Relevant bibliographies by topics / Autoimmune diseases Molecular diagnosis

Academic literature on the topic 'Autoimmune diseases Molecular diagnosis'

Author: Grafiati
Published: 10 December 2022
Last updated: 29 January 2023

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Contents

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Autoimmune diseases Molecular diagnosis.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Autoimmune diseases Molecular diagnosis"

1

Mihai, Sidonia, and Cassian Sitaru. "Immunopathology and molecular diagnosis of autoimmune bullous diseases." Journal of Cellular and Molecular Medicine 11, no. 3 (May 2007): 462–81. http://dx.doi.org/10.1111/j.1582-4934.2007.00033.x.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Andrade, Luis E. C. "Future perspective for diagnosis in autoimmune diseases." Anais da Academia Brasileira de Ciências 81, no. 3 (September 2009): 367–80. http://dx.doi.org/10.1590/s0001-37652009000300004.

Full text
Abstract:
Human beings have taken successive approaches for the understanding and management of diseases. Initially brewed in supernatural concepts and mystical procedures, a vigorous scientific approach has emerged on the grounds of fundamental disciplines such as anatomy, microbiology, biochemistry, physiology, immunology, pathology, and pharmacology. The resulting integrated knowledge contributed to the current classification of diseases and the way Medicine is carried out today. Despite considerable progress, this approach is rather insufficient when it comes to systemic inflammatory conditions, such as systemic lupus erythematosus, that covers clinical conditions ranging from mild pauci-symptomatic diseases to rapidly fatal conditions. The treatment for such conditions is often insufficient and novel approaches are needed for further progress in these areas of Medicine. A recent breakthrough has been achieved with respect to chronic auto-inflammatory syndromes, in which molecular dissection of underlying gene defects has provided directions for target-oriented therapy. Such approach may be amenable to application in systemic auto-immune diseases with the comprehension that such conditions may be the consequence of interaction of specific environmental stimuli and an array of several and interconnected gene polymorphisms. On the bulk of this transformation, the application of principles of pharmacogenetics may lead the way towards a progressively stronger personalized Medicine.
APA, Harvard, Vancouver, ISO, and other styles
3

Martinescu, Alina, Irina Franciuc, and Loredana-Mariana Aftenie. "HLA typing in autoimmune diseases." ARS Medica Tomitana 18, no. 3 (August 1, 2012): 130–34. http://dx.doi.org/10.2478/v10307-012-0025-7.

Full text
Abstract:
Abstract Genome scan, linkage and association studies have identified CMH genes in the genetic determinism of most autoimmune diseases, affecting approximately 5% of the population. The susceptibility conferred by HLA alleles does not influence the development of autoimmunity in general, but rather the probability of some disorders. From extremely high number of known HLA alleles, less than 30 are associated with diseases, and fewer than 10 are involved in the strongest associations. The aim of this study was to determine HLA genes in autoimmune diseases. The method used for the assignment of HLA alleles was molecular genotyping, primarily by the sequence specific oligonucleotide hybridization method (SSO), and when required, by the sequence specific primers method (SSP). Molecular genotyping was performed in 282 cases of diabetes mellitus type 1, Hashimoto thyroiditis, Graves’ disease and ankylosing spondylitis. HLA typing in patients with autoimmune diseases is important for determining prognosis and genetic counseling. In ankylosing spondylitis HLA typing is used for differential diagnosis. In such studies it’s important to be aware that there is a particular HLA gene expression depending on the geographic area.
APA, Harvard, Vancouver, ISO, and other styles
4

Fisenko, Andrey P., and I. E. Smirnov. "MOLECULAR DIAGNOSIS OF FIBROSIS IN DIFFUSE LIVER DISEASES." Russian Pediatric Journal 22, no. 2 (October 7, 2019): 106–15. http://dx.doi.org/10.18821/1560-9561-2019-22-2-106-115.

Full text
Abstract:
Chronic liver diseases (CLD) held an important place in the structure of pediatric hepatology including viral and autoimmune hepatitis, various forms of liver pathology caused by metabolic disorders. They are characterized by a variety of clinical manifestations, a progressive course with the formation of fibrosis and the possibility of its outcome in liver cirrhosis (LC). Liver puncture biopsy with morphological examination of its tissue is the leading method for determining the stage of liver fibrosis (LF) in CLD children. However, it is not always safe for the patient. Using non-invasive imaging methods, it is impossible to detect intermediate stages of fibrosis and it is not always possible to detect signs of CL. Therefore, non-invasive markers of LF, based on the identification of various molecular compounds involved in the formation of components of the extracellular matrix (ECM) or acting as activators of fibrogenesis, are necessary. Hyaluronic acid, collagen type IV, matrix metalloproteinases-2 and -9, a tissue inhibitor of matrix metalloproteinases-1, transforming growth factor beta1, showing diagnostic value for non-invasive monitoring of the development of LF, are well studied among them.
APA, Harvard, Vancouver, ISO, and other styles
5

Fournel, S., and S. Muller. "Synthetic Peptides in the Diagnosis of Systemic Autoimmune Diseases." Current Protein & Peptide Science 4, no. 4 (August 1, 2003): 261–76. http://dx.doi.org/10.2174/1389203033487126.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Toro-Domínguez, Daniel, and Marta E. Alarcón-Riquelme. "Precision medicine in autoimmune diseases: fact or fiction." Rheumatology 60, no. 9 (May 18, 2021): 3977–85. http://dx.doi.org/10.1093/rheumatology/keab448.

