The intravascular administration of iodine-based contrast media is a common cause of acute kidney injury (AKI). This study investigated whether changes in the urinary concentration of neutrophil gelatinase-associated lipocalin (uNGAL) before and after coronary angiography they are able to predict the development of AKI independently of previously established absolute cut-off values. A total of 125 outpatients undergoing elective coronary angiography were enrolled and divided into 2 subgroups: G1 (n = 103), patients with changes in their serum creatinine after coronary angiography of < 0.3 mg/dL, and G2 (n = 22), patients with changes in their serum creatinine after coronary angiography &#8805; 0.3 mg/dL. The primary study endpoint was AKI defined as AKI network stages 1. uNGAL was measured before coronary arteriography and 2 and 4 hours afterwards. To determine the sensitivity and specificity for the absolute and relative variations of uNGAL, a receiver operator characteristic (ROC) curve analysis was performed. Based on the ROC curve for the relative difference in uNGAL before and after coronary angiography, a 50% increase in the uNGAL value over baseline was 60% sensitive and 81% specific for AKI. The area under the curve for relative differences 2 hours after coronary angiography was 0.82. The percentage variations in the concentration of uNGAL detected the early stages of AKI regardless of the absolute cut-off established. / A administração intravascular dos meios de contraste à base de iodo é uma causa comum da injúria renal aguda. Este estudo investigou se mudanças na concentração da Lipocalina Urinária Associada com Gelatinase de Neutrófilos Humanos (NGALu), antes e após angiografia coronariana eletiva, são capazes de prever o desenvolvimento da injúria renal aguda, independentemente de pontos de corte previamente estabelecidos. Foram avaliados 125 pacientes ambulatoriais submetidos a cinecoronariografia eletiva. Os pacientes foram divididos em dois subgrupos; G1 (n=103), pacientes com alterações nos valores da creatinina sérica < 0,3 mg/dL e G2 (n=22), aqueles em que a creatinina sérica se elevou &#8805; 0,3 mg/dL. O endpoint primário dessa pesquisa foi a injúria renal aguda definida pelo acute kidney injury network estágio 1. Foram realizadas dosagens da Lipocalina urinária Associada com Gelatinase de Neutrófilos imediatamente antes, 2 e 4 horas após a cinecoronariografia. Para determinar a sensibilidade e especificidade das variações absolutas e relativas de NGALu utilizamos receiver operating characteristic (ROC). Com base na curva ROC para diferença relativa no NGALu antes e após a angiografia coronariana eletiva, um aumento de 50% no valor do NGALu após o procedimento, foi 60% sensível e 81% específico para detecção da injúria renal aguda. A área sob a curva para diferença relativa 2 horas após a cinecoronariografia foi 0,82. Variações percentuais na concentração de NGALu foram capazes de prever a injúria renal aguda 2 horas após a angiografia coronariana independentemente de pontos de corte estabelecido em valores absolutos. / Mestre em Ciências da Saúde

East of Lake Winnipeg is what conservationists call the ‘east shore wilderness’ / ‘heart of the boreal.’ The largest contiguous tract of unindustrialized boreal forest on Earth, this area has been the focus of 15 years of discussion and planning in Manitoba. The area is also designated Waabanong Nakaygum, a homeland to the Anishinaabek of this bush-meets-lake region. Waabanong has seen limited access during the industrial period of personal mechanized mobility due to a lack of constructed all-weather roads. However, an older pattern of travel and mobility does exist across the land, for centuries constituting traditional Anishinaabek patterns of land use and trade. As all-weather roads are being constructed along Lake Winnipeg, oral interviews will examine the question: will the older trails remain in the collective culture of the people or shall the north-south cultural and economic flows replace the east-west bush history traced by the rivers that wind through?

