Periodate activation and pH regulation using ball-milled metal-oxide-mineral-biochar composite for removal of antibiotics from contaminated water.

The inclusion of mineral salts in carbon activators are beneficial for advanced oxidation processes (AOPs). Herein, we present the application of ball-milled biochar with phosphate salt for periodate (IO4-) activation and degradation of antibiotics in contaminated water. Physical characterization results showed that the catalyst is infused with Mg3(PO4)2 and ball-milling increased the specific surface area to 216 m2 g-1 from 46 m2 g-1 while reducing the particle size to less than 1.0 µ. The optimized system successfully eliminated >99% of diclofenac while maintaining the pH of the reaction medium to circumneutral levels. Scavenger and ESR experiments revealed the degradation is triggered by O2•-, 1O2 and •OH species within the system. Electrochemical studies confirmed electron transfer during diclofenac degradation. The reported system demonstrated high degradation efficiency under both neutral and acidic pH conditions. Based on the by-product analysis, the degradation pathway of diclofenac was elucidated. Further, the toxicity assessment for the identified intermediates showed minimum toxicity of the degraded products. This mineral-biochar composite exhibited promising performance in eliminating other antibiotic substances. Therefore, the present finding highlights the importance of raw materials selection for producing mineral-biochar composite that provide new insights into IO4- activation for antibiotic removal by maintaining the natural pH.

Sustainable utilization of Fe3O4-modified activated lignite for aqueous phosphate removal and ANN modeling.

Lignites are widely available and cost-effective in many countries. Sustainable methods for their utilization drive innovation, potentially advancing environmental sustainability and resource efficiency. In the present study, Fe3O4 (∼25.1 nm) supported on KOH-activated lignite (A-L) displayed 8 times higher phosphate removal than pristine A-L (67.6 mg/g vs. 8.5 mg/g at pH 5, 50 mg of absorbent in 25 mL of 1500 ppm [phosphate]), owing to its abundant Fe3O4 (10 wt.% of Fe) nanoparticle content. The removal occurred within ∼2 hours, following a pseudo-second-order kinetic model. Across pH levels ranging from 5.0 to 9.0, Fe3O4-A-L's phosphate removal occurs via both chemisorption and precipitation, as evident by kinetic, pH, and XPS analyses. The phosphate adsorption fits better with the Freundlich isotherm. The combined benefits of facile recovery, rapid phosphate uptake, straightforward regeneration, and attractive post-adsorption benefits (e.g., possibly use as a Fe, P-rich fertilizer) make magnetic Fe3O4-A-L a promising candidate for real-world applications. Artificial Neural Network (ANN) modeling indicates an excellent accuracy (R2 = 0.99) in predicting the amount of phosphate removed by Fe3O4-A-L. Sensitivity analysis revealed both temperature and initial concentration as the most influencing factors. Leveraging lignite in environmentally friendly applications not only addresses immediate challenges but also aligns with sustainability goals. The study clearly articulates the potential benefits of utilizing lignite for sustainable phosphate removal and recovery, offering avenues for mitigating environmental concerns while utilizing resources efficiently.

Gossypetin Prevents the Progression of Nonalcoholic Steatohepatitis by Regulating Oxidative Stress and AMP-Activated Protein Kinase.

