Human biodistribution and radiation dosimetry for the tau tracer [18F]Florzolotau in healthy subjects.

BACKGROUND: Tau pathology plays a crucial role in neurodegeneration diseases including Alzheimer's disease (AD) and non-AD diseases such as progressive supranuclear palsy. Tau positron emission tomography (PET) is an in-vivo and non-invasive medical imaging technique for detecting and visualizing tau deposition within a human brain. In this work, we aim to investigate the biodistribution of the dosimetry in the whole body and various organs for the [18F]Florzolotau tau-PET tracer. A total of 12 healthy controls (HCs) were enrolled at Chang Gung Memorial Hospital. All subjects were injected with approximately 379.03 ± 7.03 MBq of [18F]Florzolotau intravenously, and a whole-body PET/CT scan was performed for each subject. For image processing, the VOI for each organ was delineated manually by using the PMOD 3.7 software. Then, the time-activity curve of each organ was acquired by optimally fitting an exponential uptake and clearance model using the least squares method implemented in OLINDA/EXM 2.1 software. The absorbed dose for each target organ and the effective dose were finally calculated. RESULTS: From the biodistribution results, the elimination of [18F]Florzolotau is observed mainly from the liver to the intestine and partially through the kidneys. The highest organ-absorbed dose occurred in the right colon wall (255.83 µSv/MBq), and then in the small intestine (218.67 µSv/MBq), gallbladder wall (151.42 µSv/MBq), left colon wall (93.31 µSv/MBq), and liver (84.15 µSv/MBq). Based on the ICRP103, the final computed effective dose was 34.9 µSv/MBq with CV of 10.07%. CONCLUSIONS: The biodistribution study of [18F]Florzolotau demonstrated that the excretion of [18F]Florzolotau are mainly through the hepatobiliary and gastrointestinal pathways. Therefore, a routine injection of 370 MBq or 185 MBq of [18F]Florzolotau leads to an estimated effective dose of 12.92 or 6.46 mSv, and as a result, the radiation exposure to the whole-body and each organ remains within acceptable limits and adheres to established constraints. TRIAL REGISTRATION: Retrospectively Registered at Clinicaltrials.gov (NCT03625128) on 12 July, 2018, https://clinicaltrials.gov/study/NCT03625128 .

Advanced sustainable processes via functionalized Fe-N co-doped fishbone biochar for the remediation of plasticizer di-(2-ethylhexyl) phthalate-contaminated marine sediment.

Sediments are important sinks for di-(2-ethylhexyl) phthalate (DEHP), a plasticizer, and thus, maintaining the sediment quality is essential for eliminating plasticizers in aqueous environments and recovering the sediment ecological functions. To mitigate the potential risks of endocrine-disrupting compounds, identifying an effective and eco-friendly degradation process of organic pollutants from sediments is important. However, sustainable and efficient utilization of slow pyrolysis for converting shark fishbone to generate shark fishbone biochar (SFBC) has rarely been explored. Herein, SFBC biomass was firstly produced by externally incorporating heteroatoms or iron oxide onto its surface in conjunction with peroxymonosulfate (PMS) to promote DEHP degradation and explore the associated benthic bacterial community composition from the sediment in the water column using the Fe-N-SFBC/PMS system. SFBC was pyrolyzed at 300-900 °C in aqueous sediment using a carbon-advanced oxidation process (CAOP) system based on PMS. SFBC was rationally modified via N or Fe-N doping as a radical precursor in the presence of PMS (1 × 10-5 M) for DEHP removal. The innovative SFBC/PMS, N-SFBC/PMS, and Fe-N-SFBC/PMS systems could remove 82%, 65%, and 90% of the DEHP at pH 3 in 60 min, respectively. The functionalized Fe3O4 and heteroatom (N) co-doped SFBC composite catalysts within a hydroxyapatite-based structure demonstrated the efficient action of PMS compared to pristine SFBC, which was attributed to its synergistic behavior, generating reactive radicals (SO4•-, HO•, and O2•-) and non-radicals (1O2) involved in DEHP decontamination. DEHP was significantly removed using the combined Fe-N-SFBC/PMS system, revealing that indigenous benthic microorganisms enhance their performance in DEHP-containing sediments. Further, DEHP-induced perturbation was particularly related to the Proteobacteria phylum, whereas Sulfurovum genus and Sulfurovum lithotrophicum species were observed. This study presents a sustainable method for practical, green marine sediment remediation via PMS-CAOP-induced processes using a novel Fe-N-SFBC composite material and biodegradation synergy.

