Sfermion masses in Nelson-Strassler type of models: SUSY standard models coupled with SCFTs

We study soft SUSY breaking parameters in the Nelson-Strassler type of models: SUSY standard models coupled with SCFTs. In this type of models, soft SUSY breaking parameters including sfermion masses can be suppressed around the decoupling scale of SCFTs. We clarify the condition to derive exponential suppression of sfermion masses within the framework of pure SCFTs. Such behavior is favorable for degeneracy of sfermion masses. However, the realistic sfermion masses are not quite degenerate due to the gauge couplings and the gaugino masses in the SM sector. We show the sfermion mass spectrum obtained in such models. The aspect of suppression for the soft SUSY breaking parameters is also demonstrated in an explicit model. We also give a mechanism generating the $\mu$-term of the Electro-Weak scale by a singlet field coupled with the SCFT.Comment: 28 pages, 8 figures, LaTeX file; corrected typos and references adde

Revisiting superparticle spectra in superconformal flavor models

We study superparticle spectra in the superconformal flavor scenario with non-universal gaugino masses. The non-universality of gaugino masses can lead to the wino-like or higgsino-like neutralino LSP. Furthermore, it is shown that the parameter space for the higgsino-like LSP includes the region where the fine-tuning problem can be improved. The degeneracy of soft scalar masses squared does not drastically change by taking ratios of gaugino masses of order one. The degeneracy of scalar masses for squarks and left-handed sleptons would be good to avoid the FCNC problem but that of right-handed slepton masses is weak. However, the overall size of right-handed slepton masses become larger when the bino becomes heavier. It is also pointed out that such region can be realized, and thus, that would be favorable to avoid the FCNC problem for soft scalar masses as well as A-terms.Comment: 18 pages, 12 figures, reference added, minor correction

Lepton Dipole Moments and Rare Decays in the CP-violating MSSM with Nonuniversal Soft-Supersymmetry Breaking

We investigate the muon anomalous magnetic dipole moment (MDM), the muon electric dipole moment (EDM) and the lepton-flavour-violating decays of the $\tau-$lepton, $\tau \to \mu \gamma$ and $\tau\to 3\mu$, in the CP-violating Minimal Supersymmetric Standard Model (MSSM) with nonuniversal soft-supersymmetry breaking. We evaluate numerically the muon EDM and the branching ratios $B(\tau \to \mu\gamma)$ and $B(\tau \to 3\mu)$, after taking into account the experimental constraints from the electron EDM and muon MDM. Upon imposition of the experimental limits on our theoretical predictions for the aforementioned branching ratios and the muon MDM, we obtain an upper bound of about $10^{-23} e\cdot cm$ on the muon EDM which lies well within the explorable reach of the proposed experiment at BNL.Comment: Latex, 26 pages, 8 figures, accepted for publication in Phys. Rev.

CP Violation in Kaon System in Supersymmetric SU(5) Model with Seesaw-Induced Neutrino Masses

CP violations in the kaon system are studied in supersymmetric SU(5) model with right-handed neutrinos. We pay a special attention to the renormalization group effect on the off-diagonal elements of the squark mass matrices. In particular, if the Yukawa couplings and mixings in the neutrino sector are sizable, off-diagonal elements of the right-handed down-type squark mass matrix are generated, which affect CP and flavor violations in decay processes of the kaon. We calculate supersymmetric contributions to epsilon (as well as Delta m_K), Br(K_L -> pi^0 nu \bar{nu}), and epsilon'/epsilon in this framework. We will see that the supersymmetric contribution to the epsilon parameter can be as large as (and in some case, larger than) the experimentally measured value. We also discuss its implication to future tests of the unitarity triangle of the Kobayashi-Maskawa matrix.Comment: 30 pages, 5 figue

Electric charge quantization and the muon anomalous magnetic moment

We investigate some proposals to solve the electric charge quantization puzzle, which simultaneously explain the recent measured deviation on the muon anomalous magnetic moment. For this we assess extensions of the Electro-Weak Standard Model spanning modifications on the scalar sector only. It is interesting to verify that one can have modest extensions which easily account for the solution for both problems.Comment: 20 pages, 1 figures, needs macro axodraw.st

An extended window of opportunity for G-CSF treatment in cerebral ischemia

BACKGROUND: Granulocyte-colony stimulating factor (G-CSF) is known as a powerful regulator of white blood cell proliferation and differentiation in mammals. We, and others, have shown that G-CSF is effective in treating cerebral ischemia in rodents, both relating to infarct size as well as functional recovery. G-CSF and its receptor are expressed by neurons, and G-CSF regulates apoptosis and neurogenesis, providing a rational basis for its beneficial short- and long-term actions in ischemia. In addition, G-CSF may contribute to re-endothelialisation and arteriogenesis in the vasculature of the ischemic penumbra. In addition to these trophic effects, G-CSF is a potent neuroprotective factor reliably reducing infarct size in different stroke models. RESULTS: Here, we have further delayed treatment and studied effects of G-CSF on infarct volume in the middle cerebral artery occlusion (MCAO) model and functional outcome in the cortical photothrombotic model. In the MCAO model, we applied a single dose of 60 μg/kg bodyweight G-CSF in rats 4 h after onset of ischemia. Infarct volume was determined 24 h after onset of ischemia. In the rat photothrombotic model, we applied 10 μg/kg bodyweight G-CSF daily for a period of 10 days starting either 24 or 72 h after induction of ischemia. G-CSF both decreased acute infarct volume in the MCAO model, and improved recovery in the photothrombotic model at delayed timepoints. CONCLUSION: These data further strengthen G-CSF's profile as a unique candidate stroke drug, and provide an experimental basis for application of G-CSF in the post-stroke recovery phase

