A new classification for surgical NEC during exploratory laparotomy: introduction and reproducibility assessment.

PURPOSE: Variability in necrosis patterns and operative techniques in surgical necrotizing enterocolitis (NEC) necessitates a standardized classification system for consistent assessment and comparison. This study introduces a novel intraoperative reporting system for surgical NEC, focusing on reliability and reproducibility. METHODS: Analyzing surgical NEC cases from January 2018 to June 2023 at two tertiary neonatal and pediatric surgery units, a new classification system incorporating anatomical details and intestinal involvement extent was developed. Its reproducibility was quantified using kappa coefficients (κ) for interobserver and intraobserver reliability, assessed by four specialists. Furthermore, following surgery, the occurrence of mortality and enteric autonomy were evaluated on the basis of surgical decision-making of the novel intraoperative classification system for surgical NEC. RESULTS: In total, 95 patients with surgical NEC were included in this analysis. The mean κ value of the intra-observer reliability was 0.889 (range, 0.790-0.941) for the new classification, indicating excellent agreement and the inter-observer reliability was 0.806 (range, 0.718-0.883), indicating substantial agreement. CONCLUSION: The introduced classification system for surgical NEC shows high reliability, deepening the understanding of NEC's intraoperative exploration aspects. It promises to indicate operative strategies, enhance prognosis prediction, and substantially facilitate scholarly communication in pediatric surgery. Importantly, it explores the potential for a standardized report and may represent a step forward in classifying surgical NEC, if pediatric surgeons are open to change.

Complement Proteins in Serum Astrocyte-Derived Exosomes Are Associated with Poststroke Cognitive Impairment in Type 2 Diabetes Mellitus Patients.

Background: The complement system plays crucial roles in cognitive impairment and acute ischemic stroke (AIS). High levels of complement proteins in plasma astrocyte-derived exosomes (ADEs) were proven to be associated with Alzheimer's disease. We aimed to investigate the relationship of complement proteins in serum ADEs with poststroke cognitive impairment in type 2 diabetes mellitus (T2DM) patients. Methods: This study analyzed 197 T2DM patients who suffered AIS. The Beijing version of the Montreal Cognitive Assessment (MoCA) was used to assess cognitive function. Complement proteins in serum ADEs were quantified using ELISA kits. Results: Mediation analyses showed that C5b-9 and C3b in serum ADEs partially mediate the impact of obstructive sleep apnea (OSA), depression, small vessel disease (SVD), and infarct volume on cognitive function at the acute phase of AIS in T2DM patients. After adjusting for age, sex, time, and interaction between time and complement proteins in serum ADEs, the mixed linear regression showed that C3b and complement protein Factor B in serum ADEs were associated with MoCA scores at three-, six-, and twelve-months after AIS in T2DM patients. Conclusions: Our study suggested that the impact of OSA, depression, SVD, and infarct volume on cognitive impairment in the acute stage of AIS may partially mediate through the complement proteins in serum ADEs. Additionally, the complement proteins in serum ADEs at the acute phase of AIS associated with MoCA scores at three-, six-, twelve months after AIS in T2DM patients.REGISTRATION: URL: http://www.chictr.org.cn/,ChiCTR1900021544.

Neurodevelopmental impairment following surgical necrotizing enterocolitis with gestational age ≥ 28 weeks: who is at risk?

