RISK AND RESILIENCY FACTORS IN PREDICTING RECIDIVISM AMONG NATIVE AMERICANS ON A MONTANA RESERVATION

Background: According to a 2014 report, approximately 1 in 100 American adults are incarcerated, which represents a 500% increase over the past 40 years and accounts for the largest population of prisoners in the world. Despite research that suggests incarceration is not an effective deterrent for crime, incarceration continues to increase at a historically unprecedented rate. Mass incarceration disproportionately affects communities of color. In Montana, Native Americans are overrepresented at all levels of the correctional system. In addition, Native American ex-offenders are just over twice as likely as non-Native Americans to recidivate and be returned to a correctional institution, mostly for technical violations. Many of these technical violations could be due to an invalid risk assessment that places them in higher or lower risk categories than the risk they actually pose for re-offense. There is a general lack of research regarding the predictive ability for general risk assessment with Native American offenders, and the research that is available is mixed. The Level of Service Inventory-Revised (LSI-R) is one of the most widely used recidivism risk assessments. Studies have shown low to moderate predictive ability for the LSI-R in Native American offender populations. Critics have argued that Native American offenders have culturally-specific risk and resiliency factors that are not captured by current risk assessment tools. Method: This study utilized de-identified archival data collected in partnership with the Flathead Reservation Reentry Program (FRRP). Participants included 166 federally recognized adult male (n = 101, 60%) and female (n = 65, 40%) tribal members who were criminally involved and currently living on or planning to return to the Flathead Reservation upon release from a correctional facility. Intake data was collected from February 2016 through February 2017. Outcome data, collected until February 2018, included any new charge that resulted in a conviction for up to one year from the participant’s intake date. Results: Hierarchical Binary logistic regression analysis showed that culturally-specific factors (i.e., Historical Loss Scale, Historical Loss Associated Symptoms Scale, and the Cultural Connectedness Scale) predicted recidivism over and above the offender’s risk level, as determined by the LSI-R. Additionally, ROC analysis (AUC = .65) and scale reliability (Cronbach’s alpha = .48) found poor utility for the LSI-R within the present Native American sample. Post-hoc analysis identified education/employment, family/marital discord, and anger/avoidance from the Historical Loss Associated Symptom Scale as risk factors and frequent thoughts about historical loss, increased cultural connection (specifically increased cultural participation) as resiliency factors. Discussion: These results begin to address the gap in recidivism research on risk assessment of Native American offenders and illustrate the need for inclusion of culturally specific factors in risk assessment with Native American offenders

Estimating Extent of Mortality Associated with the Douglas-Fir Beetle in the Central and Northern Rockies

Data collected from Douglas-fir stands infected by the Douglas-fir beetle in Wyoming, Montana, Idaho, and Utah, were used to develop models to estimate amount of mortality in terms of basal area killed. Models were built using stepwise linear regression and regression tree approaches. Linear regression models using initial Douglas-fir basal area were built for all study sites but produce low precision estimates. Regression tree models using initial Douglas-fir basal area of stand density index or both were also build for all sites. Regression tree models provide a more realistic approach to estimate potential mortality by creating more homogenous mortality classes with reduced variance. The models developed provide land managers with a basis for determining the potential mortality should a Douglas-fir beetle outbreak develop

Methods to Standardize a Multicenter Acupuncture Trial Protocol to Reduce Aromatase Inhibitor-related Joint Symptoms in Breast Cancer Patients

AbstractRobust methods are needed to efficiently conduct large, multisite, randomized, controlled clinical trials of acupuncture protocols. The Southwest Oncology Group (SWOG) S1200 trial is a randomized, controlled (i.e., sham-controlled and waitlist-controlled) trial of a standardized acupuncture protocol for treating aromatase inhibitor (AI)-associated arthralgias in early-stage breast cancer patients (n = 228). The primary objective of this study was to determine whether true acupuncture administered twice weekly for 6 weeks, as compared to sham acupuncture or a waitlist control, reduced AI-associated joint pain at 6 weeks as assessed by patient reports. The study was conducted at 11 institutions across the United States. The true acupuncture protocol was developed using a consensus-based process. The true acupuncture and the sham acupuncture protocols each consisted of 12 sessions administered for 6 weeks, followed by one weekly session for 6 weeks. The true acupuncture protocol used standardized protocol points, and the standardized acupoints were tailored to a patient's joint symptoms. The similarly standardized sham acupuncture protocol utilized superficial needling of nonacupoints. Standardized methods were developed to train and monitor acupuncturists and included online and in-person training, study manuals, monthly phone calls, and remote quality assurance monitoring throughout the study period. The research staff similarly received online and in-person training and monthly phone calls

