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Background: We examined the significance of neutrophil lymphocyte ratio(NLR)in gastric cancer and colon cancer in the perioperative period., Method: There were 46 patients(21 with gastric cancer and 25 with colon cancer). We examined the association between preoperative NLR and other indicators of nutritional status, as well as the relationship between preoperative NLR and the incidence of postoperative complications(all complications/infectious complications)., Result: NLR was higher in those with zinc<65 mg, prognostic nutritional index(PNI)≤40, and modified Glasgow prognostic score(mGPS)of 2 (p<0.05). NLR showed no difference among all patients with complications(12 cases), but was higher in patients with infectious complications(p<0.05)., Conclusion: Preoperative NLR is correlated with PNI as a predictor of infectious complications.

We isolated a cDNA clone encoding the human prostaglandin (PG) E receptor EP4 subtype and examined the gene expression in human blood cells. Northern blot analysis revealed that the EP4 gene is expressed at a high level in peripheral blood mononuclear cells, and at lower levels in cultured human blood cell lines, THP-1 and U937 (monocytoid cell lines), MOLT-4 and Jurkat (T-cell lines), and Raji (B-cell line). To examine regulation of the EP4 gene expression in the immune system, we studied the effects of phorbol 12-myristate 13-acetate (PMA) on these cell lines. Gene expression was upregulated in THP-1, U937, and Raji cells by PMA, and was downregulated in MOLT-4 and Jurkat cells. In THP-1 cells the effects of PMA were further analyzed, and the upregulation of the EP4 gene was shown to be followed by an increase in PGE2 binding sites and in PGE2-induced cAMP accumulation. In the striking contrast, other PGE receptor subtypes (EP1, EP2 and EP3) and other prostanoid receptors (IP and DP) were shown not to be upregulated by PMA. Therefore, this is the first demonstration of a highly specific upregulation of the EP4 subtype in THP-1 cells treated with PMA, suggesting the importance of the EP4 subtype in the immune system. In the present study we also clarified that EP4 gene expression is regulated differently among human monocytoid and lymphoid lineage cells, thus leading to the better understanding of the regulatory mechanisms for the human EP4 gene expression in the immune system.

The introduction of hybridoma technology has greatly contributed to the identification and the characterization of a variety of cell surface antigens present on human lymphoid cells. Rapid progress has recently been made in generating monoclonal antibodies against human lymphoid cells and extensive studies in clinical medicine have defined the potential application of these monoclonal antibodies. In this review, we summarize the main similarities and differences among these monoclonal antibodies.

For extracting free amino acids from human leukocytes, we find that disruption of the cells by ultrasonication is more reliable than freezing and thawing. The amount of free amino acids extracted by the latter method depends on the temperature and duration of thawing. We extracted free amino acids from leukocytes of healthy men by ultrasonication and compared their concentrations in lymphocytes and granulocytes. The amino acid content of granulocytes significantly (p less than 0.001) exceeded that of lymphocytes. Of the amino acids extracted from granulocytes, 76% was taurine; for lymphocytes taurine, aspartic acid, and glutamic acid were predominant, respectively composing 44%, 17%, and 26% of the total. Taurine is proposed as an index of cell disruption.

Exogenous adenine strongly inhibited mitogen-stimulated transformation, cytoplasmic immunoglobulin production, and natural killer activity of human mononuclear leukocytes at the high concentration of 1.0 mM. These inhibitions by adenine were not due to cytotoxicity, because the viability of cultured cells was not affected by adenine up to 1.0 mM. As the magnitude of inhibition by adenine of these in vitro immunological functions was similar in normal and adenine phosphoribosyltransferase-deficient cells, its inhibition was not mediated by corresponding nucleotides. Adenine at the concentration of 0.1 mM caused 50% inhibition of cytoplasmic immunoglobulin production without alternating cell proliferation or viability. This suggests that an appropriate concentration of adenine may inhibit the differentiation of B cells to plasma cells rather than affecting cell proliferation. Understanding the mechanisms of adenine inhibition may lead to new approaches for the regulation of immune responses.

Human peripheral blood lymphocytes were examined for rosette formation with autologous erythrocytes. When normal human lymphocytes were stimulated with phorbol myristate acetate (PMA) in the presence of autologous serum, the levels of autorosette forming cells (ARFC) were strongly enhanced. Pre-culture was necessary for the generation of ARFC by PMA and the maximal level of ARFC was observed at 72 hr of culture. ARFC appear to belong to a T cell subset and the induction of ARFC by PMA was noted in monocyte depleted lymphocyte fractions, indicating monocyte independency.

The induction of autorosette forming cells (ARFC) with phytohaemagglutinin (PHA) in human peripheral blood lymphocytes (PBL) was examined. After 24 h of incubation with PHA, the level of ARFC in PBL was markedly increased but subsequently decreased to about one-third of the peak level at 96 h of culture. When PBL were pre-treated with actinomycin D, or cultured with puromycin, the induction of ARFC was completely blocked. Pre-treatment of PBL with mitomycin C (MMC) had no effect on induction of ARFC, whereas DNA synthesis was completely blocked. These data indicate that the generation of autologous red blood cell receptors is a relatively early event in PHA activated PBL, and that it is independent of DNA synthesis but dependent on RNA and protein synthesis.

The structural characteristics of autologous red blood cell (ARBC) receptors on human peripheral blood lymphocytes (PBL) induced by phytohaemagglutinin (PHA) were examined. Tunicamycin, which is known to be a blocker of the protein glycosylation of N-glycosidic type glycoprotein, significantly inhibited the production of ARBC receptors. When trypsinized PBL were cultured in the presence of tunicamycin, the inhibitory effect was enhanced. When several monosaccharides were added to the mixture of ARBC and PBL pre-treated with PHA for 24 h, D-mannose caused the most inhibition, and galactose and D-fucose also caused significant inhibition. These data suggest that N-glycosidic type glycoproteins play an important role in binding sites to ARBC on PBL surface membranes and that more than one type of glycose may be involved.

