Background: We compared the type and duration of diabetes mellitus (DM), patient demography, high sensitivity C-reactive protein (hsCRP), Homocysteine and other variables with IMT, to determine if these markers were correlated in diabetes (in whom technetium myocardial perfusion scan were negative) and would it be appropriate biomarkers for arthrosclerosis detection in this group of diabetics.
Methods: Forty patients with DM, without CHD history, were screened with stress sintigraphy imaging using 2 days stress/rest Technetium 99 tetrafosmin protocol, employing the standard Bruce protocol. Echocardiography study requested for each patient, two blood samples for hsCRP, were requested for each candidate three weeks apart, Lipid profiles, plasma homocysteine, and hemoglobin A1C were also requested. Finally Intima-media thickness were measured for all patients.
Results: There were no relationships between hsCRP level and DM duration or with the type of DM; also there were no relation between DM duration and homocysteine or between DM type and Homocysteine. Intimal media thickness was increased proportionally with the serum level of Homocysteine.
Conclusions: This study did not show any role for the inflammatory markers in predicating the presence of coronary artery disease in participants with DM, without medium size artery disease, which may support that DM is not the only player in initiating atherosclerosis.
Keywords: Diabetes mellitus; Inflammatory markers; C-reactive protein; Myocardial ischemia; Homocysteine; Intima-media thickness.
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http://dx.doi.org/10.4021/jocmr2009.05.1239 | DOI Listing |
Alzheimers Dement
December 2024
Columbia University Irving Medical Center, New York, NY, USA.
Background: Genetic studies indicate a causal role for microglia, the innate immune cells of the central nervous system (CNS), in Alzheimer's disease (AD). Despite the progress made in identifying genetic risk factors, such as CD33, and underlying molecular changes, there are currently limited treatment options for AD. Based on the immune-inhibitory function of CD33, we hypothesize that inhibition of CD33 activation may reverse microglial suppression and restore their ability to resolve inflammatory processes and mitigate pathogenic amyloid plaques, which may be neuroprotective.
View Article and Find Full Text PDFBackground: Neuroinflammation is a critical factor of Alzheimer's Disease (AD). Dysregulation of complement leads to excessive inflammation, direct damage to self-cells and propagation of injury. This is likely of particular relevance in the brain where inflammation is poorly tolerated and brain cells are vulnerable to direct damage by complement.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of Missouri, Columbia, MO, USA.
Background: Despite data showing nutritional interventions high in antioxidant/anti-inflammatory properties (anthocyanin-rich foods such as blueberries/elderberries) may decrease risk of memory loss and cognitive decline, evidence for such effects in mild cognitive impairment (MCI) patients is limited. Therefore, we examined preliminary effects of American elderberry (Sambucus nigra canadensis) juice on cognition and inflammatory markers in MCI patients in a double-blind placebo-controlled trial.
Method: MCI patients (N = 24, M = 76.
Alzheimers Dement
December 2024
University of Georgia, College of Pharmacy, Athens, GA, USA.
Background: Reducing chronic inflammation has been linked to anti-inflammatory foods and may be implicated in treating Alzheimer's disease (AD). Plants produce antioxidants, such as phytochemicals, that appear to reduce the incidence of chronic inflammatory diseases. Phytochemicals may include active substances like polyphenols.
View Article and Find Full Text PDFImmunotherapy
January 2025
Blauvelt Consulting, LLC, Lake Oswego, OR, USA.
Aim: Lebrikizumab is an interleukin (IL)-13 inhibitor that specifically blocks IL-13 signaling. Here, we report the effects of lebrikizumab on asthma serum biomarkers in 2 phase 3 clinical studies.
Methods: LAVOLTA I and LAVOLTA II are replicate, double-blind, placebo-controlled trials with 52-week placebo-controlled treatment periods that evaluated lebrikizumab 37.
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