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  • 1
    Keywords: Life sciences ; Plant science ; Botany ; Life sciences ; Plant Sciences ; Springer eBooks
    Description / Table of Contents: Hydrotropism: Analysis of the Root Response to a Moisture Gradient.-℗ Assessing Gravitropic Responses in Arabidopsis.-℗ Physiological Analysis of Phototropic Responses in Arabidopsis -- Automatic Chloroplast Movement Analysis.-℗ Microscopic and Biochemical Visualization of Auxins in Plant Tissues.-℗ Immunolocalization of PIN and ABCB Transporters in Plants -- Analysis of Circadian Leaf Movements -- Sample Preparation of Arabidopsis Thaliana Shoot Apices for Expression Studies of Photoperiod-Induced Genes.-℗ A Luciferase-Based Assay to Test Whether Gene Expression Responses to Environmental Inputs are Temporally Restricted by the Circadian Clock.-℗ Identification of Arabidopsis Transcriptional Regulators by Yeast One-Hybrid Screens Using a Transcription Factor ORFeome.-℗ ℗ Monitoring Alternative Splicing Changes in Arabidopsis Circadian Clock Genes.-℗ Assessing the Impact of Photosynthetic Sugars on the Arabidopsis Circadian Clock.-℗ Assessing Protein Stability Under Different Light and Circadian Conditions.-℗ Screening for Abiotic Stress Tolerance in Rice: Salt, Cold, and Drought.-℗ Basic Techniques to Assess Seed Germination Responses to Abiotic Stress in Arabidopsis Thaliana.-℗ Assessing Tolerance to Heavy-Metal Stress in 〈 Arabidopsis Thaliana Seedlings -- Assessing Drought Responses Using Thermal Infrared Imaging.-℗ Generating Targeted Gene Knockout Lines in Physcomitrella Patens to Study Evolution of Stress-Responsive Mechanisms.-℗ Screening Stress Tolerance Traits in Arabidopsis Cell Cultures.-℗ Using Arabidopsis Protoplasts to Study Cellular Responses to Environmental Stress.-℗ Construction of Artificial miRNAs to Prevent Drought Stress in Solanum Tuberosum.-℗ Virus-Induced Gene Silencing for Gene Function Studies in Barley.-℗ Methods for Long-Term Stable Storage of Colletotrichum Species.-℗ Plant Inoculation With the Fungal Leaf Pathogen Colletotrichum higginsianum.-℗ Tracing Plant Defense Responses in Roots Upon MAMP/DAMP Treatment.-℗ Analysis of the Immunity-Related Oxidative Bursts by a Luminol-Based Assay.-℗ Quantitative Analysis of Microbe- Associated-Molecular-Pattern (MAMP)-Induced Ca2+ Transients in Plants -- Rapid Assessment of DNA Methylation Changes in Response to Salicylic Acid by Chop-qPCR.-℗ Determining Nucleosome Position at Individual Loci after Biotic Stress Using MNase-qPCR.-℗ Phosphoprotein Enrichment Combined with Phosphopeptide Enrichment to Identify Putative Phosphoproteins During Defense Response in Arabidopsis thaliana
    Abstract: This volume describes different up-to-date methodological approaches, ranging from physiological assays to imaging and molecular techniques, to study a wide variety of plant responses to environmental cues. Environmental Responses in Plants: Methods and Protocols is divided into four sections: Tropisms, Photoperiodism and Circadian Rhythms, Abiotic Stress Responses, and Plant-Pathogen Interactions. The chapters in these sections include detailed protocols to investigate some of the many key biological processes underlying plant environmental responses, mostly in the model organism Arabidopsis thaliana, but also in Physcomitrella patens and in different crop species such as rice, potato, barley, or tomato. Written in the highly successful Methods in Molecular Biology series format, chapters include introductions to their respective topics, lists of the necessary materials and reagents, step-by-step, readily reproducible laboratory protocols, and tips on troubleshooting and avoiding known pitfalls. Authoritative and practical, Environmental Responses in Plants: Methods and Protocols, is a great resource for plant physiologists, biochemists, and cell and molecular scientists interested in this exciting and fast-growing research topic. ℗
    Pages: XIV, 387 p. 79 illus., 21 illus. in color. : online resource.
