Relevant bibliographies by topics / Inflammatory signature

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Inflammatory signature'

Author: Grafiati
Published: 9 March 2023
Last updated: 10 March 2023

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Journal articles on the topic "Inflammatory signature"

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Rigolet, Muriel, Cyrielle Hou, Yasmine Baba Amer, Jessie Aouizerate, Baptiste Periou, Romain K. Gherardi, Peggy Lafuste, and François Jérôme Authier. "Distinct interferon signatures stratify inflammatory and dysimmune myopathies." RMD Open 5, no. 1 (February 2019): e000811. http://dx.doi.org/10.1136/rmdopen-2018-000811.

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ObjectiveThe role of interferons (IFN) in the pathophysiology of primary inflammatory and dysimmune myopathies (IDM) is increasingly investigated, notably because specific neutralisation approaches may constitute promising therapeutic tracks. In present work we analysed the muscular expression of specific IFNα/β and IFNγ-stimulated genes in patients with various types of IDM.Methods39 patients with IDM with inclusion body myositis (IBM, n=9), dermatomyositis (DM, n=10), necrotising autoimmune myopathies (NAM, n=10) and antisynthetase myositis (ASM, n=10), and 10 controls were included. Quantification of expression levels of IFNγ, ISG15, an IFNα/β-inducible gene and of six IFNγ-inducible genes (GBP2, HLA-DOB, HLA-DPB, CIITA, HLA-DRB and HLA-DMB) was performed on muscle biopsy samples.ResultsDM usually associated with strong type I IFNα/β signature, IBM and ASM with prominent type II IFNγ signature and NAM with neither type I nor type II IFN signature. Immunofluorescence study in ASM and IBM showed myofibre expression of major histocompatibility class 2 (MHC-2) and CIITA, confirming the induction of the IFNγ pathway. Furthermore, MHC-2-positive myofibres were observed in close proximity to CD8+ T cells which produce high levels of IFNγ.ConclusionDistinct IFN signatures allow a more distinct segregation of IDMs and myofibre MHC-2 expression is a reliable biomarker of type II IFN signature.
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Wu, Zhong, Martin Schlumpberger, Sameen Raza, Jiaye Yu, John DiCarlo, Yexun Wang, and Vikram Devgan. "Pathway Signature PCR Array: a novel method for studying inflammatory responses (173.11)." Journal of Immunology 188, no. 1_Supplement (May 1, 2012): 173.11. http://dx.doi.org/10.4049/jimmunol.188.supp.173.11.

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Abstract Signaling pathways play central roles in cellular physiology, and assessing the state of pathways helps clarify molecular mechanisms of disease and inflammatory responses. Gene expression signatures of pathway activation status enable reliable measurement of pathway activity. Our group developed Pathway Signature PCR Arrays to analyze gene expression and determine pathway activity within a single real-time PCR experiment. This study identified a set of genes that provide a gene signature for evaluating IL6/STAT3 pathway activity. A set of 88 signature genes were derived from microarray profiling on HepG2 and MCF10A cells treated with IL-6 protein and STAT3-specific siRNA. Genes were selected on the basis of statistically significant expression changes in response to IL-6 and reversion of altered expression upon treatment with STAT3 siRNA. These 88 IL-6/STAT3 response genes were further verified by real-time PCR, using a panel of 14 different cell lines stimulated with IL-6 or inhibited with STAT3 siRNA. Using a mathematical classifier method, a subset of genes was identified as a gene expression signature for assessing IL-6/STAT3 pathway activity. These signature genes, along with IL-6 pathway-related genes identified by literature mining, constitute the IL-6 Pathway Signature PCR Array. This array provides a useful tool for studying regulation of pathway activity via gene expression changes during inflammatory responses. Array is for molecular biology applications only.
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Li, Xinyu, Shuqiao Zhang, Shijun Zhang, Weihong Kuang, and Chunzhi Tang. "Inflammatory Response-Related Long Non-Coding RNA Signature Predicts the Prognosis of Hepatocellular Carcinoma." Journal of Oncology 2022 (March 17, 2022): 1–13. http://dx.doi.org/10.1155/2022/9917244.

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Background. Hepatocellular carcinoma (HCC) is a high mortality malignant tumor with genetic and phenotypic heterogeneity, making predicting prognosis challenging. Meanwhile, the inflammatory response is an indispensable player in the tumorigenesis process and regulates the tumor microenvironment, which can affect the prognosis of tumor patients. Methods. Using HCC samples in the TCGA-LIHC dataset, we explored lncRNA expression profiles associated with the inflammatory response. The inflammatory response-related lncRNA signature was constructed by univariate Cox regression, LASSO regression, and multivariate Cox regression methods based on inflammatory response-related differentially expressed lncRNAs in HCC. Results. Seven inflammatory response-related lncRNA signatures were identified in predicting HCC prognosis. Kaplan–Meier (K-M) survival analysis indicated that high-risk group HCC patients were associated with poor prognosis. The utility of the inflammatory response-related lncRNA signatures was proved by the AUC and DCA analysis. The nomogram further confirmed the accuracy of the novel signature in predicting HCC patients’ prognoses. In validation, our novel signature is more accurate than traditional clinicopathological performance for prognosis prediction of HCC patients. GSEA analysis further elucidated the underlying mechanisms and pathways of HCC progression in the low- and high-risk groups. Moreover, immune cells infiltration responses and immune function analyses revealed a significant difference between high- and low-risk groups in cytolytic activity, MHC class I, type I INF response, type II INF response, inflammation-promoting, and T cell coinhibition. Finally, HHLA2, NRP1, CD276, TNFRSF9, TNFSF4, CD80, and VTCN1 were expressed higher in high-risk groups in the immune checkpoint analysis. Conclusions. A novel inflammatory response-related lncRNA signature (AC145207.5, POLHAS1, AL928654.1, MKLN1AS, AL031985.3, PRRT3AS1, and AC023157.2) is capable of predicting the prognosis of HCC patients and providing new immune targeted therapies insight.
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Vasunilashorn, Sarinnapha, Long H. Ngo, Simon Dillon, Hasan Otu, Bridget Tripp, Sharon Inouye, Towia A. Libermann, and Edward R. Marcantonio. "AN INFLAMMATORY SIGNATURE OF POSTOPERATIVE DELIRIUM." Innovation in Aging 3, Supplement_1 (November 2019): S820—S821. http://dx.doi.org/10.1093/geroni/igz038.3027.

