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Strain-dependent interactions of Streptococcus gallolyticus subsp. gallolyticus with human blood cells.

Streptococcus gallolyticus subsp. gallolyticus (S. gallolyticus) is the causative pathogen in up to 20% of streptococcal-induced infective endocarditis (IE) cases. However, the underlying mechanisms of pathogenesis in S. gallolyticus have not yet been solved. Pathogens causing IE need to employ virulent strategies to initiate and establish infections, such as escape the bloodstream, invade the host-cell, and persist intracellularly. In this study, we examined the induction of inflammation by different S. gallolyticus strains in relation to their survival in whole blood and cell culture models as well as their ability to induce platelet aggregation. Phagocytosis of these bacteria by macrophages, followed by intracellular survival, was also quantified.

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Human Cord Blood CD34+ Ce Human Red Blood Cells Uni AccuPrep Genomic DNA Extr Astra Blue 6GLL, Stain fo Rabbit Anti-Human Red Blo Anti C Reactive Protein A Epidermal Growth Factor ( Epidermal Growth Factor ( anti A1, A2 human blood a Macrophage Colony Stimula anti A1, A2, A3 human blo anti B human blood antige

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Holi colours contain PM10 and can induce pro-inflammatory responses.

At Holi festivals, originally celebrated in India but more recently all over the world, people throw coloured powder (Holi powder, Holi colour, Gulal powder) at each other. Adverse health effects, i.e. skin and ocular irritations as well as respiratory problems may be the consequences. The aim of this study was to uncover some of the underlying mechanisms.

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CA125, Ovarian Cancer An CA125, Ovarian Cancer An CA125, Ovarian Cancer An Non-sterile canine serum Non-sterile canine serum Canine serum albumin lyo Canine serum albumin lyo Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon BACTERIOLOGY CANDIDA PARA

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Anti-inflammatory effects of 5-HT3 receptor antagonists in interleukin-1beta stimulated primary human chondrocytes.

Chondrocytes are one of the main cell types involved in rheumatoid inflammation, releasing mediators which add to cartilage destruction, bone damage and consequently disability. Current evidence suggests that serotonin 5-HT(3) receptor antagonists (5-HT(3)RA) show anti-inflammatory and antioxidant properties in vitro and in vivo. Yet, the mechanisms of the anti-inflammatory effects of 5-HT(3)RA have not been elucidated in detail.

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Acid‑induced cell injury and death in lung epithelial cells is associated with the activation of mitogen‑activated protein kinases.

Gastric hydrochloric acid (HCl) has been regarded as a causative factor of acute lung injury (ALI). The activation of mitogen‑activated protein kinases (MAPKs) has been suggested to be a mechanism involved in the pathogenesis of ALI in vivo. However, the effects of HCl on MAPK activation in lung epithelial cells remain to be fully elucidated. Further investigation into the role of MAPK activation in acid‑induced cell injury and death is also needed. In the present study, BEAS‑2B cells were treated with HCl (pH 4.0 medium) for 5, 15 and 30 min, and the acidified medium was then removed. Cell viability and death were detected by MTT assay and trypan blue exclusion staining, respectively. The activation of MAPKs [c‑Jun N‑terminal kinase (JNK), p38 MAPK and extracellular signal‑regulated kinase (ERK) 1/2] was analyzed by western blot analysis. Cytotoxicity was assessed by lactate dehydrogenase (LDH) release, and IL‑8 levels in culture supernatants were measured by enzyme‑linked immunosorbent assay (ELISA). Cell apoptosis was detected as changes in the levels of capase‑3, Bad and fas by western blot analysis and the number of apoptotic cells by using Annexin V/propidium iodide (PI) staining. Following pre‑treatment with the JNK inhibitor II (10 µmol/l), the p38 inhibitor SB202190 (10 µmol/l) or the ERK inhibitor U0126 (10 µmol/l) for 30 min, BEAS‑2B cells were exposed to HCl for 30 min. Cell viability, cytotoxicity, IL‑8 levels and apoptosis were detected 4 h following acid stimulation. The viability of BEAS‑2B cells was inhibited and cell death was increased in the presence of HCl. HCl stimulation induced activation of MAPKs in a time‑dependent manner. HCl exposure increased the levels of IL‑8 and the release of LDH, and induced apoptosis in BEAS‑2B cells. JNK and p38 inhibitors increased cell viability and decreased cytotoxicity and cell apoptosis, while ERK inhibitor had no effect on cell viability, cytotoxicity or apoptosis. These results indicate that acid exposure induced epithelial cell injury and death. The activation of JNK and p38 is involved in HCl‑induced epithelial lung cell injury and death.

