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H Morii

Publications and source records attributed to H Morii.

At least 37 records · Page 2Linked to original sources

tPA via infusion catheters followed by continuous IV infusion for 3 days prevents intimal hyperplasia after balloon injury.

A rabbit model was used to examine the effects of tissue plasminogen activator (tPA) on development of intimal hyperplasia following balloon injury. Thirty-two hereditary hypercholesterolemic (KHC) rabbits underwent percutaneous transluminal coronary artery balloon catheterization and injury to the common iliac artery, after which they were divided into four groups: untreated (control); Dispatch catheterized-30 minutes local saline delivery [D(+)-tPA(-)]; D(+)-30 minutes local tPA delivery (0.6 mg/kg) [D(+)-tPA(30 min)]; and D(+)-30 minutes local tPA + 3 days intravenous infusion (0.6 mg/kg/24 h) [(D(+)-tPA(30 min + 3 d)]. Twenty-eight days later, the intimal cross-sectional areas of all three Dispatch catheterized groups were significantly smaller than those of control groups, as were the intimal/medial area ratios. Moreover, the intima/media ratios of the D(+)-tPA(30 min + 3 d) group were significantly smaller than those of the D(+)-tPA(-) group. Thus, local delivery of tPA via Dispatch catheters followed by continuous intravenous infusion of tPA for 3 days prevented intimal hyperplasia after angioplasty.

Angioplasty, Balloon, Coronary↗

Increased retinal blood flow in patients with Graves' disease: influence of thyroid function and ophthalmopathy.

OBJECTIVE: Graves' ophthalmopathy (GO), resulting from the inflammation of retro-orbital tissue, is one of the major complications of Graves' disease (GD). We investigated the clinical usefulness of the measurement of retinal blood flow (RBF) in the evaluation of GO and its activity. MEASUREMENT: RBF was quantitated by pulsed Doppler mode at just below the branch of central retinal artery, from which the resistance index (RI) was calculated. PATIENTS: Forty-seven euthyroid GD patients and 70 gender- and age-matched normal controls were measured for RI to investigate the effect of GO on RBF. To investigate the effect of hyperthyroidism, 20 GD patients were measured for RI changes during antithyroid drug (ATD) therapy. Furthermore, 17 GD patients with clinically overt GO were measured for RI changes during treatment with glucocorticoid plus retro-orbital radiation. RESULTS: RI and exophthalmos showed a significant positive correlation in 47 treated euthyroid GD patients without clinically overt GO (r=0.307, P<0.05), but not in 70 age- and sex-matched normal subjects (r=0.185, P=0.161). Furthermore, RI, but not exophthalmos, significantly correlated with serum TSH receptor antibodies, an indicator for the disease activity of GO. ATD therapy significantly reduced RI in GD patients from 0.719+/-0.041 in the hyperthyroid state to 0.661+/-0.051 in the euthyroid state, but not to the levels observed in normal subjects having the similar exophthalmos (0.640+/-0.049). The fractional reduction of RI during ATD therapy significantly correlated with those of pulse pressure and ultrasonographic distensibility in carotid artery, but not with those of serum vascular injury markers. In 17 GD patients with clinically overt GO, all four patients having adipose tissue enlargement but not extraocular muscle hypertrophy (inactive GO) showed RI within the mean +/- 1 s.d. for treated GD patients without GO. In the other 13 GD patients having extraocular muscle hypertrophy (active GO), four and eight patients showed RI outside mean +/- 2 s.d. and mean +/- 1 s.d. respectively. Treatment with glucocorticoid plus radiation moved RI in 8 out of 10 patients toward the mean values of GD patients without GO, in spite of little improvement of exophthalmos. CONCLUSIONS: It was suggested that GD patients showed altered retinal hemodynamics, possibly resulting either from the cardiovascular effect of hyperthyroidism or from retro-orbital inflammation, particularly in extraocular muscle.

Adult↗

[A system of health education using dietary assessment].

