Immigration Cyber Prisons: Ending the Use of Electronic Ankle Shackles

The call to end immigration detention has garnered strong support in recent years due to a growing public awareness of its devastating impact on the individuals locked away, their families, and entire communities. Throughout the nation, communities, organizers, advocates, and public officials have demanded the shutdown of Immigration and Customs Enforcement (ICE) detention centers, particularly those operated by private prison companies. However, less attention has been paid to another form of detention that has been insidiously expanding alongside ICE’s brick-and-mortar jails: the Intensive Supervision Assistance Program (ISAP), the primary component of ICE’s so-called “Alternatives to Detention” program. ISAP surveils, monitors, and restricts immigrants by using invasive and evolving forms of technology. Like much of ICE’s sprawling detention system, ISAP is fueled by a multi-billion-dollar contract with the subsidiary of a private prison corporation that profits from detaining and surveilling immigrants. One of the most common and dehumanizing forms of surveillance in ISAP is a GPS enabled ankle monitor that shackles individuals both visibly and invisibly. This report recommends that ICE immediately wind down ISAP and cease its use of electronic ankle shackles, first by removing them from all individuals currently subject to ISAP. To the extent that ankle shackles continue being used while phasing out ISAP, the administration should mandate ICE to track the data needed to prevent discriminatory practices; provide both a clear written justification and review process when deciding to subject an individual to ankle shackles; and allow those subject to ankle shackles to secure employment, participate in family and community activities, and seek medical treatment. This report also recommends a severance of the link between immigration enforcement and service provision through community-based programs, as well as allocation of government funding for community support and legal representation services. As the harms of electronic ankle shackling demonstrate, ISAP is by no means an acceptable reform to the existing detention apparatus; rather it is another form of confinement that must be dismantled alongside physical detention. While the coercive and dehumanizing shackling of humans is unacceptable in any form, the data demonstrating the comparable or superior efficacy of more holistic intervention also lay bare the animus and profit motives at the heart of ICE’s shackling regime. Ending shackling is not just good policy; it is an issue of racial, economic, and health justice

Diabetes Reduces Mesenchymal Stem Cells in Fracture Healing Through a TNFα-Mediated Mechanism

Aims/hypothesis Diabetes interferes with bone formation and impairs fracture healing, an important complication in humans and animal models. The aim of this study was to examine the impact of diabetes on mesenchymal stem cells (MSCs) during fracture repair. Methods Fracture of the long bones was induced in a streptozotocin-induced type 1 diabetic mouse model with or without insulin or a specific TNFα inhibitor, pegsunercept. MSCs were detected with cluster designation-271 (also known as p75 neurotrophin receptor) or stem cell antigen-1 (Sca-1) antibodies in areas of new endochondral bone formation in the calluses. MSC apoptosis was measured by TUNEL assay and proliferation was measured by Ki67 antibody. In vitro apoptosis and proliferation were examined in C3H10T1/2 and human-bone-marrow-derived MSCs following transfection with FOXO1 small interfering (si)RNA. Results Diabetes significantly increased TNFα levels and reduced MSC numbers in new bone area. MSC numbers were restored to normal levels with insulin or pegsunercept treatment. Inhibition of TNFα significantly reduced MSC loss by increasing MSC proliferation and decreasing MSC apoptosis in diabetic animals, but had no effect on MSCs in normoglycaemic animals. In vitro experiments established that TNFα alone was sufficient to induce apoptosis and inhibit proliferation of MSCs. Furthermore, silencing forkhead box protein O1 (FOXO1) prevented TNFα-induced MSC apoptosis and reduced proliferation by regulating apoptotic and cell cycle genes. Conclusions/interpretation Diabetes-enhanced TNFα significantly reduced MSC numbers in new bone areas during fracture healing. Mechanistically, diabetes-enhanced TNFα reduced MSC proliferation and increased MSC apoptosis. Reducing the activity of TNFα in vivo may help to preserve endogenous MSCs and maximise regenerative potential in diabetic patients

Disordered structure for long-range charge density wave order in annealed crystals of magnetic kagome FeGe

