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PDF file - 343K, p53 function in BRAFV600E/ARF-/- murine melanoma cells.

PDF file - 407K, DNA damage induced by BRAFV600E in human melanoma cells.

PDF file - 155K, Tumor formation in BRAFV600E/ARF-/- mice.

PDF file - 23K, Primer sequences.

The nucleolus is the organelle for ribosome biogenesis and sensing various types of stress. However, its role in regulating stem cell fate remains unclear. Here, we present evidence that nucleolar stress induced by interfering rRNA biogenesis can drive the 2-cell stage embryo-like (2C-like) program and induce an expanded 2C-like cell population in mouse embryonic stem (mES) cells. Mechanistically, nucleolar integrity maintains normal liquid-liquid phase separation (LLPS) of the nucleolus and the formation of peri-nucleolar heterochromatin (PNH). Upon defects in rRNA biogenesis, the natural state of nucleolus LLPS is disrupted, causing dissociation of the NCL/TRIM28 complex from PNH and changes in epigenetic state and reorganization of the 3D structure of PNH, which leads to release of Dux, a 2C program transcription factor, from PNH to activate a 2C-like program. Correspondingly, embryos with rRNA biogenesis defect are unable to develop from 2-cell (2C) to 4-cell embryos, with delayed repression of 2C/ERV genes and a transcriptome skewed toward earlier cleavage embryo signatures. Our results highlight that rRNA-mediated nucleolar integrity and 3D structure reshaping of the PNH compartment regulates the fate transition of mES cells to 2C-like cells, and that rRNA biogenesis is a critical regulator during the 2-cell to 4-cell transition of murine pre-implantation embryo development., The role of the nucleolus in cell fate is not well known. Here the authors show nucleolar integrity maintained by rRNA-mediated liquid-liquid phase separation and 3D chromatin structure of perinucleolar heterochromatin regulates the fate transition of mouse embryonic stem cells to 2 cell-stage embryo-like cells, and that rRNA biogenesis regulates the 2-cell-to-4-cell transition of development.

To predict the epidemiological trend of coronavirus disease 2019 (COVID-19) by mathematical modeling based on the population mobility and the epidemic prevention and control measures. : As of February 8，2020，the information of 151 confirmed cases in Yueqing，Zhejiang province were obtained，including patients' infection process，population mobility between Yueqing and Wuhan，etc. To simulate and predict the development trend of COVID-19 in Yueqing, the study established two-stage mathematical models，integrating the population mobility data with the date of symptom appearance of confirmed cases and the transmission dynamics of imported and local cases. : It was found that in the early stage of the pandemic，the number of daily imported cases from Wuhan (using the date of symptom appearance) was positively associated with the number of population travelling from Wuhan to Yueqing on the same day and 6 and 9 days before that. The study predicted that the final outbreak size in Yueqing would be 170 according to the number of imported cases estimated by consulting the population number travelling from Wuhan to Yueqing and the susceptible-exposed-infectious-recovered (SEIR) model; while the number would be 165 if using the reported daily number of imported cases. These estimates were close to the 170，the actual monitoring number of cases in Yueqing as of April 27，2020. : The two-stage modeling approach used in this study can accurately predict COVID-19 epidemiological trend.

ObjectiveAntimicrobial peptides (AMPs) play essential roles in maintaining gut health and are associated with IBD. This study is to elucidate the effect of angiogenin (ANG), an intestine-secreted AMP, on gut microbiota and its relevance with IBD.DesignThe effect of ANG on microbiota and its contribution to colitis were evaluated in different colitis models with co-housing and faecal microbiota transplantation. ANG-regulated bacteria were determined by 16S rDNA sequencing and their functions in colitis were analysed by bacterial colonisation. The species-specific antimicrobial activity of ANG and its underlying mechanism were further investigated with microbiological and biochemical methods. ANG level and the key bacteria were characterised in IBD faecal samples.ResultsANG regulated microbiota composition and inhibited intestinal inflammation. Specifically, Ang1 deficiency in mice led to a decrease in the protective gut commensal strains of Lachnospiraceae but an increase in the colitogenic strains of α-Proteobacteria. Direct binding of ANG to α-Proteobacteria resulted in lethal disruption of bacterial membrane integrity, and consequently promoted the growth of Lachnospiraceae, which otherwise was antagonised by α-Proteobacteria. Oral administration of ANG1 reversed the dysbiosis and attenuated the severity of colitis in Ang1-deficient mice. The correlation among ANG, the identified bacteria and IBD status was established in patients.ConclusionThese findings demonstrate a novel role of ANG in shaping gut microbe composition and thus maintaining gut health, suggesting that the ANG-microbiota axis could be developed as a potential preventive and/or therapeutic approach for dysbiosis-related gut diseases.

