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Biomedical subjects

S Ando

Publications and source records attributed to S Ando.

At least 199 records · Page 11Linked to original sources
PubMed1994

Role of nitric oxide in exercise-induced vasodilation of the forearm.

BACKGROUND: We wished to determine the role of NO in exercise-induced metabolic forearm vasodilation. METHODS AND RESULTS: Young healthy volunteers (n = 11) underwent static handgrip exercise (4 to 5 kg, 3 minutes). Forearm blood flow (FBF) measured by strain plethysmography increased from 4.1 +/- 0.7 mL.min-1.100 mL-1 at rest to 9.8 +/- 1.2 mL.min-1.100 mL-1 immediately after exercise and gradually decreased thereafter. Exercise was repeated after intrabrachial artery infusion of NG-monomethyl-L-arginine (L-NMMA) at 4.0 mumol/min for 5 minutes. L-NMMA did not alter blood pressure and heart rate. L-NMMA decreased FBF at rest to 2.9 +/- 0.4 mL.min-1.100 mL-1 (P < .01), peak FBF immediately after exercise to 7.2 +/- 0.7 mL.min-1.100 mL-1 (P < .01), and FBF during the mid to late phase of metabolic vasodilation (P < .01). Calculated oxygen consumption during peak exercise was comparable before and after L-NMMA. Intra-arterially infused L-arginine (10 mg/min, 5 minutes) reversed the inhibitory effect of L-NMMA. To determine the effect of the decrease in resting FBF on exercise-induced hyperemia, we normalized FBF after exercise by resting FBF. The percent increases in FBF after exercise from resting FBF were similar before and after L-NMMA. Furthermore, we examined the effect of intra-arterially infused angiotensin II on FBF at rest and after exercise (n = 7). Angiotensin II decreased FBF at rest from 3.1 +/- 0.3 to 1.8 +/- 0.3 mL.min-1.100 mL-1 (P < .01), peak FBF after exercise from 8.1 +/- 0.5 to 5.6 +/- 0.5 mL.min-1.100 mL-1 (P < .01), and FBF during the mid to late phase of metabolic vasodilation. The effects of L-NMMA and angiotensin II on FBF at rest and exercise were similar. CONCLUSIONS: Our results suggest that L-NMMA decreased FBF after exercise largely by decreasing resting FBF. These results suggest that NO may not play a significant role in exercise-induced metabolic arteriolar vasodilation in the forearm of healthy humans.

Adult↗
PubMed1994

A multi-centre study of the efficacy and safety of pravastatin in hypercholesterolaemic patients with non-insulin-dependent diabetes mellitus.

A multi-centre, non-randomized clinical study of 12-months' duration was performed in 112 patients with hyperlipidaemia associated with non-insulin-dependent diabetes mellitus to evaluate the clinical efficacy and tolerability of pravastatin and to assess its effect on glycaemic control. Patients were eligible for this trial if they fulfilled the following criteria; a high plasma total cholesterol level greater than 220 mg/dl associated with stable glycaemic control for at least 3-months' observation period. On entry, patients received 10 mg pravastatin per day (5 mg twice daily) for 12 months. Clinical efficacy was evaluated in 108 patients. The results showed that pravastatin induced a significant decrease in serum cholesterol level mainly with LDL-cholesterol. Total cholesterol levels were decreased significantly from 275 +/- 3 mg/dl to 222 +/- 4 mg/dl within 3 months of the start of treatment, and LDL-cholesterol decreased from 192 +/- 4 mg/dl to 137 +/- 4 mg/dl. After 12 months' treatment, total cholesterol and LDL-cholesterol levels were 216 +/- 4 mg/dl (p < 0.001) and 137 +/- 5 mg/dl (p < 0.001), respectively. HDL-cholesterol levels were increased from 51 +/- 2 mg/dl to 56 +/- 2 mg/dl at 3 months (p < 0.001) and 55 +/- 2 mg/dl at 12 months (p < 0.01). Triglyceride concentrations were also decreased from 173 +/- 11 mg/dl to 156 +/- 13 mg/dl at 3 months and 137 +/- 10 mg/dl at 12 months (p < 0.01). Fasting plasma glucose and glycated haemoglobin levels were not affected by pravastatin. Adverse events observed in 5 cases were always mild and reversible. These results indicate a clinical usefulness of pravastatin with high compliance in patients with hyperlipidaemia associated with non-insulin-dependent diabetes mellitus.

Adult↗
PubMed1994

Influence of arotinolol hydrochloride on heart rate spectrum in hypertensive subjects.

