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Purpose: Simulating the interaction of the human body with electromagnetic fields is an active field of research. Individualized models are increasingly being used, as anatomical differences affect the simulation results. We introduce a processing pipeline for creating individual surface-based models of the human head and torso for application in simulation software based on unstructured grids. The pipeline is designed for easy applicability and is publicly released on figshare. Methods: The pipeline covers image acquisition, segmentation, generation of segmentation masks, and surface mesh generation of the single, external boundary of each structure of interest. Two gradient-echo sequences are used for image acquisition. Structures of the head and body are segmented using several atlas-based approaches. They consist of bone/skull, subarachnoid cerebrospinal fluid, gray matter, white matter, spinal cord, lungs, the sinuses of the skull, and a combined class of all other structures including skin. After minor manual preparation, segmentation images are processed to segmentation masks, which are binarized images per segmented structure free of misclassified voxels and without an internal boundary. The proposed workflow is applied to 2 healthy subjects. Results: Individual differences of the subjects are well represented. The models are proven to be suitable for simulation of the RF electromagnetic field distribution. Conclusion: Image segmentation, creation of segmentation masks, and surface mesh generation are highly automated. Manual interventions remain for preparing the segmentation images prior to segmentation mask generation. The generated surfaces exhibit a single boundary per structure and are suitable inputs for simulation software.

Humans have a unique capacity to induce intense emotional states in others by simple acts of verbal communication, and simple messages such as bad can elicit strong emotions in the addressee. However, up to now, research has mainly focused on general emotional meaning aspects and paradigms of low personal relevance (e.g., word reading), thereby possibly underestimating the impact of verbal emotion. In the present study, we recorded ERPs while presenting emotional words differing in word-inherent person descriptiveness (in that they may or may not refer to or describe a person; e.g., winner vs. sunflower). We predicted stronger emotional responses to person-descriptive words. Additionally, we enhanced the relevance of the words by embedding them in social-communicative contexts. We observed strong parallels in the characteristics of emotion and descriptiveness effects, suggesting a common underlying motivational basis. Furthermore, word-inherent person descriptiveness affected emotion processing at late elaborate stages reflected in the late positive potential, with emotion effects found only for descriptive words. The present findings underline the importance of factors determining the personal relevance of emotional words.

The intranasal (IN) route enables the delivery of insulin to the central nervous system in the relative absence of systemic uptake and related peripheral side effects. Intranasally administered insulin is assumed to travel along olfactory and adjacent pathways and has been shown to rapidly accumulate in cerebrospinal fluid, indicating efficient transport to the brain. Two decades of studies in healthy humans and patients have demonstrated that IN insulin exerts functional effects on metabolism, such as reductions in food intake and body weight and improvements of glucose homeostasis, as well as cognition, ie, enhancements of memory performance both in healthy individuals and patients with mild cognitive impairment or Alzheimer's disease; these studies moreover indicate a favourable safety profile of the acute and repeated use of IN insulin. Emerging findings suggest that IN insulin also modulates neuroendocrine activity, sleep-related mechanisms, sensory perception and mood. Some, but not all studies point to sex differences in the response to IN insulin that need to be further investigated along with the impact of age. "Brain insulin resistance" is an evolving concept that posits impairments in central nervous insulin signalling as a pathophysiological factor in metabolic and cognitive disorders such as obesity, type 2 diabetes and Alzheimer's disease, and, notably, a target of interventions that rely on IN insulin. Still, the negative outcomes of longer-term IN insulin trials in individuals with obesity or Alzheimer's disease highlight the need for conceptual as well as methodological advances to translate the promising results of proof-of-concept experiments and pilot clinical trials into the successful clinical application of IN insulin.

Background and Purpose — Thrombolytic treatment of stroke carries the risk of hemorrhagic transformation. Therefore, the potential of MRI for prediction of recombinant tissue plasminogen activator (rtPA)–induced bleeding is explored to identify patients in whom rtPA treatment may provoke such complications. Methods — Spontaneously hypertensive rats (SHR) (n=9) were submitted to middle cerebral artery (MCA) clot embolism, followed 3 hours later by intra-arterial infusion of 10 mg/kg rtPA. Untreated SHR (n=9) were infused with saline. MRI imaging was performed before treatment and included apparent diffusion coefficient (ADC), T2, and perfusion mapping and contrast enhancement with gadolinium-DTPA. The distribution of intracerebral hemorrhages was studied 3 days later by histological staining. Results — Clot embolism led to the rapid decline of ADC in the territory of the occluded artery. Tissue lesion volume derived from ADC imaging increased by 155±69% in the untreated animals and by 168±87% in the treated animals ( P =NS), determined on the histological sections after 3 days. This same lesion growth in both groups indicated absence of therapeutic effect after 3-hour treatment delay. Hemorrhagic transformations were significantly more frequent in treated SHR ( P <0.05). In untreated rats, hemorrhages were found in the border zone of the ischemic territory; in treated animals, hemorrhagic transformations occurred in the ischemic core region. rtPA-induced hemorrhages were predicted by a disturbance of the blood-brain barrier in 3 of 4 animals before treatment by Gd-DTPA contrast enhancement but not by ADC, T2, or perfusion imaging. The region of contrast enhancement colocalized with subsequent bleeding in these animals. Conclusions — The disturbance of blood-brain barrier but not of other MR parameters allows risk assessment for hemorrhagic transformation induced by subsequent thrombolytic treatment.

