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1.  Search for lepton flavour violation in the eμ continuum with the ATLAS detector in \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$\sqrt{s} = 7~\mbox{TeV}$\end{document}pp collisions at the LHC 
Aad, G. | Abbott, B. | Abdallah, J. | Abdelalim, A. A. | Abdesselam, A. | Abdinov, O. | Abi, B. | Abolins, M. | Abramowicz, H. | Abreu, H. | Acerbi, E. | Acharya, B. S. | Adams, D. L. | Addy, T. N. | Adelman, J. | Adomeit, S. | Adragna, P. | Adye, T. | Aefsky, S. | Aguilar-Saavedra, J. A. | Aharrouche, M. | Ahlen, S. P. | Ahles, F. | Ahmad, A. | Ahsan, M. | Aielli, G. | Akdogan, T. | Åkesson, T. P. A. | Akimoto, G. | Akimov, A. V. | Akiyama, A. | Aktas, A. | Alam, M. S. | Alam, M. A. | Albrand, S. | Aleksa, M. | Aleksandrov, I. N. | Aleppo, M. | Alessandria, F. | Alexa, C. | Alexander, G. | Alexandre, G. | Alexopoulos, T. | Alhroob, M. | Aliev, M. | Alimonti, G. | Alison, J. | Aliyev, M. | Allport, P. P. | Allwood-Spiers, S. E. | Almond, J. | Aloisio, A. | Alon, R. | Alonso, A. | Alviggi, M. G. | Amako, K. | Amelung, C. | Ammosov, V. V. | Amorim, A. | Amorós, G. | Amram, N. | Anastopoulos, C. | Andeen, T. | Anders, C. F. | Anderson, K. J. | Andreazza, A. | Andrei, V. | Anduaga, X. S. | Angerami, A. | Anghinolfi, F. | Anjos, N. | Annovi, A. | Antonaki, A. | Antonelli, M. | Antonelli, S. | Antonov, A. | Antos, J. | Anulli, F. | Aoun, S. | Aperio Bella, L. | Apolle, R. | Arabidze, G. | Aracena, I. | Arai, Y. | Arce, A. T. H. | Archambault, J. P. | Arfaoui, S. | Arguin, J-F. | Arik, E. | Arik, M. | Armbruster, A. J. | Arnaez, O. | Arnault, C. | Artamonov, A. | Artoni, G. | Arutinov, D. | Asai, M. | Asai, S. | Asfandiyarov, R. | Ask, S. | Åsman, B. | Asner, D. | Asquith, L. | Assamagan, K. | Astbury, A. | Astvatsatourov, A. | Atoian, G. | Aubert, B. | Auge, E. | Augsten, K. | Aurousseau, M. | Austin, N. | Avolio, G. | Avramidou, R. | Axen, D. | Azuelos, G. | Azuma, Y. | Baak, M. A. | Baccaglioni, G. | Bacci, C. | Bach, A. M. | Bachacou, H. | Bachas, K. | Bachy, G. | Backes, M. | Backhaus, M. | Badescu, E. | Bagnaia, P. | Bahinipati, S. | Bai, Y. | Bailey, D. C. | Bain, T. | Baines, J. T. | Baker, O. K. | Baker, M. D. | Baker, S. | Baltasar Dos Santos Pedrosa, F. | Banas, E. | Banerjee, P. | Banerjee, Sw. | Banfi, D. | Bangert, A. | Bansal, V. | Bansil, H. S. | Barak, L. | Baranov, S. P. | Barbaro Galtieri, A. | Barber, T. | Barberio, E. L. | Barberis, D. | Barbero, M. | Bardin, D. Y. | Barillari, T. | Barisonzi, M. | Barklow, T. | Barlow, N. | Barnett, B. M. | Barnett, R. M. | Baroncelli, A. | Barr, A. J. | Barreiro, F. | Barreiro Guimarães da Costa, J. | Barrillon, P. | Bartoldus, R. | Barton, A. E. | Bartsch, D. | Bartsch, V. | Bates, R. L. | Batkova, L. | Batley, J. R. | Battaglia, A. | Battistin, M. | Battistoni, G. | Bauer, F. | Bawa, H. S. | Beare, B. | Beau, T. | Beauchemin, P. H. | Beccherle, R. | Bechtle, P. | Beck, G. A. | Beck, H. P. | Beckingham, M. | Becks, K. H. | Beddall, A. J. | Beddall, A. | Bedikian, S. | Bednyakov, V. A. | Bee, C. P. | Begel, M. | Behar