Academic literature on the topic 'GFP reporter assay'
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Journal articles on the topic "GFP reporter assay"
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Sasuga, Shintaro, and Toshiya Osada. "The Reporter System for GPCR Assay with the Fission YeastSchizosaccharomyces pombe." Scientifica 2012 (2012): 1–11. http://dx.doi.org/10.6064/2012/674256.
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G protein-coupled receptors (GPCRs) are associated with a great variety of biological activities. Yeasts are often utilized as a host for heterologous GPCR assay. We engineered the intense reporter plasmids for fission yeast to produce green fluorescent protein (GFP) through its endogenous GPCR pathway. As a control region of GFP expression on the reporter plasmid, we focused on seven endogenous genes specifically activated through the pathway. When upstream regions of these genes were used as an inducible promoter in combination with LPI terminator, themam2upstream region produced GFP most rapidly and intensely despite the high background. Subsequently, LPI terminator was replaced with the corresponding downstream regions. The SPBC4.01 downstream region enhanced the response with the low background. Furthermore, combining SPBC4.01 downstream region with the sxa2 upstream region, the signal to noise ratio was obviously better than those of other regions. We also evaluated the time- and dose-dependent GFP productions of the strains transformed with the reporter plasmids. Finally, we exhibited a model of simplified GPCR assay with the reporter plasmid by expressing endogenous GPCR under the control of the foreign promoter.
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Collins, L. A., M. N. Torrero, and S. G. Franzblau. "Green Fluorescent Protein Reporter Microplate Assay for High-Throughput Screening of Compounds againstMycobacterium tuberculosis." Antimicrobial Agents and Chemotherapy 42, no. 2 (February 1, 1998): 344–47. http://dx.doi.org/10.1128/aac.42.2.344.
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ABSTRACT An optimal assay for high-throughput screening for new antituberculosis agents would combine the microplate format and low cost of firefly luciferase reporter assays and redox dyes with the ease of kinetic monitoring inherent in the BACTEC system. The green fluorescent protein (GFP) of the jellyfish Aequorea victoria is a useful reporter molecule which requires neither substrates nor cofactors due to the intrinsically fluorescent nature of the protein. The gene encoding a red-shifted, higher-intensity GFP variant was introduced by electroporation into Mycobacterium tuberculosis H37Ra and M. tuberculosisH37Rv on expression vector pFPV2. A microplate-based fluorescence assay (GFP microplate assay [GFPMA]) was developed and evaluated by determining the MICs of existing antimycobacterial agents. The MICs of isoniazid, rifampin, ethambutol, streptomycin, amikacin, ofloxacin, ethionamide, thiacetazone, and capreomycin, but not cycloserine, determined by GFPMA were within 1 log2dilution of those determined with the BACTEC 460 system and were available in 7 days. Equivalent MICs of antituberculosis agents in the BACTEC 460 system for both the reporter and parent strains suggested that introduction of pFPV2 did not influence drug susceptibility, in general. GFPMA provides a unique tool with which the dynamic response of M. tuberculosis to the existing and potential antituberculosis agents can easily, rapidly, and inexpensively be monitored.
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Beck, Verena, Angelika Pfitscher, and Alois Jungbauer. "GFP-reporter for a high throughput assay to monitor estrogenic compounds." Journal of Biochemical and Biophysical Methods 64, no. 1 (July 2005): 19–37. http://dx.doi.org/10.1016/j.jbbm.2005.05.001.
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Simonen, Marjo, Yvonne Ibig-Rehm, Gabriele Hofmann, Johann Zimmermann, Genevieve Albrecht, Maxime Magnier, Valerie Heidinger, and Daniela Gabriel. "High-Content Assay to Study Protein Prenylation." Journal of Biomolecular Screening 13, no. 6 (July 2008): 456–67. http://dx.doi.org/10.1177/1087057108318757.
