Attentional, anticipatory and spatial cognition fluctuate throughout the menstrual cycle: Potential implications for female sport.

Current research suggests that menstruating female athletes might be at greater risk of musculoskeletal injury in relation to hormonal changes throughout the menstrual cycle. A separate body of work suggests that spatial cognition might also fluctuate in a similar manner. Changes in spatial cognition could, in theory, be a contributing risk factor for injury, especially in fast-paced sports that require precise, millisecond accuracy in interactions with moving objects in the environment. However, existing theories surrounding causes for increased injury risk in menstruating females largely focus on biomechanical mechanisms, with little consideration of possible cognitive determinants of injury risk. Therefore, the aim of this proof-of-principle study was to explore whether menstruating females exhibit fluctuations in cognitive processes throughout their cycle on a novel sport-oriented cognitive test battery, designed to measure some of the mental processes putatively involved in these sporting situations. A total of 394 participants completed an online cognitive battery, a mood scale and a symptom questionnaire twice, 14 days apart. After exclusions, 248 eligible participants were included in the analyses (mean: 28 ± 6 years) (male = 96, female(menstruating) = 105, female(contraception) = 47). Cycle phase for menstruating females was based on self-reported information. The cognitive battery was designed to measure reaction times, attention, visuospatial functions (including 3D mental rotation) and timing anticipation. Three composite scores were generated using factor analysis with varimax rotation (Errors, Reaction Time, Intra-Individual Variability). Mixed model ANOVAs and repeated measures ANOVAs were performed to test for between and within-subject effects. There was no group difference in reaction times and accuracy between males and females (using contraception and not). However, within subject analyses revealed that regularly menstruating females performed better during menstruation compared to being in any other phase, with faster reaction times (10ms c.ca, p < 0.01), fewer errors (p < 0.05) and lower dispersion intra-individual variability (p < 0.05). In contrast they exhibited slower reaction times (10ms c.ca, p < 0.01) and poorer timing anticipation (p < 0.01) in the luteal phase, and more errors in the predicted ovulatory phase (p < 0.01). Self-reported mood, cognitive and physical symptoms were all worst during menstruation (p < 0.01), and a significant proportion of females felt that their symptoms were negatively affecting their cognitive performance during menstruation on testing day, which was incongruent with their actual performance. These findings suggest that visuospatial and anticipatory processes may fluctuate throughout the menstrual cycle in the general population, with better performance during the menstrual phase and poorer performance during the luteal phase. If these extend to associations between phase-specific cognitive performance and injury incidence, they would support a cognitive theory of determinants of injury risk in cycling female athletes, opening an opportunity to develop mitigation strategies where appropriate.

Nonlinear effects at the electrode-tissue interface of deep brain stimulation electrodes.

Objective.The electrode-tissue interface provides the critical path for charge transfer in neurostimulation therapies and exhibits well-established nonlinear properties at high applied currents or voltages. These nonlinear properties may influence the efficacy and safety of applied stimulation but are typically neglected in computational models. In this study, nonlinear behavior of the electrode-tissue interface impedance was incorporated in a computational model of deep brain stimulation (DBS) to simulate the impact on neural activation and safety considerations.Approach.Nonlinear electrode-tissue interface properties were incorporated in a finite element model of DBS electrodesin vitroandin vivo,in the rat subthalamic nucleus, using an iterative approach. The transition point from linear to nonlinear behavior was determined for voltage and current-controlled stimulation. Predicted levels of neural activation during DBS were examined and the region of linear operation of the electrode was compared with the Shannon safety limit.Main results.A clear transition of the electrode-tissue interface impedance to nonlinear behavior was observed for both current and voltage-controlled stimulation. The transition occurred at lower values of activation overpotential for simulatedin vivothanin vitroconditions (91 mV and 165 mV respectively for current-controlled stimulation; 110 mV and 275 mV for voltage-controlled stimulation), corresponding to an applied current of 30µA and 45µA, or voltage of 330 mV at 1 kHz. The onset of nonlinearity occurred at lower values of the overpotential as frequency was increased. Incorporation of nonlinear properties resulted in activation of a higher proportion of neurons under voltage-controlled stimulation. Under current-controlled stimulation, the predicted transition to nonlinear behavior and Faradaic charge transfer at stimulation amplitudes of 30µA, corresponds to a charge density of 2.29µC cm-2and charge of 1.8 nC, well-below the Shannon safety limit.Significance.The results indicate that DBS electrodes may operate within the nonlinear region at clinically relevant stimulation amplitudes. This affects the extent of neural activation under voltage-controlled stimulation and the transition to Faradaic charge transfer for both voltage- and current-controlled stimulation with important implications for targeting of neural populations and the design of safe stimulation protocols.

