Multi-omics analysis provides new insights into mechanism of didymin on non-alcoholic fatty liver disease in rats.

BACKGROUND: Non-alcoholic fatty liver disease (NAFLD) is one of the most common liver diseases accompanied by lipid and glucose metabolism disorder. Didymin has been reported to have various hepatoprotective effects, however, its potential effects and mechanisms on NAFLD remain unclear from the perspective of the whole. PURPOSE: To investigate the underlying mechanism of didymin against NAFLD using multi-omics technologies. METHODS: Rats were fed with a high-fat diet (HFD) for 8 weeks to induce NAFLD, followed by didymin treatment for 8 weeks. Next, biochemical analysis and histopathological examinations were performed to evaluate the effects of didymin. The key regulating pathways were predicted using transcriptomics, metabolomics and proteomics, and the target pathways were then verified by detecting the key genes/proteins using various experiments. RESULTS: Didymin markedly mitigated liver injury and excessive lipid droplet accretion. An integrative multi-omics analysis suggested that the PPAR signaling cascade and insulin signaling pathway might serve as pivotal mechanisms underlying the modulation of lipid and glucose homeostasis by didymin. Further dissection identified five pivotal genes (PPARα, PPARß, FABP4, ANGPTL4, and PLIN2) and four genes (HK1, HK3, GCK, and PTPN1) as potential hubs within these pathways. Subsequent validation experiments, including qPCR and Western blot, demonstrated upregulated expression of PPARα and PPARß, indicating the activation of the PPAR pathway by didymin. Concurrently, didymin appeared to modulate the insulin signaling pathway, as evidenced by the upregulated expression of HK1 and downregulated expression of PTPN1. Notably, the manipulation of PPARα, PPARß, and PTPN1 expression in LO2 cells through silence or overexpression confirmed that didymin significantly reduced lipid accumulation, with its molecular targets likely being the PPAR and insulin pathways. CONCLUSIONS: Our findings demonstrate that didymin has a protective effect on NAFLD, and its underlying mechanism may be associated with the regulation of the PPAR and insulin signaling pathways.

pH and thiosulfate dependent microbial sulfur oxidation strategies across diverse environments.

Sulfur oxidizing bacteria (SOB) play a key role in sulfur cycling in mine tailings impoundment (TI) waters, where sulfur concentrations are typically high. However, our understanding of SOB sulfur cycling via potential S oxidation pathways (sox, rdsr, and S4I) in these globally ubiquitous contexts, remains limited. Here, we identified TI water column SOB community composition, metagenomics derived metabolic repertoires, physicochemistry, and aqueous sulfur concentration and speciation in four Canadian base metal mine, circumneutral-alkaline TIs over four years (2016 - 2019). Identification and examination of genomes from nine SOB genera occurring in these TI waters revealed two pH partitioned, metabolically distinct groups, which differentially influenced acid generation and sulfur speciation. Complete sox (csox) dominant SOB (e.g., Halothiobacillus spp., Thiomonas spp.) drove acidity generation and S2O3 2- consumption via the csox pathway at lower pH (pH ~5 to ~6.5). At circumneutral pH conditions (pH ~6.5 to ~8.5), the presence of non-csox dominant SOB (hosting the incomplete sox, rdsr, and/or other S oxidation reactions; e.g. Thiobacillus spp., Sulfuriferula spp.) were associated with higher [S2O3 2-] and limited acidity generation. The S4I pathway part 1 (tsdA; S2O3 2- to S4O6 2-), was not constrained by pH, while S4I pathway part 2 (S4O6 2- disproportionation via tetH) was limited to Thiobacillus spp. and thus circumneutral pH values. Comparative analysis of low, natural (e.g., hydrothermal vents and sulfur hot springs) and high (e.g., Zn, Cu, Pb/Zn, and Ni tailings) sulfur systems literature data with these TI results, reveals a distinct TI SOB mining microbiome, characterized by elevated abundances of csox dominant SOB, likely sustained by continuous replenishment of sulfur species through tailings or mining impacted water additions. Our results indicate that under the primarily oxic conditions in these systems, S2O3 2- availability plays a key role in determining the dominant sulfur oxidation pathways and associated geochemical and physicochemical outcomes, highlighting the potential for biological management of mining impacted waters via pH and [S2O3 2-] manipulation.

Operando chemo-mechanical evolution in LiNi0.8Co0.1Mn0.1O2 cathodes.

