Internet abusers associate with a depressive state but not a depressive trait.

AIM: The present study investigated three issues: (i) whether Internet abusers display a depressive state without a depressive trait; (ii) which symptoms are shared between Internet abuse and depression; and (iii) which personality characteristics were shown in Internet abusers. METHODS: Ninety-nine male and 58 female participants aged 18-24 years were screened with the Chen Internet Addiction Scale. After screening, subjects were separated into the high- (n = 73) and low-risk (n = 84) Internet abuser groups. Participants were respectively administered the Chinese version of the Beck Depression Inventory-II to assess a depressive state and the Minnesota Multiphasic Personality Inventory-2 to assess a depressive trait. RESULTS: The present results showed that high-risk Internet abusers exhibited a stronger depressive state than low-risk Internet abusers in the Beck Depression Inventory-II. However, high-risk Internet abusers didnot show a depressive trait in the Minnesota Multiphasic Personality Inventory-2 compared to low-risk Internet abusers. Therefore, high-risk Internet abuse participants exhibited a depressive state without a depressive trait. CONCLUSIONS: In a comparison of the symptoms of depression and Internet abuse, it was found that high-risk Internet abuse participants shared some common behavioral mechanisms with depression, including the psychiatric symptoms of loss of interest, aggressive behavior, depressive mood, and guilty feelings. High-risk Internet abuse participants may be more susceptible to a temporal depressive state but not a permanent depressive trait. The present findings have clinical implications for the prevention and treatment of Internet abuse.

Genetic variants in DNA repair pathway genes and risk of esophageal squamous cell carcinoma and gastric adenocarcinoma in a Chinese population.

The DNA repair pathways help to maintain genomic integrity and therefore genetic variation in the pathways could affect the propensity to develop cancer. Selected germline single nucleotide polymorphisms (SNPs) in the pathways have been associated with esophageal cancer and gastric cancer (GC) but few studies have comprehensively examined the pathway genes. We aimed to investigate associations between DNA repair pathway genes and risk of esophageal squamous cell carcinoma (ESCC) and GC, using data from a genome-wide association study in a Han Chinese population where ESCC and GC are the predominant cancers. In sum, 1942 ESCC cases, 1758 GC cases and 2111 controls from the Shanxi Upper Gastrointestinal Cancer Genetics Project (discovery set) and the Linxian Nutrition Intervention Trials (replication set) were genotyped for 1675 SNPs in 170 DNA repair-related genes. Logistic regression models were applied to evaluate SNP-level associations. Gene- and pathway-level associations were determined using the resampling-based adaptive rank-truncated product approach. The DNA repair pathways overall were significantly associated with risk of ESCC (P = 6.37 × 10(-4)), but not with GC (P = 0.20). The most significant gene in ESCC was CHEK2 (P = 2.00 × 10(-6)) and in GC was CLK2 (P = 3.02 × 10(-4)). We observed several other genes significantly associated with either ESCC (SMUG1, TDG, TP53, GTF2H3, FEN1, POLQ, HEL308, RAD54B, MPG, FANCE and BRCA1) or GC risk (MRE11A, RAD54L and POLE) (P < 0.05). We provide evidence for an association between specific genes in the DNA repair pathways and the risk of ESCC and GC. Further studies are warranted to validate these associations and to investigate underlying mechanisms.

[The expression of T cell immune-related gene mRNAs in peripheral blood mononuclear cells from patients with venous thromboembolism].

OBJECTIVE: To explore the role of T cell-mediated immunity in the pathogenesis of venous thromboembolism (VTE) by analyzing the differential expression of T cell immune-related gene mRNAs peripheral blood mononuclear cells (PBMCs) between VTE patients and controls with GeneChip Human Genome. METHODS: Human cDNA microarray analysis was employed in PBMCs from 20 VTE patients and 20 hypertensive controls, and random variant model (RVM) corrected t-test was used for statistical analysis of differential gene expression. RESULTS: Six mRNA stripes including CD(247), CD(3D), CD(3G), Granzyme A (GzmA), Granzyme B (GzmB) and Zeta-chain-associated protein kinase 70 (ZAP70) were found to be associated with T cell-mediated immunity. Significant down-regulation of these six mRNAs was found in the VTE group compared with the controls (15.3050 ± 0.6346 vs 15.8053 ± 0.5567, 13.7878 ± 0.7731 vs 14.3820 ± 0.4857, 13.3299 ± 0.9104 vs 14.1246 ± 0.6011, 14.8893 ± 0.8675 vs 15.5305 ± 0.4624, 15.9113 ± 0.8123 vs 16.4553 ± 0.5055, 14.3652 ± 0.7717 vs 14.3652 ± 0.7717; all P values < 0.05). CONCLUSIONS: T cells' function including antigen recognition, signal transduction and cytotoxicity was impaired in VTE patients. T cell-mediated immunity dysfunction probably plays an important role in the pathogenesis of VTE.

