[Isolation of Legionella bozemanii from the lung tissue].
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Biomedical subjects
Publications and source records attributed to Y Taguchi.
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A case of male cystic prolactinoma is reported. And six cases of male prolactinoma including the present case were experienced in our department, and they were studied clinically. A 40-year-old male was admitted to our hospital with complaints of decreased libido and bitemporal visual depression. Physical examination revealed neither gynecomastia nor galactorrhea. Decreased visual acuity, bitemporal hemianopia, and pale optic disc were disclosed. On endocrinological study, high serum level of prolactin and hyposecretion of the other pituitary hormones were shown. Plain skull x-ray films showed ballooning of the sella turcica. CT scan revealed a low density area in the pituitary fossa extending to the suprasellar region. This was visualized as a homogeneous high signal intensity in the T1 weighted magnetic resonance imaging. Surgical treatment was made by transsphenoidal approach. A considerable amount of dark reddish fluid was suctioned through an incision of the thinned dura mater. Postoperative course was uneventful, and the bitemporal hemianopia was much improved. The serum level of prolactin was normalized after administration of bromocriptine. Male prolactinomas were thought to constitute 20% of all prolactinomas and male cystic prolactinoma was a rare clinical entity. Since the serum level of prolactin became to be measured routinely, six male prolactinomas have been experienced in our department. Their clinical feature were summarized as follows; Mean age of the patients was 33.2 +/- 9.8 years. Marked suprasellar extension and associated visual disturbance were common. All lesions except in the present case were solid tumor. Mean serum level of prolactin was 3398.3 +/- 2758.4 ng/ml. Pituitary apoplexy during the test of insulin, TRH and LH-RH simultaneous loading was noted in two cases.(ABSTRACT TRUNCATED AT 250 WORDS)
Our earlier studies have shown that local cortical blood flow (CoBF) in the rabbit has been autoregulated in a narrow range of mean arterial blood pressure (MABP) and autoregulation of cortical oxygen tension (bPO2) has been maintained in a wider range (75-110 mmHg) than that of CoBF. In the present studies, bPO2, NAD/NADH redox state, and CoBF were measured under the various conditions of hypoxia and hyperoxia to discuss the critical level of cortical oxidative metabolism and autoregulation of CoBF in relation to oxidative metabolism. New Zealand white rabbits were anesthetized with pentobarbital sodium intraperitoneally and paralyzed with gallamine triethiodide intravenously. They were ventilated artificially maintaining normal blood gas analysis. NAD/NADH redox state was measured with a compensated fluorometer with a reflectance device to correct for hemodynamic artefacts and bPO2 was monitored continuously with the polarographical method. They were measured simultaneously. CoBF was monitored with the thermal diffusion cerebral blood flow monitor of Flowtronics. Hypoxia and hyperoxia were produced by decreasing or increasing the inspired oxygen concentration. Arterial blood samples were obtained for blood gas determination before and during the episode of hypoxia or hyperoxia. A definite reduction of NADH began at a 50% decrease of PaO2. It corresponded to 70 mmHg of PaO2. Below 50% decrease of PaO2, NADH was reduced largely. This was statistically significant (p less than 0.01). Although, the oxidation of NADH occurred in the moderate hyperoxic state, no oxidation of NADH occurred more than 6.1% of full scale even in the condition of higher PaO2.(ABSTRACT TRUNCATED AT 250 WORDS)
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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.
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.
Hemangioblastomas of the medulla oblongata were successfully excised in two separate cases. The uncertainties of this procedure involve the value of preoperative radiation therapy, the relationship between the tumor and the medulla oblongata, and the surgical techniques themselves. Cardiovascular and respiratory disorders often complicate this type of surgery, and postoperative dysphagia is a frequent sequela.
