Libraries can make Open Access Happen Today by Simply Redirecting Subscription Funds: An Update on the SCOAP3 Initiative

This article reviews the SCOAP3 initiative which aims to redirect the subscription funds used for the core journals in High Energy Physics, to make them Open Access. This model re-interprets the role of librarians in the Open Access debate. As they are the pivot of the current system, by keeping the lifeblood of scientific information flowing to their scientists, the authors argue that they are the best placed to make it change and take advantage of it

Collect and survey: results of the EU project SOAP

Das EU-Projekt Study of Open Access Publishing (SOAP, http://soap-fp7.eu), das bis zum Deutschen Bibliothekartag in Berlin abgeschlossen sein wird, beschreibt und analysiert die Landschaft des Open Access-Publizierens. Projektpartner sind Verlage wie Biomed Central, Sage und Springer sowie Wissenschaftseinrichtungen wie CERN, MPG und STFC. In diesem Bericht wird ein Überblick über die Ansätze und Ergebnisse des Projekts gegeben. Der eine Hauptansatz des Projekts bestand in einer umfassenden Analyse bestehender Open Access-Publikationsmodelle auf Basis angereicherter Daten aus dem Directory of Open Access Journals (DOAJ). Dabei konnten neue Daten über die unterschiedlichen Einnahmequellen von Open Access-Zeitschriften gesammelt und Unterschiede zwischen großen und kleinen Verlagen und Fachgesellschaften aufgezeigt werden. Der zweite Hauptansatz des Projekts bestand in der Auswertung einer weltweiten Umfrage unter Wissenschaftlern zu deren Haltung zu Open Access. Rund 50.000 Wissenschaftler haben sich an dieser Umfrage beteiligt. Abgerundet wird das Projekt durch weitergehende Analysen zu der Frage, wie der Übergang zum Open Access-Publizieren organisiert werden könnte

The Effect of Hydroxyethyl Starches (HES 130/0.42 and HES 200/0.5) on Activated Renal Tubular Epithelial Cells

Background: Acute renal failure is a frequent complication of sepsis. Hydroxyethyl starch (HES) is widely used in the treatment of such patients. However, the effect of HES on renal function during sepsis remains controversial. We established an in vitro model of tumor necrosis factor-alpha (TNF-alpha)-stimulated human proximal tubular epithelial (HK-2) cells to assess the possible effects of HES 130/0.42 and HES 200/0.5 on these activated cells. Methods: HK-2 cells were stimulated with TNF-alpha in the presence or absence of HES 130/0.42 or 200/0.5. After 4, 10, and 18 h of incubation, monocyte chemoattractant protein-1 (MCP-1), a key chemoattractant for neutrophils and macrophages, was measured. In addition, viability and cytotoxicity assays were performed. Results: MCP-1 expression was doubled upon TNF-alpha exposure. In the presence of 2% and 4% HES 200/0.5 in 98% (96%) medium over a stimulation time period of 10 h and 18 h, the MCP-1 concentration was decreased between 26% and 56% (P < 0.05). TNF-alpha stimulation resulted in a significant decrease of viability by 53%-63%, whereas viability decreased by only 32%-40% in coincubation with HES 130/0.42 (P < 0.005) and remained even less affected by TNF-alpha in the presence of HES 200/0.5 (P < 0.001). The TNF-alpha-induced cell death rate was attenuated in the presence of HES 200/0.5 (P < 0.05). Conclusions: This in vitro study shows that both HES products modulate cell injury upon inflammatory stimulation. The effect was more pronounced in the HES 200/0.5 group than for HES 130/0.42, suggesting a possible biological difference between the HES types

Histochemical Study of the Progenetic Trematode Alloglossidium renale

A histochemical study of the progenetic trematode Alloglossidium renale has demonstrated the absence of any secreted material between the adult worm and the host (freshwater shrimp) antennal gland tubules. Host tissue is affected only by the compression, abrasion, and ingestion by the parasite, and host tubule cells near the worm have the same staining patterns as those distant from the parasite. The trematode sometimes dies within the host, leaving a necrotic mass whose histochemical staining differs significantly from the living organism. In the necrotic mass, the only recognizable features were the ova and the vitellarium, which atrophied and resulted in tyrosine-positive staining within the mass. A melanin reaction was not observed in the host using a specialized ferro-ferricyanide stain. The only apparent host response to infection was a layer of damaged squamous host cells adhering to the necrotic worm. The results confirm benign host-parasite effects and a highly evolved relationship between the host and parasite, perhaps bordering on commensalism

Role of chemokines and cytokines in a reactivation model of arthritis in rats induced by injection with streptococcal cell walls

