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Biomedical subjects

Y Imai

Publications and source records attributed to Y Imai.

At least 541 records · Page 30Linked to original sources
PubMed1995

Surgical management of tricuspid malinsertion in the Rastelli operation: conal flap method.

From June 1986 to May 1994, 25 patients underwent the Rastelli operation for complete transposition of the great arteries with ventricular septal defect and pulmonary stenosis or atresia. Fourteen patients whose tricuspid valve chordae were normal underwent the conventional Rastelli procedure (conventional group), whereas 11 patients who had tricuspid malinsertion into the infundibular septum underwent the Rastelli operation concomitant with mobilization of the infundibular septal flap, with the tricuspid valve chordae, to the right ventricular side of the intraventricular conduit (conal flap method) (conal flap group). In relation to the mobilization of the tricuspid valve chordae, right heart function and tricuspid regurgitation were compared between the two groups. There was one early death after the conventional Rastelli procedure and no early death after the Rastelli operation with a conal flap. There was one late death in the conventional group and two late deaths in the conal flap group. The mean follow-up was 50.8 +/- 5.1 months in the conventional group and 54.9 +/- 7.5 months in the conal flap group (p = 0.43). Reoperation was necessary for 1 patient in the conal flap group during follow-up. At the most recent follow-up, all patients in both groups were in New York Heart Association functional class I. Tricuspid regurgitation was estimated from the echocardiograms. Mild to moderate regurgitation was noted in 6 patients in the conventional group and 8 in the conal flap group. However, postoperative right heart catheterization data did not show any significant differences.(ABSTRACT TRUNCATED AT 250 WORDS)

Abnormalities, Multiple↗
PubMed1995

Altered lipid composition and differential changes in activities of membrane-bound enzymes of erythrocytes in hepatic cirrhosis.

Lipid composition, fluidity, and Na+,K(+)-adenosine triphosphatase (ATPase), Mg(2+)-ATPase, and acetylcholinesterase (AChE) activities of erythrocyte membranes were examined in comparison to plasma lipid composition and lecithin:cholesterol acyltransferase (LCAT) activities in 39 patients with hepatic cirrhosis due to viral hepatitis (Child-Pugh class A, n = 12; class B, n = 13; and class C, n = 14). Plasma LCAT activities decreased and the plasma free-cholesterol to phospholipid molar ratio (C/PL) increased with progressive severity of hepatic cirrhosis. C/PL and fluorescence polarization (inverse of fluidity) of erythrocyte membranes also increased with disease progression (C/PL: Child-Pugh A, 0.911 +/- 0.010; B, 0.941 +/- 0.011; C, 0.979 +/- 0.028; and normal, 0.798 +/- 0.010; fluorescence polarization: Child-Pugh A, 0.348 +/- 0.002; B, 0.351 +/- 0.002; C, 0.355 +/- 0.002; and normal, 0.340 +/- 0.002). There was a correlation between C/PL and fluorescence polarization of erythrocyte membranes (r = .629, P < .001). Na+,K(+)-ATPase activity of erythrocyte membranes did not differ between cirrhotic patients and normal subjects. On the other hand, Mg(2+)-ATPase activity decreased in Child-Pugh C cirrhosis. AChE activity was decreased in Child-Pugh A cirrhosis, and decreased further in Child-Pugh B and C cirrhosis. AChE and Mg(2+)-ATPase activities correlated inversely with fluorescence polarization (r = -.652, P < .001 and r = -.381, P < .01, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholinesterase↗
PubMed1995

Primer for bonding resin to metal.

