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opencc-by-4.0Dec 2021View details →

Ecological dataset from: 'Rats and the city: implications of urbanization on zoonotic disease risk in Southeast Asia'

This dataset includes the ecological and environmental data, a description of the analysis steps, and the related R code associated with the manuscript: "Rats and the city: implications of urbanization on zoonotic disease risk in Southeast Asia" by Kim R. Blasdell, Serge Morand, Susan G.W. Laurance, Stephen L Doggett, Amy Hahs, David Perera, and Cadhla Firth, available at: https://www.pnas.org/doi/abs/10.1073/pnas.2112341119 This dataset also relates to the preprint: "Rats in the city: implications for zoonotic disease risk in an urbanizing world" available at: https://www.biorxiv.org/content/10.1101/2021.03.18.436089v1 A detailed description of the files can be found in README.txt

opencc-by-4.0Apr 2023View details →

Questionnaire: Co-occurrence of behavioural risk factors for non-communicable diseases among 40-year and above aged community members in three regions of Myanmar

This questionnaire was applied as data collection tool for the dataset of "Co-occurrence of behavioural risk factors for non-communicable diseases among 40-year and above aged community members in three regions of Myanmar".

opencc-by-4.0May 2023View details →

Polygenic risk scores validated in patient-derived cells stratify for mitochondrial subtypes of Parkinson's disease

Background Parkinson’s disease (PD) is the fastest growing neurodegenerative disorder, with affected individuals expected to double during the next 20 years. This raises the urgent need to better understand the genetic architecture and downstream cellular alterations underlying PD pathogenesis, in order to identify more focused therapeutic targets. While only &sim;10% of PD cases can be clearly attributed to monogenic causes, there is mounting evidence that additional genetic factors could play a role in idiopathic PD (iPD). In particular, common variants with low to moderate effect size in multiple genes regulating key neuroprotective activities may act as risk factors for PD. In light of the well-established involvement of mitochondrial dysfunction in PD, we hypothesized that a fraction of iPD cases may harbour a pathogenic combination of common variants in nuclear-encoded mitochondrial genes, ultimately resulting in neurodegeneration. Methods to capture this mitochondria-related “missing heritability”, we leveraged on existing data from previous genome-wide association studies (GWAS) – i.e., the large PD GWAS from Nalls and colleagues. We then used computational approaches based on mitochondria-specific polygenic risk scores (mitoPRSs) for imputing the genotype data obtained from different iPD case-control datasets worldwide, including the Luxembourg Parkinson’s Study (412 iPD patients and 576 healthy controls) and the COURAGE-PD cohorts (7270 iPD cases and 6819 healthy controls). Results applying this approach to gene sets controlling mitochondrial pathways potentially relevant for neurodegeneration in PD, we demonstrated that common variants in genes regulating Oxidative Phosphorylation (OXPHOS-PRS) were significantly associated with a higher PD risk both in the Luxembourg Parkinson’s Study (odds ratio, OR=1.31[1.14-1.50], p=5.4e-04) and in COURAGE-PD (OR=1.23[1.18-1.27], p=1.5e-29). Functional analyses in primary skin fibroblasts and in the corresponding induced pluripotent stem cells-derived neuronal progenitor cells from Luxembourg Parkinson’s Study iPD patients stratified according to the OXPHOS-PRS, revealed significant differences in mitochondrial respiration between high and low risk groups (p < 0.05). Finally, we also demonstrated that iPD patients with high OXPHOS-PRS have a significantly earlier age at disease onset compared to low-risk patients. Conclusions our findings suggest that OXPHOS-PRS may represent a promising strategy to stratify iPD patients into pathogenic subgroups – in which the underlying neurodegeneration is due to a genetically defined mitochondrial burden – potentially eligible for future, more tailored mitochondrially targeted treatments.

opencc-by-4.0May 2023View details →

Dataset for the intervention effects and long-term changes in physical activity and cardiometabolic outcomes among children at risk of noncommunicable diseases in South Africa

Dataset used to evaluate the short-term effects of the physical and health KaziKidz intervention on cardiometabolic risk factors and the long-term changes thereof among school-aged children at risk of NCDs from disadvantaged communities in South Africa. It encompasses anonymized, unique, identification numbers, anthropometric and clinical measures, such as blood pressure, blood sugar and blood lipids, and Actigraphy-measured physical activity levels. Assigned categories to each cardiovascular risk factor and the overall classification as at risk or not is available too.

opencc-by-4.0Aug 2023View details →

A more accurate risk biomarkers recognition for Progressive Multifocal Leukoencephalopathy (PML) caused by Polyomavirus JC in patients with multiple sclerosis during treatment with disease-modifying therapies (DMTs): an ongoing clinical challenge.

The therapeutic scenario for the treatment of MS has recently been characterized by a veritable revolution, which has included the introduction, for the first time, of drug treatment guidelines and the entry, in the therapeutic landscape of the last decade, of numerous new drugs that, in varying but significantly relevant ways, have proven capable of modifying the course of the disease (Disease-Modifying Therapies - DMTs).  While the arsenal of available drugs has resulted in advances in efficacy and selectivity, it has also exposed them to the danger of side effects, potentially serious and in some cases even fatal. Among the most important side effects, complications of infectious origin, characterized by cases of viral infection/reactivation, as in the case of JCPyV, the etiologic agent of PML, are the most represented. This study, based on the follow-up of MS patients treated with different DMTs, contributes to implementing the data in the literature regarding a greater understanding of the risks related to the administration of these drugs and more appropriate monitoring of MS treatment. The risk of JCPyV reactivation with Fingolimod and Dimethyl fumarate is lower than the risk of viral reactivation associated with natalizumab. In light of the data obtained, it is possible to conclude that, in the case of natalizumab, testing for JC viruria would seem to be more useful in identifying those patients with a JCPyV-specific humoral response that is not yet detectable. In addition, our results, draw attention to the importance of analyzing the NCCR rearrangements of JCPyV. Indeed, the particular rearrangements found in plasma and PBMCs of patients with RRMS treated with natalizumab could represent an alert of neuroinvasiveness in order to detect early those patients with a higher risk of developing PML. In the case of dimethyl fumarate, it seems likely that monitoring of lymphopenia would identify a higher risk group of patients in whom alternative therapy should be sought. Prolonged lymphopenia, with absolute lymphocyte counts less than 750 lymphocytes/mL, might be the major risk factor for PML although, a greater risk might lie in the loss of CD8+ cells that are crucial for JCPyV control. For fingolimod, this strategy cannot be applied because the number of circulating lymphocytes decreases while the actual lymphocyte function appears largely normal therefore, monitoring viruria and viremia along with identification of the neurotrophic variant of the virus seems a more exploitable means for risk stratification. In conclusion, the results of this study can be considered directly transferable to the National Health System in that, both the monitoring of JCPyV reactivation by viruria and the sequence analysis of viral NCCR and host immune set-up could play the role of translatable biomarkers in clinical practice in order to assess the risk of PML onset. In addition to improving risk stratification of this disease, these biomarkers of viral reactivation and pathogenicity could facilitate timely diagnosis, optimizing the use of health care resources and contributing to the reduction of direct and indirect costs of MS disease. Prezioso Carla was supported by the Italian Ministry of Health (Starting Grant: SG-2018-12366194).

opencc-by-4.0Sep 2023View details →

Financial dimensions of global zoonotic disease risks

The CSV files contain cleaned lists of companies and shareholders used in the study "Financial dimensions of global zoonotic disease risks". Code for the analysis is available at <a href="https://github.com/juanrocha/finance_tipping">https://github.com/juanrocha/finance_tipping</a> and a preprint of the study at <a href="https://beijer.kva.se/publication/financial-dimensions-of-global-zoonotic-disease-risks/">https://beijer.kva.se/publication/financial-dimensions-of-global-zoonotic-disease-risks/</a>

Assessing the Drug Exposure Risk of Infants Breastfed by Women With Inflammatory Bowel Disease

ClinicalTrials.gov study NCT03397108. IPD Sharing: YES. Countries: 1. Publications: 2.

Study of Semaglutide for Non-Alcoholic Fatty Liver Disease (NAFLD), a Metabolic Syndrome With Insulin Resistance, Increased Hepatic Lipids, and Increased Cardiovascular Disease Risk (The SLIM LIVER St

ClinicalTrials.gov study NCT04216589. IPD Sharing: YES. Countries: 2. Publications: 2.

Reducing Cardiovascular Disease Risk in Perimenopausal Latinas

ClinicalTrials.gov study NCT04313751. IPD Sharing: YES. Countries: 1. Publications: 3.

Triple Combination Therapy in High Risk Crohn's Disease (CD)

ClinicalTrials.gov study NCT02764762. IPD Sharing: YES. Countries: 2. Publications: 1.

Edoxaban for Prevention of Blood Vessels Being Blocked by Clots (Thrombotic Events) in Children at Risk Because of Cardiac Disease

ClinicalTrials.gov study NCT03395639. IPD Sharing: YES. Countries: 14. Publications: 1.

Families-At-risk for Interstitial Lung Disease Study

ClinicalTrials.gov study NCT03641742. IPD Sharing: YES. Countries: 1. Publications: 5.

Cardiovascular Risk Reduction Study (Reduction in Recurrent Major CV Disease Events)

ClinicalTrials.gov study NCT01327846. IPD Sharing: YES. Countries: 40. Publications: 18.

publicNov 2024View details →

dryad40/100

Seagrass ecosystems reduce disease risk and economic loss in marine farming production

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dryad40/100

Data for: Developmental origins of Parkinson’s disease risk: perinatal exposure to the organochlorine pesticide dieldrin leads to sex-specific DNA modifications in critical neurodevelopmental pathways in the mouse midbrain

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publicJul 2024View details →

dryad40/100

Gut microbiome of multiple sclerosis patients and paired household healthy controls reveal associations with disease risk and course

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publicSep 2022View details →

opencc-zeroSep 2020View details →

The last moves: the effect of hunting and culling on the risk of disease spread from a population of reindeer

