A Comparison Between Two Different Definitions of Contrast-Associated Acute Kidney Injury for Long-Term Mortality in Patients with Chronic Kidney Disease Undergoing Coronary Angiography.

Background: Contrast-associated acute kidney injury (CA-AKI) is a prevalent complication following coronary angiography (CAG). However, there is ongoing controversy surrounding its precise definition. Although previous studies have demonstrated the successful application of appropriate definitions in managing high-risk CA-AKI patients, there remains limited research on the association between different definitions and prognosis specifically in patients with chronic kidney disease (CKD). Methods: A total of 4197 CKD patients undergoing coronary angiography (CAG) were included in this study. Two definitions of contrast-associated acute kidney injury (CA-AKI) were used: CA-AKIA, which was defined as an increase of ≥0.5 mg/dL or >25% in serum creatinine (SCr) from baseline within 72 hours after CAG, and CA-AKIB, which was defined as an increase of ≥0.3 mg/dL or >50% in SCr from baseline within 48 hours after CAG. Cox regression analysis was employed to assess the association between these two definitions and long-term mortality. Additionally, population attributable risks (PARs) were calculated to evaluate the impact of CA-AKI definitions on long-term prognosis. Results: During the median follow-up period of 4.70 (2.50-7.78) years, the overall long-term mortality was 23.6%, and the long-term mortality in patients with CA-AKI according to both CA-AKIA and CA-AKIB criteria were 33.5% and 33.8%, respectively. We found that CA-AKIA (HR: 1.45, 95% CI: 1.23-1.70, p<0.001) and CA-AKIB (HR: 1.44, 95% CI: 1.23-1.69, p<0.001) were associated with long-term mortality. The PARs were the highest for CA-AKIA (5.87%), followed by CA-AKIB (5.70%). Conclusion: Contrast-associated acute kidney injury (CA-AKI) is a frequently observed complication in CKD patients undergoing coronary angiography (CAG), and both definitions of CA-AKI are significantly correlated with a poor long-term prognosis. Consequently, in the clinical management of CKD patients, it is crucial to prioritize CA-AKI, irrespective of the specific CA-AKI definition used.

Land use, stratified wastewater and sediment, and microplastic attribute factors jointly influence the microplastic prevalence and bacterial colonization patterns in sewer habitats.

The capacity of microplastics to harbor and propagate bacteria has been the focus of attention over the last decade. Such microplastic-supported bacterial colonization behavior in the municipal sewer system could be a critical ecological link influencing the biogeochemical activities and risks in receiving waters in urban areas, given the alarming microplastic loads discharged there. This study conducted a large-scale survey covering a wide range of residential and industrial catchments in Shanghai, China. We aimed to assess the microplastic prevalence and bacterial colonization patterns in different sewer habitats and to explore the role of land use, stratified wastewater and sediment, and microplastic attributes in shaping the patterns. We found that the sewer system formed a temporal but pronounced microplastic pool, with land use playing a significant role in the variability of microplastic prevalence. Industrial sewers contained a high abundance of microplastics with large particle sizes, diverse polymer compositions, and shapes. However, while there was a spatial discrepancy between urban and suburban areas in the abundance of microplastics in residential sewers, their predominant polymer and shape types were simple, i.e., polyethylene terephthalate (PET) and fibers. Sewer habitat characteristics, particularly the stratified wastewater and sediment determined microbial colonization patterns. The latter acted as a long-term sink for microplastics and supported the high growth of colonizers. In contrast, the wastewater plastisphere presented novel niches, hosting communities with a marked proportion of unique bacterial genera after colonization. Besides, statistics showed a highly positive and dense co-occurrence network of the plastisphere communities, especially those from the industrial sewer sediment, with enhanced metabolic activity, cellular processes and systems, and increased human pathogenic potential. Findings indicated a coarse and uncertain effect of the selective pressure of microplastic attributes on plastisphere community structure differentiation.

High-throughput absolute quantification sequencing reveals the adaptive succession and assembly pattern of plastisphere communities in municipal sewer systems: Influence of environmental factors and microplastic polymer types.

