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Objective To analyze the risk factors of delayed recovery after laparoscopic prostate or bladder cancer radical surgery, and to provide information for early clinical prevention. Methods Three hundred and twenty-two cases of patients who underwent laparoscopic radical prostatectomy or bladder cancer surgery from September 2016 to January 2019 were enrolled in this study. The clinical data and surgical data of the patients were collected, the incidence of postoperative recovery delay was counted, and the risk factors of delayed recovery were analyzed by Logistic regression analysis. Results Six-noe cases of delayed recovery of laparoscopic prostate or bladder cancer were detected, the incidence rate was 18.1% (61/327) ; Univariate analysis found that delayed laparoscopic recovery of prostate or bladder cancer after radical surgery and age, combined with coronary heart disease, diabetes, respiratory disease, anemia, smoking, alcohol consumption, American Society of Anesthesiologists (ASA) classification, anesthesia time, intraoperative infusion, location clarity of anatomical landmarks were related. There was a correlation between the total amount, combined epidural anesthesia and intraoperative blood transfusion (P<0.05). Multivariate logistic regression analysis found that the age, diabetes, respiratory disease, anemia, smoking, alcohol consumption, location clarity of anatomical landmarks and intraoperative total infusion were independent risk factors for delayed recovery after laparoscopic prostate cancer or radical surgery for bladder cancer (P<0.05). Conclusion There is correlation between delayed laparoscopic recovery of prostate cancer or bladder cancer after radical operation and age, diabetes, respiratory disease, anemia, smoking, alcohol consumption, location clarity of anatomical landmarks and intraoperative total infusion. Accurate anatomical location can reduce the risk of postoperative recovery delay. It is conducive to the recovery of the patients after operation, and the corresponding hospitalization time of the patients is greatly shortened.
ABSTRACT
Chronic obstructive pulmonary disease (COPD) is a heterogeneous disease characteristic of small airway inflammation, obstruction, and emphysema. It is well known that spirometry alone cannot differentiate each separate component. Computed tomography (CT) is widely used to determine the extent of emphysema and small airway involvement in COPD. Compared with the pulmonary function test, small airway CT phenotypes can accurately reflect disease severity in patients with COPD, which is conducive to improving the prognosis of this disease. CT measurement of central airway morphology has been applied in clinical, epidemiologic, and genetic investigations as an inference of the presence and severity of small airway disease. This review will focus on presenting the current knowledge and methodologies in chest CT that aid in identifying discrete COPD phenotypes.
Subject(s)
Humans , Airway Obstruction , Phenotype , Pulmonary Disease, Chronic Obstructive/diagnostic imaging , Pulmonary Emphysema/diagnostic imaging , Tomography, X-Ray ComputedABSTRACT
<p><b>OBJECTIVE</b>To investigate effects of paraquat on the mRNA expression of key elements of Notch signaling (Notch1, Jagged1 and DTX1) during differentiation process of human neural stem cells (hNSCs).</p><p><b>METHODS</b>hNSCs exposed to PQ at the concentrations 0.10, 1.00, 10.00 M. Cell proliferation ability was assessed using MTT assay and mRNA expressions of Notch1, Jagged1 and DTX1 were detected by Real-time RT-PCR at 2, 4, 8, 12 d of differentiation.</p><p><b>RESULTS</b>Compared with control group, NOTCH1, JAG1 mRNA expression levels exposed to PQ at the concentration of 0.10 M significantly reduced at 2, 4, 8 d and significantly went up at 12d (P < 0.01). Compared with control group, NOTCH1, JAG1 and DTX1 mRNA expression levels exposed to PQ at the concentration of 10.00 M significantly reduced at 2, 8, 12 d (P < 0.01). PQ could down-regulate Notch1, Jagged1 and DTX1 mRNA expressions at the early stage of differentiation, then up-regulate Notch1 mRNA expression, and down-regulate Notch1, Jagged1 and DTX1 mRNA expressions at the end of differentiation.</p><p><b>CONCLUSION</b>Notch signaling pathway may be involved in differentiation of neural stem cell exposed to PQ.</p>
Subject(s)
Humans , Calcium-Binding Proteins , Metabolism , Cell Differentiation , Cells, Cultured , Embryonic Stem Cells , Cell Biology , Metabolism , Intercellular Signaling Peptides and Proteins , Metabolism , Jagged-1 Protein , Membrane Proteins , Metabolism , Neural Stem Cells , Cell Biology , Metabolism , Paraquat , Pharmacology , Receptor, Notch1 , Metabolism , Serrate-Jagged Proteins , Signal Transduction , Ubiquitin-Protein Ligases , MetabolismABSTRACT
