Pandectes françaises périodiques : Recueil mensuel de jurisprudence et de législation...

1894 (T9,PART1).

Pandectes françaises périodiques : Recueil mensuel de jurisprudence et de législation...

1886 (T1).

Pandectes françaises périodiques : Recueil mensuel de jurisprudence et de législation...

1920 (T34).

Pandectes françaises périodiques : Recueil mensuel de jurisprudence et de législation...

1890 (T5).

Pandectes françaises périodiques : Recueil mensuel de jurisprudence et de législation...

1901 (T16).

Gazette des tribunaux de commerce : journal spécial de la législation et de la jurisprudence commerciale

1828/01/01 (A2,N66)-1828/08/12 (A2,N162).

Gazette des tribunaux de commerce : journal spécial de la législation et de la jurisprudence commerciale

1827/07/28 (A1,N1)-1827/12/29 (A1,N65).

Gazette des tribunaux de commerce : journal spécial de la législation et de la jurisprudence commerciale

1830/02/04 (A4,N317)-1831/06/26 (A5,N454).

Gazette des tribunaux de commerce : journal spécial de la législation et de la jurisprudence commerciale

1829/01/02 (A3,N203)-1830/01/31 (A4,N316).

Gazette des tribunaux de commerce : journal spécial de la législation et de la jurisprudence commerciale

1828/08 (A2,N163)-1828/12/30 (A2,N202).

Gazette des tribunaux de commerce : journal spécial de la législation et de la jurisprudence commerciale

Périodicité : Trois fois par semaine (27 juillet 1827-12 août 1828) ; deux fois par semaine ([14] août 1828-26 juin 1830)

Therapeutic Properties of Superoxide Dismutase 3 and Mesenchymal Stromal Cells in Peripheral Ischemia

The aim of this study was to characterize the cellular mechanisms leading to the beneficial effect of anti-oxidative gene therapy and pro-angiogenic stem cell therapy in acute peripheral ischemia. Post-ischemic events aim to re-establish tissue blood perfusion, to clear cellular debris, and to regenerate lost tissue by differentiation of satellite cells into myoblasts. Although leukocytes have an essential role in clearing cellular debris and promoting angiogenesis, they also contribute to tissue injury through excessive ROS production. First, we investigated the therapeutic properties of extracellular superoxide dismutase (SOD3) gene transfer. SOD3 was shown to reduce oxidative stress, to normalize glucose metabolism, and to enhance cell proliferation in the ischemic muscle. Analysis of the mitogenic Ras-Erk1/2 pathway showed SOD3 mediated induction offering a plausible explanation for enhanced cell proliferation. In addition, SOD3 reduced NF-κB activity by enhancing IκBα expression thus leading to reduced expression of inflammatory cytokines and adhesion molecules with consequent reduction in macrophage infiltration. Secondly, we sought to determine the fate and the effect of locally transplanted mesenchymal stem/stromal cells (MSCs) in acute ischemia. We showed that a vast majority of the transplanted cells are cleared from the injury site within 24 hours after local transplantation. Despite rapid clearance, transplantation was able to temporarily promote angiogenesis and cell proliferation in the muscle. Lack of graft-derived growth factor expression suggests other than secretory function to mediate this observed effect. In conclusion, both SOD3 and MSCs could be utilized to alleviate peripheral ischemia induced tissue injury. We have described a previously unidentified growth regulatory role for SOD3, and suggest a novel mechanism whereby transplanted MSCs enhance the reparative potential of the recipient tissue through physical contacts.

Dissecting the molecular mechanisms of breast cancer bone metastasis for therapeutic targeting

Breast cancer that has metastasized to bone is currently an incurable disease, causing significant morbidity and mortality. The aim of this thesis work was to elucidate molecular mechanisms of bone metastasis and thereby gain insights into novel therapeutic approaches. First, we found that L‐serine biosynthesis genes, phosphoglycerate dehydrogenase (PHGDH), phosphoserine aminotransferase 1 (PSAT1) and phosphoserine phosphatase (PSPH), were up‐regulated in highly bone metastatic MDA‐MB‐231(SA) cells as compared with the parental breast cancer cell line. Knockdown of serine biosynthesis inhibited proliferation of MDA‐MB‐231(SA) cells, and L‐serine was essential for the formation of bone resorbing osteoclasts. Clinical data demonstrated that high expression of PHGDH and PSAT1 was associated with decreased relapse‐free and overall survival and with features typical of poor outcome in breast cancer. Second, RNA interference screening pointed out heparan sulfate 6‐O‐sulfotransferase 2 (HS6ST2) as a critical gene for transforming growth factor β (TGF‐β)‐induced interleukin 11 (IL‐11) production in MDA‐MB‐231(SA) cells. Exogenous heparan sulfate glycosaminoglycans heparin and K5‐NSOS also inhibited TGF‐β‐induced IL‐11 production in MDA‐MB‐231(SA) cells. Furthermore, K5‐NSOS decreased osteolytic lesion area and tumor burden in bone in mice. Third, we discovered that the microRNAs miR‐204, ‐211 and ‐379 inhibited IL‐11 expression in MDA‐MB‐231(SA) cells through direct targeting of the IL‐11 mRNA. MiR‐379 also inhibited Smad‐mediated signaling. Gene expression profiling of miR‐204 and ‐379 transfected cells indicated that these microRNAs down‐regulate several bone metastasis‐relevant genes, including prostaglandin‐endoperoxide synthase 2 (PTGS2). Taken together, this study identified three potential treatment strategies for bone metastatic breast cancer: inhibition of serine biosynthesis, heparan sulfate glycosaminoglycans and restoration of miR‐204/‐211/‐379.

Journal des commissaires de police : recueil mensuel de législation, de jurisprudence et de doctrine

1905 (A51).

Journal des commissaires de police : recueil mensuel de législation, de jurisprudence et de doctrine

1910 (A56,N6,N11).