OBJECTIVE To explore the effects of Tianma xiongling zhixuan tablet on autophagy in vascular endothelial cells of rats and its potential mechanism. METHODS The rat aortic endothelial cells （RAECs） were divided into normal group， model group， blank serum group， traditional Chinese medicine （TCM） medicated serum group， autophagy blocker group， autophagy agonist group， and TCM combined with autophagy agonist group. Except for normal group， other groups were given 10 μg/mL lipopolysaccharide for 24 hours to induce RAECs inflammation injury model. Blank serum group was treated with 10% blank serum； TCM medicated serum group received 10% medicated serum derived from Tianma xiongling zhixuan tablet； autophagy blocker group was treated with 20 μmol/L of PD98059； autophagy agonist group was administered 50 μmol/L Honokiol. Lastly， the TCM combined with autophagy agonist group was given both 10% medicated serum derived from Tianma xiongling zhixuan tablet and 50 μmol/L Honokiol. The morphological characteristics of RAECs in each group were observed. The cell viability of each group， the contents of endothelin-1 （ET-1） and nitric oxide （NO）， mitochondrial reactive oxygen species， mitochondrial membrane potential， and the expression levels of PTEN-induced kinase 1 （PINK1）， Parkin， ubiquitin-binding protein （p62）， and microtubule-associated protein 1 light chain 3 （LC3） were detected. RESULTS Compared with model group， the levels of ET-1， mitochondrial reactive oxygen species， and the relative expressions of PINK1， Parkin， and LC3 proteins in the autophagy blocker group and TCM medicated serum group were decreased or down-regulated significantly （P＜0.05 or P＜0.01）； the cell viability rate （only autophagy blocker group）， NO level， mitochondrial membrane potential， and the E-mail：46164660@qq.com relative expression level of p62 protein were increased or up-regulated significantly （P＜0.05 or P＜0.01）； the pathological damage of RAECs was significantly improved， the number of cells increased significantly， and the typical paving stone-like characteristics were restored. The levels of ET-1， mitochondrial reactive oxygen species， and the relative expression levels of Parkin and LC3 proteins in the autophagy agonist group were increased or up-regulated significantly （P＜0.05 or P＜0.01）， while cell viability rate was decreased significantly （P＜0.05）， the damage of RAECs was aggravated. Compared with the autophagy agonist group， the cell viability rate and the relative expression level of p62 protein in TCM combined autophagy agonist group were increased or up-regulated significantly （P＜0.05 or P＜0.01）， while the levels of ET-1， the relative expression levels of PINK1， Parkin， and LC3 proteins were down-regulated significantly （P＜ 0.01）， the damage of RAECs was reversed to a certain extent. CONCLUSIONS Tianma xiongling zhixuan tablet protects vascular endothelial function by regulating mitochondrial autophagy， the mechanism of which may be associated with the regulation of PINK1/Parkin signaling pathway and the inhibition of mitochondrial autophagy.

Ursodeoxycholic acid(UDCA)is a naturally occurring,low-toxicity,and hydrophilic bile acid(BA)in the human body that is converted by intestinal flora using primary BA.Solute carrier family 7 member 11(SLC7A11)functions to uptake extracellular cystine in exchange for glutamate,and is highly expressed in a variety of human cancers.Retroperitoneal liposarcoma(RLPS)refers to liposarcoma originating from the retroperitoneal area.Lipidomics analysis revealed that UDCA was one of the most significantly down-regulated metabolites in sera of RIPS patients compared with healthy subjects.The augmentation of UDCA concentration(≥25 μg/mL)demonstrated a suppressive effect on the proliferation of liposarcoma cells.[15N2]-cystine and[13Cs]-glutamine isotope tracing revealed that UDCA impairs cystine uptake and glutathione(GSH)synthesis.Mechanistically,UDCA binds to the cystine transporter SLC7A11 to inhibit cystine uptake and impair GSH de novo synthesis,leading to reactive oxygen species(ROS)accumulation and mitochondrial oxidative damage.Furthermore,UDCA can promote the anti-cancer effects of ferroptosis inducers(Erastin,RSL3),the murine double minute 2(MDM2)inhibitors(Nutlin 3a,RG7112),cyclin dependent kinase 4(CDK4)inhibitor(Abemaciclib),and glutaminase inhibitor(CB839).Together,UDCA functions as a cystine exchange factor that binds to SLC7A11 for antitumor activity,and SLC7A11 is not only a new transporter for BA but also a clinically applicable target for UDCA.More importantly,in combination with other antitumor chemotherapy or physiotherapy treatments,UDCA may provide effective and promising treatment strategies for RLPS or other types of tumors in a ROS-dependent manner.

