Eating when depressed, anxious, bored, or happy: Are emotional eating types associated with unique psychological and physical health correlates?

Publication date: 1 June 2018
Source:Appetite, Volume 125
Author(s): Abby Braden, Dara Musher-Eizenman, Tanya Watford, Elizabeth Emley
The majority of research on emotional eating has examined general emotional eating, to the exclusion of more distinct emotions such as boredom and positive emotions. The current study aimed to examine whether specific types of emotional eating (i.e., eating in response to depression (EE-D), anxiety/anger (EE-A), boredom (EE-B), and positive emotions (EE-P)) were related to a range of psychological (i.e., global psychological well-being, eating disorder symptoms, emotion regulation) and physical health variables. A sample of adults (n = 189) with overweight/obesity were recruited via Amazon Mechanical Turk. Participants self-reported height and weight and completed a battery of questionnaires. Correlational analyses showed that more frequent EE-D, EE-A, and EE-B were related to poorer psychological well-being, greater eating disorder symptoms, and more difficulties with emotion regulation. EE-P was not significantly related to outcome variables. In regression analyses, eating in response to depression (EE-D) was the type of emotional eating most closely related to psychological well-being, eating disorder symptoms, and emotion regulation difficulties. Exploratory analyses revealed associations between EE-D, EE-A, and EE-B and facets of emotion regulation and specific disordered eating symptoms. Findings suggest that unique patterns exist between specific types of emotional eating and psychological outcomes.



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Developing DNA methylation-based diagnostic biomarkers

Publication date: Available online 17 February 2018
Source:Journal of Genetics and Genomics
Author(s): Hyerim Kim, Xudong Wang, Peng Jin
An emerging paradigm shift for disease diagnosis is to rely on molecular characterization beyond traditional clinical and symptom-based examinations. Although genetic alterations and transcription signature were first introduced as potential biomarkers, clinical implementations of these markers are limited due to low reproducibility and accuracy. Instead, epigenetic changes are considered as an alternative approach to disease diagnosis. Complex epigenetic regulation is required for normal biological functions and it has been shown that distinctive epigenetic disruptions could contribute to disease pathogenesis. Disease-specific epigenetic changes, especially DNA methylation, have been observed, suggesting its potential as disease biomarkers for diagnosis. In addition to specificity, the feasibility of detecting disease-associated methylation marks in the biological specimens collected non-invasively, such as blood samples, has driven the clinical studies to validate disease-specific DNA methylation changes as a diagnostic biomarker. Here, we highlight the advantages of DNA methylation signature for diagnosis in different diseases and discuss the statistical and technical challenges to be overcome before clinical implementation.



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Precision medicine in hearing loss

Publication date: Available online 16 February 2018
Source:Journal of Genetics and Genomics
Author(s): Jason R. Rudman, Christine Mei, Sara E. Bressler, Susan H. Blanton, Xue-Zhong Liu
Precision medicine (PM) proposes customized medical care based on a patient's unique genome, biomarkers, environment and behaviors. Hearing loss (HL) is the most common sensorineural disorder worldwide and is frequently caused by a single genetic mutation. With recent advances in PM tools such as genetic sequencing and data analysis, the field of HL is ideally positioned to adopt the strategies of PM. Here, we review current and future applications of PM in HL as they relate to the four core qualities of PM (P4): predictive, personalized, patient-centered, and participatory. We then introduce a strategy for effective incorporation of HL PM into the design of future research studies, electronic medical records, and clinical practice to improve diagnostics, prognostics, and, ultimately, individualized patient treatment. Finally, specific anticipated ethical and economic concerns in this growing era of genomics-based HL treatment are discussed. By integrating PM principles into translational HL research and clinical practice, hearing specialists are uniquely positioned to effectively treat the heterogeneous causes and manifestations of HL on an individualized basis.



