Machine learning-based identification and immune characterization of ferroptosis-related molecular clusters in osteoarthritis and validation.

Osteoarthritis (OA), a degenerative joint disease, involves synovial inflammation, subchondral bone erosion, and cartilage degeneration. Ferroptosis, a regulated non-apoptotic programmed cell death, is associated with various diseases. This study investigates ferroptosis-related molecular subtypes in OA to comprehend underlying mechanisms. The Gene Expression Omnibus datasets GSE206848, GSE55457, GSE55235, GSE77298 and GSE82107 were used utilized. Unsupervised clustering identified the ferroptosis-related gene (FRG) subtypes, and their immune characteristics were assessed. FRG signatures were derived using LASSO and SVM-RFE algorithms, forming models to evaluate OA's ferroptosis-related immune features. Three FRG clusters were found to be immunologically heterogeneous, with cluster 1 displaying robust immune response. Models identified nine key signature genes via algorithms, demonstrating strong diagnostic and prognostic performance. Finally, qRT-PCR and Western blot validated these genes, offering consistent results. In addition, some of these genes may have implications as new therapeutic targets and can be used to guide clinical applications.

Airborne environmentally persistent free radicals (EPFRs) in PM2.5 from combustion sources: Abundance, cytotoxicity and potential exposure risks.

As an emerging atmospheric pollutant, airborne environmentally persistent free radicals (EPFRs) are formed during many combustion processes and pose various adverse health effects. In health-oriented air pollution control, it is vital to evaluate the health effects of atmospheric fine particulate matter (PM2.5) from different emission sources. In this study, various types of combustion-derived PM2.5 were collected on filters in a partial-flow dilution tunnel sampling system from three typical emission sources: coal combustion, biomass burning, and automobile exhaust. Substantial concentrations of EPFRs were determined in PM2.5 samples and associated with significant potential exposure risks. Results from in vitro cytotoxicity and oxidative potential assays suggest that EPFRs may cause substantial generation of reactive oxygen species (ROS) upon inhalation exposure to PM2.5 from anthropogenic combustion sources, especially from automobile exhaust. This study provides important evidence for the source- and concentration-dependent health effects of EPFRs in PM2.5 and motivates further assessments to advance public health-oriented PM2.5 emission control.

Comparative in vitro toxicological effects of water-soluble and insoluble components of atmospheric PM2.5 on human lung cells.

Fine particulates in city air significantly impact human health, but the hazardous compositional mechanisms are still unclear. Besides the toxicity of environmental PM2.5 to in vitro human lung epithelial cells (A549), the independent cytotoxicity of PM2.5-bound water-soluble (WS-PM2.5) and water-insoluble (WIS-PM2.5) fractions were also compared by cell viability, oxidative stress (reactive oxygen species, ROS), and inflammatory injury (IL-6 and TNF-α). The cytotoxicity of PM2.5 varied significantly by sampling season and place, with degrees greater in winter and spring than in summer and autumn, related to corresponding trend of air PM2.5 level, and also higher in industrial than urban site, although their PM2.5 pollution levels were comparable. The PM2.5 bound metals (Ni, Cr, Fe, and Mn) may contribute to cellular injury. Both WS-PM2.5 and WIS-PM2.5 posed significant cytotoxicity, that WS-PM2.5 was more harmful than WIS-PM2.5 in terms of decreasing cell viability and increasing inflammatory cytokines production. In particular, industrial samples were usually more toxic than urban samples, and those from summer were generally less toxic than other seasons. Hence, in order to mitigate the health risks of PM2.5 pollution, the crucial targets might be components of heavy metals and soluble fractions, and sources in industrial areas, especially during the cold seasons.

Tetracycline and sulfadiazine toxicity in human liver cells Huh-7.

As typical antibiotics, tetracycline (TC) and sulfadiazine (SDZ) enter the human body through the food chain. Therefore, it is necessary to understand their individual and combined toxicity. In this study, the effects of TC, SDZ, and their mixture on cell viability, cell membrane damage, liver cell damage, and oxidative damage were evaluated in in vitro assays with human liver cells Huh-7. The results showed cytotoxicity of TC, SDZ, and their mixture, which induced oxidative stress and caused membrane and cell damage. The effect of antibiotics on Huh-7 cells increased with increasing concentration, except for lactate dehydrogenase (LDH) activity that commonly showed a threshold concentration response and cell viability, which commonly showed a biphasic trend, suggesting the possibility of hormetic responses where proper doses are included. The toxicity of TC was commonly higher than that of SDZ when applied at the same concentration. These findings shed light on the individual and joint effects of these major antibiotics on liver cells, providing a scientific basis for the evaluation of antibiotic toxicity and associated risks.

