Baxian Formula （八仙方） is a folk pediatric prescription in Quanzhou， Fujian Province. This paper summarized the clinical experience of Professor LI Candong in treating pediatric diseases with Baxian Formula. By analyzing the distinctive composition and theoretical underpinnings of the Baxian Formula for treating pediatric lung， liver and spleen diseases， it is considered that the formula prioritizes wind medicinals， aimed at restoring the dynamics of qi movement within the zang fu （脏腑） organs. It excels in dispelling and dispersing wind， promoting digestion， calming the mind， invigorating the spleen and draining dampness， clearing heat and soothing the liver， extinguishing wind and arresting convulsion. The prescription can treat pediatric disorders caused by pathological factors such as wind， phlegm， dampness， food， heat and constraint. Moreover， this paper summarized the clinical thinking of Baxian Formula in treating pediatric diseases of the lung system （common cold， cough， eczema）， spleen system （diarrhea， food retention） and liver system （fright from external stimuli， tic disorder）， aiming at providing reference for diagnosing and treating pediatric diseases in clinical practice.

Diabetic kidney disease （DKD） is one of the main causes of chronic kidney disease. Both traditional Chinese medicine （TCM） and western medicine have their own advantages in the prevention and treatment of DKD， but there are also many difficulties. By analysis of the difficulties faced by TCM and western medicine in the differentiation and treatment of DKD， based on the theory of "miniature masses in the renal collaterals"， combined with long-term clinical practice， "internal heat leading to mass" is proposed as the core pathogenesis of DKD. Therefore， a trinity model of "disease-syndrome-symptom" for differentiation and treatment of DKD based on the core pathogenesis has been proposed. This model highlights the status of the core pathogenesis of "internal heat leading to mass" in DKD， and conducts a three-dimensional identification from the perspectives of disease， syndrome and symptom， so as to inspire clinical practice.

ObjectiveTo explore the mechanism of total saponins of Dioscoreae Nipponicae Rhizoma （TSDN） in treating gouty arthritis （GA） by regulating cyclooxygenase-2 （COX-2）-mediated M1 macrophage reprogramming by in vivo and in vitro experiments. MethodsIn vivo experiment： 24 male SD rats were randomly allocated into blank， model （GA）， TSDN， and celecoxib groups， with 6 rats in each group. After 7 days of administration， pathological changes in the ankle synovial tissue were observed via hematoxylin-eosin （HE） staining. Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） was used to quantify the mRNA levels of NOD-like receptor protein 3 （NLRP3） inflammasome， apoptosis-associated speck-like protein （ASC）， Caspase-1， COX-2， interleukin-1β （IL-1β）， and tumor necrosis factor-α （TNF-α） in the synovial tissue. Enzyme-linked immunosorbent assay （ELISA） was employed to measure the serum levels of inducible nitric oxide synthase （iNOS）， IL-1β， CD86， CD80， CD206， and arginase-1 （Arg-1）. In vitro experiment： The GA model was established by lipopolysaccharide （LPS） + MSU induction， and the inhibitor concentration was screened by the methyl thiazolyl tetrazolium （MTT） assay. RAW264.7 cells were allocated into blank， model， TSDN， dexamethasone， COX-2 inhibitor （celecoxib）， and TSDN + COX-2 inhibitor groups. The levels of iNOS， IL-1β， CD86， CD80， CD206， and Arg-1 in the cell supernatant of each group were determined by enzyme-linked immunosorbent assay （ELISA）. The mRNA and protein levels of NLRP3 inflammasome， COX-2， IL-1β， and TNF-α in each group were determined by Real-time PCR and Western blot， respectively. ResultsIn vivo experiment： compared with the model group， TSDN reduced the mRNA levels of NLRP3 inflammasome， COX-2， IL-1β， and TNF-α in the synovial tissue （P<0.05， P<0.01）. ELISA results showed that TSDN lowered the serum levels of iNOS， IL-1β， CD86， and CD80 （P<0.01） while increasing the serum levels of CD206 and Arg-1 （P<0.01）. In vitro experiment： compared with the model group， TSDN and inhibitor down-regulated the mRNA levels of NLRP3 inflammasome， COX-2， IL-1β， and TNF-α and the protein levels of NLRP3 inflammasome， COX-2， cleaved IL-1β， and TNF-α （P<0.01）. Compared with TSDN alone， TSDN + COX-2 inhibitor further reduced the mRNA and protein levels of the markers above （P<0.01）. Compared with the model group， TSDN and COX-2 inhibitor decreased the levels of IL-1β， iNOS， CD80， and CD86 （P<0.01） and increased the levels of CD206 and Arg-1 （P<0.01） in cells. Compared with TSDN alone， TSDN + COX-2 inhibitor reduced IL-1β， iNOS， CD80， and CD86 levels （P<0.05， P<0.01） and elevated CD206 and Arg-1 levels （P<0.01） in cells. ConclusionTSDN can alleviate GA by downregulating COX-2-mediated M1 macrophage reprogramming and suppressing the inflammatory factors.

