Molar distalization in orthodontics: a bibliometric analysis.

OBJECTIVES: The study endeavors to undertake a bibliometric analysis on molar distalization, with the objective of illuminating its evolutionary trajectory, current status, and prognosticating future research hotspots and trends. MATERIAL AND METHODS: A comprehensive exploration of the literature on molar distalization was carried out by conducting a search in the Web of Science (WOS) core database of the University of Hong Kong Electronic Library. The search for topic terms employed included "molar distalization," "molar distalisation," "move molar distally," "molar distal movement," and "molar backwards." The search results were subsequently subjected to meticulous analysis using CiteSpace software. This analysis encompassed various facets such as the citation count; the geographical distribution of the countries, institutions, and journals responsible for publishing the articles; the distribution of the authors; the utilization of keywords within the articles; and the analysis of references. RESULTS: A total of 516 articles were included in the analysis. The top 5 countries in terms of the number of published papers were the United States (USA), South Korea, Turkey, Italy, and Germany, and the top 5 institutions in terms of the number of published papers were Kyung Hee University, A.T. Still University of Health Sciences, Catholic University of Korea, Seoul St. Mary's Hospital, and Universidade de Sao Paulo. The top 5 authors in terms of the number of published papers were Park, Kook, Bayome, Janson, and Lee. There was little cooperation overall. The top 3 journals in terms of the most published related articles were all orthodontic-related journals. After molar distalization and anchorage, the most frequently used keywords were distalization, movement, and pendulum appliance. Kinzinger GSM is the most frequently cited author in references, and one of his articles also has the highest centrality score in references. CONCLUSIONS: As the tides of time shift and scholars display an ever-growing dedication to unraveling the intricacies of this therapeutic modality, the realm of molar distalization has undergone notable advancements in technology. Initially, the traditional appliance suffered from aesthetic drawbacks and discomfort. However, contemporary iterations of the appliance have transcended these limitations, boasting enhanced elegance and convenience while concurrently elevating their efficacy. Nevertheless, limitations of current appliances, including their durability and propensity for recurrence post-treatment, continue to necessitate further advancement. Hence, the ongoing scientific inquiry aims to delve deeper into refining treatment modalities and fabricating cutting-edge appliances within this realm. CLINICAL RELEVANCE: This study holds the potential to significantly enhance the ability of orthodontists to devise treatment protocols and offer state-of-the-art clinical recommendations, thereby empowering them to deliver advanced and refined orthodontic interventions.

Synergistic antibacterial mechanism of silver-copper bimetallic nanoparticles.

The excessive use of antibiotics in clinical settings has resulted in the rapid expansion, evolution, and development of bacterial and microorganism resistance. It causes a significant challenge to the medical community. Therefore, it is important to develop new antibacterial materials that could replace traditional antibiotics. With the advancements in nanotechnology, it has become evident that metallic and metal oxide nanoparticles (MeO NPs) exhibit stronger antibacterial properties than their bulk and micron-sized counterparts. The antibacterial properties of silver nanoparticles (Ag NPs) and copper nanoparticles (Cu NPs) have been extensively studied, including the release of metal ions, oxidative stress responses, damages to cell integrity, and immunostimulatory effects. However, it is crucial to consider the potential cytotoxicity and genotoxicity of Ag NPs and Cu NPs. Numerous experimental studies have demonstrated that bimetallic nanoparticles (BNPs) composed of Ag NPs and Cu NPs exhibit strong antibacterial effects while maintaining low cytotoxicity. Bimetallic nanoparticles offer an effective means to mitigate the genotoxicity associated with individual nanoparticles while considerably enhancing their antibacterial efficacy. In this paper, we presented on various synthesis methods for Ag-Cu NPs, emphasizing their synergistic effects, processes of reactive oxygen species (ROS) generation, photocatalytic properties, antibacterial mechanisms, and the factors influencing their performance. These materials have the potential to enhance efficacy, reduce toxicity, and find broader applications in combating antibiotic resistance while promoting public health.

Long noncoding RNA TUG1 promotes cardiac fibroblast transformation to myofibroblasts via miR­29c in chronic hypoxia.

Cardiac fibroblast­myofibroblast transformation (FMT) contributes to the fibrotic deterioration evoked by chronic hypoxia. Growing evidence implicates long noncoding RNAs (lncRNAs) in various types of cardiac physiological and pathological processes, especially in cardiac fibrosis. In the present study, the lncRNA Taurine Upregulated Gene 1 (TUG1), reported as a regulator of hypoxia fibrosis in the lungs, was found to also be an important regulator of cardiac FMT. Specifically, the possible role of TUG1 in cardiac FMT and fibrosis under chronic hypoxia was investigated. It was revealed that the degree of fibrosis in heart tissues collected from congenital heart surgery patients with low pulse oxygen saturation and mice housed under chronic hypoxic and atmospheric pressure conditions was negatively correlated with pulse oxygen saturation. Moreover, TUG1 expression was positively correlated with the degree of fibrosis but negatively correlated with pulse oxygen saturation. Cardiac fibroblasts showed increased myofibroblast marker, collagen I and α­SMA expression levels as the hypoxia time increased. TUG1 knockdown ameliorated the hypoxia­induced FMT. A bioinformatics analysis predicted that TUG1 had miR­29c binding sites in its 3'­UTR and miR­29c is a key regulator of cardiac fibrosis. The present study demonstrated that TUG1, along with miR­29c, may contribute to cardiac FMT activation and promote fibrosis in chronic hypoxia.

