12 research outputs found
Freezing line of the Lennard-Jones fluid: a Phase Switch Monte Carlo study
- Publication venue
- 'AIP Publishing'
- Publication date
- 07/11/2005
- Field of study
We report a Phase Switch Monte Carlo (PSMC) method study of the freezing line
of the Lennard-Jones (LJ) fluid. Our work generalizes to soft potentials the
original application of the method to hard sphere freezing, and builds on a
previous PSMC study of the LJ system by Errington (J. Chem. Phys. {\bf 120},
3130 (2004)). The latter work is extended by tracing a large section of the
Lennard-Jones freezing curve, the results for which we compare to a previous
Gibbs-Duhem integration study. Additionally we provide new background regarding
the statistical mechanical basis of the PSMC method and extensive
implementation details.Comment: 18 pages, 6 figure
Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease
- Author
- A Abbate
- A Abhyankar
- A Adams
- A Agafina
- A Akyea-Djamson
- A Alan
- A Alfieri
- A Alfrey
- A Alvarisqueta
- A Amos
- A Anadiotis
- A Anneveldt
- A Antolick
- A Arthur
- A Aslam
- Abaci F
- Abdullakutty J
- Abhaichand R
- Abib E Jr
- Aboufakher R
- Abrantes J
- Abreu M
- Abulencia K
- Acampora D
- Acampora M
- Accini Mendoza Jl
- Aceto L
- Acevedo B
- Acevedo L
- Acheatel R
- Actis Mv
- Adams M
- Adjic Nc
- Affaki Gs
- Agarwal Dk
- Aggarwal Rk
- Agosta Gf
- Aguilar M
- Aguilar M
- Ahire N
- Ahmad I
- Ahmed Sh
- Ahn Y
- Aish B
- Aiub F
- Aiub J
- Ajax K
- Ajioka M
- Akai Y
- Akatova E
- Akrap B
- Al Joundi T
- Al-Khalili F
- Albisu J
- Alcalde Jm
- Alcide P
- Alfonso T
- Allen J
- Alllison Dc
- Almaliky T
- Amerena J
- Andersen K
- Andor M
- Angelova I
- Angiolillo D
- Anita S
- Anker Sd
- Antalik L
- Antonicelli R
- Aparicio Cv
- Apel T
- Apostolovic S
- Ara M
- Aragorn L
- Arango Jl
- Araujo Fonseca M
- Ardissino D
- Arenas Leon Jl
- Arevalo S
- Argiolas G
- Arif I
- Armas E
- Aron G
- Arora S
- Asafu-Adjaye N
- Ashcom T
- Ashford M
- Ashino K
- Asim Oktay Ao
- Assarsson E
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- Atieh M
- Aull L
- Avalos V
- Avdonina N
- Awasthi Ak
- Axthelm C
- Ayala M
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- Ayasse M
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- B Becker
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- Ichisawa M
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- Publication venue
- 'Massachusetts Medical Society'
- Publication date
- 01/01/2017
- Field of study
Background: Experimental and clinical data suggest that reducing inflammation without affecting lipid levels may reduce the risk of cardiovascular disease. Yet, the inflammatory hypothesis of atherothrombosis has remained unproved. Methods: We conducted a randomized, double-blind trial of canakinumab, a therapeutic monoclonal antibody targeting interleukin-1β, involving 10,061 patients with previous myocardial infarction and a high-sensitivity C-reactive protein level of 2 mg or more per liter. The trial compared three doses of canakinumab (50 mg, 150 mg, and 300 mg, administered subcutaneously every 3 months) with placebo. The primary efficacy end point was nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. RESULTS: At 48 months, the median reduction from baseline in the high-sensitivity C-reactive protein level was 26 percentage points greater in the group that received the 50-mg dose of canakinumab, 37 percentage points greater in the 150-mg group, and 41 percentage points greater in the 300-mg group than in the placebo group. Canakinumab did not reduce lipid levels from baseline. At a median follow-up of 3.7 years, the incidence rate for the primary end point was 4.50 events per 100 person-years in the placebo group, 4.11 events per 100 person-years in the 50-mg group, 3.86 events per 100 person-years in