Objective: To explore the effects of the school based integrated horticulture curriculum intervention on 24 hour activity behaviors among third grade primary school students, so as to provide reference for promoting children s health. Methods: In September 2023, a convenience sampling method was used to select 90 third grade primary school students from a primary school in Changsha. Participants were randomly assigned to an intervention group ( n =45) and a control group ( n =45) using a random number table. From February to May 2024, the intervention group received a 12 week integrated curriculum intervention, consisting of two 60 minute sessions per week and covering horticultural practice, home-school collaborative tasks and nutrition knowledge education. The control group continued with routine labor education courses. The triaxial accelerometer and multi sensor sleep monitoring device were used to objectively measure light intensity physical activity (LPA), moderate to vigorous physical activity (MVPA), screen based sedentary behavior (SSB) and sleep (SLP), durations in both groups. Data were analyzed using generalized estimating equations (GEE) and Mann-Whitney U tests. Results: The time, group and interaction effects of MVPA time and SLP time before and after intervention in two groups of primary school students were not statistically significant (Wald χ 2=1.54, 2.97, 0.85 ; 0.75, 1.05, 0.48), and the group effect of LPA time (Wald χ 2=1.24) and the time and group effects (Wald χ 2=3.02, 1.18 ) were not statistically significant (all P >0.05). There were statistically significant time and interaction effects for LPA time, as well as interaction effect for SSB time in two groups of primary school students before and after intervention (Wald χ 2=4.78, 3.95, 12.60, all P <0.05). After intervention, LPA time of intervention group [152.23(59.15, 245.80)min] was higher than that of control group [120.70(29.90, 201.20)min], and SSB time of intervention group [55.50(30.00, 125.50)min] was lower than that of control group [220.00(60.00, 285.00)min], with statistically significant differences ( Z =-2.46, -4.48, both P <0.05). Conclusion The school horticulture curriculum effectively enhances daily LPA and reduces SSB among third grade primary school students.

Chronic pain is a complex condition shaped by long-standing alterations in both physiological and psychological processes. Rather than representing a simple continuation of acute nociceptive signaling, chronic pain is increasingly understood as the outcome of progressive dysregulation within distributed neural systems that govern sensation, affect, motivation, and cognitive control. Neuroimaging and electrophysiological studies indicate that this state is accompanied by extensive plastic changes in deep brain structures and large-scale networks. Beyond well-described central sensitization processes, chronic pain is characterized by disrupted oscillatory rhythms and altered connectivity within large-scale brain networks, including thalamo-cortical circuits and prefrontal-limbic-reward networks. These findings support a conceptual shift from viewing chronic pain as a focal, lesion-driven phenomenon toward recognizing it as a disorder of distributed network pathology. Pharmacological treatments remain central to clinical practice, yet their long-term efficacy is often limited and frequently accompanied by substantial side effects. The ongoing concerns about opioid-related risks and the inadequate therapeutic response in a subset of patients highlight the need for safe, non-pharmacological approaches that can address not only pain but also comorbid disturbances in mood, sleep, and social functioning. Neuromodulation provides a promising path toward mechanism-based and non-pharmacological management of chronic pain by employing physical or chemical stimulation to alter the excitability and synchrony of specific neural populations within central, peripheral, and autonomic systems. While invasive deep brain stimulation demonstrates that targeting deep brain structures can be effective, its clinical application is restricted by surgical risks and cost, highlighting the importance of non-invasive techniques capable of reaching deep targets. Current non-invasive approaches, such as transcranial electric stimulation, are constrained by limited penetration depth and insufficient spatial precision. These limitations hinder reliable engagement of deep regions implicated in pain, including the thalamus and nucleus accumbens, and tend to produce broad, non-specific modulation of cross-network oscillatory activity. Temporal interference (TI) stimulation has emerged as a means of overcoming these obstacles. By delivering interacting high-frequency currents that generate a low-frequency envelope within the head, TI enables focal stimulation of deep targets while minimizing superficial current delivery. Recent multiscale modeling and animal studies indicate that TI exploits the nonlinear rectification properties of neuronal membranes in response to high-frequency carriers, as well as their phase-locked responses to low-frequency envelopes, to generate “peak-focused” electric fields in deep regions under relatively low superficial current loads. Moreover, TI appears to exhibit potential advantages in terms of cell-type selectivity and rhythm-specific engagement, including differential responses across neuronal subtypes and distinct coupling to θ-, β-, and γ-band oscillations. These features suggest a promising avenue for correcting abnormal rhythms and network dynamics that contribute to chronic pain. This review summarizes current knowledge of the neural mechanisms underlying chronic pain and recent advances in TI research. It examines functional disturbances across key pain-related regions and networks, outlines the principles and technical characteristics of TI, and discusses potential deep-brain targets and stimulation strategies relevant to chronic pain. Evidence to date indicates that TI, with its non-invasiveness, tolerability, and capacity for precise deep brain modulation, holds great promise for the management of treatment-resistant chronic pain and may evolve into a new generation of precise and efficient non-pharmacological analgesic strategies.

