Previously deported unauthorized immigrants are over 2.5 times more likely to be arrested again than those who have not been deported

Since 2008, U.S. federal immigration has operated its ‘Secure Communities’ policy where arrestee’s identifiers are checked against immigration records. Federal immigration also identifies unauthorized immigrants who have been previously removed as a group that poses a risk to the community. Using a sample of nearly 3,000 foreign born inmates Jennifer Wong and Laura J. Hickman find that 91 percent of those who had previously been removed were rearrested within nine years, and that they were likely to be rearrested more frequently, and more quickly, compared to those who have never been removed

Conserved noncoding sequences highlight shared components of regulatory networks in dicotyledonous plants

Conserved noncoding sequences (CNSs) in DNA are reliable pointers to regulatory elements controlling gene expression. Using a comparative genomics approach with four dicotyledonous plant species (Arabidopsis thaliana, papaya [Carica papaya], poplar [Populus trichocarpa], and grape [Vitis vinifera]), we detected hundreds of CNSs upstream of Arabidopsis genes. Distinct positioning, length, and enrichment for transcription factor binding sites suggest these CNSs play a functional role in transcriptional regulation. The enrichment of transcription factors within the set of genes associated with CNS is consistent with the hypothesis that together they form part of a conserved transcriptional network whose function is to regulate other transcription factors and control development. We identified a set of promoters where regulatory mechanisms are likely to be shared between the model organism Arabidopsis and other dicots, providing areas of focus for further research

Oklahoma's dirty dozen: Unwanted invasive plants

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Longitudinal Evolution of the Pseudomonas-Derived Cephalosporinase (PDC) Structure and Activity in a CysticFibrosis Patient Treated with b-Lactams

