Effect of tunicamycin on molecular heterogeneity of colony stimulating factor in cultured mouse mammary carcinoma FM3A cells.
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Biomedical subjects
Publications and source records attributed to Y Yamamoto.
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A female infant with del(21)(pter leads to q22.1--2:) constitution identified by G, Q, and R banding is reported. She had marked mental and physical retardation, generalized hypertonia, microphthalmia with persistent hypoplastic primary vitreous, blepharochalasia, high nasal bridge, micrognathia, malformed ears with preauricular pits, and overlying fingers. The assay for superoxide dismutase-1 (SOD-1) activity in the patient revealed a normal value and it was suggested that the gene locus for SOD-1 in 21q22.2 leads to qter is not compatible with the presence of the gene dosage effect in the monosomic state.
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A strain with both the polA12 and the alk-1 mutation is only slightly more sensitive to methyl methane sulfonate (MMS) than isogenic strains with only one of the mutations. On the other hand, alk-1 recA1 double mutant is much more sensitive to MMS than are strains carrying either one of alk or recA mutation. It was suggested that the alk and the polA gene products are involved in the same DNA repair process whereas the recA function is independent from the process. The yield of MMS-induced mutation (Arg- (argE) to Arg+ reversion) in alk mutant is considerably higher than that in wild type strain. Thus, the repair process in which the alk gene product is involved is relatively accurate. When MMS-treated lambda phages were plated on MMS-treated bacteria, there were considerable increases in survival of treated phage even in recA alk double mutant. It seems that a new repair pathway, which is specific for alkylating agent-induced damages and is not dependent on the RecA function, may be induced on exposure of bacteria to the alkylating agent.
A high-performance liquid chromatographic procedure has been developed for the separation and fluorometric detection of guanidino compounds in physiologic fluids. All guanidino compounds were separated on a 17 X 0.46 cm cation-exchange column using a stepwise pH gradient. The chromatographic system was designed to enable the use of the specific reagent 9,10-phenanthrenequinone as a means of monitoring the guanidino compounds of physiologic fluids. This new analytical method is so sensitive that it enables the analysis at the picomole level. Our automatic guanidino-compound analyzer was successfully applied to the quantitative determination of all guanidino compounds in physiologic fluids from normal controls and uremic patients.
A rapid and sensitive high-performance liquid chromatographic method has been developed for the quantitative analysis of methylguanidine and guanidine in physiological fluids. These quanidino compounds are separated on a 6 x 0.23 cm cation-exchange column with 0.5 M sodium hydroxide solution. The guanidino compounds are detected with a fluorometer, which monitors the fluorescent guanidine derivatives produced by the reaction of the eluted constituents with 9,10-phenanthrenequinone. Sensitivity to sub-nanomole levels of methylguanidine and guanidine is demonstrated. The method was successfully applied to physiological fluids such as serum and cerebrospinal fluid from uremic patients.
Prolidase deficiency occurred in a 13-year-old girl. Determinations were made of prolidase and prolinase activities in cultured fibroblasts, and thin layer chromatographic studies of skin prolidase were performed. The patient had chronic, recurrent ulcers on the legs and feet, diffuse telangiectasia, shallow scar-like atrophic lesions on the face and arms, soft and thin abdominal skin, and premature gray hairs. Prolidase in the patient's skin fibroblasts was absent. Greatly reduced prolidase activity was demonstrated in the patient's skin. A review of hitherto reported cases of this disease showed such skin manifestations as (1) skin ulceration or skin fragility with scar formation, (2) purpuric lesions, (3) telangiectasia and/or photosensitivity, and (4) thickening of the skin with lymphedema.