Chronic pain is a complex condition shaped by long-standing alterations in both physiological and psychological processes. Rather than representing a simple continuation of acute nociceptive signaling, chronic pain is increasingly understood as the outcome of progressive dysregulation within distributed neural systems that govern sensation, affect, motivation, and cognitive control. Neuroimaging and electrophysiological studies indicate that this state is accompanied by extensive plastic changes in deep brain structures and large-scale networks. Beyond well-described central sensitization processes, chronic pain is characterized by disrupted oscillatory rhythms and altered connectivity within large-scale brain networks, including thalamo-cortical circuits and prefrontal-limbic-reward networks. These findings support a conceptual shift from viewing chronic pain as a focal, lesion-driven phenomenon toward recognizing it as a disorder of distributed network pathology. Pharmacological treatments remain central to clinical practice, yet their long-term efficacy is often limited and frequently accompanied by substantial side effects. The ongoing concerns about opioid-related risks and the inadequate therapeutic response in a subset of patients highlight the need for safe, non-pharmacological approaches that can address not only pain but also comorbid disturbances in mood, sleep, and social functioning. Neuromodulation provides a promising path toward mechanism-based and non-pharmacological management of chronic pain by employing physical or chemical stimulation to alter the excitability and synchrony of specific neural populations within central, peripheral, and autonomic systems. While invasive deep brain stimulation demonstrates that targeting deep brain structures can be effective, its clinical application is restricted by surgical risks and cost, highlighting the importance of non-invasive techniques capable of reaching deep targets. Current non-invasive approaches, such as transcranial electric stimulation, are constrained by limited penetration depth and insufficient spatial precision. These limitations hinder reliable engagement of deep regions implicated in pain, including the thalamus and nucleus accumbens, and tend to produce broad, non-specific modulation of cross-network oscillatory activity. Temporal interference (TI) stimulation has emerged as a means of overcoming these obstacles. By delivering interacting high-frequency currents that generate a low-frequency envelope within the head, TI enables focal stimulation of deep targets while minimizing superficial current delivery. Recent multiscale modeling and animal studies indicate that TI exploits the nonlinear rectification properties of neuronal membranes in response to high-frequency carriers, as well as their phase-locked responses to low-frequency envelopes, to generate “peak-focused” electric fields in deep regions under relatively low superficial current loads. Moreover, TI appears to exhibit potential advantages in terms of cell-type selectivity and rhythm-specific engagement, including differential responses across neuronal subtypes and distinct coupling to θ-, β-, and γ-band oscillations. These features suggest a promising avenue for correcting abnormal rhythms and network dynamics that contribute to chronic pain. This review summarizes current knowledge of the neural mechanisms underlying chronic pain and recent advances in TI research. It examines functional disturbances across key pain-related regions and networks, outlines the principles and technical characteristics of TI, and discusses potential deep-brain targets and stimulation strategies relevant to chronic pain. Evidence to date indicates that TI, with its non-invasiveness, tolerability, and capacity for precise deep brain modulation, holds great promise for the management of treatment-resistant chronic pain and may evolve into a new generation of precise and efficient non-pharmacological analgesic strategies.

BACKGROUND:Types II,IIA,and III of Hangman fractures often require surgical treatment,and the selection of surgical methods is controversial.Current surgeries have shortcomings such as incomplete reduction and malunion after surgery.In the early stage,our team used C2-3 lag screws combined with a bucking bar.Intermittent pushing of the C2 vertebral body in the oropharynx has achieved satisfactory clinical results.However,the preliminary studies included few samples and lacked a control group for comparison. OBJECTIVE:To compare the clinical efficacy of posterior C2-3 fixation combined with the bucking bar technique and posterior C2-3 fixation alone in the treatment of unstable Hangman fractures. METHODS:The clinical and imaging data of 55 patients with unstable Hangman fractures who underwent posterior C2-3 internal fixation in Affiliated Hospital of Southwest Medical University were retrospectively analyzed.According to the surgical plan,the patients were divided into two groups.Among them,23 patients received posterior cervical C2-3 internal fixation combined with the bucking bar technique(group A),and 32 patients received simple posterior C2-3 internal fixation(group B).Operation time,intraoperative blood loss,complications,pain visual analog scale score,neck disability index,American Spinal Injury Association classification,and patient satisfaction(Odom's classification)preoperation and during follow-up were compared between the two groups.The changes in C2-3 displacement and angulation and other imaging indicators were compared at each observation time point. RESULTS AND CONCLUSION:(1)There was no statistically significant difference in operation time,intraoperative blood loss,and postoperative complications between the two groups(P>0.05).(2)The neck pain visual analog scale and neck disability index scores of the two groups of patients at the final follow-up were significantly improved compared with those before surgery(P<0.05).The Odom standard classification showed that 21 cases(91%)in group A were excellent and 29 cases(91%)were excellent and good in group B.There was no statistically significant difference in the clinical efficacy indicators between the two groups(all P>0.05).(3)There was no significant difference in C2-3 angulation and displacement between the two groups before operation(P>0.05).Postoperation and at the last follow-up,the angle and displacement of C2-3 in both groups were significantly smaller than before surgery,and the difference was statistically significant(P<0.01).There was no statistically significant difference in the above indicators after surgery and at the last follow-up(P>0.05).After surgery and at the last follow-up,the displacement and angle of C2-3 in group A were significantly smaller than those in group B(P<0.05).(4)At the last follow-up,no patients in group A had residual deformity,and 4 cases(13%,4/32)in group B had residual deformity.(5)Therefore,posterior C2-3 fixation combined with transoral bucking bar technology may be beneficial to the reduction and stabilization of the vertebral body,reduces malunion,and can achieve better reduction.

