Partial Evaluation for Java Malware Detection

The fact that Java is platform independent gives hackers the opportunity to write exploits that can target users on any platform, which has a JVM implementation. Metasploit is a well-known source of Java exploits and to circumvent detection by Anti Virus (AV) software, obfuscation techniques are routinely applied to make an exploit more difficult to recognise. Popular obfuscation techniques for Java include string obfuscation and applying reflection to hide method calls; two techniques that can either be used together or independently. This paper shows how to apply partial evaluation to remove these obfuscations and thereby improve AV matching. The paper presents a partial evaluator for Jimple, which is a typed three-address code suitable for optimisation and program analysis, and also demonstrates how the residual Jimple code, when transformed back into Java, improves the detection rates of a number of commercial AV products

Differential effects of lung inflammation on insulin resistance in humans and mice

BACKGROUND: The rates of obesity, its associated diseases, and allergies are raising at alarming rates in most countries. House dust mites (HDM) are highly allergenic and exposure often associates with an urban sedentary indoor lifestyle, also resulting in obesity. The aim of this study was to investigate the epidemiological association and physiological impact of lung inflammation on obesity and glucose homeostasis. METHODS: Epidemiological data from 2207 adults of the population-based KORA FF4 cohort were used to test associations between asthma and rhinitis with metrics of body weight and insulin sensitivity. To obtain functional insights, C57BL/6J mice were intranasally sensitized and challenged with HDM and simultaneously fed with either low-fat or high-fat diet for 12 weeks followed by a detailed metabolic and biochemical phenotyping of the lung, liver, and adipose tissues. RESULTS: We found a direct association of asthma with insulin resistance but not body weight in humans. In mice, co-development of obesity and HDM-induced lung inflammation attenuated inflammation in lung and perigonadal fat, with little impact on body weight, but small shifts in the composition of gut microbiota. Exposure to HDM improved glucose tolerance, reduced hepatosteatosis, and increased energy expenditure and basal metabolic rate. These effects associate with increased activity of thermogenic adipose tissues independent of uncoupling protein 1. CONCLUSIONS: Asthma associates with insulin resistance in humans, but HDM challenge results in opposing effects on glucose homeostasis in mice due to increased energy expenditure, reduced adipose inflammation, and hepatosteatosis

Associations between anthropometric indicators in early life and low-grade inflammation, insulin resistance and lipid profile in adolescence

Background and AimsThe long-term relations between excessive adiposity in early childhood and unfavourable cardiometabolic profiles in later ages are not yet completely understood. We aimed to assess the associations between birth weight (BW) and BMI from 6 months to 6 years of age, with biomarkers indicative of low-grade inflammation, insulin resistance and lipid profiles in adolescence.Methods and ResultsRetrospective school-based study with 415 Portuguese adolescents (220 girls), mean age of 14.08±1.6 years old. Anthropometric data from birth to 6 years old was extracted from individual child health book records. Actual weight and height were measured and BMI calculated. Participants were classified at each time point as normal weight or overweight according to WHO reference values. Biomarkers were obtained from venous blood samples. Linear regressions were used to explore the associations between the biomarkers and early life anthropometric indicators. From 2 years onwards, BMI associated positively with the inflammatory score and HOMA-IR in adolescence. Children who were overweight/obese from 2 to 6 years of age presented significantly higher inflammatory score and HOMA-IR later in adolescence. TC/HDL ratio was also positively associated with BMI from the age of 5 years onwards. The associations between BMI and cardiometabolic outcomes remained positive in adolescence, with overweight adolescents presenting a higher inflammatory score, HOMA-IR and TC/HDL than normal weight adolescents.ConclusionA high BMI from an early age was consistently associated with worse inflammatory and lipid profiles and insulin resistance in adolescence. No associations were found between BW and the same studied outcomes

Physical activity, sedentary behaviour, and childhood asthma: a European collaborative analysis

