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Deformation twinning plays a vital role in accommodating plastic deformation of hexagonal-close-packed (hcp) metals, but its mechanisms are still unsettled under high strain rate shock compression. Here we investigate deformation twinning in shock-compressed Mg as a typical hcp metal with in situ, ultrafast synchrotron x-ray diffraction. Extension twinning occurs upon shock compression along $⟨11\overline{2}0⟩$ and $⟨10\overline{1}0⟩$, but only upon release for loading along $⟨0001⟩$. Such deformation mechanisms are a result of the polarity of deformation twinning, which depends on directionality and relative magnitude of resolved shear stress and may be common for Mg and its alloys in a wide range of strain rates.

To explore the effects of fine particulate matter on the level of nuclear factor erythroid-2 related factor 2 (Nrf2) in pulmonary tissues of chronic obstructive pulmonary disease (COPD) mouse models and its relationship with oxidative stress.Totally 40 BALB/c mice were randomly divided into normal control group, normal PM2.5 group, COPD control group and COPD PM2.5 group.COPD mice were established using exposure of cigarette smoking.PM2.5 (20 mg/kg) was intratracheally instilled in PM2.5 group mice.Mice pulmonary function was measured by mice noninvasive body plethysmograph and lung histopathology was observed in normal control group and normal PM2.5 group mice.The mRNA and protein expression of Nrf2 was measured with real-time polymerase chain reaction (PCR) and Western blot methods.Total antioxidative capacity (TAC) was measured by O-phenanthroline colorimetry.Glutathione peroxidase (GSH-PX) was measured by improved Hafeman colorimetry and malondialdehyde (MDA) by thiobarbiturieacid colorimetry.Nrf2 mRNA and protein in normal control group, normal PM2.5 group, COPD control group and COPD PM2.5 group were 1.00, 4.46±0.42, 4.93±0.63, 6.41±0.35 and 0.92±0.08, 1.23±0.07, 1.20±0.09, 1.43±0.10.Nrf2 mRNA and protein in COPD control group were increased than those in normal control group while those in normal PM2.5 group and COPD PM2.5 group were respectively higher than each control group.Comparing to normal PM2.5 group, the Nrf2 mRNA and protein in COPD PM2.5 group were increased (all P0.01). TAC and GSH-PX in each group were (5.1±0.4), (2.9±0.4), (3.3±0.3), (1.8±0.3) and (13.4±0.5), (9.9±0.7), (9.8±0.7), (7.0±0.6) U/mgpro.TAC and GSH-PX in COPD control group were decreased than those in normal control group while those in normal PM2.5 group and COPD PM2.5 group were respectively lower than each control group.Comparing to normal PM2.5 group, the Nrf2 mRNA and protein in COPD PM2.5 group were decreased (all P0.01). MDA in each group were (2.9±0.4), (4.8±0.5), (4.5±0.3), and (6.2±0.4) nmol/mgpro.MDA in COPD control group were increased than those in normal control group while those in normal PM2.5 group and COPD PM2.5 group were respectively higher than each control group.Comparing to normal PM2.5 group, the MDA in COPD PM2.5 group were increased (all P0.01). Positive correlations were observed between Nrf2 mRNA, protein and MDA, while negative correlations were observed between Nrf2 mRNA, protein and TAC, GSH-PX in all groups (all P0.05).PM2.5 can induce Nrf2 expression and aggravate oxidative stress in COPD mice.The increased expression of Nrf2 is closely associated with oxidative stress.

