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Our results suggest that environmental concentrations of AgNPs affected microbial biomass but had little impact on microbial diversity and may have little effects on the soil biogeochemical cycles mediated by extracellular enzyme activities. Sediment microbial communities were exposed for 21 days to an environmental concentration of copper to assess Cu-induced composition changes and resulting effects on microbial sensitivity to acute Cu and As toxicity. Chronic Cu exposure reduced the diversity of the bacterial and archaeal communities from Day 0 to Day 21. The pollution-induced community tolerance concept (PICT) predicts that loss of the most sensitive taxa and gain of more tolerant ones should increase the capacity of Cu-exposed communities to tolerate acute Cu toxicity. Although diversity loss and functional costs of adaptation could have increased their sensitivity to subsequent toxic stress, no increased sensitivity to As was observed. PICT responses varied according to heterotrophic activity, selected as the functional endpoint for toxicity testing, with different results for Cu and As. This suggests that induced tolerance to Cu and As was supported by different species with different metabolic capacities. Ecological risk assessment of contaminants would gain accuracy from further research on the relative contribution of tolerance acquisition and co-tolerance processes on the functional response of microbial communities. Short activated carbon fibers (ACF) with high surface area were fabricated via carbonization in N2 and activation in CO2 at high temperatures, with cellulose fibers as the raw materials. The obtained ACF were subsequently deposited into the support layer of a polyethersulfone (PES) ultrafiltration membrane by a facile filtration process to obtain the sandwich structured ACF-PES composite membrane. The hormone (17β-estradiol, E2) adsorption kinetics and isotherm of ACF in static conditions, as well as E2 removal by filtration with the ACF-PES composite membrane were investigated. In static conditions, ACF rapidly and efficiently adsorbs E2 evidenced by a high removal of >97 %. The fitting of second order kinetics and linear (Henry) adsorption isotherm models indicated the availability of easily accessible adsorption sites. Besides, such efficient E2 adsorption was contributed by many interactions between E2 and ACF, namely hydrophobic interactions, hydrogen bonding and π-π stacking. The incorporation of ACF in a PES membrane resulted in a minor loss of filtration flux compared with the control membrane, but significantly improved E2 removal through adsorption pathway. With only 1.0 mg ACF incorporated (loading 2.0 g/m2), the composite membrane could reject 76 % of E2 from a 100 ng/L solution at a flux of 450 L/m2∙h, demonstrating that ACF-PES can overcome the permeability-selectivity trade-off of traditional UF membranes. Smoothened Agonist cost V.Heavy metal(loid)s are natural constituents of the Earth's crust, and apportionment of their sources in surface soils is a challenging task. This study evaluated the application of positive matrix factorization (PMF) model, assisted with regression modeling and geospatial mapping, in the quantitative source apportionment of heavy metal(loid)s in the agricultural soils of Handan, a region covering >12,000 km2. Obvious enrichment of As, Cd, Cu, Pb, and Zn was found in the surface soils, with Cd alone accounted for 73 % of the overall potential ecological risk. PMF model revealed that Cd (56.9 %) and Pb (47.8 %) in the region's agricultural soils were predominantly contributed by industrial sources, Fe (71.8 %), Cr (60.0 %), V (52.9 %), Cu (50.7 %), Ni (42.2 %), and Mn (41.4 %) were primarily of lithogenic origin, while Co (54.1 %), As (42.9 %), and Zn (40.0 %) mainly came from the mixed sources of natural background, agricultural sources, and vehicle emissions. Uncertainty analysis showed that the contributions of pollution sources to the soil heavy metal(loid)s estimated by PMF model had considerable variations. While quantitative source apportionment of heavy metal(loid)s in soils could be achieved with PMF based on their spatial distributions, combination with emission inventory and reactive transport are probably necessary to obtain more accurate results. Owning to highly mechanical strength and non-interference effectivity, silica dioxide is often explored as a stable supporter commonly with mesopore. It is known that a macroporous framework has larger mass transfer channel, possibly beneficial to adsorption process. Herein highly ordered macroporous silica dioxide framework (homogeneous pore size of 194.20 nm) was synthesized and embedded with supramolecular (CC/OMS). Cs cation adsorption onto CC/OMS was explored under different pH (presence or absence of humic acid), initial cesium concentration, shaking time, competing ions. The robust cesium uptake capacity demonstrated by a theory adsorption amount of 150.01 mg/g highlighted unique CC/OMS properties combining large mass transfer channel and superior complex capacity of supramolecular. The adsorption was well fit with Langmuir and pseudo-second-order model. Sodium and potassium at a lower concentration showed little influence on cesium adsorption. The results demonstrated that CC/OMS was an alternative material for cesium capture from acidic aqueous solution. V.Atherosclerosis is regarded as a chronic inflammatory disease which immune response is regulated by multiple factors. Pseudorlaric acid D (PLAD) is the main bioactive component of Pseudolarix kaempferi Gorden, but little of its property has been found in the literature. We aimed to investigate the anti-inflammatory activity and the underlying mechanisms of PLAD