The relationship of ALPK1, hyaluronic acid and M1 macrophage polarization in the temporomandibular joint synovitis.

M1 macrophage polarization and synovitis play an important role in the pathogenesis of temporomandibular joint osteoarthritis (TMJOA). Reduced molecular weight of hyaluronic acid (HA) in synovial fluid of patients with TMJOA. In addition, high molecular weight hyaluronic acid (HMW-HA) is often used clinically to treat TMJ inflammation. As a pattern recognition receptor of the cytoplasm, ALPK1 was found to be pro-inflammatory in a variety of diseases. However, the relationship of ALPK1, HA and M1 macrophage polarization in TMJ synovitis remains unclear. We aimed to investigate the role of ALPK1 and HA in macrophage polarization and TMJ synovitis and the underlying mechanisms. The results demonstrated that ALPK1 was highly upregulated in the synovial macrophages in the inflamed TMJ synovium of patients. Low molecular weight hyaluronic acid (LMW-HA) promoted the expression of ALPK1 and M1 macrophage-associated genes. Besides, rhALPK1 promoted the expression of M1 macrophage-associated factors and the nuclear translocation of PKM2. Furthermore, ALPK1 knockout mice exhibited limited infiltration of macrophages and decreased expression levels of M1 macrophage-associated genes in CFA-induced TMJ synovitis. While HMW-HA inhibited the expression of ALPK1 and M1 macrophage polarization. Our results elucidated that ALPK1 promoted TMJ synovitis by promoting nuclear PKM2-mediated M1 macrophage polarization, whereas HMW-HA inhibited the expression of ALPK1 as well as M1 macrophage polarization.

Wheat Protein Hydrolysates Improving the Stability of Purple Sweet Potato Anthocyanins under Neutral pH after Commercial Sterilization at 121 °C.

Anthocyanins are prone to degradation and color fading after sterilization. This work examined the potential of wheat protein hydrolysates (WPHs, 40 g/L) in improving the stability of purple sweet potato anthocyanins (PSPAs) under a pH of 6.8 after sterilization at 121 °C followed by storage. Results showed that WPHs increased the thermal degradation half-life of PSPAs 1.65 times after sterilization. Compared to PSPAs alone, after being stored at 37 °C and 45 °C for 7 days, the retention concentration of PSPAs with WPHs was 5.4 and 32.2 times higher, and the color change of PSPAs with WPHs decreased from 6.19 and 10.46 to 0.29 and 0.77, respectively. AFM data, fluorescence and UV spectrograms indicated the formation of complexes between PSPAs and WPHs by hydrophobic attraction confirmed by zeta-potential data. PSPAs with WPHs had stable particle size and zeta potential, which may also significantly increase the concentrations after digestion and antioxidant power of PSPAs. This work indicated that the assembled PSPAs composite structure by WPHs significantly reduced the degradation of PSPAs at a pH of 6.8 after sterilization at 121 °C followed by long-term storage.

Tet-dependent 5-hydroxymethyl-Cytosine modification of mRNA regulates axon guidance genes in Drosophila.

Modifications of mRNA, especially methylation of adenosine, have recently drawn much attention. The much rarer modification, 5-hydroxymethylation of cytosine (5hmC), is not well understood and is the subject of this study. Vertebrate Tet proteins are 5-methylcytosine (5mC) hydroxylases and catalyze the transition of 5mC to 5hmC in DNA. These enzymes have recently been shown to have the same function in messenger RNAs in both vertebrates and in Drosophila. The Tet gene is essential in Drosophila as Tet knock-out animals do not reach adulthood. We describe the identification of Tet-target genes in the embryo and larval brain by mapping one, Tet DNA-binding sites throughout the genome and two, the Tet-dependent 5hmrC modifications transcriptome-wide. 5hmrC modifications are distributed along the entire transcript, while Tet DNA-binding sites are preferentially located at the promoter where they overlap with histone H3K4me3 peaks. The identified mRNAs are preferentially involved in neuron and axon development and Tet knock-out led to a reduction of 5hmrC marks on specific mRNAs. Among the Tet-target genes were the robo2 receptor and its slit ligand that function in axon guidance in Drosophila and in vertebrates. Tet knock-out embryos show overlapping phenotypes with robo2 and both Robo2 and Slit protein levels were markedly reduced in Tet KO larval brains. Our results establish a role for Tet-dependent 5hmrC in facilitating the translation of modified mRNAs primarily in cells of the nervous system.

