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Academic literature on the topic 'Distal suppressor'

Author: Grafiati

Published: 6 September 2023

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Journal articles on the topic "Distal suppressor"

1

Maine, E. M., and J. Kimble. "Suppressors of glp-1, a gene required for cell communication during development in Caenorhabditis elegans, define a set of interacting genes." Genetics 135, no. 4 (December 1, 1993): 1011–22. http://dx.doi.org/10.1093/genetics/135.4.1011.

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Abstract The glp-1 gene is essential for two cell interactions that control cell fate in Caenorhabditis elegans: induction of anterior pharynx in the embryo and induction of mitotic proliferation in the germ line. To identify other genes involved in these cell interactions, we have isolated suppressors of two temperature sensitive alleles of glp-1. Each of 14 recessive suppressors rescues both embryonic and germline glp-1(ts) defects. These suppressors are extragenic and define a set of six genes designated sog, for suppressor of glp-1. Suppression of glp-1 is the only obvious phenotype associated with sog mutations. Mutations in different sog genes show allele-specific intergenic noncomplementation, suggesting that the sog gene products may interact. In addition, we have analyzed a semidominant mutation that suppresses only the glp-1 germline phenotype and has a conditional feminized phenotype of its own. None of the suppressors rescues a glp-1 null mutation and therefore they do not bypass a requirement for glp-1. Distal tip cell function remains necessary for germline proliferation in suppressed animals. These suppressor mutations identify genes that may encode other components of the glp-1 mediated cell-signaling pathway or regulate glp-1 expression.

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Haverkamp., Jessica, and Timothy Ratliff. "Regulatory function of myeloid-derived suppressor cells is restricted to inflammatory site. (98.25)." Journal of Immunology 184, no. 1_Supplement (April 1, 2010): 98.25. http://dx.doi.org/10.4049/jimmunol.184.supp.98.25.

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Abstract Myeloid-derived suppressor cells (MDSC) are identified in mice as Gr-1+CD11b+ cells able to suppress T cell proliferation. Suppressive function of MDSC is linked to expression of arginase I and inducible nitric oxide synthase (iNOS) and can be augmented by inflammation. While inflammation is linked to MDSC function, it is unknown if MDSC isolated from the inflammatory site possess equal regulatory function as those in distal sites such as the spleen. Using the POET-3 model of prostate inflammation, we show Gr-1+CD11b+ cells isolated from inflamed prostates express elevated levels of ARG I and iNOS. In contrast, cells from the spleens of mice with prostate inflammation do not express detectable levels of ARG I or iNOS. However, when function of Gr-1+CD11b+ cells from spleens or the inflammatory site were tested in conventional suppression assays, all cells demonstrated suppressive function. RT-PCR analysis revealed that arginase I and iNOS mRNA were induced in MDSC during suppression assays, in part through IFN-γ. Thus conventional suppression assays induce functional suppressor cells and do not test their actual activation state in vivo. To better evaluate the function of Gr-1+CD11b+ cells we developed a short term suppression assay designed to limit exposure to IFN-γ during culture. Only cells from the inflammatory site suppressed T cell proliferation. These data demonstrate the novel finding that only Gr-1+CD11b+ cells at the inflammatory site are functional MDSC.

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Käfer, Etta. "MMS Sensitivity of All Amino Acid-Requiring Mutants in Aspergillus and Its Suppression by Mutations in a Single Gene." Genetics 115, no. 4 (April 1, 1987): 671–76. http://dx.doi.org/10.1093/genetics/115.4.671.

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ABSTRACT All available amino acid-requiring mutants of Aspergillus nidulans were found to be hypersensitive to MMS (methyl methanesulfonate) to various degrees. On MMS media, secondary mutations could be selected which suppress this MMS sensitivity but do not affect the requirement. Many such mutations were analyzed and found to be alleles of one gene, smsA (=suppressor of MMS sensitivity), which mapped distal on the right arm of chromosome V. This gene is more likely to be involved in general regulation of amino acid biosynthesis than MMS uptake, since a variety of pathway interactions were clearly modified by smsA suppressors in the absence of MMS.

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Hollingsworth, N. M., and A. D. Johnson. "A conditional allele of the Saccharomyces cerevisiae HOP1 gene is suppressed by overexpression of two other meiosis-specific genes: RED1 and REC104." Genetics 133, no. 4 (April 1, 1993): 785–97. http://dx.doi.org/10.1093/genetics/133.4.785.

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Abstract The HOP1 gene of Saccharomyces cerevisiae is believed to encode a protein component of the synaptonemal complex, the structure formed when homologous chromosomes synapse during meiotic prophase. Five new mutant alleles (three conditional, two nonconditional) of HOP1 were identified by screening EMS-mutagenized cells for a failure to complement the spore viability defect of a hop1 null allele. Two high copy plasmids were found that partially suppress the temperature-sensitive spore inviability phenotype of one of these alleles, hop1-628. The suppression is allele-specific; no effect of the plasmids is observed in hop1 null diploids. Mutation of either of the two suppressor genes results in recessive spore lethality, indicating that these genes play important roles during meiosis. The DNA sequence of one high copy suppressor gene matched that of RED1, a previously identified meiosis-specific gene. Our data strongly support the idea that RED1 protein is also a component of the synaptonemal complex and further suggest that the RED1 and HOP1 gene products may interact. The second suppressor maps to the right arm of chromosome VIII distal to CDC12 and is REC104, a meiosis-specific gene believed to act early in meiosis.

