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Biomedical subjects

N Kawada

Publications and source records attributed to N Kawada.

At least 127 records · Page 7Linked to original sources
PubMed1992

[The reactivity of dispersed human lung mast cells and peripheral blood basophils to acetylcholine].

To clarify the relation between human lung mast cells and parasympathetic nerve function as well as IgE mediated allergic reactions, highly purified dispersed human lung mast cells were obtained by using the techniques of scissors dispersion, enzymatic treatment, percoll centrifugation and exclusion of adherent cells. The reactivity to acetylcholine was examined by observing the histamine release of purified mast cells. Moreover, peripheral blood basophils, which have many functional similarities with mast cells, were also examined in the same manner. The following results were obtained; 1) Histamine was significantly released from dispersed human lung mast cells at a final concentration of 10(-5) M acetylcholine (p less than 0.05); the peak of histamine release was 10(-4) M of acetylcholine. Acetylcholine had the additional effect of releasing histamine in response to anti-IgE. Histamine release was partially inhibited by 10(-5) M atropine. 2) Basophils had no response to acetylcholine. These results suggest that human lung mast cells play an important role in the defensive mechanism as an effector cell of acetylcholine-mediated autonomic nerve system as well as IgE-mediated allergic reaction.

Acetylcholine↗
PubMed1992

[Purification and reactivity of human lung mast cells].

To clarify the pathogenesis of allergic pulmonary diseases by analysis of the reactivity of human lung mast cells, we established a method of dispersion and purification of mast cells from human lung tissue. This method consisted of 4 steps; 1) mincing by scissors, 2) enzymatic treatment by a pronase-chymopapain and collagenase-elastase mixture, 3) percoll centrifugation and 4) exclusion of adherent cells. Using this method, dispersed human lung mast cells were obtained with 38.8% purity and more than 95% viability. These mast cells contained 4.1 pg of histamine per cell, which showed these cells had mild spontaneous histamine release after treatment. The mast cells released histamine in a dose-dependent manner after treatment with calcium ionophore A 23187 and anti-IgE, and these phenomena were dependent on extracellular calcium ions. However, the cells did not release histamine with less than 100 micrograms/ml of compound 48/80. These results indicate that the human lung mast cells obtained by this method are useful to make immunological and pharmacological analyses in allergic lung diseases.

Humans↗
PubMed1992

[Rapid spontaneous postpartum remission in a case of chronic inflammatory demyelinating polyradiculoneuropathy associated with pregnancy].

A 28-year-old woman developed numbness and weakness of the hands and arms when she was 8 months pregnant, and weakness worsened gradually. However, weakness started to spontaneously subside immediately after delivery and she felt almost recovered several hours later. But weakness and numbness recurred one week after delivery and she was admitted to our hospital. Neurological examination revealed moderate weakness and disturbance of the deep and cutaneous sensations in the upper and lower extremities, and marked decrease of the deep tendon reflexes. The upper extremities were more severely affected. Nerve conduction study showed marked decrease in the motor conduction velocities. Cerebrospinal fluid showed increase of protein without pleocytosis. Teased preparation of the biopsied sural nerve showed occasional internodal segments with thin myelination, indicating demyelination and remyelination. A diagnosis of chronic inflammatory demyelinating polyradiculoneuropathy was made. Treatment with prednisolone markedly improved the weakness and hyporeflexia as well as the cerebrospinal fluid protein. Postpartum rapid remission may have been produced by rapid increase of endogenous steroid hormone in the blood by its massive excretion during delivery.

Adult↗
PubMed1991

Effects of irsoglandine maleate in an experimentally-induced acute hepatic failure model using mice.

When heat-killed Propionibacterium acnes was intravenously injected into mice followed by an intravenous injection of a small amount of Gram-negative lipopolysaccharide seven days later, most of the mice died of massive hepatic cell necrosis within 24 hours. However, when irsoglandine maleate, an anti-ulcer agent, was administered to mice during the period of experimental induction of acute hepatic failure, the survival rate, serum transaminase levels and histological changes of the liver remarkably improved. These results suggested that irsoglandine maleate may have protective effects on the liver in our experimentally-induced acute hepatic failure model using mice. Therefore, in the absence of a definitive therapy for fulminant hepatitis, irsoglandine maleate may be a promising therapeutic agent.

