bluuebunny/crossref_metadata_2025_split huggingface dataset:
Contrasting patterns of neutral and functional genetic diversity in stable and disturbed environments
Authors: Yıldırım Yeşerin , Tinnert Jon , Forsman Anders 
Published: November 2018

AbstractGenetic structure among and diversity within natural populations is influenced by a combination of ecological and evolutionary processes. These processes can differently influence neutral and functional genetic diversity and also vary according to environmental settings. To investigate the roles of interacting processes as drivers of population‐level genetic diversity in the wild, we compared neutral and functional structure and diversity between 20 Tetrix undulata pygmy grasshopper populations in disturbed and stable habitats. Genetic differentiation was evident among the different populations, but there was no genetic separation between stable and disturbed environments. The incidence of long‐winged phenotypes was higher in disturbed habitats, indicating that these populations were recently established by flight‐capable colonizers. Color morph diversity and dispersion of outlier genetic diversity, estimated using AFLP markers, were higher in disturbed than in stable environments, likely reflecting that color polymorphism and variation in other functionally important traits increase establishment success. Neutral genetic diversity estimated using AFLP markers was lower in disturbed habitats, indicating stronger eroding effects on neutral diversity of genetic drift associated with founding events in disturbed compared to stable habitats. Functional diversity and neutral diversity were negatively correlated across populations, highlighting the utility of outlier loci in genetics studies and reinforcing that estimates of genetic diversity based on neutral markers do not infer evolutionary potential and the ability of populations and species to cope with environmental change.
A likelihood for correlated extreme series
Authors: Zhu L. , Liu X. , Lund R. 
Published: November 2018

AbstractThis paper develops a likelihood for sequences of extremes when observations are dependent in time. The likelihood allows researchers to obtain more realistic standard errors of the generalized extreme‐value parameters. As a motivating example, annual minimum temperatures are examined from the Faraday/Vernadsky research station in Antarctica. Here, the year‐to‐year correlation in the series is about 0.46. Our likelihood allows the series to have temporal correlation but also keeps a generalized extreme‐value marginal distribution at each point in time. An analysis of the Faraday/Vernadsky annual minimum temperatures is conducted. While the standard error of the estimated trend increases when dependence is taken into account, it does not change the correlation‐ignored inference that annual minimum temperatures at the station are increasing.
Examining How College Promise Programs Promote Student Academic and Financial Readiness
Authors: Millett Catherine M. , Saunders Stephanie R. , Fishtein Daniel 
Published: November 2018

AbstractCurrently college promise programs are proliferating in number at the local and state levels. Most promise programs provide financial resources beyond conventional state and federal student aid to students who live in designated places and meet local‐ or state‐defined eligibility criteria. There is an immense variety of models and funding designs for these programs. In this study, we conducted a rigorous content analysis of the public web sites for a diverse subsample of 35 promise programs to explore how college promise programs promote student academic and financial readiness. Although our analysis made it clear that there is more to learn about promise programs, including understanding general administrative processes and program operations, we highlight several design and implementation considerations that may increase the capacity of these programs to promote equity in higher education access and success.
ON EXACTITUDE IN SCIENCE: A MAP OF THE EMPIRE THE SIZE OF THE EMPIRE
Authors: Van Ijzendoorn Marinus H. , Steele Miriam , Granqvist Pehr 
Published: November 2018

ABSTRACTIn the service of children's best interests, we argue for a sharpening of the evidentiary standards used in family court decision making, from preponderance of (occasionally substandard) evidence to “beyond a reasonable doubt.” Second, we call for a move in child protection cases from static diagnoses (e.g., attachment classifications) to assessments of the potential for enhanced parenting. Finally, informed by the implications of the replication crisis in the biomedical and psychological sciences, we applaud the move of the attachment field forward to large‐scale, collective research agendas and goals.
Characterization of mitochondrial proteomes of nonbilaterian animals
Authors: Muthye Viraj , Lavrov Dennis V. 
Published: November 2018

