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Biomedical subjects

H Azuma

Publications and source records attributed to H Azuma.

At least 235 records · Page 13Linked to original sources
PubMed1989

Rotational acetabular osteotomy in congenital dysplasia of the hip.

Rotational acetabular osteotomy was carried out in 127 patients (147 hips) with acetabular dysplasia, some of whom showed early or progressive degenerative changes. Complications occurring during and after operation were transient lesions of the lateral femoral cutaneous nerve in 20 patients, of the femoral nerve in 2, fracture of the acetabulum in 1, inadequate rotation of the acetabulum in 11, and infection in 3 patients. Later complications were breakage of Kirschner wires in 3, ectopic bone formation in 2 and acute chondrolysis in 3 patients. Sixty-six patients (69 hips) were followed for an average of 5 years and 4 months, and in most of them satisfactory results were achieved in spite of these complications.

Acetabulum↗
PubMed1989

Alpha 1-adrenoceptor antagonist activity of novel pyrimidine derivatives (SHI437 and IK29) in rabbit aorta and trigone of the bladder.

1. In the rabbit isolated aorta and trigone of the bladder, noradrenaline, phenylephrine and clonidine elicited concentration-dependent contractions, which may be caused through activation of postsynaptic alpha 1-adrenoceptors. 2. SHI437, IK29, prazosin and yohimbine competitively antagonized the contractile responses induced by noradrenaline in the aorta and trigone. The pA2 values of SHI437, IK29, prazosin and yohimbine were 7.35 +/- 0.09, 7.47 +/- 0.10, 8.55 +/- 0.02 and 6.28 +/- 0.05 in the aorta, and 8.07 +/- 0.04, 8.30 +/- 0.03, 8.22 +/- 0.04 and 6.46 +/- 0.04 in the trigone, respectively. 3. SHI437, IK29, prazosin and yohimbine also possessed competitive alpha 2-adrenoceptor blocking properties, judging from their antagonism of the clonidine-induced inhibitory effect on the twitch responses in the electrically stimulated vas deferens of the rat. The pA2 values of SHI437, IK29, prazosin and yohimbine were determined to be 4.76 +/- 0.02, 4.74 +/- 0.02, 5.06 +/- 0.03 and 7.86 +/- 0.04, respectively. 4. SHI437, IK29 and prazosin inhibited the contractile responses elicited by transmural electrical stimulation without affecting the evoked 3H-overflow from the [3H]-noradrenaline-preloaded rabbit aorta. Yohimbine augmented the contractile responses and 3H-overflow. 5. SHI437 and IK29 at a concentration sufficient to inhibit noradrenaline-induced contraction failed to attenuate the contractile responses of aorta to KCl, 5-hydroxytryptamine and prostaglandin F2 alpha, and of the trigone to acetylcholine and histamine. 6. The present results suggest that SHI437 and IK29 are highly selective alpha 1-adrenoceptor antagonists, especially in the trigone of the bladder.

Adrenergic alpha-Antagonists↗
PubMed1989

Inhibition of fibrin monomer polymerization by Bence Jones protein in a patient with primary amyloidosis.

The mechanism of inhibition of fibrin monomer polymerization was studied in a patient with primary amyloidosis. Thrombin and reptilase times of the patient's purified fibrinogen (Fbg) were remarkably prolonged, and polymerization of the patient's fibrin monomer was disturbed. Fbg-Bence Jones protein (BJP) complex was demonstrated by immunoelectrophoresis and sodium dodecyl sulfate-polyacrylamide gel electrophoresis on the patient's purified Fbg. The patient's BJP not only prolonged the thrombin time of normal Fbg but also inhibited the polymerization of normal fibrin monomer. These results suggested that in this patient fibrin monomer polymerization was inhibited by binding of BJP to Fbg.

Aged↗
PubMed1989

[Problems on the determination of intracellular free calcium concentration when measured by fura-2/AM in mast cells].

When rat peritoneal mast cells which had been loaded with fluorescent Ca2+ indicator fura-2/AM were exposed to compound 48/80, fura-2 fluorescence was increased in the presence of 1mM extracellular Ca2+, but remained unchanged in the Ca2(+)-eliminated medium. Only in the presence of 1mM extracellular Ca2+, both fura-2 fluorescence and histamine release were increased in response to compound 48/80, depending on the concentration of the stimulant. Both of these responses were attenuated in the same degree by such release inhibitors as disodium cromoglycate and HSR-6071. Fluorescent microscopic observation of fura-2/AM-loaded mast cells revealed that fura-2 fluorescence was densely localized in the granules and the nucleus, but less in the cytoplasm. All these results strongly suggest that increase in the fura-2 fluorescence might not result from the increase in cytoplasmic free Ca2+ concentration, but from binding of fura-2, which had been released together with chemical mediators from granules following stimulation, to extracellular Ca2+. Therefore, it seems likely that the fura-2/AM loading method is inadequate to investigate whether or not the increase in cytoplasmic free Ca2+ concentration triggers release of chemical mediators from mast cells.

