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Biomedical subjects

K Fujiwara

Publications and source records attributed to K Fujiwara.

At least 397 records · Page 22Linked to original sources
PubMed1995

DNA-based typing of human platelet antigen systems by polymerase chain reaction-single-strand conformation polymorphism method.

Polymerase chain reaction-single-strand conformation polymorphism (PCR-SSCP) method has been established to discriminate genotypes for the human platelet antigen (HPA) systems HPA-1, HPA-2, HPA-3, HPA-4, and HPA-5. Gene fragments which contain polymorphic sequences corresponding to the HPA-1, HPA-2, HPA-3, HPA-4, and HPA-5 systems were PCR-amplified with specific primers. The amplified DNA was denatured and subjected to non-denaturing polyacrylamide gel electrophoresis followed by silver staining. The results obtained by the PCR-SSCP method were in good agreement with those of the allotypes determined by serological typing. Furthermore, the results agreed with those obtained by other DNA-based typing methods such as PCR-allele-specific restriction enzyme analysis and PCR-sequence-specific primer. These results indicate that PCR-SSCP is a simple and sensitive method for determining HPA genotypes and identifying unknown polymorphisms.

Antigens, Human Platelet↗
PubMed1995

Role of adhesion between activated macrophages and endothelial cells in the development of two types of massive hepatic necrosis in rats.

Sinusoidal endothelial cell damage is produced by activation of hepatic macrophages after endotoxin administration in rats pretreated with Cornyebacterium parvum or undergoing 70% hepatectomy. Such damage causes fibrin deposition in the hepatic sinusoids leading to massive hepatic necrosis. In the C. parvum model, cytotoxic mediators, such as tumour necrosis factor (TNF)alpha and superoxide anions released from activated hepatic macrophages directly destroy sinusoidal endothelial cells. In contrast, in the partial hepatectomy model, endothelial cell damage occurs as a result of fibrin deposition due to derangement of the coagulation equilibrium regulated by tissue factor and thrombomodulin expressed on hepatic macrophages and sinusoidal endothelial cells, respectively. Immunohistological examination revealed that the expression of ICAM-1 in sinusoidal endothelial cells and LFA-1 in hepatic macrophages was greater in both models than in normal rats preceding the development of hepatic necrosis. The extent of liver injury was significantly attenuated by treatment with monoclonal antibodies against both adhesion molecules in the C. parvum model, but aggravated in the partial hepatectomy model, compared to control rats. We conclude that adhesion of activated macrophages to endothelial cells via LFA-1 and ICAM-1 in the hepatic sinusoids is essential for endothelial cell destruction in the C. parvum model, but can act protectively against provocation of fibrin deposition in the hepatectomy model.

Animals↗
PubMed1995

Possible cause of primary graft non-function after orthotopic liver transplantation: a hypothesis with rat models.

The cause of primary graft non-function after orthotopic liver transplantation (OLTX) is uncertain, but its clinical features are similar to fulminant hepatic failure with coagulopathy. In preserved livers, endothelial cell damage in the hepatic sinusoids is characteristic, indicating that fibrin deposition in the hepatic sinusoids, which can cause massive hepatic necrosis, might occur in the liver after OLTX. When rat liver was preserved in University of Wisconsin solution at 1 degree C, detachment of endothelial linings into sinusoidal lumens developed with fat-storing cell damage after 18 h. In this liver, hepatic macrophages were activated after reperfusion. Tissue factor activity in hepatic macrophages isolated from livers after OLTX was significantly increased compared to the control liver and this increase was enhanced by addition of endotoxin. In the preserved and transplanted livers, thrombomodulin expression in endothelial cells disappeared and fibrin deposition was seen in the hepatic sinusoids. Intravenous infusion therapy with antithrombin III attenuated liver injury 24 h after OLTX following preservation for 18 h. These results suggest that intravascular coagulation in the hepatic sinusoids associated with liver injury occurs in the liver after OLTX following cold preservation. This coagulopathy may be caused by sinusoidal endothelial cell damage due to regulatory imbalance in coagulation as a result of increased tissue factor activity in hepatic macrophages and decreased thrombomodulin activity in sinusoidal endothelial cells. Fat-storing cell damage may also contribute to the endothelial cell damage. A hypothesis regarding the cause of primary graft non-function after OLTX is proposed.

Adenosine↗
PubMed1995

Desmosomal dissolution in Grover's disease, Hailey-Hailey's disease and Darier's disease.

