WorldCat Identities

Barnard, M. R. (Mordaunt Roger)

Works: 14 works in 49 publications in 2 languages and 475 library holdings
Genres: Juvenile works  History  Biography 
Roles: Translator, Author
Classifications: DL312, 914.912
Publication Timeline
Most widely held works by M. R Barnard
A summer in Iceland by Carl Wilhelm Paijkull( Book )

7 editions published between 1868 and 2014 in English and held by 82 WorldCat member libraries worldwide

Fridtjof Nansen; a book for the young by Jacob B Bull( Book )

11 editions published between 1898 and 1903 in English and held by 56 WorldCat member libraries worldwide

Die culturpflanzen Norwegens by F. C Schübeler( Book )

3 editions published in 1862 in English and Danish and held by 4 WorldCat member libraries worldwide

Margaretting church and parish : past and present by M. R Barnard( Book )

in English and held by 1 WorldCat member library worldwide

A brief history of the organization and development of the Independent Order of Good Templars, from 1851 to 1855 by M. R Barnard( Book )

1 edition published in 1891 in English and held by 1 WorldCat member library worldwide

Reversible Hypothermia-Induced Inhibition of Human Platelet Activation in Whole Blood in Vitro and in Vivo( )

1 edition published in 1992 in English and held by 0 WorldCat member libraries worldwide

Platelets and other blood components are often transfused in clinical settings associated with hypothermia and a bleeding diathesis, such as cardiopulmonary bypass surgery, other major surgery, and multiple trauma. We examined the hypothesis that hypothermia reversibly inhibits human platelet activation in vitro and in vivo. Platelet activation was studied in normal human volunteers by whole blood flow cytometric analysis of modulation of platelet surface GMP-140 and the glycoprotein (GP) Ib-IX complex in: (a) shed blood emerging from a standardized in vivo bleeding time wound and (b) peripheral blood activated in vitro with either x-thrombin (in the presence of gly-pro-arg-pro, an inhibitor of fibrin polymerization) or the stable thromboxane A2 analogue U46619. Platelets in peripheral whole blood were activated at temperatures between 22 and 37 deg C. The skin temperature of the forearm was maintained at temperatures between 22 and 37 deg C prior to and during the bleeding time incision. Platelet aggregation was studied in shed blood by flow cytometry using a gate on both GPIb-positivity and light scatter and in peripheral blood by aggregometry. In vitro, hypothermia inhibited the rate and extent of both thrombin and U46619-induced: (a) upregulation of GMP-140, (b) downregulation of the GPIb-IX complex, (c) platelet aggregation, (d) platelet shape change, and (e) thromboxane B2 generation. These inhibitory effects of hypothermia were all completely reversed by rewarming the blood to 37 C. In vivo, platelet activation was inhibited by hypothermia as shown by 5 independent assays of shed blood: (1) upregulation of GMP-140, (2) downregulation of the GPIb-IX complex, (3) platelet aggregate formation, (4) thromboxane B2 generation, and (5) the bleeding time
The Odyssey by Homer( )

1 edition published in 1876 in English and held by 0 WorldCat member libraries worldwide

In Vivo Tracking of Platelets: Circulating Degranulated Platelets Rapidly Lose Surface P-Selectin but Continue to Circulate and Function( )

1 edition published in 1995 in English and held by 0 WorldCat member libraries worldwide

To examine the hypothesis that surface P-selectin-positive (degranulated) platelets are rapidly cleared from the circulation, we developed novel methods for tracking of platelets and measurement of platelet function in vivo. Washed platelets prepared from non-human primates (baboons) were labeled with PKH2 (a lipophilic fluorescent dye), thrombin-activated, washed, and re-infused into the same baboons. Three color whole blood flow cytometry was used to simultaneously: (1) identify platelets with a monoclonal antibody directed against GPIIb-IIIa (integrin alpha sub IIb Beta sub 3), (2) distinguish infused platelets by their PKH2 fluorescence, and (3) analyze platelet function with monoclonal antibodies. Two hours after infusion of autologous thrombin-activated platelets (P-selectin-positive, PKH2-labeled), 95 +/- 1% (mean +/- SEM, n = 5) of the circulating PKH2-labeled platelets had become P-selectin-negative. Compared with platelets not activated with thrombin pre-infusion, the recovery of these circulating PKH2-labeled, P-selectin-negative platelets was similar 24 hours after infusion and only slightly less 48 hours after infusion. The loss of platelet surface P-selectin was fully accounted for by a 67.1 +/- 16.7 ng/mL increase in the plasma concentration of soluble P selectin. The circulating PKH2-labeled, P-selectin-negative platelets were still able to function in vivo, as determined by their: (a) participation in platelet aggregates emerging from a bleeding time wound, (b) binding to Dacron in an arteriovenous shunt, (c) binding of monoclonal antibody PAC1 (directed against the fibrinogen binding site on GPIIb-IIIa), and (d) generation of procoagulant platelet-derived microparticles
Decreased Platelet Inhibition by Nitric Oxide in Two Brothers With a History of Arterial Thrombosis( )

1 edition published in 1995 in English and held by 0 WorldCat member libraries worldwide

Highly reactive oxygen species rapidly inactivate nitric oxide (NO), an endothelial product which inhibits platelet activation. We studied platelet inhibition by NO in two brothers with a cerebral thrombotic disorder. Both children had hyperreactive platelets, as determined by whole blood platelet aggregometry and flow cytometric analysis of the platelet surface expression of P-selectin. Mixing experiments showed that the patients' platelets behaved normally in control plasma; however, control platelets suspended in patient plasma were not inhibited by NO. As determined by flow cytometry, in the presence of plasma from either patient there was normal inhibition of the thrombin-induced expression of platelet surface P-selectin by prostacyclin, but not NO. Using a scopoletin assay, we measured a 2.7-fold increase in plasma H2O2 generation in one patient and a 3.4-fold increase in the second patient, both compared with control plasma. Glutathione peroxidase (GSH-Px) activity was decreased in the patients' plasmas compared with control plasma. The addition of exogenous GSH-Px led to restoration of platelet inhibition by NO. These data show that, in these patients' plasmas, impaired metabolism of reactive oxygen species reduces the bioavailability of NO and impairs normal platelet inhibitory mechanisms. These findings suggest that attenuated NO-mediated platelet inhibition produced by increased reactive oxygen species or impaired antioxidant defense may cause a thrombotic disorder in humans
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Audience Level
  Kids General Special  
Audience level: 0.69 (from 0.28 for Rules and ... to 0.97 for The Odysse ...)

English (34)

Danish (1)