1,663 research outputs found

    Knowledge-Attitudes-Practices About Malaria Among Communities in Southern Benin

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    Malaria still remains the main public health problem in Benin. We explored the determinants that influenced malaria treatment as well as protective behaviors, to generate a framework of useful ideas as alternative strategies against malaria. A cross-sectional survey of the knowledge, attitudes and practices (KAP) was conducted at Hozin, Vakon and Agblangandan districts in southern region of Benin. Descriptive statistics were computed and mixed logistic regression helped evaluating the relationship between frequency of each category of severity of malaria and sex group, educational level, treatment, means of self-protection against mosquitoes and identification of the cause of malaria. A significant proportion 750 (81.3%) (p<0.001) of participants stated that malaria was caused by mosquitoes. The respondents who mentioned sun as the cause of malaria, have trivialized more malaria in a proportion of about 59.30% (OR=2.67 [95% CI 1.61-4.44]) followed by those who have reported the cause of body weakness (43.68%) (OR=2.97 [95% CI 1.68-5.28]). Poor knowledge justifies the trivialization of the disease and poor management of malaria control means. National Malaria Control Programs should improve access to education, especially for women and could help improving prevention and control behaviours against malaria in communities

    Gastrointestinal Parasites of Two Populations of Arctic Foxes (<em>Vulpes lagopus</em>) from Northeast Greenland

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    Parasitological examination of 275 faecal samples from Arctic foxes (Vulpes lagopus) collected at Zackenberg Valley and Karupelv Valley in north-east Greenland from 2006 to 2008 was conducted using sieving and microscopy. Overall, 125 (45.5%) samples contained parasite eggs of Taenia crassiceps, Taenia serialis, Toxascaris leonina, Eucoleus boehmi, Physalopteridae and Ancylostomatidae, and Strongyloides-like larvae. As long-term ecological studies are conducted at both sampling locations, the present findings constitute a baseline data set for further parasitological monitoring

    Statistical mechanics of error exponents for error-correcting codes

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    Error exponents characterize the exponential decay, when increasing message length, of the probability of error of many error-correcting codes. To tackle the long standing problem of computing them exactly, we introduce a general, thermodynamic, formalism that we illustrate with maximum-likelihood decoding of low-density parity-check (LDPC) codes on the binary erasure channel (BEC) and the binary symmetric channel (BSC). In this formalism, we apply the cavity method for large deviations to derive expressions for both the average and typical error exponents, which differ by the procedure used to select the codes from specified ensembles. When decreasing the noise intensity, we find that two phase transitions take place, at two different levels: a glass to ferromagnetic transition in the space of codewords, and a paramagnetic to glass transition in the space of codes.Comment: 32 pages, 13 figure

    Mean field and corrections for the Euclidean Minimum Matching problem

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    Consider the length LMMEL_{MM}^E of the minimum matching of N points in d-dimensional Euclidean space. Using numerical simulations and the finite size scaling law =ÎČMME(d)N1−1/d(1+A/N+...) = \beta_{MM}^E(d) N^{1-1/d}(1+A/N+... ), we obtain precise estimates of ÎČMME(d)\beta_{MM}^E(d) for 2≀d≀102 \le d \le 10. We then consider the approximation where distance correlations are neglected. This model is solvable and gives at d≄2d \ge 2 an excellent ``random link'' approximation to ÎČMME(d)\beta_{MM}^E(d). Incorporation of three-link correlations further improves the accuracy, leading to a relative error of 0.4% at d=2 and 3. Finally, the large d behavior of this expansion in link correlations is discussed.Comment: source and one figure. Submitted to PR

    A random cell motility gradient downstream of FGF controls elongation of amniote embryos

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    Vertebrate embryos are characterized by an elongated antero-posterior (AP) body axis, which forms by progressive cell deposition from a posterior growth zone in the embryo. Here, we used tissue ablation in the chicken embryo to demonstrate that the caudal presomitic mesoderm (PSM) has a key role in axis elongation. Using time-lapse microscopy, we analysed the movements of fluorescently labelled cells in the PSM during embryo elongation, which revealed a clear posterior-to-anterior gradient of cell motility and directionality in the PSM. We tracked the movement of the PSM extracellular matrix in parallel with the labelled cells and subtracted the extracellular matrix movement from the global motion of cells. After subtraction, cell motility remained graded but lacked directionality, indicating that the posterior cell movements associated with axis elongation in the PSM are not intrinsic but reflect tissue deformation. The gradient of cell motion along the PSM parallels the fibroblast growth factor (FGF)/mitogen-activated protein kinase (MAPK) gradient1, which has been implicated in the control of cell motility in this tissue2. Both FGF signalling gain- and loss-of-function experiments lead to disruption of the motility gradient and a slowing down of axis elongation. Furthermore, embryos treated with cell movement inhibitors (blebbistatin or RhoK inhibitor), but not cell cycle inhibitors, show a slower axis elongation rate. We propose that the gradient of random cell motility downstream of FGF signalling in the PSM controls posterior elongation in the amniote embryo. Our data indicate that tissue elongation is an emergent property that arises from the collective regulation of graded, random cell motion rather than by the regulation of directionality of individual cellular movements

    Spatial and topological organization of DNA chains induced by gene co-localization

