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Biomedical subjects

T W Chang

Publications and source records attributed to T W Chang.

At least 91 records · Page 5Linked to original sources
PubMed1983

Chronic diarrhea associated with Clostridium difficile in children.

Clostridium difficile toxin was associated with chronic diarrhea without classic symptoms of colitis in seven children (age range, 7 weeks to 7 years). All patients had received antibiotics. Six of the seven were treated with vancomycin hydrochloride and demonstrated improvement. After treatment, four patients suffered relapses, and three required further therapy. One patient had four relapses. During all clinical relapses, toxin reappeared in the stool; recovery was always associated with its disappearance. Fifty-six percent of family contacts examined had positive cultures. These findings document C difficile as a probable cause of chronic diarrhea in childhood and emphasize its infectious potential.

Bacterial Toxins↗
PubMed1983

Quantitative of anti-NP (4-hydroxy-3-nitrophenyl)-acetyl idiotype expression on spleen and thymus cells.

Direct binding of 125I-labeled rabbit anti-NPb idiotype antibodies (RaId) was used to quantitate the expression by immune spleen and thymus cells of NPbId, the characteristic Id of the lambda 1-containing antibodies made by C57BL/6 (B6) mice to the (4-hydroxy-3-nitrophenyl)acetyl (NP) group. Direct binding of RaId by B and T cell preparations reached a maximum of 12 ng RaId per 10(8) cells at 7 days after immunization. Spleen T cell preparations maintained similar levels of binding after positive selection for Thy-1.2+ cells and overnight culture. RaId binding was also demonstrated for immune B6 thymus cells and for spleen and thymus cells of immune SJL mice, which have the appropriate heavy chain allotype for NPbId expression but have only barely detectable serum Id. However, the NPbId of T and B cell preparations were indistinguishable by (a) the susceptibility of RaId binding by the cells to inhibition by hapten or by antibodies to the variable regions of lambda light chains (anti-V lambda) and by (b) the ability of anti-V lambda and of monoclonal antibodies to the constant region of lambda 1 chains (anti-C lambda 1) to immunoprecipitate antigen (NP10-bovine serum albumin)-binding proteins from detergent extracts of isotopically labeled cells. The results strongly imply that virtually all of the NPbId of T cell preparations is due to conventional NPbId antibody that is tightly bound to T cells. The results do not, however, exclude the possibility that the T cell preparations contain a trace amount (less than or equal to 1 ng/10(8) cells) of unusual NPbId-like molecules that lack lambda chains.

Animals↗
PubMed1982

Rapid identification of Clostridium difficile by toxin detection.

Rapid identification of Clostridium difficile in a stool specimen could be accomplished within 24 h by detection of toxin elaborated in an agar or broth culture containing cycloserine and cefoxitin. Broth culture seemed to give a more rapid and sensitive result than the agar plate culture. For cultivation of C. difficile in stool, we recommend the use of chopped meat broth and blood agar plate, the former for toxin detection in 1 to 2 days and the latter for colonial morphology and isolation of a pure culture.

Bacterial Toxins↗
PubMed1982

Cellular origin and interactions involved in gamma-interferon production induced by OKt3 monoclonal antibody.

OKT3 monoclonal antibody, a human T cell mitogen, induced interferon production by cultured mononuclear cells at 10(-11) M concentrations. Interferon was secreted only under conditions wherein OKT3 was mitogenic, and production was correlated with cell proliferation. Thus, like mitogenesis, interferon secretion reached a peak 3 days after OKT3 stimulation, was inhibited by a factor(s) in human serum, and required 1000 times higher concentrations of Fab and F(ab')2 fragments of OKT3 for induction. The interferon was most likely of "gamma" (immune) type, because pH 2 and 56 degrees C treatments denatured it, whereas anti-alpha or -beta interferon antibodies did not. Mononuclear cells were fractionated into subpopulations that contained OKT4+ cells (helper/inducer T cells), OKT8+ cells (cytotoxic/suppressor T cells), and OKM1+ cells (monocytes) by combining sheep red blood cell rosetting and complement-mediated lysis using monoclonal antibodies against specific cell types. Both OKT4+ and OKT8+ cells proliferated upon OKT3 stimulation with the absolute requirement of OKM1+ cells. However, OKT4+ cells plus OKM1+ cells were necessary for the secretion of interferon. Studies with selective pretreatments with mitomycin C suggested that gamma-interferon was secreted by the OKT4+ cells and that the OKM1+ population subserved an accessory function.