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The mevalonate pathway leads to synthesis of cholesterol and isoprenoid lipids. Prenyltransferases attach the isoprenoid lipids to the C-terminus of several small guanosine triphosphate—binding proteins. The prenyl groups are essential for the biological activity of these proteins. The prenyltransferases and other components of the mevalonate pathway are either present or potential drug targets for cancer, osteoporosis, restenosis, or high serum cholesterol level. Until recently, cellular assays to study protein prenylation have been tedious, low-throughput assays. The authors have developed a high-content imaging-based assay to study protein prenylation. The assay is based on a green fluorescent protein (GFP) reporter, which is tagged with the prenylation motif of human H-Ras. The C-terminus of H-Ras targets GFP to the plasma membrane. When protein prenylation is inhibited, the tagged GFP cannot be localized to plasma membrane but is soluble in the cells. The localization of the GFP reporter can be analyzed in the 96- or 384-well format using automated microscopy and automated image analysis. Information about cell number and nuclear intensity can be obtained from the same images. In compound screening, these readouts provide valuable information about the toxicity of the compounds. The authors have validated their assay using several inhibitors of the mevalonate pathway as well as siRNA against farnesyl pyrophosphate synthase, a critical enzyme in the synthesis of the isoprenoid lipids. ( Journal of Biomolecular Screening 2008:456-467)
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Brandsma, Inger, Nynke Moelijker, Remco Derr, and Giel Hendriks. "Aneugen Versus Clastogen Evaluation and Oxidative Stress-Related Mode-of-Action Assessment of Genotoxic Compounds Using the ToxTracker Reporter Assay." Toxicological Sciences 177, no. 1 (July 3, 2020): 202–13. http://dx.doi.org/10.1093/toxsci/kfaa103.
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Abstract Understanding the mode-of-action (MOA) of genotoxic compounds and differentiating between direct DNA interaction and indirect genotoxicity is crucial for their reliable safety assessment. ToxTracker is a stem cell-based reporter assay that detects activation of various cellular responses that are associated with genotoxicity and cancer. ToxTracker consists of 6 different GFP reporter cell lines that can detect the induction of DNA damage, oxidative stress, and protein damage in a single test. The assay can thereby provide insight into the MOA of compounds. Genotoxicity is detected in ToxTracker by activation of 2 independent GFP reporters. Activation of the Bscl2-GFP reporter is associated with induction of DNA adducts and subsequent inhibition of DNA replication and the Rtkn-GFP reporter is activated following the formation of DNA double-strand breaks. Here, we show that the differential activation of these 2 genotoxicity reporters could be used to further differentiate between a DNA reactive and clastogenic or a non-DNA-reactive aneugenic MOA of genotoxic compounds. For further classification of aneugenic and clastogenic compounds, the ToxTracker assay was extended with cell cycle analysis and aneuploidy assessment. The extension was validated using a selection of 16 (genotoxic) compounds with a well-established MOA. Furthermore, indirect genotoxicity related to the production of reactive oxygen species was investigated using the DNA damage and oxidative stress ToxTracker reporters in combination with different reactive oxygen species scavengers. With these new extensions, ToxTracker was able to accurately classify compounds as genotoxic or nongenotoxic and could discriminate between DNA-reactive compounds, aneugens, and indirect genotoxicity caused by oxidative stress.
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Standage-Beier, Kylie, Stefan J. Tekel, Nicholas Brookhouser, Grace Schwarz, Toan Nguyen, Xiao Wang, and David A. Brafman. "A transient reporter for editing enrichment (TREE) in human cells." Nucleic Acids Research 47, no. 19 (August 20, 2019): e120-e120. http://dx.doi.org/10.1093/nar/gkz713.
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Abstract Current approaches to identify cell populations that have been modified with deaminase base editing technologies are inefficient and rely on downstream sequencing techniques. In this study, we utilized a blue fluorescent protein (BFP) that converts to green fluorescent protein (GFP) upon a C-to-T substitution as an assay to report directly on base editing activity within a cell. Using this assay, we optimize various base editing transfection parameters and delivery strategies. Moreover, we utilize this assay in conjunction with flow cytometry to develop a transient reporter for editing enrichment (TREE) to efficiently purify base-edited cell populations. Compared to conventional cell enrichment strategies that employ reporters of transfection (RoT), TREE significantly improved the editing efficiency at multiple independent loci, with efficiencies approaching 80%. We also employed the BFP-to-GFP conversion assay to optimize base editor vector design in human pluripotent stem cells (hPSCs), a cell type that is resistant to genome editing and in which modification via base editors has not been previously reported. At last, using these optimized vectors in the context of TREE allowed for the highly efficient editing of hPSCs. We envision TREE as a readily adoptable method to facilitate base editing applications in synthetic biology, disease modeling, and regenerative medicine.
