Relevant bibliographies by topics / Notch

Academic literature on the topic 'Notch'

Author: Grafiati
Published: 4 June 2021
Last updated: 6 July 2024

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Journal articles on the topic "Notch"

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Yuan, Xiyu, Xue Hu, Yating Zheng, and Mengli Huang. "Abstract 5095: Investigation of NOTCH mutation and correlation with immunotherapy biomarker in Chinese colorectal cancer patients." Cancer Research 82, no. 12_Supplement (June 15, 2022): 5095. http://dx.doi.org/10.1158/1538-7445.am2022-5095.

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Abstract Background: NOTCH pathway, a highly conserved signaling system, is regulated by short-range cell-cell interaction between NOTCH receptor (NOTCH1-4) and “canonical” ligand, or non-canonically through activation of other pathways. Previous research on the NOTCH gene revealed that NOTCH signaling is associated with tumorigenesis, mutagenesis, and immune tolerance in several tumors, indicating its association with the clinical benefit of immune checkpoint inhibitors (ICIs). However, the NOTCH characteristics, its correlation with immunogenic marker, and the predictive value of immunotherapy in colorectal cancer (CRC) was unknown. Methods: An independent cohort (the MSKCC study cohort) with next-generation sequencing (NGS) data from 109 patients with CRC of pan-cancer, were used to analyze the prognostic effect of NOTCH1-4 on immunotherapy. Tumor tissue samples from Chinese head and neck cancer were analyzed using NGS (panel on 381/733-gene). TMB was defined as the total number of somatic non-synonymous mutations in coding region. MSI was evaluated by NGS of 500 known MSI loci. PD-L1 expression was evaluated using immunohistochemistry (Dako 22C3). Result: In the MSKCC cohort, there were 49 (45.0%) patients harbored NOTCH mutation(NOTCHmut), including 16 (14.7%) patients of NOTCH1, 7 (6.4%) patients of NOTCH2, 16 (14.7%) patients of NOTCH3, and 10 (10.9%) patients of NOTCH4. NOTCH1 mutation (median, 65.4 Muts/Mb) was associated with higher TMB (P<0.001) than NOTCH1 wild-type (NOTCHwt) (median, 6.8 Muts/Mb), same as NOTCH2 (median, 61.4 Muts/Mb vs 7.8 Muts/Mb; P<0.001), NOTCH3 (median, 64.9 Muts/Mb vs 6.8 Muts/Mb; P<0.001), and NOTCH4 (median, 76.7 Muts/Mb vs 7.8 Muts/Mb; P<0.001). In terms of prognostic effect, there was significant difference on overall survival (OS) (HR = 0.17, P=0.008) between NOTCH3mut (median, 11.5 months) and NOTCH3wt (median, 8 months), but there was no difference in others of NOTCH. In Chinese patients, genetic mutation of 1166 CRC patients were analyzed using NGS, of which 157 (13.5%) harbored NOTCH mutation, including NOTCH1 (123, 10.5%), NOTCH2 (221, 18.9%), NOTCH3 (135, 11.6%), and NOTCH4 (55, 4.7%). NOTCH3mut (median, 47,5 Muts/Mb) was associated with higher TMB (P<0.001) than NOTCH3wt (median, 7.3 Muts/Mb), which was significant difference, same as the other three. For the TMB, there was also significant difference in MSI between NOTCH1-4mut and NOTCH1-4wt (all of the four P<0.001). There was significant difference in PD-L1 expression between NOTCHwt with NOTCH1mut (P =0.005) and NOTCH2mut (P<0.001), but not with NOTCH3mut and NOTCH4mut. Conclusions: The results showed that the NOTCH genes had a high correlation with TMB and MSI in CRC, and the NOTCH3 might a potential biomarker for immune checkpoint therapy. Citation Format: Xiyu Yuan, Xue Hu, Yating Zheng, Mengli Huang. Investigation of NOTCH mutation and correlation with immunotherapy biomarker in Chinese colorectal cancer patients [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 5095.
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Rojas, Katerin Ingrid, M. Rocio Martín, Federico Rojo, Angelo Gámez-Pozo, Francisco J. De Castro, Elena Filipovich, Jaime Ceballos, M. Rosario Hernández, and Jose Ales-Martinez. "Transcriptomic mapping on Notch signaling in A luminal phenotype breast cancer." Journal of Clinical Oncology 39, no. 15_suppl (May 20, 2021): e12539-e12539. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.e12539.

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e12539 Background: The Notch signaling pathway plays an important role in cell-differentiation, survival, proliferation, stem-cell renewal, and in determining cell fate during development and morphogenesis. The dysregulation of the Notch pathways contributes to carcinogenesis, cancer stem cell renewal, angiogenesis, and chemo-resistance. Elevated levels of Notch receptors and ligands have been associated with cancer-progression and poor survival. A less explored function of Notch pathways in cancer is their role in leukocyte homing and activation. Understanding their role and relationship with immune infiltrates is an area of interest in cancer research. Methods: The expression of four different Notch genes (Notch1, Notch2, Notch3 and Notch4) was explored in relation with A luminal breast cancer patient outcome using transcriptomic data (Affymetrix dataset, exploratory cohort) and the METABRIC study (validation cohort). The TIMER online tool was used to explore the association of the identified notch and immune infiltration, and the TCGA and METABRIC studies to analyze the correlation between notch1 - 4 expression and genomic signatures of immune activation. Results: We identified 2 individual genes called Notch1 and Notch2, which predict favorable prognosis in luminal A breast cancer. Their expression positively correlated with the presence of immune infiltrates within the tumor (dendritic cells, CD4+ T cells, neutrophils, CD8+ T cells and B cells), with markers of T cell activation and antigen presentation, and with gene signatures of immune surveillance (cytotoxic T lymphocyte activation and IFN gamma signature). By contrast Notch3 and Notch4 which predicted for detrimental outcome were not associated with any of these parameters. Conclusions: Our analysis identifies a Notch signature composed of 2 genes with potential to recognize immune infiltrated and activated A luminal phenotype breast cancers with favorable prognosis.
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Pross, Seth, John M. Millholland, Hong Sai, Andrew P. Weng, Jon C. Aster, Warren S. Pear, and Ivan Maillard. "Efficient Inhibition of Notch3 and Notch4 Family Members In Vivo by a Dominant Negative Mutant of Mastermind." Blood 104, no. 11 (November 16, 2004): 1617. http://dx.doi.org/10.1182/blood.v104.11.1617.1617.