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Abstract Delirium is a common, morbid, and costly geriatric syndrome, yet its pathophysiology remains poorly understood. In a nested matched case-control study within the Successful Aging after Elective Surgery (SAGES) study, a cohort of adults age ≥70 without dementia undergoing major non-cardiac surgery, we previously identified inflammatory proteins to be associated with delirium. Using the entire SAGES cohort, the current study examines the independent associations of these inflammatory proteins with postoperative delirium. Plasma was collected preoperatively (PREOP) and on postoperative day 2 (POD2). Neuroinflammatory marker chitinase-3-like protein [CHI3l1 or YKL-40]; PREOP and POD2) and systemic inflammatory markers interleukin [IL]-6 (POD2 only) and C-reactive protein (CRP; PREOP and POD2) were measured using enzyme-linked immunosorbent assays. Generalized linear models were used to determine the independent (multivariable) associations between the inflammatory markers, measured in sample-based quartiles (Q). All models adjusted for age, sex, baseline cognition, surgery type, Charlson comorbidity index, and medical complications. Among the 555 patients (mean age 77 years, standard deviation, SD 5.2), 58% were female and 86% underwent orthopedic surgeries. Postoperative delirium occurred in 24%. High YKL-40 PREOP and IL-6 at POD2 (Q4 vs. Q1) were significantly associated with an increased risk of delirium: relative risk (RR) [95% confidence interval (CI)] 2.2[1.1-4.4] and 2.7[1.3-5.7], respectively. CRP (PREOP and POD2) was not significantly associated with delirium (p=0.37 and p=0.73, respectively). This work underscores the importance of inflammation (YKL-40 and IL-6) in the pathophysiology of postoperative delirium.
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Gallay, Laure, Guy Mouchiroud, and Bénédicte Chazaud. "Interferon-signature in idiopathic inflammatory myopathies." Current Opinion in Rheumatology 31, no. 6 (November 2019): 634–42. http://dx.doi.org/10.1097/bor.0000000000000653.

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Yang, Xiangchou, Yangyang Zhou, Linjing Huang, Shang Lin, Haihao Ye, and Yujuan Shan. "Fibroblast Common Serum Response Signature-Related Classification Affects the Tumour Microenvironment and Predicts Prognosis in Bladder Cancer." Oxidative Medicine and Cellular Longevity 2022 (October 19, 2022): 1–29. http://dx.doi.org/10.1155/2022/5645944.

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Abnormal oncogenic signatures provide important clues regarding cancer prognosis and treatment. We analysed the variations in 189 oncogenic signature gene sets between normal and tumourous tissues from The Cancer Genome Atlas (TCGA) and found that the “CSR_LATE_UP” signature was the most upregulated oncogenic signature gene set in bladder cancer. Next, we developed a common serum response (CSR) risk score (CRS) model based on fibroblast CSR genes and systematically analysed the correlations of these genes or the CRSs with survival, previously reported molecular subtypes, clinicopathological features, cancer signalling pathways, chemotherapeutic responses, and the tumour microenvironment using TCGA and validation cohorts. The CRS could predict the malignant phenotype, chemotherapeutic efficacy, immune invasion, and disease prognosis. Inflammatory signalling pathways (e.g., inflammatory response, TNFA signalling via NFƘB, IFNα response, and IL2-STAT5 signalling) were markedly upregulated in patients with high CRS. Notably, the CSR-related gene ANLN was positively correlated with CD8+ immune cell infiltration, PD-L1 expression, and sensitivity to PD-L1 inhibitors and could thus provide guidance for clinical immunotherapy. This study highlights the crucial role of the CSR signature in bladder cancer and provides a CRS model for accurate predictions of the disease prognosis and chemotherapy and immunotherapy responses.
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Imami, Ali S., Sinead M. O’Donovan, Justin F. Creeden, Xiaojun Wu, Hunter Eby, Cheryl B. McCullumsmith, Kerstin Uvnäs-Moberg, Robert E. McCullumsmith, and Elissar Andari. "Oxytocin’s anti-inflammatory and proimmune functions in COVID-19: a transcriptomic signature-based approach." Physiological Genomics 52, no. 9 (September 1, 2020): 401–7. http://dx.doi.org/10.1152/physiolgenomics.00095.2020.

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The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused a worldwide pandemic, infecting over 16 million people worldwide with a significant mortality rate. However, there is no current Food and Drug Administration-approved drug that treats coronavirus disease 2019 (COVID-19). Damage to T lymphocytes along with the cytokine storm are important factors that lead to exacerbation of clinical cases. Here, we are proposing intravenous oxytocin (OXT) as a candidate for adjunctive therapy for COVID-19. OXT has anti-inflammatory and proimmune adaptive functions. Using the Library of Integrated Network-Based Cellular Signatures (LINCS), we used the transcriptomic signature for carbetocin, an OXT agonist, and compared it to gene knockdown signatures of inflammatory (such as interleukin IL-1β and IL-6) and proimmune markers (including T cell and macrophage cell markers like CD40 and ARG1). We found that carbetocin’s transcriptomic signature has a pattern of concordance with inflammation and immune marker knockdown signatures that are consistent with reduction of inflammation and promotion and sustaining of immune response. This suggests that carbetocin may have potent effects in modulating inflammation, attenuating T cell inhibition, and enhancing T cell activation. Our results also suggest that carbetocin is more effective at inducing immune cell responses than either lopinavir or hydroxychloroquine, both of which have been explored for the treatment of COVID-19.
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Luo, Yong, Xiaopeng Liu, Jingbo Lin, Weide Zhong, and Qingbiao Chen. "Development and validation of novel inflammatory response-related gene signature to predict prostate cancer recurrence and response to immune checkpoint therapy." Mathematical Biosciences and Engineering 19, no. 11 (2022): 11345–66. http://dx.doi.org/10.3934/mbe.2022528.

