6 research outputs found
Analysis of the potential of cancer cell lines to release tissue factor-containing microvesicles: correlation with tissue factor and PAR2 expression
- Author
- A Bharthuar
- A Delluc
- A Falanga
- A Rank
- A Rank
- AA Khorana
- AA Khorana
- Anthony Maraveyas
- AS Wolberg
- BA Lwaleed
- C Ettelaie
- C Ettelaie
- C Hernández
- C Sapet
- Camille Ettelaie
- E Camerer
- E Campello
- E Cocco
- ES Breimo
- F Doormaal van
- F Langer
- GW Tormoen
- H Kothari
- I Pabinger
- J Ahamed
- J Thaler
- J Thaler
- J Thaler
- JA Bastarache
- JE Geddings
- JH Morrissey
- John Greenman
- K Haubold
- KG Livak
- L Hu
- LV Rao
- M Davila
- Mary EW Collier
- ME Collier
- ME Collier
- ME Collier
- ME Collier
- ME Tesselaar
- ML Rand
- N Satta
- N Tavoosi
- Naima E. Benelhaj
- NS Key
- P Bucciarelli
- R Flaumenhaft
- RI Kushak
- S Butenas
- SJ Compton
- SK Dasgupta
- Sophie Featherby
- T Kawamoto
- V Combes
- W Ruf
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 19/01/2016
- Field of study
BackgroundDespite the association of cancer-derived circulating tissue factor (TF)-containing microvesicles and hypercoagulable state, correlations with the incidence of thrombosis remain unclear.MethodsIn this study the upregulation of TF release upon activation of various cancer cell lines, and the correlation with TF and PAR2 expression and/or activity was examined. Microvesicle release was induced by PAR2 activation in seventeen cell lines and released microvesicle density, microvesicle-associated TF activity, and phoshpatidylserine-mediated activity were measured. The time-course for TF release was monitored over 90 min in each cell line. In addition, TF mRNA expression, cellular TF protein and cell-surface TF activities were quantified. Moreover, the relative expression of PAR2 mRNA and cellular protein were analysed. Any correlations between the above parameters were examined by determining the Pearson’s correlation coefficients.ResultsTF release as microvesicles peaked between 30–60 min post-activation in the majority of cell lines tested. The magnitude of the maximal TF release positively correlated with TF mRNA (c = 0.717; p
Analysis of the potential of cancer cell lines to release tissue factor-containing microvesicles: correlation with tissue factor and PAR2 expression
- Author
- A Bharthuar
- A Delluc
- A Falanga
- A Rank
- A Rank
- AA Khorana
- AA Khorana
- Anthony Maraveyas
- AS Wolberg
- BA Lwaleed
- C Ettelaie
- C Ettelaie
- C Hernández
- C Sapet
- Camille Ettelaie
- E Camerer
- E Campello
- E Cocco
- ES Breimo
- F Doormaal van
- F Langer
- GW Tormoen
- H Kothari
- I Pabinger
- J Ahamed
- J Thaler
- J Thaler
- J Thaler
- JA Bastarache
- JE Geddings
- JH Morrissey
- John Greenman
- K Haubold
- KG Livak
- L Hu
- LV Rao
- M Davila
- Mary EW Collier
- ME Collier
- ME Collier
- ME Collier
- ME Collier
- ME Tesselaar
- ML Rand
- N Satta
- N Tavoosi
- Naima E. Benelhaj
- NS Key
- P Bucciarelli
- R Flaumenhaft
- RI Kushak
- S Butenas
- SJ Compton
- SK Dasgupta
- Sophie Featherby
- T Kawamoto
- V Combes
- W Ruf
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- Field of study
Inflammation control and improvement of cognitive function in COVID-19 infections: is there a role for kynurenine 3-monooxygenase inhibition?
- Author
- Publication venue
- Publication date
- 18/02/2021
- Field of study
The novel respiratory virus severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which causes coronavirus disease 2019 (COVID-19), emerged during late 2019 and spread rapidly across the world. It is now recognised that the nervous system can be affected in COVID-19, with several studies reporting long-term cognitive problems in patients. The metabolic pathway of tryptophan degradation, known as the kynurenine pathway (KP), is significantly activated in patients with COVID-19. KP metabolites have roles in regulating both inflammatory/immune responses and neurological functions. In this review, we speculate on the effects of KP activation in patients with COVID-19, and how modulation of this pathway might impact inflammation and reduce neurological symptoms
Advantages of brain penetrating inhibitors of kynurenine-3-monooxygenase for treatment of neurodegenerative diseases
- Author
- Publication venue
- Publication date
- 01/12/2020
- Field of study
Kynurenine-3-monooxygenase (KMO) is an important therapeutic target for several brain disorders that has been extensively studied in recent years. Potent inhibitors towards KMO have been developed and tested within different disease models, showing great therapeutic potential, especially in models of neurodegenerative disease. The inhibition of KMO reduces the production of downstream toxic kynurenine pathway metabolites and shifts the flux to the formation of the neuroprotectant kynurenic acid. However, the efficacy of KMO inhibitors in neurodegenerative disease has been limited by their poor brain permeability. Combined with virtual screening and prodrug strategies, a novel brain penetrating KMO inhibitor has been developed which dramatically decreases neurotoxic metabolites. This review highlights the importance of KMO as a drug target in neurological disease and the benefits of brain permeable inhibitors in modulating kynurenine pathway metabolites in the central nervous system
