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Biomedical subjects

S Yagi

Publications and source records attributed to S Yagi.

At least 127 records · Page 7Linked to original sources
PubMed1995

Adenovirus mixture isolated from the brain of an AIDS patient with encephalitis.

A mixture of adenoviruses 31 and 49 was isolated from the brain of an AIDS patient with encephalitis. Adenovirus hexon protein was detected in neurons by indirect immunofluorescence. By restriction endonuclease analysis both adenovirus 31 and 49 were shown to be new genotypes. This is the first report of the isolation of a mixture of adenoviruses from adenovirus encephalitis and the first association of adenovirus 49, a new candidate serotype, with encephalitis.

AIDS-Related Opportunistic Infections↗
PubMed1995

Changes of P300 latency with age in childhood epilepsy.

Auditory event-related potentials (P300 latency; odd-ball paradigm) were examined in 129 patients with childhood epilepsies and 53 controls. The P300 latency in the patients with epilepsies (373 +/- 39.4 ms) was significantly longer than in controls (356 +/- 38.4), and the prolongation was greatest in the patients with symptomatic partial epilepsies (390 +/- 40.5), mild in those with idiopathic generalized epilepsies (370 +/- 24.3), and minimum in those with idiopathic partial epilepsies (363 +/- 28.9). Abnormal P300 latency occurred at all ages during childhood in patients with symptomatic partial epilepsies, and at older ages in patients with idiopathic generalized epilepsies. The shortening of latency with age was relatively small in patients with epilepsies compared with controls. These results suggest that the prolongation of P300 latency (i.e., existence of cognitive disturbance) displays characteristic changes with age in each epileptic syndrome.

Adolescent↗
PubMed1995

Ventricular gradient variability. New ECG method for detection of ischemic heart disease.

The usefulness of ventricular gradient variability for detecting the presence of ischemic heart disease was evaluated in 38 patients with coronary artery disease (group 1), 21 patients with chest pain and no coronary artery disease (group 2), and 33 healthy control subjects. The ventricular gradient of each consecutive heartbeat at rest over a 22-second interval was calculated using a microcomputer. The SD and coefficient of variation for azimuth, elevation, and magnitude were used as indices of ventricular gradient variability. The SD and coefficient of variation of both the magnitude and elevation of ventricular gradient in group 1 were significantly greater than those of the other two groups (P < .01, respectively). When the normal upper limit was defined as 2SD above the mean value in the control group, a comparison between the findings for group 1 and group 2 revealed that the coefficient of variation of magnitude of the ventricular gradient was the most sensitive (82%) and specific (91%) index for coronary artery disease (chi-square test, P < .001). This study suggests that the variability in the magnitude of the ventricular gradient is a reliable index of ischemic heart disease.

Electrocardiography↗
PubMed1995

Establishment of a cell line constitutively expressing E2 glycoprotein of hepatitis C virus and humoral response of hepatitis C patients to the expressed protein.

A Chinese hamster ovary cell line was established which abundantly expresses the second envelope protein (E2) of hepatitis C virus under the control of an exogenous promoter. The expressed E2 protein was found to be a glycoprotein of 58 kDa by immunoprecipitation with sera from patients that had chronic hepatitis C. Using this cell line as antigen in immunofluorescence tests, as high as 93% of patients with non-A non-B hepatitis had antibodies against E2 protein. In Western blots using SDS-denatured E2 protein, however, the detectability of the antibody was drastically reduced to 30%. Immunoprecipitation assays and ELISA, using both native and denatured E2 protein, revealed that antibodies to E2 protein were present in most of the chronic hepatitis C patients and that they reacted only to the native forms.

Animals↗
PubMed1995

Gene cloning, nucleotide sequence, and expression of a cephalosporin-C deacetylase from Bacillus subtilis.

The gene encoding a cephalosporin-C deacetylase (CAH) from Bacillus subtilis SHS 0133 was cloned and sequenced. The nucleotide sequence contained an open reading frame encoding a polypeptide consisting of 318 amino acids, the molecular weight of which was in good agreement with the value obtained by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The deduced amino acid sequence contained the common sequence Gly-X-Ser-X-Gly found in many esterases, lipases, and serine proteases. This indicates that CAH is a serine enzyme. A possible promoter sequence which is very similar to the consensus sequences of -35 and -10 regions recognized by B. subtilis RNA polymerase utilizing sigma factor H was found in the 5'-flanking region of the CAH structural gene. Two repeated A+T-rich blocks consisting of 24 bp were also found in the upstream region of the initiation codon. We constructed a series of expression plasmids by inserting the CAH gene into Escherichia coli ATG vectors. The degree of CAH gene expression depended on promoters and vector plasmids, which have different replication origins. The expressed CAH protein was an active form in the soluble fraction obtained after cell disruption. The highest expression level was accomplished with an expression plasmid, pCAH400, which has the trp promoter and the replication origin derived from pAT153. In the fermentation using a 30-liter jar fermentor, the transformant E. coli JM103(pCAH400) produced 440 U of CAH per ml of culture during a 24-h incubation. This value corresponded to 2.1 g of CAH protein in 1 liter of culture broth.

