A feasibility study of hand kinematics for EVA analysis using magnetic resonance imaging

A new method of analyzing the kinematics of joint motion is developed. Magnetic Resonance Imaging (MRI) offers several distinct advantages. Past methods of studying anatomic joint motion have usually centered on four approaches. These methods are x-ray projection, goniometric linkage analysis, sonic digitization, and landmark measurement of photogrammetry. Of these four, only x-ray is applicable for in vivo studies. The remaining three methods utilize other types of projections of inter-joint measurements, which can cause various types of error. MRI offers accuracy in measurement due to its tomographic nature (as opposed to projection) without the problems associated with x-ray dosage. Once the data acquisition of MR images was complete, the images were processed using a 3D volume rendering workstation. The metacarpalphalangeal (MCP) joint of the left index finger was selected and reconstructed into a three-dimensional graphic display. From the reconstructed volumetric images, measurements of the angles of movement of the applicable bones were obtained and processed by analyzing the screw motion of the MCP joint. Landmark positions were chosen at distinctive locations of the joint at fixed image threshold intensity levels to ensure repeatability. The primarily two dimensional planar motion of this joint was then studied using a method of constructing coordinate systems using three (or more) points. A transformation matrix based on a world coordinate system described the location and orientation of a local target coordinate system. Future research involving volume rendering of MRI data focusing on the internal kinematics of the hand's individual ligaments, cartilage, tendons, etc. will follow. Its findings will show the applicability of MRI to joint kinematics for gaining further knowledge of the hand-glove (power assisted) design for extravehicular activity (EVA)

Na(v )1.8-null mice show stimulus-dependent deficits in spinal neuronal activity

BACKGROUND: The voltage gated sodium channel Na(v )1.8 has a highly restricted expression pattern to predominantly nociceptive peripheral sensory neurones. Behaviourally Na(v )1.8-null mice show an increased acute pain threshold to noxious mechanical pressure and also deficits in inflammatory and visceral, but not neuropathic pain. Here we have made in vivo electrophysiology recordings of dorsal horn neurones in intact anaesthetised Na(v )1.8-null mice, in response to a wide range of stimuli to further the understanding of the functional roles of Na(v )1.8 in pain transmission from the periphery to the spinal cord. RESULTS: Na(v )1.8-null mice showed marked deficits in the coding by dorsal horn neurones to mechanical, but not thermal, -evoked responses over the non-noxious and noxious range compared to littermate controls. Additionally, responses evoked to other stimulus modalities were also significantly reduced in Na(v )1.8-null mice where the reduction observed to pinch > brush. The occurrence of ongoing spontaneous neuronal activity was significantly less in mice lacking Na(v )1.8 compared to control. No difference was observed between groups in the evoked activity to electrical activity of the peripheral receptive field. CONCLUSION: This study demonstrates that deletion of the sodium channel Na(v )1.8 results in stimulus-dependent deficits in the dorsal horn neuronal coding to mechanical, but not thermal stimuli applied to the neuronal peripheral receptive field. This implies that Na(v )1.8 is either responsible for, or associated with proteins involved in mechanosensation

EVA Glove Research Team

The goal of the basic research portion of the extravehicular activity (EVA) glove research program is to gain a greater understanding of the kinematics of the hand, the characteristics of the pressurized EVA glove, and the interaction of the two. Examination of the literature showed that there existed no acceptable, non-invasive method of obtaining accurate biomechanical data on the hand. For this reason a project was initiated to develop magnetic resonance imaging as a tool for biomechanical data acquisition and visualization. Literature reviews also revealed a lack of practical modeling methods for fabric structures, so a basic science research program was also initiated in this area

High-resolution Fourier-transform XUV photoabsorption spectroscopy of 14N15N

The first comprehensive high-resolution photoabsorption spectrum of 14N15N has been recorded using the Fourier-transform spectrometer attached to the Desirs beamline at the Soleil synchrotron. Observations are made in the extreme ultraviolet (XUV) and span 100,000-109,000 cm-1 (100-91.7 nm). The observed absorption lines have been assigned to 25 bands and reduced to a set of transition energies, f values, and linewidths. This analysis has verified the predictions of a theoretical model of N2 that simulates its photoabsorption and photodissociation cross section by solution of an isotopomer independent formulation of the coupled-channel Schroedinger equation. The mass dependence of predissociation linewidths and oscillator strengths is clearly evident and many local perturbations of transition energies, strengths, and widths within individual rotational series have been observed.Comment: 14 pages, 8 figures, one data archiv