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Strand, D. J., and J. F. McDonald. "Insertion of a copia element 5' to the Drosophila melanogaster alcohol dehydrogenase gene (adh) is associated with altered developmental and tissue-specific patterns of expression." Genetics 121, no. 4 (April 1, 1989): 787–94. http://dx.doi.org/10.1093/genetics/121.4.787.

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Abstract The Drosophila melanogaster alcohol dehydrogenase gene (adh) is under the control of two separate promoters (proximal and distal) which are preferentially utilized at the larval and adult life stages, respectively. A variant alcohol dehydrogenase allele (RI-42) isolated from a natural population contains a copia retroviral-like transposable element inserted 240 bp upstream from the distal (adult) adh transcriptional start site. Levels of adh transcripts in the RI-42 variant are reduced in tissues and at life stages where copia is actively expressed and are affected in trans- by mutant alleles at the suppressor-of-white-apricot (su(wa] and suppressor-of-forked (su(f] loci. These suppressor genes have no effect on adh expression in wild-type Drosophila.

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Lissemore, J. L., P. D. Currie, C. M. Turk, and E. M. Maine. "Intragenic dominant suppressors of glp-1, a gene essential for cell-signaling in Caenorhabditis elegans, support a role for cdc10/SWI6/ankyrin motifs in GLP-1 function." Genetics 135, no. 4 (December 1, 1993): 1023–34. http://dx.doi.org/10.1093/genetics/135.4.1023.

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Abstract The glp-1 gene product mediates cell-cell interactions required for cell fate specification during development in Caenorhabditis elegans. To identify genes that interact with glp-1, we screened for dominant suppressors of two temperature-sensitive glp-1 alleles and recovered 18 mutations that suppress both germline and embryonic glp-1 phenotypes. These dominant suppressors are tightly linked to glp-1 and do not bypass the requirement for a distal tip cell, which is thought to be the source of a signal that is received and transduced by the GLP-1 protein. Using single-strand conformation polymorphism (SSCP) analysis and DNA sequencing, we found that at least 17 suppressors are second-site intragenic revertants. The suppressors, like the original glp-1(ts) mutations, are all located in the cdc10/SWI6/ankyrin domain of GLP-1. cdc10/SWI6/ankyrin motifs have been shown to mediate specific protein-protein interactions in other polypeptides. We propose that the glp-1(ts) mutations disrupt contact between GLP-1 and an as yet unidentified target protein(s) and that the dominant suppressor mutations restore appropriate protein-protein interactions.

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Alleva, D. G., C. J. Burger, and K. D. Elgert. "Tumor-induced regulation of suppressor macrophage nitric oxide and TNF-alpha production. Role of tumor-derived IL-10, TGF-beta, and prostaglandin E2." Journal of Immunology 153, no. 4 (August 15, 1994): 1674–86. http://dx.doi.org/10.4049/jimmunol.153.4.1674.

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Abstract In vitro-activated macrophages (Mphi) co-express cytotoxicity for tumor cells and suppression of lymphocyte proliferation. These Mphi functions increase during tumor growth and are mediated by soluble molecules. Because Mphi-derived nitric oxide (NO) and TNF-alpha mediate both cytotoxicity and suppression, we determined whether fibrosarcoma (Meth-KDE) growth increased Mphi-mediated suppression of T cell proliferation by increasing Mphi NO and TNF-alpha production. Tumor-bearing host peritoneal Mphi produced more NO and TNF-alpha than normal host Mphi when activated with IFN-gamma or LPS, respectively. This tumor-induced increase in Mphi NO and TNF-alpha production mediated suppression of alloantigen-driven T cell proliferation, because treatment with either NG-monomethyl-L-arginine or anti-TNF-alpha Ab blocked tumor-bearing host Mphi-mediated suppression. TNF-alpha did not directly suppress T cells, but it induced Mphi NO production that down-regulated proliferation. When non-tumor-infiltrating peritoneal Mphi were cultured with Meth-KDE cell supernatants, Mphi production of NO and TNF-alpha was strongly down-regulated. The tumor-derived molecules responsible for this inhibition were IL-10, TGF-beta 1, and prostaglandin E2. The experimental evidence leading to this conclusion included: 1) The Meth-KDE cells produced significant levels of these cytokines. 2) Recombinant forms of these cytokines suppressed NO and TNF-alpha production. 3) Ab-mediated absorption of these cytokines from tumor cell supernatants restored NO and TNF-alpha production. 4) Anti-IL-10 and anti-TGF-beta 1 Ab addition to IFN-gamma-stimulated Mphi restored NO production. Culture supernatants of two human carcinoma cell lines and another murine fibrosarcoma suppressed Mphi NO and TNF-alpha production, which was partly mediated by TGF-beta 1 and prostaglandin E2. Collectively, these results suggest that tumor growth promotes distal Mphi suppressor activity by increasing Mphi production of cytotoxic molecules and concomitantly down-regulating the local production of these antitumor molecules.

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Welshons, W. J., and H. J. Welshons. "ENHANCEMENT AND SUPPRESSION OF A EUCHROMATIC POSITION EFFECT AT NOTCH IN DROSOPHILA." Genetics 113, no. 2 (June 1, 1986): 337–54. http://dx.doi.org/10.1093/genetics/113.2.337.