Amino Acid Sequence↗
PubMed1995

Observation of vasospasm after subarachnoid hemorrhage by magnetic resonance angiography--a preliminary study.

Serial evaluation of cerebral vasospasm following subarachnoid hemorrhage was attempted in 11 patients using magnetic resonance (MR) angiography. MR angiography demonstrated vasospasm with angiographic confirmation in three patients as a segmental narrowing or loss of flow signal, usually accompanied by decreased distal flow signal. MR angiography also showed decreased flow signal suggestive of vasospasm in another patient with clinical evidence of vasospasm but no angiographic confirmation was possible because of poor condition. MR angiography showed no vasospasm in five patients without clinical evidence of vasospasm, except in one patient with disappearance of the unilateral anterior cerebral artery signal, shown to be involvement of the clipped artery. MR angiography is a potential method for detection of vasospasm with further improvement of the technique.

Acute Disease↗
PubMed1995

Cross-bridge activation rate constant determined from systolic time intervals in patients with systemic lupus erythematosus.

Cardiac adrenergic activity was investigated in 38 patients with systemic lupus erythematosus (SLE) who were not receiving cardiovascular agents using a new index of the adrenergic tone of the working left ventricular (LV) myocardium and using the heart rate to represent sinus node adrenergic tone. According to the active cross-bridge model employed in this study, the cross-bridge activation rate constant (Ka) of the LV myocardium, corresponding to the rate constant for the binding of Ca2+ to troponin C, can be approximately expressed as Ka = 3/electromechanical systole (sec-1). The Ka value corrected for heart rate (Kac) remains nearly constant in normal individuals, but is increased without change of the heart rate by dobutamine infusion. Fifty patients who fulfilled the American Rheumatism Association criteria for SLE underwent echocardiography, as well as simultaneous recording of the electrocardiogram, phonocardiogram, and carotid pulse wave tracing. Kac was calculated from the interval between the onset of the QRS complex to the second heart sound (QS2 interval) and the heart rate (HR) as follows: Kac = 3/QS2 + 0.0249 (66-HR). The 38 SLE patients were divided into a normal Kac group (n = 26, 6.9 < Kac < 8.3 sec-1) and a high Kac group (n = 12, Kac > or = 8.3 sec-1).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

[Augmentation of clonidine on Bezold-Jarisch reflex control of renal sympathetic nerve activity in cats].

The present study was undertaken to examine the possible augmentation of clonidine on the control of renal sympathetic nerve activity by Bezold-Jarisch reflex in anesthetized cats. Veratrine (3-20 micrograms/kg) produced dose-dependent decreases in arterial blood pressure (BP), heart rate (HR) and renal sympathetic nerve activity (RNA). Clonidine (3 micrograms/kg) resulted in decreases in BP, HR and RNA. Clonidine significantly potentiated the influence of Bezold-Jarisch reflex on RNA, but did not potentiate the influence of Bezold-Jarisch reflex on BP and HR. Bezold-Jarisch reflex gain calculated as percent inhibition of renal sympathetic nerve activity divided by decreases in mean blood pressure was significantly higher after the administration of clonidine.

Animals↗
PubMed1995

Subpressor dose of angiotensin II increases susceptibility to the haemodynamic injury of blood pressure in Dahl salt-sensitive rats.

OBJECTIVE: To investigate the effects of subpressor doses of angiotensin II (Ang II) on the progression of renal injuries in Dahl salt-sensitive (Dahl-S) rats with hypertension. METHODS: Rats were fed a high-salt (4% NaCl) diet and given an Ang II infusion (10 or 50 ng/kg per min, subcutaneously) for 4 weeks. RESULTS: The plasma Ang II concentration achieved in the high-dose Ang II infusion was lower than that in low-salt (0.3% NaCl) normotensive rats. The Ang II infusion did not affect systolic blood pressure, cardiac hypertrophy or weight of thoracic aorta. However, the high-dose Ang II infusion increased proteinuria by 58%, enhanced the urinary N-acetyl-beta-D-glucosaminase index by 77% and reduced the glomerular filtration rate by 37%. The impaired renal function was associated with a progression of glomerulosclerotic lesions. Neither tubular nor arterial lesions were exacerbated. The infusion did not influence prostacyclin production or urinary cyclic GMP excretion. CONCLUSION: A subpressor dose of Ang II infusion impairs renal function with progression of glomerulosclerosis, and these alterations may be due to increased susceptibility of the glomerulus in Dahl-S rats to Ang II-induced injuries. Such a mechanism might underlie a predisposition to hypertension-induced organ damage seen in Dahl-S rats with salt-induced hypertension.

