Practical Resources for Talking to Children with Autism about Systemic Racism.

As part of the child-rearing process, situations that invite difficult conversations will inevitably arise. Oftentimes, there are no guidelines or structure for how to discuss topics such as sex education, systemic racism, bullying, grieving, and gun violence. Accordingly, adults may feel at a loss for how to address difficult topics and may even avoid difficult conversations completely. When adults choose to have these conversations, they may imitate the conversations their caregivers had with them, and therefore further the cycle of systemic racism, often unknowingly and unintentionally. Racial injustice has been a core part of the American experience since the founding of the republic; hence, conversations about systemic racism are long overdue. The need has significantly increased, given the current socio-political climate. Social justice may be a sensitive topic for some, but it is a needed conversation for all, including children with Autism Spectrum Disorder (ASD). Currently available curricula and teaching manuals in the Applied Behavior Analysis (ABA) literature include little or no resources for caregivers on how to address systemic racism with their children on the spectrum. Children with ASD should be educated about how they, and their families, can combat systemic racism in their everyday lives. The present paper addresses this gap in available treatment resources by offering practical suggestions and guidelines for how adults can address the topic of systemic racism with children on the autism spectrum to educate them and prepare them to contribute to a more equitable and just future.

Ultrasound-triggered antibiotic release from PEEK clips to prevent spinal fusion infection: Initial evaluations.

Despite aggressive peri-operative antibiotic treatments, up to 10% of patients undergoing instrumented spinal surgery develop an infection. Like most implant-associated infections, spinal infections persist through colonization and biofilm formation on spinal instrumentation, which can include metal screws and rods for fixation and an intervertebral cage commonly comprised of polyether ether ketone (PEEK). We have designed a PEEK antibiotic reservoir that would clip to the metal fixation rod and that would achieve slow antibiotic release over several days, followed by a bolus release of antibiotics triggered by ultrasound (US) rupture of a reservoir membrane. We have found using human physiological fluid (synovial fluid), that higher levels (100-500 µg) of vancomycin are required to achieve a marked reduction in adherent bacteria vs. that seen in the common bacterial medium, trypticase soy broth. To achieve these levels of release, we applied a polylactic acid coating to a porous PEEK puck, which exhibited both slow and US-triggered release. This design was further refined to a one-hole or two-hole cylindrical PEEK reservoir that can clip onto a spinal rod for clinical use. Short-term release of high levels of antibiotic (340 ±â€¯168 µg), followed by US-triggered release was measured (7420 ±â€¯2992 µg at 48 h). These levels are sufficient to prevent adhesion of Staphylococcus aureus to implant materials. This study demonstrates the feasibility of an US-mediated antibiotic delivery device, which could be a potent weapon against spinal surgical site infection. STATEMENT OF SIGNIFICANCE: Spinal surgical sites are prone to bacterial colonization, due to presence of instrumentation, long surgical times, and the surgical creation of a dead space (≥5 cm3) that is filled with wound exudate. Accordingly, it is critical that new approaches are developed to prevent bacterial colonization of spinal implants, especially as neither bulk release systems nor controlled release systems are available for the spine. This new device uses non-invasive ultrasound (US) to trigger bulk release of supra-therapeutic doses of antibiotics from materials commonly used in existing surgical implants. Thus, our new delivery system satisfies this critical need to eradicate surviving bacteria, prevent resistance, and markedly lower spinal infection rates.

Induction of ischemic stroke in awake freely moving mice reveals that isoflurane anesthesia can mask the benefits of a neuroprotection therapy.

Anesthetics such as isoflurane are commonly used to sedate experimental animals during the induction of stroke. Since these agents are known to modulate synaptic excitability, inflammation and blood flow, they could hinder the development and discovery of new neuroprotection therapies. To address this issue, we developed a protocol for inducing photothrombotic occlusion of cerebral vessels in fully conscious mice and tested two potential neuroprotectant drugs (a GluN2B or α4ß2 nicotinic receptor antagonist). Our data show in vehicle treated mice that just 20 min of exposure to isoflurane during stroke induction can significantly reduce ischemic cortical damage relative to mice that were awake during stroke. When comparing potential stroke therapies, none provided any level of neuroprotection if the stroke was induced with anesthesia. However, if mice were fully conscious during stroke, the α4ß2 nicotinic receptor antagonist reduced ischemic damage by 23% relative to vehicle treated controls, whereas the GluN2B antagonist had no significant effect. These results suggest that isoflurane anesthesia can occlude the benefits of certain stroke treatments and warrant caution when using anesthetics for pre-clinical testing of neuroprotective agents.