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Hepatocytes in a normal adult liver are derived solely from the embryonic hepatocytes

Publication date: Available online 14 February 2018
Source:Journal of Genetics and Genomics
Author(s): Ce Gao, Zhihui Zhu, Yuqi Gao, Li Jan Lo, Jun Chen, Lingfei Luo, Jinrong Peng




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Novel DYW-type pentatricopeptide repeat (PPR) protein BLX controls mitochondrial RNA editing and splicing essential for early seed development of Arabidopsis

Publication date: Available online 14 February 2018
Source:Journal of Genetics and Genomics
Author(s): Yan Sun, Jiaying Huang, Sheng Zhong, Hongya Gu, Shan He, Li-Jia Qu
In plants, RNA editing is a post-transcriptional process that changes specific cytidine to uridine in both mitochondria and plastids. Most pentatricopeptide repeat (PPR) proteins are involved in organelle RNA editing by recognizing specific RNA sequences. We here report the functional characterization of a PPR protein from the DYW subclass, Baili Xi (BLX), which contains five PPR motifs and a DYW domain. BLX is essential for early seed development, as plants lacking the BLX gene was embryo lethal and the endosperm failed to initiate cellularization. BLX was highly expressed in the embryo and endosperm, and the BLX protein was specifically localized in mitochondria, which is essential for BLX function. We found that BLX was required for the efficient editing of 36 editing sites in mitochondria. Moreover, BLX was involved in the splicing regulation of the fourth intron of nad1 and the first intron of nad2. The loss of BLX function impaired the mitochondrial function and increased the reactive oxygen species (ROS) level. Genetic complementation with truncated variants of BLX revealed that, in addition to the DYW domain, only the fifth PPR motif was essential for BLX function. The upstream sequences of the BLX-targeted editing sites are not conserved, suggesting that BLX serves as a novel and major mitochondrial editing factor (MEF) via a new non-RNA-interacting manner. This finding provides new insights into how a DYW-type PPR protein with fewer PPR motifs regulates RNA editing in plants.



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Overexpressing dominant-negative FGFR2-IIIb impedes lung branching morphogenesis in pigs

Publication date: Available online 14 February 2018
Source:Journal of Genetics and Genomics
Author(s): Qin Chen, Bin Fang, Ying Wang, Chu Li, Xiaoxue Li, Ronggen Wang, Qiang Xiong, Lining Zhang, Yong Jin, Manling Zhang, Xiaorui Liu, Lin Li, Lisha Mou, Rongfeng Li, Haiyuan Yang, Yifan Dai
Genetic studies with mouse models have shown that fibroblast growth factor receptor 2-IIIb (FGFR2-IIIb) plays crucial roles in lung development and differentiation. To evaluate the effect of FGFR2-IIIb in pig lung development, we employed somatic cell nuclear transfer (SCNT) technology to generate transgenic pig fetuses overexpressing the transmembrane (dnFGFR2-IIIb-Tm) and soluble (dnFGFR2-IIIb-HFc) forms of the dominant-negative human FGFR2-IIIb driven by the human surfactant protein C (SP-C) promoter, which was specifically expressed in lung epithelia. Eight dnFGFR2-IIIb-Tm transgenic and twelve dnFGFR2-IIIb-HFc transgenic pig fetuses were collected from three and two recipient sows, respectively. Repression of FGFR2 in lung epithelia resulted in smaller lobes and retardation of alveolarization in both forms of dnFGFR2-IIIb transgenic fetuses. Moreover, the dnFGFR2-IIIb-HFc transgenic ones showed more deterioration in lung development. Our results demonstrate that disruption of FGFR2-IIIb signaling in the epithelium impedes normal branching and alveolarization in pig lungs, which is less severe than the results observed in transgenic mice. The dnFGFR2-IIIb transgenic pig is a good model for the studies of blastocyst complementation as well as the mechanisms of lung development and organogenesis.



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Turning the corner from observation to intervention in human genetics

Publication date: Available online 21 February 2018
Source:Journal of Genetics and Genomics
Author(s): David L. Nelson




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Current strategies for the treatment of inborn errors of metabolism

Publication date: Available online 14 February 2018
Source:Journal of Genetics and Genomics
Author(s): Michael J. Gambello, Hong Li
Inborn errors of metabolism (IEMs) are a large group of inherited disorders characterized by disruption of metabolic pathways due to deficient enzymes, cofactors, or transporters. The rapid advances in the understanding of the molecular pathophysiology of many IEMs, have led to significant progress in the development of many new treatments. The institution and continued expansion of newborn screening provide the opportunity for early treatment, leading to reduced morbidity and mortality. This review provides an overview of the diverse therapeutic approaches and recent advances in the treatment of IEMs that focus on the basic principles of reducing substrate accumulation, replacing or enhancing absent or reduced enzyme or cofactor, and supplementing product deficiency. In addition, the challenges and obstacles of current treatment modalities and future treatment perspectives are reviewed and discussed.



