[Eosinophilic granuloma of the mandible--a case report].
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Biomedical subjects
Publications and source records attributed to S C Lin.
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The effects of cellular cations and ATP on calcium transport in and out of the nerve endings (synaptosomes) of mice brain were studied. The synaptosomes accumulated 45Ca time-dependently in the absence of ATP or other additions for at least 10 min. When ATP was present, the overall 45Ca accumulation was decreased and was maximal at about 4 min, after which it started to decline. Studies on the effects of cations with or without ATP at 4 min revealed selective activities for different cations. Mg2+ inhibited 45Ca accumulation in the absence of ATP but increased 45Ca accumulation when ATP was present. Similarly, ATP increased 45Ca accumulation only when Mg2+ was present. Na+, on the other hand, inhibited 45Ca accumulation both in the presence and absence of ATP and/or Mg2+. K+ increased 45Ca accumulation in the presence of ATP with or without Mg2+; however, K+-stimulation was not noted in the presence of 100 mM Na+, and in fact, K+ became inhibitory. The ATP-stimulated 45Ca accumulation in the presence of Mg2+ peaked within 4-6 min and then declined, suggesting release of 45Ca. Compatible with this notion, in 45Ca-loaded synaptosomes, ATP evoked 45Ca release which was accompanied by the appearance of Pi in the medium. Although ATP-activated 45Ca-release can occur in the presence of Mg2+, Mg2+ is not required and, in fact, is inhibitory. Rapid release of 45Ca was also noted when 45Ca-loaded synaptosomes were incubated in the presence of Na+ without ATP. It is concluded that Mg2+, Na+, K+ and ATP each has a specific role in regulating Ca2+ permeability of the plasma membrane, calcium binding and calcium extrusion.
The properties of Ca2+-activated and Mg2+-activated ATPases of nerve endings from mouse brain were investigated. Ca2+ and Mg2+ each can activate ATP hydrolysis in synaptosomes and its subfractions. Both Ca2+-ATPase and Mg2+-ATPase exhibit high and low affinity for their respective cations. At millimolar concentrations of Ca2+ or Mg2+, several nucleoside triphosphates could serve as substrate for the two enzymes and their specific activities were about three to four times higher in synaptic vesicles than in synaptosomal plasma membranes (SPM). Both in SPM and in synaptic vesicles the relative activity in the presence of Ca2+ was in the order of CTP greater than UTP greater than GTP = ATP, but with Mg2+ the activity was higher with ATP than with the other three triphosphates. Mg2+-ATPase was more active than Ca2+-ATPase in SPM, but in synaptic vesicles the two enzymes exhibited similar activity. Kinetic studies revealed that Mg2+-ATPase was inhibited by excess ATP and not by excess Mg2+. The simultaneous presence of Na+ + K+ stimulated Mg2+-ATPase and inhibited Ca2+-ATPase activity in intact synaptosomes and SPM. The stimulation of Mg2+-ATPase by Na+ + K+ was further increased by increasing Mg2+ concentration and was inhibited by Ca2+ and by ouabain. When Ca2+ and Mg2+ are present together in SPM or synaptic vesicles, the total Pi liberated by the two cations may either increase or decrease, depending on their relative concentrations. Kinetic analyses indicate that Ca2+ and Mg2+ bind independently to the enzyme alone or together at different sites. The results suggest that Ca2+-ATPase and Mg2+-ATPase in SPM or synaptic vesicles may be separate and distinct systems.
Opiate agonists, morphine, levorphanol and beta-endorphin increased calcium accumulation in rat peritoneal mast cells. This effect was dose dependent and beta-endorphin was 10 times more potent than morphine. The stimulation was stereospecific and inhibited by naloxone. The site of the opiate action appears to be on the outer surface of the plasma membrane since lysis of the mast cell did not alter the response to morphine. Tolerance to the opiate effect was not seen after chronic morphine administration. Morphine did not stimulate histamine release even at relatively high doses in vivo or high concentrations in vitro. It is reasoned that the enhancing effects on external calcium accumulation may reduce the critical cytosol calcium level for effecting histamine release.
