Relevant bibliographies by topics / Pathogenesis

Academic literature on the topic 'Pathogenesis'

Author: Grafiati
Published: 4 June 2021
Last updated: 26 July 2024

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Journal articles on the topic "Pathogenesis"

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Orazov, M. R., V. E. Radzinsky, E. D. Dolgov, and Yu G. Abramashvili. "Pathogenesis and pathogenetic options in endometriosis management." Voprosy ginekologii, akušerstva i perinatologii 22, no. 1 (2023): 92–104. http://dx.doi.org/10.20953/1726-1678-2023-1-92-104.

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This article provides a literature review on the etiopathogenesis of endometriosis. Particular attention was paid to genetic and molecular biological aspects of endometriosis. The issues of conservative management of patients with confirmed endometriosis were also considered. The use of dienogest in the treatment of patients with endometriosis was substantiated. Key words: endometriosis, etiopathogenesis, genetic and molecular determinants, dienogest
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Roy, Saumendu Deb. "Pathogenesis of COVID-19." INDIAN RESEARCH JOURNAL OF PHARMACY AND SCIENCE 7, no. 4 (September 2020): 2354–58. http://dx.doi.org/10.21276/irjps.2020.7.3.3.

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Strokov, I. A., and V. V. Oganov. "Pathogenesis, evaluation and pathogenetic therapy of diabetic polyneuropathy." Neurology, Neuropsychiatry, Psychosomatics 13, no. 3 (June 24, 2021): 99–106. http://dx.doi.org/10.14412/2074-2711-2021-3-99-106.

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The increase in the number and life expectancy of patients with diabetes mellitus (DM) worldwide determines the high prevalence of late complications of diabetes, including diabetic polyneuropathy (DPN), the most common type of polyneuropathy. Oxidative stress is considered the main reason for the cellular pathology development in diabetes mellitus, which determines the use of antioxidants for the DPN treatment. Alpha-lipoic acid (ALA), a natural fat-soluble antioxidant, is the most effective drug for reducing DPN symptoms. Furthermore, the symptom-modifying effect of ALA has been shown in numerous randomized controlled trials. The article discusses the possible disease-modifying effect of ALA.
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Galante, Iv. "A. Bakk & Gh. Tamasescu Ueber die Aetiologie und Pathogenese der Epilepsie und deren Therapie. Wiener Med. W. No. 17, 1933." Kazan medical journal 29, no. 5-6 (January 12, 2022): 489. http://dx.doi.org/10.17816/kazmj89620.

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Bakk and Tamasescu (A. Bakk Gh. Tamasescu Ueber die Aetiologie und Pathogenese der Epilepsie und deren Therapie. Wiener Med. W. No. 17, 1933) give a good concise overview of the etiology, pathogenesis and treatment of epilepsy. Epilepsy is an organic syndrome with a different etiology and multiple pathogenetic factors, which explains that the methods of treatment for epilepsy vary enormously.
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A, Abdelmoktader. "Mycobacterial Tuberculosis Epidemiology and Pathogenesis." Virology & Immunology Journal 4, no. 4 (November 19, 2020): 1–7. http://dx.doi.org/10.23880/vij-16000259.

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Mycobacterium tuberculosis (MTB) is an acid fast bacterium (AFB); it has tough cell wall and circular chromosome. It is transmitted through the airborne route and cause tuberculosis (TB). The distribution of tuberculosis is not uniform across the globe; about 80% of the population in many Asian and African countries and it is the second most common cause of death from infectious disease after HIV. Organisms deposited mainly in the upper lung zones, kidneys and bones. In persons with intact cell-mediated immunity (CMI), collections of activated T cells and macrophages form granulomas that limit multiplication and spread of the organism. The Status of CMI will determine if the patient will get active or latent TB infection.
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Kim, Young Kyoon, and Younsuck Koh. "Pathogenesis." Tuberculosis and Respiratory Diseases 50, no. 5 (2001): 525. http://dx.doi.org/10.4046/trd.2001.50.5.525.

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Witz, Craig, and Robert Schenken. "Pathogenesis." Seminars in Reproductive Medicine 15, no. 03 (August 1997): 199–208. http://dx.doi.org/10.1055/s-2008-1068749.

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Gollnick, Harald P. M., Christos C. Zouboulis, Hirohiko Akamatsu, Ichiro Kurokawa, and Anja Schulte. "Pathogenesis and Pathogenesis Related Treatment of Acne." Journal of Dermatology 18, no. 9 (September 1991): 489–99. http://dx.doi.org/10.1111/j.1346-8138.1991.tb03122.x.

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Bilalova, K. A., and L. A. Yusupova. "ROSACEA: FEATURES OF PATHOGENESIS AND THERAPY." European Journal of Natural History, no. 2 2022 (2022): 18–21. http://dx.doi.org/10.17513/ejnh.34252.

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Tuor, Paula, and Jenkins Zhao. "Pathogenesis of Brain: Autism Spectrum Disorders." Neuroscience and Neurological Surgery 2, no. 2 (April 20, 2018): 01–02. http://dx.doi.org/10.31579/2578-8868/029.

