A unique Z_4^R symmetry for the MSSM

We consider the possible anomaly free Abelian discrete symmetries of the MSSM that forbid the mu-term at perturbative order. Allowing for anomaly cancellation via the Green-Schwarz mechanism we identify discrete R-symmetries as the only possibility and prove that there is a unique Z_4^R symmetry that commutes with SO(10). We argue that non-perturbative effects will generate a mu-term of electroweak order thus solving the mu-problem. The non-perturbative effects break the Z_4^R symmetry leaving an exact Z_2 matter parity. As a result dimension four baryon- and lepton-number violating operators are absent while, at the non-perturbative level, dimension five baryon- and lepton-number violating operators get induced but are highly suppressed so that the nucleon decay rate is well within present bounds.Comment: 6 page

Discrete R symmetries for the MSSM and its singlet extensions

We determine the anomaly free discrete R symmetries, consistent with the MSSM, that commute with SU(5) and suppress the $\mu$ parameter and nucleon decay. We show that the order M of such $Z_M^R$ symmetries has to divide 24 and identify 5 viable symmetries. The simplest possibility is a $Z_4^R$ symmetry which commutes with SO(10). We present a string-derived model with this $Z_4^R$ symmetry and the exact MSSM spectrum below the GUT scale; in this model $Z_4^R$ originates from the Lorentz symmetry of compactified dimensions. We extend the discussion to include the singlet extensions of the MSSM and find $Z_4^R$ and $Z_8^R$ are the only possible symmetries capable of solving the $\mu$ problem in the NMSSM. We also show that a singlet extension of the MSSM based on a $Z_{24}^R$ symmetry can provide a simultaneous solution to the $\mu$ and strong CP problem with the axion coupling in the favoured window.Comment: 44+1 pages, 2 figure

Rosiglitazone Inhibits Transforming Growth Factor-β1 Mediated Fibrogenesis in ADPKD Cyst-Lining Epithelial Cells

BACKGROUND: Interstitial fibrosis plays an important role in progressive renal dysfunction in autosomal dominant polycystic kidney disease (ADPKD). In our previous studies, we confirmed that PPAR-γ agonist, rosiglitazone could protect renal function and prolong the survival of a slowly progressive ADPKD animal model by reducing renal fibrosis. However, the mechanism remains unknown. METHODS: Primary culture epithelial cells pretreated with TGF-β1 were incubated with rosiglitazone. Extracellular matrix proteins were detected using real-time PCR and Western blotting. MAPK and Smad2 phosphorylation were measured with western blot. ERK1/2 pathway and P38 pathway were inhibited with the specific inhibitors PD98059 and SB203580. The Smad2 pathway was blocked with the siRNA. To address whether PPAR-γ agonist-mediated inhibition of TGF-β1-induced collagen type I expression was mediated through a PPAR-γ dependent mechanism, genetic and pharmaceutical approaches were used to block the activity of endogenous PPARγ. RESULTS: TGF-β1-stimulated collagen type I and fibronectin expression of ADPKD cyst-lining epithelia were inhibited by rosiglitazone in a dosage-dependent manner. Smad2, ERK1/2 and P38 pathways were activated in response to TGF-β1; however, TGF-β1 had little effect on JNK pathway. Rosiglitazone suppressed TGF-β1 induced Smad2 activation, while ERK1/2 and P38MAPK signals remained unaffected. Rosiglitazone could also attenuate TGF-β1-stimulated collagen type I and fibronectin expression in primary renal tubular epithelial cells, but had no effect on TGF-β1-induced activation of Smad2, ERK1/2 and P38 pathways. There was no crosstalk between the Smad2 and MAPK pathways in ADPKD cyst-lining epithelial cells. These inhibitory effects of rosiglitazone were reversed by the PPARγ specific antagonist GW9662 and PPARγ siRNA. CONCLUSION: ADPKD cyst-lining epithelial cells participate in TGF-β1 mediated fibrogenesis. Rosiglitazone could suppress TGF-β1-induced collagen type I and fibronectin expression in ADPKD cyst-lining epithelia through modulation of the Smad2 pathway. Our study may provide therapeutic basis for clinical applications of rosiglitazone in retarding the progression of ADPKD

Searching for the Standard Model in the String Landscape : SUSY GUTs

The goal of the present review article is to describe the ingredients necessary to find the Standard Model in the string landscape.Comment: 70 pages, 20 figures, this review article will be published in Reports on Progress in Physic

Extranodal diffuse non hodgkin lymphoma in the thigh

<p>Abstract</p> <p>Diffuse large B-cell lymphoma usually starts as a rapidly growing mass in an internal lymph node and can grow in other areas such as the bone or intestines. About 1/3 of these lymphomas are confined to one part of the body when they are localized. In the case of a 78-year-old man, an extensive tumour was located on the right thigh. Biopsies of the tumour revealed diffuse proliferation of large lymphoid cells which have totally affected the normal architecture of striated muscle. The patient received multimodality treatment including chemotherapy of the CHOP regimen and adjuvant radiotherapy. Despite this being a fast growing lymphoma, about 3 out of 4 people will have no signs of disease after initial treatment, and about half of all people with this lymphoma are cured with therapy.</p