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Abstract The four mammalian Notch receptors play multiple roles in the hematolymphoid system. Notch1 is critical for the generation of hematopoietic stem cells (HSCs) during embryonic development and for commitment to the T cell lineage, while Notch2 regulates marginal zone B cell development. In addition, important roles for Notch are starting to be identified in peripheral T cells, in which all four Notch family members are upregulated upon T cell activation. Canonical Notch signaling involves proteolytic cleavage of Notch receptors and translocation of intracellular Notch (ICN) to the nucleus where it interacts with the transcription factor CSL/RBP-J and recruits Mastermind-like proteins (MAMLs) for transcriptional activation. By inhibiting Notch1 and Notch2-dependent developmental decisions with a dominant negative mutant of MAML1 (DNMAML1), we have previously demonstrated that MAMLs critically regulate Notch signaling in vivo (Maillard et al., Blood 2004). However, it is unclear if Notch3 and Notch4 are equally dependent on the activity of MAMLs in vivo, and if DNMAML1 can thus be used as a true pan-Notch inhibitor. To address this question, we used a modified fetal thymic organ culture (FTOC) system and Notch-mediated T lineage commitment as a readout for Notch function. Fetal liver cells (FLCs) were transduced with retroviruses expressing ICN1, ICN3 or ICN4 and a retrovirus expressing DNMAML1. Irradiated fetal thymic lobes were reconstituted with transduced FLCs and cultured in the presence of gamma secretase inhibitors to inhibit the activation of endogenous Notch receptors. In this manner the effect of a specific ICN could be evaluated in the absence of endogenous Notch signals. Gamma secretase inhibitors resulted in a profound block in T cell development and in the generation of intrathymic B cells, consistent with Notch1 inhibition. ICN1, ICN3 and ICN4 were all able to rescue commitment to the T cell lineage and to block B cell development, indicating that each ICN can deliver appropriate signals for T lineage commitment in the absence of endogenous Notch1 signaling. In cells doubly transduced with specific ICNs and DNMAML1, the rescuing effect of ICN1, ICN3 or ICN4 was blocked, leading to the generation of B cells. In this competitive situation, DNMAML1 only partially inhibited ICN1, the most potent of all four Notch family members, but it was able to completely inhibit ICN3 and ICN4. We conclude that DNMAML1 can efficiently inhibit Notch3 and Notch4 in vivo. The results validate the use of DNMAML1 as a bona fide pan-Notch inhibitor in multiple settings, including studying the role of Notch in HSCs and peripheral T cells.
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Shah, Heer, Mittal Mistry, Nupur Patel, and Hemangini Vora. "Clinical significance of Notch receptors in triple negative breast cancer." Breast Disease 42, no. 1 (March 21, 2023): 85–100. http://dx.doi.org/10.3233/bd-220041.

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BACKGROUND: The Notch signaling pathway is an evolutionary conserved cell signaling pathway that plays an indispensable role in essential developmental processes. Aberrant activation of Notch pathway is known to initiate wide array of diseases and cancers. OBJECTIVE: To evaluate the clinical significance of Notch receptors in Triple Negative Breast Cancer. METHODS: We evaluated the association between Notch receptors and clinicopathological parameters including disease-free survival and overall survival of one hundred TNBC patients by immunohistochemistry. RESULTS: Positive expression of nuclear Notch1 receptor (18%) was found be significantly correlated with positive lymph node (p = 0.009), high BR score (p = 0.02) and necrosis (p = 0.004) while cytoplasmic expression of Notch2 receptor (26%) was significantly correlated with metastasis (p = 0.05), worse DFS (p = 0.05) and poor OS (p = 0.02) in TNBC patients. Membrane (18%) and cytonuclear (3%) Notch3 expression were significantly associated with poorly differentiated tumors (p = 0.007), high BR score (p = 0.002) and necrosis (p = 0.03) respectively. However, cytoplasmic Notch3 and Notch4 expression were negatively correlated with poor prognostic factors. CONCLUSIONS: Our data indicated that Notch receptors play a key role in promoting TNBC and mainly, Notch2 may contribute to poor prognosis of the disease. Hence, it is implicated that Notch2 may serve as a potential biomarker and therapeutic target for TNBC.
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Hubmann, Rainer, Martin Hilgarth, Susanne Schnabl, Elena Ponath, Dita Demirtas, Marlies Reiter, Ulrich Jäger, and Medhat Shehata. "Differential Expression and Functions of NOTCH Family Members and Involvement of NR4A1 in the Regulation of Apoptosis in CLL." Blood 120, no. 21 (November 16, 2012): 3919. http://dx.doi.org/10.1182/blood.v120.21.3919.3919.

