Exact, E=0, Solutions for General Power-Law Potentials. I. Classical Orbits

For zero energy, $E=0$, we derive exact, classical solutions for {\em all} power-law potentials, $V(r)=-\gamma/r^\nu$, with $\gamma>0$ and $-\infty <\nu<\infty$. When the angular momentum is non-zero, these solutions lead to the orbits $\r(t)= [\cos \mu (\th(t)-\th_0(t))]^{1/\mu}$, for all $\mu \equiv \nu/2-1 \ne 0$. When $\nu>2$, the orbits are bound and go through the origin. This leads to discrete discontinuities in the functional dependence of $\th(t)$ and $\th_0(t)$, as functions of $t$, as the orbits pass through the origin. We describe a procedure to connect different analytic solutions for successive orbits at the origin. We calculate the periods and precessions of these bound orbits, and graph a number of specific examples. Also, we explain why they all must violate the virial theorem. The unbound orbits are also discussed in detail. This includes the unusual orbits which have finite travel times to infinity and also the special $\nu = 2$ case.Comment: LaTeX, 27 pages with 12 figures available from the authors or can be generated from Mathematica instructions at end of the fil

Path Crossing Exponents and the External Perimeter in 2D Percolation

2D Percolation path exponents $x^{\cal P}_{\ell}$ describe probabilities for traversals of annuli by $\ell$ non-overlapping paths, each on either occupied or vacant clusters, with at least one of each type. We relate the probabilities rigorously to amplitudes of $O(N=1)$ models whose exponents, believed to be exact, yield $x^{\cal P}_{\ell}=({\ell}^2-1)/12$. This extends to half-integers the Saleur--Duplantier exponents for $k=\ell/2$ clusters, yields the exact fractal dimension of the external cluster perimeter, $D_{EP}=2-x^{\cal P}_3=4/3$, and also explains the absence of narrow gate fjords, as originally found by Grossman and Aharony.Comment: 4 pages, 2 figures (EPSF). Revised presentatio

A20 protects cells from TNF-induced apoptosis through linear ubiquitin-dependent and -independent mechanisms

The cytokine TNF promotes inflammation either directly by activating the MAPK and NF-kappa B signaling pathways, or indirectly by triggering cell death. A20 is a potent anti-inflammatory molecule, and mutations in the gene encoding A20 are associated with a wide panel of inflammatory pathologies, both in human and in the mouse. Binding of TNF to TNFR1 triggers the NF-kappa B-dependent expression of A20 as part of a negative feedback mechanism preventing sustained NF-kappa B activation. Apart from acting as an NF-kappa B inhibitor, A20 is also well-known for its ability to counteract the cytotoxic potential of TNF. However, the mechanism by which A20 mediates this function and the exact cell death modality that it represses have remained incompletely understood. In the present study, we provide in vitro and in vivo evidences that deletion of A20 induces RIPK1 kinase-dependent and -independent apoptosis upon single TNF stimulation. We show that constitutively expressed A20 is recruited to TNFR1 signaling complex (Complex I) via its seventh zinc finger (ZF7) domain, in a cIAP1/2-dependent manner, within minutes after TNF sensing. We demonstrate that Complex I-recruited A20 protects cells from apoptosis by stabilizing the linear (M1) ubiquitin network associated to Complex I, a process independent of its E3 ubiquitin ligase and deubiquitylase (DUB) activities and which is counteracted by the DUB CYLD, both in vitro and in vivo. In absence of linear ubiquitylation, A20 is still recruited to Complex I via its ZF4 and ZF7 domains, but this time protects the cells from death by deploying its DUB activity. Together, our results therefore demonstrate two distinct molecular mechanisms by which constitutively expressed A20 protect cells from TNF-induced apoptosis

Tuning trion binding energy and oscillator strength in a laterally finite 2D system: CdSe nanoplatelets as a model system for trion properties

We present a theoretical study combined with experimental validations demonstrating that CdSe nanoplatelets are a model system to investigate the tunability of trions and excitons in laterally finite 2D semiconductors. Our results show that the trion binding energy can be tuned from 36 meV to 18 meV with the lateral size and decreasing aspect ratio, while the oscillator strength ratio of trions to excitons decreases. In contrast to conventional quantum dots, the trion oscillator strength in a nanoplatelet at low temperature is smaller than that of the exciton. The trion and exciton Bohr radii become lateral size tunable, e.g. from ∼3.5 to 4.8 nm for the trion. We show that dielectric screening has strong impact on these properties. By theoretical modeling of transition energies, binding energies and oscillator strength of trions and excitons and comparison with experimental findings, we demonstrate that these properties are lateral size and aspect ratio tunable and can be engineered by dielectric confinement, allowing to suppress e.g. detrimental trion emission in devices. Our results strongly impact further in-depth studies, as the demonstrated lateral size tunable trion and exciton manifold is expected to influence properties like gain mechanisms, lasing, quantum efficiency and transport even at room temperature due to the high and tunable trion binding energies.EC/H2020/714876/EU/Photonics in Flatland: Band Structure Engineering of 2D Excitons in Fluorescent Colloidal Nanomaterials/PHOCONATU Berlin, Open-Access-Mittel - 202

Spectral Libraries for SWATH-MS Assays for Drosophila melanogaster and Solanum lycopersicum.

