Hemolytic Properties of Fine Particulate Matter (PM2.5) in In Vitro Systems.

Epidemiological studies have suggested that inhalation exposure to particulate matter (PM) air pollution, especially fine particles (i.e., PM2.5 (PM with an aerodynamic diameter of 2.5 microns or less)), is causally associated with cardiovascular health risks. To explore the toxicological mechanisms behind the observed adverse health effects, the hemolytic activity of PM2.5 samples collected during different pollution levels in Beijing was evaluated. The results demonstrated that the hemolysis of PM2.5 ranged from 1.98% to 7.75% and demonstrated a clear dose-response relationship. The exposure toxicity index (TI) is proposed to represent the toxicity potential of PM2.5, which is calculated by the hemolysis percentage of erythrocytes (red blood cells, RBC) multiplied by the mass concentration of PM2.5. In a pollution episode, as the mass concentration increases, TI first increases and then decreases, that is, TI (low pollution levels) < TI (heavy pollution levels) < TI (medium pollution levels). In order to verify the feasibility of the hemolysis method for PM toxicity detection, the hemolytic properties of PM2.5 were compared with the plasmid scission assay (PSA). The hemolysis results had a significant positive correlation with the DNA damage percentages, indicating that the hemolysis assay is feasible for the detection of PM2.5 toxicity, thus providing more corroborating information regarding the risk to human cardiovascular health.

Iron alloys of volatile elements in the deep Earth's interior.

Investigations into the compositional model of the Earth, particularly the atypical concentrations of volatile elements within the silicate portion of the early Earth, have attracted significant interest due to their pivotal role in elucidating the planet's evolution and dynamics. To understand the behavior of such volatile elements, an established 'volatility trend' has been used to explain the observed depletion of certain volatile elements. However, elements such as Se and Br remain notably over-depleted in the silicate Earth. Here we show the results from first-principles simulations that explore the potential for these elements to integrate into hcp-Fe through the formation of substitutional alloys, long presumed to be predominant constituents of the Earth's core. Based on our findings, the thermodynamic stability of these alloys suggests that these volatile elements might indeed be partially sequestered within the Earth's core. We suggest potential reservoirs for volatile elements within the deep Earth, augmenting our understanding of the deep Earth's composition.

BMP2 induces osteogenic differentiation through ACKR3 in mesenchymal stem cells.

In recent years, bone loss related diseases have attracted more and more attention, such as osteoporosis and osteonecrosis of the femoral head exhibited symptoms of osteopenia or insufficient bone mass in a certain stage. Mesenchymal stem cells (MSCs), which can be induced to differentiate into osteoblasts under certain conditions can provide a new solution bone disease. Herein, we deciphered the possible mechanism by which BMP2 drives the transduction of MSCs to the osteoblast lineage through ACKR3/p38/MAPK signaling. The levels of ACKR3 in femoral tissues of samples from humans with different ages and sexes were measured firstly and found that ACKR3 protein levels increase with age. In vitro cellular assays showed that ACKR3 inhibits BMP2-induced osteo-differentiation and promotes adipo-differentiation of MSCs, whereas siACKR3 exhibited the opposite effects. In vitro embryo femur culture experiment showed that inhibition of ACKR3 enhanced BMP2-induced trabecular bone formation in C57BL6/J mouse. In terms of molecular mechanisms, we found that p38/MAPK signaling might play the key role. ACKR3 agonist TC14012 suppressed the phosphorylation of p38 and STAT3 in BMP2 induced MSCs differentiation. Our findings suggested that ACKR3 might be a novel therapeutic target for the treatment of bone-associated diseases and bone-tissue engineering.

Microplastic atmospheric dustfall pollution in urban environment: Evidence from the types, distribution, and probable sources in Beijing, China.

