Twisted Light Transmission over 143 kilometers

Spatial modes of light can potentially carry a vast amount of information, making them promising candidates for both classical and quantum communication. However, the distribution of such modes over large distances remains difficult. Intermodal coupling complicates their use with common fibers, while free-space transmission is thought to be strongly influenced by atmospheric turbulence. Here we show the transmission of orbital angular momentum modes of light over a distance of 143 kilometers between two Canary Islands, which is 50 times greater than the maximum distance achieved previously. As a demonstration of the transmission quality, we use superpositions of these modes to encode a short message. At the receiver, an artificial neural network is used for distinguishing between the different twisted light superpositions. The algorithm is able to identify different mode superpositions with an accuracy of more than 80% up to the third mode order, and decode the transmitted message with an error rate of 8.33%. Using our data, we estimate that the distribution of orbital angular momentum entanglement over more than 100 kilometers of free space is feasible. Moreover, the quality of our free-space link can be further improved by the use of state-of-the-art adaptive optics systems.Comment: 12 pages, 4 figure

Twisted photon entanglement through turbulent air across Vienna

Photons with a twisted phase front can carry a discrete, in principle unbounded amount of orbital angular momentum (OAM). The large state space allows for complex types of entanglement, interesting both for quantum communication and for fundamental tests of quantum theory. However, the distribution of such entangled states over large distances was thought to be infeasible due to influence of atmospheric turbulence, indicating a serious limitation on their usefulness. Here we show that it is possible to distribute quantum entanglement encoded in OAM over a turbulent intra-city link of 3 kilometers. We confirm quantum entanglement of the first two higher-order levels (with OAM=$\pm 1 \hbar$ and $\pm 2 \hbar$). They correspond to four new quantum channels orthogonal to all that have been used in long-distance quantum experiments so far. Therefore a promising application would be quantum communication with a large alphabet. We also demonstrate that our link allows access to up to 11 quantum channels of OAM. The restrictive factors towards higher numbers are technical limitations that can be circumvented with readily available technologies.Comment: 11 pages, 4 figure

Communication with spatially modulated Light through turbulent Air across Vienna

The transverse spatial modes of light offer a large state-space with interesting physical properties. For exploiting it in future long-distance experiments, spatial modes will have to be transmitted over turbulent free-space links. Numerous recent lab-scale experiments have found significant degradation in the mode quality after transmission through simulated turbulence and consecutive coherent detection. Here we experimentally analyze the transmission of one prominent class of spatial modes, the orbital-angular momentum (OAM) modes, through 3 km of strong turbulence over the city of Vienna. Instead of performing a coherent phase-dependent measurement, we employ an incoherent detection scheme which relies on the unambiguous intensity patterns of the different spatial modes. We use a pattern recognition algorithm (an artificial neural network) to identify the characteristic mode pattern displayed on a screen at the receiver. We were able to distinguish between 16 different OAM mode superpositions with only ~1.7% error, and use them to encode and transmit small grey-scale images. Moreover, we found that the relative phase of the superposition modes is not affected by the atmosphere, establishing the feasibility for performing long-distance quantum experiments with the OAM of photons. Our detection method works for other classes of spatial modes with unambiguous intensity patterns as well, and can further be improved by modern techniques of pattern recognition.Comment: 11 pages, 4 figure

Neurophysiology of epidurally evoked spinal cord reflexes in clinically motor-complete posttraumatic spinal cord injury

