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The goal of the study was to determine the effectiveness of nitrification and denitrification and the kinetics of ammonia removal from a mixture of wastewater and anaerobic sludge digester supernatant in an SBR at limited oxygen concentration. In addition, the COD removal efficiency and sludge production were assessed. In the SBR cycle alternating aerobic and anaerobic phases occurred; in the aeration phase the dissolved oxygen (DO) concentration was below 0.7 mg O(2)/L. The low DO concentration did not inhibit ammonia oxidation-nitrification and the efficiency was ca. 96-98%. However, a relatively high COD concentration in the effluent was detected. The values of K(m) and V(max), calculated from the Michaelis-Menten equation, were 43 mg N-NH(4)/L and 15.64 mg N-NH(4)/L h, respectively. Activated sludge production was almost stable (0.62-0.66 g MLVSS/g COD). A high net biomass production resulted from a low specific biomass decay rate of 0.0015 d(-1)., (Copyright © 2011 Elsevier Ltd. All rights reserved.)

Background: Post-acute myocardial infarction (AMI) ventricular septal defect (VSD) is a rare but catastrophic complication. The aim of study was to delineate the incidence and risk factors of VSD in patients after AMI treated with successful primary percutaneous coronary intervention (pPCI)., Methods and Results: In the years 2004-2006, a total of 1835 patients with AMI underwent successful pPCI in our hospital. Thirteen patients (0.71%) developed VSD after pPCI. Mean time of occurrence of VSD was 24.46 ± 9.32 h. Patients with VSD had longer time from the AMI onset to pPCI vs. patients without VSD (7.77 ± 2.83 vs. 4.49 ± 4.45, P<.001). In the VSD group, most of the patients were nonsmokers, had arterial hypertension, and had no previous history of coronary artery disease (CAD). Neither group differed in administered antiplatelet therapy. According to univariate log-regression analysis, the presence of VSD was strongly associated with age >70 years (OR=4.66; P=.007), female gender (OR=5.73; P=.004), anterior infarction (OR=3.86; P=.04), single-vessel CAD (OR=3.74; P=.03), body mass index (BMI) <25 (OR=2.98; P=.04), and left ventricular wall hypertrophy (OR=3.39; P=.03)., Conclusions: Our study demonstrated that the incidence of VSD after AMI appears to have declined in patients treated with pPCI. The pathomechanism of VSD in the invasive treatment era is the consequence of several processes and needs further investigation. Advanced age, female gender, anterior infarction, single-vessel CAD, left ventricular wall hypertrophy, and low BMI are strong risk factors of this complication after AMI, which remain invariable over the years., (Copyright © 2011 Elsevier Inc. All rights reserved.)

The pathogenesis of hepatic encephalopathy (HE) is associated with hyperammonemia (HA) and subsequent exposure of the brain to excess of ammonia. Alterations of the NO/cGMP pathway and increased glutamine (Gln) content are collectively responsible for many HE symptoms, but how the two events influence each other is not clear. Previously we had shown that Gln administered intracerebrally inhibited the NO/cGMP pathway in control rats and even more so in rats with HA, and we speculated that this effect is due to inhibition by Gln of arginine (Arg) transport (Hilgier et al., 2009). In this study we demonstrate that a 3-day HA in the ammonium acetate model increases the expression in the brain of y(+)LAT2, the heteromeric transporter which preferentially stimulates Arg efflux from the cells in exchange for Gln. The expression of the basic amino acid transporter CAT1, transporting Arg but not Gln remained unaffected by HA. Multiple parameters of Arg or Gln uptake and/or efflux and their mutual dependence were altered in the cerebral cortical slices obtained from HA rats, in a manner indicating enhanced y(+)LAT2-mediated transport. HA elevated Gln content and decreased cGMP content as measured both in the cerebral cortical tissue and microdialysates. Intracortical administration of 6-diazo-5-oxo-L-norleucine (DON), which inhibits Gln fluxes between different cells of the CNS, attenuated the HA-induced decrease of cGMP in the microdialysates of HA rats, but not of control rats. The results suggest that, reduced delivery of Arg due to enhanced y(+)LAT2-mediated exchange of extracellular Gln for intracellular Arg may contribute to the decrease of NO/cGMP pathway activity evoked in the brain by HA., (Copyright © 2010 Elsevier Ltd. All rights reserved.)

Oesophageal atresia is a congenital defect of alimentary tract concerning the interruption of oesophagus with or without connection with the trachea. Its incidence is 1:3000-3500 of live-born. Associated anomalies including genetic disorders occur in 50% of patients. Edwards syndrome which is trisomy of chromosome 18 with poor prognosis. The incidence of Edwards syndrome is 1:5000 of live-born. About 5% of these children live more than 1 year. The aim of this article is a retrospective analysis of the course of treatment of newborn with oesophageal atresia and Edwards syndrome and making of therapeutic decision. The authors from different medical specializations: clinical genetics, paediatric surgery, paediatrics and neonatology, paediatric intensive care and palliative medicine, have undertaken a discussion regarding surgical treatment of children with oesophageal atresia and chromosomal, lethal syndrome.

Glutamine (Gln) is found abundantly in the central nervous system (CNS) where it participates in a variety of metabolic pathways. Its major role in the brain is that of a precursor of the neurotransmitter amino acids: the excitatory amino acids, glutamate (Glu) and aspartate (Asp), and the inhibitory amino acid, γ-amino butyric acid (GABA). The precursor-product relationship between Gln and Glu/GABA in the brain relates to the intercellular compartmentalization of the Gln/Glu(GABA) cycle (GGC). Gln is synthesized from Glu and ammonia in astrocytes, in a reaction catalyzed by Gln synthetase (GS), which, in the CNS, is almost exclusively located in astrocytes (Martinez-Hernandez et al., 1977). Newly synthesized Gln is transferred to neurons and hydrolyzed by phosphate-activated glutaminase (PAG) to give rise to Glu, a portion of which may be decarboxylated to GABA or transaminated to Asp. There is a rich body of evidence which indicates that a significant proportion of the Glu, Asp and GABA derived from Gln feed the synaptic, neurotransmitter pools of the amino acids. Depolarization-induced-, calcium- and PAG activity-dependent releases of Gln-derived Glu, GABA and Asp have been observed in CNS preparations in vitro and in the brain in situ. Immunocytochemical studies in brain slices have documented Gln transfer from astrocytes to neurons as well as the location of Gln-derived Glu, GABA and Asp in the synaptic terminals. Patch-clamp studies in brain slices and astrocyte/neuron co-cultures have provided functional evidence that uninterrupted Gln synthesis in astrocytes and its transport to neurons, as mediated by specific carriers, promotes glutamatergic and GABA-ergic transmission. Gln entry into the neuronal compartment is facilitated by its abundance in the extracellular spaces relative to other amino acids. Gln also appears to affect neurotransmission directly by interacting with the NMDA class of Glu receptors. Transmission may also be modulated by alterations in cell membrane polarity related to the electrogenic nature of Gln transport or to uncoupled ion conductances in the neuronal or glial cell membranes elicited by Gln transporters. In addition, Gln appears to modulate the synthesis of the gaseous messenger, nitric oxide (NO), by controlling the supply to the cells of its precursor, arginine. Disturbances of Gln metabolism and/or transport contribute to changes in Glu-ergic or GABA-ergic transmission associated with different pathological conditions of the brain, which are best recognized in epilepsy, hepatic encephalopathy and manganese encephalopathy.