Zinc determinations were made in a 5 month-old female with the Chediak-Higashi syndrome. Zinc concentrations in plasma, erythrocytes, lymphocytes and granulocytes from the patient were significantly higher than those in healthy children of a similar age, and were higher than--or equal to--those of healthy adults. Lymphocyte zinc levels in the parents were significantly lower than those of healthy adults. Although the cause of the high zinc concentrations in these samples cannot be fully explained , abnormally high zinc levels may be partially responsible for impairment of some leukocyte functions in patients with CHS since zinc plays a central role in cellular metabolism.

Human T lymphocyte colonies were grown in methylcellulose semi-solid cultures in the presence of phytohaemagglutinin (PHA) and/or phorbol myristate acetate (PMA). Surface marker analysis showed lower percentages of OKT3- and OKT4-positive cells in PMA-induced colonies than those in PHA-indoced colonies. The percentage of OKIa1-positive cells in PMA-induced colonies was approximately twice that in PHA-induced colonies The percentage of OKT9- positive cells in PMA-induced colonies was significantly lower than that in PHA-induced colonies. These data suggest that the subsets of PMA-induced colony cells express a more immature phenotype than that of PHA-induced colony cells and that, among PMA-induced colony cells, there are fewer T cells in the proliferative status at the time tested. When 3 × 105/ml monocyte-depleted T cells, at which concentration of seeded cells neither PHA nor PMA could induce colony growth, were cultured in the presence of both PHA and PMA. T cell colony growth was observed. In T cell colonies induced by a combination of PHA and PMA, the percentages of OKT3-, OKT4- and OKT8-positive cells were different from those in colonies induced by either PHA or PMA alone. These results suggest that PMA acts not only as a substitute for monocytes and/or interleukin-1, but may directly affect lymphocyte proliferation induced by a combination of PHA and PMA. [ABSTRACT FROM AUTHOR]

Colony growth of human lymphocytes by phorbol myristate acetate (PMA) was studied. PMA was able to induce lymphocyte colony growth in methylcellulose semi-solid cultures in the absence of lectin mitogens, phytohaemagglutinin or concanavalin A. PMA-induced colonies were found in cultures of mononuclear cells, monocyte-depleted mononuclear cells and the T-enriched cell fraction, whereas no colonies were obtained from the non-T cell fraction. At least one million mononuclear cells were required to form colonies by PMA. The colony cells were mainly I cells as judged from sheep red blood cell rosette formation. Surface immunoglobulin positive cells and peroxidase positive cells were not detected in colony cells. Non-specific esterase positive cells were only found to be less than 1% of colony cells. T cells formed more colonies than did mononuclear cells, presumably because of a concentration of colony forming cells and/or co-operating cells. Colony formation by PMA was induced from monocyte-depleted mononuclear cells and monocyte-depleted I cells, suggesting independence of monocytes. When mononuclear cells were precultured at 37° for 5 mm or 30 mm with PMA and then cultured in the semi-solid medium without PMA, only a small number of colonies grew. Further studies of PMA- induced T-cell colonies will provide information the identification and characterization of immunological states in various immunological diseases. [ABSTRACT FROM AUTHOR]

We demonstrated that a primary exposure to the lymphocytosis promoting factor (LPF) of Bordetella pertussis-induced T cell colony formation. Colony formation was observed when mononuclear cells(MNC) were cultured at concentrations of more than 1 x 106/ml, and reached a peak on day 8. However, the number of colonies generated with LPF was about one-third induced with phytohaemagglutinin (PHA). Removal of monocytes from MNC or T cells resulted in the failure of colony formation, but colony growth could be restored by the addition of monocytes or B enriched cells, indicating that they were required for the optimal colony growth induced by LPF. In the absence of accessory cells, optimal colony growth from monocyte depleted T cells could be obtained when an appropriate concentration of phorbol myristate acetate (PMA) or interleukin-2 (IL-2) was added in the cultures with LPF. PMA did not enhance LPF-induced colony formation in the cultures containing a sufficient amount of exogeneous IL-2. These findings suggest that IL-2 is essential to LPF-induced colony formation. Surface marker analysis showed that most of LPF-induced colony cells were T cells. The percentages of T4+ and Tγ cells of LPF-induced colony cells were more, and T8+ cells less, than those of PHA-induced colony cells, Ial. T9 and Tac antigens were detected on many colony cells induced by LPF or PHA. These results indicate that the phenotype of LPF-induced colony cells differs from those of PHA, but the sequential antigen expression on lymphocytes triggered by IL-2 might be similar in both LPF- and PHA-induced colony formation. [ABSTRACT FROM AUTHOR]

We studied the effect of lymphocytosis promoting factor (LPF). derived from the supernatant fluid of a culture of phase I Bordetella pertussis strain Tohama. on human lymphocyte proliferation. LPF was a potent mitogen for human mononuclear cells. specifically T cells. LPF failed to induce cytoplasmic immunoglobulin production by B cells. Removal of the monocytes from the T cell fraction diminished responses to LPF. but the response could be restored completely by the addition of 50",, monocytes. These results suggest that LPF-induced cell proliferation is at least partially dependent on monocytes. In contrast to PHA, LPF stimulated T&lamda; cells to a greater extent than non-T&lamda; cells., but the magnitude of the T&lamda; or non-T&lamda; cell response was less than that of T cells, indicating that synergistic interactions between T&lamda; and non-T&lamda; cells are required for maximal response. [ABSTRACT FROM AUTHOR]