Biomedical subjects
Publications and source records attributed to T Hirose.
We conclude that auricular deformities of the early neonate are corrigible by nonsurgical correction. Ideally, the correction should be started immediately after birth (realistically, at latest by the third day after birth) in order to obtain satisfactory and irreversible results.
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An unusual tumor of the trachea was found in a 76-year-old woman. The tumor resembled an adenoid cystic carcinoma in having many cystic spaces, but the fairly uniform tumor cells gradually merged with the myxomatous or hyalinous stroma, and foci of squamous metaplasia and glycogen-rich adenoma-like components were also observed. S-100 protein was demonstrated immunohistochemically in the tumor cells. This tumor was diagnosed as a pleomorphic adenoma (benign mixed tumor) of the trachea.
A living related kidney transplant recipient with normal renal functioning and hypertension secondary to renal artery stenosis was treated with captopril and developed reversible granulocytopenia. Complications caused by captopril, an angiotensin converting enzyme inhibitor, have been reported previously in hypertensive patients with systemic lupus erythematosus or with renal artery stenosis after renal transplantation. It is recommended that this drug be used with caution in this setting.
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To examine the effect of script type and/or script frequency on the semantic access to words, 34 undergraduates were required to category decision for each word presented tachistoscopically. Three classes of words were used as stimuli; Kana words with low Kana script frequency (Kana-Low), Kana words with high Kana script frequency (Kana-High), and Kanji words with high Kanji script frequency (Kanji). Mean decision latency for Kana-High was shorter than that for Kana-Low, while there was no difference of latency between Kana-High and Kanji. These results show that the speed of semantic access depends on script frequency rather than script type.
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The nicotinic acetylcholine receptor (AChR) from the electroplax of the ray Torpedo californica is composed of five subunits present in a molar stoichiometry of alpha 2 beta gamma delta (refs 1-3) and contains both the binding site for the neurotransmitter and the cation gating unit (reviewed in refs 4-6). We have recently elucidated the complete primary structures of the alpha-, beta- and delta-subunit precursors of the T. californica AChR by cloning and sequencing cDNAs for these polypeptides. Here, we report the whole primary structure of the gamma-subunit precursor of the AChR deduced from the nucleotide sequence of the cloned cDNA. Comparison of the amino acid sequences of the four subunits reveals marked homology among them. The close resemblance among the hydrophilicity profiles and predicted secondary structures of all the subunits suggests that these polypeptides are oriented in a pseudosymmetric fashion across the membrane. Each subunit contains four putative transmembrane segments that may be involved in the ionic channel. The transmembrane topology of the subunit molecules has also been inferred.
Previously, Guillemin and Rosenberg and Saffran and Schally demonstrated the presence of hypothalamic factors that stimulated the secretion of adrenocorticotropic hormone (ACTH) by the pituitary gland. Recently, Vale et al. have isolated and sequenced an ovine hypothalamic peptide of 41 amino acids, which is believed to represent the major physiological corticotropin-releasing factor (CRF) (reviewed in refs 5, 6). Available data suggest that hypothalamic CRF enhances both the synthesis and secretion of ACTH and related peptides such as beta-endorphin and beta-lipotropin (beta-LPH) (reviewed in ref. 6), which are all derived from the common precursor, termed ACTH-beta-LPH precursor or preproopiomelanocortin (reviewed in ref. 7). Because CRF mediates the neural control of the pituitary-adrenocortical system, the characterization of its biosynthetic precursor and the gene encoding it is essential for understanding the molecular mechanism underlying the endocrine response to stress. We have now cloned DNA sequences complementary to the ovine hypothalamic mRNA encoding the CRF precursor (referred to hereafter as prepro-CRF). The nucleotide sequence of the cloned cDNA, reported here, has revealed the primary structure of prepro-CRF. The carboxyl end represents the CRF sequence preceded by the tetrapeptide, Arg-Lys-Arg-Arg, and followed by the dipeptide, Gly-Lys. Comparison of the amino acid sequence of prepro-CRF with those of the ACTH-beta-LPH precursor and the arginine vasopressin-neurophysin II precursor suggests that these precursor proteins may be evolutionarily related.
The nicotinic acetylcholine receptor (AChR) from fish electric organ and mammalian skeletal muscle is the best characterized neurotransmitter receptor (reviewed in refs 1-3). The AChR from the electroplax of the ray Torpedo californica consists of five subunits present in a molar stoichiometry of alpha 2 beta gamma delta (refs 4-6); the apparent molecular weights of the alpha-, beta-, gamma- and delta-subunits are 40,000 (40K), 50K, 60K and 65K, respectively. Knowledge of the primary structures of these constituent polypeptides would facilitate the understanding of the molecular mechanism underlying the function of the neurotransmitter receptor. Recently, we have cloned cDNA for the alpha-subunit precursor of the T. californica AChR and have deduced the primary structure of this polypeptide from the nucleotide sequence of the cloned cDNA. Here we report the cloning and nucleotide analysis of cDNAs for the AChR beta- and delta-subunit precursors. The primary structures of the two polypeptides deduced from the cDNA sequences reveal conspicuous amino acid sequence homology among these and the alpha-subunits. The three subunits contain several highly conserved regions which may be essential for the receptor function or inter-subunit interaction.
