The feasibility of a telecommunications service in support of outpatient congestive heart failure care in a diverse patient population.

A home telemonitoring system for patients with congestive heart failure was studied for feasibility and efficacy in a diverse patient population. Fifty patients used the service, in which they weighed themselves and answered yes/no questions about symptoms. Changes in patient weights or symptoms prompted a nurse to call the patient and/or the physician.

Conditional expression of a Gi-coupled receptor causes ventricular conduction delay and a lethal cardiomyopathy.

Cardiomyopathy is a major cause of morbidity and mortality. Ventricular conduction delay, as shown by prolonged deflections in the electrocardiogram caused by delayed ventricular contraction (wide QRS complex), is a common feature of cardiomyopathy and is associated with a poor prognosis. Although the G(i)-signaling pathway is up-regulated in certain cardiomyopathies, previous studies suggested this up-regulation was compensatory rather than a potential cause of the disease.

Benzocaine-induced methemoglobinemia--two case reports related to transesophageal echocardiography premedication.

Benzocaine-induced methemoglobinemia is a potentially life-threatening complication. We report two cases of methemoglobinemia due to topical benzocaine spray used as premedication for transesophageal echocardiography. A high index of suspicion is needed for this readily treatable condition.

Thrombin receptor activating mutations. Alteration of an extracellular agonist recognition domain causes constitutive signaling.

Constitutively active thrombin receptors were generated while constructing chimeric receptors to identify the structural basis for thrombin receptor agonist specificity. Substitution of eight amino acids from the Xenopus receptor's second extracellular loop (XECL2B) for the cognate sequence in the human thrombin receptor was sufficient to confer robust constitutive activity. Smaller substitutions within the XECL2B site yielded less constitutive activation, and substitution of several unrelated sequences at this site caused no activation.

Mechanisms of thrombin receptor agonist specificity. Chimeric receptors and complementary mutations identify an agonist recognition site.

Identification of the docking interactions by which peptide agonists activate their receptors is critical for understanding signal transduction at the molecular level. The human and Xenopus thrombin receptors respond selectively to their respective hexapeptide agonists, SFLLRN and TFRIFD. A systematic analysis of human/Xenopus thrombin receptor chimeras revealed that just two human-for-Xenopus amino acid substitutions, Phe for Asn87 in the Xenopus receptor's amino-terminal exodomain and Glu for Leu260 in the second extracellular loop, conferred human receptor-like specificity to the Xenopus receptor.