oalib
Search Results: 1 - 10 of 100 matches for " "
All listed articles are free for downloading (OA Articles)
Page 1 /100
Display every page Item
Naturally occurring anti M complicating ABO grouping  [cached]
Khalid Safoorah,Dantes Roelyn,Varghese Sunu,Al Hakawati Imadeddin
Indian Journal of Pathology and Microbiology , 2011,
Abstract: Anti M is considered a naturally occurring antibody that is usually active at temperatures below 37°C and is thus of no clinical significance. This antibody, if present in an individual, can lead to a discrepancy between forward and reverse ABO grouping and thus creates diagnostic difficulties for blood bank staff. We report a case of a 58-year-old lady who had an unexpected reaction in reverse grouping due to anti M that posed a problem for us in the interpretation of results of her blood group. We also reviewed the literature to find out the significance of such discrepancy in blood grouping.
IS CARDIOVASCULAR RISK MORE IN DIABETICS BECAUSE OF LOWER APOLIPOPROTEIN A1 LEVELS RATHER THAN HIGHER APO B /APOA1 RATIO?  [cached]
Rajni Dawar,Sakshi Singal,Ritu Singh
International Journal of Biomedical Research , 2013, DOI: 10.7439/ijbr.v2i2.87
Abstract: Diabetics are known to have increased risk of cardiovascular diseases. Apolipoprotein B/ A1 ratio is considered to be a good biochemical marker for Coronary Artery Disease (CAD) risk assessment. The study was designed to estimate serum levels of apolipoprotein A1 , B and calculate Apo B/Apo A1 ratio in thirty diagnosed patients of type II diabetes attending the diabetic clinic in Lady Hardinge Medical College and Associated SSK Hospital, comparing them with age and sex matched controls and assessing their significance levels. Fasting Plasma Glucose ,Apolipoprotein A1 and apolipoprotein B in serum were measured by on fully automated analyser SYNCHRON CX9 using Kit from Randox . Statistical analysis was done by using SPSS version 17.0.It was found that Fasting plasma glucose was significantly higher in the study group compared to control group (p<0.0001). Apolipoprotein A1 was lower in patients of diabetes mellitus as compared to controls and the difference was very highly significant p<0.0001. Apolipoprotein B levels as well as Apo B/Apo A1 were significantly higher in diabetics compared to controls with p<0.01 for both. It emerged from the study that apolipoprotein A1 levels are more significant compared to apolipoprotein B and ratio of Apo B/Apo A1 and therefore is a better assessor of CAD risk in diabetics.
IS CARDIOVASCULAR RISK MORE IN DIABETICS BECAUSE OF LOWER APOLIPOPROTEIN A1 LEVELS RATHER THAN HIGHER APO B /APOA1 RATIO?
Rajni Dawar,Sakshi Singal,Ritu Singh
International Journal of Biomedical Research , 2011, DOI: 10.7439/ijbr.v2i2.87
Abstract: Diabetics are known to have increased risk of cardiovascular diseases. Apolipoprotein B/ A1 ratio is considered to be a good biochemical marker for Coronary Artery Disease (CAD) risk assessment. The study was designed to estimate serum levels of apolipoprotein A1 , B and calculate Apo B/Apo A1 ratio in thirty diagnosed patients of type II diabetes attending the diabetic clinic in Lady Hardinge Medical College and Associated SSK Hospital, comparing them with age and sex matched controls and assessing their significance levels. Fasting Plasma Glucose ,Apolipoprotein A1 and apolipoprotein B in serum were measured by on fully automated analyser SYNCHRON CX9 using Kit from Randox . Statistical analysis was done by using SPSS version 17.0.It was found that Fasting plasma glucose was significantly higher in the study group compared to control group (p<0.0001). Apolipoprotein A1 was lower in patients of diabetes mellitus as compared to controls and the difference was very highly significant p<0.0001. Apolipoprotein B levels as well as Apo B/Apo A1 were significantly higher in diabetics compared to controls with p<0.01 for both. It emerged from the study that apolipoprotein A1 levels are more significant compared to apolipoprotein B and ratio of Apo B/Apo A1 and therefore is a better assessor of CAD risk in diabetics.
