05). The cytokinesis-blockage micronucleus test (CBMN), used to evaluate the mutagenicity and antimutagenicity of different concentrations of the wasp venom, was performed according to the protocol described by Natarajan and Darroudi (1991), with some modifications. For the mutagenicity and antimutagenicity

test, 5 × 105 cells were seeded in culture flasks of 25 cm2. The flasks were incubated for 24 h in incubator at 37 °C, 5% CO2 in humid atmosphere, for a stabilization period. After this period, two evaluations were made, one to assess the mutagenicity, where the cells were exposed to the different concentrations of the wasp venom for 3 h and another to assess the antimutagenicity, performed by 4 different types of treatment, as already described for the comet assay. After the treatments, both for the evaluation of the mutagenicity and antimutagenicity, selleck screening library the cells were washed with PBS. The medium was changed and it was added to the culture cytochalasin B (final concentration of 3 μg/mL). The

cells were then incubated for more 28 h, collected, treated with hypotonic solution (sodium citrate 1%) and selleck chemical fixed with formaldehyde (40%) and ethanol-acetic acid (3:1). The slides were stained with Giemsa 5% for 8 min. It was counted 2000 binucleated cells per replica, and it was counted micronuclei, nucleoplasmic bridges and nuclear buds (Fenech and Crott, 2002). The analysis of the significance of the results was made by the ANOVA (one way) parametric statistic test, followed by the Dunnet’s comparison test (p < 0.05). The MTT test is a cytotoxicity assay in which it is measured the cell viability. This test is based on the ability of the viable cells on converting the MTT salt (Thyazolyl Blue Tetrazolium Bromide). This salt is soluble in water Protein tyrosine phosphatase and is converted, by the viable cells, into an insoluble salt of purple colouration. This product cannot cross the cell membranes of viable cells, and, therefore, accumulates in their

interior (Fotakis and Timbrell, 2006). In this study it was tested the concentrations of 160 μg/mL, 80 μg/mL, 40 μg/mL, 20 μg/mL, 10 μg/mL, 5 μg/mL, 1 μg/mL of the venom of the wasp P. paulista. The results obtained for the MTT assay are shown in Table 1, Fig. 1. From the results obtained, it was observed that the concentrations of 10 μg/mL, 5 μg/mL and 1 μg/mL were not statistically different from the negative control. Thus, it could be inferred that these concentrations were not cytotoxic for the cells exposed, after the period of 3 h of exposure. The other concentrations were significant in relation to the negative control, showing cytotoxicity and, therefore, were not suitable for use in the genotoxicity and mutagenicity tests, since these tests need viability equal or superior to 80% to be performed.

Comets were visualized with an excitation filter of 450–490 nm and an emission filter of 515 nm and fluorescent images of single cells were captured at 200 × magnification. A minimum of 100 randomly chosen cells per experimental group were scored for comet parameters such as tail length and percentage of DNA in tail [28] using the Tritek CometScore Freeware v1.5 image analysis software. Results from the Alamar Copanlisib cost Blue® assay showed that hydroquinone treatment reduced the viability of human primary fibroblasts and colon cancer HCT116 cells in a dose-dependent manner. As shown in Fig. 1, high concentrations of hydroquinone (227 μM, 454 μM, 908 μM, 2270 μM and 4541 μM) greatly decreased cell viability.

Compared to control, metabolic activity drastically dropped after exposure to any concentration equal or above 227 μM of hydroquinone. This negative effect on metabolic activity is more effective in HCT116 cells (11.25%) than fibroblasts cells (43.22%). EC50 for cytotoxicity in fibroblasts and HCT116 cells was 329.2 ± 4.8 μM and 132.3 ± 10.7 μM, respectively. There is a good fit between the dose response curve and the data points for cytotoxic effects on HCT116 cells and fibroblasts cells after 24 h (r2 = 0.9175 and r2 = 0.9773, respectively). One of the possible ways by which hydroquinone reduces cell survival could be through induction of DNA damage. We then addressed whether

hydroquinone induced DNA damage in primary human skin fibroblasts and Doxorubicin HCT116 cells, using the same range of concentrations previously demonstrated to reduce survival of both cells. To this end, we exposed HCT116 cells to increasing concentrations of hydroquinone (9.08, 45.4, 90.8, 227.0 and 454.1 μM; Table 1) for 24 h using as controls cells exposed to either no drug (solvent alone; negative control), or to etoposide for 15 min learn more (50 μM; positive control), a well-known potent inducer of DNA breaks [10]. Since fibroblasts cells were less sensitive to hydroquinone as shown