Airborne microplastics (MPs) pollution is an environmental problem of increasing concern, due to the ubiquity, persistence and potential toxicity of plastics in the atmosphere. In recent years, most studies on MPs have focused on aquatic and sedimentary environments, but little research has been done on MPs in the urban atmosphere. In this study, a total of ten dustfall samples were collected in a transect from north to south across urban Beijing. The compositions, morphologies, and sizes of the MPs in these dustfall samples were determined by means of Laser Direct Infrared (LDIR) imaging and Field Emission Scanning Electron Microscopy (FESEM). The number concentrations of MPs in the Beijing dustfall samples show an average of 123.6 items/g. The MPs concentrations show different patterns in the central, southern, and northern zones of Beijing. The number concentration of MPs was the highest in the central zone (224.76 items/g), as compared with the southern zone (170.55 items/g), and the northern zone (24.42 items/g). The LDIR analysis revealed nine compositional types of MPs, including Polypropylene (PP), Polyamide (PA), Polystyrene (PS), Polyethylene (PE), Polyethylene Terephthalate (PET), Silicone, Polycarbonate (PC), Polyurethane (PU) and Polyvinylchloride (PVC), among which PP was overall dominant. The PP dominates the MPs in the central zone (76.3%), and the PA dominates the MPs in the southern zone (55.86%), while the northern zone had a diverse combination of MPs types. The morphological types of the individual MPs particle include fragments, pellets, and fibers, among which fragments are dominant (70.9%). FESEM images show the presence of aged MPs in the Beijing atmosphere, which could pose a yet unquantified health risk to Beijing's residents. The average size of the MPs in the Beijing samples is 66.62 µm. Our study revealed that the numbers of fibrous MPs increase with the decrease in size. This pollution therefore needs to be carefully monitored, and methods of decreasing the sources and mitigations developed.

CDK5RAP3 acts as a putative tumor inhibitor in papillary thyroid carcinoma via modulation of Akt/GSK-3ß/Wnt/ß-catenin signaling.

Cyclin-dependent kinase 5 regulatory subunit-associated protein 3 (CDK5RAP3) has been documented as a vital cancer-related protein that is implicated in numerous cancer types. However, the relevance of CDK5RAP3 in papillary thyroid carcinoma (PTC) is less well understood. The goal of this work was to understand the relationship between CDK5RAP3 and PTC. Our data showed significant decreases in CDK5RAP3 levels in PTC tissues and cell lines. Functional studies revealed that upregulation of CDK5RAP3 in PTC cell lines resulted in significant reduction of cellular proliferation. Moreover, overexpression of CDK5RAP3 induced apoptosis and cell cycle arrest in PTC cells. In addition, the migration, invasion and epithelial-mesenchymal transition in PTC cells were markedly suppressed via overexpression of CDK5RAP3. Further investigation documented that overexpression of CDK5RAP3 remarkably downregulated the levels of phospho-Akt, phospho-GSK-3ß, and active ß-catenin, leading to a significant decrease in activation of the Wnt/ß-catenin pathway. Notably, knockdown of Akt abolished CDK5RAP3-silencing-mediated effects on the Wnt/ß-catenin pathway. Reactivation of the Wnt/ß-catenin pathway partially reversed CDK5RAP3-mediated tumor-inhibitory effects in PTC cells. Overexpression of CDK5RAP3 also weakened the tumorigenic potential of PTC cells in vivo. In summary, our work demonstrates that CDK5RAP3 is underexpressed in PTC and acts as a putative tumor suppressor of PTC. Our findings reveal that CDK5RAP3 exerts a tumor-suppressive role in PTC through downregulation of Wnt/ß-catenin signaling via modulation of the Akt/GSK-3ß axis.

Oxidative potential and water-soluble heavy metals of size-segregated airborne particles in haze and non-haze episodes: Impact of the "Comprehensive Action Plan" in China.

