Nanoscale textured superconductivity in Ru-substituted BaFe2As2 : a challenge to a universal phase diagram for the pnictides

75As NMR experiments were performed in Ba(Fe1-xRux)2As2 for x=0 to 80%. Magnetic fractions and NMR lineshapes demonstrate that Ru substitution destroys the antiferromagnetic (AF) order inhomogeneously with a magnetic moment distributed from 0.9 to 0 uB. Superconductivity emerges at intermediate Ru doping and coexists with AF order only in the regions where moments are smaller than ~0.3uB, resulting in an original nanoscale texture. This situation contrasts with that of Co substitution, challenging the apparent universality of the phase diagram in Fe-based superconductors

EJNMMI Res

Inflammatory vascular disease of the arteries, such as inflamed atheromatous plaques or arteritis, may cause aneurysms or ischemic strokes. In this context, using positron emission tomography (PET) to image inflammation may help select patients who would benefit from appropriate therapeutic interventions. This study sought to assess the usefulness of the 18 kDa translocator protein (TSPO) tracers [C]-PBR28 and [F]-PBR06 for imaging inflammatory vascular disease in vitro and in vivo. Immunohistochemistry for macrophage infiltration as well as autoradiography with [F]-PBR06 were performed on eight paraffin-embedded, formalin-fixed atherosclerosis plaques prospectively collected after carotid endarterectomy of eight patients affected by ischemic stroke. Six different patients, one of whom was also included in the in vitro study, underwent PET imaging. Two patients with carotid stenosis associated with ischemic stroke were imaged with [F]-PBR06 PET/CT, and four other patients (three with large vessel vasculitis and one with bilateral carotid stenosis but without stroke) were imaged with [C]-PBR28. All in vitro sections showed specific binding of [F]-PBR06, which co-localized with immunohistochemistry markers for inflammation. However, in vivo TSPO imaging with either [C]-PBR28 or [F]-PBR06 was negative in all participants. Despite good uptake on surgical samples in vitro, [C]-PBR28 and [F]-PBR06 are not viable clinical tools for imaging inflammatory vascular disease. NCT02513589, registered 31 July 2015 and NCT00547976, registered 23 October 2007. https://clinicaltrials.gov

The effect of body weight on altered expression of nuclear receptors and cyclooxygenase-2 in human colorectal cancers

<p>Abstract</p> <p>Background</p> <p>Epidemiological studies on risk factors for colorectal cancer (CRC) have mainly focused on diet, and being overweight is now recognized to contribute significantly to CRC risk. Overweight and obesity are defined as an excess of adipose tissue mass and are associated with disorders in lipid metabolism. Peroxisome proliferator-activated receptors (PPARs) and retinoid-activated receptors (RARs and RXRs) are important modulators of lipid metabolism and cellular homeostasis. Alterations in expression and activity of these ligand-activated transcription factors might be involved in obesity-associated diseases, which include CRC. Cyclooxygenase-2 (COX-2) also plays a critical role in lipid metabolism and alterations in COX-2 expression have already been associated with unfavourable clinical outcomes in epithelial tumors. The objective of this study is to examine the hypothesis questioning the relationship between alterations in the expression of nuclear receptors and COX-2 and the weight status among male subjects with CRC.</p> <p>Method</p> <p>The mRNA expression of the different nuclear receptor subtypes and of COX-2 was measured in 20 resected samples of CRC and paired non-tumor tissues. The association between expression patterns and weight status defined as a body mass index (BMI) was statistically analyzed.</p> <p>Results</p> <p>No changes were observed in PPARγ mRNA expression while the expression of PPARδ, retinoid-activated receptors and COX-2 were significantly increased in cancer tissues compared to normal colon mucosa (<it>P </it>≤ 0.001). The weight status appeared to be an independent factor, although we detected an increased level of COX-2 expression in the normal mucosa from overweight patients (BMI ≥ 25) compared to subjects with healthy BMI (<it>P </it>= 0.002).</p> <p>Conclusion</p> <p>Our findings show that alterations in the pattern of nuclear receptor expression observed in CRC do not appear to be correlated with patient weight status. However, the analysis of COX-2 expression in normal colon mucosa from subjects with a high BMI suggests that COX-2 deregulation might be driven by excess weight during the colon carcinogenesis process.</p

Thrombine et protéine C activée dans la fibrogénèse et la carcinogénèse hépatiques

