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An immunization regimen was evaluated in rabbits consisting of the soluble, oligomeric form of envelope glycoprotein of HIV-1, strain R2 (gp140R2), or the surface component of the same envelope (Env), gp120R2, in the adjuvant AS02A. The gp140R2 was selected based on its unusual CD4-independent phenotype and the exceptionally broad neutralizing response in the infected donor. The gp140R2 immunogen induced antibodies that achieved 50% neutralization of 48/48, and 80% neutralization of 43/46 primary strains of diverse HIV-1 subtypes tested. The strains tested included members of standard panels of subtype B and C strains, and other diverse strains known to be neutralization resistant. The gp120R2 induced antibodies that neutralized 9/48 of the same strains. Neutralization was IgG-mediated and HIV-1-specific. These results demonstrate that induction of truly broad spectrum neutralizing antibodies is an achievable goal in HIV-1 vaccine development. [ABSTRACT FROM AUTHOR]

The correct name is: Neelakantan T Vasudevan. Reference 1 Zhou L, Lapping S, Liao X, Lu Y, Zhou G, et al. (2020) The thromboprotective effect of traditional Chinese medicine Tongji 2 granules is dependent on anti-inflammatory activity by suppression of NF- B pathways. Correction: The thromboprotective effect of traditional Chinese medicine Tongji 2 granules is dependent on anti-inflammatory activity by suppression of NF- B pathways. [Extracted from the article]

Background: Oesophageal cancer is the fourth leading cause of cancer death in China where essentially all cases are histologically oesophageal squamous cell carcinoma (ESCC). Agnostic pathway-based analyses of genome-wide association study (GWAS) data combined with tissue-specific expression quantitative trait loci (eQTL) analysis and publicly available functional data can identify biological pathways and/or genes enriched with functionally-relevant disease-associated variants., Method: We used the adaptive multilocus joint test to analyse 1827 pathways containing 6060 genes using GWAS data from 1942 ESCC cases and 2111 controls with Chinese ancestry. We examined the function of risk alleles using in silico and eQTL analyses in oesophageal tissues., Results: Associations with ESCC risk were observed for 36 pathways predominantly involved in apoptosis, cell cycle regulation and DNA repair and containing known GWAS-associated genes. After excluding genes with previous GWAS signals, candidate pathways (and genes) for ESCC risk included taste transduction (KEGG_hsa04742; TAS2R13, TAS2R42, TAS2R14, TAS2R46,TAS2R50), long-patch base excision repair (Reactome_pid; POLD2) and the metabolics pathway (KEGG_hsa01100; MTAP, GAPDH, DCTD, POLD2, AMDHD1). We identified and validated CASP8 rs13016963 and IDH2 rs11630814 as eQTLs, and CASP8 rs3769823 and IDH2 rs4561444 as the potential functional variants in high-linkage disequilibrium with these single nucleotide polymorphisms (SNPs), respectively. Further, IDH2 mRNA levels were down-regulated in ESCC (tumour:normal-fold change = 0.69, P =  .75E-14)., Conclusion: Agnostic pathway-based analyses and integration of multiple types of functional data provide new evidence for the contribution of genes in taste transduction and metabolism to ESCC susceptibility, and for the functionality of both established and new ESCC risk-related SNPs., (Published by Oxford University Press on behalf of the International Epidemiological Association 2015. This work is written by US Government employees and is in the public domain in the US.)

