[Novel endoscopic antireflux procedures - time for critical appraisal].

GERD is the most prevalent gastrointestinal disorder in the Western world and the extent of anatomic alterations underlying the mechanisms of GERD can be viewed upon as a spectrum from a single anatomic alteration (e.g.  incompetent lower esophageal sphincter) to multiple anatomic alterations, such as diaphragmatic hiatal hernia.

[Management of patients with gastroesophageal reflux disease can be optimized].

Gastroesophageal reflux disease (GERD) often requires lifelong treatment to return to and maintain a normal quality of life. Proton pump inhibitors (PPIs) offer effective medical treatment and can be used for a long time with good safety margins. The diagnostic criteria for GERD must be strictly based on current guidelines and the need for maintained treatment must be regularly evaluated.

Laparoscopic Heller myotomy or pneumatic dilatation in achalasia: results of a prospective, randomized study with at least a decade of follow-up.

Background And Objectives: The most efficient long-term treatment strategy for achalasia has yet to be established. This study compared the long-term results (≥ 10 years) after either pneumatic dilatations or laparoscopic myotomy using treatment failure as the primary outcome. Secondary objectives were; the frequency and degree of dysphagia and effects on health-related quality of life (QoL).

Mechanisms behind COX-1 and COX-2 inhibition of tumor growth in vivo.

Non-steroidal anti-inflammatory drugs (NSAIDs) attenuate tumor net growth in clinical and experimental cancer. Evaluations in cell culture experiments have implied involvement of growth factor and G-protein related signaling pathways to explain decreased proliferation, angiogenesis, increased cell adhesion and apoptosis. Sparse information is however available from studies on growing tumors in vivo.

Global tumor RNA expression in early establishment of experimental tumor growth and related angiogenesis following COX-inhibition evaluated by microarray analysis.

Altered expression of COX-2 and overproduction of prostaglandins, particularly prostaglandin E(2), are common in malignant tumors. Consequently, non-steroidal anti-inflammatory drugs (NSAIDs) attenuate tumor net growth, tumor related cachexia, improve appetite and prolong survival. We have also reported that COX-inhibition (indomethacin) interfered with early onset of tumor endothelial cell growth, tumor cell proliferation and apoptosis.

Cyclooxygenase inhibition in early onset of tumor growth and related angiogenesis evaluated in EP1 and EP3 knockout tumor-bearing mice.

It is well established that prostanoids are essential for local inflammation including cell proliferation and apoptosis. Accordingly, prostaglandin E2 (PGE(2)) is a critical factor in wound healing, tumor invasiveness and progression. Therefore, the aim of the present work was to evaluate effects by PGE(2) on tumor vascular density at early onset of tumor growth where hypoxia is limited.