A Review of Cognitive and Behavioral Interventions for Tic Disorder.

OBJECTIVES: Tic disorder is a neurodevelopmental disorder characterized by multiple involuntary movements of muscles or vocalization. Although tic symptoms subside as the patient ages, some patients suffer from significant functional impairments related to severe tic symptoms. This manuscript aimed to review the latest scientific evidences for the effect of cognitive-behavioral interventions on tic disorder. METHODS: The relevant studies were identified by searching medical research databases. We focused our search on studies published between 2000 and 2020 in order to reflect the latest scientific evidence. A total of 821 articles were identified in the initial database search and 27 articles were finally included for the review after the exclusion of duplicated and irrelevant articles. RESULTS: Behavioral therapies including habit reversal training, Comprehensive Behavioral Intervention for Tics, and exposure and response prevention were the most widely studied interventions for tic disorder and are recommended as first-line treatments for tic disorders with high confidence. Cognitive psychophysiologic approaches were also reported to be effective. CONCLUSION: Further studies are needed to support the future treatment of tics with low-cost and more widely available treatments, in order to ensure better treatment outcomes.

Clinical Characteristics and Associated Risk Factors of Prediabetes in the Southwestern Region of Korea from 2010-2019.

This study investigated the clinical characteristics and associated risk factors of prediabetes in the southwestern region of Korea. A total of 323 subjects from 13 prediabetes studies were included in the data analysis. Subjects with prediabetes were divided into the following subtypes: (1) normal glucose tolerance (NGT) with HbA1c 5.7%-6.4%; (2) isolated impaired fasting glucose (I-IFG); (3) isolated impaired glucose tolerance (I-IGT); and (4) combined I-IFG and I-IGT (C-IFG/IGT). Clinical and biochemical variables were compared among subtypes, and multivariate logistic regression analysis was used to identify risk factors for prediabetes subtypes. The overall proportion of subjects with NGT, I-IFG, I-IGT and C-IFG/IGT was 8.4%, 20.7%, 33.1% and 37.8%, respectively. In men, C-IFG/IGT was the most common subtype, while in women, I-IGT was the most common. The parameters related to dysglycemia, atherosclerosis and liver dysfunction were higher in subjects in the C-IFG/IGT subtype than in other subtypes. Multiple linear regression analysis revealed independent risk factors for increased FPG, 2h-PPG and HbA1c levels. This study identified the clinical features and independent risk factors for prediabetes subtypes.

Phosphoglucomutase1 is necessary for sustained cell growth under repetitive glucose depletion.

Phosphoglucomutase (PGM)1 catalyzes the reversible conversion reaction between glucose-1-phosphate (G-1-P) and glucose-6-phosphate (G-6-P). Although both G-1-P and G-6-P are important intermediates for glucose and glycogen metabolism, the biological roles and regulatory mechanisms of PGM1 are largely unknown. In this study we found that T553 is obligatory for PGM1 stability and the last C-terminal residue, T562, is critical for its activity. Interestingly, depletion of PGM1 was associated with declined cellular glycogen content and decreased rates of glycogenolysis and glycogenesis. Furthermore, PGM1 depletion suppressed cell proliferation under long-term repetitive glucose depletion. Our results suggest that PGM1 is required for sustained cell growth during nutritional changes, probably through regulating the balance of G-1-P and G-6-P in order to satisfy the cellular demands during nutritional stress.

Changes in longitudinal craniofacial growth in subjects with normal occlusions using the Ricketts analysis.

OBJECTIVE: This study was designed to define the Korean norm values for the Ricketts analysis. METHODS: In this longitudinal study, lateral cephalograms of 31 subjects with normal occlusion were taken biennially from ages 9-19 years. Cephalometric measurements were performed. Parameters for which the 10-year change did not exceed one standard deviation were defined as unchanged. The means and standard deviations for the measured parameters were determined for each age group. RESULTS: No significant changes in growth were observed in the molar relationship, incisor overjet, incisor overbite, mandibular incisor extrusion, interincisor angle, lower incisor tip (B1) to A point-Pogonion (A-PO) plane, upper incisor tip (A1) to A-PO plane, B1 inclination to A-PO, A1 inclination to A-PO, B1 inclination to Frankfurt plane (FH), convexity, lower facial height, facial axis, maxillary depth, maxillary height, palatal plane to FH, cranial deflection, ramus Xi position, or porion location. Continual changes over the 10 years of growth were observed in the maxillary first molar distal position to pterygoid true vertical plane, facial depth, mandibular plane to FH, anterior cranial length, mandibular arc, and corpus length. CONCLUSIONS: Clinicians can apply the Korean norms at age 9 as determined in this study when using the Ricketts analysis. The patient's age at the beginning of treatment and their sex should be taken into consideration when drawing visual treatment objectives.

Lipin1 regulates PPARγ transcriptional activity.

