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Biomedical subjects

H Inoue

Publications and source records attributed to H Inoue.

At least 667 records · Page 37Linked to original sources
PubMed1998

[Treatment with beta-blockers in patients with acute coronary syndrome].

The effects of beta-blockers on acute myocardial infarction can be divided into those that are immediate and long-term (secondary prevention). beta-blockers given early in the course of infarction may diminish myocardial oxygen demand and therefore reduce chest pain and infarct size. Many clinical trials have clearly shown that both early and long-term treatment with beta-blockers reduce cardiac mortality and the rate of re-infarction. As seen in recommendations of ACC (American College of Cardiology)/AHA (American Heart Association) guidelines for management of acute myocardial infarction, all patients without a contraindication to beta-blockers should be treated with beta-blockers from very early course of the onset and be continued indefinitely.

Acute Disease↗
PubMed1998

[Endoscopic diagnosis of early cancer in the esophagogastric junctional region].

The endoscopic diagnosis of early esophageal and gastric cancers located within 2 cm above and below the esophagogastric junction (EGJ) is discussed. We reviewed 25 cases (10 mucosal cancers and 15 submucosal cancers). Histologically, early cancers frequently appeared as type IIc lesions (16/25: 64%). There was no relationship between tumor size and the depth of invasion of cancer lesions, and most of the lesions were well or moderately differentiated carcinomas. Endoscopically, homogenous redness with a thin white coating, some granular appearance, and easy bleeding were very important factors for the diagnosis of early gastric cancer. For superficial esophageal cancer, differential diagnosis from reflux esophagitis is correctly performed with the endoscopic dye (lugol)-staining method and biopsy. In order not to overlook early cancer at the EGJ, this area should be observed with sufficient air inflation by the U-turn or J-turn method using a frontal-view panendoscope.

Adult↗
PubMed1998

Three cases of primary lung cancer undetected by an annual checkup.

An annual check by chest roentgenogram is very important for the early detection of lung cancer. We present three cases of primary lung cancer which were not detected by the double check system or previous examination. The three patients visited our hospital for evaluation of an ill-defined opacity in the upper lobe of the lung. In the three cases, no abnormality had been reported in the previous year's annual chest X-ray, and we concurred in the decisions. The correct diagnoses of the three cases were well or poorly differentiated adenocarcinoma, and were still amenable for surgical therapy. A poorly defined tumor in this region is very difficult to detect because of superimposed opacities of other anatomical structures. When a questionable shadow in this region is found but without the typical radiological features of lung cancer, it is important to search for indirect indications of adenocarcinoma. These may include fibrotic changes and absence of inflammation. In our cases, the increased number of normal-size bronchi penetrating the ill-defined tumor, seem to have diagnostic significance.

Adenocarcinoma↗
PubMed1998

[Cerebral infarction associated with nephrotic syndrome in a young adult: a case report].

We report a 19-year-old man who developed a cerebral infarction in the territory of the anterior choroidal artery and showed a hypercoagulable state and nephrotic syndrome after diarrhea and appetite loss. He had suffered from nephrotic syndrome from the age of three and had been treated for five years. MR-angiography showed an occlusion originating in the right internal carotid artery. The right anterior and middle cerebral arteries were imaged from the left internal carotid artery via the anterior communication artery. He showed symptoms of left hemiparesis, agnosia, loss of activity, anasarca and left hypacusis following his clinical course, but had recovered from all but left hemiparesis following medical treatments including steroid therapy. The histologic finding by a renal biopsy revealed focal glomerulosclerosis. In this case, we considered that when he was in a hypercoagulable state and had a second attack of nephrotic syndrome because of inflammation and dehydration due to diarrhea and appetite loss, his hypercoagulable state grew worse, and he then developed a cerebral infarction. When one see a patient with nephrotic syndrome, one should be attentive to the possibility of a complication of cerebral infarction.

Adult↗
PubMed1997

Sequence of the FRA3B common fragile region: implications for the mechanism of FHIT deletion.

