Rapunzel syndrome is a rare presentation of a trichobezoar, with 24 cases having been reported in literature so far. This syndrome has been reported in 23 female and 1 male patient with a mean age of 10.8 years. The patients commonly present with abdominal pain, nausea, vomiting and signs of obstruction. The distal end of the bezoar may be in the jejunum, ileum or the colon. We evaluate the various cases reported and discuss the various modes of presentation of this uncommon syndrome, and also present a series of 3 cases, all females, aged 16, 18 and 21 years, and had a trichobezoar in the stomach with a tail extending into the ileum.

Objective-The aim of this study was to determine the effects of oxidized versus native omega-3 fatty acids on the endothelial expression of chemokines MCP-1 and IL-8, and, if effective in inhibiting chemokine expression, to determine the mechanism for the inhibition of chemokine expression. Methods and Results-Using enzyme-linked immunosorbent assays, we show that oxidized EPA and DHA but not unoxidized EPA or DHA inhibit cytokine-induced endothelial expression of monocyte chemoattractant protein (MCP)-1 and, to a lesser extent, IL-8. In electrophoretic mobility shift assays, oxidized EPA but not unoxidized EPA potently inhibited cytokine-induced activation of endothelial nuclear factor-B (NF-B). Using Western blot analyses, we show that the inhibition of NF-B activation was not caused by prevention of phosphorylation of I B␣ because oxidized EPA did not inhibit cytokine-induced phosphorylation and ubiquination of I B␣. Furthermore, oxidized EPA inhibited NF-B activation in endothelial cells derived from wild-type mice but had no inhibitory effects on NF-B activation in endothelial cells derived from peroxisome proliferator-activated receptor ␣ (PPAR␣)-deficient mice, indicating that oxidized EPA requires PPAR␣ for its inhibitory effects on NF-B. Conclusions-These studies show that the antiinflammatory effects of fish oil may result from the inhibitory effects of oxidized omega-3 fatty acids on NF-B activation via a PPAR␣-dependent pathway. (Arterioscler Thromb Vasc Biol. 2004;24:1621-1627.)Key Words: monocyte chemoattractant protein-1 Ⅲ oxidized omega-3 fatty acids Ⅲ oxidized eicosapentaenoic acid Ⅲ nuclear factor-B Ⅲ PPARa C onsumption of marine fish oil has been reported to improve the prognosis of several chronic inflammatory diseases characterized by leukocyte accumulation and leukocyte-mediated tissue injury, including atherosclerosis, IgA nephropathy, inflammatory bowel disease, rheumatoid arthritis, etc. [1][2][3][4] These beneficial effects of fish oil have been associated with the omega-3 polyunsaturated fatty acids (PUFAs), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA), which are abundant in marine fish oil.EPA and DHA are highly polyunsaturated and easily undergo auto-oxidation. 5,6 In fact, it is very difficult to avoid the oxidation of these very labile fatty acids. More importantly, in vivo, a large increase in tissue and plasma accumulation of both omega-3 fatty acids and fatty acid oxidation products is noted in subjects consuming fish oil, even after addition of antioxidant supplements to the diet. [7][8][9][10] This suggests the possibility that oxidized omega-3 fatty acids may be an important component of the observed antiinflammatory effects of fish oil. Indeed, our previous studies have shown that oxidized EPA, and not unoxidized EPA, potently inhibits leukocyte-endothelial interactions, both in vitro and in vivo, through a peroxisome proliferator-activated receptor (PPAR)␣-dependent mechanism. 11,12 One of the early events in inflammation is the upregulation of endothelial ch...

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Increasing evidence suggests that cardiac pacemaking is the result of two sinoatrial node (SAN) cell mechanisms: a 'voltage clock' and a Ca 2+ dependent process, or 'Ca 2+ clock.' The voltage clock initiates action potentials (APs) by SAN cell membrane potential depolarization from inward currents, of which the pacemaker current (I f ) is thought to be particularly important. A Ca 2+ dependent process triggers APs when sarcoplasmic reticulum (SR) Ca 2+ release activates inward current carried by the forward mode of the electrogenic Na + /Ca 2+ exchanger (NCX). However, these mechanisms have mostly been defined in rodents or rabbits, but are unexplored in single SAN cells from larger animals. Here, we used patch-clamp and confocal microscope techniques to explore the roles of the voltage and Ca 2+ clock mechanisms in canine SAN pacemaker cells. We found that ZD7288, a selective I f antagonist, significantly reduced basal automaticity and induced irregular, arrhythmia-like activity in canine SAN cells. In addition, ZD7288 impaired but did not eliminate the SAN cell rate acceleration by isoproterenol. In contrast, ryanodine significantly reduced the SAN cell acceleration by isoproterenol, while ryanodine reduction of basal automaticity was modest (∼14%) and did not reach statistical significance. Importantly, pretreatment with ryanodine eliminated SR Ca 2+ release, but did not affect basal or isoproterenol-enhanced I f . Taken together, these results indicate that voltage and Ca 2+ dependent automaticity mechanisms coexist in canine SAN cells, and suggest I f and SR Ca 2+ release cooperate to determine baseline and catecholaminedependent automaticity in isolated dog SAN cells.

Background Catecholamines increase heart rate by augmenting the cAMP responsive HCN4 ‘pacemaker current’ (If) and/or by promoting inward Na+/Ca2+ exchanger current (INCX), by a ‘Ca2+ clock’ mechanism in sinoatrial nodal cells (SANCs). The importance, identity and function of signals that connect If and Ca2+ clock mechanisms are uncertain and controversial, but the multifunctional Ca2+ and calmodulin-dependent protein kinase II (CaMKII) is required for physiological heart rate responses to β-adrenergic receptor (β-AR) stimulation. The aim of this stuy is to measure the contribution of the Ca2+ clock and CaMKII to cardiac pacing independent of β-AR agonist stimulation. Methods and Results We used the L-type Ca2+ channel agonist BayK 8644 (BayK) to activate the SANC Ca2+ clock. BayK and isoproterenol were similarly effective in increasing rates in SANCs and Langendorff-perfused hearts from WT control mice. In contrast, SANCs and isolated hearts from mice with CaMKII inhibition by transgenic expression of an inhibitory peptide (AC3-I) were resistant to rate increases by BayK. BayK only activated CaMKII in control SANCs, but increased ICa equally in all SANCs, indicating that increasing ICa was insufficient and suggesting CaMKII activation was required for heart rate increases by BayK. BayK did not increase If or protein kinase A (PKA)-dependent phosphorylation of phospholamban (at Ser16), indicating that increased SANC Ca2+ by BayK did not augment cAMP/PKA signaling at these targets. Late diastolic intracellular Ca2+ release and INCX were significantly reduced in AC3-I SANCs and the response to BayK was eliminated by ryanodine in all groups. Conclusions The Ca2+ clock is capable of supporting physiological fight or flight responses, independent of β-AR stimulation or If increases. Complete Ca2+ clock and β-AR stimulation responses require CaMKII.