What are the indications for 99mTc-sestamibi scintigraphy in hyperparathyroidism?
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Biomedical subjects
Publications and source records attributed to S Satake.
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Rat liver is known to contain a regulatory protein (RP) that inhibits glucokinase competitively with respect to glucose. By an immunohistochemical technique and by cell fractionation in glycerol, we investigated the distribution of RP in rat liver and its changes in response to high glucose. RP was detected almost exclusively in the nuclei of the parenchymal cells of both fed and fasted rats. In situ perfusion of the liver with 20 mM glucose for 10 min caused a marked decrease in nuclear RP and an increase in cytoplasmic RP. These results indicate that RP is present predominantly in the nuclei of hepatocytes and is translocated from the nucleus to the cytoplasm in response to high glucose.
To determine the mechanism of the antiatherosclerotic effect of estrogen, we investigated the effect of estrogen on endothelial nitric oxide synthase (NOS-3). Preincubation with a physiologic concentration of 17 beta-estradiol (10(-12)-10(-8) M) over 8 hours significantly enhanced the activity of NOS-3 in endothelial cells of cultured human umblical vein (HUVEC) and of bovine aortas (BAEC). 17 beta-estradiol also enhanced the release of nitric oxide (NO) as measured by an NO selective meter and NO2-/NO3-, metabolites of NO, from endothelial cells. Western blot showed a similar effect of 17 beta-estradiol on NOS-3. The estrogen receptor antagonists, tamoxifen and ICI182780, each inhibited the effect of 17 beta-estradiol by 80%. The effect of 17 beta-estradiol gradually decreased in cells beyond the 10th passage and was not significant in cells beyond the 16th passage. Immunocytochemistry showed the existence of estrogen receptor in HUVEC and BAEC (less than 5 passages) and the sparseness of the existence in BAEC beyond the 16th passage. Estrogen increases NOS-3 via a receptor-mediated system, and estrogen receptor, which appeared to be altered by cell senescence, could be important in the release of NO from endothelium.
Evaluation of four beta-lactamase inhibitors in terms of their outer membrane permeability in Pseudomonas aeruginosa revealed that sulbactam and tazobactam diffused most efficiently and equally well. That of BRL42715 appeared to be a factor of ten lower than that of the above two, but it showed the strongest beta-lactamase inhibitory activity. This is most likely due to its better beta-lactamase inactivating activity. BRL42715 at 1.56 micrograms ml-1 lowered the minimum inhibitory concentrations of ceftazidime and imipenem in a strain producing fully derepressed beta-lactamase and an undetectable level of the outer membrane protein OprD2.
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The development of atherosclerotic plaque is associated with neovascularization in the thickened intima and media of vascular walls. Neovascularization may have a role in the progression of atherosclerotic plaque as well as in the development of intraplaque hemorrhage. However, the mechanism and stimulus for neovascularization in atherosclerotic plaque are unknown. We postulated that smooth muscle cells (SMCs), a major cellular component in the vascular wall, might contribute to the induction of neovascularization in atherosclerotic plaque through the secretion of an angiogenic factor. We observed that endothelial cells (ECs) cultured on collagen gel with SMC-conditioned medium became spindle shaped, invaded the underlying collagen gel, and organized a capillary-like branching cord structure in the collagen gel. The conditioned medium also stimulated EC proliferation and increased the EC-associated plasminogen activator activity. The angiogenic factor in SMC-conditioned medium was retained in a heparin-Sepharose column and eluted with 0.9 M NaCl. Neutralizing anti-vascular endothelial growth factor (VEGF) antibody attenuated the angiogenic activity in the conditioned medium, including the induction of morphologic changes in ECs, mitogenic activity, and increased plasminogen activator activity associated with ECs. Immunoblotting analysis confirmed the secretion of VEGF from SMCs. These observations indicate that SMC may be responsible for the neovascularization in atherosclerotic plaque through the secretion of VEGF.
The insect brain neuropeptide, prothoracicotropic hormone (PTTH), elicits the molting process by stimulating ecdysteroidogenesis in the prothoracic glands. Changes in the subcellular distribution of PTTH during the fifth larval instar and larval-pupal metamorphosis of Bombyx were investigated using immunogold electron microscopy and computerized image analysis. A time-resolved fluoroimmunoassay was employed to quantify the hemolymph PTTH titer and the hemolymph ecdysteroid titer was determined by radioimmunoassay. Immunoreactivity was apparent only in the cytoplasm of two pairs of dorsal-lateral neurosecretory cells (La) in the brain, the prothoracicotropes, and their axons that traverse the peripheral area of the brain neuropil and then enter the neurohemal lobes of the corpora cardiaca and end in the corpora allata. Immunospecificity was evident as noted by the restriction of the 5-nm gold particles to the neurosecretory granules. Synaptic contacts were noted frequently between the dendritic collaterals of the prothoracicotropes and neighboring collaterals from other neurons. The morphological data suggest that PTTH is synthesized and released throughout the fifth larval instar. The concentration of gold particles in the neurosecretory granules and the number of neurosecretory granules increased five times during the fifth instar, and these increases were correlated with surges in the hemolymph PTTH and ecdysteroid titers. The data suggest that PTTH biosynthesis, secretory granule formation, and secretion are three continuous and almost synchronized events.
