Functional Brain Imagery and Jungian Analytical Psychology: An Interesting Dance?

Jung’s original neuroscience research project looked at the neurophysiological responses to the word association test (WAT) in an effort to understand ‘complexes’, those emotionally laden fixations that bother us all, and can be inferred from certain painful responses in the WAT. He measured breathing rates, skin conductance and electrocardiography, but there was no brain functional imaging technology available at the time. One hundred years later, a wide range of brain functional technologies are available, and this chapter describes two studies in which the WAT was performed under functional magnetic resonance imaging and quantitative electroencephalography conditions. In essence, a complexed response first activates the amygdala (many right-sided). This is followed in the next 3 s by bilateral brain activity in the anterior insula, the supplementary motor area and the dorsal cingulum; the premotor mirror neuron areas, the so-called resonance circuitry, which is central to mindfulness (awareness of self) and empathy (sense of the other), negotiations between self-awareness and the ‘internal other’, and has been well described by Dan Siegel. But over the following 2 s, activity shifts to the left hemisphere, seemingly the way the brain deals with a complex in the moment, possibly to dull the pain of the complexed response

Comparison of morphological variation indicative of ploidy-level in Phragmites australis (Poaceae) from Eastern North America.

ABSTRACT. Variation in ploidy levels in Phragmites australis is a welldocumented phenomenon although North American populations are less studied than European ones. It has been suggested, based on morphological measurements, that native and introduced P. australis subspecies in North America represent different ploidy levels. The objectives of this study were to assess whether guard cell size and stomatal density, morphological differences indicative of variation in ploidy level between native and introduced P. australis, are truly associated with different ploidy levels as measured by flow cytometry. Significant differences in guard cell size and stomatal densities were found between subspecies, with native plants having larger guard cells and lower stomatal density. However, no differences in 2C DNA content were found. Although these morphological measurements are significantly correlated with subspecies and can be added to the list of useful morphological characters distinguishing the two subspecies, it does not appear that they are accurate indicators of ploidy levels. Potential implications of these differences on the invasion biology of introduced P. australis are discussed

Mitochondrial abnormalities in spinal and bulbar muscular atrophy

Spinal and bulbar muscular atrophy (SBMA) is a motor neuron disease caused by polyglutamine expansion mutation in the androgen receptor (AR). We investigated whether the mutant protein alters mitochondrial function. We found that constitutive and doxycycline-induced expression of the mutant AR in MN-1 and PC12 cells, respectively, are associated with depolarization of the mitochondrial membrane. This was mitigated by cyclosporine A, which inhibits opening of the mitochondrial permeability transition pore. We also found that the expression of the mutant protein in the presence of ligand results in an elevated level of reactive oxygen species, which is blocked by the treatment with the antioxidants co-enzyme Q10 and idebenone. The mutant protein in MN-1 cells also resulted in increased Bax, caspase 9 and caspase 3. We assessed the effects of mutant AR on the transcription of mitochondrial proteins and found altered expression of the peroxisome proliferator-activated receptor γ coactivator 1 and the mitochondrial specific antioxidant superoxide dismutase-2 in affected tissues of SBMA knock-in mice. In addition, we found that the AR associates with mitochondria in cultured cells. This study thus provides evidence for mitochondrial dysfunction in SBMA cell and animal models, either through indirect effects on the transcription of nuclear-encoded mitochondrial genes or through direct effects of the mutant protein on mitochondria or both. These findings indicate possible benefit from mitochondrial therapy for SBMA

RANTES/CCL5 and Risk for Coronary Events: Results from the MONICA/KORA Augsburg Case-Cohort, Athero-Express and CARDIoGRAM Studies

BACKGROUND: The chemokine RANTES (regulated on activation, normal T-cell expressed and secreted)/CCL5 is involved in the pathogenesis of cardiovascular disease in mice, whereas less is known in humans. We hypothesised that its relevance for atherosclerosis should be reflected by associations between CCL5 gene variants, RANTES serum concentrations and protein levels in atherosclerotic plaques and risk for coronary events. METHODS AND FINDINGS: We conducted a case-cohort study within the population-based MONICA/KORA Augsburg studies. Baseline RANTES serum levels were measured in 363 individuals with incident coronary events and 1,908 non-cases (mean follow-up: 10.2±4.8 years). Cox proportional hazard models adjusting for age, sex, body mass index, metabolic factors and lifestyle factors revealed no significant association between RANTES and incident coronary events (HR [95% CI] for increasing RANTES tertiles 1.0, 1.03 [0.75-1.42] and 1.11 [0.81-1.54]). None of six CCL5 single nucleotide polymorphisms and no common haplotype showed significant associations with coronary events. Also in the CARDIoGRAM study (>22,000 cases, >60,000 controls), none of these CCL5 SNPs was significantly associated with coronary artery disease. In the prospective Athero-Express biobank study, RANTES plaque levels were measured in 606 atherosclerotic lesions from patients who underwent carotid endarterectomy. RANTES content in atherosclerotic plaques was positively associated with macrophage infiltration and inversely associated with plaque calcification. However, there was no significant association between RANTES content in plaques and risk for coronary events (mean follow-up 2.8±0.8 years). CONCLUSIONS: High RANTES plaque levels were associated with an unstable plaque phenotype. However, the absence of associations between (i) RANTES serum levels, (ii) CCL5 genotypes and (iii) RANTES content in carotid plaques and either coronary artery disease or incident coronary events in our cohorts suggests that RANTES may not be a novel coronary risk biomarker. However, the potential relevance of RANTES levels in platelet-poor plasma needs to be investigated in further studies