OBJECTIVES: The purpose was to examine the effect on the bond strength and durability of a resin bond to metal of modification of a primer consisting of thiophosphoric methacrylate with phosphoric methacrylates and/or benzoyl peroxide. METHODS: Acrylic rods were bonded with a luting resin consisting of poly(methyl methacrylate) powder and a mixture of methyl methacrylate and tributylborane initiator to silver-palladium alloy (Ag-Pd), gold-silver alloy (Au-Ag), cobalt-chromium alloy (Co-Cr), and titanium (Ti) surfaces treated with various primers. The bonded samples were thermocycled for 2,000 cycles and the mean bond strengths were compared using one-way ANOVA and Duncan's new multiple range test at p < 0.05. RESULTS: Using primers of thiophosphoric methacrylate or phosphoric methacrylates alone, the bond strengths of Ag-Pd decreased significantly (p < 0.05) after thermocycling. The durability was significantly improved (p < 0.05) when thiophosphoric methocrylate was used in combination with the phosphate monomers. The additional use of benzoyl peroxide and heat treatment resulted in a significant increase (p < 0.05) in the durability of two groups; the mean bond strengths over 20 MPa and the lowest values remained unchanged even after 2,000 thermocycles. SIGNIFICANCE: The highest level of bond strength and durability to dental noble metals was achieved using a mixture of thiophosphoric and phosphoric methacrylates and benzoyl peroxide. These bond strength results are comparable to values obtained for base metals.

Acetone↗
PubMed1995

Potent vitamin D3 analogs: their abilities to enhance transactivation and to bind to the vitamin D3 response element.

1,25 dihydroxyvitamin D3 [1,25(OH)2D3] mediates its biological activities through specific binding to the vitamin D3 receptor (VDR) and subsequent association with vitamin D3 responsive elements (VDRE) in genes modulated by 1,25(OH)2D3. Several novel vitamin D3 compounds (Cmpds) have recently been identified which have 5- to 1000-fold greater abilities to induce differentiation and to inhibit proliferation of HL-60 leukemic blast cells as compared to the parental 1,25(OH)2D3 (code name, Cmpd C). To clarify the mechanism by which five of these vitamin D3 analogs [1,25(OH)2-16ene-D3, (Cmpd HM); 1,25(OH)2-16ene-23yne-D3, (Cmpd V); 1,25(OH)2-16ene-23yne-26,27 F6-D3; 22-Oxa-1,25(OH)2D3; 1,25(OH)2-23yne-D3] mediate their remarkably potent biological activities, we have investigated their abilities in HL-60 cells to transactivate a chloramphenicol acetyl transferase (CAT) reporter gene containing a VDRE from the human osteocalcin gene attached to a thymidine kinase minimal promoter. Also, the abilities of the analogs to enhance the binding of the human recombinant VDR/retinoic X receptor alpha (RXR alpha) heterodimer to the VDRE were examined in gel mobility shift assays. In serumless cultures, a series of potent vitamin D3 analogs had comparable abilities to transactivate the reporter gene as did the biologically less potent 1,25(OH)2D3 (approximately 15-20-fold stimulation in cultures containing 2 x 10(-8)M of vitamin D3 cmpds). Biologically very weak inducers of differentiation of HL-60 [24R,25(OH)2D3; 25(OH)-16ene-23yne-D3] had markedly diminished abilities to induce transactivation. Dose-response studies of Cmpds C, V, HM (10(-7)-10(-11)M) showed that in serumless culture conditions, transactivation of the VDRE-CAT was similar; however, in the presence of serum, Cmpd C at 10(-9)M had 20-fold less activity than analogs V and HM. These results may reflect increased binding of Cmpd C to the D binding protein (DBP) in serum as compared to the lower binding affinities for DBP by Cmpds HM and V. Affinities of the biologically potent analogs for VDR did not parallel their abilities either to transactivate VDRE-CAT or to mediate a biological affect on HL-60 cells. In further studies, gel mobility shift assays showed that VDR alone did not have detectable binding to VDRE; likewise, VDR plus RXR had little binding to VDRE in the absence of ligand. In contrast, biologically active vitamin D3 compounds (Cmpds HM, C, V) in a dose-dependent fashion enhanced the VDR/RXR (retinoid X receptor)-VDRE retarded band.(ABSTRACT TRUNCATED AT 400 WORDS)

Base Sequence↗
PubMed1995

Cloning of a retinoic acid-induced gene, GT1, in the embryonal carcinoma cell line P19: neuron-specific expression in the mouse brain.