Submitted by Rosangela Silva (rosangela.silva3@unioeste.br) on 2018-05-24T17:46:38Z No. of bitstreams: 2 Isabel Cristina Moresco.pdf: 778049 bytes, checksum: 0c5c3dc6a4ac6f42d2f9a40313cd38c6 (MD5) license_rdf: 0 bytes, checksum: d41d8cd98f00b204e9800998ecf8427e (MD5) / Made available in DSpace on 2018-05-24T17:46:39Z (GMT). No. of bitstreams: 2 Isabel Cristina Moresco.pdf: 778049 bytes, checksum: 0c5c3dc6a4ac6f42d2f9a40313cd38c6 (MD5) license_rdf: 0 bytes, checksum: d41d8cd98f00b204e9800998ecf8427e (MD5) Previous issue date: 2018-03-08 / In the last 20 years, with the emergence of multiresistant gram-negative bacteria, polymyxins, which had fallen into disuse due to their high toxicity, were once again used as an alternative for the treatment of these infections. This antibiotic group is active against most enterobacteria and non-fermenting gram-negative bacteria, ocular, urinary tract, meninges, and bloodstream infections. The recommended dose of polymyxin B (PMB) in patients with normal renal function is 1.5 to 2.5 mg.kg-1.day-1 and the dose can be divided twice. For patients with impaired renal function, it is recommended to adjust the dose according to creatinine clearance. Because nephrotoxicity is the major limiting factor in the use of this class of antibiotics, a retrospective observational study was conducted to identify possible risk factors for the development of acute renal injury (ARF) in patients using the antibiotic PMB. The necessary information was collected to perform the study in medical records, medical prescriptions and results of laboratory tests from the patients who used PMB in a period of 5 years in a Brazilian hospital. Inclusion criteria for the study were: patients over 18 years of age who used intravenous PMB for more than 72 hours. To classify ARI levels, baseline creatinine was calculated by the average of the last five serum creatinine tests before the first dose of the antibiotic. This calculated value and the highest level of serum creatinine during treatment were used to identify and classify renal damage according to the criteria of the RIFLE (Risk, Injury and Failure and Loss and End-stage renal disease) filtration rate. The study included 120 patients, most of them male (89; 74.2%) with an average age of 50 years. The most frequent pre-existing comorbidities were systemic hypertension (50; 41.7%), diabetes mellitus (21; 17.5%), nephropathies (14; 11.7%) and obesity (13; 10.8%). The main infection was pneumonia (35.8%) and the most frequently identified infectious agent was Acinetobacter baumannii (67.9%). PMB treatments were performed for 13 days and the average daily dose was 191.5 mg. The high incidence of mortality in the studied population (46.7%) may be related to the critical clinical status of the patients, because at some point of hospitalization, 111 patients (92.5%) needed intensive care. In the population studied to evaluate risk factors, 12 patients (13.5%) presented risk, 22 (25.0%) injury, 30 (34.1%) renal failure, according to RIFLE criteria. In addition, in the group that patients developed ARF, 51.9% died, whereas in the group that did not present, only 12.5% died. There was a statistically significant difference between the groups that developed or not ARF, for the following variables: treatment time greater than 10 days, accumulated PMB dose, hypoalbuminemia and concomitant use of furosemide. However, the variables that remained in the final multivariate logistic regression model were treatment time greater than 10 days and hypoalbuminemia. Several factors inherent to the patient and the drug are related to ARF and strategies should be created in order to minimize these effects. The monitoring of renal function in all patients, especially those at risk, and the follow-up of the infection to reduce the time of treatment are highlighted. / Nos últimos 20 anos, com o surgimento de bactérias gram-negativas multirresistentes, as polimixinas, que tinham caído em desuso pela elevada toxicidade, voltaram a ser utilizadas como uma alternativa para tratamento dessas infecções. Esse grupo de antibiótico