4 research outputs found
Expression of the Frizzled Receptors and their Co-receptors in Calcified Human Aortic Valves
No full textThe cellular mechanisms that induce calcific aortic stenosis are yet to be unravelled. Wnt signaling is increasingly being considered as a major player in the disease process. However, the presence of Wnt Frizzled receptors (Fzd) and co-receptors LRP5 and 6 in normal and diseased human aortic valves remains to be elucidated. Immunohistochemistry and qPCR were used to determine Fzd receptor expression in normal and calcified human aortic valve tissue, as well as human aortic valve interstitial cells (HAVICs) isolated from calcified and normal human aortic valves. There was significantly higher mRNA expression of 4 out of the 10 Fzd receptors in calcified aortic valve tissues and 8 out of the 10 in HAVICs, and both LRP5/6 co-receptors in calcified aortic valves (PThe accepted manuscript in pdf format is listed with the files at the bottom of this page. The presentation of the authors' names and (or) special characters in the title of the manuscript may differ slightly between what is listed on this page and what is listed in the pdf file of the accepted manuscript; that in the pdf file of the accepted manuscript is what was submitted by the author
RETRACTED ARTICLE: In vitro and in vivo biocompatibility study of polyacrylate TiO2@Ag coated nanoparticles for the radiation dose enhancement
No full textWe, the Editors and Publisher of the journal Artificial Cells, Nanomedicine, and Biotechnology, have retracted the following article:Ateeque Ur Rehman, Muhammad Hassan, Sadia Bano, Khizir Farooq, Aun Raza & Muhammad Naeem Anjum (2021) In vitro and in vivo biocompatibility study of polyacrylate TiO2@Ag coated nanoparticles for the radiation dose enhancement. Artificial Cells, Nanomedicine, and Biotechnology, 49(1), 185–193, DOI: 10.1080/21691401.2021.1889574Since publication, concerns were raised about the methods and some images in this article. Specifically, some images in Figure 7 have been duplicated and rotated. When approached for an explanation, the authors were unable to provide a satisfactory explanation for this. The corresponding author has been informed of our decision to retract.We have been informed in our decision-making by our policy on publishing ethics and integrity and the COPE guidelines on retractions.The retracted article will remain online to maintain the scholarly record, but it will be digitally watermarked on each page as “Retracted”
COVID-19 and neuropathy in type 2 diabetes
No full textThis study investigated the risk factors for COVID-19 and its impact on diabetic peripheral neuropathy (DPN) in patients with type 2 diabetes (T2D). Patients with T2D underwent assessments with the NICE post-COVID questionnaire, DN4 questionnaire, vibration perception threshold (VPT), and corneal confocal microscopy (CCM) before and 11.0 ± 8.9 months after developing COVID-19. Of 76 participants with T2D, 35 (46.1%) developed COVID-19, of whom 8 (22.9%) developed severe COVID-19 and 9 (25.7%) developed long-COVID. The development of COVID-19 was associated with lower systolic blood pressure (P < 0.05). The presence and severity of DPN were not associated with developing COVID-19, severe COVID-19, or long-COVID (P = 0.42–0.94). Women were eight times more likely to develop long-COVID (P < 0.05) and elevated body weight, LDL, and VPT were associated with the development of long-COVID (P < 0.05 − 0.01). The long-COVID group exhibited significant changes in triglycerides and LDL (P < 0.05 for both) and body weight (P < 0.01) at follow-up. Their impact on clinical and neuropathy measures was comparable in patients with and without COVID-19 (P = 0.08–0.99). There was a significant reduction in corneal nerve measures (P < 0.05-0.0001) in patients with and without COVID-19. A low systolic blood pressure, altered lipids, body weight, higher VPT, and gender may determine the impact of COVID-19 in patients with T2D, but there was no evidence of an impact of COVID-19 on the development or progression of DPN
