OBJECTIVE To investigate the application value of narrow-band CE-Chirp ASSR(NB CE-Chirp ASSR)and modulated acoustic ASSR in the assessment of hearing threshold in children with hearing impairment.METHODS Forty-eight children with sensorineural hearing loss were tested by pure tone audiometry(PTA),NB CE-Chirp ASSR and modulated acoustic ASSR.According to the results of pure tone audiometry,they were divided into mild to moderate group(48 ears)and severe to profound group(48 ears).The difference and correlation between pure tone hearing threshold and ASSR response threshold of different stimuli were compared between 500-4 000 Hz.RESULTS The absolute differences between the NB CE-Chirp ASSR response threshold and the PTA threshold in 48 children were all smaller than the differences between the modulated acoustic ASSR response threshold and the PTA threshold,and the differences were statistically significant(P<0.001).Under the same stimulus sound,the absolute difference between ASSR response threshold and pure tone hearing threshold in the mild to moderate group was higher than that in the severe to very severe group.The correlation coefficients between NB CE-Chirp ASSR threshold and pure tone hearing threshold are higher than those between modulated sound ASSR threshold and pure tone hearing threshold at 500-4 000 Hz.The test time of NB CE-Chirp ASSR[(20.92±9.33)min]was significantly shorter than that of modulated acoustic ASSR[(33.68±10.97)min](P=0.004).CONCLUSION NB CE-Chirp ASSR can more accurately assess the hearing threshold of children with different degrees of hearing loss than modulated acoustic ASSR.

POEMS syndrome is a rare condition associated with plasma cell disorders， and it often involves multiple systems and has diverse clinical manifestations. This article reports two cases of POEMS syndrome with hepatosplenomegaly as the initial manifestation. During the course of the disease， the patients presented with lower limb weakness， hepatosplenomegaly， lymph node enlargement， ascites， hypothyroidism， positive M protein， and skin hyperpigmentation， and ¹⁸F-FDG PET-CT imaging revealed bone lesions mainly characterized by osteolytic changes and plasma cell tumors. There was an increase in the serum level of vascular endothelial growth factor. The patients were finally diagnosed with POEMS syndrome， and the symptoms were relieved after immunomodulatory treatment.

The master protocol design encompasses a comprehensive clinical trial protocol containing multiple sub-protocols, which can be used to evaluate the clinical intervention effects of various drugs or vaccines on various diseases. Particularly, this design strategy represents an efficient and innovative approach to trial design in the context of precision medicine. The master protocol design can be used for emerging infectious diseases and urgent vaccine development in complex situations. This review aims to outline the types and concepts of master protocol design, analyze the key points and details, and discuss its application scenarios in vaccine clinical evaluations. Additionally, it will explore potential challenges that may arise during implementation to provide references for optimizing emergency clinical trial designs of infectious disease vaccines in China.

Patients with aortic dissection are critically ill and face enormous challenges in postoperative rehabilitation nursing, and research in this area has started late. This paper reviews the development history and content of postoperative rehabilitation nursing for patients with aortic dissection, analyzes the hotspots and difficulties in the current research status of postoperative rehabilitation nursing for patients with aortic dissection, and reflects on and looks forward to the direction of the subsequent development of this field, with the aim of providing reference for postoperative rehabilitation nursing for patients with aortic dissection in China.

Frailty, an increasingly prominent clinical syndrome in the elderly population, is characterized by declining physiological reserves, weaker homeostatic maintenance, and increased sensitivity to environmental stress. Incidence of frailty increases with age and is a risk factor for a wide range of adverse health outcomes. This paper reviews the evolution of the definition of frailty, theoretical models, and commonly used methods of frailty assessment in elderly patients with coronary heart disease, further analyzes the current status of frailty in elderly patients after PCI and its association with poor prognosis, and identifies the next key research directions, aiming to provide valuable references and insights for the research and practice of nursing staff and scientific researchers.

Recruitment is a critical part of human resource management.Conducting recruitment with competency models can significantly enhance match candidates to positions.This paper outlines the theoretical support for competency models.By analyzing the construction process of competency models in public hospitals and their application in recruitment,it aims to explore problems in the implementation of competency models in recruitment and provide suggestions.

Objective To provide basis for the formation of acute exacerbation of chronic obstructive pulmonary disease(AECOPD-STES),the item weight of the syndrome therapeutic evaluation scale for AECOPD-STES was determined.Methods Based on the clinical survey data of 387 AECOPD patients,the random forest method was adopted,and the Spyder integrated development environment.Anaconda navigator software was used to call the"random forest Classifier"in the sklearn package to establish the initial random forest model and calculate the item weights.Factor analysis was used to extract common factors with cumulative variance contribution>80%,and the item weight was calculated according to the cumulative variance contribution and component score coefficient of common factors.The percentage weight method was used to calculate the item weight based on the importance score of each item by 29 experts.Finally,40%,30%and 30%of the above three methods were given respectively to determine the final weight of the items.Results The random forest method showed that the weights of wind cold syndrome,cold Yin syndrome,phlegm heat syndrome,phlegm dampness syndrome and blood stasis syndrome were 0.014-0.170,0.076-0.194,0.017-0.183,0.010-0.183 and 0.069-0.298,respectively.Factor analysis showed that the weights of wind cold syndrome,cold yin Syndrome,phlegm heat syndrome,phlegm dampness syndrome and blood stasis syndrome were 0.030-0.111,0.100-0.182,0.037-0.095,0.022-0.141 and 0.054-0.185,respectively.The percentage weight method shows that the weight ranges of wind cold syndrome,cold yin Syndrome,phlegm heat syndrome,phlegm dampness syndrome and blood stasis syndrome were 0.072-0.102,0.146-0.182,0.057-0.077,0.075-0.111 and 0.115-0.185,respectively.According to the three methods,the weights of wind cold syndrome,cold yin Syndrome,phlegm heat syndrome,phlegm dampness syndrome and blood stasis syndrome were 0.050-0.121,0.117-0.174,0.040-0.117,0.056-0.130 and 0.092-0.188,respectively.Conclusion This study determined the weight of each item of AECOPD-STES,providing a basis for the calculation of syndrome score.

