Relevant bibliographies by topics / S100A8

Academic literature on the topic 'S100A8'

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Published: 4 June 2021
Last updated: 20 February 2023

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Journal articles on the topic "S100A8"

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Broome, Ann-Marie, David Ryan, and Richard L. Eckert. "S100 Protein Subcellular Localization During Epidermal Differentiation and Psoriasis." Journal of Histochemistry & Cytochemistry 51, no. 5 (May 2003): 675–85. http://dx.doi.org/10.1177/002215540305100513.

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S100 proteins are calcium-activated signaling proteins that interact with target proteins to modulate biological processes. Our present studies compare the level of expression, and cellular localization of S100A7, S100A8, S100A9, S100A10, and S100A11 in normal and psoriatic epidermis. S100A7 and S100A11 are present in the basal and spinous layers in normal epidermis. These proteins appear in the nucleus and cytoplasm in basal cells but are associated with the plasma membrane in spinous cells. S100A10 is present in basal and spinous cells, in the cytoplasm, and is associated with the plasma membrane. S100A8 and S100A9 are absent or are expressed at minimal levels in normal epidermis. In involved psoriatic tissue, S100A10 and S100A11 levels remain unchanged, whereas, S100A7, S100A8, and S100A9 are markedly overexpressed. The pattern of expression and subcellular localization of S100A7 is similar in normal and psoriatic tissue. S100A8 and S100A9 are strongly expressed in the basal and spinous layers in psoriasis-involved tissue. In addition, we demonstrate that S100A7, S100A10, and S100A11 are incorporated into detergent and reducing agent-resistant multimers, suggesting that they are in vivo trans-glutaminase substrates. S100A8 and S100A9 did not form these larger complexes. These results indicate that S100 proteins localize to the plasma membrane in differentiated keratinocytes, suggesting a role in regulating calcium-dependent, membrane-associated events. These studies also indicate, as reported previously, that S100A7, S100A8, and S100A9 expression is markedly altered in psoriasis, suggesting a role for these proteins in disease pathogenesis.
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Mitrović Ajtić, Olivera, Tijana Subotički, Miloš Diklić, Dragoslava Đikić, Milica Vukotić, Teodora Dragojević, Emilija Živković, Darko Antić, and Vladan Čokić. "Regulation of S100As Expression by Inflammatory Cytokines in Chronic Lymphocytic Leukemia." International Journal of Molecular Sciences 23, no. 13 (June 22, 2022): 6952. http://dx.doi.org/10.3390/ijms23136952.

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The calcium-binding proteins S100A4, S100A8, and S100A9 are upregulated in chronic lymphocytic leukemia (CLL), while the S100A9 promotes NF-κB activity during disease progression. The S100-protein family has been involved in several malignancies as mediators of inflammation and proliferation. The hypothesis of our study is that S100A proteins are mediators in signaling pathways associated with inflammation-induced proliferation, such as NF-κB, PI3K/AKT, and JAK/STAT. The mononuclear cells (MNCs) of CLL were treated with proinflammatory IL-6, anti-inflammatory IL-10 cytokines, inhibitors of JAK1/2, NF-κB, and PI3K signaling pathways, to evaluate S100A4, S100A8, S100A9, and S100A12 expression as well as NF-κB activation by qRT-PCR, immunocytochemistry, and immunoblotting. The quantity of S100A4, S100A8, and S100A9 positive cells (p < 0.05) and their protein expression (p < 0.01) were significantly decreased in MNCs of CLL patients compared to healthy controls. The S100A levels were generally increased in CD19+ cells compared to MNCs of CLL. The S100A4 gene expression was significantly stimulated (p < 0.05) by the inhibition of the PI3K/AKT signaling pathway in MNCs. IL-6 stimulated S100A4 and S100A8 protein expression, prevented by the NF-κB and JAK1/2 inhibitors. In contrast, IL-10 reduced S100A8, S100A9, and S100A12 protein expressions in MNCs of CLL. Moreover, IL-10 inhibited activation of NF-κB signaling (4-fold, p < 0.05). In conclusion, inflammation stimulated the S100A protein expression mediated via the proliferation-related signaling and balanced by the cytokines in CLL.
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Peterova, Eva, Jan Bures, Paula Moravkova, and Darina Kohoutova. "Tissue mRNA for S100A4, S100A6, S100A8, S100A9, S100A11 and S100P Proteins in Colorectal Neoplasia: A Pilot Study." Molecules 26, no. 2 (January 14, 2021): 402. http://dx.doi.org/10.3390/molecules26020402.

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S100 proteins are involved in the pathogenesis of sporadic colorectal carcinoma through different mechanisms. The aim of our study was to assess tissue mRNA encoding S100 proteins in patients with non-advanced and advanced colorectal adenoma. Mucosal biopsies were taken from the caecum, transverse colon and rectum during diagnostic and/or therapeutic colonoscopy. Another biopsy was obtained from adenomatous tissue in the advanced adenoma group. The tissue mRNA for each S100 protein (S100A4, S100A6, S100A8, S100A9, S100A11 and S100P) was investigated. Eighteen biopsies were obtained from the healthy mucosa in controls and the non-advanced adenoma group (six individuals in each group) and thirty biopsies in the advanced adenoma group (ten patients). Nine biopsies were obtained from advanced adenoma tissue (9/10 patients). Significant differences in mRNA investigated in the healthy mucosa were identified between (1) controls and the advanced adenoma group for S100A6 (p = 0.012), (2) controls and the non-advanced adenoma group for S100A8 (p = 0.033) and (3) controls and the advanced adenoma group for S100A11 (p = 0.005). In the advanced adenoma group, differences between the healthy mucosa and adenomatous tissue were found in S100A6 (p = 0.002), S100A8 (p = 0.002), S100A9 (p = 0.021) and S100A11 (p = 0.029). Abnormal mRNA expression for different S100 proteins was identified in the pathological adenomatous tissue as well as in the morphologically normal large intestinal mucosa.
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McLachlan, Julia L., Alastair J. Sloan, Anthony J. Smith, Gabriel Landini, and Paul R. Cooper. "S100 and Cytokine Expression in Caries." Infection and Immunity 72, no. 7 (July 2004): 4102–8. http://dx.doi.org/10.1128/iai.72.7.4102-4108.2004.

