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Biomedical subjects

T Chiang

Publications and source records attributed to T Chiang.

125 records · Page 7Linked to original sources
PubMed1982

Inhibition of chlortetracycline activity by magnesium ions.

Up to 50% of the antimicrobial activity of chlortetracycline (CTC) can be inhibited by the presence of MgSO4 in microbiological turbidimetric assays. From 50 to 200 mM MgSO4 inhibited CTC activity, and the relationship between CTC inhibition and MgSO4 concentration is linear. The possible mechanism of this inhibition and its potential implication are discussed.

Chlortetracycline↗
PubMed1982

Inhibition of lung metastases in mice bearing a malignant fibrosarcoma by treatment with liposomes containing human C-reactive protein.

Recent studies suggest an immune modulator role for C-reactive protein (CRP). We have tested the effect of CRP in a tumor system designed for study of metastases. Fibrosarcoma T241 was implanted on one hind foot of syngeneic C57BL/6 mice. After 17 days, the tumor-bearing feet were amputated, and i.v. therapy of liposomes containing CRP or control reagents was started. Examination of the lungs on Day 35 showed that CRP:liposome-treated animals had significantly fewer and smaller metastases as compared with those in the control groups. Moreover, 38% of the animals in the former groups were completely free of metastases as compared with 0 to 2% of the controls. Significantly, enhanced survival was also noted in the CRP liposome-treated group. CRP may have biological response modifier" function of value in cancer therapy.

Animals↗
PubMed1980

Location of ribosome-binding sites in the nin5 region of bacteriophage lambda.

Seven ribosome-binding sites on DNA have been located within the region defined by the nin5 deletion as well as several ribosome-binding sites on each side of the nin5 region. These were mapped by electron microscopy relative to the end points of the nin5 deletion and two Tn903 transposons, one inserted into gene Rz and another inserted near gene Q. These ribosomes binding sites within the nin5 region may correspond to polypeptide initiation sites for up to seven new dispensible lambda genes.

Bacteriophage lambda↗
PubMed1979

Serum alpha-tocopherol, lipids, potassium, and creatine phosphokinase in normal and malabsorption patients.

Serum alpha-tocopherol, lipids, potassium, and creatine phosphokinase levels were measured in 20 adult male control patients and eight malabsorption patients. The malabsorption group had significantly lower serum alpha-tocopherol levels than the control group. This change was independent of serum total lipid levels that were not significantly different among the two groups. Serum potassium and creatine phosphokinase levels that are normally used to assess muscle pathology in man did not correlate with serum alpha-tocopherol levels in either the control of the malabsorption groups. Body mass indices that are directly related to adiposity of the individuals were calculated. Among the control patients, there was a significant increase in serum alpha-tocopherol and serum total lipids with increase in body mass index. Similar correlations did not exist in the malabsorption group. In the latter group serum alpha-tocopherol levels may have reached low enough levels to be independent of factors such as adiposity and serum total lipids.

Adipose Tissue↗
PubMed1979

Enhancing effect of thyroxine on tumor growth and metastases in syngeneic mouse tumor systems.

We studied the effect of thyroxine treatment on tumor growth and metastases resulting from tumor implants on the hind feet of mice in two syngeneic systems. In control, untreated A/Jax mice, tumor Sarcoma 1 at Day 14 after implantation had average tumor weight of 582 +/- 60 (S.D.) mg and showed an incidence of 57% metastases to regional popliteal nodes and 5% metastases to thymus. In contrast, the thyroxine-treated group (40 microgram/mouse s.c., 5 times/week for 1 month) had an average tumor weight of 808 +/- 56 mg (p less than 0.001), and metastases to popliteal nodes and thymus were 90 and 35%, respectively. In another syngeneic tumor system, Lewis fibrosarcoma was implanted in C57BL/6J mice, and the tumor weight and metastatic index (derived from the number and size of the pulmonary tumor foci) were determined at Day 28. Again, the synthetic L-thyroxine treated group showed a significant enhancement tumor growth and metastatic index. The mean tumor weight in the treated group was 385 +/- 26 mg (control, 694 +/- 25 mg; p less than 0.005) and metastatic index was 84 +/- 29 (control, 30 +/- 25; p less than 0.001). Induced hypothyroidism (treatment with 131I, 100 microCi/mouse i.p.) showed the reverse effect on both tumor systems. These results suggest that both tumor systems are dependent on thyroid hormones for their growth and spread.

Animals↗
PubMed1976

On the lack of host-cell reactivation of UV-irradiated phage T5. I. Interference of T5 infection with the host-cell reactivation of phage T1.

UV-irradiated phage T5, in contrast to T1, T3 and T7, fail to display host-cell reactivation (HCR) when infecting excision-repair proficient Escherichia coli cells. Possible causes of this lack of HCR (which T5 shares with the T-even phages) have been investigated by studying HCR of T1 under conditions of superinfection by T5. Repair-proficient B/r cells were infected at low multiplicity with UV-irradiated phage T1 in the presence of 1.8 mg/ml caffeine and were superinfected after 15 min with heavily UV-irradiated T5 amber mutants at highly multiplicity. The caffeine, which is later diluted out, prevents any T1 repair prior to T5 superinfection, and UV (254 nm) irradiation of T5 with 144 J/m2 reduces the ability of this phage to exclude T1, thus permitting a reasonable fraction of the mixedly infected complexes to produce T1 progeny. Under these conditions, T5 superinfection causes loss of HCR in about 90% of the T1-producing complexes. Superinfection with unirradiated T5 likewise inhibits HCR of T1, but superinfection with irradiated T3 (a host-cell reactivable phage) does not. This indicates that the observed HCR inhibition of T1 results from T5 infection rather than from competition of irradiated foreign DNA for the excision-repair enzymes of the bacterial host. Employment of appropriate T5 amber mutants has shown that "first-step transfer" (FST) of T5 DNA (involving only 8% of the T5 genome) is sufficient for HCR inhibition, but that transfer of the remainder DNA in addition inhibits a previously described minor T1 recovery process. HCR inhibition of T1, and thus presumably lack of HCR in T5 itself, is ascribed to a substance which is produced either post infection by a gene located in the FST segment of the T5 genome, or which is transferred from extracellular T5 together with the FST DNA.

