[A case of aortic regurgitation due to spontaneous rupture of an aortic commissure].
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Biomedical subjects
Publications and source records attributed to M Ando.
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A case of a 20-year-old man with superoinferior ventricular heart complicating situs inversus, levo-loop and dextro-malposition (I,L,D), and double-outlet right ventricle is described. The associated anomalies were hypoplastic right ventricle, ventricular septal defect, atrial septal defect secundum, infundibular and valvular pulmonary stenosis, and mitral regurgitation. Intraventricular conduit repair was successfully performed.
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A novel substrate, beta-2-chloro-4-nitrophenylmaltopentaoside (beta CNPG5), was used for the enzyme-coupled determination of alpha-amylase in biological fluids. It was hydrolyzed specifically by alpha-amylase to about 90% producing beta-2-chloro-4-nitrophenylmaltoside (beta CNPG2) and maltotriose. Under the assay conditions, the absorption of 2-chloro-4-nitrophenol (CNP) generated by the secondary reaction of alpha-glucosidase and beta-glucosidase as auxiliary enzymes is about twice the absorption of 4-nitrophenol (PNP), which is the end product currently measured in some alpha-amylase assay methods. The sensitivity of the assay using beta CNPG5 was thus much higher than that using 4-nitrophenyl-maltopentaoside (PNPG5) as substrate. The absorption of CNP did not fluctuate with temperature or with pH between 6.8 and 7.2, which are the conditions normally used for determination of amylase activity in biological fluids.
It is currently believed that the thyroid stimulating immunoglobulin (TSI) of Graves' disease is involved in the pathogenesis of hyperthyroidism through the stimulation of the adenylate cyclase-cyclic AMP system. To evaluate this mechanism, TSI in the serum of patients with Graves' disease was determined by its ability to generate cyclic AMP (cAMP) in monolayer cells prepared from a normal thyroid gland. The thyroid tissue was digested with collagenase, and the liberated follicles were collected from the supernatant and cultured for 7 days. One gram of thyroid tissue yielded more than 1 X 10(7) monolayer cells which were stored in aliquots at -80C. Cells (1 approximately 2 X 10(4)/0.28 cm2 microtiter well) were incubated for 4 hours in 0.2 ml Hanks solution poor in NaCl, with various amounts of bovine TSH (bTSH) or 1.5 mg/ml Graves' serum IgG extracted by polyethylene glycol. cAMP accumulated in medium and cells was measured by RIA. Total cAMP (both medium and cells) was about 4 times higher when NaCl was deleted from Hanks solution. Moreover, as more than 90% of the cAMP was released into the medium, it was possible to omit the measurement of cellular cAMP, which requires extraction. The increase in medium cAMP concentration was dependent upon the number of cells, incubation time, and dose of bTSH. Time course and dose response curves in medium cAMP stimulated by IgG from 3 Graves' patients paralleled those of bTSH equivalent units. Accordingly, TSI activity could be expressed in bTSH equivalent units (bTSH microUeq). The assay could detect 1.0 or 3.3 microU/ml of bTSH and was highly reproducible. TSI activity in all of 16 IgGs from normal subjects was under 3.3 bTSH microUeq/ml, while it was greater than 3.3 bTSH microUeq/ml in IgGs from 33 of 37 (89%) untreated patients with Graves disease. Of the 13 patients followed for 2 to 7 months while on antithyroid drugs, 12 had greater than 3.3 bTSH microUeq/ml and, with the exception of one, all showed a decrease in their TSI activity. Moreover, 5 of 12 patients treated continuously for more than 1 year were TSI negative (less than 3.3 bTSH microUeq/ml), and except for one case, all had TSI values below 8 bTSH microUeq/ml (a value found in only 25% of untreated patients). This in vitro bioassay for TSI is simple and sensitive. It detects the presence of TSI in virtually 90% of untreated patients with Graves' disease. TSI activity showed a clear decrease during the course of antithyroid drug therapy.
HCB was detected in all preparations of human placenta, maternal blood, milk, and cord blood. It was confirmed that HCB transferred from mother to fetus through the placenta. A significant linear correlation exists between the HCB concentration in placenta and that in cord blood. Therefore, the placental concentration of HCB is an accurate indicator of HCB contamination in pregnant women and in the newborn baby. It was decided that the commercial pesticides, PCNB and PCP, contained HCB at a concentration of about 0.7 and 0.4% of pesticides, respectively. The animals which consumed PCNB diet accumulated large amounts of HCB in lipid-rich tissues, especially in adipose tissue. On the other hand, PCNB was metabolized to methylthiopentachlorobenzene and bis(methylthio)tetrachlorobenzene. One of the main sources of HCB contamination in the general population in Japan may be derived from the commercial pesticides, PCNB and PCP.