Recently, charge density wave (CDW) has been observed well below the order of antiferromagnetism (AFM) in kagome FeGe in which magnetism and CDW are intertwined to form an emergent quantum ground state. The mechanism of CDW precipitating from an A-type AFM of Fe kagome sublattice is intensively debated. The structural distortion originating from the CDW has yet to be accurately determined in FeGe. Here we resolved the structure model of the CDW in annealed FeGe crystals through single crystal x-ray diffraction via a synchrotron radiation source. The annealed crystals exhibit strong CDW transition signals exemplified by sharp magnetic susceptibility drop and specific heat jump, as well as intense superlattice reflections from 2 $\times$ 2 $\times$ 2 CDW order. Occupational disorder of Ge atoms resulting from short-range CDW correlations above $T_\mathrm{CDW}$ has also been identified from the structure refinements. The dimerization of Ge atoms along c axis has been demonstrated to be the dominant distortion for CDW. The Fe kagome and Ge honeycomb sublattices only undergo subtle distortions. Occupational disorder of Ge atoms is also proved to exist in the CDW phase due to the random selection of partial Ge sites to be dimerized to realize the structural distortion. Our work paves the way to understanding the unconventional nature of CDW in FeGe not only by solving the structural distortion below $T_\mathrm{CDW}$ and identifying fluctuations above it but also by rationalizing the synthesis of high-quality crystals for in-depth investigations in the future.Comment: 18 pages, 4 figures. Comments are welcom

Sixty years from discovery to solution: crystal structure of bovine liver catalase form III

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/86968/1/S0907444911024486.pd

Adolescents with metabolic syndrome have a history of low aerobic fitness and physical activity levels

Abstract: Purpose: Metabolic syndrome (MS) is a clustering of cardiovascular disease risk factors that identifies individuals with the highest risk for heart disease. Two factors that may influence the MS are physical activity and aerobic fitness. This study determined if adolescent with the MS had low levels of aerobic fitness and physical activity as children. Methods: This longitudinal, exploratory study had 389 participants: 51% girls, 84% Caucasian, 12% African American, 1% Hispanic, and 3% other races, from the State of North Carolina. Habitual physical activity (PA survey), aerobic fitness (VO2max), body mass index (BMI), blood pressure, and lipids obtained at 7–10 y of age were compared to their results obtained 7 y later at ages 14–17 y. Results: Eighteen adolescents (4.6%) developed 3 or more characteristics of the MS. Logistic regression, adjusting for BMI percentile, blood pressure, and cholesterol levels, found that adolescents with the MS were 6.08 (95%CI = 1.18–60.08) times more likely to have low aerobic fitness as children and 5.16 (95%CI = 1.06–49.66) times more likely to have low PA levels. Conclusion: Low levels of childhood physical activity and aerobic fitness are associated with the presence of the metabolic syndrome in adolescents. Thus, efforts need to begin early in childhood to increase exercise

Oxygen Tension Is a Determinant of the Matrix-Forming Phenotype of Cultured Human Meniscal Fibrochondrocytes

BACKGROUND: Meniscal cartilage displays a poor repair capacity, especially when injury is located in the avascular region of the tissue. Cell-based tissue engineering strategies to generate functional meniscus substitutes is a promising approach to treat meniscus injuries. Meniscus fibrochondrocytes (MFC) can be used in this approach. However, MFC are unable to retain their phenotype when expanded in culture. In this study, we explored the effect of oxygen tension on MFC expansion and on their matrix-forming phenotype. METHODOLOGY/PRINCIPAL FINDINGS: MFC were isolated from human menisci followed by basic fibroblast growth factor (FGF-2) mediated cell expansion in monolayer culture under normoxia (21%O(2)) or hypoxia (3%O(2)). Normoxia and hypoxia expanded MFC were seeded on to a collagen scaffold. The MFC seeded scaffolds (constructs) were cultured in a serum free chondrogenic medium for 3 weeks under normoxia and hypoxia. Constructs containing normoxia-expanded MFC were subsequently cultured under normoxia while those formed from hypoxia-expanded MFC were subsequently cultured under hypoxia. After 3 weeks of in vitro culture, the constructs were assessed biochemically, histologically and for gene expression via real-time reverse transcription-PCR assays. The results showed that constructs under normoxia produced a matrix with enhanced mRNA ratio (3.5-fold higher; p<0.001) of collagen type II to I. This was confirmed by enhanced deposition of collagen II using immuno-histochemistry. Furthermore, the constructs under hypoxia produced a matrix with higher mRNA ratio of aggrecan to versican (3.5-fold, p<0.05). However, both constructs had the same capacity to produce a glycosaminoglycan (GAG) -specific extracellular matrix. CONCLUSIONS: Our data provide evidence that oxygen tension is a key player in determining the matrix phenotype of cultured MFC. These findings suggest that the use of normal and low oxygen tension during MFC expansion and subsequent neo-tissue formation cultures may be important in engineering different regions of the meniscus

