Paris Descartes University

About: Paris Descartes University is a government organization based out in Paris, France. It is known for research contribution in the topics: Population & Transplantation. The organization has 20987 authors who have published 37456 publications receiving 1206222 citations. The organization is also known as: Université Paris V-Descartes & Université de Paris V.

Construction of iron oxide nanoparticle-based hybrid platforms for tumor imaging and therapy

Abstract: The aim of this original review is to highlight and analyze the most recent progress and challenges in the synthesis and surface modifications of superparamagnetic iron oxide (Fe3O4) nanoparticles (NPs) for multimodal imaging and therapy applications, which represent important fields in medicine in general and cancer in particular Thus, the oncology domain is rapidly moving to a more personalized medicine including precision imaging and theranostic approaches Novel biocompatible Fe3O4 nanoparticulate systems have been designed for enhanced and targeted cellular uptake by surface layer coating modifications, to have improved r2 relaxivity for sensitive magnetic resonance (MR) imaging applications, to have the ability to be used for dual mode imaging, and to be used for imaging-guided cancer therapy In this review, we analyzed in depth the new strategies for generating biocompatible multifunctional Fe3O4 nanoplatforms for both the diagnosis and therapy of cancer

Nicotinamide phosphoribosyltransferase protects against ischemic stroke through SIRT1-dependent adenosine monophosphate-activated kinase pathway.

Abstract: Objective: Stroke is a leading cause of mortality and disability. Nicotinamide phosphoribosyltransferase (Nampt) is the rate-limiting enzyme in mammalian nicotinamide adenine dinucleotide (NAD) þ biosynthesis and contributes to cell fate decisions. However, the role of Nampt in brain and stroke remains to be investigated. Methods: We used lentivirus-mediated Nampt overexpression and knockdown to manipulate Nampt expression and explore the effects of Nampt in neuronal survival on ischemic stress both in vivo and in vitro. We also used adenosine monophosphate (AMP)-activated kinase-a2 (AMPKa2) and silent mating type information regulation 2 homolog 1 (SIRT1) knockout mice to investigate the underlying mechanisms of Nampt neuroprotection. Results: Nampt inhibition by a highly-specific Nampt inhibitor, FK866, aggravated brain infarction in experimentally cerebral ischemia rats, whereas Nampt overexpression in local brain and Nampt enzymatic product nicotinamide mononucleotide (NMN) reduced ischemia-induced cerebral injuries. Nampt overexpression and knockdown regulated neuron survival via the AMPK pathway. Neuroprotection of Nampt was abolished in AMPKa2 � /� neurons. In neurons, Nampt positively modulated NAD þ levels and thereby controlled SIRT1 activity. SIRT1 coprecipitated with serine/threonine kinase 11 (LKB1), an upstream kinase of AMPK, and promoted LKB1 deacetylation in neurons. Nampt-induced LKB1 deacetylation and AMPK activation disappeared in SIRT1 � /� neurons. In contrast, Ca 2þ / calmodulin-dependent protein kinase kinase-b (CaMKK-b), another upstream kinase of AMPK, was not involved in the neuroprotection of Nampt. More important, Nampt overexpression-induced neuroprotection was abolished in SIRT1 þ/� and AMPKa2 � /� mice. Interpretation: Our findings reveal that Nampt protects against ischemic stroke through rescuing neurons from death via the SIRT1-dependent AMPK pathway and indicate that Nampt is a new therapeutic target for stroke. ANN NEUROL 2011;69:360–374

Characterisation of retinoblastomas without RB1 mutations: genomic, gene expression, and clinical studies.

Abstract: Summary Background Retinoblastoma is the childhood retinal cancer that defined tumour-suppressor genes. Previous work shows that mutation of both alleles of the RB1 retinoblastoma suppressor gene initiates disease. We aimed to characterise non-familial retinoblastoma tumours with no detectable RB1 mutations. Methods Of 1068 unilateral non-familial retinoblastoma tumours, we compared those with no evidence of RB1 mutations ( RB1 +/+ ) with tumours carrying a mutation in both alleles ( RB1 −/− ). We analysed genomic copy number, RB1 gene expression and protein function, retinal gene expression, histological features, and clinical data. Findings No RB1 mutations ( RB1 +/+ ) were reported in 29 (2·7%) of 1068 unilateral retinoblastoma tumours. 15 of the 29 RB1 +/+ tumours had high-level MYCN oncogene amplification (28–121 copies; RB1 +/+ MYCN A ), whereas none of 93 RB1 −/− primary tumours tested showed MYCN amplification (p RB1 +/+ MYCN A tumours expressed functional RB1 protein, had fewer overall genomic copy-number changes in genes characteristic of retinoblastoma than did RB1 −/− tumours, and showed distinct aggressive histological features. MYCN amplification was the sole copy-number change in one RB1 +/+ MYCN A retinoblastoma. One additional MYCN A tumour was discovered after the initial frequencies were determined, and this is included in further analyses. Median age at diagnosis of the 17 children with RB1 +/+ MYCN A tumours was 4·5 months (IQR 3·5–10), compared with 24 months (15–37) for 79 children with non-familial unilateral RB1 −/− retinoblastoma. Interpretation Amplification of the MYCN oncogene might initiate retinoblastoma in the presence of non-mutated RB1 genes. These unilateral RB1 +/+ MYCN A retinoblastomas are characterised by distinct histological features, only a few of the genomic copy-number changes that are characteristic of retinoblastoma, and very early age of diagnosis. Funding National Cancer Institute–National Institutes of Health, Canadian Institutes of Health Research, German Research Foundation, Canadian Retinoblastoma Society, Hyland Foundation, Toronto Netralaya and Doctors Lions Clubs, Ontario Ministry of Health and Long Term Care, UK-Essen, and Foundations Avanti-STR and KiKa.

Deep endometriosis infiltrating the recto-sigmoid: critical factors to consider before management

Abstract: Background Deep endometriosis invading the bowel constitutes a major challenge for the gynecologist. In addition to the greater impact on pain, the high incidence of surgical morbidity involved with bowel endometriosis poses a therapeutic dilemma for the surgeon. Intestinal involvement by deep endometriotic nodules has been estimated to occur in 8-12% of women with endometriosis. Individual and clinical factors, pre-operative morphologic characteristics from imaging, surgical considerations and impact on quality of life are critical variables that should be considered in determining the best therapeutic strategy for a patient with deep endometriosis involving the sigmoid and/or the rectum. Pre-operative planning is fundamental for defining the optimal therapeutic strategy; patient counseling of treatment options, and when surgery is indicated, involvement of a multidisciplinary surgical team is required. Methods The PubMed and Cochrane database were searched for all original and review articles published in English, French and Italian, until June 2014. Search terms included 'deep endometriosis', 'surgical and clinical approach', 'bowel disease', 'quality of life', 'management of deep endometriosis'. Special attention was paid to articles comparing features of discoid and segmental resection. Results The rationale for the best therapeutic options for patients with deep endometriosis has been shown and an evidence-based treatment algorithm for determining when and which surgical intervention may be required is proposed. In deciding the best treatment option for patients with deep endometriosis involving the sigmoid and rectum, it is important to understand how the different clinical factors and pre-operative morphologic imaging affect the algorithm. Surgery is not indicated in all patients with deep endometriosis, but, when surgery is chosen, a complete resection by the most appropriate surgical team is required in order to achieve the best patient outcome. Conclusion In women with deep endometriosis, surgery is the therapy of choice for symptomatic patients when deep lesions do not improve with a medical treatment.