Technion – Israel Institute of Technology

About: Technion – Israel Institute of Technology is a education organization based out in Haifa, Israel. It is known for research contribution in the topics: Population & Upper and lower bounds. The organization has 31714 authors who have published 79377 publications receiving 2603976 citations. The organization is also known as: Technion Israel Institute of Technology & Ṭekhniyon, Makhon ṭekhnologi le-Yiśraʼel.

LIF/STAT3 Signaling Fails to Maintain Self‐Renewal of Human Embryonic Stem Cells

Abstract: Murine embryonic stem (mES) cells remain undifferentiated in the presence of leukemia inhibitory factor (LIF), and activation of signal transducer and activator of transcription 3 (STAT3) via LIF receptor (LIFR) signaling appears sufficient for maintenance of mES cell pluripotency. Anecdotal and contradictory accounts exist for the action of LIF in the culture of human embryonic stem cells, and the nature of LIF signaling and whether the LIF-STAT3 pathway is conserved in human embryonic stem cells (hESCs) has not been systematically explored. In this study, we show that the LIFRbeta and the signaling subunit gp130 are expressed in hESCs and that human LIF can induce STAT3 phosphorylation and nuclear translocation in hESCs. Nevertheless, despite the functional activation of the LIF-STAT3 signaling pathway, human LIF is unable to maintain the pluripotent state of hESCs. Feeder-free culture conditions that maintain hESCs in an undifferentiated state do not show activation of STAT3, suggesting that distinct signaling mechanisms govern the self-renewal of hESCs.

What Makes a Patch Distinct

Abstract: What makes an object salient? Most previous work assert that distinctness is the dominating factor. The difference between the various algorithms is in the way they compute distinctness. Some focus on the patterns, others on the colors, and several add high-level cues and priors. We propose a simple, yet powerful, algorithm that integrates these three factors. Our key contribution is a novel and fast approach to compute pattern distinctness. We rely on the inner statistics of the patches in the image for identifying unique patterns. We provide an extensive evaluation and show that our approach outperforms all state-of-the-art methods on the five most commonly-used datasets.

Workload: An examination of the concept.

Abstract: The relations between task difficulty and workload and workload and performance are examined. The architecture and limitations of the central processor are discussed. Various procedures for measuring workload are described and evaluated. Consideration is given to normative and descriptive approaches; subjective, performance, and arousal measures; performance operating characteristics; and psychophysiological measures of workload.

Exact and Approximate Solutions of Source Localization Problems

Abstract: We consider least squares (LS) approaches for locating a radiating source from range measurements (which we call R-LS) or from range-difference measurements (RD-LS) collected using an array of passive sensors. We also consider LS approaches based on squared range observations (SR-LS) and based on squared range-difference measurements (SRD-LS). Despite the fact that the resulting optimization problems are nonconvex, we provide exact solution procedures for efficiently computing the SR-LS and SRD-LS estimates. Numerical simulations suggest that the exact SR-LS and SRD-LS estimates outperform existing approximations of the SR-LS and SRD-LS solutions as well as approximations of the R-LS and RD-LS solutions which are based on a semidefinite relaxation.

The deoxyguanosine kinase gene is mutated in individuals with depleted hepatocerebral mitochondrial DNA.

Abstract: Mitochondrial DNA (mtDNA)-depletion syndromes (MDS; OMIM 251880) are phenotypically heterogeneous, autosomal-recessive disorders characterized by tissue-specific reduction in mtDNA copy number. Affected individuals with the hepatocerebral form of MDS have early progressive liver failure and neurological abnormalities, hypoglycemia and increased lactate in body fluids. Affected tissues show both decreased activity of the mtDNA-encoded respiratory chain complexes (I, III, IV, V) and mtDNA depletion. We used homozygosity mapping in three kindreds of Druze origin to map the gene causing hepatocerebral MDS to a region of 6.1 cM on chromosome 2p13, between markers D2S291 and D2S2116. This interval encompasses the gene (DGUOK) encoding the mitochondrial deoxyguanosine kinase (dGK). We identified a single-nucleotide deletion (204delA) within the coding region of DGUOK that segregates with the disease in the three kindreds studied. Western-blot analysis did not detect dGK protein in the liver of affected individuals. The main supply of deoxyribonucleotides (dNTPs) for mtDNA synthesis comes from the salvage pathway initiated by dGK and thymidine kinase-2 (TK2). The association of mtDNA depletion with mutated DGUOK suggests that the salvage-pathway enzymes are involved in the maintenance of balanced mitochondrial dNTP pools.