Miracle-dz/UniFAR-FTUs huggingface dataset:
Robust Sketching and Aggregation of Distributed Data Streams

The data streaming modelprovides an attractive framework for one-pass summarization of massive data sets at a single observation point. However, in an environment where multiple data streams arrive at a set of distributed observation points, sketches must be computed remotely and then must be aggregated through a hierarchy before queries may be conducted. As a result, many sketchbased methods for the single stream case do not apply directly, as either the error introduced becomes large, or because the methods assume that the streams are non-overlapping. These limitations hinder the application of these techniques to practicalprobl ems in network traffic monitoring and aggregation in sensor networks. To address this, we develop a framework for evaluating and enabling robust computation of duplicate-sensitive aggregate functions (e.g., SUM and QUANTILE), over data produced by distributed sources. We instantiate our approach by augmenting the Count-Min and Quantile Digest sketches to apply in this distributed setting, and analyze their performance. We conclude with an experimental evaluation to validate our analysis.
Curvas de rendimento da cavala, Scomberomorus cavalla (Cuvier), e da serra, Scomberomorus maculatus (Mitchill), no Estado do Ceará (Brasil).

GESTEIRA, Tereza Cristina Vasconcelos. Curvas de rendimento da cavala, Scomberomorus cavalla (Cuvier), e da serra, Scomberomorus maculatus (Mitchill), no Estado do Ceara (Brasil). Arquivos de Ciencias do Mar. Fortaleza, v.13. n.1, p.13-15, mar.1973.
Dynamic combinatorial chemistry: the unexpected choice of receptors by guest molecules.

Although our knowledge in the broad field of chemistry has increased enormously over the past decades, we are still unable to give precise predictions on the behavior of molecules in solution. Therefore, combinatorial approaches and high-throughput experimentation have become increasingly important by facilitating the rapid discovery of lead compounds and the optimization of processes in which trial-and-error is the dominant approach. In the mid-1990s, a fundamentally new concept in this area, dynamic combinatorial chemistry (DCC), was introduced by the groups of Sanders, Lehn, and others. Whereas traditional combinatorial libraries are based on the preparation of kinetically stable compounds and subsequent screening for their function, this new concept takes advantage of reversible bonds, covalent or noncovalent, by generating a random (virtual) library whose members are in dynamic equilibrium. The formation of the library is under thermodynamic control, which gives rise to new properties such as adaptation; that is, the library readjusts its distribution by external stimuli. Upon addition of a target molecule, the mixture of potential receptors in the library reequilibrates in favor of the best receptor(s) for the target. By using this strategy the preparation and screening of the receptor for a certain target is integrated in one step, as the receptor is chosen by the target. Libraries of receptors of variable complexity have been constructed, with the simplest comprised of a mixture of macrocycles of variable sizes based on identical building blocks (type A; Figure 1a).
Impact of Novel Human Immunodeficiency Virus Type 1 Reverse Transcriptase Mutations P119S and T165A on 4′-Ethynylthymidine Analog Resistance Profile

ABSTRACT 2′,3′-Didehydro-3′-deoxy-4′-ethynylthymidine (4′-Ed4T), a derivative of stavudine (d4T), has potent activity against human immunodeficiency virus and is much less inhibitory to mitochondrial DNA synthesis and cell growth than its progenitor, d4T. 4′-Ed4T triphosphate was a better reverse transcriptase (RT) inhibitor than d4T triphosphate, due to the additional binding of the 4′-ethynyl group at a presumed hydrophobic pocket in the RT active site. Previous in vitro selection for 4′-Ed4T-resistant viral strains revealed M184V and P119S/T165A/M184V mutations on days 26 and 81, respectively; M184V and P119S/T165A/M184V conferred 3- and 130-fold resistance to 4′-Ed4T, respectively. We investigated the relative contributions of these mutations, engineered into the strain NL4-3 background, to drug resistance, RT activity, and viral growth. Viral variants with single RT mutations (P119S or T165A) did not show resistance to 4′-Ed4T; however, M184V and P119S/T165A/M184V conferred three- and fivefold resistance, respectively, compared with that of the wild-type virus. The P119S/M184V and T165A/M184V variants showed about fourfold resistance to 4′-Ed4T. The differences in the growth kinetics of the variants were not more than threefold. The purified RT of mutants with the P119S/M184V and T165A/M184V mutations were inhibited by 4′-Ed4TTP with 8- to 13-fold less efficiency than wild-type RT. M184V may be the primary resistance-associated mutation of 4′-Ed4T, and P119S and T165A are secondary mutations. On the basis of our findings and the results of structural modeling, a virus with a high degree of resistance to 4′-Ed4T (e.g., more than 50-fold resistance) will be difficult to develop. The previously observed 130-fold resistance of the virus with P119S/T165A/M184V to 4′-Ed4T may be partly due to mutations both in the RT sequence and outside the RT sequence.
Regulation of Wnt signaling by the nuclear pore complex.

