Publications by authors named "Takakuwa T"

We determined the plasma concentrations of interleukin 8 (IL-8), polymorphonuclear leukocyte elastase (PMNE), and endotoxin in patients with septic shock in order to investigate the role of IL-8 and PMNE in the development of septic shock, especially in septic adult respiratory distress syndrome (ARDS). The IL-8 concentration in patients with septic shock was 6.28 +/- 9.

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The in vivo occurrence of apoptosis in neuroblastomas was investigated. Histologically, a number of tumour cells showed typical apoptotic changes, including cell shrinkage, condensed and fragmented nuclei, eosinophilic cytoplasm, and absence of the inflammatory response. These cells coincided closely with the so-called karyorrhectic cells.

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The relations between type II phospholipase A2 (PLA2) and PAF acetylhydrolase (PAFAH) levels and those of endothelin-1 (ET-1) and thrombomodulin (TM) were examined in samples containing the maximum amount of TNF-alpha detected over the clinical course for each patient with burn wound infection. The study included 23 patients with a total burn surface area of > 20%. Plasma levels of tumor necrosis factor-alpha (TNF-alpha), type II PLA2, PAFAH, TM, and ET-1 were 174.

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The expression of manganese superoxide dismutase (Mn-SOD) was studied immunohistochemically, using a specific monoclonal antibody, in surgically resected hepatocellular carcinoma (HCC) and noncancerous tissues from 47 patients (2 with well-differentiated HCC, 36 with moderately differentiated HCC, 8 with poorly differentiated HCC, and 1 with undifferentiated carcinoma). Cancer cells in 44 patients (93.6%) were positive for Mn-SOD.

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Objectives: The roles of cytokines and endotoxin in hemorrhagic shock, particularly the translocation of endotoxin and bacteria during hemorrhagic shock, were investigated.

Design: Prospective study.

Setting: Critical care and emergency center of a university hospital.

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We measured serum levels of endotoxin, cytokines, and eicosanoids and investigated their relationship to serum complement levels in patients with sepsis. Serum endotoxin (Et) levels (5.3 +/- 2.

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To examine the relationship between arachidonic acid metabolism and sepsis, we determined the blood concentration of platelet-activating factor acetylhydrolase (PAFAH) and of arachidonic acid cascade substances, leukotriene B4 (LTB4), thromboxane B2 (TXB2), and 6-keto-prostaglandin Fla (PGF1a), in patients with clinical sepsis. Blood concentrations of PAFAH, LTB4, TXB2 and PGF1a at the time of the initial diagnosis of sepsis were 23.9 +/- 9.

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We determined the plasma levels of type-II phospholipase A2 (type II PLA2), platelet-activating factor acetylhydrolase (PAFAH) leukotriene B4 (LTB4) and of several complements (C3a, C4a, and C5a), which are considered to be among the cytokines and eicosanoids involved in vascular endothelial disorders and that vary in concentration during sepsis. We investigated the relationship between those levels and those of ET-1 and TM levels in plasma. Plasma levels of type II PLA2, PAFAH, LTB4, C3a, C4a, ET-1, and TM at the time that sepsis was diagnosed in 30 patients were 218.

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To investigate the roles of tumor necrosis factor-alpha (TNF-alpha), endothelin-1 (ET-1) and thrombomodulin (TM) in the plasma of patients with sepsis, plasma levels of endotoxin (Et), TNF-alpha, ET-1 and TM were determined in 30 such patients. Plasma levels of Et, TNF-alpha, ET-1 and TM at the time sepsis was diagnosed were 4.0 +/- 6.

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Two cases of penetrating craniocerebral injuries which occurred during alpine skiing were presented. The first was a 25-year-old lady whose calvarium was impaled with a ski pole in the anterior part of the orbital roof following an interpersonal collision. She was brought to the Critical Care and Emergency Center, Iwate Medical University.

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The activities (C3a, C4a, C5a) and concentrations (CH50, C3, C4, C5) of serum complement were measured to evaluate the involvement of complement in sepsis. We studied 27 patients with sepsis who were divided into the survivors (Group 1) and the nonsurvivors (Group 2). The levels of C3a, C4a, and C5a were all significantly higher in Group 2 than in Group 1 and closely reflected the severity of sepsis.

