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S Arii

Publications and source records attributed to S Arii.

At least 109 records · Page 6Linked to original sources

Enhancement and hepatocyte-modulating effect of chemical mediators and monokines produced by hepatic macrophages in rats with induced sepsis.

We investigated the production of chemical mediators by hepatic macrophages from rats with sepsis and the modulation of hepatocyte function by these hepatic macrophages. The chemical mediators we measured were superoxide (O2-), TNF, IL-1, and PGE2. Production of these mediators by hepatic macrophages from rats with sepsis was significantly increased. Furthermore, protein synthesis by cultured hepatocytes was inhibited in a co-culture system of hepatocytes and hepatic macrophages from rats with sepsis, and it was even inhibited by the supernatant of cultured hepatic macrophages from septic rats. These results demonstrate that hepatic macrophages are activated in sepsis and may play a role in inducing hepatic dysfunction in sepsis.

Animals↗

Enhancement of hepatic macrophages in septic rats and their inhibitory effect on hepatocyte function.

In the present study, the function of hepatic macrophages and the modulation of hepatocytes by sepsis-elicited hepatic macrophages were investigated in rats with induced sepsis. The functional state of hepatic macrophages was determined by the following indicators: phagocytic index, protein-synthesizing capacity, and superoxide (O2-) producing capacity. These indices of changes in hepatic macrophages were much higher in rats with sepsis than in healthy controls. Moreover, the activated hepatic macrophages had some biological properties which were different from those of the resident Kupffer cells. It was found that protein synthesis by cultured hepatocytes was inhibited in the co-culture system of hepatocytes and sepsis-elicited hepatic macrophages, and that the supernatant of hepatic macrophages from rats with sepsis also reduced the protein-synthesizing capacity of cultured hepatocytes. Thus, activated hepatic macrophages may play a role in inducing hepatic dysfunction in sepsis.

Animals↗

Postoperative erythroderma with change of HLA phenotypes from heterozygotes to homozygotes: a report of two cases.

Fatal "postoperative erythroderma" (POE) developed in 2 patients treated with liver lobectomy and the transfusion of fresh blood. Their clinical features and skin-histological findings were indicative of acute graft-versus-host disease (GVHD). The HLA phenotypes of circulating lymphocytes of the 2 patients were heterozygous but became homozygous late in the clinical course and were identical with those of the blood donors. One of the patient's haplotypes was identical with the donor's homozygous haplotype. These findings suggest the mechanism of development of POE in apparently immunocompetent patients. The donor's T lymphocytes are histocompatible with the patient's tissues, are not rejected, and become engrafted. The patient's tissues are not histocompatible with the donor's, so that GVHD develops.

Blood Donors↗

Differentiation-dependent expression of I and sialyl I antigens in the developing lung of human embryos and in lung cancers.

The localization of two carbohydrate antigens, I and sialyl I antigens, in the lungs of developing human embryos was investigated using specific monoclonal antibodies and compared with the distribution patterns of the known embryonic antigen, stage-specific embryonic antigen-1 (Lex hapten). When the future bronchi were actively developing from the bronchial buds in the lungs of 50- to 53-day-old embryos, the immature bronchial bud cells were I-, Lex+, while the fully differentiated epithelial cells of the larger bronchus were I+, Lex-. When the bronchiolar bud cells matured into bronchiolar epithelial cells in the lung of a 12-week-old embryo, the immature bronchiolar bud cells were I-,Lex+, while the fully differentiated epithelial cells of the bronchioles were I+,Lex-. Sialylated forms of the antigens finally appeared in the lungs of 18-week-old embryos, when the terminal bud cells actively proliferated and underwent the differentiation process into epithelial cells of alveoli and alveolar ducts. The immature terminal bud cells at this stage were I-, sialyl I-, Lex+, sialyl Lex-i+, while the fully differentiated alveolar epithelial cells were I+, sialyl I+, Lex-, sialyl Lex-i-. After 8 months, the flattened mature alveolar epithelial cells were strongly positive for both I and sialyl I antigens, the strong expression of which continued after birth and even into the adult stage. These distribution patterns indicate that the I and sialyl I antigens are specific markers for the differentiated type cells in each stage of development, while Lex and related embryonic antigens were specific to the immature bud cells in every stage. The above-described differentiation-dependent expression patterns of these antigens seem to be reflected in the distribution of these antigens in human lung cancers, i.e., I and sialyl I antigens were expressed in lung cancer cells more weakly than in normal lung cells, while the Lex and sialyl Lex-i were expressed in cancer cells much more strongly than in normal lung cells. This was further reflected in the serum levels of these antigens in the patients with respiratory disorders. The distribution pattern of the serum levels of these antigens in patients with lung cancers showed sialyl Lex-i greater than sialyl I, indicating that these serum antigens originated from the lung cancer lesion where sialyl Lex-i is much more dominant than sialyl I antigen.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenocarcinoma↗

Depressed function of Kupffer cells in rats with CCl4-induced liver cirrhosis.

