Cardiac arrest resuscitation: neurologic prognostication and brain death.

Purpose Of Review: Persistent coma after cardiac arrest is a source of great emotional and financial cost to grieving family members in particular and the healthcare system in general. Neurologic prognostication helps guide appropriate discussions between family members and healthcare providers. Recent advances in therapeutic care increase the challenges, both medical and financial, on local practitioners.

Asthma, allergy, and airway hyperresponsiveness are not linked to the beta(2)-adrenoceptor gene.

Study Objectives: To exclude genetic linkage between the beta(2)-adrenoceptor gene and asthma, allergy, and methacholine airway hyperresponsiveness.

Design: The current study used six distinct intragene markers within the beta(2)-adrenoceptor gene, and evaluated genetic linkage between the beta(2)-adrenoceptor and asthma, allergy, or methacholine airway hyperresponsiveness in eight multiplex families.

Patients: Forty-nine members of eight multiplex families with a high incidence of asthma.

Genetic linkage analysis of susceptibility to particle exposure in mice.

Particle-induced increases in respiratory morbidity and mortality have been observed worldwide in industrialized cities but the toxicologic mechanisms have not been elucidated. It is hypothesized that subpopulations including the elderly and individuals with cardiopulmonary disease are particularly at risk to the effects of exposure. Genetic background is another important host factor that may contribute to interindividual responsivity to particulate exposure.

Facile detection of mitochondrial DNA mutations in tumors and bodily fluids.

Examination of human bladder, head and neck, and lung primary tumors revealed a high frequency of mitochondrial DNA (mtDNA) mutations. The majority of these somatic mutations were homoplasmic in nature, indicating that the mutant mtDNA became dominant in tumor cells. The mutated mtDNA was readily detectable in paired bodily fluids from each type of cancer and was 19 to 220 times as abundant as mutated nuclear p53 DNA.