Angiotensin II↗
PubMed1994

Cloning of the cDNA for the deleted syk kinase homologous to ZAP-70 from human basophilic leukemia cell line (KU812).

Syk kinase is one of the protein tyrosine kinases and forms a family with ZAP-70. We isolated two different sized cDNA clones of syk (Syk11 and Syk41) from a cDNA library of human KU812 (human basophilic leukemia cell line). The obtained two clones carried different messages, that Syk41 had a 69 bp-long insertion between the SH2 domain and the kinase domain compared with Syk11. Alignment of the two human syk predicted polypeptides with those of the porcine syk and ZAP-70 revealed that human syk was 5 amino acid longer than the porcine syk at the N-termini and that the insertion of the 23 amino acid found in Syk41 was present in the porcine syk and absent in ZAP-70. Reverse transcribed polymerase chain reaction targeting this region showed that both forms of the polyA RNA were expressed in Jurkat cells, human peripheral leukocytes and also KU812 cells and that the inserted form was dominant.

Amino Acid Sequence↗
PubMed1994

Molecular cloning of cDNA for rat ovarian 20 alpha-hydroxysteroid dehydrogenase (HSD1).

20 alpha-Hydroxysteroid dehydrogenase (20 alpha-HSD, EC 1.1.1.149) catalyses the conversion of progesterone into 20 alpha-dihydroprogesterone (20 alpha-OHP). Previously, we purified the enzyme (37 kDa) from rat ovary and determined its N-terminal amino acid sequence. In the present study we succeeded in cloning a full-length 20 alpha-HSD cDNA. mRNA was extracted from immature rat ovaries after successive treatment with equine chorionic gonadotropin (eCG) and human chorionic gonadotropin (hCG). A cDNA library was constructed in lambda ZAP. For screening, a 576 bp probe was amplified by the PCR using mixed primers based on the N-terminal sequence of 20 alpha-HSD, and labelled with [32P]dCTP. Eight positive clones were isolated from 1.2 x 10(4) recombinants. Analysis of the nucleotide sequence revealed that one clone of 1.2 kbp cDNA (pHSD12-07) contained a polyadenylation site and an open reading frame encoding 323 amino acids with the N-terminal sequence of 20 alpha-HSD. The fusion protein of pHSD12-07 produced by Escherichia coli reacted with a specific polyclonal antibody generated against rat ovarian 20 alpha-HSD. In addition, the in vitro transcription-translation product produced by Xenopus oocytes showed 20 alpha-HSD activity and Northern-blotting analysis revealed that the ovaries from normal adult rats contained a 1.2 kb mRNA. Thus we succeeded in isolating a clone encoding the full length of rat ovarian 20 alpha-HSD. The sequence showed high similarity with those of rat liver 3 alpha-hydroxysteroid dehydrogenase (3 alpha-HSD), bovine lung prostaglandin F synthase (PGFS), human liver chlordecone reductase (CDR), frog lens rho-crystallin and aldose reductases, indicating that 20 alpha-HSD belongs to the aldo-keto reductase family.

20-Hydroxysteroid Dehydrogenases↗
PubMed1994

High-level expression of the truncated alpha chain of human high-affinity receptor for IgE as a soluble form by baculovirus-infected insect cells. Biochemical characterization of the recombinant product.

The binding subunit of human high-affinity receptor for IgE (Fc epsilon RI alpha) was efficiently expressed as a truncated form in insect cells. The soluble (s)Fc epsilon RI alpha purified from culture medium by affinity chromatography with an anti-(alpha chain) mAb was nearly homogeneous and had an IgE-binding activity. The amino acid composition and the revealed N-terminal amino acid sequence of sFc epsilon RI alpha suggested that it was properly processed in insect cells. The apparent molecular mass (35 kDa) of purified sFc epsilon RI alpha was smaller than that of sFc epsilon RI alpha produced by CHO transfectants. The reduction of the apparent molecular mass after N-glycanase treatment showed the recombinant product was N-glycosylated. Peptide mapping of native and deglycosylated sFc epsilon RI alpha indicated that three Asn residues (Asn21, Asn42 and Asn166) should be almost fully glycosylated, and that two Asn residues (Asn74 and Asn135) were partially glycosylated.

