Ruthenium-Based Electrocatalysts for Hydrogen Evolution Reaction: from Nanoparticles to Single Atoms.

Benefiting from similar hydrogen bonding energy to Pt and much lower price compare with Pt, Ru based catalysts are promising candidates for electrocatalytic hydrogen evolution reaction (HER). The catalytic activity of Ru nanoparticles can be enhanced through improving their dispersion by using different supports, and the strong metal supports interaction can further regulate their catalytic performance. In addition, single-atom catalysts (SACs) with almost 100% atomic utilization attract great attention and the coordinative atmosphere of single atoms can be adjusted by supports. Moreover, the syngenetic effects of nanoparticles and single atoms can further improve the catalytic performance of Ru based catalysts. In this review, the progress of Ru based HER electrocatalysts are summarized according to their existing forms, including nanoparticles (NPs), single atoms (SAs) and the combination of both NPs and SAs. The common supports such as carbon materials, metal oxides, metal phosphides and metal sulfides are classified to clarify the metal supports interaction and coordinative atmosphere of Ru active centers. Especially, the possible catalytic mechanisms and the reasons for the improved catalytic performance are discussed from both experimental results and theoretical calculations. Finally, some challenges and opportunities are prospected to facilitate the development of Ru based catalysts for HER.

Current Progress of Mo-Based Metal Organic Frameworks Derived Electrocatalysts for Hydrogen Evolution Reaction.

As an important half-reaction for electrochemical water splitting, electrocatalytic hydrogen evolution reaction suffers from sluggish kinetics, and it is still urgent to search high efficiency non-platinum-based electrocatalysts. Mo-based catalysts such as Mo2 C, MoO2 , MoP, MoS2 , and MoNx have emerged as promising alternatives to Pt/C owing to their similar electronic structure with Pt and abundant reserve of Mo. On the other hand, due to the adjustable topology, porosity, and nanostructure of metal organic frameworks (MOFs), MOFs are extensively used as precursors to prepare nano-electrocatalysts. In this review, for the first time, the progress of Mo-MOFs-derived electrocatalysts for hydrogen evolution reaction is summarized. The preparation method, structures, and catalytic performance of the catalysts are illustrated based on the types of the derived electrocatalysts including Mo2 C, MoO2 , MoP, MoS2 , and MoNx . Especially, the commonly used strategies to improve catalytic performance such as heteroatoms doping, constructing heterogeneous structure, and composited with noble metal are discussed. Moreover, the opportunities and challenges in this area are proposed to guide the designment and development of Mo-based MOF derived electrocatalysts.

MicroRNA-223-3p Targeting SGK1 Regulates Apoptosis and Inflammation in Sepsis-Associated Acute Kidney Injury.

INTRODUCTION: Sepsis and septic shock are significant contributors to the development of acute kidney injury (AKI) in critically ill patients. This study aimed to elucidate the role and mechanism of microRNA-223-3p in sepsis-associated AKI (SA-AKI). METHODS: Bioinformatics methods were used to analyze the expression of microRNA-223-3p in sepsis patients, its correlation with inflammatory cytokines, and to predict the binding site of microRNA-223-3p with SGK1. The binding relationship between microRNA-223-3p and SGK1 was validated using a dual-luciferase reporter gene assay. The expression of microRNA-223-3p was assayed using qPCR in patient serum or lipopolysaccharide (LPS)-treated HK-2 cells. Cell apoptosis; expression of Bax, Bcl-2, cleaved caspase-3; and levels of TNF-α, IL-1ß, and IL-6 were measured using TUNEL assay, Western blot (WB), and ELISA, respectively. SGK1 expression of HK-2 cells with different treatments was detected using qPCR and WB. RESULTS: The expression of microRNA-223-3p was found to be upregulated in sepsis patients and HK-2 cells treated with LPS. Furthermore, microRNA-223-3p promoted apoptosis and inflammation in LPS-induced HK-2 cells. This promotion was mediated by the negative regulation of SGK1 by microRNA-223-3p. CONCLUSION: The microRNA-223-3p was found to regulate SGK1 and promote apoptosis and inflammation in LPS-induced HK-2 cells. Our study has elucidated the mechanism of microRNA-223-3p in SA-AKI, providing a potential target for sepsis treatment.

Salicylic Acid's impact on Sedum alfredii growth and cadmium tolerance: Comparative physiological, transcriptomic, and metabolomic study.

