Search

IL-33 attenuates cardiac remodeling following myocardial infarction via inhibition of the p38 MAPK and NF- B pathways The Editor deeply regrets the grievance that this matter has caused to the authors of the previously published article, and also any inconvenience caused to the readership of the Journal. Mol Med Rep 9: 1834-1838, 2014; DOI: 10.3892/mmr.2014.2051 An interested reader of an article published in the journal I Circulation Research i [Krishnamurthy P, Rajasingh J, Lambers E, Qin G, Losordo DW and Kishore R: L-10 inhibits inflammation and attenuates left ventricular remodeling after myocardial infarction via activation of STAT3 and suppression of HuR. [Extracted from the article]

3 and 4, which showed apoptotic induction as evaluated by fluorescence microscopy and TEM evaluation of ferruginol-induced apoptosis in OVCAR-3 human ovary cancer cells, respectively. Mol Med Rep 16: 7013-7017, 2017; DOI: 10.3892/mmr.2017.7484 Following the publication of the above paper, an interested reader drew to our attention that a number of apparent anomalies existed with the data presented in a couple of the figures in the above paper. [Extracted from the article]

The authors confirm that there are no further errors in the study, and all the authors agree to this correction. Mol Med Rep 22: 3316-3326, 2020, DOI: 10.3892/mmr.2020.11392 Following the publication of this paper, the authors have realized that they overlooked indicating that Ting Liu and Jingjing Meng contributed equally to this work. [Extracted from the article]

Therefore, the revised version of the Funding section paragraph should read as follows: Funding The present study was supported by a grant from Poznan University of Medical Sciences (grant no. 502-14-02227367-10694). The authors confirm that there are no further errors in the study, and all the authors agree to this correction. Mol Med Rep 20: 4403-4414, 2019, DOI: 10.3892/mmr.2019.10709 Following the publication of this paper, the authors have requested that, on p. 4412 of the above article in the Funding section of the Declarations, the acknowledgement to one of the funding sources should be removed from the paper; essentially, the reference to grant no. 2018/31/B/NZ5/02475, formulated by the Polish National Science Centre (grant providing institution), should be removed from the paper. [Extracted from the article]

Mol Med Rep 12: 4843-4850, 2015; DOI: 10.3892/mmr.2015.4074 Following the publication of the above paper, a concerned reader drew to the Editor's attention that several figures (Figs. 8 in another paper published in I Molecular Medicine Reports i , which has now been retracted [Zhu Y-Y, Huang H-Y and Wu Y-L: Anticancer and apoptotic activities of oleanolic acid are mediated through cell cycle arrest and disruption of mitochondrial membrane potential in HepG2 human hepatocellular carcinoma cells. [Extracted from the article]

Mol Med Rep 13: 4541-4548, 2016; DOI: 10.3892/mmr.2016.5105 Following the publication of the above paper, a concerned reader drew to the Editor's attention that several figures (Figs. 6 in another paper published in I Molecular Medicine Reports i , which has now been retracted [Zhu Y-Y, Huang H-Y and Wu Y-L: Anticancer and apoptotic activities of oleanolic acid are mediated through cell cycle arrest and disruption of mitochondrial membrane potential in HepG2 human hepatocellular carcinoma cells. [Extracted from the article]

Note that all that authors agree with the retraction of this paper, and the Editor and the authors apologize to the readership of the Journal for any inconvenience caused. Mol Med Rep 19: 5275-5280, 2019; DOI: 10.3892/mmr.2019.10191 Following the publication of the above paper, the authors drew to the Editor's attention that they had identified some errors in Fig. [Extracted from the article]

Mol Med Rep 22: 4351-4359, 2020; DOI: 10.3892/mmr.2020.11501 Following the publication of this paper, an interested reader drew to the attention of the Editorial Office that there were potentially concerns regarding the manner in which the botulinum toxin animal studies had been performed, and also in terms of the novelty of the study, wherein the authors had claimed that their study was the first to have explored the use of botulinum toxin for endometriosis-related pain. Furthermore, the authors have subsequently re-reviewed the field of botulinum toxin usage in endometriosis, and concede that their study has made only an incremental advance in knowledge in this area. Therefore, on the grounds that this study may have contained procedural errors in the animal experiments which the authors were unable to verify on account of having lost contact with the person who performed them, and in view of the misinformation regarding the novelty of the study, the authors have requested that the paper be retracted from the publication. [Extracted from the article]