PPARγ (peroxisome-proliferator-activated receptor γ) is a master transcription factor involved in adipogenesis through regulating adipocyte-specific gene expression. Recently, lipin1 was found to act as a key factor for adipocyte maturation and maintenance by modulating the C/EBPα (CCAAT/enhancer-binding protein α) and PPARγ network; however, the precise mechanism by which lipin1 affects the transcriptional activity of PPARγ is largely unknown. The results of the present study show that lipin1 activates PPARγ by releasing co-repressors, NCoR1 (nuclear receptor co-repressor 1) and SMRT (silencing mediator of retinoid and thyroid hormone receptor), from PPARγ in the absence of the ligand rosiglitazone. We also identified a novel lipin1 TAD (transcriptional activation domain), between residues 217 and 399, which is critical for the activation of PPARγ, but not PPARα. Furthermore, this TAD is unique to lipin1 since this region does not show any homology with the other lipin isoforms, lipin2 and lipin3. The activity of the lipin1 TAD is enhanced by p300 and SRC-1 (steroid receptor co-activator 1), but not by PCAF (p300/CBP-associated factor) and PGC-1α (PPAR co-activator 1α). The physical interaction between lipin1 and PPARγ occurs at the lipin1 C-terminal region from residues 825 to 926, and the VXXLL motif at residue 885 is critical for binding with and the activation of PPARγ. The action of lipin1 as a co-activator of PPARγ enhanced adipocyte differentiation; the TAD and VXXLL motif played critical roles, but the catalytic activity of lipin1 was not directly involved. Collectively, these data suggest that lipin1 functions as a key regulator of PPARγ activity through its ability to release co-repressors and recruit co-activators via a mechanism other than PPARα activation.

FoxO1 regulates Tlr4 inflammatory pathway signalling in macrophages.

The macrophage-mediated inflammatory response is a key etiologic component of obesity-related tissue inflammation and insulin resistance. The transcriptional factor FoxO1 is a key regulator of cell metabolism, cell cycle and cell death. Its activity is tightly regulated by the phosphoinositide-3-kinase-AKT (PI3K-Akt) pathway, which leads to phosphorylation, cytoplasmic retention and inactivation of FoxO1. Here, we show that FoxO1 promotes inflammation by enhancing Tlr4-mediated signalling in mature macrophages. By means of chromatin immunoprecipitation (ChIP) combined with massively parallel sequencing (ChIP-Seq), we show that FoxO1 binds to multiple enhancer-like elements within the Tlr4 gene itself, as well as to sites in a number of Tlr4 signalling pathway genes. While FoxO1 potentiates Tlr4 signalling, activation of the latter induces AKT and subsequently inactivates FoxO1, establishing a self-limiting mechanism of inflammation. Given the central role of macrophage Tlr4 in transducing extrinsic proinflammatory signals, the novel functions for FoxO1 in macrophages as a transcriptional regulator of the Tlr4 gene and its inflammatory pathway, highlights FoxO1 as a key molecular adaptor integrating inflammatory responses in the context of obesity and insulin resistance.

Mechanical properties of self-drilling orthodontic micro-implants with different diameters.

OBJECTIVE: The hypothesis to be tested is that peak-insertion torque of self-drilling micro-implants of an appropriate diameter correlates with peak-removal torque mechanically. MATERIALS AND METHODS: A total of 360 self-drilling micro-implants composed of five different types were used. They (24 of each group) were inserted in three types of artificial bone with the use of a driving torque tester at a speed of 15 rpm. Insertion torque was measured during the placement, while the removal torque was measured within 3 days after insertion. RESULTS: Most of the micro-implants in type A sheared before they were completely inserted in 40-pounds per cubic foot bone. The implants in other types were successfully inserted without implant breakage and bone fracture in all bone densities. There was a statistically significant correlation between insertion torque and removal torque (r > or = 0.43543, P = .0001). There were significant differences in insertion and removal torque among the diameters of implants and bone densities with an increasing tendency. The torque loss rates reduced as the diameter of the implant and bone density increased. CONCLUSIONS: Micro-implants with a diameter of less than 1.3 mm are unsuitable for insertion into a bone with a density greater than 40 pounds per cubic foot mechanically when one is using a self-drilling technique.

Vertically aligned carbon-nanotube arrays showing Schottky behavior at room temperature.

Vertically aligned carbon-nanotube (CNT) arrays were fabricated in the thin-film anodic aluminum oxide (AAO) templates on silicon wafers utilizing a niobium (Nb) thin film as the source electrode. The average diameter of the CNTs was 25 nm, and the number density was 3 x 10(10) cm(-2). The CNT arrays synthesized at 700 degrees C and above exhibited Schottky behavior even at 300 K, with energy gaps between 0.2 eV and 0.3 eV. However, individual CNTs obtained by removal of the template behaved as resistors at 300 K. The CNT/Nb oxide/Nb junction is thought to be responsible for the Schottky behavior. This structure can be a useful cornerstone in the fabrication of nanotransistors operating at room temperature.