Blood cyanide concentration was determined in rabbits intoxicated orally or by inhalation. Experiments were carried out under urethane anaesthesia. In the inhalation experiments, rabbits inhaled a combustion product containing HCN via the tracheal cannula and in the oral studies animals were administered NaCN solution into the stomach. In addition to the carotid artery and jugular vein blood samples, postmortem samples were obtained from both sides of the heart and the descending vena cava. The arterial cyanide concentration in the inhalation group showed a close relationship with ventilation. After an initial rise, blood levels decreased a little, in some cases with transient apnea. At the last stage it again increased with gasping, reaching its maximal value. After ultimate apnea, the blood cyanide concentration declined. The blood cyanide values were higher in the oral group than in the inhalation group. The difference between the two groups became larger in the inferior order, the left heart blood--the right heart blood--blood in the descending vena cava. The left heart/right heart ratio of the inhalation group was significantly higher than that of the oral group (1.28+/- 0.28 vs. 0.95+/- 0.09). The coefficient of variation (c.v.) of the inhalation group was larger than that of the other group. Within the inhalation group, the left heart blood showed the largest c.v. values and this was probably due to redistribution of the cyanide by bloodstream after attainment of the maximal concentration.
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Binding of L cell interferon to lectins, Wistaria floribunda agglutinin (WFA) and concanavalin A (Con A) was studied by affinity chromatography. Of the two molecular species of L cell interferon, F (mol. wt. 24,000) and S (mol. wt. 36,000), only the latter was bound efficiently to WFA-Sepharose and eluted quantitatively with D-galactose followed by a pH 3 buffer, suggesting a substantial difference between the two interferon species in their carbohydrate structure. Both were partially bound to Con A-Sepharose and eluted with alpha-methyl-D-glucoside, indicating that at least some of the F species are also glycoprotein, and that both F and S interferon are heterogeneous as regards their affinity to this lectin.
Although activated charcoal and alumina have been used extensively as sorbents in uremic patients, the following problems remain to be solved: 1) elution of SO4--from activated charcoal which does not adsorb it; 2) production of methylguanidine from creatinine on the surface of activated charcoal; 3) production of lipoperoxide from fatty acids by chemical reaction of activated charcoal; 4) adsorption of Ca++ and Mg++ when alumina adsorbs inorganic phosphate. These problems are studied in vitro and clinically.
In the capillary tube migration system a synthetic muramyl dipeptide (MDP; N-acetylmuramyl-L-alanyl-D-isoglutamine), a part of bacterial cell wall peptidoglycans, inhibited the migration of peritoneal exudate macrophages from normal guinea pigs or rats. The migration inhibition was also caused by some MDP-containing peptidoglycan fragments from cell walls of Lactobacillus plantarum and Staphylococcus epidermidis. The migration inhibition could not be explained on the basis of macrophage migration inhibitory factor. A stereochemically highly specific structure of MDP required for its adjuvant activity was also required for the macrophage migration inhibition. These findings suggest that MDP and MDP-containing cell wall fragments may activate macrophages and that this activation may be important in the exertion of their adjuvant activity.
A case of partial trisomy 17 with partial monosomy X resulting from a maternal X-autosomal translocation t(X;17)(q13;q21) is presented. Three previously reported cases are reviewed and the phenotypic features of trisomy 17 are discussed.
Interference between two different in vivo antigen-antibody reactions which occurred simultaneously was studied in guinea pigs. Animals were presensitized with an aqueous fraction (CP) extracted from cells of Corynebacterium equi, strain KO-85. Skin reactions of the Arthus type elicited by the CP fraction inhibited passive cutaneous anaphylaxis (PCA) induced by bovine serum albumin (BSA) and rabbit anti-BSA serum. PCA reactions of the CP-sensitized animals were also inhibited upon simultaneous challenges of BSA and the CP as evidence by reduction of PCA titer of the anti-BSA serum.
Parinaud syndrome, associated with a left thalamic hemorrhage, disappeared completely in a 57-year-old woman after ventriculoperitoneal shunt. The syndrome may be attributed to increased intracranial pressure owing to mass effect on the pretectal region and tectum, or to tightness in the incisura causing hydrocephalus secondary to aqueduct compression. The lesions responsible for the syndrome may not be irreversible.
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