by the Alamar Blue® assay, we exposed fibroblasts cells to concentrations of 454.1 and 908.2 μM of hydroquinone (Table 1). DNA breaks were detected using the highly sensitive alkaline comet assay, an electrophoresis-based assay that allows detection of both single and double-stranded DNA breaks at the single cell level. As expected, etoposide induced significant DNA damage on fibroblasts and HCT116 cells with ∼50% and 80%, respectively, of the DNA leaving the nucleus and migrating as the comet tail (Table 1). Importantly, treatment of HCT116 cells with 227 or 454 μM hydroquinone induced DNA damage similar to that caused by sub-apoptotic levels of etoposide in the same cell line. In fibroblasts, however, exposure to 454.1 μM of hydroquinone induced a much higher % of tail DNA in comets compared to etoposide (Table 1). To investigate if the presence of a fungal strain capable of degrading phenols, P. chrysogenum var.

The formation of FA in plants occurs through the metabolic route of shikimate pathway starting with aromatic amino acids, l-phenylalanine and l-tyrosine as key entities. Initially, phenylalanine and tyrosine are converted into cinnamic and p-coumaric acid with

the help of phenylalanine ammonia lyase and tyrosine ammonia lyase, respectively [17]. The p-coumaric acid gets converted into FA by hydroxylation and methylation reaction [16]. Oxidation and methylation of FA and other aromatic compounds give di- and tri-hydroxy derivatives of cinnamic acid, which takes part in the lignin formation together with learn more FA. The conversion reactions occur during the formation of FA and other aromatic compounds, which are schematically represented in Fig. 2. In vivo studies on FA metabolism suggests that it gets converted into a variety of metabolites such as ferulic acid-sulfate, ferulic acid-glucuronide, ferulic acid-sulfoglucuronide (major metabolites in the plasma and urine of rats), ferulic acid-diglucuronide, feruloylglycine, Tofacitinib m-hydroxyphenylpropionic acid, dihydroferulic acid, vanillic acid and vanilloylglycine [90] and [91]. The data obtained from these outcomes recommends that the major pathway of FA metabolism is the conjugation reaction with glucuronic acid and/or sulfate. The conjugation of FA takes place mainly in the liver through the activities of

sulfotransferases and uridine diphosphate (UDP) glucuronosyl transferases, while small amount of conjugation reaction also takes place in the intestinal mucosa and kidney [10],

[32] and [90]. A small portion of free FA possibly metabolized through β-oxidation in the liver [11]. A study was carried out by Overhage et al. with the help of Pseudomonas sp. strain HR199 at the end of twentieth century which revealed that the genes involved in the catabolic mechanism of FA were present on a DNA region, which was covered by two EcoRI fragments, E230 and E94, respectively. These genes were fcs, ech, and aat encoding for feruloyl coenzyme A synthetase, enoyl-CoA hydratase/aldolase, and β-ketothiolase, respectively [63]. Report on the degradation of FA into vanillin and other useful organic compounds through protocatechuate 4,5-cleavage (PCA) Org 27569 pathway in Sphingomonas paucimobilis SYK-6 confirmed that FA got converted into feruloyl-CoA by feruloyl-CoA synthetase (FerA), and further into HMPMP-CoA (4-hydroxy-3-methoxyphenyl-β-hydroxypropionyl-coenzyme A) with the help of feruloyl-CoA hydratases/lyases (FerB and FerB2). It subsequently resulted into vanillin with the removal of CH3COSCoA (acetyl coenzyme A), and finally vanillin transformed into pyruvate and oxaloacetate through the PCA pathway [43]. The end products of FA catabolism enter into the TCA (tricarboxylic acid cycle), and produce energy in the biological system as shown in Fig. 3.

3 In a difficult case with broad spectrum differential, this proved to be invaluable by rapidly pointing to a NHL and by improving the diagnostic certainty of the pathology analysis obtained later on. It raises the question as to whether echoendoscopists should systematically obtain FC samples in patients with HL. The authors Small Molecule Compound Library declare that no experiments were performed on humans or animals for this investigation. The authors declare that they have followed the protocols of their work centre on the publication of patient

data and that all the patients included in the study have received sufficient information and have given their informed consent in writing to participate in that study. The authors declare that they have obtained the informed consent of the patients and/or subjects mentioned in the article. The author

