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Childhood abuse linked with tripled adult SLE incidenceBackground and aims: Patients with systemic lupus erythematosus Sle prevalence have a significantly higher incidence of atherosclerosis than the general population. Studies on atherosclerosis prediction models specific for SLE patients are very limited. This study aimed to build a risk prediction model for atherosclerosis in SLE. Subsequently, differential expression analysis was carried out on 19 pairs of age-matched SLE patients with AT group or without Non-AT group atherosclerosis using peripheral venous blood.
Background
We used logistic least absolute shrinkage and selection operator regression to select variables among differentially expressed DE genes and clinical features and utilized backward stepwise logistic regression https://digitales.com.au/blog/wp-content/custom/african-slaves-during-the-nineteenth-century/inductive-and-deductive-method.php build an atherosclerosis risk prediction model with all 67 patients. The performance of the prediction model was evaluated by area under the curve AUCsle prevalence curve, and decision curve analyses.
Results: The 67 patients had a median age of Pathway analyses revealed that the AT group had upregulated atherosclerosis signaling, oxidative phosphorylation, and interleukin IL related pathways but downregulated T cell and B cell receptor sle prevalence. Keratin 10, age, and hyperlipidemia were selected as variables for the risk prediction model. The prediction model had a higher net benefit in the decision curve analysis than that when predicting with age ;revalence hyperlipidemia only.
Conclusions: We built an atherosclerotic risk prediction model with one gene and two clinical factors. This model may greatly assist clinicians to identify SLE patients with atherosclerosis, especially asymptomatic atherosclerosis. Systemic lupus erythematosus SLE is a chronic autoimmune disease that affects multiple systems including the cardiovascular system 1.
The incidence of cardiovascular events in SLE patients is significantly higher than that in the general population 2 — 4. Among females aged 35—44 years, SLE patients are 50 times more likely to develop myocardial infarction than healthy control subjects 4. Atherosclerosis is the main cause of CVD. Patients with SLE also exhibit a higher prevalence of atherosclerosis than the general population 89.
In SLE, atherosclerosis is related to both traditional risk factors, such as age, sex, prevaldnce, and SLE-related features, such as disease duration, disease activity, and medications 3 Slr sequencing is currently being applied to investigate atherosclerosis in SLE 12 — Although some interesting findings have been reported, art is an expression number of studies is relatively small, and the biological pathways that contribute to the increased atherosclerosis in SLE are not fully understood.
Early identification of SLE patients with atherosclerosis, which is often asymptomatic at the early sle prevalence, is important for prevention of atherosclerosis progression and future CVD. However, traditional prediction models, such as the Framingham risk score, largely underestimate the prevalence of atherosclerosis or cardiovascular events in SLE patients continue reading16and studies on specific prediction models sle prevalence atherosclerosis in SLE patients are limited.
Nevertheless, the four biomarkers were derived from a limited number sle prevalence candidate biomarkers.
Thus, it remains unclear whether combinations of untested biomarkers or genes can achieve better prediction accuracy. The objective of this study was to use RNA sequencing RNA-seq analysis to investigate the underlying mechanisms of atherosclerosis in SLE patients and to establish a diagnositic sle prevalence model for atherosclerosis in SLE that combines high-throughput sequencing data and clinical risk factors.
References
link There were five patients from the AT group who had several age- and sex-matching patients from the non-AT group. Venous blood was sle prevalence between and A. Cardiac enzymes including creatine kinase, creatine kinase isoenzyme, cardiac troponin I, and N-terminal pro-B-type natriuretic peptide were evaluated by a fully automated integrated biochemical analyzer Dimension EXL; Siemens, Erlangen, Germany. The erythrocyte sedimentation rate ESR was also measured. Clinical data were collected from the patients by physicians. The carotid intima media thickness CIMT was measured by a doctor specialized in diagnostic ultrasound.
The detection range included the region 1 cm distal to the common carotid artery, 1 cm to the carotid bifurcation, and 1 cm to the proximal end of the internal carotid artery For each patient, the maximum CIMT values for three sites sle prevalence the left and right sides were recorded.]
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