Electroless Copper Plating on a Cotton Surface: Effect of Metal Ion Ligand Stability Constant on Reduction Deposition.

Electroless plating facilitates the metallization of nonconductive substrate surfaces, and of note, the precise control of the bath stability constant influences the deposition process of metal particles. In this paper, trisodium citrate, potassium sodium tartrate, nitrogen triacetic acid, thiourea, and ethylenediamine tetraacetic acid disodium were selected as coordination agents, and the effect of the metal ion ligand stability constant on the reduction deposition was studied. Coordination bonds can be established between the Cu2+ and O/N/S particles in the ligand because paired electrons in O/N/S hybrid orbitals tend to occupy empty Cu2+ hybrid orbitals and establish coordination bonds. More importantly, the copper-potassium sodium tartrate ligand exhibits the lowest stability constant and lowest reduction barrier. As an exception, a consecutive Cu-plated coating with an excellent crystallinity property was deposited on the cotton surface when potassium sodium tartrate was used as the coordination agent in the plating solution. The deposition amounts are 55.2% and 74.1% after 1 and 4 h of electroless copper plating, respectively. The surface resistivity of Cu-plated cotton is 0.38 Ω/cm2, and additionally, the surface resistivity ratio before and after 1000 cycles fluctuated between 0.9 and 1.1, indicating that the Cu-plated cotton exhibits outstanding flexibility. In this paper, the deposition rate can be optimized by adjusting the copper particle ligand stability constant in the plating solution, aiming to achieve optimal results.

The chromatin remodeling protein BRG1 mediates Ang II induced pro-fibrogenic response in renal fibroblasts.

AIMS: Renal fibrosis is an important pathophysiological process commonly observed in patients chronic kidney disease (CKD). Angiotensin II (Ang II) is a major risk factor for CKD in part by promoting renal fibrosis. In the present study we investigated Brahma-Related Gene 1 (BRG1, encoded by Smarca4) in Ang II induced pro-fibrogenic response in renal fibroblasts. METHODS AND MATERIALS: CKD was induced by chronic angiotensin II infusion. Fibroblast- and myofibroblast-specific BRG1 deletion was achieved by crossing the BRG1f/f mice to the Col1a1-CreERT2 mice and the Postn-CreERT2 mice, respectively. KEY FINDINGS: BRG1 expression was up-regulated when fibroblasts were exposed to Ang II in vitro and in vivo. BRG1 silencing in primary renal fibroblasts blocked transition to myofibroblasts as evidenced by down-regulation of myofibroblast marker genes and reduction in cell proliferation, migration, and contraction. Consistently, deletion of BRG1 from fibroblasts or from myofibroblasts significantly attenuated renal fibrosis in mice subjected to chronic Ang II infusion. Transcriptomic analysis indicated that BRG1 primarily regulated expression of genes involved in cell migroproliferative behavior and extracellular matrix remodeling. Importantly, administration of PFI-3, a small-molecule BRG1 inhibition, markedly ameliorated Ang II induced renal fibrosis in mice. SIGNIFICANCE: Our data support a role for BRG1 in Ang II induced fibrogenic response in renal fibroblasts and suggest that targeting BRG1 could be considered as a reasonable approach for the intervention of CKD.

Acupoint Catgut-Embedding Therapy Inhibits NF-κB/COX-2 Pathway in an Ovalbumin-Induced Mouse Model of Allergic Asthma.

Allergic asthma is associated with T helper (Th) 2 cell-biased immune responses and characterized by the airway hyperresponsiveness (AHR). Studies have shown that the acupoint catgut-embedding therapy (ACE) has a therapeutic effect on allergic asthma. However, the relevant mechanism is poorly understood. In present study, female BALB/c mice were sensitized and challenged with ovalbumin (OVA) to establish a model of allergic asthma. AHR was evaluated by using airway resistance (R L ) and lung dynamic compliance (Cdyn). Airway inflammation and mucus hypersecretion were observed by HE and PAS staining. Inflammatory cells were counted, and related cytokines in bronchoalveolar lavage fluid (BALF) were detected by enzyme-linked immunosorbent assay (ELISA). Pulmonary group 2 innate lymphoid cell (ILC2s) proportions were analyzed by flow cytometry. The expression of nuclear factor κB (NF-κB) and cyclooxygenase-2 (COX-2) was detected by immunostaining. Our results showed that OVA induction resulted in a significant increase in R L , accompanied by a significant decrease in Cdyn. The levels of interleukin- (IL-) 4, IL-13, OVA-specific IgE in BALF, and the percentage of ILC2 in the lungs were markedly increased accompanied by a significant decreased in interferon-γ (IFN-γ). Furthermore, the expressions of p-NF-κB p65 and COX-2 in airways were significantly upregulated. After ACE treatment, the indicators above were significantly reversed. In conclusion, ACE treatment inhibited the secretion of Th2 cytokines and the proliferation of ILC2s in the lungs, thereby dampening the inflammatory activity in allergic asthma. The underlying mechanism might be related to the inhibition of NF-κB/COX-2 pathway.