The "Puck" energetic charged particle detector: Design, heritage, and advancements.

Energetic charged particle detectors characterize a portion of the plasma distribution function that plays critical roles in some physical processes, from carrying the currents in planetary ring currents to weathering the surfaces of planetary objects. For several low-resource missions in the past, the need was recognized for a low-resource but highly capable, mass-species-discriminating energetic particle sensor that could also obtain angular distributions without motors or mechanical articulation. This need led to the development of a compact Energetic Particle Detector (EPD), known as the "Puck" EPD (short for hockey puck), that is capable of determining the flux, angular distribution, and composition of incident ions between an energy range of ~10 keV to several MeV. This sensor makes simultaneous angular measurements of electron fluxes from the tens of keV to about 1 MeV. The same measurements can be extended down to approximately 1 keV/nucleon, with some composition ambiguity. These sensors have a proven flight heritage record that includes missions such as MErcury Surface, Space ENvironment, GEochemistry, and Ranging and New Horizons, with multiple sensors on each of Juno, Van Allen Probes, and Magnetospheric Multiscale. In this review paper we discuss the Puck EPD design, its heritage, unexpected results from these past missions and future advancements. We also discuss high-voltage anomalies that are thought to be associated with the use of curved foils, which is a new foil manufacturing processes utilized on recent Puck EPD designs. Finally, we discuss the important role Puck EPDs can potentially play in upcoming missions.

Pancreatoduodenectomy for pancreatic cancer in a low volume institution.

PURPOSE: To report the patient morbidity and mortality rates following pancreatoduodenectomy (PD) carried out in our low volume institution, and compare our results with results from other high volume institutions. METHODS: A retrospective analysis was conducted on patients with pancreatic malignancies surgically treated with PD from 2005 to 2010 in our institution. Data were collected with particular emphasis on morbidity and mortality rates. All patients were followed from the date of discharge to the date of death or status at the last follow-up (July 2011). RESULTS: In a period of 5 years 42 patients underwent PD. Morbidity rates were as follows: 11.9% wound infections, 21.4% pancreatic fistulae, 23.8% delayed gastric emptying (DGE), 14.3% hemorrhage, and 7.1% biliary leak. Two patients required re-laparotomy one for delayed hemorrhage and one for sepsis. The mortality rate was 7.1%. The 2-year survival rate was 45.17 percent; and the median survival 22 months. CONCLUSION: PD in our low volume institution had high morbidity and mortality rates compared with results published in the literature. There is a need, however, to establish a policy for referral of patients with pancreatic cancer to other centers with a higher number of resections, in order to decrease morbidity and mortality rates.

Glucocorticoid treatment inhibits annexin-1 expression in rheumatoid arthritis CD4+ T cells.

OBJECTIVE: Annexin-1 (Anx-A1) has been recently shown to play a key role in T-cell activation and to be highly expressed in T cells from RA patients. Here, we investigated the effects of glucocorticoids (GCs) on Anx-A1 expression in T cells in vitro and in vivo. METHODS: To evaluate the effects of dexamethasone (Dex) on Anx-A1 expression, human peripheral blood T cells were incubated with Dex and then analysed by real-time PCR and western blotting. Similar experiments were carried out in vivo by measuring Anx-A1 levels in T cells from patients with RA before and after administration of steroids. RESULTS: Incubation of T cells with Dex decreased Anx-A1 levels in a time-dependent fashion and almost abolished its expression after 12 h. Stimulation of T cells pre-incubated with Dex for 12 h with anti-CD3/CD28 led to significant reduction of IL-2 production. Addition of human recombinant Anx-A1 to Dex-treated cells reversed the inhibitory effects of the steroids on anti-CD3/CD28-induced IL-2 production. Treatment of RA patients with steroid decreased Anx-A1 expression in T cells. CONCLUSIONS: GCs suppress Anx-A1 expression in T cells in vitro and in vivo. These results provide evidence for a novel pathway by which steroids regulate the adaptive immune response and suggest that Anx-A1 may represent a target for the treatment of autoimmune diseases.