Hydrolysis of milk oligosaccharides by the oral bacterium Streptococcus sanguis atcc 10557.
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Biomedical subjects
Publications and source records attributed to H Nonaka.
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The galactosyltransferase has been purified from human parotid saliva by ammonium sulfate precipitation (25-70% saturation), followed by repeated affinity chromatography on Sepharose-alpha-lactalbumin. The molecular weight of the enzyme was estimated to be approximately 56,000. The enzyme catalyzes the transfer of galactose from UDP-galactose to the exposed N-acetylglucosamine residues derived from glycoproteins, forming a Gal beta (1-4)GlcNAc linkage.
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A case of craniometaphysial dysplasia with extensive degeneration of the cerebral white matter is presented. The cortex of the swollen part of the long bones was quite thin and there was striking trabecular atrophy. Both the vault and base of the skull showed marked thickening and sclerosis, leaving no interlaminal zone. It is probable that the diffuse degenerative change of the cerebral white matter with gliosis bears some resemblance to that produced by a circulatory disturbance of the great vein of Galen. Due to the narrowed foramen magnum, deformed atlase and axis, and the surrounding postoperative scar, the upper cervical cord was compressed, markedly atrophic and degenerated. Other segments of the cervical and thoracic cord displayed secondary wallerian degeneration and focal neurolytic lesions in the white matter. At the level of Th11 there was a pencil-like malacic lesion, suggesting an apparent interference of circulatory disturbance due possibly to the deformed vertebral column.
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Studies were made on the hemodynamics in the liver and kidney during hemorrhage and retransfusion, using 20 dogs with or without hepatic periarterial nerve plexus, anaesthetized with sodium pentobarbital. The results were as follows. In 14 dogs in which the hepatic periarterial nerve plexus was left intact (Group A), the averages of the hepatic arterial flow (HAF), portal venous pressure (PVP), portal venous flow (PVF), and flow in the right renal artery (RAF) decreased significantly to 38, 64, 35, and 25%, respectively of the control levels when the abdominal aortic pressure (ABP) fell to 40 mm Hg (36% of the control level) during hemorrhage. At the same time the portal venous resistance (PVR) and the right renal vascular resistance (RVR) increased greatly and the hepatic arterial resistance (HAR) either increased or decreased in different dogs. During retransfusion the ABP and vascular resistance returned to nearly the control levels, the PVF increased beyond the control level. In 6 dogs in which the nerve plexus was resected (Group B), the decreases in the HAF and RAF during hemorrhage were not significantly different from those in Group A. These results may suggest the following. The decrease in the HAF during hemorrhage seems to be mostly a passive change resulting from decrease in the systemic blood pressure. Neurogenic regulation may be a little. Further, the existence of the humoral regulation and autoregulation in the HAF were suggested in some cases. While, the responsibilities to hemorrhage and retransfusion appear to be different among the examined three vessels, i.e. the hepatic artery, portal vein, and renal artery. No definite interrelation was seen between the hepatic and renal circulations.
Finger-tip plethysmograms were recorded photoelectrically on 200 young males and females each. The relation between the left ventricular ejection time (ET) and the preceding heart rate (HR) and a method for correcting ET for the heart rate were studied. The values calculated by the formula ET/S-S or ET/square root S-S varied with the HR, so these formulae cannot be used for correcting the ET for HR. Thus from the relationship between ET and HR, a formula for converting the measured ET to the ET at an HR OF 70, I.E. ETc, was deduced. ETc equals ET + HR - 70. This formula can be used for both sexes of Japanese juveniles and the values obtained by it can be directly compared, irrespective of the HR.
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