New hadrons as ultra-high energy cosmic rays

Ultra-high energy cosmic ray (UHECR) protons produced by uniformly distributed astrophysical sources contradict the energy spectrum measured by both the AGASA and HiRes experiments, assuming the small scale clustering of UHECR observed by AGASA is caused by point-like sources. In that case, the small number of sources leads to a sharp exponential cutoff at the energy E<10^{20} eV in the UHECR spectrum. New hadrons with mass 1.5-3 GeV can solve this cutoff problem. For the first time we discuss the production of such hadrons in proton collisions with infrared/optical photons in astrophysical sources. This production mechanism, in contrast to proton-proton collisions, requires the acceleration of protons only to energies E<10^{21} eV. The diffuse gamma-ray and neutrino fluxes in this model obey all existing experimental limits. We predict large UHE neutrino fluxes well above the sensitivity of the next generation of high-energy neutrino experiments. As an example we study hadrons containing a light bottom squark. These models can be tested by accelerator experiments, UHECR observatories and neutrino telescopes.Comment: 17 pages, revtex style; v2: shortened, as to appear in PR

Velocity-space sensitivity of the time-of-flight neutron spectrometer at JET

The velocity-space sensitivities of fast-ion diagnostics are often described by so-called weight functions. Recently, we formulated weight functions showing the velocity-space sensitivity of the often dominant beam-target part of neutron energy spectra. These weight functions for neutron emission spectrometry (NES) are independent of the particular NES diagnostic. Here we apply these NES weight functions to the time-of-flight spectrometer TOFOR at JET. By taking the instrumental response function of TOFOR into account, we calculate time-of-flight NES weight functions that enable us to directly determine the velocity-space sensitivity of a given part of a measured time-of-flight spectrum from TOFOR

Relationship of edge localized mode burst times with divertor flux loop signal phase in JET

A phase relationship is identified between sequential edge localized modes (ELMs) occurrence times in a set of H-mode tokamak plasmas to the voltage measured in full flux azimuthal loops in the divertor region. We focus on plasmas in the Joint European Torus where a steady H-mode is sustained over several seconds, during which ELMs are observed in the Be II emission at the divertor. The ELMs analysed arise from intrinsic ELMing, in that there is no deliberate intent to control the ELMing process by external means. We use ELM timings derived from the Be II signal to perform direct time domain analysis of the full flux loop VLD2 and VLD3 signals, which provide a high cadence global measurement proportional to the voltage induced by changes in poloidal magnetic flux. Specifically, we examine how the time interval between pairs of successive ELMs is linked to the time-evolving phase of the full flux loop signals. Each ELM produces a clear early pulse in the full flux loop signals, whose peak time is used to condition our analysis. The arrival time of the following ELM, relative to this pulse, is found to fall into one of two categories: (i) prompt ELMs, which are directly paced by the initial response seen in the flux loop signals; and (ii) all other ELMs, which occur after the initial response of the full flux loop signals has decayed in amplitude. The times at which ELMs in category (ii) occur, relative to the first ELM of the pair, are clustered at times when the instantaneous phase of the full flux loop signal is close to its value at the time of the first ELM

Is a Serotonergic Mechanism Involved in 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced Appetite Suppression in the Sprague-Dawley Rat?.

The major cause of TCDD-induced death in rats is a progressive voluntary feed refusal which has been correlated with reduced gluconeogenesis. Since centrally administered TCDD does not cause death or decreased feed intake in rats, the ability of TCDD to suppress appetite via peripheral mechanisms acting on the central nervous system was examined in two experimental models. First, it was found that the feed intake of rats on scheduled feeding cycles was not decreased by blood transfused from rats with TCDD-induced appetite suppression (8 days after a lethal dose of TCDD, i.p.). In contrast, a similar transfusion from normal, satiated rats did reduce feed intake of recipient rats by approximately 40%, suggesting that TCDD-treated rats are not satiated but rather that they are not hungry. In the second study tryptophan (the amino acid precursor of the neurotransmitter serotonin) was measured in the plasma and tryptophan, serotonin, norepinephrine and dopamine in the hypothalamus as well as dopamine and its metabolites in the striatum 4, 8, and 16 days after TCDD dosage (125 &mu;g/kg, i.p.). Progressive time-dependent increases in tryptophan levels in plasma and brain were paralleled by increases in brain serotonin and 5-hydroxyindoleacetic acid (the primary metabolite of serotonin) in TCDD-treated rats. No changes were observed regarding the other biogenic amines. It is suggested based on these data and on substantial evidence from the published literature that a serotonergic mechanism may be involved in TCDD-induced feed intake reduction

Inhibition of Phosphoenolpyruvate Carboxykinase Activity Appears to be the Key Biochemical Lesion in the Acute Toxicity of 2,3,7,8-tretrachlorodibenzo-p-dioxin in Rats.

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) exerts its acute toxicity by inducing a gradually increasing voluntary feed refusal. However, this seems not to be caused by a direct effect on the central nervous system, as far higher concentrations of TCDD were found in the brain after intracerebroventricular (i.c.v.) than after lethal intravenous (i.v.) injections, but were not accompanied by a wasting syndrome. TCDD causes inhibition of several key enzymes of gluconeogenesis, with phosphoenolpyruvate carboxykinase (PEPCK) responding earliest and strongest to the insult. Responses of pyruvate carboxylase (PC) and glucose-6-phosphatase (G-6-Pase) are less pronounced and begin at later time points. Blood and brain levels of tryptophan increase following TCDD treatment with a lag period of about three days, shortly after the decrease of PEPCK activity becomes apparent. Since thi samino acid is the precursor of the appetite suppressant neurotransmitter serotonin, and since it is normally degraded via gluconeogenesis, a series of events can be suggested to explain the TCDD-induced wasting syndrome. By an as yet unrevealed mechanism TCDD decreases the activity of PEPCK to about 40 percent of normal, leading to a back-up of gluconeogenic substrates, among them tryptophan, which in turn can further inhibit PEPCK activity in vivo. This causes an increase in serotonin turnover in brain and possibly in other tissues. Increased serotonergic activity in turn is likely to play an important role in the increasing feed refusal of TCDD-treated rats which eventually leads to death