Background: Influenza A virus (IAV) is a negative-sense RNA virus of the Orthomyxoviridae family and is the etiological agent of a highly contagious acute respiratory disease that can lead to acute lung injury. Objective: To elucidate the molecular mechanisms of IAV infection, an integrative research approach combining gene expression profiling, multinetwork analysis, and in vivo experimental validations was employed. Methods: First, a series of network-based analyses were performed, including protein-protein interaction network construction, weighted gene co-expression network analysis, and subsequent gene set enrichment analysis, to identify the major underlying mechanisms of IAV infection. Following gene expression analysis, core targets, both direct and indirect regulators, were screened. An IAV (H1N1) strain A/PR/8/34-induced acute lung injury mouse model was constructed for in vivo validations. Batch one included two groups to evaluate findings from the multi-network analysis: Mock (n = 10; 5 males and 5 females) and IAV (n = 10; 5 males and 5 females). Batch two included three groups to assess the role of toll-like receptor 3 (TLR3) in IAV infection: Mock (n = 6; 3 males and 3 females), IAV (n = 6; 3 males and 3 females), and TLR3 inhibitor (n = 6; 3 males and 3 females). Body weight was measured on days 0, 3, and 5 after infection. On day 5, lung tissues were collected to assess viral load and histopathological changes. Key targets were examined using enzyme-linked immunosorbent assay, Western blotting, and immunofluorescence staining, both in sera and lung tissues. Results: IAV infection was significantly associated with dysregulation of the immune-inflammation system, such as the LTR, nucle-otide-binding oligomerization domain-(NOD) like receptor, retinoic acid-inducible gene I-like receptor, and nuclear factor kappa-B signaling pathways. Gene set enrichment analysis further indicated that the TLR and necroptosis signaling pathways played crucial roles in the progression of IAV infection (TLR signaling pathway normalized enrichment score = 2.3941, P = 1.00 × 10 ⁻¹⁰; necroptosis normalized enrichment score = 1.9421, P = 6.21 × 10 ⁻⁷). Among the core targets, TLR3 and mixed lineage kinase domain-like protein (MLKL) may regulate gene expression at the transcriptional level (all P < 0.05). In vivo validation using an IAV (PR8) infected acute lung injury mouse model demonstrated increased viral load and lung index, alveolar structural damage, and inflammatory cell infiltration. Immunofluorescence staining exhibited large gaps in Lamin B1 staining and breaches in Emerin signals following IAV-PR8 infection. Expression levels of TLR3, p-receptor-interacting serine/threonine-protein kinase 3 (RIPK3)/RIPK3, and p-mixed lineage kinase domain-like protein (MLKL)/MLKL proteins in lung tissues, as well as proinflammatory factors and mediators in sera, were significantly elevated after IAV infection. Moreover, enhanced neutrophil infiltration (myeloperoxidase) and citrullinated histone H3 (a neutrophil extracellular trap-specific marker), both established indicators of neutrophil extracellular trap formation, were observed. Notably, treatment with a TLR3 inhibitor significantly ameliorated IAV-induced acute lung injury by regulating necroptosis-related targets. Conclusion: Our study provides network-based in vivo evidence that TLR3-receptor-interacting serine/threonine-protein kinase 3-MLKL-mediated necroptosis may underlie IAV-induced acute lung injury and could serve as a potential therapeutic target in severe influenza cases.

