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To better understand the epidemiology of SARS-CoV-2 reinfections, we analyzed national data from South Korean who were followed longitudinally from January 2020 to April 2022. We conducted a nationwide retrospective cohort study to estimate possible SARS-CoV-2 reinfection rates in all residents in South Korea, with at least two episodes of laboratory-confirmed SARS-CoV-2 infection by reverse-transcriptase polymerase chain reaction or rapid antigen test (RAT) performed at least 45 or more days between both episodes, between January 2020 and April 2022. There were 16 130 855 laboratory-confirmed SARS-CoV-2 cases in South Korea, with 55 841 (346.2 per 100 000; or 0.3% of all infections) cases of possible reinfections. The reinfection rate has increased from 6.0 cases per 100 000 during Pre-Delta period to 128.0 cases per 100 000 and 355.1 cases per 100 000 during Delta and Omicron periods, respectively. Persons with one dose of vaccination had the highest reinfection rate of 642.2 per 100 000, followed by unvaccinated persons (536.2/100 000) and two-dose vaccinated persons (406.3/100 000). Our finding suggests that the majority of possible reinfections occurred following the emergence of new variants.

Hepatic glucose production (HGP) is crucial for the maintenance of normal glucose homeostasis. Although hepatic insulin resistance contributes to excessive glucose production, its mechanism is not well understood. Here, we show that inositol polyphosphate multikinase (IPMK), a key enzyme in inositol polyphosphate biosynthesis, plays a role in regulating hepatic insulin signaling and gluconeogenesis both in vitro and in vivo. IPMK-deficient hepatocytes exhibit decreased insulin-induced activation of Akt-FoxO1 signaling. The expression of messenger RNA levels of phosphoenolpyruvate carboxykinase 1 (Pck1) and glucose 6-phosphatase (G6pc), key enzymes mediating gluconeogenesis, are increased in IPMK-deficient hepatocytes compared to wild type hepatocytes. Importantly, re-expressing IPMK restores insulin sensitivity and alleviates glucose production in IPMK-deficient hepatocytes. Moreover, hepatocyte-specific IPMK deletion exacerbates hyperglycemia and insulin sensitivity in mice fed a high-fat diet, accompanied by an increase in HGP during pyruvate tolerance test and reduction in Akt phosphorylation in IPMK deficient liver. Our results demonstrate that IPMK mediates insulin signaling and gluconeogenesis and may be potentially targeted for treatment of diabetes.

Changepoint detection methods are used in many areas of science and engineering, for example, in the analysis of copy number variation data to detect abnormalities in copy numbers along the genome. Despite the broad array of available tools, methodology for quantifying our uncertainty in the strength (or the presence) of given changepoints post-selection are lacking. Post-selection inference offers a framework to fill this gap, but the most straightforward application of these methods results in low-powered hypothesis tests and leaves open several important questions about practical usability. In this work, we carefully tailor post-selection inference methods toward changepoint detection, focusing on copy number variation data. To accomplish this, we study commonly used changepoint algorithms: binary segmentation, as well as two of its most popular variants, wild and circular, and the fused lasso. We implement some of the latest developments in post-selection inference theory, mainly auxiliary randomization. This improves the power, which requires implementations of Markov chain Monte Carlo algorithms (importance sampling and hit-and-run sampling) to carry out our tests. We also provide recommendations for improving practical useability, detailed simulations, and example analyses on array comparative genomic hybridization as well as sequencing data.

The p75 neurotrophin receptor (p75NTR ) is required for maintaining peripheral sensory neuron survival and function; however, the underlying cellular mechanism remains unclear. The general view is that expression of p75NTR by the neuron itself is required for maintaining sensory neuron survival and myelination in the peripheral nervous system (PNS). Adopting a neuronal-specific conditional knockout strategy, we demonstrate the partial depletion of p75NTR in neurons exerts little influence upon maintaining sensory neuron survival and peripheral nerve myelination in health and after demyelinating neuropathy. Our data show that the density and total number of dorsal root ganglion (DRG) neurons in 2-month-old mice is not affected following the deletion of p75NTR in large-diameter myelinating neurons, as assessed by stereology. Adopting experimental autoimmune neuritis induced in adult male mice, an animal model of demyelinating peripheral neuropathy, we identify that deleting p75NTR in myelinating neurons exerts no influence upon the disease progression, the total number of DRG neurons, and the extent of myelin damage in the sciatic nerve, indicating that the expression of neuronal p75NTR is not essential for maintaining peripheral neuron survival and myelination after a demyelinating insult in vivo. Together, results of this study suggest that the survival and myelination of peripheral sensory neurons is independent of p75NTR expressed by a subtype of neurons in vivo. Thus, our findings provide new insights into the mechanism underpinning p75NTR -mediated neuronal survival in the PNS.