Air pollution is a major environmental health challenge in megacities, and as such a Comprehensive Action Plan (CAP) was issued in 2017 for Beijing, the capital city of China. Here we investigated the size-segregated airborne particles collected after the implementation of the CAP, intending to understand the change of oxidative potential and water-soluble heavy metal (WSHM) levels in 'haze' and 'non-haze' days. The DNA damage and the levels of WSHM were analyzed by Plasmid Scission Assay (PSA) and High-Resolution Inductively Coupled Plasma Mass Spectrometry (HR-ICP-MS) techniques. The PM mass concentration was higher in the fine particle size (0.43-2.1 µm) during haze days, except for the samples affected by mineral dust. The particle-induced DNA damage caused by fine sized particles (0.43-2.1 µm) exceeded that caused by the coarse sized particles (4.7-10 µm). The DNA damage from haze day particles significantly exceeded those collected on non-haze days. Prior to the instigation of the CAP, the highest value of DNA damage decreased, and DNA damage was seen in the finer size (0.43-1.1 µm). The Pearson correlation coefficient between the concentrations of water-soluble Pb, Cr, Cd and Zn were positively correlated with DNA damage, suggesting that these WSHM had significant oxidative potential. The mass concentrations of water-soluble trace elements (WSTE) and individual heavy metals were enriched in the finer particles between 0.43 µm to 1.1 µm, implying that smaller sized particles posed higher health risks. In contrast, the significant reduction in the mass concentration of water-soluble Cd and Zn, and the decrease of the maximum and average values of DNA damage after the CAP, demonstrated its effectiveness in restricting coal-burning emissions. These results have demonstrated that the Beijing CAP policy has been successful in reducing the toxicity of 'respirable' ambient particles.

Effect of high-quality care on limb function recovery and quality of life after osteoporotic hip fracture surgery in the elderly.

OBJECTIVES: To evaluate the effect of high-quality care on limb function recovery and quality of life (QOL) after osteoporotic hip fracture (OHF) surgery in the elderly. METHODS: 116 elderly patients with OHF enrolled in our hospital from January 2017 to December 2019 were assigned into observation group (high-quality care, n=58) and control group (routine care, n=58). After one month of intervention, Harris Hip Score (HHS) and Barthel Index (BI) were used to evaluating limb function and self-care ability, pain intensity numerical rating scale (PINRS) for pain assessment, self-rating anxiety scale (SAS), and self-rating depression scale (SDS) for emotion assessment. Besides, postsurgical complications, QOL and patient satisfaction were examined. RESULTS: HHS and BI were higher in observation group (P<0.05); PINRS, SAS and SDS were lower in observation group (P<0.05); incidence of postsurgical complications in the observation group was significantly lower than that in the control group (P<0.05); QOL and patient satisfaction in the observation group were higher than those in the control group (P<0.05). CONCLUSION: High-quality care promotes the recovery of limb function, the QOL and the satisfaction of elderly patients.

MicroRNA-497-5p stimulates osteoblast differentiation through HMGA2-mediated JNK signaling pathway.

BACKGROUND: Osteoporosis (OP) has the characteristics of the decline in bone mineral density and worsening of bone quality, contributing to a higher risk of fractures. Some microRNAs (miRNAs) have been validated as possible mediators of osteoblast differentiation. We herein aimed to clarify whether miR-497-5p regulates the differentiation of osteoblasts in MC3T3-E1 cells. METHODS: The expression of miR-497-5p in OP patients and controls was measured by RT-qPCR, and its expression changes during osteoblast differentiation were determined as well. The effects of miR-497-5p on the differentiation of MC3T3-E1 cells were studied using MTT, ALR staining, and ARS staining. The target gene of miR-497-5p was predicted by TargetScan, and the effects of its target gene on differentiation and the pathway involved were investigated. RESULTS: miR-497-5p expressed poorly in OP patients, and its expression was upregulated during MC3T3-E1 cell differentiation. Overexpression of miR-497-5p promoted mineralized nodule formation and the expression of RUNX2 and OCN. miR-497-5p targeted high mobility group AT-Hook 2 (HMGA2), while the upregulation of HMGA2 inhibited osteogenesis induced by miR-497-5p mimic. miR-497-5p significantly impaired the c-Jun NH2-terminal kinase (JNK) pathway, whereas HMGA2 activated this pathway. Activation of the JNK pathway inhibited the stimulative role of miR-497-5p mimic in osteogenesis. CONCLUSIONS: miR-497-5p inhibits the development of OP by promoting osteogenesis via targeting HMGA2.

Particle-induced oxidative damage by indoor size-segregated particulate matter from coal-burning homes in the Xuanwei lung cancer epidemic area, Yunnan Province, China.

