Acute adriamycin-induced cardiotoxicity is exacerbated by angiotension II

Adriamycin (ADR) increases the production of reactive oxygen species (ROS), which diminishes mitochondrial function. Angiotensin-II stimulates mitochondrial ROS generation. The aim of the study was to examine whether angiotensin converting enzyme (ACE) or renin inhibitors protect against ADR-induced mitochondrial function impairment. Rats were divided into five groups as control, ADR, co-treatment ADR with captopril, co-treatment ADR with aliskiren, co-treatment ADR with both captopril and aliskiren. Left ventricular function and blood pressures were assessed at the end of treatment period. Mitochondrial membrane potential (MMP) and ATP levels were determined. ADR treatment decreased the left ventricular pressure and increased the left ventricular end-diastolic pressure. ADR decreased MMP and ATP levels in myocyte mitochondria due to increasing oxidative stress. ADR decreased MMP and ATP levels due to increased oxidative stress in the heart. Inhibitors of ACE and renin caused the elevation of the decreased of MMP and ATP levels. The pathologic changes in electrocardiogram, blood pressure and left ventricular function were decreased by inhibition of Ang-II production. We concluded that inhibitors of angiotensin II are effective against ADR cardiotoxicity via the restoration of MMP and ATP production and prevention of mitochondrial damage in vivo.     

A rare case of monosomy 18p: translocation between chromosomes 18 and 21

A rare case of monosomy 18p with molecular cytogenetic characterization of 18;21 whole arm translocation is presented. An 8-year-old gril with mental deficiency and growth deficiency was the child of a 45-year-old healthy mother and 50-year-old nonconsanguineous father with unremarkable prenatal history. She had a round face, flat nasal bridge, micrognathia and hypotonia. Cytogenetic studies revealed de novo 45,XX,del(18)t(18;21) karyotype, which was confirmed by fluorescence in situ hybridization (FISH).     

Immunogenicity and protective efficacy of recombinant iron superoxide dismutase protein from Bordetella pertussis in mice models

Whooping cough (pertussis) is a highly contagious respiratory infection caused by Bordetella pertussis. Although availability of effective pertussis vaccines reportedly decreases the incidence of the disease, B. pertussis circulation in populations has not been eliminated. Thus, it is necessary to find new protein candidates with greater immune protective capacities than the currently available acellular pertussis vaccines. In this study, iron superoxide dismutase (FeSOD) gene (sodB) was cloned, expressed in Escherichia coli and recombinant FeSOD protein thence purified. The recombinant protein (rFeSOD) was formulated with aluminum hydroxide (Alum) or monophosphoryl lipid A (MPLA) and injected intraperitoneally to immunize mice, after which IgG1, IgG2a and IFN‐γ titers were measured to assess humoral and cellular responses, respectively, to these immunizations. The extent of bacterial colonization in lungs of intranasally challenged mice was determined 5, 8 and 14 days post‐challenge. IgG1 and IgG2a responses were significantly stronger in mice that had been immunized with rFeSOD–MPLA than in those that had received rFeSOD‐Alum (P < 0.05). Additionally, IgG2a titers were higher in mice vaccinated with recombinant protein FeSOD (rFeSOD) formulated with MPLA, especially after the second immunization. Immunization with rFeSOD–MPLA also provided a modest, but significant decrease in bacterial counts in lungs of mice (P < 0.05). Antigen specific‐IFN‐γ responses were significantly stronger in the group vaccinated with rFeSOD–MPLA, which could account for the lower bacterial counts. These findings suggest that rFeSOD protein formulated with MPLA has potential as an acellular pertussis vaccine candidate component.     

