Functional dyspepsia （FD） is a prioritized disease category where traditional Chinese medicine （TCM） demonstrates distinct therapeutic advantages. The current western medicine treatment for FD is mainly based on proton pump inhibitors and prokinetic agents， with digestive enzymes， probiotics and antidepressants serving as adjuvant medication， yet such therapies still have certain limitations. TCM treatment for FD includes oral administration of Chinese herbal formulas and Chinese patent medicines， as well as external TCM therapies such as acupuncture and moxibustion， acupoint application， hot medicinal compress therapy， rubbing with ointment， medicinal iontophoresis， auricular acupoint therapy and tui na （Chinese medical massage）. The combined treatment of FD with integrated TCM and western medicine can significantly improve clinical effectiveness and reduce adverse reactions. The common mechanisms underlying the therapeutic effects of both TCM and western medicine revolve around the core pathological processes of FD， mainly focusing on restoring gastrointestinal motility， regulating the levels of brain-gut peptides， modulating intestinal microecology， and ameliorating inflammatory status. The differential mechanisms lie in the precise targeting feature of western medicine versus the holistic-regulating and multi-target characteristics of TCM， and the two approaches exert a synergistic effect to enhance efficacy. This paper proposes to leverage the advantages of TCM in holistic regulation and the strengths of western medicine in targeted treatment， so as to provide personalized and comprehensive treatment regimens for FD patients.

Water resources are crucial for environmental protection and the health of humans, plants, and animals. Contamination of water by pathogens such as bacteria, viruses, and protozoa can lead to outbreaks of various water-related infectious diseases, posing serious threats to public health and causing significant economic and social losses. Therefore, accurate and timely detection of pathogens in water sources and related substances is vital for preventing water-borne infectious diseases. In recent years, various molecular techniques have been extensively used to address water quality issues, including emerging isothermal amplification techniques such as loop-mediated isothermal amplification (LAMP), nucleic acid sequence-based amplification (NASBA), recombinase polymerase amplification (RPA), and helicase-dependent amplification (HDA). These techniques have significantly enhanced the capacity to detect and monitor pathogens in diverse aquatic systems and wastewater. This review focused on commonly used isothermal amplification techniques in water quality assessment and their recent advancements in environmental pathogens detection.

Objective To evaluate the role of distortion product otoacoustic emissions (DPOAE) testing in evaluating early hearing loss among noise-exposed workers. Methods A total of 174 noise-exposed workers in a metal shipbuilding enterprise were selected as the research subjects by the convenience sampling method. Pure tone audiometry (PTA), DPOAE and the level of noise exposure were conducted on the workers. The rank correlation analysis was used to analyze the correlation between DPOAE amplitude and PTA threshold. The multilevel model was used to analyze the effects of gender, age, noise exposure intensity, cumulative noise exposure (CNE), hearing loss classification and PTA threshold on DPOAE results. Results At the frequencies of 0.50, 1.00, 2.00, 3.00, 4.00, 6.00 and 8.00 kHz, the DPOAE amplitude was negatively correlated with the PTA threshold (rank correlation coefficients were -0.12, -0.48, -0.47, -0.18, -0.23, -0.44, -0.19, respectively, all P<0.01). At the most frequencies, DPOAE amplitude was negatively correlated with age and CNE (all P<0.05). The results of multilevel model analysis showed that there were significant differences in DPOAE amplitudes at certain frequencies across gender, age, noise intensity, CNE, and hearing loss classification (all P<0.05). Significant differences in DPOAE responses were found among different CNE and hearing loss groups (all P<0.01). Conclusion DPOAE testing can objectively reflect the hearing status of noise-exposed workers and could be considered for inclusion in routine hearing monitoring to facilitate early detection of noise-induced hearing loss.