Ni-rich LiNi x Co y Mn z O2 (NCMxyz, x + y + z = 1, x ≥ 0.8) layered oxide materials are considered the main cathode materials for high-energy-density Li-ion batteries. However, the endless cracking of polycrystalline NCM materials caused by stress accelerates the loss of active materials and electrolyte decomposition, limiting the cycle life. Hence, understanding the chemo-mechanical evolution during (de)lithiation of NCM materials is crucial to performance improvement. In this work, an optical fiber with µÎµ resolution is designed to in operando detect the stress evolution of a polycrystalline LiNi0.8Co0.1Mn0.1O2 (P-NCM811) cathode during cycling. By integrating the sensor inside the cathode, the stress variation of P-NCM811 is completely transferred to the optical fiber. We find that the anisotropy of primary particles leads to the appearance of structural stress, inducing the formation of microcracks in polycrystalline particles, which is the main reason for capacity decay. The isotropy of primary particles reduces the structural stress of polycrystalline particles, eliminating the generation of microcracks. Accordingly, the P-NCM811 with an ordered arrangement structure delivered high electrochemical performance with capacity retention of 82% over 500 cycles. This work provides a brand-new perspective with regard to understanding the operando chemo-mechanical evolution of NCM materials during battery operation, and guides the design of electrode materials for rechargeable batteries.

Prognostic and immunotherapeutic significances of M2 macrophage-related genes signature in lung cancer.

Objective: We aimed to investigate the immunological significance of M2 macrophage-related genes in lung cancer (LC) patients, specifically focusing on constructing a risk score to predict patient prognosis and response to immunotherapy. Methods: We developed a novel risk score by identifying and incorporating 12 M2 macrophage-related genes. The risk score was calculated by multiplying the expression levels of risk genes by their respective coefficients. Through comprehensive enrichment analysis, we explored the potential functions distinguishing high- and low-risk groups. Moreover, we examined the relationship between patients in different risk groups and immune infiltration as well as their response to immunotherapy. The single-cell RNA sequencing data were acquired to ascertain the spatial pattern of RNF130 expression. The expression of RNF130 was examined using TCGA datasets and verified by HPA. The qRT-PCR was employed to examine RNF130 expression in LC cells. Finally, in vitro experiments were carried out to validate the expression and function of RNF130. Results: Our results indicated that the risk score constructed from 12 M2 macrophage-related genes was an independent prognostic factor. Patients in the high-risk group had a significantly worse prognosis compared to those in the low-risk group. Functional enrichment analysis showed a significant relationship between the risk score and immunity. Furthermore, we explored immune infiltration in different risk groups using seven immune algorithms. The results demonstrated a negative correlation between high-risk group patients and immune infiltration of B cells, CD4+ cells, and CD8+ cells. We further validated these findings using an immunotherapy response database, which revealed that high-risk patients were more likely to exhibit immune evasion and might have poorer immunotherapy outcomes. Additionally, drug sensitivity analysis indicated that patients in the high-risk group were more sensitive to certain chemotherapeutic and targeted drugs than those in the low-risk group. Single-cell analysis indicated that macrophages were the primary site of RNF130 distribution. The results from the TCGA and HPA database demonstrated a trend toward a low expression of RNF130 in LC. Finally, in vitro experiments further validated the expression and function of RNF130 in LC cells. Conclusions: The high-risk group constructed with M2 macrophage-related genes in LC was closely associated with poor prognosis, low immune cell infiltration, and poorer response to immunotherapy. This risk score can help differentiate and predict the prognosis and immune status of LC patients, thereby aiding in the development of precise and personalized immunotherapy strategies.

Harmine inhibits the proliferation and migration and promotes the apoptosis of colon cancer cells via inhibition of the FAK/AKT and ERK1/2/CREB signaling pathways.

Harmine is present in a variety of medicinal plants, and its effects on colon cancer cells remain unclear. Here, we found that harmine exhibited significant inhibitory effects on the proliferation of colon cancer cells by inhibiting the phosphorylation levels of the FAK/AKT and ERK1/2/CREB. Furthermore, harmine also inhibited the migration of colon cancer cells and suppressed the expression levels of MMP-2, MMP-9, and VEGF. Additionally, harmine-induced apoptosis in colon cancer cells by regulating the expression of Bcl-2 and Bax. In conclusion, our findings suggest that harmine exerts a significant inhibitory effect on the development of colon cancer cells.

Wavelength-tunable high-fidelity entangled photon sources enabled by dual Stark effects.

