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Biomedical subjects

R Baumal

Publications and source records attributed to R Baumal.

At least 127 records · Page 7Linked to original sources
PubMed1982

Immunohistochemical localization of prekeratin filaments in benign and malignant cells in effusions. Comparison with intermediate filament distribution by electron microscopy.

An immunoperoxidase technique employing antibody to prekeratin was used to study distribution and pattern of staining of prekeratin filaments in cytological smears obtained from 42 specimens of pleural and peritoneal effusions (27 benign, 15 malignant). The smears were either air-dried or ethanol-fixed. Both benign and malignant mesothelial cells showed distinctive peripheral or perinuclear staining patterns which differed from the characteristic arborizing pattern in adenocarcinoma cells. The ultrastructure of these 2 cell types studied in 27 body fluids (12 benign, 15 malignant) and in 13 malignant tumors (3 mesotheliomas, 10 adenocarcinomas) showed a distinctive localizaton of intermediate filaments which corresponded to and could explain the pattern of staining obtained using the immunoperoxidase technique. The immunohistochemical and ultrastructural findings appeared characteristic for benign and malignant mesothelial cells as well as for adenocarcinoma cells, and could be used as markers to differentiate mesothelial tumors and reactive mesothelial cells from adenocarcinomas.

Adenocarcinoma↗
PubMed1982

Arrangement of lambda light chain genes in mutant clones of the MOPC 315 mouse myeloma cells.

The synthesis of lambda light chains and the arrangement of the lambda-chain genes was examined in cells of the mouse myeloma MOPC 315, which is an alpha lambda 2 producer, and in several mutants derived from it. The mutants produce lambda 2 chains only (MOPC 315.26, MOPC 315.34, and MOPC 315.37) or fail to produce alpha and lambda 2 chains (MOPC 315.25 and MOPC 315.36). Messenger RNA from the lambda 2 chain-producing cells directed the synthesis of a lambda 2 chain precursor and a fragment of the lambda 1 chain (lambda 1 F) in a wheat embryo cellfree system, whereas mRNA from the cells that do not produce lambda 2 chains directed the synthesis of lambda 1 F only. DNA from the parental MOPC 315 cells and from the lambda 2 chain-producing cells contained discrete EcoRI restriction fragments coding for rearranged lambda 1 and lambda 23 chain genes and their respective germ-line V and J-C regions. DNA from the no-Ig-producing cells contained fragments coding for the rearranged lambda 1 chain gene and the germ-line V lambda 2 region, but it lacked the sequences coding for the rearranged lambda 2 chain gene and the germ-line V lambda 1 and J-C lambda 1 regions. These results suggest that rearrangements of the lambda 1 and lambda 2 chain genes occur on different chromosomes in MOPC 315 cells and imply that rearrangements of the lambda 1 and lambda 2 chain genes on the same chromosome may be mutually exclusive.

Animals↗
PubMed1982

Extraglomerular dense deposits in dense deposit disease.

A search was made for dense deposits in sites other than kidney with the use of skin biopsy specimens obtained from patients with dense-deposit disease (DDD) and tissues from autopsy material. Dense deposits were not present in basement membranes at the epidermal-dermal junction or around dermal capillaries in three skin biopsy specimens. Three cases of DDD involving the kidneys (from 1937, 1940, and 1945) were found on reviewing 200 autopsy cases in which the cause of death was renal failure. Paraffin blocks of various tissues from these cases were examined by electron microscopy. Dense deposits were noted in sinusoidal basement membranes of the spleen in the two cases in which spleen was available. No dense deposits were found in brain, heart, lungs, liver, adrenals, or pancreas. We conclude that DDD involves the kidneys and spleen.

Basement Membrane↗
PubMed1982

Variants of an interspecies hybridoma with altered tumorigenicity and protective ability against mouse myeloma tumors.

Recent isolates of RX54-3 hybridoma cells (new cells) protect BALB/c mice against subsequent challenge with the tumorigenic myeloma parent cells used to construct this hybridoma. In contrast, hybridoma cells which have been maintained in tissue culture for long periods of time (old cells) are not protective. In the present study, we compared a number of properties of the new and old hybridoma cells and determined which line was more similar to the parent myeloma. We found that new hybridoma cells resembled myeloma cells in: (a) possessing A- and C-type viral particles on transmission electron microscopy and a relatively smooth surface on scanning electron microscopy; (b) being sensitive to a hypotonic solution containing the dye propidium iodide; (c) having similar DNA histograms on flow cytometric analysis; (d) being sensitive to the bacteriocin colicin HSC 10; and (e) being tumorigenic in nude mice. In contrast, old hybridoma cells differed in all of these characteristics from new hybridoma and myeloma cells. Therefore, in order to protect against challenge with the tumorigenic myeloma parent, hybridoma cells must retain properties of that parent.

Animals↗
PubMed1982

Acute renal failure of short duration in minimal lesion nephrotic syndrome of childhood.

Two boys 12 and 8 years of age with biopsy proven minimal lesion nephrotic syndrome developed acute renal failure during the course of their illness. Renal failure developed in the first boy at the time of onset of his nephrotic syndrome while in the second boy it occurred at the time of a relapse of his disease, 5 1/2 years after onset. Both patients had a complete resolution of renal failure and nephrosis following peritoneal dialysis and oral prednisone. Acute renal failure requiring dialysis is an unexplained and rare complication of minimal lesion nephrotic syndrome in adults and children.

Acute Kidney Injury↗
PubMed1981

Protective effect of an interspecies hybridoma on the tumorigenicity of mouse myeloma cells.