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Abstract Abstract 3919 Chronic lymphocytic leukemia (CLL) cells express constitutively activated NOTCH2 in a protein kinase C (PKC) dependent manner linking NOTCH2 to the activated state of the leukemic cells. The transcriptional activity of NOTCH2 is associated with the expression of CD23 and enhanced CLL cell viability. However, the regulation and possible functions of the individual NOTCH family members (NOTCH1–4) in CLL cells remain to be clarified. We took advantage of targeting nuclear NOTCH2 using the recently identified NOTCH2 transactivation inhibitor gliotoxin (WO 2006/135949). We also analysed the regulation and possible function of NOTCH1–4 in PKC stimulated CLL cells using a PMA model (Hubmann et al., BJH 2010) and a microenvironment model where CLL lymphocytes were co-cultured with primary bone marrow stromal cells (BMSC) (Shehata et al., BLOOD 2010). Electrophoretic mobility shift assays (EMSA) demonstrated that gliotoxin inhibited DNA-bound NOTCH2 complexes in PMA stimulated CLL cells in parallel to increasing the rate of apoptosis (mean±SD: 67±31% in gliotoxin treated cells versus 13±14% in the untreated controls, n=21). This was associated with downregulation of CD23A mRNA expression and CD23 surface expression (mean±SD: 42±32% versus 83±17%, n=21) as assessed by RT-PCR and FACS analysis. Exceptionally, one CLL case with a recently described NOTCH1 gain of function mutation appeared to be less sensitive to gliotoxin and had a persistent high expression of CD23. We next tested whether NOTCH2 inhibition by gliotoxin is a selective process or indirectly mediated by effects on proteasome regulated apoptosis. Proteasome assays showed that gliotoxin had a minimal or no effect on the chymotrypsin like activity of the proteasome in CLL cells. In addition, the activity of the proteasome regulated transcription factor NFκB and the expression of its target genes like BCL2 and MCL1 were also not influenced by gliotoxin. These data point to the selectivity of targeting NOTCH2 signaling by gliotoxin rather than indirectly through the regulation of proteasome activity. Short term (4 hours) exposure of CLL cells revealed that NOTCH1 was equally transcribed in unstimulated and in PMA activated CLL cells. NOTCH2 was upregulated in PMA activated CLL lymphocytes whereas NOTCH4 was only weakly detectable in unstimulated CLL cells. Gliotoxin treatment resulted in the downregulation of NOTCH1, NOTCH2 and NOTCH4 mRNA expression. Interestingly, the inhibition of NOTCH2 activity by gliotoxin was associated with the concomitant induction of NOTCH3 signaling especially in the presence of PMA. This was indicated by the induced mRNA expression of NOTCH3 and its preferred target gene HEY1. Moreover, the induced transcription of HEY1 correlated with the upregulation of NR4A1, a key regulator of apoptosis in activated lymphocytes. These data may thus point to a pro-apoptotic role for NOTCH3/HEY1/NR4A1 signaling in CLL cells. The data also suggest that gliotoxin induced apoptosis is associated with differential regulation of the anti-apoptotic and pro-apoptotic arms of NOTCH signalling in CLL cells. RT-PCR revealed that NOTCH1 and NOTCH2 are the main NOTCH family members which are expressed in CLL cells under co-culture conditions with BMSC and in freshly isolated CLL cells. Exposure to gliotoxin in co-culture selectively induced apoptosis in CLL cells and led to downregulation of NOTCH1 and NOTCH2 together with upregulation of NOTCH3 mRNA expression. In summary, the data suggest that nuclear NOTCH2 activity might protect activated CLL cells from apoptosis by modulating the expression of NR4A1. The induced expression of NOTCH3 and its target gene HEY1 by gliotoxin reveals the complex role of different NOTCH family members in the regulation of apoptosis in CLL cells. Therefore, the individual NOTCH receptors may have opposite effects on CLL cell viability which should be considered in therapeutic approaches aimed to target NOTCH signaling in CLL. Disclosures: No relevant conflicts of interest to declare.
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Ito, T., N. Udaka, T. Yazawa, K. Okudela, H. Hayashi, T. Sudo, F. Guillemot, R. Kageyama, and H. Kitamura. "Basic helix-loop-helix transcription factors regulate the neuroendocrine differentiation of fetal mouse pulmonary epithelium." Development 127, no. 18 (September 15, 2000): 3913–21. http://dx.doi.org/10.1242/dev.127.18.3913.

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To clarify the mechanisms that regulate neuroendocrine differentiation of fetal lung epithelia, we have studied the expression of the mammalian homologs of achaete-scute complex (Mash1) (Ascl1 - Mouse Genome Informatics); hairy and enhancer of split1 (Hes1); and the expression of Notch/Notch-ligand system in the fetal and adult mouse lungs, and in the lungs of Mash1- or Hes1-deficient mice. Immunohistochemical studies revealed that Mash1-positive cells seemed to belong to pulmonary neuroendocrine cells (PNEC) and their precursors. In mice deficient for Mash1, no PNEC were detected. Hes1-positive cells belong to non-neuroendocrine cells. In the mice deficient in Hes1, in which Mash1 mRNA was upregulated, PNEC appeared precociously, and the number of PNEC was markedly increased. NeuroD (Neurod1 - Mouse Genome Informatics) expression in the lung was detected in the adult, and was enhanced in the fetal lungs of Hes1-null mice. Expression of Notch1, Notch2, Notch3 and Notch4 mRNAs in the mouse lung increased with age, and Notch1 mRNA was expressed in a Hes1-dependent manner. Notch1, Notch2 and Notch3 were immunohistochemically detected in non-neuroendocrine cells. Moreover, analyses of the lungs from the gene-targeted mice suggested that expression of Delta-like 1 (Dll1 - Mouse Genome Informatics) mRNA depends on Mash1. Thus, the neuroendocrine differentiation depends on basic helix-loop-helix factors, and Notch/Notch-ligand pathways may be involved in determining the cell differentiation fate in fetal airway epithelium.
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Mizuta, Ikuko, Yumiko Nakao-Azuma, Hideki Yoshida, Masamitsu Yamaguchi, and Toshiki Mizuno. "Progress to Clarify How NOTCH3 Mutations Lead to CADASIL, a Hereditary Cerebral Small Vessel Disease." Biomolecules 14, no. 1 (January 18, 2024): 127. http://dx.doi.org/10.3390/biom14010127.

