Printable and filament-drawable PDMS based adhesive assisted manufacturing of highly conductive copper micro-patterns.

Manufacturing of copper micro-patterns is crucial in electronics for its utilization as high conductivity transparent conductive films (TCFs) and circuits. In the preparation process of current TCFs, a plethora of materials have emerged that can replace traditional indium tin oxide (ITO). However, even for the most promising metal-based nanowire materials, there are issues such as high cost, complex welding, and high contact resistance. To address these problems, this paper proposes a printable and filament-drawable polydimethylsiloxane (PDMS)-based adhesive, which, through a novel additive patterning technology, efficiently and economically manufactures self-welding copper micro-meshes and circuits. The adhesive can be processed into micro-patterns through printing and filament drawing, on which ionic Ag can be in situ reduced and anchored, thereby eliminating the need for tedious pre- and post-treatment steps. The fully exposed Ag particles dramatically minimize the usage of precious metal catalyst, thus efficiently catalyzing electroless copper deposition (ECD) reaction. Highly conductive (1.03 × 107 S m-1) copper circuits can be fabricated on the printed adhesive patterns, exhibiting versatile applicability to diverse substrates. Highly precise copper micro-meshes (∼50 µm) can be fabricated on the filament networks drawn by the adhesive. The copper meshes undergo complete self-welding at junctions during the ECD process, thus exhibiting ultra-low square resistance of 0.45 Ω sq-1 while maintaining a high transmittance of 82.2 %. This is far superior to most of TCFs in published literature.

Fibroblast growth factor-2 alleviates the capillary leakage and inflammation in sepsis.

BACKGROUND: Acute lung injury (ALI), which is induced by numerous pathogenic factors, especially sepsis, can generate alveolar damage, pulmonary edema and vascular hyper-permeability ultimately leading to severe hypoxemia. Fibroblast growth factor-2 (FGF2) is an important member of the FGF family associated with endothelial cell migration and proliferation, and injury repairment. Here, we conducted this study aiming to evaluate the therapeutic effect of FGF2 in sepsis-induced ALI. METHODS: Recombinant FGF2 was abdominally injected into septic mice induced by cecal ligation and puncture (CLP), and then the inflammatory factors of lung tissue, vascular permeability and lung injury-related indicators based on protein levels and gene expression were detected. In vitro, human pulmonary microvascular endothelial cells (HPMEC) and mouse peritoneal macrophages (PMs) were challenged by lipopolysaccharides (LPS) with or without FGF2 administration in different groups, and then changes in inflammation indicators and cell permeability ability were tested. RESULTS: The results revealed that FGF2 treatment reduced inflammation response, attenuated pulmonary capillary leakage, alleviated lung injury and improved survival in septic mice. The endothelial injury and macrophages inflammation induced by LPS were inhibited by FGF2 administration via AKT/P38/NF-κB signaling pathways. CONCLUSION: These findings indicated a therapeutic role of FGF2 in ALI through ameliorating capillary leakage and inflammation.

Phospho-Tyr705 of STAT3 is a therapeutic target for sepsis through regulating inflammation and coagulation.

BACKGROUND: Sepsis is an infection-induced aggressive and life-threatening organ dysfunction with high morbidity and mortality worldwide. Infection-associated inflammation and coagulation promote the progression of adverse outcomes in sepsis. Here, we report that phospho-Tyr705 of STAT3 (pY-STAT3), not total STAT3, contributes to systemic inflammation and coagulopathy in sepsis. METHODS: Cecal ligation and puncture (CLP)-induced septic mice were treated with BP-1-102, Napabucasin, or vehicle control respectively and then assessed for systemic inflammation, coagulation response, lung function and survival. Human pulmonary microvascular endothelial cells (HPMECs) and Raw264.7 cells were exposed to lipopolysaccharide (LPS) with pharmacological or genetic inhibition of pY-STAT3. Cells were assessed for inflammatory and coagulant factor expression, cell function and signaling. RESULTS: Pharmacological inhibition of pY-STAT3 expression by BP-1-102 reduced the proinflammatory factors, suppressed coagulation activation, attenuated lung injury, alleviated vascular leakage and improved the survival rate in septic mice. Pharmacological or genetic inhibition of pY-STAT3 diminished LPS-induced cytokine production in macrophages and protected pulmonary endothelial cells via the IL-6/JAK2/STAT3, NF-κB and MAPK signaling pathways. Moreover, the increase in procoagulant indicators induced by sepsis such as tissue factor (TF), the thrombin-antithrombin complex (TAT) and D-Dimer were down-regulated by pY-STAT3 inhibition. CONCLUSIONS: Our results revealed a therapeutic role of pY-STAT3 in modulating the inflammatory response and defective coagulation during sepsis. Video Abstract.

Inhibition of Fibroblast Growth Factor Receptor by AZD4547 Protects Against Inflammation in Septic Mice.

Sepsis is a life-threatening condition caused by the dysregulated host immune response to infection characterized by excessive secretion of inflammatory factors. AZD4547 is a selective inhibitor of fibroblast growth factor receptors that participates in the inflammatory response. The aim of this study was to investigate the inflammation-targeting effects and related molecular mechanisms of AZD4547 in sepsis using a cecal ligation and puncture model and RAW264.7 macrophages stimulated with lipopolysaccharide. AZD4547 improved the survival of CLP mice and exhibited a robust protective function against lung damage histologically. Pretreatment with AZD4547 significantly alleviated the expression of the pro-inflammatory factors IL-1ß, IL-6, TNF-α, MMP9, and CXCL10 both in vivo and in vitro. In addition, AZD4547 suppressed the proliferative activity of macrophages in lung tissue and RAW264.7 macrophages. In addition, the LPS-induced phosphorylation of key proteins of NF-κB/MAPK/STAT3 pathways in RAW264.7 macrophages, such as p65, IκB-α, Erk1/2, JNK, and STAT3 proteins, could be inhibited by AZD4547 pretreatment. In conclusion, AZD4547 exerts a protective effect against excessive inflammatory damage in septic mice and may have the potential for use as an effective drug for the management of sepsis.