OBJECTIVE To upgrade the drug traceability code management system for a pediatric hospital under the “payment by code” background， aiming to comprehensively enhance traceability integrity， efficiency， and compliance. METHODS Taking Xiamen Children’s Hospital as the implementation setting， a before-and-after control design was adopted to construct an intelligent drug traceability code management system through systematic upgrades involving the technology platform， core mechanisms， and coordination with medical insurance. Key interventions included： upgrading a traceability code management platform and designing a dynamic code pool； innovating differentiated traceability mechanisms for routine， split-dose， and special drugs； establishing a tiered early-warning and emergency response system； and constructing a data coordination and quality control system. The drug traceability code upload rate served as the primary outcome. Process indicators such as the root causes distribution of failed uploads and the duration of medication returns， and a comprehensive outcome （the number of insurance-flagged abnormal prescriptions） were also analyzed. The data between the baseline period （April 2025） and the observation period （June-August 2025） were compared and evaluated. RESULTS After the upgrade， the overall upload rate of drug traceability codes increased from 9.21% （baseline） to 99.86% （August 2025）. The upload rate of traceability codes in previously unmanaged areas， such as the inpatient pharmacy and pharmacy intravenous admixture services， soared from 0 to nearly 100%. The proportion of non-uploads due to system issues fell from 66.44% （June 2025） to 2.62% （August Additionally， the number of insurance-flagged） abnormal prescriptions dropped sharply from 2 275.00 in the first “payment by code” policy month （July 2025） to 212.00 by the end of the observation period （August 2025）， a 90.70% decrease. CONCLUSIONS The developed management system effectively addresses complex scenario challenges such as high-frequency drug splitting. It significantly enhances traceability code upload performance and ensures a high degree of compliance with medical insurance data requirements. These outcomes contribute to proactive risk mitigation against insurance claim denials and demonstrate a concurrent optimization of pharmacy operations.

Objective: Neuronal apoptosis is considered to be a critical process in spinal cord injury (SCI). Despite growing evidence of the antiapoptotic, anti-inflammatory, and modulation of ischemic injury tolerance effects of extracellular ubiquitin (eUb), existing studies have paid less attention to the impact of eUb in neurological injury disorders, particularly in SCI. This study aimed to investigate whether eUb can play a protective role in neurons, both in vitro and in vivo, and explores the underlying mechanisms. Methods: By utilizing an oxygen glucose deprivation cellular model and a SCI rat model, we firstly investigated the therapeutic effects of eUb on SCI and further explored its effects on neuronal autophagy and mitochondria-dependent apoptosis-related indicators, as well as the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mechanical target of rapamycin (mTOR) signaling pathway. Results: In the SCI models both in vivo and in vitro, early intervention with eUb enhanced neuronal autophagy and inhibited mitochondrial apoptotic pathways, significantly mitigating SCI. Further studies had shown that this protective effect of eUb was mediated through its receptor, CXC chemokine receptor type 4 (CXCR4). Additionally, eUb-enhanced autophagy and antiapoptotic effects were possibly associated with inhibiting the PI3K/Akt/mTOR pathway. Conclusion In summary, the study demonstrates that early eUb intervention can enhance autophagy and inhibit mitochondrial apoptotic pathways via CXCR4, protecting neurons and promoting SCI repair.

Objective: Neuronal apoptosis is considered to be a critical process in spinal cord injury (SCI). Despite growing evidence of the antiapoptotic, anti-inflammatory, and modulation of ischemic injury tolerance effects of extracellular ubiquitin (eUb), existing studies have paid less attention to the impact of eUb in neurological injury disorders, particularly in SCI. This study aimed to investigate whether eUb can play a protective role in neurons, both in vitro and in vivo, and explores the underlying mechanisms. Methods: By utilizing an oxygen glucose deprivation cellular model and a SCI rat model, we firstly investigated the therapeutic effects of eUb on SCI and further explored its effects on neuronal autophagy and mitochondria-dependent apoptosis-related indicators, as well as the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mechanical target of rapamycin (mTOR) signaling pathway. Results: In the SCI models both in vivo and in vitro, early intervention with eUb enhanced neuronal autophagy and inhibited mitochondrial apoptotic pathways, significantly mitigating SCI. Further studies had shown that this protective effect of eUb was mediated through its receptor, CXC chemokine receptor type 4 (CXCR4). Additionally, eUb-enhanced autophagy and antiapoptotic effects were possibly associated with inhibiting the PI3K/Akt/mTOR pathway. Conclusion In summary, the study demonstrates that early eUb intervention can enhance autophagy and inhibit mitochondrial apoptotic pathways via CXCR4, protecting neurons and promoting SCI repair.

