ve To study the way of oxidative stress induced by soot rat pulmonary cells type Ⅱ ?Methods Before exposure to soot extracts, the rat pulmonary cells were pretreated with anti-oxidative agent, N-acetylcysteine (NAC), vitamin C, vitamin E and mannitol for 30 minutes, then the ceils were exposed to the soot extracts for 24 hours. MTT assay was applied to detect the cytotoxicity. Results It showed that NAC, vitamin C and vitamin E could reduce the cytotoxicity of rat pulmonary cell caused by soot, but no same change was observed in that of man-nitol. Conclusion It was suggested that the DNA oxidative stress of soot may be caused by multi-ways, such as in-duction of oxygen free radical and lipid peroxide etc.

Objective To investigate the micronucleus frequency in mice peripheral blood reticulocytes induced by air particulate pollutants in a railway transport station of chemical dangerous goods (RTSCDG) Methods Male BALB/C mice were selected and randomly divided into exposure groups and control groups One time exposure experiment was carried out among mice exposed to acetone extracts of air particulate pollutants at doses of 20,40,80,160 mg/kg by intraperitoneal injection Multiple time exposure experiment was carried out among mice exposed to acetone extacts of air particulate pollutants at dose of 10 mg/kg by consecutive intraperitoneal injection one time per day for 5 days The peripheral blood was sampled from mice tails and the micronucleus frequencies in reticulocytes were observed at 24, 48 and 72 h after the exposure Results The frequencies of micronuclei in peripheral blood reticulocytes revealed good time response relationship and reached the highest levels at 48 h after exposure,at the same time the frequencies of micronuclei in dose groups of 20,40,80,160 mg/kg were all higher than those in control group The multiple frequencies exposure experiment with lower dose showed that the frequencies of micronuclei in peripheral blood reticulocytes in exposure group always revealed significantly higher levels compared with those in control group during the 24th~72th hour after the exposure ( P

Objective To explore the mechanism of the skin lesion induced by oxidation hair dyes Methods The effects of subjects,such as oxidation hair dyes,hydrogen peroxide (H 2O 2) and p phenylenediamine (PPD) and their mixture which were main components of oxidation hair dyes,on the proliferation of rat's keratinocytes were detected by primary culture technique of rat's keratinocytes and MTT colorimetric assay Results All of the observed groups presented a certain inhibition on proliferation of the rat's keratinocytes,except the group exposed to PPD at the lowest dose for the shorter period The OD values decreased with the increase of exposure levels and periods Dose response relationship was observed between the exposure levels and inhibition rates of cell survival(the r values after 24 h exposue: r H 2O 2 =0 981, r PPD =0 949, r PPD-H 2O 2 =0 963, r hair dyes =0 887) Conclusion The skin lesion induced by oxidation hair dyes might associated with its cytotoxicity

The porous scaffolds for bone tissue engineering were prepared by foam impregnation. The magnesium and aluminum acid phosphates were used as bonder and the hydroxyapatite ((Ca10 (PO4)6(OH)2, HA) powder as raw materials. Scanning electron microscopy (SEM) examination indicated that the 3D interconnected porous structure of the organic foam was replicated well by the scaffolds calcined at high temperature and the structural requirement of tissue engineering was satisfied. XRD analysis showed that the scaffold was composed of HA and Ca7Mg2P6O24 while calcined at 1150 degrees C for shorter time and of (Ca, Mg)3(PO4)2 when the time prolonged to 2 h. There was no peak of CaO found in the scaffolds by XRD. According to the culture in vitro, the scaffold possesses good biocompatibility and certain degree of degradability.
Aluminum Compounds ; chemistry ; Biocompatible Materials ; Bone Substitutes ; chemistry ; Calcium Phosphates ; chemistry ; Durapatite ; chemistry ; Phosphates ; chemistry ; Porosity ; Tissue Engineering