The increase of histidine decarboxylase (HDC) activity during late pregnancy in the whole bodies of fetal mice and the kidneys of their mothers were almost completely inhibited by i.p. administration of 25 mg/kg of alpha-fluoromethylhistidine (alpha-FMH), a suicide inhibitor of HDC, starting on day 13 of pregnancy. The increase of HDC in fetal mice was previously shown to be in mast cells [T. Watanabe et al., Proc. Natl. Acad. Sci. U.S.A. 78, 4209-4212 (1981)]. The increase of HDC in maternal kidneys was examined by using estrogen and W/WV mice, which were devoid of mast cells and infertile. Treatment of castrated mice with 17-beta-estradiol increased the HDC activity of the kidney, and this increase was antagonized by concomitant treatment with clomiphene, an antiestrogen, confirming that the increase is mediated through an estrogen receptor. HDC activity in the kidney of W/WV mice was also increased by estradiol treatment, indicating that HDC activity was associated with non-mast cells.
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Bacterial growth rate was evaluated by estimating the increase in ATP content of cultures of bacterial suspensions using luciferase assay, and the method was applied to the estimation of bactericidal activity of serum and anti-bacterial activity of antibiotics. The results obtained were as follows: The bacterial numbers or bacterial growth rate determined by the ATP-Bioluminescence method was in accordance with those by CFU assay and spectrometrical assay by optical density readings. Furthermore this method was confirmed to be non-time-consuming and more simple than other methods. Using this method, anti-bacterial activity of fresh serum was evaluated. The serum suppressed the growth rate of E. coli, Str. fecalis, CBS, Kleb. pneumoniae and Staph. aureus at least for 2 hours. Heat-inactivated serum and absorbed serum with bacteria tended to lose such suppressive effect. Thus the main effective factors seem to be complements and specific antibody. The anti-microbial activity of antibiotics was enhanced by addition of fresh serum to bacterial cultures, and the results were not in accordance with those by the conventional Disc method. Thus the sensitivity test under the influence of fresh serum is recommended in order to know the clinical effect of antibiotics. These results suggest the usefulness of ATP-Bioluminescence method in the clinical laboratory examinations or investigations.
Autoregulation and CO2 response of cortical blood flow and their relationship to cortical oxygen tension is not fully known. We have examined autoregulation and CO2 response of local cortical blood flow (CoBF) and cortical oxygen tension (bPO2), using 41 New Zealand white rabbits. CoBF was measured continuously by using the heated thermocouple technique and bPO2 was monitored by the polarographic method. Intravenous injection of phenylephrine hydrochloride or trimethaphan camsylate was used to test for autoregulation by increasing or decreasing perfusion pressure. The data was analyzed in the range between 50 and 140 mmHg of mean arterial blood pressure (MABP). The range of autoregulation was determined by our own analytical method. PaCO2 was manipulated between 18.3 and 63.2 mmHg. It was increased by raising the concentration of CO2 in the inspired gas mixture. Hypocapnia was induced by hyperventilation. The mean values of CoBF and bPO2 were 36.2 +/- 5.3 ml/100 g/min and 32.9 +/- 12.8 mmHg respectively at 90 mmHg of MABP during the test for autoregulation. The changes in both CoBF and bPO2 with changing perfusion pressure were often relatively small at near baseline blood pressure and became more pronounced with large increase or decrease in MABP. On returning from high MABP to baseline blood pressure, a hysteresis effect on CoBF was observed in 20 out of twenty two cases. The autoregulation of CoBF was maintained in the range between 80 and 100 mmHg of MABP. On the other hand, bPO2 was maintained constant in the range between 75 and 110 mmHg of MABP.(ABSTRACT TRUNCATED AT 250 WORDS)
The origins of histamine-containing fibers in the cerebral cortex were examined by means of the retrograde tracer technique of horseradish peroxidase (HRP)-immunohistochemistry with histidine decarboxylase (HDC) as a marker for the histamine neuron system. Total transection of the brain rostral to the posterior hypothalamus resulted in disappearance of HDC-like immunoreactive (HDCI) fibers in the cerebral cortex, but total transection caudal to the posterior hypothalamus did not decrease the number of HDCI fibers in the cortex, suggesting that HDCI fibers in the cerebral cortex originate in the posterior hypothalamus. The projection of HDCI neurons from the posterior hypothalamus to the cerebral cortex seemed to be bilateral because hemi-transection of the brain rostral to the posterior hypothalamus resulted in a bilateral decrease of HDCI fibers in the cerebral cortex with ipsilateral predominance. After injection of HRP into the cerebral cortex, numerous cells containing both HRP granules and HDCI structures were found bilaterally in the tuberal, caudal and postmamillary magnocellular nuclei, with ipsilateral predominance. These findings indicate that HDCI cells in the above nuclei give rise to axons extending bilaterally to the cerebral cortex.
