Effect of dorsal nerve fascial island flap on repairing distal soft tissue defects at the proximal segment of the index, middle, ring, and little fingers.

BACKGROUND: To investigate the effect of the dorsal nerve fascial island (DNFI) flap on repairing finger soft tissue defects at the distal segments. METHODS: Fifty patients with distal soft tissue defects at the index, middle, ring, or little fingers were treated with a DNFI flap at the proximal phalanx between February 2008 and May 2018. The nutrient vascular chain around the dorsal branch of the proper palmar digital nerves served as the flap axis. The dorsal branch of the proper palmar digital arteries provided blood supply. The fascia pedicle served as the venous system. All patients were followed for 6 months. RESULTS: All 50 flaps survived. The appearance, color, and texture of the skin returned to normal. The sensory function was partially restored. The two-point discrimination of the finger flap was 7-10 mm. CONCLUSIONS: The DNFI flap at the proximal phalanges of the index, middle, ring, and little fingers is an effective surgical option. The technique has a high flap survival rate and long pedicle, which can repair different parts of the finger. The flap also restores the sensory function of the finger without damaging the main nerves or blood vessels. The flap treatment is an optimal option for finger soft tissue defects at the distal segments.

Mechanisms of microRNA­142 in mitochondrial autophagy and hippocampal damage in a rat model of epilepsy.

Researchers have confirmed the microRNA (miRNA/miR)­epilepsy association in rodent models of human epilepsy via a comprehensive database. However, the mechanisms of miR­142 in epilepsy have not been extensively studied. In the present study, a rat model of epilepsy was first established by an injection of lithium chloride­pilocarpine and the successful establishment of the model was verified via electroencephalogram monitoring. The levels of miR­142, phosphatase and tensin homolog deleted on chromosome 10 (PTEN)­induced putative kinase 1 (PINK1), marker proteins of mitochondrial autophagy, and apoptosis­related proteins were measured. Additionally, the pathological changes in the hippocampus, the ultrastructure of the mitochondria, and degeneration and the apoptosis of neurons were observed using different staining methods. The malondialdehyde (MDA) content and superoxide dismutase (SOD) activity in the hippocampus, mitochondrial membrane potential (MTP) and reactive oxygen species (ROS) generation were detected. Furthermore, the targeting association between miR­142 and PINK1 was predicted and verified. Consequently, apoptosis increased, and mitochondrial autophagy decreased, in the hippocampus of epileptic rats. Following miR­142 inhibition, the epileptic rats exhibited an increased Bax expression, a decreased Bcl­2 expression, upregulated marker protein levels of mitochondrial autophagy, a reduced MDA content, an enhanced SOD activity, an increased MTP and decreased ROS generation. PINK1 is a target gene of miR­142, and its overexpression protected against hippocampal damage. Taken together, the results of the present study demonstrated that miR­142 inhibition promotes mitochondrial autophagy and reduces hippocampal damage in epileptic rats by targeting PINK1. These findings may provide useful information for the treatment of epilepsy.