é ativo contra a maioria das enterobactérias e das bactérias gram-negativas não fermentadoras, em infecções oculares, do trato urinário, das meninges e da corrente sanguínea. A dose recomendada de polimixina B (PMB), em pacientes com função renal normal, é de 1,5 a 2,5 mg Kg-1 dia-1 e a dose pode ser dividida em duas vezes. Para os pacientes com alteração da função renal, recomenda-se ajustar a dose de acordo com a depuração de creatinina. Como a nefrotoxicidade é o maior limitante do uso dessa classe de antibióticos, um estudo observacional retrospectivo foi realizado com o objetivo de identificar os possíveis fatores de risco para o desenvolvimento de injúria renal aguda (IRA) em pacientes que utilizaram o antibiótico PMB. Foram coletadas as informações necessárias para realizar o estudo em prontuários, prescrições médicas e resultados de exames laboratoriais dos pacientes que utilizaram PMB em um período de 5 anos em um hospital brasileiro. Os critérios de inclusão para o estudo foram: pacientes maiores de 18 anos que utilizaram PMB por via endovenosa por mais de 72 horas. Para classificar os níveis de IRA, a creatinina basal foi calculada pela média entre os cinco últimos exames de creatinina sérica antes da primeira dose do antibiótico. Esse valor calculado e o maior nível de creatinina sérica durante o tratamento foram usados para identificar e classificar o dano renal segundo os critérios da taxa de filtração glomerular de RIFLE (Risk, Injury and Failure and Loss, and End-stage renal disease). Foram inclusos no estudo 120 pacientes, a maioria do sexo masculino (89; 74,2%) com média de idade de 50 anos. As comorbidades pré-existentes presentes com maior frequência foram hipertensão arterial sistêmica (50; 41,7%), diabetes mellitus (21; 17,5%) nefropatias (14; 11,7%) e obesidade (13; 10,8%). A principal infecção tratada foi pneumonia (35,8%) e o agente infeccioso mais identificado foi o Acinetobacter baumannii (67,9%). Os tratamentos com a PMB foram realizados durante 13 dias e a dose média diária de 191,5 mg. A alta incidência de mortalidade da população estudada (46,7%) pode estar relacionada ao estado clínico crítico dos pacientes, pois, em algum momento do internamento, 111 pacientes (92,5%) precisaram de cuidados intensivos. Na população estudada para avaliar os fatores de risco, 12 pacientes (13,5%) apresentam risco, 22 (25,0%) injúria, 30 (34,1%) falência renal, segundo os critérios de RIFLE. Além disso, no grupo que os pacientes desenvolveram IRA, 51,9% foram a óbito, enquanto que no grupo que não apresentou foram apenas 12,5%. Houve diferença estatisticamente significativa entre os grupos que desenvolveram, ou não, IRA, para as seguintes variáveis: tempo de tratamento superior a 10 dias, dose acumulada de PMB, hipoalbuminemia e uso concomitante de furosemida. Porém, as variáveis que permaneceram no modelo final de regressão logística multivariável foram o tempo de tratamento superior a 10 dias e a hipoalbuminemia. Vários fatores inerentes ao paciente e à droga estão relacionados à IRA e estratégias devem ser criadas com o intuito de minimizar esses efeitos. Destacam-se a monitorização da função renal em todos os pacientes, principalmente os de risco, e o acompanhamento da infecção para diminuir o tempo de tratamento.

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Introduction : La mortalité associée à l’insuffisance rénale aiguë (acute kidney injury ‘’AKI’’) aux soins intensifs pédiatriques (SIP) dépasse les 50%. Des études antérieures sur la thérapie de remplacement rénal (TRR) ont fait ressortir plusieurs facteurs de risque de mortalité dont le syndrome de défaillance multiviscérale (SDMV) et la surcharge liquidienne ≥ 10 à 20% avant l’initiation de la TRR. L’objectif de cette étude était d’identifier les principaux facteurs de risque de mortalité à 28 jours après l’initiation de la TRR chez les patients atteints d’AKI aux SIP. Méthode : Il s’agit d’une étude de cohorte rétrospective aux SIP d’un centre tertiaire. Tous les enfants ayant reçus de la TRR continue ou de l’hémodialyse intermittente pour AKI, entre janvier 