[The effect of changes in body position on the Holter electrocardiogram].
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Biomedical subjects
Publications and source records attributed to M Hirano.
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The patient, a 5-year-old male, was diagnosed as having pernicious anemia at our hospital in 1969. By means of an upper G-I series, he was found to have a gastric protruded lesion on the greater curvature of the upper corpus in 1983. After an endoscopic polypectomy, a type II a early gastric cancer was diagnosed which, histologically, showed a well-differentiated adenocarcinoma and a total gastrectomy was performed. From the histologic findings of the resected stomach, the were multiple endocrine cell micronests, that coincided with the distribution of intestinal metaplasia localized in the fundic gland area.
A phase I study of N4-palmitoyl-1-beta-D-arabinofuranosylcytosine (PLAC) was conducted in 88 patients; 36 with solid tumors and 52 with hematological malignancies, using 2 different schedules. Schedule 1 employed a single oral administration and Schedule 2, 5-day consecutive daily oral administration. In Schedule 1, the daily dose was initiated with 1 mg kg-1 which was escalated up to 24 mg kg-1 according to the modified Fibonacci's method. Side effects included nausea, vomiting and skin rashes, but myelosuppression was not seen within this dose range. In Schedule 2, the daily dose was started with 1 mg kg-1 which was escalated up to 24 mg kg-1. Major side effects were nausea, vomiting and anorexia, and mild myelosuppression was noted at 12 mg kg-1 or more. The dose-limiting toxicity was gastrointestinal toxicity, which appeared at 3.3 mg kg-1 or more and became frequent at 7 mg kg-1 or more. Pharmacokinetic study revealed that the plasma concentrations of PLAC and ara-C, obtained by the oral intake of 3.3 mg kg-1 or more of PLAC, were sufficient for these compounds to exert cytotoxic effects on various human leukemia cells in vitro. Based on these observations and plausible mechanism of action of PLAC, further clinical study should be carried out in a treatment schedule of considerably prolonged administration period with 3.3-6 mg kg-1 day-1 of PLAC.
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N4-Palmitoyl-1-beta-D-arabinofuranosylcytosine (PLAC) was administered PO to 76 patients with acute leukemia, myelodysplastic syndromes (MDSs), and myeloproliferative disorders (MPDs). Of 20 patients with acute myelogenous leukemia, 2 achieved complete remission, and the only patient with acute lymphoblastic leukemia achieved partial remission. Remission was reached with PLAC 100-300 mg/day 25-66 days after the start of therapy. Among 22 patients with MDS, 1 patient achieved a good response and 8 achieved partial response. Responses were reached with PLAC 50-200 mg/day 7-153 days (median, 33 days) after the start of therapy. Improvement of polycythemia was observed in all 5 patients with polycythemia vera, and reduction of thrombocytosis was observed in 5 out of 6 patients with essential thrombocythemia and myelofibrosis. An antileukemia effect was noted in 1 of 5 with chronic myelogenous leukemia. Major side effects were gastrointestinal toxicities and myelosuppression. In spite of the disadvantages, such as unpredictable absorption and a lower response rate to acute leukemia compared with its parent compound, this antileukemia Ara-C analogue that is administrable PO will be useful in the treatment of MDSs and MPDs, which do not necessarily require admission to hospital, and in the treatment of acute leukemia of the aged, a condition for which intensive chemotherapy is not appropriate.
A rapid and simple one-pot method for O-sulfation of nonsulfated cholecystokinin octapeptide (CCK-8) was developed using sulfuric acid and dicyclohexylcarbodiimide (DCC) without protection of the amino acid side chains. The extent of sulfation was increased with increasing the amount of reactants, sulfuric acid, and DCC, and reached maximum (40%) with fourfold molar excess of sulfuric acid and 40-fold molar excess of DCC. The excess of nonsulfated peptide inhibited the sulfation. The sulfation product was purified by HPLC or TLC to give a pure sulfated substance which showed exactly the same behavior as that of an authentic O-sulfated CCK-8 on HPLC or TLC. The purified sulfated peptide was active in stimulating amylase secretion from rat pancreatic fragments, and amino acid analysis showed that the tyrosine residue in the peptide existed in O-sulfated form. Sulfation with [35S]sulfuric acid-DCC produced a radioactive substance, from which O-[35S]sulfated CCK-8 could be easily purified by two-dimensional TLC.
