First Record of Steinernema kraussei (Rhabditida: Steinernematidae) from Turkey and Its Virulence against Agrotis segetum (Lepidoptera: Noctuidae)

During a survey of entomopathogenic nematodes (EPNs) in the eastern Black Sea region of Turkey in 2009–2012, a steinernematid species was recorded and isolated using the Galleria-baiting method. The isolate was identified as Steinernema kraussei based on its morphological and molecular properties. The analysis of the ITS rDNA sequence placed the Turkish population of S. kraussei in the “feltiae-kraussei” group in the clade that contains different isolates of the species. This is the first record of S. kraussei from Turkey. The efficacy of S. kraussei was tested on Agrotis segetum (Lepidoptera: Noctuidea) larvae at different densities (100, 300, and 500 infective juveniles (IJs) g⁻¹ dry sand ) in laboratory conditions at 25 °C. The highest mortality (98%) was obtained with 500 IJs g⁻¹ dry sand within 7 d after inoculation. Our results indicate that the new isolate is a highly promising biological control agent against A. segetum, one of the most serious soil pests of agricultural area and fruits worldwide.     

Nitric oxide mediates protective effect of endothelin receptor antagonism during myocardial ischemia and reperfusion

Endothelin (ET) receptor antagonism protects from ischemia-reperfusion injury. We hypothesized that the cardioprotective effect is related to nitric oxide (NO) bioavailability. Buffer-perfused rat and mouse hearts were subjected to ischemia and reperfusion. At the onset of ischemia, the rat hearts received vehicle, the dual endothelin type A/type B (ETA/ETB) receptor antagonist bosentan (10 microM), the NO synthase inhibitor NG-monomethyl-L-arginine (L-NMMA; 100 microM), the combination of bosentan and L-NMMA or the combination of bosentan, L-NMMA, and the NO substrate L-arginine (1 mM). Hearts from wild-type and endothelial NO synthase (eNOS)-deficient mice received either vehicle or bosentan. Myocardial performance, endothelial function, NO outflow, and eNOS expression were monitored. Bosentan significantly improved myocardial function during reperfusion in rats and in wild-type mice, but not in eNOS-deficient mice. The functional protection afforded by bosentan was inhibited by L-NMMA, whereas it was restored by L-arginine. Myocardial expression of eNOS (immunoblotting) increased significantly in bosentan-treated rat hearts compared with vehicle hearts. Recovery of NO outflow during reperfusion was enhanced in the bosentan-treated rat heart. The endothelium-dependent vasodilator adenosine diphosphate increased coronary flow by 18 +/- 9% at the end of reperfusion in the bosentan group, whereas it reduced coronary flow by 7 +/- 5% in the vehicle group (P < 0.001). The response to the endothelium-independent dilator sodium nitroprusside was not different between the two groups. In conclusion, the dual ETA/ETB receptor antagonist bosentan preserved endothelial and cardiac contractile function during ischemia and reperfusion via a mechanism dependent on endothelial NO production.     

The effect of calcitonin treatment on plasma nitric oxide levels in post-menopausal osteoporotic patients

Several recent studies have revealed a wide role for nitric oxide (NO) in bone metabolism. Low doses of NO cause bone resorption, but higher doses of NO inhibit bone resorbing activity. Cytokines are potent stimulators of NO production. NO is a very short-lived molecules. It exists for only 6-10 s only before it is converted by oxygen and water into the end-products nitrates and nitrites. Osteoporosis is a metabolic bone disease, characterized by a decreased amount of bone and increased susceptibility to fracture. NO may be involved as a mediator of bone disease such as post-menopausal osteoporosis. Calcitonin is a peptide hormone that inhibits bone resorption. The function of calcitonin in some cells is often unclear. In this study 30 post-menopausal osteoporotic women of ages ranging between 55 and 59 years without systemic diseases and free of any drug therapy were included. Twenty of them, randomly chosen, were treated with calcium (500 mg day(-1))+calcitonin (nasal spray 100 U day(-1)) and the other 10 women (control group) were treated with calcium only. This treatment was applied for 6 months and NO values were measured in each of the two groups before and after treatment. Our findings demonstrate that NO regulates osteoclastic bone resorption activity in association with calcitonin.     

