OBJECTIVES: Mobile phone dependence has become increasingly prominent among university students, posing significant risks to their social functioning and mental health. Previous studies suggest that perfectionistic personality traits may be key psychological predictors of mobile phone dependence, but the underlying mechanisms remain unclear. This study aims to identify core symptoms of mobile phone dependence among university students and to examine the pattern of associations between different dimensions of perfectionism and mobile phone dependence. METHODS: A cross-sectional questionnaire survey was conducted among 1404 university students nationwide. The Mobile Phone Involvement Questionnaire (MPIQ) and the Forst Multidimensional Perfectionism Scale (FMPS) were used to assess mobile phone use and perfectionism traits. The EBIC-GLASSO network model was constructed to analyze the network structure linking perfectionism and mobile phone dependence. RESULTS: A total of 56.48% of university students in the sample met the criteria for mobile phone dependence. The total FMPS score was positively correlated with the total MPIQ score (r=0.47, P<0.001). Results of multiple linear regression controlling for demographic variables showed that dimensions of FMPS score significantly predicted MPIQ score (all P<0.05). Network analysis revealed that the central dimension in perfectionism is "organization" (expected influence=2.69) and the core symptom of mobile phone dependence was "I lose track of how much I am using my smartphone" (expected influence= 0.78). Bridge centrality analysis identified "organization" as a key bridging factor linking perfectionism and mobile phone dependence (bridge strength=1.96). Among the symptom-to-symptom connections, "parental expectations" showed the strongest positive association with "arguments have arisen with others because of my mobile phone use" (partial correlation coefficient=0.15), serving as a risk factor. In contrast, "organization" was most strongly negatively associated with the same symptom (partial correlation coefficient=-0.13), serving as a protective factor, suggesting a protective effect. CONCLUSIONS Mobile phone dependence is common among college students and is primarily characterized by a lack of self-control in phone use. Although perfectionism is generally positively associated with mobile phone dependence, its internal dimensions appear to exert a dual effect. Specifically, "parental expectations" and "doubt over actions" may increase the risk of mobile phone dependence, whereas "organization" serves as a protective factor, particularly against interpersonal conflicts related to phone dependency.
Humans ; Perfectionism ; Students/psychology* ; Cell Phone ; Universities ; Cross-Sectional Studies ; Male ; Female ; Surveys and Questionnaires ; China ; Young Adult ; Adult ; Adolescent ; Personality

T-cell acute lymphoblastic leukemia (T-ALL) is a highly aggressive hematologic malignancy with a poor prognosis, despite advancements in treatment. Many patients struggle with relapse or refractory disease. Investigating the role of the super-enhancer (SE) regulated gene ubiquitin-specific protease 20 (USP20) in T-ALL could enhance targeted therapies and improve clinical outcomes. Analysis of histone H3 lysine 27 acetylation (H3K27ac) chromatin immunoprecipitation sequencing (ChIP-seq) data from six T-ALL cell lines and seven pediatric samples identified USP20 as an SE-regulated driver gene. Utilizing the Cancer Cell Line Encyclopedia (CCLE) and BloodSpot databases, it was found that USP20 is specifically highly expressed in T-ALL. Knocking down USP20 with short hairpin RNA (shRNA) increased apoptosis and inhibited proliferation in T-ALL cells. In vivo studies showed that USP20 knockdown reduced tumor growth and improved survival. The USP20 inhibitor GSK2643943A demonstrated similar anti-tumor effects. Mass spectrometry, RNA-Seq, and immunoprecipitation revealed that USP20 interacted with hypoxia-inducible factor 1 subunit alpha (HIF1A) and stabilized it by deubiquitination. Cleavage under targets and tagmentation (CUT&Tag) results indicated that USP20 co-localized with HIF1A, jointly modulating target genes in T-ALL. This study identifies USP20 as a therapeutic target in T-ALL and suggests GSK2643943A as a potential treatment strategy.