ObjectiveTo explore the mechanism of total saponins of Dioscoreae Nipponicae Rhizoma （TSDN） in treating gouty arthritis （GA） by regulating cyclooxygenase-2 （COX-2）-mediated M1 macrophage reprogramming by in vivo and in vitro experiments. MethodsIn vivo experiment： 24 male SD rats were randomly allocated into blank， model （GA）， TSDN， and celecoxib groups， with 6 rats in each group. After 7 days of administration， pathological changes in the ankle synovial tissue were observed via hematoxylin-eosin （HE） staining. Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） was used to quantify the mRNA levels of NOD-like receptor protein 3 （NLRP3） inflammasome， apoptosis-associated speck-like protein （ASC）， Caspase-1， COX-2， interleukin-1β （IL-1β）， and tumor necrosis factor-α （TNF-α） in the synovial tissue. Enzyme-linked immunosorbent assay （ELISA） was employed to measure the serum levels of inducible nitric oxide synthase （iNOS）， IL-1β， CD86， CD80， CD206， and arginase-1 （Arg-1）. In vitro experiment： The GA model was established by lipopolysaccharide （LPS） + MSU induction， and the inhibitor concentration was screened by the methyl thiazolyl tetrazolium （MTT） assay. RAW264.7 cells were allocated into blank， model， TSDN， dexamethasone， COX-2 inhibitor （celecoxib）， and TSDN + COX-2 inhibitor groups. The levels of iNOS， IL-1β， CD86， CD80， CD206， and Arg-1 in the cell supernatant of each group were determined by enzyme-linked immunosorbent assay （ELISA）. The mRNA and protein levels of NLRP3 inflammasome， COX-2， IL-1β， and TNF-α in each group were determined by Real-time PCR and Western blot， respectively. ResultsIn vivo experiment： compared with the model group， TSDN reduced the mRNA levels of NLRP3 inflammasome， COX-2， IL-1β， and TNF-α in the synovial tissue （P<0.05， P<0.01）. ELISA results showed that TSDN lowered the serum levels of iNOS， IL-1β， CD86， and CD80 （P<0.01） while increasing the serum levels of CD206 and Arg-1 （P<0.01）. In vitro experiment： compared with the model group， TSDN and inhibitor down-regulated the mRNA levels of NLRP3 inflammasome， COX-2， IL-1β， and TNF-α and the protein levels of NLRP3 inflammasome， COX-2， cleaved IL-1β， and TNF-α （P<0.01）. Compared with TSDN alone， TSDN + COX-2 inhibitor further reduced the mRNA and protein levels of the markers above （P<0.01）. Compared with the model group， TSDN and COX-2 inhibitor decreased the levels of IL-1β， iNOS， CD80， and CD86 （P<0.01） and increased the levels of CD206 and Arg-1 （P<0.01） in cells. Compared with TSDN alone， TSDN + COX-2 inhibitor reduced IL-1β， iNOS， CD80， and CD86 levels （P<0.05， P<0.01） and elevated CD206 and Arg-1 levels （P<0.01） in cells. ConclusionTSDN can alleviate GA by downregulating COX-2-mediated M1 macrophage reprogramming and suppressing the inflammatory factors.

