Vein graft (VG) failure (VGF) is associated with VG intimal hyperplasia, which is characterized by abnormal accumulation of vascular smooth muscle cells (VSMCs). Most neointimal VSMCs are derived from pre-existing VSMCs via a process of VSMC phenotypic transition, also known as dedifferentiation. There is increasing evidence to suggest that ginger or its bioactive ingredients may block VSMC dedifferentiation, exerting vasoprotective functions; however, the precise mechanisms have not been fully characterized. Therefore, we investigated the effect of ginger on VSMC phenotypic transition in VG remodeling after transplantation. Ginger significantly inhibited neointimal hyperplasia and promoted lumen (L) opening in a 3-month VG, which was primarily achieved by reducing ferroptotic stress. Ferroptotic stress is a pro-ferroptotic state. Contractile VSMCs did not die but instead gained a proliferative capacity and switched to the secretory type, forming neointima (NI) after vein transplantation. Ginger and its two main vasoprotective ingredients (6-gingerol and 6-shogaol) inhibit VSMC dedifferentiation by reducing ferroptotic stress. Network pharmacology analysis revealed that 6-gingerol inhibits ferroptotic stress by targeting P53, while 6-shogaol inhibits ferroptotic stress by targeting 5-lipoxygenase (Alox5), both promoting ferroptosis. Furthermore, both ingredients co-target peroxisome proliferator-activated receptor gamma (PPARγ), decreasing PPARγ-mediated nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 1 (Nox1) expression. Nox1 promotes intracellular reactive oxygen species (ROS) production and directly induces VSMC dedifferentiation. In addition, Nox1 is a ferroptosis-promoting gene that encourages ferroptotic stress production, indirectly leading to VSMC dedifferentiation. Ginger, a natural multi-targeted ferroptotic stress inhibitor, finely and effectively prevents VSMC phenotypic transition and protects against venous injury remodeling.

OBJECTIVES: This study aimed to investigate the perception of dental outpatient care quality from multiple perspectives of administrators, physicians, nurses, and patients and propose nursing care quality evaluation indices that are consistent with the clinical reality to provide reference for the construction of a scientific, systematic, and comprehensive dental outpatient care quality evaluation system. METHODS: A total of 39 interviewees, including 7 administrators, 11 doctors, 11 nurses, and 10 patients, were selected for semi-structured in-depth interviews in five regionally representative tertiary-level A stomatological specialty hospitals nationwide during January-April 2024 by using a multistage sampling method. Colaizzi 7-step analysis was used to analyze and summarize the interview data. Themes were extracted on the basis of the Structure-Process-Outcome (SPO) three-dimensional quality assessment model. RESULTS: Five main themes and 15 secondary themes were extracted from three quality dimensions: structure, process, and result. The related topics of structural quality were as follows: disinfection and isolation norms, equipment and consumable management, nursing manpower ratio and nurse education structure, and emergency capability. The related topics of process quality were as follows: pre-diagnosis risk assessment, patient triage and guidance, communication and attitude, health education, humanistic care, continuous care, specialty operation, and four-hand operation. The related topics of result quality were as follows: satisfaction, adverse event management and analysis, effective complaints and disputes. CONCLUSIONS Structure quality is the foundation, process quality is the core, and result quality is the key in the evaluation of the quality of oral outpatient care. The standardization of disinfection and isolation, equipment and consumable management, allocation of reasonable nursing manpower and post capacity, implementation of high-quality nursing services, and improvement of the quality and satisfaction of medical cooperation are necessary guarantees to ensure the quality of oral outpatient care.
Humans ; Quality of Health Care ; Ambulatory Care/standards* ; Dental Care/standards* ; Outpatients

