Biomedical subjects
Publications and source records attributed to M Inada.
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(a) The thyroxine-binding proteins were investigated in 23 cases of untreated thyrotoxicosis and 16 cases of untreated hypothyroidism, employing reverse flow paper electrophoresis with the glycine acetate system at pH 8.6 in the Durrum type cell.(b) In active thyrotoxicosis, all sera exhibited diminished thyroxine-binding prealbumin (TBPA) capacities. however, 17 of the 23 sera also had diminished thryroxine-binding alpha globulin (TBG) capacities, as well as markedly elevated free thyroxine fractions. In contrast, six thyrotoxic sera had normal TBG capacities and normal or slightly elevated free thyroxine fractions.(c) In hypothyroidism, the TBPA capacities showed no consistent deviation from the normal range. 11 of the 16 sera had elevated TBG capacities as well as markedly diminished free thyroxine fractions. In contrast, five hypothyroid sera had normal TBG capacities and normal or nearly normal free thyroxine fractions.(d) In thyrotoxicosis and hypothyroidism, the inverse correlation between free thyroxine fraction and TBG was much closer than that with TBPA. When diagnostic categories were considered separately, only TBG bore a significant inverse relation to the free thyroxine fraction. It is therefore suggested that in thyroid diseases TBG may sometimes play a more important role than TBPA in determining the free thyroxine fraction.(e) The demonstrated variations in the binding proteins were considered sufficient to explain the abnormalities of the free thyroxine fractions in thyroid disease.
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A single oral dose of mefenamic acid significantly depressed plasma thyroxine (T4) within 3 h in man. Similarly, mefenamic acid depressed plasma T4 within 3 h in thyroidectomized, T4-maintained rats. Plasma free fractions of T4 and tri-iodothyronine (T3) increased significantly after a single oral administration of mefenamic acid in man. In vitro addition of mefenamic acid to plasma also increased the plasma free fraction of T4. Three times more T3 was excreted into urine after an acute administration of mefenamic acid. In vitro conversion of T4 to T3 by liver homogenate was stimulated when T4 was displaced from plasma binding protein by mefenamic acid. Pituitary content of T3 increased when mefenamic acid displaced T4 and T3 from the binding protein. Simultaneously, thyrotropin (TSH) secretion in response to thyrotropin releasing hormone (TRH) was completely blocked by mefenamic acid. Prolactin release in response to TRH and luteinizing hormone (LH) and follicle stimulating hormone (FSH) release in response to luteinizing hormone releasing hormone (LH-RH) were not affected by mefenamic acid. It is concluded that mefenamic acid displaces T3 and T4 from their plasma binding protein and more T4 and T3 are available to peripheral tissues for excretion, degradation and TSH regulation.
The clinical significance of the urinary oxygen tension (PuO2) was evaluated in 60 patients with ischemic heart disease. The PuO2 had fair relations to cardiac index and serum creatinine level (r = 0.73 and r = 0.73, respectively). Although the PuO2 had a fair relation to serum creatinine in patients with a low cardiac index, there was no relation to the cardiac index. In patients with increases in PuO2 from day 1 to day 2, the cardiac index increased, and the serum creatinine level decreased on the 2nd day, whereas a sustained decrease in cardiac index and an increase in serum creatinine were observed in patients with a decrease in PuO2 from day 1 to day 2. Thus, PuO2 can be used as an indicator of the renal function in patients with ischemic heart disease.
Two cases of intestinal Behçet's disease, which developed in the state of myelodysplastic syndrome with trisomy 8, are presented. Both cases are included in the incomplete type of Behçet's disease, with recurrent aphthous stomatitis, skin lesions, genital ulcers or vascular involvement and punched-out ulcers in the cecum, without ocular involvement. The chromosomal analyses revealed chromosomal abnormalities, including trisomy 8, in both cases. Chromosomal trisomy 8 was shown in all 6 cases with the intestinal Behçet's disease associated with myelodysplastic syndrome reported previously, including our patients. Their histories indicated that myelodysplastic syndrome might have started before the development of intestinal Beçet's disease. Theses findings suggested that chromosomal trisomy 8 might play an important role in the pathogenesis, at least in some groups, of intestinal Behçet's disease.
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We previously reported that EBC-1, a non-small cell lung cancer (NSCLC) cell line, produces immunoreactive neutrophil elastase (NE). In the present study, we examined the effects of ONO-5046.Na, a specific NE inhibitor, on the in vivo growth and spontaneous pulmonary metastasis of EBC-1 transplanted into severe combined immunodeficiency (scid) mice. In control mice, EBC-1 tumors inoculated subcutaneously grew steadily throughout 8-week observation period. The daily intraperitoneal injection of ONO-5046.Na (50 mg/kg/day) from day 1 completely suppressed the tumor growth. When ONO-5046.Na treatment was initiated 14 days after EBC-1 inoculation, it also caused a significant delayed growth of this cell line. Furthermore, ONO-5046.Na treatment completely inhibits the appearance of metastatic foci in lung at 8 weeks not only when it was administered from day 1 but also when treatment was initiated 14 days after tumor inoculation, when solid tumors started to grow. The weight of the mice treated with ONO-5046.Na was similar to that of the control mice at 8 weeks, and they appeared as healthy as the control mice during the treatment. These results indicated that a NE inhibitor, ONO-5046.Na, inhibited both primary and metastatic growth of NSCLC with no marked side effects.
BACKGROUND/AIMS: We studied the effect of initial daily administration of interferon for the treatment of chronic hepatitis C, to clarify a more effective treatment protocol for the eradication of the hepatitis C virus. METHODOLOGY: Consecutive patients who met the inclusion criteria were randomly enrolled in two groups in this study. One hundred and five patients were randomized and assigned to two groups. Patients, who enrolled in group A, were treated with 6 million units of natural interferon-alpha given subcutaneously daily for an initial two weeks and then thrice a week for 22 weeks. Patients, who were enrolled in group B, were treated with the same dose of interferon-alpha given for 26 weeks thrice a week from the first administration. RESULTS: In groups A and B, 58 and 47 patients were analyzed, respectively. At the end of treatment, 37 patients in group A (63.8%) had negative serum HCV-RNA test, compared with 26 in group B (55.3%), but at 6 months after discontinuation of interferon administration, 27 patients in group A (46.6%), compared with 8 in group B (21.3%). The rate of complete remission in group A (46.6%) was higher than that in group B (21.3%) (P<0.01). In patients with genotype 1b virus, the rate of complete remission was higher in group A (31.3%) than in group B (12.5%) (not significantly), and the relapse rate was lower in group A (9.4%) than in group B (37.5%), significantly (p<0.05). CONCLUSIONS: This study suggests that initial daily interferon administration is necessary to gain a higher rate of serum HCV-RNA eradication in patients with chronic hepatitis C.