How the Commonwealth of the Northern Mariana Islands Stalled COVID-19 for 22 Months and Managed its First Significant Community Transmission

OBJECTIVE: The Commonwealth of the Northern Mariana Islands (CNMI) is a remote Pacific island territory with a population of 47 329 that successfully prevented the significant introduction of coronavirus disease (COVID-19) until late 2021. This study documents how the response to the introduction of COVID-19 in CNMI in 2021 was conducted with limited resources without overwhelming local clinical capacity or compromising health service delivery for the population. METHODS: Data from COVID-19 case investigations, contact tracing, the Commonwealth\u27s immunization registry and whole genome sequencing were collated and analysed as part of this study. RESULTS: Between 26 March 2020 and 31 December 2021, 3281 cases and 14 deaths due to COVID-19 were reported in CNMI (case fatality rate, 0.4%). While notification rates were highest among younger age groups, hospitalization and mortality rates were disproportionately greater among those aged \u3e 50 years and among the unvaccinated. The first widespread community transmission in CNMI was detected in October 2021, with genomic epidemiology and contact tracing data indicating a single introduction event involving the AY.25 lineage and subsequent rapid community spread. Vaccination coverage was high before widespread transmission occurred in October 2021 and increased further over the study period. DISCUSSION: Robust preparedness and strong leadership generated resilience within the public health sector such that COVID-19 did not overwhelm CNMI\u27s health system as it did in other jurisdictions and countries around the world. At no point was hospital capacity exceeded, and all patients received adequate care without the need for health-care rationing

Measurement of the Inclusive Semi-electronic D0D^0 Branching Fraction

Using the angular correlation between the $\pi^+$ emitted in a $D^{*+} \rightarrow D^0 \pi^+$ decay and the $e^+$ emitted in the subsequent $D^0 \rightarrow Xe^+\nu$ decay, we have measured the branching fraction for the inclusive semi-electronic decay of the $D^0$ meson to be: {\cal B}(D^0 \rightarrow X e^+ \nu) = [6.64 \pm 0.18 (stat.) \pm 0.29 (syst.)] \%. The result is based on 1.7 fb$^{-1}$ of $e^+e^-$ collisions recorded by the CLEO II detector located at the Cornell Electron Storage Ring (CESR). Combining the analysis presented in this paper with previous CLEO results we find, \frac{{\cal B} (D^0 \rightarrow X e^+ \nu)} {{\cal B} (D^0 \rightarrow K^- \pi^+)} = 1.684 \pm 0.056 (stat.) \pm 0.093(syst.) and \frac{{\cal B}(D\rightarrow K^-e^+\nu)} {{\cal B}(D\rightarrow Xe^+\nu)} = 0.581 \pm 0.023 (stat.) \pm 0.028(syst.). The difference between the inclusive rate and the sum of the measured exclusive branching fractions (measured at CLEO and other experiments) is $(3.3 \pm 7.2) \%$ of the inclusive rate.Comment: Latex file, 33pages, 4 figures Submitted to PR

Impact of Aspergillus fumigatus in allergic airway diseases

For decades, fungi have been recognized as associated with asthma and other reactive airway diseases. In contrast to type I-mediated allergies caused by pollen, fungi cause a large number of allergic diseases such as allergic bronchopulmonary mycoses, rhinitis, allergic sinusitis and hypersensitivity pneumonitis. Amongst the fungi, Aspergillus fumigatus is the most prevalent cause of severe pulmonary allergic disease, including allergic bronchopulmonary aspergillosis (ABPA), known to be associated with chronic lung injury and deterioration in pulmonary function in people with chronic asthma and cystic fibrosis (CF). The goal of this review is to discuss new understandings of host-pathogen interactions in the genesis of allergic airway diseases caused by A. fumigatus. Host and pathogen related factors that participate in triggering the inflammatory cycle leading to pulmonary exacerbations in ABPA are discussed

The evolving SARS-CoV-2 epidemic in Africa: Insights from rapidly expanding genomic surveillance

