Graphene Modified TiO2 Composite Photocatalysts: Mechanism, Progress and Perspective

Graphene modified TiO2 composite photocatalysts have drawn increasing attention because of their high performance. Some significant advancements have been achieved with the continuous research, such as the corresponding photocatalytic mechanism that has been revealed. Specific influencing factors have been discovered and potential optimizing methods are proposed. The latest developments in graphene assisted TiO2 composite photocatalysts are abstracted and discussed. Based on the primary reasons behind the observed phenomena of these composite photocatalysts, probable development directions and further optimizing strategies are presented. Moreover, several novel detective technologies—beyond the decomposition test—which can be used to judge the photocatalytic performances of the resulting photocatalysts are listed and analyzed. Although some objectives have been achieved, new challenges still exist and hinder the widespread application of graphene-TiO2 composite photocatalysts, which deserves further study

Effects of soil factors on dimethyl disulfide desorption and the risk of phytotoxicity to newly-planted seedlings

Dimethyl disulfide (DMDS) is a relatively new soil fumigant used in agro-industrial crop production to control soil-borne pests that damage crops and reduce yield. The emissions of DMDS after fumigation reduce soil concentrations thus reducing the risk of phytotoxicity to newly planted crops. However, the factors affecting the desorption of DMDS from soil are unclear. In our study, the desorption characteristics of DMDS from soil were measured in response to continuous ventilation. The degradation of DMDS in soil was examined by thermal incubation. The phytotoxic response of newly-planted cucumber (Cucumis sativus) seedlings to DMDS residues was measured by a sand culture experiment. The results showed DMDS desorption and degradation rates fit a first-order model; that 92% of the DMDS desorption occurred in the first hour after fumigant application; and that residue concentrations in the soil at the end of the ventilation period were unlikely to be phytotoxic to newly-planted cucumber seedlings. By the third day of ventilation, the average desorption rate (ADR) of DMDS in Wenshan soil was 4.0 and 3.6 times, respectively, faster than that in Shunyi and Suihua soils and the ADR of DMDS in soil decreased by 40.0% when the soil moisture content increased from 3% to 12% (wt/wt). Moreover, within one hour of ventilation, the ADR of DMDS in soil decreased by 20.1% when the soil bulk density increased from 1.1 to 1.3 g cm-3. The degradation of DMDS in soil, however, was mostly influenced by soil type and moisture content. A slow degradation rate resulted in a high initial desorption concentration of DMDS in soil. Our results indicated that DMDS desorption from soil in response to continuous ventilation was affected by the soil type, moisture content and bulk density. Rapid degradation of DMDS in soil will lower the risk of phytotoxic residues remaining in the soil and reduce emissions during the waiting period. Acceleration of emissions early in the waiting period by managing soil moisture content or increasing soil porosity may shorten the duration of emissions. Alternatively, soil extraction technology could be developed to recover and reduce fumigant emissions

Scalable Green Method to Fabricate Magnetically Separable NiFe₂O₄‑Reduced Graphene Oxide Nanocomposites with Enhanced Photocatalytic Performance Driven by Visible Light

A reduced graphene oxide (RGO)-supported nickel ferrite (NiFe₂O₄) photocatalyst was prepared by a simple mechanical ball-milling method. No additional solvents, toxic chemical reductants, or ultrasonic or high-temperature heat treatments were needed. The exfoliation and reduction of graphite oxide (GO) and the <i>in situ</i> anchoring of NiFe₂O₄ nanoparticles on graphene sheets were fulfilled simultaneously under the strong shear force. The structure characterization shows that the NiFe₂O₄ nanoparticles were uniformly dispersed on RGO sheets. Amazingly, after coupling with an appropriate amount of RGO, the photocatalytically inert NiFe₂O₄ exhibited superior photodegradation performance and recycling stability for the degradation of organic pollutant under visible-light irradiation at room temperature. It suggested that the synergistic effect between RGO and NiFe₂O₄ improved the photocatalytic performance of the composite. Moreover, the NiFe₂O₄-RGO is magnetically separable for recycling. Hopefully, this work could shed light on the environment-friendly large-scale production of graphene-based composites through the efficient ball-milling method

Chemoselective Peptide Modification via Photocatalytic Tryptophan β‑Position Conjugation

Targeting tryptophan is a promising strategy to achieve high levels of selectivity for peptide or protein modification. A chemoselective peptide modification method via photocatalytic tryptophan β-position conjugation has been discovered. This transformation has good substrate scope for both peptide and Michael acceptor, and has good chemoselectivity versus other amino acid residues. The endogenous peptides, glucagon and GLP-1 amide, were both successfully conjugated at the tryptophan β-position. Insulin was studied as a nontryptophan control molecule, resulting in exclusive B-chain C-terminal-selective decarboxylative conjugation. This transformation provides a novel approach toward peptide modification to support the discovery of new therapeutic peptides, protein labeling and bioconjugation

Histone deacetylase (HDAC) inhibitors targeting HDAC3 and HDAC1 ameliorate polyglutamine-elicited phenotypes in model systems of Huntington's disease.

