scholarly journals Early-life exposure to a herbicide has enduring effects on pathogen-induced mortality

2013 ◽  
Vol 280 (1772) ◽  
pp. 20131502 ◽  
Author(s):  
Jason R. Rohr ◽  
Thomas R. Raffel ◽  
Neal T. Halstead ◽  
Taegan A. McMahon ◽  
Steve A. Johnson ◽  
...  
Keyword(s):  
Early Life ◽  
Disease Susceptibility ◽  
Developmental Stages ◽  
Cost Effective ◽  
Amphibian Declines ◽  
Early Life Exposure ◽  
Risk Of Mortality ◽  
Fungal Load ◽  
Herbicide Atrazine ◽  
The Impact

Exposure to stressors at formative stages in the development of wildlife and humans can have enduring effects on health. Understanding which, when and how stressors cause enduring health effects is crucial because these stressors might then be avoided or mitigated during formative stages to prevent lasting increases in disease susceptibility. Nevertheless, the impact of early-life exposure to stressors on the ability of hosts to resist and tolerate infections has yet to be thoroughly investigated. Here, we show that early-life, 6-day exposure to the herbicide atrazine (mean ± s.e.: 65.9±3.48 µg l −1 ) increased frog mortality 46 days after atrazine exposure (post-metamorphosis), but only when frogs were challenged with a chytrid fungus implicated in global amphibian declines. Previous atrazine exposure did not affect resistance of infection (fungal load). Rather, early-life exposure to atrazine altered growth and development, which resulted in exposure to chytrid at more susceptible developmental stages and sizes, and reduced tolerance of infection, elevating mortality risk at an equivalent fungal burden to frogs unexposed to atrazine. Moreover, there was no evidence of recovery from atrazine exposure. Hence, reducing early-life exposure of amphibians to atrazine could reduce lasting increases in the risk of mortality from a disease associated with worldwide amphibian declines. More generally, these findings highlight that a better understanding of how stressors cause enduring effects on disease susceptibility could facilitate disease prevention in wildlife and humans, an approach that is often more cost-effective and efficient than reactive medicine.

scholarly journals The Potential Role of Nonhuman Primate Models to Better Comprehend Early Life Immunity and Maternal Antibody Transfer

Vaccines ◽  
2021 ◽  
Vol 9 (4) ◽  
pp. 306
Author(s):  
Julie Sartoretti ◽  
Christiane S. Eberhardt
Keyword(s):  
Nonhuman Primate ◽  
Early Life ◽  
Cost Effective ◽  
Maternal Antibody ◽  
Maternal Antibodies ◽  
Immunological Methods ◽  
Human Pathogens ◽  
Childhood Immunization ◽  
Primate Model ◽  
The Impact

Early life immunity is a complex field of research and there are still gaps in knowledge regarding the detailed mechanism of maternal antibody transfer, the impact of maternal antibodies on infant vaccine responses and the ontogeny of human early life immunity. A comprehensive understanding is necessary to identify requirements for early life vaccines and to improve early childhood immunization. New immunological methods have facilitated performing research in the youngest, however, some questions can only be addressed in animal models. To date, mostly murine models are used to study neonatal and infant immunity since they are well-described, easy to use and cost effective. Given their limitations especially in the transfer biology of maternal antibodies and the lack of infectivity of numerous human pathogens, this opinion piece discusses the potential and prerequisites of the nonhuman primate model in studying early life immunity and maternal antibody transfer.

scholarly journals Peanut sensitisation and allergy: influence of early life exposure to peanuts

2010 ◽  
Vol 103 (9) ◽  
pp. 1278-1286 ◽  
Author(s):  
Rachel L. Thompson ◽  
Lisa M. Miles ◽  
Joanne Lunn ◽  
Graham Devereux ◽  
Rebecca J. Dearman ◽  
...  
Keyword(s):  
Systematic Review ◽  
Early Life ◽  
Animal Studies ◽  
Human Subjects ◽  
Subsequent Development ◽  
Human Studies ◽  
Case Control Studies ◽  
Cross Sectional ◽  
Early Life Exposure ◽  
The Impact