Under the condition of immune cell balancing function collapse, acute venous thrombosis originates from intravenous immune adhesive inflammations triggered by cells which are infected by foreign pathogenic microorganism and malignant cells. With the condition of immune cell balancing function collapse, the human body lost the function of clearing intravenous foreign pathogenic microorganism and malignant cells timely and effectively. Thus, integrins β2 and β3 on the membrane of white blood cells and platelets are activated to combine with the ligand fibrinogen into a reversible mesh-like structure, which is like the intravenous biological filter and acts as physical defense of the human body to prevent the cells which are infected by foreign pathogenic microorganism and malignant cells in the distal veins from flowing back to the whole body. Meanwhile, blood cells mainly red blood cells stagnate and fulfill the filter, which blocks the blood flow in the local veins and thus results in venous thrombotic diseases. People with collapsed immune cell balancing functions are the certain groups of people who will develop venous thromboembolism. Anyone who had venous thromboembolism indicates alloantigen cells in the veins, which are mainly pathogenic microorganism infected cells and malignant cells and trigger the onset of venous thromboembolism. Only under the condition of immune cell balancing function collapse, the risk factors, such as advanced age, infection, trauma, surgery, autoimmune disease, pregnancy as well as long trip syndrome, could cause venous thromboembolism.

Background: To evaluate the activity of natural killer cells through their inhibitory and activating receptors and quantity in peripheral blood mononuclear cells extracted from patients with acute myocardial infarction, stable angina pectoris and the controls., Methods: 100 patients with myocardial infarction, 100 with stable angina, and 20 healthy volunteers were recruited into the study. 20 randomly chosen people per group were examined for the whole human genome microarray analysis to detect the gene expressions of all 40 inhibitory and activating natural killer cell receptors. Flow cytometry analysis was applied to all 200 patients to measure the quantity of natural killer cells., Results: In myocardial infarction group, the mRNA expressions of six inhibitory receptors KIR2DL2, KIR3DL3, CD94, NKG2A, KLRB1, KLRG1, and eight activating receptors KIR2DS3, KIR2DS5, NKp30, NTB-A, CRACC, CD2, CD7 and CD96 were significantly down-regulated (P<0.05) compared with both angina patients and the controls. There was no statistical difference in receptor expressions between angina patients and control group. The quantity of natural killer cells was significantly decreased in both infarction and angina patients compared with normal range (P<0.001)., Conclusions: The significant mRNAs down-regulation of several receptors in myocardial infarction group and reduction in the quantity of natural killer cells in both myocardial infarction and angina patients showed a quantitative loss and dysfunction of natural killer cells in myocardial infarction patients.

Objective: To investigate the differential gene expression of cytokines and compare their impacts on the immune functions among the acute myocardial infarction patients (AMI), the stable angina patients (SA) and the controls., Methods: 20 patients with AMI, 20 patients with SA and 20 healthy volunteers were recruited into the study. Whole human genome microarray analysis was used to detect the gene expression differences in interferons, interleukins, chemokines, tumor necrosis factors and associated receptors in peripheral blood mononuclear cells (PBMCs) among three groups., Results: Compared with SA patients and the controls respectively, in AMI patients, IFNα2, IFNαR1, IFNαR2, IFNγR1, IFNγR2, L1β, IL16, IL18, Cxcl1, Cxcl2, Cxcl6, CxcR2, CxcR4, LIGHT, TNFR1, LT-βR, CD137, TRAILR, and TWEAKR mRNA expressions were significantly up-regulated (P<0.05), while Ccl5, Ccl24, Ccl28, CcR5, TWEAK, CD40, CD27, and BAFFR mRNA expressions were significantly down-regulated (P<0.05). But, there was no significant difference in cytokine expression between the SA patients and the controls., Conclusion: In AMI patients, mRNA expression levels of cytokines were imbalanced, indicating the dysfunction of the immune system. Together with no significant change of cytokines was observed between the SA and controls, showing the different cytokine related immune activity in the AMI and SA patients.

