129 research outputs found
Topological Chern-Simons Sigma Model
We consider topological twisting of recently constructed Chern-Simons-matter
theories in three dimensions with N=4 or higher supersymmetry. We enumerate
physically inequivalent twistings for each N, and find two different twistings
for N=4, one for N=5,6, and four for N=8. We construct the two types of N=4
topological theories, which we call A/B-models, in full detail. The A-model has
been recently studied by Kapustin and Saulina. The B-model is new and it
consists solely of a Chern-Simons term of a complex gauge field up to
BRST-exact terms. We also compare the new theories with topological Yang-Mills
theories and find some interesting connections. In particular, the A-model
seems to offer a new perspective on Casson invariant and its relation to
Rozansky-Witten theory.Comment: 31 pages, no figure; v2. references adde
Janus and Multifaced Supersymmetric Theories
We investigate the various properties Janus supersymmetric Yang-Mills
theories. A novel vacuum structure is found and BPS monopoles and dyons are
studied. Less supersymmetric Janus theories found before are derived by a
simpler method. In addition, we find the supersymmetric theories when the
coupling constant depends on two and three spatial coordinates.Comment: 20 pages, no figures, typos, equations corrected. Additional comment
On instantons as Kaluza-Klein modes of M5-branes
Instantons and W-bosons in 5d maximally supersymmetric Yang-Mills theory
arise from a circle compactification of the 6d (2,0) theory as Kaluza-Klein
modes and winding self-dual strings, respectively. We study an index which
counts BPS instantons with electric charges in Coulomb and symmetric phases. We
first prove the existence of unique threshold bound state of (noncommutative)
U(1) instantons for any instanton number, and also show that charged instantons
in the Coulomb phase correctly give the degeneracy of SU(2) self-dual strings.
By studying SU(N) self-dual strings in the Coulomb phase, we find novel
momentum-carrying degrees on the worldsheet. The total number of these degrees
equals the anomaly coefficient of SU(N) (2,0) theory. We finally show that our
index can be used to study the symmetric phase of this theory, and provide an
interpretation as the superconformal index of the sigma model on instanton
moduli space.Comment: 54 pages, 2 figures. v2: references added, figure improved, added
comments on self-dual string anomaly, added new materials on the symmetric
phase index, other minor correction
Superconformal Index with Duality Domain Wall
We study a superconformal index for super Yang-Mills on with a half BPS duality domain wall inserted at the great
two-sphere in . The index is obtained by coupling the 3d generalized
superconformal index on the duality domain wall with 4d half-indices. We
further consider insertions of line operators to the configuration and propose
integral equations which express that the 3d index on duality domain wall is a
duality kernel relating half indices of two line operators related by the
duality map. We explicitly check the proposed integral equations for various
duality domain walls and line operators in the SU(2) theory. We
also briefly comment on a generalization to Gaiotto
theories with a simple example, SU(2) SYM with four flavors.Comment: v1: 25 pages, 4 figures. v2: comments and a reference added, minor
corrections. v3: 30 pages, new results and discussions added to sec 4.5 and
sec 5.1, eq 49 and eq 51 corrected, text improved; to appear in JHE
Opposing Regulation of PROX1 by Interleukin-3 Receptor and NOTCH Directs Differential Host Cell Fate Reprogramming by Kaposi Sarcoma Herpes Virus
Lymphatic endothelial cells (LECs) are differentiated from blood vascular endothelial cells (BECs) during embryogenesis and this physiological cell fate specification is controlled by PROX1, the master regulator for lymphatic development. When Kaposi sarcoma herpes virus (KSHV) infects host cells, it activates the otherwise silenced embryonic endothelial differentiation program and reprograms their cell fates. Interestingly, previous studies demonstrated that KSHV drives BECs to acquire a partial lymphatic phenotype by upregulating PROX1 (forward reprogramming), but stimulates LECs to regain some BEC-signature genes by downregulating PROX1 (reverse reprogramming). Despite the significance of this KSHV-induced bidirectional cell fate reprogramming in KS pathogenesis, its underlying molecular mechanism remains undefined. Here, we report that IL3 receptor alpha (IL3Rα) and NOTCH play integral roles in the host cell type-specific regulation of PROX1 by KSHV. In BECs, KSHV upregulates IL3Rα and phosphorylates STAT5, which binds and activates the PROX1 promoter. In LECs, however, PROX1 was rather downregulated by KSHV-induced NOTCH signal via HEY1, which binds and represses the PROX1 promoter. Moreover, PROX1 was found to be required to maintain HEY1 expression in LECs, establishing a reciprocal regulation between PROX1 and HEY1. Upon co-activation of IL3Rα and NOTCH, PROX1 was upregulated in BECs, but downregulated in LECs. Together, our study provides the molecular mechanism underlying the cell type-specific endothelial fate reprogramming by KSHV
RacB Regulates Cytoskeletal Function in \u3ci\u3eDictyostelium\u3c/i\u3e spp.
