An Unexpected Lymphoma: A Rare Case of Primary Gastric Burkitt's Lymphoma.

Primary gastric Burkitt's lymphoma is an aggressive non-Hodgkin's lymphoma that has been rarely reported in the literature. The majority of primary gastric lymphomas are diffuse large B-cell lymphomas and mucosa-associated lymphoid tissue (MALT) lymphomas. Patients with primary gastric Burkitt's lymphoma can present with abdominal pain, hematemesis, melena, perforation, and obstruction.

A rare case of primary diffuse large B-cell lymphoma of the colon.

The gastrointestinal tract is the most common site in the United States for extra-nodal lymphoma involvement. Primary colorectal involvement is very rare, only accounting for 0.3% of the large intestine cancers.

Usefulness of PA32540 in Protecting the Gastric Layer While Providing Secondary Prevention for Coronary Artery Disease.

Aspirin has been the mainstay for secondary prevention of coronary artery disease to decrease early recurrence and severity of recurrent cardiovascular events. However, an increase in gastrointestinal bleeding due to aspirin is preventing many patients from adhering to this daily regimen. PA32540, a combination pill with aspirin and omeprazole, is a newly emerging intervention that has the potential to reinforce patient compliance with the aspirin regimen due to fewer gastrointestinal adverse effects.

Erosive Esophagitis in the Obese: The Effect of Ethnicity and Gender on Its Association.

Background. Data examining the association between obesity and erosive esophagitis (ErE) have been inconsistent, with very little known about interracial variation. Goals.

Hiatus Hernia: A Rare Cause of Acute Pancreatitis.

Hiatal hernia (HH) is the herniation of elements of the abdominal cavity through the esophageal hiatus of the diaphragm. A giant HH with pancreatic prolapse is very rare and its causing pancreatitis is an even more extraordinary condition. We describe a case of a 65-year-old man diagnosed with acute pancreatitis secondary to pancreatic herniation.

Establishing the link between hepatitis B virus infection and colorectal adenoma.

Background: Chronic hepatitis B (CHB) infection has been associated with malignancy, most notably hepatocellular carcinoma. Previous research has shown that hepatitis C is associated with increased colorectal adenomas and neoplasia. Currently, there are no studies on the association of CHB and colorectal adenomas.

Low bone mineral density linked to colorectal adenomas: a cross-sectional study of a racially diverse population.

Background: Epidemiologic studies suggest that lower bone mineral density (BMD) is associated with an increased risk for colorectal adenoma/cancer, especially in postmenopausal women. The aim of this study is to investigate the association between osteopenia and/or osteoporosis and colorectal adenomas in patients from a New York community hospital.

Methods: We performed a cross-sectional observational study on 200 patients who underwent screening colonoscopies and bone density scan (dual-energy X-ray absorptiometry) at Nassau University Medical Center from November 2009 to March 2011.

The association of H. pylori and colorectal adenoma: does it exist in the US Hispanic population?

Background: Although data on the association between colorectal adenomas and Helicobacter pylori (H. pylori) exists in White and Black patients, there is no data on this association in a US Hispanic population. Our aim was to study the association of adenoma detection and biopsy proven H.

Ethnic disparities in the risk of colorectal adenomas associated with lipid levels: a retrospective multiethnic study.

Background: Although data exists showing that uncontrolled lipid levels in white and black patients is associated with colorectal adenomas, there are currently no studies looking only at the Hispanic population.

Purpose: With the rapid increase in the Hispanic population, we aimed to look at their risk of colorectal adenomas in association with lipid levels.

Methods: We retrospectively analyzed 1473 patients undergoing colonoscopy from 2009 to 2011 at a community hospital.

Ethnic disparities in the risk of colorectal adenomas associated with aspirin and statin use: a retrospective multiethnic study.

