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Objective To explore the influence of apical dense bone islands on tooth movement during orthodontic treatment and its complications, and to provide a reference for orthodontic clinical treatment. Methods This study obtained approval from the hospital ethics committee. A retrospective analysis was conducted on 33 patients with apical dense bone islands who received full-mouth fixed orthodontic treatment in the Orthodontics Department of Huizhou Stomatological Hospital from 2018 to 2022. Cone-beam CT (CBCT) was used to determine the location, distribution, and wrapping severity of the apical dense bone islands before treatment. The number of loose teeth located in the apical dense bone islands and the degree of external apical root resorption in the apical area of teeth were analyzed before treatment, immediately after treatment, and 12 months after treatment. Results There were 33 orthodontic patients (aged 11 to 42 years, with an average age of 16.7 years and a median age of 15 years) included in this study, including 12 males (36.4%) and 21 females (63.6%). All apical dense bone islands involved a single tooth located in the mandible, mainly in the premolar-molar area. No gender differences were present in the location of the dense bone islands (P>0.05). The apical dense bone islands were mildly wrapped in 23 cases (69.7%), moderately wrapped in 10 cases (30.3%), and severely wrapped in no cases. No difficulty in tooth movement or incomplete closure of extraction space was found in the apical dense bone islands with different degrees of wrapping during orthodontic treatment. For teeth located in apical dense bone islands, 1 patient (3.0%) had loose teeth before treatment, 6 patients (18.2%) had loose teeth after treatment, and 2 patients (6.1%) had loose teeth 12 months after treatment. The number of patients with grade I loose teeth increased after treatment and 12 months after treatment. There was a statistically significant difference in the number of loose teeth before and after treatment (PP>0.05), and no statistically significant difference in the number of loose teeth after treatment and 12 months after treatment (P>0.05). After treatment, apical dense bone islands showed mild resorption in 26 cases (78.8%), moderate resorption in 7 cases (21.2%), and severe resorption in no cases. The apical dense bone islands showed mild resorption in 25 cases (75.8%), moderate resorption in 8 cases (24.2%), and severe resorption in no cases 12 months after treatment. For the severity of root resorption, there was a statistically significant difference between before and after treatment (PPP>0.05). Conclusion Apical dense bone islands were not found to affect tooth movement during orthodontic treatment. After orthodontic treatment, the number of loose teeth increased and mild-to-moderate tooth external apical root resorption occurred, which may be a potential risk of external apical root resorption. Thus, it is recommended to pay close attention during the orthodontic process.

Abstract Background Potassium (K) is an essential nutrient for plant growth and development. Maize (Zea mays) is a widely planted crops in the world and requires a huge amount of K fertilizer. Arbuscular mycorrhizal fungi (AMF) are closely related to the K uptake of maize. Genetic improvement of maize K utilization efficiency will require elucidating the molecular mechanisms of maize K uptake through the mycorrhizal pathway. Here, we employed transcriptome and gene family analysis to elucidate the mechanism influencing the K uptake and utilization efficiency of mycorrhizal maize. Methods and results The transcriptomes of maize were studied with and without AMF inoculation and under different K conditions. AM symbiosis increased the K concentration and dry weight of maize plants. RNA sequencing revealed that genes associated with the activity of the apoplast and nutrient reservoir were significantly enriched in mycorrhizal roots under low-K conditions but not under high-K conditions. Weighted gene correlation network analysis revealed that three modules were strongly correlated with K content. Twenty-one hub genes enriched in pathways associated with glycerophospholipid metabolism, glycerolipid metabolism, starch and sucrose metabolism, and anthocyanin biosynthesis were further identified. In general, these hub genes were upregulated in AMF-colonized roots under low-K conditions. Additionally, the members of 14 gene families associated with K obtain were identified (ARF: 38, ILK: 4, RBOH: 12, RUPO: 20, MAPKK: 89, CBL: 14, CIPK: 44, CPK: 40, PIN: 10, MYB: 174, NPF: 79, KT: 19, HAK/HKT/KUP: 38, and CPA: 8) from maize. The transcript levels of these genes showed that 92 genes (ARF:6, CBL:5, CIPK:13, CPK:2, HAK/HKT/KUP:7, PIN:2, MYB:26, NPF:16, RBOH:1, MAPKK:12 and RUPO:2) were upregulated with AM symbiosis under low-K conditions. Conclusions This study indicated that AMF increase the resistance of maize to low-K stress by regulating K uptake at the gene transcription level. Our findings provide a genome-level resource for the functional assignment of genes regulated by K treatment and AM symbiosis in K uptake-related gene families in maize. This may contribute to elucidate the molecular mechanisms of maize response to low K stress with AMF inoculation, and provided a theoretical basis for AMF application in the crop field.