Impact of gut microbiota and associated mechanisms on postprandial glucose levels in patients with diabetes.

Diabetes and its complications are serious medical and global burdens, often manifesting as postprandial hyperglycemia. In recent years, considerable research attention has focused on relationships between the gut microbiota and circulating postprandial glucose (PPG). Different population studies have suggested that PPG is closely related to the gut microbiota which may impact PPG via short-chain fatty acids (SCFAs), bile acids (BAs) and trimethylamine N-oxide (TMAO). Studies now show that gut microbiota models can predict PPG, with individualized nutrition intervention strategies used to regulate gut microbiota and improve glucose metabolism to facilitate the precision treatment of diabetes. However, few studies have been conducted in patients with diabetes. Therefore, little is known about the relationships between the gut microbiota and PPG in this cohort. Thus, more research is required to identify key gut microbiota and associated metabolites and pathways impacting PPG to provide potential therapeutic targets for PPG.

The Bcr-Abl inhibitor DCC-2036 inhibits necroptosis and ameliorates osteoarthritis by targeting RIPK1 and RIPK3 kinases.

Osteoarthritis (OA) is a chronic progressive degenerative joint disease. Owing to its complex pathogenesis, OA treatment is typically challenging. Necroptosis is a form of programmed cell death mainly mediated by the serine/threonine kinases, RIPK1 and RIPK3, and mixed lineage kinase-like domain (MLKL). In this study, we found that the multi-targeted kinase inhibitor DCC-2036 can inhibit TSZ (TNF-α, Smac mimetic, and z-VAD-FMK)-induced necroptosis of chondrocytes and synovial fibroblast cells (SFs). In addition, we found that oral DCC-2036 inhibited chondrocyte damage in a rat model of OA induced by intra-articular injection of monosodium iodoacetate (MIA). A mechanistic study showed that DCC-2036 directly inhibited the activities of RIPK1 and RIPK3 kinases to block necroptosis, inhibiting the inflammatory response and protecting chondrocytes. In summary, our research suggests that DCC-2036, a new necroptosis inhibitor targeting RIPK1 and RIPK3 kinase activity, may be useful for the clinical treatment of OA and provides a new direction for the research and treatment of OA.

Ginsenoside Compound K Ameliorates Osteoarthritis by Inhibiting the Chondrocyte Endoplasmic Reticulum Stress-Mediated IRE1α-TXNIP-NLRP3 Axis and Pyroptosis.

Osteoarthritis (OA) is a common joint disease, and studies have reported that the endoplasmic reticulum stress (ERS) in chondrocytes caused by the cartilage tissue damage could mediate the activation of Nod-like receptor protein 3 (NLRP3) inflammasomes through inositol-requiring enzyme 1 alpha (IRE1α) and thioredoxin interacting protein (TXNIP). Ginsenoside compound K (CK) has an inhibitory effect on IRE1α activation. However, the role of IRE1α-TXNIP and its interaction with CK are still unclear. In this study, we examined the role and mechanism of action of CK in OA. We found that CK ameliorated OA and ERS in IL-1ß-treated chondrocytes and a monoiodoacetate-induced rat OA model. The effect of CK on inflammation, pyroptosis, and ERS was blocked by the ERS inducer tunicamycin. In conclusion, CK hindered OA progression by inhibiting the ERS-IRE1α-TXNIP-NLRP3 axis. Overall, our data indicate that CK could be useful in the treatment of OA and other chronic inflammatory diseases.

Effects of contralateral nephrectomy timing and ischemic conditions on kidney fibrosis after unilateral kidney ischemia-reperfusion injury.