Full text
Abstract:
Abstract Much is said about precision medicine, but its real significance and potential are far from certain. Several studies in each of the autoimmune diseases have provided important insights into molecular pathways, but the use of molecular studies, particularly those looking into transcriptome pathways, has seldom approached the possibility of using the data for disease stratification and then for prediction, or for diagnosis. Only the type I IFN signature has been considered for therapeutic purposes, particularly in the case of SLE. This review provides an update on precision medicine, on what can be translated into clinical practice and on what single-cell molecular studies contribute to our knowledge of autoimmune diseases, focusing on a few examples. The main message is that we should try to move from precision medicine of established diseases to preventive medicine in order to predict the development of disease.
APA, Harvard, Vancouver, ISO, and other styles
7

Mesko, Bertalan, Szilard Poliska, and Laszlo Nagy. "Gene expression profiles in peripheral blood for the diagnosis of autoimmune diseases." Trends in Molecular Medicine 17, no. 4 (April 2011): 223–33. http://dx.doi.org/10.1016/j.molmed.2010.12.004.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Lee, Diane. "Locating the PTPN22 Gene in Families with Multiple Diagnosis of Autoimmune Disorders (41.5)." Journal of Immunology 184, no. 1_Supplement (April 1, 2010): 41.5. http://dx.doi.org/10.4049/jimmunol.184.supp.41.5.

Full text
Abstract:
Abstract While working at NIAID, I examined the PTPN22 gene, which encodes for the lymphoid protein tyrosine phosphatase (PTP), and has been shown to be associated with susceptibility to autoimmune disorders. PTP functions in a coordinated manner with protein tyrosine kinases in the regulation of signaling responses. Kinases are involved with controlling the amplitude of a signaling response and phosphatases are important for controlling the rate and duration of the response. From this laboratory experience, I developed an immunology unit for high school molecular biology and biotechnology classes. This is an intensive month long unit which introduces the first and second lines of defense in the immune system. This unit incorporates routine laboratory practices, such as polymerase chain reaction or PCR, restriction digest and analysis to identify individuals’ susceptibility towards autoimmune diseases. Upon completion of this unit, students will gain an understanding of the immune system through the PTPN22 allele and its effects on autoimmune diseases. The concluding unit activity has students study a family pedigree chart with multiple autoimmune diseases. The PTPN22 gene is isolated from the DNA of non-affected members from this pedigree chart, through the process of PCR. Using restriction digest and analysis, individuals’ DNA is tested to determine the presence of the PTPN22 allele and to establish autoimmune disease susceptibility.
APA, Harvard, Vancouver, ISO, and other styles
9

Alghamdi, Mohammed F., and Elrashdy M. Redwan. "Advances in the diagnosis of autoimmune diseases based on citrullinated peptides/proteins." Expert Review of Molecular Diagnostics 21, no. 7 (June 7, 2021): 685–702. http://dx.doi.org/10.1080/14737159.2021.1933946.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Yeste, Ada, and Francisco J. Quintana. "Antigen Microarrays for the Study of Autoimmune Diseases." Clinical Chemistry 59, no. 7 (July 1, 2013): 1036–44. http://dx.doi.org/10.1373/clinchem.2012.194423.

Full text
Abstract:
BACKGROUND The immune response involves the activation of heterogeneous populations of T cells and B cells that show different degrees of affinity and specificity for target antigens. Although several techniques have been developed to study the molecular pathways that control immunity, there is a need for high-throughput assays to monitor the specificity of the immune response. CONTENT Antigen microarrays provide a new tool to study the immune response. We reviewed the literature on antigen microarrays and their advantages and limitations, and we evaluated their use for the study of autoimmune diseases. Antigen arrays have been successfully used for several purposes in the investigation of autoimmune disorders: for disease diagnosis, to monitor disease progression and response to therapy, to discover mechanisms of pathogenesis, and to tailor antigen-specific therapies to the autoimmune response of individual patients. In this review we discuss the use of antigen microarrays for the study of 4 common autoimmune diseases and their animal models: type 1 diabetes, systemic lupus erythematosus, rheumatoid arthritis, and multiple sclerosis. CONCLUSIONS Antigen microarrays constitute a new tool for the investigation of the immune response in autoimmune disorders and also in other conditions such as tumors and allergies. Once current limitations are overcome, antigen microarrays have the potential to revolutionize the investigation and management of autoimmune diseases.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Autoimmune diseases Molecular diagnosis"

1

Narayanan, Harish Anandha. "Molecular Understanding of Selected Autoimmune Diseases." Thesis, The University of Arizona, 2010. http://hdl.handle.net/10150/146614.

