Potential Diagnostic (potential + diagnostic)

Distribution by Scientific Domains

Terms modified by Potential Diagnostic

  • potential diagnostic marker
  • potential diagnostic pitfall
  • potential diagnostic tool

  • Selected Abstracts


    Maximizing management of patients with decompensated heart failure

    CLINICAL CARDIOLOGY, Issue S3 2000
    E. Loh M.D.
    Abstract Patients with decompensated congestive heart failure can be categorized into those with either acute or chronic presentations. Patients with acute decompensated heart failure most often have an acute injury that affects either myocardial performance (i.e., myocardial infarction) or valvular/chamber integrity (mitral regurgitation, ventricular septal rupture), which leads to an acute rise in left ventricular (LV) filling pressures resulting in pulmonary edema and dyspnea. Therapy for these patients is aimed at treating the underlying cause of the myocardial injury as well as pharmacologic strategies to reduce LV filling pressures and to improve cardiac performance. In contrast, the therapy of patients presenting with decompensated heart failure in the setting of chronic LV systolic dysfunction, treated with angiotensin-converting enzyme inhibitors, digoxin, diuretics, and maybe beta blockers, represent a poorly defined clinical entity that lacks clear guidelines for treatment. These patients can present with symptoms of volume overload and/or low cardiac output without evidence for a volume overloaded state. Potential diagnostic and therapeutic approaches include (1) a pulmonary artery catheter for invasive hemodynamic monitoring, (2) intravenous inotropic therapy, (3) LV mechanical assist device therapy, and (4) cardiac transplantation. This review presents some of the advantages and disadvantages of each of these interventions for patients with chronic systolic dysfunction who present with decompensated symptoms and require specialized management in the hospital setting. [source]


    How different are luminal A and basal breast cancers?

    INTERNATIONAL JOURNAL OF CANCER, Issue 6 2009
    François Bertucci
    Abstract Heterogeneity of breast cancer makes its evolution difficult to predict, and its treatment far from being optimal. At least 5 main molecular subtypes exist. Two major subtypes are luminal A and basal subtypes, which have opposite features, notably survival. To characterize these 2 subtypes better, with the hope of better understanding their different biology and clinical outcome, we have profiled a series of 138 tumours (80 luminal A and 58 basal) using Affymetrix whole-genome DNA microarrays. We have identified 5,621 probe sets as differentially expressed between the 2 subtypes in our series. These differences were validated in 6 independent public series (more than 600 tumours) profiled using different DNA microarrays platforms. Analysis of functions and pathways related to these probe sets, and the extent of the observed differences, confirmed that the 2 subtypes represent very distinct entities. Genes associated with proliferation, cell cycle, cell motility, angiogenesis, and NFkB signalling were overexpressed in basal tumours. Genes involved in fatty acid metabolism, TGFB signalling, and oestrogen receptor (ER) signalling were overexpressed in luminal A samples. Half of the genes overexpressed in luminal tumours contained ER-binding sites. The number of differentially expressed genes was as high as the set of genes discriminating 2 cancers of different anatomical origin (breast and colon) or discriminating acute myeloid and lymphoid leukaemia. We provide a comprehensive list of genes/pathways that define potential diagnostic, prognostic and therapeutic targets for these 2 subtypes, which should be treated differently given the profound differences observed at the molecular level. © 2008 Wiley-Liss, Inc. [source]


    A two-dimensional electrophoresis preliminary approach to human hepatocarcinoma differentiation induced by PPAR-agonists

    JOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 2 2005
    Patrizia Bottoni
    Abstract Adopting biochemical and proteomic approaches, we investigated the effect of some PPAR-agonists, a new class of differentiating agents, on human hepatocellular carcinoma Hep-G2 cell line. Cancer differentiation was assayed by checking albumin, transferrin and ,-fetoprotein synthesis. Cell metabolism was studied by NMR spectroscopy of cell culture supernatants and by evaluation of mitochondrial respiratory chain enzyme activities. The two dimensional electrophoresis approach was employed to analyze modifications in the expression of cellular proteins linked to cell phenotype differentiation in the attempt to identify potential diagnostic and prognostic biomarkers of hepatocellular carcinoma. Results indicate that PPAR-agonists are able to act as differentiating inducers in human hepatocellular carcinoma Hep-G2 cell line as well as to inhibit mitochondrial respiratory chain Complex I, provoking a selective derangement of cellular oxidative metabolism. Lastly, two dimensional electrophoresis showed interesting modifications in the pattern of expression of cellular proteins that confirm biochemical data (increase in albumin and transferrin, decrease of alpha -fetoprotein synthesis) and, moreover, emphasize the meaning of these data by the increase of spots indicatively ascribed to HSP70 and catalase. [source]


    Deregulation of E-cadherin,catenin complex in precancerous lesions of gastric adenocarcinoma

    JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 5 2003
    ANNIE ON-ON CHAN
    Abstract Background and Aim: Decrease in expression of the E-cadherin,catenin complex is an important element in gastric carcinogenesis. However, the expression of the complex in gastric precancerous lesions has not been well studied. The present study aimed to examine the serial change in expression of E-cadherin,catenin complex in the precancerous lesions of gastric cancer patients. Methods: Gastrectomy specimens of 40 patients with gastric cancer were retrieved. Areas with chronic gastritis, atrophic gastritis, intestinal metaplasia and adenocarcinoma were identified and immunostained for ,-catenin, ,-catenin and E-cadherin. The results were scored semiquantitatively by two independent pathologists using a validated scoring system. Results: A significant decrease in score was observed in 5% (1/22) of ,-catenin, 0% (0/22) of ,-catenin and 9% (2/22) of E-cadherin in chronic atrophic gastritis patients, and in 28% (5/18) of ,-catenin, 67% (10/15) of ,-catenin and 57% (8/14) of E-cadherin in intestinal metaplasia patients. The scoring of ,-catenin, ,-catenin and E-cadherin correlated with each other. Forty-three percent of patients had concordant changes of scores along the gastritis,adenocarcinoma sequence. There was no association between Helicobacter pylori status and E-cadherin,catenin complex expression. Conclusion: Deregulation of the E-cadherin,catenin complex was observed in the majority of precancerous lesions in patients with gastric adenocarcinoma, which has potential diagnostic and therapeutic implications. © 2003 Blackwell Publishing Asia Pty Ltd [source]


    Transcriptome dissection of gastric cancer: Identification of novel diagnostic and therapeutic targets from pathology specimens

    PATHOLOGY INTERNATIONAL, Issue 3 2009
    Wataru Yasui
    Gastric cancer is the fourth most common malignancy in the world, and mortality due to gastric cancer is second only to that from lung cancer. ,Transcriptome dissection' is a detailed analysis of the entire expressed transcripts from a cancer, for the purpose of understanding the precise molecular mechanism of pathogenesis. Serial analysis of gene expression (SAGE) is a suitable technique for performing transcriptome dissection. Gastric cancers of different stages and histology were analyzed on SAGE, and one of the largest gastric cancer SAGE libraries in the world was created (GEO accession number GSE 545). Through SAGE, many candidate genes have been identified as potential diagnostic and therapeutic targets for the treatment of gastric cancer. Regenerating islet-derived family, member 4 (Reg IV) participated in 5-fluorouracil (5-FU) resistance and peritoneal metastasis, and its expression was associated with an intestinal phenotype of gastric cancer and with endocrine differentiation. GW112 expression correlated with advanced tumor stage. Measurement of Reg IV and GW112 levels in sera indicated a sensitivity of 57% for detection of cancer. SPC18 participated in tumor growth and invasion through transforming tumor growth factor-, upregulation. Palate, lung, and nasal epithelium carcinoma-associated protein (PLUNC) was a useful marker for gastric hepatoid adenocarcinoma. Expression of SOX9, HOXA10, CDH17, and loss of claudin-18 expression were associated with an intestinal phenotype of gastric cancer. Information obtained from transcriptome dissection greatly contributes to diagnosis and treatment of gastric cancer. [source]