Long non-coding RNA MEG3 mediates the miR-149-3p/FOXP3 axis by reducing p53 ubiquitination to exert a suppressive effect on regulatory T cell differentiation and immune escape in esophageal cancer.

BACKGROUND: Long non-coding RNA (lncRNA) maternally expressed gene 3 (MEG3) has been implicated in the progression of esophageal cancer (EC). However, the specific mechanism of the involvement of MEG3 in EC development in relation to the regulation of immune escape remains uncertain. Thus, the aim of the current study was to investigate the effect of MEG3 on EC via microRNA-149-3p (miR-149-3p). METHODS: Gain- and loss-of-function experiments were initially performed in EC cells in addition to the establishment of a 4-nitroquinoline 1-oxide-induced EC mouse model aimed at evaluating the respective roles of forkhead box P3 (FOXP3), MEG3, miR-149-3p, mouse double minute 2 homolog (MDM2) and p53 in T cell differentiation and immune escape observed in EC. RESULTS: EC tissues were found to exhibit upregulated FOXP3 and MDM2 while MEG3, p53 and miR-149-3p were all downregulated. FOXP3 was confirmed to be a target gene of miR-149-3p with our data suggesting it reduced p53 ubiquitination and degradation by means of inhibiting MDM2. P53 was enriched in the promoter of miR-149-3p to upregulate miR-149-3p. The overexpression of MEG3, p53 or miR-149-3p or silencing FOXP3 was associated with a decline in CD25+FOXP3+CD4+ T cells, IL-10+CD4+ T cells and IL-4+CD4+ T cells in spleen tissues, IL-4, and IL-10 levels as well as C-myc, N-myc and Ki-67 expression in EC mice. CONCLUSION: Collectively, MEG3 decreased FOXP3 expression and resulted in repressed regulatory T cell differentiation and immune escape in EC mice by upregulating miR-149-3p via MDM2-mediated p53.

Notch1-Nrf2 signaling crosstalk provides myocardial protection by reducing ROS formation.

Both the Notch1 and Keap1-Nrf2 signaling pathways have cardioprotective effects, but the role of Notch1-Nrf2 crosstalk in myocardial ischemia-reperfusion injury is unclear. In this study, we established hypoxia-reoxygenation in neonate rat myocardial cells and employed γ-secretase inhibitor and curcumin to inhibit and activate the Notch1 and Keap1-Nrf2 signaling pathways, respectively. We found that the combined action of the Notch1 and Keap1-Nrf2 signaling pathways significantly increased cardiomyocyte viability, inhibited cardiomyocyte apoptosis, reduced the formation of reactive oxygen species, and increased antioxidant activities. In conclusion, these findings suggest that Notch1-Nrf2 crosstalk exerts myocardial protection by reducing the formation of reactive oxygen species.

Inhibition of mitochondrial autophagy protects donor lungs for lung transplantation against ischaemia-reperfusion injury in rats via the mTOR pathway.

Impaired mitochondrial function is a key factor attributing to lung ischaemia-reperfusion (IR) injury, which contributes to major post-transplant complications. Thus, the current study was performed to investigate the role of mitochondrial autophagy in lung I/R injury and the involvement of the mTOR pathway. We established rat models of orthotopic left lung transplantation to investigate the role of mitochondrial autophagy in I/R injury following lung transplantation. Next, we treated the donor lungs with 3-MA and Rapamycin to evaluate mitochondrial autophagy, lung function and cell apoptosis with different time intervals of cold ischaemia preservation and reperfusion. In addition, mitochondrial autophagy, and cell proliferation and apoptosis of pulmonary microvascular endothelial cells (PMVECs) exposed to hypoxia-reoxygenation (H/R) were monitored after 3-MA administration or Rapamycin treatment. The cell apoptosis could be inhibited by mitochondrial autophagy at the beginning of lung ischaemia, but was rendered out of control when mitochondrial autophagy reached normal levels. After I/R of donor lung, the mitochondrial autophagy was increased until 6 hours after reperfusion and then gradually decreased. The elevation of mitochondrial autophagy was accompanied by promoted apoptosis, aggravated lung injury and deteriorated lung function. Moreover, the suppression of mitochondrial autophagy by 3-MA inhibited cell apoptosis of donor lung to alleviate I/R-induced lung injury as well as inhibited H/R-induced PMVEC apoptosis, and enhanced its proliferation. Finally, mTOR pathway participated in I/R- and H/R-mediated mitochondrial autophagy in regulation of cell apoptosis. Inhibition of I/R-induced mitochondrial autophagy alleviated lung injury via the mTOR pathway, suggesting a potential therapeutic strategy for lung I/R injury.

