[1,25-Dihydroxyvitamin D3 and glucocorticoid regulation of alkaline phosphatase in isolated rat osteoblast-rich cells].
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Biomedical subjects
Publications and source records attributed to T Kawase.
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Eighteen cases of Ramsay Hunt syndrome were examined with electrocochleography and auditory brainstem response. Hearing was normal in 4 cases, while the other 14 exhibited sensorineural hearing loss ranging from mild to moderate in severity. Although the I-V interwave latency in all cases was within or slightly outside of the normal limits, the N1 latency was significantly prolonged in 8 cases proportionately to the degree of hearing loss at 4 and 8 kHz. The histopathological findings reported so far have indicated that the main lesion in this syndrome is in the internal auditory canal (2, 3, 4, 5). The results obtained in the present study, however, clearly show that the main site responsible for the hearing loss is not in the retrocochlear region, but in the cochlea. The possible mechanism of the cochlear involvement in this syndrome was discussed.
Electrogustometry (EGM) of the soft palate, innervated by the gustatory fibers running via the greater petrosal nerve, was performed in 10 cases with facial paralysis due to suprageniculate lesions to evaluate its clinical validity as a topographic diagnostic method. Lacrimal function was also examined for comparison. The results obtained from EGM showed a significantly increased threshold on the affected side in 90% of the cases. However, the lacrimal secretion decreased only in 40% using Schirmer No. 2 test. The results of the present study strongly suggest that EGM of the soft palate reflects the function of this nerve better than Schirmer test, and EGM is clinically useful for the topographic diagnosis of peripheral facial nerve lesions.
A case of giant internal carotid ophthalmic aneurysm was presented. In order to clarify whether the patient could tolerate carotid occlusion, a balloon clamping test was performed. before surgery. The cerebral blood flow was measured using early imaging by single photon emission computed tomography (SPECT) with N-isopropyl-(iodine-123)-p-iodoamphetamine (123I-IMP). When the balloon clamping test was performed the tracer was injected, and scanning was performed 35 minutes after removing the catheter. This tracer enabled a "memory of blood flow" during temporary ischemia to determine the character of quick diffusion and slow wash out, that could not be performed by other methods of cerebral blood flow measurement. SPECT with 123I-IMP can simplify the measurement of cerebral blood flow during the balloon clamping test.
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Devitalized, neonatal, rat calvariae incubated in a buffered solution release Ca2+ and Pi during the first day into the medium until levels reach 1.2 mM and 2.6 mM, respectively. Thereafter levels gradually decrease to stabilize by the fifth day at 0.5 mM and 2 mM. Comparison of these solubility changes with those of known calcium phosphate salts suggests that calvarial solubility is controlled by a mixture of impure, soluble, apatite precursors, which at cell death transform to an impure apatite. Increasing concentrations of Mg2+ increased the rate of Ca2+ release and, at 3 mM, stabilized Ca2+ by the fifth day at 0.9 mM. Decreasing the pH from 7.4 to 7.2 produced similar solubility changes as did the addition of citrate at 0.3 mM, phosphocitrate at 0.3 mM, ATP at 0.1 mM, and the bisphosphonate, HEBP, at 0.1 mM. Osteocalcin did not increase calvarial solubility but was able to slow the rate of calcium phosphate phase transition if present at the time of in vitro crystal formation. Phosphocitrate and HEBP were also more effective when present during in vitro crystal formation. HEBP was most effective when present during biological crystal formation, as shown by the increased solubility of devitalized calvariae removed after in vivo administration of HEBP. In vivo manipulations of osteoclast activity produced changes in plasma calcium which correlated with the solubility of the corresponding calvariae after removal and devitalization. Low milk intake increased calvarial solubility. Increasing doses of 1,25(OH)2D3 increased plasma calcium and calvarial solubility, both of which were reversed by injection of acetazolamide. It was concluded from this survey of devitalized bone solubility that calcium exchange between bone and body fluids can buffer calcium homeostasis in the young rat. The exchange is passive. The active components appear to be osteoblastic formation of soluble apatite precursors and their stabilizers and, in reverse, osteoclastic transformation of apatite to precursors by H2CO3 secretion.
We report a case of an extracranial chondroma of the skull base. This tumor occupied mainly the skull base, the nasopharynx and the parapharyngeal space. Magnetic resonance imaging was effective in diagnosis and determining the extent of the lesion. Total extirpation of the lesion was performed via an external cervical approach. A survey of the available literature revealed only three similar cases treated to date.