Histidine decarboxylase was purified from fetal rat liver about 3,000-fold by the method described previously (Watanabe, T., Nakamura, H., Leu, Y.L., Yamatodani, A., and Wada, H. (1979) Biochem. Pharmacol. 28, 1149-1155) except that DEAE-cellulose column chromatography, Sephacryl S-300 gel filtration, and preparative polyacrylamide gel electrophoresis were added. The enzyme had a molecular weight of 110,000 in the native state and gave a single band of protein on sodium dodecyl sulfate-polyacrylamide gel electrophoresis in a position corresponding to a molecular weight of 54,000, indicating that it was a dimer. Its isoelectric point was pH 5.1. Antibody raised in rabbits against the enzyme gave single fused precipitation lines with the enzymes from fetal rat liver and adult rat brain and stomach in Ouchterlony's double diffusion test, and inhibited these three enzymes similarly and strongly. Using this antibody, histidine decarboxylase-like immunoreactive structures were located in fetal liver and peritoneal mast cells, stomach and brain of rats.
The mechanism of inactivation by (S)-alpha-fluoromethylhistidine (FMH) of L-histidine decarboxylase (HDC, L-histidine carboxy-lyase, EC 4.1.1.22) purified from whole bodies of fetal rats was studied. FMH inhibited the activities of HDC purified from fetal HDC as well as HDCs from the brain and stomach of adult rats. The activity was not restored by extensive dialysis, indicating that the inhibition was irreversible. The inactivation of HDC was time and concentration dependent and followed pseudo first-order kinetics. L-Histidine, a substrate, protected HDC against inactivation, but D-histidine did not. Apo-HDC was not inactivated by FMH. On labeling of HDC with [3H]FMH, a correlation was found between the extent of incorporation of radioactivity into the enzyme and the degree of inactivation. Two moles of the inhibitor were incorporated into one mole of HDC (108,000 daltons). Experiments with [carboxyl-14C]FMH and [ring 2-14C]FMH showed that decarboxylation was necessary for the inactivation and that one molecule of FMH moiety was incorporated into an HDC monomer during every three decarboxylations of FMH.
The distribution of histidine decarboxylase-like immunoreactivity (HDCI) in the rat central nervous system was studied by the indirect immunofluorescence technique. HDCI cell bodies were concentrated in the posterior hypothalamic area, such as in the tuberal magnocellular nucleus, caudal magnocellular nucleus, posterior hypothalamic nucleus and lateral hypothalamus just lateral to the fasciculus mammillothalamicus at the level of the posterior hypothalamic nucleus. Extensive networks of HDCI fibers of various densities were found in many areas of the brain; they were particularly dense in the hypothalamus but were also found in the following areas: rostrally in the cerebral cortex, olfactory nuclei, medial amygdaloid nucleus, n. tractus diagonalis, and bed nucleus of the stria terminalis, and caudally in the central gray matter of the midbrain and pons, auditory system, n. vestibularis medialis, n. originis nervi facialis, n. parabrachialis, n. commissuralis, n. tractus solitarii, and n. raphe dorsalis.