The Effect of the Short-Range Correlations on the Generalized Momentum Distribution in Finite Nuclei

The effect of dynamical short-range correlations on the generalized momentum distribution $n(\vec{p},\vec{Q})$ in the case of $Z=N$, $\ell$-closed shell nuclei is investigated by introducing Jastrow-type correlations in the harmonic-oscillator model. First, a low order approximation is considered and applied to the nucleus $^4$He. Compact analytical expressions are derived and numerical results are presented and the effect of center-of-mass corrections is estimated. Next, an approximation is proposed for $n(\vec{p}, \vec{Q})$ of heavier nuclei, that uses the above correlated $n(\vec{p},\vec{Q})$ of $^4$He. Results are presented for the nucleus $^{16}$O. It is found that the effect of short-range correlations is significant for rather large values of the momenta $p$ and/or $Q$ and should be included, along with center of mass corrections for light nuclei, in a reliable evaluation of $n(\vec{p},\vec{Q})$ in the whole domain of $p$ and $Q$.Comment: 29 pages, 8 figures. Further results, figures and discussion for the CM corrections are added. Accepted by Journal of Physics

Proteomic characterization of HIV-modulated membrane receptors, kinases and signaling proteins involved in novel angiogenic pathways

<p>Abstract</p> <p>Background</p> <p>Kaposi's sarcoma (KS), hemangioma, and other angioproliferative diseases are highly prevalent in HIV-infected individuals. While KS is etiologically linked to the human herpesvirus-8 (HHV8) infection, HIV-patients without HHV-8 and those infected with unrelated viruses also develop angiopathies. Further, HIV-Tat can activate protein-tyrosine-kinase (PTK-activity) of the vascular endothelial growth factor receptor involved in stimulating angiogenic processes. However, Tat by itself or HHV8-genes alone cannot induce angiogenesis <it>in vivo </it>unless specific proteins/enzymes are produced synchronously by different cell-types. We therefore tested a hypothesis that <it>chronic </it>HIV-<it>replication in non-endothelial cells </it>may produce novel factors that provoke angiogenic pathways.</p> <p>Methods</p> <p>Genome-wide proteins from HIV-infected and uninfected T-lymphocytes were tested by subtractive proteomics analyses at various stages of virus and cell growth <it>in vitro </it>over a period of two years. Several thousand differentially regulated proteins were identified by mass spectrometry (MS) and >200 proteins were confirmed in multiple gels. Each protein was scrutinized extensively by protein-interaction-pathways, bioinformatics, and statistical analyses.</p> <p>Results</p> <p>By functional categorization, 31 proteins were identified to be associated with various signaling events involved in angiogenesis. 88% proteins were located in the plasma membrane or extracellular matrix and >90% were found to be essential for regeneration, neovascularization and angiogenic processes during embryonic development.</p> <p>Conclusion</p> <p>Chronic HIV-infection of T-cells produces membrane receptor-PTKs, serine-threonine kinases, growth factors, adhesion molecules and many diffusible signaling proteins that have not been previously reported in HIV-infected cells. Each protein has been associated with endothelial cell-growth, morphogenesis, sprouting, microvessel-formation and other biological processes involved in angiogenesis (p = 10^-4to 10^-12). Bioinformatics analyses suggest that overproduction of PTKs and other kinases in HIV-infected cells has <it>suppressed </it>VEGF/VEGFR-PTK expression and promoted <it>VEGFR-independent </it>pathways. This unique mechanism is similar to that observed in neovascularization and angiogenesis during embryogenesis. Validation of clinically relevant proteins by gene-silencing and translational studies <it>in vivo </it>would identify specific targets that can be used for early diagnosis of angiogenic disorders and future development of inhibitors of angiopathies. This is the first comprehensive study to demonstrate that HIV-infection alone, without any co-infection or treatment, can induce numerous "embryonic" proteins and kinases capable of generating novel <it>VEGF-independent </it>angiogenic pathways.</p

Matrix metalloproteinase 3 haplotypes and plasma amyloid beta levels: The Rotterdam Study

Experimental studies suggest that matrix metalloproteinases (MMPs) are involved in the degradation of amyloid beta (A beta) protein which plays a key role in the pathogenesis of Alzheimer's disease Whether MMPs are associated with changes in beta amyloid levels in humans remains unclear We related common haplotypes within the gene encoding MMP-3 with plasma levels of A beta(1-10) and A beta(1-12) in 1621 non-demented participants of the population-based Rotterdam Study In non-demented persons. plasma A beta concentration reflect levels of A beta in the brain DNA was genotyped for polymorphisms 1187 (5A6A, rs3025058), 2092A>G (rs522616). 9775T>A (rs563096) and 6658T>C (rs3025066) and haplotypes reconstructed (coding from 1187 (5A6A), 2092A>G. 9775-1>A and 6658T>C haplotype 1 = 5A-A-T-T. haplotype 2 = 6A-G-T-T, haplotype 3 = 6A-A-T-T. haplotype 4 = 6A-A-A-T and haplotype 5 = 5A-A-T-C) Then the associations of these haplotypes with plasma A beta(1-10) and A beta(1-42) levels were assessed using the program Stats Compared with haplotype I. haplotype 4 was associated with significantly lower levels of plasma A beta(1-40) (beta=8 04. 95% CI (-14 79 -1 28), p =0 02) after adjusting for age and sex Haplotype 2 was associated with significantly higher levels of plasma A beta(1-42) (beta=3 70,95% CI (1 75.5 65),p = 0 0002) Our observations suggest that variation in the gene encoding MMP-3 is associated with changes in amyloid beta levels in humans Factors modulating secretion or activity of MMP-3 may have the potential to in the amount of An concentration and deposition in the brain (C) 2008 Elsevier Inc. All rights reserve

Central Bank Intervention and Heterogeneous Exchange Rate Expectations: Evidence from the Daily DEM/US-Dollar Exchange Rate

In this paper we propose a generalisation of the noise trader transmission mechanism to examine the impact of central bank intervention on exchange rates. Within a heterogeneous expectation exchange rate model intervention operations are supposed to provide support for chartist or fundamentalist forecasts, which forces portfolio managers to adjust their foreign currency positions. The empirical examination of the hypothesis is done by applying a Markov regime-switching approach to daily DEM/US-dollar exchange rates and intervention data of the Deutsche Bundesbank and the Federal Reserve from 1979 to 1992. It is shown that chartist’s profits rose whenever these central banks intervened on the foreign exchange market. This is not true for those who follow a fundamentalist approach. Copyright Springer Science + Business Media, Inc. 2005exchange rates, intervention, regime-switching,