123 research outputs found
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Psychosocial risks in Europe: prevalence and strategies for prevention
- Author
- Publication venue
- Publications Office of the European Union
- Publication date
- 17/10/2014
- Field of study
1-methylnicotinamide and its structural analog 1,4-dimethylpyridine for the prevention of cancer metastasis
- Author
- A Blazejczyk
- A Crino
- A Jakubowski
- A Mogielnicki
- A Mogielnicki
- A Wozniacka
- AA Khorana
- AC Chen
- Agnieszka Blazejczyk
- AM Algra
- Andrzej Marcinek
- Anna Nasulewicz-Goldeman
- B Kalaska
- BH Majed
- C Chen
- C Xu
- CN Limjeerajarus
- D Sartini
- F Fei
- G Bendas
- G Sava
- GM Masclee
- GN Tzanakakis
- GW Daneker
- H Yasuda
- HC Bi
- HM Peshavariya
- IK Toliopoulos
- J Gebicki
- J Zhang
- Jerzy Gebicki
- JM Buonato
- Joanna Wietrzyk
- JS Palumbo
- K Bryniarski
- K Maiese
- KV Honn
- L Larue
- L Mateuszuk
- M Bartus
- M Milczarek
- M Schirner
- M Schirner
- M Shi
- M Sternak
- M Wieczorkowska
- Marcin Nowak
- Marta Switalska
- N Weidner
- N Yoshida
- OA Ulanovskaya
- R Biedron
- RB Parsons
- RB Parsons
- S Aksoy
- S Chlopicki
- S Gebremeskel
- S Hong
- S Mezouar
- SE Kispert
- Stefan Chlopicki
- T Brzozowski
- T Nojiri
- T Osawa
- T Placke
- T Wang
- T Yu
- TA Alston
- TB Domagala
- V Audrito
- V Pozzi
- VP Chauhan
- W Zhou
- X Li
- Y Aburakawa
- Y Hiromatsu
- Y Naruse
- Y Yoshitomi
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 01/01/2016
- Field of study
Background: 1-methylnicotinamide (1-MNA), an endogenous metabolite of nicotinamide, has recently gained interest due to its anti-inflammatory and anti-thrombotic activities linked to the COX-2/PGI2 pathway. Given the previously reported anti-metastatic activity of prostacyclin (PGI2), we aimed to assess the effects of 1-MNA and its structurally related analog, 1,4-dimethylpyridine (1,4-DMP), in the prevention of cancer metastasis. Methods: All the studies on the anti-tumor and anti-metastatic activity of 1-MNA and 1,4-DMP were conducted using the model of murine mammary gland cancer (4T1) transplanted either orthotopically or intravenously into female BALB/c mouse. Additionally, the effect of the investigated molecules on cancer cell-induced angiogenesis was estimated using the matrigel plug assay utilizing 4T1 cells as a source of pro-angiogenic factors. Results: Neither 1-MNA nor 1,4-DMP, when given in a monotherapy of metastatic cancer, influenced the growth of 4T1 primary tumors transplanted orthotopically; however, both compounds tended to inhibit 4T1 metastases formation in lungs of mice that were orthotopically or intravenously inoculated with 4T1 or 4T1-luc2-tdTomato cells, respectively. Additionally, while 1-MNA enhanced tumor vasculature formation and markedly increased PGI2 generation, 1,4-DMP did not have such an effect. The anti-metastatic activity of 1-MNA and 1,4-DMP was further confirmed when both agents were applied with a cytostatic drug in a combined treatment of 4T1 murine mammary gland cancer what resulted in up to 80 % diminution of lung metastases formation. Conclusions: The results of the studies presented below indicate that 1-MNA and its structural analog 1,4-DMP prevent metastasis and might be beneficially implemented into the treatment of metastatic breast cancer to ensure a comprehensive strategy of metastasis control
p53 Activation following Rift Valley Fever Virus Infection Contributes to Cell Death and Viral Production
- Author
- A Baer
