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Biomedical subjects

S Sakaguchi

Publications and source records attributed to S Sakaguchi.

At least 253 records · Page 14Linked to original sources
PubMed1984

Clinical significance of acidic pI isoenzyme of ribonuclease in human serum.

Employing isoelectric focusing with an Ampholine column, the presence of three major pI isoenzymes (basic, neutral and acidic) of human ribonuclease (RNase) is demonstrated. The acidic pI isoenzyme was observed in pancreatic and hepatic cancer cells and in fetal pancreas and liver tissues, and was frequently detected in the sera of patients with pancreatic and hepatic cancer. This isoenzyme was not, however, detected in the sera of non-cancerous patients. In pancreatic cancer tissues, other pI isoenzymes, except for the acidic one, were markedly suppressed and the isoelectrophoretic patterns of the cancerous tissues closely resembled those obtained from fetal pancreatic tissue. These results suggest that the acidic pI isoenzyme could represent one of the carcinofetal proteins and that the detection of this pI isoenzyme in the patient's serum may be useful for the diagnosis of pancreatic and hepatic cancer.

Biliary Tract Neoplasms↗
PubMed1984

Nonfunctioning islet cell carcinoma presenting bleeding gastric varices and splenomegaly.

This is a report of a 63-year-old Japanese woman with a nonfunctioning islet cell carcinoma of the pancreas presenting bleeding gastric varices and splenomegaly. These manifestations are extremely rare in patients with nonfunctioning islet cell tumor. The tumor originated in the tail of the pancreas and grew mainly within the spleen. The gastric varices due to increased blood flow to the tumor and arteriovenous fistulas within the tumor were confirmed by angiography and operation. The tumor was resected and she is in a good health for 14-months after the operation.

Adenoma, Islet Cell↗
PubMed1984

Calcium behavior in endotoxin-poisoned mice: especially calcium accumulation in mitochondria.

A possible role of intracellular Ca2+ and participation of calmodulin in cellular metabolism in endotoxin-poisoned mice were investigated. The levels of calcium in liver cytosol and liver mitochondria fractions in poisoned mice were markedly higher 18-48 hr after endotoxin injection than in the control mice. On the other hand, the levels of serum calcium in the poisoned mice were about 20% lower at 18 hr than in the controls. The serum calcium levels in mice injected with 50 and 100 micrograms of endotoxin showed no dose-response effect, but a dose-response effect was observed at a dose of 200-400 micrograms. The serum Ca2+ levels in endotoxin-tolerant mice were similar to those in the control mice. The levels in mice injected with glucocorticoid-antagonizing factor mice were about 14% lower at 3 hr than in the controls. The mice fed a vitamin D3- and calcium-free diet showed a higher mortality rate in the early stage (12-18 hr) of endotoxication than that of the mice fed a normal diet. The lipid peroxide levels and Ca2+-ATPase activity in the liver mitochondria fraction in endotoxin-poisoned mice showed a higher level than those of the control mice. There was little or no difference in the levels of serum glucose between the mice injected with calmodulin antagonist (trifluoperazine, TFP) plus endotoxin and those given endotoxin alone. However, the liver glycogen levels in TFP plus endotoxin-treated mice were markedly higher than that in mice given endotoxin alone. Furthermore, calcium antagonist (verapamil) plus endotoxin-treated mice had about a 40% higher survival rate after 72 hr than those given endotoxin alone. The findings suggest that there is a possibility of participation of the Ca2+-calmodulin system in carbohydrate metabolic disorders during endotoxemia and that the changes in intracellular Ca2+ may result in various metabolic disorders.

Animals↗
PubMed1984

[Successful resection of giant hepatocellular carcinoma with hypoglycemic attack].

