Connecting magnetic towers with Faraday rotation gradients in active galactic nuclei jets

The idea that systematic Faraday Rotation gradients across the parsec-scale jets of active galactic nuclei (AGNs) can reveal the presence of helical magnetic (B) fields has been around since the early 1990s, although the first observation of this phenomenon was about ten years later. These gradients are taken to be due to the systematic variation of the line-of-sight B field across the jet. We present here, the parsec-scale Faraday Rotation distributions for the BL Lac objects 0716+714 and 1749+701, based on polarization data obtained with the Very Long Baseline Array at two wavelengths near each of the 2 cm, 4 cm and 6 cm bands (0716+714) and at four wavelengths in the range 18-22 cm (1749+701). The Rotation Measure (RM) maps for both these sources indicate systematic gradients across their jets, as expected if these jets have helical B fields. The significance of these transverse RM gradients is >3 sigma in all cases. We present the results of Monte Carlo simulations directly demonstrating the possibility of observing such transverse RM gradients even if the intrinsic jet structure is much narrower than the observing beam. We observe an intriguing new feature in these sources, a reversal in the direction of the gradient in the jet as compared to the gradient in the core region. This provides new evidence to support models in which field lines emerging from the central region of the accretion disc and closing in the outer region of the accretion disc are both 'wound up' by the differential rotation of the disc. The net observed RM gradient will essentially be the sum effect of two regions of helical field, one nested inside the other. The direction of the net RM gradient will be determined by whether the inner or outer helix dominates the RM integrated through the jet, and RM gradient reversals will be observed if the inner and outer helical fields dominate in different regions of the jet. This potentially provides new insights about the overall configuration of the jet B fields

Strategic communication and the entrepreneurial role of the corporate communication officer

Considering the recent evolution of the communication/PR profession in large organizations both private and public, many scholars agree that a process of institutionalization is occurring. In other words, communication’s importance has been growing, reaching in recent years a strategic position as a lever for companies’ governance. A first objective of this chapter is to describe, looking at management and communication/PR literature, how and to what extent communication has become strategic. The main hypothesis is that communication has become strategic within companies’ governance in order to help each organization to develop consistently – mainly in terms of values – within its environment. A second objective is to describe, looking at the entrepreneurial organization theory and communication/PR literature, another side of the strategic evolution of communication, which is to help each organization to develop – mainly in terms of services, products and reputation – as a different, or preferably unique, entity as compared to the other organizations. The evolution of the strategic contribution of communication/PR within organizations’ decision-making has a strong impact on the role that corporate communication officers (CCOs) play in organizations both on the isomorphic and on the entrepreneurial–innovative sides of the communicational activity they carry out to support the evolution of their organizations

Aberrant Otx2 Expression Enhances Migration and Induces Ectopic Proliferation of Hindbrain Neuronal Progenitor Cells

Dysregulation of Otx2 is a hallmark of the pediatric brain tumor medulloblastoma, yet its functional significance in the establishment of these tumors is unknown. Here we have sought to determine the functional consequences of Otx2 overexpression in the mouse hindbrain to characterize its potential role in medulloblastoma tumorigenesis and identify the cell types responsive to this lineage-specific oncogene. Expression of Otx2 broadly in the mouse hindbrain resulted in the accumulation of proliferative clusters of cells in the cerebellar white matter and dorsal brainstem of postnatal mice. We found that brainstem ectopia were derived from neuronal progenitors of the rhombic lip and that cerebellar ectopia were derived from granule neuron precursors (GNPs) that had migrated inwards from the external granule layer (EGL). These hyperplasias exhibited various characteristics of medulloblastoma precursor cells identified in animal models of Shh or Wnt group tumors, including aberrant localization and altered spatiotemporal control of proliferation. However, ectopia induced by Otx2 differentiated and dispersed as the animals reached adulthood, indicating that factors restricting proliferative lifespan were a limiting factor to full transformation of these cells. These studies implicate a role for Otx2 in altering the dynamics of neuronal progenitor cell proliferation