BACKGROUND:Dysfunction of macrophage efferocytosis can induce local and systemic inflammatory damage and is associated with a variety of obesity-related metabolic diseases.Moreover,compounds targeting efferocytosis have shown good therapeutic effects. OBJECTIVE:By reviewing the effects of obesity on macrophage efferocytosis,to analyze the key mechanism by which obesity inhibits efferocytosis,to summarize the research progress in compounds targeting efferocytosis to treat obesity-related metabolic diseases,so as to provide new ideas for fully understanding efferocytosis and its relationship with metabolic diseases,aiming to provide new strategies for disease prevention and treatment. METHODS:The English search terms were"efferocytosis,metabolism,obesity,obese,atherosclerosis,non-alcoholic steatohepatitis,neurodegeneration,tumor,osteoarthritis,diabetes,compound,medicine,treatment,"which were used for literature retrieval in PubMed and Web of Science.The Chinese search term was"efferocytosis,"which was used for literature retrieval in CNKI,VIP and WanFang datebases.Ninety-nine papers were finally included in the review analysis after a rigorous screening process. RESULTS AND CONCLUSION:In the process of efferocytosis,the"Find me"and"Eat me"processes involving a large number of apoptotic cell derived factors are mainly regulated by apoptotic cells.The efferocytosis factor involved in cytoskeletal remodeling and digestion are mainly derived from macrophages,which are crucial for efferocytosis activity.These results suggest that the"Find me"and"Eat me"factors mainly reflect the condition of apoptosis,and it is more scientific to select the expression of factors involved in cytoskeletal remodeling and digestion when evaluating the efferocytosis activity of macrophages.Obesity inhibits efferocytosis,and shows an inhibitory effect on most digestive factors,but has a stress-induced activation effect on most"Find me,""Eat me"and cytoskeletal recombination factors,which further indicates the decisive effect of digestive stage on efferocytosis and suggests that it is not reliable for some studies to evaluate the efferocytosis based on the increased expression of"Find me"and"Eat me"factors.Targeting cytokines in the digestive phase may be more effective when discussing future intervention strategies targeting macrophages efferocytosis.The efferocytosis activators of macrophages are effective in the treatment of various metabolic diseases,but the efferocytosis inhibitors in tumor tissue show good anticancer effects,suggesting that the role of efferocytosis should be rationally evaluated according to the characteristics of tissue inflammation.Efferocytosis is a relatively new concept proposed in 2003,with a short research history and complex efferocytosis factors.Current studies on obesity and efferocytosis only involve a tip of the iceberg and most of them are at a superficial level and a large number of scientific experiments are needed to further validate the mechanisms.

OBJECTIVE To evaluate the cost-effectiveness of finerenone combined with standard of care （SoC） in the treatment of heart failure with mildly reduced ejection fraction （HFmrEF） or preserved ejection fraction （HFpEF）. METHODS Based on a phase Ⅲ clinical trial， a Markov model was constructed from the perspective of China’s healthcare system to compare the treatment outcomes of finerenone combined with SoC regimen versus SoC regimen alone in the treatment of different cardiac functional statuses of HFmrEF/HFpEF. Using quality-adjusted life year （QALY） as the health output index， 3 times China’s per capita GDP in 2023 as the willingness-to-pay （WTP） threshold， a simulation was conducted with a 3-month cycle length and a 10- year time horizon， incorporating an annual discount rate of 5%. The dynamic changes across various stages of HFmrEF/HFpEF treated with finerenone combined with SoC versus SoC alone were simulated to evaluate the long-term effectiveness and costs of the two treatment strategies. Additionally， one-way sensitivity analysis and probabilistic sensitivity analysis were performed， to test the robustness of the results. RESULTS The incremental cost-effectiveness ratio （ICER） of the finerenone combined with SoC regimen versus SoC regimen alone was 179 504.75 yuan/QALY， which was below the WTP threshold set in this study， indicating that the finerenone combined with SoC regimen possessed certain economic advantages. The results of one-way sensitivity analysis showed that the utility value of NYHA Ⅱ status， the drug price of finerenone， the discount rate， and the probability of hospital transfer for both groups had a great influence on ICER， but did not affect the robustness of the model. The probabilistic sensitivity analysis also confirmed the robustness of the model. CONCLUSIONS Under the WTP threshold set in this study， finerenone combined with SoC is cost-effective in the treatment of HFmrEF/HFpEF， compared with the SoC regimen.

Non-small cell lung cancer （NSCLC）， as the most common subtype of lung cancer， has a high incidence and mortality rate among global cancer cases. Although modern medicine has made remarkable progress in the treatment of NSCLC with advances in screening technologies and continuous optimization of therapeutic regimens， current treatments inevitably result in adverse outcomes such as high tumor recurrence rates， significant toxic side effects， and poor quality of life for patients. Traditional Chinese medicine （TCM） holds that the core pathogenesis of lung cancer lies in ''deficiency of healthy Qi and excess of pathogenic factors''. It originates from congenital insufficiency or acquired malnourishment， leading to an imbalance of Yin and Yang， deficiency of healthy Qi， and inability to eliminate pathogenic factors. The interactions among Qi stagnation， phlegm accumulation， blood stasis， and toxins give rise to disease. The root is deficiency， while the manifestation is excess. Therefore， the treatment of lung cancer in TCM is generally guided by the principle of "supporting the healthy Qi and eliminating the pathogens". A large number of clinical and pharmacological studies have shown that TCM and its active components can， through multiple targets and mechanisms， alleviate postoperative and chemoradiotherapy-related adverse reactions， inhibit tumor growth and recurrence， and improve the quality of life of patients with NSCLC. It is worth noting that although extensive studies have been conducted on the therapeutic patterns and pharmacological mechanisms of TCM and its active substances in NSCLC treatment， issues such as the diversity of medicinal materials， the complexity of chemical components， the scientific basis of herbal compatibility， and the flexibility of dosage indicate that there is still considerable room for further clinical and basic research. This review summarizes recent literature on the clinical syndromes， drug selection， medication patterns， and pharmacological mechanisms of TCM and its active components in the treatment of NSCLC， aiming to provide guidance for clinical medication in TCM therapy for NSCLC and to deepen the understanding and research of its therapeutic mechanisms.