- A Billecocq
- A Kelekar
- A Kurihara
- A Zamoto-Niikura
- Aarthi Narayanan
- Alan Baer
- Annalise Schoonmaker
- B Kalveram
- BA Werness
- BH Bird
- C Myskiw
- CA Pise-Masison
- Charles Bailey
- D Sir
- Dana Austin
- DW Meek
- E Turpin
- Fatah Kashanchi
- G Blakqori
- GJ Milczarek
- Jean Jacques Panthier
- K Oda
- KW Kohn
- Kylene Kehn-Hall
- Lindsay Lundberg
- LR Devireddy
- M Bouloy
- M Bouloy
- M Habjan
- M Pepin
- M Pepin
- M Scheffner
- MR Yang
- N Le May
- Nazly Shafagati
- P Di Lello
- P Verbruggen
- P Vialat
- P Vialat
- P Wang
- PA Lazo
- R Daubney
- RM Elliott
- S Won
- S Won
- S Won
- SR Gerrard
- SR Gerrard
- SY Shieh
- SY Shieh
- T Ikegami
- T Ikegami
- T Ikegami
- T Ikegami
- T Ikegami
- T Ikegami
- Taissia Popova
- Tetsuro Ikegami
- TG Popova
- TG Popova
- UM Moll
- UM Moll
- VS Thakur
- WT Steegenga
- X Chen
- Y Haupt
- Y Tabakin-Fix
- Y Zhang
- Z Mansuroglu
- Publication venue
- Public Library of Science
- Publication date
- 01/01/2012
- Field of study
Rift Valley fever virus (RVFV) is an emerging viral zoonosis that is responsible for devastating outbreaks among livestock and is capable of causing potentially fatal disease in humans. Studies have shown that upon infection, certain viruses have the capability of utilizing particular cellular signaling pathways to propagate viral infection. Activation of p53 is important for the DNA damage signaling cascade, initiation of apoptosis, cell cycle arrest and transcriptional regulation of multiple genes. The current study focuses on the role of p53 signaling in RVFV infection and viral replication. These results show an up-regulation of p53 phosphorylation at several serine sites after RVFV MP-12 infection that is highly dependent on the viral protein NSs. qRT-PCR data showed a transcriptional up-regulation of several p53 targeted genes involved in cell cycle and apoptosis regulation following RVFV infection. Cell viability assays demonstrate that loss of p53 results in less RVFV induced cell death. Furthermore, decreased viral titers in p53 null cells indicate that RVFV utilizes p53 to enhance viral production. Collectively, these experiments indicate that the p53 signaling pathway is utilized during RVFV infection to induce cell death and increase viral production
p53 Regulates Cell Cycle and MicroRNAs to Promote Differentiation of Human Embryonic Stem Cells
- Author
- A Ito
- A Krek
- A Yang
- A. A Mills
- A. J Levine
- A. K Jain
- A. L Gartel
- Abhinav K. Jain
- B. E Bernstein
- B. P Lewis
- B. P Lewis
- C Lois
- C Melton
- C Tarantino
- C. A Jost
- C. L Brooks
- Connie J. Eaves
- D Bosnakovski
- D. P Bartel
- E Stead
- Elisabeth Mahen
- F Anokye-Danso
- F Murray-Zmijewski
- F Sun
- G Liu
- G Liu
- G. A Lang
- H Hermeking
- H Hong
- H Li
- H Qin
- H Song
- I Lipchina
- J Hanna
- J Kim
- J Utikal
- J White
- J Yu
- J. A Thomson
- J. F Armstrong
- J. W Harper
- K Allton
- K Balasubramanyam
- K Meletis
- K Takahashi
- K. A Becker
- K. A Becker
- K. H Vousden
- K. W Orford
- Kendra Allton
- L Jirmanova
- L. A Boyer
- L. C Laurent
- M Ashcroft
- M Li
- M Sachdeva
- M Yamakuchi
- M. F Pera
- M. I Aladjem
- M. K Han
- Michael Kyba
- Michelina Iacovino
- Michelle Craig Barton
- N Ivanova
- N Kim
- N Xu
- N. A Barlev
- N. Y Chia
- P Gu
- P Neveu
- P Savatier
- R Jaenisch
- R Montes de Oca Luna
- R. C Perlingeiro
- R. D Morin
- R. M Marion
- Robert J. Milczarek
- S Agha-Mohammadi
- S Griffiths-Jones
- S Ruiz
- T Kawamura
- T Lin
- T Maimets
- T. C Chang
- T. I Lee
- Thomas P. Zwaka
