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Biomedical subjects

J Suzuki

Publications and source records attributed to J Suzuki.

At least 163 records · Page 9Linked to original sources
PubMed1999

[Pharmacological characteristics and clinical application of losartan, an orally active AT1 angiotensin II receptor antagonist].

Losartan is the first orally active angiotensin II receptor type 1 antagonist for a new class of cardiovascular therapeutic agent. Losartan is converted to an active metabolite (E3174) after oral administration in humans and rats. Both losartan and E3174 contribute to the net angiotensin II receptor blockade and produce anti-hypertensive effect. Losartan not only blocks the vasoconstrictive effect of angiotensin II but also inhibits its mitogenic effect; thus losartan is expected to protect against end-organ-damage-related hypertension and chronic heart failure. Unlike angiotensin-coverting-enzyme inhibitor, losartan does not elicit adverse effects of cough and angioneurotic edema by its blockade of angiotensin II receptor. It is also expected to reduce proteinuria in nephropathy. In addition to its blockade of angiotensin II receptor, losartan blocks thromboxane A2 receptor and facilitates excretion of uric acid, although therapeutic importance of these effects are under investigation. In summary, losartan, an angiotensin II type 1 receptor antagonist is a new class of antihypertensive agent and its therapeutic potentials are not merely reduction of blood pressure but total protection from end-organ damage resulting from activation of both the systemic and local renin-angiotensin system.

Angiotensin Receptor Antagonists↗
PubMed1999

An adult case with an abnormal right ventricular structure causing intraventricular pressure gradient and a history of aphthous stomatitis and thrombophlebitis.

We report a 50-year-old man with a right ventricular structure causing an intraventricular pressure gradient. He had been diagnosed as vasculo-Behçet with a history of aphthous stomatitis and thrombophlebitis. He had also been suffering from atrial flutter and mild right-side heart failure. Echocardiography showed that there was an abnormal structure attached to the right ventricular free wall and protruding into the cavity, and that it caused the pressure gradient estimated to be approximately 19 mmHg. Chest X-ray computed tomography demonstrated that the structure was partially calcified. Magnetic resonance imaging depicted the structure separating the right ventricle into two chambers. Angiographic study revealed a markedly enlarged right atrium and a filling defect at the mid-portion of the right ventricle, which divided the right ventricular cavity into two parts. Hemodynamic study showed a slightly elevated right atrial pressure (mean 7 mmHg) and a peak-to-peak intraventricular pressure difference of 18 mmHg in the right ventricle. The diastolic pressure tracing of the right ventricular low pressure chamber showed a 'dip and plateau' pattern. Although the pathological features of the abnormal right ventricular structure in this case were not fully clarified, abnormal muscle bundle and/or endocardial fibrosis, which were reported to be associated with Behçet's disease, may have contributed to its generation.

Atrial Flutter↗
PubMed1999

Clinical implication of left precordial T wave inversions in the presence of complete right bundle branch block.

This study was designed to elucidate whether left precordial negative T waves are electrocardiographic indicators for the diagnosis of hypertrophic cardiomyopathy (HCM) even in the presence of complete right bundle branch block (CRBBB). In 7 consecutive patients with CRBBB accompanied by negative T waves in at least one of the left precordial leads (V4, V5, V6, maximal negativity; 1.06 +/- 0.40 mVol) (left precordial negative T wave group) and in 15 randomly selected CRBBB patients without left precordial T wave inversions (control group), echocardiography was performed to rule out underlying diseases causing left ventricular overload and to identify candidates for magnetic resonance (MR) imaging. None had anginal pain indicating ischemic heart disease. When 2-dimensional echocardiography indicated left ventricular hypertrophy with wall thickness > or = 15 mm, the magnitude and distribution of hypertrophy were scrutinized on contiguous left ventricular MR short-axis images. The diagnostic criterion of HCM was the demonstration of hypertrophy with a wall thickness of 20 mm or more on the left ventricular MR short-axis images. All patients in the left precordial negative T wave group had negative T waves in both I (negativity; 0.27 +/- 0.17 mVol) and aVL (negativity; 0.23 +/- 0.14 mVol), whereas none in the control group did. The diagnostic criterion for HCM was fulfilled in six patients in the left precordial negative T wave group. However there were no patients who fulfilled the criterion in the control group. Negative T waves were recorded in the I (negativity; 0.30 +/- 0.17 mVol), aVL (negativity; 0.25 +/- 0.14 mVol), V4 (negativity; 1.03 +/- 0.46 mVol), V5 (negativity; 0.83 +/- 0.37 mVol) and V6 leads (negativity; 0.31 +/- 0.31 mVol) in all patients with HCM, while they were recorded in only 6% of the patients without HCM. In conclusion, the existence of left precordial negative T waves in the presence of CRBBB strongly indicates HCM.

