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Biomedical subjects

I Kosugi

Publications and source records attributed to I Kosugi.

At least 37 records · Page 2Linked to original sources
PubMed1996

Second cancer during long-term survival after resection of biliary tract carcinoma.

Curative surgery for biliary tract malignancy has improved the prognosis of patients; however, during long-term follow up after extensive surgery, four of our patients (two with gallbladder carcinoma and two with bile duct carcinoma) developed a second primary cancer (one each in the duodenum, skin, descending colon, and lung). Regular examination of the upper gastrointestinal tract, colorectum, and lungs, and testing for tumor markers (carcinoembryonic antigen and CA19-9) were performed as follow-up studies. As a result, the second cancers were all found at a relatively early stage and all four patients are still alive 6-14 years after the initial operation. A review of the annual autopsy reports over the last 5 years in Japan showed that the incidence of second cancer was 14.8% in patients with gallbladder carcinoma and 13.5% in those with bile duct carcinoma. Furthermore, the rate of second gastric and colorectal carcinoma was significantly higher in patients with primary bile duct cancer than in those with primary gallbladder cancer. In conclusion, the incidence of a second cancer after resection of biliary tract malignancy is more than 10%, but this second cancer can be detected relatively easily and treated at an early stage during the course of regular long-term follow up for the first cancer.

Adult↗
PubMed1996

Role of Kupffer cells and the spleen in modulation of endotoxin-induced liver injury after partial hepatectomy.

The hypothesis that both activated Kupffer cells and the spleen may be responsible for endotoxin-induced liver injury following partial hepatectomy was investigated. Male rats were divided into a sham group receiving laparotomy alone and three groups receiving a two-thirds hepatectomy; one group was given normal saline (NS) solution as a vehicle control, one group received intravenous gadolinium chloride (GC group) (7 mg/kg body weight) for 2 days before intravenous injection of endotoxin to inhibit Kupffer cell phagocytosis, and the third group simultaneously underwent splenectomy and partial hepatectomy (SH group). As endotoxin, lipopolysaccharide (LPS) (1 mg/kg body weight) was administered intravenously 2 days after surgery. In the GC and SH groups, phagocytic activity was reduced to approximately 40% of that in the sham group. The highest plasma tumor necrosis factor alpha (TNF-alpha) level (8,544 +/- 1,223 pg/mL) was observed in the NS group at 1 hour after LPS administration, and the level was significantly reduced by GdCl3 or splenectomy (P < 0.05). Inhibition of Kupffer cell function and splenectomy attenuated functional and structural liver damage associated with the decreased hepatic infiltration of polymorphonuclear leukocytes (PMNs) and reduced priming of circulating PMNs in the early stage of endotoxemia following partial hepatectomy. Consequently, the 24-hour survival rate of the SH and GC groups was significantly improved to 50% and 80%, respectively (P < .05), while that of the NS group was 12.5%. These findings indicate that the modification of inflammatory mediator generation by splenectomy or inhibition of Kupffer cell function may be beneficial for the prevention of endotoxin-induced liver injury after partial hepatectomy.

Animals↗
PubMed1996

Assessment of early radiation effects on the liver. Comparison of SPECT and MR.

PURPOSE: To evaluate the early effects of radiation on the liver using single photon emission CT (SPECT) with 99mTc-phytate combined with a pinhole collimator and MR imaging with superparamagnetic iron oxide (SPIO) and to compare 2 modalities regarding the assessment of the reticuloendothelial cell function. MATERIAL AND METHODS: The right sides of the livers of 12 anesthetized rats were irradiated with X-rays (4000 cGy). On the 3rd and 4th days postirradiation, SPECT and MR imaging pre- and postcontrast were performed. RESULTS: On SPECT, the irradiated areas appeared as areas with reduced 99mTc-phytate uptake in 9 rats. In the remaining 3 rats, irradiated lesions were not evident on SPECT. On the early postcontrast MR images, differential negative enhancement of the irradiated and nonirradiated areas in the same 9 rats as on SPECT was apparent. However, on the later postcontrast images of 3 of these rats, the irradiated areas, which were brighter than the nonirradiated areas, were visually less clear than those on the earlier postcontrast images. In the remaining 3 rats, no radiation damage was evident on MR images. CONCLUSION: SPECT with 99mTc-phytate and early postcontrast MR imaging with SPIO can show early radiation damage of the liver. The serial assessment of the postcontrast MR images provides functional information on the Kupffer cells.

