Mitochondrial quality control protects photoreceptors against oxidative stress in the H2O2-induced models of retinal degeneration diseases

Retinal degeneration diseases (RDDs) are common and devastating eye diseases characterized by the degeneration of photoreceptors, which are highly associated with oxidative stress. Previous studies reported that mitochondrial dysfunction is associated with various neurodegenerative diseases. However, the role of mitochondrial proteostasis mainly regulated by mitophagy and mitochondrial unfolded protein response (mtUPR) in RDDs is unclear. We hypothesized that the mitochondrial proteostasis is neuroprotective against oxidative injury in RDDs. In this study, the data from our hydrogen peroxide (H₂O₂)-treated mouse retinal cone cell line (661w) model of RDDs showed that nicotinamide riboside (NR)-activated mitophagy increased the expression of LC3B II and PINK1, and promoted the co-localization of LC3 and mitochondria, as well as PINK1 and Parkin in the H₂O₂-treated 661w cells. However, the NR-induced mitophagy was remarkably reversed by chloroquine (CQ) and cyclosporine A (CsA), mitophagic inhibitors. In addition, doxycycline (DOX), an inducer of mtUPR, up-regulated the expression of HSP60 and CHOP, the key proteins of mtUPR. Activation of both mitophagy and mtUPR increased the cell viability and reduced the level of apoptosis and oxidative damage in the H₂O₂-treated 661w cells. Furthermore, both mitophagy and mtUPR played a protective effect on mitochondria by increasing mitochondrial membrane potential and maintaining mitochondrial mass. By contrast, the inhibition of mitophagy by CQ or CsA reversed the beneficial effect of mitophagy in the H₂O₂-treated 661w cells. Together, our study suggests that the mitophagy and mtUPR pathways may serve as new therapeutic targets to delay the progression of RDDs through enhancing mitochondrial proteostasis.Subject terms: Cell death, Diseases     

Hydrolyzed polyacrylamide biotransformation in an up-flow anaerobic sludge blanket reactor system: key enzymes,functional microorganisms,and biodegradation mechanisms

Hydrolyzed polyacrylamide (HPAM) biotransformation in an up-flow anaerobic sludge blanket reactor including biodegradation performances, biodegradation mechanisms, key enzymes, and functional microorganisms was explored. Response surface methodology was applied to further improve HPAM degradation. The predicted degradation ratios of HPAM and COD_Cr were 46.2% and 83.4% under the optimal conditions. HPAM biodegradation ratio and total organic carbon removal ratio reached 40.5% and 38.9%. Total nitrogen concentration was dramatically decreased with the increasing fermentation time during the fermentation, while low ammonia nitrogen (NH₄⁺–N) and nitrite nitrogen (NO₂⁻–N) were generated. NH₄⁺–N and NO₂⁻–N increased slightly on the whole. Enzyme activity change was correlated with HPAM biodegradation. Dehydrogenase activity had a decline of 21.3–41.0%, and the minimum value occurred at 300 mg/L of HPAM. Urease activity was varied from 28.7 to 78.7% and the maximal inhibition ratio occurred at 200 mg/L of HPAM. Mechanisms for the biodegradation of HPAM were also explored by FT-IR, HPLC, and SEM. The results indicated that long-chain HPAM was broken into micromolecule compounds and the amide groups of HPAM were transformed into carboxyl groups. Based on the sequencing results on an Illumina MiSeq platform, Proteobacterias, Bacteroidetes, and Chloroflexi were turned out to be the critical microorganisms involved in HPAM degradation. This work lays a basis for HPAM-containing wastewater treatment and offers a support for water saving and emission reduction. It is of great significance to the sustainable development of oilfield.

     

Graphene-MoS2 Hybrid Structure Enhanced Fiber Optic Surface Plasmon Resonance Sensor

Plasmonics - In this paper, a fiber optic surface plasmon resonance sensor based on graphene-MoS2 hybrid structure is presented. The wavelength interrogation method is employed to analyze the...     

PACS和远程放射系统的发展和联系

本文综述了PACS和远程放射系统的构成及其关键技术,阐述了它们的联系和区别,以及两者目前集成情况,并对两者可能的集成模型进行了探讨。     

Cook Your Samples: The Application of Microwave Irradiation in Speeding Up Biological Processes

Classic and conventional procedures in molecular cloning are inherent compositions in modern molecular biological experiments and are frequently involved in daily laboratory activities. They take up the majority of the total time input in spite of the availability of well-designed specialized commercial kits. A similar situation is also in the field of biotechnology. Fortunately, microwave/ultrasonic irradiation has been found to be capable of speeding up these processes, such as proteolysis in sample preparation for proteomics research, and digestion, ligation, (de)phosphorylation of DNA with the corresponding enzymes, even the introduction of DNA samples to recipient cells, and biotransformation (e.g., the production of biodiesel). Microwave/ultrasonic irradiation, when used solely or in combination with other existing operations, makes it possible to finish these time-consuming processes in as short as 1 min with comparable or even improved efficiency, and there is no need of reagent upgradation. The adoption of irradiation is ideal because it eliminates any possible side effects of the chemicals used as performance enhancer(s) that will inevitably make the system more complicated at least. More notably, the needed irradiation in the laboratory can be generated by a common microwave oven or ultrasonic cleaner. Taken together, microwave/ultrasonic irradiation provides an accessible method to make the procedures mentioned above time- and cost- efficient. In this article, we reviewed the relevant literature and discussed the experiment and mechanism details.     

Degradation Mechanism and Enhancing Strategies of Oxygen Reduction Reaction Catalyzed by Carbon-Based Metal Free Catalysts in Acidic Solution

Carbon-based metal free catalysts (CMFCs) are far away from commercial availability mainly attributed to their poor oxygen reduction reaction (ORR) performance in acidic environment with the causes remaining obscure. By investigating the heteroatoms (N, B, P, S, Se, and Te)-doped reduced graphene oxides, the degradation mechanism of acidic ORR performance of CMFCs is found to be correlated with the oxygen-baring defects in the carbon sp² lattice, which exhibit overpotentials as low as 0.44 V but weak trapping capabilities for oxygen molecules. These findings not only revise the previously reported strategy of modeling the active sites in the basal plane of CMFCs but also highlight the connections between those active sites and the triple-coordinated VIA group elements (XC₃). Further calculations demonstrate that the XC₃ dimer can efficiently enhance the acidic ORR performance and the 2D trigonal carbon-chalcogenides C₆X (X = S, Se, and Te) are accordingly designed toward acidic ORR, which contain homogeneously distributed basal plane active sites and exhibit low overpotentials but strong trapping capabilities for oxygen molecules. This work will help to cease the debates on the active sites in CMFCs for ORR in both acidic and alkaline solutions and to open a new avenue to design CMFCs independent on doping strategy.     

The HIV core protein p24 inhibits interferon-gamma-induced increase of HLA-DR and cytochrome b heavy chain mRNA levels in the human monocyte-like cell line THP1

Cells from the human monocytic cell-line THP1 were incubated prior to activation with IFN-gamma or LPS with varying amounts of p24, the main product of the HIV gag gene and the major component of the virus core. The IFN-gamma-dependent increase of mRNA for HLA-DR and for the heavy chain of cytochrome b was markedly decreased by p24 but not by gp120. This effect was abrogated by anti-p24 antibodies. On the other hand, preincubation of THP1 cells with p24 did not affect the accumulation of the LPS-dependent mRNA for TNF alpha and IL1-beta. These results indicate that p24 at concentrations similar to those found in the serum of HIV-infected individuals specifically affects IFN-gamma-induced activation markers.