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ABSTRACT The recessive visible rough-eye mutant facet-strawberry, faswb, is caused by the deletion of 0.8 kb of base sequences from the 5' end of the Notch locus. Visible deficiencies adjacent to faswb suppress this mutant effect of the Notch locus, and in the same region (between salivary bands 3C1 and 3C7), we have demonstrated the presence of at least one partial suppressor and one enhancer of the faswb position effect at Notch.—The enhancer seems to be a small inversion approximately equal to the salivary-band doublet 3C2, 3, and the partial suppressor lies between the inversion in 3C2, 3 and the small deletion in faswb immediately distal to 3C7. Neither the enhancer, e(faswb), nor the partial suppressor, su(faswb), can be detected except when linked in cis to faswb. The e(faswb) and the su(faswb), in unison, act antagonistically on the faswb position effect.—The faswb mutant is interpreted to be a nonvariegating position effect at the Notch locus resulting from a novel euchromatic—euchromatic association of base sequences caused by the small deletion.

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Quaresma, Luisa, Antonio CALDEIRA Fradique, Fernanda Cabrita, Alexandra Pupo, Guedes DA Silva, Gualdino Silva, Jorge Esteves, et al. "The prognostic value of P53 in the nodal metastization of gastric cancer." Journal of Clinical Oncology 30, no. 15_suppl (May 20, 2012): e14673-e14673. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.e14673.

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e14673 Background: Lymph node Metastases play a major role as an independent prognostic factor in gastric cancer. Presence of distal lymph node metastases assumes a pejorative prognostic significance, and represents a problem in terms of therapeutic approach. For this reason it’s of major interest to find predictive markers of distal lymph node chain involvement. The P53 tumor suppressor gene, a product of the TP53 gene works normally as a brake on DNA replication, as suppressor of angiogenesis and triggering of apoptosis. The gene most frequently mutated in gastric cancer is the TP53, that is responsible for the production of P53 mutant protein, which forms inactive complex with the native protein, and manifest by the overexpression of p53 in immunocytochemistry. The overexpression of P53 gene has been considered a bad prognostic factor associated mainly with lymph node metastases. Methods: This study seeks to determine the relation between the expression of P53 and the presence of distal lymph node metastases as an indicator for an extended lymphadenectomy. A total of 50 patients undergoing surgery with D2 lymphadenectomy for gastric carcinoma with curative intent were enrolled in this work. Therefore it was evaluated in 1,786 lymph nodes the correlation between the P53 expression with tumor location, size, histological type, depth , number of nodes involved, number of distal lymph node metastases and the TNM stage. Results: In all parameters, mutant P53 protein related with indicators of poor prognosis. In particular has demonstrated a statistical significant correlation (p=0.019) with the presence of distal lymph node metastases. The main objective of this study which was finding a prognostic predictor of distal nodal metastases has been reached. Conclusions: Mutant P53 protein is a good prognostic indicator, for the presence of distal lymph node involvement in gastric carcinoma.

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Nahar, Rahul, Parham Ramezani-Rad, Sinisa Dovat, Maike Buchner, Thomas G. Graeber, and Markus Muschen. "Mechanisms of Ikaros-Mediated Tumor Suppression." Blood 118, no. 21 (November 18, 2011): 408. http://dx.doi.org/10.1182/blood.v118.21.408.408.

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Abstract Abstract 408 Background: The Ikaros (IKZF1) tumor suppressor is deleted in >80% of the cases of Ph+ ALL. While Ikaros cooperates with pre-B cell receptor signaling to induce cell cycle exit in Ph+ ALL (Trageser et al., J Exp Med, 2009), the mechanism of Ikaros-mediated tumor suppression is poorly understood. Here we report on a series of genetic experiments that show that Ikaros (i) interferes with key survival pathways downstream of the BCR-ABL1 kinase, (ii) inhibits leukemia cell proliferation through interaction with the pre-B cell receptor signaling pathway and (iii) activates the tumor suppressors p53, p21 and p27. Results: To elucidate the mechanism of Ikaros-dependent tumor suppression in BCR-ABL1-driven B cell lineage leukemia, we studied regulation of critical phosphorylation events downstream of the BCR-ABL1 kinase as a central mediators of survival and proliferation. Reconstitution of Ikaros expression in BCR-ABL1-transformed pre-B ALL cells resulted in rapid and global dephosphorylation comparable to the effect of Imatinib. A detailed analysis showed that Ikaros-induced dephosphorylation events affect activation of Stat5 (Y694), AKT (S473), ERK1/2 (T202 and Y204) and SRC (Y416). Interestingly, both Imatinib-treatment and reconstitution of pre-B cell receptor signaling using retroviral vectors for expression of the m heavy chain or the BLNK adapter molecule have the same effects as reconstitution of Ikaros. In fact, a comprehensive gene expression analysis demonstrated that Ikaros reconstitution resulted in similar gene expression changes as reconstitution of pre-B cell receptor signaling (m heavy chain or BLNK), reconstitution of PAX5, Cre-mediated deletion of Stat5 or Myc, or treatment with Imatinib. The signature of common gene expression changes shared between reconstitution of Ikaros, Pax5, m heavy chain, BLNK and inducible deletion of Stat5 or Myc and Imatinib-treatment involves known tumor suppressors including SPIB, BTG1, and BTG2. These findings suggest that reconstitution of tumor suppressive transcription factor (Ikaros, Pax5) converges with pre-B cell receptor-mediated tumor suppression. To better understand how pre-B cell receptor signaling and Ikaros intersect, we combined reconstitution of Ikaros with genetic deletion of either the (more proximal) SYK kinase or the (more distal) BLNK adapter molecule. While inducible Cre-mediated deletion of Syk had no effect on Ikaros-mediated tumor suppression, deletion of the BLNK adapter compromised the ability of Ikaros to function as tumor suppressor. These findings were confirmed in an in vivo transplantation experiment. While mice transplanted with Ikaros+ BLNK+ leukemia cells survived indefinitely, mice transplanted with Ikaros- BLNK+, Ikaros+ BLNK- or Ikaros- BLNK- leukemia cells died after 24 to 31 days post transplantation. While these findings provide genetic evidence for collaboration between the Ikaros and pre-B cell receptor tumor suppressor pathways, Ikaros and pre-B cell receptor signaling differ with respect to activation of classical tumor suppressor pathways. While reconstitution of pre-B cell receptor signaling failed to activate Arf, p53 or p27, protein levels of all these molecules were strongly upregulated by Ikaros. In agreement with these findings, reconstitution of pre-B cell receptor signaling had the same tumor suppressive effect in wildtype leukemia cells as in Arf−/−, p53−/− as well as p27−/− leukemia cells. Conversely, deletion of Arf and p53 significantly diminished the ability of Ikaros to function as tumor suppressor. Conclusion: Ikaros deletion represents a near-obligatory lesion in the pathogenesis of Ph+ ALL. Here we provide genetic evidence for three novel pathways of Ikaros-mediated tumor suppression. Like PAX5, Ikaros reconstitution results in multiple dephosphorylation events (Stat5, AKT, ERK1/2 and SRC are affected). In collaboration with the pre-B cell receptor and its downstream adapter molecule BLNK, Ikaros suppressed MYC and inhibits cell cycle progression. Induction of the Arf/p53 pathway represents a distinct function of Ikaros, which is not shared with the pre-B cell receptor signaling pathway. Disclosures: No relevant conflicts of interest to declare.

