ObjectiveThis paper aims to investigate and evaluate the staged efficacy and safety of the representative empirical prescription of the “Zhu Ke Jiao” theory， Qijia Rougan prescription， combined with entecavir in the treatment of hepatic fibrosis in chronic hepatitis B. MethodsA multicenter randomized controlled clinical study was conducted， and 101 patients diagnosed with chronic hepatitis B-related hepatic fibrosis （CHB-HF） who met the diagnosis and inclusion criteria were randomly assigned to an observation group （Qijia Rougan prescription + entecavir） and a control group （entecavir）. The treatment duration was 24 weeks. Liver stiffness measurement （LSM）， fibrosis-4 index （FIB-4）， portal vein diameter， hepatitis B serology， biochemical indicators， hepatic fibrosis markers in serum ［hyaluronic acid （HA）， laminin （LN）， procollagen Ⅲ peptide （PⅢP）， and type Ⅳ collagen （Ⅳ-C）］， and traditional Chinese medicine syndrome scores were used as efficacy evaluation indicators. Efficacy assessments and explorations of different staged subgroups of Qijia Rougan prescription were conducted according to LSM values based on the Metavir pathological staging standard. ResultsA total of 98 cases were included for statistical analysis， with 49 cases in the observation group and 49 in the control group. The general data of the patients in both groups were comparable. Compared with the same group before treatment， the observation group showed a significant reduction in LSM and FIB-4 （P<0.01）， as well as notable improvements in LN， Ⅳ-C， and various TCM syndrome scores （P<0.05， P<0.01）. When compared to the control group after treatment， the observation group demonstrated significant improvements in LSM， FIB-4， and various TCM syndrome score indicators （P<0.05， P<0.01）， indicating that the observation group performed better than the control group. Subgroup analysis of the regression of hepatic fibrosis stages showed that compared to the same group before treatment， the observation group had better improvement in regression of stages F2 and F3 （P<0.05）. When compared to the control group after treatment， the observation group exhibited superior improvement in regression of stage F3 （P<0.05）. No adverse events occurred in either group during the treatment period. ConclusionCompared with entecavir alone， the combination of Qijia Rougan prescription and entecavir significantly improves the degree of hepatic fibrosis and clinical TCM symptoms in patients. The optimal intervention period is primarily during stage F3， which is a potential “interception” point of the “Zhu Ke Jiao” theory.

OBJECTIVE: To investigate the relationship between physical activity and genetic risk and their combined effects on the risk of developing chronic obstructive pulmonary disease. METHODS: This prospective cohort study included 318,085 biobank participants from the UK. Physical activity was assessed using the short form of the International Physical Activity Questionnaire. The participants were stratified into low-, intermediate-, and high-genetic-risk groups based on their polygenic risk scores. Multivariate Cox regression models and multiplicative interaction analyses were used. RESULTS: During a median follow-up period of 13 years, 9,209 participants were diagnosed with chronic obstructive pulmonary disease. For low genetic risk, compared to low physical activity, the hazard ratios ( HRs) for moderate and high physical activity were 0.853 (95% confidence interval [ CI]: 0.748-0.972) and 0.831 (95% CI: 0.727-0.950), respectively. For intermediate genetic risk, the HRs were 0.829 (95% CI: 0.758-0.905) and 0.835 (95% CI: 0.764-0.914), respectively. For participants with high genetic risk, the HRs were 0.809 (95% CI: 0.746-0.877) and 0.818 (95% CI: 0.754-0.888), respectively. A significant interaction was observed between genetic risk and physical activity. CONCLUSION Moderate or high levels of physical activity were associated with a lower risk of developing chronic obstructive pulmonary disease across all genetic risk groups, highlighting the need to tailor activity interventions for genetically susceptible individuals.
Humans ; Pulmonary Disease, Chronic Obstructive/epidemiology* ; Exercise ; Male ; Female ; Middle Aged ; Prospective Studies ; Aged ; Genetic Predisposition to Disease ; Risk Factors ; United Kingdom/epidemiology* ; Incidence ; Adult

[This corrects the article DOI: 10.11909/j.issn.1671-5411.2017.08.005.].

