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Biomedical subjects

M Arai

Publications and source records attributed to M Arai.

At least 325 records · Page 18Linked to original sources
PubMed1995

Platelets with 10% of the normal amount of glycoprotein VI have an impaired response to collagen that results in a mild bleeding tendency.

Platelet glycoprotein VI (GPVI), a 62kD membrane protein, has been identified as one of the platelet receptors for collagen, since GPVI-deficient platelets exhibit abnormal responses to collagen and an abnormal bleeding tendency. We report a female patient with a mild bleeding history whose platelets expressed 10% GPVI of normal platelets. Shape change, aggregation and ATP release of the patient's platelets were completely absent in response to 1-5 micrograms/ml collagen but present normally in response to ADP and Ca2+ ionophore A23187. Adhesion of the patient's platelets to coated collagen was mildly affected (40-60% of normal platelets) in spite of only 10% expression of GPVI. Flow cytometrical studies revealed that the patient's platelets expressed normal amounts of the GPIa/IIa complex. These results suggest that platelet GPVI is less involved in adhesion to collagen than shape change and aggregation induced by collagen.

Adenosine Diphosphate↗
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

Species-specific PCR detection of malaria parasites by microtiter plate hybridization: clinical study with malaria patients.

A simple and convenient PCR method that amplifies the 18S rRNA genes has been developed for the purpose of detecting and differentiating four species causing malaria in humans. The advantage of the assay is that the biotinylated PCR product is visualized following hybridization with specific probes which are immobilized on plate wells (microtiter plate hybridization). This method has been previously evaluated in a field study and was found to be sensitive and specific for the detection of Plasmodium falciparum and Plasmodium vivax. In the current study, the microtiter plate hybridization PCR method was evaluated by using blood specimens from malaria patients. All of 36 cases of falciparum malaria, 26 of 27 cases of vivax malaria, all of 11 cases of ovale malaria, and 2 cases of malariae malaria were diagnosed species specifically by the PCR method. There were four smear-negative, PCR-positive cases that seemed to correspond to the convalescent stage of malaria. In contrast, 30 cases for which the diagnosis of malaria has been excluded on the basis of microscopy and clinical courses showed negative PCR results. By comparing parasite densities and PCR results following antimalarial treatment of some patients, it was revealed that the PCR results largely paralleled the parasite densities and that PCR could detect as few as 10 parasites per microliter of blood. We conclude that this PCR method is highly sensitive and specific for the detection of all four parasite species and can serve as a useful supplement to microscopy for the clinical management of malaria.

Animals↗
PubMed1995

Endothelin-1 and its binding sites are upregulated in pressure overload cardiac hypertrophy.

The purpose of this study was to determine whether endothelin and endothelin receptors play an important role in the development of cardiac hypertrophy due to pressure overload in vivo. Cardiac hypertrophy was produced by placing a constricting clip around the suprarenal abdominal aorta of rats. Hemodynamic parameters and plasma and ventricular concentrations of endothelin-1 (ET-1) were measured in control unoperated rats, and 30 min, 2 and 6 h, and 1 and 8 days after operation in pressure overload rats and sham-operated rats. The density and dissociation constant of ET-1 binding sites were also measured in control rats and 1 and 8 days after pressure overload and sham operation. Additionally, in situ mRNA hybridization for preproendothelin-1 (preproET-1) mRNA was performed to determine which cells were responsible for increased ET-1 levels. Ventricular ET-1 levels increased markedly on day 8 of pressure overload, whereas plasma ET-1 levels increased transiently only 30 min after operation, quickly returning to control level. In addition, ventricular ET-1 levels on day 8 showed a significant positive correlation with the degree of cardiac hypertrophy. In situ mRNA hybridization revealed that cardiac myocytes expressed preproET-1 mRNA in hypertrophied hearts in vivo. In accord with the elevation of ventricular ET-1 levels, the density of ET-1 binding sites was increased significantly, without affecting their binding affinity, on day 8 of pressure overload. These data are compatible with the hypothesis that increases in locally produced ET-1 and the density of ET-1 binding sites have an important relationship with the development of cardiac hypertrophy in vivo.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Expression of transmembrane-type protein tyrosine phosphatase mRNA along rat nephron segments.

