37 research outputs found
Direct CP Violation, Branching Ratios and Form Factors B→π, B→K in B Decays
- Author
- A W Thomas
- Abbaneo D (ALEPH Collaboration)
- Abe K
- Abe K (BELLE Collaboration)
- Aubert B (BABAR Collaboration)
- Aubert B (BABAR Collaboration)
- Aubert B (BABAR Collaboration)
- Aubert B (BABAR Collaboration)
- Aubert B (BABAR Collaboration)
- Aubert B (BABAR Collaboration)
- Aubert B (BABAR Collaboration)
- Aubert B (BABAR Collaboration)
- Ball P
- Ball P
- Bauer C W
- Bauer M
- Beneke M
- Beneke M
- Beneke M
- Beneke M Buchalla G Neubert M Sachrajda C T
- Bornheim A
- Buchalla G
- Buchalla G Safir A S
- Buras A J
- Buras A J
- Buras A J
- Cabibbo N
- Carter A B
- Charles J (CKMfitter Group Collaboration)
- Christenson J H
- Feldmann T
- Feldmann T
- Fleischer R
- Fleischer R
- Gardner S
- Gardner S
- Gardner S
- Gardner S
- Gardner S O'Connell H B Thomas A W
- Guo X H
- Guo X H
- Guo X-H Thomas A W Sevior M
- Huang H C (BELLE Collaboration)
- Keum Y Y
- Keum Y Y
- Keum Y Y Sanda A I
- Kobayashi M
- Leitner O
- Leitner O
- Li H N
- Novikov V A
- O Leitner
- O'Connell H B
- Quinn H R
- Sachrajda C T
- Sakurai J J
- Stech B
- Tomura T
- Wirbel M
- Wolfenstein L
- X-H Guo
- Publication venue
- 'IOP Publishing'
- Publication date
- 30/11/2004
- Field of study
The B→π and B→K transitions involved in hadronic B decays are
investigated in a phenomenological way through the framework of QCD
factorization. By comparing our results with experimental branching ratios from
the BELLE, BABAR and CLEO Collaborations for all the B decays including either
a pion or a kaon, we propose boundaries for the transition form factors B→π and B→K depending on the CKM matrix element parameters ρ and
η. From this analysis, the form factors required to reproduce the
experimental data for branching ratios are FB→π=0.31±0.12 and
FB→K=0.37±0.13. We calculate the direct CP violating asymmetry
parameter, aCP, for B→π+π−π and B→π+π−K decays, in the case where ρ−ω mixing effects are taken into
account. Based on these results, we find that the direct CP asymmetry for
B−→π+π−π−, Bˉ0→π+π−π0,
B−→π+π−K−, and Bˉ0→π+π−Kˉ0, reaches its maximum when the invariant mass π+π− is
in the vicinity of the ω meson mass. The inclusion of ρ−ω
mixing provides an opportunity to erase, without ambiguity, the phase
uncertainty mod(π) in the determination of the CKM angles α in case
of b→u and γ in case of b→s.Comment: 74 pages, 15 figures, 8 tables. A few misprints corrected, two
references adde
Rho-Omega Mixing and Direct CP Violation in Hadronic B-Decays
- Author
- A. Deandrea
- A. E. Snyder
- A. J. Buras
- A. J. Buras
- A. S. Dighe
- A. S. Dighe
- A. W. Thomas
- B. Costa de Beauregard
- D. Atwood
- D. Atwood
- D. Atwood
- F. Klingl
- G. Eilam
- G. Kramer
- H. B. O'Connell
- H. B. O'Connell
- H. J. Lipkin
- J. Gasser
- K. Maltman
- L. M. Barkov
- M. Bander
- M. Bauer
- M. Bauer
- M. Gronau
- M. Gronau
- N. G. Deshpande
- R. Enomoto
- R. Fleischer
- R. Fleischer
- R. Fleischer
- R. M. Barnett
- S. Gardner
- Y. Grossman
- Publication venue
- 'American Physical Society (APS)'
- Publication date
- 29/05/1997
- Field of study
The extraction of CKM-matrix-element information from hadronic B-decays
generally suffers from discrete ambiguities, hampering the diagnosis of physics
beyond the Standard Model. We show that a measurement of the rate asymmetry,
which is CP-violating, in
B±→ρ±ρ0(ω)→ρ±π+π−, where the
invariant mass of the π+π− pair is in the vicinity of the ω
resonance, can remove the mod(π) uncertainty in α≡arg[−VtdVtb∗/(VudVub∗)] present in standard analyses.Comment: 9 pages, REVTeX, 1 ps figure, major style changes, results unchange
Whole-genome sequencing reveals host factors underlying critical COVID-19
- Author
- Abd Elghafar M. S.
- Abdel-Aziz M.
- Abdelrazik M.
- Abdollahi H.
- Abdullah T.
- Abecasis G. R.
- Abedalthagafi M.
- Abel L.
- Abernathy C.
- Abraheem A.
- Abul-Husn N. S.
- Acquilini D.
- Adams C.
- Adams E. L.
- Adams K.
- Adamsara A.
- Adanini O.
- Adeleye O.
- Adra D.
- Afilalo J.
- Afilalo M.
- Afolabi D.
- Afrasiabi Z.
- Agasou A.
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- Akinkugbe O.
- Aksentijevich A.
- Al-Afghani H.
- Al-Awdah L.
- Alaamery M.
- Alahmadey Z. Z.
- Alaverdian D.
- Alavere H.
- Albader A.
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- Albesher N.
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- Aldridge J.
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- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 01/01/2022
- Field of study
Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease
Prognostic model to predict postoperative acute kidney injury in patients undergoing major gastrointestinal surgery based on a national prospective observational cohort study.
