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Subsequently to the publication of the above paper, an interested reader drew to the authors' attention that the 'Control' and 'NC' data panels shown in Fig. 2E on p. 981, showing the results of Transwell invasion assay experiments, appeared to contain overlapping sections of data, such that they were potentially derived from the same original source where these panels were intended to show the results from differently performed experiments. After having asked the authors to provide an explanation of these data, they realized that this figure had been inadvertently assembled incorrectly. A revised version of Fig. 2, containing replacement data for the experiments portrayed in Fig. 2E, is shown on the next page. Note that these errors did not adversely affect either the results or the overall conclusions reported in this study. All the authors agree with the publication of this corrigendum, and are grateful to the Editor of Molecular Medicine Reports for allowing them the opportunity to publish this. They also wish to apologize to the readership of the Journal for any inconvenience caused. [Molecular Medicine Reports 20: 977‑984, 2019; DOI: 10.3892/mmr.2019.10332].

Heart disease (HD) is a general term for various diseases affecting the heart. An increasing body of evidence suggests that the pathogenesis of HD is closely related to mitochondrial dysfunction. Peroxisome proliferator‑activated receptor γ coactivator‑1α (PGC‑1α) is a transcriptional coactivator that plays an important role in mitochondrial function by regulating mitochondrial biogenesis, energy metabolism and oxidative stress. The present review shows that PGC‑1α expression and activity in the heart are controlled by multiple signaling pathways, including adenosine monophosphate‑activated protein kinase, sirtuin 1/3 and nuclear factor κB. These can mediate the activation or inhibition of transcription and post‑translational modifications (such as phosphorylation and acetylation) of PGC‑1α. Furthermore, it highlighted the recent progress of PGC‑1α in HD, including heart failure, coronary heart disease, diabetic cardiomyopathy, drug‑induced cardiotoxicity and arrhythmia. Understanding the mechanisms underlying PGC‑1α in response to pathological stimulation may prove to be beneficial in developing new ideas and strategies for preventing and treating HDs. Meanwhile, the present review explored why the opposite results occurred when PGC‑1α was used as a target therapy.

Adults with attention-deficit/hyperactivity disorder (ADHD) experience impairing levels of inattention and/or hyperactivity-impulsivity, while individuals without ADHD experience these symptoms to a lesser extent. Yet, ADHD self-report scales so far hardly captured continuous distributions across the general population. In addition, they focused on weaknesses and ignored strengths. To address these shortcomings, we present here the Strengths and Weaknesses of ADHD and Normal-Behavior Scale Self-Report (SWAN-DE-SB). The normal distribution of the data collected and the scale's internal consistency, and factorial and convergent validity were assessed using data from a general population sample. Its clinical utility was evaluated by comparing scores from a clinical sample and a sample of individuals without ADHD and by calculating optimal cut-off values for specificity and sensitivity. The SWAN-DE-SB demonstrated normal distribution of the data collected, high internal consistency, and factorial and convergent validity. It reliably discriminated individuals with and without ADHD, with high specificity and sensitivity. It should therefore be considered a psychometrically convincing measure to assess strengths and weaknesses of ADHD symptoms and normal behavior in clinical and general population samples.

Operant conditioning and social learning theories suggest that positive cannabis use-related outcomes are a primary contributor to maintained use and risk for dependence. However, currently there does not exist a reliable, validated measure of positive cannabis-related outcomes. This study sought to develop and psychometrically evaluate the Positive Outcomes of Cannabis Use Scale (POCUS). We collected three samples, college students (N = 883), community adults (N = 214), and college students (N = 615), of predominantly White adults in the United States who completed an online survey. Exploratory and confirmatory factor analyses evaluated scale structure and identified four factors: social enhancement, mood enhancement, cognitive enhancement, and sexual enhancement. Positive outcomes were positively associated with recent use, controlling for expectancies and negative outcomes. Positive outcomes were also differentiated from positive expectancies and more influential in predicting typical use frequency. Findings indicate that the POCUS is psychometrically sound and clinically useful for measuring positive cannabis use-related outcomes among predominantly White adults in the United States.

