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Biomedical subjects

I Okada

Publications and source records attributed to I Okada.

At least 19 recordsLinked to original sources
PubMed1992

Spin-echo M-mode NMR imaging.

A nuclear magnetic resonance (NMR) imaging and display method for the observation of the continuous motion of objects is presented. By modifying a line scan technique, the spin-density distribution along a line is displayed in succession. Although spatial information is limited to only one dimension, the motion of the object is recorded at intervals of 55 ms by using a commercially available NMR imaging system. In a phantom study, this method yielded accurate velocity measurements along a single axis. When the method was applied to the human chest, an image analogous to that of M-mode echocardiography was obtained. This method, which can be called spin-echo M-mode NMR imaging, approaches the functional analysis of cardiac wall motion in regions where echocardiography is not possible. The effects of respiratory motion on the left ventricular wall were recorded in addition to its intrinsic contractile motion in an image obtained along a line parallel to the cranio-caudal axis of the body. The advantages of this method to assess cardiac wall motion in a patient with an arrhythmia were also demonstrated.

Atrial Fibrillation↗
PubMed1992

Successive infection of coxsackievirus B3 and encephalomyocarditis virus: an animal model of chronic myocarditis.

Successive infection of coxsackievirus B3 and encephalomyocarditis virus was investigated as a disease model of chronic myocarditis. Four-week-old C3H/He mice were inoculated with coxsackievirus B3 and then inoculated with encephalomyocarditis virus at 8 weeks old. The hearts were evaluated on histopathological changes compared with those of non-infected mice and mice infected with either virus alone. At 10 weeks old, the hearts of the mice infected successively with both viruses showed co-existence of fibrosis surrounding calcified lesions and marked cellular infiltration with myocardial necrosis. These findings resembled chronic active myocarditis in humans, unlike the lesions due to either virus alone. At 12 weeks old, the hearts of all the infected mice showed fibrosis with scarce cellular infiltration. The successively infected hearts also showed a significantly higher heart weight to body weight ratio than that of the non-infected control mice, and localized wall thinning in the damaged regions. Thus, we conclude that successive infection additively causes myocardial damage that resembles chronic myocarditis and may produce a heart condition similar to dilated cardiomyopathy.

Animals↗
PubMed1992

Cardiac persistence of cardioviral RNA detected by polymerase chain reaction in a murine model of dilated cardiomyopathy.

BACKGROUND: In our model of dilated cardiomyopathy (DCM), cardiac dilatation and hypertrophy developed after inoculation of encephalomyocarditis virus (EMCV), but the infectious virus was isolated only early after infection. In this study, we investigated whether viral RNA could be detected at later times using the polymerase chain reaction (PCR). METHODS AND RESULTS: In the in vitro study, FL (human amnion) cells infected with EMCV were harvested for RNA extraction, and viral cDNA was synthesized by reverse transcription with random hexamers. Using oligonucleotide primers with homology to the 5' noncoding region of EMCV, we enzymatically amplified a 121-base pair band, which was homologous to a probe specific for EMCV as demonstrated by Southern blot hybridization. The sensitivity of this PCR technique was at the level of about 10(2)-10(3) copies of viral RNA genome. In the in vivo study, four-week-old DBA/2 mice were inoculated with EMCV intraperitoneally (10 pfu/mouse) and killed on days 1,2,3,5,7,10,14,18,28,60, and 90. The hearts were divided into three parts for purification of total RNA, histopathological examination, and to culture for infectious virus. The infectious virus was isolated from the heart after the second day but never after the 14th day. The viral genome was detectable by PCR on the second day, when very little mononuclear cell infiltration around the blood vessels was histologically visible. Positive PCR signals were observed in all hearts through day 14. Viral RNA was also detected in four of six 28-day samples, four of six 60-day samples, and two of seven 90-day samples when diffuse myocardial fibrosis was prominent, but myocardial necrosis or cellular infiltration had disappeared. CONCLUSIONS: The persistence of EMCV RNA was shown by PCR in the chronic stage of EMCV-induced myocarditis, a time when the inflammatory reaction had largely subsided. The PCR is a potentially useful method to test possible viral etiologies in idiopathic heart muscle disease or DCM.

Animals↗
PubMed1992

The effect of alpha 1-blocker, bunazosin on a murine model of congestive heart failure induced by viral myocarditis.