Acute kidney injury (AKI) is an important cause of chronic kidney disease (CKD), but the underlying mechanisms are unclear. Animal models are tools for studying the AKI-CKD progression. Kidney ischemia-reperfusion injury (IRI) models, especially the unilateral IRI (uIRI) model with delayed contralateral kidney resection, are commonly used to induce fibrotic progression to CKD after AKI. However, in previous studies, we found that details of the operation had a significant impact on the long-term outcomes of the kidney in this uIRI model. In this study, we investigated the effects of resection timing of the contralateral intact kidney, core body temperatures during ischemia, and time length of kidney ischemia on kidney function, histological injury and kidney fibrosis after AKI, using a mouse uIRI model with delayed contralateral nephrectomy. The results showed that all these parameters significantly affected the AKI-CKD transition. The post-AKI fibrosis worsened and the survival rate declined with a longer interval between contralateral nephrectomy and uIRI, higher ischemic body temperature, or longer ischemic duration when the other two variables were fixed. In conclusion, in the uIRI model with delayed contralateral nephrectomy, kidney fibrosis after AKI is influenced by many factors. Strictly controlling the experimental conditions is very important for the stability and consistency of the model.

Role of adiponectin in osteoarthritis.

Osteoarthritis (OA) is a widespread and most common joint disease which leads to social cost increasing accompany with aging population. Surgery is often the final treatment option. The major progression of OA includes cartilage degradation caused by chondrocytes metabolism imbalance. So, the molecular mechanisms of action in chondrocytes may provide insights into treatment methods for OA. Adiponectin is an adipokine with many biological functions in the cell metabolism. Numerous studies have illustrated that adiponectin has diverse biological effects, such as inhibition of cell apoptosis. It regulates various functions in different organs, including muscle, adipose tissue, brain, and bone, and regulates skeletal homeostasis. However, the relationship between adiponectin and cell death in the progression of OA needs further investigation. We elaborate the structure and function and the effect of adiponectin and state the correlation and intersection between adiponectin, autophagy, inflammation, and OA. From the perspective of oxidative stress, apoptosis, pyroptosis, and autophagy, we discuss the possible association between adiponectin, chondrocyte metabolism, and inflammatory factor efforts in OA. What's more, we summarize the possible treatment methods, including the use of adiponectin as a drug target, and highlight the potential future mechanistic research. In this review, we summarize the molecular pathways and mechanisms of action of adiponectin in chondrocyte inflammation and death and the pathogenesis of OA. We also review the research on adiponectin as a target for treating OA. These studies provide a novel perspective to explore more effective treatment options considering the complex interrelationship between inflammation and metabolism in OA.

Modification effects of ambient temperature on ozone-mortality relationships in Chengdu, China.

A multitude of epidemiological studies have demonstrated that both ambient temperatures and air pollution are closely related to health outcomes. However, whether temperature has modification effects on the association between ozone and health outcomes is still debated. In this study, three parallel time-series Poisson generalized additive models (GAMs) were used to examine the effects of modifying ambient temperatures on the association between ozone and mortality (including non-accidental, respiratory, and cardiovascular mortality) in Chengdu, China, from 2014 to 2016. The results confirmed that the ambient high temperatures strongly amplified the adverse effects of ozone on human mortality; specifically, the ozone effects were most pronounced at > 28 °C. Without temperature stratification conditions, a 10-µg/m3 increase in the maximum 8-h average ozone (O3-8hmax) level at lag01 was associated with increases of 0.40% (95% confidence interval [CI] 0.15%, 0.65%), 0.61% (95% CI 0.27%, 0.95%), and 0.69% (95% CI 0.34%, 1.04%) in non-accidental, respiratory, and cardiovascular mortality, respectively. On days during which the temperature exceeded 28 °C, a 10-µg/m3 increase in O3-8hmax led to increases of 2.22% (95% CI 1.21%, 3.23%), 2.67% (95% CI 0.57%, 4.76%), and 4.13% (95% CI 2.34%, 5.92%) in non-accidental, respiratory, and cardiovascular mortality, respectively. Our findings validated that high temperature could further aggravate the health risks of O3-8hmax; thus, mitigating ozone exposure will be brought into the limelight especially under the context of changing climate.

Obesity and Coronavirus Disease 2019.