Animals↗
PubMed1991

Effect of gomisin A in the prevention of acute hepatic failure induction.

Nearly all rats develop massive hepatic cell necrosis and die upon intravenous administration of heat-killed Propionibacterium acnes followed by a small amount of Gram-negative lipopolysaccharide 7 days later. However, when such an experimental liver disorder is induced in rats raised for 4 or more weeks on food containing 0.06% of gomisin A extracted and purified from Schizandra chinensis, the survival rate rises, histological changes of the liver improve remarkably, and splenocyte reactivity to phytohemagglutinin and pokeweed mitogen as well as splenocyte interleukin 1 productivity are retained. These results suggested the possibility that the development of acute hepatic failure may be prevented with the oral administration of gomisin A.

Animals↗
PubMed1991

An autopsy case of metastatic foci of hepatocellular carcinoma in adenomatous hyperplasias of the liver.

Adenomatous hyperplasia of the liver is known as a preneoplastic or early developmental stage of hepatocellular carcinoma, in which overt malignant foci occasionally develop. We have recently experienced an autopsy case (a 70-year-old male) of liver cirrhosis with hepatocellular carcinoma and two nodules of adenomatous hyperplasia. The latter two nodules contained several microscopic foci of moderately differentiated hepatocellular carcinoma. There were a number of tumor microemboli in portal vein branches within areas of adenomatous hyperplasia in addition to areas surrounding cirrhotic liver, some of which grew into the parenchyma of adenomatous hyperplasia and cirrhotic regenerative nodules. These findings and the fact that adenomatous hyperplasia contained portal tracts including portal venous branches, suggest that malignant foci in adenomatous hyperplasia contained portal tracts including represent metastases from hepatocellular carcinoma in other parts of the liver via the intrahepatic portal venous system.

Aged↗
PubMed1991

Interferon gamma modulates production of interleukin 1 and tumor necrosis factor by murine Kupffer cells.

When mononuclear phagocytes, including Kupffer cells, are activated by various agents, they synthesize and release cytokines such as interleukin 1 (IL-1) and tumor necrosis factor (TNF). In this study, we examined the effect of in vitro Kupffer cell activation by recombinant murine interferon gamma (IFN gamma) on IL-1 and TNF secretion. IFN gamma enhanced TNF production in the presence or absence of lipopolysaccharide (LPS), but suppressed IL-1 production by Kupffer cells. Because IFN gamma also stimulated prostaglandin E2 (PGE2) production, the effect of indomethacin, which is an inhibitor of cyclooxygenase and which inhibits PGE2 biosynthesis, on IL-1 and TNF production by Kupffer cells was examined. As a result, indomethacin enhanced TNF production by Kupffer cells, but had no effect on IL-1 synthesis. These results suggested that IFN gamma modulates the production of IL-1 and TNF by Kupffer cells through different mechanisms.

Animals↗
PubMed1991

The effect of lipo-prostaglandin E1 on the production of interleukin 1 and platelet-activating factor by hepatic sinusoidal endothelial cells in mice.

We first studied the production of interleukin 1 (IL1) and platelet-activating factor (PAF) by mouse hepatic sinusoidal endothelial cells and then the effect of Lipo-prostaglandin E1 (Lipo-PGE1) on IL1 and PAF production by these cells. The incubation of mouse hepatic sinusoidal endothelial cells with lipopolysaccharide (LPS) or calcium-ionophore (CaI) A23187 resulted in a concentration-dependent production of IL1 and PAF. However, Lipo-PGE1 dose-dependently decreased the LPS- or CaI A23187-induced production of IL1 and PAF. These results suggested that Lipo-PGE1 acts on hepatic sinusoidal endothelial cells to decrease the production of IL1 and PAF, thereby ameliorating inflammatory reactions in the liver.

