A Crowded Room or the Perfect Fit? Exploring Affirmative Action Treatment in College and University Admissions for Self-Identified LGBT Individuals

This Article explores affirmative action treatment for self-identified LGBT individuals in college and university admissions. This Article seeks to explain that while granting affirmative action treatment to self-identified students in the admission process is constitutional, under the current affirmative action precedent, there is a lack of sufficient justification for such an expansion. This Article will also explore the advantages and disadvantages should colleges and universities choose to implement affirmative action programs for LGBT applicants. Section I of this Article will begin by depicting the evolution of affirmative action programs since their inception in the early 1960s. This section will also include a discussion of relevant Supreme Court jurisprudence to date (including the Court’s recent rulings in Fisher v. University of Texas). Section II will discuss the varying views that support and oppose affirmative action programs and public opinion concerning affirmative action. Next, Section III will discuss LGBT civil rights and the strides that the LGBT community has made in seeking equality (including the Court’s recent decisions in U.S. v. Windsor and Hollingsworth v. Perry). Section IV will provide analysis depicting the parallels and pitfalls of arguments supporting and opposing affirmative action for LGBT individuals. This section will also include a discussion of the constitutionality of extending these programs to benefit self-identified LGBT students. This section will conclude with a discussion of possible pros and cons of extending affirmative action benefits to LGBT students

Promoting the achievement of looked after children and young people in the London Borough of Hounslow

As of March 2016, there were 70,440 children and young people in care in England. The number of looked after children has continued to increase steadily over the last eight years. Sixty per cent of these children are in care because of abuse or neglect and three-quarters are placed in foster care arrangements. Children and young people who are in or have experienced care remain one of the lowest performing groups in terms of educational outcomes. Last year, 14% of looked after children achieved five or more A*–C GCSEs or equivalent, including English and mathematics. As a consequence, they also experience poorer employment and health outcomes after leaving school compared to their peers. They are over-represented amongst the offender population and those who experience homelessness. However, research is emerging to show that children and young people in care can have very positive experiences of school and are supported effectively to reach their full potential academically and socially. The purpose of this report is to share practice in selected Hounslow schools and colleges that is contributing to improved outcomes and school experiences for children and young people in care. In July 2015, the Hounslow Virtual School (VS) collaborated with UCL Institute of Education to run their Promoting the Achievement of Looked After Children (PALAC) programme with seven schools in the local authority (LA). This report presents an account of the programme, including the activities undertaken by the participants and the outcomes of the programme to date for students in care and staff in the participating schools

Iga-Biome Profiles Correlate With Clinical Parkinson\u27s Disease Subtypes

BACKGROUND: Parkinson\u27s disease is a heterogeneous neurodegenerative disorder with distinctive gut microbiome patterns suggesting that interventions targeting the gut microbiota may prevent, slow, or reverse disease progression and severity. OBJECTIVE: Because secretory IgA (SIgA) plays a key role in shaping the gut microbiota, characterization of the IgA-Biome of individuals classified into either the akinetic rigid (AR) or tremor dominant (TD) Parkinson\u27s disease clinical subtypes was used to further define taxa unique to these distinct clinical phenotypes. METHODS: Flow cytometry was used to separate IgA-coated and -uncoated bacteria from stool samples obtained from AR and TD patients followed by amplification and sequencing of the V4 region of the 16 S rDNA gene on the MiSeq platform (Illumina). RESULTS: IgA-Biome analyses identified significant alpha and beta diversity differences between the Parkinson\u27s disease phenotypes and the Firmicutes/Bacteroides ratio was significantly higher in those with TD compared to those with AR. In addition, discriminant taxa analyses identified a more pro-inflammatory bacterial profile in the IgA+ fraction of those with the AR clinical subclass compared to IgA-Biome analyses of those with the TD subclass and with the taxa identified in the unsorted control samples. CONCLUSION: IgA-Biome analyses underscores the importance of the host immune response in shaping the gut microbiome potentially affecting disease progression and presentation. In the present study, IgA-Biome analyses identified a unique proinflammatory microbial signature in the IgA+ fraction of those with AR that would have otherwise been undetected using conventional microbiome analysis approaches