Abstract Chemoresistance is a main reason for treatment failure in patients with nasopharyngeal carcinoma, but the exact regulatory mechanism underlying chemoresistance in nasopharyngeal carcinoma remains to be elucidated. Here, we identify PJA1 as a key E3 ubiquitin ligase involved in nasopharyngeal carcinoma chemoresistance that is highly expressed in nasopharyngeal carcinoma patients with nonresponse to docetaxel-cisplatin-5-fluorouracil induction chemotherapy. We find that PJA1 facilitates docetaxel resistance by inhibiting GSDME-mediated pyroptosis in nasopharyngeal carcinoma cells. Mechanistically, PJA1 promotes the degradation of the mitochondrial protein PGAM5 by increasing its K48-linked ubiquitination at K88, which further facilitates DRP1 phosphorylation at S637 and reduced mitochondrial reactive oxygen species production, resulting in suppression of GSDME-mediated pyroptosis and the antitumour immune response. PGAM5 knockdown fully restores the docetaxel sensitization effect of PJA1 knockdown. Moreover, pharmacological targeting of PJA1 with the small molecule inhibitor RTA402 enhances the docetaxel sensitivity of nasopharyngeal carcinoma in vitro and in vivo. Clinically, high PJA1 expression indicates inferior survival and poor clinical efficacy of TPF IC in nasopharyngeal carcinoma patients. Our study emphasizes the essential role of E3 ligases in regulating chemoresistance and provides therapeutic strategies for nasopharyngeal carcinoma based on targeting the ubiquitin-proteasome system.

Abstract In recent years, UAV techniques are developing very fast, and UAVs are becoming more and more popular in both civilian and military fields. An important application of UAVs is rescue and disaster relief. In post-earthquake evaluation scenes where it is difficult or dangerous for human to reach, UAVs and sensors can form a wireless sensor network and collect environmental information. In such application scenarios, task allocation algorithms are important for UAVs to collect data efficiently. This paper firstly proposes an improved immune multi-agent algorithm for the offline task allocation stage. The proposed algorithm provides higher accuracy and convergence performance by improving the optimization operation. Then, this paper proposes an improved adaptive discrete cuckoo algorithm for the online task reallocation stage. By introducing adaptive step size transformation and appropriate local optimization operator, the speed of convergence is accelerated, making it suitable for real-time online task reallocation. Simulation results have proved the effectiveness of the proposed task allocation algorithms.