OBJECTIVE To investigate the effects and mechanisms of Lycium ruthenicum Murr. in improving sleep. METHODS Network pharmacology was employed to identify the active components of L. ruthenicum and their associated disease targets， followed by enrichment analysis. A caffeine‑induced zebrafish model of sleep deprivation was established ， and the zebrafish were treated with L. ruthenicum Murr. extract （LRME） at concentrations of 0.1， 0.2 and 0.4 mg/mL， respectively； 24 h later， behavioral changes of zebrafish and pathological alterations in brain neurons were subsequently observed. The levels of inflammatory factors [interleukin-6 （IL-6）， IL-1β， IL-10， tumor necrosis factor-α （TNF-α）]， oxidative stress markers [superoxide dismutase （SOD）， malondialdehyde （MDA）， glutathione peroxidase （GSH-Px）， catalase （CAT）]， and neurotransmitters [5- hydroxytryptamine （5-HT）， γ-aminobutyric acid （GABA）， glutamic acid （Glu）， dopamine （DA）， and norepinephrine （NE）] were measured. The protein expression levels of protein kinase B1 （AKT1）， phosphorylated AKT1 （p-AKT1）， epidermal growth factor receptor （EGFR）， B-cell lymphoma 2 （Bcl-2）， sarcoma proto-oncogene，non-receptor tyrosine kinase （SRC）， and heat shock protein 90α family class A member 1 （HSP90AA1） in the zebrafish were also determined. RESULTS A total of 12 active components and 176 intersecting disease targets were identified through network pharmacology analysis. Among these， apigenin， naringenin and others were recognized as core active compounds， while AKT1， EGFR and others served as key targets； EGFR tyrosine kinase inhibitor resistance signaling pathway was identified as the critical pathway. The sleep improvement rates in zebrafish of LRME low-， medium-， and high-dose groups were 54.60%， 69.03% and 77.97%， 开发。E-mail：hjp_yft@163.com respectively， while the inhibition ratios of locomotor distance were 0.57， 0.83 and 0.95， respectively. Compared with the model group， the number of resting counts， resting time and resting distance were significantly increased/extended in LRME medium- and high-dose groups （P＜0.05）. Neuronal damage in the brain was alleviated. Additionally， the levels of IL-6， IL-1β， TNF-α， MDA， Glu， DA and NE， as well as the protein expression levels of AKT1， p-AKT1， EGFR， SRC and HSP90AA1， were markedly reduced （P＜0.05）， while the levels of IL-10， SOD， GSH-Px， CAT， 5-HT and GABA， as well as Bcl-2 protein expression， were significantly elevated （P＜0.05）. CONCLUSIONS L. ruthenicum Murr. demonstrates sleep-improving effects， and its specific mechanism may be related to the regulation of inflammatory responses， oxidative stress， neurotransmitter balance， and the EGFR tyrosine kinase inhibitor resistance signaling pathway.

Purpose: The aim of this study is to determine the impact of solute carrier family 3 member 2 (SLC3A2) on the malignant phenotype of gliomas and its role in regulating ferroptosis sensitivity. Materials and Methods: The malignant phenotype of glioma was assessed by cell proliferation assay, colony formation assay, EdU assay, wound healing, and Transwell experiments. We further validated the impact of reduced SLC3A2 expression on the sensitivity to ferroptosis in glioma cells through Cell Counting Kit-8 assays, flow cytometry, western blotting, and transmission electron microscopy. Western blot was used to explore how SLC3A2 affects glioma sensitivity to ferroptosis through the AKT/NF-E2-related factor 2 (NRF2)/glutathione peroxidase 4 (GPX4) axis. By establishing a subcutaneous xenograft tumor model in BALB/c-nude mice, we investigated the growth of tumors following the knockout of SLC3A2 in glioma cells. Results: Downregulation of SLC3A2 suppressed the malignant phenotype of glioma by blocking the cell cycle and epithelial-mesenchymal transition processes. On the other hand, loss of SLC3A2 not only downregulated SLC7A11 but also prevented the activation of the AKT/NRF2/GPX4 axis. These lead to increased accumulation of reactive oxygen species and lipid peroxides, ultimately enhancing the susceptibility of glioma to ferroptosis. Conclusion Our findings suggest that SLC3A2 is an oncogene in gliomas, promoting their occurrence and development. It plays a critical role in ferroptosis resistance through the AKT/NRF2/GPX4 axis.

With the accelerating trend of population aging, the number of elderly patients with lung cancer continues to rise, and the disease burden is becoming increasingly heavy. The clinical management of these patients faces severe challenges due to their decreased physiological reserve, complex comorbidities, and significant individual heterogeneity. Consequently, under traditional diagnosis and treatment models, doctors often struggle to identify the individualized risks of elderly patients in a timely and comprehensive manner, which can easily lead to decision biases such as undertreatment or overtreatment. In view of this, this study advocates for the establishment of an umbrella decision-making model specifically tailored for elderly lung cancer patients. Grounded in a multidisciplinary team (MDT) platform, this model deeply integrates oncological indicators with the comprehensive geriatric assessment (CGA) system. By holistically considering multidimensional variables including tumor burden, organ function, frailty index, cognitive status, and social support, the model establishes an operational mechanism characterized by "single entry, precise stratification, and targeted selection". Accordingly, patients can be scientifically triaged into distinct intervention tiers, such as active surveillance, minimally invasive surgery, drug therapy, radiotherapy, and best supportive care, thereby achieving real-time alignment between treatment intensity and patient fitness. This article elaborates on the construction logic and key operational procedures of this novel decision-making framework, aiming to guide clinical practice beyond the limitations of a tumor-centric perspective toward a holistic, dynamic, whole-course management strategy. This transition seeks to ensure optimal quality of life and clinical net benefit for elderly patients alongside survival prolongation.