Full text
Abstract:
Pathogens that affect the immune system, or defects in the immune system contribute to numerous autoimmune diseases. In this paper, we are going to review, analyze and understand recent findings in literature. The papers that are to be reviewed explore the observation of loss of regulatory T cells in individuals with multiple sclerosis, the importance of CD4+ during HIV infection, the role of CCR6 in the immune system and the importance of Pan-DR-Binding Hsp60 self-epitopes in rheumatoid arthritis. So this literary review is limited to understanding major defects in specific parts of the immune system and its role in causing the specific autoimmune disease. The reason for this focus is to highlight the importance of the immune system in the functioning of many processes in our body and more specifically the importance of T cells and its regulators in maintaining the immune system.
APA, Harvard, Vancouver, ISO, and other styles
2

Halonen, Maria. "Monogenic model for autoimmune diseases : molecular basis of autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED)." Helsinki : University of Helsinki, 2003. http://ethesis.helsinki.fi/julkaisut/laa/haart/vk/halonen/.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Hall, Richard James, and n/a. "Chromosome 18 and autoimmune disease." University of Otago. Department of Biochemistry, 2005. http://adt.otago.ac.nz./public/adt-NZDU20070221.141018.

Full text
Abstract:
The autoimmune diseases embody a diverse range of common human conditions that are caused by a loss of self-tolerance in the host immune system to a specific organ or tissue type. Approximately 5% of the general population are affected by autoimmune diseases which include type 1 diabetes (T1D), rheumatoid arthritis (RA) and Graves disease (GD). The majority of the autoimmune diseases are multifactorial in origin, brought about by a combination of both environmental and genetic factors. Numerous susceptibility loci have been identified for each autoimmune disease and a number of these loci have been shown to be shared amongst the autoimmune diseases. The fine-mapping of susceptibility loci to the underlying disease genes remains the current challenge facing complex disease genetics. This project aimed to further characterise the autoimmune disease susceptibility locus IDDM6 on chromosome 18q12-21. This was achieved by using a comparative mapping approach that incorporates the study of genetic association in human autoimmune disease alongside the consomic mapping of the orthologous region in the non-obese diabetic (NOD) mouse model of autoimmunity. Deleted in colorectal carcinomas (DCC) provided a strong candidate gene at IDDM6 and the resident R201G polymorphism was identified as a functional candidate A potential mechanism for the R201G polymorphism involvement in T1D aetiology was identified where the polymorphism may affect the ability of DCC to induce apoptosis in vitro. However, no evidence for R201G association could be detected in autoimmune disease case-control datasets from the New Zealand (NZ) population (T1D n = 428, RA n = 730, autoimmune thyroid disease n = 192 (AITD); versus n = 1246 healthy controls). In addition, no evidence for R201G involvement in T1D could be provided in a transmission disequilibrium test (TDT) incorporating 382 affected sib-pair families (54.2% transmission; P = 0.15). Significant association of R201G with GD was detected in a United Kingdom (UK) dataset (P = 0.002) from the Newcastle population (423 cases vs. 393 controls) but this was not replicated in an additional dataset from the UK Birmingham population (731 cases vs 668 controls; P = 0.81). It was concluded that the R201G polymorphism may encode susceptibility to GD but is unlikely to be the sole aetiological variant that accounts for the linkage previously observed at IDDM6 in autoimmune disease. To further investigate DCC as a positional candidate at IDDM6, five SNPs were selected from a 100 kb window surrounding a DCC-resident microsatellite that had previously been associated with T1D, called "88,21". The five SNPs were genotyped in the NZ T1D dataset, and the ascertainment of estimated haplotypes in this dataset revealed association of a rare haplotype with T1D, called haplotype H (3.31% cases vs 1.17% controls; P = 0.0044), in addition to global association of all haplotypes (P = 0.018). Haplotype H was also associated in an independent case-control dataset from the UK comprised of 400 T1D subjects and 443 healthy controls (P = 0.038). Maximum support for association of haplotype H was extended when both the UK and NZ T1D datasets were combined (P = 0.0017). Association of haplotype H could not be verified in a family-based test for association using the 382 UK T1D families (P = 0.40). However, the inclusion of the DCC SNPs in a TDT analysis of the published DCC-resident microsatellites "88,21" and "55,26", that had been used to identify IDDM6, extends support for the previously-associated 2-10 haplotype (2-10 refers to the published allele nomenclature at "88,21" and "55,26" respectively; 2-10-haplotype A; 59.6% T; P = 0.0058). There was no evidence for association of the five SNPs with RA or AITD when using either individual SNP analyses or estimated haplotypes in the NZ datasets. A similar lack of association was reported for the UK Newcastle GD dataset. Taken together, these data further support DCC, or a nearby gene, as conferring susceptibility to T1D. The human genetic data that supports IDDM6 involvement in autoimmune disease is further strengthened by consomic mapping of the orthologous region in mouse, using the non-obese diabetic mouse (NOD) model of autoimmune disease. In this thesis, the first evidence for a diabetes and thyroiditis susceptibility locus on mouse chromosome 18 is presented, which have been designated Idd21 and Sat1 respectively. This was achieved by using a chromosome-replacement strain with chromosome 18 derived from the diabetes-resistant Biozzi ABH strain on a diabetes-susceptible NOD genome, called NOD.ABH[Chr�⁸]. Mouse chromosome 18 contains orthology to both IDDM6 and the rat diabetes-susceptibility locus Iddm3. The NOD.ABH[Chr�⁸] mice showed a dramatic and significant reduction in diabetes incidence (30% of females were affected by 7 months of age versus 85% in NOD; P <0.0001) and that of thyroiditis (15.5% at 12 months compared to 37.4% in NOD; P <0.002). The comparative mapping of the chromosome 18 autoimmune susceptibility locus IDDM6 in human and mouse presented in this thesis provides further support for this locus. This research also clearly defines the next steps required to fine-map IDDM6 to the underlying disease genes, especially in regard to the DCC gene.
APA, Harvard, Vancouver, ISO, and other styles
4