- Author
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- Abbas J
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- Abbott TEF
- Abdalla M
- Abdikadir H
- Abuhussein N
- Acquaah F
- Adamson R
- Adeleye O
- Adeogun A
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- Akhtar A
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- Leong SH
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- Oh SY
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- Omar I
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- Pakenham A
- Palaniappan SV
- Palazzo F
- Palkhi A
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- Pantelidou M
- Paraskeva B
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- Paterson HM
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- Patrick Y
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- Peakall L
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- Peiris GB
- Pek G
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- Pinkney TD
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- Poolovadoo Y
- Poonawala R
- Popat K
- Popova P
- Porter T
- Potluri S
- Potts S
- Powell B
- Powell C
- Powell-Chandler A
- Power A
- Powers N
- Prabakaran P
- Prabhudesai A
- Pradhan A
- Prakash R
- Pranesh N
- Pratumsuwan T
- Preece R
- Premakumar Y
- Price M
- Printz V
- Prior A
- Pronin S
- Prowle J
- Prudence-Taylor AJ
- Puddy H
- Pullinger M
- Punjabi N
- Pursnani K
- Qadeer A
- Qamar I
- Qamar MA
- Quek R
- Qureshi A
- Rabiu R
- Radford A
- Radhakrishnan A
- Radotra A
- Rafferty C
- Rafiq NM
- Raghuvir V
- Rahunathan N
- Rai A
- Raja M
- Rajagopal R
- Rajendran S
- Ramakrishnan D
- Ramanujam N
- Ramjas D
- Rammell J
- Ramsden J
- Ramwell A
- Rana S
- Randhawa R
- Rangarajan S
- Rao R
- Rashed F
- Ravi F
- Rayne T
- Razaq A
- Rea E
- Redgrave N
- Redmond A
- Reehal R
- Reeves T
- Regan H
- Reid F
- Reid N
- Rembacken R
- Renju M
- Renukanthan A
- Renwick P
- Reynolds J
- Reza N
- Richards C
- Richards T
- Richardson E
- Rickard L
- Rickards C
- Ridgway P
- Riley BJ
- Rimmer L
- Rinkoff S
- Riyat H
- Roberts B
- Roberts G
- Roberts J
- Robertson D
- Robinson A
- Robinson H
- Robinson K
- Robinson SD
- Rockall T
- Rodman L
- Roe T
- Rogers A
- Rogers D
- Roper L
- Roscoe HW
- Ross F
- Rothnie K
- Rothwell L
- Rotundo A
- Roy C
- Runkel M
- Rushd A
- Russell J
- Rutherford A
- Rutherford D
- Rutler L
- Ryan G
- Saad M
- Saat MI
- Sadanand KS
- Sadhra SS
- Sadiq S
- Saeed F
- Saggar S
- Sagoo H
- Saha A
- Sait MS
- Sait S
- Saito R
- Sajid M
- Salciccioli J
- Saleem H
- Salekin D
- Sales A
- Salman M
- Samaraweera S
- Sammut T
- Samuel R
- Sanders E
- Sandhu A
- Sandhu J
- Sandhu N
- Sandland-Taylor L
- Sangal P
- Sansome S
- Sarathy PP
- Saravanabavan S
- Sardar M
- Sarens N
- Sasapu K
- Sathiyakeerthy A
- Sattar M
- Sattar Z
- Saunders I
- Saunders M
- Sawers N
- Sawkins H
- Schade A
- Schinle P
- Schramm M
- Scotcher S
- Scott K
- Scott M
- Searle C
- Seehra H
- Seehra J
- Seelarbokus A
- Seetharam P
- Sellahewa C
- Selvadurai S
- Sen P
- Seraj SS
- Serry M
- Seth I
- Sethi R
- Shafi A
- Shafiq N
- Shaid M
- Shaman S
- Shang E
- Sharif I
- Sharkey E
- Sharma A
- Sharma E
- Sharma S
- Shaw A
- Shaw C
- Sheik-Ali S
- Sheikh A
- Sheikh S
- Sheikh Z
- Shergill M
- Shergill S
- Sherlock J
- Shields P
- Shingles C
- Shirazi S
- Shurovi BN
- Siddiqui A
- Siddiqui I
- Silke E
- Sim DPY
- Sim R
- Simmonds L
- Simon A
- Simpson L
- Simpson R
- Sinclair E
- Singagireson S
- Singh K
- Singh KKR
- Sinha C
- Sivagnanasithiyar T
- Sivakumar C
- Sivakumar R
- Skulsky S
- Slade G
- Slade RD
- Sleight S
- Small S
- Smallwood J
- Smart B
- Smart G
- Smart YW
- Smith ACD
- Smith C
- Smith F
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- Smith J
- Smith M
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- Sonagara V
- Song A
- Soonawalla Z
- Soor P
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- Spiers H
- Spoor H
- Springford LR
- Srikanthan M
- Sriram A
- Stageman N
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- Stanger S
- Stanier P
- STARSurg Collaborative Writing Committee, Data analysis, Steering committee, Advisory group, Regional leads, Collaborators and validators
- STARSurg Collaborative Writing Committee, Data analysis, Steering committee, Advisory group, Regional leads, Collaborators and validators, Nepogodiev, D
- Stechman M
- Stewart D
- Stewart E
- Stewart H
- Stewart R
- Stickler E
- Stoddart MT
- Stokes E
- Stott G
- Strang S
- Stringer H
- Stringfellow TD
- Stubbing-Moore A
- Sturrock S
- Subar D
- Subratty SM
- Sukirthan N
- Sukumar S
- Sulaiman SK
- Sultan S
- Sun L
- Sundaram K
- Suresh R
- Suresh S
- Sureshkumar A
- Suri A
- Svolkinas D
- Swan A
- Swan I
- Swaray A
- Swartbol T
- Symons L
- Szczap A
- Szuman A
- Tailor S
- Tam J
- Tam JP
- Tan CY
- Tan KL
- Tan L
- Tan LC
- Tan S
- Tan TSE
