[Magnetic resonance imaging of spinal cord lesions in multiple sclerosis--detection of lesions and serial T1 relaxation time values].
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Adolescent↗
Biomedical subjects
S Kojima
Publications and source records attributed to S Kojima.
In vitro cultivation of Paragonimus miyazakii and P. ohirai.
Excysted metacercariae of Paragonimus miyazakii and P. ohirai were cultured in various media at 37.5 C in a 5% CO2 atmosphere. Paragonimus miyazakii grew rapidly and showed a well-developed ovary, uterus, and testes at 172 days in NCTC 109 supplemented with 30% rabbit serum, 50% egg yolk-109, and rabbit red blood cells (RBC's). However, none of the worms formed yolk or eggs in these cultures. On the other hand, P. ohirai grew to the adult stage, in which vitellaria and imperfect ova were formed, in NCTC 109 supplemented with 30% dog serum, 10% yeast extract Earle's solution (YLE), and dog RBC's at 252 days. The maximum body length of these worms measured 7.0 mm (mean 5.5 mm) at 252 days. The dog RBC's were an essential ingredient of the culture medium for the development of P. ohirai. Additions of liver concentrate, chick embryo extract (CEE), and egg yolk-109 in the medium did not provide any additional benefits for the development of worms. Using this supplemented medium, adult worms of P. ohirai removed from rats were maintained in vitro to examine their ability to lay eggs. Egg laying occurred during the first 10-13 days for worms that survived more than 60 days. The number of eggs deposited in this medium was about 2 times that found when Hanks' BSS and NCTC 109 were used.
Animals↗
[Survey on patients with senile dementia and subsequent nursing activities--an attempt by a public health clinic in cooperation with a local government].
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Aged↗
[Dementia and disturbance of consciousness in thalamic degeneration].
A 53-year-old male with thalamic degeneration is presented. He had double vision, cerebellar signs, and pyramidal and extrapyramidal tracts signs in addition to hypersomnia, decrease in spontaneity and attention, and impairment of memory as psychic symptoms. These signs and symptoms were progressive, and he subsequently developed akinetic mutism and died of pneumonia 17 months after the onset of the disease. His clinical diagnosis was considered as Gerstmann-Sträussler syndrome due to progressive dementia, cerebellar signs and the other signs mentioned above. The postmortem pathological investigations, however, revealed thalamic degeneration. The pathological observations showed marked loss of nerve cells and glial proliferation in the medial and anterior nuclei of thalamus. The same pathological changes were more or less demonstrated in the pulvinar, the periaqueductal gray matter of midbrain, inferior olivary nucleus, the medial parts of globus pallidus, the substantia nigra and the dentate nucleus. In the early stage of the clinical course, it was difficult to know whether the main symptoms were caused by dementia or by the disturbance of consciousness. Retrospective considerations, however, showed that dementia had appeared at first, and subsequently the disturbance of consciousness had joined. As the result, it seems that they finally caused akinetic mutism. It is known as thalamic dementia that in the cerebrovascular disease the lesions in the medial and anterior parts of bilateral non-specific thalamic nuclei cause dementia.(ABSTRACT TRUNCATED AT 250 WORDS)
Brain Stem↗
T-cell acute lymphoblastic leukemias with a t(8;14) possibly involving a c-myc locus and T-cell-receptor alpha-chain genes.
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Child↗
Formation of mast cell colonies in methylcellulose by mouse peritoneal cells and differentiation of these cloned cells in both the skin and the gastric mucosa of W/Wv mice: evidence that a common precursor can give rise to both "connective tissue-type" and "mucosal" mast cells.