Objective: Neuronal apoptosis is considered to be a critical process in spinal cord injury (SCI). Despite growing evidence of the antiapoptotic, anti-inflammatory, and modulation of ischemic injury tolerance effects of extracellular ubiquitin (eUb), existing studies have paid less attention to the impact of eUb in neurological injury disorders, particularly in SCI. This study aimed to investigate whether eUb can play a protective role in neurons, both in vitro and in vivo, and explores the underlying mechanisms. Methods: By utilizing an oxygen glucose deprivation cellular model and a SCI rat model, we firstly investigated the therapeutic effects of eUb on SCI and further explored its effects on neuronal autophagy and mitochondria-dependent apoptosis-related indicators, as well as the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mechanical target of rapamycin (mTOR) signaling pathway. Results: In the SCI models both in vivo and in vitro, early intervention with eUb enhanced neuronal autophagy and inhibited mitochondrial apoptotic pathways, significantly mitigating SCI. Further studies had shown that this protective effect of eUb was mediated through its receptor, CXC chemokine receptor type 4 (CXCR4). Additionally, eUb-enhanced autophagy and antiapoptotic effects were possibly associated with inhibiting the PI3K/Akt/mTOR pathway. Conclusion In summary, the study demonstrates that early eUb intervention can enhance autophagy and inhibit mitochondrial apoptotic pathways via CXCR4, protecting neurons and promoting SCI repair.

Objective: Neuronal apoptosis is considered to be a critical process in spinal cord injury (SCI). Despite growing evidence of the antiapoptotic, anti-inflammatory, and modulation of ischemic injury tolerance effects of extracellular ubiquitin (eUb), existing studies have paid less attention to the impact of eUb in neurological injury disorders, particularly in SCI. This study aimed to investigate whether eUb can play a protective role in neurons, both in vitro and in vivo, and explores the underlying mechanisms. Methods: By utilizing an oxygen glucose deprivation cellular model and a SCI rat model, we firstly investigated the therapeutic effects of eUb on SCI and further explored its effects on neuronal autophagy and mitochondria-dependent apoptosis-related indicators, as well as the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mechanical target of rapamycin (mTOR) signaling pathway. Results: In the SCI models both in vivo and in vitro, early intervention with eUb enhanced neuronal autophagy and inhibited mitochondrial apoptotic pathways, significantly mitigating SCI. Further studies had shown that this protective effect of eUb was mediated through its receptor, CXC chemokine receptor type 4 (CXCR4). Additionally, eUb-enhanced autophagy and antiapoptotic effects were possibly associated with inhibiting the PI3K/Akt/mTOR pathway. Conclusion In summary, the study demonstrates that early eUb intervention can enhance autophagy and inhibit mitochondrial apoptotic pathways via CXCR4, protecting neurons and promoting SCI repair.

