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  • 1
    ISSN: 1540-8159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Thrombosis of the innominate vein and SVC is a serious complication in patients with pacemakers, inducing puhnonary embolism or SVC syndrome. Venography is the definitive method for its diagnosis; however, it is too invasive for related studies. The purpose of this study was to validate sonography, pulse Doppler, and color flow in detecting noninvasively innominate vein or SVC thrombosis in patients with pacemakers. In 53 patients with pacemakers, the 1 severe SVC stenosis and 18 severe innominate vein stenoses due to thrombosis were diagnosed by digital subtraction angiography. Sonography accurately showed the severe SVC stenosis due to thrombosis, but had limitations on the innominate vein thrombosis. Color flow demonstrated mosaic flow, indicating poststenotic turbulence due to stenosis of the innominate vein and SVC caused by thrombosis in 15 of 16 patients, and pulse Doppler disclosed absence of flow due to complete occlusion of the innominate vein in 2 of 2 patients. Sensitivity and specificity for detecting severe innominate vein stenosis due to thrombosis using combined color flow and pulse Doppler was 94% and 100%, respectively. In conclusion, sonography, pulse Doppler, and color flow allow accurate detection of severe innominate vein or SVC stenosis due to thrombosis, and are therefore useful for the follow-up of patients with a pacemaker.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Dental traumatology 6 (1990), S. 0 
    ISSN: 1600-0595
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract The development of an experimental model in which a standardized traumatic injury is given to dental tissues of experimental animals is necessary to understand the tissue reactions of luxated human teeth. In this study we contrived a rat molar luxation device by which bilateral upper first molars are pushed horizontally toward the palate to cause a constant amount of dislocation. The pushing force is controlled with regard to strength, direction and duration. Using this device, molars of 3-week-old Wistar rats weighing 45-60 g were luxated, and damage to the pulps and periodontal tissues was evaluated histologically. Every luxated tooth had approximately equal hemorrhage, cell degeneration, and irregularity of periodontal fibers in the palatal cervical region. In the buccal cervical and in the bifurcation regions, the periodontium suffered edema and hemorrhage. The periodontal fibers in these regions were elongated and, in some areas, torn. Periodontal hemorrhage was also observed at the distobuccal root apex. The severity and distribution of the tissue injury were nearly equal in almost all of the molars. Few alveolar bone fractures or root fractures were observed. From these results, it is concluded that a standardized luxational trauma can be delivered to rat molars by the use of this experimental method.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1437-9813
    Keywords: Extracorporeal membrane oxygenation (ECMO) ; Artificial pulmonary surfactant
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Extracorporeal membrane oxygenation (ECMO) is gaining widespread acceptance as a therapy for newborns with severe respiratory distress. However, in some cases with pulmonary opacification or air-bronchograms on chest radiograph during ECMO, pulmonary function does not readily improve despite successful ECMO practice. We applied artificial pulmonary surfactant in two such cases. The effect was remarkable, and successful weaning from ECMO could be achieved. It appears likely that alveolar collapse due to deficient pulmonary surfactant is one cause of abnormal pulmonary shadows on chest radiographs and delayed resolution of pulmonary function during ECMO.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-0843
    Keywords: Key words Monoclonal antibody ; A33 ; Gastric cancer ; Immunohistochemistry ; Tumor targeting
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Murine monoclonal antibody A33 (mA33) was developed by the Memorial Sloan-Kettering Cancer Center and by the New York Branch of the Ludwig Institute for Cancer Research. It is an immunoglobulin (Ig)G2a antibody that detects a protease- and neuraminidase-resistant, periodate-sensitive epitope. Serological analysis of the antigen showed that it is expressed in a few colorectal cancer cell lines and a pancreatic cancer cell line, but is basically not reactive with other types of cell line. Normal fibroblasts and normal kidney cell lines reacted negatively to mA33. Immunohistochemical study of normal tissues identified the large and small intestinal mucosa as the principal site of A33 expression. Tests in tumor samples demonstrated that only tumors of the gastrointestinal tract are consistently A33 positive. A33 is found in 95% of primary and metastatic colorectal cancers, with uniform expression throughout the tumors in most cases. A33 is also detected in 63% of gastric cancers, with uniform