Biomass is among the most promising renewable resources to provide a sustainable solution to meet the world's increasing usage of it in biochemical and thermochemical conversion technologies. Thermochemical conversion processes (pyrolysis, gasification, and combustion) thermally convert biomass into energy-dense intermediates that can be, in turn, converted to power, liquid fuels, and chemicals. The performance of the processes and quality of the intermediates are strongly affected by endogenic and technogenic inorganics. This review highlights investigations on the effect and the fate of inorganics during pyrolysis, gasification, and combustion of lignocellulosic biomass and critically and comprehensively presents pretreatment and post-treatment approaches for inorganic removal. During pyrolysis process, the inorganic contents can have significant catalytic effects and change the thermal degradation rate, chemical pathway, and bio-oil yield. During combustion process, the inorganic contents can bring various technological problems, environmental risks, and health concerns. During gasification process, the inorganic contents cause diversified downstream hazards. In recent years, several pre-treatment (mechanical, thermal, and chemical pre-treatment) and post-treatment (gas product and liquid product post-treatment) approaches have been employed to control and diminish the impact of inorganics during thermochemical conversion. Effective pre-treatment technologies exist to remove inorganic contaminants to lower concentration limits. However, the main drawbacks of these pre-treatments are that they (i) reduce the overall efficiency due to the need of further drying process of wet biomass after pre-treatment and (ii) increase chemicals, facilities, and drying costs. Post-treatment technologies are utilized to meet the strict levels of cleanup demands for the downstream applications. A great number of technologies exist to purify the raw synthesis gas stream that is produced by thermochemical conversion of biomass.

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Background Ulcerative colitis (UC) is an intestinal disease which was characterized by intestinal inflammation, mucosal injury and fibrosis. In this paper, the effect of Huanglian Jiedu Decoction (HJD), a well-known traditional Chinese medicine with significant anti-inflammatory effect, on dextran sulphate sodium (DSS)-induced UC in mice and inhibition of JAK2/STAT3 pathway were investigated. Methods BALB/c mice were randomly divided into 6 groups: HJD group (high, medium and low dose), USAN group, UC group, and control group. UC in mice were induced through free access to 3% DSS solution. After being treated with HJD for 8 days, all animals were sacrifice. Pathological examination of colonic specimen was performed by H&E staining. Cytokines (TNF-α, IL-6, and IL-1β) in colon were assayed by ELISA and immunofluorescence, MPO in colon and ATT in serum were detected by ELISA. Moreover, mice in HJD group and UC group were treated with AG490 to inhibit the expression of JAK2 protein, then the expression of JAK2 and STAT3 protein in colon was determined by western blotting and immunofluorescence staining. Furthermore, KI67 in colon was examined by immunohistochemistry, and apoptosis was detected by TUNEL staining, and collagen deposition was assayed by Masson staining after JAK2/STAT3 pathway in UC mice was inhibited by HJD. Results After mice being treated with HJD, the symptoms (weight loss and haematochezia) of UC were alleviated, and the contents of inflammatory cytokines (TNF-α, IL-6 and IL-1β) and MPO in colon were significantly decreased. The expression of JAK2 and STAT3 protein was reduced after administration with HJD. After JAK2/STAT3 pathway being inhibited with HJD, the cell apoptosis, collagen deposition and immunoreactivity of macrophage in colon were significantly reduced, but the expression of Ki67 was markedly enhanced in both UC group and HJD group compare with control group. Conclusions HJD treatment can alleviate intestinal mucosal damage and has the protective effect on UC by downregulating JAK2 and STAT3 expression to reduce inflammation via JAK2/STAT3 pathway.

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