the 150-mg group, and 3.90 events per 100 person-years in the 300-mg group. The hazard ratios as compared with placebo were as follows: in the 50-mg group, 0.93 (95% confidence interval [CI], 0.80 to 1.07; P = 0.30); in the 150-mg group, 0.85 (95% CI, 0.74 to 0.98; P = 0.021); and in the 300-mg group, 0.86 (95% CI, 0.75 to 0.99; P = 0.031). The 150-mg dose, but not the other doses, met the prespecified multiplicity-adjusted threshold for statistical significance for the primary end point and the secondary end point that additionally included hospitalization for unstable angina that led to urgent revascularization (hazard ratio vs. placebo, 0.83; 95% CI, 0.73 to 0.95; P = 0.005). Canakinumab was associated with a higher incidence of fatal infection than was placebo. There was no significant difference in all-cause mortality (hazard ratio for all canakinumab doses vs. placebo, 0.94; 95% CI, 0.83 to 1.06; P = 0.31). Conclusions: Antiinflammatory therapy targeting the interleukin-1β innate immunity pathway with canakinumab at a dose of 150 mg every 3 months led to a significantly lower rate of recurrent cardiovascular events than placebo, independent of lipid-level lowering. (Funded by Novartis; CANTOS ClinicalTrials.gov number, NCT01327846.
Impact of primary kidney disease on the effects of empagliflozin in patients with chronic kidney disease: secondary analyses of the EMPA-KIDNEY trial
- Author
- Abat S.
- Abd Rahman R.
- Abdul Cader R.
- Abdul Hafidz M. I.
- Abdul Wahab M. Z.
- Abdul-Samad T.
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- 01/01/2024
- Field of study
Background: The EMPA KIDNEY trial showed that empagliflozin reduced the risk of the primary composite outcome of kidney disease progression or cardiovascular death in patients with chronic kidney disease mainly through slowing progression. We aimed to assess how effects of empagliflozin might differ by primary kidney disease across its broad population. Methods: EMPA-KIDNEY, a randomised, controlled, phase 3 trial, was conducted at 241 centres in eight countries (Canada, China, Germany, Italy, Japan, Malaysia, the UK, and the USA). Patients were eligible if their estimated glomerular filtration rate (eGFR) was 20 to less than 45 mL/min per 1·73 m2, or 45 to less than 90 mL/min per 1·73 m2 with a urinary albumin-to-creatinine ratio (uACR) of 200 mg/g or higher at screening. They were randomly assigned (1:1) to 10 mg oral empagliflozin once daily or matching placebo. Effects on kidney disease progression (defined as a sustained ≥40% eGFR decline from randomisation, end-stage kidney disease, a sustained eGFR below 10 mL/min per 1·73 m2, or death from kidney failure) were assessed using prespecified Cox models, and eGFR slope analyses used shared parameter models. Subgroup comparisons were performed by including relevant interaction terms in models. EMPA-KIDNEY is registered with ClinicalTrials.gov, NCT03594110. Findings: Between May 15, 2019, and April 16, 2021, 6609 participants were randomly assigned and followed up for a median of 2·0 years (IQR 1·5–2·4). Prespecified subgroupings by primary kidney disease included 2057 (31·1%) participants with diabetic kidney disease, 1669 (25·3%) with glomerular disease, 1445 (21·9%) with hypertensive or renovascular disease, and 1438 (21·8%) with other or unknown causes. Kidney disease progression occurred in 384 (11·6%) of 3304 patients in the empagliflozin group and 504 (15·2%) of 3305 patients in the placebo group (hazard ratio 0·71 [95% CI 0·62–0·81]), with no evidence that the relative effect size varied significantly by primary kidney disease (pheterogeneity=0·62). The between-group difference in chronic eGFR slopes (ie, from 2 months to final follow-up) was 1·37 mL/min per 1·73 m2 per year (95% CI 1·16–1·59), representing a 50% (42–58) reduction