With the acceleration of industrialization, Cd pollution has emerged as a major threat to soil ecosystem health and food safety. Hyperaccumulating plants like Sedum alfredii Hance are considered to be used as part of an effective strategy for the ecological remediation of Cd polluted soils. This study delved deeply into the physiological, transcriptomic, and metabolomic responses of S. alfredii under cadmium (Cd) stress when treated with exogenous salicylic acid (SA). We found that SA notably enhanced the growth of S. alfredii and thereby increased absorption and accumulation of Cd, effectively alleviating the oxidative stress caused by Cd through upregulation of the antioxidant system. Transcriptomic and metabolomic data further unveiled the influence of SA on photosynthesis, antioxidant defensive mechanisms, and metal absorption enrichment pathways. Notably, the interactions between SA and other plant hormones, especially IAA and JA, played a central role in these processes. These findings offer us a comprehensive perspective on understanding how to enhance the growth and heavy metal absorption capabilities of hyperaccumulator plants by regulating plant hormones, providing invaluable strategies for future environmental remediation efforts.

TCF7 and LEF-1 downregulation in sepsis promotes immune suppression by inhibiting CD4+ T cell proliferation.

BACKGROUND: Previous studies have shown that sepsis is implicated in a reduction in the number and function of CD4+ T cells. TCF7 and LEF-1 facilitate early T cell development and lineage selection of CD4+ T cells. However, the function and mechanism of TCF7 and LEF-1 in sepsis are uncharacterized. This study intended to delineate effect of TCF7 and LEF-1 on sepsis and the impact on proliferation of CD4+ T cells in sepsis. METHODS: A mouse sepsis model was constructed by cecal ligation and puncture (CLP) method. Expression of TCF7 and LEF-1 in sepsis was investigated using bioinformatics analysis and molecular experiments. We then constructed TCF7 and LEF-1 overexpression cell lines to investigate their effects on proliferation, apoptosis, effector activation, and immunosuppressive molecules of CD4+ T cells in sepsis. RESULTS: TCF7 and LEF-1 were downregulated in sepsis. As the duration of sepsis induction increased, the levels of TCF7 and LEF-1 gradually decreased, as did the number of CD4+ T cells. Cell experiments showed that overexpression of TCF7 and LEF-1 enhanced proliferation and effector activation of CD4+ T cells, reduced apoptosis, decreased PD-1 and LAG3 expression, and promoted immune response in sepsis. CONCLUSION: In conclusion, this study confirmed that downregulation of TCF7 and LEF-1 expression in sepsis inhibited proliferation of CD4+ T cells, leading to immune suppression. This finding suggested that TCF7 and LEF-1 were potential biological targets for sepsis and indicated that immunotherapy aimed at improving CD4+ T cell proliferation may be a new strategy for immune therapy in sepsis patients.

Actin Gamma 1, a new skin cancer pathogenic gene, identified by the biological feature-based classification.

Skin cancer is the most common form of cancer that accounting for at least 40% of cancer cases around the world. This study aimed to identify skin cancer-related biological features and predict skin cancer candidate genes by employing machine learning based on biological features of known skin cancer genes. The known skin cancer-related genes were fetched from database and encoded by the enrichment scores of gene ontology and pathways. The optimal features of the skin cancer related genes were selected with a series of feature selection methods, such as mRMR, IFS, and Random Forest algorithm. Quantitative PCR (Q-PCR) was performed for the predicted genes. Effects on proliferation and metastasis of skin cancer cell line A431 were detected through MTT and transwell assay. The effects on myosin light chain (MLC) phosphorylation of Actin Gamma 1 (ACTG1) were detected by Western blot. A total of 1233 GO terms and 55 KEGG pathway terms were identified as the optimal features for the depiction of skin cancer. According to those terms, 1134 possible skin cancer-related genes were predicted. We further identified 16 new biomarkers in expression and the classification model can predict skin cancer cases with 100% accuracy. Among the 16 genes, ACTG1 had significantly high expression in skin cancer tissue. Our investigation suggested that ACTG1 can regulate the cell proliferation and migration through ROCK signaling pathway.

Interleukin-17A antagonist attenuates radiation-induced lung injuries in mice.