Nonalcoholic steatohepatitis (NASH) is a severe liver metabolic disorder, however, there are still no effective and safe drugs for its treatment. Previous clinical trials used various therapeutic approaches to target individual pathologic mechanisms, but these approaches were unsuccessful because of the complex pathologic causes of NASH. Combinatory therapy in which two or more drugs are administered simultaneously to patients with NASH, however, carries the risk of side effects associated with each individual drug. To solve this problem, we identified gossypetin as an effective dual-targeting agent that activates AMP-activated protein kinase (AMPK) and decreases oxidative stress. Administration of gossypetin decreased hepatic steatosis, lobular inflammation and liver fibrosis in the liver tissue of mice with choline-deficient high-fat diet and methionine-choline deficient diet (MCD) diet-induced NASH. Gossypetin functioned directly as an antioxidant agent, decreasing hydrogen peroxide and palmitate-induced oxidative stress in the AML12 cells and liver tissue of MCD diet-fed mice without regulating the antioxidant response factors. In addition, gossypetin acted as a novel AMPK activator by binding to the allosteric drug and metabolite site, which stabilizes the activated structure of AMPK. Our findings demonstrate that gossypetin has the potential to serve as a novel therapeutic agent for nonalcoholic fatty liver disease /NASH. SIGNIFICANCE STATEMENT: This study demonstrates that gossypetin has preventive effect to progression of nonalcoholic steatohepatitis (NASH) as a novel AMP-activated protein kinase (AMPK) activator and antioxidants. Our findings indicate that simultaneous activation of AMPK and oxidative stress using gossypetin has the potential to serve as a novel therapeutic approach for nonalcoholic fatty liver disease /NASH patients.

Knockdown of PTK7 Reduces the Oncogenic Potential of Breast Cancer Cells by Impeding Receptor Tyrosine Kinase Signaling.

Protein tyrosine kinase 7 (PTK7), a catalytically defective receptor tyrosine kinase (RTK), is often upregulated in various cancers. This study aimed to validate PTK7 as a target for breast cancer (BC) and investigate its oncogenic signaling mechanism. BC tissue analysis showed significantly elevated PTK7 mRNA levels, especially in refractory triple-negative breast cancer (TNBC) tissues, compared with normal controls. Similarly, BC cell lines exhibited increased PTK7 expression. Knockdown of PTK7 inhibited the proliferation of T-47D and MCF-7 hormone-receptor-positive BC cell-lines and of HCC1187, MDA-MB-231, MDA-MB-436, and MDA-MB-453 TNBC cells. PTK7 knockdown also inhibited the adhesion, migration, and invasion of MDA-MB-231, MDA-MB-436, and MDA-MB-453 cells, and reduced the phosphorylation levels of crucial oncogenic regulators including extracellular signal-regulated kinase (ERK), Akt, and focal adhesion kinase (FAK). Furthermore, PTK7 interacts with fibroblast growth factor receptor 1 (FGFR1) and epidermal growth factor receptor (EGFR) expressed in MDA-MB-231 cells. Knockdown of PTK7 decreased the growth-factor-induced phosphorylation of FGFR1 and EGFR in MDA-MB-231 cells, indicating its association with RTK activation. In conclusion, PTK7 plays a significant role in oncogenic signal transduction by enhancing FGFR1 and EGFR activation, influencing BC tumorigenesis and metastasis. Hence, PTK7 represents a potential candidate for targeted BC therapy, including TNBC.

Degradation of phenol using Fe(II)-activated CaO2: effect of ball-milled activated carbon (ACBM) addition.

In-situ chemical oxidation (ISCO) based on peroxide activation is one of the most promising technologies for removing organic contaminants from natural groundwater (NGW). However, use of the most common form of hydrogen peroxide (H2O2) is limited owing to its significantly rapid reaction rate and heat generation. Therefore, in the present study, the activation of calcium peroxide (CaO2), a slow H2O2 releasing agent, by Fe(II) was proposed (CaO2/Fe(II)), and the phenol degradation mechanisms and feasibility of NGW remediation were investigated. The optimum molar ratio of [phenol]/[CaO2]/[Fe(II)] (phenol = 0.5 mM) was 1/10/10, resulting in 87.0-92.5% phenol removal within 120 min under a broad initial pH range of 3-9. HCO3-, PO43-, and humic acid significantly inhibited degradation, whereas the effects of Cl-, NO3-, and SO42- were negligible. Reactive oxygen species (ROS) were identified based on the results of phenol degradation in the presence of scavengers and electron spin resonance (ESR) spectroscopy, which demonstrated that 1O2 played the dominant role, supported by •OH, in CaO2/Fe(II). Phenol removal in NGW (67.81%) was less than that in distilled and deionized water (DIW, 92.5%) at a [phenol]/[CaO2]/[Fe(II)] ratio of 1/10/10. However, phenol removal was significantly improved (∼100%) by increasing the CaO2 and Fe(II) doses to 1/20/20-40. Furthermore, when 125-250 mg L-1 of ball-milled activated carbon (ACBM) was added (CaO2/Fe(II)-ACBM), phenol removal was enhanced from 67.81% to 90.94-100% in the NGW. CaO2/Fe(II)-ACBM exhibited higher total organic carbon (TOC) removal than CaO2/Fe(II). In addition, no notable by-products were detected using CaO2/Fe(II)-ACBM, whereas the polymerisation products of hydroxylated and/or ring-cleaved compounds, that is, aconitic acid, gallocatechin, and 10-hydroxyaloin, were found in the reaction with CaO2/Fe(II). These results strongly suggest that CaO2/Fe(II)-ACBM is highly promising for groundwater remediation, minimizing degradation byproducts and the adverse effects caused by the NGW components.

