[A case of ulcerative colitis showing anti-Rh (e)autoantibody associated with autoimmune hemolytic anemia].
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Biomedical subjects
Publications and source records attributed to Y Yamano.
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The nucleotide and amino acid sequences for rat type I angiotensin II receptor were deduced through molecular cloning and sequence analysis of its complementary DNAs. The rat angiotensin II receptor consists of 359 amino acid residues and has a sequence similar to G protein-coupled receptors. The expression of this receptor gene was detected in the adrenal, liver and kidney by Northern blotting. Sodium deprivation positively modulated the expression of the receptor gene in the adrenal. No detectable change was observed in the expression levels of this receptor gene between spontaneously hypertensive rats and Wistar-Kyoto rats in the tissues examined including the adrenal, brain, kidney and liver. Interestingly the expression of this receptor gene was developmentally regulated.
Angiotensin II elicits different responses which affect cardiovascular, neuronal and electrolyte transport regulation. To understand the mechanisms responsible for its various actions, the receptor for angiotensin II has long been sought, but numerous attempts to purify the receptor have been unsuccessful owing to its instability and low concentration. We report here the expression cloning of a complementary DNA encoding a bovine angiotensin II receptor to overcome these difficulties. The receptor cDNA encodes a protein of 359 amino-acid residues with a transmembrane topology similar to that of other G protein-coupled receptors. COS-7 cells transfected with the cDNA expressed specific and high-affinity binding sites for angiotensin II, angiotensin II antagonist and a non-peptide specific antagonist for type-1 receptor. Dithiothreitol inhibited ligand binding. The concentration of intracellular Ca2+ and of inositol-1,4,5-trisphosphate increased in the transfected COS-7 cells in response to angiotensin II or angiotensin III, indicating that this receptor is the type-1 receptor for angiotensin II. Northern blot analysis revealed that the messenger RNA for this receptor is expressed in bovine adrenal medulla, cortex and kidney.
We report a case of lambda-AL amyloidosis which manifested prominent hepatic cholestasis. The patient was a 71-year-old Japanese male who was admitted to our hospital because of abdominal distension and jaundice. Laboratory examination revealed a marked deterioration of liver function with cholestasis. Gastric biopsy revealed amyloid deposition. Under a diagnosis of primary amyloidosis he was treated with corticosteroid and dimethylsulfoxide. However, jaundice progressed, renal function deteriorated rapidly, and he died two weeks after admission. Autopsy revealed a profound deposition of lambda-AL amyloid not only in the liver but also in the kidneys, spleen, lungs, heart and intestine.
A case of giant metastatic liver VIPoma manifesting WDHA syndrome is described. The patient was a 33-year-old Japanese male who was admitted because of persisting watery diarrhea and weight loss. Laboratory examinations revealed marked hypokalemia, mild hypercalcemia and highly elevated plasma vasoactive intestinal peptide (VIP) and glucagon levels. Intensive imaging examinations disclosed two large tumors in the liver but not in other organs, including the pancreas. Laparoscopy disclosed a slightly elevated purplish-colored large tumor on the surface of the apparently normal liver. At operation, however, a small hard nodule was observed in the tail of the pancreas. Histologically, it was revealed to be a VIPoma resembling a carcinoid or an islet cell tumor, and was identical to the liver tumors. Thus, this neoplasm was considered to be a VIPoma of pancreatic origin, with metastatic lesions in the liver.
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Subjective symptoms and blood findings were studied in 16 construction workers and 30 vehicle repairmen using organic solvent and compared to 30 workers who were not exposed to organic solvents. A statistically significant increase was observed in the prevalence of subjective symptoms, serum phospholipid, lipoprotein fraction and IgE in construction workers and vehicle repairmen. A statistically significant decrease in neutrophils function was observed in construction workers.
Two clones that contain goat growth hormone (gGH) genes were isolated from goat genomic library using goat growth hormone cDNA as a probe. One clone CgGH contained gGH1 gene, and another clone, EgGH, contained gGH2 and gGH3 genes. The clone EgGH contained 491 bp inserted sequence, just upstream of the gGH3 gene, which was not present in the clone CgGH. From the sequencing data of the flanking regions of these gGH genes, short interspersed repetitive sequences (SINES) were found. Four SINES's existed in the CgGH clone and eight SINES's existed in the EgGH clone. The number of the repetitive DNA sequences in the goat genome was estimated about 10(2) copies from the analysis of the reassociation rate. As the number of gGH genes (gGH1, gGH2, and gGH3) per genome was different among individual goats, DNA fragments containing gGH1 gene, and that containing gGH2 and gGH3 genes, were estimated to be allelic on the goat chromosome.
We examined the airway injury of the guinea pig exposed to sulfuric acid submicron aerosols (1 mg/m3). The animals were exposed to filtered air (sham control) or to submicrometer-sized sulfuric acid aerosols for 4 hr/day, 6 days/week, with sacrifices after 4 hours, 3 days, 1, 2, and 4 weeks of acid exposure. Light and electron microscopic examinations revealed that epithelial injury such as disappearance of cilia in the central airways was observed and the severity of the injury increased with exposure duration. This experimental study shows that submicrometer particles of sulfuric acid induces significant alterations in the central airways and may be involved in the incidence of asthma attack.
