Background Aluminum (Al) is a lightweight metal that is widely present in the environment and the human body. It has been documented to cause various adverse health effects including the suppression of humoral immunity. Objective To investigate the role of oxidative stress in Al-induced humoral immunity suppression and to evaluate the possible protective effects of iron supplementation on this process. Methods Adult C57BL/6J mice were exposed to Al at concentrations of 0, 200, or 800 μg·mL⁻¹ via drinking water for three consecutive months. The expression of major histocompatibility complex class Ⅱ (I-A), proliferating cell markr-67 (Ki-67), and 2',7'-dichlorodihydrofluorescein diacetate (DCFH-DA) in splenic B cells was evaluated through flow cytometry. Splenic B cells from the mice treated with 800 μg·mL⁻¹ Al or the control were sorted and treated in vitro with glutathione (GSH), N-Acetyl-L-cysteine (NAC), or a control vehicle. After 24 h, the expression of I-A was evaluated; and the hydroxyl radical (·OH)-generating potential, ·OH production, malondialdehyde (MDA) production, and iron content were assessed using commercial kits. Sixteen mice treated with 800 μg·mL⁻¹ Al received an intravenous injection of either a ferric chloride solution containing 0.3 g·L⁻¹ iron or a 0.9% sodium chloride solution, while eight control mice received 0.9% sodium chloride solution; the injection volume was 0.1 mL per mouse. Two and a half days after injection, I-A and Ki-67 expressions, ·OH-generating potential, ·OH production, and MDA production in splenic B cells were measured; and the concentrations of serum immunoglobulin (Ig) M and IgG were measured through (enzyme-linked immunosorbent assay) ELISA. The splenic B cells sorted from untreated mice were exposed to 0, 12.5, 25, or 50 μg·L⁻¹ Al in vitro. The splenic B cells treated with 50 μg·L⁻¹ Al and the splenic B cells sorted from 800 μg·mL⁻¹ Al-treated mice were additionally treated with GSH and NAC in vitro. The iron supplementation groups, which included the 50 μg·L⁻¹ Al-treated group and splenic B cells sorted from 800 μg·mL⁻¹ Al-treated mice, were treated with a culture medium containing 30 μmol·L⁻¹ iron in vitro. I-A and Ki-67 expressions, ·OH-generating potential, ·OH production, and MDA production in B cells were detected after a 24-h treatment period. Results In the in vivo mouse model, exposure to 800 μg·mL⁻¹ Al significantly inhibited the I-A and Ki-67 expressions (P<0.05), increased DCFH-DA expression and ·OH-generating potential (P<0.05, P<0.01), decreased iron content (P<0.01) and ·OH and MDA production (P<0.01, P<0.001) of splenic B cells, as well as serum IgM and IgG concentrations (P<0.05, P<0.01) in the mice. Exposure to 200 μg·mL⁻¹ Al showed a tendency to decrease the I-A and Ki-67 expressions, and to increase the DCFH-DA expression in splenic B cells, but these differences were not significant. In the in vitro splenic B-cell model, Al (12.5, 25, and 50 μg·L⁻¹) inhibited I-A and Ki-67 expressions (P<0.05, P<0.01) across all concentrations; 50 μg·L⁻¹ Al increased the ·OH-generating potential (P<0.05), and decreased ·OH and MDA production (P<0.01, P<0.05) in B cells. Treatment with GSH and NAC further suppressed I-A expression (P<0.05) in B cells. Iron supplementation increased the ·OH and MDA production (P<0.05), restored I-A and Ki-67 expressions (P<0.05, P<0.01) in B cells, and elevated the serum IgM and IgG concentrations (P<0.05) in Al-treated mice. Conclusion Al suppresses humoral immunity and ·OH production in B cells. The underlying mechanism may involve the decreased iron content and the subsequent retardation of the Fenton reaction in B cells. Supplementing with iron can restore the Fenton reaction in B cells and potentially reverse Al-induced impairment of humoral immunity.

