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Biomedical subjects

S Tasaka

Publications and source records attributed to S Tasaka.

At least 55 records · Page 3Linked to original sources
PubMed1995

[A case of Mycobacterium fortuitum pulmonary disease in a healthy young woman successfully treated with ciprofloxacin and doxycycline].

A 22 year-old woman was admitted to our hospital complaining of subtle fever and productive cough. She did not smoke and had no underlying disease. Her chest radiograph showed infiltration in the right upper lung field. A diagnosis of Mycobacterium fortuitum pulmonary disease was made on the basis of isolation of M. fortuitum from repeated sputum cultures. On admission, we administered standard antimycobacterial agents, but found the M. fortuitum isolated in this case to be completely resistant to them. We then administered antibiotics including 600 mg of ciprofloxacin and 200 mg of doxycycline. The pneumonic findings on chest X-ray and her clinical symptoms gradually improved thereafter. The in vitro susceptibility tests confirmed the efficacy of ciprofloxacin and doxycycline. We concluded that these drugs contributed significantly to improve the disease.

Adult↗
PubMed1995

[Effects of intravascular latex injection on factors responsible for acute lung injury].

To study the contribution of phagocytosis to the development of acute lung injury, latex particles (2 x 10(9)/kg; mean diameter, 2.84 microns) were injected intravenously or intra-arterially into guinea pigs. 125I-labelled albumin was injected to estimate the degree of lung injury, and 51Cr-labelled red blood cells were injected to correct for blood contamination in the samples. A control group was given saline. Four hours after the injections, the animals were killed, bronchoalveolar lavage was done, and the lungs were examined histopathologically. Animals that had received intravenous and intra-arterial injections of latex particles had more lung water and more pulmonary albumin leakage than animals that had received saline. Histopathological examination revealed massive accumulation of latex in the reticuloendothelial system. These findings suggest that the phagocytic process in the reticuloendothelial system plays a role in the development of lung injury in guinea pigs.

Acute Disease↗
PubMed1994

Regional lung hematocrit variation and assessment of acute lung injury.

Estimating blood content in the lung remains a key step in calculating lung water volume and microvascular permeability. We studied the effect of regional lung hematocrit (Hct) variation on assessment of acute lung injury. Escherichia coli endotoxin was administered in guinea pigs intravenously. Lung injury was evaluated by measuring the wet-to-dry weight ratio (W/D) and transvascular 125I-labeled albumin leakage for 3 h [tissue-to-plasma 125I-albumin ratio (T/P)] in five tissue samples from each animal. Residual blood content was corrected using either 51Cr-red blood cells as a blood cell marker, 99mTc-albumin as a plasma marker, or both, injected 10 min before the guinea pigs were killed. Lung Hct, estimated from the marker counts of lung and peripheral blood samples, was lower than peripheral blood Hct; intraindividual variation, represented by the standard deviation in each subject, was 0.024 +/- 0.015 for the control group (coefficient of variation 8.0 +/- 5.1%) and 0.026 +/- 0.013 for the endotoxin group (coefficient of variation 8.5 +/- 4.1%). Uncorrected W/D for residual blood content was greater than the corrected W/D. 99mTc-albumin correction gave values closer to the W/D corrected by both markers. T/P corrected by 99mTc-albumin showed smaller data variations than the values obtained with 51Cr-red blood cell correction, which was affected by variations in lung Hct. We recommend using a plasma marker to correct for blood content in assessing acute lung injury by W/D and T/P.

Animals↗
PubMed1994

Granulocyte colony-stimulating factor exacerbates acute lung injury induced by intratracheal endotoxin in guinea pigs.

