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Biomedical subjects

S Inoue

Publications and source records attributed to S Inoue.

At least 91 records · Page 5Linked to original sources
PubMed1996

[Detection of angina-related coronary artery in patients with unstable angina pectoris by using 123I-BMIPP myocardial scintigraphy].

To evaluate the diagnostic accuracy of detection of angina-related coronary arteries in patients with unstable angina pectoris. Twenty patients with unstable angina pectoris underwent 123I-BMIPP scintigraphy at rest. A mean duration from last anginal attack to 123I-BMIPP scintigraphy was 408 +/- 3.2 days. Seventeen of 20 angina-related coronary territories were detected by reduced 123I-BMIPP uptake. The sensitivity and specificity for detection of angina-related coronary arteries were 85% and 95%, respectively. The decrease in myocardial uptake of 123I-BMIPP agreed with the decrease in regional wall motion by using ultrasonic echocardiography. 123I-BMIPP scintigraphy may be useful for detection of angina-related coronary artery in a routine clinical examination in patients with unstable angina pectoris.

Aged↗
PubMed1996

Effect of poly(vinylsulfonate) on murine AA amyloid: a high-resolution ultrastructural study.

In experimental murine inflammation-associated amyloidosis (AA amyloidosis), an interaction between heparan sulfate and serum amyloid A (SAA), the AA precursor, has been demonstrated and is believed to play an important role in AA amyloidogenesis. Poly(vinylsulfonate) sodium salt (PVS) can arrest AA amyloid induction and cause established amyloid deposits to regress. PVS is thought to have this property by virtue of limited anionic structural similarities it has to heparan sulfate. In the present study, a comparison has been made of the in situ light microscopic and high-resolution ultrastructure of amyloid deposits before and after PVS treatment. As shown recently in situ, AA fibrils from untreated mice are composed of an outer layer of heparan sulfate proteoglycan and a 1- to 2-nm filament network of AA protein. This layer encloses a microfibril-like structure composed of chondroitin sulfate proteoglycan wound around a core of amyloid P component. After treatment with PVS, both the heparan sulfate proteoglycan and the AA filament network are lost from the fibrils, and the more central portion disintegrates into the chondroitin sulfate proteoglycan with associated amyloid P subunits. These findings add further support to the concept that heparan sulfate proteoglycan is important in amyloid fibril structure, and interference with its binding interactions with the amyloid filament protein provides a point of therapeutic attack.

Amyloidosis↗
PubMed1996

[Bucillamin induced lung injury in rheumatoid arthritis].

Thirteen cases with rheumatoid arthritis who experienced lung injury during the treatment with bucillamine (Bc), about whom the questionnaires were answered by the physicians and whose X-ray films could be rechecked, were studied. Nine cases out of the 13 showed patchy mottled infiltrates in the bilateral center sparing the periphery, and the other 4 showed diffuse infiltrates. In these 9, serum gamma-globulin level decreased when lung injury appeared. The gamma-globulin level before the start of Bc administration, the level when lung injury appeared, the gamma-globulin decrease, and its ratio to the level before Bc were 1790 +/- 661 mg/dl, 1297 +/- 666 mg/dl, 459 +/- 320 mg/dl and 29.1 +/- 18.0%, respectively. In 5 out of the 9, gamma-globulin level reincreased when they recovered from the injury: 2 out of the 5 showed the reincrease even after steroid therapy. The data were obtained only from 2 out of the 4 with diffuse pattern in X-ray, and the decrease and the decrease ratio were 200 mg/dl (5.8%) in 1, and 49 mg/dl (3.6%) in the other. The characteristics of Bc-induced lung injury might be mottled infiltrates in the center appearing concurrently with serum immunoglobulin decrease.

Aged↗
PubMed1996

Facial nerve palsy as an early manifestation of relapse in T-cell acute lymphoblastic leukemia.

We describe a 14-year-old girl with T-cell acute lymphoblastic leukemia (ALL) who developed peripheral type facial palsy alternately on each side during remission. The cerebrospinal fluid examination and imaging studies of the brain including the temporal area failed to identify the etiology. Fully 10 weeks after the onset of the facial nerve palsy, she showed cytological findings of meningeal and bone marrow relapse. Review of the literature revealed that an isolated facial nerve palsy due to leukemic cell infiltration is a rare occurrence. Nonetheless one needs to keep in mind that it may represent the initial sign of a relapse in a patient with leukemia, particularly with T-cell ALL.

