Expiratory muscle action is prominent during anaesthesia and can impair lung function. This activity is exaggerated by the use of opioids. Airway pressure during occlusion of expiration would be a valuable measure

in the study of expiratory muscle activation. However, this would only be valid if the imposed occlusion did not itself alter muscle activation. This possibility can be checked by directly assessing muscle activity by electromyography; varying arterial carbon dioxide tensions and opioid action should be considered.\n\nMethods. We studied seven spontaneously breathing patients, anaesthetized with nitrous oxide and isoflurane, in four conditions: during an infusion of fentanyl and after naloxone, breathing normally and with breathing stimulated with CO2. We compared selleck chemicals diaphragm and external oblique abdominal electromyogram (EMG) signals during normal find protocol and occluded breaths. We also measured chest wall volume and compared airway occlusion pressure, during inspiration and expiration, with the EMG results.\n\nResults. Inspiratory occlusion increased the duration of inspiration during hypercapnia

by 20%, but not the rate of electrical activation of the diaphragm, indicating that occlusion does not cause a reflex increase in diaphragm contraction. In contrast, expiratory occlusion did not affect either the duration of expiration or the electrical activity of the external oblique muscles.\n\nConclusions. In these conditions, except for a change in inspiratory duration, respiratory muscle activity is unaffected by airway occlusion. Airway occlusion will permit valid measures of muscle activity in inspiration and expiration and provide simple measurements of respiratory muscle function during anaesthesia.”
“Escherichia coli DksA and GreB bind to RNA polymerase (RNAP), reaching inside the

secondary channel, with similar affinities but have different cellular functions. DksA destabilizes promoter complexes whereas VS-6063 GreB facilitates RNA cleavage in arrested elongation complexes (ECs). Although the less abundant GreB may not interfere with DksA regulation during initiation, reports that DksA acts during elongation and termination suggest that it may exclude GreB from arrested complexes, potentially triggering genome instability. Here, we show that GreB does not compete with DksA during termination whereas DksA, even when present in several hundredfold molar excess, does not inhibit GreB-mediated cleavage of the nascent RNA. Our findings that DksA does not bind to backtracked or active ECs provide an explanation for the lack of DksA activity on most ECs that we reported previously, raising a question of what makes a transcription complex susceptible to DksA. Structural modeling suggests that i6, an insertion in the catalytic trigger loop, hinders DksA access into the channel, restricting DksA action to a subset of transcription complexes.