We have previously shown that dysregulation of miR-21 functioned as an oncomiR in breast cancer. The aim of the present study was to elucidate the mechanisms by which miR-21 regulate breast tumor migration and invasion. We applied pathway analysis on genome microarray data and target-predicting algorithms for miR-21 target screening, and used luciferase reporting assay to confirm the direct target. Thereafter, we investigated the function of the target gene phosphoinositide-3-kinase, regulatory subunit 1 (α) (PIK3R1), and detected PIK3R1 coding protein (p85α) by immunohistochemistry and miR-21 by RT-qPCR on 320 archival paraffin-embedded tissues of breast cancer to evaluate the correlation of their expression with prognosis. First, we found that PIK3R1 suppressed growth, invasiveness, and metastatic properties of breast cancer cells. Next, we identified the PIK3R1 as a direct target of miR-21 and showed that it was negatively regulated by miR-21. Furthermore, we demonstrated that p85α overexpression phenocopied the suppression effects of antimiR-21 on breast cancer cell growth, migration and invasion, indicating its tumor suppressor role in breast cancer. On the contrary, PIK3R1 knockdown abrogated antimiR-21-induced effect on breast cancer cells. Notably, antimiR-21 induction increased p85α, accompanied by decreased p-AKT level. Besides, antimiR-21/PIK3R1-induced suppression of invasiveness in breast cancer cells was mediated by reversing epithelial-mesenchymal transition (EMT). p85α downregulation was found in 25 (7.8%) of the 320 breast cancer patients, and was associated with inferior 5-year disease-free survival (DFS) and overall survival (OS). Taken together, we provide novel evidence that miR-21 knockdown suppresses cell growth, migration and invasion partly by inhibiting PI3K/AKT activation via direct targeting PIK3R1 and reversing EMT in breast cancer. p85α downregulation defined a specific subgroup of breast cancer with shorter 5-year DFS and OS, which may require more aggressive treatment.

This report reviews our experience in venoarterial extracorporeal membrane oxygenation (ECMO) support treatment in adult patients with cardiac failure, as well as analysis of the risk factors of early mortality. From February 2005 to June 2008, 45 patients undergoing cardiogenic shock required temporary ECMO support. They were divided into three groups: post-cardiotomy (n=31) and post-transplantation (n=5) heart failure, decompensated heart failure (n=9). ECMO implantation was performed through the femoral vessels, or axillary artery, or through the right atrium and ascending aorta. Average support duration was 126.7+/-104.3 h. Twenty-seven patients could be successfully weaned from support (60%); additionally, five were bridged to heart transplantation. The in-hospital mortality was 42% (19/45). Twenty-six patients (58%) could be successfully discharged. Additional intra-aortic balloon pumps were used in 11 patients, and six of them were successfully discharged. The mortality rate was obviously high for patients with acute renal failure treated by continuous renal replacement therapy (CRRT) under ECMO support (7/9 patients). The dominant mode of death was multisystem organ failure (9/19). ECMO offers effective cardiopulmonary support in adults. The better outcome requires a multidisciplinary approach to prevent complications unique to itself and limit organ injury before and during this support.

Recent studies provide convincing evidence that a combined immunohistochemical or fluorescence in situ hybridization (FISH) score of MYC, BCL2, BCL6 proteins and MYC translocations predicted outcome in diffuse large B-cell lymphoma (DLBCL) patients treated with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP). However, by far, all these researches are based on Western populations. Therefore, we investigate the prognostic relevance of MYC-, BCL2- and BCL6-rearrangements and protein expression by immunohistochemistry and FISH from 336 de novo DLBCL, NOS treated with CHOP or R-CHOP. Breaks in MYC and BCL6, and fusion in IGH/BCL2 were detected in 9.7%, 20.0%, and 11.1% of the cases, respectively, and were not significantly associated with clinical outcomes. Protein overexpression of MYC (≥40%), BCL2 (≥70%) and BCL6 (≥50%) was encountered in 51%, 51% and 36% of the tumors, respectively. On the basis of MYC, BCL2 and BCL6 expression, double-hit scores (DHSs) and triple-hit score (THS) were assigned to all patients with DLBCL. Patients with high MYC/BCL2 DHS, high MYC/BCL6 DHS and high THS had multiple adverse prognostic factors including high LDH level, poor performance status, advanced clinical stage, high International Prognostic Index (IPI) score, and non-germinal center B-cell. In univariate analysis, high MYC/BCL2 DHS, high MYC/BCL6 DHS and high THS were associated with inferior OS and PFS in both CHOP and R-CHOP cohorts (P<0.05). The highly significant correlations with OS and PFS were maintained in multivariate models that controlled for IPI (P<0.05). DLBCLs with high DHSs and high THS share the clinical features and poor prognosis of double-hit lymphoma (P>0.05). These data together suggest that the immunohistochemical DHSs and THS defined a large subset of DLBCLs with double-hit biology and was strongly associated with poor outcome in patients treated with R-CHOP or CHOP.

The modified classification system for ruptured sinus of Valsalva aneurysm is simple and practical for clinical use.

Cardiac fibrosis, as a pathological process, plays an important role in various cardiac diseases. microRNA-155 (miR-155) is one of the most important miRNAs, and previous studies have shown that it is a regulatory factor in various fibrotic diseases. However, the mechanism by which miR-155 affects myocardial fibrosis remains unclear. In this study, we aim to establish the biological function of miR-155 in myocardial fibrosis induced by diabetes in mice. We used normal C57BL/6 wild type (WT) and miR-155 knockout (KO) mice to establish the diabetic model by intraperitoneal injection of streptozotocin, and we utilized echocardiography to evaluate the cardiac function at 30 and 60 days post-modeling. Hematoxylin-eosin (HE) and sirius-red (SR) staining were used to evaluate the degree of myocardial lesions. Furthermore, we extracted cardiac fibroblasts (CFs) from the WT mice and transfected them with miR-155 inhibitors, mimics and negative control siRNAs to analyze the specific mechanism involved in the development of myocardial fibrosis. The results showed that miR-155 deficiency could prevent cardiac fibrosis induced by diabetes in mice and also that attenuated collagen synthesis is induced by high glucose (HG) in CFs. We found that miR-155 regulated cardiac fibrosis via the TGF-β1-Smad 2 signaling pathway. These findings suggest that miR-155 may be a therapeutic target for preventing cardiac fibrosis induced by diabetes.

Patients with acute type A aortic dissection and certain serious medical conditions were more likely to die in the hospital if they underwent emergency nighttime surgical procedures.

No abstract

A study was conducted to evaluate the outcomes of the bidirectional Glenn shunt technique performed off-pump. Between April 1999 and April 2001, 36 patients underwent bidirectional Glenn shunt, unilateral in 28 patients and bilateral in 8 patients, without using cardiopulmonary bypass. The patients consisted of 25 males and 11 females with a mean age of 5.7 +/- 5.4 years and a mean body surface area of 0.72 +/- 0.34 m2. Preoperative percutaneous oxygen saturation was 75% +/- 7%, and pulmonary arterial pressure was 14.3 +/- 3.6 mmHg. There was no operative mortality. Chylothorax occurred in 1 patient in the early postoperative period. All the other patients were discharged without complications. Mean arterial oxygen saturation at discharge was 92.7% +/- 4.0%. This shunt technique is easy to perform and is helpful in the early management of patients with a functionally univentricular heart. However, much remains to be learned about this unusual physiological system.