Animals↗
PubMed1995

Fc receptors in liver sinusoidal endothelial cells in NZB/W F1 lupus mice: a histological analysis using soluble immunoglobulin G-immune complexes and a monoclonal antibody (2.4G2).

In systemic lupus erythematosus accompanied by the abnormal appearance of circulating immune complexes (ICs), Fc gamma receptor (FcR)-mediated IC handling in macrophages including Kupffer cells has been shown previously. However, sinusoidal endothelial cells (SECs) largely ingest soluble immunoglobulin (Ig) G-ICs through FcRs. In this study, the character, antigenic expression, and activity (i.e., ligand-binding capacity of SEC FcRs in NZB/NZW F1 lupus and NZW nonautoimmune mice) were immunohistochemically analyzed using monoclonal antibody (MAb) 2.4G2 to FcRs and peroxidase-antiperoxidase IgG as a ligand on cryosections. MAb 2.4G2 stained SECs and blocked the ligand binding of SEC FcRs in both mice strains. The staining intensities with MAb 2.4G2 in SECs and the FcR activities in SECs alone and all sinusoidal cells in both mice strains reached their maximum values at the age of 5 months. Staining intensities in NZB/W F1 were significantly higher at 1 and 2 months and lower at 9 months than those in NZW. The number of Kupffer cells detected by MAb F4/80 to macrophages in both mice strains gradually increased until 5 months, but their number in NZB/W F1 at 9 months was twice as large as that in NZW. In conclusion, SEC FcRs in mice are low-affinity FcRs that react with MAb 2.4G2. The data of FcR activity suggest no impairment of the FcR-mediated IgG-IC binding on SECs in NZB/W F1 in early life.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Prolonged infection of mouse brain neurons with murine cytomegalovirus after pre- and perinatal infection.

The susceptibility of mice at different developmental stages to a relatively low titer of cell culture-passaged murine cytomegalovirus (MCMV) infection was compared in terms of the urinary excretion of MCMV examined by plaque assay and in terms of the distribution of viral infection, determined by immunohistochemistry, using antibodies specific to the early nuclear antigen of MCMV. Viral infection on day 8.5 of gestation (E8.5) into the conceptus and intraperitoneal infection on day 15.5 of gestation (E15.5), postnatal day 2 (P2), postnatal day 11 (P11), and 30 days after birth (P30), respectively, were performed. Embryonal and perinatal mice were more susceptible to MCMV in terms of urinary excretion of the virus and the presence of viral antigen-positive cells in the brain, lungs, and kidneys. In the embryonal and perinatal infection, the viral antigen-positive cells in the neurons of the cerebral cortex and hippocampus were retained late after birth, even though the positive cells in the lungs and kidneys had disappeared. In the mice infected on E8.5, small clusters of viral antigen-positive cells were detected only in the cortex and hippocampus late after birth, without the urinary excretion of virus. These results suggest that when mice are infected with MCMV at the embryonal and perinatal stages, elimination of the infected neurons is delayed compared with that of the other cells in the lungs and kidneys. These findings provide a model for the analysis of pathogenesis of the subclinical congenital CMV infection that manifested clinically late after birth in humans as brain disorders.

Animals↗
PubMed1993

Defect of Fc receptors and phenotypical changes in sinusoidal endothelial cells in human liver cirrhosis.