OBJECTIVES: This study aimed to construct an evaluation index system for nursing quality management in outpatient dental clinics based on the structure-process-outcome model and provide an objective standard for the evaluation of nursing quality in outpatient dental clinics. METHODS: Through literature review, multi-subject interviews, and expert meetings, the first draft of the evaluation index for nursing quality management in outpatient dental clinics was formulated. The Delphi method was adopted to select and invite 15 experts in the fields of hospital infection management, nursing management, and specialized oral care from across the country to modify the first draft. RESULTS: The positive coefficients of the experts in the two rounds of consultation were 86.7% and 92.3%, respectively. The total authority coefficients of the experts were 0.791 and 0.717, respectively. The mean scores of the importance and feasibility of the third-level indices in the two rounds of consultation were all ≥4.333; the coefficients of variation were all ≤0.150; and the Kendall's coordination coefficients were 0.308 and 0.184 respectively, with P<0.05 for all. These results indicated that the experts were motivated to participate in this study. They recognized the importance and feasibility of the overall items in this index system, and their opinions were relatively consistent. Finally, an evaluation index system, which included 3 first-level indices, 7 second-level indices, 22 third-level indices, and 69 index connotations, for nursing quality management in outpatient dental clinics was determined. The weights of the three first-level indicators were all 0.333. Patient satisfaction (0.076, outcome dimension), hand hygiene (0.061, outcome dimension), chair care ratio (0.057, structural dimension), and turnover rate (0.057, structural dimension) were the top tertiary indicators in terms of portfolio weight. CONCLUSIONS The construction method of the evaluation index system for nursing quality management in outpatient dental clinics is scientific and reliable. It can provide a reference for the evaluation of the management level of nursing quality in outpatient dental clinics and promote the continuous improvement of nursing quality in outpatient dental clinics.
Humans ; Dental Clinics ; Delphi Technique

Tissue engineering envisions functional substitute creation for damaged tissues. Insulin-like growth factor-1 (IGF-1) plays roles in bone marrow mesenchymal stem cell (BMSC) osteogenic differentiation (OD), and we investigated its specific mechanism. BMSCs were cultured and OD was induced. Surface antigens (CD105, CD90, CD44, CD45, CD34) were identified by flow cytometry. Adipogenic, chondrogenic, and osteogenic differentiation abilities of BMSCs were observed. BMSCs were cultured in osteogenic medium containing 80 ng/mL IGF-1 for 3 weeks. Alkaline phosphatase activity, calcification level, osteogenic factor (runt related protein 2 [RUNX2], osteocalcin [OCN], osterix [OSX]), total (t-) ERK1/2 and phosphorylated-(p-) ERK1/2 levels, and SRY-related high-mobility-group box 4 (SOX4) levels were assessed by alkaline phosphatase staining and Alizarin Red staining, Western blot, and reverse transcription-quantitative polymerase chain reaction. The mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) pathway inhibitor (PD98059) was used to inhibit the MAPK/ERK pathway in IGF-1-treated BMSCs. Small interfering-SOX4 was transfected into BMSCs to down-regulate SOX4.IGF-1 increased alkaline phosphatase activity, cell calcification, and osteogenic factor (RUNX2, OCN, OSX) levels in BMSCs, indicating that IGF-1 induced rat BMSC OD. SOX4, and p-ERK1/2 and t-ERK1/2 levels were elevated in IGF-1-induced BMSCs, which were annulled by PD98059. PD98059 partly averted IGF-1-induced rat BMSC OD. SOX4 levels, alkaline phosphatase activity, cell calcification, and osteogenic factor (RUNX2, OCN, OSX) levels were reduced after SOX4 down-regulation, showing that downregulation of SOX4 averted the effect of IGF-1 on inducing rat BMSC OD. IGF-1 induced rat BMSC OD by stimulating SOX4 via the MAPK/ERK pathway.

Tissue engineering envisions functional substitute creation for damaged tissues. Insulin-like growth factor-1 (IGF-1) plays roles in bone marrow mesenchymal stem cell (BMSC) osteogenic differentiation (OD), and we investigated its specific mechanism. BMSCs were cultured and OD was induced. Surface antigens (CD105, CD90, CD44, CD45, CD34) were identified by flow cytometry. Adipogenic, chondrogenic, and osteogenic differentiation abilities of BMSCs were observed. BMSCs were cultured in osteogenic medium containing 80 ng/mL IGF-1 for 3 weeks. Alkaline phosphatase activity, calcification level, osteogenic factor (runt related protein 2 [RUNX2], osteocalcin [OCN], osterix [OSX]), total (t-) ERK1/2 and phosphorylated-(p-) ERK1/2 levels, and SRY-related high-mobility-group box 4 (SOX4) levels were assessed by alkaline phosphatase staining and Alizarin Red staining, Western blot, and reverse transcription-quantitative polymerase chain reaction. The mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) pathway inhibitor (PD98059) was used to inhibit the MAPK/ERK pathway in IGF-1-treated BMSCs. Small interfering-SOX4 was transfected into BMSCs to down-regulate SOX4.IGF-1 increased alkaline phosphatase activity, cell calcification, and osteogenic factor (RUNX2, OCN, OSX) levels in BMSCs, indicating that IGF-1 induced rat BMSC OD. SOX4, and p-ERK1/2 and t-ERK1/2 levels were elevated in IGF-1-induced BMSCs, which were annulled by PD98059. PD98059 partly averted IGF-1-induced rat BMSC OD. SOX4 levels, alkaline phosphatase activity, cell calcification, and osteogenic factor (RUNX2, OCN, OSX) levels were reduced after SOX4 down-regulation, showing that downregulation of SOX4 averted the effect of IGF-1 on inducing rat BMSC OD. IGF-1 induced rat BMSC OD by stimulating SOX4 via the MAPK/ERK pathway.

