Dictionary Matching with One Gap

The dictionary matching with gaps problem is to preprocess a dictionary $D$ of $d$ gapped patterns $P_1,\ldots,P_d$ over alphabet $\Sigma$, where each gapped pattern $P_i$ is a sequence of subpatterns separated by bounded sequences of don't cares. Then, given a query text $T$ of length $n$ over alphabet $\Sigma$, the goal is to output all locations in $T$ in which a pattern $P_i\in D$, $1\leq i\leq d$, ends. There is a renewed current interest in the gapped matching problem stemming from cyber security. In this paper we solve the problem where all patterns in the dictionary have one gap with at least $\alpha$ and at most $\beta$ don't cares, where $\alpha$ and $\beta$ are given parameters. Specifically, we show that the dictionary matching with a single gap problem can be solved in either $O(d\log d + |D|)$ time and $O(d\log^{\varepsilon} d + |D|)$ space, and query time $O(n(\beta -\alpha )\log\log d \log ^2 \min \{ d, \log |D| \} + occ)$, where $occ$ is the number of patterns found, or preprocessing time and space: $O(d^2 + |D|)$, and query time $O(n(\beta -\alpha ) + occ)$, where $occ$ is the number of patterns found. As far as we know, this is the best solution for this setting of the problem, where many overlaps may exist in the dictionary.Comment: A preliminary version was published at CPM 201

Complete measurements of quantum observables

We define a complete measurement of a quantum observable (POVM) as a measurement of the maximally refined version of the POVM. Complete measurements give information from the multiplicities of the measurement outcomes and can be viewed as state preparation procedures. We show that any POVM can be measured completely by using sequential measurements or maximally refinable instruments. Moreover, the ancillary space of a complete measurement can be chosen to be minimal.Comment: Based on talk given in CEQIP 2012 conferenc

Three Phases of Transforming a Project-Based IT Company Into a Lean and Design-Led Digital Service Provider

AbstractDigital transformation requires a continuous review of value creation, value capture, and resourcing. In this article, we define a systematical service design concept to enable all stakeholders to achieve better outcomes in cocreation activities.Abstract Digital transformation requires a continuous review of value creation, value capture, and resourcing. In this article, we define a systematical service design concept to enable all stakeholders to achieve better outcomes in cocreation activities

Expression of iron-related genes in human brain and brain tumors

<p>Abstract</p> <p>Background</p> <p>Defective iron homeostasis may be involved in the development of some diseases within the central nervous system. Although the expression of genes involved in normal iron balance has been intensively studied in other tissues, little is known about their expression in the brain. We investigated the mRNA levels of hepcidin (<it>HAMP</it>), HFE, neogenin (<it>NEO1</it>), transferrin receptor 1 (<it>TFRC</it>), transferrin receptor 2 (<it>TFR2</it>), and hemojuvelin (<it>HFE2</it>) in normal human brain, brain tumors, and astrocytoma cell lines. The specimens included 5 normal brain tissue samples, 4 meningiomas, one medulloblastoma, 3 oligodendrocytic gliomas, 2 oligoastrocytic gliomas, 8 astrocytic gliomas, and 3 astrocytoma cell lines.</p> <p>Results</p> <p>Except for hemojuvelin, all genes studied had detectable levels of mRNA. In most tumor types, the pattern of gene expression was diverse. Notable findings include high expression of transferrin receptor 1 in the hippocampus and medulla oblongata compared to other brain regions, low expression of HFE in normal brain with elevated HFE expression in meningiomas, and absence of hepcidin mRNA in astrocytoma cell lines despite expression in normal brain and tumor specimens.</p> <p>Conclusion</p> <p>These results indicate that several iron-related genes are expressed in normal brain, and that their expression may be dysregulated in brain tumors.</p

Idiopathic radiographic apical root resorption in wind instrument players

Root resorption of the permanent teeth involves an elaborate interaction among inflammatory cells resulting in loss of dental hard tissues. This report describes three clinical cases where idiopathic root resorption occurred in wind instrument playing patients. These patients produce adequate non-orthodontic forces, while playing their instruments, to expose their teeth to root resorbing force. Careful clinical monitoring of patients' teeth should be undertaken, as the additive effects of orthodontic treatment and musical habits are unknown

Staphylococcal protein Ecb impairs complement receptor-1 mediated recognition of opsonized bacteria

