Objective: To explore the association role of anxiety and depressive symptoms with Internet gaming disorder (IGD) and emotional-behavioral problems among junior high school students, so as to provide references for preventing the occurrence and progression of emotional-behavioral problems in middle school students. Methods: From September to October 2024, a random cluster sampling method was adopted to select 38 069 students from 28 junior high schools in 14 counties (cities and districts) and functional areas of Jining City, Shandong Province. Surveys were conducted by Nine item Internet Gaming Disorder Scale-Short Form, Generalized Anxiety Disorder-7, Patient Health Questionnaire-9, and Strengths and Difficulties Questionnaire. The correlation of emotional and behavioral issues, online game addiction, anxiety and depressive symptoms among junior high school students was analyzed by Speaman correlation analysis. Mediation analysis was used to explore the role of anxiety and depressive symptoms between IGD and emotional-behavioral problems among junior high school students. Results: The detection rates of emotional-behavioral problems, anxiety symptoms, depressive symptoms, and IGD among junior high school students were 19.24 %, 9.48%, 16.69%, and 19.68%, respectively. The scores of emotional-behavioral problems, anxiety symptoms, depressive symptoms and IGD were 10.00 (6.00, 15.00), 3.00 (0.00, 7.00), and 4.00 (1.00, 8.00), 13.00 (10.00, 19.00), respectively. There were positive correlations between each pair of emotional-behavioral problem, IGD, anxiety symptoms, and depressive symptoms scores ( r =0.51-0.81, all P <0.01). Anxiety and depressive symptoms played mediating roles between IGD and emotional-behavioral problems among junior high school students, with mediating effect values of 0.16 (95% CI =0.15-0.17) and 0.12 (95% CI =0.11-0.14), respectively (both P <0.01). Conclusions Anxiety and depressive symptoms mediate the relationship between IGD and emotional-behavioral problems among junior high school students. It is necessary to identify early signs of IGD among junior high school students, strengthen intervention for anxiety and depressive symptoms, to prevent the occurrence and development of emotional and behavioral issues.

Eight butyl-phthalides, senkyunolide K(1), senkyunolide N(2), butylphthalide(3), senkyunolide I(4), senkyunolide H(5),(Z)-butylidenephthalide(6),(Z)-ligustilide(7), and 3-butylidene-7-hydroxyphthalide(8) were isolated from the aerial part of Ligusticum sinense by column chromatography on silica gel column, ODS, Sephadex LH-20 and semi-preparative HPLC. Their structures were elucidated on the basis of spectroscopic and chemical data, especially NMR and MS. Compound 1 was a new butyl-phthalide and compounds 2-8 were isolated from the aerial part of L. sinense for the first time. Furthermore, the inhibitory activities of compounds 1-8 against the nitric oxide(NO) production induced by lipopolysaccharide(LPS) in mouse RAW264.7 macrophages in vitro were evaluated. The results showed that compounds 1-8 exerted inhibitory activities on NO production with IC_(50) of 19.34-42.16 μmol·L~(-1).
Animals ; Mice ; Nitric Oxide/biosynthesis* ; Ligusticum/chemistry* ; Benzofurans/isolation & purification* ; Drugs, Chinese Herbal/isolation & purification* ; Macrophages/immunology* ; RAW 264.7 Cells ; Molecular Structure

Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection,with a high mortality rate.Sirtuin 3,a deacetylase within mitochondria,plays an important regulatory role in cellular metabolism,oxidative stress,and inflammatory responses.In recent years,significant progress has been made in the study of the function and regulatory role of sirtuin 3 in sepsis-related diseases.Research has shown that sirtuin 3 can alleviate organ damage caused by sepsis by regulating mitochondrial function,reducing oxidative stress,and inhibiting inflammatory responses.The specific mechanisms include the regulation of mitochondrial bioenergetics,activation of antioxidant enzyme systems,and inhibition of inflammatory mediator expression.In addition,sirtuin 3 plays a protective role in the pathological process of sepsis by interacting with multiple signaling pathways.This article summarizes the functions and regulatory mechanisms of sirtuin 3 in various sepsis-related diseases,aiming to provide new targets and strategies for the prevention and treatment of sepsis in the future.
Sepsis/metabolism* ; Sirtuin 3/physiology* ; Humans ; Animals ; Oxidative Stress ; Mitochondria/metabolism* ; Signal Transduction

