Hepatic fibrosis refers to excessive accumulation and abnormal proliferation of fibrous connective tissue in the liver triggered by multiple pathogenic factors， and it may progress to liver cirrhosis， portal hypertension， and liver cancer. The pathological mechanisms of hepatic fibrosis involve hepatocyte injury， inflammatory cell infiltration with the release of inflammatory mediators， hepatic stellate cell activation， and extracellular matrix deposition. Recent studies have focused on mitochondrial dysfunction in disease progression， including the molecular pathways for hepatic fibrosis driven by metabolic disorders， energy deficiency， oxidative stress， mitochondrial dynamic imbalance， and autophagic dysfunction， all of which can induce liver injury. This article reviews the latest advances in hepatic fibrosis， in order to provide new therapeutic strategies for clinical management.

[Objective]To summarize the clinical academic experience of Professor HU Guojun,a famous Chinese medicine doctor,in the treatment of ankylosing spondylitis based on the theory of"host and client interaction".[Methods]Professor HU Guojun's experience in the treatment of ankylosing spondylitis based on the theory of"host and client interaction"was summarized from four aspects,including theoretical tracing,etiology,pathogenesis,treatment and medication characteristics,by consulting doctors,collating typical medical records and consulting relevant literature,and a medical case was attached to support it.[Results]Professor HU believes that the etiology and pathogenesis of ankylosing spondylitis are highly consistent with the"interaction between host and client"theory.In clinical practice,he emphasizes the principle of"supporting the vital energy and dispelling pathogenic factors,while differentiating between host and guest."He advocates that tonifying deficiency should involve examining the differences between Yin and Yang,and expelling pathogenic factors should involve distinguishing the characteristics of the pathogenic Qi.He skillfully uses blood-enriching and flesh-tonifying substances,insect-based medicines,vine and stem herbs and warming and tonifying drugs to strengthen the host energy and expel the client energy,resulting in significant therapeutic effects.In the attached case study,Professor HU used the principle of dissolving the entanglement between host and guest as the main treatment approach.By addressing both the root cause and symptoms simultaneously,he ultimately achieved the strengthening of the host energy and the expulsion of the pathogenic factors,leading to the resolution of the chronic condition.[Conclusion]Professor HU has innovatively applied the"host and client interaction"theory in the treatment of ankylosing spondylitis,yielding excellent results.This approach can serve as a new reference for the clinical diagnosis and treatment of ankylosing spondylitis.

Wang Ji is an outstanding representative of Xin'an medicine,he has made a lot of achievements in academic thought of acupuncture and moxibustion,which mainly contains the academic features such as"acupuncture treatment mainly purging excessive pathogen"and"use of moxibustion with caution for the disease-free person",as well as"no selection of fixed acupoints for treating diseases".The scholars in past dynasties did a lot of research on his theory of"acupuncture treatment mainly purging excessive pathogen"and"use of moxibustion with caution for the disease-free person",but did less research on his theory of"no selection of fixed acupoints for treating diseases",this paper explores Wang Ji's life and his representative works,and analyzes the theory of"no selection of fixed acupoints for treating diseases".Wang Ji advocates the disease treatment principle of differentiation of meridians and collaterals,qi and blood,as well as yin and yang,and his acupoint selection rules focuses on flexible prescription according to syndrome differentiation,point selection according to disease differentiation,which critically criticizes the dogmatic behavior of the conventional theory that"a certain acupoint corresponding treatment for a certain disease",he reminded the physicians that in treating disease by acupuncture and moxibustion,syndrome differentiation should be according to meridians and collaterals differentiation,acupoint application should be flexible and changeable.

[Objective]To summarize the clinical academic experience of Professor HU Guojun,a famous Chinese medicine doctor,in the treatment of ankylosing spondylitis based on the theory of"host and client interaction".[Methods]Professor HU Guojun's experience in the treatment of ankylosing spondylitis based on the theory of"host and client interaction"was summarized from four aspects,including theoretical tracing,etiology,pathogenesis,treatment and medication characteristics,by consulting doctors,collating typical medical records and consulting relevant literature,and a medical case was attached to support it.[Results]Professor HU believes that the etiology and pathogenesis of ankylosing spondylitis are highly consistent with the"interaction between host and client"theory.In clinical practice,he emphasizes the principle of"supporting the vital energy and dispelling pathogenic factors,while differentiating between host and guest."He advocates that tonifying deficiency should involve examining the differences between Yin and Yang,and expelling pathogenic factors should involve distinguishing the characteristics of the pathogenic Qi.He skillfully uses blood-enriching and flesh-tonifying substances,insect-based medicines,vine and stem herbs and warming and tonifying drugs to strengthen the host energy and expel the client energy,resulting in significant therapeutic effects.In the attached case study,Professor HU used the principle of dissolving the entanglement between host and guest as the main treatment approach.By addressing both the root cause and symptoms simultaneously,he ultimately achieved the strengthening of the host energy and the expulsion of the pathogenic factors,leading to the resolution of the chronic condition.[Conclusion]Professor HU has innovatively applied the"host and client interaction"theory in the treatment of ankylosing spondylitis,yielding excellent results.This approach can serve as a new reference for the clinical diagnosis and treatment of ankylosing spondylitis.

