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K Taga

Publications and source records attributed to K Taga.

At least 55 records · Page 3Linked to original sources

[Expression of Le(y) antigen in adenocarcinoma and its related lesions of the human uterine cervix].

The natural history and biological behavior of adenocarcinoma and related lesion of the uterine cervix remain controversial issues, but the dynamic alterations in glycosylation in the cancer cells are well known. Recently, it was recently documented that the Ley antigen might be correlated with apoptosis. Over the past eight years, we have encountered 12 cases of invasive adenocarcinoma (AD), 11 cases of early adenocarcinoma (early AD) including 6 adenocarcinoma in situ and 5 microinvasive adenocarcinoma, 16 cases of endocervical glandular dysplasia (EGD) and 10 patients with normal endocervix (control) among 2,165 postoperative cases. Immunohistochemical localizations of Le(y), sialyl Le(x) and epidermal growth factor receptor (EGFR) antigens were examined in serial sections. The localization of Le(y) antigen was predominant in the subcolumnar reserve cells in controls. The localization of sialyl Le(x) was predominant in the perinuclear portion of cells in cases of EGD. The localization of EGFR was presented in cases of tubal metaplasia, tubal type EGD, early AD and AD. These antigens were present in cases of EGD, early AD and AD, with AD cases showing the highest concentrations. To conclude, the presence of the Le(y) antigen might be correlated with differentiation, development and oncogenesis rather than with apoptosis in these lesions, EGD might indicate a precancerous lesion, and localization of the EGFR antigen indicates that tubal metaplasia, tubal type EGD, early AD and AD may have a common origin.

Adenocarcinoma↗

Interleukin-10 suppresses human immunodeficiency virus-1 replication in vitro in cells of the monocyte/macrophage lineage.

The cytokine interleukin-10 (IL-10) has been implicated in the pathogenesis of a number of disease states, including Epstein-Barr virus and human immunodeficiency virus (HIV-1) infections. In the acquired immunodeficiency syndrome (AIDS), it has been suggested that IL-10 may have a deleterious effect by suppressing cell-mediated immunity. However, there are few data on its direct effects on HIV-1 replication. In the present study, we have found that recombinant human IL-10 (rhIL-10), present during days 0 through 2, potently inhibits HIV production in elutriated monocyte/macrophage (M/M) cultures with a 50% inhibitory concentration (IC50) of approximately 0.03 U/mL. This effect did not appear to be caused by toxicity to M/M because there was no change in cell viability, ability to phagocytose latex beads, or protein synthesis as measured by [3H]-leucine incorporation, at doses of rhIL-10 that inhibit viral replication. In addition, lipopolysaccharide-induced production of IL-1 beta, IL-6, or tumor necrosis factor-alpha was not affected at these doses, nor were human mononuclear cell proliferative responses to phytohemagglutinin, OKT3 antibody, or tetanus toxoid. HIV-1 replication was similarly decreased by rhIL-10 in the monocytoid line U937 without signs of cellular toxicity. However, these effects required much higher concentrations of rhIL-10, and viral production was only partially suppressed. rhIL-10 also slightly inhibited HIV-induced cytopathicity in ATH-8, a tetanus toxoid-specific, retrovirally immortalized T-cell line, but had no effect on HIV replication in the H9 and MOLT-4 T cell lines. Thus, rhIL-10 appears to inhibit HIV replication predominantly in cells of the M/M lineage. This effect may serve to reduce viral production in patients with AIDS. However, additional studies will be needed to more precisely define its physiologic role in this disease.

CD4-Positive T-Lymphocytes↗

Regression of experimental Burkitt's lymphoma induced by Epstein-Barr virus-immortalized human B cells.

Epstein-Barr virus (EBV)-immortalized human B cells survive only transiently when injected subcutaneously into athymic mice, whereas Burkitt's lymphoma cells give rise to progressively growing subcutaneous tumors. In this study, we tested whether these Burkitt's tumors could be induced to regress via a bystander effect induced by EBV-immortalized B cells. Simultaneous inoculation of EBV-immortalized B cells and Burkitt's lymphoma cells in the same subcutaneous site resulted in tumors that regressed with necrosis and scarring. Similarly, simultaneous inoculation of EBV-immortalized B cells and Burkitt's lymphoma cells in separate subcutaneous sites resulted in regression of a proportion of the Burkitt's tumors. Furthermore, most of the established human Burkitt's tumors regressed with necrosis and scarring after intratumor inoculations with EBV-immortalized B cells. The EBV-immortalized B cells continued to exert this antitumor effect even when killed with irradiation. The experimental approach to Burkitt's lymphoma treatment described here exploits the ability of athymic mice to reject EBV-immortalized B cells to target an effective antitumor response to malignant cells normally incapable of eliciting it.

