Tissue Relaxation

Breast MRI ◽  
2008 ◽  
pp. 19-29 ◽  
Keyword(s):  
NeuroImage ◽  
2019 ◽  
Vol 186 ◽  
pp. 782-793 ◽  
Author(s):  
Yong Chen ◽  
Meng-Hsiang Chen ◽  
Kristine R. Baluyot ◽  
Taylor M. Potts ◽  
Jordan Jimenez ◽  
...  

2021 ◽  
Author(s):  
Hanqing Guo ◽  
Michael Swan ◽  
Shicheng Huang ◽  
Bing He

Apical constriction driven by non-muscle myosin II (″myosin″) provides a well-conserved mechanism to mediate epithelial folding. It remains unclear how contractile forces near the apical surface of a cell sheet drive out-of-plane bending of the sheet and whether myosin contractility is required throughout folding. By optogenetic-mediated acute inhibition of myosin, we find that during Drosophila mesoderm invagination, myosin contractility is critical to prevent tissue relaxation during the early, ″priming″ stage of folding but is dispensable for the actual folding step after the tissue passes through a stereotyped transitional configuration, suggesting that the mesoderm is mechanically bistable during gastrulation. Combining computer modeling and experimental measurements, we show that the observed mechanical bistability arises from an in-plane compression from the surrounding ectoderm, which promotes mesoderm invagination by facilitating a buckling transition. Our results indicate that Drosophila mesoderm invagination requires a joint action of local apical constriction and global in-plane compression to trigger epithelial buckling.


Author(s):  
T Alja'afreh

This paper develops a mechatronic grasper that can be used to investigate a preliminary experiment of a simple model-independent approach to control soft-tissue grasping based on, first, measurement of the total tangential grasp force and, second, discrimination of relaxation and frictional forces by imposing a limited basis set of grasper motions. The main motivation for this work is that tissue grasping is an important component of surgical procedures. However, there is a major criterion which should be achieved: maintaining grasp stability while avoiding damage due to excessive grip force. Thus, the automation of grasping force control requires a controller to apply grasping forces just sufficient to maintain grasp stability. This task is complicated by the serially connected dynamics of grasp friction and tissue relaxation.


2013 ◽  
Vol 67 (3-4) ◽  
pp. 245-257
Author(s):  
Slavoljub Jovic ◽  
Jelka Stevanovic ◽  
Suncica Borozan ◽  
Blagoje Dimitrijevic ◽  
Svetlana Fister ◽  
...  

In living sistems synthesis of nitric oxide occurs during metabolism from Larginin, nitrite and ascorbate. Being very significant carrier of information within numerous both physiological and pathological proceses in mammals' organisms, nitric oxid could possibly be useful as well as harmful. Nitric oxide synthesis is adjuvant in a healthy organism because it represents the basic molecule for understanding numerous processes in neurology, psychology, immunology and varios related fields. In other words, nitric oxide participate in number of physiological processes, such as: transmission of nerve signals (neurotransmitter role), regulation of smooth muscle tissue relaxation (eg. vasodilatation), peristaltic movements, immunomodulation, mastocyte activation, development of inflammatory response, apoptosis regulation, angiogenesis and glucose metabolism, normal heart functioning and antioxidation role. Besides being useful, nitric oxide can be harmful as well, because it has one unpaired electron, so consequently it is susceptible to oxidation becoming a stable free radical. Being such, it reacts quickly with superoxide-anion radical, givind at first an extremely reactive peroxinitrite anion, and subsequently peroxidnitrite acid. This acid is very dangerous causing thiol groups oxidation, tyrosine and phenylalanine nitrosylation, lipid oxidation, DNK chain splitting, nitrification and nucleic bases deamination. These damages of macromolecules can cause a series of undesirable changes which subsequently distub functions of molecules, and thus of cells, tissues and even organs.


