[Application of endocardial balloon electrodes to ventricular tachycardia].
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Publications and source records attributed to H Ando.
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The strong association of Behçet's disease with HLA-B51 in several ethnic groups is well known. Because the HLA-B51 antigen has been recently identified to comprise three alleles, HLA-B* 5101, HLA-B* 5102, and HLA-B* 5103, we sought to investigate whether there is any correlation of one particular allele among them with B51-positive patients with Behçet's disease. Forty-six Japanese patients with Behçet's disease and HLA-B51 were typed by using the alloantisera, which allowed the subdivision of B51 antigen by the microlymphocyte toxicity assay. All the patients were found to carry HLA-B* 5101. This result suggests that amino acid substitutions at residue 167 or 171 prevent the development of Behçet's disease, because HLA-B* 5101 differs from HLA-B* 5102 and HLA-B* 5103 by single amino acid substitution at residues 171 and 167, respectively, or that another non-HLA gene tightly linked to the HLA-B* 5101-associated haplotype around the HLA class I gene region is responsible for the susceptibility to Bechçet's disease. This study provides insight into the molecular mechanism underlying an HLA association with Behçet's disease.
A patient with vasospastic angina who developed myocardial ischemia following ethanol ingestion but not after exercise was described. Myocardial ischemia was evidenced by electrocardiograms (ECGs) and thallium-201 scintigrams. The blood acetaldehyde level after ethanol ingestion was abnormally high. The time course and severity of myocardial ischemia coincided with those of the blood ethanol and acetaldehyde level. Coronary arteriography showed ergonovine maleate-induced coronary vasospasm at the left anterior descending coronary artery. ECG changes similar to those induced by ethanol ingestion were observed at the same time. These findings suggest that the high blood acetaldehyde level might be responsible for the development of coronary vasospasm and myocardial ischemia in this patient.
To elucidate whether breast milk, vaginal discharge and contamination with maternal blood at birth are possible routes of mother-to-child transmission of hepatitis C virus (HCV), we examined HCV RNA in the cord and peripheral blood of infants, and in the blood, vaginal discharge, and breast milk of anti-HCV seropositive mothers. From July 1991 to July 1992, we studied 20 healthy pregnant women, who were seropositive with the Ortho anti-HCV EIA, and their infants. Using a sensitive nested polymerase chain reaction (nested PCR), we investigated the presence or absence of hepatitis C virus in the above-mentioned specimens. Moderate elevation of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) was observed in only one woman in the first and third trimesters. The nested PCR and subsequent Southern hybridization detected 0.5-5.5 copies of HCV c-DNA. HCV RNA was detected in 17/20 blood samples (85%), 7/14 vaginal discharge samples (50%) and 4/10 cord blood samples (40%). However, no HCV RNA was identified in the peripheral blood of infants or breast milk. The mother-to-child transmission of HCV at delivery or via breast milk does not appear to contribute much to maintaining the global HCV reservoir.
The calcium channel blockers, diltiazem and verapamil, and the beta agonist orciprenaline sulfate all demonstrated significant protection against methacholine-induced bronchoconstriction in 11 stable asthmatics (5 males and 6 females). Ten and 20 mg of inhaled diltiazem, 5 mg of verapamil or 30 mg of orciprenaline administered 15 min before stepwise increasing doses of methacholine hydrochloride produced significant reduction in respiratory resistance (Rrs), minimum dose of methacholine hydrochloride required for Rrs increase (Dmin) and bronchial reactivity measured with an Astograph. The mechanism of action of the calcium channel blockers is presumably at the level of the smooth muscle cells themselves. The combination of positive influence and lack of any adverse effect on blood pressure or heart rate with any of the agents tested indicates that their clinical application for alleviation of acute asthma can be recommended.
OBJECTIVE: Although ritodrine crosses the placenta, its direct effect on fetal cell proliferation has not been reported. We hypothesized that beta 2-adrenergic receptor stimulation could promote fetal liver growth. STUDY DESIGN: Ritodrine was added to serum- and hormone-free primary cultures of fetal, neonatal, or adult rat hepatocytes. We measured both tritiated thymidine incorporation into deoxyribonucleic acid and nucleus number. The effect of ritodrine on cell cycle was also analyzed with flow cytometry. RESULTS: Ritodrine enhanced the proliferation of fetal rat hepatocytes. Ritodrine remarkably stimulated deoxyribonucleic acid synthesis of fetal and neonatal but not adult hepatocytes. The effect was dose dependent and was antagonized by propranolol. Analysis of the nuclear deoxyribonucleic acid content derived from flow cytometry revealed that cells stimulated by ritodrine entered S phase. CONCLUSION: These results indicate that ritodrine may promote the proliferation of fetal hepatocytes through the stimulation of beta 2-adrenergic receptors, followed by induction of deoxyribonucleic acid synthesis.