1. Hunting and culling are frequently used to combat infectious wildlife diseases. The aim is to markedly lower population density in order to limit disease transmission or to eradicate the host. Massive host culling can yield a trade-off when combating wildlife disease; it follows that intrusive actions may have unintended behavioural side-effects, leading to the geographic spread of disease. The manner in which such excessive hunting and culling of hosts can affect the movement and dispersion of cervids has not been studied. 2. In this study, we quantified the behaviour (daily movements and habitat use) and dispersion of GPS-marked reindeer (n = 24) before and during the eradication of an entire population (>2000 reindeer) infected with chronic wasting disease (CWD) in Norway. We compared behaviour and dispersion during 10 ordinary hunting seasons (2007-16), an extended hunt in 2017 and marksmen culling (2017/18). 3. Seasonality had a major impact on movements. Reindeer movements during the early hunting season (20 August–20 September) did not increase the overall movements compared to that in the pre-hunt season (20 July–19 August), while extended hunting into October (as in 2017) and marksmen culling from November to February markedly increased daytime movements relative to that normally observed in this time of the year. Towards the end of the eradication, the remaining reindeer sought refuge at restricted high-elevation areas with limited forage production. Reindeer used novel areas towards the perimeter of the range, but active herding during culling stopped one herd from leaving the CWD zone. 4. Synthesis and applications: With emerging wildlife diseases, host culling is becoming a more frequently used tool for managers in Europe. Our study highlights the potential trade-off between combating disease transmission within a population and the risk of geographic spread. Such insight is important to design mitigation measures, such as perimeter fencing or herding, to avoid the risk of the geographic spread of disease in cases of severe and economically important wildlife diseases.

opencc-zeroNov 2020View details →

Risk factors for non-communicable diseases in Bangladesh: Findings of the population-based cross-sectional national survey 2018

Objectives: To determine the national prevalence of risk factors of non-communicable diseases (NCD) in the adult population of Bangladesh. Design: The study was a population-based national cross-sectional study. Setting: This study used 496 primary sampling units (PSUs) developed by the Bangladesh Bureau of Statistics. The PSUs were equally allocated to each division and urban and rural stratum within each division. Participants: The participants were adults aged 18-69 years, who were usual residents of the households for at least six months, and stayed the night before the survey. Out of 9900 participants, 8185 (82.7%) completed STEP-1 and STEP-2, and 7208 took part in STEP-3. Primary and secondary outcome: The prevalence of behavioral, physical, and biochemical risk factors of NCD. Data were weighted to generate national estimates. Results: Tobacco use was significantly (p<0.05) higher in the rural (45.2%) than the urban (38.8%) population. Inadequate fruit/vegetable intake was significantly (P<0.05) higher in the urban (92.1%) than in the rural (88.9%) population. The mean salt intake per day was higher in the rural (9.0 gm) than urban (8.9 gm) population. Among all, 3.0% had no, 70.9% had 1-2, and 26.2% had ≥3 NCD risk factors. The urban population was more likely to have insufficient physical activity (AOR: 1.2, 95% CI: 1.2–1.2), obesity (AOR: 1.5, 95% CI: 1.5–1.5), hypertension (AOR: 1.3, 95% CI: 1.3–1.3), diabetes (AOR: 1.6, 95% CI: 1.6–1.6), and hyperglycemia (AOR: 1.1, 95% CI: 1.1–1.1). Conclusions: Considering the high prevalence of the behavioral, physical, and biochemical risk factors, diverse population and high-risk group targeted interventions are essential to combat the rising burden of NCDs.

opencc-zeroNov 2020View details →

Longitudinal proteomic profiling of high-risk patients with COVID-19 reveals markers of severity and predictors of fatal disease

End-stage kidney disease (ESKD) patients are at high risk of severe COVID-19. We performed dense serial blood sampling in hospitalised and non-hospitalised ESKD patients with COVID-19 (n=256 samples from 55 patients) and used Olink immunoassays to measure 436 circulating proteins. Comparison to 51 non-infected ESKD patients revealed 221 proteins differentially expressed in COVID-19, of which 69.7% replicated in an independent cohort of 46 COVID-19 patients. 203 proteins were associated with clinical severity scores, including IL6, markers of monocyte recruitment (e.g. CCL2, CCL7), neutrophil activation (e.g proteinase-3) and epithelial injury (e.g. KRT19). Random Forests machine learning identified predictors of current or future severity such as KRT19, PARP1, PADI2, CCL7, and IL1RL1 (ST2). Survival analysis with joint models revealed 69 predictors of death including IL22RA1, CCL28, and the neutrophil-derived chemotaxin AZU1 (Azurocidin). Finally, longitudinal modelling with linear mixed models uncovered 32 proteins that display different temporal profiles in severe versus non-severe disease, including integrins and adhesion molecules. Our findings point to aberrant innate immune activation and leucocyte-endothelial interactions as central to the pathology of severe COVID-19. The data from this unique cohort of high-risk individuals provide a valuable resource for identifying drug targets in COVID-19.