Tissue engineering envisions functional substitute creation for damaged tissues. Insulin-like growth factor-1 (IGF-1) plays roles in bone marrow mesenchymal stem cell (BMSC) osteogenic differentiation (OD), and we investigated its specific mechanism. BMSCs were cultured and OD was induced. Surface antigens (CD105, CD90, CD44, CD45, CD34) were identified by flow cytometry. Adipogenic, chondrogenic, and osteogenic differentiation abilities of BMSCs were observed. BMSCs were cultured in osteogenic medium containing 80 ng/mL IGF-1 for 3 weeks. Alkaline phosphatase activity, calcification level, osteogenic factor (runt related protein 2 [RUNX2], osteocalcin [OCN], osterix [OSX]), total (t-) ERK1/2 and phosphorylated-(p-) ERK1/2 levels, and SRY-related high-mobility-group box 4 (SOX4) levels were assessed by alkaline phosphatase staining and Alizarin Red staining, Western blot, and reverse transcription-quantitative polymerase chain reaction. The mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) pathway inhibitor (PD98059) was used to inhibit the MAPK/ERK pathway in IGF-1-treated BMSCs. Small interfering-SOX4 was transfected into BMSCs to down-regulate SOX4.IGF-1 increased alkaline phosphatase activity, cell calcification, and osteogenic factor (RUNX2, OCN, OSX) levels in BMSCs, indicating that IGF-1 induced rat BMSC OD. SOX4, and p-ERK1/2 and t-ERK1/2 levels were elevated in IGF-1-induced BMSCs, which were annulled by PD98059. PD98059 partly averted IGF-1-induced rat BMSC OD. SOX4 levels, alkaline phosphatase activity, cell calcification, and osteogenic factor (RUNX2, OCN, OSX) levels were reduced after SOX4 down-regulation, showing that downregulation of SOX4 averted the effect of IGF-1 on inducing rat BMSC OD. IGF-1 induced rat BMSC OD by stimulating SOX4 via the MAPK/ERK pathway.

Infant, Newborn ; Humans ; Infant, Premature ; Infant, Low Birth Weight ; Blood Transfusion ; Infant, Premature, Diseases

Objective:To investigate the relationship between cerebrovascular variation and the occurrence and recurrence of cerebral infarction, and provide a theoretical basis for the precise prevention and treatment of cerebral infarction.Methods:Totally 13 939 patients who underwent magnetic resonance imaging(MRI) and magnetic resonance angiography(MRA) examination at the Second Affiliated Hospital of Shandong First Medical University from January 2020 to December 2021 were grouped according to clinical symptoms combined with the imaging report, including 4 412 cases in the cerebral infarction group and 9 527 cases in the control group.2 048 patients in the cerebral infarction group were eventually enrolled in the study according to the inclusion and exclusion criteria, including 1 479 cases of initial cerebral infarction and 569 cases of recurrent cerebral infarction.SPSS 25.0 statistical software was used for data analysis.The χ2 test was used to compare the incidence of cerebral infarction with different cerebrovascular variations.Univariate analysis of suspected risk factors for recurrent cerebral infarction was performed with χ2 test, nonparametric test and t test.The binary logistic regression was used to analyze independent risk factors of recurrent cerebral infarction. Results:The incidence of cerebral infarction in the dual-system cerebrovascular variant patients, the single-system cerebrovascular variant patients, and the non-cerebrovascular variant patients were 40.9%, 30.7% and 31.8% respectively.The incidence of cerebral infarction in the dual-system cerebrovascular variant patients was the highest compared with those in the single-system cerebrovascular variant patients and the non-cerebrovascular variant patients (both P<0.05). The incidence rates of embryonic posterior cerebral artery, vertebral artery dominance, and bilateral common origin anterior cerebral arteries were 14.09%, 10.76% and 5.32%, respectively.The incidence of bilateral common origin anterior cerebral arteries in the cerebral infarction group was significantly higher than that in the control group and the difference was statistically significant.Patients with cerebral infarction who were familial aggregation ( OR=2.207, 95% CI=1.591-3.062), hyperhomocysteinemia ( OR=1.262, 95% CI=1.014-1.570), hypertension ( OR=1.461, 95% CI=1.114-1.918), diabetes mellitus ( OR=1.348, 95% CI=1.072-1.694), coronary heart disease ( OR=1.491, 95% CI=1.196-1.858) were more likely to recurrent cerebral infarction ( P<0.05), and patients with cerebral infarction had a significantly increased risk of recurrent cerebral infarction with age ( OR=1.031, 95% CI=1.020-1.042, P<0.05). Conclusion:Dual-system cerebrovascular variation and bilateral common origin anterior cerebral arteries are risk factors for cerebral infarction.

