Treatment of Darier Disease with Radiation Therapy: Case Report and Literature Review.

Darier's disease (DD) is an autosomal dominant genodermatosis characterized by hyperkeratotic papules, often accompanied by scaling and crusting. Managing DD presents significant challenges due to the absence of an effective cure, with only symptom targeting treatments currently available. This study presents a case of refractory DD that showed poor response to established pharmacological treatments but demonstrated improvement with low-dose superficial X-ray radiotherapy (SRT). The radiation was delivered as a single 200 cGy treatment, which visibly improved the condition. Considering the different degrees of side effects, sequelae, and risk of developing radiation-induced cancer after exposure to moderate levels of radiation, it may be considered that we attempt to treat recalcitrant DD initially by applying a low dose of radiation in order to mitigate these undesired side effects. If larger doses or additional courses are necessary due to inadequate response, the risks and benefits must be carefully evaluated and discussed with patients.

Interfacial self-healing polymer electrolytes for Long-Cycle silicon anodes in High-Performance solid-state lithium batteries.

For all-solid-state lithium-ion batteries (ASSLIBs), silicon (Si) stands out as an appealing anodes material due to its high energy density and improved safety compared to lithium metal. However, the substantial volume changes during cycling result in poor solid-state physical contact and electrolyte-electrode interface issues, leading to unsatisfactory electrochemical performance. In this study, we employed in-situ polymerization to construct an integrated Si anodes/self-healing polymer electrolyte for ASSLIBs. The polymer chain reorganization stems from numerous dynamic bonds in the constructed self-healing dynamic supermolecular elastomer electrolyte (SHDSE) molecular structure. Notably, SHDSE also serves as a Si anodes binder with enhanced adhesive capability. As a result, the well-structured Li|SHDSE|Si-SHDSE cell generates subtle electrolyte-electrode interface contacts at the molecular level, which can offer a continuous and stable Li+ transport pathway, reduce Si particle displacement, and mitigate electrode volume expansion. This further enhances cyclic stability (>500 cycles with 68.1 % capacity retention and >99.8 % Coulombic efficiency). More practically, the 2.0 Ah wave-shaped Si||LiCoO2 soft-pack battery with in-situ cured SHDSE exhibits strongly stabilized electrochemical performance (1.68 Ah after 700 cycles, 86.2 % capacity retention) in spite of a high operating temperatures up to 100 °C and in various bending tests. This represents a groundbreaking report in flexible solid-state soft-pack batteries containing Si anodes.

Steric molecular combing effect enables Self-Healing binder for silicon anodes in Lithium-Ion batteries.

Silicon is a promising anode material for lithium-ion batteries with its superior capacity. However, the volume change of the silicon anode seriously affects the electrode integrity and cycle stability. The waterborne guar gum (GG) binder has been regarded as one of the most promising binders for Si anodes. Here, a unique steric molecular combing approach based on guar gum, glycerol, and citric acid is proposed to develop a self-healing binder GGC, which would boost the structural stability of electrode materials. The GGC binder is mainly designed to weaken van der Waals' forces between polymers through the plasticizing effect of glycerol, combing and straightening the guar molecular chain of GG, and exposing the guar hydroxyl sites of GG and the carboxyl groups of citric acid. The condensation reaction between the hydroxyl sites of GG and the carboxyl groups of citric acid forms stronger hydrogen bonds, which can help achieve self-healing effect to cope with the severe volume expansion effect of silicone-based materials. Silicon electrode lithium-ion batteries prepared with GGC binders exhibit outstanding electrochemical performance, with a discharge capacity of up to 1579 mAh/g for 1200 cycles at 1 A/g, providing a high capacity retention rate of 96%. This paper demostrates the great potential of GGC binders in realizing electrochemical performance enhancement of silicon anode.

[Retracted] Astragaloside IV inhibits platelet­derived growth factor­BB­stimulated proliferation and migration of vascular smooth muscle cells via the inhibition of p38 MAPK signaling.

[This retracts the article DOI: 10.3892/etm.2014.1905.].

The Latest View on the Mechanism of Ferroptosis and Its Research Progress in Spinal Cord Injury.