Abstract Poly-l-lactide/beta-tricalcium phosphate (PLLA/betaTCP) composite was obtained by combining ground beta-TCP with PLLA, and absorbable rods were prepared by injection moulding. Degradations of the rods were investigated by scanning electron microscope (SEM), mass loss, molecular weight and bending strength changes. At the beginning of in vivo degradation of the rods, the molecular weight of PLLA decreases sharply with the less mass losses of the rods. As in vivo degradation progress, the surfaces of the rods changed roughly, while micropores and fine groove were observed in the inner part of the rods. The bending strength of composite rods decreased from 151 MPa to 106 MPa after in vivo degradation of 12 weeks. Tissue test reveal that PLLA/beta-TCP composite has good tissue compatibility compared with PLLA.
Absorbable Implants ; Animals ; Biocompatible Materials ; chemistry ; Calcium Phosphates ; chemistry ; Fractures, Bone ; therapy ; Internal Fixators ; Lactic Acid ; chemistry ; Materials Testing ; Polyesters ; Polymers ; chemistry ; Rabbits

To investigate the ability of composite graft of osteobalsts and deproteinized bone-titanium mesh (DPB-TM) scaffold to repair cranial bone defect. 30 rabbits were randomly divided into 3 groups. The passage 3 fetal rabbit osteoblasts were seeded into porous DPB-TM scaffolds at the density of 5 x 10(6) ml(-1) as the experimental group. The same defects were respectively reconstructed by DPB-TM or osteoblasts as the control groups. After 12 weeks, the result was evaluated by three-dimensional computed tomographic scanning, gross inspection, scanning electron microscopy, histological examination and mechanics test, respectively. In the experimental group, bone trabecula was observed to pass the defect and interface was mixed. No demarcation between the region of the bone defect and the normal bone was observed. There was plenty of new bone on the scaffold. Part of the scaffold was absorbed. In view of mechanics, the intensity of artificial bone (18.93+/-1.12 MPa) was higher than that of normal bone (16.96+/-1.60 MPa) (P<0.05). In the control groups, only fibrous tissue was observed in the defect region, there was no new bone formation. The tissue engineering bone constructed by osteoblasts and DPB-TM scaffold can be applied to the repair of bone defect.
Animals ; Bone Regeneration ; Bone Substitutes ; Cell Separation ; Cells, Cultured ; Female ; Fetus ; Guided Tissue Regeneration ; Implants, Experimental ; Male ; Osteoblasts ; cytology ; Osteogenesis ; Prostheses and Implants ; Rabbits ; Random Allocation ; Skull ; injuries ; surgery ; Swine ; Tissue Engineering ; Titanium

OBJECTIVECytochrome P450 2E1 (CYP2E1) is an important metabolizing enzyme involved in oxidative stress responses to benzene, a chemical associated with bone marrow toxicity and leukemia. We aimed to identify the CYP2E1 genetic biomarkers of susceptibility to benzene toxicity in support of environmental and occupational exposure prevention, and to test whether a model using immortal human lymphocytes might be an efficient tool for detecting genetic biomarkers.

METHODSImmortalized human lymphocyte cell lines with independent genotypes on four CYP2E1 SNP sites were induced with 0.01% phenol, a metabolite of benzene. CYP2E1 gene function was evaluated by mRNA expression and enzyme activity. DNA damage was measured by Single-Cell Gel Electrophoresis (SCGE).

RESULTSAmong the four SNPs, cells with rs2070673TT and rs2030920CC showed higher levels of CYP2E1 transcription and enzymatic activity than the other genotypes in the same SNP site. Cells with higher gene expression genotypes also showed higher comet rates compared with lower gene expression genotypes.

CONCLUSIONThese results suggest that CYP2E1 rs2070673 and rs2030920 might be the genetic biomarkers of susceptibility to benzene toxicity and that the immortalized human lymphocytes model might be an efficient tool for the detection of genetic biomarkers of susceptibility to chemicals.

