scholarly journals CORRELATION BETWEEN C- REACTIVE PROTEIN AND LIPID ABNORMALITIES IN SUBJECTS WITH ISCHEMIC STROKE

2021 ◽  
Vol 9 (09) ◽  
pp. 106-107
Author(s):  
Susmitha Vasanth Pentyala ◽  
Abhilash Tadiboina

Cerebrovascular accident, which has considerable mortality and morbidity,deservesattention towards its prevention. The first lines of defense in stroke prevention are detecting and adequately treating manageable risk factors, C-Reactive protein, an acute phase reactant is an indicator ofunderlying systemic inflammation and a novel marker for atherothrombotic disease. Present study is an attempt to study the levels of C-Reactive protein in acute thromboembolic stroke and to correlate between serum C Reactive protein levels and lipid profile in acute ischemic stroke.

2015 ◽  
Vol 396 (11) ◽  
pp. 1181-1197 ◽  
Author(s):  
Yi Wu ◽  
Lawrence A. Potempa ◽  
Driss El Kebir ◽  
János G. Filep

Abstract The prototypic acute-phase reactant C-reactive protein (CRP) has long been recognized as a useful marker and gauge of inflammation. CRP also plays an important role in host defense against invading pathogens as well as in inflammation. CRP consists of five identical subunits arranged as a cyclic pentamer. CRP exists in at least two conformationally distinct forms, i.e. native pentameric CRP (pCRP) and modified/monomeric CRP (mCRP). These isoforms bind to distinct receptors and lipid rafts, and exhibit distinct functional properties. Dissociation of pCRP into its subunits occurs within the inflammatory microenvironment and newly formed mCRP may then contribute to localizing the inflammatory response. Accumulating evidence indicates that pCRP possesses both pro- and anti-inflammatory actions in a context-dependent manner, whereas mCRP exerts potent pro-inflammatory actions on endothelial cells, endothelial progenitor cells, leukocytes and platelets, and thus may amplify inflammation. Here, we review recent advances that may explain how conformational changes in CRP contribute to shaping the inflammatory response and discuss CRP isomers as potential therapeutic targets to dampen inflammation.


1990 ◽  
Vol 266 (1) ◽  
pp. 283-290 ◽  
Author(s):  
A S Whitehead ◽  
K Zahedi ◽  
M Rits ◽  
R F Mortensen ◽  
J M Lelias

A full-length C-reactive protein (CRP) cDNA clone has been isolated from a CBA/J-strain-mouse acute-phase liver library. The 1614-nucleotide cDNA specifies mRNA 5′ and 3′ untranslated regions of 81 and 858 bases respectively that flank 675 bases encoding mouse pre-CRP. The derived amino acid sequence predicts a 19-residue leader peptide followed by a 206-residue mature mouse CRP that shows considerable sequence identity with both human and rabbit CRP. Northern-blot analysis of mouse liver CRP mRNA concentrations after inflammatory stimuli and comparison with hepatic induction of mRNA for the major mouse acute-phase protein serum amyloid P component established that CRP, a major acute-phase reactant in human and rabbit, is a minor acute-phase reactant in mouse. The size and organization of the mouse CRP mRNA 5′ and 3′ untranslated regions are significantly different from those of human and rabbit CRP mRNA and may have implications for its anomalous minimal induction during acute inflammation.


2017 ◽  
Vol 24 (10) ◽  
pp. 1039-1047 ◽  
Author(s):  
Kazuo Kitagawa ◽  
Naohisa Hosomi ◽  
Yoji Nagai ◽  
Tatsuo Kagimura ◽  
Toshiho Ohtsuki ◽  
...  

