[The characteristics of RR-Lorenz plot in persistent atrial fibrillation patients complicating with escape beats and rhythm].

OBJECTIVE: To explore the characteristics of RR-Lorenz plot in persistent atrial fibrillation (AF) patients complicating with escape beats and rhythm though ambulatory electrocardiogram. METHODS: The 24-hour ambulatory electrocardiogram of 291 persistent AF patients in second affiliated hospital of Zhengzhou university from July 2005 to April 2013 were retrospectively analyzed and the RR interval and the QRS wave were measured. Patients were divided into two groups according to the distribution of the RR-Lorenz point [AF without escape beats and rhythm group (Group A, n = 259) and AF with escape beats and rhythm group (Group B, n = 32)]. The characteristics of RR-Lorenz plot between the two groups were compared. RESULTS: (1) Fan-shaped RR-Lorenz plots were evidenced in Group A. (2)In Group B, 30 cases showed fan-shaped with L-shaped and a short dense rods along 45° line. The proportion of escape beats and rhythm was 0.28% (275/98 369) -14.06% (11 263/80 112) . The other 2 cases in group B showed no typical RR-Lorenz plots features. CONCLUSION: RR-Lorenz plot could help to quickly diagnose persistent AF complicating with escape beats and rhythm according to the typical RR-Lorenz plot characteristics in 24-hour ambulatory electrocardiogram.

Copper induces cellular senescence in human glioblastoma multiforme cells through downregulation of Bmi-1.

Most human tumor cells, including glioblastoma multiforme (GBM) cells, have aberrant control of cell aging and apoptosis. Subcytotoxic concentrations of oxidative or stress­causing agents, such as hydrogen peroxide, may induce human cell senescence. Thus, induction of tumor cells into premature senescence may provide a useful in vitro model for developing novel therapeutic strategy to combat tumors. In the present study, we assessed the molecular mechanism(s) underlying senescence in GBM cells induced by copper sulfate. Following pretreatment with subcytotoxic concentrations of copper sulfate, U87-MG tumor cells showed typical aging characteristics, including reduced cell proliferation, cell enlargement, increased level of senescence-associated ß-galactosidase (SA ß-gal) activity, and overexpression of several senescence-associated genes, p16, p21, transforming growth factor ß-1 (TGF-ß1), insulin growth factor binding protein 3 (IGFBP3) and apolipoprotein J (ApoJ). We further demonstrated that the Bmi-1 pathway was downregulated in GBM cells in parallel with the induced senescence. The present study for the first time demonstrates the ability of copper to induce GBM cell senescence by downregulating Bmi-1.

Prenatal allergen and diesel exhaust exposure and their effects on allergy in adult offspring mice.

BACKGROUND: Multiple studies have suggested that prenatal exposure to either allergens or air pollution may increase the risk for the development of allergic immune responses in young offspring. However, the effects of prenatal environmental exposures on adult offspring have not been well-studied. We hypothesized that combined prenatal exposure to Aspergillus fumigatus (A. fumigatus) allergen and diesel exhaust particles will be associated with altered IgE production, airway inflammation, airway hyperreactivity (AHR), and airway remodeling of adult offspring. METHODS: Following sensitization via the airway route to A. fumigatus and mating, pregnant BALB/c mice were exposed to additional A. fumigatus and/or diesel exhaust particles. At age 9-10 weeks, their offspring were sensitized and challenged with A. fumigatus. RESULTS: We found that adult offspring from mice that were exposed to A. fumigatus or diesel exhaust particles during pregnancy experienced decreases in IgE production. Adult offspring of mice that were exposed to both A. fumigatus and diesel exhaust particles during pregnancy experienced decreases in airway eosinophilia. CONCLUSION: These results suggest that, in this model, allergen and/or diesel administration during pregnancy may be associated with protection from developing systemic and airway allergic immune responses in the adult offspring.

Chronological changes in metabolism and functions of cultured adipocytes: a hypothesis for cell aging in mature adipocytes.

The growth and aging of 3T3-L1 adipocytes were investigated in a synchronized tissue-culture system. We systematically characterized several major aspects of adipocyte metabolism and functions as variables of cell age. We found that terminal differentiation of 3T3-L1 cells is followed by a near-linear hypertrophic growth (increase in triglyceride content) of the cultured adipocytes throughout a 20-day study period. However, three metabolically and functionally distinct stages are recognized. The first stage overlaps with differentiation and is represented by small immature adipocytes. The second stage is characterized by fully mature adipocytes that show peaked overall metabolic activities. The third stage is marked by cell aging, with deterioration in every major aspect of the cell's functionality except for the function of net energy storage, which is preserved even in aged adipocytes. Compared with young mature adipocytes, older cells are increasingly insulin resistant, have decreased glucose uptake and fuel consumption, and show impaired glycerokinase-mediated fatty acid reesterification. Moreover, aged adipocytes show reduced gene expression for adiponectin and leptin, each of which is important in systemic regulation of energy metabolism. The characterization of these cell age-dependent changes in adipocyte functionality provides a model for understanding dynamic changes at the tissue level and suggests that adipose tissue is modifiable via adipocyte aging.