TI-201 uptake in an intracranial primary malignant melanoma.
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Biomedical subjects
Publications and source records attributed to T Miyazaki.
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Primary localized amyloidosis of the penile urethra is rare. We report a case in which the urethra was obstructed by amyloid tissue without evidence of systemic amyloidosis. After urethral dilatation, the patient reported a markedly improved urinary stream with minimal dysuria.
Pulmonary cryptococcosis was diagnosed by nested PCR. Extraction of DNA was performed by mechanical destruction of the capsules of Cryptococcus neoformans by the glass bead technique. Nested PCR was positive for 4 of 5 culture-positive specimens but negative for 1 culture-positive specimen, 10 culture-negative specimens, and 1 specimen with undetermined culture results.
We compared the specificities and sensitivities of four tests used for the serodiagnosis of candidemia in 39 patients with candidemia, including 10 patients with superficial Candida colonization, 10 patients with deep mycosis, and 20 healthy subjects. The results obtained by the dot immunoblotting assay for detecting the enolase antigen (48 kDa) were compared with those of assays for detecting mannan antigen, heat-labile antigen (a threshold titer of four times), and beta-glucan (> or = 60 pg/ml). Enolase antigen was detected in 28 (71.8%) patients with candidemia, while 30 (76.9%), 10 (25.6%), and 27 (84.4%) patients were positive for the heat-labile antigen by the Cand-Tec assay, the mannan antigen by the Pastorex Candida assay, and beta-glucan by the limulus test, respectively. Ten patients with superficial Candida colonization, 5 patients with invasive pulmonary aspergillosis, 5 patients with cryptococcosis, and 20 healthy subjects were negative for both enolase antigen and mannan antigen. Two patients with superficial Candida colonization, one patient with invasive pulmonary aspergillosis, and two patients with cryptococcosis were positive by the Cand-Tec assay. The beta-glucan concentration was more than 60 pg/ml in all patients with invasive pulmonary aspergillosis; however, it was less than 10 pg/ml in all patients with cryptococcosis. The specificity of enolase antigen in the serodiagnosis of candidemia was 100%, but the sensitivity was 71.8%. The specificity and sensitivity of Cand-Tec, the assay for mannan antigen, and the assay for beta-glucan were 76.9 and 87.5%, 25.6 and 100%, and 84.4 and 87.5%, respectively. Our results demonstrated that antigen detection tests are useful for the diagnosis of candidemia; however, none is satisfactory for the serodiagnosis of candidemia. We suggest that a combination of two assays may increase the accuracy of diagnosis of candidiasis.
The authors evaluated magnetic resonance (MR) angiography of the portal vein performed with a breath-hold, gadolinium-enhanced, magnetization-prepared rapid acquisition gradient-echo sequence in five volunteers and 24 patients. The main portal vein and its branches and the liver were depicted clearly in all images. The hepatic vein was clearly depicted in 21 of the 24 patients. MR angiography performed with this sequence allowed high-quality imaging of the portal and hepatic veins.
We examined the responses of epicardial (Epi) and endocardial (Endo) layers to ATP-sensitive K+ (KATP) channel modulators during regional ischemia in anesthetized dogs. Five-minute occlusion of the left anterior descending coronary artery was repeated at 30-min interval. Monophasic action potentials (MAPs) and extracellular K+ concentrations ([K+]o) were measured at Epi and Endo layers. 5-Hydroxydecanoate (5-HD, 30 mg/kg iv), a KATP channel blocker, or nicorandil (NCR, 0.2-0.5 mg/kg iv), an opener, was administered before the third or fourth occlusion. Shortening rate of action potential duration at 90% repolarization (APD90) was greater at the Epi layer than at the Endo layer during the first 4 min after the second control occlusion (19.7 +/- 1.5 vs. 13.1 +/- 2.4%, n = 14, P < 0.05). 5-HD suppressed the shortening preferentially at the Epi layer and reduced the difference between the two layers (11.0 +/- 3.5 vs. 11.5 +/- 3.7%, n = 6, NS). In contrast, NCR augmented the shortening preferentially at the Epi layer and increased the difference between the two layers at 4 min (29.0 +/- 2.0 vs. 5.9 +/- 3.0%, n = 6, P < 0.05). The time differentiation of [K+]o rise was similar at the two layers during the control occlusion (0.44 vs. 0.50 mM/min, n = 12). 5-HD reduced the rate of [K+]o rise at both layers (0.34 vs. 0.40 mM/min), whereas NCR augmented the rate at the Epi layer (0.82 vs. 0.50 mM/min). Activation of KATP channels appears to be involved in ischemia-induced APD shortening and [K+]o rise. The different responses of the two layers suggest a lower threshold for activation and/or a denser distribution of KATP channels or other K+ channels at the Epi layer.