Blood ◽  
1985 ◽  
Vol 65 (2) ◽  
pp. 264-269
Author(s):  
BA Fiedel

C-reactive protein is the prototypic acute phase reactant. A self- complexed form (H-CRP) can induce isolated platelets to undergo aggregation, secretion of dense and alpha-granule constituents, and generation of thromboxane A2, but fails to function in platelet-rich plasma (PRP) as a direct agonist. In contrast, when PRP was activated with an amount of adenosine diphosphate (ADP) that produced only reversible platelet aggregation, the presence of H-CRP resulted in irreversible aggregation and the secretion of adenosine triphosphate (ATP). Following a maximum stimulus with ADP alone, where platelet secretion occurred late during the aggregation response, the presence of H-CRP shifted and increased the secretory burst to a time simultaneous with the onset of aggregation. This hypersecretion required H-CRP to be present prior to platelet stimulation or to be added within 15 to 30 seconds following the addition of ADP. H-CRP also potentiated platelet activation stimulated with epinephrine, thrombin, and collagen. When the synergism generated in PRP by H-CRP in the presence of ADP or epinephrine was compared to the synergism similarly produced by aggregated human IgG, collagen, or thrombin, it more closely resembled that of collagen, as reflected by the kinetics and characteristics of synergism and sensitivity to creatine phosphate/creatine phosphokinase or 5,8,11,14-eicosatetraynoic acid. These data provide a philosophically ideal niche for the acute phase (and C-reactive protein) in that a platelet-directed activity associated with this acute phase reactant is not utilized unless platelets are otherwise challenged.


2021 ◽  
Vol 12 ◽  
Author(s):  
Alessandro Cuomo ◽  
Despoina Koukouna ◽  
Alessandro Spiti ◽  
Giovanni Barillà ◽  
Arianna Goracci ◽  
...  

Introduction: Compared to the general population, people with severe mental illness (SMI) have a poorer health status and a higher mortality rate, with a 10–20-year reduction in life expectancy. Excess mortality and morbidity in SMI have been explained by intertwined components. Inflammatory processes could increase the morbidity and mortality risk in patients with bipolar disorder (BD) because of a bidirectional interaction between BD and conditions related to inflammation. This pilot study aimed to evaluate the relationship between C-Reactive-Protein (CRP) and bipolar disorder severity.Methods: A retrospective observational study was conducted on 61 hospitalized patients with bipolar disorder. CRP was measured at admission to inpatient treatment (T0) and after seven days from the admission (T1). Clinical Global Impression for Depression, Mania and Overall Bipolar Illness were recorded at T0 and T1. Comparisons among the recorded CRP values were determined through the paired t-test. Correlations between CRP and CGI scores were determined through Spearman's correlation coefficient at T0 and T1.Results: A statistically significant decrease in CRP values was observed after 7 days of hospitalization (p < 0.001) and positive significant correlations emerged between CRP and CGI scores at T0 and T1.Conclusion: Patients admitted to the inpatient unit reported a statistically significant decrease of CRP values during the first 7 days of treatment. Although the direction of the relationship between BP severity and inflammation status continues to remain unclear, this study showed a relationship between the improvement of bipolar disease symptoms and the improvement of the inflammatory marker CRP.


1993 ◽  
Vol 295 (2) ◽  
pp. 379-386 ◽  
Author(s):  
N O Ku ◽  
R F Mortensen

C-reactive protein is a serum acute-phase reactant that increases several thousand-fold in concentration during inflammation in most mammals. However, mouse C-reactive protein is considered to be a minor acute-phase reactant, since its blood level increases only from approx. 0.1 to 1-2 micrograms/ml. A mouse genomic clone of approximately 5 kb was obtained to determine the molecular basis for the regulation of the expression of mouse C-reactive protein. Several cis-acting elements in the 5′ flanking region that potentially regulate transcription were identified: two glucocorticoid-responsive elements, two CCAAT-enhancer-binding protein C (C/EBP) consensus elements that are required for the interleukin-1 responsiveness of some acute-phase reactant genes, an interleukin-6-responsive element, two hepatocyte nuclear factor-1 (HNF-1) elements and a single heat-shock element. Transfection of the hepatoma cell line Hep 3B.2 with a pCAT expression vector containing the 5′ flanking sequence from -1083 to -3 bp from the transcriptional start site, and truncations of this sequence, localized elements that control the tissue-specific expression of mouse C-reactive protein to the two HNF-1 elements and a C/EBP, interleukin-1-responsive element located between -220 and -153, and -90 and -50 bp from the transcriptional start site. A constitutive nuclear protein from mouse-liver hepatocytes specifically binds to the HNF-1 elements. These findings explain the tissue-specific expression of the gene, as well as its limited expression during the acute-phase response.


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