1998 et décembre 2014, ont été inclus. Les facteurs de risque de mortalité ont été préalablement identifiés par quatre intensivistes et deux néphrologues pédiatres et analysés à l’aide d’une régression logistique multivariée. Résultats : Quatre-vingt-dix patients ont été inclus. L’âge médian était de 9 [2-14] ans. La principale indication d’initiation de la TRR était la surcharge liquidienne (64,2%). La durée médiane d’hospitalisation aux SIP était de 18,5 [8,0-31,0] jours. Quarante patients (44,4%) sont décédés dans les 28 jours suivant l’initiation de la TRR et quarante-cinq (50,0%) avant la sortie des SIP. Le score de PELOD ≥ 20 (OR 4,66 ; 95%CI 1,68-12,92) et la surcharge liquidienne ≥ 15% (OR 9,31; 95%CI 2,16-40,11) à l’initiation de la TRR étaient associés de façon indépendante à la mortalité. Conclusion : Cette étude a permis de faire ressortir deux facteurs de risque de mortalité à 28 jours à l’initiation de la TRR : la surcharge liquidienne et la sévérité du SDMV mesurée par le score de PELOD. / Introduction: Mortality rate associated with acute kidney injury (AKI) in pediatric intensive care units (PICU) exceeds 50%. Prior studies on renal replacement therapy (RRT) have highlighted different mortality risk factors including the presence of a multiple organ dysfunction syndrome (MODS) and fluid overload ≥ 10 to 20% before starting RRT. The aim of this study was to identify most important risk factors of 28-day mortality in patients with AKI at RRT initiation in PICU. Methods: We conducted a retrospective cohort study in a tertiary care pediatric center. All critically ill children who underwent acute continuous RRT or intermittent hemodialysis for AKI between January 1998 and December 2014 were included. A case report form was developed and specific risk factors were identified by a panel of four pediatric intensivists and two nephrologists. Risk factors analysis was made using logistic regression in SPSS and SAS software. Results: Ninety patients were included. The median age was 9 [2-14] years. The most common indication for RRT initiation was fluid overload (FO) (64.2%). The median PICU length of stay was 18.5 [8.0-31.0] days. Forty of the 90 patients (44.4%) died within 28 days after RRT initiation and forty-five (50.0%) died before PICU discharge. In a multivariate logistic regression analysis, a PELOD score ≥ 20 (OR 4.66; 95%CI 1.68-12.92) and percentage of FO ≥ 15% (OR 9.31; 95%CI 2.16-40.11) at RRT initiation were independently associated with mortality. Conclusion: This study suggests that fluid overload and severity of MODS measured by PELOD score are two risk factors of 28-day mortality in PICU patients on RRT.

Création Dans le roman Sous la Tiffany, Mikaël Langevin, le personnage principal, vit une pénible remise en question. Dans les derniers mois, il a délibérément sabordé son couple, sa vie sociale et même sa santé en misant tout sur sa réussite professionnelle en tant qu'enseignant. Tout pour une carrière où, selon sa perception, il ne réussit pas comme il l'aurait souhaité. Une nuit de la fin d'août, attablé devant des dizaines de cahiers noircis de sa main, il revisite un journal tenu chaque soir de l'été qui s'achève, un été pendant lequel de nombreuses fenêtres sur le passé auront été ouvertes, puis refermées. Le jour poindra dans quelques heures, il le sait bien. Mais nul éclairage ne le sert mieux que celui de la vieille Tiffany. Réflexion La deuxième partie, une réflexion d'ordre narratologique sur la dynamique de l'écart et ses procédés (analepse, prolepse, sommaire, scène, pause, ellipse, digression), vise à expliciter ce qui m'a tant séduit dans Hotaru, d'Aki Shimazaki, et dans L'Attrape-coeurs, de Jerome David Salinger, deux romans primés1 où les procédés d'écart sont habilement exploités. J'indiquerai aussi où, comment et pourquoi j'ai utilisé ces procédés dans Sous la Tiffany. Le but, au final, est de montrer comment la dynamique de l'écart contribue à accrocher le lecteur et à enrichir le récit, à conférer au texte le caractère évocateur si présent dans les oeuvres littéraires de Shimazaki et de Salinger.