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Autism spectrum disorders (ASDs) affect as many as 1 in 45 children and are characterized by deficits in sociability and communication, as well as stereotypic movements. Many children also show severe anxiety.
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Dissertations / Theses on the topic "Pathogenesis"

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Booler, Helen. "Pathogenetic mechanisms in the dystroglycanopathies pathogenesis." Thesis, Royal Veterinary College (University of London), 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.669190.

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Khamas, E. J. "Pathogenesis of staphylococcosis." Thesis, University of Nottingham, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.234678.

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deLeeuw, Ronald John. "Mantle cell lymphoma pathogenesis." Thesis, University of British Columbia, 2009. http://hdl.handle.net/2429/12469.

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Mantle cell lymphoma (MCL) is an aggressive non-Hodgkin’s lymphoma with a median patient survival time of 3 years. Although the characteristic t(11;14)(q13;q32) is found in virtually all cases, experimental evidence suggests that this event alone is insufficient to result in lymphoma and secondary genomic alterations are required. Therefore, secondary genetic alterations have been proposed as essential in MCL pathogenesis. Within this thesis I describe the creation of a novel assay to determine segmental copy number alterations at a previously unprecedented resolution. This new assay necessitated the development of new analytical software to visualize and analyze the high density data sets created. The creation of this software is described in detail. With these tools in place we assayed model genomes of MCL for recurrent segmental copy number alterations. These recurrent regions were defined; however, among these were copy number variations that appeared in both cases and controls. Investigation of these natural copy number variations in this thesis revealed that the human genome has a higher plasticity than previously appreciated. In fact, thousands of loci within the genome were found to be variable in copy number that may influence sensory perception and possibly disease susceptibility. I next investigated the genomes of MCL tumor samples to determine which somatic copy number alterations are related to a poor clinical course. Among the numerous loci that showed frequent copy number alterations in MCL genomes, many were associated with poor patient outcome. Among these, the loss of 9p21 was a strong factor in determining the clinical course of patients with MCL (P=0.0004). Three additional loci (4q13, 8q24, and 13q14) were combined with 9p21 to create a survival model that was very predictive of patient outcome (P=5.87 x 10-6). Interestingly, a previously uncharacterized locus (4q13) was within this survival model. Investigating this locus further revealed that the expression of two genes (CCNG2 and CCNI) influences the overall survival of patients with MCL (P=0.0292 and 0.0201, respectively).
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Sissons, James Robert. "Pathogenesis of Alanthamoeba encephalitis." Thesis, Birkbeck (University of London), 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.429097.

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Cowie, Danielle. "Iron and Tuberculosis pathogenesis." Thesis, Stellenbosch : Stellenbosch University, 2014. http://hdl.handle.net/10019.1/86566.

