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The role of miRNAs in the pathogenesis of PF was also reviewed. In addition, emerging diagnostic and therapeutic properties of exosomes and exosomal miRNAs in PF were described, in order to highlight the potential applications of exosomal miRNAs in PF.Ewing sarcoma is a challenging cancer entity, which, besides the characteristic presence of a fusion gene, is driven by multiple alternative splicing events. So far, splice variants in Ewing sarcoma cells were mainly analyzed for EWSR1‑FLI1. The present study provided a comprehensive alternative splicing study on CADO‑ES1, an Ewing model cell line for an EWSR1‑ERG fusion gene. Based on a well‑-characterized RNA‑sequencing dataset with extensive control mechanisms across all levels of analysis, the differential spliced genes in Ewing cancer stem cells were ATP13A3 and EPB41, while the main population was defined by ACADVL, NOP58 and TSPAN3. All alternatively spliced genes were further characterized by their Gene Ontology (GO) terms and by their membership in known protein complexes. These results confirm and extend previous studies towards a systematic whole‑transcriptome analysis. A highlight is the striking segregation of GO terms associated with five basic splice events. This mechanistic insight, together with a coherent integration of all observations with prior knowledge, indicates that EWSR1‑ERG is truly a close twin to EWSR1‑FLI1, but still exhibits certain individuality. Thus, the present study provided a measure of variability in Ewing sarcoma, whose understanding is essential both for clinical procedures and basic mechanistic insight.Following the publication of the above paper, the authors have realized that they made an error during the assembly of the western blotting data in Fig. 4; essentially, the western blotting data shown for the FAP experiment in Fig. 5 were mistakenly inserted into Fig. 4 to show the metalloproteinase‑9 (MMP‑9) data. The authors re‑examined their original data, and discovered how the error in the compilation of Fig. 4 arose. The corrected version of Fig. 4, incorporating the correct data for the MMP‑9 experiment, is shown below. Note that this error did not affect the overall conclusions reported in the study. The authors are grateful to the Editor of Oncology Reports for allowing them the opportunity to publish this Corrigendum; furthermore, they apologize for any inconvenience caused to the readership of the Journal. [the original article was published in Oncology Reports 43 1125‑1132, 2020; DOI 10.3892/or.2020.7496].Long intergenic nonprotein coding RNA 649 (LINC00649) is a functional regulator in acute myeloid leukaemia. However, the contribution of LINC00649 in colorectal cancer (CRC) has yet to be confirmed. Accordingly, the present investigation was devoted to exploring the detailed functions of LINC00649 and reveal the mechanisms underlying the LINC00649‑induced promotion of CRC progression. LINC00649 expression in CRC was investigated by reverse transcription‑quantitative PCR. Knockdown of LINC00649 was achieved using small interfering RNAs or short hairpin RNA, followed by functional experiments. The binding between LINC00649 and microRNA (miR)‑432‑5p was predicted by a bioinformatics tool, and corroborated by luciferase reporter assay and RNA immunoprecipitation. In the present study, LINC00649 was expressed at a high level in CRC. The aberrant expression of LINC00649 exhibited an inverse association with CRC patient prognosis. Functionally, the downregulation of LINC00649 exerted anticarcinogenic activities in CRC by decreasing cell proliferation, migration, and invasion and inducing cell apoptosis. Furthermore, the growth of CRC cells in vivo was attenuated after LINC00649 deficiency. Mechanistically, LINC00649 functioned as a competitive endogenous RNA by competitively binding to miR‑432‑5p in CRC cells, inducing an increase in hepatoma‑derived growth factor (HDGF). Ultimately, functional rescue experiments highlighted that the exogenous introduction of miR‑432‑5p inhibitor or HDGF overexpression plasmid partially abated the inhibitory effects of LINC00649 silencing. In conclusion, LINC00649 promoted the aggressiveness of CRC cells by adjusting the miR‑432‑5p/HDGF axis. Thus, the LINC00649/miR‑432‑5p/HDGF pathway may be a promising target for CRC therapy.Dihydromyricetin (DMY) is a natural flavonoid that possesses a wide range of pharmacological properties. The aim of the present study was to determine whether DMY could protect against nerve cell injury following ischemic stroke through antioxidant and neuroprotective effects. The effects of DMY on the viability, oxidative stress and apoptosis of HT22 cells following oxygen‑glucose deprivation and re‑oxygenation (OGD/R) were examined using MTT, lactate dehydrogenase (LDH), superoxide (SOD), malondialdehyde (MDA), western blot and TUNEL assays. Furthermore, Wnt/β‑catenin signaling proteins in OGD/R‑stimulated HT22 cells were detected in the presence or absence of DMY. In a separate experiment, the effect of DMY on OGD/R‑induced HT22 cell injury was also observed in the presence of the Wnt/β‑catenin inhibitor, XAV939. The results demonstrated that DMY had no impact on the survival of untreated HT22 cells, although DMY treatment significantly increased cell viability and inhibited cytotoxicity, oxidative stress and apoptosis following OGD/R. In addition, DMY upregulated the expression of Wnt/β‑catenin in OGD/R‑stimulated HT22 cells. In conclusion, DMY protected HT22 cells from OGD/R‑induced oxidative stress and apoptosis, and its effects may be mediated by the activation of the Wnt/β‑catenin signaling pathway.Following the publication of this article, the authors have realized that they mistakenly used the total AKT blot