Myxomatous mitral valve degeneration(MMVD)is one of the important pathogenic factors of primary mitral regurgitation.The pathological manifestations of MMVD include thickening,redundancy,and prolapse of the valve leaflets,which lead to structural and functional abnormalities of the mitral valve,eventually cause mitral regurgitation.The pathogenesis of MMVD involves abnormalities in three main cell types:valvular interstitial cells,endothelial cells,and monocyte-macrophages.Therefore,a deep understanding of the regulatory mechanisms of these cell types in MMVD is crucial for the diagnosis and treatment of MMVD.This article provides a comprehensive review of the normal tissue structure characteristics of the mitral valve,the morphological features of MMVD,and the research progress on the regulatory roles of the aforementioned cell types in MMVD,aiming to provide a scientific basis for early intervention and precise treatment of MMVD.

BACKGROUND: Double-stranded RNA-specific adenosine deaminase 1 (ADAR1) binds to double-stranded RNA and catalyzes the deamination of adenosine (A) to inosine (I). The functional mechanism of ADAR1 in non-small cell lung cancer (NSCLC) remains incompletely understood. This study aimed to investigate the prognostic significance of ADAR1 in NSCLC and to elucidate its potential role in regulating tumor cell proliferation and migration. METHODS: Data from The Cancer Genome Atlas (TCGA) and cBioPortal were analyzed to assess the correlation between high ADAR1 expression and clinicopathological features as well as prognosis in lung cancer. We performed Western blot (WB), cell proliferation assays, Transwell invasion/migration assays, and nude mouse xenograft modeling to examine the phenotypic changes and molecular mechanisms induced by ADAR1 knockdown. Furthermore, the ADAR1 p150 overexpression model was utilized to validate the proposed mechanism. RESULTS: ADAR1 expression was significantly elevated in lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC) tissues compared with adjacent non-tumor tissues (LUAD: P=3.70×10-15, LUSC: P=0.016). High ADAR1 expression was associated with poor prognosis (LUAD: P=2.03×10-2, LUSC: P=2.81×10-2) and distant metastasis (P=0.003). Gene Set Enrichment Analysis (GSEA) indicated that elevated ADAR1 was associated with mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) pathway activation, matrix metalloproteinase-9 (MMP-9) expression, and cell adhesion. ADAR1 and MMP-9 levels showed a strongly positive correlation (P=6.45×10-34) in 10 lung cancer cell lines, highest in H1581. Knockdown of ADAR1 in H1581 cells induced a rounded cellular morphology with reduced pseudopodia. Concomitantly, it suppressed cell proliferation, invasion, migration, and in vivo tumorigenesis. It also suppressed ERK phosphorylation and downregulated cellular Finkel-Biskis-Jinkins murine osteosarcoma viral oncogene homolog (c-FOS), MMP-9, N-cadherin, and Vimentin. Conversely, ADAR1 p150 overexpression in PC9 cells enhanced ERK phosphorylation and increased c-FOS and MMP-9 expression. CONCLUSIONS High ADAR1 expression is closely associated with poor prognosis and distant metastasis in NSCLC patients. Mechanistically, ADAR1 may promote proliferation, invasion, migration, and tumorigenesis in lung cancer cells via the ERK/c-FOS/MMP-9 axis.
Humans ; Lung Neoplasms/physiopathology* ; Adenosine Deaminase/genetics* ; Matrix Metalloproteinase 9/genetics* ; Cell Proliferation ; Carcinoma, Non-Small-Cell Lung/physiopathology* ; Cell Movement ; Animals ; Mice ; RNA-Binding Proteins/genetics* ; Female ; Male ; Cell Line, Tumor ; Proto-Oncogene Proteins c-fos/genetics* ; Middle Aged ; MAP Kinase Signaling System ; Gene Expression Regulation, Neoplastic ; Mice, Nude ; Extracellular Signal-Regulated MAP Kinases/genetics*

Poly(ADP-ribose) polymerase 1 (PARP1) is a multifunctional protein involved in diverse cellular functions, notably DNA damage repair. Pharmacological inhibition of PARP1 has therapeutic benefits for various pathologies. Despite the increased use of PARP inhibitors, challenges persist in achieving PARP1 selectivity and effective blood-brain barrier (BBB) penetration. The development of a PARP1-specific positron emission tomography (PET) radioligand is crucial for understanding disease biology and performing target occupancy studies, which may aid in the development of PARP1-specific inhibitors. In this study, we leverage the recently identified PARP1 inhibitor, AZD9574, to introduce the design and development of its ¹⁸F-isotopologue ([¹⁸F]AZD9574). Our comprehensive approach, encompassing pharmacological, cellular, autoradiographic, and in vivo PET imaging evaluations in non-human primates, demonstrates the capacity of [¹⁸F]AZD9574 to specifically bind to PARP1 and to successfully penetrate the BBB. These findings position [¹⁸F]AZD9574 as a viable molecular imaging tool, poised to facilitate the exploration of pathophysiological changes in PARP1 tissue abundance across various diseases.