BACKGROUND:The exact pathogenesis of temporomandibular joint osteoarthritis is currently unclear.Traditional clinical treatment strategies for temporomandibular joint osteoarthritis are symptomatic treatments such as pain relief and reduction of inflammation,which can stop the progression of the disease to a certain degree but cannot reverse the destruction of the cartilage.Cartilage degeneration,as one of the most prominent pathologic features in the development of temporomandibular joint osteoarthritis,has been the subject of an increasing number of studies that focus on its pathogenesis.Consequently,we hope to provide an ideal radical solution for the regeneration of the temporomandibular joint.OBJECTIVE:To review the progress of research on cartilage degeneration in temporomandibular joint osteoarthritis.METHODS:The search terms were"temporomandibular joint osteoarthritis,degradation of cartilage matrix,synovitis,oxidative stress,chondrocyte hypertrophy,chondrocyte apoptosis,ferroptosis,autophagy,angiogenesis,extracellular vesicles"in Chinese and English.Literature search was conducted in PubMed database and CNKI,and the time limit for the search was from January 2004 to October 2024.Screening was performed by analyzing and reading the literature,and according to the inclusion and exclusion criteria,81 papers were finally included for review.RESULTS AND CONCLUSION:(1)Increased secretion of cartilage matrix degrading enzymes causes degradation of the cartilage matrix,leading to cartilage degeneration.(2)Synovitis promotes cartilage degeneration through macrophage M1-type polarization and production of inflammatory mediators.(3)Oxidative stress promotes cartilage degeneration by exacerbating the inflammatory response through overproduction of reactive oxygen species.(4)Chondrocyte phenotypic changes and death lead to the decrease of cartilage matrix synthesis,resulting in cartilage degeneration.(5)Blood vessels of subchondral bone penetrate the calcified cartilage layer to reach the superficial cartilage layer,which destroys the cartilage structure and leads to cartilage degeneration.(6)Bioactive substances carried by serum-derived extracellular vesicles in inflammatory states also promote cartilage degeneration in temporomandibular joint osteoarthritis.

BACKGROUND:The exact pathogenesis of temporomandibular joint osteoarthritis is currently unclear.Traditional clinical treatment strategies for temporomandibular joint osteoarthritis are symptomatic treatments such as pain relief and reduction of inflammation,which can stop the progression of the disease to a certain degree but cannot reverse the destruction of the cartilage.Cartilage degeneration,as one of the most prominent pathologic features in the development of temporomandibular joint osteoarthritis,has been the subject of an increasing number of studies that focus on its pathogenesis.Consequently,we hope to provide an ideal radical solution for the regeneration of the temporomandibular joint.OBJECTIVE:To review the progress of research on cartilage degeneration in temporomandibular joint osteoarthritis.METHODS:The search terms were"temporomandibular joint osteoarthritis,degradation of cartilage matrix,synovitis,oxidative stress,chondrocyte hypertrophy,chondrocyte apoptosis,ferroptosis,autophagy,angiogenesis,extracellular vesicles"in Chinese and English.Literature search was conducted in PubMed database and CNKI,and the time limit for the search was from January 2004 to October 2024.Screening was performed by analyzing and reading the literature,and according to the inclusion and exclusion criteria,81 papers were finally included for review.RESULTS AND CONCLUSION:(1)Increased secretion of cartilage matrix degrading enzymes causes degradation of the cartilage matrix,leading to cartilage degeneration.(2)Synovitis promotes cartilage degeneration through macrophage M1-type polarization and production of inflammatory mediators.(3)Oxidative stress promotes cartilage degeneration by exacerbating the inflammatory response through overproduction of reactive oxygen species.(4)Chondrocyte phenotypic changes and death lead to the decrease of cartilage matrix synthesis,resulting in cartilage degeneration.(5)Blood vessels of subchondral bone penetrate the calcified cartilage layer to reach the superficial cartilage layer,which destroys the cartilage structure and leads to cartilage degeneration.(6)Bioactive substances carried by serum-derived extracellular vesicles in inflammatory states also promote cartilage degeneration in temporomandibular joint osteoarthritis.