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Transition from polyclonal to monoclonal gammopathy resulted in myeloma in the course of cirrhosis is rare but of interest. We treated such a case of multiple myeloma of IgG-kappa type associated with alcoholic cirrhosis. The case was a 72-year-old Japanese male patient who was admitted because of ascites and edema. Physical examination and laboratory findings including liver histology were compatible with alcoholic cirrhosis. Serum electrophoresis revealed monoclonal hypergammaglobulinemia of IgG-kappa. Bence Jones protein in urine was positive. Bone scintigraphy and roentgenography revealed small punched out lesions in the skull. A bone marrow clot section showed marked infiltration of atypical plasma cells. From these findings multiple myeloma associated with alcoholic cirrhosis was diagnosed. On the basis of a review of the reported cases, the possible relationship between monoclonal gammopathy and chronic liver diseases was discussed.
A patient of Coombs negative autoimmune hemolytic anemia was massively transfused of 162 units concentrated red blood cells in 3 months and developed iron overload disease which was confirmed by liver biopsy. Hemolysis was successfully treated with high-dose methyl-prednisolone therapy and splenectomy. To treat iron overload, we administered recombinant human erythropoietin (Epo) in combination with phlebotomy. Total iron removed for 5 months was about 4 g. Thus, combination of Epo and phlebotomy was effective for the treatment of iron overload disease. Furthermore, we compared a degree of clinical effect of subcutaneous administration of Epo with that of intravenous administration in the clinical course and found the former more effective.
The objectives of this study were to determine the LC50 of methyl bromide (MeBr) and the dose-response curve and to study the detoxication effect of reduced glutathione (GSH) on MeBr poisoning in mice. 1) The LC50 of 4-h exposure to MeBr was 405 ppm in male mice with 95% confidence limits of 386-425 ppm. 2) The mortality rates of mice exposed to 500 ppm MeBr for 105, 120, 130, 140, 150 and 180 min were 0, 0, 10.7, 15.0, 85.0 and 90.0%, respectively. 3) In contrast, the mortality rate of mice pretreated with GSH (i.p 500 mg/kg; GSH-group) was only 5.3% after exposure to 500 ppm MeBr for 150 min. 4) Metabolic substances (Br-, GSH, formaldehyde, formic acid and beta-glucuronidase) were analyzed after exposure to 500 ppm MeBr and compared with the GSH-group and the distilled water treated group (DW-group). Except for GSH, concentrations of all other substances were significantly lower in the GSH-group than in the DW-group. Erythrocyte osmotic fragility test showed a significant increase in fragility in the DW-group. These results suggested that the onset of symptoms or death due to MeBr poisoning suddenly occurs at some point of concentration and time exposure. It was also shown that pretreatment with GSH effectively reduced mortality due to MeBr exposure.
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A case of hemodialysis-associated amyloidosis in a patient who had been on hemodialysis for 10 years is described. Bone lesions were found in the humeral heads, carpal bones, and femoral heads and necks. Specimens obtained from the pathologically fractured left femoral neck revealed amyloid deposits histologically. Immunoperoxidase staining for beta-2 microglobulin was positive in the amyloid at the light-microscopic level. We reconfirmed that bone lesions associated with long-term hemodialysis are manifestations of amyloidosis of beta-2 microglobulin origin. Hemodialysis-associated amyloidosis should be considered in the treatment of long-term hemodialysis patients.
Porin-deficient mutants of Pseudomonas aeruginosa PAO1 were selected by isolating latamoxef-resistant mutants following chemical mutagenesis. Highly latamoxef-resistant mutants had alterations in both the outer membrane proteins and penicillin-binding protein 3, a lethal target of latamoxef. Both of these alterations may be essential for cells to acquire high resistance to latamoxef. Many of the latamoxef-resistant mutants were also resistant to new quinolones and chloramphenicol. Resistance to these compounds was simultaneously co-transduced from one mutant into strain PAO1 when selection was made for transduction of ofloxacin resistance. Study of these transductants indicated that decreased amounts of outer membrane proteins C, D2, E1, and E2 lowered the outer membrane permeability and resulted in resistance. Three of these proteins were apparently identical to proteins previously reported to function as small pores. The results suggested that at least one of the four proteins was functioning as a porin for the antibacterial agents studied.
Using surgical specimens from patients with lung tumor, alveolar apertures and alveolar sizes were quantitatively assessed using scanning electron microscopy. Compared with smoking habits, increased apertures, defined as alveolar destruction were observed in patients smoking more than 35 years, whereas alveolar size was increased in patients, with a 15-year smoking history. Experimental studies with exposure to NO2, O3 and H2SO4 mist showed that exposure of NO2 and H2SO4 could induce epithelial injury such as disappearance of cilia in the central airways.