45 research outputs found

    Decoupled Local Aggregation for Point Cloud Learning

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    The unstructured nature of point clouds demands that local aggregation be adaptive to different local structures. Previous methods meet this by explicitly embedding spatial relations into each aggregation process. Although this coupled approach has been shown effective in generating clear semantics, aggregation can be greatly slowed down due to repeated relation learning and redundant computation to mix directional and point features. In this work, we propose to decouple the explicit modelling of spatial relations from local aggregation. We theoretically prove that basic neighbor pooling operations can too function without loss of clarity in feature fusion, so long as essential spatial information has been encoded in point features. As an instantiation of decoupled local aggregation, we present DeLA, a lightweight point network, where in each learning stage relative spatial encodings are first formed, and only pointwise convolutions plus edge max-pooling are used for local aggregation then. Further, a regularization term is employed to reduce potential ambiguity through the prediction of relative coordinates. Conceptually simple though, experimental results on five classic benchmarks demonstrate that DeLA achieves state-of-the-art performance with reduced or comparable latency. Specifically, DeLA achieves over 90\% overall accuracy on ScanObjectNN and 74\% mIoU on S3DIS Area 5. Our code is available at https://github.com/Matrix-ASC/DeLA

    Glutamate Excitotoxicity Inflicts Paranodal Myelin Splitting and Retraction.

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    Paranodal myelin damage is observed in white matter injury. However the culprit for such damage remains unknown. By coherent anti-Stokes Raman scattering imaging of myelin sheath in fresh tissues with sub-micron resolution, we observed significant paranodal myelin splitting and retraction following glutamate application both ex vivo and in vivo. Multimodal multiphoton imaging further showed that glutamate application broke axo-glial junctions and exposed juxtaparanodal K+ channels, resulting in axonal conduction deficit that was demonstrated by compound action potential measurements. The use of 4-aminopyridine, a broad-spectrum K+ channel blocker, effectively recovered both the amplitude and width of compound action potentials. Using CARS imaging as a quantitative readout of nodal length to diameter ratio, the same kind of paranodal myelin retraction was observed with applications of Ca2+ ionophore A23187. Moreover, exclusion of Ca2+ from the medium or application of calpain inhibitor abolished paranodal myelin retraction during glutamate exposure. Examinations of glutamate receptor agonists and antagonists further showed that the paranodal myelin damage was mediated by NMDA and kainate receptors. These results suggest that an increased level of glutamate in diseased white matter could impair paranodal myelin through receptor-mediated Ca2+ overloading and subsequent calpain activation

    Eff ect of a comprehensive programme to provide universal access to care for sputum-smear-positive multidrugresistant tuberculosis in China: a before-and-after study

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    Background China has a quarter of all patients with multidrug-resistant tuberculosis (MDRTB) worldwide, but less than 5% are in quality treatment programmes. In a before-and-after study we aimed to assess the eff ect of a comprehensive programme to provide universal access to diagnosis, treatment, and follow-up for MDRTB in four Chinese cities (population 18 million). Methods We designated city-level hospitals in each city to diagnose and treat MDRTB. All patients with smear-positive pulmonary tuberculosis diagnosed in Center for Disease Control (CDC) clinics and hospitals were tested for MDRTB with molecular and conventional drug susceptibility tests. Patients were treated with a 24 month treatment package for MDRTB based on WHO guidelines. Outpatients were referred to the CDC for directly observed therapy. We capped total treatment package cost at US4644.Insurancereimbursementandprojectsubsidieslimitedpatientsexpensesto10(2011)tothosefromaretrospectivesurveyofallpatientswithMDRTBdiagnosedinthesamecitiesduringabaselineperiod(200609).Findings243patientswerediagnosedwithMDRTBorrifampicinresistanttuberculosisduringthe12monthprogrammeperiodcomparedwith92patients(equivalentto24peryear)duringthebaselineperiod.172(71243individualswereenrolledintheprogramme.Timefromspecimencollectionforresistancetestingtotreatmentinitiationdecreasedby90startedonappropriatedrugregimenincreased27times(fromnine[35172),andfollowupbytheCDCafterinitialhospitalisationincreased24times(fromone[4163[99increasedtentimes(fromtwo[8programmeperiodhadnegativeculturesorclinicalradiographicimprovement.PatientsexpensesforhospitaladmissionafterMDRTBdiagnosisdecreasedby784644. Insurance reimbursement and project subsidies limited patients’ expenses to 10% of charges for services within the package. We compared data from a 12 month programme period (2011) to those from a retrospective survey of all patients with MDRTB diagnosed in the same cities during a baseline period (2006–09). Findings 243 patients were diagnosed with MDRTB or rifampicin-resistant tuberculosis during the 12 month programme period compared with 92 patients (equivalent to 24 per year) during the baseline period. 172 (71%) of 243 individuals were enrolled in the programme. Time from specimen collection for resistance testing to treatment initiation decreased by 90% (from median 139 days [IQR 69–207] to 14 days [10–21]), the proportion of patients who started on appropriate drug regimen increased 2·7 times (from nine [35%] of 26 patients treated to 166 [97%] of 172), and follow-up by the CDC after initial hospitalisation increased 24 times (from one [4%] of 23 patients to 163 [99%] of 164 patients). 6 months after starting treatment, the proportion of patients remaining on treatment increased ten times (from two [8%] of 26 patients to 137 [80%] of 172), and 116 (67%) of 172 patients in the programme period had negative cultures or clinical–radiographic improvement. Patients’ expenses for hospital admission after MDRTB diagnosis decreased by 78% (from 796 to $174), reducing the ratio of patients’ expenses to annual household income from 17·6% to 3·5% (p<0·0001 for all comparisons between baseline and programme periods). However, 36 (15%) patients did not start or had to discontinue treatment in the programme period because of fi nancial diffi culties. Interpretation This comprehensive programme substantially increased access to diagnosis, quality treatment, and aff ordable treatment for MDRTB. The programme could help China to achieve universal access to MDRTB care but greater fi nancial risk protection for patients is needed

