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Peripheral Cells (peripheral + cell)
Selected AbstractsReverse cholesterol transport in type 2 diabetes mellitusDIABETES OBESITY & METABOLISM, Issue 6 2009K. C. B. Tan High-density lipoprotein (HDL) plays an important protective role against atherosclerosis, and the anti-atherogenic properties of HDL include the promotion of cellular cholesterol efflux and reverse cholesterol transport (RCT), as well as antioxidant, anti-inflammatory and anticoagulant effects. RCT is a complex pathway, which transports cholesterol from peripheral cells and tissues to the liver for its metabolism and biliary excretion. The major steps in the RCT pathway include the efflux of free cholesterol mediated by cholesterol transporters from cells to the main extracellular acceptor HDL, the conversion of free cholesterol to cholesteryl esters and the subsequent removal of cholesteryl ester in HDL by the liver. The efficiency of RCT is influenced by the mobilization of cellular lipids for efflux and the intravascular remodelling and kinetics of HDL metabolism. Despite the increased cardiovascular risk in people with type 2 diabetes, current knowledge on RCT in diabetes is limited. In this article, abnormalities in RCT in type 2 diabetes mellitus and therapeutic strategies targeting HDL and RCT will be reviewed. [source] P2Y13 receptor is critical for reverse cholesterol transport,HEPATOLOGY, Issue 4 2010Aurélie C. Fabre A major atheroprotective functionality of high-density lipoproteins (HDLs) is to promote "reverse cholesterol transport" (RCT). In this process, HDLs mediate the efflux and transport of cholesterol from peripheral cells and its subsequent transport to the liver for further metabolism and biliary excretion. We have previously demonstrated in cultured hepatocytes that P2Y13 (purinergic receptor P2Y, G protein,coupled, 13) activation is essential for HDL uptake but the potential of P2Y13 as a target to promote RCT has not been documented. Here, we show that P2Y13 -deficient mice exhibited a decrease in hepatic HDL cholesterol uptake, hepatic cholesterol content, and biliary cholesterol output, although their plasma HDL and other lipid levels were normal. These changes translated into a substantial decrease in the rate of macrophage-to-feces RCT. Therefore, hallmark features of RCT are impaired in P2Y13 -deficient mice. Furthermore, cangrelor, a partial agonist of P2Y13, stimulated hepatic HDL uptake and biliary lipid secretions in normal mice and in mice with a targeted deletion of scavenger receptor class B type I (SR-BI) in liver (hypomSR-BI,knockoutliver) but had no effect in P2Y13 knockout mice, which indicate that P2Y13 -mediated HDL uptake pathway is independent of SR-BI,mediated HDL selective cholesteryl ester uptake. Conclusion: These results establish P2Y13 as an attractive novel target for modulating RCT and support the emerging view that steady-state plasma HDL levels do not necessarily reflect the capacity of HDL to promote RCT. (HEPATOLOGY 2010) [source] Evidence of thymic reconstitution after highly active antiretroviral therapy in HIV-1 infectionHIV MEDICINE, Issue 2 2004G Hardy Objectives We aimed to provide evidence of thymic reconstitution after highly active antiretroviral therapy (HAART) in HIV-1 infected patients and to correlate this with the restoration of peripheral naďve T cells. Methods Positron emission tomography (PET) enables definitive evidence of thymic activity, indicating functional potential. In this case study, a single patient who initiatiated HAART demonstrated reconstitution of the naďve T-cell pool and underwent thymic PET scans at baseline and 2 and 6 months following initiation of therapy. Two patients who failed to demonstrate such reconstitution acted as controls. These patients (mean age 27 years) had chronic HIV infection with low CD4 T-cell counts (mean 82, range 9,160 cells/,L blood). Increased function of the thymus visualized by PET was correlated with phenotypic changes in CD4 and CD8 T cells in the periphery measured by flow cytometry, and with numbers of recent thymic emigrants measured by quantification of the numbers of T-cell receptor excision circles (TRECs) in peripheral cells. Results In one patient, clear correlations could be drawn between visible activity within the thymus, as measured by increased [F18]fluorodeoxyglucose (FDG) uptake, and regeneration of naďve CD4 (CD45RA/CD62L) T cells, increased numbers of CD4 T cells, controlled viraemia and increased numbers of recent thymic emigrants. A second patient displayed no increase in peripheral CD4 count and no increase in thymic activity. The third patient elected to stop