ObjectiveAs a second messenger in intracellular signal transduction, Ca²⁺ plays an important role in cell migration. Previous studies have demonstrated that extracellular Ca²⁺ influx can promote electric field-guided cell migration, known as electrotaxis. However, the effect of intracellular Ca²⁺ flow on electrotaxis is unclear. Therefore, in this study, we investigate the effect of Ca²⁺ flux on the electrotaxis of Dictyostelium discoideum. MethodsThe electrotaxis of Dictyostelium discoideum was investigated by applying a direct current (DC) electric field. Cell migration was recorded using a real-time imaging system. Calcium channel inhibitors, the extracellular Ca²⁺ chelator EGTA, Ca²⁺-free DB buffer, and caffeine were applied to investigate the impact of intra- and extracellular Ca²⁺ flow on electrotaxis. The involvement of G proteins and ERK2 in directed cell migration mediated by endoplasmic reticulum Ca²⁺ release was explored using mutants. ResultsDictyostelium discoideum migrated toward the cathode in the electric field in a voltage-dependent manner. The intracellular Ca²⁺ concentration of the cells was significantly increased in the electric field. Inhibition of both extracellular Ca²⁺ influx and intracellular Ca²⁺ release suppressed cell electrotaxis migration. Inhibition of endoplasmic reticulum Ca²⁺ release induced by caffeine significantly impaired the electrotaxis of Dictyostelium discoideum. Deletion of Gα2, Gβ, Gγ, and Erk2 notably reduced the electrotaxis of the cells. Enhancing Ca²⁺ release mediated by caffeine restored the electrotaxis of the Gα2^-, Gβ ^-, and Erk2^- mutant cells partially or completely, but did not restore electrotaxis in the Gγ^- mutant cells. ConclusionCa²⁺ release from the endoplasmic reticulum regulates electrotaxis migration in Dictyostelium discoideum and is involved in the regulation of cell electrotaxis by G proteins and ERK2.

ObjectiveNon-invasive magnetic stimulation technology has been widely used in the treatment of Alzheimer’s disease (AD), but there is a lack of convenient and timely methods for evaluating and providing feedback on the effectiveness of the stimulation, which can be used to guide the adjustment of the stimulation protocol. This study aims to explore the possibility of heart rate variability (HRV) in diagnosing AD and guiding AD magnetic stimulation intervention techniques. MethodsIn this study, we used a 40 Hz, 10 mT pulsed magnetic field to expose AD mouse models to whole-body exposure for 18 d, and detected the behavioral and electroencephalographic signals before and after exposure, as well as the instant electrocardiographic signals after exposure every day. ResultsUsing one-way ANOVA and Pearson correlation coefficient analysis, we found that some HRV indicators could identify AD mouse models as accurately as behavioral and electroencephalogram(EEG) changes (P<0.05) and significantly distinguish the severity of the disease (P<0.05), including rMSSD, pNN6, LF/HF, SD1/SD2, and entropy arrangement. These HRV indicators showed good correlation and statistical significance with behavioral and EEG changes (r>0.3, P<0.05); HRV indicators were significantly modulated by the magnetic field exposure before and after the exposure, both of which were observed in the continuous changes of electrocardiogram (ECG) (P<0.05), and the trend of the stimulation effect was more accurately observed in the continuous changes of ECG. ConclusionHRV can accurately reflect the pathophysiological changes and disease degree, quickly evaluate the effect of magnetic stimulation, and has the potential to guide the pattern of magnetic exposure, providing a new idea for the study of personalized electromagnetic neuroregulation technology for brain diseases.

