[Ultrasonographic detection of metastatic axillary lymph nodes in breast cancer].
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Biomedical subjects
Publications and source records attributed to M Nishida.
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An enzyme-linked immunosorbent assay (ELISA) system for the quantitation of human monocytic colony-stimulating factor (hM-CSF) was established, which was based on the "dual antibody immunometric sandwich" principle using horse and rabbit polyvalent antibodies against human urinary colony-stimulating factor (CSF-HU). The minimal detectable level of hM-CSF was 10 U/mL, and the assays showed good reproducibility. As measured by this method, the average serum hM-CSF level of 20 normal adults was 540 +/- 110 U/mL (range, 300 to 800 U/mL). The peak of hM-CSF measured by ELISA was identical to that measured by bioassay when semipurified CSF-HU was fractionated by reversed-phase high performance liquid chromatography (HPLC). This method detected two types of hM-CSF, which had approximate molecular weights of 85 Kd (CSF-HU) and 45 Kd in human serum and urine; the ratio of 85:45 Kd was very high in serum and the amounts of the two types were nearly equal in urine. After anticancer chemotherapy, the serum hM-CSF level of one half of the patients with hematological malignancy was elevated according to the reduction in neutrophil number, while it was almost in the normal range in the other half of the patients, indicating the possibility that anticancer chemotherapy damaged the hM-CSF-producing cells. This ELISA method may be useful for monitoring the serum hM-CSF level after anticancer chemotherapy.
The authors measured preoperative rCBF and intraoperative cortical artery pressure (CAP) during STA-MCA anastomosis to investigate cerebral hemodynamics in moyamoya disease. Six of 13 patients including 3 children showed ischemic attack and the remaining presented hemorrhagic attack. rCBF was measured by single photon ECT with Xe-133 inhalation technique. CAP's and rCBF's in moyamoya disease were compared to those in the 22 internal carotid artery (ICA) and 8 middle cerebral artery (MCA) occlusion. Systemic arterial blood pressure (SABP) was obtained at the radial artery. Mean rCBF in the MCA territory in moyamoya disease, ICA occlusion, and MCA occlusion were 39, 37, and 33 ml/100 g/min respectively. Mean SABP and CAP in moyamoya disease were 103 and 28 mmHg, respectively. In ICA occlusion, mean SABP and CAP were 98 and 45 mmHg, respectively. In MCA occlusion, mean SABP and CAP were 89 and 36 mmHg, respectively. To clarify the hemodynamics, vascular resistance was obtained from the following equations: The proximal vascular resistance (Rp), which was produced from the cervical ICA to cortical artery, was obtained by (mean SABP - mean CAP)/(rCBF). And distal vascular resistance (Rd) which was produced from the cortical artery to jugular vein, was obtained by (mean CAP)/(rCBF). Mean Rp in moyamoya disease ICA occlusion and MCA occlusion were 2.01, 1.21 and 1.70, respectively. Rd in moyamoya disease, ICA occlusion and MCA occlusion were 0.79, 1.37 and 1.22, respectively. There were significant differences in Rp and Rd between moyamoya disease and ICA or MCA occlusion. In ischemic group in moyamoya disease, rCBF, SABP, CAP, Rp and Rd were 41 ml/100 g/min, 111 mmHg, 28 mmHg, 1.92 and 0.70, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
Short-latency somatosensory evoked potential (SEP) was serially monitored in head-injured patients and its clinical significance was evaluated in relation to auditory brain stem response (ABR), prognosis and other parameters such as intracranial pressure (ICP). SEP, ABR, and ICP were monitored serially and automatically in 16 patients with acute head injury. Glasgow Coma Scale (GCS) score was equal to or less than 8 in 14 cases. High dose barbiturate therapy was performed in 7 cases and intracranial hematoma was removed operatively in 14 cases. SEP was recorded from C3'or C4'-Fz leads on the lesion side following stimulation of the contralateral median nerve, and the difference between the two potentials (N20, N13) defined as central conduction time (CCT) was followed at a basic time interval of 10-20 min. The patients were divided into 3 groups according to N20 finding and the prognosis of each group was analyzed. The final outcome (assessed 6 months after injury) was graded according to Glasgow Outcome Scale as follows: good (good recovery, moderate disability), poor (severe disability, persistent vegetative state), death (death). Three patients with no CCT change showed good recovery (table, 11). Out of 7 patients with no N20 on admission, 5 died due to severely increased ICP and the prognosis for the other 2 cases was poor. The last group consisted of 6 patients in whom CCT varied during hospitalization. In 3 out of these 6 cases N20 finally disappeared due to increased ICP and they died in the acute stage.(ABSTRACT TRUNCATED AT 250 WORDS)
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To obtain, an accurate outline of a tumor lesion in deep-seated organs with X-ray images in proton therapy, an implantation procedure of markers to determine the margins of the lesion has been developed. Nonradioactive Au grains were used as the markers and produced sufficiently clear images. The procedure consists of implanting the markers with a specially designed injector for endoscopic, palpative and intraoperative approaches to the lesions, which was performed without any adverse effects. Due to application of this procedure, the accuracy of treatment planning and pinpointing the site of the treatment field has improved greatly.