Ammonia is a major neurotoxin implicated in hepatic encephalopathy (HE). Here we discuss evidence that many aspects of ammonia toxicity in HE-affected brain are mediated by glutamine (Gln), synthesized in excess from ammonia and glutamate by glutamine synthetase (GS), an astrocytic enzyme. The degree to which Gln is increased in brains of patients with HE was found to positively correlate with the grade of HE. In animals with HE, a GS inhibitor, methionine sulfoximine (MSO), reversed a spectrum of manifestations of ammonia toxicity, including brain edema and increased intracranial pressure, even though MSO itself increased brain ammonia levels. MSO inhibited, while incubation with Gln reproduced the oxidative stress and cell swelling observed in ammonia-exposed cultured astrocytes. Recent studies have shown that astrocytes swell subsequent to Gln transport into mitochondria and its degradation back to ammonia, which then generates reactive oxygen species and the mitochondrial permeability transition. This sequence of events led to the formulation of the "Trojan Horse" hypothesis. Further verification of the role of Gln in the pathogenesis of HE will have to account for: (1) modification of the effects of Gln by interaction of astrocytes with other CNS cells; and (2) direct effects of Gln on these cells. Recent studies have demonstrated a "Trojan Horse"-like effect of Gln in microglia, as well as an interference by Gln with the activation of the NMDA/NO/cGMP pathway by ammonia as measured in whole brain, a process that likely also involves neurons., (Copyright © 2010 Elsevier Inc. All rights reserved.)

Oxidative and nitrosative stress contribute to ammonia-induced astrocytic dysfunction in hepatic encephalopathy. Treatment of cultured astrocytes with 5 mmol/L ammonium chloride ('ammonia') increased the production of reactive oxygen species (ROS), including the toxic NADPH oxidase reaction product, •O(2)(-). Atrial natriuretic peptide (ANP), natriuretic peptide C and a selective natriuretic peptide receptor (NPR)-C ligand, cANP((4-23),) each decreased the total ROS content both in control cells and cells treated with ammonia. However, attenuation of •O(2)(-) accumulation by ANP and cANP((4-23),) was observed in ammonia-treated cells only and the effect of cANP((4-23)) was decreased when the NADPH oxidase-regulatory protein G(iα-2) was blocked with a specific anti-G(iα-2) antibody. Although in contrast to ANP, cANP((4-23)) did not elevate the cGMP content in control astrocytes, it decreased cAMP content and reduced the expression of G(iα-2), the NADPH oxidase-regulatory protein. The results show the presence of functional NPR-C in astrocytes, activation of which (i) attenuates basal ROS production, and (ii) prevents excessive accumulation of the toxic ROS species, •O(2)(-) by ammonia. Ammonia, ANP and cANP((4-23)) added separately, each stimulated formation of NO(x) (nitrates + nitrites) which was associated with up-regulation of the activity [cANP((4-23))] or/and expression (ammonia) of the endothelial isoform of nitric oxide synthase. However, the ammonia-induced increase of NO(x) was not augmented by co-addition of ANP, and was reduced to the control level by co-addition of cANP((4-23)) , indicating that activation of NPR-C may also reduce nitrosative stress. Future hepatic encephalopathy therapy might include the use of cANP((4-23)) or other NPR-C agonists to control oxidative/nitrosative stress induced by ammonia., (© 2010 The Authors. Journal of Neurochemistry © 2010 International Society for Neurochemistry.)

Development and advances in heart pacing over the last nearly half a century allowed to save numerous lives by providing pacing support in bradycardia and complete heart block. Nevertheless, long-term follow up of patients with implanted pacemaker showed unfavorable remodeling of the heart, both from hemodynamic as well as electrical standpoint. The optimal programmed pacemaker setting, apart from the optimal place for ventricular stimulation, is essential to obtain the best hemodynamic and the clinical after-effects of the stimulation of the heart and to minimize potential unfavorable effects. In patients with dual-chamber pacemaker (DDD) the correct function of the left ventricle of the heart depends mainly on the electric delays between the stimulated chambers. Atrio-ventricular delay (AVD) during dual-chamber pacing influences left ventricle contraction function through preload modulation. Improperly programmed AVD in the DDD pacemaker can have unfavorable hemodynamic results. Various methods have been developed during last few decades (right heart catheterization, ventriculography, peak endocardial acceleration, echocardiography, and impedance cardiography), however only echocardiography and reocardiography are currently in general use. There should be noticed too, that also the application of special algorithms present in modern pacemakers allowing for dynamic changes of the time of the delay represents certain alternative to individual AVD optimization., (Copyright (c) 2009 Elsevier Ireland Ltd. All rights reserved.)

Wastewater treatment systems tend to be engineered to select for a few functional microbial groups that may be organized in various spatial structures such as activated sludge flocs, biofilm or granules and represented by single coherent phylogenic groups such as ammonia-oxidizing bacteria (AOB) and polyphosphate-accumulating organisms (PAO). In order to monitor and control engineered microbial structure in wastewater treatment systems, it is necessary to understand the relationships between the microbial community structure and the process performance. This review focuses on bacterial communities in wastewater treatment processes, the quantity of microorganisms and structure of microbial consortia in wastewater treatment bioreactors. The review shows that the application of molecular techniques in studies of engineered environmental systems has increased our insight into the vast diversity and interaction of microorganisms present in wastewater treatment systems.

Brain L-glutamine (Gln) accumulation and increased activity of the NO/cGMP pathway are immediate consequences of acute exposure to ammonia. This study tested whether excess Gln may influence NO and/or cGMP synthesis. Intrastriatal administration of the glutaminase inhibitor 6-diazo-5-oxo-L-norleucine or the system A-specific Gln uptake inhibitor methylaminoisobutyrate increased microdialysate Gln concentration and reduced basal and ammonia-induced NO and cGMP accumulation. Gln applied in vivo (via microdialysis) or in vitro (to rat brain cortical slices) reduced NO and cGMP accumulation in the presence and/or absence of ammonia, but not cGMP synthesis induced by the NO donor sodium nitroprusside. Attenuation of cGMP synthesis by Gln was prevented by administration of L-arginine (Arg). The L-arginine co-substrates of y(+)LAT2 transport system, L-leucine and cyclo-leucine, mimicked the effect of exogenous Gln, suggesting that Gln limits Arg supply for NO synthesis by interfering with y+LAT2-mediated Arg uptake across the cell membrane.

Prinzmetal's angina is a distinct syndrome characterized by episodes of chest pain and transient ST-segment elevation caused by coronary vasospasm. This variant form of angina is sometimes associated with complete atrioventricular block and ventricular arrhythmias. We report here a case of variant angina with documented severe heart rhythm disturbances and syncope in a 66 year-old woman. Due to recurrent episodes of high-degree atrioventricular block, a DDD pacemaker was implanted. No further symptoms of angina or cardiac arrhythmias were detected on optimal therapy.

Oxidative stress and inflammation are involved in the development of obesity. Beetroot (Beta vulgaris var. rubra) is a food ingredient containing betalain pigments that show antioxidant activity. The in vitro effect of beetroot juice and chips on oxidative metabolism and apoptosis in neutrophils from obese individuals has been investigated. Fifteen obese women (aged 45 +/- 9 years, BMI >30 kg/m2) and nine healthy controls (women, aged 29 +/- 11 years, BMI = 22.2 +/- 1.6 kg/m2) were examined. The investigated products were used as concentrates and after transport and digestion in an artificial gastrointestinal tract. Neutrophil oxidant production, in response to phorbol 12-myristate 13-acetate, was characterized by luminol-dependent chemiluminescence and a flow cytometric dichlorofluorescin oxidation assay. Caspase-3 activity, a marker of apoptosis, was measured by cleavage of the fluorogenic substrate Ac-DEVD-AMC. Neutrophils from obese individuals had a significantly higher ROS production compared with the controls (p < 0.05). Beetroot products inhibited neutrophil oxidative metabolism in a concentration-dependent manner. Also observed were the pro-apoptotic effects of beetroot at a concentration range of 0.1-10% in 24 h culture of stimulated neutrophils. These natural products (in both the liquid and solid state) have antioxidant and antiinflammatory capacity, and could be an important adjunct in the treatment of obesity., (Copyright 2008 John Wiley & Sons, Ltd.)

