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B Patton

Publications and source records attributed to B Patton.

8 recordsLinked to original sources
PubMed2006

New insights on the mechanism of palladium-catalyzed hydrolysis of sodium borohydride from 11B NMR measurements.

To gain insight on the mechanistic aspects of the palladium-catalyzed hydrolysis of NaBH(4) in alkaline media, the kinetics of the reaction has been investigated by (11)B NMR (nuclear magnetic resonance) measurements taken at different times during the reaction course. Working with BH(4)(-) concentration in the range 0.05-0.1 M and with a [substrate]/[catalyst] molar ratio of 0.03-0.11, hydrolysis has been found to follow a first-order kinetic dependence from concentration of both the substrate and the catalyst (Pd/C 10 wt %). We followed the reaction of NaBH(4) and its perdeuterated analogue NaBD(4) in H(2)O, in D(2)O and H(2)O/D(2)O mixtures. When the process was carried out in D(2)O, deuterium incorporation in BH(4)(-) afforded BH(4)(-)(n)D(n)(-) (n = 1, 2, 3, 4) species, and a competition between hydrolysis and hydrogen/deuterium exchange processes was observed. By fitting the kinetics NMR data by nonlinear least-squares regression techniques, the rate constants of the elementary steps involved in the palladium-catalyzed borohydride hydrolysis have been evaluated. Such a regression analysis was performed on a reaction scheme wherein the starting reactant BH(4)(-) is allowed both to reversibly exchange hydrogen with deuterium atoms of D(2)O and to irreversibly hydrolyze into borohydroxy species B(OD)(4)(-). In contrast to acid-catalyzed hydrolysis of sodium borohydride, our results indicate that in the palladium-catalyzed process the rate constants of the exchange processes are higher than those of the corresponding hydrolysis reactions.

Journal Article↗
PubMed2005

Coherent control and polarization readout of individual excitonic states.

We present measurements and simulations of coherent control and readout of the polarization in individual exciton states. The readout is accomplished by transient four-wave mixing detected by heterodyne spectral interferometry. We observe Rabi oscillations in the polarization, which show half the period of the Rabi oscillations in the population. A decrease of the oscillation amplitude with pulse area is observed, which is not accompanied by a change in the dephasing time. This suggests the transfer of the excitation to other states as the origin of the Rabi-oscillation damping. Detuning of the excitation enables the control of the polarization in phase and amplitude and is in qualitative agreement with simulations for a two-level system. Additionally, simultaneous Rabi flopping of several spatially and energetically close exciton states is demonstrated.

Journal Article↗
PubMed2002

Fast nuclear spin relaxation in hyperpolarized solid 129Xe.

We report extensive new measurements of the longitudinal relaxation time T1 of 129Xe nuclear spins in solid xenon. For temperatures T<120 K and magnetic fields B>0.05 T, we found T1 on the order of hours, in good agreement with previous measurements and with the predicted phonon-scattering limit for the spin-rotation interaction. For T>120 K, our new data show that T1 can be much shorter than the phonon scattering limit. For B = 0.06 T, a field often used to accumulate hyperpolarized xenon, T1 is approximately 6 s near the Xe melting point T(m) = 161.4 K. From T = 50 K to T(m), the new data are in excellent agreement with the theoretical prediction that the relaxation is due to (i) modulation of the spin-rotation interaction by phonons, and (ii) modulation of the dipole-dipole interaction by vacancy diffusion.

Journal Article↗
PubMed2001

Functional abrogation of p53 is required for T-Ag induced proliferation in cardiomyocytes.

Targeted expression of the SV40 large T-antigen oncoprotein (T-Ag) induces cardiomyocyte proliferation in the atria and ventricles of transgenic mice. Previous studies have identified the p53 tumor suppressor, p107 (a homologue of the retinoblastoma tumor suppressor), and p193 (a novel BH3 only proapoptosis protein) as prominent TAg binding proteins in cardiomyocyte cell lines derived from these transgenic mice. To further explore the significance of these protein-protein interactions in the regulation of cardiomyocyte proliferation, a transgene comprising the human atrial natriuretic factor (ANF) promoter and sequences encoding a mutant T-Ag lacking the p53 binding domain was generated. Repeated micro-injection of this DNA gave rise to genetically mosaic animals with minimal transgene content, suggesting that widespread cardiac expression of mutant T-Ag was deleterious. This notion was supported by the observation that the transgene was selectively lost from the cardiac myocytes (but not the cardiac fibroblasts) in the mosaic animals. Crosses between the mosaic mice and animals expressing a cardiac restricted dominant negative p53 resulted in transgene transmission with ensuing overt cardiac tumorigenesis. Transfection of the mutant T-Ag in embryonic stem (ES) cell-derived cardiomyocytes resulted in wide-spread cell death with characteristics typical of apoptosis. Co-transfection with a dominant negative p53 transgene rescued mutant TAg-induced cell death in the ES-derived cardiomyocyte cultures, resulting in a marked proliferative response similar to that seen in vivo with the rescued transgenic mouse study. These results indicate that T-Ag expression in the absence of p53 functional abrogation results in cardiomyocyte death.

Animals↗
PubMed2000

Simian virus 40 large T antigen binds a novel Bcl-2 homology domain 3-containing proapoptosis protein in the cytoplasm.

A 193-kDa SV40 large T antigen (T-Ag)-binding protein, designated p193, was identified and cloned. Inspection of the deduced amino acid sequence revealed the presence of a short motif similar to the Bcl-2 homology (BH) domain 3, suggesting that p193 may be a member of a family of apoptosis promoting proteins containing only BH3 motifs. In support of this, p193 expression promoted apoptosis in NIH-3T3 cells. Deletion of the BH3 motif abolished p193 apoptosis activity. p193-induced apoptosis was antagonized by co-expression of Bcl-X(L). Immune cytologic analysis indicated that p193 is localized to the cytoplasm of transfected cells. p193-induced apoptosis was also antagonized by co-expression of T-Ag, which resulted in the cytoplasmic localization of both proteins. The p193 binding site was mapped to an N-terminal region of T-Ag previously implicated in transforming activity. These results suggest that T-Ag possesses an antiapoptosis activity, independent of p53 sequestration, which is actuated by T-Ag/p193 binding in the cytoplasm.

3T3 Cells↗
PubMed2000

Ciliary neurotrophic factor is required for motoneuron sprouting.

We used mutant mice that lack the gene for ciliary neurotrophic factor (CNTF) to test the hypothesis that it is an endogenous sprouting factor. Fibers in the lateral gastrocnemius muscle were either partially denervated by transection of one of the branches of its nerve or paralyzed by intramuscular injection of botulinum toxin. This results in a significant sprouting response at the terminals of intact motoneurons in normal animals. We did not detect sprouting produced by either stimulus in mice lacking CNTF. When exogenous CNTF was administered to CNTF knockout mice following partial muscle denervation, they mounted a typical sprouting response. Thus CNTF is a critical factor in the process of sprout formation after both partial denervation injury and neuromuscular paralysis. It may function as part of a cellular compensatory mechanism after neuronal injury.

Animals↗