Effects of ethanol and lead on mouse chromosomes.
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Animals↗
Biomedical subjects
T Imai
Publications and source records attributed to T Imai.
[Insulin binding to erythrocytes in chronic glucocorticoid deficiency--investigation before and during replacement therapy].
The effect of chronic glucocorticoid deficiency on insulin binding to erythrocyte was evaluated in 2 cases of ACTH deficiency, 2 of Sheehan's syndrome and a case of Addison's disease before and after the replacement therapy with cortisone acetate. 75 gram oral glucose tolerance test (OGTT) was also performed. Mean fasting plasma glucose (FPG) and insulin (FIRI) before (70.2 mg/dl, 3.6 microU/ml) and after (75.4 mg/dl, 7.8 microU/ml) therapy were significantly lower than those in normal control (97.0 mg/dl, 12.0 microU/ml). The ratio of FIRI/FPG before and after treatment were also significantly lower than that in control subjects. Glucose areas during OGTT before and after treatment were not different from that in control subjects. However, insulin area before treatment was significantly lower than that in control group. There were significant increases in FIRI/FPG and insulin area, but not in FPG and glucose area before and after treatment. Insulin binding to erythrocytes before treatment (11.9 +/- 1.1%, mean +/- SD) was greater than that in normal subjects (7.7 +/- 1.9%, n = 19, p less than 0.05). It was significantly decreased and normalized to 7.8 +/- 2.0% by the treatment. Analysis of binding parameters revealed the increases in receptor concentration at high affinity site (R1) and in average affinity at empty site by average affinity profile (Ke) before treatment in comparison with control subjects. There was no significant difference in binding parameters after treatment and in control group. High R1 or low R2 observed before treatment was significantly decreased or increased after treatment, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
Addison Disease↗
Fluorescent investigations of binding of phenprocoumon to alpha 1-acid glycoprotein.
The fluorescence of phenprocoumon is greatly enhanced on binding to a single site on alpha 1-acid glycoprotein (alpha 1-AGP). Advantage is taken of this phenomenon to estimate a binding constant for the binding of phenprocoumon to alpha 1-AGP. The fluorescence intensity and binding constant of the phenprocoumon: alpha 1-AGP complex decreased with pH from 6.5 to 8.5, suggesting that phenprocoumon binding to alpha 1-AGP is significantly affected by microenvironmental change in alpha 1-AGP. A variety of drugs, including chlorpromazine and dicumarol, significantly inhibited phenprocoumon binding to alpha 1-AGP. Fatty acids seem to displace phenprocoumon from its binding site on alpha 1-AGP, whereas the addition of neutral salts and sialic acid did not cause the displacement of phenprocoumon. It is concluded that the phenprocoumon binding site is located in the hydrophobic protein structure of alpha 1-AGP.
Binding Sites↗
A case of diabetes mellitus associated with anti-insulin autoantibodies without previous insulin injection.
A case of diabetes mellitus who had high levels of fasting immunoreactive insulin (IRI) and low levels of immunoreactive C-peptide (CPR) is reported. Examination of her serum disclosed the presence of IgG class k + lambda type anti-insulin autoantibodies. She has never been treated with insulin, nor had drugs which have been reported to be responsible for inducing insulin autoimmune syndrome. Despite the presence of autoantibodies against insulin, she has never experienced hypoglycemia. Significance of the production of autoantibodies against insulin and physicochemical parameters of anti-insulin antibodies in her serum are discussed.
Autoantigens↗
Metabolism of nicotinamide mononucleotide in beef liver.