Following the publication of the above article, a number of errors were identified in the paper, and after having consulted with the editor of I Molecular Medicine Reports i , a corrigendum was published last year ("[Corrigendum] Differential miRNAomics of the synovial membrane in knee osteoarthritis induced by bilateral anterior cruciate ligament transection in rats." However, following publication of the above corrigendum, the paper was re-examined by the authors, and additional errors were identified; therefore, the authors are going to retract this paper from the publication. [Extracted from the article]

Mol Med Rep 21: 883-893, 2020, DOI: 10.3892/mmr.2019.10849 Following the publication of this paper, the authors have realized that the final article did not indicate in the Authors' Contribution section that Fangce Wang and Zheng Li made equal contributions to this work (FW and ZL performed most of the statistical analyses and drafted the initial version of the manuscript). The authors and the Editor apologize for any inconvenience caused. [Extracted from the article]

Mol Med Rep 12: 2919-2925, 2015; DOI: 10.3892/mmr.2015.3757 Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that the western blotting data featured in Figs. 4B and 6B (wherein there was also a duplicated set of data bands) were strikingly similar to data appearing in different form in other articles at different research institutes. [Extracted from the article]

Therefore, the affiliations for this paper should have been written as follows: ZHIKUN CHEN SP 1* sp , QIN CHE SP 2* sp and CHUNXUE XIE SP 3 sp Departments of SP 1 sp Emergency, SP 2 sp Infectious Diseases and SP 3 sp General Practice, Jingmen No. 1 People's Hospital, Jingmen, Hubei 448000, P.R. China B *Contributed equally b The authors confirm that there are no further errors in the study, and all the authors agree to this correction. Mol Med Rep 23: Article no. 111, 2021; DOI: 10.3892/mmr.2020.11750 Following the publication of this paper, the authors have realized that they overlooked indicating that Zhikun Chen and Qin Che contributed equally to this work. [Extracted from the article]

3, 6 and 8) contained data that bore striking similarities to data published in other papers, some of which had been published around the same time and written by different authors based at different research institutions. Mol Med Rep 12: 5012-5018, 2015; DOI: 10.3892/mmr.2015.4033 Following the publication of the above paper, a concerned reader drew to the Editor's attention that several figures (principally, Figs. [Extracted from the article]

Mol Med Rep 16: 6506-6511, 2017; DOI: 10.3892/mmr.2017.7440 Following the publication of this paper, the authors have contacted the Editorial Office to request that their article be retracted. Following further discussion, all authors and the Editor of I Molecular Medicine Reports i are in agreement that the paper should be retracted; moreover, the authors apologize to the readership for any inconvenience caused. [Extracted from the article]

Butein induces cell apoptosis and inhibition of cyclooxygenase-2 expression in A549 lung cancer cells. [Extracted from the article]

Multiple endocrine neoplasia type 1 (MEN1) is a rare genetic disorder that is inherited in an autosomal dominant manner. The characteristics of the disease are the combined occurrence of tumors in glands of the endocrine system, such as the parathyroid glands, pituitary gland and endocrine pancreas. Germline mutations in the MEN1 gene are associated with the occurrence of MEN1 and genetic testing for this gene is generally used as a basis for diagnosis. In this paper, a case of MEN1 in a middle‑aged Japanese woman is reported. Direct sequencing analysis of the patient's DNA was performed and it revealed a MEN1 gene heterozygous germline (NM_130799.2:c.930delG) mutation in exon 5. This deletion/frameshift mutation produced a stop codon in the downstream sequence (NP_570711.1:p.Glu273LysfsTer7). To the best of our knowledge, this is the first report describing the NM_130799.2:c.930delG mutation as the basis for MEN1. [ABSTRACT FROM AUTHOR]

