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Biomedical subjects

M Araki

Publications and source records attributed to M Araki.

At least 109 records · Page 6Linked to original sources
PubMed1996

[The production of high sensitive anti-myeloperoxidase monoclonal antibodies and their sensitivity and specificity].

We produced anti-myeloperoxidase(MPO) monoclonal antibodies(moAb) to detect MPO sensitivity in leukemic cells by visual light microscopy. We got seven kinds of moAbs which showed different properties to MPO. These antibodies reacted to MPO in immature and mature neutrophils, monocytes and HL-60(human myeloid leukemic cell line) by immunochemical detection using the avidin-biotin complex(ABC) staining method, but the amounts of immune complex products were significantly different at each moAb. MPO2, MPO4, MPO9 and MPO13 moAbs blocked MPO activities but MPO5 showed no such inhibition. Most of the moAbs reacted to 59kD MPO moAb using the western blotting method, while MPO4 and MPO5 reacted to both 81kD and 89kD MPO precursors. This data suggests that these moAbs are useful to demonstrate a small amount of MPO in leukemic cells.

Antibodies, Monoclonal↗
PubMed1995

High potassium promotes differentiation of retinal neurons but does not favor rod differentiation.

Neural retinal cells of newborn rats were cultured under dissociated culture conditions. Differentiation of several types of retinal cells was confirmed by immunohistochemical detection of type-specific neural phenotypes. We used Thy-1.1 antigen as a ganglion cell marker, HPC-1 or GABA as an amacrine cell marker and rhodopsin as a rod cell marker. With a high concentration of potassium (38 mM), expression of the respective neural phenotypes were differentially affected. High K+ increased the number of Thy-1.1 positive cells 6 to 8 fold, and drastically promoted their neurite extension. The same culture conditions, however, reduced considerably the number of rhodopsin positive cells, possibly due to the unique membrane properties of photoreceptors. A high K+ concentration also promoted differentiation of HPC-1 positive and GABA positive cells, but to a lesser extent than the Thy-1.1 positive cells. Several possibilities were examined to understand the effect of a high K+ concentration on retinal neural cells. The total cell number in cultures with a high K+ concentration was approximately half of that in control cultures at day 3 and slightly smaller at day 11, suggesting that high K+ did not have a positive general effect on the proliferation or survival of retinal cells. Naturally occurring neuronal death (apoptosis) is a well-known phenomenon during retinal development. A histochemical method for detecting DNA fragmentation, a step preceding apoptosis, showed that high K+ had no preventive effect. BrdU (bromodeoxyuridine) immunohistochemistry showed that high K+ did not seem to enhance proliferation of neural precursor cells. These results indicate that a high K+ concentration promotes the expression of neuronal phenotypes but is not a favorable condition for rod differentiation. Since a high K+ concentration is considered to induce depolarization of nerve cells, the present results suggest an anterograde influence from surrounding neuronal cells, through chronic depolarization by elevated K+, is essential for the differentiation and maturation of retinal cells.

Animals↗
PubMed1995

Site-specific recombination of a transgene in fertilized eggs by transient expression of Cre recombinase.

An efficient method of transgene modulation in fertilized eggs has been developed that uses the Cre/loxP recombination system. Twelve transgenic mouse lines carrying a chicken beta-actin promoter-loxP-chloramphenicol acetyltransferase (CAT) gene-loxP-beta-galactosidase gene construct were produced. After selection of the line showing the highest expression of the CAT gene in a variety of tissues, eggs of this line were injected in the male or female pronucleus with a Cre expression vector placed under the control of the chicken beta-actin promoter and kept in a circular form to avoid genomic integration. This resulted in a transient expression of Cre in the eggs, leading to recombination of the transgene as detected by galactosidase expression and DNA analysis. Recombination was completed before the morula stage with both types of pronuclear injections and occurred with a very high frequency; no mosaicism, no incomplete recombination, and no integration of the Cre sequence were observed in 18 mice born with this modified transgene. The beta-galactosidase gene was expressed in various tissues at levels comparable to those found for the CAT gene in the founder line. This Cre transient expression system should be useful for breeding transgenic lines in which transgene expression leads to sterility or lethality--in particular, for selecting transgenic lines with high expression of a potentially lethal transgene whose full activity is difficult to explore in a conventional transgenic system because of the risk of selecting for transgenic lines carrying only poorly expressed transgenes.