Braida, Claudia. "Molecular analysis of myotonic dystrophy type 1 patients with an unusual molecular diagnosis." Thesis restricted. Connect to e-thesis to view abstract, 2008. http://theses.gla.ac.uk/359/.

Full text
Abstract:
Thesis (Ph.D.) - University of Glasgow, 2008.
Ph.D. thesis submitted to the Division of Molecular Genetics, Institute of Biomedical and Life Sciences, University of Glasgow, 2008. Includes bibliographical references. Print version also available.
APA, Harvard, Vancouver, ISO, and other styles
5

Yang, Min, and 杨敏. "Role of regulatory B cells in autoimmune disease." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B48079832.

Full text
Abstract:
Although B cells are well-known for their functions in antibody production and antigen presentation, certain B cell subsets have been recently identified as regulatory B cells to modulate immune responses through cytokine production. However, the microenvironmental factors involved in the induction of regulatory B cells remain largely uncharacterized. B cell-activating factor (BAFF), a member of TNF family cytokines produced by myeloid cells, is a key regulator for B cell maturation and function. However, it remains unknown whether BAFF plays a role in modulating the generation of regulatory B cells and how regulatory B cells suppress autoimmune pathogenesis. In this study, treatment with BAFF significantly increased IL-10-producing B cells in culture of mouse splenic B cells, an effect specifically abrogated by neutralization with TACI-Fc. BAFF-induced IL-10-producing B cells showed a distinct CD1dhiCD5+(B10) phenotype. Phenotypic analysis further indicated that these BAFF-induced B10 cells were marginal-zone (MZ)-like B cells. Interestingly, BAFF treatment in vivo also increased the number of IL-10-producingB cells in splenic MZ regions. Moreover, chromatin immunoprecipitation analysis revealed that BAFF activated the transcription factor AP-1 for binding to IL-10 promoter, demonstrating a novel function for BAFF in inducing IL-10 production. Furthermore, those BAFF-induced B10 cells exhibited significant suppressive effects on CD4+T cell proliferation and Th1 cytokine production in culture. To explore whether these BAFF-induced B10 cells possess a regulatory function in suppressing autoimmune progression in vivo, collagen-induced arthritis (CIA) mouse model was employed. In vitro-expanded B10 cells and other control B cells were intravenously transferred into DBA/1J mice on the day of 2ndcollagen II (CII)-immunization. After adoptive transfer of BAFF-induced B10 cells, CII-immunized mice exhibited a delayed onset of arthritis and substantially reduced severity of clinical symptoms. The pathogenesis of IL-17-producing CD4+T cells (Th17) in the development of arthritis has been well-recognized, which has led me to test the hypothesis whether B10 cells ameliorate the development of arthritis via modulating Th17 cells. During the progression of CIA, IL-10-producing B cells were decreasedwhereasTh17 cells were significantly increased at the acute phase of CIA. Upon transfer of BAFF-induced B10 cells, a substantially reduction ofTh17 cells in both lymphoid organs and inflamed joints were detected. To verify whether B10 cells inhibit Th17 cell generation in culture, CFSE-labeled na?ve CD4+T cells were cocultured with B10 cells in Th17 cell polarization medium. It was found that B10 cells suppressed Th17 cell differentiation via reducing STAT3 phosphorylation and RORt expression. Although adoptive transfer of Th17 cells triggered the development of CIA in IL-17-/-DBA mice, cotransfer of B10 cells with Th17 cells profoundly delayed the onset of delayed the onset of arthritisand remarkably reduced the infiltration of Th17 cells in synovial fluid. Taken together, I have identified a novel function of BAFF in the induction of IL-10-producing regulatory B cells. My findings that adoptive transfer of BAFF-expanded B10 cells can effectively suppress the development of experimental arthritisin mice via the inhibition of Th17 cell generation may contribute to the development of new therapeutic strategies in treating human rheumatoid arthritis.
published_or_final_version
Pathology
Doctoral
Doctor of Philosophy
APA, Harvard, Vancouver, ISO, and other styles
6

Mulcahy, Anthony Francis. "The molecular cloning and characterisation of autoantigens." Thesis, University of Newcastle Upon Tyne, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.242453.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Hudspith, Karl Alexander Zhivojin. "Application of genomic technologies for molecular diagnosis of genetic diseases." Thesis, University of Oxford, 2015. https://ora.ox.ac.uk/objects/uuid:b4addaed-e9f9-4762-846a-87eb73f77235.

