Objective:To evaluate the efficacy and safety of therapeutic temperature control in patients with severe traumatic brain injury (sTBI).Methods:The full-text databases of Chinese Medical Journal, China National Knowledge Infrastructure, Wanfang Data Knowledge Service Platform, VIP Database, China Biomedical Database, PubMed, Embase, and Cochrane Library were searched for randomized controlled trials (RCTs) of hypothermia treatment and conventional treatment in patients with sTBI. The search period was from January 2016 to June 2025. Meta-analysis was performed using RevMan 5.3 software. The evaluation indicators included intracranial pressure before treatment, at 3 and 5 days after treatment, favorable prognosis rate and mortality rate within 6 months after treatment, and incidence of pulmonary infection, intracranial infection, epilepsy, acute gastrointestinal dysfunction, deep vein thrombosis, abnormal coagulation function, and arrhythmia during treatment; publication bias.Results:A total of 33 studies involving 3 322 patients were included, with 1 696 patients in the temperature treatment group and 1 626 in the conventional treatment group. There was no statistically significant difference in intracranial pressure between the two groups before treatment ( SMD=0, 95% CI -0.13, 0.14, P>0.05). However, at 3 and 5 days after treatment, the intracranial pressure was lower in the temperature treatment group than that in the conventional treatment group ( SMD=-2.29, 95% CI -2.76, -1.82, P<0.01; SMD=-2.66, 95% CI -3.43, -1.89, P<0.01). Within 6 months after treatment, the favorable prognosis rate was higher in the temperature treatment group than that in the conventional treatment group ( RR=1.41, 95% CI 1.32, 1.50, P<0.01), and mortality rate was lower than that in the conventional treatment group ( RR=0.64, 95% CI 0.55, 0.75, P<0.01). Compared with the conventional treatment group, the incidences of epilepsy and acute gastrointestinal dysfunction in the temperature treatment group were statistically reduced ( RR=0.33, 95% CI 0.13, 0.83, P<0.05; RR=0.43, 95% CI 0.25, 0.74, P<0.05). There were no statistically significant differences in the incidence of pulmonary infection ( RR=0.96, 95% CI 0.85, 1.08, P>0.05), intracranial infection ( RR=0.56, 95% CI 0.20, 1.56, P>0.05), deep vein thrombosis ( RR=0.93, 95% CI 0.69, 1.25, P>0.05), abnormal coagulation function ( RR=1.19, 95% CI 0.43, 3.31, P>0.05) or arrhythmia ( RR=0.51, 95% CI 0.23, 1.12, P>0.05) between the two groups. Egger′s test indicated the presence of publication bias and the results remained robust after trim and fill analysis. Conclusions:For patients with sTBI, temperature control therapy shows lowered intracranial pressure and mortality rate as well as improved favorable prognosis rate at 6 months posttreatment, and decreased incidence of epilepsy and acute gastrointestinal dysfunction during treatment, while reveals similar incidence of pulmonary infection, intracranial infection, deep vein thrombosis, abnormal coagulation function, and arrhythmia when compared with conventional treatment.

AIM:To identify the expression characteristics of transfer RNA-derived small RNAs(tsRNAs)re-sponding to DNA damage in human hepatoblastoma HepG2 cells,and to investigate their potential functions.METHODS:Based on paired HepG2 cells and TP53 gene knockout HepG2 cells,we successfully constructed a DNA damage cellular model using adriamycin(ADR).Transcriptome analysis of small noncoding RNAs was performed to systematically identi-fy a set of tsRNAs responding to ADR and involved in p53 regulation.Functional enrichment analysis was conducted using the Kyoto Encyclopedia of Genes and Genomes(KEGG).Additionally,after silencing the expression of target tsRNA genes,the biological functions of these tsRNAs in HepG2 cells were initially confirmed through CCK-8 assay and plate colo-ny formation assay.RESULTS:DNA damage induced a set of tsRNAs involved in p53 regulation,among which tRF-5-1(tRF-5_tRNA-Gly-TCC-2-1)and tRF-i-1(tRF i_tRNA-Tyr-GTA-11-1)showed the most significant up-regulation in HepG2 cells(P<0.05).Silencing of either tRF-5-1 or tRF-i-1 gene inhibited the proliferative activity of HepG2 cells(P<0.05).CONCLUSION:A group of tsRNAs responding to DNA damage can be identified in HepG2 cell model,and tsRNAs can promote the proliferative activity of HepG2 cells,suggesting that tsRNAs may play an important role in the de-velopment and progression of liver malignancies.