Decent work, work engagement, and turnover intention among registered nurses: a cross-sectional study.

BACKGROUND: Nurses face substantial career challenges arising from global pandemics, economic crises, and their roles in conflict-ridden areas. In this context, the rights of nurses pertaining to decent work, such as freedom, fairness, safety, and dignity, are not adequately safeguarded. This study examines decent work status among Chinese nurses and its links to demographics, work engagement, and turnover intention. METHODS: A cross-sectional study design was used following STROBE guidelines. Through a convenient sampling method, a total of 476 nurses were surveyed. These participants were drawn from three esteemed tertiary Grade A hospitals in Hangzhou, with data collection spanning from June to August in 2023. We used a comprehensive set of assessment instruments, encompassing an evaluation of demographic characteristics, the Decent Work Perceptions Scale (DWPS), the Utrecht Work Engagement Scale (UEWS), and turnover intention questionnaire. Bootstrapping procedures were used to ensure the robustness and reliability of the model. RESULTS: The study revealed that nurses' perceptions of decent work significantly impacted work engagement (ß = 0.603, p < 0.001) and turnover intention (ß = -0.275, p < 0.001). Work engagement operated as a mediator between decent work and turnover intention, decreasing the likelihood of nurses leaving their positions (ß = -0.062, p < 0.001). Factors such as age, years of working experience, professional title, job category, and attendance at professional conferences significantly influenced nurses' perceptions of decent work (all p < 0.05). CONCLUSIONS: This study examines factors affecting decent work among nurses and explores its connection with work engagement and the intention to leave. Despite limitations (sample, social desirability bias), the study offers valuable insights for nursing practice. This suggests managers improve decent work for young nurses through rational shift schedules and continuous education. Policymakers should consider adjusting nursing policies for better employment conditions.

Assessing the mediation pathways: How decent work affects turnover intention through job satisfaction and burnout in nursing.

AIM: This study aimed to assess the potential mediating roles of nurses' job satisfaction and burnout in the association between decent work and turnover intention. BACKGROUND: There is a global challenge of nursing shortages in healthcare systems worldwide. Decent work is crucial for safeguarding the rights and professional development outcomes of nurses. However, there is currently limited research on decent work among nurses, and there is a lack of studies exploring the relationships between nurses' decent work, job satisfaction, burnout, and turnover intention. METHODS: A cross-sectional survey design was employed with a sample of 460 nurses from three hospitals: The Affiliated Hospital of Hangzhou Normal University, Hangzhou Third People's Hospital, and Hangzhou Red Cross Hospital. The STROBE checklist was used. Mediation analysis using the PROCESS Macro was used to examine the relationships between decent work, job satisfaction, burnout, and turnover intention. RESULTS: The results showed that nurses' perception of decent work directly influences their turnover intention. Additionally, these findings strongly support the role of job satisfaction and burnout as mediating factors in the relationship between decent work and turnover intention. CONCLUSIONS: Decent work reduces nurse burnout and turnover intention of enhancing their job satisfaction. IMPLICATIONS FOR NURSING AND HEALTH POLICY: This study's findings have important implications for healthcare organizations and policymakers. Recognizing the pivotal role of decent work in nurses' job satisfaction and well-being can guide the development of strategies to improve working conditions and reduce turnover rates. It is imperative for healthcare institutions to prioritize creating safe, supportive, and equitable work conditions for nurses, as this can contribute to higher job satisfaction and, subsequently, lower turnover rates.

The value of radiographic features in predicting postoperative facial nerve function in vestibular schwannoma patients: A retrospective study and nomogram analysis.

