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Burn injury differentially alters whole-blood and organ glutathione synthesis rates: An experimental model

Burns & Trauma 2013年第2期1卷 87-94页

作者： Zhe-Wei Fei Vernon r. Young Xiao-Ming Lu Andrew B. rhodes r.nald g.tompkins Alan J. Fischman Yong-Ming Yu Shriners Burns Hospital and Burn & Trauma Service Massachusetts General Hospital Harvard Medical School Boston MA 02114 Shriners Burns Hospital and Burn & Trauma Service Massachusetts General Hospital Harvard Medical School Boston MA 02114 Laboratory of Human Nutrition Massachusetts Institute of Technology Cambridge MA 02142 USA

Previous studies from our laboratories revealed a reduced rate of whole-blood (WB) glutathione (gSH) synthesis in severely burned patients. To determine whether WB gSH metabolism is an indicator of the status of gSH metabolism in one or more of the major organs, we used a burn rabbit model to determine gSH concentrations and rates of synthesis in WB, liver, lungs, kidney, and skeletal muscle. L-[1-13C]-cysteine was infused intravenously for 6 h in rabbits at 3 days post-burn and in sham burn controls. WB and organ 13C-enrichment of cysteine and gSH was determined by gas chromatography/mass spectrometry. Plasma cysteine metabolic flux was increased significantly (P g burn injury. WB, liver, and lung gSH concentrations (P = 0.054, P respectively) and fractional rates of gSH synthesis (P respectively) were reduced at 3 days post-burn. Kidney was unaffected. There also appears to be an increased rate of gSH transport out of the liver after burn injury. Hence, there is a differential impact of burn injury on tissue and organ gSH status, with WB qualitatively reflecting the changes in lung and liver. It will be important to determine whether these changes are due to alterations in the intrinsic capacity for gSH synthesis and/or availability of amino acid precursors of gSH.

关键词： Burn injury glutathione glutathione concentration synthesis rate whole blood

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Performance and calibration of quark/gluon-jet taggers using 140 fb^(-1) of pp collisions at √s=13 TeV with the ATLAS detector

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Chinese Physics C 2024年第2期48卷 1-25页

作者： g. Aad B. Abbott K. Abeling N.J. Abicht S.H. Abidi A. Aboulhorma H. Abramowicz H. Abreu Y. Abulaiti B.S. Acharya C. Adam Bourdarios L. Adamczyk S.V. Addepalli M.J. Addison J. Adelman A. Adiguzel T. Adye A.A. Affolder Y. Afik M.N. Agaras J. Agarwala A. Aggarwal C. Agheorghiesei A. Ahmad F. Ahmadov W.S. Ahmed S. Ahuja X. Ai g. Aielli A. Aikot M. Ait Tamlihat B. Aitbenchikh I. Aizenberg M. Akbiyik T.P.A. Åkesson A.V. Akimov D. Akiyama N.N. Akolkar K. Al Khoury g.L. Alberghi J. Albert P. Albicocco g.L. Albouy S. Alderweireldt M. Aleksa I.N. Aleksandrov C. Alexa T. Alexopoulos F. Alfonsi M. Algren M. Alhroob B. Ali H.M.J. Ali S. Ali S.W. Alibocus M. Aliev g. Alimonti W. Alkakhi C. Allaire B.M.M. Allbrooke J.F. Allen C.A. Allendes Flores P.P. Allport A. Aloisio F. Alonso C. Alpigiani M. Alvarez Estevez A. Alvarez Fernandez M. Alves Cardoso M.g. Alviggi M. Aly Y. Amaral Coutinho A. Ambler C. Amelung M. Amerl C.g. Ames D. Amidei S.P. Amor Dos Santos K.r. Amos V. Ananiev C. Anastopoulos T. Andeen J.K. Anders S.Y. Andrean A. Andreazza S. Angelidakis A. Angerami A.V. Anisenkov A. Annovi C. Antel M.T. Anthony E. Antipov M. Antonelli F. Anulli M. Aoki T. Aoki J.A. Aparisi Pozo M.A. Aparo L. Aperio Bella C. Appelt A. Apyan N. Aranzabal S.J. Arbiol Val C. Arcangeletti A.T.H. Arce E. Arena J-F. Arguin S. Argyropoulos J.-H. Arling O. Arnaez H. Arnold g. Artoni H. Asada K. Asai S. Asai N.A. Asbah J. Assahsah K. Assamagan r. Astalos S. Atashi r.J. Atkin M. Atkinson H. Atmani P.A. Atmasiddha K. Augsten S. Auricchio A.D. Auriol V.A. Austrup g. Avolio K. Axiotis g. Azuelos D. Babal H. Bachacou K. Bachas A. Bachiu F. Backman A. Badea P. Bagnaia M. Bahmani A.J. Bailey V.r. Bailey J.T. Baines L. Baines O.K. Baker E. Bakos D. Bakshi gupta V. Balakrishnan r. Balasubramanian E.M. Baldin P. Balek E. Ballabene F. Balli L.M. Baltes W.K. Balunas J. Balz E. Banas M. Bandieramonte A. Bandyopadhyay S. Bansal L. Barak M. Barakat E.L. Barberio D. Barberis M. Barbero M.Z. Barel K.N. Barends T. Barillari M-S. Barisits T. Barklow P. Baron D.A. Baron Mo The ATLAS Collaboration

