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Back pain is a common health complaint that contributes globally to medical burden and costs, particularly in elderly populations. Nuclear medicine techniques using PET tracers offer diagnostic information about various spine disorders, including malignant, degenerative, inflammatory, and infectious diseases. Herein, the authors briefly review applications of PET in the evaluation of spine disorders in elderly patients.

In recent years, radiologic imaging has undergone tremendous technological advances and is now a pillar of diagnostic and treatment algorithms in clinical medicine. The increased complexity and volume of medical imaging has led clinicians to become ever more reliant on radiologists to both identify and interpret patient studies. A radiologist’s report provides key insights into a patient’s immediate state of health, information that is vital when choosing the most appropriate next steps in management. As errors in imaging interpretation or miscommunication of results can greatly impair patient care, identifying common error sources is vital to minimizing their occurrence. Although mistakes in medical imaging are practically inevitable, changes to the delivery of imaging reporting and the addition of artificial intelligence algorithms to analyze clinicians’ communication skills can minimize the impact of these errors, keep up with the continuously evolving landscape of medical imaging, and ultimately close the communication gap.

Immune challenge of invading macrophages at sites of infection is associated with release of TNF, which triggers a local cytokine storm as part of the normal inflammatory response. Whereas this response maybe beneficial in fighting off infections, similar responses triggered in autoimmune diseases contribute significantly to the underlying damaging pathology associated with these diseases. Here we show that Takinib, a highly discriminatory inhibitor of transforming growth factor Beta-activated kinase 1 (TAK1), selectively and potently reduces TNF production in pro-inflammatory THP-1 macrophages. A complete survey of 110 cytokines, showed robust loss of proinflammatory cytokine responsiveness to lipopolysaccharide (LPS) and interferon gamma (IFNg) challenge in response to Takinib. The mechanisms of action of Takinib was recapitulated in TAK1 KO macrophages. TAK1 KO cells showed significant loss of TNF production as well as release of IL-6 in response to LPS challenge. Furthermore, Takinib blocked the ability of exogenously added LPS to promote phosphorylation of, c-Jun, p38 protein kinases as well as downstream transcription factors regulated by nuclear factor κ-light-chain-enhancer of activated B cells (NFκB). In a mouse LPS challenge model, Takinib significantly reduced TNF serum levels. Our findings demonstrate that Takinib has utility in the treatment inflammatory disease by locally suppressing TNF production from invading macrophages.