Beyond dumping: New strategies in the separation of preservative salt from tannery waste mixed salt and its reuse for tannery industrial application.

The tannery effluent treatment plants produce tonnes of waste in the form of mixed salts containing sodium chloride, sulfate, calcium, and magnesium salts. Disposal of these mixed salts may create an environmental problem. The proposed method broadly consists of the separation of sodium chloride from reverse osmosis (RO) reject and raw-hide waste salt (preservative salt) of the tannery. This study used the physicochemical method to treat waste salt from tannery industrial waste. The addition of sodium hydroxide and sodium carbonate improved calcium and magnesium removal efficiency in the RO reject and preservative waste salts. The optimization of the sodium salt of hydroxide and carbonate is very important to remove an unwanted substance from waste salt. The sodium chloride was recovered, and the purity was about >98% which was successfully reused as preservative salt as well as in the pickling process in the tannery industry.

Anti-PTK7 Monoclonal Antibodies Exhibit Anti-Tumor Activity at the Cellular Level and in Mouse Xenograft Models of Esophageal Squamous Cell Carcinoma.

PTK7 is a catalytically defective receptor protein tyrosine kinase upregulated in various cancers, including esophageal squamous cell carcinoma (ESCC). In previous studies, we observed a positive correlation between PTK7 expression levels and tumorigenicity in various ESCC cell lines and xenograft mice with ESCC KYSE-30 cells. In this study, we analyzed the effects of anti-PTK7 monoclonal antibodies (mAbs) on the tumorigenic activity in KYSE-30 cells and in mouse xenograft models. PTK7 mAb-32 and mAb-43 bind with a high affinity to the extracellular domain of PTK7. PTK7 mAbs significantly reduced three-dimensional cell proliferation, adhesion, wound healing, and migration. PTK7 mAbs also reduce chemotactic invasiveness by decreasing MMP-9 secretion. PTK7 mAbs decreased actin cytoskeleton levels in the cortical region of KYSE-30 cells. PTK7 mAbs reduced the phosphorylation of ERK, SRC, and FAK. In a mouse xenograft model of ESCC using KYSE-30 cells, PTK7 mAbs reduced tumor growth in terms of volume, weight, and the number of Ki-67-positive cells. These results demonstrated that PTK7 mAbs can inhibit the tumorigenicity of ESCC at the cellular level and in vivo by blocking the function of PTK7. Considering the anticancer activities of PTK7 mAbs, we propose that PTK7 mAbs can be used in an effective treatment strategy for PTK7-positive malignancies, such as ESCC.

PTK7, a Catalytically Inactive Receptor Tyrosine Kinase, Increases Oncogenic Phenotypes in Xenograft Tumors of Esophageal Squamous Cell Carcinoma KYSE-30 Cells.