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The current landscape for the treatment of mitochondrial disorders

Publication date: Available online 14 February 2018
Source:Journal of Genetics and Genomics
Author(s): Jesse Slone, Baoheng Gui, Taosheng Huang
The mitochondrial organelle is crucial to the energy metabolism of the eukaryotic cell. Defects in mitochondrial function lie at the core of a wide range of disorders, including both rare primary mitochondrial disorders and more common conditions such as Parkinson's disease and diabetes. Inherited defects in mitochondrial function can be found in both the nuclear genome and the mitochondrial genome, with the latter creating unique challenges in the treatment and understanding of disease passed on through the mitochondrial genome. In this review, we will describe the limited treatment regimens currently used to alleviate primary mitochondrial disorders, as well as the potential for emerging technologies (in particular, those involving direct manipulation of the mitochondrial genome) to more decisively treat this class of disease. We will also emphasize the critical parallels between primary mitochondrial disorders and more common ailments such as cancer and diabetes.



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AQR is a novel type 2 diabetes-associated gene that regulates signaling pathways critical for glucose metabolism

Publication date: Available online 14 February 2018
Source:Journal of Genetics and Genomics
Author(s): Chun Song, Han Yan, Han-Ming Wang, Yan Zhang, Huiqing Cao, Yiqi Wan, Lingbao Kong, Shenghan Chen, Hong Xu, Bing-Xing Pan, Jin Zhang, Guo-Huang Fan, Hong-Bo Xin, Zicai Liang, Weiping Jia, Xiao-Li Tian
Type 2 diabetes mellitus (T2DM) is a common metabolic disease influenced by both genetic and environmental factors. In this study, we performed an in-house genotyping and meta-analysis study using three independent GWAS datasets of T2DM and found that rs3743121, located 1 kb downstream of AQR, was a novel susceptibility SNP associated with T2DM. The risk allele C of rs3743121 was correlated with the increased expression of AQR in white blood cells, similar to that observed in T2DM models. The knockdown of AQR in HepG2 facilitated the glucose uptake, decreased the expression level of PCK2, increased the phosphorylation of GSK-3β, and restored the insulin sensitivity. Furthermore, the suppression of AQR inhibited the mTOR pathway and the protein ubiquitination process. Our study suggests that AQR is a novel type 2 diabetes-associated gene that regulates signaling pathways critical for glucose metabolism.



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Genetic profiling of cancer with circulating tumor DNA analysis

Publication date: Available online 5 February 2018
Source:Journal of Genetics and Genomics
Author(s): Ling Lu, Junqin Bi, Liming Bao
Circulating cell-free tumor DNA (ctDNA) in the blood is DNA released from apoptotic, circulating, and living tumor cells. ctDNA is about 140 nt in length and has a half-life of about 1.5 h. ctDNA analysis provides a noninvasive means to assess the genetic profile of cancer in real time. With the advent of molecular technologies, including digital PCR and massively parallel sequencing (MPS), ctDNA analysis has shown promise as a highly sensitive and specific alternative to conventional tissue biopsy in cancer detection, longitudinal monitoring, and precision therapy. This review provides an overview of the latest development in our understanding of the biologic characteristics, detection methodologies, and potential clinical implications of ctDNA, as well as the challenges in translating ctDNA analysis from the research arena to patient care.