- Tang A
- Tang M
- Tanna A
- Taribagil P
- Tariq A
- Tate S
- Tayeh S
- Taylor K
- Taylor O
- Taylor R
- Taylor Z
- Telfer R
- Teng T
- Tenters F
- Teo R
- Thachettu A
- Thakrar D
- Thatcher A
- Theodoropoulou K
- Thomas A
- Thomas D
- Thomas M
- Thomas O
- Thomas S
- Thompson G
- Thompson J
- Thoms BL
- Thomson F
- Thorley N
- Thorn C
- Thornton T
- Thorpe O
- Tilliridou V
- Titu L
- Tod N
- Toellner H
- Toh C
- Toma T
- Tonks A
- Torrance HD
- Townsend D
- Traish M
- Trenear R
- Tresidder S
- Trevett J
- Triniman MC
- Trotter M
- Tsang JCH
- Tsang K
- Tseu B
- Tsui A
- Tullett A
- Tummon R
- Turlejski T
- Turner J
- Turner S
- Tyson N
- Ubhi HK
- Ujjal S
- Underhill R
- Vadgama N
- Vaidya A
- Vakharia A
- Van Den Berg N
- Van der Laan S
- Van Winsen K
- Vara S
- Varathan Y
- Varatharasasingam K
- Varcada M
- Vaughan R
- Vella-Baldacchino M
- Ventre C
- Venturini S
- Verma N
- Vernet G
- Victor L
- Vig S
- Vine M
- Vipond M
- Virani N
- Vizor R
- Vyas M
- Wadood Q
- Waite K
- Wakeford W
- Walford B
- Walker EY
- Walker G
- Walker K
- Walker L
- Walker NR
- Walls L
- Walsh T
- Wang H
- Wang L
- Wang X
- Ward AE
- Ward J
- Ward N
- Ward T
- Warren L
- Warren O
- Warusavitarne J
- Waterman A
- Waters S
- Watkinson G
- Watson L
- Watson N
- Waugh D
- Wayman J
- Webb E
- Webb R
- Weegenaar C
- Wei R
- Welsh K
- Whewell H
- Whitcroft I
- White C
- White F
- White P
- Whitham R
- Whyte M
- Widdison A
- Wiffen L
- Wigley C
- Wijeyaratne M
- Williams C
- Williams G
- Williams H
- Williams I
- Williams LM
- Williams P
- Williams S
- Wilson H
- Wilson J
- Wilson R
- Wilson V
- Wimalathasan A
- Woin E
- Wong C
- Wong E
- Wong J
- Wong MHY
- Wood CM
- Woodhams K
- Woolley A
- Wootton E
- Worley E
- Worsfold M
- Wright OW
- Wright R
- Wright S
- Wroe N
- Wynell-Mayow W
- Xu Y
- Yahaya AA
- Yalamarthi S
- Yang DD
- Yang N
- Yap J
- Yardimci E
- Yarham E
- Yasin IH
- Yasin T
- Yates J
- Ye W
- Yeo A
- Yeoh T
- Yeung J
- Yin ZD
- Yip J
- Yoganayagam N
- Yogeswara T
- York J
- Yousaf A
- Youssef H
- Yu T
- Yule A
- Zaat S
- Zanichelli D
- Zaver V
- Zeng R
- Zhang Y
- Zheleniakova T
- Zhu Y
- Zornoza A
- Zubikarai G
- Zulkifli A
- Zuzarte L
- Publication venue
- 'Wiley'
- Publication date
- 18/05/2018
- Field of study
Background: Acute illness, existing co-morbidities and surgical stress response can all contribute to postoperative acute kidney injury (AKI) in patients undergoing major gastrointestinal surgery. The aim of this study was prospectively to develop a pragmatic prognostic model to stratify patients according to risk of developing AKI after major gastrointestinal surgery. Methods: This prospective multicentre cohort study included consecutive adults undergoing elective or emergency gastrointestinal resection, liver resection or stoma reversal in 2-week blocks over a continuous 3-month period. The primary outcome was the rate of AKI within 7 days of surgery. Bootstrap stability was used to select clinically plausible risk factors into the model. Internal model validation was carried out by bootstrap validation. Results: A total of 4544 patients were included across 173 centres in the UK and Ireland. The overall rate of AKI was 14·2 per cent (646 of 4544) and the 30-day mortality rate was 1·8 per cent (84 of 4544). Stage 1 AKI was significantly associated with 30-day mortality (unadjusted odds ratio 7·61, 95 per cent c.i. 4·49 to 12·90; P < 0·001), with increasing odds of death with each AKI stage. Six variables were selected for inclusion in the prognostic model: age, sex, ASA grade, preoperative estimated glomerular filtration rate, planned open surgery and preoperative use of either an angiotensin-converting enzyme inhibitor or an angiotensin receptor blocker. Internal validation demonstrated good model discrimination (c-statistic 0·65). Discussion: Following major gastrointestinal surgery, AKI occurred in one in seven patients. This preoperative prognostic model identified patients at high risk of postoperative AKI. Validation in an independent data set is required to ensure generalizability
Recommended from our members
Common genetic variants in the CLDN2 and PRSS1-PRSS2 loci alter risk for alcohol-related and sporadic pancreatitis
- Author
- Albert Marilyn S.
- Albin Roger L.
- Alkaade Samer
- Amann Stephen T.
- Anderson Michelle A.
- Apostolova Liana G.
- Arnold Steven E.
- Baillie John
- Baldwin Clinton T.
- Banks Peter A.
- Barber Robert
- Barmada M. Michael
- Barnes Lisa L.
- Beach Thomas G.
- Beecham Gary W.
- Beekly Duane
- Bennett David A.
- Bigio Eileen H.
- Bird Thomas D.
- Blacker Deborah
- Boxer Adam
- Brand Randall E.
- Burke James R.
- Buxbaum Joseph D.
- Cairns Nigel J.
- Cantwell Laura B.
- Cao Chuanhai
- Carney Regina M.
- Carroll Steven L.
- Chui Helena C.
- Clark David G.
- Conwell Darwin
- Cotton Peter B.
- Coté Gregory A.
- Cribbs David H.