The aim of the present systematic review was to evaluate the influence of early life exposure (maternal and childhood) to peanuts and the subsequent development of sensitisation or allergy to peanuts during childhood. Studies were identified using electronic databases and bibliography searches. Studies that assessed the impact of non-avoidance compared with avoidance or reduced quantities of peanuts or peanut products on either sensitisation or allergy to peanuts, or both outcomes, were eligible. Six human studies were identified: two randomised controlled trials, two case–control studies and two cross-sectional studies. In addition, published animal and mechanistic studies, relevant to the question of whether early life exposure to peanuts affects the subsequent development of peanut sensitisation, were reviewed narratively. Overall, the evidence reviewed was heterogeneous, and was limited in quality, for example, through lack of adjustment for potentially confounding factors. The nature of the evidence has therefore hindered the development of definitive conclusions. The systematic review of human studies and narrative expert-led reviews of animal studies do not provide clear evidence to suggest that either maternal exposure, or early or delayed introduction of peanuts in the diets of children, has an impact upon subsequent development of sensitisation or allergy to peanuts. Results from some animal studies (and limited evidence from human subjects) suggest that the dose of peanuts is an important mediator of peanut sensitisation and tolerance; low doses tend to lead to sensitisation and higher doses tend to lead to tolerance.

scholarly journals Early-Life Exposure to Low-Dose Cadmium Accelerates Diethylnitrosamine and Diet-Induced Liver Cancer

2021 ◽  
Vol 2021 ◽  
pp. 1-15
Author(s):  
Hongbo Men ◽  
Jamie L. Young ◽  
Wenqian Zhou ◽  
Haina Zhang ◽  
Xiang Wang ◽  
...  
Keyword(s):  
Liver Cancer ◽  
Early Life ◽  
Low Dose ◽  
Liver Tumors ◽  
Cadmium Exposure ◽  
Male Mice ◽  
Nonalcoholic Fatty Liver ◽  
Early Life Exposure ◽  
The Impact

Maternal exposure to cadmium causes obesity and metabolic changes in the offspring, including nonalcoholic fatty liver disease-like pathology. However, whether maternal cadmium exposure accelerates liver cancer in the offspring is unknown. This study investigated the impact of early-life exposure to cadmium on the incidence and potential mechanisms of hepatocellular carcinoma (HCC) in offspring subjected to postweaning HCC induction. HCC in C57BL/6J mice was induced by diethylnitrosamine (DEN) injection at weaning, followed by a long-term high-fat choline-deficient (HFCD) diet. Before weaning, liver cadmium levels were significantly higher in mice with early-life cadmium exposure than in those without cadmium exposure. However, by 26 and 29 weeks of age, hepatic cadmium fell to control levels, while a significant decrease was observed in copper and iron in the liver. Both male and female cadmium-exposed mice showed increased body weight compared to non-cadmium-treated mice. For females, early-life cadmium exposure also worsened insulin intolerance but did not significantly promote DEN/HFCD diet-induced liver tumors. In contrast, in male mice, early-life cadmium exposure enhanced liver cancer induction by DEN/HFCD with high incidence and larger liver tumors. The liver peritumor tissue of early-life cadmium-exposed mice exhibited greater inflammation and disruption of fatty acid metabolism, accompanied by higher malondialdehyde and lower esterified triglyceride levels compared to mice without cadmium exposure. These findings suggest that early-life exposure to low-dose cadmium accelerates liver cancer development induced by a DEN/HFCD in male mice, probably due to chronic lipotoxicity and inflammation caused by increased uptake but decreased consumption of fatty acids.

Early Life Exposure to Air Pollution, Cognitive Development, and Labor Market Outcome

2019 ◽  
Vol 18 (2) ◽  
pp. 77-95
Author(s):  
Rashesh Shrestha
Keyword(s):  
Air Pollution ◽  
Labor Market ◽  
Cognitive Development ◽  
Cognitive Ability ◽  
Forest Fires ◽  
Early Life ◽  
Cognitive Test ◽  
Early Life Exposure ◽  
Pollution Exposure ◽  
The Impact

In this paper, I study the impact of early life exposure to air pollution caused by the 1997 Indonesian forest fires on cognitive ability, an important determinant of success in the labor market. To isolate the effect of pollution exposure, I use a difference-in-differences approach where exposure to pollution is determined by timing and region of birth. The results suggest that pollution lowered cognitive test score at age 8–9 years by 6 percent. I also estimate how this might translate into lost earnings on a different but comparable sample. The estimates suggest that natural disasters can reduce earnings by 5 to 8 percent by hampering cognitive ability. Lost earnings due to interrupted cognitive development could be an additional cost of exposure to air pollution.