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ABSTRACT The molecular immune response of the pulpal tissue during chronic carious infection is poorly characterized. Our objective was to examine the expression of potential molecular mediators of pulpal inflammation, correlate their levels with disease severity, and determine the cellular localization of key molecules. Results indicated that there was significantly increased transcriptional activity in carious compared to healthy pulp, and the increase correlated positively with disease severity. Semiquantitative reverse transcriptase PCR analysis in 10 carious and 10 healthy pulpal tissue samples of the S100 family members S100A8, S100A9, S100A10, S100A12, and S100A13; the cytokines tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β), IL-8, IL-6, and epithelial cell-derived neutrophil attractant 78 (ENA-78); and the structural protein collagen-1α indicated that all genes tested, with the exception of S100A10, were more abundantly expressed in carious teeth. In addition, we found that the closer the carious lesion front was to the pulpal chamber the higher the expression was for all genes except S100A10. Multiple-regression analysis identified a significant positive correlation between the expression levels of S100A8 and IL-1β, ENA-78, and IL-6 and between collagen-1α and S100A8, TNF-α, IL-1β, IL-8, IL-6, and ENA-78. Immunohistochemical studies in carious pulpal tissue indicated that S100A8 and the S100A8/S100A9 complex were predominantly expressed by infiltrating neutrophils. Gene expression analyses in immune system cells supported these findings and indicated that bacterial activation of neutrophils caused upregulation of S100A8, S100A9, and S100A13. This study highlights the complex nature of the molecular immune response that occurs during carious infection.
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Roszkowski, Leszek, Bożena Jaszczyk, Magdalena Plebańczyk, and Marzena Ciechomska. "S100A8 and S100A12 Proteins as Biomarkers of High Disease Activity in Patients with Rheumatoid Arthritis That Can Be Regulated by Epigenetic Drugs." International Journal of Molecular Sciences 24, no. 1 (December 31, 2022): 710. http://dx.doi.org/10.3390/ijms24010710.

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Rheumatoid arthritis (RA) is an autoimmune chronic inflammatory disease that is still not well understood in terms of its pathogenesis and presents diagnostic and therapeutic challenges. Monocytes are key players in initiating and maintaining inflammation through the production of pro-inflammatory cytokines and S100 proteins in RA. This study aimed to test a specific DNA methylation inhibitor (RG108) and activator (budesonide) in the regulation of pro-inflammatory mediators—especially the S100 proteins. We also searched for new biomarkers of high disease activity in RA patients. RNA sequencing analysis of healthy controls (HCs) and RA monocytes was performed. Genes such as the S100 family, TNF, and IL-8 were validated by qRT-PCR following DNA-methylation-targeted drug treatment in a monocytic THP-1 cell line. The concentrations of the S100A8, S100A11, and S100A12 proteins in the sera and synovial fluids of RA patients were tested and correlated with clinical parameters. We demonstrated that RA monocytes had significantly increased levels of S100A8, S100A9, S100A11, S100A12, MYD88, JAK3, and IQGAP1 and decreased levels of IL10RA and TGIF1 transcripts. In addition, stimulation of THP-1 cells with budesonide statistically reduced the expression of the S100 family, IL-8, and TNF genes. In contrast, THP-1 cells treated with RG108 had increased levels of the S100 family and TNF genes. We also revealed a significant upregulation of S100A8, S100A11, and S100A12 in RA patients, especially in early RA compared to HC sera. In addition, protein levels of S100A8, S100A11, and S100A12 in RA synovial fluids compared to HC sera were significantly increased. Overall, our data suggest that the S100A8 and S100A12 proteins are strongly elevated during ongoing inflammation, so they could be used as a better biomarker of disease activity than CRP. Interestingly, epigenetic drugs can regulate these S100 proteins, suggesting their potential use in targeting RA inflammation.
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Holmannová, Drahomíra, Barbora Císařová, Pavel Borský, Zdeněk Fiala, Ctirad Andrýs, Květoslava Hamaková, Tereza Švadláková, et al. "Goeckerman Regimen Reduces Alarmin Levels and PASI Score in Paediatric Patients with Psoriasis." Acta Medica (Hradec Kralove, Czech Republic) 64, no. 4 (2021): 204–12. http://dx.doi.org/10.14712/18059694.2022.3.

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Background. Psoriasis is a chronic systemic inflammatory disease with (extra-)cutaneous manifestations. Inflammation is associated with cellular stress and tissue damage which lead to the release of alarmins (signals of danger). Goeckerman regimen (GR) is a highly efficacious treatment consisting of the application of pharmaceutical crude tar and UVB light exposure. The reduction of inflammatory processes in the skin is accompanied by changes in the levels of inflammatory markers - alarmins (HMBG-1, S100A7, S1000A8, S100A9, S100A12, IL-17, IL-22, and IL-33). Methods. The alarmin levels in sera of 19 paediatric patients with psoriasis were determined before and after GR using commercial ELISA kits. The Psoriasis area severity index (PASI) was used to determine the disease severity. Results. GR reduced both PASI and the levels of all measured alarmins. The levels of S100A7, S100A9, IL-22, IL-33, and HMGB-1 were significantly decreased. Positive correlations between IL-22 and PASI, between S100A9 and IL-17, S100A9 and IL-22, and a negative correlation between S100A8 and IL-33 were found. Conclusions. Goeckerman regimen is a very effective, safe and low-cost therapy. We confirmed, it modulates the immune system reactivity, ameliorates the severity of the disease and reduces the levels of alarmins reflecting the presence and intensity of inflammation.
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Leach, Steven T., Hazel M. Mitchell, Carolyn L. Geczy, Philip M. Sherman, and Andrew S. Day. "S100 Calgranulin Proteins S100A8, S100A9 and S100A12 are Expressed in the Inflamed Gastric Mucosa ofHelicobacter Pylori-Infected Children." Canadian Journal of Gastroenterology 22, no. 5 (2008): 461–64. http://dx.doi.org/10.1155/2008/308942.