Harpaz, S. | Behera, P. K. | Beimforde, M. | Belanger-Champagne, C. | Bell, P. J. | Bell, W. H. | Bella, G. | Bellagamba, L. | Bellina, F. | Bellomo, G. | Bellomo, M. | Belloni, A. | Beloborodova, O. | Belotskiy, K. | Beltramello, O. | Ben Ami, S. | Benary, O. | Benchekroun, D. | Benchouk, C. | Bendel, M. | Benedict, B. H. | Benekos, N. | Benhammou, Y. | Benjamin, D. P. | Benoit, M. | Bensinger, J. R. | Benslama, K. | Bentvelsen, S. | Beretta, M. | Berge, D. | Bergeaas Kuutmann, E. | Berger, N. | Berghaus, F. | Berglund, E. | Beringer, J. | Bernardet, K. | Bernat, P. | Bernhard, R. | Bernius, C. | Berry, T. | Bertin, A. | Bertolucci, F. | Besana, M. I. | Besson, N. | Bethke, S. | Bhimji, W. | Bianchi, R. M. | Bianco, M. | Biebel, O. | Bieniek, S. P. | Biesiada, J. | Biglietti, M. | Bilokon, H. | Bindi, M. | Binet, S. | Bingul, A. | Bini, C. | Biscarat, C. | Bitenc, U. | Black, K. M. | Blair, R. E. | Blanchard, J.-B. | Blanchot, G. | Blocker, C. | Blocki, J. | Blondel, A. | Blum, W. | Blumenschein, U. | Bobbink, G. J. | Bobrovnikov, V. B. | Bocchetta, S. S. | Bocci, A. | Boddy, C. R. | Boehler, M. | Boek, J. | Boelaert, N. | Böser, S. | Bogaerts, J. A. | Bogdanchikov, A. | Bogouch, A. | Bohm, C. | Boisvert, V. | Bold, T. | Boldea, V. | Bona, M. | Bondioli, M. | Boonekamp, M. | Boorman, G. | Booth, C. N. | Booth, P. | Bordoni, S. | Borer, C. | Borisov, A. | Borissov, G. | Borjanovic, I. | Borroni, S. | Bos, K. | Boscherini, D. | Bosman, M. | Boterenbrood, H. | Botterill, D. | Bouchami, J. | Boudreau, J. | Bouhova-Thacker, E. V. | Boulahouache, C. | Bourdarios, C. | Bousson, N. | Boveia, A. | Boyd, J. | Boyko, I. R. | Bozhko, N. I. | Bozovic-Jelisavcic, I. | Bracinik, J. | Braem, A. | Brambilla, E. | Branchini, P. | Brandt, A. | Brandt, G. | Brandt, O. | Bratzler, U. | Brau, B. | Brau, J. E. | Braun, H. M. | Brelier, B. | Bremer, J. | Brenner, R. | Bressler, S. | Breton, D. | Brett, N. D. | Bright-Thomas, P. G. | Britton, D. | Brochu, F. M. | Brock, I. | Brock, R. | Brodet, E. | Broggi, F. | Bromberg, C. | Brooijmans, G. | Brooks, W. K. | Brown, G. | Brubaker, E. | Bruckman de Renstrom, P. A. | Bruncko, D. | Bruneliere, R. | Brunet, S. | Bruni, A. | Bruni, G. | Bruschi, M. | Buanes, T. | Bucci, F. | Buchanan, J. | Buchanan, N. J. | Buchholz, P. | Buckingham, R. M. | Buckley, A. G. | Buda, S. I. | Budagov, I. A. | Budick, B. | Büscher, V. | Bugge, L. | Buira-Clark, D. | Buis, E. J. | Bulekov, O. | Bunse, M. | Buran, T. | Burckhart, H. | Burdin, S. | Burgess, T. | Burke, S. | Busato, E. | Bussey, P. | Buszello, C. P. | Butler, B. | Butler, J. M. | Buttar, C. M. | Butterworth, J. M. | Buttinger, W. | Byatt, T. | Caballero, J. | Cabrera