Biomedical subjects

H Aihara

Publications and source records attributed to H Aihara.

At least 19 recordsLinked to original sources

PubMed1992

Extramedullary plasmacytoma of the thyroid, associated with follicular colonization and stromal deposition of polytypic immunoglobulins and major histocompatibility antigens. Possible categorization in MALT lymphoma.

A 78-year-old woman complaining of a neck mass underwent right hemithyroidectomy. The 7 x 6 cm thyroid tumor consisted predominantly of mildly atypical, epithelial membrane antigen-positive plasma cells and scattered lymphoid follicles. Features of follicular colonization (plasma cell infiltration into germinal centers) were noted. Numerous CD45RO-positive reactive T cells and a smaller number of CD20-positive blast-like B cells were also distributed among the plasma cell infiltrate. IgG, kappa-type monoclonality with J-chain reactivity was identified in the plasma cells, including those in the lymphoid follicles. The association of pre-existing lymphocytic thyroiditis was confirmed histologically in the non-tumorous thyroid tissue. The tumor exhibited deposition of reticulin fiber-rich, amorphous eosinophilic substances, provoking pronounced foreign body reactions. The deposit, polytypically immunoreactive for immunoglobulin gamma-, mu-, kappa- and lambda-chains, beta 2-microglobulin and HLA-DR, was scarcely reactive upon amyloid staining, and consisted ultrastructurally of electron-dense, non-fibrillar material and entrapped collagen fibers. Multiple myeloma was ruled out by laboratory, histologic and clinical examinations. The possible categorization of this extramedullary plasmacytoma of the thyroid within low-grade B cell lymphoma of the mucosa-associated lymphoid tissue (MALT) is discussed.

Aged↗

PubMed1992

[A clinical study of combined therapy of aspoxicillin and ceftazidime on intractable respiratory infections].

Both aspoxicillin (ASPC) and ceftazidime (CAZ) were administered together to 55 patients with intractable respiratory tract infections. ASPC and CAZ were administered at daily doses of 4 g and 2 to 4 g, respectively. Clinical effects were excellent in 11 cases, good in 33, fair in 7 and poor in 4, thus the efficacy rate was 80.0%. Bacteriologically, identified organisms were eradicated in 14 cases out of 21, decreased in 3, exchanged in 2 and unchanged in 2. The eradication rate was 76.2%. As a side effect, diarrhea was found in only one case, and abnormal laboratory test values were observed in 4 cases. However, these adverse reactions were not severe, therefore it was possible to continue the chemotherapy. These results indicate that the combination antimicrobial chemotherapy of ASPC and CAZ is effective against intractable respiratory tract infections.

Adult↗

PubMed1991

Sustained activation of protein kinase C is essential to HL-60 cell differentiation to macrophage.

Although a single dose of phorbol 12-myristate 13-acetate (PMA) allowed HL-60 cells to differentiate to macrophages, a single dose of membrane-permeant diacylglycerol (DAG), 1,2-dioctanoylglycerol (1,2-DiC8), was normally insufficient to differentiate these cells. These cells metabolized 1,2-DiC8 very rapidly, and 1,2-DiC8 available to protein kinase C (PKC) activation was removed from the incubation medium at a rate proportional to cell density. However, increasing the duration of exposure of HL-60 cells to this DAG either by its repeated addition or by decreasing the cell density greatly enhanced their differentiation to macrophages as measured by CD11b expression. During this differentiation induced by DAG, neither measurable translocation nor depletion (down-regulation) of PKC was observed. When the cells were exposed to PMA, on the other hand, some PKC subspecies were instantaneously translocated to membranes and subsequently disappeared very quickly, whereas the alpha-subspecies was decreased to the level of approximately 60% of the resting cell, but thereafter its activity was maintained at a nearly constant level in membranes. After approximately 4 hr, the PKC subspecies, once depleted, reappeared gradually in the membrane fraction. The results suggest that sustained activation of PKC is essential to differentiation of HL-60 cells to macrophages, and depletion of the enzyme is not needed. Perhaps translocation of PKC represents an extreme state of the active form of the enzyme, which may result from PMA action, and the alpha-subspecies presumably plays a key role in HL-60 cell differentiation.