<p><b>OBJECTIVE</b>To establish a method for determination 1-bromopropane (1-BP) in workplace air by gas chromatography-flame ionization detector (GC-FID).</p><p><b>METHOD</b>1-bromopropane in workplace air was collected with activated charcoal tube, then desorbed by carbon disulfide and determined by GC-FID. 1-bromopropane was quantitatively measured using retention time and peak area.</p><p><b>RESULTS</b>Linear regression formula was Y = 3353.4x-10064 in a range of 2.50 ∼ 500.00 µg/ml with regression coefficient R = 0.9998. Detection limit was 0.25 µg/ml and the lowest detection concentration of 1-brmopropane in air was 0.14 mg/m(3) (at air volume 1.8L). The mean recoveries of 1-BP were between 96.8% and 102.6%, and relative standard deviation of inter and intra-assay was less than 10%. The average desorption efficiencies were between 93.2% and 104.4%. The samples in activated charcoal tube could be stably stored for 5 days at room temperature.</p><p><b>CONCLUSION</b>The method could be feasible to determine 1-bromopropane in workplace air.</p>
Subject(s)
Air , Air Pollutants, Occupational , Chromatography, Gas , Methods , Hydrocarbons, Brominated , WorkplaceABSTRACT
<p><b>OBJECTIVE</b>To observe the expressions of α-SMA, integrin α5 and fibronectin (Fn) in acute paraquat poisoned rats and the effect of PDTC. To investigate the mechanism of paraquat-induced pulmonary fibrosis.</p><p><b>METHODS</b>Sprague-Dawley rats were randomly divided into three experimental groups: Control group (6 rats), PQ group (36 rats) and PQ+PDTC group (36 rats). On the 1st, 3rd, the 7th, the 14th, the 28th and the 56th day after exposure, the protein expression of α smooth muscle actin (α-SMA) was evaluated by western blot. The mRNA levels of integrin α5 and fibronectin (Fn) were analyzed with real-time quantitative PCR (RT-PCR). Meanwhile, the lung pathological changes were observed and semi-quantified.</p><p><b>RESULTS</b>T With the time passing, the expression of α-SMA in PQ group increased gradually compared with control group (P < 0.05 or P < 0.01). The increasing extent was gently on the 3 rd, the 7 th day. While increasing extent was rapidly from the 28 th to the 56 th day. RT-PCR showed PQ significantly increased Fn mRNA level on all time points and increased integrin α5 mRNA level from the 7 rd to 56 th day compared with control group (P < 0.05 or P < 0.01). PDTC treatment significantly deceased α-SMA, Fn, and integrin α5 levels compared with PQ group in corresponding time points (P < 0.05 or P < 0.01) Noteworthy, in PQ+PDTC group, the occurrence of pathological changes were drastically attenuated and pathologic score significantly decreased (P < 0.05 or P < 0.01).</p><p><b>CONCLUSIONS</b>α-SMA, integrin α5 and fibronectin could play an important role in the development of pulmonary fibrosis caused by paraquat poisoning. PDTC, asa strong NF-κB inhibitor, may inhibit NF-κB activity and further significantly decreased expressions of α-SMA, integrin α5 and fibronectin which were important part of ECM, leading to drastically attenuated pulmonary fibrosis. However, the mechanisms of PDTC intervention still remains to be explored.</p>
Subject(s)
Animals , Male , Rats , Actins , Metabolism , Disease Models, Animal , Fibronectins , Metabolism , Integrin alpha5 , Metabolism , Paraquat , Poisoning , Pulmonary Fibrosis , Metabolism , Pyrrolidines , Pharmacology , Rats, Sprague-Dawley , Thiocarbamates , PharmacologyABSTRACT
<p><b>OBJECTIVE</b>To observe the changes in the expression of connective tissue growth factor (CTGF), type I collagen (Col I), and type III collagen (Col III) among the rats with acute paraquat (PQ) poisoning and the intervention effect of pyrrolidine dithiocarbamate (PDTC) on their expression, and to investigate the mechanism of PQ-induced pulmonary fibrosis and the intervention effect of PDTC on the disease.</p><p><b>METHODS</b>Sprague-Dawley rats were randomly divided into control group (n = 6), PQ group (n = 36), and PQ + PDTC group (n = 36). The PQ group and PQ + PDTC group were given a single dose of saline-diluted PQ (80 mg/kg) by gavage; 2 h later, the PQ + PDTC group was intraperitoneally injected with a single dose of PDTC (100 mg/kg), and the PQ group was intraperitoneally injected with the same amount of saline. The control group was given saline (1 ml/kg) by gavage and was intraperitoneally injected with the same amount of saline 2h later. At 1, 3, 7, 14, 25, and 56 days after operation, the protein expression of CTGF was evaluated by Western blot; the mRNA expression of CTGF, Col I, and Col III was analyzed by real-time quantitative PCR; the content of hydroxyproline in lung tissue was measured, and the pathological changes of lung tissue of the poisoned rats were observed.