Municipal sewer systems have received increasing attention due to the magnitude of the microplastic stock and its potential ecological impacts. However, as a critical aspect of the adverse impacts, little is known about the plastisphere that forms in these engineered environments. Using high-throughput absolute quantification sequencing, we conducted a systemic study combining field survey and laboratory batch test to explain the general plastisphere pattern and the role of environmental and polymeric factors in driving plastisphere succession and assembly there. We demonstrated the capacity of microplastics to support high levels of microbial colonization, increasing by 8.7-56.0 and 1.26-5.62 times at field and laboratory scales, respectively, despite the less diverse communities hosted in the resulting plastisphere. Sediment communities exhibited higher diversity but greater loss of specific operational taxonomic units in their plastisphere than in the wastewater. The former plastisphere had primarily an enhanced methanogenesis-oriented metabolic network linked to hydrolysis fermentation, hydrogen-producing acetogenesis, and denitrification, while the latter had a pronounced niche partitioning and competitive interaction network. Exogenous substrate flux and composition were key in stimulating plastisphere community growth and succession. Furthermore, the high nitrogen baseline facilitated alternative niche formation for plastisphere nitrifiers and denitrifiers, and the plastisphere pathogens associated with denitrification and plastic biodegradation functions increased significantly. The aerobic state also promoted a 1.71 times higher colonizer load and a denser interaction pattern than the anaerobic state. Selective filtering by polymers was evident: polyethylene supported higher plastisphere diversity than polypropylene. This study provides new insights into the mechanisms driving colonizer loads and the adaptive succession and assembly of the plastisphere in such a typically hydrodynamic and highly contaminated environment. The results help to fill the knowledge gap in understanding the potential role of microplastics in shaping the microecology of sewers and increasing health risks and substrate loss during sewer transfer.

Eriocitrin Alleviates Inflammation and Oxidative Stress in Subarachnoid Hemorrhage by Regulating DUSP14.

BACKGROUND: Inflammation and oxidative stress (OS) are major causes of aneurysmal subarachnoid hemorrhage (aSAH)-induced early brain injury (EBI). Eriocitrin (EC), a flavonoid compound, has anti-inflammatory and antioxidant actions. However, there is still no relevant studies on the role of EC in SAH. Accordingly, this research aims to clarify the anti-OS and anti-inflammatory efficacy of EC in SAH. METHOD: Rat SAH model was established in vivo and administered with Eriocitrin (25 mg/kg). In vitro, BV2 cells were exposed to oxyhemoglobin (OxyHb) for 24 hours and pretreated with Eriocitrin (1 uM/mL, 2 uM/mL, 4 uM/mL) for 30 minutes. Water maze experiments and neurological function scores were conducted to assess cognitive and motor function. TdT-mediated dUTP Nick-End Labeling (TUNEL) staining was used to detect cortical cell apoptosis. Enzyme-linked immunosorbent assay (ELISA) and polymerase chain reaction (PCR) were used to detect the inflammatory factors and malondialdehyde (MDA), as well as the expression of superoxide dismutase (SOD) and glutathione peroxidase (GSH-px). Western blots were used to semi quantify nuclear factor erythroid-2-related factor 2 (Nrf2), nuclear factor-κB (NF-κB), dual specificity phosphatase 14 (DUSP14) expression. RESULTS: The findings suggest that EC (25 mg/kg) reduced SAH-induced central nervous system (CNS) damage, neuronal apoptosis, inflammatory reactions and OS. Regarding a mechanistic study, EC enhanced Nrf2 and NF-κB by increasing DUSP14 activation, thereby reducing the inflammatory cytokines interleukin (IL)-1ß, tumor necrosis factor (TNF)-α, and IL-6. In addition, EC decreased MDA while markedly elevating SOD and enhancing GSH-px. Furthermore, specifically inhibiting DUSP14 expression via using protein-tyrosine-phosphatase (PTP) inhibitor IV, neutralized the protective action of EC and aggravated inflammation and OS. In vitro experiments of OxyHb-induced BV2 cells revealed that EC promoted Nrf2 while markedly suppressing NF-κB by increasing DUSP14 activation, thereby reducing the concentrations of the above inflammatory cytokines. Moreover, EC decreased MDA while evidently increasing SOD and GSH-px. CONCLUSION: In summary, this paper lays a theoretical grounding for EC treatment of SAH-induced inflammatory reactions and OS by regulating DUSP14.

