Objective: To observe the effects of moxibustion at Huantiao (GB30) acupoint on nerve repair, regeneration, and function in rats with sciatic nerve injury (SNI), and explore the possible mechanism of SNI improvement via moxibustion. Methods: A total of 70 specific pathogen-free (SPF) grade male Sprague-Dawley (SD) rats were randomly assigned to control group (n = 10) and model group (n = 60). Following replication of SNI to model group rats, 60 SNI model rats were randomly allocated to SNI groups of 1 d, 3 d, and 7 d and moxibustion groups of 1 d, 3 d, and 7 d with 10 rats in each group. Moxibustion groups were given moxibustion at the Huantiao (GB30) acupoint on the affected side with a 5 cm distance from the skin under isoflurane respiratory anesthesia and treated once a day for 20 min for 1 d, 3 d, and 7 d, respectively. Control and SNI groups were anesthetized with isoflurane daily for 20 min. Open field tests and thermal pain threshold tests were conducted, and the general condition of rats was observed in each group pre-modeling and on treatment day 1, 3, and 7. At the end of the treatment, immunofluorescence was used to detect the axonal growth rate, axonal growth density, and Schwann cells (SCs) proliferation in the middle 1-mm cross-section of the crush injury segment in rats. The gastrocnemius muscles on both sides of the rats were taken and weighed to calculate the wet weight ratio of the gastrocnemius muscles on both sides to observe the muscle atrophy of the rats, and hematoxylin-eosin (HE) staining was used to observe the pathomorphological changes of the gastrocnemius muscles on the affected side. Quantitative real-time polymerase chain reaction (qPCR) was used to detect the expression levels of nerve growth factor (NGF), interferon (IFN), macrophage migration inhibitory factor (MIF), interleukin (IL)-4, and transforming growth factor (TGF)-β in the sciatic nerve tissue of the rats. Results: After modeling, rats in both moxibustion and SNI groups showed typical signs of pain behaviors (bending and curling of the hind soles of the affected side, licking claws, and lameness) and decreased activity compared with control group. The main benefits of moxibustion were evident from day 3: compared with SNI group, rats in moxibustion group had marked relief of pain behavior, increased activity levels and movement, and a lower response to thermal pain. At the same time, moxibustion significantly promoted the repair of SNI, as evidenced by the significantly better axonal growth rate, growth density, and SCs proliferation density in the crush injury segment compared with SNI group (P < 0.01). Moxibustion also regulated the local microenvironment of the injury, up-regulated the pro-nerve repair factors NGF, IL-4, and TGF-β (P < 0.05), and down-regulated the pro-inflammatory factors IFN-γ (P < 0.01) and MIF (P < 0.05). By day 7, the histomorphology of the gastrocnemius muscle in moxibustion group was improved, as indicated by enlarged muscle fibers, elevated regular myocyte morphology and wet weight ratio of the affected and unaffected sides (P < 0.05), as well as a sustained high expression levels of NGF, IL-4, and TGF-β (P < 0.05, P < 0.05, and P < 0.01, respectively), and a maintenance of low level of IFN-γ (P < 0.01). Concurrently, the MIF level was not significantly different from SNI group (P > 0.05). Conclusion Moxibustion at the Huantiao (GB30) acupoint effectively improves motor function and promotes recovery of sensory function and nerve regeneration in SNI rats, which may be related to the regulation of local inflammatory response, the promotion of nerve growth factor expression, the improvement of regenerative microenvironment, and the acceleration of SCs proliferation and axonal growth rate in damaged nerves.

The integrin alpha 2（ITGA2）gene locates on chromosome 5q11.2，encodes the α 2 subunit of the integrin family.The α 2 subunit is found on many cell surfaces.The α 2 subunit plays an important role in the regulation of platelet aggregation，cell migration，cell proliferation and angiogenesis.Through a wide range of studies conducted in recent years，researchers have discovered that this gene is linked to some diseases，such as rheumatoid arthritis，pediatric sickle cell disease，Kawasaki disease，malignant tumor and biliary atresia.These studies have contributed to the early identification of diseases associated with this gene and the exploration of diagnostic and therapeutic solutions for them.This article reviews the advancements in research concerning the association of ITGA2 gene with various diseases.

