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  • 1
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    A Novel Segmentation-Based Algorithm for the Quantification of Magnified Cells (2014)
    Wiley
    Details
    Publication Date: 2014-07-16
    Description: Cell segmentation and counting is often required in disciplines such as biological research and medical diagnosis. Manual counting, although still employed suffers from being time consuming and sometimes unreliable. As a result, several automated cell segmentation and counting methods have been developed. A main component of automated cell counting algorithms is the image segmentation technique employed. Several such techniques were investigated and implemented in the present study. The segmentation and counting was performed on antibody stained brain tissue sections that were magnified by a factor of 40. Commonly used methods such as the circular Hough transform and watershed segmentation were analysed. These tests were found to over-segment and therefore over-count samples. Consequently, a novel cell segmentation and counting algorithm was developed and employed. The algorithm was found to be in almost perfect agreement with the average of four manual counters, with an intraclass correlation coefficient (ICC) of 0.8. © 2014 Wiley Periodicals, Inc.
    Electronic ISSN: 0091-7419
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Published by Wiley
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  • 2
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    Reprogramming towards pluripotency requires AID-dependent DNA demethylation (2009)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2009-12-23
    Description: Reprogramming of somatic cell nuclei to yield induced pluripotent stem (iPS) cells makes possible derivation of patient-specific stem cells for regenerative medicine. However, iPS cell generation is asynchronous and slow (2-3 weeks), the frequency is low (〈0.1%), and DNA demethylation constitutes a bottleneck. To determine regulatory mechanisms involved in reprogramming, we generated interspecies heterokaryons (fused mouse embryonic stem (ES) cells and human fibroblasts) that induce reprogramming synchronously, frequently and fast. Here we show that reprogramming towards pluripotency in single heterokaryons is initiated without cell division or DNA replication, rapidly (1 day) and efficiently (70%). Short interfering RNA (siRNA)-mediated knockdown showed that activation-induced cytidine deaminase (AID, also known as AICDA) is required for promoter demethylation and induction of OCT4 (also known as POU5F1) and NANOG gene expression. AID protein bound silent methylated OCT4 and NANOG promoters in fibroblasts, but not active demethylated promoters in ES cells. These data provide new evidence that mammalian AID is required for active DNA demethylation and initiation of nuclear reprogramming towards pluripotency in human somatic cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2906123/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2906123/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bhutani, Nidhi -- Brady, Jennifer J -- Damian, Mara -- Sacco, Alessandra -- Corbel, Stephane Y -- Blau, Helen M -- AG009521/AG/NIA NIH HHS/ -- AG024987/AG/NIA NIH HHS/ -- AI007328/AI/NIAID NIH HHS/ -- R01 AG009521/AG/NIA NIH HHS/ -- R01 AG009521-25/AG/NIA NIH HHS/ -- R01 AG024987/AG/NIA NIH HHS/ -- R01 AG024987-05/AG/NIA NIH HHS/ -- T32 AI007328/AI/NIAID NIH HHS/ -- U01 HL100397/HL/NHLBI NIH HHS/ -- England -- Nature. 2010 Feb 25;463(7284):1042-7. doi: 10.1038/nature08752.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Baxter Laboratory for Stem Cell Biology, Institute for Stem Cell Biology and Regenerative Medicine, Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California 94305-5175, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20027182" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Division ; Cell Fusion ; Cell Line ; Cells, Cultured ; Cellular Reprogramming/genetics/*physiology ; Chromatin Immunoprecipitation ; Cytidine Deaminase/deficiency/genetics/*metabolism ; DNA/chemistry/genetics/metabolism ; *DNA Methylation ; DNA Replication ; Embryonic Stem Cells/cytology/metabolism ; Fibroblasts/cytology/metabolism ; Gene Expression Regulation ; Gene Knockdown Techniques ; Homeodomain Proteins/genetics ; Humans ; Induced Pluripotent Stem Cells/*cytology/enzymology/*metabolism ; Lung/cytology/embryology ; Mice ; Models, Biological ; Octamer Transcription Factor-3/genetics ; Promoter Regions, Genetic/genetics ; Time Factors
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 3
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    SIRT6 is a histone H3 lysine 9 deacetylase that modulates telomeric chromatin (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-03-14