Animals↗

Interleukin-10 inhibits apoptotic cell death in infectious mononucleosis T cells.

T lymphocytes from patients with acute EBV-induced infectious mononucleosis rapidly die by apoptosis in vitro. Because human and viral IL-10 are likely to be induced during acute EBV infection and display a variety of functions on human T cells, we examined IL-10 effects on infectious mononucleosis T cell death. After 12 h of incubation in medium alone, only 35.6 (+/- 8.2%) of the originally seeded infectious mononucleosis T cells were viable. Addition of human IL-10 (100 U/ml) to T cell cultures significantly improved recovery of viable cells (71.3 +/- 6.2%, P = 0.0156). Viral IL-10 had comparable effects to human IL-10 in this system. Protection from death by human and viral IL-10 (100 U/ml) was dose dependent and continued over a 6-d culture period. The human IL-10 effect was neutralized by the anti-human IL-10 mAb 19F1. Morphology and analysis of DNA after separation on agarose gels showed that IL-10 inhibits loss of cell volume, chromatin condensation, and DNA fragmentation, characteristics of death by apoptosis. As assessed by [3H]thymidine incorporation, the T cells were not induced to proliferate by IL-10 above the level exhibited when first removed from blood. T cells protected from death by IL-10 proliferated to IL-2 and spontaneously killed sensitive targets as effectively as medium-precultured T cells. Thus, IL-10 promotes the survival of infectious mononucleosis T cells otherwise destined to die by apoptosis and may be critical for the establishment of immunologic memory after resolution of the illness.

Adolescent↗

Human interleukin-10 can directly inhibit T-cell growth.

Human interleukin-10 (IL-10) inhibits T-cell proliferation and cytokine production in the presence of monocytes. In this study, we have investigated whether IL-10 can directly inhibit T cells. Highly purified peripheral blood T cells containing less than 0.1% CD14+ cells and unresponsive to phytohemagglutinin (PHA), were growth-inhibited by IL-10 when stimulated with immobilized OKT3 monoclonal antibody (MoAb; 55.4% inhibition). This effect was neutralized by the murine MoAb 19F1 directed against human IL-10. In addition, IL-10 inhibited by 52.5% the proliferation of a human tetanus toxoid-specific T-cell clone (TM11) induced by immobilized OKT3 MoAb in the absence of antigen-presenting function. T-cell growth inhibition by IL-10 did not reflect a cytokine-induced change in the kinetics of T-cell response to immobilized OKT3 MoAb, and was observed over a wide range of cell and OKT3 MoAb concentrations. Addition of 1% to 5% monocytes to highly purified peripheral blood T cells resulted in the emergence of proliferation to PHA and to soluble OKT3 MoAb, but did not significantly affect levels of growth inhibition by IL-10 in the presence of immobilized OKT3 MoAb. Similarly, addition of 10% monocytes to the TM11 T-cell clone resulted in the emergence of proliferation in response to tetanus toxoid, but did not significantly influence growth inhibition by IL-10 in the presence of immobilized OKT3 MoAb. When stimulated with immobilized OKT3 MoAb in the absence of accessory cells, T cells secreted IL-2. Secretion of IL-2 under these conditions was inhibited by IL-10 (51.5% inhibition). Thus, IL-10 can directly inhibit growth and IL-2 production in T cells triggered by immobilized OKT3 MoAb in the absence of monocytes.

CD3 Complex↗

IL-10 inhibits apoptotic cell death in human T cells starved of IL-2.