Nicotinamide mononucleotide (NMN) is not only an intermediate for the biosynthesis but also a degradation product of pyridine cofactors in animal tissues. Among the animal tissues tested, the highest NMN catabolizing activity was detected in beef liver (5.6 mumol/min/g tissue). This activity was 16 times higher than the NAD hydrolysis catalyzed by the liver NAD glycohydrolase. As a result of enzymatic analysis of the NMN splitting process, two types of enzyme responsible for this catabolism were partially purified and identified as a membrane-bound 5'-nucleotidase and a cytoplasmic nicotinamide riboside (NR) phosphorylase. No specific NMN glycohydrolase could be found in contrast to results observed in bacterial systems. The 5'-nucleotidase and NR phosphorylase constitute an obligatory process of the pyridine nucleotide cycle. The dephosphorylation and phosphorolysis catalyzed suggest that these enzymes could serve as an important mechanism for salvaging the ribose and nicotinamide moieties of NMN and pyridine nucleotides in the cell and a process that could be regulated at the mononucleotide level by this "NMN cycle" rather than by a NAD glycohydrolase cycle. In addition to the enzymatic properties of these enzymes, a regulatory mechanism by nucleotides such as ATP was also demonstrated.
5'-Nucleotidase↗
Nicotinamide riboside phosphorylase from beef liver: purification and characterization.
Nicotinamide riboside phosphorylase (NR phosphorylase) from beef liver has been purified to apparent homogeneity at 300-fold purification with a 35% yield. Kinetic constants for the enzyme-catalyzed phosphorolysis were as follows Knicotinamide riboside, 2.5 +/- 0.4 mM; Kinorganic phosphate, 0.50 +/- 0.12 mM; Vmax, 410 +/- 30 X 10(-6) mol min-1 mg protein-1, respectively. The molecular weights of the native enzyme and subunit structure were determined to be 131,000 and 32,000, respectively, suggesting the beef liver NR phosphorylase to be tetrameric in structure and consistent with the presence of identical subunits. The amino acid composition was shown to be very similar to that reported for human erythrocyte purine-nucleoside phosphorylase but differing considerably from that found for rat liver purine-nucleoside phosphorylase. In addition to catalytic activity with nicotinamide riboside, the beef liver enzyme catalyzed a phosphorolytic reaction with inosine and guanosine exhibiting activity ratios, nicotinamide riboside:inosine: guanosine of 1.00:0.35:0.29, respectively. These ratios of activity remained constant throughout purification of the beef liver enzyme and no separation of these activities was detected. Phosphorolysis of nicotinamide riboside was inhibited competitively by inosine (Ki = 75 microM) and guanosine (Ki = 75 microM). Identical rates of thermal denaturation of the beef liver enzyme were observed when determined for the phosphorolysis of either nicotinamide riboside or inosine. These observations coupled with studies of pH and specific buffer effects indicate the phosphorolysis of nicotinamide riboside, inosine, and guanosine to be catalyzed by the same enzyme.
Amino Acids↗
Isolation and characterization of an activator for Azotobacter vinelandii nicotinamide mononucleotide glycohydrolase.
Azotobacter vinelandii NMN glycohydrolase [EC 3.2.2.14] has been shown to require absolutely GTP or a high-molecular-weight and heat-stable component for its function. The intracellular activator could be purified from its sonicate by heat treatment, acetone precipitation, phenol extraction, and acid precipitation in a good yield. The purified activator showed high affinity and effectiveness for NMN glycohydrolase (KA = 0.012 optical density unit at 257 nm/ml; Vmax standardized by the activity at 1 mM GTP = 88%). Negative cooperativity of the enzyme activation with the activator was also shown. On treatment with either micrococcal nuclease or pancreatic RNase, the activator activity was completely abolished, whereas pronase and trypsin had no effect. The activator could be replaced by yeast RNA as well as calf liver RNA, whereas DNAs purified from Micrococcus lysodeikticus, T 7 and calf thymus had no effect on the enzyme. Furthermore, poly(G) and poly(I) could function as activators with the same effectiveness as the purified activator, and the enzyme activation with these RNA homopolymers was inhibited by poly(C), suggesting that the activation mechanism is specific with respect to base composition. Based on a kinetic analysis of the enzyme activation with commercial RNAs, together with the results from enzymatic digestion, specific inhibition of the enzyme by spermine, and its chemical properties, the activator was identified as an RNA. A model is described for NMN glycohydrolase regulation in which the RNA activator plays an important role in the NMN salvage cycles.
Azotobacter↗
Properties of allosteric nicotinamide mononucleotide glycohydrolase from Azotobacter vinelandii: activation and inhibition.
