Who Owns Christmas Trees? The Disposition of Property Used by a Partnership

Two partners form an enterprise. One (the K partner) supplies the assets used by the enterprise. The other partner (the L partner) supplies only labor. When the enterprise ends, the partners disagree about how to divide the property used in the partnership business. The K partner wants his or her property returned. The L partner wants his or her share of the business assets. If some of the property has appreciated while in partnership use, the dispute will be especially complicated. How do the partners divide the value of the property as originally brought into the business? Who benefits from the previously unrealized appreciation? This Article explores the property allocation issues that arise when the members of a K and L partnership lack a dispositive agreement. In such circumstances the default rules should provide clear guidance, and the Uniform Partnership Act (U.P.A.) seeks to do so. Unfortunately, many of the decided cases misapply or distort the U.P.A. As a body, the decided cases point in three different and mutually exclusive directions. Individually, they often ignore basic principles of partnership law. This Article takes those basic principles as its lodestar and seeks to determine how the law of partnership should analyze a K and L dispute over property disposition. Part II sets the context for the analysis, introducing partnership law as the applicable law. Part III explains the four basic partnership law concepts necessary to a proper analysis of the Christmas tree paradigm. Part IV describes the three different and mutually exclusive ways that courts have applied partnership concepts to evaluate the courts\u27 incompatible approaches. The analysis presented in Part IV suggests outcomes that some readers may find unfair. Part V confronts the problem of unfairness and tries to determine why courts find K and L property disputes so troublesome. Part V begins by highlighting some of the unbalanced results produced by strict application of partnership law principles. Part V then explores the rationale behind those principles and suggests that courts sometimes disregard the letter of the law in order to serve that underlying, and largely hidden, rationale. Part V next identifies the philosophical and practical problems that arise when courts disregard the clear letter of the law in favor of hidden rationales and instead twist a generally applicable statute in order to avoid reaching a particular unpalatable result. Part V concludes by offering an approach to the Christmas tree problem that substantially alleviates the unfairness problem while remaining faithful to the law. Part VI exemplifies the suggested approach, using concepts developed in previous Parts to resolve correctly the actual Christmas tree case

Colossal magnetostriction and negative thermal expansion in the frustrated antiferromagnet ZnCr2Se4

A detailed investigation of ZnCr2Se4 is presented which is dominated by strong ferromagnetic exchange but orders antiferromagnetically at T_N = 21 K. Specific heat C and thermal expansion Delta L/L exhibit sharp first-order anomalies at the antiferromagnetic transition. T_N is strongly reduced and shifted to lower temperatures by external magnetic fields and finally is fully suppressed suggesting a field induced quantum critical behavior close to 60 kOe. Delta L/L(T) is unusually large and exhibits negative thermal expansion below 75 K down to T_N indicating strong frustration of the lattice. Magnetostriction Delta L/L(H) reveals colossal values (0.5x10^{-3}) comparable to giant magnetostriction materials. Electron-spin resonance, however, shows negligible spin-orbital coupling excluding orbitally induced Jahn-Teller distortions. The obtained results point to a spin-driven origin of the structural instability at T_N explained in terms of competing ferromagnetic and antiferromagnetic exchange interactions yielding strong bond frustration.Comment: 5 pages 4 figure

Spin-driven Phonon Splitting in Bond-frustrated ZnCr2S4

Utilizing magnetic susceptibility, specific heat, thermal expansion and IR spectroscopy we provide experimental evidence that the two subsequent antiferromagnetic transitions in ZnCr_2S_4 at T_N1 = 15 K and T_N2= 8 K are accompanied by significant thermal and phonon anomalies. The anomaly at T_N2 reveals a strong temperature hysteresis typical for a first-order transformation. Due to strong spin-phonon coupling both magnetic phase transitions induce a splitting of phonon modes, where at T_N1 the high-frequency and at T_N2 the low-frequency modes split. The anomalies and phonon splitting observed at T_N2 are strongly suppressed by magnetic field. Regarding the small positive Curie-Weiss temperature Theta= 8 K, we argue that this scenario of two different magnetic phases with concomitant different magneto-elastic couplings results from the strong competition of ferromagnetic and antiferromagnetic exchange of equal strength.Comment: 4 pages, 4 figure

Spin-driven Phase Transitions in ZnCr2_2Se4_4 and ZnCr2_2S4_4 Probed by High Resolution Synchrotron X-ray and Neutron Powder Diffraction

