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Biomedical subjects

C C Chang

Publications and source records attributed to C C Chang.

At least 649 records · Page 36Linked to original sources
PubMed1980

Antibody-producing cells in bovine lacteal secretions after local immunization.

The indirect Jerne plaque assay was used to determine the presence of antibody-forming cells in lacteal secretions of 2 cows inoculated in the mammary gland with T4 phage. Two adjacent mammary glands of 2 nonlactating 7-months pregnant cows were inoculated by intramammary injection 4 times at 3- to 5-day intervals. The presence of plaque-forming cells (PFC) was assessed in each quarter beginning on postinoculation day 8 and at 4- to 14-day intervals thereafter. Amounts of antibodies in serum and secretions were measured by an indirect hemagglutination test. The PFC were detected in secretions from all quarters of both cows between postinoculation days 8 and 32. Concentrations of PFC fluctuated within quarters during the course of the experiment but no relationship was evident between numbers of PFC in a quarter and its inoculation status. The use of monospecific antiglobulin sera at 1 sample-collection period revealed that cells synthesizing immunoglobulin (Ig)G and IgA antibodies were predominant in lacteal secretions. Antibody amounts in serum and secretions rose after inoculation, and titers in secretions were markedly higher in most instances. Antibody-forming cells were thus demonstrated to accumulate in the mammary gland after intramammary inoculation. The presence of antibody-forming cells in non-inoculated glands may have been the result of antigen transfer among quarters, but was considered more likely to have resulted from systemic migration of antigen-stimulated cells with migration into all quarters, regardless of inoculation status. Antibodies in lacteal secretions may have accumulated through a combination of local synthesis and selective transport from the bloodstream.

Animals↗
PubMed1980

Changes of serum protein and immunoglobulin in toxemia of pregnancy.

The immune mechanism theoretically may play an important role in toxemia of pregnancy. Serum proteins, immunoglobulins and C3 were measured in 20 women with normal pregnancy and in 10 women with toxemia of pregnancy. Compared with the normal pregnancy, the toxemia group exhibited decreased albumin and IgG, and significant increases in alpha 1 globulin and IgE. The immunological implication of these changes deserves further investigation.

Blood Proteins↗
PubMed1979

Elimination of metabolic cooperation in Chinese hamster cells by a tumor promoter.

Wild-type Chinese hamster V79 cells (6-thioguanine-sensitive) reduce the recovery of 6-thioguanine-resistant cells when they are cultured together at high densities, through a form of intercellular communication (metabolic cooperation). Cooperation is inhibited by 12-O-tetradecanoyl phorbol-13-acetate, rescuing the 6-thioguanine-resistant cells. These results may be useful in the study of an aspect of the mechanism of tumor promotion and in assaying for promoters.

Animals↗
PubMed1979

Proton nuclear magnetic resonance study of cobrotoxin.

Cobrotoxin (Mr 6949), which binds tightly to the acetylcholine receptors, contains no phenylalanines and only two histidines, two tyrosines, and one tryptophan that result in well-resolved aromatic proton resonances in D2O at 360 MHz. His-32, Tyr-25, and the Trp are essential for toxicity and may interact with the acetylcholine receptor. We assign two titratable resonances (pKa = 5.1) at delta = 9.0 and 7.5 ppm at pH 2.5 and at 7.7 and 7.1 ppm at pH 9.5 to the C-2 and C-4 ring protons, respectively, of His-4. Two other titratable resonances (pKa = 5.7) at delta = 8.8 and 6.9 ppm at pH 2.5 and at 7.8 and 6.7 ppm at pH 9.5 are assigned to the C-2 and C-4 ring protons of His-32, respectively. The differences in delta values of the two histidines reflect chemically different microenvironments while their low pKa values could arise from nearby positive charges. A methyl resonance gradually shifts upfield to delta approximately 0.4 ppm as His-4 is deprotonated and is tentatively assigned to the methyl group of Thr-14 or Thr-15 which, from published X-ray studies of neurotoxins, are located in the vicinity of His-4. Further, we have identified the aromatic resonances of the invariant tryptophan and individual tyrosines and the methyl resonance of one of the two isoleucines in the molecule. Several broad nontitrating resonances of labile protons which disappear at pH greater than 9 may arise from amide groups of the beta sheet in cobrotoxin.