OBJECTIVE: The purpose of this study was to identify significant prognostic factors associated with facial paralysis after vestibular schwannoma (VS) surgery and develop a novel nomogram for predicting facial nerve (FN) outcomes. METHODS: Retrospective data were retrieved from 355 patients who underwent microsurgery via the retrosigmoid approach for VS between December 2017 and December 2022. Univariate and multivariate logistic regression analysis were used to construct a radiographic features-based nomogram to predict the risk of facial paralysis after surgery. RESULTS: Following a thorough screening process, a total of 185 participants were included. The univariate and multivariate logistic regression analysis revealed that tumor size (p = 0.005), fundal fluid cap (FFC) sign (p = 0.014), cerebrospinal fluid cleft (CSFC) sign (p < 0.001), and expansion of affected side of internal auditory canal (IAC) (p = 0.033) were independent factors. A nomogram model was constructed based on these indicators. When applied to the validation cohort, the nomogram demonstrated good discrimination and favorable calibration. Then we generated a web-based calculator to facilitate clinical application. CONCLUSION: Tumor size, FFC and CSFC sign, and the expansion of the IAC, serve as good predictors of postoperative FN outcomes. Based on these factors, the nomogram model demonstrates good predictive performance.

Resatorvid alleviates experimental inflammatory TMJOA by restraining chondrocyte pyroptosis and synovial inflammation.

OBJECTIVES: Innate immunity plays a significant role in the pathogenesis of temporomandibular joint osteoarthritis (TMJOA), which is characterized by synovial inflammation and condylar cartilage degradation. We are urged to investigate the impact of Resatorvid, a preventative drug that inhibits Toll-like receptor 4 (TLR4), on experimental inflammatory TMJOA pathology. METHODS: An intra-articular injection of complete Freund's adjuvant (CFA) was used to induce an experimental inflammatory mouse TMJOA model, and TLR4 expression was identified by immunofluorescent labeling. Intraperitoneal injections of Resatorvid were administered to CFA-induced TMJOA mice, and the pathology of TMJOA animals with and without Resatorvid treatment was examined by H&E, Safranin-O/Fast Green, and TRAP staining, as well as micro-CT, immunohistochemistry, and immunofluorescence. The impact of Resatorvid on chondrocyte pyroptosis and macrophage inflammation was further investigated using ATDC5 chondrocytes and RAW264.7 macrophages pretreated with relevant antagonists. RESULTS: CFA-induced TMJOA mice revealed remarkable synovial inflammation, together with a time course of cartilage degradation and bone destruction, with TLR4 elevated in the synovium and condylar cartilage. Prophylactic treatment with Resatorvid mitigated synovial inflammation, cartilage degeneration, and bone destruction in CFA-induced TMJOA mice and downregulated MyD88/NF-κB expression. Ex vivo studies demonstrated that Resatorvid treatment alleviated NOD-like receptor protein 3 (NLRP3)-mediated chondrocyte pyroptosis and degeneration and relieved macrophage inflammation by preventing reactive oxygen species (ROS) production through NLRP3 signaling. CONCLUSION: Prophylactic treatment with Resatorvid alleviates TMJOA pathology by inhibiting chondrocyte pyroptosis and degeneration, as well as ROS-induced macrophage inflammation, through TLR4/MyD88/NF-κB/NLRP3.

Phenomenological characteristics of autobiographical future thinking in nurses with burnout: a case-control study.

Objective: Nurses constitute the largest group of healthcare workers worldwide, and job burnout is very common among them. This study aims to explore abnormal future thinking in nurses with burnout. Additionally, the study investigates whether these manifestations worsen as burnout progresses. Methods: The study was conducted in inpatient ward nurses at a tertiary hospital in Hangzhou, China. In the first phase, two group of nurses were recruited: nurses with burnout (N = 70) and nurses without burnout (N = 70). In the second phase, three groups were recruited according to the burnout levels: mild burnout (N = 43), moderate burnout (N = 42) and severe burnout (N = 43). Data on job burnout were obtained using the Chinese Maslach Burnout Inventory. The Sentence Completion for Events in the Future Test (SCEFT) was employed to measure the content of future thinking, which was evaluated by two raters in terms of the specificity, emotional valence, and concrete content of the imagined future events. The proportions of specific types of events among all the produced events were calculated. Results: The results revealed that nurses with burnout, compared to nurses without burnout, imagined fewer specific future events, positive events, and events related to relationships and achievement. They also had more omissions. As the level of burnout increased, their impairment in future thinking worsened. Furthermore, the results also revealed that the scores of emotional exhaustion, depersonalization, and personal accomplishment had significant correlations with the proportions of positive events and events related to relationships and achievement/mastery in nurses' future thinking content. Conclusion: The future thinking ability of nurses with burnout was impaired, and this impairment worsened as the symptoms of burnout progressed. The findings of the present study have important implications for nurse caring and advocate effective interventions targeting positive future thinking to mitigate nurses' burnout.

