Effect of the valence state of Mn in MnO x /Ti4O7 composites on the catalytic performance for oxygen reduction reaction and oxygen evolution reaction.

Manganese oxide composites with mixed valence states were prepared through the hydrothermal method by compositing with Ti4O7 and calcining at different temperatures, and their ORR and OER catalytic performance were investigated. The prepared catalysts were characterized by XRD, SEM-EDS, HRTEM-EDS, and XPS methods to analyse their phase constitution, morphology feature, and surface composition. The major phase of manganese oxides was Mn3O4, which is a one-dimensional structure, and its growth was induced by Ti4O7. The ORR and OER catalytic activity can be enhanced due to the preferred orientation of manganese oxides. Electrochemical measurements, namely CV, LSV and EIS, were utilized for determining the ORR and OER catalytic activity, whereas CA and ADT were used for studying the durability and stability. A Li-O2 battery was assembled to test the electrochemical behavior and properties in practical application. MnO x /Ti4O7 calcined at 300 °C exhibited the best catalytic activity of 0.72 V vs. RHE half-wave potential for ORR and 0.67 V vs. RHE overpotential for OER. The proportion of Mn3+ was also highest in all the MnO x /Ti4O7 composites. The assembled Li-O2 battery shows high performance with a voltage gap of only 0.85 V. Therefore, it can be affirmed that the inducement of Ti4O7 could strengthen the preferred orientation in manganese oxide growth and Mn3+ in MnO x /Ti4O7 plays a vital role in catalyzing ORR and OER, with both improving the ORR and OER bifunctional catalytic performance of manganese oxides.

Analysis of FK506-mediated functional recovery and neuroprotection in a rat model of spinal cord injury indicates that EGF is modulated in astrocytes.

The present study aimed to evaluate whether the application of tacrolimus (FK506) could improve functional recovery in spinal cord injury (SCI) rat models by activating astrocytes, and to further investigate the underlying mechanisms of this action. Male Sprague-Dawley rats (n=56) were used to establish moderate SCI models, which were induced at the T10 spinal segment by dropping a 10-g weight from a height of 25 mm using a New York University Impactor device. The rats were randomly separated into the FK506 or control group (n=28 per group). Rats were treated with FK506 (0.5 mg/kg) or saline intravenously 30 min after sustaining the injury. Functional recovery was evaluated over 42 days following the injury, and epidermal growth factor (EGF) levels were detected. The astrocytes were treated with FK506 in vitro, and the EGF mRNA and protein expression levels were analyzed using reverse transcription-quantitative polymerase chain reaction and ELISA, respectively. DNA microarray analysis was also performed to evaluate the genes in astrocytes. Rats in the FK506 group had improved locomotor functional recovery compared with those of control group. Furthermore, FK506 upregulated EGF expression of astrocytes both in vivo and in vitro. Subsequent to treatment with FK506-conditioned medium (CM), the length of neuronal cells increased 61.06% on the first day, and increased 56.4% on the third day compared with those of C-CM group. Furthermore, addition of anti-EGF neutralizing antibodies could interrupt the promotion of neurite outgrowth by FK506-CM. The present study indicates that astrocytes have an important role as mediators of FK506-improved spinal cord function recovery, and this partially clarifies the role of cell-cell interaction through modulating EGF in this process.

Endoplasmic reticulum stress signaling is involved in mitomycin C (MMC)-induced apoptosis in human fibroblasts via PERK pathway.

Endoplasmic reticulum (ER) stress-mediated cell apoptosis has been implicated in various cell types, including fibroblasts. Previous studies have shown that mitomycin C (MMC)-induced apoptosis occurs in fibroblasts, but the effects of MMC on ER stress-mediated apoptosis in fibroblasts have not been examined. Here, MMC-induced apoptosis in human primary fibroblasts was investigated by exposing cells to a single dose of MMC for 5 minutes. Significant inhibition of cell proliferation and increased apoptosis were observed using a cell viability assay, Annexin V/propidium iodide double staining, cell cycle analysis, and TUNEL (terminal deoxynucleotidyl transferase dUTP nick-end labeling) staining. Upregulation of proapoptotic factors, including cleaved caspase-3 and poly ADP-ribose polymerase (PARP), was detected by Western blotting. MMC-induced apoptosis was correlated with elevation of 78-kDa glucose-regulated protein (GRP78) and C/EBP homologous protein (CHOP), which are hallmarks of ER stress. Three unfolded protein response (UPR) sensors (inositol-requiring enzyme 1, IRE1; activating transcription factor 6, ATF6; and PKR-like ER kinase, PERK) and their downstream signaling pathways were also activated. Knockdown of CHOP attenuated MMC-induced apoptosis by increasing the ratio of BCL-2/BAX and decreasing BIM expression, suggesting that ER stress is involved in MMC-induced fibroblast apoptosis. Interestingly, knockdown of PERK significantly decreased ER stress-mediated apoptosis by reducing the expression of CHOP, BIM and cleaved caspase-3. Reactive oxygen species (ROS) scavenging also decreased the expression of GRP78, phospho-PERK, CHOP, and BIM. These results demonstrate that MMC-induced apoptosis is triggered by ROS generation and PERK activation.