- Crocco Elizabeth A.
- Cruchaga Carlos
- DeCarli Charles
- Demirci F. Yesim
- Devlin Bernie
- Dick Malcolm
- Dickson Dennis W.
- DiSario James
- Duara Ranjan
- Ertekin-Taner Nilufer
- Faber Kelley M.
- Fallon Kenneth B.
- Farlow Martin R.
- Farrer Lindsay A.
- Ferris Steven
- Foroud Tatiana M.
- Forsmark Chris E.
- Frosch Matthew P.
- Galasko Douglas R.
- Ganguli Mary
- Gardner Timothy B.
- Gearing Marla
- Gelrud Andres
- Geschwind Daniel H.
- Ghetti Bernardino
- Gilbert John R.
- Gilman Sid
- Glass Jonathan D.
- Goate Alison M.
- Graff-Radford Neill R.
- Green Robert C.
- Greenhalf William
- Growdon John H.
- Guda Nalini M.
- Haines Jonathan L.
- Hakonarson Hakon
- Hamilton Ronald L.
- Hamilton-Nelson Kara L.
- Harrell Lindy E.
- Hartman Douglas J.
- Hawes Robert A.
- Head Elizabeth
- Honig Lawrence S.
- Hulette Christine M.
- Hyman Bradley T.
- Jicha Gregory A.
- Jin Lee-Way
- Johnstone Marianne
- Jun Gyungah
- Kamboh M. Ilyas
- Karydas Anna
- Kaye Jeffrey A.
- Kienholz Michelle L.
- Kim Ronald
- Klei Lambertus
- Koo Edward H.
- Kowall Neil W.
- Kramer Joel H.
- Kramer Patricia
- Krasinskas Alyssa M.
- Kukull Walter A.
- LaFerla Frank M.
- Lah James J.
- LaRusch Jessica
- Lawrence Christopher
- Lerch Markus M.
- Leverenz James B.
- Levey Allan I.
- Lewis Michele
- Li Ge
- Lieberman Andrew P.
- Lin Chiao-Feng
- Lopez Oscar L.
- Lunetta Kathryn L.
- Lyketsos Constantine G.
- Mack Wendy J.
- Marson Daniel C.
- Martin Eden R.
- Martiniuk Frank
- Mash Deborah C.
- Masliah Eliezer
- Mayerle Julia
- Mayeux Richard
- McKee Ann C.
- Melhem Nadine M.
- Mesulam Marsel
- Miller Bruce L.
- Miller Carol A.
- Miller Joshua W.
- Money Mary E.
- Montine Thomas J.
- Morris John C.
- Muniraj Thiruvengadam
- Murrell Jill R.
- Naj Adam C.
- Neoptolemos John P.
- O'Connell Michael R.
- Olichney John M.
- Orlichenko Lidiya
- Papachristou Georgios I.
- Parisi Joseph E.
- Pericak-Vance Margaret A.
- Peskind Elaine
- Petersen Ronald C.
- Pierce Aimee
- Poon Wayne W.
- Potter Huntington
- Quinn Joseph F.
- Raj Ashok
- Raskind Murray
- Reiman Eric M.
- Reisberg Barry
- Reitz Christiane
- Ringman John M.
- Roberson Erik D.
- Roeder Kathryn
- Romagnuolo Joseph
- Rosen Howard J.
- Rosenberg Roger N.
- Sandhu Bimaljit S.
- Sano Mary
- Saykin Andrew J.
- Schellenberg Gerard D.
- Schneider Julie A.
- Schneider Lon S.
- Seeley William W.
- Sherman Stuart
- Simon Peter
- Singh Vijay K.
- Slivka Adam
- Smith Amanda G.
- Smith Jill P.
- Sonnen Joshua A.
- Spina Salvatore
- Stern Robert A.
- Stolz Donna
- Sutton Robert
- Tanzi Rudolph E.
- Tector Matt
- Trojanowski John Q.
- Troncoso Juan C.
- Tsuang Debby W.
- Valladares Otto
- Van Deerlin Vivianna M.
- Van Eldik Linda J.
- Vardarajan Badri N.
- Vinters Harry V.
- Vonsattel Jean Paul
- Wang Li-San
- Weintraub Sandra
- Weiss Frank Ulrich
- Welsh-Bohmer Kathleen A.
- Whitcomb David C.
- Wilcox C. Mel
- Williamson Jennifer
- Wisniewski Stephen R.
- Woltjer Randall L.
- Wright Clinton B.
- Yadav Dhiraj
- Younkin Steven G.
- Yu Chang-En
- Yu Lei
- Zarnescu Narcis Octavian
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 13/02/2014
- Field of study
Pancreatitis is a complex, progressively destructive inflammatory disorder. Alcohol was long thought to be the primary causative agent, but genetic contributions have been of interest since the discovery that rare PRSS1, CFTR, and SPINK1 variants were associated with pancreatitis risk. We now report two significant genome-wide associations identified and replicated at PRSS1-PRSS2 (1×10-12) and x-linked CLDN2 (p < 1×10-21) through a two-stage genome-wide study (Stage 1, 676 cases and 4507 controls; Stage 2, 910 cases and 4170 controls). The PRSS1 variant affects susceptibility by altering expression of the primary trypsinogen gene. The CLDN2 risk allele is associated with atypical localization of claudin-2 in pancreatic acinar cells. The homozygous (or hemizygous male) CLDN2 genotype confers the greatest risk, and its alleles interact with alcohol consumption to amplify risk. These results could partially explain the high frequency of alcohol-related pancreatitis in men – male hemizygous frequency is 0.26, female homozygote is 0.07
Global burden and strength of evidence for 88 risk factors in 204 countries and 811 subnational locations, 1990–2021: a systematic analysis for the Global Burden of Disease Study 2021
- Author
- Abate K.H.
- Abate Y.H.
- Abbafati C.
- Abbasgholizadeh R.
- Abbasi M.A.
- Abbasi-Kangevari M.