In order to clarify the regulation mechanism of NMN glycohydrolase, a number of purine and pyrimidine nucleotides were tested as activators for the enzyme. Among naturally occurring nucleotides, pppGpp was shown to be the most potent activator (KA = 0.0087 mM). The effectiveness of these nucleotides estimated from Vmax/KA was in the order: pppGpp greater than ppGpp greater than pppppG greater than ppppG greater than pGpp greater than GTP greater than or equal to 2'-GMP greater than or equal to GppppG greater than dGTP greater than ITP greater than GDP = 2'-O-methylGTP. XTP, UTP, dTTP gave no effect. In contrast, ATP, CTP, and 7-methylGTP were inhibitory. A comparison of the data indicated that activation of the enzyme is specific for the base structure, guanine, and that effectiveness of nucleotides as activators results from the negatively charged phosphate moiety. Consistent with these results, inorganic polyphosphates (tri-, tetra-, and pentaphosphate) and 5-phosphoribose 1-pyrophosphate were shown to function as inhibitors of the enzyme. The inhibition mechanism was shown to be competitive with GTP. However, apparent Ki values for these inhibitors were dependent on the activator concentration. Furthermore, a shift of cooperativity type and progressive increase of positive cooperativity concomitant with increase of PRPP concentration were observed. These results indicate that this enzyme may be allosteric and an important regulatory component of pyridine nucleotide cycle metabolism.
Allosteric Regulation↗
Multiple necrotizing fasciitis: its etiology and histopathological features.
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Adult↗
A comparative study of the interaction of warfarin with human alpha 1-acid glycoprotein and human albumin.
The interaction of warfarin with human alpha 1-acid glycoprotein (alpha 1-AGP) and human albumin (HA) has been investigated using fluorescence and circular dichroism techniques. The fluorescence of warfarin is greatly enhanced following binding to alpha 1-AGP or HA, the binding constant for a single site being estimated by the Scatchard method. The binding constants for the two serum proteins are similar, but the thermodynamic parameters differ. The binding constants increase as the pH is raised to 9.0. Various basic drugs, such as chlorpromazine, propranolol and imipramine, markedly inhibited the binding of warfarin to alpha 1-AGP. But, some acidic drugs, including phenylbutazone, effectively displaced warfarin bound to HA. The difference in CD spectra observed for alpha 1-AGP and HA indicated that the drug-binding sites of the two proteins might have different asymmetries. It thus appears that the mode of interaction of warfarin with the two proteins differs.
Circular Dichroism↗
13 trisomy born to a mother treated with bromocriptine: incidental or not?
A case of 13 trisomy born to a mother treated with bromocriptine is described. She, 27 years old, was treated with bromocriptine (5 mg/day) as a galactorrhea amenorrhea syndrome with hyperprolactinemia (basal 34-122 ng/ml). After the treatment for about a month, disappearance of galactorrhea and occurrence of menstruation were observed. She became pregnant on the second ovulation. On the 34th week she got a male 13 trisomy (47, XY, +13) baby with premature delivery. The baby died 11 hr after his birth. After the first delivery, bromocriptine was readministered. Following the induced abortion on the second pregnancy, she borned a healthy baby on the third pregnancy in spite of taking bromocriptine. This case of 13 trisomy might be incidental. However, the effect of bromocriptine on chromosome should be further evaluated in detail.
Adult↗
Histogenesis and characterization of minimal bronchogenic carcinoma observed in heavy smokers.