Staphyloccus aureus is a major human pathogen leading frequently to sepsis and soft tissue infections with abscesses. Multiple virulence factors including several immune modulating molecules contribute to its survival in the host. When S. aureus invades the human body, one of the first line defenses is the complement system, which opsonizes the bacteria with C3b and attract neutrophils by release of chemotactic peptides. Neutrophils express Complement receptor-1 [CR1, CD35) that interacts with the C3b-opsonized particles and thereby plays an important role in pathogen recognition by phagocytic cells. In this study we observed that a fraction of S. aureus culture supernatant prevented binding of C3b to neutrophils. This fraction consisted of S. aureus leukocidins and Efb. The C-terminus of Efb is known to bind C3b and shares significant sequence homology to the extracellular complement binding protein [Ecb). Here we show that S. aureus Ecb displays various mechanisms to block bacterial recognition by neutrophils. The presence of Ecb blocked direct interaction between soluble CR1 and C3b and reduced the cofactor activity of CR1 in proteolytic inactivation of C3b. Furthermore, Ecb could dose-dependently prevent recognition of C3b by cell-bound CR1 that lead to impaired phagocytosis of NHS-opsonized S. aureus. Phagocytosis was furthermore reduced in the presence of soluble CR1 [sCR1). These data indicate that the staphylococcal protein Ecb prevents recognition of C3b opsonized bacteria by neutrophil CR1 leading to impaired killing by phagocytosis and thereby contribute to immune evasion of S. aureus.Peer reviewe

Biochem Soc Trans

Abnormal protein aggregation and intracellular or extracellular accumulation of misfolded and aggregated proteins are key events in the pathogenesis of different neurodegenerative diseases. Furthermore, endoplasmic reticulum stress and impairment of the ubiquitin-proteasome system probably contribute to neurodegeneration in these diseases. A characteristic feature of AD (Alzheimer's disease) is the abnormal accumulation of Abeta (amyloid beta-peptide) in the brain. Evidence shows that the AD-associated PS (presenilin) also forms aggregates under certain conditions and that another AD-associated protein, ubiquilin-1, controls protein aggregation and deposition of aggregated proteins. Here, we review the current knowledge of ubiquilin-1 and PS in protein aggregation and related events that potentially influence neurodegeneration

Prodromal and Early bvFTD : Evaluating Clinical Features and Current Biomarkers

AbstractDespite the current diagnostic criteria, early diagnostics of behavioral variant of frontotemporal dementia (bvFTD) has remained challenging. Patients with bvFTD often present with misleading psychiatric phenotype, and, on the other hand, impairment in memory functions have increasingly been reported. However, impaired episodic memory is currently considered as an exclusion criterion for bvFTD. Single biofluid-based or imaging biomarkers do not currently provide sufficient sensitivity or specificity for early bvFTD diagnosis at single-subject level, although studies have suggested improved accuracy with different biomarker combinations. In this mini review, we evaluate the core clinical features of early bvFTD and summarize the most potential imaging and fluid biomarkers for bvFTD diagnostics.Abstract Despite the current diagnostic criteria, early diagnostics of behavioral variant of frontotemporal dementia (bvFTD) has remained challenging. Patients with bvFTD often present with misleading psychiatric phenotype, and, on the other hand, impairment in memory functions have increasingly been reported. However, impaired episodic memory is currently considered as an exclusion criterion for bvFTD. Single biofluid-based or imaging biomarkers do not currently provide sufficient sensitivity or specificity for early bvFTD diagnosis at single-subject level, although studies have suggested improved accuracy with different biomarker combinations. In this mini review, we evaluate the core clinical features of early bvFTD and summarize the most potential imaging and fluid biomarkers for bvFTD diagnostics

Microbes Bind Complement Inhibitor Factor H via a Common Site

To cause infections microbes need to evade host defense systems, one of these being the evolutionarily old and important arm of innate immunity, the alternative pathway of complement. It can attack all kinds of targets and is tightly controlled in plasma and on host cells by plasma complement regulator factor H (FH). FH binds simultaneously to host cell surface structures such as heparin or glycosaminoglycans via domain 20 and to the main complement opsonin C3b via domain 19. Many pathogenic microbes protect themselves from complement by recruiting host FH. We analyzed how and why different microbes bind FH via domains 19–20 (FH19-20). We used a selection of FH19-20 point mutants to reveal the binding sites of several microbial proteins and whole microbes (Haemophilus influenzae, Bordetella pertussis, Pseudomonas aeruginosa, Streptococcus pneumonia, Candida albicans, Borrelia burgdorferi, and Borrelia hermsii). We show that all studied microbes use the same binding region located on one side of domain 20. Binding of FH to the microbial proteins was inhibited with heparin showing that the common microbial binding site overlaps with the heparin site needed for efficient binding of FH to host cells. Surprisingly, the microbial proteins enhanced binding of FH19-20 to C3b and down-regulation of complement activation. We show that this is caused by formation of a tripartite complex between the microbial protein, FH, and C3b. In this study we reveal that seven microbes representing different phyla utilize a common binding site on the domain 20 of FH for complement evasion. Binding via this site not only mimics the glycosaminoglycans of the host cells, but also enhances function of FH on the microbial surfaces via the novel mechanism of tripartite complex formation. This is a unique example of convergent evolution resulting in enhanced immune evasion of important pathogens viautilization of a “superevasion site.