Soluble tumor necrosis factor receptor type 1 is an alternative marker of urinary albumin-creatinine ratio and estimated glomerular filtration rate for predicting the decline of renal function in subjects with type 2 diabetes mellitus.

BACKGROUND: Urinary albumin-creatinine ratio (UACR) and estimated glomerular filtration rates (eGFR) help predict worsening diabetic kidney disease (DKD) but have their limitations. Soluble tumor necrosis factor receptor type 1 (sTNFR1) is a biomarker of DKD. The predictive abilities of sTNFR1 and UACR plus eGFR have not been compared. METHODS: This prospective cohort study included patients with type 2 diabetes (T2D) to identify the risk factors of worsening DKD. Renal events were defined as > 30 % loss in eGFR based on consecutive tests after 6 months. The associations of sTNFR1, UACR, and eGFR levels and the risks of renal events were tested using a Cox regression model and the area under the curve (AUC) was compared between sTNFR1 levels and UACR plus eGFR using receiver-operating characteristic (ROC) analysis. The accuracy of stratification was evaluated using Kaplan-Meier analysis. RESULTS: Levels of sTNFR1 and UACR were associated with risks of > 30 % decline in eGFR after adjusting for relevant factors. The association between sTNFR1 levels and renal outcomes was independent of UACR and eGFR at baseline. The AUC of sTNFR1 level was comparable with that of combined UACR and eGFR (0.73 vs. 0.71, respectively, p = 0.72) and the results persisted for quartile groups of sTNFR1 and risk categories of Kidney Disease: Improving Global Outcomes (KDIGO) (0.70 vs. 0.71, respectively, p = 0.84). Both stratifications by sTNFR1 levels and KDIGO were accurate. CONCLUSION: sTNFR1 could be an alternative marker for identifying patients with diabetes at risk of declining renal function.

A Biomimetic Synthetic Strategy Can Provide Keratan Sulfate I and II Oligosaccharides with Diverse Fucosylation and Sulfation Patterns.

Keratan sulfate (KS) is a proteoglycan that is widely expressed in the extracellular matrix of various tissue types, where it performs multiple biological functions. KS is the least understood proteoglycan, which in part is due to a lack of panels of well-defined KS oligosaccharides that are needed for structure-binding studies, as analytical standards, to examine substrate specificities of keratinases, and for drug development. Here, we report a biomimetic approach that makes it possible to install, in a regioselective manner, sulfates and fucosides on oligo-N-acetyllactosamine (LacNAc) chains to provide any structural element of KS by using specific enzyme modules. It is based on the observation that α1,3-fucosides, α2,6-sialosides and C-6 sulfation of galactose (Gal6S) are mutually exclusive and cannot occur on the same LacNAc moiety. As a result, the pattern of sulfation on galactosides can be controlled by installing α1,3-fucosides or α2,6-sialosides to temporarily block certain LacNAc moieties from sulfation by keratan sulfate galactose 6-sulfotransferase (CHST1). The patterns of α1,3-fucosylation and α2,6-sialylation can be controlled by exploiting the mutual exclusivity of these modifications, which in turn controls the sites of sulfation by CHST1. Late-stage treatment with a fucosidase or sialidase to remove blocking fucosides or sialosides provides selectively sulfated KS oligosaccharides. These treatments also unmasked specific galactosides for further modification by CHST1. To showcase the potential of the enzymatic strategy, we have prepared a range of poly-LacNAc derivatives having different patterns of fucosylation and sulfation and several N-glycans decorated by specific arrangements of sulfates.

Safinamide, an inhibitor of monoamine oxidase, modulates the magnitude, gating, and hysteresis of sodium ion current.

