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Flax and jute fibres are inexpensive and easily available bast fibres and they are extensively used as reinforcement in polymer matrix composites. However, due to their susceptibility to moisture absorption, their application is restricted to non-structural interior products. In this study, flax- and jute fibre-reinforced bioresin-based epoxy biocomposites were fabricated using hand lay-up method and their nanoindentation and flexural properties were investigated. In order to study the effects of water absorption on the nanoindentation and flexural properties, the biocomposites were subjected to water immersion tests by immersing specimens in a de-ionised water bath at 25℃ for a period of 961 h. The nanoindentation behaviour and flexural properties of water-immersed specimens were evaluated and compared alongside with dry specimens. The percentage of moisture uptake and diffusion coefficient (D) was recorded higher for jute-reinforced specimens compared with flax. The flexural properties for both types of specimens were found to decrease with increase in percentage moisture uptake. Comparison of flexural strength and flexural modulus between flax dry and flax wet biocomposites showed that wet samples lost almost 40% of strength and 69% of modulus compared with dry flax samples. The jute wet samples lost 60% of strength and 80% of modulus compared with dry samples. The nanohardness value decreased from 0.207 to 0.135 GPa for dry flax sample after immersion in water. [ABSTRACT FROM AUTHOR]

Oral Diseases (2012) 19, 80-84 Objective: To determine the role of cigarette filter on the incidence risk of oral squamous cell cancer among male smokers in a Chinese population. Subjects and Methods: A multicentric hospital-based case-control study was applied. Three hundred and nineteen male cases and 428 male controls matching for age (±3 years) were identified from January 2008 to December 2010. Detailed smoking histories were obtained by interviews. Logistic regression model was used to compare the influence of filter and non-filter cigarettes on oral cancer risk. Results: The adjusted odd ratios (ORs) for oral cancer were 1.30 (95% CI 1.15, 1.48) of filter cigarette smokers, 2.06 (95% CI 1.17, 3.62) of non-filter cigarette smokers, and 1.73 (95% CI 1.33, 2.25) of mixed smokers, as compared with non-smokers. When classified current smokers according to smoking pack year, the ORs of mixed smokers were 2.27 (95% CI 1.06, 4.85) in <20 pack year, 0.81 (95% CI 0.57, 1.14) in 20-39 pack year, and 0.86 (95% CI 0.57, 1.29) in ≥40 pack year, as compared to filter cigarette smokers. Conclusions: The protective effect against oral cancer of cigarette filter was limited, restricted to smokers of small amount of smoking accumulation. For most smokers, the difference was non-significant between filter and non-filter cigarettes on the risk of developing oral cancer. [ABSTRACT FROM AUTHOR]

In our previous study, we established an in vitro cellular carcinogenesis model of oral squamous cell carcinoma (OSCC), including a human immortalized oral epithelial cell (HIOEC) and a cancerous cell line (HB96). Microarray analysis showed that the gene encoding Yes-associated protein (YAP) was significantly increased in HB96 cells compared with HIOEC cells. But the underlying mechanism of YAP on oncogenesis, especially its downstream targets, are still not clear. YAP expression in OSCC cell lines and tissue specimens were investigated by using real-time PCR, western blotting and immunohistochemistry staining. YAP put-back plasmid with four mutation sites after YAP-siRNA interference was constructed by site-directed mutagenesis. Cell growth and colony formation were observed after YAP-siRNA interference or YAP put-back again in CAL27 cells. YAP expression was increased in the cellular carcinogenesis models and the clinical samples from primary OSCC patients. Inhibition of YAP by siRNA interference in CAL27 cells significantly inhibited cell proliferation and colony formation in soft agar, but these abilities were rescued when YAP was put-back again. At the same time, Fos Related Activator-1 (Fra-1) was down-regulated when YAP was inhibited by siRNA interference while Fra-1 was rescued when YAP was put-back again. Immunohistochemistry results also indicated that higher levels of YAP were significantly associated with Fra-1 overexpression in OSCC clinical samples. YAP could promote cell proliferation by activating transcription factor Fra-1 in oral squamous cell carcinoma. [ABSTRACT FROM AUTHOR]

