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Biomedical subjects

M Arai

Publications and source records attributed to M Arai.

At least 397 records · Page 22Linked to original sources
PubMed1993

In vivo and in vitro study of the effects of chlorpromazine on tooth mineralization in rats and mice.

The effects of chlorpromazine (CPZ) on tooth mineralization were examined using incisor dentine in adult rats and cultured tooth germs of mandibular first molars dissected from mouse embryos. CPZ (10, 50 and 250 mg/kg, s.c.) substantially inhibited dentine mineralization as evaluated by contact microradiographs. Plasma calcium and phosphorus concentrations were not decreased by CPZ (10 and 50 mg/kg). Physicochemical effects were not involved in the action of CPZ on the mineralization. In vitro experiments showed that CPZ (1 and 10 microM) inhibited mineralization and alkaline phosphatase (ALP) activity in the tooth germs. As CPZ has the properties of a calmodulin antagonist, the calmodulin antagonists W-7 and W-5 were also examined. Both inhibited mineralization and ALP activity in tooth germs; W-5 had less effect than W-7. These in vivo and in vitro findings suggest that CPZ inhibited cell-mediated mineralization in dentine without affecting the calcium-regulating system and physicochemical mineral deposition. In addition, calmodulin could be involved in cell-mediated mineralization.

Alkaline Phosphatase↗
PubMed1993

Sinusoidal endothelial cell damage by activated macrophages in rat liver necrosis.

BACKGROUND: Massive hepatic necrosis caused by fibrin deposition in the hepatic sinusoids develops with hepatic macrophage activation in rats given endotoxin after administration of heat-killed Corynebacterium parvum. Targeted cells of such macrophages were investigated. METHODS: In C. parvum-treated rats, the pathological appearance of liver cells was serially measured in serum following endotoxin administration and compared with the appearance in the perfusate during closed liver perfusion with endotoxin. RESULTS: Serum activities of tumor necrosis factor, purine nucleoside phosphorylase present in both hepatocytes and sinusoidal endothelial cells, and levels of alanine aminotransferase were higher after 30 minutes, 1 hour, and 3 hours, respectively. Pretreatment of rats with gadolinium chloride, an inhibitor of macrophage function, reduced this liver injury. Although alanine aminotransferase activity remained almost unchanged in the liver perfusate, purine nucleoside phosphorylase activity increased. This increase was reduced when rats were pretreated with gadolinium chloride. There was sinusoidal endothelial cell damage around hepatic macrophages in the liver perfused with endotoxin. CONCLUSIONS: Activated hepatic macrophages may cause sinusoidal endothelial cell damage leading to hepatocyte necrosis in rats given C. parvum and endotoxin.

Alanine Transaminase↗
PubMed1993

Steroidogenesis in isolated adrenocortical cells during development in rats.

After postnatal day 1 (d1), the hypothalamo-pituitary-adrenal axis of neonatal rats becomes less responsive to certain stimuli for up to 2 weeks. The present study was designed to quantify the development of adrenocortical cell responsiveness to its normal secretagogue, adrenocorticotropic hormone (ACTH), and to better localize intracellular sites of adrenal cell hyporesponsivity. Maximum steroidogenic responses of collagenase-dispersed adrenocortical cells (using two isolation methods) to ACTH varied significantly in the order adult > d1 > d10. The response pattern to dibutyryl cAMP ((Bu)2cAMP) was identical to that observed for ACTH (adult > d1 > d10), suggesting that neonatal adrenal responsiveness is limited by a site distal to cAMP formation. Sensitivity (EC50) of adult cells to ACTH was approximately 3-fold greater than in neonatal cells, but there was no age-dependent shift in sensitivity to (Bu)2cAMP. 20 alpha-Hydroxycholesterol (20 alpha-OHCHOL), a membrane permeable analog of cholesterol, also failed to normalize the d10 adrenal response to ACTH. This result indicates that one site of refractoriness is apparently distal to cholesterol transport, and strongly suggests possible differential cytochrome P450 enzyme expression or activity in neonatal rat adrenal cells. Finally, although stimulated secretion was lower in neonatal cells, basal corticosterone secretion was significantly greater in neonatal adrenals, suggesting that constitutive activity of neonatal adrenal cells is high compared to that of adult cells.

Adrenal Cortex↗
PubMed1993

Alteration of in vitro bone metabolism and tooth formation by zinc.

