David R

References (4)

Title : Parathyroid hormone is a DPP-IV inhibitor and increases SDF-1-driven homing of CXCR4(+) stem cells into the ischaemic heart - Huber_2011_Cardiovasc.Res_90_529
Author(s) : Huber BC , Brunner S , Segeth A , Nathan P , Fischer R , Zaruba MM , Vallaster M , Theiss HD , David R , Gerbitz A , Franz WM
Ref : Cardiovascular Research , 90 :529 , 2011
Abstract : AIMS: Parathyroid hormone (PTH) has been shown to promote stem cell mobilization into peripheral blood. Moreover, PTH treatment after myocardial infarction (MI) improved survival and myocardial function associated with enhanced homing of bone marrow-derived stem cells (BMCs). To unravel the molecular mechanisms of PTH-mediated stem cell trafficking, we analysed wild-type (wt) and green fluorescent protein (GFP)-transgenic mice after MI with respect to the pivotal stromal cell-derived factor-1 (SDF-1)/chemokine receptor type 4 (CXCR4) axis. METHODS AND RESULTS: WT and GFP-transgenic mice (C57BL/6J) were infarcted by coronary artery ligation and PTH (80 mug/kg/day) was injected for 6 days afterwards. Number of BMCs was analysed by flow cytometry. SDF-1 protein levels and activity of dipeptidyl peptidase-IV (DPP-IV) were investigated by ELISA and activity assay. Functional analyses were performed at day 30 after MI. PTH-treated animals revealed an enhanced homing of CXCR4(+) BMCs associated with an increased protein level of the corresponding homing factor SDF-1 in the ischaemic heart. In vitro and in vivo, PTH inhibited the activity of DPP-IV, which cleaves and inactivates SDF-1. Functionally, PTH significantly improved myocardial function after MI. Both stem cell homing as well as functional recovery were reversed by the CXCR4 antagonist AMD3100. CONCLUSION: In summary, PTH is a DPP-IV inhibitor leading to an increased cardiac SDF-1 level, which enhances recruitment of CXCR4(+) BMCs into the ischaemic heart associated with attenuated ischaemic cardiomyopathy. Since PTH is already clinically used our findings may have direct impact on the initiation of studies in patients with ischaemic disorders.
ESTHER : Huber_2011_Cardiovasc.Res_90_529
PubMedSearch : Huber_2011_Cardiovasc.Res_90_529
PubMedID: 21245057

Title : [Treatment of behavioral disorders in Alzheimer's disease] - David_2011_Rev.Prat_61_939
Author(s) : David R , Piano J , Robert P
Ref : Rev Prat , 61 :939 , 2011
Abstract : Behavioural and psychological symptoms (BPSD) are now known to be frequently associated to cognitive and functional decline in Alzheimer's disease and related disorders. Recommendations for the management of BPSD have been proposed. Non-pharmacological interventions should be the first-line treatment. Anti-dementia agents (cholinesterase inhibitors, memantine) and psychotropic drugs (antipsychotics, antidepressants and anticonvulsivants) could be associated to non-pharmacological interventions only in case of limited response with non pharmacologic approaches. Low-dose antipsychotics should only be prescribed for limited periods of time, in case of psychotic and/or aggressive refractory symptoms.
ESTHER : David_2011_Rev.Prat_61_939
PubMedSearch : David_2011_Rev.Prat_61_939
PubMedID: 22039732

Title : Biochemical and functional properties of distinct nicotinic acetylcholine receptors in the superior cervical ganglion of mice with targeted deletions of nAChR subunit genes - David_2010_Eur.J.Neurosci_31_978
Author(s) : David R , Ciuraszkiewicz A , Simeone X , Orr-Urtreger A , Papke RL , McIntosh JM , Huck S , Scholze P
Ref : European Journal of Neuroscience , 31 :978 , 2010
Abstract : Nicotinic acetylcholine receptors (nAChRs) mediate fast synaptic transmission in ganglia of the autonomic nervous system. Here, we determined the subunit composition of hetero-pentameric nAChRs in the mouse superior cervical ganglion (SCG), the function of distinct receptors (obtained by deletions of nAChR subunit genes) and mechanisms at the level of nAChRs that might compensate for the loss of subunits. As shown by immunoprecipitation and Western blots, wild-type (WT) mice expressed: alpha 3 beta 4 (55%), alpha 3 beta 4 alpha 5 (24%) and alpha 3 beta 4 beta 2 (21%) nAChRs. nAChRs in beta 4 knockout (KO) mice were reduced to < 15% of controls and no longer contained the alpha 5 subunit. Compound action potentials, recorded from the postganglionic (internal carotid) nerve and induced by preganglionic nerve stimulation, did not differ between alpha 5 beta 4 KO and WT mice, suggesting that the reduced number of receptors in the KO mice did not impair transganglionic transmission. Deletions of alpha 5 or beta2 did not affect the overall number of receptors and we found no evidence that the two subunits substitute for each other. In addition, dual KOs allowed us to study the functional properties of distinct alpha 3 beta4 and alpha 3 beta 2 receptors that have previously only been investigated in heterologous expression systems. The two receptors strikingly differed in the decay of macroscopic currents, the efficacy of cytisine, and their responses to the alpha-conotoxins AuIB and MII. Our data, based on biochemical and functional experiments and several mouse KO models, clarify and significantly extend previous observations on the function of nAChRs in heterologous systems and the SCG.
ESTHER : David_2010_Eur.J.Neurosci_31_978
PubMedSearch : David_2010_Eur.J.Neurosci_31_978
PubMedID: 20377613