BACKGROUND: The adenomatous polyposis coli (APC) gene at chromosome 5q21 that is responsible for familial adenomatous polyposis (FAP) was recently isolated, and germ-line mutations in a substantial number of FAP families were characterized. Based on this information, the authors attempted to develop a presymptomatic diagnosis test for members of families that carry FAP. METHODS: A rapid screening procedure using a polymerase chain reaction (PCR) method without radioisotopes, if necessary, coupled with digestion of restriction enzymes has been performed by detection of germ-line mutations that alter the size of DNA fragments or affect the recognition site of restriction enzymes in the APC locus. RESULTS: A rapid screening procedure to detect germ-line mutations at 12 loci that cause adenomatous polyposis was established. CONCLUSIONS: Using these 12 systems, presymptomatic diagnoses can be made with 100% accuracy within 24 hours. The procedures will be useful for counselling of members in some FAP families, which accounted for nearly 40% of the 95 FAP kindreds that have been detected by the germ-line mutations so far.
Recently, the survival of patients with gastroschisis has been dramatically improved and it has reached more than 90%. Over the last 10 years, 20 of 21 cases (95%) survived in our hospital. We have been using the primary fascial closure of the abdominal wall as a standard operative procedure. The umbilical cord was usually excised at the operation in order to secure the suture line and prevent wound infection. The survivors sometimes complained of the absence of the umbilicus. However, it was somewhat difficult to create a new umbilicus later by use of the surrounding skin. In the last five cases, we tried to carry out the primary fascial closure with preservation of the umbilical cord. All patients could obtain good cosmetic results with near-normal appearance. Omphalitis or cellulitis was never observed, but a small umbilical hernia occurred in one case.
The HLA-C locus frequently has a serologically undefined "blank" (CwBL) specificity. A cDNA clone derived from the HLA-C gene with a blank specificity (Cx52) strongly associated with the most common haplotype in a Japanese population, A24-CwBL-B52-DR2-DQ6-DP9, has been recently cloned and sequenced in our laboratory and officially designated Cw*1201 as an allelic name, indicating that the inability to define the HLA-C antigen serologically in this haplotype is not due to an HLA-C antigen gene deletion or mutation, but to the absence of typing sera. In this paper, a mouse L-cell transfectant expressing this Cw*1201 gene product was constructed and employed for screening of alloantisera recognizing the HLA-C antigen with the Cw*1201 specificity. Two alloantisera against Cw*1201 were thus identified and characterized using HLA homozygous B-cell lines and local panel PBL cells, indicating that a transfectant expressing a single HLA provides an efficient screening system for collection of HLA-typing sera, especially reacting with serologically unclassifiable "blank" antigens.
