Objective To evaluate the inhibitory effect of butyric acid (BA) as a histone deacetylase (HDAC) inhibitor on lipopolysaccharide (LPS)-induced pulmonary fibrosis and its mechanism. Methods Thirty C57/BL6 mice were randomly divided into three groups according to the random number method, namely control group (physiological saline was given intraperitoneally and by gavage), LPS challenge group (LPS-induced murine model of pulmonary fibrosis was reproduced with intraperitoneal injection of 10 mg/kg LPS), and BA preconditioning + LPS challenge group (10 mg/kg BA was given followed by intraperitoneal injection of 10 mg/kg LPS), with 10 mice in each group. Mice were sacrificed painlessly, and lung tissue samples were harvested at 2 weeks and 4 weeks respectively (five samples every group each time). HDAC activity was evaluated with fluorescence analysis kit. Protein expression of acetylated-histone H3 (Ace-H3), acetylated-histone H4 (Ace-H4) and thymocyte differentiation antigen 1 (Thy-1) were determined by Western Blot. The mRNA expression of Thy-1 was assessed by real-time reverse transcription- polymerase chain reaction (real-time RT-PCR). The degree of lung inflammation and fibrosis were microscopic detected after hematoxylin-eosin (HE) staining and Masson collagen staining. The deposition of lung collagen was detected by hydroxyproline content measurement kit. Results Compared to control group, the degree of lung inflammation and fibrosis was aggravated after LPS challenge, as manifested by increased hydroxyproline content (μg/mg, 2 weeks: 8.384±0.632 vs. 4.388±0.334, 4 weeks: 8.308±0.244 vs. 4.370±0.342, both P < 0.01), increased HDAC activity (μmol/L, 2 weeks: 7.243±0.384 vs. 3.628±0.641, 4 weeks: 6.479±0.202 vs. 3.238±0.524, both P < 0.01), increased deacetylation degree of histone H3 and H4 [relative expression of Ace-H3 (gray value): 0.516±0.115 vs. 1.005±0.359 at 2 weeks, 0.633±0.143 vs. 1.092±0.193 at 4 weeks, both P < 0.05; relative expression of Ace-H4 (gray value): 0.402±0.164 vs. 0.759±0.187 at 2 weeks, P > 0.05; 0.426±0.098 vs. 0.858±0.177 at 4 weeks, P < 0.01], and lowered Thy-1 mRNA and protein expression [Thy-1 mRNA (2-ΔΔCt): 0.606±0.066 vs. 1.005±0.109 at 2 weeks, P < 0.01; 0.824±0.101 vs. 1.210±0.400 at 4 weeks, P > 0.05; relative expression of Thy-1 protein (gray value): 0.725±0.284 vs. 1.249±0.297 at 2 weeks, 0.589±0.139 vs. 1.372±0.343 at 4 weeks, both P < 0.05]. Compared with LPS group, BA precondition could inhibit above processes, as manifested by decreased hydroxyproline content (μg/mg: 5.943±0.726 vs. 8.384±0.632 at 2 weeks, 4.938±0.209 vs. 8.308±0.244 at 4 weeks, both P < 0.01), decreased HDAC activity (μmol/L: 4.386±0.117 vs. 7.243±0.384 at 2 weeks, 4.863±0.096 vs. 6.479±0.202 at 4 weeks, both P < 0.01), increased Thy-1 mRNA expression at 2 weeks (2-ΔΔCt: 0.884±0.216 vs. 0.606±0.066, P < 0.05), increased acetylation degree of histone H4 and Thy-1 protein expression at 4 weeks [relative expression of Ace-H4 (gray value): 0.715±0.145 vs. 0.426±0.098, P < 0.05; relative protein expression of Thy-1 (gray value): 0.939±0.098 vs. 0.589±0.139, P < 0.01]. Conclusions LPS-induced pulmonary fibrosis was related with activation of HDAC, deacetylation of histone H3 and H4 and Thy-1 gene silencing. HDAC inhibitor BA could inhibit LPS-induced pulmonary fibrosis and Thy-1 gene silencing through inhibiting activation of HDAC and deacetylation of histone H4.

