9 results on '"Shimizu-Suganuma M"'
Search Results
2. Defferencial response to [formula omitted] by coat colors in mongolian gerbils
- Author
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Shimizu-Suganuma, M, Shichinohe, K, Mwanatambwe, M, Haga, K, Iedokoro, T, Tsukidate, S, and Fujita, K
- Published
- 1998
- Full Text
- View/download PDF
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3. Cerebellar ataxia due to Toxocara infection in Mongolian gerbils, Meriones unguiculatus.
- Author
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Akao N, Tomoda M, Hayashi E, Suzuki R, Shimizu-Suganuma M, Shichinohe K, and Fujita K
- Subjects
- Animals, Disease Models, Animal, Female, Immunohistochemistry, Toxocara canis immunology, Cerebellar Ataxia parasitology, Cerebellar Ataxia veterinary, Gerbillinae parasitology, Toxocara canis growth & development, Toxocariasis parasitology
- Abstract
We assessed the usefulness of gerbils as an experimental model for neurologic toxocarosis. Mongolian gerbils, Meriones unguiculatus, infected with Toxocara canis or Toxocara cati (1000 eggs/gerbil) showed progressive neurologic disorders from 50 days after infection in T. canis-infected gerbils or from 120 days after infection in T. cati-infected gerbils. The incidence of the onset was 6 of the 13 gerbils (49%) in the T. canis-gerbils and 5 of the 7 gerbils (71%) in the T. cati-gerbils. Histopathologically, the cerebellum was the most affected in both groups. We observed loss of Purkinje cells, glial nerve fibers, and nerve sheaths. We also found foci consisting of aggregated macrophages scattered in the white matter of the cerebellum. The affected gerbils showed ataxia and ultimately died of cachexia. Our findings suggest that irreversible neurologic toxocarosis in gerbils can be induced by infection with either T. canis or T. cati. more...
- Published
- 2003
- Full Text
- View/download PDF
4. Supplementation of heterologous complement induces anti-Thy-1.1 nephritis in the Mongolian gerbil (Meriones unguiculatus).
- Author
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Shichinohe K, Shimizu-Suganuma M, Ghazizadeh M, and Ishizaki M
- Subjects
- Animals, Disease Models, Animal, Glomerulonephritis, Membranoproliferative pathology, Guinea Pigs, Hemolysis, Immunohistochemistry veterinary, Male, Microscopy, Electron veterinary, Rabbits, Rats, Rats, Wistar, Complement System Proteins pharmacology, Gerbillinae immunology, Glomerulonephritis, Membranoproliferative immunology, Glomerulonephritis, Membranoproliferative veterinary, Kidney pathology, Thy-1 Antigens immunology
- Abstract
Anti-Thy-1.1 nephritis in the rat is a popular experimental model for mesangial proliferative glomerulonephritis (GN). This model is characterized by direct binding of anti-Thy-1.1 antibody with Thy-1.1 antigen expressed on mesangial cells (MCs) of glomeruli in the rat. A single injection of anti-rat thymocyte serum (ARTS) results in GN with proteinuria and extensive mesangiolysis. Development of mesangiolysis and proteinuria are complement-dependent. We previously demonstrated Thy-1.1 antigen, similar to the rat, in thymocytes, brain cells and MCs of the kidney in the Mongolian gerbil (MG). In this study, we attempted to develop a MG nephritis model, but an injection of ARTS did not induce GN. An additional injection of guinea pig serum as a complement after ARTS injection resulted in anti-Thy-1.1 nephritis in MG. Degeneration of MCs and neutrophil infiltration were observed 1 hr after GP serum injection. Mesangiolysis and fibrin exudation occurred 12 hr after the injection and MC proliferation was apparent 7 days after the injection. In the complement-dependent hemolytic test, MG serum could not hemolyze sheep erythrocytes. These results suggested low activity, or depletion of some factors, in complements of MG serum. more...
- Published
- 2002
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5. Ebola hemorrhagic fever (EHF): mechanism of transmission and pathogenicity.