for correspondence must be in possession of this document. The authors have no conflicts of interest to declare. “
“Artigo relacionado com:http://dx.doi.org/10.1016/j.jpg.2012.07.010 A peritonite bacteriana espontânea (PBE) é uma infeção grave e frequente, que ocorre em 10 a 30% dos doentes com cirrose hepática e ascite hospitalizados1. Esta entidade define-se pela presença de mais de 250 polimorfonucleares BKM120 research buy neutrófilos/mm3no líquido ascítico (LA), na ausência de um foco infeccioso intra-abdominal ou de malignidade1 and 2. A PBE surge devido à translocação bacteriana através do intestino, um processo pelo qual bactérias entéricas e os seus produtos (endotoxinas, ADN) atravessam a barreira mucosa intestinal e infetam os gânglios linfáticos, entrando na circulação sanguínea e no LA. Os doentes com redução da capacidade defensiva do LA têm maior suscetibilidade para PBE. Os 3 principais

mecanismos de defesa que previnem a PBE, que são a estabilidade da flora intestinal, a integridade do epitélio intestinal e as defesas do hospedeiro, estão alterados nos doentes com cirrose em estádio avançado. Nestes casos há redução da motilidade intestinal por hiperativação do sistema nervoso simpático, conduzindo a sobrecrescimento bacteriano, que favorece a ocorrência de PBE. Por outro lado, a permeabilidade da mucosa está aumentada, Dichloromethane dehalogenase em consequência da hipertensão portal e de acontecimentos pró-inflamatórios locais, desencadeados pela libertação de endotoxinas. Por último, os mecanismos de defesa locais e sistémicos estão alterados (os neutrófilos e macrófagos têm fagocitose reduzida, estando também diminuída a função efctora das células imunocompetentes circulantes no sangue), limitando a atividade bacteriostática do soro e do LA. A capacidade de opsonização do LA está relacionada com os níveis de proteínas totais, estando claramente demonstrado um maior risco de PBE em doentes em que esses valores são mais baixos.

Patients contacted the hospital either by an admission at the emergency department or were referred by their house physician at the outpatient TIA and stroke clinic. Patients with an ischemic event of more than six weeks ago were excluded for this study. All patients were followed up for three months. The protocol included a prompt start of an anti-thrombotic drug regime in every

patient (300 mg acetylsalicylic acid for 14 days in case of a minor stroke Selleck AG 14699 or an initial dose of 300 mg acetylsalicylic acid on day 1 followed by a prescription of 100 mg daily in TIA patients). All patients underwent laboratory examinations, ECG, duplex examination of the carotid and vertebral arteries and a CT and/or MR of the brain. If duplex revealed a stenosis of more than 50% or the TCD embolus detection revealed active cerebral embolism a CT angiography was performed from the aortic arc including the basal arteries of

the brain. Therapeutic drug interventions included the prescription of anti-thrombotic drug such as acetylsalicylic acid in combination with dipyridamole acid (in case of atrial fibrillation: anti-coagulants), statines and anti-hypertensive treatment. Patients used clopidogrel for six months; in case of persistent cerebral embolization (for instance after carotid surgery or when cerebral embolism was still present after the administration of acetylsalicylic acid) the drug this website regimes were switched to a combination of anti-thrombotic drugs that more effectively reduced the level of cerebral embolism. In case of a symptomatic carotid stenosis patients were asked to participate in the International Carotid Stenting Study (ICSS). The ICSS is an international multicenter trial which compares the efficacy of stenting versus surgery in the treatment of symptomatic carotid artery stenosis [5]. Patients scheduled for stent were treated with clopidogrel for at least six months,

after carotid surgery they received acetylsalicylic acid and dipyridamole acid. Patients scheduled for surgery and stenting were observed for two days at the stroke unit. Monitoring mafosfamide during stent procedure was done in awake patients by a neurologist. During carotid surgery the patients were exposed to general anesthesia and monitored by a clinical neurophysiologist. Monitoring techniques during surgery included both TCD and electro-encephalography. Based on monitoring results patients were electively shunted during the carotid endarterectomy. TCD monitoring was performed in all patients in the first hours after surgery and stenting procedures to detect persistent cerebral embolism or malignant cerebral hyperperfusion.

