Biomedical subjects
Publications and source records attributed to Y Ueda.
A 61-year-old woman with a giant aneurysm of the coronary arterial fistula between the left anterior descending coronary artery and the main pulmonary artery underwent aneurysmal resection and closure of the fistula. This was a very unusual case with rare congenital malformation with secondary atherosclerotic change.
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We performed two studies to investigate the effect of probucol on atherogenesis in vivo in the Watanabe heritable hyperlipidemic (WHHL) rabbit. In the first study (Study A), probucol was administered to 2-month-old WHHL rabbits, to evaluate its long-term effect. When killed at about 1.5 years of age, the percentage area of aorta covered with atherosclerotic plaque in probucol-treated rabbits was markedly less than that seen in non-treated rabbits (23.0 +/- 11.4% vs. 87.7 +/- 8.1%, M +/- S.D., P less than 0.001). In the second study (study B), administration of probucol was commenced with 8-month-old WHHL rabbits to investigate whether the drug was effective for limiting atherosclerosis in rabbits in which plaques had already developed. When killed after 6 months of treatment, the percentage area of aorta covered with plaque was 38.1 +/- 12.1% in treated rabbits and 82.7 +/- 22.6% in non-treated rabbits (P less than 0.02). Microscopic observations of lesions also supported the effect of probucol. Probucol treatment resulted in a change not only in the size but also the composition of lesions. Thus, probucol was effective in preventing atherosclerosis in long-term studies at both early and late stages.
In order to study the effect of jugular venous outflow obstruction on intracranial pressure and cerebrospinal fluid (CSF) reabsorption capability, changes in epidural pressure (EDP) and CSF outflow resistance (Ro) were examined following bilateral jugular vein ligation in cats. EDP increased significantly (P less than 0.01) immediately after ligation from the control value of 4.9 +/- 0.5 mmHg (mean +/- SEM) to 15.9 +/- 0.9 mmHg. Thereafter, EDP gradually decreased back toward the control value. The pressure level had decreased to 6.7 +/- 0.5 mmHg by 20 minutes after ligation. The mean Ro was significantly (P less than 0.01) higher in the ligation group (200.4 +/- 9.7 mmHg/ml/min) that in the non-ligation group (120.0 +/- 9.9 mmHg/ml/min). These results suggest that bilateral jugular vein ligation impairs CSF reabsorption.
From 1987 to February 1991, we have repaired or replaced the aortic arch in ten patients using deep hypothermic systemic circulatory arrest with continuous retrograde cerebral perfusion (CRCP). CRCP can be implemented using the bypass connecting the arterial and venous lines of the extracorporeal circuit to reverse the flow into the superior vena cava cannula after induction of circulatory arrest. CRCP flow required to maintain an internal jugular vein pressure of 20 mmHg ranged from 100 to 500 ml/min. After completion of suturing of the aortic arch graft, air is evacuated retrogradely from the open arch vessels prior to reestablishing the usual arterial return. Two patients died, one from sepsis and the other from liver cirrhosis 1 month postoperatively. CRCP times ranged from 11 to 56 min, and minimal nasopharyngeal temperatures ranged from 16 degrees to 18 degrees C. The difference in oxygen content between the perfused blood and the blood draining from the arch vessels during CRCP most likely reflected the steady-state metabolism of the brain during the deep hypothermic state. This technique offers advantages including the need for dissecting and clamping the arch branches, providing sufficient metabolic support to the brain during deep hypothermia, and eliminating embolism of particulate debris from the aortic arch.
We describe five patients with IgA-nephropathy complicating diabetes mellitus. In four cases, diabetic glomerulosclerosis was present at the same time. One patient suffered from dermatitis herpetiformis. The observation of the present five cases together with the notion of an increased prevalence in diabetes mellitus of celiac disease and dermatitis herpetiformis suggests that the occurrence of IgA-nephropathy in diabetic patients is not mere coincidence.
