Outcome after complete percutaneous removal of infected pacemaker systems and implantable cardiac defibrillators.

The mortality of retained, infected pacemaker systems is high. We assessed the safety and rate of relapse of infection after complete percutaneous removal of leads of infected pacemaker systems. None of the 40 subjects experienced procedure-related mortality and there were no cases of relapse after a median duration of follow up of 8 years (range, 3 months to 12 years).

Writing-skills development in the health professions.

Background: Studies have found that students in the medical professions often lack the writing skills required during their education and career. One contributing factor to this deficiency is that writing tends to be discipline specific, rather than requiring general skills acquired in undergraduate schools.

Purpose: To determine the extent to which a rigorous writing exercise impacted the quality of students' medical writing based on a specified rubric.

Microdomains of high calcium are not required for exocytosis in RBL-2H3 mucosal mast cells.

We have previously shown that store-associated microdomains of high Ca(2+) are not essential for exocytosis in RBL-2H3 mucosal mast cells. We have now examined whether Ca(2+) microdomains near the plasma membrane are required, by comparing the secretory responses seen when Ca(2+) influx was elicited by two very different mechanisms. In the first, antigen was used to activate the Ca(2+) release-activated Ca(2+) (CRAC) current (I(CRAC)) through CRAC channels.

Calcium influx through L-type channels is required for selective activation of extracellular signal-regulated kinase by gonadotropin-releasing hormone.

The hypothalamic decapeptide gonadotropin-releasing hormone stimulates mobilization of two discrete pools of calcium in clonal (alphaT3-1) and primary pituitary gonadotropes. A multidisciplinary approach was implemented to investigate the effects of discrete calcium fluctuations on the signaling pathways linking the gonadotropin-releasing hormone receptor to activation of mitogen-activated protein kinases and immediate early genes. Blockade of calcium influx through nifedipine-sensitive voltage-gated calcium channels reduced buserelin-induced activation of extracellular signal-regulated kinase (ERK) and c-Fos while activation of c-Jun N-terminal kinase and c-Jun was unaffected.