OBJECTIVE: To investigate the effects of acupuncture on the neurotransmitter levels and gut microbiota in a mouse model of Tourette syndrome (TS). METHODS: Thirty-six male C57/BL6 mice were randomly divided into 4 groups using a random number table method: 3,3'-iminodipropionitrile (IDPN) group, control group, acupuncture group, and tiapride group, with 9 mice in each group. In the IDPN group, acupuncture group, and tiapride group, mice received daily intraperitoneal injections of IDPN (300 mg/kg body weight) for 7 consecutive days to induce stereotyped behaviors. Subsequently, in the acupuncture intervention group, standardized acupuncture treatment was administered for 14 consecutive days to IDPN-induced TS model mice. The selected acupoints included Baihui (DU 20), Yintang (DU 29), Waiguan (SJ 5), and Zulinqi (GB 41). In the tiapride group, mice were administered tiapride (50 mg/kg body weight) via oral gavage daily for 14 consecutive days. The control group, IDPN group, and acupuncture group received the same volume of saline orally for 14 consecutive days. Stereotypic behaviors were quantified through behavioral assessments. Neurotransmitter levels, including dopamine (DA), glutamate (Glu), and aspartate (ASP) in striatal tissue were measured using enzyme-linked immunosorbent assay. Dopamine transporter (DAT) expression levels were additionally quantified through quantitative polymerase chain reaction (qPCR). Gut microbial composition was analyzed through 16S ribosomal RNA gene sequencing, while metabolic profiling was conducted using liquid chromatography-mass spectrometry (LC-MS). RESULTS: Acupuncture administration significantly attenuated stereotypic behaviors, concurrently reducing striatal levels of DA, Glu and ASP concentrations while upregulating DAT expression compared with untreated TS controls (P<0.05 or P<0.01). Comparative analysis identified significant differences in Muribaculaceae (P=0.001), Oscillospiraceae (P=0.049), Desulfovibrionaceae (P=0.001), and Marinifilaceae (P=0.014) following acupuncture intervention. Metabolomic profiling revealed alterations in 7 metabolites and 18 metabolic pathways when compared to the TS mice, which involved various amino acid metabolisms associated with DA, Glu, and ASP. CONCLUSIONS Acupuncture demonstrates significant modulatory effects on both central neurotransmitter systems and gut microbial ecology, thereby highlighting its dual therapeutic potential for TS management through gut-brain axis regulation.
Animals ; Tourette Syndrome/metabolism* ; Gastrointestinal Microbiome ; Neurotransmitter Agents/metabolism* ; Acupuncture Therapy ; Male ; Mice, Inbred C57BL ; Mice

Objective: In the present study, we compare the influence of oxidized lipoprotein(a) [Lp(a)] and unoxidized Lp(a) on plasminogen activation in the process of fibrinolysis and elucidate the potential atherogenic mechanisms of oxidized Lp(a), focusing on its role in thrombosis. Methods: Chromogenic substrate assays were conducted to study the kinetics of plasminogen activation. Fibrin clots were generated by incubating fibrinogen with thrombin, and plasminogen activation was triggered with tissue plasminogen activator (tPA). Experiments were performed in low and high concentrations of Lp(a) or oxidized Lp(a) to evaluate their respective effects on plasmin generation. Oxidized Lp(a) was prepared by chemical oxidation of isolated Lp(a) samples. Results: Low concentrations of Lp(a) enhanced plasminogen activation and fibrinolysis, reflecting its physiological role. However, at higher concentrations, oxidized Lp(a) exhibited a significant inhibitory effect on plasminogen activation. Compared to unoxidized Lp(a), oxidized Lp(a) led to earlier plateauing of plasmin generation and reduced overall plasmin levels. The inhibitory effects of oxidized Lp(a) are likely due to its structural similarity to plasminogen and higher oxidized phospholipid content, which competes with plasminogen for fibrin binding—the enhanced competition with fibrin fragments and tPA by oxidized Lp(a) further impaired fibrinolysis. Conclusion This study demonstrates that while low levels of Lp(a) may support fibrinolysis, oxidized Lp(a) impairs this process by inhibiting plasminogen activation through structural and functional competition. These findings highlight the atherogenic potential of oxidized Lp(a) and its contribution to thrombotic cardiovascular risk.

