Highly sulfonated poly ether ether ketone chelated with Cu2+ as a proton exchange membrane at sub-zero temperatures.

Improving the proton conductivity (σ) of proton exchange membranes at low temperatures is very important for expanding their application areas. Here, sulfonated poly ether ether ketone (SPEEK) membranes were prepared with different sulfonation degrees, and its maximum ion exchange capacity is 3.15 mmol/g for 10 h at 60 °C. Highly sulfonated SPEEK membrane exhibits ultra-high water uptake and excellent proton conductivity of 0.074 S/cm at -25 °C due to its abundant -SO3H. Nevertheless, its high swelling ratio and low mechanical strength are not conducive to the practical application of the membrane. Luckily, by employing the chelation of Cu2+ with -SO3- on the SPEEK chain, Cu2+-coordinated SPEEK membranes were prepared, and they not only retain high -SO3H content but also possess robust mechanical properties and good dimensional stability compared to pristine SPEEK membrane. Meanwhile, the σ of the SPEEK-Cu membrane reaches 0.054 S/cm at -25 °C, and its fuel cell maximum power (Wmax) reaches 0.42 W/cm2 at -10 °C, demonstrating superior low-temperature performance in comparison to other reported materials. Particularly, water states in the prepared membranes are quantified by low-temperature differential scanning calorimetry. Because much more water bound to the plentiful -SO3H and Cu2+ inside the membrane endows it with anti-freezing performance, the decay of the σ and the Wmax for the SPEEK-Cu membrane is retarded at sub-zero temperatures. It is envisioned that composite membranes comprising metal ions such as Cu2+-SPEEK have a high potential for sub-zero fuel cell applications.

Morphology regulation of conductive metal-organic frameworks in situ grown on graphene oxide for high-performance supercapacitors.

In this work, nickel-catecholate (Ni-CAT) nanorods were in situ compounded on graphene oxide (GO) to form a composite Ni-CAT@GO (NCG) with a special "blanket-shape" structure, which was used as an electrode material for supercapacitors. The morphology of Ni-CATs in situ grown on GO was modulated by introducing various contents of GO. With increasing GO, the length of nanorods of Ni-CATs is obviously shortened, and the charge transfer resistance of NCG is significantly reduced as the GO content is relatively low while it increases with further addition of GO, because excessive GO in NCG results in smaller crystal sizes accompanied by smaller stacking pores. Both the over-long Ni-CAT nanorods and the smaller stacking pores can restrict the accessible surface areas for the electrolyte. Optimal nanorod sizes are crucial to achieve good electrochemical performance for electrode materials. Galvanostatic charge-discharge analysis of NCG electrodes shows that their capacity initially increases and then decreases with the addition of more and more GO, and Ni-CAT@GO-0.5 (NCG0.5) with minimal charge transfer resistance exhibits the best electrochemical performance. The results demonstrate that the NCG0.5 electrode with optimal morphology possesses an excellent capacitance of 563.8 F g-1 at 0.5 A g-1 and a good rate performance of 61.9% at 10 A g-1, indicating that Ni-CAT@GO is a new type of promising electrode material for supercapacitors based on conductive metal-organic frameworks.

Light convolutional neural network by neural architecture search and model pruning for bearing fault diagnosis and remaining useful life prediction.

Convolutional Neural Network (CNN) has been extensively used in bearing fault diagnosis and Remaining Useful Life (RUL) prediction. However, accompanied by CNN's increasing performance is a deeper network structure and growing parameter size. This prevents it from being deployed in industrial applications with limited computation resources. To this end, this paper proposed a two-step method to build a cell-based light CNN by Neural Architecture Search (NAS) and weights-ranking-based model pruning. In the first step, a cell-based CNN was constructed with searched optimal cells and the number of stacking cells was limited to reduce the network size after influence analysis. To search for the optimal cells, a base CNN model with stacking cells was initially built, and Differentiable Architecture Search was adopted after continuous relaxation. In the second step, the connections in the built cell-based CNN were further reduced by weights-ranking-based pruning. Experiment data from the Case Western Reserve University was used for validation under the task of fault classification. Results showed that the CNN with only two cells achieved a test accuracy of 99.969% and kept at 99.968% even if 50% connections were removed. Furthermore, compared with base CNN, the parameter size of the 2-cells CNN was reduced from 9.677MB to 0.197MB. Finally, after minor revision, the network structure was adapted to achieve bearing RUL prediction and validated with the PRONOSTIA test data. Both tasks confirmed the feasibility and superiority of constructing a light cell-based CNN with NAS and pruning, which laid the potential to realize a light CNN in embedded systems.

Deficiency of macrophage migration inhibitory factor attenuates tau hyperphosphorylation in mouse models of Alzheimer's disease.

BACKGROUND: Pathological features of Alzheimer's disease (AD) include aggregation of amyloid beta (Aß) and tau protein. Macrophage migration inhibitory factor (MIF), a proinflammatory cytokine, has been implicated in the toxicity of aggregated Aß. It remains unclear whether MIF affects hyperphosphorylation and aggregation of tau. METHODS: The effects of MIF deficiency in tau hyperphosphorylation were examined in Mif (-/-) mice receiving intracerebroventricular (ICV) injection of streptozotocin (STZ) and in APP/PS1 transgenic mice mated with Mif (-/-) mice. MIF expression and astrocyte activation were evaluated in ICV-STZ mice using immunofluorescence staining. Cultured primary astrocytes were treated with high glucose to mimic STZ function in vitro, and the condition medium (CM) was collected. The level of tau hyperphosphorylation in neurons treated with the astrocyte CM was determined using Western blotting. RESULTS: MIF deficiency attenuated tau hyperphosphorylation in mice. ICV injection of STZ increased astrocyte activation and MIF expression in the hippocampus. MIF deficiency attenuated astrocyte activation in ICV-STZ mice. CM from high glucose-treated WT astrocytes increased tau hyperphosphorylation in cultured primary neurons, an effect absent from Mif (-/-) astrocytes and WT astrocytes treated with the MIF inhibitor ISO-1. ISO-1 had no direct effect on tau phosphorylation in cultured primary neurons. CONCLUSIONS: These results suggest that MIF deficiency is associated with reduced astrocyte activation and tau hyperphosphorylation in the mouse AD models tested. Inhibition of MIF and MIF-induced astrocyte activation may be useful in AD prevention and therapy.