Animals↗
PubMed1982

Induction of T cell proliferation and lymphokine production by monoclonal antibody.

The studies of the biological effects of OKT3 monoclonal antibody on mature human T cells demonstrate that binding to a differentiation antigen by an antibody can modulate the specialized functions of the cells bearing the antigen. OKT3 induces T cells to proliferate and to secrete gamma interferon. The antibody also inhibits cytotoxic T cells from lysing target cells. The mechanisms involved and the nature of the antigen to which OKT3 binds are discussed.

Antibodies, Monoclonal↗
PubMed1981

OKT3 monoclonal antibody inhibits cytotoxic T lymphocyte mediated cell lysis.

Human alloreactive cytotoxic T lymphocytes (CTLs) were generated in culture by stimulating peripheral blood lymphocytes against lymphocytes of unrelated donors. OKT3 monoclonal antibody, which reacts with all human peripheral T cells, inhibited more than 50% of the lysis of the allogeneic cells by the CTLs in the four-hour cytotoxicity assay at a concentration of 1 microgram ml-1. OKT4, which reacts with inducer/helper T cells, did not demonstrate this effect. OKT5 and OKT8, both of which react with cytotoxic/suppressor T cells, had a small but distinct inhibitory effect (about 20-30% maximally). OKT3 antibody is also known to induce mitogenesis of peripheral T cells, but this mitogenic effect is probably of itself not the cause of the inhibitory effect of OKT3 on CTLs. Human plasma abolished OKT3-induced mitogenesis of T cells but not OKT3-mediated inhibition of CTL activity. In addition, there exist conditions that allow both full mitogenesis and intact CTL activity, suggesting CTLs can maintain cytolytic activity under mitogenic conditions. The generation of CTLs in the 6-day mixed lymphocyte culture was also inhibited by OKT3. Several possible mechanisms for this effect are discussed.

Antibodies, Monoclonal↗
PubMed1981

Does OKT3 monoclonal antibody react with an antigen-recognition structure on human T cells?

OKT3 monoclonal antibody to human T cells inhibits the target cell lysis mediated by allogeneic cytotoxic T cells and the generation of these effector cells in mixed lymphocyte culture. This marked inhibition of cell-mediated lysis is not found with other monoclonal antibodies also reactive with cell surface antigens of human T cells (OKT1, OKT4, OKT5, OKT6, OKT8, and OKT11). OKT3 antibody is mitogenic and this effect appears to require receptor activation in that it occurs at low concentrations (10(-12) M range) of OKT3 antibody, requires intact OKT3 IgG, and is inhibited by a factor(s) in human plasma. By contrast, the inhibition of allogeneic cell-mediated lysis by OKT3 antibody appears to be due to steric hindrance in that it requires higher concentrations of OKT3 antibody (10(-8) M range), Fab fragments retain approximately 10% activity, and inhibition is demonstrable in the presence of human plasma. These findings are consistent with the suggestion that OKT3 antibody reacts with the human T-cell antigen-recognition structure.

Adult↗
PubMed1981

Ribavirin and inosiplex: a review of their present status in viral diseases.