OBJECTIVES: To develop an E-selectin-targeting nanomedicine delivery system that competitively inhibits E-selectin-neutrophil ligand binding to block neutrophil adhesion to vessels and suppress their recruitment to the lesion sites. METHODS: Doxorubicin hydrochloride (DOX)-loaded liposomes (IEL-Lip/DOX) conjugated with E-selectin-affinity peptide IELLQARC were developed using a post-insertion method. Two formulations [2-1P: Mol(PC): Mol(DPI)=100:1; 2-3P: 100:3] were prepared and their modification density and in vitro release characteristics were determined. Their targeting efficacy was assessed in a cell model of LPS-induced inflammation, a mouse model of acute lung injury (ALI), a rat femoral artery model of physical injury-induced inflammation, and a zebrafish model of local inflammation. RESULTS: The prepared IEL-Lip/DOX 2-1P and 2-3P had peptide modification densities of 4.76 and 7.57 pmoL/cm², respectively. Compared with unmodified liposomes, IEL-Lip/DOX exhibited significantly reduced 48-h cumulative release rates at pH 5.5. In the inflammation cell model, IEL-Lip/DOX showed increased uptake by activated inflammatory endothelial cells, and 2-1P exhibited a higher trans-endothelial ability. In ALI mice, the fluorescence intensity of IEL-Lip/Cy5.5 increased significantly in lung tissues by 53.71% [Z-(2-1P)] and 93.41% [Z-(2-3P)], and 2-1P had an increased distribution by 24.19% in the inflammatory lung tissue compared to normal mouse lung tissue. In rat femoral artery models, 2-1P had greater injured/normal vessel fluorescence intensity contrast. In the zebrafish models, both 2-1P and 2-3P showed increased aggregation at the site of inflammation. CONCLUSIONS This E-selectin-targeting nanomedicine delivery system efficiently targets activated inflammatory endothelial cells to increase drug concentration at the inflammatory site, which sheds light on new strategies for treating neutrophil-mediated inflammatory diseases and practicing the concept of "one drug for multiple diseases".
Animals ; Liposomes ; Rats ; Nanomedicine ; E-Selectin ; Drug Delivery Systems ; Inflammation/drug therapy* ; Mice ; Doxorubicin/analogs & derivatives* ; Zebrafish ; Acute Lung Injury/drug therapy*

Objective To investigate the effectiveness of intravenous thrombolytic therapy mode led by fast-track specialist nurses on patients with acute ischemic stroke(AIS).Methods This study involved 124 AIS patients who underwent intravenous thrombolytic therapy in the Department of Emergency of our hospital from March 2021 to February 2023.Among the patients,61 admitted between March 2021 and February 2022 received conventional AIS thrombolytic therapy were assigned to a control group.While the 63 patients who received AIS thrombolytic therapy under the specialist nurse-led intravenous thrombolytic therapy mode between March 2022 and February 2023 were assigned to an observation group.The two groups were compared in terms of the time from admission to completion of CT examination,time for signing the informed consent for thrombolytic therapy,door to needle time and percentage of DTN<60 minutes,as well as the post-thrombolysis scores according to the National Institute of Health Stroke Scale(NIHSS)and satisfaction to medical consultation.Results The observation group exhibited a significantly shorter time from admission to completion of CT examination,a shorter time for signing an informed consent for thrombolytic therapy,a shorter door to needle time and a higher percentage of DTN<60 minutes,all with significant difference in comparison with those in the control group.After thrombolysis,the NIHSS score of the observation group decreased more than that of the control group(P<0.05).The patients and their families in the observation group reported significantly higher satisfaction compared to those in the control group(both P<0.05).Conclusion The fast-track specialist nurse-led intravenous thrombolytic therapy mode demonstrates the superiority in reduction of the time from admission to completion of CT examination,time for signing an informed consent for thrombolytic therapy,door to needle time and the NIHSS scores,higher percentage of DTN<60 minutes as well as improvement of patient satisfaction.