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<abstract> <p>The aim of this study is to construct an inflammatory response-related genes (IRRGs) signature to monitor biochemical recurrence (BCR) and treatment effects in prostate cancer patients (PCa). A gene signature for inflammatory responses was constructed on the basis of the data from the Cancer Genome Atlas (TCGA) database, and validated in external datasets. It was analyzed using receiver operating characteristic curve, BCR-free survival, Cox regression, and nomogram. Distribution analysis and external model comparison were utilized. Then, enrichment analysis, tumor mutation burden, tumor immune microenvironment, and immune cell infiltration signatures were investigated. The role of the signature in immunotherapy was evaluated. The expression patterns of core genes were verified by RNA sequencing. We identified an IRRGs signature in the TCGA-PRAD cohort and verified it well in two other independent external datasets. The signature was a robust and independent prognostic index for predicting the BCR of PCa. The high-risk group of our signature predicted a shortened BCR time and an aggressive disease progression. A nomogram was constructed to predict BCR-free time in clinical practices. Neutrophils and CD8+ T cells were in higher abundance among the low-risk individuals. Immune functions varied significantly between the two groups and immune checkpoint therapy worked better for the low-risk patients. The expression of four IRRGs showed significant differences between PCa and surrounding benign tissues, and were validated in BPH-1 and DU145 cell lines by RNA sequencing. Our signature served as a reliable and promising biomarker for predicting the prognosis and evaluating the efficacy of immunotherapy, facilitating a better outcome for PCa patients.</p> </abstract>
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Pachner, Andrew R., Krista DiSano, Darlene B. Royce, and Francesca Gilli. "Clinical utility of a molecular signature in inflammatory demyelinating disease." Neurology - Neuroimmunology Neuroinflammation 6, no. 1 (November 9, 2018): e520. http://dx.doi.org/10.1212/nxi.0000000000000520.

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ObjectiveWe sought to develop molecular biomarkers of intrathecal inflammation to assist neurologists in identifying patients most likely to benefit from a range of immune therapies.MethodsWe used Luminex technology and index determination to search for an inflammatory activity molecular signature (IAMS) in patients with inflammatory demyelinating disease (IDD), other neuroinflammatory diagnoses, and noninflammatory controls. We then followed the clinical characteristics of these patients to find how the presence of the signature might assist in diagnosis and prognosis.ResultsA CSF molecular signature consisting of elevated CXCL13, elevated immunoglobulins, normal albumin CSF/serum ratio (Qalbumin), and minimal elevation of cytokines other than CXCL13 provided diagnostic and prognostic value; absence of the signature in IDD predicted lack of subsequent inflammatory events. The signature outperformed oligoclonal bands, which were frequently false positive for active neuroinflammation.ConclusionsA CSF IAMS may prove useful in the diagnosis and management of patients with IDD and other neuroinflammatory syndromes.Classification of evidenceThis study provides Class IV evidence that a CSF IAMS identifies patients with IDD.
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Van Laere, S. J., I. Van der Auwera, G. G. Van den Eynden, X. Trinh, P. Van Hummelen, P. van Dam, E. A. Van Marck, P. B. Vermeulen, and L. Y. Dirix. "Confirmation of the distinct molecular phenotype of inflammatory breast cancer compared to non-inflammatory breast cancer using Affymetrix-based genome-wide gene expression analysis." Journal of Clinical Oncology 25, no. 18_suppl (June 20, 2007): 21055. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.21055.

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21055 Background: We have shown with cDNA microarrays that inflammatory breast cancer (IBC) and non-IBC are distinct biological entities. The purpose of this study was to confirm our previous results using Affymetrix chips. Methods: RNA was extracted from 19 IBC samples and 42 non-stage matched non-IBC samples. RNA was hybridized onto Affymetrix HG U133 Plus 2.0 chips. Gene expression data were normalized using GCRMA and genes with a gene expression of at least 250 in 50% of the cases were filtered in. Hierarchical clustering and principle component analysis was executed. Identification of the different cell-of-origin subtypes in our expression data set was done using the intrinsic gene list. A NFkB signature, a MAPK signature and our own IBC signature were tested by clustering analysis. Results: Clustering using 11341 genes resulted in the identification of two clusters: one containing 14/19 IBC samples and a second containing 32/42 non-IBC (Pearson χ2; p<0.0001). Principle component analysis separated IBC from non-IBC samples along the first principle component. Interestingly, IBC samples more closely resemble T1 - T2 tumours than T3 - T4 tumours. Application of the intrinsic gene set to our IBC/non-IBC data set resulted in the classification of 14/19 IBC samples as basal-like or ErbB2-overexpressing tumours compared to only 4/42 non-IBC tumours (Pearson χ2; p<0.0001). Our own IBC signature was confronted with the new data set and performed well in separating IBC specimens form non-IBC specimens. Clustering identified three clusters from which one cluster contained 18 samples, including 12 IBC specimens (p<0.0001). Using the NFkB and MAPK signatures, similar results were obtained. Conclusions: These results confirm our findings that IBC is a distinct biologic phenotype, characterized by activation of NFkB, possibly through activation of MAPK's. IBC tumours more often demonstrate characteristics from basal-like and ErbB2-overexpressing breast tumours. The fact that IBC tumours are rapidly developing tumours instead of longstanding tumourigenic processes might explain the close resemblance of the IBC gene expression profile to the gene expression profile of T1 and T2 tumours. No significant financial relationships to disclose.
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Dissertations / Theses on the topic "Inflammatory signature"

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TORRI, ANNA. "Gene expression profiling in host-pathogen interactions and identification of the molecular mechanisms involved in dendrictic cells activation." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2009. http://hdl.handle.net/10281/7609.

