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Biomedical subjects

T Matsubara

Publications and source records attributed to T Matsubara.

At least 217 records · Page 12Linked to original sources

Can esophagectomy cure cancer of the thoracic esophagus involving the major airways?

To evaluate the effects of aggressive operation for esophageal cancer invading the trachea and main bronchi, we investigated retrospectively 62 patients with proven tracheobronchial involvement who underwent thoracotomy for esophagectomy between 1973 and 1993. We operated unless the tumor was assessed to be definitely unresectable. Esophagectomy was possible in 55 patients, and the resectability rate was 95% after preoperative computed tomography and bronchoscopy became routine. After esophagectomy, no residual cancer lesion was recognizable macroscopically in 53% of patients. The hospital mortality rate in esophagectomy cases was 7% in the past 8 years. The outcome in patients who underwent curative resection was significantly favorable (p < 0.0001), and the 2-year survival was 51%. The patients with nonresectable cancer all died within 6 months compared with a 23% 1-year survival rate for palliative esophagectomy cases (p < 0.006). Among patients with tracheobronchial involvement assessed as resectable on computed tomography and bronchoscopy, a considerable proportion benefited from aggressive therapy with esophagectomy. The possibility of complete cure was high, especially when the cancer responded well to preoperative therapy and no lymph nodes were involved.

Adult↗

Pressor response induced by the hippocampal administration of neostigmine is suppressed by M1 muscarinic antagonist.

We investigated the roles played by three muscarinic receptors (M1, M2, and M3) in the pressor response with bradycardia that followed the injection of neostigmine (5 x 10(-8) mol) into the hippocampus of anesthetized rats. These changes were blocked by the co-administration of methylatropine (5 x 10(-8) mol). The intrahippocampal injection of pirenzepine (M1 antagonist) (5 x 10(-9) - 5 x 10(-7) mol) suppressed the neostigmine-induced pressor response dose-dependently. However injection of gallamine (M2 antagonist) (5 x 10(-8) - 5 x 10(-7) mol) and of 4-DAMP (M1 and M3 antagonist) (5 x 10(-8) - 5 x 10(-7) mol) did not suppress this hypertensive response. These findings suggest that the neostigmine-induced pressor response with bradycardia is mediated through the M1 muscarinic receptor subtype.

Animals↗

Comparison of 99Tcm-pyrophosphate, 201T1 perfusion, 123I-labelled methyl-branched fatty acid and sympathetic imaging in acute coronary syndrome.

Among a group of patients (n = 15) with acute coronary syndrome, the results of using two new myocardial radiopharmaceuticals--123I-labelled 15-(p-iodo-phenyl)-3,R,S-methylpentadecanoic acid (BMIPP) and 123I-meta-iodobenzyl guanidine (MIBG)--were compared with dual 201Tl/99Tcm-pyrophosphate (Tl-PYP) imaging using single photon emission tomography (SPET). Defect scores were evaluated on a segment-by-segment basis for a total of 270 segments. For the 201Tl, BMIPP, and early and delayed MIBG studies, the mean (+/- S.D.) sums of defect scores were 9 +/- 8, 18 +/- 9, 22 +/- 12 and 29 +/- 9, respectively, revealing significantly higher scores for BMIPP and MIBG than 201Tl (P < 0.005). This was the case irrespective of various functional conditions, such as successful recanalization, failure of coronary angioplasty or restenosis. The culprit coronary artery was best identified using BMIPP, while MIBG SPET showed the most extensive defects. Normal perfusion with decreased BMIPP and MIBG uptake was frequently observed and associated with hypokinesis. 123I-BMIPP and MIBG are more sensitive for the detection of damaged myocardium, and the difference between perfusion and metabolism seems to reflect myocardial stunning.

3-Iodobenzylguanidine↗

Mutagenicity of bile and pancreatic juice from patients with pancreatico-biliary maljunction.

