BackgroundObsessive-compulsive disorder （OCD） is a common neuropsychiatric illness and is listed as one of the top ten disabling conditions causing loss of income and reduced quality of life. Psychological distress is an important cause of anhedonia in OCD patients， and is closely related to psychosomatic symptoms. Therefore， exploring the role of anhedonia in the relationship between psychological distress and psychosomatic symptoms is of great significance for optimizing clinical psychological treatment protocols for OCD patients. ObjectiveTo explore the role of anhedonia in the relationship between psychological distress and psychosomatic symptoms in OCD patients， with the aim of providing references for managing psychosomatic symptoms in patients. MethodsA total of 90 patients who met the diagnostic criteria for OCD according to the International Classification of Diseases， tenth edition （ICD-10）， and who visited the Mental Health Center outpatient clinic of General Hospital of Ningxia Medical University from September 2023 to November 2024 were selected as the study objects. The instruments and techniques used for the evaluation were： Dimensional Anhedonia Rating Scale （DARS）， 10-item Kessler Psychological Distress Scale （K10） and Psychosomatic Symptom Scale （PSSS）. Model 4 of the Process for SPSS 26.0 was used to test the mediating role of anhedonia in the relationship between psychological distress and psychosomatic symptoms， with Bootstrapping used to assess the significance of mediating effect. ResultsA total of 84 patients （93.33%） completed the valid questionnaire. K10 score was positively correlated with PSSS total score， psychological symptom score and physical symptom score （r=0.559， 0.460， 0.551， P<0.01）. K10 score was negatively correlated with DARS total score （r=-0.527， P<0.01）. The total score of DARS was negatively correlated with PSSS total score （r=-0.497， P<0.01）. Anhedonia mediated the relationship between psychological distress and psychosomatic symptoms， with an indirect effect value was 0.148 （95% CI： 0.042~0.278）， accounting for 26.48% of the total effect. ConclusionPsychological distress can affect the psychosomatic symptoms in OCD patients both directly and indirectly via anhedonia.

ObjectiveTo investigate the antidepressant effects and mechanisms of total flavonoids from Cuscutae Semen （TFCC） in the mouse model of chronic unpredictable mild stress （CUMS）. MethodsFifty male 4-week-old ICR mice were randomized into five groups （n=10 per group）： blank control， model， Cuscutae Semen decoction （10.2 g·kg^-1·d^-1）， paroxetine （2.6 mg·kg^-1·d^-1）， and TFCC （173.2 mg·kg^-1·d^-1）. The other groups except the blank control group underwent chronic unpredictable mild stress （CUMS） for 4 weeks. Behavioral assessments were conducted post-modeling. Then， the model group received distilled water （10 mL·kg^-1·d^-1）， while treatment groups were administrated with respective agents via oral gavage （10 mL·kg^-1） for 4 weeks. Depression-like behaviors were evaluated by the sucrose preference test （SPT）， forced swimming test （FST）， and tail suspension test （TST）. Hippocampal neuronal morphology was observed via hematoxylin-eosin staining， and apoptosis in the brain tissue was assessed via terminal- deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling （TUNEL）. Enzyme-linked immunosorbent assay （ELISA） was employed to measure the hippocampal levels of inflammatory cytokines ［interleukin （IL）-1β， IL-6， and TNF-α）］ and neurotransmitters ［5-hydroxytryptamine （5-HT）， dopamine （DA）， and brain-derived neurotrophic factor （BDNF）］， while the reactive oxygen species （ROS） levels were quantified via the DCFH-DA probe. Real-time PCR was performed to measure the mRNA levels of NOD-like receptor protein 3 （NLRP3）， apoptosis-associated Speck-like protein containing a CARD （ASC）， cysteinyl aspartate-specific proteinase-1 （Caspase-1）， IL-1β， and inducible nitric oxide synthase （iNOS）. Western blot was employed to evaluate the protein levels of NLRP3， ASC， Caspase-1， uncoupling protein 2 （UCP2）， and thioredoxin-interacting protein （TXNIP）. ResultsCompared with the blank control group， the model group exhibited weight loss （P<0.01）， reduced sucrose