[The expression of interferon associated genes mRNA in patients with pulmonary embolism].

OBJECTIVE: To investigate the gene expression difference of IFN and their receptors in peripheral blood mononuclear cells (PBMC) of pulmonary embolism (PE) patients. METHODS: Twenty cases of PE patients and twenty sex and age matched controls were recruited into the study. Human cDNA microarray analysis was used to detect the gene expression difference of IFN associated genes between the two groups, and random variance model corrected t test was used to analyze the statistical data. RESULTS: In comparison with the control group, mRNA expression of type I IFN, including IFNα(5) mRNA, IFNα(6) mRNA, IFNα(8) mRNA, IFNα(14) mRNA, IFNκ mRNA, IFNω(1) mRNA, IFNε(1) mRNA in PBMC of PE patients were down-regulated (P < 0.05). There was no significant difference in gene expression of type I IFN receptors IFNαR(1) and IFNαR(2) between the PE and control groups (P > 0.05). In comparison with the control group, mRNA expression of IFNγ gene was down-regulated (P < 0.05). The mRNA expression of IFNγR(1) and IFNγR(2) genes were upregulated compared with the control (P > 0.05). CONCLUSION: mRNA expression of type I and type II IFN in PE are significantly down-regulated, but not the IFN receptors. Reduced immune function may play an important role in the PE patients who are susceptible to virus, intracellular bacteria and parasites.

[Effects of exercise therapy at the intensity of anaerobic threshold for exercise tolerance in patients with chronic stable coronary artery disease].

OBJECTIVE: To investigate the effects of exercise therapy at the intensity of anaerobic threshold (AT) for exercise tolerance in patients with chronic stable coronary artery disease. METHODS: Forty-three patients with chronic stable coronary artery disease (3 patients after coronary arterial bypass graft (CABG) surgery, 22 patients with old myocardial infarction and 18 unstable angina pectoris undergoing successful percutaneous coronary intervention (PCI) finished twice cardiopulmonary exercise test (CPET) and followed their rehabilitation program for 3 months. Thirty-two patients finished their aerobic exercise therapy based on their individual anaerobic thresholds while 11 patients had no exercise therapy. RESULTS: The heart rate at AT intensity (97 ± 9/min) was lower than their traditional minimal target heart rate (112 ± 7/min) and lower than heart rate (115 ± 11/min) at ischemic threshold post-CPET. The O(2) consumption (10.7 ± 2.4 to 12.6 ± 2.9 ml×min(-1)×kg(-1)) (P = 0.04) and workload (37 ± 18 to 47 ± 13 J/s) (P = 0.04) at AT level and the O(2) consumption (15.3 ± 3.1 to 20.6 ± 4.2 ml×min(-1)×kg(-1), P = 0.02) and workload(68 ± 12 and 87 ± 14 J/s, P = 0.01) at peak level markedly increased after 3 months in the exercise group. And the O(2) consumption (15.3 ± 2.9 to 16.2 ± 3.1 ml×min(-1)×kg(-1)) and workload (65 ± 13 to 73 ± 16 J/s) at peak level mild increased after 3 months in the non-exercise group, but their O(2) consumption (11.0 ± 2.7 to 11.3 ± 2.8 ml×min(-1)×kg(-1)) and workload (38 ± 11 to 37 ± 9 J/s) at AT level had no obvious change. CONCLUSION: AT exercise intensity was lower than ischemic threshold post-CPET. Exercise therapy at the intensity of anaerobic threshold can improve oxygen capacity and exercise tolerance.

