Homotypic targeting and drug delivery in glioblastoma cells through cell membrane-coated boron nitride nanotubes
In: Materials and design, Band 192, S. 108742
ISSN: 1873-4197
3 Ergebnisse
Sortierung:
In: Materials and design, Band 192, S. 108742
ISSN: 1873-4197
In: The international journal of social psychiatry, Band 61, Heft 7, S. 693-699
ISSN: 1741-2854
Introduction/Objective: The aim was to measure the lifetime prevalence of panic disorder (PD) in an Italian community sample, and to estimate the burden attributable to PD in compromising the quality of life (QoL) of people diagnosed with it. Methods: Community survey was conducted on a sample of 4,999 randomly selected adult subjects. Instruments used were semi-structured clinical interview Advanced Neuropsychiatric Tools and Assessment Schedule (ANTAS), administered by clinicians and allowing diagnosis according to Diagnostic and Statistical Manual of Mental Disorder (4th ed.; DSM-IV); Short Form Health Survey (SF-12). Results: The lifetime prevalence of PD was 3.6% (4.4% in females, 2.5% in males; p = .002). People with PD had a lower SF-12 score than the standardized community sample (35.5 ± 6.5 vs. 38.4 ± 5.9; p < .0001) with a mean difference (attributable burden) of 2.9 ± 0.7, that is, lower than PD with agoraphobia (AP; 4.2 ± 2.4). Wilson Disease (WD), Multiple Sclerosis, Major Depressive Disorder and Eating Disorders (ED) show a higher attributable burden in impaired QoL than PD, while the attributable burden of PD with AP is not lower than in ED and WD. Conclusions: The burden attributable to the impairment of QoL following a lifetime diagnosis of PD was found to be not so great compared to the impairment caused by Major Depressive Disorder (MDD) or neurological conditions. The comorbidity of PD with AP worsens QoL significantly.
A complex array of inhibitory interneurons tightly controls hippocampal activity, but how such diversity specifically affects memory processes is not well understood. We find that a small subclass of type 1 cannabinoid receptor (CB1R)-expressing hippocampal interneurons determines episodic-like memory consolidation by linking dopamine D1 receptor (D1R) signaling to GABAergic transmission. Mice lacking CB1Rs in D1-positive cells (D1-CB1-KO) display impairment in long-term, but not short-term, novel object recognition memory (NOR). Re-expression of CB1Rs in hippocampal D1R-positive cells rescues this NOR deficit. Learning induces an enhancement of in vivo hippocampal long-term potentiation (LTP), which is absent in mutant mice. CB1R-mediated NOR and the associated LTP facilitation involve local control of GABAergic inhibition in a D1-dependent manner. This study reveals that hippocampal CB1R-/D1R-expressing interneurons control NOR memory, identifying a mechanism linking the diversity of hippocampal interneurons to specific behavioral outcomes. ; We thank Delphine Gonzales, Nathalie Aubailly, and the personnel of the Animal Facilities of the NeuroCentre Magendie for mouse care. We thank the Biochemistry Platform of Bordeaux NeuroCampus and the members of Marsicano's lab for useful discussions. This work was funded by INSERM; the European Research Council (Endofood ERC-2010-StG-260515, CannaPreg ERC-2014-PoC-640923, and MiCaBra ERC-2017-AdG-786467 to G.M.); Fondation pour la Recherche Medicale (FRM; DRM20101220445 to G.M. and DT20160435664 to J.F.O.d.C.); the Human Frontiers Science Program, Region Aquitaine, Agence Nationale de la Recherche (ANR; NeuroNutriSens ANR-13-BSV4-0006, ORUPS ANR-16-CE37-0010-01, and CaCoVi ANR-18-CE16-0001-02 to G.M.); BRAIN ANR-10-LABX-0043 (to G.M.); NIH/NIDA (1R21DA037678-01); the European Regional Development Fund; the European Union Horizon 2020 Research and Innovation Program (grant agreement 686009); French State/Agence Nationale de la Recherche/IdEx (ANR-10-IDEX-03-02), Eu-Fp7 (FP7-PEOPLE-2013-IEF-623638), and MINECO/AEI (RYC-2017-21776) (to A.B.-G.); FRM (ARF20140129235 to L.B.); and Ikerbasque (The Basque Foundation for Science) and MINECO (Ministerio de Economía y Competitividad) PGC2018-093990-A-I00 (MICIU/AEI/FEDER, UE) (to E.S.-G.).
BASE