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  • Book
    Dayong Wang.
    Summary: This book introduces readers to intestinal and epidermal barriers, and to toxicity induction of environmental toxicants or stresses in the intestine, epidermis, neurons, muscle, and reproductive organs in Caenorhabditis elegans. In addition, it discusses the protective responses of various organs and nematodes' avoidance behaviour with regard to environmental toxicants or stresses. The intestinal, epidermal, neuronal, and germline signalling pathways required for the regulation of toxicity of environmental toxicants or stresses are also introduced and discussed. As a classic model animal with well-described genetic and developmental backgrounds, the nematode Caenorhabditis elegans has been successfully and widely used in both toxicity assessments and toxicological studies on various environmental toxicants and stresses. Once exposure to certain environmental toxicants has occurred, the toxicants can enter into the primary targeted organs (such as intestinal cells), and even be translocated into secondary targeted organs (such as reproductive organs and neurons). Based on related available data, this book provides a systematic understanding of target organ toxicology in C. elegans.

    Contents:
    Intro; Preface; Contents;
    Chapter 1: Protective Responses of Different Organs to Environmental Toxicants or Stresses; 1.1 Introduction; 1.2 Protective Responses to Environmental Toxicants or Stresses in the Intestine; 1.2.1 Superoxide Dismutase (SOD) Proteins; 1.2.2 MTL-1 and MTL-2; 1.2.3 Heat Shock Proteins (HSPs); 1.2.4 PMK-1, SKN-1/Nrf, and GST-4; 1.2.5 Transcriptional Factor DAF-16; 1.2.6 Antimicrobial Proteins; 1.2.7 Mitochondrial Unfolded Protein Response (UPR); 1.2.8 Endoplasmic Reticulum (ER) UPR; 1.2.9 Autophagy 1.3 Protective Responses to Environmental Toxicants or Stresses in Epidermis1.3.1 Antimicrobial Proteins; 1.3.2 Autophagy; 1.4 Protective Responses to Environmental Toxicants or Stresses in Neurons; 1.4.1 SKN-1/Nrf; 1.4.2 JNK Signaling; 1.4.3 ERK Signaling; 1.4.4 Antimicrobial Proteins; 1.4.5 Autophagy; 1.5 Protective Responses to Environmental Toxicants or Stresses in Muscle; 1.6 Perspectives; References;
    Chapter 2: Avoidance Behavior of Nematodes to Environmental Toxicants or Stresses; 2.1 Introduction 2.2 Neurons Involved in the Regulation of Avoidance Behavior to Environmental Toxicants or Stress2.2.1 ASH Sensory Neurons; 2.2.1.1 Involvement of ASH Sensory Neurons in Response to Environmental Toxicants or Stresses; 2.2.1.2 Molecular Basis for ASH Sensory Neurons in Response to Environmental Toxicants or Stresses; 2.2.1.2.1 G Proteins; 2.2.1.2.2 Seven-Transmembrane Protein DCAR-1; 2.2.1.2.3 Neurotransmitter Signals; 2.2.2 ADL Sensory Neurons; 2.2.2.1 Involvement of ADL Sensory Neurons in Response to Environmental Toxicants or Stresses 2.2.2.2 Molecular Basis for ADL Sensory Neurons in Response to Environmental Toxicants or Stresses2.2.3 ASK Sensory Neurons; 2.2.4 ASJ Sensory Neurons; 2.2.4.1 Involvement of ASJ Sensory Neurons in Response to Environmental Toxicants or Stresses; 2.2.4.2 Molecular Basis for ASJ Sensory Neurons in Response to Environmental Toxicants or Stresses; 2.2.5 ADF Sensory Neurons; 2.2.6 ASI Sensory Neurons; 2.2.7 AWB Sensory Neurons; 2.2.8 AWC Sensory Neurons; 2.2.9 BAG Sensory Neurons; 2.2.9.1 Involvement of BAG Sensory Neurons in Response to Environmental Toxicants or Stresses 2.2.9.2 Molecular Basis for BAG Sensory Neurons in Response to Environmental Toxicants or Stresses2.2.10 OLL Sensory Neurons; 2.2.11 Interneurons; 2.3 Neuronal Circuit for the Avoidance Behavior to Environmental Toxicants or Stresses and the Underlying Molecular Basis; 2.3.1 ASI-ADF-ASH and ASH-RIC-ASI Neuronal Circuits; 2.3.1.1 ASI-ADF-ASH Neuronal Circuit; 2.3.1.2 ASH-RIC-ASI Neuronal Circuit; 2.3.1.3 Cross-Inhibitory Neural Circuitry Between ASHs and ASIs; 2.3.2 ADL-AIB Neuronal Circuit; 2.3.3 ASJ-RIM/RIC Neuronal Circuit; 2.3.4 AWB-AIZ/RMG Neuronal Circuit; 2.3.5 OLL-RMG Neuronal Circuit
    Digital Access Springer 2019
  • Article
    Hirst BH, Reed JD, Shaw B, Coy DH, Schally AV.
    Acta Hepatogastroenterol (Stuttg). 1978 Jun;25(3):208-12.
    Somatostatin inhibition of gastric acid and pepsin secretion stimulated by insulin-hypoglycaemia was quantified in six conscious cats prepared with cannulated gastric fistulae. Somatostatin 0.5-5 microgram kg-1h-1 produced a dose dependent reduction of both acid and pepsin secretions stimulated by insulin 0.2 u kg-1h-1. The doses of somatostatin which produced 50% inhibition of pepsin and acid secretions (ID50) were not significantly different (0.70 +/- 0.16 and 0.93 +/- 0.11 microgram kg-1h-1 respectively). The slope of the calculated correlation line relating % inhibition of pepsin and % inhibition of acid is within experimental error of unity indicating equality of action of somatostatin on insulin-stimulated acid and pepsin secretion. The results indicate that somatostatin is a more potent inhibitor of insulin 0.2 u kg-1h-1 stimulated acid secretion than pentagastrin 8 microgram kg-1h-1 stimulated acid secretion, but is a more potent inhibitor of pentagastrin--than insulin--stimulated pepsin secretion. As insulin stimulates less acid and more pepsin secretion than pentagastrin, the differences in sensitivities to somatostatin of these secretions produced by the two stimulants is thought to be a result of the different absolute amounts of secretion produced by the stimulants.
    Digital Access Access Options