In the present study, the Kupffer cell function of rats with CCl4-induced liver cirrhosis was tested by analyzing the changes in the host defense system. In rats without liver cirrhosis injected with CCl4 for 3 weeks concomitant with the high opsonic activity the endocytic index was significantly increased. Rats treated for 9 and 13 weeks developed cirrhosis, and their endocytic indices were not increased despite the rise in their opsonic activity. Particularly, the endocytic index of 13-week-treated rats with advanced liver cirrhosis was significantly lower than that of the other groups. The organic distribution of 51Cr-endotoxin injected intravenously exhibited characteristic changes in 9-week- and 13-week-treated rats: decreased hepatic uptake and increased splenic uptake. In contrast, pulmonary uptake was increased in all CCl4-treated rats. The superoxide production by Kupffer cells from 13-week-treated rats was greatly reduced, accompanied by the decreased superoxide dismutase activity of liver homogenate. Thus, results of this study suggest that Kupffer cell dysfunction is one of the main factors affecting host defenses in liver cirrhosis.

Animals↗

Clinicopathological features of malignancy in hepatocellular carcinoma.

The clinicopathological features showing the malignancy of hepatocellular carcinoma were investigated by retrospectively analyzing the postoperative prognosis after hepatic resection. The long-term prognosis was strongly affected by the existence of portal tumor invasion or intrahepatic metastasis as indicated by the following results. The 3-year cumulative survival rates were 61% and 38% for patients in portal vein tumor invasion groups (Vp0 and Vp1 (P less than 0.05). No patients with Vp2 or Vp3 could survive beyond 3 years after hepatic resection. Similarly, patients with intrahepatic metastasis IM0 showed a better prognosis, compared to those with IM2 or IM3 (P less than 0.05). In addition, the grade of tumor cell anaplasia to some extent affected the prognosis, but not the tumor growth pattern at the tumor/non-tumor boundary. The tumor growth rate, estimated by the alpha-fetoprotein doubling time, was not connected with venous invasion or intrahepatic metastasis, but it became shorter at the time of a recurrence. It is concluded that, from the standpoint of a long-term prognosis, the pathological features showing malignancy appear in venous invasion and intrahepatic metastasis.

Carcinoma, Hepatocellular↗

Sialyl SSEA-1 antigen as a carbohydrate marker of human natural killer cells and immature lymphoid cells.

The distribution of a carbohydrate antigen, the sialyl SSEA-1 (sialyl Lex-i), in human lymphoid cells was investigated by flow cytometry with a specific monoclonal antibody, MoAb FH-6. We concluded that the lymphocytes positive for the sialyl SSEA-1 antigen present in normal peripheral blood (PB) are natural killer (NK) cells since the positive cells had an NK activity toward K562 cells, and most of the sialyl SSEA-1+ cells were simultaneously positive for Leu-11 (CD-16) and Leu-19. Essentially, no T and B cells, defined by Leu-4 (CD3) and Leu-16 (CD20), were positive for the sialyl SSEA-1 antigen in PB samples taken from healthy donors and patients with disorders unrelated to lymphoid malignancies. Among the malignant lymphoid cells, many sialylated SSEA-1+ cells were observed in large granular lymphocyte (LGL) leukemia cells and some acute lymphoblastic leukemia (ALL) blasts, but not in CLL cells or malignant lymphoma cells. Sialyl SSEA-1 was also positive in some cultured human lymphoid cell lines. We conclude that expression of the sialyl SSEA-1 antigen is strictly limited to a distinct population of NK cells among the mature lymphocytes in normal PB, but the antigen is present in a wide range of immature lymphoblasts of T- and B-cell lineages as well as the NK-cell lineage. The sialyl SSEA-1 antigen disappears from the surface of immature lymphocytes of T- and B-cell lineages during the course of maturation.

Antibodies, Monoclonal↗

Significance of 2-3 and 2-6 sialylation of Lewis a antigen in pancreas cancer.

