Damage Factor Research Articles

Typhoon-Induced Forest Damage Mapping in the Philippines Using Landsat and PlanetScope Images

Forests provide valuable resources for households in the Philippines, particularly in poor and upland communities. This makes forests an integral part of building resilient communities. This relationship became complex during extreme events such as typhoon occurrence as forests can be a contributor to the intensity and impact of disasters. However, little attention has been paid to forest cover losses due to typhoons during disaster assessments. In this study, forest damage caused by typhoons was measured using harmonic analysis of time series (HANTS) with Landsat-8 Operation Land Imager (OLI) images. The ΔHarmonic Vegetation Index was computed by calculating the difference between HANTS and the actual observed vegetation index value. This was used to identify damaged areas in the forest regions and create a damage map. To validate the reliability of the results, the resulting maps produced using ΔHarmonic VI were compared with the damage mapped from PlanetScope’s high-resolution pre- and post-typhoon images. The method achieved an overall accuracy of 69.20%. The accuracy of the results was comparable to the traditional remote sensing techniques used in forest damage assessment, such as ΔVI and land cover change detection. To further the understanding of the relationship between forest and typhoon occurrence, the presence of time lag in the observations was investigated. Additionally, different contributing factors in forest damage were identified. Most of the forest damage observed was in forest areas with slopes facing the typhoon direction and in vulnerable areas such as near the coast and hill tops. This study will help the government and forest management sectors preserve forests, which will ultimately result in the development of a more resilient community, by making it easier to identify forest areas that are vulnerable to typhoon damage.

Protein glycation products associate with progression of kidney disease and incident cardiovascular events in individuals with type 1 diabetes

BackgroundDespite improved glycemic treatment, the impact of glycation on pathological consequences may persist and contribute to adverse clinical outcomes in diabetes. In the present study we investigated the association between serum protein glycation products and progression of kidney disease as well as incident major adverse cardiovascular events (MACE) in type 1 diabetes.MethodsFructosamine, advanced glycation end products (AGEs), and methylglyoxal-modified hydro-imidazolone (MG-H1) were measured from baseline serum samples in the FinnDiane study (n = 575). Kidney disease progression was defined as steep eGFR decline (> 3 mL/min/1.73 m2/year) or progression of albuminuria (from lower to higher stage of albuminuria). MACE was defined as acute myocardial infarction, coronary revascularization, cerebrovascular event (stroke), and cardiovascular death.ResultsFructosamine was independently associated with steep eGFR decline (OR 2.15 [95% CI 1.16–4.01], p = 0.016) in the fully adjusted model (age, sex, baseline eGFR). AGEs were associated with steep eGFR decline (OR 1.58 per 1 unit of SD [95% CI 1.07–2.32], p = 0.02), progression to end-stage kidney disease (ESKD) (HR 2.09 per 1 unit of SD [95% CI 1.43–3.05], p < 0.001), and pooled progression (to any stage of albuminuria) (HR 2.72 per 1 unit of SD [95% CI 2.04–3.62], p < 0.001). AGEs (HR 1.57 per 1 unit of SD [95% CI 1.23–2.00], p < 0.001) and MG-H1 (HR 4.99 [95% CI 0.98–25.55], p = 0.054) were associated with incident MACE. MG-H1 was also associated with pooled progression (HR 4.19 [95% CI 1.11–15.89], p = 0.035). Most AGEs and MG-H1 associations were no more significant after adjusting for baseline eGFR.ConclusionsOverall, these findings suggest that protein glycation products are an important risk factor for target organ damage in type 1 diabetes. The data provide further support to investigate a potential causal role of serum protein glycation in the progression of diabetes complications.

PFHpA alters lipid metabolism and increases the risk of metabolic dysfunction-associated steatotic liver disease in youth-a translational research framework.

