Four highly polymorphic dinucleotide microsatellites in rainbow trout (Oncorhynchus mykiss).
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Biomedical subjects
Publications and source records attributed to N Okamoto.
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We retrospectively studied 3 patients with Kawasaki disease (KD) and acute myocardial infarction (AMI) who were treated with intracoronary administration of tissue-type plasminogen activator (t-PA). Two-dimensional echocardiogram on the next day of the treatment revealed reduction of thrombus and improvement of the cardiac function in all 3 patients. However, a 12-month-old patient treated with 200,000 U/kg of t-PA at 48 h after the onset of AMI died of recurrent myocardial infarction. The other 2 patients treated with 400,000 and 800,000 U/kg, respectively, showed clear, though not prompt, improvement in clinical symptoms and laboratory data. The intracoronary thrombolytic therapy using high-dose t-PA appears effective in treating AMI associated with KD.
BACKGROUND: Serous cystadenoma of the pancreas is generally considered as having no malignant potential. Thus, of clinical importance is a differential diagnosis of this neoplasm from other solid tumors that are often malignant. RESULTS: We report a case of microcystic serous cystadenoma of the pancreas. Abdominal ultrasonography, computed tomography, and endoscopic ultrasonography showed a solid mass in the body of the pancreas with a diameter of 15 mm, but magnetic resonance imaging revealed it as a unilocular cystic lesion. Histological examinations on the surgically resected tissue specimen showed a honeycombed tumor with innumerable tiny cysts appearing grossly as a solid mass. The discrepant finding between magnetic resonance imaging and other imaging modalities observed in this case is suggestive of and might be specific to microcystic serous cystadenoma of the pancreas. CONCLUSIONS: Magnetic resonance imaging is a mandatory modality to identify pancreatic serous cystadenoma that contains no visible cystic compartments on computed tomography and ultrasonography.
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PURPOSE: To determine the relative level and localization of bone morphogenetic protein (BMP-4 mRNA in the retina and retinal pigmented epithelium (RPE) under normal and pathologic conditions, to seek clues regarding possible functions. METHODS: Clones isolated from an RPE cDNA library were sequenced and used as probes for northern blot analysis. Expression in the retina and RPE was investigated in mouse models using reverse transcription-polymerase chain reaction (RT-PCR) and in situ hybridization. The effect of recombinant proteins on RPE proliferation was investigated by thymidine incorporation. RESULTS: Bovine clones with high homology to BMP-2 and BMP4 were isolated from a subtracted RPE cDNA library. Northern blot analysis using the clones as probes demonstrated abundant and differential expression in adult bovine RPE, but with RT-PCR and in situ hybridization, expression was also demonstrated in mouse retinal neurons. In mice with oxygen-induced ischemic retinopathy there was a striking decrease in BMP-4 mRNA in the retina within 6 hours of the onset of hypoxia that was maintained for at least 5 days. In mice with inherited photoreceptor degeneration, there was a dramatic decrease in BMP4 mRNA in retina and RPE during and after the degeneration. mRNA for the type II BMP receptor was observed in freshly isolated and cultured RPE cells, isolated retina, and freshly isolated bovine aortic endothelial cells. Thymidine incorporation in early-passage RPE cells showed a 14-fold stimulation above control with 5% serum that was decreased to 322%, 393%, and 313% in the presence of BMP-2 (10 ng/ml), BMP4 (10 ng/ml), and transforming growth factor (TGF)-,1 (2 ng/ml), respectively. CONCLUSIONS: BMP-2 and BMP-4 may serve as negative growth regulators in the retina and RPE that are downregulated by injury, to allow tissue repair. Modulation of expression of the BMPs may provide a means to control the exaggerated wound repair that occurs in proliferative retinopathies.
PURPOSE: Vascular endothelial growth factor (VEGF) is upregulated by hypoxia and is a major stimulatory factor for retinal neovascularization in ischemic retinopathies such as diabetic retinopathy. This study sought to determine if VEGF is a stimulatory factor in a murine model of choroidal neovascularization (CNV). METHODS: Mice with laser-induced ruptures in Bruch's membrane were treated with vehicle alone; a drug that inhibits both VEGF and platelet-derived growth factor (PDGF) receptor kinases; a drug that inhibits PDGF, but not VEGF receptor kinase; or genistein, a nonspecific kinase inhibitor. After two weeks, CNV was quantified and compared. RESULTS: Blockade of phosphorylation by VEGF and PDGF receptors caused dramatic, almost complete inhibition of CNV. Genistein also had an inhibitory effect, but less so than the VEGF/PDGF receptor blocker. Blockade of phosphorylation by PDGF receptors, but not VEGF receptors, had no significant effect on CNV. CONCLUSIONS: These data and our previous study, which demonstrated that a kinase inhibitor that blocks VEGF and PDGF receptors and several isoforms of protein kinase C causing dramatic inhibition of CNV, suggest that VEGF signaling plays a critical role in the development of CNV in this model. If safety is established, the effect of inhibiting VEGF receptor kinase activity should be investigated in patients with CNV.
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PURPOSE: To detect mutations in the RDH5 gene encoding 11-cis retinol dehydrogenase in patients from Japan with fundus albipunctatus. METHODS: Polymerase chain reaction and direct genomic sequencing techniques were used to detect mutations of the RDH5 coding exons (exons 2-5) in two unrelated patients with fundus albipunctatus. Selected alleles that altered the coding region or intron splice sites were evaluated further through segregation analysis in the families of the index cases. RESULTS: Two novel RDH5 mutations were identified. One of these was a missense mutation Val264Gly in exon 5, and the other was an in-frame insertion of 3 bp in exon 5. CONCLUSIONS: The data indicate that mutations in RDH5 are the primary cause of fundus albipunctatus.