expression in 45% of cases. Eighty-three percent of intestinal-type gastric cancers were positive for A33, and about 50% of the diffuse-type and mucinous cancers were mA33 positive. A33 was expressed in 50% of the pancreatic cancers but with marked heterogeneity. Other epithelial cancers, sarcomas, neuroectodermal tumors, and lymphoid neoplasms were generally A33 negative. A33 is the first example of a constitutively expressed, organ-specific epithelial membrane antigen permitting highly specific tumor targeting in patients with gastrointestinal cancer. Encouraged by the success of the biodistribution and imaging characteristic studies performed at Memorial Sloan-Kettering Cancer Center by the New York Branch of the Ludwig Institute in colorectal cancers, a new clinical study of humanized monoclonal antibody huA33 against A33 antigen-positive gastric cancers has been initiated in Japan.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1619-7089
    Keywords: Acute myocardial infarction ; Fatty acid metabolism ; Iodine-123 15-(p-iodophenyl)-3(R, S)-methylpentadecanoic acid ; Myocardial viability ; Single-photon emission tomography ; ylpentadecanoic acid ; Myocardial viability ; Singlephoton emission tomography
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A discrepancy between myocardial perfusion defect and wall motion abnormalities is frequently found early after coronary reperfusion in patients with acute myocardial infarction. The purpose of this study was to assess recovery of impaired left ventricular function by reference to the discordance in defect size between myocardial fatty acid uptake and myocardial perfusion using combined single-photon emission tomographic (SPET) imaging early after coronary perfusion therapy. In 37 patients with acute myocardial infarction, iodine-123 15(p-iodophenyl)-3(R, S)-methylpentadecanoic acid (BMIPP) and thallium-201 SPET scans were performed early after coronary reperfusion. A severity score was determined from the extent of the imaging defect with each tracer. Left ventricular wall motion score (WMS) and ejection fraction (EF) were obtained at admission and at 4 weeks after the onset of infarction. In 32 of the 37 patients, discordance in defect sizes delineated with the two SPET studies was found during the acute stage. The severity score for BMIPP was larger than that for201Tl during the acute stage (7.7±2.4 vs 4.4±2.5,P 〈0.001). There was a fair correlation between the severity score for BMIPP and WMS (r=0.82,P 〈0.0001), but a poor correlation between that for201Tl and WMS. The extent of discordance in severity scores between BMIPP and201Tl during the acute stage correlated well with the extent of the improvement in WMS (r=0.86,P 〈0.0001) and that of EF (r=0.85,P 〈0.0001). We conclude that the discordance in defect size on BMIPP and201TI SPET images during the acute stage of infarction is an early predictor of the viability of the myocardium at risk of infarction.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1546-170X
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] Bone-marrow minimal residual disease (MRD) causes relapse after chemotherapy in patients with acute myelogenous leukemia (AML). We postulate that the drug resistance is induced by the attachment of very late antigen (VLA)-4 on leukemic cells to fibronectin on bone-marrow stromal cells. We found ...
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  • 7
    ISSN: 1435-5922
    Keywords: alcoholic liver diseases ; autoantibody ; HepG2 cells ; 125I-protein A binding assay
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Sera from 14 normal control subjects, 30 patients with alcoholic liver diseases (fatty liver,n=8; hepatitis,n=13; liver cirrhosis,n=9), 7 controls with chronic hepatitis B, and 8 controls with chronic hepatitis C were masured for their concentrations of antibodies against HepG2 membrane protein by a binding assay utilizing125I-labeled protein A. When the cut-off level was set as the mean value plus 2 SD of normal control subjects, the incidence of positivity was 75%, 69.2%, and 77.8% in patients with alcoholic fatty liver, alcoholic hepatitis, and alcoholic cirrhosis, respectively. Both the mean serum antibody values and the positive incidence were significantly higher in patients with alcoholic liver diseases than in either the normal controls or in the control patients with chronic hepatitis. Sodium dodecylsulfate polyacrylamide gel electrophoresis of125I-labeled HepG2 membrane protein precipitated with IgG from patients with alcoholic liver diseases revealed an immunoreactive band at a molecular weight of 78 000 daltons (gp78). The antibody activity remained after immunoabsorption by human liver-specific lipoprotein (LSP) but decreased when HepG2 cells were pre-treated with trypsin or neuraminidase. Consequently, gp78 appears to be a glycoprotein distinct from LSP, and is specifically recognized by IgG from patients with alcoholic liver diseases. This assay may provide a new system to measure autoantibody to hepatocytes in alcoholic liver diseases.
