The esthetic outcome of recipient sites of gracilis muscle flaps versus anterolateral thigh flaps: A retrospective study.

BACKGROUND: Anterolateral thigh (ALT) and gracilis muscle flaps have been described as comparable reconstructive options regarding maximal flap dimension and indications. However, split-thickness skin-grafted muscle flaps are generally believed to be inferior to perforator flaps regarding the esthetic outcome of the recipient site. The purpose of this study was to challenge this assumption, comparing the long-term esthetic outcome of the gracilis and the ALT flap. METHODS: One hundred forty-eight patients who had undergone free flap reconstruction with either free split-thickness skin-grafted gracilis muscle flaps (n = 86) or ALT flaps (n = 62) were evaluated in the study. Patients' satisfaction with the esthetic outcome, rates of flap loss, wound healing disorders and the necessity for thinning the flap or scar correction procedures were assessed. RESULTS: Flap loss occurred in 4 of 86 gracilis flaps (4.7%) and 2 of 62 (3.2%) ALT flaps (p > .9999). Thinning or scar correction procedures were necessary for 6 of 86 gracilis (7.0%) and 4 of 62 (6.5%; p > .9999) ALT flap recipient sites. Regarding the overall patients' satisfaction with the esthetic outcome, scores were similar in both groups (2.667 [ALT] vs. 2.348 [gracilis]; p = .3739). Contour deformity, scar hypertrophy, and difference in flap color/texture in relation to the surrounding skin were comparable throughout the ALT and gracilis group (2.667 vs. 2.174, p = .2099; 3.333 vs. 2.739, p = .0912 and 2.500 vs. 2.174, p = .3159, respectively). CONCLUSION: The gracilis and ALT flap are two equivalent reconstructive options regarding the esthetic outcome of the recipient site and long-term patient satisfaction.

Effects of antiepileptic drugs on GABA release from rat and human neocortical synaptosomes.

In epilepsy, allegedly, a neurotransmitter imbalance between the inhibitory GABA and the excitatory glutamate prevails. Therefore, some antiepileptic drugs (AEDs) are thought to increase GABA release. Because little is known about corresponding presynaptic effects of AEDs in the human brain, this study investigated the effects of carbamazepine, lamotrigine, phenytoin, gabapentin, pregabalin, levetiracetam, and valproate on (3)H-GABA release from human neocortical synaptosomes preincubated with (3)H-GABA. To obtain information on possible species differences, rat neocortical synaptosomes were investigated concomitantly. Release was evoked by either veratridine (1, 3.2, or 10 µM), which prevents activated voltage-dependent Na(+) channels from closing, or elevation of extracellular [K(+)] from 3 to 15 mM. The exocytosis inhibitor tetanus toxin (TeT) or withdrawal of buffer Ca(2+) (Ca (e) (2+) ) reduced K(+)-evoked release in both species, while blockade of Na(+) channels with tetrodotoxin had no effect. K(+)-evoked release was characterized as predominant, Ca(2+)-dependent and Na(+)-independent, exocytosis. Carbamazepine and phenytoin in the rat and carbamazepine, phenytoin, lamotrigine, and valproate in human tissue reduced K(+)-evoked (3)H-GABA release. With respect to veratridine-evoked release, Ca (e) (2+) withdrawal did not reduce release in the rat; it even increased the release in human tissue. TeT was slightly inhibitory in the rat. Blockade of GABA transport diminished veratridine-evoked (3)H-GABA release in either species. This release was characterized as mediated mainly by transporter reversal. Carbamazepine, lamotrigine, and phenytoin in rat tissue and carbamazepine and phenytoin in human decreased veratridine-induced (3)H-GABA release. Interestingly, no AED increased (3)H-GABA release. The reduction by AEDs of veratridine-evoked release was more intense than that of K(+)-evoked release. In conclusion, reduction of GABA release by AEDs may be the actual objective in a pathologically altered neuronal network where GABA acts in a depolarizing fashion.

Lysosomal membrane permeabilization and cathepsin release is a Bax/Bak-dependent, amplifying event of apoptosis in fibroblasts and monocytes.

Apoptotic stimuli have been shown to trigger lysosomal membrane permeability (LMP), leading to the release of cathepsins, which activate death signaling pathways in the cytosol. However, it is unknown whether this process is an initiating or amplifying event in apoptosis. In this study, we used fibroblasts and monocytes exposed to etoposide, ultraviolet light, FasL or deprived of interleukin-3 (IL-3) to show that LMP and the cytosolic release of cathepsins B, L and D consistently depends on Bax/Bak and components of the apoptosome. Neither Bax nor Bak resided on the lysosomes, indicating that lysosomes were not directly perforated by Bax/Bak but by effectors downstream of the apoptosome. Detailed kinetic analysis of cells lacking cathepsin B or L or treated with the cysteine protease inhibitor, E64d, revealed a delay in these cells in etoposide- and IL-3 deprivation-induced caspase-3 activation and apoptosis induction but not clonogenic survival, indicating that cathepsins amplify rather than initiate apoptosis.