Biomedical subjects
Publications and source records attributed to T Mitsui.
The case of a 67-year-old male with double-vessel coronary artery disease combined with a severely calcified ascending aorta, moderate aortic insufficiency, cholecystic stones, and unruptured intracranial aneurysm is presented. Successful coronary artery bypass reoperation is described using the right gastroepiploic artery through an additional left anterior thoracotomy on the beating heart.
The intracellular localization of dystrophin and beta-dystroglycan mRNA in skeletal muscles of patients with Duchenne muscular dystrophy (DMD) or Becker muscular dystrophy (BMD) and normal subjects was examined by in situ hybridization using biotinylated oligonucleotide probes. These mRNAs were found preferentially in sarcolemma in the skeletal muscles of both normal subjects and affected patients. Quantitative analysis of mRNA signals demonstrated no prominent reduction of dystrophin or beta-dystroglycan mRNA in DMD/BMD muscles. These results suggest that even mRNAs with deletions contain specific information that affects their localization, and the characteristic defect of dystrophin in DMD/BMD muscles seems to be caused mainly by the instability of dystrophin protein, as a post-transcriptional event.
BACKGROUND: The systemic use of prostaglandin E1 (PGE1) in the treatment of peripheral vascular disease is well documented. It is known that the liposomal formulation of some drugs enhances their transdermal absorption. OBJECTIVE: The potential of topical application of lipid microspheres containing PGE1 (lipo-PGE1) to treat ischemic ulcers was evaluated. METHODS: Lipo-PGE1 ointment (1 microgram/g) was applied topically to peripheral ischemic ulcers in 10 patients for 5.8 weeks (range 4-9 weeks). The patients were followed up for 6 months, and response was assessed comparing photographs of the lesions. RESULTS: Nine of 10 patients responded to treatment, but in 3 patients, the ulcers recurred after cessation of treatment. CONCLUSION: It is concluded that lipo-PGE1 ointment provides an alternative to the management of patients with incurable peripheral ischemic ulcers.
A 66-year-old male with the congestive heart failure was diagnosed grade 4 aortic valve regurgitation due to quadricuspid valve associated with bacterial endocarditis, widely patent left coronary artery ostium, chronic renal failure, and secondary hyperparathyroidism. Coronary arteriography showed that the size of left coronary ostium was widely patent 10 mm in diameter, and trans-esophageal echo cardiogram revealed perforation and vegetations on the coronary cusps of the aortic valve.
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We describe an 11-year-old girl with a mild bleeding disorder since early childhood. The disorder was characterized by a prolonged bleeding time, and the patient's platelets showed defective aggregation responses to thromboxane A2 (TXA2) mimetic U46619 and arachidonic acid. In contrast, the platelets showed normal responses to thrombin and Ca ionophore A23187. When the platelet TXA2 receptor was examined with the [3H]-labeled TXA2 agonist U46619, the equilibrium dissociation rate constants (kd) and the maximal concentration of binding sites (Bmax) of the patient's platelets were within normal ranges. Normal GTPase activity was also induced in the patient's platelets by stimulation with U46619, however, inositol 1,4,5-triphosphate (IP3) formation was not induced by U46619. These results suggests that the patient's platelets had a defect in phospholipase C activation beyond TXA2 receptors.
Two-months-old baby underwent complete correction by Barbero-Marcial's procedure for type I truncus arteriosus. Postoperative hemo-dynamics was fairly stable immediately after the operation. However, the acute rise in pulmonary pressure occurred on the 2nd postoperative day. The pulmonary vasodilation therapy with prostaglandin E1 and amrinone had failed. Thirty ppm of inhaled nitric oxide (NO) was started and it resulted in an immediate decrease in pulmonary arterial pressure. Complete weaning from NO was achieved 9 days after surgery by simultaneous administration of PGE1 and amrinone. Although inhalation of NO reduced pulmonary arterial pressure, combination of PGE1 and amrinone with NO inhalation exerted a pulmonary vasodilation and brought the patient to full recovery in this case with pulmonary hypertensive crisis.