ObjectiveHepatocellular carcinoma (HCC) represents 90% of all primary liver cancers. The main risk factors associated with HCC include viral hepatitis (B and/or C), alcohol abuse, and metabolic dysfunction-associated steatotic liver disease (MASLD), which progressively advance to liver fibrosis, cirrhosis, and ultimately evolve into HCC. Surgical resection represents the most effective treatment for HCC, while recent advances in immunotherapy, including immune checkpoint inhibitors and adoptive cell therapies, have provided improved treatment prospects for patients with unresectable HCC. However, the complex metabolic heterogeneity of HCC limits the therapeutic efficacy. Metabolic intermediates acyl-CoA not only provide energy and substrates for numerous biochemical reactions but also serve as donors for protein lysine acylation, a major class of post-translational modification (PTM). Therefore, a deeper understanding of the molecular mechanisms underlying protein lysine acylation and hepatocarcinogenesis is urgently needed. MethodsThe levels of protein lysine acylation and silence information regulator 5 (SIRT5) expression levels in clinical HCC samples were analyzed by Western blot. Quantitative malonylome and succinylome of HCC samples were analyzed by antibody-based affinity enrichment coupled with tandem mass spectrometry. The proliferation of HCC cells was analyzed with Cell Counting Kit-8 (CCK-8) assays, the apoptosis was quantified by Annexin V-FITC/propidium iodide (PI) staining coupled with flow cytometry, and the ability of cells to migrate was assayed by Transwell assays. The enzymatic activity of glutathione S-transferase Mu 1 (GSTM1) was quantified. Transgenic mice with hepatic overexpression of SIRT5 were constructed using CRISPR-Cas9, and primary hepatocarcinogenesis was induced by administration of diethylnitrosamine. ResultsWestern blot analysis indicated that the expression level of SIRT5 was elevated in clinical samples from HCC patients, and the levels of lysine malonylation, glutarylation, and succinylation were significantly reduced in HCC tissues. Knockout of SIRT5 in MHCC-97H and MHCC-97L hepatoma cells suppressed cell proliferation, and increased the percentage of apoptotic cells significantly. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses of the differentially malonylome and succinylome of HCC samples revealed significant enrichment in two major classes of biological processes: core energy metabolism (e.g., glycolysis/gluconeogenesis, tricarboxylic acid metabolic process, fatty acid beta oxidation) and detoxification and oxidative stress response (e.g., response to toxic substance, chemical carcinogenesis, reactive oxygen species (ROS)). SIRT5 removes malonylation from lysine residues in GSTM1 and restores its detoxification activity, which is crucial for the survival of hepatocytes under stressed conditions. More importantly, in vivo experiment indicated that hepatic-specific overexpression of SIRT5 in mice accelerated diethylnitrosamine-induced liver fibrosis and hepatocarcinogenesis, indicating the critical role of SIRT5 in HCC progression. ConclusionThis study highlights the previously unrecognized SIRT5-GSTM1 axis as a key regulator in hepatocarcinogenesis, and suggests a potential target for the treatment of patients with HCC.