Biological Transport↗

PubMed1991

Inhibition of gastric H+,K(+)-ATPase by the anti-ulcer agent, sofalcone.

Effects of the anti-ulcer agent, sofalcone, on gastric H+,K(+)-ATPase were studied as well as those of other chalcone derivatives, chalcone and sophoradin. These drugs inhibited pig gastric H+,K(+)-ATPase in a dose-dependent manner. They were 5-10-fold less inhibitory toward Na+,K(+)-ATPase than H+,K(+)-ATPase. The potencies of these drugs on the inhibition of enzymes were as follows: sophoradin greater than sofalcone greater than chalcone. Kinetic studies showed that the inhibition of H+,K(+)-ATPase by sofalcone was competitive with respect to ATP and was non-competitive with respect to K+. Sofalcone also inhibited H+,K(+)-ATPase mediated proton transport and reduced the phosphoenzyme level. These results suggest that sofalcone inhibits gastric H+,K(+)-ATPase competitively with ATP at the ATP site and thereby blocks the phosphorylation of the enzyme. This may be the cause of the anti-secretory activity of sofalcone.

Adenosine Triphosphatases↗

PubMed1991

Protective effects of minaprine in infarction produced by occluding middle cerebral artery in stroke-prone spontaneously hypertensive rats.

1. We examined the effects of minaprine on cerebral infarction produced by occluding of unilateral middle cerebral artery (MCA) above the rhinal fissure in stroke-prone spontaneously hypertensive rats (SHRSP). 2. Oral administration of minaprine (60 mg/kg/day) and vehicle were started 30 min after the occlusion of MCA, and continued for 6 days. 3. The brain was dissected out and 36 coronal multiple sections of the whole brain were histologically prepared to determine the location and extension of infarction. 4. The infarcted area produced by the occlusion of MCA was limited to the cerebral cortex. 5. Body weight of the minaprine-treated rats gradually decreased within 4 days after the occlusion of MCA and thereafter increased, whereas in the vehicle-treated rats, there was a gradual decrease during the experimental period. 6. Size of the infarcted area was serially measured, in each section, using a microcomputer imaging device. In all animals with an occluded MCA, there was a typical pattern of ischemic damage. 7. Post-treatment of MCA occluded SHRSP with minaprine resulted in reduction in infarct size, as compared to findings in the vehicle-treated controls. 8. The pharmacological and histopathological effects of minaprine on the progress of cerebral infarction produced by the occlusion of MCA in SHRSP are discussed.

Animals↗

PubMed1991

Electrophysiological effects of CD-349, a dihydropyridine-type calcium antagonist, on goat cardiac Purkinje fibers.

We examined the calcium antagonistic action of CD-349, a dihydropyridine derivative, on goat cardiac Purkinje fibers using the two-microelectrode voltage-clamp method. CD-349 at a concentration of 10(-5) M shortened the action potential duration without changing the maximum rise in the action potential (Vmax) in goat Purkinje fibers. CD-349 at 3 x 10(-7) to 3 x 10(-6) M inhibited the slow inward current (Isi) in a concentration-dependent manner. At the holding potential of -55 mV, CD-349 exerted a tonic block of Isi, and, furthermore, it exerted a use-dependent block at a frequency range of 1 Hz, but it did not exert a use-dependent block at 0.5 and 0.2 Hz. This may be because CD-349 delayed the recovery process from the inactivation of Isi. The amplitude of the block of Isi was larger at the holding potential of -45 mV than at -55 mV. The inactivation curve of Isi shifted toward a negative potential in the presence of CD-349. Nifedipine also exerted a tonic block of Isi. The onset of the action of nifedipine was quicker than that of CD-349 or nitrendipine. A use-dependent block at 1 Hz and delay of the recovery process from inactivation was also observed with nifedipine. The inactivation curve shifted toward the negative potential with nifedipine. On washout of the drugs, the effects of CD-349 or nitrendipine were not readily reversed compared with those of nifedipine. CD-349 had no effect on either inward rectifying (IK1) or delayed outward potassium (IK) or hyperpolarization-activated inward (If) currents. These observations suggest that, in cardiac tissues, CD-349 selectively inhibits the calcium current, presumably by acting on the inactivated channel.