preference （P<0.01）， prolonged immobility time in FST and TST （P<0.01）， neuron disarrangement with nuclear pyknosis in hippocampal CA3 region， increased apoptosis in the brain tissue， elevated levels of IL-1β， IL-6， and TNF-α （P<0.01）， declined levels of 5-HT， DA， and BDNF （P<0.01）， increased ROS accumulation （P<0.01）， upregulated mRNA levels of NLRP3， ASC， Caspase-1， IL-1β， and iNOS （P<0.01）， down-regulated protein level of UCP2 （P<0.01）， and up-regulated protein levels of NLRP3， ASC， Caspase-1， and TXNIP （P<0.01）. Compared with the model group， the interventions restored sucrose preference （P<0.01）， shortened immobility time （P<0.01）， repaired hippocampal neuronal structure， reduced apoptosis， lowered the levels of inflammatory cytokines （P<0.01）， restored the levels of neurotransmitters （P<0.01）， alleviated ROS accumulation （P<0.01）， downregulated the mRNA levels of NLRP3， ASC， Caspase-1， IL-1β， and iNOS （P<0.01）， upregulated the protein level of UCP2 （P<0.01）， and reduced the protein levels of NLRP3， ASC， Caspase-1， and TXNIP （P<0.01）. Moreover， TFCC outperformed Cuscutae Semen decoction in ameliorating depressive behaviors. TFCC excelled in neuronal repair， neurotransmitter regulation， anti-inflammatory effects， and modulation of the UCP2/TXNIP/NLRP3 pathway （P<0.05）. ConclusionTFCC modulates the hippocampal UCP2/TXNIP/NLRP3 pathway to inhibit inflammasome activation， reduce oxidative stress， restore neurotransmitters， thus suppressing neuronal apoptosis and promoting the rearrangement and morphology recovery of hippocampal cells. It outperforms Cuscutae Semen decoction in the antidepressant efficacy.

ObjectiveTo investigate the antidepressant effects and mechanisms of total flavonoids from Cuscutae Semen （TFCC） in the mouse model of chronic unpredictable mild stress （CUMS）. MethodsFifty male 4-week-old ICR mice were randomized into five groups （n=10 per group）： blank control， model， Cuscutae Semen decoction （10.2 g·kg^-1·d^-1）， paroxetine （2.6 mg·kg^-1·d^-1）， and TFCC （173.2 mg·kg^-1·d^-1）. The other groups except the blank control group underwent chronic unpredictable mild stress （CUMS） for 4 weeks. Behavioral assessments were conducted post-modeling. Then， the model group received distilled water （10 mL·kg^-1·d^-1）， while treatment groups were administrated with respective agents via oral gavage （10 mL·kg^-1） for 4 weeks. Depression-like behaviors were evaluated by the sucrose preference test （SPT）， forced swimming test （FST）， and tail suspension test （TST）. Hippocampal neuronal morphology was observed via hematoxylin-eosin staining， and apoptosis in the brain tissue was assessed via terminal- deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling （TUNEL）. Enzyme-linked immunosorbent assay （ELISA） was employed to measure the hippocampal levels of inflammatory cytokines ［interleukin （IL）-1β， IL-6， and TNF-α）］ and neurotransmitters ［5-hydroxytryptamine （5-HT）， dopamine （DA）， and brain-derived neurotrophic factor （BDNF）］， while the reactive oxygen species （ROS） levels were quantified via the DCFH-DA probe. Real-time PCR was performed to measure the mRNA levels of NOD-like receptor protein 3 （NLRP3）， apoptosis-associated Speck-like protein containing a CARD （ASC）， cysteinyl aspartate-specific proteinase-1 （Caspase-1）， IL-1β， and inducible nitric oxide synthase （iNOS）. Western blot was employed to evaluate the protein levels of NLRP3， ASC， Caspase-1， uncoupling protein 2 （UCP2）， and thioredoxin-interacting protein （TXNIP）. ResultsCompared with the blank control group， the model group exhibited weight loss （P<0.01）， reduced sucrose preference （P<0.01）， prolonged immobility time in FST and TST （P<0.01）， neuron disarrangement with nuclear pyknosis in hippocampal CA3 region， increased apoptosis in the brain tissue， elevated levels of IL-1β， IL-6， and TNF-α （P<0.01）， declined levels of 5-HT， DA， and BDNF （P<0.01）， increased ROS accumulation （P<0.01）， upregulated mRNA levels of NLRP3， ASC， Caspase-1， IL-1β， and iNOS （P<0.01）， down-regulated protein level of UCP2 （P<0.01）， and up-regulated protein levels of NLRP3， ASC， Caspase-1， and TXNIP （P<0.01）. Compared with the model group， the interventions restored sucrose preference （P<0.01）， shortened