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Dissertations / Theses on the topic "Distal suppressor"

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Wroe, Stephanie Fay. "Identification of imprinted genes on mouse distal Chr 2 by suppression subtractive hybridisation and a candidate gene approach." Thesis, University of Oxford, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.343038.

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Fonseca, Mario Alberto. "The transcriptional regulation of intestinal epithelial development and adenomatous polyposis coli tumour suppressor gene expression by Dlx homeobox genes." 2011. http://hdl.handle.net/1993/4517.

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Introduction: Colorectal cancer (CRC) is the fourth-most common cancer in Canada with a high mortality rate. Familial adenomatous polyposis (FAP) is a hereditary form of CRC; FAP patients carry germline mutations of the tumour suppressor gene adenomatous polyposis coli (APC). The function of Dlx genes in the gastrointestinal tract (GIT) has not been previously explored. Methods: Immunofluorescence (IF) was performed to identify Dlx2+ intestinal cells. Chromatin immunoprecipitation (ChIP) was performed to identify DLX2-Apc promoter interaction. Quantitative real time polymerase chain reaction (qRT-PCR) was performed on mouse small and large intestines (normal and Dlx1/Dlx2 mutant mice). Electrophoretic mobility shift assays (EMSA) and reporter assays were carried out to investigate direct binding and activity, respectively, of DLX2 on the Apc promoter in-vitro. Dlx2 expression was explored in ApcMIN mice and human CRC tumor specimens. Results: Dlx2 is highly expressed in mouse embryonic and adult intestinal epithelia. Moreover, Dlx2 is expressed in the ApcMIN mice GIT as well as in some human CRC tumor specimens. ChIP, EMSA and reporter gene assays demonstrated that DLX2 protein specifically interacts with the Apc promoter in-situ and activates its expression in vitro. In-vivo and in-vitro, β-catenin protein levels are increased when DLX2 is absent or reduced by shRNA to Dlx2. Conclusions: Regulation of APC expression during development is poorly understood. We have evidence that DLX2 interacts with the Apc promoter in-vivo. We have shown that DLX2 induces Apc transcription by directly binding to the Apc promoter in-vitro. We also showed that β-catenin expression is altered in the Dlx1/Dlx2 mutant GIT. This finding implicates the involvement of DLX2 in the canonical Wnt signalling pathway. Ultimately, restoring APC expression may be a novel strategy towards preventing progression of intestinal polyps to adenocarcinoma. This research will contribute to our knowledge of the genetic and epigenetic regulatory pathways that control intestinal development, mucosal self-renewal and CRC.

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Tran, Nhat. "smig-1(ev809) is a Novel Suppressor of Distal Tip Cell Migration Mutants in Caenorhabditis elegans." Thesis, 2014. http://hdl.handle.net/1807/44068.

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smig-1(ev809) is a novel suppressor of multiple distal tip cell (DTC) migration mutants in the nematode Caenorhabditis elegans. In the C. elegans hermaphrodite, the two U-shaped gonad arms develop and form as a result of the migration of two DTCs. smig-1(ev809) suppresses DTC migration defects of mutants encoding components of intracellular glycosylation pathways as well as extracellular basement membrane glycoproteins. The smig-1(ev809) mutation bypasses the requirement for a fully functional chondroitin pathway and MIG-17 metalloprotease in DTC pathfinding. I found that i) suppression of the hypomorphic chondroitin mutant mig-22(k141) is not completely dependent on MIG-17 activity; ii) the smig-1(ev809) mutant is likely to be a loss- of-function suppressor; and iii) SMIG-1 does not visibly affect the localization of poorly glycosylated MIG-17 on the gonad surface. Understanding SMIG-1 function will shed light on the role of glycosylation, the extracellular matrix and basement membranes in cell migration during development.

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Books on the topic "Distal suppressor"

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M, Faust Robert, United States. Agricultural Research Service., and United States Forest Service, eds. USDA-ARS national research action plan for development of technologies for management and suppression of the gypsy moth, Lymantia dispar. [Beltsville, MD]: U.S. Dept. of Agriculture, Agricultural Research Service, 1993.