Static mechanical stress induces apoptosis in rat endplate chondrocytes through MAPK and mitochondria-dependent caspase activation signaling pathways.

Mechanical stress has detrimental effects on cartilaginous endplate chondrocytes due to apoptosis in vivo and in vitro. In this study, we investigated the possible apoptosis signaling pathways induced by mechanical stress in cultured rat cervical endplate chondrocytes. Static mechanical load significantly reduced cell viability in a time- and load-dependent manner, as demonstrated by the Cell Counting Kit-8 (CCK-8) assay. Chondrocyte apoptosis induced by mechanical stress was confirmed by annexin V/propidium iodide (PI) staining and terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL). Western blot analysis revealed that static load-induced chondrocyte apoptosis was accompanied by increased phosphorylation of c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase 1/2 (ERK1/2), and p38 mitogen-activated protein kinase (MAPK). The loss of mitochondrial membrane potential (ΔΨm), increased Cytochrome c release, and activated Caspase-9 and Caspase-3, indicating that the mitochondrial pathway is involved in mechanical stress-induced chondrocyte apoptosis. Treatment with inhibitors of JNK (SP600125), p38 MAPK (SB203580), and ERK (PD98059) prior to mechanical stimulation reversed both the static load-induced chondrocyte apoptosis and the activation of JNK, p38 MAPK, and ERK. Taken together, the data presented in this study demonstrate that mechanical stress induces apoptosis in rat cervical endplate chondrocytes through the MAPK-mediated mitochondrial apoptotic pathway.

Rapid identification of spinal ventral and dorsal roots using a quartz crystal microbalance.

The fast and accurate identification of nerve tracts is critical for successful nerve anastomosis. Taking advantage of differences in acetylcholinesterase content between the spinal ventral and dorsal roots, we developed a novel quartz crystal microbalance method to distinguish between these nerves based on acetylcholinesterase antibody reactivity. The acetylcholinesterase antibody was immobilized on the electrode surface of a quartz crystal microbalance and reacted with the acetylcholinesterase in sample solution. The formed antigen and antibody complexes added to the mass of the electrode inducing a change in frequency of the electrode. The spinal ventral and dorsal roots were distinguished by the change in frequency. The ventral and dorsal roots were cut into 1 to 2-mm long segments and then soaked in 250 µL PBS. Acetylcholinesterase antibody was immobilized on the quartz crystal microbalance gold electrode surface. The results revealed that in 10 minutes, both spinal ventral and dorsal roots induced a frequency change; however, the frequency change induced by the ventral roots was notably higher than that induced by the dorsal roots. No change was induced by bovine serum albumin or PBS. These results clearly demonstrate that a quartz crystal microbalance sensor can be used as a rapid, highly sensitive and accurate detection tool for the quick identification of spinal nerve roots intraoperatively.

Short-lived chlorine-36 in a Ca- and Al-rich inclusion from the Ningqiang carbonaceous chondrite.

Excesses of sulfur-36 in sodalite, a chlorine-rich mineral, in a calcium- and aluminum-rich inclusion from the Ningqiang carbonaceous chondrite linearly correlate with chorine/sulfur ratios, providing direct evidence for the presence of short-lived chlorine-36 (with a half-life of 0.3 million years) in the early solar system. The best inferred (36Cl/35Cl)o ratios of the sodalite are approximately 5 x 10(-6). Different from other short-lived radionuclides, chlorine-36 was introduced into the inclusion by solid-gas reaction during secondary alteration. The alteration reaction probably took place at least 1.5 million years after the first formation of the inclusion, based on the correlated study of the 26Al-26Mg systems of the relict primary minerals and the alteration assemblages, from which we inferred an initial ratio of (36Cl/35Cl)o > or = 1.6 x 10(-4) at the time when calcium- and aluminum-rich inclusions formed. This discovery supports a supernova origin of short-lived nuclides [Cameron, A. G. W., Hoeflich, P., Myers, P. C. & Clayton, D. D. (1995) Astrophys. J. 447, L53; Wasserburg, G. J., Gallino, R. & Busso, M. (1998) Astrophys. J. 500, L189-L193], but presents a serious challenge for local irradiation models [Shu, F. H., Shang, H., Glassgold, A. E. & Lee, T. (1997) Science 277, 1475-1479; Gounelle, M., Shu, F. H., Shang, H., Glassgold, A. E., Rehm, K. E. & Lee, T. (2001) Astrophys. J. 548, 1051-1070]. Furthermore, the short-lived 36Cl may serve as a unique fine-scale chronometer for volatile-rock interaction in the early solar system because of its close association with aqueous and/or anhydrous alteration processes.