The effects of recombinant human granulocyte colony-stimulating factor (rG-CSF) on the lung injury induced by intratracheal endotoxin were studied using guinea pigs. Animals were divided into four groups: (1) saline control, (2) endotoxin alone, (3) cyclophosphamide (CPA)+endotoxin, and (4) CPA+rG-CSF+endotoxin. CPA was injected intraperitoneally to suppress hematopoietic function 7 d before the study. rG-CSF at a dose of 100 micrograms/kg was administered subcutaneously twice a day for 5 consecutive d beginning 2 d after the CPA pretreatment. Saline or 0.2 mg/kg of endotoxin was administered via the airway, and the animals were observed for 4 h. 99mTc-labeled macroaggregated albumin was mixed with saline or endotoxin to obtain a lobar distribution. Lung injury was assessed by the concentration ratio of 125I-labeled albumin in lung tissue to plasma (T/P) and lung wet-dry weight ratio (W/D). We also counted the number of neutrophils in bronchoalveolar lavage (BAL) fluid and fixed lung tissues. T/P, but not W/D, increased in endotoxin-alone and CPA+endotoxin groups compared with the saline control group (p < 0.01). Both T/P and W/D of the CPA+rG-CSF+endotoxin group were significantly higher than those of the endotoxin-alone and CPA+endotoxin groups (p < 0.01). In the CPA+rG-CSF+endotoxin group, histopathologic examination of the lung sections showed neutrophil recruitment into the lung, and neutrophil counts in BAL fluid were elevated. In conclusion, pretreatment with rG-CSF increased sequestration of neutrophils into the lung and exacerbated the lung injury induced by intratracheal endotoxin in CPA-treated guinea pigs.

Acute Disease↗
PubMed1994

Effects of ONO-1078, a peptide leukotriene antagonist, on endotoxin-induced acute lung injury.

The role of lipoxygenase metabolites in the pathogenesis of endotoxin (LPS)-induced lung injury remains to be clarified. We investigated the contribution of peptide leukotrienes to LPS-induced acute lung injury using a potent antagonist, ONO-1078 (ONO). Experimental groups consisted of a saline group (n = 10), an LPS group (n = 9) injected intravenously with 2 mg E. coli LPS, an ONO group (n = 8) receiving 30 mg/kg of intraperitoneal ONO, and an LPS+ONO group (n = 6) receiving 30 mg/kg of ONO intraperitoneally 10 min before the LPS injection. The [125I]albumin lung plasma ratio, which is a parameter of acute lung injury, was significantly increased (p < 0.01) in the LPS group compared with the saline, ONO, and LPS+ONO groups. The [125I]albumin BAL fluid plasma ratio was also increased (p < 0.01) in the LPS group compared with the other groups. ONO pretreatment attenuated the LPS-induced increases in neutrophil counts in the BAL fluid. In vitro studies showed that ONO suppresses the neutrophil chemotaxis induced by LTB4, zymosan-activated serum, and FMLP. We conclude that (1) ONO-1078 attenuates LPS-induced acute lung injury; and (2) this effect appears mainly a result of its potent antagonistic actions against peptide leukotrienes and also, in part, the suppression of neutrophil chemotaxis.

Albumins↗
PubMed1994

Clinical significance of measuring myeloperoxidase, thiobarbituric acid reactive material and 7S collagen in plasma of patients with adult respiratory distress syndrome.

We measured myeloperoxidase (MPO), thiobarbituric acid reactive material (TBARM), and Type IV collagen 7S domain (7S collagen) in the plasma of 21 patients with acute lung injury (ALI). Sixteen healthy subjects served as a control group. There was no significant difference in MPO between the control and ALI groups. The TBARM and 7S collagen concentrations in ALI (TBARM; 3.05 +/- 0.65 nMol/ml, 7S collagen 9.06 +/- 5.96 ng/ml: Mean +/- SD) were significantly higher than those in the control group (2.54 +/- 0.33 and 3.43 +/- 1.05, p < 0.05). TBARM and 7S collagen levels of deceased ALI patients were higher than those of surviving ALI patients (p < 0.05). There were significant correlations between the plasma levels of these two parameters and the lung injury scores. Our findings suggest that plasma TBARM and 7S collagen are useful markers for the assessment of the severity of ARDS.

Adolescent↗
PubMed1993

A case of aldosterone producing adenoma associated with high PRA after long-term angiotensin converting enzyme inhibitor treatment.

A 62-year-old patient with non-insulin dependent diabetes (NIDDM) was admitted to our hospital for blood pressure control. He had been treated with angiotensin converting enzyme inhibitor (ACEI) for 7 years and showed marked hypokalemia with increased urinary potassium excretion. Hormonal examination revealed a normal plasma aldosterone concentration and increased plasma renin activity (PRA, 13.4 ng/ml/h), so potassium losing nephropathy was suspected. After discontinuation of the ACEI, PRA decreased to normal. An adrenal adenoma was found on abdominal magnetic resonance imaging (MRI) and adrenalectomy was performed to confirm aldosterone producing adenoma (APA). Although ACEIs are said not to alter PRA in APA, this drug was primarily responsible for the increased PRA in this case. This is a rare case of APA, which showed markedly increased PRA during ACEI treatment.