Protein phosphorylation on tyrosine residues is one of the main cell signaling mechanisms. Cellular phosphotyrosyl levels are regulated by the activities of protein tyrosine kinases (PTK) and protein tyrosine phosphatases (PTPase). We have previously reported cDNA cloning of several types of PTPase from rat kidney, including LRP (leukocyte common antigen-related protein; also known as the transmembrane-type tyrosine phosphatase, i.e., RPTP alpha). LRP mRNA was shown to be abundant in the kidney; however, our understanding of the functional role of LRP in the kidney is very limited. To gain keener insight into the function of LRP in the kidney, our first approach was to reveal its mRNA distribution along rat nephron segments. Large signals were found in inner medulla by Northern blot analysis. By using a reverse transcription and polymerase chain reaction assay of individual microdissected tubule segments along the nephron [proximal convoluted tubule (PCT), medullary thick ascending limb (MTAL), cortical collecting duct (CCD), outer medullary collecting duct (OMCD), and inner medullary collecting duct (IMCD)] and glomeruli, we revealed intrarenal localization of LRP mRNA. LRP mRNA was detected in all nephron segments tested but was relatively rich in the IMCD. Rank order of the signal intensity was IMCD > PCT = OMCD > CCD > MTAL = glomeruli. Immunohistochemistry also revealed that LRP was abundant in IMCD. This pattern of expression gives rise to an interesting possibility that LRP might be involved in the specific renal tubule function, such as urinary concentrating mechanism; however, further study is required to describe the function of LRP in more detail.

Amino Acid Sequence↗
PubMed1995

A new gastric ulcer model in rats produced by ferrous iron and ascorbic acid injection.

We developed a new gastric ulcer model in which the ulcers are induced by the local injection of a ferrous iron and ascorbic acid (Fe/ASA) solution into the gastric wall. These ulcers resemble human gastric ulcers that penetrate the muscularis mucosa. The involvement of oxygen radical-mediated lipid peroxidation as the cause of these ulcers was investigated. With ferrous iron or ascorbic acid alone, gastric ulcers did not form, whereas penetrating ulcers were produced by the simultaneous injection of the Fe/ASA solution in a dose-dependent manner. Lipid peroxides significantly accumulated in the gastric mucosa from 1 to 24 h after the injection of the Fe/ASA solution. This increase in lipid peroxides preceded grossly evident gastric ulcer. Treatment with superoxide dismutase (SOD, recombinant human CuZnSOD) significantly reduced the size of the ulcers and inhibited the accumulation in lipid peroxides in the gastric mucosa, while treatment with apo-SOD or heat-inactivated SOD did not. These results suggest that lipid peroxidation mediated by oxygen radicals plays a crucial role in the pathogenesis of the gastric ulceration induced by the Fe/ASA solution.

Animals↗
PubMed1995

Alteration of bone status with ascorbic acid deficiency in ODS (osteogenic disorder Shionogi) rats.

Rats with hereditary defects in ascorbic acid (AsA) synthesis (ODS rats) subjected to AsA-deficiency for 3 weeks showed reductions of plasma alkaline phosphatase and dry and ash weights of the tibia, but no body weight alteration. In accordance with the chemical changes, bone loss and decrease of bone formation by AsA deficiency but not by malnutrition were observed in contact microradiographs of the tibia and by a tetracycline double labeling technique, respectively. The mechanical properties of femora measured by a three point-bending procedure were also altered by AsA deficiency for 3 weeks and showed decreases of 59% in toughness, 32% in strength, 32% in ductility and 22% in stiffness. The biomechanical changes by AsA deficiency were greater than the chemical changes in bone, indicating the usefulness of measuring mechanical properties as a sensitive method for the evaluation of the bone status. The second moment of the area of the femur was not changed by AsA deficiency. These results suggest that AsA deficiency in ODS rats causes marked bone loss and reduction in bone formation, which is accompanied by a greater reduction in biomechanics of the femur without causing macroarchitectural changes.