Chapter II: Heating, Ventilation, and Sanitation in School Buildings
- Author
- Albert FC
- Alt Harold L
- Atwater DW
- Atwater DW
- Barker Howard
- Bass Frederick
- Bass Frederick
- Bass Frederick
- Beery Clinton E
- Beggs EW
- Bennett Ralph
- Berestneff AA
- Billings JS
- Bishop LW
- Brown Jean Collier
- Brown-Séquard and d’Arsonval
- Butsch Russell LC
- Carey PC
- Carpenter WW
- Challman SA
- Challman SA
- Challman SA
- Cooper Frank Irving
- Correll Marie
- Crane AM
- Duffield Thomas J
- Duffield Thomas J
- Duffield Thomas J
- Eddy CA
- Edison Lamp Works
- Ewart Joseph A
- Feldman AM
- Fluegge C
- Frandsen DJ
- Franklin MW
- Freeman Frank N
- Frostic FW
- Hallett ES
- Hamon Ray L
- Harrison Ward
- Hart Chester
- Hart Chester
- Hartman Frank E
- Hartman Frank E
- Hathaway Winifred
- Heath RF
- Henderson Olive Grace
- Hermans JTF
- Hill E Vernon
- Hill E Vernon
- Hill E Vernon
- Hill E Vernon
- Holmes Warren S
- Hopkinson George M
- Houghten FC
- Hubbard CL
- Ireland Allen G
- Ittner WB
- Ives James E
- Jackson Edward
- Jedlicka AI
- Keiser W
- Keller Paul GW
- Knight George W
- Kocher A Lawrence
- Lansingh VR
- Larson GL
- Larson GL
- Leblanc F
- Lewis LL
- Lieb JW
- Logan HL
- MacDonald AJ
- Mackey HD
- Mahar James J
- Martin AJ
- McConnell WJ
- Milligan JM
- National Lamp Works
- National Lamp Works
- Nesbitt AJ
- Nesbitt John J
- Oday AB
- Pennsylvania State Department of Health
- Peppe Michael
- Pettenkofer Max von
- Pilkey Thomas A
- Pleins Leo H
- Powell AL
- Powell AL
- Ransome A
- Rauer G
- Redway Jacques W
- Robb JM
- Robb JM
- Rosenow Edward C
- Ross Nelson C
- Russo-Giliberti A
- Scherer Francis R
- Scherer Francis R
- Scherer Francis R
- Schmidt HW
- Schmidt HW
- Schmidt HW
- Schmidt HW
- Schmidt HW
- Schmidt HW
- Shawan JA
- Smith Mary E
- Smith VT
- Spaulding HT
- Sturrock Walter
- Tappan Julia B
- Tuck DH
- U. S. Public Health Service
- Walker JH
- Winslow C-EA
- Winslow C-EA
- Wisconsin Department of Public Instruction
- Wolf Carl F
- Wood Thomas D
- Zahour Robert L
- Zahour Robert L
- “Can School Buildings Be Reformed.”
- “Chicago Commission on Ventilation.”
- Publication venue
- 'American Educational Research Association (AERA)'
- Publication date
- Field of study
Mapping the human genetic architecture of COVID-19
- Author
- Abdelrazik M
- Abdullah T
- Abe R
- Abe S
- Abecasis GR
- Abel L
- Abernathy C
- Abraheem A
- Abul-Husn NS
- Acosta-Herrera M
- Acquilini D
- Acquilini D
- Adachi T
- Adachi Y
- Adams C
- Adams K
- Adanini O
- Adeleye O
- Adeniji K
- Adra D
- Afifi N
- Afilalo J
- Afilalo M
- Afolabi D
- Afrasiabi Z
- Afset JE
- Agasou A
- Aghemo A
- Agranoff D
- Agrawal S
- Aguirre LA
- Agwuh K
- Ahmad HF
- Ahmad N
- Ahmed A
- Ahmed C
- Ahmed KA
- Ai M
- Ail D
- Akeroyd L
- Akhtar MN
- Akhtar S
- Akinkugbe O
- Aksentijevich A
- Al Thani A
- Al-Muftah W
- Al-Sarraj Y
- Alarcon C
- Alarcon-Riquelme ME
- Alasdair F
- Alaverdian D
- Alavere H
- Albertos R
- Albillos A
- Albrecht W
- Albrich W
- Albrich WC
- Aldera EL
- Aldridge J
- Alegria A
- Alex B
- Alexander P
- Alfonso J
- Algera AG
- Ali A
- Ali IMA
- Ali S
- Aliberti S
- Allan A
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- Allan J
- Alldis Z
- Allen L
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- Ally SM
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- Altmueller J
- Alvaro A
- Amar D
- Amin V
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- Amiya S
- Ampuero J
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- Anania S
- Anastasescu E
- Anderson F
- Anderson J
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- Anderson S
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- Andolfo I
- Andrade V
- Andretta F
- Andreucci E
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- Uffelmann E
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- Vehreschild MJGT
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- Wyllie DH
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- Yoon KJ
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- Yoshihara T
- Yoshiya K
- Yoshiyama T
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- Zanelli G
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- Zechner M
- Zguro K
- Zhai R
- Zhang JE
- Zhang M
- Zhao JH
- Zhen J
- Zheng C
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- Zoller H
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- zu Bentrup FM
- Zucchi P
- Zwinderman AHK
- Zyndorf M
- Publication venue
- 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 diseases3,4,5,6,7. 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