[Nephropathy by food poisoning].
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Bacterial Toxins↗
Biomedical subjects
M Suda
Publications and source records attributed to M Suda.
[Renal dysfunction caused by animal poisons (snake venoms, bite and punctured poisoning)].
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Bee Venoms↗
Quadruplex formation of oligonucleotides containing G clusters and their nuclease resistance.
Oligoribonucleotides containing four G clusters, (UGnU)4 (n = 3-5), were synthesized and characterized by electrophoretic analysis and resistance to nucleases. Electrophoretic analyses indicate that the oligomers except for (UG3U)4 can form antiparallel-stranded monomeric quadruplexes in the presence of potassium cation. The oligomers used in this study are protected from endonuclease P1 and venom phosphodiesterase degradation. In addition, the oligomers indicate resistance to nucleases in human serum and E. coli S-100 fraction.
Base Composition↗
C-type natriuretic peptide as an autocrine/paracrine regulator of osteoblast. Evidence for possible presence of bone natriuretic peptide system.
C-type natriuretic peptide (CNP) is a local regulator in the brain and vascular wall. We present data to demonstrate the production and action of CNP in the osteoblast. CNP increased cGMP production, far more potently than atrial natriuretic peptide (ANP) in an osteoblastic cell line, MC3T3-E1. Since ANP and CNP are the ligands for two particulate guanylate cyclases, guanylate cyclase-A (GC-A) and guanylate cyclase-B (GC-B), respectively, these results reveal the expression of GC-B in MC3T3-E1. In addition, CNP mRNA and CNP-like immunoreactivity were detected in cell extracts from MC3T3-E1 and its culture medium, respectively. Both CNP and 8-bromo cGMP dose-dependently decreased [3H]thymidine uptake, without affecting alkaline phosphatase activity. These results indicate that CNP is a novel autocrine/paracrine regulator of osteoblast and suggest the presence of "bone natriuretic peptide system."
3T3 Cells↗
Proprotein-processing endoprotease furin decreases regulated secretory pathway-specific proteins in the pancreatic beta cell line MIN6.
Prohormone convertases PC2 and PC3, yeast Kex2-family endoproteases specific to the regulated secretory pathway, cleave proinsulin to insulin in the secretory granules of pancreatic beta cells. The well-differentiated beta cell line MIN6 expresses PC2 and PC3 and another regulated secretory pathway-specific protein chromogranin A. Furin, another yeast Kex2 endoprotease, exists in the trans-Golgi networks of many cell types. The beta cell line RINm5F (a cell line that is less differentiated than the MIN6 cell line) does not express the regulated pathway-specific proteins, but strongly expresses furin. We suspected that furin expression may cause the decrement of regulated secretory pathway-specific proteins. To test this hypothesis, we expressed a furin cDNA with a metallothionein promoter in MIN6 cells. With Zn2+ stimulation of furin expression, the messages of PC2, PC3, and chromogranin A decreased, and the processing of proinsulin to mature insulin became less efficient. The furin-expressing MIN6 cells exhibited less insulin content and weakened insulin secretion in response to a high glucose concentration. The conditioned medium from furin-expressing MIN6 cells also exerted a decrease of PC2 and PC3 expression in unaltered MIN6 cells. Thus, proteins cleaved by furin inside the cells or by truncated furin shed into the culture medium appear to cause decreased PC2 and PC3 expression, insulin content, and glucose-responsive insulin secretion in MIN6 cells.
Amino Acid Sequence↗
Progressive supranuclear palsy with asymmetric lesions in the thalamus and cerebellum, with special reference to the unilateral predominance of many torpedoes.
This report concerns a notable case of progressive supranuclear palsy exhibiting asymmetric dentate nucleus and thalamic degeneration with numerous torpedoes. The neuronal loss in the ventral lateral nucleus of the thalamus was predominant on the right side, while in the cerebellum, a quantitative study revealed the contralateral predominance of the neuronal loss in the dentate nuclei and torpedo formation, with preserved Purkinje cells. The abnormal tau-protein-related profiles in the two nuclei did not show any laterality in their distribution, indicating that the dentatothalamic tract may have been affected in a non-specific way in this case. In addition, the fact that the prominent sites of torpedo formation and loss of dentate nucleus neurons are identical supports the hypothesis that the torpedoes may be formed in association with neuronal loss in the dentate nucleus because of a plausible metabolic change in Purkinje cells through synaptic detachment of their axon terminals.
Aged↗
Chronic myelomonocytic leukaemia with t(8;9)(p11;q34) in childhood: an example of the 8p11 myeloproliferative disorder?