Distributions of sialylated derivatives of Lewis a (Lea) antigen in cancer tissue of the human pancreas and in the sera of patients with pancreas diseases have been studied; the significance of 2-3 and 2-6 sialylation of Lea antigens in pancreas cancer have been investigated using specific monoclonal antibodies. In most pancreas cancer tissue the 2-3 sialylated Lea antigen was found to be specifically distributed in cancer cells as determined by immunohistologic techniques, while a significantly smaller amount of the antigen was detected in surrounding nonmalignant pancreas tissue, which was infiltrated by cancer cells. Conversely, the 2-6 sialylated Lea antigen was abundantly present in nonmalignant pancreas tissue, while it was less frequently present in pancreas cancer cells. When the sera of 66 patients with pancreas diseases were examined for these sialylated Lea antigens, correlation studies showed that the levels of 2-3 sialylated Lea tended to be 44.1 times more than the levels of 2-6 sialylated Lea in the sera of cancer patients. The average ratio of 2-3 sialylated Lea to 2-6 sialylated Lea was 0.23 in the sera of patients with pancreatitis. These data collectively indicate that the 2-3 sialylation of Lea is remarkably enhanced, and the 2-6 sialylation of Lea antigen is suppressed in pancreas cancer. The determination of the 2-3 sialylated Lea to 2-6 sialylated Lea ratio in patients with pancreas diseases may be helpful for the differential diagnosis of pancreas cancer and nonmalignant pancreatic disorders.

Antibodies, Monoclonal↗

The three different phases of reticuloendothelial system phagocytic function in rats with liver injury.

In the present study, reticuloendothelial system (RES) phagocytic function of rats with partial hepatectomy or experimentally induced liver cirrhosis was investigated by determining the phagocytic index, the opsonic index, and uptake rate in liver, spleen, and lung of a 51Cr-labeled endotoxin-injected rat. In both the partially hepatectomized and the cirrhotic rats, all three indicators varied markedly according to the elapsed period since liver injury. The changes in RES phagocytic function were classified into three different phases: compromised, compensatory, and enhanced. The compromised phase, consisting of a decrease in the phagocytic index, was observed during the first 24 hr after 67% hepatectomy and in advanced liver cirrhosis. This represented the failure of RES phagocytic function. The compensatory phase, in which the phagocytic index was maintained at nearly normal levels mainly by a compensatory enhancement in the opsonic index, was seen during the first to second postoperative day and in moderate liver cirrhosis. The enhanced phase, with a high phagocytic index, was observed from Day 4 to approximately Day 14 after surgery, and in the cases of mild liver damage. In the compromised and compensatory phases, the liver uptake rate was significantly decreased compared with the control. However, the uptake in the spleen and lung were markedly increased. In conclusion, the phagocytic function of the RES was significantly affected to a degree which changed with the extent of liver damage.

Animals↗

[Indications for limited hepatic resection in hepatocellular carcinoma].

Indications for limited hepatic resection in patients with hepatocellular carcinoma were evaluated by retrospective and clinicopathologic analysis of postoperative cases. Particular attention was paid to hepatic functional reserve and long-term prognosis. In our department, in order to estimate the hepatic functional reserve, indocyanine green clearance test (ICG), Child's classification and the oral glucose tolerance test have been applied. For instances, the incidences of hospital deaths were 17% and 19% in cases with an ICG-K value below 0.06 and between 0.06 and 0.08, which were high, compared with 6% and 3% in cases ICG-K values of with 0.08-0.10 and 0.10-0.12. On the other hand, by clinicopathologically analyzing 18 surviving patients or those surviving without recurrence for over 3 years after hepatic resection and 41 cases of small hepatocellular cancer less than 3 cm in diameter, those with capsule formation and without portal tumor invasion, intrahepatic metastasis and capsular invasion had a good long-team prognosis without recurrence even following limited resection. Particularly, patients with a surgical margin of over 1cm between the tumor and cut surface were candidates for long, non-recurrence survival. Form these results, the indications for limited hepatic resection for hepatocellular carcinoma were considered to be on ICG-K value of less than 0.08 in hepatic function and cases without venous invasion and extracapsular tumor invasion. In other cases, it is recommended that limited resection should be followed by multidisciplinary treatment.

Carcinoma, Hepatocellular↗

[Development of the surgical therapy of malignant liver tumors].