</p><p><b>RESULTS</b>The protein expression of CTGF in the PQ group increased as the time went on, slowly from the 3rd to the 14th day and rapidly from the 28th to the 56th day, significantly higher than that in the control group at each time point (P < 0.05 or P < 0.01). The mRNA expression of CTGF in the PQ group began to rise markedly on the 1st day, increased rapidly from the 3rd to the 14th day, and remained at a relatively high level from the 28th to the 56th day, significantly higher than that in the control group at each time point (P < 0.01). The mRNA expression of Col I in the PQ group changed little on the 1st and 3rd day, increased slightly on the 7th day, and increased greatly from the 14th to the 56th day, significantly higher than that in the control group from the 7th to the 56th day (P < 0.05 or P < 0.01). The mRNA expression of Col III in the PQ group began to rise on the 1st day, reached the peak level on the 7th day, and then declined, significantly higher than that in the control group at each time point (P < 0.05 or P < 0.01). Masson staining showed that fibroblasts proliferated from the 14th to the 28th day, and collagen fibers increased gradually. Compared with the PQ group, the PQ + PDTC group showed significantly decreased protein expression of CTGF as well as mRNA expression of CTGF, Col I, and Col III (P < 0.05 or P < 0.01).</p><p><b>CONCLUSION</b>In PQ-induced pulmonary fibrosis, the expression of CTGF keeps rising, and the collagen secretion and matrix synthesis are increased probably by upregulating the transcriptional levels of Col I and Col III; CTGF plays an important role in PQ-induced pulmonary fibrosis. PDTC can inhibit the expression of CTGF, thus reducing the lung injury in rats with PQ poisoning.</p>
Subject(s)
Animals , Male , Rats , Collagen Type I , Metabolism , Collagen Type III , Metabolism , Connective Tissue Growth Factor , Metabolism , Paraquat , Poisoning , Proline , Pharmacology , Pulmonary Fibrosis , Metabolism , Rats, Sprague-Dawley , Thiocarbamates , PharmacologyABSTRACT
<p><b>OBJECTIVE</b>To study the involvement of excitatory amino acid system in astrocytes activation caused by dimethoate.</p><p><b>METHODS</b>Pure-cultured astrocytes were gained by three passages from primary cultured rat nerve cells, then treated with 10(-6),10(-5),10(-4) mol/L dimethoate for 48 h, 50 micromol/L and 100 micromol/L MK801, a NMDA receptor blocker, was used to intervene the effects induced by 10(-4) mol/L dimethoate. HPLC-FLD was utilized to measure the concentrations of excitatory amino acid (EAA), RT-PCR was used to detect the expression levels of NR2B, GLT-1, GLAST, GFAP and S100beta mRNA, and immunofluorescence staining method was applied to measure the expression levels of GFAP and S100beta proteins.</p><p><b>RESULTS</b>The expression levels of GLAST mRNA in all exposure groups were 67.8%, 68.6% and 76.2% of control level, respectively, which were significantly lower than that of control group (P < 0.05); The concentrations of EAA significantly decreased in 10(-4) mol/L dimethoate group, as compared with control group (P < 0.01); the expression levels of GFAP mRNA in 10(-4) mol/L dimethoate group, of S100beta mRNA in 10(-5) mol/L dimethoate group, of GFAP protein in 10(-4) mol/L and 10(-5) mol/L dimethoate groups and S100beta protein in 10(-4) mol/L dimethoate group were significantly higher than those in control group (P < 0.01). The expression levels of GLT-1 and GLAST mRNA in 10(-4) mol/L dimethoate plus 50 micromol/L or 100 micromol/L MK801 groups increased significantly, as compared with 10(-4) mol/L dimethoate group (P < 0.01), the expression levels of NR2B mRNA in 10(-4) mol/L dimethoate plus 50 micromol/L or 100 micromol/L MK801 groups increased significantly, as compared with control group (P < 0.05 or P < 0.01); the concentration of Glu in 10(-4) mol/L dimethoate plus 100 micromol/L MK801 group increased significantly, as compared with 10(-4) mol/L dimethoate group (P < 0.01); the expression levels of GFAP mRNA and protein in 10(-4) mol/L dimethoate plus 50 micromol/L or 100 micromol/L MK801 groups decreased significantly (P < 0.01); S100beta protein expression level in 50 micromol/L MK801 intervention group was significantly higher than thatl in control group (P < 0.01).</p><p><b>CONCLUSION</b>Excitatory amino acid system involved in astrocytes activation caused by dimethoate. MK801 was useful to control astrocytes gliosis.</p>
Subject(s)
Animals , Rats , Astrocytes , Metabolism , Cells, Cultured , Dimethoate , Toxicity , Dizocilpine Maleate , Pharmacology , Excitatory Amino Acids , Metabolism , Receptors, N-Methyl-D-AspartateABSTRACT
