A standardized elderberry extract, Sambucol (SAM), reduced hemagglutination and inhibited replication of human influenza viruses type A/Shangdong 9/93 (H3N2), A/Beijing 32/92 (H3N2), A/Texas 36/91 (H1N1), A/Singapore 6/86 (H1N1), type B/Panama 45/90, B/Yamagata 16/88, B/Ann Arbor 1/86, and of animal strains from Northern European swine and turkeys, A/Sw/Ger 2/81, A/Tur/Ger 3/91, and A/Sw/Ger 8533/91 in Madin-Darby canine kidney cells. A placebo-controlled, double blind study was carried out on a group of individuals living in an agricultural community (kibbutz) during an outbreak of influenza B/Panama in 1993. Fever, feeling of improvement, and complete cure were recorded during 6 days. Sera obtained in the acute and convalescent phases were tested for the presence of antibodies to influenza A, B, respiratory syncytial, and adenoviruses. Convalescent phase serologies showed higher mean and mean geometric hemagglutination inhibition (HI) titers to influenza B in the group treated with SAM than in the control group. A significant improvement of the symptoms, including fever, was seen in 93.3% of the cases in the SAM-treated group within 2 days, whereas in the control group 91.7% of the patients showed an improvement within 6 days (p < 0.001). A complete cure was achieved within 2 to 3 days in nearly 90% of the SAM-treated group and within at least 6 days in the placebo group (p < 0.001). No satisfactory medication to cure influenza type A and B is available. Considering the efficacy of the extract in vitro on all strains of influenza virus tested, the clinical results, its low cost, and absence of side-effects, this preparation could offer a possibility for safe treatment for influenza A and B.

BackgroundAdenosine levels rise during inflammation and modulate inflammatory responses by engaging with four different G protein-coupled receptors. It is suggested that adenosine exhibits pro-inflammatory effects through its A1 receptor (A1R), and anti-inflammatory effects through A2A receptor (A2AR). Therefore, understanding of the mechanisms that govern adenosine receptor regulation may advance treatment of various inflammatory disorders. We previously reported that peak A1R expression during leukocyte recruitment, is followed by a peak in A2AR during inflammation resolution.Principal FindingsHere, we examined whether A1R activation sequentially induces A2AR expression and by this reverses inflammation. The effect of adenosine on A1R mediated A2AR expression was examined in peritoneal macrophages (PMΦ) and primary peritoneal mesothelial cells (PMC) in vitro. Induction of A2AR was inhibited by pertussis toxin (PTX) and partly dependent on A2AR stimulation. Administration of A1R agonists to healthy mice reduced A1R expression and induced A2AR production in PMC. Mice that were preconditioned with A1R agonists 24 hours before E. coli inoculation exhibited decreased TNFα and IL-6 sera levels and reduced leukocytes recruitment. Preconditioning was blocked by pretreatment with A1R antagonist, as well as, or by late treatment with A2AR antagonist, and was absent in A2AR−/− mice.ConclusionsOur data suggest that preconditioning by an A1R-agonist promotes the resolution of inflammation by inducing the production of A2AR. Future implications may include early treatment during inflammatory disorders or pretreatment before anticipated high risk inflammatory events, such as invasive surgery and organ transplantation.

Objectives Although several works in the past have examined the effect of haemodialysis (HD) on intraocular pressure (IOP), reported findings, theories, and conclusions are very different. The objectives of this article are to resume the reported evidence of IOP changes during HD, to review the proposed hypothesis of HD influence on IOP, and to determine if ophthalmic examination is imperative in HD patients. Methods We analysed the peer-reviewed English literature and selected all possible relevant articles. Results The influence of HD on IOP is not clear, and even in recent studies opposite findings can be found. Conclusions Future studies are needed to clarify the effects of HD on IOP. In patients with glaucoma or with predisposed narrow angles, or eyes with impaired aqueous outflow, the possibility of acute IOP rise during HD could be much more frequent than in normal patients. So in these patients, a more strict ophthalmic scheduled examination seems to be feasible.

The current data suggest that the sepsis-protective antiinflammatory effects of ketamine are mediated by the release of adenosine acting through the A2A receptor.

Post-dialysis CFD level is an independent predictor of all-cause mortality in patients undergoing HD. We propose that CFD detection is an inexpensive applicable tool for identifying patients at risk and their follow-up.

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Interleukin (IL)-15 serves as a survival factor for a broad array of cells. Renal cells express both IL-15 and its receptor (IL-15R); however, the role of IL-15 in the kidney is yet to be determined. We examined IL-15 and IL-15R levels in sepsis-related renal injury, ischemia-reperfusion injury (IRI), and cisplatin-induced nephrotoxicity. To test the anti-apoptotic effect of IL-15, Bcl-2/Bax mRNA levels were assessed in kidneys of IL-15Ralpha(-/-) mice and in IL-15-stimulated renal epithelial cells (RECs). In addition, RECs were exposed to cisplatin and apoptosis was evaluated by TUNEL staining, caspase-3 activity, and cell cycle analysis. Intrarenal IL-15 levels decreased 24 h after initiation of all three examined pathologies by 5.8-fold (sepsis), 11-fold (IRI), and 23-fold (cisplatin-induced nephrotoxicity). Further experiments revealed that while addition of rIL-15 (1 ng/mL) to wild-type (WT) RECs increased Bcl-2/Bax ratio by 2-fold, kidneys of IL-15Ralpha(-/-) mice exhibited 4-fold lower Bcl-2/Bax ratio compared to WT mice. Accordingly, IL-15 lowered the apoptotic rate in cisplatin-treated cultured REC, and IL-15Ralpha(-/-) renal cells exhibited a higher rate of cisplatin-induced apoptosis. Furthermore, IL-15 levels negatively correlated with BUN of cisplatin-treated mice (R = -0.69, P = 0.003), suggesting that a decline in renal-derived IL-15 is detrimental to renal cell survival and kidney function during pathological stress.

We describe four patients who developed an encephalopathic syndrome characterized by obtundation or stupor, myoclonic jerks, and asterixis in association with cefuroxime therapy. Three patients had renal failure. These cases suggest that cefuroxime in overdose or in conventional doses in patients with renal failure can cause a reversible encephalopathy. This syndrome may have been unrecognized because it usually occurs in severely ill patients with additional causes for encephalopathy.