13,352 research outputs found
Scatteract: Automated extraction of data from scatter plots
Charts are an excellent way to convey patterns and trends in data, but they
do not facilitate further modeling of the data or close inspection of
individual data points. We present a fully automated system for extracting the
numerical values of data points from images of scatter plots. We use deep
learning techniques to identify the key components of the chart, and optical
character recognition together with robust regression to map from pixels to the
coordinate system of the chart. We focus on scatter plots with linear scales,
which already have several interesting challenges. Previous work has done fully
automatic extraction for other types of charts, but to our knowledge this is
the first approach that is fully automatic for scatter plots. Our method
performs well, achieving successful data extraction on 89% of the plots in our
test set.Comment: Submitted to ECML PKDD 2017 proceedings, 16 page
Cerebellar defects in Pdss2 conditional knockout mice during embryonic development and in adulthood
PDSS2 is a gene that encodes one of the two subunits of trans-prenyl diphosphate synthase that is essential for ubiquinone biosynthesis. It is known that mutations in PDSS2 can cause primary ubiquinone deficiency in humans and a similar disease in mice. Cerebellum is the most often affected organ in ubiquinone deficiency, and cerebellar atrophy has been diagnosed in many infants with this disease. In this study, two Pdss2 conditional knockout mouse lines directed by Pax2-cre and Pcp2-cre were generated to investigate the effect of ubiquinone deficiency on cerebellum during embryonic development and in adulthood, respectively. The Pdss2 f/-; Pax2-cre mouse recapitulates some symptoms of ubiquinone deficiency in infants, including severe cerebellum hypoplasia and lipid accumulation in skeletal muscles at birth. During early cerebellum development (E12.5-14.5), Pdss2 knockout initially causes the delay of radial glial cell growth and neuron progenitor migration, so the growth of mutant cerebellum is retarded. During later development (E15.5-P0), increased ectopic apoptosis of neuroblasts and impaired cell proliferation result in the progression of cerebellum hypoplasia in the mutant. Thus, the mutant cerebellum contains fewer neurons at birth, and the cells are disorganized. The developmental defect of mutant cerebellum does not result from reduced Fgf8 expression before E12.5. Electron microscopy reveals mitochondrial defects and increased autophagic-like vacuolization that may arise in response to abnormal mitochondria in the mutant cerebellum. Nevertheless, the mutant mice die soon after birth probably due to cleft palate and micrognathia, which may result from Pdss2 knockout caused by ectopic Pax2-cre expression in the first branchial arch. On the other hand, the Pdss2 f/-; Pcp2-cre mouse is healthy at birth but gradually loses cerebellar Purkinje cells and develops ataxia-like symptoms at 9.5months; thus this conditional knockout mouse may serve as a model for ubiquinone deficiency in adult patients. In conclusion, this study provides two mouse models of Pdss2 based ubiquinone deficiency. During cerebellum development, Pdss2 knockout results in severe cerebellum hypoplasia by impairing cell migration and eliciting ectopic apoptosis, whereas Pdss2 knockout in Purkinje cells at postnatal stages leads to the development of cerebellar ataxia. © 2011 Elsevier Inc.postprin
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Antrodia cinnamomea reduces obesity and modulates the gut microbiota in high-fat diet-fed mice.