TRAF7-targeted HOXA5 acts as a tumor suppressor in prostate cancer progression and stemness via transcriptionally activating SPRY2 and regulating MEK/ERK signaling.

Homeobox A5 (HOXA5), a homeodomain transcription factor, is considered a tumor suppressor in cancer progression; however, its function in prostate cancer (PCa) remains unclear. This study focused on the relevance of HOXA5 in PCa progression. We identified the downregulation of HOXA5 in PCa tissues based on the TCGA database and further verified in 30-paired PCa and adjacent normal tissues. Functional studies revealed that HOXA5 upregulation impaired the stem-like characteristics and malignant behaviors of PCa cells in vitro and in vivo. Mechanistically, HOXA5 was found to be regulated by tumor necrosis factor receptor-associated factor 7 (TRAF7), a putative E3-ubiquitin ligase. We observed that TRAF7 was overexpressed in PCa and subsequently enhanced the degradation of HOXA5 protein via its ubiquitin ligase activity, contributing to the acquisition of an aggressive PCa phenotype. For its downstream mechanism, we demonstrated that sprouty RTK signaling antagonist 2 (SPRY2) served as a downstream target of HOXA5. HOXA5 could directly bind to the SPRY2 promoter, thereby regulating the SPRY2-mediated MEK/ERK signaling pathway. Silencing SPRY2 largely compromised the tumor-suppressive effect of HOXA5 in PCa progression and cancer stemness. Our findings highlight the previously-underappreciated signaling axis of TRAF7-HOXA5-SPRY2, which provides a novel prognostic and therapeutic target for PCa treatment.

Systematic investigation of mitochondrial transfer between cancer cells and T cells at single-cell resolution.

Mitochondria (MT) participate in most metabolic activities of mammalian cells. A near-unidirectional mitochondrial transfer from T cells to cancer cells was recently observed to "metabolically empower" cancer cells while "depleting immune cells," providing new insights into tumor-T cell interaction and immune evasion. Here, we leverage single-cell RNA-seq technology and introduce MERCI, a statistical deconvolution method for tracing and quantifying mitochondrial trafficking between cancer and T cells. Through rigorous benchmarking and validation, MERCI accurately predicts the recipient cells and their relative mitochondrial compositions. Application of MERCI to human cancer samples identifies a reproducible MT transfer phenotype, with its signature genes involved in cytoskeleton remodeling, energy production, and TNF-α signaling pathways. Moreover, MT transfer is associated with increased cell cycle activity and poor clinical outcome across different cancer types. In summary, MERCI enables systematic investigation of an understudied aspect of tumor-T cell interactions that may lead to the development of therapeutic opportunities.

Quantifiable TCR repertoire changes in pre-diagnostic blood specimens among high-grade ovarian cancer patients.

High grade serous ovarian cancer (HGOC) is a major cause of death in women. Early detection of HGOC usually leads to a cure, yet it remains a clinical challenge with over 90% HGOCs diagnosed at advanced stages. This is mainly because conventional biomarkers are not sensitive to detect the microscopic yet metastatic early HGOC lesions. In this study, we sequenced the blood T cell receptor (TCR) repertoires of 466 ovarian cancer patients and controls, and systematically investigated the immune repertoire signatures in HGOCs. We observed quantifiable changes of selected TCRs in HGOCs that are reproducible in multiple independent cohorts. Importantly, these changes are stronger during stage I. Using pre-diagnostic patient blood samples from the Nurses' Health Study, we confirmed that HGOC signals can be detected in the blood TCR repertoire up to 4 years proceeding conventional diagnosis. Our findings may provide the basis of an immune-based HGOC early detection criterion.

[Analyzing the Pollution Sources and Mechanisms of Urban Rivers Based on Identifying the Molecular Signature of Dissolved Organic Matter].

