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Biomedical subjects

J Tseng

Publications and source records attributed to J Tseng.

At least 73 records · Page 4Linked to original sources
PubMed1982

Wound-Induced RNase Activity in Sweet Potato : EVIDENCE FOR REGULATION AT TRANSCRIPTION.

Upon wounding of sweet potato (Ipomea batatas, Lam. var. Puerto Rico) RNase activity increases rapidly following a 4-hour lag, peaks in 24 hours, and then declines. Cycloheximide inhibits induction indicating that increased activity is probably due to de novo synthesis. The half-time (t(0.5)) for RNase degradation in presence of cycloheximide (1.8 hours) is constant throughout the rise and decline in RNase activity. Induction is not affected by exogenous ethylene, but is dependent on production of endogenous ethylene. The following evidence is consistent with the hypothesis that the activity of RNase is regulated at transcription. (a) Wound induction of RNase is inhibited by actinomycin D (ACTD), cordycepin, or alpha-amanitin. (b) Addition of ACTD at 9, 12, or 24 hours causes an immediate decline in RNase. (c) Six measurements of the natural decline in RNase between 24 and 36 hours show a t(0.5) of 14.1 +/- 1 hour. (d) Use of proecdures for measurement of the t(0.5) for degradation of mRNA in bacteria and plants show a mean t(0.5) of 14 +/- 1 hour for degradation of RNase mRNA in presence of ACTD. From the fact that both the degradation of RNase in presence of ACTD and the natural decline in RNase have a t(0.5) that is very similar to the t(0.5) for degradation of RNase mRNA, it is postulated that the natural decline in sweet potato RNase is due to repression of the RNase gene as a result of which the rate of degradation of RNase follows the t(0.5) for degradation of RNase messenger.

Journal Article↗
PubMed1981

Induction of indigenous immunoglobulin-containing cells by gamma-irradiation and lymphoid cell transfer in mice.

Mice irradiated with gamma-ray develop large numbers of Ig-containing cells of various isotypes in all the lymphoid tissues examined except the thymus. The maximal dose of irradiation is approximately 500 R/mouse. These indigenous Ig-containing cells start to appear at day 3 post-irradiation, peak at day 6, and subside thereafter. The expression of the indigenous Ig-containing cells can be enhanced in the spleen of recipient mice by passive transfer of various lymphoid cells, except thymocytes. Lymphoid cells from histocompatible donors are more effective enhancers than those from nonhistocompatible donors. Cells involved in the enhancement are primarily T cells. In contrast, when T cells are eliminated from the lymphoid cell inocula, the indigenous Ig-containing cells are reduced to a level lower than that in the irradiated controls. This suppression appears to be mediated by macrophages, since recovery was found when macrophages were removed from these T cell-depleted inocula.

Animals↗
PubMed1981

Transfer of lymphocytes of Peyer's patches between immunoglobulin allotype congenic mice: repopulation of the IgA plasma cells in the gut lamina propria.

Repopulation of the IgA plasma cells in the gut lamina propria was studied by lymphocyte transfers between histocompatible, immunoglobulin allotype congenic mice (CB-20 and BALB/cJ). Among the lymphocytes transferred, Peyer's patch lymphocytes showed the highest efficiency in the repopulation. The donor IgA plasma cells appeared suddenly in the gut lamina propria in substantial numbers at day 8, increased exponentially, and repopulated essentially tne entire gut lamina propria at days 12 to 14. By sequential transfer of lymphoid cells, lymphoid cell culture, splenectomy, and jejunum-shielded total body irradiation of the recipient mice, the majority of the patch IgA precursors were found migrating directly to the spleen rather than to the gut lamina propria. The patch IgA precursors resided in the spleen for at least 5 days and then migrated to the gut lamina propria, where they further divided and matured into IgA plasma cells. However, the spleen is not a completely obligatory tissue in the migration route because the repopulation was only partially reduced when patch cells were transferred into splenectomized recipients. In the splenectomized recipients, the patch IgA precursors did not migrate directly to the gut lamina propria either, which suggests that indirect homing to the gut lamina propria is a characteristic of the patch IgA precursor cells.

Animals↗
PubMed1975

Differential susceptibility of rabbit sIgA subclasses to trypsin cleavage: characterization of the fragments obtained from the g subclass.

Rabbit secretory IgA (sIgA) was digested with trypsin at 37 degrees C for 30 min and four fractions were isolated by gel filtration. These fragments were characterized by ultracentrifugation, and by their antigenic properties as undigested sIgA, Fab and Fe (Two Fc fragments differing in their content of secretory component were obtained.) The IgA-f subclass molecules were resistant to cleavage and were found in the undigested sIgA fraction; the IgA-g subclass molecules were cleaved into Fe and Fab fragments. The g allotypic determinants of IgA-g molecules were found on both the Fc fragments and the Fab fragments. The Fc and Fab fragments obtained from trypsin-digested sIgA were compared by means of antigenic properties and peptide maps with the Fc and Fab fragments obtained from papain-digested sIgA; no differences attributable to the alpha-chain were found. Thus, papain and trypsin cleave the alpha-chain of IgA-g molecules at similar but not necessary identical positions.

