Vegetation Length is Associated with Long-term Survival in Patients Treated Surgically for Infective Endocarditis.

Background: The impact of vegetation length on therapeutic decision-making and prediction of long-term survival of patients with infective endocarditis is a highly topical issue. The aim of the study was to clarify the impact of vegetation length greater than 10 mm on long-term survival treated surgically for infective endocarditis.

Methods: Patients treated surgically for infective endocarditis in our hospital from January 2006 to November 2022 and were successfully followed up were included in the retrospective analysis.

Modifiable risk factors of immediate and long-term outcomes in the operable and inoperable with left-sided infective endocarditis.

Objectives: To evaluate the outcomes of left-sided infective endocarditis that can be operated on and cannot be operated on, and to focus on modifiable risk factors for immediate and long-term mortality.

Methods: This study retrospectively investigated patients with left-sided infective endocarditis who occurred in our medical center between January 2006 and November 2022.

Results: 48 in-hospital deaths occurred (5.

Risk factors of prolonged intensive care unit stay following cardiac surgery for infective endocarditis.

Introduction: Prolonged intensive care unit (ICU) stay is common in serious patients undergoing cardiac surgery. Prolonged ICU stay is associated with increased mortality and worse prognosis. This study was conducted to determine the risk factors for prolonged ICU stay after cardiac surgery for infective endocarditis (IE) and we try to decrease the operative risk of mortality and morbidity of cardiac surgery for IE.

Surgical treatment of left-sided infective endocarditis with symptomatic neurological complications before surgery in China.

Introduction: We aimed to investigate surgical treatment of left-sided infective endocarditis with symptomatic neurological complications before surgery.

Methods: This was a retrospective study of patients with left-sided infective endocarditis and symptomatic neurological complications before surgery undergoing cardiac surgery between January 2006 and November 2022 at our hospital.

Results: Eight hundred thirty-two patients were divided into group with symptomatic neurological complications before surgery ( = 112) and without symptomatic neurological complications before surgery ( = 720).

Impact of Vegetation Length on Clinical Complications During Surgical Intervention and Long-Term Survival in Infective Endocarditis.

We aimed to investigate the impact of vegetation length on clinical complications during surgical intervention and long-term survival in infective endocarditis. This was a retrospective study of patients with infective endocarditis who underwent cardiac surgery between January 2006 and November 2022 at our hospital. 896 patients were divided into 2 groups: group I (vegetation length <10 mm, n = 448) and group II (vegetation length ≥10 mm, n = 448).

Incomplete Pericardial Dissection, Fluid Overload, Delayed Diagnosis And Treatment, And Tuberculosis Pericarditis Are Associated With Low Cardiac Output Syndrome Following Pericardiectomy.

Background: We aimed to investigate risk factors of LCOS following pericardiectomy.

Methods: This was a retrospective study of patients undergoing pericardiectomy at three hospitals between January 1994 and May 2021.

Results: A total of 826 patients were divided into two groups: group with LCOS (N = 126) and group without LCOS (N = 700).

Analysis of risk factors of multiorgan failure after pericardiectomy for constrictive pericarditis.

Background: We aimed to investigate risk factors of multiorgan failure following pericardiectomy.

Methods: This was a retrospective study of patients undergoing pericardiectomy between January 1994 and May 2021 at three hospitals.

Results: 826 patients were included in the study and divided into two groups: group with multiorgan failure (n = 86) and group without multiorgan failure (n = 740).

Analysis of Risk Factors of Early Mortality After Pericardiectomy For Constrictive Pericarditis.

Background: We aimed to investigate risk factors of early mortality following pericardiectomy.

Methods: This was a retrospective study of patients undergoing pericardiectomy between January 1994 and May 2021 at The People's Hospital of Guangxi Zhuang Autonomous Region, Ruikang Hospital Affiliated to Guangxi University of Chinese Medicine, and The People's Hospital of Liuzhou City.

Results: This study included 826 patients, who were divided into two groups: group with operative deaths (N = 66) and group without operative deaths (N = 760).

Acute Kidney Injury: Lessons from Pericardiectomy.

Background: Acute kidney (renal) injury (AKI) is a severe and common complication that occurs in ~40% of patients undergoing cardiac surgery. AKI has been associated with increased mortality and worse prognosis. This prospective study was conducted to determine the risk factors for AKI after pericardiectomy and decrease the operative risk of mortality and morbidity.