Objective: To identify differentially expressed T cells-related genes in peripheral blood mononuclear cells and compare their differences in T cell activation and subset functions in different stages of coronary atherosclerosis disease (CAD)., Methods: 20 patients with acute myocardial infarction patients (AMI), 20 patients with stable angina pectoris (SA) and 20 healthy volunteers were recruited into the study. Whole human genome microarray analysis was used to detect the expression of T cell related genes among three groups., Results: mRNA expression of 68 genes involved in T cell was detected. 1) Antigen recognition: in the AMI patients 12 genes were down-regulated and 9 were significantly down-regulated among all 13 genes, compared with those of the SA and the control group, respectively. 2) Co-stimulators and regulators of T cell activation: among 16 genes in the AMI patients, 15 genes were lower and 8 were significantly lower than the other two groups. 3) T cell subsets, CTL: all 11 genes in the AMI patients were down-regulated, particularly GZMM and CASP8 were significantly down-regulated compared with the SA patients and controls. Th1/Th2: in the AMI patients, gene expressions including IL1 and IL18 were significantly higher, whereas GATA3 mRNA was significantly lower than those in other two groups. Th17/Treg: in the AMI group, RORC and CCR6 mRNAs were significantly down-regulated compared with the control group, while CD25 and CD127 expressions were significantly lower than SA group. There was no difference in T cell related genes between the SA patients and the controls., Conclusions: In the AMI patients, the mRNA expression of T cell antigen recognition, activation and subset functions was imbalanced or decreased, indicating the dysfunction of cellular immunity in patients with AMI. Then improving T cell mediated cellular immunity may be considered as a potential target for medical interventions in the patients with AMI.

Objective: The high morbidity, mortality and misdiagnosis rate render pulmonary embolism (PE) as a worldwide health problem. However, the etiology and pathogenesis of this disease have not been well characterized. Increasing studies indicate infection and immunity play a crucial role in PE. Natural killer (NK) cells act as a bridge between the innate immune and acquired immune. This study aimed to investigate the possible function of NK cells in PE., Methods: Human cDNA microarray analysis was employed to detect genes associated with NK cells in peripheral blood mononuclear cells (PBMCs). Random variance model corrected t-test was used for statistical analysis of differential gene expression. Flow cytometry was performed to detect the CD16+CD56+ NK cells., Results: In the present study, based on gene expression microarray analysis, we showed four inhibitory receptors (KLRB1, KLRD1, KLRF1, KLRG1) and four activating receptors (KLRC1, KLRC3, KLRK1 and NCR1) on NK cells were remarkably down-regulated and the cytological experiment demonstrated the proportion of CD16+CD56+ NK cells among PBMCs decreased in the PE group., Conclusions: We confirmed the presence of reduced expression of critical activating as well as inhibitory NK cell receptors and low proportion of CD16+CD56+ NK cells in PE. The consistence between genomic and cytological examination suggests compromised NK cells may contribute to the pathogenesis of PE.

Aim: This study was to carry out exome sequencing in a Han Chinese family with venous thromboembolism., Methods: Three venous thromboembolism (VTE) patients and five members from a Han Chinese family were evaluated by exome sequencing., Results: Among the 3 VTE patients, mutations of 2 genes including PRF1 and HTR2A were identified and predicted to be functionally damaged to their encoded proteins. In addition, the PRF1 mutation and the HTR2A mutation identified in our study were absent in 100 non-related controls, indicating that venous thromboembolism has a genetic component. The R357W mutation is located in the membrane attack complex/perforin domain of PRF1 protein, which exists in both the perforin. The steps of killing foreign or pathological antigen cells by NK cells, CD8 (+)T cells and the membrane attack complex include membrane perforation and release of the granzyme, either of which is abnormal can lead to immune dysfunction., Conclusions: The mutations of immune related genes in familial VTE might provide new understanding of the pathogenesis of familial venous thromboembolism.