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Liu, Yan Qun, and Xiong Bing Lu. "Establishing a Assay for Detection of Nonylphenol Estrogenic Effects." Applied Mechanics and Materials 71-78 (July 2011): 3003–6. http://dx.doi.org/10.4028/www.scientific.net/amm.71-78.3003.
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Environmental estrogen could mimic natural estrogens thereby disrupting the endocrine systems of human and animals. The actions of such endocrine disruptors have been studied mainly on reproduction and development. To explore the estrogenic effects of NP by reporter genebased assays we developed. pERE-GFP plamid was generated by inserting estrogen response element fragment into pGADD153-GFP. the recombinant was confirmed by restriction enzyme map and transfected into SPC-A1 cells to ensure the expression of green fluorescent protein．The assay we established in usful, NP could induce the estrogenic activities at any of the tested concentrations.
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Hughes, Chris, Adam Rabinowitz, Matthew Tate, Louise Birrell, Jodie Allsup, Nicholas Billinton, and Richard M. Walmsley. "Development of a High-Throughput Gaussia Luciferase Reporter Assay for the Activation of the GADD45a Gene by Mutagens, Promutagens, Clastogens, and Aneugens." Journal of Biomolecular Screening 17, no. 10 (July 10, 2012): 1302–15. http://dx.doi.org/10.1177/1087057112453312.
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Exposure to genotoxic carcinogens leads to increased expression of the GADD45a gene in mammalian cells. This signature of genotoxic hazard has previously been exploited in the GreenScreen HC assay, in which GADD45a expression is linked to green fluorescent protein (GFP) expression in the human TK6 lymphoblastoid cell line. This article describes the development and validation of an alternative assay (“BlueScreen HC”), in which expression is linked to Gaussia luciferase (GLuc) expression, yielding a luminescent reporter, the preferred optical output in high-throughput screening. The coelentrazine substrate of GLuc is relatively unstable, and a new buffer is reported that improves its stability. A more sensitive method is demonstrated for the measurement of cell densities in the assay, using the fluorescent cyanine dye thiazole orange. A protocol amendment also allows the assessment of pro-genotoxicity using S9 liver extracts. Compounds from the European Centre for the Validation of Alternative Methods (ECVAM) recommended list for the assessment of new or improved genotoxicity assays were evaluated with and without S9 in the new assay. The new GLuc assay was as effective as the GFP assay in producing positive results for all classes of genotoxic carcinogen and negative results for all nongenotoxins tested.
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Bui, Van Ngoc, Thi Thu Huyen Nguyen, Yvan Bettarel, Thi Hoai Thu Nguyen, Thuy Linh Pham, Thi Yen Hoang, Vu Thanh Thanh Nguyen, Ngoc Minh Nghiem, and Stefan Wölfl. "Genotoxicity of Chemical Compounds Identification and Assessment by Yeast Cells Transformed With GFP Reporter Constructs Regulated by the PLM2 or DIN7 Promoter." International Journal of Toxicology 34, no. 1 (January 2015): 31–43. http://dx.doi.org/10.1177/1091581814566870.
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Yeast cells transformed with high-copy number plasmids comprising a green fluorescent protein (GFP)-encoding gene optimized for yeast under the control of the new DIN7 or PLM2 and the established RNR2 and RAD54 promoters were used to assess the genotoxic potential of chemical compounds. The activity of potential DNA-damaging agents was investigated by genotoxicity assays and by OxoPlate assay in the presence of various test compounds. The fluorescence signal generated by GFP in response to DNA damage was related to the different concentrations of analytes and the analyte-dependent GFP synthesis. The use of distinct DNA damage-inducible promoters presents alternative genotoxicity testing strategies by selective induction of promoters in response to DNA damage. The new DIN7 and PLM2 systems show higher sensitivity than the RNR2 and RAD54 systems in detecting 4-nitroquinoline- N-oxide and actinomycin D. Both DIN7 and PLM2 systems are able to detect camptothecin while RNR2 and RAD54 systems are not. Automated laboratory systems with assay performance on 384-well microplates provide for cost-effective high-throughput screening of DNA-damaging agents, reducing compound consumption to about 53% as compared with existing eukaryotic genotoxicity bioassays.
