[A case of polypoid aberrant artery protruding into the bronchus--massive hemoptysis during laser irradiation therapy].
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Biomedical subjects
Publications and source records attributed to H Wada.
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Twenty-four hr after a single subcutaneous injection of Cd (0.024 mmol/kg), the testis showed severe and widespread degeneration. The damage was accompanied by an increase of lipoperoxide and a decrease of glutathione in the testis. Se (0.048 mmol/kg) injections 2 hr before, at the same time, and 1 hr after the Cd injection, decreased the damage. In these groups, the level of glutathione and lipoperoxides was restored to the control level. With a Se injection 6 hr after the Cd injection, the preventive effect of Se was no longer found. In the testis in which Se injection alleviated the damage caused by Cd, the changes in Ca, Mg and Zn were also restored to the control level. Uptake of Cd into the testis was stimulated by the Se injection. However, the uptake still remained at a low level in the testis in which the Se preventive effect was not found. These results suggest that the preventive effect of Se against testicular Cd toxicity is dependent on the interval between Cd and Se injections.
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A highly sensitive and specific method was developed for the determination of histamine in biological materials by high-performance liquid chromatography with a cation exchanger and an automated Shore's fluorometric detection system. Since substances causing interference in Shore's o-phthalaldehyde method, such as ammonia, histidine, spermine and spermidine, were completely separated on the column and their fluorescent intensities were much less than that of histamine in this detection system, histamine could be determined by injecting a perchloric acid extract of human plasma or mouse brain tissue directly onto the column without any previous purification procedure. The lower limit of detection of histamine by this method is 0.05 pmol, and the within-day and day-to-day variations in plasma histamine assay are less than 3%. The plasma histamine level in normal human subjects was found to be 4.0 +/- 1.6 pmol/ml (mean +/- S.D., n = 20). A good linear correlation was obtained between values for the histamine contents of mouse brain tissues determined by this method and by a radioenzymatic method with a purified histamine-N-methyltransferase preparation. The histamine levels of whole brain, hypothalamus, thalamus, brain stem and frontal cortex in male ddY mice were 367 +/- 38, 1143 +/- 70, 414 +/- 66, 196 +/- 47 and 467 +/- 91 pmol/g of wet tissue (mean +/- S.D.), respectively.
On amino acid analysis of urine of histidinemic patients, an unidentified compound was eluted in a position between beta-aminoisobutyric acid and gamma-aminobutyric acid. This compound was purified to homogeneity from the urine by a combination of extraction with 80% ethanol, repeated column chromatography on Bio-Rad AG-50, and high performance liquid chromatography on a strongly cationic ion exchanger. The compound yielded free histidine on hydrolysis in an evacuated sealed tube with 0.1-6.0 M HCl at 145 degrees C for 5 h, but not at 100 degrees C for 24 h. This compound was determined to be N tau-ribosylhistidine by 1H and 13C NMR spectroscopies. The urinary content of this material in normal and histidinemic children was 17.8 +/- 13.4 (n = 10) and 126 +/- 51 (n = 14) mumol/g creatinine (mean +/- S.D.), respectively, and were closely correlated with those of urinary histidine. The renal clearance value of N tau-ribosylhistidine in humans was 96% of that of creatinine. When rats were fed on diets rich in histidine, the urinary excretion of N tau-ribosylhistidine increased greatly and was well correlated with the intake of histidine.
L-Histidine decarboxylase [L-histidine carboxylyase, HDC, EC 4.1.1.22] is an enzyme distinct from L-DOPA decarboxylase [L-aromatic amino acid carboxylyase, DDC, EC 4.1.1.28]: the two decarboxylases from fetal rat liver were completely separated from each other by DEAE-cellulose column chromatography and by affinity chromatography with L-carnosine as a ligand. The antibody raised against this HDC inhibited the HDC's from rat and guinea-pig brains very strongly, but their DDCs very weakly. However, in immunofluorescent histochemical studies, the antibody cross-reacted with DDC-like immunoreactive structures, such as chromaffin cells of the adrenal medulla, the raphe nucleus, the substantia nigra, and the locus coeruleus of the brain of guinea-pigs, but not of rats, suggesting that these two decarboxylases share some antigenic structures.