Thus far, 14 homologues of mammalian Rac proteins have been identified in Dictyostelium. It is unclear whether each of these genes has a unique function or to what extent they play redundant roles in actin cytoskeletal organization. To investigate the specific function of RacB, we have conditionally expressed wild-type (WT-RacB), dominant negative (N17-RacB), and constitutively activated (V12-RacB) versions of the protein. On induction, cells expressing V12-RacB stopped growing, detached from the surface, and formed numerous spherical surface protrusions while cells overexpressing WT-RacB became flattened on the surface. In contrast, cells overexpressing N17-RacB did not show any significant morphological abnormalities. The surface protrusions seen in V12-RacB cells appear to be actin-driven protrusions because they were enriched in F-actin and were inhibitable by cytochalasin A treatment. The protrusions in V12-RacB cells did not require myosin II activity, which distinguishes them from blebs formed by wild-type cells under stress. Finally, we examined the functional consequences of expression of wild-type and mutant RacB. Phagocytosis, endocytosis, and fluid phase efflux rates were reduced in all cell lines expressing RacB proteins but the greatest decrease was observed for cells expressing V12-RacB. From these results, we conclude that like other members of the Rho family, RacB induces polymerization of actin but the consequences of activation appear to be different from other Dictyostelium Rac proteins so far investigated, resulting in different morphological and functional changes in cells
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Genetic predisposition to obesity and inflammation in a tri-racial/ethnic breast cancer population
Aim: Multiple genes and genetic variants may contribute to racial/ethnic disparities in obesity-associated breast cancer diagnosis and prognosis. Therefore, we evaluate whether racial/ethnic differences in polygenic risk score (PRS) contribute to obesity and inflammatory biomarker in breast cancer patients.Methods: In a tri-racial/ethnic population of 403 breast cancer patients, 21% African American (AA), 65% Hispanic White (HW), and 14% non-Hispanic White (NHW), we evaluated racial/ethnic differences in obesity PRS, the association between PRS and an inflammatory biomarker C-reactive protein (CRP), and its implication in bariatric surgery eligibility. The obesity PRS was constructed via a weighted risk allele model using 35 obesity-related single nucleotide polymorphisms (SNPs). SAS version 9.3 for Windows (SAS Institute, Cary, NC, USA) was used to perform the logistic regression analysis.Results: About 74% of our study population were overweight or obese. The mean ± SD of obesity PRS was 45.03 ± 10.66 for obese patients and 39.36 ± 8.81 for non-obese patients (P < 0.0001). AA patients had a significantly higher obesity PRS than HW and NHW (P < 0.0001). The obesity PRS significantly correlated with body mass index and CRP levels (P < 0.0001) and was associated with bariatric surgery eligibility (OR = 4.32, 95%CI: 1.89-9.87).Conclusion: In summary, multiple obesity-associated SNPs contribute to racial/ethnic disparities in obesity of breast cancer patients; the obesity PRS has application in identifying breast cancer patients with higher genetic risk for obesity who may benefit from more aggressive weight management, such as bariatric surgery to improve breast cancer clinical outcomes
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