BackgroundObesity is associated with gut microbiota dysbiosis, disrupted intestinal barrier and chronic inflammation. Given the high and increasing prevalence of obesity worldwide, anti-obesity treatments that are safe, effective and widely available would be beneficial. We examined whether the medicinal mushroom Antrodia cinnamomea may reduce obesity in mice fed with a high-fat diet (HFD).MethodsMale C57BL/6J mice were fed a HFD for 8 weeks to induce obesity and chronic inflammation. The mice were treated with a water extract of A. cinnamomea (WEAC), and body weight, fat accumulation, inflammation markers, insulin sensitivity and the gut microbiota were monitored.ResultsAfter 8 weeks, the mean body weight of HFD-fed mice was 39.8±1.2 g compared with 35.8±1.3 g for the HFD+1% WEAC group, corresponding to a reduction of 4 g or 10% of body weight (P<0.0001). WEAC supplementation reduced fat accumulation and serum triglycerides in a statistically significant manner in HFD-fed mice. WEAC also reversed the effects of HFD on inflammation markers (interleukin-1β, interleukin-6, tumor necrosis factor-α), insulin resistance and adipokine production (leptin and adiponectin). Notably, WEAC increased the expression of intestinal tight junctions (zonula occludens-1 and occludin) and antimicrobial proteins (Reg3g and lysozyme C) in the small intestine, leading to reduced blood endotoxemia. Finally, WEAC modulated the composition of the gut microbiota, reducing the Firmicutes/Bacteroidetes ratio and increasing the level of Akkermansia muciniphila and other bacterial species associated with anti-inflammatory properties.ConclusionsSupplementation with A. cinnamomea produces anti-obesogenic, anti-inflammatory and antidiabetic effects in HFD-fed mice by maintaining intestinal integrity and modulating the gut microbiota
Cell death caused by single-stranded oligodeoxynucleotide-mediated targeted genomic sequence modification
Targeted gene repair directed by single-stranded oligodeoxynucleotides (ssODNs) offers a promising tool for biotechnology and gene therapy. However, the methodology is currently limited by its low frequency of repair events, variability, and low viability of "corrected" cells. In this study, we showed that during ssODN-mediated gene repair reaction, a significant population of corrected cells failed to divide, and were much more prone to undergo apoptosis, as marked by processing of caspases and PARP-1. In addition, we found that apoptotic cell death triggered by ssODN-mediated gene repair was largely independent of the ATM/ATR kinase. Furthermore, we examined the potential involvement of the mismatch repair (MMR) proteins in this "correction reaction-induced" cell death. Result showed that while defective MMR greatly enhanced the efficiency of gene correction, compromising the MMR system did not yield any viable corrected clone, indicating that the MMR machinery, although plays a critical role in determining ssODN-directed repair, was not involved in the observed cellular genotoxic responses. © 2009. Mary Ann Liebert, Inc.published_or_final_versio
Characterization of Chlorinated Aliphatic Hydrocarbons and Environmental Variables in a Shallow Groundwater in Shanghai Using Kriging Interpolation and Multifactorial Analysis
CAHs, as a cleaning solvent, widely contaminated shallow groundwater with the development of manufacturing in China's Yangtze River Delta. This study focused on the distribution of CAHs, and correlations between CAHs and environmental variables in a shallow groundwater in Shanghai, using kriging interpolation and multifactorial analysis. The results showed that the overall CAHs plume area (above DIV) was approximately 9,000 m(2) and located in the 2-4 m underground, DNAPL was accumulated at an area of approximately 1,400 m(2) and located in the 6-8m sandy silt layer on the top of the muddy silty clay. Heat-map of PPC for CAHs and environmental variables showed that the correlation between 'Fe2+' and most CAHs such as '1,1,1-TCA', '1,1-DCA', '1,1-DCE' and '% TCA' were significantly positive (p<0.001), but '% CA' and/or '% VC' was not, and 'Cl-' was significantly positive correlated with '1,1-DCA' and '1,1-DCE' (p<0.001). The PCA demonstrated that the relative proportions of CAHs in groundwater were mostly controlled by the sources and the natural attenuation. In conclusion, the combination of geographical and chemometrics was helpful to establishing an aerial perspective of CAHs and identifying reasons for the accumulation of toxic dechlorination intermediates, and could become a useful tool for characterizing contaminated sites in general.published_or_final_versio
Brucella abortus invasion of osteocytes modulates connexin 43 and integrin expression and induces osteoclastogenesis via receptor activator of NF-ÎşB ligand and tumor necrosis factor alpha secretion