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We measured soluble CD14 (sCD14), plasma endotoxin, tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), IL-6, and interferon-gamma (IFN-gamma) in patients with multiple organ failure (MOF). The sCD14 level was significantly higher in septic patients with MOF than that in those without MOF and also higher in non-septic trauma patients with MOF than that in those without MOF. In the septic group with MOF, the sCD14 level correlated significantly with the TNF-alpha level but not the plasma endotoxin, IL-1 beta, IL-6, or IFN-gamma level.

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To examine the roles of thromboxane A2 and prostaglandin I2, which are arachidonic acid metabolites found in patients with sepsis, we measured the serum levels of their respective stable metabolites, thromboxane B2 (TXB2) and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) in 22 patients with sepsis. Results were analyzed in relation to patients' survival. The levels of both TXB2 and 6-keto-PGF1 alpha were significantly higher in patients who died than in those who survived, thus reflecting the severity of the patients' illness.

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Platelet activating factor acetylhydrolase (PAF-AH) activity was measured in patients with sepsis, and its relationships with various cytokines and endotoxin were evaluated. PAF-AH activity was significantly higher (p = 0.0136) in 17 patients who died than 13 patients who survived.

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A 21-year-old man developed signs of brainstem damage after being injured while playing rugby. Cervical x-ray films showed os odontoideum, and angiography revealed persistent occlusion of the right vertebral artery at the level of the second cervical spine. These findings indicated that atlantoaxial dislocation caused by os odontoideum may have induced vertebral artery occlusion, leading to brainstem infarction.

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The effects of intramuscular injections of minute amounts of polymyxin B were studied in 42 patients with endotoxemia. Plasma endotoxin was measured by means of an endotoxin-specific Endospecy test (Seikagaku Corp., Tokyo, Japan) after pretreatment of the plasma with a new perchloric acid method that we developed.

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To clarify the relationship between cytokines and arachidonic acid metabolites, we measured tumor necrosis factor (TNF-alpha), interleukin 8 (IL-8), and leukotriene B4 (LTB4). The subjects consisted of 30 patients with sepsis. The results were compared between patients who died (Group A) and those who survived (Group B).

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Among 231 patients with cervical injuries treated over 12 years, 15 had cervical spinal cord injury associated with ossification of the posterior longitudinal ligament. All of them were male and most had injuries due to a relatively weak external force. Four of them underwent surgery.

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Congenital generalized lipodystrophy (CGL) is a rare disease, the main symptoms of which are a reduction of systemic subcutaneous fat, characteristic facial features, hypertrichosis, and insulin-resistant diabetes. We report herein the unusual case of a 25-year-old man with CGL in whom gas gangrene developed, an association which has never before been encountered.

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A study was carried out to investigate the efficacy of therapy with recombinant human granulocyte colony-stimulating factor (rhG-CSF) in 24 patients with granulocytopenia and sepsis who had failed to respond to antibiotics. The mean leukocyte count at the start of the study was 911 +/- 334/microliter. Patients were injected subcutaneously with 75 micrograms rhG-CSF once daily for a mean of 5.

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The inhibitory actions of Ulinastatin, which is a protease inhibitor, on the production of polymorphonuclear leukocyte elastase (PMN-elastase) and interleukin 8 (IL-8) in vascular endothelial cells were evaluated. Our findings suggest that IL-8 plays a role in the production of PMN-elastase. Ulinastatin inhibited the lipopolysaccharide (LPS)-stimulated activity of polymorphonuclear leukocytes (PMN) and the production of IL-8 in vascular endothelial cells.

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The cause of liver infarction previously reported [1-4] are mainly due to occlusion of hepatic artery. Herein, we report the case of liver infarction resulted from simultaneous occlusion of hepatic artery and portal vein due to trauma and therapeutic transcatheter arterial embolization (TAE), and we followed up the infarcted lesion with computed tomography (CT), ultra sonography (US) and magnetic resonance imaging (MR imaging) until it disappeared.

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