Moral distress, psychological capital, and burnout in registered nurses.

AIMS: This study aimed to explore the relationship among moral distress, psychological capital, and burnout in registered nurses. ETHICAL CONSIDERATION: The study was approved by the Ethics Committee of the School of Nursing, Hangzhou Normal University (Approval no. 2022001). METHODS: A cross-sectional descriptive survey was conducted with a convenience sample of 397 nurses from three Grade-A tertiary hospitals in Zhejiang Province, China. Participants completed demographic information, the Nurses' Moral Distress Scale, the Nurses' Psychological Capital Scale, and the Maslach Burnout Inventory Scale. The data were analyzed using Pearson's correlation analysis, structural equation modeling, and hierarchical multiple regression analysis. RESULTS: The study found that moral distress and burnout are positively correlated, while psychological capital is negatively correlated with both moral distress and burnout. The path analysis in structural equation modeling revealed that moral distress has a significant direct effect on psychological capital, while psychological capital has a significant direct effect on burnout. In addition, moral distress also had a significant indirect effect on burnout through psychological capital. Moreover, both the direct effect of moral distress on burnout and the total effect of moral distress on burnout were significant. CONCLUSION: The findings suggest that psychological capital plays an important role in the relationship between moral distress and burnout. Promoting psychological capital among nurses may be a promising strategy for preventing moral distress and burnout in the workplace.

ALPK1 Expressed in IB4-Positive Neurons of Mice Trigeminal Ganglions Promotes MIA-Induced TMJ pain.

Pain is one of the main reasons for patients with temporomandibular joint (TMJ) disorders seeking medical care. However, there is no effective treatment yet as its mechanism remains unclear. Herein, we found that the injection of monoiodoacetate (MIA) into mice TMJs can induce typical joint pain as early as 3 days, accompanied by an increased percentage of calcitonin gene-related peptide positive (CGRP+) neurons and isolectin B4 positive (IB4+) in the trigeminal ganglions (TGs). Our previous study has discovered that alpha-kinase 1 (ALPK1) may be involved in joint pain. Here, we detected the expression of ALPK1 in neurons of TGs in wild-type (WT) mice, and it was upregulated after intra-TMJ injection of MIA. Meanwhile, the increased percentage of neurons in TGs expressing ALPK1 and CGRP or ALPK1 and IB4 was also demonstrated by the immunofluorescent double staining. Furthermore, after the MIA injection, ALPK1-/- mice exhibited attenuated pain behavior, as well as a remarkably decreased percentage of IB4+ neurons and an unchanged percentage of CGRP+ neurons, as compared with WT mice. In vitro assay showed that the value of calcium intensity was weakened in Dil+ neurons from ALPK1-/- mice of TMJ pain induced by the MIA injection, in relation to those from WT mice, while it was significantly enhanced with the incubation of recombinant human ALPK1 (rhA). Taken together, these results suggest that ALPK1 promotes mice TMJ pain induced by MIA through upregulation of the sensitization of IB4+ neurons in TGs. This study will provide a new potential therapeutic target for the treatment of TMJ pain.

The efficacy of stenting in the iliofemoral vein of patients with venous obstruction and secondary lymphedema from malignancy.