Citrus flavonoids are dietary antioxidants that may protect against oxidative stress linked to inflammation and reduce the risk of macromolecule damage caused by free radicals. Three citrus flavonoids - naringin, naringenin and hesperidin - have been examined for their ability to activate caspase-3, a marker of apoptosis execution, in human polymorphonuclear neutrophils in vitro, stimulated and non-stimulated with phorbol 12-myristate 13-acetate. The flavonoid potency to reduce reactive oxygen species generation was also assessed in measurements of superoxide radical and luminol dependent chemiluminescence. The caspase-3 activity depended on the time of flavonoid treatment and was increased markedly in phorbol-treated cells incubated with flavonoids for 24 h. Hesperidin at a concentration of 100 microm exerted the strongest stimulating effect on the enzyme (137% of control). Flavonoids inhibited the neutrophil ability to generate superoxide radical and 10-100 microM hesperidin appeared the most active phytochemical. The antioxidant capacity of the examined flavonoids was most prominently expressed in the chemiluminescent measurements. The obtained results suggest that reactive oxygen species may inhibit apoptosis via caspase-3 inhibition and the antioxidant action of citrus flavonoids may reverse this process., ((c) 2008 John Wiley & Sons, Ltd.)

In this study, we examined the intestinal uptake of thiamin (vitamin B(1)), riboflavin (vitamin B(2)) and pyridoxine (vitamin B(6)) administered at high concentration using intestinal epithelial Caco-2 cells as an in vitro model of drugs and food absorption. The effect of vitamin concentration, culture age, transport direction and incubation temperature on vitamin transport was determined. The vitamin transport was expressed as an apparent permeability coefficient and changes in cumulative fraction transported across epithelial membrane in time. It was found that transepithelial transport of these vitamins is dependent on the experimental factors. At low concentrations an active transport mechanism was observed, whereas at high vitamin concentration a passive transport dominated. At high vitamin concentration the transepithelial flux of vitamins in both directions was similar, which proves the mechanism of passive transport.

Endotracheal suction is essential to keep the respiratory capacity of the bronchial tree. The aim of this study was to establish the principles reducing potential side-effects, like hypoxia, bradycardia, hypotension, arrhythmia, nosocomial infections. Analysing the literature we have selected the following major beneficial factors: 1:2 to 2:3 cathether - tracheal tube diameter ratio, individual adjustment of the suctioning frequency, maximal duration of the procedure capped at 10-15 sec., minimal effective suctioning pressure of 80-100 mmHg. We have also determined that the following procedures should be also taken into consideration: preoxygenation (only for unstable patients), sedation and analgesia. We have concluded with the comparison of the two suction systems, pointing out that, especially for unstable patients, closed-suction system proves more suitable.

The reduced transition probabilities, B(E2; 0(gs)+ -->2(1)+), have been measured in the radioactive isotopes (108,106)Sn using subbarrier Coulomb excitation at the REX-ISOLDE facility at CERN. Deexcitation gamma rays were detected by the highly segmented MINIBALL Ge-detector array. The results, B(E2;0(gs)+ -->2(1)+)=0.222(19)e2b2 for 108Sn and B(E2; 0(gs)+-->2(1)+)=0.195(39)e2b2 for 106Sn were determined relative to a stable 58Ni target. The resulting B(E2) values are approximately 30% larger than shell-model predictions and deviate from the generalized seniority model. This experimental result may point towards a weakening of the N=Z=50 shell closure.

Recently we reported a decrease of C-type natriuretic peptide (CNP)-dependent, natriuretic peptide receptor 2 (NPR2)-mediated cyclic GMP (cGMP) synthesis in a non-neuronal compartment of cerebral cortical slices of hyperammonemic rats [Zielińska, M., Fresko, I., Konopacka, A., Felipo, V., Albrecht, J., 2007. Hyperammonemia inhibits the natriuretic peptide receptor 2 (NPR2)-mediated cyclic GMP synthesis in the astrocytic compartment of rat cerebral cortex slices. Neurotoxicology 28, 1260-1263]. Here we accounted for the possible involvement of cerebral capillary endothelial cells in this response by measuring the effect of ammonia on the CNP-mediated cGMP formation and intracellular calcium ([Ca2+]i) accumulation in a rat cerebral endothelial cell line (RBE-4). We first established that stimulation of cGMP synthesis in RBE-4 cells was coupled to protein kinase G (PKG)-mediated Ca2+ influx from the medium which was inhibited by an L-type channel blocker nimodipine. Ammonia treatment (1h, 5mM NH4Cl) evoked a substantial decrease of CNP-stimulated cGMP synthesis which was related to a decreased binding of CNP to NPR2 receptors, and depressed the CNP-dependent [Ca2+]i accumulation in these cells. Ammonia also abolished the CNP-dependent Ca2+ accumulation in the absence of Na+. In cells incubated with ammonia in the absence of Ca2+ a slight CNP-dependent increase of [Ca2+]i was observed, most likely representing Ca2+ release from intracellular stores. Depression of CNP-dependent cGMP-mediated [Ca2+]i accumulation may contribute to cerebral vascular endothelial dysfunction associated with hyperammonemia or hepatic encephalopathy.

Lifetimes of states in the ground-state bands of (70)Se and (72)Se were measured using the recoil-distance Doppler shift method. The results deviate significantly from earlier measurements, requiring a revision of the conclusions drawn from a recent Coulomb excitation experiment concerning the shape of (70)Se. The new results lead to a coherent picture of shape coexistence in the neutron-deficient selenium and krypton isotopes. The coexistence and evolution of oblate and prolate shapes in this mass region is for the first time consistently described by new Hartree-Fock-Bogolyubov-based configuration-mixing calculations which were performed using the Gogny D1S interaction.

Polymorphonuclear neutrophils (PMNs) are short-lived leukocytes that die by apoptosis. Although PMNs are crucial in the defense against infection, they have been implicated in the pathogenesis of tissue injury observed in inflammatory diseases. The induction or prevention of PMN apoptosis is currently discussed as a key event in the control of inflammation. Caspase-3 activation is the first step in the execution phase of apoptosis. In the study, effect of racemic mixtures and enantiomers of 2-arylpropionic acid derivatives: ketoprofen, flurbiprofen (FBP), and (+)-S-naproxen and 2-arylbutyric acid: indobufen on apoptosis activation via caspase-3 and phosphatidylserine (PS) translocation (annexin-V binding) in human neutrophils in vitro has been investigated. Caspase-3 activation was detected by Western blotting, fluorometric assay of DEVD-AMC cleavage, and flow cytometry with carboxyfluorescein (FAM) labeled caspase inhibitor. PMNs were isolated and cultured up to 24 h. The chiral nonsteroidal anti-inflammatory drugs (NSAIDs) were found to modulate human PMN apoptosis in a dose- and time-dependent manner. The greater activation of caspase was found at 75-150 microg/ml concentration of racemates as well enantiomers, especially for FBP, whereas NSAIDs at smaller quantities (15 microg/ml) were inactive. At concentration of 75 microg/ml, NSAIDs increased the rate of PS externalization in PMA-stimulated and non-stimulated neutrophils. Additionally, no cytotoxic effect of the NSAIDs was observed at concentration up to 75 microg/ml that induce apoptosis. Regulation of caspase activity by NSAIDs may represent a potent target to trigger apoptosis and resolve inflammatory disorders.