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We report two cases of encephalo-myelo-radiculoneuropathy, triggered by herpes simplex virus type-1 (HSV-1) infection. Patient 1 (a 25-year-old man) and patient 2 (a 52-year-old man) were admitted to the hospital because of fever, headache, abnormal behavior, and loss of consciousness. In each case, cerebrospinal fluid (CSF) showed lymphocytic pleocytosis with protein elevation, and serum and CSF IgG antibody titers to HSV-1 were elevated markedly. Although patient 1 was treated with aciclovir in the early phase of encephalitis, he developed severe quadriparesis as a sequela. Patient 2 was treated with a combination of aciclovir and corticosteroids, and he recovered completely about 4 months after the onset of the disease. There have been only a few reports of encephalo-myelo-radiculoneuropathy triggered by HSV-1 infection. Early corticosteroid therapy was effective in our patients with post-HSV-1 infectious encephalo-myelo-radiculoneuropathy. These two patients were studied with flow cytometry for peripheral blood lymphocyte subsets during the disease course. In the active stage of the disease, the helper-inducer (CD4 + CD29+), activated T cell (CD4 + CD25+), and cytotoxic/NK (CD8 Dull + CD11b Bright+) subsets were increased compared with subsets in controls. An interesting finding was mismatched responses with an increased suppressor-inducer (CD4 + Leu8+) subset and a decreased suppressor-effecter (CD8 Bright+ CD11b Dull+) subset, indicating a possible autoimmune character of encephalo-myelo-radiculoneuropathy triggered by viral infection.
The oligonucleotides containing 2'-(6-dimethylamino-2-naphthamide)uridine [U(DAN)] at the different position were synthesized by the fully automated solid phase phosphoramidite methods. The UV melting profiles for the U(DAN)-modified oligonucleotides with complementary DNA exhibited sigmoidal curves whose shapes were similar to those for the unmodified duplexes.
A model is proposed for myosin head motion along an actin filament which accommodates recent experimental data. The model includes three attached states of a myosin head and is thus similar to the classical Huxley & Simmons (1971) model, but differs in that an explicit expression is given for the spatial distribution of potential energy wells for the myosin head. Our model also differs from the classical model, in that it assumes that the proportion of myosin heads attached to actin filament is constant and independent of shortening velocity, as suggested by X-ray diffraction data. Furthermore, it posits that the crossbridge is string-like rather than spring-like. This modified model fits well to the experimental data in the following respects. (1) The calculated tension dependence of muscle stiffness agrees with the observation by Ford et al. (1985 J. Physiol. 361, 131-150). (2) A myosin head under low load can move as far as 60 nm along an actin filament during one ATP hydrolysis cycle in muscle, in agreement with the results by Yanagida et al. (1985 Nature 316, 366-369) and others. (3) The model predicts that such movements consist of a series of elementary steps of 11 nm. (4) A single myosin head hardly moves after the first step of 11 nm under the condition of in vitro experiment carried out by Finer et al. (1994 Nature 368, 113-119), in agreement with their observation. (5) The calculated energy liberation rate reproduces the characteristics of Hill's equation. (6) The "double-hyperbolic force-velocity relation" reported by Edman (1988 J. Physiol. 404, 301-321) can be understood in terms of a potential barrier against movement of a potential well in which a myosin head is trapped.
We purified the nicotinic acetylcholine receptor from digitonin-solubilized rabbit skeletal muscle by affinity chromatography and detected many proteins linked to AChR, including dystrophin, adhalin, beta-dystroglycan, utrophin, rapsyn, and actin. To determine whether or not AChR links to dystrophin-associated proteins (DAPs) without dystrophin, we studied the effects of denervation on AChR and DAPs in the skeletal muscle of a mdx mouse. Following surgical denervation, the levels of adhalin and beta-dystroglycan dramatically increased at the extrajunctional sarcolemma with AChR, suggesting that their association is independent of dystrophin. Furthermore, the diffuse extrajunctional appearance of adhalin, beta-dystroglycan, and AChR was observed after pharmacological denervation through the subcutaneous administration of succinylcholine. Since the depletion of DAPs and the subsequent disruption of sarcolemmal linkage are believed to be a primary cause of muscle cell necrosis in dystrophinopathies, pharmacological denervation may have some beneficial effect on these diseases.