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To elucidate the function of the reticuloendothelial system of liver in hepatic injury, we investigated the effect of endotoxins on superoxide anion (O-2) generating capacity and lysosomal enzyme activities of Kupffer cells isolated from rats treated with galactosamine (Gal N), with Gal N supplemented with polymyxin B (Polymyxin B-Gal N), with lipopolysaccharide (LPS) and from control rats. After collagenase digestion of the liver and centrifugation over metrizamide gradient, Kupffer cells were prepared by the dish adherence procedure. O-2 production by the cells was examined as chemiluminescence during phagocytosis of latex particles and beta-glucuronidase activities were analyzed. High titers of endotoxemia were detected in LPS and Gal N rats by limulus test, while a low endotoxemia titer was found in Polymyxin B-Gal N rats. Hepatocyte damage was found in Gal N rats, but little was recognized in LPS and Polymyxin B-Gal N rats. In the latter groups, Kupffer cells, activated by endotoxins, showed the enhancement of chemiluminescence and a release of lysosomal enzyme. Though lysosomal enzyme was released from Kupffer cells in Gal N rats, chemiluminescence was slightly suppressed in spite of the high titer of endotoxemia. These results appear to be related to the consumption of O-2 during liver injury. The functional state of Kupffer cells was thus changed by the grade of endotoxemia and hepatic injury.
The superoxide anion generating capacity of polymorphonuclear cells (PMNs) in patients with liver cirrhosis and the effect of lipopolysaccharide on rat PMNs were examined. Superoxide anion generating capacity of PMNs was measured as luminol-dependent photon emission (chemiluminescence) during phagocytosis of peptide in vitro. Chemiluminescence of PMNs from patients with liver cirrhosis was significantly enhanced compared with normal healthy volunteers, and endotoxemia was detected in 3 out of 20 cases of liver cirrhosis by the limulus gelatin test. Serial studies revealed that chemiluminescence of PMNs and endotoxin in plasma decreased after administration of polymyxin B (3 X 10(6) u/day). Chemiluminescence of rat PMNs was also markedly enhanced after the injection of lipopolysaccharide, and persisted for more than 8 days even though endotoxemia was not detected. These results indicate that the enhancement of chemiluminescence by PMNs is related to endotoxins spilling over from the liver in patients with liver cirrhosis.
The interaction between fat-storing cells (FSCs) and Kupffer cells (KCs) in vitro has been studied in an attempt to clarify certain aspects of the pathogenesis of fibrotic process in the liver. FSCs and KCs were isolated from the livers of rats either treated with CCl4 for 6 weeks, or with vitamin A for 6 weeks or from untreated rats by the pronase-collagenase digestion method. FSCs were further purified by centrifugation over a double layered metrizamide gradient, and KCs were separated from other sinusoidal cells by the dish adherence technique. FSCs from CCl4-treated rats divided rapidly, while those from vitamin A-treated rats divided slowly, as compared with untreated rats. Furthermore, the proliferation of FSCs was enhanced in the presence of KCs from CCl4-treated rats, but was slightly suppressed by KCs from normal and vitamin A-treated rats. This enhancement was mediated by a non-dialyzable, soluble factor present in the conditioned medium of KCs from CCl4-treated rats, but was not detected in the conditioned medium of KCs from normal or vitamin A-treated rats. From the present study, a growth factor secreted by KCs from CCl4-treated rats may play an important role in controlling the proliferation of FSCs during the pathogenesis of liver fibrosis.
In an attempt to elucidate the role of fat-storing cells (FSCs) in alcoholic liver fibrosis, we examined the effects of ethanol and acetaldehyde on collagen synthesis by FSCs isolated from CCl4-treated or normal rats. Isolated FSCs from normal rats showed characteristic lipid droplets in the cytoplasm. FSCs from CCl4-treated rats showed an abundant rough endoplasmic reticulum and a small number of lipid droplets. Collagen synthesis by the cells from CCl4-treated rats was 4-5-fold enhanced as compared with untreated rats. Though ethanol had an inhibitory effect on collagen synthesis by FSCs, acetaldehyde stimulated collagen production by the cells from CCl4-induced hepatic fibrosis, whereas collagen synthesis by the cells from normal rats was not influenced by acetaldehyde. From these results, FSCs are morphologically and functionally changed in liver fibrosis, and the transitional state of FSCs might be important in the pathogenesis of alcoholic liver fibrosis.
Morphological changes, proliferation and collagen synthesis of fat-storing cells (FSC) in primary culture were examined. FSC, isolated from rats treated with vitamin A, showed numerous large lipid droplets in the cytoplasm and positive desmin staining. After 4-7 days culture, these cells were transformed into fibroblast-like cells with a gradual depletion of lipid droplets and with abundant well-developed rough endoplasmic reticulum. The proliferation analysis revealed that DNA synthesis preceded the increase of cell number. Enhancement of the collagen synthesis by FSC were associated with the morphological change of the cells. Quantitative analysis revealed that these cells produced mainly type I collagen (84%) and a small amount of type III collagen (16%).