5-aminolevulinic acid-based photodynamic therapy in combination with antifungal agents for adult kerion and facial ulcer caused by Trichophyton rubrum.

Dermatophytosis is the most common fungal infectious disease in the world, which is commonly caused by Trichophyton rubrum in China. The traditional therapies for treating dermatophytosis include topical and oral antifungal agents like terbinafine, griseofulvin, and azole antifungal drugs. However, 5-aminolevulinic acid-based photodynamic therapy (ALA-PDT) as a new alternative therapy avoids the side effects and drug resistance of traditional antifungal agents. We report two cases diagnosed as kerion and tinea faciei secondary to ulcers with CARD 9 deficiency, both of whom were infected by T.rubrum. They were both successfully treated by ALA-PDT combined with antifungal drugs, providing a feasible strategy for therapeutic choice for adult kerion and ulcer treatment.

Antrodia camphorata-Derived Antrodin C Inhibits Liver Fibrosis by Blocking TGF-Beta and PDGF Signaling Pathways.

Hepatic stellate cells (HSCs) play an essential role in the development of liver fibrosis. Antrodia camphorata (A. camphorata) is a medicinal fungus with hepatoprotective effect. This study investigated whether Antrodin C, an A. camphorata-fermented metabolite, could exert a protective role on liver fibrosis both in vitro and in vivo. The anti-fibrotic effect of Antrodin C was investigated in CFSC-8B cell (hepatic stellate cell) stimulated by transforming growth factor-ß1 (TGF-ß1) or platelet-derived growth factor-BB (PDGF-BB) in vitro and in CCl4 induced liver fibrosis in mice. Antrodin C (50 µM) inhibited TGF-ß1 or PDGF-BB stimulated CFSC-8B cell activation, migration and extracellular matrix (ECM) accumulation (all p < 0.05). Antrodin C (3, 6 mg/kg/d) oral administration reduced the degree of liver fibrosis induced by CCl4 in mice. Antrodin C down-regulated the expression of α-smooth muscle actin (α-SMA) and collagen I in fibrotic livers. Furthermore, Antrodin C ameliorated alanine aminotransferase (ALT) and aspartate aminotransferase (AST) elevation in serum (all p < 0.05). Mechanistically, Antrodin C executes its anti-fibrotic activity through negatively modulate TGF-ß1 downstream SMAD Family Member 2 (Smad2), AKT Serine/Threonine Kinase 1 (AKT), extracellular signal-regulated kinase (ERK), and P38 MAP Kinase (P38), as well as PDGF-BB downstream AKT and ERK signaling pathways. Antrodin C ameliorates the activation, migration, ECM production in HSCs and CCl4-induced liver fibrosis in mice, suggesting that Antrodin C could serve as a protective molecule against liver fibrosis.

Kinematic Characteristics and Biomechanical Changes of Lower Lumbar Facet Joints Under Different Loads.

OBJECTIVE: To explore the kinematic biomechanical changes and symmetry in the left and right sides of the facet joints of lumbar spine segments under different functional loads. METHODS: Participants (n = 10) performing standing flexion and extension movements were scanned using computed tomography (CT) and dual fluoroscopy imagine system. Instantaneous images of the L3 -S1 vertebrae were captured, and by matching a three-dimensional CT model with contours from dual fluoroscopy images, in vivo facet joint movements were reproduced and analyzed. Translations and rotations of lumbar vertebral (L3 and L4 ) facet joints of data were compared for different loads (0, 5, 10 kg). The participants performed flexion and extension movements in different weight-bearing states, the translations and angles changes were calculated respectively. RESULTS: From standing to extension, there were no statistical differences in rotation angles for the facet joint processes of different vertebral segment levels under different weight loads (P > 0.05). Mediolateral axis and cranio-caudal translations under different weight loads were not statistically different for vertebral segment levels (P > 0.05). Anteroposterior translations for L3 (1.4 ± 0.1 mm) were greater than those for L4 (1.0 ± 0.1 mm) under the different load conditions (P = 0.04). Bilaterally, mediolateral, anteroposterior, and cranio-caudal translations of the facet joints under different weights (0, 10 kg) for each segment level (L3 and L4 ) were symmetric (P > 0.05). From flexion to standing, there were no statistical differences in rotation angles for different weights (0, 5, 10 kg) for each level (L3 and L4 ) (P > 0.05). There were no statistical differences between mediolateral, anteroposterior, and cranio-caudal translations at each segment level (L3 and L4 ) under different loads (P > 0.05). Under the condition of no weight (0 kg), L3 mediolateral translations on the left side (1.7 ± 1.6 mm) were significantly greater (P = 0.03) than those on the right side (1.6 ± 1.6 mm). Left side (1.0 ± 0.7 mm) L4 mediolateral translations were significantly smaller (P = 0.03) than those on the right side (1.1 ± 0.7 mm). There were no statistical differences between different weights for either anteroposterior and cranio-caudal translations (P > 0.05). There were no statistical differences for mediolateral, anteroposterior, and cranio-caudal translations for 10 kg (P > 0.05). CONCLUSION: Lumbar spine facet joint kinematics did not change significantly with increased loads. Anteroposterior translations for L3 were greater than those for L4 of the vertebral segments are related to the coronal facet joint surface. Changes in facet surface symmetry indicates that the biomechanical pattern between facet joints may change.