[Effects of aerobic exercise on exercise tolerance in patients with chronic heart failure].

OBJECTIVE: To explore the effects of aerobic exercise on exercise tolerance in patients with chronic heart failure (CHF). METHODS: A total of 50 CHF patients with left ventricular ejection fraction (LVEF) < 49% by echocardiography were enrolled. And they were randomly divided into exercise group (n = 25) and non-exercise group (n = 25). Cardiopulmonary exercise testing (CPET) was performed. The patients of exercise group underwent an aerobic exercise program in which exercise intensity was decided by anaerobic threshold (AT) before 10 J/s while those of non-exercise group performed daily activities. After 6 sessions of supervised aerobic exercise, the home-based aerobic exercise training began. CPET was re-examined 3 months later. RESULTS: The VO(2) AT, VO(2) peak, Load AT, Load peak, peak VO(2)/HR and VE/VCO(2) slope at baseline were similar between exercise group and non-exercise group (P > 0.05). The VO(2) AT, VO(2) peak, Load AT, Load peak and peak VO(2)/HR in patients of exercise group were increased compared with baseline, The differences between baseline and 3 months later expressed as ΔVO(2) AT, ΔVO(2) peak, ΔLoad AT, ΔLoad peak, Δpeak VO(2)/HR and ΔVE/VCO(2) slope, The differences of ΔVO(2) AT, ΔVO(2) peak, ΔLoad AT, ΔLoad peak and Δpeak VO(2)/HR between two groups were statistically significant [ΔVO(2) AT: 2.8 (1.2 - 3.5) ml×kg(-1)×min(-1) vs -0.3 (-2.8 - 0.1) ml×kg(-1)×min(-1), P < 0.01; ΔVO(2) peak: 3.4 (1.8 - 4.6) ml×kg(-1)×min(-1) vs -0.5 (-1.4 - 0.3) ml×kg(-1)×min(-1), P < 0.01; ΔLoad AT:15.0 (2.5 - 22.5) J/s vs 0.5(-4.2 - 3.8) J/s, P < 0.01; ΔLoad peak: 15.0 (1.3 - 25.0) J/s vs 0.0 (-8.8 - 15.0) J/s, P < 0.05; Δpeak VO(2)/HR: 2.3 (0.0 - 4.0) ml×kg(-1)×beat(-1) vs -0.1 (-0.7 - 1.2) ml×kg(-1)×beat(-1), P < 0.01]. The difference of ΔVE/VCO(2) slope was not statistically significant [-2.3 (-12.2 - 1.8) vs 1.0 (-0.4 - 2.6), P > 0.05]. CONCLUSION: After 3 months of aerobic exercise, exercise capacity may improve in the CHF patients.

[The effects of aerobic exercise on cardiac output during exercise in patients with chronic heart failure].

