(Not) going underground: rectifying a registered deed of conditions in PHG Developments Scot Limited (in liquidation), Petr

No abstract available

Perturbative QCD Fragmentation Functions for BcB_c and Bc∗B_c^* Production

The dominant production mechanism for ${\bar b} c$ bound states in high energy processes is the production of a high energy ${\bar b}$ or $c$ quark, followed by its fragmentation into the ${\bar b} c$ state. We calculate the fragmentation functions for the production of the S-wave states $B_c$ and $B_c^*$ to leading order in the QCD coupling constant. The fragmentation probabilities for ${\bar b} \rightarrow B_c$ and ${\bar b} \rightarrow B_c^*$ are approximately $2.2 \times 10^{-4}$ and $3.1 \times 10^{-4}$, while those for $c \rightarrow B_c$ and $c \rightarrow B_c^*$ are smaller by almost two orders of magnitude.Comment: Latex, 12 pages, 3 figures available upon request, NUHEP-TH-93-

Reproductive and Appetite Hormones and Bulimic Symptoms during Midlife

Eating disorders and related symptoms occur during midlife; however, little is known about their aetiology. It has been hypothesised that perimenopause represents a window of vulnerability for the development or exacerbation of eating disorder symptomatology because, like puberty, perimenopause is a period of reproductive hormone change. We compared symptoms of bulimia nervosa (bulimic symptomatology) assessed via mean scores on a self-report questionnaire in premenopausal and perimenopausal women. We also examined the association between hormone concentrations (reproductive/appetite) and bulimic symptomatology. No mean differences in bulimic symptomatology were observed between premenopause and perimenopause. However, there was a significant positive association between leptin and binge eating. Although no significant associations between reproductive hormones and bulimic symptomatology were observed, additional research is needed to provide definitive information. It is essential to learn more about the aetiology of eating disorders and related symptomatology across the lifespan in order to develop age-relevant treatment and prevention programs

Partial Dynamical Symmetry in the Symplectic Shell Model

We present an example of a partial dynamical symmetry (PDS) in an interacting fermion system and demonstrate the close relationship of the associated Hamiltonians with a realistic quadrupole-quadrupole interaction, thus shedding new light on this important interaction. Specifically, in the framework of the symplectic shell model of nuclei, we prove the existence of a family of fermionic Hamiltonians with partial SU(3) symmetry. We outline the construction process for the PDS eigenstates with good symmetry and give analytic expressions for the energies of these states and E2 transition strengths between them. Characteristics of both pure and mixed-symmetry PDS eigenstates are discussed and the resulting spectra and transition strengths are compared to those of real nuclei. The PDS concept is shown to be relevant to the description of prolate, oblate, as well as triaxially deformed nuclei. Similarities and differences between the fermion case and the previously established partial SU(3) symmetry in the Interacting Boson Model are considered.Comment: 9 figure

Hypertension Control in Adults with Diabetes Mellitus and Recurrent Cardiovascular Events: Global Results from the Trial Evaluating Cardiovascular Outcomes with Sitagliptin

Systolic blood pressure (SBP) treatment targets for adults with diabetes mellitus remain unclear. SBP levels among 12 275 adults with diabetes mellitus, prior cardiovascular disease, and treated hypertension were evaluated in the TECOS (Trial Evaluating Cardiovascular Outcomes With Sitagliptin) randomized trial of sitagliptin versus placebo. The association between baseline SBP and recurrent cardiovascular disease was evaluated using multivariable Cox proportional hazards modeling with restricted cubic splines, adjusting for clinical characteristics. Kaplan-Meier curves by baseline SBP were created to assess time to cardiovascular disease and 2 potential hypotension-related adverse events: worsening kidney function and fractures. The association between time-updated SBP and outcomes was examined using multivariable Cox proportional hazards models. Overall, 42.2% of adults with diabetes mellitus, cardiovascular disease, and hypertension had an SBP ≥140 mm Hg. The association between SBP and cardiovascular disease risk was U shaped, with a nadir ≈130 mm Hg. When the analysis was restricted to those with baseline SBP of 110 to 150 mm Hg, the adjusted association between SBP and cardiovascular disease risk was flat (hazard ratio per 10-mm Hg increase, 0.96; 95% confidence interval, 0.91-1.02). There was no association between SBP and risk of fracture. Above 150 mm Hg, higher SBP was associated with increasing risk of worsening kidney function (hazard ratio per 10-mm Hg increase, 1.10; 95% confidence interval, 1.02-1.18). Many patients with diabetes mellitus have uncontrolled hypertension. The U-shaped association between SBP and cardiovascular disease events was largely driven by those with very high or low SBP, with no difference in cardiovascular disease risk between 110 and 150 mm Hg. Lower SBP was not associated with higher risks of fractures or worsening kidney function

