Changes in smile parameters after surgical-orthodontic treatment for skeletal Class III malocclusion.

Background/purpose: Many patients pursue attractive smiles, and surgical-orthodontic treatment is a common method. We aimed to analyze the changes in smile parameters after surgical-orthodontic treatment in patients with skeletal Class III pattern and identify factors influencing postoperative outcomes. Materials and methods: This retrospective study comprised 34 patients with skeletal Class III malocclusion and pure mandible prognathism who received surgical-orthodontic treatment. Hard and soft tissue parameters were assessed through lateral cephalometry, and smile esthetics were evaluated through extraoral photography. Postoperative changes in smile parameters and between-parameter correlations were analyzed. Random forest and decision tree deep learning models were used to identify factors influencing postoperative changes. Results: Substantial postoperative changes were observed in the buccal corridor, upper lip height, and smile index. Significant between-sex differences were noted in the upper midline and right chelion. Strong, positive correlations were found between upper lip height and upper lip ratio and between lower lip height and lower lip ratio. By contrast, strong negative correlations were observed between lower teeth exposure and smile index and between interlabial gap and smile index. The highest degrees of postoperative changes were noted in asymmetry-associated smile parameters: lower lip area, interlabial gap, smile index, buccal corridor, and arc ratio. Conclusion: Considerable changes were noted in skeletal, dental, and soft tissue parameters after surgical-orthodontic treatment. However, the changes in smile esthetics were less prominent from the frontal view. As for chin asymmetry, the most to least prominent changes were in the lower lip area, interlabial gap, smile index, buccal corridor, and arc ratio, respectively.

Organic light-emitting diode therapy promotes longevity through the upregulation of SIRT1 in senescence-accelerated mouse prone 8 mice.

Phototherapy has been extensively used to prevent and treat signs of aging and stimulate wound healing, and phototherapy through light-emitting diodes (LEDs). In contrast to LED, organic LED (OLED) devices are composed of organic semiconductors that possess novel characteristics. We investigated the regenerative potential of OLED for restoring cellular potential from senescence and thus delaying animal aging. Bone marrow-derived stem cells (BMSCs) and adipose-derived stem cells (ADSCs) were isolated from the control and OLED- treated groups to evaluate their proliferation, migration, and differentiation potentials. Cellular senescence was evaluated using a senescence-associated ß-galactosidase (SA-ß-gal) activity assay and gene expression biomarker assessment. OLED treatment significantly increased the cell proliferation, colony formation, and migration abilities of stem cells. SA-ß-gal activity was significantly decreased in both ADSCs and BMSCs in the OLED-treated group. Gene expression biomarkers from treated mice indicated a significant upregulation of IGF-1 (insulin growthfactor-1). The upregulation of the SIRT1 gene inhibited the p16 and p19 genes then to downregulate the p53 expressions for regeneration of stem cells in the OLED-treated group. Our findings indicated that the survival rates of 10-month aging senescence-accelerated mouse prone 8 mice were prolonged and that their gross appearance improved markedly after OLED treatment. Histological analysis of skin and brain tissue also indicated significantly greater collagen fibers density, which prevents ocular abnormalities and ß-amyloid accumulation. Lordokyphosis and bone characteristics were observed to resemble those of younger mice after OLED treatment. In conclusion, OLED therapy reduced the signs of aging and enhanced stem-cell senescence recovery and then could be used for tissue regeneration.

Anti-Colorectal Cancer Effects of Fucoidan Complex-Based Functional Beverage Through Retarding Proliferation, Cell Cycle and Epithelial-Mesenchymal Transition Signaling Pathways.

