Description, Host-specificity, and Strain Selectivity of the Dinoflagellate Parasite Parvilucifera sinerae sp.nov. (Perkinsozoa)

17 pages, 7 figures, 2 tablesA new species of parasite, Parvilucifera sinerae sp. nov., isolated froma bloomof the toxic Dinoflagellate Alexandrium minutum in the harbor of Arenys de Mar (Mediterranean Sea, Spain), is described. This species is morphologically, behaviourally, and genetically (18S rDNA sequence) different from Parvilucifera infectans, until now the only species of the genus Parvilucifera to be genetically analyzed. Sequence análisis of the 18S ribosomal DNA supported P. Sinerae as a new species placed within the Perkinsozoa and close to P. infectans. Data on the seasonal occurrence of P. sinerae, its infective rates in natural and laboratory cultures, and intra-species strain-specific Resistance are presented. Life-cycle studies in field simples showed that the dinoflagellate resting zygote (restingcyst) was resistant to infection, but the mobile zygote (planozygote) orpelli clestage (temporary cyst) became infected. The effects of Light and salinity level son the growth of P. sinerae were examined, and the results showed that low salinity levels promote both sporangial germination and higher rates of infection. Our findings on this newly described parasite point to a complex host—parasite interaction and provide valuable information that leads to a reconsideration of the biological strategy to control dinoflagellate blooms by jeans of intentional parasitic infectionsThis research was funded by the EU Project SEED (GOCE-CT-2005-003875). R.I. Figueroa work is supported by a I3P contract and E. Garcés’ work is supported by a Ramon y Cajal grant, both from the Spanish Ministry of Education and SciencePeer reviewe

Handel und Wirtschaft der Stadt Trogir nach der Mitte des 16. Jahrhunderts

ABBILDUNGEN: nur in PRINTAUSGABE! -- Die Magisterarbeit „Handel und Wirtschaft der Stadt Trogir nach der Mitte des 16. Jahrhunderts“ untersucht Handels-, Wirtschafts- und Sozialstruktur einer Kleinstadt im venezianischen Dalmatien kurz vor dem Beginn des Zypernkrieges (1570-1573) anhand von Exportlizenzen und Schlussrelationen der venezianischen Rektoren. Die politische wie naturräumliche Grenzlage der Kommune Trogir machte die Stadt zu einem Handelsplatz. Die Grenzlage konnte aber auch zur Bedrohung werden, im 16. Jahrhundert kam diese aus dem osmanischen Hinterland und führte primär zu einer Entvölkerung des Stadtbezirks. Die Stadt wurde durch die Bedrohung auch zu einem Sicherungsposten für die wichtige Seeroute von Venedig in die Levante. Dennoch unterhielten Trogirer Händler und Kapitäne Beziehungen mit zahlreichen anderen Städten an der Adria, insbesondere mit Venedig und mit Städten an der westlichen Adriaküste. Exportiert wurden vornehmlich Feigen, Pferde, Fisch, Käse und andere Agrarprodukte, welche im Stadtbezirk produziert worden waren. Die Bedeutung Trogirs als Zwischenhandelsplatz war gering. Die Handelsintensität war zur Erntezeit im Oktober am höchsten, im April am niedrigsten. Eine winterliche Handelspause existierte nicht. Die Waren wurden mit kleineren Schiffen transportiert, welche auch für andere Aufgaben einsetzbar waren. Eine Seereise von Trogir nach Venedig dauerte im günstigsten Fall zwei Wochen. Die Handelsbeziehungen und festen Handelspartnerschaften führten auch zu einer kulturellen Einbettung der Stadt in den adriatischen Raum und insbesondere in den venezianischen Staat. So war Venedig für die Stadtbewohner nicht nur Hauptabsatzmarkt und politische Dominante, sondern auch kulturelles, soziales und architektonisches Vorbild. Durch die Schutzfunktion, welche Venedig für die Städte angesichts der osmanischen Bedrohung hatte, wurde die starke Bindung der dalmatinischen Stadtbevölkerung an Venedig noch verstärkt

Fornix deep brain stimulation enhances acetylcholine levels in the hippocampus

Deep brain stimulation (DBS) of the fornix has gained interest as a potential therapy for advanced treatment-resistant dementia, yet the mechanism of action remains widely unknown. Previously, we have reported beneficial memory effects of fornix DBS in a scopolamine induced rat model of dementia, which is dependent on various brain structures including hippocampus. To elucidate mechanisms of action of fornix DBS with regard to memory restoration, we performed c-Fos immunohistochemistry in the hippocampus. We found that fornix DBS induced a selective activation of cells in the CA1 and CA3 subfields of the dorsal hippocampus. In addition, hippocampal neurotransmitter levels were measured using microdialysis before, during and after 60 min of fornix DBS in a next experiment. We observed a substantial increase in the levels of extracellular hippocampal acetylcholine, which peaked 20 min after stimulus onset. Interestingly, hippocampal glutamate levels did not change compared to baseline. Therefore, our findings provide first experimental evidence that fornix DBS activates the hippocampus and induces the release of acetylcholine in this region.Publisher PDFPeer reviewe