Functional significance of M-type potassium channels in nociceptive cutaneous sensory endings

M-channels carry slowly activating potassium currents that regulate excitability in a variety of central and peripheral neurons. Functional M-channels and their Kv7 channel correlates are expressed throughout the somatosensory nervous system where they may play an important role in controlling sensory nerve activity. Here we show that Kv7.2 immunoreactivity is expressed in the peripheral terminals of nociceptive primary afferents. Electrophysiological recordings from single afferents in vitro showed that block of M-channels by 3 μM XE991 sensitized Aδ- but not C-fibers to noxious heat stimulation and induced spontaneous, ongoing activity at 32°C in many Aδ-fibers. These observations were extended in vivo: intraplantar injection of XE991 selectively enhanced the response of deep dorsal horn (DH) neurons to peripheral mid-range mechanical and higher range thermal stimuli, consistent with a selective effect on Aδ-fiber peripheral terminals. These results demonstrate an important physiological role of M-channels in controlling nociceptive Aδ-fiber responses and provide a rationale for the nocifensive behaviors that arise following intraplantar injection of the M-channel blocker XE991

Distinct Nav1.7-dependent pain sensations require different sets of sensory and sympathetic neurons

Human acute and inflammatory pain requires the expression of voltage-gated sodium channel Nav1.7 but its significance for neuropathic pain is unknown. Here we show that Nav1.7 expression in different sets of mouse sensory and sympathetic neurons underlies distinct types of pain sensation. Ablating Nav1.7 gene (SCN9A) expression in all sensory neurons using Advillin-Cre abolishes mechanical pain, inflammatory pain and reflex withdrawal responses to heat. In contrast, heat-evoked pain is retained when SCN9A is deleted only in Nav1.8-positive nociceptors. Surprisingly, responses to the hotplate test, as well as neuropathic pain, are unaffected when SCN9A is deleted in all sensory neurons. However, deleting SCN9A in both sensory and sympathetic neurons abolishes these pain sensations and recapitulates the pain-free phenotype seen in humans with SCN9A loss-of-function mutations. These observations demonstrate an important role for Nav1.7 in sympathetic neurons in neuropathic pain, and provide possible insights into the mechanisms that underlie gain-of-function Nav1.7-dependent pain conditions

Phenyl Saligenin Phosphate Induced Caspase-3 and c-Jun N-Terminal Kinase Activation in Cardiomyocyte-Like Cells

At present, little is known about the effect(s) of organophosphorous compounds (OPs) on cardiomyocytes. In this study we have investigated the effects of phenyl saligenin phosphate (PSP), two organophosphorothioate insecticides (diazinon and chlorpyrifos) and their acutely toxic metabolites (diazoxon and chlorpyrifos oxon) on mitotic and differentiated H9c2 cardiomyoblasts. OP-induced cytotoxicity was assessed by monitoring MTT reduction, LDH release and caspase-3 activity. Cytotoxicity was not observed with diazinon, diazoxon or chlorpyrifos oxon (48 h exposure; 200 μM). Chlorpyrifos-induced cytotoxicity was only evident at concentrations >100 μM. In marked contrast, PSP displayed pronounced cytotoxicity towards mitotic and differentiated H9c2 cells. PSP triggered the activation of JNK1/2, but not ERK1/2, p38 MAPK or PKB, suggesting a role for this pro-apoptotic protein kinase in PSP-induced cell death. The JNK1/2 inhibitor SP 600125 attenuated PSP-induced caspase-3 and JNK1/2 activation, confirming the role of JNK1/2 in PSP-induced cytotoxicity. Fluorescently labelled PSP (dansylated PSP) was used to identify novel PSP binding proteins. Dansylated PSP displayed cytotoxicity towards differentiated H9c2 cells. 2D-gel electrophoresis profiles of cells treated with dansylated PSP (25 μM) were used to identify proteins fluorescently labelled with dansylated PSP. Proteomic analysis identified tropomyosin, heat shock protein β-1 and nucleolar protein 58 as novel protein targets for PSP. In summary, PSP triggers cytotoxicity in differentiated H9c2 cardiomyoblasts via JNK1/2-mediated activation of caspase-3. Further studies are required to investigate whether the identified novel protein targets of PSP play a role in the cytotoxicity of this OP, which is usually associated with the development of OP-induced delayed neuropathy