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Changsen, Chartchai, Scott G. Franzblau, and Prasit Palittapongarnpim. "Improved Green Fluorescent Protein Reporter Gene-Based Microplate Screening for Antituberculosis Compounds by Utilizing an Acetamidase Promoter." Antimicrobial Agents and Chemotherapy 47, no. 12 (December 2003): 3682–87. http://dx.doi.org/10.1128/aac.47.12.3682-3687.2003.
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ABSTRACT The green fluorescent protein (GFP) gene offers many advantages as a viability reporter for high-throughput antimicrobial drug screening. However, screening for antituberculosis compounds by using GFP driven by the heat shock promoter, hsp60, has been of limited utility due to the low signal-to-noise ratio. Therefore, an alternative promoter was evaluated for its enhanced fluorescence during microplate-based culture and its response to 18 established antimicrobial agents by using a green fluorescent protein microplate assay (GFPMA). Mycobacterium tuberculosis strains H37Rv, H37Ra, and Erdman were transformed with pFPCA1, which contains a red-shifted gfp gene driven by the acetamidase promoter of M. smegmatis mc2155. The pFPCA1 transformants achieved higher levels of GFP-mediated fluorescence than those carrying the hsp60 construct, with signal-to-noise ratios of 20.6 to 27.8 and 3.8 to 4.5, respectively. The MICs of 18 established antimicrobial agents for all strains carrying pFPCA1 in the GFPMA were within 1 to 2 twofold dilutions of those determined by either the fluorometric or the visual microplate Alamar Blue assay (MABA). No significant differences in MICs were observed between wild-type and pFPCA1 transformants by MABA. The optimized GFPMA is sufficiently simple, robust, and inexpensive (no reagent costs) to be used for routine high-throughput screening for antituberculosis compounds.
Dissertations / Theses on the topic "GFP reporter assay"
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Vasou, Andri. "Development of a novel cell-based screening platform to identify inhibitors of viral interferon antagonists from clinically important viruses." Thesis, University of St Andrews, 2016. http://hdl.handle.net/10023/8266.
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All viruses encode for at least one viral interferon (IFN) antagonist, which is used to subvert the cellular IFN response, a powerful antiviral innate immune response. Numerous in vitro and in vivo studies have demonstrated that IFN antagonism is crucial for virus survival, suggesting that viral IFN antagonists could represent promising therapeutic targets. This study focuses on Respiratory Syncytial Virus (RSV), an important human pathogen for which there is no vaccine or virus-specific antiviral drug. RSV encodes two IFN antagonists NS1 and NS2, which play a critical role in RSV replication and pathogenicity. We developed a high-throughput screening (HTS) assay to target NS2 via our A549.pr(ISRE)GFP-RSV/NS2 cell-line, which contains a GFP gene under the control of an IFN-stimulated response element (ISRE) to monitor IFN- signalling pathway. NS2 inhibits the IFN-signalling pathway and hence GFP expression in the A549.pr(ISRE)GFP-RSV/NS2 cell-line by mediating STAT2 degradation. Using a HTS approach, we screened 16,000 compounds to identify small molecules that inhibit NS2 function and therefore relinquish the NS2 imposed block to IFN-signalling, leading to restoration of GFP expression. A total of twenty-eight hits were identified; elimination of false positives left eight hits, four of which (AV-14, -16, -18, -19) are the most promising. These four hit compounds have EC₅₀ values in the single μM range and three of them (AV-14, -16, -18) represent a chemically related series with an indole structure. We demonstrated that the hit compounds specifically inhibit the STAT2 degradation function of NS2, not the function of NS1 or unrelated viral IFN antagonists. At the current time, compounds do not restrict RSV replication in vitro, hence hit optimization is required to improve their potency. Nonetheless, these compounds could be used as chemical tools to determine the unknown mechanism by which NS2 mediates STAT2 degradation and tackle fundamental questions about RSV biology.