    Description: The Sir2 deacetylase regulates chromatin silencing and lifespan in Saccharomyces cerevisiae. In mice, deficiency for the Sir2 family member SIRT6 leads to a shortened lifespan and a premature ageing-like phenotype. However, the molecular mechanisms of SIRT6 function are unclear. SIRT6 is a chromatin-associated protein, but no enzymatic activity of SIRT6 at chromatin has yet been detected, and the identity of physiological SIRT6 substrates is unknown. Here we show that the human SIRT6 protein is an NAD+-dependent, histone H3 lysine 9 (H3K9) deacetylase that modulates telomeric chromatin. SIRT6 associates specifically with telomeres, and SIRT6 depletion leads to telomere dysfunction with end-to-end chromosomal fusions and premature cellular senescence. Moreover, SIRT6-depleted cells exhibit abnormal telomere structures that resemble defects observed in Werner syndrome, a premature ageing disorder. At telomeric chromatin, SIRT6 deacetylates H3K9 and is required for the stable association of WRN, the factor that is mutated in Werner syndrome. We propose that SIRT6 contributes to the propagation of a specialized chromatin state at mammalian telomeres, which in turn is required for proper telomere metabolism and function. Our findings constitute the first identification of a physiological enzymatic activity of SIRT6, and link chromatin regulation by SIRT6 to telomere maintenance and a human premature ageing syndrome.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2646112/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2646112/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Michishita, Eriko -- McCord, Ronald A -- Berber, Elisabeth -- Kioi, Mitomu -- Padilla-Nash, Hesed -- Damian, Mara -- Cheung, Peggie -- Kusumoto, Rika -- Kawahara, Tiara L A -- Barrett, J Carl -- Chang, Howard Y -- Bohr, Vilhelm A -- Ried, Thomas -- Gozani, Or -- Chua, Katrin F -- K08 AG028961/AG/NIA NIH HHS/ -- K08 AG028961-03/AG/NIA NIH HHS/ -- R01 AG028867/AG/NIA NIH HHS/ -- R01 AG028867-03/AG/NIA NIH HHS/ -- R01 GM079641/GM/NIGMS NIH HHS/ -- R01 GM079641-02/GM/NIGMS NIH HHS/ -- England -- Nature. 2008 Mar 27;452(7186):492-6. doi: 10.1038/nature06736. Epub 2008 Mar 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Division of Endocrinology, Gerontology and Metabolism, School of Medicine, Stanford University, Stanford, California 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18337721" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Cell Aging/genetics ; Cell Line ; Chromatin/genetics/*metabolism ; DNA Replication ; Exodeoxyribonucleases/metabolism ; Fibroblasts ; Histone Deacetylases/deficiency/genetics/*metabolism ; Histones/chemistry/metabolism ; Humans ; Lysine/metabolism ; Phenotype ; Protein Binding ; RecQ Helicases/metabolism ; Sirtuins/deficiency/genetics/*metabolism ; Telomerase/genetics/metabolism ; Telomere/genetics/*metabolism ; Werner Syndrome/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 4
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    Selective, high-contrast detection of syngeneic glioblastoma in vivo (2020)
    Springer Nature
    Details
    Publication Date: 2020-06-19
    Description: Glioblastoma is a highly malignant, largely therapy-resistant brain tumour. Deep infiltration of brain tissue by neoplastic cells represents the key problem of diffuse glioma. Much current research focuses on the molecular makeup of the visible tumour mass rather than the cellular interactions in the surrounding brain tissue infiltrated by the invasive glioma cells that cause the tumour’s ultimately lethal outcome. Diagnostic neuroimaging that enables the direct in vivo observation of the tumour infiltration zone and the local host tissue responses at a preclinical stage are important for the development of more effective glioma treatments. Here, we report an animal model that allows high-contrast imaging of wild-type glioma cells by positron emission tomography (PET) using [18 F]PBR111, a selective radioligand for the mitochondrial 18 kDa Translocator Protein (TSPO), in the Tspo−/− mouse strain (C57BL/6-Tspotm1GuMu(GuwiyangWurra)). The high selectivity of [18 F]PBR111 for the TSPO combined with the exclusive expression of TSPO in glioma cells infiltrating into null-background host tissue free of any TSPO expression, makes it possible, for the first time, to unequivocally and with uniquely high biological contrast identify peri-tumoral glioma cell invasion at preclinical stages in vivo. Comparison of the in vivo imaging signal from wild-type glioma cells in a null background with the signal in a wild-type host tissue, where the tumour induces the expected TSPO expression in the host’s glial cells, illustrates the substantial extent of the peritumoral host response to the growing tumour. The syngeneic tumour (TSPO+/+) in null background (TSPO−/−) model is thus well suited to study the interaction of the tumour front with the peri-tumoral tissue, and the experimental evaluation of new therapeutic approaches targeting the invasive behaviour of glioblastoma.