The construction of a large-scale quantum internet requires quantum repeaters containing multiple entangled photon sources with identical wavelengths. Semiconductor quantum dots can generate entangled photon pairs deterministically with high fidelity. However, realizing wavelength-matched quantum-dot entangled photon sources faces two difficulties: the non-uniformity of emission wavelength and exciton fine-structure splitting induced fidelity reduction. Typically, these two factors are not independently tunable, making it challenging to achieve simultaneous improvement. In this work, we demonstrate wavelength-tunable entangled photon sources based on droplet-etched GaAs quantum dots through the combined use of AC and quantum-confined Stark effects. The emission wavelength can be tuned by ~1 meV while preserving an entanglement fidelity f exceeding 0.955(1) in the entire tuning range. Based on this hybrid tuning scheme, we finally demonstrate multiple wavelength-matched entangled photon sources with f > 0.919(3), paving the way towards robust and scalable on-demand entangled photon sources for quantum internet and integrated quantum optical circuits.

Super-resolution diffractive neural network for all-optical direction of arrival estimation beyond diffraction limits.

Wireless sensing of the wave propagation direction from radio sources lays the foundation for communication, radar, navigation, etc. However, the existing signal processing paradigm for the direction of arrival estimation requires the radio frequency electronic circuit to demodulate and sample the multichannel baseband signals followed by a complicated computing process, which places the fundamental limit on its sensing speed and energy efficiency. Here, we propose the super-resolution diffractive neural networks (S-DNN) to process electromagnetic (EM) waves directly for the DOA estimation at the speed of light. The multilayer meta-structures of S-DNN generate super-oscillatory angular responses in local angular regions that can perform the all-optical DOA estimation with angular resolutions beyond the diffraction limit. The spatial-temporal multiplexing of passive and reconfigurable S-DNNs is utilized to achieve high-resolution DOA estimation over a wide field of view. The S-DNN is validated for the DOA estimation of multiple radio sources over 5 GHz frequency bandwidth with estimation latency over two to four orders of magnitude lower than the state-of-the-art commercial devices in principle. The results achieve the angular resolution over an order of magnitude, experimentally demonstrated with four times, higher than diffraction-limited resolution. We also apply S-DNN's edge computing capability, assisted by reconfigurable intelligent surfaces, for extremely low-latency integrated sensing and communication with low power consumption. Our work is a significant step towards utilizing photonic computing processors to facilitate various wireless sensing and communication tasks with advantages in both computing paradigms and performance over electronic computing.

The Regulatory Mechanism of Smilax China L. Saponins against Nonalcoholic Fatty Liver Is Revealed by Metabolomics and Transcriptomics.

This study was to investigate the effects of Smilax China L. saponins (SCS) on non-alcoholic fatty liver disease (NAFLD). Rats were fed a high-fat diet (HFD) for 8 weeks to induce NAFLD, followed by SCS treatment for 8 weeks. The effect of SCS on liver injury was observed by H&E staining and the regulative mechanism of SCS on lipid formation was exposed by detecting Oil red O, insulin resistance (IR), and fatty acids synthesis (FAS). Furthermore, transcriptomics and metabolomics were performed to analyze the potential targets. The experimental results indicated that SCS exerted a positive curative effect in alleviating HFD-induced overweight, hepatic injury, steatosis, and lipid formation and accumulation in rats, and the preliminary mechanism studies showed that SCS could alleviate IR, inhibit FAS expression, and reduce Acetyl-CoA levels. Besides, the integrative analysis of transcriptomics and metabolomics exposed the targets of SCS to regulate lipid production likely being the sphingolipid metabolism and glycerophospholipid metabolism pathways. This study demonstrates that SCS significantly ameliorates lipid metabolic disturbance in rats with NAFLD by relieving insulin resistance, inhibiting the FAS enzymes, and regulating the sphingolipid and glycerophospholipid metabolism pathways.

Identifying novel acute pancreatitis sub-phenotypes using total serum calcium trajectories.