The complex (1:1) was obtained by co-evaporation. MGN and β-CD, in an equimolar ratio (1:1) were added to an aqueous solution prepared with 5 mL ethanol/100 mL water. The solution was protected from light and mechanically shaken at 170 rpm at 25 °C in a Marconi MA-420 incubator shaker (São Paulo, Brazil) for 24 h. After evaporation of the ethanol from the reaction mixture, the uncomplexed MGN was removed by filtration. Then,

INK 128 cell line water was evaporated under reduced pressure in a Büchi Rotavapor (Büchi, Germany) and dried in vacuum, giving the MGN:β-CD complex. The FT-IR spectra of MGN, β-CD and MGN:β-CD complex were recorded at room temperature in a spectral region between 4000 and 500 cm−1 on an IRPrestige-21, Fourier Transform Spectrometer (Shimadzu, Kyoto, Japan). Samples were prepared as small pellets by mixing each of them in a mortar with KBr (1:100) and then pressed. A blank KBr disc was used as a background. DSC analysis was carried out for MGN, β-CD and the complex with a DSC-60 calorimeter (range 25–500 °C) (Shimadzu, Kyoto, Japan). The temperature scale Inhibitor Library in vitro was calibrated using α-alumina powder. Samples (5.0–10.0 mg) were

placed in standard aluminum pans and measurements were performed at a heating rate of 5 °C min−1 from 25 to 400 °C in a dynamic nitrogen atmosphere (flow rate = 20 mL/min). The MGN and MGN:β-CD complex were prepared with 5 mL ethanol/100 mL water. The solution of the MGN:β-CD (1:1) complex was prepared at concentrations of 50, 100 and 500 μmol L−1. The solutions were stirred (170 rpm) for 24 h at 25 °C. Initially, a concentration of 100 μmol L−1 for the solution of DPPH in only methanol was used. In order to analyze solvent effects, the concentrations of 100 μmol L−1 for MGN and 50 μmol L−1 for DPPH were used. The antioxidant activities of MGN, β-CD, MGN:β-CD complex samples and GA (positive control) were measured in terms of their radical scavenging ability (RSA), using the DPPH method. ID-8 MGN,

β-CD or MGN:β-CD complex solutions (0.30 mL) were mixed with 2.7 mL of 50 μmol L−1 DPPH solution in different proportions of methanol:water and ethanol:water (20:80, 30:70, 50:50 and 100:0 mL:mL) in a 3 mL-quartz cuvette. The DPPH absorption values were obtained at 516 nm every 5 min, during 50 min by UV–vis spectrophotometer (MultiSpec-1501, Shimadzu, Japan). The results are expressed as remaining DPPH R (%) as a function of time (Oliveira et al., 2009). All measurements were performed in triplicate. The MGN, β-CD and MGN:β-CD (1:1) complex aqueous solutions were prepared with 5 mL ethanol/100 mL water at a concentration of 100 μmol L−1. The solution was stirred (170 rpm) for 24 h in the absence of light. The ORAC analyses were carried out on a Synergy HT multidetection microplate reader, from Bio-Tek Instruments, Inc. (Winooski, USA), using 96-well polystyrene white microplates, purchased from Nunc (Denmark).

Expression of the proneural bHLH transcription factor Ascl2

is associated with stemness and is absolutely required for intestinal stem cell maintenance. Active Notch is required for Ascl2 expression and its loss results in precocious crypt cell differentiation [8 and 10]. The proneural protein Atoh1 acts as a master regulator of fate specification Epigenetic inhibitor of the secretory lineage [2 and 11]. Ascl2 expression is maintained by active Notch signalling that also acts to suppress Atoh1. Expression of Atoh1 is cell-autonomously inhibited by Hes proteins and in the absence of Notch signalling, crypt stem cells precociously differentiate into secretory goblet cells [7 and 12]. The spatial organisation of cells expressing Notch ligand and receptor in the crypt evokes a classic lateral inhibition scenario for control of stem versus secretory fate (Figure 2). Stem cells towards the crypt base found preferentially adjacent to Delta-expressing Paneth cells, express Notch receptor [13• and 14], Selleckchem Daporinad and are maintained in an undifferentiated state by constant Notch signalling

and suppression of Atoh1 [7, 9, 15 and 16], As migrating cells lose contact with Paneth cells and the high Notch signalling they confer, they become poised between secretory and non-secretory fate. Lineage selection may then arise by stochastic variation in Delta expression leading some cells to express higher levels than others. This initial stochastic imbalance in Delta expression becomes reinforced allowing only a subset of cells (Delta high, Atoh high) rising up the crypt to become committed to a secretory fate while the rest become absorptive enterocytes. This regulation and functional organisation readily explains a binary fate in a supra-Paneth cell poised population but fits less well with a subsequent downstream cascade of secretory lineage choices specified after a series of cell divisions each progressing unidirectionally towards a more restricted fate. Moreover, recent evidence derived from regenerating systems casts doubt both on the existence of stable populations of