Objective: To investigate the differences of T lymphocyte subgroups and high-sensitivity C reactive protein (HsCRP) levels among patients with venous thromboembolism (VTE), VTE patients with infection, simple infection patients and the normal controls., Method: 289 patients were enrolled in this study and divided into control group, VTE group, VTE with infection group and simple infection group., Result: Compared with the control group, the serum levels of CD3(+), CD4(+), CD8(+) T lymphocytes significantly decreased and CD4(+)/CD8(+) ratio significantly increased in simple infection group (P < 0.05); CD3(+) and CD8(+) T lymphocytes significantly decreased and CD4(+)/CD8(+) ratio significantly increased in VTE and VTE with infection group (P < 0.05); the proportion of declined CD3(+) and CD8(+) T lymphocytes increased, and the proportion of increased CD4(+)/CD8(+) ratio statistically elevated in three disease groups. As an important inflammatory factor, all HsCRP levels in three disease groups significantly increased when compared with the control group., Conclusion: Immune dysfunction exists in both of VTE and infection patients, while VTE patients tend to be accompanied with infections. The changes of T lymphocyte subgroups in VTE patients, who were independent from infection, could cause T lymphocyte immune dysfunction, suggesting that there were abnormalities of T lymphocyte immune function in VTE itself. The overall T lymphocyte functions of recognizing antigens and transducing activation signals decline in VTE patients. Besides, the function of T lymphocyte of directly killing virus microbes declines significantly and the inflammatory mechanisms are involved in the occurrence and development of venous thrombosis.

The aim of the present study was to explore the function and interaction of differentially expressed genes (DEGs) in pulmonary embolism (PE). The gene expression profile GSE13535, was downloaded from the Gene Expression Omnibus database. The DEGs 2 and 18 h post‑PE initiation were identified using the affy package in R software. The Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways of the DEGs were analyzed using Database for Annotation Visualization and Integrated Discovery (DAVID) online analytical tools. In addition, protein‑protein interaction (PPI) networks of the DEGs were constructed using the Search Tool for the Retrieval of Interacting Genes/Proteins. The PPI network at 18 h was modularized using Clusterone, and a functional enrichment analysis of the DEGs in the top three modules was performed with DAVID. Overall, 80 and 346 DEGs were identified 2 and 18 h after PE initiation, respectively. The KEGG pathways, including chemokine signaling and toll‑like receptor signaling, were shown to be significantly enriched. The five highest degree nodes in the PPI networks at 2 or 18 h were screened. The module analysis of the PPI network at 18 h revealed 11 hub nodes. A Gene Ontology terms analysis demonstrated that the DEGs in the top three modules were associated with the inflammatory, defense and immune responses. The results of the present study suggest that the DEGs identified, including chemokine‑related genes TFPI2 and TNF, may be potential target genes for the treatment of PE. The chemokine signaling pathway, inflammatory response and immune response were explored, and it may be suggested that these pathways have important roles in PE.

The minute ventilation/carbon dioxide production (VE/VCO 2 ) slope has been widely demonstrated to have strong prognostic value in patients with chronic heart failure (CHF), and the risk of mortality is believed to increase when the VE/VCO 2 slope is >32.8; however, there is little evidence concerning the prognostic value of the VE/VCO 2 slope in Chinese patients. In the present study, the prognostic value of the VE/VCO 2 slope was investigated in patients with CHF. A total of 258 subjects underwent symptom-limited cardiopulmonary exercise testing (CPET) and were divided into CHF (113 males and 16 females; LVEF <0.49) and control (106 males and 23 females) groups. The cardiac-related events over a median 33.7-month follow-up period subsequent to the CPET were evaluated using receiver operating characteristic curve analysis. The VE/VCO 2 slope was significantly different between the CHF and control groups (P<0.001). The area under the curve (AUC) for the VE/VCO 2 slope in predicting cardiac-related mortalities in the patients with CHF was 0.670 (P<0.05), and the sensitivity and specificity of the VE/VCO 2 slope were 0.667 and 0.620, respectively. The optimal threshold of the VE/VCO 2 slope for predicting cardiac-related mortalities in patients with CHF was ≥39.3. The AUC for the VE/VCO 2 slope in predicting cardiac-related hospitalizations in patients with CHF was 0.682 (P<0.05), and the sensitivity and specificity of the VE/VCO 2 slope were 0.631 and 0.778, respectively. The optimal threshold of the VE/VCO 2 slope for predicting cardiac-related hospitalizations in patients with CHF was ≥32.9. In conclusion, ventilatory efficiency decreases in patients with CHF. The VE/VCO 2 slope is a strong predictor of cardiac-related mortalities in the patients with CHF analyzed.

