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Biomedical subjects

N Konno

Publications and source records attributed to N Konno.

At least 55 records · Page 3Linked to original sources
PubMed1988

Thyroid hemiagenesis associated with the right aortic arch.

The case of a 38-year-old woman with left thyroid hemiagenesis associated with the right aortic arch is presented. The diagnosis of hemiagenesis was established by isotopic and ultrasonic imaging, and also by angiographically defined absence of the left thyroid arteries. The aortogram revealed a right aortic arch with isolation of the left subclavian artery from the aorta. Although the significance and mechanism of the concomitant development of these anomalies is unknown, this case may be the first report in the literature.

Abnormalities, Multiple↗
PubMed1988

Impairment of mitochondrial respiratory activity in the early ischemic myocardium--with special reference to electron transport system.

Impairment of mitochondrial respiration in early myocardial ischemia was studied with special reference to myocellular irreversible injury. The technique used was total ligation of the left anterior descending coronary artery, followed by reconstruction of coronary blood flow, in the dog. State 3 respiratory activity reduced significantly to 76% of that of the non-ischemic myocardium in subendocardial muscle (Endo) as early as 30 min after occlusion, and at 60 min to 84% in the subepicardium (Epi). The activity was not recovered by reperfusion. The activity of complex I of sonicated submitochondrial particles decreased at 30 min to 67% in Endo and at 60 min to 71% in Epi, and was not recovered by reperfusion. Complex II and IV activities were kept in the control level until 60 min of ischemia. DNP-stimulated ATPase activity reduced to 79% in Endo at 15 min and to 70% in Epi at 30 min, but recovered significantly by reperfusion until 30 min of ischemia. Mitochondrial respiratory activity was impaired irreversibly in ischemia for 30 min in Endo and this spread to Epi later. Degradation of complex I is considered to be one of the causes of myocardial irreversibility in early ischemia.

Adenosine Triphosphatases↗
PubMed1988

Degrading process of acute ischemic myocardial cells.

1. Development of acute ischemic myocardial injury was studied in mongrel dogs, induced by ligation of left anterior descending coronary artery (LAD), by biochemical analysis of myocardial fractions such as sarcoplasmic reticulum (SR) and mitochondria (Mt) and by electron microscopic observation of ischemic myocardial cells with lanthanum probe method. 2. Irreversible injury of ischemic myocardium initiated in subendocardial muscle as early as 20 min after occlusion of LAD as expressed degradation of major ATPase protein and phosphatidylcholine and phosphatidylethanolamine of SR and irreversible impairment of state III respiratory and dinitrophenol (DNP)-ATPase activities of Mt, and these necrotic changes advanced to subepicardial layer at about 60 min. 3. Ultrastructural irreversible findings appeared later at about 60 min following inflow of lanthanum ions in ischemia for 30 min. 4. Activation of cathepsin B inside of SR under ischemic acidic metabolism and abnormal inflow of Ca++ into ischemic cardiac myocytes are suspective of very important factors for the initiation of myocardial ischemic injury in early myocardial ischemia.

Animals↗
PubMed1988

A case of Graves' disease associated with an autonomously functioning thyroid nodule (AFTN) (Marine-Lenhalt syndrome) which spontaneously became a cold nodule.

We report a 31-year-old female with Graves' disease associated with an autonomously functioning thyroid nodule (AFTN) (Marine-Lenhalt syndrome) in which the AFTN spontaneously became a cold nodule. Initially the patient was thyrotoxic and had diffuse goiter with an elevated radioiodine uptake. She became euthyroid following six months of antithyroid drug therapy, and in addition to diffuse goiter, the solitary hot nodule was palpable in the left lobe. Fourteen months later, hyperthyroidism recurred and the thyroid scan revealed diffuse radioiodine uptake with a cold area in the nodular region. The resected nodule showed extensive degeneration and the histological diagnosis was follicular adenoma with Graves' disease. We discussed the significance of recognizing the syndrome and also compared the frequency of spontaneous degeneration in AFTN and in solitary cold nodules.

Adult↗
PubMed1988

The effects of drug metabolism inducers on the delayed neurotoxicity and disposition of tri-o-cresyl phosphate in hens following a single intravenous administration.

