Soil organic carbon (SOC) dynamics is regulated by a complex interplay of factors such as climate and potential anthropogenic activities. Livestocks play a key role in regulating the C cycle in grasslands. However, the interrelationship between SOC and these drivers remains unclear at different soil layers, and their potential relationships network have rarely been quantitatively assessed. Here, we completed a six‐year manipulation experiment of grazing exclusion (no grazing: NG) and increasing grazing intensity (light grazing: LG, medium grazing: MG, heavy grazing: HG). We tested light fraction organic carbon (LFOC) and heavy fraction organic carbon (HFOC) in 12 plots along grazing intensity in three soil layers (topsoil: 0–10 cm, mid‐soil: 10–30 cm, subsoil: 30–50 cm) to assess the drivers of SOC. Grazing significantly reduced SOC of the soil profile, but with significant depth and time dependencies. (1) SOC and SOC stability of the topsoil is primarily regulated by grazing duration (years). Specifically, grazing duration and grazing intensity increased the SOC lability of topsoil due to an increase in LFOC. (2) Grazing intensity was the major factor affecting the mid‐soil SOC dynamics, among which MG had significantly lower SOC than did NG. (3) Subsoil organic carbon dynamics were mainly regulated by climatic factors. The increase in mean annual temperature (MAT) may have promoted the turnover of LFOC to HFOC in the subsoil. Synthesis and applications. When evaluating the impacts of grazing on soil organic fraction, we need to consider the differences in sampling depth and the duration of grazing years. Our results highlight that the key factors influencing SOC dynamics differ among soil layers. Climatic and grazing factors have different roles in determining SOC in each soil layer. 相似文献
Streptococcus pneumoniae is a Gram-positive pathogen with high morbidity and mortality globally but some of its pathogenesis remains unknown. Previous research has provided evidence that aminopeptidase N (PepN) is most likely a virulence factor of S. pneumoniae. However, its role in S. pneumoniae virulence and its interaction with the host remains to be confirmed. We generated a pepN gene deficient mutant strain and found that its virulence for mice was significantly attenuated as were in vitro adhesion and invasion of host cells. The PepN protein could induce a strong innate immune response in vivo and in vitro and induced secretion of IL-6 and TNF-α by primary peritoneal macrophages via the rapid phosphorylation of MAPK and PI3K/AKT signaling pathways and this was confirmed using specific pathway inhibitors. In conclusion, PepN is a novel virulence factor that is essential for the virulence of S. pneumoniae and induces host innate immunity via MAPK and PI3K/AKT signaling.
In aquatic birds, influenza A viruses mainly replicate in the intestinal tract without significantly affecting the health of the host, but in mammals, they replicate in the respiratory tract and often cause disease. Occasionally, influenza viruses have been detected in stool samples of hospitalized patients and in rectal swabs of naturally or experimentally infected mammals. In this study, we compared the biological and molecular differences among four wild-type avian H1N1 influenza viruses and their corresponding fecal and lung isolates in DBA/2J and BALB/cJ mice. All fecal and lung isolates were more pathogenic than the original wild-type viruses, when inoculated into mice of both strains. The increased virulence was associated with the acquisition of genetic mutations. Most of the novel genotypes emerged as PB2E627K, HAF128V, HAF454L, or HAH300P variations, and double mutations frequently occurred in the same isolate. However, influenza virus strain- and host-specific differences were also observed in terms of selected variants. The avian H1N1 virus of shorebird origin appeared to be unique in its ability to rapidly adapt to BALB/cJ mice via the fecal route, compared to the adaptability of the H1N1 virus of mallard origin. Furthermore, a bimodal distribution in fecal shedding was observed in mice infected with the fecal isolates, while a normal distribution was observed after infection with the lung isolates or wild-type virus. Fecal isolates contained HA mutations that increased the activation pH of the HA protein. We conclude that influenza virus variants that emerge in fecal isolates in mammals might influence viral transmission, adaptation to mammals, and viral ecology or evolution. 相似文献
Bromodomain-containing protein 4 (BRD4) is a new therapeutic target for the treatment of diseases including cardiovascular diseases, cancer, inflammation and central nervous system (CNS) disorders. In this study, we introduced the pharmacophore of fibrates to a BRD4 inhibitor, RVX-208, to design dual-active hypolipidemic compounds, and found that some of new analogues showed favorable hypolipidemic activities. Synthetic accessibility towards this class of compounds optimized RVX-208 as well as would supply more thoughts on hypolipidemic drugs. 相似文献
Isoniazid (INH) is one of the most commonly used antituberculosis drugs, but its clinical applications have been limited by severe hepatic toxicity. Quercetin (Que), a natural flavonoid, has been proved to have many medicinal properties. This study aimed to clarify the possible protective effects of Que against INH‐induced hepatotoxicity using HepG2 cells. Our results indicated that Que significantly increased cell viability, superoxide dismutase, and GSH levels, while decreased alanine aminotransferase/aspartate aminotransferase levels. Besides, Que significantly abrogated INH‐induced cell apoptosis by upregulating the expression levels of Bcl‐2 and decreasing the levels of Bax, cleaved caspase‐3, and cleaved caspase‐9. Furthermore, Que obviously reversed the inhibition of INH on Sirtuin 1 (SIRT1) expression and extracellular signal‐regulated kinase (ERK) phosphorylation. Next, the SIRT1 inhibitor EX527 blocked the enhancement of Que upon ERK phosphorylation. Notably, EX527 partially abolished the beneficial effects of Que. In brief, our results provided the first evidence that Que protected against INH‐induced HepG2 cells by regulating the SIRT1/ERK pathway. 相似文献