Chronic heart failure （CHF） is a group of complex clinical syndromes caused by abnormal changes in the structure and/or function of the heart due to various reasons， resulting in disorders of ventricular contraction and/or diastole. CHF is a condition where primary diseases such as coronary heart disease， hypertension and pulmonary heart disease recur frequently and persist for a long time， presenting blood stasis in meridians and collaterals， stagnation of water and dampness， and accumulation of Qi in collaterals. Its pathogenesis is complex and may involve myocardial energy metabolism disorders， oxidative stress responses， myocardial cell apoptosis， autophagy， inflammatory responses， etc. According to the theory of restraining hyperactivity to acquire harmony， we believe that under normal circumstances， the adenosine monophosphate-activated protein kinase （AMPK） signaling pathway functions normally， maintaining human physiological activities and energy metabolism. Under pathological conditions， the AMPK signaling pathway is abnormal， causing energy metabolism disorders， inflammatory responses， and myocardial fibrosis. Traditional Chinese medicine （TCM） can regulate the AMPK signaling pathway through multiple mechanisms， targets， and effects， effectively curbing the occurrence and development of CHF. It has gradually become a research hotspot in the prevention and treatment of this disease. Guided by the theory of TCM， our research group， through literature review， summarized the relationship between the AMPK pathway and CHF and reviewed the research progress in the prevention and control of CHF with TCM active ingredients， TCM compound prescriptions， and Chinese patent medicines via regulating the AMPK pathway. The review aims to clarify the mechanism and targets of TCM in the treatment of CHF by regulating the AMPK pathway and guide the clinical treatment and drug development for CHF.

Primary osteoporosis （POP） is a metabolic bone disease characterized by reduced bone mass， degenerated bone microstructure， and increased bone fragility. Its pathogenesis involves the interaction of multiple factors such as genetics， aging， endocrine， and environment， which remain incompletely elucidated. Mitochondrial dysfunction can lead to insufficient adenosine triphosphate （ATP） production and abnormal accumulation of reactive oxygen species （ROS）， activating oxidative stress and inflammation pathways， thereby inhibiting osteoblast differentiation and promoting osteoclast activation， exacerbating the negative bone metabolism balance in POP. Mitochondrial autophagy， as the core mechanism of mitochondrial quality control， selectively identifies and clears damaged mitochondria to effectively reduce ROS accumulation and energy metabolism disorders， thus maintaining the balance between osteoblast and osteoclast differentiation. It plays a critical role in maintaining bone homeostasis and the prevention and treatment of POP. The traditional Chinese medicine （TCM） theory of Qi transformation shares similarities with the functions of mitochondria in energy generation and substance conversion. The pathological state of Qi deficiency and stagnation may be associated with mitochondrial autophagy dysfunction， and the pathogenic characteristics of combined phlegm and stasis align with the metabolic waste accumulation induced by obstructed autophagy flow. This article explores the correlation of the theory of Qi deficiency and stagnation with mitochondrial autophagy and elucidates its potential role in the pathogenesis of POP. Additionally， considering the pathogenesis features of POP， which involve deficiency causing stagnation and a mixture of deficiency and excess， this article proposes a novel therapeutic approach： tonifying Qi to support the body and unblocking collaterals to resolve stagnation from the perspective of mitochondrial autophagy. This article aims to provide theoretical support and research insights for further exploration of TCM in the prevention and treatment of POP.

Chronic heart failure （CHF）， as the terminal stage of various cardiovascular diseases， is characterized by a prolonged course and a high mortality rate， posing a serious threat to human health and life. According to physician Sun Yikui's theory of "Mingmen Dongqi" （dynamic Qi of life gate） in the Ming Dynasty and the modern medicine concept of mitochondrial quality control （MQC）， this paper systematically explores the pathogenic mechanisms and evolutionary patterns of CHF， as well as its intrinsic connection with microstructural homeostasis， and further proposes potential traditional Chinese medicine （TCM） intervention strategies. CHF is often caused by damage to the heart Qi at the early stage. As the disease progresses， prolonged illness affects the kidneys， leading to the dynamic Qi decline of life gate. Further， it results in the failure of the functions of sustaining and consolidating， causing the disintegration of the physical form， which corresponds to mitochondrial kinetic disorders. The deficiency in primary driving force results in impaired Qi transformation， corresponding to mitochondrial autophagy dysfunction， forming a pathological transmission chain of "life gate-mitochondrion" that ultimately leads to myocardial structural disintegration and energy metabolism failure. Modern research indicates that patients with CHF exhibit significant MQC imbalance. Disrupted mitochondrial dynamics lead to network fragmentation， and impaired autophagy causes metabolic blockage， constituting the key microscopic mechanisms underlying ventricular remodeling and pump failure. Chinese herbal medicines， such as those with the effects of warming and tonifying kidney Yang or reinforcing healthy Qi， can intervene in multiple signaling pathways-including PTEN-inducible kinase 1 （PINK1）/Parkin and AMP-activated protein kinase/dynamin-related protein 1 （AMPK/Drp1）-to regulate mitochondrial dynamics and autophagy activity. This repairs damaged MQC networks and improves the microenvironment of myocardial energy metabolism. These intervention strategies align closely with the TCM therapeutic principles of warming and tonifying life gate， replenishing Qi， and activating blood， demonstrating the advantages of holistic regulation based on kidney-centered treatment and mitochondrial-targeted approaches. By integrating the "Mingmen Dongqi" theory with the MQC mechanism， this paper establishes a theoretical framework for the integrated prevention and treatment of CHF， offering new perspectives and insights for clinical practice and future research.