therapy following the 2-month time point. Conclusions The use of PET suggests that thymic activity may increase after HAART, indicating that the thymus has the potential to be functional even in HIV-1 infected persons with low CD4 T-cell counts. [source] LDL-receptor mutations in Europe,HUMAN MUTATION, Issue 6 2004George V.Z. Dedoussis Abstract Familial hypercholesterolemia (FH) is a clinical definition for a remarkable increase of cholesterol serum concentration, presence of xanthomas, and an autosomal dominant trait of either increased serum cholesterol or premature coronary artery disease (CAD). The identification of the low-density lipoprotein (LDL)-receptor (LDLR) as the underlying cause and its genetic characterization in FH patients revealed more insights in the trafficking of LDL, which primarily transports cholesterol to hepatic and peripheral cells. Mutations within LDLR result in hypercholesterolemia and, subsequently, cholesterol deposition in humans to a variable degree. This confirms the pathogenetic role of LDLR and also highlights the existence of additional factors in determining the phenotype. Autosomal dominant FH is caused by LDLR deficiency and defective apolipoprotein B-100 (APOB), respectively. Heterozygosity of the LDLR is relatively common (1:500). Clinical diagnosis is highly important and genetic diagnosis may be helpful, since treatment is usually effective for this otherwise fatal disease. Very recently, mutations in PCSK9 have been also shown to cause autosomal dominant hypercholesterolemia. For autosomal recessive hypercholesterolemia, mutations within the so-called ARH gene encoding a cellular adaptor protein required for LDL transport have been identified. These insights emphasize the crucial importance of LDL metabolism intra- and extracellularly in determining LDL-cholesterol serum concentration. Herein, we focus on the published European LDLR mutation data that reflect its heterogeneity and phenotypic penetrance. Hum Mutat 24:443,459, 2004. © 2004 Wiley-Liss, Inc. [source] An optimized method to separate reticulocytes from peripheral blood for molecular analysisINTERNATIONAL JOURNAL OF LABORATORY HEMATOLOGY, Issue 3 2009R. PETRUZZELLI Summary A method based on immunomagnetic sorting of reticulocytes from peripheral blood was set up and combined to a commercial extraction kit for the isolation of total RNA from whole blood. This procedure resulted in high-quality RNA samples suitable for molecular analysis. We used this procedure to analyse erythroid-specific transcripts, starting from peripheral blood samples, to search for differently expressed mRNAs in patients with hereditary persistence of foetal haemoglobin. After erythrocyte lysis, CD15+and CD45+ peripheral cells were negatively sorted to remove leucocyte populations that could have affected the subsequent screening procedure. The cell sorting and RNA extraction procedure was completed within 1,2 h of erythrocyte lysis, which represents a consistent saving of time compared with other procedures. Moreover, it produced 1 ,g of total RNA per ml of blood samples, which is sufficient for molecular analysis. Therefore, our method is a reliable and efficient tool to isolate RNA from specific cell subpopulations poorly represented in peripheral blood, particularly when accurate detection and characterization of highly unstable and poorly expressed molecules is required. [source] Psychosine-induced apoptosis and cytokine activation in immune peripheral cells of Krabbe patients,JOURNAL OF CELLULAR PHYSIOLOGY, Issue 3 2007Patrizia Formichi Globoid cell leukodystrophy or Krabbe disease (KD), is a hereditary disorder caused by galactosylceramidase deficiency. Progressive accumulation of psychosine is considered to be the critical pathogenetic mechanism of cell death in the Krabbe brain. Psychosine mechanism of action has not been fully elucidated. It seems to induce apoptosis in oligodendrocytes through a mitochondrial pathway and to up-regulate inflammatory cytokines production resulting in oligodendrocyte loss. Our aim was to evaluate the role of psychosine in apoptotic cell death and inflammatory response in a group of patients affected by KD using peripheral blood lymphocytes (PBLs) and peripheral blood mononuclear cells (PBMCs) as a cellular model. PBLs from KP and healthy controls were exposed to 20 µM psychosine and analysed by flow cytometry, agarose gel electrophoresis and fluorescence microscopy. Our results showed that psychosine induces apoptosis in PBLs through a mitochondrial pathway, but the apoptotic response was quite low especially KP. The role of psychosine in the up-regulation of cytokines (TNFalpha, IL8 and MCP1) has been evaluated by ELISA in PBMCs from KP and controls after stimulation with LPS and phytohemagglutinin. Both in basal condition and after LPS stimulation, cells from KP showed a significant increase in TNF-, production, reduced MCP1 levels and no modification in IL8. These results indicate that lymphomonocytes from KP had a basal proinflammatory pattern that was amplified by psychosine. In conclusion, the reduced apoptotic response and the atypical cytokine production observed in our experiments, suggest an involvement of inflammatory pattern in immune peripheral cells of KP. J. Cell. Physiol. 