This study evaluated the association between inflammatory diets as measured by the dietary inflammatory index (DII), and inflammation biomarkers, and the development of preeclampsia among the Chinese population. We followed the reporting guidelines of the STROBE statement for observational studies. A total of 466 preeclampsia cases aged over 18 years were recruited between March 2016 and June 2019, and 466 healthy controls were 1:1 ratio matched by age (± 3 years), week of gestation (± 1 week), and gestational diabetes mellitus. The energy-adjusted DII (E-DII) was computed based on dietary intake assessed using a 79-item semiquantitative food frequency questionnaire (FFQ). Inflammatory biomarkers were analyzed by ELISA kits. The mean E-DII scores were -0.65 ± 1.58 for cases and -1.19 ± 1.47 for controls (P value <0.001). E-DII scores positively correlated with IFN-γ (rs = 0.194, P value = 0.001) and IL-4 (rs = 0.135, P value = 0.021). After multivariable adjustment, E-DII scores were positively related to preeclampsia risk (P trend <0.001). The highest tertile of E-DII was 2.18 times the lowest tertiles (95% CI = 1.52, 3.13). The odds of preeclampsia increased by 30% (95% CI= 18%, 43%, P value <0.001) for each E-DII score increase. The preeclampsia risk was positively associated with IL-2 (OR = 1.07, 95% CI = 1.03, 1.11), IL-4 (OR = 1.26, 95% CI = 1.03, 1.54) and TGF-β (OR = 1.17, 95% CI = 1.06, 1.29). Therefore, proinflammatory diets, corresponding to higher IL-2, IL-4 and TGF-β levels, were associated with increased preeclampsia risk.

Chronic inflammation exerts pleiotropic effects in the aetiology and progression of chronic obstructive pulmonary disease (COPD). Glucosamine is widely used in many countries and may have anti-inflammatory properties. We aimed to prospectively evaluate the association of regular glucosamine use with incident COPD risk and explore whether such association could be modified by smoking in the UK Biobank cohort, which recruited more than half a million participants aged 40–69 years from across the UK between 2006 and 2010. Cox proportional hazards models with adjustment for potential confounding factors were used to calculate hazard ratios (HR) as well as 95 % CI for the risk of incident COPD. During a median follow-up of 8·96 years (interquartile range 8·29–9·53 years), 9016 new-onset events of COPD were documented. We found that the regular use of glucosamine was associated with a significantly lower risk of incident COPD with multivariable adjusted HR of 0·80 (95 % CI, 0·75, 0·85; P < 0·001). When subgroup analyses were performed by smoking status, the adjusted HR for the association of regular glucosamine use with incident COPD were 0·84 (0·73, 0·96), 0·84 (0·77, 0·92) and 0·71 (0·62, 0·80) among never smokers, former smokers and current smokers, respectively. No significant interaction was observed between glucosamine use and smoking status (Pfor interaction = 0·078). Incident COPD could be reduced by 14 % to 84 % through a combination of regular glucosamine use and smoking cessation.

Intestinal stem cells, which are capable of both self-renewal and differentiation to mature cell types, are responsible for maintaining intestinal epithelial homeostasis. Recent evidence indicates that these processes are mediated, in part, through nutritional status in response to diet. Diverse dietary patterns including caloric restriction, fasting, high-fat diets, ketogenic diets and high-carbohydrate diets as well as other nutrients control intestinal stem cell self-renewal and differentiation through nutrient-sensing pathways such as mammalian target of rapamycin and AMP-activated kinase. Herein, we summarise the current understanding of how intestinal stem cells contribute to intestinal epithelial homeostasis and diseases. We also discuss the effects of diet and nutrient-sensing pathways on intestinal stem cell self-renewal and differentiation, as well as their potential application in the prevention and treatment of intestinal diseases.

Human papillomavirus (HPV) has been confirmed as the causative agent for cervical cancer. In this study, a total of 301 880 women were recruited from four different regions of Western China, with 301 880 exfoliated cervical cell samples collected from women for DNA isolation and purification. The HPV genotype was tested by polymerase chain reaction. The overall HPV prevalence rate, high-risk (HR) HPV infection rate, low-risk (LR) HPV infection rate and mixed HPV infection rate was 18.24%, 79.14%, 12.56% and 8.30%, respectively. The four most common HR HPV subtypes were HPV-52, 16, 58 and 53, which accounted for 20.49%, 19.93%, 14.54% and 10.01%, respectively. In LR HPV genotype, HPV-6 ranked the highest (28.17%), followed by HPV-81 (9.09%) and HPV-11 (3.78%). HPV genotype subgroup analysis also showed that single-type infection was the most common (77.26%) among HPV-positive individuals. Among multi-infection genotypes, double infection was the most common with frequencies of 76.04%. The overall prevalence of HPV is high in Western China, whose distribution demonstrates different patterns across different ages and regions. Viral genotypes HPV 53, 6 were frequently detected in this population, which is worth of significant clinical attention.

