PM2.5-bound metal metabolic distribution and coupled lipid abnormality at different developmental windows

2017 ◽  
Vol 228 ◽  
pp. 354-362 ◽  
Author(s):  
Tingting Ku ◽  
Yingying Zhang ◽  
Xiaotong Ji ◽  
Guangke Li ◽  
Nan Sang
Keyword(s):  
Lipid Abnormality ◽  
Developmental Windows

scholarly journals Developmental windows of breast cancer risk provide opportunities for targeted chemoprevention

2013 ◽  
Vol 319 (11) ◽  
pp. 1671-1678 ◽  
Author(s):  
Holly A. Martinson ◽  
Traci R. Lyons ◽  
Erin D. Giles ◽  
Virginia F. Borges ◽  
Pepper Schedin
Keyword(s):  
Breast Cancer ◽  
Breast Cancer Risk ◽  
Cancer Risk ◽  
Developmental Windows

Lipid Abnormality

2001 ◽  
pp. 55-62
Author(s):  
M. Mune ◽  
H. Otani ◽  
K. Kimura
Keyword(s):  
Lipid Abnormality

Lipid abnormality, current diabetes and age affect erectile hardness: An analysis of data from complete medical checkups carried out at a single hospital

2020 ◽  
Vol 27 (4) ◽  
pp. 339-343
Author(s):  
Kimiyasu Ishikawa ◽  
Haruaki Sasaki ◽  
Satoru Tanifuji ◽  
Ippei Kurokawa ◽  
Hiroo Sugishita ◽  
...  
Keyword(s):  
Lipid Abnormality

scholarly journals Age differences in prenatal testosterone’s protective effects on disordered eating symptoms: Developmental windows of expression?

2015 ◽  
Vol 129 (1) ◽  
pp. 18-36 ◽  
Author(s):  
Kristen M. Culbert ◽  
S. Marc Breedlove ◽  
Cheryl L. Sisk ◽  
Pamela K. Keel ◽  
Michael C. Neale ◽  
...  
Keyword(s):  
Disordered Eating ◽  
Age Differences ◽  
Protective Effects ◽  
Developmental Windows ◽  
Disordered Eating Symptoms

Critical windows in development of the rodent immune system

2002 ◽  
Vol 21 (9-10) ◽  
pp. 493-498 ◽  
Author(s):  
K S Landreth
Keyword(s):  
Stem Cells ◽  
Immune System ◽  
Chemical Exposure ◽  
Anatomical Location ◽  
Hematopoietic Stem ◽  
Windows Of Vulnerability ◽  
The Impact ◽  
Timing Of Exposure ◽  
Developmental Immunotoxicity ◽  
Developmental Windows

The immune system of rodents, like that in humans, develops from a population of pluripotential hematopoietic stem cells (HSC) that are generated early in gestation from uncommitted mesenchymal stem cells in the intra-embryonic splanchnoplure surrounding the heart. This early population of HSC gives rise to all circulating blood cell lineages, including cells of the innate and acquired immune system. To access the impact of chemical exposure on the developing immune system and establish developmental windows of potential vulnerability to these exposures, it is essential to first consider the anatomical development of hematopoietic and lymphopoietic tissues and the sequence of appearance of cells that give rise to the immune system. This is particularly true in embryonic development because, after they initially appear in intra-embryonic mesenchyme early in gestation, HSC migrate through an orderly series of tissues before establishing residence in the bone marrow and thymus. The effect of exposure to chemical insults in utero, then, may differ depending on the specific timing of exposure and anatomical location of hematopoiesis. Mechanisms and consequences of developmental immunotoxicity in experimental animals will need to be considered in that context. This review presents an overview of developmental hematopoiesis and a working hypothesis of critical developmental windows of vulnerability of this developmental system to toxic insult by chemical exposure.

Epigenetics and post-transcriptional regulation of cardiovascular development

2018 ◽  
Author(s):  
Jin Yang ◽  
Pei Han ◽  
Wei Li ◽  
Ching-Pin Chang
Keyword(s):  
Heart Development ◽  
Genetic Information ◽  
Cardiovascular Development ◽  
Control Of Gene Expression ◽  
Correct Sequence ◽  
Non Coding Rnas ◽  
Combinatorial Interactions ◽  
Post Transcriptional Regulation ◽  
Rna Complexes ◽  
Developmental Windows