Fluid Balance of the Second Day Following Operation is Associated with Early Mortality and Multiorgan Failure After Pericardiectomy for Constrictive Pericarditis.

Background: The operative mortality of pericardiectomy still is high. This retrospective study was conducted to determine the risk factors of early mortality and multiorgan failure.

Methods: We retrospectively analyzed patients undergoing pericardiectomy from January 2009 to June 2020 at our hospital.

Preoperative Pericardial Effusion is Associated with Low Cardiac Output Syndrome After Pericardiectomy for Constrictive Pericarditis.

Background: Low cardiac output syndrome is the main cause of death after pericardiectomy.

Methods: Patients who underwent pericardiectomy for constrictive pericarditis from January 2009 to October 2020 at our hospital were included in the study. Histopathologic studies of pericardium tissue from every patient were performed.

Diagnosis and Treatment of Mechanical Hemolysis after Mitral Repair in Adult.

Background: Mitral repair has been widely used in the treatment of secondary mitral lesions in recent years. Hemolytic anemia is known to be a rare complication after mitral repair. This study aimed to investigate the diagnosis and treatment of mechanical hemolysis after mitral repair in adults.

APC/C is essential for hematopoiesis and impaired in aplastic anemia.

Anaphase promoting complex/cyclosome (APC/C) is essential for cell cycle progression. Recently, its non-mitotic functions were also reported but less studied in several tissues including hematopoietic cells. Here, we developed an inducible (a core subunit of APC/C) knockout mice.

Clinical comparative analysis of histidine-tryptophan-ketoglutarate solution and St. Thomas crystalloid cardioplegia: A 12-year study from a single institution.

Cardioplegic reperfusion during a long-term ischemic period interrupts cardiac surgery and increases cellular edema due to repeated administration. The present clinical study compared the protective effects of histidine-ketoglutarate-tryptophan (HTK) solution and St. Thomas crystalloid cardioplegia.

DNMT1-maintained hypermethylation of Krüppel-like factor 5 involves in the progression of clear cell renal cell carcinoma.

Clear cell renal cell carcinoma (ccRCC) is the major subtype of renal cell carcinoma (RCC) that is resistant to conventional radiation and chemotherapy. It is a challenge to explore effective therapeutic targets and drugs for this kind of cancer. Transcription factor Krüppel-like factor 5 (KLF5) exerts diverse functions in various tumor types.

Inhibition of Snail Family Transcriptional Repressor 2 (SNAI2) Enhances Multidrug Resistance of Hepatocellular Carcinoma Cells.

China accounts for almost half of the total number of liver cancer cases and deaths worldwide, and hepatocellular carcinoma (HCC) is the most primary liver cancer. Snail family transcriptional repressor 2 (SNAI2) is known as an epithelial to mesenchymal transition-inducing transcription factor that drives neoplastic epithelial cells into mesenchymal phenotype. However, the roles of endogenous SNAI2 remain controversial in different types of malignant tumors.

Pure curcumin increases the expression of SOCS1 and SOCS3 in myeloproliferative neoplasms through suppressing class I histone deacetylases.

Suppressors of cytokine signaling, SOCS1 and SOCS3, are important negative regulators of Janus kinase 2/signal transducers and activators of transcription signaling, which is constitutively activated in myeloproliferative neoplasms (MPNs) and leukemia. Curcumin has been shown to possess anticancer activity through different mechanisms. However, whether curcumin can regulate the expression of SOCS1 and SOCS3 is still unknown.

Synergistic induction of galectin-1 by CCAAT/enhancer binding protein alpha and hypoxia-inducible factor 1alpha and its role in differentiation of acute myeloid leukemic cells.

Galectin-1 is a member of the galectin family and has a high affinity for galactose and N-acetylglucosamine moieties of glycoproteins. It mediates multiple signal transduction pathways to modulate cellular proliferation, survival, differentiation, and migration. However, the mechanisms for the regulation of its expression remain greatly elusive.

Oestrogen causes degradation of KLF5 by inducing the E3 ubiquitin ligase EFP in ER-positive breast cancer cells.