Dysregulation of Anti-Inflammatory Annexin A1 Expression in Progressive Crohns Disease  [PDF]
Angela Sena, Irina Grishina, Anne Thai, Larissa Goulart, Monica Macal, Anne Fenton, Jay Li, Thomas Prindiville, Sonia Maria Oliani, Satya Dandekar, Luiz Goulart, Sumathi Sankaran-Walters
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0076969
Abstract: Background Development of inflammatory bowel disease (IBD) involves the interplay of environmental and genetic factors with the host immune system. Mechanisms contributing to immune dysregulation in IBD are not fully defined. Development of novel therapeutic strategies is focused on controlling aberrant immune response in IBD. Current IBD therapy utilizes a combination of immunomodulators and biologics to suppress pro-inflammatory effectors of IBD. However, the role of immunomodulatory factors such as annexin A1 (ANXA1) is not well understood. The goal of this study was to examine the association between ANXA1 and IBD, and the effects of anti-TNF-α, Infliximab (IFX), therapy on ANXA1 expression. Methods ANXA1 and TNF-α transcript levels in PBMC were measured by RT PCR. Clinical follow up included the administration of serial ibdQs. ANXA1 expression in the gut mucosa was measured by IHC. Plasma ANXA1 levels were measured by ELISA. Results We found that the reduction in ANXA1 protein levels in plasma coincided with a decrease in the ANXA1 mRNA expression in peripheral blood of IBD patients. ANXA1 expression is upregulated during IFX therapy in patients with a successful intervention but not in clinical non-responders. The IFX therapy also modified the cellular immune activation in the peripheral blood of IBD patients. Decreased expression of ANXA1 was detected in the colonic mucosa of IBD patients with incomplete resolution of inflammation during continuous therapy, which correlated with increased levels of TNF-α transcripts. Gut mucosal epithelial barrier disruption was evident by increased plasma bacterial 16S levels. Conclusion Loss of ANXA1 expression may support inflammation during IBD and can serve as a biomarker of disease progression. Changes in ANXA1 levels may be predictive of therapeutic efficacy.
Anti-Inflammatory Preconditioning by Agonists of Adenosine A1 Receptor  [PDF]
Sigal Nakav, Cidio Chaimovitz, Yuval Sufaro, Eli C. Lewis, Gad Shaked, David Czeiger, Moshe Zlotnik, Amos Douvdevani
PLOS ONE , 2008, DOI: 10.1371/journal.pone.0002107
Abstract: Background Adenosine levels rise during inflammation and modulate inflammatory responses by engaging with four different G protein-coupled receptors. It is suggested that adenosine exhibits pro-inflammatory effects through its A1 receptor (A1R), and anti-inflammatory effects through A2A receptor (A2AR). Therefore, understanding of the mechanisms that govern adenosine receptor regulation may advance treatment of various inflammatory disorders. We previously reported that peak A1R expression during leukocyte recruitment, is followed by a peak in A2AR during inflammation resolution. Principal Findings Here, we examined whether A1R activation sequentially induces A2AR expression and by this reverses inflammation. The effect of adenosine on A1R mediated A2AR expression was examined in peritoneal macrophages (PMΦ) and primary peritoneal mesothelial cells (PMC) in vitro. Induction of A2AR was inhibited by pertussis toxin (PTX) and partly dependent on A2AR stimulation. Administration of A1R agonists to healthy mice reduced A1R expression and induced A2AR production in PMC. Mice that were preconditioned with A1R agonists 24 hours before E. coli inoculation exhibited decreased TNFα and IL-6 sera levels and reduced leukocytes recruitment. Preconditioning was blocked by pretreatment with A1R antagonist, as well as, or by late treatment with A2AR antagonist, and was absent in A2AR?/? mice. Conclusions Our data suggest that preconditioning by an A1R-agonist promotes the resolution of inflammation by inducing the production of A2AR. Future implications may include early treatment during inflammatory disorders or pretreatment before anticipated high risk inflammatory events, such as invasive surgery and organ transplantation.
