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In order to improve the surface performance of PCB epoxy resin board for sensor, sodium hypophosphate system was used for vacuum evaporation copper plating on its surface. Sodium benzenesulfonate SBS and polyethylenimine PEI were selected as additives to analyze their influence on the performance of copper plating layer, and the suitable additives for vacuum evaporation copper plating process were obtained. Results showed that the optimal content of PEI was 16～28 mg/L, that of SBS was 54～62 mg/L, and the vacuum evaporation copper plating temperature was 40～50 ℃ under the condition of continuous deposition of copper for 0.5 h at 65 ℃, based on the deposition rate and plate color. Copper was precipitated from the plating solution at approximately 20 min, and the vacuum evaporation copper plating solution with combined additives had the longest duration and showed the optimal stability. With additives, the coating had better microstructure and particle size became finer, and the number of holes decreased significantly, resulting in a denser structure and a smoother grain shape. The coating prepared by the combined additive had smaller porosity and better performance than that prepared by the single additive.

In recent years, there has been a growing interest in pure organic materials with ultralong room temperature phosphorescence (RTP) and afterglow duration time (tag) in the range of second level. However, it is extremely difficult to achieve tag >60 s in the polymer fields. Herein, this work proposes a highly versatile ultrasound‐synchronized B‐O‐Click strategy that can firmly immobilize various types of polycyclic aromatic boronic acids (PABAs) as single‐molecular states in a tight and rigid matrix of poly(vinyl alcohol) (PVA), achieving a series of record‐breaking ultralong afterglow polymeric RTP materials. Based on this approach, a polymeric material is reported exhibiting a record‐breaking tag = 130 s, accompanied with an ultralong lifetime of 7.24 s and a good phosphorescence efficiency of 14.26%. Three other polymeric materials with tag over 60 s are also realized via the same strategy by changing the phosphor. In addition, record‐breaking ultralong green (tag = 115 s) and red (tag = 80 s) afterglow are further achieved based on the phosphorescence resonance energy transfer (PRET) effect. [ABSTRACT FROM AUTHOR]

Liver fibrosis is a disease largely driven by resident and recruited macrophages. The phenotypic switch of hepatic macrophages can be achieved by chemo-attractants and cytokines. During a screening of plants traditionally used to treat liver diseases in China, paeoniflorin was identified as a potential drug that affects the polarization of macrophages. The aim of this study was to evaluate the therapeutic effects of paeoniflorin in an animal model of liver fibrosis and explore its underlying mechanisms. Liver fibrosis was induced in Wistar rats via an intraperitoneal injection of CCl4. In addition, the RAW264.7 macrophages were cultured in the presence of CoCl2 to simulate a hypoxic microenvironment of fibrotic livers in vitro. The modeled rats were treated daily with either paeoniflorin (100, 150, and 200 mg/kg) or YC-1 (2 mg/kg) for 8 weeks. Hepatic function, inflammation and fibrosis, activation of hepatic stellate cells (HSC), and extracellular matrix (ECM) deposition were assessed in the in vivo and in vitro models. The expression levels of M1 and M2 macrophage markers and the NF- κ B/HIF-1 α pathway factors were measured using standard assays. Paeoniflorin significantly alleviated hepatic inflammation and fibrosis, as well as hepatocyte necrosis in the CCl4-induced fibrosis model. Furthermore, paeoniflorin also inhibited HSC activation and reduced ECM deposition both in vivo and in vitro. Mechanistically, paeoniflorin restrained M1 macrophage polarization and induced M2 polarization in the fibrotic liver tissues as well as in the RAW264.7 cells grown under hypoxic conditions by inactivating the NF- κ B/HIF-1 α signaling pathway. In conclusion, paeoniflorin exerts its anti-inflammatory and anti-fibrotic effects in the liver by coordinating macrophage polarization through the NF- κ B/HIF-1 α pathway. [ABSTRACT FROM AUTHOR]

The structures, stabilities and electronic properties of Cu n Na ( n = 1–8) clusters have been systematically investigated by using density-functional approach. According to optimized doped clusters, growth behaviors are organized as follows: Na added Cu n clusters or Na substituted Cu n +1 clusters as well as Cu added Cu n −1 Na clusters. The calculated averaged binding energies, fragmentation energies, and second-order difference of energies exhibit a pronounced even–odd alternation phenomenon as a function of the cluster size. Electronic properties of doped clusters are studied by calculating the HOMO–LUMO gaps, the contour maps of HOMOS and electrostatic potential. At last, the molecular orbitals, VIP, VEA and chemical hardness are also analyzed. [ABSTRACT FROM AUTHOR]