To address the growing epidemic of liver disease, particularly in pediatric populations, it is crucial to identify modifiable risk factors for the development and progression of metabolic dysfunction-associated steatotic liver disease (MASLD). Per- and polyfluoroalkyl substances (PFAS) are persistent ubiquitous chemicals and have emerged as potential risk factors for liver damage. However, their impact on the etiology and severity of MASLD remains largely unexplored in humans. This study aims to bridge the gap between human and in vitro studies to understand how exposure to perfluoroheptanoic acid (PFHpA), one of the emerging PFAS replacements which accumulates in high concentrations in the liver, contributes to MASLD risk and progression. First, we showed that PFHpA plasma concentrations were significantly associated with increased risk of MASLD in obese adolescents. Further, we examined the impact of PFHpA on hepatic metabolism using 3D human liver spheroids and single-cell transcriptomics to identify major hepatic pathways affected by PFHpA. Next, we integrated the in vivo and in vitro multi-omics datasets with a novel statistical approach which identified signatures of proteins and metabolites associated with MASLD development triggered by PFHpA exposure. In addition to characterizing the contribution of PFHpA to MASLD progression, our study provides a novel strategy to identify individuals at high risk of PFHpA-induced MASLD and develop early intervention strategies. Notably, our analysis revealed that the proteomic signature exhibited a stronger correlation between both PFHpA exposure and MASLD risk compared to the metabolomic signature. While establishing a clear connection between PFHpA exposure and MASLD progression in humans, our study delved into the molecular mechanisms through which PFHpA disrupts liver metabolism. Our in vitro findings revealed that PFHpA primarily impacts lipid metabolism, leading to a notable increase of lipid accumulation in human hepatocytes after PFHpA exposure. Among the pathways involved in lipid metabolism in hepatocytes, regulation of lipid metabolism by PPAR-a showed a remarkable activation. Moreover, the translational research framework we developed by integrating human and in vitro data provided us biomarkers to identify individuals at a high risk of MASLD due to PFHpA exposure. Our framework can inform policies on PFAS-induced liver disease and identify potential targets for prevention and treatment strategies.

Changes in the cardiovascular risk profile in children approaching kidney replacement therapy

Despite significant cardiovascular (CV) morbidity in children on dialysis and after kidney transplantation, data on the evolution of CV damage in children with chronic kidney disease (CKD) approaching kidney replacement therapy (KRT) is unknown. The burden, progression, and predictors of CV damage before KRT onset were explored in two prospective multicenter cohorts from Europe and Canada: Cardiovascular Comorbidity in Children with CKD (4C) and Haemodiafiltration, Heart and Height (3H) studies, conducted from 2009-19 and 2013-16, respectively. CV damage and risk factors were evaluated (i) cross sectionally at KRT-start (n=248), and (ii) longitudinally over the 2-years preceding KRT start (n=157; 331 patient-visits). Longitudinal analyses with mixed-effects models estimated associations of modifiable CV risk factors with change in carotid intima-media thickness (cIMT) standard deviation score (SDS), pulse wave velocity (PWV-SDS), left ventricular (LV) mass and systolic dysfunction. 248 patients, age 14.3 (12.2, 16.2) years were evaluated at median 35 (28-114) days before KRT start. Elevated cIMT-SDS and PWV-SDS were present in 43% and 25%, and LV hypertrophy and systolic dysfunction in 49% and 33%. Aortic stiffness and LV hypertrophy significantly increased, especially in the year before KRT start (adjusted odds ratio, OR 0.33, P=0.002 and OR 0.54, P=0.01, respectively). 79% of children had >3 modifiable CV risk factors at KRT onset. Diastolic BP and BMI were strongly associated with a linear increase in all CV measures. After controlling for CV risk factors, the time to KRT onset no longer predicted the burden of CV damage. This comprehensive CV evaluation shows the progressive accrual of modifiable risk factors and a high burden of CV damage in the years preceding KRT onset. CV damage in the pre-KRT period is preventable. Supported by EU4Health Programme (101085068) and Kidney Research UK (RP39/2013).

Acoustic emission responses and damage estimation of coal with carbon fiber-reinforced polymer confinement under uniaxial compression

Fiber-reinforced polymer (FRP) wrapping is a potential technique for coal pillar reinforcement. In this study, an acoustic emission (AE) technique was employed to monitor coal specimens with carbon FRP (CFRP) jackets during uniaxial compression, which addressed the inability to observe the cracks inside the FRP-reinforced coal pillars by conventional field inspection techniques. The spatiotemporal fractal evolution of the cumulated AE events during loading was investigated based on fractal theory. The results indicated that the AE response and fractal features of the coal specimens were closely related to their damage evolution, with CFRP exerting a significant influence. In particular, during the unstable crack development stage, the evolutionary patterns of the AE count and energy curves of the CFRP-confined specimens underwent a transformation from the slight shock–major shock type to the slight shock–sub-major shock–slight shock–major shock type, in contrast to the unconfined coal specimens. The AE b-values decreased to a minimum and then increased marginally. The AE spatial fractal dimension increased rapidly, whereas the AE temporal fractal dimension fluctuated significantly during the accumulation and release of strain energy. Ultimately, based on the AE count and AE energy evolution, a damage factor was proposed for the coal samples with CFRP jackets. Furthermore, a damage constitutive model was established, considering the CFRP jacket and the compaction characteristics of the coal. This model provides an effective description of the stress–strain relationship of coal specimens with CFRP jackets.