Radiation induced CNS toxicity – molecular and cellular mechanisms

Radiotherapy of tumours proximal to normal CNS structures is limited by the sensitivity of the normal tissue. Prior to the development of prophylactic strategies or treatment protocols a detailed understanding of the mechanisms of radiation induced CNS toxicity is mandatory. Histological analysis of irradiated CNS specimens defines possible target structures prior to a delineation of cellular and molecular mechanisms. Several lesions can be distinguished: Demyelination, proliferative and degenerative glial reactions, endothelial cell loss and capillary occlusion. All changes are likely to result from complex alterations within several functional CNS compartments. Thus, a single mechanism responsible cannot be separated. At least four factors contribute to the development of CNS toxicity: (1) damage to vessel structures; (2) deletion of oligodendrocyte-2 astrocyte progenitors (O-2A) and mature oligodendrocytes; (3) deletion of neural stem cell populations in the hippocampus, cerebellum and cortex; (4) generalized alterations of cytokine expression. Several underlying cellular and molecular mechanisms involved in radiation induced CNS toxicity have been identified. The article reviews the currently available data on the cellular and molecular basis of radiation induced CNS side effects.   http://www.bjcancer.com © 2001 Cancer Research Campaig

Normalization of impaired emotion inhibition in bipolar disorder mediated by cholinergic neurotransmission in the cingulate cortex

The muscarinic-cholinergic system is involved in the pathophysiology of bipolar disorder (BD), and contributes to attention and the top-down and bottom-up cognitive and affective mechanisms of emotional processing, functionally altered in BD. Emotion processing can be assessed by the ability to inhibit a response when the content of the image is emotional. Impaired regulatory capacity of cholinergic neurotransmission conferred by reduced M2-autoreceptor availability is hypothesized to play a role in elevated salience of negative emotional distractors in euthymic BD relative to individuals with no history of mood instability. Thirty-three euthymic BD type-I (DSM-V-TR) and 50 psychiatrically-healthy controls underwent functional magnetic resonance imaging (fMRI) and an emotion-inhibition paradigm before and after intravenous cholinergic challenge using the acetylcholinesterase inhibitor, physostigmine (1 mg), or placebo. Mood, accuracy, and reaction time on either recognizing or inhibiting a response associated with an image involving emotion and regional functional activation were examined for effects of cholinergic challenge physostigmine relative to placebo, prioritizing any interaction with the diagnostic group. Analyses revealed that (1) at baseline, impaired behavioral performance was associated with lower activation in the anterior cingulate cortex in BD relative to controls during emotion processing; (2) physostigmine (vs. placebo) affected behavioral performance during the inhibition of negative emotions, without altering mood, and increased activation in the posterior cingulate cortex in BD (vs. controls); (3) In BD, lower accuracy observed during emotion inhibition of negative emotions was remediated by physostigmine and was associated with cingulate cortex overactivation. Our findings implicate abnormal regulation of cholinergic neurotransmission in the cingulate cortices in BD, which may mediate exaggerated emotional salience processing, a core feature of BD

Development of a psychiatric disorder linked to cerebellar lesions

Cerebellar dysfunction plays a critical role in neurodevelopmental disorders with long-term behavioral and neuropsychiatric symptoms. A 43-year-old woman with a cerebellum arteriovenous malformation and history of behavioral dysregulation since childhood is described. After the rupture of the cerebellar malformation in adulthood, her behavior morphed into specific psychiatric symptoms and cognitive deficits occurred. The neuropsychological assessment evidenced impaired performance in attention, visuospatial, memory, and language domains. Moreover, psychiatric assessment indicated a borderline personality disorder. Brain MRI examination detected macroscopic abnormalities in the cerebellar posterior lobules VI, VIIa (Crus I), and IX, and in the posterior area of the vermis, regions usually involved in cognitive and emotional processing. The described patient suffered from cognitive and behavioral symptoms that are part of the cerebellar cognitive affective syndrome. This case supports the hypothesis of a cerebellar role in personality disorders emphasizing the importance of also examining the cerebellum in the presence of behavioral disturbances in children and adults