We describe the case of a 10-year-old girl with chronic myelomonocytic leukaemia with the chromosomal translocation t(8;9)(p11;q34), who had developed tonsillar lymphoma as extramedullary involvement at the initial presentation. The cytogenetic study of the cells in both bone marrow and tonsils demonstrated t(8;9)(p11;q34), despite no malignant features in the bone marrow specimens. She developed acute leukaemic transformation 8 months after diagnosis during chemotherapy for lymphoma. Although etoposide reduced the number of blasts, t(8;9)(p11;q34)-bearing cells were not eradicated. Complete remission was obtained following an unrelated bone marrow transplantation. The clinical characteristics of this patient are similar to those of the patients with t(8;9)(p11;q34 or q32) or t(8;13)(p11;q11 or q12) reported previously. The unusual progression of the disease might be associated with the presence of (8;9)(p11;q34), suggesting a part in the 8p11 myeloproliferative syndrome.
Child↗
Granulocyte transfusion: stimulation of low dose granulocyte colony-stimulating factor in donors for leukapheresis.
In order to assess the clinical utility of granulocyte transfusions (GT), the stimulating effects of donor granulopoiesis for GT therapy were examined using either low dose recombinant human granulocyte colony-stimulating factor (rhG-CSF) or dexamethasone (DEX). The increment of leukocytes, polymorphonuclear cells (PMN) and monocytes in the subjects stimulated with rhG-CSF (0.7 microgram/kg SC) surpassed each increment in those with DEX alone (1 mg PO). The lymphocyte counts after DEX stimulation decreased in contrast to those after G-CSF stimulation. This dose of G-CSF did not enhance the priming effects on the superoxide release from PMN. The serum levels of lysozyme, but not of lactate dehydrogenase, in G-CSF stimulated donors were higher than those in DEX-treated donors. The serum macrophage/monocyte-colony stimulating factor (M-CSF) levels in DEX stimulation were lower than in either G-CSF stimulation or no stimulation. The net yield of the PMN in GT on G-CSF stimulation was practically larger than that on DEX stimulation. One of the two patients who received GT collected by DEX stimulation died of aspergillosis. Two of the five patients who received PMN mobilized by G-CSF died of fungal infections or necrotizing fasciitis, although two of the remaining patients overcame severe bacterial infections. These results suggest that low dose G-CSF effectively and safely mobilizes a sufficient quantity of PMN from GT-donors without excessive superoxide generation from the transfused cells. This low dose G-CSF stimulation may be substituted for conventional DEX stimulation for GT.
Adult↗
Kupffer cells play important roles in the metabolic degradation of a soluble anti-tumor (1-->3)-beta-D-glucan, SSG, in mice.
Metabolic degradation of a soluble highly branched (-->3)-beta-D-glucan, SSG, was examined in mice using a macrophage blocker, gadolinium chloride (GdCl3). Intraperitoneally administered SSG distributed in the liver was slowly degraded, and after 5 weeks about 30% of the SSG became anionic. In addition, it is suggested that the metabolites would contain fewer branching points as assessed by the reactivity to limulus factor G. On the other hand, in the spleen, the molecular weight and the degree of branching of SSG were not changed for at least 5 weeks. Blockade of Kupffer cells by GdCl3 did not significantly change the distribution ratio of SSG in the liver. However, the treatment significantly delayed the degradation of SSG. These results suggested that Kupffer cells play important roles, not in the distribution, but in the oxidative degradation of SSG in the liver. In addition, splenic macrophages did not significantly contribute to the metabolic degradation of SSG.
Animals↗
Prostaglandin E receptor subtypes in mouse osteoblastic cell line.
PGE2 is one of the key molecules in the osteoblast. It is the major prostanoid in the bone, and its production is under the control of both systemic and local factors. PGE2 has been reported to have multiple actions in the osteoblast, such as growth promotion and cell differentiation. To better understand the action of PGE2 in the osteoblast, we determined the PGE receptor subtypes in MC3T3-E1, an osteoblastic cell line derived from the normal mouse calvaria. Northern blot analysis revealed that EP1 and EP4 subtypes are expressed in MC3T3-E1. In contrast, EP3 subtype was not detected by either Northern blot analysis or RT-PCR. The contribution of each subtype was evaluated by studying the effects of subtype-specific analogs on osteoblastic function at confluency and 5 days after confluency. An EP1 agonist, 17-phenyl-omega-trinor PGE2, increased DNA synthesis and decreased alkaline phosphatase activity. 11-Deoxy-PGE1, and EP2 and EP4 agonist, decreased DNA synthesis and increased alkaline phosphatase activity at both stages. Butaprost, an EP2-selective agonist, showed effects similar to those of 11-deoxy-PGE1 only at confluency. Another and more differentiated osteoblastic marker, osteocalcin production, was detectable and was stimulated by 11-deoxy-PGE1 only 5 days after confluency. The exposure of these cells to EP1 agonist changed the cell shape to a more fibroblastic appearance. These results indicate that EP1, EP4, and probably EP2 are present in MC3T3-E1 cells; EP1 promotes cell growth, and EP2 and EP4 mediate differentiation of the osteoblast. Furthermore, the decreased response to EP2-specific agonist 5 days after confluency suggests that the expression of PGE receptor subtype is dependent on the stage of osteoblastic differentiation. This is the first report to determine PGE receptor subtypes in the bone.