BACKGROUND: Safinamide (SAF), an α-aminoamide derivative and a selective, reversible monoamine oxidase (MAO)-B inhibitor, has both dopaminergic and nondopaminergic (glutamatergic) properties. Several studies have explored the potential of SAF against various neurological disorders; however, to what extent SAF modulates the magnitude, gating, and voltage-dependent hysteresis [Hys(V)] of ionic currents remains unknown. METHODS: With the aid of patch-clamp technology, we investigated the effects of SAF on voltage-gated sodium ion (NaV) channels in pituitary GH3 cells. RESULTS: SAF concentration-dependently stimulated the transient (peak) and late (sustained) components of voltage-gated sodium ion current (INa) in pituitary GH3 cells. The conductance-voltage relationship of transient INa [INa(T)] was shifted to more negative potentials with the SAF presence; however, the steady-state inactivation curve of INa(T) was shifted in a rightward direction in its existence. SAF increased the decaying time constant of INa(T) induced by a train of depolarizing stimuli. Notably, subsequent addition of ranolazine or mirogabalin reversed the SAF-induced increase in the decaying time constant. SAF also increased the magnitude of window INa induced by an ascending ramp voltage Vramp. Furthermore, SAF enhanced the Hys(V) behavior of persistent INa induced by an upright isosceles-triangular Vramp. Single-channel cell-attached recordings indicated SAF effectively increased the open-state probability of NaV channels. Molecular docking revealed SAF interacts with both MAO and NaV channels. CONCLUSION: SAF may interact directly with NaV channels in pituitary neuroendocrine cells, modulating membrane excitability.

An IoT Real-Time Potable Water Quality Monitoring and Prediction Model Based on Cloud Computing Architecture.

In order to achieve the Sustainable Development Goals (SDG), it is imperative to ensure the safety of drinking water. The characteristics of each drinkable water, encompassing taste, aroma, and appearance, are unique. Inadequate water infrastructure and treatment can affect these features and may also threaten public health. This study utilizes the Internet of Things (IoT) in developing a monitoring system, particularly for water quality, to reduce the risk of contracting diseases. Water quality components data, such as water temperature, alkalinity or acidity, and contaminants, were obtained through a series of linked sensors. An Arduino microcontroller board acquired all the data and the Narrow Band-IoT (NB-IoT) transmitted them to the web server. Due to limited human resources to observe the water quality physically, the monitoring was complemented by real-time notifications alerts via a telephone text messaging application. The water quality data were monitored using Grafana in web mode, and the binary classifiers of machine learning techniques were applied to predict whether the water was drinkable or not based on the data collected, which were stored in a database. The non-decision tree, as well as the decision tree, were evaluated based on the improvements of the artificial intelligence framework. With a ratio of 60% for data training: at 20% for data validation, and 10% for data testing, the performance of the decision tree (DT) model was more prominent in comparison with the Gradient Boosting (GB), Random Forest (RF), Neural Network (NN), and Support Vector Machine (SVM) modeling approaches. Through the monitoring and prediction of results, the authorities can sample the water sources every two weeks.

HBV DNA Integration into Telomerase or MLL4 Genes and TERT Promoter Point Mutation as Three Independent Signatures in Subgrouping HBV-Related HCC with Distinct Features.

Introduction: A set of genetic mutations to classify hepatocellular carcinoma (HCC) useful to clinical studies is an unmet need. Hepatitis B virus-related HCC (HBV-HCC) harbors a unique genetic mutation, namely, the HBV integration, among other somatic endogenous gene mutations. We explored a combination of HBV DNA integrations and common somatic mutations to classify HBV-HCC by using a capture-sequencing platform. Methods: A total of 153 HBV-HCCs after surgical resection were subjected to capture sequencing to identify HBV integrations and three common somatic mutations in genomes. Three mutually exclusive mutations, HBV DNA integration into the TERT promoter, HBV DNA integration into MLL4, or TERT promoter point mutation, were identified in HBV-HCC. Results: They were used to classify HBV-HCCs into four groups: G1 with HBV-TERT integration (25.5%); G2 with HBV-MLL4 integration (10.5%); G3 with TERT promoter mutation (30.1%); and G4 without these three mutations (34.0%). Clinically, G3 has the highest male-to-female ratio, cirrhosis rate, and associated with higher early recurrence and mortality after resection, but G4 has the best outcome. Transcriptomic analysis revealed a grouping different from the published ones and G2 with an active immune profile related to immune checkpoint inhibitor response. Analysis of integrated HBV DNA provided clues for HBV genotype and variants in carcinogenesis of different HCC subgroup. This new classification was also validated in another independent cohort. Conclusion: A simple and robust genetic classification was developed to aid in understanding HBV-HCC and in harmonizing clinical studies.