Objective: Neuronal apoptosis is considered to be a critical process in spinal cord injury (SCI). Despite growing evidence of the antiapoptotic, anti-inflammatory, and modulation of ischemic injury tolerance effects of extracellular ubiquitin (eUb), existing studies have paid less attention to the impact of eUb in neurological injury disorders, particularly in SCI. This study aimed to investigate whether eUb can play a protective role in neurons, both in vitro and in vivo, and explores the underlying mechanisms. Methods: By utilizing an oxygen glucose deprivation cellular model and a SCI rat model, we firstly investigated the therapeutic effects of eUb on SCI and further explored its effects on neuronal autophagy and mitochondria-dependent apoptosis-related indicators, as well as the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mechanical target of rapamycin (mTOR) signaling pathway. Results: In the SCI models both in vivo and in vitro, early intervention with eUb enhanced neuronal autophagy and inhibited mitochondrial apoptotic pathways, significantly mitigating SCI. Further studies had shown that this protective effect of eUb was mediated through its receptor, CXC chemokine receptor type 4 (CXCR4). Additionally, eUb-enhanced autophagy and antiapoptotic effects were possibly associated with inhibiting the PI3K/Akt/mTOR pathway. Conclusion In summary, the study demonstrates that early eUb intervention can enhance autophagy and inhibit mitochondrial apoptotic pathways via CXCR4, protecting neurons and promoting SCI repair.

Objective:To observe the effects of Alpiniae Oxyphyllae Fructus-Linderae Radix on miR-155-5p/SOCS1/inflammatory factor axis and cell apoptosis in hippocampus of depressed rats.Methods:A total of 60 SPF male Wistar rats were divided into six groups: control group, model group, fluoxetine group and Alpiniae Oxyphyllae Fructus-Linderae Radix low-, middle- and high-dosage groups, with 10 rats in each group. Except for the control group, all other groups used chronic mild unpredictable stimuli combined with solitary confinement to construct a depression rat model. Following an 8-week modeling period, the fluoxetine group received oral administration of 2 mg/kg Fluoxetine liquid daily and the Alpiniae Oxyphyllae Fructus-Linderae Radix groups received oral administration of 1 g/kg, 2 g/kg and 4 g/kg Alpiniae Oxyphyllae Fructus-Linderae Radix liquid daily, whereas the control group and model group were given an equivalent volume of distilled water for continuous drug intervention over a span of 3 weeks. The rats' behavioral variations were assessed through an open field test; miR-155-5p expression in the hippocampus was determined via RT-PCR; SOCS1 protein expression in the hippocampus was evaluated by Western Blot; TNF-α, IL-6 and IL-1β levels in the serum were quantified using ELISA; hippocampal cell apoptosis was examined through HE staining.Results:Compared with the model group, the fluoxetine group and Alpiniae Oxyphyllae Fructus-Linderae Radix middle- and high-dosage groups showed an increase in open field test scores ( P<0.05), a decrease in miR-155-5p expression in the hippocampus ( P<0.05), an increase in SOCS1 protein expression in the hippocampus ( P<0.05), a decrease in serum TNF-α, IL-1β, IL-6 levels ( P<0.05), and a reduction in apoptosis of hippocampal CA3 cells ( P<0.05). Conclusion:Alpiniae Oxyphyllae Fructus-Linderae Radix probably amplifies the indirect negative regulation of SOCS1 protein on inflammatory factors by suppressing miR-155-p expression in the hippocampus of depressed rats, thereby ameliorating cell apoptosis in the hippocampal area and manifesting antidepressant properties.

