Biomedical subjects

K Pai

Publications and source records attributed to K Pai.

25 records · Page 2Linked to original sources

PubMed1992

Studies on the natural killer cell activity of human nonadherent mononuclear cells (nMNC) with tumor necrosis factor, interleukin-1, interferon-gamma and cisplatin.

The potential for additive or synergistic augmentation of NK cell activity of nMNC with recombinant tumor necrosis factor (TNF-alpha), interleukin-1 (IL-1), interferon-gamma (IFN-gamma) and cisplatin in different combinations was examined. Significant augmentation in NK activity of nMNC was observed when treated with cisplatin, rIFN-gamma, rIL-1 or rTNF-alpha in vitro. Combined treatment of nMNC with rIL-1 and rTNF-alpha resulted in moderate increase in NK cell activity. However, killing of K 562 target cells was markedly augmented by co-stimulation of nMNC with rIL-1 plus rIFN-gamma and rIL-1 plus cisplatin. Further, only a moderate augmentation of NK activity was observed when nMNC were treated with cisplatin plus TNF or IFN-gamma. These observations demonstrated the individual and co-stimulative effects on NK function of nMNC in vitro by rTNF-alpha, rIL-1, cisplatin and rIFN-gamma.

Antineoplastic Combined Chemotherapy Protocols↗

PubMed1992

Studies on the intracellular Ca2+, protein kinase activity, and ATP contents of cisplatin- and rIFN-Y-treated non-adherent mononuclear cells.

The in vitro effect of cisplatin or rIFN-Y on the intracellular free calcium, protein kinase activity and ATP content of non-adherent mononuclear cells (nMNC) from human peripheral blood was assessed. We observed that treatment of nMNC with cisplatin enhanced the [Ca2+]i, ATP level, and protein kinase activity; whereas rIFN-Y-treated nMNC showed significant rises in ATP level and protein kinase activity only. We also observed that cisplatin-treated nMNC showed an instantaneous rise in [Ca2+]i when NK-sensitive K562 cells were added to the effector cells.

Adenosine Triphosphate↗

PubMed1991

Effect of cisplatin, rIFN-Y, LPS and MDP on release of H2O2, O2- and lysozyme from human monocytes in vitro.

Increased secretion of H2O2, O2- and lysozyme by human monocytes in vitro on treatment with cisplatin, rIFN-Y (interferon-Y), LPS (lipopolysaccharide) and MDP (muramyl dipeptide) is reported. It is suggested that increased production of these secretory products represent the activated state of monocytes. These in vitro activated monocytes could either kill the tumor cells via increased contact mediated cytolysis or cytolysis mediated via the release of the secretory products like H2O2, O2- and lysozyme.

Acetylmuramyl-Alanyl-Isoglutamine↗

PubMed1991

Release of tumor cytolytic/cytostatic factor(s) by in vitro cisplatin treated macrophages: enhanced tumoricidal activity by increase in osmotic fragility of target cells.

In vitro cisplatin treatment of murine macrophages results in the release of tumor cytolytic/cytostatic factor(s) (TCF) into the culture medium. These cytolytic factors are cytotoxic/cytostatic only against Dalton's lymphoma and L929 tumor cells but not to normal splenocytes. The cisplatin-activated macrophages retain the capacity to lyse the tumor cells even after removal of the medium containing cisplatin. The mechanism of tumoricidal activity by the TCF was investigated. TCF containing medium was found to enhance the osmotic fragility of the tumor cells.

Animals↗

PubMed1990

Activation of murine macrophages by tumor necrosis factor, interleukin-1, interferon-gamma and cisplatin.

Murine peritoneal macrophages were rendered tumoricidal to Dalton's lymphoma (DL) cells on incubation with recombinant tumor necrosis factor alpha (rTNF-alpha), recombinant interleukin-1 (rIL-1) and cisplatin in vitro. Simultaneous treatment of macrophages with suboptimal doses of rTNF-alpha and rIL-1 had additive effect on the activation of macrophages. Priming of macrophages with recombinant interferon gamma (rIFN-gamma) significantly enhanced the rTNF-alpha and rIL-1-induced macrophage cytotoxicity. Cisplatin was found to up-regulate rIL-1-induced macrophage activation but inhibited the activation of macrophages with rTNF-alpha. These studies indicate the potential of appropriate combination of these Biological Response Modifiers (BRMs) against neoplasia.

Animals↗

PubMed1990

Activation of human NK cells and monocytes with cisplatin in vitro.

Human natural killer (NK) cells and monocytes treated in vitro concomitantly with cisplatin and rIFN-gamma enhanced lysis of K562 cells. Lysis was dependent upon the duration of treatment. Cisplatin and rIFN-gamma treated monocytes were equally cytotoxic to NK sensitive (K562) and NK resistant (Daudi & Raji) cell lines whereas NK cells were not rendered cytotoxic against NK resistant tumor cells. NK- and monocyte-mediated cytotoxicity against K562 cells was further enhanced when the effector cells were primed with rIFN-gamma and were subsequently treated with cisplatin.

Cisplatin↗

PubMed1983

Central venous catheters for out-patient management of malignant disorders.

The use of tunnelled central venous catheters in children with malignant disorders is an effective and safe way of giving out-patient chemotherapy and supportive care. The benefits include ready venous access, ease of administration of chemotherapy, decreased time spent in the out-patient clinic, and less anticipatory vomiting and emotional trauma for patients, parents, and staff.

Adolescent↗