Detection of RASSF1A promoter hypermethylation in serum from gastric and colorectal adenocarcinoma patients

AIM：To evaluate the diagnostic role of serum RASSF1A promoter hypermethylation in gastric and colorectal adenocarcinoma. METHODS：Methylation-specific polymerase chain reaction （MSPCR） was used to examine the promoter methylation status of the serum RASSF1A gene in 47 gastric adenocarcinoma patients, 45 colorectal adenocarcinoma patients, 60 patients with benign gastrointestinal disease （30 with benign gastric disease and 30 with benign colorectal disease）, and 30 healthy donor controls. Apaired study of RASSF1A promoter methylation status in primary tumor, adjacent normal tissue, and postopertive serum were conducted in 25 gastric and colorectal adenocarcinoma patients who later were underwent surgical therapy. RESULTS：The frequencies of detection of serum RASSF1A promoter hypermethylation in gastric （34.0%） and colorectal （28.9%） adenocarcinoma patients were significantly higher than those in patients with benign gastric （3.3%） or colorectal （6.7%） disease or in healthy donors （0%） （P 〈 0.01）. The methylation status of RASSF1A promoter in serum samples was consistent with that in paired primary tumors, and the MSPCR results for RASSF1A promoter methylation status in paired preoperative samples were consistent with those in postoperative serum samples. The serum RASSF1A promoter hypermethylation did not correlate with patient sex, age, tumor differentiation grade, surgical therapy, or serum carcinoembryonic antigen level. Although the serum RASSF1A promoter hypermethylation frequency tended to be higher in patients with distant metastases, there was no correlation between methylation status and metastasis. CONCLUSION：Aberrant CpG island methylation within the promoter region of RASSF1A is a promising biomarker for gastric and colorectal cancer.

Brain-derived neurotrophic factor protects against acrylamide-induced neuronal and synaptic injury via the TrkB-MAPK-Erk1/2 pathway

Acrylamide has been shown to be neurotoxic.Brain-derived neurotrophic factor(BDNF)can alleviate acrylamide-induced synaptic injury;however,the underlying mechanism remains unclear.In this study,dibutyryl-cyclic adenosine monophosphate-induced mature human neuroblastoma(NB-1)cells were exposed with 0–100μg/mL acrylamide for 24–72 hours.Acrylamide decreased cell viability and destroyed synapses.Exposure of co-cultured NB-1 cells and Schwann cells to 0–100μg/mL acrylamide for 48 hours resulted in upregulated expression of synapsin I and BDNF,suggesting that Schwann cells can activate self-protection of neurons.Under co-culture conditions,activation of the downstream TrkB-MAPK-Erk1/2 pathway strengthened the protective effect.Exogenous BDNF can increase expression of TrkB,Erk1/2,and synapsin I,while exogenous BDNF or the TrkB inhibitor K252a could inhibit these changes.Taken together,Schwann cells may act through the BDNF-TrkB-MAPK-Erk1/2 signaling pathway,indicating that BDNF plays an important role in this process.Therefore,exogenous BDNF may be an effective treatment strategy for acrylamide-induced nerve injury.This study was approved by the Laboratory Animal Welfare and Ethics Committee of the National Institute of Occupational Health and Poison Control,a division of the Chinese Center for Disease Control and Prevention(approval No.EAWE-2017-008)on May 29,2017.

Epitaxial Growth of Multi-structure SnO_2 by Chemical Vapor Deposition

The nanowire and whisker heterostructures of tin dioxide were fabricated by the chemical vapor deposition technique.It was demonstrated that various structures of tin oxide can be obtained by controlling the thickness of gold layer and the partial pressure of source vapor at growing sites.12.5 and 25 nm thicknesses are preferable for the epitaxial growth of nanowires and heterostructure through vapor–liquid–solid mechanism,respectively.The tin dioxide whiskers with core-shell structure were fabricated by vapor–solid mechanism.Meanwhile,the influences of various factors on the tin dioxide growth are also discussed.

Health implications of engineered nanoparticles in infants and children

Background:The nanotechnology boom and the ability to manufacture novel nanomaterials have led to increased production and use of engineered nanoparticles(ENPs).However,the increased use of various ENPs inevitably results in their release in or the contamination of the environment,which poses significant threats to human health.In recent years,extraordinary economic and societal benefits of nanoproducts as well as their potential risks have been observed and widely debated.To estimate whether ENPs are safe from the onset of their manufacturing to their disposal,evaluation of the toxicological effects of ENPs on human exposure,especially on more sensitive and vulnerable sectors of the population(infants and children)is essential.Data sources:Papers were obtained from PubMed,Web of Science,and Google Scholar.Literature search words included:"nanoparticles","infants","children","exposure","toxicity",and all relevant cross-references.Results:A brief overview was conducted to 1)characterize potential exposure routes of ENPs for infants and children;2)describe the vulnerability and particular needs of infants and children about ENPs exposure;3)investigate the current knowledge about the potential health hazards of ENPs;and 4)provide suggestions for future research and regulations in ENP applications.Conclusions:As the manufacturing and use of ENPs become more widespread,directed and focused studies are necessary to measure actual exposure levels and to determine adverse health consequences in infants and children.