Graph theoretical analysis of limestone fracture network damage patterns based on uniaxial compression test

The topological attributes of fracture networks in limestone, subject to intense hydrodynamics and intricate geological discontinuities, substantially influence the mechanical and hydraulic characteristics of the rock mass. The dynamical evolution of fracture networks under stress is crucial for unveiling the interaction patterns among fractures. However, existing models are undirected graphs focused on stationary topology, which need optimization to depict fractures' dynamic development and rupture process. To compensate for the time and destruction terms, we propose the damage network model, which defines the physical interpretation of fractures through the ternary motif. We focus primarily on the evolution of node types, topological attributes, and motifs of the fracture network in limestone under uniaxial stress. Observations expose the varying behavior of the nodes' self-dynamics and neighbors' adjacent dynamics in the fracture network. This approach elucidates the impact of micro-crack behaviors on large brittle shear fractures from a topological perspective and further subdivides the progressive failure stage into four distinct phases (isolated crack growth phase, crack splay phase, damage coalescence phase, and mechanical failure phase) based on the significance profile of the motif. Regression analysis reveals a positive linear and negative power correlation between fracture network density and branch number to the rock damage resistance, respectively. The damage network model introduces a novel methodology for depicting the interaction of two-dimensional (2D) projected fractures, considering the dynamic spatiotemporal development characteristics and fracture geometric variation. It helps dynamically characterize properties such as connectivity, permeability, and damage factors while comprehensively assessing damage in rock mass fracture networks.

Targeting gut microbiota and metabolism profiles with coated sodium butyrate to ameliorate high-energy and low-protein diet-induced intestinal barrier dysfunction in laying hens

High energy diet are a risk factor for intestinal barrier damage. Butyrate, a major energy source for intestinal epithelial cells, has been shown to improve barrier dysfunction and modulate the gut microbiota. In this trial, we examined the preventative effect of coated sodium butyrate (CSB) on high-energy low-protein (HELP)-induced intestinal barrier injury in laying hens, and also worked to determine the underlying mechanisms by an integrative analysis of gut microbiota and the metabolome. A total of 216 healthy 28-weeks-old Huafeng laying hens were randomly assigned to 3 groups with 6 replicates each: the CON group (normal diet), HELP group (high-energy and low-protein diet) and CH500 group (500 mg/kg CSB added to HELP diet). The duration of the trial encompassed a period of 10 weeks. The results revealed that CSB treatment improved the laying rate (P<0.05) and mitigated the detrimental effects on intestinal barrier function and the inflammatory response induced by the HELP diet in laying hens (P<0.05). Microbial profiling analysis revealed that the CSB treatment reshaped the HELP-perturbed gut microbiota, and promoted the growth of beneficial bacteria (P<0.05). Untargeted metabolomics analysis revealed that CSB reduced the metabolites associated with intestinal inflammation (P<0.05). In conclusion, CSB did not merely modulate alterations in the gut microbiota composition and microbial metabolites but also yielded increased egg production, while mitigating intestinal barrier dysfunction and inflammatory responses induced by HELP in laying hens.

SIC Position paper: Treat to prevent the first event - intensive LDL cholesterol lowering in patients at very high cardiovascular risk without a previous cardiovascular event. From ESC guidelines to clinical practice

Cardiovascular (CV) diseases account for over 4 million deaths every year in Europe and over 220 000 deaths in Italy, representing the leading cause of morbidity and mortality worldwide. The European Society of Cardiology (ESC) guidelines have visionary included in the at very high CV risk group patients without previous acute ischemic events, such as those with subclinical atherosclerosis, chronic coronary syndrome or peripheral arterial disease, familial hypercholesterolemia, diabetes mellitus with target organ damage or multiple associated risk factors, and those with high calculated CV risk score, recommending to consider them and to achieve the same LDL-cholesterol targets as for secondary prevention patients. The aim of this position paper is to provide an updated overview of ESC guidelines that focuses on these patient categories to raise awareness within the clinical community regarding CV risk reduction in this specific epidemiological context.

