Age, Pulse, Urea, and Albumin Score: A Tool for Predicting the Short-Term and Long-Term Outcomes of Community-Acquired Pneumonia Patients With Diabetes.

Objective: The predictive performances of CURB-65 and pneumonia severity index (PSI) were poor in patients with diabetes. This study aimed to develop a tool for predicting the short-term and long-term outcomes of CAP in patients with diabetes. Methods: A retrospective study was conducted on 531 CAP patients with type 2 diabetes. The short-term outcome was in-hospital mortality. The long-term outcome was 24-month all-cause death. The APUA score was calculated according to the levels of Age (0-2 points), Pulse (0-2 points), Urea (0-2 points), and Albumin (0-4 points). The area under curves (AUCs) were used to evaluate the abilities of the APUA score for predicting short-term outcomes. Cox regression models were used for modeling relationships between the APUA score and 24-month mortality. Results: The AUC of the APUA score for predicting in-hospital mortality was 0.807 in patients with type 2 diabetes (P<0.001). The AUC of the APUA score was higher than the AUCs of CURB-65 and PSI class (P<0.05). The long-term mortality increased with the risk stratification of the APUA score (low-risk group (0-1 points) 11.5%, intermediate risk group (2-4 points) 16.9%, high risk group (≥5 points) 28.8%, P<0.05). Compared with patients in the low-risk group, patients in the high-risk group had significantly increased risk of long-term death, HR (95%CI) was 2.093 (1.041~4.208, P=0.038). Conclusion: The APUA score is a simple and accurate tool for predicting short-term and long-term outcomes of CAP patients with diabetes.

Association between thymosin beta4 and non-alcoholic fatty liver disease

Background and aims: non-alcoholic fatty liver disease (NAFLD) is the most common type of chronic liver injury worldwide. Some studies have shown that thymosin beta4 (Tß4) is closely related to liver diseases. Nevertheless, only a few published studies have reported the relationship between Tß4 and NAFLD. The purpose of this study was to evaluate the levels of Tß4 in patients with NAFLD compared with controls and to validate their relationship in a larger cohort. Patients and methods: a total of 76 NAFLD patients and 130 healthy controls were included in the study. Serum levels of Tß4, IL-6 and adiponectin were determined by ELISA. Serum glucose, insulin and lipids, as well as liver function were measured. Multivariate statistical analyses were performed via logistic regression modelling to determine the predictors with a significant relevance to NAFLD. The association between serum Tß4 and study variables was tested using correlation coefficients calculations. Results: serum Tß4 content was 3.20 +/- 0.98 mg/l in NAFLD patients (n = 76) and 5.53 +/- 1.24 mg/l in healthy controls (n = 130); the difference between the two groups was statistically significant (p = 0.000). Multivariate logistic regression analysis identified Tß4 (OR = 0.343, 95% CI 0.240-0.491, p < 0.001), LDL (OR = 1.019, 95% CI 1.007-1.030, p = 0.001), ALT (OR = 1.021, 95% CI 1.001-1.041, p = 0.040) and IL-6 (OR = 1.443, 95% CI 1.079-1.929, p = 0.013) as independent predictors of NAFLD diagnosis. Serum Tß4 levels had a significant negative correlation with total cholesterol, TG, AST, GGT and IL-6 (p < 0.05 for all) and the correlation coefficient values were -0.163, -0.253, -0.143, -0.245 and -0.155, respectively. Serum Tß4 levels were positively correlated with serum adiponectin levels, with a correlation coefficient value of 0.143. Conclusion: serum Tß4 may play a defensive role in the development of NAFLD. Further studies are needed to confirm the role of Tß4 in NAFLD

No disponible

Association between thymosin beta4 and non-alcoholic fatty liver disease.

BACKGROUND AND AIMS: non-alcoholic fatty liver disease (NAFLD) is the most common type of chronic liver injury worldwide. Some studies have shown that thymosin beta4 (Tß4) is closely related to liver diseases. Nevertheless, only a few published studies have reported the relationship between Tß4 and NAFLD. The purpose of this study was to evaluate the levels of Tß4 in patients with NAFLD compared with controls and to validate their relationship in a larger cohort. PATIENTS AND METHODS: a total of 76 NAFLD patients and 130 healthy controls were included in the study. Serum levels of Tß4, IL-6 and adiponectin were determined by ELISA. Serum glucose, insulin and lipids, as well as liver function were measured. Multivariate statistical analyses were performed via logistic regression modelling to determine the predictors with a significant relevance to NAFLD. The association between serum Tß4 and study variables was tested using correlation coefficients calculations. RESULTS: serum Tß4 content was 3.20 ± 0.98 mg/l in NAFLD patients (n = 76) and 5.53 ± 1.24 mg/l in healthy controls (n = 130); the difference between the two groups was statistically significant (p = 0.000). Multivariate logistic regression analysis identified Tß4 (OR = 0.343, 95% CI 0.240-0.491, p < 0.001), LDL (OR = 1.019, 95% CI 1.007-1.030, p = 0.001), ALT (OR = 1.021, 95% CI 1.001-1.041, p = 0.040) and IL-6 (OR = 1.443, 95% CI 1.079-1.929, p = 0.013) as independent predictors of NAFLD diagnosis. Serum Tß4 levels had a significant negative correlation with total cholesterol, TG, AST, GGT and IL-6 (p < 0.05 for all) and the correlation coefficient values were -0.163, -0.253, -0.143, -0.245 and -0.155, respectively. Serum Tß4 levels were positively correlated with serum adiponectin levels, with a correlation coefficient value of 0.143. CONCLUSION: serum Tß4 may play a defensive role in the development of NAFLD. Further studies are needed to confirm the role of Tß4 in NAFLD.