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In this thesis we used a functional genomic approach to study host-pathogen interactions [1]. We analyzed the interaction from the host point of view and in particular from the dendritic cells point of view. Dendritic cells (DCs) constitute a heterogeneous group of antigen-presenting leukocytes important in activation of both innate and adaptive immunity [2]. In the first part of this thesis we explored the possibility to use dendritic cell transcriptomes to generate biomarkers of inflammation that may be useful to test DC activation in vitro and in vivo. We considered DC transcriptomes upon stimulation with different microorganisms and molecules able to induce activation (Schistosoma mansoni eggs, Leishmania Mexicana promastigote, Listeria monocytogenes, LPS, CpG, polyIC, Pam3cys, zymosan) or inhibition (Schistosoma SLA, Leishmania Mexicana amastigote, dexamethasone). We applied a supervised classification method, random forest algorithm, in order to identify an inflammatory signature that can describe, at molecular level, the dendritic cells status in terms of inflammation. The informative genes were selected using a training set (77 samples) and then validated on a testing set (38 samples). The 54 predictive genes selected are able to distinguish very accurately between inflammatory and non inflammatory samples. Amongst these we found genes well known to be involved in the inflammatory process (Icam1, IL-6), as well as genes not tightly correlated with inflammation (Hdac5, Gadd45b). Surprisingly, some genes with unknown function (Txndc16, Isg15) were also selected. The diagnostic performance of the generated signature was assessed against an independent set of samples (D1 cells treated with IFNa, DEX, vitamin D, IL-10, Lactobacillus paracasei, Listeria monocytogenes, LPS, poly I:C, PAM3CYS, zymosan for 24h), by qPCR. Moreover, we validated the inflammatory signature in vivo, by testing the response in splenic DCs isolated from mice treated with LPS and dexamethasone. Most of the studied genes (80%), successfully characterized the activation state of splenic DCs, and differentiated the profile of these cells from that of DCs derived from untreated mice. The small number of genes in our signature allows to use simple, conventional assays, such as quantitative reverse transcriptase-polymerase chain reaction. The increasing availability of laboratory diagnosis by polymerase chain reaction has opened up new possibilities for genomic testing based on the use of genetic signatures, in routine clinical conditions. A second major outcome from whole gene expression studies is the discovery of the molecular pathways induced in complex systems such as host-bacteria interactions [3]. Therefore, in the second part of this thesis we analyzed dendritic cells-bacteria interactions and we focused on the identification of the specific molecular mechanisms induced in DCs upon infections. Among the 1500 genes modulated in DCs by bacteria, we have detected the up-regulation of the cytokine IL22. This interleukin has been shown to have both pro- and anti-inflammatory activity in different chronic inflammatory diseases, in mouse models of infection and in liver injury [4,5]. IL-22 was described to be produced mainly by CD4+ T cells, in particular by Th17, and by NK cells. Only few and controversial data are available on IL-22 production by DC. IL-22 does not seem to influence directly immune cells since the IL-22R1 chain of IL-22 heterodimeric receptor complex is present only in a range of non immune tissues (skin, liver, respiratory system and gastrointestinal tract) [6]. Therefore, in this study we focused on how IL-22 is produced and regulated in DCs. We first demonstrated that IL-22 is produced by DCs in different in vitro systems (D1 cells, BMDC, splenic DCs) and in vivo by using mouse models of systemic inflammation and infection induced by LPS and gram+ bacteria. We showed that IL-22 up-regulation by LPS reaches the maximum level within 2 h post stimulation. Instead IL-22 is induced by IL-23 in total splenocytes with a different kinetic suggesting the existence of different regulatory pathways in different cell types. Using cellular systems (BMDC and splenocytes) derived from wt or Myd88 ko mice, we established that Myd88 has a key role in IL-22 up-regulation induced by LPS, as well as, by IL-23. We identified a Myd88-dependent and IL-23-independent production of IL-22 in BMDC upon LPS stimulation. Moreover, we found an IL-23-dependent and Myd88-dependent up-regulation of IL-22 after induction with IL-23 in total splenocytes and in splenic DCs. Finally, we performed a preliminary experiment in order to unravel IL-22 role in the liver since we could measure IL-22 receptor expression in this organ. Microarray experiment on primary hepatocytes, stimulated for 24 h with recombinant IL-22, suggests a role for IL-22 in the liver as a cytokine that promotes innate immune activation in terms of induction of antimicrobial peptides and secretion of chemokines that recruit phagocytes. The cellular source of IL-22 in the liver is currently under investigation.
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Martínez, García Antonio 1992. "Infiltrating myeloid cells and angiogenesis during skeletal muscle regeneration : role of p38γ/δ MAPKs in macrophage-phenotype acquisition." Doctoral thesis, Universitat Pompeu Fabra, 2019. http://hdl.handle.net/10803/668157.

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I joined the lab of Dra. Pura Muñoz to study the capacity of self-repair of skeletal muscle after an acute injury. During this process many different cell types interact to coordinate and regulate muscle repair. During those years I worked to shed light in how inflammation contributes to regulate skeletal muscle regeneration. Concretely, I worked in the characterization of a new macrophage’s population, characterized by the upregulation of MHC2, which appear at last stages of the regenerative process. Those cells seem to be essential in this context. In this work, we could be able to characterize the transcriptomes of all muscle-infiltrating myeloid populations and attribute a key role to p38 g/d MAPKs in their phenotypical acquisition and function. In addition, my work has demonstrated that myeloid-lack of both MAPK kinases leads in impaired muscle regeneration. In addition, during this thesis I has been working in the study of angiogenesis, concretely, in deciphering how microvascular network is reconstructed during muscle regeneration
Decidí hacer la tesis en el laboratorio de la Dra. Pura Muñoz para estudiar la capacidad de auto reparación del músculo esquelético. En este proceso, muchos tipos diferentes de células interactúan para coordinar y regular la reparación muscular. Durante esos años he trabajado para desentrañar cómo la inflamación contribuye a regular la regeneración del músculo esquelético. Concretamente, he trabajado en la caracterización de una nueva población de macrófagos, caracterizada por la sobreexpresión de MHC2, que aparece en las últimas etapas de la regeneración y que parece ser esencial para el proceso. En este trabajo hemos podido caracterizar los transcriptomas de todas las poblaciones mieloides que infiltran el músculo , así como atribuir un papel clave a las MAP quinasas p38 g / d en su la función y adquisición fenotípica de estas células. Además, mi trabajo ha demostrado que la falta de ambas MAPK quinasas solo en células mieloides conduce a defectos en la regeneración muscular. Además, durante esta tesis he trabajado en el estudio de la angiogénesis, en descifrar cómo se reconstituye la red micro-vascular durante la regeneración muscular.
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Imgenberg-Kreuz, Juliana. "Epigenetic and Gene Expression Signatures in Systemic Inflammatory Autoimmune Diseases." Doctoral thesis, Uppsala universitet, Molekylär medicin, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-310388.

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Autoimmune diseases are clinical manifestations of a loss-of-tolerance of the immune system against the body’s own substances and healthy tissues. Primary Sjögren’s syndrome (pSS) and systemic lupus erythematosus (SLE) are two chronic inflammatory autoimmune diseases characterized by autoantibody production and an activated type I interferon system. Although the precise mechanisms leading to autoimmune processes are not well defined, recent studies suggest that aberrant DNA methylation and gene expression patterns may play a central role in the pathogenesis of these disorders. The aim of this thesis was to investigate DNA methylation and gene expression in pSS and SLE on a genome-wide scale to advance our understanding of how these factors contribute to the diseases and to identify potential biomarkers and novel treatment targets. In study I, differential DNA methylation was analyzed in multiple tissues from pSS patients and healthy controls. We identified thousands of CpG sites with perturbed methylation; the most prominent finding was a profound hypomethylation at regulatory regions of type I interferon induced genes in pSS. In study II, a cases-case study comparing DNA methylation in pSS patients with high fatigue to patients with low fatigue, we found methylation patterns associated to the degree of fatigue. In study III, RNA-sequencing was applied to investigate the transcriptome of B cells in pSS in comparison to controls. Increased expression of type I and type II interferon regulated genes in pSS was observed, indicating ongoing immune activation in B cells. In study IV, the impact of DNA methylation on disease susceptibility and phenotypic variability in SLE was investigated. We identified DNA methylation patterns associated to disease susceptibility, SLE manifestations and different treatments. In addition, we mapped methylation quantitative trait loci and observed evidence for genetic regulation of DNA methylation in SLE.   In conclusion, the results presented in this thesis provide new insights into the molecular mechanisms underlying autoimmunity in pSS and SLE. The studies confirm the central role of the interferon system in pSS and SLE and further suggest novel genes and mechanisms to be involved in the pathogenesis these autoimmune diseases.
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Deeke, Shelley. "Biomarker Discovery and Extracellular Vesicle Proteomic Signatures in Pediatric Inflammatory Bowel Disease." Thesis, Université d'Ottawa / University of Ottawa, 2019. http://hdl.handle.net/10393/38660.