Adenoma↗
PubMed1993

[Measurement of myeloperoxidase and thiobarbituric acid-reactive material in plasma and bronchoalveolar lavage in E. coli-induced acute lung injury].

Myeloperoxidase (MPO), which is exclusively contained in neutrophils, is released on their activation. Therefore, MPO may possibly be used as a parameter of neutrophil activation. Thiobarbituric acid-reactive material (TBARM) reflects lipid peroxidation and is a parameter of oxygen radical-mediated cell membrane damage. Using our guinea pig model of septic lung injury we measured MPO and TBARM in the setting of acute lung injury. The two experimental groups were saline controls (n = 8) and an E. coli septic group to which 2 x 10(9) live E. coli were administered intravenously (n = 8). Lung damage was assessed by measuring wet to dry lung weight ratio (W/D) and lung tissue to plasma accumulation of 125I-albumin (AL: albumin leakage). We measured MPO and TBARM in plasma and BAL fluid. Increased W/D and AL were observed in the E. coli group suggesting the development of acute lung injury. In the E. coli group, plasma MPO increased and MPO in BAL fluid was significantly increased as compared with the saline control group. There was no difference in plasma TBARM between the two groups, while TBARM in BAL fluid of the E. coli group was greater than in that of controls. Although BAL fluid TBARM correlated with both W/D and AL, there was no relation between BAL fluid MPO and either of these parameters. We conclude that TBARM in BAL fluid may be useful for assessing E. coli-induced acute lung injury in guinea pigs.

Animals↗
PubMed1993

[A case of congenital antithrombin III deficiency with pulmonary thromboembolism and cerebellar infarction].

A 41-year old woman was admitted to a local hospital because of leg pain, chest pain and dyspnea after taking estrogen for two months for irregular menstruation. On admission to the hospital, her lung scintigram showed multiple segmental perfusion defects in the right lung. Pulmonary angiography showed several thrombi in the proximal pulmonary artery. A diagnosis of pulmonary thromboembolism was made. AT-III activity was found to be only 50% of normal value, indicating that the pulmonary thromboemboli were due to AT-III deficiency. The patient was then put on anticoagulants for two years. When she was 43-year-old, she was admitted to Keio University Hospital because of worsening of dyspnea. After admission her dyspnea had got better due to bed rest. Her brain CT, which was performed because of her gait disturbance, indicated past right cerebellar infarction. We gave her 2 mg of warfarin and maintained a thrombotest of about 30%. The investigation of her family revealed that her son also showed decrease AT-III activity, indicating a congenital abnormality. 26 families with this disease have been reported in Japan. Most had venous thromboemboli, but only a few cases had brain infarction as well. In addition, it is suggested that an estrogen therapy for irregular menstruation may have contributed, in this particular case, to the onset of thromboemboli.

Adult↗
PubMed1987

Bilateral sensorineural hearing loss associated with Mycoplasma pneumoniae infection.

Three cases of persistent bilateral sensorineural hearing loss following Mycoplasma pneumoniae (MP) infection are reported. These cases were characterized by highly elevated MP complement fixation titer and cold hemagglutinin titer. All the patients had bilateral acute otitis media with a moderate to high degree of mixed hearing loss in the early stage following primary atypical pneumonia (PAP).

Adult↗
PubMed1986

The microvascular architecture of the vestibule and the endolymphatic duct and sac of the rat in vascular corrosion casts.

The blood vessels of the vestibule and the endolymphatic duct and sac (ES) of the rat were reproduced with methacrylate casting medium and observed under a scanning electron microscope. Dense capillary networks of the macula utriculi and the macula sacculi were observed. The collecting venules from the vestibule emptied into the vein of the vestibular aqueduct (VVAQ). The plexus of the vessels in the ES was triangular in shape and had anastomoses with vessels of the bone and dura and drained into the VVAQ. The posterior meningeal artery (PMA) gave off two branches to the ES. These findings supported the similarity of the vascularization of the vestibule and the ES between the human and the rat.

Animals↗