BACKGROUND: A recently discovered non-A-E hepatitis virus has been designated hepatitis GB virus C (HGBV-C), but little is known about its mode of transmission and its clinical manifestations. We studied 519 patients on maintenance hemodialysis to determine whether they were infected with HGBV-C. METHODS: HGBV-C RNA was identified in serum by a reverse-transcription-polymerase-chain-reaction assay with nested primers deduced from a non-structural region. A nucleotide sequence of 100 bp in the nonstructural region was determined on HGBV-C clones. RESULTS: HGBV-C RNA was detected on 3.1 percent of the patients on hemodialysis (16 of 519), as compared with 0.9 percent of healthy blood donors (4 of 448, P<0.03). None of the 16 patients had evidence of active liver disease, although 7 were also infected with hepatitis C virus. Eight patients with HGBV-C infection were followed for 7 to 16 years. In two patients the virus was present at the start of hemodialysis. One had a history of transfusion, and HGBV-C persisted over a period of 16 years; the other became free of HGBV-C after 10 years. In five patients, HGBV-C RNA was first detected 3 to 20 weeks after blood transfusion and persisted for up to 13 years. One patient with no history of transfusion was infected with an HGBV-C variant with the same sequence as in two of the patients with post-transfusion HGBV-C infections. CONCLUSIONS: Patients on maintenance hemodialysis are at increased risk for HGBV-C infection. This virus produces persistent infections, which may be transmitted by transfusions but may also be transmitted by other means.
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From 1983 to 1994, 12 advanced thymomas with invasion to the great vessels were initially treated by irradiation (mean dose, 18.3 Gy) and subsequent surgical resection. In nine patients, complete resection was possible by concomitant resection of the surrounding tissues, mainly pericardium and/or brachiocephalic vein. Histologically, all tumors showed prominent fibrosis. Ten patients also received postoperative radiotherapy (mean dose, 42.3 Gy). Tumor-related deaths occurred in only two patients; one who did not receive postoperative irradiation 21 months and one who had viable cells at the surgical margin 10 months after operation. However, there were also 2 patients who died of respiratory failure due to operation and/or irradiation, one 45 days and the other 7 years after the treatment. Preoperative radiotherapy could facilitate complete resection of the advanced thymomas. The prognosis of the patients treated with preoperative radiotherapy seemed fair if followed by adequate resection and subsequent irradiation.
The localization and amounts of myoglobin (Mb) and Mb mRNA in ragged-red fibers (RRF) in skeletal muscle of 6 patients with mitochondrial encephalomyopathy were examined immunohistochemically and by in situ hybridization. The amounts of Mb and Mb mRNA were expressed in terms of optical densities (ODs) of Mb immunostaining and Mb mRNA signals. In nonatrophic RRF, Mb was predominantly seen in the ragged-red region and Mb mRNA signals were increased throughout the sarcoplasm. The amounts of Mb and Mb mRNA in nonatrophic RRF were greater than those in nonatrophic non-RRF. In contrast, the localization and amount in atrophic RRF were similar to those in atrophic non-RRF. Thus, Mb synthesis in nonatrophic RRF may increase to compensate for mitochondrial dysfunction and to supply sufficient oxygen to mitochondria, but this compensatory function may be impaired in atrophic RRF.
Human T-lymphotropic virus type l (HTLV-I) protein and messenger RNA (mRNA) for HTLV-I were examined in thyroid tissues from two patients with Hashimoto's thyroiditis and serum anti-thyroid antibody. The virus envelope protein and signals for the mRNA were detected in many of the follicular epithelial cells of the thyroid tissue from one of the patients, respectively, by immunohistochemistry and in situ hybridization. PCR-Southern blotting revealed the presence of HTLV-I DNA in the thyroid tissue, in which the viral protein and mRNA were detected, although no virus particles were found in the epithelial cells by electron microscopy. HTLV-I virus was not present in the thyroid tissue from the second patient. The present findings suggest that infection of thyroid tissue with HTLV-I is associated with the pathogenesis of Hashimoto's thyroiditis in some patients.