in the rate of chronic eGFR decline. This relative effect of empagliflozin on chronic eGFR slope was similar in analyses by different primary kidney diseases, including in explorations by type of glomerular disease and diabetes (p values for heterogeneity all >0·1). Interpretation: In a broad range of patients with chronic kidney disease at risk of progression, including a wide range of non-diabetic causes of chronic kidney disease, empagliflozin reduced risk of kidney disease progression. Relative effect sizes were broadly similar irrespective of the cause of primary kidney disease, suggesting that SGLT2 inhibitors should be part of a standard of care to minimise risk of kidney failure in chronic kidney disease. Funding: Boehringer Ingelheim, Eli Lilly, and UK Medical Research Council
Understanding and Assessing Traumatic Responses of Guilt, Shame, and Anger among Children, Adolescents, and Young Adults
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- A Cook
- A H Buss
- A H Buss
- A Hazzard
- A Mezulis
- A Sourander
- A W Wagner
- American Psychiatric Association
- B Andrews
- B Kolk van der
- C A Cuevas
- C D Spielberger
- C D Spielberger
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- D M Amodio
- D Marschall
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- D Watson
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- E Walster
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- Kenneth E. Fletcher
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- Publication venue
- 'Informa UK Limited'
- Publication date
- Field of study
Infant mental health: an emerging field for children with developmental disabilities
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- R.P. Solis-Camara R.A. Fox, B.C. Nicholson
- R.P. Weissberg K.L. Kumpfer, M.E. Seligman
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- S. Eyberg
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- S.H. McConaughy P.J. Kay, M. Fitzgerald
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- Publication date
- 01/01/2008
- Field of study
Impact of primary kidney disease on the effects of empagliflozin in patients with chronic kidney disease: secondary analyses of the EMPA-KIDNEY trial
- Author
- Abat S
- Abd Rahman R
- Abdul Cader R
- Abdul Hafidz MI
- Abdul Wahab MZ
- Abdul-Samad T
- Abdullah NK
- Abe M
- Abraham N
- Acheampong S
- Achiri P
- Acosta JA
- Adeleke A
- Adell V
- Adewuyi-Dalton R
- Adnan N
- Africano A
- Agharazii M
- Aguilar F
- Aguilera A
- Ahmad Miswan N
- Ahmad Rosdi H
- Ahmad M
- Ahmad MK
- Ahmad NA
- Ahmad NH
- Ahmad NI
- Ahmed I
- Ahmed S
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- Aiello J
- Aitken A
- AitSadi R
- Aker S
- Akimoto S
- Akinfolarin A
- Akram S
- Al-Rabadi L
- Al-Zeer B
- Alberici F
- Albert C
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- Publication venue
- Publication date
- 01/01/2023
- Field of study
Background: The EMPA-KIDNEY trial showed that empagliflozin reduced the risk of the primary composite outcome of kidney disease progression or cardiovascular death in patients with chronic kidney disease mainly through slowing progression. We aimed to assess how effects of empagliflozin might differ by primary kidney disease across its broad population. Methods: EMPA-KIDNEY, a randomised, controlled, phase 3 trial, was conducted at 241 centres in eight countries (Canada, China, Germany, Italy, Japan, Malaysia, the UK, and the USA). Patients were eligible if their estimated glomerular filtration rate (eGFR) was 20 to less than 45 mL/min per 1·73 m2, or 45 to less than 90 mL/min per 1·73 m2 with a urinary albumin-to-creatinine ratio (uACR) of 200 mg/g or higher at screening. They were randomly assigned (1:1) to 10 mg oral empagliflozin once daily or matching placebo. Effects on kidney disease progression (defined as a sustained ≥40% eGFR decline from randomisation, end-stage kidney disease, a sustained eGFR below 10 mL/min per 1·73 m2, or death from kidney failure) were assessed using prespecified Cox models, and eGFR slope analyses used shared parameter models. Subgroup comparisons were performed by including relevant interaction terms in models. EMPA-KIDNEY is registered with ClinicalTrials.gov, NCT03594110. Findings: Between May 15, 2019, and April 16, 2021, 6609 participants were randomly assigned and followed up for a median of 2·0 years (IQR 1·5-2·4). Prespecified subgroupings by primary kidney disease included 2057 (31·1%) participants with diabetic kidney disease, 1669 (25·3%) with glomerular disease, 1445 (21·9%) with hypertensive or renovascular disease, and 1438 (21·8%) with other or unknown causes. Kidney disease progression occurred in 384 (11·6%) of 3304 patients in the empagliflozin group and 504 (15·2%) of 3305 patients in the placebo group (hazard ratio 0·71 [95% CI 0·62-0·81]), with no evidence that the relative effect size varied significantly by primary kidney disease (pheterogeneity=0·62). The between-group difference in chronic eGFR slopes (ie, from 2 months to final follow-up) was 1·37 mL/min per 1·73 m2 per year (95% CI 1·16-1·59), representing a 50% (42-58) reduction in the rate of chronic eGFR decline. This relative effect of empagliflozin on chronic eGFR slope was similar in analyses by different primary kidney diseases, including in explorations by type of glomerular disease and diabetes (p values for heterogeneity all >0·1). Interpretation: In a broad range of patients with chronic kidney disease at risk of progression, including a wide range of non-diabetic causes of chronic kidney disease, empagliflozin reduced risk of kidney disease progression. Relative effect sizes were broadly similar irrespective of the cause of primary kidney disease, suggesting that SGLT2 inhibitors should be part of a standard of care to minimise risk of kidney failure in chronic kidney disease. Funding: Boehringer Ingelheim, Eli Lilly, and UK Medical Research Council
Effects of empagliflozin on progression of chronic kidney disease: a prespecified secondary analysis from the empa-kidney trial
- Author
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- Abd Rahman R
- Abdul Cader R
- Abdul Hafidz MI
- Abdul Wahab MZ
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- Publication venue
- Publication date
- 01/01/2023
- Field of study
Background: Sodium-glucose co-transporter-2 (SGLT2) inhibitors reduce progression of chronic kidney disease and the risk of cardiovascular morbidity and mortality in a wide range of patients. However, their effects on kidney disease progression in some patients with chronic kidney disease are unclear because few clinical kidney outcomes occurred among such patients in the completed trials. In particular, some guidelines stratify their level of recommendation about who should be treated with SGLT2 inhibitors based on diabetes status and albuminuria. We aimed to assess the effects of empagliflozin on progression of chronic kidney disease both overall and among specific types of participants in the EMPA-KIDNEY trial. Methods: EMPA-KIDNEY, a randomised, controlled, phase 3 trial, was conducted at 241 centres in eight countries (Canada, China, Germany, Italy, Japan, Malaysia, the UK, and the USA), and included individuals aged 18 years or older with an estimated glomerular filtration rate (eGFR) of 20 to less than 45 mL/min per 1·73 m2, or with an eGFR of 45 to less than 90 mL/min per 1·73 m2 with a urinary albumin-to-creatinine ratio (uACR) of 200 mg/g or higher. We explored the effects of 10 mg oral empagliflozin once daily versus placebo on the annualised rate of change in estimated glomerular filtration rate (eGFR