Intravenous (iv) administration of tri-o-cresyl phosphate (TOCP) caused a delayed neurotoxic effect in hens similar to that produced by oral and dermal administration. The iv ED50s for producing ataxia and paralysis were estimated to be 15.9 mg/kg and 31.7 mg/kg respectively. The tissue disposition of unaltered TOCP was determined in hens following a single iv injection of 40 mg/kg of TOCP. One hour (hr) after the injection, the leg muscle contained the highest concentration, 26.99 micrograms/g fresh weight followed by the adipose tissue. Among the nerve tissues, the sciatic nerve had the highest concentration, 9.63 micrograms/g followed by the spinal cord and the brain. Except the adipose tissue and the sciatic nerve, the concentration in all analyzed tissues dropped below 1.0 microgram/g (ml) after 24 hr. An unidentified metabolite appeared in bile taken 1 and 3 hr after the injection. Pretreatment of hens with 3-methylcolathrene (3-MC) and beta-naphthoflavone (B-NF) protected against the TOCP-induced delayed neurotoxicity, whereas phenobarbital (PB) failed to protect against the neurotoxicity. Plasma creatine phosphokinase (CK) activity in paralytic birds increased approximately 4 times of the control or symptomless hens on the 21st day. 3-MC-, B-NF- and PB-treatment depressed substantially the concentration of unaltered TOCP in brain and plasma 1 hr after iv dosing with 40 mg/kg of TOCP. Only B-NF pretreatment lowered the level of TOCP in spinal cord. There was no effect of these inducers on the level of TOCP in sciatic nerve and adipose tissue. B-NF and 3-MC lowered significantly the TOCP level in leg muscle, whereas PB had no such effect. More attention should be paid to the role of TOCP in muscle, especially to the leg muscle, judging from the present toxicological and metabolic studies.

Animals↗
PubMed1987

Measurements of serum-free thyroid hormone concentrations by ultrafiltration--a comparison with equilibrium dialysis and mathematical calculation.

An ultrafiltration method (UF) for measuring free thyroxine (FT4) and free triiodothyronine (FT3) using the Diaflow YM membrane (Centricon-10) is described. The results are compared with those by equilibrium dialysis (ED) and also by mathematical calculations derived from T4, T3, and binding protein concentrations. The precision with the UF method was excellent. The normal ranges of FT4 and FT3 by the three methods are all comparable. There was a high degree of correlation of FT4 or FT3 results by UF with those by ED and by calculation (r = 0.940-0.974, n = 161, P less than 0.001). FT4 and FT3 by all methods agreed well for hyperthyroidism, hypothyroidism, and for patients with low T4-binding globulin. The mean FT3 in pregnancy was lower than the normal value for all methods, and FT4 concentrations by UF and calculation also decreased in late pregnancy. The mean FT4 by UF and ED in low T3 syndrome were significantly higher than in the normal controls, while the calculated FT4 was lower. The FT3 in low T3 syndrome distributed normal to subnormal in all methods. These results indicate that a) the UF method is a reliable reference method for measuring FT4 and FT3 concentrations; b) the UF results agree well with those by ED and also with theoretically derived values in subjects with thyroid diseases and TBG abnormalities; c) for patients with low T3 syndrome, the FT4 results obtained by UF and ED are similarly discrepant from the calculated results, implying the existence of binding inhibitor(s) which affect both UF and ED measurements.

Adult↗
PubMed1987

Alterations in phospholipids in acute ischemic myocardium.

Alterations in the phospholipid component of membranes were studied in acute myocardial ischemia with respect to sarcoplasmic reticulum (SR) and mitochondria (Mt) in the canine heart and compared with changes in the phospholipid composition of intact membrane treated with exogenous phospholipases (PLases) A2 and C, in order to examine the mechanism of ischemic degradation. As early as 30 min after coronary ligation, the total phospholipid content of SR and Mt decreased significantly, 16.0% and 5.6%, respectively. The patterns of SR and Mt phospholipids from the ischemic myocardia did not differ on the chromatograms from those of the non-ischemic myocardia, and no significant increases in lysophospholipids were found for up to 3 hrs. Among the components of phospholipids, phosphatidylcholine (PC) and phosphatidylethanolamine (PE) decreased mainly during ischemia, and depletion of PC exceeded that of PE in SR. PLase C hydrolysed phospholipids yielded no lysophospholipids, compared to the production of a large amount of lysophospholipids by PLase A2. It was concluded that degradation of membrane phospholipids occurs in the early stage of myocardial ischemia mainly in PC and PE, which are the major components of membrane phospholipids. This may be an expression of irreversible changes, and the activation of PLase C was considered to play an important role in their degradation.