Injection of anti-Thy-1 antibody into a rat induces immediate glomerular cell death and subsequent development of glomerulonephritis. Whether the immediate cell death in this model is apoptotic has yet to be determined. Recent in vivo studies on thymocyte death have elucidated that the Thy-1 molecule can activate intracellular signaling for apoptosis. This observation prompted us to re-examine whether stimulation with anti-Thy-1 antibody can provoke apoptosis in the rat glomerulus. We found that anti-Thy-1 antibody could induce laddered DNA fragmentation of isolated glomeruli and mesangial cells in culture, definite biochemical evidence for random double-stranded breaks through apoptosis. Such DNA laddering was also demonstrated in the isolated glomeruli of rats that had been infused with anti-Thy-1 antibody several hours before. Furthermore, the terminal deoxynucleotidyl-transferase-mediated oligonucleotide nick end labeling technique stained a cell in the mesangium. Although apoptosis may be considered a candidate mechanism mediating resolution of hypercellularity in the anti-Thy-1 model, we propose that it is also involved in the immediate cell death in this model.
We identified and quantified indoxyl-beta-D-glucuronide in uremic serum and urine to determine the metabolism of indoles including indoxyl sulfate in uremic patients. Serum levels of indoxyl-beta-D-glucuronide were markedly increased in undialyzed uremic patients, in patients on hemodialysis, and in patients on continuous ambulatory peritoneal dialysis. Urinary excretion of indoxyl-beta-D-glucuronide was also increased in undialyzed uremic patients. Urinary indoxyl-beta-D-glucuronide was significantly correlated with serum indoxyl sulfate, indicating that a high serum level of indoxyl sulfate leads to the enhanced synthesis of indoxyl-beta-D-glucuronide. Oral sorbent (AST-120) administration markedly decreased the serum and urine levels of indoxyl-beta-D-glucuronide as well as indoxyl sulfate in the undialyzed uremic patients. Serum indoxyl-beta-D-glucuronide could be efficiently removed by hemodialysis despite its high protein-binding ratio of about 50%. In conclusion, the serum level of indoxyl-beta-D-glucuronide increases in uremic patients due to renal insufficiency and its increased production. The production of indoxyl-beta-D-glucuronide can be suppressed by oral sorbent treatment, and serum indoxyl-beta-D-glucuronide can be efficiently removed by hemodialysis.
3-Carboxy-4-methyl-5-propyl-2-furanpropionic acid (CMPF) is accumulated in uremic serum as a major albumin-bound organic acid. We determined both serum and urine levels of total CMPF to calculate renal clearance of CMPF in healthy subjects and undialyzed uremic patients. Urinary excretion of CMPF and renal clearance were significantly decreased in the uremic patients. The relative clearance ratios of CMPF to creatinine were as low as 0.43% in healthy subjects and 0.45% in uremic patients, indicating that only the protein-unbound, free form of serum CMPF (about 0.4%) is ultrafiltrated in the glomeruli and then excreted into urine. In conclusion, CMPF is accumulated in uremic serum as a consequence of its reduced renal clearance. Urinary excretion of CMPF may be explained only by glomerular filtration of free CMPF in the blood.