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Thesis (MSc)--Stellenbosch University, 2014.
ENGLISH ABSTRACT: Iron is an essential element that plays a role in the process of respiration, oxygen transport and as a principle cofactor to several enzymes. Iron homeostasis is a finely regulated process since excess levels become toxic to healthy cells via the production of reactive oxygen species. A plethora of genes that control several key points throughout this regulatory process have been identified. Research focusing on changes in expression levels and downstream functional effects of these genes has become increasingly important over the past decade. One area of particular interest has emerged since a link between iron status and host response to Mycobacterium tuberculosis infection was discovered. Although the prevalence of Tuberculosis has decreased across the globe with the exception of Africa and parts of Europe, the mortality rate remains high. Therefore, research that focuses on understanding an individual’s predetermined susceptibility to TB infection at the genetic level could provide health care practitioners with the tools required to identify and educate at-risk individuals prior to TB infection. RT-qPCR was utilised to determine expression profiles for eight iron genes (CP, CYBRD1, FTH, FTL, LTF, HFE, HMOX1, and SCL40A1) normalised to three reference genes (ACTB, GUSB, and RPL37A1). Up-regulation is demonstrated in the TB group for transcript levels recorded for CYBRD1, HFE, HMOX1, and SLC40A1. Several measured serum parameters including conjugated, unconjugated, total bilirubin, and total protein were increased in the TB group while albumin was significantly lower in this group. Correlation analysis demonstrated that a positive correlation exists between transferrin saturation and iron and a negative correlation exists between transferrin and ferritin levels. Individuals categorised with low serum iron levels demonstrated lower CP/GUSB levels and higher HMOX1/GUSB levels. Individuals categorised with low transferrin saturation levels demonstrated higher FTL/GUSB and SLC40A1/GUSB levels and lower CP/GUSB. Results from this study provide further evidence for the relationship between iron status and TB infection rates, although protein studies are required to confirm these results. The data obtained illustrate the important role that these profiles and iron parameters may play in the clinical field when identifying at-risk individuals. Further investigation that focuses on which gene profile and parameter combinations show the most distinctive utility in the clinical setting is warranted.
AFRIKAANSE OPSOMMING: Yster is ‘n noodsaaklike element wat ‘n rol speel in die proses van respirasie en die vervoer van suurstof en ook ‘n belangrike ko-faktor vir verskeie ensieme is. Yster homeostase is op ‘n fyn manier gereguleer omdat oormatige vlakke toksies kan wees vir gesonde selle wanneer reaktiewe suurstofspesies geproduseer word. ‘n Magdom gene wat verskeie sleutelpunte in hierdie proses kontroleer is voorheen identifiseer. Navorsing wat fokus op die veranderinge in geenuitdrukkingsvlakke en die funksionele gevolge daarvan het oor die afgelope dekade toenemend belangrik geword. Een gebied van spesifieke belang het na vore gekom nadat ‘n verband tussen ystervlakke en die manier waarop die immuunstelsel reageer op Mycobacterium tuberculosis infeksie, ontdek is. Alhoewel die voorkoms van Tuberkulose wêreldwyd, behalwe in Afrika en sekere dele van Europa, afgeneem het, bly die sterftesyfer hoog. Daarom kan navorsing wat daarop fokus om ‘n individu se voorafbepaalde vatbaarheid vir TB-infeksie op die genetiese vlak te verstaan dalk aan gesondheidswerkers die regte instrumente verskaf om hoë-risiko individue te identifiseer en op te voed voordat hulle TB ontwikkel. RT-qPKR is gebruik om die geenuitdrukkingsvlakke van agt ystergene, wat met drie verwysings-gene (ACTB, GUSB, en RPL37A1) genormaliseer is, te bepaal. ‘n Toename in die uitdrukkingsvlakke van CYBRD1, HFE, HMOX1, en SLC40A1 is in die TB-groep waargeneem. Die bloedvlakke van verskeie parameters insluitend gekonjugeerde, ongekonjugeerde, totale bilirubin, en totale proteïen was hoër in die TB-groep, terwyl albuminvlakke laer was in hierdie groep. Korrelasie-analise het ‘n positiewe korrelasie tussen transferrin-versadiging en yster getoon, terwyl daar ‘n negatiewe korrelasie tussen transferrin- en ferritinvlakke gevind is. Individue met lae ystervlakke het laer CP/GUSB-vlakke en hoër HMOX1/GUSB-vlakke getoon. Individue met lae transferrin-versadiging het hoër FTL/GUSB- en SLC40A1/GUSB-vlakke en laer CP/GUSB-vlakke getoon. Resultate uit hierdie studie verskaf verdere getuienis dat daar ‘n verwantskap tussen ystervlakke en TB-infeksiekoerse bestaan, alhoewel proteïenstudies nodig is om hierdie resultate te bevestig. Die data dui op die belangrike rol wat hierdie profiele en ystervlakke in die kliniese veld mag speel in die identifisering van hoë-risiko individue. Verdere ondersoek, gefokus op watter geenprofiel en parameterkombinasies die grootste nut in die kliniese omgewing bied, is geregverdig.
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Yau, Belinda. "Pathogenesis of pneumococcal meningitis." Thesis, The University of Sydney, 2014. http://hdl.handle.net/2123/12485.

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Streptococcus pneumoniae (SP) meningitis remains a significant cause of global childhood mortality, and a potential epidemic pathogen despite improving vaccinations schemes. Neuropathology in pneumococcal meningitis (PM) is attributed to both bacterial products and the host-mediated proinflammatory response. Proinflammatory cytokine interferon-gamma (IFNγ) is associated with macrophage activation and regulating MHC Class I expression in innate immunity. IFNγ gene knockout (GKO) mice inoculated with ~5 x 103 CFU of SP/mouse were significantly protected against fatal PM, compared to C57Bl/6 WT mice, in both serotype 3 WU2 and serotype 4 TIGR4 strains. TIGR4 PM was comparatively more virulent than WU2 PM. In murine PM, IFNγ regulated induction of chemokines MCP1, CXCL9, CXCL10, the IRGM1, IRGM3 proteins and nitric oxide synthase 2 (NOS2). In WU2 PM, production of IFNγ was attributed to infiltrating Natural Killer (NK) cells, and dependent upon activation of the inflammasome complex and interleukin-18. NOS2 GKO exhibited a significantly improved survival phenotype, and reduced blood brain barrier dysfunction, compared to WT mice. Intracellular staining revealed Ly6Chi monocytes and NK cells as the source of IFNγ-dependent NOS2 in PM. Overall, this thesis addresses IFNγ production and its contribution to experimental PM pathology.
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Cartón, García Fernando. "Myosin VB in intestinal pathogenesis." Doctoral thesis, Universitat Autònoma de Barcelona, 2017. http://hdl.handle.net/10803/458251.