OBJECTIVE: To investigate the safety and effectiveness of venous stenting in patients with chronic iliofemoral venous obstruction and secondary lymphedema from malignancy. METHODS: From July 2012 to December 2020, patients with iliofemoral venous obstruction and secondary lymphedema who underwent venous stenting in our institution were reviewed retrospectively. Clinical characteristics, surgical complications, and symptom relief were assessed. Stent patency was evaluated with duplex ultrasound or computed tomographic venography. Twelve-month outcomes were reported. RESULTS: Fifty-three patients with concurrent secondary lymphedema who had stents placed for iliofemoral venous obstruction were included. There were 42 females, and the mean age was 56.9 years. Nonthrombotic iliac vein lesions were identified in 16 patients (30.1%). Immediate technical success was 100%, with an average of two stents implanted. The median Villalta score, and Chronic Venous Disease Quality of Life quality of life questionnaire scores decreased from 12 (IQR, 10-15) and 58 (IQR, 50-66) at baseline, respectively, to 5 (interquartile range [IQR], 4-6) and 28 (IQR, 22-45) at 12 months after the procedure (P < .05), showing significant improvement in the quality of life. At the end of a median follow-up of 12 months (range, 3-25 months), the cumulative primary, assisted primary, and secondary patency rates were 70.8%, 76.9%, and 90.1%, respectively. CONCLUSIONS: In patients with secondary lymphedema from malignancy, venous stent placement is safe and effective for iliofemoral venous obstruction.

Tet-dependent 5-hydroxymethyl-Cytosine modification of mRNA regulates the axon guidance genes robo2 and slit in Drosophila.

Modifications of mRNA, especially methylation of adenosine, have recently drawn much attention. The much rarer modification, 5-hydroxymethylation of cytosine (5hmC), is not well understood and is the subject of this study. Vertebrate Tet proteins are 5-methylcytosine (5mC) hydroxylases enzymes catalyzing the transition of 5mC to 5hmC in DNA and have recently been shown to have the same function in messenger RNAs in both vertebrates and in Drosophila. The Tet gene is essential in Drosophila because Tet knock-out animals do not reach adulthood. We describe the identification of Tet-target genes in the embryo and larval brain by determining Tet DNA-binding sites throughout the genome and by mapping the Tet-dependent 5hmrC modifications transcriptome-wide. 5hmrC-modified sites can be found along the entire transcript and are preferentially located at the promoter where they overlap with histone H3K4me3 peaks. The identified mRNAs are frequently involved in neuron and axon development and Tet knock-out led to a reduction of 5hmrC marks on specific mRNAs. Among the Tet-target genes were the robo2 receptor and its slit ligand that function in axon guidance in Drosophila and in vertebrates. Tet knock-out embryos show overlapping phenotypes with robo2 and are sensitized to reduced levels of slit. Both Robo2 and Slit protein levels were markedly reduced in Tet KO larval brains. Our results establish a role for Tet-dependent 5hmrC in facilitating the translation of modified mRNAs, primarily in developing nerve cells.

A SERS-Based Dual-Parameter Monitoring Nanoprobe of ROS and PI3K/Akt during Ginsenoside Rg3-Induced Cell Apoptosis.

Both the reactive oxygen species (ROS) level and Phosphatidylinositol 3 Kinase (PI3K) protein content are two crucial parameters for characterizing states of cell apoptosis. Current methods measure these parameters with two different techniques, respectively, which usually lead to evaluation contingency. Ginsenoside Rg3 exhibits an excellent anticancer effect, which is enacted by the Phosphatidylinositol 3 Kinase/Protein Kinase B (PI3K/Akt) pathway involving ROS; however, the precise mechanism that induces cell apoptosis remains unknown. This is due to the lack of information on quantitative intracellular ROS and PI3K. Here, we used a surface-enhanced Raman scattering (SERS)-based boric acid nanoprobe to monitor the intracellular ROS level and phosphatidylinositol-3,4,5-triphosphate (PI(3,4,5)P3) content, which reflects the regulatory effect of the PI3K/Akt pathway. After treatment with ginsenoside Rg3, the PI3K/Akt content first increased and then decreased as the ROS level increased. Moreover, when the ROS level significantly increased, the mitochondrial membrane potential reduced, thus indicating the dynamic regulation effect of intracellular ROS level on the PI3K/Akt pathway. Importantly, in addition to avoiding evaluation contingency, which is caused by measuring the aforementioned parameters with two different techniques, this SERS-based dual-parameter monitoring nanoprobe provides an effective solution for simultaneous ROS level and PI3K content measurements during cell apoptosis. Furthermore, the intracellular ROS level was also able to have a dynamic regulatory effect on the PI3K/Akt pathway, which is essential for studying ROS/PI3K/Akt-pathway-related cell apoptosis and its activation mechanism.

