Notes

A neuropeptide producing reminiscences.
Nanoplastics are more likely to be suspended in air and pose a risk of respiratory exposure. However, the early health effects of low-dose nanoplastics on the respiratory system, which are expected to reflect the risk of atmospheric nanoplastics, need to be further evaluated. In this study, nanoparticles of polyethylene terephthalate, a representative plastic polymer in air, were prepared by a precipitation method. The toxicity impacts of nano-PET at environmental concentrations on the human lung carcinoma cell A549 cells were evaluated. Although the nano-PET was identified to enter the cells by confocal microscope observation and alkali-assisted thermal depolymerization coupled with LC-MS/MS analysis, the nano-PET exhibited low toxicity on mitochondrial membrane potential levels and cell apoptosis. At low concentrations of 0.10 and 0.98 μg/mL, the nano-PET had a slight promotion effect on cell viability, while an inhibitory effect on cell viability presented at higher nano-PET concentrations of 98.40 and 196.79 μg/mL. The cell survival rate at 98.4 and 196.79 μg/mL of nano-PET are lower than that of the control, and significant oxidative stress in cells caused by the nano-PET exposure at 49.2 μg/mL was observed. A decrease tendency of mitochondrial membrane potential with the increasing nano-PET exposure presents, which is consistent with the change of reactive oxygen species. selleckchem Furthermore, nano-PET at ≦ 98.4 μg/mL could not increase the sum of apoptotic in the cells, but the late apoptotic cells increased with the increase of the exposure dose. The major mechanism of the toxic effect of nano-PET on cells may be the increase of reactive oxygen species caused by oxidative stress, which in turn induces a decrease in the mitochondrial membrane potential. This study provides information on the toxicity of nano-PET at environmental concentrations in human lung cells, which helps to enrich the risk cognition of nanoplastics in the respiratory system.We read with interest the narrative review authored by Kiser et al. (2021), which discussed extensively the antioxidant effect and anti-inflammatory effect of sulforaphane, a dietary supplement found in high amounts in cruciferous vegetables that ais orally accessible and well-tolerated. Notably, in their review, the authors also discussed the potential use of sulforaphane in patients with coronavirus disease 2019 (COVID-19). Sulforaphane mediates the inhibitory effect on NLRP3 inflammasome activation and we believe that this could be the main mechanism where sulforaphane is useful for patients with COVID-19.Kawasaki disease (KD) is the leading cause of acquired heart disease in children. The cause remains unknown; however, epidemiologic and demographic data support a single preceding infectious agent may lead to KD. A variety of pathophysiologic responses have been proposed, including direct invasion of the coronary arteries, a superantigen response, and a post-infectious autoimmune phenomenon. A role for B cell responses during KD are supported by numerous findings including B cell specific markers identified in genome wide association studies. We have recently published data showing children with KD have similar plasmablast (PB) responses to children with infections. Since during other infections, cells expressing antibodies against the preceding infection are enriched in PBs, we sought to explore the specific antibodies encoded by PBs during KD. In one child we see a massive expansion in IGHV4-34 utilizing antibodies, which has been associated with autoimmunity in the past. We further explored this expansion of IGHV4-34 utilization during the peripheral PB rise with next generation sequencing (NGS) analysis and utilizing newer techniques of chromium chip single cell separation (10x Genomics®). We also utilized peptide array screening to attempt to identify an antigen to the most prolific clones.
An increasing number of studies have reported neonicotinoid insecticides (NEOs), the emerging alternatives to conventional insecticides, may increase oxidative stress and cause adverse health effects, but limited is known about the prenatal NEOs exposures and their impact on birth outcomes.

We investigated the levels of prenatal exposure to NEOs/metabolites, to assess their associations with birth outcomes, and investigate whether these associations could be mediated by oxidative stress using 8-OHdG as the biomarker.

We studied 296 mother-infant pairs recruited from Laizhou Wan Birth Cohort in 2010 - 2013. Two NEOs (IMI and ACE), three metabolites (6-CN, ND-ACE, and 2CTCA), and 8-OHdG were measured in maternal urine collected before delivery. Birth outcomes including birth weight, birth length, ponderal index (PI), head circumference, and gestational age, were acquired. We examined the associations between NEOs/metabolites and birth outcomes using multivariable linear regression. Mediation analysis was may partly mediate these associations.
Pregnant women were widely exposed to NEOs/metabolites in China. Results suggested the potential impacts of prenatal exposure to certain neonicotinoid insecticides on head circumference. Urinary 8-OHdG may partly mediate these associations.
Diabetes affects millions of people worldwide with a continued increase in incidence occurring within the pediatric population. The potential contribution of persistent organic pollutants (POPs) to diabetes in youth remains poorly known, especially regarding type 1 diabetes (T1D), generally the most prevalent form of diabetes in youth.

We investigated the associations between POPs and T1D in youth and studied the impacts of POPs on pancreatic β-cell function and viability in vitro.

