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Biomedical subjects

C C Chang

Publications and source records attributed to C C Chang.

At least 631 records · Page 35Linked to original sources
PubMed1981

Immune response in the bovine mammary gland after intestinal, local, and systemic immunization.

The immune response in mammary glands of cattle was measured after intestinal, local, and systemic immunization with T4 bacteriophage. Nonlactating pregnant cows were immunized by infusions into the intestine or mammary gland and by subcutaneous injections in the region of the prescapular or external inguinal lymph nodes. Titers of antibodies of different isotypes were measured in serum and in lacteal secretions by enzyme-linked immunosorbent assay, and numbers of cells producing antibodies of each isotype were determined in lacteal secretions by the Jerne plaque assay. Substantial increases in immunoglobulin G subclass 1 (IgG1) and IgG2 antibody titers were detected in serum and lacteal secretions of animals immunized through an intestinal fistula. IgM and IgA antibody responses were low or undetectable. Low numbers of IgA and IgG1 plaque-forming cells were occasionally detected. It is proposed on the basis of these data that migration of antigen-stimulated IgG lymphoblasts, and perhaps of antigen, to spleen and peripheral lymph nodes may be dominant events after intestinal immunization of ruminants. This is consistent with the predominance of serum-derived IgG antibodies in colostrum and milk. Intramammary infusion of antigen gave rise to increases in antibody titers in all classes which were greater not only in lacteal secretions but also in blood serum than with either systemic route used. There was clear evidence from relative antibody titers for local synthesis of antibodies, principally IgA and IgG1, in the immunized glands. Comparison of IgA titers in secretions from the immunized glands with those in serum also suggested that locally synthesized IgA antibodies may have contributed in some measure to serum titers. Local synthesis in both immunized and nonimmunized glands was also reflected by the presence of increased numbers of IgA and IgG1 plaque-forming cells. It is hypothesized that antibody-forming cells responsible for local synthesis originated in lymphoid tissue within the mammary gland or from peripheral lymph nodes, depending upon the route of immunization.

Animals↗
PubMed1981

PBB inhibits metabolic cooperation in Chinese hamster cells in vitro: its potential as a tumor promoter.

Using an in vitro assay system, polybrominated biphenyl (PBB) was assessed for its ability to inhibit metabolic cooperation between 6-thioguanine sensitive and resistant Chinese hamster V79 cells. Using a nonlethal range of the chemical, PBB was shown to inhibit metabolic cooperation (a form of cell-cell communication) in a manner similar to other known tumor promoters. Results suggest that PBB could act, epigenetically, as a teratogen and a carcinogenic promoter.

Animals↗
PubMed1981

A synthetic peptide capable of eliciting antibodies that neutralize human chorionic gonadotropin.

Antisera generated to the human chorionic gonadotropin beta-subunit (hCGbeta) have been shown not only to neutralize the biologic activity of hCG but also to cross-react with human luteinizing hormone (hLH). In an attempt to reduce such cross-reactivity, a peptide fragment analogous to the amino acid sequence of the carboxylterminal 45 residues (101-145) of the hCGbeta-subunit with alpha-aminobutyric acid substituting for cysteine at position 110 was synthesized and tested for ability to produce antibodies interacting with hCG. Antisera were generated in rabbits to a conjugate of this peptide with tetanus toxoid emulsified with Freund's complete adjuvant. Antibody titers and specificity were assessed by the double-antibody technique. The results show that the antisera to the synthetic hCGbeta fragment bound 125I-labeled hCG and did not cross-react with hLH in the radioimmunoassay system. Most importantly, the antisera effectively neutralized the biologic activity of hCG as determined by the rat uterine weight assay.

Amino Acid Sequence↗
PubMed1980

Applicability of the phosphorus-31 (oxygen-17) nuclear magnetic resonance method in the study of enzyme mechanism involving phosphorus.