Action Potentials↗

PubMed1991

Time-dependent interaction of a new H2-receptor antagonist, IT-066, with the receptor in the atria of guinea pig.

3-Amino-4-[4-[4-(1-piperidinomethyl)-2-pyridyloxy]-cis-2- butenylamino]-3-cyclobutene-1,2-dione hydrochloride (IT-066) showed a highly potent and long lasting H2-receptor blocking action in guinea pig atria. The inhibitory effect of IT-066 on the histamine-induced positive chronotropic response increased concentration- and time-dependently. A short period of treatment with IT-066 shifted the concentration-response curve of histamine to the right in parallel, without decreasing the maximal response to histamine. With prolongation of the treatment, the concentration-response curve shifted further to the right with time-dependent suppression of the maximal response to histamine. The inhibitory effect of IT-066 was irreversible. The dissociation constant for histamine (KA) was not changed by prolongation of the time of incubation with IT-066. The dissociation constant for IT-066 (KB) was decreased with the prolongation of the treatment. Kinetic analysis of the time-dependent inhibition showed a two-step reaction: the first was reversible and the second was irreversible. Preincubation of the atria with ranitidine, however, protected the H2-receptor from the apparently irreversible antagonism of IT-066. These results suggest that IT-066 has a time-dependent and irreversible interaction with the H2-receptor and that the interaction may be responsible for the potent and long lasting H2-receptor blocking action of IT-066.

Animals↗

PubMed1991

[A case with a diagnosis of apparent functional sylvian aqueductal stenosis].

A case with a presumptive diagnosis of a functional sylvian aqueductal stenosis is presented. The patient was a 64-year-old female, who suffered from progressive gait disturbance and dementia. On admission, CT-scan showed lateral and third ventricular dilatations. The pattern of the ventricular dilatation suggested an aqueductal stenosis. But CT-scan showed no tumorous lesion. RI-cisternography, RI-ventriculography, aqueductgraphy, and continuous monitoring of the intraventricular pressure of the third ventricle were performed in order to make a diagnosis. The results of these examinations led to the following conclusion. "Although there was no apparent mechanical obstruction or stenosis, the presence of circulatory failure of CSF, demonstrated apparent functional stenosis of the aqueduct sylvii." A VP-shunt operation was performed a month after her admission. Her symptoms improved remarkably.

Cerebral Aqueduct↗

PubMed1990

Interaction of the dihydropyridine calcium antagonist, CD-349, with calmodulin.