Adolescent ; Adult ; Asian Continental Ancestry Group ; Benzene ; metabolism ; pharmacology ; Cell Line ; Cell Proliferation ; drug effects ; Cytochrome P-450 CYP2E1 ; genetics ; Humans ; Lymphocytes ; drug effects ; metabolism ; Middle Aged ; Phenol ; metabolism ; pharmacology ; Young Adult

Objective: To investigate the benzene concentration in the workplace of benzene-related enterprises in Yangzhou City from 2014 to 2018, and the abnormal blood routine of workers exposed to benzene, and to assess their occupational hazards. Methods: The environmental monitoring data of benzene-related enterprises and the health examination data of benzene exposed workers were collected in March 2019. The inhalation risk assessment model of the National Environmental Protection Agency (EPA) was used to assess the carcinogenic and non-carcinogenic risks of benzene workers. Results: The qualified rate of benzene detection in the workplace was 100% from 2014 to 2018, the highest concentration was 1.42 mg/m³ in five years. The abnormal rates of blood routine detection in benzene exposed workers in five years was 7.10% (213/2 998) 、5.17% (218/4 214) 、5.61% (196/3 493) 、7.65% (288/3 767) 、7.83% (280/3 574) and 7.83%. respectively. The results of risk assessment showed that the minimum carcinogenic risk value was 7.56×10^-6 and the maximum carcinogenic risk value was 31.33×10^-6 in 2014-2018. The hazard quotient values were than 1. Conclusion Benzene monitoring concentration in benzene-related enterprises in Yangzhou City from 2014 to 2018 was low, which meets the occupational exposure limit in China. However, the abnormal rate of blood routine in five years is still high, and there are both carcinogenic and non-carcinogenic risks. We should pay more attention to the health risk of workers exposed to low concentrat in benzene.

Background N6-methyladenosine (m6A) RNA methylation may play an important role in the process of malignant transformation of cells induced by environmental carcinogens. However, the specific roles and mechanisms need to be further explored. Objective To explore the role and mechanism of m6A binding protein insulin-like growth factor 2 mRNA-binding protein 3 (IGF2BP3) in the malignant transformation of human gastric mucosal epithelial cells GES-1 induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). Methods Based on the GES-1 malignant transformation cells MC-30, a stable knockdown IGF2BP3 MC-30 cell line (MC30-shIGF2BP3, abbreviated as MC30-shI3) was constructed by lentiviral transfection technology, and a negative control group (MC30-NC) was also prepared. Real-time quantitative polymerase chain reaction (qRT-PCR) and Western blotting were applied to detect the mRNA expression and protein levels of IGF2BP3. RNA binding protein immunoprecipitation (RIP-qPCR) was used to examine the combination between IGF2BP3 protein and MYC mRNA in malignant cells MC-30. Furthermore, the stability of MYC mRNA was detected by actinomycin D assay. CCK-8 and Transwell respectively were employed to detect cell proliferation, migration, and invasion. Western blotting was applied to detect the expression of EMT markers (N-cadherin, Vimentin, α-SMA, and Snail). The role of the downstream target gene MYC was further elucidated by a rescue assay in MC30-shI3 cells transfected with a plasmid overexpressing MYC to observe changes in cellular phenotypes (proliferation, migration, invasion) and expression of key EMT proteins. Results Compared with the control group, the expression of IGF2BP3 mRNA was up-regulated after 5, 10, 20, and 40 μmol·L⁻¹ MNNG infection of GES-1 cells (P<0.05). After 20 μmol·L⁻¹ MNNG infection, the expression level of IGF2BP3 mRNA increased with prolongation of exposure time (P<0.05). Compared with the control group, the mRNA and protein expression levels of IGF2BP3 were up-regulated in the 10th, 20th, and 30th generations of 5 μmol·L⁻¹ MNNG malignant transformation (P<0.05). The results of qRT-PCR and Western blotting showed that, compared with the MC30-NC group, the IGF2BP3 and MYC mRNA expression and protein expression decreased in the MC30-shI3 group (P<0.01). The CCK8 and transwell assay results showed that, compared with the MC30-NC group, the cell proliferation, migration, and invasion abilities significantly reduced in the MC30-shI3 group (P<0.01). The results of the Western blotting showed that, compared with the MC30-NC group, the protein levels of EMT markers N-cadherin, Vimentin, α-SMA, and Snail decreased in the MC30-shI3 group (P<0.01). The results of RIP-qPCR showed that, compared with the IgG group, the mRNA level was higher for the enriched MYC in the IGF2BP3 group (P<0.01); the results of the actinomycin D assay showed that, compared with the MC30-NC group, the stability of MYC mRNA significantly reduced in the MC30-shI3 group (P<0.01). While the rescue experiment showed that, compared with the IGF2BP3 knock-down+vector group, the MYC protein level significantly increased in the IGF2BP3 knock-down + MYC over-expression group (P<0.01), the proliferation, migration, and invasion abilities significantly enhanced (P<0.01), and the EMT key proteins (N-cadherin, Vimentin, α-SMA, Snail) increased in the MC30-shI3+MYC group (P<0.01). Conclusion Exposure to MNNG could result in up-regulation of IGF2BP3 expression in GES-1 cells. IGF2BP3 may enhance the proliferation, migration, and invasion of malignantly transformed human gastric epithelial cells by binding to MYC mRNA and increasing its stability and expression level and thus promoting the EMT process, which in turn affects the progression of malignant transformation.