Pretreatment of marine sediment for the removal of di-(2-ethylhexyl) phthalate by sulfite in the presence of sorghum distillery residue-derived biochar and its effect on microbiota response.

This study investigates the mechanism behind the oxidation di-(2-ethylhexyl) phthalate (DEHP) in marine sediment by coupling sulfite using biochar prepared from sorghum distillery residue (SDRBC). The rationale for this investigation stems from the need to seek effective methods for DEHP-laden marine sediment remediation. The aim is to assess the feasibility of sulfite-based advanced oxidation processes for treating hazardous materials such as DEHP containing sediment. To this end, the sediment in question was treated with 2.5 × 10-5 M of sulfite and 1.7 g L-1 of SDRBC700 at acidic pH. Additionally, the study demonstrated that the combination of SDRBC/sulfite with a bacterial system enhances DEHP removal. Thermostilla bacteria were enriched, highlighting their role in sediment treatment. This study concludes that sulfite-associated sulfate radicals-driven carbon advanced oxidation process (SR-CAOP) offers sustainable sediment pretreatment through the SDRBC/sulfite-mediated microbial consortium, in which the SO3•- and 1O2 were responsible for DEHP degradation. SDRBC/sulfite offers an effective and environmentally friendly method for removing DEHP. Further, these results can be targeted at addressing industry problems related to sediment treatment.

Analyzing (3-Aminopropyl)triethoxysilane-Functionalized Porous Silica for Aqueous Uranium Removal: A Study on the Adsorption Behavior.

This study synthesized (3-aminopropyl)triethoxysilane-functionalized porous silica (AP@MPS) to adsorb aqueous uranium (U(VI)). To comprehensively analyze the surface properties of the AP@MPS materials, a combination of SEM, BET, XPS, NMR, and zeta potential tests were conducted. The adsorption experiments for U(VI) revealed the rapid and efficient adsorption capacity of AP@MPS, with the solution condition of a constant solution pH = 6.5, an initial U(VI) concentration of 600 mg × L-1, a maximum U(VI) capacity of AP@MPS reaching 381.44 mg-U per gram of adsorbent, and a removal rate = 63.6%. Among the four types of AP@MPS with different average pore sizes tested, the one with an average pore size of 2.7 nm exhibited the highest U(VI) capacity, particularly at a pH of 6.5. The adsorption data exhibited a strong fit with the Langmuir model, and the calculated adsorption energy aligned closely with the findings from the Potential of Mean Force (PMF) analysis. The outcomes obtained using the Surface Complex Formation Model (SCFM) highlight the dominance of the coulombic force ΔG0coul as the principal component of the adsorption energy (ΔG0ads). This work garnered insights into the adsorption mechanism by meticulously examining the ΔG0ads across a pH ranging from 4 to 8. In essence, this study's findings furnish crucial insights for the future design of analogous adsorbents, thereby advancing the realm of uranium(VI) removal methodologies.

Cumulative blood pressure load and hypertensive nephropathy in Han Chinese hypertensive patients.

The study aims to assess the relationship between cumulative blood pressure load (cBPL) and the risk of renal function decline in hypertensive patients and determine the blood pressure (BP) threshold required to prevent hypertensive nephropathy. A single-center prospective cohort study was conducted on hypertensive patients. The cBPL was defined as the proportion of area beyond variable BP cutoffs under ambulatory BP monitoring. Renal events were defined as > 25% (minor) or > 50% (major) decline of baseline estimated glomerular filtration rate (eGFR). Cox regression analysis was conducted between cBPL, other ambulatory BP parameters, and renal events. The results revealed a total of 436 Han Chinese hypertensive patients were eligible for enrollment. During an average follow-up period of 5.1 ± 3.3 years, a decline of > 25% and > 50% in eGFR was observed in 77 and eight participants, respectively. Cox regression analysis revealed that cSBPL140 (hazard ratio [HR], 1.102; 95% confidence interval [CI], 1.017-1.193; p = .017), cSBPL130 (HR, 1.076; 95% CI, 1.019-1.137; p = .008), and cSBPL120 (HR, 1.054; 95% CI, 1.010-1.099; p = .015) were independently associated with minor renal events. Similarly, cSBPL140 (HR, 1.228; 95% CI, 1.037-1.455; p = .017), cSBPL130 (HR, 1.189; 95% CI, 1.045-1.354; p = .009), and cSBPL120 (HR, 1.155; 95% CI, 1.039-1.285; p = .008) were independently associated with major renal events. In conclusion, cBPL is associated with renal function decline in hypertensive patients. Minimizing cBPL120 may decrease the risk of hypertensive nephropathy.