INTRODUCTION Investment in Africa over the past year with regard to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) sequencing has led to a massive increase in the number of sequences, which, to date, exceeds 100,000 sequences generated to track the pandemic on the continent. These sequences have profoundly affected how public health officials in Africa have navigated the COVID-19 pandemic. RATIONALE We demonstrate how the first 100,000 SARS-CoV-2 sequences from Africa have helped monitor the epidemic on the continent, how genomic surveillance expanded over the course of the pandemic, and how we adapted our sequencing methods to deal with an evolving virus. Finally, we also examine how viral lineages have spread across the continent in a phylogeographic framework to gain insights into the underlying temporal and spatial transmission dynamics for several variants of concern (VOCs). RESULTS Our results indicate that the number of countries in Africa that can sequence the virus within their own borders is growing and that this is coupled with a shorter turnaround time from the time of sampling to sequence submission. Ongoing evolution necessitated the continual updating of primer sets, and, as a result, eight primer sets were designed in tandem with viral evolution and used to ensure effective sequencing of the virus. The pandemic unfolded through multiple waves of infection that were each driven by distinct genetic lineages, with B.1-like ancestral strains associated with the first pandemic wave of infections in 2020. Successive waves on the continent were fueled by different VOCs, with Alpha and Beta cocirculating in distinct spatial patterns during the second wave and Delta and Omicron affecting the whole continent during the third and fourth waves, respectively. Phylogeographic reconstruction points toward distinct differences in viral importation and exportation patterns associated with the Alpha, Beta, Delta, and Omicron variants and subvariants, when considering both Africa versus the rest of the world and viral dissemination within the continent. Our epidemiological and phylogenetic inferences therefore underscore the heterogeneous nature of the pandemic on the continent and highlight key insights and challenges, for instance, recognizing the limitations of low testing proportions. We also highlight the early warning capacity that genomic surveillance in Africa has had for the rest of the world with the detection of new lineages and variants, the most recent being the characterization of various Omicron subvariants. CONCLUSION Sustained investment for diagnostics and genomic surveillance in Africa is needed as the virus continues to evolve. This is important not only to help combat SARS-CoV-2 on the continent but also because it can be used as a platform to help address the many emerging and reemerging infectious disease threats in Africa. In particular, capacity building for local sequencing within countries or within the continent should be prioritized because this is generally associated with shorter turnaround times, providing the most benefit to local public health authorities tasked with pandemic response and mitigation and allowing for the fastest reaction to localized outbreaks. These investments are crucial for pandemic preparedness and response and will serve the health of the continent well into the 21st century

Trait anxiety impairs cognitive flexibility when overcoming a task acquired response and a preexisting bias

Individuals with high trait anxiety tend to be worse at flexibly adapting goal-directed behavior to meet changing demands relative to those with low trait anxiety. Past research on anxiety and cognitive flexibility has used tasks that involve overcoming a recently acquired rule, strategy, or response pattern after an abrupt change in task requirements (e.g., choice X led to positive outcomes but now leads to negative outcomes). An important limitation of this research is that many decision making situations require overcoming a preexisting bias (e.g., deciding whether to withdraw a historically winning investment that has experienced recent losses). In the present study we examined whether anxiety differences in the ability to overcome an acquired response extend to the ability to overcome a preexisting bias, when the bias produces objectively disadvantageous decisions. High anxiety (n = 78) and low anxiety participants (n = 76) completed a commonly used measure of cognitive flexibility, reversal learning, and a novel Framed Gambling Task that assessed the extent to which they could make advantageous decisions when the normatively correct choice was inconsistent with a preexisting framing bias. High anxiety participants showed the expected diminished reversal learning performance and also had poorer ability to make advantageous choices that were inconsistent with the framing bias. Worse performance in the Framed Gambling Task was not driven by poor knowledge of risk contingencies, because high anxiety participants reported the same explicit knowledge as low anxiety participants. Instead, the results suggest high anxiety is associated with general deficits in resolving interference from prepotent responses

Working memory loads differentially influence frame-induced bias and normative choice in risky decision making.

Risky decision making can be biased by several types of contextual factors-in particular, framing of outcomes. A popular explanation for outcome framing effects is based on presumed affective reactions that contribute to accepting sure gains and avoiding sure losses. Other theories propose that selective weighting of information about gains and losses contributes to framing bias. Prior research on framing bias has focused on preferences rather than on decisions in which choices can be classified as advantageous (correct) or disadvantageous (incorrect) by a normative criterion. The current study used a novel hypothetical risky decision making task offering choices between a sure option and a gamble option. The gamble was advantageous or disadvantageous on different trials based on the normative criterion of expected value. Results showed risk avoidance with a gain frame and risk seeking with a loss frame, comparable to findings when choices involve preferences. We also examined the impact of working memory loads of either non-affective stimuli, most likely to interfere with acquisition of choice information, or affective stimuli, which might influence affective processes contributing to framing. The results were that non-affective working memory load produced the greatest framing magnitude, while affective load produced changes in framing magnitude across trials that varied by valence. In addition, only the non-affective load decreased advantageous choices and reduced the accuracy of answers to knowledge probe questions about the choices. The findings are consistent with the notion that framing effects may arise from cognitive non-engagement with the task, rather than arising by way of affective processes. Affective loads had a limited influence on framing and no reliable impact on choice accuracy or choice knowledge, suggesting that the affective loads influenced the weighting of choice information

Shortcomings of the behavioral competition theory of contrast: Reanalysis of McLean (1992)

McLean (1992) presented significant data showing that the occurrence of behavioral contrast in a multiple schedule was correlated with shifts in the frequency of reinforcers from a second source between components of the schedule, and interpreted his results as showing that contrast was due to changes in the degree of response competition within the constant component of the multiple schedule. Reanalysis of his data shows that there was an effect of reinforcement in the alternative component of the schedule independent of the shifts in reinforcers between components. Thus, the effect of relative rate of reinforcement cannot be ascribed, at least entirely, to the mechanisms proposed by the behavioral competition theory of contrast