Objective To investigate the risk factors for inflammatory complications after radical gastrectomy for gastric cancer and construct a nomogram model for risk prediction. Methods The clinical data of 402 patients with primary gastric cancer who underwent radical gastrectomy were retrospectively analyzed. All patients underwent preoperative Nutritional Risk Screening 2002 (NRS2002) score, Patient-Generated Subjective Global Assessment (PG-SGA) grading, Lumbar 3 Skeletal Muscle Index (L3-SMI) assessment, and serological index testing. Univariate analysis was used to screen for influencing factors of postoperative inflammatory complications of gastric cancer, and multivariate Logistic regression analysis was conducted to determine independent risk factors. A nomogram model for predicting postoperative inflammatory complications after radical gastrectomy was constructed based on the results of multivariate Logistic regression analysis, and the predictive performance of the model was evaluated using the receiver operating characteristic (ROC) curve and calibration curve. Results Univariate analysis revealed that age, TNM stage, body mass index, preoperative hemoglobin, preoperative albumin, preoperative globulin, NRS2002 score, PG-SGA grade, and L3-SMI were influencing factors of postoperative inflammatory complications in patients undergoing radical gastrectomy (P < 0.05). Multivariate Logistic regression analysis showed that age ≤60 years, preoperative hemoglobin ≤130 g/L(male) or ≤115 g/L(female), TNM staging of Ⅳ stage, NRS2002 score≥3, and L3-SMI ≤52.4 cm²/m²(male) or ≤38.5 cm²/m²(female) were independent risk factors for postoperative inflammatory complications in gastric cancer patients (P < 0.05). A nomogram model was constructed based on age, preoperative hemoglobin, TNM stage, and NRS2002 score. The ROC curve showed that the area under the curve of the nomogram model was 0.930, with sensitivity and specificity of 93.2% and 89.2%, respectively. The calibration curve demonstrated good consistency between the predicted probability of inflammatory complications and the actual outcomes. Conclusion Age≤60 years, low preoperative hemoglobin, TNM staging of Ⅳ stage, NRS2002 score ≥3, and low L3-SMI are independent risk factors for postoperative inflammatory complications in gastric cancer patients. The nomogram model constructed based on age, preoperative hemoglobin, TNM stage, and NRS2002 score can accurately predict postoperative inflammatory complications after gastrectomy for gastric cancer.

Objective: To delineate the clinical features, inheritance pattern, and genotype-phenotype correlation of a Chinese patient with a 17q25.3 duplication. Methods: Whole exome sequencing(WES), chromosomal microarray analysis (CMA), chromosomal karyotyping and fluorescence in situ hybridization(FISH) were employed for the analysis of the proband and his family members. Results: A 5.7 Mb duplication at 17q25.3→qter was identified by WES and CMA in the 4-year-old boy with multiple congenital anomalies, which was classified as a clinically pathogenic variant. This duplication was confirmed by FISH, and was inherited from his unaffected mother who carried a balanced translocation. Further study revealed that his grandmother also carried the balanced translocation but had gestated three healthy children and had no abortion history. His uncle also carried the balanced translocation, while his aunt was normal. Conclusion Above results have enriched the clinical phenotypes of 17q25.3 duplication. Genetic counseling was provided for the family.P4HB, ACTG1, BAIAP2 and TBCD genes may underlie the clinical features for the 17q25.3 duplication.

Objective To construct the rheumatoid arthritis fibroblast-like synoviocytes(RAFLS)model,and to investigate the effects of usnic acid on the inflammatory pathway of high-mobility group protein B1(HMGB1)/receptor for activated glycation end products(RAGE)and the expression levels of vascular en-dothelial growth factor(VEGF),interleukin(IL)-6 and IL-1β.Methods The patients with RA undergoing joint replacement surgery in the orthopedic department of the Second Affiliated Hospital of Guizhou Universi-ty of Traditional Chinese Medicine were selected and the synovial tissues were obtained during operation.The cells were divided into the blank control group(fetal calf serum),solvent control group(fetal calf serum+10％hydroxypropyl betacyclodextrin),usnic acid high dose group(usnic acid 50 μg/mL),usnic acid middle dose group(usnic acid 10 μg/mL),usnic acid low dose group(usnic acid 2.5 μg/mL)and hydroxychloroquine group(hydroxychloroquine 50 mmol/L).The cell proliferation after different concentrations of usnic acid treatment was detected by MTT,the HMGB1 and RAGE protein expression in cells of each group was detec-ted by Western blot,and the expression levels of HMGB1,VEGF,IL-6 and IL-1β were detected by ELISA.Re-sults Compared with the blank control group,the proportions of cellular apoptosis in the usnic acid high,middle and low doses groups and hydroxychloroquine group were increased(P＜0.05);the expression levels of HMGB1 and RAGE protein in the usnic acid high,middle and low doses groups and hydroxychloroquine group were significantly decreased(P＜0.05),the expression levels of HMGB1,VEGF,IL-6 and IL-1β were decreased(P＜0.05);compared with the hydroxychloroquine group,the cellular apoptosis proportions of the usnic acid high,middle and low doses groups were decreased(P＜0.05),the HMGB1 protein expression level in the usnic acid low dose group was significantly increased(P＜005),the RAGE protein expression level in the the usnic acid middle amd low doses groups was significantly increased(P＜0.05).Conclusion Usnic acid alleviates the inflammatory reaction of synoviocytes possibly by regulating HMGB1/RAGE inflammatory pathway and VEGF,IL-6 and IL-1β inflammatory factors expression levels.

