The role and regulation of SIRT1 in pulmonary fibrosis.

Pulmonary fibrosis (PF) is a progressive and fatal lung disease with high incidence and a lack of effective treatment, which is a severe public health problem. PF has caused a huge socio-economic burden, and its pathogenesis has become a research hotspot. SIRT1 is a nicotinamide adenosine dinucleotide (NAD)-dependent sirtuin essential in tumours, Epithelial mesenchymal transition (EMT), and anti-aging. Numerous studies have demonstrated after extensive research that it is crucial in preventing the progression of pulmonary fibrosis. This article reviews the biological roles and mechanisms of SIRT1 in regulating the progression of pulmonary fibrosis in terms of EMT, oxidative stress, inflammation, aging, autophagy, and discusses the potential of SIRT1 as a therapeutic target for pulmonary fibrosis, and provides a new perspective on therapeutic drugs and prognosis prospects.

Improving Rate Performance of Encapsulating Lithium-Polysulfide Electrolytes for Practical Lithium-Sulfur Batteries.

The cycle life of high-energy-density lithium-sulfur (Li-S) batteries is severely plagued by the incessant parasitic reactions between Li metal anodes and reactive Li polysulfides (LiPSs). Encapsulating Li-polysulfide electrolyte (EPSE) emerges as an effective electrolyte design to mitigate the parasitic reactions kinetically. Nevertheless, the rate performance of Li-S batteries with EPSE is synchronously suppressed. Herein, the sacrifice in rate performance by EPSE is circumvented while mitigating parasitic reactions by employing hexyl methyl ether (HME) as a co-solvent. The specific capacity of Li-S batteries with HME-based EPSE is nearly not decreased at 0.1 C compared with conventional ether electrolytes. With an ultrathin Li metal anode (50 µm) and a high-areal-loading sulfur cathode (4.4 mgS cm-2 ), a longer cycle life of 113 cycles was achieved in HME-based EPSE compared with that of 65 cycles in conventional ether electrolytes at 0.1 C. Furthermore, both high energy density of 387 Wh kg-1 and stable cycle life of 27 cycles were achieved in a Li-S pouch cell (2.7 Ah). This work inspires the feasibility of regulating the solvation structure of LiPSs in EPSE for Li-S batteries with balanced performance.

Electrolyte Design for Improving Mechanical Stability of Solid Electrolyte Interphase in Lithium-Sulfur Batteries.

Practical lithium-sulfur (Li-S) batteries are severely plagued by the instability of solid electrolyte interphase (SEI) formed in routine ether electrolytes. Herein, an electrolyte with 1,3,5-trioxane (TO) and 1,2-dimethoxyethane (DME) as co-solvents is proposed to construct a high-mechanical-stability SEI by enriching organic components in Li-S batteries. The high-mechanical-stability SEI works compatibly in Li-S batteries. TO with high polymerization capability can preferentially decompose and form organic-rich SEI, strengthening mechanical stability of SEI, which mitigates crack and regeneration of SEI and reduces the consumption rate of active Li, Li polysulfides, and electrolytes. Meanwhile, DME ensures high specific capacity of S cathodes. Accordingly, the lifespan of Li-S batteries increases from 75 cycles in routine ether electrolyte to 216 cycles in TO-based electrolyte. Furthermore, a 417 Wh kg-1 Li-S pouch cell undergoes 20 cycles. This work provides an emerging electrolyte design for practical Li-S batteries.

Disruption of mitochondrial redox homeostasis as a mechanism of antimony-induced reactive oxygen species and cytotoxicity.

Occupational and environmental Sb exposure has been associated with increased risk of respiratory diseases and lung cancer, but the toxicities and molecular mechanisms of Sb have been less investigated. In the present study, we first analyzed the Sb toxicity profile of lung adenocarcinoma A549 cells, and found that Sb dose-dependently decreased the cell viability and arrested cell cycle at G2/M but did not induce apoptosis. We next investigated the role of reactive oxygen species (ROS) involved in Sb-induced cytotoxicity. The results showed that Sb did not significantly induce cytosolic ROS production by NADPH oxidase (NOX) and the NOX inhibitors did not ameliorate the Sb-induced cell viability loss in A549 cells. However, the level of mitochondrial ROS (mtROS) was significantly increased in Sb-exposed cells and the mitochondria-targeted antioxidant significantly improved cell viability. These results suggested that mitochondria but not NOX is the major source of ROS production and mtROS plays a critical role in Sb-induced cytotoxicity. Furthermore, we found that Sb induced mitochondria dysfunction including the significant decrease of ATP level and mitochondrial membrane potential. Finally, Sb exposure decreased the activity of complex I and complex III, the level of -SH and GSH in mitochondria, and the activity of mitochondrial GR, GPx and TrxR, but increased the mitochondrial SOD activity, suggesting the disruption of mitochondrial redox homeostasis. Taken together, these findings suggested that Sb impaired mitochondrial redox homeostasis, resulting in formation of mtROS, thereby inhibited mitochondrial function and led to cytotoxicity.

