Simultaneous expression of CD4 and CD8 antigens by a substantial proportion of resting porcine T lymphocytes

The existence of four subpopulations in resting porcine T lymphocytes is documented. In addition to the two known subpopulations which are typified by a mutually exclusive expression of either the CD8 or the CD4 differentiation antigen, CD4-CD8+ and CD4+CD8- T lymphocytes, respectively, two unusual subpopulations were prominent not only in peripheral blood, but also in lymphoid tissues: CD4-CD8- T lymphocytes expressing neither of these antigens and CD4+CD8+ T lymphocytes coexpressing both antigens. While CD4+CD8+ lymphoblasts have been found also in other species, resting T lymphocytes with that phenotype are without precedent among all species analyzed to date. This unique composition of the porcine T lymphocyte population has to be taken into consideration when the swine is used as a large animal model in experimental medicine

Effects of Trisomic Dyrk1a and EGCG Treatment on Craniofacial Development in Ts65Dn Down Syndrome Mice

poster abstractDown syndrome (DS), also known as Trisomy 21, is a genetic disorder caused by an extra copy of human chromosome 21. Individuals with DS exhibit various phenotypes such as cognitive, skeletal and craniofacial abnormalities. The Ts65Dn mouse model displays similar craniofacial abnormalities as observed in humans with DS including a small, undersized mandible. To gain a better understanding of craniofacial abnormalities, we study the molecular and cellular mechanisms underlying these abnormalities. Previous studies conducted in our lab identified a deficit in neural crest (NC) cells in the first pharyngeal arch (PA1) or mandibular precursor by embryonic day 9.5 (E9.5). We hypothesize that the inherent molecular mechanism responsible for the small, undersized mandible is overexpression of dual-specificity tyrosine (Y) phosphorylation regulated kinase 1A (Dyrk1a), a gene that is found in three copies in individuals with DS and Ts65Dn mice. To test our hypothesis, we bred Ts65Dn mice with Dyrk1a knockout mice, thus reducing Dyrk1a copy number to normal levels. This study provides the foundation for understanding the function of Dyrk1a. We also treated embryos with Epigallocatechin gallate (EGCG), a green tea polyphenol that is known to inhibit Dyrk1a activity. We will examine the molecular and cellular effects of Dyrk1a and EGCG on the developing PA1 on E9.5 embryos. In both the genetic and pharmacological manipulations, we expect to find a larger overall embryonic size, a larger PA1 size and increased number of NC cells

Correction of Craniofacial Deficits using Epigallocatechin-3’-gallate Treatment in a Down Syndrome Mouse Model

poster abstractDown syndrome (DS) is caused by trisomy of human chromosome (HSA21). Individuals with DS display distinct craniofacial abnormalities including an undersized, dismorphic mandible which leads to difficulty with eating, breathing, and swallowing. Using the Ts65Dn DS mouse model (three copies of ~50% HSA21 homologs), we have traced the mandibular deficit to a neural crest cell (NCC) deficiency and reduction in first pharyngeal arch (PA1 or mandibular precursor) at embryonic day 9.5. Previous studies have shown that this deficit is caused when NCC fail to migrate from the neural tube to populate the PA1 and fail to proliferate in the PA1. At E9.5, Dyrk1A, a triplicated DS candidate gene, is overexpressed in the PA1 and may cause the NCC and PA1 deficits. We hypothesize that treatment of pregnant Ts65Dn mothers with Epigallocatechin-3’-gallate (EGCG), a known Dyrk1A inhibitor, will correct NCC deficits and rescue the undersized PA1 in trisomic E9.5 embryos. To test our hypothesis, we treated pregnant Ts65Dn mothers with EGCG, where embryos received treatment from either E7-E8 or E0-E9.5. Our preliminary study found variable increases in PA1 volume and NCC number between treatment regimens, with several treatment groups indicating EGCG treatment has the potential to rescue the NCC deficit in the mandibular precursor. We found an increase in NCC number and PA1 volume with E7-E8 EGCG treatment in 21-24 somite embryos from trisomic mothers and in euploid embryos from euploid mothers treated from E0-E9.5. With EGCG treatment, we also observed a decrease in the average somite number of embryos from trisomic mothers, but an increase in those mothers’ average litter size. This study is important because it helps define the specific dosage and timing of ECGC and how it may affect specific DS phenotypes. These findings provide preclinical testing for a potential therapy for craniofacial disorders linked to DS

Treatment with a Green Tea Polyphenol Corrects Craniofacial Deficits Associated with Down Syndrome

poster abstractDown syndrome (DS) is caused by trisomy of human chromosome 21 (HSA21). Individuals with DS present craniofacial abnormalities including an undersized, dismorphic mandible leading to difficulty with eating, breathing, and swallowing. Using the Ts65Dn DS mouse model (three copies of ~50% HSA21 homologs), we have traced the mandibular deficit to a neural crest cell (NCC) deficiency and reduction in first pharyngeal arch (PA1 or mandibular precursor) size at embryonic day 9.5. At E9.5, Dyrk1A, a triplicated DS candidate gene, is overexpressed and may cause the NCC and PA1 deficits. We hypothesize that treatment of pregnant Ts65Dn mothers with Epigallocatechin gallate (EGCG), a known Dyrk1A inhibitor, will correct NCC deficits and rescue the undersized PA1 in trisomic E9.5 embryos. To test our hypothesis, we treated pregnant Ts65Dn mothers with EGCG from either E7-E8 or E0-E9.5. Our preliminary study found an increase in PA1 volume and NCC number in trisomic E9.5 embryos after treatment, but observed differences between treatment regimens. Differential gene expression was also quantified in trisomic treated embryos. This preliminary data suggests EGCG treatment has the potential to rescue the mandibular phenotype caused by trisomy. These findings provide preclinical testing for a potential therapy for craniofacial disorders linked to DS

