Inflating bacterial cells by increased protein synthesis.

Understanding how the homeostasis of cellular size and composition is accomplished by different organisms is an outstanding challenge in biology. For exponentially growing Escherichia coli cells, it is long known that the size of cells exhibits a strong positive relation with their growth rates in different nutrient conditions. Here, we characterized cell sizes in a set of orthogonal growth limitations. We report that cell size and mass exhibit positive or negative dependences with growth rate depending on the growth limitation applied. In particular, synthesizing large amounts of "useless" proteins led to an inversion of the canonical, positive relation, with slow growing cells enlarged 7- to 8-fold compared to cells growing at similar rates under nutrient limitation. Strikingly, this increase in cell size was accompanied by a 3- to 4-fold increase in cellular DNA content at slow growth, reaching up to an amount equivalent to ~8 chromosomes per cell. Despite drastic changes in cell mass and macromolecular composition, cellular dry mass density remained constant. Our findings reveal an important role of protein synthesis in cell division control

Undulation Instability of Epithelial Tissues

Treating the epithelium as an incompressible fluid adjacent to a viscoelastic stroma, we find a novel hydrodynamic instability that leads to the formation of protrusions of the epithelium into the stroma. This instability is a candidate for epithelial fingering observed in vivo. It occurs for sufficiently large viscosity, cell-division rate and thickness of the dividing region in the epithelium. Our work provides physical insight into a potential mechanism by which interfaces between epithelia and stromas undulate, and potentially by which tissue dysplasia leads to cancerous invasion.Comment: 4 pages, 3 figure

Stress Clamp Experiments on Multicellular Tumor Spheroids

The precise role of the microenvironment on tumor growth is poorly understood. Whereas the tumor is in constant competition with the surrounding tissue, little is known about the mechanics of this interaction. Using a novel experimental procedure, we study quantitatively the effect of an applied mechanical stress on the long-term growth of a spheroid cell aggregate. We observe that a stress of 10 kPa is sufficient to drastically reduce growth by inhibition of cell proliferation mainly in the core of the spheroid. We compare the results to a simple numerical model developed to describe the role of mechanics in cancer progression.Comment: 5 pages, 4 figure

Rolling-sliding-contact fatigue damage of the gear tooth flanks

Bokovi zuba evolventnih zupčanika izloženi su tijekom zahvata cikličkom djelovanju kontaktnih pritisaka te kombinaciji kotrljanja i klizanja. Spomenuto opterećenje može izazvati specifičnu vrstu zamora materijala koja se naziva kotrljajno-klizno-kontaktni zamor. U radu su opisane faze procesa zamaranja materijala izloženog djelovanju cikličkih opterećenja. Klasificirana su zamorna oštećenja boka zuba zupčanika te su za svaku vrstu navedeni njezini uzroci i značajke. Navedene informacije mogu poslužiti kao pomoć pri sprečavanju ili naknadnoj identifikaciji i uklanjanju problema sa zamornim oštećenjima zupčanika u prijenosnicima snage.During the meshing of involute gears, their teeth flanks are subjected to cyclic contact pressure loading and simultaneous rolling and sliding. The mentioned loading can induce a specific type of material fatigue that is commonly denoted as rolling-sliding-contact fatigue. In this work, individual phases of fatigue occurring due to the cyclic loading are described. Furthermore, different types of fatigue damage of gear teeth flanks are classified and for each type, its causes and features are given. The information presented can be used for prevention or subsequent identification and remedial action in the case of fatigue damage of gears in power transmissions

Homeostatic competition drives tumor growth and metastasis nucleation

We propose a mechanism for tumor growth emphasizing the role of homeostatic regulation and tissue stability. We show that competition between surface and bulk effects leads to the existence of a critical size that must be overcome by metastases to reach macroscopic sizes. This property can qualitatively explain the observed size distributions of metastases, while size-independent growth rates cannot account for clinical and experimental data. In addition, it potentially explains the observed preferential growth of metastases on tissue surfaces and membranes such as the pleural and peritoneal layers, suggests a mechanism underlying the seed and soil hypothesis introduced by Stephen Paget in 1889 and yields realistic values for metastatic inefficiency. We propose a number of key experiments to test these concepts. The homeostatic pressure as introduced in this work could constitute a quantitative, experimentally accessible measure for the metastatic potential of early malignant growths.Comment: 13 pages, 11 figures, to be published in the HFSP Journa