A considerable amount of information has accumulated during the past 10 years in the search for antiviral agents. Ribavirin and inosiplex are 2 interesting developments to come out of this search. Ribavirin, a synthetic nucleoside, has an unusually wide spectrum of antiviral activity, especially when tested in vitro. A large number of RNA and DNA viruses are sensitive, especially herpes viruses, poxvirus, influenza, parainfluenza, reovirus, togavirus, and RNA tumour viruses. The in vivo antiviral spectrum of activity is much narrower, with activity against herpes virus, influenza, parainfluenza, measles and adenoviruses. However, controlled clinical trials have not been uniformly successful in treating influenza, hepatitis, herpes simplex and herpes zoster. Inosiplex has been shown to have antiviral activity in vivo against influenza, herpes simplex, rhinovirus and vaccinia virus infections. However, antiviral activity has not been consistently demonstrated, and this observation led to further studies which revealed its immunomodulating effects. The accumulated evidence has indicated that inosiplex is more a prohost agent rather than an antiviral drug. Immune functions which are depressed during viral infection can be restored to normal by inosiplex therapy. At present, neither ribavirin nor inosiplex alone has been shown to be uniformly successful in the treatment of human viral diseases. Nevertheless, their potential place in chemotherapy should not be neglected, although further data are needed to determine what this place will be. Whether combining them with other antiviral agents such as interferon, acyclovir, Ara-A, and so on, would produce a potentiation of action and improved antiviral chemotherapy, will be an interesting area for further study.

Animals↗
PubMed1981

Regulation of influenza virus-specific cytotoxic T cell responses by monoclonal antibody to a human T cell differentiation antigen.

The results in this report indicate that the OKT3 monoclonal antibody, which is specific for a human T cell differentiation antigen present on 90 to 95% of peripheral T cells, can exert several effects that regulate the generation and expression of human influenza virus-immune cytotoxic T lymphocytes (CTL). The OKT3 antibody, but not OKT1 or OKT11 (which bind to all peripheral T cells), is able to inhibit anti-influenza CTL effector cell activity. An F(ab')2 preparation of OKT3 IgG were as effective as whole IgG for the inhibition of CTL effectors, indicating that the inhibitory activity of the antibody was not a function of the Fc portion of the molecule. OKT3 IgG and OKT3 F(ab')2 fragments (but not OKT4, OKT8, or OKI were able to inhibit the generation of anti-influenza CTL. The culture of human lymphoid cells with OKT3 in the presence or absence of influenza virus induced radioresistant cells that could suppress the CTL response of fresh autologous lymphocytes to influenza. These results suggest that T cell functions can be regulated by signals that are initiated by the binding of antibody to cell surface molecules that may not be related to the T cell antigen-specific receptor(s).

Animals↗
PubMed1980

Inhibition of binding of Clostridium difficile toxin by steroids.

No detectable inhibition of binding of Clostridium difficile toxin to human erythrocyte lysate was found with alpha-D-(+)-fucose, 1-(-)-fucose, ribose, arabinose, mannose, galactose, xylose, galactosamine, glucosamine, mannosamine, N-acetyl glucosamine, N-acetyl galactosamine, N-acetyl mannosamine, N-acetyl neuraminic acid, lactose, sucrose, lactulose, neuraminidase, saponin, or amantadine. Inhibition was found, however, with a number of sterols and bile acids. In general, bile acids were more active than cholesterol and related compounds. When the bile salts were added greater than or equal to 10 min after exposure to toxin, inhibition was no longer observed. These results suggest that the membrane receptor for C. difficile toxin is not likely to be a carbohydrate component. On the other hand, the inhibitory activity by steroids suggests that a lipid component may play an important role in toxin binding.

Binding, Competitive↗
PubMed1980

Bacitracin treatment of antibiotic-associated colitis and diarrhea caused by Clostridium difficile toxin.

Four cases of antibiotic-associated colitis and diarrhea caused by Clostridium difficile were successfully treated with oral bacitracin, 25,000 units four times daily for 7-10 days. Diarrhea resolved in all of the cases, in 2 days, with disappearance of Clostridium difficile toxin in the stools in 3 out of 4 patients so measured. Two of the patients treated had relapses after vancomycin, while the other 2 were experiencing the first episodes. One patient relapsed after bacitracin treatment, but was treated successfully with vancomycin. Our preliminary experience indicates that bacitracin, being less expensive and more readily available world-wide than vancomycin, could be used as an alternative drug for toxin-induced colitis or diarrhea.

Adult↗