Size-segregated samples of airborne particulate matter were collected at the coal-burning homes of the Hutou high lung cancer epidemic village and a comparison site Xize village of the Xuanwei County, Yuanan Province, by an Anderson Cascade Impact Sampler in winter and spring to study the toxicological characteristics of different-sized particles. The DNA damage caused by the water-soluble fractions of these size-segregated particles was analyzed by the plasmid scission assay, and the trace element compositions were determined by Inductively Coupled Plasma Mass Spectrometry. The DNA damage rate from the airborne particles in the high lung cancer incidence area was higher than that in Xize village. The different-sized particles have highly varying DNA damage rates, with the values being greater in the small size range than in the large size range. The particle-induced DNA damage rates had a significantly positive correlation with total water-soluble trace elements. Further analysis of the individual elements indicated that the water-soluble heavy metals Zn, Cu, Cd, Rb, Cs, and Sb had a positive correlation with the particle-induced DNA damage, implying that these water-soluble heavy metals played an important role in the DNA damage. The Sr had a negative correlation with the particle-induced DNA damage, suggesting that the water-soluble Sr might counter DNA damage. The mass concentrations of the total and individual water-soluble trace elements were mostly enriched in the small particle size ranges, thus implying the indoor airborne particles in the small size ranges would have a higher health risk.

Identification of Three Differentially Expressed miRNAs as Potential Biomarkers for Lung Adenocarcinoma Prognosis.

OBJECTIVE: The aim of this study areto screen MicroRNAs (miRNAs) related to the prognosis of lung adenocarcinoma (LUAD) and to explore the possible molecular mechanisms. METHODS: The data for a total of 535 patients with LUAD data were downloaded from The Cancer Genome Atlas (TCGA) database. The miRNAs for LUAD prognosis were screened by both Cox risk proportional regression model and Last Absolute Shrinkage and Selection Operator (LASSO) regression model. The performances of the models were verified by time-dependent Receiver Operating Characteristic (ROC) curve. The possible biological processes linked to the miRNAs' target genes were analyzed by Gene Ontology (GO), Kyoto gene and genome encyclopedia (KEGG). RESULTS: Among 127 differentially expressed miRNAs identified from the screening analysis, there are 111 up-regulated and 16 down-regulated miRNAs. Three of them, hsa-miR-1293, hsa-miR-490 and hsa-miR- 5571, were also significantly associated with the survival of the LUAD patients. The targets of the three miRNAs are significantly enriched in systemic lupus erythematosus pathways. CONCLUSION: Hsa-miR-1293, hsa-miR-490 and hsa-miR-5571 can be potentially used as novel biomarkers for the prognosis prediction of LUAD.

Effects of polycyclic aromatic hydrocarbon exposure and miRNA variations on peripheral blood leukocyte DNA telomere length: A cross-sectional study in Henan Province, China.

Telomeres play a major role in human aging and disease, especially in most cancers. Telomere length was shortened in workers exposed to polycyclic aromatic hydrocarbons (PAHs) and influenced by individual genetic variations in telomere-binding proteins. MicroRNAs (miRNAs) can affect the progress of messenger RNA (mRNA) transcription; however, whether polymorphisms in miRNA can act on the telomere length is still unknown. Therefore, we aimed to explore the relationships between telomere damage and genetic polymorphisms in miRNA or environmental exposure. A total of 544 coke oven workers and 238 healthy controls were recruited. After collecting peripheral blood and extracting the genomic DNA of the study subjects, the telomere length (TL) in their leucocytes was detected by a real-time quantitative polymerase chain reaction (PCR), and polymorphisms in miRNAs were genotyped using the flight mass spectrometry technique. The concentrations of the four urine OH-PAHs were determined by high performance liquid chromatography (HPLC), and the Soxhlet extraction method was used to detect the concentration of coke oven emissions (COEs) in the air. We found that the peripheral blood leucocyte DNA TL was significantly shorter in the exposure group (0.75; 0.51, 1.08) than that in the control group (1.05; 0.76, 1.44) (Z = 7.692, P < 0.001). The total cumulative exposure dose (CED), 1-hydroxypyrene, 2-hydroxynaphthalene, and 3-hydroxyphenanthrene were significantly negatively correlated with TL (r = -0.307, P < 0.001; r = -0.212, P < 0.001; r = -0.110, P = 0.025; r = -0.251, P < 0.001, respectively). MiR-145 rs353291 GG, miR-30a rs2222722 CT/CC, and miR-197 rs1889470 AA could protect the telomere end in the exposed workers (P < 0.05). The interaction between miR-197 rs1889470 and the CED had an effect on TL (ß = 0.066, P = 0.034). This is the first study to evaluate gene-environmental interactions for miRNA polymorphisms and PAH exposure in coke oven workers.

