A facile approach to fabricate highly sensitive, flexible strain sensor based on elastomeric/graphene platelet composite film

This work developed a facile approach to fabricate highly sensitive and flexible polyurethane/graphene platelets composite film for wearable strain sensor. The composite film was fabricated via layer-by-layer laminating method which is simple and cost-effective; it exhibited outstanding electrical conductivity of 1430 ± 50 S/cm and high sensitivity to strain (the gauge factor is up to 150). In the sensor application test, the flexible strain sensor achieves real-time monitoring accurately for five bio-signals such as pulse movement, finger movement, and cheek movement giving a great potential as wearable-sensing device. In addition, the developed strain sensor shows response to pressure and temperature in a certain region. A multifaceted comparison between reported flexible strain sensors and our strain sensor was made highlighting the advantages of the current work in terms of (1) high sensitivity (gauge factor) and flexibility, (2) facile approach of fabrication, and (3) accurate monitoring for body motions

Intense isolectin-B4 binding in rat dorsal root ganglion neurons distinguishes c-fiber nociceptors with broad action potentials and high nav1.9 expression

Binding to isolectin-B4 (IB4) and expression of tyrosine kinase A (trkA) (the high-affinity NGF receptor) have been used to define two different subgroups of nociceptive small dorsal root ganglion (DRG) neurons. We previously showed that only nociceptors have high trkA levels. However, information about sensory and electrophysiological properties in vivo of single identified IB4-binding neurons, and about their trkA expression levels, is lacking. IB4-positive (IB4+) and small dark neurons had similar size distributions. We examined IB4-binding levels in >120 dye-injected DRG neurons with sensory and electrophysiological properties recorded in vivo. Relative immunointensities for trkA and two TTX-resistant sodium channels (Nav1.8 and Nav1.9) were also measured in these neurons. IB4+ neurons were classified as strongly or weakly IB4+. All strongly IB4+ neurons were C-nociceptor type (C-fiber nociceptive or unresponsive). Of 32 C-nociceptor-type neurons examined, ~50% were strongly IB4+, ~20% were weakly IB4+ and ~30% were IB4–. A{delta} low-threshold mechanoreceptive (LTM) neurons were weakly IB4+ or IB4–. All 33 A-fiber nociceptors and all 44 A{alpha}/beta-LTM neurons examined were IB4–. IB4+ compared with IB4– C-nociceptor-type neurons had longer somatic action potential durations and rise times, slower conduction velocities, more negative membrane potentials, and greater immunointensities for Nav1.9 but not Nav1.8. Immunointensities of IB4 binding in C-neurons were positively correlated with those of Nav1.9 but not Nav1.8. Of 23 C-neurons tested for both trkA and IB4, ~35% were trkA+/IB4+ but with negatively correlated immunointensities; 26% were IB4+/trkA–, and 35% were IB4–/trkA+. We conclude that strongly IB4+ DRG neurons are exclusively C-nociceptor type and that high Nav1.9 expression may contribute to their distinct membrane properties

Challenges of measuring body temperatures of free-ranging birds and mammals

The thermal physiology of most birds and mammals is characterised by considerable spatial and temporal variation in body temperature. Body temperature is, therefore, a key parameter in physiological, behavioural and ecological research. Temperature measurements on freely moving or free-ranging animals in the wild are challenging but can be undertaken using a range of techniques. Internal temperature may be sampled using thermometry, surgically implanted loggers or transmitters, gastrointestinal or non-surgically placed devices. Less invasive approaches measure peripheral temperature with subcutaneous passive integrated transponder tags or skin surface-mounted radio transmitters and data loggers, or use infrared thermography to record surface temperature. Choice of technique is determined by focal research question and region of interest that reflects appropriate physiological or behavioural causal mechanisms of temperature change, as well as welfare and logistical considerations. Particularly required are further studies that provide opportunities of continuously sampling from multiple sites from within the body. This will increase our understanding of thermoregulation and temperature variation in different parts of the body and how these temperatures may change in response to physiological, behavioural and environmental parameters. Technological advances that continue to reduce the size and remote sensing capability of temperature recorders will greatly benefit field research

Aerospace medicine and biology: A continuing bibliography with indexes, supplement 218, April 1981

This bibliography lists 161 reports, articles, and other documents introduced into the NASA scientific and technical information system in March 1981