Objective To investigate the effect of Saikosaponin A(SSA)on the differentiation,apoptosis and function of mouse bone marrow derived macrophages(BMDM)-derived M1/M2 macrophages,and to explore its molecular mechanism.Methods BMDM was induced to differentiate into M1/M2 macrophages in vitro,and SSA was added at the same time:CCK-8 assay was used to detect the viability of BMDM and M1/M2 macrophages.The morphology of M1/M2 macrophages was observed by inverted fluorescence microscopy.Flow cytometry(FCM)and ELISA were used to detect the levels of surface markers and cytokines in M1/M2 macrophages.Real-time fluorescent quantitative PCR(qPCR)was used to detect the mRNA levels of IL-6,TNF-α and arginase-1(Arg-1).FCM was used to detect the phagocytosis of peritoneal macrophages to fluorescent microsphere particles.Immunofluorescence(IF)assay and Western blotting were used to detect the molecular mechanism of SSA regulating M1/M2 macrophages.Results No significant effect on viability of M1/M2 macrophages was observed at SSA concentration of 10.0 mg/L,and obvious inhibition was seen at a concentration of 15.0 mg/L(P<0.01).Treatment of 10.0 mg/L SSA induced obvious morphologic changes in M1/M2 macrophages,with M1 macrophages in irregular shape,a few having pseudopods,and some showing unclear boundaries;while some M2 macrophages presenting round or irregular(P<0.001)with unclear boundaries.SSA treatment also resulted in significantly decreased proportion of M1/M2 macrophages after BMDM differentiation(P<0.05),with reduced contents of IL-6 and TNF-α secreted by M1 macrophages and their mRNA levels(P<0.05),but increased secretion of Arg-1 and mRNA levels by M2 macrophages(P<0.05).SSA treatment also inhibited the phagocytosis ability of peritoneal macrophages to fluorescent microsphere particles(P<0.01)in a concentration-dependent manner.SSA decreased the phosphorylation of NF-kappaB(p-NF-κB)(P<0.01)and enhanced the phosphorylation of signal transducer and activator of transcription 6(p-STAT6)in M2 macrophages(P<0.05).Conclusion SSA may affect the differentiation and function of M1/M2 macrophages by regulating NF-κB and STAT6 signaling pathways.

Objective To investigate the effects of cinnamic aldehyde(CA)on Bcl-2-associated X protein(Bax)and Bcl-2 homologous antagonist/killer(Bak)in vascular endothelial cells of diabetic ulcer wound tissues,as well as on cell apoptosis.Methods ① Forty-eight healthy SPF-grade male SD rats(5 weeks old,weighing 180～220 g)were randomly assigned to a control group(12 rats)and a diabetes group(36 rats).The diabetic model was established with an intraperitoneal injection of 50 mg/kg STZ-citrate sodium solution and high-fat diet feeding.The diabetes group was further randomly divided into Model group,CA group,and the rb-bFGF group,with 12 animals in each group.Wounds in the Con and Model groups were disinfected and topically treated with normal saline,CA group received topical application of 4 μmol/L CA in PEG 400 gel,and those of the rb-bFGF group were treated with bevacizumab gel.The wound healing rate of each group was calculated at 3,7 and 14 d after intervention.At 14 d after intervention,pathological changes in the wounds were observed with HE staining,and the expression levels of Bax and Bak were detected by Western blotting.② Human umbilical vein endothelial cell line EA.hy926 was treated with 175 mmol/L glucose for 48 h to establish a cell model of high glucose injury.The experimental cells were divided into control group,model group and CA treatment group.Cell scratch test and tube formation test were performed respectively to determine the migration ability and angiogenesis of the cells.The expression levels of Bax and Bak was detected with immunofluorescence assay,and cell apoptosis was detected by TUNEL staining.Results ①The diabetic rats in the Model group exhibited significantly higher blood glucose level(P<0.05),declined wound healing rate at 7 and 14 d after intervention(P<0.05),and enhanced expression levels of Bax and Bak(P<0.05)when compared with the control group.Pathological observation revealed that,at 14 d after intervention,accompanied with inflammatory reactions,dense infiltration of inflammatory cells,fewer new blood vessels,and continuous fluid exudation in the wound were observed in the Model group,but the control group presented complete epithelialization in full-thickness skin.Compared with the conditions in the Model group,both CA and rb-bFGF treatment improved the epithelialization process,with mature granulation tissues,showing good healing condition,promoted wound healing rate(P<0.05),and decreased the expression levels of Bax and Bak(P<0.05).② The results of cell experiments showed that the cells of the model group showed significantly reduced migration ability and tube formation ability(P<0.05),reduced protein levels of Bax and Bak(P<0.05),and lower apoptotic rate(P<0.05)when compared with the cells in the model group.Conclusion CA can inhibit the expression of apoptosis-related proteins Bax and Bak,promote the migration and tube formation of vascular endothelial cells,and inhibit the cell apoptosis under high glucose condition,which may be an important reason for its promoting wound healing in diabetic ulcer rats.