The phosphorus-31 (oxygen-17) [31P (17O)] NMR method [Tsai, M.-D. (1979) Biochemistry 18, 1448-1472] is tested for its general applicability by correlation with the line widths of the 17O NMR signals for the following compounds: trimethyl [17O4]phosphate (1), [17O4]phosphate (2), [alpha-17O2]adenosine 5'-(thiophosphate) (3), [alpha-17O, alpha beta-17O]-adenosine 5'-(1-thiotriphosphate) (4) [gamma-17O3]adenosine 5'-triphosphate (5), [alpha beta, beta gamma-17O2, beta-17O2]adenosine 5'-triphosphate (6), magnesium [gamma-17O3]adenosine 5'-triphosphate (7), and magnesium [alpha beta, beta gamma-17O2, beta-17O2]adenosine 5'-triphosphate (8). It is found that the line broadening effect of 17O on the 31P signals of the directly bonded 31P nuclei is present for all the functional groups in the above compounds which include examples of small 17O line widths (1 and 2), of intermediate 17O line widths (3, 5, and the nonbridge 17O of 4 and 6), and of very large 17O line widths (7, 8, and the bridge 17O of 4 and 6). On the basis of the established approximate relationship delta chi delta Q approximately aJ2, where delta chi and delta Q are the 31P and 17O line widths, respectively, of the 31P-17O groups, alpha is a constant, and J is the 31P-17O coupling constant, the results suggest that for most of the phosphate derivatives of biochemical interest, the line broadening effect of 17O should be present and detectable; i.e., delta chi should be larger than the limiting value (approximately 20 Hz). It is also found that Mg2+ causes the 17O signal of 5 and 6 to broaden (delta Q increases), which in turn causes the 31P signal to sharpen (delta chi decreases). The finding suggests that the 31P (17O) NMR methods, in combination with 17O NMR, could become a tool to study diamagnetic metal ion-nucleotide interactions.

Adenosine Triphosphate↗
PubMed1980

Saccharin may act as a tumour promoter by inhibiting metabolic cooperation between cells.

The possible role of saccharin in the carcinogenic process is, at present, still unclear. Carcinogenesis is a complex process involving, in many test systems, initiation and promotion phases. Current evidence favours the hypothesis that initiation is due to a mutagenic event, while promotion (at least the early portion) is the result of epigenetic changes. Although saccharin has been reported to be a weak mutagen in various in vitro test systems and a weak initiator in mouse skin, there is increasing evidence from in vitro, as well as in vivo, studies that it might act as a tumour promoter, rather than as a mutagen. Recently L.P.Y. et al and J.E.T. et al. developed an in vitro assay to detect tumour promoters, which has been independently reported by Murray and Fitzgerald. The assay is based on the principle that phorbol ester-type tumour promoters block 'metabolic cooperation' or a type of cell-cell communication between cells. We report here a series of experiments demonstrating the elimination of metabolic cooperation in the hypoxanthine guanine phosphoribosyltransferase (HGPRT) system in Chinese hamster V79 cells, indicating that saccharin shares properties similar to those of other known promoters.

Animals↗
PubMed1980

Ultraviolet light induction of diphtheria toxin-resistant mutations in normal and DNA repair-deficient human and Chinese hamster fibroblasts.

The role of unrepaired DNA lesions in the production of mutations is suspected of contributing to the initiation phase of carcinogenesis. Since the molecular basis of mutagenesis is not understood in eukaryotic cells, development of new genetic markers for quantitative in vitro measurement of mutations for mammalian cells is needed. Furthermore, mammalian cells, genetically deficient for various DNA repair enzymes, will be needed to study the role of unrepaired DNA lesions in mutagenesis. The results in this report relate to preliminary attempts (1) to characterize the diphtheria toxin resistance marker as a useful quantitative genetic marker in human cells and (2) to isolate and characterize various DNA repair-deficient Chinese hamster cells.

Animals↗
PubMed1980

An integrative hypothesis linking cancer, diabetes and atherosclerosis: the role of mutations and epigenetic changes.

It appears that the disease states of cancer, altherosclerosis and diabetes might share a common etiology. These chronic diseases appear to be multi-staged in their progression, with genetic, nutritional, psycho-social, environmental and viral factors influencing their appearance. We offered a hypothesis (a "mutation theory of disease"), stating that these diseases can be described by initiation and promotion phases; initiation being the result of the production of mutated cells after unrepaired damaged DNA is replicated; promotion being the selective proliferation of the initiated cells to form clones of mutated cells. It was further postulated that promotion affects cell proliferation by altering a membrane-Ca++ regulatory system. Depending on the nature of the mutation in the clone of cells, specific disease states would result. The roles of radiations, chemicals, viruses, genes, nutrition and psycho-social stress were related to either the initiation (mutation production) or the promotion (cell proliferation) phase of these diseases.

Arteriosclerosis↗