The crystal and magnetic structures of the spinel compounds ZnCr$_2$S$_4$ and ZnCr$_2$Se$_4$ were investigated by high resolution powder synchrotron and neutron diffraction. ZnCr$_2$Se$_4$ exhibits a first order phase transition at $T_N=21$ K into an incommensurate helical magnetic structure. Magnetic fluctuations above $T_N$ are coupled to the crystal lattice as manifested by negative thermal expansion. Both, the complex magnetic structure and the anomalous structural behavior can be related to magnetic frustration. Application of an external magnetic field shifts the ordering temperature and the regime of negative thermal expansion towards lower temperatures. Thereby, the spin ordering changes into a conical structure. ZnCr$_2$S$_4$ shows two magnetic transitions at $T_{N1}=15$ K and $T_{N2}=8$ K that are accompanied by structural phase transitions. The crystal structure transforms from the cubic spinel-type (space group $Fd$\={3}$m$) at high temperatures in the paramagnetic state, via a tetragonally distorted intermediate phase (space group $I4_1$ / $amd$) for $T_{N2} < T < T_{N1}$ into a low temperature orthorhombic phase (space group $I m m a$) for $T < T_{N2}$. The cooperative displacement of sulfur ions by exchange striction is the origin of these structural phase transitions. The low temperature structure of ZnCr$_2$S$_4$ is identical to the orthorhombic structure of magnetite below the Verwey transition. When applying a magnetic field of 5 T the system shows an induced negative thermal expansion in the intermediate magnetic phase as observed in ZnCr$_2$Se$_4$.Comment: 11 pages, 13 figures, to be published in PR

Human-Computer Music Performance: From Synchronized Accompaniment to Musical Partner

Live music performance with computers has motivated many research projects in science, engineering, and the arts. In spite of decades of work, it is surprising that there is not more technology for, and a better understanding of the computer as music performer. We review the development of techniques for live music performance and outline our efforts to establish a new direction, Human-Computer Music Performance (HCMP), as a framework for a variety of coordinated studies. Our work in this area spans performance analysis, synchronization techniques, and interactive performance systems. Our goal is to enable musicians to ncorporate computers into performances easily and effectively through a better understanding of requirements, new techniques, and practical, performance-worthy implementations. We conclude with directions for future work

Real Time Hand Movement Trajectory Tracking for Enhancing Dementia Screening in Ageing Deaf Signers of British Sign Language

Real time hand movement trajectory tracking based on machine learning approaches may assist the early identification of dementia in ageing Deaf individuals who are users of British Sign Language (BSL), since there are few clinicians with appropriate communication skills, and a shortage of sign language interpreters. Unlike other computer vision systems used in dementia stage assessment such as RGB-D video with the aid of depth camera, activities of daily living (ADL) monitored by information and communication technologies (ICT) facilities, or X-Ray, computed tomography (CT), and magnetic resonance imaging (MRI) images fed to machine learning algorithms, the system developed here focuses on analysing the sign language space envelope(sign trajectories/depth/speed) and facial expression of deaf individuals, using normal 2D videos. In this work, we are interested in providing a more accurate segmentation of objects of interest in relation to the background, so that accurate real-time hand trajectories (path of the trajectory and speed) can be achieved. The paper presents and evaluates two types of hand movement trajectory models. In the first model, the hand sign trajectory is tracked by implementing skin colour segmentation. In the second model, the hand sign trajectory is tracked using Part Afinity Fields based on the OpenPose Skeleton Model [1, 2]. Comparisons of results between the two different models demonstrate that the second model provides enhanced improvements in terms of tracking accuracy and robustness of tracking. The pattern differences in facial and trajectory motion data achieved from the presented models will be beneficial not only for screening of deaf individuals for dementia, but also for assessment of other acquired neurological impairments associated with motor changes, for example, stroke and Parkinsons disease

The adenovirus E4orf4 protein targets PP2A to the ACF chromatin-remodeling factor and induces cell death through regulation of SNF2h-containing complexes