Bundle-Branch Block↗
PubMed1999

Embryonic smooth muscle myosin heavy chain SMemb is expressed in pressure-overloaded cardiac fibroblasts.

Left ventricular hypertrophy (LVH) is a secondary adaptation to increased external load. Various qualitative and quantitative changes in myocytes and extracellular components occur during the development of LVH. It has recently been demonstrated that alpha-smooth muscle actin (alpha-SMA)-expressing myofibroblasts appear in the interstitium of the heart subjected to increased workload suggesting that cardiac fibroblasts as well as myocytes alter their phenotype in response to pressure overload. In the present study, to explore the load-induced response and phenotypic modulation of cardiac fibroblasts, the localization of embryonic smooth muscle myosin heavy chain (SMemb) and alpha-SMA in thoracic aorta-constricted rat hearts was investigated by immunohistochemistry, and the morphology of the SMemb-expressing cells was examined by electron microscopy. In addition, to clarify the mechanisms by which SMemb is induced in pressure-overloaded hearts, mRNA expression of SMemb in aorta-constricted rat hearts and in transforming growth factor-beta1 (TGF-beta1)-treated or mechanically-stretched cultured cardiac fibroblasts was investigated. Enhanced staining of SMemb and alpha-SMA was detected in the interstitial spindle-shaped cells in the fibrotic lesions of the pressure-overloaded left ventricles by immunohistochemistry. These cells were demonstrated by electron microscopy to have features specific for activated fibroblasts such as serrated nuclei or prominent rough endoplasmic reticulum. These cells also had characteristic features of myofibroblasts, i.e. irregularly arranged actin filaments and scattered dense bodies. Northern blot analysis revealed increased mRNA levels of SMemb both in aorta-constricted rat hearts and in cultured cardiac fibroblasts stimulated by TGF-beta1 or by mechanical stretch. These results suggest that SMemb may be a molecular marker both for the detection of activated cardiac fibroblasts that may play important roles in the remodeling of pressure-overloaded cardiac interstitium, and for the identification of the regu latory mechanisms that control the phenotypic modulation of cardiac fibroblasts in response to pressure overload.

Actins↗
PubMed1999

[Pulmonary nocardiosis associated with Cushing's syndrome].

A 54-year-old man was admitted for further investigation of multiple nodules disclosed by a chest roentgenogram. Adrenocorticotropic hormone (ACTH)-dependent Cushing's syndrome was diagnosed because serum ACTH and serum cortisol levels were elevated with a loss of diurnal rhythm. Because several extensive examinations, including inferior petrosal sinus sampling, did not detest ACTH-producing tumors, the patient was also given a diagnosis of occult ectopic ACTH syndrome. The nodules disclosed on chest roentgenograms increased gradually in size and number, and some were cavitary. Bronchial secretion samples obtained by fiberoptic bronchoscopy contained numerous Nocardia asteroides bacteria. After treatment with sulfamethoxazole-trimethoprim, the nodules gradually disappeared, leaving only scars. Although mitotane had been continuously administered to inhibit the synthesis of intrinsic corticosteroids, pulmonary nocardiosis relapsed in the patient following the termination of sulfamethoxazole-trimethoprim therapy.

ACTH Syndrome, Ectopic↗
PubMed1999

Effect of oleanolic acid-cyclodextrin inclusion compounds on dental caries by in vitro experiment and rat-caries model.