Protein tyrosine kinase 7 (PTK7), a catalytically defective receptor protein tyrosine kinase, is upregulated in tumor tissues and cell lines of esophageal squamous cell carcinoma (ESCC). We showed that PTK7 plays an oncogenic role in various ESCC cell lines. However, its role as an oncogene has not been demonstrated in vivo. Here, we examined the influence of PTK7 on the tumorigenic potential of ESCC KYSE-30 cells, which are known to establish xenograft tumors. Overexpression of PTK7 enhanced the proliferation, adhesion, wound healing, and migration of KYSE-30 cells, and these effects were reversed by the knockdown of PTK7. PTK7 overexpression and knockdown, respectively, increased and decreased the tyrosine phosphorylation of cellular proteins and the phosphorylation of ERK, AKT, and FAK, which are important for cell proliferation, survival, adhesion, and migration. Additionally, PTK7 overexpression and silencing, respectively, increased and decreased the weight, volume, and number of Ki-67-positive proliferating cells in xenograft tumors of KYSE-30 cells. Therefore, we propose that PTK7 plays an important role in the tumorigenesis of ESCC cells in vivo and is a potential therapeutic target for ESCC.

Remediation of phenol contaminated soil using persulfate activated by ball-milled colloidal activated carbon.

The degradation of phenolic compounds through persulfate (PS) activation is a valuable approach for soil/groundwater remediation. Several reports have been made related to PS activation and contaminant degradation using carbo-catalysts; however, there is no detailed study on soil remediation by colloidal activated carbon. This study demonstrates the phenol (PhOH) degradation efficiency in spiked and field-contaminated soils by a novel and low-cost ball-milled colloidal activated carbon (CACBM) catalyst. The CACBM/PS system exhibited outstanding degradation performance for PhOH in both spiked and field-contaminated soils. Optimum condition for degradation of 5.63 mmol PhOH kg soil-1 was achieved at 2.5 mg CACBM g soil-1, 5 mM PS, and a solid-liquid ratio of 1:5 at 25 °C in the wide pH range of 3-11. Radical scavenger experiments and electron spin resonance (ESR) spectroscopy revealed that both radical (•OH and SO4•-) and non-radical (1O2) species were involved in the CACBM/PS system. PhOH degradation in soil phase followed several degradation pathways, resulting in various intermediate byproducts such as acetic acid, maleic acid, p-benzoquinone, fumaric acid, and ferulic acid as analyzed by ultra-high-performance liquid chromatography with mass spectroscopy (UPLC-MS). The CACBM/PS system showed a promising potential in the remediation of organic-contaminated soil.

The catalytically defective receptor protein tyrosine kinase EphA10 promotes tumorigenesis in pancreatic cancer cells.

EphA10 (erythropoietin-producing hepatocellular carcinoma receptor A10) is a catalytically defective receptor protein tyrosine kinase in the ephrin receptor family. Although EphA10 is involved in the malignancy of some types of cancer, its role as an oncogene has not been extensively studied. Here, we investigated the influence of EphA10 on the tumorigenic potential of pancreatic cancer cells. Analysis of expression profiles from The Cancer Genome Atlas confirmed that EphA10 was elevated and higher in tumor tissues than in normal tissues in some cancer types, including pancreatic cancer. EphA10 silencing reduced the proliferation, migration, and adhesion of MIA PaCa-2 and AsPC-1 pancreatic cancer cells. These effects were reversed by overexpression of EphA10 in MIA PaCa-2 cells. Importantly, overexpression and silencing of EphA10 respectively increased and decreased the weight, volume, and number of Ki-67-positive proliferating cells in MIA PaCa-2 xenograft tumors. Further, EphA10 expression was positively correlated with invasion and gelatin degradation in MIA PaCa-2 cells. Moreover, overexpression of EphA10 enhanced the expression and secretion of MMP-9 in MIA PaCa-2 cells and increased the expression of MMP-9 and the vascular density in xenograft tumors. Finally, expression of EphA10 increased the phosphorylation of ERK, JNK, AKT, FAK, and NF-κB, which are important for cell proliferation, survival, adhesion, migration, and invasion. Therefore, we suggest that EphA10 plays a pivotal role in the tumorigenesis of pancreatic epithelial cells and is a novel therapeutic target for pancreatic cancer.