OBJECTIVES: To investigate the associations of physical activity (PA) and sedentary behaviour in early childhood with asthma and reduced lung function in later childhood within a large collaborative study. DESIGN: Pooling of longitudinal data from collaborating birth cohorts using meta-analysis of separate cohort-specific estimates and analysis of individual participant data of all cohorts combined. SETTING: Children aged 0-18 years from 26 European birth cohorts. PARTICIPANTS: 136 071 individual children from 26 cohorts, with information on PA and/or sedentary behaviour in early childhood and asthma assessment in later childhood. MAIN OUTCOME MEASURE: Questionnaire-based current asthma and lung function measured by spirometry (forced expiratory volume in 1 s (FEV1), FEV1/forced vital capacity) at age 6-18 years. RESULTS: Questionnaire-based and accelerometry-based PA and sedentary behaviour at age 3-5 years was not associated with asthma at age 6-18 years (PA in hours/day adjusted OR 1.01, 95% CI 0.98 to 1.04; sedentary behaviour in hours/day adjusted OR 1.03, 95% CI 0.99 to 1.07). PA was not associated with lung function at any age. Analyses of sedentary behaviour and lung function showed inconsistent results. CONCLUSIONS: Reduced PA and increased sedentary behaviour before 6 years of age were not associated with the presence of asthma later in childhood. © Author(s) (or their employer(s)) 2024. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.The authors received no specific funding for this article. Funding information per cohort: ABCD: The ABCD study has been supported by grants from The Netherlands Organisation for Health Research and Development (ZonMW) and The Netherlands Heart Foundation. ABIS: Special thanks to the participating families in the ABIS study, and all staff at Obstetric departments and Well-Baby Clinics. ABIS has been supported by Swedish Research Council (K2005-72X-11242-11A and K2008-69X-20826-01-4) and the Swedish Child Diabetes Foundation (Barndiabetesfonden), JDRF Wallenberg Foundation (K 98-99D-12813-01A), Medical Research Council of Southeast Sweden (FORSS), and the Swedish Council for Working Life and Social Research (FAS2004-1775) and Östgöta Brandstodsbolag. BAMSE: This BAMSE birth cohort was supported by grants from the Swedish Research Council, the Swedish Research Council for Health, Working Life and Welfare, Formas, the Swedish Heart-Lung Foundation, the Swedish Asthma and Allergy Research Foundation, Region Stockholm (ALF project, and for cohort and database maintenance), and the European Research Council (TRIBAL, grant agreement 757919). CHOP: The CHOP study reported herein have been carried out with partial financial support from the Commission of the European Community, specific RTD Programme 'Quality of Life and Management of Living Resources', within the European Union's Seventh Framework Programme (FP7/2007-2013), project EarlyNutrition under grant agreement no. 289346, partial financial support from Polish Ministry of Science and Higher Education (2571/7.PR/2012/2), the EU H2020 project PHC-2014-DynaHealth under grant no. 633595 and the European Research Council Advanced Grant META-GROWTH (ERC-2012-AdG-no.322605). COPSAC2000: All funding received by COPSAC is listed on www.copsac.com. The Lundbeck Foundation (Grant no R16-A1694); The Ministry of Health (Grant no 903516); Danish Council for Strategic Research (Grant no 0603-00280B) and The Capital Region Research Foundation have provided core support to the COPSAC research center. DNBC: The Danish National Birth Cohort was established with a significant grant from the Danish National Research Foundation. Additional support was obtained from the Danish Regional Committees, the Pharmacy Foundation, the