- Abbasian M.
- Abbasifard M.
- Abd ElHafeez S.
- Abd-Elsalam S.
- Abdi P.
- Abdollahi M.
- Abdoun M.
- Abdulah D.M.
- Abdullahi A.
- Abebe M.
- Abedi A.
- Abedi A.
- Abegaz T.M.
- Abeldaño Zuñiga R.A.
- Abiodun O.
- Abiso T.L.
- Aboagye R.G.
- Abolhassani H.
- Abouzid M.
- Aboye G.B.
- Abreu L.G.
- Abu-Gharbieh E.
- Abu-Zaid A.
- Abualruz H.
- Abubakar B.
- Abukhadijah H.J.J.
- Aburuz S.
- Adane M.M.
- Addo I.Y.
- Addolorato G.
- Adedoyin R.A.
- Adekanmbi V.
- Aden B.
- Adetunji J.B.
- Adeyeoluwa T.E.
- Adha R.
- Adibi A.
- Adnani Q.E.S.
- Adzigbli L.A.
- Afolabi A.A.
- Afolabi R.F.
- Afshin A.
- Afyouni S.
- Afzal M.S.
- Afzal S.
- Agampodi S.B.
- Agbozo F.
- Aghamiri S.
- Agodi A.
- Agrawal A.
- Agyemang-Duah W.
- Ahinkorah B.O.
- Ahmad A.
- Ahmad D.
- Ahmad F.
- Ahmad N.
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- Zyoud S.H.
- Ärnlöv J.
- Publication venue
- Elsevier BV
- Publication date
- 16/05/2024
- Field of study
Background: Understanding the health consequences associated with exposure to risk factors is necessary to inform public health policy and practice. To systematically quantify the contributions of risk factor exposures to specific health outcomes, the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2021 aims to provide comprehensive estimates of exposure levels, relative health risks, and attributable burden of disease for 88 risk factors in 204 countries and territories and 811 subnational locations, from 1990 to 2021. Methods: The GBD 2021 risk factor analysis used data from 54 561 total distinct sources to produce epidemiological estimates for 88 risk factors and their associated health outcomes for a total of 631 risk–outcome pairs. Pairs were included on the basis of data-driven determination of a risk–outcome association. Age-sex-location-year-specific estimates were generated at global, regional, and national levels. Our approach followed the comparative risk assessment framework predicated on a causal web of hierarchically organised, potentially combinative, modifiable risks. Relative risks (RRs) of a given outcome occurring as a function of risk factor exposure were estimated separately for each risk–outcome pair, and summary exposure values (SEVs), representing risk-weighted exposure prevalence, and theoretical minimum risk exposure levels (TMRELs) were estimated for each risk factor. These estimates were used to calculate the population attributable fraction (PAF; ie, the proportional change in health risk that would occur if exposure to a risk factor were reduced to the TMREL). The product of PAFs and disease burden associated with a given outcome, measured in disability-adjusted life-years (DALYs), yielded measures of attributable burden (ie, the proportion of total disease burden attributable to a particular risk factor or combination of risk factors). Adjustments for mediation were applied to account for relationships involving risk factors that act indirectly on outcomes via intermediate risks. Attributable burden estimates were stratified by Socio-demographic Index (SDI) quintile and presented as counts, age-standardised rates, and rankings. To complement estimates of RR and attributable burden, newly developed burden of proof risk function (BPRF) methods were applied to yield supplementary, conservative interpretations of risk–outcome associations based on the consistency of underlying evidence, accounting for unexplained heterogeneity between input data from different studies. Estimates reported represent the mean value across 500 draws from the estimate's distribution, with 95% uncertainty intervals (UIs) calculated as the 2·5th and 97·5th percentile values across the draws. Findings: Among the specific risk factors analysed for this study, particulate matter air pollution was the leading contributor to the global disease burden in 2021, contributing 8·0% (95% UI 6·7–9·4) of total DALYs, followed by high systolic blood pressure (SBP; 7·8% [6·4–9·2]), smoking (5·7% [4·7–6·8]), low birthweight and short gestation (5·6% [4·8–6·3]), and high fasting plasma glucose (FPG; 5·4% [4·8–6·0]). For younger demographics (ie, those aged 0–4 years and 5–14 years), risks such as low birthweight and short gestation and unsafe water, sanitation, and handwashing (WaSH) were among the leading risk factors, while for older age groups, metabolic risks such as high SBP, high body-mass index (BMI), high FPG, and high LDL cholesterol had a greater impact. From 2000 to 2021, there was an observable shift in global health challenges, marked by a decline in the number of all-age DALYs broadly attributable to behavioural risks (decrease of 20·7% [13·9–27·7]) and environmental and occupational risks (decrease of 22·0% [15·5–28·8]), coupled with a 49·4% (42·3–56·9) increase in DALYs attributable to metabolic risks, all reflecting ageing populations and changing lifestyles on a global scale. Age-standardised global DALY rates attributable to high BMI and high FPG rose considerably (15·7% [9·9–21·7] for high BMI and 7·9% [3·3–12·9] for high FPG) over this period, with exposure to these risks increasing annually at rates of 1·8% (1·6–1·9) for high BMI and 1·3% (1·1–1·5) for high FPG. By contrast, the global risk-attributable burden and exposure to many other risk factors declined, notably for risks such as child growth failure and unsafe water source, with age-standardised attributable DALYs