Amino Acid Sequence↗
PubMed1979

Ultraviolet light induction of diphtheria toxin-resistant mutants of normal and xeroderma pigmentosum human fibroblasts.

The UV induction of diphtheria toxin-resistant (DTr) mutants in normal and xeroderma pigmentosum human fibroblasts has been quantitatively characterized. A concentration of diphtheria toxin at which DTr cells are cross-resistant to Pseudomonas aeruginosa exotoxin A was determined and used in the selection of resistant mutants. Recovery of mutants was not influenced by the presence of wild-type cell densities of 1-8 x 10(5) per 9-cm plate, indicating no metabolic cooperation exists, in contrast to what is seen in the selection of some other variant phenotypes. Expression periods for UV-induced mutations differed with the severity of mutagen treatment and cell strain used. A relatively long (10-15 days after UV treatment) expression period was required for the maximum recovery of DTr mutants. Maximum recovery was followed by a decrease in mutation frequency on subsequent days evaluated. An apparent linear dose response within the dose range used was observed for UV-induced mutations in both normal and xeroderma pigmentosum fibroblasts. Our results indicate that xeroderma pigmentosum fibroblasts have higher UV-induced mutation frequencies per unit UV dose but similar frequencies per unit survival compared to normal cells within the range of UV doses tested.

Cells, Cultured↗
PubMed1978

Characterization of ultraviolet light-induced ouabain-resistant mutations in Chinese hamster cells.

Ouabain-resistant mutations in Chinese hamster cells have been quantitatively characterized. The mutation frequencies were found to be induced curvilinearly with treatments of increasing doses of ultraviolet light (UV). For the range of UV doses tested (5--20 J/m(2)), the observed frequency, Y, as a function of UV dose X, follows a curvilinear function, Y = (-28 + 13.37 X--1.52X(2) + 0.08X(3)) . 10(-6). The frequencies of UV-induced mutations were directly correlated with cell survival, indicating a similar causal relationship between cell killing and mutation induction. Under the same experimental conditions, X-rays induced 6--thioguanine-, but not ouabain-, resistant mutations. UV-induced ouabain-resistant (ouar) mutants exhibit a selection disadvantage. Their phenotypic expressions are modifiable by various agents. Wild type and 16 ouar mutants were compared with respect to their sensitivity to ouabain inhibition of 86Rb uptake by whole cells. All the ouar mutants assayed are less sensitive to the drug than are wild-type cells. In the absence of ouabain, the Na+--K+--ATPase activities can be significantly higher or lower than that of the wild-type cells.

Adenosine Triphosphatases↗
PubMed1978

Modification of UV-induced mutation frequencies in Chinese hamster cells by dose fractionation, cycloheximide and caffeine treatments.

Chinese hamster (V79) cells were irradiated with a fractionated regime of ultraviolet light (UV1 + UV2). The fractionation of a UV dose always increased the colony-forming ability but reduced (or it did not change) the mutation frequencies. Treatment with cycloheximide between the two UV irradiations resulted in two types of effects, depending on the protocols used. Long exposures to cycloheximide (i.e., greater than 6 h) for the entire period between UV1 and UV2 or partial treatment of cycloheximide (i.e., 3 h) long before UV2 always resulted in reduced colony-forming ability and enhanced or unchanged mutation frequencies. Exposure to cycloheximide for the entire period in the short fractionated regime (i.e., 4 h) between UV1 and UV2 or partial treatment of cycloheximide just prior to UV2 tended to give the opposite effects. Caffeine treatment before UV2, with or without UV1, significantly increased the mutation frequencies. These results suggest that an error-free postreplication repair system exists in Chinese hamster cells which is inhibitable by particular cycloheximide or caffeine treatments.

Caffeine↗
PubMed1978

Environmental carcinogenesis: an integrative model.