Forty-five patients with a central retinal vein occlusion were divided into three groups: those with venous stasis retinopathy (VSR, n = 27), those with hemorrhagic retinopathy (HR, n = 6), and those with undetermined retinopathy (n = 12). The electroretinogram (ERG) was recorded in all cases. The average b/a-wave amplitude ratio of the single white-flash ERG was 1.67 for the VSR group and 0.70 for the HR group. The ERG responses in the group with undetermined retinopathy helped to assess the degree of retinal ischemia and to further categorize the disorder as either VSR or HR. The b/a amplitude ratio reflected the degree of retinal ischemia and had prognostic value in predicting in which cases neovascular glaucoma may develop. The average b/a ratio in the six cases in which neovascular glaucoma developed was 0.84. This complication did not develop in any patient with a b/a ratio greater than 1. Four patients with low b/a ratios (average, 0.73) were treated with panretinal photocoagulation; neovascular glaucoma developed in none.
Prostacyclin (PG I2) generated by vascular endothelium is a strong antiaggregating substance. As platelet aggregation and release of humoral factor(s) have been reported to be crucial in the pathogenesis of acute lung injury following pulmonary microembolization, PG I2 could have a protective effect against microembolic lung vascular injury. Following unilateral microembolization, we have observed a large increase in the filtration coefficient in the nonembolized lung with a significant increase in 6-keto PG F1 alpha, the stable metabolite of PG I2, in arterial blood. The pretreatment with indomethacin (10 mg/kg) prevented the increase in 6-keto PG F1 alpha and potentiated the lung injury after microembolization. Exogenously administered PG I2 (20 ng/kg/min) prevented completely the increase in the filtration coefficient without any effects on hemodynamics, although these effects of indomethacin and PG I2 did not relate to their effects on platelet aggregation. Based on these results, we could conclude that prostacyclin could play an important role in preserving cell integrity of the lung and in prevention of increased lung vascular permeability following pulmonary microembolization.
Escherichia coli endotoxin (1 mg/kg) infusion over 30 min into anesthetized artificially ventilated dogs caused a biphasic response: an early phase of pulmonary hypertension and a late phase of increased lung vascular permeability. During an early phase, PG F2 alpha, Tx A2 (as Tx B2) and prostacyclin (as 6-keto-PG F1 alpha) concentrations increased in plasma or right duct lymph of dogs. During a late phase, the concentrations of PG F2 alpha and Tx A2 decreased to near the base-line values, while the concentration of prostacyclin remained elevated. Administrations of PG synthetase inhibitors 45 min prior to endotoxin inhibited the increase in concentration of prostacyclin following the infusion of endotoxin and potentiated the increase in lung vascular permeability at the beginning of the late phase. Continuous infusion of prostacyclin (20 ng/kg/min) starting one hour before endotoxin for 5 hour periods prevented the increase in lung vascular permeability induced by endotoxin. Based on these results, we could conclude that endogenous prostacyclin might play an important role in preserving cell integrity of lungs and counteract the deleterious effects of endotoxin.
Prostacyclin (PG I2) generated by vascular endothelium is a strong antiaggregating substance. As platelet aggregation and release of humoral factor(s) have been reported to be crucial in the pathogenesis of acute lung injury following pulmonary microembolization, prostacyclin could have a protective effect against microembolic lung vascular injury. Following unilateral microembolization, the filtration coefficient in the nonembolized lung increased significantly to 0.14 +/- 0.02 from the base line value of 0.07 +/- 0.01 ml/min/mmHg/100g. Prostacyclin as measured as 6-keto PG F1 alpha in arterial blood increased significantly to 4.15 +/- 1.76 at 30 min from the base line value of 1.90 +/- 0.45 ng/ml and increased further to 5.67 +/- 1.49 ng/ml at 60 min following microembolization. Exogenously administered PG I2 methylester (20 ng/kg/min) prevented completely the increase in the filtration coefficient without any effects on hemodynamics, although the effects of PG I2 methylester did not depend on its action on platelet aggregation. Based on these results, we conclude that prostacyclin could play an important role in preserving cell integrity of the lung and prevention of increased lung vascular permeability following pulmonary microembolization.
To evaluate the potential beneficial effect of a thromboxane synthetase inhibitor, OKY-1581, on increased pulmonary vascular permeability in pulmonary microembolization, we have measured the filtration coefficient in the nonembolized lung after unilateral microembolization in dogs. The unilateral microembolization caused marked elevations in pulmonary artery pressure and blood flow to the nonembolized lung, while pulmonary venous pressure in nonembolized lung did not change. The pulmonary vascular resistance in nonembolized lung did not increase significantly. The filtration coefficient (Kf) in nonembolized lung increased to 0.14 +/- 0.02 from the baseline value of 0.07 +/- 0.01 ml/min/mmHg/100g at 30 min after microembolization when the initial hemodynamic changes reduced toward the baseline value. In OKY-1581 treated dogs, similar hemodynamic changes did not result in the increase in the filtration coefficient in nonembolized lung. Platelet aggregation was also inhibited after microembolization in OKY-1581 treated dogs. Based on these results, we could conclude that OKY-1581 could prevent the increase in pulmonary vascular permeability following pulmonary microembolization by inhibiting platelet aggregation and possibly by preventing the release of thromboxane A2.