Objective To evaluate the clinical efficacy of Long's spinal manipulation therapy combined with four postures of rotational tendon-releasing maneuver in treating lumbar disc herniation(LDH).Methods Sixty-eight patients diagnosed with LDH were enrolled from the Department of Acupuncture and Rehabilitation at Guangdong Second Traditional Chinese Medicine Hospital between July 2024 and December 2024.Patients were randomly divided into an observation group and a control group using a random number table,with 34 cases in each group.The control group received Long's spinal manipulation therapy,while the observation group received additional training in four postures of rotational tendon-releasing maneuver.Both groups were treated for 2 weeks,with a 1-month follow-up.Clinical efficacy was evaluated after treatment by comparing Visual Analogue Scale(VAS)scores,Oswestry Disability Index(ODI)scores,and Japanese Orthopaedic Association(JOA)scores before and after intervention.Spinal parameters including maximum lumbar curvature angle,pelvic tilt angle,and maximum vertebral rotation angle were assessed using the DIERS formetric 3D evaluation system.Results(1)The total effective rate was 94.12%(32/34)in the observation group and 91.18%(31/34)in the control group,and both groups achieved ideal therapeutic efficacy,but the difference was not statistically significant(P＞0.05).(2)After treatment,the VAS scores of patients in the two groups significantly improved(P＜0.05),and the observation group was significantly superior to the control group in improving VAS scores,with statistically significant differences(P＜0.05).At the 1-month follow-up after treatment,the VAS score of the observation group significantly improved(P＜0.05),and the observation group was significantly superior to the control group,and the difference was statistically significant(P＜0.05).(3)After treatment,the JOA and ODI scores of the patients in the two groups significantly improved(P＜0.05),and the observation group was significantly superior to the control group in improving the JOA and ODI scores,and the difference was statistically significant(P＜0.05).At 1-month follow-up after treatment,JOA and ODI scores of the observation group significantly improved(P＜0.05),and the observation group was significantly superior to the control group,with statistically significant differences(P＜0.05).(4)After treatment,the maximum angle of lumbar flexion,pelvic torsion angle,and maximum rotation angle of the vertebral body of the two groups of patients were significantly improved(P＜0.05),and the observation group was significantly better than the control group,and the difference was statistically significant(P＜0.05).At the 1-month follow-up after treatment,the maximum angle of lumbar flexion,pelvic torsion angle,and maximum vertebral rotation angle of the observation group were significantly improved(P＜0.05),and the observation group was significantly superior to the control group,and the difference was statistically significant(P＜0.05).Conclusion The combination of Long's spinal manipulation therapy and four postures of rotational tendon-releasing maneuve significantly improves spinal alignment,reduces pain and disability,and enhances quality of life in patients with LDH,demonstrating notable clinical efficacy.

Objective To analyze acupoint selection law of Professor Fu Wenbin in using acupuncture for the treatment of insomnia based on data mining technology;To provide references for the formulation and optimization of clinical treatment plans.Methods The cases of insomnia treated by acupuncture in the Acupuncture and Moxibustion Department of Guangdong Provincial Hospital of Traditional Chinese Medicine from January 1,2020 to December 31,2021 and in the Acupuncture and Moxibustion Department of Shenzhen Bao'an Hospital of Traditional Chinese Medicine from August 1,2018 to December 31,2021 were collected.A database of prescription information for acupuncture treatment for insomnia was established.The law of acupoint selection frequency,meridians,specific acupoints,correlation analysis and hidden structure analysis for acupuncture treatment of insomnia was mined.Results A total of 517 prescriptions were collected.Acupoints were mainly taken from Baihui(DU20,516 times),Yintang(DU29,499 times),Zhongwan(RN12,482 times)and Taichong(LR3,410 times),and meridians were mainly from Conception Vessel(2 120 times,11 acupoints),Governor Vessel(1 074 times,5 acupoints),liver meridian(410 times,1 acupoint),stomach meridian(401 times,8 acupoints)and kidney meridian(300 times,6 acupoints).The main specific acupoints were the Jiaohui(2 723 times,20 acupoints),Mu(892 times,4 acupoints),and Yuan(746 times,8 acupoints).The core acupoint combination based on Zhongwan-Baihui,Yintang(RN12-DU20-DU29)was formed by the correlation analysis of high-frequency acupoints,and the hidden structure of high-frequency acupoints was analyzed to obtain four comprehensive clustering models corresponding to the evidence of heart-kidney disharmony,liver depression and kidney deficiency,liver depression and kidney deficiency,and heart and gallbladder dysregulation.Conclusion Professor Fu Wenbin uses acupuncture to treat insomnia,with balancing yin and yang,regulating Conception Vessel and Conception Vessel as the basic treatment principle,dredging the liver to regulate the spirit,harmonizing the stomach to calm the spirit,communicating with the heart and kidney,and treating the heart and gallbladder as the treatment method.