96 research outputs found
Importance of Non-Selective Cation Channel TRPV4 Interaction with Cytoskeleton and Their Reciprocal Regulations in Cultured Cells
- Author
- A Lieuvin
- A Mizuno
- AD Bershadsky
- AF Odell
- B Malik
- B Nilius
- C Blase
- C Goswami
- C Goswami
- C Goswami
- C Goswami
- C Goswami
- C Goswami
- C Goswami
- C Martinez-Salgado
- C Wetzel
- Chandan Goswami
- CS Chen
- D Becker
- D Becker
- D Becker
- D Platika
- DM Beltramo
- DR Webster
- F Luo
- F Xu
- FJ Ahmad
- FJ Alenghat
- FL Bender
- G Bhave
- G Landouré
- G Piperno
- GC McCarter
- GC McCarter
- H Peng
- H Shigematsu
- H Watanabe
- H Watanabe
- H Watanabe
- HC Fan
- HF Cantiello
- Hiroaki Matsunami
- HW Jin
- HX Deng
- HY Kwan
- I Lauritzen
- IM Lorenzo
- J Kuhn
- J Waning
- JA Rodriguez
- JD Levine
- Julia Kuhn
- K Shibasaki
- K Tabuchi
- KD Tanner
- KS Topp
- L Cardone
- LJ Drew
- M Arniges
- M Huang
- M LeDizet
- M Suzuki
- MJ Rock
- MP Cuajungco
- MR Kaazempur Mofrad
- N Alessandri-Haber
- N Alessandri-Haber
- N Alessandri-Haber
- N Alessandri-Haber
- N Alessandri-Haber
- N Boulais
- N Boulais
- NC Shaner
- OA Dina
- OA Dina
- P Boukamp
- P Han
- Paul A. Heppenstall
- PF Maness
- PW Baas
- R Kohler
- R Ramadass
- R Strotmann
- R Strotmann
- S Belmadani
- S Earley
- S Khawaja
- SA Gradilone
- SC Teilmann
- SG Khasar
- T Hucho
- T Wegierski
- TB Hucho
- TB Hucho
- TE Kreis
- Tim Hucho
- V Benfenati
- W Liedtke
- WA Voter
- X Gao
- X Liu
- Y Gluzman
- Y Wang
- YN Andrade
- YY Ma
- Z Pan
- Publication venue
- Public Library of Science
- Publication date
- 01/01/2010
- Field of study
BACKGROUND: TRPV4 and the cellular cytoskeleton have each been reported to influence cellular mechanosensitive processes as well as the development of mechanical hyperalgesia. If and how TRPV4 interacts with the microtubule and actin cytoskeleton at a molecular and functional level is not known. METHODOLOGY AND PRINCIPAL FINDINGS: We investigated the interaction of TRPV4 with cytoskeletal components biochemically, cell biologically by observing morphological changes of DRG-neurons and DRG-neuron-derived F-11 cells, as well as functionally with calcium imaging. We find that TRPV4 physically interacts with tubulin, actin and neurofilament proteins as well as the nociceptive molecules PKCepsilon and CamKII. The C-terminus of TRPV4 is sufficient for the direct interaction with tubulin and actin, both with their soluble and their polymeric forms. Actin and tubulin compete for binding. The interaction with TRPV4 stabilizes microtubules even under depolymerizing conditions in vitro. Accordingly, in cellular systems TRPV4 colocalizes with actin and microtubules enriched structures at submembranous regions. Both expression and activation of TRPV4 induces striking morphological changes affecting lamellipodial, filopodial, growth cone, and neurite structures in non-neuronal cells, in DRG-neuron derived F11 cells, and also in IB4-positive DRG neurons. The functional interaction of TRPV4 and the cytoskeleton is mutual as Taxol, a microtubule stabilizer, reduces the Ca2+-influx via TRPV4. CONCLUSIONS AND SIGNIFICANCE: TRPV4 acts as a regulator for both, the microtubule and the actin. In turn, we describe that microtubule dynamics are an important regulator of TRPV4 activity. TRPV4 forms a supra-molecular complex containing cytoskeletal proteins and regulatory kinases. Thereby it can integrate signaling of various intracellular second messengers and signaling cascades, as well as cytoskeletal dynamics. This study points out the existence of cross-talks between non-selective cation channels and cytoskeleton at multiple levels. These cross talks may help us to understand the molecular basis of the Taxol-induced neuropathic pain development commonly observed in cancer patients
