Ni-EDTA Containing Wastewater Treatment Using Electrochemical Advanced Oxidation Processes

The treatment of electroless plating wastewaters containing ethylenediamine tetraacetic acid complexed Ni (i.e. Ni-EDTA) has become a major problem due to the high stability and low biodegradability. Electrochemical advanced oxidation processes (EAOP) have been widely applied in removing persistent compounds by generation of highly oxidative reactive species such as hydroxyl radicals. We investigate the feasibility of treatment of Ni-EDTA containing wastewaters via EAOP employing a range of anodes and operating conditions. Both bismuth and nickel doped lead oxide anodes prepared via a co-electrodeposition process exhibit excellent electrochemical degradation of Ni-EDTA complexes and facilitate concomitant removal of Ni from solution via deposition of elemental Ni on the cathode surface. The effects of Bi/Ni doping ratio and electrodeposition current density on the electrode properties were thoroughly investigated. Our results show that minor deterioration in Ni-EDTA degradation performance was observed with minimal lead leakage. Compared with pure PbO2 and Bi-doped PbO2 electrodes, Ni doping increased the oxygen evolution potential as well as the reactive site concentration and reduced the electron transfer resistance thereby resulting in superior Ni-EDTA degradation performance. To increase the extent of Ni removal, we investigated the efficacy of five cathode materials. Our results show that carbon felt provides the best Ni removal efficiency as a result of its high surface area and low interference from side reactions such as the hydrogen evolution reaction. The Ni accumulated on the carbon felt surface was successfully recovered either as a nickel salt solution by acid leaching or as high purity NiO by calcinating the Ni-loaded carbon felt cathode. Our results also show that the performance of the regenerated carbon felt after acid leaching is comparable to that of the fresh cathode. We also developed a computational fluid dynamics (CFD) model to investigate flow behaviour and its impact on the Ni-EDTA in a flow-through reactor. The CFD model was used to investigate the effect of electrode aperture size and shape on Ni-EDTA degradation with the end goal of optimising electrode design. Additionally, we have developed a mathematical kinetic model that satisfactorily describes Ni-EDTA removal, Ni recovery, and TOC removal over a range of Ni and EDTA concentrations and provides a good description of the oxidation of various EDTA degradation intermediates

TRPC1 regulates calcium-activated chloride channels in salivary gland cells

Calcium-activated chloride channel (CaCC) plays an important role in modulating epithelial secretion. It has been suggested that in salivary tissues, sustained fluid secretion is dependent on Ca2+ influx that activates ion channels such as CaCC to initiate Cl- efflux. However direct evidence as well as the molecular identity of the Ca2+ channel responsible for activating CaCC in salivary tissues is not yet identified. Here we provide evidence that in human salivary cells, an outward rectifying Cl- current was activated by increasing [Ca2+]i, which was inhibited by the addition of pharmacological agents niflumic acid (NFA), an antagonist of CaCC, or T16Ainh-A01, a specific TMEM16a inhibitor. Addition of thapsigargin (Tg), that induces store-depletion and activates TRPC1-mediated Ca2+ entry, potentiated the Cl- current, which was inhibited by the addition of a non-specific TRPC channel blocker SKF96365 or removal of external Ca2+. Stimulation with Tg also increased plasma membrane expression of TMEM16a protein, which was also dependent on Ca2+ entry. Importantly, in salivary cells, TRPC1 silencing, but not that of TRPC3, inhibited CaCC especially upon store depletion. Moreover, primary acinar cells isolated from submandibular gland also showed outward rectifying Cl- currents upon increasing [Ca2+]i. These Cl- currents were again potentiated with the addition of Tg, but inhibited in the presence of T16Ainh-A01. Finally, acinar cells isolated from the submandibular glands of TRPC1 knockout mice showed significant inhibition of the outward Cl- currents without decreasing TMEM16a expression. Together the data suggests that Ca2+ entry via the TRPC1 channels is essential for the activation of CaCC.Fil: Sun, Yuyang. University Of North Dakota; Estados UnidosFil: Birnbaumer, Lutz. National Institutes of Health; Estados Unidos. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Singh, Brij B.. University Of North Dakota; Estados Unido

Boosting Method in Approximately Solving Linear Programming with Fast Online Algorithm