Regulation of A1 by OX40 Contributes to CD8+ T Cell Survival and Anti-Tumor Activity  [PDF]
Fengyang Lei, Jianyong Song, Rizwanul Haque, Mohammad Haque, Xiaofang Xiong, Deyu Fang, Michael Croft, Jianxun Song
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0070635
Abstract: The TNFR family member OX40 (CD134) is critical for optimal clonal expansion and survival of T cells. However, the intracellular targets of OX40 in CD8 T cells are not fully understood. Here we show that A1, a Bcl-2 family protein, is regulated by OX40 in effector CD8 T cells. In contrast to wild-type T cells, OX40-deficient CD8 T cells failed to maintain A1 expression driven by antigen. Conversely, enforced OX40 stimulation promoted A1 expression. In both situations, the expression of A1 directly correlated with CD8 T cell survival. In addition, exogenous expression of A1 in OX40-deficient CD8 T cells reversed their survival defect in vitro and in vivo. Moreover, forced expression of A1 in CD8 T cells from OX40-deficient mice restored the ability of these T cells to suppress tumor growth in a murine model. These results indicate that OX40 signals regulate CD8 T cell survival at least in part through maintaining expression of the anti-apoptotic molecule A1, and provide new insight into the mechanism by which OX40 may impact anti-tumor immunity.
The Lantibiotic Peptide Labyrinthopeptin A1 Demonstrates Broad Anti-HIV and Anti-HSV Activity with Potential for Microbicidal Applications  [PDF]
Geoffrey Férir, Mariya I. Petrova, Graciela Andrei, Dana Huskens, Bart Hoorelbeke, Robert Snoeck, Jos Vanderleyden, Jan Balzarini, Stefan Bartoschek, Mark Br?nstrup, Roderich D. Süssmuth, Dominique Schols
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0064010
Abstract: Lantibiotics are peptides, produced by bacteria, that contain the noncanonical amino acid lanthionine and many of them exhibit antibacterial activities. The labyrinthopeptin A1 (LabyA1) is a prototype peptide of a novel class of carbacyclic lantibiotics. Here, we extensively evaluated its broad-spectrum activity against HIV and HSV in vitro, studied its mechanism of action and evaluated potential microbicidal applications. LabyA1 exhibited a consistent and broad anti-HIV activity (EC50s: 0.70–3.3 μM) and anti-HSV activity (EC50s: 0.29–2.8 μM) in cell cultures. LabyA1 also inhibited viral cell-cell transmission between persistently HIV-infected T cells and uninfected CD4+ T cells (EC50:2.5 μM) and inhibited the transmission of HIV captured by DC-SIGN+-cells to uninfected CD4+ T cells (EC50:4.1 μM). Time-of-drug addition studies revealed that LabyA1 acts as an entry inhibitor against HIV and HSV. Cellular and virus binding studies combined with SPR/FLIPR technology showed that LabyA1 interacted with the HIV envelope protein gp120, but not with the HIV cellular receptors. LabyA1 also demonstrated additive to synergistic effects in its anti-HIV-1 and anti-HSV-2 activity with anti(retro)viral drugs in dual combinations such as tenofovir, acyclovir, saquinavir, raltegravir and enfuvirtide. LabyA1 can be considered as a novel lead peptide as it had profound antiviral activity against HIV and HSV. Pre-treatment of PBMCs with LabyA1 neither increased the expression of the activation markers CD69 and CD25, nor enhanced HIV replication, nor significantly induced various inflammatory cytokines/chemokines. LabyA1 also did not affect the growth of vaginal Lactobacilli populations. Based on the lack of toxicity on the vaginal Lactobacillus strains and its synergistic/additive profile in combination with clinically approved anti(retro)virals, it deserves further attention as a potential microbicide candidate in the prevention of sexual transmitted diseases.
