The"ying-wei imbalance"theory originates from Inner Canon of Yellow Emperor,which refers to the dynamic pathological process of yingfen and weifen circulation,distribution,posture,strength,and weakness due to internal and external disturbance,emphasizing that"ying-wei imbalance"is the key to disease occurrence.The sanjiao,as the"envoy of primordial qi,"is central to yingfen and weifen,and the coordinated operation of yingfen and weifen depends on the promotion of the qi of sanjiao.Therefore,based on the yingfen and weifen theory and sanjiao differentiation and treatment,this paper discusses the etiology and pathogenesis of chronic pulmonary heart disease,as well as the syndrome differentiation approach."Ying-wei imbalance"is the core of this mechanism:in the early stage,the loss of yingfen and weifen nutrition,combined with the deficiency of the qi of sanjiao,allows exogenous pathogens to invade the lungs.During progression,dysfunction in the transportation function of yingfen and weifen,along with the stagnation of the qi of sanjiao,results in pulmonary and cardiac involvement,accompanied by phlegm accumulation and stagnation.The end stage is characterized by the failure of both ying and wei,along with dysfunction of the sanjiao and zang-fu organs,which interact to form a pathological chain of"qi disease involving body."Accordingly,the treatment principle of"harmonizing yingfen and weifen,giving sanjiao treatment"was proposed.This is implemented through three therapeutic strategies:"harmonizing""returning",and"astringing"aimed at restoring balance.In the early stage,treatment focuses on tonifying the lungs and consolidating the exterior to eliminate pathogenic factors and activate stagnation.The selected formula is Buyuan Decoction with modifications to harmonize sanjiao.During the developmental stage,treatment focuses on promoting collaterals and dispersing phlegm,utilizing the modified Xuefu Zhuyu Decocotion to facilitate the restoration of function to the sanjiao.In the final stage,Fuyang Decoction,with modifications,is used to resolve fluid retention and nourish both qi and blood.Discussions are closely focused on the syndrome differentiation system of"sanjiao-yingfen and weifen,"in order to offer a novel perspective on the management of chronic pulmonary heart disease.

Objective To investigate the effect of miR-486-5P on ferroptosis in H9c2 cardiomyocytes after hypoxia/reoxygenation(H/R),and to analyze its mechanism.Methods Using H9c2 cardiomyocytes as the research object,a H/R injury model was established using cobalt chloride(CoCl2)and fresh culture medium.The cells were divided into control group,H/R group,H/R+miR-486-5P mimic NC group,H/R+miR-486-5P mimic group,H/R+miR-486-5P inhibitor NC group and H/R+miR-486-5P inhibitor group.The relative expression level of miR-486-5P was detected by quantitative reverse transcription-polymerase chain reaction(qRT-PCR).The cell viability was detected by CCK-8 method.The activities or levels of lactate dehydrogen-ase(LDH),glutathione(GSH),Fe2+and malondialdehyde(MDA)were detected by colorimetric method.The levels of reactive oxygen species(ROS)and mitochondrial membrane potential(MMP)were detected by DCFH-DA fluorescent probe and JC-1 assay,respectively.Western blot was used to detect the levels of AkT/mTOR signaling pathway proteins and ferroptosis related protein solute carrier family 7 member 11(SLC7A11),glutathione peroxidase 4(GPX4)and acyl-coa synthetase long chain family member 4(ACSL4).Results Compared with the control group,the level of miR-486-5P and cell viability in the H/R group de-creased significantly(P＜0.05),while LDH activity,MDA,Fe2+level,ROS level and ACSL4 protein level in-creased significantly(P＜0.05).The GSH,MMP,SLC7A11 and GPX4 levels and p-Akt/Akt and p-mTOR/mTOR ratios were significantly decreased(P＜0.05).After H/R treatment,compared with the H/R+miR-486-5P mimic NC group,the cell viability of the H/R+miR-486-5P mimic group was significantly increased(P＜0.05).The LDH activity,MDA,Fe2+level,ROS level and ACSL4 protein level were significantly de-creased(P＜0.05),while GSH,MMP,SLC7A11 and GPX4 levels and p-Akt/Akt and p-mTOR/mTOR ratios were significantly increased(P＜0.05).Compared with the H/R+miR-486-5P inhibitor NC group,the trend of the above indicators in the H/R+miR-486-5P inhibitor group was opposite.Conclusion miR-486-5P allevi-ates hypoxia/reoxygenation-induced ferroptosis in H9c2 cells by regulating Akt/mTOR signaling pathway,and thus alleviates hypoxia/reoxygenation induced cardiomyocyte injury.

This article introduced the experience of physician Chen Shiduo of the Qing Dynasty in treating hyperhidrosis as documented in Bian Zheng Lu.Chen Shiduo proposed several syndromes for hyperhidrosis,including insufficient lung qi,imbalance between the heart and kidney,depletion of kidney yin,excessive stomach fire,and deficiency of heart blood.In terms of treatment,he advocated for methods that focus on reinforcing deficiency and consolidating the exterior while also nourishing yin,clearing heart heat and nourishing kidney water,replenishing true yin to harmonize yin and yang,nourishing stomach yin to reduce fire and stop sweating,and nourishing the heart to enrich blood and drain fire.His medication approach emphasizes harmonizing the internal organs,with a particular expertise in using Mori Folium.His diagnosis and treatment of hyperhidrosis have been remarkably effective and serve as a reference for later generations.