PURPOSE: Surgical necrotizing enterocolitis (NEC) is a severe medical condition that, even after surgery, a portion of the survival infants may still have neurological sequelae. The objective of this study was to identify the risk factors associated with the development of permanent neurodevelopmental impairment (NDI) in neonates with surgical NEC. METHODS: Between January 2016 and June 2022, a retrospective data collection was conducted on 98 individuals who experienced surgical NEC with gestational age ≥ 28 weeks. Among these patients, 27 patients were diagnosed with NDI, while the remaining 71 patients did not have NDI. Based on this division, the patients were categorized into the NDI group and the Non-NDI group. Demographics, comorbidities, and admission lab results were analyzed using univariate and logistic regression analyses. RESULTS: Of the 98 neonates following surgical NEC, 27(27.6%) developed permanent neurodevelopmental impairment (NDI). Predictors of NDI were identified through the final multivariable logistic regression analysis, which revealed that gestational age ≤ 32 weeks (p = 0.032; odds ratio [OR], 5.673), assisted mechanical ventilation after NEC onset (p = 0.047; OR, 5.299), postoperative acute kidney injury (p = 0.040; OR, 5.106), CRP day 3 after NEC onset (p = 0.049; OR, 1.037), time from presentation to surgery (p = 0.003; OR, 1.047) were significant risk factors. CONCLUSIONS: Our study identified gestational age ≤ 32 weeks, assisted mechanical ventilation after NEC onset, postoperative acute kidney injury, CRP day 3 after NEC onset, and time from presentation to surgery as significant risk factors for NDI in neonates with surgical NEC. These factors would be helpful to refine treatment modalities for better disease outcomes. We also determined the cut-off values of CRP day 3 after NEC onset and time from presentation to surgery, allowing for the individualized evaluation of NDI risk and the implementation of earlier targeted laparotomy.

High efficiency removal of NO using waste calcium carbide slag by facile KOH modification.

Waste calcium carbide slags (CS), which are widely applied to desulfurisation, are not typically used in denitration. Herein, to well achieve waste control by waste, a facile and high-efficiency denitration strategy is developed using KOH to modify the calcium carbide slags (KCS). Various KCS samples were investigated using a series of physical and chemical characterisations. The performance test results showed that the KOH concentration and reaction temperature are the main factors affecting the denitration efficiency of KCS, and CS modified with 1.5 mol/L KOH (KCS-1.5) can achieve 100% denitration efficiency at 300°C. Such excellent removal efficiency is due to the catalytic oxidation of the oxygen-containing functional groups derived from the KCS. Further studies showed that KOH treatment significantly increased the concentration of oxygen vacancies, nitro compounds, and basic sites of CS. This study provides a novel strategy for the resource utilisation of waste CS in the future.

Acute motor-sensory axonal polyneuropathy variant of Guillain-Barré syndrome with a thalamic lesion and COVID-19: a case report and discussion on mechanism.

Background: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) primarily affects the respiratory system. During the global coronavirus disease (COVID-19) pandemic, COVID-19-associated neurological diseases have been increasingly reported, including peripheral nervous system diseases, such as Guillain-Barré syndrome (GBS). Acute motor-sensory axonal polyneuropathy (AMSAN), is a GBS variant associated with COVID-19. To date, there are no reports of GBS cases with thalamic injury and dynamic evolution with fluctuating GBS symptoms. In this report, we describe the first case of COVID-19-associated AMSAN accompanied by a thalamic lesion and discuss the magnetic resonance imaging (MRI) findings. Case presentation: A 76-year-old woman, with known co-morbid type 2 diabetes mellitus, presented to the emergency room with complaints of weakness and paraesthesia in both her legs and arms for 4 days, and fever and dry cough for the past 5 days. A nasopharyngeal swab for SARS-CoV-2 returned positive. The patient had not received specific treatment for COVID-19 infection. Neurological examination disclosed symmetric weakness (Medical Research Council grade upper limbs 4/5, lowers limbs 2/5) and areflexia in both the legs and feet. No cranial nerves were involved. Following a neuro-electro-physiology study to evaluate neurological symptoms, AMSAN was suggested. Cerebrospinal fluid (CSF) analysis showed elevated protein levels that confirmed the diagnosis of GBS. The patient was subsequently treated with intravenous immune globulin (IVIG), which improved her neurological symptoms (upper limbs 4/5, lowers limbs 4/5). However, urinary retention, dysarthria, dysphagia, bilateral facial paralysis, facial diplegia, bucking, and motor alalia gradually appeared, followed by aggravated paralysis (upper limbs 3/5, lowers limbs 1/5). After being hospitalized for 16 days, the patient underwent continuous plasma exchange (PE) treatment for a duration of 3 days. Following treatment, the patient's neurological symptoms and paralysis gradually improved (upper limbs 4/5, lowers limbs 4/5) over 2 weeks. Meanwhile, we observed that the patient's cerebral magnetic resonance imaging (MRI) findings dynamically evolved along with the fluctuation of her GBS symptoms, mainly in terms of the changes in T2 hyperintensity in the right thalamus accompanied by microhaemorrhages. The inflammation index was normal. We considered a wide range of possible causes including hypoxia, drugs, toxins, and metabolic derangements but these were excluded. Conclusion: The AMSAN variant of GBS secondary to COVID-19 infection is severe and can cause extensive damage to the peripheral nerves system. The deterioration of symptoms in the patient after early immunotherapy may indicate treatment-related fluctuation (TRF) and could be attributed to immune rebound. Moreover, an excessive immune response post-COVID-19 infection may trigger concurrent damage to the central nervous system, indicating secondary harm to brain small blood vessels and nerve units. For suspected cases of GBS complicated by COVID-19, it is essential to conduct early brain MRI examinations in addition to routine peripheral nervous system evaluations to promptly detect any intracranial lesions. This facilitates appropriate immunotherapy and improves patient prognosis.