Background::Genetic variants of dopaminergic transcription factor-encoding genes are suggested to be Parkinson’s disease (PD) risk factors; however, no comprehensive analyses of these genes in patients with PD have been undertaken. Therefore, we aimed to genetically analyze 16 dopaminergic transcription factor genes in Chinese patients with PD.Methods::Whole-exome sequencing (WES) was performed using a Chinese cohort comprising 1917 unrelated patients with familial or sporadic early-onset PD and 1652 controls. Additionally, whole-genome sequencing (WGS) was performed using another Chinese cohort comprising 1962 unrelated patients with sporadic late-onset PD and 1279 controls.Results::We detected 308 rare and 208 rare protein-altering variants in the WES and WGS cohorts, respectively. Gene-based association analyses of rare variants suggested that MSX1 is enriched in sporadic late-onset PD. However, the significance did not pass the Bonferroni correction. Meanwhile, 72 and 1730 common variants were found in the WES and WGS cohorts, respectively. Unfortunately, single-variant logistic association analyses did not identify significant associations between common variants and PD. Conclusions::Variants of 16 typical dopaminergic transcription factors might not be major genetic risk factors for PD in Chinese patients. However, we highlight the complexity of PD and the need for extensive research elucidating its etiology.

Rheumatoid arthritis(RA)is a chronic systemic autoimmune disease characterized by the hyperplasia of synovial cells,an increase in inflammatory cells,and the destruction of cartilage.The pathogenesis of RA is complex and closely related to genetic factors,immune system abnormalities,and mitochondrial dysfunction.Mitochondria,known as the powerhouse of the cell,play a pivotal role in the development of RA.Their dysfunction is manifested as abnormal energy metabolism,excessive accumulation of reactive oxygen species(ROS),and abnormal activation of the innate immune system,which in turn promotes inflammation and tissue damage.The pathogenic environment of RA influences mitochondrial dysfunction through hypoxic conditions,DNA mutations,and oxidative stress.Hypoxia impairs mitochondrial function,promoting inflammation and angiogenesis;mutations in mitochondrial DNA(mtDNA)exacerbate mitochondrial dysfunction and advance the progression of RA;oxidative stress directly damages cartilage and the extracellular matrix,altering protein structure.Therefore,investigating the relationship between mitochondrial dysfunction and the pathogenesis of RA is of significant importance for understanding the disease's mechanisms and developing novel therapeutic strategies.

Rheumatoid arthritis(RA)is a chronic systemic autoimmune disease characterized by the hyperplasia of synovial cells,an increase in inflammatory cells,and the destruction of cartilage.The pathogenesis of RA is complex and closely related to genetic factors,immune system abnormalities,and mitochondrial dysfunction.Mitochondria,known as the powerhouse of the cell,play a pivotal role in the development of RA.Their dysfunction is manifested as abnormal energy metabolism,excessive accumulation of reactive oxygen species(ROS),and abnormal activation of the innate immune system,which in turn promotes inflammation and tissue damage.The pathogenic environment of RA influences mitochondrial dysfunction through hypoxic conditions,DNA mutations,and oxidative stress.Hypoxia impairs mitochondrial function,promoting inflammation and angiogenesis;mutations in mitochondrial DNA(mtDNA)exacerbate mitochondrial dysfunction and advance the progression of RA;oxidative stress directly damages cartilage and the extracellular matrix,altering protein structure.Therefore,investigating the relationship between mitochondrial dysfunction and the pathogenesis of RA is of significant importance for understanding the disease's mechanisms and developing novel therapeutic strategies.

ObjectiveTo investigate the mortality and years of life lost of pancreatic cancer in Baoshan District of Shanghai，from 2009 to 2021， and to provide scientific evidence for the prevention and control of pancreatic cancer in the future. MethodsThe death surveillance data of Baoshan District from 2009 to 2021 were collected from the Shanghai chronic disease surveillance information management system. Crude mortality， standardized mortality，potential years of life lost （PYLL）， potential years of life lost rate （PYLLR） ， average years of potential life lost （AYLL） ， annual percentage change （APC） were calculated to analyze the trend of mortality and life loss of pancreatic cancer. ResultsFrom 2009 to 2021， a total of 2117 deaths of pancreatic cancer were reported in Baoshan District， accounting for 7.05% of all cancer deaths. The average age of the death cases was （71.18±10.97）years. The youngest was 3 years old and the oldest was 96 years old. The death component ratio of pancreatic cancer increased with time （P<0.05）， and the average death age of women was higher than that of men （P<0.05）. The crude mortality of pancreatic cancer was 17.38/10⁵ in Baoshan District from 2009 to 2021， showing a rising tendency （P<0.05） with APC of 3.74%. The standardized mortality of pancreatic cancer was 7.84/10⁵. The crude mortality of pancreatic cancer was 19.71/10⁵ in men and 14.89/10⁵ in women， both showed a tendency towards a rise （P<0.05 ） with APC of 4.44% and 2. 89%， respectively. The crude mortality of pancreatic cancer showed a tendency towards a decline in residents at ages of 45 to 60 years （ P<0.05 ）， with APC of 4.74%. The PYLL and PYLLR of pancreatic cancer were 8 115 person-years and 0.67‰ in Baoshan District from 2009 to 2021， while the AYLL of pancreatic cancer was 3.83 years per person. The PYLL was higher in men than in women. ConclusionThe mortality rate of pancreatic cancer in Baoshan District shows an increasing trend. The healthy life of elderly and men is affected largely by pancreatic cancer. It is necessary to strengthen the health education on the prevention/control of pancreatic cancer and healthy life style， thereby improving the tertiary prevention system of pancreatic cancer.