RNA polymerase I (Pol I) synthesizes about 60% of cellular RNA by transcribing multiple copies of the ribosomal RNA gene (rDNA). The transcriptional activity of Pol I controls the level of ribosome biogenesis and cell growth. However, there is currently a lack of methods for monitoring Pol I activity in real time. Here, we develop LiveArt (live imaging-based analysis of rDNA transcription) to visualize and quantify the spatiotemporal dynamics of endogenous ribosomal RNA (rRNA) synthesis. LiveArt reveals mitotic silencing and reactivation of rDNA transcription, as well as the transcriptional kinetics of interphase rDNA. Using LiveArt, we identify SRFBP1 as a potential regulator of rRNA synthesis. We show that rDNA transcription occurs in bursts and can be altered by modulating burst duration and amplitude. Importantly, LiveArt is highly effective in the screening application for anticancer drugs targeting Pol I transcription. These approaches pave the way for a deeper understanding of the mechanisms underlying nucleolar functions.

Mature microRNA (miRNA) decay is a key step in miRNA turnover and gene expression regulation. Angiogenin (ANG), the first human tumor-derived angiogenic protein and also a member of the RNase A superfamily, can promote tumor growth and metastasis by regulating rRNA biogenesis and tiRNA production. However, its effect on miRNA has not been explored. In this study, we find that ANG exclusively downregulates mature miR-141 in human umbilical endothelial cells (HUVECs) via its ribonuclease activity and preferably cleaves single-stranded miR-141 at the A5/C6, U7/G8, and U14/A15 sites via endonucleolytic digestion. By downregulating miR-141, ANG promotes HUVECs proliferation, migration, tube formation, and angiogenesis both in vitro and in vivo. Conversely, downregulated ANG inhibits ANG-mediated miR-141 decay, thus decreasing the angiogenesis process of HUVECs. We also find an inverse correlation between ANG and miR-141 expression in colorectal cancer (CRC) tissues. Our study indicates that ANG regulates CRC progression by disrupting miR-141 and its regulation on angiogenesis-related target genes, not only revealing a new mechanism of ANG action but also newly identifying miR-141 as a substrate of ANG. This study suggests that targeting ANG nuclease activity might be valuable in treating angiogenesis-related diseases through coordinately regulating the metabolism of rRNA, tiRNA, and miRNA.

As a common complication of diabetes, diabetic foot ulcers serious affect the life quality even lead to amputation if it's not properly treated. In this paper, we developed a Low Temperature Plasma Jet (LTPJ) system for treating diabetic foot ulcers on streptozotocin-induced diabetic mice. This system generates time-dependent reactive nitrogen and oxygen species (RNOS), which have temperature below 40°C. The wound area of normal mice was significantly reduced after LTPJ treatment. Histological and immunohistochemistry analysis showed faster deposition of collagen and more vessel formation both in plasma-treated normal and diabetic mice on Day 3. However, diabetic wounds showed poor collagen deposition and angiogenesis on Day 8, which might be the reason of slow wound healing. Reactive nitrogen species (RNS) that generated by LTPJ can promote endogenous nitric oxide (NO) production in diabetic wounds, thus promoting inflammation, stromal deposition, angiogenesis, cell proliferation and remodeling, while excess reactive oxygen species (ROS) will exacerbate oxidative stress in wound tissues of diabetic mice. In conclusion, LTPJ improved acute wound healing in normal mice, increased collagen deposition and angiogenesis in initial diabetic wound healing, but had no significant effect on diabetic wound healing rate.