[Distribution, Sources, and Risk Assessment of Microplastics in Surface Sediments of Yellow River Delta Wetland].

Estuarine habitats are a critical zone of the Earth with strong land-sea interactions, that are strongly influenced by human activities. Microplastics (MPs) pollution in the Yellow River Delta (YRD) wetland, a typical young warm-temperate estuarine wetland, has not been comprehensively studied. The morphology, abundance, particle size, and polymer composition of MPs in the surface sediments of the YRD wetland were determined, and the pollution status and ecological risk in the study area were evaluated using the pollution load index (PLI) and potential pollution risk index (PRI). The results showed that the abundance of MPs in the YRD wetland was 20-520 n·kg-1, with a median value of 150 n·kg-1. The MPs were primarily fibers in shape and black in color, with particle size over 1 mm. The polymer components were primarily rayon, polyethylene, polyester, and polyethylene terephthalate. The PLI and PRI values of the MPs in the area were between 0.04-0.96 and 0.00-171.60, respectively, indicating that the pollution of MPs in the YRD wetland was at a slightly polluted level with low ecological risk.

Hydrogen sulfide alleviates mitochondrial damage and ferroptosis by regulating OPA3-NFS1 axis in doxorubicin-induced cardiotoxicity.

Ferroptosis is a major cause of cardiotoxicity induced by doxorubicin (DOX). Previous studies have shown that hydrogen sulfide (H2S) inhibits ferroptosis in cardiomyocytes and myoblasts, but the underlying mechanism has not been fully elucidated. In this study, we investigated the role of H2S in protecting against DOX-induced cardiotoxicity both in vivo and in vitro, and elucidated the potential mechanisms involved. We found that DOX downregulated the expression of glutathione peroxidase 4 (GPX4) and NFS1, and upregulated the expression of acyl-coenzyme A synthetase long-chain family member 4 (ACSL4) expression level, resulting in increased lipid peroxidation and ferroptosis. Additionally, DOX inhibited MFN2 expression and increased DRP1 and FIS1 expression, leading to abnormal mitochondrial structure and function. In contrast, exogenous H2S inhibited DOX-induced ferroptosis by restoring GPX4 and NFS1 expression, and reducing lipid peroxidation in H9C2 cells. This effect was similar to that of the ferroptosis antagonist ferrostatin-1 (Fer-1) in protecting against DOX-induced cardiotoxicity. We further demonstrated that the protective effect of H2S was mediated by the key mitochondrial membrane protein optic atrophy 3 (OPA3), which was downregulated by DOX and restored by exogenous H2S. Overexpression of OPA3 alleviated DOX-induced mitochondrial dysfunction and ferroptosis both in vivo and in vitro. Mechanistically, NFS1 has an inhibitory effect on ferroptosis, and NFS1 deficiency increases the susceptibility of cardiomyocytes to ferroptosis. OPA3 is involved in the regulation of ferroptosis by interacting with NFS1. Post-translationally, DOX promoted OPA3 ubiquitination, while exogenous H2S antagonized OPA3 ubiquitination by promoting OPA3 s-sulfhydration. In summary, our findings suggested that H2S protects against DOX-induced cardiotoxicity by inhibiting ferroptosis via targeting the OPA3-NFS1 axis. This provides a potential therapeutic strategy for the treatment of DOX-induced cardiotoxicity.