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Ghent, J. H. The spray swath of the DC-3 for gypsy moth suppression using Bacillus thuringiensis. 1994.

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Lovett, Alexandra, and Whitney W. Woodmansee. A Woman with Weight Gain and Fatigue. Edited by Angela O’Neal. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190609917.003.0011.

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Cushing’s syndrome is a descriptive term of a syndrome secondary to elevated levels of steroids or cortisol, while Cushing’s disease is hypercortisolemia that results from an adrenocorticotropic (ACTH)-secreting pituitary adenoma. Patients will present with cushingoid features on physical examination and can be myopathic with proximal rather than distal muscle weakness. Diagnosis can be obtained by multiple avenues including but not limited to checking 24 hour urine cortisol, a dexamethasone suppression test, checking ACTH levels, a CRH (corticotrophin-releasing hormone) stimulation test, and inferior petrosal sinus sampling (IPSS). Once Cushing’s disease is confirmed, treatment is via transsphenoidal resection of the pituitary adenoma.

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Dean, Michael, and Karobi Moitra. Biology of Neoplasia. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0002.

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The term “cancer” encompasses a large heterogeneous group of diseases that involve uncontrolled cell growth, division, and survival, culminating in local invasion and/or distant metastases. Cancer is fundamentally a genetic disease at the cellular level. Tumors occur because clones of abnormal cells acquire multiple lesions in DNA, nearly always involving mutations, chromosomal rearrangements, and extensive alteration of the epigenome. Up to 10% of cancers also involve inherited germline mutations that are moderately to highly penetrant. Cancers begin as localized growths or premalignant lesions that may regress or disappear spontaneously, or progress to a malignant primary tumor. The somatic changes that drive abnormal growth involve activating mutations of specific oncogenes, inactivation of tumor suppressor genes, and/or disruption of epigenetic controls. The latter can result from methylation or the modification of histones and other proteins that affect the remodeling of chromosomes. Numerous non-inherited factors can cause cancer by accelerating these events.

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Purdon, James, ed. British Literature in Transition, 1900–1920: A New Age? Cambridge University Press, 2021. http://dx.doi.org/10.1017/9781108648714.

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During the first two decades of the twentieth century, Britain's imperial power and influence was at its height. These were years of daring, when adventurers sounded the mysteries of the deep sea and the distant poles, aviators sped through the skies, and new media technologies transformed communication. They were years of social upheaval, during which long-suppressed voices – particularly those of women, of the labouring classes, and of colonial subjects – grew louder and demanded to be heard. They were years of violence, of insurrection and political agitation, and of imperial conflicts that would encompass continents. By subjecting specific developments in literature and related culture to a fine-grained and historically-informed analysis, British Literature in Transition, 1900–1920: A New Age? explores the writing of this extraordinary period in all its complexity and vibrancy.

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Bloom, Lisa E. Climate Change and the New Polar Aesthetics. Duke University Press, 2022. http://dx.doi.org/10.1215/9781478018643.

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In Climate Change and the New Polar Aesthetics, Lisa E. Bloom considers the ways artists, filmmakers, and activists engaged with the Arctic and Antarctic to represent our current environmental crises and reconstruct public understandings of them. Bloom engages feminist, Black, Indigenous, and non-Western perspectives to address the exigencies of the experience of the Anthropocene and its attendant ecosystem failures, rising sea levels, and climate-led migrations. As opposed to mainstream media depictions of climate change that feature apocalyptic spectacles of distant melting ice and desperate polar bears, artists such as Katja Aglert, Subhankar Banerjee, Joyce Campbell, Judit Hersko, Roni Horn, Isaac Julien, Zacharias Kunuk, Connie Samaras, and activist art collectives take a more complex poetic and political approach. In their films and visual and conceptual art, these artists link climate change to its social roots in colonialism and capitalism while challenging the suppression of information about environmental destruction and critiquing Western art institutions for their complicity. Bloom’s examination and contextualization of new polar aesthetics makes environmental degradation more legible while demonstrating that our own political agency is central to imagining and constructing a better world.

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Donahue, Thomas J. Unfreedom for All. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780190051686.001.0001.

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It is often said that we live in global systems of injustice. But if so, what are they, and what are their moral consequences? This book offers a theory of global injustice—“Unfreedom for All.” The theory explores and defends the old adage that “No one is free while others are oppressed” by putting five questions: Why and when ought we to combat injustices done to distant others, and does this require joining in solidarity against them? Do we live under global systems of injustice? What counts as systematic injustice or oppression? Who if anyone is made unfree by such injustices? What harms do they do? Unfreedom for All shows that the “No one is free” creed either answers or results from each of these questions. It defends that creed by considering how systematic injustices—such as global severe poverty, male supremacy, or racial oppression—are perpetuated. The book argues that where your society does such an injustice, it systematically suppresses anyone’s resistance to the injustice—including yours. It uses authoritarian tactics against everyone, so you too are subject to arbitrary power. Hence you too are unfree. This holds just as true of systematic injustices done by global society, and this should be the main reason for joining in solidarity against injustice.

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Book chapters on the topic "Distal suppressor"

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Lee, Christine U., and James F. Glockner. "Case 4.13." In Mayo Clinic Body MRI Case Review, edited by Christine U. Lee and James F. Glockner, 210–11. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199915705.003.0111.