Catalytically inactive receptor tyrosine kinase PTK7 activates FGFR1 independent of FGF.

Protein tyrosine kinase 7 (PTK7), a catalytically defective receptor protein tyrosine kinase (RPTK), plays an oncogenic role by activating an unidentified TKI-258 (dovitinib)-sensitive RPTK in esophageal squamous cell carcinoma (ESCC) cells. Here, we demonstrate that among TKI-258-sensitive RPTKs, fibroblast growth factor receptor (FGFR) 1 is significantly up-regulated in ESCC tissues and cell lines. We show that PTK7 colocalizes with FGFR1 and binds it via its extracellular domain in human embryonic kidney 293 and ESCC TE-10 cells. PTK7 knockdown not only reduced ligand-free and fibroblast growth factor (FGF)-induced phosphorylation of FGFR1 but also the interaction of signaling adaptor proteins with FGFR1 and activation of downstream signaling proteins in TE-10 cells. In addition, PTK7 knockdown reduced FGF-induced oncogenic phenotypes including proliferation, anchorage-independent colony formation, wound healing, and invasion in ESCC cells. Taken together, our data demonstrate that PTK7 binds and activates FGFR1 independent of FGF and thus increases oncogenicity of PTK7- and FGFR1-positive cancers such as ESCC.-Shin, W.-S., Lee, H. W., Lee, S.-T. Catalytically inactive receptor tyrosine kinase PTK7 activates FGFR1 independent of FGF.

Activation of Persulfate by Nanosized Zero-Valent Iron (NZVI): Mechanisms and Transformation Products of NZVI.

The mechanisms involved in the activation of persulfate by nanosized zero-valent iron (NZVI) were elucidated and the NZVI transformation products identified. Two distinct reaction stages, in terms of the kinetics and radical formation mechanism, were found when phenol was oxidized by the persulfate/NZVI system. In the initial stage, lasting 10 min, Fe0(s) was consumed rapidly and sulfate radicals were produced through activation by aqueous Fe2+. The second stage was governed by Fe catalyzed activation in the presence of aqueous Fe3+ and iron (oxyhydr)oxides in the NZVI shells. The second stage was 3 orders of magnitude slower than the initial stage. An electron balance showed that the sulfate radical yield per mole of persulfate was more than two times higher in the persulfate/NZVI system than in the persulfate/Fe2+ system. Radicals were believed to be produced more efficiently in the persulfate/NZVI system because aqueous Fe2+ was supplied slowly, preventing sulfate radicals being scavenged by excess aqueous Fe2+. In the second stage, the multilayered shell conducted electrons, and magnetite in the shell provided electrons for the activation of persulfate. Iron speciation analysis (including X-ray absorption spectroscopy) results indicated that a shrinking core/growing shell model explained NZVI transformation during the persulfate/NZVI process.

PTK6 Localized at the Plasma Membrane Promotes Cell Proliferation and MigratiOn Through Phosphorylation of Eps8.

Protein tyrosine kinase 6 (PTK6; also known as Brk) is closely related to the Src family kinases, but lacks a membrane-targeting myristoylation signal. Sublocalization of PTK6 at the plasma membrane enhances its oncogenic potential. To understand the mechanism(s) underlying the oncogenic property of plasma---membrane-associated PTK6, proteins phosphorylated by membrane-targeted myristoylated PTK6 (Myr-PTK6) were enriched and analyzed using a proteomics approach. Eps8 which was identified by this method is phosphorylated by Myr-PTK6 in HEK293 cells. Mouse Eps8 expressed in HEK293 cells is phosphorylated by Myr-PTK6 at residues Tyr497, Tyr524, and Tyr534. Compared to wild-type Eps8 (Eps8 WT), the phosphorylation-defective 3YF mutant (Eps8 3YF) reverts the increased proliferation, migration, and phosphorylation of ERK and FAK mediated by Eps8 WT in HEK293 cells overexpressing PTK6. PTK6 knockdown in T-47D breast cancer cells decreased EGF-induced phosphorylation of Eps8. Endogenous PTK6 phosphorylates ectopically expressed Eps8 WT, but not Eps8 3YF mutant, in EGF-stimulated T-47D cells. The EGF-induced Eps8 phosphorylation enhances activation of ERK and FAK, cell adhesion, and anchorage-independent colony formation in T-47D cells, but not in the PTK6-knokdown T-47D cells. These results indicate that plasma-membrane-associated PTK6 phosphorylates Eps8, which promotes cell proliferation, adhesion, and migration and, thus, tumorigenesis. J. Cell. Biochem. 118: 2887-2895, 2017. © 2017 Wiley Periodicals, Inc.