    Edition: 1st ed. 2016.
    ISBN: 9781493933563
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  • 2
    Keywords: Medicine ; Endocrinology ; Orthopedics ; Medicine & Public Health ; Endocrinology ; Orthopedics ; Biomedicine general ; Springer eBooks
    Pages: : digital
    ISBN: 9780857292933
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  • 3
    Keywords: Aging ; Developmental Biology ; Geriatrics ; Endocrinology  ; Biogerontology ; Geriatrics/Gerontology ; Endocrinology ; Springer eBooks
    Description / Table of Contents: Dedication -- Foreword -- Preface -- Acknowledgements -- PART I Biology of Muscle and Bone -- Muscle and Bone Biology -- Mesenchymal stem cells as regulators of bone, muscle, and fat formation -- Age-related changes in muscle and bone -- Cross-talk between muscle and bone -- Role of connexins and pannexins in bone and muscle mass and function -- Osteosarcopenia as a Lipotoxic Disease -- The endocrine actions of undercarboxylated osteocalcin in skeletal muscle: effects and mechanisms -- Sex steroid hormones and osteosarcopenia -- Calciotropic hormones and osteosarcopenia -- Genetics of Osteosarcopenia -- PART II Clinical Characteristics -- Diagnosis of Osteosarcopenia – clinical -- Diagnosis of Osteosarcopenia – Imaging -- Diagnosis of osteosarcopenia – Biochemistry and pathology -- Osteosarcopenic obesity -- Non-pharmacological interventions for osteosarcopenia -- The Falls and Fractures Clinic – An integrated model of care for osteosarcopenic patients -- Index
    Abstract: This edited work presents the most current evidence on osteosarcopenia from bench to bedside, which is expected to facilitate the understanding of this syndrome and to develop preventive and therapeutic strategies. With our aging population, chronic diseases such as osteoporosis and sarcopenia are becoming highly prevalent. Fortunately, our understanding of the bone and muscle interactions has increased in recent years. This has allowed to the coining of the term osteosarcopenia to describe a syndrome in which these two diseases overlap. This overlap between osteoporosis and sarcopenia has major negative effects not only on our older adults but also on health systems worldwide. Readers will find a highly translational approach that starts with a summary of recent discoveries on stem cells biology, muscle and bone interactions – including the role of local bone and muscle fat – followed by comprehensive reviews on myokines (i.e. myostatin), osteokines (i.e. osteocalcin) and adipokines (i.e. interleukins) as major players and determinants of bone and muscle loss with aging. In addition, the role of sex steroids (i.e. estrogens, androgens), and calciotropic hormones (i.e. parathyroid hormone, vitamin D) in the pathogenesis of this syndrome is also reviewed. Moreover, using practical diagnostic and therapeutic tips, this book summarizes the clinical characteristics of osteosarcopenic patients thus facilitating the diagnosis and treatment of this syndrome in clinical practice. Finally, the book presents the case for the Falls and Fractures Clinic as the optimal model of care for this syndrome, aimed to avoid fragmentation and optimize osteosarcopenia care, and simultaneously prevent falls and fractures in older persons. This book offers relevant information on the mechanisms of osteosarcopenia, and a practical guide on how to identify and treat this geriatric syndrome and its adverse outcomes, which are dramatically affecting our aging population. The work is written by leaders in the field and is especially suited not only to any researcher in the musculoskeletal arena but also to medical specialists and allied health professionals involved in the care of older persons
    Pages: XVI, 383 p. 42 illus., 28 illus. in color. : online resource.
    Edition: 1st ed. 2019.