To investigate the inhibitory effects of codonopsis pilosula polysaccharides (CPP) on the deterioration of impaired phagocytosis of alveolar macrophage (AM) induced by fine particulate matter with a mean aerodynamic diameter ≤2.5 μm (PM2.5) in chronic obstructive pulmonary disease (COPD) mice.Sixty BALB/c male mice were randomly divided into control group, COPD group, PM2.5 group, PM2.5 COPD group, CPP COPD group and CPP+ PM2.5 COPD group. COPD mice were established using exposure of cigarette smoking. Meanwhile PM2.5 group, PM2.5 COPD group and CPP+ PM2.5 COPD group were exposed to PM2.5 (770 μg/m(3)) for 90 days. CPP COPD group and CPP+ PM2.5 COPD group were fed with CPP (300 mg/kg) for 90 days whilst other groups were fed with isovolumetric saline. After the models were established, mice peak inspiratory flow (PIF) and peak expiratory flow (PEF) were measured by noninvasive body plethysmograph and lung histopathology and mean linear intercept (MLI) were observed. AMs were isolated from lung tissue by discontinuous density gradient centrifugation. Mean fluorescence intensity (MFI) and the ability of AM phagocytosing flurescein isothiocyanate-labeled Escherichia coli (FITC-E.coli) (AM%) were detected by flow cytometry. Total antioxidative capacity (TAC) was measured by O-phenanthroline colorimetry. Malondialdehyde (MDA) was measured by thiobarbiturieacid colorimetry and glutathione peroxidase (GSH-PX) by improved Hafeman colorimetry.MFI in control group, COPD group, PM2.5 group, PM2.5 COPD group, CPP COPD group and CPP+ PM2.5 COPD group were 10 267±1 358, 4 817±399, 8 469±240, 3 176±501, 5 886±516 and 4 067±453. AM% in each group were (69.0±5.4)%, (30.7±3.0)%, (51.5±2.4)%, (20.4±3.5)%, (38.7±2.6)% and (28.7±4.3)%. MFI and AM% in COPD group and PM2.5 group were decreased than those in control group while those in PM2.5 COPD group were lower than in COPD group (all P0.01). Comparing to COPD group and PM2.5 COPD group respectively, MFI and AM% in CPP COPD group and CPP + PM2.5 COPD group were increased (all P0.01). TAC and GSH-PX in each group were (17.99±0.09), (6.83±0.36), (13.84±1.12), (3.61±0.29), (8.80±0.26), (5.43±0.30) U/mg protein and (84.3±5.7), (46.5±2.6), (62.0±2.2), (32.4±3.8), (53.4±4.0), (42.4±4.0) U/mg. TAC and GSH-PX in COPD group and PM2.5 group were lower than those from control group while those from PM2.5 COPD group were decreased than in COPD group (all P0.01). Comparing to COPD group and PM2.5 COPD group, TAC and GSH-PX in CPP COPD group and CPP+ PM2.5 COPD group were increased respectively (all P0.01). MDA in each group were (1.74±0.37), (2.73±0.22), (2.01±0.13), (3.55±0.33), (2.22±0.28) and (2.72±0.44) nmol/mg protein. MDA in COPD group and PM2.5 group were higher than that from control group while that from PM2.5 COPD group was higher than in COPD group; MDA in CPP COPD group and CPP+ PM2.5 COPD group were respectively decreased than those in COPD group and PM2.5 COPD group (all P0.05). Positive correlations were existed between MFI, AM% and TAC, GSH-PX, while negative correlations were existed between MFI, AM% and MDA in COPD group, PM2.5 group, PM2.5 COPD group, CPP COPD group and CPP+ PM2.5 COPD group.PM2.5 further impaired the defective phagocytosing capacity of AM and exacerbated oxidative stress in COPD mice. CPP can inhibit these effects. The protection of CPP may be closely related to its antioxidative effects.

The synthesis process of LiCoO2 prepared by l-apple acid (l-HOOCCH(OH)CH2COOH) assisted sol–gel method is studied by using Fourier transforms infrared spectroscopy, mass spectroscopy, simultaneous thermogravimetric and differential thermal analysis, X-ray diffraction analysis, and elemental analysis. The results show that lithium and cobalt ions are trapped homogeneously on an atomic scale throughout the precursor. Lithium carbonate and Co3O4 are intermediate products during heat treatment of the precursor. Moreover, the kinetics for formation of LiCoO2 by l-apple acid assisted sol–gel method is faster than the case of the conventional solid-state reaction between lithium carbonate and Co3O4. In comparison with the solid-state reaction, the sol–gel method significantly shortens the required reaction time for synthesizing LiCoO2, and also reduces the particle size. In the electrochemical test, it is found that the specific discharge/charge capacities as well as the coulomb efficiency substantially increase with increasing the calcination temperature. It is considered that LiCoO2 with a good-layered structure facilitates the insertion and de-insertion of lithium ions in aqueous electrolyte. As a result, the combination of the sol–gel method with proper calcination processes is highly successful in producing LiCoO2 powders with large specific capacity and good cycle performance in aqueous lithium-ion battery.

Magnetically recyclable Co–B hollow nanospindles have been prepared by using poly(styrene-co-methacrylic acid) nanospindles as scarified templates for the first time. The effect of the weight ratio of poly(styrene-co-methacrylic acid) to Co(OAc)2 on the structure of Co–B hollow nanospindles is not significant. In the hydrolysis of ammonia borane to release H2, the activity of Co–B hollow nanospindles was much higher than that of regular Co–B prepared without templates. Their catalytic performance is comparable to that of the reported Pt black concerning hydrogen yield. The favorable activity is attributed to the large specific surface area and hollow structure. In addition, Co–B hollow nanospindles have good reusability in the application due to their unique magnetic properties.

We investigate physical properties of bromoform (liquid CHBr3) including compressibility and refractive index under dynamic extreme conditions of shock compression. Planar shock experiments are conducted along with high-speed laser interferometry. Our experiments and previous results establish a linear shock velocity−particle velocity relation for particle velocities below 1.77 km/s, as well as the Hugoniot and isentropic compression curves up to ∼21 GPa. Shock-state refractive indices of CHBr3 up to 2.3 GPa or ∼26% compression, as a function of density, can be described with a linear relation and follows the Gladstone-Dale relation. The velocity corrections for laser interferometry measurements at 1550 nm are also obtained.