Mouse P19 embryonal carcinoma cells can be reproducibly differentiated into neurons and glial cells upon treatment with high concentrations of retinoic acid (RA). To understand the molecular mechanisms that control early neural differentiation, we constructed P19 cell lines carrying an insertion of a gene-trap vector containing lacZ as the reporter gene and a G418 resistance gene. We tested expression of the lacZ gene during the RA-induced differentiation process of 300 clones selected with G418. Ten of these clones were stained with X-gal, and five of these ten clones showed up- or down-regulation of lacZ expression. We analyzed one clone, GT1, in which expression of the lacZ gene was markedly up-regulated. The 5'-flanking genomic DNA of the GT1 gene present at the site of integration was isolated by the plasmid rescue method, and we screened a cDNA library using this DNA gene as a probe. The GT1 cDNA is about 9000 bp long, with an open reading frame encoding 1840 amino acids. This amino acid sequence has a potential glycosaminoglycan attachment site (Ser-Gly-Gly-Gly) and three N-linked glycosylation sites, but no signal peptide. The sequence of GT1 does not show significant homology with any other known proteins, suggesting that GT1 may be a novel proteoglycan core protein. In situ hybridization revealed that GT1 mRNA was expressed ubiquitiously in the adult mouse brain. This expression was specifically localized in neurons but not in glial cells. Immunohistochemistry revealed that GT1 protein was also localized in neurons. These results suggest that this protein may play a fundamental role in neurons.

Amino Acid Sequence↗
PubMed1995

Expression and distribution of low density lipoprotein receptor-related protein mRNA in the rat central nervous system.

The low density lipoprotein receptor-related protein (LRP) is a multifunctional cell surface receptor that binds to the protease inhibitor alpha 2-macroglobulin (alpha 2 M). LRP has also been identified as the apolipoprotein E (apoE) receptor that mediates lipid metabolism. Recently it has been reported that apoE4, one of three common isoforms of apoE, is a main risk factor of Alzheimer's disease (AD). Moreover, all three of these proteins are reported to accumulate in the senile plaques in the brains of Alzheimer's patients. To understand the roles of LRP in the normal development of the central nervous system (CNS) and in the pathogenesis of AD, we studied the developmental expression and localization of LRP mRNA in the CNS. We used Northern blot analysis to investigate the developmental profile of LRP mRNA in the rat brain. LRP mRNA was first detected as early as in 18-day-old embryonic rat brain and was continuously expressed thereafter. A particularly high level of expression of the mRNA was observed in the perinatal stage. We also determined the cellular distribution of LRP mRNA in the CNS of 20-day-old embryonic and 6-week-old adult rat brains by in situ hybridization using a digoxigenin-labeled antisense riboprobe to LRP mRNA. In the embryonic rat brain, LRP mRNA was highly expressed in most of the cells, mainly neurons and glial cells. In the adult rat, LRP mRNA was expressed mostly in neurons in both the brain and the spinal cord. These results suggest that LRP plays crucial roles in development of the brain.

Alzheimer Disease↗
PubMed1995

Chronic opioid antagonist administration upregulates mu opioid receptor binding without altering mu opioid receptor mRNA levels.

Chronic administration of opioid antagonists has been shown to increase radioligand binding to brain opioid receptors. The present study was conducted to determine whether chronic exposure to the opioid antagonist naltrexone would similarly increase mu opioid receptor gene expression as measured by mRNA levels. Male Sprague-Dawley rats were administered naltrexone, 7-8 mg/kg/day, or saline by osmotic minipumps for 7 days. As expected, the density of mu opioid receptor binding sites was significantly higher in the brains of animals treated chronically with naltrexone as compared with saline-treated control animals. However, mu opioid receptor mRNA content determined by a solution hybridization RNase protection assay was not significantly altered in any brain region investigated. These results indicate that the upregulation of mu opioid receptors as measured by radioligand binding is not accompanied by increased levels of mu receptor mRNA.