The objective of the present study was to examine the effects of hydrocolloidal silver nanoparticles (Ag-nano) on microbial profile of caecum and morphology of enterocytes in duodenum of Japanese quail, as a model animal for poultry. Quails (Coturnix coturnix japonica) (10 d old) were randomly divided into four groups (15 quails each) and located into four cages for 12 days. Quails were fed with granulated diets given ad libitum and had free access to drinking water. Ag-nano were added to drinking water at concentrations of 0, 5, 15 and 25 mg/kg. At the end of the experiment, the animals were killed and samples of duodenum and caeca microflora were collected. This initial investigation demonstrated that silver nanoparticles did not influence emphatically microflora of quail caecum; however, water containing 25 mg/kg of Ag-nano significantly increased the population of lactic acid bacteria. Furthermore, Ag-nano did not show any damaging properties on enterocytes of duodenal villi.

The decrease of cyclic GMP (cGMP) level in the brain, contributing to cognitive and memory deficit in hyperammonemia (HA), has been attributed to the interference of ammonia with the NMDA/nitric oxide/soluble guanylate cyclase (GC)/cGMP pathway in neurons. The present study tested the hypotheses that (a) HA also affects cGMP synthesis elicited by stimulation of the natriuretic peptide receptor 2 (NPR-2) with its natural ligand, C-type natriuretic peptide (CNP) and (b) the latter effect may involve astrocytes, the ammonia-sensitive cells. In the cerebral cortical slices of control rats, CNP stimulated cGMP synthesis in a degree comparable to the NO donor, S-nitroso-N-acetylpenicillamine (SNAP) used at an optimal concentration. Fluoroacetate (FA), a metabolic inhibitor specifically affecting astrocytic mitochondria, inhibited the CNP-dependent cGMP synthesis by about 50%. Ammonium acetate-induced HA decreased by 68% the CNP-dependent cGMP generation in slices incubated in the absence of FA. In slices incubated in the presence of FA, cGMP synthesis in slices derived from HA rats did not differ from that in control slices. The results indicate that HA inhibits CNP-dependent cGMP synthesis in the FA-vulnerable, astrocytic compartment, but not in the FA-resistant compartment(s) of the brain. HA did not affect the expression of NPR-2 mRNA in the cerebral cortex tissue as tested using real-time PCR, indicating that the effect of ammonia involves as yet unidentified events occurring posttranscriptionally. Deregulation of NPR-2 function in astrocytes by ammonia may contribute to neurophysiological symptoms of HA.

Neutron-rich, radioactive Zn isotopes were investigated at the Radioactive Ion Beam facility REX-ISOLDE (CERN) using low-energy Coulomb excitation. The energy of the 2(1)+ state in 78Zn could be firmly established and for the first time the 2+ --> 0(1)+ transition in 80Zn was observed at 1492(1) keV. B(E2,2(1)+ --> 0(1)+) values were extracted for (74,76,78,80)Zn and compared to large scale shell model calculations. With only two protons outside the Z=28 proton core, 80Zn is the lightest N=50 isotone for which spectroscopic information has been obtained to date. Two sets of advanced shell model calculations reproduce the observed B(E2) systematics. The results for N=50 isotones indicate a good N=50 shell closure and a strong Z=28 proton core polarization. The new results serve as benchmarks to establish theoretical models, predicting the nuclear properties of the doubly magic nucleus 78Ni.

Unlabelled: Before the widespread use of primary percutaneous coronary intervention (PCI) and glycoprotein llb/Illa inhibitors (GP lIb/Illa) the left ventricular thrombus (LVT) was reported to complicate up to 20% of acute myocardial infarctions (AMI). It still remains unknown how these modern therapies impact on LVT occurrence., The Aim of the Study: We tried to define the frequency of LVT among the patients (pts) who underwent successful primary PCI and received aggressive antiplatelet therapy at the same time. We also wanted to assess the clinical and echocardiographic predictors of LVT formation., Material and Methods: 3158 pts who had underwent successful primary PCI within 12 hours from onset of AMI were retrospectively analyzed. Two-dimensional and Doppler echocardiographic examinations were performed in all these pts within three to four days after the PCI. LVT was defined as an echodense mass with definite margins, distinct from the endocardium and adjacent to an area of hypo- or akinetic myocardium. Baseline demographic characteristics, angiographic findings, type of intervention and medical treatment were analyzed., Results: LVT was detected in 79 pts (2.5%). Pts with LVT and ones without it (n=3079, control group) were the same age (61.2+/-11.4 vs. 61.8 +/- 12.8 years, ns) and suffered from diabetes mellitus (29.1% vs. 22.4%, ns), lipid disorders (46.8% vs. 42.7%, ns) at the same frequency. Percentage of smokers was also similar in both groups (51.9% vs. 56%, ns). LVT pts had a history of hypertension more frequently (62.01% vs. 49.4%, p < 0.05). There were more men in LVT group (82.3% vs. 70.8%, p < 0.05). It included also more pts with anterior AMI (93.7% vs. 41.8%, p < 0.001). LVT pts had also a lower ejection fraction (43.4+/-12.4% vs. 55.7+/-12.7%, p < 0.001) and a higher wall motion score index (2.08+/-0.44 vs. 1.56+/-0.62, p < 0.001) than pts without LVT Percentage of stent implantations was similar in both groups (92.4% vs. 92.2%, ns), which also did not differ in treatment of glycoprotein llb/llla inhibitors (63.3% vs. 54.2%, ns) as well as administration of thienopyridines (92.4% vs. 92,2%). According to results of multiple log regression analysis, the presence of LVT was strongly associated with anterior AMI (adds ratio OR =25), male gender (OR = 2.21), EF < 40% (OR = 2.19) and previous hypertension (OR = 2.2)., Conclusions: The prevalence of LV thrombus early after AMI is very low in the era of primary PCI and aggressive antiplatelet treatment. The highest rate of LVT occurrence was found among male patients with anterior AMI, reduced left ventricular function and previous arterial hypertension.

Using a method whereby molecular and atomic ions are independently selected, an isobarically pure beam of 70Se ions was postaccelerated to an energy of 206 MeV using REX-ISOLDE. Coulomb-excitation yields for states in the beam and target nuclei were deduced by recording deexcitation gamma rays in the highly segmented MINIBALL gamma-ray spectrometer in coincidence with scattered particles in a silicon detector. At these energies, the Coulomb-excitation yield for the first 2+ state is expected to be strongly sensitive to the sign of the spectroscopic quadrupole moment through the nuclear reorientation effect. Experimental evidence is presented here for a prolate shape for the first 2+ state in 70Se, reopening the question over whether there are, as reported earlier, deformed oblate shapes near to the ground state in the light selenium isotopes.