Animals↗
PubMed1995

Purification and some properties of six chitinases from Aeromonas sp. no. 10S-24.

Six chitinases were purified from a culture supernatant of Aeromonas sp. no. 10S-24 by ammonium sulfate precipitation, DEAE-Sephadex A-50, Butyl-Toyopearl 650M, and chromatofocusing. These enzymes were most active at pH 3.5-4.5 and the optimum temperature were 50 degrees C. The molecular weights of the enzymes were 89,000 to 120,000 from SDS-polyacrylamide gel electrophoresis. N-Terminal amino acid sequences of the enzymes were similar to that of chitinase I.

Aeromonas↗
PubMed1995

Effects of transforming growth factor alpha (TGF-alpha) on DNA synthesis and thyrotropin-induced iodine metabolism in cultured porcine thyroid cells.

Transforming growth factor alpha (TGF-alpha) is a potent mitogen that is similar structurally to epidermal growth factor (EGF). As EGF is a potent growth stimulator and an inhibitor of iodine metabolism in cultured thyroid cells of several species, we studied whether TGF-alpha has similar effects using porcine thyroid cells in culture. Recombinant human TGF-alpha dose-dependently stimulated DNA synthesis of thyroid cells, with maximal stimulation (eight- to ninefold above basal) occurring at 2 nmol/l. The potency was approximately 50% that of mouse EGF and correlated with the ability to compete with EGF for receptor binding, suggesting that the action of TGF-alpha is mediated by interaction with EGF receptors. When thyroid cells were cultured for 3 days with thyrotropin (TSH) in the presence of TGF-alpha, TSH-induced iodide uptake was inhibited in a dose-dependent manner. The potency of TGF-alpha again was approximately 50% that of EGF. Transforming growth factor alpha did not inhibit TSH-stimulated cAMP production. Moreover, iodide uptake stimulated by either forskolin or 8-bromo-cAMP also was inhibited by TGF-alpha. Thus, we conclude that TGF-alpha inhibits TSH-induced iodine metabolism largely by acting at the steps distal to cAMP production. Northern blot analysis revealed expression of TGF-alpha mRNA in porcine thyroid cells. These observations suggest that TGF-alpha acts as an autocrine modulator of growth and differentiated functions in porcine thyroid cells.

Animals↗
PubMed1995

Study on vomiting related to the vestibulo-autonomic reflex.

The purpose of this study was to investigate the neural pathway from the vestibular labyrinth to the medullary vomiting center in the cat, using electrophysiological techniques. During electrical stimulation of the canal nerve, we found conflicting results: the pressure in the stomach sometimes increased, and sometimes decreased. There might be several neural structures between the semicircular canal nerve and the vomiting center in the dorsolateral portion of the reticular formation of medulla oblongata. Retching or vomiting-like behavior during both respiration and movement of the stomach was recorded during stimulation at several sites in the lateral medullary reticular formation. However, the evoked unit activities were not always induced by stimulation of the canal nerve.

Animals↗
PubMed1995

[Optokinetic afternystagmus: its classification, sexual difference and relation to age in normal subjects].