Stimulation-induced changes at the electrode-tissue interface and their influence on deep brain stimulation.

Objective. During deep brain stimulation (DBS) the electrode-tissue interface (ETI) forms a critical path between device and brain tissue. Although changes in the electrical double layer (EDL) and glial scar can impact stimulation efficacy, the effects of chronic DBS on the ETI have not yet been established.Approach. In this study, we characterised the ETI surrounding chronically implanted DBS electrodes in rats and compared the impedance and histological properties at the electrode interface in animals that received daily stimulation and in those where no stimulation was applied, up to 8 weeks post-surgery. A computational model was developed based on the experimental data, which allowed the dispersive electrical properties of the surrounding encapsulation tissue to be estimated. The model was then used to study the effect of stimulation-induced changes in the ETI on the electric field and neural activation during voltage- and current-controlled stimulation.Main results. Incorporating the observed changes in simulationsin silico, we estimated the frequency-dependent dielectric properties of the EDL and surrounding encapsulation tissue. Through simulations we show how stimulation-induced changes in the properties of the ETI influence the electric field and alter neural activation during voltage-controlled stimulation. A substantial increase in the number of stimulated collaterals, and their distance from the electrode, was observed during voltage-controlled stimulation with stimulated ETI properties.In vitroexamination of stimulated electrodes confirmed that high frequency stimulation leads to desorption of proteins at the electrode interface, with a concomitant reduction in impedance.Significance. The demonstration of stimulation-induced changes in the ETI has important implications for future DBS systems including closed-loop systems where the applied stimulation may change over time. Understanding these changes is particularly important for systems incorporating simultaneous stimulation and sensing, which interact dynamically with brain networks.

Utility of exercise testing to assess athletes for post COVID-19 myocarditis.

Purpose: This study assessed a functional protocol to identify myocarditis or myocardial involvement in competitive athletes following SARS-CoV2 infection. Methods: We prospectively evaluated competitive athletes (n = 174) for myocarditis or myocardial involvement using the Multidisciplinary Inquiry of Athletes in Miami (MIAMI) protocol, a median of 18.5 (IQR 16-25) days following diagnosis of COVID-19 infection. The protocol included biomarker analysis, ECG, cardiopulmonary stress echocardiography testing with global longitudinal strain (GLS), and targeted cardiac MRI for athletes with abnormal findings. Patients were followed for median of 148 days. Results: We evaluated 52 females and 122 males, with median age 21 (IQR: 19, 22) years. Five (2.9%) had evidence of myocardial involvement, including definite or probable myocarditis (n = 2). Three of the 5 athletes with myocarditis or myocardial involvement had clinically significant abnormalities during stress testing including ventricular ectopy, wall motion abnormalities and/or elevated VE/VCO2, while the other two athletes had resting ECG abnormalities. VO2max, left ventricular ejection fraction and GLS were similar between those with or without myocardial involvement. No adverse events were reported in the 169 athletes cleared to exercise at a median follow-up of 148 (IQR108,211) days. Patients who were initially restricted from exercise had no adverse sequelae and were cleared to resume training between 3 and 12 months post diagnosis. Conclusions: Screening protocols that include exercise testing may enhance the sensitivity of detecting COVID-19 related myocardial involvement following recovery from SARS-CoV2 infection.