IL-10 was originally described as an inhibitory factor produced by murine Th2 lymphocytes that suppresses IFN-gamma production by activated murine Th1 lymphocytes. In this study, we have analyzed the effect of human IL-10 on human T cell death induced by IL-2 deprivation. IL-2-dependent T lymphocytes rapidly die when deprived of IL-2. This cell death was found to involve loss of cell volume, chromatin condensation, and DNA fragmentation, all characteristic of apoptosis. After 2 days incubation in culture medium without IL-2, the viability of TM11 cells (a tetanus toxoid-specific T cell line) and of activated peripheral blood T cells decreased from > 98% to 34.3 (+/- 2.9) and 39.7 (+/- 5.5%) respectively. Addition of purified human IL-10 (100 U/ml) to these IL-2-starved cells significantly improved cell viability (66.0 +/- 6.0 and 73.1 +/- 12.3% respectively, P = 0.0051). This protective effect of IL-10 was dose-dependent and was neutralized by the anti-human IL-10 mAb 19F1. It was neither accompanied by T cell growth stimulation as judged by [3H]thymidine incorporation nor neutralized by anti-IL-2 or anti-IL-2 receptor (CD25) antibodies. Analysis of DNA after separation on agarose gels revealed that IL-10 inhibits DNA fragmentation in IL-2-starved T cells. T cells protected from death by IL-10 were indistinguishable from IL-10-untreated viable T cells in the ability to proliferate in response to IL-2. Thus, another property of IL-10 is to promote the survival of IL-2-dependent T cells otherwise destined to die by apoptosis.

Apoptosis↗

Endothelium dependence of effects of high PCO2 on agonist-induced contractility of rat aorta.

To investigate the modulation of CO2 and endothelium of vascular contraction induced by various agonists, we studied the influence of high PCO2 (PCO2 = 91 mmHg, pH = 6.99) on the response of endothelium-intact and -rubbed rat aortic preparations to KCl, phenylephrine (PE), and human-porcine endothelin-1 (ET-1). Response of endothelium-intact aortic preparations to KCl was not influenced by both high PCO2 and the pH-matched acidotic solution (7.00) with normal PCO2, whereas that of endothelium-rubbed preparations was attenuated solely by high PCO2. With cyclooxygenase inhibitors or a thromboxane A2 receptor antagonist, high PCO2 attenuated the respose of both preparations to KCl. The dose-response curve of endothelium-intact and -rubbed preparations to PE was shifted to the right by both high PCO2 and the pH-matched acidotic solution with normal PCO2. The maximal response of endothelium-intact preparation to PE was attenuated by high PCO2. Indomethacin augmented the inhibitory action of high PCO2 on the PE-induced contraction. Contractile responses of endothelium-intact and -rubbed preparations to ET-1 were not influenced by high PCO2. With indomethacin, high PCO2 also had no influence on the ET-1-induced contraction of endothelium-intact preparations. Endothelium modified the high PCO2 effects on the time-contraction responses to the three agonists. CO2 and endothelium may variously modify the responses of rat aorta to different agonists. Cyclooxygenase-related eicosanoid(s) may be involved in the effects of high PCO2 on the response of rat aortic smooth muscle cells to KCl and PE.

Animals↗

IL-10 inhibits human T cell proliferation and IL-2 production.

Human IL-10 has been reported previously to inhibit the secretion of IFN-gamma in PBMC. In this study, we have found that human IL-10 inhibits T cell proliferation to either mitogen or anti-CD3 mAb in the presence of accessory cells. Inhibited T cell growth by IL-10 was associated with reduced production of IFN-gamma and IL-2. Studies of T cell subset inhibition by human IL-10 showed that CD4+, CD8+, CD45RA high, and CD45RA low cells are all growth inhibited to a similar degree. Dose response experiments demonstrated that IL-10 inhibits secretion of IFN-gamma more readily than T cell proliferation to mitogen. In addition, IL-2 and IL-4 added exogenously to IL-10 suppressed T cell cultures reversed completely the inhibition of T cell proliferation, but had little or no effect on inhibition of IFN-gamma production. Thus, in addition to its previously reported biologic properties, IL-10 inhibits human T cell proliferation and IL-2 production in response to mitogen. Inhibition of IFN-gamma production by IL-10 appears to be independent of the cytokine effect of IL-2 production.

Humans↗

[Digital imaging microscopy for intracellular Ca2+ in cultured single rat vascular smooth muscle cells using fluorescent Ca2+ indicator "fura-2"].

We presented the principle and methodology of digital imaging microscopy for intracellular Ca2+ in cultured single vascular smooth muscle cells of the rat using fluorescent Ca2+ indicator "fura-2". The methods seemed useful for studying the physiological and pathological phenomena in a single smooth muscle cell. Analysis of the spatial and temporal dynamics of intracellular Ca2+ might be crucial for studying the active sites of vasoactive or anesthetic drugs in a vascular smooth muscle cell as well as for understanding pathophysiology of the arterial spasm.

Animals↗

High sensitivity of porcine cerebral arteries to endothelin.