Traditional studies on the evolution of antibiotic resistance development use approaches that can range from laboratory-based experimental studies, to epidemiological surveillance, to sequencing of clinical isolates. However, evolutionary trajectories also depend on the environment in which selection takes place, compelling the need to more deeply investigate the impact of environmental complexities and their dynamics over time. Herein, we explored the within-patient adaptive long-term evolution of a Pseudomonas aeruginosa hypermutator lineage in the airways of a cystic fibrosis (CF) patient by performing a chronological tracking of mutations that occurred in different subpopulations; our results demonstrated parallel evolution events in the chromosomally encoded class C β-lactamase (blaPDC). These multiple mutations within blaPDC shaped diverse coexisting alleles, whose frequency dynamics responded to the changing antibiotic selective pressures for more than 26 years of chronic infection. Importantly, the combination of the cumulative mutations in blaPDC provided structural and functional protein changes that resulted in a continuous enhancement of its catalytic efficiency and high level of cephalosporin resistance. This evolution was linked to the persistent treatment with ceftazidime, which we demonstrated selected for variants with robust catalytic activity against this expanded-spectrum cephalosporin. A “gain of function” of collateral resistance toward ceftolozane, a more recently introduced cephalosporin that was not prescribed to this patient, was also observed, and the biochemical basis of this cross-resistance phenomenon was elucidated. This work unveils the evolutionary trajectories paved by bacteria toward a multidrug-resistant phenotype, driven by decades of antibiotic treatment in the natural CF environmental setting. IMPORTANCE Antibiotics are becoming increasingly ineffective to treat bacterial infections. It has been consequently predicted that infectious diseases will become the biggest challenge to human health in the near future. Pseudomonas aeruginosa is considered a paradigm in antimicrobial resistance as it exploits intrinsic and acquired resistance mechanisms to resist virtually all antibiotics known. AmpC β-lactamase is the main mechanism driving resistance in this notorious pathogen to β-lactams, one of the most widely used classes of antibiotics for cystic fibrosis infections. Here, we focus on the β-lactamase gene as a model resistance determinant and unveil the trajectory P. aeruginosa undertakes on the path toward a multidrug-resistant phenotype during the course of two and a half decades of chronic infection in the airways of a cystic fibrosis patient. Integrating genetic and biochemical studies in the natural environment where evolution occurs, we provide a unique perspective on this challenging landscape, addressing fundamental molecular mechanisms of resistance.Fil: Colque, Claudia A. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Departamento de Química Biológica; Argentina.Fil: Albarracín Orio, Andrea G. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Departamento de Química Biológica; Argentina.Fil: Hedemann, Laura G. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Departamento de Química Biológica; Argentina.Fil: Feliziani, Sofía. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Departamento de Química Biológica; Argentina.Fil: Moyano, Alejandro J. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Departamento de Química Biológica; Argentina.Fil: Smania, Andrea M. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Departamento de Química Biológica; Argentina.Fil: Colque, Claudia A. Universidad Nacional de Córdoba. Centro de Investigaciones en Química Biológica de Córdoba (CIQUIBIC-CONICET); Argentina.Fil: Albarracín Orio, Andrea G. Universidad Nacional de Córdoba. Centro de Investigaciones en Química Biológica de Córdoba (CIQUIBIC-CONICET); Argentina.Fil: Hedemann, Laura G. Universidad Nacional de Córdoba. Centro de Investigaciones en Química Biológica de Córdoba (CIQUIBIC-CONICET); Argentina.Fil: Feliziani, Sofía. Universidad Nacional de Córdoba. Centro de Investigaciones en Química Biológica de Córdoba (CIQUIBIC-CONICET); Argentina.Fil: Moyano, Alejandro J. Universidad Nacional de Córdoba. Centro de Investigaciones en Química Biológica de Córdoba (CIQUIBIC-CONICET); Argentina.Fil: Smania, Andrea M. Universidad Nacional de Córdoba. Centro de Investigaciones en Química Biológica de Córdoba (CIQUIBIC-CONICET); Argentina.Fil: Tomatis, Pablo E. Universidad Nacional de Rosario. Instituto de Biología Molecular y Celular de Rosario (IBR-CONICET); Argentina.Fil: Dotta, Gina. Universidad Nacional de Rosario. Instituto de Biología Molecular y Celular de Rosario (IBR-CONICET); Argentina.Fil: Vila, Alejandro J. Universidad Nacional de Rosario. Instituto de Biología Molecular y Celular de Rosario (IBR-CONICET); Argentina.Fil: Tomatis, Pablo E. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas; Argentina.Fil: Moreno, Diego M. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas; Argentina.Fil: Vila, Alejandro J. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas; Argentina.Fil: Albarracín Orio, Andrea G. Universidad Católica de Córdoba. Facultad de Ciencias Agropecuarias. (IRNASUS-CONICET); Argentina.Fil: Moreno, Diego M. Universidad Nacional de Rosario. Instituto de Química de Rosario (IQUIR-CONICET); Argentina.Fil: Hickman Rachel A. Department of Clinical Microbiology; Denmark.Fil: Sommer, Lea M. Department of Clinical Microbiology; Denmark.Fil: Johansen, Helle K. Department of Clinical Microbiology; Denmark.Fil: Hickman Rachel A. Technical University of Denmark, Lyngb. Novo Nordisk Foundation Centre for Biosustainability; Denmark.Fil: Sommer, Lea M. Technical University of Denmark, Lyngb. Novo Nordisk Foundation Centre for Biosustainability; Denmark.Fil: Johansen, Helle K. Technical University of Denmark, Lyngb. Novo Nordisk Foundation Centre for Biosustainability; Denmark.Fil: Bonomo, Robert A. Case Western Reserve University. Departments of Molecular Biology and Microbiology, Medicine, Biochemistry, Pharmacology, and Proteomics and Bioinformatics; United States.Fil: Bonomo, Robert A. Senior Clinical Scientist Investigator. Louis Stokes Cleveland Department of Veterans Affairs; United States.Fil: Johansen, Helle K. University of Copenhagen. Department of Clinical Medicine; Denmark

Examining subgroup effects by socioeconomic status of public health interventions targeting multiple risk behaviour in adolescence

Multiple risk behaviour (MRB) refers to two or more risk behaviours such as smoking, drinking alcohol, poor diet and unsafe sex. Such behaviours are known to co-occur in adolescence. It is unknown whether MRB interventions are equally effective for young people of low and high socioeconomic status (SES). There is a need to examine these effects to determine whether MRB interventions have the potential to narrow or widen inequalities. Two Cochrane systematic reviews that examined interventions to reduce adolescent MRB were screened to identify universal interventions that reported SES. Study authors were contacted, and outcome data stratified by SES and intervention status were requested. Risk behaviour outcomes alcohol use, smoking, drug use, unsafe sex, overweight/obesity, sedentarism, peer violence and dating violence were examined in random effects meta-analyses and subgroup analyses conducted to explore differences between high SES and low SES adolescents. Of 49 studies reporting universal interventions, only 16 also reported having measured SES. Of these 16 studies, four study authors provided data sufficient for subgroup analysis. There was no evidence of subgroup differences for any of the outcomes. For alcohol use, the direction of effect was the same for both the high SES group (RR 1.26, 95% CI: 0.96, 1.65, p = 0.09) and low SES group (RR 1.14, 95% CI: 0.98, 1.32, p = 0.08). The direction of effect was different for smoking behaviour in favour of the low SES group (RR 0.83, 95% CI: 0.66, 1.03, p = 0.09) versus the high SES group (RR 1.16, 95% CI: 0.82, 1.63, p = 0.39). For drug use, the direction of effect was the same for both the high SES group (RR 1.29, 95% CI: 0.97, 1.73, p = 0.08) and the low SES group (RR 1.28, 95% CI: 0.84, 1.96, p = 0.25). The majority of studies identified did not report having measured SES. There was no evidence of subgroup difference for all outcomes analysed among the four included studies. There is a need for routine reporting of demographic information within studies so that stronger evidence of effect by SES can be demonstrated and that interventions can be evaluated for their impact on health inequalities.https://doi.org/10.1186/s12889-018-6042-