Background: Pulmonary rehabilitation (PR) is able to improve dyspnea, endurance capacity, and health-related quality of life in chronic obstructive pulmonary disease (COPD) patients, but it is rarely used in China. This study aimed to assess the effectiveness and safety of PR after exacerbation of COPD., Material and Methods: Patients admitted to hospital due to an exacerbation of COPD were randomized to receive either PR or routine care (control group). The PR program was performed from the second day of admission until discharge. The pre-post changes in 6-minute walk distance (6MWD), self-reported quality of life (QOL) assessed by CAT score and CRQ-SAS score, and activity of daily life assessed by ADL-D score were determined. The perceived end-effort dyspnea (Borg scale) was measured throughout the study., Results: A total of 101 patients were enrolled, of whom 7 withdrew after randomization, and 94 completed this study. There were 66 patients in the PR group and 28 in the control group. The 6MWD, resting SpO2, and exercise Borg dyspnea score were significantly improved in the PR group. In addition, the PR group had greater improvement in the total CRQ-SAS score and had a lower CAT score. Significant improvements were also found in the ADL-D and BODE index in the PR group. No adverse events were recorded during exercise., Conclusions: Our study provides evidence that it is safe and feasible to apply an early PR in patients with acute exacerbation of COPD.

Background: To compare different expression of core proteins among venous thromboembolism (VTE) and those with risk factor groups and analyze the relative risk for VTE after integrating integrin β1, β2 and β3 expression., Methods: A total of 1006 subjects were recruited and divided into VTE group, risk factor groups and control (non- risk factor) group. Flow cytometry was performed to detect the expression of integrin β1, β2 and β3. The relative risk for VTE was evaluated with independent, parallel and serial methods., Results: The expression of integrin β1 increased markedly in VTE patients, and those with risk factors (acute infection, malignancy, and autoimmune diseases), respectively (P < 0.001 or 0.01). The expression of integrin β1 in trauma/surgery group was not significantly different with control group (P > 0.05). The expression of integrin β2 or β3 significantly increased in VTE group, but that in risk factor groups was not significantly increased (P > 0.05). Multivariate analysis revealed the trauma/surgery groups had no significantly increased risk for VTE., Conclusions: VTE group patients have significantly increased expression of integrin β1, β2 and β3, and risk factor groups (acute infection, malignancy and autoimmune disease) have significantly increased expression of integrin β1. The significant increase in integrin β2, β3 expression is a marker differentiating of VTE group patients with other risk factor groups. Trauma/surgery group has no increased expression of integrin β1, β2 and β3 as other risk factors. Thus, that trauma/surgery may be not the "true" risk factor for VTE.

The aim of the present study was to identify differentially expressed B‑cell‑associated genes in peripheral blood mononuclear cells and investigate the gene expression characteristics of the different stages of B‑cell activation. A total of 20 patients with pulmonary embolisms (PE) and 20 age‑ and gender‑matched controls were enrolled in the present study. Human complementary DNA microarray analysis was used in order to detect the differential expression of B‑cell‑associated genes between the PE and control groups. Messenger (m)RNA expression was detected for 82 genes involved in B‑cell activation. The results showed that PE patients exhibited significantly increased expression levels of the B‑cell receptor genes LYN, CD22, SYK, BTK, PTPRC and NFAM1, whereas expression levels of FYN, FCRL4 and LAX1 were significantly decreased compared to those of the control group. Expression levels of T‑cell‑dependent B‑cell‑activation genes, including EMR2, TNFSF9, CD86, ICOSLG, CD37 and CD97, were significantly upregulated in PE patients, whereas SPN mRNA expression was significantly downregulated compared with those of the control group. LILRA1 and TLR9 T cell‑independent B‑cell activation mRNAs were significantly upregulated in PE patients compared with those of the control group. In addition, the expression levels of B‑cell‑activation regulator genes, including CR1, LILRB4 and VAV1, were significantly increased, whereas SLAMF7 expression levels were significantly decreased in PE patients compared with those of the control group. Furthermore, the expression levels of B‑cell‑activation‑associated cytokine genes demonstrated a significant upregulation of LTA and IL10 and downregulation of L1A, IFNA5, IFNA6, IFNA8, IFNA14, IL2, IL13 and IFNG in PE patients compared to those of the control group. In conclusion, the differential gene expression at different stages of B‑cell activation between healthy controls and PE patients indicated that B‑cell function was reduced or disorganized in patients with symptomatic PE.