Influence of arotinolol hydrochloride and atenolol on the balance between the sympathetic and parasympathetic nervous systems was evaluated in 8 hypertensive subjects by spectral analysis of heart rate (HR) and systemic blood pressure (BP). Before and after administration of either arotinolol (n = 7) or atenolol (n = 7) for 2 weeks, BP was continuously and non-invasively monitored by a finger-cuff manometry (Finapres). A time series of instantaneous HR was constructed from the BP signal. A time series of mean BP was also constructed. Spectral analysis was performed by the use of an autoregressive algorithm on these time series (approximately 180 sec). Each spectrum was subdivided into low-(0.05-0.15 Hz, LF) and high-frequency (0.15-0.4 Hz, HF) components, and each component was divided by the sum of the two for normalization. As a measure of the balance between the sympathetic and parasympathetic nervous systems, the ratio of LF to HF (LF/HF) was evaluated. Arotinolol increased fractional HF in the HR spectrum from 0.45 +/- 0.12 to 0.73 +/- 0.08 (p < 0.01) and decreased fractional LF from 0.55 +/- 0.12 to 0.27 +/- 0.08 (p < 0.01); consequently, it decreased LF/HF from 1.4 +/- 0.5 to 0.4 +/- 0.2 (p < 0.01). Atenolol had similar effects on these parameters. Neither of these beta-adrenergic blockades produced a discernible decrease in LF/HF in the BP spectrum. In conclusion, these beta-adrenergic blockades decreased LF/HF in the HR spectrum in hypertensive subjects, which suggests that they improved the balance between the sympathetic and parasympathetic nervous systems.

Adrenergic beta-Antagonists↗
PubMed1994

Isolated adrenocorticotrophin deficiency associated with anti-pituitary antibodies, pituitary cyst, sphenoidal cyst and pineal tumor.

This paper reports a rare case of isolated ACTH deficiency associated with anti-pituitary antibodies, pituitary cyst, sphenoidal cyst and pineal tumor. A 68-year-old man consulted our clinic for general fatigue. Laboratory data showed low plasma adrenocorticotrophin (ACTH) and cortisol levels with blunted responses to insulin-induced hypoglycemia and corticotrophin releasing factor (CRF). Urinary 17-OHCS was low but responded to ACTH-Z administration. No other pituitary functions were impaired. Antibodies to the cytoplasm of rat pituitary and the surface of GH3 cells were detected in the serum. The magnetic resonance imaging (MRI) showed a high signal intensity mass in the anterior pituitary and in the sphenoidal sinus in both T1 and T2 weighted images as well as a low signal intensity mass in a T1 weighted image of the pineal region. Transsphenoidal surgery was performed to resect the mass in the sphenoid sinus and in the pituitary. Pathological studies showed a benign cyst in the sphenoid sinus, and fibrous degeneration and decreased basophils in the pituitary. No infiltrative mononuclear cells were detected in the pituitary. Immunohistochemical studies revealed a decrease in the number of ACTH-producing cells in the pituitary. The patient was well maintained by glucocorticoid replacement without any growth of a possibly benign pineal tumor.

Adrenocorticotropic Hormone↗
PubMed1994

[Basic and clinical studies on biapenem (L-627) in obstetrics and gynecology].

UNLABELLED: We investigated biapenem (BIPM, L-627) a newly carbapenem antibiotic, for its antibacterial activity, tissue penetration, clinical efficacy and bacteriological effect in obstetric and gynecological infections, and obtained the following results. 1. Antibacterial activity: MICs of L-627 against 149 strains isolated from 80 patients in this clinical trial were examined and compared with those of imipenem (IPM) and ceftazidime (CAZ). The MIC50 and MIC90 of L-627 against the isolates were 0.2 and 12.5 micrograms/ml, respectively. Those of IPM were 0.2 and 6.25 micrograms/ml, respectively. The antibacterial activity of L-627 was quite similar to that of IPM, and was superior to that of CAZ. 2. Tissue and retroperitoneal fluid penetration: The peak levels in venous and uterine arterial sera were 24.0 and 26.2 micrograms/ml, respectively, after 300 mg drip infusion. The peak levels in the uterine or adnexal tissues were 2.39-9.60 micrograms/g, and 0.2 microgram/g of L-627 was detected at 275 minutes after administration. Peak levels in retroperitoneal fluid were 8.7 +/- 1.7 micrograms/ml at 1 hour after the completion of 30 minutes drip infusion (300 mg) and 7.9 +/- 0.2 micrograms/ml at 30 minutes after 300 mg 60 minutes drip infusion (300 mg). These levels expected the MICs against main pathogenic organisms. 3. CLINICAL RESULTS: L-627 was given to the following 144 patients (No. of analytical subjects) at a daily dose of 0.3-1.2 g for 2-13 days: intrauterine infections (54), adnexitis (36), parametritis (17), pelvic peritonitis (27), bartholins abscess (6) and other infections (4). The clinical efficacy was 93.1% (134/144) and the eradication rate against isolated organisms was 88.7% (110/124). Side effects were observed in 2 patients: eruption (1) and vomiting with numbness of the tongue (1). Abnormal change in laboratory test results included increase in eosinophils in 1, increase in GOT, GPT and gamma-GTP in 1 and increase in GPT and A1-P in 1, but all of these abnormalities were very mild and withdrawal of the drug was not required. Our results suggest that this drug is useful in the treatment of gynecological infections.