Objective To investigate the regulatory effect of artemisinin derivative dihydroartemisinin(DHA)on anti-tumor immune function of CD8+T cells induced by non-small cell lung cancer(NSCLC)cells.Methods NSCLC A549 cells were divided into DMSO control group and DHA treatment group.A549 cells were treated with DMSO and DHA at different concentrations(25,50 and 100 μmol/L),and the optimal concentration of DHA was selected to treat A549 cells for 0,24,48 and 72 h according to half maximal inhibitory concentrate(IC50).CCK-8 method and colony formation test were used to detect the effect of DHA on the proliferation and colony formation ability of A549 cells.Peripheral blood mononuclear cells(PBMCs)of healthy individuals were isolated by density gradient centrifugation.After monocytes were removed by adhesion method,A549 cells pretreated with mitomycin C were co-cultured with PBMCs at 10:1 ratio.After 2 weeks,flow cytometry was used to detect the proportion of CD8+T cells and the expression levels of perforin and granzyme B.Results Compared with the control group,the proliferation inhibition rates of A549 cells increased after treatment with 25,50 and 100 μmol/L DHA for 24 h(P<0.01).The IC50 of DHA on A549 cells was46.26 μmol/L.According to IC50 concentration analysis,the inhibi-tion rates of A549 cells treated with 50 μmol/L DHA for 0,24,48 and 72h were 1.53%,53.50%,63.84%and 69.91%,and the cells inhibition rates of A548 cells increased compared with the previous observation time point,namely 0,24 and 48 h(P<0.01).The colony formation assay showed that the colony formation number of A549 cells in DHA treated group decreased compared with the control group(P<0.01).Flow cytometry results showed that compared with the control group,the proportion of CD8+T cells induced by A549 cells in the co-culture system and the proportion of CD8+T cells expressing perforin and granzyme B were higher in DHA pretreatment group(P<0.01).Conclusion DHA inhibits the growth of NSCLC cells and promotes anti-tumor immune response of CD8+T cells induced by NSCLC cells.

Objective To investigate the feasibility of leucocyte-reduced pooled platelet concentrates from whole blood stored at 4℃,and provide theoretical basis for the components preparation.Methods The collected 400 mL ACD-B antico-agulant whole blood was randomly divided into two groups,stored at 4℃and room temperature.The buffy coat was prepared within 6 hours and store at 22℃until next day to prepare leucocyte-reduced pooled platelet concentrates.Platelet samples on day 1,3,5 and 7 were taken for the blood cell count and related parameter detection.The pH,glucose and lactic acid con-tent were determined to reflect the metabolic status,and the thromboelastography,platelet aggregation rate and PAC-1 and CD62P expression were determined to reflect the function and activation of platelets.The difference in platelets between two groups were analyzed.Results With the extension of storage time,the count of leucocyte-reduced pooled platelet concen-trates decreased gradually,but the platelets distribution width(PDW),mean platelet volume(MPV)and platelet-larger cell ratio(P-LCR)increased gradually in two groups,with no statistical significance(P＞0.05).The pH and glucose con-tents in two groups gradually decreased,but the lactic acid content gradually increased,with no significant difference(P＞0.05).The thrombelastogram showed MA value that reflecting platelet function has no significant change during the storage,and there was no significant difference between the two groups(P＞0.05).The aggregation rates decreased while the expres-sion of PAC-1 and CD62P increased gradually with the prolongation of preservation time,with no significant difference be-tween the two groups(P＞0.05).Conclusion There is no significant difference in platelet count,function and activation between whole blood stored at 4℃and at room temperature within 6 hours.Whole blood stored at 4℃within 6 hours can be considered as the raw material for leucocyte-reduced pooled platelet concentrates.

Pyridaben is a broad-spectrum acaricide widely used in agriculture, accidental or self-administration of large doses of pyridaben can cause multiple organ failure in patients. Due to its damage to multiple organs and no specific antidote, the mortality rate is high. This paper reports two patients who took a large amount of pyridaben, developed severe metabolic acidosis, hyperlactatemia, toxic encephalopathy, and liver, kidney, heart and digestive tract damage. After timely gastric lavage, catharsis, organ support andblood purification treatment, the condition improved and discharged. It is expected to provide clinical ideas for the treatment of pyridaben poisoning.