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Ram n Cantero-Cid Karla Marina Montalb n-Hern ndez Jenny Guevara Alejandro Pascual-Iglesias Elisa Pulido Jos Carlos Casalvilla Crist bal Marcano Cristina Barrag n Serrano Jaime Valent n Gloria Cristina Bonel-P rez Jos Avenda o-Ortiz Ver nica Terr n Roberto Lozano-Rodr guez Alejandro Mart n-Quir s Elvira Mar n Eva Pena Laura Guerra-Pastri n Eduardo L pez-Collazo Luis Augusto Aguirre 《World journal of gastrointestinal oncology》2022,14(1):295-318
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Francisco Arnalich Maria Constanza Maldifassi Enrique Ciria Angustias Quesada Rosa Codoceo Rafael Herruzo Carlos Garcia-Cerrada Fernando Montoya Juan José Vazquez Eduardo López-Collazo Carmen Montiel 《Clinica chimica acta; international journal of clinical chemistry》2010,411(17-18):1269-1274
BackgroundDiagnosing patients with acute mesenteric ischemia (AMI) in the emergency ward is challenging. This study assesses the usefulness of plasma DNA in patients with clinically suspected AMI.Methods130 consecutive patients who underwent laparotomy were studied. Cell-free plasma DNA was measured by real-time quantitative PCR assay for the β-globin gene. The primary endpoint was the accuracy of plasma DNA for predicting 30-day mortality.ResultsSurgery revealed AMI in 99 patients and alternative diagnoses in 31 patients. Forty-six patients with AMI died (46.6%) as compared to 6 (19.4%) in the non-AMI group (p < 0.05). The DNA concentration at admission was significantly higher in patients with AMI (median 7340 GE/ml, versus, 2735 GE/ml, p < 0.01) and in AMI patients who died (8830 GE/ml, versus 4970 GE/ml, p < 0.05). The area under the ROC curves for plasma DNA as a marker for mesenteric ischemia and independent predictor for 30-day mortality were 0.708 (95% CI 0.701–0.890) and 0.815 (95% CI 0.735–0.894). Multiple logistic regression analysis showed that the risk of hospital mortality increased 1.52-fold for every 1000 GE/ml increase in plasma DNA.ConclusionsPlasma DNA levels may be a useful biomarker in predicting the outcome of patients with AMI. 相似文献
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González-León MC Soares-Schanoski A del Fresno C Cimadevila A Goméz-Piña V Mendoza-Barberá E García F Marín E Arnalich F Fuentes-Prior P López-Collazo E 《Journal of endotoxin research》2006,12(5):296-306
In contrast to the thoroughly characterized mechanisms of positive regulation within cytokine signaling pathways, our knowledge of negative feedback loops is comparatively sparse. We and others have previously reported that IRAK-M down-regulates inflammatory responses to multiple stimuli. In particular, we could show that the nitric oxide (NO) donor, GSNO, induces IRAK-M overexpression in human monocytes. Here we study the expression of another important negative regulator of cytokine signaling, SOCS-1, in human monocytes exposed to GSNO. The NO donor induced significant levels of SOCS-1 mRNA and protein, 6 h and 16 h after stimulation, respectively. Monocytes stimulated with GSNO for longer periods (24 h and 48 h) failed to express IL-6 and IP-10 upon LPS challenge. In addition, and in line with previous reports of NO-mediated induction of TNF-alpha, we have found that exposure to this cytokine induces SOCS-1 mRNA in human monocytes. A blocking antibody against TNF-alpha impaired SOCS-1 expression upon GSNO treatment and re-instated IL-6 and IP-10 mRNA levels after LPS challenge in cultures pretreated with the NO donor. We conclude that NO stimulates SOCS-1 overexpression in a pathway at least partially regulated by TNF-alpha. 相似文献
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Circulating cell-free DNA (cf-DNA) mainly comes from apoptotic cells and can reflect the extent of cellular damage. Increased
plasma levels of cf-DNA have been found in many acute disorders, including septic and clinically ill patients, and usually
correlate well with clinical outcome. Acute respiratory failure, the most frequent organ failure in ICU patients, can be related
to various acute diseases that may cause cell death and release of DNA into the bloodstream. In a recent issue of Critical Care, Okkonen and colleagues evaluate levels of cf-DNA in plasma as a prognostic marker in patients needing mechanical ventilation.