    ISBN: 9783030258900
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  • 4
    Keywords: POPULATION ; ASSOCIATION ; SCHIZOPHRENIA ; PERVASIVE DEVELOPMENTAL DISORDERS ; INDIVIDUALS ; SPECTRUM DISORDERS ; Copy number variation ; GENETIC ARCHITECTURE ; NEUROPSYCHIATRIC CONDITIONS ; PTEN MUTATIONS
    Abstract: Although autism spectrum disorders (ASDs) have a substantial genetic basis, most of the known genetic risk has been traced to rare variants, principally copy number variants (CNVs). To identify common risk variation, the Autism Genome Project (AGP) Consortium genotyped 1558 rigorously defined ASD families for 1 million single-nucleotide polymorphisms (SNPs) and analyzed these SNP genotypes for association with ASD. In one of four primary association analyses, the association signal for marker rs4141463, located within MACROD2, crossed the genome-wide association significance threshold of P 〈 5 x 10(-8). When a smaller replication sample was analyzed, the risk allele at rs4141463 was again over-transmitted; yet, consistent with the winner's curse, its effect size in the replication sample was much smaller; and, for the combined samples, the association signal barely fell below the P 〈 5 x 10(-8) threshold. Exploratory analyses of phenotypic subtypes yielded no significant associations after correction for multiple testing. They did, however, yield strong signals within several genes, KIAA0564, PLD5, POU6F2, ST8SIA2 and TAF1C
    Type of Publication: Journal article published
    PubMed ID: 20663923
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  • 5
    Keywords: EXPRESSION ; POPULATION ; RISK ; GENE ; POLYMORPHISMS ; SCHIZOPHRENIA ; COPY NUMBER ; SNP ; NEURONS ; MENTAL-RETARDATION ; GENOME-WIDE ASSOCIATION ; GLUTAMATE-RECEPTOR-6 GENE ; LINKAGE ANALYSES ; RUNS
    Abstract: Autism spectrum disorder (ASD) is a highly heritable disorder of complex and heterogeneous aetiology. It is primarily characterized by altered cognitive ability including impaired language and communication skills and fundamental deficits in social reciprocity. Despite some notable successes in neuropsychiatric genetics, overall, the high heritability of ASD (round 90%) remains poorly explained by common genetic risk variants. However, recent studies suggest that rare genomic variation, in particular copy number variation, may account for a significant proportion of the genetic basis of ASD. We present a large scale analysis to identify candidate genes which may contain low-frequency recessive variation contributing to ASD while taking into account the potential contribution of population differences to the genetic heterogeneity of ASD. Our strategy, homozygous haplotype (HH) mapping, aims to detect homozygous segments of identical haplotype structure that are shared at a higher frequency amongst ASD patients compared to parental controls. The analysis was performed on 1,402 Autism Genome Project trios genotyped for 1 million single nucleotide polymorphisms (SNPs). We identified 25 known and 1,218 novel ASD candidate genes in the discovery analysis including CADM2, ABHD14A, CHRFAM7A, GRIK2, GRM3, EPHA3, FGF10, KCND2, PDZK1, IMMP2L and FOXP2. Furthermore, 10 of the previously reported ASD genes and 300 of the novel candidates identified in the discovery analysis were replicated in an independent sample of 1,182 trios. Our results demonstrate that regions of HH are significantly enriched for previously reported ASD candidate genes and the observed association is independent of gene size (odds ratio 2.10). Our findings highlight the applicability of HH mapping in complex disorders such as ASD and offer an alternative approach to the analysis of genome-wide association data.