Objective To retrospectively analyze the distribution and differences of oral behavior among patients with acute and chro-nic painassociated with temporomandibular disorders(TMD).Methods A total of 212 patients with pain TMD in West China Hospital of Stomatology completed oral behaviors checklist(OBC).SPSS statistical software was used to analyze all the data.Results The pa-tients with pain-related TMD had specific oral behaviors,such as"pressure on the jaw during sleep"(49.5%),"unilateral chewing"(49.5%),"upper and lower teeth contact when not eating"(37.7%),etc.Scores of"upper and lower teeth contact when not eating"and"muscle tension when teeth are not clenched or teeth are not in contact"in patients with chronic pain TMD were higher than those of acute patients,and the difference was statistically significant(P＜0.05).The total OBC scores and daytime OBC scores of chronic pain TMD patients were higher than those of acute pain patients,and the difference was statistically significant(P＜0.05).There was no significant difference in OBC scores of patients with acute and chronic pain TMD during sleep(P＞0.05).Conclusion Pain-related TMD patients had specific oral behaviors,and patients with chronic pain TMD exhibited higher levels of total OBC,daytime OBC,"upper and lower teeth contact when not eating"and"muscle tension when teeth do not bite or teeth are not in contact"oral behavior than acute pain TMD patients.In the treatment of patients with painful TMD,correcting the patient's bad oral behavior can help the treatment of pain-related TMD.

Aim To explore the mechanism by which dioscin regulates IL-17+γδT cells in the treatment of arthritis.Methods A collagen-induced arthritis(CIA)model was established in DBA/1 mice using bovine type Ⅱ collagen.The mice were randomly divid-ed into the CIA model group,methotrexate(MTX)positive control group,and dioscin low-dose(Dioscin-L),medium-dose(Dioscin-M),and high-dose(Dios-cin-H)groups.After intervention,the therapeutic effects were evaluated using scoring methods.Joint pathological damage was analyzed by hematoxylin and eosin(HE)staining.The levels of anti-collagen-spe-cific antibodies and the pro-inflammatory cytokine IL-17 were measured by ELISA.The expressions of γδT cells and their subtypes,as well as the secretion level of IL-17,were detected by flow cytometry.Results Dioscin significantly reduced the arthritis severity score in collagen-induced arthritis(CIA)mice,alleviated joint pathological damage,inhibited the production of IL-17 by splenic lymphocytes and the levels of anti-col-lagen-specific antibodies total IgG and IgG3,and de-creased the proportion of γδT cells in the lymph nodes,splenic γδT cells,and the Vδ4+T-cell subset.The level of IL-17 produced by the Vδ4 subtype in the lymph nodes of the intervention groups was lower than that in the model group,but the difference was not sta-tistically significant.Conclusion Dioscin has signifi-cant therapeutic effect on CIA,and its mechanism may be through the inhibition of γδT cells,but it is unlikely to be related to IL-17 derived from γδT cells.

Objective To investigate the application effect of cold snare endoscopic mucosal resection(CS-EMR)in the treatment of 6 to 9 mm colorectal small polyps.Methods A total of 82 patients with small colonic polyps in our hospital from March 2022 to August 2023 were collected and divided into the observation group(45 cases received CS-EMR)and the control group[37 cases received hot snare endoscopic mucosal resection(HS-EMR)]according to different surgical methods.The clinical efficacy,polyp resection status,complete polyp resection rate,perioperative indicators and occurrence of complications were compared between the two groups.Results Follow-up for 1 month after operation,the effective rate of treatment in the observation group was higher than that in the control group(P<0.05).There was no statistically significant difference in the polyp resection status or perioperative indicators between the two groups(P>0.05).There was no statistically significant difference in the complete polyp resection rates of patients with different pathological types or total complete resection rate between the two groups(P>0.05).The incidence of delayed bleeding and endoscopic hemostasis rate in the observation group were lower than those in the control group(P<0.05).Conclusion The complete resection rate of 6～9 mm colorectal polyps through CS-EMR was comparable to that of HS-EMR,and CS-EMR has a better efficacy and lower risk of perioperative bleeding,along with higher safety.