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To investigate a role of the Maillard reaction in the pathogenesis of diabetic nephropathy, we measured serum levels of 3-deoxyglucosone (3-DG), a potent protein cross-linking intermediate of the Maillard reaction, and tissue contents of advanced glycation end products (AGEs) in streptozotocin (STZ)-induced diabetic rats. We quantified serum 3-DG using gas chromatography/mass spectrometry, and measured AGE contents in tissues using a competitive enzyme-linked immunosorbent assay with a monoclonal anti-AGE antibody. The STZ-induced diabetic rats showed nephropathy with proteinuria, hypoproteinemia, hyperlipidemia and reduced creatinine clearance. Serum levels of 3-DG in the STZ-induced diabetic rats (mean +/- 3.46 +/- 0.23 mumol/l) were significantly (p < 0.01) higher than those in control rats (1.23 +/- 0.13 mumol/l). AGE contents in the kidney and the lens obtained from the STZ-induced diabetic rats (398 +/- 45 and 816 +/- 200 arbitrary units, respectively) were also significantly (p < 0.01) higher than those in the control rats (122 +/- 10 and 299 +/- 50 arbitrary units, respectively). The results indicate that increased levels of serum 3-DG and renal tissue. AGEs may be related to the occurrence of diabetic nephropathy.
A new series of 2-arylmethyl-1,4-benzoquinones (2) was synthesized for evaluation of their pharmacological activities. These compounds showed significant inhibition of platelet aggregation induced by arachidonic acid (AA) and some of them possessed a protective effect against endothelial cell injury caused by hydrogen peroxide.
We report a patient with Brugada syndrome who developed sustained monomorphic ventricular tachycardia (SMVT). The patient was a 29-year-old man who experienced recurrent episodes of palpitation and syncope after drinking alcohol. Electrocardiogram showed right bundle branch block and ST-segment elevation in precordial leads V1-3 without Q-Tc prolongation. Organic heart disease and coronary artery disease were excluded by noninvasive and invasive tests. Ventricular fibrillation was induced by the application of a single extra-stimulus to the right ventricular outflow tract. During isoproterenol infusion, SMVT of left bundle branch block morphology (240/min) was induced by the application of a single extrastimulus to the right ventricular apex. SMVT also developed spontaneously. Pace mapping disclosed that SMVT originated at the free wall of the right ventricular outflow tract. Head-up tilt test and an alcohol provocation test both induced similar SMVT that was associated with hypotension and near syncope. SMVT was not terminated by intravenous administration of lidocaine, procainamide or adenosine triphosphate (10 mg), but was terminated by propranolol. Thus, a beta-adrenoceptor-mediated mechanism appears to play an important role in SMVT in this patient. The site of origin of SMVT might be closely related to the lesion that causes ST-segment elevation.
Polyclonal antibodies against P-1, a pectic polysaccharide fraction extracted with 0.5 M NaOH from the kernels of Prunus mume and consisted of arabino-galacturonan, and I-3, the partial acid (0.1 M trifluoroacetic acid) hydrolysate of P-1, were prepared in Japanese white rabbits. Competitive ELISA experiments strongly suggested that anti P-1 and anti I-3 antibodies were different but P-1 and I-3 cross-reacted with each other to recognize a partly similar epitope structure. The reactivities of polysaccharide fractions from the raw flesh of P. mume, and the kernels of apricot and peach extracted with either water or sodium hydroxide were examined using both antisera by the indirect competitive ELISA method. The polysaccharide fractions extracted with sodium hydroxide solutions had the reactivities but not those extracted with cold and hot water. These facts suggested that the similar structure of polysaccharides to P-1 was present in the flesh of P. mume and the kernels of apricot and peach. However, neither pectin of apple nor citrus had reactivity with each antiserum. P-1 would be different in chemical structure from a commercially available pectin, a water-soluble polysaccharide from apple and citrus.
P-1 was partially hydrolyzed with 0.01, 0.05, and 0.1 M trifluoroacetic acid (TFA), successively, and the dialyzable (E-1, E-2, and E-3) and non-dialyzable (I-1, I-2, and I-3) fractions were prepared and analyzed chemically and immunochemically. Either I-1 or E-1 reacted with anti P-1 serum as strongly as P-1 and were mitogenic. The cross-reactivity of I-2 and I-3 was less than I-1 with anti P-1 serum. However, they were as mitogenic as I-1. The cross-reactivity of E-2 and E-3 to anti P-1 serum was also very weak, and they were not mitogenic. The E-1 fraction had a similar sugar composition to I-1 and P-1. E-2 was a monosaccharide, all of Ara, and would be from the linkage of furanosyl residues in P-1. The composition of E-3 was free from Ara and the structure of E-3 was similar to that of I-3. E-3 would be considered to be deleted arabinofuranose from E-1. These results suggest that the mitogenic activity measured by the alkaline phosphatase assay is a property of the core part, I-3, but that P-1 contains several epitopes other than the core part by the immunochemical analysis.
