Analysis of charged particle emission sources and coalescence in E/A = 61 MeV 36^{36}Ar + 27^{27}Al, 112^{112}Sn and 124^{124}Sn collisions

Single-particle kinetic energy spectra and two-particle small angle correlations of protons ($p$), deuterons ($d$) and tritons ($t$) have been measured simultaneously in 61A MeV $^{36}$Ar + $^{27}$Al, $^{112}$Sn and $^{124}$Sn collisions. Characteristics of the emission sources have been derived from a ``source identification plot'' ($\beta_{source}$--$E_{CM}$ plot), constructed from the single-particle invariant spectra, and compared to the complementary results from two-particle correlation functions. Furthermore, the source identification plot has been used to determine the conditions when the coalescence mechanism can be applied for composite particles. In our data, this is the case only for the Ar + Al reaction, where $p$, $d$ and $t$ are found to originate from a common source of emission (from the overlap region between target and projectile). In this case, the coalescence model parameter, $\tilde{p}_0$ -- the radius of the complex particle emission source in momentum space, has been analyzed.Comment: 20 pages, 5 figures, submitted to Nuclear Physics

A Three-Dimensional Code for Muon Propagation through the Rock: MUSIC

We present a new three-dimensional Monte-Carlo code MUSIC (MUon SImulation Code) for muon propagation through the rock. All processes of muon interaction with matter with high energy loss (including the knock-on electron production) are treated as stochastic processes. The angular deviation and lateral displacement of muons due to multiple scattering, as well as bremsstrahlung, pair production and inelastic scattering are taken into account. The code has been applied to obtain the energy distribution and angular and lateral deviations of single muons at different depths underground. The muon multiplicity distributions obtained with MUSIC and CORSIKA (Extensive Air Shower simulation code) are also presented. We discuss the systematic uncertainties of the results due to different muon bremsstrahlung cross-sections.Comment: 24 pages, 11 Postscript figures, LaTeX, to be published in Astroparticle Physic

Temperature increase inside LED-based illuminators for in vitro aPDT photodamage studies

Abstract Antimicrobial PhotoDynamic Therapy (aPDT) is an emerging strategy aimed at the eradication of bacterial infections, with a special focus on antibiotic-resistant bacteria. This method is easy to apply, not expensive and particularly interesting in case of bacteria that spontaneously produce the required photosensitizers. In the framework of a project aimed at the development of an ingestible pill for the application of aPDT to gastric infections by Helicobacter pylori, a LED-based illuminating prototype (LED-BIP) was purposely designed in order to evaluate the photodamage induced by light of different wavelengths on porphyrin-producing bacteria. This short paper reports about temperature tests performed to assess the maximum exposure time and light dose that can be administered to bacterial cultures inside LED-BIP without reaching temperatures exceeding the physiological range

Prion protein amyloidosis with divergent phenotype associated with two novel nonsense mutations in PRNP

Stop codon mutations in the gene encoding the prion protein (PRNP) are very rare and have thus far only been described in two patients with prion protein cerebral amyloid angiopathy (PrP-CAA). In this report, we describe the clinical, histopathological and pathological prion protein (PrPSc) characteristics of two Dutch patients carrying novel adjacent stop codon mutations in the C-terminal part of PRNP, resulting in either case in hereditary prion protein amyloidoses, but with strikingly different clinicopathological phenotypes. The patient with the shortest disease duration (27 months) carried a Y226X mutation and showed PrP-CAA without any neurofibrillary lesions, whereas the patient with the longest disease duration (72 months) had a Q227X mutation and showed an unusual Gerstmann-Sträussler-Scheinker disease phenotype with numerous cerebral multicentric amyloid plaques and severe neurofibrillary lesions without PrP-CAA. Western blot analysis in the patient with the Q227X mutation demonstrated the presence of a 7 kDa unglycosylated PrPSc fragment truncated at both the N- and C-terminal ends. Our observations expand the spectrum of clinicopathological phenotypes associated with PRNP mutations and show that a single tyrosine residue difference in the PrP C-terminus may significantly affect the site of amyloid deposition and the overall phenotypic expression of the prion disease. Furthermore, it confirms that the absence of the glycosylphosphatidylinositol anchor in PrP predisposes to amyloid plaque formation