An Energetic Model of Low Frequency Isometric Neuromuscular Electrical Stimulation.

The objective of this study was to evaluate whether an adapted Hill-type model of muscle energetics could account for the relatively high energy turnover observed during low frequency isometric Neuromuscular Electrical Stimulation (NMES). A previously validated Hill-based model was adapted to estimate the energy consumption due to muscle activation, force maintenance and internal shortening of the muscle during isometric NMES. Quadriceps muscle model parameters were identified for 10 healthy subjects based on the experimentally measured torque response to isometric stimulation at 8 Hz. Model predictions of torque and energy consumption rates across the stimulation range 1-12 Hz were compared with experimental data recorded from the same subjects. The model provided estimates in close agreement with the experimental values for the group mean energy consumption rate across the frequency range tested, (R adj (2) = 0.98), although prediction of individual data points for all frequencies and all subjects was more variable, (R adj (2) = 0.70). The model suggests that approximately one-third of the energy between 4 and 6 Hz is due to shortening heat. The model provides a means of identifying optimal therapeutic stimulation patterns for sustained incremental oxygen uptake at minimum torque output for a given muscle and provides insight into the energetic components involved.

A phase II, open-label, multicenter study to evaluate the antitumor efficacy of CO-1.01 as second-line therapy for gemcitabine-refractory patients with stage IV pancreatic adenocarcinoma and negative tumor hENT1 expression.

BACKGROUND: Nucleotide transporters such as human equilibrative nucleoside transporter-1 (hENT1) play a major role in transporting gemcitabine into cells. CO-1.01 (gemcitabine-5'-elaidate) is a novel cytotoxic agent consisting of a fatty acid derivative of gemcitabine, which is transported intracellularly independent of hENT1. CO-1.01 was postulated to have efficacy as a second-line treatment in gemcitabine-refractory pancreatic adenocarcinoma in patients with negative tumor hENT1 expression. METHODS: Eligibility criteria included patients with either a newly procured or archival biopsy tumor confirming the absence of hENT1 and either gemcitabine-refractory metastatic pancreas adenocarcinoma or with progression of disease following resection during or within 3 months of adjuvant gemcitabine therapy. Patients were treated with intravenous infusion of CO-1.01 dosed at 1250 mg/m(2) on Days 1, 8, and 15 of a 4-week cycle. The primary end point was disease control rate (DCR). RESULTS: Nineteen patients were enrolled of which 18 patients were evaluable for efficacy assessment. Thirteen patients (68%) had liver metastases, 6 (32%) had lymph node metastases, and 10 (53%) had lung metastases. Two of 18 patients (11%) achieved disease control. The median survival time was 4.3 (95% CI 2.1-8.1) months. All patients experienced at least one treatment-related adverse event with the majority of events being mild or moderate. CONCLUSION: This study did not meet its primary endpoint and no efficacy signal was identified for CO-1.01 in treating progressive metastatic pancreas adenocarcinoma.

Genomics and pharmacogenomics of pancreatic adenocarcinoma.