Adsorption↗
PubMedDate not supplied

The secretory IgA system of the gut.

Most commonly, humoral immunity manifested in the gastrointestinal tract of mammals is due to the presence of secretory IgA antibodies. Antibody specificities have been detected in the secretory IgA of gut secretions to a wide range of naturally occurring viral and bacterial components and to test antigens such as chemically modified proteins. Much of the IgA found in gut secretions is synthesized and secreted locally by the abundant plasma cells of the lamina propria. Development of methods for establishing local protective immunity in the gut requires knowledge of the origins of these plasma cells and of the whereabouts of their precursors when they are susceptible to antigen-driven proliferation and/or maturation. The Peyer's patches have been shown to contain a population of B lymphocytes especially rich in precursors for IgA plasma cells and in cells which can repopulate gut lamina propria with such IgA plasma cells. The Peyer's patches also appear to 'sample' gut antigens, in that small amounts of antigens are passed intact through their dome epithelial cells. Recent experiments bearing on the origins, differentiation and maturation, antigen sensitivity, migration and lodging of precursors for gut IgA plasma cells are discussed. We use the following three systems: (1) congenic transfer of cells from different murine lymphoid cell sources or mixtures of these (CB20 leads to BALB/c or BALB/c leads to CB20) and the use of allo-antisera to IgA allotypic determinants to assess their potential to impart an adoptive IgA antibody response to the recipient and to repopulate its histocompatible lamina propria with IgA plasma cells; (2) clonal precursor analysis (the method of Klinman) both to enumerate antigen-sensitive cells in different tissues of mice and to evaluate their potential to generate plasma cells making particular isotypes and idiotypes of antibodies; (3) use of pairs of Thiry-Vella loops in rabbits, each member either bearing or lacking a Peyer's patch, and quantitation of antibodies of each isotype and of total secretory IgA to assess the response of each loop with the time after local immunization. The results from all three systems provide strong evidence for the importance of Peyer's patches in supplying cells responsible for local humoral immunity and suggest both a differentiative pathway for IgA precursors and their whereabouts when antigen may cause the expansion of a population of specific cells.

Animals↗
PubMedDate not supplied

Induction of Fas and Fas-ligand expression in plasmacytoma cells by a cytotoxic factor secreted by murine macrophages.

Induction of tumoricidal activity is one of the major functions of activated macrophages. Our previous study demonstrated that P388D1 murine macrophage-like cells secreted a plasmacytoma cytotoxic factor (PCF) that selectively killed certain tumor cell lines including MOPC-315 plasmacytoma in vitro. Our subsequent studies demonstrated that PCF killed MOPC-315 cells by induction of apoptosis. In this report, the involvement of Fas and Fas ligand (FasL) in PCF-induced apoptosis was investigated. Results suggest that expression of Fas mRNA time-dependently increased in PCF-treated cells and reached an optimal level after 36 h of treatment. The augmented effect of PCF on Fas mRNA expression was significantly reduced by the addition of CB7.C2, an anti-PCF monoclonal antibody. The expression of FasL mRNA was also induced by PCF and reached an optimal level at 24 h, but sharply decreased after 36 h of treatment. Caspase-3 is one of the proteolytic enzymes that can be activated by the Fas-FasL interaction. In our studies, the enzymatic activity of caspase-3 was significantly induced by PCF after 6 h of treatment and reached an optimal level at 12 h. The augmented effect of PCF on caspase activity was significantly reduced by the addition of CB7.C2 and the caspase-3-specific inhibitor, DEVD-fmk. Therefore, PCF-treated plasmacytoma cells might undergo apoptosis via interaction between Fas and FasL.

Animals↗
PubMedDate not supplied

Cellular and cytokine responses in the circulation and tissue reactions in the lung of rhesus monkeys (Macaca mulatta) pretreated with cyclosporin A and challenged with staphylococcal enterotoxin B.

Cyclosporin A (CsA), an inhibitor of T cell cytokine production, protects mice against staphylococcal enterotoxin B (SEB) intoxication. To determine whether CsA treatment would work in a species closer to humans. 4 rhesus monkeys were given 50 mg/kg CsA followed by an intratracheal challenge with approximately 6 LD50 of SEB. The CsA was not protective: one of the monkeys died and the other three had to be euthanised when they became moribund. All monkeys made IL-2, TNF, and IFN-gamma in response to SEB. In addition, there was about a 10-fold increase in ACTH levels 2 hr after SEB challenge. CsA significantly suppressed in vitro proliferation of lymphocytes from treated monkeys. Both CsA-treated monkeys and monkeys that had been challenged in a previous experiment with a lethal dose of SEB but had received no cyclosporin had pathologic changes in several organs. The most prominent changes were marked edema and leukocytic infiltration of the bronchial and bronchiolar mucosa. The CsA treatment appeared to reduce the intensity of lung inflammation, but this effect was not sufficient to protect the monkeys. The results suggest that CsA alone may not be an effective therapeutic agent for humans suffering from SEB intoxication or gram-positive septic shock.

Adrenocorticotropic Hormone↗