
CHU Bordeaux
Articles
Exon location of glycine substitutions impacts kidney survival in autosomal dominant Alport Syndrome
Jan 14, 2025 |
academic.oup.com | CHU Lille |CHU Bordeaux |Univ. Lille
Unlike X-linked or autosomal recessive Alport Syndrome, no clear genotype/phenotype correlation has yet been demonstrated in patients carrying a single variant of COL4A3 or COL4A4. We carried out a multicenter retrospective study to assess the risk factors involved in renal survival in patients presenting a single pathogenic variant on COL4A3 or COL4A4. 97 patients presenting a single pathogenic variant of COL4A3 or COL4A4 were included.
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Dec 10, 2024 |
onlinecjc.ca | Quebec Heart |Quebec City |Hôpital Haut-Lévêque |CHU Bordeaux
aQuebec Heart & Lung Institute, Laval University, Quebec City, Quebec, Canada bUnité Médico-Chirurgicale des Valvulopathies, Hôpital Haut-Leveque, CHU Bordeaux, Pessac, France cDepartment of Cardiology, Hospital Bichat Claude-Bernard, Paris, France dDepartment of Cardiology, Hospital Universitario Central de Asturias, Oviedo, Spain eSouthlake Regional Health Centre, Newmarket, Ontario, Canada fCardiology Department, Hospital Universitario Marqués de Valdecilla,IDIVAL, Santander, Spain...
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Mar 26, 2024 |
diabetesjournals.org | CHU Bordeaux
We were interested in the recent article in Diabetes Care by Umapathysivam et al. (1), who reported two cases of euglycemic ketoacidosis after introduction of sodium–glucose cotransporter 2 inhibitor (SGLT2i) for heart failure with reduced ejection fraction in patients without diabetes. Reporting such adverse events is especially important, because SGLT2i may play a role in the recent rise of mortality from hyperglycemic crises in the U.S. (2).
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Nov 22, 2023 |
academic.oup.com | CHU Bordeaux
Caspofungin is an echinocandin antifungal agent that inhibits synthesis of glucan required for the fungal cell wall. Resistance is mediated by mutation of Fks1 glucan synthase, among which S645P is the most common resistance-associated polymorphism. Rapamycin is a macrolide that inhibits the mechanistic target of rapamycin (mTOR) protein kinase activity.
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