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Background: Reliable biomarkers are needed to evade the risk of injury, invasiveness and discomfort of endoscopies, which are required for inflammatory bowel disease (IBD) diagnosis and extent of disease assessment in ulcerative colitis (UC) patients. The need for biomarkers is accentuated in children, wherein the most frequently used IBD biomarker yields low specificity. Proteomics of clinical samples or their enriched components is a means to evaluate and identify alterations in proteins reflective of disease, with the potential for use as biomarkers and for providing insight on disease pathogenesis. Methods: Proteins were isolated from the intestinal mucosal-luminal interface (MLI), collected from the ascending and descending colon of pediatric treatment-naive patients. The intestinal MLI proteomes of 42 IBD and 18 control patients were analyzed by high resolution mass spectrometry (HRMS). Multivariate analysis and receiver operating characteristics curves were performed to develop protein biomarker panels to discriminate IBD from control, and for UC extent of disease. ELISAs were used to assess a subset of biomarker candidates in stool samples from an independent pediatric cohort (n=24). Extracellular vesicles (EVs) were isolated by ultracentrifugation from the intestinal MLI of 11 IBD and seven control patients, and analyzed by electron microscopy, nanoparticle tracking analysis and HRMS. Results: A biomarker panel of four proteins classified patients as either controls or active IBD with 97.5% accuracy. A second biomarker panel correctly classified 100% of UC patients as presenting with pancolitis or non-pancolitis. The differential protein expression of two biomarker candidates (catalase and leukotriene A-4 hydrolase) identified from the intestinal MLI was comparable in stool samples. Comparison of EV proteomes isolated from IBD patients and controls identified differential expression of processes related to host defense and immunity. Conclusions: Proteomic analysis of clinical samples identified differentially expressed proteins that can classify IBD patients from non-IBD controls and distinguish UC patients with pancolitis from those without pancolitis; proteins identified in intestinal aspirates displayed consistent differential expression in stool. Furthermore enrichment of EVs from the intestinal MLI indicates that these may contribute to the dysregulated host response against the intestinal microbiota which is observed in IBD.
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Bakhta, Oussama. "Métabolites circulants induits par le conditionnement ischémique à distance et mécanismes cardioprotecteurs de la colchicine à la phase aigue de l'infarctus du myocarde Metabolic Signature of Remote Ischemic Preconditioning Involving a Cocktail of Amino Acids and Biogenic Amines Cardioprotective role of colchicine against inflammatory injury in a rat 2 model of acute myocardial infarction." Thesis, Angers, 2017. http://www.theses.fr/2017ANGE0089.

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La reperfusion précoce à la phase aiguë de l’infarctus du myocarde améliore le pronostic des patients. Elle induit cependant une partie des lésions d’ischémie-reperfusion (I/R) liées à l’activation de mécanismes métaboliques et inflammatoires. Le conditionnement ischémique à distance (RIC) d’une part et les approches pharmacologiques d’autre part, constituent un espoir dans la prévention des lésions de reperfusion contre lesquelles nous ne disposons pas de traitement validé chez l’homme. L’objectif de cette thèse était d’explorer ces stratégies de cardioprotection à la phase aiguë de l’infarctus du myocarde. Grace à une approche métabolomique, nous avons identifié la kynurénine et glycine comme métabolites associés au RIC sur des plasmas de rats et confirmés dans une cohorte de patients. Nous avons ainsi validé in vivo l’action bénéfique de la kynurénine et de la glycine dans un modèle d’infarctus du myocarde. Nous avons ensuite étudié la modulation de la voie des kynurénines dans la cardioprotection induite par le RIC. Nous avons observé une activation de la voie de synthèse du NAD+ associée à une déacétylation des protéines mitochondriales hépatiques. Dans un dernier travail réalisé in vivo et in vitro, nous avons étudié le rôle cardioprotecteur de la colchicine dans l’I/R et analysé ces effets sur la modulation de l’inflammation et l’activation des voies de survie
The introduction of early reperfusion in the acute phase of myocardial infarction has improved the prognosis of patients. However, it induces irreversible damages called ischemia-reperfusion (I / R) injury followed by myocardial metabolic and inflammatory disorders. Remote ischemic conditioning (RIC) on the one hand and pharmacological approaches on the other hand, constitute a hope in the prevention of reperfusion injury against which we do not have validated treatment in humans.The aim of this thesis was to explore cardioprotection strategies in the acute phase of myocardial infarction. Using a metabolomics approach, we identified kynurenine and glycine as RIC-associated metabolites in rat plasmas and confirmed in a cohort of patients. We have also validated in vivo the beneficial effect of kynurenine and glycine in a model of myocardial infarction. We then studied the modulation of the kynurenine pathway in RIC-induced cardioprotection. We observed an activation of the NAD + synthesis pathway associated with deacetylation of hepatic mitochondrial proteins. In a last work carried out in vivo and in vitro, we studied the cardioprotective role of colchicine in I / R and analyzed its immunomodulatory effect and activation of survival pathways
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Steinbrich-Zöllner, Marta [Verfasser]. "Polychromatic flow cytometry and immune cell-specific gene expression profiling : an integrated approach to identify and validate new biomarkers and signatures of immune responses in chronic inflammatory rheumatic diseases / Marta Steinbrich-Zöllner." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2013. http://d-nb.info/1031098763/34.

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Craven, Kelly E. "Angiogenic gene signature in human pancreatic cancer correlates with TGF-beta and inflammatory transcriptomes." Diss., 2016. http://hdl.handle.net/1805/10984.

