“Thinking about Not-Thinking”: Neural Correlates of Conceptual Processing during Zen Meditation

Recent neuroimaging studies have identified a set of brain regions that are metabolically active during wakeful rest and consistently deactivate in a variety the performance of demanding tasks. This “default network” has been functionally linked to the stream of thoughts occurring automatically in the absence of goal-directed activity and which constitutes an aspect of mental behavior specifically addressed by many meditative practices. Zen meditation, in particular, is traditionally associated with a mental state of full awareness but reduced conceptual content, to be attained via a disciplined regulation of attention and bodily posture. Using fMRI and a simplified meditative condition interspersed with a lexical decision task, we investigated the neural correlates of conceptual processing during meditation in regular Zen practitioners and matched control subjects. While behavioral performance did not differ between groups, Zen practitioners displayed a reduced duration of the neural response linked to conceptual processing in regions of the default network, suggesting that meditative training may foster the ability to control the automatic cascade of semantic associations triggered by a stimulus and, by extension, to voluntarily regulate the flow of spontaneous mentation

Abnormal Brain Activation in Neurofibromatosis Type 1: A Link between Visual Processing and the Default Mode Network

Neurofibromatosis type 1 (NF1) is one of the most common single gene disorders affecting the human nervous system with a high incidence of cognitive deficits, particularly visuospatial. Nevertheless, neurophysiological alterations in low-level visual processing that could be relevant to explain the cognitive phenotype are poorly understood. Here we used functional magnetic resonance imaging (fMRI) to study early cortical visual pathways in children and adults with NF1. We employed two distinct stimulus types differing in contrast and spatial and temporal frequencies to evoke relatively different activation of the magnocellular (M) and parvocellular (P) pathways. Hemodynamic responses were investigated in retinotopically-defined regions V1, V2 and V3 and then over the acquired cortical volume. Relative to matched control subjects, patients with NF1 showed deficient activation of the low-level visual cortex to both stimulus types. Importantly, this finding was observed for children and adults with NF1, indicating that low-level visual processing deficits do not ameliorate with age. Moreover, only during M-biased stimulation patients with NF1 failed to deactivate or even activated anterior and posterior midline regions of the default mode network. The observation that the magnocellular visual pathway is impaired in NF1 in early visual processing and is specifically associated with a deficient deactivation of the default mode network may provide a neural explanation for high-order cognitive deficits present in NF1, particularly visuospatial and attentional. A link between magnocellular and default mode network processing may generalize to neuropsychiatric disorders where such deficits have been separately identified

Joining S100 proteins and migration:for better or for worse, in sickness and in health

The vast diversity of S100 proteins has demonstrated a multitude of biological correlations with cell growth, cell differentiation and cell survival in numerous physiological and pathological conditions in all cells of the body. This review summarises some of the reported regulatory functions of S100 proteins (namely S100A1, S100A2, S100A4, S100A6, S100A7, S100A8/S100A9, S100A10, S100A11, S100A12, S100B and S100P) on cellular migration and invasion, established in both culture and animal model systems and the possible mechanisms that have been proposed to be responsible. These mechanisms involve intracellular events and components of the cytoskeletal organisation (actin/myosin filaments, intermediate filaments and microtubules) as well as extracellular signalling at different cell surface receptors (RAGE and integrins). Finally, we shall attempt to demonstrate how aberrant expression of the S100 proteins may lead to pathological events and human disorders and furthermore provide a rationale to possibly explain why the expression of some of the S100 proteins (mainly S100A4 and S100P) has led to conflicting results on motility, depending on the cells used. © 2013 Springer Basel

Refractures in cemented vertebrae after percutaneous vertebroplasty: a retrospective analysis

Percutaneous vertebroplasty is an efficient procedure to treat pain due to osteoporotic vertebral compression fractures. However, refracture of cemented vertebrae occurs occasionally after vertebroplasty. It is unclear whether such fractures are procedure-related or part of the natural course of osteoporosis. The effect of potentially important covariates on refracture risk in cemented vertebrae has not been evaluated previously. We retrospectively analyzed the incidence and possible causative mechanism of refracture in patients who had received only one vertebroplasty for a single level of vertebral compression fracture. We assessed the following covariates: age, sex, body weight, height, lumbar spine bone mineral density, treated vertebral level, pre-existing untreated vertebral compression fracture, and gas-containing vertebrae before treatment. Surgical variables, including surgical approach, cement injected, and anterior vertebral height restoration, were also analyzed. Anti-osteoporotic treatment after surgery was recorded. Multiple logistic regression analysis was used to determine the relative risk of refractures of cemented vertebrae. Over all, 98 patients were evaluated with a mean follow-up of 26.9 ± 12.4 months (range, 7–55 months). We identified 62 refractures and the mean loss of anterior vertebral height was 13.3% (range 3.2–40.3%). The greater the anterior vertebral height obtained from vertebroplasty, the greater the risk of refracture occurring (P < 0.01). Gas-containing vertebrae were also prone to refracture after the procedure (P = 0.01). Anti-osteoporotic treatment was of borderline significance between refractured and non-refractured vertebrae (P = 0.07). Only restoration of anterior vertebral height was positively associated with refracture during the follow-ups (P < 0.01). In conclusion, refractures of cemented vertebrae after vertebroplasty occurred in 63% of osteoporotic patients. Significant anterior vertebral height restoration increases the risk of subsequent fracture in cemented vertebrae