Animals↗
PubMed1995

Successful treatment of hyperphosphatemic tumoral calcinosis with long-term acetazolamide.

We describe a patient with tumoral calcinosis, in which acetazolamide (ACZ) was, for the first time, tested for its therapeutic efficacy. The 19-year-old Japanese man had been suffering from multiple recurrent calcific masses with tenderness around the finger, knee, and toe joints since 10 months of age. Radiographs revealed several calcific subcutaneous masses around the finger joints, and calcific myelitis around the right knee joint and in the calvarium. The patient had hyperphosphatemia with elevated maximal threshold of renal phosphate excretion in the presence of normal kidney function and normocalcemia, suggesting a reduced ability to excrete phosphorus in the urine. A delay of disappearance of orally administered phosphate from the blood stream was found. A serum parathyroid hormone (PTH) level was normal, and responses to PTH and ACZ were also normal regarding the induction of phosphaturia. Since the masses tended to recur easily despite repeated surgical resections, we started medical treatment with phosphorus deprivation by oral aluminum hydroxide. However, the drug alone had no effect on hyperphosphatemia or calcific lesions, and ACZ was added in expectation of making the patient's phosphorus balance negative by its phosphaturic effect. Fourteen years of administration of the two drugs apparently improved the patient's symptoms, the biochemical findings, and the calcific lesions on radiographs. Thus, ACZ appeared to be useful for tumoral calcinosis resistant to phosphorus deprivation by aluminum hydroxide alone.

Acetazolamide↗
PubMed1995

Regulation of the aortic valve opening. In vivo dynamic measurement of aortic valve orifice area.

Aortic valve orifice area was dynamically measured in anesthetized dogs with a new measuring system involving electromagnetic induction. This system permits us real-time measurement of the valve orifice area in beating hearts in situ. The aortic valve was already open before aortic pressure started to increase without detectable antegrade aortic flow. Maximum opening area was achieved while flow was still accelerating at a mean of 20 to 35 msec before peak blood flow. Maximum opening area was affected by not only aortic blood flow but also aortic pressure, which produced aortic root expansion. The aortic valve orifice area's decreasing curve (corresponding to valve closure) was composed of two phases: the initial decrease and late decrease. The initial decrease in aortic valve orifice area was slower (4.1 cm2/sec) than the late decrease (28.5 cm2/sec). Aortic valve orifice area was reduced from maximum to 40% of maximum (in a triangular open position) during the initial slow closing. These measurements showed that (1) initial slow closure of the aortic valve is evoked by leaflet tension which is produced by the aortic root expansion (the leaflet tension tended to make the shape of the aortic orifice triangular) and (2) late rapid closure is induced by backflow of blood into the sinus of Valsalva. Thus, cusp expansion owing to intraaortic pressure plays an important role in the opening and closing of the aortic valve and aortic blood flow.

Animals↗
PubMed1995

A computerized control system for cardiopulmonary bypass.

A pump control system using a microcomputer for cardiopulmonary bypass has been developed. The parameters monitored by the computer are central venous pressure, aortic pressure, blood volume in a reservoir, and collapsing of a small vinyl bag in a venous withdrawal tube. Both pumps in the arterial infusion and the venous withdrawal lines are automatically controlled through an interface unit throughout cardiopulmonary bypass. The system regulates central venous pressure with a proportional-integral control algorithm to maintain intravascular volume constant. A screening algorithm is devised to remove artifacts introduced to the pressure measurement. During the weaning period, a perfusionist can select either the central venous pressure control or a reservoir blood volume control. Computerized pump perfusion was applied on 15 children during cardiac operations. Perfusion flow and central venous pressure were controlled satisfactorily with stable operation. Compared with conventional manually controlled pump perfusion, no significant difference was noted in mean aortic pressure, central venous pressure, net fluid balance, total urination, blood chemistry, and urinalysis. This system is useful and is expected to improve the safety of pump perfusion.

