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Search Results: 1 - 10 of 303 matches for " Bodo Schniewind "
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Combination phenylbutyrate/gemcitabine therapy effectively inhibits in vitro and in vivo growth of NSCLC by intrinsic apoptotic pathways
Schniewind Bodo,Heintz Kirsten,Kurdow Roland,Ammerpohl Ole
Journal of Carcinogenesis , 2006, DOI: 10.1186/1477-3163-5-25
Abstract: Background Standard chemotherapy protocols in NSCLC are of limited clinical benefit. Histone deacetylase (HDAC) inhibitors represent a new strategy in human cancer therapy. In this study the combination of the HDAC inhibitor phenylbutyrate (PB) and the nucleoside analogue gemcitabine (GEM) was evaluated and the mechanisms underlying increased cell death were analyzed. Methods Dose escalation studies evaluating the cytotoxicity of PB (0.01–100 mM), GEM (0.01–100 μg/ml) and a combination of the two were performed on two NSCLC cell lines (BEN and KNS62). Apoptotic cell death was quantified. The involvement of caspase-dependent cell death and MAP-kinase activation was analyzed. Additionally, mitochondrial damage was determined. In an orthotopic animal model the combined effect of PB and GEM on therapy was analyzed. Results Applied as a single drug both GEM and PB revealed limited potential to induce apoptosis in KNS62 and Ben cells. Combination therapy was 50–80% (p = 0.012) more effective than either agent alone. On the caspase level, combination therapy significantly increased cleavage of the pro-forms compared to single chemotherapy. The broad spectrum caspase-inhibitor zVAD was able to inhibit caspase cleavage completely, but reduced the frequency of apoptotic cells only by 30%. Combination therapy significantly increased changes in MTP and the release of cyto-c, AIF and Smac/Diabolo into the cytoplasm. Furthermore, the inhibitors of apoptosis c-IAP1 and c-IAP2 were downregulated and it was shown that in combination therapy JNK activation contributed significantly to induction of apoptosis. The size of the primary tumors growing orthotopically in SCID mice treated for 4 weeks with GEM and PB was significantly reduced (2.2–2.7 fold) compared to GEM therapy alone. The Ki-67 (KNS62: p = 0.015; Ben: p = 0.093) and topoisomerase IIα (KNS62: p = 0.008; Ben: p = 0.064) proliferation indices were clearly reduced in tumors treated by combination therapy, whereas the apoptotic index was comparably low in all groups. Conclusion Therapy combining GEM and the HDAC inhibitor PB initiates a spectrum of apoptosis-inducing mitochondrial and further JNK-dependent events, thereby overcoming the therapeutic resistance of NSCLC tumor cells. In vivo, the combination therapy substantially reduced tumor cell proliferation, suggesting that the well tolerated PB is a useful supplemental therapeutic agent in NSCLC.
A new technique for bedside placement of enteral feeding tubes: a prospective cohort study
Günther Zick, Alexander Frerichs, Markus Ahrens, Bodo Schniewind, Gunnar Elke, Dirk Sch?dler, Inéz Frerichs, Markus Steinfath, Norbert Weiler
Critical Care , 2011, DOI: 10.1186/cc9407
Abstract: This was a prospective cohort study in 27 critically ill patients subjected to transnasal endoscopy and intubation of the pylorus. Attending intensive care physicians were trained in the handling of the new endoscope for transnasal gastroenteroscopy for two days. A jejunal feeding tube was advanced via the instrument channel and the correct position assessed by contrast radiography. The primary outcome measure was successful postpyloric placement of the tube. Secondary outcome measures were time needed for the placement, complications such as bleeding and formation of loops, and the score of the placement difficulty graded from 1 (easy) to 4 (difficult). Data are given as mean values and standard deviation.Out of 34 attempted jejunal tube placements, 28 tubes (82%) were placed correctly in the jejunum. The duration of the procedure was 28 ± 12 minutes. The difficulty of the tube placement was judged as follows: grade 1: 17 patients, grade 2: 8 patients, grade 3: 7 patients, grade 4: 2 patients. In three cases, the tube position was incorrect, and in another three cases, the procedure had to be aborted. In one patient bleeding occurred that required no further treatment.Fast and reliable transnasal insertion of postpyloric feeding tubes can be accomplished by trained intensive care physicians at the bedside using the presented procedure. This new technique may facilitate early initiation of enteral feeding in intensive care patients.Feeding the critically ill patient should be preferentially accomplished via the enteral route [1,2]. A recent meta-analysis revealed that mortality and the incidence of pneumonia were significantly reduced in patients with enteral nutrition within 24 hours [3]. Parenteral nutrition may be associated with higher mortality [4].Intolerance of gastric feeding and high gastric volumes are the main obstacles for enteral nutrition [5]. If intragastric feeding fails despite prokinetic therapy with erythromycin and metoclopramide it is recommende
Applied Mathematical Theory for Monetary-Fiscal Interaction in a Supranational Monetary Union  [PDF]
Bodo Herzog
Journal of Applied Mathematics and Physics (JAMP) , 2014, DOI: 10.4236/jamp.2014.28081
Abstract:

I utilize a differentiable dynamical system á la Lotka-Voletrra and explain monetary and fiscal interaction in a supranational monetary union. The paper demonstrates an applied mathematical approach that provides useful insights about the interaction mechanisms in theoretical economics in general and a monetary union in particular. I find that a common central bank is necessary but not sufficient to tackle the new interaction problems in a supranational monetary union, such as the free-riding behaviour of fiscal policies. Moreover, I show that supranational institutions, rules or laws are essential to mitigate violations of decentralized fiscal policies.