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Abacavir, didanosine and tenofovir do not induce inflammatory, apoptotic or oxidative stress genes in coronary endothelial cells.

The use of abacavir and didanosine in HAART has been associated with an increased risk of myocardial infarction in HIV-infected patients. The aim of this study was to address the development of endothelial dysfunction in cultivated coronary artery endothelial cells (HCAECs) in response to abacavir, didanosine and tenofovir. We examined the impact of these drugs on the expression levels of the proinflammatory, oxidative stress and apoptosis regulating genes in HCAECs.

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Asiatic acid inhibits pro-angiogenic effects of VEGF and human gliomas in endothelial cell culture models.

Malignant gliomas are one of the most devastating and incurable tumors. Sustained excessive angiogenesis by glioma cells is the major reason for their uncontrolled growth and resistance toward conventional therapies resulting in high mortality. Therefore, targeting angiogenesis should be a logical strategy to prevent or control glioma cell growth. Earlier studies have shown that Asiatic Acid (AsA), a pentacyclic triterpenoid, is effective against glioma and other cancer cells; however, its efficacy against angiogenesis remains unknown. In the present study, we examined the anti-angiogenic efficacy of AsA using human umbilical vein endothelial cells (HUVEC) and human brain microvascular endothelial cells (HBMEC). Our results showed that AsA (5-20 µM) inhibits HUVEC growth and induces apoptotic cell death by activating caspases (3 and 9) and modulating the expression of apoptosis regulators Bad, survivin and pAkt-ser473. Further, AsA showed a dose-dependent inhibition of HUVEC migration, invasion and capillary tube formation, and disintegrated preformed capillary network. AsA also inhibited the VEGF-stimulated growth and capillary tube formation by HUVEC and HBMEC. Next, we analyzed the angiogenic potential of conditioned media collected from human glioma LN18 and U87-MG cells treated with either DMSO (control conditioned media, CCM) or AsA 20 µM (AsA20 conditioned media, AsA20CM). CCM from glioma cells significantly enhanced the capillary tube formation in both HUVEC and HBMEC, while capillary tube formation in both endothelial cell lines was greatly compromised in the presence of AsA20CM. Consistent with these results, VEGF expression was lesser in AsA20CM compared to CCM, and indeed AsA strongly inhibited VEGF level (both cellular and secreted) in glioma cells. AsA also showed dose-dependent anti-angiogenic efficacy in Matrigel plug assay, and inhibited the glioma cells potential to attract HUVEC/HBMEC. Overall, the present study clearly showed the strong anti-angiogenic potential of AsA and suggests its usefulness against malignant gliomas.

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Human Small Intestine Mic Human Large Intestine Mic Human Internal Mammary Ar GFP Expressing Human Inte CELLKINES Natural Human I Human Endocrine Gland Vas Human Vascular Endothelia Human Vascular Endothelia Goat Anti-Human Endotheli Macrophage Colony Stimula Macrophage Colony Stimula Recombinant Human VEGF VE

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Phytoestrogen calycosin-7-O-β-D-glucopyranoside ameliorates advanced glycation end products-induced HUVEC damage.

