113 research outputs found
Coulomb-Excitation of the Giant-Dipole Resonance in Light-Ion Inelastic-Scattering from Pb-208
Journals published by the American Physical Society can be found at http://publish.aps.org
Relations between fusion cross sections and average angular momenta
We study the relations between moments of fusion cross sections and averages
of angular momentum. The role of the centrifugal barrier and the target
deformation in determining the effective barrier radius are clarified. A simple
method for extracting average angular momentum from fusion cross sections is
demonstrated using numerical examples as well as actual data.Comment: 16 REVTeX pages plus 8 included Postscript figures (uses the epsf
macro); submitted to Phys. Rev. C; also available at
http://nucth.physics.wisc.edu/preprint
Distorted wave impulse approximation analysis for spin observables in nucleon quasi-elastic scattering and enhancement of the spin-longitudinal response
We present a formalism of distorted wave impulse approximation (DWIA) for
analyzing spin observables in nucleon inelastic and charge exchange reactions
leading to the continuum. It utilizes response functions calculated by the
continuum random phase approximation (RPA), which include the effective mass,
the spreading widths and the \Delta degrees of freedom. The Fermi motion is
treated by the optimal factorization, and the non-locality of the
nucleon-nucleon t-matrix by an averaged reaction plane approximation. By using
the formalism we calculated the spin-longitudinal and the spin-transverse cross
sections, ID_q and ID_p, of 12C, 40Ca (\vec{p},\vec{n}) at 494 and 346 MeV. The
calculation reasonably reproduced the observed ID_q, which is consistent with
the predicted enhancement of the spin-longitudinal response function R_L.
However, the observed ID_p is much larger than the calculated one, which was
consistent with neither the predicted quenching nor the spin-transverse
response function R_T obtained by the (e,e') scattering. The Landau-Migdal
parameter g'_N\Delta for the N\Delta transition interaction and the effective
mass at the nuclear center m^*(r=0) are treated as adjustable parameters. The
present analysis indicates that the smaller g'_{N\Delta}(\approx 0.3) and
m^*(0) \approx 0.7 m are preferable. We also investigate the validity of the
plane wave impulse approximation (PWIA) with the effective nucleon number
approximation for the absorption, by means of which R_L and R_T have
conventionally been extracted.Comment: RevTex 3, 29 pages, 2 tables, 8 figure
Quantum Tunneling in Nuclear Fusion
Recent theoretical advances in the study of heavy ion fusion reactions below
the Coulomb barrier are reviewed. Particular emphasis is given to new ways of
analyzing data, such as studying barrier distributions; new approaches to
channel coupling, such as the path integral and Green function formalisms; and
alternative methods to describe nuclear structure effects, such as those using
the Interacting Boson Model. The roles of nucleon transfer, asymmetry effects,
higher-order couplings, and shape-phase transitions are elucidated. The current
status of the fusion of unstable nuclei and very massive systems are briefly
discussed.Comment: To appear in the January 1998 issue of Reviews of Modern Physics. 13
Figures (postscript file for Figure 6 is not available; a hard copy can be
requested from the authors). Full text and figures are also available at
http://nucth.physics.wisc.edu/preprints
LEDGF/p75-Independent HIV-1 Replication Demonstrates a Role for HRP-2 and Remains Sensitive to Inhibition by LEDGINs
Lens epithelium–derived growth factor (LEDGF/p75) is a cellular cofactor of HIV-1 integrase (IN) that interacts with IN through its IN binding domain (IBD) and tethers the viral pre-integration complex to the host cell chromatin. Here we report the generation of a human somatic LEDGF/p75 knockout cell line that allows the study of spreading HIV-1 infection in the absence of LEDGF/p75. By homologous recombination the exons encoding the LEDGF/p75 IBD (exons 11 to 14) were knocked out. In the absence of LEDGF/p75 replication of laboratory HIV-1 strains was severely delayed while clinical HIV-1 isolates were replication-defective. The residual replication was predominantly mediated by the Hepatoma-derived growth factor related protein 2 (HRP-2), the only cellular protein besides LEDGF/p75 that contains an IBD. Importantly, the recently described IN-LEDGF/p75 inhibitors (LEDGINs) remained active even in the absence of LEDGF/p75 by blocking the interaction with the IBD of HRP-2. These results further support the potential of LEDGINs as allosteric integrase inhibitors
Cancer Genomics Identifies Regulatory Gene Networks Associated with the Transition from Dysplasia to Advanced Lung Adenocarcinomas Induced by c-Raf-1
Background: Lung cancer is a leading cause of cancer morbidity. To improve an understanding of molecular causes of disease a transgenic mouse model was investigated where targeted expression of the serine threonine kinase c-Raf to respiratory epithelium induced initialy dysplasia and subsequently adenocarcinomas. This enables dissection of genetic events associated with precancerous and cancerous lesions. Methodology/Principal Findings: By laser microdissection cancer cell populations were harvested and subjected to whole genome expression analyses. Overall 473 and 541 genes were significantly regulated, when cancer versus transgenic and non-transgenic cells were compared, giving rise to three distinct and one common regulatory gene network. At advanced stages of tumor growth predominately repression of gene expression was observed, but genes previously shown to be upregulated in dysplasia were also up-regulated in solid tumors. Regulation of developmental programs as well as epithelial mesenchymal and mesenchymal endothelial transition was a hall mark of adenocarcinomas. Additionaly, genes coding for cell adhesion, i.e. the integrins and the tight and gap junction proteins were repressed, whereas ligands for receptor tyrosine kinase such as epi- and amphiregulin were up-regulated. Notably, Vegfr- 2 and its ligand Vegfd, as well as Notch and Wnt signalling cascades were regulated as were glycosylases that influence cellular recognition. Other regulated signalling molecules included guanine exchange factors that play a role in an activation of the MAP kinases while several tumor suppressors i.e. Mcc, Hey1, Fat3, Armcx1 and Reck were significantly repressed. Finally, probable molecular switches forcing dysplastic cells into malignantly transformed cells could be identified. Conclusions/Significance: This study provides insight into molecular pertubations allowing dysplasia to progress further to adenocarcinoma induced by exaggerted c-Raf kinase activity
Mutant-IDH1-dependent chromatin state reprogramming, reversibility, and persistence
Mutations in IDH1 and IDH2 (encoding isocitrate dehydrogenase 1 and 2) drive the development of gliomas and other human malignancies. Mutant IDH1 induces epigenetic changes that promote tumorigenesis, but the scale and reversibility of these changes are unknown. Here, using human astrocyte and glioma tumorsphere systems, we generate a large-scale atlas of mutant-IDH1-induced epigenomic reprogramming. We characterize the reversibility of the alterations in DNA methylation, the histone landscape, and transcriptional reprogramming that occur following IDH1 mutation. We discover genome-wide coordinate changes in the localization and intensity of multiple histone marks and chromatin states. Mutant IDH1 establishes a CD24+ population with a proliferative advantage and stem-like transcriptional features. Strikingly, prolonged exposure to mutant IDH1 results in irreversible genomic and epigenetic alterations. Together, these observations provide unprecedented high-resolution molecular portraits of mutant-IDH1-dependent epigenomic reprogramming. These findings have substantial implications for understanding of mutant IDH function and for optimizing therapeutic approaches to targeting IDH-mutant tumors
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