Actins↗
PubMed1995

Transgenic mice expressing high levels of soluble TNF-R1 fusion protein are protected from lethal septic shock and cerebral malaria, and are highly sensitive to Listeria monocytogenes and Leishmania major infections.

Mice bearing a transgene coding for a soluble tumor necrosis factor receptor type 1 (TNFR1)-FcIgG3 fusion protein and placed under the control of the alpha-1-antitrypsin gene promoter were generated. Depending on the mouse line, blood levels of the protein ranged from 25 ng/ml to over 100 micrograms/ml; this level of expression was most often transmitted to the transgene-bearing progeny as a relatively stable feature. High-expressor mice were completely resistant to lipopolysaccharide-induced shock and lethality, including after D-galactosamine sensitization, and mice expressing about 1 microgram of the fusion protein/ml were partially (60%) protected. In contrast, mice expressing less than 0.1 microgram of the protein/ml were more sensitive than controls with respect to incidence and time of death, even though the biological activity of serum tumor necrosis factor (TNF) was partially neutralized. High-expressor mice of the adequate genetic background were markedly, although not completely, protected from death by cerebral malaria after injection with Plasmodium berghei. They were highly susceptible to Listeria monocytogenes, dying from bacterial dissemination after sublethal infection, and to Leishmania major, displaying severe, non-healing lesions after local infection. Under the same conditions, mice expressing about 1 microgram protein/ml were only partially sensitive to these last agents, compared to non-transgenic littermate mice which were fully resistant. These transgenic mice represent a model of permanent, complete or partial, impairment of TNF use, which compares favorably, for ease of breeding and for the range of effects, to mice bearing gene disruptions.

Animals↗
PubMed1995

Primary tubular adenocarcinoma arising in the duodenal limb of reconstructed gastroduodenostomy for signet-ring cell carcinoma of the stomach.

Adenocarcinoma of the small intestine is uncommon. Due to this paucity and the lack of specificity of symptoms, patients are usually seen late in the course of their illness, when curative therapy, mainly represented by extensive surgical resection, is unlikely. The authors report a case of primary well-differentiated tubular adenocarcinoma (T4N0M0) arising in the duodenal limb of a reconstructed Billroth I gastroduodenostomy, 9 years after a distal gastrectomy for signet-ring cell carcinoma of the stomach (T4N0M0). Evidence for excluding the possibility of a recurrence of the primary gastric cancer was based on the different histologic pattern, the long disease-free interval, and other features of the second neoplasm. Relatively early diagnosis of the neoplasm, followed by curative surgical therapy was made possible by the early onset of the obstructive symptoms and the favorable anatomical location of the tumor.

Adenocarcinoma↗
PubMed1995

Role of neutrophils and platelets in the pathogenesis of focal hepatocellular necrosis in endotoxaemia.

To clarify whether neutrophils and platelets are implicated in the pathogenesis of focal hepatocellular necrosis in endotoxaemia, we examined the relationship between the changes in neutrophils and platelets in peripheral blood and the degree of focal hepatocellular necrosis and serum transaminase activity in rats after endotoxin injection. The number of neutrophils in the peripheral blood decreased rapidly during the first hour after endotoxin injection and then increased. This initial decrease might be caused by the adhesion of neutrophils to pulmonary capillary walls, and the subsequent increase might be caused by granulocyte colony-stimulating factor mediated by endotoxin. However, there was no relationship between the degree of focal hepatocellular necrosis and the number of neutrophils sticking to the walls of hepatic sinusoids or the changes in the neutrophil count in the peripheral blood. The number of platelets in the peripheral blood decreased rapidly after endotoxin injection. There was a statistically significant relationship between the number of platelets in the peripheral blood and the level of serum transaminase activity: the fewer the platelets, the more severe was focal hepatocellular necrosis. The present study suggests that rapid and extensive consumption of platelets, rather than neutrophils sticking to the sinusoidal walls, is involved in the pathogenesis of focal hepatocellular necrosis in endotoxaemia.

Animals↗
PubMed1995

Comparative effects of losartan, captopril, and enalapril on murine acute myocarditis due to encephalomyocarditis virus.

