The effects of short-term, long-term, and reapplication of biochar on the remediation of heavy metal-contaminated soil.

Biochar, a cost-effective amendment, has been reported to play pivotal roles in improving soil fertility and immobilizing soil pollutants due to its well-developed porous structure and tunable functionality. However, the properties of biochar and soils can vary inconsistently after field application. This may affect the remediation of biochar on heavy metal (HM)-contaminated soil being altered. Therefore, we selected lettuce as a model crop to determine the effects of short-term, long-term, and reapplication of biochar on soil physicochemical properties, microbial community, HM bioavailability, and plant toxicity. Our investigation revealed that the long-term application of biochar remarkably improved soil fertility, increased the relative abundance of the phylum Proteobacteria which was highly resistant to HMs, and reduced the abundance of phylum Acidobacteria. These changes in soil properties decreased the accumulation of Cd and Pb in lettuce tissues. The short- and long-term applications of biochar had no substantial effects on biomass, quality, and photosynthesis of lettuce. Moreover, the short-term and reapplication of biochar had no significant effects on soil bacterial communities but decreased the accumulation of Cd and Pb in lettuce tissues. It showed that the changes in the physical, chemical, and biological properties of soil after long-term application of biochar promoted the remediation of HM-contaminated soil. Furthermore, microbial community compositions varied with metal stress and biochar application, while the relative abundance of the phylum Actinobacteria in HM-contaminated soil with long-term biochar application was markedly higher than in HM-contaminated soil without biochar application.

Study on the physicochemical properties changes of field aging biochar and its effects on the immobilization mechanism for Cd2+ and Pb2.

It has been widely reported that biochar can be used as a cost-effective amendment to immobilize of heavy metal contaminants in soil. While less research has been conducted on effect of biochar long-term field aging on its properties and the adsorption capability. In this study, the characteristics of aged biochar were investigated by comprehensive characterization to elucidate its mechanism transformation for heavy metal immobilization. Our results showed that, compared to fresh biochar, the relative content of C of aged biochar was reduced by 34.12%, while O was increased by 8.79%. Additionally, the specific surface area, pore volume, pore size and oxygen-containing functional groups of aged biochar were significantly increased compared to the fresh biochar. Batch adsorption experiment indicated that the maximum adsorption for Cd2+ (Qm = 32.157 mg/g) and Pb2+ (Qm = 39.216 mg/g) on aged biochar surface was much larger than that of Cd2+ (Qm = 7.573 mg/g) and Pb2+ (Qm = 8.134 mg/g) on fresh biochar. The underlying adsorption mechanisms for Cd2+ and Pb2+ on fresh biochar were dominated by coprecipitation, cation exchange and cation-π interaction, whereas surface complexation and cation exchange appeared to be more vital for aged biochar, as more active adsorption sites and Oxygen-containing functional groups were formed on its surface during aging, which was well explained by BET, XPS, FTIR and Elemental Analysis. Our study found that the physicochemical properties of biochar changed significantly during field aging. Although these changes increased the adsorption of heavy metals by biochar, the reduced stability of biochar to passivated heavy metal ions.

Dietary astaxanthin-rich extract ameliorates atherosclerosis/retinopathy and restructures gut microbiome in apolipoprotein E-deficient mice fed on a high-fat diet.

Scope: Atherosclerosis (AS) is the leading cause of ischemic disease. However, the anti-AS effects of astaxanthin and its potential mechanisms remain unclear. This study is aimed to investigate the function of astaxanthin-rich extract (ASTE) on AS and gut microbiota as well as the difference from atorvastatin (ATO) in apolipoprotein E-deficient (ApoE-/-) mice. Methods and results: Wild type (WT) and ApoE-/- mice were divided into seven groups: the low-fat diet (LFD) and high-fat diet (HFD) groups (in both types) as well as three ApoE-/- groups based on HFD added with two doses of ASTE and one dose of ATO, respectively. After 30 weeks of intervention, results showed that ASTE significantly inhibited body weight increase, lipids accumulation in serum/liver, and AS-lesions in the aorta. Furthermore, fundus fluorescein angiography and retinal CD31 immunohistochemical staining showed that ASTE could alleviate the occurrence of AS-retinopathy. H&E staining showed that ASTE could protect the colon's mucosal epithelium from damage. The gas chromatographic and gene expression analyses showed that ASTE promoted the excretion of fecal acidic and neutral sterols from cholesterol by increasing LXRα, CYP7A1, and ABCG5/8 and decreasing FXR, NPC1L1, ACAT2, and MTTP expressions. Remarkably, the ASTE administration maintained the gut barrier by enhancing gene expression of JAM-A, Occludin, and mucin2 in the colon and reshaped gut microbiota with the feature of blooming Akkermansia. Conclusion: Our results suggested that ASTE could prevent AS in both macrovascular and/or microvascular as well as used as novel prebiotics by supporting the bile acid excretion and growth of Akkermansia.

