Implementation of Tai Chi Among Individuals with Dementia in Long-Term Memory Care

This project focused on a dementia population within long-term care, where increased disablement occurs. A Tai Chi program was implemented into the daily routine of individuals in a long-term memory care facility to improve dynamic sitting balance for the performance of daily occupations.https://soar.usa.edu/otdcapstonessummer2023/1048/thumbnail.jp

ZFOURGE: Using Composite Spectral Energy Distributions to Characterize Galaxy Populations at 1<z<4

We investigate the properties of galaxies as they shut off star formation over the 4 billion years surrounding peak cosmic star formation. To do this we categorize $\sim7000$ galaxies from $1<z<4$ into $90$ groups based on the shape of their spectral energy distributions (SEDs) and build composite SEDs with $R\sim 50$ resolution. These composite SEDs show a variety of spectral shapes and also show trends in parameters such as color, mass, star formation rate, and emission line equivalent width. Using emission line equivalent widths and strength of the 4000\AA\ break, $D(4000)$, we categorize the composite SEDs into five classes: extreme emission line, star-forming, transitioning, post-starburst, and quiescent galaxies. The transitioning population of galaxies show modest H$\alpha$ emission ($EW_{\rm REST}\sim40$\AA) compared to more typical star-forming composite SEDs at $\log_{10}(M/M_\odot)\sim10.5$ ($EW_{\rm REST}\sim80$\AA). Together with their smaller sizes (3 kpc vs. 4 kpc) and higher S\'ersic indices (2.7 vs. 1.5), this indicates that morphological changes initiate before the cessation of star formation. The transitional group shows a strong increase of over one dex in number density from $z\sim3$ to $z\sim1$, similar to the growth in the quiescent population, while post-starburst galaxies become rarer at $z\lesssim1.5$. We calculate average quenching timescales of 1.6 Gyr at $z\sim1.5$ and 0.9 Gyr at $z\sim2.5$ and conclude that a fast quenching mechanism producing post-starbursts dominated the quenching of galaxies at early times, while a slower process has become more common since $z\sim2$.Comment: Accepted for publication in The Astrophysical Journa

Identification of target antigens of anti-endothelial cell and anti-vascular smooth muscle cell antibodies in patients with giant cell arteritis: a proteomic approach

International audienceABSTRACT: INTRODUCTION: Immunological studies of giant cell arteritis (GCA) suggest that a triggering antigen of unknown nature could generate a specific immune response. We thus decided to detect autoantibodies directed against endothelial cells (ECs) and vascular smooth muscle cells (VSMCs) in the serum of GCA patients and to identify their target antigens. METHODS: Sera from 15 GCA patients were tested in 5 pools of 3 patients' sera and compared to a sera pool from 12 healthy controls (HCs). Serum immunoglobulin G (IgG) reactivity was analysed by 2-D electrophoresis and immunoblotting with antigens from human umbilical vein ECs (HUVECs) and mammary artery VSMCs. Target antigens were identified by mass spectrometry. RESULTS: Serum IgG from GCA patients recognised 162 ± 3 (mean ± SD) and 100 ± 17 (mean ± SD) protein spots from HUVECs and VSMCs, respectively, and that from HCs recognised 79 and 94 protein spots, respectively. In total, 30 spots from HUVECs and 19 from VSMCs were recognised by at least two-thirds and three-fifths, respectively, of the pools of sera from GCA patients and not by sera from HCs. Among identified proteins, we found vinculin, lamin A/C, voltage-dependent anion-selective channel protein 2, annexin V and other proteins involved in cell energy metabolism and key cellular pathways. Ingenuity pathway analysis revealed that most identified target antigens interacted with growth factor receptor-bound protein 2. CONCLUSIONS: IgG antibodies to proteins in the proteome of ECs and VSMCs are present in the sera of GCA patients and recognise cellular targets that play key roles in cell biology and maintenance of homeostasis. Their potential pathogenic role remains to be determined

A Multilevel Model for Comorbid Outcomes: Obesity and Diabetes in the US

Multilevel models are overwhelmingly applied to single health outcomes, but when two or more health conditions are closely related, it is important that contextual variation in their joint prevalence (e.g., variations over different geographic settings) is considered. A multinomial multilevel logit regression approach for analysing joint prevalence is proposed here that includes subject level risk factors (e.g., age, race, education) while also taking account of geographic context. Data from a US population health survey (the 2007 Behavioral Risk Factor Surveillance System or BRFSS) are used to illustrate the method, with a six category multinomial outcome defined by diabetic status and weight category (obese, overweight, normal). The influence of geographic context is partly represented by known geographic variables (e.g., county poverty), and partly by a model for latent area influences. In particular, a shared latent variable (common factor) approach is proposed to measure the impact of unobserved area influences on joint weight and diabetes status, with the latent variable being spatially structured to reflect geographic clustering in risk