Biphasic effect of PTK7 on KDR activity in endothelial cells and angiogenesis.

Protein tyrosine kinase 7 (PTK7) is a member of the defective receptor protein tyrosine kinase family which lacks catalytic activity. Expression of PTK7 is increased in various cancers but its role in carcinogenesis is not well understood. We previously showed that disruption of PTK7 function suppresses VEGF-induced angiogenic phenotypes in HUVECs and mice. Here, we investigated molecular mechanisms for modulating VEGF-induced physiological effects by PTK7. Treatment with a high concentration of extracellular domain of PTK7 (soluble PTK7; sPTK7) or knockdown of PTK7 inhibited VEGF-induced phosphorylation of kinase insert domain receptor (KDR) but did not inhibit phosphorylation of fms-related tyrosine kinase 1 (FLT-1) in HUVECs. PTK7, more specifically sPTK7, interacted with KDR but not with FLT-1 in HUVECs and HEK293 cells. In vitro binding assay showed that sPTK7 formed oligomers with the extracellular domain of KDR (sKDR) up to an approximately 1:3 molar ratio, and vice versa. sPTK7 at lower molar ratios than sKDR enhanced the binding of VEGF to sKDR. At the same or higher molar ratios, it reduced the binding of VEGF to sKDR. Increasing concentrations of sPTK7 or increasing levels of PTK7 expression first increased and then decreased VEGF-induced KDR phosphorylation, migration, and capillary-like tube formation of HUVECs, as well as in vivo angiogenesis. Taken together, our data demonstrates that PTK7 regulates the activity of KDR biphasically by inducing oligomerization of KDR molecules at lower concentrations and by surrounding KDR molecules at higher concentrations.

Loop-Mediated Isothermal Amplification Targeting Actin DNA of Trichomonas vaginalis.

Trichomoniasis caused by Trichomonas vaginalis is a common sexually transmitted disease. Its association with several health problems, including preterm birth, pelvic inflammatory disease, cervical cancer, and transmission of human immunodeficiency virus, emphasizes the importance of improved access to early and accurate detection of T. vaginalis. In this study, a rapid and efficient loop-mediated isothermal amplification-based method for the detection of T. vaginalis was developed and validated, using vaginal swab specimens from subjects suspected to have trichomoniasis. The LAMP assay targeting the actin gene was highly sensitive with detection limits of 1 trichomonad and 1 pg of T. vaginalis DNA per reaction, and specifically amplified the target gene only from T. vaginalis. Validation of this assay showed that it had the highest sensitivity and better agreement with PCR (used as the gold standard) compared to microscopy and multiplex PCR. This study showed that the LAMP assay, targeting the actin gene, could be used to diagnose early infections of T. vaginalis. Thus, we have provided an alternative molecular diagnostic tool and a point-of-care test that may help to prevent trichomoniasis transmission and associated complications.

Prevalence of Trichomonas vaginalis in Women Visiting 2 Obstetrics and Gynecology Clinics in Daegu, South Korea.

