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Biomedical subjects

H X Bui

Publications and source records attributed to H X Bui.

25 records · Page 2Linked to original sources

Extragenital primary mixed malignant mesodermal tumor.

Malignant mixed mesodermal tumors (MMMT) are infrequent neoplasms characteristically arising in the endometrium. Extragenital MMMTs are extremely rare, with but 11 cases reported in the literature. Previous extragenital MMMTs have been associated with endometriosis, Wolfian duct remnants, and ovarian cyst adenocarcinoma and have been presumed to arise from coelomic and subcoelomic structures. We report a case of a MMMT arising extragenitally in the cul-de-sac in a 54-year-old White female patient in whom disseminated intraperitoneal serosal papillary serous adenocarcinoma of the peritoneum was present. The histogenesis of this rare neoplasm is discussed along with a brief review of previously reported cases.

Carcinoma, Squamous Cell↗

Impaired oxygenation of gastric mucosa in portal hypertension. The basis for increased susceptibility to injury.

Increased susceptibility to mucosal damage is a prominent feature of portal hypertensive gastropathy. Since the portal hypertensive gastric mucosa has extensive microvascular changes, we postulated that the increased sensitivity to mucosal damage could have an ischemic basis. We measured distribution of gastric serosal and mucosal oxygenation in a group of portal hypertensive and sham-operated rats, and then studied the effects of intragastric aspirin. In the basal state, gastric mucosa of portal hypertensive rats had significantly reduced oxygenation compared to controls (24 +/- 5 vs 45 +/- 7 mm Hg PO2, P less than 0.02), while serosal oxygenation was similar between the two groups. Intragastric aspirin produced significantly greater mucosal damage to portal hypertensive rats and mucosal oxygenation was almost one third that of sham-operated controls. Systemic arterial pressures and oxygenation were similar between the two groups. We conclude that there is impairment of gastric mucosal oxygenation and increased mucosal damage by aspirin in portal hypertensive rats compared with sham-operated controls. These results support our hypothesis that the increased sensitivity of the portal hypertensive mucosa to damage is a consequence of impaired mucosal oxygenation.

Animals↗

Protective effect of pentoxifylline on gastric mucosa.

Pentoxifylline (PF) has been shown to increase tissue oxygen tension. This study was performed to determine if PF has a protective effect on the gastric mucosa against alcohol (EtOH)-induced injury. Fasted Sprague-Dawley rats were pretreated with randomized test solution (control, normal saline, or PF, 75 mg/kg) intraperitoneally (ip). At 30 min, 100% EtOH (pH 8.5) was given intragastric. At 90 min, laparotomy was performed and gastric serosal stomach surface oxygen tensions (pO2) were measured. Stomachs were excised and opened and pH was measured. Photographs were taken and sections were obtained for histologic analysis to determine mucosal injury. The PF-pretreated rats had significantly higher serosal pO2 and significantly lower intragastric pH than control animals. There was significantly less gross and histologic mucosal injury in PF-treated animals. We conclude that PF is protective against EtOH gastric mucosal injury. This effect correlates with increased gastric serosal pO2 and is likely due to improved microcirculatory blood flow following PF administration.

Animals↗

Histochemistry and ultrastructure of gastric submucosal vasculature in portal hypertensive rats.

We studied histochemical and ultrastructural characteristics of the gastric submucosal blood vessels in portal hypertensive (PHT) rats. PHT was induced by two-stage ligation of the portal vein. Control rats were sham operated (SO). On the fifth day after surgery portal vein blood pressure was measured and rats were killed under nembutal anesthaesia. Gastric specimens were obtained for histological, histochemical and ultrastructural assessment. PHT rats showed thickening and increased cellularity of submucosal vessels including increase in number and size of endothelial cells. All these mesenchymal cells were vimentin-positive. Thickening of vascular wall in submucosal vessels was also observed ultrastructurally together with prominent elaboration of luminal surface of endothelial cells. These changes were not observed in SO rats. All changes in PHT rats reflect vasculopathic involvement of gastric wall in portal hypertension.

