Mindfulness meditation (MM) practices constitute an important group of meditative practices that have received growing attention. The aim of the present paper was to systematically review current ...evidence on the neurobiological changes and clinical benefits related to MM practice in psychiatric disorders, in physical illnesses and in healthy subjects.
A literature search was undertaken using Medline, ISI Web of Knowledge, the Cochrane collaboration database and references of retrieved articles. Controlled and cross-sectional studies with controls published in English up to November 2008 were included.
Electroencephalographic (EEG) studies have revealed a significant increase in alpha and theta activity during meditation. Neuroimaging studies showed that MM practice activates the prefrontal cortex (PFC) and the anterior cingulate cortex (ACC) and that long-term meditation practice is associated with an enhancement of cerebral areas related to attention. From a clinical viewpoint, Mindfulness-Based Stress Reduction (MBSR) has shown efficacy for many psychiatric and physical conditions and also for healthy subjects, Mindfulness-Based Cognitive Therapy (MBCT) is mainly efficacious in reducing relapses of depression in patients with three or more episodes, Zen meditation significantly reduces blood pressure and Vipassana meditation shows efficacy in reducing alcohol and substance abuse in prisoners. However, given the low-quality designs of current studies it is difficult to establish whether clinical outcomes are due to specific or non-specific effects of MM.
Despite encouraging findings, several limitations affect current studies. Suggestions are given for future research based on better designed methodology and for future directions of investigation.
Magnetic molecules, modelled as finite-size spin systems, are test-beds for quantum phenomena1 and could constitute key elements in future spintronics devices2–5, long-lasting nanoscale memories6 or ...noise-resilient quantum computing platforms7–10. Inelastic neutron scattering is the technique of choice to probe them, characterizing molecular eigenstates on atomic scales11–14. However, although large magnetic molecules can be controllably synthesized15–18, simulating their dynamics and interpreting spectroscopic measurements is challenging because of the exponential scaling of the required resources on a classical computer. Here, we show that quantum computers19–22 have the potential to efficiently extract dynamical correlations and the associated magnetic neutron cross-section by simulating prototypical spin systems on a quantum hardware22. We identify the main gate errors and show the potential scalability of our approach. The synergy between developments in neutron scattering and quantum processors will help design spin clusters for future applications.Inelastic neutron scattering is used to probe the spin dynamics of molecular nanomagnets, but extensive supporting computations make the technique challenging. Proof-of-principle experiments now show that quantum computers may solve these computations efficiently.
Sexual dysfunction (SD) is an important underestimated adverse effect of antidepressant drugs. Patients, in fact, if not directly questioned, tend to scarcely report them. The aim of the present ...meta-analysis was to quantify SD caused by antidepressants on the basis of studies where sexual functioning was purposely investigated through direct inquiry and specific questionnaires.
A literature search was conducted using MEDLINE, ISI Web of Knowledge, and references of selected articles. Selected studies performed on patients without previous SD were entered in the Cochrane Collaboration Review Manager (RevMan version 4.2). Our primary outcome measure was the rate of total treatment-emergent SD. Our secondary outcome measures were the rates of treatment-emergent desire, arousal, and orgasm dysfunction.
Our analyses indicated a significantly higher rate of total and specific treatment-emergent SD and specific phases of dysfunction compared with placebo for the following drugs in decreasing order of impact: sertraline, venlafaxine, citalopram, paroxetine, fluoxetine, imipramine, phenelzine, duloxetine, escitalopram, and fluvoxamine, with SD ranging from 25.8% to 80.3% of patients. No significant difference with placebo was found for the following antidepressants: agomelatine, amineptine, bupropion, moclobemide, mirtazapine, and nefazodone.
Treatment-emergent SD caused by antidepressants is a considerable issue with a large variation across compounds. Some assumptions, such as the inclusion of open-label studies or differences in scales used to assess SD, could reduce the significance of our findings. However, treatment-emergent SD is a frequent adverse effect that should be considered in clinical activity for the choice of the prescribed drug.
We show that molecular nanomagnets have a potential advantage in the crucial rush toward quantum computers. Indeed, the sizable number of accessible low-energy states of these systems can be ...exploited to define qubits with embedded quantum error correction. We derive the scheme to achieve this crucial objective and the corresponding sequence of microwave/radiofrequency pulses needed for the error correction procedure. The effectiveness of our approach is shown already with a minimal S = 3/2 unit corresponding to an existing molecule, and the scaling to larger spin systems is quantitatively analyzed.
