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Biomedical subjects

K Iida

Publications and source records attributed to K Iida.

At least 379 records · Page 21Linked to original sources

The influence of exercise on left ventricular outflow tract obstruction, left ventricular performance and electrocardiogram in hypertrophic cardiomyopathy.

To investigate exertional changes in hypertrophic cardiomyopathy (HCM), 42 patients with HCM were studied by echocardiography and ECG at a supine ergometer exercise. In 12 cases with left ventricular (LV) outflow tract obstruction at rest (Group I), systolic anterior movement (SAM) of mitral valve was intensified during exercise; and among 30 cases without obstruction at rest (Group II), in 6 cases (Group IIA) SAM appeared during exercise. SAM might be further intensified 1 minute after exercise. Inverted T-wave was seen at rest especially in Group IIB (no SAM both at rest and during exercise), and tended to become less deep during exercise with an increase of LV wall motion. In conclusion, in HCM, LV outflow tract obstruction may be produced or intensified during exercise. Inverted T-wave in HCM may become less deep during exercise, with accelerated LV function.

Adolescent↗

[Fundamental and clinical study of T-1982 (cefbuperazone) in the field of obstetrics and gynecology].

Laboratory and clinical investigation of T-1982 (cefbuperazone) in the field of obstetrics and gynecology were carried out and the following results were obtained. The peak concentrations of 18.1-36.0 micrograms/ml were noted in pelvic cavity fluid at 1-3 hours after intravenous injection or drip infusion of 1 g of T-1982 in 3 cases after total hysterectomy for diffuse uterine cancer, then the concentrations decreased very slowly and were over 10 micrograms/ml at 6 hours after administration. Transfer rate of the drug into pelvic cavity fluid was 33-66% of the serum concentrations. In clinical trial, a total of 5 cases including 4 cases of external genital infections and 1 case of pelvic infection were treated with T-1982, and the results were evaluated as good in 3 cases, poor in 1 case and unknown in 1 case. Side effects were observed in 1 case who showed slight increase of GOT and GPT.

Abscess↗

[Clinical experience with cefoperazone in respiratory tract infections and studies on its penetration into pleural effusion].

Patients with bronchopulmonary infections were treated with cefoperazone (CPZ), and the serum and pleural effusion concentrations were determined after 2g CPZ drip infusion. The following results were obtained: Eight of 10 patients treated with CPZ responded with a significant clinical improvement. Side effects were found in 4 cases; eruption in 1 case, fever and granulocytopenia in 1 case, elevation of GPT in 1 case, and thrombocytopenia in 1 case. But these side effects disappeared immediately after cessation of CPZ treatment. Intravenous drip infusion of 2 g CPZ yielded a peak serum concentration of 112.0 --210.0 micrograms/ml immediately after the end of drip infusion, and a peak pleural effusion concentration of 8.8--43.0 micrograms/ml at 2--6 hours after the end of drip infusion. The ratio of peak pleural effusion concentration to peak serum concentration was 4.4--26.9%.

Adolescent↗

[Isoproterenol infusion stress two-dimensional echocardiography in detecting coronary artery disease].