    Electronic ISSN: 2045-2322
    Topics: Natural Sciences in General
    Published by Springer Nature
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  • 5
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    Heparin Activates β-Secretase (BACE1) of Alzheimer's Disease and Increases Autocatalysis of the Enzyme† (2006)
    American Chemical Society
    Details
    Publication Date: 2006-05-01
    Print ISSN: 0006-2960
    Electronic ISSN: 1520-4995
    Topics: Biology , Chemistry and Pharmacology
    Published by American Chemical Society
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  • 6
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    Altered Brain Adiponectin Receptor Expression in the 5XFAD Mouse Model of Alzheimer’s Disease (2020)
    Molecular Diversity Preservation International
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    Publication Date: 2020-07-12
    Description: Metabolic syndromes share common pathologies with Alzheimer’s disease (AD). Adiponectin, an adipocyte-derived protein, regulates energy metabolism via its receptors, AdipoR1 and AdipoR2. To investigate the distribution of adiponectin receptors (AdipoRs) in Alzheimer’s, we examined their expression in the aged 5XFAD mouse model of AD. In age-matched wild-type mice, we observed neuronal expression of both ARs throughout the brain as well as endothelial expression of AdipoR1. The pattern of receptor expression in the aged 5XFAD brain was significantly perturbed. Here, we observed decreased neuronal expression of both ARs and decreased endothelial expression of AdipoR1, but robust expression of AdipoR2 in activated astrocytes. We also observed AdipoR2-expressing astrocytes in the dorsomedial hypothalamic and thalamic mediodorsal nuclei, suggesting the possibility that astrocytes utilise AdipoR2 signalling to fuel their activated state in the AD brain. These findings provide further evidence of a metabolic disturbance and demonstrate a potential shift in energy utilisation in the AD brain, supporting imaging studies performed in AD patients.
    Electronic ISSN: 1424-8247
    Topics: Chemistry and Pharmacology
    Published by Molecular Diversity Preservation International
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  • 7
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    Altered Brain Leptin and Leptin Receptor Expression in the 5XFAD Mouse Model of Alzheimer’s Disease (2020)
    Molecular Diversity Preservation International
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    Publication Date: 2020-11-18
    Description: Alzheimer’s disease (AD) is a complex neurodegenerative disorder characterized by the accumulation of amyloid plaques and neurofibrillary tangles. Interestingly, individuals with metabolic syndromes share some pathologies with those diagnosed with AD including neuroinflammation, insulin resistance and cognitive deficits. Leptin, an adipocyte-derived hormone, regulates metabolism, energy expenditure and satiety via its receptor, LepR. To investigate the possible involvement of leptin in AD, we examined the distribution of leptin and LepR in the brains of the 5XFAD mouse model of AD, utilizing immunofluorescent staining in young (10–12-weeks; n = 6) and old (48–52-weeks; n = 6) transgenic (Tg) mice, together with age-matched wild-type (WT) controls for both age groups (young-WT, n = 6; old-WT, n = 6). We also used double immunofluorescent staining to examine the distribution of leptin and leptin receptor expression in astrocytes. In young 5XFAD, young-WT and old-WT mice, we observed neuronal and endothelial expression of leptin and LepR throughout the brain. However, neuronal leptin and LepR expression in the old 5XFAD brain was significantly diminished. Reduced neuronal leptin and LepR expression was accompanied by plaque loading and neuroinflammation in the AD brain. A marked increase in astrocytic leptin and LepR was also observed in old 5XFAD mice compared to younger 5XFAD mice. We postulate that astrocytes may utilize LepR signalling to mediate and drive their metabolically active state when degrading amyloid in the AD brain. Overall, these findings provide evidence of impaired leptin and LepR signalling in the AD brain, supporting clinical and epidemiological studies performed in AD patients.
    Electronic ISSN: 1424-8247
    Topics: Chemistry and Pharmacology
    Published by Molecular Diversity Preservation International
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  • 8
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    A Novel Segmentation-Based Algorithm for the Quantification of Magnified Cells (2014)
    Wiley
    Details
    Publication Date: 2014-07-01
    Print ISSN: 0730-2312
    Electronic ISSN: 1097-4644
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Published by Wiley
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  • 9
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    The Astro-E/XRS Calibration Program and Results (1999)
    In:  Other Sources
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    Publication Date: 2011-08-23
    Description: XRS is the microcalorimeter X-ray detector aboard the US-Japanese ASTRO-E observatory, which is scheduled to be launched in early 2000. XRS is a high resolution spectrometer- with less than 9 eV resolution at 3 keV and better than 14 eV resolution over its bandpass ranging from about 0.3 keV to 15 keV. Here we present the results of our first calibration of the XRS instrument. We describe the methods used to extract detailed information about the detection efficiency and spectral redistribution of the instrument. We also present comparisons of simulations and real data to test our detector models.
    Keywords: Instrumentation and Photography
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  • 10
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    The Astro -E/XRS Calibration Program and Results (1999)
    In:  Other Sources
    Details
    Publication Date: 2011-08-23
    Description: XRS is the microcalorimeter X-ray detector aboard the US-Japanese ASTRO-E observatory, which is scheduled to be launched in early 2000. XRS is a high resolution spectrometer- with less than 9 eV resolution at 3 keV and better than 14 eV resolution over its bandpass ranging from about 0.3 keV to 15 keV. Here we present the results of our first calibration of the XRS instrument. We describe the methods used to extract detailed information about the detection efficiency and spectral redistribution of the instrument. We also present comparisons of simulations and real data to test our detector models
    Keywords: Astronomy
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    NASA TECHNICAL REPORTS
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