La polykystose rénale autosomique dominante (ADPKD) est une des maladies génétiques les plus communes. ADPKD se manifeste le plus souvent au stade adulte par la présence de kystes rénaux, et bien souvent de kystes hépatiques, avec une progression très variable. ADPKD mène à une insuffisance rénale: les seuls recours sont la dialyse puis la transplantation rénale. Les mutations dispersées sur les gènes PKD1 (majoritairement; la protéine polycystine-1, PC1) et PKD2 (la protéine polycystine-2, PC2) sont responsables de l’ADPKD. Le mécanisme pathogénétique de perte de fonction (LOF) et donc d’un effet récessif cellulaire est évoqué comme causatif de l’ADPKD. LOF est en effet supporté par les modèles murins d’inactivation de gènes PKD1/PKD2, qui développent de kystes, quoique in utéro et avec une rapidité impressionnante dans les reins mais pas dans le foie. Malgré de nombreuses études in vitro, le rôle de PC1/PC2 membranaire/ciliaire reste plutôt hypothétique et contexte-dépendant. Ces études ont associé PC1/PC2 à une panoplie de voies de signalisation et ont souligné une complexité structurelle et fonctionnelle exceptionnelle, dont l’implication a été testée notamment chez les modèles de LOF. Toutefois, les observations patho-cellulaires chez l’humain dont une expression soutenue, voire augmentée, de PKD1/PC1 et l’absence de phénotypes extrarénaux particuliers remet en question l’exclusivité du mécanisme de LOF. Il était donc primordial 1) d’éclaircir le mécanisme pathogénétique, 2) de générer des outils in vivo authentiques d’ADPKD en terme d’initiation et de progression de la maladie et 3) de mieux connaitre les fonctions des PC1/PC2 indispensables pour une translation clinique adéquate. Cette thèse aborde tous ces points. Tout d’abord, nous avons démontré qu’une augmentation de PKD1 endogène sauvage, tout comme chez l’humain, est pathogénétique en générant et caractérisant en détail un modèle murin transgénique de Pkd1 (Pkd1TAG). Ce modèle reproduit non seulement les caractéristiques humaines rénales, associées aux défauts du cil primaire, mais aussi extrarénales comme les kystes hépatiques. La sévérité du phénotype corrèle avec le niveau d’expression de Pkd1 ce qui supporte fortement un modèle de dosage. Dans un deuxième temps, nous avons démontré par les études de complémentations génétiques que ces deux organes reposent sur une balance du clivage GPS de Pc1, une modification post-traductionelle typique des aGPCR, et dont l’activité et l’abondance semblent strictement contrôlées. De plus, nous avons caractérisé extensivement la biogénèse de Pc1 et de ses dérivés in vivo générés suite au clivage GPS. Nous avons identifié une toute nouvelle forme et prédominante à la membrane, la forme Pc1deN, en plus de confirmer deux fragments N- et C-terminal de Pc1 (NTF et CTF, respectivement) qui eux s’associent de manière non-covalente. Nous avons démontré de façon importante que le trafic de Pc1deN i.e., une forme NTF détachée du CTF, est toutefois dépendant de l’intégrité du fragment CTF in vivo. Par la suite, nous avons généré un premier modèle humanisant une mutation PKD1 non-sens tronquée au niveau du domaine NTF(E3043X) en la reproduisant chez une souris transgénique (Pkd1extra). Structurellement, cette mutation, qui mimique la forme Pc1deN, s’est également avérée causative de PKD. Le modèle Pkd1extra a permis entre autre de postuler l’existence d’une cross-interaction entre différentes formes de Pc1. De plus, nos deux modèles murins sont tous les deux associés à des niveaux altérés de c-Myc et Pc2, et soutiennent une implication réelle de ces derniers dans l’ADPKD tou comme une interaction fonctionnelle entre les polycystines. Finalement, nous avons démontré un chevauchement significatif entre l’ADPKD et le dommage rénal aigüe (ischémie/AKI) dont une expression augmentée de Pc1 et Pc2 mais aussi une stimulation de plusieurs facteurs cystogéniques tel que la tubérine, la β-caténine et l’oncogène c-Myc. Nos études ont donc apporté des évidences cruciales sur la contribution du gène dosage dans l’ADPKD. Nous avons développé deux modèles murins qui serviront d’outil pour l’analyse de la pathologie humaine ainsi que pour la validation préclinique ADPKD. L’identification d’une nouvelle forme de Pc1 ajoute un niveau de complexité supplémentaire expliquant en partie une capacité de régulation de plusieurs voies de signalisation par Pc1. Nos résultats nous amènent à proposer de nouvelles approches thérapeutiques: d’une part, le ciblage de CTF i.e., de style chaperonne, et d’autre part le ciblage de modulateurs intracellulaires (c-Myc, Pc2, Hif1α). Ensemble, nos travaux sont d’une importance primordiale du point de vue informatif et pratique pour un avancement