Dynamic exercise two-dimensional (2-D) echocardiography has been utilized as a valuable method in the diagnosis of coronary artery disease (CAD). However, there are some limitations in this technique including inability to apply for patients whose physical capacity is limited. Moreover, appropriate echocardiographic recordings are frequently difficult because of bodily movements and/or hyperventilation during exercise. In order to overcome these limitations, we examined whether isoproterenol (ISP) infusion stress 2-D echocardiography could detect transient LV asynergy or not. The subjects consisted of 19 cases with angina pectoris (AP), 16 with old myocardial infarction (OMI), nine with atypical chest pain syndrome and six with miscellaneous heart disease. ISP stress test was performed prospectively as follows: ISP was infused at a rate of 0.02 microgram/kg/min until anginal pain occurred or significant ST depression (elevation) developed. Real time 2-D echocardiograms were obtained in the short-axis or apical RAO views of the LV before and every one minute during ISP infusion test. Coronary artery stenosis was considered to be present if the narrowing was 50% or more in the luminal diameter. The results were as follows: Adequate echocardiographic recordings were obtained in 86.1% of LV segments at rest, and in 82.2% during ISP infusion. Echocardiographic recordings during ISP infusion were feasible in almost all cases. LV wall motion abnormalities were detected in 12 (86%) of the 14 subjects with OMI and two (29%) of the seven subjects with AP at rest, while induced or exaggerated in nine (64%) of the 14 subjects with OMI and all of the 7 subjects with AP during ISP infusion. On the other hand, LV wall motion remained entirely normal during ISP infusion in 11 (92%) of the 12 subjects without CAD. In 4 (40%) of these 10 subjects without CAD, electrocardiographic judgements were positive in the ISP stress test. None had hazardous arrhythmias or severe anginal pain. ISP infusion stress 2-D echocardiography possessed feasibility of detecting LV wall motion abnormalities because this method could exclude difficulty of recordings due to bodily movements and/or hyperventilation seen in exercise echocardiography. Compared with ISP stress electrocardiography, 2-D echocardiography seemed to be superior with respect to the specificity in detecting CAD. In conclusion, ISP stress echocardiography is a safe and useful method in the diagnosis of CAD.

Adult↗

[Clinical experience in patients with Pancoast's tumor treated by fast neutron therapy].

We review our results with fast neutron therapy in Pancoast's tumor, and compare them with results obtained by photon beam therapy. 13 patients with Pancoast's tumor were divided into two groups; Group I (8 patients) received fast neutron therapy. Group II (5 patients) were treated by voltage X-ray therapy. 1. Group I was comprised of 3 patients receiving mixed beam therapy (TDF 80-100) and 5 patients subjected to boost therapy. All group II patients received 3100 to 8000 rads. 2. Fast neutron therapy was effective in 7 patients. In group II, high voltage X-ray therapy was effective in only 3 patients. 3. Two group I patients are still alive without signs of recurrence. The others died with a mean survival of 11 months. All group II patients died; their mean survival was 4.2 months. Our results suggest that fast neutron therapy is suitable and effective in patients with Pancoast's tumor.

Adenoma↗

Unique role of the complement receptor CR1 in the degradation of C3b associated with immune complexes.

The main finding of this paper is that CR1, the membrane receptor for C3b and C4b, together with C3b/C4b-inactivator (I), degrades C3b bound to immune complexes (C3b*). Two fragments are generated: C3c, which is released from the immune complexes, and C3d*. The C3c fragment released from the cell intermediate EAC1423b prepared with 125I-C3 was analyzed by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) and radioautography. It has a 135,000 mol wt and contains disulfide bonded labeled polypeptide chains of 75,000 and 31,000 mol wt, which presumably represent the beta and a fragment of the alpha-chain of C3b*. Silver staining of the SDS-PAGE gels revealed other C3-derived bands with 39-42,000 mol wt. Human erythrocytes + I also cleave C3b* into C3c and C3d*. The activity of the erythrocytes is CR1 mediated because it can be totally inhibited by monoclonal antibodies to CR1. In contrast with these results, I together with the serum protein beta 1H (H) transform EAC1423b into hemolytically inactive EAC1423bi and cleave the alpha' chain of C3b* into fragments of 70,000 and 40,000 mol wt. Small amounts of C3c are also released at relatively high concentrations of H. On a molar basis, the efficiency of CR1 in the generation of C3c and C3d is 10(4)-10(5) greater than H. An additional observation was that C3c could be released by treating EAC1423bi with CR1 + I and that this reaction was also inhibited by monoclonal antibodies to CR1. Therefore, it is likely that CR1 has binding affinity for iC3b and that the degradation of C3b* proceeds as follows: C3b (formula, see text) C3c + C3d*. Taken together, our findings argue that the processing of C3b* in vivo occurs in solid phase, that is, on the surface of cells bearing CR1.

Antigen-Antibody Complex↗

Complement receptor (CR1) deficiency in erythrocytes from patients with systemic lupus erythematosus.