1. The effects of zinc on bone metabolism and tooth formation was examined in organ cultures of calvaria and tooth germ, and in cell cultures of osteoblast-like cells, MC3T3-E1. 2. Treatment of calvaria with zinc (10, 100 microM) for 4 days both increased alkaline phosphatase (ALP) activity in bone and reduced the secretion of N-acetyl beta-glucosaminidase from bone, without affecting bone mineral or collagen content. The increase in ALP activity produced by zinc (10 microM) was inhibited neither by actinomycin D (5 micrograms/ml) nor by cycloheximide (0.5 micrograms/ml). 3. Treatment of MC3T3-E1 cells with zinc (50, 100 microM) for 25 days also increased ALP activity, but reduced calcium content in cells and in the matrix layer. 4. These results indicate that zinc increases ALP activity in osteoblasts without affecting de novo enzyme synthesis, and that it inhibits bone mineralization, in accordance with the inhibition of osteoclastic activity. 5. Treatment of tooth germ with zinc (100 microM) for 7 days also produced an increase in ALP activity and inhibition of mineralization. These results indicate that the increased ALP activity produced by zinc is a common phenomenon in hard tissues, and, further, that zinc inhibits mineralization during tissue formation.

Acetylglucosaminidase↗
PubMed1993

Myocardial atrial natriuretic factor gene expression after coronary ligation in rats.

The atrial natriuretic factor (ANF) messenger RNA (mRNA) content was determined in a rat model of acute myocardial infarction. Non-infarcted tissue of left and right ventricles were examined soon after ligation of the left descending anterior coronary artery. In the left ventricles, ANF mRNA/alpha-actin mRNA ratio increased to reach a maximum on day 7 and was sustained while in the right ventricle, the maximum was reached on day 1. The plasma ANF was significantly (p < 0.01) elevated from days 1 to 28 after coronary ligation. The primary compensatory response of ANF within the first 7 days may be attributed not only its synthesis in the left ventricle but also to its generation in the right ventricle in acute heart failure.

Actins↗
PubMed1993

Iodine regulation of endothelin-1 gene expression in cultured porcine thyroid cells: possible involvement in autoregulation of the thyroid.

We studied the regulation of endothelin (ET)-1 gene expression in porcine thyroid cells in culture. First, we demonstrated prepro-ET-1 mRNA in porcine thyroid cells. The level of the mRNA was increased by phorbol 12-myristate 13-acetate (TPA), a protein kinase C stimulator, but was decreased by TSH (1 mU/mL). However, transforming growth factor-beta and interleukin-1 beta had no effect. The amount of immunoreactive (ir)-ET-1 secreted from the cells was also increased by TPA and was decreased by TSH. Next, we studied the effect of iodide, as iodide has various effects on thyroid cells. NaI (100 microM) increased the prepro-ET-1 mRNA level. The effect of NaI was attenuated by 1 mM methimazole (MMl). The amount of ir-ET-1 released from the cells was also increased by the NaI treatment and the increase was also attenuated by MMl. These observations indicate that ET-1 gene expression is induced by organified iodine compounds in thyroid cells in a manner very similar to the inhibitory actions of iodide on thyroid cell function. The protein synthesis inhibitor, cycloheximide, superinduced prepro-ET-1 mRNA within 4 h, but NaI did not. The difference between cycloheximide and NaI suggests that the iodine effect on the gene expression is not due to nonspecific inhibition of protein synthesis. Together with our previous findings that porcine thyroid cells have ET-1 receptors and that ET-1 modulates iodine metabolism, we speculate that ET-1 produced by thyroid cells is involved in thyroid autoregulation including thyroid blood flow.

Animals↗
PubMed1993

A 3-year follow-up study of ocular hypertension by pattern electroretinogram.

A 3-year following-up study of the pattern electroretinogram (PERG) was performed in 15 eyes of 8 ocular hypertensive (OHT) patients. At first PERG recording, the amplitude of the first positive wave P1 was statistically significantly reduced in the OHT patients compared with age-matched controls (p < 0.05). There was no difference in the amplitude of the second negative wave N2 (p > 0.05). At 40 months, the amplitude of both P1 and N2 decreased and the latency of P1 was elongated. Among the changes, the decrease in N2 amplitude was the most drastic (p = 0.0001 compared with the control, p < 0.05, compared with the first recording). Glaucomatous visual field defects developed 5 years after the first PERG recording and 2 years after the reduction in N2 amplitude in 1 patient. Decreased N2 amplitude of the PERG may be an important warning sign predicting the development of glaucoma in OHT patients.

Adult↗
PubMed1993

Alterations in sarcoplasmic reticulum gene expression in human heart failure. A possible mechanism for alterations in systolic and diastolic properties of the failing myocardium.