Case-control study to identify the causative agents of ophthalmia and conjunctivitis in goats in Savannakhet province of Lao PDR

Pinkeye is a highly contagious disease of goats with different aetiologies. Surveys in Lao PDR have identified eye lesions typical of pinkeye as a common condition, however, this has not been confirmed diagnostically, and the responsible pathogens have not been identified. A matched case-control study was implemented in 70 goat holdings from Savannakhet province, Lao PDR, to detect agents causing pinkeye and conduct phylogenetic analysis of the identified pathogens. Fifty eye swabs from goats with infected eyes (cases) and 50 paired samples from unaffected cohorts (controls) were collected from 25 holdings. Samples were tested using quantitative PCR assays targeting known pinkeye pathogens at the genus and species levels. The prevalence of pathogens in case and control goats was as follows: Mycoplasma conjunctivae (94% and 74% respectively, P = 0.006, OR = 5.5), Chlamydia pecorum (4%, 10%), Moraxella ovis (30%, 30%), Moraxella bovis (0%, 0%) and Moraxella bovoculi (0%, 0%). M. conjunctivae was present in a high proportion of goats in both groups revealing that Lao goats are carriers of M. conjunctivae. However, the mean log10 genome copy number/µL of DNA extract was significantly higher in case goats than control goats (P < 0.05). Thus, M. conjunctivae is likely the principal causative agent of pinkeye in Lao goats with carrier status converting to clinical infection following corneal damage or other causative factors. M. conjunctivae detected in samples from different goats and districts showed low genetic diversity. Identifying the causes of pinkeye in Lao goats will assist in designing appropriate treatment and control strategies.

YTHDC1 m6A-dependent and m6A-independent functions converge to preserve the DNA damage response

Cells have evolved a robust and highly regulated DNA damage response to preserve their genomic integrity. Although increasing evidence highlights the relevance of RNA regulation, our understanding of its impact on a fully efficient DNA damage response remains limited. Here, through a targeted CRISPR-knockout screen, we identify RNA-binding proteins and modifiers that participate in the p53 response. Among the top hits, we find the m6A reader YTHDC1 as a master regulator of p53 expression. YTHDC1 binds to the transcription start sites of TP53 and other genes involved in the DNA damage response, promoting their transcriptional elongation. YTHDC1 deficiency also causes the retention of introns and therefore aberrant protein production of key DNA damage factors. While YTHDC1-mediated intron retention requires m6A, TP53 transcriptional pause-release is promoted by YTHDC1 independently of m6A. Depletion of YTHDC1 causes genomic instability and aberrant cancer cell proliferation mediated by genes regulated by YTHDC1. Our results uncover YTHDC1 as an orchestrator of the DNA damage response through distinct mechanisms of co-transcriptional mRNA regulation.

Research on Viscoelastic Impact Damage Constitutive Model and Its Behavioral Characteristics

To investigate the damage characteristics of viscoelastic materials under various impact scenarios, this study presents a viscoelastic impact damage constitutive model that incorporates a material coefficient, a variable fractional-order differential operator, and a damage factor. Split Hopkinson Pressure Bar experiments are conducted under single-impact and repeated-impact conditions. The results indicate that nonlinear features in stress-strain curves at different stages, exhibiting prominent strain rate dependency near the stress peak point in the single-impact scenario. In the repeated-impact scenario, the stress peak points decrease as the impact times increase, resulting in a corresponding decline in the material's load-bearing capacity. Furthermore, strain rate escalates the strain rate increases with an increase in impact times, making the material more susceptible to deformation. Parameter fitting and Sobol sensitivity analysis utilizing experimental data from both scenarios have been employed to explore the effects and patterns of single-parameter and multi-parameter coupling on the model, accurately delineating their influence. The findings reveal a strong coupling relationship among various parameters of the viscoelastic impact damage constitutive model in multiple impact scenarios, showing higher sensitivity to fluctuations in the viscoelastic coefficient and damage factor. These analyses have demonstrated the accuracy of the viscoelastic impact damage constitutive model in capturing dynamic impact damage characteristics of viscoelastic materials across various scenarios.

