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Biomedical subjects

L Jia

Publications and source records attributed to L Jia.

119 records · Page 7Linked to original sources
PubMed1994

Tumor metastasis to brain: role of endothelial cells, neurotrophins, and paracrine growth factors.

An important clinical endpoint in patients with cancer is formation of metastases in the brain. Understanding this phenomenon is important in several types of malignancies, including melanoma, lung and breast cancers. Metastatic tumor cells use specific adhesion molecules to home to brain, and there they must attach to microvessel endothelial cells and respond to brain endothelial cell-derived motility factors and brain invasion factors to invade the CNS. Neurotrophins are important invasion factors in this process, and the ability to invade into the brain may well depend on metastatic cell responses to neurotrophins and production of basement membrane-degradative enzymes capable of locally destroying the blood-brain barrier. Brain-metastatic human melanoma cells express low-affinity p75 receptor for neurotrophins such as nerve growth factor, but they do not express the high-affinity-type receptors for nerve growth factor encoded by the protooncogene trkA. Tumor cells can proliferate in the CNS in response to local paracrine growth factors and inhibitors, but their growth also depends on their producing and responding to autocrine growth factors. A major organ-derived (paracrine) growth factor has been isolated that differentially stimulates the growth of cells metastatic to the brain. Characterization of this mitogen demonstrated that it is a transferrin-like glycoprotein; cells that are metastatic to brain express greater numbers of transferrin receptors on their surfaces than cells that are poorly metastatic or metastatic to other sites. Transferrin-like factors are expressed in fetal brain and could represent the transferrin-like factors that stimulate growth of brain-metastatic melanoma and breast cancer cells. These and other factors are probably important in determining whether metastatic cells can successfully invade, colonize, and grow in the CNS.

Animals↗
PubMed1993

Inhibition by sulfhydryl compounds of vascular relaxation induced by nitric oxide and endothelium-derived relaxing factor.

On rings of rabbit thoracic aorta precontracted with phenylephrine, L-cysteine (Cys) and dithiothreitol (DTT) (1-100 microM), but not glutathione (GSH), produced dose-dependent augmentation of contraction in endothelium-intact, but not in endothelium-denuded rings. The augmentation appeared to be due to inhibition of basally released endothelium-derived relaxing factor (EDRF), and was abolished by pretreatment with superoxide dismutase (SOD, 15 U/ml). At a high dose (1 mM), Cys and GSH produced transient, and DTT produced sustained endothelium-independent relaxation, not influenced by SOD. Cys and DTT (10 microM), but not GSH, produced a small but significant inhibition of acetylcholine-induced endothelium-dependent relaxation, and this inhibition was prevented by SOD. In a perfusion-bioassay system in which EDRF was released by acetylcholine from endothelium of a perfused segment of rabbit aorta, Cys and DTT (20 microM), but not GSH, infused into the perfusate between the segment and an endothelium-denuded bioassay ring, partially inhibited relaxation by the EDRF, but not when SOD was present. In organ chamber experiments, the large transient relaxation of endothelium-denuded rings produced by 75 nM nitric oxide (NO) was partially inhibited in a concentration-dependent manner by Cys, DTT and GSH (0.1-100 microM). Moderate relaxation by 15 nM NO was almost completely inhibited by each compound at 10 microM. The order of potency was Cys > DTT > GSH. Cystine, glutathione disulfide and alanine did not inhibit. Inhibition of NO-induced relaxation was largely attenuated by SOD.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1992

Regulation of beta-endorphin receptor expression in mouse spleen cells with Con A and rIL-2.