Alprostadil↗
Idiopathic hypertrophic cranial pachymeningitis associated with hydrocephalus and myocarditis: remarkable steriod-induced remission of hypertrophic dura mater.
We describe a patient with idiopathic hypertrophic cranial pachymeningitis (IHCP) associated with hydrocephalus and myocarditis in whom steroids caused remission of the hypertrophic dura and enlarged ventricles. Myocarditis induced complete atrioventricular block that responded to steroids initially but later required permanent pacemaker implantation. Serum ANA and anti-dsDNA antibody were positive. Our case suggests that IHCP and myocarditis may share a common autoimmune etiology.
Aged↗
Oxyphil parathyroid adenoma associated with primary hyperparathyroidism and marked post-operative hungry bone syndrome.
A rare case of functioning oxyphil parathyroid adenoma associated with primary hyperparathyroidism and marked hungry bone syndrome was revealed in a 29-year-old man with hypercalcemia and elevated circulating parathyroid hormone (PTH) level. A large parathyroid tumor weighing 8.4 g was resected and proved to be an oxyphil adenoma. Hypocalcemia was sustained after the operation, despite intensive calcium supplementation. During the postoperative 8 months, bone mineral density at the lumbar spine increased dramatically from 0.892 g/cm2 to 1.244 g/cm2, and whole body bone mineral content increased from 1,913.4 g to 2,419.2 g. This case gives insight to the reversibility of bone loss in this disorder.
Adenoma, Oxyphilic↗
Spontaneous remission of primary hyperparathyroidism due to hemorrhagic infarction in the parathyroid adenoma.
A 59-year-old man visited Kyoto University Hospital because of general malaise, polyuria, and polydipsia. The diagnosis of primary hyperparathyroidism was made based on hypercalcemia and an elevated circulating PTH level. A nodule was palpable in the left anterior neck. Two weeks later, the serum calcium level was normalized and his symptoms subsided. A temporary expansion, followed by reduction of the tumor size was observed by serial ultrasonography. Histology of the resected tumor showed central necrotic tissue, with some peripherally remaining glandular tissue. We report here a rare case of primary hyperparathyroidism with spontaneous remission due to hemorrhagic infarction in the adenoma.
Adenoma↗
[Scanning and transmission microscopic observations on circulating primitive erythroblasts of yolk sac origin in the mouse embryo].
The earliest hemopoietic tissues which appear during the ontogeny of mammals are the blood islands of the yolk sac, and the blood cells produced therein begin to circulate between the embryo and visceral yolk sac at the establishment of the circulatory system. Primitive erythroblasts derived from the yolk sac have a short life span of only several days, and they form a majority of the embryonic blood cells prior to the start of liver hemopoiesis. To clarify cell fragmentation of primitive erythroblasts at the ultrastructural level, using 18 embryos of ICR-mice at 10 and 11 days of gestation, we observed circulating erythroblasts by scanning and transmission electron microscopy. The circulating erythroblasts generally had an irregularly ovoid contour, and they showed a great deal of micropinocytosis on their cell surface. The nuclei of the erythroblasts were round and possessed one or two nucleoli which were in contact with the nuclear membrane. Their nuclear chromatin was dispersed, and the cytoplasm was rich in polyribosomes and mitochondria. The majority of circulating erythroblasts were at the stage of either basophilic or polychromatophilic erythroblasts. Cytoplasmic projections could occasionally be seen extending from the erythroblast surface, and some of the projections appeared to be liberated into the vascular lumen as cell fragments. On the basis of their size and shape, the cytoplasmic projections could be classified into three types; finger-like projections, vesicular projections and microvesicular projections. The finger-like projections were approximately 1 micron in diameter and 3 microns in length. The vesicular projections, connected with the cell by a narrow stalk, were teardrop in shape, and approximately 0.8 microns in diameter and 1.5 microns in length. The microvesicular projections were approximately 0.2 microns in diameter and 0.2-0.5 microns in length. The finger-like projections had micropinocytotic invaginations on their surface, but no invaginations could be seen on the vesicular and microvesicular projections. Not only the finger-like but also the vesicular projections contained cytoplasmic matrix with a few polyribosomes. The microvesicular projections, on the other hand, occasionally contained myelinic-like figures. These projections were seen on the surface of erythroblasts at various maturation stages. The cytoplasmic fragments released from the erythroblasts were engulfed and eliminated from the embryonic peripheral blood by intravascular macrophages. The fragmentation of cytoplasmic projections was considered to be related to the development of microfilaments involved in the cytoskeleton of the erythroid elements.
