Short-term Exposure Research Articles

Short-term ozone exposure on stroke mortality and mitigation by greenness in rural and urban areas of Shandong Province, China

BackgroundShort-term exposure to ozone (O3) has been associated with higher stroke mortality, but it is unclear whether this association differs between urban and rural areas. The study aimed to compare the association between short-term exposure to O3 and ischaemic and haemorrhagic stroke mortality across rural and urban areas and further investigate the potential impacts of modifiers, such as greenness, on this association.MethodsA multi-county time-series analysis was carried out in 19 counties of Shandong Province from 2013 to 2019. First, we employed generalized additive models (GAMs) to assess the effects of O3 on stroke mortality in each county. We performed random-effects meta-analyses to pool estimates to counties and compare differences in rural and urban areas. Furthermore, a meta-regression model was utilized to assess the moderating effects of county-level features.ResultsShort-term O3 exposure was found to be associated with increased mortality for both stroke subtypes. For each 10-µg/m3 (lag0-3) rise in O3, ischaemic stroke mortality rose by 1.472% in rural areas and 1.279% in urban areas. For each 0.1-unit increase in the Enhanced Vegetation Index (EVI) per county, the ischaemic stroke mortality caused by a 10-µg/m3 rise in O3 decreased by 0.60% overall and 1.50% in urban areas.ConclusionsOur findings add to the evidence that short-term O3 exposure increases ischaemic and haemorrhagic stroke mortality and has adverse effects in urban and rural areas. However, improving greenness levels may contribute to mitigating the detrimental effects of O3 on ischaemic stroke mortality.

Ambient air pollution exposure is associated with liver fat and stiffness in Latino youth with a more pronounced effect in those with PNPLA3 genotype and more advanced liver disease

BackgroundExposure to ambient air pollutants has emerged as a risk for metabolic-dysfunction associated steatotic liver disease (MASLD). ObjectivesWe sought to examine associations between short-term (prior month) and long-term (prior year) ambient air pollution exposure with hepatic fat fraction (HFF) and liver stiffness in Latino youth with obesity. A secondary aim was to investigate effect modification by patatin-like phospholipase domain-containing protein 3 (PNPLA3) genotype and liver disease severity. MethodsData was analyzed from 113 Latino youth (age 11–19) with obesity in Southern California. Individual exposure to particulate matter with aerodynamic diameter ≤ 2.5μm (PM2.5), ≤ 10μm (PM10), nitrogen dioxide (NO2), 8-hour maximum ozone (8hrMax-O3), 24-hr O3, and redox-weighted oxidative capacity (Oxwt) were estimated using residential address histories and United States Environmental Protection Agency air quality observations. HFF and liver stiffness were measured using magnetic resonance imaging. Linear models were used to determine associations between short-term and long-term exposure to air pollutants with HFF and liver stiffness. Modification by PNPLA3 and liver disease severity was then examined. ResultsShort-term exposure to 8hrMax-O3 was positively associated with HFF. Relationships between air pollution exposure and HFF were not impacted by PNPLA3 genotype or liver disease severity. Long-term exposure to 8hrMax-O3 and Oxwt were positively associated with liver stiffness. Associations between air pollution exposure and liver stiffness depended on PNPLA3 genotype, such that individuals with GG genotypes exhibited stronger, more positive relationships between short-term exposure to PM10, 8hrMax-O3, 24-hr O3, and Oxwt and liver stiffness than individuals with CC/CG genotypes. In addition, relationships between short-term exposure to NO2 and liver stiffness were stronger in those with severe liver disease. DiscussionAir pollution exposure may be a risk factor for liver disease among Latino youth with obesity, particularly in those with other preexisting risks for liver damage.