Background: Although data on the inverse association between colorectal adenomas (CRA) and daily aspirin or statin therapy exists in white and black patients, scarce data exists on these associations in the Hispanic population. With a rapidly increasing Hispanic population in the United States, defining the association in Hispanics is crucial.

Methods: The study sample included 1,843 consecutive patients who underwent a colonoscopy (screening or diagnostic) from 2009 to 2011 at a community hospital in East Meadow, New York.

Rectal ulcers and massive bleeding after hemorrhoidal band ligation while on aspirin.

Endoscopic hemorrhoidal band ligation is a well-established nonoperative method for treatment of bleeding internal hemorrhoids (grade 1 to 3). It is a safe and effective technique with a high success rate. Complications with this procedure are uncommon.

Functional Interactions between Distinct Sodium Channel Cytoplasmic Domains through the Action of Calmodulin.

Sodium channels are fundamental signaling molecules in excitable cells, and are molecular targets for local anesthetic agents and intracellular free Ca(2+) ([Ca(2+)](i)). Two regions of Na(V)1.5 have been identified previously as [Ca(2+)](i)-sensitive modulators of channel inactivation.

Sex, age, and regional differences in L-type calcium current are important determinants of arrhythmia phenotype in rabbit hearts with drug-induced long QT type 2.

In congenital and acquired long QT type 2, women are more vulnerable than men to torsade de pointes. In prepubertal rabbits (and children), the arrhythmia phenotype is reversed; however, females still have longer action potential durations than males. Thus, sex differences in K(+) channels and action potential durations alone cannot account for sex-dependent arrhythmia phenotypes.

Potential role of isoketals formed via the isoprostane pathway of lipid peroxidation in ischemic arrhythmias.

Unabated reactive oxygen species (ROS) are potentiated by an ischemia-induced shift in anaerobic metabolism, which generates superoxide anion upon reperfusion and reintroduction of oxygen. ROS can modify protein structure and function in fundamental ways, one of which is by forming reactive lipid species from the oxidation of lipids. In this review, we discuss these pathways and discuss the literature that shows that these species can produce dramatic effects on cardiac ion channel function (eg, Na+ channel function).

Mutation in glycerol-3-phosphate dehydrogenase 1 like gene (GPD1-L) decreases cardiac Na+ current and causes inherited arrhythmias.

Background: Brugada syndrome is a rare, autosomal-dominant, male-predominant form of idiopathic ventricular fibrillation characterized by a right bundle-branch block and ST elevation in the right precordial leads of the surface ECG. Mutations in the cardiac Na+ channel SCN5A on chromosome 3p21 cause approximately 20% of the cases of Brugada syndrome; most mutations decrease inward Na+ current, some by preventing trafficking of the channels to the surface membrane. We previously used positional cloning to identify a new locus on chromosome 3p24 in a large family with Brugada syndrome and excluded SCN5A as a candidate gene.

A sodium channel pore mutation causing Brugada syndrome.

Background: Brugada and long QT type 3 syndromes are linked to sodium channel mutations and clinically cause arrhythmias that lead to sudden death. We have identified a novel threonine-to-isoleucine missense mutation at position 353 (T353I) adjacent to the pore-lining region of domain I of the cardiac sodium channel (SCN5A) in a family with Brugada syndrome. Both male and female carriers are symptomatic at young ages, have typical Brugada-type electrocardiogram changes, and have relatively normal corrected QT intervals.

HERG is protected from pharmacological block by alpha-1,2-glucosyltransferase function.

The HERG (human ether-à-go-go-related gene) protein, which underlies the cardiac repolarizing current I(Kr), is the unintended target for many pharmaceutical agents. Inadvertent block of I(Kr), known as the acquired long QT syndrome (aLQTS), is a leading cause for drug withdrawal by the United States Food and Drug Administration. Hence, an improved understanding of the regulatory factors that protect most individuals from aLQTS is essential for advancing clinical therapeutics in broad areas, from cancer chemotherapy to antipsychotics and antidepressants.