Diagnostic Value of Plasma MicroRNAs for Lung Cancer Using Support Vector Machine Model.

Aim: Small single-stranded non-coding RNAs (miRNAs) play an important role in carcinogenesis through degrading target mRNAs. However, the diagnostic value of miRNAs was not explored in lung cancers. In this study, a support-vector-machine (SVM) model for diagnosis of lung cancer was established based on plasma miRNAs biomarkers, clinical symptoms and epidemiology material. Methods: The expressions of plasma miRNA were examined with SYBR Green-based quantitative real-time PCR. Results: We identified that the expressions of 10 plasma miRNAs (miR-21, miR-20a, miR-210, miR-145, miR-126, miR-223, miR-197, miR-30a, miR-30d, miR-25), smoking status, fever, cough, chest pain or tightness, bloody phlegm, haemoptysis, were significantly different between lung cancer and control groups (P<0.05). The accuracies of the combined SVM, miRNAs SVM, symptom SVM, combined Fisher, miRNAs Fisher and symptom Fisher were 96.34%, 80.49%, 84.15%, 84.15%, 75.61%, and 80.49%, respectively; AUC of these six model were 0.976, 0.841, 0.838, 0.865, 0.750, and 0.801, respectively. The accuracy and AUC of combined SVM were higher than the other 5 models (P<0.05). Conclusions: Our findings indicate that SVM model based on plasma miRNAs biomarkers may serve as a novel, accurate, noninvasive method for auxiliary diagnosis of lung cancer.

Telomere length in workers was effected by omethoate exposure and interaction between smoking and p21 polymorphisms.

Omethoate is an organophosphorus pesticide that poses a major health hazard, especially DNA damage. The purpose of this study was to investigate the factors affecting telomere length in workers exposed to omethoate by analyzing the interaction between cell cycle gene polymorphism and environmental factors. The exposure group consisted of 118 workers exposed to omethoate for 8-10 years, the control group comprised 115 healthy people without occupational toxicant exposure history. The telomere length of genomic DNA from peripheral blood leucocyte was determined with real-time PCR. Polymerase chain reaction and restriction fragment length polymorphism was used to detect the polymorphisms in p53, p21 and MDM2 gene. The telomere length in the (CA + AA) genotypes for p21 rs1801270 polymorphism was longer than that in the CC genotype in control group (P = 0.015). The generalized linear model analysis indicated the interaction of the p21 rs1801270 polymorphic (CA + AA) genotypes and smoking has a significant effect on telomere length (ß = -0.258, P = 0.085). The prolongation of telomere length in omethoate-exposed workers was associated with genotypes (CA + AA) of p21 rs1801270, and interactions of (CA + AA) genotypes and smoking factor.

Benchmark dose assessment for coke oven emissions-induced telomere length effects in occupationally exposed workers in China.

Telomeres are DNA-protein structures that protect chromosome ends from degradation and fusion, which are shortened by oxidative stress, for example air pollution including benzene, toluene, Coke Oven Emissions (COEs), and so on. As a biomarker of health and disease, telomere length is associated with cardiovascular, diabetes and cancers. The aim of this study was to estimate the effects of COEs exposure on telomere length and the benchmark dose (BMD) of COEs. A total of 542 coke oven workers and 235 healthy controls without exposure to toxicants were recruited. Quantitative PCR was used to determine the telomere length in human peripheral blood leukocytes DNA. Propensity scoring was used to match coke oven workers to healthy controls. Linear regression models and trend tests were used to the relationship between COEs exposure and telomere length. Telomere length in COEs exposed group 0.764 (0.536, 1.092) was significantly shorter than that in the control group 1.064(0.762, 1.438), (P < 0.001). There were significantly dose-response relationships between COEs exposure and telomere damage with telomere length as a biomarker. A BMDL value lower than the present occupational exposure limits (OELs) of COEs exposure was evaluated using the BMD approach in coke oven workers. Our results suggested that shorter telomere length is related to occupational exposure to COEs and the level of COEs exposure lower than the current national OELs in China and many other countries could induce telomere damage.