NSD2 promotes ventricular remodelling mediated by the regulation of H3K36me2.

Histone lysine methylation plays an important role in the regulation of ventricular remodelling. NSD2 is involved in many types of tumours through enhancing H3K36me2 expression. However, the role of NSD2 in the regulation of histone lysine methylation during ventricular remodelling remains unclear. In this study, we established cardiac hypertrophy model in C57BL/6 mice by transverse aortic constriction and found that histone lysine methylation participated in ventricular remodelling regulation via the up-regulation of H3K27me2 and H3K36me2 expression. In addition, we constructed transgenic C57BL/6 mice with conditional knockout of NSD2 (NSD2-/- ) in the myocardium. NSD2-/- C57BL/6 mice had milder ventricular remodelling and significantly improved cardiac function compared with wild-type mice, and the expression of H3K36me2 but not H3K27me2 was down-regulated. In conclusion, NSD2 promotes ventricular remodelling mediated by the regulation of H3K36me2.

Notch signaling inhibits cardiac fibroblast to myofibroblast transformation by antagonizing TGF-ß1/Smad3 signaling.

PURPOSE: During myocardial infarction (MI), cardiac fibroblasts (CFs) transform into myofibroblast (CMT). This study aimed to investigate the crosstalk of Notch1 and transforming growth factor-ß1 (TGF-ß1)/Smad3 signaling in the regulation of CMT and myocardial fibrosis. METHODS: Primary CFs were isolated from young rats and treated with TGF-ß1 or adenovirus to overexpress or knockdown Notch1 intracellular domain (N1ICD) or Smad3. RESULTS: TGF-ß1 decreased the expression of fibroblast markers but increased the expression of myofibroblast markers in rat CFs. TGF-ß1 increased the proliferation, invasion, and adhesion, and the secretion of collagen I of CFs, and these effects were inhibited by N1ICD overexpression. Moreover, endogenous Smad3 phosphorylation in CFs was enhanced by N1ICD knockdown, whereas TGF-ß1 induced Smad3 phosphorylation was antagonized by the N1ICD overexpression. Conversely, endogenous N1ICD activation in CFs was antagonized by Smad3, whereas TGF-ß1 induced N1ICD inactivation was antagonized by Smad3 knockdown. Coimmunoprecipitation showed that N1ICD interacted with Smad3 and immunostaining revealed the colocalization of N1ICD and Smad3 in the nuclei of CFs. Moreover, we demonstrated the functional antagonism of N1ICD and Smad3 on the phenotypes of CFs. Finally, TGF-ß1/Smad3 signaling promoted whereas Notch signaling inhibited myocardial fibrosis in rat MI model. CONCLUSION: Notch signaling inhibits CMT by antagonizing TGF-ß1/Smad3 signaling. Notch signaling activators and TGF-ß1/Smad3 signaling inhibitors could be exploited for therapeutic intervention to inhibit myocardial fibrosis after MI.

Notch1 provides myocardial protection by improving mitochondrial quality control.