Collagen hydrolysates improve the efficiency of sodium alginate-encapsulated tea polyphenols in beads and the storage stability after commercial sterilization.

This study showed that sodium alginates (SA)-based beads reinforced with collagen hydrolysates (CHs) significantly increased an encapsulation rate of tea polyphenols (TP) from 34.54 % to 85.06 % when the mass ratio of SA: CHs increased from1.5:0 to 1.5:0.5. And after the 30-day storage at 37 °C, the retention rate of TP in beads with CHs at the solutions with pH = 4.0 or pH = 7.0 increased from 61.10 % to 80.21 %, or from 67.72 % to 80.47 % after sterilization at 98 °C or 121 °C for 30 min, respectively. Also, the addition of CHs at 0.5 % resulted in a greater retention of the polyphenolic compositions values of TP determined by UPLC-Orbitrap-MS system. Additionally, the DPPH and ABTS+ free-radical scavenging capacities and ferric-reducing antioxidant power of beads with CHs after sterilization at 98 °C or 121 °C for 30 min were significantly higher than which without CHs. Physical phenomena based on ζ-potential, particle size, fluorescence, UV spectroscopy and confocal laser scanning microscope showed that tightly non-covalent complexes of CHs in combination to TP could be uniformly and stably distributed in the network of SA solution for encapsulating TP in SA-based beads. These findings provided suggestions for the co-encapsulation design and development of hydrophilic nutritive compounds based on CHs in SA-based beads.

Tet-dependent 5-hydroxymethyl-Cytosine modification of mRNA regulates axon guidance genes in Drosophila.

Modifications of mRNA, especially methylation of adenosine, have recently drawn much attention. The much rarer modification, 5-hydroxymethylation of cytosine (5hmC), is not well understood and is the subject of this study. Vertebrate Tet proteins are 5-methylcytosine (5mC) hydroxylases and catalyze the transition of 5mC to 5hmC in DNA. These enzymes have recently been shown to have the same function in messenger RNAs in both vertebrates and in Drosophila. The Tet gene is essential in Drosophila as Tet knock-out animals do not reach adulthood. We describe the identification of Tet-target genes in the embryo and larval brain by mapping one, Tet DNA-binding sites throughout the genome and two, the Tet-dependent 5hmrC modifications transcriptome-wide. 5hmrC modifications are distributed along the entire transcript, while Tet DNA-binding sites are preferentially located at the promoter where they overlap with histone H3K4me3 peaks. The identified mRNAs are preferentially involved in neuron and axon development and Tet knock-out led to a reduction of 5hmrC marks on specific mRNAs. Among the Tet-target genes were the robo2 receptor and its slit ligand that function in axon guidance in Drosophila and in vertebrates. Tet knock-out embryos show overlapping phenotypes with robo2 and both Robo2 and Slit protein levels were markedly reduced in Tet KO larval brains. Our results establish a role for Tet-dependent 5hmrC in facilitating the translation of modified mRNAs primarily in cells of the nervous system.

Cystic Adventitial Disease of the Popliteal Vein: A Case Report.

Venous cystic adventitial disease (VCAD) is a rare vascular anomaly located in the common femoral vein in most cases. We describe the case of a 59-year-old female patient with right leg edema who was misdiagnosed with deep vein thrombosis of the lower extremity at another hospital. Magnetic resonance angiography revealed a round mass in the popliteal vein, with a narrow lumen. Considering the location of the lesion, absence of a history of deep venous thrombosis and trauma, and clinical manifestations, the diagnosis is likely a popliteal vein adventitial cyst. Segmental popliteal vein resection and reconstruction were performed using a cylindrical great saphenous vein graft. No joint connection was found during the operation, and the postoperative pathology confirmed VCAD.

Clinical Application of CAD/CAM-Guided Modified Dautrey's Procedure in Recurrent Temporomandibular Joint Luxation.

