ABSTRACT
Objective: To investigate the regulatory mechanisms of piwi-interacting RNA (piRNA) in bisphenol A (BPA)-induced prostate cancer cell invasion and migration. Methods: The Cancer Genome Atlas (TCGA) data was used to analyze and screen for piRNAs with significantly increased expression in prostate cancer tissues. PC-3 cells were treated with different concentrations of BPA for 12, 24, and 48 h, respectively, and the 20% inhibitory concentration (IC20) was measured using a CCK-8 assay. The expression levels of piRNAs before and after BPA treatment were determined by reverse transcription-quantitative PCR. Target genes regulated by BPA and associated with prostate cancer were screened in the Comparative Toxicogenomics Database (CTD). Dual-luciferase reporter gene assay was performed to verify the relationship between piRNA and target genes, and the expression change of the piRNA target gene was detected by Western blotting. Cell migration and invasion assays were used to determine the effects of piRNA on the malignant phenotype of prostate cancer cells. Results: After treatment of PC-3 cells with 160 μmol/L BPA, the expression of piR-sno48 was most significantly increased (P<0.05). Transfection of piR-sno48 antagomir resulted in decreased expression of endogenous piR-sno48 and a significant increase in the expression of its target gene GSTP1 (P<0.05). However, the expression of GSTP1 did not change significantly in BPA-treated PC-3 cells after transfection with piR-sno48 antagomir (P>0.05). The dual-luciferase reporter gene confirmed that piR-sno48 inhibited the expression of GSTP1 by forming an inversely complementary sequence with the 3'-UTR of GSTP1. The Transwell assay results showed that treatment with BPA significantly increased the invasion and migration ability of prostate cancer cells (P<0.01), whereas piR-sno48 antagonists significantly inhibited the effects above (P<0.01). Conclusion: BPA promotes the invasion and migration of prostate cancer cells by upregulating the expression of piR-sno48 and suppressing the expression of GSTP1. Interfering with the expression of endogenous piR-sno48 may inhibit the malignant phenotype of prostate cancer cells caused by BPA.
Subject(s)
Male , Humans , Prostate , RNA, Small Interfering , Antagomirs , Prostatic Neoplasms/geneticsABSTRACT
Objective: To investigate the regulatory mechanisms of piwi-interacting RNA (piRNA) in bisphenol A (BPA)-induced prostate cancer cell invasion and migration. Methods: The Cancer Genome Atlas (TCGA) data was used to analyze and screen for piRNAs with significantly increased expression in prostate cancer tissues. PC-3 cells were treated with different concentrations of BPA for 12, 24, and 48 h, respectively, and the 20% inhibitory concentration (IC20) was measured using a CCK-8 assay. The expression levels of piRNAs before and after BPA treatment were determined by reverse transcription-quantitative PCR. Target genes regulated by BPA and associated with prostate cancer were screened in the Comparative Toxicogenomics Database (CTD). Dual-luciferase reporter gene assay was performed to verify the relationship between piRNA and target genes, and the expression change of the piRNA target gene was detected by Western blotting. Cell migration and invasion assays were used to determine the effects of piRNA on the malignant phenotype of prostate cancer cells. Results: After treatment of PC-3 cells with 160 μmol/L BPA, the expression of piR-sno48 was most significantly increased (P<0.05). Transfection of piR-sno48 antagomir resulted in decreased expression of endogenous piR-sno48 and a significant increase in the expression of its target gene GSTP1 (P<0.05). However, the expression of GSTP1 did not change significantly in BPA-treated PC-3 cells after transfection with piR-sno48 antagomir (P>0.05). The dual-luciferase reporter gene confirmed that piR-sno48 inhibited the expression of GSTP1 by forming an inversely complementary sequence with the 3'-UTR of GSTP1. The Transwell assay results showed that treatment with BPA significantly increased the invasion and migration ability of prostate cancer cells (P<0.01), whereas piR-sno48 antagonists significantly inhibited the effects above (P<0.01). Conclusion: BPA promotes the invasion and migration of prostate cancer cells by upregulating the expression of piR-sno48 and suppressing the expression of GSTP1. Interfering with the expression of endogenous piR-sno48 may inhibit the malignant phenotype of prostate cancer cells caused by BPA.