Ferroptosis is a recently identified nonapoptotic form of cell death whose major markers are iron dependence and accumulation of lipid reactive oxygen species, accompanied by morphological changes such as shrunken mitochondria and increased membrane density. It appears to contribute to the death of tumors, ischemia-reperfusion, acute renal failure, and nervous system diseases, among others. The generative mechanism of ferroptosis includes iron overloading, lipid peroxidation, and downstream execution, while the regulatory mechanism involves the glutathione/glutathione peroxidase 4 pathway, as well as the mevalonate pathway and the transsulfuration pathway. In-depth research has continuously developed and enriched knowledge on the mechanism by which ferroptosis occurs. In recent years, reports of the noninterchangeable role played by selenium in glutathione peroxidase 4 and its function in suppressing ferroptosis and the discovery of ferroptosis suppressor protein 1, identified as a ferroptosis resistance factor parallel to the glutathione peroxidase 4 pathway, have expanded and deepened our understanding of the mechanism by which ferroptosis works. Ferroptosis has been reported in spinal cord injury animal model experiments, and the inhibition of ferroptosis could promote the recovery of neurological function. Here, we review the latest studies on mechanism by which ferroptosis occurs, focusing on the ferroptosis execution and the contents related to selenium and ferroptosis suppressor protein 1. In addition, we summarize the current research status of ferroptosis in spinal cord injury. The aim of this review is to better understand the mechanisms by which ferroptosis occurs and its role in the pathophysiological process of spinal cord injury, so as to provide a new idea and frame of reference for further exploration.

Topical 5-aminolevulinic acid photodynamic therapy for intra anal-rectal warts.

Background: Condylomata acuminata (CA) are a common sexually transmitted disease. The recurrence rate of condyloma acuminatum using traditional treatments is higher than that of applying photodynamic therapy, and a variety of adverse reactions after treatment. At the same time, different parts of condyloma acuminatum after treatment recurrence rate is also different, especially for intra anal-rectal warts.Objective: To evaluate whether using photodynamic therapy (PDT) can effectively reduce recurrence of condylomata acuminata for intra anal-rectal warts.Methods: After the confirmation of the diagnosis of intra anal-rectal warts, the patients were treated with PDT with 5-aminolevulinic acid hydrochloride (ALA). PDT was performed with irradiation of 18-36 J/cm2 at an irradiance of 20-40 mW/cm2 with light-emitting diode (LED) light energy, wavelength 635 nm. We used a special PDT light equipment for intra anal-rectal area warts. PDT was repeated once every week for 4 weeks.Results: After PDT, the complete clearance rate was 76.1% (35 of 46 patients). At the end of the 12 weeks followed, recurrence occurred in five cases. We recorded pain in all 46 patients and the average visual analog scale (VAS) pain score was 6.96 ± 1.41 points.Conclusion: The treatment with PDT is effective in reducing the high rate of recurrence for intra anal-rectal warts. Pain is still a great challenge for the therapy.

Inflammatory microenvironment contributes to epithelial-mesenchymal transition in gastric cancer.

Gastric cancer (GC) is the fifth most common malignancy in the world. The major cause of GC is chronic infection with Helicobacter pylori (H. pylori). Infection with H. pylori leads to an active inflammatory microenvironment that is maintained by immune cells such as T cells, macrophages, natural killer cells, among other cells. Immune cell dysfunction allows the initiation and accumulation of mutations in GC cells, inducing aberrant proliferation and protection from apoptosis. Meanwhile, immune cells can secrete certain signals, including cytokines, and chemokines, to alter intracellular signaling pathways in GC cells. Thus, GC cells obtain the ability to metastasize to lymph nodes by undergoing the epithelial-mesenchymal transition (EMT), whereby epithelial cells lose their epithelial attributes and acquire a mesenchymal cell phenotype. Metastasis is a leading cause of death for GC patients, and the involved mechanisms are still under investigation. In this review, we summarize the current research on how the inflammatory environment affects GC initiation and metastasis via EMT.

CCR7 enhances TGF-ß1-induced epithelial-mesenchymal transition and is associated with lymph node metastasis and poor overall survival in gastric cancer.

