The journal club.

As the body of medical literature continues to expand, physicians must develop the necessary skills to keep up with the vast amount of information available. The journal club provides a forum to allow residents to remain current with the literature while also teaching them the methods to evaluate it critically. Those readers wishing to start a journal club or revive an existing one should begin by designating a leader and defining the conference goals. Emphasizing the importance of this conference in the educational process while allowing it to be structured to optimise resident interest and attendance will help to ensure its success. Periodic evaluation of this conference will allow the organisers to assess the concordance of the resident''s goals with those of the faculty. Formal evaluation will also provide an objective assessment of the knowledge gained by the house-staff through participation in journal club.     

Gastro-oesophageal reflux disease: Medical or surgical treatment? Report of an interactive workshop

Gastroesophageal reflux disease (GERD) is the most common disease of the upper gastrointestinal tract. With the introduction of proton pump inhibitors medical treatment of GERD has been significantly improved. However, the development of laparoscopic antireflux surgery resulted in an increasing interest of surgeons in this disease. An interactive meeting was organized in order to develop an agreement between gastoenterologists and surgeons regarding therapeutic decisions and this is the main topic of this paper.     

Motor neuron disease and optic neuropathy after acute exposure to a methanol-containing solvent mixture.

A 34-years-old floor-layer developed optic neuropathy and motor neuron disease after being accidentally exposed to a solvent mixture containing methanol and other substances. Optic neuropathy is a complication of methanol poisoning, but the onset of a motor neuron disorder resembling amyotrophic lateral sclerosis after the exposure to these substances has not been previously described. The temporal onset of the clinical symptoms, biological plausibility, young age of the patient and absence of neurological disorders in the family history raises suspicion of a possible causative relationship.     

Ueber die Bildungsstätte des Gallenfarbstoffs beim Kaltblüter

Ohne Zusammenfassung     

L-carnitine and platelet aggregation in uremic patients subjected to hemodialysis

It has been reported that treatment with L-carnitine at a daily dose of 3 g orally may cause a rise in platelet aggregation and serum triglyceride concentration in hemodialyzed patients. The present double-blind cross-over study has been performed to evaluate the influence of L-carnitine when compared with placebo on platelet aggregation and plasma concentrations of various factors involved in platelet activation. In addition, the concentration of triglycerides, cholesterol and HDL-cholesterol has been evaluated. 18 uremic patients on maintenance hemodialysis for at least 1 year were randomly allocated either to a control group receiving placebo or to a group treated with L-carnitine. Statistical analysis performed by means of ANOVA did not show any significant change in the serum concentration of cholesterol, HDL-cholesterol and triglycerides. Furthermore, platelet aggregation tests (performed with adenosine 5'-diphosphate, epinephrine, thrombin and collagen) and plasma beta-thromboglobulin concentration did not show any statistically significant difference. In addition, the plasma concentration of several coagulation markers, such as factor VIIIc, antithrombin III, alpha 2-antiplasmin, and fibrinopeptide A, did not show any significant variation. The results suggest that under our experimental conditions L-carnitine neither increases the risk of thromboembolism nor alters the serum lipid content in uremic patients on chronic hemodialysis.     

Beta-defensin genomic copy number is not a modifier locus for cystic fibrosis

Human beta-defensin 2 (DEFB4, also known as DEFB2 or hBD-2) is a salt-sensitive antimicrobial protein that is expressed in lung epithelia. Previous work has shown that it is encoded in a cluster of beta-defensin genes at 8p23.1, which varies in copy number between 2 and 12 in different individuals. We determined the copy number of this locus in 355 patients with cystic fibrosis (CF), and tested for correlation between beta-defensin cluster genomic copy number and lung disease associated with CF. No significant association was found.