Articles

Characterization of the spectral phase of ultrashort light pulses
- Dorrer C.
- Joffre Manuel
Comptes Rendus de l'Academie des Sciences. Série IV, Physique, Astronomie, Elsevier , 2001, 2 (10), pp.1415-1426 . The complete characterization of a short light pulse requires the measurement of the value of the electric field as a function of time, or conversely, as a function of the optical frequency. Many different techniques have been demonstrated for this purpose. They fall in two main categories, whether a known reference pulse whose spectrum encompasses that of the unknown pulse is available or not. In the first case, linear techniques such as time-domain or frequency-domain interferometry can be directly used, with the advantage of a high sensitivity. In the latter case, non-stationary filters can be implemented using optical non-linearities, in techniques such as Frequency Resolved Optical Gating (FROG) or Spectral Phase Interferometry for Direct Electric-field Reconstruction (SPIDER). Cop. 2001 Académie des sciences/Éditions scientifiques et médicales Elsevier SAS. (10.1016/S1296-2147(01)01279-3)
DOI : 10.1016/S1296-2147(01)01279-3
NFkappaB decoy oligodeoxynucleotides reduce monocyte infiltration in renal allografts.
- Vos M
- Govers R
- Gröne H J
- Kleij L
- Schurink M
- de Weger R
- Goldschmeding R
- Rabelink T J
FASEB Journal, Federation of American Society of Experimental Biology , 2000, pp.815-22 . Monocyte influx secondary to ischemia-reperfusion conditions the renal allograft to rejection by presentation of antigens and production of cytokines. Monocyte influx depends on NFkappaB-dependent transcription of genes encoding adhesion molecules and chemokines. Here we demonstrate that cationic liposomes containing phosphorothioated oligodeoxynucleotides (ODN) with the kappaB binding site serving as competitive binding decoy, can prevent TNF-alpha-induced NFkappaB activity in endothelial cells in vitro. In an allogenic rat kidney transplantation model (BN to LEW), we show that perfusing the renal allograft with this decoy prior to transplantation abolishes nuclear NFkappaB activity in vivo and inhibits VCAM-1 expression in the donor endothelium (P<0.05). At 24 h postreperfusion, periarterial infiltration of monocytes/macrophages was significantly reduced in decoy ODN-treated allografts compared to control allografts (3.7+/-0.7 vs. 9.2+/-1.2 macrophages/vessel; P<0.01). At 72 h, there was a reduction of tubulointerstitial macrophage infiltration in decoy ODN-treated kidneys compared to controls (75.6+/-13.9 vs. 120.0+/-11.2 macrophages/tubulointerstitial area; P<0.05). In conclusion, perfusion of the renal allograft with NFkappaB decoy ODN prior to transplantation decreases the initial inflammatory response in a stringent, nonimmunosuppressed allogenic transplantation model. Therefore, the NFkappaB decoy approach may be useful to explore the role of endothelium and macrophages in graft rejection and may be developed into a graft-specific immunosuppressive strategy allowing reduction of systemic immunosuppression on organ transplantation.
Insensitivity to anti–Müllerian hormone due to a mutation in the human anti–Müllerian hormone receptor
- Imbeaud Sandrine
- Faure Emmanuelle
- Lamarre Isabelle
- Mattei Marie-Geneviève
- Di Clemente Nathalie
- Tizard Richard
- Carré-Eusèbe Danièle
- Carré-Eusèbe C
- Belville Corinne
- Tragethon Lars
- Tonkin Christopher
- Nelson Janice
- Mcauliffe A
- Bidart Jean-Michel
- Lababidi Abdul
- Josso Nathalie
- Cate Richard
- Picard Jean-Yves
Nature Genetics, Nature Publishing Group , 1995, 11 (4), pp.382 - 388 . Anti-Müllerian hormone (AMH) and its receptor are involved in the regression of Müllerian ducts in male fetuses. We have now cloned and mapped the human AMH receptor gene and provide genetic proof that it is required for AMH signalling, by identifying a mutation in the AMH receptor in a patient with persistent Müllerian duct syndrome. The mutation destroys the invariant dinucleotide at the 5' end of the second intron, generating two abnormal mRNAs, one missing the second exon, required for ligand binding, and the other incorporating the first 12 bases of the second intron. The similar phenotypes observed in AMH-deficient and AMH receptor-deficient individuals indicate that the AMH signalling machinery is remarkably simple, consisting of one ligand and one type II receptor. (10.1038/ng1295-382)
DOI : 10.1038/ng1295-382