ObjectiveTo observe ovarian microvascular damage in rats with cold coagulation and blood stasis syndrome and to explore the mechanism by which Liangfang Wenjing decoction improves this condition in rats. MethodsFifty SPF female SD rats were randomly divided into a blank group， a model group， low-dose （8.1 g·kg^-1） and high-dose groups （16.2 g·kg^-1） of Liangfang Wenjing decoction， and a 4-phenylbutyric acid （0.1 g·kg^-1） group， with 10 rats in each group. The ice-water bath method was employed to establish the rat model of cold coagulation and blood stasis syndrome. Concurrent with modeling， Liangfang Wenjing decoction was administered continuously for 21 days， once daily. The rats' syndrome manifestations and estrous cycles were recorded. The enzyme-linked immunosorbent assay （ELISA） was used to detect serum reproductive hormone levels and levels of endothelin-1 （ET-1）， nitric oxide （NO）， thrombomodulin （TM）， and von Willebrand factor （vWF） in ovarian tissue. Prothrombin time （PT）， activated partial thromboplastin time （APTT）， thrombin time （TT）， and fibrinogen （FIB） were measured. The ovarian microcirculatory blood perfusion was detected by laser speckle contrast imaging. Hematoxylin-eosin （HE） staining was performed to observe the ovarian histopathology， flow cytometry to detect ovarian apoptosis rate， and transmission electron microscopy to observe the ultrastructure of ovarian microvascular endothelial cells. Western blot was employed to detect the protein expression of endothelial nitric oxide synthase （eNOS）， phosphorylated eNOS （p-eNOS）， Caspase-3， B-cell lymphoma-2 （Bcl-2）， Bcl-2-associated X protein （Bax）， glucose-regulated protein 78 （GRP78）， C/EBP homologous protein （CHOP）， inositol-requiring enzyme1α （IRE1α）， p-IRE1α， apoptosis signal-regulating kinase 1 （ASK1）， p-ASK1， c-Jun N-terminal kinase （JNK）， and p-JNK. Immunofluorescence was used to detect ovarian Bax and Bcl-2 expression in microvascular endothelial cells. ResultsCompared with the blank group， the model group showed signs of cold coagulation and blood stasis syndrome， prolonged estrus cycles， and reproductive hormone disorders. Histopathological results revealed a decrease in follicle counts at all stages and disorganized granulosa cell arrangement. Ovarian microcirculatory perfusion was significantly decreased （P<0.01）. PT， APTT， and TT were reduced （P<0.05， P<0.01）， while FIB levels were increased （P<0.05）. In ovarian tissue， NO content was decreased， while ET-1， vWF， and TM levels were increased significantly （P<0.01）. The apoptosis rate of ovarian cells was markedly increased （P<0.01）. Furthermore， p-eNOS/eNOS and Bcl-2 were decreased （P<0.05）， whereas Bax， cleaved-Caspase-3/Caspase-3， GRP78， CHOP， p-IRE1α/IRE1α， p-ASK1/ASK1， and p-JNK/JNK expression showed significant increases （P<0.05， P<0.01）. Compared with the model group， Liangfang Wenjing decoction intervention alleviated the symptoms of cold coagulation and blood stasis， gradually restored the estrus cycle， and improved ovarian histopathology and endothelial cell ultrastructure. Microcirculatory blood perfusion was significantly elevated （P<0.05）. NO content in ovarian tissue was elevated， while ET-1， vWF， and TM levels were significantly decreased （P<0.05， P<0.01）. The p-eNOS/eNOS ratio and Bcl-2 expression were significantly elevated （P<0.05）， while the expression of Bax， cleaved-Caspase-3/Caspase-3， GRP78， CHOP， p-IRE1α/IRE1α， p-ASK1/ASK1， and p-JNK/JNK was significantly decreased （P<0.05， P<0.01）. ConclusionLiangfang Wenjing decoction may regulate the IRE1α/ASK1/JNK signaling pathway to inhibit endoplasmic reticulum stress， attenuate apoptosis， and improve microvascular endothelial injury in ovaries of rats with cold coagulation and blood stasis syndrome.