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Indiana University-Purdue University Indianapolis (IUPUI)
Pancreatic ductal adenocarcinoma (PDAC), which comprises 85% of pancreatic cancers, is the 4th leading cause of cancer death in the United States with a 5-year survival rate of 8%. While human PDACs (hPDACs) are hypovascular, they also overexpress a number of angiogenic growth factors and receptors. Additionally, the use of anti-angiogenic agents in murine models of PDAC leads to reduced tumor volume, tumor spread, and microvessel density (MVD), and improved survival. Nonetheless, clinical trials using anti-angiogenic therapy have been overwhelmingly unsuccessful in hPDAC. On the other hand, pancreatic neuroendocrine tumors (PNETs) account for only 2% of pancreatic tumors, yet they are very vascular and classically angiogenic, respond to anti-angiogenic therapy, and confer a better prognosis than PDAC even in the metastatic setting. In an effort to compare and contrast the angiogenic transcriptomes of these two tumor types, we analyzed RNA-Sequencing (RNA-Seq) data from The Cancer Genome Atlas (TCGA) and found that a pro-angiogenic gene signature is present in 35% of PDACs and that it is mostly distinct from the angiogenic signature present in PNETs. The pro-angiogenic PDAC subgroup also exhibits a transcriptome that reflects active TGF-β signaling, less frequent SMAD4 inactivation than PDACs without the signature, and up-regulation of several pro-inflammatory genes, including members of JAK signaling pathways. Consequently, targeting the TGF-β receptor type-1 kinase with SB505124 and JAK1/2 with ruxolitinib blocks proliferative crosstalk between human pancreatic cancer cells (PCCs) and human endothelial cells (ECs). Additionally, treatment of the KRC (oncogenic Kras, homozygous deletion of Rb1) and KPC (oncogenic Kras, mutated Trp53) genetically engineered PDAC mouse models with ruxolitinib suppresses murine PDAC (mPDAC) progression only in the KRC model, which shows superior enrichment and differential expression of the human pro-angiogenic gene signature as compared to KPC tumors. These findings suggest that targeting both TGF-β and JAK signaling in the 35% of PDAC patients whose cancers exhibit an pro-angiogenic gene signature should be explored in a clinical trial.
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Books on the topic "Inflammatory signature"

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Galovic, Marian, Bettina Schmitz, and Barbara Tettenborn. EEG in Inflammatory Disorders, Cerebrovascular Diseases, Trauma, and Migraine. Edited by Donald L. Schomer and Fernando H. Lopes da Silva. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190228484.003.0015.

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This chapter describes electroencephalographic (EEG) abnormalities in inflammatory and cerebrovascular diseases, traumatic brain injury, and headache. It focuses on a practical and clinical approach and covers the most important diseases from this extensive field. Particular attention has been paid to viral and autoimmune encephalitis, prion disease, ischemic stroke, posttraumatic coma, and migraine. Several signature patterns are discussed that facilitate early and accurate diagnosis. The use of EEG in guiding treatment decisions and predicting prognosis is reviewed.
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Book chapters on the topic "Inflammatory signature"

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Bertucci, François, Pascal Finetti, Max Chaffanet, Patrice Viens, and Daniel Birnbaum. "Microarray Analysis Identifies an Expression Signature for Inflammatory Breast Cancer." In Inflammatory Breast Cancer: An Update, 243–58. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-3907-9_19.

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Foti, Maria, Ottavio Beretta, Mattia Pelizzola, and Paola Ricciardi-Castagnoli. "Dendritic Cells Inflammatory Signature Induced by Microbial Pathogens." In Handbook of Tuberculosis, 23–44. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2017. http://dx.doi.org/10.1002/9783527611614.ch19.

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Tahseen, Rabia, Mohammad Parvez, G. Sravan Kumar, and Parveen Jahan. "Prognostic Importance of Th1:Th2 (IL-1β/IL-10) Cytokine Ratio in Adult Onset-Bronchial Asthma." In Proceedings of the Conference BioSangam 2022: Emerging Trends in Biotechnology (BIOSANGAM 2022), 176–87. Dordrecht: Atlantis Press International BV, 2022. http://dx.doi.org/10.2991/978-94-6463-020-6_18.

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AbstractBronchial asthma is a complex respiratory disorder, exhibits several endotypes and phenotypes due to different underlying cellular and molecular mechanisms. Globally it affects 300 million individuals, with the prevalence of 2–3% in India, contributing to morbidity and mortality. Over 50 cytokines have been identified in asthma. The dysregulation in Th1 and Th2 cytokines is implicated in the patho-mechanism of pulmonary inflammation and airway remodeling. The aim of the current study was to access the circulating levels of IL-1β (pro-inflammatory) and IL-10 (anti-inflammatory) cytokines using sandwich enzyme-linked immunosorbent assay (ELISA). In this case-control study we recruited a total of 164 subjects (104 adult onset asthma patients and 60 non-asthmatic healthy controls) from south India. Data exhibited increased levels of IL-1β and decreased levels of IL-10 in asthma patients compared to the healthy controls. Subgroup analysis revealed significant elevation in the circulating levels of IL-1β and Th1:Th2 (IL-1β/IL-10) ratio in patients with uncontrolled and long-standing disease (>10 years). Receiver operating curve analysis of individual cytokines and ratios showed good and excellent discriminating capacity respectively for health vs disease and controlled vs uncontrolled. However, IL-1β showed better incisive capacity for disease duration. Based on our observation it appears that rather than individual cytokine(s), the balance between pro and anti-inflammatory cytokines are crucial in the patho-mechanism of asthma. However, developing a signature profile of multiple cytokines using cut-off values may prove to be more promising for diagnostic, prognostic and therapeutic purposes of bronchial asthma.
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Woodward, Wendy A. "Cell Gene Expression Signatures in Inflammatory Breast Cancer." In Inflammatory Breast Cancer: An Update, 259–70. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-3907-9_20.

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Miller, Jessica E., Lindsey K. Symons, Ryan M. Marks, and Chandrakant Tayade. "Endometrial Immune-Inflammatory Gene Signatures in Endometriosis." In Endometrial Gene Expression, 141–58. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-28584-5_10.

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Laere, Steven J. Van, Peter B. Vermeulen, and Luc Y. Dirix. "cDNA Microarray Analysis of Inflammatory Breast Cancer Signatures." In Methods in Molecular Biology™, 71–98. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-530-9_6.

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Bhalla, Parinishtha, Anukriti Verma, Bhawna Rathi, Shivani Sharda, and Pallavi Somvanshi. "Exploring Molecular Signatures in Spondyloarthritis: A Step Towards Early Diagnosis." In Proceedings of the Conference BioSangam 2022: Emerging Trends in Biotechnology (BIOSANGAM 2022), 142–55. Dordrecht: Atlantis Press International BV, 2022. http://dx.doi.org/10.2991/978-94-6463-020-6_15.