A large-scale purification method for hepatitis B surface antigen produced in a recombinant yeast (Saccharomyces cerevisiae) was established. The resulting HBsAg was greater than 99% pure and suitable for vaccine use. The yeast-derived HBsAg was structurally and biochemically similar to plasma-derived HBsAg. The anti-HBs antibody producing potency of the yeast-derived vaccine in mice was significantly higher than that of the plasma-derived vaccine. The yeast-derived vaccine induced protective antibody against hepatitis B virus of either adr or ayw subtype in a chimpanzee efficacy study. These observations demonstrate the usefulness of the yeast-derived vaccine as a second-generation hepatitis B vaccine.
Vanadium was shown to be a contaminant in Sigma-grade serum albumins, fraction V. The levels of vanadium detected by neutron activation analysis were: bovine 16.7, ovine 10.0, rabbit 9.1, porcine 3.9, and human 0.19 micrograms/g protein. According to the ESR spectra, the vanadate form (+5 oxidation state) was strongly suggested as a chemical form present in albumins. Dialysis against a chelating agent was quite effective for removal of the metal ion.
3',5'-Dioctanoyl-5-fluoro-2'-deoxyuridine (FdUrd-C8), one of the lipophilic prodrugs of 5-fluoro-2'-deoxyuridine (FdUrd) was dissolved in an oily lymphographic agent (Lipiodol Ultra-Fluid), which had been studied as a carrier of the anticancer drug for hepatic cancer. The prodrug was administered into the left proper hepatic artery of rabbits bearing VX-2 tumor in the liver in order to examine the anticancer effects and possible adverse effects on nontumorous hepatic cells. Lipiodol or FdUrd-C8*Lipiodol selectively remained in the hepatic cancer area but disappeared from nontumorous parts of the liver 7 days after injection. Tumor growth rates in 1 week of the untreated group, a group given injections of 0.2 ml of Lipiodol alone, and groups given injections of 0.2 ml of Lipiodol containing 30, 50, 70, and 100 mg of FdUrd-C8 were 636, 436, 34.8, 14.9, -2.4, and -10.4% of the size at the time of treatment, respectively. Pathological observation also showed that FdUrd-C8 had a strong anticancer effect on VX-2 tumor growing in the liver of the rabbits. In contrast to the effect on the cancerous cells, that on nontumorous hepatic cells was very slight. In pathological observation, necrosis or degeneration of nontumorous hepatic cells was hardly observed. Plasma glutamic-oxaloacetic transaminase and glutamic-pyruvic transaminase levels temporarily rose 1 day after injection but returned to the initial levels within 7 days in all groups.
The presence of estrogen-independent progesterone receptors (PgR) was demonstrated in a subline of a human endometrial cancer cell line, Ishikawa cells, although the original Ishikawa cells contained estrogen-inducible PgR. Scatchard plot analysis of cytoplasmic binding data in our subline (IK-90) revealed a high affinity binding site for R5020 (Kd, 1.0 nM) with maximum binding sites of 158 fmol/mg protein. Competition experiments showed a binding specificity similar to that of typical PgR. By low-salt sucrose gradient centrifugation, radioactive 8S and 4S peaks were found. The addition of 1 microM progesterone in culture medium resulted in a rapid nuclear translocation of cytoplasmic PgR. In contrast to the original cells, estrogen receptors could not be detected in IK-90 cells, and an addition of 17 beta-estradiol (10 nM) to culture medium failed to increase PgR. Accumulation of glycogen in cytoplasm of IK-90 cells in response to R5020 (0.1-1 microM) was observed by periodic acid-Schiff staining. The addition of R5020 to culture medium (0.1-1 microM) also caused a marked decrease in the growth of IK-90 cells, whereas the other steroids including 17 beta-estradiol, tamoxifen, testosterone, and cortisol had no significant effects. These results demonstrate for the first time the presence of a progestin-responsive human endometrial cancer cell line that contains estrogen-independent functional PgR. IK-90 cells appear to be an ideal model for studying the mechanism of the antiproliferative effect of progestin on endometrial cancer cells.
