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Biomedical subjects

H Osawa

Publications and source records attributed to H Osawa.

At least 109 records · Page 6Linked to original sources

[A case of aneurysm of the descending thoracic aorta associated with Behçet's disease].

A 66-year-old male with Behçet's disease admitted again with hemoptysis. He underwent the resection and direct closure of descending aortic aneurysm 3 years ago, followed without the use of steroid. Chest CT scanning demonstrated a recurrent aneurysm of the descending aorta which was could not be detected on the previous CT only 23 days before. In the current operation, we performed resection, direct closure and wrapping of the aneurysm. The pathological examination showed a true aneurysm of Behçet's disease. The patient is free from recurrence for 17 months since the operation under steroid therapy.

Aged↗

Selective determination of chloride and bromide ions in serum by cyclic voltammetry.

Voltammetric determination of chloride and bromide ions in serum was made using a one-body type Ag electrode, whose surface was covered with a dialysis membrane for preventing interference from proteins. This determination was based on measurement of the charge of the reduction wave of silver halide formed on the Ag electrode surface in a halide ion solution during a cathodic potential sweep. In this method, depending on the potential sweep range, the charge of the reduction wave of AgI, AgI + AgBr, or AgI + AgBr + AgCl can be measured. Here, the method was used to determine the chloride and bromide ions in artificial serum. Linear concentration ranges were 1.0 x 10(-2)-2.4 x 10(-1) M for chloride ions and 5.0 x 10(-3)-1.8 x 10(-2) M for bromide ions. The correlation coefficient was 0.999 in each case. The relative standard deviation for chloride ion (1.0 x 10(-1) M) was 1.9% (n = 10), and that for bromide ion (1.5 x 10(-2) M) was 2.5% (n = 10). Bromide ions at a relatively high concentration as the component of serum had no effect on the determination of the chloride ion in the serum. This method is thus useful for the selective determination of chloride and bromide ions in serum.

Blood Substitutes↗

Identification and characterization of basal and cyclic AMP response elements in the promoter of the rat hexokinase II gene.

Hexokinases catalyze the phosphorylation of glucose and initiate cellular glucose metabolism. Hexokinase II (HKII) is the principal hexokinase isoform in skeletal muscle, heart, and adipose tissue. Isoproterenol and exogenous cyclic AMP (cAMP) increase HKII gene transcription in L6 myotubes. Various segments of the HKII promoter that direct the expression of the chloramphenicol acetyltransferase reporter gene were transfected into L6 myotubes to identify basal and cAMP response elements. The 5'-flanking region that extends 90 base pairs upstream of the transcription start site includes a CCAAT box and a cAMP response element (CRE); both contribute to basal promoter activity and each provides an independent, maximal response to cAMP. An inverted CCAAT motif, or Y box, located just upstream of the CCAAT box, contributes to basal promoter activity but is not involved in the cAMP response. Homo- and heterodimers composed of the CRE-binding protein and activating transcription factor-1 bind specifically to the CRE. The Y box and the CCAAT box specifically bind the factor NF-Y (also known as CBF).

Animals↗

Analysis of the signaling pathway involved in the regulation of hexokinase II gene transcription by insulin.

The hexokinases, by converting glucose to glucose 6-phosphate, help maintain the glucose concentration gradient that results in the movement of glucose into cells through the facilitative glucose transporters. Hexokinase II (HKII) is the major hexokinase isoform in skeletal muscle, heart, and adipose tissue. Insulin induces HKII gene transcription in L6 myotubes, and this, in turn, increases HKII mRNA and the rates of HKII protein synthesis and glucose phosphorylation in these cells. Inhibitors of distinct insulin signaling pathways were used to dissect the molecular mechanism by which HKII gene expression is induced by insulin in L6 myotubes. Treatment with wortmannin, an inhibitor of phosphatidylinositol 3-kinase (PI 3-kinase), or with rapamycin, an inhibitor of the pathway from the insulin receptor to p70/p85 ribosomal S6 protein kinase (p70(s6k)), prevented the induction of HKII mRNA by insulin. In contrast, treatment with PD98059, an inhibitor of mitogen-activated protein kinase activation, had no effect on insulin-induced HKII mRNA. In addition, rapamycin blocked the insulin-induced expression of an HKII promoter-chloramphenicol acetyltransferase fusion gene transiently transfected into L6 myotubes, whereas PD98059 had no such effect. These results suggest that a phosphatidylinositol 3-kinase/p70(s6k)-dependent pathway is required for regulation of HKII gene transcription by insulin and that the Ras-mitogen-activated protein kinase-dependent pathway is probably not involved.