OBJECTIVE: To investigate the effect of interleukin-17A (IL-17A) antibodies on radiation-induced lung injuries in mice. METHODS: The thorax of 135 mice were divided into Sham (n = 30), radiation control (RC, n = 35), treatment (n = 35, IL-17A-neutralizing antibody, 4 µg/mouse, IV, 4 days per month for 4 months) and placebo group (n = 35) before a single dose irradiation (15 Gy) to the thorax. Inflammation and collagen contents in the lung tissues were examined, and the concentration of IL-17A, TGF-ß1, and IL-6 in bronchoalveolar lavage fluid (BALF) were measured. In another 50 animals, 180-day survival rate following the irradiation and treatment was calculated by Kaplan-Meier method. RESULTS: Sixteen weeks after the irradiation and treatment, there was significant inflammatory cell infiltration and interstitial collagen depositions in the radiation control and placebo groups, whereas these changes were relatively mild in the treatment group. The percentage of grade II and III alveolitis in the treatment group (16%, P < .05) was lower than in the RC (72%) or placebo group (64%). The mean Aschcroft fibrosis scores were 2.8 (treatment group), 5.2 (RC), and 4.8 (placebo group), respectively. The scores of treatment group was lower than that of RC (P < .001) or placebo group (P < .001). The IL-17A, TGF-ß, and IL-6 concentrations in the treatment group were lower than in the RC and placebo group (P < .01) following the irradiation. The 180-day mortality rate in the treatment group was lower than in the RC group 16.7% versus 75.0%, P < .05). CONCLUSION: IL-17A antibody treatment alleviates radiation-induced pneumonitis and subsequent fibrosis, and improvise postirradiation survival.

Expression of interleukin-17A in lung tissues of irradiated mice and the influence of dexamethasone.

PURPOSE: To investigate the expressions of IL-17A in different phases of radiation-induced lung injury and the effect of dexamethasone. METHODS: The thorax of C57BL/6 mice was irradiated with 15 Gy rays. Mice from dexamethasone-treated group were injected intraperitoneally with dexamethasone (0.42 mg/kg/day) every day for the first month after irradiation. IL-17A in lung tissues was detected by immunohistochemistry. IL-17A, TGF-ß1, and IL-6 in bronchoalveolar lavage fluid were detected by ELISA. Lung inflammation and collagen deposition were observed by H&E and Masson methods. The degree of alveolitis and fibrosis was judged according to scoring. RESULTS: IL-17A expression was appreciable at 1 week, peaked at 4 weeks, and subsequently declined at 8 weeks after irradiation. IL-17A was reduced after dexamethasone application at all the observation periods. Dexamethasone also inhibited expressions of TGF-ß, IL-6, and TNF-α in bronchoalveolar lavage fluid. Moreover, dexamethasone attenuated the severity of lung injury by reducing the infiltration of inflammatory cells and collagen deposition. Terms of survival and the time of death in mice of treatment group were postponed and survival rate was improved. CONCLUSIONS: IL-17A plays an important role in the process of radiation-induced lung injury. And dexamethasone may provide a protective role in lung injury induced by radiation.

PAK1 Promotes Inflammation Induced by Sepsis through the Snail/CXCL2 Signaling Pathway.

Sepsis is a severe syndrome characterized by organ dysfunction, resulting from a systemic imbalance in response to infection. PAK1 plays a critical role in various diseases. The present study aimed to explore and delineate the mechanism of PAK1 in inflammation induced by sepsis. Bioinformatics analysis was performed to assess PAK1, snail, and CXCL2 expression in the whole blood of septic patients and the pathways enriched with PAK1. To simulate the sepsis model, THP-1 cells were stimulated with lipopolysaccharide. Gene expression was evaluated using qRT-PCR, while cell viability was assessed using CCK-8 assay. Cell apoptosis was tested with flow cytometry. Expression of inflammatory factors in cells following different treatments was analyzed using the enzyme linked immunosorbent assay (ELISA). Dual-luciferase and chromatin immunoprecipitation assays were conducted to verify the binding relationship between PAK1 and the snail. Mouse models of cecal ligation and puncture were established, and hematoxylin and eosin staining and ELISA were employed to detect the infiltration levels of inflammatory cells and the expression of related protective factors in lung, liver, and kidney tissues. The results demonstrated upregulation of PAK1, snail, and CXCL2 in the whole blood of septic patients, with PAK1 being enriched in the chemokine-related pathway. Knockdown of PAK1 significantly promoted the apoptosis of LPS-stimulated THP-1 cells and inhibited the expression of inflammatory factors. PAK1 upregulated the expression of the snail, which in turn promoted the expression of CXCL2. Thus, PAK1 mediated the sepsis-induced inflammatory response through the snail/CXCL2 pathway. In conclusion, PAK1 played a role in promoting inflammation induced by sepsis through the snail/CXCL2 axis, thereby providing a potential therapeutic target for the management of sepsis.

