Trusts - Principal and Income - Apportionment Under Pennsylvania Rule of Stock Dividends Based on Capital Surplus

Under the terms of a trust established in New York in 1915 income was to be paid to a beneficiary for life and upon his death the principal was to be distributed to certain descendants of the settlor. Two extraordinary stock distributions were received by the trust during the life of the income beneficiary. In issuing the additional shares each of the corporations had transferred to capital stock account its entire capital surplus and sufficient earned surplus to support the additional shares at their par value. At the time of creation of the trust New York applied the Pennsylvania rule for apportioning stock dividends between principal and income. The trustee determined what percentage of the amount transferred to capital stock account on the corporate books represented earned surplus and allocated to income that percentage of the additional stock received by the trustee. The remainder of the stock, which represented capitalization of capital surplus, was allocated to principal, although part of it could have been given to income without impairing the intact value of the stock given to the trust by the settlor, that is, the book value at the time of the creation of the trust plus any natural capital increments. The life beneficiary\u27s executors objected to the allocation. In a proceeding to settle the trustee\u27s accounts the lower court ordered a referee to determine whether certain items were properly includible in capital surplus for trust purposes. The appellate division upheld the apportionment as made by the trustee. On appeal, held, affirmed, two judges dissenting. The income beneficiary is entitled to no more of a stock distribution than can be connected with the capitalization of earned surplus. In re Bingham\u27s Will, (N.Y. 1959) 163 N.E. (2d) 301

Acute neuroinflammation induces AIS structural plasticity in a NOX2-dependent manner

Background Chronic microglia-mediated inflammation and oxidative stress are well-characterized underlying factors in neurodegenerative disease, whereby reactive inflammatory microglia enhance ROS production and impact neuronal integrity. Recently, it has been shown that during chronic inflammation, neuronal integrity is compromised through targeted disruption of the axon initial segment (AIS), the axonal domain critical for action potential initiation. AIS disruption was associated with contact by reactive inflammatory microglia which wrap around the AIS, increasing association with disease progression. While it is clear that chronic microglial inflammation and enhanced ROS production impact neuronal integrity, little is known about how acute microglial inflammation influences AIS stability. Here, we demonstrate that acute neuroinflammation induces AIS structural plasticity in a ROS-mediated and calpain-dependent manner. Methods C57BL/6J and NOX2−/− mice were given a single injection of lipopolysaccharide (LPS; 5 mg/kg) or vehicle (0.9% saline, 10 mL/kg) and analyzed at 6 h–2 weeks post-injection. Anti-inflammatory Didox (250 mg/kg) or vehicle (0.9% saline, 10 mL/kg) was administered beginning 24 h post-LPS injection and continued for 5 days; animals were analyzed 1 week post-injection. Microglial inflammation was assessed using immunohistochemistry (IHC) and RT-qPCR, and AIS integrity was quantitatively analyzed using ankyrinG immunolabeling. Data were statistically compared by one-way or two-way ANOVA where mean differences were significant as assessed using Tukey’s post hoc analysis. Results LPS-induced neuroinflammation, characterized by enhanced microglial inflammation and increased expression of ROS-producing enzymes, altered AIS protein clustering. Importantly, inflammation-induced AIS changes were reversed following resolution of microglial inflammation. Modulation of the inflammatory response using anti-inflammatory Didox, even after significant AIS disruption occurred, increased the rate of AIS recovery. qPCR and IHC analysis revealed that expression of microglial NOX2, a ROS-producing enzyme, was significantly increased correlating with AIS disruption. Furthermore, ablation of NOX2 prevented inflammation-induced AIS plasticity, suggesting that ROS drive AIS structural plasticity. Conclusions In the presence of acute microglial inflammation, the AIS undergoes an adaptive change that is capable of spontaneous recovery. Moreover, recovery can be therapeutically accelerated. Together, these findings underscore the dynamic capabilities of this domain in the presence of a pathological insult and provide evidence that the AIS is a viable therapeutic target

The effect of vacuum polarisation on muon-proton scattering at small energies and angles

