Green modification of biochar with poly(aspartic acid) enhances the remediation of Cd and Pb in water and soil.

Biochar is a promising adsorbent for the remediation of heavy metals in water and soil. However, pristine biochar has a limited adsorption capacity for heavy metals, which restricts its application in the field of heavy metal immobilization. In the present study, the acidic amino acid-modified biochar was prepared, and its adsorption properties for cadmium (Cd) and lead (Pb) in aqueous solution were investigated. The results showed that poly(aspartic acid)-modified biochar (PASP-BC) was more effective in removing Cd(II) from water compared to biochar modified with poly(glutamic acid) (PGA-BC), aspartic acid (ASP-BC), and glutamic acid (GA-BC). The calculated maximum adsorption capacities, derived from Langmuir fitting parameters, for Cd(II) and Pb(II) by PASP-BC were 44.2 mg/g and 126.1 mg/g, respectively, which were 3.78 and 2.70 times higher than that for pristine BC. Based on the results from Fourier transform infrared (FTIR) spectroscopy and X-ray photoelectron spectroscopy (XPS) analyses, ion exchange, complexation, and electrostatic adsorption were identified as the mechanisms for Cd(II) and Pb(II) adsorption by PASP-BC. The results of the Toxicity Characteristic Leaching Procedure (TCLP) showed that PASP-BC effectively reduced the leachability of Cd and Pb by 91.2% and 84.7%, respectively, at a dosage of 3%. The pot experiment demonstrated that PASP-BC significantly reduced the bioavailability of heavy metals in Triticum aestivum L The maximum reduction in Cd and Pb content in roots was 76.3% and 72.6% when 3% PASP-BC was applied. Importantly, the application of PASP-BC decreased the translocation factor of heavy metals in wheat. Therefore, the green modification of biochar with poly(aspartic acid) has great potential in the heavy metals removal from wastewater and remediation in contaminated soil.

LzSCL9, a Novel GRAS Transcription Factor in Lanzhou Lily (Lilium davidii var. unicolor), Participates in Regulation of Trichokonins-Primed Heat Stress Tolerance.

In our previous research, we found that trichokonins' (TKs) employment improved the thermotolerance of the Lanzhou lily, a renowned edible crop species endemic to China that is relatively susceptible to high temperatures (HTs). Here, a novel Lanzhou lily GRAS gene, LzSCL9, was identified to respond to heat stress (HS) and HS+TKs treatment based on transcriptome and RT-qPCR analysis. TKs could improve the upregulation of LzSCL9 during long-term HS. The expression profile of LzSCL9 in response to HS with or without TKs treatment showed a significant positive correlation with LzHsfA2a-1, which was previously identified as a key regulator in TKs' conferred resilience to HT. More importantly, overexpression of LzSCL9 in the lily enhanced its tolerance to HTs and silencing LzSCL9 in the lily reduced heat resistance. Taken together, this study identified the positive role of LzSCL9 in TK-induced thermotolerance, thereby preliminarily establishing a molecular mechanism on TKs regulating the thermostability of the Lanzhou lily and providing a new candidate regulator for plant heat-resistant breeding.

Association of serum folate concentrations with the mortality of cancer: a prospective cohort study.

BACKGROUND: The association between serum folate concentrations and the mortality of cancer remains unclear. We aim to investigate the association of serum folate concentrations with all-cause and cause-specific mortality among American adults with cancer. METHODS: This cohort study included 4535 patients with cancer from National Health and Nutrition Examination Survey (NHANES) 1999 to 2016 and NHANES III (1988-1994). Death outcomes were ascertained by linkage to National Death Index records through 31 December 2019. Cox proportional hazards model and two-piecewise Cox proportional hazards model were used to calculate hazard ratios and 95% confidence intervals for the associations between folate concentrations and the risk of mortality. RESULTS: During a median follow-up of 37,792 person-years, there were 1998 all-cause deaths and 616 cancer deaths. Non-linear and L-shaped associations were observed between serum folate concentrations and the risk of all-cause and cancer mortality among patients with cancer. Notably, the mortality rates reached a plateau at 23.7 ng/mL for all-cause mortality and 23.57 ng/mL for cancer mortality. When folate levels fell below these thresholds, the risk of all-cause and cancer mortality decreased by approximately 2.1% (HR 0.979; 95% CI 0.969-0.989) and 3.6% (HR 0.964; 95% CI 0.948-0.981), respectively, with each unit increase in the folate concentration up to the thresholds. CONCLUSION: Our study reveals that low serum folate concentrations are linked to an elevated risk of cancer mortality among individuals with cancer within a certain range and supplementation of folate in cancer patients to achieve specific serum folate level threshold (23.7 ng/mL) might reduce the risk of cancer mortality.

Facile fabrication of chitosan/bone/bamboo biochar beads for simultaneous removal of co-existing Cr(VI) and bisphenol a from water.