Intraarticular injection of streptococcal cell wall (SCW) antigen followed by intravenous challenge results in a T cellâ mediated monoarticular arthritis in female Lewis rats. Initial studies showed that this reactivation response to intravenous SCW antigen is dependent on the presence of interleukinâ 1 (ILâ 1) and tumor necrosis factor α (TNFâ α) and that the early phase of swelling is neutrophilâ dependent. Neutrophil depletion or passive immunization with antibodies to Pâ selectin or macrophage inflammatory proteinâ 2 reduced the intensity of ankle edema and the influx of neutrophils. After the first few days, however, the arthritic response is mediated primarily by mononuclear cells. Joint tissues showed upâ regulation of mRNA for monocyte chemotactic proteinâ 1 (MCPâ 1), which could be inhibited in part by antiâ ILâ 4; treatment of rats with antibodies to ILâ 4 or MCPâ 1 significantly suppressed development of ankle edema and histopathological evidence of inflammation. Antibodies to interferonâ γ or ILâ 10 had no effect. Treatment with antiâ MCPâ 1 also suppressed influx of 111Inâ labeled T cells into the ankle joint. These data suggest that the late, mononuclearâ dependent phase of SCWâ induced arthritis in female Lewis rats requires cytokines that upâ regulate MCPâ 1, which in turn may facilitate recruitment and extravasation of mononuclear cells into the joint. J. Leukoc. Biol. 63: 359â 363; 1998.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/142294/1/jlb0359.pd

Meiofauna and Trace Metals From Sediment Collections in Florida After the Deepwater Horizon Oil Spill

Sediment from the Florida Gulf continental shelf was collected from 18 sites during October and November 2010 for meiofauna and trace-metals analysis. Collections were obtained using a Shipek® grab on the National Oceanic and Atmospheric Administration ship Pisces and spanned from the head of the DeSoto Canyon to off the southern end of the Florida peninsula approximately following the 100–200-m contour. Mean abundance of the dominant meiofaunal groups (nematodes, copepods, and polychaetes) was unchanged when compared with 2007–2009 data. Nematodes and copepods correlated positively with each other, and negatively with latitude and longitude, suggesting that there were higher densities in southern Florida. These results contrast with those from 2007–2009 in that previously nematodes had no correlation with latitude or longitude in Florida. Nickel (Ni) and vanadium (V) concentrations were higher in the western Florida locations and correlated positively with increasing depth. No relationship was found between Ni, V, and meiofauna densities

A Phase 1 study of intravenous infusions of tigecycline in patients with acute myeloid leukemia.

Acute myeloid leukemia (AML) cells meet the higher energy, metabolic, and signaling demands of the cell by increasing mitochondrial biogenesis and mitochondrial protein translation. Blocking mitochondrial protein synthesis through genetic and chemical approaches kills human AML cells at all stages of development in vitro and in vivo. Tigecycline is an antimicrobial that we found inhibits mitochondrial protein synthesis in AML cells. Therefore, we conducted a phase 1 dose-escalation study of tigecycline administered intravenously daily 5 of 7 days for 2 weeks to patients with AML. A total of 27 adult patients with relapsed and refractory AML were enrolled in this study with 42 cycles being administered over seven dose levels (50-350 mg/day). Two patients experienced DLTs related to tigecycline at the 350 mg/day level resulting in a maximal tolerated dose of tigecycline of 300 mg as a once daily infusion. Pharmacokinetic experiments showed that tigecycline had a markedly shorter half-life in these patients than reported for noncancer patients. No significant pharmacodynamic changes or clinical responses were observed. Thus, we have defined the safety of once daily tigecycline in patients with refractory AML. Future studies should focus on schedules of the drug that permit more sustained target inhibition

Clinically relevant concentrations of lidocaine and ropivacaine inhibit TNFα-induced invasion of lung adenocarcinoma cells in vitro by blocking the activation of Akt and focal adhesion kinase

BACKGROUND Matrix-metalloproteinases (MMP) and cancer cell invasion are crucial for solid tumour metastasis. Important signalling events triggered by inflammatory cytokines, such as tumour necrosis factor α (TNFα), include Src-kinase-dependent activation of Akt and focal adhesion kinase (FAK) and phosphorylation of caveolin-1. Based on previous studies where we demonstrated amide-type local anaesthetics block TNFα-induced Src activation in malignant cells, we hypothesized that local anaesthetics might also inhibit the activation and/or phosphorylation of Akt, FAK and caveolin-1, thus attenuating MMP release and invasion of malignant cells. METHODS NCI-H838 lung adenocarcinoma cells were incubated with ropivacaine or lidocaine (1 nM-100 µM) in absence/presence of TNFα (20 ng ml(-1)) for 20 min or 4 h, respectively. Activation/phosphorylation of Akt, FAK and caveolin-1 were evaluated by Western blot, and MMP-9 secretion was determined by enzyme-linked immunosorbent assay. Tumour cell migration (electrical wound-healing assay) and invasion were also assessed. RESULTS Ropivacaine (1 nM-100 μM) and lidocaine (1-100 µM) significantly reduced TNFα-induced activation/phosphorylation of Akt, FAK and caveolin-1 in NCI-H838 cells. MMP-9 secretion triggered by TNFα was significantly attenuated by both lidocaine and ropivacaine (half-maximal inhibitory concentration [IC50]=3.29×10(-6) M for lidocaine; IC50=1.52×10(-10) M for ropivacaine). The TNFα-induced increase in invasion was completely blocked by both lidocaine (10 µM) and ropivacaine (1 µM). CONCLUSIONS At clinically relevant concentrations both ropivacaine and lidocaine blocked tumour cell invasion and MMP-9 secretion by attenuating Src-dependent inflammatory signalling events. Although determined entirely in vitro, these findings provide significant insight into the potential mechanism by which local anaesthetics might diminish metastasi