Subject(s)
Male , Humans , Prostate , RNA, Small Interfering , Antagomirs , Prostatic Neoplasms/geneticsABSTRACT
<p><b>OBJECTIVE</b>To study the effects of carbon disulfide (CS(2)) on the health of workers, and to provide the basis for the further preventive measures.</p><p><b>METHODS</b>The occupational health examination of 881 workers exposed to CS(2) in a chemical fiber factory was carried out according to the national technical standard of occupational health surveillance. The time weighted average concentrations (TWA) of CS(2) in the workshops of short silk and long silk exceeded the national standard, The workers in these two workshops served as the high exposure group. The workers of the other workshops were classified as low exposure group, in which TWA met the national standard. All exposed workers were also divided into long-term exposure group and short-term exposure group on the basis of average exposure years (16 years). The statistical analysis was used by t test, χ(2), and fisher exact test.</p><p><b>RESULTS</b>The symptom rates of numbness, fatigue, dizziness, insomnia and headache were 12.5%, 8.5%, 8.2%, 7.5%, and 7.2% respectively. The abnormal rates of superficial sensation, three fibrillation, achilles tendon reflex, patellar reflex, EMG, hypertension, triglycerides, low-density lipoprotein, and apolipoprotein B were 33.0%, 26.1%, 20.8%, 18.6%, 10.8%, 33.4%, 24.5%, 17.0% and 9.3% respectively. Among the high exposure group, the abnormal detectable rates of dizziness, headache, fatigue, insomnia, numbness, achilles tendon reflex, superficial and deep sensation, EMG, hypertension, ECG, total cholesterol, triglyceride and low density lipoprotein in long-term exposure group were significantly higher than those in short-term exposure group (P < 0.05 or P < 0.01). However, among the low exposure group, the abnormal rates of the insomnia achilles tendon reflex and superficial sensation in long term exposure group were significantly higher than those of short term exposure group (P < 0.05 or P < 0.01). The detected rates of hypertension, triglycerides, low-density lipoprotein, creatinine and uric acid were in males significantly greater than those in females (P < 0.05 or P < 0.01).</p><p><b>CONCLUSION</b>Long-term exposure to high concentrations of CS(2) could lead to the damage of nervous system, elevate blood pressure and promote the development and progression of hyperlipemia and atherosclerosis. Furthermore, CS(2) had greater effects on blood pressure and lipid in males than in females.</p>
Subject(s)
Adult , Female , Humans , Male , Middle Aged , Young Adult , Carbon Disulfide , Cardiovascular System , Chemical Industry , Health Status , Multiphasic Screening , Nervous System Diseases , Epidemiology , Occupational ExposureABSTRACT
<p><b>OBJECTIVE</b>To analyze the clinical characteristics of 267 cases with occupational chronic carbon disulfide (CS(2)) poisoning and to provide the basis for revising the items of periodical medical examination of workers occupationally exposed to CS(2).</p><p><b>METHODS</b>The subjects of present study were 267 patients with mild CS(2) poisoning diagnosed according to "Diagnostic Criteria of Occupational Chronic Carbon Disulfide Poisoning (GBZ4-2002)" from April in 2006 to May in 2010. All patients were from the same chemical fiber factory. When a subject was diagnosed as patient with CS(2) poisoning, who should interview with questionnaire which included the illness and occupational history, symptoms, individual habits. The physical examination, nervous test, cardiovascular test, biochemical test and electromyogram were performed.</p><p><b>RESULTS</b>The rate of decreased motor conduction velocity was 87.3% (233/267 roots). The highest detection rate of slowing conduction velocity was the common peroneal motor nerve which was 48.6% (138/248 roots) and the second was median motor nerve with delay rate of 37% (155/419 roots). The main symptoms of the patients were neurasthenia, numbness and paresthesia. The rates of abnormal achilles tendon reflex and knee jerk reflex in patients were were 79.4% and 49.8%, respectively. The detected rates of patients with ST-segment changes and hypertension were 19.1% and 27.5%, respectively. The rates of hypertension, systolic pressure and diastolic pressure were 27.3%, 22.5% and 21.1%, respectively. The rates of lactate dehydrogenase (LDH), triglycerides (TG) and low density lipoprotein (LDL) were high. The detected rates of urine acid, indirect bilirubin and total bilirubin in male patients were higher than those in female patients. In addition, the abnormal detected rate of urea nitrogen and indirect bilirubin increased with exposure years.