The last decade has brought significant advances in the development of molecularly targeted therapies for treatment of a variety of human malignancies. In contrast to other solid tumors, however, the impact of novel therapeutic strategies on clinical outcomes in patients with pancreas adenocarcinoma (PAC) has been limited to date. Gemcitabine was established as a standard of care for treatment of advanced PAC in 1997 based on an observed improvement in clinical benefit as adjudicated principally by pain scores and analgesic consumption, and demonstration of an overall survival (OS) benefit in a randomized comparison with 5-fluorouracil (5-FU). Since then, multiple agents targeting oncogenic signaling pathways and mediators of angiogenesis have failed to improve outcomes in phase III clinical trials when compared with gemcitabine monotherapy. An exception to this is the anti-epidermal growth factor receptor therapy erlotinib, which yielded a survival benefit in patients with advanced disease in combination with gemcitabine compared with gemcitabine alone, although this was a marginal incremental improvement for which the clinical significant has been heavily debated. More recently, the most significant therapeutic advance in PAC has come from the combination of several cytotoxic agents; infusional 5-FU, irinotecan and oxaliplatin. This combination chemotherapy regimen, known as FOLFIRINOX, improved survival in patients with an excellent functional status and stage IV disease by 4.3 months compared with gemcitabine alone. This improvement in survival did come at the cost expectedly of a significant increase in toxicities, including gastrointestinal and hematologic particularly. Other gemcitabine-based combination chemotherapy regimens including gemcitabine and platinum analogs and gemcitabine and capecitabine have consistently shown an increased response rate but no OS benefit in individual trials; albeit pooled and meta-analyses have indicated a survival benefit in good performance status patient for both these cytotoxic combinations. Accordingly, the 5-year survival for patients with PAC remains <5%, with an annual disease-specific mortality which approaches the incidence. The challenge remains therefore, to develop more effective systemic therapies against this challenging malignancy. Recent progress toward understanding the genetic events in the development of PAC, in combination with advances in the field of pharmacogenomics offer hope that we may build on achievements to-date to develop more effective therapeutic strategies for PAC in years to come.

Targeted therapies for pancreatic adenocarcinoma.

The majority of patients diagnosed with adenocarcinoma of the pancreas have advanced disease at presentation, with only 20% surviving beyond one year. Even among the 10% to 15% of patients who present with localized disease, only 20% will be alive 5 years post surgical resection. Systemic therapy for pancreatic adenocarcinoma to date has failed to provide more than a very modest survival benefit for patients with advanced disease. However, the past decade has seen significant advances in the understanding of the molecular pathogenesis of pancreatic cancer, culminating in the sequencing of the pancreatic cancer genome. New generations of therapeutic agents targeting key oncogenic cellular signaling pathways are currently under evaluation in advanced pancreatic adenocarcinoma. Although thus far only erlotinib has been shown to improve survival when compared to gemcitabine monotherapy, the authors anticipate that further developments in biomarker analysis and pharmacogenomics, along with the identification of new drugs will help maximize the benefit of novel therapeutics by directing effective use in the future. Herein the authors review the evidence to date for the use of novel cytotoxic and molecularly targeted agents in pancreatic adenocarcinoma, and discuss key areas for future therapeutic development.

Evidence of potential averaging over the finite surface of a bioelectric surface electrode.

Most bioelectric signals are not only functions of time but also exhibit a variation in spatial distribution. Surface EMG signals are often "summarized" by a large electrode. The effect of such an electrode is interpreted as averaging the potential at the surface of the skin beneath the electrode. We first introduce an electrical equivalent model to delineate this principle of averaging. Next, in a realistic finite element model of EMG generation, two outcome variables are evaluated to assess the validity of the averaging principle. One is the change in voltage distribution in the volume conductor after electrode application. The other is the change in voltage across the high impedance double layer between tissue and electrode. We found that the principle of averaging is valid, once the impedance of the double layer is sufficiently high. The simulations also revealed that skin conductivity plays a role. High-density surface EMG provided experimental evidence consistent with the simulation results. A grid with 120 small electrodes was placed over the thenar muscles of the hand. Electrical nerve stimulation assured a reproducible compound muscle response. The averaged grid response was compared with a single electrode matching the surface of the high-density electrodes. The experimental results showed relatively small errors indicating that averaging of the surface potential by the electrode is a valid principle under most practical conditions.

The effect of extracellular potassium concentration on muscle fiber conduction velocity examined using model simulation.