slope), a tertiary outcome. We studied the acute slope (from randomisation to 2 months) and chronic slope (from 2 months onwards) separately, using shared parameter models to estimate the latter. Analyses were done in all randomly assigned participants by intention to treat. EMPA-KIDNEY is registered at ClinicalTrials.gov, NCT03594110. Findings: Between May 15, 2019, and April 16, 2021, 6609 participants were randomly assigned and then followed up for a median of 2·0 years (IQR 1·5-2·4). Prespecified subgroups of eGFR included 2282 (34·5%) participants with an eGFR of less than 30 mL/min per 1·73 m2, 2928 (44·3%) with an eGFR of 30 to less than 45 mL/min per 1·73 m2, and 1399 (21·2%) with an eGFR 45 mL/min per 1·73 m2 or higher. Prespecified subgroups of uACR included 1328 (20·1%) with a uACR of less than 30 mg/g, 1864 (28·2%) with a uACR of 30 to 300 mg/g, and 3417 (51·7%) with a uACR of more than 300 mg/g. Overall, allocation to empagliflozin caused an acute 2·12 mL/min per 1·73 m2 (95% CI 1·83-2·41) reduction in eGFR, equivalent to a 6% (5-6) dip in the first 2 months. After this, it halved the chronic slope from -2·75 to -1·37 mL/min per 1·73 m2 per year (relative difference 50%, 95% CI 42-58). The absolute and relative benefits of empagliflozin on the magnitude of the chronic slope varied significantly depending on diabetes status and baseline levels of eGFR and uACR. In particular, the absolute difference in chronic slopes was lower in patients with lower baseline uACR, but because this group progressed more slowly than those with higher uACR, this translated to a larger relative difference in chronic slopes in this group (86% [36-136] reduction in the chronic slope among those with baseline uACR <30 mg/g compared with a 29% [19-38] reduction for those with baseline uACR ≥2000 mg/g; ptrend<0·0001). Interpretation: Empagliflozin slowed the rate of progression of chronic kidney disease among all types of participant in the EMPA-KIDNEY trial, including those with little albuminuria. Albuminuria alone should not be used to determine whether to treat with an SGLT2 inhibitor. Funding: Boehringer Ingelheim and Eli Lilly
Precision Electroweak Measurements on the Z resonance.
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- X Hwang
- X Lin
- X Moreno
- X Yamartino
- XC Lu
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- XL Wang
- XQ Yashima
- XW Tarjan
- Y Ask
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- Y Gracco
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- Y Izen
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- Y Oishi
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- Y Sadovsky
- Y Scott
- Y Segar
- Y Ulbricht
- Y Xu
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- Y Zhang
- YA Kang
- YD King
- YH Chaturvedi
- YS Lu
- Z Badaud
- Z Ferguson
- Z Kubinec
- Z Sztaricskai
- Z Tran
- ZA Lohmann
- Zer Zion
- ZF Grenier
- ZM Weber
- ZP Zhao
- ZY Johnson
- ZZ Yamamoto
- Publication venue
- 'Elsevier BV'
- Publication date
- 07/09/2005
- Field of study
We report on the final electroweak measurements performed with data taken at the Z resonance by the experiments operating at the electron–positron colliders SLC and LEP. The data consist of 17 million Z decays accumulated by the ALEPH, DELPHI, L3 and OPAL experiments at LEP, and 600 thousand Z decays by the SLD experiment using a polarised beam at SLC. The measurements include cross-sections, forward–backward asymmetries and polarised asymmetries. The mass and width of the Z boson, mZ and ΓZ, and its couplings to fermions, for example the ρ parameter and the effective electroweak mixing angle for leptons, are precisely measured: The number of light neutrino species is determined to be 2.9840±0.0082, in agreement with the three observed generations of fundamental fermions. The