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S Sell

Publications and source records attributed to S Sell.

At least 217 records · Page 12Linked to original sources
PubMed1977

Effects of alpha-fetoprotein on murine immune responses. II. Studies on rats.

In vitro and in vivo experiments failed to identify a consistent "immunosuppressive" or "immunoregulatory" role for alpha-fetoprotein (AFP) in the rat. Both normal and AFP-rich sera inhibited Con A, PHA, and MLR proliferation responses of lymphocyte cultures in vitro equally well, in spite of up to 100,000-fold differences in AFP concentration. AFP-rich sera also had no effect on the antibody response of the rat in vivo. Purified AFP from amniotic fluid inhibited the PHA response at concentrations of 100 in chemical contexts is converted to microgram/ml. Purified albumin was also inhibitory, but at 1 log higher concentration. Purified AFP from tumor sera was not inhibitory at 100 in chemical contexts is converted to microgram/ml for Con A, PHA, or MLR reactions and only inhibited PHA stimulation at medium concentrations greater than 1000 in chemical contexts is converted to microgram/ml. The role of AFP as an immunosuppressive agent, particularly in reference to survival of mammalian fetuses, should be reconsidered.

Animals↗
PubMed1977

Surface immunoglobulin on rabbit lymphoid cells. V. Ultrastructural distribution of b4 allotypic determinants of thymus, lymph node and bone marrow lymphocytes.

An indirect immunoferritin-labeling technique is used to localize cell surface immunoglobulin (Ig) allotypic determinants on rabbit lymph node, bone marrow and thymus lymphocytes. 47% of the lymph node cells, 62% of bone marrow small lymphocytes and less than 1% of thymic lymphocytes, are positive for surface Ig. Two Ig-positive lymph node lymphocyte populations which differ in fine structure are identified but both cell types express similar amounts of surface Ig (7,000-28,000 Ig molecules per cell). Bone marrow small lymphocytes make up only 9% of the total cell population and express less surface Ig (ca. 3,000-12,000 molecules Ig per cell) than most Ig-bearre described and both are essentially negative for surface Ig using this labeling technique.

Animals↗
PubMed1976

In vitro studies of the rabbit immune system. V. Suppressor T cells activated by concanavalin A block the proliferation, not the induction of antierythrocyte plaque-forming cells.

The late B-cell proliferative phase of the in vitro antibody response by rabbit spleen cells is highly susceptible to suppression by activated T cells. The in vitro antisheep erythrocyte plaque-forming cell (PFC) response by spleen cells from normal or primed rabbits can be suppressed by adding concanavalin A (Con A), Con A-prestimulated peripheral blood or spleen lymphocytes, or supernates from Con A-prestimulated peripheral blood lymphocytes. The suppression is not mediated by a direct interaction of Con A with responding cells as shown by the effectiveness of prestimulated cells. Primed spleen cultures remain sensitive to Con A suppression as late as 72 h after initiation, and the addition of Con A after 24-72 h rapidly stops the increase in the number of PFC. T cells are required for Con A addition to be effective but the suppression can be induced at a time when T-helper cells are no longer necessary. Further, the suppressive effect of Con A addition is abrogated by specific antisera to rabbit T cells. We propose that Con A activates suppressor T cells which then exert their effects on proliferating PFC or their immediate precursor B cells. The early inductive or recruitment phase of the response is probably not blocked by suppressor cells. Also, there is an apparent relationship between the number of proliferating B cells and the number of suppressor cells required. Finally, the difficulties in inducing a stimulatory effect by Con A and the prolonged period that Con A addition is suppressive suggests that the rabbit has relatively more and/or longer-lived suppressor cells than the mouse and may be a particularly useful species for studying suppressive phenomena and their mechanisms.

Animals↗
PubMed1976

Serum alpha-fetoprotein. A prognostic indicator of liver-cell necrosis and regeneration following experimental injury by galactosamine in rats.

The serum concentrations of alpha-fetoprotein of rats following experimental galactosamine-induced liver-cell necrosis accurately reflect the severity of preceding liver-cell damage as determined by elevation of serum transaminases. There is a very close correlation between the highest SGOT or SGPT serum activity found 1-2 days after induction of necrosis and the subsequent elevation of alpha-fetoprotein at 2-6 days. Elevations of alpha-fetoprotein are associated in time with restitutive proliferation of the damaged liver. These experimental results clarify the temporal relationship between alpha-fetoprotein and repair of liver-cell damage, which has been suggested by similar observations in cases of patients who have acute or sub-acute viral hepatitis. The correlations support the concept that serum alpha-fetoprotein concentrations may be used as a prognostic indicator of the extent and course of fulminatn or subacute hepatitis.

Alanine Transaminase↗
PubMed1976

Tissue sites of alpha fetoprotein synthesis by the rat during pregnancy and hepatoma growth.

The tissue sites of alpha1 fetoprotein (AFT) synthesis by the rat during gestation and hepatoma growth were determined by specific incorporation of a radiolabeled amino acid precursor into AFP by tissue cultures in vitro. During gestation, AFP were produced by the yolk sac, the fetal liver, and in small amounts by the fetal gastrointestinal tract; there was no synthesis by maternal rat tissues. During growth of a transplantable hepatoma, only the hepatoma tissue synthesized AFP; the nontumor tissue of the host contained AFP but did not produce it.