CCR7 is a G protein-coupled chemokine receptor. In this study, we used immunohistochemistry with tissue microarrays to measure CCR7 expression in tumor specimens from 122 patients with gastric cancer. We show that CCR7 expression is associated with lymph node metastasis (P = 0.022) and overall survival (OS; P = 0.025), and is an independent factor associated with poorer overall survival (P = 0.032). The CCR7 mechanism was predicted based on bioinformatic analysis and verified in gastric cancer cell lines and primary tumor samples. The data show that CCR7 contributes to TGF-ß1-induced epithelial-mesenchymal transition (EMT) and that the effects of TGF-ß1 are inhibited by a CCR7 neutralizing antibody or a NF-κB inhibitor. Increased TGF-ß1 expression was accompanied by nuclear localization of NF-κB-p65 and higher levels of the mesenchymal marker vimentin in human gastric cancer samples. We conclude that the CCR7 axis mediates TGF-ß1-induced EMT via crosstalk with NF-κB signaling, facilitating lymph node metastasis and poorer overall survival in patients with gastric cancer. These findings suggest CCR7 is a novel prognostic indicator and a potential target for gastric cancer therapy.

Astragaloside IV inhibits platelet-derived growth factor-BB-stimulated proliferation and migration of vascular smooth muscle cells via the inhibition of p38 MAPK signaling.

Astragaloside IV (AS-IV), the major active component extracted from Astragalus membranaceus, has been demonstrated to exhibit protective effects on the cardiovascular, immune, digestive and nervous systems; thus, has been widely used in traditional Chinese medicine. Abnormal proliferation and migration of vascular smooth muscle cells (VSMCs) is closely associated with the initiation and progression of cardiovascular diseases, including atherosclerosis and restenosis. However, the effects of AS-IV on VSMCs remain unknown. For the first time, the present study demonstrated that AS-IV markedly suppressed platelet-derived growth factor (PDGF)-BB-stimulated cellular proliferation and migration of HDMEC-a human dermal VSMCs (HDVSMCs). Further investigation into the underlying molecular mechanisms demonstrated that the administration of AS-IV attenuated the PDGF-BB-stimulated switch of HDVSMCs into a proliferative phenotype. Furthermore, AS-IV inhibited the PDGF-BB-induced expression of cell cycle-associated proteins, as well as the upregulation of matrix metalloproteinase (MMP)2, but not MMP9. In addition, AS-IV was shown to downregulate the activation of p38 mitogen-activated protein kinase (MAPK) signaling induced by PDGF-BB in HDVSMCs. Therefore, the observations of the present study indicate that AS-IV inhibits PDGF-BB-stimulated VSMC proliferation and migration, possibly by inhibiting the activation of the p38 MAPK signaling pathway. Thus, AS-IV may be useful for the treatment of vascular diseases.

DNA methylation, a hand behind neurodegenerative diseases.

Epigenetic alterations represent a sort of functional modifications related to the genome that are not responsible for changes in the nucleotide sequence. DNA methylation is one of such epigenetic modifications that have been studied intensively for the past several decades. The transfer of a methyl group to the 5 position of a cytosine is the key feature of DNA methylation. A simple change as such can be caused by a variety of factors, which can be the cause of many serious diseases including several neurodegenerative diseases. In this review, we have reviewed and summarized recent progress regarding DNA methylation in four major neurodegenerative diseases: Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), and amyotrophic lateral sclerosis (ALS). The studies of these four major neurodegenerative diseases conclude the strong suggestion of the important role DNA methylation plays in these diseases. However, each of these diseases has not yet been understood completely as details in some areas remain unclear, and will be investigated in future studies. We hope this review can provide new insights into the understanding of neurodegenerative diseases from the epigenetic perspective.

Frictional characteristics of atomically thin sheets.

Using friction force microscopy, we compared the nanoscale frictional characteristics of atomically thin sheets of graphene, molybdenum disulfide (MoS2), niobium diselenide, and hexagonal boron nitride exfoliated onto a weakly adherent substrate (silicon oxide) to those of their bulk counterparts. Measurements down to single atomic sheets revealed that friction monotonically increased as the number of layers decreased for all four materials. Suspended graphene membranes showed the same trend, but binding the graphene strongly to a mica surface suppressed the trend. Tip-sample adhesion forces were indistinguishable for all thicknesses and substrate arrangements. Both graphene and MoS2 exhibited atomic lattice stick-slip friction, with the thinnest sheets possessing a sliding-length-dependent increase in static friction. These observations, coupled with finite element modeling, suggest that the trend arises from the thinner sheets' increased susceptibility to out-of-plane elastic deformation. The generality of the results indicates that this may be a universal characteristic of nanoscale friction for atomically thin materials weakly bound to substrates.