results are compared to the predictions of the Standard Model (SM). At the Z-pole, electroweak radiative corrections beyond the running of the QED and QCD coupling constants are observed with a significance of five standard deviations, and in agreement with the Standard Model. Of the many Z-pole measurements, the forward–backward asymmetry in b-quark production shows the largest difference with respect to its SM expectation, at the level of 2.8 standard deviations. Through radiative corrections evaluated in the framework of the Standard Model, the Z-pole data are also used to predict the mass of the top quark, , and the mass of the W boson, . These indirect constraints are compared to the direct measurements, providing a stringent test of the SM. Using in addition the direct measurements of mt and mW, the mass of the as yet unobserved SM Higgs boson is predicted with a relative uncertainty of about 50% and found to be less than at 95% confidence level
Recommended from our members
Precision electroweak measurements on the Z resonance
- Author
- Abbaneo D
- Abbiendi G
- Abdallah J
- Abe K
- Abe K
- Abe T
- Abreu P
- Abt I
- Acciarri M
- Achard P
- Acton PD
- Acton PD
- Adam I
- Adam W
- Adriani O
- Adye T
- Adzic P
- Affholderbach K
- Agnew G
- Aguilar-Benitez M
- Ainsley C
- Ajaltouni Z
- Ajinenko I
- Akagi T
- Akesson PF
- Akimoto H
- Albrecht T
- Alcaraz J
- Alderweireld T
- Alekseev GD
- Alemanni G
- Alemany-Fernandez R
- Aleppo M
- Alexander G
- Allaby J
- Allen NJ
- Allison J
- Allmendinger T
- Allport PP
- Allport PP
- Almehed S
- Aloisio A
- Altekamp N
- Alviggi MG
- Amaldi U
- Amapane N
- Amaral P
- Amato S
- Ambrosi G
- Ametewee K
- Anagnostou G
- Anashkin E
- Anassontzis EG
- Anderhub H
- Anderson KJ
- Anderson S
- Andersson P
- Andreazza A
- Andreev VP
- Andringa S
- Angelescu T
- Anjos N
- Anselmo F
- Antilous P
- Antonelli A
- Antonelli M
- Antonelli M
- Apel WD
- Apollonio M
- Arcelli S
- Arefiev A
- Armitage JC
- Armstrong SR
- Arnoud Y
- Asai S
- Ash WW
- Ashby SF
- Ashton P
- Ask S
- Asman B
- Astbury A
- Aston D
- Aubert JJ
- Augustin JE
- Augustinus A
- Awunor O
- Axen D
- Azemoon T
- Aziz T
- Azuelos G
- Azzurri P
- Azzurri P
- Bacchetta N
- Badaud F
- Bagliesi G
- Bagnaia P
- Bahan GA
- Bailey I
- Baillon P
- Baines JTM
- Baird KG
- Bajo A
- Baksay G
- Baksay L
- Balandras A
- Baldew SV
- Ball AH
- Ball RC
- Ballestrero A
- Baltay C
- Bambade P
- Band HR
- Banerjee S
- Banerjee S
- Banks J
- Barakat MB
- Baranko GJ
- Barao F
- Barate R
- Barberio E
- Barberio E
- Barbiellini G
- Barbier R
- Barczyk A
- Bardin D
- Bardon O
- Barillari T
- Barillere R
- Barker G
- Barker GJ
- Barklow T
- Barklow TL
- Barlow RJ
- Barnett S
- Baroncelli A
- Barone L
- Bartalini P
- Bartoldus R
- Bashindzhagian GL
- Basile M
- Batalova N
- Batley RJ
- Battaglia M
- Battiston R
- Battiston R
- Baubillier M
- Bauer JM
- Bauerdick LAT
- Bay A
- Bazarko A
- Bazarko AO
- Bean A
- Beaudoin G
- Becattini F
- Bechtle P
- Bechtluft J
- Beck A
- Becker J
- Becker U
- Becker U
- Becks KH
- Beeston C
- Begalli M
- Behner F
- Behnke T
- Behrmann A
- Beilliere P
- Bell AN
- Bell KW
- Bell PJ
- Bella G
- Bellantoni L
- Bellerive A
- Bellodi G
- Bellucci L
- Belokopytov Y
- Belous K
- Ben-David R
- Ben-Haim E
- Benchouk C
- Bencivenni G
- Benekos N
- Benelli G
- Bentvelsen S
- Benvenuti A
- Benvenuti AC
- Berat C
- Berbeco R
- Berdugo J
- Berger R
- Berges P
- Berggren M
- Berkelman K
- Berlich P
- Berntzon L
- Bertelsen H
- Bertini D
- Bertrand D
- Bertucci B
- Besancon M
- Besson N
- Betev BL
- Bethke S
- Bettarini S
- Beuselinck R
- Bhattacharya S
- Bianchi F
- Biasini M
- Biasini M
- Biebel O
- Bienz T
- Bigi M
- Biglietti M
- Biland A
- Bilei GM
- Bilenky MS
- Binder U
- Binnie DM
- Bird F
- Bisello D
- Bizouard MA
- Black SN
- Blair GA
- Blaising JJ
- Blaylock G