immobility time （P<0.01）， repaired hippocampal neuronal structure， reduced apoptosis， lowered the levels of inflammatory cytokines （P<0.01）， restored the levels of neurotransmitters （P<0.01）， alleviated ROS accumulation （P<0.01）， downregulated the mRNA levels of NLRP3， ASC， Caspase-1， IL-1β， and iNOS （P<0.01）， upregulated the protein level of UCP2 （P<0.01）， and reduced the protein levels of NLRP3， ASC， Caspase-1， and TXNIP （P<0.01）. Moreover， TFCC outperformed Cuscutae Semen decoction in ameliorating depressive behaviors. TFCC excelled in neuronal repair， neurotransmitter regulation， anti-inflammatory effects， and modulation of the UCP2/TXNIP/NLRP3 pathway （P<0.05）. ConclusionTFCC modulates the hippocampal UCP2/TXNIP/NLRP3 pathway to inhibit inflammasome activation， reduce oxidative stress， restore neurotransmitters， thus suppressing neuronal apoptosis and promoting the rearrangement and morphology recovery of hippocampal cells. It outperforms Cuscutae Semen decoction in the antidepressant efficacy.

ObjectiveTo investigate the effect and mechanism of Shenqi Tangluo pill （SQTLP） on oxidative stress injury of skeletal muscle of type 2 diabetes mellitus （T2DM） mice based on nuclear factor erythroid 2-related factor 2 （Nrf2）/heme oxygenase-1 （HO-1）/NAD（P）H quinone oxidoreductase 1 （NQO1） pathway. MethodA total of 60 7-week-old male db/db mice ［specific pathogen-free （SPF） grade］ were selected and fed for one week for adaption. They were divided into the model control group， SQTLP low-， medium- and high-dose （19， 38， and 76 g·kg^-1） groups and metformin group （0.26 g·kg^-1） by gavage. Each group consisted of 12 mice. Twelve male db/m mice of the same age were selected as the blank group. The intervention was implemented continuously for 8 weeks. Fasting blood glucose （FBG） was detected. Fasting serum insulin （FINS） levels were detected by enzyme-linked immunosorbent assay （ELISA）， and the homeostasis model assessment-insulin resistance （HOMA-IR） index and the homeostasis model assessment-insulin sensitivity index （HOMA-ISI） were calculated. Oral glucose tolerance test （OGTT） and insulin tolerance test （ITT） were conducted. The activities of superoxide dismutase （SOD） and glutathione peroxidase （GSH-Px） and the contents of malondialdehyde （MDA） and reduced nicotinamide adenine dinucleotide phosphate （NADPH） in skeletal muscle tissues were detected by biochemical kits. Hematoxylin-eosin （HE） staining was used to observe the pathological changes in skeletal muscle tissues. The levels of reactive oxygen species （ROS） and 4-hydroxynonenal （4-HNE） in skeletal muscle tissue were detected by immunofluorescence （IF）. The expression levels of Nrf2， HO-1， NQO1 and glutamate-cysteine ligase catalytic subunit （GCLC） proteins in skeletal muscle tissues were detected by Western blot. ResultCompared with those in the blank group， FBG， FINS and HOMA-IR in the model group were significantly increased （P<0.05）， while HOMA-ISI was decreased （P<0.05）. The results of OGTT and ITT showed that blood glucose was significantly increased at all time points （P<0.05）， and glucose tolerance and insulin tolerance were significantly impaired. SOD and GSH-Px activities in skeletal muscle tissues were significantly decreased （P<0.05）， and MDA and NADPH contents were significantly increased （P<0.05）. In skeletal muscle tissues， the arrangement of muscle fibers was loose， the nucleus was disordered， and inflammatory cells were infiltrated. The expression levels of ROS and 4-HNE in skeletal muscle tissues were significantly increased （P<0.05）. The protein expression levels of Nrf2， HO-1， NQO1 and GCLC in skeletal muscle tissues were significantly decreased （P<0.05）. Compared with those in the model group， FBG， FINS and HOMA-IR in the metformin group were significantly decreased （P<0.05）， while HOMA-ISI was increased （P<0.05）. The results of OGTT and ITT showed that blood glucose in the metformin group was significantly decreased at all time points （P<0.05）. The activities of SOD and GSH-Px in skeletal muscle tissues were significantly increased （P<0.05）， while the contents of MDA and NADPH were significantly decreased （P<0.05）. No obvious abnormality was found in the skeletal