<p><b>OBJECTIVE</b>To establish the method of detecting the concentrations of bisphenol A (BPA)in air of workplaces with high performance liquid chromatographic (HPLC).</p><p><b>METHODS</b>According to standards of methods for determining the chemical substances in workplace air, BPA in the air was collected by glass fiber filter, then dissolved by acetonitrile and determined by high performance liquid chromatography with FLD.</p><p><b>RESULTS</b>There was a linear relationship within the range of 0.01-10.0 pg /ml, and the detection limit was 0.005 pg/ml. The lowest detected concentration was 3.3x10-5 mg/m3. The relative standard deviation was 2.5-5.5%. The dissolution efficiencies were 95.0%-101.9% and the sampling efficiencies were 99.6%. The samples in glass fiber filter membrane could be stored for 7 days at room temperature.</p><p><b>CONCLUSION</b>The present method could meet with the requirements of Guide for establishing occupational health standards-Part 4 Determination methods of air chemicals in workplace and be feasible for determination of BPA in workplace air.</p>
Subject(s)
Air Pollutants, Occupational , Benzhydryl Compounds , Chromatography, High Pressure Liquid , Methods , Environmental Monitoring , Methods , Reference Standards , Phenols , WorkplaceABSTRACT
<p><b>OBJECTIVE</b>To investigate the effects of controlling the specific dangerous pesticides on prevention of acute pesticide poisoning in rural area.</p><p><b>METHODS</b>The data of reported cases of pesticide poisoning were analyzed to find out the specific dangerous pesticide in acute pesticide poisoning. Then the occurrence of occupational pesticide poisoning and fatality of non-occupational pesticide poisoning were estimated under the hypothesis of removing the specific dangerous pesticides.</p><p><b>RESULTS</b>The data indicated that parathion (including methyl parathion) was the specific dangerous pesticide inducing occupational pesticide poisoning. After removing the use of parathion, the hazard of pesticides which caused occupational pesticide poisoning would be significantly decreased (P < 0.01). Parathion was also the most dangerous pesticide which caused non-occupational pesticide poisoning, with its fatality up to 15.8%. If parathion was well controlled, the fatality of non-occupational pesticide poisoning would be declined from 9.4% to 7.4%. The analyses of related literatures also revealed the similar results.</p><p><b>CONCLUSION</b>The occurrence of occupational pesticide poisoning and fatality of non-occupational pesticide poisoning may decrease if the most dangerous pesticides are well supervised.</p>
Subject(s)
Humans , Occupational Health Services , Methods , Pesticides , Poisoning , Poisoning , SuicideABSTRACT
<p><b>OBJECTIVE</b>to observe the expression of the connective tissue growth (CTGF) and a smooth muscle actin (α-SMA) in acute paraquat (PQ) poisoned rats and investigate the mechanism of paraquat-induced pulmonary fibrosis.</p><p><b>METHODS</b>sprague-Dawley rats were randomly divided into two experimental groups: control group (6 rats) and PQ group (56 rats). On the 3rd, the 7th, the 14th, the 28th and the 56th day after exposure, the expression of CTGF and α-SMA were evaluated by SABC Immunohistochemistry and Western blot; and the relationship of the expression with pathologic score, hydroxyproline were also analyzed, respectively. The lung pathological changes of rats were observed and pathological evaluation was made.</p><p><b>RESULTS</b>it was similar that the expression pattern of CTGF, α-SMA detected by immunohistochemistry and Western blot. With the time passing, their expression in PQ group increased gradually compared with control group (P < 0.05 or P < 0.01). The increasing extent of CTGF, α-SMA were gentle on the 3rd, the 7th day. While their increasing extent was rapid from the 14th to the 56th day. CTGF was positively correlated with α-SMA, pathologic score and hydroxyproline respectively (r = 0.74, r = 0.87, r = 0.71, P < 0.05 or P < 0.01). Meanwhile, the histological changes such as lung fibroblast proliferation, disorganized collagen fibers were observed in PQ group.</p><p><b>CONCLUSION</b>CTGF and α-SMA could play an important role in the development of pulmonary fibrosis caused by paraquat poisoning; CTGF may promote the transformation of fibroblasts to myofibroblasts and further strengthen the ability of synthesis collagen and extracellular matrix.</p>
Subject(s)
Animals , Male , Rats , Actins , Metabolism , Connective Tissue Growth Factor , Metabolism , Paraquat , Toxicity , Pulmonary Fibrosis , Metabolism , Pathology , Rats, Sprague-DawleyABSTRACT
