Biomedical subjects

J Xie

Publications and source records attributed to J Xie.

273 records · Page 16Linked to original sources

PubMedDate not supplied

Role of excitatory amino acids in hypoxic preconditioning.

We examined the effects of the extrinsic ionotropic NMDA receptor agonist (aspartate) and antagonist (ketamine) on the hypoxic preconditioning of mice and the concentration changes of intrinsic excitatory amino acids (EAAs), aspartate and glutamate, in the whole brain and different brain regions during preconditioning by an HPLC method. Our results showed that aspartate and ketamine significantly prolonged and shortened the standard tolerance time of mice during preconditioning and survival time in hypobaric chambers, respectively. After the 1st exposure, EAA concentrations in the whole brain and brain regions were increased. After run 4, they were decreased or maintained. It is suggested that the activation and suppression of ionotropic NMDA receptors is harmful and beneficial to hypoxic preconditioning, respectively. Degradation and/or inactivation of EAAs might be beneficial to the tolerance of mice to hypoxia.

Adaptation, Physiological↗

PubMedDate not supplied

Transforming growth factor-beta is not the major soluble immunosuppressor in the microenvironments of human breast tumours.

The immunosuppressive nature of the human breast cancer microenvironment was investigated. The soluble fraction of individual tumours was tested for its ability to influence the activation of peripheral blood lymphocytes (PBL) by interleukin-2 (IL-2) and to effect the continued proliferation of cells which had been pre-activated with IL-2. In all cases, both assays were profoundly inhibited (90-100%). None of this inhibition was due to cell killing by the tumour-derived soluble material (TDS). Sixty-two percent of TDS tested contained measurable transforming-growth factor-beta (TGF-beta) activity; following acidification TGF-beta was present in all TDS. However, in neither case was this material present in sufficient amounts to account for the degree of inhibition observed. In addition, neutralisation experiments failed to demonstrate consistent relief of inhibition in the presence of excess anti-TGF-beta antisera. These results demonstrate that TGF-beta s are not the major soluble immunosuppressive materials within human breast tumours.

Breast Neoplasms↗

PubMedDate not supplied

The ability of transforming growth factor-beta 1 to preferentially inhibit the induction of cytotoxicity in human T cells is determined by the nature of the activating signals.

TGF-beta is held to be a general inhibitor of the immune system, able to prevent the development of certain differentiated functions, such as the induction of LAK activity by IL-2. In the present study, the potential of TGF-beta 1 to inhibit anti-tumour responses was assessed by determining its relative effect on the proliferation and cytotoxicity of human T-cells, following activation by anti-CD3, anti-CD3 plus anti-CD28 or anti-CD3 plus IL-2. The results demonstrated that TGF-beta 1 inhibits the induction of cytotoxicity in human T-cells stimulated via CD3 or CD3 and CD28 (P < 0.01), without significantly altering their proliferative responses. The cytotoxic response following costimulation with IL-2 was hardly altered, while costimulation via CD28 was susceptible to suppression, suggesting that TGF-beta 1 action is affected by the nature of the costimulatory signals.

Antibodies↗