Time-Lapse Imaging of Necrosis

2013 ◽  
pp. 17-29 ◽  
Author(s):  
Fredrik Wållberg ◽  
Tencho Tenev ◽  
Pascal Meier
Keyword(s):  
Time Lapse ◽  
Time Lapse Imaging

Cleavage of Human Embryos: Options and Diversity

Acta Naturae ◽  
2016 ◽  
Vol 8 (3) ◽  
pp. 88-96
Author(s):  
Yu. K. Doronin ◽  
I. V. Senechkin ◽  
L. V. Hilkevich ◽  
M. A. Kurcer
Keyword(s):  
Time Lapse ◽  
Reproductive Technologies ◽  
Human Embryos ◽  
Imaging Data ◽  
Noninvasive Methods ◽  
Topographic Features ◽  
Time Parameters ◽  
Embryo Cleavage ◽  
Time Lapse Imaging ◽  
Developmental Dynamics

In order to estimate the diversity of embryo cleavage relatives to embryo progress (blastocyst formation), time-lapse imaging data of preimplantation human embryo development were used. This retrospective study is focused on the topographic features and time parameters of the cleavages, with particular emphasis on the lengths of cleavage cycles and the genealogy of blastomeres in 2- to 8-cell human embryos. We have found that all 4-cell human embryos have four developmental variants that are based on the sequence of appearance and orientation of cleavage planes during embryo cleavage from 2 to 4 blastomeres. Each variant of cleavage shows a strong correlation with further developmental dynamics of the embryos (different cleavage cycle characteristics as well as lengths of blastomere cycles). An analysis of the sequence of human blastomere divisions allowed us to postulate that the effects of zygotic determinants are eliminated as a result of cleavage, and that, thereafter, blastomeres acquire the ability of own syntheses, regulation, polarization, formation of functional contacts, and, finally, of specific differentiation. This data on the early development of human embryos obtained using noninvasive methods complements and extend our understanding of the embryogenesis of eutherian mammals and may be applied in the practice of reproductive technologies.

scholarly journals Evaluating the utility of time-lapse imaging in the estimation of post-mortem interval: An Australian case study

2019 ◽  
Vol 1 ◽  
pp. 204-210 ◽  
Author(s):  
Alyson Wilson ◽  
Stanley Serafin ◽  
Dilan Seckiner ◽  
Rachel Berry ◽  
Xanthé Mallett
Keyword(s):  
Time Lapse ◽  
Post Mortem ◽  
Post Mortem Interval ◽  
Australian Case ◽  
Time Lapse Imaging

scholarly journals Time-lapse imaging of CO2 migration within near-surface sediments during a controlled sub-seabed release experiment

2021 ◽  
Vol 109 ◽  
pp. 103363
Author(s):  
Ben Roche ◽  
Jonathan M. Bull ◽  
Hector Marin-Moreno ◽  
Timothy G. Leighton ◽  
Ismael H. Falcon-Suarez ◽  
...  
Keyword(s):  
Surface Sediments ◽  
Time Lapse ◽  
Near Surface ◽  
Release Experiment ◽  
Time Lapse Imaging

Segmentation and Track-Analysis in Time-Lapse Imaging of Bacteria

2016 ◽  
Vol 10 (1) ◽  
pp. 174-184 ◽  
Author(s):  
Sajith Kecheril Sadanandan ◽  
Ozden Baltekin ◽  
Klas E. G. Magnusson ◽  
Alexis Boucharin ◽  
Petter Ranefall ◽  
...  
Keyword(s):  
Time Lapse ◽  
Time Lapse Imaging ◽  
Track Analysis

scholarly journals Analysis of Ca2+ response of osteocyte network by three-dimensional time-lapse imaging in living bone

2017 ◽  
Vol 36 (5) ◽  
pp. 519-528 ◽  
Author(s):  
Tomoyo Tanaka ◽  
Mitsuhiro Hoshijima ◽  
Junko Sunaga ◽  
Takashi Nishida ◽  
Mana Hashimoto ◽  
...  
Keyword(s):  
Three Dimensional ◽  
Time Lapse ◽  
Living Bone ◽  
Time Lapse Imaging

scholarly journals Cell cycle inertia underlies a bifurcation in cell fates after DNA damage

2021 ◽  
Vol 7 (3) ◽  
pp. eabe3882
Author(s):  
Jenny F. Nathans ◽  
James A. Cornwell ◽  
Marwa M. Afifi ◽  
Debasish Paul ◽  
Steven D. Cappell
Keyword(s):  
Dna Damage ◽  
Dna Damage Response ◽  
Cell Tracking ◽  
Time Lapse ◽  
S Phase ◽  
Cdk Inhibitor ◽  
Cyclin Dependent Kinase ◽  
Cell Fates ◽  
Damage Response ◽  
Time Lapse Imaging

The G1-S checkpoint is thought to prevent cells with damaged DNA from entering S phase and replicating their DNA and efficiently arrests cells at the G1-S transition. Here, using time-lapse imaging and single-cell tracking, we instead find that DNA damage leads to highly variable and divergent fate outcomes. Contrary to the textbook model that cells arrest at the G1-S transition, cells triggering the DNA damage checkpoint in G1 phase route back to quiescence, and this cellular rerouting can be initiated at any point in G1 phase. Furthermore, we find that most of the cells receiving damage in G1 phase actually fail to arrest and proceed through the G1-S transition due to persistent cyclin-dependent kinase (CDK) activity in the interval between DNA damage and induction of the CDK inhibitor p21. These observations necessitate a revised model of DNA damage response in G1 phase and indicate that cells have a G1 checkpoint.

scholarly journals Proteins P24 and P41 Function in the Regulation of Terminal-Organelle Development and Gliding Motility in Mycoplasma pneumoniae

2007 ◽  
Vol 189 (20) ◽  
pp. 7442-7449 ◽  
Author(s):  
Benjamin M. Hasselbring ◽  
Duncan C. Krause
Keyword(s):  
Cell Division ◽  
Mycoplasma Pneumoniae ◽  
Fluorescent Protein ◽  
Time Lapse ◽  
Gliding Motility ◽  
Atypical Pneumonia ◽  
Reading Frame ◽  
Spatial Positioning ◽  
Time Lapse Imaging ◽  
Gliding Mechanism

ABSTRACT Mycoplasma pneumoniae is a major cause of bronchitis and atypical pneumonia in humans. This cell wall-less bacterium has a complex terminal organelle that functions in cytadherence and gliding motility. The gliding mechanism is unknown but is coordinated with terminal-organelle development during cell division. Disruption of M. pneumoniae open reading frame MPN311 results in loss of protein P41 and downstream gene product P24. P41 localizes to the base of the terminal organelle and is required to anchor the terminal organelle to the cell body, but during cell division, MPN311 insertion mutants also fail to properly regulate nascent terminal-organelle development spatially or gliding activity temporally. We measured gliding velocity and frequency and used fluorescent protein fusions and time-lapse imaging to assess the roles of P41 and P24 individually in terminal-organelle development and gliding function. P41 was necessary for normal gliding velocity and proper spatial positioning of new terminal organelles, while P24 was required for gliding frequency and new terminal-organelle formation at wild-type rates. However, P41 was essential for P24 function, and in the absence of P41, P24 exhibited a dynamic localization pattern. Finally, protein P28 requires P41 for stability, but analysis of a P28− mutant established that the MPN311 mutant phenotype was not a function of loss of P28.

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