The coronavirus disease 2019 (COVID-19) pandemic has brought severe challenges to global public health. Many studies have shown that obesity plays a vital role in the occurrence and development of COVID-19. Obesity exacerbates COVID-19, leading to increased intensive care unit hospitalization rate, high demand for invasive mechanical ventilation, and high mortality. The mechanisms of interaction between obesity and COVID-19 involve inflammation, immune response, changes in pulmonary dynamics, disruptions of receptor ligands, and dysfunction of endothelial cells. Therefore, for obese patients with COVID-19, the degree of obesity and related comorbidities should be evaluated. Treatment methods such as administration of anticoagulants and anti-inflammatory drugs like glucocorticoids and airway management should be actively initiated. We should also pay attention to long-term prognosis and vaccine immunity and actively address the physical and psychological problems caused by longterm staying-at-home during the pandemic. The present study summarized the research to investigate the role of obesity in the incidence and progression of COVID-19 and the psychosocial impact and treatment options for obese patients with COVID-19, to guide the understanding and management of the disease.

[Interactive Effects of the Influencing Factors on the Changes of O3 Concentrations Based on GAMs Model in Chengdu].

To explore the influence characteristics of the interaction effects between meteorological factors on ozone(O3) concentration in Chengdu, daily air pollutants and meteorological data from 2014 to 2019 were collected. Generalized additive models(GAMs) were adopted to explore the effects of different factors on O3 concentration. The results showed that the relationship between O3 and maximum temperature, sunshine hours, relative humidity, wind speed, precipitation, maximum mixed depth(MMD), and ventilation coefficient(VC) was non-linear. Specifically, the maximum temperature, sunshine hours, MMD, and relative humidity had a significant influence on O3 concentration throughout the year. It is worth noting that the influence of relative humidity and precipitation on O3 concentration during summer was more significant than that for the whole year. In the multi-meteorological factors GAMs of O3 concentration, the meteorological factors mentioned above, except average wind, had significant impacts on O3 concentration change. For the whole year, the judgment coefficient(R2) was 0.849 and the variance explanation rate was 85.1%. The maximum temperature was the most important influencing factor on O3 concentration throughout the year. During summer, corresponding R2 was 0.811 and the explanation rate of variance was 81.3%; however, maximum temperature and MMD were the dominant meteorological factors. In the interaction GAMs, for the whole year, the interaction between maximum temperature and sunshine hours, relative humidity, and precipitation, and the interaction between sunshine hours and MMD had a significant impact on O3 concentrations. The interaction between maximum temperature and sunshine hours played a leading role in changes of O3 concentration. The high temperature+strong radiation+MMD(about 2000 m) +no precipitation were conducive to the formation of O3 concentration, but in summer, only the maximum temperature, sunshine hours, and VC had the most significant effect on the O3 concentration, and strong high temperatures+strong radiation+the little horizontal wind in summer were conducive to the formation of O3 concentration near the surface. In summary, GAMs model can not only be used to identify the dominant influencing factors of O3 pollution, but also quantitatively analyze the influence of single effects and interaction of influencing factors on O3 concentration, which has great significance for the prevention and control of O3 pollution.

JUNB-FBXO21-ERK axis promotes cartilage degeneration in osteoarthritis by inhibiting autophagy.

Osteoarthritis (OA) is a heterogeneous disease that is extremely hard to cure owing to its complex regulation network of pathogenesis, especially cartilage degeneration. FBXO21 is a subunit of ubiquitin E3 ligases that degrades P-glycoprotein and EID1 by ubiquitination and activates the JNK and p38 pathways; however, its role in OA remains unknown. Here, the main objective of this study was to evaluate the potential effects and mechanism of FBXO21 in OA degeneration, we revealed that FBXO21 is upregulated in the cartilage of patients with OA, aging, and monosodium iodoacetate-induced OA rats, and chondrocytes treated with interleukin-1ß, tumor necrosis factor-α, and lipopolysaccharide. Moreover, the in vivo and in vitro knockdown of FBXO21 suppressed OA-related cartilage degeneration, as evidenced by activated autophagy, upregulated anabolism, alleviated apoptosis, and downregulated catabolism. In contrast, its overexpression promoted OA-related cartilage degeneration. In addition, using mass spectrometry and co-immunoprecipitation assay, we demonstrated that the downstream mechanism of FBXO21 inhibits autophagy by interacting with and phosphorylating ERK. Furthermore, FBXO21 alleviated anabolism and enhanced apoptosis and catabolism by inhibiting autophagy in rat chondrocytes. Interestingly, for its upstream mechanism, JUNB promoted FBXO21 expression by directly targeting the FBXO21 promoter, thus further accelerating cartilage degeneration in SW1353 cells and rat chondrocytes. Overall, our findings reveal that the JUNB-FBXO21-ERK axis regulates OA apoptosis and cartilage matrix metabolism by inhibiting autophagy. Therefore, FBXO21 is an attractive target for regulating OA pathogenesis, and its knockdown may provide a novel targeted therapy for OA.