Algorithms↗
PubMed1995

Contribution of vascular nitric oxide to basal blood pressure in conscious spontaneously hypertensive rats and normotensive Wistar Kyoto rats.

1. The aim of this study was to clarify the extent to which vascular nitric oxide contributes to basal blood pressure in conscious spontaneously hypertensive rats and normotensive Wistar Kyoto rats. 2. The contribution of vascular nitric oxide to maintenance of blood pressure was estimated by measuring the pressor response to an intravenous injection of nitric oxide synthase inhibitor, N omega-L-arginine methyl ester, given after serial injections of captopril, vasopressin V1-receptor antagonist (V1-antagonist) and ganglion blocker (pentolinium) in conscious spontaneously hypertensive and Wistar Kyoto rats aged 20-28 weeks. To estimate the 'amplifier property' of hypertrophied vasculature in spontaneously hypertensive rats, which is known to modulate pressor responses, the lower blood pressure plateau after serial injections of captopril, V1-antagonist and pentolinium and the maximum blood pressure elicited by subsequent injection of increasing doses of phenylephrine were also measured. 3. The serial injections of captopril, V1-antagonist and pentolinium decreased mean arterial pressure from 164 +/- 9 mmHg to 67 +/- 2 mmHg and from 117 +/- 2 mmHg to 49 +/- 1 mmHg in spontaneously hypertensive and Wistar Kyoto rats respectively. The subsequent injection of N omega-L-arginine methyl ester restored mean arterial pressure almost to its control levels in both spontaneously hypertensive and Wistar Kyoto rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

A polymorphism at codon 160 of human O6-methylguanine-DNA methyltransferase gene in young patients with adult type cancers and functional assay.

O6-methylguanine-DNA methyltransferase (MGMT) plays an important role in repair of alkylating agent-induced DNA damage. Among the alkylation products of DNA, O6-methylguanine is one of the most critical lesions leading to the induction of mutations. The enzyme MGMT transfers the methyl group from O6-methylguanine of DNA to its own cysteine residue. Although mutations of other DNA repair genes involved in nucleotide excision repair and mismatch repair have been proven to be related to human tumorigenesis, the question of whether MGMT gene mutation might play a role in human carcinogenesis has hitherto not been elucidated. If there is a population with decreased enzyme activity due to defective MGMT gene, the affected individuals should be at risk of developing cancer early in life because of an increased susceptibility to alkylating agents. To test this hypothesis, germ line mutations of the MGMT gene were investigated in 12 young patients with adult type cancers (mean, 16.7 years old, 8 hepatocellular carcinomas, 3 gastric cancers, 1 cholangiocellular carcinoma) and 28 elderly patients who died of non-cancer diseases as controls (mean, 66 years old). A point mutation at codon 160 in exon 5, GGA to AGA, converting glycine to arginine was found in three of the young patients (25%), while the same mutation was found in three out of 28 (10.7%) in the control group. The mutated codon was located 15 codons from a functional cysteine residue toward the carboxyl terminal. Investigation of enzyme function, even in cases of bi-allelic mutation, revealed comparable activities for both mutated and wild type MGMT. Thus, we conclude the mutation is a normal polymorphism of the MGMT gene, present in approximately 15% of the population, although this does not rule out a possible influence in other tissues.

Adolescent↗
PubMed1995

Identification of virulence-associated antigens and plasmids in Rhodococcus equi from patients with AIDS.