Objective: Cancer is one of the most common risk factor of venous thromboembolism (VTE). Our previous studies have shown that integrin subunits β1, β2 and β3 were the core proteins of venous thrombi and potential useful biomarker of VTE. This study aimed to explore the expression status of core proteins (integrin subunits β1, β2 and β3) in cancer patients., Methods: This is a case-control study. A total of 144 inpatients (54 females) with clinically proven cancers were recruited into this study, meanwhile 200 inpatients without cancer matched in sex and age were recruited as control group. Flow cytometry was done to measure the expressions of blood integrin β1, β2, β3 and cellular immunity related variables (CD3, CD4, CD8, CD4/CD8, CD16CD56 and CD19). The association degree between increased core proteins and cancers was analyzed by calculating the relative risk (RR)., Results: The expression of integrin β1 and β3 were markedly increased in patients with cancer (P=0.001 and 0.008). Integrin β2 was also mildly increased in patients with cancer (P=0.274). The relative risk ratio (RR) of increased integrin β1, β2 and β3 in cancer patients was 1.655 (95% CI: 1.321-2.074, P=0.000), 1.314 (95% CI: 1.052-1.642, P=0.021) and 1.852, (95% CI: 1.097-3.126, P=0.028), respectively. Combined analysis with integrin β1, β2 and β3 showed that the relative risk ratio (RR) of increased in cancer patients was 4.895 (95% CI: 1.645-14.563, P=0.002). CD3, CD4, CD4/CD8 and CD19 were significantly decreased (P=0.004, P=0.000, P=0.000, P=0.000, respectively) in patients with cancer, while CD8 and CD16CD56 were markedly increased in cancer patients (P=0.005, P=0.035)., Conclusions: As the core proteins of venous thrombi, integrin β1 and β3 were markedly increased expression in patients with cancer, which maybe explain the increased risk of VTE in cancer patients. A weakened or disordered immune system might be the basis of VTE in condition.

Objective: Whole human genome oligo microarrays were employed to systematically investigate the mRNA expression profile of 5-HT synthetase, transporter, receptor, and factors in 5-HT signaling pathway in peripheral blood karyocytes from pulmonary embolism (PE) patients., Methods: A total of 20 PE patients and 20 healthy subjects matched in gender and age were recruited. The human genome microarrays were performed to detect the mRNA expression profile of 5-HT synthetase, transporter, receptor, and factors in 5-HT signal pathway of two groups. The random variance model corrected t-test was used for analysis., Results: Our results showed (1) tryptophan hydroxylase (TPH1)-related gene expression was markedly down-regulated in PE patients (P < 0.01); (2) monoamine oxidases (MAO)-related gene (MAOB) expression was significantly up-regulated in PE patients (P < 0.01); (3) the expression of 17 genes of 7 5-HT receptors showed a down-regulated tendency in PE patients, and significant difference was observed in the expression of HTR1E, HTR3B, HTR4 and HTR5A between them (P < 0.05); (4) the expression of DalDAG-GEF I, Tubby, PKA and EPAC in 5-HT signal pathways was dramatically up-regulated in PE patients (P < 0.05); the expression of SPA1, RIAM, RAPL, Talin, PKC, PLC and Pyk2 was remarkably up-regulated in PE patients (P < 0.05); (5) the expression of integrin genes ITGA2B, ITGB1 and ITGB3 was significantly up-regulated in PE patients (P < 0.05)., Conclusion: In PE patients, the expression of TPH1 and HTR4 was down-regulated as a negative feedback; the MAOB expression was up-regulated. Consistent with the expression of 5-HTR1E and 5-HTR4 and the abnormally activated Tubby, the expression of integrins in platelets was activated.

