The evolution of the eutrophication of the Palić Lake (Serbia)

Eutrophication is a world-wide environmental issue. The Palic Lake is a shallow lake typical for the Pannonian plain. The Lake itself was in a very bad condition during the late sixties of the last century; polluted and hypertrophic. Due to inadequate water quality, it was dried out in 1971 and re-established in 1977 and since then its trophicity has been worsening. The lake has recreational purposes but it is also a collector for treated municipal waste waters coming from the lagoons for active sludge water treatment. The sewage discharges from rapidly developing towns in the watershed and the growing use of fertilizers in agriculture increased the nutrient load to the Lake in the last decades. A steady increase of phosphorus loading is the most important factor of the lake  eutrophication. The result of the accelerated eutrophication is the enormous amount of sediment at the bottom of the Palic Lake. Therefore, in the lake that covers an area of 565 ha and volume of 10 million m3, there was 1.900.160 m3 of sediment. The sediment thickness varied from 0.3 to 1.2 m. In summer 2010, the recreational part of the lake (sector IV) was 1.311.356 m3 of sediment, characterized with concentrations of total phosphorus (TP) of 2885 mg/kg, 4300 mg/kg total nitrogen (TN) and 39000 mg/kg total organic carbon TOC. The sediment of the Palic Lake was not loaded with high concentrations of heavy metals. Everything mentioned supports the fact that the restoration of this aquatic system is necessary and applied measures have to be grounded on the principles of ecoremediation technologies.Key words: Eutrophication, Palic Lake, sediment, total N, total P

Endothelium Derived Nitric Oxide Synthase Negatively Regulates the PDGF-Survivin Pathway during Flow-Dependent Vascular Remodeling

Chronic alterations in blood flow initiate structural changes in vessel lumen caliber to normalize shear stress. The loss of endothelial derived nitric oxide synthase (eNOS) in mice promotes abnormal flow dependent vascular remodeling, thus uncoupling mechanotransduction from adaptive vascular remodeling. However, the mechanisms of how the loss of eNOS promotes abnormal remodeling are not known. Here we show that abnormal flow-dependent remodeling in eNOS knockout mice (eNOS (−/−)) is associated with activation of the platelet derived growth factor (PDGF) signaling pathway leading to the induction of the inhibitor of apoptosis, survivin. Interfering with PDGF signaling or survivin function corrects the abnormal remodeling seen in eNOS (−/−) mice. Moreover, nitric oxide (NO) negatively regulates PDGF driven survivin expression and cellular proliferation in cultured vascular smooth muscle cells. Collectively, our data suggests that eNOS negatively regulates the PDGF-survivin axis to maintain proportional flow-dependent luminal remodeling and vascular quiescence

Антиоксидантные возможности фармацевтического препарата Неамон-Хепа при токсическом гепатите, индуцированным тетрахлоридом углерода

Scientific Center for Drug Evaluation of the Nicolae Testemitanu State Medical and Pharmaceutical University, Institut of Microbiology and Biotechnology of the Academy of Science of MoldovaThe present study was undertaken to investigate whether Neamon-Hepa treatment provides antioxidant protection from chronic liver injury induced in mice by a long-term CCl4 administration. The Neamon-Hepa capsule, a combination indigene drug, contains L-arginine, Spironolactone and biopreparation from the Spirulina platensis - BioR. Carbon tetrachloride chronic treatment for three weeks significantly decreased the hepatic antioxidant enzyme activities - almost twofold superoxide dismutase enzyme activity, catalase activity, glutathione peroxidase activity in liver tissue and induced a marked elevation almost twofold of thiobarbituric acid reactive substances levels in the plasma and liver tissue. Treatment with the Neamon-Hepa following experimental liver damage, in a dose-dependent way, resulted in a marked augmentation of antioxidant enzyme activities and reduction of lipid peroxidation levels.Целью данной работы является исследование антиоксидантного воздействия лекарственного препарата НеамонХепа у мышей с токсическим гепатитом, индуцированным тетрахлоридом углевода. В состав комбинированного медикамента Неамон-Хепа входит аргинина аспартат, БиоР и спиронолактон. Хроническая интоксикация в течении 3 недель с ССl4 снизила в два раза активность супероксиддисмутазы, каталазы, глутатионпероскидазы в печеночной ткани и повысила вдвое степень тиобарбитуровой кислоты в печеночной ткани и в сыворотке крови. Применение препарата Неамон-Хепа значительно уменьшило степень процессов липидного пероксидирования и увеличило активность антиоксидативных энзимов