Echinococcus granulosus sensu lato has complex defence mechanisms that protect it from the anti-parasitic immune response for long periods. Echinococcus granulosus cyst fluid (EgCF) is involved in the immune escape. Nevertheless, whether and how EgCF modulates the inflammatory response in macrophages remains poorly understood. Here, real-time polymerase chain reaction and enzyme-linked immunosorbent assay revealed that EgCF could markedly attenuate the lipopolysaccharide (LPS)-induced production of pro-inflammatory factors including tumour necrosis factor-α, interleukin (IL)-12 and IL-6 but increase the expression of IL-10 at mRNA and protein levels in mouse peritoneal macrophages and RAW 264.7 cells. Mechanically, western blotting and immunofluorescence assay showed that EgCF abolished the activation of nuclear factor (NF)-κB p65, p38 mitogen-activated protein kinase (MAPK) and ERK1/2 signalling pathways by LPS stimulation in mouse macrophages. EgCF's anti-inflammatory role was at least partly contributed by promoting proteasomal degradation of the critical adaptor TRAF6. Moreover, the EgCF-promoted anti-inflammatory response and TRAF6 proteasomal degradation were conserved in human THP-1 macrophages. These findings collectively reveal a novel mechanism by which EgCF suppresses inflammatory responses by inhibiting TRAF6 and the downstream activation of NF-κB and MAPK signalling in both human and mouse macrophages, providing new insights into the molecular mechanisms underlying the E. granulosus-induced immune evasion.

Sustainable and green energy sources are in high demand to meet the current human energy needs and environmental requirements. Hydrogen energy, with the highest energy density and zero carbon emission, is considered a potential solution. Hydrogen is primarily produced by splitting water. Rationally designed electrocatalysts are required to promote the cathodic hydrogen evolution reaction (HER) and the anodic oxygen evolution reaction (OER). Organic polymer matrices provide new opportunities for electrocatalytic water splitting due to their special physical and chemical characteristics and thermal stability. This article explains the role of organic polymers in electrocatalytic water decomposition from three aspects: ion-conductive polymers, conjugated conductive polymers, and carbon materials derived from organic polymers. We hope that this article will provide more rational ideas and promote the design of organic polymers for water-splitting electrocatalysis, and furnish more technical insights for the future of water electrolysis.

How do corporate bond mutual funds manage liquidity to meet investor redemptions? We show that during tranquil market conditions, these funds tend to reduce liquid asset holdings to meet redemptions, temporarily increasing relative exposures to illiquid asset classes. When aggregate uncertainty rises, however, they tend to scale down their liquid and illiquid assets proportionally to preserve portfolio liquidity. This fund-level dynamic management of liquidity appears to affect the broad financial market: Redemptions from the corporate bond fund sector lead to more corporate bond selling during high-uncertainty periods, which generates price pressures and predicts strong return reversals.

Fluorescent quantum dots (QDs) modified with polyethylene glycol (PEG) and albumin bovine serum (BSA) have profound application in the detection and treatment of hepatocellular carcinoma (HCC) cells. In the present study, the effects and mechanism of PEG and BSA modification on the cytotoxicity of QDs have been explored. It was found that the diameter of the as-prepared QDs, PEG@QDs, BSA@QDs is 3–5 nm, 4–5 nm, and 4–6 nm, respectively. With increase of the treatment time from 0 to 24 h, the HCC cell viability treated with QDs, PEG@QDs, and BSA@QDs obviously decreases, showing a certain time-dependent manner. When the concentration of several nanomaterials is increased from 10 to 90 nM, the cell viability decreases accordingly, exhibiting a certain concentration-dependent manner. Under the same concentration change conditions, the reactive oxygen species contents of cells treated by QDs, PEG@QDs, and BSA@QDs also rise from 7.9 × 103, 6.7 × 103, and 4.7 × 103 to 13.2 × 103, 14.3 × 103, and 12.3 × 103, respectively. In these processes, superoxide dismutase does not play a major role. This study provides strong foundation and useful guidance for QD applications in the diagnosis and treatment of HCC.

Reduced graphene oxide supported titanium dioxide (GO/TiO2) heterojunction composites as highly active photocatalysts were synthesized via simple ultrasonic mixing and hydrothermal reaction using TiCl3 and GO as precursors. Their structure and morphology were characterized by X-ray diffraction, Fourier transform infrared spectroscopy, Raman spectra, UV-vis spectroscopy, and thermogravimetic analysis. The GO/TiO2 heterojunction composites were used to degrade methyl orange (MO). The adsorption and photocatalytic degradation rate of the prepared GO/TiO2 composites increased by nearly three times compared with that of pristine TiO2 or GO, which reached up 90%, to degrade MO after 4 h, which provides a simple method to obtain photocatalytic materials.