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Miosina VB es una proteína que actúa como un motor molecular usando la energía del ATP para moverse a lo largo de filamentos de actina. Participa en el trafico intracelular de endosomas de reciclaje en la parte subapical de células polarizadas y no polarizadas. Su expresión es muy abundante en el intestino donde participa en el establecimiento y mantenimiento de la polaridad de los enterocitos. Mutaciones en MYO5B causan la enfermedad de inclusión de microvellosidades, in raro trastorno congénito que afecta a las células epiteliales del intestino cursando con diarrea acuosa persistente que suele ser fatal. Esta enfermedad se caracteriza por la presencia de alteraciones morfológicas en los enterocitos, atrofia de las vellosidades y deslocalización de proteínas del polo apical y basolateral del enterocito. Su patología molecular no se conoce, principalmente por la falta de modelos animales. En el presente estudio, describimos un versátil modelo murino con inactivación constitutiva de Myo5b e inactivación condicional en las células epiteliales intestinales inducida por tamoxifeno. En ambos casos, los animales muestras un cuadro clínico muy semejantes al de los pacientes con enfermedad de inclusión de microvellosidades, presentado diarrea y deshidratación que causan la muerte del animal. A nivel histológico, el intestino muestra las mismas alteraciones en los enterocitos que las presentes en pacientes humanos, incluyendo atrofia de vellosidades y deslocalización de marcadores proteicos. Además, la inactivación de Myo5b también provocó hiperproliferación de las criptas intestinales. Por lo tanto, el modelo animal presentado constituye una herramienta muy útil para investigar las causas moleculares de la enfermedad y ensayar de manera preclínica fármacos u otras opciones terapéuticas. Por otro lado, la pérdida de polaridad y diferenciación es también una de las señas de identidad de los carcinomas metastásicos avanzados y correlaciona con un mal pronóstico de los pacientes. En concreto, para el cáncer colorrectal, investigaciones previas llevadas a cabo en nuestro laboratorio ya han demostrado que la pérdida de miosina IA promueve la progresión la enfermedad y tiene actividad supresora de tumores. Dicha proteína es abundante en el borde en cepillo de los enterocitos, y participa en el mantenimiento de la estructura polarizada. Otros estudios han señalado la relación entre la inactivación de MYO5B con un incremento en la motilidad e invasión de células de cáncer gástrico, aunque todavía no se conoce nada de su relación con en el cáncer colorrectal. Para resolver esta cuestión, hemos diseñado modelos in vitro inducibles por doxiciclina para sobre expresar y reducir la expresión de dicha proteína en líneas celulares de cáncer de colon. Además, se ha empleado la tecnología CRISPR/Cas9 para inactivar la expresión de MYO5B en la línea de cáncer de colon Caco2-BBE. Los resultados muestran cambios en la polarización y diferenciación de dichas líneas celulares, de acuerdo con observaciones previas. También se ha observado una posible relación entre MYO5B y la capacidad de movilidad e invasión de las líneas de cáncer de colon. Sin embargo, la hiperproliferación observada en el intestino de los ratones no se reproduce en las líneas de cáncer de colon empleadas tras reducir o sobre expresar MYO5B, o en modelos xenograft subcutáneos in vivo de dichas líneas. Por otro lado, usando un microarray de tejidos con 155 muestras de tumores primarios de pacientes con cáncer colorrectal en estadio Dukes C se ha comprobado que una reducción en la expresión de MYO5B se asocia con una disminución en el tiempo de recaída y en la supervivencia total de los pacientes de cáncer de colon. Además, tumores con un grado de diferenciación bajo también expresan niveles de MYO5B significativamente reducidos. Finalmente, todos estos resultados indican que MYO5B juega un papel importante en la diferenciación del intestino normal y de las líneas de cáncer de colon. De la misma manera, MYO5B también podría desempeñar un papel en la progresión del cáncer colorrectal promoviendo movilidad e invasión de las células tumorales.
Myosin VB is a molecular motor protein that uses the energy of ATP to move along actin filaments. It participates in the recycling endosomes trafficking in the subapical cytoplasmic region of non-polarized and polarized cells. It is highly expressed in the small and large intestine, where its role in the establishment of polarized function in enterocytes is also well known. Inactivating mutations of MYO5B have been associated with microvillus inclusion disease (MVID), a rare congenital disorder of the intestinal epithelial cells that presents with persistent life-threatening watery diarrhea. It is characterized by morphological enterocyte abnormalities such as microvillus atrophy and mislocalization of apical and basolateral protein transporters. The molecular pathology of the disease is not well known mainly due to the lack of animal models. In the present study, we report a versatile murine model with targeted inactivation of Myo5b. This model allowed us to generate and characterized a constitutive Myo5b knockout mice and a tamoxifen-inducible intestinal-epithelium-specific Myo5b knockout. In both cases, the mice closely resemble the phenotype of MVID patients, developing watery diarrhea and dehydration causing the death of the animal. Histological study of the intestine showed all the characteristic enterocyte defects observed in MVID patients, including microvillus atrophy and mislocalization of protein markers. Moreover, the inactivation of MYO5B also originated hyperproliferation of the intestinal crypts. Therefore, our mice constitute a useful model to further investigate the underlying molecular mechanism of this disease and to preclinically assess the efficacy of novel therapeutic approaches. In addition, hyperproliferation as well as loss of cell polarity, differentiation, and tissue architecture are hallmarks of advanced metastatic carcinomas and strongly correlate with poor patient prognosis. Specifically, for colorectal cancer, the third most common type of cancer worldwide, we have previously demonstrated that the loss of brush border MYO1A, also involved in cell polarity, promotes cancer progression and has tumor suppressor activity. Other studies have indicated a relationship between MYO5B inactivation and gastric cancer, promoting invasion and motility, but little is known regarding its role in colorectal cancer. To address this question, we have developed novel doxycycline-inducible in vitro models of MYO5B overexpression and downregulation. Moreover, we have generated MYO5B knockout Caco2-BBE cells using CRISPR/Cas9 technology. Our results showed changes in the polarization and differentiation of colon cancer cells, in agreement with previous observations in the normal intestine. Moreover, we have observed a relationship between MYO5B and the motility and invasion capacity of colon cancer cells, indicating a possible role of MYO5B in colon cancer progression. However, the effect of MYO5B loss in cell proliferation observed in our Myo5b knockout mice could not be confirmed in our models in vitro and in vivo, employing cell line-derived xenografts. In addition, using a tissue microarray containing triplicate samples from 155 primary Dukes C colorectal tumors, reduced MYO5B expression was found to be associated with shorter disease-free and overall survival of the patients. Moreover, poorly differentiated tumors showed significantly reduced expression of MYO5B. Collectively, our results indicate that MYO5B plays an important role in the differentiation of the normal intestinal epithelium and colon cancer cells, as well as a possible role in cancer progression promoting cell motility and invasion.
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Hamoudi, Rifat A. "Molecular pathogenesis of MALT lymphoma." Thesis, University of Cambridge, 2010. https://www.repository.cam.ac.uk/handle/1810/238398.

