scholarly journals Animating embryos: thein totorepresentation of life

2017 ◽  
Vol 50 (3) ◽  
pp. 521-535 ◽  
Author(s):  
JANINA WELLMANN
Keyword(s):  
Developmental Biology ◽  
Systems Biology ◽  
Computational Model ◽  
Computer Model ◽  
Live Imaging ◽  
Cellular Resolution ◽  
Visualization Techniques ◽  
Over Time

AbstractWith the recent advent of systems biology, developmental biology is taking a new turn. Attempts to create a ‘digital embryo’ are prominent among systems approaches. At the heart of these systems-based endeavours, variously described as ‘in vivoimaging’, ‘live imaging’ or ‘in totorepresentation’, are visualization techniques that allow researchers to image whole, live embryos at cellular resolution over time. Ultimately, the aim of the visualizations is to build a computer model of embryogenesis. This article examines the role of such visualization techniques in the building of a computational model, focusing, in particular, on the cinematographic character of these representations. It asks how the animated representation of development may change the biological understanding of embryogenesis. By situating the animations of the digital embryo within the iconography of developmental biology, it brings to light the inextricably entwined, yet shifting, borders between the animated, the living and the computational.

The Role of Mechanical Tension in Neurons

2010 ◽  
Vol 1274 ◽  
Author(s):  
Taher Saif ◽  
Jagannathan Rajagopalan ◽  
Alireza Tofangchi
Keyword(s):  
Mechanical Response ◽  
Mechanical Forces ◽  
Active Tension ◽  
Mechanical Tension ◽  
Deformation Response ◽  
Linear Force ◽  
Tension Regulation ◽  
Over Time

AbstractWe used high resolution micromechanical force sensors to study the in vivo mechanical response of embryonic Drosophila neurons. Our experiments show that Drosophila axons have a rest tension of a few nN and respond to mechanical forces in a manner characteristic of viscoelastic solids. In response to fast externally applied stretch they show a linear force-deformation response and when the applied stretch is held constant the force in the axons relaxes to a steady state value over time. More importantly, when the tension in the axons is suddenly reduced by releasing the external force the neurons actively restore the tension, sometimes close to their resting value. Along with the recent findings of Siechen et al (Proc. Natl. Acad. Sci. USA 106, 12611 (2009)) showing a link between mechanical tension and synaptic plasticity, our observation of active tension regulation in neurons suggest an important role for mechanical forces in the functioning of neurons in vivo.

scholarly journals Role of neutrophils and α1-antitrypsin in coal- and silica-induced connective tissue breakdown

1999 ◽  
Vol 276 (2) ◽  
pp. L269-L279 ◽  
Author(s):  
K. Zay ◽  
S. Loo ◽  
C. Xie ◽  
D. V. Devine ◽  
J. Wright ◽  
...  
Keyword(s):  
Connective Tissue ◽  
Hplc Analysis ◽  
Lavage Fluid ◽  
Dust Exposure ◽  
Mineral Dusts ◽  
Methionine Residues ◽  
Over Time ◽  
Rapid Appearance

Mineral dusts produce emphysema, and administration of dust to rats results in the rapid appearance of desmosine and hydroxyproline in lavage fluid, confirming that dusts directly induce connective tissue breakdown. To examine the role of neutrophils and α1-antitrypsin (α1-AT) in this process, we instilled silica or coal into normal rats or rats that had been pretreated with antiserum against neutrophils. One day after dust exposure, lavage fluid neutrophils and desmosine and hydroxyproline levels were all elevated; treatment with antiserum against neutrophils reduced neutrophils by 75%, desmosine by 40–50%, and hydroxyproline by 25%. By 7 days, lavage fluid neutrophils and desmosine level had decreased, whereas macrophages and hydroxyproline level had increased. By ELISA analysis, lavage fluid α1-AT levels were increased four- to eightfold at both times. On Western blot, some of the α1-AT appeared as degraded fragments, and by HPLC analysis, 5–10% of the methionine residues were oxidized. At both times, lavage fluid exhibited considerably elevated serine elastase inhibitory capacity and also showed elevations in metalloelastase activity. We conclude that, in this model, connective tissue breakdown is initially driven largely by neutrophil-derived proteases and that markedly elevated levels of functional α1-AT do not prevent breakdown, thus providing in vivo support for the concept of quantum proteolysis proposed by Liou and Campbell (T. G. Liou and E. J. Campbell. Biochemistry 34: 16171–16177, 1995). Macrophage-derived proteases may be of increasing importance over time, especially in coal-treated animals.

