Katelyn E. Sadler

The paper shows that antibiotics like β-lactams, macrolides, and tetracyclines alter calcium flux in DRG neurons through mechanisms involving extracellular calcium, TRPA1, and mitochondrial ROS.

This study shows that minocycline reduces chronic pain in male sickle cell disease mice via microglia and microbiome changes, but not in females.

The paper develops a 3D agent-based model of the bilateral central amygdala to predict pain outcomes by integrating neuronal data from CGRPR and PKCδ cells.

The paper identifies an adipose-complement-lipid axis that systemically regulates sensory neuron sensitization, explaining pain-structure discordance in obesity-associated osteoarthritis.

This study identifies transcriptomic signatures in GBS patients that reveal leukocyte interactions with peripheral nerves and pain pathways, suggesting therapeutic targets for neuropathic pain.

This paper introduces a method to preserve human dorsal root ganglion neurons using Hibernate media, enabling easier access and transport for research.

This study shows that lifelong hydroxyurea treatment reduces chronic pain in sickle cell disease mice by decreasing immune activity and reversing TRPA1 sensitization.

This study shows that vaginal microbiome dysbiosis in endometriosis mice causes pain, which can be reversed by antibiotics or microbiome transplants from healthy animals.

The paper shows that keratinocyte Piezo1 contributes to paclitaxel-induced mechanical hypersensitivity by sensitizing keratinocytes to mechanical stimulation.

The paper identifies gut microbiota and metabolites as drivers of chronic sickle cell disease pain by altering vagus nerve activity.

This study identifies Piezo1 as the major mechanotransducer in keratinocytes for detecting mechanical stimuli and transmitting tactile information to sensory neurons.

This study investigates sex-based differences in endogenous opioid engagement during contextual control of pain tolerance and expectation in mice.

This study identifies TRPC5 as a mediator of inflammatory mechanical pain using knockout mice and pharmacological inhibitors, showing its role in pain behaviors induced by lysophosphatidylcholine.

This study shows keratinocytes are essential for normal cold and heat sensation in mammals through calcium release and ATP-P2X4 signaling.