ANALISA KERUSAKAN RUAS JALAN RAYA SEMARANG BOJA (Studi Kasus Pasar Jrakah – SPBU BSB)

The dense of traffic volume resulted in road damage on the Semarang Boja highway section to be precise at KM 8 – KM 14 Semarang Boja. Overcrowding and excessive tonnage are also factors in road damage in the area. The purpose of this study was to determine the LHR on Semarang Boja highway, the effect of vehicle volume on the level of damage to Jalan Raya Semarang Boja.. This research method is quantitative. The quantitative method is a method of collecting some data with primary data, namely direct surveys in the field and secondary data needed in this study. Based on the results of the analysis, the average daily traffic (LHR) on the northbound road was 1949.57 pcu/hour and on the southbound road was 1872.83 pcu/hour classified as heavy traffic. The degree of saturation (DS) value based on traffic volume &gt; 0.75 is 6.30 in morning conditions, 2.99 in afternoon conditions, 3.77 in afternoon conditions with a very saturated category

Risk factors of disease activity and renal damage in patients with systemic lupus erythematosus.

To evaluate the clinical features of patients with Systemic Lupus Erythematosus (SLE) and explore the risk factors of disease activity and renal damage. A retrospective study involving 194 patients were performed. Patients were divided into lupus nephritis (LN) group (63.40%) and non-LN group (36.60%), different disease activity group, and different renal function group according to the clinical data. Multivariate logistic regression analysis showed that albumin (ALB), uric acid (UC), total cholesterol (TC), and anti-dsDNA antibodies were the influencing factors of LN in patients with SLE (P < 0.05); ALB, UC, and complement 3(C3) were the influencing factors of lupus disease activity (P < 0.05); UC, C3, and hemoglobin (HB) were the influencing factors of abnormal renal function in SLE patients. The results of the ROC curve showed that ALB, UA, and TC had certain predictive value for combined LN in patients with SLE, and the predictive value of ALB was greater than that of TC (P < 0.05); ALB, UA, and C3 being predictors of the activity of patients with SLE; BUN, UA, and HB all had certain predictive value for the abnormal renal function in patients with LN. SLE patients have the high incidence of renal impairment. The results of this study suggest that patients with SLE should regularly monitor the levels of ALB, UA, TC, C3, and HB, as well as pay attention to the intervention of hyperlipidemia and hyperuricemia in patients with SLE to better control disease progression.

A Novel Analog of the Natural Product Fraxinellone Protects against Endogenous and Exogenous Neurotoxicants.

Numerous insults, both endogenous (e.g., glutamate) and exogenous (e.g., pesticides), compromise the function of the nervous system and pose risk factors for damage or later disease. In previous reports, limonoids such as fraxinellone showed significant neuroprotective activity against glutamate (Glu) excitotoxicity and reactive oxygen species (ROS) production in vitro, albeit with minimal mechanistic information provided. Given these findings, a library of novel fraxinellone analogs (including analogs 1 and 2 described here) was synthesized with the goal of identifying compounds exhibiting neuroprotection against insults. Analog 2 was found to be protective against Glu-mediated excitotoxicity with a measured EC50 of 44 and 39 nM for in vitro assays using PC12 and SH-SY5Y cells, respectively. Pretreatment with analog 2 yielded rapid induction of antioxidant genes, namely, Gpx4, Sod1, and Nqo1, as measured via qPCR. Analog 2 mitigated Glu-mediated ROS. Cytoprotection could be replicated using sulforaphane (SFN), a Nrf2 activator, and inhibited via ML-385, which inhibits Nrf2 binding to regulatory DNA sequences, thereby blocking downstream gene expression. Nrf2 DNA-binding activity was demonstrated using a Nrf2 ELISA-based transcription factor assay. In addition, we found that pretreatment with the thiol N-acetyl Cys completely mitigated SFN-mediated induction of antioxidant genes but had no effect on the activity of analog 2, suggesting thiol modification is not critical for its mechanism of action. In summary, our data demonstrate a fraxinellone analog to be a novel, potent, and rapid activator of the Nrf2-mediated antioxidant defense system, providing robust protection against insults.

