Probing the low-lying level structure of 94Zr through β¯ decay

223-227Low-lying states of 94Zr are populated following b- decay of 94Y, and the emitted g rays from 94Zr are detected using the 8p spectrometer composed of 20 Compton-suppressed HPGe detectors. High- statistics coincidence data have been used for the placement of very weak decay branches in the level scheme. Combining the results of level lifetimes from a previous experiment and the precisely measured branching ratio values of the weak decay branches from the present experiment, it is possible to extract the B(E2) values for all the possible decay branches from a given level. These values are helpful for proper identification of the collective and non-collective states of 94Zr. The experimental findings have been compared with predictions from shell-model calculations with a limited valence space; however, these calculations are inadequate in reproducing all of the measured spectroscopic quantities

Widespread Tau-Specific CD4 T Cell Reactivity in the General Population

Tau protein is found to be aggregated and hyperphosphorylated (p-tau) in many neurologic disorders, including Parkinson disease (PD) and related parkinsonisms, Alzheimer disease, traumatic brain injury, and even in normal aging. Although not known to produce autoimmune responses, we hypothesized that the appearance of aggregated tau and p-tau with disease could activate the immune system. We thus compared T cell responses to tau and p-tau–derived peptides between PD patients, age-matched healthy controls, and young healthy controls (<35 y old; who are less likely to have high levels of tau aggregates). All groups exhibited CD4+ T cell responses to tau-derived peptides, which were associated with secretion of IFN-γ, IL-5, and/or IL-4. The PD and control participants exhibited a similar magnitude and breadth of responses. Some tau-derived epitopes, consisting of both unmodified and p-tau residues, were more highly represented in PD participants. These results were verified in an independent set of PD and control donors (either age-matched or young controls). Thus, T cells recognizing tau epitopes escape central and peripheral tolerance in relatively high numbers, and the magnitude and nature of these responses are not modulated by age or PD disease

T cells from patients with Parkinson’s disease recognize α-synuclein peptides

Genetic studies have shown the association of Parkinson's disease with alleles of the major histocompatibility complex. Here we show that a defined set of peptides that are derived from α-synuclein, a protein aggregated in Parkinson's disease, act as antigenic epitopes displayed by these alleles and drive helper and cytotoxic T cell responses in patients with Parkinson's disease. These responses may explain the association of Parkinson's disease with specific major histocompatibility complex alleles