[摘 要] 目的：探讨lncRNA DLEU2通过EZH2/H3K27me3途径调控IKKα介导甲状腺癌（TC）放射性碘抵抗的作用机制。方法：利用TCGA数据库分析TC中DLEU2的表达及其与EZH2的相关性。构建放射性碘抵抗的TPC-1细胞（RR-TPC-1细胞）模型及裸鼠移植瘤模型，通过敲低或过表达DLEU2（si-DLEU2/OE-DLEU2）、抑制EZH2（UNC1999）、过表达IKKα（OE-IKKα）进行干预，采用qPCR、WB、RIP、ChIP、CCK-8、流式细胞术、TUNEL染色及体内成瘤实验检测基因与蛋白表达、表观修饰、细胞增殖、凋亡及肿瘤生长。结果：TCGA分析显示，DLEU2在TC组织中显著上调（P < 0.001），与患者不良预后相关（P = 0.008 4），且与EZH2表达呈正相关（r = 0.390, P < 0.001）；RIP证实EZH2与DLEU2存在相互作用/结合（P < 0.05）。体外实验表明，敲低DLEU2可显著下调RR-TPC-1细胞中EZH2、IKKα表达及H3K27me3修饰水平，抑制NF-κB通路活化（P < 0.05或P < 0.01），抑制细胞增殖、促进凋亡（均P < 0.05）。联合敲低DLEU2与抑制EZH2进一步增强上述效应，而过表达IKKα则可部分逆转上述效应（P < 0.05或P < 0.01）。体内实验进一步证实，敲低DLEU2联合抑制EZH2可显著抑制移植瘤生长，增加肿瘤细胞凋亡（均P < 0.01）；IKKα过表达则部分逆转上述抗肿瘤效应（P < 0.05或P < 0.01）。结论：lncRNA DLEU2通过招募EZH2催化H3K27me3修饰，间接激活IKKα/NF-κB信号并形成正反馈环路，介导TPC-1细胞131I抵抗。

Clinically， the occurrence of the breaking bad news is inevitable. For patients， they not only need to accept and cope with bad news， but also need to inform the bad news to their families with clear thinking and appropriate language， seeking their support and cooperation. This paper analysed the connotation and informing dilemma of bad news， investigated patients’ informing tendencies， as well as evaluated the advantages and disadvantages of three disclosure methods， including concealment， immediate informing， and staged informing. On these bases， a detailed response strategy for patients to inform their families was proposed in three parts， including pre-preparation， mid-articulation， and post-summary. In the initial phase， thorough preparation is essential. During the middle stage， when delivering bad news， use plain language and help family members adjust their emotions. In the final phase， ensure that all information and viewpoints have been fully communicated. In addition， the roles and analysis steps that doctors should play were analysed from their perspective and combined with the degree of doctor-patient trust. Effective informing of bad news is not only about communication skills， but also involves a deep understanding and respect for the psychological needs of patients and their families. Through meticulous preparation， appropriate expression， emotional support， and clear confirmation， communication and trust are promoted to face and overcome difficulties together.

Objective To summarize the perioperative nursing experience of a child with Angelman syndrome(AS)complicated with moderate scoliosis undergoing posterior 3-dimensional osteotomy correction,fusion,and internal fixation under general anesthesia.Methods The clinical data of the child with AS and moderate scoliosis who underwent surgical treatment in our hospital on Aug.4,2023,were analyzed.A multidisciplinary team was established upon admission.Relevant literatures and evidences were reviewed to develop and implement a"1+X"nursing plan,which included 2 components:"1"(core perioperative nursing priorities for scoliosis)and"X"(multiple AS-related nursing issues and corresponding strategies).Results The surgery was successful,with stable postoperative conditions and significant improvement in spinal curvature.The child's height increased by 7 cm.Discharge occurred on postoperative day 10,with 100%follow-up compliance.The child regained preoperative independent walking ability during follow-up.Conclusion The"1+X"nursing protocol for AS complicated with scoliosis can effectively ensure perioperative safety and promote recovery,which providing insights for perioperative nursing care of other rare diseases complicated with scoliosis.

Pulmonary arterial hypertension(PAH)is a serious and fatal cardiovascular disease that significantly affects patients'quality of life and survival.Current treatments offer some relief but have limited effectiveness and notable side effects.Sotatercept,as a novel drug,modulates the transforming growth factor-β(TGF-β)signaling pathway and shows promising therapeutic effects in PAH.By summarizing the pharmacological mechanisms and clinical research progress of sotatercept in PAH,assessing its application prospects,and analyzing future research directions in the light of current clinical research results,we provide an important perspective for understanding the clinical application of this drug in China,with a view to promoting its promotion and application in China.

Objective To observe the clinical and transthoracic echocardiographic manifestations of mitral annular disjunction(MAD).Methods Transthoracic echocardiographic data of 990 individuals were retrospectively analyzed.Based on the distance between the attachment point of posterior mitral valve and posterior wall of left ventricle measured on echocardiography,whether there was MAD was judged,and the subjects were divided into MAD group and non-MAD(NMAD)group,and clinical data and echocardiographic parameters were compared between groups.Taken parameters being significantly different between groups as independent variables and the presence or absence of MAD as dependent variable,multivariate binary logistic regression analysis was used to explore correlations of patients' clinical characteristics and transthoracic echocardiographic parameters of MAD.Results MAD was detected in 186 cases(186/990,18.79％).Patients' age,left atrial diameter(LAD),left ventricle diameter(LVD),late diastolic velocity of mitral valve(A)and early diastolic velocity of mitral valve orifices(E)/A in MAD group were all lower than those in NMAD group,while the proportion of moderate and above mitral regurgitation in MAD group was higher than that in NMAD group(all P＜0.05).Patients' age,A and E/A measured with transthoracic echocardiography were all correlated with MAD(all P＜0.05).Conclusion Clinical and transthoracic echocardiographic manifestations of MAD had certain characteristics.