Supported Pt-Cu bimetallic catalysts: preparation and synergic effects in their catalytic oxidative degradation of aniline.

Catalytic Fenton oxidation is an effective way to remove organic pollutants in water, and the performance of the catalyst is a key issue for the competiveness of this method. In this work, various supported bimetallic Pt-Cu catalysts were prepared by different impregnation methods and their performances for catalytic Fenton oxidation of aniline in water were investigated. In the different impregnation methods employed, factors including the reduction method of the metal precursor, type of catalytic support, and loading of metal were investigated. The effect of different reduction methods on actual loadings of the active components on the supported Pt-Cu catalysts showed the order of (i) H2 reduction > (ii) liquid phase methanal reduction. Meanwhile, compared with the monometallic catalysts, the Pt-Cu alloy phase (mainly in the form of PtCu3) was generated and the specific surface area was significantly reduced for the bimetallic catalysts. In the process of Fenton catalytic oxidation of aniline, it was found that most of the prepared catalysts had a certain catalytic activity for H2O2 accompanied with aniline degradation. It was found that Pt0.5Cu1.5/AC (where AC denotes activated carbon) exhibited superb catalytic activity compared with all other prepared catalysts. In particular, aniline was almost completely mineralized in a neutral solution (500 mg L-1 aniline, 0.098 mol L-1 H2O2) after 60 min at 50 °C using Pt-Cu/AC (Pt: 0.5%, Cu: 1.5%). The characterization results showed that the Pt and Cu components were rather evenly distributed on the AC support for this catalyst. More importantly, there was an obvious synergic effect on the supported bimetallic catalyst between the Pt and Cu components for the catalytic oxidation of aniline.

Maresin-1 suppresses IL-1ß-induced MMP-13 secretion by activating the PI3K/AKT pathway and inhibiting the NF-κB pathway in synovioblasts of an osteoarthritis rat model with treadmill exercise.

Aim: Maresin-1 is a metabolite of docosahexaenoic acid (DHA) that has potential anti-inflammatory effects. To explore whether maresin-1 changes and has a therapeutic effect in osteoarthritis (OA) model rats undergoing treadmill exercise, we examined endogenous maresin-1 in a single-session treadmill experiment and OA model rats were treated with maresin-1, moreover, we examined the effects of maresin-1 on IL-1ß induced rat fibroblast-like synoviocytes (FLSs) and possible mechanisms.Methods: In single-session treadmill experiment, 48 rats were randomly divided into 3 groups and performed three different intensities of exercise (15.2 m/min, 0°; 19.3 m/min, 5°; 26.8 m/min, 10°) for 60 min. Intra-articular lavage fluid (IALF) samples were harvested after 0, 2, and 4 h from each group (n = 4) and maresin-1 levels were evaluated by ELISA. Another 30 rats were treated with monosodium iodoacetate (MIA) to induce osteoarthritis and exogenous maresin-1 (MaR-1) and were divided into three groups (n = 10, OA: MIA, OAM: MIA+MaR1, and CG: control group). The level of injury was evaluated by OARSI and Mankin scores, and the levels of type II collagen and MMP13 were evaluated by immunohistochemistry. FLSs were obtained from the knee joint of SD rats, and the expression of MMP13 and activation of the PI3k/Akt and NF-κB p65 pathways in IL-1ß-induced FLSs were evaluated by western blotting.Results: Maresin-1 levels were increased in IALF at 4 h after exercise, and type II collagen increased in cartilage and MMP13 decreased in the synovium after treatment with maresin-1 in MIA-induced osteoarthritis. The results of vitro experiment showed decreased MMP13, activation of the PI3k/Akt pathway, and suppression of the NF-κB p65 pathway upon treatment with maresin-1 in IL-1ß-induced FLSs.Conclusions: The changes in maresin-1 in IALF, as seen in our single-section treadmill exercise, provides an explanation for the therapeutic effect of appropriate-strength treadmill exercise on osteoarthritis, and our experiments confirmed the therapeutic effect of maresin-1 both in vivo and in vitro.

