Persistent Pemphigus Vulgaris Showing Features of Tufted Hair Folliculitis

Pemphigus vulgaris is an autoimmune blistering disease that commonly involves the scalp. Lesions of pemphigus vulgaris that persist on the scalp for a long period may be accompanied by tufted hair folliculitis. Only two previous accounts of tufted hair folliculitis developing in a lesion of pemphigus vulgaris have been reported. We report a 51-year-old-man with erosions and clusters of hair on the scalp. The scalp lesion had persisted for about 20 years. A histopathological examination of the skin lesion on the scalp revealed separation of the epidermis and clusters of several adjacent hair follicles. The patient was diagnosed with persistent pemphigus vulgaris of the scalp showing features of tufted hair folliculitis

A Simple and Facile Glucose Biosensor Based on Prussian Blue Modified Graphite String

This work describes the string sensor for the simple and sensitive detection of glucose which is based on Prussian blue (PB) modified graphite utilizing dipping. First, PB modified graphite (PB-G) strings are characterized by physical and electrochemical techniques to optimize the PB-G layer thickness. Then, glucose oxidase (GOx) is immobilized on PB-G string electrode with biocompatible chitosan overlayer (Chi/GOx/PB-G). The Chi/GOx/PB-G string electrode exhibits a sensitivity of 641.3 μA·mM−1·cm−2 to glucose with a linear range of 0.03 to 1.0 mM (R2=0.9957) and a rapid response time (<3 s). Moreover, the Chi/GOx/PB-G string electrodes are less sensitive to common interference materials such as ascorbic acid, uric acid, galactose, and acetaminophen than to glucose. The Chi/GOx/PB-G string electrodes also show excellent reproducibility (<5% RSD). Therefore, our Chi/GOx/PB-G string electrodes can be simple, robust, and reliable tools for glucose sensing which can avoid complicated and difficult multistep fabrication processes. In addition, we expect that they have many potential applications in fields ranging from health care to food analysis, in particular where single use is favorable

ArrayXPath II: mapping and visualizing microarray gene-expression data with biomedical ontologies and integrated biological pathway resources using Scalable Vector Graphics

Summary: ArrayXPath () is a web-based service for mapping and visualizing microarray gene-expression data with integrated biological pathway resources using Scalable Vector Graphics (SVG). Deciphering the crosstalk among pathways and integrating biomedical ontologies and knowledge bases may help biological interpretation of microarray data. ArrayXPath is empowered by integrating gene-pathway, disease-pathway, drug-pathway and pathway–pathway correlations with integrated Gene Ontology, Medical Subject Headings and OMIM Morbid Map-based annotations. We applied Fisher's exact test and relative risk to evaluate the statistical significance of the correlations. ArrayXPath produces Javascript-enabled SVGs for web-enabled interactive visualization of gene-expression profiles integrated with gene-pathway-disease interactions enriched by biomedical ontologies

CO ameliorates cellular senescence and aging by modulating the miR-34a/Sirt1 pathway

Oxidative stress is recognised as a key factor that can lead to cellular senescence and aging. Carbon monoxide (CO) is produced by haemoxygenase-1 (HO-1), which exerts cytoprotective effects in aging-related diseases, whereas the effect of CO on cellular senescence and aging has not been elucidated. In the current study, we clearly demonstrated that CO delays the process of cellular senescence and aging through regulation of miR-34a and Sirt1 expression. CO reduced H2O2-induced premature senescence in human diploid fibroblast WI-38 cells measured with SA-beta-Gal-staining. Furthermore, CO significantly decreased the expression of senescence-associated secretory phenotype (SASP), including TNF-alpha IL-6, and PAI-1 and increased the transcriptional levels of antioxidant genes, such as HO-1 and NQO1. Moreover, CO apparently enhanced the expression of Sirt1 through down-regulation of miR-34a. Next, to determine whether Sirt1 mediates the inhibitory effect of CO on cellular senescence, we pre-treated WI-38 cells with the Sirt1 inhibitor Ex527 and a miR-34a mimic followed by the administration of H2O2 and evaluated the expression of SASP and antioxidant genes as well as ROS production. According to our results, Sirt1 is crucial for the antiaging and antioxidant effects of CO. Finally, CO prolonged the lifespan of Caenorhabditis elegans and delayed high-fat diet-induced liver aging. Taken together, these findings demonstrate that CO reduces cellular senescence and liver aging through the regulation of miR-34a and Sirt1.