Drug resistance is one of the key factors affecting the effectiveness of cancer treatment methods, including chemotherapy, radiotherapy, and immunotherapy. Its occurrence is related to factors such as mRNA expression and methylation within cancer cells. If drug resistance in patients can be accurately identified early, doctors can devise more effective treatment plans, which is of great significance for improving patients' survival rates and quality of life. Cancer drug resistance prediction based on artificial intelligence (AI) technology has emerged as a current research hotspot, demonstrating promising application prospects in guiding clinical individualized and precise medication for cancer patients. This review aims to comprehensively summarize the research progress in utilizing AI algorithms to analyze multi-omics data including genomics, transcriptomics, epigenomics, proteomics, metabolomics, radiomics, and histopathology, for predicting cancer drug resistance. It provides a detailed exposition of the processes involved in data processing and model construction, examines the current challenges faced in this field and future development directions, with the aim of better advancing the progress of precision medicine.

Objective:To explore the role of Caveolin-1 (CAV-1) in radiation-induced premature senescence of vascular endothelial cells.Methods:A cell model with stable knockdown of CAV-1 was constructed in human microvascular endothelial cells (HMEC-1) by lentiviral transfection using puromycin screening. The cells were divided into NC group and sh-CAV-1 group based on whether they were infected with lentivirus shRNA-CAV-1. The protein expression levels of CAV-1, p53 and p21 were detected by Western blot at 24, 48, and 72 h after 0, 2, and 4 Gy X-ray irradiation. The β-galactosidase staining kit was used to detect β-galactosidase in cells. CCK-8 kit was used to detect cell viability, and vascular endothelial cell function was detected by vascular tube-forming assay.Results:CAV-1 protein expression was significantly decreased at 48 h after 2 and 4 Gy X-ray irradiation ( t=3.50, 3.89, P < 0.05), and β-galactosidase in sh-CAV-1 group was significantly increased at 72 h after 0, 2 and 4 Gy X-ray irradiation ( t=12.91, 11.54, 6.04, P < 0.05) compared with the NC group. Knockdown of CAV-1 resulted in the decrease in the expression level of the cellular senescence-associated protein p53 protein ( t=4.09, 3.13, 3.43, P < 0.05), but increase in the expression level of p21 protein ( t=-3.63, -3.33, -3.06, P < 0.05). Compared with the NC group, knockdown CAV-1 significantly decreased cell viability ( t=2.97-25.89, P<0.05) and reduced vessel-forming capacity ( t=3.39-39.68, P < 0.05). Conclusions:CAV-1 is involved in the process of radiation-induced premature senescence of vascular endothelial cells through positive regulation of p53 and negative regulation of p21.