Granulocyte-colony stimulating factor for stroke treatment: mechanisms of action and efficacy in preclinical studies

G-CSF is widely employed for the treatment of chemotherapy-induced neutropenia. Recently, neuroprotective effects of G-CSF in animal stroke models were discovered including infarct size reduction and enhancement of functional recovery. The underlying mechanisms of action of G-CSF in ischemia appear to be a direct anti-apoptotic activity in neurons and a neurogenesis inducing capacity. Additional effects may be based on the stimulation of new blood-vessel formation, the stimulation of immunocompetence and -modulation as well as on bone marrow mobilization. In addition to a discussion of these mechanisms, we will review the available preclinical studies and analyze their impact on the overall efficacy of G-CSF in experimental stroke

Neuroprotection by leptin in a rat model of permanent cerebral ischemia: effects on STAT3 phosphorylation in discrete cells of the brain

In addition to its effects in the hypothalamus to control body weight, leptin is involved in the regulation of neuronal function, development and survival. Recent findings have highlighted the neuroprotective effects of leptin against ischemic brain injury; however, to date, little is known about the role performed by the signal transducer and activator of transcription (STAT)-3, a major mediator of leptin receptor transduction pathway in the brain, in the beneficial effects of the hormone. Our data demonstrate that systemic acute administration of leptin produces neuroprotection in rats subjected to permanent middle cerebral artery occlusion (MCAo), as revealed by a significant reduction of the brain infarct volume and neurological deficit up to 7 days after the induction of ischemia. By combining a subcellular fractionation approach with immunohistofluorescence, we observe that neuroprotection is associated with a cell type-specific modulation of STAT3 phosphorylation in the ischemic cortex. The early enhancement of nuclear phospho-STAT3 induced by leptin in the astrocytes of the ischemic penumbra may contribute to a beneficial effect of these cells on the evolution of tissue damage. In addition, the elevation of phospho-STAT3 induced by leptin in the neurons after 24 h MCAo is associated with an increased expression of tissue inhibitor of matrix metalloproteinases-1 in the cortex, suggesting its possible involvement to the neuroprotection produced by the adipokine

Axotomy induces axonogenesis in hippocampal neurons through STAT3

After axotomy of embryonic hippocampal neurons in vitro, some of the axotomized axons lose their identity, and new axons arise and grow. This axotomy-induced axonogenesis requires importin, suggesting that some injury-induced signals are transported via axons to elicit axonogenesis after axotomy. In this study, we show that STAT3 is activated in response to axotomy. Because STAT3 was co-immunoprecipitated with importin β in the axotomized neurons, we suggest that STAT3 is retrogradely transported as molecular cargo of importin α/β heterodimers. Indeed, inhibition of importin α binding with STAT3 resulted in the attenuation of axonogenesis. Silencing STAT3 blocked the axonogenesis, demonstrating that STAT3 is necessary for axotomy-induced axonogenesis. Furthermore, the overexpression of STAT3 enhanced axotomy-induced axonogenesis. Taken together, these results demonstrate that activation and retrograde transport of STAT3 in injured axons have key roles in the axotomy-induced axonogenesis of hippocampal neurons

Synergetic Effects of Granulocyte-Colony Stimulating Factor and Cognitive Training on Spatial Learning and Survival of Newborn Hippocampal Neurons

Granulocyte-Colony Stimulating Factor (G-CSF) is an endogenous hematopoietic growth factor known for its role in the proliferation and differentiation of cells of the myeloic lineage. Only recently its significance in the CNS has been uncovered. G-CSF attenuates apoptosis and controls proliferation and differentiation of neural stem cells. G-CSF activates upstream kinases of the cAMP response element binding protein (CREB), which is thought to facilitate the survival of neuronal precursors and to recruit new neurons into the dentate gyrus. CREB is also essential for spatial long-term memory formation. To assess the role and the potential of this factor on learning and memory-formation we systemically administered G-CSF in rats engaged in spatial learning in an eight-arm radial maze. G-CSF significantly improved spatial learning and increased in combination with cognitive training the survival of newborn neurons in the hippocampus as measured by bromodeoxyuridine and doublecortin immunohistochemistry. Additionally, G-CSF improved re-acquisition of spatial information after 26 days. These findings support the hypothesis that G-CSF can enhance learning and memory formation. Due to its easy applicability and its history as a well-tolerated hematological drug, the use of G-CSF opens up new neurological treatment opportunities in conditions where learning and memory-formation deficits occur