212:737,743, 2007. © 2007 Wiley-Liss, Inc. [source] Altered expression of collagen XVII in ameloblastomas and basal cell carcinomasJOURNAL OF ORAL PATHOLOGY & MEDICINE, Issue 10 2001Mataleena Parikka Abstract: Background: Collagen XVII (BP180) is an epithelial transmembrane protein, which presumably plays a role in cell migration and differentiation under both physiological and pathological conditions. Ameloblastoma, the most common odontogenic neoplasm, and basal cell carcinoma (BCC) of the skin exhibit similar growth patterns and share histological features. Methods: Here, we examined the distribution and expression of collagen XVII in ameloblastomas and BCCs using immunohistochemistry and non-radioactive in situ hybridization. In both tumors, the distribution of collagen XVII varied in different parts of the lesions. Results: In ameloblastomas, immunostaining for collagen XVII was usually localized in the basal and suprabasal cells of the tumor nests, although in some tumors, a diffuse intracellular staining was detected in the central cells of the neoplastic islands. In BCCs, collagen XVII was mostly seen as diffuse cytoplasmic staining in some central and peripheral cells of the tumor islands and also at the cell membranes in the basal keratinocytes of the epidermis overlying the tumor nests. Double immunostaining with antibody against ,2 chain of laminin-5 showed that these two components of the keratinocyte adhesion complex are usually co-localized in ameloblastomas and BCCs. In both tumors, collagen XVII mRNA was found in the basal epithelial cells and in some central and peripheral cells of the tumor islands, while the stromal cells were negative. Conclusions: These findings indicate that the expression of collagen XVII may be differentially regulated in various parts of the tumor. Diffuse intracellular distribution of collagen XVII and a consequent loss of critical cellular attachments may contribute to the infiltrative and progressive growing potential of tumors. [source] SEDIMENTARY IMPRINT OF MICROCYSTIS AERUGINOSA (CYANOBACTERIA) BLOOMS IN GRANGENT RESERVOIR (LOIRE, FRANCE),JOURNAL OF PHYCOLOGY, Issue 3 2007Delphine Latour Analysis of a sediment core taken from the Grangent reservoir in 2004 showed the presence of high concentrations of Microcystis aeruginosa Kütz. colonies at the sediment surface (250 colonies,·,mL sediment,1) and also at depths of 25,35 cm (2300 colonies·mL sediment,1) and 70 cm (600 colonies,·,mL sediment,1). Measurements of radioactive isotopes (7Be, 137Cs, and 241Am) along with photographic analysis of the core were used to date the deep layers: the layer located at ,30 cm dates from summer 2003, and that located at ,70 cm from 1990 to 1991. The physiological and morphological conditions of those benthic colonies were compared with those of planktonic colonies using several techniques (environmental scanning electron microscopy [ESEM], TEM, DNA markers, cellular esterases, and toxins). The ESEM observations showed that, as these colonies age, peripheral cells disappear, with no cells remaining in the mucilage of the deepest colonies (70 cm), an indication of the survival thresholds of these organisms. In the benthic phase, the physiological conditions (enzyme activity, cell division, and intracellular toxins) and ultrastructure (particularly the gas vesicles) of the cells surviving in the heart of the colony are comparable to those of the planktonic form, with all the potential needed for growth. Maintaining cellular integrity requires a process that can provide sufficient energy and is expressed in the reduced, but still existing, enzymatic activity that we measured, which is equivalent to a quiescent state. [source] T lymphocytes expressing CCR3 are increased in allergic rhinitis compared with non-allergic controls and following allergen immunotherapyALLERGY, Issue 1 2007J. N. Francis Background:, In T cell-associated allergic inflammation, homing of T-helper 2 (Th2) effector cells to mucosal sites may be influenced by chemokine receptor expression. Previous studies have identified CCR3 