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Notch signaling is conserved in C. elegans, Drosophila, and mammals. Among the four NOTCH genes in humans, NOTCH1, NOTCH2, and NOTCH3 are known to cause monogenic hereditary disorders. Most NOTCH-related disorders are congenital and caused by a gain or loss of Notch signaling activity. In contrast, cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) caused by NOTCH3 is adult-onset and considered to be caused by accumulation of the mutant NOTCH3 extracellular domain (N3ECD) and, possibly, by an impairment in Notch signaling. Pathophysiological processes following mutant N3ECD accumulation have been intensively investigated; however, the process leading to N3ECD accumulation and its association with canonical NOTCH3 signaling remain unknown. We reviewed the progress in clarifying the pathophysiological process involving mutant NOTCH3.
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Zanotti, Stefano, and Ernesto Canalis. "Notch Suppresses Nuclear Factor of Activated T Cells (Nfat) Transactivation and Nfatc1 Expression in Chondrocytes." Endocrinology 154, no. 2 (December 21, 2012): 762–72. http://dx.doi.org/10.1210/en.2012-1925.

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Notch1 to Notch4 transmembrane receptors determine cell fate, and release of the Notch intracellular domain (NICD) in the cytoplasm induces gene expression. Notch regulates endochondral ossification, but it is not clear whether Notch interacts with signals controlling chondrocyte differentiation. Nuclear factor of activated T cells (Nfatc) transcription factors regulate chondrogenesis, and we asked whether Notch modifies Nfat signaling in chondrocytes. Notch was induced in teratocarcinoma ATDC5 chondrogenic cells infected with a retroviral vector, where the cytomegalovirus (CMV) promoter directs NICD expression. NICD suppressed chondrocyte differentiation and inhibited Nfat transactivation and Nfatc1 expression. Notch was activated in chondrocytes from RosaNotch mice, where the Rosa26 promoter is upstream of a loxP-flanked STOP cassette and NICD. To excise the STOP cassette and express NICD, RosaNotch chondrocytes were infected with an adenoviral vector where the CMV promoter directs Cre expression (Ad-CMV-Cre). Notch1 and Notch2 mediate the effects of Notch in skeletal cells, and to inhibit Notch signaling, chondrocytes from mice homozygous for Notch1 and Notch2 alleles targeted with loxP sites were infected with Ad-CMV-Cre. NICD suppressed chondrogenic nodules formation and expression of selected chondrocyte gene markers, induced Col10a1 and Mmp13, and suppressed Nfat transactivation and Nfatc1 expression, whereas inactivation of Notch1 and Notch2 did not affect chondrocyte differentiation. To investigate Nfatc1 function in chondrocytes, Nfatc1 was induced in RosaNotch chondrocytes overexpressing NICD or controls. Nfatc1 suppressed chondrocyte differentiation and opposed Col10a1 induction by Notch. In conclusion, Notch suppresses Nfat transactivation in chondrocytes and Notch and Nfatc1 regulate chondrocyte differentiation.
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Takam Kamga, Paul, Giada Dal Collo, Federica Resci, Riccardo Bazzoni, Angela Mercuri, Francesca Maria Quaglia, Ilaria Tanasi, et al. "Notch Signaling Molecules as Prognostic Biomarkers for Acute Myeloid Leukemia." Cancers 11, no. 12 (December 6, 2019): 1958. http://dx.doi.org/10.3390/cancers11121958.

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The role of Notch signaling in acute myeloid leukemia (AML) is still under investigation. We have previously shown that high levels of Notch receptors and ligands could interfere with drug response. In this study, the protein expression of 79 AML blast samples collected from newly diagnosed patients was examined through flow cytometry. Gamma-secretase inhibitors were used in AML mouse xenograft models to evaluate the contribution of Notch pharmacological inhibition to mouse survival. We used univariate analysis for testing the correlation and/or association between protein expression and well-known prognostics markers. All the four receptors (Notch1–4) and some ligands (Jagged2, DLL-3) were highly expressed in less mature subtypes (M0–M1). Notch3, Notch4, and Jagged2 were overexpressed in an adverse cytogenetic risk group compared to good cytogenetic risk patients. Chi-square analysis revealed a positive association between the complete remission rate after induction therapy and weak expression of Notch2 and Notch3. We also found an association between low levels of Notch4 and Jagged2 and three-year remission following allogeneic stem cell transplantation (HSCT). Accordingly, Kaplan–Meier analysis showed improved OS for patients lacking significant expression of Notch4, Jagged2, and DLL3. In vivo experiments in an AML mouse model highlighted both improved survival and a significant reduction of leukemia cell burden in the bone marrow of mice treated with the combination of Notch pan-inhibitors (GSIs) plus chemotherapy (Ara-C). Our results suggest that Notch can be useful as a prognostic marker and therapeutic target in AML.
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Mao, Yongzhong, Shaotao Tang, Li Yang, and Kang Li. "Inhibition of the Notch Signaling Pathway Reduces the Differentiation of Hepatic Progenitor Cells into Cholangiocytes in Biliary Atresia." Cellular Physiology and Biochemistry 49, no. 3 (2018): 1115–23. http://dx.doi.org/10.1159/000493290.

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Background/Aims: Viral infections, especially with rotavirus, are often considered an initiator of the pathogenesis of biliary atresia (BA). However, the mechanism by which rotavirus induces BA is still unclear. Methods: A BA mouse model was induced in newborn mice by i.p. inoculation with rhesus rotavirus within 6 h of birth. The expression of Notch pathway-associated molecules (JAG1, JAG2, Notch1, Notch2, Notch3, Notch4, DII1, DII3, and DII4) was measured by quantitative PCR and western blot analysis. Bile duct obstruction was detected by hematoxylin and eosin staining and CK-19 immunohistochemical staining. DAPT was used to inhibit the Notch pathway in vivo and in vitro. Results: In the livers of patients with BA and rotavirus-induced BA mice, the expression of JAG1 and Notch2 was significantly increased. Inhibition of the Notch pathway by DAPT in vivo ameliorated bile duct obstruction and delayed BA-induced mortality. The serum levels of inflammation cytokines (TNF-α, IL-2, IL-8, and IL-18) were reduced by inhibiting the Notch pathway. The expression of CK19, Sox9, and EpCAM was significantly increased in BA liver, while DAPT treatment decreased the expression of CK19, Sox9, and EpCAM. Conclusion: Notch activation is involved in the pathogenesis of BA by promoting the differentiation of hepatic progenitor cells into cholangiocytes.
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Dissertations / Theses on the topic "Notch"

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Maxe, Liza, Kiana Entezarjo, and Douglas Karegren. "Swap Notch." Thesis, Högskolan i Halmstad, Akademin för ekonomi, teknik och naturvetenskap, 2019. http://urn.kb.se/resolve?urn=urn:nbn:se:hh:diva-40654.

