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The maximal steady-state force values were 13,137 ± 3647, 12,921 ± 3684, and 21,673 ± 7189 N/m 2 for control, normotensive, and preeclamptic samples at 10-μmol/L histamine (P ≤.05, compared with control placental extracts).
Interestingly, despite seizure abolishment, diazepam significantly enhanced tramadol-induced increase in the brain serotonin (p < 0.01), histamine (p < 0.01), dopamine (p < 0.05) and norepinephrine (p < 0.05) while no significant modifications were observed with the other tested pretreatments.
The addition of vasoactive drugs produced an approximately 3-fold increase with an increase to a mean tumour:liver ratio of 3.24 (s.d. = 1.39) for histamine (P less than 0.001 compared to systemic delivery), 3.21 (s.d. = 1.13, P less than 0.001) for leukotriene C4 and 3.80 (s.d. = 1.53, P less than 0.001) for interleukin-2.
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Three subjects in each group used histamine antagonists (p = 1.0, Fisher exact test).
Results from this experiment revealed that histamine significantly (P < 0.01) suppressed food intake with no effect on water consumption.
These mediators serotonin, bradykinin, histamine, substance P, and atrial natriuretic factor exhibit a potent vasodilating action on the brain [22, 30, 31].
Histamine, substance P and Kp-10 injection caused significant plasma extravasation formation in the dorsal skin 15 minutes post-injection when compared to control (saline) (Figure 3).
Many other untested cytokines (e.g. IL1, IL4), chemokines (e.g. MCP-1, IL8), proteases (e.g. neutrophil elastase, tryptase, cysteinyl cathepsins), and other inflammatory mediators (e.g. histamine, substance P, and angiotensin-II) may also contribute to endothelium activation via various mechanisms.
Treatment with OVA and PNA significantly induced plasma histamine concentrations (p < 0.05).
Acetic acid induces pain by liberating endogenous substances (bradykinin, serotonin, histamine, substance P) [ 39], which in turn excite the pain nerve endings.
Our results showed that significant increase of histamine release (P < 0.05) occurs during anaphylaxis (10.35 10.45 · 10−8 μM) in the absence of glucagon (Table 2).
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