Search PubMed⌕ Search

Biomedical subjects

C D Kim

Publications and source records attributed to C D Kim.

61 records · Page 4Linked to original sources

Associations of major histocompatibility complex haplotypes with body weight and egg production traits in S1 White Leghorn chickens.

Body weights at 8, 20, and 32 wk, total egg production, average egg weight, egg production during a 4-wk period, and age at first egg laid were measured in 652 female progeny of heterozygous x heterozygous (F1) or heterozygous x homozygous (backcross) matings of the Iowa State University S1 White Leghorn chicken line. Hens were classified by B-haplotypes (B1 or B19) and haplotype-associated immune responses (high or low) to the amino acid polymer glutamic acid-alanine-tyrosine (Ir-GAT). Body weights were affected by parental mating group, sire, and dam, but they were not affected by haplotype (B/Ir-GAT). Sexual maturity and egg production were not affected by any factors except hatch. Average egg weight was affected by parental mating group, sire, dam, and genotype, with homozygous B19B19 birds having a heavier mean egg weight (41.71 g +/- .20) than homozygous B1B1 Ir-GAT-high and - low birds (40.8 g +/- .38 and 39.2 g +/- .54, respectively); mean egg weights of heterozygous birds were approximately intermediate to the others.

Analysis of Variance↗

Genetic associations of body weight and immune response with the major histocompatibility complex in White Leghorn chicks.

Survival, body weight, and humoral immune response to sheep red blood cells (SRBC) were measured in 256 chicks of the Iowa State University S1 Leghorn line. The chicks were produced from breeders selected for serological Ea-B blood type (B1 or B19), high or low humoral immune response to the amino acid polymer, glutamic acid-alanine-tyrosine (Ir-GAT), and response to Rous sarcoma virus-induced (RSV) tumors (progression or regression). Chicks were hatched from sublines representing all eight triple homozygous genotypes. Survival was significantly (P less than .01) associated with Ir-GAT, but not with Ea-B or RSV response. Body weight was affected by Ea-B, Ir-GAT, and the interaction between Ea-B and Ir-GAT, but not by interaction with RSV response. The SRBC antibody titer was affected by the interaction of Ea-B and Ir-GAT. The SRBC antibody titer was also lowest in the B19 low group. There were positive significant correlations (.21 to .31) between SRBC antibody titer and body weights at all ages except hatch in the Ir-GAT low group, but there were no significant correlations between SRBC antibody titer and body weights in the Ir-GAT high group. In this population of White Leghorn chicks, the heritabilities of body weight ranged from .43 to .27 for weights at 2 to 6 wk of age, and the heritability of SRBC antibody titer at 4 wk was .34 +/- .25.

Animals↗

The effect of prostaglandin and its inhibitor on antibody-dependent cellular cytotoxicity against human squamous cell carcinoma of head and neck.

The effects of chimeric monoclonal antibodies (cMAbs), prostaglandin E2(PGE2), and indomethacin (INDO) on antibody-dependent cellular cytotoxicity (ADCC) against human squamous cell carcinoma of head and neck (SCCHN) cell line were examined. Using the PCI-50 SCCHN cell line as target and normal human peripheral blood mononuclear cells as the effector, ADCC was enhanced by the treatment of cMAbs (1.25 micrograms/ml), but was inhibited by exogenous PGE2(5 x 10-7M). The effects of cMAb and PGE2 were dose-dependent. Maximal suppression of activity occurred when PGE2 was present during the entire 4 hour 51Cr-release assay period, whereas pretreatment of effector cells with PGE2 had minimal inhibitory effect after washing. These results indicate that decreased ADCC seen with SCCHN targets treated with PGE2 is related to post-binding events, such as binding of effector and target cells. Pre-treatment of effector cells with INDO (1 microgram/ml) resulted in restoration of NK activity which was inhibited by PGE2. Our in vitro results suggest that INDO can increase tumor cell killing by the reversal of the suppression for many immune functions by PGE2.

Antibody-Dependent Cell Cytotoxicity↗

Effect of GM-CSF and IL-2 co-expression on the anti-tumor immune response.

We evaluated the effect of potential therapeutic genes, GM-CSF and IL-2 respectively, or in combination of both cytokines, on the activation of systemic antitumor responses. CT26 tumor cells were modified to secrete GM-CSF and/or IL-2. The growth rate of the modified tumor cells versus the parental CT26 cells did not show any difference. When we implanted the CT26 tumor cells which secrete either GM-CSF or IL-2, delayed and suppressed tumorigenicity was observed. However, another CT26 cell line which expresses both GM-CSF and IL-2 (CT26/GMCSF/IL-2) did not form any tumor mass in the immunocompetent syngeneic Balb/c mice, showing the potential immune responses. Immunohistochemical examination of the modified tumor masses implanted with the cells expressing GM-CSF or IL-2 showed increased necrosis and infiltration of NK (CD56+) lineage cells and macrophage/monocytes. In the vaccination model, the growth of rechallenged wild-type CT26 was more suppressed int he mice which were injected with GM-CSF or IL-2, however, the wild-type CT26 tumor formed normal tumor mass in the mice vaccinated with CT26/GM-CSF/IL-2 showing acute non-T-cell mediated immune response. As a treatment, we injected those modified tumor cells into the established tumor. There we could find tumor growth suppression by the injection of cytokine-modified CT26 cells, especially by the CT26/GM-CSF/IL-2. In the present study we could induce the eradication of tumorigenicity by the transfection of both GM-CSF and IL-2 genes and a potent role in the growth suppression of an established tumor.

Animals↗

Relaxant effects of cromakalim and ATP depletion in dog and rat mesenteric arteries--species differences.

In the present study, the effects of cromakalim on tension and 86Rb+ efflux rate were evaluated in strips of dog and rat mesenteric arteries and compared with the variables obtained from ATP-depleted strips of both species. The cromakalim-induced relaxation was competitively antagonized by glibenclamide, with similar pA2 values, in both dog and rat mesenteric arteries. Glibenclamide caused an enhancement of the precontraction or a reversal of the cromakalim-induced inhibition in the mesenteric arteries of both species when cromakalim was applied prior to or during phenylephrine-contraction. The 86Rb+ efflux rate from the mesenteric arteries was significantly increased in both species after application of cromakalin (10 microM). However, in the ATP-depleted mesenteric artery (verified by high performance liquid chromatography), an increase in 86Rb+ efflux and a glibenclamide-induced enhancement of contraction were observed in the rat, but not in the dog. Taken together, between dog and rat mesenteric arterial strips, a differential effect of ATP depletion with 2-deoxyglucose plus oligomycin was identified in the activation of ATP-sensitive K+ channels, but not of cromakalim.

Adenosine Triphosphate↗