We investigated the issue of mast cell heterogeneity by cloning mast cell colonies from peritoneal cells in methylcellulose, injecting the cloned cells into the skin and stomach of mast cell-deficient (WB X C57BL/6)F1-W/Wv (WBB6F1-W/Wv) mice, and staining the mast cells that developed in these sites with Berberine sulfate, a fluorescent dye that identifies heparin-containing mast cells. When peritoneal cells of nontreated WBB6F1-+/+ mice were plated in methylcellulose containing pokeweed mitogen-stimulated spleen cell conditioned medium, pure mast cell colonies developed. In contrast, the peritoneal cavity of genetically mast cell-deficient WBB6F1-W/Wv mice lacked the progenitor cells that made mast-cell colonies. The clonal nature of the mast cell colonies was determined by using the giant granules of C57BL/6-bgJ/bgJ mice as a marker: even when mixture of peritoneal cells of C57BL/6-bgJ/bgJ mice and C57BL/6-+/+ mice were plated, all of the resulting colonies consisted of either bgJ/bgJ-type mast cells alone or +/+-type mast cells alone. Individual mast c 11 colonies of WBB6F1-+/+ mouse origin were divided into two parts; one part was directly injected into the wall of the glandular stomach of a WBB6F1-W/Wv mouse, and another part was injected into the skin of the same W/Wv mouse. Injections of 14 of 46 such colonies resulted in development of mast cells in both the "connective tissues" (skin or stomach muscle or both) and the stomach mucosa. Mast cells in the connective tissues were stained with Berberine-sulfate, indicating that they contained heparin, whereas mast cells in the stomach mucosa were not. These results suggest that a single precursor cell can give rise to both "connective tissue-type" and "mucosal" mast cells.
Animals↗
Application of lectins to tumor imaging radiopharmaceuticals.
We investigated the in vitro binding of 125I-lectins to Ehrlich ascites tumor (EAT) cells and in vivo uptake of 125I-lectins in Ehrlich solid tumor (EST) bearing mice. In in vitro binding assays, phaseolus vulgaris agglutinin (PHA), pisum sativum agglutinin(PSA), and concanavalia agglutinin(Con A) showed a high affinity for EAT cells. The in vivo biodistribution of 125I-lectins showed 125I-I-PSA to be significantly taken up into EST tissues 24 h postinjection. After IV injection of 125I-PSA, uptake of the radioactivity into the tumor tissues reached a maximum at 6 h, and thereafter decreased. Rapid clearance of the radioactivity from blood and its excretion into kidney soon after injection of 125I-PSA were observed. When compared with the biodistribution of 67Ga-citrate in EST bearing mice 24 h postinjection, tumor to liver (T/B), tumor to muscle (T/M), and tumor to blood (T/B) ratios were superior for 125I-PSA. At 6 h postinjection, the T/B-ratio of 125I-PSA was 2.5, and this value may be sufficient to enable discernible diagnostic images. Our results suggest that PSA might be a useful tumor imaging radiopharmaceutical.
Animals↗
67Ga uptake and heparan sulfate content of Ehrlich solid tumor in mice.
The relationship between 67Ga uptake and heparan sulfate (HS) content in Ehrlich solid tumor (EST) of mice was investigated, and the effect of cyanomethylamine, papain, streptozotocin, or bleomycin pretreatment on 67Ga uptake in EST was studied. 67Ga uptakes in EST and kidney were much higher than other tissues, and these tissues also contained large amounts of HS. 67Ga uptakes and HS synthesis in the EST were inhibited by pretreatment with cyanomethylamine or papain (inhibitors of fibrosis). Parallel reductions of 67Ga uptake and HS synthesis in EST were observed in EST transplanted into streptozotocin-induced diabetic mice. The weight of EST in the bleomycin-injected group was decreased to less than half of the control, but no effect was observed on 67Ga uptake per gram of EST. These results suggest that 67Ga uptake in the tumor and inflammatory lesions are related to the quantity of HS in these tissues, and the correlation between the uptake of 67Ga and the rate of cellular proliferation is secondary.
Aminoacetonitrile↗
Tumor uptake of 67Ga-carrying liposomes.