scholarly journals Design, Assessment, and in vivo Evaluation of a Computational Model Illustrating the Role of CAV1 in CD4+ T-lymphocytes

2014 ◽  
Vol 5 ◽  
Author(s):  
Brittany D. Conroy ◽  
Tyler A. Herek ◽  
Timothy D. Shew ◽  
Matthew Latner ◽  
Joshua J. Larson ◽  
...  
Keyword(s):  
T Lymphocytes ◽  
Computational Model ◽  
In Vivo Evaluation ◽  
Design Assessment

scholarly journals STIMULUS: Noninvasive Dynamic Patterns of Neurostimulation using Spatio-Temporal Interference

2017 ◽  
Author(s):  
Jiaming Cao ◽  
Pulkit Grover
Keyword(s):  
Computational Model ◽  
Electrode Pair ◽  
Modeling Framework ◽  
Model Based ◽  
Spatio Temporal ◽  
Spatial Interference ◽  
The Brain ◽  
Over Time ◽  
Do So

AbstractUsing a systematic computational and modeling framework, we provide a novel Spatio-Temporal Interference-based stiMULation focUsing Strategy (STIMULUS) for high spatial precision noninvasive neurostimulation deep inside the brain. To do so, we first replicate the results of the recently proposed temporal interference (TI) stimulation (which was only tested in-vivo) in a computational model based on a Hodgkin-Huxley model for neurons and a model of current dispersion in the head. Using this computational model, we obtain a nontrivial extension of the 2-electrode-pair TI proposed originally to multielectrode TI (> 2 electrode pairs) that yields significantly higher spatial precision. To further improve precision, we develop STIMULUS techniques for generating spatial interference patterns in conjunction with temporal interference, and demonstrate strict and significant improvements over multielectrode TI. Finally, we utilize the adaptivity that is inherent in STIMULUS to create multisite neurostimulation patterns that can be dynamically steered over time.

Strength Retention of a New Microbial Cellulose Scaffold and Existing Collagen-Based Scaffolds After In Vivo Implantation in a Rabbit Model

2009 ◽  
Author(s):  
Michael I. Dishowitz ◽  
Miltiadis H. Zgonis ◽  
Jeremy J. Harris ◽  
Constance Ace ◽  
Louis J. Soslowsky
Keyword(s):  
Mechanical Behavior ◽  
Healing Process ◽  
Rabbit Model ◽  
In Vivo Model ◽  
Microbial Cellulose ◽  
Poor Outcomes ◽  
Over Time ◽  
Pullout Loads

Rotator cuff tendon tears often require large tensions for repair [1] and these tensions are associated with poor outcomes including rerupture [2]. To address this, repairs are often augmented with collagen-based scaffolds. Microbial cellulose, produced by A. xylinum as a laminar non-woven matrix, is another candidate for repair augmentation [3]. An ideal augmentation scaffold would shield the repair site from damaging loads as they change throughout the healing process. Although the initial mechanical properties of clinically used scaffolds have been well characterized [4–6], their mechanical behavior following implantation is not known. As a result, the role of these scaffolds throughout the healing process remains unknown. Therefore, the objective of this study is to characterize the mechanical behavior of existing collagen-based scaffolds and a new, microbial cellulose scaffold over time using an in vivo model. We hypothesize that: 1) collagen-based scaffolds will show decreased stiffness (1a) and suture pullout loads (1b) over time when compared to initial values while the microbial cellulose scaffold will not; and 2) the collagen-based scaffolds will have decreased stiffness (2a) and suture pullout loads (2b) when compared to the new, microbial cellulose scaffold at all timepoints.