The role of changes in preload in maintaining stable hemodynamics during coronary obstruction was assessed in the presence of myocardial ischemia due to occlusions of the left anterior descending (LAD) and left circumflex (LCX) coronary arteries. Changes in preload (mean left atrial pressure) to maintain a constant stroke volume after coronary occlusion were examined in 18 anesthetized dogs (LAD occlusion in 9 dogs, LCX occlusion in 9 dogs). The level of ischemia was assessed sonomicrometrically. Ventricular function curves relating left atrial pressure to stroke volume were assessed during a control state and after 1 min of coronary occlusion. The extent of preload reserve after coronary occlusion was examined on the ventricular function curves and was defined as the change in mean left atrial pressure required to maintain stroke volume at the level of the control state under conditions of regional ischemia. Ischemic size was determined by a stereo-angiogram after the animals were sacrificed. The extent of preload reserve (X) was linearly related to the ischemic size (Y) in both LAD (Y = 0.90 + 0.16X, r = 0.76, p < 0.001) and LCX (Y = -1.79 + 0.19X, r = 0.79, p < 0.001) occlusions. The slopes of the regression lines in LAD and LCX occlusions were the same. The X intercepts of these lines were -5.6% and 9.4% of the left ventricular weight in LAD and LCX ischemia (p < 0.001), respectively. Thus, the presence of systolic wall motion abnormalities due to coronary occlusion can be compensated for hemodynamically by changes in the preload reserve.(ABSTRACT TRUNCATED AT 250 WORDS)
The effect of vesnarinone (OPC-8212), an orally active positive inotropic agent was studied in tracheal muscle isolated from guinea pigs, and the mechanism of its action was analyzed. Vesnarinone (10(-6)-10(-4) M) caused a concentration-dependent relaxation of tracheal muscle pre-contracted by 10(-4) M histamine. The potency of the relaxing effect of vesnarinone was greater than that of theophylline; the pD2 values for vesnarinone and theophylline were 4.9 and 4.5, respectively. Vesnarinone reduced the high-K(+)-induced contracture of depolarized tracheal muscle non-competitively (pD'2 = 3.7). Vesnarinone at the low concentration of 3 x 10(-6) M shifted the concentration-response curve for isoproterenol in a parallel fashion to the left. Vesnarinone additively acted on the relaxing effect of isobutyl methyl xanthine. Propranolol (10(-5) M) and reserpine pre-treatment (5 mg/kg, i.p., 24 hr) had no effect on the relaxing effect of vesnarinone. These results suggested that vesnarinone elevated the intracellular cyclic AMP level via phosphodiesterase inhibition, resulting in the tracheal muscle relaxation.
Criminal cases involving stimulant abuse have increased since 1970 but have now leveled off. Some of the offenders claimed to have used the Vicks Inhaler containing a stimulant (1-methamphetamine) which is used for the treatment of nasal obstruction. The aim of this experiment was to measure the amount of 1-methamphetamine contained in the Vicks Inhaler by stimulating the human respiratory system. The results are as follows: 1) The data from the stimulation experiment showed that the inhalation level of 1-methamphetamine was estimated to be 320.4ng. From this value, the level of 1-methamphetamine absorbed per one respiration was calculated to be 21ng. 2) The data from quantitative and qualitative analysis by gas-chromatography showed that menthol interfered with the methamphetamine. 3) A qualitative test for the stimulant in urine was negative when the subject inhaled the Vicks Inhaler only once. However, this test turned positive when the subject inhaled it more than 17 times.
This study examined mainly the adverse effects of 201Tl myocardial scintigraphy with dipyridamole (D-Tl) in 73 elderly patients over 70 years old in comparison with those in 65 younger patients. Fifty-five of 73 elderly patients (75%) and 49 of 65 younger patients (75%) had a persistent or dipyridamole-induced perfusion defect on D-Tl. The hemodynamic changes induced by dipyridamole as well as the incidence of cardiac and noncardiac adverse effects were similar in both groups and no serious adverse effect occurred in either group. Secondly, we examined the procedure's usefulness for detecting ischemic heart disease in elderly and younger patients. Dipyridamole induced perfusion defect was noted in 21 elderly patients and in 24 younger patients (N.S.). Among the patients in whom coronary angiography was performed, significant coronary artery stenosis was found in 5 of 8 elderly patients and 17 of 20 young patients (N.S.). In patients with one or two-vessel disease, the area with dipyridamole induced ischemia was concordant with the stenotic area seen on coronary angiography in 3 of 3 elderly patients and 12 of 13 younger patients (N.S.). Thus, the safety and usefulness of D-Tl for detecting myocardial ischemia were comparable in elderly and young patients.
In the rat under urethane anesthesia, a fast intravenous injection of a bolus of sodium azide elicited a transient cornea-positive change in transocular potential (azide response). A bolus injection of sodium thiocyanate (NaSCN) produced a cornea-negative response (SCN- response) with a similar rising phase as the azide response, but with a faster return from the peak. The peak amplitude depended on bolus volume, concentration, animal strain, and age. For more than 24 h, the azide and SCN- responses could be recorded repeatedly from a single rat with little variation in peak amplitudes. Following an administration of iodate, known to degenerate the retinal pigment epithelium (RPE), the transocular d.c. potential decreased; the azide response became smaller and then was inverted in polarity, whereas the SCN- response became larger. Azide and SCN- are assumed to depolarize and hyperpolarize the basal membrane of RPE, respectively. The equilibrium potential of ions passing through the putative azide-sensitive channels is assumed less negative than resting potential of RPE cells. The SCN- response probably represents a diffusion potential of SCN- permeating through anionic channels at a higher rate than Cl-. Results demonstrate the feasibility of in vivo electrophysiological measurement of the functional state and the structural integrity of RPE under pathological conditions.