Heavy metal Cr(VI) and organic BPA have posed harmful risks to human health, aquatic organisms and the ecosystem. In this work, Chitosan/bone/bamboo biochar beads (CS-AMCM) were synthesized by co-pyrolysis and in situ precipitation method. These microbeads featured a particle size of approximately 1 ± 0.2 mm and were rich in oxygen/nitrogen functional groups. CS-AMCM was characterized using XRD, Zeta potential, FTIR, etc. Experiments showed that adsorption processes of CS-AMCM on Cr(VI) and BPA fitted well to Langmuir model, with theoretical maximum capacities of 343.61 mg/g and 140.30 mg/g, respectively. Pore filling, electrostatic attraction, redox, complexation and ion exchange were the main mechanisms for Cr(VI), whereas for BPA, the intermolecular force (hydrogen bond) and pore filling were involved. CS-AMCM with adsorbed Cr(VI) demonstrated effective activation in producing ·OH and ·O2 from H2O2, which degraded BPA and Cr(VI) with the removal rates of 99.2% and 98.2%, respectively. CS-AMCM offers the advantages of low-cost, large adsorption capacity, high catalytic degradation efficiency, and favorable recycling in treating Cr(VI) and BPA mixed wastewater, which shows great potential in treating heavy metal and organic matter mixed pollution wastewater.

Exposure to trichloromethane via drinking water promotes progression of colorectal cancer by activating IRE1α/XBP1 pathway of endoplasmic reticulum stress.

Trichloromethane (TCM), a commonly recognized disinfection by-product formed during the chlorination of water, has been associated with the onset of colorectal cancer (CRC) in humans. Despite this, the impact of TCM on the progression of CRC remains uncertain. In this investigation, it was observed that exposure to TCM could augment the migratory capabilities of CRC cells and facilitate the advancement of colorectal tumors. To delve deeper into the mechanism responsible for TCM-induced CRC progression, we performed RNA-Seq analysis at cellular and animal levels after TCM exposure. Both the KEGG and GO enrichment analyses indicated the activation of endoplasmic reticulum stress (ERS) and the regulation of the cytoskeleton. Subsequently, we confirmed the activation of the IRE1α/XBP1 pathway of ERS through western blot and RT-qPCR. Additionally, we observed the aggregation of cytoskeletal proteins F-actin and ß-tubulin at the cell membrane periphery and the development of cellular pseudopods using immunofluorescence following exposure to TCM in vitro. The downregulation of IRE1α and XBP1 through siRNA interference resulted in the disruption of cell cytoskeleton rearrangement and impaired cell migration capability. Conversely, treatment with TCM mitigated this inhibitory effect. Moreover, chronic exposure to low concentration of TCM also triggered CRC cell migration by causing cytoskeletal reorganization, a process controlled by the IRE1α/XBP1 axis. Our study concludes that TCM exposure induces cell migration through the activation of ERS, which in turn regulates cytoskeleton rearrangement. This study offers novel insights into the mechanism through which TCM facilitates the progression of CRC.

NR2F1 overexpression alleviates trophoblast cell dysfunction by inhibiting GDF15/MAPK axis in preeclampsia.

Abnormal functions of trophoblast cells are associated with the pathogenesis of preeclampsia (PE). Nuclear receptor subfamily 2 group F member 1 (NR2F1) acts as a transcriptionally regulator in many diseases, but its role in PE remains unknown. Hypoxia/reoxygenation (H/R)-stimulated HTR-8/SVneo cells were used to mimic PE injury in vitro. NR2F1 overexpression alleviated trophoblast apoptosis, as evidenced by the decreased number of TUNEL-positive cells and the downregulation of caspase 3 and caspase 9 expression in cells. NR2F1 overexpression increased the invasion and migration ability of HTR-8/SVneo cells, accompanied by increased protein levels of matrix metalloproteinase (MMP)-2 and MMP-9. mRNA-seq was applied to explore the underlying mechanism of NR2F1, identifying growth differentiation factor 15 (GDF15) as the possible downstream effector. Dual-luciferase reporter, ChIP-qPCR, and DNA pull-down assays confirmed that NR2F1 bound to the promoter of GDF15 and transcriptionally inhibited its expression. GDF15 overexpression increased apoptosis and decreased the ability of invasion and migration in HTR-8/SVneo cells expressing NR2F1. MAPK pathway was involved in the regulation of PE. Administration of p38 inhibitor, ERK inhibitor, and JNK inhibitor reversed the effect of simultaneous overexpression NR2F1 and GDF15 on trophoblast apoptosis, invasion, and migration. Our findings demonstrated that NR2F1 overexpression inhibited trophoblast apoptosis and promoted trophoblast invasion and migration. NR2F1 might negatively regulate GDF15 expression by binding to its promoter region, which further inhibited MAPK signaling pathway in PE. Our study highlights that NR2F1 might sever as a potential target in PE.

