PPFM: Image denoising in photon-counting CT using single-step posterior sampling Poisson flow generative models

Diffusion and Poisson flow models have shown impressive performance in a wide range of generative tasks, including low-dose CT image denoising. However, one limitation in general, and for clinical applications in particular, is slow sampling. Due to their iterative nature, the number of function evaluations (NFE) required is usually on the order of $10-10^3$, both for conditional and unconditional generation. In this paper, we present posterior sampling Poisson flow generative models (PPFM), a novel image denoising technique for low-dose and photon-counting CT that produces excellent image quality whilst keeping NFE=1. Updating the training and sampling processes of Poisson flow generative models (PFGM)++, we learn a conditional generator which defines a trajectory between the prior noise distribution and the posterior distribution of interest. We additionally hijack and regularize the sampling process to achieve NFE=1. Our results shed light on the benefits of the PFGM++ framework compared to diffusion models. In addition, PPFM is shown to perform favorably compared to current state-of-the-art diffusion-style models with NFE=1, consistency models, as well as popular deep learning and non-deep learning-based image denoising techniques, on clinical low-dose CT images and clinical images from a prototype photon-counting CT system

Observation of eight-photon entanglement

Using ultra-bright sources of pure-state entangled photons from parametric down conversion, an eight-photon interferometer and post-selection detection, we demonstrate the ability to experimentally manipulate eight individual photons and report the creation of an eight-photon Schr\"odinger cat state with an observed fidelity of $0.708 \pm 0.016$.Comment: 6 pages, 4 figure

Trends in socioeconomic inequalities in smoking prevalence, consumption, initiation, and cessation between 2001 and 2008 in the Netherlands. Findings from a national population survey

<p>Abstract</p> <p>Background</p> <p>Widening of socioeconomic status (SES) inequalities in smoking prevalence has occurred in several Western countries from the mid 1970’s onwards. However, little is known about a widening of SES inequalities in smoking consumption, initiation and cessation.</p> <p>Methods</p> <p>Repeated cross-sectional population surveys from 2001 to 2008 (n ≈ 18,000 per year) were used to examine changes in smoking prevalence, smoking consumption (number of cigarettes per day), initiation ratios (ratio of ever smokers to all respondents), and quit ratios (ratio of former smokers to ever smokers) in the Netherlands. Education level and income level were used as indicators of SES and results were reported separately for men and women.</p> <p>Results</p> <p>Lower educated respondents were significantly more likely to be smokers, smoked more cigarettes per day, had higher initiation ratios, and had lower quit ratios than higher educated respondents. Income inequalities were smaller than educational inequalities and were not all significant, but were in the same direction as educational inequalities. Among women, educational inequalities widened significantly between 2001 and 2008 for smoking prevalence, smoking initiation, and smoking cessation. Among low educated women, smoking prevalence remained stable between 2001 and 2008 because both the initiation and quit ratio increased significantly. Among moderate and high educated women, smoking prevalence decreased significantly because initiation ratios remained constant, while quit ratios increased significantly. Among men, educational inequalities widened significantly between 2001 and 2008 for smoking consumption only.</p> <p>Conclusions</p> <p>While inequalities in smoking prevalence were stable among Dutch men, they increased among women, due to widening inequalities in both smoking cessation and initiation. Both components should be addressed in equity-oriented tobacco control policies.</p

Phylogenetic Detection of Recombination with a Bayesian Prior on the Distance between Trees

Genomic regions participating in recombination events may support distinct topologies, and phylogenetic analyses should incorporate this heterogeneity. Existing phylogenetic methods for recombination detection are challenged by the enormous number of possible topologies, even for a moderate number of taxa. If, however, the detection analysis is conducted independently between each putative recombinant sequence and a set of reference parentals, potential recombinations between the recombinants are neglected. In this context, a recombination hotspot can be inferred in phylogenetic analyses if we observe several consecutive breakpoints. We developed a distance measure between unrooted topologies that closely resembles the number of recombinations. By introducing a prior distribution on these recombination distances, a Bayesian hierarchical model was devised to detect phylogenetic inconsistencies occurring due to recombinations. This model relaxes the assumption of known parental sequences, still common in HIV analysis, allowing the entire dataset to be analyzed at once. On simulated datasets with up to 16 taxa, our method correctly detected recombination breakpoints and the number of recombination events for each breakpoint. The procedure is robust to rate and transition∶transversion heterogeneities for simulations with and without recombination. This recombination distance is related to recombination hotspots. Applying this procedure to a genomic HIV-1 dataset, we found evidence for hotspots and de novo recombination

