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Biomedical subjects

J Klempnauer

Publications and source records attributed to J Klempnauer.

At least 163 records · Page 9Linked to original sources
PubMed1989

Adrenal cortex transplantation after bilateral total adrenalectomy in the rat.

An experimental animal model with adrenal cortex transplantation was developed to study adrenal cortex replacement therapy in patients with multiple endocrine neoplasia type 2 who have had bilateral adrenalectomy for pheochromocytomas. Adrenal cortex of syngenetic rats was isolated from the medulla by collagenase digestion and a defined sedimentation. The cell suspension of the cortical cells was implanted under the kidney capsule of untreated syngenetic rats. After two weeks the recipients were bilaterally adrenalectomized. Serum corticosterone levels were measured as an estimate of function of the grafts. All recipients were healthy throughout the observation period, whereas all adrenalectomized controls died within 18 days. Vital cortex cells could be demonstrated in the explanted grafts by immunohistochemistry. Corticosterone levels of transplanted animals were nearly normal (9.5 ng/100 mL +/- 0.4) compared to the controls (0.20 ng/mL +/- 0.06). This animal model of adrenal cortex transplantation allows the separation of medullary from cortical cells. After transplantation, these cortical cells survived for eight weeks and were able to replace the adrenal cortex function.

Adrenal Cortex↗
PubMed1986

Detection of polymorphic rat MHC antigen determinants in cryostat sections. A method for selecting monoclonal alloantibodies.

An immunohistological method for detection of rat MHC antigens by unconjugated primary alloantibodies is described. The procedure is based on secondary reagents specific for an allotypic marker of rat kappa light chains and makes possible differentiation between specifically bound alloantibody and the ubiquitously distributed interstitial immunoglobulin in the section. This technique can be used to pre-select monoclonal antibodies to be coupled to biotin or enzymes for histological application.

Animals↗
PubMed1986

Distinct histologic patterns of acute, prolonged, and chronic rejection in vascularized rat pancreas allografts.

In a model of pancreas whole organ transplantation in streptozotocin diabetic rats distinct histologic patterns of acute, prolonged and chronic rejection were defined by light microscopy. Allotransplantation between major histocompatibility complex (MHC) congenic and recombinant rat strains allowed an immunogenetic analysis of the effect of defined histocompatibility antigens on graft morphology. The impact of surgical techniques with preserved and suppressed exocrine secretion on graft histology was sequentially assessed in pancreas isograft recipients. MHC incompatibility was associated with acute rejection, non-MHC disparity with prolonged rejection and RT1.C mismatch with chronic rejection.

Animals↗
PubMed1985

Altered distribution of class I and class II MHC antigens during acute pancreas allograft rejection in the rat.

The expression of MHC class I and class II antigens was investigated in a model of acute pancreas allograft rejection in the rat. Pancreaticoduodenal and duct-ligated DA(RT1a)-to-LEW(RT1(1] and LEW(RT1(1]-to-LEW.1U(RT1u) pancreas grafts were compared with normal organs and with LEW(RT1(1] isografts at daily intervals from day 1 to day 10 after transplantation. The results show profound changes of MHC antigen distribution in allografts during the process of rejection. Exocrine acinar cells, being class-I-antigen-negative in the normal pancreas, strongly express these antigens during rejection. Class II antigens, normally not found in pancreatic endothelia or parenchymal cells, appear in duct epithelia, acinar cells, and endothelia of big vessels. Endocrine islet cells and smooth muscle cells stay Ia-negative throughout the rejection process. Focal class I reactivity is also observed in acinar cells of pancreaticoduodenal isografts; but class II antigens are neither seen in parenchymal cells nor in endothelia of any isograft. Thus, in the rat pancreas allograft model, the induction of class II antigens is an early phenomenon characteristic of an ongoing immune response, and it provides a valuable new diagnostic criterion. Antibodies reactive exclusively with donor-haplotype antigens demonstrate an increase in donor-derived class I and class II antigen-positive interstitial cells in addition to parenchymal antigenic changes. A possible effect of the antigenic alteration described on the course of the rejection process is discussed.

Animals↗
PubMed1984

Phenotype and histological distribution of interstitial dendritic cells in the rat pancreas, liver, heart, and kidney.

The phenotype and the histological distribution of interstitial dendritic cells was investigated in the rat pancreas, liver, heart, and kidney by immunoperoxidase techniques. Monoclonal antibodies, directed against lymphocyte differentiation antigens (W3/25, W3/13, and Ox8) or against Ia antigens, revealed distinct phenotypes of these cells in all organs investigated--namely W3/25+Ia- dendritic cells, W3/25+Ia+ cells, and a small W3/25-Ia+ population. In the kidney cortex a W3/25+W3/13+ population was additionally shown. Interestingly, the phenotypically distinct cell populations also differed in their topographical distribution: W3/25+Ia+ cells were evenly scattered in the interstitium of the endocrine and exocrine pancreas, heart, and kidney. In contrast, W3/25+Ia- cells showed an additional predilection for connective tissue septa in the exocrine pancreas and for the kidney medulla. In the liver, phagocytic Kupffer cells were W3/25+Ia-, whereas the W3/25+Ia+ nonphagocytic dendritic cell population resided periportally and around central veins. These results show a marked heterogeneity of interstitial dendritic cells in the rat, which is discussed in terms of different cell lines or different activation or maturation stages of one single cell type.

Animals↗