Modified gracilis muscle flap in facial reanimation: U-shaped design.

BACKGROUND: Surgical treatment of long-term facial palsy has been reported using various techniques, including functioning muscle-free flaps. The free gracilis muscle flap is the most common because of its many advantages. Our study presents a modified way of shaping the gracilis muscle for transfer to the face to improve the restoration of natural smiles. METHODS: This retrospective study assessed 5 patients who received the classical technique and 43 patients who received modified, U-shaped, free gracilis muscle flap for smile reanimation from 2013 to 2018. The surgery is single-staged. Preoperative and postoperative photos were taken. Functional outcomes were evaluated using the Terzis and Noah score and the Chuang smile excursion score. RESULTS: The mean patient age at the time of operation was 31 years. The length of gracilis muscle harvested was 12-13 cm. Of the 43 patients who received U-shaped design-free gracilis muscle, results were excellent for 15 (34.9%), good for 20 (46.5%), and fair for 8 (18.6%) followed the Terzis and Noah score. The Chuang smile excursion score was 2 for 16.3%, 3 for 46.5%, and 4 for 37.2% of 43 patients. Of the 5 patients who underwent classical technique, there are no excellent results based on the Terzis and Noah score. The Chuang smile excursion score was only 1 and 2. CONCLUSIONS: The U-shaped modification to the gracilis muscle-free flap is a simple and effective technique to help restore a symmetrical and natural smile in patients with facial palsy.

SELENBP1 overexpression in the prefrontal cortex underlies negative symptoms of schizophrenia.

The selenium-binding protein 1 (SELENBP1) has been reported to be up-regulated in the prefrontal cortex (PFC) of schizophrenia patients in postmortem reports. However, no causative link between SELENBP1 and schizophrenia has yet been established. Here, we provide evidence linking the upregulation of SELENBP1 in the PFC of mice with the negative symptoms of schizophrenia. We verified the levels of SELENBP1 transcripts in postmortem PFC brain tissues from patients with schizophrenia and matched healthy controls. We also generated transgenic mice expressing human SELENBP1 (hSELENBP1 Tg) and examined their neuropathological features, intrinsic firing properties of PFC 2/3-layer pyramidal neurons, and frontal cortex (FC) electroencephalographic (EEG) responses to auditory stimuli. Schizophrenia-like behaviors in hSELENBP1 Tg mice and mice expressing Selenbp1 in the FC were assessed. SELENBP1 transcript levels were higher in the brains of patients with schizophrenia than in those of matched healthy controls. The hSELENBP1 Tg mice displayed negative endophenotype behaviors, including heterotopias- and ectopias-like anatomical deformities in upper-layer cortical neurons and social withdrawal, deficits in nesting, and anhedonia-like behavior. Additionally, hSELENBP1 Tg mice exhibited reduced excitabilities of PFC 2/3-layer pyramidal neurons and abnormalities in EEG biomarkers observed in schizophrenia. Furthermore, mice overexpressing Selenbp1 in FC showed deficits in sociability. These results suggest that upregulation of SELENBP1 in the PFC causes asociality, a negative symptom of schizophrenia.