Der V-Y-Lappen zur Versorgung von Fingerkuppendefekten

OBJECTIVE: Restoration of the fingertip with a neurovascular V-Y flap. INDICATIONS: Transverse or oblique defects of the fingertip, also with exposed bone of the distal phalanx. CONTRAINDICATIONS: Larger defects of the phalanx over the proximal interphalangeal joint. Crush injury of the finger. Preexisting lesions of the fingertip. Circulatory disorder. Contamination. Infection of the finger. SURGICAL TECHNIQUE: A single volar (Tranquilli-Leali, Atasoy) or a bilateral V-Y flap (Geissend?rfer, Kutler) is used for restoration of the fingertip. The incision is V-shaped and will be converted to a Y, as the flap is advanced. The subcutaneous tissue of the flap contains neurovascular structures, and provides sensibility and padding of the fingertip. A distal advancement of the flap up to 10 mm is possible with this technique. POSTOPERATIVE MANAGEMENT: Immobilization in a two-finger splint for 1 week. RESULTS: Good functional results.     

Limb trauma with arterial injury: long-term performance of venous interposition grafts

BACKGROUND: In contrast to arterial occlusive disease, data on long-term outcomes after vein grafts in limb trauma with arterial injury are sparse. PATIENTS: From 1991 through 2001, 22 trauma victims received 23 interposition vein grafts performed by an interdisciplinary team of trauma and vascular surgeons. Indications included both blunt and penetrating injuries with critical limb ischemia in the majority of cases. RESULTS: Operative treatment of the injured vessels (brachial n = 5, radial/ulnar n = 7, popliteal n = 6, tibial n = 3, pedal n = 2) encompassed venous interposition graft of either saphenous (n = 15) or cephalic vein (n = 8). All patients survived the operative procedure. 4 graft occlusions were noted and 3 major amputations had to be performed (one despite patent graft). 13 patients (76%) were available for duplex ultrasound examination after a mean follow-up of 59 months where patent grafts could be detected in all cases. CONCLUSION: A multidisciplinary approach ensures optimal treatment strategy of arterial injury in extremity trauma. Interposition vein grafts provide durable long-term results and should be attempted even in single-vessel injuries of forearm and lower leg.     

cAMP-inducible chloride conductance in mouse fibroblast lines stably expressing the human cystic fibrosis transmembrane conductance regulator.

A cAMP-inducible chloride permeability has been detected in mouse fibroblast (L cell) lines upon stable integration of a full-length cDNA encoding the human cystic fibrosis transmembrane conductance regulator (CFTR). As indicated by a Cl(-)-indicator dye, the Cl- permeability of the plasma membrane increases by 10- to 30-fold within 2 min after treatment of the cells with forskolin, an activator of adenylyl cyclase. The properties of the conductance are similar to those described in secretory epithelial cells; the whole-cell current-voltage relationship is linear and there is no evidence of voltage-dependent inactivation or activation. In contrast, this cAMP-dependent Cl- flux is undetectable in the untransfected cells or cells harboring defective cDNA constructs, including one with a phenylalanine deletion at amino acid position 508 (delta F508), the most common mutation causing cystic fibrosis. These observations are consistent with the hypothesis that the CFTR is a cAMP-dependent Cl- channel. The availability of a heterologous (nonepithelial) cell type expressing the CFTR offers an excellent system to understand the basic mechanisms underlying this CFTR-associated ion permeability and to study the structure and function of the CFTR.     

Phosphatase inhibitors activate normal and defective CFTR chloride channels.

The cystic fibrosis transmembrane conductance regulator (CFTR) chloride channel is regulated by phosphorylation and dephosphorylation at multiple sites. Although activation by protein kinases has been studied in some detail, the dephosphorylation step has received little attention. This report examines the mechanisms responsible for the dephosphorylation and spontaneous deactivation ("rundown") of CFTR chloride channels excised from transfected Chinese hamster ovary (CHO) and human airway epithelial cells. We report that the alkaline phosphatase inhibitors bromotetramisole, 3-isobutyl-1-methylxanthine, theophylline, and vanadate slow the rundown of CFTR channel activity in excised membrane patches and reduce dephosphorylation of CFTR protein in isolated membranes. It was also found that in unstimulated cells, CFTR channels can be activated by exposure to phosphatase inhibitors alone. Most importantly, exposure of mammalian cells to phosphatase inhibitors alone activates CFTR channels that have disease-causing mutations, provided the mutant channels are present in the plasma membrane (R117H, G551D, and delta F508 after cooling). These results suggest that CFTR dephosphorylation is dynamic and that membrane-associated phosphatase activity may be a potential therapeutic target for the treatment of cystic fibrosis.