An Econophysics Model of Financial Bubbles  [PDF]
Bodo Herzog
Natural Science (NS) , 2015, DOI: 10.4236/ns.2015.71006
Abstract: Usually financial crises go along with bubbles in asset prices, such as the housing bubble in the US in 2007. This paper attempts to build a mathematical model of financial bubbles from an econophysics, and thus a new perspective. I find that agents identify bubbles only with a time delay. Furthermore, I demonstrate that the detection of bubbles is different on either the individual or collective point of view. Second, I utilize the findings for a new definition of asset bubbles in finance. Finally, I extend the model to the study of asset price dynamics with news. In conclusion, the model provides unique insights into the properties and developments of financial bubbles.
Quantum Model of Decision-Making in Economics  [PDF]
Bodo Herzog
Journal of Quantum Information Science (JQIS) , 2015, DOI: 10.4236/jqis.2015.51001
Abstract: The paper designs a quantum model of decision-making (QMDM) that utilizes neuroscientific evidence. The new model provides both normative and positive implications to economics. First, it enhances the study of decision-making which is an extension of the expected utility theory (EUT) in mathematical economics. Second, we demonstrate how the quantum model mitigates drawbacks of the expected utility theory of today.
Liquidity Management at the Zero Lower Bound and an Era of Activism in Central Banking  [PDF]
Bodo Herzog
Journal of Mathematical Finance (JMF) , 2016, DOI: 10.4236/jmf.2016.61006
Abstract:

The paper studies liquidity management in the banking sector at the zero lower bound implemented by central banks. The new era of monetary policy with interest rates at zero and quantitative easing programs raise questions about the effectiveness of central banking policy and their impact on the banking sector. I find that the zero lower bound reduces liquidity reserves of banks and thus creates less credit supply. The T-LTRO program, developed by the European Central Bank, has helped to tackle this problem. However, the recently expanded asset purchase program reveals the opposite effect. Hence, the recent liquidity provisions by central banks have put incentives rather on de-leveraging than bank lending.

Pathophysiology of Hypertrophic Pyloric Stenosis Revisited: The Use of Isotonic Fluid for Preoperative Infusion Therapy Is Supported  [PDF]
Ralf-Bodo Troebs
Open Journal of Pediatrics (OJPed) , 2014, DOI: 10.4236/ojped.2014.43027
Abstract: Background: The aim of this study was to elucidate the preoperative clinical and biochemical profile of infants with IHPS to optimize infusion therapy. Patients and Method: We retrospectively analyzed data from 56 infants who were operated for IHPS. Our study includes growth and laboratory data prior to the initiation of therapy. Results: Median duration of propulsive vomiting was 4 d; the median age was 37 d (18 - 108), and the median body weight was 3840 g (2760 -5900). Metabolic alkalosis (MAlk) with a pH of 7.45 ± 0.06 and an stHCO3- of 28.7 ± 4.5 mmol/l was found. In a subgroup of the infants, negative base excess (BE) was observed. The sodium concentration was normal or reduced (mean/median of 137 mmol/l). There was a strong negative correlation between stHCO3- and K+. The carbon dioxide partial pressure tended to increase (5.72 ± 0.84 kPa). Calculations of osmolality revealed a normal osmolarity. Hypoglycemia did not occur. The creatinine clearance according to the Schwartz formula remained at a normal level (85.3 ± 24.3 ml/min/1.73 m2). Discussion: The presented case series is characterized by a short duration of preoperative vomiting. MAlk can be classified as a chloride deficiency syndrome. It is accompanied by normo- or hyponatremic dehydration with normal osmolality. Partial respiratory compensation occurred. A normal creatinine clearance indicated good glomerular renal function. Conclusion: The presented study supports the use of an isotonic infusion fluid with a low glucose concentration for preoperative infusion therapy.