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Quillard, Thibaut. "Importance de la voie Notch dans la dysfonction endothéliale en transplantation : régulation et fonctions des récepteurs Notch2 et Notch4." Nantes, 2008. https://archive.bu.univ-nantes.fr/pollux/show/show?id=6bdde4e3-76bb-4a01-9661-3ee28931b379.

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Notch joue un rôle important dans la survie, la prolifération et la transdifférenciation des cellules endothéliales (CE). Ces mécanismes sont tout particulièrement importants dans l'artériosclérose du greffon (AG). L'objectif de ce travail est de définir la régulation et le rôle de Notch dans la dysfonction des CE associée à l'AG. Nous avons tout d'abord étudié la régulation des molécules Notch (récepteurs, ligands et effecteurs) au cours de l'activation des CE. Ainsi, le TNFα oriente le profil Notch vers une forte diminution de Notch4 et une augmentation de Notch2, respectivement par les voies NF��B et PI3K. Cet effet est toutefois associé à une baisse globale de l’activité CBF1. La baisse du récepteur endothélial Notch4 est, de plus, associée à l’AG dans un modèle d’allogreffe cardiaque chez le rat où le TNFα, TGFβ et IL10 sont fortement exprimés. Le blocage de Notch4 et de hes1 par ARN interférence favorise l’expression de VCAM-1, induit l’apoptose et altère la cicatrisation endothéliale. L’expression constitutive de Notch2ICD grâce à un adénovirus recombinant induit l’apoptose des CE par une forte répression de gènes anti- (survivine, April) et pro-apoptotiques (Bim, DAPK2, HRK, DR5, CD40). La fonction pro-apoptotique de N2ICD dépend essentiellement de l’inhibition de la survivine. L'extinction de Notch2 augmente l'expression de la survivine et protège les CE de l’apoptose. L'ensemble de ces travaux montre une interaction entre les voies du TNF et Notch au cours de la dysfonction endothéliale, propose un rôle pour Notch4 dans la prévention de la dysfonction endothéliale dans l'AG et démontre l'importance de Notch2 dans la survie des CE par la régulation de la survivine
Notch plays major roles in endothelial cells (EC) survival, proliferation and transdifferentiation. These events are particularly implicated in transplant arteriosclerosis (TA). This work aims to define Notch molecules regulation and its functional relevance in graft EC. We first studied Notch family members (receptors, ligands and effectors) regulation during EC activation by cytokines. We show that TNFα induced a switch in Notch expression pattern by a strong down-regulation of Notch4 and an increase in Notch2, respectively dependent on NFkB and PI3K pathways. This effect is associated with a global decrease in CBF1 activity and an opposite regulation of hes1 and hey1. Decrease in EC-restricted Notch4 expression is also associated with TA in a rat cardiac allograft model where TNFα, TGFβ and IL10 are strongly expressed. Inhibition of Notch4 and hes1 by siRNA enhances VCAM1 expression, induces apoptosis and impairs endothelial injury repair, suggesting that Notch4 expression is required to maintain EC survival and quiescence. To study the role of Notch2 in EC, we constructed a recombinant adenovirus for Notch2ICD (N2ICD). Constitutive expression of N2ICD leads to EC apoptosis associated with a drastic repression of pro- (survivin, april) and anti-apoptotic genes (bim, DAPK2, HRK, DR5, CD40). Effect of N2ICD is mainly dependent on survivin inhibition. Accordingly, Notch2 knock-down increases survivin expression and protects EC from anoïkis. Altogether, our results reveal crosstalks between TNF and Notch signaling during endothelial dysfunction, propose a role for Notch4 in preventing TA-related EC dysfunction and for Notch2 role in EC survival through survivin regulation
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Huang, Yuchen. "Adaptive Notch Filter." PDXScholar, 1994. https://pdxscholar.library.pdx.edu/open_access_etds/4802.

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The thesis presents a new adaptive notch filter (ANF) algorithm that is more accurate and efficient and has a faster convergent rate than previous ANF algorithms. In 1985, Nehorai designed an infinite impulse response (UR) ANF algorithm that has many advantages over previous ANF algorithms. It requires a minimal number of parameters with constrained poles and zeros. It has higher stability and sharper notches than any ANF algorithm until now. Because of the special filter structure and the recursive prediction error (RPE) method, however, the algorithm is very sensitive to the initial estimate of the filter coefficient and its covariance. Furthermore, convergence to the true filter coefficient is not guaranteed since the error-performance surface of the filter has its global minimum lying on a fairly flat region. We propose a new ANF algorithm that overcomes the convergence problem. By choosing a smaller notch bandwidth control parameter that makes the error-performance surface less flat, we can more easily detect a global minimum. We also propose a new convergence criterion to be used with the algorithm and a self-adjustment feature to reset the initial estimate of the filter coefficient and its covariance. This results in guaranteed convergence with more accurate results and more efficient computations than previous ANF algorithms.
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O'Neill, Christine F. "Notch Regulation of Human Breat Cancer Progression: Contrasting Roles for Notch Signaling." Fogler Library, University of Maine, 2007. http://www.library.umaine.edu/theses/pdf/O'NeillCF2007.pdf.

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Poudel, Rajeeb. "Single Notch Versus Multi Notch Credit Rating Changes and the Business Cycle." Thesis, University of North Texas, 2015. https://digital.library.unt.edu/ark:/67531/metadc848118/.