Primary osteoporosis （POP） is a metabolic bone disease characterized by reduced bone mass， degenerated bone microstructure， and increased bone fragility. Its pathogenesis involves the interaction of multiple factors such as genetics， aging， endocrine， and environment， which remain incompletely elucidated. Mitochondrial dysfunction can lead to insufficient adenosine triphosphate （ATP） production and abnormal accumulation of reactive oxygen species （ROS）， activating oxidative stress and inflammation pathways， thereby inhibiting osteoblast differentiation and promoting osteoclast activation， exacerbating the negative bone metabolism balance in POP. Mitochondrial autophagy， as the core mechanism of mitochondrial quality control， selectively identifies and clears damaged mitochondria to effectively reduce ROS accumulation and energy metabolism disorders， thus maintaining the balance between osteoblast and osteoclast differentiation. It plays a critical role in maintaining bone homeostasis and the prevention and treatment of POP. The traditional Chinese medicine （TCM） theory of Qi transformation shares similarities with the functions of mitochondria in energy generation and substance conversion. The pathological state of Qi deficiency and stagnation may be associated with mitochondrial autophagy dysfunction， and the pathogenic characteristics of combined phlegm and stasis align with the metabolic waste accumulation induced by obstructed autophagy flow. This article explores the correlation of the theory of Qi deficiency and stagnation with mitochondrial autophagy and elucidates its potential role in the pathogenesis of POP. Additionally， considering the pathogenesis features of POP， which involve deficiency causing stagnation and a mixture of deficiency and excess， this article proposes a novel therapeutic approach： tonifying Qi to support the body and unblocking collaterals to resolve stagnation from the perspective of mitochondrial autophagy. This article aims to provide theoretical support and research insights for further exploration of TCM in the prevention and treatment of POP.

Chronic heart failure （CHF）， as the terminal stage of various cardiovascular diseases， is characterized by a prolonged course and a high mortality rate， posing a serious threat to human health and life. According to physician Sun Yikui's theory of "Mingmen Dongqi" （dynamic Qi of life gate） in the Ming Dynasty and the modern medicine concept of mitochondrial quality control （MQC）， this paper systematically explores the pathogenic mechanisms and evolutionary patterns of CHF， as well as its intrinsic connection with microstructural homeostasis， and further proposes potential traditional Chinese medicine （TCM） intervention strategies. CHF is often caused by damage to the heart Qi at the early stage. As the disease progresses， prolonged illness affects the kidneys， leading to the dynamic Qi decline of life gate. Further， it results in the failure of the functions of sustaining and consolidating， causing the disintegration of the physical form， which corresponds to mitochondrial kinetic disorders. The deficiency in primary driving force results in impaired Qi transformation， corresponding to mitochondrial autophagy dysfunction， forming a pathological transmission chain of "life gate-mitochondrion" that ultimately leads to myocardial structural disintegration and energy metabolism failure. Modern research indicates that patients with CHF exhibit significant MQC imbalance. Disrupted mitochondrial dynamics lead to network fragmentation， and impaired autophagy causes metabolic blockage， constituting the key microscopic mechanisms underlying ventricular remodeling and pump failure. Chinese herbal medicines， such as those with the effects of warming and tonifying kidney Yang or reinforcing healthy Qi， can intervene in multiple signaling pathways-including PTEN-inducible kinase 1 （PINK1）/Parkin and AMP-activated protein kinase/dynamin-related protein 1 （AMPK/Drp1）-to regulate mitochondrial dynamics and autophagy activity. This repairs damaged MQC networks and improves the microenvironment of myocardial energy metabolism. These intervention strategies align closely with the TCM therapeutic principles of warming and tonifying life gate， replenishing Qi， and activating blood， demonstrating the advantages of holistic regulation based on kidney-centered treatment and mitochondrial-targeted approaches. By integrating the "Mingmen Dongqi" theory with the MQC mechanism， this paper establishes a theoretical framework for the integrated prevention and treatment of CHF， offering new perspectives and insights for clinical practice and future research.