We decided to focus attention on healthy young people, and to conduct a survey of their diet, as well as their physical activity and health condition, so that we made diagnoses and also give instructions on each subject using a computer program to promote their health. We carried out this experiment using this method with 836 young female subjects in order to find out whether it can be applied as a useful health education approach. 1. According to the survey, when the subjects made efforts in making the instructions as convenient as possible, the percentage of subjects who could carry out advice even 4 months later was seen to be higher. 2. The advice for which a significantly high percentage of subjects said "want to improve their daily action" and could actually carry out and improve them, was as follows: they should eat vegetables, have a substantial breakfast, drink milk every day, refrain from too much salt, not go without meals, increase the frequency of eating seaweed, and refrain from snacks. 3. The two kinds of scores used to evaluate diets showed that assessment after nine months gave lower values than those obtained when this survey started. Using these two evaluating scores, changes in diets were divided into five patterns, and their relation to the question "whether they used the advice or not" was examined. As a result, the percentage showing favorable diet changes in subjects who "took advice" was showed to be significantly high. 4. Subjects who received advice on physical activity exhibited improvement in carrying out routine exercises as well as making their daily life more active. 5. With subjects who took advice on both diet and physical activity, the number who complained about fatigue was significantly reduced. Although it is difficult to improve diet and exercise habits, the results of the survey suggest that our approach should be useful for improving health.

Adult↗

Activation of prostacyclin synthesis by mechanical stimulation in the ciliated protozoan Tetrahymena thermophila.

We detected a HPLC peak corresponding to 6-keto-PGF(1alpha), a stable metabolite of prostacyclin (PGI(2)), in [1-(14)C]arachidonate metabolites from the ciliated protozoan Tetrahymena thermophila. Quantitative analysis of 6-keto-PGF(1alpha) by enzyme immunoassay revealed that the synthesis and release were rapidly activated by the mechanical stimulation of a short centrifugation. The activation was suppressed significantly by a cyclooxygenase inhibitor, ibuprofen, and was independent of the extracellular Ca(2+). External addition of PGI(2) and its stable analogue, beraprost, caused a transient increase in the tumbling frequency of swimming. Other prostanoids, PGE(2) and PGF(2alpha), have no effect on the swimming. These results indicate that a free-living ciliate, T. thermophila, synthesizes and has a specific sensitivity to PGI(2).

6-Ketoprostaglandin F1 alpha↗

CTP:2,3-di-O-geranylgeranyl-sn-glycero-1-phosphate cytidyltransferase in the methanogenic archaeon Methanothermobacter thermoautotrophicus.

CDP-2,3-di-O-geranylgeranyl-sn-glycerol synthase (CDP-archaeol synthase) activity was discovered in the membrane fraction of the methanoarchaeon Methanothermobacter thermoautotrophicus cells. It catalyzed the formation of CDP-2,3-di-O-geranylgeranyl-sn-glycerol from CTP and 2,3-di-O-geranylgeranyl-sn-glycero-1-phosphate (unsaturated archaetidic acid). The identity of the reaction product was confirmed by thin layer chromatography, fast atom bombardment-mass spectroscopy, chemical analysis, and by UV spectroscopy. One mole of the product was formed from approximately 1 mol of each of the reactants. The enzyme showed maximal activity at pH 8.5 and 55 degrees C in the presence of Mg(2+) and K(+) ions. By in vivo pulse labeling of phospholipids with (32)P(i), CDP-archaeol was found to be an intracellular intermediate. A cell-free homogenate of M. thermoautotrophicus, when incubated with l-serine, converted the product of CDP-archaeol synthase reaction to a product with the same chromatographic mobility as archaetidylserine. It was concluded from these results that both CDP-archaeol and CDP-archaeol synthase were involved in cellular phospholipid biosynthesis. Among various synthetic substrate analogs, both enantiomers of unsaturated archaetidic acid possessing geranylgeranyl chains showed similar levels of activity, while archaetidic acid with saturated or monounsaturated isoprenoid or straight chains was a poor substrate, despite having the same stereostructure as the fully active substrate. The ester analogs with geranylgeranioyl chains showed significant activities. These results suggest that the enzyme dose not recognize ether or ester bonds between glycerophosphate and hydrocarbon chains nor the stereostructure of the glycerophosphate backbone but mainly targets substrates with geranylgeranyl chains.