A high-performance liquid chromatographic (HPLC) method is reported for the determination of dopamine-3- and -4-O-sulphate isomers in human plasma and urine using an anion exchanger coupled with post-column hydrolysis and fluorimetric detection. Samples of plasma or urine are partially purified on Dowex 1 and Dowex 50 columns and separated using HPLC. These compounds are then hydrolysed and determined automatically by the p-aminobenzoic acid method in a continuous-flow reaction system. As the p-aminobenzoic acid method is very specific for dopamine, it is also possible to determine the isomers by injecting 5-20 microliter of urine or 100-200 microliter of deproteinized plasma directly into the HPLC system without clean-up. The detection limit of the method for both isomers is 0.3 pmol. In normal subjects, the plasma levels of dopamine-3- and -4-O-sulphate are 26.5 (S.D. 11.1) and 2.68 (S.D. 0.34) pmol/ml, and their urinary excretion rates are 1.73 (S.D. 0.56) and 0.27 (S.D. 0.04) nmol/min, respectively. Thus the two isomers are present in both plasma and urine and their urinary excretions reflect directly their plasma levels.
The formation of N tau-ribosylhistidine (His-R), a novel histidine derivative found in the urine of histidinemic patients, was studied. A most possible synthetic pathway catalyzed by imidazole acetic acid (ImAA) phosphoribosyltransferase was not substantiated, because p.o. administration to humans and rats of aspirin, an inhibitor of the enzyme, did not change the urinary excretion of His-R, whereas aspirin decreased the excretion of ImAA-R with concomitant increase in that of ImAA. His-R was produced on incubation of a rat liver homogenate or its membrane fraction with histidine, NAD(P)+ and MgCl2, but not with only histidine or NAD(P)+. Nicotinamide inhibited the formation of His-R. Thus the enzymes responsible for the formation of His-R were suggested to be NAD(P)+ nucleosidase, nucleotide pyrophosphatase and 5'-nucleotidase.
Histidine decarboxylase (HDC) activity increased 13-, 7-, and 2-fold in the spleen, lung and liver, respectively, but not in other tissues of C57BL/6 mice injected i.v. with 50 micrograms/kg of Staphylococcal enterotoxin A (SEA). But even in the spleen, increase in the histamine level was only 1.5 times that of untreated mice. In genetically mast cell-deficient WBB6F1 - W/Wv mice HDC activity in the spleen increased to the same extent as in wild type WBB6F1 - +/+ mice on SEA treatment, but the histamine level in the spleen also increased 20-fold, whereas it increased only 1.4-fold in +/+ mice. These results suggest that the increases in HDC and histamine resulted from interaction of SEA with non-mast cells in tissues.
The localization of cytosolic (s) or mitochondrial (m) glutamic oxaloacetic transaminase (GOT) was examined in the rat retina by means of an indirect immunofluorescence method using antibodies specific for s- and m-GOT. The m-GOT-like immunoreactive structures were seen on the inner segments of the photoreceptor cells and other outer and inner plexiform layers. These structures were dot-like in appearance. Somas were not labeled. In contrast, s-GOT-like structures were found on the inner segments and inner fibers of the photoreceptor cells, numerous cell somas in the inner nuclear layer (horizontal, amacrine and bipolar cells), and ganglion cell layer (displaced amacrine cells) and inner plexiform layer. The difference in distribution between s- and m-GOT isozymes suggests that they may be useful as markers for glutamatergic and/or aspartinergic neurons.