They report that plasma cf-DNA was higher than normal in patients with mechanical ventilation, and even higher in patients
who eventually died compared to survivors. However, its usefulness as a death predictor may be limited in the heterogeneous
group of mechanically ventilated patients, probably due to confounding effects of co-morbidities, among other factors. 相似文献
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Gómez-Piña V Martínez E Fernández-Ruíz I Del Fresno C Soares-Schanoski A Jurado T Siliceo M Toledano V Fernández-Palomares R García-Rio F Arnalich F Biswas SK López-Collazo E 《Journal of leukocyte biology》2012,91(6):933-945
The MMPs constitute a family of endopeptidases that can cleavage extracellular proteins. They are involved in a number of events; some of these include inflammatory processes. One of its targets is the TREM-1, which has emerged as an important modulator of innate immune responses in mammals. This transmembrane glycoprotein possesses an Ig-like ectodomain readily shed by MMPs to generate sTREM-1. Whereas membrane-anchored TREM-1 amplifies inflammatory responses, sTREM-1 exhibits anti-inflammatory properties. Here we show that sustained cell surface expression of TREM-1 in human monocytes, through metalloproteinase inhibition, counteracts the well-characterized down-regulation of several proinflammatory cytokines during the ET time-frame, also known as M2 or alternative activation. In addition to the cytokines profile, other features of the ET phenotype were underdeveloped when TREM-1 was stabilized at the cell surface. These events were mediated by the signal transducers PI3Ks and Syk. We also show that sTREM-1 counteracts the proinflammatory response obtained by membrane TREM-1 stabilization but failed to induce ET on na?ve human monocytes. As the sustained TREM-1 expression at the cell surface suffices to block the progress of a refractory state in human monocytes, our data indicate that TREM-1 and MMPs orchestrate an "adaptive" form of innate immunity by modulating the human monocytes response to endotoxin. 相似文献
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Juan Manuel Torres Rubén Martinez-Barricarte Sonia García-Gómez Marina S. Mazariegos Yuval Itan Bertrand Boisson Rita ρlvarez Ana?s Jiménez-Reinoso Lucia del Pino Rebeca Rodríguez-Pena Antonio Ferreira Enrique Hernández-Jiménez Victor Toledano Carolina Cubillos-Zapata Mariana Díaz-Almirón Eduardo López-Collazo José L. Unzueta-Roch Silvia Sánchez-Ramón Jose R. Regueiro Eduardo López-Granados Jean-Laurent Casanova Rebeca Pérez de Diego 《The Journal of clinical investigation》2014,124(12):5239-5248
Heterotrimers composed of B cell CLL/lymphoma 10 (BCL10), mucosa-associated lymphoid tissue lymphoma translocation protein 1 (MALT1), and caspase recruitment domain–containing (CARD) family adaptors play a role in NF-κB activation and have been shown to be involved in both the innate and the adaptive arms of immunity in murine models. Moreover, individuals with inherited defects of MALT1, CARD9, and CARD11 present with immunological and clinical phenotypes. Here, we characterized a case of autosomal-recessive, complete BCL10 deficiency in a child with a broad immunodeficiency, including defects of both hematopoietic and nonhematopoietic immunity. The patient died at 3 years of age and was homozygous for a loss-of-expression, loss-of-function BCL10 mutation. The effect of BCL10 deficiency was dependent on the signaling pathway, and, for some pathways, the cell type affected. Despite the noted similarities to BCL10 deficiency in mice, including a deficient adaptive immune response, human BCL10 deficiency in this patient resulted in a number of specific features within cell populations. Treatment of the patient’s myeloid cells with a variety of pathogen-associated molecular pattern molecules (PAMPs) elicited a normal response; however, NF-κB–mediated fibroblast functions were dramatically impaired. The results of this study indicate that inherited BCL10 deficiency should be considered in patients with combined immunodeficiency with B cell, T cell, and fibroblast defects. 相似文献
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Soares-Schanoski A Gómez-Piña V del Fresno C Rodríguez-Rojas A García F Glaría A Sánchez M Vallejo-Cremades MT Baos R Fuentes-Prior P Arnalich F López-Collazo E 《Journal of leukocyte biology》2007,82(3):700-709
Osteoclasts are large, multinucleated cells, which originate from the fusion of macrophages. They play a central role in bone development and remodeling via the resorption of bone and are thus important mediators of bone loss, which leads to osteoporosis. IL-1R-associated kinase (IRAK)-M is a pseudokinase, which acts as a negative modulator of innate immune responses mediated by TLRs and IL-1R. Recently, it has been reported that IRAK-M also participates in the control of macrophage differentiation into osteoclasts. In addition, it was shown that IRAK-M knockout mice develop a strong osteoporosis phenotype, suggesting that down-regulation of this molecule activates osteoclast-mediated bone resorption. We studied the effect of the osteoporosis-inducing glucocorticoid, 6-methylprednisolone (6-MP), on IRAK-M expression in osteoclasts. Our results showed that osteoclasts, derived from THP-1 and RAW cells as well as human blood monocytes, differentiated into osteoclasts, express high levels of IRAK-M at mRNA and protein levels. In addition, 6-MP down-regulates IRAK-M expression, which correlates with an increased activation of bone resorption. These findings suggest a mechanism of corticosteroid-induced osteoporosis and open new avenues for treating this endemic disease of Western societies. 相似文献