- U Lakshmipathy
- V Calvanese
- V Dotsch
- V Zuckerman
- V. P Sah
- W Gu
- W Hu
- W. M Keyes
- W. R Taylor
- W. S el-Deiry
- Y Liu
- Y Wang
- Y Wang
- Y. J Choi
- Publication venue
- Public Library of Science
- Publication date
- 01/01/2012
- Field of study
Multiple studies show that tumor suppressor p53 is a barrier to dedifferentiation; whether this is strictly due to repression of proliferation remains a subject of debate. Here, we show that p53 plays an active role in promoting differentiation of human embryonic stem cells (hESCs) and opposing self-renewal by regulation of specific target genes and microRNAs. In contrast to mouse embryonic stem cells, p53 in hESCs is maintained at low levels in the nucleus, albeit in a deacetylated, inactive state. In response to retinoic acid, CBP/p300 acetylates p53 at lysine 373, which leads to dissociation from E3-ubiquitin ligases HDM2 and TRIM24. Stabilized p53 binds CDKN1A to establish a G1 phase of cell cycle without activation of cell death pathways. In parallel, p53 activates expression of miR-34a and miR-145, which in turn repress stem cell factors OCT4, KLF4, LIN28A, and SOX2 and prevent backsliding to pluripotency. Induction of p53 levels is a key step: RNA-interference-mediated knockdown of p53 delays differentiation, whereas depletion of negative regulators of p53 or ectopic expression of p53 yields spontaneous differentiation of hESCs, independently of retinoic acid. Ectopic expression of p53R175H, a mutated form of p53 that does not bind DNA or regulate transcription, failed to induce differentiation. These studies underscore the importance of a p53-regulated network in determining the human stem cell state
A narrative review on the similarities and dissimilarities between myalgic encephalomyelitis/chronic fatigue syndrome (me/cfs) and sickness behavior
- Author
- A Bosutti
- A Boullerne
- A Hilgers
- A Korkmaz
- A Peters
- A Wilson
- AA Farooqui
- AC Anand
- AJ Cleare
- AJ Dunn
- AL Fitzpatrick
- AL Komaroff
- AM Wynne
- AS Papadopoulos
- AS Winkler
- B Widner
- BG Charlton
- BL Hart
- BM Carruthers
- BM Carruthers
- BM Necela
- C D'Mello
- C Garcia-Ruiz
- C Gemma
- C Hawk
- C Heesen
- C Li
- C Murr
- CA Dinarello
- CB Lawrence
- CC Chang
- CL Sherry
- D Beccano-Kelly
- D Morgan
- D Nashan
- DC Shungu
- DG Allen
- DH Streeten
- DJ Mahad
- DL Arnold
- DR van Langenberg
- E Bossy-Wetzel
- E Gottlieb
- ED Carlton
- EM Maloney
- EW Brenu
- EW Brenu
- F Camus
- F Eskandari
- F McKechnie
- F Nava
- FB Axelrod Axelrod
- G Anderson
- G Broderick
- G Kennedy
- G Mastorakos
- G Morris
- GA Mostafa
- GC Brown
- GC Brown
- GC Brown
- George Anderson
- Gerwyn Morris
- GK Sakkas
- GL Nicolson
- GL Nicolson
- H Besedovsky
- H Esterbauer
- H Naess
- HK Kang
- I Bechmann
- I Mihaylova
- IA Clark
- J Allen
- J Chen
- J Francis
- J Visser
- JA Pasco
- JE Bower
- JJ Garcia
- JJ Ochoa
- JK Chia
- JL Newton
- JM Stewart
- JP Konsman
- JR Kerr
- JS Adelman
- JS Myers
- JW Koo
- JW Murrough
- K Fukuda
- K Miwa
- K Riazi
- KB Norheim
- KD Ackerman
- KJ Tracey
- L MacDonald
- L Paul
- L Qin
- L Zhang
- LA Tiersky
- LE Hains
- LM Harden
- LM Tak
- LV Scott
- LV Scott
- LV Scott
- M Berk
- M Jaattela
- M Maes
- M Maes
- M Maes
- M Maes
- M Maes
- M Maes
- M Maes
- M Maes
- M Maes
- M Maes
- M Maes
- M Maes
- M Maes
- M Maes
- M Maes
- M Nishikai
- M Pagani
- M Viljoen
- MA Demitrack
- MA Fletcher
- MC Pascoe
- MC Wichers
- MD Buchwald
- Michael Berk
- Michael Maes
- MJ Kluger
- MJ Kluger