To analyze the pathological changes occurring in Fc receptors (FcRs) in sinusoidal endothelial cells (SECs) in chronic liver diseases, we first characterized immunohistochemically the SEC FcRs by using monoclonal antibodies (MAbs) to FcRs and then investigated the distribution of the SEC FcRs by using peroxidase-antiperoxidase IgG complexes as a ligand on frozen sections. MAb 2E1 to FcRII reacted with SECs in a similar manner to peroxidase-antiperoxidase IgG and blocked the peroxidase-antiperoxidase IgG binding to SECs, whereas MAbs 3G8 and Leu-11b to FcRIII did not. FcRs in normal liver were found along the sinusoidal walls, except for those in the outer periportal zones, but FcRs in chronic active hepatitis and cirrhosis were intermittently or focally absent. The lengths of the FcR-positive portion of sinusoids in unit areas were respectively about 54% and 76% of the normal values in active and inactive cirrhosis. Where FcRs were absent, the MAbs CD36, CD31, and EN4 revealed the presence of sinusoids and, in active cirrhosis, frequently the thickening of liver cell plates. The FcR-negative SECs in the outer periportal zones of normal livers were different from the SECs of other sites in the presence of PAL-E antigen and a rich amount of EN4 antigen, though these sinusoids possessed Kupffer cells and no perisinusoidal deposition of laminin. The FcR-negative SECs in liver diseases occasionally presented the character of ordinary blood vessels, viz., PAL-E antigen, CD34 antigen, and a deficiency of Kupffer cells, regardless of perisinusoidal laminin deposition. However, they preserved the character of normally FcR-possessing SECs, viz., CD36 antigen, and a small amount of EN4 and CD31 antigens. These findings indicate that the outer-periportal SECs in normal livers are phenotypically different from other SECs and that the SECs in diseased livers frequently undergo phenotypical changes, including loss of FcRs, regardless of perisinusoidal laminin deposition, i.e., capillarization of the sinusoids. These phenotypical changes in SECs may reduce the capacity of FcR-mediated IgG-IC metabolism in diseased livers.

Antibodies, Monoclonal↗
PubMed1992

A case of ileus caused by a spiruroid nematode.

A 34-year-old male living in Aichi Prefecture, Japan, complained of lower abdominal pain. Ileus was suspected based on his clinical history and symptoms, and a laparotomy was performed. Four sections of a nematode were found in a large eosinophilic granuloma in the intestinal wall, and were identified as the larva of a spiruroid nematode. This is the third reported case of a spiruroid nematode infection found in the ileum.

Adult↗
PubMed1992

Endocytosis of soluble IgG immune complex and its transport to lysosomes in hepatic sinusoidal endothelial cells.

Both Kupffer cells and sinusoidal endothelial cells are engaged in the hepatic uptake of soluble IgG immune complex (IgG-IC) through Fc-receptors on their surface. Hepatocytes have also been reported to take up IgG-IC. It remains unclear, however, whether the endothelial cell degrades IgG-IC and whether the hepatocyte participates in IgG-IC clearance. In this study, normal mice received a single intravenous injection of soluble immune complex preformed in antigen excess, i.e. bovine serum albumin (BSA) anti-BSA-mouse-IgG complex (BABIgG) or BSA anti-BSA-mouse-F(ab')2 complex (BABF(ab')2), or BSA alone. An immunoperoxidase study for BSA showed that from 1 to 120 min after injection only BABIgG was ingested by both endothelial cells and Kupffer cells but not by hepatocytes. The staining intensity of BABIgG was maximal at about 15 min and decreased subsequently. Endocytosis of BABIgG occurred through coated pits in the endothelial cells. Within a few minutes, endocytosed BABIgG was found in tubulovesicular structures and large vesicles. The occasional large vesicles were shown to be lysosomes by simultaneous demonstration of BABIgG with acid phosphatase. BABIgG was not found on either of the endothelial and hepatocellular surfaces facing the space of Disse or in hepatocytes. These results indicate that soluble IgG-IC is endocytosed by sinusoidal endothelial cells and degraded in the lysosomes and that the participation of hepatocytes in the clearance of IgG-IC is improbable.

