Diffusion Bonding of Al-Mg-Si Alloy and 301L Stainless Steel by Friction Stir Lap Welding Using a Zn Interlayer.

Friction stir lap welding (FSLW) is expected to join the hybrid structure of aluminum alloy and steel. In this study, the Al-Mg-Si aluminum alloy and 301L stainless steel were diffusion bonded by FSLDW with the addition of 0.1 mm thick pure Zn interlayer, when the tool pin did not penetrate the upper aluminum sheet. The characteristics of lap interface and mechanical properties of the joint were analyzed. Under the addition of Zn interlayer, the diffusion layer structure at lap interface changed from continuous to uneven and segmented. The components of the diffusion layer were more complex, including Fe-Al intermetallic compounds (IMCs), Fe-Zn IMCs and Al-Zn eutectic. The largely changed composition and thickness of uneven and segmented diffusion layer at the lap interface played a significant role in the joint strength. The tensile shear load of Zn-added joint was 6.26 kN, increasing by 41.3% than that of Zn-not-added joint. These two joints exhibited interfacial shear fracture, while the Zn interlayer enhanced the strength of diffusion bonding by extending the propagation path of cracks.

Effects of Concentration and Spin Speed on the Optical and Electrical Properties of Silver Nanowire Transparent Electrodes.

In this paper, silver nanowires (AgNWs) with a diameter of 40 nm and a length of 45 µm were dispersed into an ethanol solution to prepare AgNW solutions with concentrations of 1, 2, and 3 mg/mL, respectively. The AgNW solutions were then deposited on a glass substrate using spin-coating at 1000, 2000, and 3000 rpm for 45 s, respectively, to prepare transparent electrodes. The results showed that the distribution of AgNWs on the substrate increased in density with the increase in the AgNW solution concentration and the decrease in spin speed. The effect of concentration on the distribution of AgNWs was greater than that of the spin speed. The transmittance of each electrode was between 84.19% and 88.12% at 550 nm, the average sheet resistance was between 20.09 and 358.11 Ω/sq, the highest figure of merit (FoM) was 104.42, and the lowest haze value was 1.48%. The electrode prepared at 1000 rpm with a concentration of 2 mg/mL and that prepared at 3000 rpm with a concentration of 3 mg/mL were very similar in terms of the average sheet resistance, transmittance at 550 nm, FoM, and haze value; thus, these two electrodes could be considered equivalent. The haze value of the electrode was positively correlated with the spin speed at low concentration, but that relationship became inverse as the concentration rose. For the AgNWs used in this experiment with an aspect ratio of 1125, the concentration of the AgNW solution should reach at least 2 mg/mL to ensure that the FoM of the electrode is greater than 35.

Increasing TRPV4 expression restores flow-induced dilation impaired in mesenteric arteries with aging.

The flow-stimulated intracellular Ca(2+) concentration ([Ca(2+)]i) rise in endothelial cells is an important early event leading to flow-induced blood vessel dilation. Transient receptor potential vanilloid subtype 4 (TRPV4), a Ca(2+)-permeable cation channel, facilitates the flow-stimulated [Ca(2+)]i rise. To determine whether TRPV4 is involved in age-related flow-induced blood vessel dilation impairment, we measured blood vessel diameter and nitric oxide (NO) levels and performed Ca(2+) imaging, immunoblotting, and immunostaining assays in rats. We found that the flow-induced and TRPV4 activator 4α-PDD-induced dilation of mesenteric arteries from aged rats were significantly decreased compared with those from young rats. The flow- or 4α-PDD-induced [Ca(2+)]i rise was also markedly reduced in primary cultured mesenteric artery endothelial cells (MAECs) from aged rats. Immunoblotting and immunostaining results showed an age-related decrease of TRPV4 expression levels in MAECs. Additionally, the 4α-PDD-induced NO production was significantly reduced in aged MAECs. Compared with lentiviral GFP-treated aged rats, lentiviral vector delivery of TRPV4 increased TRPV4 expression level in aged MAECs and restored the flow- and 4α-PDD-induced vessel dilation in aged mesenteric arteries. We concluded that impaired TRPV4-mediated Ca(2+) signaling causes endothelial dysfunction and that TRPV4 is a potential target for clinical treatment of age-related vascular system diseases.

Properties of lewis lung carcinoma cells surviving curcumin toxicity.