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The Chinese garden of genetics —celebrating 40th anniversary of Genetics Society of China

Publication date: 20 January 2018
Source:Journal of Genetics and Genomics, Volume 45, Issue 1
Author(s): Yongbiao Xue




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Structure and functions of the translation initiation factor eIF4E and its role in cancer development and treatment

Publication date: 20 January 2018
Source:Journal of Genetics and Genomics, Volume 45, Issue 1
Author(s): Arianna Piserà, Adele Campo, Salvatore Campo
In eukaryotic cells, protein synthesis is a complex and multi-step process that has several mechanisms to start the translation including cap-dependent and cap-independent initiation. The translation control of eukaryotic gene expression occurs principally at the initiation step. In this context, it is critical that the eukaryotic translation initiation factor eIF4E bind to the 7-methylguanosine (m7G) cap present at the 5′-UTRs of most eukaryotic mRNAs. Combined with other initiation factors, eIF4E mediates the mRNA recruitment on ribosomes to start the translation. Moreover, the eIF4E nuclear bodies are involved in the export of specific mRNAs from the nucleus to the cytoplasm. In this review, we focus on the eIF4E structure and its physiological functions, and describe the role of eIF4E in cancer development and progression and the current therapeutic strategies to target eIF4E.



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Mouse macrophage specific knockout of SIRT1 influences macrophage polarization and promotes angiotensin II-induced abdominal aortic aneurysm formation

Publication date: 20 January 2018
Source:Journal of Genetics and Genomics, Volume 45, Issue 1
Author(s): Zhuqin Zhang, Jing Xu, Yue Liu, Tingting Wang, Jianfei Pei, Liqin Cheng, Delong Hao, Xiang Zhao, Hou-Zao Chen, De-Pei Liu
Abdominal aortic aneurysm (AAA) is a vascular degenerative disease. Macrophage polarization and the balance between classically activated macrophages (M1) and alternatively activated macrophages (M2) are crucial for AAA pathogenesis. The present study aims to investigate the roles of macrophage SIRT1 in AAA formation and macrophage polarization. We found that in mouse peritoneal macrophages, SIRT1 expression was decreased after M1 stimulation, but was enhanced after M2 stimulation. Results from SIRT1^flox/flox mice and macrophage specific SIRT1 knockout mice with treatment of angiotensin II (Ang II) for 4 weeks showed that macrophage specific deficiency of SIRT1 increased the incidence of AAA and exacerbated the severity, including more severe aneurysm types, enlarged diameter of the aneurysm and increased degradation of elastin. In mouse aortas, SIRT1 deficiency increased the pro-inflammatory M1 molecule inducible nitric oxide synthase (iNOS), and decreased M2 molecules such as arginase 1 (Arg1) and mannose receptor (MR). Furthermore, in peritoneal macrophages, SIRT1 deficiency increased the expression of M1 inflammatory molecules, but decreased the expression of M2 molecules. Overexpression of SIRT1 had the opposite effects. Thus, macrophage specific knockout of SIRT1 influences macrophage polarization and accelerates Ang II-induced AAA formation.



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Assessing resident awareness on e-waste management in Bangalore, India: a preliminary case study

Abstract

The generation of e-waste has increased significantly in India, and the informal recycling of e-waste has adverse effects on environment and public health. In this article, the E-waste management is evaluated in accordance from the resident's awareness perspective in Bangalore city, India. The survey data revealed that about 58% male and 42% female responded and 35% of the participants belong to age range between 18 and 25 years. About 60% of respondent's education level was either graduate or post graduate, 27% high school to higher school, 10% higher educated (> post graduate), and 3% primary to middle. Only 30% of the respondents were confident with e-waste rules and regulation, while 39% of the respondents were of very little information. Indian e-waste management has been improving for the last few years and it continues to develop. Therefore, the findings can be valuable for better understanding the resident's awareness for e-waste management and also need to promote the environmentally sound management of e-waste in Bangalore, India.

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COX-2 Forms Regulatory Loop with YAP to Promote Proliferation and Tumorigenesis of Hepatocellular Carcinoma Cells