The hypothesis that chromosomal fragile sites may be "weak links" that result in hot spots for cancer-specific chromosome rearrangements was supported by the discovery that numerous cancer cell homozygous deletions and a familial translocation map within the FHIT gene, which encompasses the common fragile site, FRA3B. Sequence analysis of 276 kb of the FRA3B/FHIT locus and 22 associated cancer cell deletion endpoints shows that this locus is a frequent target of homologous recombination between long interspersed nuclear element sequences resulting in FHIT gene internal deletions, probably as a result of carcinogen-induced damage at FRA3B fragile sites.

Acid Anhydride Hydrolases↗
PubMed1997

Identification of chondromodulin I as a novel endothelial cell growth inhibitor. Purification and its localization in the avascular zone of epiphyseal cartilage.

Cartilage is unique among tissues of mesenchymal origin in that it is resistant to vascular invasion due to an intrinsic angiogenic inhibitor. During endochondral bone formation, however, calcified cartilage formed in the center of the cartilaginous bone rudiment allows vascular invasion, which initiates the replacement of cartilage by bone. The transition of cartilage from the angioresistant to the angiogenic status thus plays a key role in bone formation. However, the molecular basis of this phenotypic transition of cartilage has been obscure. We report here purification of an endothelial cell growth inhibitor from a guanidine extract of bovine epiphyseal cartilage. The N-terminal amino acid sequence indicated that the inhibitor was identical to chondromodulin I (ChM-I), a cartilage-specific growth-modulating factor. Purified ChM-I inhibited DNA synthesis and proliferation of vascular endothelial cells as well as tube morphogenesis in vitro. Expression of ChM-I cDNA in COS7 cells indicated that mature ChM-I molecules were secreted from the cells after post-translational modifications and cleavage from the transmembrane precursor at the predicted processing signal. Recombinant ChM-I stimulated DNA synthesis and proteoglycan synthesis of cultured growth plate chondrocytes, but inhibited tube morphogenesis of endothelial cells. In situ hybridization and immunohistochemical studies indicated that ChM-I is specifically expressed in the avascular zone of cartilage in developing bone, but not present in calcifying cartilage. These results suggest a regulatory role of ChM-I in vascular invasion during endochondral bone formation.

Animals↗
PubMed1997

Identification of an autocrine chondrocyte colony-stimulating factor: chondromodulin-I stimulates the colony formation of growth plate chondrocytes in agarose culture.

Chondrocytes are unique among non-transformed cells in that they are capable of anchorage-independent growth in soft agar. Fibroblast growth factor (FGF) is known as a potent colony-stimulating factor for chondrocytes. However, cartilage extracts contain a potent colony-stimulating activity which is not explicable only by contaminating FGF. We previously isolated the 25 kDa cartilage-specific glycoprotein chondromodulin-I (ChM-I) which stimulates the growth of chondrocytes. In the present study, we observed that ChM-I stimulates the colony formation of rabbit growth plate chondrocytes in agarose culture. ChM-I alone weakly stimulated the formation of chondrocyte colonies, but it markedly stimulated colony formation synergistically in the presence of an optimal dose of FGF-2. This effect was dependent on the dose of ChM-I. These results suggest that ChM-I participates in an autocrine signaling mechanism for the anchorage-independent growth of chondrocytes in vitro.

Animals↗
PubMed1997

Identification of a human LMX1 (LMX1.1)-related gene, LMX1.2: tissue-specific expression and linkage mapping on chromosome 9.

LMX1 is a LIM-homeodomain (LIM-HD)-containing protein expressed selectively in insulin-producing beta-cell lines, and it it has been shown to activate insulin gene transcription. The human LMX1 gene was mapped by fluorescence in situ hybridization to chromosome region 1q22-q23, yet Church et al. (1994, Nat. Genet. 6: 98-105) identified two exon-trapping products from human chromosome 9 that were highly homologous to hamster LMX1. In the current study, we demonstrate tissue-specific expression of an LMX1 (now known as LMX1.1)-related gene, named LMX1.2. The chicken C-LMX1 gene, recently cloned using the hamster LMX1.1 sequence and shown to specify dorsal cell fate during vertebrate limb development (9), is actually more related to human LMX1.2 than LMX1.1. We have identified a unique simple sequence repeat polymorphic marker (hLMX1.2CA1) in a P1 genomic clone containing the human LMX1.2 gene and genetically mapped the marker on chromosome 9 between markers D9S1825 and D9S290 with odds of at least 1000:1. In addition, we localized the human LMX1.1 gene to three CEPH "B" yeast artificial chromosome clones (907A11, 935B12, and 947B2), along with two nearby polymorphic markers (D1S426 and D1S194)). Identification of this new LIM-HD-related gene may provide the opportunity to elucidate further the function of LIM class homeobox genes. Nearby polymorphic markers will be useful in testing the hypothesis that mutations in these LIM-HD genes result in genetic diseases such as non-insulin-dependent diabetes mellitus.