Background predation risk induces anxiety-like behaviour and predator neophobia in zebrafish

Prey face a major challenge in balancing predator avoidance with other essential activities. In environments with high risk, prey may exhibit neophobia (fear of novelty) due to the increased likelihood of novel stimuli being dangerous. The zebrafish, Danio rerio, is an established model organism for many scientific studies. Although spatial and object neophobia in zebrafish have received previous attention, little is known about the role of background risk in inducing neophobia in zebrafish. Here, we present two experiments using zebrafish to explore whether background predation risk can induce anxiety-like behaviour in a novel environment and neophobic responses when exposed to a novel odour. Over five days, we repeatedly exposed zebrafish to either high background risk in the form of chemical alarm cues (i.e., injured conspecific cues that indicate a predator attack) or a low-risk water control stimulus. In Experiment 1, when tested in a novel tank, zebrafish exposed to high predation risk displayed anxiety-like responses (reduced activity and increased bottom time spent) compared to their low-risk counterparts. Moreover, high-risk individuals showed reduced intra-session habituation to the novel tank compared to low-risk individuals. In Experiment 2, high-risk individuals exhibited fear responses toward a novel odour, unlike low-risk individuals. These results reveal that short-term repeated exposures to high risk can induce anxiety-like behaviour and predator odour neophobia in zebrafish.

Criteria air pollutants and HIV-related mortality: Insights from a nationwide case-crossover investigation

The heightened vulnerability of individuals with HIV to environmental stressors is well-recognized, yet the role of air pollution in exacerbating HIV-related mortality remains underexplored. In this nationwide, individual-level case-crossover study conducted from 2013 to 2019, we investigated the association between short-term exposure to criteria air pollutants and HIV-related mortality. Our analysis of 38,510 HIV-related deaths revealed significant associations between exposure to PM2.5, PM10, NO2, and CO and increased mortality risk. The effects of PM2.5 and PM10 persisted for two days, whereas NO2 and CO had immediate, same-day impacts. Vulnerability was heightened in individuals under 65 years, males, those with lower educational attainment, and unmarried individuals. Among causes of death, HIV-related malignant neoplasms exhibited the highest sensitivity to particulate matter. Our findings provide novel insights into the relationship between short-term air pollution exposure and HIV-related mortality, emphasizing the increased susceptibility of this immunocompromised population. The results underscore the need for targeted public health interventions to reduce pollution exposure, particularly for the most at-risk demographic groups. This study contributes to a deeper understanding of environmental health risks faced by individuals living with HIV and informs evidence-based policy recommendations.

Untargeted metabolomic analysis reveals a time-course hepatic metabolism disorder induced by short-term 6PPD exposure in rats

The tire antioxidant 6PPD has garnered extensive attention due to its widespread presence in the environment and the harmful effects of its transformation products on aquatic organisms. 6PPD has been detected in airborne dust, and it can enter mammals through inhalation exposure. While the toxic effects of 6PPD exposure have been reported in mammals, its effects on hepatic metabolism still remain poorly understood. Here, we collected the serum and liver samples at 1, 6, and 72 h following a single oral exposure of 100 mg/kg body weight (bw) 6PPD, respectively. We also investigated changes in serum and hepatic physiological indicators and metabolites, correspondingly. Results indicated that single time oral exposure a high dose of 6PPD did not significantly affect the physiological indexes of rats within a short time frame. However, untargeted metabolomics analysis of the metabolites in the liver at 1, 6, and 72 h revealed that the number of differential expression metabolites gradually increased over time and the most affected substances were lipids and lipid-like molecules. Interestingly, the KEGG pathway enrichment analysis indicated that 6PPD disrupted the riboflavin metabolism, leading to a significant decrease in FMN levels at all time points. In addition, the hepatic glucose metabolism was significantly affected at 6 and 72 h after oral administration. Taken together, short-term exposure to 6PPD disturbed lipid and riboflavin metabolism and gradually affected glucose metabolism in the liver of rats. These findings revealed the impacts of 6PPD on the hepatic metabolism in animals, and also offered some important insights into its toxicology and health risk.

The Effect of Acute High-Altitude Exposure on Oral Pathogenic Bacteria and Salivary Oxi-Inflammatory Markers.