We give a compact expression for the unpolarised differential cross section for muon-proton scattering in the one photon exchange approximation. The effect of adding the vacuum polarisation amplitude to the no-spin-flip amplitude for one photon exchange is calculated at small energies and scattering angles and is found to be negligible for present experiments.Comment: 6 pages, one figur

COMPTEL solar flare observations

COMPTEL as part of a solar target of opportunity campaign observed the sun during the period of high solar activity from 7-15 Jun. 1991. Major flares were observed on 9 and 11 Jun. Although both flares were large GOES events (greater than or = X10), they were not extraordinary in terms of gamma-ray emission. Only the decay phase of the 15 Jun. flare was observed by COMPTEL. We report the preliminary analysis of data from these flares, including the first spectroscopic measurement of solar flare neutrons. The deuterium formation line at 2.223 MeV was present in both events and for at least the 9 Jun. event, was comparable to the flux in the nuclear line region of 4-8 MeV, consistent with Solar-Maximum Mission (SSM) Observations. A clear neutron signal was present in the flare of 9 Jun. with the spectrum extending up to 80 MeV and consistent in time with the emission of gamma-rays, confirming the utility of COMPTEL in measuring the solar neutron flux at low energies. The neutron flux below 100 MeV appears to be lower than that of the 3 Jun. 1982 flare by more than an order of magnitude. The neutron signal of the 11 Jun. event is under study. Severe dead time effects resulting from the intense thermal x-rays require significant corrections to the measured flux which increase the magnitude of the associated systematic uncertainties

Transplantation of Ciliary Neurotrophic Factor-Expressing Adult Oligodendrocyte Precursor Cells Promotes Remyelination and Functional Recovery after SpinalCord Injury

Demyelination contributes to the dysfunction after traumatic spinal cord injury (SCI). We explored whether the combination of neurotrophic factors and transplantation of adult rat spinal cord oligodendrocyte precursor cells (OPCs) could enhance remyelination and functional recovery after SCI. Ciliary neurotrophic factor (CNTF) was the most effective neurotrophic factor to promote oligodendrocyte (OL) differentiation and survival of OPCs in vitro. OPCs were infected with retroviruses expressing enhanced green fluorescent protein (EGFP) or CNTF and transplanted into the contused adult thoracic spinal cord 9 d after injury. Seven weeks after transplantation, the grafted OPCs survived and integrated into the injured spinal cord. The survival of grafted CNTF-OPCs increased fourfold compared with EGFP-OPCs. The grafted OPCs differentiated into adenomatus polyposis coli (APC+) OLs, and CNTF significantly increased the percentage of APC+ OLs from grafted OPCs. Immunofluorescent and immunoelectron microscopic analyses showed that the grafted OPCs formed central myelin sheaths around the axons in the injured spinal cord. The number of OL-remyelinated axons in ventrolateral funiculus (VLF) or lateral funiculus (LF) at the injured epicenter was significantly increased in animals that received CNTF-OPC grafts compared with all other groups. Importantly, 75% of rats receiving CNTF-OPC grafts recovered transcranial magnetic motor-evoked potential and magnetic interenlargement reflex responses, indicating that conduction through the demyelinated axons in VLF or LF, respectively, was partially restored. More importantly, recovery of hindlimb locomotor function was significantly enhanced in animals receiving grafts of CNTF-OPCs. Thus, combined treatment with OPC grafts expressing CNTF can enhance remyelination and facilitate functional recovery after traumatic SCI

Escape Behavior of Quantum Two-Particle Systems with Coulomb Interactions

Quantum escapes of two particles with Coulomb interactions from a confined one-dimensional region to a semi-infinite lead are discussed by the probability of particles remaining in the confined region, i.e. the survival probability, in comparison with one or two free particles. For free-particle systems the survival probability decays asymptotically in power as a function of time. On the other hand, for two-particle systems with Coulomb interactions it shows an exponential decay in time. A difference of escape behaviors between Bosons and Fermions is considered as quantum effects of identical two particles such as the Pauli exclusion principle. The exponential decay in the survival probability of interacting two particles is also discussed in a viewpoint of quantum chaos based on a distribution of energy level spacings.Comment: 10 pages, 7 figure