Urbán, S. | Caccia, M. | Caforio, D. | Cakir, O. | Calafiura, P. | Calderini, G. | Calfayan, P. | Calkins, R. | Caloba, L. P. | Caloi, R. | Calvet, D. | Calvet, S. | Camacho Toro, R. | Camard, A. | Camarri, P. | Cameron, D. | Cammin, J. | Campana, S. | Campanelli, M. | Canale, V. | Canelli, F. | Canepa, A. | Cantero, J. | Capasso, L. | Capeans Garrido, M. D. M. | Caprini, I. | Caprini, M. | Capriotti, D. | Capua, M. | Caputo, R. | Caramarcu, C. | Cardarelli, R. | Carli, T. | Carlino, G. | Carminati, L. | Caron, B. | Caron, S. | Carpentieri, C. | Carrillo Montoya, G. D. | Carter, A. A. | Carter, J. R. | Carvalho, J. | Casadei, D. | Casado, M. P. | Cascella, M. | Caso, C. | Castaneda Hernandez, A. M. | Castaneda-Miranda, E. | Castillo Gimenez, V. | Castro, N. F. | Cataldi, G. | Cataneo, F. | Catinaccio, A. | Catmore, J. R. | Cattai, A. | Cattani, G. | Caughron, S. | Cavallari, A. | Cavalleri, P. | Cavalli, D. | Cavalli-Sforza, M. | Cavasinni, V. | Cazzato, A. | Ceradini, F. | Cerqueira, A. S. | Cerri, A. | Cerrito, L. | Cerutti, F. | Cetin, S. A. | Chafaq, A. | Chakraborty, D. | Chan, K. | Chapleau, B. | Chapman, J. D. | Chapman, J. W. | Chareyre, E. | Charlton, D. G. | Chavda, V. | Cheatham, S. | Chekanov, S. | Chekulaev, S. V. | Chelkov, G. A. | Chelstowska, M. A. | Chen, C. | Chen, H. | Chen, L. | Chen, S. | Chen, X. | Cheplakov, A. | Cherkaoui El Moursli, R. | Chernyatin, V. | Cheu, E. | Cheung, S. L. | Chevalier, L. | Chiefari, G. | Chikovani, L. | Childers, J. T. | Chilingarov, A. | Chiodini, G. | Chizhov, M. V. | Choudalakis, G. | Chouridou, S. | Christidi, I. A. | Christov, A. | Chromek-Burckhart, D. | Chu, M. L. | Chudoba, J. | Ciapetti, G. | Ciba, K. | Ciftci, A. K. | Ciftci, R. | Cinca, D. | Cindro, V. | Ciobotaru, M. D. | Ciocca, C. | Ciocio, A. | Cirilli, M. | Citterio, M. | Ciubancan, M. | Clark, A. | Clark, P. J. | Cleland, W. | Clemens, J. C. | Clement, B. | Clement, C. | Clifft, R. W. | Coadou, Y. | Cobal, M. | Coccaro, A. | Cochran, J. | Coe, P. | Coelli, S. | Cogan, J. G. | Coggeshall, J. | Cogneras, E. | Cojocaru, C. D. | Colas, J. | Colijn, A. P. | Collard, C. | Collins, N. J. | Collins-Tooth, C. | Collot, J. | Colon, G. | Coluccia, R. | Comune, G. | Conde Muiño, P. | Coniavitis, E. | Conidi, M. C. | Consonni, M. | Constantinescu, S. | Conta, C. | Conventi, F. | Cooke, M. | Cooper, B. D. | Cooper-Sarkar, A. M. | Copic, K. | Cornelissen, T. | Corradi, M. | Corriveau, F. | Corso-Radu, A. | Cortes-Gonzalez, A. | Cortiana, G. | Costa, G. | Costa, M. J. | Costanzo, D. | Costin, T. | Côté, D. | Coura Torres, R. | Courneyea, L. | Cowan, G. | Cowden, C. | Cox, B. E. | Cranmer, K. | Cranshaw, J. | Crescioli, F. | Cristinziani, M. | Crosetti, G. | Crupi, R. | Crépé-Renaudin, S. | Cuenca Almenar, C. | Cuhadar Donszelmann, T. | Cuneo, S. | Curatolo, M. | Curtis, C. J. | Cwetanski, P. | Czirr, H. | Czyczula, Z. | D’Auria, S. | D’Onofrio, M. | D’Orazio, A. | Da Rocha Gesualdi Mello, A. | Da