Animals↗
PubMed1976

Effect of anti-alpha1-fetoprotein on alpha1-fetoprotein-producing rat tumors in vivo and in vitro.

Active or passive immunization of rats to alpha1-fetoprotein (AFP) does not consistently inhibit the growth of AFP-producing transplantable hepatomas in vivo, and anti-AFP does not kill these hepatomas in vitro. However, 3 of 14 rats in 1 experiment responded to passive immunization by reversal of tumor growth as evidenced by normalization of elevated AFP serum concentrations, and 1 of 9 rats actively immunized with rat AFP in complete Freund's adjuvant had suppressed growth of transplantable hepatoma 7777.

Animals↗
PubMed1976

Expression of an oncodevelopmental gene product (alpha-fetoprotein) during fetal development and adult oncogenesis.

The expression of an "oncodevelopmental" protein, alpha-fetoprotein (AFP), has been systematically studied in rats during normal development and during regeneration of the liver by fetal rat hepatocytes in vitro, in rats bearing transplantable hepatomas, in rats fed chemical carcinogens, and in mice that spontaneously develop hematomas. AFP is a serum protein made normally during fetal and neonatal stages by liver and yolk sac cells. In newborn rats at approximately 4 weeks of age, the production of AFP is abruptly terminated, a process which is closely associated with cessation of liver cell proliferation. In adult rats, AFP production recurs following the reinitiation of hepatic DNA synthesis induced by partial hepatectomy or by the administration of heaptotoxic chemicals. Detailed metabolic and direct labeling studies of fetal rat hepatocytes in vitro also demonstrate a kinetically similar pattern of hepatocyte DNA synthesis and AFP production. In vitro studies utilizing combined autoradiography for DNA-synthesizing cells and immunofluorescence for AFP-containing cells demonstrates that replicating hepatocytes produce AFP, however, available data do not yet permit a distinction between G1 (pre- or postmitotic) and/or G2 production. During growth of an AFP- producing tumor, the serum concentration of AFP may be used as a accurate index of tumor growth, and, if a transplanted tumor is removed, as a marker for metastatic growth of the tumor. Using this model, we have shown that radiation to the lung at the time of surgical removal of a growing tumor in the leg will prevent establishment and growth of pulmonary metastases and that anti-AFP serum treatment may inhibit growth of a transplantable hepatoma that produces AFP. The exposure of rats to chemical hepatocarcinogens results in the appearance of evaluated serum AFP concentration as early as within 1 week of feeding; noncarcinogenic chemical analogs do not cause an elevation. AFP elevation also occurs with low doses of the hepatocarcinogen in the absence of detectable cell injury (by morphological examination of serum enzyme levels) or any other known morphological or biochemical change. This may represent a highly selective derepression of protein synthesis that occurs following the formation of a complex between the metabolites of the carcinogen and specific chromatin loci. Although every rat so far treated with even subcarcinogenic doses of hepatocarcinogens has elevated serum AFP concentrations, many primary carcinogen-induced hepatomas do not produce detectable AFP. Either there is a subsequent change in the preneoplastic AFP-producing cell that occurs prior to irreversible neoplastic alteration, or the hepatocytes originally influenced by the carcinogens to produce AFP are not necessarily the same cells that are the progenitors of the hepatoma produced by more prolonged exposure...

2-Acetylaminofluorene↗
PubMed1976

alpha-Fetoprotein in toxic liver injury.

The temporal sequence of alpha-fetoprotein appearance in serum was determined in both necrogenic and nonnecrogenic liver injury. Ethionine, thioacetamide, and CCl4 were used to intoxicate male and female rats for evaluating serum enzyme levels, mitotic indices, and morphological reflections of impairment. Thioacetamide- and CCl4-induced cell death preceded the mitotic wave in residual hepatocytes, and, in the case of both agents, this intoxicant-mediated necrosis preceded the emergence of alpha-fetoprotein. Yet, although there was no evidence of either cell destruction or significant mitotic activity in ethionine-poisoned animals, serum alpha-fetoprotein levels progressively increased. Thus the temporal sequence of alpha-fetoprotein synthesis and/or release and cellular reorganization for regeneration suggests that reappearance of the protein macro-molecule is an expression of the altered phenotype observed during the "step-down" phase of liver regeneration.

Alanine Transaminase↗
PubMed1975

Relationship of the biosynthesis of alpha-fetoprotein, albumin, hemopexin, and haptoglobin to the growth state of fetal rat hepatocyte cultures.

AFP and albumin are produced by arginine-synthesizing fetal rat hepatocytes in vitro. AFP and hemopexin production are coupled to hepatocellular proliferation, whereas albumin and haptoglobin production are not. During the cell cycle, AFP is synthesized prior to S and released prior to M. AFP may play a role in regulation of hepatocellular growth through estradiol binding and modulation of the intracellular concentration of lipoprotein (VLDL).

Albumins↗