Numerical modelling of light gauge cold-formed steel compression members subjected to distortional buckling at elevated temperatures

Fire safety design of building structures has received greater attention in recent times due to continuing loss of properties and lives during fires. However, fire performance of light gauge cold-formed steel structures is not well understood despite its increased usage in buildings. Cold-formed steel compression members are susceptible to various buckling modes such as local and distortional buckling and their ultimate strength behaviour is governed by these buckling modes. Therefore a research project based on experimental and numerical studies was undertaken to investigate the distortional buckling behaviour of light gauge cold-formed steel compression members under simulated fire conditions. Lipped channel sections with and without additional lips were selected with three thicknesses of 0.6, 0.8, and 0.95 mm and both low and high strength steels (G250 and G550 steels). More than 150 compression tests were undertaken first at ambient and elevated temperatures. Finite element models of the tested compression members were then developed by including the degradation of mechanical properties with increasing temperatures. Comparison of finite element analysis and experimental results showed that the developed finite element models were capable of simulating the distortional buckling and strength behaviour at ambient and elevated temperatures up to 800 °C. The validated model was used to determine the effects of mechanical properties, geometric imperfections and residual stresses on the distortional buckling behaviour and strength of cold-formed steel columns. This paper presents the details of the numerical study and the results. It demonstrated the importance of using accurate mechanical properties at elevated temperatures in order to obtain reliable strength characteristics of cold-formed steel columns under fire conditions.

Independent cinema in the Chinese film industry

Chinese independent cinema has developed for more than twenty years. Two sorts of independent cinema exist in China. One is underground cinema, which is produced without official approvals and cannot be circulated in China, and the other are the films which are legally produced by small private film companies and circulated in the domestic film market. This sort of ‘within-system’ independent cinema has played a significant role in the development of Chinese cinema in terms of culture, economics and ideology. In contrast to the amount of comment on underground filmmaking in China, the significance of ‘within-system’ independent cinema has been underestimated by most scholars. This thesis is a study of how political management has determined the development of Chinese independent cinema and how Chinese independent cinema has developed during its various historical trajectories. This study takes media economics as the research approach, and its major methods utilise archive analysis and interviews. The thesis begins with a general review of the definition and business of American independent cinema. Then, after a literature review of Chinese independent cinema, it identifies significant gaps in previous studies and reviews issues of traditional definition and suggests a new definition. After several case studies on the changes in the most famous Chinese directors’ careers, the thesis shows that state studios and private film companies are two essential domestic backers for filmmaking in China. After that, the body of the thesis provides an examination of the development of ‘within-system’ independent cinema. Specifically, three factors: government intervention, the majors’ performance (state studios and, later, the conglomerates) and the market conduct of independent cinema at various points in their trajectories are studied. The key findings of the study are as follows: First, most scholars have overlooked the existence and the significance of within-system Chinese independent cinema. Drawing on an American definition of the independent sector, this thesis proposes a definition of the sector in China: namely, any film that has not been financed, produced, and/or distributed by majors. The thesis also notes important contradictions in applying this definition: i.e. film-making is still dependent on policies that frame industry development. The thesis recognises that major tensions apply to filmmaking in China, which significantly differentiates the Chinese independents from those in the US. Second, the development of Chinese independent cinema is the result the rise of the private sector and the decline of the state studio system. As state studios encountered difficulties the private sector moved forward; consequently the environment improved for independent cinema. Third, before 2003, the film industry in China had little commercialisation. The government controlled independent cinema by means of license and censorship. State studios produced main melody films and Hollywood attracted most of the audiences. Many independent filmmakers focused on commercial films, thus contributing to film commercialisation. Fourth, after 2003, the film industry became increasingly fragmented. The government created distribution and exhibition opportunities for main melody films; conglomerates collaborated with Hong Kong players; Hong Kong co-productions and Hollywood occupied the film market; and small private film companies produced main melody films in order to earn meagre profits. The original contribution of the thesis is to advance the study of Chinese independent cinema. The study suggests a reasonable and practical definition of Chinese independent cinema. It shows how the Chinese government authorities have implemented economic measures to gain ideological control in the film industry. Finally, this the first study on Chinese independent cinema applying a synthesis of economic, political and historical perspectives.

Intrinsically photosensitive melanopsin retinal ganglion cell contributions to the post-illumination pupil response and circadian rhythm