BACKGROUND: Acute pancreatitis (AP) has heterogeneous clinical features, and identifying clinically relevant sub-phenotypes is useful. We aimed to identify novel sub-phenotypes in hospitalized AP patients using longitudinal total serum calcium (TSC) trajectories. METHODS: AP patients had at least two TSC measurements during the first 24 h of hospitalization in the US-based critical care database (Medical Information Mart for Intensive Care-III (MIMIC-III) and MIMIC-IV were included. Group-based trajectory modeling was used to identify calcium trajectory phenotypes, and patient characteristics and treatment outcomes were compared between the phenotypes. RESULTS: A total of 4518 admissions were included in the analysis. Four TSC trajectory groups were identified: "Very low TSC, slow resolvers" (n = 65; 1.4% of the cohort); "Moderately low TSC" (n = 559; 12.4%); "Stable normal-calcium" (n = 3875; 85.8%); and "Fluctuating high TSC" (n = 19; 0.4%). The "Very low TSC, slow resolvers" had the lowest initial, maximum, minimum, and mean TSC, and highest SOFA score, creatinine and glucose level. In contrast, the "Stable normal-calcium" had the fewest ICU admission, antibiotic use, intubation and renal replace treatment. In adjusted analysis, significantly higher in-hospital mortality was noted among "Very low TSC, slow resolvers" (odds ratio [OR], 7.2; 95% CI, 3.7 to 14.0), "moderately low TSC" (OR, 5.0; 95% CI, 3.8 to 6.7), and "Fluctuating high TSC" (OR, 5.6; 95% CI, 1.5 to 20.6) compared with the "Stable normal-calcium" group. CONCLUSIONS: We identified four novel sub-phenotypes of patients with AP, with significant variability in clinical outcomes. Not only the absolute TSC levels but also their trajectories were significantly associated with in-hospital mortality.

The Global and Regional Prevalence of Hospital-Acquired Carbapenem-Resistant Klebsiella pneumoniae Infection: A Systematic Review and Meta-analysis.

Background: Due to scarce therapeutic options, hospital-acquired infections caused by Klebsiella pneumoniae (KP), particularly carbapenem-resistant KP (CRKP), pose enormous threat to patients' health worldwide. This study aimed to characterize the epidemiology and risk factors of CRKP among nosocomial KP infections. Method: MEDLINE, Embase, PubMed, and Google Scholar were searched for studies reporting CRKP prevalence from inception to 30 March 2023. Data from eligible publications were extracted and subjected to meta-analysis to obtain global, regional, and country-specific estimates. To determine the cause of heterogeneity among the selected studies, prespecified subgroup analyses and meta-regression were also performed. Odds ratios of CRKP-associated risk factors were pooled by a DerSimonian and Laird random-effects method. Results: We retained 61 articles across 14 countries and territories. The global prevalence of CRKP among patients with KP infections was 28.69% (95% CI, 26.53%-30.86%). South Asia had the highest CRKP prevalence at 66.04% (95% CI, 54.22%-77.85%), while high-income North America had the lowest prevalence at 14.29% (95% CI, 6.50%-22.0%). In the country/territory level, Greece had the highest prevalence at 70.61% (95% CI, 56.77%-84.45%), followed by India at 67.62% (95% CI, 53.74%-81.79%) and Taiwan at 67.54% (95% CI, 58.65%-76.14%). Hospital-acquired CRKP infections were associated with the following factors: hematologic malignancies, corticosteroid therapies, intensive care unit stays, mechanical ventilations, central venous catheter implantations, previous hospitalization, and antibiotic-related exposures (antifungals, carbapenems, quinolones, and cephalosporins). Conclusions: Study findings highlight the importance of routine surveillance to control carbapenem resistance and suggest that patients with nosocomial KP infection have a very high prevalence of CRKP.

Modulation the Synergistic Effect of Chitosan-Sodium Alginate Nanoparticles with Ca2+: Enhancing the Stability of Pickering Emulsion on D-Limonene.

Pickering emulsions (PEs) have been regarded as an effective approach to sustaining and preserving the bioactivities of essential oils. The aim of this research is to prepare a PE stabilized by chitosan/alginate nanoparticles (CS-SA NPs) for the encapsulation and stabilization of D-limonene. In this work, the influence of calcium ions (Ca2+) on the morphology and interaction of nanoparticles was studied, and then the preparation technology of CS-SA/Ca2+ NPs was optimized. The results showed that the presence of Ca2+ reduced the size of the nanoparticles and made them assume a spherical structure. In addition, under the conditions of 0.2 mg/mL CaCl2, 0.6 mg/mL SA, and 0.4 mg/mL CS, the CS-SA/Ca2+ NPs had the smallest size (274 ± 2.51 nm) and high stability (-49 ± 0.69 mV). Secondly, the PE was prepared by emulsifying D-limonene with CS-SA/Ca2+ NPs, and the NP concentrations and homogenization speeds were optimized. The results showed that the small droplet size PE could be prepared with 2 mg/mL NP and a homogenization speed of 20,000 r/min, and it had excellent antibacterial and antioxidant activities. Most importantly, the emulsion showed higher activity, higher resistance to ultraviolet (UV) and a higher temperature than free D-limonene. This research provides a feasible solution for the encapsulation, protection and delivery of essential oils.

