89 research outputs found
Usefulness of C-reactive protein as a marker of early post-infarct left ventricular systolic dysfunction
Objective To assess the usefulness of in-hospital measurement
of C-reactive protein (CRP) concentration in
comparison to well-established risk factors as a marker of
post-infarct left ventricular systolic dysfunction (LVSD) at
discharge.
Materials and methods Two hundred and four consecutive
patients with ST-segment-elevation myocardial
infarction (STEMI) were prospectively enrolled into the
study. CRP plasma concentrations were measured before
reperfusion, 24 h after admission and at discharge with an
ultra-sensitive latex immunoassay.
Results CRP concentration increased significantly during
the first 24 h of hospitalization (2.4 ± 1.9 vs. 15.7 ± 17.0
mg/L; p\0.001) and persisted elevated at discharge
(14.7 ± 14.7 mg/L), mainly in 57 patients with LVSD
(2.4 ± 1.8 vs. 25.0 ± 23.4 mg/L; p\0.001; CRP at discharge
21.9 ± 18.6 mg/L). The prevalence of LVSD was
significantly increased across increasing tertiles of CRP
concentration both at 24 h after admission (13.2 vs. 19.1
vs. 51.5 %; p\0.0001) and at discharge (14.7 vs. 23.5 vs.
45.6 %; p\0.0001). Multivariate analysis demonstrated
CRP concentration at discharge to be an independent
marker of early LVSD (odds ratio of 1.38 for a 10 mg/L
increase, 95 % confidence interval 1.01–1.87; p\0.04).
Conclusion Measurement of CRP plasma concentration
at discharge may be useful as a marker of early LVSD in
patients after a first STEMI
Lenalidomide reduces microglial activation and behavioral deficits in a transgenic model of Parkinson’s disease
BACKGROUND: Parkinson’s disease (PD) is one of the most common causes of dementia and motor deficits in the elderly. PD is characterized by the abnormal accumulation of the synaptic protein alpha-synuclein (α-syn) and degeneration of dopaminergic neurons in substantia nigra, which leads to neurodegeneration and neuroinflammation. Currently, there are no disease modifying alternatives for PD; however, targeting neuroinflammation might be a viable option for reducing motor deficits and neurodegeneration. Lenalidomide is a thalidomide derivative designed for reduced toxicity and increased immunomodulatory properties. Lenalidomide has shown protective effects in an animal model of amyotrophic lateral sclerosis, and its mechanism of action involves modulation of cytokine production and inhibition of NF-κB signaling. METHODS: In order to assess the effect of lenalidomide in an animal model of PD, mThy1-α-syn transgenic mice were treated with lenalidomide or the parent molecule thalidomide at 100 mg/kg for 4 weeks. RESULTS: Lenalidomide reduced motor behavioral deficits and ameliorated dopaminergic fiber loss in the striatum. This protective action was accompanied by a reduction in microgliosis both in striatum and hippocampus. Central expression of pro-inflammatory cytokines was diminished in lenalidomide-treated transgenic animals, together with reduction in NF-κB activation. CONCLUSION: These results support the therapeutic potential of lenalidomide for reducing maladaptive neuroinflammation in PD and related neuropathologies. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12974-015-0320-x) contains supplementary material, which is available to authorized users
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