Background: The environment can alter the homeostasis of humans and human microbiota. Oral health is influenced by high altitude through symptoms of periodontitis, barodontalgia, dental barotrauma, and a decrease in salivary flow. Microbiota and inflammatory state are connected in the oral cavity. This study aimed to explore the effect of acute high-altitude exposure on the salivary microbiome and inflammatory indicators. Methods: Fifteen healthy expeditioners were subjected to oral examination, recording the plaque index (PII), gingival index (GI), the simplified oral hygiene index (OHI-S), and the number of teeth; unstimulated saliva samples were collected at an altitude of 1191 m (T1) and 4556 m (T2). TNF-α, sICAM1, ROS, and the oral bacterial species Porphyromonas gingivalis (Pg) and Fusobacterium nucleatum (Fn) were quantified. Results: At T2, slCAM, TNF, and ROS increased by 85.5% (IQR 74%), 84% (IQR 409.25%), and 53.5% (IQR 68%), respectively, while Pg decreased by 92.43% (IQR 102.5%). The decrease in Pg was greater in the presence of low OHI-S. The increase in slCAM1 correlated with the reduction in Fn. Individuals with high GI and OHI-S had a limited increase in TNF-α at T2. Conclusion: Short-term exposures can affect the concentration of pathogenic periodontal bacteria and promote local inflammation.

Ameliorative Effects of N-Acetyl Cysteine and Zinc Sulfate on Reproductive Dysfunction Induced by Short-Term Crude Oil Exposure in Male Wistar Rats

Background: Crude oil contamination by accidental or voluntary ingestion is prevalent in the Niger Delta region of Nigeria. One of the possible impacts of crude oil contamination is reproductive toxicity leading to infertility. The present study evaluated the potential protective effects of N-Acetyl Cysteine (NAC) and Zinc Sulfate (ZnSO4) in mitigating reproductive dysfunction caused by short-term Bonny Light Crude oil (BLCO) exposure in male Wistar rats. Materials and Methods: Fifty (50) male Wistar (180 – 200g) were used for the study. They were divided into ten (10) groups of five (5) animals each. Groups I and II served as the control and negative control and received distilled water and BLCO (600mg/kg) respectively while groups III to X served as the experimental groups and received NAC (100 and 200mg/kg) and ZnSO4 (0.5mg/kg and 1mg/kg) orally for three (3) weeks. Animals were euthanized, and blood and semen were collected for biochemical and seminal analysis. Results: The results of this current study show that BLCO exposure caused a disruption in reproductive functions in rats by decreasing reproductive hormones and semen quality parameters in Wistar rats. NAC and ZnSO4 administration significantly improved semen quality parameters by improving sperm count, sperm motility and morphology in experimental rats. Conclusion: Evidence from the present study suggests that NAC and ZnSO4 protected the testes, preventing reproductive alterations linked to BLCO exposure.

Effects of Increasing Oral Deoxynivalenol Gavage on Growth Performance, Blood Biochemistry, Metabolism, Histology, and Microbiome in Rats.

Mycotoxin-contaminated feed or food can affect physiological responses and cause illnesses in humans and animals. In this study, we evaluated the effects of deoxynivalenol (DON) toxicity on the growth performance, blood biochemistry, histology, microbiome, and metabolism of rats fed with different toxin concentrations. After 1 week of acclimatization, seven-week-old male rats received 0.9% saline as a control, 0.02 mg/kg DON as T1, and 0.2 mg/kg DON as T2 via oral gavage for 4 weeks. The final body weight of the T2 group was significantly lower than that of the control and T1; however, the average daily gain, feed intake, and feed conversion ratio did not differ. Fibrosis and apoptosis were observed in various tissues as DON concentration increased. Creatinine and alkaline phosphatase levels were significantly lower in the DON-treated group than in the control. Firmicutes and Desulfobacterota phyla dominated the cecum, whereas those in the feces were Proteobacteria and Bacteroidetes. Metabolomic profiling showed phenylalanine, tyrosine, and tryptophan biosynthesis as the most prominent pathways. Overall, our results suggest that low-dose and short-term DON exposure can trigger several adverse effects in rats. Dietary toxicants in rats may explain the physiological effects associated with the metabolism commonly reported in animals.