A patient with a new variant of multiple sulphatase deficiency (MSDv) is reported. Unlike the usual type, onset was late and progress was slow. The phenotypic changes were those usually seen in multiple sulphatase deficiency but much milder. Cytoplasmic accumulations were found in skin fibroblasts, and urinary mucopolysaccharides and sulphatides were high. Arylsulphatases A, B and C (ASA, B and C), heparan N-sulphatase sulphoiduronate sulphatase, and N-acetylgalactosamine 6-sulphatase all had low activity in lymphocytes and cultured skin fibroblasts. Complementation for ASA activity was found in hybrids between MSDv and metachromatic leukodystrophy (MLD) as well as between multiple sulphatase deficiency (MSD) and MLD. Complementation for ASC activity was also seen in hybrids between MSDv and X-linked ichthyosis (XLI), and between MSD and XLI. However, neither ASA nor ASC activity increased in hybrid cells of MSDv and MSD. These results suggested that the mutations of MSDv and of MSD were allelic, although of different phenotypes.
To define the role of arachidonate metabolites in evolving ischaemic myocardial damage 10 anaesthetised open chest dogs underwent 90 min occlusion of the left anterior descending coronary artery followed by 5 h reperfusion. Tissue extracts from ischaemic myocardium incubated in vitro were subjected to high pressure liquid chromatography for analysis of lipoxygenase products such as mono hydroxyeicosatetraenoic (HETE) acids and to radioimmunoassay for determining a cyclooxygenase product, thromboxane B2. In ischaemic myocardium the production of 12-HETE (120(35) ng.g-1, mean (SEM)) and thromboxane B2 (18.3(2.4) ng.g-1) was significantly higher than that in normal myocardium (13(2) ng.g-1, p less than 0.01, and 4.2(0.5) ng.g-1, p less than 0.001, respectively). 12-HETE production was linearly correlated with thromboxane B2 production in ischaemic myocardium (r = 0.718, p less than 0.02). The increased production of 12-HETE and thromboxane B2 was in proportion to infarct size as measured by a percentage risk area infarcted (r = 0.732, p less than 0.02, and r = 0.942, p less than 0.001, respectively). Similarly, the increase in production of these eicosanoids was related to the degree of leucocyte infiltration in ischaemic myocardium. These results indicate that altered arachidonate metabolism is strongly associated with the progression of ischaemic myocardial damage, suggesting important roles for these eicosanoids, which may be produced by blood corpuscles during the evolution of acute myocardial infarction.
Ninety-three, previously untreated epileptics were subjected to clonazepam monotherapy. The plasma clonazepam concentrations were monitored to achieve optimal therapeutic effects of the drug. Within a mean duration of follow-up of 32 months, 57 (61.3%) of the 93 cases became seizure-free. The drug showed a high efficacy for complete seizure control of more than 80% for both simple partial seizures and primary generalized tonic clonic ones. The mean plasma level of clonazepam giving complete seizure control was 14.7 ng/ml (range: 3.0-34.6 ng/ml) in cases of generalized epilepsy, and 15.6 ng/ml (range: 4.5-42.3 ng/ml) in cases of partial epilepsy. There was a high correlation between the plasma level and the dose, but no correlation between the plasma level and the clinical effect of the drug. The variable therapeutic range and great interindividual differences in the optimal plasma clonazepam level imply that individually tailored regimens are necessary to achieve optimal therapeutic effects of the drug.
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We compared amounts of lipoxygenase products with the extent of leukocyte infiltration in the ischemic myocardium with an occlusion-reperfusion model of open-chest dog. Changes in peripheral leukocyte count and leukocyte function estimated by neutrophil aggregation induced by calcium ionophore A23187 were also examined. The ischemic tissue (120 +/- 40 ng/g, mean +/- SEM) showed a marked increase in 12-hydroxyeicosatetraenoic acid (HETE) production compared with the normal tissue (13 +/- 1 ng/g, p less than 0.01). The production of 5-HETE in the ischemic tissue was also augmented as well. When we examined the correlation between production of either 12-HETE or 5-HETE and leukocyte infiltration in the ischemic tissue, the former was augmented markedly in proportion to the extent of the latter. Leukocyte count in peripheral circulation was gradually increased after reperfusion. Similarly, neutrophil aggregation was significantly augmented during reperfusion. These results indicate that production of lipoxygenase metabolites associated with leukocyte infiltration in the reperfused ischemic tissue was increased during the course of myocardial infarction, which was accompanied by activation of leukocyte in peripheral circulation. Further studies should be done to clarify the importance of lipoxygenase metabolites in the evolution of reperfusion-induced myocardial injury.