Metastasis of colorectal cancer (CRC) is the leading cause of CRC-associated mortality. Angiogenin (ANG), a member of the ribonuclease A superfamily, not only activates endothelial cells to induce tumor angiogenesis, but also targets tumor cells to promote cell survival, proliferation and/or migration. However, its clinical significance and underlying mechanism in CRC metastasis are still largely unknown. Here, we reported that ANG was upregulated in CRC tissues and associated with metastasis in CRC patients. We then revealed that ANG enhanced CRC growth and metastasis in both in vitro and in vivo systems. Intriguingly, we characterized a bunch of tRNA-derived stress-induced small RNAs (tiRNAs), produced through ANG cleavage, that was enriched in both CRC tumor tissues and highly metastatic cells, and functioned in ANG-promoted CRC metastasis. Moreover, higher level of a 5'-tiRNA from mature tRNA-Val (5'-tiRNA-Val) was observed in CRC patients and was correlated with tumor metastasis. Taken together, we propose that a novel ANG-tiRNAs-cell migration and invasion regulatory axis promotes CRC metastasis, which might be of potential target for CRC diagnosis and treatment.

Although colorectal cancer (CRC) is one of the most common causes of cancer mortality, early-stage detection dramatically improves survival rate. To explore the feasibility of serum angiogenin (ANG) as a biomarker for early detection of colorectal neoplasia, we collected serum samples from 781 participants, including 369 patients with CRC, 133 with colorectal adenoma and 279 healthy controls. We examined the levels of serum ANG by ELISA, calculated the diagnostic accuracy of ANG by plotted receiver operating characteristic curves (ROCs), and compared it with those obtained by carcinoembryonic antigen (CEA) and carbohydrate antigen 19-9 (CA19-9). We also analyzed the relationship between serum ANG level and TNM stage in CRC patients. The results showed that ANG serum levels were significantly elevated in patients with colorectal adenomas and CRC (P < 0.01). The area under the ROC curve (AUC) for ANG in distinguishing CRC patients from healthy controls was 0.740 [95% confidence interval (CI): 0.705-0.744], comparable to that of CEA (0.770; 95% CI: 0.735-0.802; P = 0.26) but significantly higher than that of CA19-9 (0.636; 95% CI: 0.598-0.674, P < 0.01), with much higher sensitivity (67.75%) than CEA (36.86%) or CA19-9 (12.20%). We observed no significant differences in ANG serum levels among CRCs at different TNM stages. Furthermore, sensitivity and specificity of ANG for distinguishing colorectal adenomas patients from healthy controls were 66.20% and 64.90%, respectively. ANG has the potential to serve as a serum biomarker for early detection of colorectal neoplasia.

Communication between myeloid cells and epithelium plays critical role in maintaining intestinal epithelial barrier integrity. Myeloid cells interact with intestinal epithelial cells (IECs) by producing various mediators; however, the molecules mediating their crosstalk remain incompletely understood. Here, we report that deficiency of angiogenin (Ang) in mouse myeloid cells caused impairment of epithelial barrier integrity, leading to high susceptibility to DSS‐induced colitis. Mechanistically, myeloid cell‐derived angiogenin promoted IEC survival and proliferation through plexin‐B2‐mediated production of tRNA‐derived stress‐induced small RNA (tiRNA) and transcription of ribosomal RNA (rRNA), respectively. Moreover, treatment with recombinant angiogenin significantly attenuated the severity of experimental colitis. In human samples, the expression of angiogenin was significantly down‐regulated in patients with inflammatory bowel disease (IBD). Collectively, we identified, for the first time to our knowledge, a novel mediator of myeloid cell‐IEC crosstalk in maintaining epithelial barrier integrity, suggesting that angiogenin may serve as a new preventive agent and therapeutic target for IBD.

N6‐methyladenosine (m(6)A) mRNA methylation has emerged as an important player in many biological processes by regulating gene expression. However, its roles in intestinal stem cell (ISC) homeostasis remain largely unknown. Here, we report that YTHDF1, an m(6)A reader, is highly expressed in ISCs and its expression is upregulated by Wnt signaling at the translational level. Whereas YTHDF1 is dispensable for normal intestinal development in mice, genetic ablation of Ythdf1 dramatically blocks Wnt‐driven regeneration and tumorigenesis with reduced ISC stemness. Mechanistically, YTHDF1 facilitates the translation of Wnt signaling effectors including TCF7L2/TCF4, while this process is enhanced during Wnt activation to augment β‐catenin activity. Targeting YTHDF1 in ISCs of established tumors leads to tumor shrinkage and prolonged survival. Collectively, our studies unveil YTHDF1 as an amplifier of Wnt/β‐catenin signaling at the translational level, which is required for the maintenance of ISCs during regeneration and tumorigenesis.

Extremely low frequency magnetic field (ELF-MF) has been classified as a possible carcinogen to humans by the International Agency for Research on Cancer [2002]. However, debate on the genotoxic effects of ELF-MF has continued due to lack of sufficient experimental evidence. Ataxia telangiectasia mutated (ATM) plays a central role in DNA damage repair; its deficiency can result in cellular sensitivity to DNA-damaging agents. To evaluate the genotoxicity of ELF-MF, we investigated the effects of 50 Hz MF on DNA damage in ATM-proficient (Atm+/+ ) mouse embryonic fibroblasts (MEFs) and ATM-deficient (Atm-/- ) MEFs, a radiosensitive cell line. Results showed no significant difference in average number of γH2AX foci per cell (9.37 ± 0.44 vs. 9.08 ± 0.28, P = 0.58) or percentage of γH2AX foci positive cells (49.22 ± 1.86% vs. 49.74 ± 1.44%, P = 0.83) between sham and exposure groups when Atm+/+ MEFs were exposed to 50 Hz MF at 2.0 mT for 15 min. Extending exposure duration to 1 or 24 h did not significantly change γH2AX foci formation in Atm+/+ MEFs. Similarly, the exposure did not significantly affect γH2AX foci formation in Atm-/- MEFs. Furthermore, 50 Hz MF exposure also did not significantly influence DNA fragmentation, cell viability, or cell cycle progression in either cell types. In conclusion, exposure to 50 Hz MF did not induce significant DNA damage in either Atm+/+ or Atm-/- MEFs under the reported experimental conditions. Bioelectromagnetics. 39:476-484, 2018. © 2018 Wiley Periodicals, Inc.

Follistatin (FST), a single-chain glycosylated protein, is expressed in various tissues. The essential biological function of FST is binding and neutralizing transforming growth factor β (TGF-β) superfamily, including activin, myostatin, and bone morphogenetic protein (BMP). Emerging evidence indicates that FST also serves as a stress responsive protein, which plays a protective role under a variety of stresses. In most cases, FST performs the protective function through its neutralization of TGF-β superfamily. However, under certain circumstances, FST translocates into the nucleus to maintain cellular homeostasis independent of its extracellular antagonism activity. This review provides integrated insight into the most recent advances in understanding the role of FST under various stresses, and the clinical implications corresponding to these findings and discusses the mechanisms to be further studied.

Angiogenin (ANG) is a ribonuclease with angiogenic activity in in vitro and in vivo angiogenesis assays, but little is known about its physiological functions. Recently, the zebrafish ribonuclease like 1 (Rnasel1) gene was cloned and found to be structurally and functionally similar to human ANG. Therefore, we investigated the effect of Rnasel1 on angiogenesis during zebrafish development. In Tg (fli1:EGFP)y1 embryos injected with Rnasel1 morpholino oligonucleotides (MOs), vasculogenesis was intact, but angiogenesis was markedly impaired resulting in defective intersegmental vessels (ISVs). The impaired angiogenesis could be rescued by co-injection with MO-resistant full-length Rnasel1 mRNA. On the other hand, Rnasel1 over-expression led to ectopic ISV branching from the dorsal aorta. Mechanistically, we found that Rnasel1 promotes kinase insert domain receptor like (Kdrl) gene expression at transcriptional level. Our results indicate that Rnasel1 plays an important role in angiogenesis during zebrafish development through regulating Kdrl gene expression.

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-1β) 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.

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. © 2016 Wiley Periodicals, Inc.

Silica nanoparticles (SiNPs) have been reported to induce pulmonary fibrosis (PF) with an unknown mechanism. Recently, the activation of autophagy, a lysosome-dependent cell degradation pathway, by SiNPs has been identified in alveolar epithelial cells (AECs). However, the underlying mechanism and the relevance of SiNPs-induced autophagy to the development of PF remain elusive. Here, we report that autophagy dysfunction and subsequent apoptosis in AECs are involved in SiNPs-induced PF. SiNPs engulfed by AECs enhance autophagosome accumulation and apoptosis both in vivo and in vitro. Mechanically, SiNPs block autophagy flux through impairing lysosomal degradation via acidification inhibition. Lysosomal reacidification by cyclic-3′,5′-adenosine monophosphate (cAMP) significantly enhances autophagic degradation and attenuate apoptosis. Importantly, enhancement of autophagic degradation by rapamycin protects AECs from apoptosis and attenuates SiNPs-induced PF in the mouse model. Altogether, our data demonstrate a repressive effect of SiNPs on lysosomal acidification, contributing to the decreased autophagic degradation in AECs, thus leading to apoptosis and subsequent PF. These findings may provide an improved understanding of SiNPs-induced PF and molecular targets to antagonize it.