vers une thérapie contre l’ADPKD. Le partage de voies communes entre AKI et ADPKD ouvre la voie aux approches thérapeutiques parallèles pour un traitement assurément beaucoup plus rapide. / Autosomal dominant polycystic kidney disease (ADPKD) is one of the most common genetic diseases. ADPKD is manifested by the presence of renal cysts detected most often in the adult stage, and frequently liver cysts, with highly variable progression. ADPKD leads to kidney failure with the only recourse of dialysis and eventual kidney transplantation. Mutations dispersed throughout the PKD1 gene (major player, the polycystin-1 protein, PC1) and the PKD2 gene (polycystin-2 protein, PC2) are responsible for ADPKD. The loss of function (LOF) pathogenetic mechanism, and therefore a cellular recessive effect, has been suggested as causative of ADPKD. LOF is indeed supported by the PKD1/PKD2 gene inactivation mouse models, which develop cysts, although in utero with impressive speed in the kidney but not in the liver. Despite many in vitro studies, the membrane/ciliary role of PC1/PC2 remains rather hypothetical and context-dependent. These studies have associated PC1/PC2 to a variety of signaling pathways and underlined exceptional structural and functional complexity, whose involvement has been tested especially in LOF models. However, pathocellular observations in humans with sustained and even increased expression of PKD1/PC1, and the absence of particular human extrarenal phenotypes questions the exclusivity of the LOF mechanism. It was therefore essential 1) to clarify the pathogenetic mechanism, 2) to generate in vivo tools authentic of ADPKD in terms of initiation and progression of the disease and 3) to better understand the essential functions of PC1/PC2 for an adequate clinical translation. This thesis addresses all of these issues. First, we demonstrated that an increase in endogenous PKD1, just like in humans, is pathogenetic by generating and characterizing in detail a transgenic mouse model of Pkd1 (Pkd1TAG). This model not only reproduces the renal human characteristics associated with defects of the primary cilium, but also the extrarenal, namely, liver cysts. The severity of the phenotype correlates with the expression level of Pkd1, which strongly supports a dosage model. Secondly, we have demonstrated with genetic complementation studies that these two organs rely on a balance of Pc1 GPS cleavage, a typical post-translational modification of aGPCR, whose activity and abundance seem strictly controlled. Furthermore, we have extensively characterized Pc1 biogenesis and its derivatives in vivo generated upon GPS cleavage. We have identified a new form, predominantly on the membrane, the Pc1deN form, in addition to confirming the two N- and C-terminal Pc1 fragments (NTF and CTF, respectively), which associate non-covalently. Importantly, we have demonstrated that traffic of Pc1deN i.e., the NTF form detached from the CTF, is still dependant on the integrity of the CTF fragment. Next, we generated a first model humanizing a PKD1 nonsense truncated mutation at the level of the NTF(E3043X) domain by reproducing it in a transgenic mouse (Pkd1extra). Structurally, this mutation, which mimics Pc1deN, has also been shown to be causative of PKD. The Pkd1extra model allowed the proposition of the existence of a cross-interaction between different forms of Pc1. In addition, our two mouse models are both associated with altered levels of c-Myc and Pc2, which is supportive of their involvement in ADPKD and a functional interaction between the polycystins. Finally, we have shown a significant overlap between ADPKD and acute renal injury (ischemia/AKI) namely increased expression of Pc1 and Pc2 but also stimulation of several cystogenic factors such as tuberin, β-catenin and the oncogene c-Myc. Our studies have therefore given crucial evidence to the contribution of PKD1 gene dosage mechanism in ADPKD. We have developed two mouse models, which can serve as a tool for the analysis of human pathology as well as for preclinical validation of ADPKD. The identification of a new form of Pc1 adds an additional level of complexity in part explaining the regulation capacity of Pc1 on several signaling pathways. Our findings lead us to propose new therapeutic approaches: firstly, targeting the CTF i.e., chaperone style, and also targeting intracellular modulators (c-Myc, Pc2, Hif1α). Together, our work is of paramount importance in an informative point of view and practical perspective for progress towards a therapy for treating ADPKD. The sharing of common pathways between AKI and ADPKD paves the way for parallel therapeutic approaches for assured much faster treatment.