Quantitative proteomics methods have emerged as powerful tools for measuring protein expression changes at the proteome level. Using MS-based approaches, it is now possible to routinely quantify thousands of proteins. However, prefractionation of the samples at the protein or peptide level is usually necessary to go deep into the proteome, increasing both MS analysis time and technical variability. Recently, a new MS acquisition method named SWATH is introduced with the potential to provide good coverage of the proteome as well as a good measurement precision without prior sample fractionation. In contrast to shotgun-based MS however, a library containing experimental acquired spectra is necessary for the bioinformatics analysis of SWATH data. In this study, spectral libraries for two widely used models are built to study crop ripening or animal embryogenesis, Solanum lycopersicum (tomato) and Drosophila melanogaster, respectively. The spectral libraries comprise fragments for 5197 and 6040 proteins for S. lycopersicum and D. melanogaster, respectively, and allow reproducible quantification for thousands of peptides per MS analysis. The spectral libraries and all MS data are available in the MassIVE repository with the dataset identifiers MSV000081074 and MSV000081075 and the PRIDE repository with the dataset identifiers PXD006493 and PXD006495

Pharmacokinetics and pharmacodynamics of sotalol in a pediatric population with supraventricular and ventricular tachyarrhythmia

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/109904/1/cptclpt200121.pd

Clinicopathological evaluation of chronic traumatic encephalopathy in players of American football

IMPORTANCE: Players of American football may be at increased risk of long-term neurological conditions, particularly chronic traumatic encephalopathy (CTE). OBJECTIVE: To determine the neuropathological and clinical features of deceased football players with CTE. DESIGN, SETTING, AND PARTICIPANTS: Case series of 202 football players whose brains were donated for research. Neuropathological evaluations and retrospective telephone clinical assessments (including head trauma history) with informants were performed blinded. Online questionnaires ascertained athletic and military history. EXPOSURES: Participation in American football at any level of play. MAIN OUTCOMES AND MEASURES: Neuropathological diagnoses of neurodegenerative diseases, including CTE, based on defined diagnostic criteria; CTE neuropathological severity (stages I to IV or dichotomized into mild [stages I and II] and severe [stages III and IV]); informant-reported athletic history and, for players who died in 2014 or later, clinical presentation, including behavior, mood, and cognitive symptoms and dementia. RESULTS: Among 202 deceased former football players (median age at death, 66 years [interquartile range, 47-76 years]), CTE was neuropathologically diagnosed in 177 players (87%; median age at death, 67 years [interquartile range, 52-77 years]; mean years of football participation, 15.1 [SD, 5.2]), including 0 of 2 pre–high school, 3 of 14 high school (21%), 48 of 53 college (91%), 9 of 14 semiprofessional (64%), 7 of 8 Canadian Football League (88%), and 110 of 111 National Football League (99%) players. Neuropathological severity of CTE was distributed across the highest level of play, with all 3 former high school players having mild pathology and the majority of former college (27 [56%]), semiprofessional (5 [56%]), and professional (101 [86%]) players having severe pathology. Among 27 participants with mild CTE pathology, 26 (96%) had behavioral or mood symptoms or both, 23 (85%) had cognitive symptoms, and 9 (33%) had signs of dementia. Among 84 participants with severe CTE pathology, 75 (89%) had behavioral or mood symptoms or both, 80 (95%) had cognitive symptoms, and 71 (85%) had signs of dementia. CONCLUSIONS AND RELEVANCE: In a convenience sample of deceased football players who donated their brains for research, a high proportion had neuropathological evidence of CTE, suggesting that CTE may be related to prior participation in football.This study received support from NINDS (grants U01 NS086659, R01 NS078337, R56 NS078337, U01 NS093334, and F32 NS096803), the National Institute on Aging (grants K23 AG046377, P30AG13846 and supplement 0572063345-5, R01 AG1649), the US Department of Defense (grant W81XWH-13-2-0064), the US Department of Veterans Affairs (I01 CX001038), the Veterans Affairs Biorepository (CSP 501), the Veterans Affairs Rehabilitation Research and Development Traumatic Brain Injury Center of Excellence (grant B6796-C), the Department of Defense Peer Reviewed Alzheimer’s Research Program (grant 13267017), the National Operating Committee on Standards for Athletic Equipment, the Alzheimer’s Association (grants NIRG-15-362697 and NIRG-305779), the Concussion Legacy Foundation, the Andlinger Family Foundation, the WWE, and the NFL