Recent studies have shown that intracellular Ca2+ handling is abnormal in the myocardium of patients with end-stage heart failure. Muscles from the failing hearts showed a prolonged Ca2+ transient and a diminished capacity to restore a low resting Ca2+ level during diastole. Accordingly, we examined whether this defect in Ca2+ transport function is due to alterations in sarcoplasmic reticulum gene expression. We determined the messenger RNA (mRNA) levels of sarcoplasmic reticulum Ca2+ transport proteins in failing human hearts from 17 cardiac transplant recipients with a diagnosis of dilated cardiomyopathy, primary pulmonary hypertension, or ischemic heart disease. The expression levels of each mRNA were compared with each other and then correlated with that of atrial natriuretic factor (ANF) mRNA in the failing ventricle. The mRNA levels for the calcium release channel (ryanodine receptor, RYR2), Ca2+ uptake pump (Ca(2+)-ATPase, SERCA2 isoform), and phospholamban differed significantly between heart samples but showed an inverse relation with that of ventricular ANF mRNA. In contrast, calsequestrin mRNA levels remained unchanged in these failing hearts. In addition, beta-myosin and alpha-cardiac actin mRNA levels also showed an inverse relation with ANF mRNA levels. These changes were observed in both right and left ventricles of hearts with congestive heart failure due to dilated cardiomyopathy, primary pulmonary hypertension, or ischemic heart disease. The results are consistent with the hypothesis that abnormal calcium handling in the sarcoplasmic reticulum of failing hearts is due to the altered expression of the genes encoding sarcoplasmic reticulum proteins.

Adolescent↗
PubMed1993

Troponin I gene expression during human cardiac development and in end-stage heart failure.

Recent reports have demonstrated the presence of two isoforms of troponin I in the human fetal heart, namely, cardiac troponin I and slow skeletal muscle troponin I. Structural and physiological considerations indicate that these isoforms would confer differing contractile properties on the myocardium, particularly on the phosphorylation-mediated regulation of contractility by adrenergic agonists. We have investigated the developmental expression of these isoforms in the human heart from 9 weeks of gestation to 9 months of postnatal life, using Western blots revealed with troponin I antibodies to detect troponin protein isoforms and Northern blots to detect the corresponding mRNAs. The results show the following: 1) Slow skeletal muscle troponin I is the predominant isoform throughout fetal life. 2) After birth, the slow skeletal isoform is lost, with cardiac troponin I being the only isoform detectable by 9 months of postnatal development. 3) The protein isoforms and their corresponding mRNAs follow the same pattern of accumulation, suggesting that the transition in troponin expression is regulated at the level of gene transcription. The developmental transition in troponin I isoform content has implications for contractility of the fetal and postnatal myocardium. We further analyzed right and left ventricular muscle samples from 17 hearts in end-stage heart failure resulting from pulmonary hypertension, ischemic heart disease, or dilated cardiomyopathy. Cardiac troponin I mRNA remained abundant in each case, and slow skeletal muscle troponin I mRNA was not detectable in any of sample. We conclude that alterations in troponin I isoform content do not therefore contribute to the altered contractile characteristics of the adult failing ventricle.

Adolescent↗
PubMed1993

Molecular cloning and expression of proteinaceous alpha-amylase inhibitor gene from Streptomyces nitrosporeus in Escherichia coli.

The proteinaceous alpha-amylase inhibitor, T-76, gene was cloned by screening a Streptomyces nitrosporeus genomic library using a deoxyinosine-containing probe corresponding to the amino acid sequence of the inhibitor. The nucleotide sequence of the insert of a positive clone had an open reading frame of 330 bp that encoded a polypeptide of 110 amino acid residues with a calculated molecular mass of 11,306 daltons. The polypeptide begins with proximal basic amino acids and a region rich in hydrophobic amino acids that possibly act as a signal peptide for secretion, which is followed by a sequence consistent with the amino-terminal amino acid sequence of the T-76 inhibitor. Escherichia coli cells harboring the plasmid derivatives for expression produced the inhibitor in their periplasmic space. The amino-terminal sequence of the inhibitor produced by an E. coli transformant was identical to that of the T-76 inhibitor secreted by S. nitrosporeus. The amino acid sequence of the inhibitor deduced from nucleotide sequence showed significant homology to other proteinaceous alpha-amylase inhibitors.

Amino Acid Sequence↗
PubMed1993

Synthesis of 2-deoxy-2-[(2R,3S)-2-fluoro-3-hydroxytetradecanamido]- 3-O-[(3R)-3-hydroxytetradecanoyl]-4-O-phosphono-D-glucopyranose and its (2S,3R)-isomer.