The threshold concentration of endothelin to induce contractions in porcine cerebral arteries (anterior cerebral, Willis ring and basilar artery) was lower than those for coronary and renal arteries. The median effective concentrations (ED50) of endothelin in cerebral arteries were also significantly lower than those for coronary and renal arteries. There was no significant difference in the sensitivity to endothelin among cerebral arteries, or between coronary and renal arteries. The maximal percentage of contractions induced by endothelin, as compared to that induced by 10(-1) M potassium chloride, was not significantly different between the arteries.

Animals↗

Multiple risk factors in coronary artery disease patients with abnormal glucose tolerance.

Two hundred twenty five anginal symptomatic patients (37-75 years) undergoing selective coronary angiography were studied to clarify the importance of risk factors for coronary artery disease (CAD). Serum lipids, apolipoproteins, fasting blood glucose, hemoglobin A1 and A1c, serum insulin levels, hypertension, smoking and obesity were examined as coronary risk factors in 64 newly diagnosed non-insulin dependent diabetic patients (60 +/- 1 (+/- SE)yr), 88 impaired glucose tolerant (IGT) patients (58 +/- 1 yr) and 73 non-diabetic patients (62 +/- 1 yr). Diabetic and IGT patients showed significantly higher coronary atherosclerosis indices than non-diabetic patients (p less than 0.05). In the diabetic and IGT groups, the plasma triglyceride concentrations were significantly higher in the patients with coronary atherosclerosis (CAS) than in either patients without CAS (p less than 0.05) or non-diabetic patients with CAS (p less than 0.05). The prevalence of hypertension in the diabetic patients with CAS was higher than in the non-diabetic patients with CAS. These data suggest that hypertriglyceridemia and hypertension might be important as risk factors in the development of coronary atherosclerosis in persons with an abnormal glucose tolerance.

Adult↗

Preferential expression of IL-2 receptor subunits on memory populations within CD4+ and CD8+ T cells.

Using anti-Tac and anti-Mik-beta 1 monoclonal antibodies to alpha and beta subunits of the interleukin-2 receptor (IL-2R), respectively, a marked difference in expression of IL-2R subunits on blood CD4+ and CD8+ T cells was demonstrated between adults and newborns. In the adult blood, reciprocal expression of IL-2R alpha and IL-2R beta was observed in CD4+ and CD8+ T cells. Some CD4+ T cells expressing IL-2R alpha were often detected, but IL-2R beta + CD4+ cells were very few. On the other hand, CD8+ T cells expressed significant IL-2R beta but little IL-2R alpha. In marked contrast to adult individuals, both CD4+ and CD8+ T cells from the newborns, which seemed to consist mainly of naive populations, showed only negligible expression of IL-2R subunits. It was found that IL-2R subunits appeared to be preferentially expressed on CD4+ and CD8+ T cells with memory phenotypes in the adult blood. Isolated memory (CD45RO+) CD4+ and CD8+ T cells, unlike naive (CD45RO-) ones, were able to proliferate in response to exogenous IL-2 as well as the recall antigen. The present results suggest that IL-2R subunits expressed on circulating T-cell subsets may play an important role in memory T-cell function.

Adult↗

Proton flow along lipid bilayer surfaces: effect of halothane on the lateral surface conductance and membrane hydration.

Impedance dispersion in liposomes measures the lateral charge transfer of lipid membrane surfaces. Depending on the choice of frequency between 1 kHz and 100 GHz, relaxation of the counterions at the interface, orientation of the head group, and relaxation of the bound and free water are revealed. This study measured the impedance dispersion in dipalmitoylphosphatidylcholine (DPPC) liposomes at 10 kHz. The surface conductance and capacitance showed breaks at pre- and main transition temperatures. Below the pre-transition temperature, the activation energy of the ion movement was 18.1 kJ.mol-1, which corresponded to that of the spin-lattice relaxation time of water (18.0 kJ.mol-1). At temperatures between pre- and main transition it increased to 51.3 kJ.mol-1, and agreed with 46.2-58.0 kJ.mol-1 of the activation energy of the dielectric relaxation of ice. Because the present system was salt-free, the ions were H3O+ and OH-, hence, their behavior represents that of water. The above results show that below the pre-transition temperature, the conductance is regulated by the mobility of free ions, or the number of free water molecules near the interface. On the other hand when the temperature exceeded pre-transition, melting of the surface-bound water crystals became the rate-limiting step for the proton flow. Halothane did not show any effect on the ion movement when the temperature was below pre-transition. When the temperature exceeded pre-transition, 0.35 mM halothane (equilibrium concentration) decreased the activation energy of the ion movement to 29.3 kJ.mol-1. This decrease indicates that halothane enhanced the release of the surface-bound water molecules at pre-transition. The surface-disordering effect of halothane was also shown by depression of the pre-transition temperature and decrease of the association energy among head groups from 9.7 kJ.mol-1 of the control to 5.2 kJ.mol-1 at 0.35 mM.