Background: Primary Carnitine Deficiency (PCD) is a potentially life-threatening autosomal recessive monogenic disorder arising from mutations in the organic cation transporter 2 (OCTN2) gene. Dilated cardiomyopathy (DCM) is a prevalent symptom associated with this condition, and episodes of metabolic disturbance may lead to sudden death. However, the pathogenic mechanism remains unclear. Here, we sought to investigate the response of cardiomyocytes and alterations in the intercellular communication in individuals with PCD DCM. Methods: The GSE211650 dataset was downloaded. Subsequently, modular analysis was performed using hdWGCNA. SCENIC was employed for transcription factor analysis. Monocle2 and SCP were applied to conduct trajectory inference and characterize dynamic features. CellChat was used to investigate intercellular interactions. Results: OCTN2-deficient cardiomyocytes displayed transcriptomic alterations indicative of reduced contractility, developmental abnormalities, and fibrosis. The reduced expression of genes encoding troponin, myosin, and calcium ion transporters may underlie the observed decrease in contractility. Suppressed Wnt signaling and downregulated transcription factors associated with myocardial development suggest potential developmental disturbances in cardiomyocytes. Growth arrest-specific 6 (GAS6) secreted by TNNC1 high cardiomyocytes is implicated in myocardial inflammation and fibrosis. Macrophages-derived secreted phosphoprotein 1 (SPP1) promotes the activation of fibroblasts. Furthermore, there was a reduction in neuronal genes in the OCTN2-deficient group. Conclusions: Our research has unveiled, for the first time, the responses of cardiomyocytes and alterations in the intercellular communication in PCD DCM, offering valuable insights for the precision treatment of this condition.

The efficiency of AlGaInP micro light-emitting diodes (micro-LEDs) was far weaker than that of GaN-based micro-LEDs in structure and performance. Consequently, there was an urgent demand to enhance their efficiency. In this study, a citric acid treatment strategy is proposed to improve the efficiency of red micro-LEDs, and the etching uniformity of different concentrations was first confirmed. We optimized the concentration of citric acid to 1:1 and modulated the wet etching time at 0, 30, 60, 90, and 120 s to treat the sidewalls of devices. Under an injection current density of 68 nA/cm2, the forward voltage (Vf) of micro-LEDs after soaking in citric acid ranged from 1.40 to 1.45 V. Compared with the sample operated at the forward voltage without citric acid sidewall treatment, AlGaInP micro-LEDs displayed significantly enhanced forward voltage. This indicates that citric acid effectively removed N-GaAs without damaging the electrical properties of the devices. Among all citric acid-treated micro-LEDs, the sample with a 60 s wet etching process showed the best improvement, with the light output power and external quantum efficiency (EQE) increased by 31.08% and 5.4%, respectively. Our proposed method to treat AlGaInP micro-LEDs presents promising opportunities for the future development of high-performance optoelectronics.

A new species of the genus Camellia (Theaceae), Camellia zijinica, discovered in the Danxia landscape from Guangdong Province, China, is characterized and illustrated. Phylogenetic analysis based on chloroplast genomes suggested its affinity with C. drupifera, C. oleifera and C. fluviatilis, however, it morphologically differs from all of the latter by leaf shape and size. Phonologically, it most closely resembles C. microphylla, but can be distinguished from the latter by its young branchlets glabrous (vs. densely pubescent), fewer bracteoles and sepals, diverse leaf shape, midvein raised slightly with sparsely pubescent or glabrous (vs. prominently with densely pubescent) and leaf adaxially matt (vs. vernicose) when dried. By morphological and molecular analyses, Camellia zijinica represented a distinct new species of C. sect. Paracamellia.

Abstract Background Metastasis has emerged as the major reason of treatment failure and mortality in patients with nasopharyngeal carcinoma (NPC). Growing evidence links abnormal DNA methylation to the initiation and progression of NPC. However, the precise regulatory mechanism behind these processes remains poorly understood. Methods Bisulfite pyrosequencing, RT-qPCR, western blot, and immunohistochemistry were used to test the methylation and expression level of NEURL3 and its clinical significance. The biological function of NEURL3 was examined both in vitro and in vivo. Mass spectrometry, co-immunohistochemistry, immunofluorescence staining, and ubiquitin assays were performed to explore the regulatory mechanism of NEURL3. Results The promoter region of NEURL3, encoding an E3 ubiquitin ligase, was obviously hypermethylated, leading to its downregulated expression in NPC. Clinically, NPC patients with a low NEURL3 expression indicated an unfavorable prognosis and were prone to develop distant metastasis. Overexpression of NEURL3 could suppress the epithelial mesenchymal transition and metastasis of NPC cells in vitro and in vivo. Mechanistically, NEURL3 promoted Vimentin degradation by increasing its K48-linked polyubiquitination at lysine 97. Specifically, the restoration of Vimentin expression could fully reverse the tumor suppressive effect of NEURL3 overexpression in NPC cells. Conclusions Collectively, our study uncovers a novel mechanism by which NEURL3 inhibits NPC metastasis, thereby providing a promising therapeutic target for NPC treatment.