and CCR4 as putative markers of Th2 cells and CCR5 and CXCR3 as markers of Th1 cells. The aim of this study was to assess differential chemokine receptor expression from symptomatic atopic grass pollen-sensitive subjects, compared with patients on high-dose allergen injection immunotherapy (IT) and healthy controls. Methods:, We examined chemokine receptor expression (CCR1,7 and CXCR1,4) by flow cytometry of peripheral blood CD4+ and CD8+ T cells. We also depleted peripheral blood mononuclear cell (PBMC) populations of CCR3+ CD4+ cells by magnetic bead separation and cells were stimulated with grass pollen allergen for 6 days. Cytokine production was measured by enzyme-linked immunosorbent assay. Results:, On freshly isolated PBMC, atopic individuals exhibited increased numbers of CCR3+ CD4+ cells compared with normal controls (P < 0.01). CCR3 expression in IT patients was reduced compared with matched atopic rhinitic controls (P < 0.05) and comparable with that observed in normal subjects. Depletion of CCR3+ CD4+ cells from allergen-stimulated PBMC cultures resulted in decreased interleukin (IL)-5 production compared with whole CD4+ populations (P < 0.05). Freshly isolated CCR3+ CD4+ cells have significantly higher intracellular IL-4 and lower IFN- , levels than CCR3, CD4+ cells. CD4+ T cells cultured from both peripheral cells and nasal biopsies demonstrated increased expression of CCR3 in the presence of IL-4 (P < 0.05). Conclusion:, CCR3+ CD4+ T cells are increased in allergic rhinitis, are reduced by allergen IT, have a Th2 phenotype and contribute to allergen-specific responses. Strategies against CCR3+ T cells may be effective in human allergic diseases. [source] Immunohistochemical demonstration of p63 in DMBA-induced hamster buccal pouch squamous cell carcinogenesisORAL DISEASES, Issue 5 2003YK Chen Objectives: Abnormalities in the p53 gene are regarded as the most consistent genetic abnormalities detected in head and neck squamous cell carcinogenesis. Two new members of the p53 gene family, p73 at the 1p36 region and p63 at the 3q27-29 region, have recently been identified. They share considerable sequence homology with p53 in the transactivation, DNA binding, and oligomerization domains, indicating possible involvement in carcinogenesis. To our knowledge, however, p63 expression in experimental oral carcinogenesis has not been studied. Materials and methods: Immunohistochemical analysis of p63 protein expression was performed in 7,12-dimethylbenz[a]anthracene (DMBA)-induced hamster buccal pouch squamous cell carcinogenesis. Fifty outbred, young (6 weeks), male, Syrian golden hamsters (Mesocricatus auratus) were randomly divided into three experimental groups (each consisting of 10 3-, 9- and 15-week DMBA treated animals), and two control groups (with 10 animals in each). The pouches of the three experimental groups were painted bilaterally with a 0.5% DMBA solution three times a week. The treatment protocol for animals in one of the control groups was identical with only mineral oil applied, while the other control group remained untreated throughout the experiment. Results: In all of the untreated and mineral oil-treated pouch mucosa, nuclear positivity for p63 was mainly observed in the basal/parabasal cell layers. The p63 nuclear positivity extended from the basal/parabasal layers to the whole epithelial layers in the 3- and 9-week DMBA-treated pouch mucosa. Furthermore, the positive nuclear-stain cells were randomly distributed throughout the entire epithelial layers in the 3- and 9-week DMBA-treated pouch-mucosa specimens. In carcinomas from 15-week DMBA-treated pouch specimens, p63 staining was more uniform and homogeneous for the less-differentiated tumor areas. By contrast, p63 expression was noted mainly in the peripheral cells of tumor nests in the well-differentiated tumor areas. Conclusions: The results of this study are consistent with those from previous analyses of p63 expression in human oral mucosa, suggesting that p63 may be associated with the regulation of epithelial differentiation and proliferation in DMBA-induced hamster buccal pouch squamous cell carcinogenesis. Further study is required to investigate which p63 isoform(s) is/are involved in hamster buccal pouch carcinogenesis. [source] Presence Of Nemathecia In Parachaetetes Asvapatii Pia, 1936 (Rhodophyta, Gigartinales?): Reproduction In ,Solenoporaceans' RevisitedPALAEONTOLOGY, Issue 6 2001J. Aguirre Parachaetetes asvapatii is a very common algal species in the Palaeogene deposits of the Tethyan realm and has been considered as a member of the heterogeneous family Solenoporaceae. This attribution is exclusively based on features