Full text
Abstract:
Methods for sequencing deoxyribonucleic acid (DNA) have improved rapidly in the past decade. Recent methods, termed "next-generation sequencing" (NGS), have made sequencing large quantities of DNA economically viable in molecular diagnostics of genetic diseases. This thesis describes some of the first investigations to use NGS for such a purpose. Several different NGS platforms, each of which differs substantially in terms of sample preparation, chemistry, and sequencing methodology, were tested, in addition to several sequence capture and enrichment technologies that allow sequencing to be targeted, and these combinations were compared to Sanger sequencing. They were each found to have different strengths and weaknesses, which affect their accuracy, reliability, time taken to results, financial cost, and ease of use, but all showed high accuracy and dramatically increased throughput over Sanger sequencing. NGS was used to identify pathogenic mutations in two groups of patients who had either inherited retinal dystrophies (IRD), or severe early onset epilepsies. NGS was able to identify pathogenic variants, demonstrating the ability of the technology to provide medically useful information for genetically heterogeneous conditions. NGS combined with a novel data analysis pipeline was able to make a secure molecular diagnosis in 25% of a cohort of IRD patients who previously did not have a genetic diagnosis. The greatest challenge presented by NGS was found to be filtering the vast amounts of data produced to identify potential pathogenic variants. In silico pathogenicity prediction programs were used, but none were 100% accurate. Other methods were also employed to provide further evidence of pathogenicity. These included family based DNA testing for cosegregation of variants with phenotype, and transcript based analysis. In some patients, despite extensive genetic testing, a secure molecular diagnosis could not be made using DNA sequencing technologies, illustrating that challenges still remain in the field of genetic diagnostics.
APA, Harvard, Vancouver, ISO, and other styles
8

Mohamed, Nahla. "Molecular Diagnosis of Common Viral Infectious Diseases Based on Real-Time PCR." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-7118.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Xu, Jiru. "Application of PCR and DNA sequencing based molecular diagnosis in infectious diseases." Thesis, University of Ulster, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.399727.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Abdelrahman, Wael Hosny Abdellatif. "Avian intestinal spirochaetosis in British egg laying flocks : molecular diagnosis, epidemiology and economic impact." Thesis, Royal Veterinary College (University of London), 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.559017.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "Autoimmune diseases Molecular diagnosis"

1

Conrad, K. Autoantibodies in systemic autoimmune diseases: A diagnostic reference. Lengerich: Pabst Science Pub., 2002.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
2

Constantin, Bona, and Theofilopoulos A. N, eds. The molecular pathology of autoimmune diseases. 2nd ed. Amsterdam: Harwood Academic, 2001.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

Autoimmune diagnostics. Berlin: De Gruyter, 2011.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
4

J, Brenner Kyle, ed. Autoimmune diseases: Symptoms, diagnosis, and treatment. Hauppauge, N.Y: Nova Science Publishers, 2010.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
5

M, Lydyard Peter, Brostoff Jonathan, and Roitt Ivan M, eds. Autoimmune disease: Aetiopathogenesis, diagnosis, and treatment. Oxford: Blackwell Science, 1994.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
6

1957-, Demaine Andrew G., Banga J.-Paul 1953-, McGregor Alan M. 1948-, and North Atlantic Treaty Organization. Scientific Affairs Division., eds. The molecular biology of autoimmune disease. Berlin: Springer-Verlag, 1990.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
7

Petrov, Maria E. Autoimmune disorders: Symptoms, diagnosis, and treatment. Hauppauge, N.Y: Nova Science Publishers, 2010.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
8

Yehuda, Shoenfeld, Cervera Ricard, and Gershwin M. Eric 1946-, eds. Diagnostic criteria in autoimmune diseases. Totowa, NJ: Humana Press, 2008.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
9

Jeffery, S. Molecular diagnosis. Oxford: BIOS Scientific, 1999.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
10

Hertl, Michael. Autoimmune diseases of the skin: Pathogenesis, diagnosis, management. 3rd ed. Wien: Springer, 2011.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Book chapters on the topic "Autoimmune diseases Molecular diagnosis"

1

Tsuruta, Daisuke, Teruki Dainichi, Takahiro Hamada, Norito Ishii, and Takashi Hashimoto. "Molecular Diagnosis of Autoimmune Blistering Diseases." In Methods in Molecular Biology, 17–32. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-227-8_2.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

