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Biomedical subjects

T Asano

Publications and source records attributed to T Asano.

At least 775 records · Page 43Linked to original sources
PubMed1985

Reduced collagen biosynthesis in oral mucosa of beige (Chediak-Higashi) mice.

Oral mucosa of beige (Chediak-Higashi) mice had decreased levels of collagen synthesis and prolyl hydroxylase activity compared with normal animals. No significant difference was observed in non-collagen protein synthesis between the two groups. These results suggest that decreased collagen biosynthesis in oral tissues may be partially involved in the increased incidence of periodontal disease in the Chediak-Higashi syndrome.

Animals↗
PubMed1985

Protection against suture insufficiency in ante-thoracic esophagogastrostomy.

In attempts to decrease suture insufficiency in case of ante-thoracic esophagogastrostomy, a gastric tube was so specially prepared that the short gastric vessels as well as the splenic vessels were severed very adjacent to the spleen. The anastomosis of the gastric tube thus prepared to the cervical esophagus was made using EEA-autosuture instruments. The suture insufficiency rate was thus markedly improved, with a value of approximately 10 per cent. Even cases of suture insufficiency with minor leakage, control was complete with simple pressure with gauze.

Adult↗
PubMed1985

Characterization of the spontaneous DNA-synthesizing and/or IgG-secreting cells in peripheral blood from patients with systemic lupus erythematosus.

Characterization of the cells responsible for spontaneous DNA synthesis and/or IgG secretion in systemic lupus erythematosus (SLE) was undertaken by fractionation of the peripheral blood mononuclear cells (PBM). Each fraction was analyzed for its capacity to incorporate [3H]thymidine [( 3H]TdR) and secrete IgG without mitogen. The non-E rosette-forming cell (non-ERRC) fraction, which consisted of the surface immunoglobulin-positive [sIg(+)] cells and null cells, revealed a markedly increased spontaneous DNA synthesis (620.0 +/- 586.9 cpm) during the first hour of culture and an elevated spontaneous IgG secretion (8639 +/- 2630 ng/ml) during 9 days of culture. Of particular interest was the finding that both increased responses were conducted by the null cells; the null cell population had approximately a fourfold relative increase of [3H]TdR incorporation and a 60-fold relative increase of IgG secretion compared with the sIg(+) cell population. These results suggest that SLE patients have a small population of preactivated B-cell lineage cells, which lack sIg or have a very low density of sIg.

Antibody Formation↗
PubMed1985

Alterations of the eicosanoid synthetic capacity of rat brain microvessels following ischemia: relevance to ischemic brain edema.

To know the mechanism underlying ischemic brain edema, a time-course analysis of the eicosanoid synthetic capacity of brain microvessels was carried out using unilateral, middle cerebral artery (MCA)-occluded rats. Concomitant with the development of brain edema the synthetic capacity of all products, including cyclooxygenase and lipoxygenase products, increased significantly. Next the effects of 15-hydroperoxyarachidonic acid (15-HPAA) on the synthetic capacity of microvessels were examined. The drug caused a generalized increase of each product, the profile of which was similar to that obtained with ischemic hemispheres, although the ratios of each product differed somewhat among them. The enhanced synthesis of eicosanoids by 15-HPAA was markedly suppressed by radical scavengers such as alpha-tocopherol, hydroquinone, and 1,2-bis(nicotineamide)-propane. Furthermore, the evolution of brain edema was virtually suppressed by the systemic administration of 1,2-bis(nicotineamide)-propane. The above result suggests that the enzyme activity of the arachidonic acid (AA) cascade of microvessels is stimulated by its own products. Such a mechanism will form a vicious cycle that accelerates the accumulation of free radicals within microvessels and thus may play a role in the progressing disruption of the blood-brain barrier (BBB) following ischemia.

Animals↗
PubMed1985

Coexisting primary hyperparathyroidism and Albright's hereditary osteodystrophy--an unusual association.

Primary hyperparathyroidism associated with Albright's hereditary osteodystrophy was diagnosed in a 22 year old Japanese woman, the second such case to be reported. Albright's hereditary osteodystrophy (AHO) appears to be associated with a larger number of disorders than the well recognized pseudohypoparathyroidism. AHO and pseudo-pseudohypoparathyroidism are essentially identical.

Adult↗
PubMed1985

TEA prevents the decline of the duration of the action potential in hypoxic cardiac muscle.