Cholesterol on the cell membrane plays a crucial role in regulating membrane proteins,influencing cell functions,and the occurrence and development of tumors.The CD44 receptor protein is closely associated with tumor invasion and metastasis.Therefore,developing biosensors capable of in-situ simultaneous monitoring of cholesterol and CD44 receptor protein on the cell membrane is of great significance for disease diagnosis.In this study,a spatially resolved strategy dual-signal multifunctional electrochemiluminescence(ECL)sensor was designed.The positive potential luminescent probe(ALC)was prepared by combining gold nanostars with luminol and cholesterol oxidase(ChOx),and the negative potential luminescent probe(CZA)was prepared by combining carbon quantum dots(CQD)with ZIF-8 and gold nanoparticles(AuNPs).The dual probes were fixed on dual working electrodes respectively to construct a spatial resolution dual signal sensor,and the signals were independently output with K2S2O8 as co-reactant.When the measurement signal of ALC probe was enhanced due to enzymatic catalysis of cholesterol,CZA synchronously output the internal reference signal,realizing ratio ECL detection of cholesterol,with a linear range of 50 nmol/L-1600 μmol/L and a detection limit of 20 nmol/L.Furthermore,after the double probes were respectively modified with folic acid(FA)and hyaluronic acid(HA),a spatially resolved dual-functional cell sensor was constructed by capturing human hepatoma cells HepG2 through ligand-receptor specific recognition.This sensor enabled the simultaneous monitoring of cholesterol-ChOx catalytic reaction and CD44-HA recognition on the cell membrane,as well as the quantitative detection of cancer cells and cholesterol on the cell membrane.The results showed that the linear detection range for HepG2 cell was 100-10000 cell/mL.By reducing cholesterol on the cell membrane using methyl-β-cyclodextrin(MβCD)downregulated CD44 expression,it was found that the cholesterol content was positively correlated with CD44 expression on the cell membrane.The control experiments showed that the analysis method was feasible.The designed ECL sensor could be used to detect cholesterol ratiometrically and provided a new method for the simultaneous analysis of multiple functional molecules in cells.

Metabolic diseases have seen a steady increase in incidence in recent years, becoming one of the main causes of sub-health status globally. Neutrophil extracellular traps(NETs) are reticular complexes containing DNA, which trap foreign microorganisms or induce an immune response. Current research indicates that NETs are widely active in various metabolic diseases and can cause severe damage to the body through multiple mechanisms, including promoting blood glucose elevation, damaging vascular endothelial cells, forming vascular embolisms, triggering intense inflammation, and promoting lipid accumulation. Therefore, intervening in NETs is an important approach to treating metabolic diseases. Research has shown a close relationship between the theory of spleen heat-turbid toxin theory and metabolic diseases-NETs mechanism. The basic pathogenesis include the internal accumulation of phlegm-dampness, qi stagnation and blood stasis, internal accumulation of dampness-heat, phlegm and blood stasis, and flourishing toxic heat. Various Chinese herbal medicines with the functions of dispelling dampness, resolving phlegm, promoting blood circulation to remove blood stasis, and clearing heat and toxins, along with their extracts and compound prescriptions, can treat metabolic diseases by regulating NETs and delaying disease progression. This paper systematically outlined the formation mechanisms of NETs, their connection to metabolic diseases, the theoretical basis in TCM, their roles in numerous metabolic diseases, and the current research status of TCM in regulating NETs to prevent and control metabolic diseases, aiming to provide effective reference ideas for developing therapeutic strategies for metabolic diseases.
Humans ; Extracellular Traps/metabolism* ; Metabolic Diseases/metabolism* ; Drugs, Chinese Herbal/therapeutic use* ; Animals ; Neutrophils/metabolism* ; Medicine, Chinese Traditional