James, Judith A., and Catriona A. Wagner. "Toward Molecular Diagnoses for Autoimmune Rheumatic Diseases." In Diagnoses Without Names, 33–41. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-04935-4_4.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Edwards, N. Lawrence. "Autoimmune Diseases." In Principles of Molecular Medicine, 299–307. Totowa, NJ: Humana Press, 1998. http://dx.doi.org/10.1007/978-1-59259-726-0_34.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Zeniya, Mikio. "Diagnosis of Autoimmune Hepatitis." In Autoimmune Liver Diseases, 67–81. Tokyo: Springer Japan, 2014. http://dx.doi.org/10.1007/978-4-431-54789-1_5.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Wayne, Sigrid. "Systematic Autoimmune Diseases." In Molecular Pathology Library, 9–19. Boston, MA: Springer US, 2010. http://dx.doi.org/10.1007/978-1-4419-1707-2_2.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Khan, Ashraf, and Otto Walter. "Autoimmune Thyroid Diseases." In Molecular Pathology Library, 37–45. Boston, MA: Springer US, 2010. http://dx.doi.org/10.1007/978-1-4419-1707-2_5.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Tanaka, Atsushi. "Diagnosis and UDCA Treatment of Primary Biliary Cirrhosis." In Autoimmune Liver Diseases, 249–59. Tokyo: Springer Japan, 2014. http://dx.doi.org/10.1007/978-4-431-54789-1_18.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Chen, Youhai H. "Apoptosis and Autoimmune Diseases." In Molecular Mechanisms of Programmed Cell Death, 67–78. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4757-5890-0_6.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Coppedè, Fabio, and Lucia Migliore. "Epigenetics of Autoimmune Diseases." In Molecular mechanisms and physiology of disease, 151–73. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-0706-9_6.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Mascaró, Jose M. "Histological and Immunofluorescence Diagnosis of Autoimmune Blistering Diseases." In Blistering Diseases, 161–91. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-45698-9_16.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Autoimmune diseases Molecular diagnosis"

1

Kasem, Maryam A. G., Marwa M. A. Hadhoud, and Mohammed A. A. ELdesoky. "Automatic diagnosis of autoimmune diseases by classifying HEp-2 cells." In 2017 13th International Computer Engineering Conference (ICENCO). IEEE, 2017. http://dx.doi.org/10.1109/icenco.2017.8289789.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Amanatidis, Dimitrios, Georgios Chatzisavvas, and Michael Dossis. "Brain MRI based diagnosis of autoimmune diseases using deep learning." In 2022 7th South-East Europe Design Automation, Computer Engineering, Computer Networks and Social Media Conference (SEEDA-CECNSM). IEEE, 2022. http://dx.doi.org/10.1109/seeda-cecnsm57760.2022.9932959.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Barturen, G., M. Kerick, D. Alvarez-Errico, R. Quintares, E. Carnero, D. Gemperline, E. Dow, et al. "S1A:5 Molecular stratification of autoimmune diseases based on epigenetic profiles." In 11th European Lupus Meeting, Düsseldorf, Germany, 21–24 March 2018, Abstract presentations. Lupus Foundation of America, 2018. http://dx.doi.org/10.1136/lupus-2018-abstract.2.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Barturen, Guillermo, Sepideh Babaei, Francesc Català-Moll, Manuel Martínez-Bueno, Zuzanna Makowska, Jordi Martorell-Marugán, Pedro Carmona-Sáez, et al. "O31 Integrative analysis reveals a molecular stratification of systemic autoimmune diseases." In 12th European Lupus Meeting. Lupus Foundation of America, 2020. http://dx.doi.org/10.1136/lupus-2020-eurolupus.42.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Gupta, Riya, Aditya M. Rao, Lara Murphy Jones, and Purvesh Khatri. "Formulating a gene signature for diagnosis of autoimmune and infectious diseases." In BCB '21: 12th ACM International Conference on Bioinformatics, Computational Biology and Health Informatics. New York, NY, USA: ACM, 2021. http://dx.doi.org/10.1145/3459930.3469497.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Dantas Pimentel, Danielly, Gizelle Gouvea Rezende, Gustavo Roberto Lourenço, Iane Tamara Dondé, Juliana de Jesus Boscolo, Luciana Akita, Viviane Alves Costa, Viviane Queiroz de Oliveira Maia, and Taisa Morete da Silva. "IDIOPATHIC PULMONARY HEMOSIDEROSIS AS A DIFFERENTIAL DIAGNOSIS OF AUTOIMMUNE DISEASES: CASE REPORT." In Congresso Brasileiro de Reumatologia 2020. Sociedade Brasileira de Reumatologia, 2021. http://dx.doi.org/10.47660/cbr.2020.17292.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Korolev, M., L. Fedotov, A. Ogloblin, B. Fedotov, and D. Luchinina. "DIAGNOSIS AND TREATMENT OF PATIENTS SUFFERING FROM AUTOIMMUNE DISEASES OF THE ESOPHAGUS, COMPLICATED BY BENIGH STRICTURE." In ESGE Days 2019. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1681886.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Seixas, Luiza Kohler, Marcio da Silva Paz, Claudia Suemi Kamoi Kay, Lineu Cesar Werneck, Paulo José Lorenzoni, Renata Dal Prá Ducc, and Rosana Herminia Scola. "Autoimmune diseases associated with inflammatory demyelinating diseases of the central nervous system – a cross sectional study." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.141.