Ru doping induced interface engineering in flower-liked CoMoO4-RuO2 boosts oxygen electrocatalysis for rechargeable Zn-air battery.

Constructing heterogeneous catalysts can significantly boost the electrocatalytic activity due to the improved intrinsic catalytic activity induced by tailored electronic structure and optimized chemisorption to the reaction intermediates. RuO2 based electrocatalysts are especially attractive due to the high catalytic activity of RuO2. To reduce the usage of noble metal and improve the catalytic activity of catalyst, CoMoO4-RuO2 micro-flower was synthesized using a facile hydrothermal-calcination method in this work. CoMoO4-RuO2 exhibits a low overpotential of 177 mV at 10 mA cm-2 for oxygen evolution reaction (OER) and a high half-wave potential of 0.858 V for oxygen reduction reaction (ORR). Moreover, the Zn-air battery assembled using CoMoO4-RuO2 exhibit shows a high maximum discharge power density of 149 mW cm-2 and a large open circuit voltage of 1.38 V. The good performance can be attributed to the incorporation of RuO2, which not only induces extra catalytic active sites, but also forms heterojunction with CoMoO4 to optimize the electronic structure of CoMoO4-RuO2, thereby achieving a better equilibrium of absorption and desorption of intermediates. The work provides insights into designing RuO2 based electrocatalysts for advanced electrocatalysis.

Hollow CoVOx/Ag nanoprism with tailored electronic structure for high efficiency oxygen evolution reaction.

Developing high-active and inexpensive electrocatalysts for oxygen evolution reaction (OER) is very important in the field of water splitting. The catalytic performance of electrocatalysts can be significantly improved by optimizing the electronic structure and designing suitable nanostructure. In this work, we represent the synthesis of hollow CoVOx/Ag-5 for OER. Due to the interaction of CoVOx and Ag nanoparticles, the electronic structure is optimized to improve the intrinsic catalytic activity. Additionally, the extrinsic catalytic activity of CoVOx/Ag is enhanced by the abundant active sites from the hollow structure. As a result, the CoVOx/Ag-5 demonstrates significantly enhanced OER catalytic activity with a low overpotential of 247 mV at 10 mA cm-2. In addition, it also exhibits excellent durability, without obvious attenuation in performance after continuous operation for 60 h. Furthermore, the catalyst can enable full water splitting with appropriate 100 % Faraday efficiency, demonstrating its practical application.

Jasmonic acid's impact on Sedum alfredii growth and cadmium tolerance: A physiological and transcriptomic study.

Soil cadmium (Cd) pollution is escalating, necessitating effective remediation strategies. This study investigated the effects of exogenous jasmonic acid (JA) on Sedum alfredii Hance under Cd stress, aiming to enhance its phytoextraction efficiency. Initially, experiments were conducted to assess the impact of various concentrations of JA added to environments with Cd concentrations of 100, 300, and 500 µmol/L. The results determined that a concentration of 1 µmol/L JA was optimal. This concentration effectively mitigated the level of ROS products by enhancing the activity of antioxidant enzymes. Additionally, JA fostered Cd absorption and accumulation, while markedly improving plant biomass and photosynthetic performance. In further experiments, treatment with 1 µmol/L JA under 300 µmol/L Cd stress was performed and transcriptomic analysis unveiled a series of differentially expressed genes (DEGs) instrumental in the JA-mediated Cd stress response. These DEGs encompass not only pathways of JA biosynthesis and signaling but also genes encoding functions that influence antioxidant systems and photosynthesis, alongside genes pertinent to cell wall synthesis, and metal chelation and transport. This study highlights that JA treatment significantly enhances S. alfredii's Cd tolerance and accumulation, offering a promising strategy for plant remediation and deepening our understanding of plant responses to heavy metal stress.

Malignant hyperthermia: Report on a successful rescue of a case with the highest temperature of 44.2°C.

