Biomedical subjects

T Usui

Publications and source records attributed to T Usui.

At least 379 records · Page 21Linked to original sources

PubMed1990

[A case of myotonic dystrophy associated with intracardiac conduction abnormalities and aortic regurgitation].

A rare case of myotonic dystrophy with mechanical derangement in a 48-year-old male is reported. The patient was admitted to Fuzisawa City Hospital because of chest discomfort. On physical examination, he had the typical facial appearance of myotonic dystrophy, and displayed grip myotonia. The blood pressure was 120/60 mmHg and the pulse 51, regular. A systolic ejection murmur at the cardiac base, an early diastolic blowing murmur along the left sternal border, and a pansystolic murmur at the apex were heard. The deep tendon reflexes were all normal. Elevation of serum creatine kinase and aldolase were noted. Chest X-ray films suggested moderate cardiomegaly. An electrocardiogram showed sinus bradycardia, atrioventricular block and left bundle branch block, suggesting diffuse involvement of the conduction system. An echocardiography confirmed the presence of left ventricular enlargement, thickened aortic valves, mitral regurgitation, and aortic regurgitation. Selective coronary angiography revealed no abnormalities. Left ventriculography demonstrated diffuse hypokinesis of the entire ventricle. Light microscopy of biopsied right myocardium revealed prominent interstitial fatty infiltration, mild interstitial fibrosis, and variation in the nuclear size. A 22-year-old son also had myotonic dystrophy and had an echocardiography indicative of thickened valves with aortic regurgitation. Myotonic dystrophy is a autosomal dominant disease. Cardiac involvement selectively disturbs the conduction system, sinus node, and to a lesser extent myocardium. Although the presence of aortic regurgitation could be a mere coincidence, we believe that this did not occur by accident, because the patient's son also had aortic regurgitation.

Echocardiography↗

PubMed1989

Study of estramustine binding protein (EMBP): purification of rat EMBP and establishment of RIA.

Estramustine binding protein (EMBP) was purified from the ventral prostate of the rat using DEAE-cellulose chromatography, concanavalin-A affinity chromatography and DEAE-sepharose chromatography. At the final step of the purification, two different peaks (Peaks A and B) of A280 nm were obtained. Peak A had a high binding activity to [3H] estramustine. On the other hand, Peak B had a low binding activity. On the analysis of polyacrylamide gel electrophoresis, Peak A gave two protein bands, whereas Peak B gave a single band. The molecular weight of the markedly stained band of Peak A was approximately 27,000, whereas that of Peak B was 18,000, as estimated by analysis of Fargusson's plot. The antibody against Peak B was used for establishing a radioimmunoassay (RIA) of EMBP. The sensitivity of this assay system was sufficient to measure of 1 ng of EMBP. The dilution curve of rat prostatic cytosol was paralleled with the standard curve. As a result obtained from this RIA, the mean concentration of immunoreactive EMBP was 8.01 ng/mg cytosol protein in human benign hyperplastic prostate (BPH) and 4.28 ng/mg protein in human prostatic carcinoma (PC), respectively. These results here obtained indicate that human prostate has an immunoreactive protein to the purified EMBP obtained from the ventral lobe of rat prostate.

Animals↗

PubMed1989

Cyclic AMP-responsive region of the human proopiomelanocortin (POMC) gene.

Transcription of the human proopiomelanocortin (POMC) gene is regulated by cAMP. To identify the region in the human POMC gene responsible for this regulation, we constructed chimeric genes containing different portions of the 5'-flanking region of the human POMC gene fused to the structural sequence encoding the bacterial reporter enzyme chloramphenicol acetyltransferase (CAT). The transcriptional activity of the fusion genes introduced into the rat glial cell line C6 was assayed by measuring CAT activity in the cell lysate. Forskolin, an adenylate cyclase-activating agent, stimulated the expression of POMC-CAT fusion genes. Deletion analysis demonstrated that the region between -417 and -97 bp from the transcriptional origin of the human POMC gene was responsible for regulation by cyclic AMP.

Animals↗

PubMed1989

Compound muscle action potentials and spinal evoked potentials in experimental spine maneuver.

In this study, the authors evaluated the effects of spine manipulations, similar to those used in scoliosis surgery, on the compound muscle action potential (CMAP) and spinal evoked potential (SEP) in 25 cats: a distraction maneuver was performed in ten, a rotation in five, and a combined (distraction and rotation) procedure in ten cats. Compound muscle action potential was only minimally changed by the rotation maneuver alone in all five cats. Distraction resulted in earlier deterioration of CMAP than SEP; when CMAP was no longer elicitable in ten cats, seven still showed measurable SEP. All ten cats became paraplegic. With the combined procedure, both CMAP and SEP were abolished earlier than with distraction alone. This was observed in all ten cats becoming paraplegic. The authors further extended the study to ten rabbits having experimentally induced scoliosis. Following corrective surgery with distraction and derotation, eight rabbits lost both CMAP and SEP. Two lost CMAP with still recordable SEP. All ten rabbits became paraplegic. These findings suggest that monitoring CMAP is a more sensitive measure than SEP, and that the spinal cord is more vulnerable to a combined distraction and derotation maneuver than to either one alone.