Targeting of FSP1 regulates iron homeostasis in drug-tolerant persister head and neck cancer cells via lipid-metabolism-driven ferroptosis.

BACKGROUND: Research has demonstrated that some tumor cells can transform into drug-tolerant persisters (DTPs), which serve as a reservoir for the recurrence of the disease. The persister state in cancer cells arises due to temporary molecular reprogramming, and exploring the genetic composition and microenvironment during the development of head and neck squamous cell carcinoma (HNSCC) can enhance our comprehension of the types of cell death that HNSCC, thus identifying potential targets for innovative therapies. This project investigated lipid-metabolism-driven ferroptosis and its role in drug resistance and DTP generation in HNSCC. METHODS: High levels of FSP1 were discovered in the tissues of patients who experienced relapse after cisplatin treatment. RNA sequencing indicated that a series of genes related to lipid metabolism were also highly expressed in tissues from these patients. Consistent results were obtained in primary DTP cells isolated from patients who experienced relapse. The Cancer Genome Atlas database confirmed this finding. This revealed that the activation of drug resistance in cancer cells is influenced by FSP1, intracellular iron homeostasis, and lipid metabolism. The regulatory roles of ferroptosis suppressor protein 1 (FSP1) in HNSCC metabolic regulation were investigated. RESULTS: We generated human oral squamous cell carcinoma DTP cells (HNSCC cell line) to cisplatin and observed higher expression of FSP1 and lipid-metabolism-related targets in vitro. The shFSP1 blockade attenuated HNSCC-DTP cell stemness and downregulated tumor invasion and the metastatic rate. We found that cisplatin induced FSP1/ACSL4 axis expression in HNSC-DTPC cells. Finally, we evaluated the HNSCC CSC-inhibitory functions of iFSP1 (a metabolic drug and ferroptosis inducer) used for neo-adjuvant chemotherapy; this was achieved by inducing ferroptosis in a patient-derived xenograft mouse model. CONCLUSIONS: The present findings elucidate the link between iron homeostasis, ferroptosis, and cancer metabolism in HNSCC-DTP generation and acquisition of chemoresistance. The findings may serve as a suitable model for cancer treatment testing and prediction of precision treatment outcomes. In conclusion, this study provides clinically oriented platforms for evaluating metabolism-modulating drugs (FSP1 inhibitors) and new drug candidates of drug resistance and ferroptotic biomarkers.

Effect of Solute on Interfacial Properties and Micelle Structure of Dodecylbenzenesulfonate (DBS): Experimental and Molecular Dynamics Studies.

A combined experimental and molecular dynamic simulation approach was used to examine the structure and interfacial properties of solute-saturated micelles. The properties of dodecylbenzenesulfonate (DBS) micelles were examined in dodecane and benzene hydrocarbon systems. Pyrene fluorescence was used to determine the aggregation number of surfactant monomers in the micelle systems. Molecular dynamic (MD) simulations using energy minimization applying the CHARMm force field with the TIP3P model for water. Comparison of the DBS/benzene and DBS/Dodecane micelles equilibrium structures via radial distribution function (RDF) and probability distribution function (PDF) analysis indicates that the area per head group for the DBS/Benzene micelle interface is significantly larger than that of the DBS/Dodecane at the interface. It was also determined that benzene molecules can move freely within the micelle while dodecane is strictly confined in the core of the micelle. The increased interfacial area per monomer caused by the insertion of benzene also reduces the effectiveness of the surfactant, which has implications for use in various environmental applications. However, the DBS/benzene micelle can solubilize many more hydrocarbon molecules in one micelle with less surfactant monomer (i.e., lower aggregation number) per micelle due to the increased available packing positions within the micelle. This, in turn, increases the efficiency of the surfactant in real-world applications which is consistent with previous laboratory results. Understanding the differing solubilization characteristics of surfactants against various classes of hydrocarbons in single solute systems is a necessary step to beginning to understand their solubilization properties in the mixed waste systems prevalent in most surfactant enhanced remediation (SEAR) strategies.