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Chien, Chia-Hung, and 簡嘉宏. "Functional Analysis of Zebrafish CTGF gene promoter by Transgenic Assay with Green Fluorescent Protein (GFP) Reporter Gene." Thesis, 2007. http://ndltd.ncl.edu.tw/handle/30067652716686339852.
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碩士臺灣大學
口腔生物科學研究所
95
Connective tissue growth factor (CTGF), a member of CCN family, is a cysteine-rich, secreted, extracellular matrix-associated protein that regulates diverse cellular functions in different cell types. It modulates many cellular functions, including cell proliferation, migration, adhesion, and extracellular matrix production. Evidence suggests that there is a distinctive function of CTGF in the skeletal development. For instance, during Meckel''s cartilage development, CTGF acts as a down-stream molecule of TGF-β to stimulate cell-cell interactions and the expression of condensation-associated genes. Actually, TGF-β response element is located on the CTGF gene, and CTGF can exert many functions by the induction of TGF-β. The aim of this study was to analyze the zebrafish CTGF promoter. Its cognate genomic DNA fragments were amplified by polymerase chain reaction (PCR). Upstream promoter (enhancer) fragments were constructed with EGFP (enhanced green fluorescent protein) reporter gene or with HSV-tymidine kinase (TK) basal promoter and analyzed in vivo by transient transgenic assays using zebrafish embryos. Results demonstrate that the constructs of pZF-CTGF(-2893/ +105)-EGFP1 [pCTGF- EGFP1] and pZF-CTGF(-1593/-1462)-HSV-TK-EGFP1 [pCTGF-E2-TK EGFP1]can drive the specific expression of GFP in zebrafish embryo(5dpf). The expression sites include mandible, cranium, cornea, heart, somite, notochord, floor plate, fin bud, and epidermis. It is identical to in situ hybridization result. Furthermore,the proximal promoter constructs of the pZF-CTGF(-195/+22)-EGFP1 [pCTGF-P200- EGFP1], pZF-CTGF(-64/+22)-EGFP1 [pCTGF-vTATA-EGFP1] and pZF-CTGF(-195/-44)- HSV-TK-EGFP1 [pCTGF-195xTATA-TK-EGFP1] can also drive expression of GFP in zebrafish embryo(5dpf). The expression sites include notochord and somite. However, the expression area is fewer. The zebrafish transgenic stable lines were not obtained from pZF-CTGF(-2893/+105)-EGFP1 [pCTGF-EGFP1] construct yet. The results suggest that the tissue-specific regulatory elements of the zebrafish CTGF reside within the upstream conserved region (-1593/-1462) and proximal promoter region (-195/ +22), and the regulatory mechanism of CTGF may be conserved among the vertebrate species.
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Chen, Chun-Yu, and 陳俊宇. "Tissue-specific Analysis of CCN1/CYR61 Gene Promoter of Zebrafish by Transgenic Assay with Green Fluorescent Protein (GFP) Reporter Gene." Thesis, 2007. http://ndltd.ncl.edu.tw/handle/96437365304079612916.
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碩士臺灣大學
口腔生物科學研究所
95
Cysteine-rich 61(Cyr61/CCN1), one of CCN family members, is an secretory matricellular protein with multiple biological functions, such as regulating cell adhesion, inducing cell migration, enhancing growth-factor-induced cell division and prolonging cell survival. It’s function is tightly associated with embryonic development, angiogenesis, chondrogenesis, tumor forming and wound healing. Moreover, CCN1/ Cyr61 is expressed in various tissues. Based on the above mentions, CCN1/Cyr61 may play an important role in normal development of an organism. The aim of this study is to identify the cis-regulatory elements of CCN1/Cyr61 gene. I cloned and constructed its promoter DNA fragments in EGFP1 vector. Those constructs were microinjected into zebrafish zygote for their functional assay. The transient transgenic assay reveals that the longest promoter fragment (-2902/+29) could induce EGFP expression in embryo’s notochord、somite、heart、hindbrain、fin、mandible (pharyngeal arches) and epithelium; on the other hand, the proximal region (-140/+29) could only induce EGFP expression in notochord、somite、heart、hindbrain and epithelium. Besides, I obtain a transgenic stable line (F1 generation) with longest promoter fragment (-2902/+29). The expression of green fluorescent protein can be observed in the previous described tissues, which corresponds with the endogenous one of Cyr61. Therefore, I demonstrated that the upstream region (-2902/+29) of zebrafish CCN1/Cyr61 gene harbors most of its cis-regulatory elements. Comparing the upstream genomic DNA sequences of CCN1/Cyr61 from eight different animal species led to the identification of a highly conserved region (-2299~-2123) in the upstream promoter region, in which several putative transcription factor binding sites are located by TRANSFAC software analysis. Furthermore, I divided it into 4 smaller fragments and constructed each with HSV-thymidine kinase basal promoter. The transient transgenic experiments show that each different conserved sub-region has differential EGFP expression patterns. Together, the cis-regulatory elements in the upstream 2.9kb promoter region of zebrafish CCN1/Cyr61 gene is functionally conserved through vertebrates’ evolutionary process.