Amino Acid Sequence↗
PubMed1997

Inhibition of human low-density lipoprotein oxidation by flavonoids in red wine and grape juice.

In the presence of red wine or grape juice, low-density lipoprotein was significantly resistant to oxidation; the biological activity of flavonoids, but not ethanol or nonflavonoid phenolic compounds, appeared to contribute to the antioxidant properties of red wine and grape juice. A significant antioxidant activity was also confirmed in low-density lipoprotein from humans after ingesting red wine but not grape juice, suggesting that flavonoids in red wine can be absorbed from the intestine more efficiently than those in grape juice.

Adolescent↗
PubMed1997

Use of high-performance liquid chromatography as an extraction procedure for analysis of triazolam in decomposed human muscle by gas chromatography-mass spectrometry.

A reliable and sensitive method for the determination of triazolam in human muscle using gas chromatography-mass spectrometry (GC-MS) is described. The drug was extracted from decomposed human muscle using three-step liquid-liquid extraction and HPLC which was performed isocratically on a conventional ODS column with a mobile phase of 0.01 M phosphate buffer (pH 6.5)-acetonitrile (7:3). Estazolam was used as an internal standard. GC-MS analysis was performed on a DB-5 capillary column. Excellent linearity was obtained over the concentration range 1-200 ng/g. The lower limit of detection was approximately 0.5 ng/g. Forensic application of the present method was also described.

Chromatography, High Pressure Liquid↗
PubMed1997

High induction of phenol UDP-glucuronosyltransferase in the kidney medulla of beta-naphthoflavone-treated rats.

Phenol UDP-glucuronosyltransferase activity was highly induced in the microsomes of the kidney medulla of rats by beta-naphthoflavone treatment. In the medulla, phenol UDP-glucuronosyltransferase and its mRNA were greatly increased in both immunoblotting and Northern blot analyses following beta-naphthoflavone treatment of the rats. In untreated rat kidneys, phenol UDP-glucuronosyltransferase was detected by immunohistochemical analysis only in proximal convolution tubular cells located in the cortex. After beta-naphthoflavone treatment of the rats, UDP-glucuronosyltransferase appeared in the epithelial cells in the straight portion of the distal tubules located in the medulla. In conclusion, the medullary distal tubular cells have high latent glucuronidation activity and are thought to play an important role in drug excretion.

Animals↗
PubMed1997

Mechanism of mustard oil-induced skin inflammation in mice.