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Issuers’ credit ratings change by one or more notches when credit rating agencies provide new ratings. Unique to the literature, I study the influences affecting multi notch versus single notch rating upgrades and downgrades. For Standard & Poors data, I show that rating changes with multiple notches provide more information to the market than single notch rating changes. Consistent with prior literature on the business cycle, I show that investors value good news rating changes (upgrades) more in bad times (recession) and that investors value bad news rating changes (downgrades) more in good times (expansion). I model and test probit models using variables capturing the characteristics of the previous issuer’s credit rating, liquidity, solvency, profitability, and growth opportunity to determine the classification of single notch versus multi notch rating changes. The determinants of multi notch versus single notch rating changes for upgrades and downgrades differ. Business cycle influences are evident. Firms that have multi notch rating upgrades and downgrades have significantly different probit variables vis-à-vis firms that have single notch rating upgrades and downgrades. The important characteristics for determining multiple notch upgrades are a firm’s prior rating change, prior rating, cash flow, total assets and market value. The important characteristics for determining multiple notch downgrades are a firm’s prior rating change, prior rating, current ratio, interest coverage, total debt, operating margin, market to book ratio, capital expenditure, total assets, market value, and market beta. The variables that differ for multi notch upgrades in recessions are cash flow, net income, operating margin, market to book ratio, total assets, and retained earnings. The variables that differ for multi notch downgrades in expansions are a firm’s prior rating change, current ratio, interest coverage ratio, debt ratio, total debt, capital expenditure and market beta. The power of the explanatory tests improves when the stage of the business cycle is considered. Results are robust to consideration of rating changes across rating categories, changes from probit to logit, alternative specifications of accounting variables, lags and leads of recessions and expansions timing, Fama and French industry adjustments, and winsorization levels of variables.
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Serafin, Valentina. "Notch3 signalling promotes tumour growth in colorectal cancer: implication for Notch target therapy." Doctoral thesis, Università degli studi di Padova, 2012. http://hdl.handle.net/11577/3422188.

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It is well known that aberrant activation of the Notch pathway plays a critical role in the pathogenesis of T cell acute lymphoblastic leukaemia (T-ALL) and of certain solid tumors including lung, breast and ovarian cancer. In particular, increased Notch1 activity has been observed in intestinal adenoma, partially accomplished by β-catenin-mediated up-regulation of the Notch ligand Jagged-1. Whether further mechanisms of Notch activation exist and other Notch receptors might be involved in colorectal cancer (CRC) has not been investigated so far. In this study we investigated the possible involvement of Notch3 signaling in CRC, and the possible therapeutic implications. Intrigued by the observation that Notch3 mRNA and protein are over-expressed in a subset (20%) of human CRC, we sought to investigate how Notch3 modulates oncogenic features of CRC cells. By exploiting xenografts of CRC cells with different tumorigenic properties in mice, we found that the aggressive phenotype was associated with altered expression of components of the Notch pathway, including augmented expression of Delta-like 4 (DLL4) and Jagged-1 ligands and increased levels of the Notch3 transcript and intracellular domain (ICD). Stimulation with immobilized recombinant DLL4 dramatically increased Notch3 expression and Notch signaling. Moreover, forced expression of an active form of Notch3 mirrored effects of DLL4 stimulation and increased tumor formation. Conversely, blocking Notch3 signaling resulted in perturbation of the cell cycle followed by reduction of cell proliferation and inhibition of tumor growth. Moreover, we observed that these CRC cells have also different metastatic potential in terms of number and dimension when injected intravenously in mice. Lung metastases formed by CRC cells expressed Notch3, but the number or size was not significantly reduced by anti-Notch2/3 treatment. Overall, these findings indicate that Notch3 receptor can modulate the tumorigenic properties of CRC cells, and that DLL4 contributes to sustain Notch activity in DLL4-expressing tumors. Further studies are necessary to clarify the role of Notch3 in metastasis and design effective target therapies.
E’ ormai noto da alcuni anni che un’aberrante attivazione della via di segnalazione di Notch gioca un ruolo critico nella patogenesi della leucemia linfoblastica acuta a cellule T (T-ALL) e di alcune neoplasie solide come il cancro del polmone, della mammella e dell’ovaio. Inoltre, una marcata attivazione del recettore Notch1 è stata osservata negli adenomi intestinali ed è correlata all’aumentata espressione del ligando Jagged-1 indotta dall’attivazione del pathway Wnt-APC-β-catenina. E’ stato inoltre dimostrato che questa pathway, insieme a quella di Notch, interviene nella regolazione della proliferazione e del differenziamento delle cellule epiteliali della mucosa intestinale normale. Attualmente, non si sa ancora se altri meccanismi di attivazione della pathway di Notch, oltre a quello ligando-dipendente, siano operativi nel CRC e nemmeno se possano essere coinvolti altri recettori della stessa famiglia. In questo studio, abbiamo cercato di chiarire il possibile coinvolgimento di Notch3 nel CRC. Basandoci sull’osservazione che Notch3 risulta essere frequentemente overespresso sia a livello di mRNA che di proteina nei campioni umani di CRC, abbiamo cercato di chiarire come il recettore Notch3 potesse modulare le proprietà tumorigeniche delle cellule di CRC. A tale scopo, si sono rivelati particolarmente utili alcuni xenotrapianti di cellule umane di CRC che presentano una diversa aggressività in topi NOD/SCID. Infatti, utilizzando i tumori sperimentali, abbiamo potuto dimostrare che l’espressione dei diversi componenti del pathway di Notch risulta essere significativamente elevata nella variante aggressiva rispetto a quella dormiente. In particolare si è osservata un’ aumentata espressione dei ligandi DLL4 e Jagged-1 ed un incremento dei livelli del trascritto di Notch3 e della forma attiva del recettore nei tumori che crescono più rapidamente. Una simile up-regolazione di Notch3 con un’aumentata attivazione della via di segnalazione si è osservata in seguito a stimolazione delle cellule di CRC in vitro con il ligando DLL4 ricombinante. Analogamente, anche l’overespressione di una forma attiva del recettore Notch3 in queste stesse cellule conferisce loro una maggiore capacità proliferativa e favorisce la formazione di tumori in vivo. Al contrario, si è visto che l’inattivazione del pathway mediante silenziamento genico di Notch3 nelle cellule aggressive di CRC, determina significative alterazioni del ciclo cellulare con conseguente riduzione nella proliferazione in vitro e un ritardo nella crescita dei tumori in vivo. Complessivamente, questi risultati dimostrano che il recettore Notch3 può modulare le proprietà tumorigeniche delle cellule di CRC, in particolare contribuendo a mantenere elevata l’attivazione della via di Notch nei tumori esprimenti nel loro microambiente tumorale alti livelli di DLL4. Inoltre, l’inoculo della variante più aggressiva rispetto a quella dormiente per via endovenosa in topi NOD/SCID ha mostrato che le cellule di CRC non hanno solo una diversa capacità tumorigenica, ma anche una differente capacità metastatica a livello polmonare, sia in termine di numero che di dimensioni delle metastasi osservate. Basandoci sui risultati fin qui ottenuti, e su uno studio recentemente pubblicato in cui è stato dimostrato come il pathway di Notch sembra essere coinvolto anche nel processo di metastatizzazione, abbiamo condotto un primo esperimento pilota che prevedeva, in topi portatori di metastasi polmonari, il blocco dei recettori Notch3 e Notch2 mediante l’impiego di un anticorpo neutralizzante. Sfortunatamente i risultati ottenuti non hanno fino ad ora mostrato una riduzione significativa nel numero e nelle dimensioni delle metastasi analizzate: l’analisi dei livelli di alterazione di Notch dopo il trattamento è in corso. A conclusione dello studio le nostre osservazioni rappresentano un punto di partenza per un futuro sviluppo di terapie che abbiano Notch3 come bersaglio per il trattamento di un sottogruppo di casi di CRC.
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7

