Abstract The pyrolysis kinetics of hulless barley straw at different heating rates of 5，10, 15, 20 and 30 ºC/min were investigated via thermogravimetry, and the activation energy distribution E and pre-exponential factor k0 were calculated using the Distributed Activation Energy Model (DAEM) from thermogravimetric analysis (TGA) curves, and characterizations of pyrolysis product of biochar were analyzed by techniques of scanning electron microscopy (SEM) and X-ray diffraction (XRD). The pyrolysis process consisted mainly of the dehydration stage (50-150 ºC), the active pyrolysis stage (200-400 ºC) and the passive pyrolysis stage (400-800 ºC). The E ranged from 73.45 to 214.11 kJ/mol within the conversion rate range of 0.10-0.55, and changed from 214.11 to 141.55 kJ/mol within the conversion rate range of 0.55-0.90, and the average value of E was 172.23 kJ/mol. The values of k0 changed greatly with E values at different mass conversion. The wide E and k0 distributions obtained from the kinetic analysis are attributed to the complex chemical reactions of pyrolysis. The structure of biochar was degraded or ruptured due to the increase in temperature. The XRD analysis confirmed that the biochar was amorphous, dominated by disordered graphitic crystallites.

Abstract Streptococcus pneumoniae is one of the most frequent opportunistic pathogens worldwide. DNA processing protein A (DprA) is an important factor involved in bacterial uptake and DNA integration into bacterial genome, but its role in S. pneumoniae virulence remains unclear. The aim of this study was to characterize the effects of the pneumococcal dprA gene on the pathogenesis of S. pneumoniae. To construct a dprA-deficient pneumococcal strain, the dprA gene of the S. pneumoniae strain D39 was inactivated. The virulence of this dprA-deficient strain, designated ΔD39, was compared with that of the wild-type strain by evaluating their respective capabilities to adhere to human pulmonary epithelial cells (PEC-A549) and by analyzing their choline-binding protein expression levels. In addition, the expression profiles of genes associated with virulence and host survival assays were also conducted with the mutant and the wild-type strain. Our results indicate that the capability of ΔD39 to adhere to the PEC-A549 airway cells was significantly lower (p < 0.01) compared with D39. Additionally, the 100-KD choline-binding protein was not detected in ΔD39. The addition of competence-stimulating peptide (CSP) lead to a significantly reduction of psaA mRNA expression in the dprA-deficient mutant and an increased level of psaA transcripts in the wild-type strain (p < 0.01). The median survival time of mice intraperitoneally infected with ΔD39 was significantly higher (p < 0.01) than that of mice infected with D39. The results of this study suggest that DprA has a significant effect on virulence characteristics of S. pneumoniae by influencing the expression of choline-binding protein and PsaA.