ObjectiveTo investigate the mRNA expression profile and clinical significance of the RAB24 gene in hepatocellular carcinoma （HCC） based on multi-source database including The Cancer Genome Atlas （TCGA） and clinical cohort validation. MethodsData from TCGA （n=424） were utilized to evaluate the prognostic value of RAB24 expression via Kaplan-Meier analysis and Cox regression models. An independent clinical cohort comprising 90 HCC and 30 paracancerous tissues was established to validate protein expression and histopathological features through immunohistochemistry （IHC） and routine histological staining. The TIMER database was employed to analyze the association between RAB24 and the tumor microenvironment （TME）. Furthermore， integrated with LinkedOmics， GSEA and GSVA algorithms were used to quantitatively characterize the core molecular pathways regulated by RAB24. ResultsThe mRNA expression level of RAB24 in HCC was significantly higher than that in non-tumor liver tissues （P<0.05）. Kaplan-Meier analysis revealed that the overall survival （OS） of patients in the RAB24 low-expression group was significantly longer compared to the high-expression group （HR=1.570， Log-rank P=0.01）. Cox proportional hazards regression analysis demonstrated that RAB24 expression （HR=1.480， P=0.028）， T stage （HR=2.949， P<0.001）， M stage （HR=4.077， P=0.017）， and tumor residual status （HR=2.317， P<0.001） were independent prognostic factors for HCC. RAB24 expression was highly correlated with alpha-fetoprotein （AFP） levels and immune infiltration levels （P<0.01）， and showed a significant， low-level positive correlation with the TP53 gene （Rho=0.31， P<0.01）. Quantitative analysis of the RAB24 protein in clinical samples validated that RAB24 expression in HCC tissues was significantly elevated compared to non-tumor liver tissues （P<0.05）. TIMER analysis confirmed that RAB24 expression was highly associated with the infiltration of multiple immune cells （such as B cells and NK cells）， as well as stromal and tumor purity scores in tumor tissues （P<0.01）. GSEA/GSVA enrichment revealed that the P53， MYC， and mTORC1 signaling pathways were activated in the RAB24 high-expression group； correlation analysis confirmed that the RAB24 expression level exhibited a significant， low-level positive correlation with the ribosome pathway activity score （r=0.23， P<0.01）. ConclusionsThe RAB24 gene， as a poor prognostic factor for HCC patients， is a potential biomarker for HCC diagnosis， treatment and prognosis. The study is expected to lay a theoretical foundation for the precise diagnosis and treatment of clinical HCC.

ObjectiveTo observe the effects of Youguiwan on the localization and differentiation of embryonic stem cells transplanted into ovaries，and to preliminarily explore whether its mechanism is related to the protein kinase B （Akt）/mammalian target of rapamycin （mTOR）/4E-binding protein 1 （4EBP1）/p70S6 kinase （P70S6K） signaling pathway. MethodsA total of 81 healthy adult female C57BL/6 mice that had received ovarian transplantation of GFP-labeled embryonic stem cells were randomly allocated into a control group，a Youguiwan group，and a positive control group. The control group received normal saline via gavage，the Youguiwan group was administered Youguiwan decoction at a clinical equivalent dose of 17.1 g·kg^-1，and the positive control group received human menopausal gonadotropin （HMG） injections every 48 h. Ovarian tissue samples were collected on days 7，14，and 21 post-administration. Frozen sections were prepared to observe stem cell localization. The immunofluorescence assay was used to detect growth differentiation factor 9 （GDF9） and mTOR expression. real time polymerase chain reaction（Real-time PCR） was performed to measure the mRNA levels of follicle-stimulating hormone receptor （FSHR） and luteinizing hormone receptor （LHR）. Western blotting was conducted to assess the expression and phosphorylation levels of Akt，mTOR，4EBP1，and P70S6K. ResultsFluorescence microscopy revealed that the transplanted embryonic stem cells were predominantly localized within the granular cell layer，the cell layer of the follicular structure，and the stroma. After 14 days of drug intervention，compared with the control group，the Youguiwan group showed upregulated mRNA levels of FSHR and LHR in the ovarian tissue （P<0.01），as well as elevated phosphorylation/protein ratios of Akt，mTOR，4EBP1，and P70S6K （P<0.05）. After 21 days of drug intervention，compared with the control group，the Youguiwan group exhibited enhanced expression of GDF9 and mTOR in the ovarian tissue as detected by immunofluorescence （P<0.05），along with elevated mRNA levels of FSHR and LHR （P<0.01） and phosphorylation/protein ratios of Akt and 4EBP1 （P<0.05）. ConclusionYouguiwan can promote the localization and differentiation of mouse embryonic stem cells within the ovary and enhance the expression of GDF9，FSHR，and LHR mRNA in the ovarian tissue by influencing the Akt/mTOR/4EBP1/P70S6K pathway.