Dissolved organic matter (DOM) is an essential component of river pollutants. Under the new situation of black water treatment in urban areas of China, in view of the widespread problem of unclear sources of multiple pollutants, further analysis of DOM components in urban rivers from the molecular level is a key link to deeply explore the sources, causes, and mechanism of river pollution so as to achieve efficient management. In this study, the urban rivers in the central city were selected as the research object, and a total of five rivers were selected that were seriously affected by the discharge sewage of four combined and separated sewer systems, respectively. Using Fourier transform ion cyclotron resonance mass spectrometry (FT-ICR-MS), this study identified the molecular formulae and analyzed the elemental composition and compound groups of DOM in water and sediment samples at each site in dry and wet weather. The results showed that:①although CHO molecules and lignins were the main compounds in the urban river DOM, the high proportion of lipids, proteins, and heteroatomic compounds (especially CHOS molecules) revealed the anthropogenic pollution in rivers, which also led to the increase in DOC, TN, and NH+4-N. ②Surfactants such as C17H28O3S and C18H30O3S were ubiquitous in all urban rivers, which could be used as markers of domestic wastewater pollution. ③In wet weather, the rainfall inputs, storm runoffs, and hydraulic disturbance jointly led to the increase in the proportion of CHO molecules and lignin compounds; the decrease in proteins and lipids; the rise of DOC, TN, and NH+4-N concentrations in river water; and the decrease in DOC, TN, and NH+4-N concentrations and proteins and lipids in river sediments. ④The abundance of multi-heteroatomic compounds and condensed aromatics in the combined sewer system was higher than that in the separated sewer system, which may have been more severely polluted by domestic wastewater and storm runoff, especially kitchen wastewater. This study provides new insight for clarifying the critical causes of pollution in the new stage and provides an essential basis for further precision prevention and control of water pollution.

Loss of SYNCRIP unleashes APOBEC-driven mutagenesis, tumor heterogeneity, and AR-targeted therapy resistance in prostate cancer.

Tumor mutational burden and heterogeneity has been suggested to fuel resistance to many targeted therapies. The cytosine deaminase APOBEC proteins have been implicated in the mutational signatures of more than 70% of human cancers. However, the mechanism underlying how cancer cells hijack the APOBEC mediated mutagenesis machinery to promote tumor heterogeneity, and thereby foster therapy resistance remains unclear. We identify SYNCRIP as an endogenous molecular brake which suppresses APOBEC-driven mutagenesis in prostate cancer (PCa). Overactivated APOBEC3B, in SYNCRIP-deficient PCa cells, is a key mutator, representing the molecular source of driver mutations in some frequently mutated genes in PCa, including FOXA1, EP300. Functional screening identifies eight crucial drivers for androgen receptor (AR)-targeted therapy resistance in PCa that are mutated by APOBEC3B: BRD7, CBX8, EP300, FOXA1, HDAC5, HSF4, STAT3, and AR. These results uncover a cell-intrinsic mechanism that unleashes APOBEC-driven mutagenesis, which plays a significant role in conferring AR-targeted therapy resistance in PCa.

Bovine blastocyst-like structures derived from stem cell cultures.

Understanding the mechanisms of blastocyst formation and implantation is critical for improving farm animal reproduction but is hampered by a limited supply of embryos. Here, we developed an efficient method to generate bovine blastocyst-like structures (termed blastoids) via assembling bovine trophoblast stem cells and expanded potential stem cells. Bovine blastoids resemble blastocysts in morphology, cell composition, single-cell transcriptomes, in vitro growth, and the ability to elicit maternal recognition of pregnancy following transfer to recipient cows. Bovine blastoids represent an accessible in vitro model for studying embryogenesis and improving reproductive efficiency in livestock species.

Ginsenoside Rg5 attenuates hypoxia-induced cardiomyocyte apoptosis via regulating the Akt pathway.

Ginsenoside Rg5 has been implicated in a variety of diseases. However, it is unknown whether Ginsenoside Rg5 can protect against hypoxia-induced neonatal rat cardiomyocytes (NRMs). The purpose of this study was to look into the effect of Ginsenoside Rg5 on hypoxia-induced NRMs apoptosis as well as the underlying molecular mechanism. In this study, following isolation and culture of ventricular myocardial cells from neonatal rats, the appropriate concentration of Rg5 was determined using the MTT assay, the effect of Rg5 on apoptosis was assessed employing TUNEL staining and flow cytometry assays. Levels of apoptosis-related proteins and phosphorylated level of Akt (ser 473 and ser 308) were analyzed using the western blot analysis. Finally, the experimental results shown that Ginsenoside Rg5 significantly inhibited hypoxia-induced NRMs apoptosis, decreased the expression pro-apoptotic protein Bax, increased the expression of anti-apoptotic protein Bcl-2 ratio and the level of cleaved caspase 3. Akt signaling activation was found to be the mechanism of Ginsenoside Rg5s protective effect on hypoxia-induced NRMs apoptosis, as an Akt inhibitor eliminated the anti-apoptotic effects of Ginsenoside Rg5. Various analyses were performed and verified, ginsenoside Rg5 suppressed hypoxia-induced apoptosis in NRMs via activation of the Akt signaling.