Proteins involved in the formation of desmosomes and simpler adherens junctions were studied in three types of non-immune acantholytic diseases; specifically, four cases of Grover's disease (GD), one case of Hailey-Hailey's disease (HHD) and one case of Darier's disease (DD), and these were compared to two cases of immune-mediated acantholytic disease pemphigus vulgaris (PV). The proteins studied included: 1. The intracellular desmosomal proteins, desmoplakin I and II and plakoglobin; 2. The intercellular desmosomal proteins, desmoglein and CD44; and 3. vinculin, which is a major intracellular protein of the simpler aherens junctions. In GD, HHD and DD, immunostaining showed a loss of desmoplakin I and II and plakoglobin from the desmosomes, and a diffuse staining in the cytoplasm. In contrast, in pemphigus vulgaris, these proteins seemed intact and were localized to dot-like spots on the cell surface. Also, desmoglein, and CD44 were slightly affected in GD, and moderately affected in HHD and DD. Absence of desmosomal attachment plaques, the lack of labeling with desmoglein in the affected desmosomes and a diffusion of the labels into cytoplasm were demonstrated with electron microscopy using an immunogold technique. In PV, desmoglein III is one of the target antigens for the autoantibodies in this disease and was only partially preserved in a small number of lesional cells, while CD44 was mostly preserved. Vinculin was intact in GD, HHD and DD, but was lost in PV. This study, our previous work, and that of others, suggest that: 1. In GD, HHD and DD, the proteins of the desmosomal attachment plaque are primarily affected; 2. In PV, the intercellular glycoproteins are primarily involved; and 3. Simple adherens junctions are intact in GD, HHD and DD, but are damaged in PV.

Acantholysis↗
PubMed1995

Involvement of pituitary hormone in the sex-related regulation of hepatic epoxide hydrolase activity in mice.

The involvement of the pituitary gland in the expression of sex-related differences in the activities of epoxide hydrolase (EH) in liver was examined in hypophysectomized and neonatally monosodium L-glutamate (MSG)-treated male and female mice. In hypophysectomized mice, the hepatic microsomal EH activity of males and females increased considerably above those of the respective sham-operated controls, and the female activity exceeded that of the sham-operated males. The hypophysectomy caused a decrease in soluble EH activity in males, while the operation led to an elevation of the activity in females. Neonatal treatment with MSG resulted in marked increases of microsomal EH activity in males and females at adulthood and the activity was about 2 times that of the male control mice. Treatment of hypophysectomized males and females with growth hormone (GH) resulted in a significant decrease in microsomal EH activity below those of the corresponding hypophysectomized controls, while the hormone treatment had no effect on the soluble enzyme activities. These results suggest that murine hepatic microsomal EH activity is principally under the suppressive control of the pituitary and GH is a causal hormone involved in the expression of sexual dimorphism in the enzyme activity.

Animals↗
PubMed1995

[Brain deformation caused by hyperplasia molar teeth (macrodonts) in the Japanese field vole (Microtus montebelli)].

Protrusion of hyperplastic upper molar teeth (macrodonts) into the cranial cavity was observed in the Japanese field vole. Protrusions of the upper molars occurred on both sides, but were large on the left than on the right. The teeth invaded the cranial cavity and brain parenchyma. Large concavities on the ventral side of the brain were interposed between the lateral olfactory tract and the optic tract. Invation by one macrodont reached the basal nuclei, hypothalamic and thalamic nuclei. The brain was deformed bilaterally, and nearly the entire olfactory bulb, globus pallidus, internal capsule, and lateral preoptic nucleus, and a portion of the hypothalamus, thalamus and anterior commissure were absent on the left side.

Animals↗
PubMed1995

Cyclosporin A and FK-506 in inhibition of rat Ito cell activation in vitro.

Ito cells are the primary matrix-producing cells in the liver. In hepatic fibrosis in vivo or culture on plastic, these cells undergo activation, a process characterized by cell proliferation, fibrogenesis, and smooth muscle alpha-actin expression. The cytosolic-binding proteins of cyclosporin A (CsA) and FK506 accelerate folding of various proteins including collagen and become inactivated by binding to those agents. CsA is shown to inhibit collagen synthesis in cultured fibroblasts. These findings prompted us to examine the effect of cyclosporin A and FK506 on Ito cell activation. CsA and FK506 reduced DNA synthesis in a dose-related manner, to 26% and 45% of controls at 5 mumol/L, respectively, without affecting total protein synthesis. CsA reduced collagen synthesis in a dose-related manner, to 70% of controls at 5 mumol/L without affecting noncollagenous protein synthesis, whereas FK506 changed neither collagen synthesis nor noncollagenous protein synthesis. Moreover, smooth muscle alpha-actin expression was reduced by 0.5 mumol/L CsA, but not by FK506. CsA merits consideration for the therapy of hepatic fibrosis. FK506 may also be a candidate for such therapy through inhibitory action on Ito cell proliferation.

Actins↗
PubMed1995

Junctional proteins of keratinocytes in Grover's disease, Hailey-Hailey's disease and Darier's disease.

