Purpose -There has been a growing attention to building information modeling (BIM) globally due to its benefits to various stages of a building's life cycle. To facilitate the implementation of BIM in the construction industry effectively, the purpose of this paper is to gain a better understanding of the mechanism for BIM adoption by practitioners such as architects. Design/methodology/approach -A questionnaire survey of architects is conducted in Shenzhen, China. A structural equation model is built with survey data to identify the key factors affecting architects' BIM adoption in the design firms. Findings -It is found that motivation, technical defects of BIM and BIM capability are the statistically significant factors affecting architects' BIM adoption whereas management support and knowledge structure are not. Research limitations/implications -Only one architectural, engineering and construction (AEC) profession, i.e. architects were selected as research participants. In future, other professions such as construction engineers, project managers, etc. should be investigated with respect to their BIM adoption issues. Practical implications -BIM technology developers should improve the technology along the objectives of economic benefits, effectiveness and efficiency of BIM adoption. The compatibility and integration between BIM and other widely available software in the industry should also be improved. Moreover, AEC company and project managers should provide architects with opportunities of BIM training so that architects are more likely to apply BIM in future projects. Originality/value -A quantitative theoretical model, i.e. structural equation model is built to identify key factors affecting architects' BIM adoption, which takes one step further to reveal the BIM adoption mechanism in contrast to previous descriptive-oriented studies.

Background: A study was conducted to evaluate the effect of the empirical use of fluoroquinolones on the timing of antituberculous treatment and the outcome of patients with tuberculosis in an endemic area. Methods: All patients with culture confirmed tuberculosis aged >14 years diagnosed between July 2002 and December 2003 were included and their medical records were reviewed. Results: Seventy nine (14.4%) of the 548 tuberculosis patients identified received a fluoroquinolone (FQ group), 218 received a non-fluoroquinolone antibiotic (AB group), and 251 received no antibiotics before antituberculous treatment. Fifty two (65.8%) experienced clinical improvement after fluoroquinolone use. In the FQ group the median interval from the initial visit to starting antituberculous treatment was longer than in the AB group and in those who received no antibiotics (41 v 16 v 7 days), and the prognosis was worse (hazard ratio 6.88 (95% CI 1.84 to 25.72)). More patients in the FQ and AB groups were aged .65 years (53.2% and 61.0% v 31.5%), had underlying disease (53.2% and 46.8% v 34.3%), and were hypoalbuminaemic (67.2% and 64.9% v 35.1%). Of the nine mycobacterial isolates obtained after fluoroquinolone use from nine patients whose initial isolates were susceptible to ofloxacin, one (11.1%) was resistant to ofloxacin (after fluoroquinolone use for 7 days). Independent factors for a poor prognosis included empirical fluoroquinolone use, age .65, underlying disease, hypoalbuminaemia, and lack of early antituberculous treatment. Conclusions: 14.4% of our patients with tuberculosis received a fluoroquinolone before the diagnosis. With a 34 day delay in antituberculous treatment and more frequent coexistence of underlying disease and hypoalbuminaemia, empirical fluoroquinolone treatment was associated with a poor outcome. Mycobacterium tuberculosis isolates could obtain ofloxacin resistance within 1 week.

Regulatory T cells (Tregs) and B cells present in gut-associated lymphoid tissues (GALT) are both implicated in the resolution of colitis. However, how the functions of these cells are coordinated remains elusive. We used the dextran sulfate sodium (DSS)-induced colitis model combined with gene-modified mice to monitor the progression of colitis, and simultaneously examine the number of Tregs and B cells, and the production of IgA antibodies. We found that DSS-treated mice exhibited more severe colitis in the absence of B cells, and that the adoptive transfer of B cells attenuated the disease. Moreover, the transfer of IL-10−/− B cells also attenuated colitis, suggesting that B cells inhibited colitis through an interleukin-10 (IL-10)-independent pathway. Furthermore, antibody depletion of Tregs resulted in exacerbated colitis. Intriguingly, the number of GALT Tregs in B cell-deficient mice was significantly decreased during colitis and the adoptive transfer of B cells into these mice restored the Treg numbers, indicating that B cells contribute to Treg homeostasis. We also found that B cells induced the proliferation of Tregs that in turn promoted B-cell differentiation into IgA-producing plasma cells. These results demonstrate that B cells and Tregs interact and cooperate to prevent excessive immune responses that can lead to colitis.

Amanzio and Benedetti (J Neurosci 1999; 19: 484-494) first addressed the conditions necessary for the activation of opioid and non-opioid placebo responses in human. Here, we investigated whether placebo analgesia is subdivided into opioid and non-opioid components in mice by using the model of hot-plate test. Drug conditioning was performed by the combination of the conditioned cue stimulus with the unconditioned drug stimulus, either opioid agonist morphine hydrochloride or non-opioid aspirin. Placebo analgesic responses were evoked by an exposure to a conditioned cue previously paired with drug conditioning. Morphine conditioning produced placebo responses that were completely antagonised by naloxone. By contrast, the conditioned cue after aspirin conditioning elicited a placebo effect that was not blocked by naloxone. Therefore, we first evoked opioid and non-opioid placebo responses in mice that were either naloxone-reversible or naloxone-insensitive, depending on the drug used in conditioning procedure. These findings support that the mechanisms underlying placebo analgesia may depend on the drug conditioning that was originally performed. The present procedure of mice may serve as a model for further understanding of the opioid and non-opioid mechanisms underlying placebo responses.

Background:This study was aimed to detect post-chemotherapeutic circulating tumour cells (CTCs) in stage III colon cancer patients and identify those who were at high risk of relapse.Methods:We used human telomerase reverse transcriptase, cytokeratin-19, cytokeratin-20, and carcinoembryonic antigen (CEA) as the biomarkers to detect CTCs in 90 stage III colon cancer patients undergoing curative resection followed by mFOLFOX chemotherapy.Results:Post-chemotherapeutic relapse occurred in 30 (33.3%) patients. By univariate analysis and multivariate proportional hazards regression analysis, perineural invasion (hazard ratio (HR): 2.752; 95% confidence interval (CI): 1.026–7.381), high post-chemotherapeutic serum CEA levels (HR: 2.895; 95% CI: 1.143–7.333) and persistent presence of post-chemotherapeutic CTCs (HR: 6.273; 95% CI: 2.442–16.117) were independent predictors of post-chemotherapeutic relapse. In addition, the persistent presence of post-chemotherapeutic CTCs strongly correlated with reduced disease-free survival and overall survival. Accuracy of detecting relapse in post-chemotherapeutic stage III colon cancer patients by analysing the persistent presence of post-chemotherapeutic CTCs was higher than that by post-chemotherapeutic CEA levels (odds ratio: 50.091 vs 5.211).Conclusion:The persistent presence of post-chemotherapeutic CTCs is a potential powerful surrogate marker for determining clinical outcome in stage III colon cancer patients receiving adjuvant mFOLFOX chemotherapy.