Malignant hyperthermia (MH) is an inherited skeletal muscle disorder caused primarily by a genetic mutation, usually in the calcium channel gene of the muscle. This mutation can lead to muscle hypersensitivity to volatile anesthetics (such as sevoflurane) and the depolarizing muscle relaxant succinylcholine, resulting in hyperthermia, muscle stiffness, metabolic disturbances, and other severe physiological reactions. This condition may prove fatal unless it is recognized in its early stages and treatment is administered promptly and aggressively. We report a 13-year-old adolescent who underwent laparoscopic appendectomy and developed MH after the use of inhalational anesthetics, manifested by unremitting hyperthermia with a maximum temperature of 44.2°C, muscle rigidity, tachycardia, hypercapnia; and malignant arrhythmias, cardiogenic shock, hyperkalemia, metabolic, and respiratory acidosis. After early and timely recognition, multidisciplinary management and administration of dantrolene, the case was successfully treated. Exome sequencing revealed a point mutation (amino acid change) on the RYR1 gene: c.12700G>C(p.Val4234Leu). Due to the lack of ready-made dantrolene in our hospital, the patient in this case received dantrolene treatment only 6 h after the first observation of high body temperature. We review the development of the disease and summarize the success of treatment and what can be done to improve the chances of saving the patient's life if dantrolene is not available in time.

DOCK8 inhibits the immune function of neutrophils in sepsis by regulating aerobic glycolysis.

INTRODUCTION: This study endeavored to investigate the role of DOCK8 in modulating the immune function triggered by sepsis. METHODS: Expression of DOCK8 in the whole blood of sepsis patients and its enrichment pathways were assayed by bioinformatics. Pearson analysis was used to predict the relationship between glycolytic signaling pathway and its relevance to neutrophil function in sepsis. A sepsis mouse model was then built by performing cecal ligation and puncture treatment on male mice. Neutrophils were isolated, and their purity was tested by flow cytometry. Neutrophils were then stimulated by lipopolysaccharide to build a sepsis cell model. Next, quantitative reverse transcription polymerase chain reaction and CCK-8 were applied to test the expression of DOCK8 and cell viability, western blot to assay the expression of HK-2, PKM2, and LDHA proteins, ELISA to measure the concentrations of TNF-α, IL-1ß, and IL-6, Transwell to detect the chemotaxis of neutrophils and flow cytometry to detect the phagocytic activity of neutrophils. Finally, in different treatment groups, we used Seahorse XF 96 to analyze the extracellular acidification rate (ECAR) of sepsis cells and used enzyme-linked immunosorbent assay to detect the contents of pyruvic acid, lactic acid, and ATP in sepsis cells. RESULTS: DOCK8 was downregulated in sepsis blood and activated neutrophils. Aerobic glycolysis was positively correlated with sepsis. Activated neutrophils promoted the expression of inflammatory factors TNF-α, IL-1ß, and IL-6. Low expression of DOCK8 facilitated the proliferation, chemotaxis, and phagocytic activity of sepsis cells and promoted the expression of inflammatory factors. Bioinformatics analysis revealed that DOCK8 was enriched in the glycolytic signaling pathway. Low expression of DOCK8 induced ECAR, promoted the protein expression of HK-2, PKM2 and LDHA, and favored the increase of pyruvate, lactate, and ATP contents. While 2-DG treatment could restore these effects. CONCLUSION: DOCK8 may inhibit sepsis-induced neutrophil immune function by regulating aerobic glycolysis and causing excessive inflammation, which helps to explore potential therapeutic targets.

Biochar loaded with bacteria enhanced Cd/Zn phytoextraction by facilitating plant growth and shaping rhizospheric microbial community.

