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Biomedical subjects

K Nakata

Publications and source records attributed to K Nakata.

At least 379 records · Page 21Linked to original sources
PubMed1991

Evaluation of nontumorous tissue damage by transcatheter arterial embolization for hepatocellular carcinoma.

The serial changes in serum hepatic enzyme activities by transcatheter arterial embolization (TAE) were analyzed in 17 patients with hepatocellular carcinoma to estimate the contribution to the value by the damage of tumor or nontumorous hepatic cells. The serum levels of relatively tumor-specific fructose 1,6-diphosphate (FDP) aldolase were elevated after TAE in the cases of both superselective and nonsuperselective TAE that were performed from the segmental and the nonsegmental hepatic artery, respectively, but we found the marked elevation of FDP aldolase in the cases of the superselective TAE. In contrast, the non-tumor-specific fructose 1-phosphate (F1P) aldolase was markedly elevated only in the cases of nonsuperselective TAE. The total amount of FDP aldolase released by TAE correlated significantly with the integrated tumor tissue volume (P less than 0.005), whereas the total amount of F1P aldolase output correlated significantly with the integrated nontumorous tissue volume (P less than 0.005) as defined by lipiodol accumulation on computerized tomography scan. The consequent changes in the total nontumorous liver volumes after TAE were also analyzed by the follow-up computerized tomography scan. The nonsuperselective TAE caused the significant total nontumorous liver atrophy when compared with the superselective TAE. The progression of the total nontumorous liver atrophy correlated significantly with F1P aldolase output by TAE (P less than 0.001) but not with FDP aldolase output. These results suggest that the outputs of FDP and F1P aldolase are useful to estimate the degree of the tumorous and nontumorous tissue damage by TAE, respectively, and F1P aldolase output can be used to predict the progression of liver atrophy caused by TAE.

Adult↗
PubMed1991

Granulocyte-macrophage colony-stimulating factor promotes the proliferation of human alveolar macrophages in vitro.

The effects of granulocyte-macrophage (GM-CSF) or macrophage-CSF on in vitro proliferation of human alveolar macrophages (AM) were evaluated. AM of healthy volunteers incubated with recombinant human GM-CSF revealed incorporation of [3H]thymidine in vitro. The maximum incorporation was observed at 20 U/ml of GM-CSF on day 3. The proportion of proliferating cells incubated with 20 U/ml of GM-CSF from day 3 to day 4 was 8 to 11% of the total, whereas 3 to 5% of cells proliferated without GM-CSF. The number of cell nuclei increased 1.30- to 1.68-fold in the initial 7 days during incubation with 20 U/ml of GM-CSF, whereas there was a 1.07- to 1.13-fold increase without GM-CSF. Conditioned media obtained by the incubation with human lung tissue exhibited similar effects as recombinant human GM-CSF on macrophages. The effects were completely abrogated by antibody against human GM-CSF. Immunohistochemically, GM-CSF was detected in lung cells including AM, alveolar epithelium, alveolar interstitial cells, and endothelial cells. In contrast, recombinant macrophage-CSF did not induce the proliferation of human AM, although it has been known to promote the proliferation of murine AM. These observations suggest that GM-CSF plays an important role among the regulatory factors that locally support the population of AM in human lungs.

Adult↗
PubMed1991

Tetrasomy 8 in acute myelomonocytic leukemia developing after a gastric cancer operation.

A 70 year-old-Japanese man underwent gastrectomy for early gastric cancer with preoperative hypocellular marrow. Three weeks later, acute myelomonocytic leukemia developed with tetrasomy for chromosome 8 (48,XY,+8,+8). The patient died of leukemia on the 33rd postoperative day. Whether or not the operation triggered the leukemia remains unknown.

Adenocarcinoma↗
PubMed1991

Fluorimetric and high-performance liquid chromatographic determination of D-lactate in biological samples.

D-Lactate in biological samples was converted into a strongly fluorescent substance in a one-vial reaction. It was first converted into the pyruvate hydrazone in the presence of D-lactate dehydrogenase, an NADH-reoxidation system using diaphorase, D,L-6,8-thioctamide and hydrazine. This hydrazone was then converted into 2-hydroxy-6,7-dimethoxy-3-methylquinoxaline by 1,2-diamino-4,5-dimethoxybenzene in 1 M hydrochloric acid, and the quinoxaline was extracted and measured fluorimetrically at 432 nm (excitation at 365 nm). The calibration curve for D-lactate was linear up to at least 100 nmol/ml of the assay mixture, with a determination limit of 2 nmol/ml. The quinoxaline was also analysed by high-performance liquid chromatography with fluorimetric detection. The calibration curve for D-lactate was linear from 500 fmol to 75 nmol in the reaction mixture. This method was 4000 times more sensitive than the fluorimetric method, and could determine D-lactate in blood plasma volumes of less than 1 microliter.

