B. B. Lorenzetti

Publications45
h-index29
Citations5,148
Highly Influential Citations191
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The pivotal role of tumour necrosis factor alpha in the development of inflammatory hyperalgesia.
TLDR
The delineation of the role of TNF alpha,IL-1 beta, IL-6 and IL-8 in the development of inflammatory hyperalgesia taken together with the finding that the production of these cytokines is inhibited by steroidal anti-inflammatory drugs provides a mechanism of action for these drugs in the treatment ofinflammatory hyperalGESia.
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The pivotal role of tumour necrosis factor α in the development of inflammatory hyperalgesia
TLDR
Results show that TNFα has an early and crucial role in the development of inflammatory hyperaglesia and the finding that the production of these cytokines is inhibited by steroidal anti‐inflammatory drugs provides a mechanism of action for these drugs in the treatment ofinflammatory hyperalgesia.
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Interleukin-1β as a potent hyperalgesic agent antagonized by a tripeptide analogue
TLDR
An analgesic tripeptide analogue of IL-1β is developed which antagonizes hyperalgesia evoked by IL- 1β and by the inflammatory agent carrageenan.
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Central and peripheral antialgesic action of aspirin-like drugs.
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Bradykinin initiates cytokine‐mediated inflammatory hyperalgesia
TLDR
Data show that bradykinin can initiate the cascade of cytokine release that mediates hyperalgesic responses to carrageenin and endotoxin, and suggests that the release of hyperAlgesic cytokines can be initiated independently of bradyKinin BK2 receptors.
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Peripheral analgesia and activation of the nitric oxide-cyclic GMP pathway.
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Interleukin‐8 as a mediator of sympathetic pain
TLDR
IL‐8 is the first endogenous mediator to be identified as evoking hyperalgesia involving the sympathetic nervous system, and a new biological activity of IL-8 is described, namely the capacity to evoke hyperAlgesia by a prostaglandin‐independent mechanism.
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Cytokine‐mediated inflammatory hyperalgesia limited by interleukin‐10
TLDR
The data suggest that IL‐10 limits the inflammatory hyperalgesia evoked by carrageenin and bradykinin by two mechanisms: inhibition of cytokine production and inhibition of IL‐1β evoked PGE2 production.
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The molecular mechanism of action of peripheral morphine analgesia: stimulation of the cGMP system via nitric oxide release.
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Role of lipocortin‐1 in the anti‐hyperalgesic actions of dexamethasone
TLDR
It is suggested that, in inflammatory hyperalgesia, inhibition of the induction of cyclo‐oxygenase 2 (COX‐2), rather than phospholipase A2, by dexamethasone and lipocortin‐12–26 contributing, in part, to this role.
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