</p><p><b>CONCLUSION</b>Occupational chronic CS(2) poisoning mainly affects the nervous system, as well as liver and kidney function. Detecting the median and common peroneal motor nerve conduction velocities could be the screening indicators for the peripheral nerve injury induced by CS(2) in the occupational exposure population during the periodical occupational medical examinations.</p>
Subject(s)
Adult , Aged , Female , Humans , Male , Middle Aged , Carbon Disulfide , Poisoning , Chemical Industry , Kidney , Liver , Multiphasic Screening , Nervous System , Neural Conduction , Occupational ExposureABSTRACT
<p><b>OBJECTIVE</b>To explore the role of -1C/T single nucleotide polymorphism within Annexin A5 gene in the genetic susceptibility to coal worker's pneumoconiosis (CWP).</p><p><b>METHODS</b>Four hundred and seventy CWP Han chinese patients and 428 Han chinese controls were enclosed in present case-control study. All subjects were exposed to coal dusts. The polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was used to detect the -1C/T SNP in Annexin A5 gene for all subjects. The relationship between the -1C/T SNP in Annexin A5 gene and CWP was analyzed.</p><p><b>RESULTS</b>CT/TT genotype in -1C/T SNP was associated with a significantly decreased risk of CWP, as compared with the CC genotype among subgroups exposed to coal dusts for ≥ 27 years (adjusted OR = 0.65, 95%CI: 0.44 - 0.98, P = 0.039) and patients with CWP at stage II (adjusted OR = 0.55, 95%CI: 0.34 - 0.90, P = 0.028).</p><p><b>CONCLUSION</b>The results of present study suggest that the Annexin A5 -1C/T polymorphism may be involved in the development of CWP in Han Chinese coal miners.</p>
Subject(s)
Aged , Humans , Male , Middle Aged , Annexin A5 , Genetics , Anthracosis , Genetics , Asian People , Genetics , Case-Control Studies , Gene Frequency , Genetic Predisposition to Disease , Genotype , Polymorphism, Single NucleotideABSTRACT
<p><b>OBJECTIVE</b>The main purpose of this work was to give the evidence of reasonable and feasible dust control measures which will be taken in the future by analyzing the trend of dust concentration from 1991 to 2010 and identifying working faces with the severe dust contamination in one underground iron mine.</p><p><b>METHODS</b>The data was from routine monitoring between the years 1991 and 2010, which enclosed the total dust concentrations and silica contents. China National Standard of Occupational exposure limits for hazardous agents in the workplace used to judge whether the dust concentration exceeded the National Standard.</p><p><b>RESULTS</b>The general trend of total dust concentration from 1991 to 2010 was decreased, especially maximum and average levels. The highest exceeding rate was 43.16% in 1993 and the best years were 2009 and 2010, but the exceeding rates were still over 30%. The dust exposure levels varied with different work faces. The mining and supporting were the most severe dust pollution faces which the highest ultra exceeding rates were 51.61% and 51.48% and the maximum exceeding times were 64.6 and 16.4 respectively. The next was constructing face with 40.23% exceeding rate and 24.6 times more than standard.</p><p><b>CONCLUSION</b>The trend of total dust concentration from 1991 to 2010 was decreased, but the dust exceeding rate was still high. The strong measures should be taken to control the dust pollution in this iron mine, especially mining and supporting faces.</p>
Subject(s)
Air Pollutants, Occupational , Dust , Environmental Monitoring , Iron , Mining , Occupational ExposureABSTRACT