BACKGROUND & AIMS The function of beta-catenin as a transcriptional coactivator of T-cell factor-4 (TCF-4) is crucial for colorectal carcinogenesis. However, beta-catenin has no nuclear localization signal, and the mechanisms by which beta-catenin is imported into the nucleus and forms a complex with the TCF-4 nuclear protein are poorly understood. METHODS Proteins of 2 colorectal cancer cell lines, HCT-116 and DLD1, were immunoprecipitated with anti-TCF-4 antibody and analyzed directly by nanoflow liquid chromatography and mass spectrometry. The functional significance of nuclear pore complex (NPC) proteins in Wnt signaling was evaluated by in vitro and in vivo sumoylation, luciferase reporter, and colony formation assays. RESULTS TCF-4 interacted with a large variety of NPC proteins including ras-related nuclear protein (Ran), Ran binding protein-2 (RanBP2), and Ran GTPase-activating protein-1 (RanGAP1). The NPC protein RanBP2 functioned as the small ubiquitin-related modifier (SUMO) E3 ligase of TCF-4, and sumoylation of TCF-4 enhanced the interaction between TCF-4 and beta-catenin. The overexpression of NPC proteins increased the nuclear import of the TCF-4 and beta-catenin proteins and enhanced the transcriptional activity. NPC proteins increased the growth of colorectal cancer cells, whereas sentrin-specific protease-2 inhibited it. CONCLUSIONS Through a comprehensive proteomics approach, we revealed that NPC functions as a novel regulator of Wnt signaling and is possibly involved in colorectal carcinogenesis. A new drug targeting the interactions of TCF-4 with NPC proteins as well as their sumoylation activity might be effective for suppressing aberrant Wnt signaling and the proliferation of colorectal cancer cells.
Microenvironmental regulation of hematopoietic stem cells

A major challenge in hematopoietic biology is the description and understanding of the molecular mechanisms responsible for the regulation of the primitive stem cell compartment. In one sense there exists a wealth of functional and physical properties which provide insight into the biology of the stem cell and its clonal progeny. However, much of this information is descriptive and available only as a function of complex in vivo assays. In order to move beyond these limitations, in vitro systems which accurately recapitulate the self‐renewal, differentiation and proliferative behaviors of stem cells are required. We have approached this issue by focusing on the in vivo stem cell microenvironment. Dissection of this microenvironment into discrete cellular entities has yielded a cell line with in vitro stem cell supportive properties consistent with those which might be expected in a stem cell niche. Studies are summarized which suggest that a single stromal cell line provides a milieu which facilitates the in vitro maintenance of transplantable stem cells as well as the generation of large populations of committed progenitors. It is anticipated that this system will allow a direct analysis of stem cell regulatory pathways. Stem Cells 1997; 15(suppl 1): 63‐68
Unraveling the mechanism by which TRPV4 mutations cause skeletal dysplasias