Amino Acid Sequence↗
PubMed1994

The efficacy of monatepil, a new calcium antagonist, in the treatment of essential hypertension.

A multicenter, open-label trial in Japan examined the efficacy, safety, and optimal dose of monatepil (AJ-2615) as monotherapy and in combination therapy with angiotensin-converting enzyme (ACE) inhibitors or beta-blockers. Patients with essential hypertension who had never been treated or had been refractory to conventional antihypertensive agents were enrolled in the trial. During a 4-week control period patients assigned to monotherapy received placebo and those assigned to combination therapy received an ACE inhibitor or beta-blocker and placebo. Patients with systolic blood pressure (BP) > or = 160 mm Hg and diastolic BP > or = 95 mm Hg at the end of the control period were enrolled in the study. The initial dose of monatepil was 30 mg/day in monotherapy and 15 mg/day in combination therapy; the daily dose was titrated to 60 mg/day according to the antihypertensive response. The treatment period was 8 to 12 weeks. Blood pressure decreased from 168 +/- 8/100 +/- 6 to 142 +/- 9/85 +/- 7 mm Hg (SD) with monatepil monotherapy, from 171 +/- 11/102 +/- 6 to 141 +/- 9/84 +/- 6 mm Hg in combination with ACE inhibitors, and from 175 +/- 13/102 +/- 7 to 153 +/- 21/91 +/- 9 mm Hg in combination with beta-blockers (P < .001). When patients in whom mean BP decreased by > or = 13 mm Hg were defined as responders, the response rate was 80.4%, 78.1%, and 51.6% in the respective groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1994

Vasoconstrictors and renal protection induced by beta 1-selective adrenoceptor antagonist bisoprolol.

We investigated the role of the vasoconstrictors endothelin-1 (ET-1) and thromboxane in renal protection by the beta 1-selective adrenoceptor antagonist, bisoprolol, in Dahl salt-sensitive rats (Dahl S) and salt-resistant rats (Dahl R). Six-week bisoprolol treatment (20 mg/kg chow) reduced systolic blood pressure (SBP) by 14% in Dahl S rats fed a high-salt (4% NaCl) diet. This BP reduction was accompanied by a decrease in aortic wall thickness. ET-1 and thromboxane released from renal cortex was significantly decreased by 17 and 30% with bisoprolol, respectively. Other prostaglandin synthesis was unaffected. Renal function such as proteinuria, N-acetyl-beta-D-glucosaminidase (NAG) excretion, and glomerular filtration rate (GFR) was not influenced by bisoprolol. Morphologic investigation showed that bisoprolol significantly improved glomerular sclerosis by 29% and attenuated arterial damage by 71%, although tubular injury was not affected. The more severe the glomerulosclerotic lesions, the greater the generation of thromboxane and ET. The arterial lesions were positively correlated to thromboxane generation. These data indicate that long-term bisoprolol treatment reduces vasoconstrictive ET-1 and thromboxane generation and that these alterations may be partly responsible for the amelioration of glomerular and arterial injury in Dahl S rats.

Adrenergic beta-1 Receptor Antagonists↗
PubMed1994

New dihydropyridine calcium channel antagonist, pranidipine, attenuates hypertensive renal injury in Dahl salt-sensitive rats.

Interest in the cardiovascular protective effects of calcium channel antagonists has increased in the past decade. We investigated prevention of vascular wall remodeling by the long-acting calcium channel antagonist pranidipine in 12-week-old Dahl salt-sensitive (SS) rats with high-salt-induced (4% NaCl) hypertension. Six-week pranidipine treatment (60 mg/kg chow) decreased systolic blood pressure (SBP) by 22% in SS rats. This BP reduction was associated with decreases in cardiac mass and weight of the aortic wall. Glomerular filtration rate (GFR) was increased by 33%, but this did not lead to a decrease in urinary protein or NAG excretion. Morphologic investigation demonstrated striking resolution of arterial injury (medial necrosis and/or hyperplasia, inflammatory cell infiltration, and thrombus formation) by 87% after pranidipine treatment. Glomerular sclerosis was also attenuated by 61%, whereas tubular injury was improved by only 28%. These morphologic changes were reflected in the findings that the capacity of kidney homogenate for generating lipid peroxides was significantly decreased and that collagen levels and pattern type became similar to those of normotensive salt-resistant (SR) rats. Pranidipine also attenuated hypertensive vasculopathy in small arteries of the middle cerebral arteries. Thus, the calcium channel antagonist pranidipine can attenuate the vascular injury that occurs in salt-induced hypertension, a promising property that implicates its clinical usage, particularly in essential hypertension with cardiovascular complications.

Animals↗