Objective To propose a low-dose CT image denoising method based on an improved Corediff model to recover the detailed features of the image and enhance the image quality.Methods An RS-Corediff model was established by modifying the key component U-Net network of the Corediff model.Firstly,the residual module was introduced in the network input stage for feature extraction;secondly,a new downsampling module was designed in the U-Net network encoder,which learned the semantic information of the feature map by convolution and maintained the learning state during the downsampling process so as to fully extract the image features;thirdly,the feature splicing processing was used to further enhance the learning effect during the upsampling process of the U-Net network decoder;finally,the convolutional kernel size was modified to adjust the sensory field during the convolutional process of the whole U-Net network structure so as to obtain rich features.The RS-Corediff model was compared with the residual encoder-decoder convolutional neural network(RED-CNN)model and the Corediff model on the public dataset AAPM 2016 in order to verify its effectiveness for low-dose CT image denoising.Results The RS-Corediff model gained advantages over the RED-CNN and Corediff models with a peak signal-to-noise ratio(PSNR)of 41.269 8,structural similarity(SSIM)of 0.953 4 and root mean square error(RMSE)of 17.568 7.Conclusion The proposed method effectively preserves the texture and details of low-dose CT images during the denoising process to improve the overall quality of the images.[Chinese Medical Equipment Journal,2025,46(5):9-13]

Objective:To explore the differences in clinical efficacy between Co-Cr-Mo guided multidirectional sliding growing rod technology (CMSG) and traditional growing rod in the treatment of neurofibromatosis type 1 dysplastic early-onset scoliosis.Methods:A retrospective analysis was conducted on the data of 20 patients with neurofibromatosis type 1 dysplastic early-onset scoliosis who underwent surgical treatment in the Scoliosis Department of Zhengzhou Orthopaedic Hospital Affiliated to Henan University from January 2010 to July 2022. There were 10 patients in the traditional rod group (treated with traditional growing rod surgery) and 10 patients in the CMSG group (treated with CMSG technology). All patients were ≤10 years old and had a Cobb angle ≥45°. The number of surgeries and the occurrence of complications were recorded. The Cobb angle of the main scoliotic curve, the Cobb angle of kyphosis from T 5 to T 12, and the height from T 1 to S 1 were measured from the imaging data to evaluate the correction of deformity and spinal growth. Results:There were no significant differences in age, gender, follow - up time, preoperative Cobb angle, and preoperative Cobb angle of kyphosis from T 5-T 12 between the CMSG group and the TGR group ( P>0.05). The number of surgeries 1.3±0.67 and the total medical cost 91, 100±34, 700 yuan in the CMSG group were lower than those in the TGR group (5.3±1.77 times and 155, 800±45, 900 yuan], and the differences were statistically significant ( t=6.687, P<0.001; t=3.558, P=0.002). The Cobb angles of the main curve before surgery, after the first surgery, and at the last follow - up in the CMSG group were 69.7°±17.8°, 19.8°±9.7°, and 24.4°±9.0° respectively, while those in the TGR group were 62.0°±11.1°, 32.1°±11.4°, and 33.3°±11.6° respectively. The differences in Cobb angles after the first surgery and at the last follow-up between the two groups were statistically significant ( t=2.633, P=0.017; t=2.313, P=0.033). The Cobb angles of kyphosis from T 5 to T 12 before surgery, after the first surgery, and at the last follow - up in the CMSG group were 40.0°±24.2°, 21.0°±6.0°, and 33.6°±9.3° respectively, while those in the TGR group were 31.3°±14.5°, 26.3°±10.5°, and 32.3°±17.2° respectively. There were no significant differences in the Cobb angles of kyphosis from T 5 to T 12 after the first surgery and at the last follow-up between the two groups ( t=1.383, P=0.184; t=0.243, P=0.811). The heights from T 1 to S 1 before surgery, after the first surgery, and at the last follow-up in the CMSG group were 30.5±3.4 cm, 33.7±3.3 cm, and 37.9±4.8 cm respectively, with an annual increase of 1.18±0.39 cm. The heights from T 1 to S 1 in the TGR group were 29.1±3.0 cm, 31.4±2.9 cm, and 36.3±3.5 cm respectively, with an annual increase of 1.25±0.23 cm. There was no significant difference in the annual growth height of T 1-S 1 between the two groups ( t=1.367, P=0.189). During the follow-up period, 3 patients in the CMSG group had 3 complications: 1 case of coronal plane trunk decompensation, 1 case of rod fracture, and 1 case of distal junctional kyphosis. In the TGR group, 7 patients had 8 complications: 2 cases of wound rupture, 3 cases of screw loosening, 1 case of distal addition phenomenon, 1 case of proximal addition phenomenon, and 1 case of rod fracture. Conclusion:The Co-Cr-Mo guided multidirectional sliding growing rod technique is safe and effective in treating type 1 neurofibromatosis with malnutrition type early-onset scoliosis. It can effectively control the progression of spinal deformities,preserve the growth ability of the spine, and have a low overall incidence of complications.

