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      Soluble C-Type Lectin-Like Receptor 2 Elevation in Patients with Acute Cerebral Infarction

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          Abstract

          Background: Acute cerebral infarction (ACI) includes cardiogenic ACI treated with anticoagulants and atherosclerotic ACI treated with antiplatelet agents. The differential diagnosis between cardiogenic and atherosclerotic ACI is still difficult. Materials and Methods: The plasma sCLEC-2 and D-dimer levels were measured using the STACIA system. Results: The plasma sCLEC-2 level was significantly high in patients with ACI, especially those in patients with atherosclerotic or lacunar ACI, and plasma D-dimer levels were significantly high in patients with cardioembolic ACI. The plasma levels of sCLEC-2 and the sCLEC-2/D-dimer ratios in patients with atherosclerotic or lacunar ACI were significantly higher than those in patients with cardioembolic ACI. The plasma D-dimer levels in patients with atherosclerotic or lacunar ACI were significantly lower than those in patients with cardioembolic ACI. The plasma levels of sCLEC-2 and the sCLEC-2/D-dimer ratios were significantly higher in patients with atherosclerotic or lacunar ACI or acute myocardial infarction in comparison to patients with cardioembolic ACI or those with deep vein thrombosis. Conclusion: Using both the plasma sCLEC-2 and D-dimer levels may be useful for the diagnosis of ACI, and differentiating between atherosclerotic and cardioembolic ACI.

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          Management of acute ischemic stroke

          Michael S Phipps, Carolyn A Cronin (2020)
          Stroke is the leading cause of long term disability in developed countries and one of the top causes of mortality worldwide. The past decade has seen substantial advances in the diagnostic and treatment options available to minimize the impact of acute ischemic stroke. The key first step in stroke care is early identification of patients with stroke and triage to centers capable of delivering the appropriate treatment, as fast as possible. Here, we review the data supporting pre-hospital and emergency stroke care, including use of emergency medical services protocols for identification of patients with stroke, intravenous thrombolysis in acute ischemic stroke including updates to recommended patient eligibility criteria and treatment time windows, and advanced imaging techniques with automated interpretation to identify patients with large areas of brain at risk but without large completed infarcts who are likely to benefit from endovascular thrombectomy in extended time windows from symptom onset. We also review protocols for management of patient physiologic parameters to minimize infarct volumes and recent updates in secondary prevention recommendations including short term use of dual antiplatelet therapy to prevent recurrent stroke in the high risk period immediately after stroke. Finally, we discuss emerging therapies and questions for future research.
          Article 0 comments Cited 166 times – based on 0 reviews     Review now
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            A novel Syk-dependent mechanism of platelet activation by the C-type lectin receptor CLEC-2.

            Yukio Ozaki, Gemma Fuller, Edina Schweighoffer … (2006)
            The snake venom rhodocytin has been reported to bind to integrin alpha2beta1 and glycoprotein (GP) Ibalpha on platelets, but it is also able to induce activation independent of the 2 receptors and of GPVI. Using rhodocytin affinity chromatography, we have identified a novel C-type lectin receptor, CLEC-2, in platelets that confers signaling responses to rhodocytin when expressed in a cell line. CLEC-2 has a single tyrosine residue in a YXXL motif in its cytosolic tail, which undergoes tyrosine phosphorylation upon platelet activation by rhodocytin or an antibody to CLEC-2, but not to collagen, thrombin receptor agonist peptide (TRAP), or convulxin. Tyrosine phosphorylation of CLEC-2 and other signaling proteins by rhodocytin is inhibited by the Src family kinase inhibitor PP2. Further, activation of murine platelets by rhodocytin is abolished in the absence of Syk and PLCgamma2, and partially reduced in the absence of LAT, SLP-76, and Vav1/Vav3. These findings define a novel signaling pathway in platelets whereby activation of CLEC-2 by rhodocytin leads to tyrosine phosphorylation of its cytosolic tail, binding of Syk and initiation of downstream tyrosine phosphorylation events, and activation of PLCgamma2. CLEC-2 is the first C-type lectin receptor to be found on platelets which signals through this novel pathway.
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              A Test in Context: D-Dimer