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Mucosa associated lymphoid tissue (MALT) lymphoma is characterized by t(11;18)(q21;q21)/API2-MALT1, t(1;14)(p22;q32)/BCL10-IGH andt(14;18)(q32;q21)/IGH-MALT1, which commonly activate the NF-κB pathway. Gastric MALT lymphomas harbouring such translocation do not respond to Helicobacter pylori eradication, while those without translocation can be cured by antibiotics. To understand the molecular mechanism of MALT lymphoma with and without chromosome translocation, 24 cases (15 translocation-positive and 9 translocation-negative) of MALT lymphomas together with 7 follicular lymphomas and 7 mantle cell lymphomas were analysed by Affymetrix gene expression microarray platform. Unsupervised clustering showed that cases of MALT lymphoma were clustered as a single branch. However, within the MALT lymphoma group, translocation-positive cases were intermingled with translocation-negative cases. Gene set enrichment analysis (GSEA) of the NF-κB target genes and 4394 additional gene sets covering various cellular pathways, biological processes and molecular functions showed that translocation-positive MALT lymphomas were characterized by an enhanced expression of NF-κB target genes, particularly TLR6, CCR2, CD69 and BCL2, while translocation-negative cases were featured by active inflammatory and immune responses, such as IL8, CD86, CD28 and ICOS. Separate analyses of the genes differentially expressed between translocation-positive and negative cases and measurement of gene ontology term in these differentially expressed genes by hypergeometric test reinforced the above findings by GSEA. The differential expression of these NF-κB target genes between MALT lymphoma with and without translocation was confirmed by quantitative RT-PCR and immunohistochemistry or Western blot. Expression of TLR6, in the presence of TLR2, enhanced both API2-MALT1 and BCL10 mediated NF-κB activation in vitro. In addition, there was cooperation between expression of BCL10, MALT1 or API2-MALT1, and stimulation of the antigen receptor or CD40 or TLR in NF-κB activation as shown by both reporter assay and IκBα degradation. Interestingly, expression of BCL10 but not API2-MALT1 and MALT1, in the presence of LPS stimulation, also triggered IκBβ degradation, suggesting activation of different NF-κB dimers between these oncogenic products. Study by co-immunoprecipitation showed that BCL10 directly interacts with MALT1. Sub-cellular localisation experiments in BJAB B-cells, showed that BCL10 localisation was affected by MALT1. When BCL10 was over-expressed, the protein was predominantly expressed in the nuclei, but when MALT1 was over-expressed, BCL10 was mainly localised in the cytoplasm. When both BCL10 and MALT1 were over-expressed, BCL10 was expressed in the cytoplasm in the early hours when the protein level was low, but in both the cytoplasm and nuclei after 9 hours when the protein level was high. Over-expression of API2-MALT1 did not shown any apparent effect on BCL10 sub-cellular localisation in vitro. Finally, comparison of MALT lymphoma expression microarray with other lymphomas showed lactoferrin to be highly expressed in MALT lymphoma. This was confirmed by qRT-PCR, showing lactoferrin to be significantly over-expressed in MALT lymphoma compared to FL and MCL. Thus lactoferrin may be a potential marker for MALT lymphoma.
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Alam, Sam Mohammad Kutubul. "Pathogenesis of Langerhans Cell Histiocytosis." Thesis, Imperial College London, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.487289.