Acid Phosphatase↗
PubMed1991

[Tissue levels of pirarubicin (THP) in dogs following intra-arterial infusion].

The blood and tissue levels of pirarubicin (THP) were studied in dogs by HPLC analysis. The THP (1.5 mg/kg) was infused from the bifurcation of internal iliac artery. We measured the concentration of THP after 1 or 2 hours of intra-arterial infusion (IA) and compared with the concentration of THP administered intravenously (IV). The plasma levels of THP following IA rapidly disappeared the same as for IV. The blood cell level of THP following both IA and IV was significantly higher than the plasma level. The bladder mucosa and muscle levels of THP following IA were about 8 times as high as that of IV. The bladder muscle level of THP 2 hours after IA was about twice as high as after 1 hour and the same as the bladder mucosa level of THP after both 1 and 2 hours. It is considered that THP by the present method may have the transition from the mucosa to the muscle in the bladder. In the other intrapelvic tissues (perivesical adipose tissue, pelvic lymph node and prostate), IA also had higher concentrations compared with IV. However, the extrapelvic tissues (heart, liver and kidney) levels of THP following IA were the same as those for IV. It was concluded that THP was a reasonable agent for IA chemotherapy for bladder cancer.

Animals↗
PubMed1990

Alterations in Fc receptor activity in sinusoidal endothelial cells and Kupffer cells during D-galactosamine (GalN)-induced liver injury in rats. A histological study.

Fc receptors in sinusoidal cells and immune complex uptake were studied histologically in D-galactosamine HCl (GalN)-induced liver injury in rats. Kupffer cells and monocytes were distinguished from sinusoidal endothelial cells and from each other by endogenous peroxidase staining. Fc receptors were found along the sinusoidal endothelium throughout the lobules in normal livers. In acute injury caused by 300 or 750 mg/kg of GalN, Fc receptors were preserved within necrotic foci until the foci were infiltrated by inflammatory cells. The endothelial Fc receptor activity altered, as demonstrated by their capacity to bind immune complexes, after GalN injection. The activity decreased from 24 h after injection in the periportal areas in both dose groups, and increased transiently with dose-dependence in the remaining areas. Kupffer cell numbers also showed a transient dose-dependent increase, except in the periphery of lobules where they generally decreased. In chronic injury with 400 mg/kg, Fc receptors were lost and Kupffer cells decreased in the periportal areas. Circulating immune complexes were ingested by Kupffer cells and endothelial cells in normal and injured livers, showing the the same distribution as that of Fc receptors except that the complexes decreased gradually towards the centrilobular zones.

Animals↗
PubMed1990

Defect of sinusoidal Fc receptors and immune complex uptake in CCl4-induced liver cirrhosis in rats.

The purpose of this paper is to provide a histopathologic basis for abnormalities in immune-complex clearance in liver disease. Fc receptors in CCl4-induced liver cirrhosis in rats were studied by applying peroxidase-antiperoxidase immunoglobulin G complex as a ligand to the frozen sections. Intravenous injection of bovine serum albumin-antibovine serum albumin complexes or colloidal carbon was combined with histological staining for endogenous peroxidase, fibronectin, laminin, or a lectin, Bandeiraea simplicifolia agglutinin I. In the cirrhotic process, sinusoidal Fc receptors showed a weakened reactivity to the ligand with focal absence, and the length of the Fc receptor-positive portion of the sinusoids in unit area decreased to about 50% of the normal value in the advanced cirrhosis. Fibronectin and the lectin showed the presence of sinusoids where Fc receptors were absent. The endothelium in Fc receptor-negative areas did not take up either immune complexes or carbon, and Kupffer cells were absent in these areas. A disturbed immune-complex metabolism was thus suggested to occur in association with the defect of sinusoidal Fc receptors in liver cirrhosis. These abnormalities appeared to not be directly related to perisinusoidal laminin deposition, i.e., capillarization of the sinusoid.

Animals↗
PubMed1990

[An aggressive angiomyxoma of the vulva].