Iga-Biome Profiles Correlate With Clinical Parkinson\u27s Disease Subtypes

BACKGROUND: Parkinson\u27s disease is a heterogeneous neurodegenerative disorder with distinctive gut microbiome patterns suggesting that interventions targeting the gut microbiota may prevent, slow, or reverse disease progression and severity. OBJECTIVE: Because secretory IgA (SIgA) plays a key role in shaping the gut microbiota, characterization of the IgA-Biome of individuals classified into either the akinetic rigid (AR) or tremor dominant (TD) Parkinson\u27s disease clinical subtypes was used to further define taxa unique to these distinct clinical phenotypes. METHODS: Flow cytometry was used to separate IgA-coated and -uncoated bacteria from stool samples obtained from AR and TD patients followed by amplification and sequencing of the V4 region of the 16 S rDNA gene on the MiSeq platform (Illumina). RESULTS: IgA-Biome analyses identified significant alpha and beta diversity differences between the Parkinson\u27s disease phenotypes and the Firmicutes/Bacteroides ratio was significantly higher in those with TD compared to those with AR. In addition, discriminant taxa analyses identified a more pro-inflammatory bacterial profile in the IgA+ fraction of those with the AR clinical subclass compared to IgA-Biome analyses of those with the TD subclass and with the taxa identified in the unsorted control samples. CONCLUSION: IgA-Biome analyses underscores the importance of the host immune response in shaping the gut microbiome potentially affecting disease progression and presentation. In the present study, IgA-Biome analyses identified a unique proinflammatory microbial signature in the IgA+ fraction of those with AR that would have otherwise been undetected using conventional microbiome analysis approaches

Prion protein interacts with bace1 and differentially regulates its activity towards wild type and swedish mutant amyloid precursor protein

In Alzheimer disease amyloid-β (Aβ) peptides derived from the amyloid precursor protein (APP) accumulate in the brain. Cleavage of APP by the β-secretase BACE1 is the rate-limiting step in the production of Aβ. We have reported previously that the cellular prion protein (PrP(C)) inhibited the action of BACE1 toward human wild type APP (APP(WT)) in cellular models and that the levels of endogenous murine Aβ were significantly increased in PrP(C)-null mouse brain. Here we investigated the molecular and cellular mechanisms underlying this observation. PrP(C) interacted directly with the prodomain of the immature Golgi-localized form of BACE1. This interaction decreased BACE1 at the cell surface and in endosomes where it preferentially cleaves APP(WT) but increased it in the Golgi where it preferentially cleaves APP with the Swedish mutation (APP(Swe)). In transgenic mice expressing human APP with the Swedish and Indiana familial mutations (APP(Swe,Ind)), PrP(C) deletion had no influence on APP proteolytic processing, Aβ plaque deposition, or levels of soluble Aβ or Aβ oligomers. In cells, although PrP(C) inhibited the action of BACE1 on APP(WT), it did not inhibit BACE1 activity toward APP(Swe). The differential subcellular location of the BACE1 cleavage of APP(Swe) relative to APP(WT) provides an explanation for the failure of PrP(C) deletion to affect Aβ accumulation in APP(Swe,Ind) mice. Thus, although PrP(C) exerts no control on cleavage of APP(Swe) by BACE1, it has a profound influence on the cleavage of APP(WT), suggesting that PrP(C) may be a key protective player against sporadic Alzheimer disease

Relativistic quantum transport theory of hadronic matter: the coupled nucleon, delta and pion system