This study explored epidemiological trends in trichomoniasis in Daegu, South Korea. Wet mount microscopy, PCR, and multiplex PCR were used to test for Trichomonas vaginalis in vaginal swab samples obtained from 621 women visiting 2 clinics in Daegu. Of the 621 women tested, microscopy detected T. vaginalis in 4 (0.6%) patients, PCR detected T. vaginalis in 19 (3.0%) patients, and multiplex PCR detected T. vaginalis in 12 (1.9%) patients. Testing via PCR demonstrated high sensitivity and high negative predictive value for T. vaginalis. Among the 19 women who tested positive for T. vaginalis according to PCR, 94.7% (18/19) reported vaginal signs and symptoms. Notably, more than 50% of T. vaginalis infections occurred in females younger than 30 years old, and 58% were unmarried. Multiplex PCR, which simultaneously detects pathogens from various sexually transmitted infections, revealed that 91.7% (11/12) of patients were infected with 2 or more pathogens. Mycoplasma hominis was the most prevalent co-infection pathogen with T. vaginalis, followed by Ureaplasma urealyticum and Chlamydia trachomatis. Our results indicate that PCR and multiplex PCR are the most sensitive tools for T. vaginalis diagnosis, rather than microscopy which has been routinely used to detect T. vaginalis infections in South Korea. Therefore, clinicians should take note of the high prevalence of T. vaginalis infections among adolescent and young women in order to prevent persistent infection and transmission of this disease.

The inherent nature of N/P heteroatoms in Sargassum fusiforme seaweed biochar enhanced the nonradical activation of peroxymonosulfate for acetaminophen degradation in aquatic environments.

This study investigated the catalytic activity of biochar materials derived from algal biomass Sargassum fusiforme (S. fusiforme) for groundwater remediation. A facile single-step pyrolysis process was used to prepare S. fusiforme biochar (SFBCX), where x denotes pyrolysis temperatures (600 °C-900 °C). The surface characterization revealed that SFBC800 possesses intrinsic N and P heteroatoms. The optimum experimental condition for acetaminophen (AAP) degradation (>98.70%) was achieved in 60 min using 1.0 mM peroxymonosulfate (PMS), 100 mg L-1 SFBC800, and pH 5.8 (unadjusted). Moreover, the degradation rate constant (k) was evaluated by the pseudo-first-order kinetic model. The maximum degradation (>98.70%) of AAP was achieved within 60 min of oxidation. Subsequently, the k value was calculated to be 6.7 × 10-2 min-1. The scavenger tests showed that radical and nonradical processes are involved in the SFBC800/PMS system. Moreover, the formation of reactive oxygen species (ROS) in the SFBC800/PMS system was confirmed using electron spin resonance (ESR) spectroscopy. Intriguingly, both radical (O2•-, •OH, and SO4•-) and nonradical (1O2) ROS were formed in the SFBC800/PMS system. In addition, electrochemical studies were conducted to verify the electron transfer process of the nonradical mechanism in the SFBC800/PMS system. The scavenger and electron spin resonance (ESR) spectroscopy showed that singlet oxygen (1O2) is the predominant component in AAP degradation. Under optimal condition, the SFBC800/PMS system reached ∼81% mineralization of AAP within 5 min and continued to ∼85% achieved over 60 min of oxidation. Coexisting ions and different aqueous matrices were investigated to examine the feasibility of the catalyst system, and the SFBC800/PMS system was found to be effective in the remediation of AAP-contaminated groundwater, river water, and effluent water obtained from wastewater treatment plants. Moreover, the SFBC800-activated PMS system demonstrated reusability. Our findings indicate that the SFBC800 catalyst has excellent catalytic activity for AAP degradation in aquatic environments.

A critical review of sustainable pesticide remediation in contaminated sites: Research challenges and mechanistic insights.