Increased use of epidural Spinal Cord Stimulation (eSCS) for the rehabilitation of spinal cord injury (SCI) has highlighted the need for a greater understanding of the properties of reflex circuits in the isolated spinal cord, particularly in response to repetitive stimulation. Here, we investigate the frequency-dependence of modulation of short- and long-latency EMG responses of lower limb muscles in patients with SCI at rest. Single stimuli could evoke short-latency responses as well as long-latency (likely polysynaptic) responses. The short-latency component was enhanced at low frequencies and declined at higher rates. In all muscles, the effects of eSCS were more complex if polysynaptic activity was elicited, making the motor output become an active process expressed either as suppression, tonic or rhythmical activity. The polysynaptic activity threshold is not constant and might vary with different stimulation frequencies, which speaks for its temporal dependency. Polysynaptic components can be observed as direct responses, neuromodulation of monosynaptic responses or driving the muscle activity by themselves, depending on the frequency level. We suggest that the presence of polysynaptic activity could be a potential predictor for appropriate stimulation conditions. This work studies the complex behaviour of spinal circuits deprived of voluntary motor control from the brain and in the absence of any other inputs. This is done by describing the monosynaptic responses, polysynaptic activity, and its interaction through its input–output interaction with sustain stimulation that, unlike single stimuli used to study the reflex pathway, can strongly influence the interneuron circuitry and reveal a broader spectrum of connectivity

Effects of sustained electrical stimulation on spasticity assessed by the pendulum test

To access publisher's full text version of this article, please click on the hyperlink in Additional Links field or click on the hyperlink at the top of the page marked DownloadNeuromodulation using electrical stimulation is able to enhance motor control of individuals suffering an upper motor neuron disorder. This work examined the effect of sustained electrical stimulation to modify spasticity in the leg muscles. We applied transcutaneous spinal cord stimulation with a pulse rate of 50 Hz for 30 min. The subjects were assessed before and after the intervention using in a pendulum test setup. The motion of the free swinging leg was acquired through video tracking and goniometer measurements. The quantification was done through the R2n index which shows consistency identifying the spasticity levels. In all incomplete SCI subjects having severe spasticity, the results show that electrical stimulation is effective to modify the increased muscle tone.Consejo Nacional de Ciencia y Tecnologí

Effects of sustained electrical stimulation on spasticity assessed by the pendulum test

Neuromodulation using electrical stimulation is able to enhance motor control of individuals suffering an upper motor neuron disorder. This work examined the effect of sustained electrical stimulation to modify spasticity in the leg muscles. We applied transcutaneous spinal cord stimulation with a pulse rate of 50 Hz for 30 min. The subjects were assessed before and after the intervention using in a pendulum test setup. The motion of the free swinging leg was acquired through video tracking and goniometer measurements. The quantification was done through the R2n index which shows consistency identifying the spasticity levels. In all incomplete SCI subjects having severe spasticity, the results show that electrical stimulation is effective to modify the increased muscle tone.Research funding: This work was supported by the Mexican Council of Research and Technology (CONACYT), Grant: 264528 (www.conacyt.mx) and; Landspitali – University Hospital science found (www.landspitali.is).Peer Reviewe

Long-term high-level exercise promotes muscle reinnervation with age.

The histologic features of aging muscle suggest that denervation contributes to atrophy, that immobility accelerates the process, and that routine exercise may protect against loss of motor units and muscle tissue. Here, we compared muscle biopsies from sedentary and physically active seniors and found that seniors with a long history of high-level recreational activity up to the time of muscle biopsy had 1) lower loss of muscle strength versus young men (32% loss in physically active vs 51% loss in sedentary seniors); 2) fewer small angulated (denervated) myofibers; 3) a higher percentage of fiber-type groups (reinnervated muscle fibers) that were almost exclusive of the slow type; and 4) sparse normal-size muscle fibers coexpressing fast and slow myosin heavy chains, which is not compatible with exercise-driven muscle-type transformation. The biopsies from the old physically active seniors varied from sparse fiber-type groupings to almost fully transformed muscle, suggesting that coexpressing fibers appear to fill gaps. Altogether, the data show that long-term physical activity promotes reinnervation of muscle fibers and suggest that decades of high-level exercise allow the body to adapt to age-related denervation by saving otherwise lost muscle fibers through selective recruitment to slow motor units. These effects on size and structure of myofibers may delay functional decline in late aging