The afferent and efferent connections of the prelunate visual association area V4 of macaque monkeys were investigated by means of the horseradish peroxidase (HRP) method. The specific thalamic afferents from the dorsolateral segment of the medial pulvinar and the lateral segment of the inferior pulvinar were topographically organized. A band of cells was labelled in the intralaminar nuclei (nucl. centr. med. and lat., reaching into LD and the most dorsal part of VL), and a few cells in the interlaminar layers of the lateral geniculate body. Other diencephalic afferents included the claustrum, the nucleus basalis Meynert and the pars compacta of the substantia nigra. Ipsilateral cortical areas which projected into V4 included area 18 (V2), the inferior parietal cortex, the anterior and posterior parts of the superior temporal sulcus, the frontal eye fields and the temporo-basal association cortex on the lateral half of the parahippocampal gyrus and around the occipito-temporal sulcus. In the contralateral cortex, discontinuous regions in areas V4 and V5 on the prelunate gyrus and some cells at the 17/18-border were labelled. All regions in which labelled cells were found and, in addition a restricted region in the dorsal cap of the head and the tail of the caudate nucleus showed fibre and terminal labelling. In addition mesencephalic afferents and efferents were identified but not investigated in detail. An attempt to estimate the quantitative contribution of the various afferent systems to the prelunate cortex was made by counting the labelled cells in the different areas. The afferent and efferent organization of the prelunate visual association area indicates that it is incorporated in a network of cortical and subcortical regions involved in various aspects of visual behavior.

Neurotrophins play an important role in modulating activity-dependent neuronal plasticity. In particular, threshold levels of brain-derived neurotrophic factor (BDNF) are required to induce long-term potentiation (LTP) in acute hippocampal slices. Conversely, the administration of exogenous BDNF prevents the induction of long-term depression (LTD) in the visual cortex. A long-standing missing link in the analysis of this modulatory role of BDNF was the determination of the time-course of endogenous BDNF secretion in the same organotypic preparation in which LTP and LTD are elicited. Here, we fulfilled this requirement in slices of perirhinal cortex. Classical theta-burst stimulation patterns evoking LTP lasting >180 min elicited a large increase in BDNF secretion that persisted 5-12 min beyond the stimulation period. Weaker theta-burst stimulation patterns leading only to the initial phase of LTP (≈35 min) were accompanied by a smaller increase in BDNF secretion lasting <1 min. Sequestration of BDNF by TrkB-IgG receptor bodies prevented LTP. Low-frequency stimulations leading to LTD were accompanied by reductions in BDNF secretion that never lasted beyond the duration of the stimulation.

The activities of the 5'I-deiodinase (5'D-I), 5'II deiodinase (5'D-II) and 5III-deiodinase (5D-III) isoenzymes and tissue concentrations of thyroxine (T4) and triiodothyronine (T3) were measured in up to 10 regions of the rat brain after acute and subchronic nonpharmacological (sleep deprivation, 12 h fasting, 14 days' calorie-reduced diet) and pharmacological (ethanol, haloperidol, clozapine, lithium, carbamazepine, desipramine, fluoxetine, tranylcypromine, and mianserin) treatments. All of these treatments induced significant and sometimes dramatic changes in 5'D-II activities and tissue concentrations of thyroid hormones and, to a lesser extent, in 5D-III activity. The activity of 5'D-I remained unaffected. The results revealed a surprising specificity for each type of treatment in terms of the isoenzyme and hormone affected, the direction of the change, the brain region affected and the time of day. The changes in thyroid hormone concentrations frequently failed to correspond in any way to those in deiodinase activities and unexpected effects such as inhibition of both 5'D-II and 5D-III were seen, indicating that there may be additional pathways of iodothyronine metabolism in the CNS. In conclusion, particularly 5'D-II activity and thyroid hormone concentrations in the CNS are highly sensitive to many different kinds of influence that may induce changes in neuronal activity. However, these changes in deiodinase activities do not ensure stable tissue concentrations of T3, but were, on the contrary, in most cases accompanied by marked changes T3 levels in the tissue. The implications of these findings for the physiological role of thyroid hormones in the CNS are discussed.