Biomedical subjects
Publications and source records attributed to A Kurihara.
Rupture of one or both peroneal tendons is rare. We present a case of longitudinal ruptures in both peroneus longus and brevis tendons. We obtained a very satisfactory clinical result with surgical debridement of the abnormal granulation tissue and proliferated synovial sheath.
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A 60-years-old woman with polycythemia vera with marked thrombocytosis and intolerable erythromelalgia was presented. A single dose of 400 mg aspirin was effective to improve the pain and cyanosis. And we studied the relationship between platelet aggregation rate and symptoms after administration of several antiplatelet drugs. A single dose of 100, 200, 400 and 800 mg aspirin, 25 mg indomethacin (Id), 200 mg OKY-046, and daily dose of 300 and 600 mg dipyridamole (Dp) and 300 mg ticlopidine (Tc) were given. Aspirin, Id and OKY-046 were effective for the improvement of finger pain. The complete inhibition of spontaneous aggregation (SPA) and aggregation by 2.0 micrograms/ml of collagen were well parallel with the improvement of symptoms. But duration of effect of LKY-046 were only 6 hours. Dp and Tc were not effective for the improvement of pain, had no relation with platelet aggregation rate. The concentration level of aspirin in vivo which suppresses the platelet aggregation induced by SPA and 2.0 micrograms/ml of collagen coincided well with the concentration level of this drug which suppresses the same platelet aggregation in vitro. It seems to be useful to suppress the platelet aggregation induced by SPA and 2.0 micrograms/ml of collagen with aspirin and Id for controlling the platelet aggregation induced circulatory disturbance in patient with thrombocytosis.
To characterize the efflux system of digoxin, a cardiac glycoside, from the brain to the blood through the blood-brain barrier and blood-cerebrospinal fluid (CSF) barrier, the accumulation of digoxin by the brain microvessel or the choroid plexus isolated from guinea pig brain was investigated. The accumulation of digoxin by the brain microvessel has a saturable component (Km = 0.163 microM, Vmax = 0.142 nmol/mL of tissue/min), with a nonsaturable component [Kd = 0.203 cell-to-medium (C:M) ratio/min] that was decreased by hypothermia (Q10 = 2.9), sulfhydryl reagent, and quinidine, but not by a metabolic inhibitor [2,4-dinitrophenol (DNP)]. It was concentration- and Na+-dependent. The accumulation of digoxin by the choroid plexus was also saturable (Km = 1.9 microM, Vmax = 3.8 nmol/mL of tissue/min), and was decreased by hypothermia (Q10 = 4.4), sulfhydryl reagents, ouabain, and quinidine, but not by metabolic inhibitors (DNP, KCN); it was also concentration- and Na+-dependent. The binding of digoxin to the homogenate of choroid plexus was one-tenth of digoxin accumulation by the intact choroid plexus, suggesting that digoxin is transported into the cells and bound to the cytosol fraction. The value of (Vmax/Km + Kd) multiplied by the total tissue weight of the microvessel per guinea pig is approximately 10-fold that of Vmax/Km multiplied by the tissue weight of the choroid plexus, although (Vmax/Km + Kd) per milliliter of the microvessel is half the Vmax/Km value of the choroid plexus. These findings suggest that digoxin can be excreted from both the brain and the cerebrospinal fluid to blood by a carrier-mediated diffusion system which is inhibited by quinidine, and that a main route of digoxin efflux from the brain to the blood is not through the blood-CSF barrier, but through the blood-brain barrier.
