Carolina R | Universidad de San Buenaventura Cartagena (original) (raw)
Papers by Carolina R
Canadian Journal of Anaesthesia-journal Canadien D Anesthesie, 1990
H.-G. Feichtinger
Physics Letters B, 1994
q,10, T. Neumann q, R. S inkus q, K. Wick q, E. B adura r, B.D. B urow r, A. Ftirtjes r.ll, E. Lo... more q,10, T. Neumann q, R. S inkus q, K. Wick q, E. B adura r, B.D. B urow r, A. Ftirtjes r.ll, E. Lohrmann r, J. Milewski r, M. Nakahata r,12, N. Pavel r, G. Poelz r, W. Schott r, J. Terron r,7, E Zetsche r,
Physical Review Letters, 2003
Fuel and Energy Abstracts, 2011
A measurement of the Z/γ⁎Z/γ⁎ transverse momentum (pTZ) distribution in proton–proton collisions ... more A measurement of the Z/γ⁎Z/γ⁎ transverse momentum (pTZ) distribution in proton–proton collisions at s=7 TeV is presented using Z/γ⁎→e+e−Z/γ⁎→e+e− and Z/γ⁎→μ+μ−Z/γ⁎→μ+μ− decays collected with the ATLAS detector in data sets with integrated luminosities of 35 pb−1 and 40 pb−1, respectively. The normalized differential cross sections are measured separately for electron and muon decay channels as well as for their combination up to pTZ of 350 GeV for invariant dilepton masses 66 GeV<mℓℓ<116 GeV66 GeV<mℓℓ<116 GeV. The measurement is compared to predictions of perturbative QCD and various event generators. The prediction of resummed QCD combined with fixed order perturbative QCD is found to be in good agreement with the data.
Molecular and Cellular Biochemistry, 1998
We have blocked creatine kinase (CK) mediated phosphocreatine (PCr) ⇄ ATP transphosphorylation in... more We have blocked creatine kinase (CK) mediated phosphocreatine (PCr) ⇄ ATP transphosphorylation in mitochondria and cytosol of skeletal muscle by knocking out the genes for the mitochondrial (ScCKmit) and the cytosolic (M-CK) CK isoforms in mice. Animals which carry single or double mutations, if kept and tested under standard laboratory conditions, have surprisingly mild changes in muscle physiology. Strenuous ex vivo conditions were necessary to reveal that MM-CK absence in single and double mutants leads to a partial loss of tetanic force output. Single ScCKmit deficiency has no noticeable effects but in combination the mutations cause slowing of the relaxation rate. Importantly, our studies revealed that there is metabolic and cytoarchitectural adaptation to CK defects in energy metabolism. The effects involve mutation type-dependent alterations in the levels of AMP, IMP, glycogen and phosphomonoesters, changes in activity of metabolic enzymes like AMP-deaminase, alterations in mitochondrial volume and contractile protein (MHC isoform) profiles, and a hyperproliferation of the terminal cysternae of the SR (in tubular aggregates). This suggests that there is a compensatory resiliency of loss-of-function and redirection of flux distributions in the metabolic network for cellular energy in our mutants.
Canadian Journal of Anaesthesia-journal Canadien D Anesthesie, 1990
H.-G. Feichtinger
Physics Letters B, 1994
q,10, T. Neumann q, R. S inkus q, K. Wick q, E. B adura r, B.D. B urow r, A. Ftirtjes r.ll, E. Lo... more q,10, T. Neumann q, R. S inkus q, K. Wick q, E. B adura r, B.D. B urow r, A. Ftirtjes r.ll, E. Lohrmann r, J. Milewski r, M. Nakahata r,12, N. Pavel r, G. Poelz r, W. Schott r, J. Terron r,7, E Zetsche r,
Physical Review Letters, 2003
Fuel and Energy Abstracts, 2011
A measurement of the Z/γ⁎Z/γ⁎ transverse momentum (pTZ) distribution in proton–proton collisions ... more A measurement of the Z/γ⁎Z/γ⁎ transverse momentum (pTZ) distribution in proton–proton collisions at s=7 TeV is presented using Z/γ⁎→e+e−Z/γ⁎→e+e− and Z/γ⁎→μ+μ−Z/γ⁎→μ+μ− decays collected with the ATLAS detector in data sets with integrated luminosities of 35 pb−1 and 40 pb−1, respectively. The normalized differential cross sections are measured separately for electron and muon decay channels as well as for their combination up to pTZ of 350 GeV for invariant dilepton masses 66 GeV<mℓℓ<116 GeV66 GeV<mℓℓ<116 GeV. The measurement is compared to predictions of perturbative QCD and various event generators. The prediction of resummed QCD combined with fixed order perturbative QCD is found to be in good agreement with the data.
Molecular and Cellular Biochemistry, 1998
We have blocked creatine kinase (CK) mediated phosphocreatine (PCr) ⇄ ATP transphosphorylation in... more We have blocked creatine kinase (CK) mediated phosphocreatine (PCr) ⇄ ATP transphosphorylation in mitochondria and cytosol of skeletal muscle by knocking out the genes for the mitochondrial (ScCKmit) and the cytosolic (M-CK) CK isoforms in mice. Animals which carry single or double mutations, if kept and tested under standard laboratory conditions, have surprisingly mild changes in muscle physiology. Strenuous ex vivo conditions were necessary to reveal that MM-CK absence in single and double mutants leads to a partial loss of tetanic force output. Single ScCKmit deficiency has no noticeable effects but in combination the mutations cause slowing of the relaxation rate. Importantly, our studies revealed that there is metabolic and cytoarchitectural adaptation to CK defects in energy metabolism. The effects involve mutation type-dependent alterations in the levels of AMP, IMP, glycogen and phosphomonoesters, changes in activity of metabolic enzymes like AMP-deaminase, alterations in mitochondrial volume and contractile protein (MHC isoform) profiles, and a hyperproliferation of the terminal cysternae of the SR (in tubular aggregates). This suggests that there is a compensatory resiliency of loss-of-function and redirection of flux distributions in the metabolic network for cellular energy in our mutants.