The purpose of this study was to investigate the therapeutic effect of an alpha 1-blocker, bunazosin, using an experimental murine model of congestive heart failure induced by viral myocarditis. This model is characterized by a high incidence of severe myocarditis and subsequent congestive heart failure, and is suitable for the evaluation of the effect of drugs. To estimate myocardial damage objectively and quantitatively, we used antimyosin monoclonal antibody in addition to histopathological grading. Four-week-old BALB/c mice were inoculated with encephalomyocarditis virus. The mice were injected daily with bunazosin or saline as a placebo from the day of viral inoculation until day 7 (protocol-I) or day 14 (protocol-II), or from day 4 to day 14 (protocol-III). They were then injected with 1.5 microCi of indium-111 labeled antimyosin antibody and were killed 24 h later. The antimyosin cardiac uptake was counted and histopathological grading was performed. The heart-weight to body-weight ratio, left ventricular dimension, histopathological grades and antimyosin cardiac uptake were significantly lower in the bunazosin group than in the placebo group in protocol-II, but not in protocol-I or protocol-III. Bunazosin showed a protective effect against viral myocarditis only when it was started early after infection and continued until the stage of congestive heart failure.

Adrenergic alpha-Antagonists↗
PubMed1992

Combination treatment with ribavirin and interferon for coxsackievirus B3 replication.

The effects of combined treatment with ribavirin and recombinant human leukocyte interferon-alpha A/D against Coxsackievirus B3 replication were investigated in cultured cells. Recombinant human leukocyte interferon-alpha A/D was applied 12 hours before Coxsackievirus B3 inoculation and ribavirin was applied 1 hour after Coxsackievirus B3 inoculation on FL (human amnion) cell monolayers. These drugs inhibited Coxsackievirus B3 replication synergistically by plaque-reduction assay. This method of applying drugs may be useful in preventing and treating Coxsackie B virus infection.

Cell Line↗
PubMed1992

Detection of viral RNA in experimental coxsackievirus B3 myocarditis of mice using the polymerase chain reaction.

The presence of the viral RNA in the myocardium in experimental coxsackievirus B3 myocarditis of mice was investigated using the polymerase chain reaction (PCR). Four-week-old C3H/He mice (n = 35) were inoculated with coxsackievirus B3 (Nancy strain, 10(5) plaque-forming units/mouse). We used a pair of primers, which encompass a part of the 5' end sequence of the coxsackievirus B3 genome and can also detect many enteroviral RNAs. We found that hearts were positive for the viral RNA from 2 to 21 days after virus inoculation by PCR, but negative after day 28 and in non-infected control mice (n = 5). The viral RNA were detected by PCR later than by culture. Thus, the detection of the viral RNA using enzymatic amplification is more rapid and easier and may be more useful for clinical diagnosis of viral myocarditis than conventional culture methods. However, virus persistence in the myocardium long after virus inoculation is unusual in this model.

Animals↗
PubMed1991

Beta-blocker treatment of dilated cardiomyopathy. Beneficial effect of carteolol in mice.

BACKGROUND: The effects of carteolol, a nonselective beta-adrenergic receptor blocker with intrinsic sympathomimetic activity, were compared with those of metoprolol in a murine model of viral myocarditis and dilated cardiomyopathy caused by encephalomyocarditis virus. METHODS AND RESULTS: In the acute experiment, BALB/c and DBA/2 mice were inoculated with encephalomyocarditis virus. BALB/c mice were then given carteolol at 1 (n = 10), 10 (n = 10), 30 (n = 11), or 100 mg/kg (n = 9) daily, and DBA/2 mice were given carteolol at 1 (n = 9) or 10 mg/kg (n = 9) daily starting the day of inoculation. Controls were given distilled water (n = 23 for BALB/c mice and n = 8 for DBA/2 mice). BALB/c mice were killed on day 7, and DBA/2 mice were killed on day 14. In the subacute experiment, DBA/2 mice were inoculated with the virus and then given carteolol at 1 (n = 12) or 10 mg/kg (n = 16), or distilled water (n = 27) daily, starting on day 14. Mice were killed on day 28. Virus replication, murine survival, heart weight to body weight ratio, and histopathological findings were similar in each group in the acute and subacute experiments. In the chronic experiment, DBA/2 mice were inoculated with the virus and were then given carteolol at 1 (n = 13) or 10 mg/kg (n = 9), metoprolol at 30 mg/kg (n = 9), or distilled water (n = 31) daily, starting on day 14. Mice were killed on day 104. Heart weight to body weight ratio and histopathological scores were significantly lower in mice given carteolol than in the infected control group. Furthermore, left ventricular cavity dimension, left ventricular wall thickness, and myocardial fiber diameter of the left ventricle were significantly reduced in mice given carteolol compared with the control group. Metoprolol did not cause any significant changes compared with the control group. CONCLUSIONS: This study suggests that carteolol prevents the development of myocardial lesions similar to those in dilated cardiomyopathy after myocarditis in the chronic stage.