Osteoarticular brucellosis is the most common localization of human active disease. Osteocytes are the most abundant cells of bone. They secrete factors that regulate the differentiation of both osteoblasts and osteoclasts during bone remodeling. The aim of this study is to determine if Brucella abortus infection modifies osteocyte function. Our results indicate that B. abortus infection induced matrix metalloproteinase 2 (MMP-2), receptor activator for NF-ÎşB ligand (RANKL), proinflammatory cytokines, and keratinocyte chemoattractant (KC) secretion by osteocytes. In addition, supernatants from B. abortus-infected osteocytes induced bone marrow-derived monocytes (BMM) to undergo osteoclastogenesis. Using neutralizing antibodies against tumor necrosis factor alpha (TNF-α) or osteoprotegerin (OPG), RANKL's decoy receptor, we determined that TNF-α and RANKL are involved in osteoclastogenesis induced by supernatants from B. abortus-infected osteocytes. Connexin 43 (Cx43) and the integrins E11/gp38, integrin-α, integrin-β, and CD44 are involved in cell-cell interactions necessary for osteocyte survival. B. abortus infection inhibited the expression of Cx43 but did not modify the expression of integrins. Yet the expression of both Cx43 and integrins was inhibited by supernatants from B. abortus-infected macrophages. B. abortus infection was not capable of inducing osteocyte apoptosis. However, supernatants from B. abortus-infected macrophages induced osteocyte apoptosis in a dose-dependent manner. Taken together, our results indicate that B. abortus infection could alter osteocyte function, contributing to bone damage.Fil: Pesce Viglietti, AyelĂ©n Ivana. Consejo Nacional de Investigaciones CientĂficas y TĂ©cnicas. Oficina de CoordinaciĂłn Administrativa Houssay. Instituto de InmunologĂa, GenĂ©tica y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de InmunologĂa, GenĂ©tica y Metabolismo; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Hospital de ClĂnicas General San MartĂn; ArgentinaFil: Arriola Benitez, Paula Constanza. Consejo Nacional de Investigaciones CientĂficas y TĂ©cnicas. Oficina de CoordinaciĂłn Administrativa Houssay. Instituto de InmunologĂa, GenĂ©tica y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de InmunologĂa, GenĂ©tica y Metabolismo; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Hospital de ClĂnicas General San MartĂn; ArgentinaFil: Gentilini, Maria Virginia. Consejo Nacional de Investigaciones CientĂficas y TĂ©cnicas. Oficina de CoordinaciĂłn Administrativa Houssay. Instituto de InmunologĂa, GenĂ©tica y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de InmunologĂa, GenĂ©tica y Metabolismo; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Hospital de ClĂnicas General San MartĂn; ArgentinaFil: Velasquez, Lis Noelia. Consejo Nacional de Investigaciones CientĂficas y TĂ©cnicas. Instituto de Medicina Experimental. Academia Nacional de Medicina de Buenos Aires. Instituto de Medicina Experimental; ArgentinaFil: Fossati, Carlos Alberto. Consejo Nacional de Investigaciones CientĂficas y TĂ©cnicas. Centro CientĂfico TecnolĂłgico Conicet - La Plata. Instituto de Estudios InmunolĂłgicos y FisiopatolĂłgicos. Universidad Nacional de La Plata. Facultad de Ciencias Exactas. Instituto de Estudios InmunolĂłgicos y FisiopatolĂłgicos; Argentina. Universidad Nacional de La Plata. Facultad de Ciencias Exactas. Departamento de Ciencias BiolĂłgicas; ArgentinaFil: Giambartolomei, Guillermo Hernan. Consejo Nacional de Investigaciones CientĂficas y TĂ©cnicas. Oficina de CoordinaciĂłn Administrativa Houssay. Instituto de InmunologĂa, GenĂ©tica y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de InmunologĂa, GenĂ©tica y Metabolismo; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Hospital de ClĂnicas General San MartĂn; ArgentinaFil: Delpino, MarĂa Victoria. Consejo Nacional de Investigaciones CientĂficas y TĂ©cnicas. Oficina de CoordinaciĂłn Administrativa Houssay. Instituto de InmunologĂa, GenĂ©tica y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de InmunologĂa, GenĂ©tica y Metabolismo; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Hospital de ClĂnicas General San MartĂn; Argentin
The two PPX-GppA homologues from Mycobacterium tuberculosis have distinct biochemical activities
Inorganic polyphosphate (poly-P), guanosine pentaphosphate (pppGpp) and guanosine tetraphosphate (ppGpp) are ubiquitous in bacteria. These molecules play a variety of important physiological roles associated with stress resistance, persistence, and virulence. In the bacterial pathogen Mycobacterium tuberculosis, the identities of the proteins responsible for the metabolism of polyphosphate and (p)ppGpp remain to be fully established. M. tuberculosis encodes two PPX-GppA homologues, Rv0496 (MTB-PPX1) and Rv1026, which share significant sequence similarity with bacterial exopolyphosphatase (PPX) and guanosine pentaphosphate 5′-phosphohydrolase (GPP) proteins. Here we delineate the respective biochemical activities of the Rv0496 and Rv1026 proteins and benchmark these against the activities of the PPX and GPP proteins from Escherichia coli. We