Krüppel-like factor 5 (KLF5) has been confirmed as a key transcription factor in the occurrence and development of tumors, which is closely related to the malignant biological behaviors such as the proliferation and migration of tumor cells. This article summarizes the latest progress of KLF5 in tumor research, explores the mechanism and role of KLF5 in promoting tumor progression, aiming to further explore the potential of KLF5 as a therapeutic target and bring new thinking to the research in this field.

Objective To investigate the characteristics of peripheral blood in the treatment of aplastic anemia(AA)with Bushen Shengxue Method and Yiqi Yangxue Method combined with Western medicine.Methods Totally 492 AA patients who were treated in 19 centers including Xiyuan Hospital China Academy of Chinese Medical Sciences from September 2018 to March 2021 were selected,and were randomized into three groups:161 cases in the Bushen Shengxue group,164 cases in the Yiqi Yangxue group,and 167 cases in the control group.All three groups were orally administered cyclosporine and androgens.Bushen Shengxue group was given Bushen Shengxue Granules,Yiqi Yangxue group was given Yiqi Yangxue Granules,and the control group was given placebo(half dosage of Bushen Shengxue granules).The general data,overall efficacy,and peripheral blood at the 1st month,the 4th month,and 6th month after treatment were analyzed.Results The total effective rate of Bushen Shengxue group was 98.8％(159/161),which was significantly higher than that of Yiqi Yangxue group(79.9％)and the control group(61.7％),with statistical significance(P＜0.001);The total effective rate of Yiqi Yangxue group was significantly higher than that of the control group(P＜0.001).Compared with before treatment,the hemoglobin(HGB)levels of all three groups of patients significantly increased after treatment(P＜0.001,P＜0.01),and the platelet levels of Bushen Shengxue group and the control group significantly increased after treatment(P＜0.001);after treatment,the HGB levels in the three groups were ranked from high to low as the Bushen Shengxue group,Yiqi Yangxue group and the control group(P＜0.01).25％of patients had HGB levels exceeding 20％of baseline values,Bushen Shengxue group took 1 month,while Yiqi Yangxue group and control group took 4 months;25％of patients had an increase in HGB levels exceeding 50％of the baseline value,Bushen Shengxue group took 6 months,while Yiqi Yangxue group and control group took more than 6 months.At 6 months,the number of patients with HGB elevation exceeding 20％and 50％of baseline values in Bushen Shengxue group was higher than that in Yiqi Yangxue group and the control group(P＜0.05,P＜0.001).25％of patients had white blood cell elevation exceeding 50％of the baseline value,Bushen Shengxue group took 4 months,Yiqi Yangxue group took 6 months,and the control group took more than 6 months.25％of patients showed an increase in platelet levels exceeding 100％of the baseline value,Bushen Shengxue group took 4 months,while Yiqi Yangxue group and control group took 6 months;at 6 months,the number of patients in Bushen Shengxue group and Yiqi Yangxue group with platelet elevation exceeding 20％of the baseline value was significantly higher than that in the control group(P＜0.01,P＜0.05).Conclusion Bushen Shengxue method combined with Western medicine intreating AA is better than the method of Yiqi Yangxue method combined with Western medicine.In terms of improving HGB,it is reflected in shortening the recovery time and increasing the number of beneficiaries,and the dosage can affect the recovery time and the number of beneficiaries at the same time;in terms of improving white blood cell and platelet,it is reflected in shortening the recovery time,and the dosage can affect the recovery time.