Objective: In the present study, we compare the influence of oxidized lipoprotein(a) [Lp(a)] and unoxidized Lp(a) on plasminogen activation in the process of fibrinolysis and elucidate the potential atherogenic mechanisms of oxidized Lp(a), focusing on its role in thrombosis. Methods: Chromogenic substrate assays were conducted to study the kinetics of plasminogen activation. Fibrin clots were generated by incubating fibrinogen with thrombin, and plasminogen activation was triggered with tissue plasminogen activator (tPA). Experiments were performed in low and high concentrations of Lp(a) or oxidized Lp(a) to evaluate their respective effects on plasmin generation. Oxidized Lp(a) was prepared by chemical oxidation of isolated Lp(a) samples. Results: Low concentrations of Lp(a) enhanced plasminogen activation and fibrinolysis, reflecting its physiological role. However, at higher concentrations, oxidized Lp(a) exhibited a significant inhibitory effect on plasminogen activation. Compared to unoxidized Lp(a), oxidized Lp(a) led to earlier plateauing of plasmin generation and reduced overall plasmin levels. The inhibitory effects of oxidized Lp(a) are likely due to its structural similarity to plasminogen and higher oxidized phospholipid content, which competes with plasminogen for fibrin binding—the enhanced competition with fibrin fragments and tPA by oxidized Lp(a) further impaired fibrinolysis. Conclusion This study demonstrates that while low levels of Lp(a) may support fibrinolysis, oxidized Lp(a) impairs this process by inhibiting plasminogen activation through structural and functional competition. These findings highlight the atherogenic potential of oxidized Lp(a) and its contribution to thrombotic cardiovascular risk.

Objective: In the present study, we compare the influence of oxidized lipoprotein(a) [Lp(a)] and unoxidized Lp(a) on plasminogen activation in the process of fibrinolysis and elucidate the potential atherogenic mechanisms of oxidized Lp(a), focusing on its role in thrombosis. Methods: Chromogenic substrate assays were conducted to study the kinetics of plasminogen activation. Fibrin clots were generated by incubating fibrinogen with thrombin, and plasminogen activation was triggered with tissue plasminogen activator (tPA). Experiments were performed in low and high concentrations of Lp(a) or oxidized Lp(a) to evaluate their respective effects on plasmin generation. Oxidized Lp(a) was prepared by chemical oxidation of isolated Lp(a) samples. Results: Low concentrations of Lp(a) enhanced plasminogen activation and fibrinolysis, reflecting its physiological role. However, at higher concentrations, oxidized Lp(a) exhibited a significant inhibitory effect on plasminogen activation. Compared to unoxidized Lp(a), oxidized Lp(a) led to earlier plateauing of plasmin generation and reduced overall plasmin levels. The inhibitory effects of oxidized Lp(a) are likely due to its structural similarity to plasminogen and higher oxidized phospholipid content, which competes with plasminogen for fibrin binding—the enhanced competition with fibrin fragments and tPA by oxidized Lp(a) further impaired fibrinolysis. Conclusion This study demonstrates that while low levels of Lp(a) may support fibrinolysis, oxidized Lp(a) impairs this process by inhibiting plasminogen activation through structural and functional competition. These findings highlight the atherogenic potential of oxidized Lp(a) and its contribution to thrombotic cardiovascular risk.

Objective: In the present study, we compare the influence of oxidized lipoprotein(a) [Lp(a)] and unoxidized Lp(a) on plasminogen activation in the process of fibrinolysis and elucidate the potential atherogenic mechanisms of oxidized Lp(a), focusing on its role in thrombosis. Methods: Chromogenic substrate assays were conducted to study the kinetics of plasminogen activation. Fibrin clots were generated by incubating fibrinogen with thrombin, and plasminogen activation was triggered with tissue plasminogen activator (tPA). Experiments were performed in low and high concentrations of Lp(a) or oxidized Lp(a) to evaluate their respective effects on plasmin generation. Oxidized Lp(a) was prepared by chemical oxidation of isolated Lp(a) samples. Results: Low concentrations of Lp(a) enhanced plasminogen activation and fibrinolysis, reflecting its physiological role. However, at higher concentrations, oxidized Lp(a) exhibited a significant inhibitory effect on plasminogen activation. Compared to unoxidized Lp(a), oxidized Lp(a) led to earlier plateauing of plasmin generation and reduced overall plasmin levels. The inhibitory effects of oxidized Lp(a) are likely due to its structural similarity to plasminogen and higher oxidized phospholipid content, which competes with plasminogen for fibrin binding—the enhanced competition with fibrin fragments and tPA by oxidized Lp(a) further impaired fibrinolysis. Conclusion This study demonstrates that while low levels of Lp(a) may support fibrinolysis, oxidized Lp(a) impairs this process by inhibiting plasminogen activation through structural and functional competition. These findings highlight the atherogenic potential of oxidized Lp(a) and its contribution to thrombotic cardiovascular risk.

