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PRP in Vitiligo
Published in Vineet Relhan, Vijay Kumar Garg, Sneha Ghunawat, Khushbu Mahajan, Comprehensive Textbook on Vitiligo, 2020
Subsequent centrifugation is faster so that platelets are spun down and separate as a pellet at the bottom of the tube from platelet-poor plasma (PPP) above. Approximately 3/4 of the supernatant is discarded, and the platelet-rich pellet is resuspended in the remaining plasma. PRP is usually activated by adding Cacl2 (250 μL per 1 mL of plasma) just before its injection. The viability of the platelets is assured by carrying out the process in a refrigerated centrifuge at 20°C. Trypan blue staining can confirm the viable state of the platelet concentrate obtained by the aforementioned method.
Connective tissue disease
Published in Catherine Nelson-Piercy, Handbook of Obstetric Medicine, 2020
LA is a misnomer coined because it prolongs coagulation times in vitro. It is detected by the prolongation of the activated partial thromboplastin time or the dilute Russell's viper venom time (dRVVT). This prolongation fails to correct with the addition of platelet poor plasma, but corrects with excess phospholipid.
Anti-Phospholipid Antibodies and Impairment of Prostacyclin Synthesis by the Endothelium
Published in E. Nigel Harris, Thomas Exner, Graham R. V. Hughes, Ronald A. Asherson, Phospholipid-Binding Antibodies, 2020
Luis O. Carreras, Jos Vermylen
PGI2 production by rat aortic rings decreases upon repeated washing in buffer, but is partially restored by normal plasma. Using both fresh or such “exhausted” rings, the patient’s platelet poor plasma (PPP) consistently had an inhibitory effect on PGI2 formation, as compared with normal PPP. The inhibitory effect on PGI2 production was confined to the patient’s IgG fraction.
Platelet removal by single-step centrifugation
Published in Platelets, 2021
Linda G. Rikkert, Frank A. W. Coumans, Chi M. Hau, Leon W. M. M. Terstappen, Rienk Nieuwland
Blood was obtained from ten healthy donors with informed consent in accordance with the Declaration of Helsinki and the study protocol was waived by the medical ethics committee of the Amsterdam University Medical Center. Whole blood was drawn using a 21 G needle. The first 3.5 mL was discarded. For each of the ten donors, nine 3.2% citrate blood collection tubes of 3.5 mL (Greiner Bio-one, Kremsmünster, Austria) were collected, mixed gently with the anti-coagulant and processed within 15 minutes. Seven blood collection tubes were centrifuged at 2,500 g for 15 minutes using a Rotina 380 R centrifuge (Hettich, Tuttlingen, Germany) at 20°C without brake (see Figure 1). Platelet poor plasma was collected with a plastic Pasteur pipette (VWR, Radnor, PA), leaving 1 cm of plasma above the buffy coat and taking care not to disturb the buffy coat to circumvent cell contamination. Next, the approximately 9 mL of platelet poor plasma was pooled.
Impact of high on-treatment platelet reactivity after angioplasty in patients with peripheral arterial disease
Published in Platelets, 2021
Lucas Busch, Manuel Stern, Lisa Dannenberg, Philipp Mourikis, Michael Gröne, Göksen Özaslan, Yvonne Heinen, Christian Heiss, Roberto Sansone, Amin Polzin, Malte Kelm
Platelet function testing was performed 1 day after PTA, under continued maintenance dose 4 h after intake. Aseptic venipuncture was conducted on a dorsum manus or cubital vein with a 21 G butterfly needle (BD Vacutainer® Safety-Lok™). Blood was collected in 2.7 ml citrate vacutainers (1:10, BD Vacutainer®),) and transported at room temperature. The analysis was processed within 30 min. Pharmacodynamic response to clopidogrel was assessed by vasodilator-stimulated protein phosphorylation assay (VASP). Incubation with prostaglandin E1 or adenosine-diphosphate (ADP) and prostaglandin E1 was conducted. Afterward, VASP phosphorylation was measured. Platelet reactivity index (PRI) >50% was defined as HTPR to clopidogrel according to the expert consensus statement on platelet function and genetic testing for guiding P2Y12 receptor inhibitor treatment [17]. Aspirin antiplatelet effects were evaluated by light-transmission aggregometry (LTA). Whole blood was centrifuged to generate platelet-rich plasma (250 x g) and platelet-poor plasma (1600 x g). Platelet aggregation was induced by 0.5 µM arachidonic acid to allow specific determination of pharmacodynamic response to aspirin [18]. HTPR to aspirin was set as maximum of aggregation (MoA%) >20% as previously described [3,19,20].
In vitro effects of cobalt and chromium nanoparticles on human platelet function
Published in Nanotoxicology, 2021
Dominik Taterra, Bendik Skinningsrud, Przemysław A. Pękala, Iwona M. Tomaszewska, Krzysztof Marycz, Marek W. Radomski, Krzysztof A. Tomaszewski
A Whole Blood Lumi-aggregometer (Chrono-Log Corporation, Havertown, PA) linked to the Aggrolink data reduction system (810DR; Chrono-log) (Radomski et al. 2005) was used to test the ability of Co and Cr NPs to induce platelet aggregation. Nanoparticles dispersed in its proper medium were loaded in test tubes, placed in a water bath, and sonicated at 37 °C for 10 min prior to the aggregation assay. Platelet-rich plasma samples were incubated in the presence or absence of NPs at concentrations ranging from 5 to 50 µg/mL, and their effects were recorded for 10 min. Collagen (Chronolog) (5 µg/mL)-induced platelet aggregation was used as a positive control. Platelet-poor plasma was used as a reference blank (Santos-Martinez et al. 2012). Results were expressed as the percentage of maximal aggregation (PPP transmission set at 100%).