Adolescent↗
PubMed1994

Effects of a novel dihydropyridine calcium antagonist on venous capacitance in Wistar-Kyoto rats.

Calcium antagonists are potent dilators of resistance vessels but do not dilate capacitance vessels. CD832 is a novel dihydropyridine calcium antagonist which has a nitrate moiety in its chemical structure. The authors examined the effects of CD832 on venous capacitance in anesthetized rats. Venous capacitance was assessed by measuring mean circulatory filling pressure (MCFP) at three levels of blood volume. Nitroglycerin decreased and phenylephrine increased MCFP. CD832 did not alter MCFP. After treatment with hexamethonium to prevent reflex venoconstriction, CD832 significantly decreased MCFP but nicardipine (another dihydropyridine calcium antagonist) did not. The magnitude of hypotension caused by CD832 and nicardipine was comparable. The results suggest that CD832 is a unique calcium antagonist which has a venodilator effect.

Animals↗
PubMed1994

[Obstetrical and gynecological infection].

We discussed the current situation of the intractable bacterial infections in the gyneco-obstetrical field and the countermeasures especially to puerperal fever and pelvic abscess (polymicrobial infection). It is very important to select the proper antibiotics for the treatment, it must be according to the pathobacteriological manifestations of the individual case. We must fix the attention to the infections caused by MRSA.

Abscess↗
PubMed1993

Membrane disorganization induced by perfringolysin O (theta-toxin) of Clostridium perfringens--effect of toxin binding and self-assembly on liposomes.

theta-Toxin (perfringolysin O) of Clostridium perfringens binds to membrane cholesterol with high (Kd approximately 10(-9) M) and low (Kd approximately 10(-7) M) affinities and causes membrane lysis of intact cells and liposomes. In order to understand the lytic process at the molecular level, the lysis of liposomes was investigated in comparison with that of intact cells. The toxin dose required to cause 50% lysis (RD50) of phosphatidylcholine/phosphatidylglycerol (82:18, mol/mol) liposomes containing 36-40 mol% cholesterol was 300-1400-times higher than the RD50 value for sheep or human erythrocytes when samples with the same cholesterol concentration were compared. However, the average number of toxin molecules bound per liposome vesicle at 50% lysis was estimated as 10-18 from the RD50 values, close to the number on erythrocytes at 50% lysis, suggesting that the number of toxin molecules adsorbed per vesicle is important for lysis. As to the toxin dose required for membrane lysis, no significant difference was observed between liposomes containing both high- and low-affinity toxin-binding sites and those containing only low-affinity sites, suggesting that theta-toxin molecules bound to low-affinity sites can assemble and cause membrane lysis as well as those bound to high-affinity sites. theta-Toxin assembles on liposomal membranes, as on erythrocytes, in a high-molecular-weight polymeric form as judged from sedimentation patterns in sucrose density-gradient centrifugation. The high-molecular-weight polymers were detected only under conditions where cell or liposome lysis occurred. At low toxin doses, slower sedimenting toxin oligomers and monomers were predominant on liposomal membranes. These results indicate that toxin assembly on membranes is essential for liposome lysis as it is for cell lysis and that assembly occurs on membranes without membrane proteins.

Animals↗
PubMed1993

A novel ganglioside with a free amino group in bovine brain.