Demixing microwave signals using system-on-chip photonic processor.

The integrated photonic processor, co-packaged with electronic peripherals, is proposed for blind source separation of microwave signals, which separates signal-of-interest from dynamic interference with real-time adaptability.

[Mechanism about LMP1 of EB Virus Promoting Plasma Blast Differentiation of DLBCL Cell via mTORC1].

OBJECTIVE: To investigate possible mechanism on protien LMP1 expressed by EBV inducing plasmablast differentiation of DLBCL cell via the mTORC1 pathway. METHODS: The expression levels of LMP1 protein, CD38 and the phosphorylation levels of p70S6K in EBV+ and EBV- DLBCL cell lines were detected by Western blot. Cell lines overexpressing LMP1 gene stablely were constructed and LMP1 gene was silenced by RNAi. The expression of LMP1 gene was verified by RT-qPCR. The expression levels of LMP1 and CD38 and the phosphorylation levels of p70S6K in each group were detected by Western blot. RESULTS: Compared with EBV-DLBCL cells, the expression of LMP1 was detected on EBV +DLBCL cells (P =0.0008), EBV +DLBCL cells had higher phosphorylation levels of p70S6K (P =0.0072) and expression levels of CD38(P =0.0091). Compared with vector group, the cells of LMP1OE group had higher expression levels of LMP1 and CD38 (P =0.0353; P <0.0001), meanwhile molecular p70S6K was phosphorylated much more(P =0.0065); expression of LMP1 mRNA was verified(P <0.0001). Compared with si-NC group, expression level of LMP1 protein(P =0.0129) was not detected and phosphorylated p70S6K disappeared of LMP1KO group (P =0.0228); meanwhile, expression of CD38 decreased,although there was no significant difference (P =0.2377). CONCLUSION: LMP1 promotes DLBCL cells plasmablast differentiation via activating mTORC1 signal pathway.

Early warning system enables accurate mortality risk prediction for acute gastrointestinal bleeding admitted to intensive care unit.

Acute gastrointestinal (GI) bleeding are potentially life-threatening conditions. Early risk stratification is important for triaging patients to the appropriate level of medical care and intervention. Patients admitted to intensive care unit (ICU) has a high mortality, but risk tool is scarce for these patients. This study aimed to develop and validate a risk score to improve the prognostication of death at the time of patient admission to ICU. We developed and internally validated a nomogram for mortality in patients with acute GI bleeding from the eICU Collaborative Research Database (eICU-CRD), and externally validated it in patients from the Medical Information Mart for Intensive Care III database (MIMIC-III) and Wuhan Tongji Hospital. The performance of the model was assessed by examining discrimination (C-index), calibration (calibration curves) and usefulness (decision curves). 4750 patients were included in the development cohort, with 1184 patients in the internal validation cohort, 1406 patients in the MIMIC-III validation cohort, and 342 patients in the Tongji validation cohort. The nomogram, which incorporated ten variables, showed good calibration and discrimination in the training and validation cohorts, yielded C-index ranged from 0.832 (95%CI 0.811-0.853) to 0.926 (95CI% 0.905-0.947). The nomogram-defined high-risk group had a higher mortality than the low-risk group (44.8% vs. 3.5%, P < 0.001; 41.4% vs 3.1%, P < 0.001;53.6% vs 7.5%, P < 0.001; 38.2% vs 4.2%, P < 0.001). The model performed better than the conventional Glasgow-Blatchford score, AIMS65 and the newer Oakland and Sengupta scores for mortality prediction in both the derivation and validation cohorts concerning discrimination and usefulness. Our nomogram is a reliable prognostic tool that might be useful to identify high-risk acute GI bleeding patients admitted to ICU.