AIM:To establish a severe pneumonia mouse model induced by bacterial infection.METHODS:A total of 102 male SPF C57BL/6J mice were randomly divided into a control group and a model group.Klebsiella pneu-moniae was administered via tracheal instillation at a concentration of 5×109 CFU.Mice were euthanized on days 1,2,4,8,and 14 post-infection to assess general condition,body weight,mortality,white blood cell and neutrophil counts,in-flammatory markers,and pathological changes in lung,heart,liver,spleen,kidney,and intestinal tissues.RESULTS:Mice in the model group exhibited symptoms such as dyspnea and huddling from 6 hours to 4 days post-infection,which progressively worsened,accompanied by continuous weight loss(P<0.01).These symptoms gradually resolved between days 5 and 14.Arterial oxygen saturation in the model group dropped to 80.7%from days 1 to 8(P<0.01)but returned to normal from days 9 to 14.A total of 23 model mice died between days 1 and 9,with no deaths thereafter,resulting in a mortality rate of 31.9%(P<0.01).Pathological examination revealed inflammatory cell infiltration,congestion,and ede-ma in lung tissue from days 1 to 2,with continued inflammatory cell infiltration,alveolar structural disorganization from days 4 to 8,and alveolar rupture and fusion by day 14(P<0.05 or P<0.01).Additionally,model mice showed significant increases in neutrophil count,white blood cell count,protein content in bronchoalveolar lavage fluid,total cell count,neutrophil ratio,and levels of inflammatory factors tumor necrosis factor-α(TNF-α),interleukin-1β(IL-1β)and IL-6 in peripheral blood from days 1 to 8(P<0.05 or P<0.01).No significant pathological changes were observed in heart and liver tissues,while spleen,kidney,and intestinal tissues exhibited notable pathological changes:indistinct boundaries be-tween red and white pulp in the spleen,significant congestion and edema around renal glomeruli,renal tubules,and col-lecting ducts,and extensive inflammatory cell infiltration in the colonic mucosa.CONCLUSION:Tracheal instillation of 5×109 CFU Klebsiella pneumoniae induces severe pathological changes in the lungs of mice,offering a robust model for studying the pathogenesis and treatment of severe pneumonia.

Lipid Droplets/metabolism* ; Bacteria ; Lipid Metabolism

Objective:To investigate the role of a disintegrin and metalloprotease 12 (ADAM12) gene in chondrocyte injury in patients with Kashin-Beck disease (KBD) and its impact on genes related to insulin-like growth factor binding protein (IGFBP).Methods:Articular cartilage samples were obtained from 5 patients with KBD and 5 control subjects admitted to Honghui Hospital Affiliated to Xi'an Jiaotong University. Chondrocytes were extracted and cultured in vitro. Quantitative real-time PCR (qRT-PCR) and Western blotting were used to detect the expression levels of ADAM12 mRNA and protein in chondrocytes of patients with KBD and control subjects, respectively. Subsequently, ADAM12 gene overexpression was performed using lentivirus in chondrocytes of patients with KBD. MTT assay was used to detect changes in cell viability after ADAM12 gene overexpression, and qRT-PCR was used to detect the mRNA expression levels of chondrocyte differentiation related genes SRY-box transcription factor 9 (SOX9) and type Ⅱ collagen (COLⅡ), apoptosis-related gene B-cell lymphoma/leukaemia-2-associated X protein (BAX), and anabolic related genes IGFBP3 and IGFBP5. Results:The expression levels of ADAM12 mRNA and protein in chondrocytes of patients with KBD (0.57 ± 0.05, 0.81 ± 0.07) were significantly lower than those of control subjects (1.00 ± 0.00, 1.00 ± 0.00), and the differences were statistically significant ( t = - 24.50, - 3.61, P < 0.05). The results of MTT assay showed that the cell viability of chondrocytes in ADAM12 overexpression group (1.09 ± 0.05) was higher than that in empty vector control group (1.00 ± 0.08), and the difference was statistically significant ( t = 4.12, P = 0.031). The results of qRT-PCR showed that compared with empty vector control group, the mRNA expression levels of IGFBP3 (2.35 ± 0.79 vs 0.96 ± 0.25), IGFBP5 (2.13 ± 0.30 vs 0.98 ± 0.34), SOX9 (2.92 ± 0.51 vs 0.94 ± 0.36) and COLⅡ (6.45 ± 2.81 vs 0.87 ± 0.19) in ADAM12 overexpression group were significantly increased, and the differences were statistically significant ( t = 3.19, 5.16, 6.27, 4.10, P < 0.05); while the expression level of BAX mRNA (0.31 ± 0.06 vs 1.02 ± 0.22) was significantly decreased, and the difference was statistically significant ( t = - 11.16, P < 0.001). Conclusion:The ADAM12 gene may have a role in inhibiting apoptosis and promoting differentiation in chondrocyte injury in patients with KBD, and its overexpression can increase expression of IGFBP3 and IGFBP5.