We experienced a 68 years-old male who had frequent hypoglycemic attacks. The diagnosis of a giant hepatoma associated with hypoglycemia was established by oral glucose tolerance test (O-GTT), angiography and computed tomography. The cavography demonstrated the invasion or depression of the tumor. It was ascertained by an operative exploration that the tumor occupied most of the right trisegments of the liver and infiltrated into a part of the left lateral segment. The right hepatic trisegmentectomy along 1.5cm left side line apart from the falciform ligament was performed. Resected tumor showed 11 X 13 X 10cm in size and 1200g in weight. Microscopic findings demonstrated hepatocellular carcinoma as Edmondson's Type II. After the operation, this patient became free from the hypoglycemic attack. A fasting blood sugar became within normal limits and O-GTT demonstrated a normal blood sugar level and insulin response. No concentration of immuno-reactive insulin was found in the resected tumor, however, the blood sugar in rats which received the intravenous injection of the tumor extracts was remarkably decreased in 20 minutes. From these observation, hypoglycemia in this patient seemed to depend mainly on the factor of insulin-like activity of the tumor. In the literature, the hepatocellular carcinoma associated with paraneoplastic phenomenon, e.g. hypoglycemia, has rarely been resected because of accompanied liver cirrhosis or giant size of the tumor. This is the second patient in our country in whom the tumor was fortunately resected and the paraneoplastic syndrome disappeared postoperatively.

Aged↗
PubMed1984

[Effects of beryllium chloride on cultured cells].

The effects of beryllium on cultured cells were investigated. Three cell-lines (HeLa-S3, Vero, HEL-R66) were used in these experiments and they were cultured in Eagle's MEM plus 5 or 10% FBS (Fetal Bovine Serum) containing beryllium in various concentrations. HeLa cells or Vero cells were able to grow in the medium with 10 micrograms Be/ml (1.1 mM). On the other hand, the growth of HEL cells were strongly inhibited, even when cultured in the medium with 1 microgram Be/ml (1.1 X 10(-1) mM) and the number of living cells showed markedly low level as compared to that of the control samples cultured in the medium without beryllium. The cytotoxic effects of beryllium on these cells, which were cultured for three days in the medium with beryllium, were observed. None of cytotoxic effects were found on HeLa cells cultured with 0.5 micrograms/ml (5.5 X 10(-2) mM) and on Vero cells cultured with 0.05 micrograms Be/ml (5.5 X 10(-3) mM), while HEL cells received cytotoxic effects even when cultured in the medium containing 0.05 micrograms Be/ml (5.5 X 10(-3) mM), and these effects on the cells appeared strong when cultured in the medium without FBS. It was revealed from these experiments that HEL cells are very sensitive in terms of toxic effects of beryllium. Therefore, there cells can be used for the toxicological study on low level concentrations of the metal.

Animals↗
PubMed1983

[Studies on the cell-mediated immunity caused by beryllium compounds].

In order to examine the sensitizing ability of beryllium (Be), a footpad reaction test and a macrophage migration inhibition test were carried out using mice treated with beryllium compounds. The findings of the experiments are summarized as follows: 1) The footpad reaction test of the mice injected with BeCl2 once a week subcutaneously at their dorsal area showed the positive results after four injections. The macrophage migration inhibition test was also performed by an agarose plate method using peritoneal cells and spleen cells obtained from these mice. The ratio of the number of positive mice showed more than 50% after five injections when peritoneal cells were used and after six injections when spleen cells were used. 2) The footpad reaction test of mice injected with one of various Be-compounds six times once a week showed a cross positive reaction against these compounds, and the macrophage migration of these mice was inhibited by these Be-compounds, but not by other metals. 3) When mice were once injected with 7BeCl2, about a half dose of the injected metal was discharged from the body within 7 days after the injection, and about a half dose of the residual metal was still found in the injected site. Further investigations may be required to solve the point that the persistent remaining of this metal in situ may raise the Be sensitizing ability.

Animals↗
PubMed1983

[Surgery of the portal vein in the resection of carcinoma of the biliary tract and pancreas].