Rangarao, Kaluri Venkata. "Adaptive digital notch filtering." Thesis, Monterey, California. Naval Postgraduate School, 1991. http://hdl.handle.net/10945/26345.

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Singh, Nita. "The expression of the Notch receptors, Notch ligands, and the Fringe genes in hematopoiesis." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp04/mq29262.pdf.

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Ferreira, António Carlos Ribeiro. "Notch signaling pathway in gastric carcinogenesis: E-cadherin inactivation on Noth-dependent cell survival." Doctoral thesis, Faculdade de Medicina da Universidade do Porto, 2010. http://hdl.handle.net/10216/55364.

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Ferreira, António Carlos Ribeiro. "Notch signaling pathway in gastric carcinogenesis: E-cadherin inactivation on Noth-dependent cell survival." Tese, Faculdade de Medicina da Universidade do Porto, 2010. http://hdl.handle.net/10216/55364.

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Books on the topic "Notch"

1

Simpson, Pat. The notch receptors. Austin: R.G. Landes Co., 1994.

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Bellen, Hugo J., and Shinya Yamamoto, eds. Notch Signaling. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1139-4.

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Yasutomo, Koji, ed. Notch Signaling. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-4971-2.

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Koenig, Joseph. Smugglers notch. Bath, England: Chivers Press, 1991.

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Pinkham's Notch. Porthsmouth, N.H: P.E. Randall Publisher, 1998.

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Koenig, Joseph. Smuggler's notch. New York: Viking, 1989.

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Notch signaling: Methods and protocols. New York: Humana Press, 2014.

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Jia, Dongyu, ed. Notch Signaling Research. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2201-8.

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Notch ear's sacrifice. Evergreen, CO: Todd Lederman, 2009.

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One last notch. London: Robert Hale, 2005.

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Book chapters on the topic "Notch"

1

Park, Gibeom, and Woong-Yang Park. "Notch (Notch1, Notch2, Notch3, Notch4)." In Encyclopedia of Signaling Molecules, 3554–62. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_509.

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Horstkorte, Rüdiger, Bettina Büttner, Kaya Bork, Navdeep Sahota, Sarah Sabir, Laura O’Regan, Joelle Blot, et al. "Notch (Notch1, Notch2, Notch3, Notch4)." In Encyclopedia of Signaling Molecules, 1254–61. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_509.

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Weik, Martin H. "notch." In Computer Science and Communications Dictionary, 1117. Boston, MA: Springer US, 2000. http://dx.doi.org/10.1007/1-4020-0613-6_12548.

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Clausen, Torben, José Luis Trejo, Mark P. Mattson, Alexis M. Stranahan, Joanna Erion, Rosa Maria Bruno, Stefano Taddei, and Melinda M. Manore. "Notch." In Encyclopedia of Exercise Medicine in Health and Disease, 648. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_3207.

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Hozumi, Katsuto. "Notch Ligands for Lymphocyte Development." In Notch Signaling, 3–20. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-4971-2_1.

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Maekawa, Yoichi, Takahide Ikeda, and Piyarat Srinontong. "Notch Controls the Differentiation and Function of Cytotoxic CD8 T Cells." In Notch Signaling, 21–33. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-4971-2_2.

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Ishifune, Chieko, and Koji Yasutomo. "Notch and Myeloid Cells." In Notch Signaling, 35–55. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-4971-2_3.

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Helbig, Christina, and Derk Amsen. "Taking CD4 T Cells Up a Notch." In Notch Signaling, 57–75. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-4971-2_4.

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Chiba, Shigeru. "NOTCH in Malignant Lymphoma." In Notch Signaling, 79–92. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-4971-2_5.

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Nowell, Craig S., and Freddy Radtke. "The Two Faces of Notch in Solid Cancers." In Notch Signaling, 93–104. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-4971-2_6.

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Conference papers on the topic "Notch"

1

Ucar-Bilyeu, Deniz A., Margarite D. MATOSSIAN, VAN Hoang Barnes, Fokhrul M. Hossain, Mohit Gupta, HOPE E. BURKS, THOMAS D. WRIGHT, et al. "Abstract 967: Targeting notch one notch above." 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.am2018-967.