A number of epidermal proteins are closely related to skin barrier function, the abnormalities of which can lead to specific skin diseases. These proteins must be quantified to further investigate the changes in the skin barrier between healthy and disease states. However, the non-invasive and proteome-wide quantification of skin proteins without any labelling steps remains a challenge. In this study, 3M medical adhesive tapes were used to obtain skin samples from volunteers. Proteins were extracted from fresh skin samples and digested with trypsin. Each tryptic peptide was analysed in three replicates using liquid chromatography with tandem mass spectrometry analysis and label-free quantification. The data were searched against the Human Universal Protein Resource (UniProt) to match with known proteins. Using this method, 1,157 skin proteins recorded in the UniProt were quantified. A total of 50 identical proteins were identified in the three replicate analyses of all samples with no significant differences in abundance. The results provided an objective metric for further study of skin ageing and various skin diseases. Specifically, the non-invasive proteome-wide method used in this study can be applied to future studies of skin diseases related to barrier destruction by monitoring the changes in the levels of epidermal proteins. [ABSTRACT FROM AUTHOR]

Mol Med Rep 21: 876-882, 2020; DOI: 10.3892/mmr.2019.10862 Following the publication of the above article on modeling variants of adenosine deaminase 2 (ADA2), previously identified by Gibson I et al i [Kristen M. Gibson, Kimberly A. Morishita, Paul Dancey, Paul Moorehead, Britt Drögemöller, Xiaohua Han, Jinko Graham, Robert E. W. Hancock, Dirk Foell, Susanne Benseler, Rashid Luqmani, Rae S. M.Yeung, Susan Shenoi, Marek Bohm, Alan M. Rosenberg, Colin J. Ross, David A. Cabral and Kelly L. Brown: Identification of novel adenosine deaminase 2 gene variants and varied clinical phenotype in pediatric vasculitis. The authors would like to add that the p.Arg34Trp variant's association with DADA2 has been previously identified in a paper by Kaljas I et al i : Human adenosine deaminases ADA1 and ADA2 bind to different subsets of immune cells. [Extracted from the article]

5 contained apparent anomalies, including unexpectedly similar-looking cells and repeated patternings of the cells in terms of their layout/arrangement within the data panels. Mol Med Rep 11: 931-939, 2015; DOI: 10.3892/mmr.2014.2819 Following the publication of the above paper, a concerned reader drew to the Editor's attention that Fig. [Extracted from the article]

Long non-coding RNAs (lncRNAs) comprise a sizeable class of non-coding RNAs with a length of over 200 base pairs. Little is known about their biological function, although over 20,000 lncRNAs have been annotated in the human genome. Through a diverse range of mechanisms, their primary function is in the regulation of the transcription of protein-coding genes. lncRNA transcriptional activation can result from a group of nucleus-retained and chromatin-associated lncRNAs, which function as scaffolds in the cis/trans recruitment of transcription factors, co-activators or chromatin remodelers, and/or promoter enhancers. Exosomes are released as extracellular vesicles and they are produced by endocytic pathways. Their synthesis is initiated by various processes including ceramide synthesis, release of intracellular Ca2+ or acid-base balance disorders. Prior to vesicle creation, selective cargo loading occurs in the Endosomal Sorting Complex Required for Transport. Participation of endosomal sorting proteins such as tetraspanins or specific sumoylated proteins required for transport has been indicated in research. The endosomal-sorting complex consists of four components, these induce the formation of multivesicular bodies and the induction of membrane deformation to form exosomes. Nanovesicles could be formed inside multivesicular bodies to allow transport outside the cell or digestion in lysosomes. The molecular content of exosomes is more heterogenic than its synthesis process, with different cargoes being examined inside vesicles with regard to the type or stage of cancers. This paper will review the importance of lncRNAs as crucial molecular content of exosomes, indicating its involvement in tumour suppression, pro-tumorigenic events and the development of novel therapeutic approaches in the near future. Further studies of their mechanisms of function are essential, as well as overcoming several challenges to gain a clearer insight to the approaches for the best clinical application. [ABSTRACT FROM AUTHOR]

The role of mitochondrial (mt)DNA variations in hearing loss have been studied extensively; in particular, the well-known pathogenic A1555G mutation in the human mitochondrial 12S ribosomal RNA gene is associated with aminoglycoside-induced and non-syndromic hearing loss. The present paper described a Chinese pedigree with hearing impairments. We first performed polymerase chain reaction and direct sequence analysis for the mtDNA genes. Additionally, the GJB2 gene mutations were also genotyped. Notably, this family had a very high penetrance of deafness (66.7 and 33.3%; including and excluding aminoglycoside use, respectively). Sequence analysis of the mtDNA genes from the matrilineal relatives identified the occurrence of A1555G mutation, as well as the tRNAAsp A7551G mutation. The A7551G mutation occurred at position 37 in the anticodon stem of tRNAAsp, which is extremely conserved among various species. The nucleotide at this position is often chemically modified and thus contributes to the maintenance of functional tRNAAsp, therefore, this mutation may cause an imbalance in the level of tRNAAsp and lead to mitochondrial dysfunction which is involved in the pathogenesis of hearing loss. Taken together, the findings of the present study demonstrated that the A7551G mutation may have contributed to the deafness phenotype caused by the A1555G mutation. [ABSTRACT FROM AUTHOR]