OBJECTIVE: To observe the effects of aerobic exercise on cardiac output during exercise in patients with chronic heart failure (CHF). METHODS: A total of 50 CHF patients (echocardiography measured left ventricular ejection fraction < 0.49) were enrolled in the study and randomly divided into aerobic exercise group (n = 25) and control group (n = 25). Cardiopulmonary exercise testing (CPET) was performed. Patients of aerobic exercise group underwent aerobic exercise according to aerobic exercise prescription and exercise intensity is decided by anaerobic threshold before 10 J/s (1 minute before) of the oxygen consumption. After 6 supervised aerobic exercise training sessions in the hospital, patients were asked to perform the home-based aerobic exercise training. Patients in control group were required to maintain daily physical activities. CPET were reviewed 3 months later. RESULTS: Cardiac output (CO), peak CO, peak cardiac power output (peak CPO), resting heart rate (HR), heart rate at AT (HRAT), HR peak, resting mean arterial pressure (MAP), peak MAP at baseline were similar between aerobic exercise group and control [(4.2 ± 2.0) L/min vs. (3.3 ± 1.0) L/min, (6.2 ± 2.7) L/min vs. (5.2 ± 1.8) L/min, (1.8 ± 2.9) L/min vs. (2.0 ± 1.8) L/min, (1.3 ± 0.5) J/s vs. (1.2 ± 0.5) J/s, (76.8 ± 13.5) beats/min vs. (73.4 ± 11.9) beats/min, (91.5 ± 11.3) beats/min vs. (92.6 ± 12.4) beats/min, (106.0 ± 12.9) beats/min vs. (108.3 ± 17.4) beats/min, (80.8 ± 9.9) mm Hg (1 mm Hg = 0.133 kPa) vs. (87.6 ± 13.3) mm Hg, (98.8 ± 12.4) mm Hg vs. (102.7 ± 13.9) mm Hg, all P > 0.05]. Compared to baseline, CO, peak CO, peak CPO, HR, HRAT, HR peak, MAP, peak MAP after 3 months were similar between aerobic exercise group and control (all P > 0.05). The differences between baseline and 3 months later expressed as ΔCO, Δpeak CO, Δpeak CPO, ΔHR, ΔHRAT, ΔHR peak, ΔMAP, Δpeak MAP were also similar between aerobic exercise group and control group [(-0.7 ± 2.4) L/min vs. (0.7 ± 2.0) L/min, (1.1 ± 2.6) L/min vs. (1.4 ± 2.1) L/min, (0.1 ± 3.7) L/min vs. (-0.2 ± 2.5) L/min, (0.2 ± 1.0) J/s vs. (0.2 ± 0.5) J/s, (-0.4 ± 7.6) beats/min vs. (1.9 ± 9.9) beats/min, (3.4 ± 11.3) beats/min vs. (-2.8 ± 7.6) beats/min, (8.9 ± 14.5) beats/min vs. (3.7 ± 14.4) beats/min, (1.5 ± 12.8) mm Hg vs. (-1.3 ± 11.1) mm Hg, (6.4 ± 18.9) mm Hg vs. (1.3 ± 12.3) mm Hg, all P > 0.05]. CONCLUSION: Three months aerobic exercise training did not improve cardiac output and related parameters during exercise in this cohort patients with CHF.

[Reduced cardiopulmonary exercise capacity in patients with chronic heart failure: impact of left ventricular systolic dysfunction].

OBJECTIVE: To evaluate the cardiopulmonary exercise capacity in patients with chronic heart failure (CHF). METHODS: Cardiopulmonary exercise testing on bicycle ergometer was performed in 74 age, gender and BMI-matched patients. There were 37 patients with LVEF < 0.45 in CHF group and another 37 patients with LVEF > 0.50 in control group. VO(2)AT, VO(2)Peak, Load AT, Load peak and VE/VCO(2) slope were measured and compared. RESULTS: (1) VO(2)AT, VO(2)Peak, Load AT and Load peak were all significantly reduced in patients with CHF as compared with controls [VO(2)AT: (11.3 +/- 2.3) ml x kg(-1) x min(-1) vs (12.8 +/- 2.5) ml x kg(-1) x min(-1), P < 0.05; VO(2)peak: (15.2 +/- 4.3) ml x kg(-1) x min(-1) vs (17.3 +/- 3.9) ml x kg(-1) x min(-1), P < 0.05; Load AT: (25.2 +/- 18.8) J x s(-1) vs (45.6 +/- 18.7) J x s(-1), P < 0.01; Load peak: (54.9 +/- 22.5) J x s(-1) vs (80.3 +/- 21.6) J x s(-1), P < 0.01]; (2) VE/VCO(2) slope increased in patients with CHF as compared with controls [(36.7 +/- 6.7) vs (30.3 +/- 4.3), P < 0.01]; (3) None of VO(2)AT, VO(2), Peak Load AT, Load peak or VE/VCO(2) slope was correlated with LVEF [(r = 0.054, P > 0.05); (r = 0.03, P > 0.05); (r = 0.310, P > 0.05); (r = 0.174, P > 0.05); (r = -0.203, P > 0.05)]; VO(2)AT, VO(2)Peak, Load AT and Load peak were all correlated negatively with a higher NYHA grade [(r = -0.477, P < 0.01); (r = -0.591, P < 0.01); (r = -0.640, P < 0.01); (r = -0.672, P < 0.01)]; VE/VCO(2) slope correlated positively with a higher NYHA grade (r = 0.652, P < 0.01); None of VO(2)AT, VO(2)Peak, Load AT, Load peak or VE/VCO(2) slope was correlated with LVMI [r = 0.045, P > 0.05); (r = -0.017, P > 0.05); (r = -0.214, P > 0.05); (r = -0.123, P > 0.05); (r = 0.106, P > 0.05)]. CONCLUSION: (1) Cardiopulmonary exercise capacity is reduced in CHF patients. (2) None of VO(2)AT, VO(2)Peak, Load AT, Load peak and VE/VCO(2) slope is correlated with LVEF; VO(2)AT, VO(2)Peak, Load AT and Load peak all correlate negatively with the higher NYHA grade; VE/VCO(2) slope correlates positively with a higher NYHA grade; None of VO(2)AT, VO(2)Peak, Load AT, Load peak or VE/VCO(2) slope correlates with LVMI. An analysis of gas metabolism is a safe, accurate and scientific testing method of exercise tolerance.

[Novel GATA4 mutations identified in patients with congenital heart disease].

OBJECTIVE: To identify the novel genetic determinants in patients with congenital heart disease (CHD). METHODS: The clinical data and peripheral venous blood samples from 120 unrelated individuals with idiopathic CHD were collected and evaluated compared to 100 unrelated healthy controls. The complete coding exons and the partial flanking introns of GATA4 gene were amplified by polymerase chain reaction and sequenced by di-deoxynucleotide chain termination. The generated sequences were aligned with those retrieved from GenBank with the aid of programme BLAST to identify the sequence variations. The software Clustal W was utilized to analyze the conservation of altered amino acids. RESULTS: Three novel heterozygous missense GATA4 mutations were identified in 3 of 120 CHD cases. Namely, the triplet substitutions of AGA for AGC at codon 90, GAG for GAC at codon 95, and AAT for AAG at codon 329, predicting the conversions of serine into arginine at amino acid residue 90 (S90R), aspartic acid into glutamic acid at amino acid residue 95 (D95E) and lysine into asparagine at amino acid residue 329 (K329N), were detected. None of these three mutations were probed in 100 controls. A cross-species alignment of GATA4 encoded protein sequences displayed that the lysine at amino acid residue 329 was completely conserved evolutionarily. Additionally, a single nucleotide polymorphism c. 99G>T was observed. However, the polymorphic frequency distribution in CHD patients was not statistically different from that in controls (for genotypes, chi(2) = 0.2640, P = 0.6074; for alleles, chi(2) = 0.2514, P = 0.6161). CONCLUSION: The idiopathic CHD has a marked heterogeneity and the mutated GATA4 gene may be responsible for CHD in a subset of patients.

[The expression and significance of immunity associated genes mRNA in patients with pulmonary embolism].

OBJECTIVE: To investigate the molecular alteration of immunity associated genes in patients with pulmonary embolism (PE) so as to preliminarily elucidate its pathogenetic mechanism. METHODS: Human cDNA microarray analysis was employed in this study, random variance model (RVM) corrected t-test was used for the statistical data analysis of differential gene expression. RESULTS: In comparison with control, mRNA expression of functional genes of neutrophils, monophagocytes, IFN regulating factors, TNF, adhesion molecules and T cells were significantly different in PE patients. However, gene expressions of B cell immune function and complement activation associated factors were not significantly different between two groups. CONCLUSION: Unbalance expression of immune function associated genes, especially down-regulated expression of T cell mediated function genes, in patients with PE indicates that the etiology of PE might be related to viral infection.

[Effects of early submaximal cardiopulmonary exercise test and cardiac rehabilitation for patients with acute myocardial infarction after percutaneous coronary intervention: a comparative study].