We examined the mechanism of the inflammatory response induced by topical application of mustard oil (0.5-20.0%/20 microliters per ear) to the mouse ear compared to that of the response to capsaicin. The dose-dependent increases in plasma extravasation and ear thickness reached a maximum at approximately 30 min after mustard oil application. Topical pretreatment of ears with capsaicin (250 micrograms/ear) diminished mustard oil-induced plasma extravasation for up to day 7 but not at day 14 after treatment. However, desensitization of the exudative response was not evoked by reapplication of mustard oil to ears. The inflammatory response to mustard oil did not differ between the ears of mast cell-deficient mice and those of the congenic normal mice. Mustard oil-induced plasma extravasation was unaffected by pretreatment with histamine H1 and 5-HT2 receptor antagonists and the capsaicin-functional inhibitor, ruthenium red, which inhibit capsaicin-induced ear oedema. The endopeptidase inhibitor, phosphoramidon, enhanced the ability of mustard oil to increase dye leakage. The tachykinin NK1 receptor antagonist, SR 140333 ((S)1-[2-[3-(3,4-dichlorophenyl)-1-(3-isopropoxyphenylacetyl)pi peridin-3-yl]ethyl]-4-phenyl-1-azoniabicyclo[2.2.2.]octane, chloride), not only inhibited mustard oil-induced plasma extravasation but also blocked the enhancement by phosphoramidon of the response to mustard oil. In contrast, the tachykinin NK2 receptor antagonist, SR 48968 ((S)-N-methyl-N[4-(4-acetylamino-4-phenylpiperidino)-2-(3,4,- dichlorophenyl)butyl]benzamide), and the tachykinin NK3 receptor antagonist, SR 142801 ((S)-(N)-(1-(3-(1-benzoyl-3-(3,4-dichlorophenyl)piperidin-3-yl)pro pyl)-4- phenylpiperidin-4-yl)-N-methylacetamide), had no effect on plasma extravasation. The present results demonstrated that mustard oil induces mouse skin inflammation through a mechanism different from that for capsaicin. Mediators such as histamine and 5-HT from mast cells appear to be minor factors in the response to mustard oil. In addition, evidence supports the assumption that the tachykinin NK1 receptor is involved in this model.

Administration, Topical↗
PubMed1997

Molecular cloning of a novel receptor-type protein tyrosine phosphatase from murine fetal liver.

A cDNA fragment encoding a novel tyrosine phosphatase (PTPase), termed ptpf, was isolated from day 11.5 mouse fetal liver using reverse transcription-polymerase chain reaction (RT-PCR) with degenerate primers. The 5.5-kb cDNA encoding the complete coding region was isolated from an adult mouse kidney cDNA library. This cDNA contained a single open reading frame (ORF) encoding a predicted 1436-amino-acid protein with a molecular mass of 161,150 Da. Sequence analysis revealed that PTPf was homologous to PTPmu and PTPkappa, and a putative receptor-type PTPase. Northern blotting analysis of adult mouse mRNA indicated the existence of four major ptpf transcripts of approximately 10, 6, 3 and 2.7 kb, and these transcripts were expressed in a tissue-specific manner. During embryogenesis, only the 6-kb transcript was detected.

Amino Acid Sequence↗
PubMed1997

Suppression of tumor growth by the 3' untranslated region of mel-18 in 3Y1 cells transformed by the E6 and E7 genes of human papillomavirus type 18.

By introducing a cDNA library derived from rat embryonic fibroblast cells, we isolated several morphologically flat revertants of rat 3Y1 cells transformed by the E6 and E7 genes of human papillomavirus type 18 (HPV18). From one of the revertants, we recovered a 0.2-kb cDNA, N56, that suppresses the tumor growth of the transformed 3Y1 cells irrespective of the expression of the E6 and E7 genes. The nucleotide sequence of the cDNA was shown to be identical to that of the 3' untranslated region of a putative mammalian polycomb group gene, mel-18.

Animals↗
PubMed1997

Retinoids suppress epidermal growth factor-induced transcription of cyclooxygenase-2 in human oral squamous carcinoma cells.

Cyclooxygenase-2 (Cox-2), the inducible form of cyclooxygenase, is up-regulated in tumors and transformed cells. Because this enzyme catalyzes the formation of prostaglandins from arachidonic acid, chemopreventive strategies that suppress its expression could be useful for preventing cancer. We investigated whether retinoids suppressed basal expression of Cox-2 or EGF-mediated induction of Cox-2 in human oral squamous carcinoma cells. Treatment with retinoids [all-trans-retinoic acid (all-trans-RA), 9-cis-RA, 13-cis-RA, and retinyl acetate] suppressed both basal levels of Cox-2 and EGF-mediated induction of Cox-2 protein and synthesis of prostaglandin E2. Retinoids also suppressed the induction of Cox-2 mRNA by EGF. Transient transfection experiments showed that EGF caused about a 100% increase in Cox-2 promoter activity, an effect that was suppressed by retinoids. Levels of epidermal growth factor receptor were unaffected by retinoids. Epidermal growth factor caused a nearly 10-fold increase in mitogen-activated protein kinase activity; this effect was not blocked by retinoids.

Carcinoma, Squamous Cell↗