Objective:To investigate the impact of matrix metalloproteinase 13 (MMP13) and low-density lipoprotein receptor-related protein 1 (LRP1) on autophagy of articular chondrocytes in patients with Kashin-Beck disease (KBD).Methods:Human articular cartilage samples obtained from 4 KBD patients and 4 control subjects were collected from Shaanxi Institute for Endemic Disease Prevention and Control, and the expression levels of MMP13 and LRP1 in cartilage tissue were determined using immunohistochemistry (IHC). Chondrocytes were extracted and cultured in vitro, the mRNA and protein expression levels of LRP1 and the autophagy related genes [Beclin 1 (BECN1), microtubule associated protein 1 light chain 3 (LC3)], cartilage injury related genes [MMP13, caspase-3 (CASP3)], chondrocyte differentiation related genes [collagen type Ⅱ alpha 1 chain (COL2A1), and SRY-box transcription factor 9 (SOX9)] were detected by real-time fluorescence quantitative PCR (qRT-PCR) and Western blot (WB), respectively. Chondrocytes from 3 KBD patients were extracted, and MMP13 gene silencing experiment was performed by RNA interference (RNAi) technology, the mRNA and protein expression levels of the above genes were detected by qRT-PCR and WB, respectively. In addition, the antagonist receptor associated protein (RAP) of LRP1 was used to block the LRP1 of human normal chondrocytes (C28/I2 cells), and qRT-PCR and WB were used to detect the mRNA and protein expression levels of LRP1, chondrocyte autophagy, differentiation and cartilage injury related genes, respectively. Results:The IHC results showed that the expression levels of MMP13 (1.67 ± 0.21, 0.59 ± 0.15, 0.51 ± 0.12) in the surface, middle, and deep layers of cartilage tissue of KBD patients were significantly higher than those of control subjects (0.25 ± 0.03, 0.26 ± 0.04, 0.06 ± 0.01), and the differences were statistically significant ( t = - 11.38, P < 0.001; t = - 3.82, - 6.26, P = 0.019, 0.003). The expression levels of LRP1 (0.10 ± 0.02, 0.03 ± 0.01, 0.17 ± 0.03) were significantly lower than those of control subjects (1.63 ± 0.40, 0.44 ± 0.12, 0.34 ± 0.08), and the differences were statistically significant ( t = 6.61, 5.61, 3.64, P = 0.003, 0.005, 0.022). The mRNA and protein expression levels of MMP13, CASP3, SOX9 in chondrocytes of KBD patients were significantly higher than those of control subjects, and the differences were statistically significant ( P < 0.05). The mRNA expression levels of LRP1, LC3, COL2A1 were significantly lower than those of control subjects, and the differences were statistically significant ( P < 0.05). After silencing the MMP13 gene in chondrocytes of KBD patients, there were no significant differences in the mRNA and protein expression levels of LRP1, BECN1, LC3, CASP3, COL2A1, and SOX9 ( P > 0.05). After blocking LRP1 with RAP, the protein expression levels of LRP1, BECN1, LC3, MMP13, COL2A1 and SOX9 in chondrocytes were significantly lower than those in control group ( P < 0.05). Conclusions:There is no direct correlation between MMP13 and abnormal autophagy of articular chondrocytes in KBD patients. After blocking LRP1, the expression of the autophagy related genes BECN1 and LC3 in chondrocytes is decreased.