Primary amyloidosis is a systemic disorder caused by the clonal production and tissue deposition of immunoglobulin light chain proteins. The disease symptoms are typical of multisystem failure. Common presenting features include nephrotic syndrome, hepatomegaly, sensomotor peripheral neuropathy and, in the case of cardiac involvement, congestive heart failure. This last sign appears very seldom as alone, without any others. Cardiac involvement generally denotes a poor prognosis, regardless of the method of treatment. The median survival rate from onset of congestive heart failure is 6 months. Only the patients with earliest diagnosis made and advanced treatment (chemotherapy, autologous stem-cell transplantation, heart transplantation) introduced have the chance of the lengthening of life. The authors present a case of 52-year-old man with a primary amyloidosis, who suffered from severe, not responding to treatment, congestive heart failure. Because of lack of the other organ involvement symptoms, the correct diagnosis was made very late. The authors place emphasis on a simple diagnostic tool such as the correlation between the low voltage in the limb ECG leads and the echocardiographic sings of left ventricular hypertrophy. The combination of specific ECG, echocardiographic findings and positive extracardiac tissue biopsy may be sufficient to reach correct diagnosis. These examinations are easy accessible in non-specialist hospitals.

Neurotoxic effects of ammonia are mediated by increased accumulation of nitric oxide (NO), which combines with free radicals to form a highly toxic compound, peroxynitrite. Previous experiments in vivo and in vitro have suggested that this phenomenon engages neuron-derived NO and is coupled to changes in the accumulation of cGMP. The present study accounted for the facts that: (i) astrocytes, not neurons are the morphological target of ammonia, and (ii) both NO-dependent, soluble (sGC) and NO-independent, particulate guanylate cyclase (pGC) mediate cGMP production in the cells. Neocortical rat astrocytes were treated for 1 or 24 h with 5 mM ammonium chloride ("ammonia") and then subjected to: (i) cGMP measurement, and (ii) mRNA and/or protein expression analysis of alpha1 and beta1 subunits of sGC and two pGC forms: pGC-A and pGC-B. Treatment with ammonia for 1h increased accumulation of cGMP and sGCbeta1 mRNA expression, without producing significant changes in the protein expression. This was followed by a decrease of cGMP level at 24 h treatment, associated with a decreased expression of sGCbeta1 and sGCalpha1 mRNA and sGCbeta1 protein. Expression of pGC-A and pGC-B mRNA was elevated in ammonia-treated astrocytes after 24 h. Accordingly, increased cGMP accumulation was noted in the presence of a specific sGC inhibitor (ODQ). The results show that ammonia affects cGMP production in astrocytes, and that this may involve not only sGC but also pGC.

The inhibitory effect of silydianin, an active constituent of Silybium marianum, on the in vitro production and release of oxidative products has been examined. Polymorphonuclear neutrophils (PMNs) play a primary role in the initiation and propagation of inflammatory responses. Their apoptosis is a major mechanism associated with the resolution of inflammatory reactions. Neutrophils were assessed for caspase-3 activity, the rst step in the execution phase of apoptosis. When cells were cultured with 100 microM silydianin for 24 h, caspase-3 was activated. Induction of apoptosis by silydianin was accompanied by a decrease in luminol-enhanced chemiluminescence as well as superoxide radical (O2*-) release in freshly isolated cells and lipid peroxidation in mouse spleen microsomes. No significant effect of silydianin on PMN hydrogen peroxide production evaluated by a flow cytometric dichlorofluorescin oxidation assay was found. Such results indicate a possible antiinflammatory activity for silydianin, which regulates caspase-3 activation, affects cell membranes and acts as a free radical scavenger., (Copyright 2006 John Wiley & Sons, Ltd.)

Amyloidosis is a group of biochemical disturbances, leading to extracellular deposition of misfolded protein fibril's. It can be of primary, secondary or hereditary (familial) origin. The disorder is known from 150 years, and as already 23 fibril precursor proteins have been identified. Its symptoms can be systemic, localized; some forms don't produce any clinical manifestation. In this article amyloidosis pathogenesis, classification, epidemiology, prognosis and clinical characteristics are described, mainly with reference to the respiratory system.

The aim of this study was to evaluate the transfer frequency of plasmids encoding extended-spectrum beta-lactamases (ESBLs) from clinical isolates of Enterobacteriaceae to E. coli K12 C600 recipient strain. Additionally, resistance patterns to antimicrobial drugs of the isolates as well as transconjugants were analyzed. Fifty-four clinical strains belonging to the Enterobacteriaceae family were isolated from children hospitalized in Medical University Hospital in Wrocław. All the strains studied were identified in automatic ATB system using ID32E tests. Besides, they were ESBL-positive as was confirmed by the double-disc synergy test (DDST). The minimal inhibitory concentration (MIC) was determined for twelve selected antibiotics and chemotherapeutics. The majority of the strains (87%) were able to transfer plasmid-mediated ESBL to E. coli K12 C600 recipient strain with a frequencies ranged from 10(-5) to 10(-1) per donor cell. All the isolates studied as well as their transconjugants were susceptible to imipenem, meropenem and norfloxacin (MIC <1mg/L). On the other hand, these strains displayed high level of resistance (MIC 512 - >1024 mg/L) to cefotaxime, ceftriaxone, gentamycin, amikacin and cotrimoxazole. Genetic markers conferring resistance to aminoglycosides and cotrimoxazole were often co-transferred to recipient strain in conjugation process.

Transvenous pacemaker lead malposition in the left ventricle is a rare complication of pacemaker implantation however, at the moment of diagnosis poses the serious therapeutic problem. The usual morphology for paced events originating from the right ventricle has a left bundle branch block pattern, but sometimes right bundle branch block (RBBB) configuration is identified. The report describes two cases of RBBB configuration in the electrocardiogram (ECG) after pacemaker implantation. Case 1 demonstrates a female with unintentional pacemaker lead placement in the left ventricle through patent foramen ovale. Lead malposition was diagnosed accidentally during echocardiographic study (ECHO), 6 years after implantation. Case 2 concerns a man with a RBBB pacing configuration, but with correct pacemaker lead position in the right ventricle. Authors analyze these cases in connection with other publicized reports in order to find the safe algorithm for intraoperative estimation of correct pacemaker lead location. The following algorithm of procedures during pacemaker implantation is proposed to avoid the lead malposition in the left ventricle. First, obligatory perform 12-lead ECG in pace mode during surgery or immediately after it. Second, in case of RBBB pattern in post implant ECG, make ECHO for precise lead position description.

The primary tracheo-bronchial amyloidosis is a rare entity with long lasting and progressive course. Precise diagnosis can be established on the basis of pathological features seen in samples derived from the airways, obtained during fibreoptic bronchoscopy or during lung biopsy sometimes. Describing the case of an insidious course of primary tracheobronchial AL type amyloidoisis, that was initially recognised and treated as a chronic obstructive pulmonary disease. The authors represent its clinical course and the diagnostic difficulties. The changes in the respiratory tract, both radiological and endoscopic suggested a tuberculous or proliferative process. They were responsible for a severe increasing dyspnoea, due to bronchial obstruction, with muco-haemoptic expectoration. A forceps resection of the endobronchial lesions enabled to established the right diagnosis and further treatment limited to local procedures.

There are reports of successful pregnancies in women with haematological malignancies after either autologous or allogeneic bone marrow transplantation (BMT). We report six cases of uncomplicated pregnancies in five women treated with high-dose chemotherapy, radiotherapy and autologous bone marrow transplantation (ABMT) for acute lymphoblastic leukaemia. One patient was diagnosed as having leukaemia during pregnancy. The pregnancy ended with medical termination. Each woman received conditioning regimens without total body irradiation (TBI). Of five women, who received AMBT, all resumed spontaneous cyclical menstruation post transplantation. All of them conceived naturally between 15-52 months following ABMT. We noted one miscarriage in our 29-year-old patient. Six pregnancies went to term and each resulted in the successful delivery of a full-term baby. We did not notice any case of relapse of leukaemia in pregnancy.