Rhodococcus equi is an emerging opportunistic pathogen of human immunodeficiency virus-infected patients. However, little is known about the characteristics of R. equi isolates from humans. This study characterized the plasmid content, expression of a virulence-associated antigen, and mouse virulence of 19 R. equi isolates from patients with and without AIDS. EcoRI digestion patterns and Southern, Western, and virulence analyses of these isolates with cryptic plasmids allowed definition of a new category of R. equi. Isolates from patients with AIDS tended either to be virulent and have 15- to 17-kDa antigens and an 85-kb plasmid (10(6) bacteria needed for lethality) or have intermediate virulence (10(7) bacteria needed for lethality) and one of four distinct large plasmids that share DNA homology and express a 20-kDa antigen. Most of the non-AIDS isolates were avirulent (> 10(8) bacteria needed for lethality) and did not express any of these antigens.

AIDS-Related Opportunistic Infections↗
PubMed1995

Activation of phospholipase A2 and acylation of lysophospholipids: the major regulators for platelet activating factor production in rat neutrophils.

Rat inflammatory neutrophils induced arachidonic acid release and platelet-activating factor (PAF) production in response to opsonized zymosan (OPZ) dose-dependently. Phospholipase A2 activity also increased dose-dependently, paralleling the increases in arachidonic acid and PAF. The time courses of the activities of phospholipase A2 and acetyltransferase, and the amounts of free arachidonic acid, lyso-PAF, and PAF demonstrated that activation of the enzymes in the remodeling pathway could be required for PAF production in rat neutrophils, which agrees with the documented fact for macrophages. Phospholipase A2 could be a rate-limiting enzyme for PAF production, since an increased lyso-PAF amount or addition of exogenous lyso-PAF reflected the increase in PAF formation in the cells. This phospholipase A2 activity in rat neutrophils could be attributed to cytosolic type phospholipase A2, because the activity was mostly suppressed by a specific antibody to cytosolic phospholipase A2. As previously reported, pretreatment of neutrophils with the acyl-CoA synthetase inhibitor, triacsin C, or the acyltransferase inhibitor, merthiolate, enhanced PAF production as well as arachidonic acid release by the cells in response to OPZ. Triacsin C inhibited arachidonoyl-CoA production and merthiolate suppressed the transacylation of lyso-PAF to 1-alkyl-2-arachidonoyl-GPC. These results suggest that these inhibitors of acylation of lyso-PAF caused accumulation of lyso-PAF, which resulted in enhancement of PAF production when phospholipase A2 and acetyltransferase were activated by OPZ. Thus the activation of cytosolic phospholipase A2 and the acylation of lyso-PAF by such as arachidonic acid could be regulating factors for PAF production in stimulated rat neutrophils.

Acylation↗
PubMed1995

Effects of vasopressin V1 and V2 receptor antagonists on the development of salt-induced hypertension in Dahl rats.

To determine whether the vasopressor and antidiuretic actions of arginine vasopressin (AVP) may participate in the development of salt-induced hypertension, we examined the long-term effects of AVP V1 and V2 receptor antagonists on blood pressure (BP) in Dahl-Iwai salt-sensitive (DS) and salt-resistant (DR) rats. From age 7 weeks, DS and DR rats were fed a diet containing 8% NaCl, alone (control group); 8% NaCl and 1% OPC-21268 (V1 antagonist-treated group); or 8% NaCl and 0.05% OPC-31260 (V2 antagonist-treated group). The pressor response to AVP was significantly inhibited in DS rats treated with OPC-21268. Urinary volume and water intake were significantly increased by administration of OPC-31260; this increase was greater in DR rats than in DS rats. Indirect BP measurements obtained using tailcuff plethysmography showed that DS but not DR rats developed hypertension when fed high-salt diets. However, chronic treatment with either OPC-21268 or OPC-31260 did not alter the course of hypertension in DS rats, despite the effective blocking actions of these antagonists. This finding also was confirmed by direct BP measurements. Our results indicate that even if AVP plays a role in salt-induced hypertension peripheral blockade of either subtype of AVP receptors does not prevent the development of hypertension in DS rats.

Analysis of Variance↗