Coliphages↗
PubMed1976

On the lack of host-cell reactivation of UV-irradiated phage T5 II. Further characterization of the repair inhibition exerted by T5 infection.

Experiments reported in the preceding paper [4] had shown that host-cell reactivation (HCR) of UV-irradiated phage T1 in excision-repair proficient Escherichia coli cells is inhibited by superinfection with phage T5. Theoretical considerations have led to predictions concerning the dependence of repair inhibition on the multiplicity of superinfecting T5 phage and on the UV fluence to which they were exposed. These predicitions have been supported by experimental results described in this paper. The fluence dependence permitted calculation of the relative UV sensitivity of the gene function responsible for repair inhibition; it was found to be about 2.3% that of the plaque-forming ability of phage T5. The T5-inhibitable step in excision repair occurs early in the infective cycle of T1. Furthermore, experiments involving the presence of 400 mug/ml chloramphenicol showed that HCR inhibition of T1 is caused by a protein produced after the FST segment of T5 (i.e. the first 8% of the T5 genome) has entered the host cell. A previously described minor T1 recovery process, occurring in both excision-repair-proficient and -deficient host cells, is inhibited by T5 infection due to a different substance, which is most likely associated with the "second-step-transfer" region of T5 DNA (involving the remainder of the genome). Superinfection with T4v1 phage resulted in HCR inhibition of T1, resembling that observed after T5 superinfection. The discussion of these results suggests that inhibition of the bacterial excision repair system by T5 or T4 infection occurs at the level of UV-endonucleolytic incision, and that lack of HCR both in T-even phages and in T5 can be explained in the same manner.

Caffeine↗
PubMed1976

Bioassay for quantitating circulating tumor cells in a syngeneic mouse tumor system.

A bioassay is described for the quantitation of tumor cells in blood specimens in a syngeneic mouse tumor system (Sarcoma 1 in A/J mice). The procedure involved i.m. injection of blood containing tumor cells into each thigh of normal recipient mice and, 14 days later, examination of the sites of injection for evidence of tumor growth. For each specimen, a tumor index was calculated based on the number of tumor takes and the size of the tumors. The number of tumor cells was determined by comparison with tumor indices from standard specimens with known number of tumor cells. Optimal conditions for this assay were investigated. We have used this bioassay to quantitate tumor cells in the venous blood of tumor-bearing animals under various treatments and manipulations. At the same time, the incidence of regional node metastasis was obtained by direct histological examination. Surgical removal of a well-established primary tumor enhanced the dissemination of the tumor, as evidenced by an increased incidence in regional node metastasis and an increase in the number of tumor cells reaching the venous circulation. Similar results were obtained when the tumor-bearing feet were ligated to produce ischemia of the primary tumor. Repeated physical trauma to the primary tumor resulted in increased dissemination of tumor cells into the venous circulation, but it did not increase the incidence of regional node metastasis. Immunosuppression of the tumor-bearing animals increased the dissemination of tumor cells, whereas immunostimulation decreased the dissemination.

Animals↗
PubMed1976

Effects of the immunosuppressive drug niridazole in isogeneic and allogeneic mouse tumor systems in vivo.

In both isogeneic (Sarcoma 1 in A/JAX mice) and allogeneic (Sarcoma 180 in C57BL/6 mice) mouse tumor systems, treatment of the tumor-bearing mice with niridazole, an antiprarasitic drug, known to be a potent suppressor of cell mediated but not humoral immunity caused enhancement of metastases to regional popliteal nodes. Niridazole also inhibited tumor growth in vivo, as manifested by a significant decrease in the weight of the primary tumors. The enhancement of metastases is attributed to the suppression of cell-mediated immunity by the drug, but the mechanism of tumor-growth inhibition is not yet clear.

Animals↗
PubMed1974

Evidence against phenotypic mixing between bacteriophage T4 wild type and T4v minus.

In a recent publication Shames et al. (1973) concluded that the UV-specific T4 endonuclease (a repair enzyme coded for by the gene v of wild-type T4) is a component of extracellular phage, which is injected into the host cell and can perform an early repair step without requiring gene expression. This notion is, however, not supported by results presented in this paper. Lysates obtained from mixed multiple infection of Escherichia coli cells with T4v(1) (-) and T4v(+) (or T4v(2) (-) and T4v(+)) failed to show the expected phenotypic mixing, i.e., incorporation of UV endonuclease into capsids of v(-) phages resulting in recognizable repair. The fraction of v(+) and v(-) particles in such lysates was determined by single-plaque analysis before and after irradiation with a UV dose at which virtually all survivors are particles having undergone repair. Even though our mixed infection conditions were most favorable for the possible occurrence of phenotypic mixing, none out of several hundred individual plaques from survivors were found to be genotypically v(-), whereas 30 were expected in the case that phenotypically mixed v(-) particles were repaired like T4v(+). Our failure to observe phenotypic mixing suggests that the data by Shames et al. reflect intracellular synthesis of endonuclease after phage infection.

Coliphages↗