Mitochondrial transfer of α-synuclein mediates carbon disulfide-induced mitochondrial dysfunction and neurotoxicity

Exposure to carbon disulfide (CS2) is a recognized risk factor in the pathogenesis of Parkinson’s disease, yet the underlying mechanisms of deleterious effects on mitochondrial integrity have remained elusive. Here, through establishing CS2 exposure models in rat and SH-SY5Y cells, we demonstrated that highly expressed α-synuclein (α-Syn) is transferred to mitochondria via membrane proteins such as Tom20 and leads to mitochondrial dysfunction and mitochondrial oxidative stress, which ultimately causes neuronal injury. We first found significant mitochondrial damage and oxidative stress in CS2-exposed rat midbrain and SH-SY5Y cells and showed that mitochondrial oxidative stress was the main factor of mitochondrial damage by Mitoquinone intervention. Further experiments revealed that CS2 exposure led to the accumulation of α-Syn in mitochondria and that α-Syn co-immunoprecipitated with mitochondrial membrane proteins. Finally, the use of an α-Syn inhibitor (ELN484228) and small interfering RNA (siRNA) effectively mitigated the accumulation of α-Syn in neurons, as well as the inhibition of mitochondrial membrane potential, caused by CS2 exposure. In conclusion, our study identifies the translocation of α-Syn to mitochondria and the impairment of mitochondrial function, which has important implications for the broader understanding and treatment of neurodegenerative diseases associated with environmental toxins.

The association of structural versus load-dependent large artery stiffness mechanisms with cerebrovascular damage and cortical atrophy in humans.

Large central arterial stiffness is a risk factor for cerebrovascular damage and subsequent progression of neurodegenerative diseases, including Alzheimer's disease and dementia. However, arterial stiffness is determined by both the intrinsic components of the arterial wall (structural stiffness) and the load (i.e., arterial blood pressure) exerted upon it by the blood (load-dependent stiffness). This study aimed to determine the degree to which structural and/or load-dependent mechanisms of central arterial stiffness are associated with cerebrovascular damage. Among 128 healthy individuals (aged 63±6, age range: 50-80 years, 42% men), aortic and carotid artery stiffness was measured via carotid-femoral pulse wave velocity and B-mode ultrasonography, respectively. Using participant-specific exponential models, both aortic and carotid artery stiffness were standardized to a reference blood pressure to separate their structural and load-dependent stiffness mechanisms. Magnetic resonance imaging was used to derive total, periventricular, and deep cerebral white matter lesion volume (WMLV) and global cortical thickness. After adjusting for common cardiovascular disease risk factors, a 1 m/s increase in structural aortic stiffness was associated with 15% greater total WMLV (95% confidence interval [CI] = 0.01, 0.27, P = 0.036), 14% greater periventricular WMLV (95%CI = 0.004, 0.25, P = 0.044) and 0.011mm lower cortical thickness (95%CI = -0.022, -1.18, P = 0.028). No association was observed between structural carotid stiffness and WMLVs (total, periventricular, and deep), and neither aortic nor carotid load-dependent stiffness was associated with WMLVs or cortical thickness. Structural, not load-dependent, mechanisms of aortic stiffness are related to cerebrovascular-related white matter damage.

An experimental investigation of ship propulsion system fatigue damage during crash astern maneuver

Marine propulsion shafts are exposed to fatigue due to various maneuvers. Among them, crash astern is considered to induce a high level of torsional stress on the shaft. Torsional stress is a dominant factor in shaft fatigue damage; however, there has been limited discussion on how much this maneuver impacts shaft fatigue life. So, this study aims to calculate fractional fatigue damage resulting from crash astern maneuvers, obtaining numerical results through a marine shaft fatigue analysis method. Firstly, shaft fatigue criteria were defined to establish S-N curves. Then, crash astern maneuvers were conducted to measure torsional stress as a loading history. Raw data were analyzed to apply alternating stress values to the S-N curve, enabling the calculation of cumulative fractional damage. The crash astern maneuver was executed under two different drafts: full laden and normal ballast, allowing for a comparison of shaft fatigue levels based on draft. Torsional stress was higher in the ballast condition than in full laden. Additionally, fatigue damage in ballast is approximately 1.7 times higher than in the other condition. The results suggest that the shaft is more affected by fatigue when sailing in shallow water than when sailing in deep sea.

