Ewing’s Sarcoma

Ewing’s sarcoma is the second most common malignant tumor of the bone occurring in children and adolescents. Typically, patients present between the ages of 10 and 20, with the disease having a slight predilection for males.1 Tumors often arise in the mid-shaft with the femur being the most frequently affected bone. The most common chromosome translocation, t(11;22)(q24;q12), occurs between the EWS gene and the FLI-1 gene. This translocation has been implicated in these aggressive and malignant tumors.1–4 Oftentimes, patients present with pain and swelling in the area of the affected bone or joint.5 While there has been some improvement in survival for patients that present with localized tumors, patients presenting with metastases continue to have a poor prognosis.3,6 Current treatment options include surgical resection coupled with chemotherapy and radiation therapy. Recent molecular studies have demonstrated some promise for the development of targeted gene therapy.4 We present a case of a 16-year old boy that presented with leg pain and a mass in his left fibula

Instruction, perception, and reflection : beginning teachers\u27 habits of mind

N

Characterization on interactions between the prion protein and amyloid-beta

The cellular prion protein (PrP) has been shown to act as a receptor for soluble oligomers of amyloid-beta (Aβ), an ~4 kDa amyloidogenic peptide that is found in neuritic plaques that are a pathological hallmark of Alzheimer’s disease (AD). Oligomeric forms of the Aβ peptide are thought to be synaptotoxic, and have been shown to produce PrP-dependent dendritic spine loss, suppression of long term potentiation (LTP), and behavioral changes in mouse models of AD. However, the specific molecular interactions between PrP and Aβ have not been fully characterized. In this work, we conducted a robust examination of the kinetic processes leading to Aβ fibril formation, and present evidence that PrP significantly inhibits Aβ polymerization. Using established mathematical models of polymerization kinetics, we show that inhibition is based on binding between PrP and the ends of Aβ filaments, an interaction that blocks elongation. To support these results, we conducted multiple binding assays to show that PrP binds to monomers of Aβ with low affinity, oligomers with intermediate affinity, and to fibrils with high affinity. These results extend upon previous studies, which have focused only on the interaction between oligomeric Aβ and PrP. To better understand the molecular interactions required for binding and inhibition of polymerization, we performed assays with a series of PrP deletion mutants, which revealed that low-affinity binding to Aβ monomer is dependent on the presence of the C-terminal domain of PrP. This domain is also required for Aβ polymerization inhibition. Based on our results, we propose a model in which the unstructured N-terminal domain of PrP binds to the ends of Aβ fibrils, while the C-terminal domain interrupts the docking of new monomers to fibril ends, in part through competing for similar binding sites. This study provides an important contribution to our understanding of the PrP-Aβ interaction that leads to synaptoxicity

Alien Registration- Fenderson, Frank W. (Calais, Washington County)

https://digitalmaine.com/alien_docs/1171/thumbnail.jp

An analysis of the community development program of the Georgia Power Company as a phase of community relations.

Thesis (M.S.)--Boston Universit

Landscape genetics of the New England cottontail: Effects of habitat fragmentation on population genetic structure and dispersal

The New England cottontail (Sylvilagus transitionalis) is a species of conservation concern. Population recovery will require knowledge of genetic structure and dispersal patterns. To this end, I used microsatellite loci to assess genetic structure at two spatial scales: across the entire range (broadscale) and within the northernmost population (finescale). Range-wide, cottontails are separated into five distinct populations. There was little evidence of gene flow among populations and they have experienced extensive genetic drift. Several populations had comparatively reduced genetic diversity. Intensive fine-scale surveys revealed four genetically differentiated populations. Interstate-95 is a dispersal barrier, though other major roads did not impact gene flow. Greater fragmentation resulted in stronger spatial genetic structure. Dispersal is female-biased, yet female dispersal may be limited by patch isolation. Management efforts should focus on increasing habitat and restoring connectivity. Additional surveys may be needed across the range to identify population-specific dispersal barriers that may require special mitigation

Using World-Wide-Web technology for pathology education

In this article, we describe the development of computer-based learning programs for pathology students at Jefferson Medical College. These programs are authored using HTML (HyperText Markup Language), and are available to students on campus and via the internet. Our computer-based learning resources include scheduling information, course goals and objectives, glossary of key words, self-assessment programs and image-based case studies. These educational programs are popular with the students. We recommend the use of World Wide Web technology to improve teaching and learning in pathology education

Anthropogenic Habitats Facilitate Dispersal of an Early Successional Obligate: Implications for Restoration of an Endangered Ecosystem

Landscape modification and habitat fragmentation disrupt the connectivity of natural landscapes, with major consequences for biodiversity. Species that require patchily distributed habitats, such as those that specialize on early successional ecosystems, must disperse through a landscape matrix with unsuitable habitat types. We evaluated landscape effects on dispersal of an early successional obligate, the New England cottontail (Sylvilagus transitionalis). Using a landscape genetics approach, we identified barriers and facilitators of gene flow and connectivity corridors for a population of cottontails in the northeastern United States. We modeled dispersal in relation to landscape structure and composition and tested hypotheses about the influence of habitat fragmentation on gene flow. Anthropogenic and natural shrubland habitats facilitated gene flow, while the remainder of the matrix, particularly development and forest, impeded gene flow. The relative influence of matrix habitats differed between study areas in relation to a fragmentation gradient. Barrier features had higher explanatory power in the more fragmented site, while facilitating features were important in the less fragmented site. Landscape models that included a simultaneous barrier and facilitating effect of roads had higher explanatory power than models that considered either effect separately, supporting the hypothesis that roads act as both barriers and facilitators at all spatial scales. The inclusion of LiDAR-identified shrubland habitat improved the fit of our facilitator models. Corridor analyses using circuit and least cost path approaches revealed the importance of anthropogenic, linear features for restoring connectivity between the study areas. In fragmented landscapes, human-modified habitats may enhance functional connectivity by providing suitable dispersal conduits for early successional specialists