Transient Receptor Potential Vanilloid 4 (TRPV4) is a mechano- and osmosensitive cation channel that is highly expressed in chondrocytes, the cells in cartilage. A large number of mutations in TRPV4 have been linked to skeletal dysplasias, and the goal of this addendum is to shed light on the mechanisms by which mutations in TRPV4 can cause skeletal dysplasias by focusing on 3 recent publications. These papers suggest that skeletal dysplasia-causing TRPV4 mutations reprogram chondrocytes to increase follistatin production, which inhibits BMP signaling, thus slowing the process of endochondral ossification and leading to skeletal dysplasia. In spite of these important advances in our understanding of the disease mechanism, much remains to be elucidated. Nonetheless, these new data suggest that inhibiting aberrant TRPV4 activity in the cartilage may be a promising direction for therapeutic intervention.
NF-kappaB Signaling Pathways in Neurological Inflammation: A Mini Review

The NF-κB (nuclear factor κ-light-chain-enhancer of activated B cells) transcription factor family is a pleiotropic regulator of many cellular signaling pathways, providing a mechanism for the cells in response to a wide variety of stimuli linking to inflammation. The stimulated cells will be regulated by not only the canonical but also non-canonical NF-κB pathways. To initiate both of these pathways, IκB-degradation triggers NF-κB release and the nuclear translocated-heterodimer (or homodimer) can associate with the κB sites of promoter to regulate the gene transcriptions. NF-κB ubiquitously expresses in neurons and the constitutive NF-κB activation is associated with processing of neuronal information. NF-κB can regulate the transcription of genes such as chemokines, cytokines, proinflammatory enzymes, adhesion molecules, proinflammatory transcription factors, and other factors to modulate the neuronal survival. In neuronal insult, NF-κB constitutively active in neuron cell bodies can protect neurons against different injuries and regulate the neuronal inflammatory reactions. Besides neurons, NF-κB transcription factors are abundant in glial cells and cerebral blood vessels and the diverse functions of NF-κB also regulate the inflammatory reaction around the neuronal environment. NF-κB transcription factors are abundant in the brain and exhibit diverse functions. Several central nerve system (CNS) diseases are linked to NF-κB activated by inflammatory mediators. The RelA and c-Rel expression produce opposite effects on neuronal survival. Importantly, c-Rel expression in CNS plays a critical role in anti-apoptosis and reduces the age-related behaviors. Moreover, the different subunits of NF-κB dimer formation can modulate the neuroninflammation, neuronal protection, or neurotoxicity. The diverse functions of NF-κB depend on the subunits of the NF-κB dimer-formation which enable us to develop a therapeutic approach to neuroinflammation based on a new concept of inflammation as a strategic tool in neuronal cells. However, the detail role of NF-κB in neuroinflammation, remains to be clarified. In the present article, we provide an updated review of the current state of our knowledge about relationship between NF-κB and neuroinflammation.
Highly Efficient Single-Phase Transformerless Inverters for Grid-Connected Photovoltaic Systems

Driven by worldwide demand for renewable sources, the photovoltaic market saw in the last years a considerable amount of innovations regarding the construction and operation of inverters connected to the grid. One significant advance, among some that will be here discussed is, for example, the abolition of the galvanic isolation in inverters installed in Germany. There, transformerless topologies, like the H5 and Heric, can reach very high levels of efficiency and allow the best cost-benefit ratio for low-power grid-tied systems. This paper will follow this direction and propose a single-phase transformerless inverter circuit being composed of the association of two step-down converters. Each one modulates a half-wave of the output current, as the correct polarity of the connection to the grid is provided by low-frequency switches. Due to its straightforward design, reduced amount of semiconductors, and simple operation, it is possible to achieve a high level of efficiency and reliability. These and some other characteristics will be benchmarked against other existing circuits, being followed by a theoretical analysis on the properties of the proposed solution. The project of a laboratory prototype will be presented, along with a discussion about the obtained experimental results.
MEF 9 , an E-Subclass Pentatricopeptide Repeat Protein , Is Required for an RNA Editing Event in the nad 7 Transcript in Mitochondria of Arabidopsis 1 [ C ] [ OA ]