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The expression of the inflammatory S100 calgranulin proteins (S100A8, S100A9 and S100A12) in normal andHelicobacter pylori-infected gastric mucosa of children were examined. S100A8, S100A9 and S100A12, which were virtually absent in normal gastric mucosa, were highly expressed inH pylori-infected mucosa. This expression correlated with the severity of gastritis (r=0.9422, P<0.05). S100 calgranulins may be involved in bacterial-induced gastritis and may limit bacterial growth.
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Tardif, Mélanie R., Julie Andrea Chapeton-Montes, Alma Posvandzic, Nathalie Pagé, Caroline Gilbert, and Philippe A. Tessier. "Secretion of S100A8, S100A9, and S100A12 by Neutrophils Involves Reactive Oxygen Species and Potassium Efflux." Journal of Immunology Research 2015 (2015): 1–16. http://dx.doi.org/10.1155/2015/296149.

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S100A8/A9 (calprotectin) and S100A12 proinflammatory mediators are found at inflammatory sites and in the serum of patients with inflammatory or autoimmune diseases. These cytoplasmic proteins are secreted by neutrophils at sites of inflammation via alternative secretion pathways of which little is known. This study examined the nature of the stimuli leading to S100A8/A9 and S100A12 secretion as well as the mechanism involved in this alternative secretion pathway. Chemotactic agents, cytokines, and particulate molecules were used to stimulate human neutrophils. MSU crystals, PMA, and H2O2induced the release of S100A8, S100A9, and S100A12 homodimers, as well as S100A8/A9 heterodimer. High concentrations of S100A8/A9 and S100A12 were secreted in response to nanoparticles like MSU, silica, TiO2, fullerene, and single-wall carbon nanotubes as well as in response to microbe-derived molecules, such as zymosan or HKCA. However, neutrophils exposed to the chemotactic factors fMLP failed to secrete S100A8/A9 or S100A12. Secretion of S100A8/A9 was dependent on the production of reactive oxygen species and required K+exchanges through the ATP-sensitive K+channel. Altogether, these findings suggest that S100A12 and S100A8/A9 are secreted independently either via distinct mechanisms of secretion or following the activation of different signal transduction pathways.
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Li, Changyou, Siyuan Li, Changkai Jia, Lingling Yang, Zicheng Song, and Yiqiang Wang. "Low Concentration of S100A8/9 Promotes Angiogenesis-Related Activity of Vascular Endothelial Cells: Bridges among Inflammation, Angiogenesis, and Tumorigenesis?" Mediators of Inflammation 2012 (2012): 1–8. http://dx.doi.org/10.1155/2012/248574.

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Previous studies showed that several members of the S100A family are involved in neovascularization and tumor development. This study checked whether low concentrations of S100A8 or S100A9 has any effect on the behaviour of vascular endothelial cells. A human umbilical vascular endothelial cell (HUVEC) line was used to measure vascular endothelial cell bioactivity related to angiogenesis, such as cell proliferation, migration, and vessel formation. In the low concentration range up to 10 μg/mL, either each alone or in combination, S100A8 and S100A9 proteins promoted proliferation of HUVEC cells in a dose-dependent manner. The presence of both proteins in culture showed additive effects over each single protein. Both proteins enhanced HUVEC cells to migrate across the transwell membrane and to form tube-like structures on the Matrigel surface. When mixed in Matrigel and injected subcutaneously in Balb/c mice, both proteins increased vessel development in the gel plugs. Microarray assay of HUVEC cells treated with 10 μg/mL S100A8 revealed that ribosome pathway, pathogenicEscherichia coliinfection pathway, apoptosis, and stress response genes were modulated by S100A8 treatment. We propose that S100A8 and S100A9 proteins from either infiltrating inflammatory cells or tumor cells play an important role in the interplay among inflammation, angiogenesis, and tumorigenesis.
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Wakiya, R., T. Kameda, K. Ueeda, S. Nakashima, H. Shimada, M. F. Mansour, M. Kato, et al. "Hydroxychloroquine modulates elevated expression of S100 proteins in systemic lupus erythematosus." Lupus 28, no. 7 (May 8, 2019): 826–33. http://dx.doi.org/10.1177/0961203319846391.

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Objectives We investigated the effect of hydroxychloroquine (HCQ) on S100A8 and S100A9 serum levels in systemic lupus erythematosus (SLE) patients with low disease activity receiving immunosuppressants. Methods SELENA-SLEDAI, Cutaneous Lupus Erythematous Disease Area and Severity Index (CLASI) and serum levels of complement factors, anti-dsDNA antibodies, and white blood cell, lymphocyte, and platelet counts were used to evaluate disease activity, cutaneous disease activity, and immunological activity, respectively. Serum S100A8 and S100A9 were measured at HCQ administration and after 3 or 6 months using ELISA. Results S100A8 and S100A9 serum levels were elevated at baseline and the magnitude of decrease from baseline at 3 and 6 months after HCQ administration was greater in patients with renal involvement than in those without (baseline: S100A8, p = 0.034; S100A9, p = 0.0084; decrease: S100A8, p = 0.049; S100A9, p = 0.023). S100 modulation was observed in patients with ( n = 17; S100A8, p = 0.0011; S100A9, p = 0.0002) and without renal involvement ( n = 20; S100A8, p = 0.0056; S100A9, p = 0.0012), and was more apparent in patients with improved CLASI activity scores (improved: S100A8, p = 0.013; S100A9, p = 0.0032; unimproved: S100A8, p = 0.055; S100A9, p = 0.055). No associations were observed for immunological biomarkers. Conclusion HCQ may improve organ involvement in SLE by modulating S100 protein levels, especially in patients with renal or skin involvement.
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Dissertations / Theses on the topic "S100A8"