Propofol Inhibits the Activation of p38 through Up-Regulating the Expression of Annexin A1 to Exert Its Anti-Inflammation Effect  [PDF]
Jing Tang, Xi Chen, Weifeng Tu, Yuanbo Guo, Zhenlong Zhao, Qiong Xue, Chunshui Lin, Jinfang Xiao, Xuegang Sun, Tao Tao, Miaoning Gu, Youtan Liu
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0027890
Abstract: Inflammatory response is a kind of nonspecific immune response, with the central link of vascular response, which is mainly manifested by changes in neutrophils and vascular endothelial cells. In recent years, the in vivo and in vitro role of intravenous anesthetic propofol in inhibiting inflammatory response has been attracting more and more attention, but the anti-inflammatory mechanisms of propofol for mononuclear cells still remain undefined. In this study, proteomics analysis was applied to investigate protein expression profile changes in serum mononuclear cells following intervention of rats with endotoxemia using propofol. After two-dimensional electrophoresis and mass spectrometric identification, it has been found that the protein Annexin A1 was up-regulated in the propofol intervention group. Annexin A1 is a glucocorticoid-dependent anti-inflammatory protein. After detection using ELISA and Western blot assays, it has also been found that propofol can not only promote the expression of Annexin A1, but also inhibit the phosphorylation level of p38 and release of inflammatory factors (IL-1β, IL-6 and TNF-α) in rats with endotoxemia. In order to further determine the role of up-regulated expression of Annexin A1 in anti-inflammation of propofol, this gene was silenced in vitro in human THP-1 cells, to detect the phosphorylation status of p38 and release of inflammatory factors. The results show that Annexin A1 can negatively regulate phosphorylation of p38 and release of IL-1β, IL-6 and TNF-α in THP-1 cells following propofol intervention and lipopolysaccharide (LPS) stimulation. Our results clearly indicate that propofol can up-regulate Annexin A1 to inhibit the phosphorylation level of p38 and release of IL-1β, IL-6 and TNF-α, so as to inhibit inflammatory response. Therefore, it can be speculated that Annexin A1 might be the key signaling protein in the in vivo and in vitro anti-inflammatory mechanisms of propofol.
Anti-tumor immune response in ovarian cancer: clinical implications, prognostic significance and potential for novel treatment strategies
Nikos G. Gavalas,Meletios A. Dimopoulos,Aristotelis Bamias
Oncology Reviews , 2011, DOI: 10.4081/92
Abstract: Ovarian cancer is one of the leading causes of cancer-related death among women. Disease relapse occurs in a high number of cases and treatment currently involves the use of chemotherapy with the use of paclitaxel and platinum-based agents. Resistance to the disease occurs in more than 70% of the cases. The immune system is increasingly becoming a target for intense research in order to study the host’s immune response against ovarian cancer. T cell populations, including NK T cells and Tregs, have been associated with disease outcome indicating their increasing clinical significance, having been associated with positive prognosis and as markers of disease progress, respectively. Cytokines may also be associated with positive prognosis and they can have a direct or indirect effect in mobilizing relevant T cells, thus eliciting an immune response. Harnessing the immune system capacity in order to induce anti-tumor response is a major challenge. This is achieved via the use of antibodies that can elicit an immune response or via the use of direct administration of cytotoxic T cell populations (e.g., CD8?). This review examines the recent developments in our understanding of the mechanisms of development of the immune response in ovarian cancer as well as its prognostic significance and the existing experience in clinical studies using factors associated with immune response, such as monoclonal antibodies, cytokines, vaccines and activated or expanded relevant autologous populations from peripheral blood.
On the discrepancy principle  [PDF]
A. G. Ramm
Physics , 2003,
Abstract: A simple proof of the convergence of the variational regularization, with the regularization parameter, chosen by the discrepancy principle, is given for linear operators under suitable assumptions. It is shown that the discrepancy principle, in general, does not yield uniform with respect to the data convergence. An a priori choice of the regularization parameter is proposed and justified for some nonlinear operator equations.
Page 1 /100
Display every page Item


Home
Copyright © 2008-2017 Open Access Library. All rights reserved.