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66-year-old man with a history of a cystic pancreatic lesion and increasing abdominal pain Coronal fat-suppressed 2D SSFP images (Figure 4.13.1) reveal marked biliary and pancreatic ductal dilatation. Note also the large soft tissue nodules in the proximal and distal pancreatic duct and the small nodules at the bifurcation of the common duct. Axial fat-suppressed T2-weighted FSE image (...

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Lee, Christine U., and James F. Glockner. "Case 9.10." In Mayo Clinic Body MRI Case Review, edited by Christine U. Lee and James F. Glockner, 439–40. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199915705.003.0232.

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24-year-old man with 5-year history of Crohn disease now with worsening right lower quadrant pain, difficulty eating, and diarrhea Coronal SSFSE (Figure 9.10.1), fat-suppressed 2D SSFP (Figure 9.10.2), and postgadolinium 3D SPGR (Figure 9.10.3) images show marked thickening of the distal ileum, with matted loops of ileum in the right lower quadrant. Note the prominent enteroenteric fistula in the distal ileum....

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Lee, Christine U., and James F. Glockner. "Case 9.1." In Mayo Clinic Body MRI Case Review, edited by Christine U. Lee and James F. Glockner, 421–22. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199915705.003.0223.

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56-year-old asymptomatic woman with liver mass thought to be focal nodular hyperplasia on CT Image from a double-contrast esophagram (Figure 9.1.1) demonstrates a relatively subtle mural lesion in the distal esophagus with a small central ulceration. Axial fat-suppressed T2-weighted FSE images (...

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Lee, Christine U., and James F. Glockner. "Case 8.18." In Mayo Clinic Body MRI Case Review, edited by Christine U. Lee and James F. Glockner, 405–6. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199915705.003.0214.

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25-year-old man with 3-year history of gross hematuria Axial (Figure 8.18.1) and coronal (Figure 8.18.2) fat-suppressed FSE T2-weighted images show a large frondlike mass in the posterior left bladder. Note the dilated distal left ureter on the coronal image. Axial postgadolinium 2D SPGR images (...

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Lee, Christine U., and James F. Glockner. "Case 9.13." In Mayo Clinic Body MRI Case Review, edited by Christine U. Lee and James F. Glockner, 444–45. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199915705.003.0235.

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86-year-old man with rectal bleeding; colonoscopy demonstrated a polyp in the ascending colon Axial SSFSE images (Figure 9.13.1) and coronal fat-suppressed SSFP images (Figure 9.13.2) show focal mural thickening in the distal ileum. The underlying lumen is dilated, and no proximal obstruction is visible. Axial (...

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Lee, Christine U., and James F. Glockner. "Case 9.2." In Mayo Clinic Body MRI Case Review, edited by Christine U. Lee and James F. Glockner, 423–24. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199915705.003.0224.

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56-year-old man with progressive solid-food dysphagia and a 15-lb weight loss over the past 3 months Axial fat-suppressed FSE T2-weighted images (Figure 9.2.1) show circumferential thickening and mildly increased signal intensity in the distal esophagus. Axial diffusion-weighted images with a b value of 600 s/mm...

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Lee, Christine U., and James F. Glockner. "Case 8.19." In Mayo Clinic Body MRI Case Review, edited by Christine U. Lee and James F. Glockner, 407–8. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199915705.003.0215.

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75-year-old man with history of gross hematuria Axial fat-suppressed FSE T2-weighted images (Figure 8.19.1) show a mass in the bladder posteriorly near the right ureterovesical junction with mild increased signal intensity obstructing the distal right ureter. Arterial phase and 10-minute delayed postgadolinium coronal 3D SPGR images from an MR urogram (...

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Lee, Christine U., and James F. Glockner. "Case 3.11." In Mayo Clinic Body MRI Case Review, edited by Christine U. Lee and James F. Glockner, 152–53. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199915705.003.0081.

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66-year-old woman with upper abdominal pain radiating to her back, jaundice, nausea, and chills; CT demonstrated intra- and extrahepatic biliary dilatation MIP image from 3D FRFSE MRCP (Figure 3.11.1) demonstrates diffuse intra- and extrahepatic biliary dilatation extending to the distal CBD, which shows focal narrowing. An intraductal filling defect is seen immediately above the narrowing. Axial fat-suppressed SSFP images (...

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Connell, John M. C., and E. Marie Freel. "Primary aldosteronism and other steroid-related causes of endocrine hypertension." In Oxford Textbook of Endocrinology and Diabetes, 810–24. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199235292.003.0570.

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Mineralocorticoid hypertension is characterized by increased distal renal tubular sodium reabsorption, raised body sodium content, plasma volume expansion, markedly reduced body potassium content, with a metabolic alkalosis and suppression of renin production by the juxtaglomerular cells of the kidney (and correspondingly low levels of angiotensin II). Primary aldosteronism is the most common cause of mineralocorticoid hypertension (1); less frequent causes include the rare inborn errors of adrenal steroid synthesis (11β‎-hydroxylase and 17α‎-hydroxylase deficiency), alterations in corticosteroid metabolism (syndrome of apparent mineralocorticoid excess), and constitutive activation of the epithelial sodium channel (Liddle’s syndrome).

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Lee, Christine U., and James F. Glockner. "Case 17.20." In Mayo Clinic Body MRI Case Review, edited by Christine U. Lee and James F. Glockner, 827–28. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199915705.003.0438.

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72-year-old man with cholangiocarcinoma in the distal common bile duct VR image from 3D FRFSE MRCP (Figure 17.20.1) demonstrates moderately dilated intrahepatic ducts in the central right hepatic lobe, poorly visualized ducts in the medial left lobe, and dilated ducts in the lateral left lobe. There is an abrupt cutoff of the common bile duct near the pancreatic head, with a stent extending into the duodenum, and an apparent filling defect proximal to the obstruction. Notice also the dilated pancreatic duct. Axial fat-suppressed 3D SSFP images (...

