Collective Sensemaking Around COVID-19: Experiences, Concerns, and Agendas for our Rapidly Changing Organizational Lives

Uncertainty is at the forefront of many crises, disasters, and emergencies, and the COVID-19 pandemic is no different in this regard. In this forum, we, as a group of organizational communication scholars currently living in North America, engage in sensemaking and sensegiving around this pandemic to help process and share some of the academic uncertainties and opportunities relevant to organizational scholars. We begin by reflexively making sense of our own experiences with adjusting to new ways of working during the onset of the pandemic, including uncomfortable realizations around privilege, positionality, race, and ethnicity. We then discuss key concerns about how organizations and organizing practices are responding to this extreme uncertainty. Finally, we offer thoughts on the future of work and organizing informed by COVID-19, along with a list of research practice considerations and potentially generative research questions. Thus, this forum invites you to reflect on your own experiences and suggests future directions for research amidst and after a cosmology event

Data-driven models of dominantly-inherited Alzheimer’s disease progression

Dominantly-inherited Alzheimer's disease is widely hoped to hold the key to developing interventions for sporadic late onset Alzheimer's disease. We use emerging techniques in generative data-driven disease-progression modelling to characterise dominantly-inherited Alzheimer’s disease progression with unprecedented resolution, and without relying upon familial estimates of years until symptom onset (EYO). We retrospectively analysed biomarker data from the sixth data freeze of the Dominantly Inherited Alzheimer Network observational study, including measures of amyloid proteins and neurofibrillary tangles in the brain, regional brain volumes and cortical thicknesses, brain glucose hypometabolism, and cognitive performance from the Mini-Mental State Examination (all adjusted for age, years of education, sex, and head size, as appropriate). Data included 338 participants with known mutation status (211 mutation carriers: 163 PSEN1; 17 PSEN2; and 31 APP) and a baseline visit (age 19–66; up to four visits each, 1·1±1·9 years in duration; spanning 30 years before, to 21 years after, parental age of symptom onset). We used an event-based model to estimate sequences of biomarker changes from baseline data across disease subtypes (mutation groups), and a differential-equation model to estimate biomarker trajectories from longitudinal data (up to 66 mutation carriers, all subtypes combined). The two models concur that biomarker abnormality proceeds as follows: amyloid deposition in cortical then sub-cortical regions (approximately 24±11 years before onset); CSF p-tau (17±8 years), tau and Aβ42 changes; neurodegeneration first in the putamen and nucleus accumbens (up to 6±2 years); then cognitive decline (7±6 years), cerebral hypometabolism (4±4 years), and further regional neurodegeneration. Our models predicted symptom onset more accurately than EYO: root-mean-squared error of 1·35 years versus 5·54 years. The models reveal hidden detail on dominantly-inherited Alzheimer's disease progression, as well as providing data-driven systems for fine-grained patient staging and prediction of symptom onset with great potential utility in clinical trials

Inclusive production of ρ0(770),f0(980)\rho^{0}(770), f_0(980) and f2(1270)f_2(1270) mesons in νμ\nu_{\mu} charged current interactions

The inclusive production of the meson resonances $\rho^{0}(770)$, $f_0(980)$ and $f_2(1270)$ in neutrino-nucleus charged current interactions has been studied with the NOMAD detector exposed to the wide band neutrino beam generated by 450 GeV protons at the CERN SPS. For the first time the $f_{0}(980)$ meson is observed in neutrino interactions. The statistical significance of its observation is 6 standard deviations. The presence of $f_{2}(1270)$ in neutrino interactions is reliably established. The average multiplicity of these three resonances is measured as a function of several kinematic variables. The experimental results are compared to the multiplicities obtained from a simulation based on the Lund model. In addition, the average multiplicity of $\rho^{0}(770)$ in antineutrino - nucleus interactions is measured.Comment: 23 pages, 14 figures, 8 tables. To appear in Nucl. Phys.

Observation of the Decays B0->K+pi-pi0 and B0->rho-K+

We report the observation of B^0 decays to the K^+pi^-pi^0 final state using a data sample of 78 fb^-1 collected by the Belle detector at the KEKB e^+e^- collider. With no assumptions about intermediate states in the decay, the branching fraction is measured to be (36.6^{+4.2}_{-4.3}+- 3.0)*10^-6.We also search for B decays to intermediate two-body states with the same K^+pi^-pi^0 final state. Significant B signals are observed in the rho(770)^- K^+ and K^*(892)^+pi^- channels, with branching fractions of (15.1^{+3.4+1.4+2.0}_{-3.3-1.5-2.1})* 10^-6 and (14.8^{+4.6+1.5+2.4}_{-4.4-1.0-0.9})* 10^-6, respectively. The first error is statistical, the second is systematic and the third is due to the largest possible interference. Contributions from other possible two-body states will be discussed. No CP asymmetry is found in the inclusive K^+pi^-pi^0 or rho^-K^+ modes, and we set 90% confidence level bounds on the asymmetry of -0.12<A_{CP}<0.26 and -0.18<A_{CP}<0.64, respectively.Comment: 18 pages, 7 figure