Animals↗
PubMed1987

Degradation of the cardiac sarcoplasmic reticulum in acute myocardial ischemia.

The degradation of the sarcoplasmic reticulum (SR) in acute myocardial ischemia was studied with references to the regional irreversibility and to the mechanism of ischemic degradation by the measurements of Ca++-stimulated ATPase activity and composition of the major ATPase protein of the SR and activity of cathepsin B of the SR and lysosome (Ly) fractions. Ca++-stimulated ATPase activity decreased to 66% of that of the nonischemic portion at 20 min after coronary ligation in the subendocardium (Endo) and to 44% at 30 min in the subepicardium (Epi). Composition of the major ATPase protein decreased to 55% and 73% at 30 min in Endo and Epi, respectively. In both SR and Ly fractions cathepsin B exhibited the maximal activity at 6.0-6.5, and pH dependent. And incubation of the SR at pH 6.0 induced the degradation of the ATPase protein quite similarly to that in vivo ischemia. These results suggest that the degradation of the SR membrane of ischemic myocardial cells begins earlier in Endo 20 to 30 min after the cease of the coronary blood flow, and extends to Epi later. Cathepsin B is strongly conceivable to play an initial role of necrotic process of the ischemic myocardial cells by activation inside of the SR in ischemic acidic state.

Acute Disease↗
PubMed1987

Relationship between serum thyroxine concentration and dialyzable triiodothyronine fraction in patients with hyper- and hypothyroidism.

The interrelationship between the dialyzable triiodothyronine (T3) fraction (DFT3), T3, and thyroxine (T4) was examined in various groups of patients with hyper- and hypothyroidism. Partial correlational analysis showed that DFT3 correlated significantly with T4 (r = 0.383, N = 114, P less than 0.001), but not with T3 (r = 0.132). DFT3 exceeded the normal range when T4 was supranormal. The relation between T3 and free T3 (FT3) was quadratic (R2 = 0.944, N = 112, P less than 0.001). When the patients were divided into two groups according to T4 levels, the regression line between T3 and FT3 in patients with supranormal T4 was more than twice as steep as that obtained in patients with normal or subnormal T4 levels. In addition, the DFT3 and FT3 values were higher in patients with hyperthyroidism and both elevated T4 and T3 than in patients with hyperthyroidism and only elevated T3. The results indicate that T4 is a major factor influencing the DFT3 value, except when the T4-binding globulin concentrations vary markedly, and that the T4 level should be taken into account for a clinical evaluation of the FT3 concentration in hyper- and hypothyroidism.

Adult↗
PubMed1986

Ultrastructural changes in the sarcoplasmic reticulum in acute myocardial ischemia.

We investigated the morphologic changes in the sarcoplasmic reticulum (SR) in acute myocardial ischemia, induced by occlusion of the coronary artery in the canine heart, by freeze-fracture of SR in situ and in vitro, and they were compared to the alterations in Ca++-stimulated ATPase activity and protein composition of the isolated SR. Both SR in situ and the isolated SR exhibited typical intramembranous particles with diameters of 70 to 90 A in freeze-fracture replicas. The intramembranous particle density of the P face in SR in situ was 3,319 +/- 75 (mean +/- SE) per micrometer2 and that in the isolated SR was 2,667 +/- 60; particles were more numerous on the concave (P) face than on the convex (E) face. In ischemia for 30 to 60 min a significant decrease in the number of particles was found in SR in situ, and the corresponding change was noted in the isolated SR. Simultaneous decreases in Ca++-stimulated ATPase activity and the major ATPase protein of the SR were recognized. The close correlation of the changing pattern between the reduction in Ca++-ATPase and that in intramembranous particle density during ischemia supports the suggestion that a large part of the intramembranous particles represent ATPase protein itself. Decrease in the SR membrane particles strongly suggests the degradation of ATPase protein in the process of ischemic myocardial injury.

Adenosine Triphosphatases↗
PubMed1986

Discrepancy between uptake of serum triiodothyronine as measured by albumin and charcoal methods in nonthyroidal illnesses.

