A Theory of Poverty: Legal Immobility

The puzzle of why the cycle of poverty persists and upward socioeconomic mobility is so difficult has long captivated scholars and the public alike. Yet with all of the attention that has been paid to poverty, the crucial role of the law, particularly state and local law, in perpetuating poverty is largely ignored. This Article offers a new theory of poverty, one that introduces the concept of legal immobility. Legal immobility considers the cumulative effects of state and local laws as a mechanism through which poverty is perpetuated and upward socioeconomic mobility is stunted. The Article provides an initial description and normative account of this under-theorized aspect of our laws and argues that in order to fully understand poverty, a more complete understanding of the relationship between law and poverty is needed. After discussing several examples of laws that can contribute to legal immobility (everything from state and local tax laws to occupational licensing laws), the Article offers a three-prong theory to help understand the distinct pathways through which individual laws that contribute to legal immobility function: (1) calculated exploitation; (2) gratuitous management; and (3) routine neglect. This framework provides a guide for future work to build on legal immobility theory. By bringing to light the cumulative effects of local and state laws in perpetuating poverty, the goal is for legal immobility theory to ultimately help lawmakers develop new structural approaches to tackling poverty

Stealing (Identity) From the Poor

The law of data breaches is new, dynamic, and evolving. The number and complexity of breaches increases each year and legal scholars, courts, and policymakers scramble to respond. In 2019, 14.4 million consumers became victims of identity theft, the most problematic consequence of data breaches for consumers. Indeed, one-third of all Americans have experienced identity theft at some point in their lives. Yet despite low-income groups comprising at least thirty percent of all identity theft victims, existing discourse and debate on the regulatory regime governing data breaches and identity theft primarily reflects the experiences and concerns of middle- and high-income groups. Debates remain uninformed by detailed analysis of how the use of illegally obtained data may uniquely harm low-income individuals and how these harms may be exacerbated for low-income victims who are Black. We lack careful theoretical assessment of the complex relationship between identity theft victimization and wider structures of inequality. This Article uses original data to fill these significant descriptive, theoretical, and normative gaps in the literature. It then turns toward exploring the common and understudied problem of aligning regulatory regimes with the needs of prototypical higher-income people, leaving those who are low-income to operate within a system that was not designed to help them—what I call plutocentric regulation. Finally, the Article proposes a new federal agency, the Data Privacy and Identity Recovery Agency (DPIRA), to streamline the process for identity theft victims and make the recovery process equitable for all victims, regardless of their income

The Potential of Teledentistry in Community Oral Health for the Pediatric Population

• Dental caries is the most prevalent chronic disease of childhood in the US. • Young children are a particularly vulnerable population because of their dependence, inability to communicate needs, and relative poverty. • Furthermore, this can be exacerbated by disparities such that an increased rates of caries are observed in children who are of low socioeconomic status and minority backgrounds. • However, community oral health screenings can play a vital role in childhood caries as a predominately preventable disease. • The current emphasis on social distance during the COVID-19 pandemic has brought attention to teledentistry, which may have a valuable role in the future of community oral health outreach

Integrative analysis identifies candidate tumor microenvironment and intracellular signaling pathways that define tumor heterogeneity in NF1

Neurofibromatosis type 1 (NF1) is a monogenic syndrome that gives rise to numerous symptoms including cognitive impairment, skeletal abnormalities, and growth of benign nerve sheath tumors. Nearly all NF1 patients develop cutaneous neurofibromas (cNFs), which occur on the skin surface, whereas 40-60% of patients develop plexiform neurofibromas (pNFs), which are deeply embedded in the peripheral nerves. Patients with pNFs have a ~10% lifetime chance of these tumors becoming malignant peripheral nerve sheath tumors (MPNSTs). These tumors have a severe prognosis and few treatment options other than surgery. Given the lack of therapeutic options available to patients with these tumors, identification of druggable pathways or other key molecular features could aid ongoing therapeutic discovery studies. In this work, we used statistical and machine learning methods to analyze 77 NF1 tumors with genomic data to characterize key signaling pathways that distinguish these tumors and identify candidates for drug development. We identified subsets of latent gene expression variables that may be important in the identification and etiology of cNFs, pNFs, other neurofibromas, and MPNSTs. Furthermore, we characterized the association between these latent variables and genetic variants, immune deconvolution predictions, and protein activity predictions

Effects of Cyclic Chronic Heat Stress on the Expression of Nutrient Transporters in the Jejunum of Modern Broilers and Their Ancestor Wild Jungle Fowl

snibaThe mechanisms associated between growth rate, gut integrity and heat stress (HS) responses are not known. The current study aimed to evaluate the effect of chronic HS on jejunal nutrient transport in slow- (ACRB from 1950), moderate- (95RAN from 1995), rapid-(modern broilers, MRB) growing birds, and their ancestor wild jungle fowl (JF). One-day male chicks (n=150/line) were placed by line in environmentally controlled chambers and kept under the same environmental conditions until d28. On d29, an 8-h daily cyclic HS (36ºC) was applied to half of the chambers, which lasts until d55, while keeping the rest under thermal neutral conditions (TN, 24°C). Jejunum tissues were collected for morphology assessment and molecular analysis of carbohydrate-, amino acid- and fatty acid- transporters. MRB exhibited the highest BW followed by 95RAN under both conditions. HS decreased FI in MRB and 95RAN, which results in lower BW compared to their TN counterparts, however no effect was observed in ACRB and JF. MRB showed greater villus height to crypt depth ratio under both environmental conditions. Molecular analyses showed that GLUT2, 5, 10, and 11 were upregulated in MRB compared to some of the other populations under TN conditions. HS down regulated GLUT2, 10, 11, and 12 in MRB while it increased the expression of GLUT1, 5, 10, and 11 in JF. GLUT2 protein expression was higher in JF compared to ACRB and MRB under TN conditions. It also showed an increase in ACRB but no effect on 95RAN and MRB under HS conditions. ACRB exhibited greater expression of EAAT3 gene as compared to the rest of populations maintained under TN conditions. HS exposure did not alter the gene expression of amino acid transporters in MRB. Gene expression of CD36 and FABP2 was up-regulated in HS JF birds. Protein expression of CD36 was down-regulated in HS JF while no effect was observed in ACRB, 95RAN and MRB. Taken together, these data are the first to show the effect of HS on jejunal expression of nutrient transporters in three broiler populations known to represent 70 years of genetic progress in the poultry industr

