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Abstract Bentonite is a natural and environmentally clay mineral, and bentonite-derived mesoporous materials (BDMMs) were obtained conveniently from the alkali and acid treatment of bentonite. In the present study, BDMMs were explored for immobilization of laccase obtained from Trametes versicolor. As a result, bentonite-derived mesoporous materials- Laccase (BDMMs- Lac) was developed for the removal of tetracycline (TC). The enzyme immobilization process was carried out through physical adsorption contact (ion exchange adsorption, hydrogen bond adsorption, and Van der waals adsorption) between the BDMMs and laccase. The process of immobilization remarkably increased its operating temperature. The BDMMs- Lac exhibited over 60% removal efficiency for TC within 3 h in the presence of 1-hydroxybenzotriazole (HBT). In conclusion, BDMMs- Lac showed more promising potential than free laccase for practical continuous applications. Highlights • BDMMs were expediently obtained from alkali & acid treatment of original bentonite. • Surface areas and average pore sizes of BDMMs were improved nearly by 74 and 2 times. • The thermal stability of BDMMs- Lac was highly improved compared to free laccase. • In the presence of HBT, BDMMs- Lac could remove 60% of TC within 180 min. [ABSTRACT FROM AUTHOR]

The effect of insurance status on overall survival (OS) of patients with cutaneous T-cell lymphoma (CTCL) is unclear. We identified 11,861 patients from the US National Cancer Data Base diagnosed with CTCL from 2004–2014, of which 6088 had private insurance, 756 had Medicaid, 4536 had Medicare, and 481 are uninsured. Privately insured patients were more likely to present at an early stage (p <.001). On multivariate Cox regression analysis, privately insured patients had significantly longer OS than patients with Medicaid (HR: 1.936, 95% CI: 1.680–2.230, p <.001), Medicare (HR: 1.342, 95% CI: 1.222–1.474, p <.001), or no insurance (HR 1.849, 95% CI: 1.539–2.222, p <.001). The survival advantage of privately insured patients persisted on relative survival and propensity score-matched analyses. In conclusion, privately insured patients were more likely to present at an early stage, and had longer OS than patients who were Medicaid-, Medicare-, or not insured. [ABSTRACT FROM AUTHOR]

Background: Retinoic acid (RA) is an active metabolite of vitamin A and has been reported to improve the clinical symptoms of patients with systemic sclerosis (SSc). However, the mechanism of RA in the prevention of SSc remains unclear. Regulatory T cells (Tregs) are a subpopulation of T cells with immunosuppressive activity. The quantitative and functional defects of Tregs may mediate the immune dysfunction in SSc. The addition of all-trans retinoic acid (ATRA) to human naïve CD4+ cells could promote the maturation of Tregs and increase the stable expression of Foxp3. In this study, we explored the role of RA on Tregs in SSc CD4+ T cells and its possible epigenetic mechanisms, so as to further understand the mechanisms of RA on SSc.Methods: CD4+ T cells were isolated from peripheral blood of SSc and treated with or without ATRA and/or transforming growth factor-β (TGF-β). The percentage of CD4+CD25+FOXP3+ Tregs was counted by flow cytometry. FOXP3 mRNA and protein levels were measured by quantitative real-time reverse transcriptase polymerase chain reaction and Western blotting, respectively. Bisulfite sequencing was performed to determine the methylation status of the FOXP3 proximal promoter sequences.Results: The expression of Tregs and FOXP3 in CD4+ T cells from patients with SSc increased in response to ATRA. Moreover, combined stimulation with ATRA and TGF-β resulted in the enhancement of these effects. Further studies revealed that stimulation with ATRA increased the expression of FOXP3 in SSc CD4+ T cells by downregulating FOXP3 promoter methylation levels.Conclusions: ATRA acts as an inducer of Treg response in SSc CD4+ T cells via demethylation of the FOXP3 promoter and activation of FOXP3 expression. This may be one of the molecular mechanisms for ATRA, and therefore, RA can be used for the treatment of SSc. [ABSTRACT FROM AUTHOR]

• The aryl hydrocarbon receptor downregulated in SSc patient dermal fibroblasts. • The AhR ligand-Ficz attenuated the COL1A1 expression and upregulate the MMP1 expression by activating AhR signaling. • The AhR ligand-Ficz downregulated α-SMA expression in vivo and vitro. • AhR signaling activation partially relieve the dermal fibrosis in bleomycin-induced SSc mouse model. Systemic sclerosis (SSc) is a systemic autoimmune disease that often leads to fibrosis of multiple organs, and there are no effective treatments. Aryl hydrocarbon receptor (AhR) is a highly evolutionarily conserved transcription factor activated by endogenous and exogenous ligands and that regulate cell proliferation, tumorigenesis and immune balance. Recently, it have reported AhR signaling may participate in fibrosis process, usually consider as a negative regulator of TGF-β. However, the detailed relationship between AhR and SSc has not been reported yet. Here we firstly found that AhR and CYP1A1 downregulated in SSc fibroblast(n = 6). The AhR ligand-Ficz negatively regulates TGF-β1, COL1A1 and α-SMA expression, also enhances the MMP-1 expression via the AhR signaling activation. Conversely the AhR antagonist CH223191 could inhibit this effect. Furthermore, the antifibrosis effect of AhR signaling activation was also confirmed in bleomycin induced scleroderma mouse model. In conclusion, AhR signaling activation balances the extracellular matrix (ECM) composition and deposition, which may provide a new sight to the pathogenesis of SSc and AhR signaling activation may be a potential therapy for SSc. [ABSTRACT FROM AUTHOR]

Background: To clarify the controversy between inflammatory or autoimmune skin diseases and thyroid diseases, we performed two-sample Mendelian randomization (MR) analyses., Participants: Genetic data on factors associated with atopic dermatitis (AD, n=40,835), seborrheic dermatitis (SD, n=339,277), acne (n=363,927), rosacea (n=299,421), urticaria (n=374,758), psoriasis (n=373,338), psoriasis vulgaris (n=369,830), systemic lupus erythematosus (SLE, n=14,267), vitiligo (n=353,348), alopecia areata (AA, n=361,822), pemphigus (n=375,929), bullous pemphigoid (BP, n=376,274), systemic sclerosis (SSc, n=376,864), localized scleroderma (LS, n=353,449), hypothyroidism (n=314,995 or n=337,159), and hyperthyroidism (n=281,683 or n=337,159) were derived from genome-wide association summary statistics of European ancestry., Main Measures: The inverse variance weighted method was employed to obtain the causal estimates of inflammatory or autoimmune skin diseases on the risk of thyroid diseases, complemented by MR-Egger, weighted median, and MR-pleiotropy residual sum and outlier (MR-PRESSO)., Key Results: AD, SLE, SD, and psoriasis vulgaris were associated with an increased risk of hypothyroidism, whereas BP was associated with a lower risk of hypothyroidism (all with p < 0.05). The multivariable MR analyses showed that AD (OR = 1.053; 95%CI: 1.015-1.092; p = 0.006), SLE (OR = 1.093; 95%CI: 1.059-1.127; p < 0.001), and SD (OR = 1.006; 95%CI: 1.002-1.010; p = 0.006) independently and predominately contributed to the genetic causal effect on hypothyroidism after adjusting for smoking. The results showed no causal effects of inflammatory or autoimmune skin diseases on hyperthyroidism., Conclusion: The findings showed a causal effect of AD, SLE, SD on hypothyroidism, but further investigations should be conducted to explore the pathogenic mechanisms underlying these relationships., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 You, Duan, Zhou, Yu, Zou, Wei, Chai, Zeng, Xiao, Yuan and Xiao.)