This paper revisits the claim that members of legislative committees direct more earmark spending to their constituents. In South Korea's legislature, a national law regulating the budget committee provides an unusual source of exogenous variation in membership: members of the committee are rotated each year owing to 1‐year term limits. Using data from 226 local governments, and both within‐district and within‐member variations in membership, we find that districts represented by a budget committee member secure roughly 3% more subsidies than those represented by a nonmember. (JEL D72, D78, H70)

Global low‐carbon transition demands the development of large‐scale infrastructure, which is sand intensive. Natural sand is widely considered abundant, whereas recent research has pointed out the increasing risk of supply shortage in a number of world regions. In the current research, we examine the implication of future sand demand in the context of low‐carbon infrastructure development. We mapped the projected investments on buildings and low‐carbon infrastructure up to 2030 and estimated the sand intensity of the two types of construction. We translated these investments and sand intensity to country‐specific sand‐demand projections under three economic development scenarios. Our results indicate that China is expected to face the highest sand demand, followed by India, and that should the current sand extraction rates and construction practices be maintained, developing countries will be exposed to a significant supply risk of construction sand. Under the scenario of sustainable growth, developed economies are expected to have a relatively stable sand demand whereas South‐East Asia and Africa will see a rapid increase in their sand demand over the next 15 years. Our results call regional sand supply security into attention in low‐carbon transition planning.

Understanding the environmental consequences of actions is becoming increasingly important in the field of industrial ecology in general, and in life cycle assessment (LCA) more specifically. However, a consensus on how to operationalize this idea has not been reached. A variety of methods have been proposed and applied to case studies that cover various aspects of consequential life cycle assessment (CLCA). Previous reviews of the topic have focused on the broad agenda of CLCA and how different modeling frameworks fit into its goals. However, explicit examination of the spectrum of methods and their application to the different facets of CLCA are lacking. Here, we provide a detailed review of methods that have been used to construct models of the environmental consequences of actions in CLCA. First, we cover the following structural modeling approaches: (a) economic equilibrium models, (b) system dynamics models, (c) technology choice models, and (d) agent‐based models. We provide a detailed review of particular applications of each model in the CLCA domain. The advantages and disadvantages of each are discussed, and their relationships with CLCA are clarified. From this, we are able to map these models onto the established aspects of CLCA. We learn that structural models alone are not sufficient to quantify the uncertainty distributions of underlying parameters in CLCA, which are essential components of a robust analysis of consequences. To address this, we provide a brief introduction to a counterfactual‐based causal inference approach to parameter identification and uncertainty analysis that is emerging in the CLCA literature. We recommend that one potential research path forward is the establishment of feedback loops between empirical estimates and structural models.

In this study, we evaluated the effects of anacardic acid (AA), a phenolic lipid found in cashew nuts (Anacardium occidentale), on metabolic disorders related to obesity, fatty liver disease, and diabetes using both in vitro and in vivo models. The application of AA led to a reduction in lipid accumulation in 3T3‐L1 cells without observable cytotoxicity. Results from Western blot analysis revealed that AA treatment also led to decreased expression of fatty acid synthase and peroxisome proliferator‐activated receptor gamma. In vivo studies were performed to evaluate the effects of AA treatment on fatty liver disease and diabetes. Mice fed a high‐fat and high‐sucrose diet had significantly higher body and liver weights, and higher levels of liver fat, cholesterol, fasting glucose, and homeostasis model assessment of insulin resistance (HOMA‐IR). However, 12 weeks of oral treatment with 500 μg/kg BW AA slowed down lipid accumulation rates in the liver and mitigated insulin resistance in these mice. Thus, AA may reduce lipid levels and have an antidiabetic effect., Anacardic acid inhibits lipid accumulation in 3T3‐L1 cells. Anacardic acid reduces lipid accumulation in mice fed high‐fat and high‐sucrose diet. Anacardic acid mitigates insulin resistance in mice fed high‐fat and high‐sucrose diet.

Herein, we report a polar-radical relay strategy for α-C-H amination of cyclic amines with N-chloro-N-sodio-carbamates. The relay is initiated by in situ generation of cyclic iminium intermediate using N-iodosuccinimide (NIS) oxidant as an initiator, which then operates through a series of polar (addition and elimination) and radical (homolysis, hydrogen- and halogen atom transfer) reactions to enable the challenging C-N bond formation in a controlled manner. A broad range of α-amino cyclic amines were readily accessed with excellent regioselectivity, and the superb applicability was further demonstrated by functionalization of biologically relevant compounds.