Academic literature on the topic 'Juan Filloy'

Background:IgA vasculitis (IgAV) and IgA nephropathy (IgAN) are inflammatory conditions that share pathogenic and molecular mechanisms [1] and may represent different outcomes of a continuous spectrum of disease [2]. Interleukin (IL)17A has been identified as a common genetic risk locus for several immune-mediated diseases [3, 4].Objectives:To determine whether IgAV and IgAN exhibit a different IL17A association pattern.Methods:Five IL17A tag polymorphisms (rs4711998, rs8193036, rs3819024, rs2275913 and rs7747909) were genotyped in 388 Caucasian patients with IgAV, 99 patients with IgAN and 1,003 sex and ethnically matched healthy controls.Results:No statistically significant differences between patients with IgAV and healthy controls and between patients with IgAN and healthy controls were observed when each IL17A genetic variant was analyzed independently (Table 1). Similarly, IgAV patients exhibited similar genotype and allele IL17A frequencies than those with IgAN (Table 1). Moreover, no genotype or allele differences between IgAV patients who developed nephritis and patients with IgAN were detected. Furthermore, haplotype frequencies were similar in patients with IgAV, IgAV and nephritis and those with IgAN.Table 1.Genotype and allele frequencies of IL17A gene in patients with IgA vasculitis, patients with IgA nephropathy and healthy controls.PolymorphismChangeData set1/11/22/212rs4711998G/AIgAV53.4 (207)38.9 (151)7.7 (30)72.8 (565)27.2 (211)IgAN49.0 (48)42.9 (42)8.2 (8)70.4 (138)29.6 (58)Controls52.7 (529)41.2 (413)6.1 (61)73.3 (1471)26.7 (535)rs8193036T/CIgAV57.0 (221)38.4 (149)4.6 (18)76.2 (591)23.8 (185)IgAN64.3 (63)31.6 (31)4.1 (4)80.1 (157)19.9 (39)Controls60.3 (605)35.2 (353)4.5 (45)77.9 (1563)22.1 (443)rs3819024A/GIgAV44.1 (171)43.3 (168)12.6 (49)65.7 (510)34.3 (266)IgAN39.4 (39)54.5 (54)6.1 (6)66.7 (132)33.3 (66)Controls45.6 (457)44.6 (447)9.9 (99)67.8 (1361)32.2 (645)rs2275913G/AIgAV44.6 (172)43.3 (167)12.2 (47)66.2 (511)33.8 (261)IgAN39.8 (39)53.1 (52)7.1 (7)66.3 (130)33.7 (66)Controls44.8 (449)44.2 (443)11.1 (111)66.8 (1341)33.2 (665)rs7747909G/AIgAV53.9 (209)39.4 (153)6.7 (26)73.6 (571)26.4 (205)IgAN41.1 (39)54.7 (52)4.2 (4)68.4 (130)31.6 (60)Controls53.0 (532)39.4 (395)7.6 (76)72.7 (1459)27.3 (547)Conclusion:Our results revealed that IgAV and IgAN share a similar IL17A association pattern.References:[1]N Engl J Med 2013;368:2402-14.[2]Am J Kidney Dis 1988;12:373-7.[3]Ann Rheum Dis 2014;73:1742-5.[4]Mediators Inflamm 2018;2018:1395823.Acknowledgements:This study was supported by European Union FEDER funds and “Fondo de Investigaciones Sanitarias” (grant PI18/00042) from ‘Instituto de Salud Carlos III’ (ISCIII, Health Ministry, Spain). DP-P is a recipient of a Río Hortega programme fellowship from the ISCIII, co-funded by the European Social Fund (ESF, `Investing in your future´) [grant number CM20/00006]; SR-M is supported by funds of the RETICS Program co-funded by the European Regional Development Fund (ERDF) [grant number RD16/0012/0009]; VP-C is supported by a pre-doctoral grant from IDIVAL [grant number PREVAL 18/01]; BA-M is a recipient of a `López Albo´ Post-Residency Programme funded by Servicio Cántabro de Salud; LL-G is supported by funds of IDIVAL [grant number INNVAL20/06]; RL-M is a recipient of a Miguel Servet type I programme fellowship from the ISCIII, co-funded