ObjectiveTo investigate the epidemiological characteristics of respiratory disease mortality in Baoshan residents during the period of 2009‒2020. MethodsRespiratory disease deaths of Baoshan residents from 2009‒2020 were collected. ICD-10 codes were used to classify the causes of death， and R-4.2.1 was applied for statistical analysis. The average annual percent change （AAPC） of standardized mortality rates of different respiratory diseases were analyzed by using Joinpoint 4.9.0.0. ResultsThe average annual mortality rate of respiratory diseases in Baoshan from 2009 to 2020 was 58.86/10⁵， and the standardized mortality rate was 35.62/10⁵， which was the 3rd leading cause of mortality. The mortality rate of respiratory diseases was higher in men than in women （χ²=46.70， P<0.001）. COPD ranked first among respiratory diseases in Baoshan from 2009 to 2020， followed by pneumonia， asthma and pneumoconiosis in that order. The standardized mortality rate for COPD decreased from 38.66/10⁵ in 2009 to 19.88/10⁵ in 2020 （AAPC=-6.6%， 95%CI： -8.2% to -4.9%， P<0.001）. The standardized mortality rate of asthma decreased from 2.86/10⁵ in 2009 to 1.43/10⁵ in 2020 （AAPC=-5.8%， 95%CI： -8.8% to -2.8%， P<0.01）. The standardized mortality rate of pneumoconiosis decreased from 0.64/10⁵ in 2009 to 0.12/10⁵ in 2020 （AAPC=-7.4%， 95%CI： -13.0% to -1.5%， P<0.05）. The standardized mortality rate for pneumonia decreased from 2.63/10⁵ in 2009 to 0.70/10⁵ in 2020 （AAPC=-6.2%， 95%CI： -12.2% to 0.2%， P=0.056）， but not statistically significant. The annual average mortality rates of COPD， pneumonia and asthma were all highest in January. Crude mortality rates for COPD （χ²=2 669.01， P<0.001）， pneumonia （χ²=217.82， P<0.001）， asthma （χ²=100.09， P<0.001）， pneumoconiosis （χ²=26.46， P<0.001） and all categories of respiratory diseases （χ²=2 995.84， P<0.001） increased with age showed an increasing trend. The crude mortality rates for COPD （χ²=101.69， P<0.001）， pneumonia （χ²=7.39， P<0.01） and asthma （χ²=7.41， P<0.01） were higher in the central than in the northern part of Baoshan District， while the crude mortality rate for COPD （χ²=19.97， P<0.001） was higher in the central than in the southern part. ConclusionThe attention should be focused on COPD； increased detection in males and the elderly， especially in winter and spring； and a good balance between environmental and economic when planning the regional development.

Oligoasthenospermia is the primary cause of infertility. However, there are still enormous challenges in the screening of critical candidates and targets of oligoasthenospermia owing to its complex mechanism. In this study, stem cell factor (SCF), c-kit, and transient receptor potential vanilloid 1 (TRPV1) biosensors were successfully established and applied to studying apoptosis and autophagy mechanisms. Interestingly, the detection limit reached 2.787 × 10^-15 g/L, and the quantitative limit reached 1.0 × 10^-13 g/L. Furthermore, biosensors were used to investigate the interplay between autophagy and apoptosis. Schisandrin A is an excellent candidate to form a system with c-kit similar to SCF/c-kit with a detection constant (K_D) of 5.701 × 10^-11 mol/L, whereas it had no affinity for SCF. In addition, it also inhibited autophagy in oligoasthenospermia through antagonizing TRPV1 with a K_D of up to 4.181 × 10^-10 mol/L. In addition, in vivo and in vitro experiments were highly consistent with the biosensor. In summary, high-potency schisandrin A and two potential targets were identified, through which schisandrin A could reverse the apoptosis caused by excessive autophagy during oligoasthenospermia. Our study provides promising insights into the discovery of effective compounds and potential targets via a well-established in vitro-in vivo strategy.