Cytotoxicity of doxrubicin loaded single-walled carbon nanotubes

Carbon nanotube (CNTs) is a new alternative for efficient drug delivery and it has a great potential to change drug delivery system profile in pharmaceutical industry. One of the important advantage of CNTs is their needle-like, cylindrical shape. This shape provides a high surface area for multiple connections and adsorption onto for millions of therapeutic molecules. CNTs can be internalized by cells via endocytosis, passive diffusion and phagocytosis and release the drug with different effects like pH and temperature. The acidic nature of cancer cells and the susceptibility of CNTs to release the drug in the acidic environment have made it a promising area of research in cancer drug delivery. In this research, we investigated cell viability, cytotoxicity and drug delivery in breast cancer cell line by designing non-covalent single walled carbon nanotubes (SWNT)–doxorubicin (DOX) supramolecular complex that can be developed for cancer therapy. Applied high concentrations of DOX loaded SWNTs changed the actin structure of the cells and prevented the proliferation of the cells. It was showed that doxorubicin loaded SWNTs were more effective than free doxorubicin at relatively small concentrations. Once we applied same procedure for short and long (short: 1–1.3 µm; long: 2.5–4 µm) SWNTs and compared the results, more disrupted cell structure and reduction in cell proliferation were observed for long CNTs. DOX is bounded more to nanotubes in basic medium, less bound in acidic environment. Cancer cells were also examined for concentration at which they were effective by applying DOX and it was seen that 3.68 µM doxorubicin kills more than 55% of the cells.     

Electrophysiological and neuropsychological outcomes of severe obstructive sleep apnea: effects of hypoxemia on cognitive performance

Obstructive sleep apnea syndrome (OSAS) is a sleep disorder characterized with upper airway obstructions. Some studies showed cognitive and electrophysiological changes in patients with OSAS; however, contradictory results were also reported. The purpose of the present study was twofold: (1) to investigate cognitive changes in severe OSAS patients by using neuropsychological tests and electrophysiological methods together, (2) to investigate influence of hypoxemia levels on cognition. Fifty-four severe OSAS patients and 34 age-, gender- and education matched healthy subjects were participated. OSAS patients were further divided into two subgroups according to minimum oxygen saturation levels. All participants underwent a detailed neuropsychological test battery. A classical visual oddball task was used to elicit ERP P300 and mean P300 amplitudes were measured from F_z, C_z and P_z electrode sites. OSAS patients showed reduced mean P300 amplitudes up to 43–51% on all electrode sites compared to healthy controls. Subgroup analysis revealed significant differences in neuropsychological test scores between healthy controls and high hypoxemia OSAS group, as well as between low and high hypoxemia groups. Moreover, both low and high hypoxemia OSAS groups had lower P300 amplitudes compared with healthy controls. P300 amplitudes showed a gradual decline in parallel with increasing hypoxemia severity; however, the difference between high and low hypoxemia OSAS groups did not reach significance. Moderate correlations were found between sleep parameters, neuropsychological test scores and P300 amplitudes. These results suggest that electrophysiological measures could be better indicators of cognitive changes than neuropsychological tests in OSAS, particularly in mildly affected patients.     

Regional and seasonal variation in airborne grass pollen levels between cities of Australia and New Zealand

Although grass pollen is widely regarded as the major outdoor aeroallergen source in Australia and New Zealand (NZ), no assemblage of airborne pollen data for the region has been previously compiled. Grass pollen count data collected at 14 urban sites in Australia and NZ over periods ranging from 1 to 17 years were acquired, assembled and compared, revealing considerable spatiotemporal variability. Although direct comparison between these data is problematic due to methodological differences between monitoring sites, the following patterns are apparent. Grass pollen seasons tended to have more than one peak from tropics to latitudes of 37°S and single peaks at sites south of this latitude. A longer grass pollen season was therefore found at sites below 37°S, driven by later seasonal end dates for grass growth and flowering. Daily pollen counts increased with latitude; subtropical regions had seasons of both high intensity and long duration. At higher latitude sites, the single springtime grass pollen peak is potentially due to a cooler growing season and a predominance of pollen from C₃ grasses. The multiple peaks at lower latitude sites may be due to a warmer season and the predominance of pollen from C₄ grasses. Prevalence and duration of seasonal allergies may reflect the differing pollen seasons across Australia and NZ. It must be emphasized that these findings are tentative due to limitations in the available data, reinforcing the need to implement standardized pollen-monitoring methods across Australasia. Furthermore, spatiotemporal differences in grass pollen counts indicate that local, current, standardized pollen monitoring would assist with the management of pollen allergen exposure for patients at risk of allergic rhinitis and asthma.     

