Coupling paper-based microfluidics and lab on a chip technologies for confirmatory analysis of trinitro aromatic explosives.

A new microfluidic paper-based analytical device (µPAD) in conjunction with confirmation by a lab on chip analysis was developed for detection of three trinitro aromatic explosives. Potassium hydroxide was deposited on the µPADs (0.5 µL, 1.5 M), creating a color change reaction when explosives are present, with detection limits of approximately 7.5 ± 1.0 ng for TNB, 12.5 ± 2.0 ng for TNT and 15.0 ± 2.0 ng for tetryl. For confirmatory analysis, positive µPADs were sampled using a 5 mm hole-punch, followed by extraction of explosives from the punched chad in 30 s using 20 µL borate/SDS buffer. The extractions had efficiencies of 96.5 ± 1.7%. The extracted explosives were then analyzed with the Agilent 2100 Bioanalyzer lab on a chip device with minimum detectable amounts of 3.8 ± 0.1 ng for TNB, 7.0 ± 0.9 ng for TNT, and 4.7 ± 0.2 ng for tetryl. A simulated in-field scenario demonstrated the feasibility of coupling the µPAD technique with the lab on a chip device to detect and identify 1 µg of explosives distributed on a surface of 100 cm(2).

Cortical short-term fatigue effects assessed via rhythmic brain-muscle coherence.

This study is aimed at assessing the short-term effects of muscular fatigue on the sensorimotor areas organization in the left and right hemispheres. Magnetoencephalographic (MEG) and electromyographic (EMG) activities were simultaneously recorded during the execution of a non-fatiguing motor task, performed before and after a task known to induce muscle fatigue (Fatigue). Coherence between cerebral and muscular rhythms as well as cerebral and muscular rhythms spectral densities were estimated during this non-fatiguing task and at rest. The MEG-EMG coherence in the beta band (13-32 Hz) was higher after than before Fatigue. The background activity reduction during contraction with respect to rest (i.e. the cerebral reactivity) was less evident after than before Fatigue in the gamma (33-45 Hz) and beta bands. When differentiating subjects on the base of Fatigue endurance times, while a huge inter-subject variability was found, an evident intra-subject similarity was observed for left and right arms, suggesting that resistance to fatigue is more an individual ability than a motor skill differentiated for the dominant and non-dominant side. In conclusion, signs of a more selective neural recruitment, more coupled with muscular activity, appeared as short-term effects of muscular fatigue in primary sensorimotor cortical areas. Evidence suggested that the reduction of cortical recruitment and the increased cortico-muscular coupling are distinct mechanisms.

Shaping the excitability of human motor cortex with premotor rTMS.

Recent studies have shown that low-frequency repetitive transcranial magnetic stimulation (rTMS) to the left dorsal premotor cortex has a lasting influence on the excitability of specific neuronal subpopulations in the ipsilateral primary motor hand area (M1(HAND)). Here we asked how these premotor to motor interactions are shaped by the intensity and frequency of rTMS and the orientation of the stimulating coil. We confirmed that premotor rTMS at 1 Hz and an intensity of 90% active motor threshold (AMT) produced a lasting decrease in corticospinal excitability probed with single-pulse TMS over the left M1(HAND). Reducing the intensity to 80% AMT increased paired-pulse excitability at an interstimulus interval (ISI) of 7 ms. Opposite effects occurred if rTMS was given at 5 Hz: at 90% AMT, corticospinal excitability increased; at 80% AMT, paired-pulse excitability at ISI = 7 ms decreased. No effects were seen if rTMS was applied at the same intensities to prefrontal or primary motor cortices. These findings indicate that the intensity of premotor rTMS determines the net effect of conditioning on distinct populations of neurones in the ipsilateral M1(HAND), but it is the frequency of rTMS that determines the direction of the induced change. By selecting the appropriate intensity and frequency, premotor rTMS allows to induce a predictable up- or down-regulation of the excitability in distinct neuronal circuits of human M1(HAND).

Subthalamic somatosensory evoked potentials in Parkinson's disease.

Deep brain stimulation (DBS) of subthalamic nucleus (STN) is an effective treatment for advanced Parkinson's disease. It also provides an opportunity to record neural activity from the human basal ganglia. In this study, to investigate the involvement of the human STN in sensory functions, we recorded somatosensory evoked potentials (SEPs) elicited by contralateral median-nerve stimulation, from STN electrodes implanted for DBS in patients with Parkinson's disease. We suggest that the STN N18 component of SEPs in Parkinson's disease is a mainly local field potential elicited by muscle afferent input to the nucleus.

Focal reduction of intracortical inhibition in the motor cortex by selective proprioceptive stimulation.

The influence of proprioception on motorcortical excitability was assessed by muscle vibration (MV; 80 Hz, 0.5 mm amplitude) of the flexor carpi radialis muscle (FCR) and compared to voluntary contraction and relaxation conditions. Motor thresholds, motor-evoked potentials (MEPs) in response to single pulses of transcranial magnetic stimulation (TMS) and the intracortical inhibition (ICI) and facilitation (ICF) after paired magnetic stimuli were studied. A control experiment using TMS inducing posteriorly directed current was performed. MEPs were recorded simultaneously from the FCR, the extensor carpi radialis, the abductor pollicis brevis and the first dorsal interosseus. In the FCR, MV led to an increase of excitability shown by a decrease of motor threshold, a facilitation of MEPs in response to single-pulse TMS, a reduction of ICI and an increase of ICF. Since especially the ICI and ICF remain unchanged in other recorded muscles, this increase of excitability is specific for the vibrated muscle. With posteriorly directed current the ICI in the FCR was reduced as well, showing an involvement of later I-waves. We suggest that MV induces a focused motorcortical activation which relies on a reduced activity of intracortical inhibitory interneuronal circuits targeting selectively the motorcortical representation of the vibrated muscle.