Animals↗
PubMed1991

Transforming growth factor beta 1 differentially regulates alpha-fetoprotein and albumin in HuH-7 human hepatoma cells.

Transforming growth factor beta 1 (TGF-beta 1) is known to inhibit hepatocyte growth in vitro and in vivo. In this study, we analyzed the effect of TGF-beta 1 on alpha-fetoprotein (AFP) and albumin gene expression in HuH-7 human hepatoma cells. TGF-beta 1 inhibited cell growth in a dose dependent manner. The cellular secretion rate of AFP but not albumin was suppressed significantly by TGF-beta 1. TGF-beta 1 caused a significant reduction in the level of AFP mRNA. In contrast, the levels of albumin mRNA or beta-actin mRNA were not changed by TGF-beta 1. In transient transfection experiments, TGF-beta 1 resulted in selective repression of AFP promoter activity. These results suggest that TGF-beta 1 is one of the key factors involved in the differential regulation of the AFP gene and the albumin gene.

Carcinoma, Hepatocellular↗
PubMed1991

Combination effect of recombinant human interleukin 1 alpha with antitumor drugs on syngeneic tumors in mice.

To investigate the combination effects of recombinant human interleukin 1 alpha (rHu IL-1 alpha) and antitumor drugs, groups of 7 mice bearing syngeneic tumors (Meth A sarcoma in BALB/c mice and colon 26 adenocarcinoma in BALB/c x DBA/2 F1 mice) were treated i.v. with the antitumor drugs according to the early (once daily on days 1, 4, 7, 10, and 13) and/or late (once daily on days 7, 10, 13, 16, and 19) medication schedules in combination with rHu IL-1 alpha administered i.m. at various timings (1 day before, concurrently with, and 1 day after every drug administration). Inhibition rates of the antitumor drugs (mitomycin C, doxorubicin, cisplatin, cyclophosphamide, and 5-fluorouracil) for both the murine tumors were more or less raised by coadministration of rHu IL-1 alpha irrespective of medication schedules and combination timings. After both early and late treatments with the optimal combinations of rHu IL-1 alpha (0.1-3 micrograms/mouse) and cisplatin (2-4 mg/kg) and by the late treatment with the optimal combinations of rHu IL-1 alpha (0.3-3 micrograms/mouse) and carboplatin (32 mg/kg) or thiotepa (4 mg/kg), many mice were completely cured of colon 26 adenocarcinoma and survived for more than 90 days. Combined use of rHu IL-1 alpha and antitumor drugs seems to be beneficial in antitumor chemotherapy.

Adenocarcinoma↗
PubMed1991

Recovery from hepatic necrosis following acute portal vein embolism with special reference to reconstruction of occluded vessels.

We examined the morphological and haemodynamic changes in the livers of rats following acute obstruction of portal vein branches by the injection of agar into the portal vein. Histological and angiographic examinations of the liver were performed after measurements of portal vein pressure in vivo and portal vascular resistance by an isolated liver perfusion method. Portal vein embolism induced hepatic necrosis in the centrilobular and midzonal areas, which was rapidly resorbed and replaced by regenerated liver cells leaving no trace. This recovery from hepatic necrosis was closely related to recanalization of obstructed portal vein branches, which led to falls in both the elevated portal vein pressure and the increased portal vascular resistance following embolization.

Acute Disease↗
PubMed1991

Focal veno-occlusive lesions following metastasis of cancer in the liver with special reference to obstruction of lymphatics in hepatic veins.

Focal veno-occlusive lesions and congestion of the liver are found frequently at autopsy in patients with metastatic carcinoma in the liver. In 6 cases, intimal proliferation of loose connective tissue with dilatation of lymphatic capillaries was seen continuously from the terminal hepatic venule to the hepatic vein, and cancer cells were found only in lymphatic capillaries in the wall of the hepatic vein. In 7 cases, cancer cells infiltrated directly into the adventitia of the sublobular vein and intimal proliferation of loose connective tissue with or without formation of recent thrombi was observed. A main causative factor of hepatic veno-occlusive disease is thought to be leakage of plasma due to endothelial injury to the terminal hepatic venule and sublobular vein. Lymphatic obstruction, in addition to a direct reaction to invasion of cancer cells to the vessel wall, may also cause veno-occlusive lesions due to stasis and leakage of lymph fluid into the intima of the terminal hepatic venule, sublobular vein and hepatic vein.