BACKGROUND: Fucus vesiculosus-derived fucoidan, a multifunctional bioactive polysaccharide sourced from marine organisms, exhibits a wide range of therapeutic properties, including its anti-tumor effects. While previous research has reported on its anti-cancer potential, limited studies have explored its synergistic capabilities when combined with other natural bioactive ingredients. In this current study, we present the development of an integrative functional beverage, denoted as VMW-FC, which is composed of a fucoidan complex (FC) along with a blend of various herbal components, including vegetables (V), mulberries and fruits (M), and spelt wheat (W). OBJECTIVE: Colorectal cancer (CRC) remains a significant cause of mortality, particularly in metastatic cases. Therefore, the urgent need for novel alternative medicines that comprehensively inhibit CRC persists. In this investigation, we assess the impact of VMW-FC on CRC cell proliferation, cell cycle dynamics, metastasis, in vivo tumorigenesis, and potential side effects. METHODS: Cell growth was assessed using MTT and colony formation assays, while metastatic potential was evaluated through wound healing and transwell migration assays. The underlying signaling mechanisms were elucidated through qPCR and western blot analysis. In vivo tumor formation and potential side effects were evaluated using a subcutaneous tumor-bearing NOD/SCID mouse model. RESULTS: Our findings demonstrate that VMW-FC significantly impedes CRC proliferation and migration in a dose- and time-dependent manner. Furthermore, it induces sub-G1 cell cycle arrest and an increase in apoptotic cell populations, as confirmed through flow-cytometric analysis. Notably, VMW-FC also suppresses xenograft tumor growth in NOD/SCID mice without causing renal or hepatic toxicity. CONCLUSION: The integrative herbal concoction VMW-FC presents a promising approach for inhibiting CRC by slowing proliferation and migration, inducing cell cycle arrest and apoptosis, and suppressing markers associated with proliferation (Ki-67, PCNA, and CDKs) and epithelial-mesenchymal transition (EMT) (Vimentin, N-cadherin, and ß-catenin).

Hard Anodization Film on Carbon Steel Surface by Thermal Spray and Anodization Methods.

In this paper, we used two mass-produced industrial technologies, namely, thermal spraying and anodization methods, to enhance the surface characteristics of AISI 1045 medium carbon steel for use in special environments or products. The anodic film can effectively improve the surface properties of carbon steel. A sequence of treatments of the carbon steel substrate surface that consist of sandblasting, spraying the aluminum film, annealing, hot rolling, cleaning, grinding, and polishing can increase the quality of the anodized film. This paper proposes an anodization process for the surface of carbon steel to increase the corrosion resistance, hardness, color diversification, and electrical resistance. The resulting surface improves the hardness (from 170 HV to 524 HV), surface roughness (from 1.26 to 0.15 µm), coloring (from metal color to various colors), and corrosion resistance (from rusty to corrosion resistant). The electrochemical corrosion studies showed that the AISI 1045 steel surface with a hard anodized film had a lower corrosion current density of 10-5.9 A/cm2 and a higher impedance of 9000 ohm than those of naked AISI 1045 steel (10-4.2 A/cm2 and 150 ohm) in HCl gas.

Amelioration of Nicotine-Induced Osteoarthritis by Platelet-Derived Biomaterials Through Modulating IGF-1/AKT/IRS-1 Signaling Axis.

Besides inhalation, a few studies have indicated that the uptake of nicotine through air or clothing may be a significant pathway of its exposure among passive smokers. Nicotine is well known to exert various physiological impacts, including stimulating sympathetic nervous system, causing vascular disturbances, and inducing cell death. Therefore, we aimed to establish whether exposure of nicotine could induce articular cartilage degeneration in a mouse model of osteoarthritis (OA). We specifically assessed dose-dependent effect of nicotine in vitro to mimic its accumulation. Further, during the in vivo studies, mice subcutaneously administered with nicotine was examined for OA-associated pathologic changes. We found that nicotine significantly suppressed chondrocytes and chondrogenic markers (Sox, Col II, and aggrecan). Nicotine-treated mice also showed altered knee joint ultrastructure with reduced Col II and proteoglycans. After corroborating nicotine-induced OA characteristics, we treated this pathologic condition through employing platelet-derived biomaterial (PDB)-based regenerative therapy. The PDB significantly suppressed OA-like pathophysiological characteristics by 4 weeks. The mechanistic insight underlying this therapy demonstrated that PDB significantly restored levels of insulin-like growth factor 1 (IGF-1) signaling pathway proteins, especially pIGF-1 R, pAKT, and IRS-1, regulating extracellular matrix synthesis by chondrocytes. Taken together, the PDB exerts regenerative and reparative activities in nicotine-mediated initiation and progression of OA, through modulating IGF-1/AKT/IRS-1 signaling axis.