Objective:To investigate the efficacy and treatment adherence of digital cognitive behavioral therapy for insomnia (dCBT-I) in patients with insomnia disorder accompanied by anxiety and depressive symptoms, and to provide empirical evidence for its clinical application.Methods:From December 2023 to December 2024, 102 patients with insomnia disorder accompanied by anxiety and depressive symptoms were recruited from the outpatient department of Inner Mongolia Brain Hospital and randomly assigned to either the dCBT-I group ( n=56) or the digital sleep hygiene education (dSHE) group ( n=46). The dCBT-I group received a 4-week intervention comprising 5 core modules, while the dSHE group received 4 weeks of digital sleep hygiene education. Both groups received weekly guidance from clinical psychologists. Subjective sleep quality (Insomnia Severity Index, ISI), anxiety (Hamilton Anxiety Scale, HAMA), and depressive symptoms (17-item Hamilton Depression Scale, HAMD 17) were assessed at baseline, week 4, week 8, and week 12. Objective sleep parameters (polysomnography, PSG) and cognitive function (Repeatable Battery for the Assessment of Neuropsychological Status, RBANS) were evaluated at baseline and week 4. Linear mixed-effects model was used to analyze the effects of group, timepoint, and their interaction on outcome measures, after controlling medication history, age, sex, education level, ethnicity, and marital status as covariates. Results:A total of 76 patients (dCBT-I: n=42; dSHE: n=34) completed the 4-week intervention, yielding a treatment adherence rate of 74.5%(76/102). At weeks 4, 8, and 12, the dCBT-I group demonstrated significantly lower scores on the ISI, HAMA, and HAMD 17 scales compared to the dSHE group (β=-1.70--0.66, t=-15.38--6.21, all P<0.05), along with higher rates of medication reduction (χ 2=16.40, 9.22, 6.66, all P<0.05). No significant differences were observed in PSG parameters between the two groups. However, the dCBT-I group demonstrated significant improvements in RBANS subdomains, including immediate memory, language function, and delayed memory (β=0.45, 0.86, 1.43, t=3.09, 2.67, 4.36, all P<0.05). Conclusion:dCBT-I is an effective and well-adhered intervention for patients with insomnia disorder accompanied by anxiety and depressive symptoms, warranting broader clinical implementation.

Objective To observe the depressive behavior and neuronal damage induced by different doses of corticosterone(CORT)in mice,and to explore the optimal dose for a corticosterone-induced depression model in mice.Methods Forty male C57BL/6J mice were divided randomly into four groups:control group and low,medium,and high CORT groups(20,40,and 60 mg/kg,respectively),treated with the corresponding drug dose by subcutaneous injection for 4 weeks.Behavioral c hanges in mice after corticosterone administration for 3 and 4 weeks were detected by sugar water preference,forced swimming,tail suspension,and open field tests.Morphological changes in neurons in the hippocampal CA1 area and forebrain cortex area were observed by hematoxylin-eosin(HE)and Nissl staining.Serum levels of 5-hydroxytryptamine(5-HT)were detected by enzyme-linked immunosorbent assay.Depression-related behavioral changes induced by different doses of corticosterone were compared.Results The bodyweights of mice in all three CORT groups(20,40,and 60 mg/kg)decreased(P＜0.05)and the preference for sucrose solution decreased(P＜0.01)compared with the findings in the control group.The immobility time in the forced swimming test was prolonged in the CORT 20 and 40 mg/kg groups(P＜0.01)and the immobility time of mice in the tail suspension test was prolonged in the CORT 40 mg/kg group(P＜0.05).The total distance,the length of time spent in the peripheral area was prolonged and the time entering the central area in the open-field experiment were decreased in the CORT 40 and 60 mg/kg groups(P＜0.05),and average speed were decreased in the CORT 40 mg/kg group(P＜0.05).In addition,CORT injection result ed in abnormal neuronal cell morphology,cell deformation,and nuclear condensation in the hippocampal CA1 and forebrain cortex areas,to different degrees.Serum 5-hydroxytryptamine levels were reduced in the CORT 40 and 60 mg/kg groups(P＜0.05).Conclusions CORT 20,40,and 60 mg/kg can induce depression-like behavioral changes and neuronal damage in mice to varying degrees,with the most notable effect at 40 mg/kg.Under experimental conditions,we consider that 40 mg/kg is the best dose for replicating corticosterone-induced depression in model mice.

