Homer proteins are integral to the assembly of proteins regulating glutamate signaling and synaptic plasticity. Constitutive Homer2 gene deletion [knock-out (KO)] and rescue with adeno-associated viral (AAV) transfection of Homer2b was used to demonstrate the importance of Homer proteins in neuroplasticity produced by repeated ethanol (EtOH) administration. Homer2 KO mice avoided drinking high concentrations of EtOH and did not develop place preference or locomotor sensitization after repeated EtOH administration. The deficient behavioral plasticity to EtOH after Homer2 deletion was paralleled by a lack of augmentation in the rise in extracellular dopamine and glutamate elicited by repeated EtOH injections. The genotypic differences in EtOH-induced change in behavior and neurochemistry were essentially reversed by AAV-mediated transfection of Homer2b into accumbens cells including, differences in EtOH preference, locomotor sensitization, and EtOH-induced elevations in extracellular glutamate and dopamine. These data demonstrate a necessary and active role for accumbens Homer2 expression in regulating EtOH-induced behavioral and cellular neuroplasticity.
We report a case of azathioprine hypersensitivity syndrome and review the literature on azathioprine-induced eruptions with features of Sweet syndrome. Our patient's distribution of lesions on the extremities and the finding of suppurative folliculitis on histopathology were not classical for Sweet syndrome. Azathioprine hypersensitivity syndrome seems to be a neutrophil-driven dermatosis; therefore, many overlapping features with Sweet syndrome are not surprising. Due to the potential for anaphylaxis with azathioprine rechallenge, a better term for a Sweetlike presentation in the setting of azathioprine administration is azathioprine hypersensitivity syndrome.
Primary cutaneous inoculation blastomycosis occurs less commonly than secondary blastomycosis, in which cutaneous lesions most often originate from a primary pulmonary infection which disseminates through the blood or lymphatics to involve the skin. In secondary cutaneous blastomycosis, the primary pulmonary infection is frequently subclinical at the time cutaneous lesions manifest. Here we report two cases that illustrate the difficulty in distinguishing between primary and secondary cutaneous involvement. We also review the expanding literature on blastomycosis since its identification over a century ago.
We found no significant difference in p16 staining in Spitz nevi and Spitzoid melanomas. We conclude that p16 does not appear to be a useful immunohistochemical marker in distinguishing between Spitz nevi and Spitzoid melanomas.
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