The reliability and practicality of research findings in health economics are gradually becoming core issues of close concern for clinical and public health experts. As healthcare resources remain under increasing pressure, conducting efficient cost-effectiveness analyses and achieving rational resource allocation are becoming ever more critical. In recent years, medical laboratory health economics has transitioned from purely academic discussions to integration into clinical practice, becoming a key tool for improving the efficiency and quality of healthcare services. It has demonstrated remarkable results in optimizing patient management and medical decision-making processes. So we invited experts from the fields of medical laboratory science and health economics to share valuable experiences and unique insights on topics such as cost assessment methods, pricing strategies, quality regulation, and the role of medical laboratory health economics in enhancing clinical practice and patient benefits. These experts generally agree that, while research in medical laboratory health economics has shown significant advantages and effectively addressed urgent clinical needs in resource allocation and cost control, it still faces multiple challenges, including limitations in research methodology application, high operational costs, and insufficient standardization of management systems.

A 36-year-old male presented to the Department of Neurosurgery of the Second People′s Hospital of Hunan Province on February 12, 2024, due to "10 days of aggravated paroxysmal headache and 1 day of mental abnormality". Ten days ago, after catching a cold, the patient developed persistent low fever and paroxysmal headache. On February 12, 2024, acuted mental and behavioral abnormalities developed, including slow response, self-talk, defecation and urination, no sense of shame and other mental and behavioral abnormalities. On February 22nd, metagenomic next-generation sequencing (mNGS) in cerebrospinal fluid confirmed feline rickettsia infection. One week after doxycycline anti-rickettsia treatment, cerebrospinal fluid mNGS results indicated that the etiology turned negative, and the clinical symptoms improved. Mental disorders caused by rickettsial encephalitis in cats are rare but clinically significant. This case highlights the diagnostic value of mNGS in critical and difficult cases, and supports its integration with traditional diagnostic techniques to achieve precision medicine.

Since the introduction of the radioallergosorbent test in 1967, the in vitro diagnosis (IVD) of allergen testing has undergone 58 years of development. This paper systematically reviews the historical progression of allergen detection IVD in China, providing a detailed list of classification in terms of the major allergen detection methods currently used domestically. It also discusses the future trends in the field. Furthermore, the paper highlights the existing challenges and aims to offer clinical guidance for medical professionals working in the field of allergy medicine.

