Alpha-melanocyte-stimulating hormone protects against renal injury after ischemia in mice and rats.

Reperfusion after ischemia induces cytokines, chemoattractant chemokines, adhesion molecules, and nitric oxide (NO). The resultant neutrophil adherence and NO potentiates renal injury. alpha-Melanocyte-stimulating hormone (alpha-MSH) is a potent anti-inflammatory agent that inhibits neutrophil migration and production of neutrophil chemokines and NO. Since neutrophils and NO promote renal ischemic injury, we sought to determine if alpha-MSH inhibits renal injury in a model of bilateral renal ischemia. alpha-MSH significantly reduced ischemia-induced renal damage, measured by changes in renal histology and plasma blood urea nitrogen and creatinine in mice. alpha-MSH significantly decreased tubule necrosis, neutrophil plugging, and capillary congestion. Delay of alpha-MSH treatment for 6 h after ischemia also significantly inhibited renal damage. alpha-MSH also significantly inhibited ischemic damage in rats. To begin to determine the mechanism of action of alpha-MSH, we measured its effects on mediators of neutrophil trafficking and induction of the inducible isoform of NO synthase-II. alpha-MSH inhibited ischemia-induced increases in mRNA for the murine neutrophil chemokine KC/IL-8. alpha-MSH also inhibited induction of mRNA for the adhesion molecule ICAM-1, which is known to be critical in renal ischemic injury. alpha-MSH inhibited nitration of kidney proteins and induction of NO synthase-II. We conclude: (a) alpha-MSH protects against renal ischemia/reperfusion injury; and (b) it may act, in part, by inhibiting the maladaptive activation of genes that cause neutrophil activation and adhesion, and induction of NO synthase.     

Scanning electron microscopic observations of extracted terminal hair follicles of the adult human scalp and eyebrow with special references to the bulge area

Scanning electron microscopic studies of human terminal hair follicles of the scalp and eyebrow have previously been limited to the hair shaft. In this study we investigated EDTA-treated extracted whole hair follicles in which most of the basal cell surface of the outer root sheath was well preserved. In the bulge area of scalp follicles there were many knob-like or villous projections. These were located in some specimens on one side of the follicle, while in others they were located around the entire circumference of the follicle. These projections were thought to represent the anchoring points of the branched follicular end of the arrector muscles. Ring-like elevations with groove-like depressions above and below were also observed surrounding the entire follicle. These were thought to represent the track of circumfollicular arrector muscles which depressed the outer root sheath when they repeatedly contracted. Most anagen eyebrow follicles showed morphological variations in the bulge area such as lattice-window-like structures and undulation patterns. In telogen follicles, the bulge became indistinguishable from the clubbed end. The lower end of these telogen follicles showed irregularly shaped bulge areas, but did not show lattice-window-like structures or undulation patterns as observed in anagen follicles. Interestingly, a hole was found in some bulge areas of both anagen and telogen follicles. Serial vertical sections of follicles revealed invaginated areas, which seemed to correspond to the openings seen in whole mounts. In vertical sections of eyebrow follicles some keratinocytes of the outer root sheaths of the bulge area were seen to be melanized to various extents. This phenomen was independent of hair cycle phase.     

A unique case of extramammary Paget's disease. Derivation from eccrine porocarcinoma?

A unique case of extramammary Paget's disease is reported that may have derived from eccrine porocarcinoma. A palm-sized erythematous plaque on the patient's pubis spread to the lower abdominal wall. The center of the lesion contained a reddish tumor. Histologic findings of the erythematous plaque showed features of extra-mammary Paget's disease. Those of the reddish tumor, however, corresponded most closely to eccrine porocarcinoma, though we could not entirely rule out that the changes corresponded to larger nests of less differentiated Paget cells. The two distinct neoplastic areas showed continuity both clinically and histologically; our case differed from epidermotropic eccrine porocarcinoma in several clinicopathologic respects. Our case suggests the possibility that extramammary Paget's disease could arise from preexisting porocarcinoma.