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A typical nitrogen expanded austenite layer is formed by plasma-based low-energy nitrogen ion implantation (PBLEII) on AISI 304L austenitic stainless steel at a moderate temperature of 380 °C. The dislocation self-organization structure in the nitrogen expanded austenite layer is characterized as an evolution from partial and Lomer-Cottrell dislocations in the inner layer near the interface to multilayer stacking faults in the outer nitrided layer. The self-organized dislocation density and forms are essentially dependent on the plastic deformation, strain-gradient, and nitrogen-related stacking fault energies, respectively, due to the constrained expansion in the nitrided layer. As the nitrogen concentration in the austenitic matrix increases, the stacking fault energy gradually decreases, resulting in the transformation of the defect from Lamer-Cottrell dislocations to multilayer stacking faults. The appropriate stress, which is associated with orderly stress relief during dislocation self-organization, preserves the integrity of the nitrided layer with a combinedly improved in wear and corrosion resistance. Nitriding-induced dislocation self-organization is basically explored as the formation mechanism of the nitrogen expanded austenite layer, contributing to the development of the specific low-temperature nitriding austenitic steel.

Elongated superstructure diffraction spots were observed in perfect nitrogen-expanded austenite without stress or plastic strain, which was prepared by plasma-based low-energy nitrogen-ion implanting Fe-Cr-Ni austenitic alloy foils at low temperature of 380 °C. The Fe _4 N-like ordered nitrogen-expanded austenite ( γ ′ _N ) antiphase domains formed in the disordered nitrogen-expanded austenite ( γ _N ) matrix. Only the high Cr-content alloys presented elongated diffraction spots. The reconstruction of the diffraction spots strength distribution shows an elongated egg-shape in reciprocal space. This elongation corresponded to a pancake-like antiphase domains distribution in matrix, which was confirmed in dark field images as a lamellar structural feature. The Cr-N short-range ordering (SRO) and anisotropic elastic module rather than the constrained strain in the γ _N phase layer determine the formation of γ ′ _N antiphase domains.

Chlamydia trachomatis is an obligate intracellular bacterial pathogen that causes several significant human infectious diseases, including trachoma, urethritis, cervicitis and salpingitis, and is an important cofactor for transmission of human immunodeficiency virus. Until very recently, over three decades of research effort aimed at developing a C trachomatis vaccine had failed, due mainly to the lack of a precise understanding of the mechanisms for protective immunity. Although most studies concerning protective immunity to C trachomatis have focused on humoral immune responses, recent studies have clearly shown that T helper-1 (Th1)-like CD4 T cell-mediated immune responses play the dominant role in protective immunity. These studies suggest a paradigm for chlamydial immunity and pathology based on the concept of heterogeneity (Th1/Th2) in CD4 T cell immune responses. This concept for chlamydial immunity offers a rational template on which to base renewed efforts for development of a chlamydial vaccine that targets the induction of cell-mediated Th1 immune responses.

Improved cookstoves and fuels, such as advanced gasifier stoves, carry the promise of improving health outcomes, preserving local environments, and reducing climate-forcing air pollutants. However, low adoption and use of these stoves in many settings has limited their benefits. We aimed to improve the understanding of improved stove use by describing the patterns and predictors of adoption of a semi-gasifier stove and processed biomass fuel intervention in southwestern China. Of 113 intervention homes interviewed, 79% of homes tried the stove, and the majority of these (92%) continued using it 5–10 months later. One to five months after intervention, the average proportion of days that the semi-gasifier stove was in use was modest (40.4% [95% CI 34.3–46.6]), and further declined over 13 months. Homes that received the stove in the first batch used it more frequently (67.2% [95% CI 42.1−92.3] days in use) than homes that received it in the second batch (29.3% [95% CI 13.8−44.5] days in use), likely because of stove quality and user training. Household stove use was positively associated with reported cooking needs and negatively associated with age of the main cook, household socioeconomic status, and the availability of substitute cleaner-burning stoves. Our results show that even a carefully engineered, multi-purpose semi-gasifier stove and fuel intervention contributed modestly to overall household energy use in rural China.

OBJECTIVE: Black seed oil (BSO) is widely used as a traditional medicine for asthma and other inflammatory diseases. The aim of this study is to evaluate the effects of BSO on ovalbumin (OVA) induced acute lung remodelling in E3 inbred rats. METHOD:Rats were divided into three groups; Control, OVA and BSO. The rats were intraperitoneally sensitised and challenged intranasally with OVA and treated intraperitoneally with pure BSO for seven days. The collagen deposition and other pathological alteration were determined by Masson’s trichrome, PAS and HE staining. Activity of arginase, ornithine decarboxylase (ODC) and proline level was determined by spectrophotometry, and polyamine by HPLC. The mRNA expression of arginase І, endothelin1 (Edn1), matrix metallopeptidase 3 (MMP3) and growth factors was determined by real time RT-PCR. RESULTS: Massive inflammation and characteristics of lung remodelling including collagen deposition, goblet cell hyperplasia and proline level were observed in the lungs of OVA exposed rats. Administration of BSO in the OVA exposed rats suppressed the inflammatory cells infiltration, goblet cell hyperplasia and collagen deposition. The activity of total arginase and ODC; proline and polyamine level was decreased in the lung homogenate of BSO treated rats. Furthermore, BSO abrogated the mRNA expression of Edn1, MMP3, transforming growth factor beta (TGF-β), fibroblast growth factor 2 (FGF2) and vascular epidermal growth factor (VEGF) in the lungs of OVA challenged rats. CONCLUSION: Administration of BSO significantly reduced the level of allergen induced lung remodelling. The effect of BSO on lung remodelling is probably mediated by the inhibition of arginase pathways and the expression of Edn1, MMP3 and growth factors. Our findings suggest that BSO might have useful implications in the treatment and future research into allergen-induced lung remodelling.