A case of an aggressive angiomyxoma of the vulva in a 38-year-old lady is reported. The tumor was gelatinous and 12 x 8 x 7 cm in size. Histologically, spindle or stellate-shaped tumor cells and blood vessels were found distributed in a myxoid stroma. It was found that the tumor cells were immunoreactive to vimentin but negative to desmin and smooth muscle specific actin. Ultrastructurally the tumor cells had an intercellular junction, an abundant, rough endemic reticulum, and intracytoplasmic filaments, but no focal densities of the filaments and the basal lamina. These findings have revealed that this tumor consisted of myofibroblastic cells resembling fibroblasts rather than myofibroblasts.

Adult↗
PubMed1986

Impaired effect of dopamine on cardiac output during octopamine infusion.

The hemodynamic effects of octopamine (OCT) were studied before and during dopamine (DA) infusion in six normal dogs. Before OCT infusion, DA significantly increased cardiac index (CI) from 3.24 +/- 0.20 to 4.90 +/- 0.30 L/min X m2 and significantly decreased systemic vascular resistance index (SVRI) from 3700.2 +/- 212.5 to 2618.3 +/- 156.6 dyne X sec/cm5 X m2, without changing heart rate. During OCT infusion, DA failed to increase CI or decrease SVRI; however, it significantly increased heart rate from 153.3 +/- 12.9 to 183.0 +/- 17.0 beat/min. This suppression of a DA-related increase in cardiac output may explain why DA is ineffective in those septic patients with elevated plasma OCT levels.

Analysis of Variance↗
PubMed1985

Effect of reduced glutathione on hemodynamic responses and plasma catecholamine levels during metabolic acidosis.

The effects of reduced glutathione (GSH) on plasma catecholamine (CA) levels and hemodynamics were studied in seven severely acidotic dogs, before and after dopamine (DA) infusion. Seven other dogs, also acidotic, received lactated Ringer's solution instead of GSH. Although metabolic acidosis decreased cardiac index (CI) in both groups, the decrease was significantly less in the GSH group. The significantly increased systemic vascular resistance index (SVRI) in the control group was suppressed by GSH infusion, although similarly high plasma CA levels were maintained in both groups. This suggests that GSH has certain vasodilating effects not related to adrenosympathetic activity. CI did not improve and DA infusion significantly increased SVRI in the control group, whereas CI increased with a mild decrease of SVRI in the GSH group. The rise of plasma norepinephrine after DA infusion was low in the GSH group compared to the increase in the control group. This study suggests that during acidosis GSH improves hemodynamics and restores the effects of DA on cardiac output.

Acidosis↗
PubMed1985

Effects of dopamine and dobutamine on hemodynamics and plasma catecholamine levels during severe lactic acid acidosis.

This study was designed to evaluate the effects of dopamine and dobutamine on hemodynamics and plasma catecholamine levels during experimental lactic acid acidosis in dogs. During the normal acid-base state (pH 7.4, PCO2 40 mm Hg), cardiac output and stroke volume were significantly increased and systemic vascular resistance was decreased by the infusion of dopamine or dobutamine 20 mcg/kg/min. Dobutamine produced identical changes in cardiac output, stroke volume, and systemic vascular resistance even during severe lactic acid acidosis (pH 7.0, PCO2 40 mm Hg). Dopamine, however, failed to increase cardiac output and stroke volume and to decrease systemic vascular resistance during lactic acidosis. The plasma norepinephrine level was elevated from 0.49 to 3.01 ng/ml during normal acid-based state and from 1.76 to 9.53 ng/ml during severe lactic acid acidosis by the infusion of dopamine. Dobutamine infusion did not affect the plasma norepinephrine level during normal acid-base state but reduced the level during lactic acid acidosis. The marked increase in plasma norepinephrine following dopamine infusion may explain both the decrease in cardiac output and the increase in systemic vascular resistance in response to dopamine infusion during severe lactic acid acidosis. These results indicate that dobutamine may be more useful than dopamine in improving cardiac output during severe acidosis.

Acid-Base Equilibrium↗