Objective:To explore the relationship between serum omentin-1 and 25-hydroxyvitamin D 3 [25(OH)D 3] levels and bone age index (BAI), pelvic ultrasound findings in girls with central precocious puberty (CPP). Methods:This was a cross-sectional observational study. A total of 150 girls with CPP admitted to the Shaanxi Provincial People′s Hospital from October 2021 to October 2023 were selected as the CPP group, and 63 normal girls who underwent physical examination at the child health clinic during the same period were selected as the control group. Serum Omentin-1 and 25(OH)D 3 levels were detected; anteroposterior X-ray and pelvic ultrasound examinations were performed to obtain BAI, ovarian volume, and uterine volume. Pearson correlation analysis was used to evaluate the correlations of Omentin-1 and 25(OH)D 3 with BAI, ovarian volume, and uterine volume. Multivariate logistic regression analysis was used to screen the influencing factors of CPP, and receiver operating characteristic (ROC) curve was drawn to analyze the value of Omentin-1 and 25(OH)D 3 in diagnosing CPP. Results:The serum levels of Omentin-1 and 25(OH)D 3 in the CPP group were lower than those in the control group (all P<0.05); BAI, uterine volume, and ovarian volume in the CPP group were larger than those in the control group, and the number of follicles with diameter ≥4 mm was more than that in the control group (all P<0.05). In girls with CPP, serum Omentin-1 and 25(OH)D 3 levels were negatively correlated with BAI, uterine volume, ovarian volume, and the number of follicles with diameter ≥4 mm (all P<0.05). Multivariate logistic regression analysis showed that maternal menarche age ≤12 years, high BMI, high BAI, and high estradiol were risk factors for CPP (all P<0.05), while high Omentin-1 and high 25(OH)D 3 were protective factors for CPP (all P<0.05). The areas under the curve (AUC) of Omentin-1 and 25(OH)D 3 for diagnosing CPP were 0.799 and 0.808 respectively; the AUC of combined diagnosis was 0.886, which was higher than that of single diagnosis (all P<0.05). Conclusions:Decreased serum Omentin-1 and 25(OH)D 3 levels in girls with CPP are associated with high BAI and increased ovarian and uterine volumes. The combination of Omentin-1 and 25(OH)D 3 has high value in the diagnosis of CPP.

Objective To observe the clinical and transthoracic echocardiographic manifestations of mitral annular disjunction(MAD).Methods Transthoracic echocardiographic data of 990 individuals were retrospectively analyzed.Based on the distance between the attachment point of posterior mitral valve and posterior wall of left ventricle measured on echocardiography,whether there was MAD was judged,and the subjects were divided into MAD group and non-MAD(NMAD)group,and clinical data and echocardiographic parameters were compared between groups.Taken parameters being significantly different between groups as independent variables and the presence or absence of MAD as dependent variable,multivariate binary logistic regression analysis was used to explore correlations of patients' clinical characteristics and transthoracic echocardiographic parameters of MAD.Results MAD was detected in 186 cases(186/990,18.79％).Patients' age,left atrial diameter(LAD),left ventricle diameter(LVD),late diastolic velocity of mitral valve(A)and early diastolic velocity of mitral valve orifices(E)/A in MAD group were all lower than those in NMAD group,while the proportion of moderate and above mitral regurgitation in MAD group was higher than that in NMAD group(all P＜0.05).Patients' age,A and E/A measured with transthoracic echocardiography were all correlated with MAD(all P＜0.05).Conclusion Clinical and transthoracic echocardiographic manifestations of MAD had certain characteristics.

Pulmonary arterial hypertension(PAH)is a serious and fatal cardiovascular disease that significantly affects patients'quality of life and survival.Current treatments offer some relief but have limited effectiveness and notable side effects.Sotatercept,as a novel drug,modulates the transforming growth factor-β(TGF-β)signaling pathway and shows promising therapeutic effects in PAH.By summarizing the pharmacological mechanisms and clinical research progress of sotatercept in PAH,assessing its application prospects,and analyzing future research directions in the light of current clinical research results,we provide an important perspective for understanding the clinical application of this drug in China,with a view to promoting its promotion and application in China.