Beneficial effects of pomegranate peel extract on plasma lipid profile, fatty acids levels and blood pressure in patients with diabetes mellitus type-2: A randomized, double-blind, placebo-controlled study

Pomegranate peel contains high levels of various phytochemicals. We evaluated the effects of pomegranate peel extract (PoPEx) consumption on plasma lipid profile, fatty acids (FA) level and blood pressure (BP) in patients with diabetes mellitus type 2 (DMT2). Thirty-seven subjects were recruited in this double blind, placebo controlled randomized trial. The study group (n = 19) received over 8 week's capsules containing PoPEx twice a daily, while the placebo group received placebo. Treatment with PoPEx induced a significant lowering of both systolic and diastolic BP. The plasma levels of triglycerides, low-density lipoprotein cholesterol/high-density lipoprotein cholesterol ratio (LDL-C/HDL-C), and HbA1c were significantly decreased, while the level of HDL-C was significantly increased, compared with placebo intake. Moreover, the PoPEX treatment significantly improved the plasma lipids fatty acids content. It is concluded that consumption of PoPEx in DMT2 subject had favourable effects on some metabolic parameters, BP, lipid profile and plasma lipid FA composition

Quality assurance process within the RAdiosurgery for VENtricular TAchycardia (RAVENTA) trial for the fusion of electroanatomical mapping and radiotherapy planning imaging data in cardiac radioablation

A novel quality assurance process for electroanatomical mapping (EAM)-to-radiotherapy planning imaging (RTPI) target transport was assessed within the multi-center multi-platform framework of the RAdiosurgery for VENtricular TAchycardia (RAVENTA) trial. A stand-alone software (CARDIO-RT) was developed to enable platform independent registration of EAM and RTPI of the left ventricle (LV), based on pre-generated radiotherapy contours (RTC). LV-RTC were automatically segmented into the American-Heart-Association 17-segment-model and a manual 3D-3D method based on EAM 3D-geometry data and a semi-automated 2D-3D method based on EAM screenshot projections were developed. The quality of substrate transfer was evaluated in five clinical cases and the structural analyses showed substantial differences between manual target transfer and target transport using CARDIO-RT

Control of zeolite microenvironment for propene synthesis from methanol

Optimising the balance between propene selectivity, propene/ethene ratio and catalytic stability and unravelling the explicit mechanism on formation of the first carbon–carbon bond are challenging goals of great importance in state-of-the-art methanol-to-olefin (MTO) research. We report a strategy to finely control the nature of active sites within the pores of commercial MFI-zeolites by incorporating tantalum(V) and aluminium(III) centres into the framework. The resultant TaAlS-1 zeolite exhibits simultaneously remarkable propene selectivity (51%), propene/ethene ratio (8.3) and catalytic stability (>50 h) at full methanol conversion. In situ synchrotron X-ray powder diffraction, X-ray absorption spectroscopy and inelastic neutron scattering coupled with DFT calculations reveal that the first carbon–carbon bond is formed between an activated methanol molecule and a trimethyloxonium intermediate. The unprecedented cooperativity between tantalum(V) and Brønsted acid sites creates an optimal microenvironment for efficient conversion of methanol and thus greatly promotes the application of zeolites in the sustainable manufacturing of light olefins.We thank EPSRC (EP/P011632/1), the Royal Society, National Natural Science Foundation of China (21733011, 21890761, 21673076), and the University of Manchester for funding. We thank EPSRC for funding and the EPSRC National Service for EPR Spectroscopy at Manchester. A.M.S. is supported by a Royal Society Newton International Fellowship. We are grateful to the STFC/ISIS Facility, Oak Ridge National Laboratory (ORNL) and Diamond Light Source (DLS) for access to the beamlines TOSCA/MAPS, VISION and I11/I20, respectively. We acknowledge Dr. L. Keenan for help at I20 beamline (SP23594-1). UK Catalysis Hub is kindly thanked for resources and support provided via our membership of the UK Catalysis Hub Consortium and funded by EPSRC grant: EP/R026939/1, EP/R026815/1, EP/R026645/1, EP/R027129/1 or EP/M013219/1 (biocatalysis). We acknowledge the support of The University of Manchester’s Dalton Cumbrian Facility (DCF), a partner in the National Nuclear User Facility, the EPSRC UK National Ion Beam Centre and the Henry Royce Institute. We recognise Dr. R. Edge and Dr. K. Warren for their assistance during the 60Co γ-irradiation processes. We thank Prof. A. Jentys from the Technical University of Munich for the measurement of the INS spectrum of iso-butene. We thank C. Webb, E. Enston and G. Smith for help with GC–MS; Dr. L. Hughes for help with SEM and EDX; M. Kibble for help at TOSCA/MAPS beamlines. Computing resources (time on the SCARF compute cluster for some of the CASTEP calculations) was provided by STFC’s e-Science facility. A portion of this research used resources at the Spallation Neutron Source, a DOE Office of Science User Facility operated by ORNL. The computing resources at ORNL were made available through the VirtuES and the ICE-MAN projects, funded by Laboratory Directed Research and Development programme and Compute and Data Environment for Science (CADES

