Sublinear Algorithms for Approximating String Compressibility

We raise the question of approximating the compressibility of a string with respect to a fixed compression scheme, in sublinear time. We study this question in detail for two popular lossless compression schemes: run-length encoding (RLE) and a variant of Lempel-Ziv (LZ77), and present sublinear algorithms for approximating compressibility with respect to both schemes. We also give several lower bounds that show that our algorithms for both schemes cannot be improved significantly. Our investigation of LZ77 yields results whose interest goes beyond the initial questions we set out to study. In particular, we prove combinatorial structural lemmas that relate the compressibility of a string with respect to LZ77 to the number of distinct short substrings contained in it (its ℓth subword complexity , for small ℓ). In addition, we show that approximating the compressibility with respect to LZ77 is related to approximating the support size of a distribution.National Science Foundation (U.S.) (Award CCF-1065125)National Science Foundation (U.S.) (Award CCF-0728645)Marie Curie International Reintegration Grant PIRG03-GA-2008-231077Israel Science Foundation (Grant 1147/09)Israel Science Foundation (Grant 1675/09

Myeloid-Specific Deletion of Mcl-1 Yields Severely Neutropenic Mice That Survive and Breed in Homozygous Form

Mouse strains with specific deficiency of given hematopoietic lineages provide invaluable tools for understanding blood cell function in health and disease. Whereas neutrophils are dominant leukocytes in humans and mice, there are no widely useful genetic models of neutrophil deficiency in mice. In this study, we show that myeloid-specific deletion of the Mcl-1 antiapoptotic protein in Lyz2Cre/CreMcl1flox/flox (Mcl1ΔMyelo) mice leads to dramatic reduction of circulating and tissue neutrophil counts without affecting circulating lymphocyte, monocyte, or eosinophil numbers. Surprisingly, Mcl1ΔMyelo mice appeared normally, and their survival was mostly normal both under specific pathogen-free and conventional housing conditions. Mcl1ΔMyelo mice were also able to breed in homozygous form, making them highly useful for in vivo experimental studies. The functional relevance of neutropenia was confirmed by the complete protection of Mcl1ΔMyelo mice from arthritis development in the K/B×N serum-transfer model and from skin inflammation in an autoantibody-induced mouse model of epidermolysis bullosa acquisita. Mcl1ΔMyelo mice were also highly susceptible to systemic Staphylococcus aureus or Candida albicans infection, due to defective clearance of the invading pathogens. Although neutrophil-specific deletion of Mcl-1 in MRP8-CreMcl1flox/flox (Mcl1ΔPMN) mice also led to severe neutropenia, those mice showed an overt wasting phenotype and strongly reduced survival and breeding, limiting their use as an experimental model of neutrophil deficiency. Taken together, our results with the Mcl1ΔMyelo mice indicate that severe neutropenia does not abrogate the viability and fertility of mice, and they provide a useful genetic mouse model for the analysis of the role of neutrophils in health and disease

Amyloid-b1-42 treatment does not have a specific effect on cholinergic neurons in in vitro basal forebrain neuronal cultures of rat

The neurotoxic effect of amyloid-beta peptide (1-42) was investigated in cultures of neuronal tissue derived from the basal forebrain of embryonic rat. The axonal varicosities of the cholinergic cells were revealed by vesicular acetylcholine transporter staining, and the axonal varicosities in general by synaptophysin immunohistochemistry. The results demonstrate that the treatment of in vitro neuronal cultures with 20 mM amyloid-beta peptide (1-42) for 2 days on day 5, 12 or 15 exerted a neurotoxic effect on both the cholinergic and the non-cholinergic neurons. In the same cultures, the absolute number of synaptophysin-positive axon varicosities was reduced to greater extent (control: 203 ± 37/field vs treated: 101 ± 16/field) than the number of vesicular acetylcholine transporter-immunoreactive (control: 48 ± 4/field vs treated: 0/field) structures. It is concluded that amyloid-beta peptide (1-42) does not have a specific effect only on the cholinergic neurons, but affects non-cholinergic neurons as well