Pretreatment triglycerides-to-high density lipoprotein cholesterol ratio in postmenopausal women with endometrial cancer.

Raised triglycerides (TG) and reduced high density lipoprotein cholesterol (HDL-c) are components of metabolic syndrome. Both high TG and metabolic syndrome have been reported to be risk factors of endometrial cancer. Therefore, triglycerides-to-high density lipoprotein cholesterol ratio (TG/HDL-c ratio) may be a useful biological indicator in managing endometrial cancer. We aimed to explore the association between pretreatment TG/HDL-c ratio and endometrial cancer in postmenopausal women, and to evaluate its potential role in the disease. Pretreatment serum lipid profile and TG/HDL-c ratio were retrospectively analyzed for 167 postmenopausal women with endometrial cancer and 464 matched noncancer controls. Compared with controls, pretreatment TG/HDL-c ratio in endometrial cancer patients significantly elevated regardless of whether patients had diabetes or overweight/obesity (P < 0.05). Further analyses showed that pretreatment TG/HDL-c ratio increased significantly with advanced tumor stage. Interestingly, TG/HDL-c ratio of type I endometrial cancer patients was higher than those with type II endometrial cancer. A positive association was found between pretreatment TG/HDL-c ratio and tumor stage (adjusted r = 0.176, P = 0.027) in endometrial cancer group. Receiver operating characteristic curve analysis yielded the cut-off value of 1.52 for TG/HDL-c ratio to discriminate patients with cancer from controls (area under the curve, 0.689; sensitivity, 51.5%; specificity, 84.1%). Multivariate logistic regression model identified TG/HDL-c ratio ≥ 1.52 (odds ratio = 4.123; P < 0.001) as an independent predictor of endometrial cancer. TG/HDL-c ratio was positively associated with endometrial cancer clinical features, such as tumor stage and pathogenetic type. Accordingly, pretreatment TG/HDL-c ratio might be a potential marker for endometrial cancer.

Altered mean platelet volume in children with Henoch-Schonlein purpura and its association with disease activity.

Background Henoch-Schonlein purpura is a systemic small-vessel vasculitis that occurs mainly in children. A review of the literature has suggested a correlation between mean platelet volume and several inflammatory disorders. However, to the best of our knowledge, any potential correlation between mean platelet volume and Henoch-Schonlein purpura has not been reported in the literature. Therefore, our study aimed to evaluate the role of mean platelet volume concentrations in patients with Henoch-Schonlein purpura. Methods This study included 97 children with Henoch-Schonlein purpura and 120 healthy individuals as controls. Results Mean platelet volume concentrations were found to be significantly lower in Henoch-Schonlein purpura patients compared with healthy controls (8.1 ± 0.86 vs. 9.4 ± 0.81, P < 0.001). Similarly, significant negative correlations were observed between mean platelet volume and neutrophil count, platelet count and erythrocyte sedimentation rate in patients with Henoch-Schonlein purpura (r=-0.327, P = 0.001; r=-0.419, P < 0.001; r=-0.255, P = 0.012). Interestingly, mean platelet volume was significantly lower in the acute phase compared with the convalescent phase of Henoch-Schonlein purpura patients (7.8 ± 0.86 vs. 8.3 ± 0.77, P = 0.002). A cut-off value for mean platelet volume was 7.85 with area under the curve of 0.726 to identify acute phase vs. convalescent phase in patients with Henoch-Schonlein purpura. Mean platelet volume was independently associated with Henoch-Schonlein purpura in logistic regression analysis (odds ratio = 0.114, 95% confidence interval = 0.053-0.243, P < 0.001). Conclusions Our results suggest that mean platelet volume is inversely associated with disease in patients with Henoch-Schonlein purpura, and mean platelet volume may be a useful marker to identify active disease in Henoch-Schonlein purpura patients.

Transient appearance of EDTA-dependent pseudothrombocytopenia in a postoperative patient with sepsis: A case report.

