[Endo-beta-glucuronidase].
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Biomedical subjects
Publications and source records attributed to M Endo.
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A 35-year-old male with tetralogy of Fallot, who had undergone left Blalock-Taussig shunt at ten year old, developed severe dysfunction of right ventricle with decreased right ventricular ejection fraction of 25% and frequent premature ventricular contractions of right ventricular origin. Following intracardiac procedure, the venoarterial assist circulation was successfully employed for 9 hours, until his hemodynamic conditions were improved. This experience reemphasized the importance of right ventricular protection and mechanical circulatory assist in the surgical treatment of Fallot's tetralogy in older children and adults who developed severe right ventricular dysfunction as a natural history of this disease.
Precise determination of the arrhythmogenic area by the intraoperative cardiac mapping procedure is a prerequisite to successful surgical therapy for tachyarrhythmias. Because of the limitation of time during operation, mapping should be performed precisely and quickly. For this purpose we have developed and used an on-line portable minicomputer system (modified HPM-6500; Fukuda Denshi Co., Ltd.). A ventricular epicardial excitation sequence map is acquired by measuring the conduction time difference for 51 predetermined points on the whole ventricular surface. The measured data are instantaneously digitized and computed to be displayed as an isochornous map in real time basis. Similar program is available for atrial excitation map. With this system it takes only about ten minutes to get an epicardial isochornous map. Recently a multi-channel signal-processing unit has been incorporated in the HPM-6500. With the use of a sock electrode or a card electrode, a map can be obtained on a few cardiac contractions. Multi-point simultaneous mapping has been proved to be especially important to get a VT isochornous map, for induced VTs during operation are usually unstable and transient.
St. Jude Medical (SJM) valve replacement in 995 patients with a cumurative follow-up period of 2,730 patient-years was compared with the Björk-Shiley (BS) valve replacement in 406 patients, who had followed up for 3,779 patient-years (pt-yr). The overall survival rates of aortic, mitral, and double valve replacement with SJM (and BS) at 10 years were 60.6% (80.0%), 89.6% (81.9%), 90.3% (73.9%), respectively. The linealized incidences of thromboembolism, valve thrombosis, prosthetic valve endocarditis, anticoagulation-related hemorrhage, significant hemolysis, and structural failure in SJM (and BS) were as follows: 1.32%/pt-yr (0.82%/pt-yr), 0.11%/pt-yr (0.21%/pt-yr), 0.18%/pt-yr (0.08%/pt-yr), 0.04%/pt-yr (0.24%/pt-yr), 0.18%/pt-yr (0.13%/pt-yr), and 0%/pt-yr (0.05%/pt-yr), respectively. Reoperation (explant and re-replacement or suture repair) was required in 10 SJM patients (0.37%/pt-yr) and in 14 BS cases (0.37%/pt-yr). Actuarially over 97% of patients were free of valve-related mortality at 10 years in both groups. From these results we conclude that both SJM and BS valves are equally excellent cardiac valve prosthesis. Considering the better hemodynamic characteristics and technical feasibility, we have thus far adopted SJM, rather than BS, as a first prosthesis of choice.
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Sulfated glycoprotein was isolated by precipitation from dialyzed human pancreatic juice and purified by ion-exchange chromatography followed by repeated gel chromatography. The sulfated glycoprotein was obtained as a sulfated glycoprotein-lipid complex by Sepharose CL-2B chromatography. Lipids aggregating with the sulfated glycoprotein were glycolipids such as ceramide trihexoside, and simple lipids such as cholesterol and cholesterol ester. This glycoprotein was resistant to digestion with mucopolysaccharidases or alpha-amylase, and consisted of 60% (w/w) protein and 40% sugars. The polypeptide core was characterized by a high content of serine, threonine, aspartic acid and glycine, but lacked cysteine. Its sugar components were N-acetylglucosamine, N-acetylgalactosamine, galactose, fucose and sialic acid. Absorption at 1240 cm-1 and 820 cm-1 by infrared spectroscopy indicated the presence of a sulfate ester group. All the carbohydrate chains of this sulfated glycoprotein, which are polydisperse and heterogeneous, were O-glycosidically linked through N-acetylgalactosamine to a protein core.
The ras gene product (p21) specifically binds GDP or GTP. In analogy with the reaction mechanism of other GTP-binding proteins, only the GTP-bound conformation is believed to be the biologically active one. Previously, we reported that not only oncogenic p21(Val-12) but also proto-oncogenic p21(Gly-12) could induce morphological differentiation in rat pheochromocytoma PC12 cells when microinjected in the complexed form with GTP gamma S [(1987) Mol. Cell. Biol. 7, 4553-4556]. In the present report we transformed PC12 cells with the oncogenic ras gene placed under the metallothionein I promoter. It was found that the transformed cells, when induced with Cd2+, differentiated in the absence of NGF. Then we analyzed the guanine nucleotide bound to p21 in the intact PC12 cells. It was found that conditionally induced p21(Val-12) was mostly present in the GTP-bound form, whereas the endogenous p21(Gly-12) was in the GDP-bound form. These results indicate again that p21.GTP induces the morphological differentiation of PC12 cells.