Intensity-modulated radiation therapy(IMRT) is currently the main treatment method for nasopharyngeal carcinoma. During radiotherapy for nasopharyngeal carcinoma, factors such as body mass reduction, tumor regression, and organ displacement at risk can affect the precise implementation of radiation therapy. Applying adaptive radiotherapy (ART) technology to optimize the treatment plan at the appropriate timing can reduce the adverse effects caused by the above factors and enhance the accuracy of radiotherapy. There are no uniform standards for the necessity, timing, and case selection of ART. In this review, the research progress of ART in the radiotherapy of nasopharyngeal carcinoma in recent years was reviewed to provide a reference for further clinical application of ART in nasopharyngeal carcinoma.

OBJECTIVE: To demonstrate the mechanism of mechanical ventilation (MV) induced endoplasmic reticulum stress (ERS) promoting mechanical ventilation-induced pulmonary fibrosis (MVPF), and to clarify the role of angiotensin receptor 1 (AT1R) during the process. METHODS: The C57BL/6 mice were randomly divided into four groups: Sham group, MV group, AT1R-shRNA group and MV+AT1R-shRNA group, with 6 mice in each group. The MV group and MV+AT1R-shRNA group mechanically ventilated for 2 hours after endotracheal intubation to establish MVPF animal model (parameter settings: respiratory rate 70 times/minutes, tidal volume 20 mL/kg, inhated oxygen concentration 0.21). The Sham group and AT1R-shRNA group only underwent intubation after anesthesia and maintained spontaneous breathing. AT1R-shRNA group and MV+AT1R-shRNA group were airway injected with the adeno-associated virus one month before modeling to inhibit AT1R gene expression in lung tissue. The expressions of AT1R, ERS signature proteins [immunoglobulin heavy chain-binding protein (BIP), protein disulfide isomerase (PDI)], fibrosis signature proteins [collagen I (COL1A1), α-smooth muscle actin (α-SMA)] in lung tissues were detected by immunofluorescence and Western blotting. Hematoxylin-eosin (HE) staining was used to evaluate lung injury and Masson staining was used to evaluate pulmonary fibrosis. RESULTS: Compared with the Sham group, the degree of pulmonary fibrosis and lung injury were more significant in the MV group. In the MV group, the protein expressions of AT1R, BIP, PDI, COL1A1 and α-SMA were increased (AT1R/β-actin: 1.40±0.02 vs. 1, BIP/β-actin: 2.79±0.07 vs. 1, PDI/β-actin: 2.07±0.02 vs. 1, COL1A1/α-Tubulin: 2.60±0.15 vs. 1, α-SMA/α-Tubulin: 2.80±0.25 vs. 1, all P < 0.01). The number of E-cad⁺/AT1R⁺ and E-cad⁺/BIP⁺ cells in lung tissue increased, and the fluorescence intensity of COL1A1 and α-SMA increased. Compared with the MV group, the degree of pulmonary fibrosis and lung injury were significantly relieved in the MV+AT1R-shRNA group. In the MV+AT1R-shRNA group, the protein expressions of AT1R, BIP, PDI, COL1A1 and α-SMA were decreased (AT1R/β-actin: 0.53±0.03 vs. 1.40±0.02, BIP/β-actin: 1.73±0.15 vs. 2.79±0.07, PDI/β-actin: 1.04±0.07 vs. 2.07±0.02, COL1A1/α-Tubulin: 1.29±0.11 vs. 2.60±0.15, α-SMA/α-Tubulin: 1.27±0.10 vs. 2.80±0.25, all P < 0.01). The number of E-cad⁺/AT1R⁺ and E-cad⁺/BIP⁺ cells in lung tissue decreased, and the fluorescence intensity of COL1A1 and α-SMA decreased. There was no statistically significant difference in the indicators between AT1R-shRNA group and Sham group. CONCLUSIONS MV up-regulate the expression of AT1R in alveolar epithelial cells, activate the AT1R pathway, induce ERS and promote the progression of MVPF.
Mice ; Animals ; Pulmonary Fibrosis/chemically induced* ; Lung Injury ; Respiration, Artificial/adverse effects* ; Actins/metabolism* ; Tubulin ; Mice, Inbred C57BL ; Endoplasmic Reticulum Stress ; RNA, Small Interfering