High demand of neoplastic tissues for glutamine (Gln) is met by its active transport across cell membranes. Chronic treatment with acrylamide in rodents is associated with an increased incidence of neoplasms, including astrocytomas. In this study, 24-h acrylamide treatment significantly increased the initial rate of l-[G-3H]glutamine uptake in astrocyte cultures derived from the acrylamide-sensitive Fischer 344 rat, and this effect could be fully inhibited by histidine, a model substrate for the amino acid transport system N. RT-PCR analysis revealed that acrylamide treatment caused a significant increase in the astrocytic expression of the mRNA coding for the major system N protein, SNAT3, which is specifically overexpressed in malignant gliomas in situ. The acrylamide-induced upregulation of astrocytic Gln transport via system N is likely to affect Gln homeostasis in these cells and may be causally related to the increased astrocytoma incidence observed in Fischer 344 rats.

Unlabelled: Obese people are at high risk for developing diabetes, dyslipidemia, hypertension, and cardiovascular diseases, which lead to an increased risk of mortality. Evidence for the potential role of oxidative stress in various diseases and pathophysiological processes suggests that the dietary intake and the therapeutic use of antioxidants may have positive health effects. The aim of the study was: 1) to investigate the ability of the major tea polyphenols: (-)-epigallocatechin gallate (EGCG), theaflavins (TF) and gallic acid (GA) to protect in vitro human neutrophils from oxidative damage induced by phorbol myristate acetate (PMA), 2) estimation the level of reactive oxygen species (ROS) production in obese patient depending on the red tea Pu-Erh drinking, 3) estimation inflammatory marker: CRP., Material and Methods: We tested 14 obese patients (aged 45+/-12 years, women, BMI=34+/-5.1 kg/m2). The inclusion criteria were based on physical examination, BMI, WHR, and the body composition examination based on bioimpedance method. PMA were isolated and oxidant production, in response to 1 microg/ml PMA, was characterized by the production of hydrogen peroxide, nitric oxide and chemiluminescence intensity. CRP level was assayed by the immunoturbidimetric test in serum. Control group consisted of healthy blood donors., Results: Women consuming red tea revealed alteration in reactive oxygen species generation; the relative decrease of RFT was greater after 5 months than that after 1 month of treatment. A decrease in ROS generation after red tea consumption was accompanied by the decrease of ROS in response to tested compounds in normal cells. EGCG and TF showed similar potency in antioxidative activities. Tea polyphenols were not found to modulate CRP level in obese women., Conclusions: Tea may thus represent an important source of dietary antioxidants; there is need for more detailed studies to improve our understanding of the role of tea in reducing risk of major disease states.

Background: Circulating endothelial microparticles (EMPs), the small vesicles released from altered endothelial cells, have been established as markers of endothelial injury. The elevated count of EMPs has been described in different conditions involving endothelial injury, including acute myocardial infarction (AMI)., Aim: To assess the presence of EMP in patients with acute MI in relation to early clinical outcome and coronary angiography results., Materials and Methods: EMPs counts were determined in 66 patients pts (23 women, 43 men) with documented ST elevation AMI and in 10 control patients with no evidence of coronary artery disease. All pts with AMI underwent coronary angiography with attempted primary angioplasty. EMPs were assayed by flow cytometry in platelet-poor plasma with combinations of fluorescent antibodies (anti CD31, -51, -42) allowing distinction of EMPs from platelet microparticles. Clinical and angiography results were compared with EMP levels., Results: Three kinds of EMPs were measured: CD31+, CD51+ and CD31+/51+. The percentage of EMPs CD31+/CD51 was significantly (p=0,042) higher in patients with AMI in comparison with control subjects. However, a marker, which distinguished both groups the most, was the level of EMPs CD51+. It was significantly (p=0,024) higher in pts with AMI than in control pts. The levels of CD31+ were similar in both groups. There was no correlation between EMP levels, clinical and angiography results., Conclusion: The presence of circulating EMPs provides direct evidence of endothelial injury in AMI. The clinical and practical value of these results, however, needs further exploration.

Background: The level of 8-oxoguanine (8-oxoG), a general marker of oxidative DNA damage, in DNA is the result of both an equilibrium between the rates of its formation and removal from DNA by DNA repair enzymes and the removal of 8-oxodGTP from the cellular nucleotide pool by hydrolysis to 8-oxodGMP, preventing its incorporation into DNA. To determine the contribution of each component to the level of 8-oxoG in DNA, we compared 8-oxoG-excising activity (encoded by hOGG1), 8-oxodGTPase activity (encoded by hMTH1), and 8-oxoG levels in DNA from tumors and surrounding normal lung tissues from non-small-cell lung cancer patients., Methods: We measured the level of 8-oxoG in DNA of 47 patients by high-performance liquid chromatography/electrochemical detection (HPLC/ECD), hOGG1 activity in tissue extracts of 56 patients by the nicking assay using an oligodeoxynucleotide containing a single 8-oxoG, and hMTH1 activity in tissue extracts of 33 patients by HPLC/UV detection. All statistical tests were two-sided., Results: The 8-oxoG level was lower in tumor DNA than in DNA from normal lung tissue (geometric mean: 5.81 versus 10.18 8-oxoG/10(6) G, geometric mean of difference = 1.75; P<.001). The hOGG1 activity was also lower in tumor than in normal lung tissue (geometric mean: 8.76 versus 20.91 pmol/h/mg protein, geometric mean of difference = 2.39; P<.001), whereas the hMTH1 activity was higher in tumor than in normal lung tissue (geometric mean: 28.79 versus 8.94 nmol/h/mg protein, geometric mean of difference = 0.31; P<.001). The activity of hMTH1 was three orders of magnitude higher than that of hOGG1 (nanomoles versus picomoles per hour per milligram of protein, respectively)., Conclusions: Several different components contribute to the maintenance of 8-oxoG levels in human DNA, with the greatest contributor being the removal of 8-oxodGTP from the cellular nucleotide pool by hMTH1.

A previous study showed that treatment of C6 glioma cells with 10 mM ammonium chloride monia") for 24 h decreases taurine uptake and evokes sodium-dependent taurine efflux, indicating reversal of the taurine transporter (TauT)-mediated transport as an underlying mechanism. Consistent with the involvement of TauT we now show that the ammonia-induced changes in Tau uptake and efflux are inhibited by the protein kinase C (PKC) activator phorbol 12,13-dibutyrate (PDBu). Ammonia treatment of C6 cells resulted in increased intracellular accumulation of cAMP. Incubation of the cells with dibutyryl cAMP (dbcAMP) mimicked the effects of ammonia on both taurine uptake and efflux. The effects of dbcAMP on taurine uptake and efflux were additive to the effects of ammonia. Collectively, the results suggest that the effects of ammonia on taurine uptake and efflux may be partly mediated by cAMP. Consistent with this mechanism, the adenyl cyclase inhibitor, miconazole reduced the stimulation of efflux by ammonia.