Egmont Foundation, the March of Dimes Birth Defects Foundation, the Health Foundation and other minor grants. The DNBC Biobank has been supported by the Novo Nordisk Foundation and the Lundbeck Foundation. EDEN: EU FP7 Framework MedAll project, National Institute for Research in Public Health (IRESP TGIR Cohorte Santé 2008 Program); National Agency for Research (ANR non-thematic programme); French Speaking Association for the Study of Diabetes and Metabolism (Alfediam); Mutuelle Générale de l’Éducation Nationale; Nestlé; French National Institute for Health Education (INPES); Paris‐Sud University; French National Istitute for Population Health Surveillance (InVS); French Agency for Environment Security (AFFSET); French Ministry of Health Perinatal Program; Inserm Nutrition Research Program; Institut Fédératif de Recherche and Cohort Program; French Ministry of Research; EURIP and FIRE doctoral school–Programme Bettencourt; Fondation pour la Recherche Médicale (FRM). G21: Generation XXI was supported by the European Regional Development Fund (ERDF) through the Operational Programme Competitiveness and Internationalisation and national funding from the Foundation for Science and Technology (FCT), Portuguese Ministry of Science, Technology and Higher Education under the project 'HIneC: When do health inequalities start? Understanding the impact of childhood social adversity on health trajectories from birth to early adolescence' (POCI-01-0145-FEDER-029567; Reference PTDC/SAU-PUB/29567/2017). It is also supported by the Unidade de Investigação em Epidemiologia–Instituto de Saúde Pública da Universidade do Porto (EPIUnit) (UIDB/04750/2020), Administração Regional de Saúde Norte (Regional Department of Ministry of Health) and Fundação Calouste Gulbenkian; PhD Grant SFRH/BD/108742/2015 (to SS) co-funded by FCT and the Human Capital Operational Programme (POCH/FSE Program); ACS is founded by a FCT Investigator contracts IF/01060/2015. Generation R: The Generation R Study is made possible by financial support from the Erasmus Medical Centre, Rotterdam, the Erasmus University Rotterdam and The Netherlands Organization for Health Research and Development. The project received funding for projects from the European Union's Horizon 2020 research and innovation programme (LIFECYCLE, grant agreement No 733206, 2016; EUCAN-Connect grant agreement No 824989; ATHLETE, grant agreement No 874583). LD received funding from the European Union's Horizon 2020 cofunded programme ERA-Net on Biomarkers for Nutrition and Health (ERA HDHL) (ALPHABET project (no 696295; 2017), ZonMW The Netherlands (no 529051014; 2017)). GINIplus: The GINIplus study was mainly supported for the first 3 years of the Federal Ministry for Education, Science, Research and Technology (interventional arm) and Helmholtz Zentrum Munich (former GSF) (observational arm). The 4 years, 6 years, 10 years and 15 years follow-up examinations of the GINIplus study were covered from the respective budgets of the five study centres (Helmholtz Zentrum Munich (former GSF), Research Institute at Marien-Hospital Wesel, LMU Munich, TU Munich and from 6 years onwards also from IUF - Leibniz Research-Institute for Environmental Medicine at the University of Düsseldorf) and a grant from the Federal Ministry for Environment (IUF Düsseldorf, FKZ 20462296). Further, the 15-year follow-up examination of the GINIplus study was supported by the Commission of the European Communities, the 7th Framework Program: MeDALL project, and as well by the companies Mead Johnson and Nestlé. The authors thank all the families for their participation in the GINIplus study. Furthermore, we thank all members of the GINIplus Study Group for their excellent work. The GINIplus Study