Farm Tractors in Kansas: How to Perfect a Security Interest

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Farm Tractors in Kansas: How to Perfect a Security Interest

Widespread enactment of the Uniform Commercial Code (UCC) occurred nearly half a century ago. Even so, significant non-uniformities in commercial law remain. One is the method of perfecting a security interest in a farm tractor

Chronic recurrent Gorham-Stout syndrome with cutaneous involvement

Type IV osteolysis or Gorham-Stout syndrome is a rare condition characterized by recurrent vascular tumors that disrupt normal anatomical architecture. Gorham-Stout syndrome is most commonly associated with the skeletal system with resulting replacement of bone with scar tissue following tumor regression. The loss of entire bones has given Gorham-Stout syndrome the moniker vanishing bone disease. Natural progression of Gorham-Stout syndrome is characterized by spontaneous disease resolution. However, rare variants of recurrent, progressive, and/or systemic disease have been reported. We present a patient with a history of recurrent Gorham- Stout disease refractory to all treatment options considered. In addition to skeletal disease, our patient had soft tissue and cutaneous involvement, thus reflecting the more aggressive disease variant. Previous surgical attempts to control disease had been ineffective and the patient was referred to us for radiation therapy. Treatment with external beam radiation therapy resulted in good local control and symptom palliation, but full disease resolution was never accomplished. In addition to presentation of this patient, a review of the literature on etiological hypotheses and past/future treatment options was conducted and is included

Genome-Wide Scan and Test of Candidate Genes in the Snail Biomphalaria glabrata Reveal New Locus Influencing Resistance to Schistosoma mansoni

Background: New strategies to combat the global scourge of schistosomiasis may be revealed by increased understanding of the mechanisms by which the obligate snail host can resist the schistosome parasite. However, few molecular markers linked to resistance have been identified and characterized in snails. Methodology/Principal Findings: Here we test six independent genetic loci for their influence on resistance to Schistosoma mansoni strain PR1 in the 13-16-R1 strain of the snail Biomphalaria glabrata. We first identify a genomic region, RADres, showing the highest differentiation between susceptible and resistant inbred lines among 1611 informative restriction-site associated DNA (RAD) markers, and show that it significantly influences resistance in an independent set of 439 outbred snails. The additive effect of each RADres resistance allele is 2-fold, similar to that of the previously identified resistance gene sod1. The data fit a model in which both loci contribute independently and additively to resistance, such that the odds of infection in homozygotes for the resistance alleles at both loci (13% infected) is 16-fold lower than the odds of infection in snails without any resistance alleles (70% infected). Genome-wide linkage disequilibrium is high, with both sod1 and RADres residing on haplotype blocks >2Mb, and with other markers in each block also showing significant effects on resistance; thus the causal genes within these blocks remain to be demonstrated. Other candidate loci had no effect on resistance, including the Guadeloupe Resistance Complex and three genes (aif, infPhox, and prx1) with immunological roles and expression patterns tied to resistance, which must therefore be trans-regulated. Conclusions/Significance: The loci RADres and sod1 both have strong effects on resistance to S. mansoni. Future approaches to control schistosomiasis may benefit from further efforts to characterize and harness this natural genetic variation

Genome-Wide Scan and Test of Candidate Genes in the Snail <i>Biomphalaria glabrata</i> Reveal New Locus Influencing Resistance to <i>Schistosoma mansoni</i>

<div><p>Background</p><p>New strategies to combat the global scourge of schistosomiasis may be revealed by increased understanding of the mechanisms by which the obligate snail host can resist the schistosome parasite. However, few molecular markers linked to resistance have been identified and characterized in snails.</p><p>Methodology/Principal Findings</p><p>Here we test six independent genetic loci for their influence on resistance to <i>Schistosoma mansoni</i> strain PR1 in the 13-16-R1 strain of the snail <i>Biomphalaria glabrata</i>. We first identify a genomic region, <i>RADres</i>, showing the highest differentiation between susceptible and resistant inbred lines among 1611 informative restriction-site associated DNA (RAD) markers, and show that it significantly influences resistance in an independent set of 439 outbred snails. The additive effect of each <i>RADres</i> resistance allele is 2-fold, similar to that of the previously identified resistance gene <i>sod1</i>. The data fit a model in which both loci contribute independently and additively to resistance, such that the odds of infection in homozygotes for the resistance alleles at both loci (13% infected) is 16-fold lower than the odds of infection in snails without any resistance alleles (70% infected). Genome-wide linkage disequilibrium is high, with both <i>sod1</i> and <i>RADres</i> residing on haplotype blocks >2Mb, and with other markers in each block also showing significant effects on resistance; thus the causal genes within these blocks remain to be demonstrated. Other candidate loci had no effect on resistance, including the Guadeloupe Resistance Complex and three genes (<i>aif</i>, <i>infPhox</i>, and <i>prx1)</i> with immunological roles and expression patterns tied to resistance, which must therefore be trans-regulated.</p><p>Conclusions/Significance</p><p>The loci <i>RADres</i> and <i>sod1</i> both have strong effects on resistance to <i>S</i>. <i>mansoni</i>. Future approaches to control schistosomiasis may benefit from further efforts to characterize and harness this natural genetic variation.</p></div

Loci examined among 439 outbred snails.

<p>^aName of gene or marker</p><p>^bScaffold number in <i>B</i>. <i>glabrata</i> reference genome version BglaB1</p><p>^cNumber of genotyped and phenotyped outbred snails</p><p>^dFrequency of each allele, named alphabetically</p><p>^eOther loci showing significant linkage disequilibrium with each locus</p><p>^fMultiplicative decrease in odds of infection conveyed by each copy of a resistance allele at each locus, significance (p < 0.01) conveyed with **</p><p>^gFirst description of locus</p><p>Loci examined among 439 outbred snails.</p

Joint influence of <i>RADres1</i> and <i>sod1</i> genotypes on resistance.

<p>Genotype combinations are indicated along the x and y axes. Empirical resistance values are plotted as black circles along the z axis. Standard errors of proportions for resistance at each genotype combination are shown with a vertical yellow line. Predicted values from an additive 2-locus multiple regression model with no dominance or epistasis are indicated with green squares. The data are consistent with this simple model, although minor non-additive effects may be responsible for small nonsignificant differences between predicted and empirical values.</p

Distribution of allele frequencies among RAD sites.

<p>We characterized 1611 informative RAD sites in 19 inbred lines by minor allele count (“MAC”) (maximum of 19; i.e. 50% allele frequency) and difference in MAC between susceptible (N = 10) and resistant (N = 9) lines (“MAC difference”, theoretical maximum = 18; i.e. 9 resistant lines fixed for one allele, 10 susceptible lines fixed for another). Circle sizes are proportional to the number of RAD sites showing each pattern. The cumulative percentage of RAD sites, starting with the highest observed MAC difference, is shown on the righthand y-axis. The highest MAC difference was observed for 10 RAD sites in perfect mutual LD, with a MAC of 13 and a MAC difference of 13, which we defined as the <i>RADres</i> region and examined further (red arrow; encompasses scaffolds of subsequently examined markers <i>RADres1</i> and <i>RADres2</i>). The one remaining RAD site with an equivalent MAC difference was also in high, but not perfect, LD with <i>RADres</i> (pink arrow; scaffold not examined further). The <i>sod1</i> haplotype block had a MAC difference of 5, which was higher than average but not an outlier (blue arrow).</p