Fatty acid-binding protein-3 and renal function decline in patients with chronic coronary syndrome.

BACKGROUND: Renal dysfunction is common in patients with coronary artery disease. Due to the shared vascular pathogenesis between the two conditions, novel biomarkers such as the fatty acid-binding protein-3 (FABP-3) have been proposed for diagnosis and prognosis prediction. This multicentre prospective cohort study investigates the association between FABP-3 and renal dysfunction. HYPOTHESIS: We hypothesized that higher FABP-3 levels are correlated to worse renal outcome. METHODS: Patients with chronic coronary syndrome were classified into three groups based on the initial serum FABP-3 levels. The Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation was used to estimate the patient's renal function. Renal events were defined as >25% and >50% decline in estimated glomerular filtration rate (eGFR). Cox multivariable regression was employed to delineate the correlation between FABP-3 and renal dysfunction. RESULTS: A total of 1606 subjects were included. During a mean follow-up of 35.9 months, there were 239 patients with eGFR >25% reduction and 60 patients with >50% reduction. In the Kaplan-Meier survival curve and log-rank test, increased levels of FABP-3 were significantly correlated with eGFR >25% reduction (p < .001) and >50% reduction (p < .001). Multivariate Cox regression model revealed that subjects with higher FABP-3 exhibited a greater risk of eGFR >25% reduction (Group 2: hazard ratio [HR] = 2.328, 95% confidence interval [CI] = 1.521-3.562, p < .001; Group 3: HR = 3.054, 95% CI = 1.952-4.776, p < .001) and >50% reduction (Group 3: HR = 4.838, 95% CI = 1.722-13.591, p = .003). CONCLUSIONS: Serum FABP-3 may serve as a novel biomarker to predict eGFR decline in patients with chronic coronary syndrome.

The impacts of anemia burden on clinical outcomes in patients with out-of-hospital cardiac arrest.

BACKGROUND: Out-of-hospital cardiac arrest (OHCA) has low survival rates, and few patients achieve a desirable neurological outcome. Anemia is common among OHCA patients and has been linked to worse outcomes, but its impact following the return of spontaneous circulation (ROSC) is unclear. This study examines the relationship between anemia burden and clinical outcomes in OHCA patients. HYPOTHESIS: Higher anemia burden after ROSC may be related to higher mortality and worse neurologic outcomes. METHODS: Patients who experienced OHCA and had ROSC were enrolled retrospectively. Anemia burden was defined as the area under curve from the target hemoglobin level over a 72-h period after OHCA. Hemoglobin level was measured at 12-h intervals. The clinical outcomes of the study included mortality and neurological outcomes at Day 30. RESULTS: The study enrolled 258 nontraumatic OHCA patients who achieved ROSC between January 2017 and December 2021. Among the 162 patients who survived more than 72 h, a higher anemia burden, specifically target hemoglobin levels below 7 (hazard ratio [HR]: 1.129, 95% confidence interval [CI]: 1.013-1.259, p = .029), 8 (HR: 1.099, 95% CI: 1.014-1.191, p = .021), and 9 g/dL (HR: 1.066, 95% CI: 1.001-1.134, p = .046) was associated with higher 30-day mortality. Additionally, anemia burden with target hemoglobin levels below 7 (HR: 1.129, 95% CI: 1.016-1.248; p = .024) and 8 g/dL (HR: 1.088; 95% CI: 1.008-1.174, p = .031) was linked to worse neurological outcomes. CONCLUSIONS: Anemia burden predicts 30-day mortality and neurological outcomes in OHCA patients who survive more than 72 h. Maintaining higher hemoglobin levels within the first 72 h after ROSC may improve short-term outcomes.

