27 research outputs found
Universality in Decays and Constraints on the Slepton Masses
The leptonic decays are calculated at the 1-loop level in the Minimal
Supersymmetric Standard Model. The deviation from the
universality is studied as a function of the supersymmetric parameters and
discussed in the context of the expected improvement of the experimental
accuracy.Comment: 10 pages, standard LaTeX, report DFPD 94/TH-27,MPI-Ph/94-24,DESY
94-077. 5 figures can be obtained via conventional mail from P. Chankowski
upon reques
Complete On-Shell Renormalization Scheme for the Minimal Supersymmetric Higgs Sector
Systematic on-shell renormalization programme is carried out for the Higgs
and gauge boson sectors of the Minimal Supersymmetric Standard Model. Complete
1-loop results for the 2- and 3-point Green's functions are explicitly given.
The Higgs boson masses and the cross sections for the neutral scalar production
in the colliders are calculated.Comment: 64 pages, 10 figures (not included, availaible on request in
PostScript format), LaTeX, preprint no MPI-Ph/92-117 and DFPD 93/TH/1
Identification of Autophagy as a Functional Target Suitable for the Pharmacological Treatment of Mitochondrial Membrane Protein-Associated Neurodegeneration (MPAN) In Vitro
Mitochondrial membrane protein-associated neurodegeneration (MPAN) is a relentlessly progressive neurodegenerative disorder caused by mutations in the C19orf12 gene. C19orf12 has been implicated in playing a role in lipid metabolism, mitochondrial function, and autophagy, however, the precise functions remain unknown. To identify new robust cellular targets for small compound treatments, we evaluated reported mitochondrial function alterations, cellular signaling, and autophagy in a large cohort of MPAN patients and control fibroblasts. We found no consistent alteration of mitochondrial functions or cellular signaling messengers in MPAN fibroblasts. In contrast, we found that autophagy initiation is consistently impaired in MPAN fibroblasts and show that C19orf12 expression correlates with the amount of LC3 puncta, an autophagy marker. Finally, we screened 14 different autophagy modulators to test which can restore this autophagy defect. Amongst these compounds, carbamazepine, ABT-737, LY294002, oridonin, and paroxetine could restore LC3 puncta in the MPAN fibroblasts, identifying them as novel potential therapeutic compounds to treat MPAN. In summary, our study confirms a role for C19orf12 in autophagy, proposes LC3 puncta as a functionally robust and consistent readout for testing compounds, and pinpoints potential therapeutic compounds for MPAN.</p
Identification of Autophagy as a Functional Target Suitable for the Pharmacological Treatment of Mitochondrial Membrane Protein-Associated Neurodegeneration (MPAN) In Vitro
Mitochondrial membrane protein-associated neurodegeneration (MPAN) is a relentlessly progressive neurodegenerative disorder caused by mutations in the C19orf12 gene. C19orf12 has been implicated in playing a role in lipid metabolism, mitochondrial function, and autophagy, however, the precise functions remain unknown. To identify new robust cellular targets for small compound treatments, we evaluated reported mitochondrial function alterations, cellular signaling, and autophagy in a large cohort of MPAN patients and control fibroblasts. We found no consistent alteration of mitochondrial functions or cellular signaling messengers in MPAN fibroblasts. In contrast, we found that autophagy initiation is consistently impaired in MPAN fibroblasts and show that C19orf12 expression correlates with the amount of LC3 puncta, an autophagy marker. Finally, we screened 14 different autophagy modulators to test which can restore this autophagy defect. Amongst these compounds, carbamazepine, ABT-737, LY294002, oridonin, and paroxetine could restore LC3 puncta in the MPAN fibroblasts, identifying them as novel potential therapeutic compounds to treat MPAN. In summary, our study confirms a role for C19orf12 in autophagy, proposes LC3 puncta as a functionally robust and consistent readout for testing compounds, and pinpoints potential therapeutic compounds for MPAN
Identification of Autophagy as a Functional Target Suitable for the Pharmacological Treatment of Mitochondrial Membrane Protein-Associated Neurodegeneration (MPAN) In Vitro