The"ying-wei imbalance"theory originates from Inner Canon of Yellow Emperor,which refers to the dynamic pathological process of yingfen and weifen circulation,distribution,posture,strength,and weakness due to internal and external disturbance,emphasizing that"ying-wei imbalance"is the key to disease occurrence.The sanjiao,as the"envoy of primordial qi,"is central to yingfen and weifen,and the coordinated operation of yingfen and weifen depends on the promotion of the qi of sanjiao.Therefore,based on the yingfen and weifen theory and sanjiao differentiation and treatment,this paper discusses the etiology and pathogenesis of chronic pulmonary heart disease,as well as the syndrome differentiation approach."Ying-wei imbalance"is the core of this mechanism:in the early stage,the loss of yingfen and weifen nutrition,combined with the deficiency of the qi of sanjiao,allows exogenous pathogens to invade the lungs.During progression,dysfunction in the transportation function of yingfen and weifen,along with the stagnation of the qi of sanjiao,results in pulmonary and cardiac involvement,accompanied by phlegm accumulation and stagnation.The end stage is characterized by the failure of both ying and wei,along with dysfunction of the sanjiao and zang-fu organs,which interact to form a pathological chain of"qi disease involving body."Accordingly,the treatment principle of"harmonizing yingfen and weifen,giving sanjiao treatment"was proposed.This is implemented through three therapeutic strategies:"harmonizing""returning",and"astringing"aimed at restoring balance.In the early stage,treatment focuses on tonifying the lungs and consolidating the exterior to eliminate pathogenic factors and activate stagnation.The selected formula is Buyuan Decoction with modifications to harmonize sanjiao.During the developmental stage,treatment focuses on promoting collaterals and dispersing phlegm,utilizing the modified Xuefu Zhuyu Decocotion to facilitate the restoration of function to the sanjiao.In the final stage,Fuyang Decoction,with modifications,is used to resolve fluid retention and nourish both qi and blood.Discussions are closely focused on the syndrome differentiation system of"sanjiao-yingfen and weifen,"in order to offer a novel perspective on the management of chronic pulmonary heart disease.

This article introduced the experience of physician Chen Shiduo of the Qing Dynasty in treating hyperhidrosis as documented in Bian Zheng Lu.Chen Shiduo proposed several syndromes for hyperhidrosis,including insufficient lung qi,imbalance between the heart and kidney,depletion of kidney yin,excessive stomach fire,and deficiency of heart blood.In terms of treatment,he advocated for methods that focus on reinforcing deficiency and consolidating the exterior while also nourishing yin,clearing heart heat and nourishing kidney water,replenishing true yin to harmonize yin and yang,nourishing stomach yin to reduce fire and stop sweating,and nourishing the heart to enrich blood and drain fire.His medication approach emphasizes harmonizing the internal organs,with a particular expertise in using Mori Folium.His diagnosis and treatment of hyperhidrosis have been remarkably effective and serve as a reference for later generations.

Although the artificial intelligence diagnosis technology of traditional Chinese medicine(TCM)is constantly developing,the existing intelligent syndrome differentiation models can only output the diagnosis results and cannot display the reasoning process of TCM diagnosis.They do not have the interpretability of TCM diagnostic knowledge and are difficult to truly reflect the process of TCM's syndrome differentiation.This can be a long-standing problem that has puzzled the academic community.This article elaborates on the development process and technical characteristics of intelligent diagnosis in traditional Chinese medicine,explores multiple key technologies and bottlenecks in current research in reasoning of TCM's Syndrome Differentiation,and factors affecting diagnosis.A novel intelligent diagnosis model architecture that can infer and explain the process of TCM'ssyndrome differentiation was proposed,and the implementation process of the model and algorithm was explained,and detailed data instance analysis was conducted.This article will provide new methods for the development of intelligent syndrome differentiation of TCM and open up new research ideas for clinical decision-making assistance of TCM.