We attempted to detect mutagenic activity in bile and pancreatic juice from patients with biliary tract disease using the spore rec assay and wild (H17) and mutant (M45) strains. Three bile samples out of 5 obtained from patients with pancreatico-biliary maljunction showed positive reaction in the spore rec assay, and all contained a high level of amylase activity, while 300 microliters of bile samples obtained from 10 control patients without pancreatico-biliary maljunction did not show any positive reaction. Moreover, 300 microliters of the in vitro mixture of bile with an equal volume of pancreatic juice also showed a positive reaction after treatment for 12 days at 37 degrees C or for 10 min at 100 degrees C, suggesting that they were very stable and long-acting in vivo. These data suggest that possible mutagens might be formed by the mixing of bile with pancreatic juice regurgitated into the biliary tract, and that there might be a relationship to biliary tract cancer which often accompanies pancreatico-biliary maljunction.

Amylases↗

[Dye leakage from choroidal neovascularization with indocyanine green angiography].

The ultrastructure of experimentally induced choroidal neovascularization was studied in correlation with dye leakage in indocyanine green (ICG) infrared fluorescence angiography. Newly formed vessels which demonstrated leakage of ICG extended into the subretinal space without enclosure of retinal pigment epithelium (RPE), and the endothelial cells were immature. Choroidal neovascularization which did not demonstrate leakage of ICG was enclosed by RPE without retinal detachment, and the endothelial cells were mature. The newly formed vessels with immature endothelium in the subretinal space that were covered with multiple layers of RPE demonstrated no leakage. These results show that ICG leaks form choroidal neovascularization which has immature vessels that are not enclosed by RPE and that extend into the subretinal space.

Animals↗

[Circularity index of left ventricular shape in the assessment of heart disease].

Left ventricular volume and ejection fraction obtained by cineangiography are useful to evaluate global left ventricular function in humans. Left ventriculography provides evidence of the effect of coronary artery stenosis on regional wall motion in patients with coronary artery disease. Changes in left ventricular shape are also found in various heart diseases. The left ventricular cavity is normally ellipsoid in shape, but becomes flat in hypertrophic cardiomyopathy, globular in dilated cardiomyopathy, and aneurysmal in some patients with myocardial infarction. This study developed a new method to quantify regional and global left ventricular shape. Regional circularity index (RCI) was defined as GD divided by r (GD = distance from each 5-degree endocardial margin to the center of gravity, r = radius of the circle equal to left ventricular area). The global circularity index (GCI) was derived from the sum of magnitude of RCI-1. The end-systolic GCI was related to end-systolic left ventricular wall stress (r = 0.71, p < 0.001). The change in GCI during systole was related to left ventricular ejection fraction (r = 0.79, p < 0.001). In severe cases of dilated cardiomyopathy, the left ventricle became more spherical during ejection. End-systolic left ventricular moment around the minor axis had a good correlation with left ventricular ejection fraction (r = 0.81, p < 0.001). Quantification of regional and global left ventricular shape can be used to estimate left ventricular wall stress from left ventricular shape. Left ventricular shape change during systole and the moment around the left ventricular short axis contributes to left ventricular ejection.

Angiocardiography↗

[Local spread of carcinoma of the esophagus by perineural invasion].

For clarification of the clinico-pathological features of carcinoma of the esophagus by perineural invasion (pni), 107 resected specimens were histologically examined. A correlation between pni and other findings, including clinical results, was sought. Pni was found in 31 patients (29.0%). It was found in no cases without adventitial cancerous invasion, at 26.3% in a1, 36.5% in a2 and 66.7% in a3. Pni would thus appear to be closely correlated with the depth of invasion. It also showed correlation with lymph-canal invasion but not with venous invasion or lymph node metastasis. Pni positivity was the same regardless of patient's age and sex, as well as tumor size, location and histological differentiation. In patients who had undergone preoperative radiotherapy, lymph-canal and venous invasion were noted to have markedly decreased but not pni. Curative resection was carried out in 57.9% of the pni negative patients and in 32.3% of the pni positive. Local recurrence was observed in 30.0% of pni positive and only 4.5% of negative cases. The cumulative survival rate was not significantly less in positive compared to negative patients.