<p><b>OBJECTIVE</b>To explore the dose-effect relationship between lead exposure and nerve conduction velocity, and to assess risk characteristics of nerve conduction velocity induced by lead exposure.</p><p><b>METHODS</b>The external dose, internal dose (blood lead, urine lead) and the conduction velocity of peripheral nerve were examined. The benchmark dose of a population exposed to occupational lead was estimated to develop risk assessment of nerve conduction velocity in worker exposed to lead by use of BMDS (version 1.3.3). The BMDL in terms of blood lead and urine lead was calculated.</p><p><b>RESULTS</b>There was correlation between blood lead and urine lead. The sense nerve conduction velocity was decreased significantly in the group of lead exposure workers (P < 0.05). The BMDLs-05 for median nerve conduct velocity, ulnar nerve conduction velocity, and superficial peroneal nerve conduction velocity in terms of blood lead were 456.99, 332.36 and 468.38 microg/L respectively; the BMDLs-05 in terms of urine lead were 14.1, 9.2 and 13.6 microg/gCr respectively.</p><p><b>CONCLUSION</b>The internal dose is the better index to reflect the level of lead exposure. Blood lead is identified as a specific and sensitive biomarker for sense nerve conduction velocity reduction. Ulnar nerve conduction velocity can be used as highly sensitive biomarkers to screen the high risk population of lead exposure.</p>
Subject(s)
Adolescent , Adult , Aged , Female , Humans , Male , Middle Aged , Young Adult , Biomarkers , Blood , Lead , Blood , Lead Poisoning , Blood , Neural Conduction , Occupational Exposure , Risk Assessment , Surveys and QuestionnairesABSTRACT
<p><b>OBJECTIVE</b>To determine the long-term testicular effect after neonatal exposure to 2,2', 4,4',5,5'-hexa-chlorobiphenyl (PCB153).</p><p><b>METHODS</b>On birth day (Postnatal day 0, PNDO), the Sprague-Dawley (SD) male rats were mixed together and divided into 12 pups/litter. At PND1, the rats were grouped randomly into control and treatment groups according to different litters, 24 pups/group. They were treated by oral gavage with PCB153 in corn oil at doses of 0, 0.025, 0.250 and 2.500 mg/kg BW-day from PNDI to PND7. The rats were sacrificed at PND8 and PND90 by anesthesia. The testes were collected and weighed for histological examination and daily sperm production at PND8 or/and PND90. The epididymidis and the epididymidis cauda also were collected and weighed for determination the sperm counts at PND90.</p><p><b>RESULTS</b>The body weight of 2.500 mg/kg dose group was decreased significantly from PND3 to PND8 compared with that of control (P < 0.05). At PND8, the loose structure in seminiferous cord and the spermatogonia with enlarged volume and detached from the cord were observed in 2.500 mg/kg dose group by light microscope and electronic microscopy. With the increase of exposure doses, the testicular daily sperm production (DSP) and the sperm counts of epididymidis cauda were decreased in dose-dependent manner at PND90. The DSP in 0.250 mg/kg [30 x 10(6)/testis(g)] and 2.500 mg/kg [18 x l0(6)/testis(g)] dose groups were significantly reduced compared with that of control [36 x 10(6)/testis(g)] (P < 0.05). And there was a significant reduction in the sperm counts of epididymidis cauda in 0.250 mg/kg [42 x 10(7)/epididymidis cauda (g)] and 2.500 mg/kg [18 x 10(7)/epididymidis cauda (g)] dose groups compared with that of control [51 x 10(7)/epididymidis cauda (g)] (P < 0.05).</p><p><b>CONCLUSIONS</b>The spermatogenesis of adult testis is disturbed, which causes the decrease in the testicular DSP and the sperm counts of epididymidis cauda after neonatal exposure to PCB153. The long-term damage in male reproductive function is caused by neonatal exposure to chemicals.</p>
Subject(s)
Animals , Male , Rats , Animals, Newborn , Environmental Exposure , Polychlorinated Biphenyls , Toxicity , Rats, Sprague-Dawley , Sperm Count , Spermatogenesis , Testis , PathologyABSTRACT
<p><b>OBJECTIVE</b>To explore the dose-effect relationship between 1-bromopropane (1-BP) exposure and health effects in workers.</p><p><b>METHODS</b>Occupational field investigations were conducted in 1-BP factories. Ambient 1-BP concentrations were detected with detection tube, and the 8 h time-weighted average individual exposure levels (TWA-8 h) were measured by passive sampler. Workers underwent questionnaire survey, neurological examination, nerve conduction velocity examination, vibration sensation test. routine blood test as well as blood biochemical test. According to TWA values or TWA x duration values, workers were divided into three dose groups for dose-effect relationship analysis. USEPA BMDS 2.1 software was applied to calculate 1-BP benchmark dose (BMD) and its 95% lower limit (BMDL).</p><p><b>RESULTS</b>The TWA-8h concentrations ranged from 0.35 to 535.19 mg/m3 (geo-mean 14.08 mg/m3). Dose-dependent analysis showed that the motor nerve distal latency (linear regression coefficient was 0.066 6), vibration sensation of toes (linear regression coefficient were 0.157 2 and 0.193 9), creatine kinase (linear regression coefficient was -1.05) and thyroid stimulating hormone levels (linear regression coefficient was 0.1024) of 1-BP exposed workers changed in a dose-dependent manner (P < 0.05). BMD calculation based on DL as 1-BP toxic effect endpoint showed that TWA-8h of the BMD values and BMDL values were 50.55 mg/m3 and 30.78 mg/m3, respectively.</p><p><b>CONCLUSION</b>1-BP causes dose-dependent changes in tibial nerve DL, vibration sensation, CK and TSH levels.</p>