Alprostadil↗
PubMed1990

Arachidonic acid metabolites in carbon tetrachloride-induced liver injury.

The changes in the levels of leukotrienes (LTs) and prostaglandins (PGs) in the liver tissue of rats with carbon tetrachloride (CCl4)-induced liver injury were studied. As a result, after the administration of CCl4, the levels of LTs increased at an early stage while the levels of PGs increased at a later stage. This suggests that LTs may have an adverse effect on liver injury induced by CCl4, and that PGs may not have a direct effect on liver injury. In addition, serum GOT and GPT levels improved with the administration of AA-861, a 5-lipoxygenase inhibitor, while these levels did not change with the administration of indomethacin, a cyclooxygenase inhibitor. These results suggest that arachidonic acid metabolites may play an important role in the induction of liver cell injury.

Alanine Transaminase↗
PubMed1990

Interferon gamma stimulates prostaglandin E2 production by mouse Kupffer cells.

When mononuclear phagocytes, including Kupffer cells, are activated by various agents, they synthesize and release arachidonic acid metabolites, prostaglandins (PGs) and leukotrienes (LTs). In this study, we examined the effect of in vitro Kupffer cell activation with recombinant murine IFN gamma on PGE2 and LTB4 secretion. IFN gamma enhanced PGE2 secretion, and this effect of IFN gamma was stronger than that of IL-1 or TNF. Moreover, IFN gamma promoted LTB4 release especially in the absence of PGs. On the other hand, dexamethasone and indomethacin inhibited and, EGTA and TMB-8, which reduce intracellular Ca++ Levels, blocked IFN gamma induced PGE2 production, which suggested that the activation of phospholipase A2 and cyclooxygenase in Kupffer cells requires the elevation of intracellular Ca++ levels.

Animals↗
PubMed1990

Synthesis of eicosanoids by Propionibacterium acnes-elicited liver adherent cells and their effect on production of interleukin 1 and tumor necrosis factor.

When heat-killed Propionibacterium acnes (P. acnes) is intravenously injected into rats or mice, liver adherent cells including macrophages and Kupffer cells increase in number and they synthesize various kinds of biologically-active materials. We studied the production of eicosanoids and the cytokines, interleukin 1 (IL-1) and tumor necrosis factor (TNF), by P. acnes-elicited liver adherent cells and the regulatory mechanisms of eicosanoids in the synthesis of cytokines. As a result, P. acnes-elicited liver adherent cells synthesized not only prostaglandin (PG) E2, 6-keto-PGF1 alpha, thromboxane B2 and leukotriene B4, but also IL-1 and TNF. In addition, PGE2 and PGI2 suppressed the production of these cytokines. These results suggested that there are auto-regulatory mechanisms in production of cytokines in the liver.

Animals↗
PubMed1990

Changes in leukotrienes and prostaglandins in the liver tissue of rats in the experimental massive hepatic cell necrosis model.

When heat-killed Propionibacterium acnes is intravenously injected into rats followed by an intravenous injection of a small amount of Gram-negative lipopolysaccharide (LPS) 7 days later, massive hepatic cell necrosis is induced and most of the rats die within 24 hours of LPS injection. Using this experimental model, we studied the changes in the levels of leukotrienes (LTs) and prostaglandins (PGs) in the liver tissue and bile of rats with experimentally-induced massive hepatic cell necrosis. Both the levels of LTs and PGs in the liver tissue and LTs in the bile increased before the microscopic appearance of hepatic cell necrosis. These results suggest that arachidonic acid metabolites may play an important role in the induction of liver cell injury.

6-Ketoprostaglandin F1 alpha↗
PubMed1990

[The protective effects of glucagon and insulin in an experimental massive hepatic cell necrosis model].