RNA editing in plants alters specific nucleotides from C to U in mRNAs in plastids and in mitochondria. I here characterize the nuclear gene MITOCHONDRIAL EDITING FACTOR9 (MEF9) that is required for RNA editing of the site nad7-200 in the nad7 mitochondrial mRNA in Arabidopsis (Arabidopsis thaliana). The MEF9 protein belongs to the E subfamily of pentatricopeptide repeat proteins and unlike the three previously identified mitochondrial editing factors MEF1 and MEF11 in Arabidopsis and OGR1 in rice (Oryza sativa) does not contain a DYW C-terminal domain. In addition, the E domain is incomplete, but seems to be functionally required, since one of the two independent EMS mutants encodes a MEF9 protein truncated by a stop codon at the beginning of the E domain. In both mutant plants premature stop codons in MEF9 inactivate RNA editing at site nad7-200. The homozygous mutant plants are viable and develop rather normally. The lack of RNA editing at site nad7-200 thus seems to be tolerated although this editing event is conserved in most plant species or the genomic sequence already codes for a T at this position, resulting in a generally conserved amino acid codon.
Inhibition of Borna disease virus replication by an endogenous bornavirus-like element in the ground squirrel genome

Significance Sequences derived from ancient viruses have been shown to make up a substantial part of animal genomes. Bornaviruses, a genus of nonsegmented, negative-sense RNA virus, also have left their DNA copies in the genomes of a number of vertebrate lineages. Recent studies have demonstrated that some endogenous bornavirus-like elements (EBLs) may have acquired functions in their hosts as a result of exaptation. In this study, we show that protein encoded by an EBL in the genome of the thirteen-lined ground squirrel efficiently blocks infection and replication of extant bornavirus. To our knowledge, this is the first report showing that endogenous nonretroviral RNA virus elements may function in antiviral defense, providing a potential role for RNA virus endogenization in host evolution. Animal genomes contain endogenous viral sequences, such as endogenous retroviruses and retrotransposons. Recently, we and others discovered that nonretroviral viruses also have been endogenized in many vertebrate genomes. Bornaviruses belong to the Mononegavirales and have left endogenous fragments, called “endogenous bornavirus-like elements” (EBLs), in the genomes of many mammals. The striking features of EBLs are that they contain relatively long ORFs which have high sequence homology to the extant bornavirus proteins. Furthermore, some EBLs derived from bornavirus nucleoprotein (EBLNs) have been shown to be transcribed as mRNA and probably are translated into proteins. These features lead us to speculate that EBLs may function as cellular coopted genes. An EBLN element in the genome of the thirteen-lined ground squirrel (Ictidomys tridecemlineatus), itEBLN, encodes an ORF with 77% amino acid sequence identity to the current bornavirus nucleoprotein. In this study, we cloned itEBLN from the ground squirrel genome and investigated its involvement in Borna disease virus (BDV) replication. Interestingly, itEBLN, but not a human EBLN, colocalized with the viral factory in the nucleus and appeared to affect BDV polymerase activity by being incorporated into the viral ribonucleoprotein. Our data show that, as do certain endogenous retroviruses, itEBLN potentially may inhibit infection by related exogenous viruses in vivo.
Lymphocyte populations of AKR-J mice. I. Effect of aging on migration patterns, response to PHA and expression of theta antigen.

The present study describes abnormalities that occur in the lymph node, spleen, thymus, and blood lymphocytes of two distinct types of leukemic AKR/J mice. These two types, designated A and B leukemia, occur in a ratio of 3:1 in mice aged 7 to 10 months. Type A leukemic mice are characterized by the presence of a thymoma and enlarged peripheral lymphoid organs, and lymphocytes which 1) fail to migrate to lymph nodes, 2) exhibit normal transformation in response to PHA, and 3) have elevated sensitivity to anti-theta (θ) serum. Type B leukemic mice have an atrophic thymus and elarged peripheral lymphoid organs; their lymphocytes 1) fail to home to lymph nodes, 2) exhibit decreased transformation in response to PHA, and 3) have decreased sensitivity to anti-θ serum. The significance of the dissociation of thymus-dependent characteristics, e.g., lymphocyte recirculation, response to PHA, and expression of the θ antigen, observed in type A leukemic lymphocytes, as well as the possible origins of type A and B leukemic lymphocyte populations, are discussed.
Temperature Modulates the Effects of Ocean Acidification on Intestinal Ion Transport in Atlantic Cod, Gadus morhua