Obese people are at high risk for developing diabetes, dyslipidemia, hypertension, and cardiovascular diseases, which lead to an increased risk of mortality. Activated polymorphonuclear neutrophils (PMN) generate extremely high amounts of reactive oxygen species (ROS), but these are normally targeted at pathogens inside intracellular phagosomes. These same beneficial antimicrobial functions can cause significant local tissue injury and lead to the development of pathologic systemic inflammatory conditions. PMN apoptosis is a major mechanism associated with the resolution of inflammatory reactions. The goals of the present study were: 1) to evaluate the level of reactive oxygen species production in PMN from obese people before and during body mass reduction, 2) to investigate the in vitro effect of flavonoids: quercetin and rutin on oxidative metabolism and apoptosis of stimulated neutrophils in obese patient. We tested 30 obese patients (women) before body mass reduction and 20 patients during low calories diet. The inclusion criteria were based on physical examination, BMI, WHR, the body composition examination based on bioimpedance method and biochemical assessment. PMN were isolated and oxidant production, in response to 1 microg/ml PMA, was characterised by the production of hydrogen peroxide, nitric oxide and chemiluminescence intensity. Caspase-3 activation was assayed by the method of DEVD-AMC cleavage in PMN cultured up to 24 hours. The results of our study showed: 1) the decrease in PMN oxidant production in patient during the mass reduction, 2) the strong antioxidant activity of quercetin and rutin in obese patients before and during the body mass reduction, these effects were dose dependent and rutin was less potent than quercetin, 3) acceleration of PMN apoptosis by rutin is associated with an increase in caspase 3 activity.

Theophylline is a drug used in the treatment of obstructive pulmonary disease and a strong immunomodulator and has anti-inflammatory potential. However, its mechanism of definite action is still poorly defined. In the present study the effect of teophylline on the in vitro formation and release of reactive oxygen species in polymorphonuclear neutrophils (PMN) was studied at concentration of 0.9-130 microg/ml. The neutrophils oxygen metabolism was assessed with methods: luminol-dependent chemiluminescence, cytochrome C reduction, phenol red oxidation, and Griess reaction. In vitro theophylline treatment most effectively inhibit neutrophil hydrogen peroxide and nitric oxide generation (at 90 and 130 microg/ml), superoxide production (at 1.3 microg/ml), and diminish chemiluminescence (at the smallest concentrations 0.9 and 1.3 microg/m). We concluded that the effects of theophylline on granulocyte function are likely to contribute to the drug's clinical efficacy.

Treatment of cerebral cortical slices with 5mM ammonium acetate (ammonia) elevated the glutamine (Gln) content and increased cell volume in the slices, in agreement with the postulated contribution of glutamine to hyperammonemic brain edema [Neurochem. Int. 43 (2003) 299]. In this study we show that, unexpectedly, treatment with a glutamine synthetase inhibitor, methionine sulfoximine (MSO) (0.1-5.0mM) in the absence of ammonia increases Gln content in the slices in a dose-independent manner, to levels higher than those recorded after ammonia treatment. MSO (>0.1mM) inhibited (>0.1mM) Gln uptake in crude cerebral cortical cell membranes (P2 fraction). Since Gln uptake in this preparation was largely facilitated by the Gln efflux-promoting systems ASC and N and less so by the uptake promoting system A, MSO-induced accumulation of Gln could result from inhibition of Gln efflux. MSO did not affect cell volume in the slices, showing that Gln retention is not as a rule a causative factor in cerebral edema. MSO at 5mM concentration increased cell swelling induced by ammonia, which is consistent with earlier observations pointing to the direct excitotoxic action of MSO in vivo and in vitro. The results emphasize the limits of applicability of MSO as an inhibitor of Gln synthesis in an in vitro system.

Background: Acute myocardial infarction (AMI) is one of the main causes of death in the elderly, however, the optimal therapy of AMI in this age-group has not yet been established., Aim: To compare the early outcome of patients with AMI aged > or =75 years who underwent primary percutaneous coronary interventions (PCI) or were treated conservatively., Methods: In-hospital outcome of 180 patients aged > or =75 years, hospitalised due to AMI, was retrospectively analysed. Ninety two consecutive patients, admitted with AMI between May 2001 and October 2002, underwent primary PCI whereas 88 patients, treated for AMI between 1993 and 2002, received standard pharmacological therapy without thrombolysis., Conclusions: Primary PCI in the elderly with AMI is significantly more effective than conservative therapy, except with patients with cardiogenic shock in whom mortality is similar regardless of the therapy used.

Guillain-Barré syndrome (GBS) is the most common acquired polyradiculoneuropathy in childhood. It has been conventionally regarded as a disease exclusively of the peripheral nervous system. The involvement of the central nervous system (CNS) in patients with GBS has been rarely described. The purpose of the study was to delineate the extent of subclinical neurological changes of CNS in children and adolescents with this syndrome. Thirty patients aged 8-18 years with GBS were treated in the Chair and Department of Developmental Neurology. The upper and lower limbs paresis dominated in clinical pictures of these patients. Cranial nerve involvement was noticed in 9 children. An ascending bulbar paralysis was noted in four cases. Sensory symptoms were found in all children. The nerve conduction velocities were abnormal in all examined patients with GBS. The control group for neurophysiological studies consisted of 66 healthy children and adolescents at the matched age. Evoked potentials (EP) were registered by means of Multiliner (Toennies, Germany). Brainstem evoked potentials (BAEP) and visual evoked potentials (VEP) were always performed in the same conditions with the same equipment for the children and adolescents in the GBS and control group, according to the guidelines of the International Federation of Clinical Neurophysiology (IFCN). The following BAEP parameters were considered: the latencies of waves I to V, interpeak latencies I-III, III-V and I-V. The latencies of N75, P100, N145 as well as the amplitudes of N75/P100, P100/N145 for mono- and binocular stimulations of VEP were analysed. BAEP showed abnormalities in 6 cases and VEP in 5 cases. The statistically significant prolongation of the latencies of waves III, V and interpeak I-V were found in children and adolescents with GBS. The BAEP changes may reflect impairment at the brainstem level in these patients. In VEP recording in GBS the prolongation of latencies P100 and N145 without changes in amplitudes were found. These parameters were statistically significant in comparison to the control group. VEP results suggest the involvement of visual pathway in examined children and adolescents. EP can be used as a complementary method for the evaluation of clinically silent lesion in the auditory and optical tracts in GBS.

Unlabelled: Patent foramen ovale (PFO) represents the most common persistent abnormality of fetal origin. The aim of the study was to analyze the incidence and characteristics of PFO and to assess PFO as the risk factor of paradoxical embolism. 945 consecutive pts (442F and 503M aged 13-85, mean 53.02 +/- 14.42 years) in whom TEE was performed and flow through PFO was detected in basal conditions (colour-Doppler) and/or during provocation (Valsalva/cough manoeuvre) with contrast (saline infusion) at the period 1998-2002 was retrospectively analyzed. 183 pt had a history of systemic embolisation (SE) or transient ischemic attack (TIA). PFO was diagnosed [PFO(+)] in 57 pts (6%)-22F, 35M aged 14-77 years, mean 52.44 +/- 14.84 years. 888 pts without PFO [PFO(-)] created a control group. Two subgroups were analyzed in the study group: xPFO(+) - 28 pts with PFO as the only abnormality, yPFO(+) - 29 pts with PFO and other heart/aortic disease. Similarly, in the control group two subgroups were analysed: xPFO(-) - pts with normal TEE and negative history of heart/aortic disease and yPFO(-) - pts without PFO but with other heart/aortic disease. Aneurysmal formation of interatrial septum was detected in 24 pts, and in 6 pts it coexisted with PFO. The intensity of shunt was significantly higher in yPFO(+) than in xPFO(+) group. In 5 pts permanent shunt through PFO at the basal stage was observed (4 pts with significant regurgitation of the atrio-ventricular valves and one patient with tricuspid stenosis). Percentage of pts with the history of SE/TIA was significantly higher in group xPFO(+) than in xPFO(-) (p < 0.01)., Conclusions: (1) PFO is a risk factor of SE/TIA only in group xPFO(+). (2) Flow through PFO in group xPFO(+) is generally minimal. (3) In case of coexisting heart pathology PFO may provoke significant right-to-left or even left-to-right shunt.