    Type of Publication: Journal article published
    PubMed ID: 21996756
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  • 6
    Abstract: BACKGROUND: Over the past decade genome-wide association studies (GWAS) have been applied to aid in the understanding of the biology of traits. The success of this approach is governed by the underlying effect sizes carried by the true risk variants and the corresponding statistical power to observe such effects given the study design and sample size under investigation. Previous ASD GWAS have identified genome-wide significant (GWS) risk loci; however, these studies were of only of low statistical power to identify GWS loci at the lower effect sizes (odds ratio (OR) 〈1.15). METHODS: We conducted a large-scale coordinated international collaboration to combine independent genotyping data to improve the statistical power and aid in robust discovery of GWS loci. This study uses genome-wide genotyping data from a discovery sample (7387 ASD cases and 8567 controls) followed by meta-analysis of summary statistics from two replication sets (7783 ASD cases and 11359 controls; and 1369 ASD cases and 137308 controls). RESULTS: We observe a GWS locus at 10q24.32 that overlaps several genes including PITX3, which encodes a transcription factor identified as playing a role in neuronal differentiation and CUEDC2 previously reported to be associated with social skills in an independent population cohort. We also observe overlap with regions previously implicated in schizophrenia which was further supported by a strong genetic correlation between these disorders (Rg = 0.23; P = 9 x 10-6). We further combined these Psychiatric Genomics Consortium (PGC) ASD GWAS data with the recent PGC schizophrenia GWAS to identify additional regions which may be important in a common neurodevelopmental phenotype and identified 12 novel GWS loci. These include loci previously implicated in ASD such as FOXP1 at 3p13, ATP2B2 at 3p25.3, and a 'neurodevelopmental hub' on chromosome 8p11.23. CONCLUSIONS: This study is an important step in the ongoing endeavour to identify the loci which underpin the common variant signal in ASD. In addition to novel GWS loci, we have identified a significant genetic correlation with schizophrenia and association of ASD with several neurodevelopmental-related genes such as EXT1, ASTN2, MACROD2, and HDAC4.
    Type of Publication: Journal article published
    PubMed ID: 28540026
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  • 7
    Keywords: GENE ; DELETIONS ; MENTAL-RETARDATION ; LOCI ; GENOME-WIDE ASSOCIATION ; CNTNAP2 ; Copy number variation ; DE-NOVO MUTATIONS ; LINKAGE ANALYSES ; DEVELOPMENTAL DISORDERS
    Abstract: While it is apparent that rare variation can play an important role in the genetic architecture of autism spectrum disorders (ASDs), the contribution of common variation to the risk of developing ASD is less clear. To produce a more comprehensive picture, we report Stage 2 of the Autism Genome Project genome-wide association study, adding 1301 ASD families and bringing the total to 2705 families analysed (Stages 1 and 2). In addition to evaluating the association of individual single nucleotide polymorphisms (SNPs), we also sought evidence that common variants, en masse, might affect the risk. Despite genotyping over a million SNPs covering the genome, no single SNP shows significant association with ASD or selected phenotypes at a genome-wide level. The SNP that achieves the smallest P-value from secondary analyses is rs1718101. It falls in CNTNAP2, a gene previously implicated in susceptibility for ASD. This SNP also shows modest association with age of word/phrase acquisition in ASD subjects, of interest because features of language development are also associated with other variation in CNTNAP2. In contrast, allele scores derived from the transmission of common alleles to Stage 1 cases significantly predict case status in the independent Stage 2 sample. Despite being significant, the variance explained by these allele scores was small (Vm〈 1%). Based on results from individual SNPs and their en masse effect on risk, as inferred from the allele score results, it is reasonable to conclude that common variants affect the risk for ASD but their individual effects are modest.