In vivo assembly of the axon initial segment in motor neurons
- Author
- A Delpy
- A Duflocq
- A Iwakura
- A Lorincz
- AH Song
- AL Scain
- Amélie Fréal
- Antonny Czarnecki
- AP Barnes
- B Winckler
- B Zonta
- Barbara Le Bras
- BX Gao
- C Leterrier
- C Leterrier
- C Nakada
- CG Dotti
- D Sanchez-Ponce
- D Zhou
- DL Sherman
- E Kordeli
- Erika Bullier
- François Couraud
- G Lemaillet
- H Kuba
- H Wichterle
- JJ Devaux
- JJ Garrido
- JM Sobotzik
- JM Wilson
- JS Dasen
- KJ Bender
- KL Hedstrom
- KL Hedstrom
- LE Wentworth
- M Bouzidi
- M Komada
- M Takahashi
- Marc Davenne
- Masayuki Komada
- MH Kole
- MN Rasband
- MR Galiano
- MS Grubb
- N Alessandri-Haber
- N Matsuda
- N Ulfig
- Pascal Legendre
- Peter J. Brophy
- S Arber
- S Berghs
- S Lacas-Gervais
- S Pun
- S Tait
- SM Jenkins
- TA Maniar
- V Bernard
- Y Dzhashiashvili
- Y Ogawa
- Y Uemoto
- Z Pan
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- 01/01/2013
- Field of study
International audienceThe axon initial segment (AIS) is responsible for both the modulation of action potentials and the maintenance of neuronal polarity. Yet, the molecular mechanisms controlling its assembly are incompletely understood. Our study in single electroporated motor neurons in mouse embryos revealed that AnkyrinG (AnkG), the AIS master organizer, is undetectable in bipolar migrating motor neurons, but is already expressed at the beginning of axonogenesis at E9.5 and initially distributed homogeneously along the entire growing axon. Then, from E11.5, a stage when AnkG is already apposed to the membrane, as observed by electron microscopy, the protein progressively becomes restricted to the proximal axon. Analysis on the global motor neurons population indicated that Neurofascin follows an identical spatio-temporal distribution, whereas sodium channels and beta 4-spectrin only appear along AnkG(+) segments at E11.5. Early patch-clamp recordings of individual motor neurons indicated that at E12.5 these nascent AISs are already able to generate spikes. Using knock-out mice, we demonstrated that neither beta 4-spectrin nor Neurofascin control the distal-to-proximal restriction of AnkG
Nociceptors: a phylogenetic view
- Author
- A Babes
- A Dhaka
- A Iggo
- A Momin
- A Momin
- AB Vallbo
- AD Grant
- AJ Billy
- AJ Page
- AJ Page
- AL Kleinhaus
- AM Binshtok
- AM Rush
- AN Akopian
- AR Martin
- AW Thomas
- B Al-Anzi
- B Kenton
- B Lynn
- B Namer
- C Belmonte
- C Darwin
- C Martinez-Salgado
- C Montell
- C Weidner
- C Wetzel
- CI Bargmann
- CJ Grimmelikhuijzen
- CJ Woodbury
- CJ Woolf
- CJ Woolf
- CS Sherrington
- D Sakharov
- DD McKemy
- DJ Cosens
- DM Bautista
- DM Bautista
- DM Cain
- DM Ross
- DM Tobin
- DT Hamamoto
- DT Hamamoto
- E Lingueglia
- ER Troemel
- ES Smith
- ES Smith
- ET Walters
- ET Walters
- Ewan St. John Smith
- F Anton
- G Matthews
- G Reid
- Gary R. Lewin
- GC McCarter
- GM Story
- GR Lewin
- GR Lewin
- GR Lewin
- GS Richards
- H Adriaensen
- H Cadiou
- H Koopowitz
- HA Colbert
- HN Wenk
- HO Handwerker
- HR Koerber
- I Tracey
- J Byrne
- J Hu
- J Huang
- J Huang
- J Nordgreen
- J Pastor
- J Srinivasan
- JA Ainsley
- JB Davis
- JD Rose
- JE Mellem
- JE Mellem
- JG Nicholls
- JJ Lawson
- JM Kaplan
- JN Wood
- JS Mogil
- KD Davis
- KH Steen
- KM Albers
- KM Weston
- KY Kwan
- KY Kwan
- KY Kwan
- L Kruger
