PubMed Health⌕ Search

Biomedical subjects

Ana Petrovic

Publications and source records attributed to Ana Petrovic.

6 recordsLinked to original sources
PubMed2006

Central injections of CRF reinstate cocaine seeking in rats after postinjection delays of up to 3 h: an influence of time and environmental context.

RATIONALE: In drug addicts, the induction of drug craving is not always associated with an immediate opportunity to take drugs again. It is, therefore, important to study how delays in opportunity for drug seeking affect the time-course of relapse. Intracerebroventricular (i.c.v.) injection of corticotropin-releasing factor (CRF) is a stressor that reinstates heroin and alcohol seeking in rats, when administered just before tests for reinstatement. It is not known whether CRF reinstates cocaine seeking; moreover, the effect of delaying testing for reinstatement, after CRF injection, has not been studied. OBJECTIVES: To determine whether i.c.v. CRF induces reinstatement of cocaine seeking after postinjection delays of up to 3 h and to determine whether the context in which a delay is experienced influences the time-course of CRF-induced reinstatement. METHODS: Rats self-administered cocaine (1.0 mg/kg per infusion) for 8-10 days. Subsequently, responding for drug was extinguished and testing for reinstatement by i.c.v. CRF (0.5 microg) was conducted. Animals were tested after postinjection delays of up to 3 h; the delays were experienced either in the self-administration (SA) chamber or home cage (HC). RESULTS: When delays were spent in the SA chambers, CRF induced reinstatement in all delay groups. When delays were spent in the HC, CRF did not induce reinstatement after a 2-h delay. CONCLUSIONS: We argue that the effects we observed are consistent with a contextual conditioning account of reinstatement, whereby CRF that was experienced in the context of the SA chamber served to elicit a conditioned excitatory response developed to that context during training.

Animals↗
PubMed2004

Multiresolution segmentation of natural images: from linear to nonlinear scale-space representations.

In this paper, we introduce a framework that merges classical ideas borrowed from scale-space and multiresolution segmentation with nonlinear partial differential equations. A non-linear scale-space stack is constructed by means of an appropriate diffusion equation. This stack is analyzed and a tree of coherent segments is constructed based on relationships between different scale layers. Pruning this tree proves to be a very efficient tool for unsupervised segmentation of different classes of images (e.g., natural, medical, etc.). This technique is light on the computational point of view and can be extended to nonscalar data in a straightforward manner.

Algorithms↗
PubMed2003

Intrinsic rotation and molecular structure.

The intrinsic rotation, limiting value of specific rotation at zero concentration, of (R)-(-)-epichlorohydrin was measured in four different solvents, CH(3)OH, CH(2)Cl(2), CHCl(3) and CCl(4). It was found that the sign of rotation in CH(3)OH, and CH(2)Cl(2) solvents is opposite to that in CCl(4). The intrinsic rotation in CHCl(3) is close to zero. This observed pattern was explained using density functional calculations of specific rotation using very large basis sets. It was found that the g-I and g-II conformations of epichlorohydrin have nearly the same magnitude of specific rotation but with opposite sign. When these two conformations have equal populations, as in CHCl(3) solvent, the net rotation is close to zero. When g-II conformation dominates, as in CCl(4) solvent, the observed sign of rotation will be opposite to that when g-I conformation dominates, as in CH(2)Cl(2) and CH(3)OH solvents. A combination of intrinsic rotation measurement with density functional prediction of specific rotation is demonstrated to be a practical method for determining the structures of molecules.

Journal Article↗
PubMed2001

Reduced cell surface expression of CCR5 in CCR5Delta 32 heterozygotes is mediated by gene dosage, rather than by receptor sequestration.

Macrophage tropic (M-tropic) human immunodeficiency virus (HIV) infection of primary human T cells and macrophages requires optimal cell surface expression of the chemokine receptor CCR5 in addition to CD4. Natural mutations of CCR5 that impair surface expression bestow in the homozygous state complete resistance to M-tropic HIV infection. ccr5Delta32 is the major prototype of such mutants. ccr5Delta32 heterozygosity is associated with delayed onset of AIDS and reduced risk of initial transmission, and this correlates with reduced levels of CCR5 and reduced infectability of CD4+ cells. In addition to gene dosage, sequestration of wild type (WT) CCR5 by mutant protein has been proposed as a mechanism to explain reduced surface expression of CCR5 in cells from ccr5Delta32 and CCR5-893(-) heterozygotes. However, here we demonstrate that a molar excess of ccr5Delta32 or related deletion mutants does not significantly impair the cell surface density of co-expressed WT receptor either in human epithelial cells or Jurkat T cells. Further, ligand-dependent signaling and M-tropic HIV usage of WT receptor are also unaffected. Nascent WT receptor does associate with ccr5Delta32 and related mutant proteins and with other unrelated CC and CXC chemokine receptors under transient labeling conditions. However, using confocal microscopy, we demonstrate that in the steady state, WT and truncated CCR5 proteins segregate into nonoverlapping subcellular compartments. These findings together with the observed and known variability in the cell surface density of CCR5 on quiescent PBLs lead us to conclude that reduced CCR5 gene dosage rather than receptor sequestration is the major determinant of reduced CCR5 expression in cells from ccr5Delta32 heterozygotes.

Amino Acid Sequence↗
PubMedDate not supplied

Effects of HIV-1 Nef on cellular gene expression profiles.

The early human immunodeficiency virus (HIV) accessory protein Nef makes an important contribution to virulence, but the mechanisms by which Nef influences pathogenesis remain unclear. Many well-studied effects of Nef, like CD4 and class I MHC downregulation, occur posttranslationally. However, Nef has the potential to affect gene expression by interfering with cell signaling pathways and by virtue of structural features such as the Pro-X-X-Pro motif, which may interact with src homology region-3 domains of src-like kinases. We used a cDNA microarray screening strategy to identify cellular genes whose steady state transcriptional levels may be affected by Nef. We generated HeLa cell lines expressing wild-type or mutant HIV-1 nef protein sequences. Using cDNA microarray technology, we compared the patterns of cellular gene expression in the various cell lines to the pattern in non-Nef-expressing HeLa cells. By matching the patterns of cellular gene expression in HeLa cell lines expressing various Nefs with that of parental HeLa cells, we identified several cellular genes whose expression was modulated differentially by Nef and its mutants. We confirmed the differential expression of selected genes by RNA filter blotting. Genes expressed at higher levels included proteases, transcription factors, protein kinases, nuclear import/export proteins, adaptor molecules and cyclins, some of which have previously been implicated as being important for HIV replication and pathogenesis. The results indicate that Nef expression can alter the expression of cellular genes and suggest that this alteration in cellular gene expression may serve to optimize the cell to support the subsequent stages of viral replication.

Gene Expression↗