    Type of Publication: Journal article published
    PubMed ID: 22843504
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  • 8
    Keywords: RISK ; DELETIONS ; GENOME-WIDE ASSOCIATION ; DUPLICATIONS ; STRUCTURAL VARIATION ; COPY NUMBER VARIANTS ; FRAGILE-X-SYNDROME ; DE-NOVO MUTATIONS ; INTELLECTUAL DISABILITY ; PHENOTYPE ONTOLOGY
    Abstract: Rare copy-number variation (CNV) is an important source of risk for autism spectrum disorders (ASDs). We analyzed 2,446 ASD-affected families and confirmed an excess of genic deletions and duplications in affected versus control groups (1.41-fold, p = 1.0 x 10(-5)) and an increase in affected subjects carrying exonic pathogenic CNVs overlapping known loci associated with dominant or X-linked ASD and intellectual disability (odds ratio = 12.62, p = 2.7 x 10(-15), approximately 3% of ASD subjects). Pathogenic CNVs, often showing variable expressivity, included rare de novo and inherited events at 36 loci, implicating ASD-associated genes (CHD2, HDAC4, and GDI1) previously linked to other neurodevelopmental disorders, as well as other genes such as SETD5, MIR137, and HDAC9. Consistent with hypothesized gender-specific modulators, females with ASD were more likely to have highly penetrant CNVs (p = 0.017) and were also overrepresented among subjects with fragile X syndrome protein targets (p = 0.02). Genes affected by de novo CNVs and/or loss-of-function single-nucleotide variants converged on networks related to neuronal signaling and development, synapse function, and chromatin regulation.
    Type of Publication: Journal article published
    PubMed ID: 24768552
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  • 9
    Keywords: GENE-EXPRESSION ; NF-KAPPA-B ; RESPONSES ; IFN-GAMMA ; TRANSCRIPTION FACTOR ; HETEROGENEITY ; BET ; PROTEIN-LEVELS ; TH1 DEVELOPMENT ; RAPID ON/OFF
    Abstract: The probabilistic expression of cytokine genes in differentiated T helper (Th) cell populations remains ill defined. By single-cell analyses and mathematical modeling, we show that one stimulation featured stable cytokine nonproducers as well as stable producers with wide cell-to-cell variability in the magnitude of expression. Focusing on interferon-gamma (IFN-gamma) expression by Th1 cells, mathematical modeling predicted that this behavior reflected different cell-intrinsic capacities and not mere gene-expression noise. In vivo, Th1 cells sort purified by secreted IFN-gamma amounts preserved a quantitative memory for both probability and magnitude of IFN-gamma re-expression for at least 1 month. Mechanistically, this memory resulted from quantitatively distinct transcription of individual alleles and was controlled by stable expression differences of the Th1 cell lineage-specifying transcription factor T-bet. Functionally, Th1 cells with graded IFN-gamma production competence differentially activated Salmonella-infected macrophages for bacterial killing. Thus, individual Th cells commit to produce distinct amounts of a given cytokine, thereby generating functional intrapopulation heterogeneity.
    Type of Publication: Journal article published
    PubMed ID: 25607461
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  • 10
    Abstract: The dual leucine zipper kinase DLK induces beta-cell apoptosis by inhibiting the transcriptional activity conferred by the beta-cell protective transcription factor cAMP response element binding protein CREB. This action might contribute to beta-cell loss and ultimately diabetes. Within its kinase domain DLK shares high homology with the mixed lineage kinase (MLK) 3, which is activated by tumor necrosis factor (TNF) alpha and interleukin (IL)-1beta, known prediabetic signals. In the present study, the regulation of DLK in beta-cells by these cytokines was investigated. Both, TNFalpha and IL-1beta induced the nuclear translocation of DLK. Mutations within a putative nuclear localization signal (NLS) prevented basal and cytokine-induced nuclear localization of DLK and binding to the importin receptor importin alpha, thereby demonstrating a functional NLS within DLK. DLK NLS mutants were catalytically active as they phosphorylated their down-stream kinase c-Jun N-terminal kinase to the same extent as DLK wild-type but did neither inhibit CREB-dependent gene transcription nor transcription conferred by the promoter of the anti-apoptotic protein BCL-xL. In addition, the beta-cell apoptosis-inducing effect of DLK was severely diminished by mutation of its NLS. In a murine model of prediabetes, enhanced nuclear DLK was found. These data demonstrate that DLK exerts distinct functions, depending on its subcellular localization and thus provide a novel level of regulating DLK action. Furthermore, the prevention of the nuclear localization of DLK as induced by prediabetic signals with consecutive suppression of beta-cell apoptosis might constitute a novel target in the therapy of diabetes mellitus.
    Type of Publication: Journal article published
    PubMed ID: 26776303
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