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This study examines the determinants and consequences of firms' disclosures related to the COVID-19 pandemic in annual financial reports in China. First, we find that firms with high growth opportunity or low stock liquidity tended to disclose COVID-19 pandemic information to mitigate information asymmetry. Second, our results show that voluntary risk disclosure significantly decreased stock risks due to the reduction of information asymmetry. We further find that stock price crash risks decreased for firms that reported risk information compared with those that did not. Our results suggest that detailed voluntary risk disclosure is needed to mitigate stock risks, especially in extreme situations. [ABSTRACT FROM AUTHOR]

Gene encoding endo-β-l,4-glucanase(TM1525) is derived from Thermotoga maritima (T. maritima), which has an open reading frame of 825 bp and encodes a 274 amino acid endo-β-1, 4-glucanase. This enzyme has the same high temperature resistance as thermophilic bacteria,which is an ideal property for industrial applications. By molecular biological means, TM1525 was cloned into pHT43 vector and introduced into Bacillus subtilis (B. subtilis) WB800N by electroporation. The results showed that the WB800N expression system was successfully constructed, and extracellular expression of the recombinant gene was achieved. Cellulose hydrolyzed activity of the protein was exhibited. [ABSTRACT FROM AUTHOR]

Using Fe(III) salts and chitosan, nano iron oxide impregnated in chitosan bead (NIOC) was successfully synthesized for aqueous Cr(VI) detoxification via sol-gel technique without any additional crosslinking agent. NIOC characterization demonstrated that the iron in NIOC mainly existed as nano akaganeite (β-FeOOH) and complex with chitosan. Intraparticle diffusion was the major rate-limiting step. The maximal adsorption capacity was 69.8 mg/g (pH 5.0, 20 °C). Normal concentration of coexisting anions (SO 4 2− , CO 3 2− , SiO 3 2 −) showed insignificant competition, whereas PO 4 3− suppressed the Cr(VI) sorption. Cr(VI)-loaded NIOC could be effectively regenerated by alkaline solutions. Column adsorption runs using granular NIOC could effectively treat about 1600 bed volumes of Cr(VI) solution (from 3.7 mg Cr/L in influent to <0.5 mg Cr/L in effluent). The Cr(VI) removal mechanisms involved the direct sorption of Cr(VI) (electrostatic attraction and ligand exchange), reduction of Cr(VI) into Cr(III) and re-sorption of Cr(III) via chelation on NIOC surface. [ABSTRACT FROM AUTHOR]

Echinacoside (ECH) is a natural compound extracted from the stem of the Cistanche deserticola plant, has significant biological properties, including antioxidant, anti-inflammatory, neuroprotective, anti-tumor, hepatoprotective, and immunomodulatory properties. In this study, we aimed to explore the protection effects and mechanisms of ECH on diabetic liver injury in db/db mice. Overall, 6-week-old db/db mice (n = 20) were randomly allocated to 2 groups: diabetic model group (db/db group, intragastric administration of normal saline, n = 10) and ECH-treated group (db/db + ECH group, n = 10). Additionally, the normal control group comprised 6-week-old db/m mice (db/m group, normal saline intragastric administration, n = 10). ECH was administered once a day for 10 weeks. Weight and fasting blood glucose (FBG) were measured biweekly. HE staining and Oil O staining were used to evaluate liver tissue pathological changes and lipid accumulation respectively. Immunofluorescence staining, Western blot and RT-PCR analysis were used to detect the expression of components of the AMPK/SIRT1 signaling axis. The results showed that the administration of echinacoside for 10 weeks could significantly improve liver injury and insulin resistance in db/db mice (p < 0.01). Also, echinacoside treatment helped to reduce blood lipids and blood glucose (p < 0.01). Moreover, ECH actived AMPK/SIRT1 signaling, upregulated peroxisome proliferator-activated receptor gamma co-activator 1 alpha (PGC-1α), proliferator-activated receptor-α (PPARα), carnitine palmitoyl transferase-1A (CPT1A) in db/db mice (p < 0.01). The effect of ECH may be elicited by the activation of the liver AMPK/SIRT1 pathway and its downstream factors to improve adiposity, insulin resistance, and dyslipidemia. [ABSTRACT FROM AUTHOR]

Kidney fibrosis and renal tubular epithelial-to-mesenchymal transition (EMT) are the main pathological changes of diabetic nephropathy (DN), which eventually leads to end-stage renal disease. Previous studies have suggested that echinacoside (ECH) is antifibrotic in the liver. However, the effect of ECH on kidney fibrosis in DN and its mechanisms are unknown. This study was performed to explore the effect of ECH on kidney fibrosis and also the molecular mechanisms of ECH in a db/db mice model of DN. Our results showed that, relative to db/db mice, the mice in the ECH group had an improved general state and reduced blood glucose and 24-hour urinary protein levels. The deterioration of renal function was delayed due to treatment with ECH. We also observed that ECH can improve histopathological findings in the kidneys of db/db mice, including collagen deposition, mesangial cell and mesangial matrix hyperplasia, basement membrane thickening, and podocyte reduction. Moreover, ECH inhibited the TGF-β1/Smads signaling pathway, downregulated fibronectin (FN), collagen IV, and alpha-smooth muscle actin (α-SMA) levels, and upregulated E-cadherin level in the db/db mice model of DN. Our findings indicate that ECH has a therapeutic effect on DN, including the inhibition of renal tubular EMT and kidney fibrosis. Furthermore, ECH inhibits kidney fibrosis through regulation of the TGF-β1/Smads signaling pathway., Competing Interests: Disclosure The authors report no conflicts of interest in this work.