Objective:To investigate the drug resistance gene characteristics, plasmid characteristics and genome tracing of Shigella sonnei causing a bacillary dysentery outbreak in Shandong Province. Methods:Sixty-five Shigella sonnei strains isolated from a 2021 outbreak in a county of Shandong Province were analyzed using antimicrobial susceptibility testing, whole genome sequencing (WGS), characterization of resistance and virulence genes, plasmid profiling, core genome multilocus sequence typing (cgMLST), and single nucleotide polymorphism (SNP) analysis. Results:All isolates had the same resistance phenotype and genotypes and were multidrug-resistant ESBL-producing Shigella sonnei, carrying important virulence genes. Plasmid analysis revealed a conserved genetic arrangement, pil( M/ N/ O2/ P)-tra( F/ H/ J/ K/ N/ O/ P/ Q)-IS Ecp1- blaCTX-M-14-Tn 903- yub( J/ I/ F/ G/ E/ D), and shared across strains from diverse regions and bacterial species. The cgMLST and SNP analyses demonstrated concordant clustering, with all 65 outbreak-related strains forming a single cluster alongside human-derived strains from Guangxi. Conclusion:The ESBL-producing Shigella sonnei responsible for the outbreak shares a homologous relationship with Guangxi human-derived strains, and the detected resistance plasmids and virulence genes underscore the need to strengthen drug resistance surveillance and genome tracing.

Objective To analyse impact of low-dose CT on radiation dose and image quality of ankle fractures in children.Methods 600 suspected ankle fracture children admitted to Hangzhou Children's Hospital were selected as the research subjects from January to December 2023.All children needed to undergo conventional dose CT examination and low-dose CT examination.Image quality,radiation dose,diagnostic accuracy,and diagnostic efficacy of conventional dose CT and low-dose CT examination were compared.Results No significant difference was found between conventional-dose CT examination and low-dose CT examination in objectivity image quality index(P＞0.05).Effective dose,dose length product,and volume CT dose index of low-dose CT examination were all lower than those of conventional dose CT examination,and the difference was statistically significant(P＜0.05).The diagnostic accuracy of low-dose CT examination and conventional dose CT examination showed no significant difference(P＞0.05).Low-dose CT examination compared with conventional dose CT examination,there was no significant difference in diagnostic specificity(P＞0.05),while there was significant difference in diagnostic sensitivity and accuracy(P＜0.05).Area under the curve of effective dose,dose length product,volume CT dose index alone and combined diagnosis of ankle fractures in children were 0.899(95％CI:0.880-0.918),0.934(95％CI:0.918-0.950),0.928(95％CI:0.911-0.945),and 0.934(95％CI:0.918-0.950),respectively.Conclusion Low-dose CT examination technology has high diagnostic value for ankle fractures in children,can reduce radiation dose,and has little impact on image quality and diagnostic accuracy.It is worth popularizing and applying.

BACKGROUND:D1-3-n-butylphthalide has antioxidant and anti-inflammatory effects and has been explored to have protective role in Parkinson's disease,but the underlying mechanisms are unknown.OBJECTIVE:To investigate the protective effect of D1-3-n-butylphthalide by the approach of network pharmacology,molecular docking,and cellular experimental validation.METHODS:(1)Network pharmacology and molecular docking:The database was used to screen the targets of D1-3-n-butylphthalide and Parkinson's disease.The intersection was taken from the construction of the target protein interaction network,and then screen the core targets.The GO and KEGG pathway enrichment was used to further analyze the core targets.The interaction between the target proteins and D1-3-n-butylphthalide was verified by molecular docking.(2)Cell validation:The passage 6 PC12 cells were divided into six groups for culture.The control group was cultured with conventional culture medium.The model group was cultured with N-methyl-4-phenylpyridinium iodide to induce Parkinson's disease model.The ML385 inhibitor group was added with nuclear factor E2-related factor 2 inhibitor ML385 on the basis of inducing Parkinson's disease model.The D1-3-n-butylphthalide treatment group was added with butylphthalide on the basis of inducing Parkinson's disease model.The D1-3-n-butylphthalide combined with ML385 treatment group was added with D1-3-n-butylphthalide and ML385 on the basis of inducing Parkinson's disease model.The D1-3-n-butylphthalide group was cultured with conventional culture medium containing butylphthalide alone.Cell proliferation,intracellular reduced glutathione and malondialdehyde levels,and protein expression of protein kinase B/glycogen synthase kinase 3β/nuclear factor E2-related factor 2(AKT/GSK-3β/Nrf2)signaling pathway were detected.RESULTS AND CONCLUSION:(1)A total of 52 targets were screened for the intersection of drugs and disease targets,and the core targets including the matrix metalloproteinase 9 and GSK-3β were involved the phosphatidylinositol 3-kinase(PI3K)/AKT and oxidative stress-related signaling pathways.The molecular docking binding energy of D1-3-n-butylphthalide and GSK-3β was-18.27 kJ/mol,which indicated that D1-3-n-butylphthalide had a good binding ability with GSK-3β.(2)Compared with the model group,the PC12 cell activity and reduced glutathione level in the D1-3-n-butylphthalide treatment group were increased(P＜0.05),the malondialdehyde level was decreased(P＜0.05),and the expression of p-AKT,p-GSK-3β,Nu-Nrf2,and T-Nrf2 proteins was increased(P＜0.05).Compared with the D1-3-n-butylphthalide group,the PC12 cell activity and reduced glutathione level in the D1-3-n-butylphthalide combined with ML385 treatment group were decreased(P＜0.05),the malondialdehyde level was increased(P＜0.05),and the expression of Nu-Nrf2 and T-Nrf2 proteins was decreased(P＜0.05).(3)These results demonstrate that D1-3-n-butylphthalide can inhibit oxidative stress and improve cell activity through the AKT/GSK-3β/Nrf2 signaling pathway,and has a protective effect on the Parkinson's cell model induced by N-methyl-4-phenylpyridinium iodide.

