Indurated Plaque with Bullae Formation on the Left Arm.

A 72-year-old white man presented to the clinic with a tender, pruritic lesion on the upper part of his left arm that had progressively worsened over 4 months. Physical examination revealed an erythematous to violaceous, indurated, and sclerotic plaque with multiple foci of crusting and erosions (Figure 1). The patient denied any recent trauma, travel, fever, chills, weight loss, or constitutional symptoms.

Advanced Management of Severe Keloids.

Keloids negatively impact the health and quality of life of many affected dermatologic patients. Treating keloids is often difficult, and suboptimal responses are frequent. Fortunately, there are many treatment options available to the clinician that may lead to improved clinical outcomes.

A case of rupioid syphilis masquerading as aggressive cutaneous lymphoma.

Secondary syphilis has been known since the late 19th century as the great imitator; however, some experts now regard cutaneous lymphoma as the great imitator of skin disease. Either disease, at times an equally fastidious diagnosis, has reported to mimic each other even. It is thus vital to consider these possibilities when presented with a patient demonstrating peculiar skin lesions.

Mucinous carcinoma: a translucent blue papule on an 89-year-old man.

An 89-year-old man with no significant medical history presented with a slow-growing, asymptomatic translucent blue mass noticed 1 year prior to evaluation. Review of symptoms was negative for constitutional symptoms, gastrointestinal (GI) disturbance, and visual complaints. Physical evaluation revealed a 4-mm firm light blue translucent papule on the left medial canthus (Figure 1).

Practice trends in the treatment of actinic keratosis in the United States: 0.5% fluorouracil and combination cryotherapy plus fluorouracil are underused despite evidence of benefit.

Background: Topical fluorouracil and cryotherapy are among the most commonly used treatments for actinic keratosis. Evidence shows that 0.5% fluorouracil has similar efficacy and is better tolerated than 5% fluorouracil.

Eicosanoid signaling and vascular dysfunction: methylmercury-induced phospholipase D activation in vascular endothelial cells.

Mercury, especially methylmercury (MeHg), is implicated in the etiology of cardiovascular diseases. Earlier, we have reported that MeHg induces phospholipase D (PLD) activation through oxidative stress and thiol-redox alteration. Hence, we investigated the mechanism of the MeHg-induced PLD activation through the upstream regulation by phospholipase A2 (PLA2) and lipid oxygenases such as cyclooxygenase (COX) and lipoxygenase (LOX) in the bovine pulmonary artery endothelial cells (BPAECs).

Calcium and calmodulin regulate mercury-induced phospholipase D activation in vascular endothelial cells.

Earlier, we reported that mercury, the environmental risk factor for cardiovascular diseases, activates vascular endothelial cell (EC) phospholipase D (PLD). Here, we report the novel and significant finding that calcium and calmodulin regulated mercury-induced PLD activation in bovine pulmonary artery ECs (BPAECs). Mercury (mercury chloride, 25 microM; thimerosal, 25 microM; methylmercury, 10 microM) significantly activated PLD in BPAECs.

Phospholipase A2 activation regulates cytotoxicity of methylmercury in vascular endothelial cells.

Mercury has been identified as a risk factor for cardiovascular disease among humans. Through diet, mainly fish consumption, humans are exposed to methylmercury, the biomethylated organic form of environmental mercury. As the endothelium is an important player in homeostasis of the cardiovascular system, here, the authors tested their hypothesis that methylmercury activates the lipid signaling enzyme phospholipase A(2) (PLA(2)) in vascular endothelial cells (ECs), causing upstream regulation of cytotoxicity.

Mercury activates vascular endothelial cell phospholipase D through thiols and oxidative stress.

Currently, mercury has been identified as a risk factor of cardiovascular diseases among humans. Here, the authors tested the hypothesis that mercury modulates the activity of the endothelial lipid signaling enzyme, phospholipase D (PLD), which is an important player in the endothelial cell (EC) barrier functions. Monolayers of bovine pulmonary artery ECs (BPAECs) in culture, following labeling of membrane phospholipids with [32P]orthophosphate, were exposed to mercuric chloride (inorganic form), methylmercury chloride (environmental form), and thimerosal (pharmaceutical form), and the formation of phosphatidylbutanol as an index of PLD activity was determined by thin-layer chromatography and liquid scintillation counting.