No abstract

Cigarette smoking, which exposes the lung to high concentrations of reactive oxidant species (ROS) is the major risk factor for chronic obstructive pulmonary disease (COPD). Recent studies indicate that ROS interfere with protein folding in the endoplasmic reticulum and elicit a compensatory response termed the "unfolded protein response" (UPR). The importance of the UPR lies in its ability to alter expression of a variety of genes involved in antioxidant defense, inflammation, energy metabolism, protein synthesis, apoptosis, and cell cycle regulation. The present study used comparative proteomic technology to test the hypothesis that chronic cigarette smoking induces a UPR in the human lung. Studies were performed on lung tissue samples obtained from three groups of human subjects: nonsmokers, chronic cigarette smokers, and ex-smokers. Proteomes of lung samples from chronic cigarette smokers demonstrated 26 differentially expressed proteins (20 were up-regulated, 5 were down-regulated, and 1 was detected only in the smoking group) compared with nonsmokers. Several UPR proteins were up-regulated in smokers compared with nonsmokers and ex-smokers, including the chaperones, glucose-regulated protein 78 (GRP78) and calreticulin; a foldase, protein disulfide isomerase (PDI); and enzymes involved in antioxidant defense. In cultured human airway epithelial cells, GRP78 and the UPR-regulated basic leucine zipper, transcription factors, ATF4 and Nrf2, which enhance expression of important anti-oxidant genes, increased rapidly (< 24 h) with cigarette smoke extract. These data indicate that cigarette smoke induces a UPR response in the human lung that is rapid in onset, concentration dependent, and at least partially reversible with smoking cessation. We speculate that activation of a UPR by cigarette smoke may protect the lung from oxidant injury and the development of COPD.

In this study, we propose a versatile method for synthesizing uniform three-dimensional (3D) metal carbides, nitrides, and carbonitrides (MXenes)/metal-organic frameworks (MOFs) composites (Ti 3 C 2 T X /Cu-BTC, Ti 3 C 2 T X / Fe,Co-PBA, Ti 3 C 2 T X /ZIF-8, and Ti 3 C 2 T X /ZIF-67) that combine the advantages of MOFs and MXenes to enhance stability and improve conductivity. Subsequently, 3D hollow Ti 3 C 2 T X /ZIF-67/CoV 2 O 6 composites with excellent electronand ion-transport properties derived from Ti 3 C 2 T X /ZIF-67 were synthesized. The specific capacitance of the Ti 3 C 2 T X / ZIF-67/CoV 2 O 6 electrode was 285.5 F g À 1 , which is much higher than that of the ZIF-67 and Ti 3 C 2 T X /ZIF-67 electrode. This study opens a new avenue for the design and synthesis of MXene/MOF composites and complex hollow structures with tailorable structures and compositions for various applications.

Chemical states and electrical properties of a high-k metal oxide/silicon interface with oxygen-gettering titaniummetal-overlayer Appl.We present theoretical and experimental results regarding the thermodynamic stability of the high-k dielectrics ZrO 2 and HfO 2 in contact with Si and SiO 2 . The HfO 2 /Si interface is found to be stable with respect to formation of silicides whereas the ZrO 2 /Si interface is not. The metal-oxide/SiO 2 interface is marginally unstable with respect to formation of silicates. Cross-sectional transmission electron micrographs expose formation of nodules, identified as silicides, across the polycrystalline silicon/ZrO 2 /Si interfaces but not for the interfaces with HfO 2 . For both ZrO 2 and HfO 2 , the x-ray photoemission spectra illustrate formation of silicate-like compounds in the MO 2 /SiO 2 interface.

