20 research outputs found
Strain-driven criticality underlies nonlinear mechanics of fibrous networks
Networks with only central force interactions are floppy when their average connectivity is below an isostatic threshold. Although such networks are mechanically unstable, they can become rigid when strained. It was recently shown that the transition from floppy to rigid states as a function of simple shear strain is continuous, with hallmark signatures of criticality [Sharma et al., Nature Phys. 12, 584 (2016)]. The nonlinear mechanical response of collagen networks was shown to be quantitatively described within the framework of such mechanical critical phenomenon. Here, we provide a more quantitative characterization of critical behavior in subisostatic networks. Using finite-size scaling we demonstrate the divergence of strain fluctuations in the network at well-defined critical strain. We show that the characteristic strain corresponding to the onset of strain stiffening is distinct from but related to this critical strain in a way that depends on critical exponents. We confirm this prediction experimentally for collagen networks. Moreover, we find that the apparent critical exponents are largely independent of the spatial dimensionality. With subisostaticity as the only required condition, strain-driven criticality is expected to be a general feature of biologically relevant fibrous networks
Strain-controlled criticality governs the nonlinear mechanics of fibre networks
Disordered fibrous networks are ubiquitous in nature as major structural
components of living cells and tissues. The mechanical stability of networks
generally depends on the degree of connectivity: only when the average number
of connections between nodes exceeds the isostatic threshold are networks
stable (Maxwell, J. C., Philosophical Magazine 27, 294 (1864)). Upon increasing
the connectivity through this point, such networks undergo a mechanical phase
transition from a floppy to a rigid phase. However, even sub-isostatic networks
become rigid when subjected to sufficiently large deformations. To study this
strain-controlled transition, we perform a combination of computational
modeling of fibre networks and experiments on networks of type I collagen
fibers, which are crucial for the integrity of biological tissues. We show
theoretically that the development of rigidity is characterized by a
strain-controlled continuous phase transition with signatures of criticality.
Our experiments demonstrate mechanical properties consistent with our model,
including the predicted critical exponents. We show that the nonlinear
mechanics of collagen networks can be quantitatively captured by the
predictions of scaling theory for the strain-controlled critical behavior over
a wide range of network concentrations and strains up to failure of the
material
Second-Generation Antipsychotics and Neuroleptic Malignant Syndrome: Systematic Review and Case Report Analysis
Peri-Adrenal Hemangioma Mimicking a Pheochromocytoma on Metaiodobenzylguanidine (MIBG) Scan.
Pheochromocytomas account for less than one percent of hypertension and are usually suspected because of clinical manifestations, confirmed by laboratory evaluation and subsequently localized by radiology. Higher HU units on pre-contrast CT and hyperintense signal on T2 weighted MRI images are often seen in pheochromocytoma. Metaiodobenzylguanidine (MIBG) scans have been widely used to localize pheochromocytoma and false-positive scans are reported to be rare. We report a hypertensive patient with symptoms consistent with a pheochromocytoma, with a left adrenal mass with a pre-contrast HU of 8 but a 70 HU post-contrast value. No biochemical evidence of catecholamine excess was noted. A MIBG scan was reported as highly suspicious for a pheochromocytoma. Laparoscopic resection of the mass confirmed the presence of a peri-adrenal hemangioma with both capillary and cavernous components. We postulate that the accumulation of MIBG because of the hemangioma was responsible for the false-positive MIBG scan
The Role of Network Architecture in Collagen Mechanics
Collagen forms fibrous networks that reinforce tissues and provide an extracellular matrix for cells. These networks exhibit remarkable strain-stiffening properties that tailor the mechanical functions of tissues and regulate cell behavior. Recent models explain this nonlinear behavior as an intrinsic feature of disordered networks of stiff fibers. Here, we experimentally validate this theoretical framework by measuring the elastic properties of collagen networks over a wide range of self-assembly conditions. We show that the model allows us to quantitatively relate both the linear and nonlinear elastic behavior of collagen networks to their underlying architecture. Specifically, we identify the local coordination number (or connectivity) 〈z〉 as a key architectural parameter that governs the elastic response of collagen. The network elastic response reveals that 〈z〉 decreases from 3.5 to 3 as the polymerization temperature is raised from 26 to 37°C while being weakly dependent on concentration. We furthermore infer a Young's modulus of 1.1 MPa for the collagen fibrils from the linear modulus. Scanning electron microscopy confirms that 〈z〉 is between three and four but is unable to detect the subtle changes in 〈z〉 with polymerization conditions that rheology is sensitive to. Finally, we show that, consistent with the model, the initial stress-stiffening response of collagen networks is controlled by the negative normal stress that builds up under shear. Our work provides a predictive framework to facilitate future studies of the regulatory effect of extracellular matrix molecules on collagen mechanics. Moreover, our findings can aid mechanobiological studies of wound healing, fibrosis, and cancer metastasis, which require collagen matrices with tunable mechanical properties