progenitors and the irreversibility of lineage specification. For many years it has also been known Idelalisib that intestinal regeneration following damage is not solely a function of surviving stem cells expanding to restore homeostasis (Figure 3) [17]. Following radiation induced injury the clonogenic fraction of crypt cells is elevated suggesting that these might correspond to the abundant and immature absorptive cells present within the early transit-amplifying compartment of the lower crypt. In support, specific ablation of the key Lgr5+ population using targeted diptheria toxin is not catastrophic as non-Lgr5+ cells (Bmi1+) cells are able to act as a replacement stem cell pool at least for a limited time [18].

Activated CD4+ T cells also travel to the site of infection and, via cytokine signals, activate tissue-resident macrophages to become fully active and to destroy phagocytosed antigen/pathogens. Antibodies can enhance the effector functions of innate cells, for example, by enhancing phagocytosis. Soluble antibodies at the site of challenge

can neutralise pathogens directly by binding to their surface. Cytotoxic T cells can directly kill infected tissue/cells via molecular and chemical signalling. These cells can also induce infected cells/phagocytes to kill intracellular pathogens, or can inhibit pathogen replication via chemical and molecular signals. On secondary exposure to the same antigen or pathogen, specific adaptive effectors with a memory phenotype can rapidly proliferate and produce a new wave of adaptive immunity ZD1839 chemical structure at the site of challenge. This pathway can occur independently of further innate immune events and is the basis of vaccination. The coordination of all these phases ensures that a call for help from the periphery is relayed to the regional secondary lymphoid tissues and that appropriate effectors are directed to the site of infection by a series of chemical and molecular signals. This cycle of an immune response forms http://www.selleckchem.com/products/SRT1720.html the basis for the principles of vaccination

(Figure 2.10) and is discussed further in the next section. The modern immunology concepts described in this chapter are of great importance both for the design Idoxuridine of new vaccines and to help us understand why vaccines do – or do not – work as efficiently as desired. Vaccines aim to prevent the disease symptoms that are the consequences of a pathogenic infection. In most cases, this does not occur by completely preventing infection but by limiting the consequences of the infection. As discussed earlier, an understanding of the disease pathogenesis and natural immune control is, therefore, very useful when selecting appropriate antigens

upon which to base a vaccine. Vaccines developed from pathogens can vary in the complexity of the pathogen-derived material they contain. Our understanding of fundamental immunology, as well as the selection techniques used, has resulted in new vaccines that are better characterised than ever before, and has also initiated a more rational approach to vaccine design. The different approaches to antigen selection are discussed in depth in Chapter 3 – Vaccine antigens. The immune system is triggered by a combination of events and stimuli, as described previously. The requirement for more than the presence of a ‘foreign’ antigen to elicit an immune response must therefore always be considered in vaccine design, particularly when using highly purified or refined antigens (see Chapter 3 – Vaccine antigens).

The test section of this tunnel is rectangular with a length of 2.6 m, a width of 0.6 m and a height find more of 0.6 m. The maximum flow speed is 12 m/s, and the pressure can vary from 10 to 200 kPa. A schematic diagram of the MOERI medium-sized tunnel is shown in Fig. 7. A wake screen composed of a brass wire mesh was made to reproduce the nominal wake flow measured

behind the model ship in the MOERI towing tank. The propeller configurations and the nominal wake distributions measured at the propeller plane inside the cavitation tunnel are shown in Fig. 8. The pressure fluctuation is measured on a flat plate above the model propeller. The flat plate is away from the model propeller tip, which corresponds to the vertical clearance RG7420 of the hull. Pressure transducers, model XTM-190-25A, were used to measure the pressure values. The computation and the five measured positions on the plate are shown in Fig. 9. Using the method recommended by ITTC (1987), the full-scale pressure fluctuation amplitudes can be predicted from the model scale measurement according to the following formula. equation(9) PS=PM×ρSρM(nSnM)2(DSDM)2fSfM=nSnMwhere ρρ is the density, nn is the rotational speed, and D is the diameter; suffix S represents the ship, and M represents the model.