Adult↗
PubMed1991

Variations in radioimmunoscintigraphic detection of tumor showed by five monoclonal antibodies to carcinoembryonic antigen.

Radioimmunoscintigraphy using mouse monoclonal antibodies to various parts of a carcinoembryonic antigen (CEA) molecule was performed. Four radiolabeled antibodies (F4-82, 28A, F3-30, F33-104) were injected into tumor transplanted nude mice to compare the accumulation of these antibodies in tumors. The four antibodies were accumulated selectively in CEA- producing tumors. The tumor visualization correlated with the tumor/blood radioactivity ratio, whereas the tumor/blood radioactivity ratio did not correlate with the in vitro percent binding to tumor cells or the in vivo percent injected dose in CEA-producing tumors. Among the four antibodies, F33-104 showed the highest tumor/blood radioactivity ratio and the best image quality in any CEA-producing tumor. These results suggest that the antibody which has a high tumor/blood ratio rather than high total tumor uptake may be useful for radioimmunoscintigraphy.

Animals↗
PubMed1991

The pathogenesis of hyaline globules in liver cells after partial hepatectomy in rats.

To clarify the pathogenesis of hyaline globules in liver cells after partial hepatectomy, the present study was undertaken in rats. When partial hepatectomy was performed by the surgical procedure of Higgins and Anderson, the inferior vena cava pressure was raised, and many hyaline globules, which are very similar to those caused by condensation of the contents of vacuoles in liver cells after temporary pressure elevation of the inferior vena cava, were induced in liver cells. On the other hand, when the median lobe and the left lateral lobe were removed carefully one at a time to avoid operative narrowing of the inferior vena cava, the inferior vena cava pressure was not elevated, and only very few hyaline globules were formed. This suggests that hyaline globules in liver cells following partial hepatectomy in rats may be caused by elevation of inferior vena cava pressure due to narrowing of the inferior vena cava by surgical procedure.

Animals↗
PubMed1991

Endotoxin hepatotoxicity augmented by ethanol.

To determine whether alcohol increases endotoxin hepatotoxicity, we administered ethanol (4.8 g/kg body wt in 4 ml of water) to rats through a gastric tube, then immediately injected endotoxin (2, 2.5, or 3 mg/kg body wt). In the rats pretreated with ethanol, the injection of 2 mg/kg body wt of endotoxin induced a slight rise of serum transaminase. However, when 2.5 mg/kg body wt of endotoxin was given, there were no significant histopathological or biochemical differences between the rats pretreated with ethanol and those pretreated with water. Moreover, there was no significant difference in mortality rates between the rats pretreated with ethanol and the controls when 3 mg/kg body wt (LD50) of endotoxin was injected. These results suggest that acute administration of alcohol enhances endotoxin hepatotoxicity when the dose of endotoxin is small, but that the effect of alcohol is masked when larger doses of endotoxin are given.

Animals↗
PubMed1991

Validation of a toxicity testing model by evaluating oxygen supply and energy state in the isolated perfused rat kidney. Single-pass preparation without albumin.

Validation of a toxicity testing model concerning energy metabolism was attempted by evaluating the oxygen supply and energy state in an isolated perfused rat kidney of single-pass preparation without albumin. Perfusion was performed at a temperature of 31 degrees C, flow rate of 11.0 mL/g/min, and pressure of 81-104 mmHg. The perfusate was saturated with 95% O2/5% CO2. After preperfusion for 30 min, the redox states of cytochrome aa3 and c and pyridine nucleotides (PN) in the perfused kidney were measured to be stable for 90 min by a scanning reflectance spectrophotometry and surface fluorometry, respectively. During the same period, the contents of ATP and inorganic phosphate (Pi) in the perfused kidney were also measured to be stable by 31P-NMR spectroscopy. The oxygen supply to the cell was more than the amount required for the basal metabolism of the cell. For assessment of the effects of chemical agents on the renal cell metabolism, this preparation of the perfused rat kidney was considered to have several advantages, despite some of its inherent limitations in the function of the kidney.