muscle tissue of the metformin group. The expressions of ROS and 4-HNE in skeletal muscle tissues were decreased （P<0.05）. The protein expression levels of Nrf2， HO-1， NQO1 and GCLC in skeletal muscle tissues were significantly increased （P<0.05）. Compared with those in the model group， FBG， FINS and HOMA-IR in the SQTLP medium- and high-dose groups were significantly decreased （P<0.05）， while HOMA-ISI was increased （P<0.05）. The results of OGTT and ITT showed that the glucose tolerance and insulin tolerance of mice were improved in each dose group of SQTLP. The GSH-Px activity in the SQTLP low-dose group was significantly increased （P<0.05）， and the NADPH content was decreased （P<0.05）. The activities of SOD and GSH-Px in the SQTLP medium- and high-dose groups were significantly increased （P<0.05）， while the contents of MDA and NADPH were significantly decreased （P<0.05）. The skeletal muscle tissue injury of mice in each dose group of SQTLP was ameliorated to different degrees. In the SQTLP medium- and high-dose groups， the expressions of ROS and 4-HNE were decreased （P<0.05）， and the protein expression levels of Nrf2， HO-1， NQO1 and GCLC were significantly increased （P<0.05）. Compared with those in the SQTLP low-dose group， FBG and HOMA-IR in the SQTLP high-dose group were significantly decreased （P<0.05）， while HOMA-ISI was increased （P<0.05）. The results of OGTT and ITT showed that the SQTLP high-dose group significantly improved the glucose tolerance and insulin tolerance of mice. The activities of SOD and GSH-Px in skeletal muscle tissues were significantly increased （P<0.05）， while the contents of MDA and NADPH were significantly decreased （P<0.05）. No obvious abnormality was found in the skeletal muscle tissue， the expressions of ROS and 4-HNE were decreased （P<0.05）， and the protein expression levels of Nrf2， HO-1， NQO1 and GCLC were significantly increased （P<0.05） in the skeletal muscle tissue of the SQTLP high-dose group. ConclusionSQTLP can significantly improve IR in T2DM mice， and the mechanism is related to SQTLP activating the Nrf2/HO-1/NQO1 signaling pathway， promoting the expression of antioxidant enzymes， and thus improving the oxidative stress injury in the skeletal muscle.

OBJECTIVE To explore the phenotypic changes and possible mechanisms of lncRNA OIP5-AS1 on the proliferation, migration, apoptosis, invasion and cycle of ovarian epithelial cells IOSE80. METHODS The clinical data of patients were collected from TCGA database and GEO database. After R package analysis, the differential expression of OIP5-AS1 was visualized in the volcanic map. The correlation between survival rate and OIP5-AS1 was analyzed by Kaplan-Meier. The IOSE80 cell model of OIP5-AS1 over expression and silencing was constructed with lentivirus vector. The expression of OIP5-AS1 was verified by RT-qPCR. Cell proliferation was detected by CCK-8. Invasion was detected by Transwell. Cell migration was detected by scratch test. Cell cycle and apoptosis were detected by flow cytometry. Western blotting was used to detect the expression of E-cadherin and N-cadherin, as well as the expression of cyclin-dependent kinase(CDK) and cyclin-G-related kinase(GAK). RESULTS RT-qPCR results showed that IOSE80 cell lines over expressing and silencing OIP5-AS1 were successfully constructed. CCK-8 results showed that overexpressing OIP5-AS1 promoted the proliferation of IOSE80 cells. Scratch test results showed that overexpressing OIP5-AS1 promoted the migration of IOSE80 cells. Transwell results showed that overexpressing OIP5-AS1 would increase the invasiveness of IOSE80 cells. Flow cytometry results showed that overexpression of OIP5-AS1 weakened the apoptosis of IOSE80 cells and promoted the progress of cell cycle. Western blotting results showed that overexpression of OIP5-AS1 downregulated the expression of E-cadherin and upregulated the expression of N-cadherin, while overexpression of OIP5-AS1 increased the expression of CDK and GAK proteins. CONCLUSION LncRNA OIP5-AS1 further interferes with the regulation of IOSE80 cell cycle by up regulating the expression of CDK and GAK, and then indirectly regulates the malignant phenotype of ovarian epithelial cells.