- LJ Drew
- LM Mendell
- LM Passano
- LS Loken
- LU Sneddon
- LU Sneddon
- LU Sneddon
- LU Sneddon
- LU Sneddon
- M Chalfie
- M Hesselager
- M Huang
- M Kavaliers
- M Kavaliers
- M Koltzenburg
- M Koltzenburg
- M Kress
- M Renganathan
- M Srivastava
- M Tominaga
- M Whitear
- MA Hilliard
- MB Goodman
- MJ Caterina
- MJ Caterina
- MJ Gentle
- MJ Gentle
- MJ Millan
- MP Price
- MP Price
- MS Gold
- N Alessandri-Haber
- N Alessandri-Haber
- N Alessandri-Haber
- N Levina
- N Milenkovic
- N Milenkovic
- N Wittenburg
- NG Jones
- NR Gavva
- NT Blair
- O Caspani
- P Bessou
- P Cesare
- P Goadby
- PA Getting
- PA Illich
- PD Pezalla
- PI Baccaglini
- PJ Ashley
- PJ Snow
- PR Burgess
- PW Reeh
- Q Ma
- R Brett
- R Madrid
- R Necker
- R OâHagan
- R Schmidt
- RA Meyer
- RB Leonard
- RC Jones 3rd
- RD Treede
- RE Coggeshall
- RY Hwang
- S Frings
- S Ugawa
- S Willenbring
- S Zurborg
- SA Malin
- SE Jordt
- SE Jordt
- SG Lechner
- SG Lechner
- SI Sukharev
- SM Brierley
- SN Lawson
- SR Lockery
- SR Lockery
- SY Xu
- T Cavelier-Smith
- T Coric
- T Coric
- T Ford
- T Hadrys
- T Sokabe
- TH Bullock
- TJ Park
- V Castellucci
- WD Tracey Jr
- WR Schlue
- X Chen
- X Shu
- Y Karashima
- Y Sambongi
- YF Liang
- YF Liang
- Publication venue
- Springer-Verlag
- Publication date
- 01/12/2009
- Field of study
The ability to react to environmental change is crucial for the survival of an organism and an essential prerequisite is the capacity to detect and respond to aversive stimuli. The importance of having an inbuilt âdetect and protectâ system is illustrated by the fact that most animals have dedicated sensory afferents which respond to noxious stimuli called nociceptors. Should injury occur there is often sensitization, whereby increased nociceptor sensitivity and/or plasticity of nociceptor-related neural circuits acts as a protection mechanism for the afflicted body part. Studying nociception and nociceptors in different model organisms has demonstrated that there are similarities from invertebrates right through to humans. The development of technology to genetically manipulate organisms, especially mice, has led to an understanding of some of the key molecular players in nociceptor function. This review will focus on what is known about nociceptors throughout the Animalia kingdom and what similarities exist across phyla; especially at the molecular level of ion channels
Human keratinocytes are vanilloid resistant
- Author
- A Athanasiou
- A Gandarillas
- A Guo
- A Kofalvi
- A Liapi
- A Macho
- A Pivarcsi
- A Pivarcsi
- A Singh Tahim
- A Szallasi
- A Szallasi
- A Szallasi
- A Toth
- AD Guler
- AM Peier
- AndrĂĄs TĂłth
- B Lynn
- BS Alper
- CE Argoff
- CP Watson
- Csaba Vizler
- DC Brown
- DG Witte
- DJ Levey
- DM Simpson
- E Bodo
- E Mezey
- ErzsĂ©bet KĂșsz
- FA Bucci Jr
- G Bhave
- GC Tender
- I Nagy
- IstvĂĄn Koncz
- J Winter
- J Winter
- JB Davis
- JC Roberts
- JM Paramio
- JĂĄnos Prorok
- K Inoue
- Katalin JĂłsvay
- Kornélia Szabó
- KrisztiĂĄn KaszĂĄs
- L Karai
- LA Birder
- Lajos Kemény
- Leslie B. Vosshall
- LĂĄszlĂł Pecze
- M Denda
- M Hu-Tsai
- M Numazaki
- MD Southall
- MH Vos
- MJ Caterina
- MJ Caterina
- MK Chung
- Mårta Széll
- N Alessandri-Haber
- N Hellwig
- N Kedei
- P Boukamp
- P Facer
- P Gopinath
- PJ O'Connell
- PK Jensen
- S Basu
- S Stander
- SE Jordt
- SM Huang
- TamĂĄs Letoha
- TK Pareek
- V Sathianathan
- Z Olah
- Z Olah
- Z Olah
- ZoltĂĄn OlĂĄh
- Publication venue
- 'Public Library of Science (PLoS)'
- Publication date
- 01/01/2008
- Field of study