Adenosine Triphosphate↗
PubMed1991

The protective effects of SA3443, a novel cyclic disulfide, on chronic liver injuries in rats.

The effects of (4R)-hexahydro-7,7-dimethyl-6-oxo-1,2,5-dithiazocine-4- carboxylic acid (SA3443), a novel cyclic disulfide compound, on the development of chronic liver injury were studied in rats, using two types of models, carbon tetrachloride (CCl4)-induced chronic liver injury and heterologous serum (swine serum)-induced liver fibrosis. SA3443 (30-100 mg/kg, p.o.) significantly suppressed increases in serum transaminase and alkaline phosphatase activity induced by CCl4-treatment for 10 weeks. This compound also inhibited increases in hepatic lipids and hydroxyproline content in CCl4-treated rats. In the histopathological studies, treatment with SA3443 resulted in a decrease in the degree of hepatic necrosis, fibrosis and steatosis. On the other hand, 8-weeks treatment with swine serum revealed hepatic fibrosis without appearance of necrosis or fatty accumulation. In this model, SA3443 (30 mg/kg, p.o.) reduced the hepatic hydroxyproline level, and diminished the formation of connective tissue in the liver. These findings indicate that SA3443 protects the liver against chronic liver injuries induced by CCl4 and heterogeneous serum.

Animals↗
PubMed1991

Surface blood flow and histology of human anterior cruciate ligament allografts.

We measured surface blood flow in 53 anterior cruciate ligaments (ACLs) reconstructed with allogeneic tendon grafts using laser Doppler flowmetry and examined their histology through biopsy specimens procured during second-look arthroscopy to investigate the fate of ACL allografts on a long-term basis. The age of the grafts, i.e., time from the reconstruction to the second-look arthroscopy, ranged from 6 to 89 months. Six-month grafts showed significantly higher blood flow than the other older ones from 12 to 89 months, which showed a blood flow level equivalent to normal control ACLs. Histological studies revealed that ACL allografts remodeled with time, and that they reached stability by 18 months postimplantation. These results confirmed the concepts of age-dependent remodeling of allografts and their longevity in the human knee joint.

Adult↗
PubMed1991

Lack of correlation between the amount of eugenol released from zinc oxide-eugenol sealer and cytotoxicity of the sealer.

The purpose of this study was to examine a possible correlation between the eugenol released from a zinc oxide-eugenol sealer (Canals) and the degree of cytotoxicity. The cytotoxicity and eugenol release from root canal filling material containing eugenol was examined for test solutions at several experimental periods. No positive correlation was found between eugenol release and cytotoxicity of the root canal filling material.

Animals↗
PubMed1991

Relation of the reticuloendothelial function to endotoxin hepatotoxicity.

The present study was undertaken in rats to clarify whether endotoxin hepatotoxicity can be modified by phagocytic activity of the reticuloendothelial system. Pretreatment with cortisone acetate, diethylstilbestrol, methyl palmitate, triolein or gadolinium chloride markedly improved the mortality rate from endotoxemia and prevented the development of focal random coagulative hepatocellular necrosis and the elevation of serum transaminase activities due to endotoxemia. Cortisone acetate, methyl palmitate and gadolinium chloride are the well-known depressors of reticuloendothelial phagocytic activity: Diethylstilbestrol and triolein are the stimulators. This suggests that phagocytic activity of the reticuloendothelial system does not relate to not only the mortality rate but also the degree of hepatic injury following endotoxemia.

Animals↗
PubMed1991

The role of pericentral fibrosis in experimental portal hypertension in rats.

To clarify the relation of pericentral fibrosis to portal hypertension, measurements of portal vascular resistance in vitro and blood pressures of several key points in hepatic vascular pathways in vivo were undertaken in rats given dimethylnitrosamine. Administration of dimethylnitrosamine induced tortuosity and narrowing of the peripheral branches of the hepatic vein due to pericentral fibrosis. No significant change was produced in the sinusoids and the portal vein branches. The portal vascular resistance was increased and the portal vein pressure was elevated markedly. The blood pressure gradient was steep in the intrahepatic vein, but not in the intrahepatic portal vein or the sinusoids, as compared to control. These data suggest that deformation of the peripheral branches of the hepatic vein due to pericentral fibrosis causes a marked increase in vascular resistance in the intrahepatic hepatic vein, i.e. postsinusoidal portal hypertension.

Animals↗