Background Occupational stress and depressive symptoms of disease prevention and control personnel are serious. Objective To investigate the relationship between occupational stress, psychological capital, and depressive symptoms of disease prevention and control personnel, and analyze the potential mediating effect of psychological capital on the relationship between occupational stress and depressive symptoms. Methods From July to September 2020, a cluster random sampling method was used to select 2201 employees from 21 centers for disease control and prevention as study subjects covering all levels of administrative divisions in Jiangsu Province. A total of 2036 valid questionnaires were collected with a recovery rate of 92.5%. The Core Occupational Stress Scale, Patient Health Questionnaire, and Psychological Capital Questionnaire were used to investigate their occupational stress, depressive symptoms, and psychological capital. Stratified regression analysis was used to explore the effects of occupational stress and psychological capital on depressive symptoms. A mediating effect model was used to analyze and verify the potential mediating effect of psychological capital on the relationship between occupational stress and depressive symptoms. Results The total scores in M (P₂₅, P₇₅) of occupational stress, depressive symptoms, and psychological capital in the target population were 42.0 (37.0, 48.0), 8.0 (4.0, 9.0), and 4.6 (4.0, 5.0) respectively. The positive rate of occupational stress was 31.0% (631/2036), and the positive rate of depressive symptoms was 22.0% (448/2036). The dimensional scores of organization and reward, and demand and effort of occupational stress were positively correlated with the total score of depressive symptoms [Spearman correlation coefficients (r_s) were 0.371 and 0.269, P<0.05]. The dimensional scores of social support and autonomy of occupational stress and the score of psychological capital were negatively correlated with the total score of depressive symptoms (r_s=−0.373, −0.112, −0.494, P<0.05). The organization and reward, and demand and effort had positive effects on depressive symptoms (b=0.188, 0.177, P<0.05), while social support and autonomy had negative effects on depressive symptoms (b=−0.290, −0.078, P<0.05), and associated with a 22.5% increase of explanatory variance. Psychological capital had a negative effect on depressive symptoms (b=−0.368, P<0.05), and associated with an 11.0% increase of explanatory variance. Psychological capital had mediating effects on the associations of social support, organization and reward, and autonomy with depressive symptoms, and the mediating effect values were −0.210 (95%CI: −0.253-−0.171), 0.096 (95%CI: 0.071-0.122), and −0.164 (95%CI: −0.229-−0.103), respectively. The corresponding mediating effect percentages were 40.23%, 26.97%, and 45.56%, respectively. Conclusion Occupational stress of disease prevention and control personnel can directly affect depressive symptoms, but also indirectly through psychological capital. Psychological capital plays a partial mediating role in the associations of social support, organization and reward, and autonomy of occupational stress with depressive symptoms. The occurrence of depressive symptoms can be reduced by decreasing occupational stress and increasing psychological capital.