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    Transcriptional activity has been shown to relate to the organization of chromosomes in the eukaryotic nucleus and in the bacterial nucleoid. In particular, highly transcribed genes, RNA polymerases and transcription factors gather into discrete spatial foci called transcription factories. However, the mechanisms underlying the formation of these foci and the resulting topological order of the chromosome remain to be elucidated. Here we consider a thermodynamic framework based on a worm-like chain model of chromosomes where sparse designated sites along the DNA are able to interact whenever they are spatially close-by. This is motivated by recurrent evidence that there exists physical interactions between genes that operate together. Three important results come out of this simple framework. First, the resulting formation of transcription foci can be viewed as a micro-phase separation of the interacting sites from the rest of the DNA. In this respect, a thermodynamic analysis suggests transcription factors to be appropriate candidates for mediating the physical interactions between genes. Next, numerical simulations of the polymer reveal a rich variety of phases that are associated with different topological orderings, each providing a way to increase the local concentrations of the interacting sites. Finally, the numerical results show that both one-dimensional clustering and periodic location of the binding sites along the DNA, which have been observed in several organisms, make the spatial co-localization of multiple families of genes particularly efficient.Comment: Figures and Supplementary Material freely available on http://dx.doi.org/10.1371/journal.pcbi.100067

    Arctic marine phytobenthos of northern Baffin Island

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    This project was supported by SAMS and NFSD core funding (Oceans 2025 WP 4.5 from the UK Natural Environment Research Council), the European Commission (ASSEMBLE, grant agreement no. 227799), and the TOTAL Foundation (Paris; Project “Macroalgal and oomycete benthic diversity in the Canadian Marine Arctic”). This work also received funding from the MASTS pooling initiative (The Marine Alliance for Science and Technology for Scotland) and their support is gratefully acknowledged. MASTS is funded by the Scottish Funding Council (grant reference HR09011) and contributing institutions. We also would like to thank Laura Grenville-Briggs (KTH, Stockholm) for help with bioinformatics analyses as well as Cindy Grant and Philippe Archambault (University of Quebec, Rimouski) for help with preparing the map of the study area (Fig. 1).Peer reviewedPublisher PD

    Identification of soluble tumor necrosis factor-like weak inducer of apoptosis (sTWEAK) as a possible biomarker of subclinical atherosclerosis

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    OBJECTIVES: Assessment of vascular risk in asymptomatic patients and the response to medical therapy is a major challenge for prevention of cardiovascular events. Our aim was to identify proteins differentially released by healthy versus atherosclerotic arterial walls, which could be found in plasma and serve as markers of atherosclerosis. METHODS AND RESULTS: We have analyzed supernatants obtained from cultured human carotid plaques and healthy arteries by surface-enhanced laser-desorption/ionization time-of-flight mass spectrometry ProteinChip System. Surface-enhanced laser-desorption/ionization analysis unveiled an 18.4-kDa peak released in lower amount by carotid plaques than normal endarteries. This protein was identified as soluble tumor necrosis factor-like weak inducer of apoptosis (sTWEAK). To confirm that sTWEAK was the protein of interest, Western blot and enzyme-linked immunosorbent assay were performed. Both techniques confirmed that sTWEAK levels were decreased in carotid plaque supernatants. Subsequent measurement of sTWEAK in plasma showed a reduced concentration in subjects with carotid stenosis (N=30) compared with healthy subjects matched by sex and age (N=28) (P<0.001). Furthermore, in a test population of 106 asymptomatic subjects, we showed that sTWEAK concentrations negatively correlated with the carotid intima-media thickness (r=-0.4; P<0.001), an index of subclinical atherosclerosis. CONCLUSIONS: These results suggest that sTWEAK could be a potential biomarker of atherosclerosis

    Detection and dynamics of circulating tumor cells in patients with high-risk prostate cancer treated with radiotherapy and hormones: a prospective phase II study

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    BACKGROUND: Circulating tumor cells (CTCs) are an established prognostic marker in castration-resistant prostate cancer but have received little attention in localized high-risk disease. We studied the detection rate of CTCs in patients with high-risk prostate cancer before and after androgen deprivation therapy and radiotherapy to assess its value as a prognostic and monitoring marker. PATIENTS AND METHODS: We performed a prospective analysis of CTCs in the peripheral blood of 65 treatment-naive patients with high-risk prostate cancer. EpCAM-positive CTCs were enumerated using the CELLSEARCH system at 4 timepoints. A cut off of 0 vs >/= 1 CTC/7.5 ml blood was defined as a threshold for negative versus positive CTCs status. RESULTS: CTCs were detected in 5/65 patients (7.5%) at diagnosis, 8/62 (12.9%) following neoadjuvant androgen deprivation and 11/59 (18.6%) at the end of radiotherapy, with a median CTC count/7.5 ml of 1 (range, 1-136). Only 1 patient presented a positive CTC result 9 months after radiotherapy. Positive CTC status (at any timepoint) was not significantly associated with any clinical or pathologic factors. However, when we analyzed variations in CTC patterns following treatment, we observed a significant association between conversion of CTCs and stages T3 (P = 0.044) and N1 (P = 0.002). Detection of CTCs was not significantly associated with overall survival (P > 0.40). CONCLUSIONS: Our study showed a low detection rate for CTCs in patients with locally advanced high-risk prostate cancer. The finding of a de novo positive CTC count after androgen deprivation therapy is probably due to a passive mechanism associated with the destruction of the tumor. Further studies with larger samples and based on more accurate detection of CTCs are needed to determine the potential prognostic and therapeutic value of this approach in non-metastatic prostate cancer. TRIAL REGISTRATION: ClinicalTrials.gov ID: NCT01800058
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