1989 ◽  
Vol 257 (4) ◽  
pp. G570-G577 ◽  
Author(s):  
M. J. Muller ◽  
J. D. Huizinga ◽  
S. M. Collins

We examined changes in membrane function underlying the increased contractility of jejunal longitudinal muscle to carbachol in rats infected 6 days previously with Trichinella spiralis. Muscarinic receptor characteristics were examined in particulate fractions using [N-methyl-3H]scopolamine (NMS). There was a significant reduction in the total number of binding sites on muscle from infected rats, but the affinity for NMS was unchanged. Similarly, in competition studies, the binding of carbachol to high or low affinity sites was not significantly different in tissue from control or infected rats. However, we observed an 89% suppression of the activity of K+ -stimulated ouabain-sensitive p-nitrophenylphosphatase (pNPPase), an enzyme marker for the Na+ -K+ pump, in plasma membranes from infected compared with control rats. Similar results were obtained in 86Rb uptake studies. In contractility studies, evidence for the electrogenicity of the Na+ -K+ pump was obtained by demonstrating that pump activation by K+, Rb+, or Cs+ was associated with tissue relaxation with a rank order of potency that was identical to that for stimulation of pNPPase activity by these ions. Conversely, pump inhibition by vanadate increased tone and abolished phasic contractions in muscle from control or infected rats. This was accompanied by an increased response to carbachol in muscle from control but not infected rats. In addition, pump inhibition by removing extracellular K increased tone in control tissue but decreased tone in muscle from T. spiralis-infected rats, presumably because of preexisting pump suppression. These results are consistent with the hypothesis that suppression of electrogenic Na-pump activity contributes to the increased contractility of jejunal muscle in rats infected with T. spiralis.


2007 ◽  
Vol 103 (2) ◽  
pp. 710-716 ◽  
Author(s):  
Michael J. Emery ◽  
Randy L. Eveland ◽  
Seong S. Kim ◽  
Jacob Hildebrandt ◽  
Erik R. Swenson

CO2 regulation of lung compliance is currently explained by pH- and CO2-dependent changes in alveolar surface forces and bronchomotor tone. We hypothesized that in addition to, but independently of, those mechanisms, the parenchyma tissue responds to hypercapnia and hypocapnia by relaxing and contracting, respectively, thereby improving local matching of ventilation (V̇a) to perfusion (Q̇). Twenty adult rats were slowly ventilated with modified Krebs solution (rate = 3 min−1, 37°C, open chest) to produce unperfused living lung preparations free of intra-airway surface forces. The solution was gassed with 21% O2, balance N2, and CO2 varied to produce alveolar hypocapnia (Pco2 = 26.1 ± 2.4 mmHg, pH = 7.56 ± 0.04) or hypercapnia (Pco2 = 55.0 ± 2.3 mmHg, pH = 7.23 ± 0.02). The results show that lung recoil, as indicated from airway pressure measured during a breathhold following a large volume inspiration, is reduced ∼30% when exposed to hypercapnia vs. hypocapnia ( P < 0.0001, paired t-test), but stress relaxation and flow-dependent airway resistance were unaltered. Increasing CO2 from hypo- to hypercapnic levels caused a substantial, significant decrease in the quasi-static pressure-volume relationship, as measured after inspiration and expiration of several tidal volumes, but hysteresis was unaltered. Furthermore, addition of the glycolytic inhibitor NaF abolished CO2 effects on lung recoil. The results suggest that lung parenchyma tissue relaxation, arising from active elements in response to increasing alveolar CO2, is independent of (and apparently in parallel with) passive tissue elements and may actively contribute to V̇a/Q̇ matching.


ChemInform ◽  
2010 ◽  
Vol 27 (36) ◽  
pp. no-no
Author(s):  
K. YANG ◽  
J. D. ARTZ ◽  
J. LOCK ◽  
C. SANCHEZ ◽  
B. M. BENNETT ◽  
...  

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