SummaryMitochondria require ~1,500 proteins for their maintenance and proper functionality, which constitute the mitochondrial proteome (mt‐proteome). Although a few of these proteins, mostly subunits of the electron transport chain complexes, are encoded in mitochondrial DNA (mtDNA), the vast majority are encoded in the nuclear genome and imported to the organelle. Previous studies have shown a continuous and complex evolution of mt‐proteome among eukaryotes. However, there was less attention paid to mt‐proteome evolution within Metazoa, presumably because animal mtDNA and, by extension, animal mitochondria are often considered to be uniform. In this analysis, two bioinformatic approaches (Orthologue‐detection and Mitochondrial Targeting Sequence prediction) were used to identify mt‐proteins in 23 species from four nonbilaterian phyla: Cnidaria, Ctenophora, Placozoa, and Porifera, as well as two choanoflagellates, the closest animal relatives. Our results revealed a large variation in mt‐proteome in nonbilaterian animals in size and composition. Myxozoans, highly reduced cnidarian parasites, possessed the smallest inferred mitochondrial proteomes, while calcareous sponges possessed the largest. About 513 mitochondrial orthologous groups were present in all nonbilaterian phyla and human. Interestingly, 42 human mitochondrial proteins were not identified in any nonbilaterian species studied and represent putative innovations along the bilaterian branch. Several of these proteins were involved in apoptosis and innate immunity, two processes known to evolve within Metazoa. Conversely, several proteins identified as mitochondrial in nonbilaterian phyla and animal outgroups were absent in human, representing cases of possible loss. Finally, a few human cytosolic proteins, such as histones and cytosolic ribosomal proteins, were predicted to be targeted to mitochondria in nonbilaterian animals. Overall, our analysis provides the first step in characterization of mt‐proteomes in nonbilaterian animals and understanding evolution of animal mt‐proteome. © 2018 IUBMB Life, 70(12):1289–1301, 2018
Treatment of intractable oral ulceration with an oral mucosa equivalent
Authors: Lee Jaewang , Shin Daiha , Roh Jong‐Lyel 
Published: November 2018

AbstractThe current use of steroids or pharmacological immunomodulators for the treatment of intractable oral ulceration is ineffective, necessitating newer cell‐based therapeutic approaches. We examined the potential efficacy of an oral mucosa equivalent developed in this study in an in vivo model of repeat major oral ulceration mimicking the intractable oral ulceration observed clinically. Oral mucosal samples and plasma fibrin were obtained from Sprague–Dawley rats. The oral mucosa equivalents were prepared with cultured mucosal keratinocytes and plasma fibrin mixed with cultured fibroblasts. Ulcers were chemically induced on the rat buccal mucosa thrice in 3 weeks and covered with or without mucosa equivalents. Gross and microscopic findings and mRNA expression levels were compared between the ulcer control and mucosa equivalent groups. Oral mucosal keratinocytes and fibroblasts were cultured in vitro to achieve high viability and colony‐forming efficiency. The equivalents showed epithelial and subepithelial structures similar to those of oral mucosa and exhibited high p63 positivity. In the in vivo study, ulceration was resolved earlier without significant granulation or scarring in the equivalent group than in control group (p < 0.05). Microscopic examinations revealed rapid re‐epithelialization and less fibrosis in the equivalent group than in the control group (p < 0.05). Mucosa equivalent‐covered ulcers showed histological characteristics similar to those of the normal buccal mucosa and exhibited lower expression of TGFB1, ACTA2, and FN1 mRNAs than the control group. The in vitro‐engineered oral mucosa equivalent promotes ulcer healing without scarring and functional deficits. © 2018 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater 107B: 1779–1785, 2019.
IGF‐1 and BMP‐7 synergistically stimulate articular cartilage repairing in the rabbit knees by improving chondrogenic differentiation of bone‐marrow mesenchymal stem cells
Authors: Peng Xian‐Bo , Zhang Yuan , Wang Yue‐Qiu , He Qi , Yu Qian 
Published: November 2018