Quantum-Statistical Correlations and Single Particle Distributions for Slowly Expanding Systems with Temperature Profile

Competition among particle evaporation, temperature gradient and flow is investigated in a phenomenological manner, based on a simultaneous analysis of quantum statistical correlations and momentum distributions for a non-relativistic, spherically symmetric, three-dimensionally expanding, finite source. The parameters of the model emission function are constrained by fits to neutron and proton momentum distributions and correlation functions in intermediate energy heavy-ion collisions. The temperature gradient is related to the momentum dependence of the radius parameters of the two-particle correlation function, as well as to the momentum-dependent temperature parameter of the single particle spectrum, while a long duration of particle evaporation is found to be responsible for the low relative momentum behavior of the two-particle correlations.Comment: 20 pages + 5 ps figures, ReVTeX, uses psfig.sty, the description is extended to include final state interactions, phenomenological evaporation and to fit intermediate energy heavy ion proton and neutron spectrum and correlation dat

Allelic Origin of Protease-Sensitive and Protease-Resistant Prion Protein Isoforms in Gerstmann-Sträussler-Scheinker Disease with the P102L Mutation

Gerstmann-Sträussler-Scheinker (GSS) disease is a dominantly inherited prion disease associated with point mutations in the Prion Protein gene. The most frequent mutation associated with GSS involves a proline-to-leucine substitution at residue 102 of the prion protein, and is characterized by marked variability at clinical, pathological and molecular levels. Previous investigations of GSS P102L have shown that disease-associated pathological prion protein, or PrPSc, consists of two main conformers, which under exogenous proteolysis generates a core fragment of 21 kDa and an internal fragment of 8 kDa. Both conformers are detected in subjects with spongiform degeneration, whereas only the 8 kDa fragment is recovered in cases lacking spongiosis. Several studies have reported an exclusive derivation of protease-resistant PrPSc isoforms from the mutated allele; however, more recently, the propagation of protease-resistant wild-type PrPSc has been described. Here we analyze the molecular and pathological phenotype of six GSS P102L cases characterized by the presence of 21 and 8 kDa PrP fragments and two subjects with only the 8 kDa PrP fragment. Using sensitive protein separation techniques and Western blots with antibodies differentially recognizing wild-type and mutant PrP we observed a range of PrPSc allelic conformers, either resistant or sensitive to protease treatment in all investigated subjects. Additionally, tissue deposition of protease-sensitive wild-type PrPSc molecules was seen by conventional PrP immunohistochemistry and paraffin-embedded tissue blot. Our findings enlarge the spectrum of conformational allelic PrPSc quasispecies propagating in GSS P102L thus providing a molecular support to the spectrum of disease phenotypes, and, in addition, impact the diagnostic role of PrP immunohistochemistry in prion diseases

Frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17)

Frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17) is an autosomal dominant neurodegenerative disorder, which has three cardinal features: behavioral and personality changes, cognitive impairment, and motor symptoms. FTDP-17 was defined during the International Consensus Conference in Ann Arbor, Michigan, in 1996. The prevalence and incidence remain unknown but FTDP-17 is an extremely rare condition. It is caused by mutations in the tau gene, which encodes a microtubule-binding protein. Over 100 families with 38 different mutations in the tau gene have been identified worldwide. The phenotype of FTDP-17 varies not only between families carrying different mutations but also between and within families carrying the same mutations. The pathogenetic mechanisms underlying the disorder are thought to be related to the altered proportion of tau isoforms or to the ability of tau to bind microtubules and to promote microtubule assembly. Definitive diagnosis of FTDP-17 requires a combination of characteristic clinical and pathological features and molecular genetic analysis. Genetic counseling should be offered to affected and at-risk individuals; for most subtypes, penetrance is incomplete. Currently, treatment for FTDP-17 is only symptomatic and supportive. The prognosis and rate of the disease's progression vary considerably among individual patients and genetic kindreds, ranging from life expectancies of several months to several years, and, in exceptional cases, as long as two decades