Objective To primarily investigate the indoor radon concentrations in the urban and rural dwellings in Yinchuan, China, and to estimate the effective dose. Methods A total of 67 dwellings, which included 49 urban households and 18 rural households in Yinchuan, were selected to cumulatively measure the indoor radon concentrations for more than 3 months using solid state nuclear track detection. Results The arithmetic mean, geometric mean, median, and range of indoor radon concentrations in urban and rural areas in Yinchuan were 64 Bq/m³, 59 Bq/m³, 57 Bq/m³, and 25-172 Bq/m³, respectively. Surveillance sites with an indoor radon concentration higher than 100 Bq/m³ accounted for 7.5%. Indoor radon concentrations in rural areas were higher than those in urban areas. Indoor radon concentrations were highest in winter and lowest in summer. The effective dose of indoor radon exposure among residents in Yinchuan was 1.86 mSv/a. Conclusion The results of indoor radon concentrations measured in this investigation in Yinchuan are significantly higher than those measured in the 1990s. The annual effective dose is higher than the mean levels in the world and China.

OBJECTIVE: To investigate the serum microRNA (miRNA) expression and examine the impact of miRNA expression profiles on T helper type 17 (Th17)/regulatory T cells (Treg) imbalance among patients with cystic echinococcosis, so as to provide insights into the illustration of the mechanisms underlying chronic Echinococcus granulosus infections, and long-term pathogenesis. METHODS: Total RNA was extracted from the sera of cystic echinococcosis patients and healthy controls, and subjected to high-throughput sequencing with the Illumina sequencing platform. Known miRNAs were annotated and new miRNAs were predicted using the miRBase database and the miRDeep2 tool, and differentially expressed miRNAs were identified. The target genes of differentially expressed miRNAs were predicted using the software miRanda and TargetScan, and the intersection was selected for Gene Ontology (GO) enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis. Among the differentially expressed miRNAs with the 20 highest fold changes, miRNAs that targeted genes relating to key transcription factors RORC and FOXP3 that determine the production of Th17 and Treg cells or their important regulatory pathways (PI3K-Akt and mTOR pathways) were matched. RESULTS: A total of 53 differentially expressed miRNAs were screened in sera of cystic echinococcosis patients and healthy controls, including 47 up-regulated miRNAs and 6 down-regulated miRNAs. GO enrichment analysis showed that these differentially expressed miRNA were involved DNA transcription and translation, cell components, cell morphology, neurodevelopment and metabolic decomposition, and KEGG pathway analysis showed that the differentially expressed miRNA were mainly involved in MAPK, PI3K-Akt and mTOR signaling pathways. Among the differentially expressed miRNAs with the 20 highest fold changes, there were 3 miRNAs that had a potential for target regulation of RORC, and 15 miRNAs that had a potential to target the PI3K-Akt and mTOR signaling pathways. CONCLUSIONS Significant changes are found in serum miRNA expression profiles among patients with E. granulosus infections, and differentially expressed miRNAs may lead to Th17/Treg imbalance through targeting the key transcription factors of Th17/Treg or PI3K-Akt and mTOR pathways, which facilitates the long-term parasitism of E. granulosus in hosts and causes a chronic disease.