Measurement of the Charged Multiplicities in b, c and Light Quark Events from Z0 Decays

Average charged multiplicities have been measured separately in $b$, $c$ and light quark ($u,d,s$) events from $Z^0$ decays measured in the SLD experiment. Impact parameters of charged tracks were used to select enriched samples of $b$ and light quark events, and reconstructed charmed mesons were used to select $c$ quark events. We measured the charged multiplicities: $\bar{n}_{uds} = 20.21 \pm 0.10 (\rm{stat.})\pm 0.22(\rm{syst.})$, $\bar{n}_{c} = 21.28 \pm 0.46(\rm{stat.}) ^{+0.41}_{-0.36}(\rm{syst.})$ $\bar{n}_{b} = 23.14 \pm 0.10(\rm{stat.}) ^{+0.38}_{-0.37}(\rm{syst.})$, from which we derived the differences between the total average charged multiplicities of $c$ or $b$ quark events and light quark events: $\Delta \bar{n}_c = 1.07 \pm 0.47(\rm{stat.})^{+0.36}_{-0.30}(\rm{syst.})$ and $\Delta \bar{n}_b = 2.93 \pm 0.14(\rm{stat.})^{+0.30}_{-0.29}(\rm{syst.})$. We compared these measurements with those at lower center-of-mass energies and with perturbative QCD predictions. These combined results are in agreement with the QCD expectations and disfavor the hypothesis of flavor-independent fragmentation.Comment: 19 pages LaTex, 4 EPS figures, to appear in Physics Letters

Measurement of the Polarized Structure Function σLT′\sigma_{LT^\prime} for p(e⃗,e′π+)np(\vec{e},e'\pi^+)n in the Δ(1232)\Delta(1232) Resonance Region

The polarized longitudinal-transverse structure function $\sigma_{LT^\prime}$ has been measured using the $p(\vec e,e'\pi^+)n$ reaction in the $\Delta(1232)$ resonance region at $Q^2=0.40$ and 0.65 GeV$^2$. No previous $\sigma_{LT^\prime}$ data exist for this reaction channel. The kinematically complete experiment was performed at Jefferson Lab with the CEBAF Large Acceptance Spectrometer (CLAS) using longitudinally polarized electrons at an energy of 1.515 GeV. A partial wave analysis of the data shows generally better agreement with recent phenomenological models of pion electroproduction compared to the previously measured $\pi^0 p$ channel. A fit to both $\pi^0 p$ and $\pi^+ n$ channels using a unitary isobar model suggests the unitarized Born terms provide a consistent description of the non-resonant background. The $t$-channel pion pole term is important in the $\pi^0 p$ channel through a rescattering correction, which could be model-dependent.Comment: 6 pages, LaTex, 5 eps figures: Submitted to PRC/Brief Reports v2: Updated referenc

Limit on Tau Neutrino Mass from τ−→π−π+π−π0ντ\tau^{-}\to \pi^{-}\pi^{+}\pi^{-}\pi^{0}\nu_{\tau}

From a data sample of 29058 $\tau^\pm\to\pi^\pm\pi^+\pi^-\pi^0\nu_\tau$ decays observed in the CLEO detector we derive a 95% confidence upper limit on the tau neutrino mass of 28 MeV.Comment: 17 pages postscript, also available through http://w4.lns.cornell.edu/public/CLN

An HDAC6-dependent surveillance mechanism suppresses tau-mediated neurodegeneration and cognitive decline

Tauopathies including Alzheimer’s disease (AD) are marked by the accumulation of aberrantly modified tau proteins. Acetylated tau, in particular, has recently been implicated in neurodegeneration and cognitive decline. HDAC6 reversibly regulates tau acetylation, but its role in tauopathy progression remains unclear. Here, we identified an HDAC6-chaperone complex that targets aberrantly modified tau. HDAC6 not only deacetylates tau but also suppresses tau hyperphosphorylation within the microtubule-binding region. In neurons and human AD brain, HDAC6 becomes co-aggregated within focal tau swellings and human AD neuritic plaques. Using mass spectrometry, we identify a novel HDAC6-regulated tau acetylation site as a disease specific marker for 3R/4R and 3R tauopathies, supporting uniquely modified tau species in different neurodegenerative disorders. Tau transgenic mice lacking HDAC6 show reduced survival characterized by accelerated tau pathology and cognitive decline. We propose that a HDAC6-dependent surveillance mechanism suppresses toxic tau accumulation, which may protect against the progression of AD and related tauopathies