Mesmerized

This body of work is about looking and contemplating. Intense concentration requires solitude, which is why the figures that appear in the work are either literally isolated or seem detached from others around them. Sometimes the events the figures witness are ordinary, but more often their environments have mysterious or whimsical qualities. The whimsy comes from two places; fictional literature and childhood fantasies. Reading connects me to things and ideas outside of myself and allows the work to vacillate between the reality of normal daily observation and the mental escape of daydreaming. I want to make a place where everything is better and to which people can escape. Common iconography I’ve developed includes dogs, kites, homes, trees, blimps, and people I know. This work is asking you to notice and appreciate the details of your landscape; imagined and real

Current evidence for a modulation of low back pain by human genetic variants

The manifestation of chronic back pain depends on structural, psychosocial, occupational and genetic influences. Heritability estimates for back pain range from 30% to 45%. Genetic influences are caused by genes affecting intervertebral disc degeneration or the immune response and genes involved in pain perception, signalling and psychological processing. This inter-individual variability which is partly due to genetic differences would require an individualized pain management to prevent the transition from acute to chronic back pain or improve the outcome. The genetic profile may help to define patients at high risk for chronic pain. We summarize genetic factors that (i) impact on intervertebral disc stability, namely Collagen IX, COL9A3, COL11A1, COL11A2, COL1A1, aggrecan (AGAN), cartilage intermediate layer protein, vitamin D receptor, metalloproteinsase-3 (MMP3), MMP9, and thrombospondin-2, (ii) modify inflammation, namely interleukin-1 (IL-1) locus genes and IL-6 and (iii) and pain signalling namely guanine triphosphate (GTP) cyclohydrolase 1, catechol-O-methyltransferase, μ opioid receptor (OPMR1), melanocortin 1 receptor (MC1R), transient receptor potential channel A1 and fatty acid amide hydrolase and analgesic drug metabolism (cytochrome P450 [CYP]2D6, CYP2C9)

Absence of the mutated Trp2 allele but a common polymorphism of the COL9A2 collagen gene is associated with early recurrence after lumbar discectomy in a German population

Genetic factors seem to play a role in symptomatic lumbar disc disease (LDD). It has been shown previously that a tryptophan mutation of the COL9A2 gene is a major risk factor for LDD in a Finish population. The impact of collagen gene variations on the relapse rate after lumbar discectomy, however, has not been studied so far. Here, we conducted a cross-sectional genotyping study of patients who underwent lumbar discectomy to determine the influence of a COL9A2 mutation on the recurrence rates. Biopsy samples from 288 patients suffering from LDD with and without relapse were analyzed by PCR restriction fragment analysis and direct sequencing. The mutated Trp2 allele was not detected in the patients’ samples of the present study. However, nine patients with recurrent LDD, but only two without recurrence were homozygous for the Arg allele. Homozygosity for the Arg allele of Col9A2 seems to be more frequent in the patient group with early recurrence although the differences in the allele frequencies were statistically not significant. In contrast, the Trp2 mutation seems not to be a major susceptibility factor for LDD in a German population