Mol Med Rep 23: 212, 2021; DOI: 10.3892/mmr.2021.11851 Following the publication of this article and after having solicited the opinions of all the participating authors, the Editorial Office was contacted by the authors to explain that the following changes are required to the list of contributing authors on the paper. The corresponding author of the article should be changed to the first author (Gang Chen), and a request was made that the name of the final author in the author list (Xiaotang Yang), who was also the original corresponding author, be removed. [Extracted from the article]

Mol Med Rep 12: 4291-4297, 2015; DOI: 10.3892/mmr.2015.3964 Subsequently to the publication of the above paper, an interested reader has drawn to the authors' attention that, in Fig. Immunostaining for (A-D) OPN and (E-H) CD44 in tissue samples from rat kidneys. [Extracted from the article]

Mol Med Rep 22: 4611-4618, 2020; DOI: 10.3892/mmr.2020.11564 Subsequently to the publication of the above article, the authors have realized that the bar charts shown for Fig. 3A and B, as they appeared in the paper, were the same as the bar charts shown for Fig. MRNA expression of Col-I, Col-III, HOXA11, TGF- 1, MMP-2, MMP-9 and TIMP1 in (A) HOXA11-siRNA group and (B) TGF- 1-siRNA group. [Extracted from the article]

Aquaporins are ubiquitous proteins that belong to the major intrinsic protein family. Previous studies have indicated that aquaporins are involved in multiple physiological processes in parasites, such as nutrient absorption and end product efflux, and thus, would be promising pharmacological agents in the fight against parasite infection. In the present paper, the authors analyzed the evolutionary relationship of parasitic aquaporins by re‑constructing of a phylogenic tree using neighbor‑joining and maximum likelihood methods. In addition, the authors discussed the variation of the conserved functional sites impacting on the transportation of water molecules. The protein was concluded to be a potential drug target in parasites. [ABSTRACT FROM AUTHOR]

The authors are grateful to the editor of I Molecular Medicine Reports i for allowing them to publish this Corrigendum, and all the named authors agree to its contents. Mol Med Rep 23: 130, 2021; DOI: 10.3892/mmr.2020.11769 The authors have realized that, on p. 9 in the right-hand column, the second sentence featured in the final summary paragraph of the Discussion should have been deleted from the proofs prior to the publication of this article (the sentence that read as: 'This result indicated that downregulated BNIP3 expression may decrease the radioresistance of NPC cells.'). Therefore, this sentence has been eliminated from the paper. [Extracted from the article]

The PCR amplification products were analyzed using agarose gel electrophoresis and dissociation curves. The presence of a single band with anticipate size indicated the PCR product was specific (B) Dissociation curves for the PCR products. Mol Med Rep 12: 7721-7727, 2015; DOI: 10.3892/mmr.2015.4396 Following the publication of the above article, the authors contacted the Editorial Office to explain that Fig. [Extracted from the article]

Osteoporosis is a systemic bone disease characterized by decreased bone mass and quality and bone micro-architecture degradation. Its primary cause is disorder of bone metabolism: Over-formation of osteoclasts, resulting in increased bone resorption and insufficient osteogenesis. Traditional herbal flavonoids can be used as alternative drugs to prevent and treat osteoporosis due to their wide range of sources, structural diversity and less adverse effects. The present paper reviewed six flavonoids, including quercetin, icariin, hesperitin, naringin, chrysin and pueraria, that promote bone formation and have been widely studied in the literature over the past five years, with the aim of providing novel ideas for the development of drugs for bone-associated disease. [ABSTRACT FROM AUTHOR]