Objective:To explore the role of Caveolin-1 (CAV-1) in radiation-induced premature senescence of vascular endothelial cells.Methods:A cell model with stable knockdown of CAV-1 was constructed in human microvascular endothelial cells (HMEC-1) by lentiviral transfection using puromycin screening. The cells were divided into NC group and sh-CAV-1 group based on whether they were infected with lentivirus shRNA-CAV-1. The protein expression levels of CAV-1, p53 and p21 were detected by Western blot at 24, 48, and 72 h after 0, 2, and 4 Gy X-ray irradiation. The β-galactosidase staining kit was used to detect β-galactosidase in cells. CCK-8 kit was used to detect cell viability, and vascular endothelial cell function was detected by vascular tube-forming assay.Results:CAV-1 protein expression was significantly decreased at 48 h after 2 and 4 Gy X-ray irradiation ( t=3.50, 3.89, P < 0.05), and β-galactosidase in sh-CAV-1 group was significantly increased at 72 h after 0, 2 and 4 Gy X-ray irradiation ( t=12.91, 11.54, 6.04, P < 0.05) compared with the NC group. Knockdown of CAV-1 resulted in the decrease in the expression level of the cellular senescence-associated protein p53 protein ( t=4.09, 3.13, 3.43, P < 0.05), but increase in the expression level of p21 protein ( t=-3.63, -3.33, -3.06, P < 0.05). Compared with the NC group, knockdown CAV-1 significantly decreased cell viability ( t=2.97-25.89, P<0.05) and reduced vessel-forming capacity ( t=3.39-39.68, P < 0.05). Conclusions:CAV-1 is involved in the process of radiation-induced premature senescence of vascular endothelial cells through positive regulation of p53 and negative regulation of p21.

Objective To observe the depressive behavior and neuronal damage induced by different doses of corticosterone(CORT)in mice,and to explore the optimal dose for a corticosterone-induced depression model in mice.Methods Forty male C57BL/6J mice were divided randomly into four groups:control group and low,medium,and high CORT groups(20,40,and 60 mg/kg,respectively),treated with the corresponding drug dose by subcutaneous injection for 4 weeks.Behavioral c hanges in mice after corticosterone administration for 3 and 4 weeks were detected by sugar water preference,forced swimming,tail suspension,and open field tests.Morphological changes in neurons in the hippocampal CA1 area and forebrain cortex area were observed by hematoxylin-eosin(HE)and Nissl staining.Serum levels of 5-hydroxytryptamine(5-HT)were detected by enzyme-linked immunosorbent assay.Depression-related behavioral changes induced by different doses of corticosterone were compared.Results The bodyweights of mice in all three CORT groups(20,40,and 60 mg/kg)decreased(P＜0.05)and the preference for sucrose solution decreased(P＜0.01)compared with the findings in the control group.The immobility time in the forced swimming test was prolonged in the CORT 20 and 40 mg/kg groups(P＜0.01)and the immobility time of mice in the tail suspension test was prolonged in the CORT 40 mg/kg group(P＜0.05).The total distance,the length of time spent in the peripheral area was prolonged and the time entering the central area in the open-field experiment were decreased in the CORT 40 and 60 mg/kg groups(P＜0.05),and average speed were decreased in the CORT 40 mg/kg group(P＜0.05).In addition,CORT injection result ed in abnormal neuronal cell morphology,cell deformation,and nuclear condensation in the hippocampal CA1 and forebrain cortex areas,to different degrees.Serum 5-hydroxytryptamine levels were reduced in the CORT 40 and 60 mg/kg groups(P＜0.05).Conclusions CORT 20,40,and 60 mg/kg can induce depression-like behavioral changes and neuronal damage in mice to varying degrees,with the most notable effect at 40 mg/kg.Under experimental conditions,we consider that 40 mg/kg is the best dose for replicating corticosterone-induced depression in model mice.

