Einzelreferate und Buchbesprechungen

Ohne Zusammenfassung     

Characteristics of Epstein-Barr virus primary infection in pediatric liver transplant recipients

BACKGROUND/AIM: Pediatric liver transplant recipients are at high risk of Epstein-Barr virus infection. However the incidence of clinical symptoms and the graft function at the time of acute infection remains poorly documented. The aim of this study was to monitor the clinical and biochemical events associated with primary Epstein-Barr virus infection. METHODS: Clinical and biological patterns associated with Epstein-Barr virus infection were prospectively searched in 38 liver transplanted children. Polymerase chain reaction and anti-Epstein-Barr virus IgM antibodies were used at regular intervals to detect the timing of primary infection. RESULTS: Five children (13%) had pretransplant immunity, 26 (68.5%) developed primary Epstein-Barr virus infection 15 to 90 days after transplantation and seven (18.5%) remained Epstein-Barr virus negative. The four patients with clinical symptoms at the time of infection subsequently developed post-transplant lymphoproliferative disease. A single post-transplant lymphoproliferative disease occurred in non-symptomatic patients (overall incidence 13%). No mortality was associated with post-transplant lymphoproliferative disease. Two asymptomatic patients had abnormal liver function tests possibly related to primary Epstein-Barr virus infection. CONCLUSION: Epstein-Barr virus primary infection occurs in 80% of seronegative patients within 3 months after OLT. Clinical symptoms are rare and closely associated with post-transplant lymphoproliferative disease. Outside post-transplant lymphoproliferative disease, the consequences of infection are marginal.     

Mammalian Erv46 localizes to the endoplasmic reticulum-Golgi intermediate compartment and to cis-Golgi cisternae

Yeast endoplasmic reticulum (ER) vesicle protein Erv46p is a novel membrane protein involved in transport through the early secretory pathway. Investigation of mammalian Erv46 (mErv46) reveals that it is broadly expressed in tissues and protein-secreting cells. By immunofluorescence microscopy, mErv46 displays a crescent-shaped perinuclear staining pattern that is characteristic of the Golgi complex. Quantitative immunoelectron microscopy indicates that mErv46 is restricted to the cis face of the Golgi apparatus and to vesicular tubular structures between the transitional ER and cis-Golgi. Minor amounts of mErv46 reside in ER membranes and later Golgi cisternae. On Brefeldin A treatment, mErv46 redistributes to punctate structures that costain for ERGIC53. Depletion of mErv46 protein by RNA interference caused no apparent structural changes in the intermediate compartment or Golgi complex. These findings place mErv46 in a group of itinerant proteins that cycle between the ER and Golgi compartments such as ERGIC53 and the p24 proteins.     

No bone ingrowth into the tibia tunnel in anterior cruciate ligament-reconstructed patients: A 1-year prospective quantified CT study of 10 patients reconstructed with an autologous bone-patellar tendon-bone graft

10 patients with major instability symptoms due to an acute anterior cruciate ligament injury were operated on with a bone-patellar tendon-bone reconstruction. Tibial condyle bone mineral density (BMD), bone ingrowth and changes in diameter in the tibia bone tunnel were studied with quantified computed tomography (QCT) postoperatively and after 1, 3, 6 and 12 months. We found no sign of bone ingrowth in the form of increased bone mineral density (BMD) in the bone tunnels in any of the patients. The tunnel diameter increased in all patients during the first postoperative months. After 1 year, 5 patients had a smaller diameter than at the first postoperative examination, 2 had the same diameter as immediately after surgery and 2 patients had a larger diameter. A sclerotic zone developed in all patients along the perimeter of the tunnel during the 3-6 months of follow-up. The BMD in the tibial condyle decreased at 3 months; it then increased, but between 6 and 12 months, it levelled out and was slightly lower than postoperatively. In conclusion, we found no growth of bone into the tunnel and tendinous part of the graft during the first postoperative year.     

Changes in biochemical markers of bone metabolism and BMD during the first year after a hip fracture

We measured the levels of biochemical markers of bone formation and bone resorption in hip fracture patients preoperatively and after 6 and 12 months. Bone densitometry was done with quantitative computer tomography (QCT), dual-energy X-ray absorptiometry (DXA) and heel ultrasound. After 6 months, the biochemical markers of bone formation and bone resorption had increased. The levels remained high after 1 year and no change occurred between 6 and 12 months. We found no correlations between biochemical bone markers and bone density/ stiffness on admission and change in bone mineral density (BMD) during the first postoperative year, despite the changes in bone markers and bone density. In our opinion, biochemical bone markers can not be used to predict bone loss in the individual patient after a hip fracture.