Adolescent↗
PubMed1996

[A case of coronary artery embolism after double valve replacement].

A 69-year-old woman with combined valvular heart disease (mitral regurgitation and aortic regurgitation), ascending aortic aneurysm, and atrial fibrillation underwent double valve replacement (DVR) and, ascending aortic wall plication. The postoperative thrombo-test level was around 20%. The ST elevation on ECG (II, III, aVFm, V4 approximately V6) with chest pain were recognized on the 13 th postoperative day. She was diagnosed as having acute myocardial infarction, and percutaneous transluminal coronary recanalization was performed immediately. The coronary angiogram showed occlusion at the left anterior descending branch (#8). This lesion could be recanalized by 6,000 U plasminogen pro activator (pro-UK) administration. The cineangiogram on the 35th postoperative day, revealed complete recanalization of this occlusion. Several cases of acute myocardial infarction associated with valvular heart diseases has been reported previously in Japan. However, there has been no report, except for this case, demonstrating occlusion in the coronary artery after prosthetic replacement and successful PTCR. So, this case is the first report on that point.

Aged↗
PubMed1996

[A case with superficial siderosis of the central nervous system accompanied by sensory high tone hearing loss and recurrent headache and vomiting].

A 13-year-old boy with superficial siderosis of the central nervous system was reported. There were many members, including the proband, with sensory high tone hearing loss in his maternal family, but they did not have other neurological symptoms. Paroxysmal and pulsatile severe headache, and vomiting without aura appeared recurrently at the age of 8. His consciousness was alert and no other abnormal sign or symptom was seen during the attacks. The electroencephalogram and cranial computed tomogram revealed no abnormality. The T2 weighted magnetic resonance image of the cranium showed a superficial low intensity zone on the cerebellar vermis, frontal and parietal lobes of the cerebrum, and cervical and upper portion of the thoracic spinal cord at the age of 12, when he had severe headache and vomiting. Cerebrospinal fluid showed xanthochromia with mild elevation of the protein level during an attack, and a light bloody appearance during the asymptomatic state. The diagnosis of superficial siderosis of the central nervous system was made by these findings of magnetic resonance image and cerebrospinal fluid. The bleeding sources to the subarachnoid space could not be detected by cerebral angiography.

Adolescent↗
PubMed1996

Expression of immunoreactive activin A protein in remodeling lesions associated with interstitial pulmonary fibrosis.

The expression of activin A, one of the transforming growth factor-beta supergene family, was studied in various pulmonary conditions associated with interstitial pulmonary fibrosis (3 cases with diffuse alveolar damage, 6 cases with idiopathic pulmonary fibrosis, and 1 case with pulmonary fibrosis associated with rheumatoid arthritis) using immunohistochemical techniques on paraffin-embedded sections. Controls consisted of 10 cases with normal pulmonary parenchyma, and 2 cases with primary pulmonary hypertension and 1 case with secondary pulmonary hypertension were also studied. The lung specimens from normal parenchyma weakly expressed immunoreactive activin A on the bronchiolar epithelium. In marked contrast, all of the specimens from cases with diffuse alveolar damage and interstitial pulmonary fibrosis demonstrated strong expression of activin A on metaplastic epithelium, hyperplastic smooth muscle cells, desquamated cells, and alveolar macrophages. Pulmonary arteries from patients with primary or secondary pulmonary hypertension showed abundant immunoreactive activin A on smooth muscle cells. These findings suggest a potential role for this growth factor, activin A, in the pathogenesis of pulmonary tissue remodeling associated with interstitial pulmonary fibrosis.

Activins↗
PubMed1996

[Diagnosis of superficial-type early carcinoma of the gallbladder by endoscopic ultrasonography--comparison with ultrasonography].

The detectability of superficial-type carcinoma of the gallbladder by ultrasonography (US) and endoscopic ultrasonography (EUS) were investigated. Eight patients with such carcinoma of the gallbladder were reviewed. They had undergone both US and EUS previous to surgery. The tumor was detected in 3 patients by US, 2 patients with IIa + IIb-type carcinoma and 1 patient with IIa-type carcinoma. Those lesions were visualized as localized thickening of the gallbladder wall or as broad-based tumor. In 2 patients, lesions were not initially detected by US, but were shown by US after the examination by EUS. The tumor was detected by EUS also in 1 case of IIb + IIa-type carcinoma besides those 3 patients mentioned above. All four of these lesions were visualized as broad-based tumor by EUS. It was difficult to detect pure IIb-type or small IIa-type carcinoma even by EUS. In patients with concomitant acute cholecystitis or gallbladder stone, it was difficult to evaluate the abnormal findings of the gallbladder wall.

