Abstract
Methylphenidate (MPH) is an effective symptomatic treatment of attention deficit hyperactivity disorder (ADHD), but the mechanisms of its therapeutic action have not been fully elucidated. To address this issue, we assessed the effects of discontinuation of chronic MPH treatment on regional cerebral blood flow (rCBF) in ADHD patients. <b>Methods:</b> Twenty-two prepubescent boys with ADHD (age range, 8.2–11.5 y) and 7 healthy volunteers were studied with SPECT on and off MPH. Their rCBF data were automatically normalized to whole-brain counts and coregistered with standard anatomic space. rCBF changes were evaluated with statistical parametric mapping based on voxel-by-voxel ANOVA. <b>Results:</b> When the subjects were not taking MPH, rCBF was higher in the motor, premotor, and the anterior cingulate cortices (Brodmann’s areas 4, 6, and 32). <b>Conclusion:</b> Brief discontinuation of MPH treatment is associated with increased motor and anterior cingulate cortical activity. Our findings suggest that MPH treatment modulates motor and anterior cingulate cortical activity directly or indirectly. Alternatively, our findings may be related to MPH withdrawal. These data provide novel information on the potential mechanisms of the therapeutic action of MPH. Furthermore, they are clinically relevant to the commonly occurring brief interruptions in MPH treatment.
Highlights
Melanoma is currently the most lethal form of skin cancer
Most tumors lack significant immune infiltration prior to immune therapy, and immune therapies are hindered by a persistent lack of immune cell infiltration
Our studies found that melanoma express TLRs 2, 3, 4, 6, 7, and 9, but that without exogenous stimulation, melanoma cells produce few immune cell attracting chemokines
Summary
Melanoma is currently the most lethal form of skin cancer. Clinical efforts to combat melanoma have included approaches to induce the immune system, through T-cell directed therapies, to clear melanoma. TLR2/6 agonists and IFNg synergize to induce melanoma cells to produce T-cell recruiting chemokines From Society for Immunotherapy of Cancer 28th Annual Meeting National Harbor, MD, USA.
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