on atherosclerosis. In this study, atherosclerosis model was established by feeding with a high-fat diet in ApoE-/- mice. PLAD was administered intragastrically at a dose of 5 mg/kg for four weeks. We found that PLAD could significantly improve the lipid metabolism and decrease atherosclerotic lesion areas as well as mitigate atherosclerotic changes on vessel walls. Besides, PLAD could markedly inhibit the inflammatory response by down-regulating the levels of Ly6Chi monocytes and NETs, and restraining NETs formation. The expression of pro-inflammatory cytokines IL-1β and IL-18 was also evidently reduced by PLAD. These results indicated that modulating the activation and recruitment of Ly6Chi monocytes and NETs could be the potential anti-inflammatory mechanisms of PLAD on atherosclerosis. PLAD might be a promising therapeutic strategy for the treatment of atherosclerosis and inflammation-related diseases. Long non-coding RNA (lncRNA) LINC00173 has been previously shown to promote chemoresistance and progression of small-cell lung cancer. Herein, we examine the clinical significance and biological function of LINC00173 in triple-negative breast cancer (TNBC). Quantitative PCR analysis was performed to determine the expression of LINC00173 in TNBC and adjacent breast tissues (n = 84). The associations of LINC00173 expression with cancer features and survival of TNBC patients were analyzed. The function of LINC00173 in TNBC cell proliferation, colony formation, and invasion was explored. TNBCs expressed increased levels of LINC00173 relative to normal breast tissues. TNBC patients with high tumoral LINC00173 levels had a lower recurrence-free survival and overall survival rate than those with low LINC00173 expression. Silencing of LINC00173 inhibited the proliferation, colony formation, and invasion of TNBC cells, whereas overexpression of LINC00173 exerted opposite effects. In vivo studies confirmed the reduction of tumor growth by LINC00173 depletion. Mechanistic investigation revealed that LINC00173 suppressed miR-490-3p to promote aggressive phenotype in TNBC cells. There was an inverse correlation between miR-490-3p and LINC00173 in TNBC (r = -0.2647, P =  0.0149). Altogether, LINC00173 functions as an oncogene in TNBC through antagonization of miR-490-3p. Upregulation of LINC00173 is associated with poor prognosis in TNBC. Targeting LINC00173 provides a potential therapeutic strategy for TNBC. The promoting roles of the long non-coding RNA (lncRNA) MACC1-AS1 have been indicated in gastric and pancreatic cancer, however, its roles in nasopharyngeal carcinoma (NPC) progression are never been revealed. In this work, it was shown that lncRNA MACC1-AS1 was highly expressed in NPC tissues and cells relative to the adjacent tissues and nasal mucosa cells, respectively. Additionally, MACC1-AS1 expression was positively correlated with the high rate of lymph node metastasis and large tumor size. in vitro and in vivo experiments revealed that MACC1-AS1 knockdown reduced the stemness of NPC cells, which was indicated by the decrease of sphere-forming ability, ALDH1 activity, stemness marker expression and tumor-initiating capacity. Mechanistic research showed that MACC1-AS1 antagonized the activity of miR-145, which could target Smad2. In turn, smad2 directly bound to MACC1-AS1 promoter and thus increased MACC1-AS1 expression. Notably, knockdown of miR-145 or overexpression of Smad2 rescued the inhibition of MACC1-AS1 knockdown on the stemness of NPC cells. Therefore, these results demonstrate a novel MACC1-AS1/miR-145/Smad2 negative loop responsible for NPC cell stemness. Severe acute pancreatitis (SAP), a critical inflammatory pathological disease of the pancreas, is crucial for the manifestation of lethal multiple organ dysfunction syndrome and systemic inflammatory response syndrome. Acute kidney injury (AKI) is one of the most severe complications of severe acute pancreatitis. Yet, the specific pathogenesis of AKI following SAP is defectively understood, and involves in multiple pathological processes in a "network-regulative" pattern, including dysfunction of the intestinal barrier, prolonged activation of coagulation, elevated discharge of damage-associated molecular patterns, complication of abdominal compartment syndrome, excessive release of inflammatory mediators, overexpression of procalcitonin, and incitement of chronic metabolic diseases. Therefore, in this review, we summarize the current knowledge on the pathogenesis of kidney injury following SAP to provide a better understanding of the interactions involved and to encourage the identification of novel targeted therapies to treat SAP and associated AKI. BACKGROUND Cervical cancer (CC) is one of the most common cancers in women. Long non-coding RNAs (lncRNAs) have been proposed as therapeutic targets in CC. Hence, the present study evaluated the effect of ASB16-AS1 on CC via regulating miR-1305. METHODS Differentially expressed lncRNAs associated with CC were screened using bioinformatics database. The expression of ASB16-AS1 and miR-1305 were measured by qRT-PCR in CC tissues and CC cells. Cell proliferation was assessed by CCK-8 and colon formation assays. Cell abilities of migration and invasion were detected by Transwell migration and invasion assays. Luciferase report assays were used to explore the correction between ASB16-AS1, miR-1305 and Wnt2 in CC. Western blot assay detect the activity of Wnt/β-catenin pathway. The xenograft tumor in nude mice was observed to evaluate tumor formation in vivo. RESULTS In our study, we showed that the expression of ASB16-AS1 was increased while miR-1305 reduced was re in CC. Clinically, ASB16-AS1 and miR-1305 were correlated with poor-associated clinicopathological features of CC patients.