During fatiguing contractions muscle fiber conduction velocity (CV) decreases progressively. The exact cause of this is not yet fully known, although recent studies suggest that changes in extracellular potassium concentration play an important role. A model was developed to examine the effect of accumulation of extracellular potassium ions on the muscle fiber action potential and its CV. As the extracellular potassium concentration was increased, the action potential progressively broadened, reduced in peak-peak amplitude and its CV decreased. However, when the inward rectifier channels were blocked, the changing shape of the action potential and the reduction of its CV with increasing extracellular potassium were dramatically reduced. The simulation results support the hypothesis that the reduction in muscle fiber CV observed during sustained fatiguing contractions may be due in part, to increased accumulation of extracellular potassium ions and suggest that the inward rectifier currents play an important role on the relationships observed.

The effect of subcutaneous fat on myoelectric signal amplitude and cross-talk.

The effect of subcutaneous fat on myoelectric signal amplitude and cross-talk was studied using finite element (FE) models of electromyogram (EMG) signal propagation. A FE model of the upper arm consisted of skin, fat, muscle and bone tissues in concentric layers. Single muscle fibre action potentials were simulated for muscle fibres at a variety of depths and combined to simulate surface EMG interference patterns. As fat layers of 3, 9 and 18 mm were added to the model, the RMS (root mean square) amplitude of the surface EMG signal directly above the centre of the active muscle decreased by 31.3, 80.2 and 90.0%, respectively. Similarly, surface EMG cross-talk above the region of inactive muscle increased as the fat layer thickness increased. The surface EMG RMS amplitude fell below 5% of its value above the centre of the muscle at 14 degrees, 17 degrees, 34 degrees and 47 degrees from the edge of the active muscle with fat layers of 0, 3, 9 and 18 mm, respectively. An additional model was developed with the subcutaneous fat layer thinned from 9 mm to 3 mm in a small, focal region under a pair of recording electrodes. Reducing the fat layer in this manner caused the surface EMG amplitude at the electrodes to increase by 241% and decreased the EMG cross-talk by 68%; this was near the values for the 3 mm uniform fat layer. This demonstrates that fat reduction surgery can increase surface EMG signal amplitude and signal independence for improved prosthesis control.

Rectification and non-linear pre-processing of EMG signals for cortico-muscular analysis.

Rectification of the electromyographic (EMG) signal is a commonly used pre-processing procedure that allows detection of significant coherence between EMG and measured cortical signals. However, despite its accepted and wide-spread use, no detailed analysis has been presented to offer insight into the precise function of rectification. We begin this paper with arguments based on single motor unit action potential (AP) trains to demonstrate that rectification effectively enhances the firing rate information of the signal. Enhancement is achieved by shifting the peak of the AP spectrum toward the lower firing rate frequencies, whilst maintaining the firing rate spectra. A similar result is obtained using the analytic envelope of the signal extracted using the Hilbert transform. This argument is extended to simulated EMG signals generated using a published EMG model. Detection of firing rate frequencies is obtained using phase randomised surrogate data, where the original EMG power spectrum exceeds the averaged rectified surrogate spectra at integer multiples of firing rate frequencies. Model simulations demonstrate that this technique accurately determines grouped firing rate frequencies. Extraction of grouped firing rate frequencies prior to coherency analyses may further aid interpretation of significant cortico-muscular coherence findings.

Electromyogram median frequency, spectral compression and muscle fibre conduction velocity during sustained sub-maximal contraction of the brachioradialis muscle.

Changes in the median frequency of the power spectrum of the surface electromyogram (EMG) are commonly used to detect muscle fatigue. Previous research has indicated that changes in the median frequency are related to decreases in muscle fibre conduction velocity (MFCV) during sustained fatiguing contractions. However, in experimental studies the median frequency has been consistently observed to decrease by a relatively greater amount than MFCV. In this paper, a new estimate of EMG frequency compression, the Spectral Compression Estimate (SCE), is compared with the median frequency of the EMG power spectrum, the median frequency of the EMG amplitude spectrum and MFCV measured during sustained, isometric, fatiguing contractions of the brachioradialis muscle at 30, 50 and 80% maximum voluntary contraction (MVC). The SCE is found to provide a better estimate of the observed changes in MFCV than the median frequency of either the EMG power spectrum or EMG amplitude spectrum.

