14 research outputs found

    Phylogenetic trees of <i>Jacaranda</i> populations based on different components of simple sequence repeat (SSR) data.

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    <p>SSR variation (A), amplicon size variation (B), flanking region (FR) sequence variation (C) and amplicon sequence variation (D). Each type of data was analysed according to a pair of suitable genetic distance estimators: F<sub>ST</sub>, suitable for loci following the infinite allele model (IAM); R<sub>ST</sub>, for loci following the stepwise mutation model (SMM); and N<sub>ST</sub>, for loci following the infinite site model (ISM) model. There are four geographic populations: Counami (<i>C</i>), Paracou (<i>P</i>) and Saint-Laurent (<i>S</i>) in French Guiana; Tapajos (<i>T</i>) in Brazil. Note that scales are not the same among trees.</p

    Two alternative genealogies for simple sequence repeat (SSR) alleles containing the same number of repeats.

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    <p>SSR alleles are indicated by their number of repeats (n, n+1). The A/C letters indicate a SNP in the flanking regions. Red bars correspond to mutational events in the flanking region sequence or in the number of SSR repeats. (A) No sequence information: deduced genealogy of observed data (third line) groups alleles together according to their number of repeats and involves a single SSR mutation. Genealogy is recent. (B) Consideration of sequence information: deduced genealogy involves a SNP mutation and two SSR mutations (alternative topology will involve two identical and independent substitutions at the same nucleotide site and a unique SSR mutation, which is less likely). Genealogy is ancient and SSR alleles do not group according to their numbers of repeats.</p

    Linkage Disequilibrium (LD) for pairs of polymorphisms in the flanking regions.

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    <p>Dark cells contain LD values significantly different from zero. An asterisk next to a locus name indicates that the SSR repeat(s) is (are) located between that locus and the next. Colouring (shading) indicates the degree of significance of the test: green (light grey*), <i>P</i>>0.05; orange (grey*), 0.05<<i>P</i>>0.001; red (dark grey*), <i>P</i><0.001. * In shades-of-gray printouts.</p

    Polymorphism at each simple sequence repeat (SSR) locus differentiated by segments of the DNA amplicon. SSR1, SSR2 and SSR3: respectively first, second and third SSR occurring in each amplicon (see figure S1 for details on each amplicon’s sequence); FR: flanking regions; <i>H<sub>e</sub></i>: Nei’s genetic diversity; A: number of alleles; h: number of haplotypes. Data sets: C, <i>Citrus</i>; J, <i>Jacaranda</i>; Q, <i>Quercus</i>.

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    <p>Polymorphism at each simple sequence repeat (SSR) locus differentiated by segments of the DNA amplicon. SSR1, SSR2 and SSR3: respectively first, second and third SSR occurring in each amplicon (see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0040699#pone.0040699.s001" target="_blank">figure S1</a> for details on each amplicon’s sequence); FR: flanking regions; <i>H<sub>e</sub></i>: Nei’s genetic diversity; A: number of alleles; h: number of haplotypes. Data sets: C, <i>Citrus</i>; J, <i>Jacaranda</i>; Q, <i>Quercus</i>.</p

    Alignment of a subset of DNA fragments at simple sequence repeat (SSR) loci Jc3H10 (<i>Jacaranda copaia</i>) (A) and QrZAG30 (<i>Quercus robur</i>) (B).

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    <p>Numbers in the top line indicate positions relative to the consensus sequence of (A) 190 bp and (B) 247 bp. Bold nucleotides in brackets indicate SSR motifs and their number of repeats. Dashes indicate gaps, highlighted nucleotides in green (light grey*) indicate indels of one to three bases, highlighted nucleotides in red (dark grey*) mark mutations from one base to another, and yellow (light grey*) boxes indicate groups of insertion/deletions longer than three bases and considered as a single mutational event. * In shades-of-gray printouts.</p

