Characterization of Selenite Reduction by <i>Lysinibacillus</i> sp. ZYM‑1 and Photocatalytic Performance of Biogenic Selenium Nanospheres

This study comprehensively investigated the feasibility of biogenic selenium nanomaterials (Se NMs) as a photocatalyst in dye degradation. The marine selenite-reducing bacterium Lysinibacillus sp. ZYM-1 was isolated. This strain can reduce selenite to Se NMs over a wide range of pH (5–9), selenite concentration (1–25 mM), and temperature (20–50 °C) within 48 h. Draft genome data suggested that sulfite reductase may be responsible for selenite reduction. Biogenic Se NMs generated under different conditions were subsequently characterized. The morphology and size of Se NMs were dependent on medium composition, pH, incubation time, selenite concentration, and temperature. Se nanospheres (Se NSs) exhibited significant visible light-driven photocatalytic activity on Rhodamine B (RhB) with H₂O₂. Three N-deethylation intermediates and phthalic acid were identified as degradation products of RhB by using liquid chromatography-high resolution mass spectrometry (LC-HRMS), indicating the coexistence of chromophore cleavage and the N-deethylation pathway

Bacteria-Mediated Ultrathin Bi₂Se₃ Nanosheets Fabrication and Their Application in Photothermal Cancer Therapy

Bismuth selenide (Bi₂Se₃) attracts a lot of attention nowadays due to its unique electronic and thermoelectric properties. In this study, fabrication of Bi₂Se₃ nanosheets by selenite-reducing bacterium (SeRB) was first reported. Morphology, size, and location of the biogenic Bi₂Se₃ are bacteria-dependent. It is difficult to separate Bi₂Se₃ generated by <i>Bacillus cereus</i> CC-1 (Bi₂Se₃-C) from the biomass because of strong interaction with the cell membrane. However, Bi₂Se₃ produced by <i>Lysinibacillus</i> sp. ZYM-1 (Bi₂Se₃-Z), is highly dispersed in extracellular space with high stability. Further characterization by X-ray diffraction (XRD), scanning electron microscopy (SEM), transmission electron microscopy (TEM), and atomic force microscopy (AFM) on Bi₂Se₃-Z indicates that the product is a rhombohedral-phase, ultrathin nanosheet-like structure with an average size of ∼100 nm. Subsequently, the photothermal performance of Bi₂Se₃-Z with the irradiation of 808 nm near-infrared (NIR) laser was determined. When the Bi₂Se₃-Z concentration was 26 mg L^–1, and irradiation power was 2 W, the photothermal conversion efficiency was calculated as 30.7%. At the same condition, 100% of the MCF7 and A549 cancer cells were killed within 10 min of irradiation in vitro. Moreover, using 1% (v/v) PVP as surfactant, a novel nanodumbbell structure of Bi₂Se₃ was obtained. Overall, this bacteria-driven Bi₂Se₃ fabrication paves a new way for biocompatible photothermal nanomaterials

Table1_Calycosin attenuates renal ischemia/reperfusion injury by suppressing NF-κB mediated inflammation via PPARγ/EGR1 pathway.DOCX

Renal ischemia reperfusion injury (IRI) is a leading and common cause of acute kidney injury (AKI), and inflammation is a critical factor in ischemic AKI progression. Calycosin (CAL), a major active component of Radix astragali, has been reported to have anti-inflammatory effect in multiple organs. However, whether CAL can alleviate renal IRI and its mechanism remain uncertain. In the present study, a renal IRI model is established by bilateral renal pedicles occlusion for 35 min in male C57BL/6 mice, and the effect of CAL on renal IRI is measured by serum creatinine and pathohistological assay. Hypoxia/reoxygenation (H/R) stimulated human renal tubular epithelial cells HK-2 were applied to explore the regulatory mechanisms of CAL. Luciferase reporter assay and molecular docking were applied to identify the CAL’s target protein and pathway. In the mice with renal IRI, CAL dose dependently alleviated the renal injury and decreased nuclear factor kappa B (NF-κB) mediated inflammatory response. Bioinformatics analysis and experiments showed that early growth response 1 (EGR1) increased in mice with renal IRI and promoted NF-κB mediated inflammatory processes, and CAL dose-dependably reduced EGR1. Through JASPAR database and luciferase reporter assay, peroxisome proliferator-activated receptor γ (PPARγ) was predicted to be a transcription factor of EGR1 and repressed the expression of EGR1 in renal tubular epithelial cells. CAL could increase PPARγ in a dose dependent manner in mice with renal IRI and molecular docking predicted CAL could bind stably to PPARγ. In HK-2 cells after H/R, CAL increased PPARγ, decreased EGR1, and inhibited NF-κB mediated inflammatory response. However, PPARγ knockdown by siRNA transfection abrogated the anti-inflammation therapeutic effect of CAL. CAL produced a protective effect on renal IRI by attenuating NF-κB mediated inflammatory response via PPARγ/EGR1 pathway.</p

Kaplan-Meier analysis of peak CPO and peak VO_2:Curve 1(group B):

<p>peak VO₂≤ 13.4 ml.kg^-1.min^-1 but peak CPO > 1.1 W; Curve 2(group A): peak VO₂≤ 13.4 ml.kg^-1.min^-1 but peak CPO ≤ 1.1W. Log-Rank: 3.875, <i>P</i> = 0.04. By Kaplan Meier analysis, the patients with a peak VO₂≤13.4 ml.kg^-1.min^-1 those with peak CPO>1.1W had better survival than those with peak CPO ≤ 1.1 W (Log-Rank: 3.875, <i>P</i> = 0.04).</p

ROC analysis of peak VO₂, Peak CPO(Left panel: peak CPO; Right panel: peak VO₂).

<p>The area under ROC Curve of peak CPO for predicting cardiac-related deaths was 0.68 (<i>Ρ</i><0.05), and the sensitivity and specificity were 0.713 and 0.650 respectively, which is significantly more sensitive than peak VO₂ (the sensitivity was 0.590 and the specificity was 0.667). The optimal threshold of peak CPO for predicting cardiac-related deaths was≤ 1.1W and the optimal threshold of peak VO₂ for predicting cardiac-related deaths was ≤13.4 ml.kg^-1.min^-1 in Chinese CHF patients.</p