Extensive removal of thallium by graphene oxide functionalized with aza-crown ether

Thallium (Tl) is a highly toxic heavy metal, and its pollution and remediation in aquatic environments has attracted considerable attention. To reduce or remove Tl pollution in the environment, various strategies have been applied. Graphene oxide (GO) has abundant oxygen-containing functional groups, indicating its high application potential for pollution remediation via methods involving binding to metal ions or positively charged organic molecules or electrostatic interaction and coordination. However, the adsorption of Tl to GO occurs via physical adsorption, for which the adsorption efficiency is low. Therefore, herein, we report a new method to effectively remove Tl pollution in water. We combined GO with aza-crown ether, which enhanced the electronegativity and ability to bind metal ions. The functionalized graphene oxide (FGO) demonstrated high efficiency through a wide pH gradient of 5–10, with a dominant Tl(i) adsorption capacity (112.21 mg g⁻¹) based on the Langmuir model (pH 9.0, adsorbent concentration of 0.8 g L⁻¹). The adsorption of Tl(i) during removal fit a pseudo-second-order kinetic model well. The mechanisms of Tl removal involve physical and chemical adsorption. In summary, our study provides a new method for the detection and treatment of Tl-containing wastewater by using FGO.

Thallium (Tl) is a highly toxic heavy metal, and its pollution and remediation in aquatic environments has attracted considerable attention.     

Electrochemical performance of activated carbon fiber with hydrogen bond-induced high sulfur/nitrogen doping

The sulfur/nitrogen co-doped activated carbon fiber (S/N-ACF) is prepared by the thermal treatment of thiourea-bonded hydroxyl-rich carbon fiber, which can bond the decomposition products of thiourea through hydrogen bond interaction to avoid the significant loss of sulfur and nitrogen sources during the thermal treatment process. The sulfur/nitrogen co-doped carbon fiber (S/N-CF) is prepared by the thermal treatment of thiourea-adsorbed carbon fiber. The doping degree of the carbon fiber is improved by reasonable strategy. S/N-ACF shows a higher amount of S/N doping (4.56 at% N and 3.16 at% S) than S/N-CF (1.25 at% N and 0.61 at% S). S/N-ACF with high S/N doping level involves highly active sites to improve the capacitive performance, and high delocalization electron to improve the conductivity and rate capability when compared with the normal S/N co-doped carbon fiber (S/N-CF). Accordingly, the specific capacitance increases from 1196 mF cm⁻² for S/N-CF to 2704 mF cm⁻² for S/N-ACF at 1 mA cm⁻². The all-solid-state flexible S/N-ACF supercapacitor achieves 184.7 μW h cm⁻² at 350 μW cm⁻². The results suggest that S/N-ACF has potential application as a CF-based supercapacitor electrode material.

Sulfur/nitrogen co-doped activated carbon fiber is prepared by thermal treatment of thiourea-bonded hydroxyl-rich carbon fiber, which achieves high doping level and electrochemical performance.     

Micron-sized SiOx/N-doped carbon composite spheres fabricated with biomass chitosan for high-performance lithium-ion battery anodes

To achieve superior lithium storage performance, SiO_x is usually designed into nanostructured SiO_x/C composites by complex or expensive methods. Here, micron-sized interconnected SiO_x/N-doped carbon (NC) microspheres composed of evenly dispersed SiO_x nano-domains and NC have been fabricated by a scalable microemulsion method and following pyrolysis, using vinyltriethoxysilane and chitosan as precursors. The unique structure of the micron-sized SiO_x/NC spheres leads to enhanced structural integrity and enables stable long-term cycling (800 cycles at 2 A g⁻¹). Benefiting from the enhanced electron/Li⁺ diffusion kinetics originated from the unique structure and N-doping, SiO_x/NC-2 presents considerable capacitive-controlled Li storage capacity, which leads to outstanding rate capability. Consequently, the assembled SiO_x/NC-2//LiFePO₄ full cell exhibits superior rate capability (106 mA h g⁻¹ at 4C) and stable long-term cycling at 2C (102 mA h g⁻¹ after 350 cycles). This work opens a new door for the application of chitosan in building micron-sized high-performance SiO_x/C anode materials, and to some extent facilitates the recycling of waste seafood shells.

Chitosan is employed as a carbon precursor to fabricate micron-scale interconnected SiO_x/NC spheres that exhibit excellent lithium storage performance.     

Hyperbaric oxygen treatment mitigates liver damage in mice with noise exposure

Noise exposure relates to various pathological disorders including liver damage, preventive measures of which are being demanded. Hyperbaric oxygen treatment (HBOT), as a non-invasive procedure, exerts convincing therapeutic potency on multiple liver diseases. The efficacy of HBOT in mitigating noise induced liver damage (NILD) and associated mechanisms would be elucidated here. Mice were subject to broad band noise (20–20k Hz, 90–110 dB) for 5 days by 3 hours/day. HBOT with 2.5 atmosphere absolute (ata) was employed before noise exposure. Morphology of liver tissue was examined by hematoxylin-eosin (HE) staining. Oil Red O (ORO), transferase-mediated dUTP nick end labelling (TUNEL) test and western blot were utilized to detect lipid accumulation, apoptotic cells and protein expression, respectively. Ceramide (Cer) level was assayed by immunohistochemistry (IHC) analysis. With noise exposure, conspicuous structural derangement and lipid deposition occurred in liver tissue of mice, which was alleviated significantly by the application of HBOT. Meanwhile, HBOT reduced the proportion of apoptotic hepatocytes, restraining the superoxide production in noise exposed mice. In view of underlying mechanisms, noise enhanced the acid sphingomyelinase (ASM) protein expression and the Cer generation in liver tissue of mice which was reversed substantially by HBOT. Altogether, HBOT ameliorates the structural and functional derangement of liver by neutralizing the ASM/Cer pathway in noise exposed mice.     