Ginsenoside Rb1 Improves Post-Cardiac Arrest Myocardial Stunning and Cerebral Outcomes by Regulating the Keap1/Nrf2 Pathway.

The prognosis of cardiac arrest (CA) is dismal despite the ongoing progress in cardiopulmonary resuscitation (CPR). ginsenoside Rb1 (Gn-Rb1) has been verified to be cardioprotective in cardiac remodeling and cardiac ischemia/reperfusion (I/R) injury, but its role is less known in CA. After 15 min of potassium chloride-induced CA, male C57BL/6 mice were resuscitated. Gn-Rb1 was blindly randomized to mice after 20 s of CPR. We assessed the cardiac systolic function before CA and 3 h after CPR. Mortality rates, neurological outcome, mitochondrial homeostasis, and the levels of oxidative stress were evaluated. We found that Gn-Rb1 improved the long-term survival during the post-resuscitation period but did not affect the ROSC rate. Further mechanistic investigations revealed that Gn-Rb1 ameliorated CA/CPR-induced mitochondrial destabilization and oxidative stress, partially via the activation of Keap1/Nrf2 axis. Gn-Rb1 improved the neurological outcome after resuscitation partially by balancing the oxidative stress and suppressing apoptosis. In sum, Gn-Rb1 protects against post-CA myocardial stunning and cerebral outcomes via the induction of the Nrf2 signaling pathway, which may offer a new insight into therapeutic strategies for CA.

Development of UHPLC-MS/MS method for simultaneous determination of tacrolimus and sirolimus in human whole blood and comparisons with two immunoassays.

Tacrolimus (TAC) and sirolimus (SIR) antirejection medications are widely used in organ transplantation. We aimed to develop an ultra-high performance liquid chromatography tandem mass spectrometry (UHPLC-MS/MS) assay for quantifying TAC and SIR simultaneously and evaluating agreement with chemiluminescence microparticle immunoassay (CMIA) and electrochemiluminescence immunoassay (ECLIA). Whole blood samples collected from 209 TAC and 208 SIR patients were assessed by UHPLC-MS/MS, CMIA and ECLIA. The agreement of the three techniques was assessed using the Bland-Altman plot. The UHPLC-MS/MS assay had a calibration range of 1-100 ng/ml for TAC and SIR. The accuracy and precision were -2.73-4.32% and <4.71% for TAC, respectively, and 0.07-4.84% and <6.5% for SIR, respectively. The three methods had good correlation. In comparison with UHPLC-MS/MS, two immunoassays showed a slight deviation in proportion. An UHPLC-MS/MS method for simultaneously detecting TAC and SIR in human whole blood was developed, validated and comparatively analyzed with CMIA and ECLIA. For determining TAC and SIR, immunoassays displayed acceptable analytical performances in terms of precision and correlation compared with UHPLC-MS/MS. However, further investigation is warranted to examine the novel method.

Treatment of cadmium and zinc-contaminated water systems using modified biochar: Contaminant uptake, adsorption ability, and mechanism.

Cd and Zn contamination in water occurs frequently that threatens water supply, human health, and food production. MnFeB, a novel absorbent biochar modified using KMnO4 and hematite, was prepared and used for the treatment of Cd2+ and Zn2+solutions. MnFeB exhibits a rough surface structure, large specific surface area, higher total pore volume, massive functional groups, and abundant iron oxide, all of which contribute to higher Cd2+ and Zn2+ adsorption capacity. In single metal systems, maximum Cd2+ and Zn2+ adsorption capacities of MnFeB were 1.88 and 1.79 times higher than those of unmodified biochar (CSB). The maximum Cd2+ and Zn2+ adsorption capacities of MnFeB were 2.73 and 2.65 times higher than CSB in the binary metal system. Key adsorption mechanisms of Cd2+ and Zn2+ by MnFeB included electrostatic interaction, co-precipitation, π-π interaction, complexation, and ion exchange. Thus, MnFeB can be used as a novel absorbent to treat Cd and Zn-polluted water.

