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S Segal

Publications and source records attributed to S Segal.

At least 451 records · Page 25Linked to original sources

Characteristics of gamma-glutamyltranspeptidase in cultured skin fibroblasts from normals and cystinotics.

The characteristics of a fluorimetric method for assay of gamma-glutamyltranspeptidase (EC 2.3.2.2) in cultured human skin fibroblasts from normal donors and cystinotic patients using gamma-glutamyl-7-amino-4-coumarin as substrate are described. It is possible with this method to measure enzymatic activity in sonicates of cells with as little as 0.029 mmol/l L-cystine as acceptor-substrate with only 0.20 mg of cellular protein after 30--60 min of incubation. The properties of the enzyme in cells from patients with cystine storage disease show elevated gamma-glutamyltranspeptidase under various incubation conditions.

Cells, Cultured↗

Anesthetic drugs accelerate the progression of postoperative metastases of mouse tumors.

Experiments were made to investigate the effect of four anesthetic drugs that are commonly used in surgical practice on the postoperative growth of mouse tumors in syngeneic recipients. These experiments revealed that some of the anesthetics when applied for surgical excision of the local tumor, strongly accelerated postoperative progression of spontaneous lung metastases produced by the 3LL Lewis lung carcinoma and by the B16 melanoma. Some of the drugs caused the appearance of metastases in organs, such as the liver, in which spontaneous metastases are not usually produced by these tumors. A T10 sarcoma clone that does not produce detectable metastases in immune intact mice even following intravenous injection, did produce metastases when injected into animals treated with pentothal sodium.

Anesthetics↗

The regulation of SV40 gene expression in nonpermissive cells.

The limitations to SV40 growth in nonpermissive cells are poorly understood. In differentiated mouse cells, early mRNA and T-antigens are synthesized, but no viral DNA replication has been detected. A plausible explanation for the limitation to viral DNA synthesis in these cells might be the inability of a mouse cell-specific DNA polymerase to interact with the SV40 T-antigen-viral DNA complex. In spite of this abortive viral-cell interaction, SV40 late viral transcripts can be detected in infected mouse cells. Both early and late transcripts can be detected in infected mouse cells. Both early and late SV40 transcriptional activities peak between 10 and 15 h post infection; by 24 h after infection SV40 RNA is almost undetectable. In spite of the detection of late SV40 mRNA in mouse cells, we have been unable to detect any structural proteins (VP1, VP2, or VP3) encoded by these transcripts. A more restrictive interaction occurs between SV40 and undifferentiated mouse teratocarcinoma cell lines. Using an in vitro technique, the viral transcriptional complex (VTC) assay, we were able to demonstrate viral transcriptional activity on both the early and the late strands of SV40 in F9 embryonal carcinoma cells. Nevertheless, no mature processed mRNAs or viral encoded polypeptides were detected in these cells. After differentiation of the F9 cells with retinoic acid, however, spliced early mRNAs, as well as the SV40 T-antigen, were present.

Animals↗

Control of progression of local tumor and pulmonary metastasis of the 3LL Lewis lung carcinoma by different histocompatibility requirements in mice.

Intrafootpad inoculation of syngeneic mice with Lewis lung carcinoma (3LL) cells led to the growth of a solid tumor at the site of transplantation, followed by development of metastases in the lungs. Surgical excision of the primary tumor resulted in an accelerated growth and increased incidence of pulmonary metastases. Inasmuch as 3LL tumor cells isolated from the local tumor differed antigenically from the cells isolated from the metastases, the genetic control of the local 3LL tumor growth and that of its lung metastases were tested. The local tumor grew in allogeneic mice, yet its growth rate was higher in syngeneic and semiallogeneic F1 hybrids than in allogeneic recipients. However, lung metastases did not appear in allogeneic animals. By analysis of the rate of growth of the local tumor in congenic mouse strains, the tumor progression appeared to be linked to the host's genetic background rather than to the H-2 region. The generation of lung metastases required compatibility at both background and H-2 haplotype. Tests of the development of metastases in mice of congenic resistant recombinant strains revealed that metastases developed only in animals that shared with the tumor the gene products of the D-end of the major histocompatibility complex. Thus metastasis formation was controlled by both a non-H-2 gene(s) and a gene(s) linked to the H-2D region or another nearby region to the right of H-2D.

Animals↗

Metastatic properties conferred on nonmetastatic tumors by hybridization of spleen B-lymphocytes with plasmacytoma cells.

The P3-NSI/1-Ag4-1 (NSI) plasmacytoma, when transplanted sc in syngeneic BALB/c mice, grows locally without forming spontaneous metastases. We tested whether somatic hybridization of the NSI cells with spleen B-lymphocytes would render them metastatic in (C57BL/6 X BALB/c) F1 mice. We found that the hybridomas thus produced generated spontaneous metastases with distinct organ specificities. Some hybridomas produced metastases in both liver and spleen, whereas others produced metastases in only the liver. Cells derived from spleen-and liver-seeking hybridomas, when transplanted sc, produced tumors that metastasized to both the liver and spleen. Tumor cells derived from spleen metastasis produced, on transplantation, a tumor that generated spleen metastasis of a larger mass than did tumors derived from liver metastases. Cells derived from liver-seeking hybridomas metastasized to only the liver. Similar patterns of organ specificity were observed after iv injection of the hybridoma cells. The spleen seemed to play determining role in controlling the production of liver metastases by hybridomas that produced both liver and spleen metastases. Such hybridomas did not produce liver metastases when injected into splenectomized recipients. Hybridomas that were only liver-seeking did produce metastases in splenectomized recipients.

Animals↗

Plasma membrane microviscosity of Lewis lung carcinoma cells derived from local growth and pulmonary metastases.