The interaction effects of coke oven emissions exposure and metabolic enzyme Gene variants on total antioxidant capacity of workers.

OBJECTIVES: The aim of this study was to investigate the association between coke oven emissions (COEs) exposure and total antioxidant capacity (T-AOC), and to explore whether genetic variations in metabolic enzyme genes GSTT1, GSTM1, GSTP1, and CYP2E1 can affect these associations in coke oven workers. METHODS: 536 coke oven workers and 238 healthy controls were recruited. T-AOC of plasma was determined with kit. Five polymorphic loci of GSTT1 (+/-), GSTM1 (+/-), GSTP1 rs1695, CYP2E1 rs6413432 and CYP2E1 rs3813867 were detected by polymerase chain reaction and restriction fragment length polymorphism. RESULTS: This study shows that the T-AOC in exposure group (12.02 ±â€¯4.72) was significantly lower than that in control group (15.32 ±â€¯7.19) (P < 0.01), and the COEs exposure could decrease the T-AOC of coke oven workers significantly [ß(95% CI) = -2.663 (-4.538,-0.787), P < 0.001]. The T-AOC of female was lower than that of male in exposed and control groups (P < 0.001). The T-AOC was higher in GSTM1 (-) individuals than in GSTM1 (+) individuals in the control group (P = 0.037). The T-AOC with the AG genotype in GSTP1 rs1695 polymorphism was higher than that of the GG genotype in the control group (P = 0.043). The generalized linear model results showed that the risk factors for the decrease of T-AOC include GSTT1 (+) (b = -0.999, P = 0.009), female (b = -2.875, P < 0.01), COEs-exposed (b = -2.712, P = 0.004), GSTM1 (+) (b = -1.814, P = 0.008), and interactions of GSTM1 (+) and COEs-exposed (b = 1.872, P=0.024). CONCLUSIONS: The risk factors for the decrease of T-AOC include GSTT1 (+), female, COEs-exposed, GSTM1 (+), and interactions of GSTM1 (+) and COEs-exposed.

Genetic polymorphisms, mRNA expression levels of telomere-binding proteins, and associates with telomere damage in PAHs-Exposure workers.

Coke oven emissions (COEs), confirmed human carcinogens, are mainly composed of polycyclic aromatic hydrocarbons (PAHs). Telomere shortening in blood leukocytes has been associated with COEs, and polymorphisms in metabolic enzymes. However, the relationship between polymorphisms in telomere related genes and telomere shortening in COEs exposed workers has never been evaluated. Therefore, we measured telomere length and mRNA expression levels of telomere-binding proteins (TBPs) by qPCR method in leucocyte from 544 COEs exposed workers and 238 office staffs (referents). Flight mass spectrometry was used to perform the genotyping of selected functional and susceptible SNPs. The results showed that the telomere length in the exposure group 0.75(0.51,1.08) was significantly shorter than that in the control group 1.05(0.76,1.44) (P < 0.001). The mRNA expression levels of TPP1, TERF1 and TERF2 genes in the exposure group were significantly lower than those in the control group (P < 0.05), the mRNA expression level of POT1 in the exposure group was significantly higher than that in the control group (P < 0.05). We used the wild homozygous genotype as a reference, subjects carrying TERT rs2736109 AA, TERT rs3215401 CC and TERT rs2736100 GT + GG genotypes had significantly longer telomere length in the exposure group (P < 0.05). In conclusion, the workers exposed to COEs had shorter telomere length, which was regulated by the TPP1, TERF1, TERF2 and POT1 genes expression levels, and the gene polymorphisms of TERT gene were associated with the telomere length among PAHs-exposure workers.

Telomere Length in Workers Was Effected by Omethoate Exposure, GSTM1 Deletion, Interaction Between Smoking and GSTP1 Polymorphisms.

