Background: Chronic systemic inflammation has been implicated in the pathogenesis of hypertension and cardiovascular disease. Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by chronic inflammation and an increased risk for cardiovascular disease. Currently few studies have evaluated the potential cardiovascular benefits of exercise in SLE. It is unknown whether the favorable effect of habitual exercise on arterial stiffness observed in healthy adults can be extended to SLE. Therefore, as an initial step, we determined the association between habitual exercise, inflammatory markers, central arterial compliance, and aortic wave reflection in healthy adults and SLE patients.
Methods: We studied 41 adults, aged 33 ± 11 years (15 healthy controls, 12 sedentary SLE, and 14 physically active SLE patients).
Results: Age, body mass index, and metabolic risk factors were not different between the three groups. Carotid arterial compliance was lower whereas augmentation index (AI) and inflammatory markers (C-reactive protein (CRP), interleukin (IL)-12, tumor necrosis factor-α (TNF-α)) were higher in sedentary SLE patients compared with healthy controls, but were not different between physically active SLE patients and healthy controls. Cardiac ejection fraction was lower in sedentary SLE than physically active SLE or healthy controls. In the pooled population, carotid arterial compliance was inversely associated with TNF-α (r = -0.38; P < 0.01), and AI was positively associated with both CRP (r = 0.33; P < 0.05) and intercellular adhesion molecule-1 (r = 0.28; P < 0.05).
Conclusions: SLE-associated stiffening of the central artery and wave reflection were not observed in habitually exercising adults with SLE. Furthermore, greater arterial stiffness was associated with higher inflammatory markers, suggesting that need for studies on inflammation and SLE-associated arterial stiffening.
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http://dx.doi.org/10.1038/ajh.2011.143 | DOI Listing |
Brain Topogr
January 2025
Department of Neurology, Yale University School of Medicine, 333 Cedar Street, New Haven, CT, 06520, USA.
Aberrant large-scale resting-state functional connectivity (rsFC) has been frequently documented in ischemic stroke. However, it remains unclear about the altered patterns of within- and across-network connectivity. The purpose of this meta-analysis was to identify the altered rsFC in patients with ischemic stroke relative to healthy controls, as well as to reveal longitudinal changes of network dysfunctions across acute, subacute, and chronic phases.
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January 2025
Chaum Life Center, CHA University School of Medicine, Seoul, 06062, Korea.
No biomarker can effectively screen for early gastric cancer (EGC). Players in the A disintegrin and metalloproteinase (ADAM)-natural killer group 2 member D (NKG2D) receptor axis may have a role for that. As a proof-of-concept pilot study, the expression of ADAM8, ADAM9, ADAM10, ADAM12, ADAM17, and major histocompatibility complex (MHC) class I chain-related sequence A (MICA), a ligand for NKG2D, in gastric cancer was investigated in silico using The Cancer Genome Atlas (TCGA) database.
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January 2025
Faculty of Computer Science and Engineering, Shahid Beheshti University, Tehran, Iran.
Genetics plays a significant role in Multiple Sclerosis (MS), with approximately 12.6% of cases occurring in familial form. While previous studies have demonstrated differences in disease progression and MRI findings between familial and sporadic MS, there has been no comparison of cognitive impairment between them.
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January 2025
Department of Medical Biotechnology, College of Biotechnology, Misr University for Science and Technology, P. O. Box 77, Giza, Egypt.
Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by persistent inflammation of the synovial joints, leading to cartilage and bone destruction. This study aimed to evaluate the diagnostic utility of specific microRNAs (miRNAs) as potential biomarkers for RA. The study was conducted on 60 patients with RA disease along with 20 control participants.
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Department of Molecular Pathology, IRCCS Neuromed, Pozzilli, Italy.
Metabotropic glutamate (mGlu) receptors are candidate drug targets for therapeutic intervention in Parkinson's disease (PD). Here we focused on mGlu3, a receptor subtype involved in synaptic regulation and neuroinflammation. mGlu3 mice showed an enhanced nigro-striatal damage and microglial activation in response to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP).
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