To adapt to the new training program and requirement of MOE , a reform in Chinese curricula, textbook selection and editing, and teaching evaluation method was carried out to strengthen medical Chinese teaching and improve the students' overall Chinese proficiency. Detailed measures in-cluded adjusting the class hour, formulating Chinese reading and writing syllabus, Chinese listening and speaking syllabus and graded vocabulary, evaluating the effect through Chinese proficiency test, learning evaluation and file cover evaluation. After the reform, attendance rate was improved obviously, plagiarism rate was declined obviously and students were highly praised by teacher during the internship and practice.

Objective:To develop an HPLC-MS/MS method for the determination of rosuvastatin in plasma and study the relative bioavailability and bioequivalence of the capsules and tablets in Chinese healthy volunteers. Methods: A single oral dose (20 mg of the test or reference preparation) was given to 24 male healthy volunteers in a randomized crossover study. The plasma concentration of rosuvastatin was determined by HPLC-MS/MS. The pharmacokinetic parameters were calculated and the bioavailability and bioequiva-lence of the two preparations were evaluated by DAS 3. 0 software. Results:After a single dose, the pharmacokinetic parameters of ro-suvastatin capsules and tablets were as follows:Tmax was (3. 56 ± 1. 68) h and (3. 63 ± 1. 56) h, Cmax was (21. 17 ± 13. 74) ng· ml-1 and (26.33 ±23.22) ng·ml-1, t1/2 was (10.68 ±5.50) h and (9.04 ±6.00) h, AUC0-t was (219.31 ±146.09) ng·h· ml-1 and (252. 43 ± 194. 96) ng·h·ml-1 , AUC0-∞ was (225. 32 ± 146. 76) ng·h·ml-1 and (257. 24 ± 194. 61) ng·h·ml-1 , respectively. The 90% confidential interval of AUC0-t, AUC0-∞ and Cmax was 81. 1%-106% , 81. 8%-105. 4% and 77. 9%-104. 5%, respectively. The mean relative bioavailability of the test preparation(the capsules) to the reference preparation(the tablets) was (100. 7 ± 54. 1)%. Conclusion:The test and reference preparations are bioequivalent.

Adolescent ; Adult ; Age Factors ; Child ; Child, Preschool ; Electroencephalography ; Epilepsy, Temporal Lobe ; diagnosis ; etiology ; Humans ; Infant ; Male ; Middle Aged

Objective To investigate whether conventional protein kinase C (cPKC ) βⅡ-interacting collapsin response mediator protein-2 (CRMP-2) provides neuroprotection against cerebral ischemic (I) injuries. Methods Male BALB/c mice were randomly divided into normoxic control (Nor) , HPC, Nor + Sham, HPC + Sham, Nor + I and HPC + I groups (n = 6 per group). Using our HPC and MCAO mouse models, we applied immunoprecipita-tion, two-dimensional electrophoresis and mass spectrometry to characterize cPKCβⅡ-interacting proteins and combined with SDS-PAGE and Western blot to quantitatively analyze CRMP-2 phosphorylation and degradation levels in the brain of mice after HPC and MCAO. Results The expression level of 10 cPKCβⅡ-interacting proteins changed obviously in cerebral cortex of HPC mice when compared with Nor group. One of these proteins, CRMP-2 protein level increased in particulate fraction and decreased in cytosolic fraction of cerebral cortex of HPC mice. CRMP-2 phosphorylation level in ischemic core (Ic) of cerebral cortex decreased significantly ( P < 0. 05 , n = 6) as compared with that of Nor + sham group, but CRMP-2 phosphorylation level in HPC +I group increased significantly as compared with that of Nor +I group ( P < 0. 05, n = 6). In ischemic cortex, CRMP-2 degradation (proteolysis) was observed as the appearance of 55 ku breakdown products (BDP). However, the CRMP-2 degradation level, BDPs products decreased significantly in penumbra ( P) of ischemic cortex from HPC +I group when we compared with that of Nor +I group (P < 0. 05, n = 6 ). Conclusion CRMP-2 is involved in attenuating the decrease of CRMP-2 phosphorylation in ischemic core and in inhibiting its degradation in penumbra of cerebral cortex of mice thereby to lessen the ischemic injuries.