Resection and reconstruction of the portal vein were performed in 5 cases of total pancreatectomy for pancreatic carcinoma, and in 7 cases of right hepatic trisegmentectomy for carcinoma of the gall bladder, or for intra- or extrahepatic bile ducts. Techniques of the surgery were described, especially on the necessity of "insert anastomosis" and on the indication of vessel implantation. No postoperative mortality and morbidity due to the reconstruction of portal vein was observed. Early thrombotic obstruction was observed only in one case which was the first case of this procedure. Late stenosis of the reconstructed vein due to the invasion of carcinoma was angiographically observed in 3 cases. Conclusively, this procedure can safely be performed in the resection of carcinoma of those organs. Improvements in resectability and late prognosis of the carcinoma may be expected. However, acquirement of the basic technique of vascular surgery is necessary, especially in the reconstruction of the portal vein at the hepatic pedicle.

Adult↗
PubMed1982

Study on cellular events in postthymectomy autoimmune oophoritis in mice. I. Requirement of Lyt-1 effector cells for oocytes damage after adoptive transfer.

Neonatal thymectomy during the critical period, 2-4 d after birth, can induce various organ-specific autoimmune diseases including oophoritis in A/J mice. The oophoritis thus induced was passively transferred into neonatal mice by injection of spleen cells obtained from syngeneic donors with the disease. Recipient ovaries were rapidly damaged with remarkable mononuclear cell infiltration and destruction of follicular structures. The phenotype of effector cells responsible for successful adoptive transfer was found to be Thy-1+, Lyt-1+,23-, Ia-, Qa-1-, and was sensitive to antithymocyte serum treatment but resistant to cyclophosphamide treatment or in vitro X-ray irradiation. The compatibility between donor and recipient at the major histocompatibility complex was not required for the effector phase of transfer. The oophoritis induced in BALB/c (nu/+ or +/+) was also shown to be transferred into athymic BALB/c nude mice with resulting ovarian lesion and circulating autoantibodies against oocytes. In this transfer system, the effector cells were also demonstrated to be T cells with the Lyt-1+,23- phenotype. Adoptive transfer experiments in both systems revealed that the destruction of ovaries in postthymectomy autoimmune oophoritis was mediated by Lyt-1 T cells. Whether these T cells can be distinguished from other Lyt-1 cells, such as T helper cells and effector T cells in delayed-type hypersensitivity (DTH), is not clear at present, but the results suggest that the effector mechanisms may be closely related to a DTH reaction.

Animals↗
PubMed1982

Study on cellular events in post-thymectomy autoimmune oophoritis in mice. II. Requirement of Lyt-1 cells in normal female mice for the prevention of oophoritis.

Autoimmune oophoritis that develops in A/J mice after neonatally thymectomy (NTx) was prevented by a single intraperitoneal injection of spleen cells or thymocytes from normal adult female mice. Prevention of oophoritis was achieved when spleen cells were given within 2 wk after Tx. When spleen cells were obtained from neonatally oophorectomized mice, four times more cells were required for the prevention of oophoritis, but those from the mice oophorectomized on day 7 after birth had equivalent capacity to prevent oophoritis to those from normal female mice. The spleen cells from normal A/J mice that prevented the development of oophoritis in NTx A/J mice were Thy-1+, Lyt-1+,23-, Ia-, Qa-1-, sensitive to in vitro irradiation with 400 rad, resistant to administration of cyclophosphamide or anti-thymocyte serum, and were not eliminated by adult thymectomy. Thymocytes with oophoritis-preventing capacity were also found to be Lyt-1+,23- and TL-1,2,3-. These results seem to correlate well with the finding that the Lyt-1 subpopulation is substantially decreased in NTx mice. The results suggest that, in this post-thymectomy autoimmune oophoritis, NTx abrogates the Lyt-1 T cell subpopulation that serves as suppressive or regulatory cells over developing self-reactive cells directed toward ovarian antigens, and eventually may cause autoimmune oophoritis.

Aging↗
PubMed1982

Kinetic study on chemical modification of Taka-amylase A. II. Ethoxycarbonylation of histidine residues.