Interleukin-1β modulates lymphoid differentiation of Flt3-positive multipotent progenitors after transplantation

Myeloablative pre-conditioning facilitates the differentiation of transplanted hematopoietic stem and progenitor cells (HSPCs). However, the factors in the stress environment that regulate HSPC behavior remain elusive. Here, we investigated the mechanisms that shaped the cell fates of transplanted murine multipotent progenitors (MPPs) expressing the Fms-related receptor tyrosine kinase 3 gene (Flt3). Using lineage tracing, clonal analysis, and single-cell RNA sequencing (RNA-seq), we showed that the myeloablative environment increased lymphoid priming of Flt3+ MPPs and that their efficient B cell output required intact interleukin 1 (IL-1) signaling. The Flt3+ MPPs with short-term exposure to IL-1β underwent a myeloid-biased to lymphoid-biased cell fate switch and produced more lymphoid-biased progeny with a strongerB lymphopoiesis capacity invitro. Correspondingly, a brief exposure to IL-1β facilitated the B cell output of transplanted Flt3+ MPPs invivo. Together, our study demonstrated an unrecognized function of IL-1β in promoting B lymphopoiesis and highlighted a latent effect of IL-1β in regulating MPP cell fate dynamics.

Rapid α-Al2O3 Growth on an Iron Aluminide Coating at 600 °C in the Presence of O2, H2O, and KCl.

In this work, a slurry iron aluminide-coated ferritic steel SVM12 was subjected to a laboratory experiment mimicking superheater corrosion in a biomass-fired power boiler. The samples were exposed under model Cl-rich biomass conditions, in a KCl + O2 + H2O environment at 600 °C for 168, 2000, and 8000 h. The morphology of corrosion and the composition of the oxide scale and the coating were investigated by a combination of advanced analytical techniques such as FESEM/EDS, SEM/EBSD, and XRD. Even after short-term exposure, the coating developed a very fast-growing and up to 50 μm thick α-Al2O3 scale in contrast to the spontaneous formation of a protective, thin, dense, slow-growing, and very adhesive α-Al2O3 layer usually formed on metallic materials after high-temperature oxidation. In view of the literature on the formation of oxide scales on alloys and coatings, the formation of an α-Al2O3 scale at this relatively low temperature is very surprising in itself. The thick alumina scale was not protective as its formation resulted in fast degradation of the coating and rapid Fe2Al5 → FeAl phase transformation, which in turn generated porosity inside the coating. In all cases, the resulting thick Al2O3 scale was porous and consisted of both equiaxed α-Al2O3 grains and randomly oriented aggregated alumina whiskers. Potassium is concentrated in the outer part of the Al2O3 scale, while chlorine is concentrated close to the scale/aluminide interface. The unexpected formation of rapidly growing α-Al2O3 at relatively low temperature is attributed to the hydrolysis of aluminum chloride generated in the corrosion process.

Long-Term Neurotoxic Effects and Alzheimer's Disease Risk of Early EHDPP Exposure in Zebrafish: Insights from Molecular Mechanisms to Adult Pathology.

2-Ethylhexyl diphenyl phosphate (EHDPP), ubiquitously monitored in environmental media, is highly bioaccumulative and may pose long-term risks, even after short-term exposure. In this investigation, larval zebrafish were exposed to 0.05, 0.5, and 5.0 μg/L EHDPP from 4 to 120 h postfertilization (hpf) to examine the long-term neurotoxicity effects of early exposure. Exposure to 5.0 μg/L EHDPP yielded hyperactive locomotor behavior, which was characterized by increased swimming speed, larger turning angles, and heightened sensitivity to light-dark stimulation. The predicted targets of EHDPP (top 100 potential macromolecules) were primarily associated with brain diseases like Alzheimer's disease (AD). Comparisons of differentially expressed genes (DEGs) from AD patients (GSE48350) and RNA-seq data from EHDPP-exposed zebrafish confirmed consistently abnormal regulatory pathways. EHDPP's interaction with M1 and M5 muscarinic acetylcholine receptors likely disrupted calcium homeostasis, leading to mitochondrial dysfunction and neurotransmitter imbalance as well as abnormal locomotor behavior. Especially, 5.0 μg/L EHDPP exposure during early development (4-120 hpf) triggered early- and midstage AD-like symptoms in adulthood (180 dpf), characterized by cognitive confusion, aggression, blood-brain barrier disruption, and mitochondrial damage in brains. These findings provide deep insights into the long-term neurotoxicity effects and Alzheimer's disease risks of early EHDPP exposure at extremely low dosages.