AMES: An Automated Self-Administered Scale to Detect Incipient Cognitive Decline in Primary Care Settings.

Early identification and intervention of cognitive decline could be effective to prevent progression to dementia. We developed a self-delivered cognitive screening tool, Automated Memory and Executive Screening (AMES), to assess cognitive domains including memory, language, and executive function. 189 participants with diagnoses of mild cognitive impairment (MCI, n = 43), subjective cognitive decline (SCD, n = 29), objectively-defined subtle cognitive decline (obj-SCD, n = 18), and normal controls (NC, n = 99) completed the study. AMES had good convergent validity with conventional scales, and was good to discriminate patients with MCI (area under the curve [AUC] = 0.88; sensitivity = 86%; specificity = 80%) and obj-SCD (AUC = 0.78; sensitivity = 89%; specificity = 63%) from NC. These findings support that AMES is an easy to administer and effective instrument to screen for early cognitive impairment in community-based settings.

Malignant cancer may increase the risk of all-cause in-hospital mortality in patients with acute myocardial infarction: a multicenter retrospective study of two large public databases.

BACKGROUND: Acute myocardial infarction (AMI) and cancer are diseases with high morbidity and mortality worldwide, bringing a serious economic burden, and they share some risk factors. The purpose of this study was to determine the effect of cancer on the all-cause in-hospital mortality of patients with AMI. METHODS: This multicenter retrospective study analyzed patients with AMI from the Medical Information Mart for Intensive Care IV (MIMIC-IV) database and eICU Collaborative Research Database (eICU-CRD) in the United States. Patients were divided into two groups based on whether they had concomitant malignant cancer: cancer and noncancer groups. The outcome was all-cause in-hospital mortality. The association between the two groups and their outcomes were analyzed using Kaplan-Meier and Cox proportional-hazards regression models. Propensity score matching (PSM) and propensity score based inverse probability of treatment weighting (IPTW) were used to further adjust for confounding variables to verify the stability of the results. RESULTS: The study included 3,034 and 5,968 patients with AMI from the MIMIC-IV database and the eICU-CRD, respectively. Kaplan-Meier survival curves indicated that the probability of in-hospital survival was lower in patients with cancer than in those without cancer. After adjusting for potential confounding variables using multivariable Cox proportional hazards regression, the risk of all-cause in-hospital mortality was significantly higher in the cancer than the noncancer group, and the HR (95% CI) values for the cancer group were 1.56(1.22,1.98) and 1.35(1.01,1.79) in the MIMIC-IV database and the eICU-CRD, respectively. The same results were obtained after using PSM and IPTW, which further verified the results. CONCLUSIONS: Among the patients with AMI, the all-cause in-hospital mortality risk of those with cancer was higher than those without cancer. Therefore, when treating such patients, comprehensive considerations should be made from a multidisciplinary perspective involving cardiology and oncology, with the treatment plan adjusted accordingly.

The blackening process of black-odor water: Substance types determination and crucial roles analysis.

Black-odor water is a serious environmental issue in many developing counties. Iron sulfides and chromophoric dissolved organic matter are considered possible blackening substances. However, the specific type of blackening iron sulfides and the contributions of blackening substances are unclear. This study performed a laboratory simulation experiment to identify the blackening iron sulfides and quantify the contribution of blackening substances. The environmental conditions for forming blackening substances and their blackening process were also determined. We demonstrated that the black iron sulfide was mackinawite. Humic acid is another substance that absorbs light. The equivalent contributions of mackinawite and humic acid were 18.94 m-1/mg Fe2+ and 1.11 m-1/mg DOC, respectively. A pH of more than 6 is a precondition for producing mackinawite. The production of black substances is the foundation of the blackening process, but the suspension of black substances is essential in causing water blackening. Fulvic acid stabilizes the suspension by changing the surface charge of blackening substances. Moreover, blackening substances can also be suspended with microbial flocs. Determining blackening substances and their role during the blackening process would allow for developing precise and targeted control technologies, improving urban water over the long term.