Generation and characterisation of Friedreich ataxia YG8R mouse fibroblast and neural stem cell models

This article has been made available through the Brunel Open Access Publishing Fund.Background: Friedreich ataxia (FRDA) is an autosomal recessive neurodegenerative disease caused by GAA repeat expansion in the first intron of the FXN gene, which encodes frataxin, an essential mitochondrial protein. To further characterise the molecular abnormalities associated with FRDA pathogenesis and to hasten drug screening, the development and use of animal and cellular models is considered essential. Studies of lower organisms have already contributed to understanding FRDA disease pathology, but mammalian cells are more related to FRDA patient cells in physiological terms. Methodology/Principal Findings: We have generated fibroblast cells and neural stem cells (NSCs) from control Y47R mice (9 GAA repeats) and GAA repeat expansion YG8R mice (190+120 GAA repeats). We then differentiated the NSCs in to neurons, oligodendrocytes and astrocytes as confirmed by immunocytochemical analysis of cell specific markers. The three YG8R mouse cell types (fibroblasts, NSCs and differentiated NSCs) exhibit GAA repeat stability, together with reduced expression of frataxin and reduced aconitase activity compared to control Y47R cells. Furthermore, YG8R cells also show increased sensitivity to oxidative stress and downregulation of Pgc-1α and antioxidant gene expression levels, especially Sod2. We also analysed various DNA mismatch repair (MMR) gene expression levels and found that YG8R cells displayed significant reduction in expression of several MMR genes, which may contribute to the GAA repeat stability. Conclusions/Significance: We describe the first fibroblast and NSC models from YG8R FRDA mice and we confirm that the NSCs can be differentiated into neurons and glia. These novel FRDA mouse cell models, which exhibit a FRDA-like cellular and molecular phenotype, will be valuable resources to further study FRDA molecular pathogenesis. They will also provide very useful tools for preclinical testing of frataxin-increasing compounds for FRDA drug therapy, for gene therapy, and as a source of cells for cell therapy testing in FRDA mice. © 2014 Sandi et al

Genomic Profiling of Childhood Tumor Patient-Derived Xenograft Models to Enable Rational Clinical Trial Design.

Accelerating cures for children with cancer remains an immediate challenge as a result of extensive oncogenic heterogeneity between and within histologies, distinct molecular mechanisms evolving between diagnosis and relapsed disease, and limited therapeutic options. To systematically prioritize and rationally test novel agents in preclinical murine models, researchers within the Pediatric Preclinical Testing Consortium are continuously developing patient-derived xenografts (PDXs)-many of which are refractory to current standard-of-care treatments-from high-risk childhood cancers. Here, we genomically characterize 261 PDX models from 37 unique pediatric cancers; demonstrate faithful recapitulation of histologies and subtypes; and refine our understanding of relapsed disease. In addition, we use expression signatures to classify tumors for TP53 and NF1 pathway inactivation. We anticipate that these data will serve as a resource for pediatric oncology drug development and will guide rational clinical trial design for children with cancer

A New Panel-Estimated GFR, Including beta(2)-Microglobulin and beta-Trace Protein and Not Including Race, Developed in a Diverse Population

RATIONALE AND OBJECTIVE: GFR estimation based on creatinine and cystatin C (eGFR(cr-cys)) is more accurate than eGFR based on either creatinine or cystatin C alone (eGFR(cr) or eGFR(cys)), but the inclusion of creatinine in eGFR(cr-cys) requires specification of a person’s race. Beta-2-microglobulin (B2M) and beta-trace protein (BTP) are alternative filtration markers that appear to be less influenced by race than creatinine. STUDY DESIGN: Study of diagnostic test accuracy. SETTING AND PARTICIPANTS: Development in pooled population of seven studies with 5017 participants with and without chronic kidney disease. External validation in a pooled population of seven other studies with 2245 participants. TESTS COMPARED: Panel eGFR using B2M and BTP in addition to cystatin C (three-marker panel) or creatinine and cystatin C (four-marker panel) with and without age and sex or race. OUTCOMES: GFR measured as the urinary clearance of iothalamate, plasma clearance of iohexol, or plasma clearance of Cr-EDTA RESULTS: Mean measured GFR was 58.1 and 83.2 ml/min/1.73m(2) and the proportion of blacks was 38.6% and 24.0%, in the development and validation populations, respectively. In development, addition of age and sex improved the performance of all equations compared to equations without age and sex, but addition of race did not further improve the performance. In validation, the four-marker panels were more accurate than the three-marker panels (p<0.001). The three-marker panel without race was more accurate than eGFR(cys) [1- P(30) of 15.6 vs 17.4% (p=0.014)], and the four-marker panel without race was as accurate as eGFR(cr-cys) [1- P(30) of 8.6 vs 9.4% (p=0.17)]. Results were generally consistent across subgroups. LIMITATIONS: No representation of participants with severe comorbid illness and from geographic areas outside of North America and Europe. CONCLUSIONS: The four-marker panel eGFR is as accurate as eGFR(cr-cys), without requiring specification of race. A more accurate race-free eGFR could be an important advance