Objective: To investigate the core proteins (integrin subunits β1, β2 and β3) in the acute venous thrombi and validate the specificity and sensitivity of increased expression of integrin subunits β1, β2 and β3 in patients with venous thromboembolism., Methods: A total of 120 patients (73 females) with clinically proven acute VTE and aged between 24-90 years, and 120 non-VTE patients and healthy controls receiving physical examination matched in the sex and age were recruited. Flow cytometry was done to measure the expressions of blood integrin β1, β2 and β3. The receiver-operator characteristic (ROC) curve analysis was conducted to evaluate the diagnostic accuracy of integrin β1, β2 and β3., Results: The median levels of integrin β1, β2 and β3 were significantly higher in VTE patients than in non-VTE patients (P=0.000, 0.000 and 0.000, respectively) and healthy controls (P=0.000, 0.000 and 0.000, respectively). The ROC curves showed that integrin β1, β2 and β3 were specific diagnostic predictors of VTE with an area under the curve (AUC) of 0.870, 0.821, and 0.731, respectively. When three integrins were combined for diagnosis, the AUC of ROC curve was 0.916, and the sensitivity, specificity, positive and negative predictive values were 84.6%, 90.8%, 81.7% and 92.0%, respectively., Conclusion: The increased integrin β1, β2 and β3, as the core protein of venous thrombosis, have relatively high specificity and sensitivity for VTE and thus may serve as useful new biomarkers for the diagnoses of VTE.

In patients with pulmonary embolism (PE), forepart components of complements were activated. However there are interruption/decrease of cascade reaction and cytolytic effects in complement system. This study detected CRP, CH50, C3 and C4 levels in patients with venous thromboembolism (VTE) and compare with the imbalance of complement associated gene mRNA expression in PE patients. There was significant increase of CH50 in acute VTE patients. Even though CH50 increased significantly in acute VTE patients and had a relatively high sensitivity, cytolytic effects of complements might decrease, based on the genomics results of complement cascade reactions imbalance/interruption and increased total complements in VTE patients.

Whole human genome oligo microarrays were employed to systematically investigate the differential expression characteristics of associated mRNAs, which were found in the signal transduction pathway of β2 integrins in peripheral blood mononuclear cells (PBMCs) between patients with symptomatic pulmonary embolism (PE) and controls. A total of 20 cases of PE patients and twenty gender‑ and age‑matched controls were recruited for the study. Human cDNA microarray analysis was used to detect the differences in mRNA expression between the two groups and a random variance model corrected t‑test was used to analyze the statistical data. A total of 80 associated mRNAs were detected. The mRNA expression of chemokines, ligands, inside‑out and outside‑in signaling pathway‑associated proteins were upregulated significantly in the PE group, compared with the controls. In five subunit‑associated mRNAs, the mRNA expression of ITGAL, ITGAM, ITGAX and ITGB2, which encode for the subunits of αL, αM, αX and β2, were upregulated in the PE group and the differences, with the exception of ITGB2, were statistically significant (P<0.05). The mRNA expression of ITGAD was downregulated; however, there was no significant difference (P>0.05). The expression of Fgr mRNA was significantly downregulated (P<0.01). Thus, in PE patients, bilateral signal transduction pathways of β2 integrins in neutrophils and monocytes were activated, enhancing innate immunity.