Objective To find out whether photobiomodulation(PBM)can mitigate cognitive dysfunction caused by chronic stress by affecting levels of adenosine triphosphate(ATP)and adenosine receptors.Methods Twenty-four C57BL/6J mice were randomly divided into a control group,a stress group,and a treatment group.Chronic unpredictable mild stress was used to establish a mouse model of stress.Six weeks into modeling,the treatment group was subjected to one week of PBM interventions.Behavioral tests were conducted to observe behavioral changes in the mice.Western blotting(WB)was used to detect the expressions of A1,A2B,and A3 adenosine receptors in the hippocampus and prefrontal cortex of mice in the three groups.Twelve C57BL/6J mice were randomly divided into a control group and an intervention group.The intervention group received a week of PBM interventions and underwent behavioral testing.WB was used to detect the expression changes of A1,A2B,and A3 adenosine receptors in the hippocampus and prefrontal cortex in both groups.Immunofluorescence assay was adopted to detect the expression of c-Fos in the hippocampus of mice in the two groups.The ATP assay kit made by Beyotime Biotechnology Co.,Ltd.was used to measure changes in ATP contents in the hippocampus and prefrontal cortex tissues of mice.Cell experiments were conducted to verify the effect of PBM on intracellular ATP contents.Results Mice in the stress group covered a similar distance to the control group,but finished far fewer platform crossings.There was no significant difference between the treatment group and the control group in the number of times of platform crossings,but compared favorably with the stress group where the levels of adenosine receptors in the hippocampus and prefrontal cortex were lower,but were increased by PBM.After PBM interventions in normal mice,platform crossings were increased significantly compared to the control group.PBM also raised adenosine receptor levels and ATP contents in the hippocampus and prefrontal cortex,and increased hippocampal c-Fos expressions.In vitro,PBM elevated intracellular ATP levels.Conclusion PBM may improve chronic stress-induced cognitive dysfunction by regulating ATP levels and adenosine receptor expressions,thereby modulating neuronal responsiveness in the hippocampus.

Objective:To investigate differentially expressed lipid molecules and their associated metabolic pathways in lung tissue using lipidomic analysis in a rat model of acute lung injury (ALI).Methods:An ALI rat model was established via intratracheal instillation of lipopolysaccharide (LPS). Twenty rats were randomly allocated into an ALI group and a control group ( n = 10 per group). The left lung was subjected to histopathological evaluation, while the right lung underwent untargeted lipidomics analysis. Ultra-high-performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS) was employed for lipid profiling. Principal component analysis (PCA) and orthogonal partial least squares-discriminant analysis (OPLS-DA) were performed to assess intergroup differences and determine variable importance in projection (VIP) scores. Differential lipids were screened based on VIP and fold change.Lipid identification and metabolic pathway analysis were conducted using MetaboAnalyst 5.0 and the Kyoto Encyclopedia of Genes and Genomes (KEGG) database. Results:Among 1 022 detected lipid molecules, 47 were differentially expressed (VIP > 1, FC > 2.0 or < 0.5, P< 0.05). Subsequent analysis identified 12 structurally annotated lipids ( P < 0.05), predominantly enriched in glycerophospholipid metabolism, linoleic acid metabolism, and α-linolenic acid metabolism pathways. Notably, phosphatidylcholines (PCs) and lysophosphatidylcholines (LPCs) exhibited significant alterations in the ALI group. Conclusions:The ALI model demonstrated substantial dysregulation of lipid metabolism, particularly involving PCs and LPCs, with prominent perturbations in glycerophospholipid metabolism. This provides a scienctific basis for indepth research on the pathogenesis mechanism of ALI/acute respiratory distress syndrome (ARDS) .

Ursodeoxycholic acid (UDCA) is a naturally occurring, low-toxicity, and hydrophilic bile acid (BA) in the human body that is converted by intestinal flora using primary BA. Solute carrier family 7 member 11 (SLC7A11) functions to uptake extracellular cystine in exchange for glutamate, and is highly expressed in a variety of human cancers. Retroperitoneal liposarcoma (RLPS) refers to liposarcoma originating from the retroperitoneal area. Lipidomics analysis revealed that UDCA was one of the most significantly downregulated metabolites in sera of RLPS patients compared with healthy subjects. The augmentation of UDCA concentration (≥25 μg/mL) demonstrated a suppressive effect on the proliferation of liposarcoma cells. [¹⁵N₂]-cystine and [¹³C₅]-glutamine isotope tracing revealed that UDCA impairs cystine uptake and glutathione (GSH) synthesis. Mechanistically, UDCA binds to the cystine transporter SLC7A11 to inhibit cystine uptake and impair GSH de novo synthesis, leading to reactive oxygen species (ROS) accumulation and mitochondrial oxidative damage. Furthermore, UDCA can promote the anti-cancer effects of ferroptosis inducers (Erastin, RSL3), the murine double minute 2 (MDM2) inhibitors (Nutlin 3a, RG7112), cyclin dependent kinase 4 (CDK4) inhibitor (Abemaciclib), and glutaminase inhibitor (CB839). Together, UDCA functions as a cystine exchange factor that binds to SLC7A11 for antitumor activity, and SLC7A11 is not only a new transporter for BA but also a clinically applicable target for UDCA. More importantly, in combination with other antitumor chemotherapy or physiotherapy treatments, UDCA may provide effective and promising treatment strategies for RLPS or other types of tumors in a ROS-dependent manner.