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Betz, Christine [Verfasser], and Oliver [Akademischer Betreuer] Einsle. "Structural characterization of the metal-binding ligands S100A8/S100A9 and S100B of the receptor for advanced glycation end products = Strukturelle Charakterisierung der metallbindenden Liganden S100A8/S100A9 und S100B des Rezeptors für Advanced Glycation End Products." Freiburg : Universität, 2013. http://d-nb.info/1115813455/34.

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Leukert, Nadja. "Molekulare Charakterisierung verschiedener Komplexformen der Calcium-bindenden Proteine S100A8 und S100A9." [S.l. : s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=967777062.

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van, Hummel Annika Elise. "The Roles of S100A8 and S100A9 in Cartilage: Degradation and Formation." Thesis, The University of Sydney, 2014. http://hdl.handle.net/2123/11521.

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Osteoarthritis (OA) is a debilitating joint disease that increases in prevalence with age, with latest figures show that around 2.4 million Australians suffer from OA. There are currently no disease-modifying drugs available and due to poor management options, the number of joint replacement surgeries is increasing by nearly 10% per annum in Australia. S100A8 and S100A9 calcium-binding proteins are expressed by immune cells, and are involved in inflammatory situations, including inflammatory diseases such as rheumatoid arthritis, where there is an increase in circulating and local (synovial fluid) levels of S100A8 and S100A9. They are present in the body preferentially as a heterodimer (S100A8/S100A9) or less commonly as homodimers. Recently, S100A8 and S100A9 were found in bone and cartilage cells; however their roles in these tissues are still unknown. The aim of this research therefore was to determine the role(s) of S100A8 and S100A9 in cartilage degeneration and OA. The results presented in this thesis have provided insight into the role(s) of S100A8 and S100A9 in cartilage and in OA. S100A8 and S100A9 act as primers of cartilage degradation, through TLR4 and MAPK signalling pathways, but require a second messenger in order to achieve full biochemical breakdown. S100A8 is abundant in chondrocytes of human OA joints, but does not appear to be involved in non-inflammatory mouse models. S100A8, and to a lesser degree S100A9, are also abundant at joint margins and in osteophytes from human OA patients, and may play a role in chondrogenesis. The results presented in this thesis have determined some of the mechanisms of action of S100A8 and S100A9 in cartilage, however, the exact role of S100A8 and S100A9 in OA remain unclear, and further work will need to be performed to fully determine the significance of S100A8 and S100A9 in OA.
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Baker, Jonathan Richard. "S100A8 in development." Thesis, University College London (University of London), 2008. http://discovery.ucl.ac.uk/1444146/.

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S100 proteins are a family of Ca2+ binding EF-hand proteins. S100A8 is a cytosolic protein expressed in myeloid cells and epithelia where it forms a stable heterodimer with another S100 protein family member, S100A9. The S100A9 null mouse is viable and has no gross defect whereas the S100A8 null mouse is embryonic lethal. It was originally proposed that the S100A8 null mouse is lethal at E 9.0 in development due to lack of expression at E 6.5 in ectoplacental cone cells. This thesis shows that the S100A8 null phenotype is more complex than originally thought. S100A8 has a role in preimplantation development, which is previously unstudied. A small number of S100A8 null embryos survive to blastocyst but none survive implantation showing fatal compromise of S100A8 null embryos early in development. This thesis presents evidence that this lethality presents between fertilisation and E 2.5 of development. S100A8 also has a role in the murine decidua after implantation possibly key to normal murine development. S100A8 mRNA is highly expressed in maternal decidua yet S100A8 protein is not highly expressed. Foetal yolk sac cells do not express S100A8 mRNA yet they do stain positively for S100A8 protein. This thesis proposes that S100A8 protein is generated in the murine decidua and exported to the foetus where haematopoietic cells present the protein. The S100A8 protein has been shown to be expressed and stable independently of its myeloid partner, S100A9. These observations explain the discrepancy between the two SI00 null mouse phenotypes and add new insight to the S100A8 null phenotype.
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Raquil, Marie-Astrid. "Études des rôles pro-inflammatoires et prolifératifs des protéines S100A8 et S100A9." Thesis, Université Laval, 2008. http://www.theses.ulaval.ca/2008/25415/25415.pdf.

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Sikora, Kristin [Verfasser]. "RAGE-abhängige S100A8- und S100A9-Expression in humanen THP-1 Zellen / Kristin Sikora." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2009. http://d-nb.info/1023749920/34.

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Ludwig, Stefan [Verfasser]. "Die S100-Proteine S100A8 und S100A9 sowie der Heterodimerkomplex S100A8/A9 im Serum und Plasma als Marker des Prostatakarzinoms : Untersuchungen zu präanalytischen Einflussfaktoren und zur diagnostischen Differenzierung zwischen benigner Prostatahyperplasie und Prostatakarzinom / Stefan Ludwig." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2008. http://d-nb.info/1023022486/34.

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Laouedj, Malika. "Effets des protéines S100A8 et S100A9 dans la différenciation cellulaire dans la leucémie myéloïde aiguë." Doctoral thesis, Université Laval, 2017. http://hdl.handle.net/20.500.11794/27761.