Aged↗
PubMed1996

[Management of aortoesophageal fistula due to thoracic aortic aneurysm].

Aortoesophageal fistula (AEF) is a rare but fatal disease without prompt diagnosis and treatment. A 82-year-old woman was admitted because of repeated hematemesis. Endoscopic examination suspected submucosal tumor with blood clot at the top on the mid-esophagus. The CT scan of the thorax and the aortography revealed a thoracic aortic aneurysm. AEF was diagnosed and the operation was performed. The ruptured aneurysm was resected and patched with Dacron graft. At the same time, subtotal esophagectomy with esophagostomy and gastrostomy were performed. The reconstruction at five weeks after operation induced oral intake. She died from an aspiration pneumonia five month later.

Aged↗
PubMed1996

[Clinical effects of urokinase and sodium ozagrel in patients with acute symptomatic lacunar infarction].

The clinical effects were compared between a thrombolytic agent (urokinase) and a thromboxane synthetase inhibitor (sodium ozagrel) in patients with acute lacunar infarction. All patients had some degree of neurological deficits, which corresponded to the lesions on computerized tomography or magnetic resonance imaging. Urokinase of 420,000 units was given over two days in 11 patients, 160 mg/day of sodium ozagrel was administered for two weeks in 23 patients. The study was followed up to one month after the onset. Urokinase treatment improved motor paresis in 45.5-62.5% of the patients, sodium ozagrel in 68.4-86.7%. Using the combined score of motor paresis and conscious disorder, urokinase group revealed 44.4-45.5% improvement, but sodium ozagrel group 81.0-89.5% (p < 0.05). The rates of suppressive effect in progressing stroke and complete recovery were higher in sodium ozagrel group. Sodium ozagrel was clinically more efficient than urokinase in patients with lacunar infarction.

Acute Disease↗
PubMed1996

Clinical significance of abnormal postexercise systolic blood pressure response in patients with hypertrophic cardiomyopathy.

The clinical significance of abnormal postexercise systolic blood pressure (SBP) response in patients with hypertrophic cardiomyopathy (HCM) was assessed by treadmill exercise testing in 30 normal subjects and 96 patients with HCM. SBP recovery ratios were derived by dividing the SBP at 1 and 3 min after exercise by the peak exercise SBP. The upper normal limit of the SBP ratio was defined by two standard deviations (SD) from the mean in 30 normal subjects. A postexercise SBP ratio that exceeded the upper normal limits of the SBP ratio was considered to be an abnormal SBP response in patients with HCM. Twenty-seven (28%) of 96 patients with HCM showed an abnormal SBP response. Compared with the normal SBP response group (69 cases) among patients with HCM, the abnormal SBP response group had lower SBP response during exercise (22 +/- 25 vs 62 +/- 26 mmHg : mean +/- 1 SD, p < 0.05), more prolonged QRS width (110 +/- 21 vs 92 +/- 20 msec, p < 0.05), higher incidences of ventricular tachycardia (12 vs 7 cases, p < 0.001), and sudden death (7 vs 0 cases, p < 0.0001). The defect area of Tl-201 myocardial scintigraphy was more extensive in the abnormal SBP response group (2.9 +/- 1.7 segments) than in the normal SBP response group (1.1 +/- 1.3 segments, p < 0.05). During atrial pacing (120/min), pulmonary artery wedge pressure was slightly elevated from 10 +/- 2 (at rest) to 14 +/- 3 mmHg (during pacing) (p<0.001), cardiac index showed no significant changes, and time constant T was shortened from 58 +/- 13 to 48 +/- 10 msec (p < 0.001) in the normal SBP response group, but in the abnormal SBP response group pulmonary artery wedge pressure was highly elevated from 12 +/- 5 to 20 +/- 3 mmHg (p < 0.0001), cardiac index was decreased from 2.5 +/- 0.7 to 2.1 +/- 0.6 l/min/m2 (p < 0.05), and the time constant T had no significant changes. These observations suggest that patients with HCM and abnormal postexercise SBP response have an abnormal cardiac response during exercise and extensive myocardial damage.

Blood Pressure↗