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After an amputation, advanced prosthetic limbs can be used to interface with the nervous system and restore motor function. Despite numerous breakthroughs in the field, many of the recent research advancements have not been widely integrated into clinical practice. This review highlights recent innovations in neuromuscular implants—specifically those that interface with skeletal muscle—which could improve the clinical translation of prosthetic technologies. Skeletal muscle provides a physiologic gateway to harness and amplify signals from the nervous system. Recent surgical advancements in muscle reinnervation surgeries leverage the "bio‐amplification" capabilities of muscle, enabling more intuitive control over a greater number of degrees of freedom in prosthetic limbs than previously achieved. We anticipate that state‐of‐the‐art implantable neuromuscular interfaces that integrate well with skeletal muscle and novel surgical interventions will provide a long‐term solution for controlling advanced prostheses. Flexible electrodes are expected to play a crucial role in reducing foreign body responses and improving the longevity of the interface. Additionally, innovations in device miniaturization and ongoing exploration of shape memory polymers could simplify surgical procedures for implanting such interfaces. Once implanted, wireless strategies for powering and transferring data from the interface can eliminate bulky external wires, reduce infection risk, and enhance day‐to‐day usability. By outlining the current limitations of neuromuscular interfaces along with potential future directions, this review aims to guide continued research efforts and future collaborations between engineers and specialists in the field of neuromuscular and musculoskeletal medicine. [ABSTRACT FROM AUTHOR]

Previous work has revealed robust dorsal root ganglia neurite growth in hydrogels of chondroitin sulfate. In the current work, it was determined whether addition of a synthetic bioactive peptide could augment neurite growth in these matrices via enhanced binding and sequestering of growth factors. Fluorescence recovery after photobleaching studies revealed that addition of peptide slowed nerve growth factor diffusivity in chondroitin sulfate gels, but not in control gels of hyaluronic acid. Furthermore, cultures of chick dorsal root ganglia in gels of hyaluronic acid or chondroitin sulfate revealed enhanced growth in chondroitin sulfate gels only upon addition of peptide. Taken together, these results suggest a synergistic nerve growth factor-binding activity between this peptide and chondroitin sulfate.

Proof-of-concept studies that display the potential of using a glucose-sensitive hydrogel as a continuous glucose sensor are presented. The swelling ratio, porosity, and diffusivity of the hydrogel increased with glucose concentration. In glucose solutions of 50, 100, 200, and 300 mg/dL, the hydrogel swelling ratios were 4.9, 12.3, 15.9, and 21.7, respectively, and the swelling was reversible. The impedance across the hydrogel depended solely on the thickness and had an average increase of 47 Ω/mm. The hydrogels exposed to a hyperglycemic solution were more porous than the hydrogels exposed to a normal glycemic solution. The diffusivity of 390 Da MW fluorescein isothiocyanate in hydrogels exposed to normal and hyperglycemic solutions was examined using fluorescence recovery after photobleaching and was found to be 9.3 × 10(-14) and 41.4 × 10(-14) m(2)/s, respectively, compared to 6.2 × 10(-10) m(2)/s in glucose solution. There was no significant difference between the permeability of hydrogels in normal and hyperglycemic glucose solutions with averages being 5.26 × 10(-17) m(2) and 5.80 × 10(-17) m(2), respectively, which resembles 2-4% agarose gels. A prototype design is presented for continuous intravascular glucose monitoring by attaching a glucose sensor to an FDA-approved stent.

Background: Similar to other neurological diseases, subtle early neurological changes that occur in Alzheimer's Disease (AD) are difficult to quantify and track objectively. One relevant bio‐signal is eye movement, as it presents a unique window into cognitive processes as a direct measure of real‐time inputs to the brain. Eye‐tracking allows us to estimate timestamped activity of neural function and begin to infer and quantify attention, reprocessing (eg. word revisits), and many other aspects relevant to assessing AD. The goal of this study was to investigate the saccadic movements and trial progress during administration of the Stroop test in AD compared to normal controls. Method: 5 AD subjects and 12 age‐matched cognitively normal controls were recruited from the Johns Hopkins Memory and Alzheimer's Treatment Center and the Movement Disorders Clinic at the Johns Hopkins University School of Medicine. An Eyelink Portable Duo in head‐free‐to‐move mode was used to track eye movements. Movement of the eyes were analyzed by automatically segmenting saccade movements throughout a trial. We then analyzed the eye movements in the context of cognitive performance, by identifying when subjects progress to each word in the Stroop test. We compared the performance of each group using a Wilcoxon RankSum test with the SciPy package using Python. Result: Preliminary results show that 60% (3/5) of AD subjects were unable to complete the Stroop task in 80 seconds. Individuals with AD had more saccades (p=0.105) with greater saccadic overshoot (p=0.092) and a greater maximum saccade velocity (p=0.035) on average compared to cognitively normal controls. AD subjects also took much longer to complete the first (p=0.114) and second lines (p=0.092) compared to healthy controls, suggesting initial confusion and hesitation. Conclusion: AD subjects change their gaze more often with greater speed and less precision than age‐matched controls. These data demonstrate feasibility of using automatic quantitative evaluation of eye movements in AD. In the future, we will determine the utility of using this tool for early detection of AD and tracking its progression, along with combining other measures such as voice and handwriting (multimodal) to provide insights into early physiological changes in AD. [ABSTRACT FROM AUTHOR]

We report live animal studies that verify and quantify successful transocular transmission of data from a miniature low-power implant. To minimize damage, implantation within layers of the eye requires an ultrasmall device on a scale of just a few millimeters on each side and less than 500 [micro]m in thickness. A high-frequency transmitter integrated circuit (IC) was designed, fabricated, and bonded onto a board containing an antenna, matching network components, and interconnects. The transmitter must achieve sufficient efficiency to draw minimal power from the limited onboard storage array while outputting a sufficiently large signal to overcome tissue-induced attenuation. Two different versions of the system were developed, one using a low-temperature co-fired ceramic material for the substrate and the other using silicon. Animal studies performed using live rabbits followed by empirical measurements verified the feasibility of a wireless telemetry scheme for a low-power miniature ocular implant. Index Terms--Biological system modeling, biomedical applications of EM radiation, biomedical telemetry, implantable biomedical devices.

Abstract Background A serious complication with drug-eluting coronary stents is late thrombosis, caused by exposed stent struts not covered by endothelial cells in the healing process. Real-time detection of this healing process could guide physicians for more individualized anti-platelet therapy. Here we present work towards developing a sensor to detect this healing process. Sensors on several stent struts could give information about the heterogeneity of healing across the stent. Methods A piezoelectric microcantilever was insulated with parylene and demonstrated as an endothelialization detector for incorporation within an active coronary stent. After initial characterization, endothelial cells were plated onto the cantilever surface. After they attached to the surface, they caused an increase in mass, and thus a decrease in the resonant frequencies of the cantilever. This shift was then detected electrically with an LCR meter. The self-sensing, self-actuating cantilever does not require an external, optical detection system, thus allowing for implanted applications. Results A cell density of 1300 cells/mm2 on the cantilever surface is detected. Conclusions We have developed a self-actuating, self-sensing device for detecting the presence of endothelial cells on a surface. The device is biocompatible and functions reliably in ionic liquids, making it appropriate for implantable applications. This sensor can be placed along the struts of a coronary stent to detect when the struts have been covered with a layer of endothelial cells and are no longer available surfaces for clot formation. Anti-platelet therapy can be adjusted in real-time with respect to a patient's level of healing and hemorrhaging risks.