Losartan, a recently developed nonpeptide angiotensin II (AII) receptor antagonist, was orally administered for 14 days to mice with viral myocarditis, beginning 7 days after encephalomyocarditis virus inoculation. The angiotensin-converting enzyme inhibitors (ACEI) captopril and enalapril were also administered in the same manner to compare the therapeutic effects of these three drugs on the degree of myocarditis, acute heart failure, and left ventricular (LV) hypertrophy. Heart weight and the heart weight/body weight ratio were reduced by losartan (60 mg/kg/day) and captopril (7.5 mg/kg/day), but not by enalapril (1 mg/kg/day). LV wall thickness and cavity dimension were decreased in the losartan and captopril groups. Captopril reduced both myocardial necrosis and inflammation, whereas enalapril reduced myocardial necrosis but not inflammation. However, none of the studied losartan doses (1.2, 12, 60 mg/kg/day) influenced myocardial necrosis and inflammation resulting from viral infection. Thus, specific blockade of AII is beneficial in congestive heart failure (CHF) and LV hypertrophy but is not effective in viral-evoked inflammation and injury.

Acute Disease↗
PubMed1995

Blood pressure control during surgical operations.

In order to reduce intraoperative blood loss and spare blood transfusion, we developed a blood pressure control system using a state-predictive controller. Using adult mongrel dogs, the mean arterial pressure (MAP) was recorded from a femoral artery while trimethaphan camsilate was infused at constant rates. A pure delay plus a first-order delay model was then derived from the dose-response curves and the values of plant parameters (gain, time-constant, dead-time, and so on) were estimated based on the experimental data. For this model, a state-predictive servo system was designed to cope with the pure delay existing in the model, and simulated. In order to evaluate the accuracy and reliability of this system, we experimented on dogs. With a reference MAP set at 60 mmHg, the MAP reached the reference level in 5.8 to 26.5 min. The duration of error from the reference MAP (+/- 10%) was 2.3 +/- 3.9 min/h (n = 7). These results indicated the safety and stability of our system.

Animals↗
PubMed1995

Modulation of protein kinase C produces glucose-dependent alterations in hemodynamics and metabolism in the perfused liver in fasted rats.

Protein kinase C (PKC) has been suggested to be involved in the regulation of hepatic blood flow and metabolism. To confirm the role of PKC, we studied the effects of active and inactive PKC modulators on hemodynamics and metabolism in the perfused rat liver. In addition, the influence of glucose concentration in the medium was studied. The liver was isolated from fasted Sprague-Dawley rats and perfused through the portal vein at a constant pressure of 12 cm H2O. 4 alpha-Phorbol 12,13-didecanoate, an inactive phorbol ester for PKC, slightly decreased hepatic flow only when its initial concentration was raised to 20 microM. In contrast, 4 beta-phorbol 12,13-didecanoate, an active phorbol ester for PKC, at initial concentrations of 80 nM to 1.28 microM decreased hepatic flow and oxygen consumption in a dose-dependent manner, and increased lactate production. HA-1004, a relatively inactive PKC inhibitor, at an initial concentration of 33 microM did not modify the effects of phorbol 12-myristate 13-acetate (PMA), a potent PKC activator. However, H-7, a relatively specific PKC inhibitor, at a concentration of 33 microM attenuated the effects of PMA. The effects of PMA were enhanced by an increase in n-glucose concentration from 10 to 25 mM but not by an increase in L-glucose concentration. These results suggest that modulation of PKC exerts glucose-dependent influences on hepatic flow and metabolism.

Animals↗
PubMed1995

Effect of lidocaine injection of EOAE in patients with tinnitus.

In the present study, evoked otoacoustic emissions (EOAEs) were measured in 30 patients with tinnitus before and after intravenous lidocaine injection (1 mg/kg). For EOAE recordings, 1 kHz tone burst stimuli were used. Intravenous lidocaine injection resulted in suppression of tinnitus in 22 (73%) ears, and changes of EOAE amplitude (increase or decrease) in 18 (60%) ears. Of the 18 ears with EOAE amplitude changes, tinnitus disappeared or decreased in 17 (94%) ears. In 12 ears without changes of EOAE amplitude, tinnitus was suppressed in only 5 (42%). Changes in latency were not detected in any of the ears. These results indicate that there is a relationship between the effect of lidocaine in tinnitus suppression and changes in cochlear micromechanics caused by lidocaine.

Acoustic Stimulation↗
PubMed1995

Chronic effect of losartan in a murine model of dilated cardiomyopathy: comparison with captopril.