    Die Pseudarthrose nach Sprunggelenksarthrodese

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    Die Sprunggelenksarthrodese ist bei therapieresistenter Schmerzsymptomatik einer Sprunggelenksarthrose, nicht beherrschbarer Entzündung im Bereich des Rückfußes, Talusnekrose, schmerzhafter Pseudarthrose nach Arthrodese der Sprunggelenke sowie kontrakter Deformität des Rückfußes mit Gangstörung und Hautkomplikation indiziert. Sie stellt immer noch einen komplizierten Eingriff mit einer hohen Komplikationsrate dar. Dazu trägt neben den häufigen Wundheilungsstörungen die Pseudarthrose bei. Das Risiko für die Entstehung einer solchen Pseudarthrose hängt von klinischen Faktoren wie der sprunggelenksnahen Osteopenie, der Dauermedikation von Kortikoiden sowie dem Nikotinabusus und von operativen Faktoren wie der Komplexität des Verfahrens und Stabilität der Methode ab. Beim parallelen Auftreten dieser Faktoren mit Beeinträchtigung des biologischen und mechanischen Standbeins der Osteoneogenese potenziert sich dieses Risiko. Eine Sonderstellung unter den Risikofaktoren nimmt die sprunggelenksnahe Osteopenie ein. Nach entsprechender Analyse kommt sie hier signifikant vor. Ihre Diagnose beruft sich auf der nicht zu vernachlässigenden Anamnese, der bereits verordneten Medikation, der aussagefähigen, jedoch nicht standardisierten Knochendichtemessung und der entscheidenden Röntgendiagnostik. In Zukunft sollte präoperativ die bereits standardisierte Röntgendiagnostik mit einer Knochendichtemessung kombiniert werden. Leider ist präoperativ das Risiko, an einer Pseudarthrose nach einer Sprunggelenksarthrodese zu leiden, nur abschätzbar und nicht quantifizierbar. Neben der objektiven Befundung mittels Röntgen kann die subjektive Einschätzung des Patienten bei der Beurteilung der Pseudarthrose hilfreich sein. Somit müssen falsch positive Röntgenbefunde bei klinisch stummer Pseudarthrose im Sinne einer fibrösen Ankylosierung eingestuft und keiner Operation zugeführt werden. Bei einer Pseudarthrose nach der Sprunggelenksarthrodese mit Angabe einer Unzufriedenheit, einem moderaten Schmerz bei leichter Belastung, einem regelmäßigen Analgetikagebrauch, einem VAS-Wert ab 5, einer beschwerdefreien Gehstrecke unter 100m mit Gebrauch von 2 UAGS ist nach Aufklärung des Patienten die Re-Arthrodese zu diskutieren. Es sollten dann die Compliance jedes Patienten verbessert (Abstellen des Nikotinabusus), die präoperative Therapie von Neben- (Osteopenie) und Grunderkrankung (Umsetzung der immunsupprimierenden Therapie) optimiert und das geeignete Vorgehen (z.B. Zweizeitigkeit bei Pantalar-Arthrodese (zuerst talocrural und dann talotarsal) bzw. Nutzung interne Kompressionsmethoden mit autologem Knochenspan bei Knochendefekt) gewählt werden.In painful osteoarthrosis, arthritis and pseudarthrosis of the ankle joint, in osteonecrosis of the talus and in deformity of the foot with limp and complications of skin the arthrodesis of the hindfoot is indicated. This is a difficult operation with many comlications like infection and pseudarthrosis. The risk of a pseudarthrosis depends on clinical factors like osteopenie, corticoid medication, nicotin and operative factors like the stabilisation. These factors injure the biological and mechanic basis of osteoneogenesis. The osteopenie is a significant risk factor. The diagnosis of the osteopenie is based on the anamnesis, the medication, the measurement of the bonemass and the x-ray. In future there must be standard to combinated the measurement of bonemass and x-ray. The risk of pseudarthrosis is not to quantify. The x-ray and the pain characterize a pseudarthrosis. So a painless pseudarthrosis don´t have to operate. When a patient with a pseudarthrosis is dissatisfied, when the pain is moderate with a value in the visuel analog scale of pain higher as 5, when analgetic medication are regular used, a painless walking less than 100m, a necessary use of supports a new arthrodesis ist indicated. Now the compliance of patient, the therapie of diseases and the operation methodes are improved

    Simplified schematic part of the fatty acid pathway known in plants.

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    <p>Blue shaded boxes indicate probable negatively correlated pathway while yellow boxes indicate positively correlated pathway due to presence of mutant FAD2 genes. Action of mutant <i>FAD2A</i> and <i>FAD2B</i> in the S-population while <i>FAD2A</i> QTL in the T-population stops desaturation of oleic acid (C18:1) to linoleic acid (C18:2). The capital letters in parenthesis (A-D) indicate the pathway through which fatty acids are produced by acyl carrier protein (ACP) synthesis within the plastid. ACCase, Acetyl-CoA carboxylase; FAS, fatty acid synthase; KAS, ketoacyl ACP synthetase; Δ9DES, Δ9 desaturase; ACS, acyl-CoA synthetase; FAT B, palmitoyl-ACP thioesterase; FATA, stearoyl-ACP thioesterase; FAE, fatty acid elongase, <i>FAD2</i>, fatty acid desaturase.</p

    Phenotypic effect of <i>FAD2A</i> and <i>FAD2B</i> genes for oil quality traits in the S- and T-population.

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    <p>AA: wild A sub-genome allele for <i>FAD2A</i> gene in homozygous condition, aa: mutant A sub-genome allele for <i>FAD2A</i> gene in homozygous condition, Aa: <i>FAD2A</i> gene in heterozygous condition in A sub-genome, BB: wild B sub-genome allele for <i>FAD2B</i> gene in homozygous condition, bb: mutant B sub-genome allele for <i>FAD2B</i> gene in homozygous condition, Bb: <i>FAD2B</i> gene in heterozygous condition in B sub-genome. Since the RIL populations were genotyped and phenotyped, there should be no heterozygous Aa or Bb genotype.</p><p>*The phenotypic data taken for comparison from Pandey et al. [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0119454#pone.0119454.ref024" target="_blank">24</a>].</p><p>Phenotypic effect of <i>FAD2A</i> and <i>FAD2B</i> genes for oil quality traits in the S- and T-population.</p
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