Although there is considerable literature concerning ossification of the posterior longitudinal ligament or the ligamentous flava (OPLL or OYL) in the cervical and thoracic spine, there are only a few references about OPLL or OYL in the lumbar spine. The authors have described lumbar spinal stenosis due to OPLL or OYL as hyperostotic lumbar spinal stenosis, and analyzed 12 surgically documented cases with this condition. The symptoms and signs of hyperostotic lumbar spinal stenosis are the same as those seen in degenerative lumbar spinal stenosis, but the degree of paraparesis is much more severe in hyperostotic lumbar spinal stenosis. Computed tomography scan imaging clearly demonstrates OPLL or OYL in the lumbar spine, although some lesions can be seen on the lateral view of a plain roentgenogram. The results of 12 surgical cases suggest that decompression laminectomy produces relief of symptoms. An analysis of 2,403 plain lumbar roentgenograms showed an incidence of 8.4% OYL in the lumbar spine, with frequent involvement of the upper and middle lumbar spine. A classification system of OYL in the lumbar spine has been developed. The entire spine should be examined before surgery on a patient with hyperostotic lumbar spinal stenosis because of a tendency to ossify spinal ligaments at other levels.
This rapid, simple amidolytic assay of protein C activity in whole plasma involves activation by protein C activator from the venom of Agkistrodon contortrix contortrix (Protac) and use of a Cobas Fara spectrophotometer programmed for kinetic assay. Plasma is incubated with activator venom in the presence or absence of antibody to human protein C in the instrument, chromogenic substrate (S-2366) is added, and the absorbance is measured at 405 nm. The difference between the absorbance of the sample plasma with and without antibody to human protein C correlated well with protein C antigen as assayed by enzyme-linked immunosorbent assay (ELISA) and the Laurell rocket technique in normal subjects, patients being treated with warfarin, and patients with liver cirrhosis or disseminated intravascular coagulation. Our mean value for protein C in normal subjects is 115.9 (SD 16.7)% for amidolytic activity, 103.0 (SD 17.4)% for ELISA, and 97.2 (SD 18.1)% for the rocket technique. The high value for normal subjects presumably includes some nonspecific amidolytic activity activated by the activator venom, as indicated by measurable activity in immuno-depleted protein C-deficient plasma. Within-run and between-run CVs were less than 5% at low, normal, and high concentrations of protein C amidolytic activity.
To study the transport system of propranolol (PL), a basic drug, in the blood-brain barrier, the uptake of PL into isolated bovine brain microvessels was investigated. The uptake of PL was a concentrative one via saturable process (Km = 42.5 microM) that was decreased by hypothermia (Q10 = 2.2), but not by metabolic inhibitors (2,4-dinitrophenol, KCN, ouabain). Although basic drugs such as quinidine and imipramine decreased both the initial rate of uptake and the steady-state cell-to-medium concentration ratio (C/M) of PL, acidic drugs (phenobarbital, salicylic acid) did not affect them. These results suggest that PL is taken up by the endothelial cells of the isolated brain microvessels by facilitated diffusion which is specific for basic drugs and then binds to certain binding sites in the cells.
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We attempted to use CDDP for patients with advanced cancers of the gastrointestinal system by intra-arterial infusion, giving consideration to the side effects of CDDP. Of 19 cases treated with CDDP, 17 cases were evaluable. These 17 cases comprised 10 cases of gastric cancer, 1 of pancreatic cancer and 6 of colon cancer. Therapeutic effects were as follows. According to the criteria for judgement of solid cancers, there were 10 evaluable cases which comprised 1 case of PR, 2 of MR, 4 of NC and 3 of PD. According to the criteria for judgement of malignant ascites, there were 6 evaluable cases which comprised 4 effective and 2 non-effective cases. As to side effects, nausea and vomiting were observed in 10 cases, numbness in 1, fever in 1 and aggravation of diabetes in 2. From the above results, intra-arterial infusion of CDDP is considered to be an effective method for the treatment of advanced cancers of the gastrointestinal system, especially of malignant ascites.
Using an experimental model for allergic inflammation of the air pouch type in rats, the effects of dexamethasone and indomethacin on leukocyte infiltration and level of chemotactic activity in the inflammatory exudate were examined to clarify the mechanisms of anti-inflammatory effects of glucocorticoids. Both dexamethasone and indomethacin when locally administered inhibited leukocyte infiltration, while chemotactic activity of the exudate was reduced by dexamethasone only. Indomethacin failed to reduce the level of chemotactic activity. Suppression by dexamethasone of the level of chemotactic activity became evident prior to the decrease in the number of leukocytes in the inflammatory exudate. These results suggest that the anti-inflammatory steroids manifest their inhibitory effect on leukocyte infiltration by inhibiting the generation of chemotactic factors in the inflammatory site. Besides this, the possible production of some inhibitory factors by the steroids may be considered as an alternative mechanism.