Recourant volontiers au voilement ou à un jeu de paravents, l’écriture pudique est marquée par la précaution – souvent troublante en soi – d’éviter de provoquer le trouble chez son lecteur. Hamaguri d’Aki Shimazaki se construit autour d’un noyau apparemment contradictoire qui transcende le tabou de l’inceste. L’étude de ce roman, mis en parallèle avec L’amant de Duras et Les belles endormies de Kawabata, permet de mettre en relief un érotisme pudique dont la principale caractéristique consiste en une remise en cause de son principe transgressif, découlant de la dissolution de la limite tracée par l’interdit. Dans un phénomène de coïncidence des opposés, l’érotisme pudique aplanit le rapport dualiste entre des éléments donnés comme inconciliables : chair et esprit, Éros et Thanatos, licite et illicite. Empreint de ce type d’érotisme, Probablement personne met en scène une jeune femme et son professeur de peinture sumi-e, de quarante ans son aîné. Une passion indéfinissable, à la lisière de la hantise, les lie de plus en plus étroitement l’un à l’autre. Leur relation se joue dans le non-dit, les regards, la gestuelle; elle se révèle graduellement à travers des traits d’encre sur le papier et la symbolique de la fleur : fascinante, cueillie, flétrie… Leur drame se joue dans la zone grise entre ce qui a eu lieu et n’a jamais eu lieu. / With its active usage of veils and folding screens, modesty writing is characterized by a certain precaution – often unsettling in and of itself – that is intended to avoid exciting readers. Aki Shimazaki’s Hamaguri is constructed on such a seemingly contradictory core that transcends the taboo of incest. A comparative analysis of this novel using Duras’ The Lover and Kawabata’s The House of the Sleeping Beauties allows one to uncover a certain erotic modesty, whose defining characteristic is that it undermines transgression when the boundaries of the forbidden are broken down. In a phenomenon where opposites collide, erotic modesty bridges the dualistic gap that exists between elements once considered incompatible: body and soul, Eros and Thanatos, that which is permitted and the forbidden. Infused with this particular form of eroticism, Probablement personne acquaints readers with a young woman and her sumi-e painting professor, who is forty years her senior. An incommunicable bond develops, bordering on haunting, and ties the two closer together. Their relationship transpires in the unspoken, looks as well as gestures, gradually unveiling itself through strokes of ink on paper and floral symbolism: captivating, picked, wilted. Their drama unfolds in the grey area between what really happens, and what does not.

40% of severe acute respiratory syndrome coronavirus two (SARS-CoV-2) severe cases develop acute kidney injury (AKI). Current treatment for renal complications limits financial and material resources available. To explore alternative treatments and accelerate research in case of future coronavirus outbreaks, a mouse model of coronavirus disease 2019-associated AKI (C19-AKI) would represent a critical biomedical research tool. The surrogate model of C19-AKI (SMC) developed consisted of angiotensin-converting enzyme two (ACE2) knockout (KO) mice receiving 400 ng/kg/min of angiotensin (Ang) II by osmotic minipump for eight days with a single injection of lipopolysaccharide (LPS; 10 mg/kg) on the seventh day of Ang II and euthanasia 24 hours after LPS. Similarly, to C19-AKI, the SMC exhibited albuminuria, elevated blood urea nitrogen, electrolyte imbalance, neutrophil infiltration, and upregulation of the G-coupled protein receptor (GPR)84 and pro-inflammatory and injury markers. GPR84 was found in bronchoalveolar lavage fluid neutrophils of coronavirus disease 2019 (COVID-19) patients, suggesting a potential implication of GPR84 in the disease. We hypothesised that GPR84 deletion or antagonism with GLPG-1205 could attenuate SMC’s indices of renal injury and inflammation. GLPG-1205 and GPR84 KO had no effects in the SMC model, as suggested by unchanged albuminuria, electrolytes, and markers expression. Interestingly, neutrophil infiltration was attenuated by GLPG-1205 only. The SMC is an interesting tool for therapeutic development for infections associated with renal injury, such as SARS-CoV-2. GPR84 role in the SMC needs to be further assessed.