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Hendrix, Karen D., Charles A. Hulse, Georg J. Ockenfuss, and Robert B. Sargent. "Demonstration of narrowband notch and multi-notch filters." In Optical Engineering + Applications, edited by Jennifer D. T. Kruschwitz and Michael J. Ellison. SPIE, 2008. http://dx.doi.org/10.1117/12.795498.

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Hartmann, C. S., J. C. Andle, and M. B. King. "SAW Notch Filters." In IEEE 1987 Ultrasonics Symposium. IEEE, 1987. http://dx.doi.org/10.1109/ultsym.1987.198941.

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Owen, Harry. "Holographic notch filter." In San Diego, '91, San Diego, CA, edited by Ivan Cindrich and Sing H. Lee. SPIE, 1991. http://dx.doi.org/10.1117/12.50638.

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Panja, Ardhendu, Arnab Bhattacharya, and Tribeni Prasad Banerjee. "Design and Analysis of Notch Depth for T-Notch Filter." In 2020 National Conference on Emerging Trends on Sustainable Technology and Engineering Applications (NCETSTEA). IEEE, 2020. http://dx.doi.org/10.1109/ncetstea48365.2020.9119943.

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Pathak, Vikas, Satyasai Jagannath Nanda, Amit Mahesh Joshi, and Sitanshu Sekhar Sahu. "High Speed Implementation of Notch/Anti-notch IIR Filter on FPGA." In 2018 15th IEEE India Council International Conference (INDICON). IEEE, 2018. http://dx.doi.org/10.1109/indicon45594.2018.8986985.

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Kwok, Kam-cheung, and Ming-kam Chan. "Parallel DC notch filter." In San Diego, '91, San Diego, CA, edited by Andrew G. Tescher. SPIE, 1991. http://dx.doi.org/10.1117/12.50859.

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Ning, Alex, and Jon D. Masso. "Multiline holographic notch filters." In San Diego, '91, San Diego, CA, edited by Jeremy M. Lerner and Wayne R. McKinney. SPIE, 1991. http://dx.doi.org/10.1117/12.49408.

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Wachirarattanapornkul, Sorapong. "Active DURC notch filter." In 2014 4th Joint International Conference on Information and Communication Technology, Electronic and Electrical Engineering (JICTEE). IEEE, 2014. http://dx.doi.org/10.1109/jictee.2014.6804122.

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Hryniewicz, J. V., P. P. Absil, B. E. Little, R. A. Wilson, L. G. Joneckis, and P. T. Ho. "Microring resonator notch filters." In Conference on Lasers and Electro-Optics (CLEO 2000). Technical Digest. Postconference Edition. TOPS Vol.39. IEEE, 2000. http://dx.doi.org/10.1109/cleo.2000.907438.

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Reports on the topic "Notch"

1

Huang, Yuchen. Adaptive Notch Filter. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.6686.

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Mehta, Samir, and Kurt Hankenson. Notch Signaling in Bone Regeneration. Fort Belvoir, VA: Defense Technical Information Center, October 2011. http://dx.doi.org/10.21236/ada564010.

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Lee, Eun U., Bruce A. Pregger, Robert E. Taylor, and Charles Lei. Biaxial Fatigue Cracking from Notch. Fort Belvoir, VA: Defense Technical Information Center, March 2013. http://dx.doi.org/10.21236/ada575515.

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Mohn, Gillian. Top Notch Stitching documentation redesign. Ames (Iowa): Iowa State University, December 2021. http://dx.doi.org/10.31274/cc-20240624-1509.

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Kim, Minji. Notch in Pathological Angiogenesis and Lymphangiogenesis. Fort Belvoir, VA: Defense Technical Information Center, May 2013. http://dx.doi.org/10.21236/ada581029.

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Kim, Minji. Notch in Pathological Angiogenesis and Lymphangiogenesis. Fort Belvoir, VA: Defense Technical Information Center, May 2012. http://dx.doi.org/10.21236/ada589440.

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Kim, Minji. Notch in Pathological Angiogenesis and Lymphangiogenesis. Fort Belvoir, VA: Defense Technical Information Center, May 2011. http://dx.doi.org/10.21236/ada550314.

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Jeffries, Shawn. Molecular Mechanisms of Notch Signaling in Neoplasia. Fort Belvoir, VA: Defense Technical Information Center, August 2002. http://dx.doi.org/10.21236/ada411237.

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Maxey and Barnes. L51622 The Chevron Notched Drop-Weight-Tear-Test Specimen. Chantilly, Virginia: Pipeline Research Council International, Inc. (PRCI), September 1990. http://dx.doi.org/10.55274/r0010366.

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This research is aimed at finding a new type of notch that would produce propagation data similar to that produced by the PC DWTT. High-toughness materials and materials that had previously been studied were used assuming that if the new notch worked on these materials it would be satisfactory for lower toughness materials. Several notch modifications were tried and most were no better than the standard pressed notch used in the API specimen. A search for a new type of notch for the standard drop-weight-tear-test (DWTT) specimen has been completed. This new notch specimen is to replace the precracked DWTT specimen which has been shown to predict full-scale behavior but has received-little support from pipe manufacturers. The new notch is a chevron notch causing fracture initiation to occur at a machined point located at mid-wall thicknessand about 0.2 inch below the specimen edge (i.e., at the same depth as the pressed-in notch of the standard DWTT). No precracking or other severe prestraining, which may create strain aging problems, is required to produce the specimen. A good correlation was obtained between the chevron-notched DWTT and the Charpy V-notch specimens for conventionally rolled steels; this correlation effectively ties the chevron notched data to past fracture research data and to published correlations thatdescribe fracture in terms of Charpy upper-shelf energy. A procedure is included for preparing and conducting the Chevron notched DWTT.
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10

McGinnis, Dave, and /Fermilab. Phase Advance for Wideband Dampers With Notch Filters. Office of Scientific and Technical Information (OSTI), February 2000. http://dx.doi.org/10.2172/984605.

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