The modification of Taka-amylase A (TAA) [EC 3.2.1.1] of Aspergillus oryzae by diethylpyrocarbonate (DEP) was carried out at 25 degrees C and at pH 5.8 (0.1 M acetate buffer). Two out of the six histidine residues were modified with 4.6 mM DEP, and two or three histidine residues were modified with 23 mM DEP. In both cases, one of them was protected from modification by the presence of 15% maltose. The results suggest that two or three out of the six histidine residues are exposed on the surface of the TAA molecule, and one of them exists near the maltose binding site. Ethoxycarbonylation of histidine residues of TAA caused loss of the amylase activity and activation of the hydrolysis of phenyl alpha-maltoside (phi alpha M). The kinetic parameters of the modified TAA for several substrates and analogs were determined at 25 degrees C and at pH 5.3 (0.08 M acetate buffer). From the results, it was found that this alteration of the enzyme activity by the modification was not due to a change in Km value but to a change in k0 value. Thus, some of the histidine residues in TAA are suggested to play an important role in the enzyme catalytic function.

Amylases↗
PubMed1982

Effect of lead acetate on superoxide anion generation and its scavengers in mice given endotoxin.

The administration of endotoxin to mice rendered hypersensitive by lead acetate resulted in profound lipid peroxide formation in the liver 6 hr postintoxication. Endotoxin plus lead acetate administration depressed glutathione peroxidase and superoxide dismutase activities in mouse liver, whereas superoxide anion generation significantly increased in the livers of endotoxin plus lead acetate-treated mice compared with that in mice treated with endotoxin alone. Serum acid phosphatase and lactate dehydrogenase isozyme exhibited much more leakage in endotoxin plus lead acetate-injected mice than in sera of mice given endotoxin alone. Nonprotein SH level in the liver was reduced markedly in endotoxin-lead treated mice compared with those receiving endotoxin alone. The plasma vitamin E level was found to decline by 6 hr postintoxication in both endotoxin-lead and endotoxin alone-treated mice, and the transient elevation of the plasma level at 18 hr may be considered to indicate mobilization from other tissues into the blood.

Acid Phosphatase↗
PubMed1982

Metabolic disorders of serum lipoproteins in endotoxin-poisoned mice: the role of high density lipoprotein (HDL) and triglyceride-rich lipoproteins.

A study was performed to clarify the role of serum lipoproteins, especially high density lipoprotein (HDL) and triglyceride-rich lipoproteins in endotoxemic or endotoxin-poisoned animals. The level of HDL-cholesterol decreased markedly in mouse serum 18-24 hr postintoxication, while the amount of low density lipoprotein (LDL)-cholesterol in the sera of poisoned mice was about 175% of that of the controls. Serum lecithin-cholesterol acyltransferase activity in the poisoned mice decreased slightly for 3-6 hr after endotoxin injection, but became markedly increased at 18-24 hr as compared with that in the controls. The amount of serum very low density lipoprotein (VLDL) showed a marked increase in the poisoned mice 8-24 hr postintoxication. The HDL fraction in the electrophoretic patterns of serum was reduced according to the dose of endotoxin 18 hr postintoxication. The HDL fraction in mice injected with lead acetate plus endotoxin was markedly lower than that in the poisoned mice. When streptozotocin-diabetic mice were injected with endotoxin, the HDL fraction was higher than that in the endotoxin-poisoned mice. In endotoxin-poisoned mice a correlation was observed between the lipid peroxide and LDL levels in the serum. In disk electrophoretic patterns, the HDL fraction in mice given vitamin E-supplemented diet showed a higher level than that in mice given a normal diet. Lipoprotein lipase (LPL) activity in poisoned mice significantly decreased to 59% of the control value 18 hr postintoxication, but hepatic triglyceride lipase activity was only slightly increased in endotoxin-poisoned mice. In analysis of HDL apoprotein peptide in serum lipoprotein, the apo C-II peptide level was clearly lower in mouse serum 18 hr postintoxication than that in the controls. These results suggest that the decrease in LPL activity in endotoxin-poisoned mice may be closely related to a decrease in the apo C-II peptide level, and also that it plays an important part in HDL and triglyceride-rich lipoprotein metabolism in the poisoned mice.

Animals↗