[Corrigendum] Ouabain suppresses the growth and migration abilities of glioma U­87MG cells through inhibiting the Akt/mTOR signaling pathway and downregulating the expression of HIF­1α.

Subsequently to the publication of the above paper, an interested reader drew to the authors' attention that several pairings of panels in Fig. 5, as shown on p. 5599, were strikingly similar. After having examined their original data, the authors realized that they uploaded some images incorrectly during the process of compiling this figure, and that there were duplicated data panels in this figure. However, the authors were able to consult their original data, and had access to the correct images. The revised version of Fig. 5, showing the correct data for the Akt/Control, p­Akt/Control, mTOR/0.05 µM Ouabain, HIF­1α/0.05 µM Ouabain and Akt/0.5 µM Ouabain experiments, is shown opposite. Note that the replacement of the erroneous data does not affect either the results or the conclusions reported in this paper, and all the authors agree to this Corrigendum. The authors are grateful to the Editor of Molecular Medicine Reports for granting them this opportunity to publish a Corrigendum, and apologize to the readership for any inconvenience caused. [the original article was published in Molecular Medicine Reports 17: 5595­5600, 2018; DOI: 10.3892/mmr.2018.8587].

Ouabain suppresses the growth and migration abilities of glioma U­87MG cells through inhibiting the Akt/mTOR signaling pathway and downregulating the expression of HIF­1α.

Glioma is one of the most malignant forms of brain tumor, and has been of persistent concern due to its high recurrence and mortality rates, and limited therapeutic options. As a cardiac glycoside, ouabain has widespread applications in congestive heart diseases due to its positive cardiac inotropic effect by inhibiting Na+/K+­ATPase. Previous studies have demonstrated that ouabain has antitumor activity in several types of human tumor, including glioma. However, the exact underlying mechanism remains to be elucidated. The purpose of present study was to elucidate the effect of ouabain on human glioma cell apoptosis and investigate the exact mechanism. U­87MG cells were treated with various concentrations of ouabain for 24 h, following which cell viability and survival rate were assessed using a 3­(4,5-dimethylthiazol-2­yl)­2,5­diphenyltetrazolium bromide assay. The dynamic changes and cell motility were observed using digital holographic microscopy. Additionally, western blot analysis and high­content screening assays were used to detect the protein expression levels of phosphorylated (p­)Akt, mammalian target of rapamycin (mTOR), p­mTOR and hypoxia­inducible factor (HIF)­1α, respectively. Compared with the control group, ouabain suppressed U­87MG cell survival, and attenuated cell motility in a dose­dependent manner (P<0.01). The downregulation of p­Akt, mTOR, p­mTOR and HIF­1α were observed following treatment with 2.5 and 25 µmol/l of ouabain. These results suggested that ouabain exerted suppressive effects on tumor cell growth and motility, leading to cell death via regulating the intracellular Akt/mTOR signaling pathway and inhibiting the expression of HIF­1α in glioma cells. The present study examined the mechanism underlying the antitumor property of ouabain, providing a novel potential therapeutic agent for glioma treatment.