Nuclear Receptor NR1D1 Regulates Abdominal Aortic Aneurysm Development by Targeting the Mitochondrial Tricarboxylic Acid Cycle Enzyme Aconitase-2.

BACKGROUND: Metabolic disorder increases the risk of abdominal aortic aneurysm (AAA). NRs (nuclear receptors) have been increasingly recognized as important regulators of cell metabolism. However, the role of NRs in AAA development remains largely unknown. METHODS: We analyzed the expression profile of the NR superfamily in AAA tissues and identified NR1D1 (NR subfamily 1 group D member 1) as the most highly upregulated NR in AAA tissues. To examine the role of NR1D1 in AAA formation, we used vascular smooth muscle cell (VSMC)-specific, endothelial cell-specific, and myeloid cell-specific conditional Nr1d1 knockout mice in both AngII (angiotensin II)- and CaPO4-induced AAA models. RESULTS: Nr1d1 gene expression exhibited the highest fold change among all 49 NRs in AAA tissues, and NR1D1 protein was upregulated in both human and murine VSMCs from AAA tissues. The knockout of Nr1d1 in VSMCs but not endothelial cells and myeloid cells inhibited AAA formation in both AngII- and CaPO4-induced AAA models. Mechanistic studies identified ACO2 (aconitase-2), a key enzyme of the mitochondrial tricarboxylic acid cycle, as a direct target trans-repressed by NR1D1 that mediated the regulatory effects of NR1D1 on mitochondrial metabolism. NR1D1 deficiency restored the ACO2 dysregulation and mitochondrial dysfunction at the early stage of AngII infusion before AAA formation. Supplementation with αKG (α-ketoglutarate, a downstream metabolite of ACO2) was beneficial in preventing and treating AAA in mice in a manner that required NR1D1 in VSMCs. CONCLUSIONS: Our data define a previously unrecognized role of nuclear receptor NR1D1 in AAA pathogenesis and an undescribed NR1D1-ACO2 axis involved in regulating mitochondrial metabolism in VSMCs. It is important that our findings suggest αKG supplementation as an effective therapeutic approach for AAA treatment.

Nuclear receptor Nur77 protects against oxidative stress by maintaining mitochondrial homeostasis via regulating mitochondrial fission and mitophagy in smooth muscle cell.

Angiotensin II (AngII) induces disruption of mitochondrial homeostasis and oxidative stress. Nuclear receptor NR4A1 (Nur77) plays an important role in vascular smooth muscle cells (VSMCs) function. However, the role of Nur77 in AngII-induced mitochondrial dynamics and oxidative stress in VSMCs remains unknown. In an in vitro model of AngII-treated cells, we discovered that Nur77 knockout aggravated AngII-induced oxidative stress in VSMCs, whereas activation of Nur77 by celastrol diminished them. Concomitantly, disturbance of mitochondrial dynamics induced by AngII was further exacerbated in Nur77 deficient VSMCs compared to wild-type (WT) VSMCs. Interestingly, Nur77 deletion increased mitochondrial fission but not fusion as evidenced by upregulated fission related genes (Fis1 and Drp1) but not fusion (Opa1 and Mfn2) under AngII stimulation in VSMCs. Mechanically, Nur77 could directly bind to the promoter regions of Fis1 and Drp1 and repress their transcription. Furthermore, we observed that Nur77 additionally promoted mitochondrial homeostasis by increasing mitophagic flux in a transcription-independent manner upon AngII challenge. By using an in vivo model of AngII-induced abdominal aortic aneurysm (AAA), we finally validated the protective role of Nur77 involved in the mitochondrial fission process and mitophagic flux in aortas, which was correlated with the occurrence and development of AAA in AngII-infused mice. Our data defines an essential role of Nur77 in regulating oxidative stress by maintaining mitochondrial homeostasis in VSMCs via both transcription-dependent and transcription-independent manner, supporting the therapeutic potential of Nur77 targeting in vascular diseases.

Hydrogen helps to ameliorate Staphylococcus aureus-induced mastitis in mice.

