Free subalgebras of division algebras over uncountable fields

We study the existence of free subalgebras in division algebras, and prove the following general result: if $A$ is a noetherian domain which is countably generated over an uncountable algebraically closed field $k$ of characteristic 0, then either the quotient division algebra of $A$ contains a free algebra on two generators, or it is left algebraic over every maximal subfield. As an application, we prove that if $k$ is an uncountable algebraically closed field and $A$ is a finitely generated $k$-algebra that is a domain of GK-dimension strictly less than 3, then either $A$ satisfies a polynomial identity, or the quotient division algebra of $A$ contains a free $k$-algebra on two generators.Comment: 20 page

Prevalence and geographical distribution of Papio hamadryas papillomavirus 1 (PhPV1) in Kenyan baboons

Papio hamadryas papillomavirus (PhPV) 1, 2, and 3, are Alphapapillomaviruses that have been detected in Kenyan Olive baboons but the distribution is unknown. Therefore, cervical screening for PhPV1 was performed in baboons from various areas in Kenya using a nested polymerase chain reaction. The prevalence rate was 33%.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/135993/1/jmp12247.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/135993/2/jmp12247_am.pd

Nonhuman Primate Models Used to Study Pelvic Inflammatory Disease Caused by Chlamydia trachomatis

Pelvic inflammatory disease (PID) is a global health concern that is associated with significant morbidity and is a major cause of infertility. Throughout history animals have been used for anatomical studies and later as models of human disease. In particular, nonhuman primates (NHPs) have permitted investigations of human disease in a biologically, physiologically, and anatomically similar system. The use of NHPs as human PID models has led to a greater understanding of the primary microorganisms that cause disease (e.g., Chlamydia trachomatis and Neisseria gonorroheae), the pathogenesis of infection and its complications, and the treatment of people with PID. This paper explores historical and contemporary aspects of NHP modeling of chlamydial PID, with an emphasis on advantages and limitations of this approach and future directions for this research

Amantadine Did Not Positively Impact Cognition in Chronic Traumatic Brain Injury: A Multi-Site, Randomized, Controlled Trial

Despite limited evidence to support the use of amantadine to enhance cognitive function after traumatic brain injury (TBI), the clinical use for this purpose is highly prevalent and is often based on inferred belief systems. The aim of this study was to assess effect of amantadine on cognition among individuals with a history of TBI and behavioral disturbance using a parallel-group, randomized, double-blind, placebo-controlled trial of amantadine 100 mg twice-daily versus placebo for 60 days. Included in the study were 119 individuals with two or more neuropsychological measures greater than 1 standard deviation below normative means from a larger study of 168 individuals with chronic TBI (>6 months post-injury) and irritability. Cognitive function was measured at treatment days 0, 28, and 60 with a battery of neuropsychological tests. Composite indices were generated: General Cognitive Index (included all measures), a Learning Memory Index (learning/memory measures), and Attention/Processing Speed Index (attention and executive function measures). Repeated-measures analysis of variance revealed statistically significant between-group differences favoring the placebo group at day 28 for General Cognitive Index (p = 0.002) and Learning Memory Index (p = 0.001), but not Attention/Processing Speed Index (p = 0.25), whereas no statistically significant between-group differences were found at day 60. There were no statistically significant between-group differences on adverse events. Cognitive function in individuals with chronic TBI is not improved by amantadine 100 mg twice-daily. In the first 28 days of use, amantadine may impede cognitive processing. However, the effect size was small and mean scores for both groups were generally within expectations for persons with history of complicated mild-to-severe TBI, suggesting that changes observed across assessments may not have functional significance. The use of amantadine to enhance cognitive function is not supported by these findings