The present article describes the results of observations of 11 lesions in 8 cases of roentgenographically occult in situ or microinvasive squamous cell carcinoma with a size of 4 X 4 mm or less which were detected by detailed histologic investigations of 59 cases of occult bronchogenic carcinoma. The 59 cases were discovered mainly by mass screening for the detection of early lung cancers using chest x-ray combining sputum cytology for heavy smokers. The resected specimens were processed with the method of serial block sectioning. All the serial blocks of these minimal carcinomas were observed in detail to confirm the presence or absence of carcinoma and of morphological changes of the bronchial epithelium contiguous to carcinoma. Adjacent to carcinoma, there were normal bronchial epithelium in three lesions, squamous metaplasia with marked atypia in four, basal cell hyperplasia in two, and markedly atypical basal cells without hyperplasia in two. An inference on histogenesis of bronchogenic squamous cell carcinoma was drawn from the detailed observations as follows: (1) A carcinoma develops in the area of squamous metaplasia with marked atypia; (2) A carcinoma arises from markedly atypical basal cells with or without prior hyperplasia. Even in such small-sized carcinomas, there is a difference in type of invasion within the bronchial wall. One is the creeping type which shows a marked horizontal growth and the other is the penetrating type which shows a marked downward growth.
Aged↗
[13 trisomy born to a mother with galactorrhea-amenorrhea syndrome].
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Abnormalities, Drug-Induced↗
[Low-tone noise accompanied by hemifacial spasm. Case report].
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Facial Muscles↗
[Subacute cerebellar degeneration with HCG-beta positive seminoma of the testis].
Neurological disorders associated with a malignant neoplasm, which is not caused by a direct effect such as metastasis, infiltration or compression, is called carcinomatous neuromyopathy. Subacute cerebellar degeneration recognized in this category is characterized by acutely or subacutely progressive cerebellar ataxia and widespread loss of Purkinje cells. There have been several reports of subacute cerebellar degeneration in lung carcinoma, ovarian carcinoma and Hodgkin's disease, but rare in urogenital malignancies. We present a patient with neurological disorder considered subacute cerebellar degeneration associated with HCG-beta positive seminoma. A 29-year-old man noticed a left intrascrotal mass in the summer of 1984. The mass began to grow in April, 1985 and diplopia, gait disturbance and dysarthria appeared late in May. He consulted our hospital on July 20, 1985. Serum human chorionic gonadotropin (HCG)-beta was elevated to 200 ng/ml but alpha-fetoprotein and carcinoembryonic antigen were normal. Left high orchiectomy was performed and the tumor was diagnosed histologically as typical seminoma. Bulky metastatic tumor was recognized in retroperitoneum on abdominal CT but brain CT was normal. VAB VI chemotherapy was performed. The retroperitoneal metastatic tumor disappeared and HCG-beta was normalized and complete remission achieved, but cerebellar symptoms still remain 14 months after remission. This case is considered to be subacute cerebellar degeneration associated with seminoma and is the second case with testicular carcinoma reported.
Acute Disease↗
[A case report of multiple endocrine neoplasia type 2b].
A 10-year-old girl was admitted displaying a medullary thyroid carcinoma, accompanying neurinomas of the tongue, marfanoid habitus, megacolon, and scoliosis. Although her adrenal glands were found to be unremarkable on both CT and ultrasonogram examination an MIBG scintiscan showed a 131-1 uptake, suggesting the presence of medullary hyperplasia. Remarkable nodal involvement with invasive features witnessed in the upper mediastinum during tertiary surgery four years later, following a total thyroidectomy. The TCT and CEA profiling was not sufficient enough to predict a recurrence. At the present state there is difficulty in providing an early diagnosis; through node dissection, however, is considered to be necessary at time of primary thyroid operation in cases with MEN type 2b.
Carcinoma↗
[Microangiopathic hemolytic anemia (MAHA) and renal failure induced by anti-neoplastic agents--a case report].
A 65-year-old man underwent left-upper lobectomy for large cell carcinoma of the lung on November 8, 1984 (pT1N0M0: Stage I a). He was treated with MMC, Futraful, CDDP and CPM as adjuvant chemotherapy. In April 1985, he was re-admitted to our hospital because of progressive dyspnea. He was diagnosed as having drug-induced interstitial pneumonia, and so steroid therapy was started. In July 1985, he suffered from anemia, thrombocytopenia, proteinuria and azotemia progressively, and died due to pulmonary hemorrhage and edema. At necropsy, no cancer recurrence was found. It thus seemed that the cause of death was microangiopathic hemolytic anemia and renal failure induced by anti-neoplastic agents.
Acute Kidney Injury↗