decreasing by 71·5% (64·4–78·8) for child growth failure and 66·3% (60·2–72·0) for unsafe water source. We separated risk factors into three groups according to trajectory over time: those with a decreasing attributable burden, due largely to declining risk exposure (eg, diet high in trans-fat and household air pollution) but also to proportionally smaller child and youth populations (eg, child and maternal malnutrition); those for which the burden increased moderately in spite of declining risk exposure, due largely to population ageing (eg, smoking); and those for which the burden increased considerably due to both increasing risk exposure and population ageing (eg, ambient particulate matter air pollution, high BMI, high FPG, and high SBP). Interpretation: Substantial progress has been made in reducing the global disease burden attributable to a range of risk factors, particularly those related to maternal and child health, WaSH, and household air pollution. Maintaining efforts to minimise the impact of these risk factors, especially in low SDI locations, is necessary to sustain progress. Successes in moderating the smoking-related burden by reducing risk exposure highlight the need to advance policies that reduce exposure to other leading risk factors such as ambient particulate matter air pollution and high SBP. Troubling increases in high FPG, high BMI, and other risk factors related to obesity and metabolic syndrome indicate an urgent need to identify and implement interventions. Funding: Bill & Melinda Gates Foundation
Global burden and strength of evidence for 88 risk factors in 204 countries and 811 subnational locations, 1990–2021: a systematic analysis for the Global Burden of Disease Study 2021
- Author
- Abate Kalkidan Hassen
- Abate Yohannes Habtegiorgis
- Abbafati Cristiana
- Abbasgholizadeh Rouzbeh
- Abbasi Madineh Akram
- Abbasi-Kangevari Mohsen
- Abbasian Mohammadreza
- Abbasifard Mitra
- Abd ElHafeez Samar
- Abd-Elsalam Sherief
- Abdi Parsa
- Abdollahi Mohammad
- Abdoun Meriem
- Abdulah Deldar Morad
- Abdullahi Auwal
- Abebe Mesfin
- Abedi Aidin
- Abedi Armita
- Abegaz Tadesse M
- Abeldaño Zuñiga Roberto Ariel
- Abiodun Olumide
- Abiso Temesgen Lera
- Aboagye Richard Gyan
- Abolhassani Hassan
- Abouzid Mohamed
- Aboye Girma Beressa
- Abreu Lucas Guimarães
- Abu-Gharbieh Eman
- Abu-Zaid Ahmed
- Abualruz Hasan
- Abubakar Bilyaminu
- Abukhadijah Hana Jihad Jihad
- Aburuz Salahdein
- Adane Mesafint Molla
- Addo Isaac Yeboah
- Addolorato Giovanni
- Adedoyin Rufus Adesoji
- Adekanmbi Victor
- Aden Bashir
- Adetunji Juliana Bunmi
- Adeyeoluwa Temitayo Esther
- Adha Rishan
- Adibi Amin
- Adnani Qorinah Estiningtyas Sakilah
- Adzigbli Leticia Akua
- Afolabi Aanuoluwapo Adeyimika
- Afolabi Rotimi Felix
- Afshin Ashkan
- Afyouni Shadi
- Afzal Muhammad Sohail
- Afzal Saira
- Agampodi Suneth Buddhika
- Agbozo Faith
- Aghamiri Shahin
- Agodi Antonella
- Agrawal Anurag
- Agyemang-Duah Williams
- Ahinkorah Bright Opoku
- Ahmad Aqeel
- Ahmad Danish
- Ahmad Firdos
- Ahmad Noah
- Ahmad Shahzaib
- Ahmad Tauseef
- Ahmed Ali
- Ahmed Anisuddin
- Ahmed Ayman
- Ahmed Luai A
- Ahmed Muktar Beshir
- Ahmed Safoora
- Ahmed Syed Anees
- Ajami Marjan
- Akalu Gizachew Taddesse
- Akara Essona Matatom
- Akbarialiabad Hossein
- Akhlaghi Shiva
- Akinosoglou Karolina
- Akinyemiju Tomi
- Akkaif Mohammed Ahmed
- Akkala Sreelatha
- Akombi-Inyang Blessing
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- Yi Siyan
- Yigzaw Zeamanuel Anteneh
- Yiğit Arzu
- Yin Dehui
- Yip Paul
- Yismaw Malede Berihun
- Yon Dong Keon
- Yonemoto Naohiro
- You Yuyi
- Younis Mustafa Z
- Yousefi Zabihollah
- Yu Chuanhua
- Yu Yong
- Zadey Siddhesh
- Zadnik Vesna
- Zakham Fathiah
- Zaki Nazar
- Zakzuk Josefina
- Zamagni Giulia
- Zaman Sojib Bin
- Zandieh Ghazal G Z
- Zanghì Aurora
- Zar Heather J
- Zare Iman
- Zarimeidani Fatemeh
- Zastrozhin Mikhail Sergeevich
- Zeng Youjie
- Zhai Chunxia
- Zhang Anthony Lin
- Zhang Haijun
- Zhang Liqun
- Zhang Meixin
- Zhang Yunquan
- Zhang Zhenyu
- Zhang Zhi-Jiang
- Zhao Hanqing
- Zhao Jeff T
- Zhao Xiu-Ju George
- Zhao Yang
- Zhao Yong
- Zheng Peng
- Zhong Chenwen
- Zhou Jingjing
- Zhou Juexiao
- Zhou Shangcheng
- Zhu Bin
- Zhu Lei
- Zhu Zhaohua
- Ziaeian Boback
- Ziafati Makan
- Zielińska Magdalena
- Zimsen Stephanie R M
- Zoghi Ghazal
- Zoller Thomas
- Zumla Alimuddin
- Zyoud Sa'ed H
- Zyoud Samer H
- Publication venue
- Publication date
- 01/01/2024
- Field of study
Background: Understanding the health consequences associated with exposure to risk factors is necessary to inform public health policy and practice. To systematically quantify the contributions of risk factor exposures to specific health outcomes, the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2021 aims to provide comprehensive estimates of exposure levels, relative health risks, and attributable burden of disease for 88 risk factors in 204 countries and territories and 811 subnational locations, from 1990 to 2021. Methods: The GBD 2021 risk factor analysis used data from 54 561 total distinct sources to produce epidemiological estimates for 88 risk factors and their associated health outcomes for a total of 631 risk–outcome pairs. Pairs were included on the basis of data-driven determination of a risk–outcome association. Age-sex-location-year-specific estimates were generated at global, regional, and national levels. Our approach followed the