Fanconi Anemia: Exploration of DNA Repair Pathways from Genetic Diseases to Cancer and Prospects for Treatment / 肿瘤防治研究

Fanconi anemia (FA) is an inheritable disorder that presents with bone marrow failure, developmental anomalies, and an increased susceptibility to cancer. The etiology of this condition stems from a genetic mutation that disrupts the proper repair of interstrand DNA cross-links (ICLs). The resultant dysregulation of the DNA damage response mechanism can induce genomic instability, thereby elevating the mutation rates and the likelihood of developing cancer. The FA pathway assumes a pivotal role in safeguarding genome stability through its involvement in the repair of DNA cross-links and the maintenance of overall genomic integrity. A mutation in the germ line of any of the genes responsible for encoding the FA protein results in the development of FA. The prevalence of aberrant FA gene expression in somatic cancer, coupled with the identification of a connection between FA pathway activation and resistance to chemotherapy, has solidified the correlation between the FA pathway and cancer. Consequently, targeted therapies that exploit FA pathway gene abnormalities are being progressively developed and implemented. This review critically examines the involvement of the FA protein in the repair of ICLs, the regulation of the FA signaling network, and its implications in cancer pathogenesis and prognosis. Additionally, it explores the potential utility of small-molecule inhibitors that target the FA pathway.

Effect of Third Interstitial Fluid on Adverse Outcomes in Patients with Severe Pre-eclampsia and Twin Pregnancy: A 5-year Single-center Retrospective Study.

OBJECTIVE: This study aims to identify the effect of third interstitial fluid on adverse outcomes in twin pregnancies with severe pre-eclampsia, and explore the differences in bad ending between twins and singletons. METHODS: The present retrospective cohort study was conducted on patients with severe pre-eclampsia, who delivered in Tongji Hospital, Wuhan, China, between 2017 and 2022. The adverse outcomes in singleton and twin pregnancies with severe pre-eclampsia were initially investigated. Then, the diverse maternal and fetal consequences between singleton and twin pregnancies in patients with severe pre-eclampsia were compared after merging with the third interstitial fluid. RESULTS: A total of 709 patients were included for the present study. Among these patients, 68 patients had twin pregnancies, and 641 patients had singleton pregnancies. The rate of postpartum hemorrhage (2.81% vs. 13.24%, P<0.001), and admission rate to the Neonatal Intensive Care Unit (NICU) after birth (30.73% vs. 63.24%, P=0.011) were significantly higher in twin pregnancies. The neonatal weight of twins was statistically lower than singletons (1964.73±510.61 g vs. 2142.92±731.25 g, P=0.008). For the groups with the third interstitial fluid, the delivery week (P=0.001) and rate of admission to the NICU after birth were significantly advanced in twin pregnancy group, when compared to singleton pregnancy group (P=0.032), and the length of hospital stay was shorter (P=0.044). Furthermore, there was no statistically significant difference between the twin pregnancy group and the singletony pregnancy group without the third interstitial fluid. CONCLUSION: The maternal and fetal adverse outcomes of patients with severe pre-eclampsia increased in twin pregnancies, when compared to singleton pregnancies. Thus, when patients develop the third interstitial fluid, twin pregnancies would more likely lead to adverse fetal outcomes, when compared to singleton pregnancies, and there would be no significant difference in maternal adverse outcomes. More attention should be given to patients who merge with the third interstitial fluid.

The effect of internal salary incentives based on insurance payment on physicians' behavior: experimental evidence.

BACKGROUND: Understanding how physicians respond to payment methods is crucial for designing effective incentives and enhancing the insurance system. Previous theoretical research has explored the effects of payment methods on physician behavior based on a two-level incentive path; however, empirical evidence to validate these theoretical frameworks is lacking. To address this research gap, we conducted a laboratory experiment to investigate physicians' behavioral responses to three types of internal salary incentives based on diagnosis-related-group (DRG) and fee-for-service (FFS). METHODS: A total of 150 medical students from Capital Medical University were recruited as participants. These subjects played the role of physicians in choosing the quantity of medical services for nine types of patients under three types of salary incentives-fixed wage, constant fixed wage with variable performance wage, and variable fixed wage with variable performance wage, of which performance wage referred to the payment method balance under FFS or DRG. We collected data on the quantities of medical services provided by the participants and analyzed the results using the Friedman test and the fixed effects model. RESULTS: The results showed that a fixed wage level did not have a significant impact on physicians' behavior. However, the patients benefited more under the fixed wage compared to other salary incentives. In the case of a floating wage system, which consisted of a constant fixed wage and a variable performance wage from the payment method balance, an increase in performance wage led to a decrease in physicians' service provision under DRG but an increase under FFS. Consequently, this resulted in a decrease in patient benefit. When the salary level remained constant, but the composition of the salary varied, physicians' behavior changed slightly under FFS but not significantly under DRG. Additionally, patient benefits decreased as the ratio of performance wages increased under FFS. CONCLUSIONS: While using payment method balance as physicians' salary may be effective in transferring incentives of payment methods to physicians through internal compensation frameworks, it should be used with caution, particularly when the measurement standard of care is imperfect.