The adenovirus E4 open-reading-frame 4 (E4orf4) protein regulates the progression of viral infection and when expressed individually it induces non-classical apoptosis in transformed cells. Here we show that E4orf4 associates with the ATP-dependent chromatin-remodeling factor ACF that consists of a sucrose non fermenting-2h (SNF2h) ATPase and an Acf1 regulatory subunit. Furthermore, E4orf4 targets protein phosphatase 2A (PP2A) to this complex and to chromatin. Obstruction of SNF2h activity inhibits E4orf4-induced cell death, whereas knockdown of Acf1 results in enhanced E4orf4-induced toxicity in both mammalian and yeast cells, and Acf1 overexpression inhibits E4orf4′s ability to downregulate early adenovirus gene expression in the context of viral infection. Knockdown of the Acf1 homolog, WSTF, inhibits E4orf4-induced cell death. Based on these results we suggest that the E4orf4–PP2A complex inhibits ACF and facilitates enhanced chromatin-remodeling activities of other SNF2h-containing complexes, such as WSTF–SNF2h. The resulting switch in chromatin remodeling determines life versus death decisions and contributes to E4orf4 functions during adenovirus infection

Higher CSF sTREM2 attenuates ApoE4-related risk for cognitive decline and neurodegeneration

BACKGROUND: The Apolipoprotein E ε4 allele (i.e. ApoE4) is the strongest genetic risk factor for sporadic Alzheimer's disease (AD). TREM2 (i.e. Triggering receptor expressed on myeloid cells 2) is a microglial transmembrane protein brain that plays a central role in microglia activation in response to AD brain pathologies. Whether higher TREM2-related microglia activity modulates the risk to develop clinical AD is an open question. Thus, the aim of the current study was to assess whether higher sTREM2 attenuates the effects of ApoE4-effects on future cognitive decline and neurodegeneration. METHODS: We included 708 subjects ranging from cognitively normal (CN, n = 221) to mild cognitive impairment (MCI, n = 414) and AD dementia (n = 73) from the Alzheimer's disease Neuroimaging Initiative. We used linear regression to test the interaction between ApoE4-carriage by CSF-assessed sTREM2 levels as a predictor of longitudinally assessed cognitive decline and MRI-assessed changes in hippocampal volume changes (mean follow-up of 4 years, range of 1.7-7 years). RESULTS: Across the entire sample, we found that higher CSF sTREM2 at baseline was associated with attenuated effects of ApoE4-carriage (i.e. sTREM2 x ApoE4 interaction) on longitudinal global cognitive (p = 0.001, Cohen's f2 = 0.137) and memory decline (p = 0.006, Cohen's f2 = 0.104) as well as longitudinally assessed hippocampal atrophy (p = 0.046, Cohen's f2 = 0.089), independent of CSF markers of primary AD pathology (i.e. Aβ1-42, p-tau181). While overall effects of sTREM2 were small, exploratory subanalyses stratified by diagnostic groups showed that beneficial effects of sTREM2 were pronounced in the MCI group. CONCLUSION: Our results suggest that a higher CSF sTREM2 levels are associated with attenuated ApoE4-related risk for future cognitive decline and AD-typical neurodegeneration. These findings provide further evidence that TREM2 may be protective against the development of AD

The Cytosolic Tail of the Golgi Apyrase Ynd1 Mediates E4orf4-Induced Toxicity in Saccharomyces cerevisiae

The adenovirus E4 open reading frame 4 (E4orf4) protein contributes to regulation of the progression of virus infection. When expressed individually, E4orf4 was shown to induce non-classical transformed cell-specific apoptosis in mammalian cells. At least some of the mechanisms underlying E4orf4-induced toxicity are conserved from yeast to mammals, including the requirement for an interaction of E4orf4 with protein phosphatase 2A (PP2A). A genetic screen in yeast revealed that the Golgi apyrase Ynd1 associates with E4orf4 and contributes to E4orf4-induced toxicity, independently of Ynd1 apyrase activity. Ynd1 and PP2A were shown to contribute additively to E4orf4-induced toxicity in yeast, and to interact genetically and physically. A mammalian orthologue of Ynd1 was shown to bind E4orf4 in mammalian cells, confirming the evolutionary conservation of this interaction. Here, we use mutation analysis to identify the cytosolic tail of Ynd1 as the protein domain required for mediation of the E4orf4 toxic signal and for the interaction with E4orf4. We also show that E4orf4 associates with cellular membranes in yeast and is localized at their cytoplasmic face. However, E4orf4 is membrane-associated even in the absence of Ynd1, suggesting that additional membrane proteins may mediate E4orf4 localization. Based on our results and on a previous report describing a collection of Ynd1 protein partners, we propose that the Ynd1 cytoplasmic tail acts as a scaffold, interacting with a multi-protein complex, whose targeting by E4orf4 leads to cell death