A 49-year-old man who had undergone repair of tetralogy of Fallot underwent replacement of a thrombosed St. Jude Medical prosthesis in pulmonary position after intravenous thrombolytic therapy. Dysfunction of the prosthetic valve was detected clinically by change of heart sound and the appearance of a new diastolic murmur. Cinefluoroscopy confirmed fixation of both leaflets. Although thrombolytic therapy using urokinase was successful twice, the prosthesis was replaced with a Carpentier-Edwards bioprosthesis due to recurrent prosthetic dysfunction.
Seventy-five osteosarcomas at various grades of histologic differentiation were investigated for evidence of osteonectin. According to the results of the study, osteonectin was present in all osteosarcomas. An association between the intensity of the osteonectin antibody reaction and prognosis could not be established. Evidence of osteonectin was also found in other bone tumors. Osteonectin is therefore unsuitable for differential diagnosis, cannot be regarded as a bone specific protein and has not prognostic value.
Amino acid sequences were analyzed for two isoforms of myosin essential light chain, LC17a and LC17b [Hasegawa, Y., Ueno, H., Horie, K., & Morita, F. (1988) J. Biochem. 103, 15-18] from porcine aorta smooth muscle. Both LC17a and LC17b consisted of 150 amino acid residues and their N-terminal Cys residues were blocked by an acetyl group. The amino acid sequences of LC17a and LC17b were common from the N-terminal to Glu-141 and five amino acid substitutions were observed within the remaining C-terminal 9 residues. The amino acid sequences of LC17a and LC17b were identical to those deduced from the nucleotide sequences of bovine aortic cDNAs encoding the two isoforms [Lash, J. A., Helper, D.J., Klug, M., Nicolozakes, A.W., & Hathaway, D.R. (1990) Nucleic Acids Res. 18, 7176].
A proteinaceous protease inhibitor was isolated from the culture broth of Streptomyces lividans 66 by a series of purification steps (salting out by ammonium sulfate, ion-exchange chromatography on DEAE-cellulose, hydrophobic chromatography on Phenyl-Sepharose, and gel-filtration on Sephacryl S-200), and was named S. lividans protease inhibitor (SLPI). The purified SLPI existed in a dimeric form consisting of two identical subunits, each of which was composed of 107 amino acids. SLPI exhibited strong inhibitory activity toward subtilisin BPN'. These features were similar to those of protein protease inhibitors produced by other Streptomyces (SSI family inhibitor). In addition, SLPI was capable of inhibiting trypsin with an inhibitor constant (Ki) of about 10(-9) M. The primary structure of SLPI and location of two disulfide bridges were homologous to those of the other serine protease inhibitors of Streptomyces. The reactive site of SLPI was found to be Arg67-Glu68 from the sequence analysis of cleaved SLPI which was produced by acidification of subtilisin-SLPI complex. An Arg residue at the P1 site was consistent with the trypsin-inhibitory property of SLPI. Sequence comparison with other members of the SSI family revealed that amino acid replacements in SLPI were mainly localized on the surface of the SLPI molecule, and many of the amino acid residues in beta-sheets and hydrophobic core were well conserved.
A 34-year-old Japanese male had leg pain, edema of the legs, hypohidrosis, whorl-like opacities of the bilateral cornea, bilateral subcapsular cataracts, and chest discomfort on exercise. He had no characteristic angiokeratomas but did have telangiectases. The electrocardiogram revealed high voltage. The echocardiogram revealed mild mitral regurgitation. The alpha-galactosidase A activity in cultured lymphoblasts was deficient (0.5 nmol/h/mg protein). Electron microscopic examination of the skin revealed lamellar cytoplasmic inclusions in the endothelial cells, pericytes, and fibroblasts. He had a G--> A transition at nucleotide 982 in the coding sequence of the alpha-galactosidase A gene which resulted in a glycine to arginine amino acid substitution at residue 328. His uncle also had leg pain, edema of the legs, hypohidrosis, and chest pain on exercise. He had no characteristic angiokeratomas but did have telangiectases. Cardiovascular examination revealed hypertrophic cardiomyopathy and stenoses of coronary arteries. Electron microscopic examination of the skin revealed lamellar cytoplasmic inclusions in the endothelial cells, pericytes, and fibroblasts.
