Can we afford to let sleeping dogs lie?

In patients with chronic myelogenous leukemia (CML) mutations of the BCR-ABL kinase domain (KD) have been identified as the leading cause of acquired resistance to imatinib, while the mechanisms underlying the persistence of minimal residual disease (MRD) are unknown. In this issue of Blood, Chu and colleagues report several patients with KD mutations at the time of complete cytogenetic response (CCR), implicating mutations as a cause of disease persistence.     

Influence of pre-exercise acidosis and alkalosis on the kinetics of acid-base recovery following intense exercise

The purpose of this study was to measure the recovery kinetics of pH and lactate for the conditions of pre-exercise acidosis, alkalosis, and placebo states. Twelve trained male cyclists completed 3 exercise trials (110% workload at VO2max), ingesting either 0.3 g/kg of NH4Cl (ACD), 0.2 g/kg of Na+HCO3- and 0.2 g/kg of sodium citrate (ALK), or a placebo (calcium carbonate) (PLAC). Blood samples (heated dorsal hand vein) were drawn before, during, and after exercise. Exercise-induced acidosis was more severe in the ACD and PLAC trials (7.15 +/- 0.06, 7.21 +/- 0.07, 7.16 +/- 0.06, P < 0.05, for ACD, ALK, PLAC, respectively). Recovery kinetics for blood pH and lactate, as assessed by the monoexponential slope constant, were not different between trials (0.057 +/- 0.01, 0.050 +/- 0.01, 0.080 +/- 0.02, for ACD, ALK, PLAC, respectively). Complete recovery of blood pH from metabolic acidosis can take longer than 45 min. Such a recovery profile is nonlinear, with 50% recovery occurring in approximately 12 min. Complete recovery of blood lactate can take longer than 60 min, with 50% recovery occurring in approximately 30 min. Induced alkalosis decreases metabolic acidosis and improves pH recovery compared to acidodic and placebo conditions. Although blood pH and lactate are highly correlated during recovery from acidosis, they recover at significantly different rates.     

A novel approach to the management of persistent postpneumonectomy bronchopleural fistula

A 69-year-old man who had a left pneumonectomy for nonsmall cell lung cancer had a bronchopulmonary fistula develop that recurred after surgical closure. He had multiple organ failure develop precluding further operative intervention. Successful resolution of the fistula was achieved using a novel application of a covered expandable metallic stent.     

Rigid bronchoscopy-guided percutaneous tracheostomy

We describe a case series of seven patients that demonstratesthe usefulness of rigid bronchoscopy in percutaneous tracheostomy.The technique was used in selected patients who had a previoustracheostomy, a difficult airway, high risk of bleeding, ora tracheal stent in place.     

Electrical stimulation restores the specificity of sensory axon regeneration

Electrical stimulation at the time of nerve repair promotes motoneurons to reinnervate appropriate pathways leading to muscle and stimulates sensory neurons to regenerate. The present experiments examine the effects of electrical stimulation on the specificity of sensory axon regeneration. The unoperated rat femoral cutaneous branch is served by 2-3 times more DRG neurons than is the muscle branch. After transection and repair of the femoral trunk, equal numbers of DRG neurons project to both branches. However, 1 h of electrical stimulation restores the normal proportion of DRG neurons reinnervating skin and muscle. To ask if the redistribution of stimulated neurons results from enhanced specificity of target reinnervation, we developed a new technique of sequential double labeling. DRG neurons projecting to the femoral muscle branch were prelabeled with Fluoro Gold 2 weeks before the nerve was transected proximally and repaired with or without 1 h of 20-Hz electrical stimulation. Three weeks after repair, the muscle nerve was labeled a second time with Fluororuby. The percentage of regenerating neurons that both originally served muscle and returned to muscle after nerve repair increased from 40% without stimulation to 75% with stimulation. Electrical stimulation thus dramatically alters the distribution of regenerating sensory axons, replacing normally random behavior with selective reinnervation of tissue-specific targets. If the enhanced regeneration specificity resulting from electrical stimulation is found to improve function in a large animal model, this convenient and safe technique may be a useful adjunct to clinical nerve repair.