Liver Fibrosis Leading to Cirrhosis: Basic Mechanisms and Clinical Perspectives.

Liver fibrosis is the pathological deposition of extracellular matrix rich in fibrillar collagen within the hepatocytes in response to chronic liver injury due to various causes. As the condition advances, it can progress to cirrhosis, the late stages of which are irreversible. Multiple pathophysiological mechanisms and cell types are responsible for the progression of liver fibrosis and cirrhosis.

Early Definitive Diagnosis and Management of Incidental Neuroendocrine Tumors Found on Gastrointestinal Endoscopy.

Neuroendocrine tumors (NETs) are tumors that originate from neuroendocrine cells and can be found throughout the body but are most commonly seen in the gastrointestinal tract, pancreas, and lungs. There is an increase in the diagnosis of NETs due to advances in diagnostic modalities. Although mucosal tumors are easily visualized on upper GI endoscopic imaging, neuroendocrine tumors are often missed due to their deep mucosal origin with normal overlying mucosa.

The Role of Sphingolipids in Regulating Vascular Permeability in Idiopathic Pulmonary Fibrosis.

Idiopathic pulmonary fibrosis (IPF) is a disease that causes scarring and fibrotic transformation of the lung parenchyma, resulting in the progressive loss of respiratory function and, often, death. Current treatments that target profibrotic factors can slow the rate of progression but are unable to ultimately stop it. In the past decade, many studies have shown that increased vascular permeability may be both a predictive and perpetuating factor in fibrogenesis.

High rates of advanced gastric cancer in community of Flushing, New York.

Background: Gastric cancer remains a major public health issue and is a leading cause of death worldwide, accounting for 600,000 deaths annually. Over the last decades, there has been a steady decline in the incidence rates of gastric cancer. Furthermore, the incidence rates of gastric cancer in different parts of the country vary due to epidemiological and migration trends.

Multifocal granular cell tumor presenting as an esophageal stricture.

Introduction: Granular cell tumors are uncommonly found in the gastrointestinal tract with slow progression and are usually benign though they may have propensity for malignant transformation. Initially attributed to neuronal origin through immunohistochemistry, there has been controversy with increasing reports of granular cell tumors of non-neural origin.

Case Report: We report a case of multifocal granular cell tumor involving the esophagus and stomach in a young female with history of dysphagia for 9 years with worsening symptoms.

Thrombin induced secretion of macrophage migration inhibitory factor (MIF) and its effect on nuclear signaling in endothelium.

The procoagulant thrombin stimulates endothelial cells (EC) to undergo rapid cytoskeleton changes via signaling pathways that induce multiple phenotypic changes, including alterations in permeability, vasomotor tone, adhesion molecule synthesis, and leukocyte trafficking. We studied a novel role of thrombin's action on the endothelium that results in MIF secretion, which is linked to myosin light chain (MLC) and extracellular signal-regulated kinase (ERK(1/2))-dependent nuclear signaling. In bovine pulmonary artery EC (BPAEC), thrombin treatment induced intracellular MLC phosphorylation within 15 min, followed by a significant increase in MIF secretion within 30 min.

Successful closure of a rectovaginal fistula by using an endoscopically placed Resolution clip.

Background: Rectovaginal fistula (RVF) is an abnormal epithelium-lined communication between the wall of the rectum and the posterior vaginal wall. The incidence of RVFs is low and accounts for about 5% of all anorectal fistulas. Women who suffer from an RVF complain of uncontrollable passage of gas or feces from the vagina.

Regulation of c-Jun N-terminal kinase and p38 kinase pathways in endothelial cells.

The rapid and transient induction of E-selectin gene expression by inflammatory tumor necrosis factor (TNF)-alpha in endothelial cells is mediated by signaling pathways which involve c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK) kinase pathways. To explore this regulation, we first observed that in the continuous presence of cytokine TNF, activation of JNK-1 in both nuclear and cytoplasmic compartments peaked at 15-30 min, with activity returning to uninduced levels by 60 min. Phosphorylation of both the p38 kinase and its molecular target, the nuclear transcription factor, activating transcription factor-2, were transient after TNF-alpha or interleukin (IL)-1beta induction.