The in vivo distribution, excretion, and tumor localization of liposome-encapsulated 67Ga in normal and Ehrlich tumor (solid form)-bearing mice were studied. In normal mice, multilamellar vesicles (MLVs) were taken up mainly by the liver and spleen, whereas small unilamellar vesicles (SUVs) exhibited a broader tissue distribution. When 67Ga was encapsulated in MLVs or SUVs, the excretion of the radiotracer in the urine and feces was less than that observed for free tracer at 72 h after i.v. administration. In tumor-bearing mice, SUVs were found to accumulate preferentially in tumors. The tumor uptake of neutral, positive, and negative SUVs was 10%-13% of the administered dose per gram of tumor tissue at 24 h after their injection. These values were about three times higher than those found for free 67Ga-nitrilotriacetic acid (67Ga-NTA) or 67Ga-citrate. Significant differences in tumor uptake due to different surface charges of liposomes were not observed. Enhanced tumor-to-blood and tumor-to-muscle ratios were also observed at 24 h after injection. These results suggest that 67Ga-carrying liposomes may be a useful for tumor imaging.
Animals↗
Visible fibrinolysis by endothelial cells: effect of vitamins and sterols.
We have succeeded in corroborating the enhancing effect of vitamin A, vitamin C, sitosterol and fucosterol on the fibrinolytic activity of endothelial cells. The assay system consisted of an in situ dissolution of a fibrin layer coated onto a culture dish, over which endothelial cells were grown in a culture medium containing 10% serum. The dissolution was enhanced by the addition of these vitamins and phytosterols to the culture medium.
Animals↗
Effect of clofibrate on cholesterol metabolism in rats treated with polychlorinated biphenyls.
Serum and hepatic cholesterol content in rats treated with polychlorinated biphenyls (PCBs, KC-400) were increased compared to those of control rats. This increase of cholesterol content was reduced to control level by simultaneous administration of ethyl p-chlorophenoxyisobutyrate (CPIB). Also, when lecithin-cholesterol acyltransferase (LCAT) (EC. 2.3.1.43) activity was expressed as the net cholesterol esterification, the acyltransferase activity in rats treated with PCBs was elevated, while the elevated acyltransferase activity was brought to control level by simultaneous administration of CPIB. On the other hand, the amount of bile of rats treated with CPIB, PCBs and PCBs-CPIB was increased, but free and total cholesterol content in bile of these treated rats was decreased to 40-60% of those of control rats. Moreover, cytochrome P-450 content in liver microsomes of rats treated with CPIB, PCBs and PCBs-CPIB was increased. At the same time, cholesterol-metabolizing activity in liver microsomes of rats treated with CPIB, PCBs and PCBs-CPIB also was elevated. Similar results were obtained for drug metabolizing (aniline hydroxylation and aminopyrine N-demethylation) activity. In addition, the amount of bile acids excreted from rats treated with CPIB, PCBs and PCBs-CPIB was increased compared to that of control rats. These results suggest that hypercholesterolemia induced by oral ingestion of PCBs is recovered by CPIB treatment and that this hypocholesterolemic effect of CPIB may be related partly to the elevation of hepatic mixed function oxidase activity for cholesterol catabolism.
Animals↗
Comparative effects of intracoronary administration of propranolol with systemic administration on hypoxic canine myocardium.
Myocardial protective effects of intracoronary administration of relatively small doses of propranolol were examined and compared with systemic administration in 20 open-chest dogs. In group 1 (n = 6) rate-pressure-product (R X P) did not change during 5-minute left anterior descending artery (LAD) perfusion with deoxygenated Krebs-Henseleit solutions (KHS). However, R X P decreased by the same degree in group 2 (n = 7), which received perfusion with KHS containing 0.4 or 0.8 mg/dl of propranolol, and in group 3 (n = 7) given LAD perfusion with original KHS and systemic administration of 0.02 to 0.04 mg/kg of propranolol. Total administered doses of propranolol were the same for groups 2 and 3. Transmural biopsy after 5 minutes of perfusion revealed less severe metabolic deterioration of hypoxic myocardium in group 2 when compared with that in group 1, as evidenced by higher ATP (adenosine triphosphate) (2.81 +/- 0.35 versus 2.23 +/- 0.45 mumol/g, p less than 0.05) and lower lactate content (5.62 +/- 1.44 versus 9.01 +/- 2.62 mumol/g, p less than 0.05). On the other hand, significant metabolic preservation was not noted in group 3. Sequential changes in regional myocardial contraction did not differ among the three groups. In conclusion, intracoronary administration of propranolol showed myocardial protective effects that were not mediated by the changes in hemodynamics and myocardial contraction.
