lymphatic involvement (82%) as compared with patients with low AgNOR scores (AgNOR scores < 4.6, n = 31, 45%), regardless of the size and histologic type of the tumor, and the depth of invasion of the gastric wall. The 5-year survival rate of 33 patients with high AgNOR scores (22.7%) was significantly poorer than that of 31 patients with low AgNOR scores (55.4%, p = 0.024). Thus, the AgNOR score of cancer cells at the invasive margin of the tumor appears to be a good predictor of the prognosis of patients with advanced gastric cancer with serosal invasion.
Mast cells exhibit a biphasic (immediate and delayed) eicosanoid-biosynthetic response after stimulation with particular cytokines or Fc epsilonRI (high affinity receptor for IgE) cross-linking. Treatment of rat serosal connective tissue mast cells (CTMC) with nerve growth factor (NGF) induced only the delayed phase of PGD2 generation that depended on inducible cyclooxygenase-2 (COX-2), but not constitutive COX-1, even though the subcellular distributions of these isoforms were similar. Experiments using several phospholipase A2 (PLA2) isozyme-specific probes and inhibitors suggested that both constitutive cytosolic PLA2 and inducible type IIA secretory PLA2 (sPLA2) are involved in NGF-initiated, COX-2-dependent, delayed PGD2 generation in rat CTMC. A type IIA sPLA2 inhibitor, but neither cytosolic PLA2 nor COX inhibitors, reduced, while adding exogenous type IIA sPLA2 augmented, NGF-induced COX-2 expression and its attendant PGD2 generation, indicating that the sPLA2-mediated increase in delayed PGD2 generation was attributable mainly to enhanced COX-2 expression. Type IIA sPLA2 and its close relative type V sPLA2 associated with fibroblastic cell surfaces increased NGF-induced COX-2 expression more efficiently than the soluble enzymes, revealing a particular juxtacrine sPLA2 presentation route. Surprisingly, catalytically inactive type IIA sPLA2 mutants, which were incapable of promoting arachidonic acid release from cytokine-primed cells, retained the ability to enhance COX-2 expression in CTMC, indicating that the COX-2-inducing activities of sPLA2 are independent of their catalytic functions.
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