The geometric stability, electronic structure and magnetic properties of the Pt4clusters on graphene substrates are investigated using the first-principles methods. It is found that the Pt4clusters on the defective graphene with a single vacancy defect (SV-graphene) have larger binding energies than that on the pristine graphene. The different position of SV sites can modulate the geometric stability of Pt4clusters. The Pt4clusters provide more transferred electrons to the SV-graphene and exhibit the positively charged, which helps to weaken the CO adsorption. The results would be important for understanding that the adsorption behavior of metal clusters on graphene. [ABSTRACT FROM PUBLISHER]

Liver fibrosis is a disease largely driven by resident and recruited macrophages. The phenotypic switch of hepatic macrophages can be achieved by chemo-attractants and cytokines. During a screening of plants traditionally used to treat liver diseases in China, paeoniflorin was identified as a potential drug that affects the polarization of macrophages. The aim of this study was to evaluate the therapeutic effects of paeoniflorin in an animal model of liver fibrosis and explore its underlying mechanisms. Liver fibrosis was induced in Wistar rats via an intraperitoneal injection of CCl 4 . In addition, the RAW264.7 macrophages were cultured in the presence of CoCl 2 to simulate a hypoxic microenvironment of fibrotic livers in vitro . The modeled rats were treated daily with either paeoniflorin (100, 150, and 200[Formula: see text]mg/kg) or YC-1 (2[Formula: see text]mg/kg) for 8 weeks. Hepatic function, inflammation and fibrosis, activation of hepatic stellate cells (HSC), and extracellular matrix (ECM) deposition were assessed in the in vivo and in vitro models. The expression levels of M1 and M2 macrophage markers and the NF-[Formula: see text]B/HIF-1[Formula: see text] pathway factors were measured using standard assays. Paeoniflorin significantly alleviated hepatic inflammation and fibrosis, as well as hepatocyte necrosis in the CCl 4 -induced fibrosis model. Furthermore, paeoniflorin also inhibited HSC activation and reduced ECM deposition both in vivo and in vitro . Mechanistically, paeoniflorin restrained M1 macrophage polarization and induced M2 polarization in the fibrotic liver tissues as well as in the RAW264.7 cells grown under hypoxic conditions by inactivating the NF-[Formula: see text]B/HIF-1[Formula: see text] signaling pathway. In conclusion, paeoniflorin exerts its anti-inflammatory and anti-fibrotic effects in the liver by coordinating macrophage polarization through the NF-[Formula: see text]B/HIF-1[Formula: see text] pathway.

High-fat diet (HFD) has been associated with neuroinflammation and apoptosis in distinct brain regions. To explore the effect of short-term (7, 14 and 21 days) high-fat overfeeding on apoptosis, inflammatory signaling proteins, APP changes and glial cell activities in cerebral cortex and cerebellum. Mice were fed with HFD for different lengths (up to 21 days) and after each time body weights of mice was tested, then the apoptotic proteins, IL-1β, APP, BACE1and MAPKs, Akt and NF-κB signaling activity were evaluated by western blots. Results demonstrate that short period of high-fat overnutrition significantly promotes apoptosis, APP expression at day 21 of cerebral cortex and at day 7 of cerebellum compared to chow diet. In addition, increased GFAP + astrocytes, Iba-1 + microglia and IL-1β 30 were observed in cerebral cortex after 21 days HFD, but no changes for 7 days overfeeding of cerebellum. Serendipitously, ERK1/2 pathway was activated both in cerebral cortex and cerebellum for different time course of HFD. Furthermore, increased phospho-p38 MAPK level was observed in cerebellum only. In consistent with in vivo results, SH-SY5Y cells treatment with cholesterol (50 μM, 100 μM) for 48 h culture in vitro demonstrated that pro-apoptotic proteins were enhanced as well. In brief, short-term HFD consumption increases sensitivity to apoptosis, APP and IL-1β production as well as gliosis in cerebral cortex and cerebellum, which may be related to enhancement of ERK1/2 and p38 MAPK activation.