Adenine Nucleotides↗
Comparative effects of three chelating agents on distribution and excretion of cadmium in rats.
Sodium N-benzyl-D-glucamine dithiocarbamate (NBG-DTC), which was newly synthesized, 2,3-dimercaptopropanol (BAL), and N-methyl-D-glucamine dithiocarbamate (NMG-DTC) were compared for their relative efficacies in the distribution and excretion of cadmium in rats exposed to cadmium. Rats were injected ip with 109CdCl2 (1 mg Cd and 10 microCi 109Cd/kg) and 3 days later, they were treated with the chelating agents (400 mumol/kg) every other day for 2 weeks. These chelating agents were effective in removing cadmium from the body without increasing the amount of cadmium in the kidney. After treatment with these chelating agents, cadmium was excreted mainly in the feces through the bile and the fecal excretion of cadmium by NBG-DTC was significantly larger than that by BAL or NMG-DTC. The hepatic cadmium content after treatment with NBG-DTC was much more decreased than that with BAL or NMG-DTC. The renal cadmium content was decreased only after treatment with NBG-DTC. These chelating agents did not result in the redistribution of cadmium to brain, testes, and heart. The growth of rats was little retarded by treatment with NBG-DTC and NMG-DTC, but was retarded by treatment with BAL. The treatment with NBG-DTC decreased the tissue amounts of Zn, Fe, and Mn to a small extent as compared with the treatment with cadmium alone. The results of this study reveal that the injection of NBG-DTC to rats pretreated with cadmium can more effectively remove cadmium from the body without the mobilization of cadmium to the kidney, the critical organ in cadmium toxicity, and without redistribution of cadmium to other tissues such as brain, testes, and heart, than injection of BAL and NMG-DTC.
Animals↗
Nicotine potentiates superoxide anion generation by human neutrophils.
Cytotoxic neutrophil-derived oxygen radicals have been implicated in the pathogenesis of a variety of cardiovascular, pulmonary, and neoplastic disorders for which cigarette smoking is a prominent risk factor. Although nicotine alone failed to provoke neutrophil oxidative metabolism, the alkaloid caused dose-dependent (0.1 to 10 microM) potentiation of superoxide anion release induced by either phorbol myristate acetate or N-formyl-methionyl-leucyl-phenylalanine. The potentiating effect of nicotine was not attenuated by either atropine or hexamethonium nor was it mimicked by acetylcholine, suggesting involvement of noncholinergic receptors or a membrane-fluidizing effect of the alkaloid. Nicotine-induced exacerbation of neutrophil superoxide anion production may be involved with the enhanced risk of cardiovascular, pulmonary, or neoplastic disease in individuals who smoke.
Drug Synergism↗
Effects of chelating agents on biliary and urinary excretion and tissue distribution of cadmium in rats.