Catalysis↗

Phosphate regulation of vascular smooth muscle cell calcification.

Vascular calcification is a common finding in atherosclerosis and a serious problem in diabetic and uremic patients. Because of the correlation of hyperphosphatemia and vascular calcification, the ability of extracellular inorganic phosphate levels to regulate human aortic smooth muscle cell (HSMC) culture mineralization in vitro was examined. HSMCs cultured in media containing normal physiological levels of inorganic phosphate (1.4 mmol/L) did not mineralize. In contrast, HSMCs cultured in media containing phosphate levels comparable to those seen in hyperphosphatemic individuals (>1.4 mmol/L) showed dose-dependent increases in mineral deposition. Mechanistic studies revealed that elevated phosphate treatment of HSMCs also enhanced the expression of the osteoblastic differentiation markers osteocalcin and Cbfa-1. The effects of elevated phosphate on HSMCs were mediated by a sodium-dependent phosphate cotransporter (NPC), as indicated by the ability of the specific NPC inhibitor phosphonoformic acid, to dose dependently inhibit phosphate-induced calcium deposition as well as osteocalcin and Cbfa-1 gene expression. With the use of polymerase chain reaction and Northern blot analyses, the NPC in HSMCs was identified as Pit-1 (Glvr-1), a member of the novel type III NPCs. These data suggest that elevated phosphate may directly stimulate HSMCs to undergo phenotypic changes that predispose to calcification and offer a novel explanation of the phenomenon of vascular calcification under hyperphosphatemic conditions. The full text of this article is available at http://www.circresaha.org.

Arteries↗

Prostaglandin I(2), a possible thermo-sensory mediator in Paramecium.

Thermo-sensory mechanisms are little understood. The protozoan, Paramecium multimicronucleatum, is sensitive and responsive to a cooling stimulus. We found that inhibitors of prostaglandin (PG) biosynthesis reduced the response to the cooling stimulus. Inversely, the response suppressed by the inhibitors was recovered by application of stable PGI(2) analogs, including iloprost. Paramecium cells showed binding activity specific for [(3)H]iloprost. Moreover, an arachidonic acid metabolite, possibly PGI(2), was rapidly increased in response to the cooling stimulus, suggesting that prostaglandin biosynthesis plays a crucial role in the cooling-sensory transduction. Paramecium may be a useful model for the investigation of the molecular basis of thermo-sensory mechanisms.

Animals↗

Peroxisome proliferator-activated receptor-gamma agonists increase vascular endothelial growth factor expression in human vascular smooth muscle cells.

Vascular endothelial growth factor (VEGF), expressed in a variety of mesenchymal cells including vascular smooth muscle cells (VSMC), is a potent mitogen for endothelial cells, and is used clinically applied for ischemic disease of peripheral vessels. To determine whether peroxisome proliferator-activated receptor gamma (PPARgamma) regulates VEGF production in VSMC, we examined VEGF secretion from VSMC treated with PPAR agonists. Troglitazone increased VEGF secretion in a time- and dose-dependent manner (261 +/- 35% with 25 mM of troglitazone for 24 h), and also increased levels of VEGF mRNA. VEGF secretion was also increased by other PPARgamma agonists, pioglitazone, LY171883, and 15d-PGJ2 (224 +/- 17.1%, 247 +/- 36.8% and 171 +/- 7.8%, respectively), but not the PPARgamma agonists bezafibrate and Wy14643 (85.2 +/- 1.5%, 94.6 +/- 3.2, respectively). Our findings suggest that thiazolidinediones might be useful for the therapeutic angiogenesis for ischemic artery disease.