We used data and plasma samples from the SEARCH for Diabetes in Youth Case Control Study (SEARCH-CC). Participants were categorized as Controls, T1D with normal insulin sensitivity (T1D/IS), and T1D with insulin resistance (T1D/IR). We assessed plasma concentrations of polychlorinated biphenyls (PCBs) and organochlorine pesticides and estimated the odds of T1D through multivariable logistic regression. In addition, we performed in vitro experiments with the INS-1E pancreatic β-cells. Cells were treated with PCB-153 or p,p'-DDing from 1×10
M to 5×10
M, impaired the ability of pancreatic β-cells to produce and secrete insulin in response to glucose. These failures were paralleled by impaired Ins1 and Ins2 mRNA expression. In addition, among different targeted genes, PCB-153 significantly reduced Slc2a2 and Gck mRNA expression whereas p,p'-DDE mainly affected Abcc8 and Kcnj11. While treatment with PCB-153 or p,p'-DDE for 2days did not affect β-cell viability, longer treatment progressively killed the β-cells.

These results support a potential role of POPs in T1D etiology and demonstrate a high sensitivity of pancreatic β-cells to POPs.
These results support a potential role of POPs in T1D etiology and demonstrate a high sensitivity of pancreatic β-cells to POPs.So far, the human health impacts of nano- and microplastics are poorly understood. Thus, we investigated whether nanoplastics exposure induces inflammatory processes in primary human monocytes and monocyte-derived dendritic cells. We exposed these cells in vitro to nanoplastics of different shapes (irregular vs. spherical), sizes (50-310 nm and polydisperse mixtures) and polymer types (polystyrene; polymethyl methacrylate; polyvinyl chloride, PVC) using concentrations of 30-300 particles cell-1. Our results show that irregular PVC particles induce the strongest cytokine release of these nanoplastics. Irregular polystyrene triggered a significantly higher pro-inflammatory response compared to spherical nanoplastics. The contribution of chemicals leaching from the particles was minor. The effects were concentration-dependent but varied markedly between cell donors. We conclude that nanoplastics exposure can provoke human immune cells to secrete cytokines as key initiators of inflammation. This response is specific to certain polymers (PVC) and particle shapes (fragments). Accordingly, nanoplastics cannot be considered one homogenous entity when assessing their health implications and the use of spherical polystyrene nanoplastics may underestimate their inflammatory effects.
To investigate whether and how social support influenced frailty progression through depressive symptoms and physical activity.

Of 1235 community-dwelling older adults enrolled at baseline, 778 (63.0%) undergoing at least one yearly follow-up were included in the final analysis. Data were collected on frailty, social support, depressive symptoms, physical activity and covariates.

Two frailty trajectory classes were identified and labeled as alleviated frailty and deteriorated frailty. Subjective support prevented the deterioration of frailty through decreased depressive symptoms, while objective support and support utilization prevented the deterioration of frailty through increased physical activity.

The pathways through which social support ameliorates frailty vary by support types. Subjective support interventions should be included in the multifactorial interdisciplinary management of frailty to address social and psychological vulnerabilities, along with objective support and support utilization interventions addressing physical inactivity.
The pathways through which social support ameliorates frailty vary by support types. Subjective support interventions should be included in the multifactorial interdisciplinary management of frailty to address social and psychological vulnerabilities, along with objective support and support utilization interventions addressing physical inactivity.The serotonin transporter promoter region polymorphism (5-HTTLPR) has been implicated in stress regulation, with increased stress reactivity often being found in carriers of the low-expressing short (S) allele. Nevertheless, the role of the 5-HTTLPR in influencing parasympathetic stress reactivity, as indexed by Respiratory Sinus Arrhythmia (RSA), is still unknown. This study examined, for the first time, whether the 5-HTTLPR was associated with variations in RSA response to maternal separation in a sample of 69 healthy 5-year-old children. Preschoolers' RSA was measured during an age-adapted version of the Strange Situation Procedure (SSP). The 5-HTTLPR polymorphism was tested as a predictor of RSA dynamic response to the SSP through multilevel models. A significant interaction between 5-HTTLPR and SSP episodes was found. In particular, whereas a significant decrease in RSA levels was observed during the stranger episode in the whole sample, S allele carriers showed a significant decrease in RSA levels from the stranger episode to the first separation episode, followed by an increase for the rest of the procedure. Albeit preliminary, data support the view that the 5-HTTLPR may contribute to individual differences in RSA stress reactivity from preschool age.First-person narratives are more attentively and emotionally engaging than third-person narratives. This study examined whether and how personal perspective modulates counterfactual processing. Participants read counterfactual and causal conditionals written from the first-person or third-person perspective (e.g., If/Because I/he had read enough literature before, I/he would have finished my/his thesis easily.), followed by factual consequences that contained a critical word either consistent or inconsistent with preceding contexts (e.g., Therefore, when I/he was about to defend the thesis I/he felt panicked/confident). In both perspectives, inconsistent words showed a prolonged N400 vs. consistent words in the counterfactual condition, but a larger P600 in the causal condition. The critical word showed a larger P600 in the first- than the third-person condition in counterfactual scenarios, but not in causal scenarios. These findings suggest that personal perspective exerts different influences on counterfactual processing, presumably by modulating the amount of attentional resources involved.
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