Sodium N-benzyl-D-glucamine dithiocarbamate (NBG-DTC), which was newly synthesized, sodium N-methyl-D-glucamine dithiocarbamate (NMG-DTC), and 2,3-dimercapto-1-propanol (BAL) were evaluated for their efficacy in mobilization of cadmium from the body using rats which had received cadmium, 30 min and 24 h earlier. At both 30 min and 24 h after treatment with cadmium, these chelating agents significantly enhanced the biliary excretion of cadmium, but did not influence the urinary excretion of the metal. Such an enhancement effect of NBG-DTC on the biliary excretion of cadmium was much larger than that of NMG-DTC or BAL. These chelating agents were effective in mobilizing cadmium from the liver at 30 min after pretreatment with cadmium. NBG-DTC showed the largest effectiveness on the depression of cadmium content in the liver. However, the contents of cadmium in the liver and kidney of rats given cadmium, 24 h earlier, did not significantly change at 3 h after treatment with the chelating agents. These results show that the injection of NBG-DTC at both 30 min and 24 h after treatment with cadmium can much more effectively mobilize cadmium from the body mainly through the bile without redistribution of cadmium to tissues than injection of NMG-DTC and BAL.
Animals↗
67Ga binding to sulfated proteoglycan in normal and CCl4-damaged liver.
The binding of 67Ga and 59Fe to sulfated proteoglycan in the normal and CCl4-damaged mouse livers have been studied by means of Sepharose CL-4B column chromatography in guanidine hydrochloride. 67Ga uptake in the liver was elevated to approximately 1.8 times that of the control 2 days after a single administration of CCl4. 67Ga was bound to two types of sulfated proteoglycan (average mol. wt 1,700,000 and 35,000) in the normal and CCl4-damaged liver. However, the percentage of 67Ga bound to sulfated proteoglycan (mol. wt about 1,700,000) in the CCl4-damaged liver was increased as compared with that in the normal liver. Papain digestion of these sulfated proteoglycan fractions caused the 67Ga radioactivities to shift to a low molecular weight fraction (about 10,000). Cellulose acetate electrophoresis of this fraction (mol. wt about 10,000) isolated from the normal and CCl4-damaged livers resulted in identifying heparan sulfate (HS). The 35SO4 incorporation into HS band isolated from the CCl4-damaged liver, as an indicator of HS synthesis, was increased compared with that of the normal liver. 59Fe was not bound to sulfated proteoglycan and its gel filtration pattern was evidently different from that of 67Ga.
Animals↗
Effects of protein intake on blood pressure, sodium metabolism, and urinary kallikrein excretion in salt-loaded rats.
Fifty-five male Wistar rats were divided into four groups and were fed (1) a control diet, (2) a high-salt low-protein (HSLP) diet, (3) a high-salt standard protein (HSSP) diet, or (4) a high-salt high-protein (HSHP) diet for 17 weeks in order to assess the effects of these diets on blood pressure, sodium metabolism, and urinary kallikrein excretion. Mean blood pressure on the 17th week was 156 +/- (SE)3 mm Hg in the HSLP group, and 152 +/- 3 mm Hg in the HSSP group. These values were significantly higher than 126 +/- 4 mm Hg in the HSHP group. Blood pressure showed reciprocal relationships to both urinary sodium and kallikrein excretion. These results suggest that high protein intake suppresses the rise of blood pressure of salt-loaded rats by facilitating sodium excretion and activating the renal kallikrein-kinin system.
Animals↗
Plasma atrial natriuretic polypeptide and polyuria during paroxysmal tachycardia in Wolff-Parkinson-White syndrome patients.
The human atrial natriuretic polypeptide (hANP) concentration in plasma was measured during paroxysmal supraventricular tachycardia provoked in 2 patients with Wolff-Parkinson-White syndrome. A 10- to 20-fold increase in plasma hANP concentration was observed during the tachycardia: from 12 to 291 pg/ml in 1 case and from 14 to 174 pg/ml in the other. Although polyuria was associated with the tachycardia, urinary sodium excretion as well as urinary osmolality were decreased. The urinary arginine vasopressin was appreciably decreased during the tachycardia. These results suggest that hANP released by paroxysmal tachycardia might not act as a natriuretic factor in this range of plasma concentration. Polyuria during paroxysmal tachycardia was attributed mainly to the inhibition of arginine vasopressin release.
Adult↗