Alterations of junctional structures in non-immune mediated acantholytic diseases (Grover's, Hailey-Hailey's and Darier's diseases) were examined using monoclonal antibodies against desmosomal attachment constituents (desmoplakin I & II and plakoglobin), desmosomal intercellular cement glycoprotein (desmoglein), protein of adherens junction (vinculin), and protein of gap junction (43Kd connexin). Universal cell surface (transmembrane) glycoprotein CD44 was also studied. In acantholytic foci of these diseases, attachment plaque proteins had dissolved and diffused into the acantholytic cells. The normal dotted linear pattern of immunostaining on the cell membrane was totally lost. In contrast, CD44 was well preserved on the cell membranes of acantholytic cells. Adherens junction and gap junction proteins were mostly preserved. Acantholytic cells of pemphigus vulgaris were similarly studied. In these cells, desmosomal attachment plaque proteins were very well preserved, while intercellular cement substance (desmoglein), adherens junctional proteins (vinculin), and gap junction protein (connexin) were totally absent, either on the cell membrane or in the cytoplasm. Electron microscopy confirmed an early dissolution of attachment plaque. Internalized desmosomal structures were seldom found in acantholytic cells of non-immune diseases. It was concluded that the primary event in acantholysis in these three diseases is the dissolution of desmosomal attachment plaque.

Acantholysis↗
PubMed1995

[Surgical repair of valvular diseases in patients over 75 years of age].

From January 1985 through August 1993, 41 patients older than 70 years underwent valvular surgery. In them, 10 patients were older than 75 years old. We evaluated those operative results. First, we classified them into 3 groups; Group A: over 75 y.o. (10 cases), Group B: 70-74 y.o. (31 cases) and Group C: 60-69 y.o. (39 cases, from January 1992 through August 1993). Surgical deaths were 1 case in Group A, and 1 in Group B. Distant deaths were 1 case in Group B, and 2 in Group C. Preoperative cardiac catheterization data showed the progression of cardiac failure in proportion to aging. But postoperative data showed no difference among 3 groups, and the condition was reversible. NYHA classification and cardiothoracic ratio (CTR) showed the same results. In summary, in valvular diseases in patients over 75 years of age, the progression of the condition was recognized but it was reversible. So we conclude that the surgical repair of no influence of age is necessary.

Aged↗
PubMed1995

[A case of esophageal cancer required jejunal reconstruction because of a gastric ulcer scar].

Recently, with increase of number of esophagectomy for esophageal cancer, the cases having the lesion in the organs for esophageal substitute have been increasing. The case of esophageal cancer, required reconstruction using the pedicled jejunum, because of impaired submucosal blood perfusion of the stomach caused by a ulcer scar, was reported. The patient was a 72-year-old female, with the ulcerative and infiltrative cancer lesion in the anterior wall of the mid-thoracic esophagus. Barium swallow revealed shortening of the lesser curvature and indentation of the greater curvature of the stomach. Endoscopy showed the lesion occupying anterior two thirds of the esophageal wall circumferentialy from 30 to 34 cm from the incisor tooth. The lineal scar of ulcer on the lesser curvature of the body of the stomach was also found. Following esophagectomy through right thoracotomy, the stomach was mobilized for reconstruction by dividing left gastric artery and short gastric artery, but the stomach oral to the ulcer scar became ischemic and bleeding was not found at the tip of the stomach. Therefore, reconstruction was performed using the pedicled jejunum through antesternal route. The gastric cardia is rich in the vascular network in the submucosal layer. The ulcer or ulcer scar of this region can cause ischemia in the tip of the gastric tube for esophageal substitute. Care should be taken to detect the ulcer lesion at the stomach preoperatively. In the case with the ulcer lesion blood supply to the tip of the gastric tube should be critically evaluated.

Aged↗
PubMed1995

Xanthogranulomatous cholecystis. Cell composition and a possible pathogenetic role of cell-mediated immunity.

Thirty-three cases of xanthogranulomatous cholecystitis (XGC) exhibiting the typical morphologic features were studied by light and electron microscopy and immunohistochemical techniques. Incidence of XGC was 4.2% of the surgically resected gallbladder diseases. Histologically, the granulomatous lesion of XGC principally consisted of accumulations of foam cells and lymphocytes. Variable numbers of multinucleated giant cells, granulocytes and fibroblastic cells were also noted. With respect to the origin of foam cells, it was considered that the vast majority of foam cells were derived from monocytes/macrophages because they were invariably positive for KP1, HAM56, CD11b and CD68. Interspersed among macrophage foam cells, many T lymphocytes were identified. The subtyping of T cells indicated a heterogenous population composed of both CD4+ and CD8+ lymphocytes typically in a ratio of 1:2. Macrophages and T lymphocytes demonstrated a marked expression of HLA-DR antigen. Electron microscopic and immunohistochemical double-staining observation demonstrated intimate apposition of T lymphocytes to macrophages or macrophage foam cells. The results indicate that XGC is a granulomatous disorder characterized by accumulations of macrophage foam cells and T cells. Delayed type hypersensitivity reaction of cell-mediated immunity may be implicated in the pathogenesis of XGC.

Adult↗