199,398 research outputs found
HO-1 expression in macrophages.
No full textRepresentative sections (400x magnifications) of rat prostate MatLyLu TINT double stained for CD68+ (brow) and HO-1+ (red) cells (A), or double stained for CD163+ (brown) and HO-1+ (red) cells (B). Most cells stained both red and blown suggesting that most HO-1+ cells are macrophages, and in particular of the M2-type (CD163+).</p
Going Beyond Counting First Authors in Author Co-citation Analysis
No full textThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Dispelling the Myths Behind First-author Citation Counts
No full textWe conducted a full-scale evaluative citation analysis study of scholars in the XML research field to explore just how different from each other author rankings resulting from different citation counting methods actually are, and to demonstrate the capability of emerging data and tools on the Web in supporting more realistic citation counting methods. Our results contest some common arguments for the continued
use of first-author citation counts in the evaluation of scholars, such as high correlations between author rankings by first-author citation counts and other citation
counting methods, and high costs of using more realistic citation counting methods that are not well-supported by the ISI databases. It is argued that increasingly available digital full text research papers make it possible for citation analysis studies to go beyond what the ISI databases have directly supported and to employ more
sophisticated methods
HO-1 expression in human primary prostate tumors.
No full text(A) Representative sections of HO-1 staining (brown) in non-malignant prostate tissue, in a Gleason score (GS) 7 primary prostate tumor, and in a GS 10 primary prostate tumor (200x magnifications, inserts show higher magnifications). (B) A GS 10 tumor double stained for factor VIII positive blood vessels (green) and HO-1+ cells (brown) (400x magnifications, and insert at higher magnifications).</p
HO-1 induction promotes M2 macrophage polarisation.
No full textRAW 264.7 cells were transfected with siRNA HO-1 and siRNA NC (non-correlated). (A) RT-qPCR analysis of HO-1 mRNA in cells transfected 48 hours after transfection. Cells were treated with SP (10 μM) and/or LPS (100 ng/ml) for 24 hours and mRNA expression of selected genes was evaluated by RT-qPCR (B) IL-6 mRNA expression (C) TNF-α mRNA expression (D) Arg1 mRNA expression (E) IL-10 mRNA expression and (F) Rel A mRNA expression. The data are mean ±SD of two separate experiments, each of which was performed in triplicate. **p < 0.01 versus siRNA NC.</p
HO-1 and HIF-1α are expressed in the peri-infarct region of the ischemic mouse brain.
No full text(A) Representative image of the TTC stained regions (a, contralateral region; b, peri-infarct region; c, infarct region) in a mouse subjected to 2 h ischemia and 24 h reperfusion (I/R) (n = 3 per group). (B) DAB staining observed as brown color in the peri-infarct region (b) in wild-type (WT) and HO-1+/- mice. Scale bars = 20 μm. (C) Expression of target proteins was determined in brain tissues using western blot analysis, and their levels were quantified (n = 5 per group). **P D) WT and HO-1+/- mice were subjected to I/R, and the brain sections (a, contralateral region; b, peri-infarct region; c, infarct region) were stained with the indicated antibodies (n = 4 per group). Images are representative from three individual tissues.</p
HO-1 is rapidly increased after haptoglobin and hemopexin infusion.
No full text(A and B) SS-mice (n = 3/group) were infused with vehicle or equimolar (1 μmol/kg) Hb, Hp, Hpx, Hb + Hp, or Hb + Hpx. Livers were removed and flash frozen 1 hour after infusion. Hepatic microsomes were used to assess heme oxygenase (HO) activity (A) via bilirubin production and protein expression (B) via immunoblot. Bars are means ± SD, **p (C and D) SS-mice (n = 3/group) were untreated or infused with Hp or Hpx (1 μmol/kg) at baseline (time 0). Livers were removed and flash frozen 24, 48 or 72 hours after infusion. Hepatic microsomes were used to assess (C) HO activity and (D) HO-1 protein expression via immunoblot. Bars are means ± SD, *p (E and F) SS-mice (n = 3/group) were infused with vehicle or increasing doses (0.0156, 0.0625, 0.25 or 1.0 μmols/kg) of Hp or Hpx at baseline. Livers and kidneys were removed and flash frozen 24 hours after infusion. Hepatic (E) and kidney (F) microsomes were used to assess HO activity. Bars are means ± SD.</p
HO-1 protein expression in rat prostate tumors and in the surrounding non-malignant prostate tissue (TINT).
No full text(A) Representative sections of control rat prostate tissue and orthotopic rat prostate tumors and TINT stained for HO-1 (brown) (left panel; 100x magnifications, right panel; shows higher magnifications). (B) Antibody specificity control. No staining was seen in sections incubated with primary antibody that had been pre-incubated with an excess of a recombinant rat HO-1 peptide.</p
HMOX1 gene promoter alleles and high HO-1 levels are associated with severe malaria in Gambian children.
No full textHeme oxygenase 1 (HO-1) is an essential enzyme induced by heme and multiple stimuli associated with critical illness. In humans, polymorphisms in the HMOX1 gene promoter may influence the magnitude of HO-1 expression. In many diseases including murine malaria, HO-1 induction produces protective anti-inflammatory effects, but observations from patients suggest these may be limited to a narrow range of HO-1 induction, prompting us to investigate the role of HO-1 in malaria infection. In 307 Gambian children with either severe or uncomplicated P. falciparum malaria, we characterized the associations of HMOX1 promoter polymorphisms, HMOX1 mRNA inducibility, HO-1 protein levels in leucocytes (flow cytometry), and plasma (ELISA) with disease severity. The (GT)(n) repeat polymorphism in the HMOX1 promoter was associated with HMOX1 mRNA expression in white blood cells in vitro, and with severe disease and death, while high HO-1 levels were associated with severe disease. Neutrophils were the main HO-1-expressing cells in peripheral blood, and HMOX1 mRNA expression was upregulated by heme-moieties of lysed erythrocytes. We provide mechanistic evidence that induction of HMOX1 expression in neutrophils potentiates the respiratory burst, and propose this may be part of the causal pathway explaining the association between short (GT)(n) repeats and increased disease severity in malaria and other critical illnesses. Our findings suggest a genetic predisposition to higher levels of HO-1 is associated with severe illness, and enhances the neutrophil burst leading to oxidative damage of endothelial cells. These add important information to the discussion about possible therapeutic manipulation of HO-1 in critically ill patients
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