Functional changes in retinal pigment epithelium (RPE) associated with light-induced retinal damage were studied by measuring transocular potential changes evoked by injections of azide and thiocyanate (SCN-). The retinal damage by light in the rat is classified into two types: Type 1, rod cell death associated with RPE deterioration; Type 2, the loss of rod cells without RPE deterioration. To study the type 1 damage, littermate pairs of long-term dark-adapted adult albino rats were tested at 1 h and 10 d after the exposure to green light of 1,200 lx for 1/2 to 24 h. Time course of the damage progress was also followed for 12 h. We found that 1) RPE was affected rapidly by the damaging light, 2) the exposure length determined the ultimate degree of RPE damage, 3) damaging effects on RPE proceeded slower and weaker after exposure than during continuous light, 4) progress of the damage in RPE was two-phasic; during the first phase, the SCN- response was enhanced and the azide response was reduced; both responses were decreased rapidly in the second phase. The first phase was assumed to indicate a depolarization of the basolateral membrane of RPE, and the second phase to manifest the structural deterioration of RPE. The type 2 damage was studied in young rats with exposure to weak light for 28 d. At 30 d after the exposure, a-wave of the ERG and number of rod cells were substantially reduced but azide and SCN- responses were affected slightly.
Electrophysiological properties of the retinal pigment epithelium (RPE) were studied in the rat with hereditary retinal dystrophy (rdy). Transocular potential changes evoked by intravenous bolus injections of azide and thiocyanate (SCN-) are the only available indication of RPE state when degeneration of rods is in progress. Also determined were age-dependent decrease in retinal DNA content and in counts of cones that survive after degeneration of rods. The azide response in the pigmented and albino rdy rat was already reduced at the earliest age tested (60 d) and continued to decrease till the age of 2 years. The SCN-response was similarly affected but seemed to decline faster than the azide response. The azide/SCN- response ratio was significantly increased in albino mutants, especially around the age of 400 d. At the age of 10 months and later, the azide and SCN- responses became slower than those of normals. A prolonged exposure of 1,200 1x light to dystrophic rats older than 110 did not affect the azide and SCN- responses whereas the same exposure abolishes the responses of normal rats and of the dystrophic rats at early stages. In rdy rats, the electrophysiological changes were considered to correlate with structural changes of the junctional RPE complex and with abnormal membrane enzyme distribution discovered by others. These RPE changes may contribute to the decreasing cone cell number after rod cell disappearance.
PURPOSE: This study was performed to examine the gelatinolytic and caseinolytic activities and the levels of two proteinase inhibitors, alpha 1-proteinase inhibitor (alpha 1-antitrypsin) and alpha 2-macroglobulin, in the human aqueous humor. METHODS: Aqueous humor samples were collected during elective surgery in patients with cataracts. Zymography with gelatin- and casein-containing gels was performed. The inhibitors were examined by Western blot analyses, enzyme-linked immunosorbent assay, and dot blot assays. RESULTS: The aqueous humor contained a major band of gelatinolytic activity at a molecular weight of 66 kD and minor bands at 125, 95, and 62 kD. These gelatinases were inhibited by 10 mM ethylenediaminetetraacetic acid (EDTA) or 1,10-phenanthroline. After extended incubation (48 hours), zymography on casein-containing gels showed proteinase bands with molecular weights in the 80- to 84-kD range. Additional bands at 68 and 48 kD also were observed. All the caseinase activities were inhibited by 10 mM phenylmethylsulfonyl fluoride and 1 microgram/ml aprotinin. No inhibition was observed with 5 mM EDTA, 5 microM E-64, or 1 microM pepstatin. These results indicated that the caseinases are serine proteinases. Western blot analysis showed a 53-kD alpha 1-proteinase inhibitor band in the aqueous humor. The concentration was 32.2 +/- 9.9 micrograms/ml, constituting approximately 15% of the total protein. A 360-kD protein band immunoreactive to anti-alpha 2-macroglobulin also was detected. Its level in the aqueous humor was 3.2 +/- 1.3 micrograms/ml. CONCLUSIONS: The gelatinases, serine-like proteinases, and proteinase inhibitors found in the aqueous humor may participate in the remodeling of extracellular matrices in the trabecular meshwork and other tissues bordering the anterior chamber.