scholarly journals Temperature cycling during platelet cold storage improves in vivo recovery and survival in healthy volunteers

Transfusion ◽  
2017 ◽  
Vol 58 (1) ◽  
pp. 25-33 ◽  
Author(s):  
Jaroslav G. Vostal ◽  
Monique P. Gelderman ◽  
Andrey Skripchenko ◽  
Fei Xu ◽  
Ying Li ◽  
...  

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 720-720
Author(s):  
Fei Xu ◽  
Monique Gelderman-Fuhrmann ◽  
John Farrell ◽  
Jaroslav Vostal

Abstract Abstract 720 Platelets are currently limited to 5 days of storage at room temperature to prevent growth of bacteria to high levels. Cold storage of platelets could reduce bacterial proliferation but platelets stored in cold for over 48 hours are cleared rapidly from circulation through the hepatocyte Ashwell-Morell (AM) receptor thus limiting the applicability of cold temperatures to platelet storage. We used a temperature cycling method to store human platelets in the cold without decreasing their in vivo recovery in an immunodeficient (SCID) animal model of transfusion. Temperature cycled (TC) apheresis human platelets were stored in the cold (4°C) for 12 hours and then incubated at 37°C for 30 minutes before returning back to cold storage. The TC (37°C pulses for 30 minutes at 12 hour intervals) was continued for 2, 5 and 7 days. Human platelets stored either at room temperature (RT), cold or TC for 2, 5 and 7 days were infused into 6 to 8 SCID mice per group and their in vivo recovery in circulation was determined at 5, 20 and 60 minutes after transfusion by flow cytometry. Carbohydrate exposure on the surface of the platelets was analyzed for galactose by Erythrina cristagalli agglutinin (ECA), and for β-GlnNAc by succinyl wheat germ agglutinin (sWGA) using flow cytometry. Involvement of the AM receptor was examined by monitoring clearance of cold stored platelets in the presence of asialofetuin, a competitive ligand for the receptor. In vivo recovery of human platelets stored for two-days in SCID mice circulation is shown in Figure 1. As expected, cold platelets had significantly decreased recovery compared to RT platelets, from 22.1±2.5% to 11.1±3.3% (P<0.01), 11.5±2.9% to 5.5±3.6% (P<0.01) and 11.2±1.4% to 6.2±1.8% (P<0.01) respectively at 5, 20 and 60 min post platelets injection. Compared to cold platelets, TC platelets recovery increased significantly from 11.1±3.3% to 15.9±4.4% (P<0.01), 5.5±3.6+% to 10.5±4.7% (P<0.01) and 6.2±1.8% to 9.5±2.2% (P<0.05) respectively at 5, 20 and 60 min post platelets injection. At 20 and 60 min post injection, the TC platelets have recovery of 10.5±4.7% and 9.5±2.2% respectively, that are comparable (P>0.05%) to RT platelet recoveries of 11.5±2.9% and 11.2±1.4% for the same time points. Similar increases of in vivo recovery for TC platelets as compared to cold platelets were obtained for at 5 and 7 days.Figure 1Human Platelet Recovery (% of total platelets circulating) * p< 0.05, ** p< 0.01, *** p< 0.001Figure 1. Human Platelet Recovery (% of total platelets circulating) * p< 0.05, ** p< 0.01, *** p< 0.001 Binding of the galactose specific lectin, ECA, was increased by 142±22% from RT to cold platelets (P<0.01) as previously reported. However, binding of ECA was also increased by 134±16% from RT to TC platelets (P<0.01). β-GlnNAc exposure, as measured by sWGA lectin binding, was increased after cold and TC storage by 222±65% (P<0.01) and 197±14% (P<0.01), respectively, when compared to RT platelets. Platelets stored in the cold for >48 hours have been reported to be cleared through the hepatic AM receptor which recognizes asialocarbohydrates. Co-injection of asialofetuin significantly improved the recovery of two-day cold stored platelets from 9.5±5.1% to 18.4±7.3% (P<0.05) and 4.8±3.7% to 12.1±4.9% (P<0.01), at 5 min and 20 min post injection, respectively. Native fetuin did not alter the clearance of cold platelets. However, there was no significant increase in the recovery of TC platelets in the presence of asialofetuin as compared to fetuin injection (P>0.28), even though the TC platelets, like cold platelets, have significantly increased β-galactose exposure. Our results indicate that ‘temperature cycling' during cold storage of platelets may be an effective method to store human platelets up to 7 days without loss of in vivo recovery after transfusion when compared to RT platelets. Temperature cycling does not alter the cold induced increases in β-gal or β-GlcNAc expression which suggests that there are other mechanisms besides binding to the AM receptor that mediate clearance of platelets stored in the cold for >48 hours. The findings and conclusions in this abstract have not been formally disseminated by the Food and Drug Administration and should not be construed to represent any Agency determination or policy. Disclosures: No relevant conflicts of interest to declare.



