ABSTRACT
Overutilization and misuse of antibiotics in recent decades markedly intensified the rapid proliferation and diffusion of antibiotic resistance genes (ARGs) within the environment, thereby elevating ARGs to the status of a global public health crisis. Recognizing that soil acts as a critical reservoir for ARGs, environmental researchers have made great progress in exploring the sources, distribution, and spread of ARGs in soil. However, the microscopic state and micro-interfacial behavior of ARGs in soil remains inadequately understood. In this study, we reviewed the micro-interfacial behaviors of antibiotic-resistant bacteria (ARB) in soil and porous media, predominantly including migration-deposition, adsorption, and biofilm formation. Meanwhile, adsorption, proliferation, and degradation were identified as the primary micro-interfacial behaviors of ARGs in the soil, with component of soil serving as significant determinant. Our work contributes to the further comprehension of the microstates and processes of ARB and ARGs in the soil environments and offers a theoretical foundation for managing and mitigating the risks associated with ARG contamination.
ABSTRACT
The last two decades have seen nitrogen/iron-transforming bacteria at the forefront of new biogeochemical discoveries, such as anaerobic ammonium oxidation coupled to ferric iron reduction (feammox) and lithoautotrophic nitrate-reducing ferrous iron-oxidation (NRFeOx). These emerging findings continue to expand our knowledge of the nitrogen/iron cycle in nature and also highlight the need to re-understand the functional traits of the microorganisms involved. Here, as a proof-of-principle, we report compelling evidence for the capability of an NRFeOx enrichment culture to catalyze the feammox process. Our results demonstrate that the NRFeOx culture predominantly oxidizes NH4+ to nitrogen gas, by reducing both chelated nitrilotriacetic acid (NTA)-Fe(III) and poorly soluble Fe(III)-bearing minerals (γ-FeOOH) at pH 4.0 and 8.0, respectively. In the NRFeOx culture, Fe(II)-oxidizing bacteria of Rhodanobacter and Fe(III)-reducing bacteria of unclassified_Acidobacteriota coexisted. Their relative abundances were dynamically regulated by the supplemented iron sources. Metagenomic analysis revealed that the NRFeOx culture contained a complete set of denitrifying genes along with hao genes for ammonium oxidation. Additionally, numerous genes encoding extracellular electron transport-associated proteins or their homologs were identified, which facilitated the reduction of extracellular iron by this culture. More broadly, this work lightens the unexplored potential of specific microbial groups in driving nitrogen transformation through multiple pathways and highlights the essential role of microbial iron metabolism in the integral biogeochemical nitrogen cycle.
Subject(s)
Ammonium Compounds , Nitrates , Oxidation-Reduction , Nitrates/metabolism , Ammonium Compounds/metabolism , Anaerobiosis , Ferric Compounds/metabolism , Iron/metabolism , Ferrous Compounds/metabolism , Nitrogen/metabolism , Bacteria/metabolism , Bacteria/genetics , Bacteria/classificationABSTRACT
Groundwater contamination with arsenic and nitrate poses a pressing concern for the safety of local communities. Bioremediation, utilizing Fe(II)-oxidizing nitrate reducing bacteria, shows promise as a solution to this problem. However, the relatively weak environmental adaptability of a single bacterium hampers practical application. Therefore, this study explored the feasibility and characteristics of a mixed iron-dependent autotrophic denitrifying (IDAD) culture for effectively removing arsenic and nitrate from synthetic groundwater. The IDAD biosystem exhibited stable performace and arsenic resistance, even at a high As(III) concentration of 800 µg/L. Although the nitrogen removal efficiency of the IDAD biosystem decreased from 71.4% to 64.7% in this case, the arsenic concentration in the effluent remained below the standard (10 µg/L) set by WHO. The crystallinity of the lepidocrocite produced by the IDAD culture decreased with increasing arsenic concentration, but the relative abundance of the key iron-oxidizing bacteria norank_f_Gallionellaceae in the culture showed an opposite trend. Metagenomic analysis revealed that the IDAD culture possess arsenic detoxification pathways, including redox, methylation, and efflux of arsenic, which enable it to mitigate the adverse impact of arsenic stress. This study provides theoretical understanding and technical support for the remediation of arsenic and nitrate-contaminated groundwater using the IDAD culture.
Subject(s)
Arsenic , Autotrophic Processes , Biodegradation, Environmental , Denitrification , Groundwater , Iron , Nitrates , Water Pollutants, Chemical , Groundwater/microbiology , Groundwater/chemistry , Nitrates/metabolism , Arsenic/metabolism , Water Pollutants, Chemical/metabolism , Water Pollutants, Chemical/analysis , Iron/metabolism , Bacteria/metabolism , Bacteria/genetics , Gallionellaceae/metabolismABSTRACT
The transportation of antibiotic resistance genes (ARGs) in manure-soil-plant continuums poses risks to human health. Horizontal gene transfer, particularly for bacterial transformation, is an important way for ARG dissemination. As crucial components in soils, iron oxides impacted the fates of various abiotic and biotic contaminants due to their active properties. However, whether they can influence the transformation of ARGs is unknown, which waits to be figured out to boost the assessment and control of ARG spread risks. In this study, we have investigated the effects of goethite, hematite, and magnetite (0-250 mg/L, with sizes < 100 nm and > 100 nm) on the transfer of ampicillin resistance genes to Escherichia coli cells. At lower iron oxide concentrations, the transformation of ARGs was first facilitated (transformation frequency reached up to 3.38-fold higher), but the facilitating effects gradually weakened and eventually disappeared as concentrations further increased. Particle size and iron oxide type were not the universal determinants controlling the transformation. At lower concentrations, iron oxides interacted with proteins and phospholipids in E. coli envelope structures, and induced the overgeneration of intracellular reactive oxygen species. Consequently, they led to pore formation and permeability enhancement on the cell membrane, thus promoting the transformation. The facilitation was also associated with the carrier-like effect of iron oxides for antibiotic resistance plasmids. At higher concentrations, the weakened facilitations were attributed to the aggregation of iron oxides. In this study, we highlight the crucial roles of the concentrations (contents) of iron oxides on the dissemination of ARGs in soils; this study may serve as a reference for ARG pollution control in future agricultural production.
Subject(s)
Anti-Bacterial Agents , Ferric Compounds , Transformation, Bacterial , Humans , Anti-Bacterial Agents/pharmacology , Escherichia coli/genetics , Genes, Bacterial , Drug Resistance, Microbial/genetics , Soil/chemistry , Oxides , Iron , Soil Microbiology , Manure/microbiologyABSTRACT
Pin1, a peptide prolyl cis-trans isomerase, is overexpressed and/or overactivated in many human malignancies. However, whether Pin1 regulates the immunosuppressive TME has not been well defined. In this study, we detected the effect of Pin1 on immune cells and immune checkpoint PD-L1 in the TME of CRC and explored the anti-tumor efficacy of Pin1 inhibitor ATRA combined with PD-1 antibody. We found that Pin1 facilitated the immunosuppressive TME by raising the proportion of myeloid-derived suppressor cells (MDSCs) and declining the percentage of CD8+ T cells and CD4+ T cells. Pin1 restrained PD-L1 protein expression in CRC cells and the effect was tempered by endoplasmic reticulum (ER) stress inducers. Mechanically, Pin1 overexpression decreased the stability of PD-L1 and promoted its degradation by mitigating ER stress. Silencing or inhibiting Pin1 promoted PD-L1 protein expression by inducing ER stress. Hence, Pin1 inhibitor ATRA enhanced the anti-tumor efficacy of PD-1 antibody in the CRC allograft by upregulating PD-L1. Our results reveal the critical and pleiotropic effects of Pin1 on managing the immune cells and immune checkpoint PD-L1 in the TME of CRC, providing a new promising candidate for combination with immunotherapy.
Subject(s)
B7-H1 Antigen , Colorectal Neoplasms , Humans , Peptidylprolyl Isomerase , CD8-Positive T-Lymphocytes/metabolism , CD8-Positive T-Lymphocytes/pathology , Programmed Cell Death 1 Receptor/metabolism , Colorectal Neoplasms/pathology , Tumor MicroenvironmentABSTRACT
RESEARCH QUESTION: Are the observed associations between female reproductive factors and sex hormones with the risk of uterine leiomyoma truly causal associations? DESIGN: The putative causal relationships between female reproductive factors and sex hormones with uterine leiomyoma were investigated using two-sample Mendelian randomization. Statistics on exposure-associated genetic variants were obtained from genome-wide association studies (GWAS). The uterine leiomyoma GWAS from the FinnGen and FibroGENE consortia were used as outcome data for discovery and replication analyses, respectively. Results were pooled by meta-analysis. Sensitivity analyses ensured robustness of the Mendelian randomization analysis. RESULTS: When FinnGen GWAS were used as outcome data, a causal relationship was found between age at menarche (OR 0.84, P < 0.0001), age at menopause (OR 1.08, P < 0.0001), number of live births (OR 0.25, P < 0.001) and total testosterone levels (OR 0.90, P < 0.001) with the risk of uterine leiomyoma. When FibroGENE GWAS were used as outcome data, Mendelian randomization results for age at menopause, the number of live births and total testosterone levels were replicated. In the meta-analysis, a later age at menopause (OR 1.08, P < 0.0001) was associated with an increased risk of uterine leiomyoma. A higher number of live births (OR 0.25, P < 0.0001) and higher total testosterone levels (OR 0.90, P < 0.0001) were associated with a decreased risk of uterine leiomyoma. CONCLUSIONS: A causal relationship between later age at menopause, lower number of live births and lower total testosterone levels with increased risk of uterine leiomyoma was found.
Subject(s)
Genome-Wide Association Study , Leiomyoma , Humans , Female , Mendelian Randomization Analysis , Sex Factors , Gonadal Steroid Hormones , Leiomyoma/genetics , TestosteroneABSTRACT
Neuronal apoptosis and neuroinflammation are key factors involved in the pathological changes of Parkinson's disease (PD). Sophoricoside (SOP) has shown anti-inflammatory and anti-apoptosis effects in various diseases. However, the role of SOP in PD has not been reported. In this experiment, we found that oral administration of SOP alleviated weight loss and motor symptoms in 1-Methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP)-injected mice. Further studies revealed that SOP inhibited inflammatory responses and neuronal apoptosis in the midbrain region of MPTP-injected mice. In vitro mechanistic study, we found that SOP exerts neuroprotective effects through a two-sided action. On the one hand, SOP inhibits Lipopolysaccharide (LPS)-induced inflammatory responses in microglia by inhibiting the Nuclear factor kappa-B(NF-κB) pathway. On the other hand, SOP inhibits 1-methyl-4-phenylpyridinium (MPP+)-induced neuronal apoptosis by regulating the Adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) signaling pathway. Thus SOP is expected to be a potential therapeutic agent for PD by targeting neuroinflammation and neuronal apoptosis.
Subject(s)
Neuroprotective Agents , Parkinson Disease , Mice , Animals , Parkinson Disease/metabolism , Neuroinflammatory Diseases , 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine/metabolism , 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine/pharmacology , 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine/therapeutic use , NF-kappa B/metabolism , 1-Methyl-4-phenylpyridinium , Administration, Oral , Mice, Inbred C57BL , Disease Models, Animal , Neuroprotective Agents/pharmacology , Neuroprotective Agents/therapeutic use , Neuroprotective Agents/metabolism , Microglia , Dopaminergic Neurons , Mammals/metabolismABSTRACT
Parkinson's disease (PD) is a neurodegenerative disorder that occurs most frequently in middle-aged and elderly people. It is characterized by an insidious onset and a complex etiology, and no effective treatment has been developed. The primary characteristic of PD is the degenerative death of midbrain dopaminergic neurons. The excessive autophagy of neurons and hyperactivation of microglia were shown to be involved in the apoptosis of dopaminergic neurons. Limonin (LM), a type of pure natural compound present in grapefruit or citrus fruits (e. g., lemon, orange) has been reported to inhibit apoptosis and inflammation. However, its role and mechanism of action in PD are unclear. In this study, we explored the effect and mechanism of action of LM in PD. In vivo experiments revealed that LM ameliorated 6-OHDA-induced reduced motor activity and PD-related pathological damage in rats. In vitro experiments revealed that LM inhibited the 6-OHDA-induced apoptosis of PC12 cells by inhibiting the excessive autophagy of neurons. In addition, LM inhibited microglial inflammation by activating the AKT/Nrf-2/HO-1 pathway and protected neurons against microglial inflammation-mediated neurotoxicity. In conclusion, the findings of this experiment demonstrated that LM exerted neuroprotective effects by inhibiting neuronal autophagy-mediated apoptosis and microglial activation in 6-OHDA-injected rats, thus indicating that LM can serve as a candidate for PD by targeting neuroinflammation and neuronal autophagy to inhibit neuronal apoptosis.
Subject(s)
Limonins , Neuroprotective Agents , Parkinson Disease , Humans , Rats , Animals , Aged , Middle Aged , Oxidopamine/adverse effects , Oxidopamine/metabolism , Microglia , Neuroprotective Agents/pharmacology , Neuroprotective Agents/therapeutic use , Neuroprotective Agents/metabolism , Limonins/pharmacology , Parkinson Disease/metabolism , Neurons , Inflammation/drug therapy , Administration, Oral , AutophagyABSTRACT
Glomalin-related soil protein (GRSP) has gained widespread attention because of its benefits to carbon sequestration, improving soil quality and fixing heavy metals. However, studies on how GRSP affects the environmental fate of organic contaminants are scarce. In this study, different types of GRSPs were isolated from forest soils and characterized to study the binding of GRSPs and PAHs under different environmental conditions. The results indicated that GRSPs contain abundant functional groups (such as -NH, -COOH, and CO) and material composition, like humic acid, proteins, and lipids. For the tested GRSPs, EE-GRSP has lower DOC, SUVA260 and SUVA280 values, as well as higher E2/E3 values, indicating that EE-GRSP has lower hydrophobicity and molecular weight. These properties can lead to strong interactions between GRSP and PAHs, especially with benzopyrene, which has a high Kow and Ksw and a large molecular size, with binding constants ranging from 16,119 to 163,697 L·kg-1. Furthermore, low pH (pH = 3) and temperature (15 °C) could increase GRSP's aggregation, enhance the GRSP binding ability with PAHs, whose binding constants were 11,595 and 5067.3 L·kg-1. Therefore, the binding between GRSP and PAHs may lead to changes in the fate of PAHs in the soil and affect the environmental risk of PAHs. The results presented here will deepen our understanding of the environmental function of GRSPs and provide a theoretical basis to further elucidate the mechanisms of GRSPs and organic pollutants.
Subject(s)
Polycyclic Aromatic Hydrocarbons , Soil Pollutants , Soil/chemistry , Fungal Proteins , Glycoproteins , Polycyclic Aromatic Hydrocarbons/analysis , Soil Pollutants/analysisABSTRACT
Accumulating research has indicated that inordinate activation of microglia releases inflammatory cytokines, damages neurons, and causes neuroinflammation, which eventually could lead to neurodegenerative diseases such as Parkinson's disease and Huntington's disease, etc. Notopterol (NOT) has anti-inflammatory and anti-oxidant functions in boundary tissues, but the effects of NOT on neuroinflammation have not been covered. Therefore, this study attempts to investigate the effect of NOT on neuroinflammation and the underlying mechanisms. According to the findings, NOT dramatically decreased the expression of pro-inflammatory mediators (interleukin-6 (IL-6), inducible nitric-oxide synthase (iNOS), tumor necrosis factor-α (TNF-α), and Cyclooxygenase-2 (COX-2)) in LPS-exposed BV-2 cells. Western blot analysis revealed that NOT could promote the activation of AKT/Nrf2/HO-1 signaling pathway. Further studies have shown that anti-inflammatory property of NOT was inhibited by MK2206 (an AKT inhibitor), RA (an Nrf2 inhibitor), and SnPP IX (an HO-1 inhibitor). In addition, it was also discovered that NOT could weaken the damage of LPS to BV-2 cells and improve their survival rate. As a result, our results imply that NOT inhibits the inflammatory response of BV-2 cells through the AKT/Nrf2/HO-1 signaling axis and exerts a neuroprotective effect by inhibiting the activation of BV-2 cells.
Subject(s)
Lipopolysaccharides , Proto-Oncogene Proteins c-akt , Humans , Proto-Oncogene Proteins c-akt/metabolism , Lipopolysaccharides/pharmacology , NF-E2-Related Factor 2/metabolism , Neuroinflammatory Diseases , Signal Transduction , Inflammation/metabolism , Anti-Inflammatory Agents/pharmacology , Anti-Inflammatory Agents/therapeutic use , Anti-Inflammatory Agents/metabolism , Microglia , NF-kappa B/metabolism , Nitric Oxide Synthase Type II/metabolismABSTRACT
With low bioaccessbility, persistence of the undissolved organic pollutants in soil and sediments poses threat to health of the resident. Although ubiquitous black carbon catalyzes a wide range of biogeochemical reactions in nature, its role in biotransformation of the compounds in non-aqueous phase like 2, 2'-nitrobiphenyl remains unclear. Reduction rate constants of 2, 2'-dinitrobiphenyl by Shewanella oneidensis MR-1 increased from 0.0044 h-1 by 7-fold to 0.035 h-1 in the presence of black carbons produced at pyrolysis temperature of 250-900 °C. Accordingly, electrical conductivity of black carbon was enhanced from 0 to 5.56 Sâcm-1. The reactivity of black carbon for catalyzing the biotransformation positively correlated with its electrical conductivity (R2 > 0.89), which was strongly associated with conductive graphitic clusters in it. The surface oxygenated groups in black carbon were likely not involved in the bioreduction. This work attaches importance to role of the ubiquitous black carbon in natural biotransformation of the undissolved pollutants, and elucidates new mechanism for the biotransformation.
Subject(s)
Environmental Pollutants , Graphite , Oxidation-Reduction , Electrons , Biotransformation , Electric Conductivity , Environmental Pollutants/metabolism , CarbonABSTRACT
BACKGROUND: The stemness characteristics of cancer cells, such as self-renewal and tumorigenicity, are considered to be responsible, in part, for tumor metastasis. Epithelial-to-mesenchymal transition (EMT) plays an important role in promoting both stemness and tumor metastasis. Although the traditional medicine juglone is thought to play an anticancer role by affecting cell cycle arrest, induction of apoptosis, and immune regulation, a potential function of juglone in regulating cancer cell stemness characteristics remains unknown. METHODS: In the present study, tumor sphere formation assay and limiting dilution cell transplantation assays were performed to assess the function of juglone in regulating maintenance of cancer cell stemness characteristics. EMT of cancer cells was assessed by western blot and transwell assay in vitro, and a liver metastasis model was also performed to demonstrate the effect of juglone on colorectal cancer cells in vivo. RESULTS: Data gathered indicates juglone inhibits stemness characteristics and EMT in cancer cells. Furthermore, we verified that metastasis was suppressed by juglone treatment. We also observed that these effects were, in part, achieved by inhibiting Peptidyl-prolyl cis-trans isomerase NIMA-interacting 1 (Pin1). CONCLUSIONS: These results indicate that juglone inhibits maintenance of stemness characteristics and metastasis in cancer cells.
Subject(s)
Epithelial-Mesenchymal Transition , Naphthoquinones , Neoplasms , Neoplastic Stem Cells , Apoptosis , Blotting, Western , Neoplasms/drug therapy , Neoplasm Metastasis/prevention & control , Naphthoquinones/pharmacologyABSTRACT
BACKGROUND: Previous studies have shown a close association between an altered immune system and Parkinson's disease (PD). Neuroinflammation inhibition may be an effective measure to prevent PD. Recently, numerous reports have highlighted the potential of hydroxy-carboxylic acid receptor 2 (HCA2) in inflammation-related diseases. Notably, the role of HCA2 in neurodegenerative diseases is also becoming more widely known. However, its role and exact mechanism in PD remain to be investigated. Nicotinic acid (NA) is one of the crucial ligands of HCA2, activating it. Based on such findings, this study aimed to examine the effect of HCA2 on neuroinflammation and the role of NA-activated HCA2 in PD and its underlying mechanisms. METHODS: For in vivo studies, 10-week-old male C57BL/6 and HCA2-/- mice were injected with LPS in the substantia nigra (SN) to construct a PD model. The motor behavior of mice was detected using open field, pole-climbing and rotor experiment. The damage to the mice's dopaminergic neurons was detected using immunohistochemical staining and western blotting methods. In vitro, inflammatory mediators (IL-6, TNF-α, iNOS and COX-2) and anti-inflammatory factors (Arg-1, Ym-1, CD206 and IL-10) were detected using RT-PCR, ELISA and immunofluorescence. Inflammatory pathways (AKT, PPARγ and NF-κB) were delineated by RT-PCR and western blotting. Neuronal damage was detected using CCK8, LDH, and flow cytometry assays. RESULTS: HCA2-/- increases mice susceptibility to dopaminergic neuronal injury, motor deficits, and inflammatory responses. Mechanistically, HCA2 activation in microglia promotes anti-inflammatory microglia and inhibits pro-inflammatory microglia by activating AKT/PPARγ and inhibiting NF-κB signaling pathways. Further, HCA2 activation in microglia attenuates microglial activation-mediated neuronal injury. Moreover, nicotinic acid (NA), a specific agonist of HCA2, alleviated dopaminergic neuronal injury and motor deficits in PD mice by activating HCA2 in microglia in vivo. CONCLUSIONS: Niacin receptor HCA2 modulates microglial phenotype to inhibit neurodegeneration in LPS-induced in vivo and in vitro models.
Subject(s)
Niacin , Parkinson Disease , Receptors, G-Protein-Coupled , Animals , Male , Mice , Dopaminergic Neurons , Lipopolysaccharides , Mice, Inbred C57BL , Microglia/metabolism , Neuroinflammatory Diseases , NF-kappa B/metabolism , Niacin/pharmacology , Parkinson Disease/metabolism , PPAR gamma/metabolism , Proto-Oncogene Proteins c-akt/metabolism , Receptors, G-Protein-Coupled/agonists , Receptors, G-Protein-Coupled/metabolismABSTRACT
Parkinson's disease (PD) is a neurodegenerative disease in which neuronal apoptosis and associated inflammation are involved in its pathogenesis. However, there is still no specific treatment that can stop PD progression. Isoalantolactone (IAL) plays a role in many inflammation-related diseases. However, its effect and mechanism in PD remain unclear. In this study, results showed that IAL administration ameliorated 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP)-induced PD-related pathological impairment and decreased motor activity in mice. Results from in vitro mechanistic studies showed that IAL regulated apoptosis-related proteins by activating the AKT/Nrf2 pathway, thereby suppressing the apoptosis of SN4741 cells induced by N-methyl-4-phenylpyridinium Iodide (MPP+). On the other hand, IAL inhibited LPS-induced release of pro-inflammatory mediators in BV2 cells by activating the AKT/Nrf2/HO-1 pathway and inhibiting the NF-κB pathway. In addition, IAL protected SN4741 from microglial activation-mediated neurotoxicity. Taken together, these results highlight the beneficial role of IAL as a novel therapy and potential PD drug due to its pharmacological profile.
Subject(s)
Neurodegenerative Diseases , Parkinson Disease , Animals , Mice , 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine/adverse effects , 1-Methyl-4-phenylpyridinium , Apoptosis , Inflammation/metabolism , Inflammation Mediators/metabolism , Iodides/adverse effects , Lipopolysaccharides/adverse effects , Mice, Inbred C57BL , NF-E2-Related Factor 2 , NF-kappa B/metabolism , Parkinson Disease/metabolism , Proto-Oncogene Proteins c-akt , Pyrrolidines , SesquiterpenesABSTRACT
Objective: To explore the clinical effect and safety of 5-aminolevulinic acid photodynamic therapy (ALA-PDT) combined with 1550 nm fractional laser therapy in the treatment of rosacea. Methods: 114 patients with type I and type II rosacea treated in our hospital from March 2018 to April 2020 were recruited. They were randomly assigned (1 : 1 : 1) to receive ALA-PDT (photodynamic group), 1550 nm fractional laser (laser group), or ALA-PDT and 1550 nm fractional laser therapy (combination group). Outcome measures included skin lesion scores, efficacy, and adverse reactions. Results: After treatment, patients in the three groups showed lower skin lesion scores than before treatment, and the combination group showed significantly lower results than the other groups (P < 0.05). There was no significant difference in the total efficacy among the three groups (P > 0.05), but the combination group outperformed the other groups in the comparison of the efficacy levels (P < 0.05). Edema with lupus erythematosus, pain, and burning sensation was found in some cases but disappeared within 2 to 4 days after symptomatic treatment without interference with subsequent treatment. No patients had pigmentation, hypopigmentation, scars, or other serious adverse reactions. Conclusion: In the treatment of rosacea, ALA-PDT combined with a 1550 nm fractional laser can reduce redness and facilitate skin remodeling, with high efficacy and safety, so it is worthy of clinical promotion and application.
ABSTRACT
The capability of laccase to oxidate a broad range of polyphenols and aromatic substrates in vitro offers a new technological option for the remediation of polycyclic aromatic hydrocarbon (PAH) pollution with high cytotoxicity. However, laccase application in the remediation of PAH-contaminated sites mainly suffers from a low oxidation rate and high cost because of the difficulty in its recovery. In this study, laccases were immobilized on magnetic Fe3O4 particles coated with chitosan (Fe3O4@SiO2-chitosan) to improve the operational stability and reusability in the treatment of PAH pollution. The enzyme fixation capacity reached 158 mg g-1, and 79.1% of free laccase activities were reserved under the optimum immobilized condition of 4% glutaraldehyde, 1.0 mg mL-1 laccase, 2 h covalent bonding time, and 6 h fixation time. The degradation efficiencies of anthracene (ANT) and benzo[a]pyrene (B(a)P) by Fe3O4@SiO2-chitosan immobilized laccase in 48 h were 81.9% and 69.2%, respectively. Furthermore, it is very easy to magnetically recover the immobilized laccase from reaction systems and reuse it in a new batch. The relative activities of immobilized laccase were over 50% for the degradation of ANT and B(a)P in three catalytic runs, reaching the goal of substantially reducing cost in practice. According to the results from quantum calculations and mass spectrum analyses, the degradation products of ANT and B(a)P by laccase were anthraquinone and B(a)P-dione, respectively. The findings from this study provide valuable insight in promoting the application of immobilized laccase technology in the remediation of PAH contamination.
Subject(s)
Chitosan , Polycyclic Aromatic Hydrocarbons , Catalysis , Enzymes, Immobilized/metabolism , Laccase/metabolism , Magnetic Phenomena , Polycyclic Aromatic Hydrocarbons/metabolism , Polyporaceae , Silicon Dioxide/metabolism , TrametesABSTRACT
Parkinson's disease (PD) is a usual disease caused by degeneration of the central nervous system, which features the denaturation and death of dopaminergic neurons in the substantia nigra compact (SNc) of the midbrain. Neuroinflammation casts a consequential role in its pathogenesis, and the excessive activation of microglia as a major part of neuroinflammation cannot be ignored. Studies have indicated that Hordenine (HOR) functioned widely as an anti-oxidant and anti-inflammatory substance, but there are no reports on neuroinflammation effects. Therefore, this study is devoted to exploring the effect of HOR on neuroinflammation and its specific mechanism. In vivo, results revealed that HOR depressed the activation of microglia in SNc and protected dopaminergic neurons in the 6-hydroxydopamine (6-OHDA)-induced PD rat model, which terminally reduced movement disorders and weight loss. In vitro, studies have shown that HOR can inhibit inflammatory responses triggered by lipopolysaccharide (LPS) in BV-2 cells. More profound studies have discovered that the specific anti-inflammatory mechanism is intimately associated with the NF-κB and MAPK signaling pathways. All in it together, HOR acts as a significant role in preserving dopaminergic neurons by restraining neuroinflammation mediated by activation of microglia. This may provide a potential drug for Parkinson's treatment.
Subject(s)
Neuroprotective Agents , Parkinson Disease , Animals , Anti-Inflammatory Agents/metabolism , Anti-Inflammatory Agents/pharmacology , Anti-Inflammatory Agents/therapeutic use , Cell Line , Lipopolysaccharides/pharmacology , MAP Kinase Signaling System , Microglia , NF-kappa B/metabolism , Neuroinflammatory Diseases , Neuroprotective Agents/pharmacology , Neuroprotective Agents/therapeutic use , Parkinson Disease/drug therapy , Rats , Tyramine/analogs & derivativesABSTRACT
Soil studies have reported the effect of Hexachlorocyclohexane (HCH) on soil microbial communities. However, how soil microbial communities and function shift after HCH addition into the red and purple soil remains unclear. Here, we analyzed the HCH residue fate, and the functional composition and structure of microbial communities to HCH in the two soils. Under the 100 g/ha and 1000 g/ha treatment, the dissipation rate of HCH was 0.0386 and 0.0273 in the purple soil, 0.0145 and 0.0195 in the red soil. The enrichment of HCH degrading genes leads to a higher HCH dissipation rate in the purple soil. PCoA results demonstrated that HCH addition has a different effect on the community diversity in the two soils, and Proteobacteria and Acidobacteria were the major phyla in the two soils. The soil microbiome average variation degree values of red soil were higher than purple soil, which indicated that the soil microbiome in the purple soil was more stable than in the red soil under HCH addition. PICRUSt2 results indicated that functional genes involved in the carbon, nitrogen biogeochemical cycles and HCH degradation were more tolerant to HCH addition in the purple soil. This study provides new insights into understanding of the effect of HCH addition on soil microbial communities and function in the red and purple paddy soil.
Subject(s)
Hexachlorocyclohexane , Soil Pollutants , Bacteria/genetics , Hexachlorocyclohexane/analysis , Soil , Soil Microbiology , Soil Pollutants/analysisABSTRACT
BACKGROUND: This article presents a new method using a dermis-outer orbicularis fascia-orbicularis-levator (DOOL) fixation technique for double-eyelid blepharoplasty. METHODS: Our surgical technique preserves the preorbicular venous network (POVN) and uses mattress sutures to fix the dermis, outer fascia of the orbicularis oculi muscle, and orbicularis oculi muscle with pretarsal levator aponeurosis (DOOL). Between January 2016 and July 2018, 335 patients were treated with this POVN-preserving DOOL technique (321 women and 14 men; mean age, 29.6 y). The patients were followed up for 6-30 months. The complications were documented, and the overall outcomes of the upper eyelid folds were evaluated by both surgeons and patients as good, fair, or poor. RESULTS: Among 335 patients, 307 (91.6%) had good results, 17 (5.1%) had fair results, and 11 (3.3%) had poor results. Postoperative complications included partial (n=4) or complete (n=3) loss of the double-eyelid line and asymmetric folds (n=4). Hypertrophic/depressed scars did not occur. CONCLUSIONS: With less invasiveness and secure internal fixation, the DOOL fixation technique with POVN preservation can achieve a stable and natural double-eyelid appearance. LEVEL OF EVIDENCE IV: This journal requires that authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors www.springer.com/00266 .
Subject(s)
Blepharoplasty , Adult , Blepharoplasty/methods , Dermis/surgery , Eyelids/surgery , Facial Muscles/surgery , Fascia , Female , Humans , Male , Retrospective StudiesABSTRACT
Using biomass wastes as adsorbents is a promising option for organic waste reclamation, but unfortunately, their adsorption capacity is usually limited, especially for hydrophobic organic pollutants. To address this issue, this work prepared cetylpyridinium chloride (a cationic surfactant)-modified pine sawdust (CPC-PS) and further demonstrated their performance for hydrophobic bisphenol A (BPA) and 2,4-dichlorophenol (DCP) adsorption. Compared to the PS, the CPC-PS improved the maximum adsorption capacity for BPA and DCP by approximately 98% and 122%, respectively. The kinetic and thermodynamic analyses showed that the BPA and DCP adsorption onto the CPC-PS fitted the pseudo-second-order kinetics and the Freundlich model. After regeneration using NaOH, the adsorption capacity of the CPC-PS for BPA still maintained 80.2% of the initial value after five cycles. Based on the experimental results, the CPC-PS was proposed to enhance the BPA and DCP adsorption through the solubilization of hemimicelles for hydrophobic organic pollutants, the π-π stacking between benzene-ring structures, and the hydrogen binding between the adsorbents and the pollutants. This work provides a viable method to use surfactant-modified pine sawdust as effective adsorbents to remove hydrophobic pollutants.