Identification of a non-dividing subpopulation of mouse and human epidermal cells exhibiting high levels of persistent ultraviolet photodamage.

The distribution and persistence of cyclobutane pyrimidine dimers were investigated in mouse skin after chronic and acute exposures to ultraviolet-B radiation. We found that DNA damage accumulated in response to chronic irradiation and persisted in a unique set of epidermal cells located at the basal layer. Treatment with a tumor promoter caused the heavily damaged epidermal cells to divide and p53-immunopositive clusters to form within 24 h suggesting that these cells may be progenitors of the mutant p53 clusters associated with actinic keratoses and squamous cell carcinomas. In contrast to low fluence chronic irradiation, daily treatment with a higher fluence of ultraviolet-B produced extensive hyperplasia and considerably reduced penetration of photodamage. Exposure of chronically irradiated skin to an acute "sunburn dose" of ultraviolet-B also produced significant epidermal hyperplasia and resulted in complete loss of heavily damaged basal cells within 4 d postirradiation. The occurrence and distribution of cyclobutane dimers in human skin correlated well with putative sunlight exposure and resembled that observed in ultraviolet-B-irradiated mice. Heavily damaged basal cells were observed at various sites, including those receiving sporadic sunlight exposure, suggesting that these cells may play an important role in carcinoma formation in humans.

The impact of a clinical pathway for gastric bypass surgery on resource utilization.

BACKGROUND: Clinical pathways are believed to improve patient care and reduce costs. Our hypothesis was that a gastric bypass pathway would decrease hospital resource utilization and cost of care without adversely affecting patient care. METHODS: The prepathway (Pre) group consisted of 16 gastric bypasses (6/98 to 3/99). The postpathway (Post) group includes 12 gastric bypass procedures performed after institution of the clinical pathway (4/99 to 12/99). The impact of the clinical pathway on hospital length of stay (LOS) and resource utilization was investigated. A comparison of costs was performed using cost/charge ratios. Hospital readmissions and postoperative complications were also examined. RESULTS: Despite increased obesity/medical acuity of the Post group, hospital LOS decreased by 3 days (P < 0.0001). Total hospital costs decreased by over $1600/case (>15%). Postpathway savings were greatest for room and board (34%), supplies (41%), and lab/radiology costs (50%). An increase in OR costs (22%) was observed in the Post group. This was due to an increase in anesthesia time (epidural catheter placement) and equipment costs (ultrasonic shears). Despite reductions in hospital LOS and resource utilization, the complication rate (Pre 12%, Post 16%) was similar and two patients in each group required brief readmission. CONCLUSIONS: A pathway for gastric bypass decreased hospital LOS and resource utilization. OR-related expenses account for 34-50% of total costs and must be monitored closely for surgical patients. The reduction in costs observed with this clinical pathway was not associated with an increase in postoperative complications or hospital readmission.

Quantification of HER2/neu gene amplification by competitive pcr using fluorescent melting curve analysis.