Objective:To evaluate the efficacy and safety of therapeutic temperature control in patients with severe traumatic brain injury (sTBI).Methods:The full-text databases of Chinese Medical Journal, China National Knowledge Infrastructure, Wanfang Data Knowledge Service Platform, VIP Database, China Biomedical Database, PubMed, Embase, and Cochrane Library were searched for randomized controlled trials (RCTs) of hypothermia treatment and conventional treatment in patients with sTBI. The search period was from January 2016 to June 2025. Meta-analysis was performed using RevMan 5.3 software. The evaluation indicators included intracranial pressure before treatment, at 3 and 5 days after treatment, favorable prognosis rate and mortality rate within 6 months after treatment, and incidence of pulmonary infection, intracranial infection, epilepsy, acute gastrointestinal dysfunction, deep vein thrombosis, abnormal coagulation function, and arrhythmia during treatment; publication bias.Results:A total of 33 studies involving 3 322 patients were included, with 1 696 patients in the temperature treatment group and 1 626 in the conventional treatment group. There was no statistically significant difference in intracranial pressure between the two groups before treatment ( SMD=0, 95% CI -0.13, 0.14, P>0.05). However, at 3 and 5 days after treatment, the intracranial pressure was lower in the temperature treatment group than that in the conventional treatment group ( SMD=-2.29, 95% CI -2.76, -1.82, P<0.01; SMD=-2.66, 95% CI -3.43, -1.89, P<0.01). Within 6 months after treatment, the favorable prognosis rate was higher in the temperature treatment group than that in the conventional treatment group ( RR=1.41, 95% CI 1.32, 1.50, P<0.01), and mortality rate was lower than that in the conventional treatment group ( RR=0.64, 95% CI 0.55, 0.75, P<0.01). Compared with the conventional treatment group, the incidences of epilepsy and acute gastrointestinal dysfunction in the temperature treatment group were statistically reduced ( RR=0.33, 95% CI 0.13, 0.83, P<0.05; RR=0.43, 95% CI 0.25, 0.74, P<0.05). There were no statistically significant differences in the incidence of pulmonary infection ( RR=0.96, 95% CI 0.85, 1.08, P>0.05), intracranial infection ( RR=0.56, 95% CI 0.20, 1.56, P>0.05), deep vein thrombosis ( RR=0.93, 95% CI 0.69, 1.25, P>0.05), abnormal coagulation function ( RR=1.19, 95% CI 0.43, 3.31, P>0.05) or arrhythmia ( RR=0.51, 95% CI 0.23, 1.12, P>0.05) between the two groups. Egger′s test indicated the presence of publication bias and the results remained robust after trim and fill analysis. Conclusions:For patients with sTBI, temperature control therapy shows lowered intracranial pressure and mortality rate as well as improved favorable prognosis rate at 6 months posttreatment, and decreased incidence of epilepsy and acute gastrointestinal dysfunction during treatment, while reveals similar incidence of pulmonary infection, intracranial infection, deep vein thrombosis, abnormal coagulation function, and arrhythmia when compared with conventional treatment.