The long-term effects of losartan, an angiotensin II subtype-I receptor antagonist, were compared with those of captopril in a murine model of dilated cardiomyopathy caused by encephalomyocarditis virus. Four weeks after viral inoculation, 42 DBA/2 mice were given oral losartan 1.2 mg/kg/day (n = 8), 12 mg/kg/day (n = 8) or 60 mg/kg/day (n = 8) or captopril 7.5 mg/kg/day (n = 8) in drinking water or distilled water (n = 10). Mice were killed at the end of the 12-wk treatment period. Heart weight, left ventricular thickness, left ventricular cavity dimension and myocardial fiber diameter were significantly lower in mice given losartan 60 mg/kg as compared with the infected untreated group. Captopril had a similar effect on all parameters. The pathologic score of cardiac fibrosis was significantly lower in the mice treated with captopril but was not reduced in the mice treated with losartan. Moreover, as compared with the age- and sex-matched normal mice, cardiac mass and myocardial fiber diameter were significantly lower in normal mice treated with losartan 60 mg/kg. This study suggests that long-term treatment with losartan may prevent thickening of left ventricular wall and cavity dimension in dilated cardiomyopathy caused by encephalomyocarditis virus. The potency, and perhaps the efficacy, of losartan appear to be less than those of captopril.

Angiotensin Receptor Antagonists↗
PubMed1994

Resistance to the anti-proliferative effect of IL-1 on human melanoma cell line is associated with endogenous production of IL-1 and IL-6.

A human melanoma cell line (A375-6) became resistant to the anti-proliferative effect of human IL-1 after a long period of culture. Two stable resistant sub-clones were obtained, and the mechanism of the IL-1 resistance was investigated. Resistant cells, but not sensitive cells, appeared to produce constitutively IL-1 activity. The activity was neutralized by anti-IL-1 alpha antibody but not by anti-IL-1 beta antibody. Resistant cells expressed IL-1 alpha but not IL-1 beta mRNA. Therefore, the resistant cells appeared to produce IL-1 alpha mRNA for IL-1 receptor antagonist (IL-1Ra) was not detected in resistant cells, indicating that the resistance is not attributable to IL-1Ra. These resistant cells were also resistant to the anti-proliferative effect of human IL-6, but not to that of human TNF. Resistant cells appeared to produce constitutively IL-6 more than sensitive cells, and IL-6 production both in sensitive and in resistant cells was augmented by exogenous IL-1. Furthermore, constitutive production of IL-6 in resistant cells was inhibited by IL-1Ra. Type I IL-1 receptor (IL-1R) mRNA was expressed equally in resistant and sensitive cells. These data indicate that the resistance is not the result of loss of functional IL-1R and that IL-1 induces IL-6 in an autocrine manner. It is, therefore, conceivable that endogenous IL-1 and IL-6 contribute to IL-1 resistance.

Cell Division↗
PubMed1994

Developing rat pineal cells manifest potential of neuronal differentiation in vitro.

The pineal gland in mammals is an endocrine organ and generally does not exhibit neuronal characteristics. However, it is known that under culture conditions, cells from newborn rat pineals express properties characteristic of photoreceptors. Here, we studied the potential of rat pineal cells to differentiate into neuronal cell types using different neural markers. Three phenotype markers characteristic of nerve cells, i.e., intense GABA, neuron-specific antigen (HPC-1) and microtubule-associated protein 2 (MAP2) immunoreactivities, were detected in the pineal culture of newborn rats. Expression of the respective neuronal phenotypes appears to be controlled by different mechanisms; in the normal culture medium containing 5.4 mM KCl, numerous cells were stained intensely with anti-GABA antiserum, whereas only a few were stained intensely either with HPC-1 or MAP2 antibody. In a culture medium with a high concentration of KCl (35 mM), which may induce depolarization of nerve cells, numerous cells became strongly positive for HPC-1 or MAP2; both the cell bodies and the neuritic fibers were stained positively. Since cells intensely immunoreactive to GABA, HPC-1 or MAP2 were not found in intact pineals of the rat, the present results indicate that the neuronal potency of the rat pineal cells is expressed only in vitro and is suppressed in vivo, and that the potency is lost during postnatal development. Norepinephrine at 1 microM, which suppresses differentiation of rhodopsin immunoreactive cells, was ineffective in inducing phenotypic expression of neuronal properties in the present system, indicating that the mechanism of suppression of neuronal properties in the intact pineal may be different from the one for photoreceptors.

