On the Bhabha scattering for z=2 Lifshitz QED

In this paper, we compute and discuss the differential cross-section of the Bhabha scattering in the framework of the z = 2 Lifshitz quantum electrodynamics (QED). We start by constructing the classical solutions for the fermionic fields, in particular the completeness relations, and also derive the theory's propagators. Afterwards, we compute the photon exchange and pair annihilation contributions for the Bhabha's process, and upon achieving the results we establish the magnitude of the theory's free parameter by looking for small deviations of the QED tree results.

Genotipagem dos isolados de Giardia duodenalis em famílias de pescadores da colônia de Porto Said, Botucatu, São Paulo

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

GQ-16, a Novel Peroxisome Proliferator-activated Receptor gamma (PPAR gamma) Ligand, Promotes Insulin Sensitization without Weight Gain

The recent discovery that peroxisome proliferator-activated receptor gamma (PPAR gamma) targeted anti-diabetic drugs function by inhibiting Cdk5-mediated phosphorylation of the receptor has provided a new viewpoint to evaluate and perhaps develop improved insulin-sensitizing agents. Herein we report the development of a novel thiazolidinedione that retains similar anti-diabetic efficacy as rosiglitazone in mice yet does not elicit weight gain or edema, common side effects associated with full PPAR gamma activation. Further characterization of this compound shows GQ-16 to be an effective inhibitor of Cdk5-mediated phosphorylation of PPAR gamma. The structure of GQ-16 bound to PPAR gamma demonstrates that the compound utilizes a binding mode distinct from other reported PPAR gamma ligands, although it does share some structural features with other partial agonists, such as MRL-24 and PA-082, that have similarly been reported to dissociate insulin sensitization from weight gain. Hydrogen/deuterium exchange studies reveal that GQ-16 strongly stabilizes the beta-sheet region of the receptor, presumably explaining the compound's efficacy in inhibiting Cdk5-mediated phosphorylation of Ser-273. Molecular dynamics simulations suggest that the partial agonist activity of GQ-16 results from the compound's weak ability to stabilize helix 12 in its active conformation. Our results suggest that the emerging model, whereby "ideal" PPAR gamma-based therapeutics stabilize the beta-sheet/Ser-273 region and inhibit Cdk5-mediated phosphorylation while minimally invoking adipogenesis and classical agonism, is indeed a valid framework to develop improved PPAR gamma modulators that retain antidiabetic actions while minimizing untoward effects.

Electroweak Sudakov effects in W, Z and γ production at large transverse momentum

We study electroweak Sudakov effects in single W, Z and γ production at large transverse momentum using soft collinear effective theory. We present a factorized form of the cross section near the partonic threshold with both QCD and electroweak effects included and compute the electroweak corrections arising at different scales. We analyze their size relative to the QCD corrections as well as the impact of strong-electroweak mixing terms. Numerical results for the vector-boson cross sections at the Large Hadron Collider are presented.

Ist das Schlachten der Thiere nach jüdischem Ritus wirklich Thierquälerei? : Ein Wort der Verwahrung z. zur Abwehr

von Hermann Engelbert

Programm zur Eröffnung des jüdisch-theologischen Seminars zu Breslau "Fränckel'sche Stiftung" : den 16. Ab 5614, 10. August 1854

Enth.: Über palästinische und alexandrinische Schriftforschung / vom Direktor Z. Frankel. Zur Geschichte des jüdisch-theologischen Seminars / vom Kuratorium

Frauentypen : unseren Führerinnen z. Erinnerung an d. Esra-Tagung Fulda im Tammus 5681

von Hannah Meyer-Breuer

Devārîm aḥadîm : kôlēl ʿinyānîm šônîm derāšā we-sippûr û-māzāl ; oif welcher weize man kann be-emes reṭṭen Galitzien ...

Jitzḥak Weber

Cerebral cortical astroglia from the trisomy 16 mouse, a model for Down syndrome, produce neuronal cholinergic deficits in cell culture

Trisomy 21 (Down syndrome) is associated with a high incidence of Alzheimer disease and with deficits in cholinergic function in humans. We used the trisomy 16 (Ts16) mouse model for Down syndrome to identify the cellular basis for the cholinergic dysfunction. Cholinergic neurons and cerebral cortical astroglia, obtained separately from Ts16 mouse fetuses and their euploid littermates, were cultured in various combinations. Choline acetyltransferase activity and cholinergic neuron number were both depressed in cultures in which both neurons and glia were derived from Ts16 fetuses. Cholinergic function of normal neurons was significantly down-regulated by coculture with Ts16 glia. Conversely, neurons from Ts16 animals could express normal cholinergic function when grown with normal glia. These observations indicate that astroglia may contribute strongly to the abnormal cholinergic function in the mouse Ts16 model for Down syndrome. The Ts16 glia could lack a cholinergic supporting factor present in normal glia or contain a factor that down-regulates cholinergic function.