Tumor drug resistance is an important problem in the failure of chemotherapy and targeted drug therapy, which is a complex process involving chromatin remodeling. SWI/SNF is one of the most studied ATP-dependent chromatin remodeling complexes in tumorigenesis, which plays an important role in the coordination of chromatin structural stability, gene expression, and post-translation modification. However, its mechanism in tumor drug resistance has not been systematically combed. SWI/SNF can be divided into 3 types according to its subunit composition: BAF, PBAF, and ncBAF. These 3 subtypes all contain two mutually exclusive ATPase catalytic subunits (SMARCA2 or SMARCA4), core subunits (SMARCC1 and SMARCD1), and regulatory subunits (ARID1A, PBRM1, and ACTB, etc.), which can control gene expression by regulating chromatin structure. The change of SWI/SNF complex subunits is one of the important factors of tumor drug resistance and progress. SMARCA4 and ARID1A are the most widely studied subunits in tumor drug resistance. Low expression of SMARCA4 can lead to the deletion of the transcription inhibitor of the BCL2L1 gene in mantle cell lymphoma, which will result in transcription up-regulation and significant resistance to the combination therapy of ibrutinib and venetoclax. Low expression of SMARCA4 and high expression of SMARCA2 can activate the FGFR1-pERK1/2 signaling pathway in ovarian high-grade serous carcinoma cells, which induces the overexpression of anti-apoptosis gene BCL2 and results in carboplatin resistance. SMARCA4 deletion can up-regulate epithelial-mesenchymal transition (EMT) by activating YAP1 gene expression in triple-negative breast cancer. It can also reduce the expression of Ca²⁺ channel IP3R3 in ovarian and lung cancer, resulting in the transfer of Ca²⁺ needed to induce apoptosis from endoplasmic reticulum to mitochondria damage. Thus, these two tumors are resistant to cisplatin. It has been found that verteporfin can overcome the drug resistance induced by SMARCA4 deletion. However, this inhibitor has not been applied in clinical practice. Therefore, it is a promising research direction to develop SWI/SNF ATPase targeted drugs with high oral bioavailability to treat patients with tumor resistance induced by low expression or deletion of SMARCA4. ARID1A deletion can activate the expression of ANXA1 protein in HER2+ breast cancer cells or down-regulate the expression of progesterone receptor B protein in endometrial cancer cells. The drug resistance of these two tumor cells to trastuzumab or progesterone is induced by activating AKT pathway. ARID1A deletion in ovarian cancer can increase the expression of MRP2 protein and make it resistant to carboplatin and paclitaxel. ARID1A deletion also can up-regulate the phosphorylation levels of EGFR, ErbB2, and RAF1 oncogene proteins.The ErbB and VEGF pathway are activated and EMT is increased. As a result, lung adenocarcinoma is resistant to epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs). Although great progress has been made in the research on the mechanism of SWI/SNF complex inducing tumor drug resistance, most of the research is still at the protein level. It is necessary to comprehensively and deeply explore the detailed mechanism of drug resistance from gene, transcription, protein, and metabolite levels by using multi-omics techniques, which can provide sufficient theoretical basis for the diagnosis and treatment of poor tumor prognosis caused by mutation or abnormal expression of SWI/SNF subunits in clinical practice.

Numerous studies have shown that depression is main-ly associated with the abnormal expression of connexin 43(Cx43)in astrocytes(Astro)and its mediated dysfunction of gap junction(GJ).However,the molecular mechanism of post-translational modifications targeting Cx43 to regulate neuroin-flammation-associated depression is still unclear.Post-transla-tional modifications of Cx43 mainly include phosphorylation of specific amino acid sites by PKC,PKA,PKG,MAPK and PTK,and protein degradation of Cx43 through the K48/K63 polyubiq-uitylation and deubiquitination pathways,which ultimately lead to protein degradation through K48/K63 polyubiquitination and deubiquitination.These modifications are ultimately involved in the regulation of neuroinflammatory responses through the associ-ation of GJ function.In this paper,we systematically review the role of Cx43 post-translational modifications in neuroinflamma-tion,with the aim of further exploring the potential application of targeting these modifications to modulate the inflammatory re-sponse mechanism in improving depressive symptoms.