Transfusion ◽  
2015 ◽  
Vol 56 (1) ◽  
pp. 24-32 ◽  
Author(s):  
Andrey Skripchenko ◽  
Monique P. Gelderman ◽  
Helen Awatefe ◽  
Annette Turgeon ◽  
Dedeene Thompson-Montgomery ◽  
...  


Transfusion ◽  
2012 ◽  
Vol 53 (6) ◽  
pp. 1178-1186 ◽  
Author(s):  
Fei Xu ◽  
Monique P. Gelderman ◽  
John Farrell ◽  
Jaroslav G. Vostal


Transfusion ◽  
2006 ◽  
Vol 46 (2) ◽  
pp. 257-264 ◽  
Author(s):  
Donald M. Arnold ◽  
Nancy M. Heddle ◽  
Myron Kulczycky ◽  
Julie Carruthers ◽  
Christopher Sigouin ◽  
...  


1979 ◽  
Vol 42 (03) ◽  
pp. 825-831 ◽  
Author(s):  
Jean-Pierre Allain

SummaryIn order to determine the correlation between different doses of F. VIII and their clinical effect,. 70 children with severe hemophilia A were studied after treatment with single doses of cryoprecipitate. The relationship between plasma F. VIII levels or doses calculated in u/ kg of body weight and clinical results followed an exponential curve. Plasma F. VIII levels of 0.35 and 0.53 u/ml corresponded to 95 and 99% satisfactory treatment, respectively. Similar clinical results were obtained with 20 and 31 u/kg. When the in vivo recovery of F. VIII after lyophilized cryoprecipitate was 0.015 u/ml for each u/kg injected, plasma F. VIII levels of 0.30 and 0.47 u/ml respectively were achieved. Since home treatment is largely based on single infusions of F. VIII, it is suggested that moderate and severe hemorrhages be treated with a dose which will provide a plasma F. VIII level of 0.5 u/ml.



2019 ◽  
Vol 130 ◽  
pp. 32-43 ◽  
Author(s):  
Elias Begas ◽  
Maria Bounitsi ◽  
Thomas Kilindris ◽  
Evangelos Kouvaras ◽  
Konstantinos Makaritsis ◽  
...  


2017 ◽  
Vol 51 (4) ◽  
pp. 410-418 ◽  
Author(s):  
Rupert S. Austin ◽  
Maisalamah Haji Taha ◽  
Frederic Festy ◽  
Richard Cook ◽  
Manoharan Andiappan ◽  
...  

Swept-source optical coherence tomography (SS-OCT) shows potential for the in vivo quantitative evaluation of micro-structural enamel surface phenomena occurring during early erosive demineralization. This randomized controlled single-blind cross-over clinical study aimed to evaluate the use of SS-OCT for detecting optical changes in the enamel of 30 healthy volunteers subjected to orange juice rinsing (erosive challenge) in comparison to mineral water rinsing (control), according to wiped and non-wiped enamel surface states. Participants were randomly allocated to 60 min of orange juice rinsing (pH 3.8) followed by 60 min of water rinsing (pH 6.7) and vice versa, with a 2-week wash-out period. In addition, the labial surfaces of the right or left maxillary incisors were wiped prior to SS-OCT imaging. An automated ImageJ algorithm was designed to analyse the back-scattered OCT signal intensity (D) after orange juice rinsing compared to after water rinsing. D was quantified as the OCT signal scattering from the 33 µm sub-surface enamel, normalised by the total OCT signal intensity entering the enamel. The back-scattered OCT signal intensity increased by 3.1% (95% CI 1.1-5.1%) in the wiped incisors and by 3.5% (95% CI 1.5-5.5%) in the unwiped incisors (p < 0.0001). Wiping reduced the back-scattered OCT signal intensity by 1.7% (95% CI -3.2 to -0.3%; p = 0.02) in comparison to the unwiped enamel surfaces for both rinsing solutions (p = 0.2). SS-OCT detected OCT signal changes in the superficial sub-surface enamel of maxillary central incisor teeth of healthy volunteers after orange juice rinsing.