Publication date: April 2018
Source:Neoplasia, Volume 20, Issue 4
Author(s): Guanglin Xu, Ying Wang, Weijie Li, Yuanyuan Cao, Jinling Xu, Ziwei Hu, Yaping Hao, Li Hu, Yawen Sun
COX-2 and YAP are shown to be highly associated with hepatocellular carcinoma (HCC) and frequently upregulated during tumor formation. However, despite their importance, whether there is a mutual interaction between COX-2 and YAP and how they regulate each other are not clear. In this paper, we showed that COX-2 overexpression in HCC cell lines resulted in increased levels of YAP mRNA, protein, and its target genes. COX-2 promoted proliferation of HCC cell lines, and knockdown of YAP antagonized this effect. In addition, our results indicated that EP2 and Wnt/β-Catenin mediate the transcriptional induction of YAP by COX-2. On the other hand, YAP increased COX-2 expression at the level of transcription requiring intact TEAD binding sites in the COX-2 promoter. Collectively, these findings indicated that COX-2 is not only a stimulus of YAP but also a target of Hippo-YAP pathway, thus forming a positive feedback circuit, COX-2-PGE2-EP2-Gαs-β-catenin-YAP-COX-2. In a further study, we showed that inhibition of YAP and COX-2 acted synergistically and more efficiently reduced the growth of HCC cells and tumor formation than either of them alone, suggesting that dual governing of YAP and COX-2 may lead to the discovery of promising therapeutic strategies for HCC patients via blocking this positive feedback loop.



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Wnt Signalling Drives Context-Dependent Differentiation or Proliferation in Neuroblastoma

Publication date: April 2018
Source:Neoplasia, Volume 20, Issue 4
Author(s): Marianna Szemes, Alexander Greenhough, Zsombor Melegh, Sally Malik, Aysen Yuksel, Daniel Catchpoole, Kelli Gallacher, Madhu Kollareddy, Ji Hyun Park, Karim Malik
Neuroblastoma is one of the commonest and deadliest solid tumours of childhood, and is thought to result from disrupted differentiation of the developing sympathoadrenergic lineage of the neural crest. Neuroblastoma exhibits intra- and intertumoural heterogeneity, with high risk tumours characterised by poor differentiation, which can be attributable to MYCN-mediated repression of genes involved in neuronal differentiation. MYCN is known to co-operate with oncogenic signalling pathways such as Alk, Akt and MEK/ERK signalling, and, together with c-MYC has been shown to be activated by Wnt signalling in various tissues. However, our previous work demonstrated that Wnt3a/Rspo2 treatment of some neuroblastoma cell lines can, paradoxically, decrease c-MYC and MYCN proteins. This prompted us to define the neuroblastoma-specific Wnt3a/Rspo2-driven transcriptome using RNA sequencing, and characterise the accompanying changes in cell biology. Here we report the identification of ninety Wnt target genes, and show that Wnt signalling is upstream of numerous transcription factors and signalling pathways in neuroblastoma. Using live-cell imaging, we show that Wnt signalling can drive differentiation of SK-N-BE(2)-C and SH-SY5Y cell-lines, but, conversely, proliferation of SK-N-AS cells. We show that cell-lines that differentiate show induction of pro-differentiation BMP4 and EPAS1 proteins, which is not apparent in the SK-N-AS cells. In contrast, SK-N-AS cells show increased CCND1, phosphorylated RB and E2F1 in response to Wnt3a/Rspo2, consistent with their proliferative response, and these proteins are not increased in differentiating lines. By meta-analysis of the expression of our 90 genes in primary tumour gene expression databases, we demonstrate discrete expression patterns of our Wnt genes in patient cohorts with different prognosis. Furthermore our analysis reveals interconnectivity within subsets of our Wnt genes, with one subset comprised of novel putative drivers of neuronal differentiation repressed by MYCN. Assessment of β-catenin immunohistochemistry shows high levels of β-catenin in tumours with better differentiation, further supporting a role for canonical Wnt signalling in neuroblastoma differentiation.



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S-phase Specific Downregulation of Human O6-Methylguanine DNA Methyltransferase (MGMT) and its Serendipitous Interactions with PCNA and p21cip1 Proteins in Glioma Cells