Conference papers on the topic "GFP reporter assay"
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Mukhopadhyay, Asima, Nicola Curtin, and Richard Edmondson. "Evaluation of different methods to assess homologous recombination status and sensitivity to PARP inhibitors in ovarian cancer." In 16th Annual International Conference RGCON. Thieme Medical and Scientific Publishers Private Ltd., 2016. http://dx.doi.org/10.1055/s-0039-1685289.
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Methods: Matched samples of ascites and tumor tissue were taken from patients undergoing surgery for epithelial ovarian cancer. Tumor samples were formalin fixed and paraffin embedded (FFPE); ascites samples were used to generate primary cultures (PC). HR status was determined in PCs as previously described.[1] IC50 for the PARP inhibitor Rucaparib was estimated using SRB assays. DNA was extracted from the FFPE tissue. The following techniques were evaluated in PCs or paired FFPE samples: DR-GFP reporter assay, PARP activity assay, BRCA1 expression on immunohistochemistry, BRCA1 methylation status and BRCA1/2 mutation analysis. A next generation sequencing based assay was used to detect mutations and other genomic alterations in a large panel of cancer-associated genes, including BRCA1/2. Results: Paired samples were collected from 64 patients and characterized for HR function. 47/64 (76%) were high grade serous. 44% (28/64)) were HR defective (HRD) by Rad51 assay and correlated with Rucaparib sensitivity (PPV-92%, NPV-100%). Molecular analysis revealed that all mutations and other genomic alterations detected in ascites derived PCs were also found in matched FFPE tumor tissues. All tumors with serous histology contained p53 mutations, whilst the remaining tumors without p53 mutations were non-serous in histology. DR-GFP assay was unreliable in PC due to poor transfection. In a subset of 50 cancers there was reduced BRCA1 expression in the HRD vs. HRC tumours (34.8% vs. 22.7%, ns) whilst in a further subset of 30 cases there was no difference in endogenous or stimulated PARP activity between HRD and HRC tumours. Deleterious BRCA2 mutations were identified in 7 tumors, 6 of which were HRD. Only 1 deleterious BRCA1 mutation was detected but methylation of BRCA1 was identified in 13 of 64 (20%) tumors, 7 of which were HRD. Mutation of BRCA2 was mutually exclusive to methylation of BRCA1. HRD vs. HRC tumours showed BRCA1 methylation (25% vs. 17%) and BRCA1/2 mutation (21% vs. 0.3%). 14/28 (50%) HR defective tumors do not have BRCA1/2 mutations or BRCA1 methylation, suggesting other mechanisms can also result in a HR defective phenotype. 28/64 (43%) of samples demonstrated the HR defective phenotype. In all cases HR status correlated with sensitivity to Rucaparib. Conclusion: As expected, deleterious BRCA2 mutations conferred a HRD phenotype in cells but methylation of BRCA1 was not universally associated with HRD. This may be as a result of only partial silencing of the gene by methylation and further work is required to identify thresholds of methylation which may predict HR status. The use of BRCA1/2 mutation testing alone is unlikely to identify the majority of HR defective ovarian tumors. Assessment of functional status of HRD is the preferred option and further technologies should be developed to simplify the Rad51 assay.
