Are sTAT3 and importins novel mediators of early molecular and cellular responses in experimental duodenal ulceration?
Thus, STAT3 represents an important new molecular mechanism in experimental duodenal ulceration.
Postischemic extremities exhibited a transient, early burst of TNF release on reperfusion, which likely represented washout of TNF produced during ischemia. Suppression of TNF activity with an antibody to TNF-alpha resulted in a salutary increase in postischemic flow rates, suggesting that TNF may play a role in the no-reflow phenomenon.