The validity of the EMG and MMG techniques to examine muscle hypertrophy

Objective: The purpose of this investigation was to examine the ability of the electromyographic (EMG) and mechanomyographic (MMG) amplitude versus torque relationships to track group and individual changes in muscle hypertrophy as a result of resistance training. Approach: Twelve women performed four weeks of forearm flexion blood flow restriction (BFR) resistance training at a frequency of three times per week. The training was performed at an isokinetic velocity of 120°∙s−1 with a training load that corresponded to 30% of concentric peak torque. Muscle hypertrophy was determined using ultrasound-based assessments of muscle cross-sectional area from the biceps brachii. Training-induced changes in the slope coefficients of the EMG amplitude and MMG amplitude versus torque relationships were determined from the biceps brachii during incremental (10%–100% of maximum) isometric muscle actions. Main results: There was a significant (p \u3c 0.001; d = 2.15) mean training-induced increase in muscle cross-sectional area from 0 week (mean ± SD = 5.86 ± 0.65 cm2) to 4 weeks (7.42 ± 0.80 cm2), a significant (p = 0.023; d = 0.36) decrease in the EMG amplitude versus torque relationship (50.70 ± 20.41 to 43.82 ± 17.76 μV∙Nm−1), but no significant (p = 0.192; d = 0.17) change in the MMG amplitude versus torque relationship (0.018 ± 0.009 to 0.020 ± 0.009 m∙s−2∙Nm−1). There was, however, great variability for the individual responses for the EMG and MMG amplitude versus torque relationships. Significance: The results of the present study indicated that the EMG amplitude, but not the MMG amplitude versus torque relationship was sensitive to mean changes in muscle cross-sectional area during the early-phase of resistance training. There was, however, great variability for the individual EMG amplitude versus torque relationships that limits its application for identifying individual changes in muscle hypertrophy as a result of BFR

Mesenteric Vascular Dysregulation and Intestinal Inflammation Accompanies Experimental Spinal Cord Injury

Cervical and high thoracic spinal cord injury (SCI) drastically impairs autonomic nervous system function. Individuals with SCI at thoracic spinal-level 5 (T5) or higher often present cardiovascular disorders that include resting systemic arterial hypotension. Gastrointestinal (GI) tissues are critically dependent upon adequate blood flow and even brief periods of visceral hypoxia triggers GI dysmotility. The aim of this study was to test the hypothesis that T3-SCI induces visceral hypoperfusion, diminished postprandial vascular reflexes and concomitant visceral inflammation. We measured in vivo systemic arterial blood pressure and superior mesenteric artery (SMA) and duodenal blood flow in anesthetized T3-SCI rats at 3 days and 3 weeks post-injury either fasted or following enteral feeding of a liquid mixed-nutrient meal (Ensure™). In separate cohorts of fasted T3-SCI rats, markers of intestinal inflammation were assayed by qRT-PCR. Our results show that T3-SCI rats displayed significantly reduced SMA blood flow under all experimental conditions (p\u3c0.05). Specifically, the anticipated elevation of SMA blood flow in response to duodenal nutrient infusion (postprandial hyperemia) was either delayed or absent after T3-SCI. The dysregulated SMA blood flow in acutely-injured T3-SCI rats coincides with abnormal intestinal morphology and elevation of inflammatory markers, all of which resolve after 3 weeks. Specifically, Icam1, Ccl2 (MCP-1) and Ccl3 (MIP-1α) were acutely elevated following T3-SCI. Our data suggest that arterial hypotension diminishes mesenteric blood flow necessary to meet mucosal demands at rest and during digestion. The resulting GI ischemia and low-grade inflammation may be an underlying pathology leading to GI dysfunction seen following acute T3-SCI

Osteopontin ablation ameliorates muscular dystrophy by shifting macrophages to a pro-regenerative phenotype.

In the degenerative disease Duchenne muscular dystrophy, inflammatory cells enter muscles in response to repetitive muscle damage. Immune factors are required for muscle regeneration, but chronic inflammation creates a profibrotic milieu that exacerbates disease progression. Osteopontin (OPN) is an immunomodulator highly expressed in dystrophic muscles. Ablation of OPN correlates with reduced fibrosis and improved muscle strength as well as reduced natural killer T (NKT) cell counts. Here, we demonstrate that the improved dystrophic phenotype observed with OPN ablation does not result from reductions in NKT cells. OPN ablation skews macrophage polarization toward a pro-regenerative phenotype by reducing M1 and M2a and increasing M2c subsets. These changes are associated with increased expression of pro-regenerative factors insulin-like growth factor 1, leukemia inhibitory factor, and urokinase-type plasminogen activator. Furthermore, altered macrophage polarization correlated with increases in muscle weight and muscle fiber diameter, resulting in long-term improvements in muscle strength and function in mdx mice. These findings suggest that OPN ablation promotes muscle repair via macrophage secretion of pro-myogenic growth factors