The mechanistic basis of discrete-time population models: The role of resource partitioning and spatial aggregation

2010 ◽  
Vol 77 (3) ◽  
pp. 213-218 ◽  
Author(s):  
Masahiro Anazawa
Keyword(s):  
Discrete Time ◽  
Resource Partitioning ◽  
Population Models ◽  
Spatial Aggregation ◽  
Mechanistic Basis

scholarly journals Alleviation of carbon tetrachloride-induced hepatocellular damage and oxidative stress with a leaf extract of Glyphae brevis (Tiliaceae)

2018 ◽  
Vol 29 (6) ◽  
pp. 609-619 ◽  
Author(s):  
Lucky Legbosi Nwidu ◽  
Yibala I. Oboma ◽  
Ekramy Elmorsy ◽  
Wayne Grant Carter
Keyword(s):  
Carbon Tetrachloride ◽  
Leaf Extract ◽  
Protective Role ◽  
Lipid Peroxidation Product ◽  
Hematological Indices ◽  
Hepatocellular Damage ◽  
Antioxidant Parameters ◽  
Mechanistic Basis ◽  
Histopathological Studies

Abstract Background Glyphae brevis leaf is reported in ethnomedicine as a treatment for hepatitis and jaundice; however, no studies have hitherto investigated the mechanistic basis of these claims. Methods A hepato-protective role of G. brevis hydromethanolic (GBH) leaf extract was established against carbon tetrachloride (CCl4)-induced hepatotoxicity. Twenty-four hours after a CCl4 challenge, rats were sacrificed and serum hematological indices, lipid profile, and biochemical parameters were determined. The antioxidant enzymes parameters (glutathione, catalase, and superoxide dismutase) and lipid peroxidation product (thiobarbituric reactive substances) levels in liver homogenates were evaluated. Changes in the liver cyto-architecture of different treatment groups were also investigated. Results The GBH extract produced no significant impact on weight and hematological indices. Intoxication with CCl4 significantly (p<0.001–0.05) increased total cholesterol (TC) and low-density lipoproteins (LDL) compared with control rats. Pretreatment with GBH leaf extract significantly reduced triglycerides, TC, and LDL to approaching control levels (p<0.001–0.05). The GBH leaf extract significantly alleviated CCl4-induced elevation of alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and the CCl4-induced depression of total protein, and albumin. Liver antioxidant parameters were significantly increased in plant extract-treated rats, and this antagonized the pro-oxidant effect of CCl4. Histopathological studies also supported a hepato-protective effect of GBH. Collectively, the GBH leaf extract alleviated the CCl4-induced hepatotoxicity through improvement of innate antioxidant enzyme levels and lipid metabolism and stabilized the hepatocyte cyto-architecture of intoxicated rats. Conclusions This study establishes the ethnomedicinal role of G. brevis leaf in hepatitis and the mechanistic basis of hepato-protection against CCl4-induced hepatotoxicity.

scholarly journals Inhibition of mTOR during a postnatal critical sensitive window rescues deficits in GABAergic PV cell connectivity and social behavior caused by loss of TSC1

2020 ◽  
Author(s):  
Mayukh Choudhury ◽  
Clara A. Amegandjin ◽  
Vidya Jadhav ◽  
Josianne Nunes Carriço ◽  
Ariane Quintal ◽  
...  
Keyword(s):  
Social Behavior ◽  
Time Course ◽  
Cell Types ◽  
Developmental Time ◽  
Adult Mice ◽  
Mtorc1 Signaling ◽  
Pv Cell ◽  
Mechanistic Basis

ABSTRACTMutations in regulators of the Mechanistic Target Of Rapamycin Complex 1 (mTORC1), such as Tsc1/2, lead to neurodevelopmental disorders associated with autism, intellectual disabilities and epilepsy. Whereas the effects of mTORC1 signaling dysfunction within diverse cell types are likely critical for the onset of the diverse neurological symptoms associated with mutations in mTORC1 regulators, they are not well understood. In particular, the effects of mTORC1 dys-regulation in specific types of inhibitory interneurons are unclear.Here, we showed that Tsc1 haploinsufficiency in parvalbumin (PV)-positive GABAergic interneurons either in cortical organotypic cultures or in vivo caused a premature increase in their perisomatic innervations, followed by a striking loss in adult mice. This effects were accompanied by alterations of AMPK-dependent autophagy in pre-adolescent but not adult mice. PV cell-restricted Tsc1 mutant mice showed deficits in social behavior. Treatment with the mTOR inhibitor Rapamycin restricted to the third postnatal week was sufficient to permanently rescue deficits in both PV cell innervation and social behavior in adult conditional haploinsufficient mice. All together, these findings identify a novel role of Tsc1-mTORC1 signaling in the regulation of the developmental time course and maintenance of cortical PV cell connectivity and provide a mechanistic basis for the targeted rescue of autism-related behaviors in disorders associated with deregulated mTORC1 signaling.