Animals↗
PubMed1989

Binding of plasma fibronectin to human polymorphonuclear leukocytes in normal subjects and patients with aplastic anemia and thyroid dysfunction.

The binding of iodine 125-labeled fibronectin to polymorphonuclear leukocytes (PMNs) from human peripheral blood was examined. The optimum temperature and time for the binding were 37 degrees C and 30 minutes, respectively. On increase in the amount of 125I-labeled fibronectin, its binding to PMNs became saturated. Scatchard analysis of data on binding indicated the presence of a single class of binding sites. PMNs from 15 normal subjects had approximately 6.3 +/- 1.6 x 10(3) sites per cell and a dissociation constant of 10.2 +/- 2.4 x 10(-9) mol/L, indicating that they had high affinity for soluble fibronectin. Arg-Gly-Asp-Ser inhibited the binding of fibronectin to PMNs, strongly suggesting that the fibronectin receptor is one of the Arg-Gly-Asp receptor family. The plasma level of fibronectin was higher in patients with hyperthyroidism and lower in patients with hypothyroidism than in normal subjects, without any significant change in the number of fibronectin binding sites of the PMNs. However, the number of binding sites of fibronectin on PMNs of patients with aplastic anemia was increased, probably because of sensitization of the PMNs with immune complex and other factors.

Anemia, Aplastic↗
PubMed1989

A possible mechanism for the neural adverse reactions caused by metrizamide.

Causality of the metrizamide-induced neural adverse effects was explored among the effects on behavior, electroencephalogram (EEG), and brain glucose utilization in rats. Iotrolan, a new myelographic contrast agent, was used as a reference substance throughout the study. Supracortical subarachnoidal administration of metrizamide caused, within a few minutes, symptoms of sedation and anxiety, which were accompanied by appearance of slow wave or flattening in EEG not only of the cortex, but also of the regions of the hippocampus and thalamus. The rates of local cerebral glucose utilization (LCGU) in a wide range of the brain, measured by using 3H-2-deoxyglucose, were also altered significantly. Despite a limited distribution of metrizamide in the lateral region of the cortex, LCGU was suppressed significantly in the administered side of the parietal cortex, thalamus, subthalamic nucleus, medial geniculate body, and mammillary body and increased in the regions of hippocampus, caudate-putamen, and globus pallidus. It is concluded that, rather than inhibiting the hexokinase reaction in the brain cell, metrizamide appears to cause reduction of a net glucose transport into the cell and that this direct effect on the cortex is amplified and propagated, via neurotransmission, to the regions of the diencephalon and midbrain, causing secondarily various types of disturbance in the mental and motor functions. Iotrolan was proved to lack any biologic activity that may relate to the neural adverse effect observed with metrizamide.

Animals↗
PubMed1988

Correlations of in vivo growth of CTL-susceptible and -resistant variant tumor cell lines in CTL-responder AKR.H-2b:Fv-1b and -nonresponder AKR.H-2b mice.