Action Potentials↗

PubMed1989

Leukotriene B4 metabolism in neutrophils of patients with chronic granulomatous disease: phorbol myristate acetate decreases endogenous leukotriene B4 via NADPH oxidase-dependent mechanism.

We studied the effect of phorbol myristate acetate (PMA) on endogenous leukotriene B4 (LTB4) metabolism of calcium ionophore A23187-stimulated human neutrophils. Preincubation of normal neutrophils with PMA significantly suppressed the recovery of endogenous LTB4 induced by A23187. PMA did not suppress the recovery of LTB4 produced by neutrophils from patients with chronic granulomatous disease (CGD), which is known to be defective in NADPH oxidase activation to produce reactive oxygen species (ROS). PMA inhibited the formation of omega-oxidation products of LTB4, but enhanced arachidonic acid release in normal and CGD neutrophils. Furthermore, 5-lipoxygenase activity of 10,000 x g supernatants from normal neutrophils pretreated with PMA was equivalent to that of the controls. Decrease in LTB4 recovery was not attributed to the suppression of the intracellular Ca2+ increase. Thus, it is suggested that reactive oxygen species (ROS) produced by PMA may directly affect endogenous LTB4 and convert it into metabolite(s) distinct from omega-oxidation products.

Arachidonate 5-Lipoxygenase↗

PubMed1989

Two-site immunoradiometric assay for adrenocorticotrophin: a cautionary study about the reactivity to its precursor molecules.

The specificity of a "two-site" immunoradiometric assay (IRMA) has been reevaluated by examining its ability to detect heterogeneous adrenocorticotrophin-like immunoreactivity (ACTH-LI) separated by gel column chromatography. Plasma samples from patients with Addison's disease, Nelson's syndrome and ectopic ACTH syndrome and tissue extract of human anterior pituitary were subjected to ACTH-IRMA and the levels of ACTH-LI were compared with those measured by conventional ACTH-radioimmunoassay (RIA). The level of ACTH-LI measured by IRMA was considerably lower than that measured by RIA in the plasma of a case of ectopic ACTH syndrome and the ACTH-LI did not show a dilution curve parallel with that of the standard. Gel exclusion chromatography revealed that the plasma contained a relatively large quantity of "big ACTH" which was found to be poorly detected by the IRMA. In the plasma of Addison's disease or the extract of pituitary gland in which "big ACTH" constituted a small portion, whole ACTH-LI was apparently diluted in parallel with the ACTH standard, although the "big ACTH" also did not show full parallelism with the ACTH standard in the IRMA. These data suggest that "big ACTH" derived not only from an ectopic ACTH-producing tumour but also from a normal human pituitary gland cannot be detected as well as authentic ACTH by the ACTH-IRMA system. Therefore, samples which contain a relatively large proportion of "big ACTH" in the total ACTH-LI should be carefully evaluated by ACTH-IRMA.

ACTH Syndrome, Ectopic↗

PubMed1989

Effects of recombinant human interleukin-1 alpha, -1 beta, 2 and 6 on ACTH synthesis and release in the mouse pituitary tumour cell line AtT-20.

The effects of recombinant human interleukin (rhIL)-1 alpha, -1 beta, 2 and 6 on the release of ACTH from the ACTH-producing tumour cell line AtT-20 of the mouse were studied during relatively long periods of incubation. Levels of ACTH in the media, measured by radioimmunoassay, were increased by the addition of rhIL-1 alpha or -1 beta after latent periods of more than 4 h. RhIL-1 alpha and -1 beta were almost equally potent in this experiment and the minimum, half-maximum and maximum effective concentrations of both rhIL-1 alpha and -1 beta were about 0.1 pmol/l, 1-3 pmol/l and 10-100 pmol/l respectively. During incubation with rhIL-1 beta, immunoreactive ACTH levels and mRNA levels of the ACTH precursor pro-opiomelanocortin in cells also increased without apparent changes in the growth rate of the cells. Although the AtT-20 cells used in this study were quite insensitive to human/rat corticotrophin-releasing hormone (CRH), the cells showed a significant response to CRH after incubation with rhIL-1 beta. RhIL-6 showed similar effects to those of rhIL-1 beta on ACTH synthesis and release; increasing ACTH in cells and media after a certain latent period. On the other hand, rhIL-2 did not change ACTH levels in the AtT-20 cells in this study. These observations indicate that rhIL-1 alpha, -1 beta and rhIL-6 have direct effects on ACTH-producing cells to stimulate the release and synthesis of ACTH after a latent period.

Adrenocorticotropic Hormone↗

PubMed1989