MicroRNA­34a mediates atrial fibrillation through regulation of Ankyrin­B expression.

Atrial fibrillation (AF) has a high prevalence and recurrence rate, and is associated with substantial mortality. However, its underlying mechanisms are not thoroughly understood. Increasing attention has been paid to the roles of microRNAs (miRs) in the pathogenesis of cardiovascular disease, including miR­1 and miR­133 (in the electrophysiological response), and miR­34a (in cardiac fibrosis). Recently, Ankyrin­B (Ank­B), an adaptor protein, has been demonstrated to be associated with AF. As a predicted target gene of miR­34a, the present study aimed to investigate if miR­34a has a role in AF via regulation of Ank­B expression. Western blot analysis revealed that the expression levels of Ank­B was lower in the atrial tissue of AF patients than in individuals with sinus rate (SR); however, reverse transcription­quantitative polymerase chain reaction data demonstrated that miR­34a expression exhibited the opposite pattern. Dual­luciferase assays following the specific overexpression or inhibition of miR­34a indicated that the 3' untranslated region of Ankyrin 2 (the gene encoding Ank­B) contained binding sites for miR­34a. Furthermore, the expression levels of Ank­B and sodium­calcium exchanger 1 (an Ank­B binding partner important in Ca2+ homeostasis), as well as intracellular Ca2+ signaling detected by Fluoro­3 AM, were altered following the modulation of miR­34a expression. Thus, miR­34a may serve an important role in early electrophysiological remodeling and the development of AF via the regulation of Ank­B expression. These results offer valuable insight into the underlying mechanism of AF, and provide a promising target for developing clinical diagnostic tools and potential therapies for patients with AF.

MicroRNA-146b inhibition augments hypoxia-induced cardiomyocyte apoptosis.

MicroRNAs (miRs) regulate a number of physiological and pathological processes, including myocardial chronic hypoxia. Previous studies revealed that the expression of miR-146b is increased in vitro and in vivo following the induction of hypoxia. In the present study, the role of miR­146b in hypoxic cardiomyocytes, and the mechanisms underlying its activity, were investigated. The expression of miR­146b was measured in tissue samples from patients with congenital heart disease by reverse transcription­quantitative polymerase chain reaction. The rat H9c2 cardiomyocyte cell line was transfected with an miR­146b inhibitor or the experimental controls, and the cells were maintained under hypoxic conditions for 72 h. The expression of miR­146b increased following the induction of hypoxia. Transfection with the miR­146b inhibitor enhanced the release of lactate dehydrogenase and increased hypoxia­induced apoptosis, as determined by terminal deoxynucleotidyl transferase dUTP nick­end labeling, Hoechst 33258 staining, JC­1 assay (measuring mitochondrial membrane permeability) and annexin V/propidium iodide analysis. A decreased expression of Bcl­2 was observed, whereas the expression levels of cleaved­caspase 3 and Bax were increased. Western blot analysis and a dual luciferase reporter assay confirmed that ribonuclease L is a direct target of miR­146b. Furthermore, inhibition of miR-146b increased the activation of nuclear factor-κB and signal transducer and activator of transcription 3. In conclusion, the inhibition of miR­146b may increase hypoxia-induced cardiomyocyte apoptosis.

miR-138 protects cardiomyocytes from hypoxia-induced apoptosis via MLK3/JNK/c-jun pathway.

Cardiomyocytes experience a series of complex endogenous regulatory mechanisms against apoptosis induced by chronic hypoxia. MicroRNAs are a class of endogenous small non-coding RNAs that regulate cellular pathophysiological processes. Recently, microRNA-138 (miR-138) has been found related to hypoxia, and beneficial for cell proliferation. Therefore, we intend to study the role of miR-138 in hypoxic cardiomyocytes and the main mechanism. Myocardial samples of patients with congenital heart disease (CHD) were collected to test miR-138 expression. Agomir or antagomir of miR-138 was transfected into H9C2 cells to investigate its effect on cell apoptosis. Higher miR-138 expression was observed in patients with cyanotic CHD, and its expression gradually increased with prolonged hypoxia time in H9C2 cells. Using MTT and LDH assays, cell growth was significantly greater in the agomir group than in the negative control (NC) group, while antagomir decreased cell survival. Dual luciferase reporter gene and Western-blot results confirmed MLK3 was a direct target of miR-138. It was found that miR-138 attenuated hypoxia-induced apoptosis using TUNEL, Hoechst staining and Annexin V-PE/7-AAD flow cytometry analysis. We further detected expression of apoptosis-related proteins. In the agomir group, the level of pro-apoptotic proteins such as cleaved-caspase-3, cleaved-PARP and Bad significantly reduced, while Bcl-2 and Bcl-2/Bax ratio increased. Opposite changes were observed in the antagomir group. Downstream targets of MLK3, JNK and c-jun, were also suppressed by miR-138. Our study demonstrates that up-regulation of miR-138 plays a protective role in myocardial adaptation to chronic hypoxia, which is mediated mainly by MLK3/JNK/c-jun signaling pathway.