Bonjour,
Je suis passé récemment de l'utilisation de TexMaker à TexStudio, notamment pour la fonction d'ajout au dictionnaire disponible dans TexStudio, et l'affichage plus clair. Cependant, lorsque je colle une référence bibliographique dans mon fichier .bib dans TexStudio, des sauts de lignes apparaissent, alors qu'ils ne sont pas présents dans le texte de départ. En revanche, lorsque je colle ce même texte, toujours dans TexStudio, dans un fichier .tex par exemple, les saut de lignes n'apparaissent plus. Voyez l'exemple ci dessous pour comparer les deux résultats. Auriez vous une astuce pour éviter les sauts de ligne lorsque qu'on colle une texte dans le fichier .bib ?
Merci
Tom
Dans le fichier .bib :
Dans un fichier .tex par exemple :
Code : Sélectionner tout - Visualiser dans une fenêtre à part
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55 @article{ author = {Yamashita, M. and Emerman, M.}, title = {Capsid is a dominant determinant of retrovirus infectivity in nondividing cells}, journal = {J Virol}, volume = {78}, number = {11}, pages = {5670-8}, note = {Yamashita, Masahiro Emerman, Michael eng R01 AI51153/AI/NIAID NIH HHS/ R37 AI30927/AI/NIAID NIH HHS/ Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. 2004/05/14 05:00 J Virol. 2004 Jun;78(11):5670-8.}, abstract = {A major difference between lentiviruses such as human immunodeficiency virus (HIV) and most other retroviruses is their ability to productively infect nondividing cells. We present here genetic evidence for involvement of the capsid protein (CA) in the infectious phenotype in nondividing cells. A chimeric HIV type 1 (HIV-1) in which the MA and CA of HIV-1 are replaced with the MA, p12, and CA encoding sequences from murine leukemia virus (MLV) loses the ability to efficiently infect nondividing cells. Analysis of the accumulation of two-long-terminal-repeat circles implies that the impairment of nuclear transport of preintegration complexes is responsible for the restricted infection of this chimeric virus in nondividing cells. Incorporation of MLV MA and MLV p12 into HIV virions alone does not exert any adverse effects on viral infection in interphase cells. These results suggest that CA is the dominant determinant for the difference between HIV and MLV in the ability to transduce nondividing cells.}, keywords = {Active Transport, Cell Nucleus Capsid/*physiology Gene Products, gag/physiology HIV Long Terminal Repeat HIV-1/*physiology HeLa Cells Humans Leukemia Virus, Murine/*physiology Viral Matrix Proteins/physiology}, year = {2004} }
Code : Sélectionner tout - Visualiser dans une fenêtre à part
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28 @article{ author = {Yamashita, M. and Emerman, M.}, title = {Capsid is a dominant determinant of retrovirus infectivity in nondividing cells}, journal = {J Virol}, volume = {78}, number = {11}, pages = {5670-8}, note = {Yamashita, Masahiro Emerman, Michael eng R01 AI51153/AI/NIAID NIH HHS/ R37 AI30927/AI/NIAID NIH HHS/ Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. 2004/05/14 05:00 J Virol. 2004 Jun;78(11):5670-8.}, abstract = {A major difference between lentiviruses such as human immunodeficiency virus (HIV) and most other retroviruses is their ability to productively infect nondividing cells. We present here genetic evidence for involvement of the capsid protein (CA) in the infectious phenotype in nondividing cells. A chimeric HIV type 1 (HIV-1) in which the MA and CA of HIV-1 are replaced with the MA, p12, and CA encoding sequences from murine leukemia virus (MLV) loses the ability to efficiently infect nondividing cells. Analysis of the accumulation of two-long-terminal-repeat circles implies that the impairment of nuclear transport of preintegration complexes is responsible for the restricted infection of this chimeric virus in nondividing cells. Incorporation of MLV MA and MLV p12 into HIV virions alone does not exert any adverse effects on viral infection in interphase cells. These results suggest that CA is the dominant determinant for the difference between HIV and MLV in the ability to transduce nondividing cells.}, keywords = {Active Transport, Cell Nucleus Capsid/*physiology Gene Products, gag/physiology HIV Long Terminal Repeat HIV-1/*physiology HeLa Cells Humans Leukemia Virus, Murine/*physiology Viral Matrix Proteins/physiology}, year = {2004} }
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