Objective To investigate the protective effect of insulin-like growth factor-1(IGF-1)precondi-tioning on hypoxic injury in H9c2 rat cardiomyocytes and its mechanism.Methods H9c2 cells were randomly divided into four groups,control group,hypoxia group(CoCl2 group),hypoxia+IGF-1 pretreatment group(CoCl2+IGF-1 group),hypoxia+IGF-1 pretreatment+phosphatidylinositol 3 kinase(PI3K)/protein kinase B(Akt)pathway specific inhibitor LY294002 group(CoCl2+IGF-1+LY294002 group).CCK8 assay was used to detect the survival rate of H9c2 cells,and Tunel assay was used to detect the apoptosis of H9c2 cells,DCFH-DA probe method was used to detect the reactive oxygen species(ROS)level of H9c2 cells in each group.The activities of superoxide dismutase(SOD)and lactate dehydrogenase(LDH)in culture supernatant were detected by kit.The levels of glutathione peroxidase(GSH-Px)and malondialdehyde(MDA)in culture supernatant were detected by enzyme-linked immunosorbent assay(ELISA).Western blot was used to detect the expression of pro-apoptotic protein B cell lymphoma 2 associated X protein(Bax),Caspase-3,anti-apoptot-ic protein Bcl-2,pathway proteins Akt and phosphorylated Akt(p-Akt)in H9c2 cells.Results IGF-1 could increase cell viability(P＜0.05),reduced cell apoptosis rate(P＜0.05),reduced ROS level(P＜0.05),re-duced MDA production(P＜0.05),reduced LDH activity(P＜0.05),and increased SOD and GSH-Px activi-ties(P＜0.05).It also promoted the expression of p-Akt(P＜0.05),reduced the expression of pro-apoptotic proteins Bax and Caspase-3(P＜0.05),and increased the expression of anti-apoptotic protein Bcl-2(P＜0.05).After the addition of PI3K pathway specific inhibitor LY294002,the protective effect of IGF-1 on hy-poxic H9c2 cells disappeared.Conclusion IGF-1 protects cardiomyocytes from hypoxia injury by inhibiting oxidative stress and apoptosis of cardiomyocytes through activating PI3K/Akt pathway and improving the survival rate of cardiomyocytes.

Objective To study the effects of intramedullary pressure on the fluid flow behavior in bones.Methods Multi-scale models of macro bone tissue and macro-meso osteon groups were established using the COMSOL Multiphysics software.Considering the interrelationship of different pore scales,such as the bone marrow cavity,Haversia canal,and bone lacunar-canaliculus,the pore pressure and flow rate of hollow bone tissues and bone tissues with intramedullary pressure were compared,and the effects of the amplitude and frequency of intramedullary pressure on the pressure and flow velocity of the liquid in the bone were analyzed.Results When intramedullary pressure was considered,the pore pressure in bone tissues with intramedullary pressure was 6.4 kPa higher than that in hollow bone tissues.The flow pressure increased significantly with an increase in the intramedullary pressure amplitude,but the flow velocity remained unchanged.The frequency of intramedullary pressure had little effect on pore pressure and flow velocity.Conclusions The multi-scale pore model established in this study can accurately analyze bone fluid flow behavior.These results are of great significance for an in-depth understanding of force conduction in the bone.

Background: The incidence density of metabolic dysfunction-associated fatty liver disease (MAFLD) and the effect of a healthy lifestyle on the risk of MAFLD remain unknown. We evaluated the prevalence and incidence density of MAFLD and investigated the association between healthy lifestyle and the risk of MAFLD. Methods: A cross-sectional analysis was conducted on 37,422 participants to explore the prevalence of MAFLD. A cohort analysis of 18,964 individuals was conducted to identify the incidence of MAFLD, as well as the association between healthy lifestyle and MAFLD. Cox proportional hazards regression was used to calculate the hazard ratio (HR) and 95% confidence interval (CI) with adjustments for confounding factors. Results: The prevalence of MAFLD, non-alcoholic fatty liver disease, and their comorbidities were 30.38%, 28.09%, and 26.13%, respectively. After approximately 70 thousand person-years of follow-up, the incidence densities of the three conditions were 61.03, 55.49, and 51.64 per 1,000 person-years, respectively. Adherence to an overall healthy lifestyle was associated with a 19% decreased risk of MAFLD (HR, 0.81; 95% CI, 0.72 to 0.92), and the effects were modified by baseline age, sex, and body mass index (BMI). Subgroup analyses revealed that younger participants, men, and those with a lower BMI experienced more significant beneficial effects from healthy lifestyle. Conclusion Our results highlight the beneficial effect of adherence to a healthy lifestyle on the prevention of MAFLD. Health management for improving dietary intake, physical activity, and smoking and drinking habits are critical to improving MAFLD.

Chronic inflammation is critical in the onset and progression of atherosclerosis (AS). The lipopolysaccharide (LPS) level in the circulation system is elevated in AS patients and animal models, which is correlated with the severity of AS. Inspired by the underlying mechanism that LPS could drive the polarization of macrophages toward the M1 phenotype, aggravate inflammation, and ultimately contribute to the exacerbation of AS, LPS in the circulation system was supposed to be the therapeutic target for AS treatment. In the present study, polymyxin (PMB) covalently conjugated to PEGylated liposomes (PLPs) were formulated to adsorb LPS through specific interactions between PMB and LPS. In vitro, the experiments demonstrated that PLPs could adsorb LPS, reduce the polarization of macrophages to M1 phenotype and inhibit the formation of foam cells. In vivo, the study revealed that PLPs treatment reduced the serum levels of LPS and pro-inflammatory cytokines, decreased the proportion of M1-type macrophages in AS plaque, stabilized AS plaque, and downsized the plaque burdens in arteries, which eventually attenuated the progression of AS. Our study highlighted LPS in the circulation system as the therapeutic target for AS and provided an alternative strategy for AS treatment.