comparative risk assessment framework predicated on a causal web of hierarchically organised, potentially combinative, modifiable risks. Relative risks (RRs) of a given outcome occurring as a function of risk factor exposure were estimated separately for each risk–outcome pair, and summary exposure values (SEVs), representing risk-weighted exposure prevalence, and theoretical minimum risk exposure levels (TMRELs) were estimated for each risk factor. These estimates were used to calculate the population attributable fraction (PAF; ie, the proportional change in health risk that would occur if exposure to a risk factor were reduced to the TMREL). The product of PAFs and disease burden associated with a given outcome, measured in disability-adjusted life-years (DALYs), yielded measures of attributable burden (ie, the proportion of total disease burden attributable to a particular risk factor or combination of risk factors). Adjustments for mediation were applied to account for relationships involving risk factors that act indirectly on outcomes via intermediate risks. Attributable burden estimates were stratified by Socio-demographic Index (SDI) quintile and presented as counts, age-standardised rates, and rankings. To complement estimates of RR and attributable burden, newly developed burden of proof risk function (BPRF) methods were applied to yield supplementary, conservative interpretations of risk–outcome associations based on the consistency of underlying evidence, accounting for unexplained heterogeneity between input data from different studies. Estimates reported represent the mean value across 500 draws from the estimate's distribution, with 95% uncertainty intervals (UIs) calculated as the 2·5th and 97·5th percentile values across the draws. Findings: Among the specific risk factors analysed for this study, particulate matter air pollution was the leading contributor to the global disease burden in 2021, contributing 8·0% (95% UI 6·7–9·4) of total DALYs, followed by high systolic blood pressure (SBP; 7·8% [6·4–9·2]), smoking (5·7% [4·7–6·8]), low birthweight and short gestation (5·6% [4·8–6·3]), and high fasting plasma glucose (FPG; 5·4% [4·8–6·0]). For younger demographics (ie, those aged 0–4 years and 5–14 years), risks such as low birthweight and short gestation and unsafe water, sanitation, and handwashing (WaSH) were among the leading risk factors, while for older age groups, metabolic risks such as high SBP, high body-mass index (BMI), high FPG, and high LDL cholesterol had a greater impact. From 2000 to 2021, there was an observable shift in global health challenges, marked by a decline in the number of all-age DALYs broadly attributable to behavioural risks (decrease of 20·7% [13·9–27·7]) and environmental and occupational risks (decrease of 22·0% [15·5–28·8]), coupled with a 49·4% (42·3–56·9) increase in DALYs attributable to metabolic risks, all reflecting ageing populations and changing lifestyles on a global scale. Age-standardised global DALY rates attributable to high BMI and high FPG rose considerably (15·7% [9·9–21·7] for high BMI and 7·9% [3·3–12·9] for high FPG) over this period, with exposure to these risks increasing annually at rates of 1·8% (1·6–1·9) for high BMI and 1·3% (1·1–1·5) for high FPG. By contrast, the global risk-attributable burden and exposure to many other risk factors declined, notably for risks such as child growth failure and unsafe water source, with age-standardised attributable DALYs decreasing by 71·5% (64·4–78·8) for child growth failure and 66·3% (60·2–72·0) for unsafe water source. We separated risk factors into three groups according to trajectory over time: those with a decreasing attributable burden, due largely to declining risk exposure (eg, diet high in trans-fat and household air pollution) but also to proportionally smaller child and youth populations (eg, child and maternal malnutrition); those for which the burden increased moderately in spite of declining risk exposure, due largely to population ageing (eg, smoking); and those for which the burden increased considerably due to both increasing risk exposure and population ageing (eg, ambient particulate matter air pollution, high BMI, high FPG, and high SBP). Interpretation: Substantial progress has been made in reducing the global disease burden attributable to a range of risk factors, particularly those related to maternal and child health, WaSH, and household air pollution. Maintaining efforts to minimise the impact of these risk factors, especially in low SDI locations, is necessary to sustain progress. Successes in moderating the smoking-related burden by reducing risk exposure highlight the need to advance policies that reduce exposure to other leading risk factors such as ambient particulate matter air pollution and high SBP. Troubling increases in high FPG, high BMI, and other risk factors related to obesity and metabolic syndrome indicate an urgent need to identify and implement interventions
Mapping the human genetic architecture of COVID-19
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- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 01/01/2021
- Field of study