The transcription factors Ets1 and Sox10 interact during murine melanocyte development

Melanocytes, the pigment-producing cells, arise from multipotent neural crest (NC) cells during embryogenesis. Many genes required for melanocyte development were identified using mouse pigmentation mutants. The variable spotting mouse pigmentation mutant arose spontaneously at the Jackson Laboratory. We identified a G-to-A nucleotide transition in exon 3 of the Ets1 gene in variable spotting, which results in a missense G102E mutation. Homozygous variable spotting mice exhibit sporadic white spotting. Similarly, mice carrying a targeted deletion of Ets1 exhibit hypopigmentation; nevertheless, the function of Ets1 in melanocyte development is unknown. The transcription factor Ets1 is widely expressed in developing organs and tissues, including the NC. In the chick, Ets1 is required for the expression of Sox10, a transcription factor critical for the development of various NC derivatives, including melanocytes. We show that Ets1 is required early for murine NC cell and melanocyte precursor survival in vivo. Given the importance of Ets1 for Sox10 expression in the chick, we investigated a potential genetic interaction between these genes by comparing the hypopigmentation phenotypes of single and double heterozygous mice. The incidence of hypopigmentation in double heterozygotes was significantly greater than in single heterozygotes. The area of hypopigmentation in double heterozygotes was significantly larger than would be expected from the addition of the areas of hypopigmentation of single heterozygotes, suggesting that Ets1 and Sox10 interact synergistically in melanocyte development. Since Sox10 is also essential for enteric ganglia development, we examined the distal colons of Ets1 null mutants and found a significant decrease in enteric innervation, which was exacerbated by Sox10 heterozygosity. At the molecular level, Ets1 was found to activate an enhancer critical for Sox10 expression in NC-derived structures. Furthermore, enhancer activation was significantly inhibited by the variable spotting mutation. Together, these results suggest that Ets1 and Sox10 interact to promote proper melanocyte and enteric ganglia development from the NC

Two novel human cytomegalovirus NK cell evasion functions target MICA for lysosomal degradation

NKG2D plays a major role in controlling immune responses through the regulation of natural killer (NK) cells, αβ and γδ T-cell function. This activating receptor recognizes eight distinct ligands (the MHC Class I polypeptide-related sequences (MIC) A andB, and UL16-binding proteins (ULBP)1–6) induced by cellular stress to promote recognition cells perturbed by malignant transformation or microbial infection. Studies into human cytomegalovirus (HCMV) have aided both the identification and characterization of NKG2D ligands (NKG2DLs). HCMV immediate early (IE) gene up regulates NKGDLs, and we now describe the differential activation of ULBP2 and MICA/B by IE1 and IE2 respectively. Despite activation by IE functions, HCMV effectively suppressed cell surface expression of NKGDLs through both the early and late phases of infection. The immune evasion functions UL16, UL142, and microRNA(miR)-UL112 are known to target NKG2DLs. While infection with a UL16 deletion mutant caused the expected increase in MICB and ULBP2 cell surface expression, deletion of UL142 did not have a similar impact on its target, MICA. We therefore performed a systematic screen of the viral genome to search of addition functions that targeted MICA. US18 and US20 were identified as novel NK cell evasion functions capable of acting independently to promote MICA degradation by lysosomal degradation. The most dramatic effect on MICA expression was achieved when US18 and US20 acted in concert. US18 and US20 are the first members of the US12 gene family to have been assigned a function. The US12 family has 10 members encoded sequentially through US12–US21; a genetic arrangement, which is suggestive of an ‘accordion’ expansion of an ancestral gene in response to a selective pressure. This expansion must have be an ancient event as the whole family is conserved across simian cytomegaloviruses from old world monkeys. The evolutionary benefit bestowed by the combinatorial effect of US18 and US20 on MICA may have contributed to sustaining the US12 gene family

The route of priming influences the ability of respiratory virus–specific memory CD8+ T cells to be activated by residual antigen

After respiratory virus infections, memory CD8+ T cells are maintained in the lung airways by a process of continual recruitment. Previous studies have suggested that this process is controlled, at least in the initial weeks after virus clearance, by residual antigen in the lung-draining mediastinal lymph nodes (MLNs). We used mouse models of influenza and parainfluenza virus infection to show that intranasally (i.n.) primed memory CD8+ T cells possess a unique ability to be reactivated by residual antigen in the MLN compared with intraperitoneally (i.p.) primed CD8+ T cells, resulting in the preferential recruitment of i.n.-primed memory CD8+ T cells to the lung airways. Furthermore, we demonstrate that the inability of i.p.-primed memory CD8+ T cells to access residual antigen can be corrected by a subsequent i.n. virus infection. Thus, two independent factors, initial CD8+ T cell priming in the MLN and prolonged presentation of residual antigen in the MLN, are required to maintain large numbers of antigen-specific memory CD8+ T cells in the lung airways