We report here findings in a 51-year-old Japanese man with non-insulin-dependent diabetes mellitus who complained of exercise-induced cramps. Muscle biopsy showed scattered regenerating fibers, small angular fibers and increased PAS positive particles. Electron microscopic examination revealed an abnormal accumulation of glycogen particles in subsarcolenmmal areas and between myofibrils while chemical studies showed an increased glycogen concentration and decreased phosphoglycerate mutase (PGAM), 46.9% of the normal mean value. Thus, partial PGAM deficiency, insulin resistance and mild diabetic sensory-motor polyneuropathy can induce severe cramps.
OBJECTIVE: Images of breath-hold MR cholangiopancreatography (MRCP) using HASTE (half-Fourier acquisition single-shot turbo spin-echo) sequences were taken in healthy volunteers. The technique was then evaluated as a noninvasive alternative to direct cholangiopancreatography in patients with pancreaticobiliary diseases. SUBJECTS AND METHODS: Forty healthy volunteers and 56 patients with various pancreaticobiliary diseases were examined by MRCP using HASTE with 128 echo train lengths on a 1.5-T MR unit. A body phased-array coll was used for data collection. Imaging times were 2 sec for the single-slice technique with a 20-mm slice thickness and 18 sec for sequential acquisition by the multislice technique with a 5-mm slice thickness (effective TE, 87 msec). We used the healthy volunteers to determine our ability to detect normal structures. The results obtained by HASTE for both patient groups were correlated with imaging by percutaneous transhepatic cholangiography or endoscopic retrograde cholangiopancreatography. RESULTS: In all healthy volunteers, HASTE-MRCP showed both the common bile duct and the main pancreatic duct. Cystic ducts were visualized in 88% of these volunteers by HASTE-MRCP, and branches of pancreatic ducts were visualized in 75% by HASTE-MRCP. The diameter and length of dilated or stenotic ducts seen on HASTE-MRCP were correlated with percutaneous transhepatic cholangiography or endoscopic retrograde cholangiopancreatography images in 56 diseased patients. Not only the position of stenosis or dilatation but also the distal portion of the stenosis was visualized by HASTE-MRCP. CONCLUSION: Breath-hold HASTE-MRCP with a phased-array multicoil consistently allows for high-quality images of both normal and diseased pancreaticobiliary tracts. This technique can be used as a noninvasive screening method for pancreaticobiliary diseases in the majority of patients.
The "Cardiophone System" is a system designed to expand the relationship between patients and medical services using a transtelephonic electrocardiogram and computer-assisted answering system. The transtelephonic electrocardiogram, or so-called "Cardiophone", developed by Nihon Kohden, Inc., allows the patients to carry a "Cardiophone" to record electrocardiograms during paroxysmal occurrences of palpitation, chest pain, and other symptoms. The Cardiophone may function as a terminal of the host computer at the hospital, which stores the electrocardiogram and print it as soon as the computer receives the electrocardiogram over the phone. Cardiologists can examine the electrocardiogram immediately after it is printed. Cardiologists and operators are on duty 24 hours a day. Judgments based on the electrocardiogram are made by the cardiologist on duty, and stored in the computer by the operator. The patients may listen to the judgment over the phone within 30 min of sending the electrocardiogram. In the case of potentially lethal findings on the electrocardiogram, the cardiologist on duty calls the patient directly to give a medical advice. We studied 184 outpatients who were enrolled in the Cardiophone System of our hospital. The average number of transtelephonic electrocardiograms was 10 per day. Abnormal electrocardiographic changes were observed in 42 patients, and the diagnoses were as follows: paroxysmal supraventricular tachycardia in 18 patients, paroxysmal atrial fibrillation in 17, ventricular tachycardia in 3, and angina in 7. Among seven patients in whom ST changes were documented by Cardiophone, six were diagnosed as variant angina. In several patients with diagnoses already made by Holter monitoring, the Cardiophone was used to monitor the drug effects and the correlations between symptoms and arrhythmic events. We conclude that the Cardiophone System is useful for diagnosing the causes of paroxysmal cardiac symptoms in some patients and for improving home medical services.