Flexural failure mechanism of bamboo composite plates with different construction technologies and tectonic patterns

To investigate the failure mechanism of bamboo fiber reinforced composite (BFRC) plates with different construction technologies and tectonic patterns, flexural experiments were performed. The flexural property of the parallel bamboo strand lumbers (PBSL) is better than that of the glued laminated bamboo (GLB), where the cracking load is increased by 141 % at most and the peak load is increased by 57 % at most. The orthogonal structure for the cross-laminated bamboo (CLB) improves the flexural property to a certain extent by inhibiting the initial cracking whether it is PBSL or GLB, and the peak load is increased by 9.83 % and 11.40 %, respectively. The residual bearing capacity of the PBSL is better than that of the CLB, the PBSL can basically maintain half of the ultimate bearing capacity while the damage factor of CLB is as high as 0.84 when the structure is damaged, revealing that the orthogonal layup structure results in weak interlayer interface after explosion. Orthotropic plate theory and composite failure criteria were proposed and consistently predicted the cracking load and the ultimate load. It is found that matrix fracture controls the cracking load, while fiber fracture determines the ultimate load.

Health burden and costs attributable to the carbon footprint of the health sector in the European Union

BackgroundThe healthcare sector has an environmental impact of around 4.6% of global CO2 emissions, contributing to aggravating the climate crisis. However, the impact of the health sector’s emissions on human health is not regularly assessed. We aim to estimate the health burden and associated costs of the health sector’s carbon footprint within the European Union (EU). MethodsWe calculated disability-adjusted life years (DALYs) and associated costs based on human health damage factors (DALYs/kg-CO2e) by considering four scenarios. Three scenarios for shared socioeconomic pathways (S1 – high growth, S2 − baseline, and S3 − low growth) represented variations of global society, demographics, and economics until 2100. A fourth scenario (S4) considered the current EU’s 55% reduction goal of greenhouse gas emissions. The healthcare sector’s emissions per capita (in CO2-equivalent) in 2019 were extracted from the Lancet Countdown, and population data were retrieved from Eurostat for the same year. ResultsIn the EU, 365,047 DALYs (95%CI: 194,692–535,403) are expected to be caused by the health sector’s emissions at baseline (S2). In an S1 scenario, the burden would slightly decrease to 316,374 DALYs (95%CI: 170,355–462,393), whereas a S3 scenario would increase 486,730 DALYs (95%CI: 243,365–681,422). If EU’s carbon goals are met, the burden could be substantially reduced to 164,271 DALYs (95%CI: 87,611–240,931). Costs can amount to 25.6 billion euros, when considering DALYs monetisation. ConclusionCO2 emissions from the health sector are expected to significantly impact human health. Therefore, it is important to ensure that EU climate policies for public buildings are in line with the Paris Agreement, increase funding for climate mitigation programs within the healthcare sector, and review clinical practices at the local level.

Mechanical behaviors and meso analysis of asphalt mixtures under moisture damage induced by hydrodynamic impacts

Moisture damage significantly affects the performance and integrity of asphalt pavement. The water immersion method commonly used in laboratory is considered as a static water intrusion technique to simulate the moisture damage on asphalt mixtures. However, field conditions mainly involve dynamic water impacting due to moving tires and pressurized pore water. In this study, the in-situ moisture damage induced by repeated traffics was recurred with the Moisture Induced Sensitivity Tester (MIST), and their mechanisms and impacts on the void structure, viscoelastic properties, and fracture performance of the asphalt mixture were assessed. The findings revealed that hydrodynamic impacts with various loading cycle (0, 2000, 4000, 6000 cycles) could lead to an increase in the porosity of the mixture, with isolated voids eventually merged under water intrusion and erosion. The growth rate of the connected voids was more drastic in the initial stage and gradually decreased with the increased loading cycle. Besides, the dynamic water damage could enlarge the overall permeability of the asphalt mixtures and aggrandize the complexity of the water flow paths in a non-linear manner. The dynamic water damage factor (Dm) reflecting the variation of porosity was introduced to characterize the damage severity of the mixture. The results indicated that a severer damage was normally observed for the mixture with a higher initial porosity. Furthermore, significant effects of hydrodynamic damage on the dynamic modulus of the asphalt mixtures, especially in the high temperature (low frequency) domain, were also observed on the MIST-conditioned specimens. The CT-scanning analysis implied that the impaired adhesion between asphalt and aggregates and mechanical damage from pore water pressures were the primary causes of the damage. A degradation in crack resistance is observed from the Semi-Circular Bending (SCB) tests considering the hydrodynamic damage at various MIST-conditioning cycle.