of the vegetative tissue, since no reproductive structures have ever been recovered. However, detailed analysis of Late Cretaceous,Eocene material from Turkey has revealed nemathecia-like structures in one specimen attributable to P. asvapatii. These nemathecia are small wart-like structures protruding on the thallus surface that formed by enlargement of the most peripheral cells of the plant. Nemathecia only occur in three families of the order Gigartinales (Rhodophyta): Rhizophyllidaceae, Peyssonneliaceae and Polyideaceae. Since reproductive structures are stable characters, the presence of nemathecia leads us to tentatively refer P. asvapatii and related species (probably Elianella elegans) to the Gigartinales. [source] Expression of p73 in normal skin and proliferative skin lesionsPATHOLOGY INTERNATIONAL, Issue 12 2004Makoto Kamiya The p73 gene is a member of the p53 gene family and the structure and functions of p73 protein are similar to those of ,p53. ,However, ,these ,two ,proteins ,have ,different ,roles. In the present study, p73 protein was found immunohistochemically to be distributed in the basal cells of the epidermis, columnar basal cells in the hair follicle and peripheral cells without lipid droplets in the sebaceous and meibomian glands; it was expressed strongly in tumor cells in basal cell carcinomas and in the basal cell-like cells in seborrheic keratosis, and weakly or negatively in the squamous cell-like cells in seborrheic keratosis and in the tumor cells in squamous cell carcinomas. No relationship was detected between p73 and p53 protein distribution and between p73 protein expression and the proliferative potential, as shown by the Ki-67 immunopositive cell ratio. The present study shows that p73 protein is likely to play important roles in skin differentiation rather than proliferation or carcinogenesis of the skin. [source] Comparison of cell proliferation in the centre and advancing fronts of oral squamous cell carcinomas using Ki-67 indexCELL PROLIFERATION, Issue 5 2003U. Dissanayake A comparison was made between the indices derived from the centre of the tumours and those derived from the invasive fronts of the same tumours. There was a positive correlation between the two indices suggesting a clonal expansion of malignant cells, but the mean index derived for the invasive fronts (29.75 11.64) was significantly higher than the mean index for the body of these tumours (25.65 11.64). Thus, at a given time, more peripheral cells at the invasive front are proliferating and this compartment is likely to be more informative in prognostic and other behavioural studies involving the cell cycle. In squamous carcinomas, increased and uncontrolled cell proliferation at the invasive front may be one feature contributory to the invasion. [source] 3134: Identification of potential human corneal endothelial stem-like cell nichesACTA OPHTHALMOLOGICA, Issue 2010G THURET Purpose to study the localization of potential stem-(like) cells in human adult corneal endothelium Methods Fresh (6-12h post mortem) and organ cultured (OC) corneas were studied after flat mount. The whole endothelium and posterior limbus (PL) was observed after triple staining with Trypan blue, Alizarin red and Hoechst 33342, in order to determine cells shape, localization and viability. The level of endothelial cell (EC) differenciation was determined after immunostaining (fluorescence) for ZO-1, Na+/K+ ATPase and COX IV; the cell proliferation status was assessed using Ki67; four markers for stem cells were used: Oct-4, BCRP, Nestin and Telomerase; ability for cell migration was evaluated from Myosin IIA expression Results In several corneas, the nuclei of peripheral EC were centripetally aligned suggesting continuous slow central migration. Numerous small cells with a reduced expression of differenciation markers were accumulated near peripheral Hassall Henle bodies. In these potential niches, cells were distributed in 3-5 layers. A high expression of Myosin II was found in peripheral cells. Ki67+ cells were found in PL and peripheral EC only after OC. None of the 4 stem cell markers was found in EC, and their expression in PL was poorly reliable because of high background noise. Numerous trypan blue positive cells were located at the PL and in the extreme periphery of endothelium Conclusion several strong arguments suggest the location of corneal endothelial stem-like cell niches in endothelial periphery or in the PL, and the capacity of EC to migrate from these niches toward the centre. Trypan blue staining pattern suggests that they could rapidly die in ex vivo corneas, and be therefore hard to indentify [source] | |||||||||||||