The anti-inflammatory agent curcumin can selectively eliminate malignant rather than normal cells. The present study examined the effects of curcumin on the Lewis lung carcinoma (LLC) cell line and characterized a subpopulation surviving curcumin treatments. Cell density was measured after curcumin was applied at concentrations between 10 and 60 µM for 30 hours. Because of the high cell loss at 60 µM, this dose was chosen to select for surviving cells that were then used to establish a new cell line. The resulting line had approximately 20% slower growth than the original LLC cell line and based on ELISA contained less of two markers, NF-κB and ALDH1A, used to identify more aggressive cancer cells. We also injected cells from the original and surviving lines subcutaneously into syngeneic C57BL/6 mice and monitored tumor development over three weeks and found that the curcumin surviving-line remained tumorigenic. Because curcumin has been reported to kill cancer cells more effectively when administered with light, we examined this as a possible way of enhancing the efficacy of curcumin against LLC cells. When LLC cells were exposed to curcumin and light from a fluorescent lamp source, cell loss caused by 20 µM curcumin was enhanced by about 50%, supporting a therapeutic use of curcumin in combination with white light. This study is the first to characterize a curcumin-surviving subpopulation among lung cancer cells. It shows that curcumin at a high concentration either selects for an intrinsically less aggressive cell subpopulation or generates these cells. The findings further support a role for curcumin as an adjunct to traditional chemical or radiation therapy of lung and other cancers.

Neutralization of chemokine CXCL14 (BRAK) expression reduces CCl4 induced liver injury and steatosis in mice.

Using mouse gene expression microarray analysis, we earlier obtained dynamic profiles of whole genome expression in the CCl(4)-induced liver injury mouse model. CXCL14 expression was increased in the liver injury phase and returned to normal after liver regeneration suggesting its involvement in the liver injury or regeneration regulation. The role of CXCL14 in liver injury was investigated. The dynamic of CXCL14 transcription was analyzed in CCl(4)-induced mouse liver damage by qRT-PCR. Plasmid mediated CXCL14 overexpression and antibody neutralization of endogenous CXCL14 were used to demonstrate its effects and mechanisms on CCl(4)-induced liver injury and acute liver failure. We showed that CXCL14 expression was immediately upregulated post CCl(4) injection with a dose-dependent response. CXCL14 over-expression aggravated CCl(4)-induced liver injuries, evidenced by enhanced acidophilic change and necrosis of hepatocyte, increased fat deposition in hepatocytes (P<0.01), and inhibited hepatocyte proliferation (P<0.01). On the contrary, anti-CXCL14 antibody treatment reduced the severity of CCL4-induced liver injuries Significant reductions in hepatic necrosis area (P<0.05), the liver fat deposition (P<0.01), and the lipid peroxidation measured by serum MDA (P<0.05) were observed. Importantly, the antibody treatment reduced the mouse mortality caused by CCl4-induced liver failure (P<0.05). The data suggest that CXCL14 and its receptor present potential targets for the treatment of liver diseases.

rhIL-1Ra reduces hepatocellular apoptosis in mice with acetaminophen-induced acute liver failure.

Acute liver failure (ALF) is a life-threatening disease that has proven difficult to cure. In Western countries, acetaminophen (APAP) poisoning is the most common cause of ALF. However, the mode of cell death in APAP-induced ALF cases is controversial. Previous studies have shown that administration of anti-interleukin-1 (anti-IL-1) antibody attenuated APAP-induced liver injury, and that administration of anti-IL-1 receptor antagonist (anti-IL-1Ra) antibody exacerbated organ injury. These results prompted us to investigate the roles of IL-1Ra in APAP-induced ALF mice. Our results show that administration of recombinant human IL-1Ra (rhIL-1Ra) could significantly improve the survival rate of mice with ALF induced by APAP. Furthermore, we found that rhIL-1Ras could dramatically inhibit the activities of alanine aminotransferase and aspartate aminotransferase in serum, reduce the death of hepatocytes and accelerate the proliferation of hepatocytes. In addition, we show that hepatocellular apoptosis rather than necrosis was the major cause of ALF-induced animal death, and that the anti-apoptosis role of rhIL-1Ra was mediated by reducing the release of cytochrome c from the mitochondria, and the activities of caspase-3, caspase-8 and caspase-9 in the liver tissue. In conclusion, these data indicate that rhIL-1Ra is a promising candidate for the treatment of APAP-induced ALF in mice through the reduction of hepatocellular apoptosis.