In β‑thalassemia, excessive α‑globin chain impedes the normal development of red blood cells resulting in anemia. Numerous miRNAs, including miR‑6747‑3p, are aberrantly expressed in β‑thalassemia major (β‑TM), but there are no reports on the mechanism of miR‑6747‑3p in regulating red blood cell lineage development and fetal hemoglobin (HbF) expression. In the present study, RT‑qPCR was utilized to confirm miR‑6747‑3p expression in patients with β‑TM and the healthy controls. Electrotransfection was employed to introduce the miR‑6747‑3p mimic and inhibitor in both HUDEP‑2 and K562 cells, and red blood cell lineage development was evaluated by CCK‑8 assay, flow cytometry, Wright‑Giemsa staining and Benzidine blue staining. B‑cell lymphoma/leukemia 11A (BCL11A) was selected as a candidate target gene of miR‑6747‑3p for further validation through FISH assay, dual luciferase assay and Western blotting. The results indicated that miR‑6747‑3p expression was notably higher in patients with β‑TM compared with healthy controls and was positively related to HbF levels. Functionally, miR‑6747‑3p overexpression resulted in the hindrance of cell proliferation, promotion of cell apoptosis, facilitation of cellular erythroid differentiation and γ‑globin expression in HUDEP‑2 and K562 cells. Mechanistically, miR‑6747‑3p could specifically bind to the 546‑552 loci of BCL11A 3'‑UTR and induce γ‑globin expression. These data indicate that upregulation of miR‑6747‑3p affects red blood cell lineage development and induces HbF expression by targeting BCL11A in β‑thalassemia, highlighting miR‑6747‑3p as a potential molecular target for β‑thalassemia therapy.

Lung adenocarcinoma (LUAD) is highly associated with lung cancer‑associated mortality. Notably, S100 calcium‑binding protein A16 (S100A16) has been increasingly considered to have prognostic value in LUAD; however, the underlying mechanism remains unknown. In the present study, S100A16 expression levels in LUAD tissues and cells were respectively analyzed by the UALCAN database and western blotting. Cell Counting Kit‑8 and 5‑ethynyl‑2'‑deoxyuridine assays were used to examine cell proliferation, whereas wound healing, Transwell and tube formation assays were used to assess cell migration, invasion and angiogenesis, respectively. Western blotting was also used to examine the expression levels of proteins associated with metastasis, angiogenesis, focal adhesion and the extracellular matrix (ECM)‑receptor interaction pathways. The relationship between S100A16 and Mov10 RNA helicase (MOV10) was predicted by bioinformatics tools, and was verified using a co‑immunoprecipitation assay. Furthermore, the interaction between MOV10 and integrin α3 (ITGA3) was verified by RNA immunoprecipitation assay, and the actinomycin D assay was used to detect ITGA3 mRNA stability. The results demonstrated that S100A16 expression was increased in LUAD tissues and cell lines, and was associated with unfavorable outcomes. Knocking down S100A16 expression hindered the proliferation, migration, invasion and angiogenesis of LUAD cells. Furthermore, S100A16 was shown to bind to MOV10 and positively modulate MOV10 expression in LUAD cells, while MOV10 overexpression partially reversed the suppressive role of S100A16 knockdown on the aggressive phenotypes of LUAD cells. Furthermore, it was demonstrated that S100A16 regulated the stability of ITGA3 mRNA via MOV10 to mediate ECM‑receptor interactions. In conclusion, S100A16 may bind to MOV10 to stabilize ITGA3 mRNA and regulate ECM‑receptor interactions, hence contributing to the malignant progression of LUAD.

Significance: Intraoperative molecular imaging (IMI) enables the detection and visualization of cancer tissue using targeted radioactive or fluorescent tracers. While IMI research has rapidly expanded, including the recent Food and Drug Administration approval of a targeted fluorophore, the limits of detection have not been well-defined.

Aim: The ability of widely available handheld intraoperative tools (Neoprobe and SPY-PHI) to measure gamma decay and fluorescence intensity from IMI tracers was assessed while varying characteristics of both the signal source and the intervening tissue or gelatin phantoms.

Approach: Gamma decay signal and fluorescence from tracer-bearing tumors (TBTs) and modifiable tumor-like inclusions (TLIs) were measured through increasing thicknesses of porcine tissue and gelatin in custom 3D-printed molds. TBTs buried beneath porcine tissue were used to simulate IMI-guided tumor resection.