The characteristics of the binding of the 1,4-dihydropyridine Ca2+ antagonist, 2-nitratopropyl 3-nitratopropyl 2,6-dimethyl-4-(3-nitrophenyl)-1,4-dihydropyridine 3,5-dicarboxylate (CD-349), to calmodulin (CaM) and the effect of CD-349 on the Ca2+/CaM-dependent enzyme, cyclic GMP (cGMP) phosphodiesterase (PDE), were investigated. CD-349 showed a Ca2(+)-dependent binding to CaM, in equilibrium column binding studies. CD-349 inhibited the [3H]CD-349 binding to CaM, at a concentration producing a 50% inhibition (IC50) of 2.4 microM, whereas the CaM antagonist, trifluoperazine hydrochloride (TFP), stimulated the [3H]CD-349 binding to CaM. Scatchard plot analysis of the binding of CD-349 to CaM revealed that the apparent dissociation constant (Kapp) of CD-349 was 2.1 microM and the maximal number of binding sites (Bmax) of CD-349 was 1.0 nmol/nmol CaM. In the presence of TFP, the Kapp and Bmax values of CD-349 binding to CaM were changed to 1.1 microM and 1.5 nmol/nmol CaM respectively. Although the CaM antagonists, N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide hydrochloride (W-7) and TFP, decreased and increased, respectively, the fluorescence intensity caused by 2-p-toluidinylnaphthalene-6-sulfonic acid (TNS)-CaM binding, CD-349 only slightly decreased the fluorescence of TNS bound CaM. CD-349 inhibited both basal and Ca2+/CaM-activated cGMP PDE activity. However, CaM did not competitively antagonize the CD-349-induced inhibition of the Ca2+/CaM-activated PDE activity. In addition, the kinetic study showed that CD-349 inhibited both basal and Ca2+/CaM-activated cGMP PDE activity, competitively with cGMP, with almost the same inhibition constant (Ki). These results suggest that CD-349 binds to CaM, with Ca2+ dependency, at sites differing from those which bind to the CaM antagonist. The inhibitory activity of CD-349 on Ca2+/CaM-dependent PDE does not seem to be due to a CaM antagonistic action.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗

PubMed1990

Protein kinase C during differentiation of human promyelocytic leukemia cell line, HL-60.

Protein kinase C (PKC) from human promyelocytic leukemia HL-60 cells can be resolved into three fractions (peak, a, b and c) by hydroxyapatite column chromatography. Peak a and c enzymes are indistinguishable from the brain type II PKC having beta (beta I and beta II)-sequence and type III having alpha-sequence, respectively. Peak b enzyme is a previously unidentified PKC subspecies that has enzymological properties subtly different from type I (having gamma-sequence), type II and type III PKC. Upon treatment of HL-60 cells with 1 microM retinoic acid, this peak b enzyme is decreased dramatically within 24 h, whilst peak a enzyme (beta-PKC) is increased, and peak c (alpha-PKC) enzyme is slightly decreased within 48 h. The result implies that the PKC subspecies in HL-60 cells have distinct functions during cell differentiation.

Amino Acid Sequence↗

PubMed1990

H2-receptor antagonism by a novel compound IT-066 assessed from [14C]aminopyrine accumulation in rabbit parietal cells.

The H2-receptor antagonistic activities and properties of IT-066 were investigated in rabbit isolated gastric mucosal cell and were compared with those of famotidine and cimetidine. IT-066 inhibited dose dependently the histamine-stimulated [14C]aminopyrine ([14C]AP) accumulation in parietal cells. The antagonism was unsurmountable. The inhibitory action of IT-066 was enhanced by lengthening of its incubation time with the cells. IT-066 following 30 min preincubation with the parietal cells showed 32 and 1560 times the activity of famotidine and cimetidine, respectively, as an inhibitor of [14C]AP accumulation. The inhibitory activity of IT-066 on the histamine effect remained after repeated washing of the cells while with famotidine and cimetidine the response to histamine was restored after washout of the drugs from the cells. These data indicate that the antagonism of IT-066 on histamine H2-receptors is high and is unsurmountable in the isolated parietal cell model.

Aminopyrine↗

PubMed1990

Alteration of metabolism of acetylcholine induced by 2-deoxy-D-glucose in the gastroduodenum of the rat.