Publication date: April 2018
Source:Neoplasia, Volume 20, Issue 4
Author(s): AGM Mostofa, Surendra R. Punganuru, Hanumantha Rao Madala, Kalkunte S. Srivenugopal
Whether the antimutagenic DNA repair protein MGMT works solo in human cells and if it has other cellular functions is not known. Here, we show that human MGMT associates with PCNA and in turn, with the cell cycle inhibitor, p21^cip1 in glioblastoma and other cancer cell lines. MGMT protein was shown to harbor a nearly perfect PCNA-Interacting Protein (PIP box) motif. Isogenic p53-null H1299 cells were engineered to express the p21 protein by two different procedures. Reciprocal immunoprecipitation/western blotting, Far-western blotting, and confocal microscopy confirmed the specific association of MGMT with PCNA and the ability of p21 to strongly disrupt the MGMT-PCNA complexes in tumor cells. Alkylation DNA damage resulted in a greater colocalization of MGMT and PCNA proteins, particularly in HCT116 cells deficient in p21 expression. p21 expression in isogenic cell lines directly correlated with markedly higher levels of MGMT mRNA, protein, activity and greater resistance to alkylating agents. In other experiments, four glioblastoma cell lines synchronized at the G1/S phase using either double thymidine or thymidine-mimosine blocks and subsequent cycling consistently showed a loss of MGMT protein at mid- to late S-phase, irrespective of the cell line, suggesting such a downregulation is fundamental to cell cycle control. MGMT protein was also specifically degraded in extracts from S-phase cells and evidence strongly suggested the involvement of PCNA-dependent CRL4^Cdt2 ubiquitin-ligase in the reaction. Overall, these data provide the first evidence for non-repair functions of MGMT in cell cycle and highlight the involvement of PCNA in MGMT downregulation, with p21 attenuating the process.



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The Use of Vibrational Energy to Isolate Adipose-Derived Stem Cells

Background: Adipose-derived stem cell (ADSC)–based treatments have the potential to treat numerous soft-tissue pathologies. It would be beneficial to develop an efficient and reliable intraoperative, nonenzymatic method of isolating ADSCs for clinical use. This study aims to determine the (1) viability and proliferative capacity of ADSCs after exposure to vibrational energies and (2) efficacy of vibrational energy as a method of ADSC isolation from surgically harvested infrapatellar fat pad (IFP). Methods: Cultured ADSCs were exposed to 15 minutes of vibration (60 Hz) with displacements ranging from 0 to 2.5 mm to assess cell viability and proliferation. Then, arthroscopically harvested adipose tissue (IFP; n = 5 patients) was filtered and centrifuged to separate the stromal vascular fraction, which was exposed to 15 minutes of vibration (60 Hz; 1.3 mm or 2.5 mm displacement). A viability analysis was then performed along with proliferation and apoptosis assays. Results: Vibration treatment at all displacements had no effect on the viability or proliferation of the cultured ADSCs compared with controls. There was an increased apoptosis rate between the 2.5 mm displacement group (7.53%) and controls (5.17%; P

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The Value of Supine Chest X-Ray in the Diagnosis of Pneumonia in the Basal Lung Zones

Publication date: Available online 2 March 2018
Source:Academic Radiology
Author(s): Wolfgang G. Kunz, Maximilian Patzig, Alexander Crispin, Robert Stahl, Maximilian F. Reiser, Mike Notohamiprodjo
Rationale and ObjectivesBasal lung opacities are frequently observed on supine chest x-ray (SCXR) of intensive care patients, causing insecurity among clinicians and radiologists. We sought to determine the diagnostic accuracy of SCXR for basal pneumonia.Materials and MethodsWe identified 172 patients who received both SCXR and computed tomography within 1 hour. Two readers examined the SCXR and rated findings in both basal zones according to the following scale: 0 = "no pneumonia," 1 = "possible pneumonia," 2 = "highly suspected pneumonia." Computed tomography served as standard of reference. Sensitivity, specificity, and positive and negative predictive values (PPV/NPV) were calculated once pooling 0 and 1 as negative and once pooling 1 and 2 as positive finding.ResultsWhen pooling 0 and 1 as negative, sensitivity was 0.45 (right)/0.38 (left), specificity was 0.94/0.97, PPV was 0.76/0.79, and NPV was 0.81/0.84. When pooling 1 and 2 as positive, sensitivity was 0.80/0.75, specificity was 0.62/0.58, PPV was 0.45/0.35, and NPV was 0.88/0.89. The most common findings in false-positive cases were combined pleural effusions and lower lobe atelectasis.ConclusionsInterpreting only highly suspicious basal opacities as pneumonia considerably increases the PPV with almost constant NPV. Clinicians and radiologists should be aware of the limitations of SCXR regarding basal pneumonia.



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