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Tableau d’honneur de la Faculté des études supérieures et postdoctorales, 2016-2017
Les leucémies myéloïdes aiguës (LMA) sont des hémopathies rares, mais très agressives. Elles résultent d’un dérèglement du processus d’hématopoïèse qui se caractérise par une prolifération incontrôlée de cellules sanguines immatures engagées dans la lignée myéloïde. En dépit des traitements actuels qui reposent sur l’utilisation d’agents chimiothérapeutiques ciblant les cellules en prolifération, le pronostic des patients souffrants de LMA est très sombre. En effet, seuls 30% des patients souffrants de LMA survivent au-delà de 5 ans suivant la prise en charge thérapeutique. L’identification des acteurs participant au développement et au maintien des LMA est donc cruciale pour l’élaboration d’une stratégie thérapeutique efficace et ciblée. S100A8 et S100A9 sont des protéines fixatrices de calcium exprimées par les neutrophiles et les monocytes. Ce sont des alarmines jouant des rôles clés dans l’inflammation et dans des pathologies causées par une inflammation excessive. Les protéines S100A8 et S100A9 exercent également de multiples fonctions dans divers tumeurs solides. Elles favorisent la formation de niche pré-métastasique et inhibe la réponse immunitaire antitumorale. Une analyse du génome par séquençage a mis en évidence que S100A8 et S100A9 sont fortement exprimées chez les patients atteints de LMA. De plus, l’expression de la protéine S100A8 chez les patients souffrants de LMA serait corrélée avec un faible taux de survie. Principalement étudiées dans les tumeurs solides, les fonctions des protéines S100A8 et S100A9 dans les néoplasies hématologiques telles que les leucémies sont très peu documentées. Dans ces travaux de thèse, nous nous sommes donc intéressés aux rôles exercés par les protéines S100A8 et S100A9 dans les leucémies myéloïdes aiguës. À l’aide d’un modèle murin de LMA induit par la surexpression des facteurs HOXA9 et MEIS1 dans des cellules souches/progénitrices hématopoïétiques, nous avons démontré l’existence d’une fraction de cellules exprimant les protéines S100A8 et S100A9. Celle-ci est également retrouvée chez les patients atteints de leucémies aiguës myélomonocytaires et monocytaires (M4-M5 d’après la classification FAB). Les études menées in vivo et in vitro révèlent que la protéine S100A9 induit la différenciation des cellules leucémiques, tandis que la protéine S100A8, préviens l’effet de S100A9 permettant de maintenir ainsi le phénotype immature des cellules LMA. Le traitement par la protéine recombinante S100A9 permet d’accroitre la maturation des cellules LMA, diminue leur prolifération et prolonge la survie des souris LMA. De la même façon le traitement par les anticorps anti-S100A8 provoque un effet similaire au traitement par la protéine S100A9. Nos résultats suggèrent que de forts ratios de S100A9 sur S100A8 sont requis pour induire la différenciation des cellules LMA. Le mécanisme intracellulaire par lequel S100A9 induit la différenciation des cellules leucémiques a également été étudié dans le cadre de cette thèse. Nous avons identifié que S100A9 via la liaison au récepteur TLR (Toll-like receptor) active les voies de signalisations Mitogen Activated Protein Kinase p38, Jun N-terminal Kinase et extracellular signal-regulated kinases 1 et 2 et provoque la différenciation des cellules leucémiques. Les essais menés sur des cellules primaires de patients malades ont permis de confirmer la capacité de S100A9 et de S100A8 à réguler la différenciation des cellules leucémiques. En somme, les données présentées dans cette thèse contribuent à une meilleure compréhension des rôles des protéines S100A8 et S100A9 dans la différenciation des cellules myéloïdes. Par ailleurs, nos données permettent également d’entrevoir les bénéfices thérapeutiques liés au blocage de S100A8 ou à l’augmentation de S100A9 dans les LMA.
Acute myeloid leukemias (AMLs) are rare but still aggressive hematological diseases. They are the result of a perturbed hematopoietic process characterized by an uncontrolled proliferation of hematopoietic cells committed to the myeloid lineage. Despite current therapy based on chemotherapeutic agents, aimed at killing proliferating cells, prognosis of AML patients is dismal and only 30 % of patients survived beyond 5 years. Identification of actors involved in the initiation and sustaining LMA is crucial to the development of efficient and targeted therapy strategy. S100A8 and S100A9 are calcium-binding proteins predominantly expressed by neutrophils and monocytes, and play key roles in both normal and pathological inflammation. Recently, both proteins were found to promote tumor progression through the establishment of pre-metastatic niches and to inhibit antitumor immune responses. Although S100A8 and S100A9 have been studied in solid cancers, their functions in hematological malignancies remain poorly understood. However, S100A8 and S100A9 are highly expressed in acute myeloid leukemia (AML), and S100A8 expression has been linked to a poor prognosis in AML. Although the roles of these proteins were studies in solid tumor, little is known in their functions in hematological malignancies. We studied in this thesis the role of S100A8 and S100A9 in acute myeloid leukemia. Using AML mouse model of AML surexpressing HOXA9 and MEIS1 in hematopoietic stem and progenitor cells, we identified a small subpopulation of cells expressing S100A8 and S100A9. This subpopulation was consistently found in AML samples from patients with myelomonocytic and monocytic leukemias (M4 and M5 according FAB classification). In vitro and in vivo analyses revealed that S100A9 induces AML cell differentiation, whereas S100A8 prevents differentiation induced by S100A9 activity and maintains AML immature phenotype. Treatment with recombinant S100A9 proteins increased AML cell maturation, induced growth arrest, and prolonged survival in an AML mouse model. Interestingly, anti-S100A8 antibody treatment had effects similar to S100A9 therapy in vivo, suggesting that high ratios of S100A9 over S100A8 are required to induce differentiation. In this thesis, the mechanism of S100A9 leading to differentiation of leukemic cells was also study. Our in vitro studies on the mechanisms/pathways involved in leukemic cell differentiation revealed that binding of S100A9 to toll-like receptor 4 (TLR4) promotes activation of p38 mitogen-activated protein kinase, extracellular signal-regulated kinases 1 and 2, and Jun N-terminal kinase signaling pathways, leading to myelomonocytic and monocytic AML cell differentiation. Overall, our findings indicate that S100A8 and S100A9 are regulators of myeloid differentiation in leukemia and have therapeutic potential in myelomonocytic and monocytic AMLs.
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Defrêne, Joan. "Fonctions des protéines S100A8 et S100A9 dans la réponse inflammatoire associée aux maladies auto-immunes." Doctoral thesis, Université Laval, 2020. http://hdl.handle.net/20.500.11794/66869.

