Application of Brunauer–Emmett–Teller (BET) theory and the Guggenheim–Anderson–de Boer (GAB) equation for concentration-dependent, non-saturable cell–cell interaction dose-responses

2020 ◽  
Vol 47 (6) ◽  
pp. 561-572
Author(s):  
Van Anh Nguyen ◽  
Murali Ramanathan
Cells ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 274
Author(s):  
Matthew Antel ◽  
Mayu Inaba

The Drosophila ovary offers a suitable model system to study the mechanisms that orchestrate diverse cellular processes. Oogenesis starts from asymmetric stem cell division, proper differentiation and the production of fully patterned oocytes equipped with all the maternal information required for embryogenesis. Spatial and temporal regulation of cell-cell interaction is particularly important to fulfill accurate biological outcomes at each step of oocyte development. Progress has been made in understanding diverse cell physiological regulation of signaling. Here we review the roles of specialized cellular machinery in cell-cell communication in different stages of oogenesis.


2018 ◽  
Vol 115 (48) ◽  
pp. 12112-12117 ◽  
Author(s):  
Rebekka E. Breier ◽  
Cristian C. Lalescu ◽  
Devin Waas ◽  
Michael Wilczek ◽  
Marco G. Mazza

Phytoplankton often encounter turbulence in their habitat. As most toxic phytoplankton species are motile, resolving the interplay of motility and turbulence has fundamental repercussions on our understanding of their own ecology and of the entire ecosystems they inhabit. The spatial distribution of motile phytoplankton cells exhibits patchiness at distances of decimeter to millimeter scales for numerous species with different motility strategies. The explanation of this general phenomenon remains challenging. Furthermore, hydrodynamic cell–cell interactions, which grow more relevant as the density in the patches increases, have been so far ignored. Here, we combine particle simulations and continuum theory to study the emergence of patchiness in motile microorganisms in three dimensions. By addressing the combined effects of motility, cell–cell interaction, and turbulent flow conditions, we uncover a general mechanism: The coupling of cell–cell interactions to the turbulent dynamics favors the formation of dense patches. Identification of the important length and time scales, independent from the motility mode, allows us to elucidate a general physical mechanism underpinning the emergence of patchiness. Our results shed light on the dynamical characteristics necessary for the formation of patchiness and complement current efforts to unravel planktonic ecological interactions.


1990 ◽  
Vol 130 (2) ◽  
pp. 320-328 ◽  
Author(s):  
Marja-Liisa Lindsberg ◽  
Mark Brunswick ◽  
Achsah Keegan ◽  
James J. Mond
Keyword(s):  
B Cells ◽  

Endocrinology ◽  
2006 ◽  
Vol 147 (3) ◽  
pp. 1166-1174 ◽  
Author(s):  
Sergio R. Ojeda ◽  
Alejandro Lomniczi ◽  
Claudio Mastronardi ◽  
Sabine Heger ◽  
Christian Roth ◽  
...  

The initiation of mammalian puberty requires an increase in pulsatile release of GnRH from the hypothalamus. This increase is brought about by coordinated changes in transsynaptic and glial-neuronal communication. As the neuronal and glial excitatory inputs to the GnRH neuronal network increase, the transsynaptic inhibitory tone decreases, leading to the pubertal activation of GnRH secretion. The excitatory neuronal systems most prevalently involved in this process use glutamate and the peptide kisspeptin for neurotransmission/neuromodulation, whereas the most important inhibitory inputs are provided by γ-aminobutyric acid (GABA)ergic and opiatergic neurons. Glial cells, on the other hand, facilitate GnRH secretion via growth factor-dependent cell-cell signaling. Coordination of this regulatory neuronal-glial network may require a hierarchical arrangement. One level of coordination appears to be provided by a host of unrelated genes encoding proteins required for cell-cell communication. A second, but overlapping, level might be provided by a second tier of genes engaged in specific cell functions required for productive cell-cell interaction. A third and higher level of control involves the transcriptional regulation of these subordinate genes by a handful of upper echelon genes that, operating within the different neuronal and glial subsets required for the initiation of the pubertal process, sustain the functional integration of the network. The existence of functionally connected genes controlling the pubertal process is consistent with the concept that puberty is under genetic control and that the genetic underpinnings of both normal and deranged puberty are polygenic rather than specified by a single gene. The availability of improved high-throughput techniques and computational methods for global analysis of mRNAs and proteins will allow us to not only initiate the systematic identification of the different components of this neuroendocrine network but also to define their functional interactions.


eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Robert J Tetley ◽  
Guy B Blanchard ◽  
Alexander G Fletcher ◽  
Richard J Adams ◽  
Bénédicte Sanson

Convergence and extension movements elongate tissues during development. Drosophila germ-band extension (GBE) is one example, which requires active cell rearrangements driven by Myosin II planar polarisation. Here, we develop novel computational methods to analyse the spatiotemporal dynamics of Myosin II during GBE, at the scale of the tissue. We show that initial Myosin II bipolar cell polarization gives way to unipolar enrichment at parasegmental boundaries and two further boundaries within each parasegment, concomitant with a doubling of cell number as the tissue elongates. These boundaries are the primary sites of cell intercalation, behaving as mechanical barriers and providing a mechanism for how cells remain ordered during GBE. Enrichment at parasegment boundaries during GBE is independent of Wingless signaling, suggesting pair-rule gene control. Our results are consistent with recent work showing that a combinatorial code of Toll-like receptors downstream of pair-rule genes contributes to Myosin II polarization via local cell-cell interactions. We propose an updated cell-cell interaction model for Myosin II polarization that we tested in a vertex-based simulation.


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