Full text
Abstract:
Background: The most prevalent autoimmune diseases (AID) of the Central Nervous System (CNS) are Multiple Sclerosis (MS) and Neuromyelitis Optica Spectrum Disorder (NMOSD), both being demyelinating diseases. Recent studies show that patients with CNS demyelinating diseases have a higher risk of presenting associated diagnosis of another AIDs. Objectives: The present study aimed to evaluate the frequency of autoimmune comorbidities and autoantibodies in patients with MS and NMOSD. Design and setting: Were analyzed the medical records of 126 patients with MS or NMOSD, from the Demyelinating Diseases Outpatient Clinic in the Neurological and Psychiatric Unit in the Complexo Hospital de Clinicas da Universidade Federal do Parana (CHC-UFPR), taking in consideration the presence of AIDs and autoantibodies. Methods: The variables were organized in a Microsoft® Office Excel spreadsheet for statistical analysis. Results: Of the 126 analyzed cases, 111 (88%) corresponded to MS and 15 (12%) to NMOSD. From the total, at least one AID was associated in 11 patients (8.7%), six of which were diagnosed with MS and five with NMOSD (p<0.05). Regarding autoantibodies, there were 21 cases (16.7%) in which antinuclear antibodies (ANA) were present, and 12 cases (9.5%) in which autoantibodies other than ANA were present (p<0.05). Conclusions: The results of the study showed a higher frequency of AIDs in patients with CNS demyelinating diseases compared to the normal population. The results found in this study may contribute to improve the treatment and follow-up of patients with CNS demyelinating diseases, so that the concomitance of other AIDs is considered by the clinician.
APA, Harvard, Vancouver, ISO, and other styles
9

Blaskovich, Mark A., Wanida Phetsang, M. Rhia Stone, Urszula Lapinska, Stefano Pagliara, Rajiv Bhalla, and Matthew A. Cooper. "Antibiotic-derived molecular probes for bacterial imaging." In Photonic Diagnosis, Monitoring, Prevention, and Treatment of Infections and Inflammatory Diseases 2019, edited by Tianhong Dai, Mei X. Wu, and Jürgen Popp. SPIE, 2019. http://dx.doi.org/10.1117/12.2507329.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Remuzgo-Martínez, S., B. Atienza-Mateo, V. Pulito-Cueto, F. Genre, V. M. Mora-Cuesta, D. Iturbe-Fernández, V. Portilla, et al. "Endothelin-1 for the differential diagnosis between interstitial lung disease associated with autoimmune diseases and idiopathic pulmonary fibrosis." In ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.2310.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Reports on the topic "Autoimmune diseases Molecular diagnosis"

1

Yogev, David, Ricardo Rosenbusch, Sharon Levisohn, and Eitan Rapoport. Molecular Pathogenesis of Mycoplasma bovis and Mycoplasma agalactiae and its Application in Diagnosis and Control. United States Department of Agriculture, April 2000. http://dx.doi.org/10.32747/2000.7573073.bard.

Full text
Abstract:
Mycoplasma bovis and M. agalactiae are two phylogenetically related mycoplasmas which cause economically significant diseases in their respective bovine or small ruminant hosts. These organisms cause persistent asymptomatic infections that can result in severe outbreaks upon introduction of carrier animals into susceptible herds. Little is known about the mechanisms underlying mycoplasma-host interaction, variation in virulence, or of the factors enabling avoidance of the host immune system. In recent years it has become apparent that the ability of pathogenic microorganisms to rapidly alter surface antigenic structures and to fine tune their antigenicity, a phenomena called antigenic variation, is one of the most effective strategies used to escape immune destruction and to establish chronic infections. Our discovery of a novel genetic system, mediating antigenic variation in M. bovis (vsp) as well as in M. agalactiae (avg) served as a starting point for our proposal which included the following objectives: (i) Molecular and functional characterization of the variable surface lipoproteins (Vsp) system of M. bovis and comparison with the Vsp-counterpart in M. agalactiae (ii) Determination of the role of Vsp proteins in the survival of M. bovis when confronted by host defense factors, (iii) Assessment of Vsp-based genetic and antigenic typing of M. bovis and M. agalactiae for epidemiology of infection and (iv) Improvement of diagnostic tests for M. bovis and M. agalactiae based on the vsp-and vsp-analogous systems. We have carried out an extensive molecular characterization of the vsp system and unravelled the precise molecular mechanism responsible for the generation of surface antigenic variation in M. bovis. Our data clearly demonstrated that the two pathogenic mycoplasma species possess large gene families encoding variable lipoprotein antigens that apparently play an important role in immune evasion and in pathogen-host interaction during infection. Phase variable production of these antigens was found to be mediated by a novel molecular mechanism utilizing double site-specific DNA inversions via an intermediate vsp configuration. Studies in model systems indicate that phase variation of VspA is relevant in interaction between M. bovis and macrophages or monocytes, a crucial stage in pathogenesis. Using an ELISA test with captured VspA as an antigen, phase variation was shown to occur in vivo and under field conditions. Genomic rearrangements in the avg gene family of M. agalactiae were shown to occur in vivo and may well have a role in evasion of host defences and establishment of chronic infection. An epidemiological study indicated that patterns of vsp-related antigenic variation diverge rapidly in an M. bovis infected herd. Marked divergence was also found with avg-based genomic typing of M. agalactiae in chronically infected sheep. However, avg-genomic fingerprints were found to be relatively homogeneous in different animals during acute stages of an outbreak of Contagious Agalactiae, and differ between unrelated outbreaks. These data support the concept of vsp-based genomic typing but indicate the necessity for further refinement of the methodology. The molecular knowledge on these surface antigens and their encoding genes provides the basis for generating specific recombinant tools and serological methods for serodiagnosis and epidemiological purposes. Utilization of these methods in the field may allow differentiating acutely infected herds from chronic herds and disease-free herds. In addition the highly immunogenic nature of these lipoproteins may facilitate the design of protective vaccine against mycoplasma infections.
APA, Harvard, Vancouver, ISO, and other styles
2