Mitochondrial quality control is a new target for myocardial protection. Notch signaling plays an important role in heart development, maturation, and repair. However, the role of Notch in the myocardial mitochondrial quality control remains elusive. In this study, we isolated myocardial cells from rats and established myocardial ischemia reperfusion injury (IRI) model. We modulated Notch1 expression level in myocardial cells via infection with recombinant adenoviruses Ad-N1ICD and Ad-shN1ICD. We found that IR reduced myocardial cells viability, but Notch1 overexpression increased the viability of myocardial cells exposed to IRI. In addition, Notch1 overexpression improved ATP production, increased mitochondrial fusion and decreased mitochondrial fission, and inhibited mitophagy in myocardial cells exposed to IRI. However, N1ICD knockdown led to opposite effects. The myocardial protection role of Notch1 was related to the inhibition of Pink1 expression and Mfn2 and Parkin phosphorylation. In conclusion, Notch1 exerts myocardial protection and this is correlated with the maintenance of mitochondrial quality control and the inhibition of Pink1/Mfn2/Parkin signaling.

NSD2 silencing alleviates pulmonary arterial hypertension by inhibiting trehalose metabolism and autophagy.

Nuclear receptor binding SET domain 2 (NSD2)-mediated metabolic reprogramming has been demonstrated to regulate oncogenesis via catalyzing the methylation of histones. The present study aimed to investigate the role of NSD2-mediated metabolic abnormality in pulmonary arterial hypertension (PAH). Monocrotaline (MCT)-induced PAH rat model was established and infected with adeno-associated virus carrying short hairpin RNA (shRNA) targeting NSD2. Hemodynamic parameters, ventricular function, and pathology were evaluated by microcatheter, echocardiography, and histological analysis. Metabolomics changes in lung tissue were analyzed by LC-MS. The results showed that silencing of NSD2 effectively ameliorated MCT-induced PAH and right ventricle dysfunction, and partially reversed pathological remodeling of pulmonary artery and right ventricular hypertrophy. In addition, the silencing of NSD2 markedly reduced the di-methylation level of H3K36 (H3K36me2 level) and inhibited autophagy in pulmonary artery. Non-targeted LC-MS based metabolomics analysis indicated that trehalose showed the most significant change in lung tissue. NSD2-regulated trehalose mainly affected ABC transporters, mineral absorption, protein digestion and absorption, metabolic pathways, and aminoacyl-tRNA biosynthesis. In conclusion, we reveal a new role of NSD2 in the pathogenesis of PAH related to the regulation of trehalose metabolism and autophagy via increasing the H3K36me2 level. NSD2 is a promising target for PAH therapy.

Hes1 is upregulated by ischemic postconditioning and contributes to cardioprotection.

The expression of Hes1 is increased following myocardial infarct and other ischemic cardiomyopathies, but the role of Hes1 in cardioprotection provided by ischemic postconditioning (IPost) remains unclear. In this study, we used gain and loss of function approaches to investigate the role of Hes1 in cardioprotection during IPost. Primary cardiac myocytes exposed to ischemia reperfusion injury (IRI) and IPost were used as the experimental model. The results showed that Hes1 expression was increased during myocardial IPost, and Hes1 promoted the viability while inhibited the apoptosis of cardiomyocytes. Moreover, Hes1 inhibited the opening of mitochondrial permeability transition pore (mPTP) and the generation of reactive oxygen species in primary cardiac myocytes exposed to IRI. Mechanistically, we found that Hes1-mediated cardioprotection was related to the downregulation of phosphatase and tensin homolog and the activation of phosphatidylinositol 3-kinase/Akt and signal transducer and activator of transcription 3 signalling. These data demonstrate that Hes1 is upregulated and mediates cardioprotection provided by IPost and suggest that Hes1 is a potential new target for the treatment of ischemic cardiomyopathy.

Notch signaling activation contributes to cardioprotection provided by ischemic preconditioning and postconditioning.

