Initial Implant Stability Predicts Migration But Not Failure in Cementless Acetabular Revision with Bone Grafting

Host bone contact of less than 50% is perceived but not proven to cause migration and loosening after actetabular revision. A prospective analysis of cementless acetabular revision cases with impaction grafting was performed to determine if this was an independent risk factor for these events. Sixty-two hips in 54 patients were assessed at a mean follow-up of 84.5 months (range 61–112) yielding a probability of 94.6% of retaining the acetabular component using revision for aseptic loosening as the end point. No single factor was independently causative for loosening, although Type III fixation was associated with migration (p = 0.0159); subanalysis suggested that achieving host–bone contact in at least part of the dome and posterior column is important.     

A Case of Catamenial Pneumothorax with Diaphragmatic Fenestrations

Background: Considerable controversy exists with regards to the physiopathogenesis of catamenial pneumothorax. The rarity of catamenial pneumothorax makes understanding of its pathophysiology and verification of etiological mechanisms difficult. Objective: To contribute evidence to the knowledge base on the pathogenesis of catamenial pneumothorax. Case Report: We describe a case of catamenial pneumothorax with images that substantiate the pore hypothesis as a cause of recurrence of air in the pleural cavity in this patient. Conclusion: Our case report contributes evidence that transperitoneal migration of endometrial implants may occur through diaphragmatic fenestrations. Surgical options may be more viable to prevent recurrent pneumothoraces in such patients.     

In Vitro free radical production in rat esophageal mucosa induced by nicotine

Oxidative stress induced by nicotine was investigated in the esophageal mucosa of rats. The homogenized mucosa was incubated for 30 min with 50, 100, 200, 400, and 800 ng/mg protein/ml nicotine or with 200 ng/mg protein/ml nicotine for 15, 30, 45, and 60 min. Esophageal mucosa was also incubated for 30 min with 200 ng/mg protein/ml nicotine with or without the scavengers superoxide dismutase (SOD), catalase, SOD + catalase, inactivated SOD, inactivated catalase, or albumin. Incubation with 0.9% NaCl served as control. There was a strong correlation between chemiluminescence and the nicotine dose (r=0.75) or the nicotine incubation time (r=0.77). Thirty-minute incubation of the esophageal mucosa with 200 ng/mg protein/ml nicotine increased chemiluminescence 5.5-fold and lipid peroxidation 3.3-fold. This response was dampened by SOD or catalase and abolished by SOD + catalase. Inactivated enzymes or albumin had no scavenging effect. These results demonstrate that nicotine causes oxidative stress to the esophageal mucosa.     

Mucosal glucosamine synthetase activity in inflammatory bowel disease

Abnormalities in colonic glycoprotein synthesis have been implicated in the pathogenesis of ulcerative colitis and Crohn's disease. Glucosamine synthetase is the rate-limiting step in the biosynthesis of gastrointestinal glycoprotein and has been measured in control subjects (N=23) and patients with ulcerative colitis (N=26) or Crohn's disease of the colon (N=20) classified according to the macroscopic status of the rectum. Glucosamine synthetase activity was relatively constant around the normal colon but lower levels were found in the terminal ileum. In ulcerative colitis, glucosamine synthetase activity was similar to controls (24.0±1.9) mmol/g wet (wt/hr) irrespective of disease activity (quiescent:N=13, =27.3±1.9; activeN=16, =26.2±2.3). Rectal glucosamine synthetase activity was normal in the presence of active Crohn's proctocolitis (29.4±3.1) but raised in patients with Crohn's colitis and rectal sparing (37.2±4.9P<0.02). Glucosamine synthetase activity was strongly influence by the degree of epithelial preservation.