Animals↗
PubMed1994

Isoflurane modulates phorbol myristate acetate-, prostaglandin D2-, and prostaglandin E2-induced alterations in hepatic flow and metabolism in the perfused liver in fasted rats.

Protein kinase C (PKC) is thought to play an important role in the regulation of hepatic flow and metabolism in the liver. The activation of PKC has been implicated in pathologic responses of the organisms to immunologically active substances including endotoxin. The effects of volatile anesthetics on the hemodynamic and metabolic alterations associated with PKC activation were studied using isolated liver perfusion. The liver was isolated from overnight-fasted, male Sprague-Dawley rats, and placed in a recirculating perfusion-aeration system. The liver was perfused through the portal vein at a constant pressure of 12 cm H2O. Isoflurane at a concentration of 3% maintained hepatic flow, reduced oxygen consumption, and transiently enhanced lactate production. Phorbol 12-myristate 13-acetate (PMA), a potent activator of PKC, at an initial concentration of 80 nM decreased hepatic flow and oxygen consumption, and enhanced lactate production. Isoflurane significantly attenuated the PMA-induced alterations in hepatic flow, oxygen consumption, and lactate production. A similar inhibition of the PMA-induced alterations was observed in the liver treated with halothane at 2%. Isoflurane attenuated the flow reduction and stabilized the oxygen consumption after the administration of prostaglandin D2 (PGD2) and E2 (PGE2), possible mediators of PMA. Isoflurane, and presumably other volatile anesthetics, may elicit beneficial effects on the liver by attenuating the PKC-mediated alterations in hepatic hemodynamics and metabolism when PKC in the liver is activated through pathologic mechanisms.

Animals↗
PubMed1994

Complete atrioventricular block during left heart catheterization.

A 75-year-old male underwent cardiac catheterization for frequent ventricular premature contractions and reduced left ventricular function. ECG on admission showed complete right bundle branch block (RBBB) and left anterior hemiblock. Right heart catheterization was performed uneventfully, but complete atrioventricular block (CAVB) occurred suddenly when a pig-tail catheter was inserted into the left ventricle. Electrophysiological study identified this CAVB as HV block, and demonstrated HV prolongation in sinus rhythm. The coronary angiogram revealed no obstructive lesion or spasm with ergonovine. The reproducibility of the CAVB was demonstrated. The final CAVB developed and persisted for more than one week, requiring the implantation of a permanent pacemaker (DDD). Complete atrioventricular block induced during left heart catheterization is very rare. Pre-existing RBBB with left anterior or posterior hemiblock and reduced left ventricular function may be common factors in patients with this condition. Emergency pacing equipment should always be on-line when left heart catheterization is conducted in such patients.

Aged↗
PubMed1994

Blood viscosity and plasma viscosity in patients with sudden deafness.

Blood viscosity and plasma viscosity were measured in 51 patients with sudden deafness (SD) and 70 controls with normal hearing. Blood viscosity and plasma viscosity in patients with SD at their first medical examination were significantly higher than in the control group. The difference in viscosimetry results between the two groups was greater at higher shear rates. The data obtained in viscosimetry and pure-tone audiometry were analyzed after dividing the patients into a high viscosity group and a normal viscosity group. The correlation between average hearing level in pure-tone audiogram and blood viscosity or plasma viscosity was positive. The values of the O2-transport capacity of the blood demonstrated a negative correlation with average hearing level in patients with SD before treatment. During the course of treatment, blood viscosity and plasma viscosity decreased with the improvement of hearing impairment. When the distribution of average hearing level was 40 to 79 dB, a few of the patients with "recovery" or "good improvement" and most of patients with "fair improvement" or "no change" belonged to the low viscosity group. And, most of the patients with flat type hearing impairment and a few patients with high tone type hearing impairment belonged to the high viscosity group. These results suggest that many patients with SD have increased blood viscosity and plasma viscosity, and that this increase may play a significant role in the etiology of SD. There are also some differences in etiologic factors concerning type of hearing impairment and prognosis. In conclusion, the present study points to the importance of measuring blood viscosity and plasma viscosity in patients with SD, since blood and/or plasma viscosity may be involved in its etiology and prognosis.

Adult↗