In this paper, we develop a new algorithm combining the idea of ``boosting'' with the first-order algorithm to approximately solve a class of (Integer) Linear programs(LPs) arisen in general resource allocation problems. Not only can this algorithm solve LPs directly, but also can be applied to accelerate the Column Generation method. As a direct solver, our algorithm achieves a provable $O(\sqrt{n/K})$ optimality gap, where $n$ is the number of variables and $K$ is the number of data duplication bearing the same intuition as the boosting algorithm. We use numerical experiments to demonstrate the effectiveness of our algorithm and several variants

Self-paced Weight Consolidation for Continual Learning

Continual learning algorithms which keep the parameters of new tasks close to that of previous tasks, are popular in preventing catastrophic forgetting in sequential task learning settings. However, 1) the performance for the new continual learner will be degraded without distinguishing the contributions of previously learned tasks; 2) the computational cost will be greatly increased with the number of tasks, since most existing algorithms need to regularize all previous tasks when learning new tasks. To address the above challenges, we propose a self-paced Weight Consolidation (spWC) framework to attain robust continual learning via evaluating the discriminative contributions of previous tasks. To be specific, we develop a self-paced regularization to reflect the priorities of past tasks via measuring difficulty based on key performance indicator (i.e., accuracy). When encountering a new task, all previous tasks are sorted from "difficult" to "easy" based on the priorities. Then the parameters of the new continual learner will be learned via selectively maintaining the knowledge amongst more difficult past tasks, which could well overcome catastrophic forgetting with less computational cost. We adopt an alternative convex search to iteratively update the model parameters and priority weights in the bi-convex formulation. The proposed spWC framework is plug-and-play, which is applicable to most continual learning algorithms (e.g., EWC, MAS and RCIL) in different directions (e.g., classification and segmentation). Experimental results on several public benchmark datasets demonstrate that our proposed framework can effectively improve performance when compared with other popular continual learning algorithms

Inhibition of L-Type Ca 2+ Channels by TRPC1-STIM1 Complex Is Essential for the Protection of Dopaminergic Neurons

Loss of dopaminergic (DA) neurons leads to Parkinson’s disease; however, the mechanism(s) for the vulnerability of DA neurons is(are) not fully understood. We demonstrate that TRPC1 regulates the L-type Ca2 channel that contributes to the rhythmic activity of adult DA neurons in the substantia nigra region. Store depletion that activates TRPC1, via STIM1, inhibits the frequency and amplitude of the rhythmic activity in DA neurons of wild-type, but not in TRPC1/, mice. Similarly, TRPC1/ substantia nigra neurons showed increased L-type Ca2 currents, decreased stimulation-dependent STIM1-Cav1.3 interaction, and decreased DA neurons. L-type Ca2 currents and the open channel probability of Cav1.3 channels were also reduced upon TRPC1 activation, whereas increased Cav1.3 currents were observed upon STIM1 or TRPC1 silencing. Increased interaction between Cav1.3-TRPC1-STIM1 was observed upon store depletion and the loss of either TRPC1 or STIM1 led to DA cell death, which was prevented by inhibiting L-type Ca2 channels. Neurotoxins that mimic Parkinson’s disease increased Cav1.3 function, decreased TRPC1 expression, inhibited Tg-mediated STIM1-Cav1.3 interaction, and induced caspase activation. Importantly, restoration of TRPC1 expression not only inhibited Cav1.3 function but increased cell survival. Together, we provide evidence that TRPC1 suppresses Cav1.3 activity by providing an STIM1-based scaffold, which is essential for DA neuron survival.Fil: Sun, Yuyang. University of North Dakota; Estados UnidosFil: Zhang, Haopeng. University of North Dakota; Estados UnidosFil: Selvaraj, Senthil. University of North Dakota; Estados UnidosFil: Sukumaran, Pramod. University of North Dakota; Estados UnidosFil: Lei, Saobo. University of North Dakota; Estados UnidosFil: Birnbaumer, Lutz. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. National Institutes of Environmental Health Sciences; Estados UnidosFil: Singh, Brij B.. University of North Dakota; Estados Unido

Transient receptor potential channel 1 deficiency impairs host defense and proinflammatory responses to bacterial infection by regulating protein kinase Cα signaling