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De nos jours, les maladies auto-immunes concernent une part grandissante de la population mondiale et s’accompagnent d’une comorbidité importante, mais aussi d’un lourd fardeau économique. Parmi ces maladies les plus courantes, on distingue l'arthrite rhumatoïde et le psoriasis affectant respectivement les articulations et la peau et qui ne possèdent toujours pas de traitements curatifs. Dans la pathogenèse de ces maladies, une forte réponse inflammatoire est notamment générée et entretenue, contribuant ainsi à la dégradation des tissus ciblés. De nombreux marqueurs de l’inflammation sont sécrétés dans ces tissus, dont les protéines S100A8 et S100A9 qui sont deux motifs moléculaires associés aux dommages cellulaires. Ces deux protéines sont majoritairement exprimées par les neutrophiles et les cellules myéloïdes activées ainsi que les kératinocytes. Plusieurs études démontrent des propriétés pro-inflammatoires pour S100A8 et S100A9. S100A9 stimule la sécrétion de cytokines pro-inflammatoires par les neutrophiles et les monocytes. La protéineS100A8 est chimiotactique pour les neutrophiles et les monocytes et sa neutralisation in vivo diminue le recrutement de leucocytes dans l’inflammation aiguë. En revanche, des études suggèrent des fonctions anti inflammatoires pour S100A8. Son expression est notamment induite par l’interleukine 10 et les glucocorticoïdes. De plus, S100A8 est sensible à l’oxydation et sa forme oxydée possède des fonctions anti inflammatoires. Cependant, les fonctions de ces deux protéines dans le développement de l’inflammation associées aux maladies auto-immunes sont peu connues. Nous avons effectué la première caractérisation des souris déficientes pour S100a8 et démontré que la protéine S100A8 contrôle la différenciation des cellules myéloïdes et leur capacité à moduler la réponse inflammatoire. À l’aide du modèle d’arthrite induite par le collagène, nous avons démontré que S100A8 est anti-inflammatoire. Elle diminue l’infiltration de neutrophiles et la sécrétion de cytokines pro-inflammatoires dans les pattes. Également, nous avons démontré que S100A8 atténue l’activité des ostéoclastes in vitro et invivo. Le traitement avec un anticorps contre la protéine S100A8 nous a permis de démontrer que les fonctions anti-inflammatoires de S100A8 sont principalement extra cellulaires. En comparant les souris déficientes pour S100a8 et S100a9, nous avons étudié le rôle de S100A8 et S100A9 dans le psoriasis induit par l’imiquimod chez la souris. Dans ce modèle, S100A8 et S100A9 amoindrissent l’hyperplasie et l’inflammation de la peau. Ces travaux ont montré que S100A8 contrôle la différenciation et la prolifération des kératinocytes. Aussi, S100A8 et S100A9 contrôlent l’infiltration de neutrophiles dans le derme ainsi que la réponse des lymphocytes T producteurs d’IL-17 dans les ganglions lymphatiques et le derme.Les travaux de cette thèse démontrent que S100A8 est anti-inflammatoire dans l’arthrite et le psoriasis, mais que S100A9 possède des fonctions différentes dans l’inflammation dépendamment du type de réaction inflammatoire. Par ailleurs, nous avons révélé que deux alarmines peuvent étonnamment exercer des fonctions anti-inflammatoires. La compréhension de ces nouveaux rôles de modulation de l’inflammation pourrait contribuer au développement de nouvelles thérapies.
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Endoh, Yasumi Medical Sciences Faculty of Medicine UNSW. "New mechanisms modulating S100A8 gene expression." Publisher:University of New South Wales. Medical Sciences, 2008. http://handle.unsw.edu.au/1959.4/42942.

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S100A8 is a highly-expressed calcium-binding protein in neutrophils and activated macrophages, and has proposed roles in myeloid cell differentiation and host defense. Functions of S100A8 are not fully understood, partly because of difficulties in generating S100A8 knockout mice. Attempts to silence S100A8 gene expression in activated macrophages and fibroblasts using RNA interference (RNAi) technology were unsuccessful. Despite establishing validated small interfering RNA (siRNA) systems, enzymaticallysynthesized siRNA targeted to S100A8 suppressed mRNA levels by only 40% in fibroblasts activated with FGF-2+heparin, whereas chemically-synthesized siRNAs suppressed S100A8 driven by an S100A8-expression vector by ~75% in fibroblasts. Suppression of the gene in activated macrophages/fibroblasts was low, and some enzymatically-synthesized siRNAs to S100A8, and unrelated siRNA to GAPDH, induced/enhanced S100A8 expression in macrophages. This indicated that S100A8 may be upregulated by type-1 interferon (IFN). IFN-β enhanced expression, but did not directly induce S100A8. Poly (I:C), a synthetic dsRNA, directly induced S100A8 through IL-10 and IFN-dependent pathways. Induction by dsRNA was dependent on RNA-dependent protein kinase (PKR), but not cyclooxygenase-2, suggesting divergent pathways in LPS- and dsRNA-induced responses. New mechanisms of S100A8 gene regulation are presented, that suggest functions in anti-viral defense. S100A8 expression was confirmed in lungs from influenza virus-infected mice and from a patient with severe acute respiratory syndrome (SARS). Multiple pathways via mitochondria mediated S100A8 induction in LPS-activated macrophages; Generation of reactive oxygen species via the mitochondrial electron transport chain and de novo synthesis of ATP may be involved. This pathway also regulated IL-10 production, possibly via PKR. Extracellular ATP and its metabolites enhanced S100A8 induction. Results support involvement of cell stress, such as transfection, in S100A8 expression. A breast tumor cell line (MCF-7) in which the S100A8 gene was silenced, was established using micro RNA technology; S100A8 induction by oncostatin M was reduced by >90% in stably-transfected cells. This did not alter MCF-7 growth. The new approach to investigate the role of S100A8 in a human tumor cell line may assist in exploring its functions and lead to new studies concerning its role in cancer.
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Books on the topic "S100A8"