Subject(s)
Adult , Female , Humans , Creatine Kinase , Blood , Hydrocarbons, Brominated , Toxicity , Maximum Tolerated Dose , Neural Conduction , Occupational Exposure , Tibial Nerve , WorkplaceABSTRACT
<p><b>OBJECTIVE</b>To investigate the health effects of 1-bromopropane (1-BP) on female exposed workers.</p><p><b>METHODS</b>Four 1-BP manufacturing plants were investigated. Workers were interviewed with questionnaire and examined with neurobehavioral core test battery, nerve conduction velocity tests of nervus tibialis and nervus suralis, vibration sensation test, hematological and biochemical tests. Ambient 1-BP concentration was measured with detection tube, and time-weighed average levels of individual workers were estimated with passive samplers.</p><p><b>RESULTS</b>1-BP concentration in the plants ranged from 0 to 402.40 mg/m3 (Geomean 32.19 mg/m3). Time-weighted average exposure levels (TWA-8 h) ranged from 0.35 to 535.19 mg/m3 (Geomean 14.08 mg/m3). Compared with the control group, 1-BP exposed workers showed reduced motor nerve conduction velocity [(44.8 +/- 8.7) m/s] and sensory nerve conduction velocity [(45.5 +/- 4.9) m/s], prolonged distal latency [(7.5 +/- 2.1) ms], reduced toe vibration perception, and altered neurobehavior parameters(POMS vigor, tension, anxiety, confusion) significantly (P < 0.05). As to hematological and biochemical indicators, the exposed workers showed decreased white blood cell count [(5.6 +/- 2.17) x 10(3)/microl], red blood cell count [(3.9 +/- 0.4) x 10(6)/microl], hemoglobin [(121.1 +/- 14.5) g/L] and creatine kinase [(82.0 +/- 27.5) IU/L] (P < 0.05), and increased serum total protein (8.0 +/- 0.5 g/dl), lactate dehydrogenase [(335.2 +/- 356.6) IU/L], thyroid-stimulating hormone [(3.6 +/- 2.3) microIU/ml] and follicle-stimulating hormone levels (18.7 +/- 24.4 mIU/ml) (P < 0.05).</p><p><b>CONCLUSION</b>1-BP exposure may affect peripheral nerves and central nervous system, and lead to abnormal hematological and biomedical indicators.</p>
Subject(s)
Adult , Female , Humans , Middle Aged , Young Adult , Creatine Kinase , Metabolism , Hematologic Tests , Hemoglobins , Metabolism , Hydrocarbons, Brominated , Nervous System , Neural Conduction , Occupational ExposureABSTRACT
<p><b>OBJECTIVE</b>To explore the semen quality of the workers exposed to the xenoestrogen bisphenol A (BPA) was explored.</p><p><b>METHODS</b>A cross-sectional study of 20 BPA exposed and 16 control workers with similar age, physical activities was performed. Tests included quantifying BPA in blood samples and investigating the quantity and quality of semen. Semen parameters were determined with the method recommended by WHO.</p><p><b>RESULTS</b>94.4% exposed workers were found BPA in blood, and the median was 101.94 microg/L. However, only 18.8% control subjects were found BPA in blood, and the median level was 0 microg/L. The sperm density of exposed workers [(68.65 +/- 44.00) x 10(6)/ml] was significantly lower than that of control [(118.56 +/- 98.36) x 10(6)/ml]. Relationship analysis showed the positive relationships (r = 0.44, P < 0.01) between the sperm with quick forward progression and BPA level in blood, negative relationships between the percentage of normal sperm and BPA level in blood (r = -0.62, P = 0.01).</p><p><b>CONCLUSION</b>BPA could affect the sperm density, and may influence the semen quality. More research should be performed on the effect and the mechanism of BPA on man.</p>
Subject(s)
Humans , Male , Benzhydryl Compounds , Chi-Square Distribution , Cross-Sectional Studies , Occupational Exposure , Phenols , Pilot Projects , Semen , Semen AnalysisABSTRACT
<p><b>OBJECTIVE</b>To investigate the effect and mechanisms of dimethoate on the primary cultured cortical neuronal cell injury.</p><p><b>METHODS</b>Cortical neuronal cells were isolated and cultured in serum free medium for 6 days in vitro, and 1, 5, 10, 50 and 100 micromol/L dimethoate were added to the medium and intracellular SOD, MDA and GSH. The content of excitatory amino acid was measured after 48 hours. Flow cytometry was used to detect the neuronal cell apoptosis.