Incidental pesticide application on farmlands can result in contamination of off-target biota, soil, groundwater, and surrounding ecosystems. To manage these pesticide contaminations sustainably, it is important to utilize advanced approaches to pesticide decontamination. This review assesses various innovative strategies applied for remediating pesticide-contaminated sites, including physical, chemical, biological, and nanoremediation. Integrated remediation approaches appear to be more effective than singular technologies. Bioremediation and chemical remediation are considered suitable and sustainable strategies for decontaminating contaminated soils. Furthermore, this study highlights key mechanisms underlying advanced pesticide remediation that have not been systematically studied. The transformation of applied pesticides into metabolites through various biotic and chemical triggering factors is well documented. Ex-situ and in-situ technologies are the two main categories employed for pesticide remediation. However, when selecting a remediation technique, it is important to consider factors such as application sites, cost-effectiveness, and specific purpose. In this review, the sustainability of existing pesticide remediation strategies is thoroughly analyzed as a pioneering effort. Additionally, the study summarizes research uncertainties and technical challenges associated with different remediation approaches. Lastly, specific recommendations and policy advocacy are suggested to enhance contemporary remediation approaches for cleaning up pesticide-contaminated sites.

Exploring the environmental pathways and challenges of fluoroquinolone antibiotics: A state-of-the-art review.

Fluoroquinolone (FQ) antibiotics have become a subject of growing concern due to their increasing presence in the environment, particularly in the soil and groundwater. This review provides a comprehensive examination of the attributes, prevalence, ecotoxicity, and remediation approaches associated with FQs in environmental matrices. The paper discusses the physicochemical properties that influence the fate and transport of FQs in soil and groundwater, exploring the factors contributing to their prevalence in these environments. Furthermore, the ecotoxicological implications of FQ contamination in soil and aquatic ecosystems are reviewed, shedding light on the potential risks to environmental and human health. The latter part of the review is dedicated to an extensive analysis of remediation approaches, encompassing both in-situ and ex-situ methods employed to mitigate FQ contamination. The critical evaluation of these remediation strategies provides insights into their efficacy, limitations, and environmental implications. In this investigation, a correlation between FQ antibiotics and climate change is established, underlining its significance in addressing the Sustainable Development Goals (SDGs). The study further identifies and delineates multiple research gaps, proposing them as key areas for future investigational directions. Overall, this review aims to consolidate current knowledge on FQs in soil and groundwater, offering a valuable resource for researchers, policymakers, and practitioners engaged in environmental management and public health.

The cytosolic domain of protein-tyrosine kinase 7 (PTK7), generated from sequential cleavage by a disintegrin and metalloprotease 17 (ADAM17) and γ-secretase, enhances cell proliferation and migration in colon cancer cells.

Protein-tyrosine kinase 7 (PTK7) is a member of the defective receptor protein-tyrosine kinases and is known to function as a regulator of planar cell polarity during development. Its expression is up-regulated in some cancers including colon carcinomas. A 100-kDa fragment of PTK7 was detected in the culture media from colon cancer cells and HEK293 cells. The shed fragment was named sPTK7-Ig1-7 because its molecular mass was very similar to that of the entire extracellular domain of PTK7 that contains immunoglobulin-like loops 1 to 7 (Ig1-7). The shedding of sPTK7-Ig1-7 was enhanced by treatment with phorbol 12-myristate 13-acetate. In addition to the sPTK7-Ig1-7 found in the culture medium, two C-terminal fragments of PTK7 were detected in the cell lysates: PTK7-CTF1, which includes a transmembrane segment and a cytoplasmic domain, and PTK7-CTF2, which lacks most of the transmembrane segment from PTK7-CTF1. Analysis of PTK7 processing in the presence of various protease inhibitors or after knockdown of potential proteases suggests that shedding of PTK7 into sPTK7-Ig1-7 and PTK7-CTF1 is catalyzed by ADAM17, and further cleavage of PTK7-CTF1 into PTK7-CTF2 is mediated by the γ-secretase complex. PTK7-CTF2 localizes to the nucleus and enhances proliferation, migration, and anchorage-independent colony formation. Our findings demonstrate a novel role for PTK7 in the tumorigenesis via generation of PTK7-CTF2 by sequential cleavage of ADAM17 and γ-secretase.