An implantable sensor capable of long-term monitoring of tissue glucose concentrations by wireless telemetry has been developed for eventual application in people with diabetes. In a recent trial, the sensor-telemetry system functioned continuously while implanted in subcutaneous tissues of two pigs for a total of 222 days and 520 days respectively, with each animal in both non-diabetic and diabetic states. The sensor detects glucose via an enzyme electrode principle that is based on differential electrochemical oxygen detection, which reduces the sensitivity of the sensor to encapsulation by the body, variations in local microvascular perfusion, limited availability of tissue oxygen, and inactivation of the enzymes. After an initial two-week stabilization period, the implanted sensors maintained stability of calibration for extended periods. The lag between blood and tissue glucose concentrations was 11.8 ± 5.7 minutes and 6.5 ± 13.3 minutes respectively, for rising and falling blood glucose challenges (mean ± SD). The lag was determined mainly by glucose mass transfer in the tissues, rather than the intrinsic response of the sensor, and showed no systematic change over implant test periods. These results represent a milestone in the translation of the sensor system to human applications.

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The neural interfaces field holds great promise to enable elucidation of neural information processing and to develop new implantable devices for stimulation based therapy. Currently, this field is struggling to find solutions for reducing tissue reactions to implanted micro and nanotechnology. Prior studies have recently shown that gelatin coatings lower activation of digestive microglia and mitigate the ubiquitous loss of neurons adjacent to implanted probes, both of which impede implant function. The underlying mechanisms remain to be elucidated, however. Our findings demonstrate for the first time that gelatin has a significant effect on the BBB by promoting rapid restoration of integrity after injury. Moreover, gelatin alters microglia phenotypes and modulates gelatinase activity for up to 2weeks favoring anti-inflammation and restoration of the tissue. Given the key importance of the BBB for normal brain functions, we believe our findings have substantial significance and will be highly interesting to researchers in the biomaterial field.

mechanically in service by rod fracture. One of the mechanical failure modes of the insulators is a failure process called brittle fracture [1]-[31], which is caused by the stress corrosion cracking (SCC) of the GRP rods [32]-[51]. The process is catastrophic and unpredictable, leading to the drop of energized transmission lines [13], [18]. Several attempts have been made over the years [1]-[31] to understand this process and provide potential remedies to avoid it in service. In Fig. 2(a-d), some examples are presented of brittle fracture failures of failed nonceramic insulators operated at 115 kV (Fig. 2a, b), 345 kV (Fig. 2c), and 500 kV (Fig. 2d). It should be noted that all insulators in Fig. 2 were made by the same manufacturer and were based on the epoxy

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