Brucellosis is an infectious disease affecting humans and animals worldwide. Effective methods of control include inducing immunity in animals by vaccination and elimination. Brucella abortus S19 is one of the popular vaccines for control of cattle brucellosis, as it has low virulence. In this paper, allelic exchange plasmids of wzm and wzt genes were constructed and partially knocked out to evaluate the effects on the induction of immunity to Brucella abortus S19 mutants. Cytokine secretion in vitro, INF-γ induction in vivo and antibody dynamics were evaluated. These data suggested that the immunity-eliciting ability of the wzm and wzt gene deletion mutants was similar, although reduced compared with the S19 strain. The results demonstrated that the wzt gene may be more important in the regulation of the induction of immunity than the wzm gene. [ABSTRACT FROM AUTHOR]

Several studies have investigated the correlation between the peroxisome proliferator-activated receptor γ2 (PPAR-γ2) Pro12Ala (rs1801282) polymorphism and the risk of breast cancer, with inconsistent results. For this reason, a meta-analysis was conducted to identify the potential correlation after pooling data from eligible case-control studies. Search strategies were conducted in PubMed, EMBASE and the COCHRANE Library in English and from VIP, CNKI and Sinomed in Chinese (all the papers were published before November 11, 2012) using appropriate terms. A total of 2,279 cases and 2,360 controls from four related case-control studies were included in this meta-analysis. According to the three eligible populations, the odds ratios (ORs) and 95% confidence intervals (CIs) on the risk of breast cancer for the CG versus CC and GG versus CC genotypes and the G versus C allele were 0.84 and 0.72-0.98, 0.92 and 0.32-2.61, and 0.98 and 0.84-1.13, respectively. The OR and 95% CI for CG+GG versus CC from the four study populations were 0.85 and 0.73-0.98, respectively. This meta-analysis supported the fact that the G allele of PPAR-γ2 Pro12Ala (rs1801282) modestly affects the risk of breast cancer. Nevertheless, further studies are required to enrich the evidence of this correlation. [ABSTRACT FROM AUTHOR]

After the publication of the above article, the authors have found that they are not able to reproduce certain of the results presented in their research. The authors have expressed their concern about the choice of cell line selected for their original experiments, which may account for why their results are no longer reproducible. Both authors on the paper agree to the retraction, and regret the inconvenience that this retraction will cause to the Editor and to the readership of the Journal. [Extracted from the article]

Despite the various different candidate genetic polymorphisms of potential clinical relevance, there is not enough understanding of the inter-individual variability in analgesic administration. The cytochrome P450 2D6 (CYP2D6) genotype is thought to be one of the most studied. The aim of the present evidence-based review was to determine if there is now sufficient evidence to make clinical recommendations based on a specific genomic profile. The data sources utilized were as follows: PubMed (NLM) database, Evidence Based Medicine Guidelines and Google. Research on clinical guidance standards, systematic reviews, meta-analyses and clinical trials, published prior to January 2018, were evaluated in English, using the MeSH terms 'cancer pain', 'polymorphism', 'genetic' and 'gene polymorphism'. To assess the level of evidence, the Strength of Recommendation Taxonomy of the American Family Physician was applied. From the initial search, 12 systematic reviews and/or meta-analyses, 5 clinical trials and 10 guidelines were selected. The results indicated that genetic variation of µ-opioid receptor 1 (OPRM1) may contribute to inter-individual differences in morphine consumption with recommendation grade A for OPRM A118G single nucleotide polymorphism (rs1799971). Polymorphisms associated with the metabolization process of morphine and other opioid drugs are very relevant in opioid titration and ethnic subgroup differences which have to be taken into account (particularly, for the recommendation grade A for the CYP2D6 polymorphism). In human studies, the catechol-O-methyl transferase (COMT) genotype affects the efficacy of opioids in acute and chronic pain under different settings, with recommendation grade B to the COMT single nucleotide polymorphism rs4680 (Val/Met). Finally, polymorphisms of the ATP-binding cassette family of efflux transporters were highlighted. Consistent data on pain polymorphisms is now widely available; however, these results have had very little impact on clinical guidelines and daily oncologist practice. Persisting pain, side effects of grade 3 (NCI-CTCAE v4.0) and breakthrough pain with more than 4 episodes/day should be considered the criteria for pain multidisciplinary team discussions and for polymorphism screening. [ABSTRACT FROM AUTHOR]