Comparative study of in situ N2 rotational Raman spectroscopy methods for probing energy thermalisation processes during spin-exchange optical pumping

Spin-exchange optical pumping (SEOP) has been widely used to produce enhancements in nuclear spin polarisation for hyperpolarised noble gases. However, some key fundamental physical processes underlying SEOP remain poorly understood, particularly in regards to how pump laser energy absorbed during SEOP is thermalised, distributed and dissipated. This study uses in situ ultra-low frequency Raman spectroscopy to probe rotational temperatures of nitrogen buffer gas during optical pumping under conditions of high resonant laser flux and binary Xe/N2 gas mixtures. We compare two methods of collecting the Raman scattering signal from the SEOP cell: a conventional orthogonal arrangement combining intrinsic spatial filtering with the utilisation of the internal baffles of the Raman spectrometer, eliminating probe laser light and Rayleigh scattering, versus a new in-line modular design that uses ultra-narrowband notch filters to remove such unwanted contributions. We report a ~23-fold improvement in detection sensitivity using the in-line module, which leads to faster data acquisition and more accurate real-time monitoring of energy transport processes during optical pumping. The utility of this approach is demonstrated via measurements of the local internal gas temperature (which can greatly exceed the externally measured temperature) as a function of incident laser power and position within the cell

Neuroinflammation, Mast Cells, and Glia: Dangerous Liaisons

The perspective of neuroinflammation as an epiphenomenon following neuron damage is being replaced by the awareness of glia and their importance in neural functions and disorders. Systemic inflammation generates signals that communicate with the brain and leads to changes in metabolism and behavior, with microglia assuming a pro-inflammatory phenotype. Identification of potential peripheral-to-central cellular links is thus a critical step in designing effective therapeutics. Mast cells may fulfill such a role. These resident immune cells are found close to and within peripheral nerves and in brain parenchyma/meninges, where they exercise a key role in orchestrating the inflammatory process from initiation through chronic activation. Mast cells and glia engage in crosstalk that contributes to accelerate disease progression; such interactions become exaggerated with aging and increased cell sensitivity to stress. Emerging evidence for oligodendrocytes, independent of myelin and support of axonal integrity, points to their having strong immune functions, innate immune receptor expression, and production/response to chemokines and cytokines that modulate immune responses in the central nervous system while engaging in crosstalk with microglia and astrocytes. In this review, we summarize the findings related to our understanding of the biology and cellular signaling mechanisms of neuroinflammation, with emphasis on mast cell-glia interactions

Transcriptional dynamics driving MAMP-triggered immunity and pathogen effector-mediated immunosuppression in Arabidopsis leaves following infection with Pseudomonas syringae pv tomato DC3000

Transcriptional reprogramming is integral to effective plant defense. Pathogen effectors act transcriptionally and posttranscriptionally to suppress defense responses. A major challenge to understanding disease and defense responses is discriminating between transcriptional reprogramming associated with microbial-associated molecular pattern (MAMP)-triggered immunity (MTI) and that orchestrated by effectors. A high-resolution time course of genome-wide expression changes following challenge with Pseudomonas syringae pv tomato DC3000 and the nonpathogenic mutant strain DC3000hrpA- allowed us to establish causal links between the activities of pathogen effectors and suppression of MTI and infer with high confidence a range of processes specifically targeted by effectors. Analysis of this information-rich data set with a range of computational tools provided insights into the earliest transcriptional events triggered by effector delivery, regulatory mechanisms recruited, and biological processes targeted. We show that the majority of genes contributing to disease or defense are induced within 6 h postinfection, significantly before pathogen multiplication. Suppression of chloroplast-associated genes is a rapid MAMP-triggered defense response, and suppression of genes involved in chromatin assembly and induction of ubiquitin-related genes coincide with pathogen-induced abscisic acid accumulation. Specific combinations of promoter motifs are engaged in fine-tuning the MTI response and active transcriptional suppression at specific promoter configurations by P. syringae