BACKGROUND: Notch signaling is known to be activated following myocardial ischemia, but its role in cardioprotection provided by ischemic preconditioning (IPC) and ischemic postconditioning (IPost) remains unclear. METHODS: Lentiviral vectors were constructed to overexpress or knockdown N1ICD in H9c2 cardiomyocyte and rat heart exposed to ischemia reperfusion injury (IRI), IPC or IPost. RESULTS: Notch1 signaling was activated during myocardial IPC and IPost, and could enhance cell viability and inhibit apoptosis. Furthermore, activated Notch1 signaling stabilized mitochondrial membrane potential and reduced reactive oxygen species induced by IRI. The cardioprotection provided by activated Notch1 signaling resembled that of IPC and IPost, which was related to Stat3 activation and regulation of apoptosis related proteins. Furthermore, in langendorff heart perfusion model, activated Notch1 signaling restored cardiac function, decreased lactate dehydrogenase release and limited infarct size after myocardial ischemia. CONCLUSIONS: Notch1 signaling is activated and mediates cardioprotection provided by IPC and Ipost. Notch1 signaling may represent a potential new pharmacologic mimic for cardioprotection of ischemic heart disease.

Long non-coding RNA NCK1-AS1 functions as a ceRNA to regulate cell viability and invasion in esophageal squamous cell carcinoma via microRNA-133b/ENPEP axis.

This study is designed to explore the role of long non-coding RNAs (lncRNAs) NCK1-AS1 in proliferative and invasive activities of esophageal squamous cell carcinoma (ESCC) cells by binding to microRNA-133b (miR-133b) to regulate ENPEP. Differentially expressed lncRNAs, miRs, genes and their targeting relationships were screened on ESCC-related gene expression datasets GSE17351 and GSE6188. The targeting relationships among NCK1-AS1, miR-133b, and ENPEP were verified using functional assays. Loss- and gain- of function assays were carried out to examine the roles of NCK1-AS1, miR-133b, and ENPEP in ESCC cell proliferative, invasive, migrative and apoptotic abilities as well as tumorigenesis in vivo. Elevated NCK1-AS1 and ENPEP but reduced miR-133b expression were found in ESCC. NCK1-AS1 knockdown or miR-133b overexpression inhibited the malignant properties of ESCC cells as well as tumorigenesis in vivo. NCK1-AS1 regulated the ENPEP expression by competitively binding to miR-133b. ENPEP overexpression reversed inhibition of NCK1-AS1 knockdown on the function of ESCC cells. This study provides evidence that silencing NCK1-AS1 inhibits expression of ENPEP by sponging miR-133b, thereby suppressing ESCC.

NSD2 promotes pressure overload-induced cardiac hypertrophy via activating circCmiss1/TfR1/ferroptosis signaling.

Heart failure typically occurs early in the clinical course of sustained cardiac hypertrophy that is accompanied by maladaptive remodeling of the heart. It is critical to discover new mechanisms and effective therapeutic targets to prevent and cure pathological cardiac hypertrophy. The objective of the study was to evaluate the effects of circRNAs on NSD2-induced ventricular remodeling. We screened the dysregulated circRNAs in normal or NSD2-/- C57BL/6 mice with or without transverse aortic constriction (TAC), and found that circCmss1 significantly increased in normal TAC mice, but decreased in NSD2-/- TAC mice. Angiotensin II(Ang II)induced neonatal cardiomyocyte hypertrophy in vitro and the pressure overload-induced cardiac hypertrophy in vivo can be reduced by Knocking down circCmss1. We further investigated the downstream signaling of circCmss1 in the progression of NSD2-promoted ventricular remodeling and discovered that circCmss1 could interact with a transcription factor EIF4A3 and induce the expression of transferrin receptor 1 (TfR1), thus activating the ferroptosis in cardiomyocytes. This study highlights the significance of NSD2 activation of circCmss1/EIF4A3/TfR1 as therapeutic targets for treating pathological myocardial hypertrophy.

Exploring Dysregulated Ferroptosis-Related Genes in Septic Myocardial Injury Based on Human Heart Transcriptomes: Evidence and New Insights.