- MP Fink
- N Bassi
- N Klimas
- N Quan
- N Terrando
- NA Riobo
- ND Vaziri
- NE Booth
- NF Hill
- NL Reynolds
- O Zachrisson
- P De Becker
- P Kumar
- P Roy-Byrne
- P Skapinakis
- PC Calder
- Piotr Galecki
- PJ Robson-Ansley
- PK Peterson
- PM Soetekouw
- PS Strickland
- Q Zhu
- R Avitsur
- R Bellmann-Weiler
- R Cairns
- R Freeman
- R Klein
- R Medzhitov
- R Milczarek
- R Murayama
- R Patarca
- R Roubenoff
- R Wong
- RC Vermeulen
- RH Straub
- RJ Lane
- RK Kumar
- RR Dietert
- RS Hetem
- S Berkovitz
- S Chakraborty
- S Fukuda
- S Fulle
- S Glund
- S Kent
- S Myhill
- S Steinshamn
- S Tanaka
- SF Maier
- SM Kerfoot
- SV Arnett
- SY Hwang
- SY Kuo
- T Ishikawa
- T Kato
- T Turan
- TA Atkin
- TJ Montague
- TL Young-Pearse
- V Chesnokova
- V Marty
- VA Pavlov
- WA Banks
- WK Jerjes
- WM Behan
- Y Chen
- Y He
- Y Hokama
- Y Hokama
- Y Jammes
- YW Xie
- Z Merali
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 01/01/2013
- Field of study
It is of importance whether myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a variant of sickness behavior. The latter is induced by acute infections/injury being principally mediated through proinflammatory cytokines. Sickness is a beneficial behavioral response that serves to enhance recovery, conserves energy and plays a role in the resolution of inflammation. There are behavioral/symptomatic similarities (for example, fatigue, malaise, hyperalgesia) and dissimilarities (gastrointestinal symptoms, anorexia and weight loss) between sickness and ME/CFS. While sickness is an adaptive response induced by proinflammatory cytokines, ME/CFS is a chronic, disabling disorder, where the pathophysiology is related to activation of immunoinflammatory and oxidative pathways and autoimmune responses. While sickness behavior is a state of energy conservation, which plays a role in combating pathogens, ME/CFS is a chronic disease underpinned by a state of energy depletion. While sickness is an acute response to infection/injury, the trigger factors in ME/CFS are less well defined and encompass acute and chronic infections, as well as inflammatory or autoimmune diseases. It is concluded that sickness behavior and ME/CFS are two different conditions
Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)
- Author
- A. -G. Wu
- A. C. Ma
- A. K. Au
- Abdel-Aziz A. K.
- Abdelfatah S.
- Abdellatif M.
- Abdoli A.
- Abel S.
- Abeliovich H.
- Abildgaard M. H.
- Abudu Y. P.
- Acevedo-Arozena A.
- Adamopoulos I. E.
- Adeli K.
- Adolph T. E.
- Adornetto A.
- Aflaki E.
- Agam G.
- Agarwal A.
- Aggarwal B. B.
- Agnello M.
- Agostinis P.
- Agrewala J. N.
- Agrotis A.
- Aguilar P. V.
- Ahmad S. T.
- Ahmed Z. M.
- Ahumada-Castro U.
- Aits S.
- Aizawa S.
- Akkoc Y.
- Akoumianaki T.
- Akpinar H. A.
- Al-Abd A. M.
- Al-Akra L.
- Al-Gharaibeh A.
- Alaoui-Jamali M. A.
- Alberti S.
- Alcocer-Gomez E.
- Alessandri C.
- Ali M.
- Alim Al-Bari M. A.
- Aliwaini S.
- Alizadeh J.
- Almacellas E.
- Almasan A.
- Alonso A.
- Alonso G. D.
- Altan-Bonnet N.
- Altieri D. C.
- Alvarez E. M. C.
- Alves da Costa C.
- Alves S.
- Alzaharna M. M.
- Amadio M.
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- Amaral C.
- Ambrosio S.
- Amer A. O.
- Ammanathan V.
- An Z.
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- Antebi A.
- Anton Z.
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- Publication venue
- 'Informa UK Limited'
- Publication date
- 01/01/2021
- Field of study
Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)1.