[Expression of ADAR1 isoforms in murine acute T-ALL leukemia model].

This study was purposed to investigate the expression of ADAR1 isoforms of P110 and P150 during the development of murine leukemia. A Notch1 over-expressing murine T cell acute lymphoblastic leukemia model was used to study the expression of ADAR1. BMMNC were isolated at different stages of disease and CD45.2(+)GFP(+) leukemia cells were sorted by flow cytometry at late stage. The expression of ADAR1 was detected by real time quantitative PCR. The results showed that mouse bone marrow cells from both leukemia and control groups expressed P110 and P150. Difference of P110 and P150 mRNA expression were observed during the development of leukemia. The expression of P110 dramatically increased and was significantly higher than that in control group. However, the expression level of P150 in leukemia group decreased stably and reached one-fourth of that in control group at 14 day. Furthermore, similar expression patterns could be detected in sorted CD45.2(+)GFP(+) leukemia cells. It is concluded that the mRNA expressions of P110 and P150 show diverse patterns in the development of leukemia, suggesting that RNA editing mediated by ADAR1 isoforms may play different roles in leukemia.

Abnormal expression of ADAR1 isoforms in Chinese pediatric acute leukemias.

The posttranscriptional RNA editing by the type 1 adenosine deaminase acting on RNAs (ADAR1), expressed as p110 and p150 isoforms, is important for both physiological and pathological processes. Their expression and significance in leukemias remain unknown. Here, we investigated the expression of ADAR1 in Chinese pediatric acute leukemias by real-time PCR and Western blot. The results showed that significant high expression of p110 was detected in leukemias, especially in B-ALL, whereas a slight increase of p150 could be observed. Furthermore, the decrease of p110 expression was observed in B-ALL patients achieving complete remission. Moreover, among prognostic risk groups in ALL, the highest expressions of p110 and p150 were detected in standard-risk group, whereas their lowest expressions were in high-risk group. This observation was further confirmed in comparisons between good and poor prognostic groups based on prognostic related clinical features. These results demonstrated that ADAR1 isoforms showed different expression patterns, suggesting that they might play different roles in pediatric leukemias. Our results will help us for the better understanding of RNA editing, exploring the potential target for the treatment, and making prognostic evaluation in childhood leukemias.

Abnormal expression of P2X family receptors in Chinese pediatric acute leukemias.

Nucleotides are new players in intercellular communication network. P2X family receptors are ATP-gated plasma membrane ion channels with diverse biological functions. Their distribution patterns and significance in pediatric leukemias have not been established. Here we investigated the expression of P2X receptors in BMMC samples from Chinese pediatric acute leukemias. Real-time PCR and Western blot results showed that P2X1, P2X4, P2X5 and P2X7 receptors were simultaneously over expressed in leukemias compared with controls, whereas P2X2, P2X3 and P2X6 were absent or marginally expressed in both groups. It was worth noting that the co-expression feature of them, especially between P2X4 and P2X7, could be observed and the highest expression of P2X7 was detected in relapsed patients. Moreover, concomitant decrease of P2X4, P2X5 and P2X7 expressions was observed at CR stage in a follow-up study. Functional P2X7 was also verified. These results suggested that P2X1, P2X4, P2X5 and P2X7 were hematopoiesis-related P2X receptors, and their signaling, especially for P2X7, might play important roles in pediatric leukemias. P2X receptors might co-operatively contribute to the malignant phenotype in human pediatric leukemias.

A special linker between macrophage and hematopoietic malignant cells: membrane form of macrophage colony-stimulating factor.

The membrane form of macrophage colony-stimulating factor (mM-CSF) is an alternative splicing variant of this cytokine. Although its high expression was detected in hematopoietic malignancies, its physiologic and pathologic roles in hematopoietic system have not been established. In this report, stable transfectant clones expressing mM-CSF (Namalwa-M and Ramos-M) were obtained, which showed reduced proliferation potential in vitro. Moreover, the in vivo study showed that Namalwa-M and Ramos-M exhibited enhanced oncogenicity in tumor size in nude mice model, which could be inhibited by M-CSF monoclonal antibody. A remarkable increase in infiltrating macrophage and the vessel densities was found in tumor tissues formed by lymphoma cell lines that stably expressed mM-CSF, which suggested the involvement of macrophages in this process. The in vitro results using coculture system showed that macrophages could promote Namalwa-M and Ramos-M proliferation and activate extracellular signal-regulated kinase/mitogen-activated protein kinase signal pathway. In addition, the expression of murine origin vascular endothelial growth factor, basic fibroblast growth factor, and hepatocyte growth factor was elevated in Namalwa-M formed tumor tissues. These results suggested that mM-CSF should be a positive regulator in the development of hematopoietic malignancies by abnormally activating infiltrating macrophages, which in turn promote the malignant development. Thus, mM-CSF may be a critical linker between macrophages and malignant cells in the development of hematopoietic malignancies.