It is vital to understand the adsorption mechanisms and identify the adsorption kinetics when applying an adsorbent to remove heavy metals from aqueous solution. A Pb(II) imprinted magnetic biosorbent (Pb(II)-IMB) was developed for the removal of Pb 2+ via lead ion imprinting technology and crosslinking reactions among chitosan (CTS), Serratia marcescens and Fe 3 O 4 . The effect of different parameters such as solution pH, adsorbent dosage, selectivity sorption and desorption were investigated on the absorption of lead ion by Pb(II)-IMB. The adsorbent was characterized by a Brunauer-Emmett Teller (BET) analysis, X-ray diffraction (XRD), vibrating sample magnetometry (VSM), scanning electron microscopy (SEM) and energy dispersive spectrometry (EDS). The adsorption kinetics, equilibrium and thermodynamics of Pb(II)-IMB for Pb(II) were studied. The results of the abovementioned analyses showed that the adsorption kinetic process fit well with the second-order equation. The adsorption isotherm process of Pb(II) on the Pb(II)-IMB was closely related to the Langmuir model. Thermodynamic studies suggested the spontaneous and endothermic nature of adsorption of Pb(II) by Pb(II)-IMB. The adsorption mechanism of Pb(II)-IMB was studied by Fourier transform infrared spectroscopy (FTIR) and X-ray photoelectron spectroscopy (XPS). The results indicated that the nitrogen in the amino group and the oxygen in the hydroxyl group of Pb(II)-IMB were coordination atoms.

To study the effect of Huangzhi oral liquid (HZOL) on I/R after 2 h and 4 h and determine its regulatory function on caspase-3 and protein networks. 70 SD male rats were randomly divided into seven groups and established myocardial I/R injury model by ligating the left anterior descending coronary artery. Myocardial infarction model was defined by TTC staining and color of the heart. The levels of CK-MB, CTnI, C-RPL, SOD, and MDA were tested at 2 h and 4 h after reperfusion. HE staining and ultramicrostructural were used to observe the pathological changes. The apoptotic index (AI) of cardiomyocyte was marked by TUNEL. The expression levels of caspase-3, p53, fas, Bcl-2, and Bax were tested by immunohistochemistry and western blot. HZOL corrected arrhythmia, improved the pathologic abnormalities, decreased CK-MB, CTnI, C-RPL, MDA, AI, caspase-3, p53, fas, and Bax, and increased SOD ans Bcl-2 with different times of myocardial reperfusion; this result was similar to the ISMOC (P > 0.05). HZOL could inhibit arrhythmia at 2 and 4 h after I/R and ameliorate cardiac function, which was more significant at 4 h after reperfusion. This result may be related to decreased expression of caspase-3, p53, and fas and increased Bcl-2/Bax ratio.

Desert terrains in northern China are covered by widespread regolith sediments which mask geochemical signals from ore bodies and are major obstacles to mineral exploration. There is a critical need to study the vertical distribution of elements in the regolith, and to determine potential mechanisms for transferring elements from the ore body upwards through regolith cover to the surface, and to establish appropriate sampling media and analytical methods. The Jinwozi gold deposit, which is covered by four to several tens of metres of regolith sediment, was selected for this study. Samples were taken from different regolith horizons in two vertical profiles over the deposit. Gold and associated elements showed crescent-shaped distribution patterns in the vertical profile, i.e. elements tend to be enriched in lower and upper parts of the profile over the ore body. Enrichment of elements in weathered rocks is derived from the ore body, whereas enrichment at or near surface is due to adsorption by clays or oxide coatings. For gold, the greatest contrast between anomalous and background concentration is in the fine fraction of soils, and the Au anomalies are located directly over the ore body. Gold appears to migrate vertically to the surface to be trapped in clays and oxide coatings to produce superimposed anomalies in the regolith near or at the surface. Fine fraction samples (−120 mesh; 125 μm) from clay-rich horizons or selective leaching of elements adsorbed on clays or oxide coatings are effective for locating buried deposits.

Liver injury after experimental acetaminophen treatment is mediated both by direct hepatocyte injury through a P450-generated toxic metabolite and indirectly by activated liver Kupffer cells and neutrophils. This study was designed to investigate the role of Notch signaling in the regulation of innate immune responses in acetaminophen (APAP)-induced liver injury. Using a mouse model of APAP-induced liver injury, wild-type (WT) and toll-like receptor 4 knockout (TLR4 KO) mice were injected intraperitoneally with APAP or PBS. Some animals were injected with γ-secretase inhibitor DAPT or DMSO vehicle. For the in vitro study, bone marrow-derived macrophages (BMMs) were transfected with Notch1 siRNA, TLR4 siRNA, and non-specific (NS) siRNA and stimulated with LPS. Indeed, paracetamol/acetaminophen-induced liver damage was worse after Notch blockade with DAPT in wild-type mice, which was accompanied by significantly increased ALT levels, diminished hairy and enhancer of split-1 (Hes1), phosphorylated Stat3 and Akt but enhanced high mobility group box 1 (HMGB1), TLR4, NF-κB, and NLRP3 activation after APAP challenge. Mice receiving DAPT increased macrophage and neutrophil accumulation and hepatocellular apoptosis. However, TLR4 KO mice received DAPT reduced APAP-induced liver damage, NF-κB, NLRP3, and cleaved caspase-1 activation. BMMs transfected with Notch1 siRNA reduced Hes1, phosphorylated Stat3 and Akt but augmented HMGB1, TLR4, NF-κB, and NLRP3. Furthermore, TLR4 siRNA knockdown resulted in decreased NF-κB, NLRP3, cleaved caspase-1, and IL-1β levels following LPS stimulation. These results demonstrate that Notch signaling regulates innate NLRP3 inflammasome activation through regulation of HMGB1/TLR4/NF-κB activation in APAP-induced liver injury. Our novel findings underscore the critical role of the Notch1-Hes1 signaling cascade in the regulation of innate immunity in APAP-triggered liver inflammation. This might imply a novel therapeutic potential for the drug-induced damage-associated lethal hepatitis.