<p><b>OBJECTIVE</b>To investigate the association between the promoter polymorphism -509C/T of the transforming growth factor-β1 gene (TGFB1) and the disease severity of allergic rhinitis (AR) in childhood.</p><p><b>METHODS</b>A total of 96 Chinese patients with persistent AR aged 3 - 17 (9.4 ± 3.8) years old were enrolled in the study. Among these patients 53.1% were mild cases (n = 51) and 46.9% were moderate-to-severe cases (n = 45). Genotyping was performed on peripheral blood genomic DNA by using PCR-RFLP. Serum levels of TGF-β1 was measured by ELISA, and serum total IgE, specific IgE and eosinophil cationic protein (ECP) levels were determined using an ImmunoCAP100E system. Statistical analysis was conducted with SPSS11.0 software.</p><p><b>RESULTS</b>Significant differences were found in genotype frequencies for the TGFB1-509C/T polymorphism between mild and moderate-to-severe AR patients (χ(2) = 8.361, P = 0.015). Children with persistent AR bearing the TT genotype of the -509C/T polymorphism had significantly increased risk for moderate-to-severe AR (Fisher's exact test, P = 0.007) compared to children with the CC/CT genotypes. There was no significant association between the -509C/T polymorphism and serum TGF-β1 levels (F = 0.389, P = 0.679); however, serum total IgE (F = 4.210, P = 0.018) and ECP (H = 6.297, P = 0.043) levels were found to be significantly associated with the polymorphism.</p><p><b>CONCLUSION</b>The results suggest that the TGFB1 gene polymorphism -509C/T may play a potential role in the severity of persistent AR in childhood.</p>
Subject(s)
Adolescent , Child , Child, Preschool , Female , Humans , Male , Gene Frequency , Genetic Predisposition to Disease , Genotype , Polymorphism, Single Nucleotide , Promoter Regions, Genetic , Rhinitis, Allergic, Perennial , Genetics , Transforming Growth Factor beta1 , GeneticsABSTRACT
<p><b>OBJECTIVE</b>To study the early effects of coal dust on lung function in new underground coal miners.</p><p><b>METHODS</b>Two hundred and eighty-seven male miners were selected from new employees at the Xuzhou Mining Group Company as study group, and 132 male students at a mining technical school were selected as control. Data collection included: individual demographic parameters, family medical history, occupational history, and smoking history, measurement of dust concentrations in work areas, and lung function tests. This prospective cohort study took place over 3 years during which time total dust and respirable dust concentrations in the new coal miners' work areas were measured twice each month. For both miner and student groups, FVC and FEV(1) were tested initially before dust exposure, and then 15 times over the 3 years.</p><p><b>RESULTS</b>The average total dust and respirable dust concentrations in the miners' work areas were 23.8 mg/m(3) and 8.9 mg/m(3) respectively, which greatly exceeded national health criteria. During the first year of dust exposure, the miners's average FVC was higher than that of the controls (5.19 L vs 4.92 L, P < 0.01). During the 2nd and 3rd year the difference in average FVC between miners and control group was not significant (5.14 L vs 5.12 L, P > 0.05). Before dust exposure, the miners' FEV(1) was significantly higher than that of the control group (4.48 L vs 4.28 L). In the miners group, FEV(1) declined rapidly during the first year following dust exposure (from 4.48 L to 4.25 L), and in the 2nd and the 3rd year the average FEV(1) of the miners was significantly lower than that of controls (4.34 L vs 4.56 L, P < 0.01), although there were some fluctuations during the follow-up period. Overall, the average FEV(1) of miners group showed a significant decline during the study. There were significant correlations between FVC or FEV(1) and age, height, weight, and smoking. The three-year total loss of FVC and FEV(1) in smoking miners (154 ml, 184 ml) were greater than in non-smoking miners (83 ml, 91 ml).</p><p><b>CONCLUSION</b>There are apparent effects of coal dust on lung function in new underground coal miners, with FEV(1) being more impacted than FVC. Smoking may aggravate the effect of dust exposure on reducing lung function.</p>
Subject(s)
Adolescent , Adult , Humans , Male , Coal Mining , Cohort Studies , Dust , Forced Expiratory Volume , Inhalation Exposure , Occupational Exposure , Prospective Studies , Pulmonary Ventilation , Physiology , SmokingABSTRACT
This article considers how China's medical schools can best prepare tomorrow's doctors for coping with the health needs of a society undergoing rapid industrialization and urbanization, where most of the life-threatening infectious diseases have been controlled. Preventive medicine assumes overriding importance and this implies that students should gain practical experience as well as theoretical knowledge of social conditions