GSK-3β inhibition by curcumin mitigates amyloidogenesis via TFEB activation and anti-oxidative activity in human neuroblastoma cells

© 2020 Informa UK Limited, trading as Taylor & Francis Group.The translocation of transcription factor EB (TFEB) to the nucleus plays a pivotal role in the regulation of basic cellular processes, such as lysosome biogenesis and autophagy. Autophagy is an intracellular degradation system that delivers cytoplasmic constituents to the lysosome, which is important in maintaining cellular homeostasis during environmental stress. Furthermore, oxidative stress is a critical cause for the progression of neurodegenerative diseases. Curcumin has anti-oxidative and anti-inflammatory activities, and is expected to have potential therapeutic effects in various diseases. In this study, we demonstrated that curcumin regulated TFEB export signalling via inhibition of glycogen synthase kinase-3β (GSK-3β); GSK-3β was inactivated by curcumin, leading to reduced phosphorylation of TFEB. We further showed that H2O2-induced oxidative stress was reduced by curcumin via the Nrf2/HO-1 pathway in human neuroblastoma cells. In addition, we showed that curcumin induced the degradation of amyloidogenic proteins, including amyloid-β precursor protein and α-synuclein, through the TFEB-autophagy/lysosomal pathway. In conclusion, curcumin regulates autophagy by controlling TFEB through the inhibition of GSK-3β, and increases antioxidant gene expression in human neuroblastoma cells. These results contribute to the development of novel cellular therapies for neurodegenerative diseases.

Multiple Psoas Abscess Formation after Pharmacopuncture -A Case Report-

Acupuncture has been widely used in alternative medicine for pain relief but may have many complications due to lack of appropriate cares. Pharmacopuncture is a sort of acupuncture that injects a herbal ingredient through a thin tube for the purpose of combining the effects of the herb and acupuncture and it has many pitfalls. The agents used in pharmacopuncture are not refined for a desired effect and not produced by sterile standard processes under strict medical surveillance. We report a case of a 44-yr-old male patient who had multiple abscesses in the psoas region with fever, right low back and hip pain that began after the pharmacopuncture treatment. This case shows that although pharmacopuncture has been practiced widely, it is important that the appropriate aseptic technique should be used to prevent severe infections and other complications

Enhancement of radiation response in human cervical cancer cells in vitro and in vivo by arsenic trioxide (As2O3)

AbstractArsenic trioxide (As2O3) inhibits cell growth and induces apoptosis in certain types of cancer cells including acute promyelocytic leukemia, prostate and ovarian carcinomas, but its effect on response of tumor cells to ionizing radiation has never been explored before. Here we demonstrate that As2O3 can sensitize human cervical cancer cells to ionizing radiation both in vitro and in vivo. As2O3 in combination with ionizing radiation have a synergistic effect in decreasing clonogenic survival and in the regression of established human cervical tumor xenografts. Pretreatment of the cells with As2O3 also synergistically enhanced radiation-induced apoptosis. Apoptosis of the cells by combined treatment of As2O3 and radiation was associated with reactive oxygen species generation and loss of mitochondrial membrane potential, resulting in the activation of caspase-9 and caspase-3. The combined treatment also resulted in an increased G2/M cell cycle distribution at the concentration of As2O3 which did not alter cell cycle when applied alone. These results indicate that As2O3 can synergistically enhance radiosensitivity of human cervix carcinoma cells in vitro and in vivo, suggesting a potential clinical applicability of combination treatment of As2O3 and ionizing radiation in cancer therapies

Vaccinia-Related Kinase 2 Mediates Accumulation of Polyglutamine Aggregates via Negative Regulation of the Chaperonin TRiC

Misfolding of proteins containing abnormal expansions of polyglutamine (polyQ) repeats is associated with cytotoxicity in several neurodegenerative disorders, including Huntington&apos;s disease. Recently, the eukaryotic chaperonin TRiC hetero-oligomeric complex has been shown to play an important role in protecting cells against the accumulation of misfolded polyQ protein aggregates. It is essential to elucidate how TRiC function is regulated to better understand the pathological mechanism of polyQ aggregation. Here, we propose that vaccinia-related kinase 2 (VRK2) is a critical enzyme that negatively regulates TRiC. In mammalian cells, overexpression of wild-type VRK2 decreased endogenous TRiC protein levels by promoting TRiC ubiquitination, but a VRK2 kinase-dead mutant did not. Interestingly, VRK2-mediated downregulation of TRiC increased aggregate formation of a polyQ-expanded huntingtin fragment. This effect was ameliorated by rescue of TRiC protein levels. Notably, small interference RNA-mediated knockdown of VRK2 enhanced TRiC protein stability and decreased polyQ aggregation. The VRK2-mediated reduction of TRiC protein levels was subsequent to the recruitment of COP1 E3 ligase. Among the members of the COP1 E3 ligase complex, VRK2 interacted with RBX1 and increased E3 ligase activity on TRiC in vitro. Taken together, these results demonstrate that VRK2 is crucial to regulate the ubiquitination-proteosomal degradation of TRiC, which controls folding of polyglutamine proteins involved in Huntington&apos;s disease.open118Ysciescopu