Methylenetetrahydrofolate reductase (MTHFR) C677T polymorphism and high plasma homocysteine in chronic hepatitis C (CHC) infected patients from the Northeast of Brazil

<p>Abstract</p> <p>Background/Aim</p> <p>Hyperhomocysteinemia due to Methylenetetrahydrofolate Reductase (<it>MTHFR</it>) gene, in particular the C677T (Ala222Val) polymorphism were recently associated to steatosis and fibrosis. We analyzed the frequency of <it>MTHFR </it>gene in a cross-sectional study of patients affected by Chronic Hepatitis C (CHC) from Northeast of Brazil.</p> <p>Method</p> <p>One hundred seven-four untreated patients with CHC were genotyped for the C677T <it>MTHFR</it>. Genomic DNA was extracted from peripheral blood cells and the C677T <it>MTHFR </it>polymorphism was identified by PCR-RFLP. The homocysteine (Hcy) levels were determined by chemiluminescence method. All patients were negative for markers of Wilson's disease, hemochromatosis and autoimmune diseases and have current and past daily alcohol intake less than 100 g/week.</p> <p>Results</p> <p>Among subjects infected with CHC genotype non-1 the frequency of <it>MTHFR </it>genotypes TT was 9.8% <it>versus </it>4.4% genotype 1 (p = 0.01). Nevertheless, association was found between the <it>MTHFR </it>genotype TT × CT/CC polymorphism and the degree of steatosis and fibrosis in both hepatitis C genotype (p < 0.05). A significant difference was found on plasma Hcy levels in patients with steatosis regardless of HCV genotype (p = 0.03).</p> <p>Conclusion</p> <p>Our results indicate that plasma Hcy levels is highly prevalent in subjects with chronic hepatits C with steatosis regardless of HCV genotype and vitamin deficiency. The presence of genotype TT of <it>MTHFR </it>C677T polymorphism was more common in CHC genotype non-1 infected patient regardless of histopathological classification and genotype TT+CT frequencies were significant in the presence of fibrosis grade 1+2 and of steatosis in CHC infected patients from the northeast of Brazil regardless of HCV genotype. The genetic susceptibility of <it>MTHFR </it>C677T polymorphism should be confirmed in a large population.</p

Detectable Clonal Mosaicism from Birth to Old Age and its Relationship to Cancer

Clonal mosaicism for large chromosomal anomalies (duplications, deletions and uniparental disomy) was detected using SNP microarray data from over 50,000 subjects recruited for genome-wide association studies. This detection method requires a relatively high frequency of cells (>5–10%) with the same abnormal karyotype (presumably of clonal origin) in the presence of normal cells. The frequency of detectable clonal mosaicism in peripheral blood is low (<0.5%) from birth until 50 years of age, after which it rises rapidly to 2–3% in the elderly. Many of the mosaic anomalies are characteristic of those found in hematological cancers and identify common deleted regions that pinpoint the locations of genes previously associated with hematological cancers. Although only 3% of subjects with detectable clonal mosaicism had any record of hematological cancer prior to DNA sampling, those without a prior diagnosis have an estimated 10-fold higher risk of a subsequent hematological cancer (95% confidence interval = 6–18)

Microwave multiplexing on the Keck Array

We describe an on-sky demonstration of a microwave-multiplexing readout system in one of the receivers of the Keck Array, a polarimetry experiment observing the cosmic microwave background at the South Pole. During the austral summer of 2018-2019, we replaced the time-division multiplexing readout system with microwave-multiplexing components including superconducting microwave resonators coupled to radio-frequency superconducting quantum interference devices at the sub-Kelvin focal plane, coaxial-cable plumbing and amplification between room temperature and the cold stages, and a SLAC Microresonator Radio Frequency system for the warm electronics. In the range 5-6 GHz, a single coaxial cable reads out 528 channels. The readout system is coupled to transition-edge sensors, which are in turn coupled to 150-GHz slot-dipole phased-array antennas. Observations began in April 2019, and we report here on an initial characterization of the system performance.Comment: 9 pages, 11 figures, Accepted by the Journal of Low Temperature Physics (Proceedings of the 18th International Workshop on Low Temperature Detectors