The fibrosis of tissues and organs occurs via an aberrant tissue remodeling process characterized by an excessive deposition of extracellular matrix, which can lead to organ dysfunction, organ failure, and death. Because the pathogenesis of fibrosis remains unclear and elusive, there is currently no medication to reverse it; hence, this process deserves further study. Activating protein-1 (AP-1)-comprising Jun (c-Jun, JunB, JunD), Fos (c-fos, FosB, Fra1, and Fra2), and activating transcription factor-is a versatile dimeric transcription factor. Numerous studies have demonstrated that AP-1 plays a crucial role in advancing tissue and organ fibrosis via induction of the expression of fibrotic molecules and activating fibroblasts. This review focuses on the role of AP-1 in a range of fibrotic disorders as well as on the antifibrotic effects of AP-1 inhibitors. It also discusses the potential of AP-1 as a new therapeutic target in conditions involving tissue and organ fibrosis., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Loss of melanocytes induced by activated CD8 + T cells is the pathological hallmark of vitiligo. Melanocyte-specific CD8 + T cells are recruited to the skin via chemokines, thereby releasing perforin, granzyme, and other cytotoxic substances that destroy the melanocytes. However, the mechanism of CD8 + T cells to adhere to melanocytes is unknown. Previous transcriptome sequencing results published by our group showed that the occluding ( OCLN) gene was significantly upregulated in CD8 + T cells from skin lesions of vitiligo. Occludin is a crucial component of the tight junction between cells; in cells without tight junction, occludin mediates the adhesion of two cells in the form of a self-ligand. This study demonstrated that OCLN gene expression was elevated in the CD8 + T cells of vitiligo patients, and occludin mediates the adherence of CD8 + T cells to melanocytes. Besides, pathological changes in vitiligo skin lesions reveal that CD8 + T cells continuously persist in the skin lesions, which is related to the persistence of the disease. In this regard, we found that fibroblasts from vitiligo patients significantly express occludin, which may participate in the continuous retention of CD8 + T cells in the skin lesions. The pathogenesis of vitiligo is closely related to oxidative stress, and our data suggest that overexpression of hypoxia-inducible factor-1 α (HIF-1 α ) increases the expression of occludin. Besides, ChIP-qPCR of CD8 + T cells revealed that HIF-1 α directly binds to the OCLN promoter. Thus, occludin upregulation promotes the adhesion of CD8 + T cells and melanocytes via the HIF-1 α signaling pathway. Our study results suggested a critical role for OCLN in the occurrence, progression, and maintenance of vitiligo. Therefore, inhibiting the expression of OCLN gene may be a potential targeted treatment strategy., Competing Interests: The authors declare that there is no conflict of interest regarding the publication of this article., (Copyright © 2022 Puyu Zou et al.)

Antibiotic concentrations in surface waters far exceed the pollution limit due to the abuse of pharmaceuticals, resulting in an urgent need for an approach with potential efficiency, sustainability and eco-friendliness to remove antibiotic pollutants. A novel biochar-based nanomaterial was synthesized by hydrothermal synthesis and was investigated for its removal potential for tetracycline hydrochloride (TC) from both artificial and real wastewater. The associative facilitation between biochar and g-MoS 2 nanosheets was proposed, revealing the favorable surface structures and adsorption properties of the composite. The related adsorption kinetics, isotherms and thermodynamics were studied by several models with adsorption experimental data, turning out that biochar decorated by g-MoS 2 exhibited optimum TC removal with adsorption capacity up to 249.45 mg/g at 298 K. The adsorption behavior of TC molecules on g-MoS 2 -BC can be interpreted well by three-step process, and it is dominated by several mechanisms containing pore-filling, electrostatic force, hydrogen bond and π-π interaction. In addition, the cost-effective g-MoS 2 -BC nanocomposites demonstrated excellent adsorption and recycling performance in TC-contaminated river water, which might provide the underlying insights needed to guide the design of promising approach for contaminant removal on a large scale in practical application., (Copyright © 2018. Published by Elsevier B.V.)

This research investigated the adsorption of zinc and lead from binary metal solution with tunable selectivity. A nano adsorbent was prepared by introducing imine groups onto the surface of stability enhanced magnetic nanoparticles and then characterized by TEM and FTIR. Binary metal components adsorption was carried out in different concentration of metal and EDTA solution. Due to the interaction between metals and adsorbent in the presence of EDTA, the selective adsorption of zinc and lead could be achieved with 100% selectivity. To only remove zinc from binary metals, the solution condition was [EDTA]/[M(2+)] = 0.7 with pH of 6, and its saturated adsorption capacity was 1.25 mmol/g. For selective adsorption of lead, an equilibrium adsorption capacity of 0.81 mmol/g was obtained under the condition of [EDTA]/[M(2+)] = 0.7 and pH of 2. The exhausted adsorbent could be regenerated by simple acid or alkali wash, and high purity lead and zinc salt solutions were recovered and concentrated.