Title : The DNA sequence of the human X chromosome - Ross_2005_Nature_434_325
Author(s) : Ross MT , Grafham DV , Coffey AJ , Scherer S , McLay K , Muzny D , Platzer M , Howell GR , Burrows C , Bird CP , Frankish A , Lovell FL , Howe KL , Ashurst JL , Fulton RS , Sudbrak R , Wen G , Jones MC , Hurles ME , Andrews TD , Scott CE , Searle S , Ramser J , Whittaker A , Deadman R , Carter NP , Hunt SE , Chen R , Cree A , Gunaratne P , Havlak P , Hodgson A , Metzker ML , Richards S , Scott G , Steffen D , Sodergren E , Wheeler DA , Worley KC , Ainscough R , Ambrose KD , Ansari-Lari MA , Aradhya S , Ashwell RI , Babbage AK , Bagguley CL , Ballabio A , Banerjee R , Barker GE , Barlow KF , Barrett IP , Bates KN , Beare DM , Beasley H , Beasley O , Beck A , Bethel G , Blechschmidt K , Brady N , Bray-Allen S , Bridgeman AM , Brown AJ , Brown MJ , Bonnin D , Bruford EA , Buhay C , Burch P , Burford D , Burgess J , Burrill W , Burton J , Bye JM , Carder C , Carrel L , Chako J , Chapman JC , Chavez D , Chen E , Chen G , Chen Y , Chen Z , Chinault C , Ciccodicola A , Clark SY , Clarke G , Clee CM , Clegg S , Clerc-Blankenburg K , Clifford K , Cobley V , Cole CG , Conquer JS , Corby N , Connor RE , David R , Davies J , Davis C , Davis J , Delgado O , Deshazo D , Dhami P , Ding Y , Dinh H , Dodsworth S , Draper H , Dugan-Rocha S , Dunham A , Dunn M , Durbin KJ , Dutta I , Eades T , Ellwood M , Emery-Cohen A , Errington H , Evans KL , Faulkner L , Francis F , Frankland J , Fraser AE , Galgoczy P , Gilbert J , Gill R , Glockner G , Gregory SG , Gribble S , Griffiths C , Grocock R , Gu Y , Gwilliam R , Hamilton C , Hart EA , Hawes A , Heath PD , Heitmann K , Hennig S , Hernandez J , Hinzmann B , Ho S , Hoffs M , Howden PJ , Huckle EJ , Hume J , Hunt PJ , Hunt AR , Isherwood J , Jacob L , Johnson D , Jones S , de Jong PJ , Joseph SS , Keenan S , Kelly S , Kershaw JK , Khan Z , Kioschis P , Klages S , Knights AJ , Kosiura A , Kovar-Smith C , Laird GK , Langford C , Lawlor S , Leversha M , Lewis L , Liu W , Lloyd C , Lloyd DM , Loulseged H , Loveland JE , Lovell JD , Lozado R , Lu J , Lyne R , Ma J , Maheshwari M , Matthews LH , McDowall J , Mclaren S , McMurray A , Meidl P , Meitinger T , Milne S , Miner G , Mistry SL , Morgan M , Morris S , Muller I , Mullikin JC , Nguyen N , Nordsiek G , Nyakatura G , O'Dell CN , Okwuonu G , Palmer S , Pandian R , Parker D , Parrish J , Pasternak S , Patel D , Pearce AV , Pearson DM , Pelan SE , Perez L , Porter KM , Ramsey Y , Reichwald K , Rhodes S , Ridler KA , Schlessinger D , Schueler MG , Sehra HK , Shaw-Smith C , Shen H , Sheridan EM , Shownkeen R , Skuce CD , Smith ML , Sotheran EC , Steingruber HE , Steward CA , Storey R , Swann RM , Swarbreck D , Tabor PE , Taudien S , Taylor T , Teague B , Thomas K , Thorpe A , Timms K , Tracey A , Trevanion S , Tromans AC , d'Urso M , Verduzco D , Villasana D , Waldron L , Wall M , Wang Q , Warren J , Warry GL , Wei X , West A , Whitehead SL , Whiteley MN , Wilkinson JE , Willey DL , Williams G , Williams L , Williamson A , Williamson H , Wilming L , Woodmansey RL , Wray PW , Yen J , Zhang J , Zhou J , Zoghbi H , Zorilla S , Buck D , Reinhardt R , Poustka A , Rosenthal A , Lehrach H , Meindl A , Minx PJ , Hillier LW , Willard HF , Wilson RK , Waterston RH , Rice CM , Vaudin M , Coulson A , Nelson DL , Weinstock G , Sulston JE , Durbin R , Hubbard T , Gibbs RA , Beck S , Rogers J , Bentley DR
Ref : Nature , 434 :325 , 2005
Abstract : The human X chromosome has a unique biology that was shaped by its evolution as the sex chromosome shared by males and females. We have determined 99.3% of the euchromatic sequence of the X chromosome. Our analysis illustrates the autosomal origin of the mammalian sex chromosomes, the stepwise process that led to the progressive loss of recombination between X and Y, and the extent of subsequent degradation of the Y chromosome. LINE1 repeat elements cover one-third of the X chromosome, with a distribution that is consistent with their proposed role as way stations in the process of X-chromosome inactivation. We found 1,098 genes in the sequence, of which 99 encode proteins expressed in testis and in various tumour types. A disproportionately high number of mendelian diseases are documented for the X chromosome. Of this number, 168 have been explained by mutations in 113 X-linked genes, which in many cases were characterized with the aid of the DNA sequence.
ESTHER : Ross_2005_Nature_434_325
PubMedSearch : Ross_2005_Nature_434_325
PubMedID: 15772651
Gene_locus related to this paper: human-NLGN3 , human-NLGN4X