RATIONALE: Ethylenediaminetetraacetic acid-dependent pseudothrombocytopenia (EDTA-PTCP) is a rare phenomenon characterized by spuriously low platelet counts when EDTA reacts with harvested blood. However, to the best of our knowledge, only two cases involving EDTA-PTCP in postoperative patients with sepsis have been reported. Here, we describe a case of EDTA-PTCP that appeared transiently in a postoperative patient with sepsis. PATIENT CONCERNS: A 68-year-old female patient underwent laparoscopic tension-free hernioplasty for incisional hernia. Postoperatively, the patient developed very low platelet counts. The number of platelets in this patient had not improved following treatment with fresh-frozen plasma and platelet transfusions. DIAGNOSES: The diagnosis of EDTA-PTCP was confirmed from the discovery of platelet aggregation in peripheral blood smears. INTERVENTIONS: We used sodium citrate-anticoagulated blood samples for platelet counting. OUTCOMES: The patient's platelet counts returned to normal with the use of sodium citrate-anticoagulated blood samples. Furthermore, the phenomenon of EDTA-PTCP disappeared when the patient was cured. LESSONS: The phenomenon of low platelet counts in postoperative patients with sepsis should be considered as possible EDTA-PTCP. In addition, peripheral blood smears and the use of sodium citrate anticoagulant are effective and valuable methods that can help identify EDTA-PTCP.

The CCND1 G870A gene polymorphism and leukemia or non-Hodgkin lymphoma risk: a meta-analysis.

In recent years, mounting evidence has indicated that the CCND1 G870A gene polymorphism, which impacts the mitotic cell cycle, may influence leukemia or non-Hodgkin lymphoma risk. Unfortunately, the previous results were inconsistent. Therefore, a meta-analysis was performed to obtain a more precise estimation of any association. We conducted a search in PubMed, Embase and CNKI covering all published papers up to March, 2014. A total of 9 publications including 10 case-control studies met the inclusion criteria. Odds ratios (ORs) and their 95% confidence intervals (95%CIs) were applied to assess association. The pooled ORs showed significant association in non-Hodgkin lymphoma (comparison A vs G: OR= 1.114, 95%CI=1.053-1.179, p=0.000; homozygote comparison AA vs GG: OR=1.245, 95%CI=1.110-1.396, p=0.000; heterozygote comparison AG vs GG: OR=1.095, 95%CI=1.000-1.199, p=0.05; dominant model AA/GA vs GG: OR=1.137, 95%CI=1.043-1.239, p=0.003; and recessive model AA vs GA/GG: OR=1.177, 95%CI=1.066-1.301, p=0.001). However, there was no association between the CCND1 G870A polymorphism and leukemia risk. In conclusion, the CCND1 G870A polymorphism may increase risk of non-Hodgkin lymphoma, but not leukemia. However, more primary large scale and well-designed studies are still required to evaluate the interaction of CCND1 G870A polymorphism with leukemia and non-Hodgkin lymphoma risk.

The CCND1 G870A gene polymorphism and brain tumor risk: a meta-analysis.

BACKGROUND: In recent years, numerous studies have been performed to investigate the CCND1 G870A gene polymorphism impact on brain tumors susceptibility. Unfortunately, the results of previous studies were inconsistent. Therefore, we performed a meta-analysis to derive a more precise estimation of any association. MATERIALS AND METHODS: We conducted a search in PubMed, Embase and CNKI covering all published papers up to November, 2013. Odds ratios (ORs) and their 95% confidence intervals (95%CIs) were applied to assess associations. RESULTS: A total of 6 publications including 9 case-control studies met the inclusion criteria. The pooled ORs for the total included studies showed significant association among comparison A vs G (OR= 1.246, 95%CI= 1.092-1.423, p= 0.001), homozygote comparison AA vs GG (OR= 1.566, 95%CI= 1.194-2.054, p= 0.001), heterozygote comparison AG vs GG (OR= 1.290, 95%CI= 0.934-1.782, p= 0.122), dominant model AA/GA vs GG (OR= 1.381, 95%CI= 1.048-1.821, p= 0.022) and recessive model AA vs GA/GG (OR= 1.323, 95%CI= 1.057- 1.657, p= 0.015) especially in glioma. CONCLUSIONS: CCND1 G870A polymorphism may increase brain tumor risk, especially for gliomas. However, more primary large scale and well-designed studies are still required to evaluate the interaction of CCND1 G870A polymorphism with brain tumor risk.

Association between the XRCC3 Thr241Met polymorphism and cervical cancer risk: a meta-analysis.

BACKGROUND: Numerous epidemiological studies have been conducted to evaluate the association between variants of the DNA repair gene XRCC3 and cancer risk. Here we focused on one XRCC3 polymorphism and development of cervical cancer, performing a meta-analysis. METHODS: The pooled association between the XRCC3 Thr241Met polymorphism and cervical cancer risk was assessed by odds ratios (ORs) and their 95% confidence intervals (95%CIs). RESULTS: A total of 5 case-control studies met the inclusion criteria. The pooled ORs for the total included studies showed no association among homozygotes TT vs. CC: OR=1.93, 95%CI=0.68- 5.49, P=0.22; dominant model TT

Expression of fragile histidine triad (FHIT) and WW-domain oxidoreductase gene (WWOX) in nasopharyngeal carcinoma.

