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1

CD14 C260T promoter polymorphism and the risk of cerebrovascular diseases: a meta-analysis

100%
Banerjee I.
Journal of Applied Genetics
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2009
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vol. 50
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issue 2
153-157
EN
Cerebrovascular diseases (CVD) are dysfunctions of the brain, resulting from diseases of blood vessels supplying the brain. Atherosclerosis is one of the major underlying causes of CVD, in which inflammation plays a crucial role. One of the inflammatory mechanisms contributing to atherogenesis is the activation of monocytes and macrophages, which could be mediated by the bacterial endotoxin lipopolysaccharide (LPS) via its receptor CD14. The C260T (rs2569190) single-nucleotide polymorphism (SNP) in the promoter region of the CD14 gene was implicated in CVD. To assess the role of this SNP in CVD, a comprehensive meta-analysis of the available genetic data was conducted. All the case-control association studies evaluating the role of CD14 C260T in CVD were identified. Of these, 7 studies (comprising a total of 1488 patients and 1600 control subjects) were included in this meta-analysis. To measure the strength of genetic association for the gene variant, the odds ratios (ORs) were calculated using both fixed and random effects for comparisons of the alleles, the genotypes, and the dominant and recessive genotype models. The results showed there was no significant association between the T allele of C260T and the risk of CVD under the fixed effects model, OR = 0.99 (95% CI (0.89, 1.09)), P = 0.84; or the random effects model, OR = 0.99 (95% CI (0.88, 1.11)), P = 0.83. Similar results were obtained for the homozygotes and the dominant and recessive models. In conclusion, the results of this meta-analysis suggest the CD14 C260T polymorphism is not a risk factor for CVD. However, more studies in ethnically varied populations are needed to evaluate in a reliable manner the role of this SNP in CVD susceptibility.
2
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Challenges and possibilities of intravascular cell therapy in stroke

100%
Hicks A., Jolkkonen J.
Acta Neurobiologiae Experimentalis
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2009
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vol. 69
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issue 1
1-11
EN
Stroke is the third leading cause of death in Western countries and more importantly a leading cause of adult disability. The recovery process of stroke patients might be enhanced by intensive rehabilitation, which acts through brain plasticity mechanisms. Restorative approaches such as cell-based therapies are clinically appealing as it might be possible to help patients even when treatment is initiated days or weeks after the ischemic insult. An extensive number of experimental transplantation studies have been conducted with cells of different origins (e.g., embryonic stem, fetal neural stem, human umbilical cord blood) with promising results. Noninvasive intravascular administration of cells, which provides a broad distribution of cells to the close proximity of ischemic tissue, has perhaps the most immediate access to clinical applications. However, surprisingly little is known about whole body biodistribution of intravascularly administered cells and mechanisms leading to improved functional recovery. This review examines the recent literature concerning intravascular cell-based therapies in experimental stroke.
3
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Focal stroke in the barrel cortex of rats enhances ipsilateral response to vibrissal input

88%
Jablonka J., Kossut M.
Acta Neurobiologiae Experimentalis
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2006
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vol. 66
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issue 3
261-266
EN
Brain injury triggers spontaneous plasticity, often resulting in considerable restoration of function. To investigate mechanisms of this compensatory plasticity we followed changes in the brain's pattern of activation evoked by stimulation of vibrissae, after a focal cortical stroke which destroyed the cortical representation of vibrissae, the barrel cortex. The pattern of brain activation was visualized with [14C]-2-doexyglucose (2DG) autoradiography in rats 7 days after photothrombotic stroke. During isotope incorporation, vibrissae contralateral to stroke were stimulated. In control rats this stimulation activates the barrel cortex and the second somatosensory cortex in the contralateral hemisphere. Seven days after stroke in the barrel cortex, significant increases in activation were found in ipsilateral, uninjured hemisphere in the barrel cortex and anterior vibrissae representation, and also in regions not specifically connected to vibrissae stimulation, such as motor and auditory cortex. Shortly after cortical stroke, the intact hemisphere shows higher metabolic activation in several cortical regions, possibly due to abnormal interactions with the injured hemisphere.
4

Biomechanic shear stress in carotid arteries and atherosclerosis development

88%
Kazmierski R.
Postępy Higieny i Medycyny Doświadczalnej
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2003
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vol. 57
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issue 6
713-725
EN
One of the major hemodynamic forces acting on blood vessels is shear stress, which is, the friction force between the endothelial cell surface and flowing blood. Arterial shear stress within physiologic range (15-70 dyne/cm2) induces endothelial quiescence and an atheroprotective gene expression profile. Low shear stress (< 4 dyne/cm2 ) stimulates atherogenic phenotype, whereas, high shear stress (>70 dyne/cm2 ) induce prothrombotic state.
5

Stroke, myocardial infarction, acute and chronic inflammatory diseases: caspases and other apoptotic molecules as targets for drug development

88%
Kreuter M., Langer C., Kerkhoff C., Reddanna P., Kania A. L., Maddika S., Chlichlia C., Bui T. N., Los M.
Archivum Immunologiae et Therapiae Experimentalis
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2004
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vol. 52
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issue 3
141-155
EN
Mapping of the human and other eukaryotic genomes has provided the pharmacological industry with excellent models for drug discovery. Control of cell proliferation, differentiation, activation and cell removal is crucial for the development and existence of multicellular organisms. Each cell cycle progression, with sequences of DNA replication, mitosis, and cell division, is a tightly controlled and complicated process that, when deregulated, may become dangerous not only to a single cell, but also to the whole organism. Regulation and the proper control of the cell cycle and of programmed cell death (apoptosis) is therefore essential for mammalian development and the homeostasis of the immune system. The molecular networks that regulate these processes are critical targets for drug development, gene therapy, and metabolic engineering. In addition to the primary, intracellular apoptotic suicide machinery, components of the immune system can detect and remove cells and tissue fragments that no longer serve their defined functions. In this review we will focus on apoptotic pathways converging on caspase family proteases, summarizing pharmacological attempts that target genes, proteins, and intermolecular interactions capable of modulating apoptosis and the inflammatory response. The upcoming pharmacological development for treatment of acute pathologies, such as sepsis, SIRS, stroke, traumatic brain injury, myocardial infarction, spinal cord injury, acute liver failure, as well as chronic disorders such as Huntington's disease, Parkinson's disease, ALS, and rheumatoid arthritis, will be discussed in details. We also suggest new potential molecular targets that may prove to be effective in controlling apoptosis and the immune response in vivo.
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