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Biomedical subjects

G B Bulkley

Publications and source records attributed to G B Bulkley.

131 records · Page 8Linked to original sources
PubMed1975

Long-term spontaneous regression of malignant melanoma with visceral metastases. Report of a case with immunologic profile.

A case of a 58-year-old woman with viscerally metastatic malignant melanoma is presented 12 years after spontaneous and complete regression of disease. Diagnosis of primary and metastatic lesions was confirmed by review of tissue sections. The presence and subsequent absence of visceral metastases were documented by open liver biopsies. Sections of metastatic lesions revealed extensive necrosis of tumor and infiltration of lymphocytes and plasma cells. Skin testing showed a strongly positive delayed hypersensitivity response to dinitrochlorobenzene (DNCB), to a standard battery of bacterial and fungal antigens, and to two of four preparations of allogeneic melanoma antigens. Values for cell- and serum-mediated cytotoxicity against melanoma cells and the response of the patient's lymphocytes to phytohemagglutinin were slightly above the normal range. A review of the literature reveals 13 other cases of long-term spontaneous regression of melanoma. None of these, however, had biopsy evidence of visceral disease. In each of the 13 cases, regression was associated with an event that might be inferred to have altered the patient's hormonal or immune status. This patient also provides evidence of a complete, spontaneous, and long-term remission of metastatic disease associated with the spontaneous development of host immunity.

Autoantigens↗
PubMed1975

Tuberous xanthoma in homozygous type II hyperlipoproteinemia. A histologic, histochemical, and electron microscopical study.

Histologic, histochemical, and ultrastructural studies of a tuberous xanthoma from a patient with homozygous type II hyperlipoproteinemia showed that all of the lipid was within histiocytic foam cells; no lipid was identified in interstitial regions or in blood vessels. Primitive mesenchymal cells, elongated perivascular and fibroblast-like cells, and lysosome-filled macrophages also were present within the xanthoma, indicating possible stages in the evolution of dermal mesenchymal cells into mature, cholesterol-rich foam cells. Morphologically, the lipid was in four different forms: large droplets, which were the dominant form, and membrane-bound crystals, concentric lamellar bodies, and ceroid. The paucity of membrane-bound lipid forms, relative to the abundant free lipid droplets, indicated that lysosomal digestion was a minor metabolic pathway for the intracellular metabolism of lipid in the xanthoma. Thus, nonlysosomal lipid storage in foam cells is a characteristic tissue response to the underlying metabolic defect in type II hyperlipoproteinemia.

Adolescent↗
PubMedDate not supplied

Suppression of cytokine-induced neutrophil accumulation in rat mesenteric venules in vivo by general anesthesia.

Most studies of neutrophil-endothelial interactions in vivo necessarily require the use of general anesthetic agents which are well known to be immunosuppressive. By using whole-mount preparations of the rat mesoappendix, we were able to study tumor necrosis factor alpha (TNF-alpha) induced neutrophil adhesion to the mesenteric venular endothelium in vivo without necessarily using general anesthesia. TNF-alpha significantly increased venular-neutrophil accumulation in a dose-dependent manner, accumulation was markedly increased at 1, 2, and 4 h, but returned to baseline after 24 h. After these preliminary dose-response and time-course studies, we evaluated the influence of standard clinically effective doses of several commonly used anesthetic agents (thiopental, pentobarbital, ketamine, alpha-chloralose, methoxyflurane, and halothane) on the extent of neutrophil-venular accumulation induced 2 h after intraperitoneal injection of 0.4 mg/kg TNF-alpha, compared to unanesthetized rats. All general anesthetics tested, with the exception of methoxyflurane, significantly suppressed this response. In most cases this suppression was striking (from 60 to 85%) such that a statistically significant proinflammatory response was obscured. Although methoxyflurane also tended to suppress this response to TNF-alpha, it was the only agent that allowed the response to be clearly seen. Because anesthesia markedly suppresses cytokine-induced neutrophil-venular adhesion, this model should provide an important complementary technique to the classical in vivo microcirculatory approaches which do necessarily require general anesthesia.

Anesthesia, General↗
PubMedDate not supplied

Influence of endotoxemia on hepatic energy metabolism in rats with obstructive jaundice.

BACKGROUND/AIMS: A secondary insult in patients with obstructive jaundice can lead to multiple system organ failure. We evaluated the influence of endotoxin on hepatic energy metabolism and hepatic tissue blood flow in obstructive jaundiced rats. MATERIAL AND METHODS: Male Sprague-Dawley rats were divided into a control group, an endotoxin administration group, an obstructive jaundice group, and an obstructive jaundice with endotoxin administration group. To evaluate hepatic energy metabolism, we have measured arterial blood ketone body ratio, and arterial blood total ketone body concentration. Hepatic tissue blood flow was determined by laser Doppler velocimetry. RESULTS: In the endotoxin administration group, no change was observed in hepatic energy metabolism. However, the obstructive jaundice group was associated with decreased hepatic tissue blood flow shortly after the outset of jaundice, while no change was observed in hepatic energy metabolism until 3 weeks later. In the obstructive jaundice with endotoxin administration, a significant decrease in hepatic tissue blood flow and an increase in hepatic energy metabolism were measured. CONCLUSION: Endotoxin administration alone had no influence on hepatic energy metabolism, while endotoxin administration in the presence of obstructive jaundice results in a rapid decrease in hepatic energy metabolism. This occurred as a result of the secondary insult of endotoxin in the setting of decreased hepatic tissue blood flow caused by obstructive jaundice.

Animals↗