Animals↗

The portal hypertensive gastric mucosa: histologic, ultrastructural, and functional analysis after aspirin-induced damage.

We assessed macroscopic, histologic, ultrastructural, and functional features of aspirin-induced gastric mucosal injury in portal hypertensive and sham-operated rats. Portal hypertension was produced by staged portal vein ligation. Four hours after intragastric acidified aspirin administration, intraluminal pH in portal hypertensive rats was 6.6 +/- 0.2 and 4.3 +/- 0.5 in sham-operated controls (p less than 0.01). Gross mucosal damage was significantly greater in portal hypertensive rats compared with controls (18 +/- 2 versus 7 +/- 1% of total mucosal area). Histologic deep necrosis involved 22 +/- 2% of mucosal section lengths in portal hypertensive rats compared with 7 +/- 1% in sham-operated rats (p less than 0.01). In portal hypertensive rats, histologic and ultrastructural evaluation demonstrated capillary endothelial abnormalities, arterialization of submucosal veins, and markedly greater severity of microvascular damage than in sham-operated controls. Neutralized aspirin (pH, 7.0) did not produce any significant damage detectable grossly, histologically, or by transmission electron microscopy in portal hypertensive rats. We conclude that acid-dependent aspirin-induced gastric mucosal damage is significantly increased in portal hypertension.

Animals↗

Microvascular abnormalities of the portal hypertensive gastric mucosa.

Compared with normotensive mucosa, the portal hypertensive gastric mucosa has increased susceptibility to injury by noxious agents such as alcohol and aspirin, but the mechanism of this phenomenon is unclear. Since the microvasculature of the normal gastric mucosa is an important target of injury by these agents, we studied the histologic and ultrastructural features of gastric vasculature and mucosal microvasculature in rats with portal hypertension (produced by staged portal vein ligation) and in sham-operated rats. In portal hypertensive rats, the gastric mucosa was swollen and hyperemic and the endothelial cells of mucosal microvessels had very prominent enlarged cytoplasm obstructing capillary lumina. Quantitative analysis of transmission electron micrographs demonstrated that in portal hypertensive rats the gastric mucosal capillary endothelium had significantly increased cytoplasmic area (236%), increased pinocytic vesicular area (416%) and increased capillary basement membrane thickness (143%) compared to respective parameters in sham-operated control rats. Arterioles in the muscularis mucosae and in submucosa were thickened, and submucosal veins demonstrated features of arterialization. All these findings indicate that portal hypertension produces definite microvascular changes in the gastric mucosa resulting in compromise of the capillary lumina. These changes may be the basis for the observed morphologic and functional abnormalities of the portal hypertensive mucosa and its increased predisposition to injury.

Animals↗

True synovial metaplasia of breast implant capsules: a light and electron microscopic study.

The formation of true synovial-lined membranes at tissue sites not intimately related to an articulation or a tendon sheath has been described in a variety of pathologic and postsurgical conditions, but until recently has not been well recognized to occur in association with tissue surrounding silicone breast implants. Of 15 cases with resected periprosthetic breast capsules, 7 (47%) demonstrated true synovial metaplasia with capsule-implant interfaces lined by typical synovial cells. Histochemical and immunohistochemical staining reactions were essentially identical to those observed in synovial control cases and featured positive reactions to Alcian blue-periodic acid-Schiff, reticulin, and vimentin. Focal positive immunoreactivity was observed with alpha 1-antitrypsin, alpha 1-antichromotrypsin, lysozyme, and CD68. No immunoreactivity was observed with cytokeratin AE1/AE3, S-100 protein, carcinoembryonic antigen, or basement membrane antigens. Transmission electron microscopy of the lining cells confirmed their true synovial nature with the type A (macrophage-like) cells, type B (fibroblast-like) cells, and intermediate forms or type AB cells identified. We conclude that the cellular lining surrounding silicone breast implants is a true synovial membrane, that synovial metaplasia may occur in nearly one half of all resected periprosthetic capsules, and that awareness of this entity will enable the surgical pathologist to render an accurate histopathologic diagnosis.

Adult↗