Results: Gamma decay from TBTs and TLIs was detected through significantly thicker tissue and gelatin than fluorescence, with at least 5% of the maximum signal observed through up to 5 and 0.5 cm, respectively, depending on the overlying tissue type or gelatin.

Conclusions: We developed novel systems that can be fine-tuned to simulate variable tumor characteristics and tissue environments. These were used to evaluate the detection of fluorescent and gamma signals from IMI tracers and simulate IMI surgery.

This study aimed to evaluate the psychometric characteristics of the Social Phobia Inventory (SPIN) by employing network analysis, confirmatory factor analysis, and the Polytomous Rasch Model. A cross-sectional data set was collected comprising 1,530 participants, with 959 being women and 571 being men. The Bootstrap Exploratory Graph Analysis unveiled the presence of two dimensions, with Items 17, 15, 5, 14, 6, and 9 exhibiting the highest strength centrality index. Notably, the Network Comparison Test indicated no differences in Network Invariance and global strength between the networks of women and men. Furthermore, the confirmatory factor analysis results demonstrated that the two extracted dimensions displayed an acceptable goodness of fit. In addition, the reliability coefficient values were acceptable, exceeding the threshold of 0.70. The Rasch analysis results suggested an overall fit, but some items exhibited overlap, suggesting their potential removal. Furthermore, it was recommended to develop new items to address gaps between existing items, particularly for measuring the lower levels of Social Anxiety Disorder. In conclusion, these findings provide robust evidence supporting the reliability and validity of the SPIN as a tool for measuring Social Anxiety Disorder in Algeria.

Glioma, a type of brain tumor, is influenced by mechanical forces in its microenvironment that affect cancer progression. However, our understanding of the contribution of compression and its associated mechanisms remains limited. The objective of the present study was to create an environment in which human brain glioma H4 cells experience pressure and thereby investigate the compressive mechanosensors and signaling pathways. Subsequent time‑lapse imaging and wound healing assays confirmed that 12 h of compression significantly increased cell migration, thereby linking compression with enhanced cell motility. Compression upregulated the expression of Piezo1, a mechanosensitive ion channel, and growth differentiation factor 15 (GDF15), a TGF‑β superfamily member. Knockdown experiments targeting PIEZO1 or GDF15 using small interfering RNA resulted in reduced cell motility, with Piezo1 regulating GDF15 expression. Compression also upregulated CTLA4, a critical immune checkpoint protein. The findings of the present study therefore suggest that compression enhances glioma progression by stimulating Piezo1, promoting GDF15 expression and increasing CTLA4 expression. Thus, these findings provide important insights into the influence of mechanical compression on glioma progression and highlight the involvement of the Piezo1‑GDF15 signaling pathway. Understanding tumor responses to mechanical forces in the brain microenvironment may guide the development of targeted therapeutic strategies to mitigate tumor progression and improve patient outcomes.

Colorectal cancer (CRC) ranks fifth in terms of incidence rate and mortality among malignant tumors in China. Oxaliplatin (OXA) is a first‑line drug for the clinical treatment of CRC, but its antitumor effect is limited because of the development of drug resistance. The present study aimed to investigate whether the traditional Chinese medicine Huaier can regulate the Wnt/β‑catenin signaling pathway by affecting the expression of METTL3, thereby promoting the sensitivity of HCT‑8/L cells to OXA. The expression of METTL3 was analyzed based on the UCSC Xena and Gene Expression Omnibus databases. Silent METTL3 and overexpression METTL3 models were constructed, and Cell Counting Kit‑8 and flow cytometry were used to detect the effects of Huaier on the viability and apoptosis of HCT‑8/L cells. Western blotting, reverse transcription‑quantitative PCR, nuclear cytoplasmic separation and immunofluorescence were used to detect the effects of Huaier on the expression of METTL3, Pgp, Wnt/β‑catenin signaling pathway‑related proteins, apoptosis‑related proteins and related mRNA. The results demonstrated that patients with high expression levels of METTL3 had a shorter overall survival period. The expression level of METTL3 significantly increased in drug‑resistant CRC cells. Silencing METTL3 promoted apoptosis of CRC cells and increased their sensitivity to OXA by inhibiting the Wnt/β‑catenin signaling pathway. Huaier downregulated the expression of METTL3, thereby promoting apoptosis of drug‑resistant CRC cells and increasing their sensitivity to OXA by inhibiting the Wnt/β‑catenin signaling pathway.