Abstract Chronic Painful Temporomandibular Disorders (TMD) are challenging to diagnose and manage due to their complexity and lack of understanding of brain mechanism. In the past few decades’ neural mechanisms of pain regulation and perception have been clarified by neuroimaging research. Advances in the neuroimaging have bridged the gap between brain activity and the subjective experience of pain. Neuroimaging has also made strides toward separating the neural mechanisms underlying the chronic painful TMD. Recently, Artificial Intelligence (AI) is transforming various sectors by automating tasks that previously required humans’ intelligence to complete. AI has started to contribute to the recognition, assessment, and understanding of painful TMD. The application of AI and neuroimaging in understanding the pathophysiology and diagnosis of chronic painful TMD are still in its early stages. The objective of the present review is to identify the contemporary neuroimaging approaches such as structural, functional, and molecular techniques that have been used to investigate the brain of chronic painful TMD individuals. Furthermore, this review guides practitioners on relevant aspects of AI and how AI and neuroimaging methods can revolutionize our understanding on the mechanisms of painful TMD and aid in both diagnosis and management to enhance patient outcomes.

Abstract Emerging evidence indicates that DNA methylation plays an important role in the initiation and progression of nasopharyngeal carcinoma (NPC). DNAJA4 is hypermethylated in NPC, while its role in regulating NPC progression remains unclear. Here, we revealed that the promoter of DNAJA4 was hypermethylated and its expression was downregulated in NPC tissues and cells. Overexpression of DNAJA4 significantly suppressed NPC cell migration, invasion, and EMT in vitro, and markedly inhibited the inguinal lymph node metastasis and lung metastatic colonization in vivo, while it did not affect NPC cell viability and proliferation capability. Mechanistically, DNAJA4 facilitated MYH9 protein degradation via the ubiquitin-proteasome pathway by recruiting PSMD2. Furthermore, the suppressive effects of DNAJA4 on NPC cell migration, invasion, and EMT were reversed by overexpression of MYH9 in NPC cells. Clinically, a low level of DNAJA4 indicated poor prognosis and an increased probability of distant metastasis in NPC patients. Collectively, DNAJA4 serves as a crucial driver for NPC invasion and metastasis, and the DNAJA4-PSMD2-MYH9 axis might contain potential targets for NPC treatments.

Compound 7–16 was designed and synthesized in our previous study and was identified as a more potential selective 5-HT2A receptor antagonist and inverse agonist for treating Parkinson’s disease psychosis (PDP). Then, the metabolism, disposition, and excretion properties of 7–16 and its potential inhibition on transporters were investigated in this study to highlight advancements in the understanding of its therapeutic mechanisms. The results indicate that a total of 10 metabolites of 7–16/[14C]7–16 were identified and determined in five species of liver microsomes and in rats using UPLC-Q Exactive high-resolution mass spectrometry combined with radioanalysis. Metabolites formed in human liver microsomes could be covered by animal species. 7–16 is mainly metabolized through mono-oxidation (M470-2) and N-demethylation (M440), and the CYP3A4 isozyme was responsible for both metabolic reactions. Based on the excretion data in bile and urine, the absorption rate of 7–16 was at least 74.7%. 7–16 had weak inhibition on P-glycoprotein and no effect on the transport activity of OATP1B1, OATP1B3, OAT1, OAT3, and OCT2 transporters. The comprehensive pharmacokinetic properties indicate that 7–16 deserves further development as a new treatment drug for PDP.