Via, C. | Dabrowski, W. | Dahlhoff, A. | Dai, T. | Dallapiccola, C. | Daly, C. H. | Dam, M. | Dameri, M. | Damiani, D. S. | Danielsson, H. O. | Dankers, R. | Dannheim, D. | Dao, V. | Darbo, G. | Darlea, G. L. | Daum, C. | Dauvergne, J. P. | Davey, W. | Davidek, T. | Davidson, N. | Davidson, R. | Davies, M. | Davison, A. R. | Dawe, E. | Dawson, I. | Daya-Ishmukhametova, R. K. | De, K. | de Asmundis, R. | De Castro, S. | De Castro Faria Salgado, P. E. | De Cecco, S. | de Graat, J. | De Groot, N. | de Jong, P. | De La Taille, C. | De la Torre, H. | de Mora, L. | De Nooij, L. | De Oliveira Branco, M. | De Pedis, D. | de Saintignon, P. | De Salvo, A. | De Sanctis, U. | De Santo, A. | De Vivie De Regie, J. B. | Dean, S. | Dedovich, D. V. | Degenhardt, J. | Dehchar, M. | Deile, M. | Del Papa, C. | Del Peso, J. | Del Prete, T. | Dell’Acqua, A. | Dell’Asta, L. | Della Pietra, M. | della Volpe, D. | Delmastro, M. | Delpierre, P. | Delsart, P. A. | Deluca, C. | Demers, S. | Demichev, M. | Demirkoz, B. | Deng, J. | Deng, W. | Denisov, S. P. | Derendarz, D. | Derkaoui, J. E. | Derue, F. | Dervan, P. | Desch, K. | Devetak, E. | Deviveiros, P. 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This paper presents a search for the t-channel exchange of an R-parity violating scalar top quark (\documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$\tilde{t}$\end{document}) in the e±μ∓ continuum using 2.1 fb−1 of data collected by the ATLAS detector in \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$\sqrt{s}=7~\mbox{TeV}$\end{document}pp collisions at the Large Hadron Collider. Data are found to be consistent with the expectation from the Standard Model backgrounds. Limits on R-parity-violating couplings at 95 % C.L. are calculated as a function of the scalar top mass (\documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$m_{\tilde{t}}$\end{document}). The upper limits on the production cross section for pp→eμX, through the t-channel exchange of a scalar top quark, ranges from 170 fb for \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$m_{\tilde{t}}=95~\mbox{GeV}$\end{document} to 30 fb for \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$m_{\tilde{t}}=1000~\mbox{GeV}$\end{document}.
doi:10.1140/epjc/s10052-012-2040-z
PMCID: PMC4370899  PMID: 25814838
2.  Pathogenesis of lung cancer signaling pathways: roadmap for therapies 
Lung cancer is the major cancer killer worldwide, and 5-yr survival is extremely poor (≤15%), accentuating the need for more effective therapeutic strategies.
Significant advances in lung cancer biology may lead to customised therapy based on targeting specific genes and pathways. The main signalling pathways that could provide roadmaps for therapy include the following: growth promoting pathways (Epidermal Growth Factor Receptor/Ras/PhosphatidylInositol 3-Kinase), growth inhibitory pathways (p53/Rb/P14ARF, STK11), apoptotic pathways (Bcl-2/Bax/Fas/FasL), DNA repair and immortalisation genes.