- Author
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Mwanatambwe M, Yamada N, Arai S, Shimizu-Suganuma M, Shichinohe K, and Asano G
- Subjects
- Africa epidemiology, Animals, Haplorhini, Hemorrhagic Fever, Ebola epidemiology, Hemorrhagic Fever, Ebola physiopathology, Humans, Hemorrhagic Fever, Ebola transmission
- Abstract
Hemorrhagic fevers represent a wide spectrum of viral infectious diseases, out-breaking mostly as epidemics, some of them being highly lethal. They range from those caused by bunyaviridae, associated with renal or pulmonary syndromes and those recently emerging and caused by the filoviridae family of thread-like viruses. Among the latter, Ebola hemorrhagic fever (EHF) bears the highest mortality and morbidity rates. One form of the disease has been documented only in monkeys. The human form, has occurred mainly in areas surrounding rain forests in central Africa. Patients present with signs of hemorrhagic diathesis, fever, diarrhea and neurological disorders, leading sometimes to confusion with local endemic diseases. Fatal victims of the disease die of dehydration. Poor hygienic conditions facilitate the spread of the virus. Biologically, the virus seems to target both the host blood coagulative and immune defense systems. Intensive epidemiologic search have failed to establish the definitive natural host of the virus. Twice, with a 19-year interval, major outbreaks have taken place in the Democratic Republic of the Congo. The second major outbreak in the northwestern city of Kikwit in April 1995 will serve here to elucidate the mechanism of the viral infection. more...
- Published
- 2001
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6. Localization of extracellular matrix and mitogen-activated protein kinase (MAPK) in aorta of streptozotocin treated Mongolian gerbils.
- Author
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Naito Z, Nishigaki R, Kawahara K, Yokoyama M, Yamada N, Asano G, Shimizu-Suganuma M, and Shichinohe K
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- Animals, Gerbillinae, Immunohistochemistry, Aorta enzymology, Aorta pathology, Diabetes Mellitus, Experimental enzymology, Diabetes Mellitus, Experimental pathology, Extracellular Matrix pathology, Mitogen-Activated Protein Kinase Kinases metabolism
- Abstract
To evaluate the relationship among the extracellular matrix (ECM) and mitogen-activated protein kinase (MAPK) family for the vascular damages in hyperglycemia, we injected Mongolian gerbils intravenously with 150 mg/kg streptozotocin (STZ) and observed over the next one year the resulting aortic changes by immunohistochemical techniques. After STZ treatment, hyperglycemia was confirmed. At 4 weeks after STZ administration morphological observation revealed increased stromal components among the vascular smooth muscle cells (SMCs). Immunohistochemically, extracellular matrices such as fibronectin and laminin were localized in the aorta at 4 weeks and one year after STZ administration. The reaction products of MAPK in vascular SMCs were more increased at one year than at 4 weeks after STZ administration. After STZ administration, the increase of ECM and MAPK was observed in the aorta, which suggests these factors play important roles in the pathogenesis of macrovasculopathy in diabetes mellitus. more...
- Published
- 2001
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7. Differential susceptibility to Brugia pahangi infection in Mongolian gerbils (Meriones unguiculatus) of different coat colour.
- Author
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Shimizu-Suganuma M, Shichinohe K, Tsukidate S, and Fujita K
- Subjects
- Animals, Body Weight, Disease Models, Animal, Eosinophilia parasitology, Female, Male, Parasitemia, Splenomegaly parasitology, Splenomegaly pathology, Brugia pahangi pathogenicity, Filariasis genetics, Genetic Predisposition to Disease, Gerbillinae parasitology, Hair Color genetics, Host-Parasite Interactions genetics
- Abstract
The influence of intraspecific host variables on the response to parasitic infections is an important aspect of host-parasite relationships, yet little is known about this aspect of filariasis for lack of a model. This study presents coat colour mutants of the Mongolian gerbil (Meriones unguiculatus) as potential new models for research into the effects of host genetic variation on response to filarial infection. Peak level of microfilaraemia, eosinophil response, body weight and degree of splenomegaly in gerbils infected with Brugia pahangi varied with agouti, albino, and black coat colour. These results suggested that coat colour-related genes might influence host immune response to developmental stages of the parasite and eosinophil-mediated reaction might cause host damage. more...