Many studies have shown that hydrogen has anti-inflammatory and anti-oxidant effects. Because of its ability to quickly pass through cell membranes, hydrogen has become a hot spot in the research of inflammatory diseases. Vitamin E glycerin (VEG) and hydrogen-rich Vitamin E glycerin (HR-VEG) were prepared, aiming to explore their anti-inflammatory activities in mice mastitis induced by Staphylococcus aureus (S. aureus). In the early part of this study, the prepared vitamin E medium (VEM) and hydrogen-rich vitamin E medium (HR-VEM) were added to mammary epithelial cells infected with S. aureus. HR-VEM was found to be more effective in reducing the phosphorylation of p65 and p38 and in reducing the production of interleukin-1 beta (IL-1ß) than VEM. Whereafter, the mice model of mastitis was established by injecting S. aureus from the mammary duct. Then VEG and HR-VEG were applied to the mammary gland for seven consecutive days. After that, the clinical symptoms, histopathology, bacterial load, inflammatory factors, as well as the related pathway were analyzed. The results showed that HR-VEG can more significantly alleviate the damage of mammary tissue than VEG, and reduce the production of tumor necrosis factor-alpha (TNF-α), IL-1ß and interleukin 6 (IL-6). In addition, HR-VEG inhibited the TLR2 and Nod2 signaling pathways and reduced the phosphorylation level of MAPK and NF-κB signaling pathways in S. aureus-induced murine mastitis. This study indicates that hydrogen helps to ameliorate S. aureus-induced mastitis in mice through attenuating TLR2 and Nod2 mediated NF-κB and MAPK activation.

Regulating mitochondrial homeostasis and inhibiting inflammatory responses through Celastrol.

Background: The high morbidity and mortality rate of coronary heart disease poses a serious threat to human health. Atherosclerosis, a chronic inflammation of the blood vessel wall, is a significant pathological process leading to coronary heart disease. Macrophage inflammation plays a crucial role in the occurrence and development of atherosclerosis. Methods: Macrophage inflammation model was constructed by lipopolysaccharide (LPS), and macrophages were treated with Celastrol at different concentrations (0, 0.1, 1, 10, 100 ng/mL) and different time points (0, 1, 3, 6, 12 h). Real-time quantitative PCR (qPCR) and Western Blot were used to detect the expression of Nur77 mRNA and protein. Macrophages were then pretreated with 100 nmol/L tripterine for 40min and co-cultured with 100 ng/mL LPS. The expression levels of inflammatory factors and chemokines, phosphorylation of phospho-dynamin-related protein 1 (p-Drp1) at Ser637 and expression of mitochondrial fusion protein mitochondrial fusion protein mitofusin-2 (Mfn2) were detected by qPCR, Western blot and ELISA, respectively. The changes of mitochondrial membrane potential were detected by JC-1 probe. Results: 100 nmol/L Celastrol can significantly inhibit LPS-induced inflammatory responses and down-regulate the expression levels of cytokines such as inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX2), tumor necrosis factor-α (TNF-α), chemokines (CCL-2, and CXCL-10), as well as chemokines. And Celastrol could regulate mitochondrial fission and fusion by promoting the phosphorylation of the Drp1 at the Ser637 site, thereby inhibiting mitochondrial fission. At the same time, by up-regulating the level of the Mfn2, Celastrol also promoted mitochondrial fusion. In addition, we found that the nuclear factor-k-gene binding (NF-κB), extracellular signal-regulated kinase 1/2 (ERK1/2), and p38 signaling pathways aided the drug's anti-inflammatory effects. We also explored the relationship between Celastrol and the nuclear receptor Nur77 and found that it could up-regulate the expression of Nur77. Conclusions: Our study found that Celastrol could reduce inflammation by regulating Drp1 dependent mitochondrial fission and fusion, as well as the ERK1/2, p38, NF-κB signaling pathways. This finding provides a strong direction for the development of new anti-inflammatory drugs for atherosclerosis.

Streptococcus agalactiae-induced autophagy of bovine mammary epithelial cell via PI3K/AKT/mTOR pathway.