The Relative Permittivity Changes of EGF by 50 Hz MF Exposure Neither Affect the Interaction of EGF With EGFR Nor Its Biological Effects.

The biophysical mechanism of magnetic fields (MFs) acting on living systems is not clear. Previous research showed that, similar to epidermal growth factor (EGF), MF exposure induced EGF receptor (EGFR) clustering and activated EGFR signaling. In this study, we investigated whether MF exposure induced the changes in physical characteristics of EGF and downstream effects of EGF and EGFR interaction. The phase-interrogation surface plasmon resonance (SPR) sensing analyses showed that 50 Hz MF exposure at 4.0 mT for 1 h induced reversible relative permittivity changes of EGF solution. However, compared with sham-exposed EGF solution, the MF-exposed EGF solution did not affect the binding of EGF to EGFR, nor the cell viability and EGFR clustering in human amniotic epithelial cells (FL cells). Our data suggest that cellular EGFR clustering response to MF exposure might not be a result of changes in relative permittivity of EGF in cell culture solution. Bioelectromagnetics. © 2020 Bioelectromagnetics Society.

The decreased permittivity of zebrafish embryos culture medium by magnetic fields did not affect early development of zebrafish embryos.

Epidemiological studies have shown associations between exposure to environmental extremely low frequency magnetic fields (ELF-MF) and health effects, but the mechanisms of ELF-MF induced biological effects remain unclear. We hypothesized that ELF-MF may regulate functions of tissues or cells via its effects on surrounding environment, e.g., culture medium. To test this hypothesis, we investigated the effects of 50 Hz MF on the relative permittivity of zebrafish embryos culture medium as well as of MF-exposed medium on zebrafish embryos development. The responses of medium to 50 Hz MF exposure were evaluated by a phase-sensitive surface plasmon resonance (SPR) system. The results demonstrated that MF treatment decreased relative permittivity of zebrafish embryos medium in a dose and time-dependent way. Interestingly, the decreased permittivity induced by MF exposure gradually recovered and approached to the base level when the exposure was removed off. However, MF-exposed medium did not trigger adverse consequences of embryos during zebrafish embryonic development, including mortality, malformation, hatching and heart rate when the MF pre-exposed medium was subjected to one cell-stage embryos. Moreover, the MF-exposed medium did not induce apoptosis of zebrafish embryos at 48 and 72 h post fertilization. Our data demonstrated that the relative permittivity of zebrafish embryos medium was decreased by MF exposure, whereas this decrease failed to result in abnormal development of zebrafish embryos.

RF-EMF exposure at 1800 MHz did not elicit DNA damage or abnormal cellular behaviors in different neurogenic cells.

Despite many years of studies, the debate on genotoxic effects of radiofrequency electromagnetic fields (RF-EMF) continues. To systematically evaluate genotoxicity of RF-EMF, this study examined effects of RF-EMF on DNA damage and cellular behavior in different neurogenic cells. Neurogenic A172, U251, and SH-SY5Y cells were intermittently (5 min on/10 min off) exposed to 1800 MHz RF-EMF at an average specific absorption rate (SAR) of 4.0 W/kg for 1, 6, or 24 h. DNA damage was evaluated by quantification of γH2AX foci, an early marker of DNA double-strand breaks. Cell cycle progression, cell proliferation, and cell viability were examined by flow cytometry, hemocytometer, and cell counting kit-8 assay, respectively. Results showed that exposure to RF-EMF at an SAR of 4.0 W/kg neither significantly induced γH2AX foci formation in A172, U251, or SH-SY5Y cells, nor resulted in abnormal cell cycle progression, cell proliferation, or cell viability. Furthermore, prolonged incubation of these cells for up to 48 h after exposure did not significantly affect cellular behavior. Our data suggest that 1800 MHz RF-EMF exposure at 4.0 W/kg is unlikely to elicit DNA damage or abnormal cellular behaviors in neurogenic cells. Bioelectromagnetics. 38:175-185, 2017. © 2016 Wiley Periodicals, Inc.