The aim of the present study was to analyze the expression of FHIT and WWOX in nasopharyngeal carcinoma (NPC) and correlations with clinical pathologic features. mRNA expression of the FHIT and WWOX was assessed by real-time fluorescent relatively quantitative PCR in 61 NPC tissues and 45 non-cancerous nasopharyngeal tissues. As a result, mRNA expression levels of both FHIT and WWOX were significantly lower in NPC patients than in control samples (P=0.049 and 0.045, respectively). Moreover, the mRNA expression of both had an inverse relation with larger invasive range (P=0.035 and 0.048, respectively), poor histologic differentiation (P=0.012 and 0.016) and advanced clinical stage (P=0.026 and 0.038). Consistency was found between expression of FHIT and WWOX in the same NPC tissues (r=0.681, P=0.00). In conclusion, synergy between FHIT and WWOX may exist in the development of NPC so that the two factors may be considered as important genetic markers. Detecting the expression of FHIT and WWOX should provide clinically significant information relevatn to tumor diagnosis, progression and treatment modalities for NPC.

Cellular sources of interleukin 16 in benign and malignant pleural effusions.

BACKGROUND: Interleukin 16 (IL-16) can be detected by ELISA in pleural effusion (PE) and its concentration is higher than in serum. This study investigated the cellular sources of IL-16 in PE. METHODS: The samples of PE were collected from 34 patients who were newly diagnosed having PE in the pleural cavity. We performed cell culture to purify the pleural mesothelial cells (PMC), Wright staining to count the purity and immunocytochemical stain to identify the cultured cells. The intracellular IL-16 expression was detected by flow cytometry (FCM). The different cells in PE were first separated by magnetic cell sorting (MCAS) then the separated cells were cultured in RPMI1640 with 10% fetal calf serum (FCS). We extracted the supernatant and detected IL-16 concentration by ELISA. The IL-16 protein was detected by immunohistochemistry and double immunofluorescence staining. RESULTS: The percentages of cells which secreted IL-16 were: CD3(+)CD8(-) cells ((74.27 ± 15.56)%, n = 34); CD3(+)CD8(+) cells ((69.86 ± 18.55)%, n = 34); CD19(+) cells ((45.30 ± 18.77)%, n = 15); CD14(+) cells ((16.91 ± 16.69)%, n = 15); and PMC ((2.05 ± 1.85)%, n = 7). The concentrations of IL-16 in the supernatant from cultured cells were: CD4(+) cells ((102.50 ± 42.51) ng/L, n = 5); CD8(+) cells ((92.58 ± 18.34) ng/L, n = 5); CD19(+) cells ((79.85 ± 5.62) ng/L, n = 5); CD14(+) cells ((58.51 ± 25.38) ng/L, n = 5); and PMC ((18.14 ± 8.37) ng/L, n = 5). In lymphocytes, monocytes/macrophages and PMC, we could observe the cells that expressed IL-16 protein. In paraffin-embedded sections, we also could observe by immunohistochemistry the CD4(+)IL-16(+) cells, CD8(+)IL-16(+) cells, CD19(+)IL-16(+) cells, and CD14(+)IL-16(+) cells. CONCLUSIONS: IL-16 in PE is mainly secreted by T lymphocytes, including CD3(+)CD8(-) cells and CD3(+)CD8(+) cells. CD19(+) cells and CD14(+) cells can also secrete IL-16, but the percentage of PMC that can secrete IL-16 is very low.

[The regulation effect of liposomal transfection of antisense oligonucleotide on the alpha-globin in patients with severe beta-thalassemia].

