The present study aimed to analyse the influence of speed and power abilities in goal situations in professional football. During the second half of the season 2007/08, videos of 360 goals in the first German national league were analysed by visual inspection. For the assisting and the scoring player the situations immediately preceding the goal were evaluated. The observed actions were categorised as: no powerful action, rotation (around the body's centre-line), straight sprint, change-in-direction sprint, jump, or a combination of those categories. Two hundred and ninety-eight (83%) goals were preceded by at least one powerful action of the scoring or the assisting player. Most actions for the scoring player were straight sprints (n = 161, 45% of all analysed goals, P < 0.001) followed by jumps (n = 57, 16%), rotations and change-in-direction sprints (n = 22, 6% each). Most sprints were conducted without an opponent (n = 109, P < 0.001) and without the ball (n = 121, P < 0.001). Similarly, for the assisting player the most frequent action was a straight sprint (n = 137, P < 0.001) followed by rotations (n = 28), jumps (n = 22) and change-in-direction sprints (n = 18). The straight sprints were mostly conducted with the ball (n = 93, P = 0.003). In conclusion, straight sprinting is the most frequent action in goal situations. Power and speed abilities are important within decisive situations in professional football and, thus, should be included in fitness testing and training.

Mixed integer programs are commonly solved with linear programming based branch-and-bound algorithms. The success of the algorithm strongly depends on the strategy used to select the variable to branch on.We present a new generalization called reliability branching of today's state-of-the-art strong branching and pseudocost branching branching strategies for linear programming based branch-and-bound algorithms. After reviewing commonly used branching strategies and performing extensive computational studies we compare different parameter settings and show the superiority of our proposed new strategy.

Cell invasion through a dense three-dimensional (3D) matrix is believed to depend on the ability of cells to generate traction forces. To quantify the role of cell tractions during invasion in 3D, we present a technique to measure the elastic strain energy stored in the matrix due to traction-induced deformations. The matrix deformations around a cell were measured by tracking the 3D positions of fluorescent beads tightly embedded in the matrix. The bead positions served as nodes for a finite element tessellation. From the strain in each element and the known matrix elasticity, we computed the local strain energy in the matrix surrounding the cell. We applied the technique to measure the strain energy of highly invasive MDA-MB-231 breast carcinoma and A-125 lung carcinoma cells in collagen gels. The results were compared to the strain energy generated by non-invasive MCF-7 breast and A-549 lung carcinoma cells. In all cases, cells locally contracted the matrix. Invasive breast and lung carcinoma cells showed a significantly higher contractility compared to non-invasive cells. Higher contractility, however, was not universally associated with higher invasiveness. For instance, non-invasive A-431 vulva carcinoma cells were the most contractile cells among all cell lines tested. As a universal feature, however, we found that invasive cells assumed an elongated spindle-like morphology as opposed to a more spherical shape of non-invasive cells. Accordingly, the distribution of strain energy density around invasive cells followed patterns of increased complexity and anisotropy. These results suggest that not so much the magnitude of traction generation but their directionality is important for cancer cell invasion.

The nemaline myopathies are characterized by weakness and eosinophilic, rodlike (nemaline) inclusions in muscle fibers. Amish nemaline myopathy is a form of nemaline myopathy common among the Old Order Amish. In the first months of life, affected infants have tremors with hypotonia and mild contractures of the shoulders and hips. Progressive worsening of the proximal contractures, weakness, and a pectus carinatum deformity develop before the children die of respiratory insufficiency, usually in the second year. The disorder has an incidence of approximately 1 in 500 among the Amish, and it is inherited in an autosomal recessive pattern. Using a genealogy database, automated pedigree software, and linkage analysis of DNA samples from four sibships, we identified an approximately 2-cM interval on chromosome 19q13.4 that was homozygous in all affected individuals. The gene for the sarcomeric thin-filament protein, slow skeletal muscle troponin T (TNNT1), maps to this interval and was sequenced. We identified a stop codon in exon 11, predicted to truncate the protein at amino acid 179, which segregates with the disease. We conclude that Amish nemaline myopathy is a distinct, heritable, myopathic disorder caused by a mutation in TNNT1.

The cytoskeletal protein vinculin contributes to the mechanical link of the contractile actomyosin cytoskeleton to the extracellular matrix (ECM) through integrin receptors. In addition, vinculin modulates the dynamics of cell adhesions and is associated with decreased cell motility on two-dimensional ECM substrates. The effect of vinculin on cell invasion through dense three-dimensional ECM gels is unknown. Here, we report how vinculin expression affects cell invasion into three-dimensional collagen matrices. Cell motility was investigated in vinculin knockout and vinculin expressing wild-type mouse embryonic fibroblasts. Vinculin knockout cells were 2-fold more motile on two-dimensional collagen-coated substrates compared with wild-type cells, but 3-fold less invasive in 2.4 mg/ml three-dimensional collagen matrices. Vinculin knockout cells were softer and remodeled their cytoskeleton more dynamically, which is consistent with their enhanced two-dimensional motility but does not explain their reduced three-dimensional invasiveness. Importantly, vinculin-expressing cells adhered more strongly to collagen and generated 3-fold higher traction forces compared with vinculin knockout cells. Moreover, vinculin-expressing cells were able to migrate into dense (5.8 mg/ml) threedimensional collagen matrices that were impenetrable for vinculin knockout cells. These findings suggest that vinculin facilitates three-dimensional matrix invasion through up-regulation or enhanced transmission of traction forces that are needed to overcome the steric hindrance of ECMs.Cell migration is an important and fundamental biomechanical process that plays an essential role in inflammatory diseases, embryonic development, wound healing, and metastasis formation. Current concepts of cell migration have been established in two-dimensional models, but they can explain only partially the migratory behavior in three dimensions. For instance, the migratory capability of cells on two-dimensional substrates depends mainly on adhesion strength, adhesion dynamics, and the dynamics of cytoskeletal remodeling (1, 2), whereas the migratory capability of cells in three-dimensional connective tissue depends also on the steric hindrance of the matrix, matrix degradation by proteolytic enzyme secretion, and the generation of protrusive or contractile forces (1, 3-5). The balance of all these parameters-adhesion strength, cytoskeletal remodeling, matrix degradation, and the generation and transmission of contractile forces-is important for the migration speed in three-dimensional extracellular matrix (ECM) 2 (6). Depending on this balance, a broad variety of invasion strategies between different cell types and even within the same cell type are possible (7).The connection between the ECM and the actomyosin cytoskeleton through integrin-type cell-matrix adhesion receptors is facilitated by the mechano-coupling protein vinculin (8, 9). The effect of vinculin on the migration of cells has previously been investigated using two-dimensional ECM substrates, whe...

In this paper, we present the implementation of a branch-and-cut algorithm for solving Steiner tree problems in graphs. Our algorithm is based on an integer programming formulation for directed graphs and comprises preprocessing, separation algorithms, and primal heuristics. We are able to solve nearly all problem instances discussed in the literature to optimality, including one problem that-to our knowledge-has not yet been solved. We also report on our computational experiences with some very large Steiner tree problems arising from the design of electronic circuits. All test problems are gathered in a newly introduced library called SteinLib that is accessible via the World Wide Web.

This paper reports on the fifth version of the Mixed Integer Programming Library. The miplib 2010 is the first miplib release that has been assembled by a large group from academia and from industry, all of whom work in integer programming. There was mutual consent that the concept of the library had to be expanded in order to fulfill the needs of the community. The new version comprises 361 instances sorted into several groups. This includes the main benchmark test set of 87 instances, which

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