featured in Fig. selleck chemical 4A for the GAPDH blot in Fig. 3B on p. 116. The corrected version of Fig. 3, featured the correct data for the GAPDH experiment, is shown opposite. The authors regret that this error was not picked up upon before the paper was sent to press, and thank the Editor of International Journal of Molecular Medicine for allowing them the opportunity to publish a corrigendum. The error did not affect either the results or the conclusions reported in the study, and all the authors agree to this corrigendum. Furthermore, they regret any inconvenience caused to the readership. [the original article was published in International Journal of Molecular Medicine 34 112‑118, 2014; DOI 10.3892/ijmm.2014.1773].Genetic defects in interleukin-12/23/17 immunity are associated with an increased risk of Staphylococcus aureus and herpesvirus skin infections. This study analysed spontaneous safety reports from the WHO Pharmacovigilance Center of bacterial skin or herpesvirus infections associated with secukinumab, ustekinumab and tumour necrosis factor-α inhibitors. Associations found in disproportionality analyses were expressed as reporting odds ratios (ROR). For bacterial skin infections, ustekinumab showed the strongest association (ROR 6.09; 95% confidence interval (95% CI) 5.44-6.81), and, among the tumour necrosis factor-α inhibitors, infliximab showed the strongest association (ROR 4.18; 95% CI 3.97-4.40). Risk was comparable between infliximab and secukinumab (ROR 3.51; 95% CI 3.00-4.09). Secukinumab showed the strongest association with herpes simplex infection (ROR 4.80; 95% CI 3.78-6.10). All biologics were equally associated with herpes zoster. Infliximab was the only biologic associated with cytomegalovirus infection (ROR 5.66; 95% CI 5.08-6.31) and had the strongest association with Epstein-Barr virus infection (ROR 6.90; 95% CI 6.03-7.90). All biologics evaluated were positively associated with bacterial skin infections, herpes simplex, and herpes zoster, compared with all other drugs in the WHO database for which individual case safety reports were collected. The possibility of under-reporting, reporting bias and difference in causality assessment between countries and reporters must be taken into account when interpreting the results of disproportionality analyses.Hyperhidrosis is a dermatological condition that causes psychosocial impairment and has a negative impact on patients' quality of life. The epidemiology of hyperhidrosis is currently poorly understood. The aim of this study was to analyse comorbidities and treatments in 511 subjects with hyperhidrosis selected from the patient records of Oulu University Hospital. The mean age of patients with local hyperhidrosis was 27.9 years and the majority were female (62.7%). The most common anatomical site of symptoms in the youngest age group was the palms, whereas the axillae were a more common site in advanced age. Depression was a common comorbidity in both local (11.6%) and generalized hyperhidrosis (28.6%). Anxiety affected 12.7% of patients with generalized hyperhidrosis. In 36.8% of the patients with local hyperhidrosis there was a delay in diagnosis of more than 10 years. The most commonly used treatments included topical antiperspirants, iontophoresis and botulin toxin injections.is missing (Short communication).Leukaemia is a malignant neoplasm of the haematopoietic system. Cutaneous manifestations of leukaemia are called leukaemia cutis, and are regarded as a sign of poorer prognosis and shorter survival time. A single-institution retrospective review was performed of medical records of patients diagnosed with leukaemia cutis in the dermatology department of Seoul St Mary's Hospital between January 2012 and April 2021. Fifty-six cases with cutaneous leukaemic involvement and underlying haematological malignancy were included (40 acute myelogenous leukaemia, 8 acute lymphoblastic leukaemia, 3 chronic myeloid leukaemia, 2 chronic lymphocytic leukaemia, and 3 myelodysplastic syndrome). Male-female ratio 1.91, mean age at diagnosis 45.8 years. Plaques (28%) and papules (27%) were the most common skin lesions, followed by patches (18%) and nodules (16%). Mean time from diagnosis of leukaemia to development of leukaemia cutis was 12.3 months. Forty-six patients (84%) died during the 7-year follow-up; mean time from diagnosis of leukaemia cutis to death was 5.4 months. The results suggest that leukaemia cutis is associated with poor outcomes in patients with leukaemia. Comprehensive skin examination of these patients may help diagnose leukaemia cutis early, enabling prompt treatment.Capillary malformation-arteriovenous malformation syndrome is a rare genodermatosis with cutaneous capillary malformations and a risk of associated fast-flow malformations. We describe here a four-generation family with a novel heterozygous pathogenic variant in the EPHB4 gene (NM_004444.5 (EPHB4) c.2224G>C, p.(Ala742Pro)). A review of the literature retrieved 127 patients with capillary malformation-arteriovenous malformation syndrome and confirmed variants in EPHB4. Multiple capillary malformations were present in 114 (89.76%) patients, and 12 (9.44%) patients had a solitary capillary malformation. Arteriovenous malformations/fistulas were present in 23 (18.1%) patients, and were located within the central nervous system in 5 (3.9%) patients. Not all papers included description of epistaxis. Telangiectasias were reported in 28 (22%) patients, and Bier spots were described in 20 (15.7%) patients. The clinical characteristics of capillary malformation-arteriovenous malformation syndrome are diverse and often discrete, which can make it difficult to distinguish capillary malformation-arteriovenous malformation syndrome from hereditary haemorrhagic telangiectasia.