The identification of jets originating from quarks and gluons,often referred to as quark/gluon tagging,plays an important role in various analyses performed at the Large Hadron Collider,as Standard Model measurements and searches for new particles decaying to quarks often rely on suppressing a large gluon-induced *** paper describes the measurement of the efficiencies of quark/gluon taggers developed within the ATLAS Collaboration,using √s=13 TeV proton–proton collision data with an integrated luminosity of 140 fb^(-1) collected by the ATLAS *** taggers with high performances in rejecting jets from gluon over jets from quarks are studied:one tagger is based on requirements on the number of inner-detector tracks associated with the jet,and the other combines several jet substructure observables using a boosted decision tree.A method is established to determine the quark/gluon fraction in data,by using quark/gluon-enriched subsamples defined by the jet *** in tagging efficiency between data and simulation are provided for jets with transverse momentum between 500 geV and 2 TeV and for multiple tagger working points.

关键词： ATLAS JET QUArK gLUON TAggINg

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Imaging C-Fos gene Expression in Burns Using Lipid Coated Spion Nanoparticles

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Advances in Molecular Imaging 2012年第4期2卷 31-37页

作者： Aristarchos Papagiannaros Valeria righi george g. Day Laurence g. rahme Philip K. Liu Alan J. Fischman r.nald g. tompkins A. Aria Tzika Athinoula A. Martinos Center of Biomedical Imaging Department of Radiology Massachusetts General Hospital Boston USA Department of Surgery Massachusetts General Hospital Harvard Medical School Boston USA Molecular Surgery Laboratory Department of Surgery Massachusetts General Hospital and Shriners Burns Institute Harvard Medical School and Massachusetts General Hospital Boston USA NMr Surgical Laboratory Department of Surgery Massachusetts General Hospital and Shriners Burns Institute Harvard Medical School Boston USA