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Conference papers on the topic "Distal suppressor"

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Luchnikov, Alexander V., and Igor V. Mel'nikov. "The timing jitter suppression of subpicosecond optical solitons during their transmission over long distant fibre." In The European Conference on Lasers and Electro-Optics. Washington, D.C.: Optica Publishing Group, 1994. http://dx.doi.org/10.1364/cleo_europe.1994.cthi5.

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Limitation of the transmission rate in optical soliton high bit rate (5 Gbits/s and higher) and ultralong (up to 10,000 km) information transmission systems is mainly due to soliton timing jitter, which is concerned with interaction of solitons with the spontaneous noise of optical amplifiers (Gordon-Haus effect)1 and electrostrictional soliton long-range interaction.2 The methods of the soliton timing jitter suppression were proposed.3,4 Similar problems arise when teraherz sequence of subpicosecond solitons have to be transmitted through long fibre of up to 100 km length. In this paper we propose the original method of the timing jitter suppression of subpicosecond solitons. The method is based on the soliton frequency stabilization due to the joint action of differential spectral amplification of soliton and Raman self-frequency shift.

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Gusevsky, V. I., and O. N. Tsvetkova. "Suppression of Distant Aperture Sidelobes in Linear and Planar Phased Arrays." In 2018 Progress in Electromagnetics Research Symposium (PIERS-Toyama). IEEE, 2018. http://dx.doi.org/10.23919/piers.2018.8597725.

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Magalhães, Paolla Giovanna Rossito de, Marina Buldrini Filogonio Seraidarian, Bernardo Tardin Caetano, Barbara Oliveira Paixão, Tassila Oliveira Nery de Freitas, Daniel Vasconcelos de Pinho Tavares, Gabriella Braga da Cunha Silva, et al. "Case Report: Reversible Cerebral Vasoconstriction Syndrome in a cancer patient using ZoladexTM." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.142.

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Context: The Reversible Cerebral Vasoconstriction Syndrome (SVCR) is characterized by rapid and reversible vasoconstriction and segmental dilation of cerebral arteries, usually preceded by thunderclap headache. The involvement of second and third-order branches of the cerebral arteries is the most commom finding in a cerebral angiography. This report is about a SVCR case with atypical involvement, significantly compromising extracranial vessels and raising the hypothesis of association between the use of hormonal blocker gosserelin acetate (ZoladexTM) with SVCR. Case report: Female, 39 years old, with breast cancer and bone metastasis using ZoladexTM that presented with a sudden headache and vomiting, progressing to global afasia and paresis in the right upper limb. Magnetic resonance identified hyperacute intraparenchymal hematoma in left frontoparietal convexity and subarachnoid haemorrhage. Cerebral angiography showed irregularities in the distal branches (M3 and M4) of the middle cerebral arteries, as well as in the superficial temporal artery, characterized by focal strictures. Conclusion: Studies show that hormonal fluctuations in the postpartum period can trigger SVCR due to the drop in estrogen and progesterone (gonadotropins). During postpartum, the stimulus of breastfeeding increases prolactin levels leading to GnRH suppression, which decreases the level of gonadotropins. ZoladexTM is a GnRH analogue and its chronic administration results in suppression of these hormones - similar to the postpartum period. Therefore, there may be an association of hormonal blockers with SVCR.

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Segalman, Daniel J., Gordon G. Parker, and Daniel J. Inman. "Vibration Suppression by Modulation of Elastic Modulus Using Shape Memory Alloy." In ASME 1993 Design Technical Conferences. American Society of Mechanical Engineers, 1993. http://dx.doi.org/10.1115/detc1993-0151.

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Abstract A method is proposed for suppressing the resonances that occur as an item of rotating machinery is spun-up from rest to its operating speed. This proposed method invokes “stiffness scheduling” so that the resonant frequency of the system is shifted during spin-up so as to be distant from the excitation frequency. A strategy for modulating the stiffness through the use of shape memory alloy is also presented.

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Murakami, Kazuhiro, Arata Kawamura, Youichi Fujisaka, Nobuhiko Hiruma, and Youji Iiguni. "Distant Sound Suppression Using Spectral Phase Variance for Two Channel Blind Source Separation." In 2018 Asia-Pacific Signal and Information Processing Association Annual Summit and Conference (APSIPA ASC). IEEE, 2018. http://dx.doi.org/10.23919/apsipa.2018.8659634.

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Ferreira, Maurício J., Nuno A. Silva, and Nelson J. Muga. "Efficient Randomness Extraction in Quantum Random Number Generators." In Workshop de Comunicação e Computação Quântica. Sociedade Brasileira de Computação, 2022. http://dx.doi.org/10.5753/wquantum.2022.223591.

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Randomness extraction algorithms play an essential role in Quantum Random Number Generators (QRNGs), where they are used to suppress unwanted classical noise and distill true randomness from their biased output. By employing the SHA-512 hash function and Toeplitz matrix multiplication, we analyse two suitable constructions based on different principles and reach postprocessing rates of 8.69 Mbps and 3.68 Mbps, respectively. Finally, we develop a length-compatible Toeplitz-hashing algorithm able to achieve rates of 143.29 Mbps in a parallelized GPU implementation.