Significant differences in plasma membrane microviscosity between 3LL Lewis lung carcinoma cells, grown at the site of their original inoculation (1-3LL), and the pulmonary metastatic cells of this tumor (m-3LL) were detected by a recent improvement of the fluorescence polarization technique, especially designed for cells in suspension. Membrane microviscosity was also found to depend on the site of the growth and the stage of tumor development. The results show that lung metastases are lower in membrane microviscosity compared to 1-3LL and that, within the latter, cells grown in the muscle are characterized by higher microviscosity than those grown under the skin or in the footpad. Within one transplantation period, 3LL tumor cells tend to acquire membrane microviscosity values typical of the anatomical location of tumor growth. Tumors at advanced stages were generally found to be more rigid than young ones, where tumor size (volume) rather than its age seemed to determine the membrane microviscosity. These differences are discussed in terms of both the causes and the biological, as well as immunological, implications in relation to the newly proposed hypothesis of passive modulation of antigenic expression.

Animals↗

Treatment of malignant external otitis in its initial stage.

A method of treating malignant external otitis in its initial stage is described. The treatment is based on repeated curettage with Epontol under light general anesthesia. This method requires no systemic antibiotic treatment, can be carried out as an office procedure, and effects a complete cure in a relatively short time.

Anesthesia, General↗

Effectiveness of prophylactic antibiotic treatment in mastoid surgery.

This article describes a prospective study of the effectiveness of prophylactic antibiotic treatment in preventing infection following mastoid surgery. Seventy-two patients who underwent surgery for chronic middle ear disease served as the basis for this study. Bacteriologic findings from middle ear discharge, showing aerobic and anaerobic bacteria, are reported. The patients were randomly classified into two groups, one undergoing surgery with preventive antibiotic treatment with clindamycin and gentamycin and the other undergoing surgery without antibiotic therapy. The early postoperative inflammatory complications are presented. No significant differences were found in the incidence of these complications between the two groups. In view of the results, the effectiveness of preventive antibiotic treatment in mastoid surgery is questioned.

Adolescent↗

Effect of lactic dehydrogenase virus infection on tumor induction and tumor growth.

The ubiquitous nononcogenic lactic dehydrogenase RNA virus (LDV) is one of the most common contaminants of transplantable tumors and oncogenic viral preparations. This association of LDV with a large variety of murine tumors and the known effect of LDV infection on immune competence may suggest the existence of a possible etiological relationship between the virus and murine tumors. We have found that the inoculation of transplantable carcinoma cells to acutely LDV-infected mice is followed by an enhanced rate of tumor growth. To examine the possibility that LDV is involved in the carcinogenic process and may act as a promoter or initiator, we infected mice with LDV at various time intervals prior to, simultaneously with or after their treatment with chemical carcinogens (urethan 3-methylcholanthrene, and 9,10-dimethyl-1,2-benzanthracene) and then followed the development of the malignant disease. No differences in the rate of tumor appearance and in mortality were observed between LDV-infected and uninfected mice. In addition, LDV failed to affect the development of spontaneous reticulum cell sarcoma and lymphatic leukemia in SJL/J, AKR/Cu, and AKR/J mouse strains. It is suggested that, although LDV does not affect the induction of oncogenic processes, this virus may still be capable of promoting the progression of transplantable tumors due to its immunoregulatory properties.

Animals↗

Differential expression of H-2 gene products in tumour cells in associated with their metastatogenic properties.

Many neoplasms seem to be heterogeneous in nature, producing metastases by pre-existing variant cells with inherent biochemical and biological properties. The survival and proliferation of metastatic cells depend on various biological properties, such as enzymes which degrade basement membranes, resistance to various host defence systems, association with host cellular components, adhesiveness and expression of certain membrane glycoproteins. Recent studies have indicated that metastatic cells may differ from the local tumour cells in the expression of immune recognizable membrane-associated antigens. Such antigenic differences may result from an immunoselection of cells with distinct antigenic properties due to a specific immune response evoked against the local tumour. In view of the role of the major histocompatibility complex (MHC) system in controlling and restricting the function of immune effector cells against modified self-components, one could assume that the modulation of the expression of MHC-encoded antigens on the membrane of tumour cells influenced the interclonal relationship within a local heterogeneous tumour cell population and the subsequent generation of metastasis. The modulation of the expression of H-2 antigens on several murine tumours is well documented; however, practically no attempts were made to relate H-2 modulation with invasiveness. We now describe principal differences in the expression of H-2 parental haplotypes between a local F1 methylcholanthrene-induced tumour and its descendant pulmonary metastases. These results suggest that both the expression and the immunogenicity of MHC products strongly influence the immune relationship between the tumour and the host's immune system, thus determining the generation and dissemination of metastases.

Animals↗

The effect of azaserine on glutamine uptake by rat renal brush-border membranes.

Azaserine added directly to isolated rat renal brush-border membrane vesicles inhibits uptake of L-glutamine. Azaserine acts as a non-competitive inhibitor of the low-Km system for glutamine transport, but has no effect on the high-Km system. Preincubation of the vesicles with azaserine at 37 degrees C min is not required for transport inhibition to occur, although it is a requirement for gamma-glutamyl transpeptidase inhibition. Removal of azaserine from the vesicle preparation by repeated resuspensions in buffer results in a reversal of the transport inhibition but not in reversal of enzyme inhibition. Azaserine also inhibits vesicle uptake of L-proline and alpha-methyl D-glucoside, indicating a generalized effect on membrane transport systems. The data cast doubt on the postulate that gamma-glutamyl transpeptidase might act as the carrier mechanism for glutamine reabsorption by renal cortical cells.

Animals↗