AbstractKnee injury is known as a frequently occurred damage related to sports, which may affect the function of cartilage. This study aims to explore whether Insulin‐like growth factor 1 (IGF‐1) and bone morphogenetic protein‐7 (BMP‐7)‐modified bone‐marrow mesenchymal stem cells (BMSCs) affect the repair of cartilage damage found in the knee. Primarily, BMSCs were treated with a series of pEGFP‐C1, IGF‐1, and BMP‐7, followed by determination of IGF‐1 and BMP‐7 expression. A rabbit cartilage defect model was also established. Afterfward, cell morphology, viability, cartilage damage repair effect, and expression of collagen I and collagen II at the 6th and the 12th week were measured. BMSCs treated with pEGFP‐C1/IGF‐1, pEGFP‐C1/BMP‐7, and pEGFP‐C1/BMP‐7‐IGF‐1 exhibited elevated expression of BMP‐7 and IGF‐1. Besides, BMSCs in the P10 generation displayed decreased cell proliferation. Moreover, BMSCs treated with IGF‐1, BMP‐7, and IGF‐1‐BMP‐7 showed reduced histological score and collagen I expression while elevated collagen II expression, as well as better repair effect, especially in those treated with IGF‐1‐BMP‐7. Collectively, these results demonstrated a synergistic effect of IGF‐1 and BMP‐7 on the BMSC chondrogenic differentiation on the articular cartilage damage repair in the rabbit knees, highlighting its therapeutic potential for the treatment of articular cartilage damage.
FtsA as a cidal target for Staphylococcus aureus: Molecular docking and dynamics studies
Authors: Ragunathan Adhithya , Malathi Kullappan , Ramaiah Sudha , Anbarasu Anand 
Published: November 2018

AbstractStaphylococcus aureus infection is a healthcare problem to mankind for a considerable period of time. Once when it enters the bloodstream of an individual, it may potentially result in life‐threatening conditions. The resistance of
S. aureus to various drugs such as penicillin, methicillin, gentamicin, erythromycin, and tetracycline have been well documented. Presently vancomycin is the drug of choice for methicillin resistant
S. aureus. Scientists believe that
S. aureus would completely develop resistance to vancomycin as well. Therefore there is a commensurate need to develop a drug to replace vancomycin. In the current study, we have focussed on FtsA, an important and vital cell division protein, which is found only in
S. aureus and in other prokaryotic cells. We have carried out virtual screening process for FtsA against ZINC database, the best hit molecules obtained from the preliminary docking studies were subjected to SYBYL X 2.0 docking. The molecules ZINC74432848, ZINC37769607, and ZINC96896268 displayed the highest C‐score value of 4.89, 4.49, and 4.22, respectively. The top ranked molecule ZINC74432848 was observed to form 4 hydrogen bonds with FtsA. The simulation study reveals the greater stability of the FtsA‐ZINC74432848 complex. If the in vitro and in vivo study turns out affirmative, then ZINC74432848 could be developed as a potent drug for FtsA.
Dppa3 in pluripotency maintenance of ES cells and early embryogenesis
Authors: Zhao Shuang , Xu Jia , Liu Siying , Cui Kaige , Li Zongjin , Liu Na 
Published: November 2018

AbstractEmbryonic development is precisely regulated by a network of signal pathways and specific genes. Dppa3 (also known as Pgc7 or Stella) plays an important role in early embryonic development during the cleavage stage as a maternal effect gene. Dppa3 expresses in many species, and its homologous gene in human and rat genomes is located at the same chromosomal regions and have the same exon‐intron structure. However, unlike mouse embryonic stem (ES) cells, in which the Dppa3 promoter maintains hypomethylation that allows a high transcription level, the DPPA3 promoter region in human ES cells is methylated, much like that of mouse epiblast stem cell. Dppa3 is essential for early embryogenesis and pluripotency maintenance; however, the precise mechanism and downstream passage remains unknown. In this review, we will summarize some important functions of Dppa3 in early embryogenesis and pluripotency maintenance of mouse ES cells.
Inactivation of ADAMTS18 by aberrant promoter hypermethylation contribute to lung cancer progression
Authors: Zhang Yan , Xu Hongying , Mu Junhao , Guo Shuliang , Ye Lin , Li Dairong , Peng Weiyan , He Xiaoqian , Xiang Tingxiu 
Published: November 2018