A novel ganglioside which binds cholera-toxin B-subunit was purified from bovine brain by an h.p.l.c. system using an Aquasil column subsequent to Q-Sepharose column chromatography. T.l.c./immunostaining showed that the isolated ganglioside had about 60% of the binding reactivity of the authentic ganglioside GM1 for cholera-toxin B-subunit. On h.p.l.c., this ganglioside migrated between ganglioside GD1a and GD1b, and was found to give positive reactions with ninhydrin and fluorescamine reagents which specifically react with amino groups. The presence of a free amino group was further confirmed by chemical re-N-acetylation. The N-acetylated product had an identical RF value on h.p.l.c. and similar reactivity with cholera-toxin B-subunit as the authentic GM1. H.p.t.l.c., t.l.c./immunostaining, negative-ion fast-atom-bombardment (f.a.b.)-m.s., and 1H-n.m.r. spectroscopy of the novel ganglioside unequivocally demonstrated that it has the basal structure of GM1 with de-N-acetylated neuraminic acid instead of N-acetylneuraminic acid. In the present study we report for the first time that a ganglioside derivative containing de-N-acetylated neuraminic acid, de-N-acetylated GM1, exists in natural brain tissues.

Acetylation↗
PubMed1993

Phosphorylation of a 62 kd porcine alpha-internexin, a newly identified intermediate filament protein.

A 62 kd protein was purified from the Triton-insoluble fraction of porcine brain white matter. This protein formed 10nm filaments, in vitro. The phosphorylation of the 62 kd protein by cAMP-dependent protein kinase caused electrophoretic mobility to shift to 66 kd on SDS-PAGE and a complete loss of the filament forming ability ensued. Amino acid sequences of four peptide fragments obtained from the 62 kd protein by lysylendopeptidase were identical with that of a 66 kd rat brain alpha-internexin. Amino acid analyses of the phosphopeptide fragment derived from phosphorylated porcine alpha-internexin revealed that the phosphorylation sites by cAMP-dependent protein kinase located in the amino-terminal head domain of this protein. These results strongly suggest that alpha-internexin polymerizes into 10nm filaments in vitro and that phosphorylation of the amino-terminal domain of alpha-internexin controls its polymerizability.

Amino Acid Sequence↗
PubMed1993

Novel lacto-ganglio type gangliosides with GM2-epitope in bovine brain which react with IgM from a patient of the amyotrophic lateral sclerosis-like disorder.

A motor neuron disorder resembling that of amyotrophic lateral sclerosis was found in a patient who had received the intramuscular administration of a mixture of bovine brain gangliosides (Yuki, N., Sato, S., Miyatake, T., Sugiyama, K., Katagiri, T., and Sasaki, H. (1991) Lancet 337, 1109-1110). A very high titer of anti-GM2 IgM was detected in the patient's serum and the patient quickly recovered after plasmapheresis. The clinical course of the patient appeared to be different from amyotrophic lateral sclerosis and the anti-GM2 IgM was thought to be the culprit. The IgM reacted with GM2, GM1b-GalNAc, SPG(alpha 2-3)-GalNAc, and GD1a-GalNAc, but not with GA2 or GD2, meaning that the epitope recognized by the IgM was the GM2-like terminal structure, GalNAc beta 1-4(Neu-Ac alpha 2-3)Gal beta 1-. In this study, we found two novel GM2-epitope containing gangliosides, X1 and X2, in bovine brain gangliosides by TLC immunostaining using the patient's IgM. They were characterized as unique lacto-ganglio type gangliosides containing the following branching structures. [formula: see text] Their unusual structures may be immunogenic to humans to induce anti-GM2 antibody.

Aged↗
PubMed1993

Phosphorylation of synthetic vimentin peptides by cdc2 kinase.

Synthetic peptide representing the site Ser-41 in vimentin, Leu-Gly-Ser41-Ala42-Leu-Arg44-Arg-Arg-NH2, and its analogs in which Ala-42 was replaced by various amino acids were tested as substrates for cdc2 kinase. Among them, the analog containing sarcosine as well as proline was an excellent substrate. The result suggests that the N-substituted structure of proline immediately following the site is important for cdc2 kinase phosphorylation. Replacement of Ala-42 by polar amino acids, especially lysine, had negative effects on peptide phosphorylation. The peptides in this study were also assayed with another type of proline-directed protein kinase, tau protein kinase II. The substrate specificity differed essentially from that of cdc2 kinase.

Animals↗
PubMed1993

Combination of arachidonic acid and guanosine 5'-O-(3-thiotriphosphate) induce translocation of rac p21s to membrane and activation of NADPH oxidase in a cell-free system.