Splenectomy is a useful method of treatment in some hematological disorders (congenital microspherocytosis, ITP, hypersplenism). However in many clinical situations the unclear prognostic factors, bad patient's condition or non-typical disease's course may impede the decision to splenectomize. We present a history of three successfully splenectomized patients. In each of reported cases the complicated course required detailed disease and treatment analysis. Our results indicate that splenectomy should be considered as a therapeutic option in the thrombocytopenic patients. This group of patients should be immediately referred to specialized centres.

Swelling of CNS cells due to endogenous ammonia is a major cause of cerebral oedema in hyperammonaemic encephalopathies. In the present study, incubation in the presence of 5mM ammonium acetate ("ammonia") decreased steady-state distribution of [14C]inulin within incubated rat cerebrocortical minislices, indicating cell swelling. NMDA receptor antagonists, MK-801 ((+)-5-methyl-10,11-dihydro-5H-dibenzo [a,d]cycloheptene-5,10-imine maleate,10 microM) and DL-AP-5 (DL-2-amino-5-phosphonovaleric acid, 250 microM), a nitric oxide synthase inhibitor, L-nitroarginine (L-NNA, 500 microM), and an antioxidant, taurine (Tau, 10 mM), markedly attenuated the cell volume-increasing effect of ammonia. The effect of Tau (10mM) was abolished by the GABA(A) receptor antagonist bicuculline (100 microM), but was unaffected by the Tau transport inhibitor guanidynoethyl-sulfonate (GES, 500 microM). Ammonia increased the slice content of Gln, an amino acid whose excess accumulation has been implicated in hyperammonemic oedema. However, treatments that reduced the cell volume did not affect Gln content. These results indicate that ammonia-induced cell swelling is in a large degree mediated by overactivation of NMDA receptors and the ensuing generation of NO and free radicals.

To assess the role of oxidative stress and lipid peroxidation (LPO) in the pathogenesis of lung cancer, we measured the levels of 1,N(6)-ethenoadenine (epsilonA) and 3,N(4)-ethenocytosine (epsilonC) in the DNA by immunoaffinity/(32)P postlabeling (33 cases). We also measured the capacity for epsilonA and epsilonC repair (by the nicking assay) in normal and tumor lung tissues, as well as in blood leukocytes of lung cancer patients (56 cases). Repair activities for epsilonA and epsilonC were also assayed in leukocytes of healthy volunteers, matched with cancer patients for age, sex, and smoking habit (25 individuals). Up to 10-fold variations among individuals were observed both in adducts level and repair activities. No differences in epsilonA and epsilonC levels between tumor and nonaffected lung tissues were recorded. However, leukocytes accumulated a significantly higher number of DNA adducts than the lung tissues. Repair activities for both epsilonA and epsilonC were significantly higher in tumor than in normal lung tissue. No significant differences in epsilonA and epsilonC repair activities were associated with age, sex, or smoking habit. However, a significant difference in repair capacity was observed between two histological types of lung cancer, squamous cell carcinoma (SQ) and adenocarcinoma (AD). In individuals suffering from lung AD, epsilonA- and epsilonC-repair activities in normal lung and blood leukocytes were significantly lower than in SQ patients. Moreover, in nonaffected lung tissue of AD patients, the ratio epsilonA/epsilonC adducts was lower than in SQ patients. Differences have also been found between epsilonA and epsilonC repair activities of cancer patients and healthy volunteers. Repair capacity for epsilonA was significantly lower in blood leukocytes of lung cancer patients than in leukocytes of healthy volunteers (P = 0.012). This difference was even larger between healthy volunteers and patients developing inflammation-related AD (P = 0.00033). Repair activities for epsilonC were the same in leukocytes of healthy controls, all lung cancer patients, and SQ patients. However, individuals with ADs revealed significantly lower epsilonC-repair activity (P = 0.013). These results suggest that oxidative stress-mediated lipid peroxidation might contribute to induction and/or progression of lung cancer. Decreased activity of base excision repair pathway for epsilonA and epsilonC is associated particularly with inflammation-related lung AD.

Flavonoids are reported to be powerful antioxidants in cell free systems. They naturally occur as glycosides rather than as aglycon. In this study the ability of the flavonoid quercetin and its glycosides, quercetin-3-O-rutinoside (rutin), quercetin-3-O-glucoside and quercetin-3-O-(6″-O-acetyl)-glucoside, to protect in vitro rat C6 glioma cells from oxidative damage induced by cumene hydroperoxide was investigated. Cumene hydroperoxide induced cell death and lipid peroxidation. The cytotoxicity of cumene hydroperoxide could be prevented by the radical scavenger dimethyl thiourea and the ferric iron chelator deferoxamine, indicating that its cytotoxic activity is related to the generation of reactive oxygen radicals in the ferrous iron dependent Fenton reaction. Quercetin, in a concentration range of 10-100 μM, but neither rutin nor the other two glycosides, were able to protect C6 cells from cytotoxicity and lipid peroxidation. Furthermore, cytoprotective concentrations of quercetin proved to be cytotoxic itself. These results call in question potential beneficial effects of dietary intake or therapeutic use of naturally occurring flavonoids.

Spasmodic dysphonia is a focal laryngeal dystonia. It presents as: adductor spasmodic dysphonia with the strain-strangle voice; abductor spasmodic dysphonia with whispering voice and breathy breaks in connected speech; and adductor respiratory dystonia with paradoxical vocal fold movements and stridor. It is most commonly treated by the intramuscular injection of botulinum toxin. In this article, the authors discuss difficulties in making diagnosis and treatment in patients with laryngeal dystonia concerning their own cases.

Gamma-Aminobutyric acid (GABA) is the main inhibitory amino acid in the central nervous system (CNS). Experiments with animal models of HE, and with brain slices or cultured CNS cells treated with ammonia, have documented changes in GABA distribution and transport, and modulation of the responses of both the GABA(A)-benzodiazepine receptor complex and GABA(B) receptors. Although many of the data point to an enhancement of GABAergic transmission probably contributing to HE, the evidence is not unequivocal. The major weaknesses of the GABA theory are (1) in a vast majority of HE models, there were no alterations of GABA content in the brain tissue and/or extracellular space, indicating that exposure of neurons to GABA may not have been altered, (2) changes in the affinity and capacity of GABA receptor binding were either absent or qualitatively different in HE models of comparable severity and duration, and (3) no sound changes in the GABAergic system parameters were noted in clinical cases of HE. Taurine (Tau) is an amino acid that is thought to mimic GABA function because of its agonistic properties towards GABA(A) receptors, and to contribute to neuroprotection and osmoregulation. These effects require Tau redistribution between the different cell compartments and the extracellular space. Acute treatment with ammonia evokes massive release of radiolabeled or endogenous Tau from CNS tissues in vivo and in vitro, and the underlying mechanism of Tau release differs from the release evoked by depolarizing conditions or hypoosmotic treatment. Subacute or chronic HE, and also long-term treatment of cultured CNS cells in vitro with ammonia, increase spontaneous Tau "leakage" from the tissue. This is accompanied by a decreased potassium- or hypoosmolarity-induced release of Tau and often by cell swelling, indicating impaired osmoregulation. In in vivo models of HE, Tau leakage is manifested by its increased accumulation in the extrasynaptic space, which may promote inhibitory neurotransmission and/or cell membrane protection. In chronic HE in humans, decreased Tau content in CNS is thought to be one of the causes of cerebral edema. However, understanding of the impact of the changes in Tau content and transport on the pathogenic mechanisms of HE is hampered by the lack of clear-cut evidence regarding the various roles of Tau in the normal CNS.