Triiodothyronine (T3) uptake as determined with albumin (AT3U) and with charcoal (CT3U) as binders were compared for patients with low-T3 syndrome. Both T3U values were identical in normal subjects and in patients with thyroidal disorders, pregnancy, low thyroxin-binding globulin (TBG), or acute hepatitis with high concentration of TBG. In the low-T3 syndrome, AT3U was significantly higher than CT3U (38.5 +/- 7.2% vs 29.4 +/- 4.9%, mean +/- SD, n = 37, p less than 0.001), and this difference increased as TBG and albumin concentrations decreased. Decreasing the concentration of TBG and albumin in serum by dilution increased the AT3U more than the CT3U value. Adding albumin to serum decreased AT3U, but not CT3U, when serum TBG and albumin concentrations were low. The free-thyroxin (T4) index as calculated by the AT3U ratio and T4 more accurately reflects the concentration of free T4 in low-T3 syndrome than does the index calculated from the CT3U ratio and T4. Thus AT3U is determined primarily by changes in TBG and albumin concentrations, so that the free-T4 index based on the AT3U ratio and T4 may be more useful than the CT3U method for evaluating free-T4 concentrations in low-T3 syndrome, which frequently has concomitant decreases in TBG and albumin concentrations.

Adult↗
PubMed1985

Serum concentration of unsaturated thyroxine-binding globulin in hyper- and hypothyroidism.

The concentration of serum thyroxine (T4)-binding globulin (TBG) not binding T4 (unsaturated TBG, u-TBG) was determined in hyper- and hypothyroidism. u-TBG was expressed as the product of TBG concentration and the ratio of free TBG capacity to maximal TBG capacity as determined by reverse-flow electrophoresis. u-TBG concentration in normal sera (n = 40) was 15.5 +/- 2.3 mg/l (mean +/- SD), or 257 +/- 38 nmol/l for a molecular weight of TBG of 60 000 daltons. u-TBG levels were significantly lower in hyperthyroidism (7.1 +/- 2.3 mg/l, n = 16, P less than 0.001) and higher in hypothyroidism (21.7 +/- 5.0 mg/l, n = 22, P less than 0.001). Based on partial correlation analysis, u-TBG was inversely correlated to serum T4 (r = -0.586, P less than 0.001), but not correlated to triiodothyronine (T3) (r=-0.180, NS). There was a reciprocal correlation between u-TBG concentration and the T3 uptake value (r = 0.748, P less than 0.001). There was also a reciprocal correlation of u-TBG with both % free T4 (r = 0.425, P less than 0.001) and % free T3 (r = 0.377, P less than 0.001), when the data were subjected to partial correlation analysis. These results provide the values for u-TBG concentration in hyper- and hypothyroidism, and support the concept that the free fractions of serum thyroid hormones may be determined by the number of binding sites of the TBG molecule that are not saturated with T4 in hyper-and hypothyroidism.

Adult↗
PubMed1985

Ultrastructure of the sarcoplasmic reticulum in the ischemic myocardium.

Fine structural changes in the sarcoplasmic reticulum (SR) in myocardial ischemia, induced by occlusion of the anterior descending branch of the left coronary artery in the canine heart, were studied by the freeze-fracture technique in situ and in vitro and compared to the alterations in Ca2+-stimulated ATPase activity and sodium dodecyl sulfate gel electrophoresis of the isolated SR. Both SR in situ and the isolated SR exhibited the typical intramembranous particles of 70-90 A in freeze-fracture replicas, and the numbers of particles were more numerous in the concave face (PF) than in the convex face (EF). The numbers of particles in the PF were 2748/micron 2 on the average. In ischemia for 1-2 hr, a significant decrease in the numbers of the particles was found in SR in situ, and corresponding changes were noted in the isolated SR. Decreases in Ca2+-stimulated ATPase activity and in the major protein band of ATPase were recognized simultaneously. The close correlation of the changing patterns between the reduction in Ca2+-ATPase and that in the intramembranous particle density during ischemia supports the suggestion that a large part of the intramembranous particles represents ATPase protein itself. The decrease in the particles of SR membrane indicates the degradation of ATPase in the process of ischemic myocardial necrosis.

Animals↗