Real-time variabilities in microplastic abundance and characteristics of urban surface runoff and sewer overflow in wet weather as impacted by land use and storm factors.

Urban surface runoff (USR) and drainage system overflows during wet weather (WWF) play a key role in shaping water pollution. Particularly, the impact of large amounts of microplastic pollution on urban water bodies is unclear. We conducted an in-field investigation in six central urban drainage systems along Suzhou Creek in the Shanghai megacity of China and identified the impacts of storm factors and land use on the real-time dynamic changes in microplastic abundance and characteristics in USR and WWF. Microplastic abundances ranged from 228.3 ± 105.4-4969.51 ± 348.8, 309.3 ± 144.3-5195.8 ± 425.5, and 130.0 ± 30.0-8500.0 ± 1241.0 particles/L in the traffic and residential catchment USR, and the WWF, respectively. Under similar storm factor conditions, we observed correlations between environmental factors and microplastic abundance, especially the polymer type, verifying the significant role of land use. The microplastic abundance were 90.2 particles/L higher in the traffic catchment USR than in the residential catchment USR. Notably, we found unique microplastic polymers comprising ethylene vinyl acetate copolymer and thermoplastic elastomers in the residential and traffic catchment USR, respectively. However, land use had a minimum impact on the size and shape of microplastics: small-sized and film microplastics dominated in both USR types. We found statistical evidence of the widespread correlations between microplastic abundance and storm factors (accumulated storm depth and WWF flow) in both USR and WWF. The first flush phenomenon of microplastic dynamics was found in both USR and WWF. Microplastic characteristics also changed dynamically with storm time. With heavy storm factors, polypropylene and small-sized (<1 mm) microplastics in USR events increased and then decreased. This was also true for WWF events in granular and polyethylene terephthalate microplastics. Our results can facilitate the targeted mitigation of emerging pollutants to enhance stormwater management strategies and prevent future contamination.

Construction of TiO2(B)/Anatase Heterophase Junctions via a Water-Induced Phase Transformation Strategy for Enhanced Photocatalytic Hydrogen Production.

The development of facile and green solution-phase routes toward the fabrication of TiO2-based heterophase junctions with a delicate control of phase and structure is a challenging task. Herein, we report a simple and convenient method to controllably fabricate TiO2(B)/anatase heterophase junctions, which was successfully realized by utilizing the ideal great solvent of water to treat the presynthesized TiO2(B) nanosheet precursor at a low temperature of 80 °C. On the basis of phase structure transformation and morphology evolution data, the formation of these TiO2(B)/anatase heterophase junctions was reasonably explained by a novel water-induced TiO2(B) → anatase phase transformation mechanism. Benefiting from the desirable structural and photoelectronic advantages of more exposed active sites, enhanced light absorbance, and promoted separation of photogenerated electron-hole pairs, the thus-transformed TiO2(B)/anatase heterophase junctions exhibit fascinating photocatalytic performance in water splitting. Specifically, with the help of Pt as a cocatalyst and methanol as a sacrificial agent, the H2 production rate of optimized TiO2(B)/anatase heterophase junction reaches 6.92 mmol·g-1·h-1, which is almost 7.1 and 2.1 times higher than those of the pristine TiO2(B) nanosheets and the final anatase nanocrystals. More interestingly, the TiO2(B)/anatase heterophase junction also delivers prominent activity toward pure water splitting to simultaneously produce H2 and H2O2, with evolution rates of up to 1.10 and 0.55 mmol·g-1·h-1, respectively. Our work may advance the facile green solvent-mediated synthesis of metal oxide-based heterophase junctions for applications in energy- and environmental-related areas.

[Ecological Risk Assessment of Microplastics Occurring in Surface Water of Terrestrial Water Systems across China].