A rabbit lymphocyte-mouse myeloma hybridoma (RX54-3) was administered to BALB/c mice, in order to determine whether hybridoma cells have any protective effect on the tumorigenicity of the P3X63/Ag8 mouse myeloma cell line, one of the parents of this hybridoma. Two sublines of RX54-3 were studied. (a) "new" cells, which produce rabbit light chains and mouse immunoglobulin, are killed by anti-myeloma cell antiserum and complement and possess a high chromosome count. And (b) "old" cells, which have lost all immunoglobulin-producing capacity, are no longer killed by anti-myeloma cell antiserum and complement and possess a low chromosome count. In contrast to myeloma cells, the hybridoma cells were nontumorigenic in normal BALB/c mice, even at very high cell doses. When hybridoma cells were administered prior to challenge with P3X63/Ag8 myeloma cells, protection against development of myeloma tumors was much more effective with new cells than with old cells. Development of protection was dependent on the dose of hybridoma cells, their route of administration, their viability and ability to divide, and the time interval between administration of the hybridoma and myeloma cells. The protection produced by the new hybridoma cells was comparable to that seen after administration of a subtumorigenic dose of living myeloma cells. With both the hybridoma and myeloma cells, protection was seen only against challenge with P3X63/Ag8 myeloma cells but not against another myeloma tumor. These studies indicate that administration of somatic cell hybrids is an effective method of protecting syngeneic hosts against challenge with mouse myeloma tumor cells.

Animals↗
PubMed1981

A monoclonal antiidiotypic antibody to MOPC 315 IgA inhibits the growth of MOPC 315 myeloma cells in vitro.

Spleen cells from BALB/c mice immunized with MOPC 315 IgA were fused with P3X63/Ag8 myeloma cells. Hybrid clones were screened for antibody production by a plate-binding radioimmunoassay in which MOPC 315 IgA was reacted with culture supernatants and 125I-protein A. One antibody-producing hybridoma clone (D10) was selected and injected i.p. into BALB/c mice. Ascitic fluid of tum or-bearing animals reacted specifically with MOPC 315 IgA and the reaction was inhibited by DNP- aminocaproic acid, indicating that the monoclonal antibody was directed against the hapten-binding site of MOPC 315 IgA. The monoclonal antiidiotypic antibody was of the complement (C)-binding IgG2a subclass and inhibited IgA production and growth of MOPC 315 cells in vitro in the presence of guinea pig C, as assessed by inhibition of formation of plaques and colonies by MOPC 315 cells in agar.

Animals↗
PubMed1980

Induction of cytotoxic factors by immunization of mice with Freund's adjuvant components.

Antiidiotypic antibody (AIA) was raised in mice by immunization with MOPC 315 immunoglobulin A emulsified in Freund's adjuvant (FA). The antibody content of mouse serum was assessed by (a) its ability to inhibit rosetting of 2,4,6-trinitro-phenyl-sheep red blood cells around MOPC 315 myeloma cells, and (b) by a solid phase antigen-binding plate assay based on reactivity with 125I-Protein A and inhibition in the presence of dinitrophenyl aminocaproic acid. FA was necessary for the production of AIA to MOPC 315 immunoglobulin A. Some of the AIA-containing mouse sera were cytotoxic for MOPC 315 cells in the presence of guinea pig complement. However, cytotoxicity was not correlated with amount of AIA, as assessed by inhibition of rosette formation, nor was it specific for myeloma cells bearing the MOPC 315 idiotype. Furthermore, cytotoxicity could also be generated by immunization of mice with complete Freund's adjuvant, incomplete Freund's adjuvant, or the muramyl dipeptide portion of mycobacteria, all in the absence of MOPC 315 immunoglobulin A. Therefore, the complement-dependent cytotoxic antibodies in the AIA-containing antisera, which belonged to the immunoglobulin G and M classes, were likely directed against some component of FA. Myeloma cells which were not killed by anti-FA antiserum, as assessed by dye exclusion, were inhibited in their ability to secrete immunoglobulin and to form clones in agar.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1979

Mutations affecting immunoglobulin light chain secretion by myeloma cells. I. Functional analysis by cell fusion.

Two clones of MOPC 315 cells have been selected which synthesize but do not secrete Ig lambda light chains. These clones were analyzed by fusion with a cell line synthesizing and secreting kappa chains. Conditions were established for recovery at high frequency (approximately 10(-3)) of spontaneously fused, viable hybrid cells. The resulting hybrid cell lines synthesized both kappa and lambda chains but secreted only kappa chains. Hybrid cells produced by fusion of a lambda-secreting clone of MOPC 315 with the kappa-secreting cell line were also isolated and shown to synthesize and secrete both kappa and lambda chains. These results suggest that the nonsecretion of lambda chains was not due to a defect the secretion mechanism of the variant cells. A more likely alternative is that the lambda chains in the variant cell lines were structurally altered to a form which could not be secreted.

Animals↗
PubMed1979

Similarity of casein- and endotoxin-induced, myeloma- associated and aged SJL/J amyloid in various strains of mice.

Amyloidosis was induced in a number of strains of mice by repeated injections of casein and endotoxin. Spontaneous amyloid was obtained from Balb/C mice bearing a myeloma tumor (IgG2a producing MOPC 173 tumor) and from aged SJL/J mice. Both the induced and spontaneous forms were similar in their size, immunological reactivity, peptide maps and in the susceptibility of histological sections to oxidizing agents with or without trypsin digestion. Since case-induced murine amyloid resembles the nonimmunoglobulin from of human amyloid, it is concluded that an immunoglobulin form in mice has yet to be characterized.

Aging↗