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Moist pleurisy in patients with Mycobacterium avium Complex (MAC) is rarer than tuberculosis. We encountered an extremely rare case of MAC disease in a 75-year-old man who initially had only right pleural effusion. Gaffky VII was detected in the pleural effusion, and Mycobacterium avium was identified by culture and PCR. Although administration of antitubercular agents (RFP, INH, EB, and SM) + CAM and thoracic lavage were repeated, the Gaffky persisted strongly. Accordingly, pulmonary decortication and filling of the cavity with an omental flap were performed as surgical treatments. However, fistulas were formed between the remaining empyema cavity and the surgical wounds. Fenestration was also carried out. Postoperatively, centriacinar abnormalities appeared on computed tomography (CT). It has been reported that MAC disease begins with centriacinar abnormalities and the incidence of the lymphatic developmental pattern was low. Tuberculosis (the idiopathic pleuritis type) is considered to be caused this pattern from the primary infection focus. Therefore, the onset of unilateral effusion is extremely rare in patient with MAC disease, suggesting that the lymphatic developmental pattern occurs less frequently in patients with MAC disease. Furthermore, in this case, we speculated that centriacinar abnormalities were the MAC infection foci and could be detected by CT due to surgical invasion.
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BACKGROUND: Many studies have demonstrated in animal experiments that persistent inflammation may accelerate the development of carcinoma. In this article, the question of whether the persistent elevation of serum alanine aminotransferase (ALT) levels (which represents the inflammatory necrosis of hepatocytes) correlates with the development of hepatocellular carcinoma (HCC) was studied in patients with early stage hepatitis C virus (HCV)-associated cirrhosis. METHODS: Sixty-nine consecutive patients with biopsy proven HCV-associated cirrhosis (mostly Child's Stage A) who had been followed for >5 years for the development of HCC were studied. They were subdivided into 3 groups according to their serum ALT levels: Group A was comprised of 28 patients whose annual average serum ALT level was persistently high (>/= 80 IU) (high ALT group), Group B was comprised of 28 patients whose annual average serum ALT level was persistently low (< 80 IU) (low ALT group), and Group C was comprised of 13 unclassified patients. The patients had been studied prospectively with frequent ultrasonography and magnetic resonance imaging or computed tomography for > 5 years. RESULTS: In the high ALT group HCC developed in 71.4% of patients compared with 25.0% in the low ALT group over the observation period (P < 0.005). The 5-year rate of incidence of HCC in the high ALT group was as high as 53.6% compared with only 7.1% in the low ALT group (P < 0.001). The expected interval between the diagnosis of cirrhosis and the development of HCC was 6.0 +/- 0.7 years (mean +/- standard error) in the high ALT group and 12.7 +/- 1.2 years in the low ALT group (P < 0.001). CONCLUSIONS: The results of the current study demonstrated that the development of HCC was more rapid in the high ALT group with HCV-associated cirrhosis.
A monoclonal antibody (MAb) specific for rainbow trout thrombocytes was produced and its reactivity was demonstrated by flow cytometry and immuno-electron microscopy. Flow cytometry analysis showed that this MAb (TTL-7D11) reacted positively with about 30% of the peripheral blood leucocytes (PBL) and about 1%, 2%, and 11% of the pronephros, mesonephros, and spleen cells, respectively. Electron microscopy using immunogold labeling demonstrated that this MAb reacted strongly with thrombocytes, where gold beads could be seen attached only to the membrane and canalicular system of these cells. Positive and negative leucocytes for this MAb were obtained by magnetic cell separation. In the positive fraction, 96% of the cells were thrombocytes, while in the negative fraction no more than 3% were, which clearly showed a high purity of the positive fraction. Aggregation studies showed that about 75% of the positive fraction cells aggregated after being mixed with U-46619 thromboxane-mimetic, whereas in the negative fraction only 10% of the cells did so. Thus, utilizing the TTL-7D11 we have succeeded in isolating a pure thrombocyte population, and this would facilitate further studies, particularly on their characteristics and function(s).
BACKGROUND: Several studies have suggested that patients with dementia experience a deterioration of biological rhythms. We investigated the daily profile of serum melatonin levels in patients with dementia of the Alzheimer's type (AD), since daily melatonin rhythm is thought to reflect the functioning of the biological clock. METHODS: Seventeen inpatients with AD, 10 psychiatric inpatients without dementia, and 11 elderly healthy volunteers participated in this study. Serum melatonin was assessed every 3 hours by radioimmunoassay. RESULTS: A daily fluctuation of melatonin levels with a significant nocturnal increase was observed in all three subject groups. However, both the AD patients and psychiatric patients without dementia showed significantly higher levels of melatonin in the daytime compared with the healthy subjects. When the effect of bright light exposure on melatonin secretion was investigated in six AD patients and five psychiatric patients without dementia, the daytime levels were markedly decreased in the patients without dementia, while no change was observed in the AD patients. CONCLUSIONS: The high levels of melatonin in the daytime associated with a lack of response to light exposure in AD patients may be due to the neurodegenerative process of this disease.