How coastal strategic planning reflects interrelationships between ecosystem services: a four-step method

Explicit and integrated inclusion of ecosystem services (ESs) and their interrelationships can improve the quality of strategic plans and decision-making processes. However, there is little systematic analysis of how ES interrelationships are framed in policy language, particularly in coastal planning discourse. The objective of this paper is therefore to present a four-step method, based on content analysis, to assess ES interrelationships in coastal strategic planning documents. The method consists of: 1) selecting strategic plans; 2) identifying ESs; 3) identifying drivers, ESs and their effects; and 4) constructing relational diagrams. The four-step method is applied to a case of Jiaozhou Bay in China, demonstrating its capacity of identifying which drivers and ES trade-offs and synergies are formulated in coastal strategic plans. The method is helpful to identify overlooked ES interrelationships, inform temporal and spatial issues, and assess the continuity of plans' attention to interrelationships. The main methodological contributions are discussed by emphasizing its broad scope of drivers and ESs and an explicit distinction among the cause of relationships. The developed method also has the potential of cross-fertilizing other kinds of approaches and facilitating practical planning processes

Systemic circulatory influences on retinal microvascular function in middle-age individuals with low to moderate cardiovascular risk

Purpose: To investigate the relationship between retinal microvascular reactivity, circulatory markers for CVD risk and systemic antioxidative defence capacity in healthy middle-aged individuals with low to moderate risk of CVD. Methods: Retinal vascular reactivity to flickering light was assessed in 102 healthy participants (46-60 years) by means of dynamic retinal vessel analysis (DVA). Other vascular assessments included carotid intima-media thickness (C-IMT) and blood pressure (BP) measurements. Total cholesterol (CHOL), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), triglycerides (TG) and blood glutathione levels in its reduced (GSH) and oxidized (GSSG) forms were also determined for each participant, along with Framingham risk scores (FRS). Results: Retinal arterial baseline diameter fluctuation (BDF) was independently, significantly and negatively influenced by LDL-C levels (β = -0.53, p = 0.027). Moreover, the arterial dilation slope (SlopeAD) was independently, significantly and positively associated with redox index (GSH: GSSG ratio, β = 0.28, p = 0.016), while the arterial constriction slope (SlopeAC) was significantly and negatively influenced by blood GSH levels (β = -0.20, p = 0.042), and positively associated with FRS (β = 0.25, p = 0.009). Venous BDF and dilation amplitude (DA) were also negatively influenced by plasma LDL-C levels (β = -0.83, p = 0.013; and β = -0.22, p = 0.028, respectively). Conclusions: In otherwise healthy individuals with low to moderate cardiovascular risk, retinal microvascular dilation and constriction responses to stress levels are influenced by systemic antioxidant capacity, and circulating markers for cardiovascular risk

NCAM180 Regulates Ric8A Membrane Localization and Potentiates β-Adrenergic Response

Cooperation between receptors allows integrated intracellular signaling leading to appropriate physiological responses. The Neural Cell Adhesion Molecule (NCAM) has three main isoforms of 120, 140 and 180 kDa, with adhesive and signaling properties, but their respective functions remains to be fully identified. Here we show that the human NCAM180 intracellular domain is a novel interactor of the human guanosine exchange factor (GEF) Ric8A using the yeast two hybrid system and immunoprecipitation. Furthermore, NCAM, Ric8A and Gαs form a tripartite complex. Colocalization experiments by confocal microscopy revealed that human NCAM180 specifically induces the recruitment of Ric8A to the membrane. In addition, using an in vitro recombinant system, and in vivo by comparing NCAM knock-out mouse brain to NCAM heterozygous and wild type brains, we show that NCAM expression dose dependently regulates Ric8A redistribution in detergent resistent membrane microdomains (DRM). Previous studies have demonstrated essential roles for Ric8 in Gα protein activity at G protein coupled receptors (GPCR), during neurotransmitter release and for asymmetric cell division. We observed that inhibition of Ric8A by siRNA or its overexpression, decreases or increases respectively, cAMP production following β-adrenergic receptor stimulation. Furthermore, in human HEK293T recombinant cells, NCAM180 potentiates the Gαs coupled β-adrenergic receptor response, in a Ric8A dependent manner, whereas NCAM120 or NCAM140 do not. Finally, in mouse hippocampal neurons expressing endogenously NCAM, NCAM is required for the agonist isoproterenol to induce cAMP production, and this requirement depends on Ric8A. These data illustrate a functional crosstalk between a GPCR and an IgCAM in the nervous system