Introduction: Sepsis is currently a common condition in emergency and intensive care units, and is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection. Cardiac dysfunction caused by septic myocardial injury (SMI) is associated with adverse prognosis and has significant economic and human costs. The pathophysiological mechanisms underlying SMI have long been a subject of interest. Recent studies have identified ferroptosis, a form of programmed cell death associated with iron accumulation and lipid peroxidation, as a pathological factor in the development of SMI. However, the current understanding of how ferroptosis functions and regulates in SMI remains limited, particularly in the absence of direct evidence from human heart. Methods: We performed a sequential comprehensive bioinformatics analysis of human sepsis cardiac transcriptome data obtained through the GEO database. The lipopolysaccharide-induced mouse SMI model was used to validate the ferroptosis features and transcriptional expression of key genes. Results: We identified widespread dysregulation of ferroptosis-related genes (FRGs) in SMI based on the human septic heart transcriptomes, deeply explored the underlying biological mechanisms and crosstalks, followed by the identification of key functional modules and hub genes through the construction of protein-protein interaction network. Eight key FRGs that regulate ferroptosis in SMI, including HIF1A, MAPK3, NOX4, PPARA, PTEN, RELA, STAT3 and TP53, were identified, as well as the ferroptosis features. All the key FRGs showed excellent diagnostic capability for SMI, part of them was associated with the prognosis of sepsis patients and the immune infiltration in the septic hearts, and potential ferroptosis-modulating drugs for SMI were predicted based on key FRGs. Conclusion: This study provides human septic heart transcriptome-based evidence and brings new insights into the role of ferroptosis in SMI, which is significant for expanding the understanding of the pathobiological mechanisms of SMI and exploring promising diagnostic and therapeutic targets for SMI.

The N-classification for esophageal cancer staging: should it be based on number, distance, or extent of the lymph node metastasis?

BACKGROUND: The recently published AJCC-TNM staging system for esophageal carcinoma made an obvious modification on N-classification based on the number of metastatic regional lymph nodes (LN). However, this classification might ignore the site at which these LNs occur, a factor that might be even more important in reflecting patients' prognosis. METHODS: A retrospective study of 236 patients with carcinoma of thoracic esophagus who underwent esophagectomy between 1984 and 1989 with each at least six LNs removed was conducted, with a 10-year follow-up rate of 92.4%. The proposed scheme for N-classification according to the number (0, 1-2, 3-6, ≥7; N0-3), distance (0, 1, 2, 3 stations; S0-3), or extent (0, 1, and 2 fields; F0-2) of LN involvement was evaluated by univariate and multivariate survival analysis. RESULTS: The LN metastasis was identified in 112 patients, revealing a poorer 5-year survival in this patient group when compared to patients without node involvement. Cox regression analysis revealed that the number and distance of LN metastases and the number of metastasis fields were factors significantly influencing survival. When these factors were further analyzed by univariate log-rank test, no significant difference in survival existed between N2 and N3 patients, or among S1, S2, and S3 patients. When patients were grouped according to the extent of LN metastasis, significant differences in survival were observed overall and between each subgroup. CONCLUSIONS: Refining the current N-classification for esophageal cancer according to the extent of LN metastasis, rather than by number alone, might be a better means of staging that could subgroup patients more effectively and result in different rates of survival.

[A cross-sectional study on the industrial noise over-limit status in Guangzhou factories].

OBJECTIVE: To investigate the industrial noise over-limit status of the worksites in Guangzhou factories, so as to promote the prevention and control of occupational noise hazards. METHODS: 211 factories in Guangzhou were monitored and investigated. The analysis and assessment were developed for the properties and size of the factories, the districts of the factories being located, the industries of the factories being classified and the date of monitoring. RESULTS: In this understudied factories, most of them were national-owned and joint-ventures, medium size, located in urban, and mainly involved in the industries of manufacturing of motor vehicle, shipping, electron and electric equipment, and the industries of petroleum and chemicals. The prevalence of noise over-limit was higher in joint-ventures (36.0%) and private-run enterprises (31.2%). The over-limit status mainly presented in industries of textile, food and beverage processing, and leather producing, with getting prevalence of over-limit 46.7%, 43.1% and 41.3% respectively. Subsequence were industries of manufacturing of electron and electric equipment, motor vehicle and shipping, and industries of printing and goods producing for culture and sports, with the prevalence for all > 35%. Factories monitored during spring and summer also had higher prevalence of noise over-limit. The similar results were got after adjustment for each other using multivariable regression. The most common over-limit sites mainly focused on the operation of cutting and sawing, milling and planing, pressing, riveting, drilling, jointing, assembling and quality inspecting in industries of mechanism processing and manufacturing, on quality inspecting and packing in industries of pharmacy and food and beverage manufacture, on spinning and scutching in textile industry, and on cleaning and maintaining as assistant jobs, and patrolling and inspecting air-press machine, ventilation machine, dynamotor and pump. CONCLUSION: Noise in Guangzhou factories widely exists with different industries and districts. To strengthen noise occupational hazards prevention and control for the high risk districts, industries and worksites should be the key job in the future.