Intrinsically photosensitive retinal ganglion cells (ipRGCs) in the eye transmit the environmental light level, projecting to the suprachiasmatic nucleus (SCN) (Berson, Dunn & Takao, 2002; Hattar, Liao, Takao, Berson & Yau, 2002), the location of the circadian biological clock, and the olivary pretectal nucleus (OPN) of the pretectum, the start of the pupil reflex pathway (Hattar, Liao, Takao, Berson & Yau, 2002; Dacey, Liao, Peterson, Robinson, Smith, Pokorny, Yau & Gamlin, 2005). The SCN synchronizes the circadian rhythm, a cycle of biological processes coordinated to the solar day, and drives the sleep/wake cycle by controlling the release of melatonin from the pineal gland (Claustrat, Brun & Chazot, 2005). Encoded photic input from ipRGCs to the OPN also contributes to the pupil light reflex (PLR), the constriction and recovery of the pupil in response to light. IpRGCs control the post-illumination component of the PLR, the partial pupil constriction maintained for > 30 sec after a stimulus offset (Gamlin, McDougal, Pokorny, Smith, Yau & Dacey, 2007; Kankipati, Girkin & Gamlin, 2010; Markwell, Feigl & Zele, 2010). It is unknown if intrinsic ipRGC and cone-mediated inputs to ipRGCs show circadian variation in their photon-counting activity under constant illumination. If ipRGCs demonstrate circadian variation of the pupil response under constant illumination in vivo, when in vitro ipRGC activity does not (Weng, Wong & Berson, 2009), this would support central control of the ipRGC circadian activity. A preliminary experiment was conducted to determine the spectral sensitivity of the ipRGC post-illumination pupil response under the experimental conditions, confirming the successful isolation of the ipRGC response (Gamlin, et al., 2007) for the circadian experiment. In this main experiment, we demonstrate that ipRGC photon-counting activity has a circadian rhythm under constant experimental conditions, while direct rod and cone contributions to the PLR do not. Intrinsic ipRGC contributions to the post-illumination pupil response decreased 2:46 h prior to melatonin onset for our group model, with the peak ipRGC attenuation occurring 1:25 h after melatonin onset. Our results suggest a centrally controlled evening decrease in ipRGC activity, independent of environmental light, which is temporally synchronized (demonstrates a temporal phase-advanced relationship) to the SCN mediated release of melatonin. In the future the ipRGC post-illumination pupil response could be developed as a fast, non-invasive measure of circadian rhythm. This study establishes a basis for future investigation of cortical feedback mechanisms that modulate ipRGC activity.

Broadening of transgenic adenocarcinoma of the mouse prostate (TRAMP) model to represent late stage androgen depletion independent cancer

BACKGROUND The transgenic adenocarcinoma of the mouse prostate (TRAMP) model closely mimics PC-progression as it occurs in humans. However, the timing of disease incidence and progression (especially late stage) makes it logistically difficult to conduct experiments synchronously and economically. The development and characterization of androgen depletion independent (ADI) TRAMP sublines are reported. METHODS Sublines were derived from androgen-sensitive TRAMP-C1 and TRAMP-C2 cell lines by androgen deprivation in vitro and in vivo. Epithelial origin (cytokeratin) and expression of late stage biomarkers (E-cadherin and KAI-1) were evaluated using immunohistochemistry. Androgen receptor (AR) status was assessed through quantitative real time PCR, Western blotting, and immunohistochemistry. Coexpression of AR and E-cadherin was also evaluated. Clonogenicity and invasive potential were measured by soft agar and matrigel invasion assays. Proliferation/survival of sublines in response to androgen was assessed by WST-1 assay. In vivo growth of subcutaneous tumors was assessed in castrated and sham-castrated C57BL/6 mice. RESULTS The sublines were epithelial and displayed ADI in vitro and in vivo. Compared to the parental lines, these showed (1) significantly faster growth rates in vitro and in vivo independent of androgen depletion, (2) greater tumorigenic, and invasive potential in vitro. All showed substantial downregulation in expression levels of tumor suppressor, E-cadherin, and metastatis suppressor, KAI-1. Interestingly, the percentage of cells expressing AR with downregulated E-cadherin was higher in ADI cells, suggesting a possible interaction between the two pathways. CONCLUSIONS The TRAMP model now encompasses ADI sublines potentially representing different phenotypes with increased tumorigenicity and invasiveness.

Estrogen receptor-Beta activated apoptosis in benign hyperplasia and cancer of the prostate is androgen independent and TNF-alpha mediated

Prostate cancer (PCa) and benign prostatic hyperplasia (BPH) are androgen-dependent diseases commonly treated by inhibiting androgen action. However, androgen ablation or castration fail to target androgen-independent cells implicated in disease etiology and recurrence. Mechanistically different to castration, this study shows beneficial proapoptotic actions of estrogen receptor–β (ERβ) in BPH and PCa. ERβ agonist induces apoptosis in prostatic stromal, luminal and castrate-resistant basal epithelial cells of estrogen-deficient aromatase knock-out mice. This occurs via extrinsic (caspase-8) pathways, without reducing serum hormones, and perturbs the regenerative capacity of the epithelium. TNFα knock-out mice fail to respond to ERβ agonist, demonstrating the requirement for TNFα signaling. In human tissues, ERβ agonist induces apoptosis in stroma and epithelium of xenografted BPH specimens, including in the CD133+ enriched putative stem/progenitor cells isolated from BPH-1 cells in vitro. In PCa, ERβ causes apoptosis in Gleason Grade 7 xenografted tissues and androgen-independent cells lines (PC3 and DU145) via caspase-8. These data provide evidence of the beneficial effects of ERβ agonist on epithelium and stroma of BPH, as well as androgen-independent tumor cells implicated in recurrent disease. Our data are indicative of the therapeutic potential of ERβ agonist for treatment of PCa and/or BPH with or without androgen withdrawal.