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In this paper, we present data on the physics and phenomenology of plasma reactors based on the One Atmosphere Uniform Glow Discharge Plasma (OAUGDP™) that are useful in optimizing the conditions for plasma formation, uniformity and surface treatment applications. It is shown that the real (as opposed to reactive) power delivered to a reactor is divided between dielectric heating of the insulating material and power delivered to the plasma available for ionization and active species production. A relationship is given for the dielectric heating power input as a function of the frequency and voltage at which the OAUGDP™ discharge is operated.

This paper presents a micro electromagnetic energy harvester which can convert low level vibration energy to electrical power. It mainly consists of an electroplated copper planar spring, a permanent magnet and a copper planar coil with high aspect ratio. Mechanical simulation shows that the natural frequency of the magnetspring system is 94.5 Hz. The resonant vibration amplitude of the magnet is 259.1 lm when the input vibration amplitude is 14 lm and the magnet-spring system is at resonance. Electromagnetic simulation shows that the linewidth and the turns of the coil influence the induced voltage greatly. The optimized electromagnetic vibration energy harvester can generate 0.7 lW of maximal output power with peak-peak voltage of 42.6 mV in an input vibration frequency of 94.5 Hz and input acceleration of 4.94 m/s 2 (this vibration is a kind of low level ambient vibration). A prototype (not optimized) has been fabricated using MEMS micromachining technology. The testing results show that the prototype can generate induced voltage (peak-peak) of 18 mV and output power of 0.61 lW for 14.9 m/s 2 external acceleration at its resonant frequency of 55 Hz (this vibration is not in a low ambient vibration level).

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Systemic metabolic syndrome significantly increases the risk of morbidity and mortality in patients with non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH). However, no effective therapeutic strategies are available, practically because our understanding of its complicated pathogenesis is poor. Here we identify the tripartite motif-containing protein 31 (Trim31) as an endogenous inhibitor of rhomboid 5 homolog 2 (Rhbdf2), and we further determine that Trim31 directly binds to Rhbdf2 and facilitates its proteasomal degradation. Hepatocyte-specific Trim31 ablation facilitates NAFLD-associated phenotypes in mice. Inversely, transgenic or ex vivo gene therapy-mediated Trim31 gain-of-function in mice with NAFLD phenotypes virtually alleviates severe deterioration and progression of steatohepatitis. The current findings suggest that Trim31 is an endogenous inhibitor of Rhbdf2 and downstream cascades in the pathogenic process of steatohepatitis and that it may serve as a feasible therapeutical target for the treatment of NAFLD/NASH and associated metabolic disorders.

Background and Aims Nonalcoholic fatty liver disease (NAFLD) has been widely recognized as a precursor to metabolic complications. Elevated inflammation levels are predictive of NAFLD‐associated metabolic disorder. Inactive rhomboid‐like protein 2 (iRhom2) is regarded as a key regulator in inflammation. However, the precise mechanisms by which iRhom2‐regulated inflammation promotes NAFLD progression remain to be elucidated. Approach and Results Here, we report that insulin resistance, hepatic steatosis, and specific macrophage inflammatory activation are significantly alleviated in iRhom2‐deficient (knockout [KO]) mice, but aggravated in iRhom2 overexpressing mice. We further show that, mechanistically, in response to a high‐fat diet (HFD), iRhom2 KO mice and mice with iRhom2 deficiency in myeloid cells only showed less severe hepatic steatosis and insulin resistance than controls. Inversely, transplantation of bone marrow cells from healthy mice to iRhom2 KO mice expedited the severity of insulin resistance and hepatic dyslipidemia. Of note, in response to HFD, hepatic iRhom2 binds to mitogen‐activated protein kinase kinase kinase 7 (MAP3K7) to facilitate MAP3K7 phosphorylation and nuclear factor kappa B cascade activation, thereby promoting the activation of c‐Jun N‐terminal kinase/insulin receptor substrate 1 signaling, but disturbing AKT/glycogen synthase kinase 3β–associated insulin signaling. The iRhom2/MAP3K7 axis is essential for iRhom2‐regulated liver steatosis. Conclusions iRhom2 may represent a therapeutic target for the treatment of HFD‐induced hepatic steatosis and insulin resistance.

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