KLF5 (Krüppel-like factor 5) is a multifunctional transcription factor involved in cell proliferation, differentiation and carcinogenesis. In addition to frequent inactivation in different types of human cancers, including breast cancer, KLF5 has been identified as an essential co-factor for the TGF-β (transforming growth factor β) tumour suppressor. In our previous study demonstrating a negative regulation of ER (oestrogen receptor α) function by KLF5 in breast cancer cells [Guo, Dong, Zhao, Sun, Li and Dong (2010) Int.

Hypoxia inducible factor-1 mediates expression of galectin-1: the potential role in migration/invasion of colorectal cancer cells.

The expression of galectin-1, one of the most important lectins participating in the malignant tumor development, has been shown to be regulated by hypoxia, but its exact mechanism remains elusive. Here, we find that ectopically expressed hypoxia-inducible factor (HIF) 1alpha protein, an oxygen-sensitive subunit of HIF-1 that is a master factor for cellular response to hypoxia, significantly increases galectin-1 expression in both messenger RNA and protein levels in all four colorectal cancer (CRC) cell lines tested. However, hypoxia-induced galectin-1 expression cannot be seen in sentrin/SUMO-specific protease 1 homozygous-null mouse embryonic fibroblasts that fail to accumulate HIF-1alpha protein.

Proteomics-based identification of two novel direct targets of hypoxia-inducible factor-1 and their potential roles in migration/invasion of cancer cells.

Hypoxia-inducible factor-1 (HIF-1), consisting of oxygen-sensitive HIF-1alpha and constitutively expressed HIF-1beta subunits, is a master transcriptional activator for cellular response to hypoxia. To explore direct HIF-1 targets, here we used differential gel electrophoresis (DIGE) to compare the HIF-1-regulated proteins between leukemic U937T-cell line with and without conditional induction of HIF-1alpha protein by tetracycline-off system. Among the upregulated proteins identified, mRNA levels of annexin A1, macrophage-capping protein (CapG), S100 calcium-binding protein A4 (S100A4), S100A11, acyl-CoA-binding protein and calcyclin-binding protein also increased.

Estrogen-induced interaction between KLF5 and estrogen receptor (ER) suppresses the function of ER in ER-positive breast cancer cells.

Kruppel-like factor 5 (KLF5) is implicated in human breast cancer by frequent genomic deletion and expressional deregulation, but the molecular mechanisms by which KLF5 affects breast tumorigenesis are still unknown. This study was conducted to examine whether and how KLF5 affects the function of estrogen receptor (ER) in breast cancer cells. Using different cell lines, we found that restored expression of KLF5 inhibited estrogen-promoted cell proliferation in ER-positive MCF-7 and T-47D cell lines but had no effect on ER-negative SK-BR-3 cells.

Acetylation of KLF5 alters the assembly of p15 transcription factors in transforming growth factor-beta-mediated induction in epithelial cells.

KLF5 plays important roles in a variety of cellular processes including proliferation and differentiation. Recently KLF5 was shown to reverse its function in proliferative and p15 regulation upon transforming growth factor-beta (TGFbeta)-mediated acetylation. To understand how KLF5 acetylation functions in TGFbeta-induced p15 transcription, we characterized the interactions of KLF5 with other transcription factors and promoter DNA elements in the context of TGFbeta.

Pro-proliferative factor KLF5 becomes anti-proliferative in epithelial homeostasis upon signaling-mediated modification.

During epithelial homeostasis, stem cells divide to produce progenitor cells, which not only proliferate to generate the cell mass but also respond to cellular signaling to transition from a proliferative state to a differentiation state. Such a transition involves functional alterations of transcriptional factors, yet the underlying molecular mechanisms are poorly understood. Recent studies have implicated Kruppel-like factors (KLFs) including KLF5 in the renewal and maintenance of stem/progenitor cells.

Accumulation of hypoxia-inducible factor-1 alpha protein and its role in the differentiation of myeloid leukemic cells induced by all-trans retinoic acid.

Background: The clinical activities of all-trans retinoic acid in the treatment of acute promyelocytic leukemia, a unique subtype of acute myeloid leukemia, have triggered extensive studies aimed at defining the mechanisms by which this compound induces differentiation of leukemic cells. Recent studies show that hypoxia-inducible factor-1 alpha (HIF-1 alpha) contributes to the differentiation of acute myeloid leukemia cells via transcriptional activity-independent mechanisms. We investigated whether all-trans retinoic acid affects HIF-1 alpha protein and whether this has a role in all-trans retinoic acid-induced differentiation.