The remediation of marine sediments containing polycyclic aromatic hydrocarbons by peroxymonosulfate activated with Sphagnum moss-derived biochar and its benthic microbial ecology.

This research was to study the efficiency of Sphagnum moss-derived biochar (SMBC) in removing polycyclic aromatic hydrocarbons (PAHs) from marine sediment using a peroxymonosulfate (PMS)-based carbon-advanced oxidation process (PMS-CAOPs). Sphagnum moss-derived biochar (SMBC) was generated via a simple thermochemical process for PMS activation toward enhancing decontamination of sediments. At pH 6, the SMBC/PMS system achieved a PAH removal efficiency exceeding 78% in 12 h reaction time. Moreover, PAHs of 6-, 5-, 4-, 3-, and 2-ring structures exhibited 98%, 74%, 68%, 85%, and 91%, of removal, respectively. The SMBC activation of PMS generated both radicals (SO4•- and HO•) and nonradical (1O2), species responsible for PAHs degradation, attributed primarily to inherent iron and carbon moieties. The significant PAHs degradation efficiency showcased by the SMBC/PMS process holds promise for augmenting the performance of indigenous benthic microbial activity in sediment treatment contexts. The response of sediment microbial communities to PAH-induced stress was particularly associated with the Proteobacteria phylum, specifically the Sulfurovum genus. The findings of the present study highlight the efficacy of environmentally benign reactive radical/nonradical-based PMS-CAOP using pristine carbon materials, offering a sustainable strategy for sediment treatment.

Metal-free nitrogen and sulfur binary-doped cellulose-based biochar for efficient suppression of priority organic pollutants and environmental application.

Biochar production from cellulose biomass is an alternative solution in the search for clean and renewable biofuel. However, the rational design of cellulose biochar (CLBC) for polycyclic aromatic hydrocarbons (PAHs) reduction by integrating pyrolysis process parameters and introducing heteroatoms as inhibitors remains to be studied. Therefore, exogenous heteroatoms (N, B, S, SB, NB, and NS) were used to modify CLBC for the first time. CLBC300 pyrolyzed at 300 °C in a CO2 atmosphere achieved the highest concentrations of PAHs (4982 ± 271 ng g-1), compared with that of CLBC700 (3615 ± 71 ng g-1) formed in a N2 atmosphere without heteroatom doping. The results showed that binary nitrogen- and sulfur-doped CLBC exhibited remarkable PAH-removal performance of 99 % with the lowest toxic equivalency (TEQ) value of 9 ng g-1. Overall, this study presents novel insights into the development of a heteroatom-based modification approach for reducing CLBC-borne PAHs and creating value-added products from cellulose biomass.

Facile heteroatoms modification biochar production from mahogany (Swietenia macrophylla King) pericarps for enhanced the suppression of polycyclic aromatic hydrocarbon pollutants.

Polycyclic aromatic hydrocarbons (PAHs) are critical environmental concerns due to their intrinsic toxic aromatic nature and concomitant circumstances that potentially harm the ecological and human health. In this study, converting mahogany (Swietenia macrophylla King) pericarps to value-added biochar by pyrolysis for evaluating the potential formation/destruction of biochar-bound PAHs was studied for the first time. This study designed and optimized the thermal processing conditions at 300-900 °C in the CO2 or N2 atmosphere, and heteroatoms (N, O, B, NB, and NS) were modified for mahogany pericarps biochar (MPBC) production. The MPBC500 exhibited significantly higher pyrolysis products of PAHs (2780 ± 38 ng g-1) than that of MPBC900 (78 ± 6 ng g-1) under N2 without introducing modified elements. Specifically, the inhibition capacity of MPBC500 for PAHs under CO2 was improved most efficiently by the active nitrogen species of the pyridinic N and pyrrolic N groups. The pyrolysis conditions and heteroatom modification of MPBC altered its physicochemical properties, that is, aromaticity and hydrophobicity, affecting the PAH concentration and composition in the pyrolysis products. This study reveals sustainable approaches to reduce the environmental footprint of biochar by focusing on increases in PAHs pollution in sustainable biochar produced from a low-carbon bioeconomy perspective.

PAICS/DYRK3 Multienzyme Interactions as Coregulators of Purinosome Formation and Metabolism on Radioresistance in Oral Squamous Cell Carcinoma.

