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991.
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993.
Matthew Mazalouskas Tammy Jessen Seth Varney James S Sutcliffe Jeremy Veenstra-VanderWeele Edwin H Cook Jr Ana M D Carneiro 《Neuropsychopharmacology》2015,40(8):2015-2024
Converging lines of evidence have identified genetic interactions between the serotonin transporter (SERT) gene and ITGB3, which encodes the β3 subunit that forms the αIIbβ3 and αvβ3 integrin receptor complexes. Here we examine the consequences of haploinsufficiency in the mouse integrin β3 subunit gene (Itgb3) on SERT function and selective 5-hydroxytryptamine (5-HT) reuptake inhibitor (SSRI) effectiveness in vivo. Biochemical fractionation studies and immunofluorescent staining of murine brain slices reveal that αvβ3 receptors and SERTs are enriched in presynaptic membranes from several brain regions and that αvβ3 colocalizes with a subpopulation of SERT-containing synapses in raphe nuclei. Notably, we establish that loss of a single allele of Itgb3 in murine neurons is sufficient to decrease 5-HT uptake by SERT in midbrain synaptosomes. Pharmacological assays to elucidate the αvβ3-mediated mechanism of reduced SERT function indicate that decreased integrin β3 subunit expression scales down the population size of active SERT molecules and, as a consequence, lowers the effective dose of SSRIs. These data are consistent with the existence of a subpopulation of SERTs that are tightly modulated by integrin αvβ3 and significantly contribute to global SERT function at 5-HT synapses in the midbrain. Importantly, our screen of a normal human population for single nucleotide polymorphisms in human ITGB3 identified a variant associated with reductions in integrin β3 expression levels that parallel our mouse findings. Thus, polymorphisms in human ITGB3 may contribute to the differential responsiveness of select patients to SSRIs. 相似文献
994.
995.
Ana B. Arroyo María P. Fernndez-Prez Alberto del Monte Sonia guila Raúl Mndez Rebecca Hernndez-Antolín Nuria García-Barber Ascensin M. de los Reyes-García Paula Gonzlez-Jimnez María I. Arcas Vicente Vicente Rosario Menndez Vicente Andrs Rocío Gonzlez-Conejero Constantino Martínez 《Haematologica》2021,106(6):1636
Neutrophil extracellular traps (NET) induce a procoagulant response linking inflammation and thrombosis. Low levels of miR-146a, a brake of inflammatory response, are involved in higher risk of cardiovascular events, but the mechanisms explaining how miR-146a exerts its function remain largely undefined. The aim of this study was to explore the impact of miR-146a deficiency in NETosis both in sterile and non-sterile models in vivo, and to investigate the underlying mechanism. Two models of inflammation were used: (i) Ldlr-/- mice transplanted with bone marrow from miR-146a-/- or wild-type mice were fed a high-fat diet, generating an atherosclerosis model; and (ii) an acute inflammation model was generated by injecting lipopolysaccharide (1 mg/kg) into miR-146a-/- and wildtype mice. miR-146a deficiency increased NETosis in both models. Accordingly, miR-146a-/- mice showed significantly reduced carotid occlusion time and elevated levels of NET in thrombi following FeCl3-induced thrombosis. Infusion of DNAse I abolished arterial thrombosis in both WT and miR-146a-/- mice. Interestingly, miR-146a-deficient mice have aged, hyperreactive and pro-inflammatory neutrophils in their circulation which are more prone to form NET independently of the stimulus. Furthermore, we demonstrated that patients with community-acquired pneumonia with reduced miR-146a levels associated with the T variant of the functional rs2431697 had an increased risk of cardiovascular events due, in part, to an increased generation of NET. 相似文献
996.
Aikaterini Nanou Chrisavgi Toumpeki Pavlos Fanis Nicoletta Bianchi Lucia Carmela Cosenza Cristina Zuccato George Sentis Giorgos Giagkas Coralea Stephanou Marios Phylactides Soteroula Christou Michalis Hadjigavriel Maria Sitarou Carsten W. Lederer Roberto Gambari Marina Kleanthous Eleni Katsantoni 《Haematologica》2021,106(4):1207
997.
998.
de Souza Júlia Ruete Yokoyama Ana Paula Magnus Mariana Munari Boin Ilka de Ataide Elaine Cristina Munhoz Derli Conceição Pereira Fabrício Bíscaro Luzo Angela Orsi Fernanda Andrade 《Journal of thrombosis and thrombolysis》2022,53(4):887-897
Journal of Thrombosis and Thrombolysis - The relationship between acidosis and coagulopathy has long been described in vitro and in trauma patients, but not yet in orthotopic liver transplantation... 相似文献
999.
Fernández-Ávila Daniel Gerardo Patino-Hernandez Daniela Kowalskii Sergio Vargas-Caselles Alfredo Sapag Ana Maria Cachafeiro-Vilar Antonio Meléndez-Muñoz Lucia Santiago-Pastelín Carlos Graf Cesar Rossetto Chayanne Palleiro Daniel Trincado Daniela Fernández-Ávila Diana Arrieta Dina Reyes Gil Then Baez Jossiel Ugarte-Gil Manuel F. Cardiel Mario Colman Nelly Chávez Nilmo Burgos Paula I Montúfar Ruben Sandino Sayonara Fuentes-Silva Yurilis Soriano Enrique R. 《Clinical rheumatology》2021,40(7):2913-2920
Clinical Rheumatology - Studies conducted by various scientific societies have shown that the demand for specialized rheumatology care is greater than the projected growth of the workforce. Our... 相似文献
1000.
Natasha Aleksova Ana C. Alba Chun-Po S. Fan Faizan Amin Omid Kiamanesh Caroline McGuinty Hanna Lee Juan G. Duero Posada Heather J. Ross Filio Billia Vivek Rao 《The Canadian journal of cardiology》2021,37(3):467-475
BackgroundAs patients with advanced heart failure are living longer, defining the impact of left ventricular assist devices (LVADs) on outcomes in an aging population is of great importance. We describe overall survival, rates of adverse events (AEs), and post-AE survival in patients age ≥ 70 years vs age 50-69 years after destination-therapy (DT) LVAD implantation.MethodsA retrospective analysis was conducted with the use of the International Society for Heart and Lung Transplantation Mechanically Assisted Circulatory Support (IMACS) registry. All adults age ≥ 50 years with a continuous-flow DT LVAD from 2013 to 2017 were included. The primary outcome was all-cause mortality. The secondary outcomes were the incidence of and survival after gastrointestinal (GI) bleeding, infection, stroke, pump thrombosis, pump exchange, and right-side heart failure. Mortality and AEs were assessed with the use of competing risk models.ResultsAt total of 5,572 patients were included: 3,700 aged 50-69 and 1,872 aged ≥ 70. All-cause mortality by 42 months was 55.8% in patients aged ≥ 70 and 44.8% in patients aged 50-69 (P = 0.001). Patients aged ≥ 70 had a 37.8% higher risk of death after DT LVAD implantation (hazard ratio 1.378, 95% CI 1.251-1.517). Patients aged ≥ 70 had higher risk of GI bleeding but lower risk of right-side heart failure. There was no difference between age groups for risk of infection or stroke. Experiencing any AE was associated with an increased risk of death that did not vary with age.ConclusionsPatients aged ≥ 70 years have reduced survival after DT LVAD, in part because of increased GI bleeding, while the incidence of other AEs is similar to that of patients aged 50-69 years. Careful patient selection beyond age alone may allow for optimal outcomes after DT LVAD implantation. 相似文献