Tumor enucleation of renal cell carcinoma: operative technique, DNA cytometry results, complications.
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Biomedical subjects
Publications and source records attributed to F Steinbach.
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The release of gastric somatostatinlike immunoreactivity and gastrin was studied in rats with chronic achlorhydria induced by the substituted benzimidazole BY 308. In vitro, stimulation of gastrin release by acetylcholine was slightly enhanced after 1 day of treatment but no further effects were observed compared to placebo controls. Four weeks of treatment evoked marked gastrin hypersecretion, which was atropine-resistant. Stimulation of gastrin release was inversely correlated to enhancement of basal gastrin levels. Chronic achlorhydria distinctly reduced somatostatin responses to isoproterenol, whereas potent stimulation was observed in controls. Treatment with BY 308 for 1 wk was associated with fully developed gastrin hypersecretion but isoproterenol-stimulated somatostatin release was still unaffected. Hypergastrinemia accompanied by increased antral gastrin and reduced antral and fundic somatostatin concentrations was also found in vivo after 4 wk of treatment with BY 308. It is concluded that chronic achlorhydria not only enhances storage and secretion of gastrin but also diminishes the secretion and tissue stores of somatostatin; adaptive changes of the somatostatin cell occur, however, with a much longer delay.
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Computed tomography (CT) was performed in 28 patients 2 weeks to 120 months after enucleation of renal cell carcinoma. The postoperative defect could be exactly localized in all patients. A wedge-shaped (N = 11) or concave (N = 9) morphology was typical. No dependence between morphology of the defect and localization or size of the tumor or the operative technique was observed. The defects were smaller (1.9 cm) than the original prominent tumors (3.6 cm). Defect size was dependent on the operative technique: closure by suture of the renal capsule in smaller defects or by fat flap in larger ones. Postoperative hematomas or delayed perfusion in the adjacent parenchyma were seen in five patients. Tumor recurrence was correctly diagnosed in one patient.
Dendritic cells (DCs) are professional antigen-presenting cells (APCs), and classical DCs, such as Langerhans cells (LCs) or interdigitating DCs (IDCs) are known to be the most potent stimulators of T lymphocytes. Earlier, several groups described the generation of DCs from monocytes, starting with peripheral blood mononuclear cells (PBMCs), adherent cells or magnetic bead-purified CD14+ cells. Although modifications of the original protocols have already been described, some questions relevant to clinical application and basic studies have not yet been addressed. Granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin-4 (IL4) appear to be necessary, but are not sufficient for the differentiation of monocyte-derived dendritic cells (MoDCs), as indicated by the failure to generate such cells under serum-free conditions. Using adherence purified monocytes, we first investigated the amount of GM-CSF and IL4 required for the differentiation of DCs. Consecutive kinetic studies during the differentiation period were designed to demonstrate how monocytes acquire the phenotype and function of DCs. The results showed that small amounts of GM-CSF and IL4 were required to generate MoDC which acquired their phenotype and function within 4 days. IL13 may substitute for IL4, whereas IL10, TNF alpha or IFN gamma inhibited the generation of MoDCs.
Recent observations indicate that an antiinflammatory process may play a role in the metastatic cascade of renal cell carcinoma (RCC). Therefore, we compared the expression of cytokines from primary human RCC cultures, from established renal carcinoma cells and those from corresponding proximal renal tubulus cells. For this purpose the different cell types were treated with well defined and with bacterial substances such as the lipopolysaccharide, the staphylococcal enterotoxin B, a superantigen, or a combination of the calcium ionophore A23187 and phorbol 12-myristate-13-acetate. The resulting cell supernatants were analyzed for the proinflammatory cytokines (TNF-alpha, IL-6), the chemotactic active interleukin-8 as well as cytokines from T-helper type I (IL-2, IFN-gamma, IL-12) and type II (IL-4, IL-10). In parallel, the expression of cytokine-specific m-RNA was analyzed by multiplex-PCR. Our results clearly demonstrate that among the various cytokines analyzed a predominant release of TNF-alpha, IL-8 and IL-6 is obtained. The remainder cytokines were not detected independent whether molecular biology or cytokine release experiments were applied. Expression of the cytokines was dependent on the degree of malignancy. Among the applied stimuli, only the activation with calcium ionophore/phorbolester modulated cytokine expression and release. While TNF-alpha was induced from normal renal cells by up to 300% (2000 + 120 ng/10(5) cells) a pronounced suppression of TNF-alpha was observed in dependence on the malignancy of the cell line. In contrast, the cytokines IL-6 and IL-8 were significantly upregulated in malignant cells unlike in normal renal cells. These data suggest a differential role of the various cytokines derived from normal or tumor cells. Detailed studies will allow the understanding of the distinct roles of cytokines in renal carcinoma disease.