Effects of dexamethasone on chemotactic activity to polymorphonuclear leukocytes (PMN) of a lipophilic fraction collected with the aid of octadecylsilyl silica cartridge from exudates of an allergic inflammation were investigated. The chemotactic activity of this fraction was attributable to leukotriene B4 fraction separated by means of a reversed phase high performance liquid chromatography. Local application of dexamethasone suppressed dose-dependently the chemotactic activity of the lipophilic fraction in parallel with the inhibition of PMN infiltration in the inflammatory sites.
Rat polymorphonuclear leukocytes exposed to opsonised zymosan particles in vitro instantaneously and continuously release a chemotactic factor in the medium. The activity of this factor was mainly attributed to leukotriene B4, based on the data with high performance liquid chromatography. Preincubation of the cells with an antiinflammatory steroid, dexamethasone, at a dose of 0.25 micrograms/ml caused suppression in generation of the chemotactic factor from the leukocytes in a time-dependent manner.
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For the determination of leukocyte chemotaxis in the Boyden chamber toward zymosan-activated serum, a modification of the 51Cr-labeling method originally introduced by Gallin et al. was made using a polycarbonate filter at the top of a double filter system. By application of this method, it was demonstrated that an anti-inflammatory steroid, dexamethasone at relatively low doses, directly inhibited chemotactic movement of leukocytes after the pretreatment of the cells with dexamethasone for several hours. This inhibitory effect was proved to be a common property of glucocorticoids. The leukocyte-inhibitory effect manifested within the cell body and the release of any extracellular factors mediating the inhibitory effect of the corticoid into the medium was not demonstrated. The present data suggests that the inhibitory effect of dexamethasone on leukocyte infiltration observed in vivo is attributed to the direct inhibitory effect of dexamethasone on the motility of leukocytes.
The present study was designed to clarify molecular mechanisms underlying inhibitory effect of dexamethasone on leukocyte infiltration in the inflammatory site. For the assay of leukocyte infiltration, two or four blebs were made s.c. on the back of rats by injecting with 2% carboxymethyl cellulose solution containing a chemoattractant, casein. Leukocyte accumulation in the bleb was inhibited considerably by local application of dexamethasone at a concentration of 0.6 X 10(-6) M. Hydrocortisone mesylate, which was reported in the study with hepatoma tissue culture cells to be a long-acting antagonist against glucocorticoid in binding to the corticoid receptor, blocked the above leukocyte inhibitory effect of dexamethasone when applied simultaneously with dexamethasone. The leukocyte infiltration was unaffected by the application of hydrocortisone mesylate alone. Treatment with androstenedione, which was reported to be inactive in the hepatoma tissue culture cells, did not interfere with the inhibitory effect of dexamethasone at all. Actinomycin D, when applied simultaneously with dexamethasone, significantly suppressed the leukocyte-inhibitory effect of dexamethasone. In contrast with those observations, the inhibitory effect of dexamethasone was not affected at all in cases that actinomycin D and hydrocortisone mesylate, respectively, were applied after the administration of dexamethasone. These results indicate essential roles of glucocorticoid receptor and gene expression for the manifestation of the inhibitory effect of dexamethasone on leukocyte infiltration in the inflammatory site.
Chemotactic activity at the site of an allergic air-pouch inflammation induced with azobenzene-arsonate-conjugated acetyl bovine serum albumin as an antigen was studied and a close correlation of the chemotactic activity with the intensity of leukocyte migration was demonstrated. In the period of vigorous leukocyte immigration into the fluid in the allergic air-pouch, chemotactic activity of the exudate was maintained at a high level, while no significant activity was detected after the number of leukocytes in the pouch fluid reached maximum.
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