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The Langerhans cell (LC) is a histiocytic cell that represents a resident immigrant population in the epidermis and functions as a professional antigen presenting cell (APC). Langerhans cell histiocytosis (LCH) is a rare disorder that can affect both adults and children and can involve various organs. Clinically the disease ranges from a solitary lytic bone lesion, which may resolve following curettage, to a disseminated leukaemia-like disease with multiple organ involvement, which can be fatal. Despite considerable advances in our understanding of the disease, the aetiology ofLCH remains obscure. The aim of this study is to identify differentially expressed genes in LCH cell as compared to normal LC to gain novel insight into potential pathologic mechanisms involved in this disease. This has been carried out by using immunoaffinity cell purification against the LC marker CDla, a technique developed in our laboratory, together with a suppressive subtractive cDNA hybridisation (SSH) technique. Because of the limited LCH RNA material, an initial study was carried out to optimise conditions for SSH using HeLa cells and YCI cells, a derivative of HeLa in which CDla is constitutively expressed. By doing these experiments, it was found that the inclusion of an additional step to the subtraction protocol, namely size fractionation and purification of subtracted cDNA, allowed efficient recovery ofcDNA clones for the differentially expressed CDla gene. Using this optimised protocol, gene expression between normal LC and LCH cells obtained from bronchial alveolar lavage from one patient with LCH have been compared. A total of 291 differentially expressed clones were identified by differential screening and sequenced. The resulting sequences were used to search DNA sequence databases and the results used to classify sequences into three groups: (i) sequences that matched known human gene sequences, (ii) sequences that were found to originate from the pathogen Mycoplasma hyorhinis (M hyorhinis) and (iii) gene sequences of unknown origin. Using RT-PCR I have evaluated the expression of these in other LCH samples and have demonstrated one of the known human genes, argininosuccinate synthetase to be differentially expressed exclusively in 18 LCH-involved tissues from 17 LCH involved patients examined to date. Further, using RT-PCR, M hyorhinis sequences were also confirmed in six out of six additional LCH samples derived from bronchial alveolar lavage and two additional LCH samples involving gum. Taken together, these findings suggest that a discrete set of genes are differentially expressed in LCH, which may be important in the pathogenesis of this disease. Further, my data suggest the possible involvement of a novel infectious agent in the disease.
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Wang, Eddy Hsi Chun. "The pathogenesis of alopecia areata." Thesis, University of British Columbia, 2014. http://hdl.handle.net/2429/51360.

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The development of a hair loss disease, alopecia areata (AA), is believed to be associated with the initiation of an autoimmune response triggered by the activation of cytotoxic T-cells (CTLs) by unidentified autoantigen epitopes. The long-term sequelae of AA also have not received investigation beyond clinical observations. I hypothesized that CTLs in AA can be activated by autoantigen epitopes derived from hair follicle (HF) cells and activated CTLs may affect the viability of HF keratinocytes. Furthermore, I hypothesized the development of AA can have adverse effects on heart health and induce apoptosis of cardiomyocytes mediated in part by stress hormones. To test these hypotheses, I stimulated AA human peripheral blood mononuclear cells (PBMCs) and mouse LNCs with HF autoantigen epitope peptides. I showed that trichohyalin (TCHH) peptides induced higher frequencies of AA PBMC activation and led to keratinocyte apoptosis, while cytokeratin 16 (KRT16) peptides activate more AA mouse LNCs; both indicating the importance of keratinocyte autoantigens in AA pathogenesis. We showed that AA mice displayed significantly heavier hearts and collagen deposition in hearts compared to controls. Exposure of heart tissues to stress hormone adrenocorticotrophic hormone (ACTH) resulted in differential expression of interleukin-18 (Il18) genes and increased secretion of cardiac disease marker cardic troponin-I (cTnI). AA patients showed highest levels of cTnI compared to androgenetic alopecia (AGA) and no-hair-loss (NHL) groups. Culturing of cardiomyocytes with plasma from AA subjects with higher levels of cTnI also resulted in higher levels of apoptosis compared to cultures with plasma expressing low levels of cTnI; suggesting presence of harmful factors in the plasma. Additionally, to prove AA is a cell-mediated disease, we established a new mouse model of AA via injecting naïve C3H/HeJ mice with cultured LNCs isolated from spontaneously affected AA mice. In conclusion, AA pathogenesis is associated with higher frequencies of PBMC or LNC activation upon keratinocyte antigen epitope challenge and AA development resulted in changes in gene expression and heart morphology in mice and heart tissue remodeling markers in humans.
Medicine, Faculty of
Medicine, Department of
Experimental Medicine, Division of
Graduate
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Books on the topic "Pathogenesis"

1

M, Iglewski Barbara, and Clark Virginia L, eds. Molecular basis of bacterial pathogenesis. London: Academic Press, 1992.

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Pathogenesis. Chicago: Switchback Books, 2008.

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Kishore, Uday, ed. Microbial Pathogenesis. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-67452-6.

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Ağın, Başak, and Şafak Horzum. Posthuman Pathogenesis. New York: Routledge, 2022. http://dx.doi.org/10.4324/9781003288244.

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Nordenfelt, Pontus, and Mattias Collin, eds. Bacterial Pathogenesis. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6673-8.

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Lee, Hong Kyu, Salvatore DiMauro, Masashi Tanaka, and Yau-Huei Wei, eds. Mitochondrial Pathogenesis. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-662-41088-2.

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DeLeo, Frank R., and Michael Otto, eds. Bacterial Pathogenesis. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-60327-032-8.

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Schuitemaker, Hanneke, and Frank Miedema, eds. AIDS Pathogenesis. Dordrecht: Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-017-0685-8.

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Hanneke, Schuitemaker, and Miedema F, eds. AIDS pathogenesis. Dordrecht: Kluwer Academic, 2000.

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Neal, Nathanson, and Ahmed Rafi, eds. Viral pathogenesis. Philadelphia: Lippincott-Raven, 1997.

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Book chapters on the topic "Pathogenesis"

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Frank, J. Howard, J. Howard Frank, Michael C. Thomas, Allan A. Yousten, F. William Howard, Robin M. Giblin-davis, John B. Heppner, et al. "Pathogenesis." In Encyclopedia of Entomology, 2759. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6359-6_2799.