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AbstractSpondyloarthritis is an acute inflammatory disorder of the musculoskeletal system often accompanied by pain, stiffness, bone and tissue damage. It majorly consists of ankylosing spondylitis, psoriatic arthritis and reactive arthritis. It follows a differential diagnosis pattern for demarcation between the spondyloarthritis subtypes and other arthritic subtypes such as rheumatoid arthritis, juvenile arthritis and osteoarthritis due to the heterogeneity causing gradual chronicity and complications. Presence of definite molecular markers can not only improve diagnosis efficiency but also aid in their prognosis and therapy. This study is an attempt to compose a refined list of such unique and common molecular signatures of the considered subtypes, by employing a reductionist approach amalgamating gene retrieval, protein-protein interaction network, functional, pathway, micro-RNA-gene and transcription factor-gene regulatory network analysis. Gene retrieval and protein-protein interaction network analysis resulted in unique and common interacting genes of arthritis subtypes. Functional annotation and pathway analysis found vital functions and pathways unique and common in arthritis subtypes. Furthermore, miRNA-gene and transcription factor-gene interaction networks retrieved unique and common miRNA’s and transcription factors in arthritis subtypes. Furthermore, the study identified important signatures of arthritis subtypes that can serve as markers assisting in prognosis, early diagnosis and personalized treatment of arthritis patients requiring validation via prospective experimental studies.
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Robertson, Fredika M., Khoi Chu, Sandra V. Fernandez, Zaiming Ye, Sanford H. Barsky, and Massimo Cristofanilli. "Gene Signatures of Inflammatory Breast Cancer: Epithelial Plasticity and a Cancer Stem Cell Phenotype." In Cell and Molecular Biology of Breast Cancer, 305–22. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-634-4_14.

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Aiman, Ayesha, Seemi Farhat Basir, and Asimul Islam. "Interferons Horizon Therapeutics." In Interferon - Immune Metabolism [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.104718.

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Interferons (IFNs) are a family of multi-functional proteins, called cytokines, that are produced by immune cells such as leukocytes, natural killer (NK) cells, macrophages, fibroblasts, and epithelial cells. The minute amount of these α-helical glycoproteins, produced by mammalian cells, are firm components of the innate arm of the immune system providing rapid and broad protection against numerous types of invading pathogens. Interferons, from their discovery in the 19th century, have always held out a promise of important clinical utility first as an antiviral agent and more recently holding anti-inflammatory and regenerative effects for treating various neurological diseases such as multiple sclerosis, encephalopathies, Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS), etc. IFNs elicit anti-viral and anti-inflammatory properties by inducing transcription of multiple IFN stimulated genes (ISG), a response that is partly mediated by Interferon regulatory factors (IRFs). This chapter provides a brief introduction of the interferon system as well as an in-depth assessment of the interferon signature and the various assay procedures for synthesizing non-natural interferon analogs for structural analysis, which may be helpful in designing improved products and act as a diagnostic tool for neurodegenerative disorders.
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M., Fredika, Chu Khoi, Rita Circo, Julia Wulfkuhle, Savitri Krishnamurthy, Zaiming Ye, Annie Z., et al. "Genomic and Proteomic Pathway Mapping Reveals Signatures of Mesenchymal-Epithelial Plasticity in Inflammatory Breast Cancer." In Breast Cancer - Recent Advances in Biology, Imaging and Therapeutics. InTech, 2011. http://dx.doi.org/10.5772/23082.

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Conference papers on the topic "Inflammatory signature"

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Tantillo, E., P. Caruso, D. Colecchia, G. Pittelli, S. Pontis, M. Civelli, and M. Trevisani. "Inflammatory signature of a murine model of chronic obstructive pulmonary disease (COPD) exacerbations." In ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.1075.

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Thudi, Nanda K., Pijus K. Mandal, John S. McMurray, and Fredika M. Robertson. "Abstract 653: Stat3 as a molecular signature and therapeutic target for inflammatory breast cancer." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-653.

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Guglietta, Silvia, Lukas Weber, Bruno Fosso, Marinella Marzano, Gary Hardiman, Monica Olcina, Mark Robinson, and Carsten Krieg. "486 Complement downregulation promotes an inflammatory signature that renders colorectal cancer susceptible to immunotherapy." In SITC 37th Annual Meeting (SITC 2022) Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-sitc2022.0486.

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Frøssing, Laurits, Ditte Kjærsgaard Klein, Kathrine Baines, Peter Gibson, Vibeke Backer, and Celeste Porsbjerg. "The 6 Gene Signature in Whole Sampled Sputum provides Clinically Feasible Inflammatory Phenotyping of Asthma." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa1714.

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Wilcox, Jessica A., Jan Remsik, N. Esther Babady, Tracy A. McMillen, Behroze A. Vachha, Neil A. Halpern, Vikram Dhawan, et al. "Abstract 703: An inflammatory leptomeningeal signature in cancer patients with neurologic manifestations of COVID-19." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-703.

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Brown, R. Dale, Min Li, Charles T. Stewart, B. Alexandre McKeon, and Kurt R. Stenmark. "Cardiac Fibroblasts Contribute To The Inflammatory-Fibrotic Signature Of The Right Ventricle In Hypoxia-Induced Pulmonary Hypertension." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a3458.

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Wang, Lin, Andriy Kobryn, Kyeongah Kang, Emanuela Taioli, William Oh, Paolo Boffetta, Shu-Hsia Chen, Stuart Aaronson, and David J. Mulholland. "Abstract 695: Exposure to World Trade Center (WTC) dust initiates a pro-cancer inflammatory signature in mice." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-695.

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Van, Laere SJ, Golen KL Van, M. Joglekar, NT Ueno, P. Finetti, Dam PA Van, P. Viens, et al. "P5-01-01: Identification, Validation and Assessment of Transcriptional Relevance of a PDGFR-Activation Signature in (Inflammatory) Breast Cancer." In Abstracts: Thirty-Fourth Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 6‐10, 2011; San Antonio, TX. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/0008-5472.sabcs11-p5-01-01.

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Choi, Kwangmin, Kakajan Komurov, Jonathan S. Fletcher, Edwin Jousma, Jose A. Cancelas, Jianqiang Wu, and Nancy Ratner. "Abstract A04: An inflammatory gene signature distinguishes neurofibroma Schwann cells and macrophages from cells in the normal peripheral nervous system." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; October 20-23, 2016; Boston, MA. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/2326-6074.tumimm16-a04.