by the European Social Fund (ESF, `Investing in your future´) [grant number CP16/00033].Disclosure of Interests:Diana Prieto-Peña: None declared, Fernanda Genre: None declared, Sara Remuzgo Martinez: None declared, Verónica Pulito-Cueto: None declared, Belén Atienza-Mateo: None declared, Belén Sevilla: None declared, Javier Llorca: None declared, Norberto Ortego: None declared, Leticia Lera-Gómez: None declared, Maite Leonardo: None declared, Ana Peñalba: None declared, Luis Martín-Penagos: None declared, Jose Alberto Miranda-Filloy: None declared, J. Narváez: None declared, LUIS CAMINAL MONTERO: None declared, PAZ COLLADO: None declared, Antonio Fernandez-Nebro: None declared, Gisela Díaz-Cordoves: None declared, Secundino Cigarrán: None declared, Jesús Calviño: None declared, Carmen Cobelo: None declared, Javier Sanchez Perez: None declared, Diego de Argila: None declared, Esteban Rubio-Romero: None declared, MANUEL LEON LUQUE: None declared, Juan María Blanco-Madrigal: None declared, E. Galindez: None declared, Javier Martin Ibanez: None declared, Santos Castañeda: None declared, Ricardo Blanco Speakers bureau: Abbvie, Pfizer, Roche, Bristol-Myers, Janssen and MSD, Consultant of: Abbvie, Pfizer, Roche, Bristol-Myers, Janssen and MSD, Grant/research support from: Abbvie, MSD and Roche, Miguel A González-Gay Speakers bureau: Pfizer, Abbvie, MSD, Grant/research support from: Pfizer, Abbvie, MSD, Raquel López-Mejías: None declared

Hirigoyen, M.-F. (2014). Que sais-je? Le harcèlement moral au travail, Presses Universitaires de France, 128 p.
 Filion L.J. (2013). Innover au féminin : Savoir se dépasser – Intraprendre. Québec, Presse de l’Université du Québec, 292p.
 Fontan, J. M, Hamel, P. et Morin, R., Villes et conflits : Action collective, justice sociale et enjeux environnementaux, PUL, Québec, 2012, 227 p.
 Benoit Lévesque, Jean-Marc Fontan et Juan-Luis Klein, (sous la dir. de), L’inno-vation sociale: Les marches d’une cons-truction théorique et pratique, Québec, Presses de l’Université du Québec, 2014, 451 p.

Background:BAFF, APRIL and BAFFR are genes that encode cytokines with a key role in the development and survival of B-lymphocytes [1-4]: The B cell-activating factor (BAFF, also known as BLyS), a proliferation-inducing ligand (APRIL) and BAFF receptor (BAFF-R), respectively. Previous genetic studies have revealed that the BAFF-APRIL-BAFFR pathway is implicated in the genetic predisposition to several immune-mediated diseases [5].Objectives:To determine whether the BAFF-APRIL-BAFFR pathway represents a novel genetic risk factor for the pathogenesis of Immunoglobulin-A vasculitis (IgAV), an inflammatory disease in which IgA deposits and B-lymphocytes are crucial [6, 7].Methods:A functional BAFF polymorphism (rs374039502) and two tag variants within APRIL (rs11552708 and rs6608) and BAFFR (rs7290134 and rs77874543) were genotyped in 386 Caucasian IgAV patients (the largest series of Caucasian patients with IgAV ever assessed for genetic studies) and 806 sex and ethnically matched healthy controls by TaqMan assays.Results:No statistically significant differences in the genotype and allele frequencies between patients with IgAV and healthy controls were observed when each genetic variant of BAFF APRIL and BAFFR was analyzed independently (Table 1). Likewise, no statistically significant differences in genotype and allele frequencies of BAFF