Diagnostic algorithm for papillary urothelial tumors in the urinary bladder

Papillary urothelial neoplasms with deceptively bland cytology cannot be easily classified. We aimed to design a new algorithm that could differentiate between these neoplasms based on a scoring system. We proposed a new scoring system that enables to reproducibly diagnose non-invasive papillary urothelial tumors. In this system, each lesion was given individual scores from 0 to 3 for mitosis and cellular thickness, from 0 to 2 for cellular atypia, and an additional score for papillary fusion. These scores were combined to form a summed score allowing the tumors to be ranked as follows: 0–1 = UP, 2–4 = low malignant potential (LMP), 5–7 = low-grade transitional cell carcinoma (TCC), and 8–9 = high-grade TCC. In addition to the scoring system, ancillary studies of MIB and p53 indexes with CK20 expression pattern analyses were compared together with clinical parameters. The MIB index was strongly correlated with disease progression. Four of the 22 LMP patients (18.2%) had late recurrences, two of these four (9.1%) had progression to low-grade carcinoma. The MIB index for LMP patients was strongly associated with recurrence (recurrence vs. non-recurrence, 16.5 vs. 8.1, p < 0.001). The proposed scoring system could enhance the reproducibility to distinguish papillary urothelial neoplasms

Circadian Rhythm and Sleep Disruption: Causes, Metabolic Consequences and Countermeasures.

Circadian (∼ 24 hour) timing systems pervade all kingdoms of life, and temporally optimize behaviour and physiology in humans. Relatively recent changes to our environments, such as the introduction of artificial lighting, can disorganize the circadian system, from the level of the molecular clocks that regulate the timing of cellular activities to the level of synchronization between our daily cycles of behaviour and the solar day. Sleep/wake cycles are intertwined with the circadian system, and global trends indicate that these too are increasingly subject to disruption. A large proportion of the world's population is at increased risk of environmentally-driven circadian rhythm and sleep disruption, and a minority of individuals are also genetically predisposed to circadian misalignment and sleep disorders. The consequences of disruption to the circadian system and sleep are profound and include myriad metabolic ramifications, some of which may be compounded by adverse effects on dietary choices. If not addressed, the deleterious effects of such disruption will continue to cause widespread health problems; therefore, implementation of the numerous behavioural and pharmaceutical interventions that can help restore circadian system alignment and enhance sleep will be important

Cross-talk between circadian clocks, sleep-wake cycles, and metabolic networks: Dispelling the darkness.

Integration of knowledge concerning circadian rhythms, metabolic networks, and sleep-wake cycles is imperative for unraveling the mysteries of biological cycles and their underlying mechanisms. During the last decade, enormous progress in circadian biology research has provided a plethora of new insights into the molecular architecture of circadian clocks. However, the recent identification of autonomous redox oscillations in cells has expanded our view of the clockwork beyond conventional transcription/translation feedback loop models, which have been dominant since the first circadian period mutants were identified in fruit fly. Consequently, non-transcriptional timekeeping mechanisms have been proposed, and the antioxidant peroxiredoxin proteins have been identified as conserved markers for 24-hour rhythms. Here, we review recent advances in our understanding of interdependencies amongst circadian rhythms, sleep homeostasis, redox cycles, and other cellular metabolic networks. We speculate that systems-level investigations implementing integrated multi-omics approaches could provide novel mechanistic insights into the connectivity between daily cycles and metabolic systems.ABR is a Wellcome Trust Senior Clinical Fellow and receives funding from the Wellcome Trust (Grant No. 100333/Z/12/Z), the European Research Council (ERC Starting Grant No. 281348, MetaCLOCK), the European Molecular Biology Organization (EMBO) Young Investigators Programme, and the Lister Institute of Preventative Medicine. SR is supported by the Wellcome Trust.This is the final version of the article. It first appeared from Wiley via https://doi.org/10.1002/bies.20150005

MYO6 Regulates Spatial Organization of Signaling Endosomes Driving AKT Activation and Actin Dynamics

APPL1- and RAB5-positive signaling endosomes play a crucial role in the activation of AKT in response to extracellular stimuli. Myosin VI (MYO6) and two of its cargo adaptor proteins, GIPC and TOM1/TOM1L2, localize to these peripheral endosomes and mediate endosome association with cortical actin filaments. Loss of MYO6 leads to the displacement of these endosomes from the cell cortex and accumulation in the perinuclear space. Depletion of this myosin not only affects endosome positioning, but also induces actin and lipid remodeling consistent with endosome maturation, including accumulation of F-actin and the endosomal lipid PI(3)P. These processes acutely perturb endosome function, as both AKT phosphorylation and RAC-dependent membrane ruffling were markedly reduced by depletion of either APPL1 or MYO6. These results place MYO6 and its binding partners at a central nexus in cellular signaling linking actin dynamics at the cell surface and endosomal signaling in the cell cortex