RESUMO
BACKGROUND: The COVID-19 pandemic spurred an increase in online information regarding disease spread and symptomatology. OBJECTIVE: Our purpose is to systematically assess the quality and readability of articles resulting from frequently Google-searched COVID-19 terms in the United States. METHODS: We used Google Trends to determine the 25 most commonly searched health-related phrases between February 29 and April 30, 2020. The first 30 search results for each term were collected, and articles were analyzed using the Quality Evaluation Scoring Tool (QUEST). Three raters scored each article in authorship, attribution, conflict of interest, currency, complementarity, and tone. A readability analysis was conducted. RESULTS: Exactly 709 articles were screened, and 195 fulfilled inclusion criteria. The mean article score was 18.4 (SD 2.6) of 28, with 7% (14/189) scoring in the top quartile. National news outlets published the largest share (70/189, 36%) of articles. Peer-reviewed journals attained the highest average QUEST score compared to national/regional news outlets, national/state government sites, and global health organizations (all P<.05). The average reading level was 11.7 (SD 1.9, range 5.4-16.9). Only 3 (1.6%) articles were written at the recommended sixth grade level. CONCLUSIONS: COVID-19-related articles are vastly varied in their attributes and levels of bias, and would benefit from revisions for increased readability.
RESUMO
Cardiac hypertrophy is common in autosomal dominant polycystic kidney disease (ADPKD) patients. We found increased heart weight in Pkd1RC/RC and Pkd2WS25/+ mouse models of ADPKD. As there is a link between increased heart weight and mammalian target of rapamycin (mTOR), the aim of the study was to determine mTOR complex 1 and 2 signaling proteins in the heart in the Pkd1RC/RC mouse model of PKD. In 70 day old Pkd1RC/RC hearts, on immunoblot analysis, there was a large increase in p-AMPKThr172, a known autophagy inducer, and an increase in p-AktSer473 and p-AktThr308, but no increase in other mTORC1/2 proteins (p-S6Ser240/244, p-mTORSer2448). In 150 day old Pkd1RC/RC hearts, there was an increase in mTORC1 (p-S6Ser240/244) and mTOR-related proteins (p-AktThr308, p-GSK3ßSer9, p-AMPKThr172). As the mTOR pathway is the master regulator of autophagy, autophagy proteins were measured. There was an increase in p-Beclin-1 (BECN1), an autophagy regulator and activating molecule in Beclin-1-regulated autophagy (AMBRA1), a regulator of Beclin that play a role in autophagosome formation, an early stage of autophagy. There was a defect in the later stage of autophagy, the fusion of the autophagosome with the lysosome, known as autophagic flux, as evidenced by the lack of an increase in LC3-II, a marker of autophagosomes, with the lysosomal inhibitor bafilomycin, in both 70 day old and 150 day old hearts. To determine the role of autophagy in causing increased heart weight, Pkd1RC/RC were treated with 2-deoxyglucose (2-DG) or Tat-Beclin1 peptide, agents known to induce autophagy. 2-DG treatment from 150 to 350 days of age, a time period when increased heart weight developed, did not reduce the increased heart weight. Unexpectedly, Tat-Beclin 1 peptide treatment from 70 to 120 days of age resulted in increased heart weight. In summary, there is suppressed autophagic flux in the heart at an early age in Pkd1RC/RC mice. Increased mTOR signaling in older mice is associated suppressed autophagic flux. There was a large increase in p-AMPKThr172, a known autophagy inducer, in both young and old mice. 2-DG treatment did not impact increased heart weight and Tat-Beclin1 peptide increased heart weight.