Objective To explore the clinical effect of urapidil combined with recombinant human brain natriuretic peptide(rhBNP)in the treatment of high blood pressure complicated with acute heart failure.Methods Sixty patients with high blood pressure(HBP)and acute heart failure(AHF)were collected from May 2022 to December 2023 in the inpatient department of Yingtan People's Hospital were to conduct retrospective analysis.They were divided into two groups according to different clinical drugs,with 30 cases in each group.The control group received conventional drugs(amlodipine besylate+spirolactone)+intravenous furosemide infusion+administer urapidil intravenously,the experimental group was additionally given rhBNP.Both groups received treatment for 7 days in the hospital.Blood pressure,heart rate,N-terminal pro-brain natriuretic peptide(NT-proBNP),left heart function changes and adverse reactions during treatment were compared in two groups.Results After the treatment of those patients,the total effective rate and left ventricular ejection fraction of experimental group were higher than those of control group(P＜0.05).The changes of heart rate,NT-proBNP,left ventricular end-systolic diameter,left ventricular end-diastolic diameter and blood pressure in experimental group were lower than those in control group(P＜0.05).Two groups were no significant difference in the total incidence of adverse drug reactions(P＞0.05).Conclusion Urapidil and rhBNP is obviously superior to urapidil alone in the treatment of HBP complicated with AHF,and can obviously reduce blood pressure and heart rate,improve cardiacfunction,and is safe in clinical application.

Objective To investigate the application of the risk management information system in the nursing management .Methods On the basis of our large-scale integrated nursing information system , the nursing department and information center of nursing risk management information system was developed . Results The rates of nursing evaluation , admission assessment , pressure sores risk assessment , fall risk assessment, catheter slippage assessment and self-care capacity assessment were 93.0%, 96.0%, 95.0%, 98.0%, 95.0%and 96.0%, which were all significantly higher than 78.0%, 75.0%, 71.0%, 83.0%, 80.0%and 75.0% before the intervention (χ2 =9.074, 15.686, 10.286, 13.885, 20.411, 17.786, respectively;P<0.05).The scores of work satisfaction of nurses and the patients satisfaction were (95.14 ± 0.46) and (96.17 ±2.03), which were significantly higher than (82.13 ±1.78) and (84.10 ±4.79) before the intervention (t=79.92, 23.20, respectively;P<0.05).Conclusions Nursing information system applied in risk management can ensure patient safety and improve the quality of nursing management .

Background Chlorinated perfluoroalkyl ether sulfonate Cl-PFAES, trade name F-53B, a novel per- and polyfluoroalkyl substance (PFAS), has been shown to induce multi-organ toxicity in humans and cross the blood-brain barrier. However, its toxic effects and underlying mechanisms on neural stem cells (NSCs) remain unclear. Objective To investigate the impact of F-53B on NSCs proliferation and differentiation through oxidative stress and explore its potential molecular mechanisms in associations with mitochondrial function damage and the expression of autophagy-related gene (PINK1/Parkin). Methods Primary NSCs isolated from neonatal C57BL/6 mice were used as a model and exposed to F-53B at concentrations of 0, 33, or 100 μmol·L⁻¹ for 24 h. Cell viability was assessed using the cell counting kit-8 (CCK-8) assay, while proliferation was evaluated by the 5-ethynyl-2’-deoxyuridine (EdU) incorporation assay. Immunofluorescence staining was performed to observe differentiation phenotypes. Intracellular and mitochondrial reactive oxygen species (ROS) levels were quantified using dihydroethidium (DHE) and MitoSOX probes, respectively. Mitochondrial morphology was observed using MitoTracker Green. ATP level was measured with a commercial kit. Additionally, real-time quantitative polymerase chain reaction (qPCR) was conducted to quantify the expression of PINK1 and Parkin genes. Results Exposure to 100 μmol·L⁻¹ F-53B significantly reduced cell viability to 93.6% of the control group (P<0.01), and decreased the proportion of EdU⁺ cells (P<0.01), indicating proliferation inhibition. The differentiation analysis showed a reduction in neuronal generation, axonal shortening, and an increase in astrocytes. The 100 μmol·L⁻¹ F-53B exposure elevated intracellular ROS to 122% (P<0.01) and mitochondrial ROS (MitoROS) to 135% (P<0.001) of the control levels, leading to mitochondrial fragmentation. The ATP levels after the F-53B exposure decreased to 62.4% relative to the control group (P<0.001). Furthermore, the mRNA expression levels of PINK1 and Par after the F-53B exposure were notably reduced (P<0.05). Conclusion F-53B may induce oxidative stress, thereby disrupting mitochondrial morphology and function while inhibiting the PINK1/Parkin-mediated mitophagy pathway, ultimately leading to impaired neural stem cell proliferation and abnormal differentiation. This study provides new insights into the neurotoxicity mechanisms of F-53B.