Interaction of Cooking-Generated Aerosols on the Human Nervous System and the Impact of Caloric Restriction Post-Exposure

Background: The inhalation of cooking-generated aerosols could lead to translocation to the brain and impact its function; therefore, the effects of cooking-generated aerosols on healthy adults were investigated using an electroencephalograph (EEG) during the 2 h period post-exposure. Methods: To explore any changes from the impact of exposure to cooking-generated aerosols on the human brain due to the absence of food intake during exposure, we divided the study participants into three groups: (A) no food intake for 2 h (2 h-zero calorie intake), (B) non-zero calorie intake, and (C) control group (simulated cooking). Results: The ultrafine particle concentrations increased from 9.0 × 103 particles/cm3 at the background level to approximately 8.74 × 104 particles/cm3 during cooking. EEGs were recorded before cooking (step 1), 60 min after cooking (step 2), 90 min after cooking (step 3), and 120 min after cooking (step 4). Comparing the non-zero calorie group with the control group, it was concluded that exposure to cooking-generated aerosols resulted in a 12.82% increase in the alpha band two hours post-exposure, compared to pre-exposure. The results revealed that zero calorie intake after exposure mitigated the impacts of cooking-generated aerosols for the alpha, beta3, theta, and delta bands, while it exacerbated effects on the whole brain for the beta1 and beta2 bands. Conclusions: While these are short-term studies, long-term exposure to cooking-generated ultrafine particles can be established through successive short-term exposures. These results underscore the need for further research into the health impacts of cooking-generated aerosols and the importance of implementing strategies to mitigate exposure.

Regualtion of LAMTOR1 by Oxidative Stress in Retinal Pigment Epithelium: Implications for Age-Related Macular Degeneration Pathogenesis

Oxidative stress is a critical pathogenic factor for age-related macular degeneration (AMD). Autophagy serves as a mechanism to counteract oxidative stress. LAMTOR1 regulates mTORC1 activity by recruiting or disassembling it on the lysosome under the addition or deprivation of amino acids. This regulation inhibits or enhances autophagy. Our study investigates whether oxidative stress impacts LAMTOR1, thereby adapting to oxidative conditions. We employed oxidative stressors, menadione (VK3) and 4-hydroxynonenal (4-HNE), and observed a reduction of LAMTOR1 in both human and mouse retinal pigment epithelium (RPE) following short-term (1h) and prolonged exposures (24h). Nrf2 overexpression increased both lamtor1 mRNA and LAMTOR1 protein in the RPE. To determine if Nrf2 regulates lamtor1 transcription, we cloned the deletion mutants of the lamtor1 promoter into a luciferase reporter. Although the promoter contained antioxidant response elements, transcriptional activity depended on the interaction between Nrf2 and the constructs containing the transcriptional start site. Moreover, Nrf2-driven transcription was significantly reduced by an inhibitor of histone acetyltransferase, p300. Correspondingly, Nrf2 overexpression increased levels of acetylated histone3 and p300. The reduction in LAMTOR1 by 4-HNE was reversed by pepstatin A and NH4Cl which block lysosomal degradation. 4-HNE increased TFEB nuclear translocation which was reversed by LAMTOR1 overexpression. In vivo, LAMTOR1 levels decreased in the photoreceptor and RPE layers of NaIO3-injected mice, compared to PBS-injected controls. In conclusion, oxidative injury reduces LAMTOR1, predominantly through lysosomal degradation although Nrf2-mediated histone acetylation enhances lamtor1 transcription. This study reveals a previously unrecognized regulatory mechanism of lamtor1 by oxidative stress, suggesting a novel role for LAMTOR1 in the pathogenesis of AMD.

