International Consensus Statement on Obstructive Sleep Apnea.

Background: Evaluation and interpretation of the literature on obstructive sleep apnea (OSA) allows for consolidation and determination of the key factors important for clinical management of the adult OSA patient. Toward this goal, an international collaborative of multidisciplinary experts in sleep apnea evaluation and treatment have produced the International Consensus statement on Obstructive Sleep Apnea (ICS:OSA).

Methods: Using previously defined methodology, focal topics in OSA were assigned as literature review (LR), evidence-based review (EBR), or evidence-based review with recommendations (EBR-R) formats.

Central sleep apnea.

Central apnea syndrome is a disorder with protean manifestations and concomitant conditions. It can occur as a distinct clinical entity or as part of another clinical syndrome. The pathogenesis of central sleep apnea (CSA) varies depending on the clinical condition.

Secondary angiodysplasia-associated gastrointestinal bleeding in end-stage renal disease: Results from the nationwide inpatient sample.

Background: Chronic kidney disease is associated with angiodysplasia of gastrointestinal tract leading to increased risk of gastrointestinal bleeding.

Aim: To determine the nationwide prevalence, trends, predictors and resource utilization of angiodysplasia-associated gastrointestinal bleeding in end-stage renal disease hospitalizations.

Methods: The Nationwide Inpatient Sample database from 2009 to 2014, was utilized to conduct a retrospective study on patients with angiodysplasia associated- gastrointestinal bleeding and end-stage renal disease.

The Regulatory Role of Rac1, a Small Molecular Weight GTPase, in the Development of Diabetic Retinopathy.

Diabetic retinopathy, a microvascular complication of diabetes, remains the leading cause of vision loss in working age adults. Hyperglycemia is considered as the main instigator for its development, around which other molecular pathways orchestrate. Of these multiple pathways, oxidative stress induces many metabolic, functional and structural changes in the retinal cells, leading to the development of pathological features characteristic of this blinding disease.

Aminophylline shortage and current recommendations for reversal of vasodilator stress: An ASNC information statement endorsed by SCMR.

Pharmacologic reversal of serious or intolerable side effects (SISEs) from vasodilator stress is an important safety and comfort measure for patients experiencing such effects. While typically performed using intravenous aminophylline, recurrent shortages of this agent have led to a greater need to limit its use and consider alternative agents. This information statement provides background and recommendations addressing indications for vasodilator reversal, timing of a reversal agent, incidence of observed SISE with vasodilator stress, clinical and logistical considerations for aminophylline-based reversal, and alternative non-aminophylline based reversal protocols.

Aminophylline shortage and current recommendations for reversal of vasodilator stress: an ASNC information statement endorsed by SCMR.

Pharmacologic reversal of serious or intolerable side effects (SISE) from vasodilator stress is an important safety and comfort measure for patients experiencing such effects. While typically performed using intravenous aminophylline, recurrent shortages of this agent have led to a greater need to limit its use and consider alternative agents. This information statement provides background and recommendations addressing indications for vasodilator reversal, timing of a reversal agent, incidence of observed SISE with vasodilator stress, clinical and logistical considerations for aminophylline-based reversal, and alternative non-aminophylline based reversal protocols.

Three-dimensional echocardiography in acute heart failure: Can and should we do it in the emergency department?

Despite its proven superiority over two-dimensional transthoracic echocardiography (2DTTE) for left ventricular (LV) volumes and ejection fraction, clinical use of 3DTTE remains very limited in the acute setting. 3DTTE may have significant clinical advantages in the assessment of acute heart failure. Further exploration of 3DTTE utilization may help in more precise assessment of the regional wall-motion abnormalities, early identification of acute ischemic from nonischemic LV dysfunction with a more precise approach to the AHF management.

COPII-Dependent ER Export: A Critical Component of Insulin Biogenesis and β-Cell ER Homeostasis.

Pancreatic β-cells possess a highly active protein synthetic and export machinery in the endoplasmic reticulum (ER) to accommodate the massive production of proinsulin. ER homeostasis is vital for β-cell functions and is maintained by the delicate balance between protein synthesis, folding, export, and degradation. Disruption of ER homeostasis by diabetes-causing factors leads to β-cell death.

Methylation profile landscape in mesothelioma: possible implications in early detection, disease progression, and therapeutic options.

Malignant Pleural Mesothelioma (MPM) is an aggressive malignancy of the pleura associated with asbestos exposure. Incidence of MPM is expected to increase over the course of next decade in both Europe and the developing countries. Although significant progress has been made in terms of etiology and pathogenesis of this disease, currently available therapeutic options have not significantly improved the survival outcome of patients on standard chemotherapeutic regimens.

Liver hemangioma complicated by obstructive jaundice.

This report describes a liver hemangioma causing obstructive jaundice, an extremely rare condition that has been reported on 3 previous occasions. A hemangioma can compress the major bile ducts and require partial hepatectomy for a successful outcome.

Akt2, but not Akt1 or Akt3 mediates pressure-stimulated serum-opsonized latex bead phagocytosis through activating mTOR and p70 S6 kinase.

Monocytes and macrophages play critical roles in innate host defense and are sensitive to mechanical stimuli. Tissue pressure is often altered in association with inflammation or infection. Low pressure (20 mmHg), equivalent to normal tissue pressure, increases phagocytosis by primary monocytes and PMA-differentiated THP-1 macrophages, in part by FAK and ERK inhibition and p38 activation.

Aminopropionic acid receptors in paraventricular nucleus mediate pressor and vasopressin responses to endothelin-1 in subfornical organ.