1975 ◽  
Author(s):  
E. G. D. Tuddenham ◽  
A. L. Bloom ◽  
J. C. Giddings ◽  
C. A. Barrett

The occurrence of factor VIII inhibitor in five mild or moderately affected liaemophilic patients is described. In four patients the inhibitor inactivated endogenous factor VIII an dtemporarily converted them to severely affected haemophiliacs with factor VIII level of 0%. In the fifth patient, a brother of one of the others, the inhibitor although more potent did not inactivate the patient’s own factor VIII and did not completely inactivate normal factor VIII in vitro. This patient responded to treatment with factor-VIII concentrate but the in-vivo recovery was reduced. The patient’s plasma was tested against a panel of normal donors but it inactivated factor VIII in each to a similar extent and no evidence for normal factor-VIII groups was obtained. In the other patients the response to replacement treatment was also better than that usually seen in severely affected haemophilic patients with inhibitor. In the two related patients the inhibitors have so far persisted but in the unrelated patients the inhibitors eventually disappeared and did not always recur with subsequent therapy. The incidence of factor- VIII inhibitor in less severe haemophiliacs (factor VIII > 3% ) in this centre is 6% suggesting that the complication is more frequent in this type of patient than hitherto recognised.



Molecules ◽  
2021 ◽  
Vol 26 (12) ◽  
pp. 3602
Author(s):  
Elena Genova ◽  
Maura Apollonio ◽  
Giuliana Decorti ◽  
Alessandra Tesser ◽  
Alberto Tommasini ◽  
...  

Interferonopathies are rare genetic conditions defined by systemic inflammatory episodes caused by innate immune system activation in the absence of pathogens. Currently, no targeted drugs are authorized for clinical use in these diseases. In this work, we studied the contribution of sulforaphane (SFN), a cruciferous-derived bioactive molecule, in the modulation of interferon-driven inflammation in an immortalized human hepatocytes (IHH) line and in two healthy volunteers, focusing on STING, a key-component player in interferon pathway, interferon signature modulation, and GSTM1 expression and genotype, which contributes to SFN metabolism and excretion. In vitro, SFN exposure reduced STING expression as well as interferon signature in the presence of the pro-inflammatory stimulus cGAMP (cGAMP 3 h vs. SFN+cGAMP 3 h p value < 0.0001; cGAMP 6 h vs. SFN+cGAMP 6 h p < 0.001, one way ANOVA), restoring STING expression to the level of unstimulated cells. In preliminary experiments on healthy volunteers, no appreciable variations in interferon signature were identified after SFN assumption, while only in one of them, presenting the GSTM1 wild type genotype related to reduced SFN excretion, could a downregulation of STING be recorded. This study confirmed that SFN inhibits STING-mediated inflammation and interferon-stimulated genes expression in vitro. However, only a trend towards the downregulation of STING could be reproduced in vivo. Results obtained have to be confirmed in a larger group of healthy individuals and in patients with type I interferonopathies to define if the assumption of SFN could be useful as supportive therapy.



2019 ◽  
Vol 124 ◽  
pp. 6-18 ◽  
Author(s):  
Stephen C. Kanick ◽  
Peter A. Schneider ◽  
Bruce Klitzman ◽  
Natalie A. Wisniewski ◽  
Kerstin Rebrin


Sign in / Sign up

Export Citation Format

Share Document