Ehrlich, Marcelo, John S. Parker, and Terence S. Dermody. Development of a Plasmid-Based Reverse Genetics System for the Bluetongue and Epizootic Hemorrhagic Disease Viruses to Allow a Comparative Characterization of the Function of the NS3 Viroporin in Viral Egress. United States Department of Agriculture, September 2013. http://dx.doi.org/10.32747/2013.7699840.bard.

Full text
Abstract:
Project Title: "Development of a plasmid-based reverse genetics system for the Bluetongue and Epizootic Hemorrhagic Disease viruses to allow comparative characterization of the function of the NS3 viroporin in viral egress". Project details: No - IS-4192-09; Participants – Ehrlich M. (Tel Aviv University), Parker J.S. (Cornell University), DermodyT.S. (Vanderbilt University); Period - 2009-2013. Orbiviruses are insect-borne infectious agents of ruminants that cause diseases with considerable economical impact in Israel and the United States. The recent outbreaks of BTV in Europe and of Epizootic Hemorrhagic Disease Virus (EHDV) in Israel, underscore the need for: (i) a better comprehension of the infection process of orbiviruses, (ii) the identification of unique vs. common traits among different orbiviruses, (iii) the development of novel diagnosis and treatment techniques and approaches; all aimed at the achievement of more effective control and treatment measures. It is the context of these broad goals that the present project was carried out. To fulfill our long-term goal of identifying specific viral determinants of virulence, growth, and transmission of the orbiviruses, we proposed to: (i) develop reverse genetics systems for BTV and EHDV2-Ibaraki; and (ii) identify the molecular determinants of the NS3 nonstructural protein related to viroporin/viral egress activities. The first objective was pursued with a two-pronged approach: (i) development of a plasmid-based reverse genetics system for BTV-17, and (ii) development of an "in-vitro" transcription-based reverse genetics system for EHDV2-Ibaraki. Both approaches encountered technical problems that hampered their achievement. However, dissection of the possible causes of the failure to achieve viral spread of EHDV2-Ibaraki, following the transfection of in-vitro transcribed genomic segments of the virus, revealed a novel characteristic of EHDV2-Ibaraki infection: an uncharacteristically low fold increase in titer upon infection of different cell models. To address the function and regulation of NS3 we employed the following approaches: (i) development (together with Anima Cell Metrology) of a novel technique (based on the transfection of fluorescently-labeledtRNAs) that allows for the detection of the levels of synthesis of individual viral proteins (i.e. NS3) in single cells; (ii) development of a siRNA-mediated knockdown approach for the reduction in levels of expression of NS3 in EHDV2-Ibaraki infected cells; (iii) biochemical and microscopy-based analysis of the localization, levels and post-translational modifications of NS3 in infected cells. In addition, we identified the altered regulation and spatial compartmentalization of protein synthesis in cells infected with EHDV2-Ibaraki or the mammalian reovirus. In EHDV2-Ibaraki-infected cells such altered regulation in protein synthesis occurs in the context of a cell stress reponse that includes the induction of apoptosis, autophagy and activation of the stressrelated kinase c-Jun N-terminal Kinase (JNK). Interestingly, inhibition of such stress-related cellular processes diminishes the production of infectious virions, suggesting that EHDV usurps these responses for the benefit of efficient infection. Taken together, while the present project fell short of the generation of novel reverse genetics systems for orbiviruses, the development of novel experimental approaches and techniques, and their employment in the analysis of EHDV-infected cells, yielded novel insights in the interactions of orbiviruses with mammalian cells.
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Autoimmune diseases Molecular diagnosis' for particular source types:
Journal articles Dissertations / Theses Books
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography