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This research seeks to unpack the development of the EU as a security actor in cyberspace. Drawing on the theoretical approach of role theory, this article shows that the EU’s role in cyberspace should be understood in relationality to the other poles. On the one hand, the declining hegemonic role of the US in cyberspace as well as the divergence between the US and the EU with regard to cybersecurity governance has made the EU more aware of the need for cyber sovereignty and strategic autonomy. Therefore, the EU seeks to pursue a role of an autonomous cybersecurity player through the enactment of cybersecurity at institutional and operational level. On the other hand, under conditions of increasing interdependence, the EU has considered international cooperation to address challenges in cyberspace as a strategic priority, therefore seeking to act as a promoter of a multi-stakeholder model. Moreover, interpolariy in cyberspace determines the contestation of EU role by other poles. While the EU has recorded some small successes as a regulation-setter, emerging poles of power in the cybersecurity domain contest the EU’s desired role, promoting more state-centric approaches and seeking to transfer regulatory authority in the cybersecurity domain to the UN.

Background: Accumulating evidence has shown that disorders in the gut microbiota and derived metabolites affect the development of atherosclerotic cardiovascular disease (ASCVD). However, which and how specific gut microbial metabolites contribute to the progression of atherosclerosis and the clinical relevance of their alterations remain unclear. Methods: We performed integrated microbiome–metabolome analysis of 30 patients with coronary artery disease (CAD) and 30 age- and sex-matched healthy controls to identify CAD-associated microbial metabolites, which were then assessed in an independent population of patients with ASCVD and controls (n=256). We further investigate the effect of CAD-associated microbial metabolites on atherosclerosis and the mechanisms of the action. Results: Indole-3-propionic acid (IPA), a solely microbially derived tryptophan metabolite, was the most downregulated metabolite in patients with CAD. Circulating IPA was then shown in an independent population to be associated with risk of prevalent ASCVD and correlated with the ASCVD severity. Dietary IPA supplementation alleviates atherosclerotic plaque development in ApoE −/− mice. In murine- and human-derived macrophages, administration of IPA promoted cholesterol efflux from macrophages to ApoA-I through an undescribed miR-142-5p/ABCA1 (ATP-binding cassette transporter A1) signaling pathway. Further in vivo studies demonstrated that IPA facilitates macrophage reverse cholesterol transport, correlating with the regulation of miR-142-5p/ABCA1 pathway, whereas reduced IPA production contributed to the aberrant overexpression of miR-142-5p in macrophages and accelerated the progression of atherosclerosis. Moreover, the miR-142-5p/ABCA1/reverse cholesterol transport axis in macrophages were dysregulated in patients with CAD, and correlated with the changes in circulating IPA levels. Conclusions: Our study identify a previously unknown link between specific gut microbiota-derived tryptophan metabolite and ASCVD. The microbial metabolite IPA/miR-142-5p/ABCA1 pathway may represent a promising therapeutic target for ASCVD.

Whether and to what extent the relationship between physical activity (PA) and colorectal cancer (CRC) differs according to CRC-related genetic risk remains to be determined, and no studies to date have quantified how much genetically determined risk could be compensated for with active exercise.Genetic risk was quantified by a polygenic risk score (PRS) summarizing the estimated effect of 140 CRC-associated genetic variants. Associations of PA with CRC risk were estimated by multivariable logistic regression across PRS levels. We also compared the impact of PA and specific PA types to the PRS using "genetic risk equivalent (GRE)", a novel approach to enhance effective risk communication.Among 5058 CRC patients and 4134 controls, we observed no significant association between overall PA level in quartiles and CRC risk. However, the highest versus lowest lifetime leisure time physical activity (LTPA) was associated with a 13% lower CRC risk [odds ratio 0.87, 95% confidence interval (CI) 0.77-1.00] independent of PRS levels (adjusted p value for interaction = 0.18). This effect was equivalent to the effect of having 11 percentiles lower PRS (GRE -10.6, 95% CI -20.7 to -0.6). The GRE (95% CI) for the highest lifetime sports tertile was -23.0 (-33.9 to -12.0).LTPA was inversely associated with CRC risk irrespective of polygenic risk for CRC, which reinforces the importance of LTPA in CRC prevention among the general population. Adequate sports activity can compensate for a large share of polygenic risk for CRC.

BackgroundIncidence of colorectal cancer (CRC) in younger adults is increasing in many countries. Smoking is an established risk factor of CRC risk, but evidence on its impact on early-onset CRC (EOCRC) risk is limited. We aimed to evaluate the association of smoking exposure with EOCRC and compare it with late-onset CRC (LOCRC).MethodsSmoking history and other known or suspected CRC risk factors were ascertained in detail in personal interviews among 6264 CRC patients and 6866 controls (frequency matched for age, sex, and county of residence) who were recruited in 2003-2020 in the DACHS study (Darmkrebs: Chancen der Verhütung durch Screening [German]; Colorectal Cancer: Chances for Prevention Through Screening [English]), a population-based case-control study from Germany. Associations of smoking with EOCRC (ResultsSmoking exposure was much higher among EOCRC cases than among controls, and strong associations of smoking were observed for both EOCRC and LOCR. Adjusted odds ratios for EOCRC and LOCRC were as follows: current smoking: 1.57 (95% confidence interval [CI] = 1.20 to 2.04, P ConclusionSmoking is a strong risk factor for both EOCRC and LOCRC.

Background:Tobacco smoking is an established risk factor for colorectal cancer. However, genetically defined population subgroups may have increased susceptibility to smoking-related effects on colorectal cancer.Methods:A genome-wide interaction scan was performed including 33,756 colorectal cancer cases and 44,346 controls from three genetic consortia.Results:Evidence of an interaction was observed between smoking status (ever vs. never smokers) and a locus on 3p12.1 (rs9880919, P = 4.58 × 10−8), with higher associated risk in subjects carrying the GG genotype [OR, 1.25; 95% confidence interval (CI), 1.20–1.30] compared with the other genotypes (OR Conclusions:Our study identified novel genetic loci that may modulate the risk for colorectal cancer of smoking status and intensity, linked to tumor suppression and immune response.Impact:These findings can guide potential prevention treatments.

ImportanceExcess weight, the prevalence of which is high and increasing in many countries, is linked to multiple adverse health outcomes, including increased colorectal cancer (CRC) risk. Better communication of health risks associated with excess weight might support efforts of prevention.ObjectiveTo evaluate the individual and joint associations of body mass index (BMI) and polygenic risk with CRC, to assess potential interactions among them, and to quantify by how much increased polygenic risk for CRC can be offset by having a BMI within reference range.Design, Setting, and ParticipantsThis population-based case-control study was conducted in the Rhine-Neckar region of southwest Germany, with recruitment from 2003 to 2017. Participants with both risk factor and genetic information were included for analysis. Data analysis was conducted from December 8, 2021, to February 17, 2022.ExposuresBMI was calculated as self-reported weight in kilograms approximately 10 years before diagnosis or interview and current height in meters squared. A polygenic risk score (PRS) was built based on 140 CRC-related risk loci.Main Outcomes and MeasuresIndividual and joint associations of BMI and PRS with CRC were estimated using multiple logistic regression. Associations of excess weight with CRC were quantified by adjusted odds ratios (aORs) and genetic risk equivalents (GREs), the equivalent outcomes conveyed by defined differences in PRS percentiles.ResultsAmong 9169 participants (median [IQR] age, 69 [62-76] years; 5589 [61.0%] male participants) included, 5053 had CRC and 4116 did not. BMI of 30 or greater was associated with higher odds of having CRC compared with BMI less than 25 (aOR, 1.71; 95% CI, 1.49-1.97), independent of PRS levels (P for interaction = .45). Participants with BMI of 30 or greater and a PRS in the highest tertile had higher odds of CRC compared with participants with BMI less than 25 and a PRS in the lowest tertile (aOR, 3.82; 95% CI, 3.03-4.82). The estimated association of BMI greater than 30 with CRC risk was equivalent to that of having a 41 (95% CI, 29-53)–percentile higher PRS. BMI of 30 or greater was particularly associated with stage IV CRC (aOR, 2.21; 95% CI, 1.71-2.84).Conclusions and RelevanceThese findings suggest that excess weight was associated with CRC regardless of PRS levels. The association of having a BMI within reference range may be similar to that of having a substantially lower polygenic risk for CRC.

This research responds to an increasing volume of scholarly literature unpacking the recent dynamics of EU foreign policy discourses and practices vis-à-vis China. Drawing on the theoretical approach of collective securitisation, this article shows that EU foreign policy towards China since the mid-2010s has witnessed increasing collective securitisation moves directed at multiple policy frames, including Asian regional security frame, economic security frame, political security frame and information and technology and cybersecurity frame. The EU’s attempts to securitise China as an existential threat across multiple issue areas have been triggered by a combination of long-term trends and specific sets of precipitating events, which contributed to galvanising the EU’s collective securitising discourses and subsequent policy initiatives. However, this research finds that the EU’s securitising moves and relevant speech acts have not resulted in a coherent audience response among the EU member states. The divergent views held by the EU’s internal audience on whether China should be perceived as an existential threat have hampered the implementation of the EU’s collective policy outputs.

Background Obesity is an established risk factor for colorectal cancer (CRC), but the evidence for the association is inconsistent across molecular subtypes of the disease. Methods We pooled data on body mass index (BMI), tumor microsatellite instability status, CpG island methylator phenotype status, BRAF and KRAS mutations, and Jass classification types for 11 872 CRC cases and 11 013 controls from 11 observational studies. We used multinomial logistic regression to estimate odds ratios (OR) and 95% confidence intervals (CI) adjusted for covariables. Results Higher BMI was associated with increased CRC risk (OR per 5 kg/m2 = 1.18, 95% CI = 1.15 to 1.22). The positive association was stronger for men than women but similar across tumor subtypes defined by individual molecular markers. In analyses by Jass type, higher BMI was associated with elevated CRC risk for types 1-4 cases but not for type 5 CRC cases (considered familial-like/Lynch syndrome microsatellite instability-H, CpG island methylator phenotype-low or negative, BRAF-wild type, KRAS-wild type, OR = 1.04, 95% CI = 0.90 to 1.20). This pattern of associations for BMI and Jass types was consistent by sex and design of contributing studies (cohort or case-control). Conclusions In contrast to previous reports with fewer study participants, we found limited evidence of heterogeneity for the association between BMI and CRC risk according to molecular subtype, suggesting that obesity influences nearly all major pathways involved in colorectal carcinogenesis. The null association observed for the Jass type 5 suggests that BMI is not a risk factor for the development of CRC for individuals with Lynch syndrome.

Evidence is lacking on the impact of alcohol consumption on colorectal cancer (CRC) risk (overall and by age at diagnosis) by polygenic risk score (PRS) levels, and it is unclear how the magnitude of CRC risk associated with alcohol consumption compares to the magnitude of genetically determined risk.Multiple logistic regression was used to assess the association between alcohol consumption and colorectal cancer (CRC) across PRS levels based on 140 CRC-related loci among 5104 CRC cases and 4131 controls from a large population-based case-control study. We compared the effects for alcohol consumption and PRS on CRC risk using the "Genetic Risk Equivalent (GRE)" for effective risk communication. Specific analyses were conducted for early-onset CRC (EOCRC,55 years) and late-onset CRC (LOCRC, ≥55 years).High alcohol consumption, and to a lower extent, also alcohol abstinence were associated with increased CRC risk. Compared to low alcohol consumption (0·1-25 g/d), lifetime average alcohol consumption ≥25 g/d was more strongly associated with EOCRC [odds ratio (OR) 1·8, 95% confidence interval (CI) 1·2-2·8] than with LOCRC risk (OR 1·3, 95% CI 1·1-1·4) (Excessive alcohol use was strongly associated with EOCRC risk, independent of PRS levels. Abstaining from heavy drinking could reduce risk for CRC, in particular for EOCRC to an extent that would be equivalent to having a much lower genetically determined risk.The first author (X.C.) was supported by the Guangzhou Elite Project (GEP). The DACHS study was supported by grants from the German Research Council (BR 1704/6-1, BR1704/6-3, BR 1704/6-4, BR 1704/6-6, CH 117/1-1, BR 1704/17-1, HO 5117/2-1) and the German Federal Ministry of Education and Research (01KH0404, 01ER0814, 01ER0815, 01GL1712).

By employing discourse-historical approach and corpus linguistics, this paper examines media reports to analyze the Chinese official discourse in the context of the COVID-19 outbreak. The results demonstrate that a paradox of globalism and nationalism has been simultaneously reflected when reporting the global pandemic. Based on a polarizing discursive construction of positive "self" and negative "others," on many occasions, the globalist and nationalist arguments have been closely intertwined and complement each other to reinforce the legitimacy of the ruling party at home and the international reputation of China under the leadership of the ruling party.

Polygenic risk scores (PRSs) could help to define personalized colorectal cancer (CRC) screening strategies. The aim of this study was to evaluate whether a PRS, along with adenoma characteristics, could help to define more personalized and risk-adapted surveillance intervals.In a population-based, case-control study from Germany, detailed information on previous colonoscopies and a PRS based on 140 CRC-related, single-nucleotide polymorphisms was obtained from 4696 CRC cases and 3709 controls. Participants were classified as having low, medium, or high genetic risk according to tertiles of PRSs among controls. We calculated the absolute risk of CRC based on the PRS and colonoscopy history and findings.We observed major variations of CRC risk according to the PRS, including among individuals with detection and removal of adenomas at colonoscopy. For instance, the estimated 10-year absolute risk of CRC for 50-year-old men and women with no polyps, for whom repeat screening colonoscopy is recommended after 10 years only, was 0.2%. Equivalent absolute risks were estimated for people with low-risk adenomas and low PRS. However, the same levels of absolute risk were reached within 3 to 5 years by those with low-risk adenomas and high PRS and with high-risk adenomas irrespective of the PRS.Consideration of genetic predisposition to CRC risk, as determined by a PRS, could help to define personalized, risk-adapted surveillance intervals after detection and removal of adenomas at screening colonoscopy. However, whether the risk variation is strong enough to direct clinical risk stratification needs to be explored further.

Emerging evidence has shown the potential of oral microbiota as a noninvasive diagnostic tool in gastrointestinal (GI) cancer. PubMed, Web of Science, and Embase were systematically searched for eligible studies published until May 31, 2019. Of the 17 included studies published between 2011 and 2019, five kinds of GI cancer, including colorectal cancer (n=6), pancreatic cancer (n=5), gastric cancer (n=4), esophageal cancer (n=2) and liver cancer (n=1), were reported. Generally, the diagnostic performance of the multi-bacteria model for GI cancer was strong with the best area under the receiver operator characteristic curve (AUC) exceeding 0.90, but only one study had a validation phase. Pathogens involved in periodontal disease, such as Porphyromonas gingivalis and Tannerella forsythia, were linked to various kinds of GI cancer. Besides, more oral bacteria significantly differed between cases with upper digestive cancer and healthy controls when compared to colorectal cancer (the most common form of lower digestive cancer), probably indicating a different mechanism due to anatomical and physiological differences in the digestive tract. Oral microbiota changes were associated with risk of various kinds of GI cancer, which could be considered as a potential tool for early prediction and prevention of GI cancer, but validation based on a large population, reproducible protocols for oral microbiota research and oral-gut microbiota transmission patterns are required to be resolved in further studies.

Background The regular use of non-steroidal anti-inflammatory drugs (NSAIDs) has been associated with reduced colorectal cancer (CRC) risk. Aim To explore whether this association varies according to background polygenic risk for CRC. Methods Data were collected from a large population-based case-control study on CRC in Germany. A polygenic risk score (PRS) based on 140 CRC-related risk loci was used to quantify the genetic risk. The associations of regular use of NSAIDs (≥2times per week for at least 1 year) with CRC risk were estimated in the whole population and in subgroups according to PRS levels using multivariable logistic regression. The impact of NSAIDs on CRC risk was compared to PRS using the 'genetic risk equivalent' (GRE), a recently developed metric for effective risk communication. Results In total 5129 CRC cases and 4093 controls were included in this analysis. The regular use of NSAIDs (including aspirin) was associated with reduced CRC risk [odds ratio (OR) 0.66, 95% confidence interval (CI) 0.59, 0.74], as was regular use of aspirin only (OR 0.73, 95% CI 0.65, 0.83), without indication of interaction with the PRS (P = 0.10 and 0.22 respectively). The effect of NSAID use was equivalent to the effect of having a 32 percentiles lower PRS (GRE -32, 95% CI -41, -22). Conclusions The regular use of NSAIDs is associated with greatly reduced CRC risk regardless of individual genetic profile. With an equivalent reduction of relative risk across all polygenic risk groups, absolute risk reduction would be expected to be strongest among those with the highest polygenic risk score.

The past decade has witnessed an increasing nexus between the European Union’s trade and foreignpolicy toward Asia. On the one hand, the EU has sought to deepen economic cooperation with its keyAsian partners since this region has become central to the EU’s economic growth. On the other hand,the EU has increasingly used its trade policy as a foreign policy tool to pursue its geopolitical interestsin Asia. Against this background, the paper seeks to examine the dynamics of trade relations betweenthe EU and its Asian partners by adopting the role theory. Using this theory, this paper aims to providea holistic understanding of how the EU’s changing role in the EU-Asia trade relations has affected itspursuit of economic as well as geopolitical interests in Asia.

In this paper, we integrate inertial navigation system (INS) with wireless sensor network (WSN) to enhance the accuracy of indoor localization. Inertial measurement unit (IMU), the core of the INS, measures the accelerated and angular rotated speed of moving objects. Meanwhile, the ranges from the object to beacons, which are sensor nodes with known coordinates, are collected by time of arrival (ToA) approach. These messages are simultaneously collected and transmitted to the terminal. At the terminal, we set up the state transition models and observation models. According to them, several recursive Bayesian algorithms are applied to producing position estimations. As shown in the experiments, all of three algorithms do not require constant moving speed and perform better than standalone ToA system or standalone IMU system. And within them, two algorithms can be applied for the tracking on any path which is not restricted by the requirement that the trajectory between the positions at two consecutive time steps is a straight line.

To overcome the limitation of single search strategy of grey wolf optimizer (GWO) in solving various function optimization problems, we propose a multi-strategy ensemble GWO (MEGWO) in this paper. The proposed MEGWO incorporates three different search strategies to update the solutions. Firstly, the enhanced global-best lead strategy can improve the local search ability of GWO by fully exploiting the search space around the current best solution. Secondly, the adaptable cooperative strategy embeds one-dimensional update operation into the framework of GWO to provide a higher population diversity and promote the global search ability. Thirdly, the disperse foraging strategy forces a part of search agents to explore a promising area based on a self-adjusting parameter, which contributes to the balance between the exploitation and exploration. We conducted numerical experiments based on various functions form CEC2014. The obtained results are compared with other three modified GWO and seven state-of-the-art algorithms. Furthermore, feature selection is employed to investigate the effectiveness of MEGWO on real-world applications. The experimental results show that the proposed algorithm which integrate multiple improved search strategies, outperforms other variants of GWO and other algorithms in terms of accuracy and convergence speed. It is validated that MEGWO is an efficient and reliable algorithm not only for optimization of functions with different characteristics but also for real-world optimization problems.

Grey wolf optimizer (GWO) is an efficient swarm intelligence algorithm for kinds of optimization problems. However, GWO tends to be trapped in local optimum when solving large-scale problems. Social hierarchy is one of the main characteristics of GWO which affect the searching efficiency. Thus, an improved algorithm called hierarchy strengthened GWO (HSGWO) is proposed in this paper. First, the pack of wolves is roughly divided into two categories: dominant wolves and omega wolves. Second, the enhanced elite learning strategy is performed for dominant wolves to prevent the misguidance of low-ranking wolves and improve the collective efficiency. Then, the hybrid GWO and differential evolution (DE) strategy is executed for omega wolves to avoid falling into local optimum. In addition, a new hybrid one-dimensional and total-dimensional selection strategy is designed for omega wolves to balance the exploration and the exploitation during optimization. Finally, a perturbed operator is used to maintain the diversity of the population and further improve the exploration. To make a complete evaluation, the proposed HSGWO is first compared with six representative GWO variants for 50-dimensional problems based on CEC2014 benchmarks. The scalability of HSGWO is further tested by comparing it with eight state-of-the-art non-GWO algorithms for large-scale optimization problems with 100 decision variables. In addition, feature selection problem is used for testing the effectiveness of HSGWO on real-world applications. The experimental results demonstrated that the proposed algorithm outperforms other algorithms in terms of solution quality and convergence rate in most of the experiments.

In this paper, we propose a novel distributed digital transmission framework for two jointly sparse correlated signals. First, the non-zero coefficients of each signal are quantized by a standard quantizer or a novel distributed quantizer, as appropriate. Then, these quantized values are mapped to the elements of a finite field, except 0, while the zero coefficients are mapped to 0. Subsequently, compressed sensing over finite fields is applied to obtain measurements. We name such an order first quantization then compressed sensing. The two measurement signals are then converted to bit sequences, modulated, and transmitted through separate additive white Gaussian noise (AWGN) channels. At the central receiver, which has access to both channels, following demodulation, an innovative joint belief propagation (JBP) algorithm is performed for joint recovery. In this algorithm, we introduce a new type of constraint node, i.e., correlation constraint nodes, which connect two factor graphs that separately represent the CS encoding matrix of each signal. The experimental results prove that under the same framework the proposed scheme provides significant performance improvements compared to the scheme that ignores the correlated information between jointly sparse signals, especially when the correlation coefficient is high. Then, to answer the question of which order is better, we construct the first compressed sensing, then quantization framework, for fairness, two cutting edge jointly greedy pursuit algorithms are separately adopted at the joint decoder. Through simulations, we validate that the proposed framework provides more effective and robust transmissions.

Introduction Smoking and genetic predisposition are established risk factors for colorectal cancer (CRC). We aimed to assess and compare their individual and joint impact on CRC risk using the novel approach of genetic risk equivalent (GRE). Methods Data were extracted from the Darmkrebs: Chancen der Verhutung durch Screening study, a large population-based case-control study in Germany. A polygenic risk score (PRS) based on 140 CRC-related single nucleotide polymorphisms was derived to quantify genetic risk. Multiple logistic regression was used to estimate the individual and joint impact of smoking and PRS on CRC risk, and to quantify the smoking effect in terms of GRE, the corresponding effect conveyed by a defined difference in PRS percentiles. Results There were 5,086 patients with CRC and 4,120 controls included. Current smokers had a 48% higher risk of CRC than never smokers (adjusted odds ratio 1.48, 95% confidence interval 1.27-1.72). A PRS above the 90th percentile was significantly associated with a 3.6-, 4.3-, and 6.4-fold increased risk of CRC in never, former, and current smokers, respectively, when compared with a PRS below the 10th percentile in never smokers. The interaction between smoking and PRS on CRC risk did not reach statistical significance (P = 0.53). The effect of smoking was equivalent to the effect of having a 30 percentile higher level of PRS (GRE 30, 95% confidence interval 18-42). Discussion Both smoking and the PRS carry essentially independent CRC risk information, and their joint consideration provides powerful risk stratification. Abstinence from smoking can compensate for a substantial proportion of genetically determined CRC risk.

Background Polygenic risk scores (PRS), which are derived from results of large genome-wide association studies, are increasingly propagated for colorectal cancer (CRC) risk stratification. The majority of studies included in the large genome-wide association studies consortia were conducted in the United States and Germany, where colonoscopy with detection and removal of polyps has been widely practiced over the last decades. We aimed to assess if and to what extent the history of colonoscopy with polypectomy may alter metrics of the predictive ability of PRS for CRC risk. Methods A PRS based on 140 single nucleotide polymorphisms was compared between 4939 CRC patients and 3797 control persons of the Darmkrebs: Chancen der Verhütung durch Screening (DACHS) study, a population-based case-control study conducted in Germany. Risk discrimination was quantified according to the history of colonoscopy and polypectomy by areas under the curves (AUCs) and their 95% confidence intervals (CIs). All statistical tests were 2-sided. Results AUCs and 95% CIs were higher among subjects without previous colonoscopy (AUC = 0.622, 95% CI = 0.606 to 0.639) than among those with previous colonoscopy and polypectomy (AUC = 0.568, 95% CI = 0.536 to 0.601; difference [Δ AUC] = 0.054, P = .004). Such differences were consistently seen in sex-specific groups (women: Δ AUC = 0.073, P = .02; men: Δ AUC = 0.046, P = .048) and age-specific groups (younger than 70 years: Δ AUC = 0.052, P = .07; 70 years or older: Δ AUC = 0.049, P = .045). Conclusions Predictive performance of PRS may be underestimated in populations with widespread use of colonoscopy. Future studies using PRS to develop CRC prediction models should carefully consider colonoscopy history to provide more accurate estimates.

Incidence of colorectal cancer (CRC) in younger adults is increasing in many countries. Given the established association of body mass index (BMI) with CRC risk and the increasing obesity prevalence among younger generations, we aimed to evaluate the association of BMI at different ages during early adulthood with early-onset CRC.Among 6602 patients with CRC and 7950 matched controls who were recruited in 2003-2020 in the Darmkrebs: Chancen der Verhütung durch Screening study, a population-based case-control study from Germany, 747 patients and 621 controls were younger than 55 years and included in this analysis. Self-reported height and weight at ages 20 years and 30 years and at approximately 10 years before diagnosis or interview were recorded in personal interviews. Associations of BMI with early-onset CRC were estimated using multiple logistic regression.Compared with participants with BMI25 kg/mObesity at early adulthood is strongly associated with increased risk of early-onset CRC. German Clinical Trials Register ID: DRKS00011793.

Underwater acoustic sensor networks play an important role in assisting humans to explore information under the sea. In this work, we consider the combination of sensor selection and data routing in three dimensional underwater wireless sensor networks based on Bayesian compressive sensing and particle swarm optimization. The algorithm we proposed is a two-tier PSO approach. In the first tier, a PSO-based clustering protocol is proposed to synthetically consider the energy consumption and uniformity of cluster head distribution. Then in the second tier, a PSO-based routing protocol is proposed to implement inner-cluster one-hop routing and outer-cluster multi-hop routing. The nodes selected to constitute i-th effective routing path decide which positions in the i-th row of the measurement matrix are nonzero. As a result, in this tier the protocol comprehensively considers energy efficiency, network balance and data recovery quality. The Bayesian Cram&eacute, r-Rao Bound (BCRB) in such a case is analyzed and added in the fitness function to monitor the mean square error of the reconstructed signal. The experimental results validate that our algorithm maintains a longer life time and postpones the appearance of the first dead node while keeps the reconstruction error lower compared with the cutting-edge algorithms which are also based on distributed multi-hop compressive sensing approaches.

Previous studies have shown a strong coexistence of colorectal neoplasia (CRN) and cardiovascular diseases (CVD). This study was aimed to summarize the available evidence on association of CVD risk with early CRN detection in asymptomatic populations. PubMed, Web of Science, and Embase were systematically searched for eligible studies published until Dec 20, 2019. Studies exploring the associations of recommended CVD risk assessment methods (e.g., risk scores, carotid artery plaque, and coronary artery calcium score [CACS]) with risk of CRN were included. Meta-analyses were conducted to determine the overall association of CVD risk with the CRN. A total of 12 studies were finally included. The association of carotid artery plaque with the risk of colorectal adenoma (AD) was weakest (pooled odds ratio [OR)] 1.27, 95% confidence interval [CI), 1.12, 1.45]. Participants with CACS>100 had about 2-fold increased risk of AD than those with CACS=0. The pooled ORs were 3.36 (95% CI, 2.15, 5.27) and 2.30 (95% CI, 1.69, 3.13) for the risk of advanced colorectal neoplasia (AN) and AD, respectively, in participants with Framingham risk score (FRS)>20%, when compared to participants at low risk (FRS

Rationale: Bioavailable and free 25-hydroxyvitamin D (25(OH)D) are emerging measurements of vitamin D. Whether serum bioavailable or free 25(OH)D level is associated with mortality in patients with coronary artery disease (CAD) is unknown. Objective: Our aim is to determine the potential association between serum total, bioavailable, and free 25(OH)D levels and the risk of mortality among patients with CAD. Methods and Results: We measured serum 25(OH) levels in 1387 patients with angiographically confirmed CAD from the Guangdong Coronary Artery Disease Cohort. Serum DBP (vitamin D-binding protein) levels were measured using a polyclonal immunoassay, and serum-free 25(OH)D levels were measured using a 2-step immunoassay. Bioavailable 25(OH)D levels were calculated using a previously validated formula. By the median follow-up time of 6.7 years, 205 patients had died, including 134 deaths from cardiovascular diseases. In multivariate analyses, low serum bioavailable 25(OH)D level was significantly associated with increased risks of mortality, independent of established cardiovascular risk factors, features and treatments of CAD, factors associated with vitamin D and mineral metabolism, and CRP (C-reactive protein). The multivariable-adjusted hazard ratios across quartiles of bioavailable 25(OH)D were 1.79, 1.35, 1.36, and 1.00 for all-cause mortality ( P for trend=0.01) and 2.58, 1.85, 1.73, and 1.00 for cardiovascular mortality ( P for trend=0.001), respectively. Serum-free 25(OH)D level was inversely associated with the risk of mortality, with the extreme-quartile hazard ratios of 1.64 for all-cause mortality ( P for trend=0.024) and 1.97 for cardiovascular mortality ( P for trend=0.013). In contrast, serum total 25(OH)D level was not significantly associated with all-cause mortality or cardiovascular mortality. Conclusions: Lower serum bioavailable and free 25(OH)D levels rather than total 25(OH)D level are independently associated with an increased risk of all-cause mortality and cardiovascular mortality in a population-based CAD cohort.

This letter studies zero-delay joint source–channel coding for transmission of correlated Gaussian sources over a Gaussian interference channel. We propose to adopt a delay-free hybrid digital and analog scheme, which is transmitting the superposition of scaled source and its quantized version after applying scalar quantization to the source at each transmitter. At the corresponding receiver, two kinds of estimators are presented. It is shown that both the schemes, when optimized, beat the uncoded transmission if the channel signal-to-noise ratio is higher than a threshold value for different correlation coefficients and interference values.

