Publications by authors named "Cecile Husson"

Background: Following STRIDE-II recommendations, the discovery of novel noninvasive biomarkers, beyond the use of C-reactive protein (CRP) and fecal calprotectin, remains a medical need to further improve the monitoring of patients with inflammatory bowel disease (IBD). This study aims to evaluate the potential of serum lipopolysaccharide-binding protein (LBP) in monitoring IBD activity.

Methods: This retrospective cross-sectional study included 69 IBD patients (43 Crohn's disease and 26 ulcerative colitis) and 82 controls.

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Although cisplatin is used as a first-line therapy in many cancers, its nephrotoxicity remains a real problem. Acute kidney injuries induced by cisplatin can cause proximal tubular necrosis, possibly leading to interstitial fibrosis, chronic dysfunction, and finally to a cessation of chemotherapy. There are only a few nephroprotective actions that can help reduce cisplatin nephrotoxicity.

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  • - Aristolochic acid nephropathy (AAN) is a serious kidney condition caused by consuming substances with aristolochic acids, often found in certain Chinese herbal remedies and contaminated food, leading to kidney damage and chronic conditions.
  • - Research used rodent models to study how AAN progresses from acute kidney injury (AKI) to chronic kidney disease (CKD), revealing that initial injury leads to inflammation and eventual severe kidney deterioration.
  • - Four key players in this transition were identified: tubular epithelial cells, endothelial cells, inflammatory cells, and myofibroblasts, highlighting their roles in kidney damage and potential future research directions.
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Aristolochic acids (AAs) are powerful nephrotoxins that cause severe tubulointerstitial fibrosis. The biopsy-proven peritubular capillary rarefaction may worsen the progression of renal lesions via tissue hypoxia. As we previously observed the overproduction of reactive oxygen species (ROS) by cultured endothelial cells exposed to AA, we here investigated in vitro AA-induced metabolic changes by H-NMR spectroscopy on intracellular medium and cell extracts.

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  • Aristolochic acid nephropathy (AAN) causes kidney damage characterized by fibrosis and tubular atrophy, with a link between reduced capillary density and fibrosis severity.
  • The study found that aristolochic acid (AA) harms endothelial cells, impairing their function and leading to increased reactive oxygen species (ROS) and calcium levels, which contribute to cell death.
  • Antioxidants and AMPK activators showed promise in reversing some of the damage caused by AA, suggesting that restoring cellular balance could alleviate microcirculation issues and improve kidney health.
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Experimental aristolochic acid nephropathy is characterized by transient acute proximal tubule necrosis and inflammatory cell infiltrates followed by interstitial fibrosis and tubular atrophy. The respective role of T-cell subpopulations has never been studied in the acute phase of the mouse model, and was heretofore exclusively investigated by the use of several depletion protocols. As compared to mice injected with aristolochic acids alone, more severe acute kidney injury was observed after CD4 or CD8 T-cells depletion.

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  • Myoglobinuric acute kidney injury (AKI) is a serious condition that needs to be treated quickly to avoid severe health issues.
  • The report talks about a kidney transplant patient who got very sick because of a virus and had high levels of a protein called myoglobin in their blood, which harmed their kidneys.
  • Using a special dialysis machine helped remove up to 71% of the myoglobin from the patient’s blood in just 3 hours, and their kidney function improved fast, but doctors still need to figure out when to use this expensive treatment for the best results.
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Ethnopharmacological Relevance: The world prevalence of kidney stones is increasing and plants are frequently used to treat urolithiasis. Pistacia lentiscus L, a plant which freely grows around the Mediterranean basin areas, is widely used for various pathologies. P.

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Background: The platelet-derived growth factor receptor β (PDGFRβ)+ perivascular cell activation becomes increasingly recognized as a main source of scar-associated kidney myofibroblasts and recently emerged as a new cellular therapeutic target.

Aims: In this regard, we first confirmed the presence of PDGFRβ+ perivascular cells in a human case of end-stage aristolochic acid nephropathy (AAN) and thereafter we focused on the early fibrosis events of transforming growth factor β (TGFβ) inhibition in a rat model of AAN.

Materials And Methods: Neutralizing anti-TGFβ antibody (1D11) and its control isotype (13C4) were administered (5 mg/kg, i.

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Ethnopharmacological Relevance: Although acknowledged as toxic herbs, Aristolochia species are still widely used worldwide. The aristolochic acids (AA) they contain can induce the so-called "aristolochic acid nephropathy", leading to renal fibrosis and upper urinary tract cancer. Traditional Moroccan medicine still often uses Aristolochia species under the vernacular name of Bereztem for the treatment of numerous ailments, notably cancer, diabetes or digestive tract disorders.

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  • - Aristolochic acids (AA) are toxic to kidneys and can lead to chronic kidney disease, prompting researchers to explore if rhBMP-7 can prevent damage caused by AA.
  • - In lab tests, AA increased markers of cell damage and fibrosis while rhBMP-7 showed limited ability to counteract these changes in renal cells.
  • - In animal studies, treatment with rhBMP-7 did not prevent kidney damage or related complications caused by AA, indicating that its protective effects need further investigation.
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Background: The 2009 KDIGO (Kidney Disease: Improving Global Outcomes) chronic kidney disease-mineral and bone disorder clinical practice guideline suggests correcting 25-hydroxyvitamin D3 (25[OH]D) levels<30ng/mL in patients treated with maintenance hemodialysis, but does not provide a specific treatment protocol.

Study Design: 2-center, double-blind, randomized, 13-week, controlled trial followed by a 26-week open-label study.

Setting & Participants: 55 adult maintenance hemodialysis patients with 25(OH)D levels<30ng/mL were recruited from June 2008 through October 2009.

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  • The study aimed to evaluate existing and new diagnostic criteria for endemic nephropathy (EN), as no specific biomarker has been identified yet.
  • Researchers compared clinical and laboratory data from a population in EN-affected villages using modified WHO criteria and applied ROC analysis to determine the predictive value of various variables.
  • Findings highlighted that while certain urinary markers and kidney measurements could effectively distinguish EN patients, the cut-off values for alfa1-microglobulin needed adjustment, and family history significantly increased the risk of developing the disease.
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Objective: High glucose content of peritoneal dialysis fluids (PDFs) has been shown to contribute to loss of peritoneal function during long-term peritoneal dialysis. However, hyperosmolality and hypertonicity of PDF are usually seen as similar stress events inducing osmotic stress-induced programmed cell death. In this study, we examined the impact of various osmotic agents on apoptosis induced by hyperosmolar PDFs, focusing on the mechanisms underlying the lethal effects of PDFs on peripheral blood mononuclear cells (PBMCs).

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Background: Interstitial inflammation is a prominent feature associated with the severity of renal injury and progressive kidney failure. We utilized an animal model of aristolochic acid (AA)-induced nephropathy (AAN) to assess patterns of infiltration and inflammation during the evolution of tubulointerstitial damage and to relate them to the development of fibrosis.

Methods: Male Wistar rats receiving sc daily AA or vehicle were sacrificed between Days 1 and 35.

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Background: Experimental aristolochic acid nephropathy (AAN), characterized by interstitial fibrosis, tubular atrophy, and chronic renal failure, was reported after 35-day injections of aristolochic acids (AA) to salt-depleted male Wistar rats. The link between renal fibrosis and the renin-angiotensin system (RAS) in this model remains unknown.

Methods: We investigated the impact of sodium diets (low and normal), of RAS inhibition with enalapril (ENA) alone, or combined with candesartan (CSN) for 35 days, and ENA + CSN for 65 days on AAN development.

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