Streptococcus agalactiae (S. agalactiae) infection is a significant cause of mastitis, resulting in loss of cellular homeostasis and tissue damage. Autophagy plays an essential function in cell survival, defense, and the preservation of cellular homeostasis, and is often part of the response to pathogenic challenge. However, the effect of autophagy induced by S. agalactiae in bovine mammary epithelial cells (bMECs) is mainly unknown. So in this study, an intracellular S. agalactiae infection model was established. Through evaluating the autophagy-related indicators, we observed that after S. agalactiae infection, a significant quantity of LC3-I was converted to LC3-II, p62 was degraded, and levels of Beclin1 and Bcl2 increased significantly in bMECs, indicating that S. agalactiae induced autophagy. The increase in levels of LAMP2 and LysoTracker Deep Red fluorescent spots indicated that lysosomes had participated in the degradation of autophagic contents. After autophagy was activated by rapamycin (Rapa), the amount of p-Akt and p-mTOR decreased significantly, whilst the amount of intracellular S. agalactiae increased significantly. Whereas the autophagy was inhibited by 3-methyladenine (3MA), the number of intracellular pathogens decreased. In conclusion, the results demonstrated that S. agalactiae could induce autophagy through PI3K/Akt/mTOR pathway and utilize autophagy to survive in bMECs.

Biochar Alleviates Phytotoxicity by Minimizing Bioavailability and Oxidative Stress in Foxtail Millet (Setaria italica L.) Cultivated in Cd- and Zn-Contaminated Soil.

Soil contamination with multiple heavy metals is a global environmental issue that poses a serious threat to public health and ecological safety. Biochar passivation is an efficient and economical technology to prevent heavy metal contamination of Cd; however, its effects on compound-contaminated and weakly alkaline soil remain unclear. Further, the mechanisms mediating the immobilization effects of biochar have not been evaluated. In this study, three biochar treated at different pyrolytic temperatures [300°C (BC300), 400°C (BC400), and 500°C (BC500)] were applied to Cd-/Zn-contaminated soils, and their effects on plant growth, photosynthetic characteristics, Cd/Zn accumulation and distribution in foxtail millet were evaluated. Further, the effect of biochar application on the soil physicochemical characteristics, as well as the diversity and composition of the soil microbiota were investigated. Biochar significantly alleviated the phytotoxicity of Cd and Zn. DTPA (diethylenetriamine pentaacetic acid)-Cd and DTPA-Zn content was significantly reduced following biochar treatment via the transformation of exchangeable components to stable forms. BC500 had a lower DTPA-Cd content than BC300 and BC400 by 42.87% and 39.29%, respectively. The BC500 passivation ratio of Cd was significantly higher than that of Zn. Biochar application also promoted the growth of foxtail millet, alleviated oxidative stress, and reduced heavy metal bioaccumulation in shoots, and transport of Cd from the roots to the shoots in the foxtail millet. The plant height, stem diameter, biomass, and photosynthetic rates of the foxtail millet were the highest in BC500, whereas the Cd and Zn content in each organ and malondialdehyde and hydrogen peroxide content in the leaves were the lowest. Moreover, biochar application significantly increased the abundance of soil bacteria and fungi, as well as increasing the fungal species richness compared to no-biochar treatment. Overall, biochar was an effective agent for the remediation of heavy metal-contaminated soil. The passivation effect of biochar exerted on heavy metals in soil was affected by the biochar pyrolysis temperature, with BC500 showing the best passivation effect.

Staphylococcus aureus mediates pyroptosis in bovine mammary epithelial cell via activation of NLRP3 inflammasome.

Cell death and inflammation are intimately linked during mastitis due to Staphylococcus aureus (S. aureus). Pyroptosis, a programmed necrosis triggered by gasdermin protein family, often occurs after inflammatory caspase activation. Many pathogens invade host cells and activate cell-intrinsic death mechanisms, including pyroptosis, apoptosis, and necroptosis. We reported that bovine mammary epithelial cells (MAC-T) respond to S. aureus by NOD-like receptor protein 3 (NLRP3) inflammasome activation through K+ efflux, leading to the recruitment of apoptosis-associated speck-like protein (ASC) and the activation of caspase-1. The activated caspase-1 cleaves gasdermin D (GSDMD) and forms a N-terminal pore forming domain that drives swelling and membrane rupture. Membrane rupture results in the release of the pro-inflammatory cytokines IL-18 and IL-1ß, which are activated by caspase-1. Can modulate GSDMD activation by NLRP3-dependent caspase-1 activation and then cause pyroptosis of bovine mammary epithelial cells.