Objective To explore the correlation between serum hypoxia-inducible factor-1α(HIF-1α)levels and cerebral microbleeds(CMBs)and cognitive impairment and to assess the predictive value of HIF-1α for CSVD-related cognitive impairment.Methods A total of 104 patients with CSVD who attended the Department of Neurology,First Affiliated Hospital of Xinxiang Medical University from June 2022 to November 2023 were enrolled.All enrolled patients were subjected to basic statistics,cranial nuclear magnetic resonance examination,cognitive function assessment,and serum HIF-1α test,and the number and location of CMBs were counted.Based on the above data the enrolled patients were grouped.The correlation between HIF-1α and cognitive function and CMBs was studied the influencing factors of CMBs and cognitive impairment were analyzed,and the predictive value of HIF-1α on the occurrence of cognitive impairment was evaluated.Results There were statistically significant differences in HIF-1α levels and cognitive function among different CMBs groups.Serum HIF-1α levels were significantly negatively correlated with overall cognitive function,visuospatial and executive function,attention,and delayed recall,and serum HIF-1α was positively correlated with the number of CMBs.HIF-1α may be a risk factor for CMBs and cognitive impairment associated with CSVD,and serum HIF-1α has potential in predict the cognitive impairment caused by CSVD.Conclusion Serum levels of HIF-1α were associated with the number of CMB and CSVD-related cognitive impairment,and serum levels of HIF-1α may have a predictive value for CSVD-related cognitive impairment.

Aim To investigate the effect of tetrameth-ylpyrazine(TMP)on neuroinflammation after cerebral ischemia and hypoxia via mannose-binding lectin(MBL).Methods Patients diagnosed with ischaemic stroke at Shanxi Provincial People's Hospital were in-cluded in the study,and their clinicopathological data,as well as blood and urine samples,were collected with the consent of the patients and their families.Using these biological samples,differential proteins and tar-gets were identified by proteomic analysis and subse-quently verified with animal experiments.The mice were divided into the sham,dMCAO,and TMP(10,20,40 mg·kg-1)treatment groups.After seven days of drug administration,the modified neurological sever-ity score(mNSS)was used to assess the neurological function.TTC staining was used to detect the volume of cerebral infarction.Motor function was evaluated be-haviourally,and ELISA was used to detect MASP1,sC5b-9,TNF-α,IL-6,and IL-1β.Western blot was used to determine the expression of relevant proteins,such as MBL2,MASP2,and C3.Results Compared with the sham group,the dMCAO group exhibited in-creased neurological impairment,which was signifi-cantly ameliorated by TMP treatment.The expression levels of MBL2,C3 and MASP2 were elevated in the dMCAO group and were reduced following TMP treat-ment.Additionally,the dMCAO group showed elevat-ed expression of inflammatory factors IL-1 β,IL-6 and TNF-α,which were then suppressed by TMP treat-ment.Conclusion TMP inhibits the inflammatory re-sponse after ischemia and hypoxia by regulating MBL,thus attenuating brain injury.

Aim To explore the possible regulatory effect of leptin on acyl-CoA synthetase long chain fami-ly member ACSL5 and their effect on migration and in-vasion of breast cancer cell,and to explore the underly-ing mechanism.Methods The expression of leptin receptor was detected by immunofluorescence assay.The migration and invasion ability of MCF-7 cells were detected by wound healing assay and Transwell assay respectively.The downstream target gene of leptin was analyzed by PCR microarray data.The expression of ACSL5 in breast cancer and its correlation with the staging and prognosis of breast cancer patients were as-sessed uing bioinformatics methods.The expression of ACSL5 in MCF-7 cells treated with different concentra-tions of leptin was detected using real time fluorescence quantitative polymerase chain reaction(RT-qPCR).Overexpressing ACSL5 was constructed by lentiviral transfection;the expressions of EMT related proteins,AMPK-α and p-AMPK-α were detected by Western blot.Results Leptin promoted breast cancer cell mi-gration and invasion and EMT.ACSL5 was significant-ly low expressed in breast cancer and related to progno-sis.Leptin downregulated the expression of ACSL5 through OBR.Leptin activated AMPK pathway to downregulate ACSL5 and promote migration,invasion and EMT of breast cancer cells.Conclusions Leptin may promote the migration,invasion and EMT of breast cancer by downregulating ACSL5 through activating AMPK pathway.