Abstract. Lipoxins are endogenous lipoxygenase-derived eicosanoids, generated during inflammatory, hypersensitivity, and vascular events, that display vasodilatory, antiinflammatory, and pro-resolution activity. Here, we evaluated the efficacy of 15-epi-16-(para-fluorophenoxy)-lipoxin A 4 -methyl ester (15-epi-16-(FPhO)-LXA 4 -Me), a stable synthetic analogue of aspirin-triggered 15-epi-lipoxin A 4 in ischemic acute renal failure (ARF) in NIH Swiss mice. ARF was induced by 30-min crossclamping of renal pedicles and was associated with elevated serum creatinine, morphologic injury, polymorphonuclear leukocyte (PMN) recruitment, and increased mRNA lev- with lower IL-1␤, IL-6, and GRO1 mRNA levels, whereas ICAM-1 and VCAM-1 mRNA levels were unchanged. Compatible with these results, LXA 4 blunted chemoattractant-stimulated PMN migration across HK-2 renal epithelial cell monolayers in vitro, but it did not inhibit cytokine-induced HK-2 ICAM-1 expression or adhesiveness for PMN. Interestingly 15-epi-16-(FPhO)-LXA 4 -Me-treated animals also displayed increased renal mRNA levels for suppressors of cytokine signaling-1 (SOCS-1) and SOCS-2, but not CIS-1, endogenous inhibitors of cytokine-elicited Jak/Stat-signaling pathways. These results indicate that 15-epi-16-(FPhO)-LXA 4 -Me is protective in renal ischemia reperfusion injury in vivo, at least partially by modulating cytokine and chemokine expression and PMN recruitment, and provides a rationale for further exploration of the efficacy of LXA 4 structural analogues in ischemic ARF and other renal diseases.Ischemic acute renal failure (ARF) remains a formidable clinical problem for which there is no specific treatment (1). The pathophysiology of ARF is multifaceted and includes persistent intrarenal vasoconstriction, hypoxic tubule epithelial cell injury, and polymorphonuclear leukocyte (PMN)-mediated cytotoxicity upon reperfusion (1,2). Despite the impressive efficacy of agents that specifically target these processes in experimental models, none has proved effective in randomized controlled clinical trials (1). These disappointing results have shifted attention toward regimens that simultaneously target two or more of the aforementioned pathophysiologic events.Lipoxins (LX) are lipoxygenase-derived arachidonate metabolites that are generated in a variety of human and experimental inflammatory, hypersensitivity, and vascular diseases (reviewed in references 3-5). They are generated principally by transcellular routes during cell-cell interactions by biosynthetic pathways initiated through the action of two lipoxygenDr. Martin O. Leonard and Dr. Kieran Hannan contributed equally to this work.

Introduction: Pericardial cysts occur rarely with an incidence rate of 1 per 100,000. They are usually detected by chance and are clinically silent in most cases.

Most symptoms of Gulf War Illness (GWI) are similar to Chronic Fatigue Syndrome (CFS) and/or Fibromyalgia (FM). We investigated whether these symptoms are associated with an activated coagulation system as has been reported in some cases of CFS/FM. The coagulation assays include activation markers of the cascade, platelet activation and hereditary risk factors. Our findings show activation of the coagulation system in GWI. This evidence of a hypercoagulable state suggests that symptoms may be due to poor blood flow and, therefore, a basis for the potential utility of anticoagulant therapy.

Introduction:The standard low-phosphorus diet restricts pulses, nuts, and whole grains and other high phosphorus foods to control hyperphosphatemia. We conducted a randomized controlled trial to evaluate the effectiveness, safety, and tolerability of the modified diet, which introduced some pulses and nuts, increased the use of whole grains, increased focus on the avoidance of phosphate additives, and introduced the prescription of low-biological-value protein such as bread.Methods: We conducted a multicenter, pragmatic, parallel-arm, open-label, randomized controlled trial of modified versus standard diet in 74 adults on hemodialysis with hyperphosphatemia over 1 month. Biochemistry was assessed using monthly laboratory tests. Dietary intake was assessed using a 2-day record of weighed intake of food, and tolerability was assessed using a patient questionnaire.Results: There was no significant difference in the change in serum phosphate between the standard and modified diets. Although total dietary phosphorus intake was similar, phytate-bound phosphorus, found in pulses, nuts, and whole grains, was significantly higher in the modified diet (P < 0.001). Dietary fiber intake was also significantly higher (P < 0.003), as was the percentage of patients reporting an increase in bowel movements while following the modified diet (P ¼ 0.008). There was no significant difference in the change in serum potassium or in reported protein intake between the 2 diets. Both diets were similarly well tolerated. Conclusion:The modified low phosphorus diet was well tolerated and was associated with similar phosphate and potassium control but with a wider food choice and greater fiber intake than the standard diet.