Organic fluorescent dyes with high quantum yield are widely applied in bioimaging and biosensing. However, most of them suffer from a severe effect called aggregation-caused quenching (ACQ), which means that their fluorescence is quenched at high molecular concentrations or in the aggregation state. Aggregation-induced emission (AIE) is a diametrically opposite phenomenon to ACQ, and luminogens with this feature can effectively solve this problem. Graphene oxide has been utilized as a quencher for many fluorescent dyes, based on which biosensing can be achieved. However, using graphene oxide as a surface modification agent of fluorescent nanoparticles is seldom reported. In this article, we used nanographene oxide (NGO) to encapsulate fluorescent nanoparticles, which consisted of a type of AIE dye named TPE-TPA-FN (TTF). NGO significantly improved the stability of nanoparticles in aqueous dispersion. In addition, this method could control the size of nanoparticles' flexibly as well as increase their emission efficiency. We then used the NGO-modified TTF nanoparticles to achieve three-photon fluorescence bioimaging. The architecture of ear blood vessels in mice and the distribution of nanoparticles in zebrafish could be observed clearly. Furthermore, we extended this method to other AIE luminogens and showed it was widely feasible.

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.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-1β) 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.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.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.

Extremely low frequency magnetic field (ELF-MF) has been classified as a possible carcinogen to humans by the International Agency for Research on Cancer [2002]. However, debate on the genotoxic effects of ELF-MF has continued due to lack of sufficient experimental evidence. Ataxia telangiectasia mutated (ATM) plays a central role in DNA damage repair; its deficiency can result in cellular sensitivity to DNA-damaging agents. To evaluate the genotoxicity of ELF-MF, we investigated the effects of 50 Hz MF on DNA damage in ATM-proficient (Atm

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-1β) 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.

Background. Angiogenin (ANG) is a multifunctional angiogenic protein that participates in both normal development and diseases. Abnormal serum ANG levels are commonly reported in various diseases. However, whether ANG can serve as a diagnostic or prognostic marker for different diseases remains a matter of debate. Methods. Here, we performed a systematic review and meta-analysis of the literature utilizing PubMed, Web of Science, and Scopus search engines to identify all publications comparing plasma or serum ANG levels between patients with different diseases and healthy controls, as were studies evaluating circulating ANG levels in healthy populations, pregnant women, or other demographic populations. Results. This study demonstrated that the serum ANG concentration in healthy populations was 336.14 ± 142.83 ng/ml and remained relatively stable in different populations and regions. We noted no significant differences in serum ANG levels between patients and healthy controls, except in cases in which patients suffered from cancer or cardiovascular diseases. The serum ANG concentrations were significantly higher in patients who developed colorectal cancer, acute myeloid leukemia, multiple myeloma, myelodysplastic syndromes, and heart failure than those in healthy controls. Conclusion. ANG has the potential of being a serum biomarker for cancers and cardiovascular diseases.

This study aimed to evaluate the effects of electromagnetic fields (EMF) exposure on levels of serum lipids in workers of an electric power plant. A cross-sectional study was carried out in an electric power plant in Zhejiang province, China, from August to September 2011. All participants were divided into two groups with high occupational EMF exposure and low occupational EMF exposure. The occupational EMF exposure included radiofrequency EMF and extremely low-frequency EMF. Occupational EMF exposure was associated with an increased level of low-density lipoprotein cholesterol (LDL-c; β = 0.17 mmol/L, P = 0.022). High EMF exposure group with longer employment duration, longer daily EMF exposure duration, and more mobile phone or electric fee per month had significantly higher levels of total cholesterol, LDL-c, or triglyceride than the corresponding reference group. However, significantly decreased level of high-density lipoprotein cholesterol was only observed in high EMF exposure group with more mobile phone fee per month. Similar results were also found in 544 participants with available data of serum lipids in 2010. The findings showed that chronic EMF exposure was associated with the change of serum lipid levels. EMF exposure might modulate the process of lipid metabolism.