</p><p><b>RESULTS</b>After 48 h, the activity of SOD and the content of GSH decreased [(1.04 +/- 0.02), (0.99 +/- 0.02), (0.96 +/- 0.02), (0.91 +/- 0.02) U/mg pro] [(219.35 +/- 6.79), (205.6 +/- 6.29), (194.06 +/- 2.63), (93.68 +/- 7.56) mg/g pro], and the content of MDA increased obviously with 5, 10, 50 and 100 micromol/L dimethoate [(21.22 +/- 0.29), (24.01 +/- 0.34), (27.15 +/- 1.02), (32.91 +/- 1.39) nmol/mg pro]; The content of Asp from 10 to 100 micromol/L dose group was higher than the control group and the content of Glu from 1 to 100 micromol/L dose group was higher than the control group. The apoptosis rate had great significance between 1 to 100 micromol/L dose groups and control group. When treated with dimethoate, MDA content in neuron was positively correlated with the content of EAAs with the increase of dimethoate. The correlative coefficient was 0.937 and 0.759 respectively (P < 0.01), while it was negatively correlated with the content of GSH. The correlative coefficient was -0.868 and -0.801 respectively (P < 0.01).</p><p><b>CONCLUSION</b>The oxidative damage and changes of excitatory amino acid content induced by Dimethoate contribute to the primary cultured rat cortical neuron apoptosis.</p>
Subject(s)
Animals , Rats , Animals, Newborn , Apoptosis , Cells, Cultured , Cerebral Cortex , Cell Biology , Dimethoate , Toxicity , Excitatory Amino Acids , Metabolism , Glutathione , Metabolism , Malondialdehyde , Metabolism , Neurons , Metabolism , Pathology , Oxidative Stress , Rats, Sprague-Dawley , Superoxide Dismutase , MetabolismABSTRACT
<p><b>OBJECTIVE</b>To investigate the effects of neonatal exposure of DNA methylation inhibitor, Cadmium and PCB153 on DNA methylation, apoptosis and spermatogenesis in SD rats.</p><p><b>METHODS</b>Neonatal SD rats were randomly divided into 10 groups and received oral administrations of PCB153 (0.025, 0. 250, 2.500 mg/kg), or Cadmium (1, 2, 4 mg/kg), or positive control 5-Aza-CdR (0.025, 0.250 mg/kg), or vehicle control for five days from PND3. Half of the rats were killed 24 h after the last administration. The remains were fed until 12 weeks. Sperm numbers, apoptosis and DNA methylation levels in testis were investigated.</p><p><b>RESULTS</b>The daily sperm production was significantly decreased in each neonatal exposed group (P < 0.05). Neonatal rats exposed to 5-Aza-CdR and Cadmium reduced the global DNA methylation level, increased apoptosis, while PCB153 exposure did not significantly change DNA methylation and apoptosis.</p><p><b>CONCLUSION</b>Neonatal rats exposed to chemicals could reduce spermatogenesis via multiple pathways. Lower DNA methylation and increased neonatal apoptosis were suggested as one of the causes.</p>
Subject(s)
Animals , Male , Rats , Animals, Newborn , Apoptosis , Cadmium , Toxicity , DNA Methylation , Polychlorinated Biphenyls , Toxicity , Rats, Sprague-Dawley , Spermatogenesis , Testis , Metabolism , PathologyABSTRACT
<p><b>OBJECTIVE</b>To observe the changes of cytokine and NF-kappaB activity in acute paraquat poisoned rats and the effect of PDTC and the mechanism of lung injury caused by paraquat poisoning.</p><p><b>METHODS</b>Sprague-Dawley (SD) rats were randomly divided into three groups: Control group (6 rats), PQ group (56 rats) and PQ + PDTC group (46 rats). On the 1st, the 3rd, the 7th, the 14th, the 28th and the 56th day after treatment, the level of interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF-alpha), transforming growth factor-beta 1 (TGF-beta1) and platelet-derived growth factor (PDGF) in serum were detected; the activity of NF-kappaB in lung tissues was detected.</p><p><b>RESULTS</b>The level of IL-1 beta increased significantly on the 1st, the 3rd, the 7th day in PQ group compared with control group (P<0.01). The content of TGF-beta1 and TNF-alpha in PQ group significantly increased compared with control group (P<0.05 or P<0.01). The level of PDGF significantly increased on the 7th, the 14th, the 28th and the 56th day compared with control group (P<0.01). Meanwhile, IL-1 beta and TNF-alpha were positively correlated with lung coefficient (r=0.37, 0.46, P<0.05 or P<0.01 ); TGF-beta1 and PDGF had positive correlation with hydroxyproline (r=0.56, 0.89, P<0.01). The activity of NF-kappaB in lung tissue of PQ group significantly increased on the 1st, the 3rd, the 7th and 14th day compared with control (P<0.05 or P<0.01). There was a significant decrease of IL-1 beta, TGF-beta1, TNF-alpha and PDGF in PQ + PDTC group compared with PQ group (P<0.05 or P<0.01) in the corresponding sacrifice dates. There was a significant decrease in NF-kappaB activity on the 1st, the 3rd, the 7th day in PQ + PDTC group compared with PQ group (P<0.01).</p><p><b>CONCLUSION</b>The cytokine and NF-kappaB could play an important role in lung injury of poisoned rats. PDTC may inhibit the expression of NF-kappaB and further reduce the production of cytokines, alleviate lung injury in acute paraquat poisoned rats.</p>
Subject(s)
Animals , Male , Rats , Interleukin-1beta , Metabolism , Lung , Metabolism , Pathology , NF-kappa B , Metabolism , Paraquat , Toxicity , Rats, Sprague-Dawley , Transforming Growth Factor beta1 , Metabolism , Tumor Necrosis Factor-alpha , MetabolismABSTRACT