Is there association between Glutathione S Transferases polymorphisms and cataract risk: a meta-analysis?

BACKGROUND: Glutathione S transferase (GST) polymorphisms have been considered as risk factors for age-related cataracts, but the results remain controversial. In this study, we have performed a meta-analysis to evaluate the association between polymorphisms of GSTM1 and GSTT1 and cataract risk. METHODS: Published literature from PubMed and other databases were retrieved. The case-control studies regarding the association between GSTM1 or GSTT1 polymorphism and cataract risk were included. Pooled odds ratio (OR) and 95 % confidence interval (CI) were calculated using random- or fixed-effects model. RESULTS: Fifteen studies on GSTM1 (3,065 patients and 2,105 controls), and nine studies on GSTT1 (2,374 patients and 1,544 controls) were included. By pooling all the studies, GSTM1 null polymorphism was not associated with cataract risk, and this negative association maintained in subgroup analyses. However, GSTT1 null polymorphism was significantly associated with increased risk of posterior subcapsular (OR, 1.42; 95 % CI, 1.04-1.94) but not other subtypes of cataract. Stratified analyses demonstrated an association of GSTT1 null genotype with increased risk of cataract in Asian (OR, 1.44; 95 % CI, 1.14-1.83) but not Caucasian populations. In addition, seven pooled studies showed no association of cataract risk with the combined GSTM1 and GSTT1 null genotypes. CONCLUSIONS: This meta-analysis suggests that GSTT1 null polymorphism is associated with increased risk of posterior subcapsular cataract. Given the limited sample size, the association between GSTT1 null polymorphism and cataract risk in Asian awaits further investigation.

"As a parent, I want to do more for my child": A phenomenological approach to understanding the experiences of parents involved in surgical decision-making for children with congenital hand anomalies.

BACKGROUND: A congenital anomaly of the hand can affect both function and appearance, and places a stressful psychological burden on the family, especially parents. Surgery during infancy may prevent later disabilities, but little is known of the importance of parents' involvement in these decisions in terms of psychological adjustment or treatment satisfaction. OBJECTIVE: To understand parents' perceptions of involvement in their child's surgery for limb anomaly, and their preferences for the support of healthcare professionals. Results should lead to recommended interventions to improve familial adjustment to the child's condition. METHODS: Qualitative data was collected from semi-structured confidential self-reported interviews of 35 parents (65.7 % mothers) of children who had received reconstructive surgery for congenital hand anomaly (at age 24.89 ± 9.26 months); interviews were coincident with the 1-month postoperative follow-up. The parents ranged in age, gender, educational background, economic status, and type of anomaly. Data analysis referenced Colaizzi's phenomenological approach. RESULTS: The concerns of the parents were consolidated into three themes: attitudes toward Parental involvement in surgical decision-making; status of parental involvement in Surgical decision-making; and need for help and support. CONCLUSIONS: Some parents were comfortable leaving surgical decisions entirely to the medical staff, but most preferred active participation and were disappointed at their lack of inclusion. The maximum benefit from surgery for congenital abnormalities in infancy is achieved when the parents and extended families have access to the expertise, skills, encouragement, and psychological support of healthcare providers.

Exploring the anti-inflammatory and immune regulatory effects of Taohe Chengqi decoction in sepsis-induced lung injury.

ETHNOPHARMACOLOGICAL RELEVANCE: Sepsis presents complex pathophysiological challenges. Taohe Chengqi Decoction (THCQ), a traditional Chinese medicine, offers potential in managing sepsis-related complications, though its exact mechanisms are not fully understood. AIM OF THE STUDY: This research aimed to assess the therapeutic efficacy and underlying mechanisms of THCQ on sepsis-induced lung injury. MATERIALS AND METHODS: The study began with validating THCQ's anti-inflammatory effects through in vitro and in vivo experiments. Network pharmacology was employed for mechanistic exploration, incorporating GO, KEGG, and PPI analyses of targets. Hub gene-immune cell correlations were assessed using CIBERSORT, with further scrutiny at clinical and single-cell levels. Molecular docking explored THCQ's drug-gene interactions, culminating in qPCR and WB validations of hub gene expressions in sepsis and post-THCQ treatment scenarios. RESULTS: THCQ demonstrated efficacy in modulating inflammatory responses in sepsis, identified through network pharmacology. Key genes like MAPK14, MAPK3, MMP9, STAT3, LYN, AKT1, PTPN11, and HSP90AA1 emerged as central targets. Molecular docking revealed interactions between these genes and THCQ components. qPCR results showed significant modulation of these genes, indicating THCQ's potential in reducing inflammation and regulating immune responses in sepsis. CONCLUSION: This study sheds light on THCQ's anti-inflammatory and immune regulatory mechanisms in sepsis, providing a foundation for further research and potential clinical application.

Positive regulation of the CREB phosphorylation via JNK-dependent pathway prevents antimony-induced neuronal apoptosis in PC12 cell and mice brain.

Antimony (Sb) is a potentially toxic chemical element abundantly found in the environment. We previously reported that Sb promoted neuronal deathvia reactive oxygen species-dependent autophagy. Here, we assessed the role of cyclic adenosine monophosphate response element-binding protein (CREB) in Sb-induced neuronal damage. We found that Sb treatment induced CREB phosphorylation and neuronal apoptosis both in vitro and in vivo. Interestingly, inhibition of CREB's transcriptional activity with 666-15 dramatically enhanced apoptosis in PC12 cells by downregulating B-cell lymphoma 2 (Bcl-2). Additionally, Sb activated ERK, JNK, and p38 signaling ; however, only JNK promoted CREB phosphorylation. In conclusion, our findings suggest that CREB phosphorylation by JNK attenuates Sb-induced neuronal apoptosis via Bcl-2 upregulation. These data suggest that JNK-dependent CREB activation prevents neurons from Sb-induced apoptosis and guides the development of novel strategies to prevent Sb-induced neurotoxicity.

Akt inhibition-dependent downregulation of the Wnt/ß-Catenin Signaling pathway contributes to antimony-induced neurotoxicity.

Antimony (Sb), as a newly identified nerve poison, can lead to neuronal apoptosis. However, its neurotoxicological mechanisms remain largely unclear. Here, we evaluated the role and regulation of Wnt/ß-catenin pathway in Sb-mediated neurotoxicity. Under Sb treatment, ß-catenin was dramatically downregulated in vivo and in vitro. Moreover, overexpression of ß-catenin effectively attenuated Sb-induced survivin gene expression suppression and subsequent apoptosis in PC12 cells. In addition, Sb stimualted glycogen synthase kinase-3ß (GSK-3ß) activation, shown as decreased phosphorylation levels at Ser 9 both in PC12 cells and mice brain. Paramacological inhibition of GSK-3ß using lithium chloride (LiCl) significantly rescued ß-catenin expression. For upstream pathway analysis, we found Sb treatment decreased protein kinase B (Akt) phosphorylation, and Akt activator protected PC12 cells from GSK-3ß activation and subsequent ß-catenin suppression. In summary, our data provided a novel molecular mechanism of Sb-associated neurotoxicity, namely that Sb induces Wnt/ß-catenin pathway suppression through Akt inhibition, thus resulted in neuronal apoptosis.

The effects of 50 Hz magnetic field-exposed cell culture medium on cellular functions in FL cells.

Although extremely low frequency magnetic fields (ELF-MFs) have been classified as a possible carcinogen for humans by the International Agency for Research on Cancer (IARC), their biological effects and underlying mechanisms are still unclear. Our previous study indicated that ELF-MF exposure influenced the relative permittivity of the saline solution, suggesting that the MF exposure altered physical properties of the solution. To explore the biophysical mechanism of ELF-MF-induced biological effects, this study examined the effects of 50 Hz sinusoidal MF at 0-4.0 mT on the permittivity of culture medium with phase-interrogation surface plasmon resonance (SPR) sensing. Then, the biological effects of MF pre-exposed culture medium on cell viability, the mitogen-activated protein kinase (MAPK) signaling pathways, oxidative stress, and genetic stabilities were analyzed using Cell Counting Kit-8, western blot, flow cytometry, γH2AX foci formation, and comet assay. The results showed that SPR signals were decreased under MF exposure in a time- and dose-dependent manner, and the decreased SPR signals were reversible when the exposure was drawn off. However, MF pre-exposed culture medium did not significantly change cell viability, intracellular reactive oxygen species level, activation of the MARK signaling pathways, or genetic stabilities in human amniotic epithelial cells (FL cells). In conclusion, our data suggest that the relative permittivity of culture medium was influenced by 50 Hz MF exposure, but this change did not affect the biological processes in FL cells.

Effects of 1800 MHz RF-EMF exposure on DNA damage and cellular functions in primary cultured neurogenic cells.

PURPOSE: To systematically evaluate the effects of 1800 MHz radiofrequency electromagnetic fields (RF-EMF) exposure on DNA damage and cellular functions in primary cultured neurogenic cells. MATERIALS AND METHODS: The primary cultured astrocytes, microglia and cortical neurons were exposed to RF-EMF at a SAR of 4.0 W/kg. The DNA damage was evaluated by γH2AX foci formation assay. The secretions of pro-inflammatory cytokines (TNF-α, IL-6 and IL-1ß) in astrocytes and microglia, microglial phagocytic activity and neuronal development were examined by enzyme-linked immunosorbent assay, phagocytosis assay and immunofluorescent staining on microtubule-associated protein tau, microtubule-associated protein 2, postsynaptic density 95 and gephyrin, respectively. RESULTS: RF-EMF exposure did not significantly induce γH2AX foci formation in three primary cultured neurogenic cells. Furthermore, RF-EMF exposure did not significantly affect the secretion of cytokines in astrocytes and microglia, and the morphological indicators of dendrites or synapses of cortical neurons. However, the exposure significantly reduced the phagocytic activity of microglia and inhibited the axon branch length and branch number of cortical neurons. CONCLUSIONS: Our data demonstrated that exposure to RF-EMF did not elicit DNA damage but inhibited the phagocytic ability of microglia and the axon branch length and branch number of cortical neurons.

Association between parental occupational exposure to extremely low frequency magnetic fields and childhood nervous system tumors risk: A meta-analysis.

BACKGROUND AND OBJECTIVE: Previous epidemiological studies suggested association between parental occupational exposure to extremely low frequency magnetic fields (ELF-MF) and risk of childhood nervous system tumors, but the results were inconsistent. We conducted a meta-analysis of case-control and cohort studies to re-evaluate this association. METHODS: Relevant studies were identified by searching PubMed and Web of Science databases as well as by manual searching. Summary odds ratio (OR) with 95% confidence interval (CI) were pooled with a fixed-effects or random-effects model. RESULTS: A total of 22 eligible articles (21 case-control studies and 1 cohort study) were included for the quantitative analysis. The results showed that parental occupational ELF-MF exposure was significantly associated with an increased risk of childhood nervous system tumors (OR = 1.11, 95% CI = 1.02-1.21), and this association remained in studies on central nervous system (CNS) tumors (OR = 1.13, 95% CI = 1.02-1.27) but not neuroblastoma (OR = 1.02, 95% CI = 0.92-1.14). Furthermore, maternal (OR = 1.14, 95% CI = 1.05-1.23) but not paternal (OR = 1.05, 95% CI = 0.98-1.13) occupational ELF-MF exposure significantly increased risk of childhood nervous system tumors. Increased risk of childhood CNS tumors was significant associated with maternal (OR = 1.16, 95% CI = 1.06-1.26) but not paternal (OR = 1.15, 95% CI = 0.98-1.34) occupational ELF-MF exposure. CONCLUSION: In conclusion, our results provide limited evidence for the association between maternal occupational exposure to ELF-MF and increased risk of childhood CNS tumors, which should be explained with cautions. Future studies are needed to further evaluate the association of paternal occupational ELF-MF exposure with risk of childhood CNS tumors.

The effects of 50 Hz magnetic field exposure on DNA damage and cellular functions in various neurogenic cells.

Epidemiological studies have indicated a possible association between extremely low-frequency magnetic field (ELF-MF) exposure and the risk of nervous system diseases. However, laboratory studies have not provided consistent results for clarifying this association, despite many years of studies. In this study, we have systematically investigated the effects of 50 Hz MF exposure on DNA damage and cellular functions in both neurogenic tumor cell lines (U251, A172, SH-SY5Y) and primary cultured neurogenic cells from rats (astrocytes, microglia, cortical neurons). The results showed that exposure to a 50 Hz MF at 2.0 mT for up to 24 h did not influence γH2AX foci formation (an early marker of DNA double-strand breaks) in any of six different neurogenic cells. Exposure to a 50 Hz MF did not affect cell cycle progression, cell proliferation or cell viability in neurogenic tumor U251, A172 or SH-SY5Y cells. Furthermore, the MF exposure for 24 h did not significantly affect the secretion of cytokines (TNF-α, IL-6 or IL-1ß) in astrocytes or microglia, or the phagocytic activity of microglia. In addition, MF exposure for 1 h per day did not significantly influence expression levels of microtubule-associated protein tau, microtubule-associated protein 2, postsynaptic density 95 or gephyrin in cortical neurons, indicating an absence of effects of MF exposure on the development of cortical neurons. In conclusion, our data suggest that exposure to a 50 Hz MF at 2.0 mT did not elicit DNA damage effects or abnormal cellular functions in the neurogenic cells studied.