We studied myelodysplastic syndrome-associated inhibitory activity (MDS-IA), which inhibited colony formation in vitro of normal granulocyte-macrophage progenitors (CFU-GM). When adherent marrow cells were incubated with fetal calf serum for 21-24 d, monocyte-derived lipid containing huge macrophages (MDLM) developed. MDLM from MDS marrow (MDS-MDLMs) and their conditioned medium (MDLM-CM) consistently suppressed the growth of normal CFU-GM colony formation. MDS-IA was active on CFU-GM during the S-phase and relatively resistant to heating. Monoclonal antibody against H subunit (acidic) ferritin and polyclonal antibody against placental ferritin neutralized the inhibitory activity of MDS-MDLMs. In addition, cell lysates of MDS-MDLMs reacted to both monoclonal anti-H subunit ferritin and polyclonal anti-placental ferritin in Western blotting analysis, indicating that the inhibitory activity was predominantly acidic isoferritin. On the other hand, MDLMs obtained from normal bone marrow had a CFU-GM enhancing activity. These results suggest that MDS-MDLMs may be responsible for the suppression of granulopoiesis in patients with MDS and that the suppression may be mediated by soluble factors, notably H subunit isoferritin.
Tissue localization of collagenous and basement membrane proteins in the extracellular matrix of five sacro-coccygeal chordomas and human fetal notochords was examined immunohistochemically to assess the implications for the histogenesis and histological diagnosis of chordoma. Human fetal notochords and conventional chordomas both exhibited basement membrane proteins (such as type IV collagen and laminin) and type VI collagen on the surfaces of cellular cords. Type II collagen, a main structural protein of cartilage, was also present in both tissues. In the chordomas, however, type II collagen was not so widespread as it was in the notochords, and the predominant collagenous protein was type I. In contrast, an altered deposition of these proteins was noticed in a recurrent tumour which, histologically, showed considerable atypia and eventually metastasized to the liver. The characteristic cartilage-type and basement membrane proteins disappeared and unusual collagen types, such as types III and V, appeared in the stroma. The results further support the notochordal origin of chordoma and suggest that the immunohistochemistry of collagenous and basement membrane proteins may be a helpful criterion for the histological diagnosis and prediction of the biological aggressiveness of chordomas.
The Working Party for Legionellosis headed by the Japanese Ministry of Health and Welfare processed to standardize the diagnostic procedures for Legionella pneumonia, as the first step to clarify the actual occurrence of patients with this respiratory disease. All the clinical data were collected and analysed on the 28 culture-confirmed patients in Japan during the past 11 years, from 1980 through 1990. The 28 patients were distributed throughout Japan, from Hokkaido to Kyushu. Out of 28 patients, 18 were community-acquired and 10 were nosocomially infected. In 8 of 18 community-acquired patients, any significant underlying disease was not observed. Though it was dominant in the age group in their 60s & 70s, victims were distributed in adults over 20 years of age and even in a new born baby. Only 5 out of 28 patients recovered successfully. From the autopsy findings, in 5 out of the remaining 23 expired patients, Legionella pneumonia seemed to be successfully treated, but other disease or other bacterial pneumonia put an end to the patients. The results of clinical laboratory tests and the efficacy of antibiotics to Legionella pneumonia were essentially the same as those reported in the literature.