Adipose Tissue↗

Sonographic diagnosis of fatty liver using a histogram technique that compares liver and renal cortical echo amplitudes.

Accurate diagnosis of fatty liver using ultrasonography was attempted based on the difference between the echo intensities of the liver and kidney determined from ultrasonic histograms. Livers were then classified as having fatty infiltration, normal histology, or intermediate histology based on CT ratios established previously in earlier work comparing non-contrast-enhanced liver and spleen. The hepatorenal difference was significantly greater in the fatty liver group than in the normal liver group (8.9 +/- 2.0 dB vs 2.5 +/- 4.5 dB, p < 0.001). When a hepatorenal difference of > or = 7.0 dB was taken as the criterion, this method had a sensitivity of 91.3%, a specificity of 83.8%, and an accuracy of 86.7% for the diagnosis of fatty liver. Thus, quantitative ultrasonic diagnosis of fatty liver can be performed using echo intensity histograms.

Adult↗

Inverse relation of serum Helicobacter pylori antibody titres and extent of intestinal metaplasia.

AIMS: To clarify the relation between the serum titre of anti-Helicobacter pylori (H pylori) antibody and the extent of intestinal metaplasia of the gastric mucosa. METHODS: The serum anti-H pylori IgG titres of 95 asymptomatic individuals (mean age 65 years) undergoing an annual health examination were measured and compared with the extent of intestinal metaplasia (absent, moderate, or extensive), determined by examination of multiple endoscopic mucosal biopsy specimens. Serum pepsinogen I (PGI) levels, as a marker for gastric atrophy, were also measured. RESULTS: The prevalence of seropositivity for H pylori antibody was high (> 80%), regardless of the extent of metaplasia. However, there was a negative association between the extent of metaplasia and the anti-H pylori titre: 75% of the subjects in the group without metaplasia had high (3+) antibody levels, as did 43% with moderate, and 37% with extensive metaplasia (absent v extensive). The inverse relation between the titre and the extent of metaplasia was evident when examined in those with normal PGI (> 30 ng/ml), whereas no such relation was apparent in subjects with low PGI (< or = 30 ng/ml). CONCLUSIONS: The anti-H pylori titre correlates inversely with the extent of intestinal metaplasia, particularly in subjects with less marked gastric atrophy.

Aged↗

Case report: malignant haemobilia detected in the gallbladder--retrograde cholangiographic findings.

Haemobilia caused by gallbladder cancer is a rare condition and cholangiography rarely detects gallbladder haemorrhage because cancer cells or blood clots obstruct the cystic duct. We describe a patient with haemobilia caused by gallbladder cancer, in whom retrograde cholangiography showed a cast-like filling defect in the common bile duct and, in addition, several string-like defects in the gallbladder. The string-like defects appeared to be streams of clotted blood flowing towards the common bile duct in this case of relatively minor haemorrhage.

Adenocarcinoma↗

[Study on the morphological changes in the placenta of rats administered nitric oxide synthase inhibitor].

To clarify the roles of nitric oxide synthase (NOS) during pregnancy, histopathological changes in the placenta were observed after the administration of an NOS inhibitor [NG-nitro-L-arginine methyl ester (L-NAME)] to rats. L-NAME was infused subcutaneously from day 12 of gestation at stable concentrations of 3mg/day (group B) or 25mg/day (group C) until day 18 when the placentae were removed. The mean systolic blood pressures in groups B and C were higher than in the controls (group A). By both light and electron microscopy, morphological changes were observed and compared to those of human placenta in preeclampsia. In groups B and C, light microscopy showed that giant cells were vacuolated, degenerated and decreased in number. In the labyrinth, the stroma was extremely edematous, and the intervillous space and fetal vessels were narrowed. Electron microscopy showed that micro-fibrin clots were deposited on the maternal surface of trophoblasts. The endothelial cells of fetal vessels were irregular in shape. In group B the endothelial cells and intermediate filaments were increased. These findings suggest that decreased NO production may cause changes similar to those found in preeclampsia. Treatment with NOS inhibitor may be used in an animal model for preeclampsia.