Tear Levels of Inflammatory Cytokines in Keratoconus: A Meta-Analysis of Case-Control and Cross-Sectional Studies.

PURPOSE: To assess the tear levels of inflammatory cytokines in patients with keratoconus (KC). DESIGN: Systemic review and meta-analysis. METHODS: The following electronic databases and search engine were searched: PubMed, EMBASE, Web of Science, and Google Scholar. A systematic search of all relevant studies published through January 2021 was conducted, and the standardized mean difference (SMD) and 95% confidence interval (CI) of cytokine levels were calculated to estimate the pooled effects. Sensitivity analysis, subgroup analysis, and metaregression were applied to explore the sources of heterogeneity. RESULTS: A total of 7 studies with 374 participants (374 eyes) from clinical studies were included. The tear levels of interleukin-1 beta (IL-1ß), interleukin-6 (IL-6), and tumor necrosis factor alpha (TNF-α) were significantly increased in KC compared with normal controls. The SMD of IL-1ß was 1.93 (95% CI 0.22 to 3.65, P = 0.03). The SMD of IL-6 was 1.22 (95% CI 0.59 to 1.84, P < 0.001). The SMD of TNF-α was 1.75 (95% CI 0.66 to 2.83, P = 0.002). There was no significant difference between the two groups on interleukin-4 (IL-4) and interleukin-10 (IL-10). The SMD for IL-4 was 2.36 (95% CI -0.28 to 5.00, P = 0.08) and for IL-10 was 0.30 (95% CI -1.29 to 1.89, P = 0.71). Meta-regression analysis indicated that the heterogeneity maybe significantly correlated with the method of detection, the different ages, and the source of population. CONCLUSIONS: Our meta-analysis demonstrated that proinflammatory cytokines IL-1ß, IL-6, and TNF-α were increased, indicating that cytokine profile changed in KC tears and inflammation may play an important role in the pathogenesis and development of KC.

Effects of high-fat diet and Apoe deficiency on retinal structure and function in mice.

To investigate the effects of a high-fat diet (HFD) and apolipoprotein E (Apoe) deficiency on retinal structure and function in mice. Apoe KO mice and wild-type C57BL/6J mice were given a low-fat diet (LFD) or a HFD for 32 weeks. Blood glucose, serum lipids, body weight and visceral fat weight were evaluated. Retinal sterol quantification was carried out by isotope dilution gas chromatography-mass spectrometry. The cholesterol metabolism related genes SCAP-SREBP expressions were detected by qRT-PCR. Retinal function was recorded using an electroretinogram. The thickness of each layer of the retina was measured by optical coherence tomography. Fundus fluorescein angiography was performed to detect retinal vasculature changes. Immunohistochemical staining was used to determine the expression of NF-κB, TNF-α and VEGFR2 in the retina among HFD, HFD Apoe-/-, LFD Apoe-/- and WT mice retinas. HFD feeding caused the mice to gain weight and develop hypercholesterinemia, while Apoe-/- abnormalities also affected blood lipid metabolism. Both HFD and Apoe deficiency elevated retinal cholesterol, especially in the HFD Apoe-/- mice. No up-regulated expression of SCAP-SREBP was observed as a negative regulator. Impaired retinal functions, thinning retinas and abnormal retinal vasculature were observed in the peripheral retinas of the HFD and Apoe-/- mice compared with those in the normal chow group, particularly in the HFD Apoe-/- mice. Moreover, the expression of NF-κB in the retinas of the HFD and Apoe-/- mice was increased, together with upregulated TNF-α mRNA levels and TNF-α expression in the layer of retinal ganglion cells of the peripheral retina. At the same time, the expression level of VEGFR2 was elevated in the intervention groups, most notably in HFD Apoe-/- mice. HFD or Apoe gene deletion had certain adverse effects on retinal function and structure, which were far below the combined factors and induced harm to the retina. Furthermore, HFD caused retinal ischemia and hypoxia. Additionally, Apoe abnormality increased susceptibility to ischemia. These changes upregulated NF-κB expression in ganglion cells and activated downstream TNF-α. Simultaneously, they activated VEGFR2, accelerating angiogenesis and vascular permeability. All of the aforementioned outcomes initiated inflammatory responses to trigger ganglion cell apoptosis and aggravate retinal neovascularization.