OBJECTIVE: To investigate the safety and effects of early submaximal cardiopulmonary exercise test (CPET) and cardiac rehabilitation for patients with acute myocardial infarction (AMI) after percutaneous coronary intervention (PCI). METHODS: 94 patients with AMI after PCI were randomly divided into 2 groups: exercise group undergoing anaerobic rehabilitation training based on anaerobic threshold (AT) exercise prescription for 3 months, and control group, conducting exercise according to the needs of the patients themselves. Three months later, the exercise cardiopulmonary function was evaluated. RESULTS: In the first CPET 89 patients attained their anaerobic threshold (AT) and their heart rates were lower than their target heart rates following the exercise test. The oxygen consumption at the anaerobic threshold (VO2AT) 3 months later of the exercise group was [(12.6 +/- 2.9) ml x min(-1) x kg(1)], significantly greater and that before the exercise [(10.5 x 2.9) ml x min x kg(-1), P = 0.000]. The peak oxygen uptake (VO2 pea) 3 months of the exercise group was (20 +/- 4) ml x min(-1) x kg(-1), signficantly greater then that before exercise [(14 +/- 4) ml x min(-1) x kg(-1), P = 0.000]. The LAT 3 months of the exercise group was (42 +/- 16) J x s(-1), significantly higher than that before exercise p [(33 +/- 20) J x s(-1), P = 0.000]. The workload at peak level (Lpeak) 3 months of the exercise group was (89 +/- 14) J x s(-1) significantly greater than thatbefore exercise [(66 +/- 21) J x s(-1), P = 0.000]. And the VO2pea and Lpeak of 3 months later of the control group were [(19 +/- 4) ml x min(-l) x kg(-1)) and (80 +/- 14) J x s(-1)] respectively, both significantly higher than those before exercise [(14 +/- 4) ml x min(-1) x kg(-1) and (64 +/- 21) J x s(-1), both P = 0.000]. CONCLUSION: The early submaximal CPET and cardiac rehabilitation for patients with AMI after PCI are not only safe but also can improve their exercise capacity.

[An study on screening the gene clusters associated with pulmonary embolism-deep venous thrombosis by oligo microarray].

OBJECTIVE: To find out the gene clusters associated with pulmonary embolism-deep venous thrombosis (PE-DVT) and elucidate the molecular genetic mechanism of PE. METHODS: Peripheral venous blood samples were collected from 9 PE patients and 33 normal controls. The total RNA was extracted and purified. Nine PE cRNA probes labeled with cyanine 3 were constructed, and one standard cRNA probe labeled with cyanine 5 was synthesized based on the total RNA mixture of the controls. Hybridization with Agilent Whole Human Genome Oligo Microarray was performed. Eleven of the genes screened were randomly selected to be amplified by fluorescence quantitative PCR (FQ-PCR). RESULTS: 434 differential expression genes were screened from the 9 microarrays, including 36 gene transcripts. Associated with blood coagulation, 20 with immune or inflammatory response, 29 with metabolism, 26 with cell differentiation and apoptosis, 25 with cell growth/maintenance, 22 with cell-cell signaling or signal transduction, 14 with cytoskeleton or motility, 15 with ion channel or ion transport, 14 with transcription, and 6 with DNA/RNA binding. These 11 of these genes were randomly selected to be amplified by FQ-PCR. The differential expression of the 11 selected genes was consistent with the microarray. CONCLUSION: The differential expression of a lot of genes in the body may play a role in the process of initiation and development of PE-DVT.

Systemic inflammatory response following acute myocardial infarction.

Acute cardiomyocyte necrosis in the infarcted heart generates damage-associated molecular patterns, activating complement and toll-like receptor/interleukin-1 signaling, and triggering an intense inflammatory response. Inflammasomes also recognize danger signals and mediate sterile inflammatory response following acute myocardial infarction (AMI). Inflammatory response serves to repair the heart, but excessive inflammation leads to adverse left ventricular remodeling and heart failure. In addition to local inflammation, profound systemic inflammation response has been documented in patients with AMI, which includes elevation of circulating inflammatory cytokines, chemokines and cell adhesion molecules, and activation of peripheral leukocytes and platelets. The excessive inflammatory response could be caused by a deregulated immune system. AMI is also associated with bone marrow activation and spleen monocytopoiesis, which sustains a continuous supply of monocytes at the site of inflammation. Accumulating evidence has shown that systemic inflammation aggravates atherosclerosis and markers for systemic inflammation are predictors of adverse clinical outcomes (such as death, recurrent myocardial infarction, and heart failure) in patients with AMI.

Prognostic value of serum CYFRA21-1 and CEA for non-small-cell lung cancer.