Forecasting age-related changes in breast cancer mortality among white and black US women: a functional data approach

Background: The disparity in breast cancer mortality rates among white and black US women is widening, with higher mortality rates among black women. We apply functional time series models on age-specific breast cancer mortality rates for each group of women, and forecast their mortality curves using exponential smoothing state-space models with damping. Materials and Methods: The data were obtained from the Surveillance, Epidemiology and End Results (SEER) program of the US [1]. Mortality data were obtained from the National Centre for Health Statistics (NCHS) available on the SEER*Stat database. We use annual unadjusted breast cancer mortality rates from 1969 to 2004 in 5-year age groups (45–49, 50–54, 55–59, 60–64, 65–69, 70–74, 75–79, 80–84). Age-specific mortality curves were obtained using nonparametric smoothing methods. The curves are then decomposed using functional principal components and we fit functional time series models with four basis functions for each population separately. The curves from each population are forecast and prediction intervals are calculated. Results: Twenty-year forecasts indicate an overall decline in future breast cancer mortality rates for both groups of women. This decline appears to be steeper among white women aged 55–73 and black women aged 60–84. For black women under 55 years of age, the forecast rates are relatively stable indicating there is no significant change in future breast cancer mortality rates among young black women in the next 20 years. Conclusion: White women have smooth and consistent patterns in breast cancer mortality rates for all age-groups whereas the mortality rates for black women are much more variable. The projections suggest, for some age groups, black American women may not benefit equally from the overall decline in breast cancer mortality in the United States.     

Effects of diethylstilbestrol in human lymphocytes in vitro: A dose and time-dependent study on genotoxic, cytotoxic and apoptotic effects

Most of the biological, chemical or physical agents that cause cell death in certain doses and time of exposure may induce either apoptosis or necrosis. This study explores in what ways the genotoxic, cytotoxic and apoptotic effects of diethylstilbestrol (DES), a chemical agent currently used in the treatment of various types of cancer, on the human lymphocytes depend upon the dose and the exposure time. For this purpose, firstly it aims to determine in what dosages and durations of DES treatment, genotoxicity and cytotoxicity in human lymphocytes occur in vitro. Secondly, it explores the effects of DES on sister-chromatid exchanges (SCEs) and apoptosis and their relation with the nitric oxide (NO) levels. Finally, it investigates whether different dosages of DES and duration of treatment with it are correlated with each other. In so doing, we investigated the relationship among the viability, necrosis and apoptosis rates of human lymphocytes which were treated with five different DES concentrations (1, 5, 10, 15 and 20 μM) for 24, 48 and 72 h, DNA fragmentation analysis of these cells, their mean SCE values and NO levels. We concluded that 5 μM DES at 24 h is the most effective dosage that induces typical features of apoptosis in human lymphocytes. Despite the fact that there are many other studies on the effects of DES on the cancer cells, we thought it might be worth looking into the effects of DES on human lymphocytes in vitro. We meant the present study to contribute to the research done in the field of cancer treatment. (Mol Cell Biochem 276: 45–53, 2005)     

Melatonin reverses the oxidative stress and mitochondrial dysfunction caused by LETM1 silencing

LETM1 is a mitochondrial inner‐membrane protein, which is encoded by a gene present in a locus of 4p, which, in turn, is deleted in the Wolf–Hirschhorn Syndrome, and is assumed to be related to its pathogenesis. The cellular damage caused by the deletion is presumably related to oxidative stress. Melatonin has many beneficial roles in protecting mitochondria by scavenging reactive oxygen species, maintaining membrane potential, and improving functions. The aim of this study was to investigate the effects of melatonin administration to LETM1‐silenced mouse embryonic fibroblast cells as a cellular model for LETM1 deficiency. We transfected mouse embryonic fibroblast cells with a pair of siRNA against LETM1 and monitored the oxidative stress and mitochondrial functions with or without melatonin addition. MnSOD expression and aconitase activity decreased and oxidized protein levels increased in LETM1‐silenced cells. LETM1 suppression did not alter the expression of OXPHOS complexes, but the oxygen consumption rates decreased significantly; however, this change was not related to complex I but instead involved complex IV and complex II. Melatonin supplementation effectively normalized the parameters studied, including the oxygen consumption rate. Our findings identified a novel effect of LETM1 deficiency on cellular respiration via complex II as well as a potential beneficial role of melatonin treatment. On the other hand, these effects may be specific to the cell line used and need to be verified in other cell lines.     

The Macroecology of Airborne Pollen in Australian and New Zealand Urban Areas

The composition and relative abundance of airborne pollen in urban areas of Australia and New Zealand are strongly influenced by geographical location, climate and land use. There is mounting evidence that the diversity and quality of airborne pollen is substantially modified by climate change and land-use yet there are insufficient data to project the future nature of these changes. Our study highlights the need for long-term aerobiological monitoring in Australian and New Zealand urban areas in a systematic, standardised, and sustained way, and provides a framework for targeting the most clinically significant taxa in terms of abundance, allergenic effects and public health burden.