Objective:To investigate the impact of immunosuppressive therapy on the severity of SARS-CoV-2 infection and cytokine levels in pediatric patients with kidney diseases.Methods:A retrospective analysis was conducted on the clinical data of 40 hospitalized pediatric patients who were diagnosed with SARS-CoV-2 infection at the 900th Hospital of PLA Joint Logistic Support Force from December 2022 to February 2023. Based on their immunosuppressive status prior to SARS-CoV-2 infection, these patients were categorized into immunosuppressive group and non-immunosuppressive group. Independent sample t-tests, Mann-Whitney U tests, and χ2 test were employed to compare the clinical baseline characteristics and laboratory data, the severity of SARS-CoV-2 infection, and the levels of cytokines between the 2 groups. Results:Among the 40 patients, 11 were in the immunosuppressive group (aged 13 (8, 14) years, 9 males and 2 females) and 29 in the non-immunosuppressive group (aged 2 (1, 4) years, 15 males and 14 females). In the immunosuppressive group, 2 were asymptomatic cases, 8 were mild cases, and 1 was moderate case, and there was no severe or critical cases. In the non-immunosuppressive group, 8 were mild cases, 5 were moderate, 15 were severe cases, 1 was critical case, and no asymptomatic cases. The underlying diseases in the immunosuppressive group included nephrotic syndrome (6 cases), IgA vasculitis nephritis (2 cases), lupus nephritis (1 case), post-renal transplantation (1 case), and renal failure (1 case), with a mean total immunosuppression score (TIS) of (3.6±1.4) points. In the non-immunosuppressive group, 2 patients had a history of epilepsy, and the remaining 27 cases had no underlying conditions, all with TIS scores of 0. Compared to the children in the non-immunosuppressive group, those in the immunosuppressive group were more likely to exhibit asymptomatic or mild infection, with lower risks of severe disease, cytokine storm, fever, and cough, but a higher risk of fatigue ( OR=1.22, 2.66, 0.48, 0.12, 0.12, 0.13, 1.22; 95% CI 0.93-1.62, 0.99-7.15, 0.33-0.70, 0.03-0.57, 0.03-0.57, 0.03-0.65, 0.93-1.62; all P<0.05). The levels of cytokine IL-6, interferon-α and interferon-γ in the immunosuppressive group were all lower than those in the non-immunosuppressive group ( Z=2.23, 2.51, 2.92, respectively; all P<0.05). Conclusion:Pediatric patients with kidney diseases receiving appropriate immunosuppressive therapy may mitigate the severity of SARS-CoV-2 infection by suppressing the expression of cytokines.

In traditional Chinese medicine,jaundice is a liver and gallbladder disorder,primarily characterized by yellowing of the eyes,skin,and urine,with ocular yellowing being the most prominent feature.The understanding of jaundice pathogenesis in traditional Chinese medicine can be traced back to the Inner Canon of Huangdi.Despite the continuous development and improvement of successive generations of medical practitioners and a rich theoretical understanding of its pathogenesis being formed by the end of the Qing Dynasty,no unified view exists on whether the core pathological factor was dampness or blood stasis,nor on whether the primary disease location lay in the spleen and stomach or the liver and gallbladder.This article re-examines historical perspectives on jaundice pathogenesis within the context of traditional Chinese medicine theory,focusing on two key issues:pathological factors and the location of Zang and Fu.By integrating modern research approaches based on compound pathogenesis theory,and considering pathological factors,disease location according to Zang and Fu,and disease progression,a theoretical model is reconstructed,centered on the intermingling of dampness and blood stasis and integration of liver and spleen.Additionally,the insights and therapeutic strategies of multiple renowned clinical hepatology experts are incorporated to enrich the theoretical framework for jaundice treatment in traditional Chinese medicine and to enhance clinical efficacy.