Objective:To investigate the efficacy and treatment adherence of digital cognitive behavioral therapy for insomnia (dCBT-I) in patients with insomnia disorder accompanied by anxiety and depressive symptoms, and to provide empirical evidence for its clinical application.Methods:From December 2023 to December 2024, 102 patients with insomnia disorder accompanied by anxiety and depressive symptoms were recruited from the outpatient department of Inner Mongolia Brain Hospital and randomly assigned to either the dCBT-I group ( n=56) or the digital sleep hygiene education (dSHE) group ( n=46). The dCBT-I group received a 4-week intervention comprising 5 core modules, while the dSHE group received 4 weeks of digital sleep hygiene education. Both groups received weekly guidance from clinical psychologists. Subjective sleep quality (Insomnia Severity Index, ISI), anxiety (Hamilton Anxiety Scale, HAMA), and depressive symptoms (17-item Hamilton Depression Scale, HAMD 17) were assessed at baseline, week 4, week 8, and week 12. Objective sleep parameters (polysomnography, PSG) and cognitive function (Repeatable Battery for the Assessment of Neuropsychological Status, RBANS) were evaluated at baseline and week 4. Linear mixed-effects model was used to analyze the effects of group, timepoint, and their interaction on outcome measures, after controlling medication history, age, sex, education level, ethnicity, and marital status as covariates. Results:A total of 76 patients (dCBT-I: n=42; dSHE: n=34) completed the 4-week intervention, yielding a treatment adherence rate of 74.5%(76/102). At weeks 4, 8, and 12, the dCBT-I group demonstrated significantly lower scores on the ISI, HAMA, and HAMD 17 scales compared to the dSHE group (β=-1.70--0.66, t=-15.38--6.21, all P<0.05), along with higher rates of medication reduction (χ 2=16.40, 9.22, 6.66, all P<0.05). No significant differences were observed in PSG parameters between the two groups. However, the dCBT-I group demonstrated significant improvements in RBANS subdomains, including immediate memory, language function, and delayed memory (β=0.45, 0.86, 1.43, t=3.09, 2.67, 4.36, all P<0.05). Conclusion:dCBT-I is an effective and well-adhered intervention for patients with insomnia disorder accompanied by anxiety and depressive symptoms, warranting broader clinical implementation.

BACKGROUND:Premature birth is a major global health problem associated with high mortality and morbidity.White matter injury is the most common brain injury in preterm infants.Salvia miltiorrhiza is a traditional herbal plant that is commonly used to treat cardiovascular and cerebrovascular diseases in Asian countries. OBJECTIVE:To investigate the therapeutic effect of Salvia miltiorrhiza on white matter injury in preterm infants. METHODS:Eighteen neonatal male Sprague-Dawley rats at 3-day gestational age were selected and randomized into normal group,white matter injury group,and Salvia miltiorrhiza group.Animal models of preterm white matter injury were established by permanent ligation of the right common carotid artery in the latter two groups.Rats in the Salvia miltiorrhiza group were given intraperitoneal injection of Salvia miltiorrhiza(5 mg/kg·d)for 7 consecutive days.Normal group and white matter injury group were given the same volume of PBS for intervention.On the 14th day after modeling,the rats were sacrificed.Brains were pathologically observed by hematoxylin-eosin staining under microscope,and the expression levels of myelin basic protein and CC1 in brain tissue were visualized using immunofluorescence.Furthermore,liquid chromatography-tandem mass spectrometry was used to analyze possible pathways for the action of Salvia miltiorrhiza. RESULTS AND CONCLUSION:In the white matter injury group,the structure of the corpus callosum was irregular and the cells appeared swollen and necrotic.In addition,induction of white matter injury resulted in significantly reduced myelin formation,with irregular and loosely arranged nerve fibers and significantly decreased myelin sheaths.Interestingly,white matter injury rats treated with Salvia miltiorrhiza had reduced cellular swelling,reduced lesions,and increased myelin sheaths.The expression of myelin basic protein was closely related to myelin formation,and CC1 was a marker of myelin oligodendrocytes.Salvia miltiorrhiza significantly up-regulated the expressions of myelin basic protein and CC1 in white matter injury rats(P＜0.000 1),indicating that Salvia miltiorrhiza alleviated white matter injury.Liquid chromatography-tandem mass spectrometry analysis showed that the therapeutic effect of Salvia miltiorrhiza in the rat model of white matter injury was closely related to the regulation of complement and coagulation cascades.To conclude,Salvia miltiorrhiza may be a potential therapeutic agent for treating preterm white matter injury.