Search

Background: Demodex mites are related to some inflammatory diseases such as rosacea and blepharitis and could be harmful in patients with immunodeficiency or immunosuppression, especially notable in patients using biologic like dupilumab. In order to have an objective observation of different anti-Demodex strategies, we conducted this study, based on interventional clinical evidence with quantified Demodex mite data. Methods: We used the PubMed, Embase, ClinicalTrials.gov, Medline, and International Clinical Trials Registry Platform (ICTRP) as databases. To assess the risk of bias, the RoB2 and ROBINS-I tools were used. The certainty of evidence was assessed following the GRADE guideline. Furthermore, the effect sizes (ESs) of different strategies were compared in different time periods (0–1, 1–2, 2–3, >3 months), as well as Demodex decrease rates. Results: 1,618 studies were identified in the databases, with 21 of which included in the final quantitative synthesis. Interventions in these studies included ivermectin, tea tree oil (TTO), permethrin, crotamiton, metronidazole, light therapies, combined therapies, and other therapies. During 0–1 month, the ES varied from 0.07 (cleanser) to 1.95 (systemic ivermectin-metronidazole). During 1–2 months, the ES varied from 0.88 (topical permethrin) to 4.40 (topical ivermectin). During 2–3 months, the ES varied from 0.79 (topical permethrin) to 8.37 (topical ivermectin). During the time of 3 months, the ES varied from 0.59 (topical permethrin) to 2.25 (intense pulsed light [IPL]). In terms of Demodex decrease rates, topical ivermectin, TTO, permethrin, IPL, and baby shampoo had achieved a nearly 100% decrease. The reported adverse events were mostly mild, without severe adverse events reported in any of the studies. Conclusions: We found ivermectin (topical and systemic), ivermectin-metronidazole (topical), and TTO (topical) are promising anti-Demodex interventions. In addition to traditional pharmacotherapy, light therapies, especially IPL and skin cleansing, could also be considered as effective methods to control Demodex mite infestation.

Background: The Corona pandemic fuelled up skin pathogen challenges in young and adults, the antimicrobial efficacy of laundry detergents could be considered particularly. However, no available data focusing on the form of laundry detergent, additives and conditions affect the antimicrobial efficacy. This study simulated washing procedures to investigate the antibacterial and antifungal activity of laundry detergents.Methods and Results: Mimic laundry procedures were performed to treat Gram-positive bacteria, Gram-negative bacteria and fungus, colony counting and propidium iodide staining were used to assess the antimicrobial activity. Powder detergent A, NaBO3*4H2O with the tetraacetylethylenediamine, 2Na2co3.3H2O with tetraacetylethylenediamine could achieve a > 5-log10 reduction of three microbial colony generation. Anionic surfactant sodium dodecylbenzene sulphonate (SDBS) group had the strongest fluorescence intensity in three microbial propidium iodide staining.Conclusions: Powder form laundry detergents are superior to liquid form, peroxide-based bleaches and bleach activator in solid form, the solid surfactants with matched PH and alkyl chain length showed a considerable antimicrobial effect.

We investigated the molecular mechanism of curcumol-induced apoptosis in bladder cancer cells. The mitochondrial membrane potential was measured using JC-1 staining. ROS generation of bladder cancer cells was determined using the DCFH staining method. The apoptosis of bladder cancer cells was examined using the Annexin V-FITC and PI double-staining method. Enforced expression of EZH2 in bladder cancer cells was accomplished by transfecting an EZH2 expression plasmidinto EJ and T24 cells. siRNAs targeting EZH2 were used to inhibit endogenous expression of EZH2. Curcumol dose-dependently inhibited proliferation and colony formation and induced apoptosis in EJ and T24 bladder cancer cells. These effects correlated with decreased accumulation of EZH2. In addition, suppression of EZH2 enhanced the inhibitory effects of curcumol on cell growth and colony formation and increased curcumol-induced apoptosis. Conversely, enforced expression of EZH2 ameliorated the inhibitory effects of curcumol on cell growth and colony formation and decreased curcumol-induced apoptosis in EJ and T24 cells. We also found that suppression of EZH2 induced ROS generation and MMP loss in both EJ and T24 cells. Conversely, up-regulation of EZH2 suppressed ROS generation and MMP loss. Our data indicate that curcumol inhibits proliferation and induces apoptosis by targeting EZH2 and modulating the mitochondrial apoptosis pathway.

Bladder cancer is the second most common malignant tumor of the urinary tract worldwide and is associated with significant morbidity and mortality. EZH2, the enzymatic subunit of Polycomb repressive complex 2 (PRC2), is frequently overexpressed in multiple tumor types including Bladder cancer and plays multiple roles in tumor cell proliferation and apoptosis. Previous study showed that miR-26a has different roles in different tumors and the expression of EZH2 is identified as a potential target of miR-26a which miR-26a has been found to decrease in bladder cancer. But the mechanism between EZH2 and miR-26a is not completely clear in bladder cancer. Western blot and Real-time PCR were involved to detect both expression of mRNA and protein of EZH2. And we used mimics-miR26a to elaborate the relationship between EZH2 and miR-26a in cell proliferation and apoptosis process through lots of specific assays. The results showed that EZH2 express mainly in bladder tumor tissues than para-carcinoma tissues. Meanwhile, miR26a can down-regulate the expression of EZH2 through suppressing EZH2 activity. Both miR26a and downregulated EZH2 can induce bladder cancer cell apoptosis and increase cell at G1 stage as well as suppress cell proliferation. The further assays reveal that miR-26a can suppress cell proliferation and enhance cell apoptosis through EZH2. In this study, we found that EZH2 was overexpressed in bladder tumor tissue and miR-26a could downregulate the expression of EZH2 to inhibit proliferation and enhance apoptosis in bladder cancer.