Objective: In humans, multiple genes in the interleukin (IL)-2/IL-2 receptor (IL-2R) pathway are associated with type 1 diabetes. However, no link between IL-2 responsiveness and CD4(+)CD25(+)FOXP3(+) regulatory T-cells (Tregs) has been demonstrated in type 1 diabetic subjects despite the role of these IL-2-dependent cells in controlling autoimmunity. Here, we address whether altered IL-2 responsiveness impacts persistence of FOXP3 expression in Tregs of type 1 diabetic subjects.Research Design and Methods: Persistence of Tregs was assessed by culturing sorted CD4(+)CD25(hi) natural Tregs with IL-2 and measuring FOXP3 expression over time by flow cytometry for control and type 1 diabetic populations. The effects of IL-2 on FOXP3 induction were assessed 48 h after activation of CD4(+)CD25(-) T-cells with anti-CD3 antibody. Cytokine receptor expression and signaling upon exposure to IL-2, IL-7, and IL-15 were determined by flow cytometry and Western blot analysis.Results: Maintenance of FOXP3 expression in CD4(+)CD25(+) Tregs of type 1 diabetic subjects was diminished in the presence of IL-2, but not IL-7. Impaired responsiveness was not linked to altered expression of the IL-2R complex. Instead, IL-2R signaling was reduced in Tregs and total CD4(+) T-cells of type 1 diabetic subjects. In some individuals, decreased signal transducer and activator of transcription 5 phosphorylation correlated with significantly higher expression of protein tyrosine phosphatase N2, a negative regulator of IL-2R signaling.Conclusions: Aberrant IL-2R signaling in CD4(+) T-cells of type 1 diabetic subjects contributes to decreased persistence of FOXP3 expression that may impact establishment of tolerance. These findings suggest novel targets for treatment of type 1 diabetes within the IL-2R pathway and suggest that an altered IL-2R signaling signature may be a biomarker for type 1 diabetes. [ABSTRACT FROM AUTHOR]

Purpose: To investigate the estrogenic protective effect and mechanism of Tanshinone IIA on oxidative-injured vascular endothelial cells.Methods: We established low-estrogen atherosclerotic animal model by feeding ovariectomized apoE-/- mice a high-fat diet, and oxidative-injured cells model were induced by ox-LDL in HUVECs. Tanshinone IIA ( mice: 30mg/kg, 60mg/kg, cells: 0.1μM, 1μM, 10μM) was given to the mice and cells, and estrogen(mice: 0.00013mg/g/d, cells: 0.01μM) and estrogen receptor antagonist(ICI182780, mice: 0.065mg/g, cells: 0.1μM) were also designed to be given. The levels of NF-κB, sICAM-1, AP-1, E-selectin and 17β-estradiol (E2) in serum and the levels of NF-κB, sICAM-1, AP-1 and E-selectin in supernatant were measured by ELISA. The expression of p-ERK1/2 in cells and mice aorta and expression of ERα in cells were assessed by Western blotting.Results:Tanshinone IIA could not significantly increase the serum E2 level of ovariectomized apoE-/- mice. But it significantly inhibited the levels of NF-κB, AP-1, sICAM-1 and E-selectin in serum of ovariectomized ApoE-/- mice and supernatant of ox-LDL injured HUVECs, and Tanshinone IIA significatly inhibited the expression of p-ERK1/2 in mice aorta and cells and inhibited the expression of ERα in cells, which was similar to the estradiol, and could be inhibited by ICI182780.Conclusios: Tanshinone IIA has an anti-inflammatory effect on oxidative-injured cells, and the mechanism is that Tanshinone IIA could significantly attenuate the p-ERK1/2 to inhibit the mitogen-activated protein kinase (MAPK) signaling pathway by bonding with estrogen receptor, which is similar to the estrogen.Effect of Tanshinone IIA on p-ERK1/2 [ABSTRACT FROM AUTHOR]

Background: Nuclear factor-kappa B (NF-kappaB) signaling constitutes a key event in the multistep process of carcinogenesis, progression and treatment in many cancer types. However, the significance of NF-kappaB pathway for complex and tissue-specific aspects of head and neck cancer progression, such as invasion and metastasis, is less understood.Methods: The expression of NF-kappaB p65 in squamous cell carcinoma of the head and neck (SCCHN) clinical specimens by immunohistochemistry. The role of NF-kappaB activity in head and neck squamous cell carcinoma was determined by western blot, reporter assay and EMSA analysis in vitro and metastasis assays in vivo in different metastatic potential tumor cells. Furthermore, the apoptosis rate and expression of metastasis-related protein such as MMP9 and VEGF were examined by Annexin V/PI staining and Western blot, respectively.Results: A higher level of active nuclear-localized NF-kappaB was observed in the metastatic SCCHN specimens group (p < 0.01). The NF-kappaB activities of SCCHN cell lines with different metastatic potentials were then determined and in excellent agreement with results found in SCCHN specimens, highly metastatic SCCHN cell lines expressed high level of NF-kappaB activity. The treatment of highly metastatic SCCHN cells with NF-kappaB inhibitors reduced the in vitro cell invasion capacity of the cells without affecting the apoptotic rate. Additionally, the NF-kappaB inhibitors significantly inhibited the experimental lung metastasis of Tb cells and lymph node metastasis of TL cells in nude mice. Furthermore, the expression of metastasis-related proteins, such as matrix metalloproteinase 9 and vascular endothelial growth factor, was inhibited by pyrrolidine dithiocarbonate.Conclusions: This study suggests that NF-kappaB activity significantly contributes to tumor hematologic and lymphatic metastases and may aid in the development of early detection methods or therapies targeting non-conventional molecular targets. [ABSTRACT FROM AUTHOR]