OBJECTIVE: The aim of this study was to explore the association between telomere length and metabolizing enzyme gene polymorphisms and environmental factors in omethoate-exposed workers. METHODS: The gene-environment interactions were analyzed with generalized linear model method. RESULTS: The relative telomere lengths in the individuals with GSTM1-deletion were longer than that in non-deletion genotype in the control group (P = 0.011); the relative telomere lengths with GG+AG genotypes in GSTP1 rs1695 were longer than that of AA genotype in the exposure group (P = 0.039). The interaction between the GG+AG genotypes in GSTP1 rs1695 and smoking exposure had significant effect on telomere length (P < 0.05). CONCLUSIONS: The prolongation of relative telomere length in omethoate-exposed workers was associated with GSTM1-deletion, GG+AG genotypes, and interactions of GG+AG genotypes and smoking factor.

Pressure-Induced Large Emission Enhancements of Cadmium Selenide Nanocrystals.

Pressure quenching of optical emission largely limits the potential application of many materials in optical pressure-sensing devices, since emission intensity is crucially connected to performance. Boosting visible-light emission at high pressure is, therefore, an important goal. Here, we demonstrate that the emission of CdSe nanocrystals (NCs) can be enhanced by more than an order of magnitude by compression. The brightest emission can be achieved at pressures corresponding to the phase transitions in different sized CdSe NCs. Very bright blue emission can be obtained by exploiting the increase in band gap with increasing pressure. First-principles calculations indicate that the interaction between the capping oleic acid (OA) layer and the CdSe core is strengthened with increased Hirshfeld charge at high pressure. The effective surface reconstruction associated with the removal of surface-related trap states is highly responsible for the pressure-induced emission enhancement of these CdSe NCs. These findings pave the way for designing a stress nanogauge with easy optical readout and provide a route for tuning bright-fluorescence imaging in response to an externally applied pressure.

Interaction between polymorphisms in cell-cycle genes and environmental factors in regulating cholinesterase activity in people with exposure to omethoate.

Cholinesterase activity (ChA), the effective biomarker for organophosphate pesticide exposure, is possibly affected by single nucleotide polymorphisms (SNPs) in cell-cycle-related genes. One hundred and eighty workers with long-term exposure to omethoate and 115 healthy controls were recruited to explore the gene-gene and gene-environment interactions. The acetylthiocholine and dithio-bis-(nitrobenzoic acid) method was used to detect the cholinesterase activities in whole blood, erythrocytes and plasma. Genetic polymorphisms were determined by the PCR-RFLP and direct PCR electrophoresis methods. Statistical results showed that the cholinesterase activities of whole blood, erythrocytes and plasma in the exposure group were significantly lower than those in the control group (p < 0.001), and erythrocyte cholinesterase activities were associated with gender, smoking and drinking in the exposure group (p < 0.05). Single-locus analyses showed that there is a statistically significant difference in the ChA among the genotypes CC, CA and AA of the p21 rs1801270 locus in the control group (p = 0.033), but not in the exposure group. A significant interaction between genes and environmental factors (i.e. p53, p21, mdm2, gender, smoking and drinking) affecting ChA was found through a generalized multifactor dimensionality reduction analysis. These obtained markers will be useful in further marker-assisted selection in workers with exposure to omethoate.

Detecting the polymorphism of TERF1 gene by an improved PCR-RFLP method.

BACKGROUND: Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) is a common and mature method of detecting the single nucleotide polymorphism (SNP). But, for the polymorphism site rs3863242 of telomeric repeat binding factor 1(TERF1) gene, there is no appropriate restriction enzyme to recognize it, which limits the research between the variants of rs3863242 and human diseases. METHODS: The reverse primer was designed based on turning the 3rd base T into the mismatch base G. After PCR amplification, a new restriction enzyme site was introduced into the TERF1 gene amplification products. Two hundred forty samples from Chinese Han individuals were genotyped to evaluate this method. RESULTS: A new restriction enzyme site for CviQI was introduced into the PCR products. The genotype frequencies of 240 samples from Chinese Han individuals were 4.17% for A/A, 29.58% for A/G, 66.25% for G/G respectively. The allele frequencies were 18.96% for A and 81.04% for G respectively. The genotyping results of PCR products were consistent with the gene sequencing result. CONCLUSIONS: We developed a simple, direct and economical technique for analyzing the polymorphism of TERF1 rs3863242. It may be applied to the colony screening of other SNPs, mutation-screening of tumor-related gene or mutations in some specific genes on a large scale, in the future.