The development of surgical treatment for malignant liver tumor was reviewed. The developmental process can apparently be divided into four periods. The first period up to 1968 is when surgical trials for liver tumors were started, and much effort was directed toward the establishment of systematic procedures for hepatic resection. The second period starts form 1968, when the Liver Cancer Study Group of Japan was inaugurated to organize investigators participating in the treatment of, and basic research on liver tumors. During this period, the basis for contemporary surgical treatment and sophisticated means of diagnosis such as such as determination of serum AFP level, selective angiography, and liver scintigraphy were established. This period came to an end around 1977 when computed tomography and ultrasonography were developed and popularized. In the third period, a variety of procedures for hepatic resection such as lobectomy, segmentectomy and newly devised echo-guided sub-segmentectomy were performed, based on the close evaluation of hepatic functional reserve. However, analysis of the outcome in patients who had undergone surgery alone suggested the limitations of surgical treatment, leading to the advent of the 4th period two to three years ago. The strategy of therapy in the 4th period has been aimed at multidisciplinary treatment such as transarterial embolization, intratumoral injection of tumoricidal agents, radiotherapy, regional chemotherapy and immunotherapy.

Hepatectomy↗

Human monoclonal antibody recognizing liver-type aldolase B.

A human hybridoma clone (4E3) has been established by fusing lymphocytes from a lymph node taken from a breast cancer patient and human lymphoblastoid cells, LICR-LON-HMy2, by the poly(ethylene glycol) method. 4E3 has been stabilized and continued to secrete IgMk antibody into culture medium (greater than 10 micrograms/ml) for over 1 year. The following characteristics of the antigen strongly suggested that 4E3 recognizes liver-type aldolase B (EC 4.1.2.13): the Mr of the native molecule is 160,000 and that of the subunit is 40,000, and thus it has a tetrameric structure of identical subunits; the antigen is abundant in the liver and kidney of human, mouse and rabbit, and is localized by immunohistochemical methods in the cytoplasm of hepatocytes and in the proximal tubules of the kidney; the antigen is precipitable by 50-80% saturation with (NH4)2SO4; the antigen shows charge-dependent heterogeneity on DEAE-cellulose chromatography. To confirm this notion, aldolase B was purified to homogeneity from the liver of human, mouse and rabbit by phosphocellulose chromatography. During the chromatographic purification, the antigen activity as assayed by enzyme-linked immunosorbent assay (e.l.i.s.a.) was superimposed on the enzymic activity of aldolase. Furthermore, monoclonal antibody 4E3 strongly reacted with purified aldolase B in SDS/polyacrylamide-gel electrophoresis followed by Western blotting and also in e.l.i.s.a. using microplates coated with purified enzyme. The reaction between aldolase B and 4E3 activated the human complement system as assessed by the attachment of C3 to the immune complex of aldolase B and 4E3.

Animals↗

Changes in the reticuloendothelial phagocytic function after partial hepatectomy.

The changes in the phagocytic function of the reticuloendothelial (RE) system after 67% hepatectomy in rats were studied by use of 51Cr-endotoxin as the phagocytable material. The humoral opsonic index was significantly increased to approximately 1.2 to 1.8 (control, 1.0 +/- 0.2, mean +/- SD) until the fourteenth postoperative day. In contrast, the phagocytic index was decreased to 0.068 +/- 0.016 (control, 0.103 +/- 0.015) on the first day, then returned to the normal level on the second day. In this early postoperative period, uptake rates of 51Cr-endotoxin in the liver were remarkably decreased to about 50% to 70% of control, whereas those in the spleen and lung were increased two- to threefold of control. From the third to the fourteenth day, the phagocytic index was significantly increased compared with the preoperative level. During this period, the uptake rates in the liver and spleen were within the normal range. These results suggest that the increases in the opsonic index of 67% hepatectomized rats represent the homeostatic response for maintaining or stimulating RE system phagocytic function, and that high or normal phagocytic index, concomitant with the increase in the opsonic index, implies an enhanced or compensatory stage, respectively. The decrease in the phagocytic index despite the high opsonic index is assumed to represent a compromised stage of the RE system.

Animals↗

Changes in acetoacetate/beta-hydroxybutyrate ratio in arterial blood following hepatic artery embolization in man.

Acetoacetate/beta-hydroxybutyrate ratio in the hepatic venous blood was compared to the ratios in arterial blood and peripheral venous blood in hypoxic state following right hepatic artery embolization in 5 patients with liver cancer. Ketone body ratios in right hepatic venous blood were positively correlated with those in arterial blood (r = 0.960, p less than 0.001), but not with those in peripheral venous blood. The free NAD+/NADH ratio of the liver mitochondria, which is reflected by the ketone body ration in hepatic venous blood, can be evaluated by the ketone body ratio in the arterial blood.

3-Hydroxybutyric Acid↗