Mitochondrial membrane protein-associated neurodegeneration (MPAN) is a relentlessly progressive neurodegenerative disorder caused by mutations in the C19orf12 gene. C19orf12 has been implicated in playing a role in lipid metabolism, mitochondrial function, and autophagy, however, the precise functions remain unknown. To identify new robust cellular targets for small compound treatments, we evaluated reported mitochondrial function alterations, cellular signaling, and autophagy in a large cohort of MPAN patients and control fibroblasts. We found no consistent alteration of mitochondrial functions or cellular signaling messengers in MPAN fibroblasts. In contrast, we found that autophagy initiation is consistently impaired in MPAN fibroblasts and show that C19orf12 expression correlates with the amount of LC3 puncta, an autophagy marker. Finally, we screened 14 different autophagy modulators to test which can restore this autophagy defect. Amongst these compounds, carbamazepine, ABT-737, LY294002, oridonin, and paroxetine could restore LC3 puncta in the MPAN fibroblasts, identifying them as novel potential therapeutic compounds to treat MPAN. In summary, our study confirms a role for C19orf12 in autophagy, proposes LC3 puncta as a functionally robust and consistent readout for testing compounds, and pinpoints potential therapeutic compounds for MPAN.</p
Viable -- Yukawa Unification in SUSY SO(10)
The supersymmetric SO(10) GUT with ---- Yukawa coupling
unification has problems with correct electroweak symmetry breaking,
experimental constraints (especially ) and neutralino
abundance, if the scalar masses are universal at the GUT scale. We point out
that non-universality of the scalar masses at the GUT scale generated both by
(1) renormalization group running from the Planck scale to the GUT scale and
(2) --term contribution induced by the reduction of the rank of the gauge
group, has a desirable pattern to make the model phemenologically viable (in
fact the only one which is consistent with experimental and cosmological
constraints). At the same time the top quark mass has to be either close to its
quasi IR--fixed point value or below 170 GeV. We also briefly discuss the
spectrum of superpartners which is then obtained.Comment: 11 pages LaTeX, 2 PS figures as uuencoded tar-gzipped fil
From Flavour to SUSY Flavour Models
If supersymmetry (SUSY) will be discovered, successful models of flavour not
only have to provide an explanation of the flavour structure of the Standard
Model fermions, but also of the flavour structure of their scalar
superpartners. We discuss aspects of such "SUSY flavour" models, towards
predicting both flavour structures, in the context of supergravity (SUGRA). We
point out the importance of carefully taking into account SUSY-specific
effects, such as 1-loop SUSY threshold corrections and canonical normalization,
when fitting the model to the data for fermion masses and mixings. This
entangles the flavour model with the SUSY parameters and leads to interesting
predictions for the sparticle spectrum. We demonstrate these effects by
analyzing an example class of flavour models in the framework of an SU(5) Grand
Unified Theory with a family symmetry with real triplet representations. For
flavour violation through the SUSY soft breaking terms, the class of models
realizes a scheme we refer to as "Trilinear Dominance", where flavour violation
effects are dominantly induced by the trilinear terms.Comment: 44 pages, 10 figures, version published in Nuclear Physics
Finite Supersymmetric Threshold Corrections to CKM Matrix Elements in the Large Regime
We evaluate the finite 1-loop threshold corrections, proportional to
, to the down quark mass matrix. These result in corrections to down
quark masses and to Cabibbo-Kobayashi-Maskawa [CKM] matrix elements. The
corrections to CKM matrix elements are the novel feature of this paper. For
grand unified theories with large these corrections may
significantly alter the low energy predictions of four of the CKM matrix
elements and the Jarlskog parameter J, a measure of CP violation. The angles
and of the unitarity triangle and the ratio
, however, are not corrected to this order. We also
discuss these corrections in the light of recent models for fermion masses.
Here the corrections may be useful in selecting among the various models.
Moreover, if one model fits the data, it will only do so for a particular range
of SUSY parameters.Comment: 15 pages, 3 figures not included; hard copy of the figures may be
obtained upon reques