Disseminated trichosporonosis with atypical histologic findings in a patient with acute lymphocytic leukemia

We report a case of disseminated Trichosporon asahii in a patient on systemic antifungal therapy who presented with multiple cutaneous nodules suggestive of fungal infection. Histologic features resembled neutrophilic eccrine hidradenitis but staining with periodic acid‐Schiff and Gomori methenamine silver confirmed the clinical diagnosis. This case highlights the importance of maintaining suspicion for trichosporonosis and contextualizing histologic findings within the underlying clinical picture.     

A cut above the rest: Trimming as a painless depilatory

Shaving and other modes of epilation can cause undue anxiety, pain, or skin irritation in children. Here, we present hair trimming as a safe, painless, and cost‐effective alternative for patients with unwanted hair which may be performed indefinitely or until the child is old enough to direct management. In select cases, removing unwanted hair using this technique may facilitate dermatologic surveillance.     

Opioid, 5-HT1A and alpha 2 receptors localized to subsets of guinea-pig myenteric neurons.

The expression of mu opioid, alpha 2 and 5-hydroxytryptamine1A (5-HT1A) receptors on guinea-pig myenteric neurons was determined using receptor selective agonists during intracellular recordings in vitro. Agonists known to hyperpolarize myenteric neurons by increasing potassium conductance were tested: noradrenaline and UK 14304 (alpha 2 agonists); 5-HT, 8-hydroxydipropylaminotetralin, 5-carboxamidotryptamine (5-HT1A agonists); normorphine, [Met5]-enkephalin and D-Ala2-Phe4, Gly-ol5 enkephalin (mu agonists). The alpha 2 agonists hyperpolarized 46/67 AH cells; mu agonists hyperpolarized 11/66 AH cells and 5-HT1A agonists inhibited 28/57 AH cells. Hyperpolarizations to both alpha 2 and mu agonists were observed in 11/59 AH cells; hyperpolarizations to both alpha 2 and 5-HT1A agonists were observed in 23/49 AH cells. Hyperpolarizations mediated at alpha 2 receptors were observed in 11/54 S neurons and mu agonists hyperpolarized 17/45 S cells. alpha 2 and mu receptors were localized together on 10/43 S cells tested with receptor selective agonists. 5-HT1A-mediated hyperpolarizations were not observed in 36 S cells. Presynaptic inhibition of fast excitatory post-synaptic potentials (fast e.p.s.p.s., S neurons) was observed in all cells tested with alpha 2 agonists (n = 32); in 14/23 cells tested with 5-HT1A agonists and in 8/22 cells tested with mu agonists. Both alpha 2 and 5-HT1A agonists inhibited fast e.p.s.p.s in 15/23 cells, while alpha 2 and mu agonists both inhibited the fast e.p.s.p. in 8/21 cells. Inhibition of fast e.p.s.p.s by mu and 5-HT1A agonists occurred together in 2/19 cells. Slow non-cholinergic e.p.s.p.s were inhibited by alpha 2 agonists in 19/19 cells and by 5-HT1A agonists in 19/21 cells. alpha 2- and 5-HT1A-mediated inhibition of slow e.p.s.p.s occurred together in 12/14 cells. These data allow AH neurons to be divided into two groups: those expressing alpha 2 and 5-HT1A receptors and those expressing alpha 2 and mu receptors. alpha 2 and mu receptors coexist on S neurons which do not express 5-HT1A receptors. Terminals that release acetylcholine express either alpha 2 and mu or alpha 2 and 5-HT1A receptors, consistent with the idea that they are provided by AH cells. Terminals that release mediators of the slow e.p.s.p. express primarily alpha 2 and 5-HT1A receptors.     

Protection of early phase hepatic ischemia-reperfusion injury by cholinergic agonists

Background  

Cytokine production is critical in ischemia/reperfusion (IR) injury. Acetylcholine binds to macrophages and inhibits cytokine synthesis, through the cholinergic anti-inflammatory pathway. This study examined the role of the cholinergic pathway in cytokine production and hepatic IR- injury.