Background and objective Genetic predisposition and menopausal hormone therapy (MHT) are established risk and preventive factors for colorectal cancer (CRC), respectively. We aimed to evaluate the joint associations of a polygenic risk score (PRS) and MHT on CRC risk for informing CRC prevention. Methods We used data from 28,486 postmenopausal women (11,519 cases and 16,967 controls) of European descent from 38 studies. MHT use was assessed as the use of any MHT, estrogen-only (E-only) or combined estrogen-progestogen (E+P) therapy at reference time. A PRS based on 141 genetic variants previously identified by genome-wide association studies of CRC was modelled as categorical variable in quartiles and also as per-standard deviation difference between PRS and minimum of PRS [(PRS-min(PRS))/SD(PRS)] (PRS.minsd). Multiplicative interaction between PRS and MHT was evaluated using standard logistic regression. Additive interaction was measured using the relative excess risk due to interaction (RERI). Results The use of any MHT as well as E+P and E-only were associated with reduced CRC risk (Odds ratio [OR] 0.70, 0.71, 0.65, respectively). PRS was associated with increased CRC risk, whether as continuous variable (PRS.minsd) (OR 1.53) or in quartiles (OR 1.49, 1.92, 2.87, respectively). We identified statistically significant negative multiplicative interaction (OR: 0.92; 95%CI: 0.87, 0.98) as well as negative additive interaction (RERI: -0.13; 95%CI: -0.15, -0.10) between PRS.minsd and any MHT use. Results were limited to additive interactions with PRS.minsd for E-only use (RERI: -0.14; 95%CI: -0.18, -0.11) and E+P use (RERI: -0.12; 95%CI: -0.16, -0.08). The magnitude of negative additive interactions increased with higher quartiles of PRS for all MHT variables and was consistently significant for the highest quartile compared to the lowest quartile of PRS for any MHT use (RERI: -0.78; 95%CI: -1.03, -0.52), E-only use (RERI: -0.78; 95%CI: -1.18, -0.39), and also E+P use (RERI: -0.53; 95%CI: -0.96, -0.10). Negative multiplicative interaction was also observed for higher PRS quartiles of all MHT variables but significant only for the highest quartile with E-only use (OR: 0.73; 95%CI: 0.55, 0.97). These negative interactions on both multiplicative and additive scales indicate that MHT has a relatively more protective effect on CRC risk for those women with larger PRS scores. For example, compared to women in the lowest PRS quartile with no MHT use, the risk of CRC for women in higher quartiles of PRS was more strongly reduced with MHT use (ORPRS.Q3+noMHT: 1.93 vs ORPRS.Q3+MHT: 1.38, OR MHT/noMHT in PRS.Q3: 0.71; ORPRS.Q4+noMHT: 2.81 vs ORPRS.Q4+MHT: 1.77, OR MHT/noMHT in PRS.Q4: 0.63). Conclusions The protective effect of MHT use on the risk of CRC is stronger in women with higher genetic risk. Risk prediction models incorporating PRS may need to account for potential effect modification by non-genetic risk factors. Citation Format: Yu Tian, Yi Lin, Andre E. Kim, Stephanie A. Bien, Polly A. Newcomb, Graham Casey, Elizabeth A. Platz, Loic Le Marchand, Peter T. Campbell, Hermann Brenner, Michael Hoffmeister, Feng Guo, Xuechen Chen, Marc J. Gunter, Niki Dimou, Stephen B. Gruber, Andrew T. Chan, Amit D. Joshi, Sonja I. Berndt, Emily White, Victor Moreno, Ross L. Prentice, Ulrike Peters, William Gauderman, Li Hsu, Jenny Chang-Claude. Association of polygenic risk score and menopausal hormone therapy for colorectal cancer risk [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2021; 2021 Apr 10-15 and May 17-21. Philadelphia (PA): AACR; Cancer Res 2021;81(13_Suppl):Abstract nr 818.

// Xinrui Li 1, * , Ding Ding 1, * , Yuan Zhang 2 , Dongfang Su 1 , Min Wang 1 , Xuechen Chen 1 , Yan Yang 1 , Changjiang Hong 2 , Gang Hu 3 and Wenhua Ling 1 1 Guangdong Provincial Key Laboratory of Food, Nutrition and Health, Department of Nutrition, School of Public Health, Sun Yat-sen University, Guangzhou, Guangdong, China 2 Department of Cardiology, General Hospital of Guangzhou Military Command of People’s Liberation Army, Guangzhou, Guangdong, China 3 Chronic Disease Epidemiology Laboratory, Pennington Biomedical Research Center, Baton Rouge, LA, USA * These authors have contributed equally to this work Correspondence to: Wenhua Ling, email: lingwh@mail.sysu.edu.cn Keywords: hepcidin; coronary artery disease; mortality; cohort study Received: January 02, 2017 Accepted: July 06, 2017 Published: November 27, 2017 ABSTRACT Background: Increased blood hepcidin may be associated with the presence and promotion of atherosclerosis, the association of hepcidin with mortality among coronary artery disease (CAD) patients remains unknown. We sought to assess the relationship of hepcidin and all-cause and cardiovascular disease (CVD) mortality among CAD patients with and without acute coronary syndrome (ACS). Methods and Results: This study included 759 patients with ACS and 526 patients with stable CAD. After an average follow-up of 4.1 years, 154 deaths were recorded, 114 were due to CVD. After adjusting for CVD risk factors and inflammatory markers, the plasma hepcidin was positively associated with all-cause and CVD mortality in the ACS patients, the multivariable-adjusted hazard ratios (HRs) across tertiles of hepcidin were 1.00, 2.18 (95% CI 1.23-3.94), and 2.82 (95% CI 1.59-5.12) for all-cause mortality ( P trend =0.006), and 1.00, 2.20 (95% CI 1.12-4.05), and 2.64 (95% CI 1.41-5.65) for CVD mortality ( P trend =0.01). The C-index and net reclassification improvement when including hepcidin in traditional CVD models were 1.6% and 21.5% for all-cause mortality, 1.4% and 23.5% for CVD mortality, respectively, ( P