Design a novel integrated screw for minimally invasive atlantoaxial anterior transarticular screw fixation: a finite element analysis.

PURPOSE: To design a new type of screw for minimally invasive atlantoaxial anterior transarticular screw (AATS) fixation with a diameter that is significantly thicker than that of traditional screws, threaded structures at both ends, and a porous metal structure in the middle. The use of a porous metal structure can effectively promote bone fusion and compensate for the disadvantages of traditional AATSs in terms of insufficient fixation strength and difficulty of bone fusion. The biomechanical stability of this screw was verified through finite element analysis. This instrument may provide a new surgical option for the treatment of atlantoaxial disorders. METHODS: According to the surgical procedure, the new type of AATS was placed in a three-dimensional atlantoaxial model to determine the setting of relevant parameters such as the diameter, length, and thread to porous metal ratio of the structure. According to the results of measurement, the feasibility and safety of the new AATS were verified, and a representative finite element model of the upper cervical vertebrae was chosen to establish, and the validity of the model was verified. Then, finite element-based biomechanical analysis was performed using three models, i.e., atlantoaxial posterior pedicle screw fixation, traditional atlantoaxial AATS fixation, and atlantoaxial AATS fixation with the new type of screw, and the biomechanical effectiveness of the novel AATS was verified. RESULTS: By measuring the atlantoaxial parameters, the atlantoaxial CT data of the representative 30-year-old normal adult male were selected to create a personalized 3D printing AATS screw. In this case, the design parameters of the new screw were determined as follows: diameter, 6 mm; length of the head thread structure, 10 mm; length of the middle porous metal structure, 8 mm (a middle porous structure containing an annular cylinder ); length of the tail thread structure, 8 mm; and total length, 26 mm. Applying the same load conditions to the atlantoaxial complex along different directions in the established finite element models of the three types of atlantoaxial fusion modes, the immediate stability of the new AATS is similar with Atlantoaxial posterior pedicle screw fixation.They are both superior to traditional atlantoaxial anterior screw fixation.The maximum local stress on the screw head in the atlantoaxial anterior surgery was less than those of traditional atlantoaxial anterior surgery. CONCLUSIONS: By measuring relevant atlantoaxial data, we found that screws with a larger diameter can be used in AATS surgery, and the new AATS can make full use of the atlantoaxial lateral mass space and increase the stability of fixation. The finite element analysis and verification revealed that the biomechanical stability of the new AATS was superior to the AATS used in traditional atlantoaxial AATS fixation. The porous metal structure of the new AATS may promote fusion between atlantoaxial joints and allow more effective bone fusion in the minimally invasive anterior approach surgery.

Moderate Mechanical Stimulation Protects Rats against Osteoarthritis through the Regulation of TRAIL via the NF-κB/NLRP3 Pathway.

The aim of this study was to examine exercise-related genes in articular cartilage identified through bioinformatics analysis to dissect the potential signaling pathway involved in mechanical stimulation in osteoarthritis (OA). To this end, we evaluated the GSE74898 dataset from the Gene Expression Omnibus database for exercise-related differentially expressed miRNAs (DE-miRNAs) using the R software package and predicted potential target genes for these miRNAs using miRTarBase. Functional annotation and pathway enrichment analysis were performed for these potential DE-miRNA targets. The effects of mechanical stimulation on the tumor necrosis factor-related apoptosis-induced ligand (TRAIL)/nuclear factor-kappa B (NF-κB)/nucleotide-binding and oligomerization domain-like receptor containing protein 3 (NLRP3) signaling pathway were evaluated in articular cartilage and chondrocytes. A total of 394 DE-miRNAs were identified (103 upregulated miRNAs; 291 downregulated miRNAs) in the cartilage of rats following treadmill exercise compared to the cartilage of unexercised control rats. Thus, mechanical stimulation could modulate the TRAIL/NF-κB/NLRP3 signaling pathway on OA. Histological and protein analysis demonstrated that moderate-intensity treadmill exercise could ameliorate OA through the downregulation of TRAIL. Furthermore, moderate cyclic tensile strain (CTS) could rescue chondrocytes from the effects of TRAIL via the inhibition of the nuclear translocation of NF-κB p65 and formation of NLRP3. Our findings indicate that moderate mechanical stimulation could ameliorate the degeneration of cartilage and chondrocyte damage through the inhibition of the TRAIL/NF-κB/NLRP3 pathway.