Purified proteochondroitin sulfate was incubated at pH 4.0 with a rabbit liver lysosomal enzyme fraction. The formed degradation products were isolated by gel filtration followed by reduction with NaB3H4. After acid hydrolysis of the reduced digest, the hydrolysate was passed through Dowex 50W-X8 and 1-X2 columns. The separated neutral sugars were then subjected to paper chromatography, which demonstrated that galactose and xylose had been at the reducing termini of chondroitin sulfate after incubation with the liver lysosomal preparation. These results suggest the presence in the liver lysosomal preparation of an endo-beta-galactosidase and an endo-beta-xylosidase which act at the linkage region of proteochondroitin sulfate.
N-Acetylchondrosine was incubated at pH 4.0 with a rabbit-liver crude enzyme extract. Gel filtration of the reaction products on Sephadex G-15 revealed the presence of monosaccharide liberated from the disaccharide. The monosaccharide fraction was analyzed by gas-liquid chromatography, and identified as a mixture of glucuronic acid and N-acetylgalactosamine. These results indicate the presence of beta-glucuronidase, which degrades N-acetylchondrosine, in rabbit liver. The discovery of the presence of this enzyme may help to establish the complete degradation process of chondroitin sulfates.
An endo-beta-glucuronidase acting on chondroitin sulfate was isolated from rabbit liver and purified about 550-fold, using a combination of ammonium sulfate fractionation, DEAE-cellulose chromatography, gel filtration on Sephacryl S-300, affinity chromatography through heparin-Sepharose CL-6B and preparative polyacrylamide gel electrophoresis. The pH optimum of this enzyme was 4.0 and the Km value 7 X 10(-3) M for chondroitin sulfate (Mr 40,000). The isoelectric point of the enzyme was found to be at pH 5.4. The molecular weight, estimated by gel filtration through Sephacryl S-200 and by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, was 35,000. This enzyme, which was found in the liver, kidney, spleen, and lung, hydrolyzed the glucuronyl galactose linkage of the linkage region of chondroitin sulfate possessing a very small peptide segment. The enzyme did not hydrolyze proteoglycan. It was concluded that an endo-beta-glucuronidase is involved in the catabolism of proteoglycan chondroitin sulfates.
Calcium store of the skinned fibers of the guinea-pig portal vein, pulmonary artery and taenia caeci consisted of two classes: one with both Ca-induced Ca release (CICR) and inositol 1,4,5-trisphosphate (IP3)-induced Ca release (IICR) mechanisms (S alpha) and the other only with IICR mechanisms (S beta). Ryanodine, applied during the CICR was activated, locked the CICR channels open, but the drug had practically no effect on the IICR mechanism. Thus, after the ryanodine treatment the Ca store with the CICR (S alpha) lost its capacity to hold Ca. Changes in the agonist-evoked contraction of intact muscle due to the ryanodine treatment suggest that agonists release Ca from S alpha which produces the initial phase of contractures.
An antibody was developed against a 23-kDa fragment of myosin which contains a part of the ATP-binding site, and applied to skinned muscle fibers. The antibody abolished active tension generation of the fibers, but did not block their assumption of a rigor state nor their release from this state by ATP. The primary amino acid sequence of the antigenic site on the fragment was found to be the region containing residues 77-80. This sequence region is predicted to have interesting secondary structures, and is distinct from the proposed ATP-binding site. We discuss the possibility that the region is responsible for the energy-transducing step in muscle contraction.
An 11-yr-old girl, who had been treated with human growth hormone (h-GH) for 31 months, developed acute myeloblastic leukemia with an inv(3)(q21q26). Since GH has been suggested to influence the genesis of leukemia, and the inversion 3 has been reported only in adult leukemia patients, the GH treatment may have caused the development of leukemia or accelerated the proliferation of the leukemia cells.
The endoscopic findings and the surgical results of 131 resected cases of superficial oesophageal cancer are described. Of these 131 cases 24 (18%) had mucosal cancer. Twenty-one (88%) of 24 cases of mucosal cancer of the oesophagus had neither nodal involvement nor vascular invasion, and therefore excellent long-term results can be anticipated. In order to obtain good results in the treatment of mucosal cancer of the oesophagus, the role of oesophagoscopy is extremely important in the early diagnosis of this cancer.
In a 48-year-old woman, the diagnosis of a right coronary arteriovenous fistula communicating with the coronary sinus was made noninvasively using two-dimensional, pulsed and color Doppler echocardiography. These noninvasive techniques were superior to angiography in delineating the cardiac chamber into which the fistula emptied.
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