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Takiguchi, Kazuma, Arata Kawamura, and Youji Iiguni. "Distant Sound Source Suppression Based on Multichannel Nonnegative Matrix Factorization with Bases Distance Maximization Penalty." In 2019 International Symposium on Intelligent Signal Processing and Communication Systems (ISPACS). IEEE, 2019. http://dx.doi.org/10.1109/ispacs48206.2019.8986259.

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Scholl, Marija S. "Star-Light Suppression with a rotating Rotational-Shearing Interferometer for Extra-Solar Planet Detection." In Signal Recovery and Synthesis. Washington, D.C.: Optica Publishing Group, 1995. http://dx.doi.org/10.1364/srs.1995.rtue2.

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Star light, scattered from even most smoothly polished optical surfaces, prevents detection of a faint planet light because of the enormous brightness ratio between them. Figure 1 shows two point sources: a dark (Earth-like) planet rotates slowly around a bright star. At the time of observation the planet is assumed to be on x-axis. The wavefronts originating from the star and the planet, respectively, are incident on the aperture at a distant observation plane as plane waves with the propagation vector parallel to the optical axis and tilted with the direction cosine vector (1, 0, n).

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Tsukui, Hidenori, Rihito Kanamaru, Ai Sadatomo, Daishi Naoi, Tetsuichiro Shimizu, Makiko Tahara, Katsusuke Mori, et al. "Abstract 615: Local irradiation with systemic anti-PD1 antibody may effectively suppress the micrometastasis in distant organ through the induction of abscopal effects." 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.am2017-615.

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Morris, Zachary S., Emily Guy, David Francis, Monica M. Gressett, Eric A. Armstrong, Shyhmin Huang, Lauryn R. Werner, et al. "Abstract 4011: Effectivein situimmunization via local radiation therapy (RT) and tumor-specific immunocytokine (IC): Suppression from distant tumor is blocked by RT or Treg-depleting CTLA-4 antibody." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-4011.

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Reports on the topic "Distal suppressor"

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Chejanovsky, Nor, and Suzanne M. Thiem. Isolation of Baculoviruses with Expanded Spectrum of Action against Lepidopteran Pests. United States Department of Agriculture, December 2002. http://dx.doi.org/10.32747/2002.7586457.bard.

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Our long-term goal is to learn to control (expand and restrict) the host range of baculoviruses. In this project our aim was to expand the host range of the prototype baculovirus Autographa cali/arnica nuclear polyhedrosis virus (AcMNPV) towards American and Israeli pests. To achieve this objective we studied AcMNPV infection in the non-permissive hosts L. dispar and s. littoralis (Ld652Y and SL2 cells, respectively) as a model system and the major barriers to viral replication. We isolated recombinant baculoviruses with expanded infectivity towards L. dispar and S. littoralis and tested their infectivity towards other Lepidopteran pests. The restricted host range displayed by baculoviruses constitutes an obstacle to their further implementation in the control of diverse Lepidopteran pests, increasing the development costs. Our work points out that cellular defenses are major role blocks to AcMNPV replication in non- and semi-permissive hosts. Therefore a major determinant ofbaculovirus host range is the ability of the virus to effectively counter cellular defenses of host cells. This is exemplified by our findings showing tliat expressing the viral gene Ldhrf-l overcomes global translation arrest in AcMNPV -infected Ld652Y cells. Our data suggests that Ld652Y cells have two anti-viral defense pathways, because they are subject to global translation arrest when infected with AcMNPV carrying a baculovirus apoptotic suppressor (e.g., wild type AcMNPV carryingp35, or recombinant AcMNPV carrying Opiap, Cpiap. or p49 genes) but apoptose when infected with AcMNPV-Iacking a functional apoptotic suppressor. We have yet to elucidate how hrf-l precludes the translation arrest mechanism(s) in AcMNPV-infected Ld652Y cells. Ribosomal profiles of AcMNPV infected Ld652Y cells suggested that translation initiation is a major control point, but we were unable to rule-out a contribution from a block in translation elongation. Phosphorylation of eIF-2a did not appear to playa role in AcMNPV -induced translation arrest. Mutagenesis studies ofhrf-l suggest that a highly acidic domain plays a role in precluding translation arrest. Our findings indicate that translation arrest may be linked to apoptosis either through common sensors of virus infection or as a consequence of late events in the virus life-cycle that occur only if apoptosis is suppressed. ~ AcMNPV replicates poorly in SL2 cells and induces apoptosis. Our studies in AcMNPV - infected SL2ceils led us to conclude that the steady-state levels of lEI (product of the iel gene, major AcMNPV -transactivator and multifunctional protein) relative to those of the immediate early viral protein lEO, playa critical role in regulating the viral infection. By increasing the IEl\IEO ratio we achieved AcMNPV replication in S. littoralis and we were able to isolate recombinant AcMNPV s that replicated efficiently in S. lifforalis cells and larvae. Our data that indicated that AcMNPV - infection may be regulated by an interaction between IE 1 and lED (of previously unknown function). Indeed, we showed that IE 1 associates with lED by using protein "pull down" and immunoprecipitation approaches High steady state levels of "functional" IE 1 resulted in increased expression of the apoptosis suppressor p35 facilitating AcMNPV -replication in SL2 cells. Finally, we determined that lED accelerates the viral infection in AcMNPV -permissive cells. Our results show that expressing viral genes that are able to overcome the insect-pest defense system enable to expand baculovirus host range. Scientifically, this project highlights the need to further study the anti-viral defenses of invertebrates not only to maximi~e the possibilities for manipulating baculovirus genomes, but to better understand the evolutionary underpinnings of the immune systems of vertebrates towards virus infection.

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