Objective:To analyze the results of national external quality assessment (EQA) for transfusion compatibility test in 2023, and provide reference for quality management of clinical transfusion compatibility testing.Methods:The EQA of clinical transfusion compatibility testing by NCCL was performed 3 times in 2023 among included laboratories. The panel consisting of 22 samples was distributed to 4 186 laboratories across 31 provinces (Including 2 961 tertiary hospital laboratories, 1 085 secondary hospital laboratories, 23 primary hospital laboratories, 106 blood station laboratories and 11 independent clinical laboratories). Each panel contains 11 red blood cell and 11 plasma samples per 1.5 ml/tube. Each participant laboratory of the EQA program was required to carry out the detection and return results in expected time. Statistical analysis and evaluation on the reported results were conducted by NCCL from the aspects of regional distribution, laboratory grading, testing methodology, reagent and testing system usage.Results:The qualification rates of EQA for five items including ABO positive typing, ABO reverse typing, RhD blood type, antibody screening, and cross matching were 96.68%, 95.10%, 96.46%, 95.32%, and 91.04%, respectively. The EQA qualification rate of tertiary hospital laboratories was 87.77% (2 599/2 961), which was significantly higher than the 77.79% (844/1 085) of secondary hospital laboratories. There were significant differences in the qualification rate of participating laboratories among different regions. The utilization rates of micro column agglutination method in ABO positive typing, ABO reverse typing, RhD blood type, antibody screening, and cross matching were 80.81% (10 080/12 474), 75.06% (9 337/12 440), 81.38% (10 118/12 433), 89.59% (11 104/12 394) and 76.25% (9 495/12 453), respectively. The qualification rate of micro column agglutination method was significantly higher than that of saline slide method in ABO positive typing detection ( P<0.05). The qualification rate of micro column agglutination method was significantly higher than that of the polyamine method and anti-human globulin test tube method in antibody screening ( P<0.05). There were statistically significant differences in qualification rate of 7 reagents in ABO reverse typing, antibody screening and cross matching ( P<0.05). There was no statistically significant difference in the qualification rate between the two detection systems for other reagents, except for the ABO reverse typing where the qualification rate of reagent 1 in a single system was higher than that in a mixed system ( P<0.05). Conclusion:The testing capabilities of clinical laboratories in different regions and different type varied significantly in China. Micro column agglutination method was the most popular selection in transfusion compatibility testing. The regents used in these laboratories showed good performance. However, the detection efficiency of some reagents still need to be improved. EQA could be used to evaluate, monitor, and improve the quality of testing.

Objective:To research the mechanism of the regulation of homeobox B8(HOXB8)for lysine demethylase 6B(KDM6B)-mediated CCAAT/enhancer binding protein α(C/EBPα)axis on the metastasis of high-grade serous ovarian cancer(HGSOC),so as to provide references for the study of the pathogenesis of HGSOC patients.Methods:The tumor tissue samples and corresponding adjacent normal tissue samples of HGSOC patients admitted to Wuhan Hospital of Traditional Chinese and Western Medicine from June to December 2024 were selected,and cell lines SKOV3 and A2780 of ovarian cancer were collected.Real-time fluorescence quantitative polymerase chain reaction(RT-qPCR)was adopted to detect the mRNA levels of KDM6B in HGSOC tumor tissues and its corresponding adjacent tissues.Western blot assay and immunohistochemistry were adopted to detect the expressions of KDM6B protein in the tissue.The A2780 cells of ovarian cancer were divided into the oe-HOXB8 group that was transfected by the HOXB8 overexpression vector,and the oe-NCHOXB8 group with the negative control(NC)vector.The SKOV3 cells of ovarian cancer were divided into the si-HOXB8 group that was transfected by the HOXB8 small interference sequence,and the si-NCHOXB8 group with negative control sequence.The transfected KDM6B was divided into the si-KDM6B group with small interference sequence and the oe-KDM6B group transfected with overexpression vector.The co-transfection HOXB8 and(or)KDM6B,C/EBPα were divided into si-HOXB8+si-KDM6B group and si-HOXB8+si-C/EBPα group of small interference sequence.The chromatin immunoprecipitation-qPCR(ChIP-qPCR)and dual-luciferase reporter gene assay were used to verify the mechanism that HOXB8 transcript and regulate KDM6B in SKOV3 and