1

Tirkos, Sam. Investigation of S100A8 and S100A9 as potential genetic modifiers of the pulmonary phenotype in cystic fibrosis mice. Ottawa: National Library of Canada, 2003.

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Dubois, Josephine. Untersuchung von linearen und zirkulären Transkripten des TRAM1- und S100A6-Genlokus im Kontext des Harnblasenkarzinoms. Wiesbaden: Springer Fachmedien Wiesbaden, 2022. http://dx.doi.org/10.1007/978-3-658-40358-4.

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White, Alexander S. Photographer's guide to the canon powershot s100. [Place of publication not identified]: White Knight Press, 2011.

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Brant, Stephen. Distribution of renal S100 proteins in psysiological and pathological models. London: University of East London, 2000.

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McKendry, Amanda Jayne. Comparison of HMB45 monoclonal antibody and S100 poprtein in the immunohistochemical diagnosis of melanoma. [S.l: The Author], 1993.

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Ruiz, Rafael. S100b: Serum Detection, Functions and Clinical Significance. Nova Science Publishers, Incorporated, 2015.

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Cuna. S100 Money & Negotiable Instruments. Kendall Hunt Pub Co, 1994.

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VIDEO LESSONS S100 S135 S150. MCGRAW-HILL, 1995.

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World Cup 1994 (LADYBD/S100). Ladybird Books Ltd, 1994.

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Merklinger, Sandra Lea. Progression and regression of pulmonary vascular disease related to smooth muscle cell apoptosis, S100A4/Mts1 and fibulin-5. 2005.

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Book chapters on the topic "S100A8"

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Sreejit, Gopalkrishna, Sunil Kiran Nooti, Baskaran Athmanathan, and Prabhakara Reddy Nagareddy. "S100A8/A9 in Myocardial Infarction." In Methods in Molecular Biology, 739–54. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9030-6_46.

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Gharibyan, Anna L., Dina Raveh, and Ludmilla A. Morozova-Roche. "S100A8/A9 Amyloidosis in the Ageing Prostate: Relating Ex Vivo and In Vitro Studies." In Methods in Molecular Biology, 387–401. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-551-0_26.

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Donato, Rosario, Guglielmo Sorci, and Ileana Giambanco. "S100A6." In Encyclopedia of Signaling Molecules, 4805–13. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101531.

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Donato, Rosario, Guglielmo Sorci, and Ileana Giambanco. "S100A6." In Encyclopedia of Signaling Molecules, 1–10. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_101531-1.

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Yatime, Laure. "Structural Analysis of S100A8 Complex with Zinc and Calcium: A General Protocol for the Study of S100 Proteins in the Presence of Divalent Cations by X-Ray Crystallography." In Methods in Molecular Biology, 417–35. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9030-6_26.

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Prudovsky, Igor, Thallapuranam Krishnaswamy Suresh Kumar, and Rosario Donato. "S100a13." In Encyclopedia of Signaling Molecules, 4801–4. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101530.

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Prudovsky, Igor, Thallapuranam Krishnaswamy Suresh Kumar, and Rosario Donato. "S100a13." In Encyclopedia of Signaling Molecules, 1–4. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_101530-1.

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Gressner, A. M., and O. A. Gressner. "S100A12-Protein." In Lexikon der Medizinischen Laboratoriumsdiagnostik, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-49054-9_2726-1.

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Gressner, A. M., and O. A. Gressner. "S100A12-Protein." In Springer Reference Medizin, 2097. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_2726.

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House, Reniqua P., Sarah C. Garrett, and Anne R. Bresnick. "Moving Aggressively: S100A4 and Tumor Invasion." In Signaling Pathways and Molecular Mediators in Metastasis, 91–113. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-2558-4_4.

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Conference papers on the topic "S100A8"

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Crowe, L. A. N., M. Akbar, K. Patommel, S. M. Kitson, E. Garcia Melchor, D. S. Gilchrist, G. A. Murrell, I. B. McInnes, and N. L. Millar. "AB0068 Alarmins s100a8 and s100a9 modulate the inflammatory microenvironment in early tendinopathy." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.7019.

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Lee, Eunmi, Maria Ouzounova, Raziye Piranlioglu, Abdeljabar El Andaloussi, Sena Arbag, Gang Zhou, and Hasan Korkaya. "Abstract 2956: Chemical library screen identifies compounds that target S100A8/S100A9 complex and MDSC accumulation." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-2956.

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Ghavami, Saeid, Thomas Vogl, Johannes Roth, Helmut Unruh, and Andrew J. Halayko. "S100A8 And S100A9 Homo-, And Hetero-Dimers Affect Extracellular Matrix In Human Smooth Muscle With Different Down Stream Signalling." 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.a6682.

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Ghavami, S., T. Hynes, T. Vogl, S. Basu, C. Kerkhoff, J. Roth, and AJ Halayko. "A Role for S100A8/A9 in Allergic Airway Inflammation?." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a6326.