Endothelin-1 (ET-1) acts at selected brain loci to elicit a pressor response and secretion of vasopressin (AVP). Glutamatergic receptors of the N-methyl-D-aspartate (NMDA) subtype mediate ET-1-induced AVP secretion in vitro, but the role of glutamatergic receptors in the pressor response and the secretion of AVP in vivo has not been studied. We hypothesized that both the pressor response and AVP secretion in response to ET-1 microinjection into subfornical organ (SFO) would be suppressed by ionotropic glutamatergic receptor antagonists in the paraventricular nucleus (PVN).

Nitric oxide modulation of ET(B) receptor-induced vasopressin release by rat and mouse hypothalamo-neurohypophyseal explants.

Endothelin (ET) peptides stimulate vasopressin (AVP) secretion via ET(B) receptors at hypothalamic loci. Nitric oxide modulates the actions of ET in the cardiovascular system and also influences neurotransmission and specifically suppresses firing of magnocellular neurons. The purpose of these studies was to ascertain whether nitric oxide, generated in response to ET(B) receptor stimulation, buffers the stimulatory effect of ET and suppresses AVP release.

Neuronal nitric oxide synthase activity in the paraventricular nucleus buffers central endothelin-1- induced pressor response and vasopressin secretion.

Endothelin 1 (ET-1) injected into the lateral cerebral ventricle increases sympathetic output, arterial pressure and plasma vasopressin (AVP). These responses are mediated by glutamatergic inputs and inhibited by gamma-amino-butyric acidergic inputs in the paraventricular nucleus (PVN). It has been suggested that nitric oxide enhances these gamma-amino-butyric acidergic inhibitory inputs.

Identification of intelectin overexpression in malignant pleural mesothelioma by serial analysis of gene expression (SAGE).

Malignant pleural mesothelioma (MPM) is a fatal neoplasm with no acceptable curative approaches. We used serial analysis of gene expression (SAGE) to compare the gene expression pattern of a surgically resected MPM to the autologous normal mesothelium. Intelectin gene overexpression (>139-fold) was found in the tumor.

Acute actions of testosterone on contractile function of isolated rat ventricular myocytes.

Variation between the sexes in cardiac function have been established. The extent to which sex hormones are responsible for these differences is unclear. The current study was designed to determine whether testosterone acts acutely to enhance contractility of cultured rat ventricular myocytes.

Gonadectomy alters myosin heavy chain composition in isolated cardiac myocytes.

Sex differences in cardiac function have been identified. Studies suggest that the presence of testosterone in males may contribute to the observed differences in cardiac function. Our laboratory has shown previously that testosterone treatment of gonadectomized adult male rats enhances contractility of isolated rat ventricular myocytes.

Testosterone regulates mRNA levels of calcium regulatory proteins in cardiac myocytes.

Gender-related differences in cardiac function have been described in the literature, but whether the presence of sex hormones is responsible for these differences remains unclear. This study was designed to determine whether testosterone regulates the gene expression of calcium regulatory proteins in rat heart, thus playing a role in gender-related differences in cardiac performance. Ventricular myocytes were isolated from two-day-old rats and treated with testosterone at varying duration; the levels of gene expression for the androgen receptor (AR) and major calcium regulatory proteins were determined by quantitative real-time PCR.

Extracellular pressure stimulates macrophage phagocytosis by inhibiting a pathway involving FAK and ERK.

We hypothesized that changes in extracellular pressure during inflammation or infection regulate macrophage phagocytosis through modulating the focal adhesion kinase (FAK)-ERK pathway. Undifferentiated (monocyte-like) or PMA-differentiated (macrophage-like) THP-1 cells were incubated at 37 degrees C with serum-opsonized latex beads under ambient or 20-mmHg increased pressure. Pressure did not affect monocyte phagocytosis but significantly increased macrophage phagocytosis (29.

Paradigms for mechanical signal transduction in the intestinal epithelium. Category: molecular, cell, and developmental biology.

Diverse physical forces including deformation or strain, pressure, and shear stress affect the intestinal mucosa during normal function, and mucosal biology is altered in pathological states in which these forces alter. Taken together with evidence in other tissues and cell types that physical forces can affect cell biology, this has led to the hypothesis that repetitively applied physical forces can initiate intracellular signals that alter intestinal epithelial proliferation and phenotype. This review outlines the nature of such forces and summarizes in vivo and in vitro evidence in support of the paradigm that repetitive force is trophic for the intestinal mucosa via a complex cascade of intracellular signals.

Divalent cations modulate human colon cancer cell adhesion.

Background: Iatrogenic tumor implantation within surgical sites can compromise curative cancer surgery. Cancer cell adhesion to extracellular matrix proteins is mediated by diverse matrix receptors, most notably integrins. Divalent cations may modulate integrin-ligand interactions in some cells.

Modulation of ET(B) receptor-induced arginine-vasopressin secretion by N-methyl-D-aspartate (NMDA) and gamma-aminobutyric acid (GABA)-dependent mechanisms in hypothalamo-neurohypophysial explants.

The endothelins (ETs) stimulate the secretion of arginine-vasopressin (AVP) in vivo and in vitro. The activation of hypothalamic ET(B) receptors increases AVP release, but the neurotransmitters mediating these responses are not known. In the compartmentalized hypothalamo-neurohypophysial explant model, the overall basal release of AVP was 53+/-17 pg x h(-1) x PP(-1) (where PP is posterior pituitary).

Endothelin 1-induced pressor response and vasopressin release in rats with heart failure.

Heart failure (HF) is characterized by activation of both neurohumoral and sympathetic nervous systems. Specifically, HF is associated with increases in vasopressin (VP) and endothelin (ET) and in arterial baroreflex dysfunction. Hypothesis was that central ET-1 potentiates VP secretion in HF due to impaired pressor response and diminished arterial baroreflex inhibition.