The superoxide-generating NADPH oxidase system in phagocytes consists of membrane-associated cytochrome b558 and three cytosolic components named p67-phox, p47-phox, and rac p21s. In a cell-free system consisting of membrane and cytosol, the oxidase can be activated with guanosine 5'-O-(3-thiotriphosphate) (GTP gamma S) and an unsaturated fatty acid such as arachidonic acid (AA). Incubation of cytosol and membrane with AA alone caused clear translocation of p47-phox and p67-phox to the membrane, but only slight translocation of rac p21s. GTP gamma S alone did not significantly induce the translocation of rac p21s. However, GTP gamma S in combination with AA markedly augmented rac p21s translocation to the membrane. The translocation of rac p21s is not induced by GDP or GDP beta S. These results indicate that the GTP-bound active form of rac p21s is the entity that is translocated to the membrane by the action of AA.

Amino Acid Sequence↗
PubMed1993

Long chain fatty acid utilization of T-cells from autoimmune MRL-lpr/lpr mice.

To test the hypothesis that T-cells which exhibit abnormal immunological behavior manifest derangements in the de novo synthesis of phospholipids, the utilization of [3H]palmitic acid in B220+ T-cells from autoimmune MRL-lpr/lpr mice was investigated. The rate of incorporation of [3H]palmitic acid into membrane phospholipids was markedly increased in intact B220+ T-cells compared to that in T-cells from immunologically normal mice. The activities of two key enzymes involved in the de novo synthesis of palmitoyl-phospholipids, acyl-coenzyme (CoA) ligase and acyl-CoA; sn-glycerol-3-phosphate acyl transferase, were significantly higher in homogenates from B220+ T-cell membranes compared with those in controls. Despite these findings, the molar concentration of individual palmitoyl glycerolipids was equivalent in the membranes of B220+ T-cells and control lymph node T-cells. The results indicate that T-cells from lupus mice exhibit complex defects in the biosynthesis and turnover of membrane phospholipids and suggest the possibility that these aberrations contribute to T-cell dysfunction in autoimmune diseases.

Animals↗
PubMed1993

Antimicrobial specificity and hemolytic activity of cyclized basic amphiphilic beta-structural model peptides and their interactions with phospholipid bilayers.

We synthesized a series of cyclic antiparallel beta-sheet model peptides with various ring sizes, which were designed on the basis of a cyclic beta-structural antibiotic, gramicidin S (GS); cyclo(Val-Orn-Leu-D-Phe-Pro)2, and investigated in terms of their antimicrobial activity and specificity against Gram-positive and Gram-negative bacteria and lytic activity for human erythrocytes. In our planning, in order to compare the peptides with GS, D-Phe-Pro sequence forming beta-turn in GS molecule remained unaltered and repeating sequences of alternately hydrophobic (Leu)-hydrophilic (Orn) residue were introduced into the beta-structural parts. CD study in acidic liposomes as well as leakage study of carboxyfluorescein encapsulated in phospholipid vesicles indicated that the peptides strongly interacted with lipid bilayers by taking an amphiphilic beta-structure. Antimicrobial study showed that although GS is active only against Gram-positive bacteria, the antimicrobial spectra of the model peptides transformed gradually to be active against Gram-negative ones and finally only against Gram-negative bacteria whose repeating sequences increased. It should be noted that the designed cyclic model peptides show antibacterial activity but accompany no hemolysis. This indicates that an appropriate hydrophobicity together with a proper orientation of hydrophilic (cationic) and hydrophobic groups in cyclic beta-structural molecules can hold antimicrobial activity against both types of bacteria without damaging eukaryotic cells.

Amino Acid Sequence↗
PubMed1993

Differential fatty acid release from CA1 and CA3 regions of rat hippocampal slices under hypoxia and hypoglycemia.

Rat hippocampal slices were subjected to hypoxia and/or hypoglycemia for 10 min, and free fatty acids released in CA1 and CA3 regions were separately analyzed. Fatty acid accumulation in CA1 was not so significant under hypoglycemia, but very prominent under hypoxia. Free fatty acid levels in CA3 were much less than those in CA1 even under hypoxia plus hypoglycemia. This observation seems to be consistent with the selective vulnerability of CA1 neurons seen in in vivo ischemia. The decreasing order of accumulation of free fatty acid species in CA1 was C16:0 > C18:0 > C18:1 > C20:4 > C22:6. The increment fold as compared to control level was decreasing as follows: C22:6, 28 times; C20:4, 13 times, C18:1, 10 times; C18:0 = C16:0, 3 times. The present experimental conditions using hippocampal slices provided a good in vitro model to prove the selective hypoxic damages of the CA1 subfield in terms of free fatty acid release in association with the membrane degradation.

Animals↗