In a recent study, a unique gene expression signature was observed when comparing esophageal squamous cell carcinoma (ESCC) epithelial cells to normal esophageal epithelial cells using laser capture microdissection (LCM) and cDNA microarray technology. To validate the expression of several intriguing genes from that study (KRT17, cornulin, CD44, and EpCAM), we employed two new technologies, expression microdissection (xMD) for high-throughput microdissection facilitating protein analysis and RNAscope for the evaluation of low abundant transcripts in situ. For protein measurements, xMD technology was utilized to specifically procure sufficient tumor and normal epithelium from frozen human tissue for immunoblot analysis of KRT17 (CK17) and cornulin. A novel in situ hybridization method (RNAscope) was used to determine the transcript level of two relatively low expressed genes, CD44 and EpCAM in both individual formalin-fixed paraffin-embedded (FFPE) tissue sections and in an ESCC tissue microarray (TMA). The results successfully confirmed the initial expression pattern observed for all four genes, potentially implicating them in the pathogenesis of ESCC. Additionally, the study provides important methodological information on the overall process of candidate gene validation.

Few studies have investigated the changes of Th1- and Th2-type cytokines in pulmonary embolism (PE) patients. In this study, the gene expression of interleukins and the balance of Th1- and Th2-type cytokines in the peripheral blood mononuclear cells (PBMCs) of PE patients and controls were investigated. A total of 20 PE patients and 20 gender- and age-matched controls were included in the study. Human cDNA microarray analysis was used to detect the differences in cytokine gene expression between the two groups and a random variance model corrected t-test was used to analyze the statistical data. In comparison with the controls, 12 genes were found to be downregulated, specifically IL1A, IL9, IL17B, IL19, IL23A, IL25 (p<0.05), IL2, IL3, IL13, IL22, IL24 and IL31 (p<0.01), and 2 genes were found to be upregulated, specifically IL10 and IL28A, in the PE patients. The expression levels of IFN-γ and IL2 mRNA in the PE patients were significantly lower than those in the control group (p<0.01), while the IL20 mRNA expression levels were significantly upregulated (p<0.01). We conclude that there are significant differences in interleukin gene expression between the PE patients and the control group. A shift of the Th1/Th2 balance comprising enhanced Th2 activity and reduced Th1 activity in the PE patients is also demonstrated.

By studying the chaos attractor of cardiac magnetic induction strength B(z) generated by the electrical activity of the heart, we found that its projection in the reconstructed phase space has a similar shape with the map of the total current dipole vector. It is worth noting that the map of the total current dipole vector is computed with MCG recordings measured at 36 locations, whereas the chaos attractor of B(z) is generated by only one cardiac magnetic field recordings on the measured plan. We discuss only two subjects of different ages in this paper.

A computational study of a magneto-electrocardiogram (magneto-ECG) and a correlative locus of the total current dipole vector map are presented. Unlike the ordinary electrocardiogram (ECG), the magneto-ECG is the solution to the inverse problem of electrocardiograph), which is calculated with the magnetic field signals recorded at 36 locations of a human heart surface. Using this method we investigated 6-lead magneto-ECG, the correlative locus of the total current dipole vector during a cardiac cycle and the current density distribution map. We find that the magneto-ECG and the correlative locus of the total current dipole vector map reveal not only the properties of P-wave, QRS-wave, T-wave similar to the common ECG, but also additional information about the electrophysiological activity of the heart. We anticipate that the magneto-ECG and the locus of the total current dipole vector map may avail the early diagnosis of cardiac diseases.

Objective: To establish a clinical classification of pulmonary embolism (PE), and to evaluate the optional treatment strategies for different types of PE., Methods: From December 1995 to July 2001, 45 patients with acute PE were hospitalized, of which 33 received intravenous thrombolytic therapy or interventional treatment., Results: Misdiagnostic rate in the 45 patients with acute PE during first visit was 62.2% and mortality rate was 28.9%. Misdiagnostic rate in acute PE patients who had undergone surgery was 82% and mortality rate was 73%. The effective rate of thrombolytic therapy was 77.7%. Clinical symptoms rapidly disappeared in massive PE patients treated with interventional therapies., Conclusions: Intravenous thrombolytic therapy is one of the most effective methods for treating acute PE. Application of interventional therapy for severe acute PE is also promising.