Biochar and metal-tolerant bacteria have been widely used in the remediation of heavy metal contaminated soil. However, the synergistic effect of biochar-functional microbes on phytoextraction by hyperaccumulators remains unclear. In this study, the heavy metal-tolerant strain Burkholderia contaminans ZCC was selected and loaded on biochar to produce biochar-resistant bacterial material (BM), and the effects of BM on Cd/Zn phytoextraction by Sedum alfredii Hance and rhizospheric microbial community were explored. The results showed that, BM application significantly enhanced the Cd and Zn accumulation of S. alfredii by 230.13% and 381.27%, respectively. Meanwhile, BM alleviated metal toxicity of S. alfredii by reducing oxidative damage and increasing chlorophyll and antioxidant enzyme activity. High-throughput sequencing revealed that BM significantly improved soil bacterial and fungal diversity, and increased the abundance of genera with plant growth promoting and metal solubilizing functions such as Gemmatimonas, Dyella and Pseudarthrobacter. Co-occurrence network analysis showed that BM significantly increased the complexity of the rhizospheric bacterial and fungal network. Structural equation model analysis revealed that soil chemistry property, enzyme activity and microbial diversity contributed directly or indirectly to Cd and Zn extraction by S. alfredii. Overall, our results suggested that biochar- B. contaminans ZCC was able to enhance the growth and Cd/Zn accumulation by S. alfredii. This study enhanced our understanding on the hyperaccumulator-biochar-functional microbe interactions, and provided a feasible strategy for promoting the phytoextraction efficiency of heavy metal contaminated soils.

The relationship between expression of PD-L1 and HIF-1α in glioma cells under hypoxia.

Hypoxia inducible factor-1α (HIF-1α) up-regulates the expression of programmed death ligand-1 (PD-L1) in some extracranial malignancies. However, whether it could increase PD-L1 expression in intracranial tumor is still unknown. Here, we explored the relationship between HIF-1α and PD-L1 expression in glioma, and investigated their clinical significance. In glioma patients, HIF-1α and PD-L1 were overexpressed in high grade glioma tissues and were significantly associated with poor survival. In glioma cells, PD-L1 expression was induced under hypoxia condition, and the enhanced PD-L1 expression was abrogated by either HIF-1α knock-down or HIF-1α inhibitor treatment. Furthermore, ChIP-qPCR analysis showed the direct binding of HIF-1α to PD-L1 proximal promoter region, providing evidence that HIF-1α up-regulates PD-L1 in glioma. In glioma murine model, the combination treatment with HIF-1α inhibitor and anti-PD-L1 antibody caused a more pronounced suppressive effect on tumor growth compared to either monotherapy. Immunologically, the combination treatment improved both dendritic cell (DC) and CD8+ T cell activation. Overall, our results demonstrated that positive correlation between PD-L1 and HIF-1α in glioma, and provide an alternative strategy, inhibiting HIF-1α, as combination therapies with immunotherapies to advance glioma treatment.

Impact of acute pulmonary embolism on plasma and tissue hepatocyte growth factor: an experimental study.

This study was designed to investigate the impact of acute pulmonary embolism (PE) on plasma and tissue hepatocyte growth factor (HGF). PE was established in 16 New Zealand white rabbits by intravenous injection of autologous blood clots. Another 16 sham-operated rabbits were used as control. Plasma HGF levels and tissue HGF expression was measured by enzyme-linked immunosorbent assay (ELISA) and immunohistochemistry, respectively. The plasma HGF levels in the PE group were elevated 1 hour after PE (P < .01). In the lung tissue samples, the positive HGF expression ratio was 91.7% and 20.8%, respectively, in the PE and the control group (P < .01). The positive HGF expression ratio in the right ventricular tissue samples in the PE group was higher than in the control group (75.0% versus 20.9%; P < .01). The positive HGF expression ratio in the liver samples in the PE and the control groups was 33.3% and 16.7%, respectively (P < .05). In conclusion, acute PE was associated with a significant increase in plasma HGF. Acute PE was also associated with an enhanced HGF expression in the lungs, the right ventricle, and the liver.

[Early high-volume hemofiltration treatment in severe sepsis].

OBJECTIVE: To evaluate the effect of early application of high-volume hemofiltration treatment (HVHF) on the levels of lactic acid, pro-inflammatory cytokines and C-reactive protein (CRP) in plasma, as well as APACHE II score in patients suffering from severe sepsis. METHODS: Thirty patients meeting the diagnosis of severe sepsis were enrolled in the trial within 24 hours of insults. The level of lactic acid, interleukin-6 (IL-6) and CRP in plasma were measured before HVHF and at 24, 48 or 72 h following HVHF treatment. RESULT: The plasma levels of lactic acid and IL-6 decreased significantly at 24 h, 48 h, 72 h after HVHF (P <0.05), while, IL-10 did not differ significantly following HVHF (P>0.05), when compared with that before HVHF. CONCLUSION: The early application of HVHF could clear the plasma lactic acid and pro-inflammatory cytokines, and improve the tissue oxygenation in severe sepsis.