Epigenetic changes in lung cancer contribute strongly to cell transformation by modifying chromatin structures and the specific expression of genes; these include DNA methylation, histone and chromatin protein modification, and micro-RNA, all of which are responsible for the silencing of tumour suppressor genes while enhancing expression of oncogenes.
The genetic and epigenetic pathways involved in lung tumorigenesis differ between smokers and nonsmokers, and are tools for cancer diagnosis, prognosis, clinical follow-up and targeted therapies.
doi:10.1183/09031936.00014009
PMCID: PMC2762943  PMID: 19483050
Lung cancer pathology; molecular biology; molecular genetics; molecular pathology; molecular therapy; signal pathways
3.  Differential expression of telomerase reverse transcriptase (hTERT) in lung tumours 
British Journal of Cancer  2004;90(6):1222-1229.
doi:10.1038/sj.bjc.6601643
PMCID: PMC2410220  PMID: 15026805
lung cancer; hTERT; telomerase; immunohistochemistry; nucleolar localization
4.  Interferon-γ induced increases in intracellular calcium in T lymphocytes from patients with multiple sclerosis precede clinical exacerbations and detection of active lesions on MRI 
BACKGROUND—Interferon (IFN)-γ exerts a multiplicity of actions potentially relevant for the pathogenesis of multiple sclerosis, including the expression of a transplasmalemma calcium (Ca2+) influx leading to an intracellular Ca2+ ([Ca2+]i) increase able to lower T lymphocyte threshold of excitability. It has been previously shown in a cross sectional cumulative study that this influx is associated with clinical and MRI evidence of disease activity.
METHODS—To evaluate the temporal relation between disease activity and the IFN-γ activated Ca2+ influx in individual patients, a fluorimetric analysis was performed on peripheral blood lymphocytes from eight patients with relapsing-remitting multiple sclerosis every 15 days for one year. Results—Fluctuations of the influx were correlated with clinical events and monthly enhanced brain MRI. The influx was detected a mean of 10.4 (range 7-17) times per patient during our analysis. In 61% of the occasions, influx induced [Ca2+]i increases were recorded in each patient in more than two consecutive measurements, determining sustained [Ca2+]i increases lasting for a mean of 31.5 days. Peak [Ca2+]i increases preceded clinical attacks (P=0.04) or maximal detection of brain MRI enhancing lesions (P=0.05) by a mean of 30.8 and 34.2 days respectively. Spectral analysis of time series further indicated that the fluctuation frequency of [Ca2+]i increases due to the influx over time were superimposable on the appearance of new MRI lesions in all patients and confirmed that in two thirds of the patients these [Ca2+]i increases occurred significantly before (P<0.005) or concurred with new lesion appearance. Finally, the overall presence of the influx throughout the follow up period correlated (P=0.03) with the patients' exacerbation rates.
CONCLUSIONS—Intracellular events leading to T lymphocyte activation in multiple sclerosis occur in the peripheral blood before CNS specific events become evident and are, in part, sustained by cytokine induced Ca2+ mediated phenomena.


PMCID: PMC2169707  PMID: 9328251
5.  Bidirectional modulation of insulin action by amino acids. 
Journal of Clinical Investigation  1998;101(7):1519-1529.
Amino acids have been shown to stimulate protein synthesis, inhibit proteolysis, and decrease whole-body and forearm glucose disposal. Using cultured hepatoma and myotube cells, we demonstrate that amino acids act as novel signaling elements in insulin target tissues. Exposure of cells to high physiologic concentrations of amino acids activates intermediates important in the initiation of protein synthesis, including p70 S6 kinase and PHAS-I, in synergy with insulin. This stimulatory effect is largely due to branched chain amino acids, particularly leucine, and can be reproduced by its transamination product, ketoisocaproic acid. Concurrently, amino acids inhibit early steps in insulin action critical for glucose transport and inhibition of gluconeogenesis, including decreased insulin-stimulated tyrosine phosphorylation of IRS-1 and IRS-2, decreased binding of grb 2 and the p85 subunit of phosphatidylinositol 3-kinase to IRS-1 and IRS-2, and a marked inhibition of insulin-stimulated phosphatidylinositol 3-kinase. Taken together, these data support the hypothesis that amino acids act as specific positive signals for maintenance of protein stores, while inhibiting other actions of insulin at multiple levels. This bidirectional modulation of insulin action indicates crosstalk between hormonal and nutritional signals and demonstrates a novel mechanism by which nutritional factors contribute to insulin resistance.