Circadian Desynchrony Promotes Metabolic Disruption in a Mouse Model of Shiftwork

Shiftwork is associated with adverse metabolic pathophysiology, and the rising incidence of shiftwork in modern societies is thought to contribute to the worldwide increase in obesity and metabolic syndrome. The underlying mechanisms are largely unknown, but may involve direct physiological effects of nocturnal light exposure, or indirect consequences of perturbed endogenous circadian clocks. This study employs a two-week paradigm in mice to model the early molecular and physiological effects of shiftwork. Two weeks of timed sleep restriction has moderate effects on diurnal activity patterns, feeding behavior, and clock gene regulation in the circadian pacemaker of the suprachiasmatic nucleus. In contrast, microarray analyses reveal global disruption of diurnal liver transcriptome rhythms, enriched for pathways involved in glucose and lipid metabolism and correlating with first indications of altered metabolism. Although altered food timing itself is not sufficient to provoke these effects, stabilizing peripheral clocks by timed food access can restore molecular rhythms and metabolic function under sleep restriction conditions. This study suggests that peripheral circadian desynchrony marks an early event in the metabolic disruption associated with chronic shiftwork. Thus, strengthening the peripheral circadian system by minimizing food intake during night shifts may counteract the adverse physiological consequences frequently observed in human shift workers

CXCR3-dependent accumulation and activation of perivascular macrophages is necessary for homeostatic arterial remodeling to hemodynamic stresses

Sustained changes in blood flow modulate the size of conduit arteries through structural alterations of the vessel wall that are dependent on the transient accumulation and activation of perivascular macrophages. The leukocytic infiltrate appears to be confined to the adventitia, is responsible for medial remodeling, and resolves once hemodynamic stresses have normalized without obvious intimal changes. We report that inward remodeling of the mouse common carotid artery after ligation of the ipsilateral external carotid artery is dependent on the chemokine receptor CXCR3. Wild-type myeloid cells restored flow-mediated vascular remodeling in CXCR3-deficient recipients, adventitia-infiltrating macrophages of Gr1low resident phenotype expressed CXCR3, the perivascular accumulation of macrophages was dependent on CXCR3 signaling, and the CXCR3 ligand IP-10 was sufficient to recruit monocytes to the adventitia. CXCR3 also contributed to selective features of macrophage activation required for extracellular matrix turnover, such as production of the transglutaminase factor XIII A subunit. Human adventitial macrophages displaying a CD14+/CD16+ resident phenotype, but not circulating monocytes, expressed CXCR3, and such cells were more frequent at sites of disturbed flow. Our observations reveal a CXCR3-dependent accumulation and activation of perivascular macrophages as a necessary step in homeostatic arterial remodeling triggered by hemodynamic stress in mice and possibly in humans as well