<p><b>OBJECTIVE</b>To investigate the change of oxidative stress and nuclear factor-kappaB (NF-kappaB) activity in acute paraquat (PQ) poisoned rats and the effect of PDTC.</p><p><b>METHODS</b>144 SD rats were randomly divided into four experimental groups: control group (6 rats), PDTC group (36 rats), PQ group (56 rats) and PQ + PDTC group (46 rats). On the 1st, the 3rd, the 7th, the 14th, the 28th and the 56th day after treatment, the level of malondialdehyde (MDA), the activity of glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), catalase (CAT) and myeloperoxidase (MPO) in serum were detected; the content of hydroxyproline (Hyp) and the activity of NF-kappaB in lung tissues were detected; the lung pathological changes of rats were observed.</p><p><b>RESULTS</b>The level of MDA and MPO in serum increased and the activity of GSH-Px, SOD, CAT in serum decreased significantly in PQ group compared with control and PDTC group (P<0.05 or P<0.01) in the corresponding sacrifice dates. There were a significant decrease of MDA and increase of GPx, SOD, CAT in PQ + PDTC group compared with PQ group (P<0.05 or P<0.01) in the corresponding sacrifice dates. The activity of NF-kappaB in lung tissue of PQ group significantly increased on the 1st, the 3rd, the 7th and 14th day compared with control and PDTC group (P<0.01). There was a significant decrease in NF-kappaB activity on the 1st, the 3 rd, the 7th day in PQ + PDTC group compared with PQ group (P<0.05 or P<0.01). The MPO activity on the 14th day was (119.56 +/- 21.23) U/L, was lower than that of PQ group (P<0.05). Meanwhile, the content of Hyp in PQ group was significantly higher than control and PDTC group on the 14th, the 28th and the 56th day (P<0.01), and its content was lower in PQ + PDTC group on the 28th and the 56th day (0.89 +/- 0.05), (0.93 +/- 0.13) microg/mg compared with PQ group (P<0.01). The histological changes such as alveolitis and fibrosis in PQ + PDTC group were slighter than those in PQ group.</p><p><b>CONCLUSION</b>Oxidative stress and NF-kappaB could play an important role in lung injury of poisoned rats. PDTC may improve redox imbalance and inhibit the expression of NF-kappaB and therefore might have therapeutic effect on acute paraquat poisoning.</p>
Subject(s)
Animals , Male , Rats , Disease Models, Animal , Lung , Metabolism , Pathology , NF-kappa B , Metabolism , Oxidative Stress , Paraquat , Toxicity , Rats, Sprague-DawleyABSTRACT
<p><b>OBJECTIVE</b>To investigate the influence of pyrrolidine dithiocarbamate (PDTC) on the expression of transforming growth factor beta(1) (TGF-beta(1)), matrix metalloproteinase-2 (MMP-2) and tissue inhibitor-1 of metalloproteinase (TIMP-1) in rats with pulmonary damage induced by paraquat (PQ).</p><p><b>METHODS</b>Fifty-four healthy male SD rats were randomly assigned into the control group (normal saline), the PQ-treatment groups (4 groups) and the PDTC treatment groups (4 groups). Except the rats in the control group, the rats in the PQ group were gavaged only with 40 mg/kg PQ, and PDTC group with 40 mg/kg PQ plus immediate injection 120 mg/kg PDTC (i.p). On the 3rd, the 7th, the 14th and 28th day after treatments, one group rats of each treatments were sacrificed and lung and blood samples were collected. The level of TGF-beta(1) protein in the plasma, the mRNA expression of TGF-beta(1), MMP-2 and TIMP-1 were evaluated using RT-PCR and real-time quantitative PCR, while pathological changes of lung were examined under optical microscope and electrical microscope.</p><p><b>RESULTS</b>The TGF-beta(1) protein, TGF-beta(1) and MMP-2 mRNA expression were increased significantly in the earlier stage and then decreased after PQ administration (P < 0.05 or P < 0.01), while the mRNA level of TIMP-1 was augmented continuously (P < 0.01) throughout the study compared to the control group. In comparison with the PQ group, in the PDTC treatment group, the TGF-beta(1) mRNA expression on the 3rd and the 14th day, 0.54 +/- 0.08 and 0.72 +/- 0.04 respectively, the MMP-2 mRNA expression on the 7th and 14th day, 1.62 +/- 0.50 and 1.97 +/- 0.34 respective-ly, and the TIMP-1 mRNA on the 7th and 21st day, 1.79 +/- 0.21 and 2.00 +/- 0.34 respectively, were significantly decreased (P < 0.05 or P < 0.01).</p><p><b>CONCLUSION</b>PDTC could attenuate paraquat-induced up-regulation of TGF-beta(1) and its mRNA expression, MMP-2 and TIMP-1 mRNA levels, which indicates that PDTC may exert its protective effects on paraquat-induced pulmonary damage by alleviating the earlier inflammation damage and adjust-ing the balance between MMPs and TIMPs. However, further studies are still warranted to investigate and clarify the underlying mechanisms involved in this complicated process.</p>