MXenes have attracted great interests as supercapacitors due to their metallic conductivity, high density, and hydrophilic nature. Herein we report Ti3C2‐Cu/Co hybrids via molten salt etching in which the existence of metal atoms and their interactions with MXene via surficial O atoms were elucidated by XAFS for the first time. The electrochemical investigation of Ti3C2‐Cu electrode demonstrated the pseudocapacitive contribution of Cu and a splendid specific capacitance of 885.0 F g−1 at 0.5 A g−1 in 1.0 M H2SO4. Symmetric supercapacitor Ti3C2‐Cu//Ti3C2‐Cu was demonstrated with operating voltage of 1.6 V, areal capacitance of 290.5 mF cm−2 at 1 mA cm−2, and stability over 10 000 cycles. It delivered an areal energy density of 103.3 μWh cm−2 at power density of 0.8 mW cm−2, based on which a supercapacitor pouch was fabricated. It provides deeper insights into the molten salt mechanism and strategies for designing MXene‐based materials for electrochemical energy storage.

Release of cytochrome c (cyt c) into cytoplasm initiates caspase-mediated apoptosis, whereas activation of Akt kinase by phosphorylation at serine-473 prevents apoptosis in several cell systems. To investigate cell death and cell survival pathways, the authors studied release of cyt c, activation of caspase, and changes in Akt phosphorylation in rat brains subjected to 15 minutes of ischemia followed by varying periods of reperfusion. The authors found by electron microscopic study that a portion of mitochondria was swollen and structurally altered, whereas the cell membrane and nuclei were intact in hippocampal CA1 neurons after 36 hours of reperfusion. In some neurons, the pattern of immunostaining for cyt c changed from a punctuate pattern, likely representing mitochondria, to a more diffuse cytoplasmic localization at 36 and 48 hours of reperfusion as examined by laser-scanning confocal microscopic study. Western blot analysis showed that cyt c was increased in the cytosolic fraction in the hippocampus after 36 and 48 hours of reperfusion. Consistently, caspase-3-like activity was increased in these hippocampal samples. As demonstrated by Western blot using phosphospecific Akt antibody, phosphorylation of Akt at serine-473 in the hippocampal region was highly increased during the first 24 hours but not at 48 hours of reperfusion. The authors conclude that transient cerebral ischemia activates both cell death and cell survival pathways after ischemia. The activation of Akt during the first 24 hours conceivably may be one of the factors responsible for the delay in neuronal death after global ischemia.

Along with the development of industry and the improvement of people’s living standards, peoples’ demand on resources has greatly increased, causing energy crises and environmental pollution. In recent years, photocatalytic technology has shown great potential as a low-cost, environmentally-friendly, and sustainable technology, and it has become a hot research topic. However, current photocatalytic technology cannot meet industrial requirements. The biggest challenge in the industrialization of photocatalyst technology is the development of an ideal photocatalyst, which should possess four features, including a high photocatalytic efficiency, a large specific surface area, a full utilization of sunlight, and recyclability. In this review, starting from the photocatalytic reaction mechanism and the preparation of the photocatalyst, we review the classification of current photocatalysts and the methods for improving photocatalytic performance; we also further discuss the potential industrial usage of photocatalytic technology. This review also aims to provide basic and comprehensive information on the industrialization of photocatalysis technology.

Autophagy is the main degradation pathway responsible for eliminating abnormal protein aggregates and damaged organelles prevalent in neurons after transient cerebral ischemia. This study investigated whether accumulation of protein aggregate-associated organelles in postischemic neurons is a consequence of changes in autophagy. Electron microscopic (EM) analysis indicated that both autophagosomes (AP) and autolysosomes (AL) are significantlly upregulated in hippocampal CA1 and DG neurons after ischemia. The LC3-II conjugate, a marker for APs assessed by Western blotting, was upregulated in postischemic brain tissues. Confocal microscopy showed that LC3 isoforms were located in living postischemic neurons. Treatment with chloriquine (CQ) resulted in accumulation of LC3-II in sham-operated rats, but did not further change the LC3-II levels in postischemic brain tissues. The results indicate that at least part of the accumulation of protein aggregate-associated organelles seen following ischemia is likely to be due to failure of the autophagy pathway. The resulting protein aggregation on subcellular organelle membranes could lead to multiple organelle damage and to delayed neuronal death after transient cerebral ischemia.