- Author
- Abdel-Aziz AK
- Abdelfatah S
- Abdellatif M
- Abdoli A
- Abel S
- Abeliovich H
- Abildgaard MH
- Abudu YP
- Acevedo-Arozena A
- Adamopoulos IE
- Adeli K
- Adolph TE
- Adornetto A
- Aflaki E
- Agam G
- Agarwal A
- Aggarwal BB
- Agnello M
- Agostinis P
- Agrewala JN
- Agrotis A
- Aguilar PV
- Ahmad ST
- Ahmed ZM
- Ahumada-Castro U
- Aits S
- Aizawa S
- Akkoc Y
- Akoumianaki T
- Akpinar HA
- Al-Abd AM
- Al-Akra L
- Al-Gharaibeh A
- Alaoui-Jamali MA
- Alberti S
- Alcocer-Gómez E
- Alessandri C
- Ali M
- Alim Al-Bari MA
- Aliwaini S
- Alizadeh J
- Almacellas E
- Almasan A
- Alonso A
- Alonso GD
- Altan-Bonnet N
- Altieri DC
- Alves da Costa C
- Alves S
- Alzaharna MM
- Amadio M
- Amantini C
- Amaral C
- Ambrosio S
- Amer AO
- Ammanathan V
- An Z
- Andersen SU
- Andrabi SA
- Andrade-Silva M
- Andres AM
- Angelini S
- Ann D
- Anozie UC
- Ansari MY
- Antas P
- Antebi A
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- Anwar T
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- Apostolova N
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- Araya J
- Araújo WL
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- Arikkath J
- Arimoto H
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- Armstrong-James D
- Arnauné-Pelloquin L
- Aroca A
- Arroyo DS
- Arsov I
- Artero R
- Arévalo M-A
- Asaro DML
- Aschner M
- Ashrafizadeh M
- Ashur-Fabian O
- Atanasov AG
- Au AK
- Auberger P
- Auner HW
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- Autelli R
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- Aveic S
- Aveleira CA
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- Zimmermann CM
- Ziviani E
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- Zorov DB
- Zorzano A
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- Álvarez ÉMC
- Ávalos Y
- Önal G
- Üstün S
- Čolić M
- Đokić J
- Žerovnik E
- Publication venue
- 'Informa UK Limited'
- Publication date
- 01/01/2021
- Field of study
In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field
Iron Behaving Badly: Inappropriate Iron Chelation as a Major Contributor to the Aetiology of Vascular and Other Progressive Inflammatory and Degenerative Diseases
- Author
- A Abbott
- A Abou-Raya
- A Aljandali
- A Ambesi-Impiombato
- A Aydin
- A Balcerczyk
- A Besarab
- A Brzezinski
- A Campbell
- A Carrillo-Vico
- A Cavalli
- A Chattopadhyay
- A Chattopadhyay
- A Cherubini
- A Dey
- A Doms
- A Donovan
- A Donovan
- A Dávalos
- A Gaeta
- A Garny
- A Gnjec
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- The Long-Term Intervention with Pravastatin in Ischaemic Disease (LIPID) Study Group
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- Publication venue
- Publication date
- 09/08/2008
- Field of study
The production of peroxide and superoxide is an inevitable consequence of
aerobic metabolism, and while these particular "reactive oxygen species" (ROSs)
can exhibit a number of biological effects, they are not of themselves
excessively reactive and thus they are not especially damaging at physiological
concentrations. However, their reactions with poorly liganded iron species can
lead to the catalytic production of the very reactive and dangerous hydroxyl
radical, which is exceptionally damaging, and a major cause of chronic
inflammation. We review the considerable and wide-ranging evidence for the
involvement of this combination of (su)peroxide and poorly liganded iron in a
large number of physiological and indeed pathological processes and
inflammatory disorders, especially those involving the progressive degradation
of cellular and organismal performance. These diseases share a great many
similarities and thus might be considered to have a common cause (i.e.
iron-catalysed free radical and especially hydroxyl radical generation). The
studies reviewed include those focused on a series of cardiovascular, metabolic
and neurological diseases, where iron can be found at the sites of plaques and
lesions, as well as studies showing the significance of iron to aging and
longevity. The effective chelation of iron by natural or synthetic ligands is
thus of major physiological (and potentially therapeutic) importance. As
systems properties, we need to recognise that physiological observables have
multiple molecular causes, and studying them in isolation leads to inconsistent
patterns of apparent causality when it is the simultaneous combination of
multiple factors that is responsible. This explains, for instance, the
decidedly mixed effects of antioxidants that have been observed, etc...Comment: 159 pages, including 9 Figs and 2184 reference
Dielectric properties of lignin and glucomannan as determined by spectroscopic ellipsometry and Lifshitz estimates of non-retarded Hamaker constants
- Author
- A Venkateswaran
- AA Feiler
- Bertrand Faure
- BW Ninham
- DB Hough
- EM Lifshitz
- G Carlsson
- G Milczarek
- GS Furman
- Hans Arwin
- HC Hamaker
- HG Tompkins
- J Laine
- KG Denbigh
- L Bergström
- L Bergström
- Lars Wågberg
- Lennart Bergström
- M Holmberg
- M Norgren
- M Norgren
- MJ Heathcote
- PC Hiemenz
- PH Hermans
- Rebecca Hollertz
- RH French
- RR Dagastine
- S Barsberg
- SB Lee
- SC Fox
- SH Beis
- SM Notley
- SM Notley
- SM Notley
- VA Parsegian
- WN Stoops
- Yujia Zhang
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- Field of study
Styrene and Polystyrene Modified Polyethylenes: Characterization and Properties
- Publication venue
- 'Informa UK Limited'
- Publication date
- Field of study
- …