The canine platform: a modified method for posterior tooth eruption.
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Biomedical subjects
Publications and source records attributed to A Yaffe.
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The oligosaccharide processing and secretion of hepatitis B surface antigen (HBsAg) was studied in Chinese hamster ovary cells stably transfected with the gene coding HBsAg. HBsAg was secreted from cells with a relatively long half time (ca. 5 h). This appeared to be a characteristic of HBsAg itself, since HBsAg-producing cells infected with vesicular stomatitis virus transported the viral envelope glycoprotein to the cell surface with normal kinetics (half time of ca. 30 min). The secreted HBsAg was comprised of both the unglycosylated (P20) and the glycosylated (G25) polypeptides, characteristic of HBsAg isolated from human serum or secreted from other cell lines (C. W. Crowley, C.-C. Liu, and A. D. Levinson, Mol. Cell. Biol. 3:44-55, 1983; M. F. Dubois, C. Pourcel, S. Rousset, C. Chang, and P. Tiollais, Proc. Natl. Acad. Sci. U.S.A. 77:4549-4553, 1980; C.-C. Liu, D. Yansura, and A. D. Levinson, DNA, 1:213-221, 1982; G. M. Macnab, J. J. Alexander, G. Lecatsas, E. M. Bey, and J. M. Urbanocvicz, Br. J. Cancer, 24:509-515, 1976; A. M. Moriarity, B. H. Hoyer, J. W.-K. Shih, J. L. Gerin, and D. H. Hamer, Proc. Natl. Acad. Sci. U.S.A. 78:2606-2610, 1981; D. L. Peterson, J. Biol. Chem., 256:6975-6983, 1981). The glycosylated polypeptide (GP25) contained complex oligosaccharide chains. Cell-associated HBsAg also was comprised of both an unglycosylated and a glycosylated polypeptide; however, the glycosylated form (GP23) contained only high-mannose oligosaccharide chains. No oligosaccharide processing of the high-mannose chains could be detected within the cells. Thus, most of the time before secretion of HBsAg from cells must have been spent in a pre-Golgi or early Golgi compartment. Glycosylation was inhibited completely by tunicamycin, although unglycosylated particles were still secreted from cells and were antigenic. The secretion and oligosaccharide processing of HBsAg were inhibited with high concentrations of monensin, but at lower concentrations of monensin HBsAg was still secreted, although only half of the oligosaccharide chains were processed to the complex form.
Three wall intrabony defects were produced in 11 dogs using a round bur followed by curettes and hoes. A copper band was fixed to the tooth with stainless steel ligature wire. Six weeks later, the copper band was removed and the defect was treated with an enriched collagen solution (ECS) prepared from acid-extracted dog skin collagen. Thirty-three defects were treated with ECS and 33 defects were controls. Healing was assessed histologically 4 and 6 weeks after treatment for the presence of new cementum, periodontal ligament and alveolar bone, as well as arrested epithelial downgrowth along the dental root. Unlike the controls, treatment with ECS resulted in restoration of periodontal attachment after 4 weeks. This included formation of new cementum, new alveolar bone and dense connective tissue fiber running between bone and cementum. Control sections showed epithelial migration along the root, separating it from the adjacent connective tissue and thus preventing new attachment.
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The structural gene of Hepatitis B virus surface protein (HBsAg) was introduced into a plasmid capable of autonomous replication and selection in both the yeast Saccharomyces cerevisiae and E. coli. In this plasmid transcription of the HBsAg is initiated by the 5'-flanking sequence of the yeast 3-phosphoglycerate kinase (PGK) gene and terminated by the 3'-flanking region of the yeast TRP1 gene. Yeast cells containing this plasmid produce a new major species of mRNA of 1200 nucleotides in length coding for HBsAg. Viral surface antigen is made in nonglycosylated form at a level of about 1-2 percent of total yeast protein. A small fraction of this polypeptide (2-5 percent) is found in aggregated form upon yeast cell disruption by glass beads. This material is similar in size, density, and shape to the 22nm particle, isolated from the plasma of human hepatitis carriers, and induced comparable levels of HBsAg antibodies in mice when compared with the natural particle.
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Second premolars in both upper and lower jaws of 6 dogs were extracted and acrylic resin replicas were made of the roots. Horizontal channels were drilled across the root replica perpendicular to the long axis. Before implantation, the prepared root replicas were immersed in a solution of native collagen. One year after implantation, proliferation of connective tissue and newly-formed viable bone were observed within the channel as well as surrounding the treated implants. All control implants without collagen treatment were rejected leaving chronically inflamed implantation sites.
Occlusal interferences on right upper molars in rats produced ultrastructural changes in the calcification of ipsilateral condylar cartilage. This was characterized by premature appearance of apatite crystals within extracellular matrix vesicles present in the proliferative cell zone. The normal proliferative cell zone in the rat condyle manifested noncalcifying vesicles. The zone of calcification in rats with an occlusal splint revealed longitudinal calcifying fronts in the vicinity of the chondrocytes. These fronts were composed of haphazardly distributed apatite crystals. These ultrastructural alterations support the generally accepted view that mechanical stimuli induce changes in the process of primary mineralization.
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The effect of solutions of lidocaine, with and without adrenaline, on the blood vessels of the dental pulp and periodontal ligament in rat molars was examined. The vessels were visualized by intravascular injection of a supension of carbon particles. The results indicate that the anesthetic solution alone does have a local effect on the blood vessels. Local anesthetic solutions containing adrenaline had a more marked effect; in addition, a dose-dependent systemic effect of adrenaline was noted.
The phenomenon of occlusal wear has been generally reported, with no distinction being made between wear of the anterior or posterior teeth. This paper describes a group of patients without oral habits and exhibiting anterior tooth attrition or flaring with minimal posterior tooth attrition. The mandibular anterior movement patterns of the patients studied were evaluated using a Sirognathograph. These patterns appear to be the etiology for the anterior attrition or flaring present. A treatment mode allowing coexistence of this phenomenon with an anterior guidance that does not interfere with the mastication pattern is proposed. A hypothesis that might explain the clinical findings and a mode of treatment are described.
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