Temperature inversions in the atmospheric boundary layer and lower troposphere over the Sichuan Basin, China: Climatology and impacts on air pollution.

The Sichuan Basin (SB) is one of the four most severely polluted regions in China in terms of air quality, and the frequent generation of temperature inversions is a key factor. The deep mountain-basin topography and the geographical location adjacent to the Tibetan Plateau combine to make the inversion characteristics of this region unique. Knowledge regarding these characteristics remains limited, however. In this study, the radiosonde data at standard pressure levels and significant levels from all SB operational radiosonde stations over 2015-2018 were used to document the climatological features of the inversions from the surface to a height of 5500 m and to evaluate the impact on local air pollutant concentrations. Results revealed that the temperature inversion in the SB is a common and year-round phenomenon. The annual inversion frequency, depth, and strength values are 74.4%, 252.2 m, and 1.3 °C/100 m, respectively. The inversions are most frequent (95.4%), deepest (289.4 m), and strongest (1.6 °C/100 m) in winter. They tend to occur at one of two heights, either below 600 m or between 2200 and 3500 m. Based on their bottom heights, the inversions were divided into three groups: surface-based inversions (SIs), elevated inversions (EIs), and lower-troposphere inversions (LTIs). Annual LTI is most frequent (63.0%) and deepest (264.7 m), while annual SI is strongest (1.8 °C/100 m). Extreme contrasts exist in the seasonal properties of different inversion types. All types of inversions play a considerable role in air pollution, resulting in a high probability of severe and very serious pollution in winter. SI has a greater impact on pollutant concentrations than EI and LTI. The frequent generation of LTIs is a unique feature of the deep SB. LITs exert a significant impact on the formation of local heavy air pollution, but have not been given sufficient attention.

Unraveling How the H2 Treatment Helps Improve the Performances of Cu and Ag Loaded Y Zeolites for Adsorptive Desulfurization.

This work seeks for a better understanding on how the gas treatment process affected the structure of metal loaded zeolite Y (MY, M = Ag, Cu) adsorbants and how the structural changes affected the performances of the adsorbents for adsorptive desulfurization. A series of characterization tools including solid-state nuclear magnetic resonance were employed. Compared to the N2 treatment, the H2 treatment on the MY adsorbents led to the reduction of the loaded M components to their metallic state and, consequently, brought several structural changes to the zeolitic framework. The structural changes brought by the H2 treatment can be accounted for the decreased Brönsted acidity over the Lewis acidity of the adsorbents and thus helped in improving their adsorption capacity. This paper provides new insights on how the zeolitic framework changes affected the sulfur adsorption capacity of MY, which is helpful for designing better adsorbents for sulfur removal from oil.

Research on braking energy recovery strategy of electric vehicle based on ECE regulation and I curve.

Electric vehicles can convert the kinetic energy of the vehicle into electric energy for recycling. A reasonable braking force distribution strategy is the key to ensure braking stability and the energy recovery rate. For an electric vehicle, based on the ECE regulation curve and ideal braking force distribution (I curve), the braking force distribution strategy of the front and rear axles is designed to study the braking energy recovery control strategy. The fuzzy control method is adopted while the charging power limit of the battery is considered to correct the regenerative braking torque of the motor, the ratio of the regenerative braking force of the motor to the front axle braking force is designed according to different braking strengths, then the braking force distribution and braking energy recovery control strategies for regenerative braking and friction braking are developed. The simulation model of combined vehicle and energy recovery control strategy is established by Simulink and Cruise software. The braking energy recovery control strategy of this article is verified under different braking conditions and New European Driving Cycle conditions. The results show that the control strategy proposed in this article meets the requirements of braking stability. Under the condition of initial state of charge of 75%, the variation of state of charge of braking control strategy in this article is reduced by 8.22%, and the state of charge of braking strategy based on I curve reduces by 9.12%. The braking force distribution curves of the front and rear axle are in line with the braking characteristics, can effectively recover the braking energy, and improve the battery state of charge. Taking the using range of 95%-5% of battery state of charge as calculation target, the cruising range of vehicle with braking control strategy of this article increases to 136.64 km, which showed that the braking control strategy in this article could increase the cruising range of the electric vehicle.