    A compact integrated device for spatially selective optogenetic neural stimulation based on the Utah Optrode Array

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    Optogenetics is a powerful tool for neural control, but controlled light delivery beyond the superficial structures of the brain remains a challenge. For this, we have developed an optrode array, which can be used for optogenetic stimulation of the deep layers of the cortex. The device consists of a 10×10 array of penetrating optical waveguides, which are predefined using BOROFLOAT® wafer dicing. A wet etch step is then used to achieve the desired final optrode dimensions, followed by heat treatment to smoothen the edges and the surface. The major challenge that we have addressed is delivering light through individual waveguides in a controlled and efficient fashion. Simply coupling the waveguides in the optrode array to a separately-fabricated μLED array leads to low coupling efficiency and significant light scattering in the optrode backplane and crosstalk to adjacent optrodes due to the large mismatch between the μLED and waveguide numerical aperture and the working distance between them. We mitigate stray light by reducing the thickness of the glass backplane and adding a silicon interposer layer with optical vias connecting the μLEDs to the optrodes. The interposer additionally provides mechanical stability required by very thin backplanes, while restricting the unwanted spread of light. Initial testing of light output from the optrodes confirms intensity levels sufficient for optogenetic neural activation. These results pave the way for future work, which will focus on optimization of light coupling and adding recording electrodes to each optrode shank to create a bidirectional optoelectronic interface

    A survey of localization in wireless sensor network

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    Localization is one of the key techniques in wireless sensor network. The location estimation methods can be classified into target/source localization and node self-localization. In target localization, we mainly introduce the energy-based method. Then we investigate the node self-localization methods. Since the widespread adoption of the wireless sensor network, the localization methods are different in various applications. And there are several challenges in some special scenarios. In this paper, we present a comprehensive survey of these challenges: localization in non-line-of-sight, node selection criteria for localization in energy-constrained network, scheduling the sensor node to optimize the tradeoff between localization performance and energy consumption, cooperative node localization, and localization algorithm in heterogeneous network. Finally, we introduce the evaluation criteria for localization in wireless sensor network

    Multisite microLED optrode array for neural interfacing

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    We present an electrically addressable optrode array capable of delivering light to 181 sites in the brain, each providing sufficient light to optogenetically excite thousands of neurons in vivo, developed with the aim to allow behavioral studies in large mammals. The device is a glass microneedle array directly integrated with a custom fabricated microLED device, which delivers light to 100 needle tips and 81 interstitial surface sites, giving two-level optogenetic excitation of neurons in vivo. Light delivery and thermal properties are evaluated, with the device capable of peak irradiances >80  mW  /  mm2 per needle site. The device consists of an array of 181 80  μm  ×  80  μm2 microLEDs, fabricated on a 150-μm-thick GaN-on-sapphire wafer, coupled to a glass needle array on a 150-μm thick backplane. A pinhole layer is patterned on the sapphire side of the microLED array to reduce stray light. Future designs are explored through optical and thermal modeling and benchmarked against the current device

    An optrode array for spatiotemporally precise large-scale optogenetic stimulation of deep cortical layers in non-human primates

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    Optogenetics has transformed studies of neural circuit function, but remains challenging to apply in large brains, such as those of non-human primates (NHPs). A major challenge is delivering intense, spatiotemporally precise, patterned photostimulation across large volumes in deep tissue. Such stimulation is critical, for example, to modulate selectively deep-layer corticocortical feedback projections. To address this unmet need, we have developed the Utah Optrode Array (UOA), a 10×10 glass needle waveguide array fabricated atop a novel opaque optical interposer then bonded to an electrically addressable μLED array. In vivo experiments with the UOA demonstrated large-scale, spatiotemporally precise, activation of deep circuits in monkey cortex. Specifically, the UOA permitted both focal (confined to single layers/columns), and widespread (multiple layers/columns) optogenetic activation of deep layer neurons, simply by varying the number of activated μLEDs and/or the irradiance. Thus, the UOA represents a powerful optoelectronic device for targeted manipulation of deep-layer circuits in NHP models.Competing Interest StatementThe authors have declared no competing interest

    An optrode array for spatiotemporally-precise large-scale optogenetic stimulation of deep cortical layers in non-human primates

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    Optogenetics has transformed studies of neural circuit function, but remains challenging to apply to non-human primates (NHPs). A major challenge is delivering intense, spatiotemporally-precise, patterned photostimulation across large volumes in deep tissue. Such stimulation is critical, for example, to modulate selectively deep-layer corticocortical feedback circuits. To address this need, we have developed the Utah Optrode Array (UOA), a 10×10 glass needle waveguide array fabricated atop a novel opaque optical interposer, and bonded to an electrically addressable µLED array. In vivo experiments with the UOA demonstrated large-scale, spatiotemporally precise, activation of deep circuits in NHP cortex. Specifically, the UOA permitted both focal (confined to single layers/columns), and widespread (multiple layers/columns) optogenetic activation of deep layer neurons, as assessed with multi-channel laminar electrode arrays, simply by varying the number of activated µLEDs and/or the irradiance. Thus, the UOA represents a powerful optoelectronic device for targeted manipulation of deep-layer circuits in NHP models
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