Adult↗

In vitro studies to elucidate the metabolic pathway of (+)-S-145, a thromboxane A2 receptor antagonist, in rats. Evidence for two independent pathways in peroxisomal beta-oxidation.

The metabolism of (+)-S-145, a thromboxane A2 receptor antagonist, was investigated in vitro using isolated hepatocytes, liver homogenates, and subcellular fractions prepared from rats. The cofactor requirement and subcellular distribution of beta-oxidation and hydroxylation suggested that the chain shortening of the carboxyl side chain of (+)-S-145 was catalyzed by beta-oxidation enzyme systems in peroxisomes and hydroxylation at the C-5 and C-6 positions of the bicyclo ring was catalyzed by monooxygenases in microsomes, respectively. In the initial stage of metabolism of (+)-S-145, the potential of activation to its coenzyme A (CoA) thio ester was prominent, compared with that of the hydroxylation. The resulting (+)-S-145-CoA was beta-oxidized. There seems to be two metabolic pathways in the metabolism of (+)-S-145-CoA. One is the biotransformation of (+)-S-145-CoA to bisnor-(+)-S-145 and tetranor-(+)-S-145 in the beta-oxidation cycle, and the other is the reduction of (+)-S-145-CoA to dihydro-(+)-S-145-CoA by NADPH dependent delta 5-reductase followed by beta-oxidation to dihydrobisnor-(+)-S-145, which was scarcely beta-oxidized to tetranor-(+)-S-145. Finally, these beta-oxidized metabolites are hydroxylated by monooxygenases in microsomes at the 5- or 6-position of their bicyclo ring, whereas beta-oxidation activity of hydroxylated metabolites of (+)-S-145 was not observed in the light mitochondrial fraction nor in isolated hepatocytes.

Animals↗

Polar lipids of a non-alkaliphilic extremely halophilic archaebacterium strain 172: a novel bis-sulfated glycolipid.

Extremely halophilic archaebacteria which require high salt concentrations for growth and survival contain glycerol diether analogues of phospholipids and sulfated glycolipids as major membrane polar lipids. A non-alkaliphilic, non-pigmented rod-shaped extreme halophile, isolated from sea sand in Japan and designated 'strain 172', was found to contain two phospholipids, phosphatidylglycerol (PG) and phosphatidylglyceromethylphosphate (PGP-Me), derived from both C20-C20- and C20-C25-glycerol diethers, and a novel major glycolipid (designated SGL-X). This glycolipid has been identified as a bis-sulfated diglycosyl C20-C20- or C20-C25-glycerol diether, on the basis of its TLC mobility, positive-staining behavior with sugar and sulfate-staining reagents, its mole ratio sulfate/glycolipid = 2.2, and by spectrometric analysis (IR and FAB-MS) of the intact and the desulfated SGL-X. The sugars were identified as mannose and glucose, after acid hydrolysis of SGL-X, by paper chromatography of the free sugars and GC-MS of the derivatized sugars (alditol acetates). Permethylation analysis and 1H- and 13C-NMR analysis established the position and configuration of the sugar linkages and the positions of the sulfate groups. The final structure of SGL-X (now designated S2-DGD-1) is proposed to be: 2,3-diphytanyl- or phytanyl-sesterterpenyl-1-[2,6-(HSO3)2-alpha-Manp-1--> 2- Glcp]-sn-glycerol. This lipid is the first bis-sulfated glycolipid to be reported in extremely halophilic archaebacteria, and is the first in the biosphere that possesses two sulfate groups attached to the same monosaccaride.

Archaea↗

Chromosomal pericentric inversion detected in a sow and her piglets.