Acetophenones↗

The SCG10-related gene family in the developing rat retina: persistent expression of SCLIP and stathmin in mature ganglion cell layer.

Neuronal growth-associated proteins (GAPs), such as GAP-43 and SCG10, are thought to play crucial roles in both axonal and dendritic outgrowth during neural development and regeneration, although the underlying mechanisms remain largely unknown. The recent finding that SCG10 is a microtubule regulator and also the identification of RB3 and SCLIP as two new SCG10-related members prompted us to investigate the roles of SCG10-related family in neural development, using the retina as a model system. We determined the temporal expression and the spatial distribution of SCG10-related mRNAs in the developing rat retina. Semiquantitative analysis by RT-PCR revealed that in prenatal retina, levels of SCG10 and stathmin mRNAs were higher than those of RB3 and SCLIP. In the postnatal retina, the level of SCLIP increased, whereas the level of RB3 remained low. In situ hybridization revealed that GAP-43 and all of the SCG10-related family mRNAs were present in the retinal ganglion cells (RGCs) at all stages of retinal development, and that stathmin mRNA was present in mitotic neuroblastic cells. Differential expression of SCG10 and other members of the family became more evident as retinal development proceeded; SCG10 and RB3 expression were relatively specific in the RGCs and amacrine cells, whereas SCLIP was also evident in bipolar and horizontal cells. Stathmin mRNA was highly expressed both in the RGCs and other interneurons. These results indicate that multiple SCG10-related proteins are expressed in single neurons including RGCs, and suggest that these nGAPs play similar but distinct roles in differentiation and functional maintenance of retinal neurons.

Animals↗

Generation, Microwave Spectrum, Barrier to Internal Rotation of Methyl Group, and ab Initio MO Calculation of syn-2-Nitrosopropene, syn-CH(2)&dbond;C(CH(3))&bond;N&dbond;O.

syn-2-Nitrosopropene was generated, in the gas phase, by chemical reaction of 1-chloro-2-(hydroxyimino)propane with K(2)CO(3) and identified by microwave spectroscopy. The microwave spectrum of the reaction product was observed in the frequency range from 8.0 to 40.0 GHz. The rotational constants (MHz) were determined as A = 8744.09(6), B = 4846.07(2), and C = 3177.84(3) for CH(2)&dbond;C(CH(3))&bond;(14)NO (normal species) and A = 8664.36(5), B = 4822.15(3), and C = 3157.04(3) for CH(2)&dbond;C(CH(3))&bond;(15)NO ((15)N species) in the ground vibrational state. The values of the planar moment (P(cc) = (I(a) + I(b) - I(c))/2) obtained for the normal and (15)N species were 1.525(1) and 1.526(1) u Å(2), respectively. This suggests that the nitrogen atom lies in or is close to the ab inertial plane of the molecule and shows also that only two hydrogen atoms are located symmetrically out of the symmetry plane. The reaction product was determined to be syn-2-nitrosopropene by comparing the observed and calculated rotational constants, kappa (Ray's asymmetry parameter) and r(s) coordinates of the nitrogen atom. The dipole moments (D) were determined to be µ(a) = 2.43(5), µ(b) = 1.12(7), and µ(total) = 2.67(7). The barrier heights of the internal rotation owing to the methyl group of the normal species in the ground and first excited torsional states were determined to be 1750(50) and 1740(50) cal/mol (1 cal/mol = 4.184 J/mol), respectively. The (14)N nuclear quadrupole coupling constants (MHz) were determined to be chi(aa) = 0.25(21), chi(bb) = -7.11(40), and chi(cc) = 6.85(61). Two vibrational excited states were observed and the vibrational frequencies (cm(-1)) of the C-N and C-C torsional modes were determined to be 160(40) and 175(40), respectively. The lifetime of syn-2-nitrosopropene was found to be ca. 2 min in the waveguide cell. Copyright 2000 Academic Press.

Journal Article↗

Mechanism of atherosclerotic calcification.

