Nitrogen Microplasma Generated in Chip-Based Ingroove Glow Discharge Device for Detection of Organic Fragments by Optical Emission Spectrometry

In this study, nitrogen was successfully used to maintain the microplasma discharge to excite and detect organic compounds for the first time. A new nitrogen glow discharge microplasma-generated in-chip-based ingroove device was developed and applied as the excitation source for optical emission spectrometry. The unique ingroove design of the discharge chamber can provide good stability and sensitivity for nitrogen microplasma to detect trace organic samples. Unlike argon/helium microplasmas, the nitrogen microplasma has a strict demand on the material of electrodes, especially cathodes. We tested the effects of four common electrode materials from various aspects and obtained the most appropriate material for nitrogen glow discharge, namely, platinum. We also studied the excitation and detection mechanism of organic compounds in nitrogen microplasma and confirmed that the main means of excitation in nitrogen plasma was through energy transfer rather than penning ionization. Several organic compounds were directly injected and detected in the optimized working conditions with the limits of detection at the hundreds of picograms level. Because of the portable nitrogen generators handily and commercially available, this detection system with nitrogen as the discharge gas can overcome the limitation of noble gas supply. In addition, the advantages of small size, low energy consumption, good stability, and reproducibility demonstrate that the nitrogen ingroove microplasma source can be applied in a portable detector for on-site and real-time spectrometry detection

Evolution of a Native Oxide Layer at the a‑Si:H/c-Si Interface and Its Influence on a Silicon Heterojunction Solar Cell

The interface microstructure of a silicon heterojunction (SHJ) solar cell was investigated. We found an ultrathin native oxide layer (NOL) with a thickness of several angstroms was formed on the crystalline silicon (c-Si) surface in a very short time (∼30 s) after being etched by HF solution. Although the NOL had a loose structure with defects that are detrimental for surface passivation, it acted as a barrier to restrain the epitaxial growth of hydrogenated amorphous silicon (a-Si:H) during the plasma-enhanced chemical vapor deposition (PECVD). The microstructure change of the NOL during the PECVD deposition of a-Si:H layers with different conditions and under different H₂ plasma treatments were systemically investigated in detail. When a brief H₂ plasma was applied to treat the a-Si:H layer after the PECVD deposition, interstitial oxygen and small-size SiO₂ precipitates were transformed to hydrogenated amorphous silicon suboxide alloy (a-SiO_<i>x</i>:H, <i>x</i> ∼ 1.5). In the meantime, the interface defect density was reduced by about 50%, and the parameters of the SHJ solar cell were improved due to the post H₂ plasma treatment

Data_Sheet_1_Effects of the synbiotic composed of mangiferin and Lactobacillus reuteri 1–12 on type 2 diabetes mellitus rats.docx

Many synbiotics are effective for the prevention and treatment of type 2 diabetes mellitus (T2DM). In the treatment of T2DM, synbiotics often regulate the composition of intestinal flora, which autoinducer-2 (AI-2) may play an important role. Whether the changes of intestinal flora are related to AI-2 during synbiotics treatment of T2DM is a topic worth studying. We elucidated the effects of synbiotic composed of mangiferin and Lactobacillus reuteri 1–12 (SML) on T2DM rats. Male Spraque-Dawley rats were injected intraperitoneally with streptozotocin (STZ) and randomly grouped. After that, biochemical parameters, intestinal flora, fecal AI-2, and intestinal colonization of L. reuteri were detected. The results showed that SML had a hypoglycemic effect and mitigated the organ lesions of the liver and pancreas. Also, SML regulated biochemical parameters such as short chain fatty acids (SCFAs), lipopolysaccharides (LPS), intercellular cell adhesion molecule-1 (ICAM-1), and tumor necrosis factor-α (TNF-α). On the other hand, the proportion of probiotics, such as Lactobacillus acidophilus, L. reuteri, Bifidobacterium pseudolongum, Lactobacillus murinus, and Lactobacillus johnsonii, were elevated by the treatment of SML. In addition, SML promoted the colonization and proliferation of L. reuteri in the gut. Another thing to consider was that AI-2 was positively correlated with the total number of OTUs sequences and SML boosted AI-2 in the gut. Taken together, these results supported that SML may modulate intestinal flora through AI-2 to treat T2DM. This study provided a novel alternative strategy for the treatment of T2DM in future.</p

Increased activation of Glucogenesis pathway in human fetal hepatocytes after exposure to Sirtinol.

<p>(A) Expression of hepatic PEPCK and G6PC mRNA measured by qRT- PCR in human fetal hepatocytes exposed to +50uM Sirtinol compared to controls. (B) Immunofluorescence of S-473 AKT in human fetal hepatocytes with or without 50uM Sirtinol (10x). (C) Fluorescence intensity quantification for S-473 AKT signal (arbitrary units) using ImageJ (n≥7/group; *, P < .05). (D) Western blot analysis for S-473 AKT/AKT, S-256 FOXO1/FOXO1 in human fetal hepatocytes exposed to 50uM Sirtinol compared to controls. GAPDH was used as a loading control. (E) Immunofluorescence staining of S-256 FOXO1 in human fetal hepatocytes with or without 50uM Sirtinol (20x).</p

Expression of SIRT1 in human fetal and adult liver and isolated hepatocytes.

<p>(A) Immunohistochemistry of SIRT1 in human fetal and adult liver, (B) Immunofluorescence staining of SIRT1 in fetal and adult hepatocytes after 2 days of culture. (C) Quantification of hepatic SIRT1 mRNA expression measured by qRT- PCR in human fetal and adult hepatocytes in vitro and in vivo (n≥3/group).</p

Expression of SIRT1 in human fetal and adult liver and isolated hepatocytes.

<p>(A) Immunohistochemistry of SIRT1 in human fetal and adult liver, (B) Immunofluorescence staining of SIRT1 in fetal and adult hepatocytes after 2 days of culture. (C) Quantification of hepatic SIRT1 mRNA expression measured by qRT- PCR in human fetal and adult hepatocytes in vitro and in vivo (n≥3/group).</p

Donor Demographics.

<p>Donor Demographics.</p

Lipids and glucose levels in human fetal hepatocytes after Sirt1 inhibition.

<p>(A) Fluorescent staining of lipids (red droplets, white arrow) inside human fetal hepatocytes (HFH) with or without 50uM Sirtinol for 3 days (20x). (B) Triglycerides quantification of human fetal hepatocytes with or without +50uM Sirtinol for 3 days analyzed by a colorimetric assay. (C) Glucose concentration between normal HFH and HFH +50uM Sirtinol for 3 days. (n≥7/group; *, P < .05).</p

Representation of SIRT1 regulation of lipid and glucose balances in human fetal hepatocytes.

<p>In normal conditions, SIRT1 inhibits De Novo Lipogenesis and Gluconeogenesis through the AKT/FOXO1 pathway inside human fetal hepatocytes, keeping a normal balance inside the cells. Upon SIRT1 inhibition, both the lipid and glucose balance will be disrupted, leading to an increase of lipid and carbohydrates levels in human fetal hepatocytes.</p