The aim of the study was to assess the clinical prognostic value of serum cytokeratin 19 fragment (CYFRA21-1) and carcinoembryonic antigen (CEA) for non-small-cell lung cancer (NSCLC) patients. Literatures related to effects of serum CYFRA21-1 and CEA on the prognosis of lung cancer patients were retrieved from databases such as PubMed, Springer Link, Embase, Wanfang, and CNKI. Meta-analysis was carried out using RevMan 5.1 software. Ten literatures involving 1990 NSCLC patients were selected in this study. Total survive estimation merging hazard ratio (HR) in all NSCLC patients with high-level serum CYFRA21-1 was 1.64 (95% CI 1.46-1.84, P < 0.001) and that in all NSCLC patients with high level serum CEA was 1.46 (95% CI 1.28-1.65, P < 0.001). Serum CYFRA21-1 and CEA can be used as prognostic factors of NSCLC patients. Combinative detection of the two indices will be more reliable.

Significantly reduced function of T cells in patients with acute arterial thrombosis.

OBJECTIVES: To explore the intrinsic factors related to the pathogenesis of acute arterial thrombosis (AAT) and to elucidate the pathogenesis of AAT on the basis of differentially expressed genes. METHODS: Patients with acute myocardial infarction (AMI), stable angina (SA) and healthy controls (n = 20 per group) were recruited, and the whole human genome microarray analysis was performed to detect the differentially expressed genes among these subjects. RESULTS: Patients with AMI had disease-specific gene expression pattern. Biological functional analysis showed the function of T cells was significantly reduced, the mitochondrial metabolism significantly decreased, the ion metabolism was abnormal, the cell apoptosis and inflammatory reaction increased, the phagocytosis elevated, the neutrophil-mediated immunity increased and the post-traumatic repair of cells and tissues increased in AMI patients. The biological function in SA group and healthy controls remained stable and was comparable. CONCLUSIONS: The reduced function of T cell gene models in AAT showed the dysfunction of the immune system. The pathogenesis of AAT may be related to the inflammatory reaction after arterial intima infection caused by potential pathogenic microorganisms.

Expression characteristics of neutrophil and mononuclear-phagocyte related genes mRNA in the stable angina pectoris and acute myocardial infarction stages of coronary artery disease.

OBJECTIVE: To investigate expression differences of neutrophil and mononuclear phagocyte related gene mRNAs among acute myocardial infarction (AMI), stable angina (SA) and control groups, and then discuss their expression characteristics in the stable angina pectoris (SAP) and AMI stages of coronary artery disease (CAD). METHODS: Whole Human Genome Oligo Microarrays were applied to assess the differential expression characteristics of neutrophil and mononuclear phagocyte related mRNAs in patients with AMI (n = 20), SA (n = 20) and controls (n = 20). RESULTS: (1) Almost all colony-stimulating factors (CSF) and their receptors related mRNAs was up-regulated in AMI and SA groups compared with the control group, and the expression of granulocyte-macrophage colony stimulating factor receptor (GM-CSFR) and granulocyte colony stimulating factor receptor (G-CSFR) mRNAs in the AMI group was significantly up-regulated compared with the other two groups (P < 0.01). (2) The expression of mRNAs related to monocyte chemoattractant protein-1 (MCP-1), CCR2 (MCP-1 receptor) and CXCR2 (IL-8 receptor) was significantly up-regulated (P < 0.01) in AMI group compared with SA and control groups. IL-8 mRNA expression in the AMI group was clearly higher than the controls (P < 0.05). (3) All mRNAs expression related to opsonic receptors (IgG FcR and C3bR/C4bR) was significantly up-regulated in AMI group compared with SA and control group (P < 0.01), and the SA group showed an upward trend compared with controls. (4) Most pattern recognition receptor (PRR)-related mRNAs expression was up-regulated in AMI group compared with SA and control groups. Most toll-like receptor (TLR) mRNAs expression was significantly up-regulated (P < 0.01) than the SA and control groups; macrophage scavenger receptor (MSR) mRNA was significantly up-regulated in AMI group compared with the control group (P < 0.01), and the SA group showed an upward trend compared with the controls. CONCLUSIONS: The expression of most neutrophil and mononuclear-macrophage function related genes mRNAs was significantly up-regulated by stages during the progression of CAD, suggesting that the adhesive, chemotactic and phagocytic functions of neutrophil and mononuclear-macrophage were strengthened in the occurrence and development of coronary atherosclerosis and AMI. This also showed a stepped upward trend as the disease progressed.