2-Deoxy-2-[(2R,3S)-2-fluoro-3-hydroxytetradecanamido]-3-O-[( 3R)-3-hydroxytetradecanoyl]-4-O-phosphono-D-glucopyranose and its (2S,3R)-isomer were respectively synthesized from allyl 2-[(2R,3S)-3-(benzyloxycarbonyloxy)-2-fluorotetradecanamido] -2-deoxy-4,6-O-isopropylidene-beta-D-glucopyranoside and its corresponding (2S,3R)-isomer. Both target compounds did not activate macrophage, but the (2S,3R)-analogue strongly inhibited the binding of LPS to macrophage.

Carbohydrate Sequence↗
PubMed1993

Expression of the cellulase (FI-CMCase) gene of Aspergillus aculeatus in Escherichia coli.

FI-CMCase cDNA of Aspergillus aculeatus was expressed in Escherichia coli by using the tac promoter of E. coli. Transformants of E. coli harboring a plasmid pHEM06 containing mature form FI-CMCase cDNA produced FI-CMCase in the cytoplasm of the cells. The enzyme from E. coli cells was purified to yield 56% and it was immunological identical to that of FI-CMCase purified from A. aculeatus.

Amino Acid Sequence↗
PubMed1993

Mononeuropathy multiplex with ulcerative colitis.

We describe acute mononeuropathy multiplex in a patient with chronic ulcerative colitis. The symptoms of neuropathy were well correlated with the disease activity of colitis. Both electrophysiological study and sural nerve biopsy revealed axonal degeneration. Mononeuropathy multiplex may be an extraintestinal manifestation of ulcerative colitis.

Adult↗
PubMed1993

[Evoked otoacoustic emissions: a comparison between responses from humans and guinea pigs].

Transiently evoked otoacoustic emissions (TEOAEs) from 16 normal human ears and 26 normal guinea pig ears were measured with the ILO 88 (ver 3.91). The following results were obtained: 1) In one animal ear, waveforms of TEOAEs were unchanged after administration of muscle relaxants, and showed reversible changes before and after asphyxia. 2) In 3 guinea pig and 2 human ears, the input-output functions showed a strong saturation at higher stimulus levels, when measurement of the highest peak-to-peak amplitude was used as the output energy. 3) Highest peak frequencies (HPFs) of TEOAEs were distributed at around 1 kHz in human ears but were concentrated around frequencies of 2 kHz to 3 kHz in almost all guinea pig ears. 4) Latencies of predominant TEOAEs in human and guinea pig ears were 9.26 +/- 1.89 msec and 2.37 +/- 0.47 msec, respectively. Endpoint times of TEOAEs were 16.37 +/- 1.79 msec and 5.74 +/- 1.10 msec, respectively. Both indicators in human ears were 3-4 times longer than those in guinea pig ears. From these results, we conclude that click-evoked TEOAEs can be detected even in guinea pigs. In addition, our measurements showed that HPFs of TEOAEs in guinea pig ears were higher than those in human ears, and that latencies and durations in guinea pig ears were much shorter than those in human ears. The higher HPFs of TEOAEs in guinea pig ears may be attributable to higher resonant frequencies in the middle ear than are found in human ears.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

[Significance of serum neuron-specific enolase levels after head injury].

Enolase is an enzyme involved in glycolysis and neurospecific enolase (NSE) has two types of isoenzyme (alpha gamma and gamma gamma enolase). Found in nerve cells and axons, the NSE is reported to be released into the serum and cerebrospinal fluid following nerve injury. We recently analyzed serum NSE levels in 47 patients with solitary head injury who were transported to our center immediately after injury. There were 35 men and 12 women, with a mean age of 35.1 years. In each case, blood was sampled within 8 hours after injury. Serum NSE was measured and analyzed in relation to the level of consciousness (Japan Coma Scale) upon admission, the modified Araki's classification, the presence or absence of skull fracture, findings from computed tomography (CT) scans and the prognosis according to the Glasgow outcome scale. Differences were compared by t-test to determine significance. When the level of consciousness was compared with the serum NSE level upon admission, the NSE level was significantly higher in patients showing a three digit code disturbance of consciousness than in the other patients (p < 0.005). When NSE was analyzed in relation to the modified Araki's classification, the NSE level for the prolonged type with focal signs was higher than the NSE level for any other type (p < 0.001 compared to the transient type). The NSE level was significantly higher in patients with skull fracture than in patients without skull fracture (p < 0.01). The NSE level was significantly higher in patients showing contusion on CT scans than in patients without contusion (p < 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