Cardio-cerebrovascular complications from Nd:YAG laser treatment of lung cancer.

The laser palliation of patients with unresectable lung cancer has an acceptable complication rate. Perforation, bleeding, and pneumothorax are the main complications described. Cardiovascular morbidity has been reported to be 1% in six surgical series and has been attributed to general anesthetics or hypoxia. However, one very recent anesthesia study described a 25% incidence, and two case reports inferred an air embolism. We reviewed 62 patients who have undergone 111 treatments for endobronchial carcinoma. Eight manifested perioperative cardiac or cerebral events. Five of the eight developed bradycardia; four experienced progression to intraoperative cardiac arrest. Other electrocardiographic abnormalities appeared and resolved within 24 hours. Four patients developed stroke and electrocardiographic changes. Two of these resolved spontaneously within 1 month. Early computed tomography in one patient showed intracerebral air. These data indicate that patient disease or hypoxemia is not sufficient to explain intraoperative cardiac and postoperative cerebral changes. Air embolism to the cerebral circulation occurs during laser bronchoscopy. Reduced cooling air flow, return to helium fiber cooling, or reversion to photodynamic therapy is indicated.

Improved measurement of the positive-muon lifetime and determination of the Fermi constant.

The mean life of the positive muon has been measured to a precision of 11 ppm using a low-energy, pulsed muon beam stopped in a ferromagnetic target, which was surrounded by a scintillator detector array. The result, tau(micro)=2.197 013(24) micros, is in excellent agreement with the previous world average. The new world average tau(micro)=2.197 019(21) micros determines the Fermi constant G(F)=1.166 371(6)x10(-5) GeV-2 (5 ppm). Additionally, the precision measurement of the positive-muon lifetime is needed to determine the nucleon pseudoscalar coupling g(P).

Evidence for insulin degradation by muscle and fat tissue in an insulin resistant diabetic patient.

The period before, during and after resistance to subcutaneous insulin in a 20-year-old, non-obese insulin-dependent patient with 'brittle' diabetes is documented and clinical observations are correlated with experimental results of insulin degradation in vitro. Treatment with intravenous but not subcutaneous aprotinin markedly reduced subcutaneous insulin requirements. Insulin resistance recurred following cessation of aprotinin. Serum free insulin levels were low during the subcutaneous resistant phase compared with those during the more sensitive phase. Insulin degradation in vitro by adipose tissue and muscle taken from the patient during a resistant phase was increased compared with degradation by tissue taken during a sensitive phase and by tissue from normal subjects. Chromatography of incubation media revealed that during the resistant phase, tissue from the patient degraded insulin to small fragments. It is concluded that, in this patient, insulin resistance was caused by excessive degradation in both muscle and adipose tissue.