In order to demonstrate distribution of the laryngeal peripheral sensory nerve fibers of cats, wheat germ agglutinin-horseradish peroxidase was injected into the nodose ganglion. The results were as follows: The internal branch of the superior laryngeal nerve (SLN) innervated ipsilaterally the epiglottis, the aryepiglottic fold, the arytenoid eminence, the rostral aspect of the vocal fold, the laryngeal vestibulum and the mucosa covering the posterior cricoarytenoid muscle. The posterior branch of the recurrent laryngeal nerve (RLN) was divided into two branches. One branch formed Galen's anastomosis together with fibers of the internal branch of the SLN. The other supplied the caudal aspect of the vocal folds and the subglottis, together with fibers of the internal branch of the SLN, bilaterally with ipsilateral predominance. Some fibers of the internal branch of the SLN united with some fibers of the posterior branch of the RLN and penetrated the cricoid foramen to innervate the posterior wall of the glottis and the medial aspect of the arytenoid cartilage bilaterally with ipsilateral predominance.
Acquired laryngo-pharyngeal fistula is a very rare condition. This paper reports a 65-year-old man who presented with a laryngo-pharyngeal fistula caused by trauma to the cervical vertebra. The symptom was persistent aspiration. The fistula was located between the subglottic space and the hypopharynx through the cricoid lamina. A fluoroscopic video recording was useful in demonstrating the fistula, and a fibrescopic examination confirmed its existence and exact location. The fistula was successfully treated with closure of both larynx and pharynx with a sternomastoid muscle interposition.
Density values of the corpus callosum and ventricular brain ratio (VBR) were obtained by coronal computerized tomography (CT) in 16 chronic schizophrenic patients and 16 normal controls. The corpus callosum of schizophrenic brains showed no apparent density loss which could indicate a dysfunctional brain. A significant ventricular dilatation was found in the patient group compared with age-matched controls. This finding was compatible with several former observations with transverse scanning.
We present evidence that the expression of rho is regulated by rho-dependent attenuation of transcription. Gene fusion analysis with nested series of deletions of rho indicated that the transcription of rho is attenuated in a rho-dependent manner in the leader region and that neither a read-through transcription from the upstream gene, trxA, nor a modulation of transcription initiation of the rho promoter is involved in the self-control of rho. S1 mapping and Northern hybridization analyses localized at least six transcription attenuation or termination sites in the region ranging from the 3' end of the trxA structural gene to the middle of the rho structural gene. Among them, the most upstream site overlapping the rho promoter sequence was assigned to the terminator for the trxA gene, and the second and third sites, mapping about 80 and 50 nucleotides upstream from the start codon of rho, were suggested to function as the major attenuation sites for regulation of the rho expression. Further, the start points of the trxA and rho RNAs were determined in an in vitro transcription system to be located 111 nucleotides (U) and 255 nucleotides (G) upstream from their respective start codons. These results necessitate revisions of previous predictions on the sites of transcriptional signals in the trxA and rho genes (S. Brown, B. Albrechtsen, S. Pedersen, and P. Klemm, J. Mol. Biol. 162:283-298, 1982; C.-J. Lim, D. Geraghty, and J. A. Fuchs, J. Bacteriol. 163:311-316, 1985; B.J. Wallace and S.R. Kushner, Gene 32:399-408, 1984).
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BMY-28142, 7-[(Z)-2-(2-aminothiazol-4-yl)-2-methoxyiminoacetamido]-3- (1-methylpyrrolidinio)methyl-3-cephem-4-carboxylate, exhibited a well-balanced, extended-spectrum of antibacterial activity both in vitro and in vivo. Against Staphylococci and Streptococci, BMY-28142 was about four to ten times more active than ceftazidime and comparable to cefotaxime. Most Enterobacteriaceae were more susceptible to BMY-28142 than to ceftazidime, though strains of Pseudomonas aeruginosa were slightly more sensitive to ceftazidime. BMY-28142 showed potent activity against Gram-negative bacteria resistant to ceftazidime and/or cefotaxime. Bactericidal activity of BMY-28142 against 10 strains of P. aeruginosa was superior to that of ceftazidime. In bacterial infection models in mice, BMY-28142 was more effective than ceftazidime against three Gram-positive and three Gram-negative pathogens. The anti-pseudomonal in vivo activity of BMY-28142 was nearly comparable to that of ceftazidime. The blood levels and urinary excretion rates of BMY-28142 in mice were similar to those of ceftazidime.
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