Monogenic variants in dystonia: an exome-wide sequencing study

Background Dystonia is a clinically and genetically heterogeneous condition that occurs in isolation (isolated dystonia), in combination with other movement disorders (combined dystonia), or in the context of multisymptomatic phenotypes (isolated or combined dystonia with other neurological involvement). However, our understanding of its aetiology is still incomplete. We aimed to elucidate the monogenic causes for the major clinical categories of dystonia. Methods For this exome-wide sequencing study, study participants were identified at 33 movement-disorder and neuropaediatric specialty centres in Austria, Czech Republic, France, Germany, Poland, Slovakia, and Switzerland. Each individual with dystonia was diagnosed in accordance with the dystonia consensus definition. Index cases were eligible for this study if they had no previous genetic diagnosis and no indication of an acquired cause of their illness. The second criterion was not applied to a subset of participants with a working clinical diagnosis of dystonic cerebral palsy. Genomic DNA was extracted from blood of participants and whole-exome sequenced. To find causative variants in known disorder-associated genes, all variants were filtered, and unreported variants were classified according to American College of Medical Genetics and Genomics guidelines. All considered variants were reviewed in expert round-table sessions to validate their clinical significance. Variants that survived filtering and interpretation procedures were defined as diagnostic variants. In the cases that went undiagnosed, candidate dystonia-causing genes were prioritised in a stepwise workflow. Findings We sequenced the exomes of 764 individuals with dystonia and 346 healthy parents who were recruited between June 1, 2015, and July 31, 2019. We identified causative or probable causative variants in 135 (19%) of 728 families, involving 78 distinct monogenic disorders. We observed a larger proportion of individuals with diagnostic variants in those with dystonia (either isolated or combined) with coexisting non-movement disorder-related neurological symptoms (100 [45%] of 222;excepting cases with evidence of perinatal brain injury) than in those with combined (19 [19%] of 98) or isolated (16 [4%] of 388) dystonia. Across all categories of dystonia, 104 (65%) of the 160 detected variants affected genes which are associated with neurodevelopmental disorders. We found diagnostic variants in 11 genes not previously linked to dystonia, and propose a predictive clinical score that could guide the implementation of exome sequencing in routine diagnostics. In cases without perinatal sentinel events, genomic alterations contributed substantively to the diagnosis of dystonic cerebral palsy. In 15 families, we delineated 12 candidate genes. These include IMPDH2, encoding a key purine biosynthetic enzyme, for which robust evidence existed for its involvement in a neurodevelopmental disorder with dystonia. We identified six variants in IMPDH2, collected from four independent cohorts, that were predicted to be deleterious de-novo variants and expected to result in deregulation of purine metabolism. Interpretation In this study, we have determined the role of monogenic variants across the range of dystonic disorders, providing guidance for the introduction of personalised care strategies and fostering follow-up pathophysiological explorations

Testing association of rare genetic variants with resistance to three common antiseizure medications

Abstract Objective Drug resistance is a major concern in the treatment of individuals with epilepsy. No genetic markers for resistance to individual antiseizure medication (ASM) have yet been identified. We aimed to identify the role of rare genetic variants in drug resistance for three common ASMs: levetiracetam (LEV), lamotrigine (LTG), and valproic acid (VPA). Methods A cohort of 1622 individuals of European descent with epilepsy was deeply phenotyped and underwent whole exome sequencing (WES), comprising 575 taking LEV, 826 LTG, and 782 VPA. We performed gene- and gene set–based collapsing analyses comparing responders and nonresponders to the three drugs to determine the burden of different categories of rare genetic variants. Results We observed a marginally significant enrichment of rare missense, truncating, and splice region variants in individuals who were resistant to VPA compared to VPA responders for genes involved in VPA pharmacokinetics. We also found a borderline significant enrichment of truncating and splice region variants in the synaptic vesicle glycoprotein (SV2) gene family in nonresponders compared to responders to LEV. We did not see any significant enrichment using a gene-based approach. Significance In our pharmacogenetic study, we identified a slightly increased burden of damaging variants in gene groups related to drug kinetics or targeting in individuals presenting with drug resistance to VPA or LEV. Such variants could thus determine a genetic contribution to drug resistance