The effect of about one hundred compounds on the activity of histidine decarboxylase partially purified from whole bodies of fetal rats was determined. Most of them at their 10 mM concentration had little effect on the enzyme activity; but 12 compounds inhibited the enzyme to a greater extent than 30%. Among these, except for alpha-methylhistidine that has been known to be a strong and specific inhibitor, DOPA, homocysteine, cysteine, methionine and urocanic acid were the best inhibitors; beta-phenyllactic acid, phenylpyruvic acid and carnosine were less strong inhibitors; valine, oxaloacetic acid and N tau-methylimidazole acetic acid were weak inhibitors. Histamine had no inhibitory action. Thus, the substrate binding site of histidine decarboxylase is very rigid and specific for L-histidine.
The existence of a histidine decarboxylase (HDC)-immunoreactive diencephalo-spinal pathway in the rat was demonstrated using an antiserum raised against HDC from fetal rat liver. HDC-immunoreactive nerve cell bodies were numerous in the ventral and lateral caudal hypothalamus. More caudally, in the mesencephalon, no cell bodies were observed but fairly many, transversely cut nerve fibres were found in association with the fasiculus longitudinalis medialis bilaterally. At the most caudal medullary level these longitudinally passing fibres became displaced ventrally to a position just laterally to the pyramidal decussation. In the spinal cord the fibres were more dispersed and rather sparse in most areas. The existence of a diencephalo-spinal HDC-immunoreactive pathway was verified by analyzing material from rats which had received injections of the retrograde fluorescent tracer True Blue into the cervical spinal cord. True Blue fluorescence and HDC immunofluorescence were found to coexist in a subpopulation of the HDC-immunoreactive neurones in the hypothalamus.
Effects of alpha-fluoromethylhistidine (FMH), an irreversible inhibitor of histidine decarboxylase, on the sleep-waking parameters were studied in rats for 24 hours. Intraperitoneal administration of FMH (100 mg/kg) at 11:30 hr resulted in a longer sleep latency compared with the control values. Hour-to-hour analyses revealed that wakefulness (W) time decreased (from 20:00 to 07:00 hr) and slow wave sleep (SS) time increased (from 19:00 to 06:00 hr) in the night. Paradoxical sleep (PS) time did not parallel the SS changes; it was increased significantly from 07:00 to 11:00 hr in the next morning. The influence of FMH seemed to be divided into direct, immediate action (increase of W) and late, prolonged action (decrease of W), and the results obtained support the histamine arousal hypothesis.
Twenty one male albino rats of the Wistar strain were trained on a differential reinforcement of long latency 20 with a limited hold 36 schedule through 30 consecutive days. Six rats were injected into the medial septal area with 8 micrograms of 6-hydroxydopamine dissolved in 0.9% saline solution containing 0.1% ascorbic acid. Five rats were injected with only ascorbic acid solution and the remaining rats were not treated with any injection or surgical operation. As a result of this differential reinforcement of long latency training, the 6-hydroxydopamine-injected rats showed significantly better performance and less acceleration of lever pressing response just after nonreinforced responses (incorrect responses) compared with the other two control groups, especially in the early 10 sessions. These findings suggested that the 6-hydroxydopamine-injected rats were hardly affected by response acceleration following nonreinforcements and therefore could acquire this training schedule faster than could the controls. The authors proposed one probable hypothesis, that the catecholaminergic input to the septum mediated a frustrated emotional response such as response acceleration resulting from nonreinforcements and impaired behavioral inhibition in the time discrimination situation.
A case of aqueductal stenosis is reported. The patient was a 14-year-old Japanese girl who was suffering from bilateral tinnitus and unsteadiness of gait. A series of neuro-otological tests revealed prolonged acoustically evoked brain stem response (ABR) latency, disturbed standing reflex, inhibited optokinetic nystagmus (OKN) and ataxic eye tracking test (ETT). Marked distension of the lateral and third ventricles was noticed on CT examination of the brain. A positive contrast ventriculogram using iotalamic acid showed occlusion of the cerebral (Sylvian) aqueduct. All of these results are suggestive of benign, non-neoplastic aqueductal stenosis with associated hydrocephalus. The patient underwent ventriculo-peritoneal shunt and, following the surgery, the results of neuro-otological, including radiological, re-examination indicated a remarkable recovery.