group consists of the following: Institute of Epidemiology, Helmholtz Zentrum München, German Research Center for Environmental Health, Neuherberg (Heinrich J, Brüske I, Schulz H, Flexeder C, Zeller C, Standl M, Schnappinger M, Ferland M, Thiering E, Tiesler C); Department of Pediatrics, Marien-Hospital, Wesel (Berdel D, von Berg A); Ludwig-Maximilians-University of Munich, Dr von Hauner Children’s Hospital (Koletzko S); Child and Adolescent Medicine, University Hospital rechts der Isar of the Technical University Munich (Bauer CP, Hoffmann U); IUF- Environmental Health Research Institute, Düsseldorf (Schikowski T, Link E, Klümper C, Krämer U, Sugiri D). HUMIS: HUMIS is supported by the Research Council of Norway (NevroNor, grant number 226402). INMA Asturias: This study was funded by grants from, FIS-FEDER: PI04/2018, PI09/02311, PI13/02429, PI18/00909; Obra Social Cajastur/Fundación Liberbank, and Universidad de Oviedo. We thank Fundación NOE Alimerka. INMA Gipuzkoa: This study was funded by grants from Instituto de Salud Carlos III (FIS-PI06/0867, FIS-PI09/00090, FIS-PI13/02187 include FEDER funds), CIBERESP, Department of Health of the Basque Government (2005111093, 2009111069, 2013111089 and 2015111065), and the Provincial Government of Gipuzkoa (DFG06/002, DFG08/001 and DFG15/221) and annual agreements with the municipalities of the study area (Zumarraga, Urretxu, Legazpi, Azkoitia y Azpeitia y Beasain). INMA Menorca: This study was funded by grants from Instituto de Salud Carlos III (Red INMA G03/176; CB06/02/0041; 97/0588; 00/0021-2; PI061756; PS0901958; PI14/00677 incl. FEDER funds), CIBERESP, Beca de la IV convocatoria de Ayudas a la Investigación en Enfermedades Neurodegenerativas de La Caixa, and EC Contract No. QLK4-CT-2000-00263. INMA Sabadell: This study was funded by grants from Instituto de Salud Carlos III (Red INMA G03/176; CB06/02/0041; PI041436; PI081151 incl. FEDER funds; CPII/00018), CIBERESP, Generalitat de Catalunya-CIRIT 1999SGR 00241, Generalitat de Catalunya-AGAUR 2009 SGR 501, Fundació La marató de TV3 (090430), EU Commission (261357). ISGlobal is a member of the CERCA Programme, Generalitat de Catalunya. INMA Valencia: This study was funded by grants from UE (FP7-ENV-2011 cod 282957 and HEALTH.2010.2.4.5-1), Spain: ISCIII (Red INMA G03/176, CB06/02/0041; FIS-FEDER: PI03/1615, PI04/1509, PI04/1112, PI04/1931, PI05/1079, PI05/1052, PI06/1213, PI07/0314, PI09/02647, PI11/01007, PI11/02591, PI11/02038, PI13/1944, PI13/2032, PI14/00891, PI14/01687, PI16/1288, PI17/00663, and 19/1338; Miguel Servet-FEDER CP11/00178, CP15/00025 and CPII16/00051), Generalitat Valenciana: FISABIO (UGP 15-230, UGP-15-244, UGP-15-249, and AICO 2020/285), and Alicia Koplowitz Foundation 2017. KOALA: The KOALA cohort study was cofinanced by Friesland Foods (now FrieslandCampina), Netherlands Asthma Foundation (grant numbers 3.2.07.022 and 3.2.03.48) and Netherlands Heart Foundation (grant number 2014 T037), the Netherlands Organization for Health Research and Development (ZonMw Prevention Program number 1.210-00-090). The funding sources had no role in the study design and the collection, analysis and interpretation of data and the writing of the article and the decision to submit it for publication. Lifeways: The Lifeways study has been funded by the Health Research Board, Ireland, and the Irish Department of Health and Children’s Health Promotion Policy Unit. LISA: The LISA study was mainly supported by grants from the Federal Ministry for Education, Science, Research and Technology and in addition from Helmholtz Zentrum Munich (former GSF), Helmholtz Centre for Environmental Research—UFZ, Leipzig, Research Institute at Marien-Hospital Wesel, Pediatric Practice, Bad Honnef for the first 2 years. The 4 years, 6 years, 10 years and 15 years follow-up examinations of the LISA study were covered from the respective budgets of the involved partners (Helmholtz Zentrum Munich (former GSF), Helmholtz Centre for Environmental Research—UFZ, Leipzig, Research Institute at Marien-Hospital Wesel, Pediatric Practice, Bad Honnef, IUF—Leibniz-Research Institute for Environmental Medicine at the University of Düsseldorf) and in addition by a grant from the Federal Ministry for Environment (IUF Düsseldorf, FKZ 20462296). Further, the 15-year follow-up examination of the LISA study was supported by the Commission of the European Communities, the 7th Framework Program: MeDALL project. The authors thank all the families for their participation in the LISA study. Furthermore, we thank all members of the LISA Study Group for their excellent work. The LISA Study group consists of the following: Helmholtz Zentrum München, German Research Center for Environmental Health, Institute of Epidemiology, Munich (Heinrich J, Schnappinger M, Brüske I, Ferland M, Schulz H, Zeller C, Standl M, Thiering E, Tiesler C, Flexeder C); Department of Pediatrics, Municipal Hospital 'St. Georg', Leipzig (Borte M, Diez U, Dorn C, Braun E); Marien Hospital Wesel, Department of Pediatrics, Wesel (von Berg A, Berdel D, Stiers G, Maas B); Pediatric Practice, Bad Honnef (Schaaf B); Helmholtz Centre of Environmental Research—UFZ, Department of Environmental Immunology/Core Facility Studies, Leipzig (Lehmann I, Bauer M, Röder S, Schilde M, Nowak M, Herberth G, Müller J); Technical University Munich, Department of Pediatrics, Munich (Hoffmann U, Paschke M, Marra S); Clinical Research Group Molecular Dermatology, Department of Dermatology and Allergy, Technische Universität München (TUM), Munich (Ollert M, J. Grosch). LRC: All phases of this study were supported by the Swiss National Science Foundation (grants: SNF 320030_182628, 32003B_162820, PDFMP3 137033, 32003B_162820, 32003B_144068, PZ00P3_147987) and Asthma UK 07/048. LUCKI: This study was supported by Maastricht University and the Public Health Service South Limburg. PIAMA: The Prevention and Incidence of Asthma and Mite Allergy Study has been funded by grants from the Netherlands Organization for Health Research and Development; the Netherlands Organization for Scientific Research; the Lung Foundation of the Netherlands; the Netherlands Ministry of Planning, Housing and the Environment; the Netherlands Ministry of Health, Welfare and Sport; and the National Institute for Public Health and the Environment. SEATON: Medical Research Council, Grant number: 80219, MR/K001035/1; Asthma UK, Grant numbers: 00/011, 02/017. STEPS Study: The Academy of Finland (grant no. 123571 and 121659); the Juho Vainio Foundation; the Foundation for Pediatric Research; the Finnish Medical Foundation. SWS: The SWS was supported by grants from the Medical Research Council (MC_UU_12011/4), Dunhill Medical Trust, British Heart Foundation, Food Standards Agency (contract no N05071), British Lung Foundation. National Institute for Health Research Southampton Biomedical Research Centre, University of Southampton and University Hospital Southampton National Health Service Foundation Trust, the European Union’s Seventh Framework Programme (FP7/2007-2013), project EarlyNutrition (grant 289346) and European Union’s Horizon 2020 research and innovation programme under grant agreement No 733206 (LifeCycle). WHISTLER: The authors (from the WHISTLER birth cohort) received no specific funding for this article. The WHISTLER birth cohort was supported with a grant from the Netherlands Organization for Health Research and Development (grant no. 2001-1-1322) and by an unrestricted grant from GlaxoSmithKline Netherlands

