Check out my favorite professor Dr. Rennaker's new biotech study! His team’s clinical study showed that patients with treatment resistant PTSD who underwent standard therapy plus an implanted device that stimulates the Vagus nerve experienced complete loss of diagnosis up to six months later. That alone is astounding — PTSD often persists for life in many people, but here was a method showing actual remission in a small cohort. What’s extraordinary, in their Phase 1 trial of nine participants who had failed previous PTSD treatments, all nine lost their PTSD diagnosis and stayed symptom free for at least six months afterward. 

The system, called the ReStore System, comprises three primary parts, a very small implanted stimulator that sits on the vagus nerve in the neck, an external PCM that the patient wears in a neck band for control and power, and a smartphone app that programs and triggers the stimulator. During each therapy session the device delivers short bursts of electrical stimulation in sync with the exposure therapy work. The idea is that the vagus stimulation opens a window of neuroplasticity which makes the exposure therapy more effective. The technology enables the clinician to coordinate the psychological therapy with the stimulation, thereby leveraging the brain’s own “learning” machinery at the right moment.

In short, this is not just therapy plus device, but therapy amplified by technology designed to piggy back on the body’s natural plasticity. It really underscores how engineering, neuroscience, and clinical practice can converge. For someone like me who’s exploring biomedical applications and neurobiology, it’s a perfect example of translational science where the tech doesn’t just assist, it changes the game.

Dr. Porter’s presentation left me genuinely amazed at how far biomedical engineering has come and how creative science can be when two fields collide. Using lipid coated nanoemulsions that can vaporize into bubbles to target and destroy tumors more efficiently. Turning superheated liquid droplets into on demand bubble generators that amplify ultrasound’s heating effect. The fact that his team was able to triple the thermal dose and achieve tumor ablation at less than half the usual power is mind blowing. Even more impressive is that these droplets had the property of only vaporizing at the tumor site, completely avoiding damage to surrounding brain tissue. That kind of precision feels like science fiction becoming reality.

Dr. Porter’s finding that cavitation triggers the release of calreticulin, a molecule tied to immune activation, was especially exciting because it connects physical therapy with immunotherapy. His research is a great mechanism for target specific pharmacology and BBB modification. It’s fascinating to think one nanoparticle platform could bridge diagnostics, treatment, and immune response. His explanation of J aggregated ICG liposomes show how those molecular details can directly translate into medical innovation, it’s all about solving problems that once seemed impossible. 

In her dissertation proposal, Moreno presented fascinating research on how nociceptors differ across species. She focused on three key genes: TRPA1, TRPV1, and NTRK1, which are involved in nociception, chemoreception, and nerve growth regulation. Moreno found that mice express the TRPA1 gene much more than humans, while humans show higher expression of TRPV1, the heat sensing ion channel. From this, she proposed that TRPA1 likely evolved first to detect harmful stimuli, while TRPV1 later specialized in heat detection through gene duplication. Her research also looked at NTRK1, a gene essential for nerve growth and pain signaling, and how its regulation differs between species like humans, mice, and pigs. Using tools like RNA sequencing and computational modeling, she aims to uncover how these genes’ regulatory networks evolved and what that might mean for sensory function.  

I found Moreno’s work particularly compelling because it bridges evolutionary neurobiology with molecular genetics, areas often studied in isolation. Her focus on chromatin accessibility and transcription factor binding divergence reflects the growing importance of epigenetic regulation in comparative genomics. The discussion of NTRK1 as a direct transcriptional and epigenetic target of IL-3, regulated by EGR1, reinforced how gene environment interactions shape neuronal phenotypes. While I am curious about the clinical translational potential, particularly how interspecies nociceptor variation might inform human pain modulation, the evolutionary perspective she offers provides a valuable framework for understanding why certain pain mechanisms are conserved or lost across taxa. Overall, her proposal emphasized the importance of examining genetic and regulatory diversity to better contextualize human nociception within an evolutionary continuum.