Receptor interacting protein 1 involved in ultraviolet B induced NIH3T3 cell apoptosis through expression of matrix metalloproteinases and reactive oxygen species production.

BACKGROUND: Receptor interacting protein 1 (RIP1), which plays a key role in apoptosis, cell survival and programmed cell necrosis, is one of the most important proteins in the RIP family. The purpose of this study was to investigate the roles of RIP1 in the apoptosis, the generation of reactive oxygen species (ROS) and the expression of matrix metalloproteinases (MMPs) induced by ultraviolet B (UVB) in fibroblasts. METHODS: siRNA targeting RIP1 was used to silence RIP1 expression in the NIH3T3 fibroblasts. The mRNA and protein levels of MMP-1 and MMP-3, caspase-3 and -8 activities, and ROS activities were determined by reverse transcriptase-quantitative polymerase chain reaction (RT-qPCR), immunoblotting, caspase activity assay, immunofluorescence, and flow cytometry. RESULTS: The mRNA and protein expressions of MMP-1 and MMP-3 were significantly increased in RIP1 deficient NIH3T3 cells at 24 hours after UVB treatment. At 24 hours after exposure to UVB, RIP1 deficient NIH3T3 cells presented apoptotic morphology, and the apoptosis rate was significantly increased accompanied by pronounced increase in caspase-8 and -3 activities. ROS production was inhibited by UVB at 12 hours in RIP1 deficient NIH3T3 cells. CONCLUSION: RIP1 is involved in NIH3T3 cell damage induced by UVB via participating in the apoptosis, expression of MMPs and ROS production.

[Progress of research on the expression and function of vimentin].

As a kind of cytoskeleton protein, vimentin is a major member of intermediate filament family. Vimentin is found mainly in mesenchymal cells, and its expression and phosphorylation are regulated by many factors. In the past, vimentin was revealed as a scaffold maintaining cellular integrity, and recent studies shed lights on the evidence that vimentin played many important roles in cellular adhesion, growth, apoptosis, cell signaling as well as inflammatory response. This article summarizes the recent progress of vimentin about its expression and function.

[Effect of neuronal differentiation induced by nerve growth factor on the tolerance-dosage of ultraviolet radiation of PC12 cells].

OBJECTIVE: To evaluate the effect of neuronal differentiation induced by nerve growth factor (NGF) on the tolerance-dosage of ultraviolet radiation of PC12 Cells. METHODS: Neuron-differentiated PC12 cells and untreated PC12 cells were exposed to different ultraviolet radiation dosage of 10, 30, 60, 80, 100, and 200 mJ/cm2. Cell survival rates were determined by MTT assay. RESULTS: Neuron-differentiated PC12 cells had increased tolerance dose to ultraviolet radiation with noticeable apoptosis at the radiation dose of 100 mJ/cm2 in contrast to 30 mJ/cm2 for normal PC12 cells. CONCLUSION: Neuronal differentiation exerts the effect of increasing the tolerance dose of PC12 cells to ultraviolet radiation.

[Synergistic effects of acitretin and narrow-band ultraviolet-B in inducing retinoic acid receptor gamma mRNA expression in normal human keratinocytes].

OBJECTIVE: To investigate the changes in cell proliferation and retinoic acid receptor gamma (RARgamma) mRNA expression in normal human keratinocytes after acitretin treatment and/or narrow-band ultraviolet-B irradiation. METHODS: Normal human keratinocytes were exposed to irradiation with 100 mJ/cm square NB-UVB and/or subsequent 12-hour incubation with 1x10(-6) mol/L acitretin, and the expression of RARgamma mRNA in the cells was examined using RT-PCR and real-time quantitative RT-PCR. RESULTS: A 0.9- and a 2.3-fold increase in RARgamma mRNA expression was induced in the cells by exposure to 100 mJ/cm square NB-UVB and 10(-6) mol/L acitretin, respectively, and the expression was synergistically enhanced by 2.8-fold after their combined treatment. CONCLUSION: Upregulated expression of RARgamma mRNA can be associated with keratinocyte growth inhibition after treatment with acitretin and NB-UVB irradiation.