Biochar mitigation of soil acidification and carbon sequestration is influenced by materials and temperature.

The alleviation effects on soil acidification by different raw materials and pyrolysis temperatures can broaden the utilization of biochar. In this study, nine types of biochar produced from three raw materials, namely fruit tree branch, peanut shell, and cow dung, at three pyrolysis temperatures (300, 450, and 600 °C) were used to amend acidified brown soil; the rape growth, physiology character, soil chemical and microbial, along with soil organic carbon mineralization were also investigated. The results showed that application of biochar increased soil pH by 8.48-79.25% and reduced exchangeable acidity, exchangeable Al, and exchangeable H by 56.94-94.95%, 34.38-95.66%, and 58.72-93.27%, respectively. Biochar alleviated oxidative stress in plants, reduced malondialdehyde and glutathione content in leaves, promoted rape growth, and increased microbial community diversity and the relative abundances of Acidobacteria and Olpidiomycota in the acidic soil. Moreover, biochar reduced the mineralization rate of organic carbon and the proportion of mineral-bonded organic carbon. Overall, biochar application is an effective strategy to ameliorate soil acidification and enhance rape production and carbon sequestration. The mitigation effect of branch biochar and cow dung biochar on soil acidification was superior to that of peanut shell biochar. The effects of biochar depended on the pyrolysis temperature; the positive effects of biochar samples pyrolyzed at 450 and 600 â„ƒ were stronger than those pyrolyzed at 300 â„ƒ. In this study, the optimum biochar materials and carbonization temperature for acidified soil improvement, as well as the effects of biochar application on soil microbial and carbon mineralization were clarified, which provides a new potential strategy for acidified soil improvement and expand the application range of biochar.

Removal of SO2 from flue gas using blast furnace dust as an adsorbent.

To control the SO2 emission and achieve the target of "waste controlled by waste", a novel desulfurization method with blast furnace dust slurry was proposed. The effects of reaction temperature, oxygen concentration, and solid-liquid ratio on SO2 removal efficiency were investigated. The optimal conditions were reaction temperature of 35 ℃, oxygen concentration of 10 vol.%, and solid-liquid ratio of 0.5 g/300 mL. Under the optimal conditions, the desulfurization efficiency reached 100% for 4 h. Response surface methodology (RSM) results showed that oxygen concentration significantly influenced the SO2 removal efficiency. Finally, the possible desulfurization mechanism of blast furnace dust was proposed based on the EDX, XRD, SEM-EDS, ICP, and IC. The blast furnace dust (main components are CaZn8(SO4)2(OH)12Cl2·(H2O)9, Mn6.927Si6O15·(OH)8, ZnO, Fe2O3) reacted with H+ to form Zn2+, Fe3+, and Mn2+ which shows a key effect on the SO2 liquid catalytic oxidation. This study provides a promising, feasible, and low-cost desulfurization technology by reusing blast furnace dust.

The boosting of microwave roasting technology on the desulfurization of phosphate rock.

A green and-easy to operate method, the microwave technology, was developed to promote the desulfurization process of phosphate rock, systematically investigates the strengthening effect of microwave, and uses XRD, BET, SEM, XRF, ICP, and EDS to characterize the reactants. The results show that the main reason for the desulfurization efficiency is improved by microwave heating under microwave conditions, different thermal stress phosphate rock materials lead to the destruction of each microstructure, and a specific surface area increased 40.25% phosphate rock. In addition, after microwave irradiation, the pore size of the phosphate rock at 2-5 nm is significantly increased, and the number of mesopores is significantly increased, thereby increasing the desulfurization efficiency of the phosphate rock. By investigating the effects of temperature, oxygen content, flow rate, and solid-liquid ratio on desulfurization efficiency, the paper concludes that the optimal conditions for desulfurization of phosphate rock after microwave irradiation are C(SO2) is 2500 mg·m-3, temperature is 40 °C, φ(O2) is 5%, solid-liquid ratio is 3.5 g:200 ml, and flue gas flow is 500 ml·min-1.