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A preparation of enriched synaptosomal plasma membrane (SPM) from mouse brain was found to contain a Mg2+-independent high affinity Ca2+-activated ATPase. The preparation readily accumulated Ca2+ at micromolar concentration from the medium in the presence or absence of Mg2+ and released previously accumulated calcium upon the addition of ATP. It is concluded that SPM Ca2+-ATPase may have a functional role in removal of cytosol Ca2+.
We studied the properties of calcium-activated ATPases present in preparations of isolated presynaptic nerve ending (synaptosome) and its subfractions from mouse brain. ATPase activity in the preparation was stimulated by Ca2+ and by Mg2+, but not by Na+ and K+, when each was added alone. The substrate specificities were found to be similar. The ATPases hydrolyzed only the high-energy phosphate bond and similar activity was exhibited for all nucleoside triphosphates tested (ATP, CTP, GTP, UTP). Moreover, the enzymes were insensitive to mitochondrial markers and to ouabain, but were inhibited by La3+. La3+ produced uncompetitive inhibition of Ca2+-ATPase in intact synaptosomes. Inhibition by La3+ was greatly increased after lysis of the synaptosomes, suggesting that the active sites of the enzymes may be on the cytosolic face of the membranes. The Ca2+-ATPase activity in synaptosomes was increased by increasing concentrations of external K+, suggesting that Ca2+ influx may be involved The Ca2+-ATPase in synaptosomal plasma membranes and synaptic vesicles had higher specific activities than those of intact synaptosomes and were activated, both in the presence and the absence of Mg2+, by Ca2+ concentrations approximating the intracellular level (10(-7) M). It is concluded that the nonmitochondrial synaptosomal Ca2+-ATPase may play an important role in the regulation of intracellular Ca2+.
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Thirty-four cases of SLE treated during the past seven years (1974-1981) in Taipei Municipal Jen-Ai Hospital are reported and analyzed. Diagnosis of SLE was based on ARA preliminary criteria and Hahn's preliminary criteria. There were 32 females (94.2%) and 2 males (5.8%). The mean age at diagnosis was 28.5 years (range 14-51). Clinical manifestations were as follows: facial erythema 24 cases (70.6%), Raynaud's phenomenon 4 cases (11.4%), oral or nasopharyngeal ulceration 7 cases (20.6%), arthritis without deformity 22 cases (64.7%), proteinuria 21 cases (61.8%), pleural or pericardial effusions 13 cases (38.2%), psychosis or convulsions 9 cases (26.5%), hematological abnormalities 25 cases (73.5%). Laboratory findings were as follows: positive ANA test 33/34 (97.0%), hypocomplementemia 10/13 (76.9%), direct Coombs' test 4/18 (22.2%), indirect Coombs' test 1/13 (7.6%), LE cell 19/34 (55.9%), RA Latex 7/17 (41.7%), polyclonal gammopathy 15/17 (88.2%), anemia 25/34 (73.5%), leukopenia 12/34 (35.3%), thrombocytopenia 10/34 (29.4%). Three cases were complicated by herpes zoster, one by hyperthyroidism, and one by autoimmune thyroiditis. Ten cases died, including 4 renal failure, 2 heart failure, 2 cases of committed suicide and 1 case of CNS involvement.
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A series of 6-substituted and 6,7-disubstituted pyrimido[4,5-b][1,4]oxazines (8-oxadihydropteridines) was synthesized through the condensation of an alpha-halo ketone and 2,5-diamino-4,6-pyrimidinediol. The resulting 8-oxadihydropteridines were assayed as potential antifolates in a dihydrofolate reductase enzyme system. The 2-amino-4-hydroxyoxa-dihydropteridines were found to possess greater biological activity than the corresponding 2,4-diamino compounds. The pteroic acid homeostere 2-amino-4-hydroxy-6-phenethyl-8-oxadihydropteridine was the most potent of the compounds tested.
Radioactive plastic microspheres 50 and 200 micra in diameter labeled with Ytterbium169 were used to study distribution in the femoral circulation of living dogs under general anaesthesia. Shunting was demonstrated because radioactivity was detected in the lungs after intraarterial injection of 50 micra microspheres. When the size of the microspheres injected was 200 micra no radioactivity was detected over the lungs. This indicates that the arteriovenous anastomoses are smaller than 200 micra, they are probably located in the skin because there was less radioactivity in the skin after intrafemoral injection of the 50 micra microspheres than when the injected microspheres were 200 micra in diameter.