OBJECTIVE: To study the effect of liposomal transfection of antisense oligonucleotide (ASON) on the erythroid cell alpha-globin gene in the patients with severe beta-thalassemia, and provide a new idea for beta-thalassemia gene therapy. METHODS: A highly effective ASON targeting alpha-globin gene was transfected into severe beta-thalassemic erythroid cells cultured in vitro by liposomal at an optimal concentration. The expression level of alpha, beta, gamma-globin gene, the level of hemoglobin, and the excess alpha-globin chains precipitates in ASON group and control group were carefully analyzed by quantitative real-time PCR(Q-RT-PCR), high performance liquid chromatography (HPLC), and electron microscope, respectively. RESULTS: The mRNA expression of alpha-globin gene was significantly lower in ASON group (9.04 +/- 0.29) than in control group (24.23 +/- 0.29) (P<0.01). Simultaneously, the disequilibrium between alpha- and beta-, gamma-globin gene expression was partly modified by ASON, the ratios of ASON group and control group being 0.79 +/- 0.02 and 2.26 +/- 0.06 respectively (P<0.01). HPLC demonstrated that the levels of HbA2 and HbF increased with downregulation of alpha-globin gene in beta-thalassemic erythroid cells, particularly HbF. The precipitates of alpha-globin chains in ASON group were lessened under electron microscope, particularly in early erythroblast while no change in the control group. CONCLUSION: The high effective ASON contributes to inhibit the alpha-globin gene expression of severe beta-thalassemic erythroid cells, partly modify the disequilibrium between alpha-, beta- and gamma-globin gene expression and obviously reduce the precipitates of alpha-globin chains in erythroid cells. It might provide a new idea for gene therapy of beta-thalassemia.

Analysis of Epstein-Barr viral DNA load, EBV-LMP2 specific cytotoxic T-lymphocytes and levels of CD4+CD25+ T cells in patients with nasopharyngeal carcinomas positive for IgA antibody to EBV viral capsid antigen.

BACKGROUND: Epstein-Barr virus (EBV) is a herpesvirus commonly associated with several malignant diseases including nasopharyngeal carcinoma (NPC), which is a common cancer in Southeastern Asia. Previous studies showed that plasma levels of EBV-DNA might be a sensitive and reliable biomarker for the diagnosis, staging and evaluating of therapy for NPC. There are a few analyses of the levels of EBV-latent membrane protein 2 (LMP2)-specific cytotoxic T-lymphocytes (CTLs) in patients with NPC. This study was conducted to investigate the levels of EBV-LMP2-specific CTLs, EBV-DNA load and the level of CD4(+)CD25(+) T cells in such patients. METHODS: From February 2006 to April 2006, 62 patients with NPC, 40 healthy virus carriers positive for EBV viral capsid antigen (EBV-IgA-VCA) and 40 controls were enrolled in the study. We used a highly sensitive ELISPOT assay, real-time polymerase chain reaction (PCR) and flow cytometry to measure the EBV-LMP2-specific CTL response, the EBV DNA load and the level of CD4(+)CD25(+) T cells, respectively. RESULTS: The EBV-LMP2-specific CTL responses of the samples from the control, healthy virus carriers and patients with NPC were significantly different from the LMP2 epitopes, with the control and healthy virus carrier samples displaying a stronger response in three cases. There were significant differences in EBV DNA load in serum between NPC and the healthy groups; patients with NPC at stages III or IV had significantly higher viral loads compared with those at stages I or II. A significantly higher percentage of CD4(+)CD25(+) T lymphocytes were detected in the patients, compared with healthy virus carriers and healthy controls. Moreover, patients with advanced stages of NPC (III and IV) had significantly higher percentages than the patients with early stages (I and II). CONCLUSIONS: Patients with NPC are frequently unable to establish or maintain sufficient immunosurveillance to control proliferating B cells harboring EBV and to destroy the tumor cells that express immunodominant LMP2 proteins. Controlling the activity of CD4(+)CD25(+) T cells and elevating CD8(+) cells specific for LMP2 epitopes could be an effective immunotherapy for patients with NPC.

[Dendritic cells transfected with recombinant adenovirus Ad5F35-LMP2 induces LMP2 specific immunity mediated by cytotoxic T lymphocytes in vitro].

OBJECTIVE: To observe whether dendritic cells (DCs) transfected with recombinant adenovirus Ad5F35-LMP2 induces LMP2 specific immunity mediated by cytotoxic T lymphocytes in vitro. METHODS: Dendritic cells have been generated in vitro, and cocultured with autologous T cell after the DCs were infected with Ad5F35-LMP2, then the proliferation of the induced T cells and their cytotoxic activity against CNE-2 tumor cells which express EBV-LMP2 protein on membrane were assessed by MTT method. RESULTS: The dendritic cells could be transfected with Ad5F35-LMP2 and the CTL activated by Ad5F35-LMP2-DC could effectively suppress the proliferation of CNE-2 cells compared with control groups. CONCLUSION: The dendritic cells transfected with recombinant adenovirus Ad5F35-LMP2 showed cytotoxicity effect by activating T lymphocytes.

[Immune responses induced by recombinant adenovirus Ad5F35-LMP2 in rhesus monkeys].