Observation of B+ -> K+ eta gamma

We report measurements of radiative B decays with K eta gamma final states, using a data sample of 253 /fb recorded at the Upsilon(4S) resonance with the Belle detector at the KEKB e+e- storage ring. We observe B+ -> K+ eta gamma for the first time with a branching fraction of (8.4 +- 1.5(stat) +1.2 -0.9(syst)) X 10^{-6} for M(Keta) K0 eta gamma. We also search for B -> K3*(1780) gamma.Comment: 12 pages, 5 figures, accepted by Phys. Lett.

Clinical and Biomarker Changes in Dominantly Inherited Alzheimer's Disease

BACKGROUND: The order and magnitude of pathologic processes in Alzheimer's disease are not well understood, partly because the disease develops over many years. Autosomal dominant Alzheimer's disease has a predictable age at onset and provides an opportunity to determine the sequence and magnitude of pathologic changes that culminate in symptomatic disease. METHODS: In this prospective, longitudinal study, we analyzed data from 128 participants who underwent baseline clinical and cognitive assessments, brain imaging, and cerebrospinal fluid (CSF) and blood tests. We used the participant's age at baseline assessment and the parent's age at the onset of symptoms of Alzheimer's disease to calculate the estimated years from expected symptom onset (age of the participant minus parent's age at symptom onset). We conducted cross-sectional analyses of baseline data in relation to estimated years from expected symptom onset in order to determine the relative order and magnitude of pathophysiological changes. RESULTS: Concentrations of amyloid-beta (Aβ)(42) in the CSF appeared to decline 25 years before expected symptom onset. Aβ deposition, as measured by positron-emission tomography with the use of Pittsburgh compound B, was detected 15 years before expected symptom onset. Increased concentrations of tau protein in the CSF and an increase in brain atrophy were detected 15 years before expected symptom onset. Cerebral hypometabolism and impaired episodic memory were observed 10 years before expected symptom onset. Global cognitive impairment, as measured by the Mini-Mental State Examination and the Clinical Dementia Rating scale, was detected 5 years before expected symptom onset, and patients met diagnostic criteria for dementia at an average of 3 years after expected symptom onset. CONCLUSIONS: We found that autosomal dominant Alzheimer's disease was associated with a series of pathophysiological changes over decades in CSF biochemical markers of Alzheimer's disease, brain amyloid deposition, and brain metabolism as well as progressive cognitive impairment. Our results require confirmation with the use of longitudinal data and may not apply to patients with sporadic Alzheimer's disease. (Funded by the National Institute on Aging and others; DIAN ClinicalTrials.gov number, NCT00869817.)

Measurement of the Branching Fraction for B->eta' K and Search for B->eta'pi+

We report measurements for two-body charmless B decays with an eta' meson in the final state. Using 11.1X10^6 BBbar pairs collected with the Belle detector, we find BF(B^+ ->eta'K^+)=(79^+12_-11 +-9)x10^-6 and BF(B^0 -> eta'K^0)=(55^+19_-16 +-8)x10^-6, where the first and second errors are statistical and systematic, respectively. No signal is observed in the mode B^+ -> eta' pi^+, and we set a 90% confidence level upper limit of BF(B^+-> eta'pi^+) eta'K^+- decays is investigated and a limit at 90% confidence level of -0.20<Acp<0.32 is obtained.Comment: Submitted to Physics Letters

Time-Dependent CP Violation Effects in Partially Reconstructed B0→D∗πB^0 \to D^* \pi Decays

We report measurements of time-dependent decay rates for $B^0 \to D^{*\mp} \pi^\pm$ decays and extraction of CP violation parameters related to $\phi_3$. We use a partial reconstruction technique, whereby signal events are identified using information only from the primary pion and the charged pion from the decay of the $D^{*\mp}$. The analysis uses $140 {\rm fb}^{-1}$ of data accumulated at the $\Upsilon(4S)$ resonance with the Belle detector at the KEKB asymmetric-energy $e^{+}e^{-}$ collider. We measure the CP violation parameters $S^+ = 0.035 \pm 0.041 ({\rm stat}) \pm 0.018 ({\rm syst})$ and $S^- = 0.025 \pm 0.041 ({\rm stat}) \pm 0.018 ({\rm syst})$.Comment: 15 pages, 5 figures. To appear in Physics Letters