2-Deoxy-D-glucose (2-DG) administered intraperitoneally, dose-dependently increased the secretion of gastric acid, and the changes were comparable with those on the activity of choline acetyltransferase (CAT) and acetylcholinesterase (AChE) in the stomach. Double-reciprocal plot analysis of the increased activity of CAT and AChE, induced by 2-DG, showed that the changes were due to the increase of Vmax, with no change in the Km-value for the substrates. The uptake of [3H]choline and subsequent synthesis of [3H]ACh was observed in the forestomach, corpus and antrum of the stomach and in the duodenum. 2-Deoxy-D-glucose significantly increased the uptake of [3H]choline and synthesis of [3H]ACh in every region of the stomach and in the duodenum, in a dose-dependent manner. The increase of secretion of gastric acid, induced by 2-DG paralleled that of uptake of [3H]choline and synthesis of [3H]ACh at an early stage. The conversion of [3H]choline taken up to [3H]ACh was negligibly influenced by 2-DG. Neither the content of ACh and choline, nor the turnover rate of ACh, were changed by administration of 2-DG. 2-Buten-4-olide (2-B4O), which inhibits the activity of the vagus nerve through the central nervous system, prevented 2-DG-induced uptake of [3H]choline and subsequent synthesis of [3H]ACh, as well as the increase in secretion of gastric acid. These results suggest that the uptake of [3H]choline and subsequent synthesis of [3H]ACh are closely related to the neuronal activity of the vagus nerve, and that cholinergic neuronal activity is dependent upon quantitative changes of metabolism of ACh in the gastroduodenum.

Acetylcholine↗

PubMed1990

26,27-Hexafluoro-1,25-dihydroxyvitamin D3 (F6-1,25(OH)2D3) prevents osteoporosis induced by immobilization combined with ovariectomy in the rat.

The effect of 26,27-hexafluoro-1,25-dihydroxyvitamin D3 (F6-1,25(OH)2D3) on experimental osteoporosis in the rat induced by a combination of immobilization and ovariectomy was evaluated. F6-1,25(OH)2D3 increased the femur score and the photo-density. The administration of F6-1,25(OH)2D3 also significantly increased the dry weight, the ash weight and the ash content of the bone. Both F6-1,25(OH)2D3 and 1 alpha(OH)D3 showed a nearly dose-dependent effect and significant inhibition of the decrease of bone mass. Histomorphometry revealed a significant decrease of resorption by the administration of F6-1,25(OH)2D3. Bone formation rate in the F6-1,25(OH)2D3 treated group significantly decreased compared with the vehicle group. In conclusion, the pharmacological effective dose of F6-1,25(OH)2D3 was considered to prevent the osteoporotic decrease of bone mass by suppressing the elevated bone turnover.

Animals↗

PubMed1990

Effect of salvianolic acid A, a depside from roots of Salvia miltiorrhiza, on gastric H+,K(+)-ATPase.

Salvianolic acid A, a depside from the roots of Salvia miltiorrhiza, inhibited pig gastric H+,K(+)-ATPase and pNPPase with 50% inhibition values (IC50) of 5.2 x 10(-7) M and 1.7 x 10(-6) M, respectively. Kinetic studies revealed that the inhibition patterns induced by salvianolic acid A were competitive with respect to ATP and noncompetitive with respect to K+. Salvianolic acid A (25 mg/kg, i.p.) significantly inhibited acid secretion in pylorus-ligated rats. At the same dose it also showed a significant reduction in the formation of gastric lesion induced by water immersion and restraint stress. These results suggest that salvianolic acid A shows antisecretory and antiulcer activity by inhibiting the gastric H+,K(+)-ATPase.

Adenosine Triphosphatases↗

PubMed1990

Inhibition of gastric H+, K(+)-ATPase by chalcone derivatives, xanthoangelol and 4-hydroxyderricin, from Angelica keiskei Koidzumi.

Two chalcone derivatives, xanthoangelol (1) and 4-hydroxyderricin (II) isolated from Angelica keiskei Koidzumi, inhibited pig gastric H+, K(+)-ATPase with IC50 values of 1.8 and 3.3 microM, respectively. The inhibition by I or II was competitive with respect to ATP and was non-competitive with respect to K+ I and II also inhibited K+, stimulated p-nitrophenyl phosphatase, with IC50 values of 1.3 and 3.5 microM, respectively. Proton transport in-vitro was inhibited by I or II, in a dose-dependent manner, 1 at 100 mg kg-1, i.p. significantly inhibited acid secretion and the formation of stress-induced gastric lesions. These results suggest that the antisecretory effect of 1 is due to the inhibition of gastric H+, K(+)-ATPase.