Vasculopathy including endothelial cell (EC) apoptosis and inflammation contributes to the high incidence of stroke and myocardial infarction in diabetic patients. The aim of the present study was to investigate the effect of calycosin-7-O-β-D-glucopyranoside (CG), a phytoestrogen, on advanced glycation end products (AGEs)-induced HUVEC damage. We observed that CG can significantly ameliorate AGEs-induced HUVEC oxidative stress and apoptosis. The ratio of SOD/MDA was significantly increased to the normal level by CG pretreatment. CG preincubation dramatically increased anti-apoptotic Bcl-2 while decreased pro-apoptotic Bax and Bad expressions as detected by immunocytochemistry. Moreover, CG ameliorated macrophage migration and adhesion to HUVEC; the monocyte chemotactic protein-1 and interleukin-6 levels in the culture supernatant were dramatically reduced by CG as determined by ELISA; the expressions of inflammatory proteins including ICAM-1, TGF-β1, and RAGE in both protein and mRNA levels were significantly reduced to the normal level by CG pretreatment as determined by immunocytochemistry and real-time RT-PCR. The intracellular investigation suggests that CG can reverse AGEs-activated ERK1/2 and NF-κB phosphorylation, in which estrogen receptors were involved in. Our results strongly indicate that CG can modulate EC dysfunction by ameliorating AGEs-induced cell apoptosis and inflammation.

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Anti RAGE (Receptor for A Anti 3 DG imidazolone Mon Anti AGE 3 Monoclonal Ant Rat monoclonal anti mouse Human Anti-Advanced Glyco Advanced Glycation End Pr Advanced Glycation End Pr OxiSelect™ Cellular UV- CD31, Endothelial Cell; CD31, Endothelial Cell; CD34, Endothelial Cell; CD34, Endothelial Cell;

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[Autocrine stimulation of receptor-tyrosine kinases (RTK) in human tumor cell lines in vitro: therapeutic implications].

The VEGF/VEGFR system is known to play an important role in the development of new blood vessels during tumor formation. There is evidence that VEGFRs are not only present on endothelial cells but also on tumor cells. Since VEGF is able to induce proliferation and migration via VEGFR-2 we have studied the expression of VEGFRs and related receptor tyrosine kinases (RTKs) in different tumor cell lines and the effect of growth factor stimulation.

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Modulation of pro- and anti-inflammatory cytokine production in very preterm infants.

In premature infants, outcome of infection-associated complications is heterogeneous despite advances in antibiotic treatment and diagnosis. Information on the immune response in preterm infants is limited. Immune modulatory strategies require detailed analysis of mediators and their kinetics.

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Bcl-xL mediates a survival mechanism independent of the phosphoinositide 3-kinase/Akt pathway in prostate cancer cells.

Among various molecular strategies by which prostate cancer cells evade apoptosis, phosphoinositide 3-kinase (PI3K)/Akt signaling represents a dominant survival pathway. However, different prostate cancer cell lines such as LNCaP and PC-3 display differential sensitivity to the apoptotic effect of PI3K inhibition in serum-free media, reflecting the heterogeneous nature of prostate cancer in apoptosis regulation. Whereas both cell lines are equally susceptible to LY294002-mediated Akt dephosphorylation, only LNCaP cells default to apoptosis, as evidenced by DNA fragmentation and cytochrome c release. In PC-3 cells, Akt deactivation does not lead to cytochrome c release, suggesting that the intermediary signaling pathway is short-circuited by an antiapoptotic factor. This study presents evidence that Bcl-xL overexpression provides a distinct survival mechanism that protects PC-3 cells from apoptotic signals emanating from PI3K inhibition. First, the Bcl-xL/BAD ratio in PC-3 cells is at least an order of magnitude greater than that of LNCaP cells. Second, ectopic expression of Bcl-xL protects LNCaP cells against LY294002-induced apoptosis. Third, antisense down-regulation of Bcl-xL sensitizes PC-3 cells to the apoptotic effect of LY294002. The physiological relevance of this Bcl-xL-mediated survival mechanism is further underscored by the protective effect of serum on LY294002-induced cell death in LNCaP cells, which is correlated with a multifold increase in Bcl-xL expression. In contrast to Bcl-xL, Bcl-2 expression levels are similar in both cells lines, and do not respond to serum stimulation, suggesting that Bcl-2 may not play a physiological role in antagonizing apoptosis signals pertinent to BAD activation in prostate cancer cells.

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