Vulvodynia: What is available online? A systematic review of information on the internet.

AIM: This review aimed to evaluate the quality of medicalinformation online for patients relating to vulvodynia. To our knowledge no evaluation of online patient information exists regarding vulvodynia and, at present, there is no standardized or validated method of evaluating medical information on the internet. METHODS: A clearly defined protocol was developed to generate keywords relating to vulvodynia. The three most popular search engines worldwide; google.com, yahoo.com, and bing.com, were searched in September 2020. Three assessors evaluated eligible webpages for accuracy, credibility, readability, and reliability. RESULTS: Forty-five webpages were eligible with 38% given HON certification or Information Standard approval. Only one webpage achieved a DISCERN score of ≥63 indicating excellent reliability. No webpages scored a maximum 10 points for credibility. Eleven percent of webpages were rated "accurate" with score 17 or above. The modal Flesch Kincaid Grade Level was 9 with only 15.6% having a readability grade level of 8 or less. CONCLUSIONS: It has been shown in previous studies that patient information available online pertaining to gynecological conditions is frequently inaccurate, with limited regulation and low reliability, and our findings are in agreement with this. As patients increasingly look to the internet for medical information and education, we as clinicians, need to ensure the resources available are of a high standard and regulated. Without ensuring safe and effective healthcare resources, we risk misinformation which can negatively impact clinical care.

Oxidized Low-Density Lipoprotein Loading of Macrophages Downregulates TLR-Induced Proinflammatory Responses in a Gene-Specific and Temporal Manner through Transcriptional Control.

Hypercholesterolemia is a key risk factor for atherosclerosis and leads to the uptake of native and oxidized low-density lipoprotein (oxLDL) by macrophages (Mϕs) and foam cell formation. Inflammatory processes accompany Mϕ foam cell formation in the artery wall, yet the relationship between Mϕ lipid loading and their response to inflammatory stimuli remains elusive. We investigated proinflammatory gene expression in thioglycollate-elicited peritoneal Mϕs, bone marrow-derived Mϕs and dendritic cells, and RAW264.7 cells. Loading with oxLDL did not induce peritoneal Mϕ apoptosis or modulate basal-level expression of proinflammatory genes. Upon stimulation of TLR4, the rapid induction of IFN-ß was inhibited in cells loaded with oxLDL, whereas the induction of other proinflammatory genes by TLR4 (LPS), TLR3 (polyriboinosinic-polyribocytidylic acid), TLR2 (Pam3CSK4), and TLR9 (CpG) remained comparable within the first 2 h. Subsequently, the expression of a subset of proinflammatory genes (e.g., IL-1ß, IL-6, CCL5) was reduced in oxLDL-loaded cells at the level of transcription. This phenomenon was partially dependent on NF erythroid 2-related factor 2 (NRF2) but not on nuclear liver X receptors α and ß (LXRα,ß), peroxisome proliferator-activated receptor-γ (PPARγ), and activating transcription factor 3 (ATF3). LPS-induced NF-κB reporter activity and intracellular signaling by NF-κB and MAPK pathways were comparable in oxLDL-loaded Mϕs, yet the binding of p65/RelA (the prototypic NF-κB family member) was reduced at IL-6 and CCL5 promoters. This study revealed that oxLDL loading of Mϕs negatively regulates transcription at late stages of TLR-induced proinflammatory gene expression and implicates epigenetic mechanisms such as histone deacetylase activity.