Radiotherapy has the widest application to esophageal squamous cell carcinoma (ESCC) patients. Factors associated with DNA damage repair have been shown to function in cell radiosensitivity. Human positive cofactor 4 (PC4) has a role in nonhomologous end joining (NHEJ) and is involved in DNA damage repair. However, the clinical significance and biological role of PC4 in cancer progression and cancer cellular responses to chemoradiotherapy (CRT) remain largely unknown. The aim of the present study was to investigate the potential roles of PC4 in the radiosensitivity of ESCC. In this study, we showed that knockdown of PC4 substantially increased ESCC cell sensitivity to ionizing radiation (IR) both in vitro and in vivo and enhanced radiation-induced apoptosis and mitotic catastrophe (MC). Importantly, we demonstrated that silencing of PC4 suppressed NHEJ by downregulating the expression of XLF in ESCC cells, whereas reconstituting the expression of XLF protein in the PC4-knockdown ESCC cells restored NHEJ activity and radioresistance. Moreover, high expression of PC4 positively correlated with ESCC resistance to CRT and was an independent predictor for short disease-specific survival of ESCC patients in both of our cohorts. These findings suggest that PC4 protects ESCC cells from IR-induced death by enhancing the NHEJ-promoting activity of XLF and could be used as a novel radiosensitivity predictor and a promising therapeutic target for ESCCs.

We develop a mini gas gun system for simultaneous, single-pulse, x-ray diffraction and imaging under high strain-rate loading at the beamline 32-ID of the Advanced Photon Source. In order to increase the reciprocal space covered by a small-area detector, a conventional target chamber is split into two chambers: a narrowed measurement chamber and a relief chamber. The gas gun impact is synchronized with synchrotron x-ray pulses and high-speed cameras. Depending on a camera's capability, multiframe imaging and diffraction can be achieved. The proof-of-principle experiments are performed on single-crystal sapphire. The diffraction spots and images during impact are analyzed to quantify lattice deformation and fracture; fracture is dominated by splitting cracks followed by wing cracks, and diffraction peaks are broadened likely due to mosaic spread. Our results demonstrate the potential of such multiscale measurements for studying high strain-rate phenomena at dynamic extremes.

Selectins play a major role in the inflammatory reaction by initiating neutrophil attachment to activated vascular endothelium. Some heparin preparations can interact with L- and P-selectin; however, the determinants required for inhibiting selectin-mediated cell adhesion have not yet been characterized. We now report that carboxyl-reduced and sulfated heparin (prepared by chemical modifications of porcine intestinal mucosal heparin leading to the replacement of carboxylates by O-sulfate groups) and trestatin A sulfate (obtained by sulfation of trestatin A, a non-uronic pseudo-nonasaccharide extracted from Streptomyces dimorphogenes) exhibit strong anti-P-selectin and anti-L-selectin activity while lacking antithrombin-mediated anticoagulant activity. In vitro experiments revealed that both compounds inhibited P-selectin- and L-selectin-mediated cell adhesion under laminar flow conditions. Moreover, carboxyl-reduced and sulfated heparin and trestatin A sulfate were also active in vivo, as assessed by experiments showing 1) that microinfusion of trestatin A sulfate reduced by 96% leukocyte rolling along rat mesenteric postcapillary venules and 2) that both compounds inhibited (by 58-81%) neutrophil migration into thioglycollate-inflamed peritoneum of BALB/c mice. These results indicate that nonanticoagulant sulfated saccharides targeted at P-selectin and L-selectin may have therapeutic potential in inflammatory disorders.

Patients with severe temporal lobe epilepsy lose neurons within the CA3 and hilar regions of the hippocampus. Loss of CA3 and hilar neurons was also induced by transducing organotypic hippocampal slice cultures with a replication-defective herpes simplex virus (HSV) vector expressing the GluR6 kainate subtype of the glutamate receptor (HSVGluR6). In transduced fibroblasts, HSVGluR6 expressed a M(r) 115,000 protein that reacted with anti-GluR6 serum. After exposure of fibroblast to HSVGluR6, a kainate-dependent toxicity appeared in cells that were previously resistant to kainate. Microapplication of nanoliter amounts of recombinant HSV stocks into organotypic hippocampal slice cultures resulted in localized transduction and gene transfer at the site of microapplication. Microapplication of 100 HSVGluR6 virions into CA3 stratum pyramidale induced a large loss of CA3 pyramidal cells and hilar neurons, despite the small number of transduced neurons. This effect was not seen when 100 virions of HSVGluR6 were microapplied to CA1 stratum pyramidale. Tetrodotoxin or N-methyl-D-aspartate receptor antagonists inhibited the large loss of CA3 and hilar neurons, suggesting that the small cluster of HSVGluR6-transduced cells induced an N-methyl-D-aspartate-dependent transsynaptic loss of non-transduced neurons.