Results 211 to 220 of about 688,075 (263)

Publisher Correction: IL-33/ST2 drives inflammatory pain via CCL2 signaling and activation of TRPV1 and TRPM8. [PDF]

Commun Biol
Wang L, Zhang J, Qiu S, Huang R, Wang Y, Wang Y, Li M, Ye Q, Zhang S, Qi Z, Cao L, Li G, An Y, Xie D, Mi W, Wang H, Luo T, Xie J, Huang J.   +18 more
europepmc   +1 more source

Caffeic acid phenethyl ester attenuates inflammatory pain through promoting spinal microglial M1-to-M2 polarization by suppressing the PI3K/Akt/NF-κB pathway and attenuating peripheral inflammation. [PDF]

Mol Pain
Wang D, Li Y, Ni C, Xu L, Huang X, Zhang S, Shen G, Zhang H, Ni H, Yao M, Lin X, Liu G.   +11 more
europepmc   +1 more source

IL-33/ST2 drives inflammatory pain via CCL2 signaling and activation of TRPV1 and TRPM8. [PDF]

Commun Biol
Wang L, Zhang J, Qiu S, Huang R, Wang Y, Wang Y, Li M, Ye Q, Zhang S, Qi Z, Cao L, Li G, An Y, Xie D, Mi W, Wang H, Luo T, Xie J, Huang J.   +18 more
europepmc   +1 more source

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Prostanoids and inflammatory pain

Prostaglandins and Other Lipid Mediators, 2013
Prostanoids play pivotal roles in inflammation and pain. Cyclooxygenase (COX) inhibitors, the nonsteroidal anti-inflammatory drugs (NSAIDs), depress prostanoid formation and are widely used to treat inflammatory pain. However, their therapeutic benefit is offset by serious side-effects, primarily gastrointestinal and cardiovascular complications ...
Lihong Chen, Guangrui Yang, Tilo Groser   +2 more
exaly   +3 more sources

Bradykinin and inflammatory pain

Trends in Neurosciences, 1993
There is compelling evidence linking bradykinin (BK) with the pathophysiological processes that accompany tissue damage and inflammation, especially the production of pain and hyperalgesia. Several mechanisms have been proposed to account for hyperalgesia including the direct activation of nociceptors as well as sensitization of nociceptors through the
A, Dray, M, Perkins
openaire   +4 more sources

Inflammatory pain: kinins and antagonists

Current Opinion in Anaesthesiology, 2001
This short review focuses on the most recent findings in the rapidly expanding field of kinin research. Through a series of recent publications, the crucial relevance of this group of peptides as mediators of inflammatory pain is becoming increasingly evident.
J B, Calixto, D A, Cabrini, J, Ferreira, M M, Campos   +3 more
openaire   +2 more sources

Inflammatory pain

Current Opinion in Anaesthesiology, 1992
Traditionally, non-steroidal anti-inflammatory drugs (NSAIDs) have been advocated for inflammatory pain. Studies in arthritic rats have shown that inflammatory pain is more sensitive to opioids than other types of nociceptive pain.
openaire   +1 more source

Optogenetic Neuromodulation in Inflammatory Pain

Neuroscience
Inflammatory pain is one of the most prevalent forms of pain and negatively influences the quality of life. Neuromodulation has been an expanding field of pain medicine and is accepted by patients who have failed to respond to several conservative treatments.
Yanan Liang, Yaping Zhou, Md. Moneruzzaman, Yonghui Wang   +3 more
openaire   +2 more sources

Local control of inflammatory pain

Agents and Actions, 1981
The mechanism of the local hyperalgesic action of prostaglandin E2 has been studied using rat paw oedema. Prostaglandin E2 is a metabotropic transmitter, activating adenylate cyclase, either directly or through the release of a stimulatory protein factor. This activation of adenylate-cyclase is blocked, locally, by opiates.
openaire   +2 more sources

Physiological, Inflammatory and Neuropathic Pain

1987
The confusion amongst clinicans and basic scientists as to what precisely pain is, is emblematic of the difficulties that confront all who attempt to elucidate its pathogenesis. A major contributor to this state of affairs would appear to have been Charles Sherrington. At the turn of the century, with great insight, he focussed attention away from pain
openaire   +2 more sources