scholarly journals Mir-21 Suppression Promotes Mouse Hepatocarcinogenesis

Cancers ◽  
2021 ◽  
Vol 13 (19) ◽  
pp. 4983
Author(s):  
Marta Correia de Sousa ◽  
Nicolas Calo ◽  
Cyril Sobolewski ◽  
Monika Gjorgjieva ◽  
Sophie Clément ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Mouse Liver ◽  
Potential Therapeutic Target ◽  
Stat3 Signaling ◽  
Gene And Protein Expression ◽  
Genetic Deletion ◽  
Almost All ◽  
Over Time

The microRNA 21 (miR-21) is upregulated in almost all known human cancers and is considered a highly potent oncogene and potential therapeutic target for cancer treatment. In the liver, miR-21 was reported to promote hepatic steatosis and inflammation, but whether miR-21 also drives hepatocarcinogenesis remains poorly investigated in vivo. Here we show using both carcinogen (Diethylnitrosamine, DEN) or genetically (PTEN deficiency)-induced mouse models of hepatocellular carcinoma (HCC), total or hepatocyte-specific genetic deletion of this microRNA fosters HCC development—contrasting the expected oncogenic role of miR-21. Gene and protein expression analyses of mouse liver tissues further indicate that total or hepatocyte-specific miR-21 deficiency is associated with an increased expression of oncogenes such as Cdc25a, subtle deregulations of the MAPK, HiPPO, and STAT3 signaling pathways, as well as alterations of the inflammatory/immune anti-tumoral responses in the liver. Together, our data show that miR-21 deficiency promotes a pro-tumoral microenvironment, which over time fosters HCC development via pleiotropic and complex mechanisms. These results question the current dogma of miR-21 being a potent oncomiR in the liver and call for cautiousness when considering miR-21 inhibition for therapeutic purposes in HCC.

Computational Model of the Role of Sensory Disorganization in Focal Task-Specific Dystonia

2000 ◽  
Vol 84 (5) ◽  
pp. 2458-2464 ◽  
Author(s):  
Terence D. Sanger ◽  
Michael M. Merzenich
Keyword(s):  
Computational Model ◽  
Cortical Area ◽  
Motor Behavior ◽  
Loop Transformation ◽  
Task Specificity ◽  
Abnormal Motor ◽  
Focal Task ◽  
Over Time ◽  
And Task

We present a new computational model for the development of task-specific focal dystonia. The purpose of the model is to explain how altered sensory representations can lead to abnormal motor behavior. Dystonia is described as the result of excessive gain through a sensorimotor loop. The gain is determined in part by the sensory cortical area devoted to each motor function, and behaviors that lead to abnormal increases in sensory cortical area are predicted to lead to dystonia. Properties of dystonia including muscular co-contraction, overflow movements, and task specificity are predicted by properties of a linear approximation to the loop transformation. We provide simulations of several different mechanisms that can cause the gain to exceed 1 and the motor activity to become sustained and uncontrolled. The model predicts that normal plasticity mechanisms may contribute to worsening of symptoms over time.

Enzymatic- and renal-dependent catabolism of the intestinotropic hormone glucagon-like peptide-2 in rats

2000 ◽  
Vol 278 (1) ◽  
pp. E134-E139 ◽  
Author(s):  
Wendy Tavares ◽  
Daniel J. Drucker ◽  
Patricia L. Brubaker
Keyword(s):  
Renal Clearance ◽  
Dipeptidyl Peptidase ◽  
Dipeptidyl Peptidase Iv ◽  
Intestinal Growth ◽  
No Conversion ◽  
Glucagon Like Peptide ◽  
Over Time