Our study was designed to evaluate the effects of the K+ channel blocker tetraethylammonium TEA (20 mM), Ca++ ionophore A23187 (6.9 microM), the Ca++ channel blocker verapamil (2 microM), and CaCl2 (6 mM) on a model of heart damage, hypoxia/reoxygenation of isolated guinea-pig hearts. The right ventricular papillary muscles maintained at 37 degrees C and paced at 60 beats/min were perfused with Ringer solution equilibrated with 95% O2-5% CO2 (normoxia) or 95% N2-5% CO2 (hypoxia). After stabilization of the electrical and mechanical activity, 60 min of hypoxia was induced and then followed by 15 min of reoxygenation. During hypoxia, there was a significant decrease in the action potential duration (APD) and the contractile force (CF). The decrease in APD in the TEA-treated muscle was significantly less than that in the non-treated muscle. However, CF declined at the same rate in both groups. Neither A23187, CaCl2 nor verapamil prevented the decline in both APD and CF. To study the slow responses, the fast Na+ current was first voltage-inactivated by partial depolarization to about -40 mM using an elevated K+ solution. The rate of hypoxia-induced blockade of the slow response was not slower in the presence of 20 mM TEA. These data demonstrate that TEA significantly prevented the decline of APD in hypoxia, but this resistance in APD did not affect the rate of inhibition of mechanical activity.

Action Potentials↗
PubMed1985

[The pathomechanism underlying ischemic brain edema: the role of Na+, K+-ATPase of the brain microvessels].

In the present study, the anti-edema effect of AVS [1,2-bis (nicotineamide)-propane] was evaluated using the cat MCA occlusion model with or without recirculation. In the prolonged ischemia (PI) group, cortical edema as assessed by the changes in specific gravity, developed in those cortical areas where the mean 1-CBF was less than 25-30 ml/100 g/min during MCA occlusion (4 hours). In the recirculation group (2 hours' ischemia followed by 2 hours' recirculation: RC group), the ischemic threshold for edema development was almost the same as in the PI group. In both groups, the drop in cortical specific gravity was significantly suppressed by AVS. Regarding the time-course of 1-CBF, there was no difference between the PI-AVS-treated and PI-saline-treated groups. In the RC group, however, the postischemic hypoperfusion was significantly ameliorated by AVS. Based on the present and previous data showing the antiedema effect of AVS, the mechanism of action of AVS was discussed in relation to the pathomechanism underlying ischemic brain edema. Our new concept of ischemic brain edema is briefly stated below. Related in vitro studies have shown the followings: (i) the influx of sodium not of proteins is the principal cause of ischemic brain edema: (ii) the eicosanoid synthetic capacity of the brain microvessel (MV) is increased simultaneous to edema development (iii) an elevation in the level of hydroperoxides enhances the activities of Na+, K+-ATPase as well as the arachidonate cascade of MV. These data suggest that free fatty acids and free radicals liberated following cerebral ischemia stimulate the activity of the MV-Na+, K+-ATPase, which results in increased sodium influx across the BBB. AVS was shown to scavenge hydroxyl radicals and to inhibit the stimulatory effects of a lipid hydroperoxide (15-HPAA) on the activities of Na+, K+-ATPase and the arachidonate cascade of the MV. These actions of AVS may be linked to its antiedema effect.

Animals↗
PubMed1985

[Clinical experience of latamoxef in the field of neurosurgery on the penetration into the cerebrospinal fluid in the patients with postoperative meningitis].

Latamoxef (LMOX) at a dose of 2 g was intravenously administered to 12 cases with postoperative meningitis and the concentrations in serum and cerebrospinal fluid (CSF) were examined up to 2 hours and the results obtained were as follows; The average serum and CSF concentrations of LMOX were 125.0 micrograms/ml, 4.33 micrograms/ml at 0.5 hour, 80.7 micrograms/ml, 4.64 micrograms/ml at 1 hour and 45.8 micrograms/ml, 3.82 micrograms/ml at 2 hours, respectively. The clinical responses of LMOX against postoperative meningitis were revealed excellent in 4 cases and good in 8 cases. No side effects were observed. LMOX was thought to be effective agent in the treatment of the postoperative meningitis.

Adult↗
PubMed1985

[Identification of 11-HETE in the rat brain and its relevancy to ischemic cerebral edema].

Eicosanoids are thought to be important in the pathogenetic mechanism of ischemic brain damage. But little is known about lipoxygenase products and their roles in brain. In the present study, lipoxygenase metabolism in the brain and its relevancy to ischemic brain edema were studied using high performance liquid chromatography (HPLC) and gas chromatography-mass spectrometry (GC-MS). The rat middle cerebral artery (MCA) occlusion model was used because the time course of ischemic edema formation has been well known. The rat brain was fixed by in situ freezing 24 and 72 hours after MCA occlusion, and removed. Identification and quantitative analysis of hydroxyeicosatetraenoic acids (HETEs) in normal and ischemic brain homogenates was performed by HPLC and GC-MS. The rat brain was divided into the microvessel (MV) fraction and the rest. Then the same analysis was carried out in the both fractions obtained from the normal rat brain. Only 11-HETE was detected in the normal and ischemic brain. Quantitatively, normal brains contained 1288 +/- 66 (mean +/- SE) of 11-HETE ng/g wet weight, while the hemispheres rendered ischemic for 24 and 72 hours after MCA occlusion contained 1101 +/- 48, and 1663 +/- 147, respectively. The 11-HETE content was significantly increased 72 hours after MCA occlusion (p less than 0.05). The MV fraction of rat brain contained 11-HETE (653 ng/mg protein) ten times as much as the other fraction. The identification of 11-HETE in the rat brain is a new finding.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