demonstrate that Rv0496 functions as an exopolyphosphatase, showing a distinct preference for relatively short-chain poly-P substrates. In contrast, Rv1026 has no detectable exopolyphosphatase activities. Analogous to the E. coli PPX and GPP enzymes, the exopolyphosphatase activities of Rv0496 are inhibited by pppGpp and, to a lesser extent, by ppGpp alarmones, which are produced during the bacterial stringent response. However, neither Rv0496 nor Rv1026 have the ability to hydrolyze pppGpp to ppGpp; a reaction catalyzed by E. coli PPX and GPP. Both the Rv0496 and Rv1026 proteins have modest ATPase and to a lesser extent ADPase activities. pppGpp alarmones inhibit the ATPase activities of Rv1026 and, to a lesser extent, the ATPase activities of Rv0496. We conclude that PPX-GppA family proteins may not possess all the catalytic activities implied by their name and may play distinct biochemical roles involved in polyphosphate and (p)ppGpp metabolic pathways. © 2012 2012 Choi et al.published_or_final_versio
Near Horizon of 5D Rotating Black Holes from 2D Perspective
We study the CFT dual to five dimensional extremal rotating black holes, by
investigating the two dimensional perspective of their near horizon geometry.
From two dimensional point of view, we show that both gauge fields, related to
the two rotations, appear in the same manner in the asymptotic symmetry and in
the associated central charge. We find that, our results are in perfect
agreement with the generalization of Kerr/CFT approach to five dimensional
extremal rotating black holes.Comment: The last version to appear in the European Physical Journal
Evolution favors protein mutational robustness in sufficiently large populations
BACKGROUND: An important question is whether evolution favors properties such
as mutational robustness or evolvability that do not directly benefit any
individual, but can influence the course of future evolution. Functionally
similar proteins can differ substantially in their robustness to mutations and
capacity to evolve new functions, but it has remained unclear whether any of
these differences might be due to evolutionary selection for these properties.
RESULTS: Here we use laboratory experiments to demonstrate that evolution
favors protein mutational robustness if the evolving population is sufficiently
large. We neutrally evolve cytochrome P450 proteins under identical selection
pressures and mutation rates in populations of different sizes, and show that
proteins from the larger and thus more polymorphic population tend towards
higher mutational robustness. Proteins from the larger population also evolve
greater stability, a biophysical property that is known to enhance both
mutational robustness and evolvability. The excess mutational robustness and
stability is well described by existing mathematical theories, and can be
quantitatively related to the way that the proteins occupy their neutral
network.
CONCLUSIONS: Our work is the first experimental demonstration of the general
tendency of evolution to favor mutational robustness and protein stability in
highly polymorphic populations. We suggest that this phenomenon may contribute
to the mutational robustness and evolvability of viruses and bacteria that
exist in large populations
Metacarpophalangeal joint loads during bonobo locomotion: model predictions vs. proxies
The analysis of internal trabecular and cortical bone has been an informative tool for drawing inferences about behaviour in extant and fossil primate taxa. Within the hand, metacarpal bone architecture has been shown to correlate well with primate locomotion; however, the extent of morphological differences across taxa is unexpectedly small given the variability in hand use. One explanation for this observation is that the activity-related differences in the joint loads acting on the bone are simply smaller than estimated based on commonly used proxies (i.e. external loading and joint posture), which neglect the influence of muscle forces. In this study, experimental data and a musculoskeletal finger model are used to test this hypothesis by comparing differences between climbing and knuckle-walking locomotion of captive bonobos (Pan paniscus) based on (i) joint load magnitude and direction predicted by the models and (ii) proxy estimations. The results showed that the activity-related differences in predicted joint loads are indeed much smaller than the proxies would suggest, with joint load magnitudes being almost identical between the two locomotor modes. Differences in joint load directions were smaller but still evident, indicating that joint load directions might be a more robust indicator of variation in hand use than joint load magnitudes. Overall, this study emphasizes the importance of including muscular forces in the interpretation of skeletal remains and promotes the use of musculoskeletal models for correct functional interpretations
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