Ventricular tachycardia (VT) with right bundle branch block QRS morphology and left axis deviation originating in the inferolateral apical segment of the left ventricle was found in a 24-year-old man without overt structural heart disease. Intracardiac recordings during VT showed atrioventricular dissociation with the earliest activation at an apical inferolateral site in the left ventricle, where Purkinje fiber potentials were recorded fusing in the ventricular electrogram. Ventricular pacing was performed at this site, and yielded a QRS morphology identical to the VT. Radiofrequency current was applied and resulted in the complete elimination of VT.
OBJECTIVES: The purpose of this study was to evaluate the effects of thermal balloon percutaneous transluminal coronary angioplasty using radiofrequency energy in the treatment of patients with failed coronary angioplasty and complex lesions. In addition, we evaluated restenosis after radiofrequency thermal balloon applications. BACKGROUND: The efficacy of coronary angioplasty is limited by the relatively low success rate in complex lesions and the high frequency of restenosis. Few reports have studied the combined effects of pressure and laser thermal energy. This study describes a new device for coronary angioplasty using radiofrequency thermal energy. METHODS: Thirty-two patients with failed conventional coronary angioplasty or complex lesions were treated with radiofrequency thermal balloon coronary angioplasty. Radiofrequency energy was delivered up to 11 times in exposures ranging from 30 to 60 s in duration. This combined effect allowed the vascular wall to be heated to temperatures ranging from 60 to 70 degrees C. Follow-up coronary angiography was performed, on average, 6 months after the procedure. RESULTS: Successful radiofrequency coronary angioplasty was achieved in 28 (82%) of 34 lesions. There was one abrupt coronary artery occlusion (3%) and no death, perforation or dissection. Angiographic restenosis occurred in 14 (56%) of 25 lesions. CONCLUSIONS: In patients with failed coronary angioplasty and difficult complex lesions, radiofrequency coronary angioplasty could potentially improve angioplasty success rates and may have important implications for bailout cases with abrupt occlusion. However, restenosis remains a significant problem.
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The purpose of this study was to evaluate the sealing ability of a dentinal apical plug treated with a bonding agent. Ninety human lower premolars were used. The teeth were divided into three groups. in groups 1 and 2, to prepare an apical isthmus of 1 mm in length, the first apical seat was prepared with a #45 K file 1 mm short of the anatomical apex and with a #60 K file 2 mm short for the second apical seat. Dry dentin fillings were packed in the apical isthmus with a #60 K file. In group 1, the root canal was obturated with gutta-percha and Canals root canal sealer by the lateral condensation method. In group 2, following an application of the bonding agent to the plug, the root canal was obturated in the same way. In group 3 (control), a single apical seat was prepared with a #60 K file 1 mm short of the apex and the root canal was obturated similarly. The teeth of three groups were immersed in a 1% methylene blue solution for 1, 2, and 4 wk. Dye penetration depth from the apical foramen was determined. Group 2 showed no leakage after 4 wk. Groups 1 and 3 showed dye penetration into the root canal, and in these two groups dye penetration increased with time.
A thoroughbred horse, gelding, gray color, aged 19 years old had cutaneous melanomas from the root to the middle of the tail, and throughout the connective tissues of the whole body. Histologically, the tumors were diagnosed as mature melanotic melanomas characteristically deposited with abundant melanin pigment. Examined with an electron microscope, melanosomes were electron opaque without internal structure (stage IV), or as mature granular and lamellar types. Most of them were fused with each other, and formed compound melanosomes, which was similar to internal melanin aggregates in shape. The internal melanin aggregates gradually disintegrated, and compound melanosomes grew spherical. The compound melanosomes changed into autophagosomes.
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Brief exposure of Pseudomonas aeruginosa to a temperature of 10 degrees C or lower caused a significant leakage of the periplasmic beta-lactamase into the medium. The extent of leakage increased as the incubation temperature was lowered to 4 degrees C and reached a maximum at 0 degrees C. Cells grown in the presence of beta-lactamase inducers were unsuitable for the permeability assay. It was found that the diffusion rates of beta-lactams through the outer membrane of P. aeruginosa were much lower than those previously reported, as assayed under refined conditions. The diffusion rates of beta-lactams in one of the mutants tested were an order of magnitude lower than those of the other strains, despite the fact that the outer membrane protein profile of the strain appeared to be indistinguishable from those of the others. These results suggest that beta-lactam antibiotics diffuse through the outer membrane of P. aeruginosa, at least partly, through a non-porin pathway.
Imipenem-resistant clinical isolates of Pseudomonas aeruginosa were divided into two categories: (i) isolates that were moderately resistant to imipenem (MIC 6.25 mg/L) that produced trace amounts of protein D2 detected with immunoblotting using anti-protein D2 antibody, but not when stained with Coomassie blue and had inducible class 1 beta-lactamase expression; (ii) isolates that were highly resistant to several beta-lactams, including meropenem, with no protein D2 by staining or immunoblotting and had stably derepressed beta-lactamase. Laboratory strains were isolated and analyzed: (i) mutants lacking protein D2, or (ii) lacking protein D2 and producing stably derepressed beta-lactamase with carbapenem resistance similar to the clinical isolates. (iii) mutants producing undetectable beta-lactamase which were four-fold more susceptible to imipenem than the mutant producing stably derepressed beta-lactamase or the strain with inducible beta-lactamase. These data suggests that beta-lactamase and outer membrane permeability govern meropenem-resistance in P. aeruginosa.