Process pi p -> pi pi N at high energies and moderate momenta transferred to the nucleon and the determination of parameters of the f_0(980) and f_0(1300)

We present the results of simultaneous analysis of the S-wave pi pi-spectra in the reactions pi^- p -> (pi^0 pi^0)_S n at p_{lab}=38 GeV/c (GAMS) and pi^- p -> (pi^+ pi^-)_S n at p_{lab}=18 GeV/c (E852 Collaboration) at moderate momenta transferred to the nucleon, |t| < 1.5 (GeV/c)^2. The t-distributions are described by the reggeized pi- and a_1-exchanges provided by the leading and daughter trajectories, while the M_{pi pi}-spectra are determined by a set of scalar-isoscalar resonances. With M_{pi pi}-distributions averaged over t-intervals, we have found several solutions given by different t-channel exchange mechanisms at |t| ~ (0.5-1.5) (GeV/c)^2, with resonance parameters close to each other. We conclude that despite a poor knowledge of the structure of the t-exchange, the characteristics of resonances such as masses and widths can be reliably determined using the processes under discussion. As to pole positions, we have found (1031 +/- 10) - i(35 +/- 6) MeV for f_0(980) and (1315 +/- 20) - i(150 +/- 30) MeV for f_0(1300).Comment: 17 pages, RevTeX, 10 EPS figures, misprints correcte

Observation of the Cabibbo-suppressed decay Xi_c+ -> p K- pi+

We report the first observation of the Cabibbo-suppressed charm baryon decay Xi_c+ -> p K- pi+. We observe 150 +- 22 events for the signal. The data were accumulated using the SELEX spectrometer during the 1996-1997 fixed target run at Fermilab, chiefly from a 600 GeV/c Sigma- beam. The branching fractions of the decay relative to the Cabibbo-favored Xi_c+ -> Sigma+ K- pi+ and Xi_c+ -> X- pi+ pi+ are measured to be B(Xi_c+ -> p K- pi+)/B(Xi_c+ -> Sigma+ K- pi+) = 0.22 +- 0.06 +- 0.03 and B(Xi_c+ -> p K- pi+)/B(Xi_c+ -> X- pi+ pi+) = 0.20 +- 0.04 +- 0.02, respectively.Comment: 5 pages, RevTeX, 3 figures (postscript), Submitted to Phys. Rev. Let

Characteristics and trends in required home care by GPs in Austria: diseases and functional status of patients

BACKGROUND: Almost all societies carry responsibility towards patients who require continuous medical care at home. In many health systems the general practitioner cooperates with community based services of home care and coordinates all medical and non medical activities. In Austria the general practitioner together and in cooperation with relatives of the patient and professional organisations usually takes on this task by visiting his patients. This study was carried out to identify diseases that need home care and to describe the functional profile of home care patients in eastern Austria. METHODS: Cross sectional observational study with 17 GP practices participating during 2 study periods in 1997 and in 2004 in eastern Austria. Each GP identified patients requiring home care and assessed their underlying diseases and functional status by filling in a questionnaire personally after an encounter. Patients in nursing homes were excluded. Statistical tests used were t-tests, contingency tables, nonparametric Wilcoxon signed rank sum test and Fisher-combination test. RESULTS: Patients with degenerative diseases of the central nervous system (65%) caused by Alzheimer's disease and cerebrovascular occlusive disease and patients with degenerative diseases of the skeletal system (53%) were the largest groups among the 198 (1997) and 261 (2004) home care cases of the 11 (1997) and 13 (2004) practices. Malignant diseases in a terminal state constituted only 5% of the cases. More than two thirds of all cases were female with an average age of 80 years. Slightly more than 70% of the patients were at least partially mobile. CONCLUSION: Home care and home visits for patients with degenerative diseases of the central nervous and skeletal system are important elements of GP's work. Further research should therefore focus on effective methods of training and rehabilitation to better the mental and physical status of patients living in their private homes

A Deubiquitylating Complex Required for Neosynthesis of a Yeast Mitochondrial ATP Synthase Subunit

The ubiquitin system is known to be involved in maintaining the integrity of mitochondria, but little is known about the role of deubiquitylating (DUB) enzymes in such functions. Budding yeast cells deleted for UBP13 and its close homolog UBP9 displayed a high incidence of petite colonies and slow respiratory growth at 37°C. Both Ubp9 and Ubp13 interacted directly with Duf1 (DUB-associated factor 1), a WD40 motif-containing protein. Duf1 activates the DUB activity of recombinant Ubp9 and Ubp13 in vitro and deletion of DUF1 resulted in the same respiratory phenotype as the deletion of both UBP9 and UBP13. We show that the mitochondrial defects of these mutants resulted from a strong decrease at 37°C in the de novo biosynthesis of Atp9, a membrane-bound component of ATP synthase encoded by mitochondrial DNA. The defect appears at the level of ATP9 mRNA translation, while its maturation remained unchanged in the mutants. This study describes a new role of the ubiquitin system in mitochondrial biogenesis

Enhanced killing of androgen-independent prostate cancer cells using inositol hexakisphosphate in combination with proteasome inhibitors

Effective treatments for androgen-independent prostate cancer (AIPCa) are lacking. To address this, emerging therapeutics such as proteasome inhibitors are currently undergoing clinical trials. Inositol hexakisphosphate (IP6) is an orally non-toxic phytochemical that exhibits antitumour activity against several types of cancer including PCa. We have previously shown that treatment of PC3 cells with IP6 induces the transcription of a subset of nuclear factor-κB (NF-κB)-responsive and pro-apoptotic BCL-2 family genes. In this study, we report that although NF-κB subunits p50/p65 translocate to the nucleus of PC3 cells in response to IP6, inhibition of NF-κB-mediated transcription using non-degradable inhibitor of κB (IκB)-α does not modulate IP6 sensitivity. Treatment with IP6 also leads to increased protein levels of PUMA, BIK/NBK and NOXA between 4 and 8 h of treatment and decreased levels of MCL-1 and BCL-2 after 24 h. Although blocking transcription using actinomycin D does not modulate PC3 cell sensitivity to IP6, inhibition of protein translation using cycloheximide has a significant protective effect. In contrast, blocking proteasome-mediated protein degradation using MG-132 significantly enhances the ability of IP6 to reduce cellular metabolic activity in both PC3 and DU145 AIPCa cell lines. This effect of combined treatment on mitochondrial depolarisation is particularly striking and is also reproduced by another proteasome inhibitor (ALLN). The enhanced effect of combined MG132/IP6 treatment is almost completely inhibited by cycloheximide and correlates with changes in BCL-2 family protein levels. Altogether these results suggest a role for BCL-2 family proteins in mediating the combined effect of IP6 and proteasome inhibitors and warrant further pre-clinical studies for the treatment of AIPCa