At present, pancreatic cancer is a solid tumor with the worst prognosis. Compared with surgery and chemotherapy, radiotherapy plays an auxiliary role in the treatment of pancreatic cancer. In recent years, significant advances have been achieved in radiotherapy technology, which have been gradually applied in the diagnosis and treatment of pancreatic cancer. In this article, the progress in radiation therapy in the treatment of pancreatic cancer was reviewed, especially the clinical application of magnetic resonance imaging-guided radiation therapy in the treatment of pancreatic cancer, aiming to deepen the understand of the progress in radiation therapy for pancreatic cancer, and providing reference for improving the survival rate of pancreatic cancer patients.

Objective: To explore the effects of long noncoding-RNA (lncRNA) taurine upregulated gene 1 (TUG1) on the proliferation and osteogenic/odontoblast differentiation of human dental pulp stem cells (hDPSCs). Methods : hDPSCs were isolated and cultured. The surface antigens CD44, CD45, CD73, CD90, CD133 and STRO-1 were detected by flow cytometry. Alkaline phosphatase (ALP) staining and alizarin red staining were used to identify the ability of cells to differentiate. RNA was collected on Days 0, 7 and 14 of the osteogenic induction of hDPSCs, and qRT-PCR was used to detect the relative expression of TUG1. The hDPSCs were stably transfected with a lentiviral vector containing the TUG1-silenced pSLenti-U6-shRNA(TUG1)-CMV-EGFP-F2A-Puro-WPRE to silence TUG1. The ability of hDPSCs to proliferate was assessed with the CCK-8 method. ALP and alizarin red staining and quantitative detection were used to detect the ALP activity and formation of mineralized nodules of hDPSCs. The expression levels of dentin sialophosphoprotein (DSPP), dentin matrix protein-1 (DMP-1), Runt-associated transcription factor 2 (Runx2), osteocalcin (OCN) and osteopontin (OPN) genes and proteins were measured by qRT-PCR and Western blot. Results : The hDPSCs were successfully isolated and cultured, and TUG1 expression was significantly increased during osteogenic differentiation (P<0.05). The hDPSCs proliferation was suppressed after silencing TUG1(P<0.05). After osteogenic induction, ALP and alizarin red staining showed that ALP activity and mineralized nodules were suppressed by silencing TUG1. The expression levels of the odontogenic differentiation gene DSPP and DMP-1 and the osteogenic differentiation gene Runx2, OCN and OPN were also significantly decreased (P<0.05). Conclusion Knocking down TUG1 can inhibit the proliferation and osteogenic/odontogenic differentiation of hDPSCs.

Objective:To investigate the risk factors for axial deviation in the treatment of tibial defect susing Orthofix unilateral external fixator and proximal tibial osteotomy for bone transport.Methods:A retrospective study was performed to analyze the clinical data of 90 patients who had been treated for tibial bone defects by the Orthofix unilateral external fixator at Department of Microrepair and Reconstruction, The First Hospital Affiliated to Xinjiang Medical University from May 2012 to June 2019. There were 77 males and 13 females with a mean age of 41.2 years (from 17 to 63 years).The bone defects ranged from 4 to 13 cm in length. According to the Paley criteria for axial deviation, the 90 patients were divided into 2 groups: a deviation-free group with no axial deviation or an axial deviation ≤5° and a deviation group with an axial deviation>5°. The 2 groups were compared in terms of age, number of prior surgery, defect length, placement angle of Schanz screws, external fixation time, external fixation index and bending degree of Schanz screws at the last follow-up.The factors with P<0.05 were analyzed by multivariate logistic regression to find the risk factors for coronal axial deviation. Results:The 90 patients were followed up for an average of 23 months (from 12 to 40 months). The incidence of axial deviation in this cohort was 36.7% (33/90).The deviation group had a significantly larger number of prior surgery [5 (3, 6) times], a significantly longer defect length [8 (8, 9) cm], a significantly longer external fixation time [400.0 (341.8, 426.3) d], and a significantly greater bending degree of Schanz screws at the last follow-up [1.2° (0.4°, 3.5°)] than the deviation-free group [3 (2, 3) times, 6 (5, 8) cm, 340.8 (226.5, 422.8) d, and 0.8° (0.2°, 3.7°)] (all P<0.05). Multivariate logistic regression analysis showed that the number of prior surgery ( OR=2.581, 95% CI: 1.496-4.450, P=0.001) and the defect length ( OR=5.310, 95% CI: 1.952-14.442, P=0.001) were the risk factors for the axial deviation. Conclusion:In the treatment of tibial defect susing Orthofix unilateral external fixator and proximal tibial osteotomy for bone transport, the more prior surgeries and the longer a bone defect, the higher the risk for axial deviation.