- Published
- 2000
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8. Ultrastructural changes and immunohistochemical localization of advanced glycation end products in the heart of streptozotocin-treated Mongolian gerbils.
- Author
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Fujii T, Nishigaki R, Kawahara K, Yamada N, Onda M, Yokoyama M, Naito Z, Asano G, Shimizu-Suganuma M, and Shichinohe K
- Abstract
This study was designed to clarify the developing mechanism of cardiomyopathy and vasculopathy in streptozotocin-treated Mongolian gerbils. Twenty male Mongolian gerbils (MG; 10-12 weeks old) were used, and 150 mg/kg of streptozotocin (STZ) was injected into the left femoral vein. Six control male MG were injected intravenously with normal saline. The animals showed severe hyperglycemia (up to 330 +/- 96.4 mg/dl) by 1 week after streptozotocin administration. At 1 week after STZ treatment, cardiomyocytes revealed no significant change, but unclear striated structures were demonstrated in cardiomyocytes at 4 weeks. After 1 year, anisocytosis was observed, and in the perinuclear region granular components were stained positively with periodic acid-Schiff reagent. Ultrastructurally, at 4 weeks and 1 year after STZ treatment, cardiomyocytes were irregular in size, and oval amorphous and lysosomal electron-dense bodies were observed in perinuclear and cytoplasmic regions. In coronary arteries, endothelial and medial cells revealed increased vesicles and intercellular collagen fibrils. Capillaries showed slight swelling of endothelial cells associated with the lamellar thickening of basement membrane and collagen fibrils in the perivascular regions. Immunohistochemically, advanced glycation end products (AGE) were observed in the cytoplasm of vascular and heart cells, and ultrastructurally the reaction products were demonstrated in the endoplasmic reticulum and lysosomes of cardiomyocytes and vascular cells in the STZ-treated Mongolian gerbils. AGE may play an important role not only in angiopathy but also in cardiomyopathy of STZ-treated Mongolian gerbils after STZ treatment. more...
- Published
- 1999
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9. Nafamostat mesilate, a synthetic protease inhibitor, attenuated hypercoagulability in a canine model of hemorrhagic shock.
- Author
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Koido Y, Kato K, Shimizu-Suganuma M, and Shichinohe K
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- Animals, Benzamidines, Dogs, Partial Thromboplastin Time, Prothrombin Time, Serotonin blood, Blood Coagulation drug effects, Guanidines pharmacology, Platelet Aggregation drug effects, Protease Inhibitors pharmacology, Shock, Hemorrhagic blood
- Abstract
Hypercoagulability is known to occur in the early phase of hemorrhagic shock. The prolongation of excessive clot formation after recovery from a shock state leads to the formation of microthrombi or disseminated intravascular coagulation which disturbs microcirculation, damaging organ function. The aim of the present study is to investigate the beneficial effect of a synthetic protease inhibitor, 6-amidino-2-naphthyl p-guanidinobenzoate dimethanesulfonate (nafamostat mesilate), in the attenuation of hypercoagulability in hemorrhagic shock. A model of hemorrhagic shock that simulates the clinical course of injured patients was created in anesthetized dogs. The animals were divided into two groups: a control group (group-C, n = 9) and an experimental group (group-E, n = 9). Animals received saline or 0.2 mg/kg of nafamostat mesilate respectively when their mean arterial pressure declined to 50 mmHg. The serum concentration of hydroxytryptamine (5-HT), prothrombin time (PT), and activated partial thromboplastin time (APTT) were determined as indicators of platelet activity and blood coagulation. In group-C, serum 5-HT was elevated significantly at 60 min after hemorrhagic shock but not so in group-E. The APTT at 30 and 60 min was shorter in group-C than in group-E. The PT at 30 min was also shorter in group-C. Plasma fibrin degradation products (FDP) increased at 60 min after the induction of shock in group-C. The results indicate that inadequate tissue perfusion in shock stimulates blood coagulation and that nafamostat mesilate might be beneficial in decreasing excessive blood coagulation. more...
- Published
- 1997
- Full Text
- View/download PDF
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