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排序方式: 共有273条查询结果,搜索用时 46 毫秒
271.
Sophia Schneider Luca Schierbaum Wessel A. C. Burger Steve Seltzsam Chunyan Wang Bixia Zheng Chen-Han Wilfred Wu Makiko Nakayama Dervla M. Connaughton Nina Mann Mohamed A. Shalaby Jameela A. Kari Sherif ElDesoky Velibor Tasic Loai A. Eid Shirlee Shril David M. Thal Friedhelm Hildebrandt 《American journal of medical genetics. Part A》2023,191(8):2083-2091
Neurogenic bladder is caused by disruption of neuronal pathways regulating bladder relaxation and contraction. In severe cases, neurogenic bladder can lead to vesicoureteral reflux, hydroureter, and chronic kidney disease. These complications overlap with manifestations of congenital anomalies of the kidney and urinary tract (CAKUT). To identify novel monogenic causes of neurogenic bladder, we applied exome sequencing (ES) to our cohort of families with CAKUT. By ES, we have identified a homozygous missense variant (p.Gln184Arg) in CHRM5 (cholinergic receptor, muscarinic, 5) in a patient with neurogenic bladder and secondary complications of CAKUT. CHRM5 codes for a seven transmembrane-spanning G-protein-coupled muscarinic acetylcholine receptor. CHRM5 is shown to be expressed in murine and human bladder walls and is reported to cause bladder overactivity in Chrm5 knockout mice. We investigated CHRM5 as a potential novel candidate gene for neurogenic bladder with secondary complications of CAKUT. CHRM5 is similar to the cholinergic bladder neuron receptor CHRNA3, which Mann et al. published as the first monogenic cause of neurogenic bladder. However, functional in vitro studies did not reveal evidence to strengthen the status as a candidate gene. Discovering additional families with CHRM5 variants could help to further assess the genes' candidate status. 相似文献
272.
Ovidiu Chioncel Marianna Adamo Maria Nikolaou John Parissis Alexandre Mebazaa Mehmet Birhan Yilmaz Christian Hassager Brenda Moura Johann Bauersachs Veli-Pekka Harjola Elena-Laura Antohi Tuvia Ben-Gal Sean P. Collins Vlad Anton Iliescu Magdy Abdelhamid Jelena Čelutkienė Stamatis Adamopoulos Lars H. Lund Mariantonietta Cicoira Josep Masip Hadi Skouri Finn Gustafsson Amina Rakisheva Ingo Ahrens Andrea Mortara Ewa A. Janowska Abdallah Almaghraby Kevin Damman Oscar Miro Kurt Huber Arsen Ristic Loreena Hill Wilfried Mullens Alaide Chieffo Jozef Bartunek Pasquale Paolisso Antoni Bayes-Genis Stefan D. Anker Susanna Price Gerasimos Filippatos Frank Ruschitzka Petar Seferovic Rafael Vidal-Perez Alec Vahanian Marco Metra Theresa A. McDonagh Emanuele Barbato Andrew J.S. Coats Giuseppe M.C. Rosano 《European journal of heart failure》2023,25(7):1025-1048
Acute heart failure (AHF) represents a broad spectrum of disease states, resulting from the interaction between an acute precipitant and a patient's underlying cardiac substrate and comorbidities. Valvular heart disease (VHD) is frequently associated with AHF. AHF may result from several precipitants that add an acute haemodynamic stress superimposed on a chronic valvular lesion or may occur as a consequence of a new significant valvular lesion. Regardless of the mechanism, clinical presentation may vary from acute decompensated heart failure to cardiogenic shock. Assessing the severity of VHD as well as the correlation between VHD severity and symptoms may be difficult in patients with AHF because of the rapid variation in loading conditions, concomitant destabilization of the associated comorbidities and the presence of combined valvular lesions. Evidence-based interventions targeting VHD in settings of AHF have yet to be identified, as patients with severe VHD are often excluded from randomized trials in AHF, so results from these trials do not generalize to those with VHD. Furthermore, there are not rigorously conducted randomized controlled trials in the setting of VHD and AHF, most of the data coming from observational studies. Thus, distinct to chronic settings, current guidelines are very elusive when patients with severe VHD present with AHF, and a clear-cut strategy could not be yet defined. Given the paucity of evidence in this subset of AHF patients, the aim of this scientific statement is to describe the epidemiology, pathophysiology, and overall treatment approach for patients with VHD who present with AHF. 相似文献