BACKGROUND: Generalized pustular psoriasis (GPP), a rare and recurrent autoinflammatory disease, imposes a substantial burden on patients and society. Awareness of GPP in China remains limited. METHODS: This cross-sectional survey, conducted between September 2021 and May 2023 across 14 hospitals in China, included GPP patients of all ages and disease phases. Data collected encompassed demographics, clinical characteristics, economic impact, disease severity, quality of life, and treatment-related complications. Risk factors for GPP recurrence were analyzed. RESULTS: Among 127 patients (female/male ratio = 1.35:1), the mean age of disease onset was 25 years (1st quartile [Q1]-3rd quartile [Q3]: 11-44 years); 29.2% had experienced GPP for more than 10 years. Recurrence occurred in 75.6% of patients, and nearly half reported no identifiable triggers. Younger age at disease onset ( P  = 0.021) and transitioning to plaque psoriasis ( P  = 0.022) were associated with higher recurrence rates. The median diagnostic delay was 8 months (Q1-Q3: 2-41 months), and 32.3% of patients reported misdiagnoses. Comorbidities were present in 53.5% of patients, whereas 51.1% experienced systemic complications during treatment. Depression and anxiety affected 84.5% and 95.6% of patients, respectively. During GPP flares, the median Dermatology Life Quality Index score was 19.0 (Q1-Q3: 13.0-23.5). This score showed significant differences between patients with and without systemic symptoms; it demonstrated correlations with both depression and anxiety scores. Treatment costs caused financial hardship in 55.9% of patients, underscoring the burden associated with GPP. CONCLUSIONS The substantial disease and economic burdens among Chinese GPP patients warrant increased attention. Patients with early onset disease and those transitioning to plaque psoriasis require targeted interventions to mitigate the high recurrence risk.
Humans ; Male ; Female ; Psoriasis/pathology* ; Adult ; Cross-Sectional Studies ; Adolescent ; Child ; Young Adult ; Quality of Life ; Middle Aged ; China/epidemiology* ; Recurrence ; Risk Factors ; Surveys and Questionnaires ; East Asian People

BACKGROUND:D1-3-n-butylphthalide has antioxidant and anti-inflammatory effects and has been explored to have protective role in Parkinson's disease,but the underlying mechanisms are unknown.OBJECTIVE:To investigate the protective effect of D1-3-n-butylphthalide by the approach of network pharmacology,molecular docking,and cellular experimental validation.METHODS:(1)Network pharmacology and molecular docking:The database was used to screen the targets of D1-3-n-butylphthalide and Parkinson's disease.The intersection was taken from the construction of the target protein interaction network,and then screen the core targets.The GO and KEGG pathway enrichment was used to further analyze the core targets.The interaction between the target proteins and D1-3-n-butylphthalide was verified by molecular docking.(2)Cell validation:The passage 6 PC12 cells were divided into six groups for culture.The control group was cultured with conventional culture medium.The model group was cultured with N-methyl-4-phenylpyridinium iodide to induce Parkinson's disease model.The ML385 inhibitor group was added with nuclear factor E2-related factor 2 inhibitor ML385 on the basis of inducing Parkinson's disease model.The D1-3-n-butylphthalide treatment group was added with butylphthalide on the basis of inducing Parkinson's disease model.The D1-3-n-butylphthalide combined with ML385 treatment group was added with D1-3-n-butylphthalide and ML385 on the basis of inducing Parkinson's disease model.The D1-3-n-butylphthalide group was cultured with conventional culture medium containing butylphthalide alone.Cell proliferation,intracellular reduced glutathione and malondialdehyde levels,and protein expression of protein kinase B/glycogen synthase kinase 3β/nuclear factor E2-related factor 2(AKT/GSK-3β/Nrf2)signaling pathway were detected.RESULTS AND CONCLUSION:(1)A total of 52 targets were screened for the intersection of drugs and disease targets,and the core targets including the matrix metalloproteinase 9 and GSK-3β were involved the phosphatidylinositol 3-kinase(PI3K)/AKT and oxidative stress-related signaling pathways.The molecular docking binding energy of D1-3-n-butylphthalide and GSK-3β was-18.27 kJ/mol,which indicated that D1-3-n-butylphthalide had a good binding ability with GSK-3β.(2)Compared with the model group,the PC12 cell activity and reduced glutathione level in the D1-3-n-butylphthalide treatment group were increased(P＜0.05),the malondialdehyde level was decreased(P＜0.05),and the expression of p-AKT,p-GSK-3β,Nu-Nrf2,and T-Nrf2 proteins was increased(P＜0.05).Compared with the D1-3-n-butylphthalide group,the PC12 cell activity and reduced glutathione level in the D1-3-n-butylphthalide combined with ML385 treatment group were decreased(P＜0.05),the malondialdehyde level was increased(P＜0.05),and the expression of Nu-Nrf2 and T-Nrf2 proteins was decreased(P＜0.05).(3)These results demonstrate that D1-3-n-butylphthalide can inhibit oxidative stress and improve cell activity through the AKT/GSK-3β/Nrf2 signaling pathway,and has a protective effect on the Parkinson's cell model induced by N-methyl-4-phenylpyridinium iodide.