OBJECTIVE: To investigate the short-and med-term clinical efficacy of unicompartmental knee arthroplasty(UKA)for the treatment of medial knee osteoarthritis (OA) in elderly patients with anterior cruciate ligament deficiency(ACLD). METHODS: A retrospective analysis was conducted on 31 patients aged over 75 years old with primary medial knee OA and ACLD who underwent UKA between January 2018 and December 2022. The cohort included 12 males and 19 females, aged from 75 to 91 years with an average age of (79.56±4.54) years, with 13 left knee, 16 right knee, and 2 bilateral knees. Clinical outcomes were assessed preoperatively and at final follow-up using the visual analogue scale (VAS), Hospital for Special Surgery(HSS) score, range of motion (ROM), hip-knee-ankle angle (HKA), and tibial component posterior slope angle (TCPSA). Complications such as infection, prosthesis wear, prosthesis loosening, and dislocation were also recorded. RESULTS: All 31 patients were followed up from 12 to 63 months with an average of (28.34±10.56) months. The average postoperative TCPSA was (4.83±1.31)° ranged from 2.5° to 6.8°. At the final follow-up, there was significant improvement in VAS (3.24±0.53) vs. (6.59±0.69), HSS score (85.19±4.45) vs. (64.38±5.94), ROM (118.83±5.38)° vs. (98.85±4.08)°, and HKA (176.83±5.16)° vs. (169.57±6.28)° compared to preoperative values (P<0.05). No cases of infection, prosthesis loosening, or dislocation were reported. CONCLUSION UKA provides favorable short-and mid-term outcomes for elderly patients with medial knee OA and ACLD . However, long-term clinical efficacy needs further investigation through extended follow-up.
Humans ; Male ; Female ; Arthroplasty, Replacement, Knee/methods* ; Aged ; Osteoarthritis, Knee/physiopathology* ; Retrospective Studies ; Aged, 80 and over ; Range of Motion, Articular ; Anterior Cruciate Ligament Injuries/surgery*

Objective:To analyze the factors associated with non-radiographic bone erosion in gout pa-tients,to improve the understanding of bone erosion in gout,and to promote the early detection of bone erosion.Methods:A retrospective analysis was conducted on the medical records of gout patients treated at Beijing Jishuitan Hospital from January 2018 to January 2022.Bone erosion was detectable by ultra-sound but not detected by X-ray as non-radiographic bone erosion;no bone erosion was detected by both ultrasound and joint X-ray as undetected bone erosion.A case-control study was used,and the two groups were matched 1∶2 according to age and sex.The differences between the two groups were com-pared in terms of general information,joint involvement characteristics,laboratory indicators and compli-cations.In the univariate analysis,P＜0.1 was included in the multivariate analysis,and the conditional Logistic regression was used for the multivariate analysis.P＜0.05 was considered to have statistically significant differences.Results:Among the 41 patients with non-radiographic bone erosion,the top three joints with bone erosion before its occurrence were metatarsophalangeal joint(12 cases),ankle(10 ca-ses),and knee(7 cases).There were 82 patients undetected with bone erosion.There were no signifi-cant differences in general information between the two groups(P＞0.05),including age,gender,body mass index,and alcohol consumption history.The characteristics of affected joints in the non-radio-graphic bone erosion group were compared with those in the no bone erosion detected,and the former had more affected joints(P=0.02),and a higher proportion of patients with at least 3 attacks of gout per year(P＜0.001).There were no significant differences in serum uric acid,fasting blood glucose,cholesterol,triglycerides,low-density lipoprotein,high-density lipoprotein,creatinine,homocysteine,white blood cell count,and urine pH between the two groups(P＞0.05).The results of multivariate analysis showed that at least 3 flares of gout per year was an independent risk factor for radiologically negative bone erosion in patients with gout,with an OR(95％CI)of 5.139(1.529-17.271).Conclusion:At least 3 flares of gout per year predicts the occurrence of radiologically negative bone erosion,and these patients should be given more attention to achieving treatment targets.