Animals↗
[What can we do for cancer patients with pain to go home].
When patients suffering from cancer pain wish to stay at home, the most important condition is to relieve the cancer pain. But it is not enough; decreasing the fear of pain is another important problem. From these viewpoints, we have tried to assist these patients to go home. In this paper we report two cases of 61-year-old and 57-year-old women with severe leg pain caused by pelvic recurrence of cancer of the uterus and rectum. At first, we needed high doses of morphine by intravenous administration all day long. To control their mental condition, we talked personally with them to understand their distress and asked them to put in writing anything about their anxiety in a special notebook. After that, we advised them on how to use anodyne, how to deal with side effects of the drugs and how to use various social services in their home. Then, after their cancer pain was controlled by radiotherapy and appropriate anodyne, they overcame their anxiety and at last they could go home.
Bone Neoplasms↗
Acyl-coenzyme A: cholesterol- acyl-coenzyme A:1,2-diacylglycerol acyltransferase and phosphatidate phosphorylase activities in liver microsomes from nephrotic rats.
The lipid components of very low density lipoproteins (VLDL) were significantly elevated in the nephrotic rats. Also the nephrotic VLDL particles had a significantly higher ratio of surface lipids (FC + PL) to core lipids (TG + CE) probably indicating production of smaller sized VLDL in the nephrotic rats. Electron microscopy showed VLDL particles with a reduced mean size in the nephrotic rats. The activities of VLDL core lipid synthesizing enzymes were evaluated in experimental nephrotic syndrome. In addition, the effects of exogeneous cholesterol, 25-OH-cholesterol and low density lipoprotein (LDL) on the acyl-coenzyme A: cholesterol acyltransferase (ACAT) activity were investigated as well. ACAT activity in nephrosis was normal, but stimulated to varying extents in the presence of these factors. On the other hand, the acylcoenzyme A:1,2-diacylglycerol acyltransferase (ADGAT) and phosphatidate phosphorylase-activities were significantly increased in the nephrotic rats. The microsomal cholesterol (free and ester) and phospholipid concentrations were normal but the triglyceride level was significantly reduced in the experimental group. We speculate that an excess production of smaller-sized VLDL particles due to altered activities of microsomal lipid synthesizing enzymes may occur in puromycin amino nucleoside induced-nephrotic rats.
Acyltransferases↗
Gel-to-sol transition of 13C-labeled (1-->3)-beta-D-glucan, 13C-SSG, assessed by 13C nuclear magnetic resonance (13C-NMR) spectroscopy.
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Adjuvants, Immunologic↗
Membrane-bound glycoconjugates of fetal mouse erythropoietic cells with special reference to phagocytosis by hepatic macrophages.
Using lectin and colloidal iron (CI) stainings in combination with neuraminidase digestion, glycoconjugates on the surface of erythropoietic cells of the yolk sac and liver in fetal mice were examined. Fetal hepatic macrophages were capable of distinguishing between phagocytozed and non-phagocytozed erythroid elements as described in our previous study. Marked differences between these two elements could be ultrahistochemically detected on their cell surface. The phagocytozed elements, such as nuclei expelled from erythroblasts and degenerating primitive erythroblasts, faintly bound neuraminidase-sensitive CI, and neuraminidase digestion imparted a weak peanut agglutinin (PNA) binding. In contrast, erythroblasts at various maturation stages, erythrocytes and normal primitive erythroblasts heavily bound neuraminidase-sensitive CI, and neuraminidase digestion imparted a moderate PNA binding. No differences in binding of either concanavalin agglutinin, Ricinus communis agglutinin-I or PNA were noted between phagocytozed and non-phagocytozed erythroid elements. Desialylation appears to be one of the most important signs for the recognition mechanism of fetal macrophage phagocytosis. During maturation of hepatic erythroblasts, sialic acid changes its affinity for Limax flavus agglutinin from strong to weak, and soybean agglutinin binding sites disappear at the basophilic erythroblast stage. Glycoconjugates on polychromatophilic erythroblasts acquire similar compositions to those of erythrocytes.
Animals↗