Earlier work in vitro showed that oleanolic acid (OA) was a potential inhibitor of insoluble glucan (ISG) synthesis from mutans streptococci (MS). In this study, two oleanolic acid-cyclodextrin inclusion compounds (OA-CDs), oleanolic acid-G1-beta-cyclodextrin (OA-G1-beta CD) and oleanolic acid-beta-cyclodextrin (OA-beta CD), were assayed for their effects on ISG synthesis from Streptococcus mutans MT8148R, and on the growth of oral bacteria. OA-beta CD inhibited ISG synthesis by 55.3 and 37.4% at 62.5 and 15.6 micrograms/ml of OA, respectively. Both OA-CDs inhibited the growth of MS, S. sanguis, and S. salivarius at 4 to 8 micrograms/ml of OA. The anticariogenic effect of the OA-beta CD was examined in a rat-caries model. Rats in the infected control groups showed the highest caries score. The infected treatment group B (0.5% OA in diet) showed lower scores than the control group. These results suggest that OA-beta CD is a potential anti-caries agent.

Animals↗
PubMed1999

[A clinical study of cerebral palsy in Shiga; 1977-1986--I. Etiological analysis of various types of cerebral palsy].

Two hundred and two cases of CP in Shiga Prefecture, born between April 1977 and March 1987, were classified at 6 years of age into 5 groups: 69 with spastic diplegia (34%), 62 with tetraplegia (31%), 33 with hemiplegia (16%), 23 with the dyskinetic type (11%) and 15 with the ataxic type (7%). The rate of preterm birth was 32%, being highest in the spastic diplegia group. The etiological and risk factors were analysed in these cases. In term infants with spastic diplegia, the presumptive causes were unknown in 55%, prenatal in 28%, and perinatal in only 17%. In preterm infants with spastic diplegia, periventricular leukomalacia was the most important. In term infants with tetraplegia, brain anomalies and hypoxic-ischemic encephalopathy were the two main causes. In preterm infants with tetraplegia, the presumptive causes were perinatal in 67%. In most of the patients with hemiplegia, there were unilateral lesions such as middle cerebral artery infarction and cerebral hemiatrophy. Most of the dyskinetic cases had perinatal causes such as bilirubin encephalopathy in 9 patients. In 40% of the ataxic cases, there were brain anomalies.

Cerebral Palsy↗
PubMed1999

[A clinical study of cerebral palsy in Shiga; 1977-1986--II. Severity of the disability and complications in various types of cerebral palsy].

The severity of the disability and complications was evaluated at 6 years of age in 202 cases of cerebral palsy (CP) in Shiga Prefecture (69 with spastic diplegia, 62 with tetraplegia, 33 with hemiplegia, 23 with the dyskinetic type and 15 with the ataxic type) born between April 1977 and March 1987. The degree of gross motor disability differed among the clinical types, being mild in 45%, moderate in 17%, and severe in 39%. Gross motor disability was generally correlated with mental retardation, with some exceptions. Some non-ambulatory cases exhibited a normal or subnormal mentality, and most of such cases had been preterm infants with spastic diplegia. Most cases with mild gross motor disability and severe or moderate mental retardation had been term infants. Forty-eight percent suffered from epilepsy (25% in spastic diplegia, 86% in tetraplegia, 45% in hemiplegia, 39% in the dyskinetic type and 13% in the ataxic type). Microcephaly was noted in 35% (66% in tetraplegia and about 20% in other types).

Cerebral Palsy↗
PubMed1999

[A clinical study of cerebral palsy in Shiga; 1977-1986--III. Diagnosis and treatment of various types of cerebral palsy].

The age at the first clinical referral or diagnosis of cerebral palsy (CP), the age at the onset of treatment, the route of referral, and the kind of school entered were investigated in 202 cases of CP in Shiga Prefecture (69 with spastic diplegia, 62 with tetraplegia, 33 with hemiplegia, 23 with the dyskinetic type and 15 with the ataxic type) born between April 1977 and March 1987. In the hemiplegia, spastic diplegia and ataxic types, the age at the first clinical referral or diagnosis, was above 1 year in 42%, 39% and 33%, respectively. In the tetraplegia and the dyskinetic types, by contrast, such a delay occurred in only 9% and 4%, respectively. Cases of the former three types were referred from medical institutions less frequently (53% in the ataxic type, 52% in spastic diplegia and 40% in hemiplegia) than those of the latter two types (76% in tetraplegia and 61% in the dyskinetic type). About 30% of the cases were referred from health centers (38% in spastic diplegia, 33% in hemiplegia, 30% in the dyskinetic type, 20% in the ataxic type and 16% in tetraplegia). A considerable number of cases visited a clinic without reference (27% in hemiplegia, 27% in the ataxic type, 10% in spastic diplegia, 9% in the dyskinetic type, and 8% in tetraplegia). Fifty-three percent of the cases entered an elementary school (ordinary classes in 30% and special classes in 23%), 41% a special school, and 5% entered a protective institution. The early diagnosis of hemiplegia, spastic diplegia and the ataxic type of CP was difficult in some cases. Cases with suspected signs of CP should be referred to clinic early in the absence of definite diagnosis.