Objective To explore the related functional mechanism of Xihuang pill containing serum inter-vention in breast cancer cells based on microRNA(miR)21-5p targeting FAM13A gene.Methods Bioinfor-matics websites was used to predict potential miRNAs of FAM13A gene,double luciferase reporter experi-ments were conducted to verify the binding site relationship between FAM13A and predicted miRNAs.The Xihuang pill containing serum was prepared,and human breast cancer MDA-MB-231 cells were cultured.The proliferation of MDA-MB-231 cells was interfered by the Xihuang pill containing serum with different dilution ratios by CCK-8 test,and the best dilution ratio concentration of Xihuang pill containing serum to inhibit the proliferation of breast cancer cells was selected.Real time fluorescence quantitative PCR(RT-qPCR)was ap-plied to detect the relative expression levels of FAM13A mRNA,as well as the relative expression levels of miR21-5p,in MDA-MB-231 cells after intervention with Xihuang pill containing serum.Cell proliferation(Edu)assay and cell apoptosis detection(TUNEL)assay were used to detect the effects of Xihuang pill con-taining serum intervention on cell proliferation and apoptosis function in MDA-MB-231 cells.The siRNA lentiviral transfection on MDA-MB-231 cells was performed to knock down the FAM13A gene,and Edu assay and TUNEL assay were used to detect changes in proliferation and apoptosis ability of MDA-MB-231 cells af-ter lentiviral transfection.The expression level of miR21-5p in MDA-MB-231 cells after FAM13A gene knock-out was detected by RT-qPCR technology.Results Target Scan online website predicted the potential miR-21-5p binding sequence in the 3'UTR of FAM13A mRNA,and dual luciferase reporter assay confirmed the in-teraction between miR-21-5p and FAM13A.After intervention of MDA-MB-231 cells with Xihuang pill drug containing serum,RT-qPCR results showed that compared with the control group(NC group),the Xihuang pill drug containing serum group(XHW group)downregulated the expression levels of FAM13A mRNA(P＜0.05),and upregulated the expression level of miR21-5p(P＜0.05).Compared with the NC group,the XWH group showed reduced cell proliferation ability and promoted cell apoptosis.(P＜0.05).After silencing the FAM13A gene in MDA-MB-231 cells,compared with the control group(shCtrl group),the shFAM13A group showed a significant decrease in cell proliferation ability and promoted cell apoptosis.The RT-qPCR re-sults showed that compared with the shCtrl group,the expression level of miR21-5p was significantly upregu-lated in the shFAM13A group(P＜0.05).Conclusion Xihuang pill could participate in the anti-tumor treat-ment of breast cancer by regulating miR21-5p to affect the expression level of FAM13A gene.

Breast cancer is one of the most common malignant tumors among women worldwide, with an increasing incidence rate year by year, making it a significant public health concern. With the continuous advancement of tumor biology research, N 6-methyladenosine (m 6A) modification, as an important form of RNA modification, has attracted growing attention. The m 6A modification, the most prevalent RNA modification in eukaryotes, occurs in almost all types of RNA and plays a critical role in the occurrence, progression, and metastasis of breast cancer. It influences cell proliferation, apoptosis, and alterations in the tumor microenvironment, though the specific mechanisms underlying these effects require further in-depth investigation. Moreover, the specific patterns of m 6A modification demonstrate its potential as a novel biomarker for breast cancer, which could provide new directions for early diagnosis and prognosis evaluation.