Arsenic projects in SE Asia

2016 ◽  
Vol 31 (1) ◽  
Author(s):  
Panida Navasumrit ◽  
Krittinee Chaisatra ◽  
Mathuros Ruchirawat
Keyword(s):  
Early Life ◽  
Arsenic Exposure ◽  
Inorganic Arsenic ◽  
Human Beings ◽  
Disease Outcomes ◽  
Early Life Exposure ◽  
Wide Range ◽  
Southern Thailand ◽  
Health And Development ◽  
The Impact

AbstractEarly life exposure to inorganic arsenic is associated with a wide range of malignant and chronic disease outcomes in humans. Prenatal arsenic exposure may give rise to adverse effects on child health and development as arsenic readily passes through the placenta in human beings. The impact of maternal arsenic exposure on fetal gene expression was conducted in pregnant women living in Southern Thailand. Arsenic exposed newborns had significantly higher levels of arsenic in cord blood, and a set of genes associated with numerous biological pathways, including cell signaling, apoptosis, inflammatory and stress response. A slight increase in promoter methylation of

scholarly journals Serotonin-related rodent models of early-life exposure relevant for neurodevelopmental vulnerability to psychiatric disorders

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Tamara S. Adjimann ◽  
Carla V. Argañaraz ◽  
Mariano Soiza-Reilly
Keyword(s):  
Psychiatric Disorders ◽  
Early Life ◽  
Life Experience ◽  
Behavioral Outcomes ◽  
Behavioral Effects ◽  
Rodent Models ◽  
Environmental Perturbations ◽  
Early Life Experience ◽  
Early Life Exposure ◽  
The Impact

AbstractMental disorders including depression and anxiety are continuously rising their prevalence across the globe. Early-life experience of individuals emerges as a main risk factor contributing to the developmental vulnerability to psychiatric disorders. That is, perturbing environmental conditions during neurodevelopmental stages can have detrimental effects on adult mood and emotional responses. However, the possible maladaptive neural mechanisms contributing to such psychopathological phenomenon still remain poorly understood. In this review, we explore preclinical rodent models of developmental vulnerability to psychiatric disorders, focusing on the impact of early-life environmental perturbations on behavioral aspects relevant to stress-related and psychiatric disorders. We limit our analysis to well-established models in which alterations in the serotonin (5-HT) system appear to have a crucial role in the pathophysiological mechanisms. We analyze long-term behavioral outcomes produced by early-life exposures to stress and psychotropic drugs such as the selective 5-HT reuptake inhibitor (SSRI) antidepressants or the anticonvulsant valproic acid (VPA). We perform a comparative analysis, identifying differences and commonalities in the behavioral effects produced in these models. Furthermore, this review discusses recent advances on neurodevelopmental substrates engaged in these behavioral effects, emphasizing the possible existence of maladaptive mechanisms that could be shared by the different models.

scholarly journals Early-life exposure to Ivermectin alters long-term growth and disease susceptibility

PLoS ONE ◽  
2021 ◽  
Vol 16 (10) ◽  
pp. e0258185
Author(s):  
Taegan A. McMahon ◽  
Shannon Fernandez-Denmark ◽  
Jeffrey M. Grim
Keyword(s):  
Growth Rates ◽  
Early Life ◽  
Disease Susceptibility ◽  
Batrachochytrium Dendrobatidis ◽  
Pathogenic Fungus ◽  
Exponential Growth Phase ◽  
Long Term Effects ◽  
Lower Growth ◽  
Early Life Exposure

Ivermectin is a broad-spectrum antiparasitic medicine, which is often used as a treatment for parasites or as a prophylaxis. While studies have looked at the long-term effects of Ivermectin on helminths, studies have not considered the long-term impacts of this treatment on host health or disease susceptibility. Here, we tracked the effects of early life Ivermectin treatment in Cuban tree frogs (Osteopilus septentrionalis) on growth rates, mortality, metabolically expensive organ size, and susceptibility to Batrachochytrium dendrobatidis (Bd) infection. One year after exposure, there was no effect of Ivermectin exposure on frog mass (X21 = 0.904, p = 0.34), but when tracked through the exponential growth phase (~2.5 years) the Ivermectin exposed individuals had lower growth rates and were ultimately smaller (X21 = 7.78, p = 0.005; X21 = 5.36, p = 0.02, respectively). These results indicate that early life exposure is likely to have unintended impacts on organismal growth and potentially reproductive fitness. Additionally, we exposed frogs to Bd, a pathogenic fungus that has decimated amphibian populations globally, and found early life exposure to Ivermectin decreased disease susceptibility (disease load: X21 = 17.57, p = 0.0002) and prevalence (control: 55%; Ivermectin: 22%) over 2 years after exposure. More research is needed to understand the underlying mechanism behind this phenomenon. Given that Ivermectin exposure altered disease susceptibility, proper controls should be implemented when utilizing this drug as an antiparasitic treatment in research studies.

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