Objective:To investigate the clinical characteristics and genetic etiology of Duchenne muscular dystrophy (DMD) with myogenic tumors.Methods:The clinical data of 2 children with DMD combined with myogenic tumors diagnosed in Children′s Hospital Affiliated to Zhengzhou University in July 2021 and February 2022 were collected. The relevant literature was reviewed to summarize the clinical characteristics and explore the mechanism of the dystrophin ( DMD) gene in myogenic tumors. Results:A 6-year and 10-month-old boy with DMD (deletion of exon 45) and a 12-year-old boy with DMD (deletion of exon 51) were diagnosed with tumors. They were diagnosed with DMD for delayed motor development in the Department of Neurology of Children′s Hospital Affiliated to Zhengzhou University. They presented with painless masses in the waist. Postoperative pathological diagnosis: the pathology and immunohistochemistry of case 1 showed an alveolar rhabdomyosarcoma (ARMS) and both myogenin and myogenic differentiation 1 positive; the pathology and immunohistochemistry of case 2 showed an alveolar soft part sarcoma(ASPS) and transcription factor enhancer 3 positive; both cases were myogenic tumors. Literature review (including this paper) showed that there were in total 14 cases with DMD combined with myogenic tumors including 13 cases of rhabdomyosarcoma (RMS) and 1 case of ASPS. All of them are male, and the age of onset of the tumors was 4-17 years. Pathological subtypes were described in 6 cases of ARMS and 5 cases of embryonal RMS, and were not described in 2 cases. The 9 cases described all had large deletions in the DMD gene which can change the reading frame of the DMD gene, and all gene mutations did not exceed exon 62. Conclusions:DMD gene with deletion may increase the risk of having myogenic tumors, and RMS is more common, which is manifested as painless mass in early stage. All DMD gene deletions do not exceed exon 62 and lead to change of the gene reading frame with severe clinical phenotype and degenerative changes in muscle function.

Objective To investigate the distribution and antimicrobial resistance profiles of clinically isolated Haemophilus influenzae and Moraxella catarrhalis in hospitals across China from 2015 to 2021,and provide evidence for rational use of antimicrobial agents.Methods Data of H.influenzae and M.catarrhalis strains isolated from 2015 to 2021 in CHINET program were collected for analysis,and antimicrobial susceptibility testing was performed by disc diffusion method or automated systems according to the uniform protocol of CHINET.The results were interpreted according to the CLSI breakpoints in 2022.Beta-lactamases was detected by using nitrocefin disk.Results From 2015 to 2021,a total of 43 642 strains of Haemophilus species were isolated,accounting for 2.91％of the total clinical isolates and 4.07％of Gram-negative bacteria in CHINET program.Among the 40 437 strains of H.influenzae,66.89％were isolated from children and 33.11％were isolated from adults.More than 90％of the H.influenzae strains were isolated from respiratory tract specimens.The prevalence of β-lactamase was 53.79％in H.influenzae strains.The H.influenzae strains isolated from children showed higher resistance rate than the strains isolated from adults.Overall,779 strains of H.influenzae did not produce β-lactamase but were resistant to ampicillin(BLNAR).Beta-lactamase-producing strains showed significantly higher resistance rates to these antimicrobial agents than the β-lactamase-nonproducing strains.Of the 16 191 M.catarrhalis strains,80.06％were isolated from children and 19.94％isolated from adults.M.catarrhalis strains were mostly susceptible to both amoxicillin-clavulanic acid and cefuroxime,evidenced by resistance rate lower than 2.0％.Conclusions The emergence of antibiotic-resistant H.influenzae due to β-lactamase production poses a challenge for clinical anti-infective treatment.Therefore,it is very important to implement antibiotic resistance surveillance for H.influenzae and guide rational antibiotic use.All local clinical microbiology laboratories should actively improve antibiotic susceptibility testing and strengthen antibiotic resistance surveillance for H.influenzae.