- Blobel V
- Bloch D
- Bloch-Devaux B
- Blom M
- Blondel A
- Bloodworth IJ
- Bloomer JE
- Blucher E
- Bluj M
- Blumenschein U
- Blyth SC
- Bobbink BJ
- Boccali T
- Bock P
- Boden B
- Boeriu O
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- Trigger I
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- Yamartino JM
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- Yeaman A
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- Yellin SJ
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- Yurko M
- Yushchenko O
- Yuta H
- Zacek V
- Zachariadou K
- Zachariadou K
- Zacharov I
- Zaitsev A
- Zalewska A
- Zalewski P
- Zalite A
- Zalite Y
- Zapalac G
- Zavrtanik D
- Zdarko RW
- Zeitlin C
- Zeitnitz C
- Zer-Zion D
- Zerwas D
- Zeuner W
- Zevgolatakos E
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- Zhuang HL
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- Zichichi A
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- Zilizi G
- Zimin NI
- Zimmermann B
- Zintchenko A
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- Zucchelli GC
- Zumerle G
- Zupan M
- Publication venue
- SelectedWorks
- Publication date
- 20/10/2010
- Field of study
Precision electroweak measurements on the Z resonance
- Author
- Abbaneo D
- Abbiendi G
- Abdallah J
- Abe K
- Abe K
- Abe T
- Abreu P
- Abt I
- Acciarri M
- Achard P
- Acton PD
- Acton PD
- Adam I
- Adam W
- Adriani O
- Adye T
- Adzic P
- Affholderbach K
- Agnew G
- Aguilar-Benitez M
- Ainsley C
- Ajaltouni Z
- Ajinenko I
- Akagi T
- Akesson PF
- Akimoto H
- Albrecht T
- Alcaraz J
- Alderweireld T
- Alekseev GD
- Alemanni G
- Alemany-Fernandez R
- Aleppo M
- Alexander G
- Allaby J
- Allen NJ
- Allison J
- Allmendinger T
- Allport PP
- Allport PP
- Almehed S
- Aloisio A
- Altekamp N
- Alviggi MG
- Amaldi U
- Amapane N
- Amaral P
- Amato S
- Ambrosi G
- Ametewee K
- Anagnostou G
- Anashkin E
- Anassontzis EG
- Anderhub H
- Anderson KJ
- Anderson S
- Andersson P
- Andreazza A
- Andreev VP
- Andringa S
- Angelescu T
- Anjos N
- Anselmo F
- Antilous P
- Antonelli A
- Antonelli M
- Antonelli M
- Apel WD
- Apollonio M
- Arcelli S
- Arefiev A
- Armitage JC
- Armstrong SR
- Arnoud Y
- Asai S
- Ash WW
- Ashby SF
- Ashton P
- Ask S
- Asman B
- Astbury A
- Aston D
- Aubert JJ
- Augustin JE
- Augustinus A
- Awunor O
- Axen D
- Azemoon T
- Aziz T
- Azuelos G
- Azzurri P
- Azzurri P
- Bacchetta N
- Badaud F
- Bagliesi G
- Bagnaia P
- Bahan GA
- Bailey I
- Baillon P
- Baines JTM
- Baird KG
- Bajo A
- Baksay G
- Baksay L
- Balandras A
- Baldew SV
- Ball AH
- Ball RC
- Ballestrero A
- Baltay C
- Bambade P
- Band HR
- Banerjee S
- Banerjee S
- Banks J
- Barakat MB
- Baranko GJ
- Barao F
- Barate R
- Barberio E
- Barberio E
- Barbiellini G
- Barbier R
- Barczyk A
- Bardin D
- Bardon O
- Barillari T
- Barillere R
- Barker G
- Barker GJ
- Barklow T
- Barklow TL
- Barlow RJ
- Barnett S
- Baroncelli A
- Barone L
- Bartalini P
- Bartoldus R
- Bashindzhagian GL
- Basile M
- Batalova N
- Batley RJ
- Battaglia M
- Battiston R
- Battiston R
- Baubillier M
- Bauer JM
- Bauerdick LAT
- Bay A
- Bazarko A
- Bazarko AO
- Bean A
- Beaudoin G
- Becattini F
- Bechtle P
- Bechtluft J
- Beck A
- Becker J
- Becker U
- Becker U
- Becks KH
- Beeston C
- Begalli M
- Behner F
- Behnke T
- Behrmann A
- Beilliere P
- Bell AN
- Bell KW
- Bell PJ
- Bella G
- Bellantoni L
- Bellerive A
- Bellodi G
- Bellucci L
- Belokopytov Y
- Belous K
- Ben-David R
- Ben-Haim E
- Benchouk C
- Bencivenni G
- Benekos N
- Benelli G
- Bentvelsen S
- Benvenuti A
- Benvenuti AC
- Berat C
- Berbeco R
- Berdugo J
- Berger R
- Berges P
- Berggren M
- Berkelman K
- Berlich P
- Berntzon L
- Bertelsen H
- Bertini D
- Bertrand D
- Bertucci B
- Besancon M
- Besson N
- Betev BL
- Bethke S
- Bettarini S
- Beuselinck R
- Bhattacharya S
- Bianchi F
