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Previous studies have shown that patients with systemic lupus erythematosus (SLE) tend to have a higher risk of cardiovascular disease (CVD), but the potential causal relationship between genetic susceptibility to SLE and CVD risk is not clear. This study systematically investigated the potential association between genetically determined SLE and the risk of CVD. The genetic tools were obtained from genome-wide association studies of SLE and CVD, with no overlap between their participating populations. Mendelian randomization (MR) analysis was performed using inverse variance weighting as the primary method. Simultaneously, a series of repeated analyses, sensitivity analyses, and instrumental variable strength evaluations were performed to verify the reliability of our results. MR analysis showed that genetic susceptibility to SLE was associated with a higher risk of heart failure (OR=1.025, 95% CI [1.009-1.041], P=0.002), ischemic stroke (OR=1.020, 95% CI [1.005-1.034], P=0.009), and venous thromboembolism (OR=1.001, 95% CI [1.000-1.002], P=0.014). However, genetic susceptibility to SLE was negatively correlated with the risk of type 2 diabetes (OR=0.968, 95% CI [0.947-0.990], P=0.004). Sensitivity analysis found no evidence of horizontal pleiotropy or heterogeneity. Our MR study explored the causal role of SLE in the etiology of CVD, which would help improve our understanding of the basic disease mechanisms of SLE and provide comprehensive CVD assessment and treatment for SLE patients.

BackgroundA large number of observational studies showed that patients with psoriasis have a higher risk of cardiovascular disease (CVD), but most studies did not fully adjust for confounding factors, so it is not clear whether the risk of CVD is directly attributed to psoriasis. We used Mendelian randomization (MR) to evaluate the potential causal relationship between psoriasis and CVD.MethodsWe used genetic instruments from the genome-wide association study (GWAS) of European descent for psoriasis to investigate its relationship with CVD. Inverse variance-weighted (IVW) MR analyses were used for the primary analysis. In addition, a variety of other methods were used to replicate the analysis.ResultsThe fixed-effects IVW method indicated that genetic susceptibility to psoriasis was associated with a higher risk of heart failure (HF) [odds ratio (OR) = 1.04; 95% CI, 1.01–1.06, P = 2.72E-03], atrial fibrillation (AF) (OR = 1.04; 95% CI, 1.02–1.07, P = 3.27E-04), myocardial infarction (MI) (OR = 1.07; 95% CI, 1.01–1.12, P = 0.01), valvular heart disease (VHD) (OR = 1.001; 95% CI, 1.000–1.002, P = 1.85E-03), and large artery stroke (LAS) (OR = 1.11; 95% CI, 1.05–1.18, P = 5.37E-04) but not with the other two subtypes of ischemic stroke (IS) [cardioembolic stroke (CES) (OR = 1.03; 95% CI, 0.98–1.07, P = 0.27) and small vessel stroke (SVS) (OR = 1.00; 95% CI, 0.95–1.07), P = 0.88)]. Sensitivity analysis found weak evidence of horizontal diversity and heterogeneity to ensure the stability of the results.ConclusionOur study provided evidence for a potential causal link between psoriasis and CVD. These findings partly suggest that early monitoring of cardiovascular risk in patients with psoriasis is intentional.

At present, elucidating the cortical origin of EEG microstates is a research hotspot in the field of EEG. Previous studies have suggested that the prefrontal cortex is closely related to EEG microstate C and D, but whether there is a causal link between the prefrontal cortex and microstate C or D remains unclear. In this study, pretrial EEG data were collected from ten patients with prefrontal lesions (mainly located in inferior and middle frontal gyrus) and fourteen matched healthy controls, and EEG microstate analysis was applied. Our results showed that four classical EEG microstate topographies were obtained in both groups, but microstate C topography in patient group was obviously abnormal. Compared to healthy controls, the average coverage and occurrence of microstate C significantly reduced. In addition, the transition probability from microstate A to C and from microstate B to C in patient group was significantly lower than those of healthy controls. The above results demonstrated that the damage of prefrontal cortex especially inferior and middle frontal gyrus could lead to abnormalities in the spatial distribution and temporal dynamics of microstate C not D, showing that there is a causal link between the inferior and middle frontal gyrus and the microstate C. The significance of our findings lies in providing new evidence for elucidating the cortical origin of microstate C.

It is well-documented that rheumatoid arthritis (RA), ankylosing spondylitis (AS), and juvenile idiopathic arthritis (JIA) often exhibit skin manifestations, with psoriasis typically occurring around the time of diagnosis. Thus, it is essential to investigate the potential causal relationship between these forms of arthritis and psoriasis. The OpenGWAS provided traitIDs for exposure factors (RA (bbj-A-74), AS (ebi-A-GCST005529), and JIA (finn-b-JUVEN-ARTHR)) and outcome (psoriasis, finn-b-L12-PSORIASIS). bbj-A-74 had 19,190 samples (9,739,303 SNPs), ebi-A-GCST005529 had 22,647 samples (99,962 SNPs), finn-b-JUVEN-ARTHR had 173,622 samples (16,380,296 SNPs), and psoriasis had 216,752 samples (16,380,464 SNPs). Initially, 57 RA SNPs, 25 AS SNPs, and 5 JIA SNPs were acquired. Causal links were explored via univariate Mendelian Randomization (UVMR) analysis, with sensitivity analyses ensuring reliability. Additionally, multivariate MR (MVMR) analysis was conducted to further estimate the effect of each exposure factor on psoriasis. Significant causal links (P < 0.05, OR > 1) were found between bbj-A-74, ebi-A-GCST005529, finn-b-JUVEN-ARTHR, and finn-b-L12-PSORIASIS, indicating associations of RA, AS, and JIA with psoriasis. Sensitivity analyses ensured the reliability of these finding, showing no heterogeneity, horizontal pleiotropy, or SNP locus oversensitivity in UVMR results. Furthermore, MVMR analysis revealed AS and JIA as psoriasis risk factors, while RA showed non-significant protective effects. This suggests AS and JIA may contribute to psoriasis onset or exacerbation when coexisting. MR analyses were conducted to investigate the causal links between RA, AS, JIA, and psoriasis, enhancing our grasp of the underlying mechanisms of psoriasis.

The paper aims to highlight the decisive role of supranational and national courts in the recognition of a fundamental right to a healthy environment and in widening the scope of its protection. It analyses, in a critical sense, the doctrine that defines this trend as jurisprudential activism and that raises concerns regarding the principle of separation of powers.

The ‘causal link’ requirement for the adoption of safeguard measures, under Article 4.2(b) of the Agreement on Safeguards, has been one of the most controversial disciplines under the WTO Agreement. Some critics, such as Alan O. Sykes, point out logical and practical defects in the WTO panels’ and the Appellate Body’s findings on this topic. This article attempts to clarify the requirements of the ‘causal link’, adopting a new microeconomic analytical model that accounts for the precise conditions of competition between imported and domestic products. The analysis reveals that the ‘causal link’ requirement calls for a demonstration that the factors falling into the category of ‘unforeseen developments’ under Article XIX:1(a) of the GATT 1994 have caused both increased imports and domestic injury.

This chapter contains sections titled: Description of the Method Historical Origins and Influences Key Epistemological Assumptions What Kind of Research Questions is Thematic Analysis Most Suited to Addressing? What Kinds of Data are Most Appropriate and From Whom Should They be Collected? What Approach is Taken to the Involvement of Research Participants, Including Mental Health Service Users? How to Use This Method What Makes for a Better Quality Thematic Analysis? What are the Recent Developments and Innovations Concerning this Method? Conclusions Acknowledgements References

(1) Background. A definition of healthcare-associated infections is essential also for the attribution of the restorative burden to healthcare facilities in case of harm and for clinical risk management strategies. Regarding M. chimaera infections, there remains several issues on the ecosystem and pathogenesis. We aim to review the scientific evidence on M. chimaera beyond cardiac surgery, and thus discuss its relationship with healthcare facilities. (2) Methods. A systematic review was conducted on PubMed and Web of Science on 7 May 2024 according to PRISMA 2020 guidelines for reporting systematic reviews, including databases searches with the keyword “Mycobacterium chimaera”. Article screening was conducted by tree authors independently. The criterion for inclusion was cases that were not, or were improperly, consistent with the in-situ deposition of aerosolised M. chimaera. (3) Results. The search yielded 290 eligible articles. After screening, 34 articles (377 patients) were included. In five articles, patients had undergone cardiac surgery and showed musculoskeletal involvement or disseminated infection without cardiac manifestations. In 11 articles, respiratory specimen reanalyses showed M. chimaera. Moreover, 10 articles reported lung involvement, 1 reported meninges involvement, 1 reported skin involvement, 1 reported kidney involvement after transplantation, 1 reported tendon involvement, and 1 reported the involvement of a central venous catheter; 3 articles reported disseminated cases with one concomitant spinal osteomyelitis. (4) Conclusions. The scarce data on environmental prevalence, the recent studies on M. chimaera ecology, and the medicalised sample selection bias, as well as the infrequent use of robust ascertainment of sub-species, need to be weighed up. The in-house aerosolization, inhalation, and haematogenous spread deserve experimental study, as M. chimaera cardiac localisation could depend to transient bacteraemia. Each case deserves specific ascertainment before tracing back to the facility, even if M. chimaera represents a core area for healthcare facilities within a framework of infection prevention and control policies.

Purpose This paper aims to understand if buy-now-pay-later (BNPL) services, a digital type of credit that targets young consumers, acts as a protective or a risk factor for food insecurity among young consumers in Australia. Design/methodology/approach The study uses survey data from a representative sample of young consumers aged 18–24 from all internal states and territories in Australia. Propensity score matching is used to test two hypotheses: BNPL drives young consumers to food insecurity, and food insecurity leads young consumers to use BNPL. Findings There is evidence that BNPL use is driving young Australian consumers to experience food insecurity, but there is no evidence of food insecurity driving the use of BNPL services. Practical implications The evidence of BNPL driving young consumers to experience food insecurity calls for the adoption of practices and stronger regulation to ensure that young users from being overindebted. Originality/value Although the link with more traditional forms of credit (such as personal loans) and consumer wellbeing has been explored more broadly, this project is the first attempt to have causal evidence of the link between BNPL and food insecurity in a high-income country, to the best of the authors’ knowledge. This evidence helps to fill the gap about the protective or risky nature of this type of digital financial product, as experienced by young Australians.

When a new bug report is assigned to developers, they first need to understand what the bug report expresses (what) and why this bug occurs (why). To do so, developers usually explore different bug related data sources to investigate whether there are historical bugs with similar symptoms and causes related to the bug at hand. Automatic bug classification with respect to what and why information of bugs would enable developers to narrow down their search of bug resources and improve the bug fixing productivity. To achieve this goal, we propose an approach, BugClass, which applies a deep neural network classification approach based on Hierarchical Attention Networks (HAN) to automatically classify the bugs into different what and why categories by exploiting the bug repository and commit repository. Then, we explore the causal link relationship between what and why categories to further improve the accuracy of the bug classification. Experimental results demonstrate that BugClass is effective to classify the given bug reports into what and why categories, and can be also effectively used for identifying the why category for new bugs based on the causal link relations.