Calcification is almost invariably associated with atherosclerotic plaque lesions. Recent data suggest that plaque calcification is an active, regulated process similar to osteogenesis. In order to clarify the mechanism of plaque calcification, we developed an in vitro model of vascular calcification by utilizing bovine vascular smooth muscle cells (BVSMCs). This model is useful in that diffuse and massive calcification can be induced within 2 weeks and thereby biochemical analyses of vascular calcification can be performed. We have analyzed several aspects of vascular calcification by using this model and demonstrated as follows: 1) in vitro calcification of BVSMCs is regulated by calciotropic hormones and BVSMCs are equipped with a unique autocrine and/or paracrine system regulating calcium metabolism. 2) Sodium-dependent phosphate cotransport plays a crucial role in BVSMC calcification as well as in mineralization of skeletal tissues. 3) BVSMCs acquire osteoblastic phenotype under certain conditions. Finally, we discuss the roles of macrophages in the development of atherosclerotic calcification. Interferon-gamma (IFN-gamma) induces gene expression of 25-hydrovitamin D-1 alpha-hydroxylase (1 alpha OHase) and its activity in macrophages. Since 1 alpha OHase can locally convert 25-hydroxyvitamin D into 1 alpha, 25-dihydroxyvitamin D (1,25(OH)2D), an active metabolite of vitamin D, it is suggested that local production of 1,25(OH)2D by macrophages may promote atherosclerotic calcification. Moreover, macrophages may be involved in the phenotypic changes of vascular smooth muscle cells (VSMCs) to acquire calcifying capacity. Therefore, the phenotypic changes of VSMCs in atherosclerotic plaque may contribute to the development of atherosclerotic calcification.

Animals↗

Inverse relationship between circulating oxidized low density lipoprotein (oxLDL) and anti-oxLDL antibody levels in healthy subjects.

Oxidized low density lipoprotein (oxLDL) has been implicated in the pathogenesis of atherosclerosis. Recent studies have shown that immunization of animals with oxLDL results in suppression of atherogenesis. Antibody against oxLDL (oxLDL Ab) is detectable in human sera, although its biological significance is not well established. We examined the relationship between oxLDL Ab titer and circulating oxLDL level in 130 healthy Japanese subjects. OxLDL was measured as apolipoprotein (apo) B-containing lipoproteins carrying oxidized phosphatidylcholines by a sensitive ELISA. IgG class oxLDL Ab titer was measured by ELISA. Plasma oxLDL concentration was very low and it corresponded on average to one to two out of 1000 apoB-containing lipoproteins in plasma. Plasma oxLDL correlated positively with LDL cholesterol and inversely with oxLDL Ab titer. These associations remained significant and independent in multiple regression analysis including age, gender, smoking, and high-density lipoprotein cholesterol. These data indicate that healthy subjects have a very low concentration of oxLDL in the circulation, and that oxLDL Ab titer is in an inverse relationship with plasma oxLDL concentration in this population. Although these results suggest that oxLDL Ab may play a role in maintaining the low level of plasma oxLDL, its role in atherogenesis awaits further studies.

Adult↗

Pathophysiology and diagnosis of primary hyperparathyroidism--strategy for asymptomatic primary hyperparathyroidism.

Primary hyperparathyroidism (PHPT), the most common cause of hypercalcemia due to excessive secretion of PTH, is usually associated with hypophosphatemia and elevated serum chloride. Although PHPT was often complicated by renal stone disease and osteitis fibrosa in the past, routine screening of serum calcium (Ca) and development of sophisticated assay of parathyroid hormone have contributed to earlier detection of asymptomatic PHPT (APHPT). The proportion of APHPT patients, who have a mild elevation of serum Ca levels, usually within 1.0 mg/dL above the upper limit of normal, rose from 10-20% to approximately 45% of all PHPT patients in 1990-1995 in our clinic. Although it has been reported that the prevalence of PHPT is about 0.1% of the American population, the prevalence of PHPT appears to be far less in the Japanese population. Determination of a strategy for the increasing number of APHPT patients, is a pressing need but has yet to be accomplished. Treatment with bone antiresorptive drugs has met with some success, although the long-term efficacy of this treatment is not clear. The therapeutic effects of Ca-sensing receptor agonists appear promising.