BACKGROUND: Use of capsaicin or resiniferatoxin (RTX) as analgesics is an attractive therapeutic option. RTX opens the cation channel inflammatory pain/vanilloid receptor type 1 (TRPV1) permanently and selectively removes nociceptive neurons by Ca(2+)-cytotoxicity. Paradoxically, not only nociceptors, but non-neuronal cells, including keratinocytes express full length TRPV1 mRNA, while patient dogs and experimental animals that underwent topical treatment or anatomically targeted molecular surgery have shown neither obvious behavioral, nor pathological side effects. METHODS: To address this paradox, we assessed the vanilloid sensitivity of the HaCaT human keratinocyte cell line and primary keratinocytes from skin biopsies. RESULTS: Although both cell types express TRPV1 mRNA, neither responded to vanilloids with Ca(2+)-cytotoxicity. Only ectopic overproduction of TRPV1 rendered HaCaT cells sensitive to low doses (1-50 nM) of vanilloids. The TRPV1-mediated and non-receptor specific Ca(2+)-cytotoxicity ([RTX]>15 microM) could clearly be distinguished, thus keratinocytes were indeed resistant to vanilloid-induced, TRPV1-mediated Ca(2+)-entry. Having a wider therapeutic window than capsaicin, RTX was effective in subnanomolar range, but even micromolar concentrations could not kill human keratinocytes. Keratinocytes showed orders of magnitudes lower TRPV1 mRNA level than sensory ganglions, the bona fide therapeutic targets in human pain management. In addition to TRPV1, TRPV1b, a dominant negative splice variant was also noted in keratinocytes. CONCLUSION: TRPV1B expression, together with low TRPV1 expression, may explain the vanilloid paradox: even genuinely TRPV1 mRNA positive cells can be spared with therapeutic (up to micromolar) doses of RTX. This additional safety information might be useful for planning future human clinical trials
Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)
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- 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.
- Amantini C.
- Amaral C.
- Ambrosio S.
- Amer A. O.
- Ammanathan V.
- An Z.
- Andersen S. U.
- Andrabi S. A.
- Andrade-Silva M.
- Andres A. M.
- Angelini S.
- Ann D.
- Anozie U. C.
- Ansari M. Y.
- Antas P.
- Antebi A.
- Anton Z.
- Anwar T.
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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-GĂłmez 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
- AntĂłn Z
- Anwar T
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- Apostolova N
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- Arasaki K
- Araya J
- AraĂșjo WL
- Arden C
- Arguelles S
- Arias E
- Arikkath J
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- Ariosa AR
- Armstrong-James D
- Arnauné-Pelloquin L
- Aroca A
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- Arsov I
- Artero R
- Arévalo M-A
- Asaro DML
- Aschner M
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- Ashur-Fabian O
- Atanasov AG
- Au AK
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- ĂstĂŒn S
- ÄoliÄ M
- ÄokiÄ J
- Ćœerovnik 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
Transient decrease in nociceptor GRK2 expression produces long-term enhancement in inflammatory pain
- Publication venue
- eScholarship, University of California
- Publication date
- 01/10/2012
- Field of study
