Distributed Testing of Excluded Subgraphs

We study property testing in the context of distributed computing, under the classical CONGEST model. It is known that testing whether a graph is triangle-free can be done in a constant number of rounds, where the constant depends on how far the input graph is from being triangle-free. We show that, for every connected 4-node graph H, testing whether a graph is H-free can be done in a constant number of rounds too. The constant also depends on how far the input graph is from being H-free, and the dependence is identical to the one in the case of testing triangles. Hence, in particular, testing whether a graph is K_4-free, and testing whether a graph is C_4-free can be done in a constant number of rounds (where K_k denotes the k-node clique, and C_k denotes the k-node cycle). On the other hand, we show that testing K_k-freeness and C_k-freeness for k>4 appear to be much harder. Specifically, we investigate two natural types of generic algorithms for testing H-freeness, called DFS tester and BFS tester. The latter captures the previously known algorithm to test the presence of triangles, while the former captures our generic algorithm to test the presence of a 4-node graph pattern H. We prove that both DFS and BFS testers fail to test K_k-freeness and C_k-freeness in a constant number of rounds for k>4

Impaired CK1 Delta Activity Attenuates SV40-Induced Cellular Transformation In Vitro and Mouse Mammary Carcinogenesis In Vivo

Simian virus 40 (SV40) is a powerful tool to study cellular transformation in vitro, as well as tumor development and progression in vivo. Various cellular kinases, among them members of the CK1 family, play an important role in modulating the transforming activity of SV40, including the transforming activity of T-Ag, the major transforming protein of SV40, itself. Here we characterized the effects of mutant CK1δ variants with impaired kinase activity on SV40-induced cell transformation in vitro, and on SV40-induced mammary carcinogenesis in vivo in a transgenic/bi-transgenic mouse model. CK1δ mutants exhibited a reduced kinase activity compared to wtCK1δ in in vitro kinase assays. Molecular modeling studies suggested that mutation N172D, located within the substrate binding region, is mainly responsible for impaired mutCK1δ activity. When stably over-expressed in maximal transformed SV-52 cells, CK1δ mutants induced reversion to a minimal transformed phenotype by dominant-negative interference with endogenous wtCK1δ. To characterize the effects of CK1δ on SV40-induced mammary carcinogenesis, we generated transgenic mice expressing mutant CK1δ under the control of the whey acidic protein (WAP) gene promoter, and crossed them with SV40 transgenic WAP-T-antigen (WAP-T) mice. Both WAP-T mice as well as WAP-mutCK1δ/WAP-T bi-transgenic mice developed breast cancer. However, tumor incidence was lower and life span was significantly longer in WAP-mutCK1δ/WAP-T bi-transgenic animals. The reduced CK1δ activity did not affect early lesion formation during tumorigenesis, suggesting that impaired CK1δ activity reduces the probability for outgrowth of in situ carcinomas to invasive carcinomas. The different tumorigenic potential of SV40 in WAP-T and WAP-mutCK1δ/WAP-T tumors was also reflected by a significantly different expression of various genes known to be involved in tumor progression, specifically of those involved in wnt-signaling and DNA repair. Our data show that inactivating mutations in CK1δ impair SV40-induced cellular transformation in vitro and mouse mammary carcinogenesis in vivo

Is there an influence of body mass on digesta mean retention time in herbivores? A comparative study on ungulates

The relation between body mass (BM) and digesta mean retention time (MRT) in herbivores was the focus of several studies in recent years. It was assumed that MRT scaled with BM0.25 based on the isometric scaling of gut capacity (BM1.0) and allometric scaling of energy intake (BM0.75). Literature studies that tested this hypothesis produced conflicting results, arriving sometimes at higher or lower exponents than the postulated 0.25. This study was conducted with 8 ruminants (n=2–6 per species) and 6 hindgut fermenting species/breeds (n=2–6, warthog n=1) with a BM range of 60–4000 kg. All animals received a ration of 100% grass hay with ad libitum access. Dry matter intake was measured and the MRT was estimated by the use of a solute and a particle (1–2 mm) marker. No significant scaling of MRTparticle with BM was observed for all herbivores (32 BM0.04, p=0.518) and hindgut fermenters (32 BM0.00, p=1.00). The scaling exponent for ruminants only showed a tendency towards significance (29 BM0.12, p=0.071). Ruminants on average had an MRTparticle 1.61-fold longer than hindgut fermenters. Whereas an exponent of 0.25 is reasonable from theoretical considerations, much lower exponents were found in this and other studies. The energetic benefit of increasing MRT is by no means continuous, since the energy released from a given food unit via digestion decreases over time. The low and non-significant scaling factors for both digestion types suggest that in ungulates, MRT is less influenced by BM (maximal allometric exponent≤0.1) than often reported