Hormone Antagonists↗

Control of neurotransmission, behaviour and development, by photo-dynamic manipulation of tissue redox state of brain targets.

Reversible manipulation of local neurotransmission in brain areas, using controlled spatial and temporal resolution, is one of the powerful techniques used to investigate integrative aspects of brain function. We have developed a novel technique for rapidly inactivating local synaptic transmission, from outside the brain, within seconds or minutes via oxidation of target tissue using a photosensitive dye followed by photoirradiation (photo-dynamic tissue oxidation; PDTO). PDTO applied through a defined slit, sharply suppressed excitatory synaptic transmission in rat hippocampal slices and also suppressed in vivo hippocampal neurotransmission reversibly. Furthermore, we manipulated the voluntary movement of gerbils in free-field activity by application of PDTO to the striatum. Also, in freely moving kittens, the development of the visual cortex was manipulated by long-lasting application of PDTO to the eye. Thus, PDTO enables external manipulation of in vivo or in vitro neurotransmission in various clearly defined regions on the submillimeter scale. Suppression of neurotransmission occurred only within the photo-oxidized area which can be histochemically visualized.

Animals↗

Chemopreventive effect of 24R,25-dihydroxyvitamin D(3) in N, N'-dimethylhydrazine-induced rat colon carcinogenesis.

In this study we investigated the effects of 24R,25-dihydroxyvitamin D(3) [24R,25(OH)(2)D(3)] on N,N'-dimethylhydrazine (DMH)-induced rat colon carcinogenesis. For experiments 1 and 2, 50 F344 male, 6-week-old rats were divided into five groups in each experiment. Animals were given s.c. injections of DMH once a week for 4 weeks. Those in groups 1-5 were given 24R,25(OH)(2)D(3) in the diet (10, 5, 2.5, 1.25 or 0 p.p.m., respectively) during the post-initiation stage in experiment 1 and during the initiation stage in experiment 2. At termination, the numbers of aberrant crypt foci (ACF) in the rat colonic mucosa were decreased dose-dependently in rats treated with 24R,25(OH)(2)D(3) during the post-initiation stage, but not in the initiation stage. For experiment 3, 15 male, 9-week-old rats were divided into three groups and given 24R,25(OH)(2)D(3) in the diet (10, 5 or 0 p.p.m.). Animals were injected with 5-bromo-2'-deoxyuridine (BrdU) i.p. 1 h before death to examine DNA synthesis in the colon mucosa. BrdU labeling indices were decreased dose-dependently in colonic crypts of rats treated with 24R, 25(OH)(2)D(3). In experiment 4, using the multicarcinogenic protocol we could analyze our data with respect to not only one separate organ, but at the organism level. Sixty-eight male, 6-week-old rats were treated with DMH, N-methylnitrosourea, 2, 2'-dihydroxy-di-n-propylnitrosamine, diethylnitrosamine and N-butyl-N-(4-hydroxybutyl)nitrosamine in weeks 1-4 and were then given 24R,25(OH)(2)D(3) in the diet (5, 1 or 0 p.p.m.) throughout weeks 5-30. Examination of the development of tumors and preneoplastic lesions in various organs revealed that 24R, 25(OH)(2)D(3) inhibited colonic tumor development significantly but exerted no effects on tumor induction in other organs. In conclusion, these results strongly indicate that 24R,25(OH)(2)D(3) inhibits colon carcinogenesis specifically, without any enhancement of carcinogenesis in other organs, when administered in the post-initiation phase.

1,2-Dimethylhydrazine↗

Hyperparathyroidism is augmented by ovariectomy in Nagase analbuminemic rats.