Rare and low-frequency exonic variants and gene-by-smoking interactions in pulmonary function

Genome-wide association studies have identified numerous common genetic variants associated with spirometric measures of pulmonary function, including forced expiratory volume in one second (FEV1), forced vital capacity, and their ratio. However, variants with lower minor allele frequencies are less explored. We conducted a large-scale gene-smoking interaction meta-analysis on exonic rare and low-frequency variants involving 44,429 individuals of European ancestry in the discovery stage and sought replication in the UK BiLEVE study with 45,133 European ancestry samples and UK Biobank study with 59,478 samples. We leveraged data on cigarette smoking, the major environmental risk factor for reduced lung function, by testing gene-by-smoking interaction effects only and simultaneously testing the genetic main effects and interaction effects. The most statistically significant signal that replicated was a previously reported low-frequency signal in GPR126, distinct from common variant associations in this gene. Although only nominal replication was obtained for a top rare variant signal rs142935352 in one of the two studies, interaction and joint tests for current smoking and PDE3B were s

Investigating the causal effect of smoking on hay fever and asthma: a Mendelian randomization meta-analysis in the CARTA consortium

AbstractObservational studies on smoking and risk of hay fever and asthma have shown inconsistent results. However, observational studies may be biased by confounding and reverse causation. Mendelian randomization uses genetic variants as markers of exposures to examine causal effects. We examined the causal effect of smoking on hay fever and asthma by using the smoking-associated single nucleotide polymorphism (SNP) rs16969968/rs1051730. We included 231,020 participants from 22 population-based studies. Observational analyses showed that current vs never smokers had lower risk of hay fever (odds ratio (OR) = 0·68, 95% confidence interval (CI): 0·61, 0·76; P &lt; 0·001) and allergic sensitization (OR = 0·74, 95% CI: 0·64, 0·86; P &lt; 0·001), but similar asthma risk (OR = 1·00, 95% CI: 0·91, 1·09; P = 0·967). Mendelian randomization analyses in current smokers showed a slightly lower risk of hay fever (OR = 0·958, 95% CI: 0·920, 0·998; P = 0·041), a lower risk of allergic sensitization (OR = 0·92, 95% CI: 0·84, 1·02; P = 0·117), but higher risk of asthma (OR = 1·06, 95% CI: 1·01, 1·11; P = 0·020) per smoking-increasing allele. Our results suggest that smoking may be causally related to a higher risk of asthma and a slightly lower risk of hay fever. However, the adverse events associated with smoking limit its clinical significance.</jats:p

Association of Forced Vital Capacity with the Developmental Gene <i>NCOR2</i>

Background Forced Vital Capacity (FVC) is an important predictor of all-cause mortality in the absence of chronic respiratory conditions. Epidemiological evidence highlights the role of early life factors on adult FVC, pointing to environmental exposures and genes affecting lung development as risk factors for low FVC later in life. Although highly heritable, a small number of genes have been found associated with FVC, and we aimed at identifying further genetic variants by focusing on lung development genes. Methods Per-allele effects of 24,728 SNPs in 403 genes involved in lung development were tested in 7,749 adults from three studies (NFBC1966, ECRHS, EGEA). The most significant SNP for the top 25 genes was followed-up in 46,103 adults (CHARGE and SpiroMeta consortia) and 5,062 chi

Genome-wide association analysis identifies six new loci associated with forced vital capacity

Forced vital capacity (FVC), a spirometric measure of pulmonary function, reflects lung volume and is used to diagnose and monitor lung diseases. We performed genome-wide association study meta-analysis of FVC in 52,253 individuals from 26 studies and followed up the top associations in 32,917 additional individuals of European ancestry. We found six new regions associated at genome-wide significance (P < 5 × 10−8) with FVC in or near EFEMP1, BMP6, MIR129-2–HSD17B12, PRDM11, WWOX and KCNJ2. Two loci previously associated with spirometric measures (GSTCD and PTCH1) were related to FVC. Newly implicated regions were followed up in samples from African-American, Korean, Chinese and Hispanic individuals. We detected transcripts for all six newly implicated genes in human lung tissue. The new loci may inform mechanisms involved in lung development and the pathogenesis of restrictive lung disease