Le but de ce travail était d'étudier le rôle de la thrombine et de la protéine C activée (PCA) dans la fibrose hépatique et le carcinome hépatocellulaire (CHC). Nous montrons que des souris KO ou hétérozygotes pour le récepteur à la thrombine PAR-1 ont une susceptibilité réduite à la fibrose hépatique. Dans le CHC humain, PAR-1 est exprimé par les myofibroblastes hépatiques et par de rares cellules tumorales. L'expression du facteur tissulaire (FT), initiateur de la coagulation, est réduite dans les CHC par rapport au foie non tumoral et n'a pas de valeur pronostique. Enfin, la PCA, inhibiteur de la génération de thrombine, a des effets profibrogéniques sur les myofibroblastes hépatiques humains via PAR-1. Son rôle reste à préciser car la préincubation avec la thrombine abolit ses effets. PAR-1 semble être une cible thérapeutique d'avenir dans la prévention de la fibrose hépatique mais son rôle dans le CHC semble mineur comme celui du FT. Le rôle de la PCA reste à définir in vivo.The aim of this work was to study the role of thrombin and Activated Protein (APC) in liver fibrosis and hepatocellular carcinoma (HCC). We found that KO and heterozygous mice for the main receptor of thrombin, PAR-1, had a reduced susceptibility to CC14-induced fibrosis. In human HCC, liver myofibroblasts and few tumor cells expressed PAR-1. The expression of tissue factor, the main iniitiator of coagulation, was lower in HCC than in non tumoral liver and its expression had no pronostic significance. Finally, PCA, an inhibitor of thrombin generation, had profibrogenic effects in human liver myofibroblasts via PAR-1. Its role is still ill-defined because preincubation with thrombin abolished its effects. PAR-1 could be a promising target for antifibrotic liver treatment. The role of PCA must be addressed in vivo. PAR-1 and tissue factor do not appear as major actors of liver carcinogenesis.BORDEAUX2-BU Santé (330632101) / SudocSudocFranceF

L'hépatite chronique virale C chez les sujets co-infectés par le virus de l'immunodéficience humaine (histologie, étude de la fibrose, détection intrahépatique du virus de l'hépatite C et comparaison avec les sujets immunocompétents)

BORDEAUX2-BU Santé (330632101) / SudocPARIS-BIUM (751062103) / SudocSudocFranceF

Reply to a comment published in Physical Review Letters

International audienceIn the preceding Comment, Ramos-Álvarez, Mosqueira, and Vidal [1] criticize the analysis of our magnetoresistance data in LiFeAs [2] and conclude that this " poses serious doubts about the conclusions drawn in our Letter about the 2D nature of fluctuation effects in LiFeAs "

Liver myofibroblasts activate protein C and respond to activated protein C

AIM: To study the protein C activation system in human liver myofibroblasts, and the effects of activated protein C (APC) on these cells

Unexpected discovery of 2 cases of hepatocyte nuclear factor 1α-mutated infracentimetric adenomatosis

We present 2 cases of hepatocyte nuclear factor 1α (HNF1α)-mutated adenomatosis, discovered for reasons unrelated to this disease, and identified using immunohistochemical methods. These new tools may further our understanding of the link between adenomas/adenomatosis subtypes and their complications, and their association with other abnormalities

Halofuginone suppresses the lung metastasis of chemically induced hepatocellular carcinoma in rats through MMP inhibition

Halofuginone, an inhibitor of collagen synthesis, appears to be a promising antitumoral drug in preclinical studies. We used a relevant rat model of autochthonous, chemically induced, spontaneously metastasizing hepatocellular carcinoma (HCC) to test the efficacy of halofuginone on tumor progression and matrix metalloproteinase (MMP) expression. Following sequential administration of diethylnitrosamine and N-nitrosomorpholine for 14 weeks, all animals developed HCC and then received halofuginone or its solvent for 10 weeks. The final number of liver tumors was lower in the halofuginone group than in the solvent group (57.2 ± 4.6 vs 68 ± 5.0; P < .01). The percentage of the lung surface infiltrated by metastasis was much smaller in the halofuginone group (0.3 ± 0.2%) than in the solvent group (13.5 ± 10.1%; P < .02). MMP-9 activity was decreased in the halofuginone group by 89% and 63% in non-neoplastic parts of the liver and tumor, respectively. The percentage of active MMP-2 was reduced by 90% in non-neoplastic parts of the liver and by 61% in tumors. This was likely subsequent to a decreased expression of both MMP-14 and tissue inhibitor of matrix metalloproteinase-2, which are required for pro-MMP-2 activation. These results, obtained from a clinically relevant model, further suggest the potential benefit of halofuginone in HCC