9 research outputs found

    Pottery from the interstage of Neolithic and Bronze Age and from later epochs

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    <div><p>Meniere's disease is an episodic vestibular syndrome associated with sensorineural hearing loss (SNHL) and tinnitus. Patients with MD have an elevated prevalence of several autoimmune diseases (rheumatoid arthritis, systemic lupus erythematosus, ankylosing spondylitis and psoriasis), which suggests a shared autoimmune background. Functional variants of several genes involved in the NF-κB pathway, such as <i>REL</i>, <i>TNFAIP3</i>, <i>NFKB1</i> and <i>TNIP1</i>, have been associated with two or more immune-mediated diseases and allelic variations in the <i>TLR10</i> gene may influence bilateral affectation and clinical course in MD. We have genotyped 716 cases of MD and 1628 controls by using the ImmunoChip, a high-density genotyping array containing 186 autoimmune loci, to explore the association of immune system related-loci with sporadic MD. Although no single nucleotide polymorphism (SNP) reached a genome-wide significant association (p<10<sup>−8</sup>), we selected allelic variants in the NF-kB pathway for further analyses to evaluate the impact of these SNPs in the clinical outcome of MD in our cohort. None of the selected SNPs increased susceptibility for MD in patients with uni or bilateral SNHL. However, two potential regulatory variants in the <i>NFKB1</i> gene (rs3774937 and rs4648011) were associated with a faster hearing loss progression in patients with unilateral SNHL. So, individuals with unilateral MD carrying the C allele in rs3774937 or G allele in rs4648011 had a shorter mean time to reach hearing stage 3 (>40 dB HL) (log-rank test, corrected p values were p = 0.009 for rs3774937 and p = 0.003 for rs4648011, respectively). No variants influenced hearing in bilateral MD. Our data support that the allelic variants rs3774937 and rs4648011 can modify hearing outcome in patients with MD and unilateral SNHL.</p></div

    Single nucleotide polymorphisms in the NF-κB pathway with reported associations.

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    a<p>NCBI human genome build 37 coordinates.</p>b<p>http://<a href="http://www.ncbi.nlm.nih.gov/gap" target="_blank">www.ncbi.nlm.nih.gov/gap</a><a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0112171#pone.0112171-Tryka1" target="_blank">[38]</a>.</p><p>Single nucleotide polymorphisms in the NF-κB pathway with reported associations.</p

    Epidemic curve and vector infestation level reported for each epidemiological week during 2014 and 2015 in Panama and San Miguelito districts.

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    <p><b>(A)</b> Epidemic curve of CHIKV infections (97/107) from epidemiological week 19 in 2014 to 26 in 2015; autochthonous (red) and impor (blue) cases reported. (<b>B)</b> Time serial analysis showing data collected (black), interpolated (grey) and predicted (red) of <i>Ae</i>. <i>aegypti</i> and <i>Ae</i>. <i>albopictus</i> infestation level. (<b>C)</b> Abundance tendency of <i>Ae</i>. <i>aegypti</i> (blue bars) and <i>Ae. albopictus</i> (black line).</p

    Epidemic curve of chikungunya and dengue cases reported in Panama country from 2014 to July 2015.

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    <p><b>A.</b> Red bar represents Chikungunya imported cases and blue bar autochthonous cases. <b>B.</b> Blue dots represent dengue positive cases in the country of Panama from the National Dengue surveillance program (left axis). From this surveillance ICGES detected ~10% (577/6459) of the national dengue positive cases (green broken line, right axis). All the positive Chikungunya cases (red bar, right axis) from the National Chikungunya Surveillance program were analyzed at ICGES.</p
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