Aesthetic Theory in Performance: A Comparative Study on Aristotle\u27s Catharsis and Bharata Mundi\u27s Rasa and Their Applications for Modern Theatre Practices

As a storytelling species, theatre offers a powerful tool to explore our human nature. Theatre influences us. It affects our brains, especially our emotions. The key to discovering what happens to us while we watch theatre can be analyzed through aesthetic theories—two in particular. One popular theory derives from ancient Greece; the other from ancient India. Ancient Greece provides us with Aristotle and his theory of catharsis while ancient India gives us Bharata Mundi and his theory of rasa. Catharsis and rasa are aesthetic theories that seek to validate or measure the emotional reaction towards a work of art that can change people. Both of them measure this change by outward reactionary signs like crying, or by giving one goosebumps. The time has come for a major paradigm shift in terms of how we understand emotion in theatre. In this paper I compare Aristotle’s Poetics and catharsis to Mundi’s Natyasastra and rasa. A study with broad implications, this comparison reveals the ethnocentric limitations of the dominant theory of catharsis and highlights how an application of rasa creates a more collectivist and instinct driven understanding of theatrical practice

Mandibular and Neural Crest Cell Deficits Seen in TsDn65 Down Syndrome Mouse Model Rescued By Green Tea Polyphenol, EGCG

poster abstractDown Syndrome (DS) is caused by trisomy of the human chromosome 21 (Hsa21) and occurs in ~1 of every 700 births. DS is distinguished by over 80 phenotypic abnormalities including skeletal deficits and craniofacial phenotypes characterized by a flattened skull, slanted eyes, and a smaller mandible. To study these abnormalities, we utilize the Ts65Dn DS mouse model containing a triplication of approximately half of the gene homologues found on Hsa21 and mirrors the skeletal and mandibular phenotypes observed in DS. In Ts65Dn mice, the origin of the mandibular deficits were traced to a reduction in size of the 1st branchial arch (BA1), the developmental precursor to the mandible, occurring at embryonic day 9.5 (E9.5). At E9.5, we observe a lack of proliferation and migration of neural crest cells (NCC) from the neural tube (NT) into the BA1, causing a reduced BA1. We hypothesize that an overexpression of Dyrk1a, a Hsa21 homologue, contributes to the mandibular deficit seen in E9.5 Ts65Dn embryos. We propose that EGCG, a green tea polyphenol, will inhibit DYRK1a activity, rescuing the BA1 deficit. To test our hypothesis, Ts65Dn mothers were treated with EGCG from E0-E9.5 and sacrificed to retrieve the E9.5 embryos. Our results from unbiased stereological assessments show that E0-E9.5 EGCG in vivo treatment has the potential to increase NCC number, BA1 volume, and embryo volume of trisomic embryos. This data provide preclinical testing for a potential therapy of DS craniofacial disorders, which may extend to treating bone deficits in DS and osteoporosis

Taking Ownership of Grain Belt Agriculture and Rural Economic Development

Community/Rural/Urban Development,

Intragenic CFTR Duplication and 5T/12TG Variant in a Patient with Non-Classic Cystic Fibrosis

Cystic fibrosis (CF) is an autosomal recessive disorder characterized by the accumulation of sticky and heavy mucus that can damage several organs. CF shows variable expressivity in affected individuals, but it typically causes respiratory and digestive complications as well as congenital bilateral absence of the vas deferens in males. Individuals with classic CF usually have variants that produce a defective protein from both alleles of the CFTR gene. Individuals with other variants may present with classic, non-classic, or milder forms of CF due to lower levels of functional CFTR protein. This article reports the genetic analysis of a female with features of asthma and mild or non-classic CF. CFTR sequencing demonstrated that she is a carrier for a maternally derived 5T/12TG variant. Deletion/duplication analysis by multiplex ligation-dependent probe amplification (MLPA) showed the presence of an intragenic paternally derived duplication involving exons 7-11 of the CFTR gene. This duplication is predicted to result in the production of a truncated CFTR protein lacking the terminal part of the nucleotide-binding domain 1 (NBD1) and thus is likely to be a non-functioning allele. The combination of this large intragenic duplication and 5T/12TG is the probable cause of the mild or non-classic CF features in this individual

Comfort Food for All: The Scalability of LMS-Embedded Librarianship

Embedded librarianship provides information literacy instruction right where students prefer to do course related research: online. The learning management system (LMS) provides an effective arena for librarians to collaborate with professors and reach students with library services alongside course content. How scalable, though, is this service so that it can meet the needs of all students? Presenters will share data from a 2011 international survey, material from the professional literature, and the experiences of LMS embedded librarians to help answer this question. Time will be spent discussing how to reorganize information literacy efforts and workflow within the library to address the scalability question head-on. Observant library administrators would do well to reallocate staff responsibilities to ensure LMS embedded librarianship becomes standard fare, as it reaches the many at their point of need. The presenters will address questions such as the following: Is it just too time-consuming to undertake? Is it meant for a select few classes? Which information literacy instruction methods can be incorporated to innovatively meet the needs of students? What time-saving tools can be employed to sustain the program long-term? Librarians must re-envision themselves as virtual information literacy instructors because that is where users prefer to slice and dice research assignments. Come learn tools, techniques, and staffing innovations to make LMS embedded librarianship sustainable on your campus