Background and Aims:Laparoscopic cholecystectomy(LC)is a common surgical method for the treatment of gallbladder diseases.However,some patients experience symptoms such as dyspepsia after surgery,which can affect their quality of life.Compound azinomide enteric-coated tablets,a novel drug,may improve dyspeptic symptoms after LC.This study was conducted to explore the clinical efficacy of compound azinomide enteric-coated tablets in treating post-LC dyspepsia symptoms through a multicenter clinical trial.Methods:A multicenter,superior efficacy,open-label,parallel-controlled design was used.Patients with postoperative dyspepsia were enrolled in 7 centers between January 2023 and May 2024.Patients were randomly assigned to either the observation or control groups using a random number table.The observation group received compound azinomide enteric-coated tablets,while the control group was treated with a combination of oryzae pancreatin tablets and ursodeoxycholic acid tablets.Both groups were treated for 4 weeks.The primary endpoints included gastrointestinal symptom scores and quality of life scores assessed before and at 14 and 28 d after treatment.Additionally,the incidence of adverse reactions and cost-effectiveness ratio(CER)were compared between the groups.Results:A total of 303 patients were included,with 150 in the observation group and 153 in the control group.Baseline characteristics were balanced between the groups before treatment(all P>0.05).After treatment,the observation group showed significantly higher effective rates at 14 d and 28 d than the control group(44.7%vs.29.4%;98.0%vs.73.9%,both P<0.05).The observation group also had significantly lower symptom scores and quality of life scores at both 14 and 28 d,with a significantly higher improvement rate in symptom scores compared to the control group(all P<0.05).Further analysis of the improvement rate and treatment efficacy for individual symptoms revealed that,except for the 14-d improvement in abdominal pain/discomfort,the observation group showed better improvement in all other symptoms at 14 d and in all symptoms at 28 d compared to the control group(all P<0.05).No adverse reactions were observed in either group.The CER for the observation group was 283.78 yuan/efficacy rate at 14 d and 128.57 yuan/efficacy rate at 28 d,while the control group's CER was 729.93 yuan/efficacy rate at 14 d and 290.22 yuan/efficacy rate at 28 d.Conclusion:Compound azinomide enteric-coated tablets demonstrated good clinical efficacy in treating dyspepsia symptoms after LC with excellent safety and high cost-effectiveness.Despite some limitations,the results provide a new treatment option for dyspepsia after LC.Larger-scale randomized controlled trials are needed to validate this study's conclusions further.

Objective:To investigate the changes in iodine intake and iodine nutrition trends of pregnant women in a certain district of Beijing, as well as their related influencing factors, to provide a basis for formulating iodine supplementation strategies for pregnant women.Methods:According to the National Monitoring Program for Iodine Deficiency Disorders, a stratified random sampling method was used to select 100 pregnant women (balanced in early, middle, and late pregnancy) for monitoring each year from 2021 to 2024. Based on the salt iodine and urinary iodine levels of pregnant women, combined with their intake of iodine supplements and other medications, a generalized linear model (GLM) was used to analyze the annual trends in salt iodine and urinary iodine levels. Generalized linear mixed-effects models (GLMMs) were employed to evaluate the variations in salt iodine and urinary iodine levels of pregnant women during different pregnancy periods.Results:From 2021 to 2024, a total of 400 pregnant women were enrolled, with salt iodine levels of (19.23 ± 6.18), (21.31 ± 6.41), (22.38 ± 6.86), and (15.87 ± 9.43) mg/kg, respectively. There was a statistically significant differences between different years ( F = 15.21, P < 0.001). By 2024, the proportion of non-iodized salt consumed reached 25.0% (25/100). The median urinary iodine levels in each year were 136.02, 151.27, 117.83, and 122.94 μg/L, respectively, and the differences between different years were statistically significant ( H = 31.89, P < 0.001). The GLM results showed that compared with 2021, the salt iodine level increased by 2.21 mg/kg (β = 2.21, P = 0.038) in 2022, increased by 3.24 mg/kg (β = 3.24, P = 0.002) in 2023, and decreased by 3.28 mg/kg (β = - 3.28, P = 0.002) in 2024. The urinary iodine level decreased by 24.53 μg/L (β = - 24.53, P = 0.030) in 2024. The GLMMs results showed that compared with early pregnancy, urinary iodine levels increased by 33.68 μg/L (β = 33.68, P = 0.008) in middle pregnancy and 43.17 μg/L (β = 43.17, P = 0.001) in late pregnancy. Conclusions:From 2021 to 2024, the iodine intake of pregnant women in a certain district of Beijing shows an overall trend of first increasing and then decreasing, especially with an increase in the proportion of non iodized salt consumption in 2024. And the iodine nutrition status varies during different pregnancy periods. It is necessary to strengthen the promotion of iodized salt and the publicity of iodine deficiency disorders prevention and control, to ensure that pregnant women can obtain sufficient iodine nutrition through other means when their intake of iodized salt is reduced.