We derive the relativistic quantum transport equation for the pion distribution function based on an effective Lagrangian of the QHD-II model. The closed time-path Green's function technique, the semi-classical, quasi-particle and Born approximation are employed in the derivation. Both the mean field and collision term are derived from the same Lagrangian and presented analytically. The dynamical equation for the pions is consistent with that for the nucleons and deltas which we developed before. Thus, we obtain a relativistic transport model which describes the hadronic matter with $N$, $\Delta$ and $\pi$ degrees of freedom simultaneously. Within this approach, we investigate the medium effects on the pion dispersion relation as well as the pion absorption and pion production channels in cold nuclear matter. In contrast to the results of the non-relativistic model, the pion dispersion relation becomes harder at low momenta and softer at high momenta as compared to the free one, which is mainly caused by the relativistic kinetics. The theoretically predicted free $\pi N \to \Delta$ cross section is in agreement with the experimental data. Medium effects on the $\pi N \to \Delta$ cross section and momentum-dependent $\Delta$-decay width are shown to be substantial.Comment: 66 pages, Latex, 12 PostScript figures included; replaced by the revised version, to appear in Phys. Rev.

Spleen tyrosine kinase-mediated autophagy is required for epithelial-mesenchymal plasticity and metastasis in breast cancer

The ability of breast cancer cells to transiently transition between epithelial and mesenchymal states contributes to their metastatic potential. Therefore, driving tumor cells into a stable mesenchymal state, as opposed to complete tumor cell eradication, presents an opportunity to pharmacologically limit disease progression by promoting an asymptomatic state of dormancy. Here we compare a reversible model of epithelial-mesenchymal transition (EMT) induced by TGF-β to a stable mesenchymal phenotype induced by chronic exposure to the ErbB kinase inhibitor lapatinib. Only cells capable of returning to an epithelial phenotype resulted in skeletal metastasis. Gene expression analyses of the two mesenchymal states indicated similar transition expression profiles. A potently downregulated gene in both datasets was spleen tyrosine kinase (SYK). In contrast to this similar diminution in mRNA, kinome analyses using a peptide array and DNA-conjugated peptide substrates showed a robust increase in SYK activity upon TGF-β-induced EMT only. SYK was present in cytoplasmic RNA processing depots known as P-bodies formed during the onset of EMT, and SYK activity was required for autophagy-mediated clearance of P-bodies during mesenchymal-epithelial transition (MET). Genetic knockout of autophagy related 7 (ATG7) or pharmacological inhibition of SYK activity with fostamatib, a clinically approved inhibitor of SYK, prevented P-body clearance and MET, inhibiting metastatic tumor outgrowth. Overall, the current study suggests assessment of SYK activity as a biomarker for metastatic disease and the use of fostamatinib as a means to stabilize the latency of disseminated tumor cells

Polymorphisms at codons 108 and 189 in murine PrP play distinct roles in the control of scrapie incubation time

Rona Barron - ORCID: 0000-0003-4512-9177 https://orcid.org/0000-0003-4512-9177Item not available from this repository.Susceptibility to transmissible spongiform encephalopathies (TSEs) is associated strongly with PrP polymorphisms in humans, sheep and rodents. In mice, scrapie incubation time is controlled by polymorphisms at PrP codons 108 (leucine or phenylalanine) and 189 (threonine or valine), but the precise role of each polymorphism in the control of disease is unknown. The L108F and T189V polymorphisms are present in distinct structural regions of PrP and thus provide an excellent model with which to investigate the role of PrP structure and gene variation in TSEs. Two unique lines of transgenic mice, in which 108F and 189V have been targeted separately into the endogenous murine Prnp a gene, have been produced. TSE inoculation of inbred lines of mice expressing all allelic combinations at codons 108 and 189 has revealed a complex relationship between PrP allele and incubation time. It has been established that both codons 108 and 189 control TSE incubation time, and that each polymorphism plays a distinct role in the disease process. Comparison of ME7 incubation times in mouse lines that are heterozygous at both codons has also identified a previously unrecognized intramolecular interaction between PrP codons 108 and 189.https://doi.org/10.1099/vir.0.80525-086pubpub