Fornix deep brain stimulation enhances acetylcholine levels in the hippocampus

Deep brain stimulation (DBS) of the fornix has gained interest as a potential therapy for advanced treatment-resistant dementia, yet the mechanism of action remains widely unknown. Previously, we have reported beneficial memory effects of fornix DBS in a scopolamine-induced rat model of dementia, which is dependent on various brain structures including hippocampus. To elucidate mechanisms of action of fornix DBS with regard to memory restoration, we performed c-Fos immunohistochemistry in the hippocampus. We found that fornix DBS induced a selective activation of cells in the CA1 and CA3 subfields of the dorsal hippocampus. In addition, hippocampal neurotransmitter levels were measured using microdialysis before, during and after 60 min of fornix DBS in a next experiment. We observed a substantial increase in the levels of extracellular hippocampal acetylcholine, which peaked 20 min after stimulus onset. Interestingly, hippocampal glutamate levels did not change compared to baseline. Therefore, our findings provide first experimental evidence that fornix DBS activates the hippocampus and induces the release of acetylcholine in this region

Biocompatible PVDF nanofibers with embedded magnetite nanodiscs enable wireless magnetoelectric stimulation in premotor cortex

Wireless neuromodulation technologies aim to eliminate the need for invasive hardware and enhance tissue compatibility. Magnetoelectric (ME) materials enable magnetic field-induced electrical stimulation, offering a minimally invasive neural activation. However, conventional ME systems use rigid ceramic components with limited biocompatibility. Here, a flexible, predominantly organic ME platform composed of polyvinylidene fluoride (PVDF) nanofibers embedded with anisotropic magnetite nanodiscs (MNDs) is reported. These MNDs are selected for their unique ability to exert magnetic torque due to vortex magnetization and their intrinsic magnetostrictive behaviour. The resulting ME fibers preserve the piezoelectric β-phase of PVDF and exhibit a magnetoelectric voltage coefficient of 1.26 Vcm Oe . Two magnetic activation strategies are compared, torque-based and high-frequency magnetostriction, finding that magnetostriction more effectively triggers neuronal responses. In vitro calcium imaging reveals robust activation in primary cortical neurons cultured on ME fibers. Biocompatibility post-stimulation is confirmed on ex vivo human brain tissue, with no increased cell death. Implanted into the premotor cortex of freely moving mice, the fibers enabled wireless modulation of motor behaviour under an alternating magnetic field. This work presents the first demonstration of wireless magnetoelectric neuromodulation using soft, biocompatible fiber composites, paving the way for future bioelectronic interfaces free from rigid components and tethered systems

Ventromedial prefrontal cortex stimulation enhances memory and hippocampal neurogenesis in the middle-aged rats

© 2015, eLife Sciences Publications Ltd. All Rights Reserved. Memory dysfunction is a key symptom of age-related dementia. Although recent studies have suggested positive effects of electrical stimulation for memory enhancement, its potential targets remain largely unknown. In this study, we hypothesized that spatially targeted deep brain stimulation of ventromedial prefrontal cortex enhanced memory functions in a middle-aged rat model. Our results show that acute stimulation enhanced the short-, but not the long-term memory in the novel-object recognition task. Interestingly, after chronic high-frequency stimulation, both the short- and long-term memories were robustly improved in the novel-object recognition test and Morris water-maze spatial task compared to sham. Our results also demonstrated that chronic ventromedial prefrontal cortex high-frequency stimulation upregulated neurogenesis-associated genes along with enhanced hippocampal cell proliferation. Importantly, these memory behaviors were strongly correlated with the hippocampal neurogenesis. Overall, these findings suggest that chronic ventromedial prefrontal cortex high-frequency stimulation may serve as a novel effective therapeutic target for dementia-related disorders.published_or_final_versio

Memory prosthesis: is it time for a deep neuromimetic approach?

Memory loss, one of the most dreaded afflictions of the human condition, presents considerable burden on the world’s health care system and it is recognized as a major challenge in the elderly. There are only a few neuro-modulation treatments for memory dysfunctions. Open loop deep brain stimulation is such a treatment for memory improvement, but with limited success and conflicting results. In recent years closed-loop neuropros-thesis systems able to simultaneously record signals during behavioural tasks and generate with the use of inter-nal neural factors the precise timing of stimulation patterns are presented as attractive alternatives and show promise in memory enhancement and restoration. A few such strides have already been made in both animals and humans, but with limited insights into their mechanisms of action. Here, I discuss why a deep neuromimetic computing approach linking multiple levels of description, mimicking the dynamics of brain circuits, interfaced with recording and stimulating electrodes could enhance the performance of current memory prosthesis systems, shed light into the neurobiology of learning and memory and accelerate the progress of memory prosthesis research. I propose what the necessary components (nodes, structure, connectivity, learning rules, and physi-ological responses) of such a deep neuromimetic model should be and what type of data are required to train/ test its performance, so it can be used as a true substitute of damaged brain areas capable of restoring/enhancing their missing memory formation capabilities. Considerations to neural circuit targeting, tissue interfacing, elec-trode placement/implantation and multi-network interactions in complex cognition are also provided