Interactive effect of biogenic nanoparticles and UV-B exposure on physio-biochemical behavior and secondary metabolism of Artemisia annua L

Biosynthesized silver nanoparticles (AgNPs) are key nanomaterials with unique physio-chemical characteristics and diverse applications. Their strong absorption potential and antibacterial activity make them useful for agriculture, medicine and other industries. AgNPs boost plant growth and metabolism, especially under stress. However, the combined effects of AgNPs and UV-B exposure on plants are unknown. To elucidate the interactive effects of biosynthesized silver nanoparticles (AgNPs) and exposure of ultraviolet B (UV-B) on plant growth and metabolic processes, this study assessed the response of Artemisia annua under controlled in vitro conditions. In total, eight sets of plants were used with the alone/combined treatment of AgNPs and UV-B. For this purpose, spherical and averaged ∼ 31.8 nm in size AaAgNPs were synthesized. The photosynthetic pigments were calculated maximum with the alone treatment of 0.5 mg L−1 AaAgNPs and combined treatment of 0.5 mg L−1 AaAgNPs with 3 h UV-B, respectively. The results evidenced that the co-exposure of AaAgNPs and UV-B led to a significant balance in ROS production of A. annua; as well as improved antioxidative enzyme activity. Fluorescence and scanning electron microscopic (SEM) analysis indicated the enhancement of glandular trichomes (GT) area and density with the combined treatment of AaAgNPs and 3 h UV-B. In accordance with correlation between microscopic GT results, high concentration of artemisinin and up-regulation of related transcripts were found in A. annua plants treated with low concentrations of AaAgNPs and UV-B. Thus, it may be inferred that two distinct plant growth modulators, namely low-concentration biosynthesized AgNPs and short-term UV-B exposure, can enhance the physio-biochemical characteristics and production of secondary metabolites (specially artemisinin) in A. annua synergistically.

Rapid onset fibrotic remodeling and ventricular dysfunction induced by phenylephrine involve targeted reprogramming of myocyte and fibroblast transcriptomes.

Catecholamine dysregulation is a common feature of multiple acute and chronic cardiac conditions, including heart failure. To investigate the role of altered α-adrenergic stimulation on cardiac function, we developed a short-term exposure model, administering phenylephrine subcutaneously to mice for one week. Compared to vehicle-injected controls, phenylephrine-treated animals exhibited increased ejection fraction, decreased chamber size, diastolic dysfunction and ventricular hypertrophy in the absence of hypertension. Remarkably, these animals developed extensive fibrotic remodeling of the tissue that plateaued at 24 hours and myocyte hypertrophy localized to regions of fibrotic deposition after 3 days of treatment. Transcriptome analyses of purified myocyte and fibroblast populations from these hearts revealed an unexpected role for myocytes in the production of extracellular matrix. Comparison with other models of cardiac stress, including pressure overload hypertrophy and cytokine activation of fibroblasts, identified stimulus-specific transcriptional circuits associated with cardiac pathology. Given the rapid, robust fibrotic response that preceded myocyte hypertrophy, intercellular communication analyses were conducted to investigate fibroblast to myocyte signaling, identifying potential crosstalk between these cells. These studies thoroughly describe and phenotypically characterize a new model of short-term catecholamine stress and provide an atlas of transcriptional remodeling in myocytes and fibroblasts.

Wildland Fire-Related Smoke PM 2.5 and Cardiovascular Disease ED Visits in the Western United States.

The impact of short-term exposure to fine particulate matter (PM 2.5 ) due to wildland fire smoke on the risk of cardiovascular disease (CVD) remains unclear. We investigated the association between short-term exposure to wildfire smoke PM 2.5 and Emergency Department (ED) visits for acute CVD in the Western United States from 2007 to 2018. ED visits for primary or secondary diagnoses of atrial fibrillation (AF), acute myocardial infarction (AMI), heart failure (HF), stroke, and total CVD were obtained from hospital associations or state health departments in California, Arizona, Nevada, Oregon, and Utah. ED visits included those that were subsequently hospitalized. Daily smoke, non-smoke, and total PM 2.5 were estimated using a satellite-driven multi-stage model with a high resolution of 1 km. The data were aggregated to the zip code level and a case-crossover study design was employed. Temperature, relative humidity, and day of the year were included as covariates. We analyzed 49,759,958 ED visits for primary or secondary CVD diagnoses, which included 6,808,839 (13.7%) AFs, 1,222,053 (2.5%) AMIs, 7,194,474 (14.5%) HFs, and 808,396 (1.6%) strokes. Over the study period from 2007-01-01 to 2018-12-31, the mean smoke PM 2.5 was 1.27 (Q1: 0, Q3: 1.29) µg/m 3 . A 10 µg/m 3 increase in smoke PM 2.5 was associated with a minuscule decreased risk for AF (OR 0.994, 95% CI 0.991-0.997), HF (OR 0.995, 95% CI 0.992-0.998), and CVD (OR 0.9997, 95% CI 0.996-0.998), but not for AMI and stroke. Adjusting for non-smoke PM 2.5 did not alter these associations. A 10 µg/m 3 increase in total PM 2.5 was linked to a small increased risk for all outcomes except stroke (OR for CVD 1.006, 95% CI 1.006-1.007). Associations were similar across sex and age groups. We identified an unexpected slight lower risk of CVD ED visits associated with short-term wildfire smoke PM 2.5 exposure. Whether these findings are due to methodological issues, behavioral changes, or other factors requires further investigation.