Animals↗

Tissue factor pathway inhibitor production by human mesangial cells in culture.

Fibrin formation within the glomeruli has been observed in various forms of human and experimental glomerulonephritis and it may play an important role in progressive glomerular injury. Furthermore it has been hypothesized that glomerular fibrin deposition may occur through activation of either the intrinsic or extrinsic coagulation pathway. It has been demonstrated that a procoagulant activity (PCA) which is compatible with tissue factor is present in the glomeruli and becomes increased in human proliferative glomerulonephritis and in animal models of nephritis. Tissue factor pathway inhibitor (TFPI) regulates the extrinsic pathway of blood coagulation through its ability to inhibit tissue factor activity. TFPI is present in plasma and in platelets, and it is now thought to be produced mainly by endothelial cells. We examined whether human mesangial cells (HMC) could produce TFPI and attempted to clarify regulatory factors which affect TFPI production. Cultured HMC were used and TFPI in the cell supernatants was measured by ELISA using a specific antibody. Cultured HMC showed the production of TFPI. Immunoblot analysis revealed 40 kD protein of TFPI. The concentration of TFPI was significantly increased following the incubation with thrombin and heparin, including low molecular weight heparin, in a dose- and time-dependent manner. However, fetal calf serum, phorbol myristate acetate, lipopolysaccharide, IL-1 beta and tissue factor did not stimulate TFPI synthesis. Our data show that cultured HMC have the ability to produce TFPI which inhibits fibrin formation. It is possible that thrombin-induced enhancement of TFPI synthesis may be caused by the autoregulatory system of blood coagulation and that with heparin it may represent another anticoagulatory effect of heparin.

Anticoagulants↗

Deterioration of urinary findings after tonsil stimulation in patients with IgA nephropathy.

We studied whether urinary findings are affected by stimulation of tonsils in patients with IgA nephropathy. In 62 patients with IgA nephropathy and 20 patients with other renal diseases tonsils were stimulated by an ultra short wave for 10 min. Changes in amount of urinary protein, urinary sediment, blood leucocyte count, concentrations of serum IgA and serum secretory IgA were evaluated after tonsil stimulation. Forty of 62 patients with IgA nephropathy (65%) showed deterioration of urinary findings after the stimulation compared with 6 of 20 patients with other renal diseases (30%). The deterioration was significantly more frequent in IgA nephropathy than in other renal diseases (p <0.005). Previous episodes of gross hematuria following upper respiratory tract infections had occurred in 17 of 40 patients who showed deterioration of urinary findings after tonsil stimulation (43%) as against in 4 of 22 without deterioration (18%). The level of serum secretory IgA was higher in patients who showed deterioration of urinary findings after tonsil stimulation than in those who did not show it. Though tonsil stimulation increased blood leucocyte count it did not affect the concentrations of serum IgA or secretory IgA. It is concluded that tonsil stimulation often deteriorates urinary findings in patients with IgA nephropathy; therefore chronic tonsillitis may play a part in the pathogenesis of IgA nephropathy.

Adolescent↗

Rupture of an isolated internal iliac artery aneurysm into the rectum: report of a case.

Aneurysmal rupture into the intestinal tract is a rare but disastrous complication of an internal iliac artery aneurysm. We report herein the successful surgical repair of a fistula between a huge aneurysm of the right internal iliac artery and the rectum in an 81-year-old man. After a femoro-femoral cross-over bypass had been performed, the aneurysm was opened and its patent arterial branches were ligated with sutures. The fistula was then intra-aneurysmally sutured and covered with an omental flap. The diagnostic and therapeutic approaches to this severe complication are discussed with a review of the literature following the presentation of this case.

Aged↗

Membranoproliferative glomerulonephritis associated with hepatitis C virus infection responsive to interferon-alpha.

A 42-year-old man with hepatitis C virus infection, cryoglobulinemia, hypocomplementemia, and nephrotic syndrome is reported. The kidney biopsy showed membranoproliferative glomerulonephritis. The patient was treated with interferon-alpha for 2 months. After the treatment, serum hepatitis C virus RNA became negative and nephrotic syndrome remitted. Repeat biopsy of the kidney revealed an improvement in renal histology. This case confirms an association between hepatitis C virus infection and membranoproliferative glomerulonephritis and the usefulness of interferon-alpha for treatment.

Adult↗