Formation of pea protein amyloid-like nanofibrils-derived hydrogels mediated by epigallocatechin gallate.

This study investigated the interaction between pea protein amyloid-like nanofibril and epigallocatechin gallate, constructed and characterized the novel pea protein nanofibrils-derived hydrogel mediated by epigallocatechin gallate, and researched the functionalities of the hydrogel. Epigallocatechin gallate remodeled the structure of pea protein nanofibrils, and a stable and strong hydrogel was formed at a relatively low protein concentration (4.5%). Additionally, the hydrogels exhibited various surface structures and hydrogel properties dependent on the mass ratio. Strongest gel strength (51 g) was attained at 0.25 epigallocatechin gallate/pea protein nanofibrils mass ratio. Whereas, the hydrogels exhibited the highest water holding capacity (87%) at 0.05 mass ratio. The primary driving forces in the formation and maintaining of the hydrogels were hydrophobic interactions and ionic bonds. Progressive rise of ß-sheet content of pea protein nanofibrils occurred increasing epigallocatechin gallate concentration. This hydrogel holds great potential for applications in food processing, targeted delivery of nutraceuticals and biomedicine.

EBV-Positive Pleomorphic Variant Transformation of CD5-Negative Mantle Cell Lymphoma: A Rare Case Report and Literature Review.

Mantle cell lymphoma (MCL) is a mature B-cell lymphoma associated with cyclin D family rearrangements and typically expresses CD5 and cyclin D1. Epstein-Barr virus- (EBV-) positive MCL is rare, and the role of EBV infection and its transformation in MCL remains unclear. We present a case of CD5-negative classic MCL that progressed to an EBV + pleomorphic MCL six years after the initial diagnosis. Molecular studies confirmed the same clonal origin. To the best of our knowledge, the EBV-positive transformation of CD5-negative MCL into a pleomorphic variant has rarely been reported, and its recognition is important for the diagnosis and the management of patients with MCL.

The double-edged effects of IL-6 in liver regeneration, aging, inflammation, and diseases.

Interleukin-6 (IL-6) is a pleiotropic cytokine and exerts its complex biological functions mainly through three different signal modes, called cis-, trans-, and cluster signaling. When IL-6 binds to its membrane or soluble receptors, the co-receptor gp130 is activated to initiate downstream signaling and induce the expression of target genes. In the liver, IL-6 can perform its anti-inflammatory activities to promote hepatocyte reprogramming and liver regeneration. On the contrary, IL-6 also exerts the pro-inflammatory functions to induce liver aging, fibrosis, steatosis, and carcinogenesis. However, understanding the roles and underlying mechanisms of IL-6 in liver physiological and pathological processes is still an ongoing process. So far, therapeutic agents against IL­6, IL­6 receptor (IL­6R), IL-6-sIL-6R complex, or IL-6 downstream signal transducers have been developed, and determined to be effective in the intervention of inflammatory diseases and cancers. In this review, we summarized and highlighted the understanding of the double-edged effects of IL-6 in liver homeostasis, aging, inflammation, and chronic diseases, for better shifting the "negative" functions of IL-6 to the "beneficial" actions, and further discussed the potential therapeutic effects of targeting IL-6 signaling in the clinics.

AHNAK2 Regulates NF-κB/MMP-9 Signaling to Promote Pancreatic Cancer Progression.

Early metastasis of pancreatic cancer (PaC) is a major cause of its high mortality rate. Previous studies have shown that AHNAK2 is involved in the progression of some tumors and is predicted to be an independent prognostic factor for PaC; however, the specific mechanisms through which AHNAK2 regulates PaC remain unclear. In this study, we examined the role of AHNAK2 in PaC and its potential molecular mechanisms. AHNAK2 mRNA and protein expression in PaC tissues and cells were measured using qRT-PCR and western blot analysis. After AHNAK2 knockdown using small interfering RNA, PaC cells were subjected to CCK-8 scratch, and Transwell assays to assess cell proliferation, migration, and invasion, respectively. Furthermore, the validation of the mechanistic pathway was achieved by western blot analysis. AHNAK2 mRNA and protein levels were up-regulated in PaC and silencing AHNAK2 significantly inhibited the proliferation, migration, and invasion of PaC cells. Mechanistically, AHNAK2 knockdown decreased the expression of phosphorylated p65, phosphorylated IκBα, and matrix metalloproteinase-9 (MMP-9), suggesting that activation of the NF-κB/MMP-9 signaling pathway was inhibited. Importantly, activation of NF-κB reversed the effects of AHNAK2 knockdown. Our findings indicate that AHNAK2 promotes PaC progression through the NF-kB/MMP-9 pathway and provides a theoretical basis for targeting AHNAK2 for the treatment of PaC.