Relationships between urinary antimony levels and both mortalities and prevalence of cancers and heart diseases in general US population, NHANES 1999-2010.

The effects of antimony (Sb) exposure on mortalities, cancers and cardiovascular diseases were controversial in occupational workers, and the evidence from the general population is limited. The objective of this study is to investigate the relationships between Sb exposure and specific health events in the general population. Totally, 7781 participants aged ≥20years were selected from the National Health and Nutrition Examination Survey (NHANES) 1999-2010 and were followed for an average of 6.04years. The Cox and logistic regression models were applied to evaluate the effects of urinary Sb (U-Sb) levels on the risks of all-cause and cause-specific mortalities, and the likelihoods of self-reported cancers and heart diseases, respectively. When setting quartile 1 of U-Sb levels as reference, the hazard ratios (HRs) [95% confidence intervals (CIs)] of the quartile 2 through 4 for all-cause mortality were 1.21 (0.84, 1.74), 1.49 (1.08, 2.04) and 1.66 (1.20, 2.28). The HR of quartile 3 of U-Sb levels for heart disease mortality was 2.18 (1.24, 3.86). Furthermore, increased odds ratios (ORs) from quartile 2 to 4 were 1.69 (1.05, 2.74), 1.42 (0.79, 2.55) and 2.11 (1.26, 3.55) for self-reported congestive heart failure, and 1.37 (0.95, 1.99), 1.96 (1.37, 2.82) and 1.81 (1.16, 2.83) for heart attack. Elevated U-Sb levels were not significantly related to mortality of malignant neoplasms, and self-reported cancers. The data demonstrated associations of increased U-Sb levels with all-cause and heart diseases mortalities, and prevalent congestive heart failure and heart attack, suggesting public concerns on the health hazards of Sb exposure in the general population.

Mobile phone signal exposure triggers a hormesis-like effect in Atm+/+ and Atm-/- mouse embryonic fibroblasts.

Radiofrequency electromagnetic fields (RF-EMFs) have been classified by the International Agency for Research on Cancer as possible carcinogens to humans; however, this conclusion is based on limited epidemiological findings and lacks solid support from experimental studies. In particular, there are no consistent data regarding the genotoxicity of RF-EMFs. Ataxia telangiectasia mutated (ATM) is recognised as a chief guardian of genomic stability. To address the debate on whether RF-EMFs are genotoxic, we compared the effects of 1,800 MHz RF-EMF exposure on genomic DNA in mouse embryonic fibroblasts (MEFs) with proficient (Atm+/+) or deficient (Atm-/-) ATM. In Atm+/+ MEFs, RF-EMF exposure for 1 h at an average special absorption rate of 4.0 W/kg induced significant DNA single-strand breaks (SSBs) and activated the SSB repair mechanism. This effect reduced the DNA damage to less than that of the background level after 36 hours of exposure. In the Atm-/- MEFs, the same RF-EMF exposure for 12 h induced both SSBs and double-strand breaks and activated the two repair processes, which also reduced the DNA damage to less than the control level after prolonged exposure. The observed phenomenon is similar to the hormesis of a toxic substance at a low dose. To the best of our knowledge, this study is the first to report a hormesis-like effect of an RF-EMF.

Associations of parental occupational exposure to extremely low-frequency magnetic fields with childhood leukemia risk.

Previous studies on the association of parental occupational exposure to extremely low-frequency magnetic fields (ELF-MF) with childhood leukemia risk have produced inconsistent results. To reevaluate this association, we performed a meta-analysis by pooling 11 case-control and one cohort studies. The overall results showed that neither maternal nor paternal occupational exposure was associated with childhood leukemia risk. For paternal occupational exposure, significant association was found when pooling studies with small number of cases (OR =1.96; 95% CI, 1.03-3.74) or with lower quality score (OR =1.52; 95% CI, 1.07-2.15). However, this association was not confirmed when pooling studies with large number of cases or high quality score. In conclusion, our data indicate no association between parental occupational ELF-MF exposure and childhood leukemia risk, and the elevated OR under certain subgroup analysis is likely due to chance. Further studies with precise ELF-MF exposure assessment are suggested.