We have previously demonstrated amelioration of Huntington's disease (HD)-related phenotypes in R6/2 transgenic mice in response to treatment with the novel histone deacetylase (HDAC) inhibitor 4b. Here we have measured the selectivity profiles of 4b and related compounds against class I and class II HDACs and have tested their ability to restore altered expression of genes related to HD pathology in mice and to rescue disease effects in cell culture and Drosophila models of HD. R6/2 transgenic and wild-type (wt) mice received daily injections of HDAC inhibitors for 3 days followed by real-time PCR analysis to detect expression differences for 13 HD-related genes. We find that HDACi 4b and 136, two compounds showing high potency for inhibiting HDAC3 were most effective in reversing the expression of genes relevant to HD, including Ppp1r1b, which encodes DARPP-32, a marker for medium spiny striatal neurons. In contrast, compounds targeting HDAC1 were less effective at correcting gene expression abnormalities in R6/2 transgenic mice, but did cause significant increases in the expression of selected genes. An additional panel of 4b-related compounds was tested in a Drosophila model of HD and in STHdhQ111 striatal cells to further distinguish HDAC selectivity. Significant improvement in huntingtin-elicited Drosophila eye neurodegeneration in the fly was observed in response to treatment with compounds targeting human HDAC1 and/or HDAC3. In STHdhQ111 striatal cells, the ability of HDAC inhibitors to improve huntingtin-elicited metabolic deficits correlated with the potency at inhibiting HDAC1 and HDAC3, although the IC50 values for HDAC1 inhibition were typically 10-fold higher than for inhibition of HDAC3. Assessment of HDAC protein localization in brain tissue by Western blot analysis revealed accumulation of HDAC1 and HDAC3 in the nucleus of HD transgenic mice compared to wt mice, with a concurrent decrease in cytoplasmic localization, suggesting that these HDACs contribute to a repressive chromatin environment in HD. No differences were detected in the localization of HDAC2, HDAC4 or HDAC7. These results suggest that inhibition of HDACs 1 and 3 can relieve HD-like phenotypes in model systems and that HDAC inhibitors targeting these isotypes might show therapeutic benefit in human HD

Histone deacetylase (HDAC) inhibitors targeting HDAC3 and HDAC1 ameliorate polyglutamine-elicited phenotypes in model systems of Huntington's disease.

We have previously demonstrated amelioration of Huntington's disease (HD)-related phenotypes in R6/2 transgenic mice in response to treatment with the novel histone deacetylase (HDAC) inhibitor 4b. Here we have measured the selectivity profiles of 4b and related compounds against class I and class II HDACs and have tested their ability to restore altered expression of genes related to HD pathology in mice and to rescue disease effects in cell culture and Drosophila models of HD. R6/2 transgenic and wild-type (wt) mice received daily injections of HDAC inhibitors for 3 days followed by real-time PCR analysis to detect expression differences for 13 HD-related genes. We find that HDACi 4b and 136, two compounds showing high potency for inhibiting HDAC3 were most effective in reversing the expression of genes relevant to HD, including Ppp1r1b, which encodes DARPP-32, a marker for medium spiny striatal neurons. In contrast, compounds targeting HDAC1 were less effective at correcting gene expression abnormalities in R6/2 transgenic mice, but did cause significant increases in the expression of selected genes. An additional panel of 4b-related compounds was tested in a Drosophila model of HD and in STHdhQ111 striatal cells to further distinguish HDAC selectivity. Significant improvement in huntingtin-elicited Drosophila eye neurodegeneration in the fly was observed in response to treatment with compounds targeting human HDAC1 and/or HDAC3. In STHdhQ111 striatal cells, the ability of HDAC inhibitors to improve huntingtin-elicited metabolic deficits correlated with the potency at inhibiting HDAC1 and HDAC3, although the IC50 values for HDAC1 inhibition were typically 10-fold higher than for inhibition of HDAC3. Assessment of HDAC protein localization in brain tissue by Western blot analysis revealed accumulation of HDAC1 and HDAC3 in the nucleus of HD transgenic mice compared to wt mice, with a concurrent decrease in cytoplasmic localization, suggesting that these HDACs contribute to a repressive chromatin environment in HD. No differences were detected in the localization of HDAC2, HDAC4 or HDAC7. These results suggest that inhibition of HDACs 1 and 3 can relieve HD-like phenotypes in model systems and that HDAC inhibitors targeting these isotypes might show therapeutic benefit in human HD

The cost of Alzheimer\u27s disease in China and re-estimation of costs worldwide

INTRODUCTION: The socioeconomic costs of Alzheimer\u27s disease (AD) in China and its impact on global economic burden remain uncertain. METHODS: We collected data from 3098 patients with AD in 81 representative centers across China and estimated AD costs for individual patient and total patients in China in 2015. Based on this data, we re-estimated the worldwide costs of AD. RESULTS: The annual socioeconomic cost per patient was US $19,144.36, and total costs were US$167.74 billion in 2015. The annual total costs are predicted to reach US $507.49 billion in 2030 and US$1.89 trillion in 2050. Based on our results, the global estimates of costs for dementia were US $957.56 billion in 2015, and will be US$2.54 trillion in 2030, and US $9.12 trillion in 2050, much more than the predictions by the World Alzheimer Report 2015. DISCUSSION: China bears a heavy burden of AD costs, which greatly change the estimates of AD cost worldwide