The expression of the beta-endorphin receptor on both activated and unstimulated mouse spleen cells was studied. Results showed that unstimulated cells have only one type of beta-endorphin receptor with a specific low affinity (Kd = 1.034 +/- 0.0237 x 10(-7) M, 25,000 sites/cell). After Con A stimulation, cells express two types of receptors, one with a low affinity (Kd = 1.034 +/- 0.024 x 10(-7) M, 320,000 sites/cell) and the other with a high affinity (Kd = 1.052 +/- 0.033 x 10(-9) M, 49,000 sites/cell). The kinetic experiments during 4 days after Con A activation indicated that the receptor of high affinity emerged from 24 to 72 h, while the low affinity one increased in number after stimulation. The receptor numbers of both high and low affinity ones reached a maximum peak at 72 h, then began to decline. The addition of exogenous rIL-2 depressed the Con A-induced increment of the receptor numbers of both the high and low affinity ones, but enhanced the proliferative response of the cells. It is suggested that the degree of the expression of the receptors does not simply depend on the mitogenic degree of the cells. In addition, our experiment demonstrated that splenocytes cultured in medium with or without Con A or Con A + rIL-2 for 96 h did not secrete any detectable amount of beta-endorphin with use of the RIA assay, which is sensitive enough to detect the much lower levels of beta-endorphin than that necessary for biological effects. We suggest that the expression of the high affinity beta-endorphin receptor on the activated T-lymphocytes may have to precede the production of IL-2 to potentiate the T-cell proliferative response. The mechanisms and modes of interaction between the neuroendocrine system and the immune system were discussed.

Animals↗
PubMed1992

Construction of an Rb gene expression plasmid.

We obtained an 844 bp Bg1II fragment from an Rb cDNA clone and inserted it into the expression vector pWR-13 to construct an Rb gene expression plasmid. When the Rb Bg1II fragment was fused in-frame into pWR-13, it was operated by a Lac Z promoter and produced a fusion protein which consisted of expressed Rb protein and a small peptide from Lac Z. The recombinants were transformed into E. coli with the CaCl2 method, screened by in situ hybridization, and restriction mapped. Total cellular protein of transformed clones was analyzed by SDS-PAGE and Commassie blue staining. The sense clones showed a unique band at 28,000. On Western blot, this band specifically reacted with 125I-labelled antibody against synthetic Rb peptide. This protein comprised more than 5% of total bacterial protein.

Amino Acid Sequence↗
PubMed1989

[The characteristic changes of immune function with aging].

It is well-known that the most prominent age-related immunological abnormalities were reduced immune response against foreign antigens and increased auto-antibody production against intrinsic antigens. To explain these immunological abnormalities, we examined the various functions of human lymphocytes from aged and young groups at cellular, molecular and genetic levels. The results indicate: The first, T cells from the aged showed significantly reduced proliferative response not only to specific antigen TAP but also to mitogen PHA or combined stimulation of PMA and ionomycin. The second, the number of IL-2 receptor, particularly high affinity ones, on aged T cells were significantly reduced in the aged after TAP and PHA stimulation. The third, the ability to express Tac (p55) and p70/75 of IL-2R and to internalize the rIL-2 bound to the receptor were reduced in aged T cells. The fourth, although the ability to proliferate in response to SAC stimulation was two folds less in the aged B cells than that in the young ones, the capacity to differentiate into IgG and IgA class ISC after the combined stimulation with SAC and partially purified BCDF were rather increased on the basis of the number of viable cells recovered. The fifth, the amount of IL-2 activity produced by aged T cells was ten fold less than that by young ones, but the amount of BCDF activity produced by aged T cells was three folds higher than that by young ones after PHA stimulation. An inverse correlation between IL-2 activity and BCDF activity was found when the both activities were determined in the same sample. The sixth, the combined stimulation with PMA and ionomycin could induce proliferative response to highly purified T cells, T cell subsets and B cells. The degree of age-related decline of the proliferative response of CD-8 positive T cells was most significant, that of CD-4 positive ones was next and that of B cells was least. The seventh, although the maximum of c-myc mRNA level was attained at 2 hr after the stimulation and similar amount between the both age groups, the amount of mRNA at 8 or 24 hr was rather higher in the aged T cells than in the young ones. The reduction of the degradation rate of c-myc mRNA seemed to be the cause. We found no difference of the maximum amount and kinetics of c-myb mRNA between both age groups in T cells.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1987

[Misdiagnosis of malignant lymphoma--report of 45 patients].

A series of 50 patients with malignant lymphoma, proven by biopsy, was retrospectively studied. 39 were non-Hodgkin's lymphoma and 11 Hodgkin's disease. 45 (90%) had been misdiagnosed because of lack of initial specific symptoms. It is suggested that for patients with a painless progressively enlarging superficial lymph node without adhering to its surrounding tissues and irresponsive to general management, having irregular fever, bloody stool, abdominal pain or mass, complication of partial intestinal obstruction, sharp vigilance be kept for the possibility of malignant lymphoma.

Adolescent↗