The Major of Medical Imaging Technology (Radiotherapy Technology Orientation) in West China Medical School, Sichuan University, has been devoted to training therapists, dosimetrists, and physicists in tumor radiotherapy, and it is urgently needed to improve the practice ability of interns and standardize the teaching system. In view of the current status of the practice of students in radiotherapy technology, this article analyzes and summarizes the teaching staff construction, teaching contents, teaching methods, and other aspects, finds out the problems and challenges in the current teaching system, and puts forward suggestions for practice teaching reform.

Objective: To explore the application effect of secondary personalized chairside education on changing the knowledge and behavior of patients with oral periodontal disease. Methods: A total of 124 patients experiencing initial periodontal disease were selected. Sixty-two patients were observed in the observation group, and 62 patients were observed in the control group. After the doctor checked and determined the periodontal condition of the patients, the nurse conducted a targeted, personalized secondary one-on-one chairside mission for the observation group; in the control group, the nurses provided routine one-to-one health education to the patients before treatment. Statistical analysis was conducted to assess periodontal knowledge mastery, self-care behaviors, rate of return for periodontal treatment and patient satisfaction after 3 months. The plaque index and scale index were statistically analyzed before and 3 months after treatment. Results : No statistical difference was found in the general data between the two groups of patients (P > 0.05); however, the degree of mastery of periodontal knowledge in the observation group was higher than that in the control group. The degrees of mastery of the clinical manifestations, hazards and treatment methods were 96.7%, 93.5%, and 91.9% in the observation group and 72.5%, 48.3%, and 69.3% in the control group, respectively; the difference was statistically significant (P < 0.05). The patients in the observation group were more likely than those in the control group to brush more than 2 times daily, use dental floss and use an interdental brush; 100%, 96.7%, and 77.4% of patients in the observation group and 80.6%, 56.4%, and 40.3% of patients in the control group participated in these oral health care behaviors, respectively. The difference was statistically significant (P < 0.05). The rate of recovery and patient satisfaction were higher in the observation group than in control group at 3 months; the rate of recovery and patient satisfaction were 80.6% and 96%, in the observation group and 41.9% and 88.7% in the control group, respectively. The difference was statistically significant (P < 0.05). After 3 months, the plaque index in the observation group was lower than that in the control group (1.71 ± 1.12, 2.35 ± 0.78), and the difference was statistically significant (P < 0.05). Conclusion Secondary personalized chairside education can significantly improve the patient’s cognition of the disease, allow the formation of accurate oral health awareness, and change the patient’s bad oral hygiene habits and medical behavior. Thus, this method is an effective oral health education method and can change the knowledge and beliefs of patients with oral periodontitis.

Coding with high-frequency stimuli could alleviate the visual fatigue of users generated by the brain-computer interface (BCI) based on steady-state visual evoked potential (SSVEP). It would improve the comfort and safety of the system and has promising applications. However, most of the current advanced SSVEP decoding algorithms were compared and verified on low-frequency SSVEP datasets, and their recognition performance on high-frequency SSVEPs was still unknown. To address the aforementioned issue, electroencephalogram (EEG) data from 20 subjects were collected utilizing a high-frequency SSVEP paradigm. Then, the state-of-the-art SSVEP algorithms were compared, including 2 canonical correlation analysis algorithms, 3 task-related component analysis algorithms, and 1 task discriminant component analysis algorithm. The results indicated that they all could effectively decode high-frequency SSVEPs. Besides, there were differences in the classification performance and algorithms' speed under different conditions. This paper provides a basis for the selection of algorithms for high-frequency SSVEP-BCI, demonstrating its potential utility in developing user-friendly BCI.
Humans ; Brain-Computer Interfaces ; Evoked Potentials, Visual ; Algorithms ; Discriminant Analysis ; Electroencephalography