Mr imaging of gene transcription is important as it should enable the non-invasive detection of mrNA alterations in disease. A range of MrI methods have been proposed for in vivo molecular imaging of cells based on the use of ultra- small super-paramagnetic iron oxide (USPIO) nanoparticles and related susceptibility weighted imaging methods. Al-though immunohistochemistry can robustly differentiate the expression of protein variants, there is currently no direct gene assay technique that is capable of differentiating established to differentiate the induction profiles of c-Fos mrNA in vivo. To visualize the differential FosB gene expression profile in vivo after burn trauma, we developed Mr probes that link the T2* contrast agent [superparamagnetic iron oxide nanoparticles (SPION)] with an oligodeoxynucleotide (ODN) sequence complementary to FosB mrNA to visualize endogenous mrNA targets via in vivo hybridization. The presence of this SPION-ODN probe in cells results in localized signal reduction in T2*-weighted Mr images, in which the rate of signal reduction (r2*) reflects the regional iron concentration at different stages of amphetamine (AMPH) exposure in living mouse tissue. Our aim was to produce a superior contrast agent that can be administered using sys- temic as opposed to local administration and which will target and accumulate at sites of burn injury. Specifically, we developed and evaluated a PEgylated lipid coated Mr probe with ultra-small super-paramagnetic iron oxide nanoparti- cles (USPION, a T2 susceptibility agent) coated with cationic fusogenic lipids, used for cell transfection and gene de- livery and covalently linked to a phosphorothioate modified oligodeoxynucleotide (sODN) complementary to c-Fos mrNA (SPION-cFos) and used the agent to image mice with leg burns. Our study demonstrated the feasibility of monitoring burn injury using Mr imaging of c-Fos transcription in vivo, in a clinically relevant mouse model of burn injury for the first ti

关键词： Positive Contrast Transverse relaxation in the rotating Frame (T2r) Superparamagnetic Iron-Oxide (Uspio) Burn Skeletal Muscle C-Fos

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regulation of IgF-1 signal pathways by androgen in skeletal muscle of glucocorticoid-treated rats

Regulation of IGF-1 signal pathways by androgen in skeletal ...

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第八届全国烧伤外科学年会

作者：尹会男柴家科尢永明申传安吴焱秋姚咏明刘辉 r.nald g. tompkins 盛志勇 Department of Burns and Plastic Surgery Burns InstituteFirst Affiliated Hospital of General Hospital of PLA(Formerly 304th Hospital) Department of Surgery Department of Surgery Massachusetts General HospitalShriners Burns Institute and Harvard Medical School

＜正＞The mechanisms by which androgens ameliorate glucocorticoid-induced muscle wasting are still under *** studies suggest that the anabolic effects of testosterone on muscle protein metabolism are mediated by the IgF-1 signal *** therefore examined the effects of testosterone on IgF-1 signal pathway activation in the skeletal muscle of glucocorticoid-treated *** female SD rats were randomly divided into four groups:control group,dexamethasone group,testosterone group and testosterone+dexamethasone *** attenuated the loss of body weight,gastrocnemius muscle weight and the reduction of muscle fiber cross-sectional area induced by dexamethasone. Testosterone prevented the dexamethasone-induced decrease of IgF-1 expression in skeletal muscle but did not change its serum *** prevented dexamethasone-induced dephosphorylation of protein kinase B （Akt） and p70 ribosomal protein S6 kinase （p70S6K）,two downstream targets of IgF-1 associated with protein *** both control and dexamethasone groups,testosterone was found to increase the phosphorylation of glycogen synthase kinase-3beta （gSK-3beta）,another downstream target of *** total amount of Akt,p70S6K or gSK-3beta proteins was not changed among these groups. The expression of two proteolysis related ubiquitin E3-ligases,muscle atrophy F-box （MAFbx） and muscle rINg finger-1 （MurF1） that are regulated by IgF-1 were also *** did not show any effect on the expression of MAFbx and MurF1 mrNA in both control and dexamethasone *** findings suggest that the anabolic effects of testosterone in reversing dexamethasone-induced muscle atrophy involve a mechanism of sharing the IgF-1 downstream signal transduction pathways in promoting muscle protein synthesis.

关键词： protein kinase B (Akt) p70 ribosomal protein S6 kinase (p70S6K) glycogen synthase kinase-3beta (gSK-3beta) muscle atrophy F-box (MAFbx) muscle rINg finger-1 (MurF1)

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带微处理机的医学仪器的设计

带微处理机的医学仪器的设计

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作者： W.J.·汤普金斯(W.J. tompkins) J.g.·韦勃斯特(J.g. Webster)

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