Thermally stimulated luminescence glow curve structure of β‐irradiated CaB4O7:Dy

Thermally stimulated luminescence glow curves of CaB₄O₇:Dy samples after β‐irradiation showed glow peaks at ~335, 530 and 675 K, with a heating rate of 2 K/s. The main peak at 530 K was analyzed using the T_max–T_stop method and was found to be composed of at least five overlapping glow peaks. A curve‐fitting program was used to perform computerized glow curve deconvolution (CGCD) analysis of the complex peak of the dosimetric material of interest. The kinetic parameters, namely activation energy (E) and frequency factor (s), associated with the main glow peak of CaB₄O₇:Dy at 520 K were evaluated using peak shape (PS) and isothermal luminescence decay (ILD) methods. In addition, the kinetics was determined to be first order (b =1) by applying the additive dose method. The activation energies and frequency factors obtained using PS and ILD methods are calculated to be 0.72 and 0.72 eV and 8.76 × 10⁵ and 1.44 × 10⁶/s, respectively. Copyright © 2014 John Wiley & Sons, Ltd.     

Thiamine-responsive megaloblastic anemia syndrome: a novel mutation

The thiamine-responsive megaloblastic anemia syndrome (TRMA) is an autosomal recessive disorder characterized by diabetes mellitus, megaloblastic anemia and sensorineural hearing loss due to mutations in SLC 19A2 that encodes a thiamine transporter protein. The disease can manifest at any time between infancy and adolescence, and not all cardinal findings are present initially. The anemia typically improves significantly with pharmacological doses of thiamine. Variable improvement in diabetes is also noted. However, the hearing loss is apparently irreversible, although a delay in the onset of deafness may be possible. We present a 2-year old girl with non-autoimmune diabetes mellitus and anemia in whom we found a novelc.95T>A (leu32X) mutation in the SLC19A2 gene in this study.Our patient with this new mutation did not suffer from hearing loss.     

Antifungal activity of olive leaf (Olea Europaea L.) extracts from the Trilye Region of Turkey

Antimicrobial properties of olive leaf extract on some yeast were examined in this study. Fresh olive leaf extracts were prepared using various solvents (water, ethanol, acetone, ethyl acetate) in Soxhlet apparatus. Antimicrobial effects of these extacts were tested againstSaccharomyces cerevisiae ATCC 9763,Schizosaccharomyces pombe, Saccharomyces uvarum, Candida oleophila, Metschnikowia fructicola andKloeckera apiculata. The antifungal activities of these extracts were tested by the disc diffusion assay, minimum inhibitory concentration (MIC) and minimum fungicidal concentration (MFC). All extracts showed various degrees of antifungal effects with 10–28 μg/ml MIC, 20–48 μg/ml MFC and 1.5–9.3 mm inhibitory zone values against yeasts utilised, except water. The results indicated that the tested yeasts were sensitive to acetone and ethyl acetate extracts. It was determined thatSaccharomyces cerevisiae ATCC 9763 was the most resistant among the yeasts.     

Elements of disease in a changing world: modelling feedbacks between infectious disease and ecosystems

An overlooked effect of ecosystem eutrophication is the potential to alter disease dynamics in primary producers, inducing disease‐mediated feedbacks that alter net primary productivity and elemental recycling. Models in disease ecology rarely track organisms past death, yet death from infection can alter important ecosystem processes including elemental recycling rates and nutrient supply to living hosts. In contrast, models in ecosystem ecology rarely track disease dynamics, yet elemental nutrient pools (e.g. nitrogen, phosphorus) can regulate important disease processes including pathogen reproduction and transmission. Thus, both disease and ecosystem ecology stand to grow as fields by exploring questions that arise at their intersection. However, we currently lack a framework explicitly linking these disciplines. We developed a stoichiometric model using elemental currencies to track primary producer biomass (carbon) in vegetation and soil pools, and to track prevalence and the basic reproduction number (R₀) of a directly transmitted pathogen. This model, parameterised for a deciduous forest, demonstrates that anthropogenic nutrient supply can interact with disease to qualitatively alter both ecosystem and disease dynamics. Using this element‐focused approach, we identify knowledge gaps and generate predictions about the impact of anthropogenic nutrient supply rates on infectious disease and feedbacks to ecosystem carbon and nutrient cycling.