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Holmgren, Jan. "Pathogenesis." In Cholera, 199–208. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4757-9688-9_10.

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Heemskerk, Dorothee, Maxine Caws, Ben Marais, and Jeremy Farrar. "Pathogenesis." In SpringerBriefs in Public Health, 9–16. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-19132-4_2.

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Chae, Jae Jin, and Daniel L. Kastner. "Pathogenesis." In Rare Diseases of the Immune System, 13–30. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-14615-7_2.

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van Duinen, Martin Th A. "Pathogenesis." In The Transorbital Intracranial Penetrating Injury, 39–47. Dordrecht: Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-011-4457-5_8.

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Gonzalez-Scarano, F., M. J. Endres, and N. Nathanson. "Pathogenesis." In Current Topics in Microbiology and Immunology, 217–49. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-76018-1_8.

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Cheli, Rodolfo, Alessandro Perasso, and Attilio Giacosa. "Pathogenesis." In Gastritis, 98–109. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71845-8_7.

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Modrow, Susanne, Dietrich Falke, Uwe Truyen, and Hermann Schätzl. "Pathogenesis." In Molecular Virology, 39–47. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-20718-1_4.

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Bond, Ross. "Pathogenesis." In Veterinary Allergy, 247–51. Oxford, UK: John Wiley & Sons, Ltd, 2013. http://dx.doi.org/10.1002/9781118738818.ch38.

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Poolman, Jan T. "Pathogenesis." In Gonococci and Meningococci, 619–20. Dordrecht: Springer Netherlands, 1988. http://dx.doi.org/10.1007/978-94-009-1383-7_96.

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Conference papers on the topic "Pathogenesis"

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"26th Annual Midwest Microbial Pathogenesis Conference (MMPC)." In 26th Annual Midwest Microbial Pathogenesis Conference (MMPC). Frontiers Media SA, 2020. http://dx.doi.org/10.3389/978-2-88963-591-7.

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Worcester, Elaine M., Andrew P. Evan, Fredric L. Coe, James C. Williams, Andrew P. Evan, James E. Lingeman, and James A. McAteer. "Pathogenesis of Stone Disease." In RENAL STONE DISEASE 2: 2nd International Urolithiasis Research Symposium. AIP, 2008. http://dx.doi.org/10.1063/1.2998058.

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Chen, Chang-Lin, Jia-Chen Tsai, Wei-Ling Huang, Ying-Hsuan Meng, Ju-Chun Huang, Ying-Chieh Chen, and Chuang-Rung Chang. "Mitochondria dynamics and pathogenesis." In PROCEEDINGS OF THE 3RD INTERNATIONAL SEMINAR ON METALLURGY AND MATERIALS (ISMM2019): Exploring New Innovation in Metallurgy and Materials. AIP Publishing, 2020. http://dx.doi.org/10.1063/5.0002464.

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Hybiske, Kevin. "PL09.1 Understanding chlamydia pathogenesis." In Abstracts for the STI & HIV World Congress (Joint Meeting of the 23rd ISSTDR and 20th IUSTI), July 14–17, 2019, Vancouver, Canada. BMJ Publishing Group Ltd, 2019. http://dx.doi.org/10.1136/sextrans-2019-sti.12.

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Chandran, Vinod. "Pathogenesis of Psoriatic Arthritis." In The 6th IFPA World Psoriasis and Psoriatic Arthritis Congress. Baarn, the Netherlands: Medicom Medical Publishers, 2023. http://dx.doi.org/10.55788/c9ea6682.

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Chandran, Vinod. "Pathogenesis of Psoriatic Arthritis." In 6th IFPA-WPPAC 2021. Baarn, the Netherlands: Medicom Medical Publishers, 2023. http://dx.doi.org/10.55788/d1cace39.

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Yoshida, Masahiro, Shunsuke Minagawa, Jun Araya, Hiromichi Hara, Akihiro Ichikawa, Nayuta Saito, Nahoko Sato, et al. "Involvement ferroptosis in COPD pathogenesis." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa4451.

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ZIEGLER, JOHN L. "INFECTIOUS AGENTS AND CANCER: PATHOGENESIS." In International Seminar on Nuclear War and Planetary Emergencies 38th Session. WORLD SCIENTIFIC, 2008. http://dx.doi.org/10.1142/9789812834645_0039.

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HARDY, JOHN. "ALZHEIMER'S DISEASE: GENETICS TO PATHOGENESIS." In International Seminar on Nuclear War and Planetary Emergencies 38th Session. WORLD SCIENTIFIC, 2008. http://dx.doi.org/10.1142/9789812834645_0035.

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Saito, Nayuta, Jun Araya, Akihiko Ito, Yusuke Hosaka, Akihiro Ichikawa, Tsukasa Kadota, Takayuki Nakano, et al. "Lysosomal dysfunction in COPD pathogenesis." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa1673.

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Reports on the topic "Pathogenesis"

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Roop, R. M. Mid-Atlantic Microbial Pathogenesis Meeting. Fort Belvoir, VA: Defense Technical Information Center, March 2003. http://dx.doi.org/10.21236/ada413150.