PMCID: PMC508730  PMID: 9525995
6.  Interferon-gamma activated calcium influx in peripheral blood lymphocytes from patients with primary and secondary progressive multiple sclerosis. 
Interferon-gamma (IFN-gamma) contributes to the early events leading to T cell activation in relapsing-remitting (RR) multiple sclerosis (MS) by activating a transplasmalemma calcium influx, the detection of which is closely associated with clinical and MRI evidence of disease activity. The appearance of this influx represents one of the earliest peripheral events in the pathogenesis of RRMS. It is still questioned whether the same immune mediated mechanisms also operate in primary progressive (PP)MS. Fluorimetric evidence of the IFN-gamma activated calcium influx was sought in 16 patients with PPMS and 39 patients with secondary progressive (SP)MS. To compare peripheral versus CNS evidence of immune activation 11 of the patients with PPMS and 27 of the patients with SPMS underwent gadolinium enhanced brain MRI. The IFN-gamma activated influx was detected in peripheral blood lymphocytes from eight of 16 (50%) patients with PPMS, and 20 of 39 (51%) patients with SPMS, a frequency similar to that previously reported in patients with RRMS during phases of disease stability. Gadolinium enhancing brain MRI lesions were found in only one of 11 (9%) patients with PPMS and 12 of 27 (41%) with SPMS. Our study shows that peripheral blood lymphocytes from patients with PPMS and patients with SPMS express with the same frequency as patients with RRMS, an IFN-gamma dependent intracellular process leading to T cell activation able to trigger disease activity.
PMCID: PMC1074051  PMID: 8937348
7.  Metabolic effects of successful intraportal islet transplantation in insulin-dependent diabetes mellitus. 
Journal of Clinical Investigation  1996;97(11):2611-2618.
The intraportal injection of human pancreatic islets has been indicated as a possible alternative to the pancreas transplant in insulin-dependent diabetic patients. Aim of the present work was to study the effect of intraportal injection of purified human islets on: (a) the basal hepatic glucose production; (b) the whole body glucose homeostasis and insulin action; and (c) the regulation of insulin secretion in insulin-dependent diabetes mellitus patients bearing a kidney transplant. 15 recipients of purified islets from cadaver donors (intraportal injection) were studied by means of the infusion of labeled glucose to quantify the hepatic glucose production. Islet transplanted patients were subdivided in two groups based on graft function and underwent: (a) a 120-min euglycemic insulin infusion (1 mU/kg/min) to assess insulin action; (b) a 120-min glucose infusion (+75 mg/di) to study the pattern of insulin secretion. Seven patients with chronic uveitis on the same immunosuppressive therapy as grafted patients, twelve healthy volunteers, and seven insulin-dependent diabetic patients with combined pancreas and kidney transplantation were also studied as control groups. Islet transplanted patients have: (a) a higher basal hepatic glucose production (HGP: 5.1 +/- 1.4 mg/kg/ min; P < 0.05 with respect to all other groups) if without graft function, and a normal HGP (2.4 +/- 0.2 mg/kg/min) with a functioning graft; (b) a defective tissue glucose disposal (3.9 +/- 0.5 mg/kg/min in patients without islet function and 5.3 +/- 0.4 mg/kg/min in patients with islet function) with respect to normals (P < 0.01 for both comparisons); (c) a blunted first phase insulin peak and a similar second phase secretion with respect to controls. In conclusion, in spite of the persistence of an abnormal pattern of insulin secretion, successful intraportal islet graft normalizes the basal HGP and improves total tissue glucose disposal in insulin-dependent diabetes mellitus.
PMCID: PMC507348  PMID: 8647955

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