The intestinotropic hormone glucagon-like peptide (GLP)-2-(1—33) is cleaved in vitro to GLP-2-(3—33) by dipeptidyl peptidase IV (DP IV). To determine the importance of DP IV versus renal clearance in the regulation of circulating GLP-2-(1—33) levels in vivo, GLP-2-(1—33) or the DP IV-resistant analog [Gly2]GLP-2 was injected in normal or DP IV-negative rats and assayed by HPLC and RIA. Normal rats showed a steady degradation of GLP-2-(1—33) to GLP-2-(3—33) over time, whereas little or no conversion was detected for GLP-2-(1—33) in DP IV-negative rats and for [Gly2]GLP-2 in normal rats. To determine the role of the kidney in clearance of GLP-2-(1—33) from the circulation, normal rats were bilaterally nephrectomized, and plasma immunoreactive GLP-2 levels were measured. The slope of the disappearance curves for both GLP-2-(1—33) and [Gly2]GLP-2 were significantly reduced in nephrectomized compared with nonnephrectomized rats ( P < 0.01). In contrast to both GLP-2-(1—33) and [Gly2]GLP-2, GLP-2-(3—33) did not stimulate intestinal growth in a murine assay in vivo. Thus the intestinotropic actions of GLP-2-(1—33) are determined both by the actions of DP IV and by the kidney in vivo in the rat.

Mitochondrial matrix calcium ions regulate energy production in myocardium: A cytochemical study

1990 ◽  
Vol 48 (2) ◽  
pp. 166-167
Author(s):  
W.A. Jacob ◽  
R. Hertsens ◽  
A. Van Bogaert ◽  
M. De Smet
Keyword(s):  
Energy Metabolism ◽  
Calcium Ions ◽  
Energy Production ◽  
Regulation Of Respiration ◽  
Free Calcium ◽  
Mitochondrial Matrix ◽  
Cytochemical Study ◽  
Nmr Techniques

In the past most studies of the control of energy metabolism focus on the role of the phosphorylation potential ATP/ADP.Pi on the regulation of respiration. Studies using NMR techniques have demonstrated that the concentrations of these compounds for oxidation phosphorylation do not change appreciably throughout the cardiac cycle and during increases in cardiac work. Hence regulation of energy production by calcium ions, present in the mitochondrial matrix, has been the object of a number of recent studies.Three exclusively intramitochondnal dehydrogenases are key enzymes for the regulation of oxidative metabolism. They are activated by calcium ions in the low micromolar range. Since, however, earlier estimates of the intramitochondnal calcium, based on equilibrium thermodynamic considerations, were in the millimolar range, a physiological correlation was not evident. The introduction of calcium-sensitive probes fura-2 and indo-1 made monitoring of free calcium during changing energy metabolism possible. These studies were performed on isolated mitochondria and extrapolation to the in vivo situation is more or less speculative.

Meiotic CENP-C is a shepherd: bridging the space between the centromere and the kinetochore in time and space

2020 ◽  
Vol 64 (2) ◽  
pp. 251-261
Author(s):  
Jessica E. Fellmeth ◽  
Kim S. McKim
Keyword(s):  
Chromosome Segregation ◽  
New Technologies ◽  
Early Prophase ◽  
Unique Role ◽  
Kinetochore Assembly ◽  
M Phase ◽  
In Vivo Analysis ◽  
Meiosis I

Abstract While many of the proteins involved in the mitotic centromere and kinetochore are conserved in meiosis, they often gain a novel function due to the unique needs of homolog segregation during meiosis I (MI). CENP-C is a critical component of the centromere for kinetochore assembly in mitosis. Recent work, however, has highlighted the unique features of meiotic CENP-C. Centromere establishment and stability require CENP-C loading at the centromere for CENP-A function. Pre-meiotic loading of proteins necessary for homolog recombination as well as cohesion also rely on CENP-C, as do the main scaffolding components of the kinetochore. Much of this work relies on new technologies that enable in vivo analysis of meiosis like never before. Here, we strive to highlight the unique role of this highly conserved centromere protein that loads on to centromeres prior to M-phase onset, but continues to perform critical functions through chromosome segregation. CENP-C is not merely a structural link between the centromere and the kinetochore, but also a functional one joining the processes of early prophase homolog synapsis to late metaphase kinetochore assembly and signaling.

Sign in / Sign up

Export Citation Format

Share Document