Intraocular tumour necrosis factor ligand related molecule 1 A links disease progression of proliferative diabetic retinopathy after primary vitrectomy

Tumour necrosis factor ligand related molecule 1 A (TL1A), a member of tumour necrosis factor superfamily, has been identified as a crucial regulator for vascular homeostasis and inflammation. However, the function of TL1A in diabetic retinopathy (DR) is largely unknown. This study aims to examine levels of TL1A in serum and intraocular fluid in patients with proliferative diabetic retinopathy (PDR), and to explore the correlation of intraocular TL1A with the prognosis of PDR progression after primary vitrectomy. Seventy-five patients (75 eyes) with PDR who underwent pars plana vitrectomy (PPV) and 19 patients (19 eyes) who received vitrectomy for idiopathic macular holes (IMH) as non-diabetic control group were enrolled in this prospective study. Serum, aqueous and vitreous fluid samples were collected during cataract and PPV surgery. Protein expressions of TL1A as well as other angiogenic and inflammatory cytokines in serum and intraocular fluid were measured. Correlations of intraocular TL1A concentrations with inflammatory cytokines were analyzed. We found both aqueous and vitreous TL1A levels were significantly higher in the PDR group than in control group (P_aqueous = 0.026; P_vitreous <0.001). Angiogenic and inflammatory cytokines such as VEGF, IL-6, IL-8, MCP-1, MIP-1α, and MIP-1β were significantly higher in intraocular fluid in PDR group than in controls, which MCP-1 and MIP-1α showed positive correlation with intraocular TL1A levels. There is no significant difference in the levels of serum TL1A as well as other inflammatory cytokines between PDR patients and controls. Intraocular levels of TL1A were significantly lower in PDR progression group than in the stable group (P_aqueous <0.001; P_vitreous <0.001). Multivariate logistic regression analyses revealed that lower levels of intraocular TL1A was an important risk factor for predicting PDR progression after primary PPV (OR_aqueous = 0.717, P_aqueous = 0.001; OR_vitreous = 0.684; P_vitreous = 0.002). In conclusion, TL1A and multiple inflammatory cytokines were highly enriched in the intraocular fluid of PDR patients compared with the controls. Lower levels of intraocular TL1A were associated with development of PDR complications after primary PPV and might be used as prognostic factor in predicting the vitrectomy outcome in PDR patients.     

Tryptophan 387 and 390 residues in ADAMTS13 are crucial to the ability of vascular tube formation and cell migration of endothelial cells

A disintegrin and metalloproteinase with thrombospondin motifs 13 (ADAMTS13) was mainly generated and secreted from endothelial cells (ECs). Our previous study showed that tryptophan (Trp) residues at 387 and 390 in ADAMTS13 are required for its secretion and enzymatic activity. However, the effects on its host cell as well as the potential mechanism have not been clear. The aim of the study was to examine the effects of Trp residues 387 and 390 of ADAMTS13 on the biological processes of ECs. Herein, Trp was substituted with alanine in ADAMTS13 to generate ADAMTS13 mutants at 387 (W387A), 390 (W390A), and double mutants at 387 and 390 (2WA), respectively. We found that substitution mutation impaired vascular endothelial growth factor (VEGF) secretion and the downstream JAK1/STAT3 activation, the binding ability to Von Willebrand factor, cell proliferation, migration, and vascular tube formation. Overall, our study concluded that Trp³⁸⁷ and Trp³⁹⁰ of ADAMTS13 play vital roles in the biological function of ECs.     

131I治疗分化型甲状腺癌颈部摄碘组织的吸收剂量与疗效分析

目的 评估分化型甲状腺癌（DTC）术后行131I治疗后,甲状腺残余灶、DTC转移灶内照射的吸收剂量与治疗反应的关系。 方法 收集2017年2月至9月中山大学附属第三医院核医学科22例DTC术后行131I治疗的患者,其中男性10例、女性12例,年龄21~59岁,中位年龄39.5岁。在患者服药后多个时间点行131I全身平面显像及局部SPECT/CT显像,测算甲状腺残余灶、DTC转移灶的吸收剂量及患者的平均吸收剂量。按照《2015美国甲状腺协会成人甲状腺结节与分化型甲状腺癌指南》评估患者的治疗后反应。使用Mann-Whitney U检验评估残余灶与转移灶在不同疗效及分组之间的吸收剂量差异,受试者工作特征（ROC）曲线评估吸收剂量预测治疗效果的性能。 结果 100%（28/28）的甲状腺残余灶及34.8%（8/23）的DTC转移灶为完全反应。完全反应的DTC转移灶吸收剂量（M=79.3 Gy）高于未完全反应（M=29.8 Gy）的转移灶（Z=?2.195,P=0.028）。ROC曲线分析提示,DTC转移灶的吸收剂量可用于预测病灶行131I治疗后的疗效反应,曲线下面积达0.783（Z=?2.195,P=0.028）,预测病灶达完全反应的截止值为70.6 Gy。患者平均吸收剂量可预测治疗后病情的缓解状况,曲线下面积达0.823（Z=?2.285,P=0.022）。 结论 DTC转移灶的吸收剂量需要达到足量才可达到治疗完全反应。摄碘组织的吸收剂量与患者平均吸收剂量均可作为碘治疗后治疗反应的预测指标。