APRIL or BAFFR were found when patients with IgAV were stratified according to the age at disease onset or to the presence/absence of gastrointestinal or renal manifestations. Similar results were disclosed when haplotype frequencies of APRIL and BAFFR were compared between patients with IgAV and healthy controls as well as patients with IgAV stratified according to the age at disease onset or to the presence/absence of gastrointestinal or renal manifestations.Conclusion:Our results suggest that the BAFF-APRIL-BAFFR pathway does not contribute to the genetic network underlying IgAV.References:[1]J Exp Med 1999;190:1697-710; [2] Science 1999;285:260-3; [3] Nat Genet 2005;37:829-34; [4] Nat Immunol 2002;3:822-9; [5] N Engl J Med 2017;376:1615-26; [6] N Engl J Med 2013;368:2402-14; [7] Autoimmun Rev 2018;17:301-315.Table 1.Genotype and allele frequencies of BAFF, APRIL and BAFFR genes in patients with IgA vasculitis and healthy controls.PolymorphismLocus1/2Data set1/11/22/212rs374039502BAFFT/APatients91.9 (353)8.1 (31)095.9 (737)4.1 (31)Controls91.5 (733)8.1 (65)0.4 (3)95.6 (1531)4.4 (71)rs11552708APRILG/APatients78.1 (299)20.6 (79)1.3 (5)88.4 (677)11.6 (89)Controls77.9 (625)20.4 (1641.6 (13)88.1 (1414)11.9 (190)rs6608APRILC/TPatients71.9 (277)26.0 (100)2.1 (8)84.9 (654)15.1 (116)Controls70.0 (561)27.6 (221)2.5 (20)83.7 (1343)16.3 (261)rs7290134BAFFRA/GPatients58.0 (224)36.3 (140)5.7 (22)76.2 (588)23.8 (184)Controls57.2 (459)36.4 (292)6.5 (52)75.3 (1210)24.6 (396)rs77874543BAFFRG/CPatients82.7 (316)16.0 (61)1.3 (5)90.7 (693)9.3 (71)Controls83.0 (666)16.6 (133)0.4 (3)91.3 (1465)8.7 (139)Acknowledgements:This study was supported by European Union FEDER funds and “Fondo de Investigaciones Sanitarias” (grant PI18/00042) from ‘Instituto de Salud Carlos III’ (ISCIII, Health Ministry, Spain). DP-P is a recipient of a Río Hortega programme fellowship from the ISCIII, co-funded by the European Social Fund (ESF, `Investing in your future´) [grant number CM20/00006]; SR-M is supported by funds of the RETICS Program co-funded by the European Regional Development Fund (ERDF) [grant number RD16/0012/0009]; VP-C is supported by a pre-doctoral grant from IDIVAL [grant number PREVAL 18/01]; BA-M is a recipient of a `López Albo´ Post-Residency Programme funded by Servicio Cántabro de Salud; LL-G is supported by funds of IDIVAL [grant number INNVAL20/06]; RL-M is a recipient of a Miguel Servet type I programme fellowship from the ISCIII, co-funded by the European Social Fund (ESF, `Investing in your future´) [grant number CP16/00033].Disclosure of Interests:Diana Prieto-Peña Speakers bureau: Abbvie, Pfizer, Roche, Bristol-Myers, Janssen and MSD, Consultant of: Abbvie, Pfizer, Roche, Bristol-Myers, Janssen and MSD, Grant/research support from: Abbvie, MSD and Roche, Sara Remuzgo Martinez: None declared, Fernanda Genre: None declared, Verónica Pulito-Cueto: None declared, Belén Atienza-Mateo: None declared, Belén Sevilla: None declared, Javier Llorca: None declared, Norberto Ortego: None declared, Leticia Lera-Gómez: None declared, Maite Leonardo: None declared, Ana Peñalba: None declared, J. Narváez: None declared, Luis Martín-Penagos: None declared, Jose Alberto Miranda-Filloy: None declared, LUIS CAMINAL MONTERO: None declared, PAZ COLLADO: None declared, Javier Sanchez Perez: None declared, Diego de Argila: None declared, Esteban Rubio-Romero: None declared, MANUEL