In heterozygous mice, attenuation of G-protein-coupled receptor kinase 2 (GRK2) level in nociceptors is associated with enhanced and prolonged inflammatory hyperalgesia. To further elucidate the role of GRK2 in nociceptor function we reversibly decreased GRK2 expression using intrathecal antisense oligodeoxynucleotide (AS-ODN). GRK2 AS-ODN administration led to an enhanced and prolonged hyperalgesia induced by prostaglandin E(2), epinephrine and carrageenan. Moreover, this effect persisted unattenuated 2weeks after the last dose of antisense, well after GRK2 protein recovered, suggesting that transient attenuation of GRK2 produced neuroplastic changes in nociceptor function. Unlike hyperalgesic priming induced by transient activation of protein kinase C epsilon (PKCΔ), (Aley et al., 2000; Parada et al., 2003b), the enhanced and prolonged hyperalgesia following attenuation of GRK2 is PKCΔ- and cytoplasmic polyadenylation element binding protein (CPEB)-independent and is protein kinase A (PKA)- and Src tyrosine kinase (Src)-dependent. Finally, rats treated with GRK2 AS-ODN exhibited enhanced and prolonged hyperalgesia induced by direct activation of second messengers, adenyl cyclase, Epac or PKA, suggesting changes downstream of G-protein-coupled receptors. Because inflammation can produce a decrease in GRK2, such a mechanism could help explain a predilection to develop chronic pain, after resolution of acute inflammation
Heat and hyposmotic stimulation increase in [Ca2+]i by Ca2+ influx in rat synoviocytes
- Author
- B. Nilius
- E. Hinoi
- E. M. Gallo
- Fen Hu
- H. Takeda-Nakazawa
- H. Tosuji
- H. Watanabe
- I. B. McInnes
- J. Shou
- J. Vriens
- J. Vriens
- M. K. Chung
- M. Salmon
- M. Silva de
- M. Y. Kochukov
- N. Alessandri-Haber
- N. Alessandri-Haber
- N. Alessandri-Haber
- S. Mangos
- S. Shanfield
- T. Tsubaki
- W. Liedtke
- W. Liedtke
- WenWu Sun
- WenXiu Yang
- X. Gao
- X. Liu
- Y. Fu
- Y. M. Jiu
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- Field of study
4-isopropylcyclohexanol has potential analgesic effects through the inhibition of anoctamin 1, TRPV1 and TRPA1 channel activities
- Author
- A Caputo
- A Manglik
- A Wright
- AD Grant
- AM Peier
- B Billen
- B Lee
- B Nilius
- B Xiao
- BC Schroeder
- CJ Proudfoot
- D Julius
- DD McKemy
- F Huang
- F Huang
- H Cho
- H Chun
- H Salazar
- HS Smith
- JD Brunner
- JP Sapio
- JP White
- K Nagatomo
- K Talavera
- LJ Macpherson
- M Bandell
- M Gees
- M Takaishi
- MJ Caterina
- N Alessandri-Haber
- N Alessandri-Haber
- N Alessandri-Haber
- N Alessandri-Haber
- NR Gavva
- P Kanju
- P Scudieri
- RJ Laing
- SE Jordt
- T Ohta
- W Everaerts
- WM Knowlton
- X Jin
- Y Chen
- Y Karashima
- Y Takayama
- Y Takayama
- YA Alpizar
- YD Yang
- Z Xu
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- Field of study
Kinin Receptors Sensitize TRPV4 Channel and Induce Mechanical Hyperalgesia: Relevance to Paclitaxel-Induced Peripheral Neuropathy in Mice
- Author
- A Fox
- AD Grant
- C Kilkenny
- D Sachs
- DM Bautista
- E Rivera
- Elizabeth S. Fernandes
- F Marceau
- F Yanaga
- Fabiana Chaves Dias
- FC Meotti
- Gabriela C. Segat
- H Zhang
- HC Fan
- HH Chuang
- J Ferreira
- J Ferreira
- J Ferreira
- JB Calixto
- JL Hylden
- JoĂŁo B. Calixto
- K Mizumura
- KO Aley
- M Bandell
- Marianne N. Manjavachi
- MaĂra A. Bicca
- N Alessandri-Haber
- N Alessandri-Haber
- N Alessandri-Haber
- N Alessandri-Haber
- OA Dina
- P Cesare
- P Cesare
- PM Dougherty
- QP Ma
- QP Ma
- QP Ma
- R Costa
- R Costa
- R Costa
- RC Dutra
- RC Polomano
- Robson Costa
- S Materazzi
- S Wang
- TM Cunha
- W Everaerts
- W Liedtke
- WJ Dixon
- Y Chen
- Publication venue
- 'Springer Science and Business Media LLC'
- Publication date
- Field of study
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