AbstractLung cancer is the most frequently diagnosed cancer worldwide. Epigenetic regulation contributes to lung cancer pathogenesis. The ADAMTS18 tumor suppressor gene is inactivated in some cancers, but its involvement in lung cancer has not been shown. Immunohistochemistry, quantitative reverse‐transcription polymerase chain reaction (qRT‐PCR), and methylation‐specific PCR were used to assay ADAMTS18 expression and promoter methylation in lung tumor tissues and adjacent tissues. Cell viability, transwell, and wound‐healing assays, as well as flow cytometry were used to characterize the biological activity of ADAMTS18. The influence of ADAMTS18 on protein expression was assayed using western blots analysis, and its effect on chemosensitivity was assayed by the response to cisplatin. We found that
ADAMTS18 was silenced in lung cancer cells by promoter methylation. Demethylation by the DNA methyltransferase inhibitor 5‐aza‐2′‐deoxycytidine, with or without the histone deacetylase inhibitor trichostatin A, restored
ADAMTS18 expression. Compared with normal lung tissue,
ADAMTS18 in lung tumors was frequently methylated. Overexpression of ADAMTS18 in lung cancer cells inhibited cell proliferation, migration, and invasiveness and induced G0/G1 cell cycle arrest. Furthermore, ADAMTS18 suppressed epidermal growth factor receptor/protein kinase B (EGFR/AKT) signaling, which sensitized lung cancer cells to cisplatin. Thus, our results demonstrated that the tumor suppressor gene
ADAMTS18 was downregulated in lung cancer by promoter CpG methylation, and it promoted sensitivity to cisplatin via EGFR/AKT signaling. Our study suggests that
ADAMTS18 promoter methylation is a potential epigenetic biomarker for early detection of lung cancer and warrants investigation as a therapeutic target for early‐stage lung cancer.
The effect of Activin‐A on periodontal ligament fibroblasts‐mediated osteoclast formation in healthy donors and in patients with fibrodysplasia ossificans progressiva
Authors: Schoenmaker Ton , Wouters Fenne , Micha Dimitra , Forouzanfar Tim , Netelenbos Coen , Eekhoff E. Marelise W. , Bravenboer Nathalie , de Vries Teun J. 
Published: November 2018

AbstractFibrodysplasia ossificans progressiva (FOP) is a genetic disease characterized by heterotopic ossification (HO). The disease is caused by a mutation in the activin receptor type 1 (ACVR1) gene that enhances this receptor's responsiveness to Activin‐A. Binding of Activin‐A to the mutated ACVR1 receptor induces osteogenic differentiation. Whether Activin‐A also affects osteoclast formation in FOP is not known. Therefore we investigated its effect on the osteoclastogenesis‐inducing potential of periodontal ligament fibroblasts (PLF) from teeth of healthy controls and patients with FOP. We used western blot analysis of phosphorylated SMAD3 (pSMAD3) and quantitative polymerase chain reaction to assess the effect of Activin‐A on the PLF. PLF‐induced osteoclast formation and gene expression were studied by coculturing control and FOP PLF with CD14‐positive osteoclast precursor cells from healthy donors. Osteoclast formation was also assessed in control CD14 cultures stimulated by macrophage colony‐stimulating factor (M‐CSF) and receptor activator of nuclear factor kappa‐B ligand (RANK‐L). Although Activin‐A increased activation of the pSMAD3 pathway in both control and FOP PLF, it increased ACVR1, FK binding protein 12 (FKBP12), an inhibitor of DNA binding 1 protein (ID‐1) expression only in FOP PLF. Activin‐A inhibited PLF mediated osteoclast formation albeit only significantly when induced by FOP PLF. In these cocultures, it reduced M‐CSF and dendritic cell‐specific transmembrane protein (DC‐STAMP) expression. Activin‐A also inhibited osteoclast formation in M‐CSF and RANK‐L mediated monocultures of CD14+ cells by inhibiting their proliferation.This study brings new insight on the role of Activin A in osteoclast formation, which may further add to understanding FOP pathophysiology; in addition to the known Activin‐A‐mediated HO, this study shows that Activin‐A may also inhibit osteoclast formation, thereby further promoting HO formation.
A review of the anti‐inflammatory properties of antidiabetic agents providing protective effects against vascular complications in diabetes
Authors: Yaribeygi Habib , Atkin Stephen L. , Pirro Matteo , Sahebkar Amirhossein 
Published: November 2018

AbstractThe global prevalence of Type 2 diabetes mellitus and its associated complications are growing rapidly. Although the role of hyperglycemia is well recognized in the pathophysiology of diabetic complications, its exact underlying mechanisms are not fully understood. In this regard, accumulating evidence suggests that the role of inflammation appears pivotal, with studies showing that most diabetic complications are associated with an inflammatory response. Several classes of antidiabetic agents have been introduced for controlling glycemia, with evidence that these pharmacological agents may have modulatory effects on inflammation beyond their glucose‐lowering activity. Here we review the latest evidence on the anti‐inflammatory effects of commonly used antidiabetic medications and discuss the relevance of these effects on preventing diabetic complications.
The roles of moonlight ribosomal proteins in the development of human cancers
Authors: Molavi Ghader , Samadi Nasser , Hosseingholi Elaheh Zadeh 
Published: November 2018

