Adult ; Haploidy ; Hematopoietic Stem Cell Transplantation ; Hemorrhage ; Humans ; Lung Diseases ; Male ; Pulmonary Alveoli

Humans ; Leukemia, Lymphocytic, Chronic, B-Cell ; Societies, Medical ; United States

OBJECTIVE To investigate the clinical characteristics of imipenem-resistant Pseudomonas aeruginosa sepsis in neutropenic hematological malignancy patients. METHODS A retrospective review of the medical records of 3 cases in neutropenic hematological malignancy patients with P.aeruginosa sepsis in June 2008 were taken. RESULTS All they died within 3 days,2 times blood culture results indicated.With imipenem-resistant P.aeruginosa growth. CONCLUSIONS Neutropenic hematological malignancy patients with imipenem-resistant P.aeruginosa sepsis have rapid progress of the disease and high mortality rates,we should step up surveillance.

Humans ; Leukemia, Large Granular Lymphocytic

Angiotensin II ; pharmacology ; Cells, Cultured ; Focal Adhesion Protein-Tyrosine Kinases ; metabolism ; Humans ; Myocytes, Smooth Muscle ; cytology ; Pulmonary Artery ; cytology

Humans ; Leukemia, Lymphocytic, Chronic, B-Cell ; metabolism ; Wnt Proteins ; metabolism ; Wnt Signaling Pathway

Bacteremia ; etiology ; Catheterization ; adverse effects ; Child ; Coagulase ; metabolism ; Cross Infection ; etiology ; Drug Resistance, Bacterial ; drug effects ; Endocarditis, Bacterial ; etiology ; Humans ; Methicillin ; pharmacology ; Quinolones ; pharmacology ; Staphylococcal Infections ; complications ; drug therapy ; microbiology ; Staphylococcus ; classification ; drug effects ; pathogenicity ; Urinary Tract Infections ; etiology ; Vancomycin ; pharmacology

Adenocarcinoma ; metabolism ; pathology ; Adult ; Aged ; Carcinoma, Non-Small-Cell Lung ; metabolism ; pathology ; Carcinoma, Squamous Cell ; metabolism ; pathology ; Female ; Humans ; Immunohistochemistry ; Lung ; chemistry ; pathology ; Lung Neoplasms ; metabolism ; pathology ; Male ; Middle Aged ; Oxidoreductases ; metabolism ; Sex Factors ; Smoking ; Tumor Suppressor Proteins ; metabolism ; WW Domain-Containing Oxidoreductase

Objective To explore the effects of estrogen on stress-induced senescence of vascular smooth muscle cells (VSMCs) and the underlying mechanisms. Methods The VSMCs of passage 2-3 cultured from female SD rats were induced into senescence by exposing to 150μmol/L H2O2 in the presence or absence of different concentrations(10-10mol/L-10-8mol/L) of 17β-estradiol (E2). The expressions or activities of senescence associated marker DcR2, senescence-associated beta-galactosidase (SA-β-Gal), oncogene Ras and p21WAF1 were detected by flow cytometry, cytochemical staining, pull-down assay or Western blotting analysis. Results Flow cytometry analysis showed that in the physiological concentrations, E2 significantly inhibited the H2O2-promoted high-level expression of DcR2 of VSMCs in a dose-dependent manner, with a highest inhibitive rate at 14.48%±0.6%(E2=10-8 mol/L;P<0.05, n =3);this inhibitive effect could be blocked by a E2 receptors inhibitor ICI 182,780. Cytochemistry staining showed that the rate of SA-β-Gal positive VSMCs induced by H2O2 decreased in presence of 10-8mol/L E2 (20.5%±1.4% vs 9.6%±0.9%;P<0.05, n =9). Pull-down assay and Western blotting analysis revealed that administration of 10-8mol/L E2 obviously reduced the H2O2-induced activity of Ras (0.60±0.06 vs 0.26±0.04;P<0.05, n =3) and expression of p21WAF1 (0.46±0.04 vs 0.33±0.02;P<0.05, n =3). Conclusion E2 exerts, an inhibitive effects on stress-induced senescence of VSMCs by suppressing the activity of Ras and expression of p21WAF1. This finding suggests a novel mechanism for the hormone's anti-atheroschlerotic effects.