We analyzed the initial and follow-up chest radiographs of 28 patients with culture-positive Legionella pneumonia, and developed a scoring system to quantitate the severity of radiological findings for pneumonia. Intrapulmonary shadows were observed on the initial chest radiograph in 26 patients, but pleural effusion was noted in only one. In one patient the initial chest radiograph had probably been obtained too early to reveal any pulmonary change. Alveolar shadows were noted on the initial radiograph in 21 (81%) patients, and interstitial shadows in 5 (19%). In ten (38%) patients shadows were present in both lung fields. Shadows were prominent in the middle and lower lung fields. A cavity was noted in only one patient, and pleural effusion was also noted at some time during the clinical course in 19 (70%). A large amount of pleural effusion was observed in four patients. The average pneumonia severity score was 3.3 in the 9 patients who survived, and 5.1 in the 17 who died (p > 0.05). The mortality rate was 53% in the 17 patients with pneumonia severity score of 5 or less and 89% in the 9 patients with a score of 6 or more (p > 0.05). Twelve patients died within one week after the initial chest radiograph was obtained. There were no differences among patients with community-acquired infection with or without underlying disease and those with nosocomial infection in characteristic and extension of shadow, presence of pleural effusion, or pneumonia score. The chest radiograph of Legionella pneumonia include bilateral shadow findings characteristic, pleural effusion and rapid progression of shadow, and are clinically useful for diagnosis.
We examined the effects of moxibustion on primary sensory neurons in the skin of rats using immunocytochemistry combined with a fluorescent retrograde tracer dye, fluoro gold (FG). Galanin-like immunoreactive (IR) fibers were often observed in the dermis of treated skin at 18 hours after moxibustion, while such fibers were rarely detected in untreated (control) skin. Moreover, most of galanin-IR fibers also displayed substance P (SP)-like immunoreactivity. About 20-30% of the dorsal root ganglion (DRG) neurons labeled when FG was injected intradermally into the moxibustion-treated skin showed galanin-like immunoreactivity, while the proportion of FG-labeled neurons with such immunoreactivity was less than 10% in control DRGs. These results show that moxibustion induced galanin expression by primary sensory neurons containing SP. The possible functions of this peptide are discussed in relation to the effects of moxibustion.
1. Horizontal cells of the cat retina were isolated by enzymatic dissociation. Two types of horizontal cells were identified: the axonless (A-type) horizontal cell having four to six thick, long (approximately 100 microns) dendrites, and the short-axon (B-type) horizontal cell having many (> 5) fine, short (approximately 30 microns) dendrites. 2. Membrane properties of isolated horizontal cells were analyzed under current-clamp and voltage-clamp conditions. In the A-type cell, the average resting potential was -55 mV and the mean membrane capacitance was 110 pF, whereas values in the B-type cell were -58 mV and 40 pF, respectively. The A-type cell showed long-lasting Ca spikes, but B-type cells had no Ca spikes. 3. Five types of voltage-dependent ionic currents were recorded: a sodium current (INa), a calcium current (ICa), and three types of potassium currents. Potassium currents consisted of potassium current through the inward rectifier (Ianomal), transient outward potassium current (IA), and potassium current through the delayed rectifier (IK(v)). INa was recorded only from A-type cells. Other currents were recorded from both types of cells. 4. INa activated when cells were depolarized from a holding potential (Vh) of -95 mV, and it was maximal at -25 mV. This current was blocked by tetrodotoxin. Approximately half of the A-type cells had INa, but no B-type cell had this current. 5. L-type ICa, an inward-going sustained current, was activated with depolarization more positive than -25 mV. Current amplitude reached a maximal value near 15 mV and became smaller with further depolarization.(ABSTRACT TRUNCATED AT 250 WORDS)
The role of the reactive oxygen species (ROS) in the induction of tissue injury has been well documented. Regarding glomerular injury, the focus of past studies has been on superoxide, hydrogen peroxide, hydroxyl radical and C10-. However, whether singlet oxygen, an exceptionally reactive oxygen metabolite, may cause glomerular lesions has not been investigated. In the present study we documented the effects of locally generated singlet oxygen in the kidney. To generate singlet oxygen, kidneys were perfused with the pigment pheophorbide a, which was followed by exposure to light. One hour after irradiation, severe morphological damage of the glomerular cell had developed. Extensive deposits of fibrin and accumulation of platelets were seen in the glomerular capillary lumina. By contrast, kidneys not exposed to light showed no, or only minimal, abnormalities. Glomerular injury was not inhibited by pretreatment with superoxide dismutase. These results suggest that singlet oxygen produced by pheophorbide a by photodynamic reaction leads to tissue injury in vivo.