Spontaneously occurring lymphoma/leukemias in AKR and AKR.H-2b mice are characterized by their expression of the Gross cell surface antigen (GCSA) and their weak immunogenicity. Although of a responder H-2 type, AKR.H-2b mice could not raise cytolytic T lymphocytes (CTLs) against a syngeneic GCSA+ tumor (AKR.H-2bSL1). In contrast, AKR.H-2b:Fv-1b mice served as a source for "antiviral" CTLs specific for GCSA+ tumors such as AKR.H-2bSL1, but not for CTLs against the cl.18-5 variant tumor, an antiviral CTL-resistant subclone derived from AKR.H-2bSL1. In the present study in vivo tumor challenge experiments demonstrated that both the ability of the recipient strain to raise CTLs and the sensitivity of the tumor to the CTLs were critical factors which determine tumor growth and recipient mortality. Furthermore, the ability to raise protective immunity against AKR.H-2bSL1 and cl.18-5 tumor challenge by preimmunization was investigated. It was not possible to raise protective immunity in CTL-nonresponder AKR.H-2b mice. In the case of AKR.H-2b:Fv-1b mice, immunization with allogeneic GCSA+ E male G2 tumor cells leads to complete protective immunity--not only against parental AKR.H-2bSL1 but, somewhat surprisingly, also against cl.18-5 variant, tumor challenge. Consistent with these findings and at the same time with an in vivo role for antiviral CTL, however, CTLs directed to the E male G2, AKR.H-2bSL1, and cl.18-5 tumors could be generated from the spleens of mice which had rejected cl.18-5 tumor cells. Interestingly, immunization of AKR.H-2b:Fv-1b mice with syngeneic AKR.H-2bSL1 tumor cells failed to raise any protective immunity. Thus, the data suggested that the concurrent recognition of allogeneic components with tumor-associated transplantation antigens (TATA) might be important in the induction of sufficient protective immunity against syngeneic GCSA+ tumors. Finally, the possible relationship of TATA and retroviral antigens, such as gp70 and p30 or as defined by CTL clones, is discussed.

AKR murine leukemia virus↗
PubMed1988

[Stimulatory effects of lisuride on local cerebral blood flow and local cerebral glucose utilization in rats].

Effects of lisuride, a central dopamine agonist of the ergot type, on local cerebral blood flow (LCBF) and local cerebral glucose utilization (LCGU) were studied using the autoradiographical 14C-iodoantipyrine and 3H-deoxyglucose method, respectively, in conscious rats. Lisuride significantly stimulated LCBF in the cerebellar gray matter. LCBF in some other regions including the cerebral cortex, caudate-putamen, thalamus, geniculate body and substantia nigra were also stimulated by lisuride. No changes were observed in the hippocampus, hypothalamus and white matter. A close correlation was observed between LCBF and LCGU. Region specificity of the stimulatory effect by lisuride on LCBF and LCGU was coincident. Lisuride shortened the lethal time in the anoxia model. In conclusion, lisuride stimulated not only glucose utilization but also blood flow in local regions of the brain.

Animals↗
PubMed1988

Augmentation of adenosine-induced relaxation response with hydralazine in aortic strips.

Adenosine produced a slight but concentration-dependent relaxation in rabbit aortic strips preconstricted with norepinephrine. The effect of adenosine was markedly augmented in the presence of hydralazine. On the other hand, the adenosine-induced relaxation was attenuated by 8-phenyltheophylline, but was unaffected by indomethacin, nordihydroguaiaretic acid and quinacrine, indicating that adenosine acts via purinergic receptors and that vasodilating metabolites of arachidonic acid are not involved in the relaxation. The adenosine-induced relaxation remained unaffected by S-(p-nitrobenzyl)-6-thioguanosine (NBTG) or 2'-deoxycoformycin (2'DCF), alone or combined. NBTG significantly inhibited the incorporation of [3H] adenosine, while the content of [3H] compound was increased by 2'DCF, but was unchanged by hydralazine. Hydralazine also augmented the 2-chloroadenosine-induced relaxation. These results suggest that the augmentation of adenosine-induced relaxation with hydralazine does not result from an inhibition of adenosine transport and/or adenosine deaminase. When adenosine was added, relaxation was elicited with concomitant increase in cAMP, but with no significant change in cGMP. In the presence of hydralazine, the cAMP increasing effect of adenosine was augmented, and the level of cGMP increased with adenosine. These changes in cyclic nucleotide levels might at least in part explain the augmentation of adenosine-induced relaxation with hydralazine.

Adenosine↗
PubMed1988

Thrombin-induced membrane depolarization of platelets and its inhibition by cetiedil.

When 50 microM cetiedil alone was added to a platelet suspension, increase in Na+ content, decrease in K+ content, and depolarization of platelet membrane were observed without change in the intracellular concentration of free Ca2+ ([Ca2+]1) or in the morphology of platelets. The cetiedil-induced depolarization was attenuated by the reduction of extracellular sodium concentration, while sodium transport inhibitors such as procaine and tetrodotoxin failed to modify the depolarization. On the other hand, thrombin caused such changes in platelets as increases in Na+ content, 22Na space and [Ca2+]1, decrease in K+ content, and membrane depolarization. All these changes caused by thrombin were inhibited by cetiedil. It is suggested that cetiedil brought the increased ion transport and subsequent partial depolarization, which might lead to modification of the reaction of platelet membrane induced by thrombin.

Azepines↗