1,2-Dipalmitoylphosphatidylcholine↗

Differential expression of CD45RO (UCHL1) and its functional relevance in two subpopulations of circulating TCR-gamma/delta+ lymphocytes.

We examined the developmental profile of TCR-gamma/delta+ cells with respect to CD45RO expression. Although total TCR-gamma/delta+ cells were negligible in the neonatal blood and increased with advancing age, most blood TCR-gamma/delta+ cells markedly expressed CD45RO without a distinction of age, probably reflecting a different CD45RO expression of two subsets defined by BB3 and delta TCS1 mAbs. The vast majority of BB3+ cells expressed CD45RO, whereas expression of CD45RO was virtually absent in the delta TCS1+ population. Functional studies revealed that, while both TCR-gamma/delta+ cell subsets showed CD3-mediated activation, only BB3+ (or Ti gamma A+) cells, but not delta TCS1+ cells, appeared to proliferate in response to PPD in PPD-reactive individuals. The results suggested that the CD45RO+ (BB3+ or Ti gamma A+) subset among blood TCR-gamma/delta+ cells may be mainly involved in the memory or primed component of the immune system responding to some foreign antigens.

Adolescent↗

Effects of thiopental, pentobarbital, and ketamine on endothelin-induced constriction of porcine cerebral arteries.

Contractile mechanisms of endothelin, a newly isolated vasoactive substance from endothelium, were evaluated in anterior cerebral arteries (ACA). Furthermore, the effects of thiopental, pentobarbital, ketamine, and diltiazem on the endothelin-induced cerebral vasoconstriction were also studied. Endothelin induced cerebral arterial contractions in concentrations above 3 X 10(-10) M. The median effective concentration (ED50: X10(-9) M) of endothelin was 2.1 +/- 0.7 (n = 6). Endothelin did not elicit contractions in preparations soaked in Ca2(+)-free solution, but addition of 2.5 mM Ca2+ to the baths induced marked contractions. Thiopental and pentobarbital attenuated endothelin-induced contractions at concentrations above 3 X 10(4) M, while ketamine was effective above 10(-3) M. In contrast, diltiazem decreased endothelin-induced vasoconstriction at 10(-6) M. The findings suggest that endothelin may cause contractions of porcine cerebral arteries by influx of Ca2+ through Ca2+ channels. The cerebral vasomotion induced by endothelin, however, does not seem to be influenced by clinical doses of barbiturates and ketamine.

Animals↗

Anginal attack following a sodium bicarbonate and hydrocortisone injection.

A case of a 73-year-old man with variant angina who developed chest pain and shock following an injection of sodium bicarbonate and hydrocortisone is reported. The electrocardiogram (ECG) during the chest pain attack revealed ST elevation in leads II, III and aVF. It returned to a normal pattern 10 min later. Coronary angiography, performed 2 hours after the anginal attack, showed no significant coronary arterial stenosis. One month later, an injection of ergonovine (16 micrograms) into the right and left coronary arteries induced spasms in segments 4 and 13, with ischemic ECG changes. Possible causes of the anginal attack are a coronary arterial spasm induced by the allergic reaction to hydrocortisone and/or serum alkalosis due to the sodium bicarbonate injection triggered by hyperventilation.

Aged↗

[Anesthesia for pectus excavatum].

The incidence of arrhythmia, postoperative complication and pulmonary oxygenation (PaO2) were studied in 48 patients with pectus excavatum scheduled for the Ravitch operation under halothane-nitrous oxide-oxygen (GOF) and enflurane-nitrous oxide-oxygen (GOE) anesthesia. Preoperative abnormalities of ECG were observed in 36 of 18 cases. Main abnormalities were incomplete right bundle branch block, left atrium enlargement, and sinus arrhythmia. Ventricular arrhythmia was observed in 4 of 12 cases during GOF anesthesia, whereas no arrhythmia was observed during GOE anesthesia. In postoperative chest X-ray, pulmonary atelectasis (60%), pleural effusion (48%), and pneumothorax (8%) were observed. The results suggest that GOE is more advantageous for pectus excavatum operation than GOF. Postoperative pulmonary surveillance is important for pectus excavatum operation.

Adolescent↗