Common genetic variants related to vitamin D status are not associated with esophageal squamous cell carcinoma risk in China.

BACKGROUND: Few studies have examined the association of common genetic variants related to vitamin D metabolism and signaling to esophageal squamous cell carcinoma (ESCC). METHODS: We evaluated the association between 12 single nucleotide polymorphisms (SNPs) in four genes related to vitamin D levels and ESCC risk using data from a genome-wide association study. Participants were recruited from the Shanxi Upper Gastrointestinal Cancer Genetics Project and the Linxian Nutrition Intervention Trials, and included 1942 ESCC cases and 2111 controls. We used logistic models to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for the SNP associations, after controlling for age and gender. RESULTS: None of the 12 evaluated SNPs in the four vitamin D-related genes were significantly associated with risk of ESCC. The strongest associations were for rs3794060 (P=0.07) and rs12800438 (P=0.08) in the DHCR7/NADSYN1 gene. No association between vitamin D-related SNPs and risk of ESCC was observed in a genotype score analysis that included all 12 SNPs. ORs for quartiles 2, 3 and 4 of the genotype scores were 0.83 (95% CI: 0.68, 1.01), 1.02 (0.85, 1.21), and 1.08 (0.89, 1.30), respectively, with no evidence for a significant monotonic trend (P=0.120). CONCLUSIONS: Our results suggested that common genetic variants related to vitamin D levels are not associated with risk of ESCC in this Chinese population.

Venous thromboembolism is a product in proliferation of cancer cells.

The pathogenesis of venous thromboembolism (VTE) in patients with cancer is related to the destruction of small veins and the intravenous formation of filamentous mesh-like structure by fibrinogen. The filamentous mesh-like filter can block hematogenous metastasis of cancer cells and also can stagnate blood cells, leading to venous thrombosis. Cancer cells have characteristics of malignancy and fast proliferation, and ischemic necrosis frequently occurs, and small veins were invaded and damaged. The formation of filamentous mesh-like structure has defense function and also may cause the occurrence of VTE. VTE is a product of the proliferation process of malignant cells.

Activation of circulated immune cells and inflammatory immune adherence are involved in the whole process of acute venous thrombosis.

OBJECTIVE: To investigate localization and distribution of integrin subunit ß1, ß2 and ß3 and morphological changes of ligand-recepter binding in thrombi of acute pulmonary embolism (PE) patients and explore activation of circulated immune cells, inflammatory immune adherence and coagulation response in acute venous thrombosis. METHODS: Thrombi were collected from patients with acute PE. Immunohistochemistry was done to detect the expression and distribution of integrin ß1, ß2 and ß3 in cells within thrombi, and ligands of integrin subunit ß1, ß2 and ß3 were also determined by immunohistochemistry within the thrombi. RESULTS: 1) Acute venous thrombi were red thrombi composed of skeletons and filamentous mesh containing large amounts of red blood cells and white blood cells; 2) Integrin subunit ß1, ß2 and ß3 were expressed on lymphocytes, neutrophils and platelets; 3) No expression of integrin ß1 ligands: Laminin, Fibronectin, Collagen I or Collagen-II on lymphocytes; integrin ß2 ligands including ICAM, factor X and iC3b are distributed on neutrophils, and ligand fibrinogen bound to neutrophils; integrin ß3 was expressed on platelets which form the skeleton of thrombi and bound to fibrinogen to construct mesh structure; 4) Factor Xa was expressed on the filamentous mesh; 5) Filamentous mesh was fully filled with red blood cell dominant blood cells. CONCLUSION: Acute venous thrombosis is an activation process of circulated lymphocytes, neutrophils and platelets mainly, and a whole process including integrin subunit ß2 and ß3 binding with their ligands. Activation of immune cells, inflammatory immune adherence and coagulation response are involved in the acute venous thrombosis.