OBJECTIVE: To observe the specific cellular and humoral immune responses after immunization with recombinant adenovirus Ad5F35-LMP2 in rhesus monkeys. METHODS: Sixteen rhesuses were immunized with Ad5F35-LMP2 through intra-muscular injection in three groups: high dosage group (1.5 x 10(10) TCID(50)/rhesus), medium dosage group (1.5 x 10(9)TCID(50)/rhesus), low dosage group (1.5 x 10(8)TCID50/rhesus) and the last group was control (PBS 4 ml/rhesus). They were totally immunized three times at intervals of one month. The EBV-LMP2 specific cellular immune responses were tested during the 0, 4, 8, 12 weeks by Elispot after immunization respectively. And the titers of anti-LMP2 antibody were tested by EIA at the same time. RESULTS: EBV-LMP2 specific cellular and humoral immune responses which were induced by recombinant adenovirus Ad5F35-LMP2 can be found in all the three dosage groups. The potency of immune responses was related with the dosage of immunization. Higher dosage elicited more potent immune response. CONCLUSION: The recombinant adenovirus Ad5F35-LMP2 could elicit LMP2 specific cellular and humoral immune responses in rhesus.

[Determination and significance of interleukin-16 in tuberculous and malignant pleural effusion].

OBJECTIVE: Interleukin-16 (IL-16) is a chemoattractant of CD4+ lymphocytes, and it has been implicated in the pathogenesis of various inflammatory diseases. The aim of the present study was to measure IL-16 in pleural effusions caused by tuberculosis and malignancy and its relationship with cell and differential counts as well as lymphocyte subsets. METHODS: Pleural effusion and venous blood samples were collected from 32 patients with tuberculous pleuritis and 30 lung cancer patients with malignant effusion. Analysis of pleural effusion for total leukocytes and cell differentials of leukocytes was performed. Three-color flow cytometry was performed to determine T lymphocyte subsets in cell pellets of pleural effusion. The concentration of IL-16 in cell-free supernatants of pleural effusion and sera was measured by a sandwich enzyme-linked immunosorbent assay. RESULTS: In all the studied patients, the level of IL-16 was significantly higher in pleural effusion than in serum. The levels of IL-16 were significantly higher in tuberculous than in malignant effusions. In pleural effusion, positive correlations were found between the IL-16 levels and total cell counts, lymphocytes, CD3+ T cells, as well as CD4+ T cells. CONCLUSIONS: Compared to malignant pleural effusion, IL-16 appeared to be increased in tuberculous pleural effusion. The pleural effusion IL-16 levels were positively related to the numbers of CD4+ T cells, suggesting that IL-16 might be capable of inducing CD4+ T cell infiltration into pleural space.

CD4+CD25+ regulatory T lymphocytes in malignant pleural effusion.

BACKGROUND: Active suppression by CD4(+)CD25(+) regulatory T lymphocytes plays an important role in the downregulation of T-cell responses to foreign and self-antigens. OBJECTIVE: To analyze whether the CD4(+)CD25(+) regulatory T lymphocytes exist and function normally in malignant pleural effusion. METHODS: The percentages of CD4(+)CD25(+) T lymphocytes in pleural effusion and peripheral blood from patients with lung cancer with malignant effusion, pleural lavage and peripheral blood from patients with lung cancer without effusion, and peripheral blood from healthy control subjects were determined by flow cytometry. The expressions of forkhead transcription factor Foxp3 and cytotoxic lymphocyte-associated antigen-4 were also examined. CD4(+)CD25(+) and CD4(+)CD25(-) T cells from pleural effusion and peripheral blood were isolated, and were cultured to observe the effects of CD4(+)CD25(+) cells on proliferation response of CD4(+)CD25(-) T cells in vitro. MAIN RESULTS: There were increased numbers of CD4(+)CD25(+) T cells in malignant pleural effusion from patients with lung cancer compared with pleural lavage from patients with lung cancer without pleural effusion, and that these cells have constitutive high-level expression of Foxp3 and cytotoxic lymphocyte-associated antigen-4. Furthermore, CD4(+)CD25(+) T cells mediate potent inhibition of proliferation response of CD4(+)CD25(-) T cells, and anticytotoxic lymphocyte-associated antigen-4 monoclonal antibody could reduce the inhibitory activity of CD4(+)CD25(+) T cells. CONCLUSIONS: The increased CD4(+)CD25(+) T cells found in malignant pleural effusion express high levels of Foxp3 transcription factor and potently suppress the proliferation of CD4(+)CD25(-) T cells, and cytotoxic lymphocyte-associated antigen-4 is involved in the suppressive activity of pleural CD4(+)CD25(+) T cells.