Objective:To investigate the diagnostic efficiency of the 2020 Chinese Thyroid Imaging Reporting and Data System (C-TIRADS) and the 2017 American College of Radiology Thyroid Imaging Reporting and Data System (ACR-TIRADS) in the diagnosis of benign and malignant thyroid nodules.Methods:A retrospective analysis of the two-dimensional ultrasound image results of 324 thyroid nodules in 289 patients with thyroid nodules and thyroid nodules were performed in the physical examination of the Health Management Department of the Guangdong Second Provincial General Hospital from January 2018 to January 2019. A superficial professional doctor with a senior professional title simultaneously uses the C-TIRADS and ACR-TIRADS methods to evaluate the above nodules. The results are all pathologically referenced for the χ2 test and the receiver operating characteristic curve is drawn. Results:The sensitivity of C-TIRADS in diagnosing benign and malignant thyroid nodules was 81.90%, specificity was 97.72%, accuracy was 92.59%, negative predictive value was 91.85%, positive predictive value was 84.51%; ACR-TIRADS diagnosis The sensitivity of benign and malignant thyroid nodules was 59.05%, specificity was 99.54%, accuracy was 86.42%, negative predictive value was 83.52%, and positive predictive value was 98.41%. The area under the ROC curve was 0.958 and 0.935( Z=2.31 P=0.021). Conclusion:C-TIRADS classification based on counting method is better than ACR-TIRADS classification based on sub-method in the diagnosis of thyroid nodules. It has better efficacy and is more suitable for the current status of diagnosis and treatment of thyroid nodules in China.

Objective:To determine the effect of miR-122-5p on microglia polarization, apoptosis and inflammation after traumatic brain injury (TBI).Methods:A mouse model and an in vitro TBI model were established. Astrocytes were stimulated to synthesize and release exosomes by brain extracts. microRNA microarray analysis was used to analyze the significantly altered microRNAs. Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was applied to detect the expression of miR-122-5p in the in vivo and in vitro TBI model. TUNEL, immunofluorescence, and Western blot were performed to detect the effects of miR-122-5p inhibitors on microglia apoptosis, microglia M1/M2 phenotype transformation and the activation of NLRP3 inflammasome pathway and the phosphorylation of NF-κB after TBI.Results:The results of microRNA microarray analysis showed that 83 miRNAs were downregulated significantly (altered more than 2 folds, P < 0.05), among which miR-122-5p was significantly down-regulated ( P < 0.01). Expression of miR-122-5p was significantly decreased in the in vivo and in vitro TBI model [(1.00±0.00) vs. (0.41±0.15), P < 0.001; (1.00±0.00) vs. (0.34±0.07), P < 0.001]. TUNEL and immunofluorescence showed that miR-122-5p inhibitor significantly alleviated microglia apoptosis[(8.03±1.30) vs. (3.17±0.34), P < 0.001] and promoted microglia M1→M2 phenotype transformation ,M1 phenotype polarization was reduced [(56.96±13.70) vs. (34.70±3.47), P =0.002] and M2 phenotype polarization was increased [(30.46±3.67) vs. (40.74±2.49), P =0.005]. Western blot showed that NLRP3 inflammasome activation was inhibited and NF-κB phosphorylation was decreased when miR-122-5p was downregulated[(0.77±0.10) vs. (0.51±0.11), P =0.02; (0.73±0.08) vs. (0.50±0.07), P =0.003]. Conclusions:miR-122-5p is downregulated in microglia and exosomes secreted by astrocytes after TBI. miR-122-5p inhibitor can attenuate the microglia inflammatory response after TBI by inhibiting the activation of NLRP3 inflammasome pathway and the phosphorylation of NF-κB, promoting the microglia M1→M2 phenotypic transformation and reducing microglia apoptosis, thereby reducing the microglia inflammatory injury after TBI.