Although prostaglandin E1 (PGE1), a potent vasodilator, is known to affect cerebral vasculature, its effects on cerebrospinal fluid (CSF) dynamics have yet to be determined. Accordingly, this experiment was designed to investigate the rate of CSF formation (Vf), intracranial pressure (ICP), sagittal sinus pressure (SSP), carotid blood flow (CaBF), and regional cerebral blood flow (r-CBF) in anesthetized cats during and after decrease of arterial pressure induced by intravenous PGE1. It was found that there were no significant changes in Vf, ICP, or SSP during deliberately induced PGE1 hypotension. r-CBF was maintained during induced hypotensive states regardless of diminished CaBF. Findings indicated that under experimental conditions employed here, PGE1 does not significantly affect dynamics of ICP. PGE1 therefore appears potentially useful for purposes of deliberate induction of hypotension during general anesthesia.
The degree of obturation of dentinal tubules as well as the dentinal uptake of F, Zn and Sr was investigated after placement of glass ionomer cement (GIC) containing variable proportions of the tannin-fluoride preparation, HY agent, into freshly prepared cavities. It was found that when HY agent was incorporated into the cement powder, there was both increase in electrical resistance in the dentinal floor of the GIC-restored cavity in addition to inhibition of dye penetration. Further, these changes were directly proportional to the concentration of HY agent. Electron probe microanalysis of the principal constituents of HY agent (F, Zn and Sr) revealed that the penetration depth for F and Zn was also directly proportional to the relative amount of incorporated HY agent, whereas Sr could not be detected regardless of HY concentration. Results clearly demonstrated that the higher the concentration of HY agent incorporated into GIC, the greater the degree of dentinal tubular obturation.
Root canal models were implanted in rats in order to investigate histologically the movement of granulation tissue invading apical canals and dead spaces and changes in cell proliferative activity as indicated by 3H-thymidine. The models were prepared to have 1, 2, and 3 mm apical canals, with and without dead spaces, to simulate preparations short of the apex and obturation to several levels. After 12 wks implantation of the models without dead spaces, granulation tissue invading 1 mm apical canals did not degenerate and cell proliferative activity remained high. However, tissue invading the 2 and 3 mm apical canals tended to be necrotic and cell proliferative activity was decreased. In the models with dead spaces, the tissue in the 1 and 2 mm apical canals developed and invaded the dead spaces, and still possessed proliferative activity 12 wks after implantation. In contrast, the tissue in the 3 mm apical canals did not invade the dead spaces, even after 12 wks, and no proliferative activity was observed.
We investigated the chondroitin sulfate in human periodontal samples (gingiva, periodontal ligament, cementum and alveolar bone) collected for orthodontic reasons. Glycosaminoglycans (GAGs) were extracted from the periodontium by enzyme digestion, and unsaturated disaccharide isomers of chondroitin sulfate were obtained by chondroitinase AC II and hyaluronidase digestion. The isomers were analyzed by high-performance liquid chromatography. Chondroitin sulfate was found in all four types of periodontal tissue; its unsaturated disaccharide isomers consisted in ΔDi-0S, ΔDi-6S, ΔDi-4S, ΔDi-diSE and ΔDi-triS. These four types of periodontal tissue showed different molar ratios of the unsaturated disaccharides. The ratio of ΔDi-4S to ΔDi-6S was greater in the calcified than in the uncalcified tissue.
β-Glycosidases (N-acetyl-β-glucosaminidase, N-acetyl-β-galactosaminidase, β-glucuronidase) were assayed in temporomandibular joint (TMJ) synovial fluid obtained from 23 patients with closed lock TMJ internal derangement (ID), four with closed-lock TMJ osteoarthritis (OA), and 13 with normal controls (N). Synovial fluid was collected from the upper joint space after injecting 1.5 ml of 1% lidocaine three times. The specific activity of N-acetyl-β-glucosaminidase increased significantly both with ID (p<0.01) and with OA (p<0.001), along with increases in the activity of N-acetyl-β-galactosaminidase (p<0.05 with ID and p<0.01 with OA) and in β-glucuronidase (p<0.05 both with ID and OA). The N-acetyl-β-glucosaminidase activity with OA was also significantly higher (p<0.001) than with ID. These findings suggest that N-acetyl-β-glucosaminidase activity in the TMJ synovial fluid reflects the degree of TMJ dysfunction.
We used immunohistochemical methods to investigate whether in vitro labeling with bromodeoxyuridine (BrdU) of oral cancer tissues is useful in pathological diagnosis. BrdU-positive cells were found around the basal region of the epithelium in normal oral mucosa, in a papilloma specimen and in tissue with moderate dysplasia. The labeling rates (percentage of BrdU-positive cells, LR) for these cases were 1.2%, 6.9% and 7.5%, respectively. In well-differentiated carcinoma, more layers of BrdU positive cells were observed from the basal layer toward the surface. The LR in this region was 13.9-17.0%. In vitro BrdU labeling of oral tumors may be useful in pathological diagnosis, since the LR is lowest in normal tissues, higher in benign tumors, and highest in malignant tumor tissues.
The effect of various glycosaminoglycans on the growth of cultured Tawa sarcoma cells (CTS cells) were determined under both fast and slow growth conditions. Hyaluronic acid, chondroitin, chondroitin 4-sulfate, and chondroitin 6-sulfate (all of which have only one type of uronic acid, glucuronic acid) inhibited the growth of CTS cells during fast growth and accelerated it during slow growth. Both keratan sulfate and keratan polysulfate (containing galactose) inhibited the growth of CTS cells during both growth conditions. Only glycosaminoglycans containing iduronic acid (heparin, heparan sulfate, and dermatan sulfate) accelerated the growth of the cells during fast growth. However, heparin inhibited the growth during slow growth while heparan sulfate and dermatan sulfate accelerated it. Growth regulation seems to require complete structural integrity of the glycosaminoglycans. The component subunits alone lack such activity when not linked together.