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Gemicioglu, Bilun, Ozgur Yasar, and Tulay Akcay. "Significance of serum YKL-40, S100A8, S100A9, calprotectin, periostin and LRG1 levels in patients with newly diagnosed, controlled and uncontrolled asthma." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa2023.

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Liya, LI, Zuo Xiaoxia, Xiao Yizhi, DI Liu, Luo Hui, and Zhu Honglin. "AB0211 NEUTROPHIL-DERIVED EXOSOME S100A8/A9 INHIBITS ANGIOGENESIS IN SYSTEMIC SCLEROSIS." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.6484.

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Popp, D., F. Rühle, W. de Jager, T. Vogl, and J. Roth. "OP0091 S100a8 triggers a novel immune-regulatory mechanism in developing dendritic cells." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.4960.

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Kruisbergen, N., S. van Dalen, M. van den Bosch, A. Blom, and P. van Lent. "SAT0067 Role of nox2-derived reactive oxygen species in s100a8/a9-driven inflammatory osteoarthritis." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.5421.

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Li, Si, Fangying Xu, Lili Wang, Hui Li, and Maode Lai. "Abstract 4723: Improving prognosis or promoting progression? Double sword of S100A8 in colorectal cancer." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-4723.

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Zervides, Kristoffer Alexander, Andreas Jern, Jessica Nystedt, Petra Nilsson, Pia C. Sundgren, Birgitta Gullstrand, Anders A. Bengtsson, and Andreas Jönsen. "P43 Serum S100A8/A9 concentrations are associated with neuropsychiatric involvement and fatigue in SLE." In 12th European Lupus Meeting. Lupus Foundation of America, 2020. http://dx.doi.org/10.1136/lupus-2020-eurolupus.91.

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Reports on the topic "S100A8"

1

Emberley, Ethan D., and Peter Watson. The Role of S100A7/RANBPM Interaction in Human Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 2001. http://dx.doi.org/10.21236/ada396984.

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Emberley, Ethan, and Peter Watson. The Role of S100A7/RANBPM Interaction in Human Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 2002. http://dx.doi.org/10.21236/ada412819.

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Emberley, Ethan D., and Peter Watson. The Role of S100A7/RANBPM Interaction in Human Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 2003. http://dx.doi.org/10.21236/ada418754.

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West, Nathan. Exploring and Exploiting the Protein S100A7 as a New Target for Breast Cancer Therapy. Fort Belvoir, VA: Defense Technical Information Center, January 2010. http://dx.doi.org/10.21236/ada520729.

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Kim, Edward J., and David Helfman. Characterization of Molecular Factors Critical to the S100A4 (A Metastasis-Associated Protein) - Dependent Increase in Motility of Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, April 2004. http://dx.doi.org/10.21236/ada424207.

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State Savings Bank of Tasmania - Hobart (Chief Office) - Depositors Ledgers - Hobart - Accounts - S1 - S1000 -1908-1912. Reserve Bank of Australia, March 2021. http://dx.doi.org/10.47688/rba_archives_2006/20525.

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OVERHANG EFFECT ON WEB CRIPPLING CAPACITY OF COLDFORMED AUSTENITIC STAINLESS STEEL SHS MEMBERS: AN EXPERIMENTAL STUDY. The Hong Kong Institute of Steel Construction, August 2022. http://dx.doi.org/10.18057/icass2020.p.343.

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This paper studies the overhang effects on ultimate bearing capacities of cold-formed austenitic stainless steel square hollow section (SHS) members undergoing web crippling between EndTwo-Flange (ETF) and Interior-Two-Flange (ITF) loading conditions. A total of 16 web crippling tests were conducted with specimens covering various overhang lengths. Tensile coupon tests were performed to obtain the material properties of the test specimens. The web crippling capacities obtained from the tests were compared with the nominal capacities predicted by the SEI/ASCE 8-22 Specification for the design of cold-formed stainless steel structural members. It is shown that the SEI/ASCE 8-22 Specification leads to overly conservative web crippling capacity predictions for the tubular specimens with overhangs. The applicability of the overhang effect enhancement factor codified in the AISI S100- 16 Specification to the studied stainless steel specimens was evaluated. It is revealed that the accuracy and consistency of the web crippling capacity predictions can be enhanced by employing the enhancement factor codified in the AISI S100-16 Specification, yet such a treatment still leads to rather scatter predictions and can lead to unconservative capacity estimations. An extended investigation is currently underway to propose improved design rules for cold-formed stainless steel tubular members with overhangs under ETF loading condition.
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Government Savings Bank of New South Wales - Balmain - Depositors Ledgers - Friendly Society (Loose Leaf System) Cheque Accounts S1-S100 (incl. Continuation) - 1930-1933. Reserve Bank of Australia, March 2021. http://dx.doi.org/10.47688/rba_archives_2006/22603.

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A SURROGATE MODEL TO ESTIMATE THE AXIAL COMPRESSIVE CAPACITY OF COLD-FORMED STEEL OPEN BUILT-UP SECTIONS. The Hong Kong Institute of Steel Construction, August 2022. http://dx.doi.org/10.18057/icass2020.p.316.

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This paper proposed a surrogate model to simplify the process of estimating the axial compressive capacity of cold-formed steel (CFS) open built-up sections composed of lipped channels with different section sizes, thickness, length, and connector spacing. The surrogate model was developed based on the current design methods, i.e., the Effective Width Method (EWM) and Direct Strength Method (DSM), which are codified in the North American Specification AISI S100-16. This new model features two surface regression equations with a boundary inequality criteria, anchored on two important parameters, i.e., modified slenderness ratio, (KL/r)m and minimum thickness-to-width ratio (t/w)min of the built-up sections. The model was validated with 1089 sets of the experimental results data collected from previous research tested on the axial capacity of CFS open built-up sections with the different design configurations. The proposed surrogate model is aimed to simplify the design process among practising engineers for a quick preliminary calculation of the axial compressive capacity of these new CFS open built-up sections.
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