This case report describes skeletal anchorage-supported maxillary protraction performed with the Alternate Rapid Maxillary Expansion and Constriction (AltRAMEC) protocol over a treatment duration of 14 months in a 16-year-old female patient who was in the late growth-development period. Miniplates were applied to the patient's aperture piriformis area to apply force from the protraction appliance. After 9 weeks of following the Alt-RAMEC protocol, miniplates were used to transfer a unilateral 500-g protraction force to a Petit-type face mask. A significant improvement was observed in the soft tissue profile in measurements made both cephalometrically and in three dimensional photographs. Subsequently, the second phase of fixed orthodontic treatment was started and the treatment was completed with the retention phase. Following treatment completion, occlusion, smile esthetics, and soft tissue profile improved significantly in response to orthopedic and orthodontic treatment.

OBJECTIVE: α-synuclein, Nogo-A and Ubiquitin C-terminal hydrolase L1 (UCH-L1) have neuromodulatory roles for human brain. Therefore, abnormalities of these molecules are associated with neuropsychiatric disorders. Although some serum studies in the other disorders have been made, serum study of α-synuclein, Nogo-A and UCH-L1 is not present in patients with schizophrenia and healthy controls. Therefore, our aim was to compare serum levels of α-synuclein, Nogo-A and UCH-L1 of the patients with schizophrenia and healthy controls. METHODS: Forty-four patients with schizophrenia who is followed by psychotic disorders unit, and 40 healthy control were included in this study. Socio-demographic form and Positive and Negative Syndrome Scale (PANSS) was applied to patients, and sociodemographic form was applied to control group. Fasting bloods were collected and the serum levels of α-synuclein, Nogo-A and UCH-L1 were measured by ELISA method. RESULTS: Serum α-synuclein [patient: 12.73 (5.18–31.84) ng/mL; control: 41.77 (15.12–66.98) ng/mL], Nogo-A [patient: 33.58 (3.09–77.26) ng/mL; control: 286.05 (136.56–346.82) ng/mL] and UCH-L1 [patient: 5.26 (1.64–10.87) ng/mL; control: 20.48 (11.01–20.81) ng/mL] levels of the patients with schizophrenia were significianly lower than healthy controls (p<0.001). CONCLUSION: Our study results added new evidence for explaining the etiopathogenesis of schizophrenia on the basis of neurochemical markers.
Biomarkers ; Brain ; Enzyme-Linked Immunosorbent Assay ; Fasting ; Humans ; Methods ; Psychotic Disorders ; Schizophrenia* ; Ubiquitin Thiolesterase