              Jeffrey Weitz, James C Fredenburgh, John W Eikelboom (2017)
              D-dimer is a soluble fibrin degradation product that results from ordered breakdown of thrombi by the fibrinolytic system. Numerous studies have shown that D-dimer serves as a valuable marker of activation of coagulation and fibrinolysis. Consequently, D-dimer has been extensively investigated for the diagnosis of venous thromboembolism (VTE) and is used routinely for this indication. In addition, D-dimer has been evaluated for determining the optimal duration of anticoagulation in VTE patients, for diagnosing and monitoring disseminated intravascular coagulation, and as an aid in the identification of medical patients at high risk for VTE. Thus, quantification of D-dimer levels serves an important role in guiding therapy. This review: 1) describes how D-dimer is generated; 2) reviews the assays used for its detection; and 3) discusses the role of D-dimer determination in these various conditions.
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                Author and article information

                Contributors
                Tadeusz Robak: Role: Academic Editor
                Journal
                Journal ID (nlm-ta): J Clin Med
                Journal ID (iso-abbrev): J Clin Med
                Journal ID (publisher-id): jcm
                Title: Journal of Clinical Medicine
                Publisher: MDPI
                ISSN (Electronic): 2077-0383
                Publication date (Electronic): 30 July 2021
                Publication date Collection: August 2021
                Volume: 10
                Issue: 15
                Electronic Location Identifier: 3408
                Affiliations
                [1 ]Department of Neurology, Mie Prefectural General Medical Center, Yokkaichi 510-8561, Japan; nishigaki-a@ 123456med.mie-u.ac.jp (A.N.); ksuzu6161@ 123456gmail.com (K.S.); ak1233maggot@ 123456gmail.com (K.T.); toshi9031@ 123456yahoo.co.jp (T.K.); holly.0639-bj@ 123456i.softbank.jp (S.H.)
                [2 ]Department of Central Laboratory, Mie Prefectural General Medical Center, Yokkaichi 510-8561, Japan; ichi911239@ 123456yahoo.co.jp (Y.I.); ajbyd06188@ 123456yahoo.co.jp (M.E.)
                [3 ]Department of Emergency and Critical Care Center, Mie Prefectural General Medical Center, Yokkaichi 510-8561, Japan; akitaka-yamamoto@ 123456mie-gmc.jp
                [4 ]Department of Cardiovascular Medicine, Mie Prefectural General Medical Center, Yokkaichi 510-8561, Japan; jun-masuda@ 123456mie-gmc.jp (J.M.); katsutoshi-makino@ 123456mie-gmc.jp (K.M.)
                [5 ]Department of Laboratory and General Medicine, Mie Prefectural General Medical Center, Yokkaichi 510-8561, Japan; katsuya-shiraki@ 123456mie-gmc.jp
                [6 ]Mie Prefectural General Medical Center, Yokkaichi 510-8561, Japan; hideto-shimpo@ 123456mie-gmc.jp
                [7 ]Department of Molecular Pathobiology and Cell Adhesion Biology, Mie University Graduate School of Medicine, Tsu 514-8507, Japan; motomushimaoka@ 123456gmail.com
                [8 ]Department of Clinical and Laboratory Medicine, University of Yamanashi, Yamanashi 409-3898, Japan; katsuei@ 123456yamanashi.ac.jp
                Author notes
                [* ]Correspondence: wadahide@ 123456clin.medic.mie-u.ac.jp ; Tel.: +81-59-345-2321
                Author information
                https://orcid.org/0000-0003-1930-3397
                https://orcid.org/0000-0001-9021-8633
                Article
                Publisher ID: jcm-10-03408
                DOI: 10.3390/jcm10153408
                PMC ID: 8348423
                PubMed ID: 34362190
                SO-VID: 9d5546a9-fac9-4b9e-a783-ab51268c8a5c
                Copyright © © 2021 by the authors.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( https://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 03 July 2021
                Date accepted : 28 July 2021
                Categories
                Subject: Article

                Keywords: platelet activation,sclec-2,acute cerebral infarction (aci),atherosclerotic aci,cardioembolic aci
                Data availability:
                Keywords: platelet activation, sclec-2, acute cerebral infarction (aci), atherosclerotic aci, cardioembolic aci

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