Effects of nerve growth factor (NGF) on the uptake of non-metabolizable alpha-aminoisobutyric acid (AIB) and on Na,K-ATPase activity in superior cervical sympathetic ganglia (SCG) excised from adult rats were examined during aerobic incubation in vitro. Active uptake of labelled AIB into isolated SCG during 1 to 5 hours incubation at 37 degrees C was significantly accelerated by the addition of NGF to the incubation medium in a dose-dependent manner. Although the Km value of the AIB uptake by the SCG did not change with the addition of NGF, Vmax was nearly doubled. The NGF-evoked increase in AIB uptake was antagonized by the further addition of its specific antiserum in a dose-dependent fashion, and was largely suppressed in a medium containing ouabain. In SCG, axotomized one week prior to the examination, from which most of the neurons had disappeared and reactive proliferation of satellite glial components was in progress, the NGF-induced acceleration of AIB uptake was completely absent. The ganglionic Na,K-ATPase activity was greatly stimulated in the presence of NGF, and the effect was completely eliminated in the axotomized SCG. These results strongly suggest that the NGF-induced acceleration of active AIB uptake by the isolated SCG occurs not in glial cells but exclusively in the neuronal components with the apparent coupling of an Na ion extrusion process.
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Some new aspects of damage to cytochrome P-450 peroxidase activities by a toxic peroxide were investigated. Methyl ethyl ketone peroxide (MEKP) damage to cytochrome P-450 and inhibition of cytochrome P-450-mediated peroxidase activities were studied. In vivo, hepatic microsomal NADH- and NADPH-peroxidase activities were induced in rats by phenobarbital and 3-methylcholanthrene. Phenobarbital treatment induced more NADH- and NADPH-peroxidase activity than did 3-methylcholanthrene treatment. In vitro, microsomal cytochrome P-450 from rat liver was more sensitive to damage by MEKP than was this protein from rat kidney. Destruction of cytochrome P-450 hemoprotein and inhibition of its associated peroxidase activities by MEKP increased as a function of time of exposure to the peroxide. The addition of MEKP to microsomes resulted in a progressive increase in spectral absorbance at 433 nm. MEKP was an irreversible inhibitor of NADH- and NADPH-peroxidase, and NADH-peroxidase was more sensitive to damage than was NADPH-peroxidase. At 0 time and low concentration, MEKP was immediately bound to microsomal cytochrome P-450 and it exhibited competitive inhibition of NADH- and NADPH-peroxidase. At high concentration, MEKP was a mixed inhibitor of NADH- and NADPH-peroxidase. This study also showed that MEKP is a substrate for microsomal P-450 peroxidase activities and suggests that these peroxidase activities may play an important role in metabolism of toxic lipophilic organic peroxides that enter the endoplasmic reticulum.
A case of subtotal reconstruction of the thumb is described. The reconstruction was carried out as a staged procedure with an intact index finger transposition, followed by opposition transfer using the abductor digiti quinti muscle after three weeks. Twenty-eight months postoperatively, power grip and precision grip were restored despite destruction of the thenar muscles.
The effect of dietary vitamin E on in vivo and in vitro damage by methyl ethyl ketone peroxide (MEKP) to cytochrome P-450 and its associated enzymatic activity was studied. In vivo, MEKP damaged microsomal cytochrome P-450 and cytochrome P-450-mediated peroxidases in vitamin E-deficient rat liver. Dietary vitamin E treatment of rats protected the microsomal enzymes from peroxide damage. In vitro, the extent of MEKP inhibition was different for tetramethylphenylenediamine (TMPD)-peroxidase, NADH-peroxidase, and aminopyrine demethylase. In vitro addition of MEKP induced production of more thiobarbituric acid reacting substances (TBARS) in liver microsomes from vitamin E-deficient rats than from vitamin E-supplemented rats. When NADH and/or NADPH were supplied as reductants of MEKP, the inhibition of aminopyrine demethylase activity and the generation of TBARS by added MEKP were markedly reduced. In vivo, adequate levels of vitamin E and of NADH and NADPH are probably necessary to provide important protection to the endoplasmic reticulum during metabolism of toxic organic peroxides, such as MEKP.