Niche Occupancy and the Relative Role of Micro-Habitat and Diet in Resource Partitioning Among Pond Dwelling Tadpoles

2009 ◽  
Vol 4 (3) ◽  
pp. 275-285 ◽  
Author(s):  
Vitor H. M. Do Prado ◽  
Mariluce G. Fonseca ◽  
Fernanda V. R. De Almeida ◽  
Orlando Necchi Junior ◽  
Denise De C. Rossa-Feres
Keyword(s):  
Resource Partitioning ◽  
Relative Role

scholarly journals Protein kinase CK2: structure, regulation and role in cellular decisions of life and death

2003 ◽  
Vol 369 (1) ◽  
pp. 1-15 ◽  
Author(s):  
David W. LITCHFIELD
Keyword(s):  
Protein Kinase ◽  
Protein Kinase Ck2 ◽  
Current Knowledge ◽  
Cellular Functions ◽  
Serine Threonine Kinase ◽  
Life And Death ◽  
Dual Specificity ◽  
Mechanistic Basis ◽  
Kinase Ck2

Protein kinase CK2 ('casein kinase II') has traditionally been classified as a messenger-independent protein serine/threonine kinase that is typically found in tetrameric complexes consisting of two catalytic (α and/or α′) subunits and two regulatory β subunits. Accumulated biochemical and genetic evidence indicates that CK2 has a vast array of candidate physiological targets and participates in a complex series of cellular functions, including the maintenance of cell viability. This review summarizes current knowledge of the structural and enzymic features of CK2, and discusses advances that challenge traditional views of this enzyme. For example, the recent demonstrations that individual CK2 subunits exist outside tetrameric complexes and that CK2 displays dual-specificity kinase activity raises new prospects for the precise elucidation of its regulation and cellular functions. This review also discusses a number of the mechanisms that contribute to the regulation of CK2 in cells, and will highlight emerging insights into the role of CK2 in cellular decisions of life and death. In this latter respect, recent evidence suggests that CK2 can exert an anti-apoptotic role by protecting regulatory proteins from caspase-mediated degradation. The mechanistic basis of the observation that CK2 is essential for viability may reside in part in this ability to protect cellular proteins from caspase action. Furthermore, this anti-apoptotic function of CK2 may contribute to its ability to participate in transformation and tumorigenesis.

scholarly journals New Frontiers: Approaches to Understand the Mechanistic Basis of Renal Toxicity

2018 ◽  
Vol 46 (8) ◽  
pp. 1002-1005
Author(s):  
Mary B. Nabity ◽  
Joseph W. Polli ◽  
Vishal Vaidya ◽  
Andrzej Krolewski ◽  
Warren E. Glaab
Keyword(s):  
Renal Toxicity ◽  
Kidney Injury ◽  
Scientific Session ◽  
Diabetic Patients ◽  
Drug Induced ◽  
Research Areas ◽  
Novel Biomarkers ◽  
Mechanistic Basis ◽  
New Research

A scientific session entitled “New Frontiers: Approaches to Understand the Mechanistic Basis of Renal Toxicity” focused on novel biomarkers to monitor kidney injury both preclinically and clinically, as well as providing mechanistic insight of the induced injury. Further, the role and impact of kidney membrane transporters in drug-induced kidney toxicity provided additional considerations when understanding kidney injury and the complex role of drug transporters in either sensitivity or resistance to drug-induced injury. The onset of nephropathy in diabetic patients was also presented, focusing on the quest to discover novel biomarkers that would differentiate diabetic populations more susceptible to nephropathy and renal failure. The session highlighted exciting new research areas and novel biomarkers that will enhance our understanding of kidney injury and provide tools for ensuring patient safety clinically.

scholarly journals A61 Large RNA genomes: Is RNA polymerase fidelity enough?

2019 ◽  
Vol 5 (Supplement_1) ◽  
Author(s):  
F Ferron ◽  
B Canard
Keyword(s):  
Rna Polymerase ◽  
Rna Synthesis ◽  
Rna Virus ◽  
Virus Genome ◽  
Gene Products ◽  
Dna Viruses ◽  
Viral Rdrp ◽  
Polymerase Fidelity ◽  
Mechanistic Basis

Abstract Large-genome Nidoviruses and Nidovirus-like viruses reside at the current boundary of largest RNA genome sizes. They code for an unusually large number of gene products matching that of small DNA viruses (e.g. DNA bacteriophages). The order of appearance and distribution of enzyme genes along various virus families (e.g. helicase and ExoN) may be seen as an evolutionary marker in these large RNA genomes lying at the genome size boundary. A positive correlation exists between (+)RNA virus genome sizes and the presence of the RNA helicase and the ExoN domains. Although the mechanistic basis of the presence of the helicase is still unclear, the role of the ExoN activity has been linked to the existence of an RNA synthesis proofreading system. In large Nidovirales, ExoN is bound to a processive replicative RNA-dependent RNA polymerase (RdRp) and corrects mismatched bases during viral RNA synthesis. Over the last decade, a view of the overall process has been refined in Coronaviruses, and in particular in our lab (Ferron et al., PNAS, 2018). We have identified genetic markers of large RNA genomes that we wish to use to data-mine currently existing metagenomic datasets. We have also initiated a collaboration to sequence and explore new viromes that will be searched according to these criteria. Likewise, we have a collection of purified viral RdRps that are currently being used to generate RNA synthesis products that will be compared to existing NGS datasets of cognate viruses. We will be able to have an idea about how much genetic diversity is possibly achievable by viral RdRp (‘tunable fidelity’) versus the detectable diversity (i.e. after selection in the infected cell) that is actually produced.

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