Emerging evidence has been revealed that high fat diet (HFD) correlate with insulin resistance (IR) which could be induced by endoplasmic reticulum stress (ERS). Recently, obesity or HFD induced nonalcoholic fatty liver disease (NAFLD) could promote alteration of iron metabolism. Disorder of iron metabolism have been linked to unnormal metabolism of glucose and lipid. Herein, we investigated the effect of impaired iron homeostasis on hepatic IR, focusing on ferritinophagy. Male C57/6J mice were administered with HFD (60% energy from fat) or LFD (10% energy from fat) for 10 weeks (n = 10), and Palmitic acid (PA)-insulin treated HepG2 cells were also established. Hepatic IR as evidenced by increased hepatic steatosis and decreased of p-AKT (48%, p < 0.0005), p-GSK-3β (34%, p < 0.05) in the liver of HFD mice. In addition, decreased iron level and expression NCOA4, as well as increased up-regulation of IRE1α and EIF2α were observed in HFD liver. By using desferrioxamine (DFO) and ferric ammonium citrate (FAC), we examined iron level on IRE1α and EIF2α. And glucose uptake assay shown that FAC supplementation, and ERS inhibitors of 4-PBA and STF could improve the glucose uptake of HepG2 cells in the presence of PA. Furthermore, we evaluated the glucose uptake of HepG2 cells incubated with adenovirus which mediated overexpression of NCOA4, FAC, 4-PBA (ERS inhibitor) or STF (IRE1 inhibitor). Taken together, deficiency of iron induced by impaired ferritinophagy induced hepatic IR, partly by aggravating hepatic ERS, especially IRE1 signal pathway in vivo and vitro. These findings provide evidence and new insight for therapeutic strategy of iron deficiency in NAFLD.

The present study investigated the effects of condensed tannins (CT) on intestinal immune function in on-growing grass carp (Ctenopharyngodon idella). A total of 540 healthy grass carp were fed six diets containing different levels of CT (0, 10·00, 20·00, 30·00, 40·00 and 50·00 g/kg diet) for 70 d and then challenged with Aeromonas hydrophila for 14 d. The results showed that, compared with the control group, dietary CT (1) induced intestinal histopathological lesions and aggravated enteritis; (2) decreased lysozyme and acid phosphatase activities, complement 3 (C3), C4 and IgM contents and down-regulated the Hepcidin, liver-expressed antimicrobial peptide (LEAP)-2A, LEAP-2B, Mucin2 and β-defensin-1 mRNA levels in the proximal intestine (PI), mid intestine (MI) and distal intestine (DI) (P < 0·05); (3) down-regulated the mRNA levels of anti-inflammatory cytokines transforming growth factor (TGF)-β1, TGF-β2 (not in MI and DI), IL-4/13A (not IL-4/13B), IL-10 and IL-11 partly correlated with target of rapamycin (TOR) signalling; and (4) up-regulated the mRNA levels of pro-inflammatory cytokines interferon-γ2, IL-1β, IL-6, IL-8 (not in PI), IL-12p35, IL-12p40, IL-15 and IL-17D partly related to NF-κB signalling in the intestine of on-growing grass carp. Overall, the results indicated that CT could impair the intestinal immune function, and its potential regulation mechanisms were partly associated with the TOR and NF-κB signalling pathways. Finally, based on the percentage weight gain and enteritis morbidity, the maximum allowable levels of CT for on-growing grass carp (232·22–890·11 g) were estimated to be 18·6 and 17·4 g/kg diet, respectively.

Laboratory experiments have shown that thermal gradients in silicate melts can lead to isotopic fractionation; this is known as the Richter effect. However, it is perplexing that the Richter effect has not been documented in natural samples as thermal gradients commonly exist within natural igneous systems. To resolve this discrepancy, theoretical analysis and calculations were undertaken. We found that the Richter effect, commonly seen in experiments with wholly molten silicates, cannot be applied to natural systems because natural igneous samples are more likely to be formed out of partially molten magma and the presence of minerals adds complexity to the behaviour of the isotope. In this study, we consider two related diffusion-rate kinetic isotope effects that originate from chemical diffusion, which are absent from experiments with wholly molten samples. We performed detailed calculations for magnesium isotopes, and the results indicated that the Richter effect for magnesium isotopes is buffered by kinetic isotope effects and the total value of magnesium isotope fractionation can be zero or even undetectable. Our study provides a new understanding of isotopic behaviour during the processes of cooling and solidification in natural magmatic systems.