Effects of High-Temperature Stress on Biological Characteristics of Coccophagus japonicus Compere.

The parasitoid, Coccophagus japonicus Compere (Hymenoptera: Aphelinidae) is a dominant natural enemy of Parasaissetia nigra Nietner (Hemiptera: Coccidae), an important pest of rubber trees. Much of Chinese rubber is cultivated in hotter regions such as Yunnan and Hainan, exposing applied parasitoids to non-optimal temperatures. Therefore, C. japonicus must adapt to avoid temperature-related impacts on survival and population expansion. In this study, we monitored the survival rate, developmental duration, parasitism rate, and fecundity of C. japonicus during short-term exposures to 36 °C, 38 °C, and 40 °C for 2, 4, and 6 h, as well as continuous exposures to 32 °C and 34 °C for 3 days. The results show that short-term exposure to high-temperature stress leads to decreased survival rate of C. japonicus larvae and pupae, with survival rates declining as temperature and duration increase. High-temperature stress also delayed insect development, reduced mature egg production, shortened the body length of newly emerged females, and decreased female lifespans. Moreover, continuous high-temperature stress was found to significantly impact the development and reproduction of C. japonicus. Compared with the CK (27 °C), 3 d of continuous exposure to 34 °C prolonged developmental duration, shortened the body length and lifespan of newly emerged females, reduced survival rate and single female fecundity, and significantly decreased offspring numbers and parasitism rates. Temperatures of 36 °C, 38 °C, and 40 °C decreased the mortality time of adult females to 28.78, 16.04, and 7.91 h, respectively. Adverse temperatures also affected the insects' functional response, with 8 h of stress at 36 °C, 38 °C, and 40 °C causing the control efficiency of C. japonicus on P. nigra. This level of stress in the parasitoids was found to reduce the immediate attack rate and search effect, prolong processing time, and attenuate interference between small prey. Parasitoid efficiency was lowest following exposure to 40 °C. In this study, we determined the range of high temperatures that C. japonicus populations can tolerate under short- or long-term stress, providing guidance for future field applications.

Unveiling the Molecular Effects of Replacement and Legacy PFASs: Transcriptomic Analysis of Zebrafish Embryos Reveals Surprising Similarities and Potencies.

The prevalence of per- and poly fluoroalkyl substances (PFASs) in the environment has prompted restrictions on legacy PFASs due to their recognized toxic effects. Consequently, alternative "replacement" PFASs have been introduced and are prevalent in environmental matrices. Few studies have investigated the molecular effects of both legacy and replacement PFASs under short-term exposures. This study aimed to address this by utilizing transcriptomic sequencing to compare the molecular impacts of exposure to concentrations 0.001-5 mg/L of the legacy PFOS and two of its replacements, PFECHS and FBSA. Using zebrafish embryos, the research assessed apical effects (mortality, morphology, and growth), identified differentially expressed genes (DEGs) and enriched pathways, and determined transcriptomic points of departure (tPoDs) for each compound. Results indicated that PFOS exhibited the highest relative potency, followed by PFECHS and then FBSA. While similarities were observed among the ranked DEGs across all compounds, over-representation analysis revealed slight differences. Notably, PFOS demonstrated the lowest tPoD identified to date. These findings raise concerns regarding the safety of emerging replacement PFASs and challenge assumptions about PFAS toxicity solely resulting from their accumulative potential. As replacement PFASs proliferate in the environment, this study underscores the need for heightened scrutiny of their effects and questions current regulatory thresholds.