When heat-killed Propionibacterium acnes was intravenously injected into mice and seven days later, a small amount of gram-negative lipopolysaccharide (LPS) was also intravenously injected, most of them died of massive hepatic cell necrosis. However, then glucagon (0.5 mg/kg body weight) and insulin (0.5 units/kg body weight) or glucagon (0.5 mg/kg body weight) individually were administered during this experimental induction of massive hepatic cell necrosis, the survival rate of mice increased and serum transaminase levels improved. Also, the histological changes of the liver improved remarkably. But, insulin (0.5 units/kg body weight) individually was not effective in an experimental massive cell necrosis model. These results suggested that glucagon and insulin was effective in our experimental massive hepatic cell necrosis model.

Animals↗
PubMed1990

[Adenomyoma in association with early gastric carcinoma].

Described is a gastric adenomyoma associated with superficial gastric adenocarcinoma that was found in a 72-year-old male. This uncommon benign gastric lesion is believed to be developmental in origin and sometimes categorized as belonging to a subgroup of a heterotopic pancreas. Besides its rarity, an adenomyoma is also known to be a possible cause of a gastric malignancy. Although the focus of the carcinoma in our case was located in the center of the adenomyoma, this finding cannot support the etiology of a gastric carcinoma originating in an adenomyoma. However, the present case appears to imply some relationship between an adenomyoma and a gastric carcinoma.

Adenocarcinoma↗
PubMed1990

[Serotonin and tryptamine metabolism in the acute hepatic failure model--changes in tryptophan and its metabolites in the liver, brain, kidney and serum].

When trinitrophenylated (TNP) hepatocytes and lipopolysaccharide (LPS) are intravenously injected into TNP-liver protein sensitized guinea pigs, massive hepatic cell necrosis was induced in most of mice. Using this experimental acute hepatic failure model, the tryptophan metabolism in the liver, brain, kidney and serum was studied. As a result, the tryptophan level was remarkably high in all three organs and serum, and the metabolism of both the tryptamine pathway and serotonin pathway was induced. Also, in the brain, the tryptamine metabolism was more induced compared to the serotonin. These results suggest that the metabolites of tryptophan may be involved in this acute hepatic failure model.

Acute Disease↗
PubMed1989

T lymphocyte subsets in the peripheral blood in patients with primary biliary cirrhosis.

T lymphocyte subsets and natural killer (NK) cells in the peripheral blood of 10 patients with primary biliary cirrhosis (PBC) were examined by using various kinds of monoclonal antibodies directed to the surface markers of the lymphocytes. We found that the population of Leu 2a+, Leu 15- cytotoxic T cells was decreased in PBC patients compared to normal controls, especially in those with a high serum titer of anti-mitochondria antibodies. However, there was no significant difference in the population of Leu 2a+, Leu 15+ suppressor T cells between PBC patients and normal controls. Although the population of Leu 3a+, Leu 8- helper T cells was not significantly different, the population of Leu 3a+, Leu 8+ suppressor-inducer T cells was remarkably increased in PBC patients compared to normal controls. On the other hand, no such difference was seen for the NK cells. Furthermore, the Leu 3a+/Leu 2a+ ratio was significantly higher in PBC patients especially in those with a high serum anti-mitochondria antibody titer, which was thought to be due to the decreased population of cytotoxic T cells.

Adult↗
PubMed1989

Serotonin and tryptamine metabolism in the acute hepatic failure model: changes in tryptophan and its metabolites in the liver, brain and kidney.

When heat-killed Propionibacterium acnes, a gram-positive anaerobe, is intravenously injected into mice followed by an intravenous injection of gram-negative lipopolysaccharide (LPS) 7 days later, most of the mice die of massive hepatic cell necrosis within 24 hours of LPS injection. Using this experimental model, acute hepatic failure was induced in mice, and the tryptophan metabolism in the liver, brain and kidney was studied. As a result, the tryptophan level was remarkably high in all three organs, and the metabolism of both the tryptamine pathway and serotonin pathway was induced. However, in the brain, the tryptamine metabolism was more induced compared to the serotonin, suggesting that the metabolites of tryptamine, may be involved in hepatic encephalopathy.

Acute Disease↗