Oral squamous cell carcinoma (OSCC) is a prevalent type of oral cancer. While therapeutic innovations have made strides, radioresistance persists as a significant hindrance in OSCC treatment. Despite identifying numerous targets that could potentially suppress the oncogenic attributes of OSCC, the exploration of oncogenic protein kinases for cancer therapy remains limited. Consequently, the functions of many kinase proteins in OSCC continue to be largely undetermined. In this research, we aim to disclose protein kinases that target OSCC and elaborate their roles and molecular mechanisms. Through the examination of the kinome library of radiotherapy-resistant/sensitive OSCC cell lines (HN12 and SAS), we identified a key gene, the tyrosine phosphorylation-regulated kinase 3 (DYRK3), a member of the DYRK family. We developed an in vitro cell model, composed of radiation-resistant OSCC, to scrutinize the clinical implications and contributions of DYRK3 and phosphoribosylaminoimidazole carboxylase and phosphoribosylaminoimidazolesuccinocarboxamide synthase (PAICS) signaling in OSCC. This investigation involves bioinformatics and human tissue arrays. We seek to comprehend the role of DYRK3 and PAICS signaling in the development of OSCC and its resistance to radiotherapy. Various in vitro assays are utilized to reveal the essential molecular mechanism behind radiotherapy resistance in connection with the DYRK3 and PAICS interaction. In our study, we quantified the concentrations of DYRK3 and PAICS proteins and tracked the expression levels of key pluripotency markers, particularly PPAT. Furthermore, we extended our investigation to include an analysis of Glut-1, a gene recognized for its linkage to radioresistance in oral squamous cell carcinoma (OSCC). Furthermore, we conducted an in vivo study to affirm the impact of DYRK3 and PAICS on tumor growth and radiotherapy resistance, focusing particularly on the role of DYRK3 in the radiotherapy resistance pathway. This focus leads us to identify new therapeutic agents that can combat radiotherapy resistance by inhibiting DYRK3 (GSK-626616). Our in vitro models showed that inhibiting PAICS disrupts purinosome formation and influences the survival rate of radiation-resistant OSCC cell lines. These outcomes underscore the pivotal role of the DYRK3/PAICS axis in directing OSCC radiotherapy resistance pathways and, as a result, influencing OSCC progression or therapy resistance. Our findings also reveal a significant correlation between DYRK3 expression and the PAICS enzyme in OSCC radiotherapy resistance.

Soluble tumor necrosis factor receptor type 1 predicts cardiorenal outcomes and better associated with distinct cardiovascular or renal outcomes than precedential renal or cardiovascular events in type 2 diabetes mellitus.

Background: Inflammations are the crucial pathogenesis of chronic complications of type 2 diabetes mellitus (T2DM). Objectives: The timeline of cardiovascular and renal complications of T2DM and whether soluble tumor necrosis factor receptor type 1 (sTNFR1) levels predict cardiorenal outcomes were still elusive. Design: Prospectively observational study. Methods: Chinese patients with T2DM were enrolled. Cardiorenal composite events defined by either cardiovascular composite events (all-cause mortality, acute coronary syndrome, or non-fatal stroke) or renal composite events (a decline of >30% of renal function or worsening status of albuminuria) were followed. Associations of sTNFR1 levels and cardiovascular, renal, and cardiorenal composite events were analyzed in regression models presented by hazard ratio (HR) and 95% confidence interval (95% CI). Results: Among 370 subjects, 42 cardiovascular and 86 renal composite events occurred. Higher sTNFR1 levels were related to higher frequency and risks of cardiovascular composite events (HR 1.07, 95% CI 1.01-1.13, p = 0.009) and renal composite events (HR 1.05, 95% CI 1.02-1.09, p < 0.001). Occurrences of cardiovascular composite events were not predicted by precedential renal composite events. sTNFR1 levels were proved to be associated with risks of cardiorenal composite events in Cox regression sequential models (adjusted HR 1.04, 95% CI 1.00-1.08, p = 0.03). The results were consistent in all subgroup analyses. Conclusion: Levels of sTNFR1 were associated with cardiorenal complications of T2DM and the predictabilities of TNFR1 levels were better than precedential cardiovascular or renal events.