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- Rykaczewski H
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- Schotanus DJ
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- Schwiening J
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- Szumilo A
- Szumlak T
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- Taffard AC
- Tafirout R
- Takahashi T
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- Tomaradze A
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- Torrence E
- Torrence E
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- Towers S
- Toya D
- Tran P
- Trandafir AI
- Transtromer G
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- Travnicek P
- Trefzger T
- Treille D
- Tresilian NJ
- Tricomi A
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- Trigger I
- Tristram G
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- Trocme B
- Trocsanyi Z
- Trombini A
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- Turluer ML
- Turnbull RM
- Tyapkin IA
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- Tysarczyk-Niemeyer G
- Tzamarias S
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- Uvarov V
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- van Dalen JA
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- van der Aa O
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- Veszpremi V
- Vesztergombi G
- Vetlitsky I
- Vicinanza D
- Videau H
- Videau I
- Viertel G
- Vikas P
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- Villegas M
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- Virtue CJ
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- Vlasov E
- Vodopianov I
- Vodopyanov AS
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- Vorobyov AA
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- Wang XL
- Wang ZM
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- Ward JJ
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- Wermes N
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- Whalley MA
- Whitaker JS
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- White SL
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- Wiedenmann W
- Wiedenmann W
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- Williams DC
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- Williams SH
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- Wilson GW
- Wilson JA
- Wilson RJ
- Wingerter I
- Winter M
- Winterer VH
- Wisniewski WJ
- Witek M
- Wittlin JL
- Wlodek T
- Wlodek T
- Wolf G
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- Wood NC
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- Wu SL
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- Yamamoto RK
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- Yamartino JM
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- Yang BZ
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- Yang HJ
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- Young CC
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- Yushchenko O
- Yuta H
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- Zachariadou K
- Zacharov I
- Zaitsev A
- Zalewska A
- Zalewski P
- Zalite A
- Zalite Y
- Zapalac G
- Zavrtanik D
- Zdarko RW
- Zeitlin C
- Zeitnitz C
- Zer-Zion D
- Zerwas D
- Zeuner W
- Zevgolatakos E
- Zhang J
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- Zhang ZP
- Zhao J
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- Zhuravlov V
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- Zilizi G
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- Zimmermann B
- Zintchenko A
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- Zoller M
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- Zucchelli GC
- Zumerle G
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- Publication venue
- Publication date
- 01/01/2006
- Field of study