CO2-driven seawater acidification has been demonstrated to enhance intestinal bicarbonate secretion rates in teleosts, leading to an increased release of CaCO3 under simulated ocean acidification scenarios. In this study, we investigated if increasing CO2 levels stimulate the intestinal acid–base regulatory machinery of Atlantic cod (Gadus morhua) and whether temperatures at the upper limit of thermal tolerance stimulate or counteract ion regulatory capacities. Juvenile G. morhua were acclimated for 4 weeks to three CO2 levels (550, 1200, and 2200 μatm) covering present and near-future natural variability, at optimum (10°C) and summer maximum temperature (18°C), respectively. Immunohistochemical analyses revealed the subcellular localization of ion transporters, including Na+/K+-ATPase (NKA), Na+/H+-exchanger 3 (NHE3), Na+/HCO3− cotransporter (NBC1), pendrin-like Cl−/HCO3− exchanger (SLC26a6), V-type H+-ATPase subunit a (VHA), and Cl− channel 3 (CLC3) in epithelial cells of the anterior intestine. At 10°C, proteins and mRNA were generally up-regulated for most transporters in the intestinal epithelium after acclimation to higher CO2 levels. This supports recent findings demonstrating increased intestinal HCO3− secretion rates in response to CO2 induced seawater acidification. At 18°C, mRNA expression and protein concentrations of most ion transporters remained unchanged or were even decreased, suggesting thermal compensation. This response may be energetically favorable to retain blood HCO3− levels to stabilize pHe, but may negatively affect intestinal salt and water resorption of marine teleosts in future oceans.
Pre-existing diabetes mellitus increases the risk of gastric cancer: a meta-analysis.

AIM To systematically assess the association between diabetes and incidence of gastric cancer. METHODS We searched MedLine (PubMed), EMBASE, and the Cochrane Library without any limitations with respect to publication date or language, we also searched the references of qualifying articles. Case-control studies and cohort studies comparing the risk of gastric cancer between diabetic patients and control subjects were included. We excluded studies reporting only standardized incidence ratios without control groups and those that investigated only mortality but not incidence. Seventeen studies met our criteria, and the qualities of these studies were assessed using the Newcastle-Ottawa Quality Assessment Scale. We performed a meta-analysis of pre-existing diabetes and gastric cancer incidence using the DerSimonian-Laird method for random-effects. For subgroup analyses, we separated the studies by study type, region, sex and method to determine confounding factors and reliability. We also conducted subgroup analyses to examine the effects of smoking, Helicobacter pylori (H. pylori) infection, and cancer site. Publication bias was evaluated using Begg's test. RESULTS A random-effects model meta-analysis showed an increased gastric cancer risk in diabetic patients [relative risk (RR) = 1.19; 95%CI: 1.08-1.31]. Subgroup analyses indicated that this result persisted in cohort studies (RR = 1.20; 95%CI: 1.08-1.34), in studies on populations of both Western (RR = 1.18; 95%CI: 1.03-1.36) and Eastern countries (RR = 1.19; 95%CI: 1.02-1.38), in a female subgroup (RR=1.24; 95%CI: 1.01-1.52), and in highly qualified studies (RR = 1.17; 95%CI: 1.05-1.31). Moreover, these results persisted when the analysis was confined to studies adjusted for well-known gastric cancer risk factors such as smoking (RR = 1.17; 95%CI: 1.01-1.34) and H. pylori infection (RR = 2.35; 95%CI: 1.24-4.46). CONCLUSION Pre-existing diabetes mellitus may increase the risk of gastric cancer by approximately 19%. This effect seems to be unrelated to geographical region.