Curcumin induces apoptosis in tumor necrosis factor-alpha-treated HaCaT cells.

Psoriasis is a benign, chronic skin disease characterized by keratinocyte hyperproliferation and abnormal differentiation. Curcumin, a selective phosphorylase kinase inhibitor, is a natural phytochemical present in turmeric. Curcumin has been confirmed to have anti-inflammatory properties as well as the ability to inhibit proliferation and decrease the expression of pro-inflammatory cytokines in psoriatic keratinocytes. However, the pro-apoptotic effect of curcumin in keratinocytes remains unclear. In the present study, we investigated the effect of curcumin on apoptosis induction in TNF-α-treated HaCaT cells. These results show that curcumin exhibited a significant pro-apoptotic effect on HaCaT cells only in the presence of TNF-α and/or TRAIL. The pro-apoptotic effect of curcumin resulted from the increased expression of TRAIL-R1/R2 and the decreased expression of anti-apoptotic proteins. Our results indicate that both curcumin and TNF-α up-regulated the expression of TRAIL-R1/R2. In addition, the expression of anti-apoptotic proteins (IAP1, IAP2, Bcl-X(L)) was up-regulated by TNF-α but suppressed by curcumin in HaCaT cells. Because these proteins are regulated by NF-κB, we examined the role of curcumin in NF-κB activation. As expected, curcumin inhibited TNF-α-induced activation of NF-κB, including NF-κB-P65. Curcumin also inhibited the TNF-α-induced production of IL-6/IL-8 in HaCaT cells. These results imply that curcumin-induced apoptosis of HaCaT cells only occurs when TNF-α or/and TRAIL are present. Therefore, we believe that curcumin is able to reverse the anti-apoptotic function of TNF-α in HaCaT cells and thus expect curcumin to be successful in the treatment of psoriasis.

A modified LC-MS/MS method for determination of tetramethylpyrazine in microdialysis samples and calibration of home-made linear probes.

Tetramethylpyrazine (TMP) is one of the most important active ingredients of a Chinese herb Ligusticum wallichii Franchat, which is widely used for the treatment of cardiovascular diseases. Several factors may affect TMP exposure after topical administration, resulting in large variability and demanding further elucidation of drug distribution. This paper describes a new efficient reliable LC-MS/MS assay for the determination of TMP in dermal microdialysate, where TMP was separated on an Agilent C(18) column (3.5 µm, 100 mm × 2.1 mm i.d.) using a mixture of methanol, water and acetic acid (50:50:0.6, v/v/v) at a flow-rate of 0.3 mL/min. The retention time was 1.89 min for TMP and 1.17 min for the internal standard (caffeine). Histological analysis confirmed an inflammatory response to the microdialysis probes and the presence of a collagen capsule. The membrane extraction efficiency (percentage delivered to the tissue space) for TMP was not altered through the implant lifetime. The validation and sample analysis results showed that the method is precise, accurate and well suited to support dermal microdialysis experiments.

Camptothecin fails to induce apoptosis in tumor necrosis factor-alpha-treated HaCaT cells.

Camptothecin (CPT), a DNA topoisomerase I inhibitor, was originally isolated from the fruits of the Chinese Camptotheca acuminata tree. CPT and its derivatives have been used in the treatment of psoriasis and cancer in China for decades. It is well known that tumor necrosis factor-α (TNF-α) is a key proinflammatory cytokine in the pathogenesis of psoriasis. In this study, we investigated the effect of CPT on TNF-α-treated HaCaT cells. The results indicated that CPT in the concentration range of 0.5-2.0 µg·ml(-1) failed to show any proapoptotic effect in HaCaT cells. It was found that both CPT and TNF-α up-regulated the expression of TRAIL receptor 1/2 but not TRAIL in HaCaT cells. Furthermore, the expression of antiapoptotic proteins (IAP1, IAP2, and Bcl-X(L)) was up-regulated by TNF-α and suppressed by CPT in HaCaT cells. Because these gene products are known to be regulated by nuclear factor-kappa B (NF-κB), we examined the role of CPT on NF-κB activation. It was found that CPT not only failed to inhibit TNF-α-induced NF-κB activation but also contributed to NF-κB activation. In addition to these effects, CPT also promoted the production of interleukin-6, similar to TNF-α, in HaCaT cells. In conclusion, despite ample evidence supporting CPT-induced carcinoma cell apoptosis, our study clearly shows that CPT fails to show any proapoptotic effects in HaCaT cells, even though it enhanced TRAIL receptor 1/2 expression and inhibited the expression of TNF-α-induced antiapoptotic proteins. Taken together, this study demonstrates that CPT fails to block the activity of TNF-α. With respect to the NF-κB-activating role of CPT, we suggest that the benefit of CPT in the treatment of psoriasis should be reevaluated.