Objective:To explore if there is premature senescence of chondrocytes in patients with Kashin-Beck disease (KBD) and osteoarthritis.Methods:Five knee cartilage samples of KBD, osteoarthritis and control groups were collected, respectively, from the Second Affiliated Hospital of Xi'an Jiaotong University. DNA was then extracted from cartilage samples and DNA methylation was analyzed by Illumina Infinium HumanMethylation450 BeadChip. At the same time, based on genome-wide methylation data, the online DNA methylation aging clock calculator (https://dnamage.genetics.ucla.edu/home) was used to calculate the DNA methylation age (DNAm age) of samples, and the results were compared with their actual ages.Results:In the comparison between KBD group and control group, 1 212 differentially methylated CpG sites were found, including 497 hypermethylated CpG sites and 715 hypomethylated CpG sites, corresponding to 264 hypermethylated genes and 368 hypomethylated genes, respectively. In the comparison between osteoarthritis group and control group, 656 differentially methylated CpG sites were found, including 343 hypermethylated CpG sites and 313 hypomethylated CpG sites, corresponding to 177 hypermethylated genes and 174 hypomethylated genes, respectively. In the above comparison, 367 overlapped CpG sites (corresponding to 182 genes) were found, which were differentially methylated in both KBD and control groups and osteoarthritis and control groups. The results of DNA methylation aging clock showed that the average age acceleration differences between DNAm age and actual age of KBD, osteoarthritis and control groups were 2.549, 0.017, and - 5.364 years, respectively, the DNAm ages of KBD and osteoarthritis groups were greater than the actual ages.Conclusion:The chondrocytes show premature senescence in both KBD and osteoarthritis.

Objective: To propose the concept of a novel regional control and prevention (RCP) system for the outbreak of COVID-19 infectious disease, design an emergency epidemic prevention information system based on the existing network architecture and information system in the region, and a remote intelligent medical consultation and remote office platform, research and develop the technology of risk assessment and early warning for people in the region, and improve the regions’prevention and control ability facing emergency of major infectious diseases. Methods: Taking colleges, affiliated (teaching) hospitals, and cloud applications as typical RCP regional units, the existing local area network interaction methods between the cloud and universities and affiliated (teaching) hospitals are established to realize remote work in the network environment, remote medical imaging, psychological and ethical consultation and interaction; applying multi-agent propagation model based on complex network, combining Global Positioning System (GPS), Radio Frequency Identification (RFID), and electronic fence technology, to realize the risk classification and early warning of units and personnel in the area. Results: In the RCP, a system architecture combining campus network, affiliated (teaching) hospital intranet, and the Internet is used. Dynamic connection is made using distributed technology and cloud storage. The data buffer mechanism of the intermediary database in the network realized telemedicine consultation and telecommuting. Relying on the platform, multi-agent propagation model based on complex network and cellular automaton model are used to realize the score and early warning of population exposure risk in the region by using GPS, RFID and electronic fence technology. Conclusions In the epidemic phase of major infectious diseases, the construction of RCP can improve the response speed of wartime epidemic prevention, provide reasonable data-based warnings and risk ratings, and reduce the exposure risk of susceptible people. The design and development of RCP is a systematic project that needs to combine regional structural and functional characteristics, and the foundation of the early informatization work in the region and the level of the emergency development team determine the development progress, maintenance, and actual application effects. It is recommended to establish a peacetime and wartime combined RCP mode and incorporate it into the government's disease control system to improve the national and regional level of prevention and control of major infectious diseases.