Impact of Giving Patients Your Personal Phone Number in Otolaryngology-Head & Neck Surgery.

Objective: Patient-provider communication is a major barrier to care, with some providers giving their personal phone number (PPN) to patients for increased accessibility. We investigated participant utilization of provider's PPN, its effect on participant satisfaction, provider's ability to predict abuse of this practice, and evolving provider perceptions.

Study Design: Prospective, randomized study.

Transabdominal laparoscopic adrenalectomy of a large adrenal lipoma: A case report and review of literature.

The exponential increase in use of computer tomography (CT) and magnetic resonance imaging (MRI) has lead to a significant increase in the detection of asymptomatic adrenal masses. The prevalence of adrenal "incidentalomas" is approximately 4-10%. We present a case of a 55-year-old male with a large right adrenal mass that was followed by serial computer tomography scans and multiple non-diagnostic core biopsies.

The role of cardiac troponin T quantity and function in cardiac development and dilated cardiomyopathy.

Background: Hypertrophic (HCM) and dilated (DCM) cardiomyopathies result from sarcomeric protein mutations, including cardiac troponin T (cTnT, TNNT2). We determined whether TNNT2 mutations cause cardiomyopathies by altering cTnT function or quantity; whether the severity of DCM is related to the ratio of mutant to wildtype cTnT; whether Ca(2+) desensitization occurs in DCM; and whether absence of cTnT impairs early embryonic cardiogenesis.

Methods And Findings: We ablated Tnnt2 to produce heterozygous Tnnt2(+/-) mice, and crossbreeding produced homozygous null Tnnt2(-/-) embryos.

Leptin signalling reduces the severity of cardiac dysfunction and remodelling after chronic ischaemic injury.

Aims: Leptin is elevated under conditions of both obesity and heart failure (HF), and activation of leptin receptor (ObR) signalling is known to increase in vivo cardiac contractility and to have anti-hypertrophic effects on the left ventricle (LV). However, it is unknown whether ObR signalling is altered in cardiomyocytes after myocardial infarction (MI) leading to HF, or if a deficiency in ObR signalling leads to worse HF.

Methods And Results: In separate experimental protocols, C57BL/6J and leptin-deficient (ob/ob) mice underwent open-chest surgery to induce permanent left coronary artery ligation (CAL) or had a sham operation.

A PRKAG2 mutation causes biphasic changes in myocardial AMPK activity and does not protect against ischemia.

Dominant mutations in the gamma2 regulatory subunit of AMP-activated protein kinase (AMPK), encoded by the gene PRKAG2, cause glycogen storage cardiomyopathy. We sought to elucidate the effect of the Thr400Asn (T400N) human mutation in a transgenic mouse (TGT400N) on AMPK activity, and its ability to protect the heart against ischemia-reperfusion injury. TGT400N hearts had markedly vacuolated myocytes, excessive accumulation of glycogen, hypertrophy, and preexcitation.

In vivo alpha-adrenergic responses and troponin I phosphorylation: anesthesia interactions.

The mechanisms by which alpha-adrenergic stimulation of the heart in vivo can cause contractile dysfunction are not well understood. We hypothesized that alpha-adrenergic-mediated contractile dysfunction is mediated through protein kinase C phosphorylation of troponin I, which in in vitro experiments has been shown to reduce actomyosin Mg-ATPase activity. We studied pressure-volume loops in transgenic mice expressing mutant troponin I lacking protein kinase C phosphorylation sites and hypothesized altered responses to phenylephrine.