Hidden Voices of Black Men

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/66982/2/10.1177_002193479402500102.pd

Lambda Hyperons in 2 A*GeV Ni + Cu Collisions

A sample of Lambda's produced in 2 A*GeV Ni + Cu collisions has been obtained with the EOS Time Projection Chamber at the Bevalac. Low background in the invariant mass distribution allows for the unambiguous demonstration of Lambda directed flow. The transverse mass spectrum at mid-rapidity has the characteristic shoulder-arm shape of particles undergoing radial transverse expansion. A linear dependence of Lambda multiplicity on impact parameter is observed, from which a total Lambda + Sigma^0 production cross section of $112 +/- 24 mb is deduced. Detailed comparisons with the ARC and RVUU models are made.Comment: Revised version accepted for publication in Phys. Lett.

Michigan's Continuing Abolition of the Death Penalty and the Conceptual Components of Symbolic Legislation

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/68316/2/10.1177_096466399300200304.pd

Effects of sleep deprivation on neural functioning: an integrative review

Sleep deprivation has a broad variety of effects on human performance and neural functioning that manifest themselves at different levels of description. On a macroscopic level, sleep deprivation mainly affects executive functions, especially in novel tasks. Macroscopic and mesoscopic effects of sleep deprivation on brain activity include reduced cortical responsiveness to incoming stimuli, reflecting reduced attention. On a microscopic level, sleep deprivation is associated with increased levels of adenosine, a neuromodulator that has a general inhibitory effect on neural activity. The inhibition of cholinergic nuclei appears particularly relevant, as the associated decrease in cortical acetylcholine seems to cause effects of sleep deprivation on macroscopic brain activity. In general, however, the relationships between the neural effects of sleep deprivation across observation scales are poorly understood and uncovering these relationships should be a primary target in future research

Punishing Terrorists: A Re-Examination of U.S. Federal Sentencing in the Postguidelines Era

The empirical literature on the theory and practice of sentencing politically motivated offenders such as terrorists in U.S. federal courts is limited. Thus, we know relatively little about the dealings between terrorist offenders and the criminal justice system or how these interactions may be influenced by changes in American legal or political context. This study summarizes previous findings relative to sentencing disparity among terrorists and nonterrorists in U.S. federal courts prior to the imposition of the U.S. Sentencing Guidelines. We then identify events occurring after the advent of the guidelines, including the early acts of terrorism on American soil. We evaluate the sentencing of terrorists versus nonterrorists following the confluence imposition of the guidelines and these events. We determine whether and how the sentencing disparity between terrorist and nonterrorist has changed since the implementation of the U.S. Sentencing Guidelines and the terrorist events of the early 1990s. Based on our findings, we put forth suggestions as to the possible ways these conditions may have affected sentencing outcomes.Yeshttps://us.sagepub.com/en-us/nam/manuscript-submission-guideline

Association of Immunosuppression and Human Immunodeficiency Virus (HIV) Viremia with Anal Cancer Risk in Persons Living with HIV in the United States and Canada

Background: People living with human immunodeficiency virus (HIV; PLWH) have a markedly elevated anal cancer risk, largely due to loss of immunoregulatory control of oncogenic human papillomavirus infection. To better understand anal cancer development and prevention, we determined whether recent, past, cumulative, or nadir/peak CD4+ T-cell count (CD4) and/or HIV-1 RNA level (HIV RNA) best predict anal cancer risk. Methods: We studied 102 777 PLWH during 1996-2014 from 21 cohorts participating in the North American AIDS Cohort Collaboration on Research and Design. Using demographics-adjusted, cohort-stratified Cox models, we assessed associations between anal cancer risk and various time-updated CD4 and HIV RNA measures, including cumulative and nadir/peak measures during prespecified moving time windows. We compared models using the Akaike information criterion. Results: Cumulative and nadir/peak CD4 or HIV RNA measures from approximately 8.5 to 4.5 years in the past were generally better predictors for anal cancer risk than their corresponding more recent measures. However, the best model included CD4 nadir (ie, the lowest CD4) from approximately 8.5 years to 6 months in the past (hazard ratio [HR] for <50 vs ≥500 cells/μL, 13.4; 95% confidence interval [CI], 3.5-51.0) and proportion of time CD4 <200 cells/μL from approximately 8.5 to 4.5 years in the past (a cumulative measure; HR for 100% vs 0%, 3.1; 95% CI, 1.5-6.6). Conclusions: Our results are consistent with anal cancer promotion by severe, prolonged HIV-induced immunosuppression. Nadir and cumulative CD4 may represent useful markers for identifying PLWH at higher anal cancer risk

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease