Non-perturbative Landau gauge and infrared critical exponents in QCD

We discuss Faddeev-Popov quantization at the non-perturbative level and show that Gribov's prescription of cutting off the functional integral at the Gribov horizon does not change the Schwinger-Dyson equations, but rather resolves an ambiguity in the solution of these equations. We note that Gribov's prescription is not exact, and we therefore turn to the method of stochastic quantization in its time-independent formulation, and recall the proof that it is correct at the non-perturbative level. The non-perturbative Landau gauge is derived as a limiting case, and it is found that it yields the Faddeev-Popov method in Landau gauge with a cut-off at the Gribov horizon, plus a novel term that corrects for over-counting of Gribov copies inside the Gribov horizon. Non-perturbative but truncated coupled Schwinger-Dyson equations for the gluon and ghost propagators $D(k)$ and $G(k)$ in Landau gauge are solved asymptotically in the infrared region. The infrared critical exponents or anomalous dimensions, defined by $D(k) \sim 1/(k^2)^{1 + a_D}$ and $G(k) \sim 1/(k^2)^{1 + a_G}$ are obtained in space-time dimensions $d = 2, 3, 4$. Two possible solutions are obtained with the values, in $d = 4$ dimensions, $a_G = 1, a_D = -2$, or $a_G = [93 - (1201)^{1/2}]/98 \approx 0.595353, a_D = - 2a_G$.Comment: 26 pages. Modified 2.25.02 to update references and to clarify Introduction and Conclusio

Alterations of EGFR, p53 and PTEN that mimic changes found in basal-like breast cancer promote transformation of human mammary epithelial cells

Breast cancer can be classified into different molecular subtypes with varying clinical and pathological characteristics. The basal-like breast cancer subtype represents one of the most aggressive and lethal types of breast cancer, and due to poor mechanistic understanding, it lacks targeted therapy. Many basal-like breast cancer patient samples display alterations of established drivers of cancer development, including elevated expression of EGFR, p53 inactivating mutations and loss of expression of the tumor suppressor PTEN; however, their contribution to human basal-like breast cancer pathogenesis remains ill-defined. Using non-transformed human mammary epithelial cells, we set out to determine whether altering EGFR, p53 and PTEN in different combinations could contribute to basal-like breast cancer progression through transformation of cells. Altering PTEN in combination with either p53 or EGFR in contrast to any of the single alterations caused increased growth of transformed colonies in soft agar. Concomitantly modifying all three genes led to the highest rate of cellular proliferation and the greatest degree of anchorage-independent colony formation. Results from our effort to engineer a model of BBC expressing alterations of EGFR, p53 and PTEN suggest that these changes are cooperative and likely play a causal role in basal-like breast cancer pathogenesis. Consideration should be given to targeting EGFR and restoring p53 and PTEN signaling simultaneously as a strategy for treatment of this subtype of breast cancer

2019 American College of Rheumatology/Arthritis Foundation Guideline for the Management of Osteoarthritis of the Hand, Hip, and Knee

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/153772/1/acr24131.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/153772/2/acr24131_am.pd

The E3 ubiquitin ligase TRIM25 regulates adipocyte differentiation via proteasomemediated degradation of PPAR gamma

Peroxisome proliferator-activated receptor gamma (PPAR??) is a ligand-dependent transcription factor that regulates adipocyte differentiation and glucose homeostasis. The transcriptional activity of PPAR?? is regulated not only by ligands but also by post-translational modifications (PTMs). In this study, we demonstrate that a novel E3 ligase of PPAR??, tripartite motif-containing 25 (TRIM25), directly induced the ubiquitination of PPAR??, leading to its proteasome-dependent degradation. During adipocyte differentiation, both TRIM25 mRNA and protein expression significantly decreased and negatively correlated with the expression of PPAR??. The stable expression of TRIM25 reduced PPAR?? protein levels and suppressed adipocyte differentiation in 3T3-L1 cells. In contrast, the specific knockdown of TRIM25 increased PPAR?? protein levels and stimulated adipocyte differentiation. Furthermore, TRIM25-knockout mouse embryonic fibroblasts (MEFs) exhibited an increased adipocyte differentiation capability compared with wild-type MEFs. Taken together, these data indicate that TRIM25 is a novel E3 ubiquitin ligase of PPAR?? and that TRIM25 is a novel target for PPAR??-associated metabolic diseases

SS18 Together with Animal-Specific Factors Defines Human BAF-Type SWI/SNF Complexes

Contains fulltext : 94049.pdf (publisher's version ) (Open Access

Guidelines for designing travel surveys for statewide transportation planning. Final report.

Federal Highway Administration, Office of Highway Planning, Washington, D.C.Mode of access: Internet.Author corporate affiliation: Peat, Marwick, Mitchell and Company, Washington, D.C.Subject code: SDBSubject code: WMEGSubject code: WTSubject code: WWDSubject code: YCDHSubject code: YCDRSubject code: YE

Travel Survey Procedures for Statewide Transportation Planning

DOT-FH-11-8592This report describes and evaluates alternative travel survey procedures that have been used for or are potentially applicable to statewide transportation planning. The types of survey procedures discussed in the report include household, roadside, and modal passenger survey techniques. The potential uses, strengths, and weaknesses of each type of survey are assessed. The report presents illustrative survey instruments, survey .costs, and procedures for administering surveys for statewide transportation planning