LEON LUQUE: None declared, Juan María Blanco-Madrigal: None declared, E. Galindez: None declared, Javier Martin Ibanez: None declared, Santos Castañeda: None declared, Ricardo Blanco Speakers bureau: Abbvie, Pfizer, Roche, Bristol-Myers, Janssen and MSD, Consultant of: Abbvie, Pfizer, Roche, Bristol-Myers, Janssen and MSD, Grant/research support from: Abbvie, MSD and Roche, Miguel A González-Gay Speakers bureau: Pfizer, Abbvie, MSD, Grant/research support from: Pfizer, Abbvie, MSD, Raquel López-Mejías: None declared

ABSTRAKHasil penelitian menyimpulkan, bahewa akibat hukum dari peralihan hak milik atas tanah yang belum lunas pembayarannya adalah sah secara jual beli, akan tetapi apabila pembayaran harga tanahnya tersebut belum dilunasi terlebih dahulu maka peralihan hak nya dapat ditangguhkan (sesuai perjanjian pengikatan jual beli lunas). Setelah pembayaran harganya dilunasi baru proses peralihan haknya dilanjutkan (pembuatan Akta Jual Beli dan proses sertifikat). PPAT membuatkan Akta Jual Beli selanjutnya akta tersebut dijadikan alat bukti autentik yang menerangkan telah terjadi peralihan hak atas tanah melalui jual beli selanjutnya untuk didaftarkan. Sedangkan jual beli tanah yang menganut hukum adat bersifat konkret, kontan, nyata dan riil. Artinya peran PPAT dalam melaksanakan amanat Undang-Undang tersebut harus benar-benar terlaksana dan kaitannya dengan peralihan hak milik atas tanah yang belum lunas pembayarannya, PPAT harus menentukan sikap tegas untuk tidak membuatkan Akta Jual Beli tersebut sebelum seluruh pembayaran harganya lunas meskipun cara pembayarannya secara bertahap. Solusinya apabila ada permasalahan seperti itu maka PPAT harus membuatkan perjanjian pengikatan jual beli lunas sebelum dibuatkan Akta Jual Belinya. Hal tersebut dilakukan supaya terwujud rasa keadilan dan meminimalisir wanprestasi antara penjual dan pembeli dalam kaitannya dengan jual beli tanah.Kata Kunci : Akibat Hukum, Jual Beli Tanah, Belum Lunas. ABSTRACT The result of this study concludes that the legal effect of the transfer of ownership of land that has not paid off is valid for the sale and purchase, but if the payment of the land price has not been paid in advance then the transfer of its rights can be suspended (in accordance with the agreement of sale and purchase settlement paid). After payment of the price is paid a new process of transfer of rights continue (making Deed of Sale and Purchase certificate process). PPAT makes the Deed of Sale and then the deed is used as authentic proof that there has been a transfer of land rights through subsequent sale and sale to be registered. While the sale and purchase of land that adheres to customary law is concrete, cash, real and real. This means that the role of PPAT in carrying out the mandate of the Act must be fully implemented and related to the transfer of ownership rights to land that has not paid off, PPAT must determine the firm stance to not make the Deed and Sell before all payment of the price paid in full even though the payment method gradually . The solution if there are problems like that then PPAT must make a binding agreement to buy and sell paid before the Deed of Sale. This is done in order to realize the sense of justice and minimize the default between the seller and the buyer in relation to the sale and purchase of land.Keywords: Legal Effect, Sale and Purchase Land, Not Filled.