4-Nitrophenylphosphatase↗

PubMed1990

Effect of minaprine and other reference drugs on passive avoidance impairment induced by cerebral ischemia in Mongolian gerbils.

We examined the characteristics of cerebral ischemia-induced behavioral deficit in the passive avoidance task and the effect of minaprine and other cytoprotective drugs on passive avoidance deficit induced by cerebral ischemia in Mongolian gerbils. Severe impairment of passive avoidance was apparent when the duration of the ischemia exceeded 2 min. Histopathological ischemic neuronal damage in CA1 neurons at 7 days after occlusion was also induced when the ischemia was over 2 min. Otherwise, although cerebral ischemia was carried out at 5 min, 2 hr, 5 hr or 24 hr after the training session, the passive avoidance deficit was produced 24 hr after the training session. When the training session was carried out 24 hr before the occlusion, minaprine, which was administered 30 min before the occlusion, led to a recovery of the response latency. Pentobarbital, diazepam and ethylapovincamine improved the passive avoidance deficit induced by 5-min bilateral carotid artery occlusion. On the other hand, the passive avoidance deficit was not ameliorated by Ca(++)-hopantenate, nicardipine and idebenone. The hippocampal damage at 7 days after occlusion was prevented by the drugs that ameliorated the passive avoidance deficit. The relationship between passive avoidance deficit and CA1 neuronal death in the hippocampus induced by cerebral ischemia warrants further attention.

Animals↗

PubMed1990

Effects of minaprine and sulpiride injected into the amygdaloid nucleus on the duration of immobility in rats forced to swim.

We examined the effects of minaprine and sulpiride injected into the medial amygdaloid nucleus on the duration of immobility in rats forced to swim. Minaprine (50 micrograms/microliter) significantly reduced the duration of immobility, while sulpiride (50 micrograms/microliters) remarkedly enhanced it. These results suggest that the medial amygdaloid nucleus might be involved in the suppressive effect of minaprine on the duration of immobility, as was seen with the tricyclic antidepressants. The pattern of behavior seen with sulpiride administrations differs considerably from that seen with the tricyclic antidepressants.

Amygdala↗

PubMed1990

Clinicopathological differences between early-onset and late-onset sepsis and pneumonia in very low birth weight infants.

We performed clinicopathological studies on early-onset sepsis (5 infants, less than 72 hours of life, EOS) and late-onset sepsis (15 infants, greater than 72 hours, LOS) of very low birth weight, less than 1500 g (VLBW). In EOS, the clinical features mimic the respiratory distress syndrome and hematological changes were not observed. The lungs showed slight interstitial pneumonia with structural immaturity, hyaline membranes, hemorrhage, and minimal infiltration by polymorphonuclear neutrophils (PMNs). The pathogen was group B streptococcus or weakly gram-negative bacilli. In LOS, pneumonia proceeded to sepsis and neutropenia with elevated numbers of circulating immature neutrophils, and increased levels of C-reactive protein were observed at the onset of sepsis. Severe pneumonia with infiltration of numerous PMNs and bacterial colonies and polymicrobial infection by nosocomial pathogens such as Staphylococcus aureus and Pseudomonas aeruginosa were common. The thymus and spleen weights varied but retained normal structure in EOS. The thymus was depleted of lymphocytes, and the spleen was hypertrophic but poorly reactive against infection in LOS. The pathogenesis of EOS is regarded as being more closely correlated with lung immaturity and circulatory disorder in early life, whereas that of LOS is associated with immunological defenses of the host, potency of the pathogens, and terminal multiple organ failure.

Blood Cell Count↗