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Geisbert, Thomas W., Peter B. Jahrling, Tom Larsen, Kelly J. Davis, and Lisa Hensley. Filovirus Pathogenesis in Nonhuman Primates. Fort Belvoir, VA: Defense Technical Information Center, January 2002. http://dx.doi.org/10.21236/ada421420.

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Altier, Craig, and Daniel Wozniak. Mid-Atlantic Microbial Pathogenesis Meeting. Fort Belvoir, VA: Defense Technical Information Center, December 2005. http://dx.doi.org/10.21236/ada461976.

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Adami, Hans-Olov. The Infectious Pathogenesis of Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, March 2009. http://dx.doi.org/10.21236/ada503532.

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Sood, Anil K. Early Events in Ovarian Cancer Pathogenesis. Fort Belvoir, VA: Defense Technical Information Center, January 2012. http://dx.doi.org/10.21236/ada608121.

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Adami, Hans-Olov. The Infectious Pathogenesis of Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, March 2010. http://dx.doi.org/10.21236/ada526530.

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Sood, Anil K. Early Events in Ovarian Cancer Pathogenesis. Fort Belvoir, VA: Defense Technical Information Center, November 2010. http://dx.doi.org/10.21236/ada542176.

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Adami, Hans-Olov, and Lorelei Mucci. The Infectious Pathogenesis Of Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, April 2011. http://dx.doi.org/10.21236/ada549351.

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Adami, Hans-Olov, and Lorelei A. Mucci. The Infectious Pathogenesis of Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, March 2008. http://dx.doi.org/10.21236/ada482578.

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Splitter, Gary, and Menachem Banai. Microarray Analysis of Brucella melitensis Pathogenesis. United States Department of Agriculture, 2006. http://dx.doi.org/10.32747/2006.7709884.bard.

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Original Objectives 1. To determine the Brucella genes that lead to chronic macrophage infection. 2. To identify Brucella genes that contribute to infection. 3. To confirm the importance of Brucella genes in macrophages and placental cells by mutational analysis. Background Brucella spp. is a Gram-negative facultative intracellular bacterium that infects ruminants causing abortion or birth of severely debilitated animals. Brucellosis continues in Israel, caused by B. melitensis despite an intensive eradication campaign. Problems with the Rev1 vaccine emphasize the need for a greater understanding of Brucella pathogenesis that could improve vaccine designs. Virulent Brucella has developed a successful strategy for survival in its host and transmission to other hosts. To invade the host, virulent Brucella establishes an intracellular niche within macrophages avoiding macrophage killing, ensuring its long-term survival. Then, to exit the host, Brucella uses placenta where it replicates to high numbers resulting in abortion. Also, Brucella traffics to the mammary gland where it is secreted in milk. Missing from our understanding of brucellosis is the surprisingly lillie basic information detailing the mechanisms that permit bacterial persistence in infected macrophages (chronic infection) and dissemination to other animals from infected placental cells and milk (acute infection). Microarray analysis is a powerful approach to determine global gene expression in bacteria. The close genomic similarities of Brucella species and our recent comparative genomic studies of Brucella species using our B. melitensis microarray, suqqests that the data obtained from studying B. melitensis 16M would enable understanding the pathogenicity of other Brucella organisms, particularly the diverse B. melitensis variants that confound Brucella eradication in Israel. Conclusions Results from our BARD studies have identified previously unknown mechanisms of Brucella melitensis pathogenesis- i.e., response to blue light, quorum sensing, second messenger signaling by cyclic di-GMP, the importance of genomic island 2 for lipopolysaccharide in the outer bacterial membrane, and the role of a TIR domain containing protein that mimics a host intracellular signaling molecule. Each one of these pathogenic mechanisms offers major steps in our understanding of Brucella pathogenesis. Strikingly, our molecular results have correlated well to the pathognomonic profile of the disease. We have shown that infected cattle do not elicit antibodies to the organisms at the onset of infection, in correlation to the stealth pathogenesis shown by a molecular approach. Moreover, our field studies have shown that Brucella exploit this time frame to transmit in nature by synchronizing their life cycle to the gestation cycle of their host succumbing to abortion in the last trimester of pregnancy that spreads massive numbers of organisms in the environment. Knowing the bacterial mechanisms that contribute to the virulence of Brucella in its host has initiated the agricultural opportunities for developing new vaccines and diagnostic assays as well as improving control and eradication campaigns based on herd management and linking diagnosis to the pregnancy status of the animals. Scientific and Agricultural Implications Our BARD funded studies have revealed important Brucella virulence mechanisms of pathogenesis. Our publication in Science has identified a highly novel concept where Brucella utilizes blue light to increase its virulence similar to some plant bacterial pathogens. Further, our studies have revealed bacterial second messengers that regulate virulence, quorum sensing mechanisms permitting bacteria to evaluate their environment, and a genomic island that controls synthesis of its lipopolysaccharide surface. Discussions are ongoing with a vaccine company for application of this genomic island knowledge in a Brucella vaccine by the U.S. lab. Also, our new technology of bioengineering bioluminescent Brucella has resulted in a spin-off application for diagnosis of Brucella infected animals by the Israeli lab by prioritizing bacterial diagnosis over serological diagnosis.
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