Transient receptor potential channel 1 (TRPC1) is a nonselective cation channel that is required for Ca2+ homeostasis necessary for cellular functions. However, whether TRPC1 is involved in infectious disease remains unknown. Here, we report a novel function for TRPC1 in host defense against Gram-negative bacteria. TRPC1-/- mice exhibited decreased survival, severe lung injury, and systemic bacterial dissemination upon infection. Furthermore, silencing of TRPC1 showed decreased Ca2+ entry, reduced proinflammatory cytokines, and lowered bacterial clearance. Importantly, TRPC1 functioned as an endogenous Ca2+ entry channel critical for proinflammatory cytokine production in both alveolar macrophages and epithelial cells. We further identified that bacterium-mediated activation of TRPC1 was dependent on Toll-like receptor 4 (TLR4), which induced endoplasmic reticulum (ER) store depletion. After activation of phospholipase Cγ (PLC-γ), TRPC1 mediated Ca2+ entry and triggered protein kinase Cα (PKC-α) activity to facilitate nuclear translocation of NF-kB/Jun N-terminal protein kinase (JNK) and augment the proinflammatory response, leading to tissue damage and eventually mortality. These findings reveal that TRPC1 is required for host defense against bacterial infections through the TLR4-TRPC1-PKCγ signaling circuit.Fil: Zhou, Xikun. University Of North Dakota; Estados Unidos. West China Hospital Of Sichuan University; ChinaFil: Ye, Yan. University Of North Dakota; Estados UnidosFil: Sun, Yuyang. University Of North Dakota; Estados UnidosFil: Li, Xuefeng. West China Hospital Of Sichuan University; China. University Of North Dakota; Estados UnidosFil: Wang, Wenxue. University Of North Dakota; Estados UnidosFil: Privratsky, Breanna. University Of North Dakota; Estados UnidosFil: Tan, Shirui. University Of North Dakota; Estados UnidosFil: Zhou, Zongguang. West China Hospital Of Sichuan University; ChinaFil: Huang, Canhua. West China Hospital Of Sichuan University; ChinaFil: Wei, Yu-Quan. West China Hospital Of Sichuan University; ChinaFil: Birnbaumer, Lutz. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. National Institute Of Environmental Health Sciences; Estados UnidosFil: Singh, Brij B.. University Of North Dakota; Estados UnidosFil: Wu, Min. University Of North Dakota; Estados Unido

Experimental Study on Uniaxial Compression of Bamboo Poles with Different Reinforcements

The natural round bamboo is a kind of ecological building material with many excellent physical and mechanical characteristics, such as fast growth, high strength and good environmental performance. However, the natural round bamboos were barely used for its worse durability and easiness to crack compared other bamboo productions after secondary operation. In order to improve the safety and durability of the round bamboo structure, the axial compression test of the GFRP (glass fiber-reinforced polymer) and/or mortar reinforcing cracked bamboo was conducted. The 20 cm tall round bamboo column specimens were divided into five categories: the first without cracks and reinforcement, the second with cracks but without reinforcement, the third with cracks and full GFRP reinforcement, the forth with cracks and fulfil of cement motrar, and the last with cracks and reinforced using both GFRP and cement mortar. The bearing capacity and the failure modes were observed and studied. It was found that the composite reinforcement of GFRP and mortar could significantly increase the bearing capacity of the cracked round bamboos, and avoid brittle failure through improving the ductility of the specimens

Experimental Study on Uniaxial Compression of Bamboo Nodes Using 3D Scanning Technique

Bamboo is a kind of ecological building material for its physical and mechanical characteristics, such as fast growth, high yield, high strength, high toughness and good environmental performance. However, there are few studies on the influence of bamboo node structure about the mechanical properties of bamboo, and it is difficult to accurately determine the cross-section area of the bamboo node. In this paper, the three-dimensional scanner was combined with the reverse modeling technology to accurately obtain the cross-sectional area of the bamboo node. The bamboo node was subjected to axial compression test. Based on the experimental results, it was confirmed that the compressive strength of the bamboo node increased from the bottom to the top. The experimental results also showed that the difference in the degree of cracks has an effect on the bamboo break mode. Bamboo nodes with severe cracks and uneven distribution on the surface had the largest degree of expansion at the original deep cracks or the original surface through cracks. Bamboo nodes with slight cracks and even distribution or without cracks on the surface were uniformly expanding at the lower part when they were broken