Cerebral Palsy↗
PubMed1999

Relationship between hydrophobicity and beta-blocking potencies, affinities or dissociation of beta-blockers from beta-adrenoceptors.

The present study was performed to assess the relationship between the hydrophobicity of drugs and (1) inhibitory strength (pA2) on chronotropic or inotropic actions, (2) displacemental potencies of 3H-CGP12177 or 125I-iodocyanopindolol binding to beta-adrenoceptors (beta-ARs) (pKi) or (3) dissociating potencies of these drugs from beta-ARs of atria strips pretreated with drugs. The beta-blockers used in the present study were bopindolol, active metabolite of bopindolol (18-502), atenolol, propranolol, pindolol, nadolol, alprenolol, oxprenolol, metoprolol, labetalol and acebutolol. The value of the partition coefficient of propranolol was the highest, and that of the beta1-selective blocker atenolol was the lowest. Although low correlation coefficients between hydrophobicity and inhibitory beta-blocking potencies determined by pharmacological experiments or displacemental potencies by the radioligand binding assay using 3H-CGP12177 and 125I-iodocyanopindolol were observed, significant relationships between hydrophobicities of these drugs and dissociating potencies from beta-ARs were observed. These results suggest that the hydrophobicity of drugs may be important for the slow dissociation from beta-ARs, but not for the beta-blocking action.

Adrenergic beta-Antagonists↗
PubMed1998

Synergistic action of R-Ras and IGF-1 on Bcl-xL expression and caspase-3 inhibition in BaF3 cells: R-Ras and IGF-1 control distinct anti-apoptotic kinase pathways.

R-Ras and insulin-like growth factor-1 (IGF-1) synergistically inhibit apoptosis of BaF3 cells upon interleukin-3 deprivation. To characterize the mechanism of this synergistic inhibition, we examined the effect of R-Ras and IGF-1 on several apoptosis-related proteins. Extracellular signal-regulated kinase (ERK) was activated by IGF-1, but not by R-Ras. In contrast, Akt was activated strongly by R-Ras, but weakly by IGF-1. It was also found that R-Ras and IGF-1 cooperatively induced Bcl-xL expression and inhibited caspase-3 activation.

Apoptosis↗
PubMed1998

Omega-3 polyunsaturated fatty acids--modulation of voltage-dependent L-type Ca2+ current in guinea-pig tracheal smooth muscle cells.

Omega-3 polyunsaturated fatty acids have been reported to be associated with favorable changes in the respiratory system. To determine one of the mechanisms for this effect, membrane currents were recorded in guinea-pig tracheal myocytes by using the whole-cell voltage clamp technique. Without EGTA in the patch pipette containing the Cs-internal solution, command voltage pulses positive to +0 mV from a holding potential of -60 mV elicited a voltage-dependent L-type Ca2+ current (I(Ca x L)) and a subsequent outward current. Upon repolarization, slowly decaying inward tail currents were recorded. The outward currents and the inward tail current were enhanced by methyl-1,4,-dihydro-2,6-dimethyl-3-nitro-4-(2-trigluromethylphenyl )-pyridine-5-carboxylate, and blocked by Cd2+ or nifedipine. Inclusion of EGTA (5 mM) in the patch pipette also abolished these currents, indicating that they were Ca2+-dependent. When [Cl-]o or [Cl-]i was changed, the reversal potential of these currents shifted, thus behaving like a Cl(-)-sensitive ion channel. 4,4'-Diisothiocyanatostilbene-2,2'-disulphonic acid. a Cl- channel blocker, inhibited the currents. The omega-3 polyunsaturated fatty acids eicosapentaenoic acid (3-30 microM) and docosahexaenoic acid (30 microM) suppressed I(Ca x L) and then inhibited I(Ca x Cl) in a reversible manner. Similar inhibitory effects of eicosapentaenoic acid on I(Ca x L) were observed with 5 mM EGTA in the patch pipette. Neurokinin A (1 microM) and caffeine (10 mM) also transiently activated I(Cl x Ca), probably due to Ca2+ release from Ca2+ storage sites. Pretreatment of the cells with eicosapentaenoic acid markedly suppressed the activation of I(Cl x Ca) by neurokinin A or caffeine. These results suggest that omega-3 polyunsaturated fatty acids inhibit voltage-dependent L-type Ca2+ currents and also Ca2+-activated Cl- currents in tracheal smooth muscle cells from the guinea-pig, which may play a role in modulation of tracheal smooth muscle tone.