To assess the ecological risk of microplastics (MPs) occurring in the surface water of terrestrial water systems across China, this study obtained relevant literature and data by searching keywords including microplastics, urban, and river on websites such as Science Direct and Web of Science. We constructed an evaluation method of ecological risk characterization ratio (RCR) based on chemical hazard data, as well as data of MPs abundance and polymer proportion originating in studies from 2017 to 2021 that covered 33 water bodies in 15 provinces. The results showed that the average abundance of MPs in natural water bodies in China reached (3604.2±5926.4) n·m-3, and the average abundance of MPs in urban water bodies was (7722.6±9505.7) n·m-3. The corresponding average RCR of natural water bodies was 22.09±45.2, and the average RCR of urban water bodies was 15.67±34.8. Therefore, according to the value of RCR, the ecological risk could be rated as four levels. Of these, no significant risk (RCR ≤ 1) was found in 17 water bodies, accounting for 42.5%; low ecological risks (RCR 1-10) were found in 12 water bodies (30%); medium ecological risks (RCR 10-100) were found in 9 water bodies (22.5%); and high ecological risks (RCR>100) were found in 2 water bodies (5%). Data analysis showed a significant correlation between MPs abundance and RCR values in natural water bodies (R2=0.875, P<0.01), though not in urban water bodies. This suggested that the high abundance of MPs could not precisely indicate a high degree of ecological risk in the area. In addition, RCR values were observed to be positively correlated with the watershed area (R2=0.864, P<0.01), and MPs abundance was correlated with GDP (R2=0.679, P<0.05) and watershed resident population (R2=0.922, P<0.05). This study provides baseline data for evaluating the ecological risk of MPs and a feasible method for evaluating the ecological risk of MPs in surface water of terrestrial water systems.

Occurrence of macroplastics and microplastics in biogenic waste digestate: Effects of depackaging at source and dewatering process.

Plastic debris, including macroplastics (>5 mm) and microplastics (0.1-5 mm), has proven to be an emerging contaminant. Anaerobic digestion, coupled with energy recovery, can be an effective valorization technology for biogenic waste. But the use of the resulting digestate as a soil conditioner is a source for plastic debris release into the environment. The preprocess and postprocess used could influence the quantity of plastic debris found in the digestate, but the specifics of these effects are relatively unknown. Therefore, we measured the quantity of plastic debris in raw digestate under a variety of preprocessing scenarios. We also investigated the occurrence of plastic debris in solid and liquid digestates resulting from the dewatering of raw digestate. The quantity of plastic debris ranged from 41 to 3298 particles/kg (WW) for raw digestate, 319-3604 particles/kg (WW) for solid digestate and 7-38 particles/kg (WW) for liquid digestate. We observed that depackaging at source by citizens themselves (removing the package of biogenic waste when dropping it into bins), significantly reduced the quantities of plastic debris in raw digestate by an order of magnitude. Furthermore, the number of polymer types in raw digestate, where depackaging occurred at source, were lower than that where this rule was not in place. The average size of plastic debris in solid digestate was significantly smaller than that in raw digestate, which indicated that the process of mechanical dewatering could generate MPs. It is recommended to depackage for biogenic waste at source to reduce the quantities of MPs in digestate.

Ectopic JAK-STAT activation enables the transition to a stem-like and multilineage state conferring AR-targeted therapy resistance.

Emerging evidence indicates that various cancers can gain resistance to targeted therapies by acquiring lineage plasticity. Although various genomic and transcriptomic aberrations correlate with lineage plasticity, the molecular mechanisms enabling the acquisition of lineage plasticity have not been fully elucidated. We reveal that Janus kinase (JAK)-signal transducer and activator of transcription (STAT) signaling is a crucial executor in promoting lineage plasticity-driven androgen receptor (AR)-targeted therapy resistance in prostate cancer. Importantly, ectopic JAK-STAT activation is specifically required for the resistance of stem-like subclones expressing multilineage transcriptional programs but not subclones exclusively expressing the neuroendocrine-like lineage program. Both genetic and pharmaceutical inhibition of JAK-STAT signaling resensitizes resistant tumors to AR-targeted therapy. Together, these results suggest that JAK-STAT are compelling therapeutic targets for overcoming lineage plasticity-driven AR-targeted therapy resistance.