BACKGROUND: Molecular detection methods for HER2/neu gene amplification include fluorescence in situ hybridization (FISH) and competitive PCR. We designed a quantitative PCR system utilizing fluorescent hybridization probes and a competitor that differed from the HER2/neu sequence by a single base change. METHODS: Increasing twofold concentrations of competitor were coamplified with DNA from cell lines with various HER2/neu copy numbers at the HER2/neu locus. Competitor DNA was distinguished from the HER2/neu sequence by a fluorescent hybridization probe and melting curve analysis on a fluorescence-monitoring thermal cycler. The percentages of competitor to target peak areas on derivative fluorescence vs temperature curves were used to calculate copy number. RESULTS: Real-time monitoring of the PCR reaction showed comparable relative areas throughout the log phase and during the PCR plateau, indicating that only end-point detection is necessary. The dynamic range was over two logs (2000-250 000 competitor copies) with CVs < 20%. Three cell lines (MRC-5, T-47D, and SK-BR-3) were determined to have gene doses of 1, 3, and 11, respectively. Gene amplification was detected in 3 of 13 tumor samples and was correlated with conventional real-time PCR and FISH analysis. CONCLUSION: Use of relative peak areas allows gene copy numbers to be quantified against an internal competitive control in < 1 h.

Effects of chronic exposure to ultraviolet B radiation on DNA repair in the dermis and epidermis of the hairless mouse.

It has previously been shown that chronic exposure to low fluences of ultraviolet B radiation reduced DNA repair capacity in mouse skin. In this study we now extend this to examine the concentration dependence and tissue dependence of this phenomenon. We found that (6-4) photoproducts were repaired considerably faster than cyclobutane dimers and that the kinetics for photoproduct removal were comparable in the dermis and epidermis. Chronic ultraviolet B irradiation significantly reduced the initial rate and extent of DNA repair. After low daily doses of ultraviolet B (6-4) photoproduct repair was most affected and after high daily doses the repair of both cyclobutane and (6-4) dimers was reduced. Whereas cyclobutane dimer repair was most affected in the dermis, reduced (6-4) photoproduct repair was observed in both tissues. The deleterious effects of chronic ultraviolet exposure were sustained for a considerable time after the chronic treatment ended.

Attenuation of DNA damage in the dermis and epidermis of the albino hairless mouse by chronic exposure to ultraviolet-A and -B radiation.

Mammalian skin is vulnerable to the photocarcinogenic and photoaging effects of solar UV radiation and defends itself using a variety of photoprotective responses including epidermal thickening, tanning and the induction of repair and antiradical systems. We treated Skh-1 albino hairless mice for 60 days with ultraviolet-A (UVA) or ultraviolet-B (UVB) radiation and measured the frequency of cyclobutane pyrimidine dimers and pyrimidine(6-4)pyrimidone photoproducts induced by a single acute sunburn dose of UVB at different stages of the chronic treatment. We found that both UVA and UVB exposure produced a photoprotective response in the dermis and epidermis and that the degree of photoproduct attenuation was dependent on dose, wavelength and the type of damage induced. Although epidermal thickening was important, our data suggest that UV protective compounds other than melanin may be involved in mitigating the damaging effects of sunlight in the skin.

Finite element modeling of electromagnetic signal propagation in a phantom arm.

Improving the control of artificial arms remains a considerable challenge. It may be possible to graft remaining peripheral nerves in an amputated limb to spare muscles in or near the residual limb and use these nerve-muscle grafts as additional myoelectric control signals. This would allow simultaneous control of multiple, degrees of freedom (DOF) and could greatly improve the control of artificial limbs. For this technique to be successful, the electromyography (EMG) signals from the nerve-muscle grafts would need to be independent of each other with minimal crosstalk. To study EMG signal propagation and quantify crosstalk, finite element (FE) models were developed in a phantom-arm model. The models were validated with experimental data collected by applying sinusoidal excitations to a phantom-arm model and recording the surface electric potential distribution. There was a very high correlation (r > 0.99) between the FEM data and the experimental data, with the error in signal magnitude generally less than 5%. Simulations were then performed using muscle dielectric properties with static, complex, and full electromagnetic solvers. The results indicate that significant displacement currents can develop (> 50% of total current) and that the fall-off of surface signal power varies with how the signal source is modeled. Index Terms-Control, electromyography (EMG), finite element (FE), modeling, prosthesis.