Dynamics of Galactic Disks and Mergers at z~1.6: Spatially Resolved Spectroscopy with Keck Laser Guide Star Adaptive Optics

We present 0.2" resolution near-infrared integral field spectroscopy of H-alpha emission from six star forming galaxies at z~1.6 (look-back time of ~9.6 Gyr). These observations were obtained with OSIRIS using the Keck Laser Guide Star Adaptive Optics system. All sources have a compact spatial extent of ~1", with an average half light radius of r=2.9 kpc and average dereddened star formation rate of 22 Msolar per year. Based on H-alpha kinematics we find that these six galaxies are dynamically distinguishable, and we classify them as either merger or disk candidate systems. We find three merger systems (HDF-BX1287, HDF-BX1315, and Q1623-BX491) with varying geometries and dynamical properties. Three galaxies (HDF-BMZ1299, Q2343-BX344, and Q2343-BM145) are well-fit by an inclined-disk model with low velocity residuals (20 to 46 km/sec). An average plateau velocity of v_p=185 km/sec is achieved within 1.0 kpc. The majority of observed velocity dispersions (~88 km/sec) can be explained by the residual seeing halo, and are not intrinsic to our sources. However, one merger and one disk candidate have high velocity dispersions (> 200 km/sec) that cannot be solely explained by beam smearing. For two disk candidates, we detect [NII] emission and are able to map the [NII]/H-alpha ratio on kiloparsec scales. In both cases, [NII] emission is more concentrated than H-alpha emission (< 0.2"), and peak ratios are best explained by the presence of an AGN. These are among the weakest known AGN at high redshift, however their emission is strong enough to impact high redshift metallicity studies that use nebular ratios. All disk candidates have likely completed only a few orbital periods, and if left unperturbed are excellent candidates to become present-day spiral galaxies.Comment: 45 pages, 12 figures, resubmitted to Ap

Effects of antiplatelet therapy on stroke risk by brain imaging features of intracerebral haemorrhage and cerebral small vessel diseases: subgroup analyses of the RESTART randomised, open-label trial

Background Findings from the RESTART trial suggest that starting antiplatelet therapy might reduce the risk of recurrent symptomatic intracerebral haemorrhage compared with avoiding antiplatelet therapy. Brain imaging features of intracerebral haemorrhage and cerebral small vessel diseases (such as cerebral microbleeds) are associated with greater risks of recurrent intracerebral haemorrhage. We did subgroup analyses of the RESTART trial to explore whether these brain imaging features modify the effects of antiplatelet therapy

Burden of Risk Alleles for Hypertension Increases Risk of Intracerebral Hemorrhage

Background and Purpose-Genetic variation influences risk of intracerebral hemorrhage (ICH). Hypertension (HTN) is a potent risk factor for ICH and several common genetic variants (single nucleotide polymorphisms [SNPs]) associated with blood pressure levels have been identified. We sought to determine whether the cumulative burden of blood pressure-related SNPs is associated with risk of ICH and pre-ICH diagnosis of HTN. Methods-We conducted a prospective multicenter case-control study in 2272 subjects of European ancestry (1025 cases and 1247 control subjects). Thirty-nine SNPs reported to be associated with blood pressure levels were identified from the National Human Genome Research Institute genomewide association study catalog. Single-SNP association analyses were performed for the outcomes ICH and pre-ICH HTN. Subsequently, weighted and unweighted genetic risk scores were constructed using these SNPs and entered as the independent variable in logistic regression models with ICH and pre-ICH HTN as the dependent variables. Results-No single SNP was associated with either ICH or pre-ICH HTN. The blood pressure-based unweighted genetic risk score was associated with risk of ICH (OR, 1.11; 95% CI, 1.02-1.21; P=0.01) and the subset of ICH in deep regions (OR, 1.18; 95% CI, 1.07-1.30; P=0.001), but not with the subset of lobar ICH. The score was associated with a history of HTN among control subjects (OR, 1.17; 95% CI, 1.04-1.31; P=0.009) and ICH cases (OR, 1.15; 95% CI, 1.01-1.31; P=0.04). Similar results were obtained when using a weighted score. Conclusion-Increasing numbers of high blood pressure-related alleles are associated with increased risk of deep ICH as well as with clinically identified HTN. (Stroke. 2012; 43: 2877-2883.