The role of albumin in bone metabolism was studied in Nagase analbuminemic (NA) rats. Serum calcium (Ca), inorganic phosphate (Pi) and magnesium (Mg) concentrations did not differ between female NA and control Sprague-Dawley (SD) rats at the time of ovariectomy (ovx), although serum ionized Ca was significantly lower in NA rats than in SD rats. Serum parathyroid hormone (PTH) and osteocalcin (OC) concentrations and urinary Ca excretion were significantly greater in NA rats than in SD rats, suggesting hyperparathyroidism and the resultant enhanced bone turnover in NA rats. Paradoxically, ovx increased serum PTH and OC in NA rats but not in SD rats. Ovx-induced exacerbation of hyperparathyroidism was confirmed by significantly greater conversion of 25-hydroxyvitamin D to 1, 25-dihydroxyvitamin D in ovx NA rats even after normalization to vitamin D-binding protein. Bone mineral density (BMD) in proximal tibia increased similarly in a time-dependent manner in sham-operated NA and SD rats. However, ovx ablated the time-dependent increase of BMD in SD rats and significantly decreased BMD in NA rats by 2 wk after ovx, resulting in a significantly lower BMD in ovx NA rats than in ovx SD rats. In summary, NA rats, which are analbuminemic with compensatory increases in lipid and protein synthesis, developed hyperparathyroidism, possibly due to an increase in serum Pi and a reduction of ionized Ca, and ovx induced a greater BMD reduction in NA rats than in SD rats, probably by exacerbating hyperparathyroidism.

Albumins↗

Chemically prepared hevein domains: effect of C-terminal truncation and the mutagenesis of aromatic residues on the affinity for chitin.

Chemically prepared hevein domains (HDs), N-terminal domain of an antifungal protein from Nicotiana tabacum (CBP20-N) and an antimicrobial peptide from Amaranthus caudatus (Ac-AMP2), were examined for their affinity for chitin, a beta-1,4-linked polymer of N-acetylglucosamine. An intact binding domain, CBP20-N, showed a higher affinity than a C-terminal truncated domain, Ac-AMP2. The formation of a pyroglutamate residue from N-terminal Gln of CBP20-N increased the affinity. The single replacement of any aromatic residue of Ac-AMP2 with Ala resulted in a significant reduction in affinity, suggesting the importance of the complete set of three aromatic residues in the ligand binding site. The mutations of Phe18 of Ac-AMP2 to the residues with larger aromatic rings, i.e. Trp, beta-(1-naphthyl)alanine or beta-(2-naphthyl)alanine, enhanced the affinity, whereas the mutation of Tyr20 to Trp reduced the affinity. The affinity of an HD for chitin might be improved by adjusting the size and substituent group of stacking aromatic rings.

Amino Acid Substitution↗

Percutaneous transluminal coronary angioplasty performed 24-48 hours after the onset of acute myocardial infarction improves chronic-phase left ventricular regional wall motion.

The authors investigated the capacity of percutaneous transluminal coronary angioplasty (PTCA) performed 24-48 hours after the onset of acute myocardial infarction (AMI) to improve regional left ventricular wall motion. Twenty-four patients were divided into two groups: a PTCA group who received successful PTCA (14 cases) and a non-PTCA group (10 cases) who did not receive PTCA. Left ventricular end-diastolic volume (LVEDV) increased significantly (p<0.01) from 57+/-14 mL/m2 during the acute phase to 83+/-16 mL/m2 during the chronic phase in the non-PTCA group, whereas no significant change in LVEDV was seen in the PTCA group (69+/-26 vs. 76+/-16 mL/m2). In addition, in patients with 99% stenosis/thrombolysis in myocardial infarction (TIMI) grade 3 flow, increases in regional left ventricular wall motion (delta(sd)/chord) at the infarcted site between the acute and chronic phases were significantly greater in the PTCA group than in the non-PTCA group (2.49+/-1.05 vs. 0.67+/-0.65, p<0.01). PTCA performed 24-48 hours after the onset of AMI improved wall motion at the infarcted site.

Aged↗