Adrenergic beta-Antagonists↗
PubMed1991

Pathogenesis of myocardial injury in myocarditis and cardiomyopathy.

The pathogenesis of myocardial cell injury in myocarditis and cardiomyopathy was investigated. The presence of viral genomes in the murine heart in experimental coxsackievirus B3 myocarditis was studied by Northern blotting analysis using a 32P-labeled cDNA probe from the 5' end sequence. The strongest signal of positive autoradiograms was always at about 7.4 kilobases, corresponding to the size of the complete genome of the virus. Successive infections with coxsackievirus and encephalomyocarditis (EMC) virus infection showed simultaneous acute myocarditis and healed myocarditis, and the results suggest that successive virus infections cause additional myocardial damage, and develop lesions similar to chronic myocarditis or dilated cardiomyopathy. Anti-heart auto-antibody, induced during EMC virus infection, reacted predominantly with myosin. Indium-111 antimyosin scintigraphy showed positive in some of the patients with cardiomyopathy, and the uptake was inversely correlated with left ventricular function. When mice were injected with antimyosin antibody, mouse immunoglobulin G was detected in hearts in the chronic stage of EMC virus myocarditis, in myocytes surrounding fibrosis and calcification, suggesting deposition of antimyosin antibody. Although further study is necessary to clarify the mechanism of uptake of antimyosin in cardiomyopathy, antimyosin antibody may accumulate in viable myocytes with ongoing degeneration as well as in necrosis.

Animals↗
PubMed1991

The effect of cyclosporine on the immunopathogenesis of viral myocarditis in mice.

The effect of cyclosporine on the immunopathogenesis of viral myocarditis was studied using a murine viral myocarditis model. Mice in the treated group had a higher mortality rate compared with those of the infected control group before day 15 (47/67 vs. 14/31, p less than 0.05). On day 7, treated mice showed higher titers of anti-heart autoantibody than the control group (12 +/- 7 vs 4 +/- 2, p less than 0.05), but no significant difference was seen on day 14 (28 +/- 15 vs. 39 +/- 34). Histologic lesions, lymphocyte subsets in the peripheral blood and heart in situ, the neutralizing antibody, and virus concentrations in the heart showed no significant differences between these groups. This study suggests that with the use of cyclosporine the production of anti-heart autoantibody was enhanced in the early stages of viral myocarditis in mice, and was associated with higher mortality rate.

Animals↗
PubMed1991

Genetic resistance to a Marek's disease transplantable tumor cell line in chicken lines selected for different immunological characters.

The tumor incidence and mortality of Marek's disease (MD) were determined for 471 progeny from four pairs of lines two-way selected for different immunological characters: graft versus host reaction (GVHR) competence, IgG levels, antibody response to rabbit serum albumin (RSA), and anaphylactic shock to BSA. All chicks were inoculated at 1 wk of age with 1 to 2 x 10(6) viable cells of a MD lymphoblastoid cell line, MDCC-MSB1-41C (41 C). Tumor incidence differed significantly between the high (H) and low (L) lines of each GVHR-, IgG-, RSA-, or BSA-selected group. There were also significant differences in mortality rates between H and L lines of all selected groups. The IgG-H, BSA-H, and RSA-H lines were more resistant than their respective L lines. The H line of the GVHR-selected lines was more susceptible than the L line. Tumor regression could be detected only in the IgG- and RSA-selected lines. No definite correlation could be found between genetic resistance to 41C and genetic resistance to MD virus.

Anaphylaxis↗
PubMed1990

Hearing screening in health examination services for young children at health centers in Japan.

The infant hearing screening program (IHSP) was devised for the early discovery of severe to profound hearing impairments in children. The program has been planned for use in the ordinary health examination services (with a follow-up program) for young children in health centers. The IHSP consists of a three-part test battery: a high-risk register for deafness, a developmental test of auditory function, and an auditory behavioral test. From 1977 to 1983, 22,443 young children were screened in four health centers in Osaka City. Ten of these children were identified as having serious hearing loss. Five of these 10 children were below 11 months of age. The incidence of children with severe to profound hearing impairment was inferred to be approximately 0.04% in the general population of young children. Certain problems occurred in the IHSP, and included a high level of over-referrals. However, the IHSP was considered to be a useful screening method for the early detection of severe hearing impairments when used in general health check-ups in health centers.