An integrative theory is proposed in which environmental carcinogenesis is viewed as a process by which the genetic control of cell division and differentiation is altered by carcinogens. In this theory, carcinogens include physical, chemical, and viral "mutagens," as well as chemical and viral gene modulators. Existing explanations of carcinogenesis can be considered either as somatic mutation theories or as epigenetic theories. Evidence seems to support the hypothesis that both mutations and epigenetic processes are components of carcinogenesis. The mutational basis of cancer is supported by the clonal nature of tumors, the mutagenicity of most carcinogens, high mutation frequencies in cells of cancer-prone human fibroblasts lacking DNA repair enzymes, the correlation of in vitro DNA damage and in vitro mutation and transformation frequencies with in vivo tumorigenesis, age-related incidences of various hereditary tumors, and the correlation between photoreactivation of DNA damage and the biological amelioration of UV-induced neoplasms. Since both mutagens and gene modulators can be carcinogenic it may be that carcinogens affect genes which control cell division. An integration of the mutation and epigenetic theories of cancer with the "two-stage" theory and Comings's general theory of carcinogenesis is proposed. This integrative theory postulates that carcinogens can affect regulatory genes which control a series of "transforming genes." A general hypothesis is advanced that involves a common mechanism of somatic mutagenesis via error-prone repair of DNA damage which links carcinogenesis, teratogenesis, atherosclerosis and aging. Various concepts are presented to provide a framework for evaluating the scientific, medical, and social implications of cancer.

Aging↗
PubMed1978

Purification and properties of non-precipitating antibodies to cobrotoxin.

The heterogeneity of precipitating and non-precipitating antibodies to cobrotoxin was demonstrated by their elution pattern on cobrotoxin-Sepharose and chromatography on DEAE-cellulose column. Gel filtration patterns on a Sepharose 6B column revealed that the soluble complexes formed from non-precipitating antibody and HNB-cobrotoxin at a different molar ratio all emerged in the void volume, indicating that the molecular weight of the soluble complex is around 4,000,000 or larger. Unreacted free non-precipitating antibody coincided with the peak of IgG and was proved to be free from HNB-cobrotoxin. The molar ratio of antibody to antigen for the soluble complex was found to be 0.79 to 0.97 indicating that 1.58--1.94 molecules of non-precipitating antibody are bound to HNB-cobrotoxin instead of three molecules as in the case of precipitating antibody.

Antibodies↗
PubMed1978

Effect of crotamine, a toxin of South American rattlesnake venom, on the sodium channel of murine skeletal muscle.

1 Crotamine (0.5 mug/ml) augmented the single twitch response of the rat and mouse isolated diaphragm to direct stimulation and prolonged the time course of contraction. At higher doses (10 to 50 mug/ml), contracture was observed with spontaneous fibrillation.2 The resting membrane potential of diaphragm was rapidly depolarized to about -50 mV within 5 minutes. No increase of depolarization occurred on prolongation of the incubation time or increase of crotamine concentration from 0.5 mug/ml to 50 mug/ml. The effect was not reversed by washing.3 Tetrodotoxin, low Na(+) (12 mM), Ca(2+) (10 mM) and procaine (1 mM) prevented the crotamine-depolarization. However, depolarization resumed when crotamine and the antagonists were removed.4 Low Cl(-) (8.5 mM) and pretreatment with ouabain enhanced depolarization by crotamine.5 High K(+) (25 to 50 mM) prevented the further depolarization by crotamine and the membrane potential was restored to normal on washout of crotamine with normal Tyrode solution.6 Effective membrane resistance was decreased by about 50% by crotamine.7(24)Na-influx of the rat diaphragm was increased by crotamine. (42)K-influx was slightly increased if tetrodotoxin was also present but was decreased in the absence of tetrodotoxin.8 No effect on the miniature and evoked endplate potential of the rat diaphragm was observed. Skeletal muscles from frog and chick were not affected.9 It is inferred that crotamine acts on a molecule regulating the Na(+) - permeability of the Na(+) channel of murine muscles. It is proposed that extracellular K(+) depresses the permeability of the Na(+) channel by acting on the same regulator molecule.

Animals↗