This study aimed to introduce the clinical application of the CAD/CAM-guided modified Dautrey's procedure in recurrent anterior temporomandibular joint luxation and evaluate its clinical effects. Four selected patients were treated by the CAD/CAM-guided modified Dautrey's procedure and were followed-up to access their curative effect. Joint pain and sound, recurrence rate, mandibular function, maximum mouth opening (MMO), symptoms of facial nerve injury, and changes in zygomatic facial appearance were observed in postoperative follow-up. The followed-up period ranged from 3 months to 1 year with an average time of 7.5 months. There was no recurrence in all 4 patients, and no symptoms of facial nerve injury and zygomaticofacial appearance changes were found. All patients showed improvement in MMO, with a mean preoperative and postoperative MMO of 4.74 and 3.74 cm, respectively. All of them showed relief of joint pain or sound 3 months or more after the operation and could exercise mandibular normally. This results showed that the CAD/CAM-guided modified Dautrey's procedure was effective in the treatment of recurrent temporomandibular joint luxation and could be used as a good alternative treatment for it.

Long noncoding RNA TUG1 induces angiogenesis of endothelial progenitor cells and dissolution of deep vein thrombosis.

OBJECTIVE: Long non-coding RNA (lncRNA) essentially controls many physiological and pathological processes of deep vein thrombosis (DVT). Based on that, lncRNA taurine upregulated gene 1 (TUG1)-involved angiogenesis of endothelial progenitor cells (EPCs) and dissolution of DVT was explored. METHODS: In the in-vitro experiments, EPCs were engineered with mimic, inhibitor, siRNA, and plasmid, after which tube formation, proliferation, migration, and apoptosis were checked. In the in-vivo experiments, a DVT mouse model was established. Before the DVT operation, the mice were injected with agomir, antagomir, siRNA, and plasmid. Subsequently, thrombosis and damage to the femoral vein were pathologically evaluated. TUG1, miR-92a-3p, and 3-Hydroxy-3-methylglutaryl coenzyme A reductase (Hmgcr) expression in the femoral vein was tested. The relationship between TUG1, miR-92a-3p, and Hmgcr was validated. RESULTS: DVT mice showed suppressed TUG1 and Hmgcr expression, and elevated miR-92a-3p expression. In EPCs, TUG1 overexpression or miR-92a-3p inhibition promoted cellular angiogenesis, whereas Hmgcr silencing blocked cellular angiogenesis. In DVT mice, elevated TUG1 or inhibited miR-92a-3p suppressed thrombosis and damage to the femoral vein whilst Hmgcr knockdown acted oppositely. In both cellular and animal models, TUG1 overexpression-induced effects could be mitigated by miR-92a-3p up-regulation. Mechanically, TUG1 interacted with miR-92a-3p to regulate Hmgcr expression. CONCLUSION: Evidently, TUG1 promotes the angiogenesis of EPCs and dissolution of DVT via the interplay with miR-92a-3p and Hmgcr.

ALPK1 Accelerates the Pathogenesis of Osteoarthritis by Activating NLRP3 Signaling.

Alpha-kinase 1 (ALPK1), a member of the alpha-kinase family, has been shown to be involved in mediating inflammatory responses and is strongly associated with gout; however, its modulatory role in osteoarthritis (OA) remains unclear. Here, we uncovered elevation of ALPK1 in degraded cartilage of destabilized medial meniscus (DMM) and collagenase-induced osteoarthritis (CIOA), two different mouse OA models induced by mechanical stress or synovitis. Intraarticular administration of recombinant human ALPK1 (rhALPK1) in vivo exacerbated OA pathogenesis in both DMM and CIOA mice, whereas ALPK1 knockout reversed this process. In vitro study demonstrated that ALPK1 aggravates metabolic disturbances in chondrocytes by enhancing the production of NOD-like receptor protein 3 (NLRP3), an inflammasome sensors driving interlukin-1ß (IL-1ß)-mediated inflammatory conditions. Furthermore, the selective inhibition of nuclear factor-κB (NF-κB) or NLRP3 indicates that NLRP3 is a downstream signaling governed by NF-κB in ALPK1-activated chondrocytes. Collectively, these results establish ALPK1 as a novel catabolic regulator of OA pathogenesis, and targeting this signaling may be a promising treatment strategy for OA. © 2022 American Society for Bone and Mineral Research (ASBMR).