This study reports quantitative information on the concentration of complement receptor for C3b and C4b (CR1) on erythrocytes from normal individuals and patients with immune complex disease. The measurements were performed by an immunoradiometric assay using monoclonal antibodies against CR1. The antibody specificity was confirmed by immunoprecipitation of CR1 from extracts of surface-labeled cells, by inhibition of rosette formation between B lymphocytes and the erythrocytes intermediate EAC14oxy23b, and by the characteristic distribution of the antigen among cells of human peripheral blood. The number of CR1 molecules in erythrocytes from 52 normal individuals was estimated as 1,410 +/- 620. No significant differences in CR1 levels were observed when individuals were grouped by sex, age, or blood groups. In patients with SLE and rheumatoid arthritis, the number of CR1 molecules per RBC was significantly lower, i.e., 600 +/- 307 and 903 +/- 417, respectively. CR1 levels were normal in asthmatics undergoing long-term treatment with prednisone. In SLE patients, significant correlations were found between CR1 levels, C4 hemolytic titers, and levels of circulating immune complexes. In two out of four patients with SLE, CR1 levels increased significantly during remission, showing that the deficiency is, at least in part, reversible. The deficiency in CR1 could be genetically controlled or could represent an epiphenomenon caused by the interaction of the receptor with a ligand present in the circulation of patients.

Adolescent↗

A case of cerebrotendinous xanthomatosis: effects of ursodeoxycholic acid administration on serum bile acids and cholestanol.

Cerebrotendinous xanthomatosis (CTX) is a rare familiar disease characterized by tendon xanthomas, cataracts, cerebellar ataxia, dementia and an elevated serum cholestanol level. In this paper, a 50-year-old man with typical signs and symptoms of CTX is described. Serum cholestanol and chelesterol concentrations were 17.9-28.6 micrograms/ml and 109-153 mg/dl, respectively. The determination of non-sulfated bile acid concentration in the serum assayed by mass fragmentography disclosed an abnormal profile. The concentration of cholic acid (0.30-0.52 microgram/ml) was higher than normal, while those of chenodeoxycholic acid, ursodeoxycholic acid, deoxycholic acid and lithocholic acid were extremely low or undetectable. Administration of ursodeoxycholic acid (300 mg per day, orally) for 2 weeks resulted in a marked reduction of serum cholic acid concentration. However, serum cholestanol levels remained unchanged.

Bile Acids and Salts↗

Complement receptor is an inhibitor of the complement cascade.

A glycoprotein from the membrane of human erythrocytes has been identified as a receptor for C3b (CR1). It promotes the dissociation of the alternative pathway C3 convertase C3b,Bb and the cleavage of C3b by C3b/C4b inactivator. We find that CR1 also inactivates the C3 and C5 convertases of the classical pathway. CR1 inhibits the consumption of C3 by C3 convertase EAC142 and enhances the decay of C4b,2a sites. On a weight basis, CR1 is approximately 5-10 times more active than C4 binding protein, a serum inhibitor of C4b,2a. The binding of 125I-CR1 to EAC14 cells is inhibited by C2. Therefore, it is likely that CR1 and C2 compete for a site on C4b. CR1 inhibited C5 convertase even more effectively, but had no effect on the assembly of the late complement components. At high concentrations, CR1 alone has no irreversible effects on cell-bound C4b. In the fluid phase, CR1 can function as a cofactor for the cleavage of the alpha' chain of C4b by C3b/C4b inactivator. A well-known function of CR1 is to promote adherence of microbes or immune complexes bearing C3b and C4b to cells. This interaction could result in a microenvironment damaging to the plasma membrane of the responding cell because the extrinsic C3b and C4b fragments can serve as additional sites of assembly of enzymes of the cascade. We therefore wish to propose that CR1 on the surface of cells supplies an increased local concentration of a strong inhibitor of the amplifying enzymes of the complement system and provides cells with a mechanism for circumventing damage when they bind C3b- and C4b-bearing substrates.

Complement C3-C5 Convertases↗