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1.
Adv Med Educ Pract ; 13: 167-175, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-35228827

RESUMO

PURPOSE: This study aimed to investigate the perceptions and habits of different emergency department (ED) workers (nurses, residents, and attending physicians) and their pre- or post-shift routines. The study also examined the effect of night shifts on personal life, social life, and health. PATIENTS AND METHODS: An anonymous, online, cross-sectional, multiple-choice, self-rating (5-point Likert scale) survey was administered to the participants. All analyses were performed using the SPSS version 22.0. Ethical approval was obtained from the Institutional Review Board (IRB) of King Saud University Medical City (KSUMC) in Riyadh, Saudi Arabia. RESULTS: Thirty-three nurses, 51 residents, and 39 attending physicians participated in the survey (response rates of 21%, 100%, and 100%, respectively). A significant difference was noted in the need to use physical sleeping aids between the three groups (P < 0.003), with more nurses using humidifiers as a sleeping aid (21.2%) than residents or attending physicians. However, there was no difference in the use of pharmacological aids between the three groups. All groups utilized coffee as the preferred stimulant, especially residents (76.5%, P <0.032). Nurses and attending physicians wake up 2 hours before their shift, while residents prefer 3 hours (P <0.001). Attending physicians reported the highest accident rates post-night shifts of 17.9% (P < 0.001). Residents reported satisfaction while working night shifts and were least in agreement with night shifts reducing life span. Attending physicians were more in agreement with the increasing risk of drug/alcohol misuse and the incidence of depression in relation to night shifts. CONCLUSION: Participants shared many commonalities, yet residents were less likely to use sleeping aids and enjoy night shifts more than the other groups. All groups consumed coffee for stimulation. Attending physicians reported the highest accident rates post night shifts.

2.
Kidney Int ; 98(5): 1225-1241, 2020 11.
Artigo em Inglês | MEDLINE | ID: mdl-32610050

RESUMO

Polycystin-1 (PC1) and -2 (PC2), products of the PKD1 and PKD2 genes, are mutated in autosomal dominant polycystic kidney disease (ADPKD). They localize to the primary cilia; however, their ciliary function is in dispute. Loss of either the primary cilia or PC1 or PC2 causes cyst formation. However, loss of both cilia and PC1 or PC2 inhibits cyst growth via an unknown pathway. To help define a pathway, we studied cilium length in human and mouse kidneys. We found cilia are elongated in kidneys from patients with ADPKD and from both Pkd1 and Pkd2 knockout mice. Cilia elongate following polycystin inactivation. The role of intraflagellar transport proteins in Pkd1-deficient mice is also unknown. We found that inactivation of Ift88 (a gene expressing a core component of intraflagellar transport) in Pkd1 knockout mice, as well as in a new Pkd2 knockout mouse, shortened the elongated cilia, impeded kidney and liver cystogenesis, and reduced cell proliferation. Multi-stage in vivo analysis of signaling pathways revealed ß-catenin activation as a prominent, early, and sustained event in disease onset and progression in Pkd2 single knockout but not in Pkd2.Ift88 double knockout mouse kidneys. Additionally, AMPK, mTOR and ERK pathways were altered in Pkd2 single knockout mice but only AMPK and mTOR pathway alteration were rescued in Pkd2.Ift88 double knockout mice. Thus, our findings advocate an essential role of polycystins in the structure and function of the primary cilia and implicate ß-catenin as a key inducer of cystogenesis downstream of the primary cilia. Our data suggest that modulating cilium length and/or its associated signaling events may offer novel therapeutic approaches for ADPKD.


Assuntos
Cistos , Doenças Renais Policísticas , Rim Policístico Autossômico Dominante , Animais , Cílios , Cistos/genética , Humanos , Rim , Fígado , Camundongos , Camundongos Knockout , Rim Policístico Autossômico Dominante/genética , Canais de Cátion TRPP/genética
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