Abstract The treatment of recessive dystrophic epidermolysis bullosa (RDEB) remains challenging. Elevated IgE levels have previously been reported in several RDEB patients. In this prospective, single‐centre, open intervention study, elevated IgE levels were seen in 11 out of 12 patients with intense pruritus, and the patients with elevated IgE levels received anti‐IgE therapy every 4 weeks for at least three cycles. Compared with the baseline, 10 patients with RDEB had good clinical outcomes with enhanced wound healing, a reduction in Birmingham (epidermolysis bullosa) EB severity score by 15%, a reduction in affected body surface area by 23.3%, amelioration of skin inflammation, and an increase in type VII collagen deposition by 13.1‐fold. All the patients had a good tolerance to anti‐IgE therapy. Furthermore, patients with higher IgE levels tended to have higher disease severity and more favorable clinical outcomes. Our report also suggested the potential role of IgE in the pathogenesis of inflammatory conditions associated with RDEB. (ChiCTR1900021437).
The present study presents a kind of novel ultrafiltration membrane which can be applied to purify water containing hexavalent chromium (Cr(VI)) ions and was prepared via the immersion phase inversion method. 2-Amino-4-thiazoleacetic acid was used as the additive of the novel ultrafiltration (UF) membrane and the membrane material was polyvinylidene fluoride (PVDF). The effects of technical parameters on the performance of the novel UF membranes were investigated. The prepared polymer blend membrane was characterized using Fourier transform infrared (FTIR) spectroscopy, scanning electron microscopy (SEM) and contact angle measurements. The experimental results showed that the pure water flux of the membrane was 318.11 L/m2·h, the contact angle was 81.2° and the adsorption capacity of chromium ion was 165 µg/cm2. The modified PVDF membrane presented better adsorption abilities for chromium ion than that of the traditional membrane.
Abstract. Dust is a major source of atmospheric aerosols. Its chemical composition is often assumed to be similar to the parent soil. However, this assumption has not been rigorously verified. Here, we generated dust aerosols from soils to determine if there is particle size-dependent selectivity of heavy metals in the dust generation. Mn, Cd, Pb and other heavy metals were found to be highly enriched in fine (PM2.5) dust aerosols, which can be up to ~6.5-fold. To calculate the contributions of dust to atmospheric heavy metals, regional air quality models usually use the dust chemical profiles from the US EPA’s SPECIATE database, which does not capture the correct size-dependent selectivity of heavy metals in dust aerosols. Our air quality modeling for China demonstrates that the calculated contribution of fine dust aerosols to atmospheric heavy metals, as well as their cancer risks, could have significant errors without using proper dust profiles.
Sleep deprivation negatively influences cognition, however, the regulatory mechanisms to counteract this effect have not been identified. IGF-1 has been shown to be anti-inflammatory and neuroprotective in CNS injury models. In this study, we determined the impact of IGF-1 on brain injury and inflammation while modeling sleep deprivation. We found that IGF-1 was downregulated in human peripheral blood and in mice subjected to sleep deprivation for 5 days, with reduced activation of the downstream PI3K/AKT/GSK-3β pathway in mice brains. In addition, we found reduced levels of the anti-apoptosis enzyme Bcl-2 and increased levels of pro-apoptosis enzyme Caspase-9 expression, together with increased pro-inflammatory factors. The administration of IGF-1 after sleep deprivation induced activation of the PI3K/AKT/GSK-3β pathway, reversed changes in Bcl-2, Caspase-9, and pro-inflammatory factors, and alleviated cognitive impairment. Notably, IGF-1 also induced activation of the PI3K/AKT/GSK-3β pathway, and displayed anti-apoptosis and anti-inflammatory properties under normal sleep conditions,while IGF-1 did not improve the cognition under normal sleep conditions. These results suggest that the IGF-1/PI3K/AKT/GSK-3β pathway is involved in the regulation of cognitive function after sleep deprivation through modulation of apoptosis and inflammatory response. IGF-1 could be a viable therapeutic target, though further investigation is required to better understand its role in sleep deprivation.
Lapatinib, a double-target receptor tyrosine kinase inhibitor, is an oral-targeted anticancer drug developed by GlaxoSmithKline (GSK). It mainly acts on epidermal growth factor receptor 1 (EGFR1) a...
Abstract Background: Sleep deprivation negatively influences cognition, although inflammatory and immune responses participate in sleep deprivation,the molecular regulators of neuroinflammation after sleep deprivation remain to be defined. IGF-1 have shown anti-inflammatory and neuroprotective properties in models of CNS injury. This study investigated the role of IGF-1 on neuroinflammation and cognition deficits after sleep deprivation. Methods: Human periphery blood were obtained from chronic insomia(CI) patients to evaluated the levels of IGF-1. Mouse model of modified multiple platforms method (MMPM) was used to examine the role of IGF-1 in sleep deprivation. Behavior was evaluated by water maze tests.Inflammatory markers, and neuroinflammation were assessed by western blot and quantitative real-time PCR. Results: We found down-regulation of IGF-1 in human peripheral blood and in mice subjected to sleep deprivation for 5 days, and reduced activation of downstream the PI3K/AKT/GSK-3β pathway in mice brain. In conjunction, we found reduced levels of anti-apoptosis enzyme Bcl-2 and increased levels of pro-apoptosis enzyme Caspase-9, together with increased pro-inflammatory factors. Administration of IGF-1 induced activation of the PI3K/AKT/GSK-3β pathway, reversed changes in Bcl-2, Caspase-9 and pro-inflammatory factors, and prevented cognitive decline. Conclusion: These findings indicate that the IGF-1 reduces neuroinflammation and cogniton deficits after sleep deprivation. The effects may be mediated by the interaction among IGF-1 and PI3K/AKT/GSK-3β signaling. IGF-1 may be a viable therapeutic target that requires further investigations in sleep deprivation.
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