Significance of tumor mutation burden and immune infiltration in thymic epithelial tumors.

BACKGROUND: Thymic epithelial tumors (TETs) are relatively rare malignant thoracic tumors. Tumor mutation burden (TMB) and immune infiltration play important roles in tumorigenesis. METHODS: Research data was obtained using the Cancer Genome Atlas (TCGA) database to evaluate the landscape of tumor mutations, related factors, and relationship of prognosis. The CIBERSORT algorithm was used to evaluate immune cell infiltration in TETs and its relationship with TMB. Immune-related differentially expressed genes (irDEGs) were identified. Hub irDEGs independently related to prognosis were analyzed using univariate and multivariate Cox proportional hazard models. A survival signature was constructed from hub irDEGs. RESULTS: A total of 122 patients were included in this study. GTF2I was the most common gene mutation. Higher TMB was significantly associated with the later stage, more advanced pathological type, and older age. The overall survival (OS) of patients in the low-TMB group was significantly better. There was no significant correlation between TMB levels and PD-L1 expression. Enrichment analysis showed that DEGs were mainly involved in the P13K-Akt signaling pathway. There were significant differences in macrophage and other types of immune cell infiltration between the high- and low-TMB groups. CCR5, FASLG, and CD79A independently relating to prognosis were screened from 391 irDEGs. The low-risk group had a significantly better prognosis than the high-risk group based on the signature, which has a good predictive effect on OS. CONCLUSIONS: In this study, TETs patients with high TMB had a significantly poor prognosis and an immune-related gene signature was found to effectively evaluate the long-term prognosis.

[Esophagogastrostomy by side-to-side anastomosis in prevention of anastomotic stricture: a randomized clinical trial].

OBJECTIVE: To compare a side-to-side esophagogastric anastomosis with conventional hand-sewn or stapled esophagogastrostomy for prevention of anastomotic stricture by randomized clinical trial. METHODS: Between November 2007 and September 2008, 160 patients with esophageal carcinoma or gastric cardia cancer were consecutively admitted and underwent surgical treatment. After excluding 5 patients (2 refused to participate in and 3 did not meet inclusion criteria), the remaining 155 patients were completely randomized to receive either a side-to-side esophagogastric anastomosis (SS group), or the conventional hand-sewn (HS group), or a circular stapled (CS group) anastomosis, after the removal of esophageal tumor. The primary outcome measured the incidence of anastomotic stricture at 3 months after the operation (defined as the diameter of the anastomotic orifice

[Mercury concentration in cerebrospinal fluid in patients with chronic mercury poisoning].

OBJECTIVE: To investigate the changes of mercury (Hg) levels in cerebrospinal fluid (CSF) in patients with chronic mercury poisoning and elucidate the neurotoxic mechanism of mercury. METHODS: Nine patients with chronic mercury poisoning (poisoning group) as well as eight patients without exposure to mercury were included in this study. Mercury concentrations of 24 hour urine (U-Hg) and CSF (CSF-Hg) were measured with cold-vapor atomic absorption spectrometry-alkali stannous chloride method. The concentration of blood (B-Hg) at the same day was measured with cold-vapor atomic absorption spectrometry-acidic stannous chloride method. In five patients of poisoning group, these concentrations before chelation therapy were compared with those after chelation therapy. RESULTS: The levels of B-Hg, U-Hg, and CSF-Hg in poisoning group (250.00 +/- 48.54, 160.07 +/- 91.15, 20.22 +/- 10.21 nmol/L, respectively) were significantly higher than those in control group (81.04 +/- 63.01, 24.73 +/- 9.96 nmol/L, undetectable, respectively; P < 0.01). In nine patients of poisoning group, CSF-Hg concentrations were correlated with B-Hg (r = 0.675, P < 0.05), but not U-Hg. After chelation therapy with dimercaptopropane sulfonate in five patients of poisoning group, the levels of B-Hg, U-Hg, and CSF-Hg were decreased significantly (P < 0.05). The reduction of CSF-Hg was not related with B-Hg and U-Hg. CONCLUSION: CSF-Hg concentration in chronic mercury poisoning patient is increased with the rise of B-Hg, but not U-Hg. When the levels of B-Hg and U-Hg drop to normal, the CSF-Hg level is still high enough to be detected. It indicates that mercury is combined with protein after entering brain and this complex is difficult to cross through blood-cerebral barrier. The complex may cause neuromuscular disorder and fremitus in chronic mercury poisoning.