Abstract“Moonlighting protein” is a term used to define a single protein with multiple functions and different activities that are not derived from gene fusions, multiple RNA splicing, or the proteolytic activity of promiscuous enzymes. Different proteinous constituents of ribosomes have been shown to have important moonlighting extra‐ribosomal functions. In this review, we introduce the impact of key moonlight ribosomal proteins and dependent signal transduction in the initiation and progression of various cancers. As a future perspective, the potential role of these moonlight ribosomal proteins in the diagnosis, prognosis, and development of novel strategies to improve the efficacy of therapies for human cancers has been suggested.
Retracted: TMEM206 promotes the malignancy of colorectal cancer cells by interacting with AKT and extracellular signal‐regulated kinase signaling pathways
Authors: Zhao Jinbo , Zhu Dehua , Zhang Xiupeng , Zhang Yong , Zhou Jianping , Dong Ming 
Published: November 2018

AbstractBackgroundThe roles of TMEM206, a new transmembrane protein, in cancer, including colorectal cancer (CRC), are unknown. Related family members, including TMEM16A, TMEM132A, and TMEM176B, have been shown to be involved in various biological behaviors. In addition, TMEM88 has been reported to promote non‐small‐cell lung cancer. In this study, we examined the roles of TMEM206 in CRC.MethodReal‐time reverse transcription polymerase chain reaction was used to measure TMEM206 messenger RNA (mRNA) levels in clinical specimens and transfected cell lines. Immunohistochemistry was used to determine the relationship between TMEM206 expression levels and clinical data. Plasmids and small interfering RNA were used to upregulate and silence TMEM206, respectively. Protein expression levels and signaling pathway modulation were validated through western blot analysis. Colony formation, MTT, cell migration and invasion assays, and flow cytometry analyses were used to test the potential roles of TMEM206 in CRC. Co‐immunoprecipitation was used to evaluate the interaction between TMEM206 and AKT.ResultsInvestigation of the clinical significance of TMEM206 expression in CRC tissues revealed that TMEM206 mRNA and protein levels were higher in CRC tissues than in paired normal adjacent tissues (p < 0.05). TMEM206 overexpression was positively associated with T stage of cancer and UICC stage (
p < 0.05) and negatively related to differentiation of CRC (
p = 0.015). Upregulation or silencing of TMEM206 promoted or inhibited the proliferation of CRC cells and positively or negatively regulated the levels of phospho‐AKT and downstream signaling pathway components (phospho‐glycogen synthase kinase 3β and cyclin D1), respectively. Moreover, silencing of TMEM206 in cell lines arrested CRC cells in the G1 stage of the cell‐cycle. In addition, upregulating or silencing TMEM206 increased or decreased cell invasion and migration in vitro and positively or negatively altered levels of the phospho‐extracellular signal‐regulated kinase (ERK) and phospho‐focal adhesion kinase 397, respectively. Co‐immunoprecipitation demonstrated that AKT and TMEM206 proteins interacted. Furthermore, TMEM206 promoted the development and progression of CRC by enhancing the interactions between the AKT and ERK signaling pathways.ConclusionTMEM206 controlled the progression of CRC by accelerating CRC cell proliferation and promoting CRC cell migration and invasion. The target of TMEM206 may be AKT, which is known to be involved in modulating the biological behaviors of various cancers.
Mitochondrial dysfunction in diabetes and the regulatory roles of antidiabetic agents on the mitochondrial function
Authors: Yaribeygi Habib , Atkin Stephen L. , Sahebkar Amirhossein 
Published: November 2018

AbstractThe prevalence of type 2 diabetes mellitus (T2DM) is increasing rapidly with its associated morbidity and mortality. Many pathophysiological pathways such as oxidative stress, inflammatory responses, adipokines, obesity‐induced insulin resistance, improper insulin signaling, and beta cell apoptosis are associated with the development of T2DM. There is increasing evidence of the role of mitochondrial dysfunction in the onset of T2DM, particularly in relation to the development of diabetic complications. Here, the role of mitochondrial dysfunction in T2DM is reviewed together with its modulation by antidiabetic therapeutic agents, an effect that may be independent of their hypoglycemic effect.