A2780 cells of ovarian cancer.The effects of overexpression or silencing of HOXB8 in A2780 and SKOV3 cells on the proliferation,invasion,migration and KDM6B expression of ovarian cancer cells were detected.The effects of overexpression or silencing of KDM6B in SKOV3 cells on the trimethylation modification of lysine 27 at histone H3(H3K27me3)and the expression of C/EBPα were detected.The effects of silencing KDM6B and C/EBPα on HOXB8-induced cell proliferation,invasion and migration were analyzed through functional rescue experiments.Results:In tumor tissues,the mRNA and protein expression levels of KDM6B were 1.02±0.03 and 1.02±0.04,respectively,which were significantly higher than those in the adjacent tissues,and the differences were statistically significant(t=62.440,38.737,P<0.01).The optical density value of proliferation,invasion rate and migration rate of A2780 cells in the oe-HOXB8 group that was transfected by the HOXB8 overexpression vector were respectively(1.74±0.15),(89.71±6.60)%and(85.33%±7.02)%,which were significantly higher than those in the oe-NCHOXB8 group,and the differences were statistically significant(t=7.778,7.353,4.759,P<0.01).The optical density value of proliferation,invasion rate and migration rate of SKOV3 cells in the si-HOXB8 group were respectively(0.54±0.06),(47.23±3.41)%and(43.20±3.12)%,all of which were significantly lower than those in the si-NCHOXB8 group,and the differences were statistically significant(t=9.400,8.615,9.040,P<0.01).The optical density value of proliferation,invasion rate and migration rate of SKOV3 cells in the si-HOXB8+si-KDM6B group were(1.04±0.09),(73.11±4.98)%and(68.65±4.45)%,respectively,which were significantly higher than those in the si-HOXB8 group,and the differences were all statistically significant(t=6.875,6.852,7.562,P<0.01).The optical density value of proliferation,invasion rate and migration rate of SKOV3 cells in the si-HOXB8+si-C/EBPα group were respectively(0.97±0.07),(75.87±5.12)%and(70.59±4.81)%,all of which were significantly higher than those in the si-HOXB8 group,and the differences were all statistically significant(t=6.355,7.500,7.884,P<0.01).Conclusion:HOXB8 can inhibit the C/EBPα expression and promote the HGSOC metastasis by regulating and controlling H3K27me3 modification of KDM6B-mediated C/EBPα histone.

Objective:To investigate the situation of computed tomography(CT)equipment and socio economic development of various grades and classifications of medical institutions in Jiangsu Province,and to analyze the interrelationship between them.Methods:From October 20,2023 to November 20,2023,a questionnaire survey was conducted on imported and domestic CT equipment of various grades and classifications of medical institutions in 13 prefecture-level cities in Jiangsu Province through online questionnaire survey of"questionnaire star".The gross domestic product(GDP)of each prefecture-level city in Jiangsu province was used as an indicator of measuring the level of socio-economic development in the region.The CT number,the row number of detector,quality of image,the total examination case number of daily average and the daily average case number of single machine examination of medical institutions of various grades and classifications of 13 prefecture-level cities were used to conduct correlation analysis with GDP values of various districts.Results:A total of 910 questionnaires were distributed,and 512 questionnaires were retrieved.There were 482 valid questionnaires in the 512 questionnaires,and the valid rate was 94.15,which involved to 482 various grade and classification institutions of 13 prefecture-level cities in Jiangsu province.The number of imported and domestic CT equipment in the 13 prefecture-level cities of Jiangsu Province positively correlated with the GDP of each city(r=0.882,0.880,P<0.001).The number of imported CT equipment with 64 rows and more than 64 rows,and with less than 64 rows,and the number of domestic CT equipment with 64 rows and more than 64 rows,and with less than 64 rows all positively correlated with the GDP of each city(r=0.880,0.881,0.736,0.897,P<0.05).The total number of daily average of examinations for imported and domestic CT equipment of 13 prefecture-level cities positively correlated with the GDP of each city(r=0.774,0.814,P<0.05).There were no significant difference in the image quality and the daily average case number of single machine examination between the domestic CT equipment and the imported CT equipment(P>0.05).Conclusion:The medical institutions of city with high level of economic development have more quantitative and more high-end CT equipment,and the quality of image of domestic CT equipment is equal to that of imported CT equipment regardless of the high and low level of economic development.