Neuroinflammation commences decades before Alzheimer's disease (AD) clinical onset and represents one of the earliest pathomechanistic alterations throughout the AD continuum. Large-scale genome-wide ...association studies point out several genetic variants-
, and
-potentially linked to neuroinflammation. Most of these genes are involved in proinflammatory intracellular signaling, cytokines/interleukins/cell turnover, synaptic activity, lipid metabolism, and vesicle trafficking. Proteomic studies indicate that a plethora of interconnected aberrant molecular pathways, set off and perpetuated by TNF-α, TGF-β, IL-1β, and the receptor protein TREM2, are involved in neuroinflammation. Microglia and astrocytes are key cellular drivers and regulators of neuroinflammation. Under physiological conditions, they are important for neurotransmission and synaptic homeostasis. In AD, there is a turning point throughout its pathophysiological evolution where glial cells sustain an overexpressed inflammatory response that synergizes with amyloid-β and tau accumulation, and drives synaptotoxicity and neurodegeneration in a self-reinforcing manner. Despite a strong therapeutic rationale, previous clinical trials investigating compounds with anti-inflammatory properties, including non-steroidal anti-inflammatory drugs (NSAIDs), did not achieve primary efficacy endpoints. It is conceivable that study design issues, including the lack of diagnostic accuracy and biomarkers for target population identification and proof of mechanism, may partially explain the negative outcomes. However, a recent meta-analysis indicates a potential biological effect of NSAIDs. In this regard, candidate fluid biomarkers of neuroinflammation are under analytical/clinical validation, i.e., TREM2, IL-1β, MCP-1, IL-6, TNF-α receptor complexes, TGF-β, and YKL-40. PET radio-ligands are investigated to accomplish
and longitudinal regional exploration of neuroinflammation. Biomarkers tracking different molecular pathways (body fluid matrixes) along with brain neuroinflammatory endophenotypes (neuroimaging markers), can untangle temporal-spatial dynamics between neuroinflammation and other AD pathophysiological mechanisms. Robust biomarker-drug codevelopment pipelines are expected to enrich large-scale clinical trials testing new-generation compounds active, directly or indirectly, on neuroinflammatory targets and displaying putative disease-modifying effects: novel NSAIDs, AL002 (anti-TREM2 antibody), anti-Aβ protofibrils (BAN2401), and AL003 (anti-CD33 antibody). As a next step, taking advantage of breakthrough and multimodal techniques coupled with a systems biology approach is the path to pursue for developing individualized therapeutic strategies targeting neuroinflammation under the framework of precision medicine.
We pinpoint the key ingredients ruling decoherence in multispin clusters, and we engineer the system Hamiltonian to design optimal molecules embedding quantum error correction. These are ...antiferromagnetically coupled systems with competing exchange interactions, characterized by many low-energy states in which decoherence is dramatically suppressed and does not increase with the system size. This feature allows us to derive optimized code words, enhancing the power of the quantum error correction code by orders of magnitude. We demonstrate this by a complete simulation of the system dynamics, including the effect of decoherence driven by a nuclear spin bath and the full sequence of pulses to implement error correction and logical gates between protected states.
Understanding chiral-induced spin selectivity (CISS), resulting from charge transport through helical systems, has recently inspired many experimental and theoretical efforts but is still the object ...of intense debate. In order to assess the nature of CISS, we propose to focus on electron-transfer processes occurring at the single-molecule level. We design simple magnetic resonance experiments, exploiting a qubit as a highly sensitive and coherent magnetic sensor, to provide clear signatures of the acceptor polarization. Moreover, we show that information could even be obtained from time-resolved electron paramagnetic resonance experiments on a randomly oriented solution of molecules. The proposed experiments will unveil the role of chiral linkers in electron transfer and could also be exploited for quantum computing applications.
Since the introduction of psychiatric medications with relatively good safety profiles, such as selective serotonin reuptake inhibitors (SSRIs) and serotonin norepinephrine reuptake inhibitors, ...increasing attention has been given to side effects such as sexual dysfunction (SD), which, although unrelated to risks of mortality, could undermine compliance with treatment regimens and impair quality of life. Indeed, there is consistent evidence to suggest that a large number of psychiatric medications adversely affect one or more of the three phases of normal sexual response: desire, arousal, and orgasm. 1,2
Clinical Pharmacology & Therapeutics (2011) 89 1, 142–147. doi: 10.1038/clpt.2010.70
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