Child Health Services↗
PubMed1990

The viral genome in experimental murine Coxsackievirus B3 myocarditis: a Northern blotting analysis.

The presence of viral genomes in the murine heart in experimental coxsackievirus B3 myocarditis was investigated by Northern blotting analysis. Four-week-old C3H/He mice were inoculated with coxsackievirus B3. After sacrifice, the hearts were divided into 3 parts. Total RNA was extracted from one part of the heart. The other two parts were used for investigation of histopathology and of virus titer by plaque assay. The 32P-labeled cDNA probe was derived from the 5' end sequence of the coxsackievirus B3 genome. Northern blot autoradiograms of heart RNA were positive for viral RNA until day 7 and negative after day 10 and in control (uninfected) hearts. Positive autoradiograms always had the strongest signal at about 7.4 kilobase, corresponding to the size of the complete genome of the virus. The viral genomes were detected earlier than the appearance of the histopathologic changes in the murine heart. This type analysis of the viral genome in the murine myocardium may be useful in evaluating the effects of specific drugs on experimental viral myocarditis at the level of the viral genome.

Animals↗
PubMed1990

[Magnetic resonance angiography using a magnetic resonance flow tagging technique].

A direct bolus imaging method, which was developed for flow quantitation, was applied to the cervical regions of four normal volunteers to perform magnetic resonance angiography. A transverse section of 10 mm thickness was selectively excited to tag blood flow in the supraclavicular region and a projected image of the tagged bolus viewed in terms of anteroposterior direction was obtained after the echo time (TE). Like cine magnetic resonance imaging, multiple images representing four to 16 cardiac phases were obtained with repeated excitations. With a relatively long TE, ranging from 50 to 200 msec, we advanced tagged blood farther downstream, so as to elongate the visualized bolus along the vessel. Within the visualized bolus, the outer layer close to the vessel wall, where the blood flow velocity was slow, stretched like long tails behind the central part of the bolus producing arrow-head shapes, and the tails were assumed to represent the vascular structure. Bilateral common carotid and vertebral arteries were visualized in each image size approximately 5 cm obtained at the systolic phase. Since prolonged TE yielded less signal intensity, the bolus was not clearly visualized when TE was longer than 100 msec. The cine display of images with multiple cardiac phases produced good evaluations of dynamic changes of pulsatile flow, and this method is expected to be a useful diagnostic tool which combines the capability of flow quantitation with non-invasive angiography. The accuracy of this method in delineating a stenotic lesion was also evaluated using phantom with steady flow, since it is one of the most important capabilities of a clinically used angiographic method.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiography↗
PubMed1989

Myocardial uptake of antimyosin monoclonal antibody in a murine model of viral myocarditis.

The myocardial uptake of 125I- and 131I-antimyosin monoclonal antibody Fab in experimental myocarditis in BALB/c mice induced by encephalomyocarditis virus was studied. The biodistribution of 125I-antimyosin demonstrated that the highest ratio of radioactivity appears in the heart of infected mice on day 14 (the ratio of percent dose per gram for the organ to percent dose per milliliter for blood; 9.75 +/- 2.79 vs. 1.27 +/- 0.78 at 24 hours in inoculated mice vs. control mice). There was no statistically significant difference between the mean activity ratios of tissues other than the heart in control and inoculated mice. The uptake ratio for the heart increased significantly 3 days after virus inoculation and reached a maximum on day 14 when myocardial lesions were most extensive and prominent. The uptake ratio decreased significantly, but it still remained high compared with controls on day 28 when cellular infiltration had decreased and fibrosis was evident. The scintigraphic images obtained with 131I-antimyosin monoclonal antibody clearly demonstrated that visualization of the heart in experimental myocarditis was possible 24 hours after administration of radiotracer, and localized activity was still observed in the 48-hour image. We conclude that antimyosin monoclonal antibodies localize selectively in the heart from the acute to subacute stage of viral myocarditis. These findings indicate that antimyosin scintigraphy is a reliable noninvasive method for the evaluation of patients suspected of having myocarditis.

Animals↗