Echinococcosis/genetics* ; Gene Expression Profiling ; Humans ; MicroRNAs/metabolism* ; Phosphatidylinositol 3-Kinases/genetics* ; Proto-Oncogene Proteins c-akt/genetics* ; T-Lymphocytes, Regulatory ; TOR Serine-Threonine Kinases/genetics* ; Th17 Cells ; Transcription Factors/genetics*

ObjectiveTo observe the effects of transcranial direct current stimulation (tDCS) on insomnia, anxiety and depression in patients with post-sroke insomnia (PSI). MethodsFrom January, 2020 to May, 2021, 44 patients with PSI from Beijing Bo'ai Hospital were randomly divided into control group (n = 22) and experimental group (n = 22). On the basis of conventional treatment, the experimental group accepted tDCS, and the control group accepted sham stimulation for four weeks. Pittsburgh Sleep Quality Index (PSQI) and sleep monitoring system based on cardiopulmonary coupling technology were used to evaluate the sleep quality of the patients before and after treatment. Hamilton Anxiety Scale (HAMA) and Hamilton Depression Scale (HAMD) were used to evaluate mood. ResultsTwo cases dropped out in each group. After treatment, the scores of PSQI, HAMA and HAMD decreased in both groups (t > 8.575, P < 0.001), and the scores of PSQI and HAMA were better in the experimental group than in the control group (t > 2.811, P < 0.01), however, there was no significant difference in the scores of HAMD between two groups (t = 1.756, P > 0.05). After treatment, the sleep quality index, total sleep time, sleep latency, sleep efficiency and wake conversion times improved (|t| > 4.721, P < 0.001), and the rapid eye movement time prolonged in the experimental group (t = -2.851, P = 0.010); the sleep quality index, total sleep time, sleep efficiency and wake conversion times were better in the experimental group than in the control group (t > 2.190, P < 0.05), however, no significant difference was found in the sleep latency and rapid eye movement time between two groups (|t| < 1.073, P > 0.05). ConclusiontDCS could improve the sleep quality and anxiety in PSI patients, and has little effect on sleep structure.

【Objective】 To evaluate the performance of the magnetic artificial blood vessel device for fast non-suture anastomosis of caval reconstruction with artificial blood vessel transplantation after resection in canines. 【Methods】 Sixteen adult mongrel dogs of either gender were randomly divided into two groups for vena cava reconstruction with artificial blood vessel transplantation after inferior vena cava (IVC) resection. Group MCA (n=8): magnetic artificial blood vessel device for IVC reconstruction; Group manual sewing (MS) (n=8): hand suturing for IVC reconstruction. Operation time and stoma errhysis were recorded during operation. Patency and stoma stenosis were confirmed via color Doppler ultrasound scanning and X-ray cholangiography at different time points as late as 4 weeks after surgery. 【Results】 The time required to perform the vascular anastomosis was significantly shorter for the magnetic artificial blood vessel device (6.25±2.25)min than for MS (27.32±5.12)min (P<0.001). There were four cases of stoma errhysis in MS group which had to be repaired (P=0.077). Vascular X-ray angiography and color Doppler ultrasound found normal blood flow and no stoma stenosis in MCA group, but three cases of stoma stenosis in MS groups (P=0.200). Compared with MS group, the magnetic ring device stoma was associated with smooth re-endothelialization and depressed infiltration of inflammatory cells at the anastomotic site. 【Conclusion】 The magnetic artificial blood vessel device offers a simple, fast, reliable, and efficacious technique for vena cava reconstruction with artificial blood vessel transplantation.

OBJECTIVE: To explore the clinical phenotype and genetic diagnosis of a patient featuring secondary amenorrhea, breast dysplasia and mental retardation. METHODS: Peripheral venous blood samples were collected from the patient and her family members and subjected to G-banding karyotyping and single nucleotide polymorphism array (SNP-array) analysis. RESULTS: The patient was found to have a karyotype of 46,X,der(X)(12qter→ 12q22::Xq23→ Xpter)mat, her mother had a karyotype of 46,X,t(X;12)(Xpter→ Xq23::12q22→ 12qter;12pter→ 12q22::Xq23→ Xqter), while her father and brother were both 46,XY. SNP-array analysis suggested the patient to be arr[hg19]12q22q24.33(94 792 972-133 777 562)× 3, Xq23q28(108 786 070-155 233 098)×1. CONCLUSION The abnormal phenotypes of the patient can probably be attributed to the presence of Xq23-qter deletion and 12q22-qter duplication, both have derived from her mother's balanced t (X;12) translocation.