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1435-5922
    Keywords: Key words: ethanol ; asialoglycoprotein receptor ; IL-1β ; IL-6 ; TNF-α
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract: Blood levels of inflammatory-related cytokines, including interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α, are elevated in patients with alcoholic liver diseases. We investigated the effects of these cytokines and ethanol on the expression of hepatic asialoglycoprotein receptors (AGPRs) in a human hepatoblastoma cell line, HepG2. An [125I]-asialo-orosomucoid binding assay showed significant increases in surface AGPR numbers in HepG2 cells by treatment with IL-1β, IL-6, and TNF-α, to levels which were approximately 130% of the values in untreated control cells. However, the enhanced AGPR numbers induced by treatment with these cytokines were markedly suppressed, to 70%–80% of the number in the untreated cells, by treatment with ethanol. Immunological detection of AGPR with a specific antibody demonstrated that the modulation of surface AGPR numbers was correlated with the cellular expression levels of AGPR. These results suggest that, although IL-1β, IL-6, and TNF-α stimulate the synthesis of hepatic AGPR, ethanol suppresses the expression of AGPR augmented by these cytokines. This leads to an increase in serum asialo-orosomucoid levels caused by the disordered catabolism mediated by AGPR in patients with alcoholic liver disease.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1435-5922
    Keywords: fulminant hepatitis ; hepatitis C virus ; multiple sclerosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A 55-year-old woman was treated at our hospital for multiple sclerosis. Therapy consisted of glucocorticosteroids and cyclosporin. In the 7th week after these drugs were discontinued the patient developed acute liver failure due to fulminant hepatitis (FH) and died. Post-mortem examination showed massive liver necrosis. Serologic examination was negative for hepatitis B virus-related markers. Anti-hepatitis C virus (anti-HCV) antibody and serum HCV RNA were negative on admission, but HCV RNA appeared concurrently with the onset of FH. Although HCV infection rarely causes FH, it was considered to be the cause of FH in this patient, since there were no other causes of acute liver injury. We suspect that underlying immunologic abnormalities in conjunction with HCV infection may have precipitated the FH.
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1435-5922
    Keywords: asialoglycoprotein receptor ; cytokine ; acute phase protein
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The asialoglycoprotein receptor (AGPR) is responsible for the catabolism of acute phase proteins. The effects of inflammation-related cytokines on the expression of AGPR were investigated in HepG2 cells derived from a human hepatoblastoma cell line. Binding studies, using a [125I]-labeled asialo-orosomucoid ligand, revealed that AGPR numbers on cell surfaces were increased by interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor (TNF). In cells treated with IL-1, IL-6, or TNF, immunohistochemical staining with an anti-AGPR monoclonal antibody demonstrated augmented expression. Pulse labeling analysis, using [35S]-labeled methionine, showed newly synthesized AGPR in both the precursor and the mature forms. When IL-1, IL-6, and TNF were added to the culture medium, total synthesis of AGPR (sum of the mature and precursor forms) was increased. In addition, the relative proportion of the synthesized precursor form of AGPR was higher in cytokine-treated than in untreated cells, suggesting that these cytokines augment the synthesis of AGPR, particularly in the stage prior to glycosylation.
    Type of Medium: Electronic Resource
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