A rare case of plasma cell granuloma of the lung in a 5-year-old girl showing extrapulmonal extension to the adjoining thoracic wall was reported. Intrapulmonal and thoracic wall granulomas revealed the same histopathologic features; proliferation of plasma cells and fibrous connective tissue. Although slightly atypical plasma cells were observed among many mature ones, immunohistochemical examination revealed polyclonal proliferation, confirming their inflammatory nature. Cellular components of fibrous connective tissue were identified as fibroblastic cells and myofibroblasts by electron microscopy. The present case and literature suggested the importance of the fact that "infiltrative" plasma cell granuloma had a tendency to occur in children.
The effects of nifedipine, a calcium channel blocker, on human bronchial smooth muscle contractions induced by leukotrienes C4 and D4 (LTC4, LTD4), prostaglandin F2 alpha (PGF2 alpha), and potassium were studied in vitro. The LTC4, LTD4, PGF2 alpha, and potassium caused bronchial smooth muscle contractions. After incubation with nifedipine at 2.9 X 10(-6)M, the contractions caused by LTC4, LTD4, PGF2 alpha, and potassium were significantly decreased. Nifedipine also significantly reversed human bronchial smooth muscle contractions previously initiated by these agonists. The effect of nifedipine on potassium contraction was significantly greater than that on LTC4, LTD4, and PGF2 alpha-induced contractions. The pharmacologic feature of nifedipine is that it inhibits the calcium influx associated with membrane depolarization. Therefore, these results suggest that there are two mechanisms of calcium movements in human bronchial smooth muscle contractions induced by LTC4, LTD4, and PGF2 alpha: membrane-depolarization-dependent and -independent mechanisms.
Three cases of criss-cross heart which we have observed during last five years are described. All of these cases were diagnosed by angiocardiography and two-dimensional echocardiography, and one of them was verified by autopsy. Two of them are unique among cases reported thus far. Case 1 shows ordinary criss-crossing with supero-inferior ventricle, and case 2, extreme crossing atrioventricular (A-V) valves, in which the right-sided right atrium connects to the left posteriorly positioned right ventricle through the tricuspid valve, and the left-sided left atrium to the right anterior left ventricle via a posteriorly positioned mitral valve. In case 3, the criss-cross appearance is secondary to displacement of the heart by compression caused by a diaphragmatic hernia. Findings in these cases suggest that criss-cross heart is caused not only by primary rotation of the ventricles during cardiac morphogenesis but also by secondary rotation of a formed heart induced by extracardiac compression. The degree of rotation in these cases revealed a wide spectrum from minimal to extreme. In addition, subxiphoid two-dimensional contrast echocardiography is recommended as the only accurate method of non-invasive diagnosis of this condition.
A 61 year old Japanese man with a diagnosis of Addison's disease was admitted to Kyushu University Hospital for further investigation of high ACTH levels and hyperpigmentation which 37.5 mg of cortisone acetate failed to alleviate. The basal level of plasma ACTH was 700-1000 pg/ml, and following 25-37.5 mg cortisone acetate or 1 mg dexamethasone the levels were 300-600 pg/ml. The general pigmentation showed little improvement with such medication. Radiographic studies revealed a double floor of the sella turcica and cisternal herniation. These observations suggested the existence of a pituitary ACTH-secreting tumour. Plasma ACTH showed a circadian rhythm ranging from 440 to 1570 pg/ml and it was not suppressed to a normal range by oral administration of dexamethasone, 8 mg/day or by continuous infusion of dexamethasone, 1.25 mg/h for 2 h. Plasma ACTH responses of 80% above basal level to lysine-vasopressin (LVP), and 12% above basal to synthetic ovine corticotrophin releasing factor (CRF) were observed. FK 33-824, a methionine-enkephalin analogue, suppressed plasma ACTH to 85% of basal level, while bromocriptine (CB-154) caused no significant change. These findings led to a diagnosis of pituitary ACTH-secreting adenoma (corticotropinoma) in association with Addison's disease. The persistent circadian rhythm of plasma ACTH suggested that this adenoma may not be completely free from regulation by the central nervous system. This case may be clinically significant for investigation of the pathogenesis of pituitary adenoma, particularly in Nelson's syndrome.