Cardiac organogenesis requires the control of gene expression at distinct developmental windows in order to organize morphogenetic steps in the correct sequence for heart development. This is facilitated by concerted regulation at three levels: chromatin, transcription, and post-transcriptional modifications. Epigenetic regulation at the chromatin level changes the chromatin scaffold of DNA to regulate accessibility of the DNA sequence to transcription factors for genetic activation or repression. At the genome, long non-coding RNAs work with epigenetic factors to alter the chromatin scaffold or form DNA-RNA complexes at specific genomic loci to control the transcription of genetic information. After RNA transcription, the expression of genetic information can be further modified by microRNAs. Each layer of gene regulation requires the participation of many factors, with their combinatorial interactions providing variations of genetic expression at distinct pathophysiological phases of the heart. The major functions of chromatin remodellers and non-coding RNAs are discussed.

scholarly journals Epigenetic modifications associated with in utero exposure to endocrine disrupting chemicals BPA, DDT and Pb

2019 ◽  
Vol 34 (4) ◽  
pp. 309-325 ◽  
Author(s):  
Chinonye Doris Onuzulu ◽  
Oluwakemi Anuoluwapo Rotimi ◽  
Solomon Oladapo Rotimi
Keyword(s):  
Endocrine Disruptors ◽  
Endocrine Disrupting Chemicals ◽  
Endocrine System ◽  
Environmental Chemicals ◽  
Epigenetic Mechanisms ◽  
Epigenetic Alterations ◽  
Endocrine Disrupting ◽  
Non Coding Rnas ◽  
Hormone System ◽  
Developmental Windows

Abstract Endocrine disrupting chemicals (EDCs) are xenobiotics which adversely modify the hormone system. The endocrine system is most vulnerable to assaults by endocrine disruptors during the prenatal and early development window, and effects may persist into adulthood and across generations. The prenatal stage is a period of vulnerability to environmental chemicals because the epigenome is usually reprogrammed during this period. Bisphenol A (BPA), lead (Pb), and dichlorodiphenyltrichloroethane (DDT) were chosen for critical review because they have become serious public health concerns globally, especially in Africa where they are widely used without any regulation. In this review, we introduce EDCs and describe the various modes of action of EDCs and the importance of the prenatal and developmental windows to EDC exposure. We give a brief overview of epigenetics and describe the various epigenetic mechanisms: DNA methylation, histone modifications and non-coding RNAs, and how each of them affects gene expression. We then summarize findings from previous studies on the effects of prenatal exposure to the endocrine disruptors BPA, Pb and DDT on each of the previously described epigenetic mechanisms. We also discuss how the epigenetic alterations caused by these EDCs may be related to disease processes.

Retinoic acid treatment at different developmental windows: Neurofunctional deficits and cerebellar phenotype in the rat

2008 ◽  
Vol 180 ◽  
pp. S45
Author(s):  
Domenico Belfiore ◽  
Addolorata Coluccia ◽  
Pietro Borracci ◽  
Arcangela Giustino ◽  
Antonella Bizzoca ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Acid Treatment ◽  
Retinoic Acid Treatment ◽  
Developmental Windows

scholarly journals Commonly dysregulated genes in murine APL cells

Blood ◽  
2006 ◽  
Vol 109 (3) ◽  
pp. 961-970 ◽  
Author(s):  
Wenlin Yuan ◽  
Jacqueline E. Payton ◽  
Matthew S. Holt ◽  
Daniel C. Link ◽  
Mark A. Watson ◽  
...  
Keyword(s):  
Gene Expression ◽  
Expression Patterns ◽  
Cathepsin G ◽  
Hematopoietic Progenitors ◽  
Cell Functions ◽  
Maturation In Vitro ◽  
Myeloid Development ◽  
Genetic Events ◽  
Developmental Windows

Abstract To identify genes that are commonly dysregulated in a murine model of acute promyelocytic leukemia (APL), we first defined gene expression patterns during normal murine myeloid development; serial gene expression profiling studies were performed with primary murine hematopoietic progenitors that were induced to undergo myeloid maturation in vitro with G-CSF. Many genes were reproducibly expressed in restricted developmental “windows,” suggesting a structured hierarchy of expression that is relevant for the induction of developmental fates and/or differentiated cell functions. We compared the normal myeloid developmental transcriptome with that of APL cells derived from mice expressing PML-RARα under control of the murine cathepsin G locus. While many promyelocyte-specific genes were highly expressed in all APL samples, 116 genes were reproducibly dysregulated in many independent APL samples, including Fos, Jun, Egr1, Tnf, and Vcam1. However, this set of commonly dysregulated genes was expressed normally in preleukemic, early myeloid cells from the same mouse model, suggesting that dysregulation occurs as a “downstream” event during disease progression. These studies suggest that the genetic events that lead to APL progression may converge on common pathways that are important for leukemia pathogenesis.

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