Animals↗
PubMed1998

Heart rate variability during the first month of smoking cessation.

BACKGROUND: Heart rate variability (HRV) is known to increase after smoking cessation. However, no work has been performed concerning HRV immediately after smoking cessation. METHODS AND RESULTS: We studied HRV before and from 1 day to 1 month after smoking cessation and also determined whether there is a relation between HRV and the withdrawal syndrome immediately after smoking cessation. We determined HRV by using a two-channel 24-hour ambulatory ECG system before and 1, 2, 3, 7, 14, 21, and 28 days after smoking cessation in 20 healthy male volunteers who had smoked one or more packs per day for 2 or more years. One day after smoking cessation, heart rate decreased significantly, and all 24-hour time and frequency domain indices of HRV increased except the standard deviations of the normal R-R intervals and the 5-minute mean R-R. The magnitude of increase in these indices peaked 2 to 7 days after smoking cessation and gradually decreased thereafter. The increase in HRV persisted 1 month after smoking cessation. In the 16 subjects with signs of withdrawal syndrome and in the four subjects without evidence of withdrawal before and immediately and 1 month after smoking cessation, HRV increased immediately after smoking cessation and remained elevated after 1 month. CONCLUSIONS: HRV increases immediately after smoking cessation and gradually declines thereafter, which suggests that the effect of smoking on autonomic activity rapidly disappears immediately after smoking cessation. HRV remained unaffected by the presence or absence of the withdrawal syndrome.

Adult↗
PubMed1998

Sensitive diagnosis of cardiac allograft rejection by detection of cytokine transcription in situ.

OBJECTIVE: In situ transcription of cytokines which are important in the development of cardiac rejection has not been evaluated for diagnosing rejection. The objective was to evaluate the usefulness of in situ reverse transcriptase polymerase chain reaction (RT-PCR) for sensitive detection of acute cardiac rejection. METHODS: We studied interferon (IFN)-gamma and interleukin (IL)-2 expression using immunohistochemistry and in situ RT-PCR in murine cardiac transplant models. Hearts were heterotopically transplanted (BALB/c to C3H/He) and some mice were not treated (n = 23); others were treated with anti-intercellular adhesion molecule (ICAM)-1 and anti-lymphocyte function associated antigen (LFA)-1 monoclonal antibodies (mAbs) (n = 23). Allografts were removed at days 1 to 7. For control, isografts were harvested at day 7 (n = 2). RESULTS: Mice without treatment rejected allografts within 7 days, while all mAb-treated recipients accepted allografts for the same period. At day 1, allografts of both groups showed scattered myocardial cell infiltration which increased in non-treated allografts, but remained stable in mAb-treated grafts thereafter. In situ RT-PCR showed that IL-2 and IFN-gamma mRNA positive cells were present in non-treated allografts, while few mRNA positive cells were expressed in infiltrating cells in the mAb-treated allografts (IL-2, day 3: 88.8 +/- 28.3 vs. 7.2 +/- 6.4, p < 0.05, positive cells within 10 fields per section). However, immunohistochemistry could not reveal the difference at day 3. CONCLUSION: In situ RT-PCR is a sensitive method for diagnosing acute rejection, and it reveals the characteristics of myocardial infiltrate cells to determine their role in the process of rejection.

Animals↗