Phthalate monoesters affect membrane fluidity and cell-cell contacts in endometrial stromal adherent cell lines and spheroids

Phthalate monoesters have been identified as endocrine disruptors in a variety of models, yet understanding of their exact mechanisms of action and molecular targets in cells remains incomplete. Here, we set to determine whether epidemiologically relevant mono(2-ethyl-5-hydroxyhexyl) phthalate (MEHHP) can affect biological processes by altering cell plasma membrane fluidity or formation of cell-cell contacts. As a model system, we chose endometrial stromal cell lines, one of which was previously used in a transcriptomic study with MEHHP or MEHHP-containing mixtures. A short-term exposure (1 h) of membrane preparations to endocrine disruptors was sufficient to induce changes in membrane fluidity/rigidity, whereas different mixtures showed different effects at various depths of the bilayer. A longer exposure (96 h) affected the ability of cells to form spheroids and highlighted issues with membrane integrity in loosely assembled spheroids. Finally, in spheroids assembled from T-HESC cells, MEHHP interfered with the formation of cell-cell contacts as indicated by the immunostaining of zonula occludens 1 protein. Overall, this study emphasized the need to consider plasma membrane, membrane-bound organelles, and secretory vesicles as possible biological targets of endocrine disruptors and offered an explanation for a multitude of endocrine disruptor roles documented earlier.

Dynamic BMP gene expression regulation in chick RPE during recovery from short term optical defocus and form-deprivation.

This study investigated the differential gene expression of BMPs in chick retinal pigment epithelium (RPE) during recovery from short term exposure to optical defocus and form-deprivation (FD) treatments. 14-day old White-Leghorn chicks wore either monocular +10 or -10 D lenses, or diffusers for 2 or 48 h, after which eyes were allowed unobstructed vision for up to 96 h. Over this recovery period, refractive errors and choroidal thickness (ChT) were tracked using retinoscopy and high-frequency A-scan ultrasonography. Real-time PCR was used to examine the expression of BMP2, 4, and 7 genes in RPE samples collected 0, 15 min, 2, 24, 48, and 96 h after the termination of treatments. Expression levels in treated eyes and their contralateral control eyes were compared. After the termination of the lens and diffuser treatments, eyes gradually recovered from induced shifts in refractive error. With all three treatments, ChT changes reached statistical significance after 48 h of treatment, be it thinning with the -10 D lens and diffuser treatments (-0.06 ± 0.03mm, p < 0.05; -0.11 ± 0.04 mm, p < 0.05, resp.), or thickening with the +10 D lens (0.31 ± 0.04 mm, p < 0.001). BMP2 gene expression was rapidly upregulated in eyes wearing the +10 D lens, being statistical significance after 2 h, as well as 48 h of treatment. With the 2 h treatment, the latter gene expression pattern persisted for 15 min into the recovery period, before decreasing to the same level as that of contralateral control eyes, with a short-lived rebound, i.e., upregulation, 24 h into the recovery period. With the longer, 48 h treatment, BMP2 gene expression decreased more gradually, from 739 ± 121% at the end of the treatment period, to 72 ± 14% after 48 h of recovery. Two and 48 h of both -10 D and FD treatments resulted in BMP2 gene expression downregulation, with the time taken for gene expression levels to fully recover varying with the duration of initial treatments. In both cases, BMP2 gene expression downregulation persisted for 15 min into the recovery period, but reversed to upregulation by 2 h. Similar gene expression patterns were also observed for BMP4, although the changes were smaller. The observed changes in BMP gene expression in chick RPE imply dynamic, albeit complex regulation, with the duration of exposure and recovery being critical variables for all three types of visual manipulations. This study provides further evidence for a role of the RPE as an important signal relay linking the retina to the choroid and sclera in eye growth regulation.