Publications by authors named "H Daoud"

In this paper, an automated feature selection (FS) method is presented to optimize machine learning (ML) models' performances, enhancing early keratoconus screening. A total of 448 parameters were analyzed from a dataset comprising 3162 observations sourced from the swept source optical coherence tomography imaging system developed by the Chinese Academy of Sciences Institute of Automation (SS-1000 CASIA OCT) and electronic health records (EHR). To identify the most relevant features, the analysis of variance (ANOVA) method was used in this study.

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Low-level laser therapy (LLLT) is a non-invasive application of non-thermogenic light that is proven to promote tissue healing and alleviate pain. The authors aim to conduct the first meta-analysis, evaluating the effects of LLLT on wound healing and pain in skin wounds by comparing it to skin wounds not treated with LLLT. The Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines were followed by searching the electronic databases.

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Background: Ang-II (angiotensin II) impairs the function of the antihypertensive enzyme ACE2 (angiotensin-converting enzyme 2) by promoting its internalization, ubiquitination, and degradation, thus contributing to hypertension. However, few ACE2 ubiquitination partners have been identified, and their role in hypertension remains unknown.

Methods: Proteomics and bioinformatic analyses were used to identify ACE2 ubiquitination partners in the brain, heart, and kidney of hypertensive C57BL6/J mice of both sexes.

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Cumulative evidence suggests that ATP-sensitive potassium (K) channels act as a key regulator of cerebral blood flow (CBF). This implication seems to be complicated, since K channels are expressed in several vascular-related structures such as smooth muscle cells, endothelial cells and pericytes. In this systematic review, we searched PubMed and EMBASE for preclinical and clinical studies addressing the involvement of K channels in CBF regulation.

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Article Synopsis
  • Angiotensin-II negatively affects ACE2, an important antihypertensive enzyme, by promoting its breakdown, contributing to high blood pressure.
  • Researchers identified UBR1 as a key protein that helps in the ubiquitination of ACE2, particularly heightened in hypertensive conditions and showing sex-specific regulation by testosterone.
  • Silencing UBR1 in mice led to increased ACE2 levels and a temporary drop in blood pressure, suggesting that targeting UBR1 and related proteins could be a new treatment strategy for hypertension.
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