Forward modeling of pile-up events in liquid scintillator detectors for neutron emission spectroscopy.

When using liquid scintillator detectors to measure the neutron emission spectrum from fusion plasmas, the problem of pile-up distortion can be significant. Because of the large neutron rates encountered in many fusion experiments, some pile-up distortion can remain even after applying traditional pile-up elimination methods, which alters the shape of the measured light-yield spectrum and influences the spectroscopic analysis. Particularly, pile-up events appear as a high-energy tail in the measured light-yield spectrum, which obfuscates the contribution that supra-thermal ions make to the energy spectrum. It is important to understand the behavior of such "fast ions" in fusion plasmas, and it is hence desirable to be able to measure their contribution to the neutron spectrum as accurately as possible. This paper presents a technique for incorporating distortion from undetected pile-up events into the analysis of the light-yield spectrum, hence compensating for pile-up distortion. The spectral contribution from undetected pile-up events is determined using Monte Carlo methods and is included in the spectroscopic study as a pile-up component. The method is applied to data from an NE213 scintillator detector at JET and validated by comparing with results from the time-of-flight spectrometer TOFOR, which is not susceptible to pile-up distortion. Based on the results, we conclude that the suggested analysis method helps counteract the problem of pile-up effects and improves the possibilities for extracting accurate fast-ion information from the light-yield spectrum.

Altered PKR Signalling and C / EBPß Expression is Associated with HLA-B27 Expression in Monocytic Cells.

Infection caused by certain gram-negative bacteria, e.g. Salmonella, can trigger inflammatory joint disease reactive arthritis (ReA). It is suggested that the disease-triggering bacteria or bacterial components persist in patients for an abnormally long time. Development of ReA is strongly associated with tissue antigen HLA-B27. Previously, we reported an enhanced replication of Salmonella enteritidis and altered p38 MAP kinase signalling in HLA-B27-expressing monocytic cells. Here we aimed to investigate the role of HLA-B27 in regulation of double-stranded RNA-activated kinase (PKR)-related signalling in Salmonella-infected or Salmonella lipopolysaccharide (LPS)-stimulated human U937 monocytic cells, as PKR has been reported to modify p38 signalling in Salmonella-infected cells. In cells expressing HLA-B27, PKR is overexpressed and hypophosphorylated, and the expression of transcription factor CCAAT enhancer binding protein beta (C/EBPß) is increased upon Salmonella infection and LPS stimulation. The expression of C/EBPß is PKR-dependent in LPS-stimulated mock cells, whereas in LPS-stimulated B27 cells the majority of C/EBPß is expressed in a PKR-independent manner. Our results show that the expression of HLA-B27 disturbs the PKR-mediated signalling pathway. Moreover, altered signalling is related to misfolding-linked Glu45 in the B pocket of the HLA-B27 heavy chain. We suggest that the expression of HLA-B27 HCs modulates the intracellular environment of monocyte/macrophages and the mechanisms that are important in eliminating intracellular S. enteritidis by altering the intracellular signalling. This phenomenon is at least partly dependent on the misfolding feature of the B27 molecule. These observations offer a novel mechanism by which HLA-B27 may modulate inflammatory response induced by ReA-triggering bacteria.