Quantitation of protein kinase A-mediated trafficking of cardiac sodium channels in living cells.

Objective: Na(+) current derived from expression of the principal cardiac Na(+) channel, Na(v)1.5, is increased by activation of protein kinase A (PKA). This effect is blocked by inhibitors of cell membrane recycling, or removal of a cytoplasmic endoplasmic reticulum (ER) retention motif, suggesting that PKA stimulation increases trafficking of cardiac Na(+) channels to the plasma membrane.

Recreating an artificial biological pacemaker: insights from a theoretical model.

Background: Normal cardiac rhythm is critically dependent on the sinoatrial (SA) node, the natural biological pacemaker. Although recent studies have focused on the development of "artificial" biological pacemakers using gene transfer, less is known about the functional consequences of such interventions.

Objective: The purpose of this study was to investigate the electrophysiological consequences of two approaches used to create a biological pacemaker: overexpression of the hyperpolarization-activated cyclic nucleotide gated channel (HCN "pacemaker" channels) and suppression of the inward-rectifier potassium current, I(K1).

New mechanism contributing to drug-induced arrhythmia: rescue of a misprocessed LQT3 mutant.

Background: The cardiac sodium channel (SCN5A) mutation L1825P has been identified in a patient with drug-induced torsade de pointes precipitated by the IKr blocker cisapride. Although L1825P generates late sodium current typical of SCN5A-linked long-QT syndrome (LQT3) in vitro, the patient reported had a normal QT interval before administration of the drug. To address this discrepancy, we tested the hypothesis that this mutant channel is not processed normally.

Oxidative mediated lipid peroxidation recapitulates proarrhythmic effects on cardiac sodium channels.

Sudden cardiac death attributable to ventricular tachycardia/fibrillation (VF) remains a catastrophic outcome of myocardial ischemia and infarction. At the same time, conventional antagonist drugs targeting ion channels have yielded poor survival benefits. Although pharmacological and genetic models suggest an association between sodium (Na+) channel loss-of-function and sudden cardiac death, molecular mechanisms have not been identified that convincingly link ischemia to Na+ channel dysfunction and ventricular arrhythmias.

Genetics of acquired long QT syndrome.

The QT interval is the electrocardiographic manifestation of ventricular repolarization, is variable under physiologic conditions, and is measurably prolonged by many drugs. Rarely, however, individuals with normal base-line intervals may display exaggerated QT interval prolongation, and the potentially fatal polymorphic ventricular tachycardia torsade de pointes, with drugs or other environmental stressors such as heart block or heart failure. This review summarizes the molecular and cellular mechanisms underlying this acquired or drug-induced form of long QT syndrome, describes approaches to the analysis of a role for DNA variants in the mediation of individual susceptibility, and proposes that these concepts may be generalizable to common acquired arrhythmias.

Compound-specific Na+ channel pore conformational changes induced by local anaesthetics.

Upon prolonged depolarizations, voltage-dependent Na+ channels open and subsequently inactivate, occupying fast and slow inactivated conformational states. Like C-type inactivation in K+ channels, slow inactivation is thought to be accompanied by rearrangement of the channel pore. Cysteine-labelling studies have shown that lidocaine, a local anaesthetic (LA) that elicits depolarization-dependent ('use-dependent') Na+ channel block, does not slow recovery from fast inactivation, but modulates the kinetics of slow inactivated states.

SCN5A-linked disease syndromes: complex monogenic disorders of cardiac rhythm.

Significant advances in the field of molecular biology have enabled the identification of genes that confer susceptibility to disease. Inherited arrhythmia syndromes resulting from genetic alterations of various cardiac ion channels and proteins have been invaluable to further our understanding of the molecular basis of cardiac excitability. Mutations in SCN5A, the gene encoding the pore-forming subunit of the cardiac sodium channel, have been associated with distinct life-threatening cardiac rhythm syndromes.