The genetic make-up of an individual contributes to the susceptibility and response to viral infection. Although environmental, clinical and social factors have a role in the chance of exposure to SARS-CoV-2 and the severity of COVID-191,2, host genetics may also be important. Identifying host-specific genetic factors may reveal biological mechanisms of therapeutic relevance and clarify causal relationships of modifiable environmental risk factors for SARS-CoV-2 infection and outcomes. We formed a global network of researchers to investigate the role of human genetics in SARS-CoV-2 infection and COVID-19 severity. Here we describe the results of three genome-wide association meta-analyses that consist of up to 49,562 patients with COVID-19 from 46 studies across 19 countries. We report 13 genome-wide significant loci that are associated with SARS-CoV-2 infection or severe manifestations of COVID-19. Several of these loci correspond to previously documented associations to lung or autoimmune and inflammatory diseases3–7. They also represent potentially actionable mechanisms in response to infection. Mendelian randomization analyses support a causal role for smoking and body-mass index for severe COVID-19 although not for type II diabetes. The identification of novel host genetic factors associated with COVID-19 was made possible by the community of human genetics researchers coming together to prioritize the sharing of data, results, resources and analytical frameworks. This working model of international collaboration underscores what is possible for future genetic discoveries in emerging pandemics, or indeed for any complex human disease
Climate Change and the Integrity of Science
- Author
- A. Bax
- A. Cazenave
- A. Fersht
- A. J. Bebbington
- A. J. Ciechanover
- A. K. Romney
- A. Kerr
- A. Klug
- A. L. Mabogunje
- A. Landy
- A. R. Cashmore
- A. Salmond
- A. T. Brunger
- A. T. Jagendorf
- A. Walker
- B. A. Larkins
- B. Asfaw
- B. D. Smith
- B. F. Reskin
- B. H. Singer
- B. Hille
- B. Moss
- B. Skyrms
- C. D. Michener
- C. Dean
- C. Frieden
- C. H. Langmuir
- C. J. R. Garrett
- C. J. Shatz
- C. O. Lovejoy
- C. S. Cox
- C. S. Goodman
- C. S. Jencks
- C. S. Spencer
- C. Wu
- C. Wunsch
- D. B. Wake
- D. Branton
- D. E. Canfield
- D. E. Clapham
- D. H. Janzen
- D. H. Thomas
- D. J. Anderson
- D. J. Derosier
- D. J. Futuyma
- D. J. Meltzer
- D. Kennedy
- D. L. Hartl
- D. M. Crothers
- D. M. Hunten
- D. P. Delmer
- D. R. Davies
- D. R. Piperno
- D. S. Massey
- D. W. Russell
- D. W. Schindler
- D. Weigel
- E. A. Boyle
- E. Anders
- E. B. Cowling
- E. B. Leopold
- E. B. Watson
- E. Blackburn
- E. F. Delong
- E. H. Fischer
- E. L. Miles
- E. L. Simons
- E. M. Conwell
- E. Medina
- E. Ostrom
- E. S. Mosley-Thompson
- E. W. Nester
- F. J. Ayala
- F. M. M. Morel
- F. S. Chapin
- F. Sherman
- G. A. Petsko
- G. B. Dalrymple
- G. B. Nair
- G. Bell
- G. C. Daily
- G. E. Likens
- G. F. Oster
- G. Feher
- G. H. Pettengill
- G. Hammel
- G. M. Woodwell
- G. S. Khush
- H. A. Mooney
- H. E. Wright
- H. J. Melosh
- H. Kornberg
- H. R. Kaback
- I. A. Izquierdo
- I. Fridovich
- J. A. Ferejohn
- J. A. Sabloff
- J. A. Wood
- J. C. Carrington
- J. C. Castilla
- J. C. Lagarias
- J. C. McWilliams
- J. Cairns
- J. D. Roberts
- J. Deisenhofer
- J. E. Blamont
- J. E. Dixon
- J. E. Kutzbach
- J. E. Walker
- J. F. O'Connell
- J. Frank
- J. H. Brown
- J. L. Bennetzen
- J. L. Dangl
- J. L. van Etten
- J. Lippincott-Schwartz
- J. M. Hayes
- J. Marcus
- J. Nathans
- J. P. Klinman
- J. Pedlosky
- J. R. Sanes
- J. S. Boyer
- J. S. House
- J. S. Valentine
- J. Schellnhuber
- J. Schmitt
- J. Terborgh
- J. W. Valentine
- K. A. Emanuel
- K. B. Strier
- K. E. van Holde
- K. Hawkes
- K. Kirk
- K. Lambeck
- K. Sieh
- K. V. Flannery
- L. E. Anselin
- L. G. Thompson
- L. Knopoff
- L. Lorand
- M. B. Davis
- M. D. Coe
- M. D. Sahlins
- M. F. Singer
- M. G. Kivelson
- M. G. Rossmann
- M. G. Turner
- M. Goodman
- M. Hout
- M. J. Donoghue
- M. J. West-Eberhard
- M. K. Arroyo
- M. L. Zoback
- M. Levitt
- M. Lynch
- M. R. Berenbaum
- M. R. Botchan
- M. V. L. Bennett
- M. Vaughan
- N. D. Opdyke
- N. H. Sleep
- N. Myers
- N. R. Pace
- O. B. Berlin
- P. A. Frey
- P. A. Reichard
- P. B. Moore
- P. B. Price
- P. E. Olsen
- P. G. Falkowski
- P. Greengard
- P. H. Gleick
- P. H. von Hippel
- P. J. Bjorkman
- P. J. Crutzen
- P. J. Watson
- P. Kay
- P. O. Brown
- P. R. Ehrlich
- P. V. de Camilli
- P. V. Kirch
- R. A. Nicoll
- R. B. Croteau
- R. B. Goldberg
- R. C. Kessler
- R. D. Palmiter
- R. Dirzo
- R. E. Lenski
- R. E. Ricklefs
- R. F. Doolittle
- R. Fischer
- R. Haselkorn
- R. J. Britten
- R. Jeanloz
- R. L. Rivest
- R. L. Sidman
- R. M. Adams
- R. M. Amasino
- R. M. Cowling
- R. N. Clayton
- R. P. Novick
- R. R. Sederoff
- R. R. Sokal
- R. S. Defries
- R. Schekman
- R. T. Paine
- R. T. Tjian
- R. V. Wolfenden
- R. Z. Sagdeev
- S. A. Darst
- S. A. Kay
- S. A. Levin
- S. C. Harrison
- S. G. Philander
- S. H. Schneider
- S. H. Snyder
- S. Hake
- S. Hanson
- S. Manabe
- S. N. Eisenstadt
- S. P. Briggs
- S. R. Carpenter
- S. R. Hart
- S. R. Wessler
- S. S. Taylor
- S. Uyeda
- S. Verba
- S. W. Englander
- S. W. Kieffer
- T. A. Steitz
- T. C. Sudhof
- T. D. Pollard
- T. D. White
- T. Dunne
- T. Eisner
- T. F. Malone
- T. Hokfelt
- T. Kailath
- T. O. Diener
- V. L. Schramm
- W. A. Jury
- W. C. Clark
- W. G. Ernst
- W. Gilbert
- W. H. Goodenough
- W. H. Munk
- W. J. Brill
- W. J. Rutter
- W. J. Wilson
- W. R. Briggs
- W. R. Gardner
- W. S. Broecker
- W. W. Anderson
- X. T. Le Pichon
- Publication venue
- 'American Association for the Advancement of Science (AAAS)'
- Publication date
- Field of study