Forty-four pigs with the suspicious symptoms of porcine stress syndrome (PSS) were selected for chromosome analysis. Cytogenetic evaluation by means of the G-banding technique revealed that one sow had an abnormal (38,XX, inv (1p+q-) (2.1;1.1) karyotype. The same abnormality was also detected in 8 of 13 offspring of this sow. However, there was no correlation between the chromosome abnormality and PSS. The chromosome abnormality did not give rise to a reduction in the fertility of this sow or in the viability of her offspring. This case represents the first reported instance of pericentric inversion in swine.

Journal Article↗

The involvement of the stimulatory G protein in sexual dimorphism of beta-adrenergic receptor-mediated functions in rat liver.

In rat hepatocytes, beta-adrenergic receptor (beta-AR)-mediated cAMP generation was found to be higher in the female than in the male. As compared to the male, the number of beta-AR, detected by [125I]iodocyanopindolol, was elevated in the female. In agonist competition experiments, the proportion of beta-AR in the high-affinity state was promoted in the female than in the male. The alpha subunit of the stimulatory G protein (Gs alpha) was quantified using ADP-ribosylation catalyzed by cholera toxin. The amount of Gs alpha, both small, 42 kDa (Gs alpha S), and large, 47 kDa (Gs alpha L), forms increased in parallel with enhancement of catecholamine-sensitive adenylate cyclase activity in the female. The female showed a disproportionate increase in Gs alpha L, which is preferentially coupled to beta-AR, compared with Gs alpha S. In addition, 17 beta-estradiol facilitated isoproterenol-induced cAMP generation in both male and female rats, whereas castration or testosterone had no effect on this response. It is proposed that the cellular sites for sexual dimorphism in hepatic beta-adrenergic functions are the coupling state of beta-AR to Gs and the amount of Gs alpha as well as the level of beta-AR.

Adrenergic beta-Antagonists↗

Heart rate variability before the occurrence of silent myocardial ischemia during ambulatory monitoring.

Thirty-three ischemic episodes in 19 patients with stable coronary artery disease were studied to clarify changing autonomic nervous system activity during daily life before the occurrence of myocardial ischemia. Nonischemic points were studied for comparison of control data with ischemic episodes. These were defined as (1) patient showing no ischemic ST-T change while having the same heart rate with onset of ischemic episodes, and (2) presence within 1 to 2 hours before or after onset of ischemic episodes in the same patient. We analyzed heart rate (HR) variability during the 30-minute period before the onset and after the end of ischemic episodes during 24-hour monitoring. The period of 30 to 40 minutes before ischemia was regarded as the baseline, and HR variability was analyzed at 10-minute intervals before each ischemic episode and nonischemic point. HR variability was quantified on the band of 2 components: low frequency (0.04 to 0.15 Hz; LF) and high frequency (0.15 to 0.40 Hz; HF). Of the 33 episodes, 24 (73%) had a greater LF/HF value during the 30-minute period before ischemia than that before the nonischemic points. Distribution of the number of the 24 episodes demonstrated circadian rhythm with a peak from 8 to 10 A.M. HF power began to decrease from the last 10 minutes before ischemia, compared with baseline. A significant decrease in HF power with a background of greater value of LF/HF may explain the reduced ischemic threshold for ischemia during daily life.

Aged↗

Frequent loss of heterozygosity in the region including BRCA1 on chromosome 17q in squamous cell carcinomas of the esophagus.

Ninety-four esophageal squamous cell carcinomas were examined for loss of heterozygosity at several loci on the long arm of chromosome 17 (17q), using restriction fragment length polymorphism markers. Loss of heterozygosity was observed in 56 (62%) of 91 tumors that were informative with at least one marker. Comparison of these results with clinicopathological data indicated that the losses on chromosome 17q had occurred at an early stage of carcinogenesis. Detailed deletion mapping in these tumors revealed that the region commonly deleted was within the segment between loci defined by two markers at chromosomal band 17q21.3.

Alleles↗