Optokinetic afternystagmus, or OKAN, was investigated in 147 normal subjects (69 males and 78 females aged 20-78) for the purpose of obtaining the normal duration range and total number of beats in OKAN of the 1st phase. OKAN was recorded nystagmographically with the eyes open in darkness immediately after the sudden cessation of horizontal optokinetic stimulation with a constant speed of 60 degrees/sec. for 45 sec. The duration data for OKAN of the 1st. phase were distributed in a very wide range, between 0 and 180 sec., in all 294 samples. Therefore, the author arbitrarily divided the times into 3 categories: hypo-response with a duration below 10 sec., middle response above 10 sec. but below 60 sec. and hyper-response above 60 sec. OKAN were classified into 6 groups, with 3 subgroups, based on durations of OKAN of the 1st. phase, as results varied widely. 1. Classified OKAN groups and their rates: symmetric bilateral middle response (1a) was 10.9%, asymmetric bilateral middle response (1b) 15.0%, symmetric bilateral hyper-response (2a) 2.7%, asymmetric bilateral hyper-response (2b) 1.4%, bilateral hypo-response (bilateral no response (3a) and others (3b)) 25.2%, unilateral hypo response with contralateral middle response (4) 31.3%, unilateral hypo-response with contralateral hyper-response (5) 4.1%, and, unilateral middle response with contralateral hyper-response (6) 9.5%. 2. Classified OKAN groups for each sex and in different age groups: Generally, characteristic changes in the rate of classified OKAN for each sex and in different age groups could not be detected, for example, bilateral hypo-response (3a and 3b) appeared in all age groups from different decades. 3. The mean value of the maximal velocity in the slow phase of OKAN of the 1st. phase was 8.6 degrees/sec, the mean value of the total number of beats in OKAN of the 1st. phase was 22.8 and the average durations of OKAN of the 1st phase, to the right and to the left, were 27.3 sec and 21.7 sec., respectively. OKAN of the 2nd phase appeared in 9 (6.1%) but OKAN of 3rd phase was not observed in any of the subjects.

Adult↗
PubMed1995

[Left diaphragmatic hernia due to blunt chest trauma complicated with intrapleural gastric perforation].

A 17-year-old male was injured by traffic accidents. Multiple left rib fractures, radiopacity of left hemithorax and rightward mediastinal shift lead us to the diagnosis of traumatic hemothorax. But left tube thoracostomy could not obtain any fluid. After this finding we suspected diaphragmatic hernia. Neither inserted nasogastric tube nor abdominal echogram could not lead to definitive diagnosis. Chest CT could identify stomach and spleen in the thoracic cavity. Insufflation of 300 ml air through nasogastric tube could not expand the stomach. By insertion of another thoracic tube some coffee-ground like materials could be obtained. Laparotomy disclosed rupture of left hemidiaphragm and intrathoracic displacement of the stomach and spleen. After reposition of stomach, we discovered 5 cm fissure of the stomach and left thoracic cavity filled with leaked gastric contents. Though reports of combined diaphragmatic hernia and gastric rupture are rare, these combination could occur if a patient with diaphragmatic hernia encounters blunt chest trauma on a full stomach.

Accidents, Traffic↗
PubMed1995

[Massive and progressive hepatosplenomegaly caused by disseminated nontuberculous mycobacteriosis in a patient with acquired immunodeficiency syndrome].

A 28-year-old hemophilia A patient was admitted to our hospital in July, 1991 because of high fever, chronic diarrhea and anemia. The patient had been recognized as a asymptomatic carrier of human immunodeficiency virus (HIV) in 1985 and had developed Pneumocystis carinii pneumonia and had been diagnosed as acquired immunodeficiency syndrome (AIDS) in 1990. Hematologic laboratory examinations on admission revealed pancytopenia and a CD4+ cell count of 3/mm3. X-ray findings of chest and abdomen were normal and bacterial cultures of sputum, urine, blood, stool, cerebrospinal fluid and bone marrow yielded no pathogenic microorganisms. Microscopical examination of the stained specimens showed no acid-fast bacilli. On his fifth hospital day, his liver and spleen enlarged markedly and an abdominal CT scan obtained on the 13th day revealed high-grade hepatosplenomegaly. Administration of several kinds of antibiotics, antifungal agents, antiviral agents, antituberculous agents and gamma-globulin medicines did not relieve the symptoms. On the 28th day the patient had developed a subarachnoid hemorrhage and died five days later. Retrospectively all cultures for acid-fast bacilli of the specimens on his admission yielded nontuberculous mycobacteria. The bacteria were identified as Mycobacterium avium by polymerase chain reaction and his disease was eventually diagnosed as disseminated Mycobacterium avium complex (MAC) infection. The liver and spleen weighed 2,660 g and 1,840 g respectively at autopsy. Although hepatosplenomegaly is commonly recognized in AIDS patients with disseminated MAC infection, such massive and rapid enlargement has been rarely observed. This case study emphasize the importance of diagnosis and rapid treatment at the early stage of MAC infection.

AIDS-Related Opportunistic Infections↗