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Castelino, Kenneth, Veljko Milanovic, Daniel T. McCormick, Norman Tien, and Arun Majumdar. "Multiplexed Label-Free Biosensor Chip Based on Nanoscale Electrical Double Layer Capacitance Sensing." In ASME 2004 3rd Integrated Nanosystems Conference. ASMEDC, 2004. http://dx.doi.org/10.1115/nano2004-46051.
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We report the design, fabrication and testing of a microchip that exploits a capacitive detection scheme for multiplexed label-free biomolecular assays. The detection scheme is based on the nanoscale gap parallel-plate capacitor formed by the electrical double layer at the interface of a metal electrode and an ionic solution, which is sensitive to biological reactions at the electrode surface. Since the nanogap is obtained by electrical and chemical control, no nano-patterning techniques are needed and the simple device structure facilitates sensor readout, multiplexing, and packaging. Finally, this sensing technique is universal and can be applied to detection of diverse biological entities such as proteins and cells.
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Seidl, S. "SCREENING PROCEDURES TO PREVENT TRANSMISSION OF HEPATITIS B, NON-A,NON-B, AND AIDS BY BLOOD TRANSFUSION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644753.
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Although the number of infectious agents capable of being transmitted through blood and blood products is vast, only a few cause problems in recipients of a magnitude which warrants the need for screening tests. The most important agents are Hepatitis B Virus (HBV), Hepatitis non-A,non-B (HNANB) - agents causing posttransfusion hepatitis (PTH) and the human immundeficiency viruses (HIV) responsible for transfusion associated AIDS (TAA).PTH: Prospective studies in open-heart-surgery patients demonstrated a high prevalence (8-17%) *in Spain, Italy, the United States and Israel whereas low percentages (2-5%) were observed in Australia, Finland and West-Germany. Among haemophiliacs acute and chronic hepatitis is a rather frequent complication. Serologic markers of HBV infection have been observed in the majority of patients. Since HBsAg screening has been introduced most cases of PTH (>90%) are due to infection with HNANB-agents. For this type of hepatitis no specific assay exists. It has been suggested that surrogate tests (ALT, anti-HBc screening) might serve as interim screening measure. In prospective studies in the USA a correlation has been observed between donor ALT and recipient hepatitis, but not more than 30% of PTH can be prevented at a loss of 1,5 to 3,0% of the donor population. Similar data have been reported when blood donors were screened for anti-HBc. There was a significantly higher incidence of PTH in recipients receiving at least one unit of anti HBc positive blood. This was recently confirmed in a study in which patients received blood with ALT-levels below 30 IU/ml. The incidence of HNANB was 2,1% after transfusion with anti HBc negative blood whereas 10,1% developed HNANB when anti HB positive blood was transfused (P=< 0.0001). However, these two markers (ALT, anti HBc) do not identify the same NANB carrier population. - ALT screening and testing for anti-HBc have been recently instituted in the USA as “surrogate tests” for detecting HNANB carriers.TAA: Among the total number of AIDS cases there ist a small percentage caused by transfusion of blood and blood products. In the USA approximately 2% of TAA have been reported, 1 % of AIDS patients are haemophiliacs but the majority of haemophiliacs are HIV-antibody positive. According to a survey of the Council of Europe (March 1986) the percentages of HIV positive European haemophiliacs varies between 4 to 8% (Belgium, Norway) and 30 to 60% in other European countries. The number of TAA-cases is around 1%, AIDS among European haemophiliacs has been observed up to 5% of the total AIDS cases. - Screening for HIV antibodies in blood donors was introduced in most European countries and the USA in early summer 1985, but several thousands of recipients of HIV positive blood (issued before) are now virus carriers. This has been confirmed in “look back” programmes: A substantial number of recipient (50 to 90%) has been found to be HIV positive.-A major disadvantage of the HIV antibody test is the fact that antibodies appear several weeks after infection. The gap between infection and detecting HIV antibodies may be reduced by an antigen test, which recognizes the HIV infection as early as two weeks after infection. - The recent detection of HIV 2 implies the necessity of developing tests for the identification of variants of HIV.