The cavitation patterns of the model propellers are obtained for the selected blade′s angular position, and the corresponding numerical flow analysis results are shown in Fig. 10, Fig. 11 and Fig. 12. The angular positions of a key blade shown in these figures are measured from the vertically upward position in a clockwise direction when the propeller is viewed from behind. Fig. 13 shows the computed sheet cavitation volume variations. Fig. 14, Fig. 15 and Fig. 16 are the comparison results. The experimental result, the potential-based prediction results, and the results of the newly developed time domain prediction method are compared at positions ‘P’, ‘C’, and ‘S’. As shown Table 4 and Fig. 17, the maximum value of the pressure fluctuation is experimentally measured

and numerically predicted at a slightly starboard side of the propeller. There are two reasons. The first reason is that sheet cavitation volume is occurred analogously symmetric shape whose maximum volume is located slightly starboard side as shown in Fig. 13. The second reason is Succinyl-CoA the source movement. Because sources are moving from port side to starboard side, induced pressure fluctuation at the starboard side is higher than that of port side. The newly developed time domain prediction results show good agreement with the experimental results, and the developed method is qualitatively and quantitatively superior to the potential-based prediction method. A new time domain prediction method has been presented with the aim of computing the pressure fluctuation induced by a propeller sheet cavitation. Modern acoustic theory is applied to the source modeling of the pressure fluctuation.

Interaktionen zwischen Fe und Mn wurden bereits intensiv diskutiert, jedoch müssen weitere Metalle wie Cu, Zn oder Ca in die Überlegungen einbezogen werden. Es ist bekannt, dass ein komplexes Netzwerk existiert, in dem diese Elemente die biologische Funktion der jeweils anderen positiv oder negativ beeinflussen. Ungleichgewichte in Bezug auf Metallionen könnten zu der Schädigung der Neuronen beitragen, die primär durch eine Mn-Überexposition

verursacht wurde. Was diese Metalle betrifft, ist die Rolle des Transports über den Riechnerv ins Gehirn ebenfalls von großem Interesse und sollte weiter untersucht werden. Des Weiteren ist die Bestimmung von Mn-Spezies in verschiedenen menschlichen Körperflüssigkeiten this website wie Serum und Liquor eine leistungsfähige Methode im Rahmen eines Mn-Biomonitoring. Wenn die entsprechende Technik gut etabliert ist, handelt es sich im Vergleich zur MRT oder hochauflösenden

Massenspektrometrie um eine praktikable und sogar kostengünstige Methode. So kann mithilfe eines geeigneten Mn-Biomonitorings die Belastung des menschlichen Körpers durch hohe Mn-Konzentrationen frühzeitig nachgewiesen werden, was die Prävention des Manganismus oder des durch langfristige Mn-Exposition induzierten Parkinsonismus durch möglichst weitgehenden Schutz der Neuronen gegen Mn (wie für Silymarin diskutiert) erleichtert. Andererseits sollten Informationen über spezifische Mn-Spezies weiter dazu benutzt werden, Fragen zur Wechselbeziehung zwischen den Spezies und den molekularen Mechanismen der Mn-induzierten Toxizität in Neuronen zu klären: Gibt es Wechselbeziehungen oder PS-341 cell line sogar eine deutliche Korrelation zwischen bestimmten Mn-Spezies im Gehirn und Konzentrationsänderungen oder sonstigen Einflüssen auf Neurotransmitter oder die Aktivität der Acetylcholinesterase? Gibt es eine Korrelation zwischen einer bestimmten Mn-Spezies und Ungleichgewichten anderer Metallspezies, insbesondere Störungen des Fe(II)/Fe(III)-Gleichgewichts, Dichloromethane dehalogenase die zu oxidativem Stress führen könnten? Schließlich: Welche anderen Stoffwechselwege werden durch spezifische

Mn-Spezies beeinflusst? Vorläufige Experimente unseres Labors mittels ESI-FT-ICR-MS weisen darauf hin, dass im Gehirn eine enorme Zahl an Metaboliten und Stoffwechselwegen durch Mn beeinflusst wird und dass in der Zukunft Rückschlüsse auf den Zusammenhang mit bestimmten Mn-Spezies gezogen werden können. Bei keinem der Autoren besteht ein Interessenkonflikt. Dieser Review ist Teil der Serie von Übersichtsartikeln über Spurenelemente in dieser Zeitschrift, die von der Gesellschaft für Mineralstoffe und Spurenelemente e. V. initiiert wurde. “
“Nickel kommt zu etwa 0,01 % in der Erdkruste vor, hauptsächlich in Form von Sulfid-, Oxid- und Silikatmineralien [1]. Natürliche geologische Prozesse wie Verwitterung und Vulkanismus haben nur zu einem geringen Gehalt an Nickel in der natürlichen Umwelt geführt.