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Jibril, Aisha, Prakrit Kumar, Charlotte Hellmich, Jamie A. Moore, Jayna J. Mistry, Victoria Willimott, Kristian M. Bowles, and Stuart A. Rushworth. "Abstract 2799: Multiple myeloma derived mitochondrial DAMPs induce a pro-inflammatory signature in the bone marrow microenvironment to promote pro-tumoral expansion." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-2799.

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Reports on the topic "Inflammatory signature"

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Shpigel, Nahum Y., Ynte Schukken, and Ilan Rosenshine. Identification of genes involved in virulence of Escherichia coli mastitis by signature tagged mutagenesis. United States Department of Agriculture, January 2014. http://dx.doi.org/10.32747/2014.7699853.bard.

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Mastitis, an inflammatory response of the mammary tissue to invading pathogenic bacteria, is the largest health problem in the dairy industry and is responsible for multibillion dollar economic losses. E. coli are a leading cause of acute mastitis in dairy animals worldwide and certainly in Israel and North America. The species E. coli comprises a highly heterogeneous group of pathogens, some of which are commensal residents of the gut, infecting the mammary gland after contamination of the teat skin from the environment. As compared to other gut microflora, mammary pathogenic E. coli (MPEC) may have undergone evolutionary adaptations that improve their fitness for colonization of the unique and varied environmental niches found within the mammary gland. These niches include competing microbes already present or accompanying the new colonizer, soluble and cellular antimicrobials in milk, and the innate immune response elicited by mammary cells and recruited immune cells. However, to date, no specific virulence factors have been identified in E. coli isolates associated with mastitis. The original overall research objective of this application was to develop a genome-wide, transposon-tagged mutant collection of MPEC strain P4 and to use this technology to identify E. coli genes that are specifically involved in mammary virulence and pathogenicity. In the course of the project we decided to take an alternative genome-wide approach and to use whole genomes bioinformatics analysis. Using genome sequencing and analysis of six MPEC strains, our studies have shown that type VI secretion system (T6SS) gene clusters were present in all these strains. Furthermore, using unbiased screening of MPEC strains for reduced colonization, fitness and virulence in the murine mastitis model, we have identified in MPEC P4-NR a new pathogenicity island (PAI-1) encoding the core components of T6SS and its hallmark effectors Hcp, VgrG and Rhs. Next, we have shown that specific deletions of T6SS genes reduced colonization, fitness and virulence in lactating mouse mammary glands. Our long-term goal is to understand the molecular mechanisms of host-pathogen interactions in the mammary gland and to relate these mechanisms to disease processes and pathogenesis. We have been able to achieve our research objectives to identify E. coli genes that are specifically involved in mammary virulence and pathogenicity. The project elucidated a new basic concept in host pathogen interaction of MPEC, which for the best of our knowledge was never described or investigated before. This research will help us to shed new light on principles behind the infection strategy of MPEC. The new targets now enable prevalence and epidemiology studies of T6SS in field strains of MPEC which might unveil new geographic, management and ecological risk factors. These will contribute to development of new approaches to treat and prevent mastitis by MPEC and perhaps other mammary pathogens. The use of antibiotics in farm animals and specifically to treat mastitis is gradually precluded and thus new treatment and prevention strategies are needed. Effective mastitis vaccines are currently not available, structural components and effectors of T6SS might be new targets for the development of novel vaccines and therapeutics.
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Shpigel, Nahum, Raul Barletta, Ilan Rosenshine, and Marcelo Chaffer. Identification and characterization of Mycobacterium paratuberculosis virulence genes expressed in vivo by negative selection. United States Department of Agriculture, January 2004. http://dx.doi.org/10.32747/2004.7696510.bard.

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Mycobacterium avium subsp. paratuberculosis (MAP) is the etiological agent of a severe inflammatory bowel disease (IBD) in ruminants, known as Johne’s disease or paratuberculosis. Johne’s disease is considered to be one of the most serious diseases affecting dairy cattle both in Israel and worldwide. Heavy economic losses are incurred by dairy farmers due to the severe effect of subclinical infection on milk production, fertility, lower disease resistance and early culling. Its influence in the United States alone is staggering, causing an estimated loss of $1.5 billion to the agriculture industry every year. Isolation of MAP from intestinal tissue and blood of Crohn's patients has lead to concern that it plays a potential pathogenic role in promoting human IDB including Crohn’s disease. There is great concern following the identification of the organism in animal products and shedding of the organism to the environment by subclinically infected animals. Little is known about the molecular basis for MAP virulence. The goal of the original proposed research was to identify MAP genes that are required for the critical stage of initial infection and colonization of ruminants’ intestine by MAP. We proposed to develop and use signature tag mutagenesis (STM) screen to find MAP genes that are specifically required for survival in ruminants upon experimental infection. This research projected was approved as one-year feasibility study to prove the ability of the research team to establish the animal model for mutant screening and alternative in-vitro cell systems. In Israel, neonatal goat kids were repeatedly inoculated with either one of the following organisms; MAP K-10 strain and three transposon mutants of K-10 which were produced and screened by the US PI. Six months after the commencement of inoculation we have necropsied the goats and taken multiple tissue samples from the jejunum, ileum and mesenteric lymph nodes. Both PCR and histopathology analysis indicated on efficient MAP colonization of all the inoculated animals. We have established several systems in the Israeli PI’s laboratory; these include using IS900 PCR for the identification of MAP and using HSP65-based PCR for the differentiation between MAV and MAP. We used Southern blot analysis for the differentiation among transposon mutants of K-10. In addition the Israeli PI has set up a panel of in-vitro screening systems for MAP mutants. These include assays to test adhesion, phagocytosis and survival of MAP to/within macrophages, assays that determine the rate of MAPinduced apoptosis of macrophages and MAP-induced NO production by macrophages, and assays testing the interference with T cell ã Interferon production and T cell proliferation by MAP infected macrophages (macrophage studies were done in BoMac and RAW cell lines, mouse peritoneal macrophages and bovine peripheral blood monocytes derived macrophages, respectively). All partners involved in this project feel that we are currently on track with this novel, highly challenging and ambitious research project. We have managed to establish the above described research systems that will clearly enable us to achieve the original proposed scientific objectives. We have proven ourselves as excellent collaborative groups with very high levels of complementary expertise. The Israeli groups were very fortunate to work with the US group and in a very short time period to master numerous techniques in the field of Mycobacterium research. The Israeli group has proven its ability to run this complicated animal model. This research, if continued, may elucidate new and basic aspects related to the pathogenesis MAP. In addition the work may identify new targets for vaccine and drug development. Considering the possibility that MAP might be a cause of human Crohn’s disease, better understanding of virulence mechanisms of this organism might also be of public health interest as well.
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