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Background: Tinea of vellus hair is a dermatophyte infection with or without localised infection of adjacent skin. The epidemiology and pathogenesis of this disorder have insufficiently been established. Objectives: To gain insight into the epidemiology and analysis dissection of patterns of vellus hair infection. Methods: A comprehensive examination of our series of cases and existing literature, clinical information was performed. Microsporum species were assayed for levels of keratinase and SUB1‐3 level after different keratin‐induced cultures. Results: The infection affects both children and adults, with a male‐to‐female ratio of 1:1.3. The most afflicted areas are the face, neck and upper limbs. Both typical (ringworm‐like) and atypical (tinea incognito) tinea lesions can be observed. The disorder is caused primarily by the zoophilic Microsporum canis (40.39%). Topical antifungal drugs alone are ineffective; mycological cure is achieved in combination with systemic antifungal therapy for 4–8 weeks. In vitro, M. canis exhibited significantly elevated levels of secreted protease and SUB1 and SUB3 transcripts in cat hair cultures. Conversely, the findings of anthropophilic dermatophytes M. audouinii and M. ferrugineum demonstrated the opposite trend, suggesting that there are associations between keratinase activity and expression of SUB1 and SUB3 induced by different keratin substrates among M. canis complex members. Conclusions: The epidemiological characteristics of tinea of vellus hair help us to understand its transmission patterns and develop effective prevention strategies. There are associations between keratinase activity and expression of SUB1‐3 induced by different substrates, which may explain the host shift and adaptation from pet animals to particular micro‐habitats on the human host. [ABSTRACT FROM AUTHOR]

Isoleucine is a branched chain amino acid. The role of isoleucine in cerebral ischemia–reperfusion injury remains unclear. Here, we show that the concentration of isoleucine is decreased in cerebrospinal fluid in a rat model of cerebral ischemia–reperfusion injury, the rat middle cerebral artery occlusion (MCAO). To our surprise, the level of intraneuronal isoleucine is increased in an in vitro model of cerebral ischemia injury, the oxygen–glucose deprivation (OGD). We found that the increased activity of LAT1, an L‐type amino acid transporter 1, leads to the elevation of intraneuronal isoleucine after OGD insult. Reducing the level of intraneuronal isoleucine promotes cell survival after cerebral ischemia–reperfusion injury, but supplementing isoleucine aggravates the neuronal damage. To understand how isoleucine promotes ischemia‐induced neuronal death, we reveal that isoleucine acts upstream to reduce the expression of CBFB (core binding factor β, a transcript factor involved in cell development and growth) and that the phosphatase PTEN acts downstream of CBFB to mediate isoleucine‐induced neuronal damage after OGD insult. Interestingly, we demonstrate that direct‐current stimulation reduces the level of intraneuronal isoleucine in cortical cultures subjected to OGD and that transcranial direct‐current stimulation (tDCS) decreases the cerebral infarct volume of MCAO rat through reducing LAT1‐depencent increase of intraneuronal isoleucine. Together, these results lead us to conclude that LAT1 over activation‐dependent isoleucine‐CBFB‐PTEN signal transduction pathway may mediate ischemic neuronal injury and that tDCS exerts its neuroprotective effect by suppressing LAT1 over activation‐dependent signalling after cerebral ischemia–reperfusion injury. [ABSTRACT FROM AUTHOR]

Doxorubicin (Dox) is an effective chemotherapeutic drug for the treatment of various cancers. Due to its potential fatal cardiotoxic side effects, the clinical application is often limited. Dexrazoxane (Dex) is the only drug approved by the Food and Drug Administration (FDA) for the prevention of Dox-induced cardiotoxicity but has side effects. Thus, more protective strategies should be explored. If NAD+ plays a role in maintaining heart function, its precursor prospectively alleviates Dox-induced cellular injury. Here, we studied the protective effects of nicotinic acid riboside (NAR) on Dox-induced cardiotoxicity in vivo and in vitro. We found that NAR significantly improved the cardiac function of Dox-treated mice by restoring ejection fraction (EF), fractional shortening (FS), and serum level of cardiac troponin (cTnI). NAR not only reduced malondialdehyde (MDA), lactate dehydrogenase (LDH), and reactive oxygen species (ROS) levels in Dox-treated cardiomyocytes but also further promoted the activities of cardiac superoxide dismutase (SOD) and glutathione (GSH). Following exposure to 5 μM Dox, cotreatment with NAR exhibited increased cell viability with a decrease in the apoptosis cell population. Moreover, the levels of apoptosis-related proteins, as well as proteins involved in oxidative stress and autophagy, were altered after NAR treatment. Collectively, these findings underline the protective potential of NAR against Dox-induced cardiomyocyte injury by regulating Nrf-2/P62-related oxidative stress and autophagy, which could potentially promote survival. [ABSTRACT FROM AUTHOR]

Long noncoding RNA (lncRNA) growth arrest‐specific 5 (GAS5) is implicated in several cancers via modulating microRNAs (miRs). However, little information is available about the correlation between GAS5 and miR‐10b. Therefore, we sought out to investigate the biological role of GAS5‐miR‐10b node mainly in glioma cells. We artificially modulated GAS5 to explore its roles in viability assayed by cell counting kit‐8 (CCK‐8), motile activities by 24‐Transwell assay, as well as apoptosis by a flow cytometer and Western blot assay. miR‐10b and Sirtuin 1 (Sirt1) were quantified by qRT‐PCR. After co‐transfection, we analyzed the viability, migration, invasion, apoptosis, and Sirt1 expression. Western blot was implemented to detect the phosphorylated forms of PTEN, PI3K, AKT, MEK, and ERK. GAS5 inhibited proliferation and motile behaviors, and fortified apoptosis. As for the viability and motile activities, the property of GAS5 was reversed in miR‐10b‐replenished U251 and A172 cells, while maintained in miR‐10b‐deficient cells. Additionally, GAS5‐induced apoptosis was abolished by miR‐10b overexpression while fortified by miR‐10b silence. Besides, GAS5 negatively modulated Sirt1 via miR‐10b. Moreover, Sirt1 negatively modulated PTEN and positively mediated the abovementioned regulators. GAS5 represses the process of glioma cells by decreasing miR‐10b, which as accompanied by Sirt1 silence‐induced inactivation of PTEN/PI3K/AKT and MEK/ERK cascades. [ABSTRACT FROM AUTHOR]