[A study on lymphocyte DNA damage in traffic policemen in Guangzhou].

OBJECTIVE: To study the effect of occupational exposure to traffic exhaust and smoking on DNA damage in traffic policemen. METHODS: 812 traffic policemen (741 men and 71 women, 130 of office-work and 682 of outside work) from 8 districts in Guangzhou were investigated. Blood samples were taken by venipuncture and lymphocytes were collected by using lymphocyte separation medium and centrifugation. The comet assay was used to measure DNA damage. RESULTS: The office-work policemen [(37.7 +/- 9.5) years] were older than the outside-work ones [(32.3 +/- 8.1) years, P < 0.001]. No significant difference was observed in sex (P = 0.08) and age (P = 0.45). Comet assay showed that occupational exposure to traffic exhaust significantly increased tail length [4.20 micro m, 95% CI: (3.98 - 4.42) micro m vs 3.23 micro m, 95% CI: (2.82 - 3.7) micro m, P < 0.001]. Smokers had longer tail length [4.66 micro m, 95% CI: (4.37 - 4.97) micro m] than ex-smokers [3.28 micro m, 95% CI: (2.57 - 4.17) micro m] and nonsmokers [3.47 micro m, 95% CI: (3.21 - 3.75) micro m, P < 0.001]. In nonsmokers, significant increase in tail length was observed by passive smoking at home (P = 0.004) but not at work (P = 0.22). When out-door nonsmokers were excluded, passive smoking at work also significantly increased tail length (P = 0.007). Analysis of covariance showed that occupational exposure to traffic exhaust, tobacco smoking, and female had independent effect on lymphocyte DNA damage (P < 0.001) after these factors were adjusted. Passive smoking and age had no effect on lymphocyte DNA damage. CONCLUSIONS: Occupational exposure to traffic exhaust and tobacco smoking respectively increase lymphocyte DNA damage. Female traffic policemen may have more severe DNA damage than male.

[Association between number of lymphadenectomy and postoperative complication in surgery for esophageal carcinoma].

OBJECTIVE: To investigate the association between the number of lymph nodes retrieval and the incidence of postoperative complications in patients with esophageal carcinoma. METHOD: From January 2008 to December 2009, 794 patients with esophageal carcinoma underwent esophagectomy and lymphadenectomy in the Department of Thoracic Surgery at the West China Hospital of Sichuan University. The clinical data, surgeons, the extent of lymphadenectomy and its association with operative morbidity were retrospectively analyzed. RESULTS: There was no operative death. A total of 84 patients with complication(10.6%) were documented. There were 11,770 lymph nodes harvested in total with an average of 14.8. Multivariate logistic regression showed that gender, number of metastatic lymph nodes, level of anastomosis, and surgeons' experience were risk factors associated with postoperative complications (all P<0.05), while the number and group of lymph node resection were not(all P>0.05). CONCLUSION: Within a rational range of lymphadenectomy(<50) following esophagectomy, the postoperative complications are significantly associated with the gender, extent of regional lymph nodes metastasis, site of anastomosis and the expertise of the surgeons, but not associated with the number and group of lymph nodes resection.