Metabolic Signature of Electrosurgical Liver Dissection
Witigo von Sch?nfels, Oliver von Kampen, Eleonora Patsenker, Felix Stickel, Bodo Schniewind, Sebastian Hinz, Markus Ahrens, Katharina Balschun, Jan-Hendrik Egberts, Klaus Richter, Andreas Landrock, Bence Sipos, Olga Will, Patrizia Huebbe, Stefan Schreiber, Michael Nothnagel, Christoph R?cken, Gerald Rimbach, Thomas Becker, Jochen Hampe, Clemens Schafmayer
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0072022
Abstract: Background and Aims High frequency electrosurgery has a key role in the broadening application of liver surgery. Its molecular signature, i.e. the metabolites evolving from electrocauterization which may inhibit hepatic wound healing, have not been systematically studied. Methods Human liver samples were thus obtained during surgery before and after electrosurgical dissection and subjected to a two-stage metabolomic screening experiment (discovery sample: N = 18, replication sample: N = 20) using gas chromatography/mass spectrometry. Results In a set of 208 chemically defined metabolites, electrosurgical dissection lead to a distinct metabolic signature resulting in a separation in the first two dimensions of a principal components analysis. Six metabolites including glycolic acid, azelaic acid, 2-n-pentylfuran, dihydroactinidiolide, 2-butenal and n-pentanal were consistently increased after electrosurgery meeting the discovery (p<2.0×10?4) and the replication thresholds (p<3.5×10?3). Azelaic acid, a lipid peroxidation product from the fragmentation of abundant sn-2 linoleoyl residues, was most abundant and increased 8.1-fold after electrosurgical liver dissection (preplication = 1.6×10?4). The corresponding phospholipid hexadecyl azelaoyl glycerophosphocholine inhibited wound healing and tissue remodelling in scratch- and proliferation assays of hepatic stellate cells and cholangiocytes, and caused apoptosis dose-dependently in vitro, which may explain in part the tissue damage due to electrosurgery. Conclusion Hepatic electrosurgery generates a metabolic signature with characteristic lipid peroxidation products. Among these, azelaic acid shows a dose-dependent toxicity in liver cells and inhibits wound healing. These observations potentially pave the way for pharmacological intervention prior liver surgery to modify the metabolic response and prevent postoperative complications.
Surface Area and Curvature of the general Ellipsoid
Daniel Poelaert,Joachim Schniewind,Frank Janssens
Mathematics , 2011,
Abstract: This paper gives a detailed derivation of the surface of a tri-axial ellipsoid. The general result is in terms of the elliptic integrals of the first and second kind. It is in checked for all special cases included and the corresponding simplified formulae are given. Next, expressions for the mean and Gaussian curvature are derived. These curvatures depend only on: a) the three axes, and from the point under consideration, b) its distance to the centre and c) the length of the perpendicular from centre to the tangent plane of that point. Finally, it is noticed that at the four umbilic points of an ellipsoid, where the cicular sections degenerate to a point, the two principal curvatures are equal and have the simple expression (a c / b^3)where a>b>c are the half-axes.
Duodenal Atresia-Tandler’s “Epithelial Plug Stage” Revisited  [PDF]
Ralf-Bodo Tr?bs
Open Journal of Pediatrics (OJPed) , 2019, DOI: 10.4236/ojped.2019.91010
Abstract: Background: Duodenal atresia is the most common type of intestinal atresia. Pathogenesis of duodenal atresia can be explained by an embryological theory that involves persistent physiologic epithelial occlusion (“epithelial plug”), first published in 1900. Tandlers developmental arrest theory has been accepted by the majority of recognized modern textbooks to date. The aim of the presented study is to re-evaluate the relevance of Tandler’s observations. Method: Tandler’s paper was reviewed retrospectively and discussed from the point of view of subsequent research. Results and Discussion: Local epithelial proliferation, vacuolization failure and mesenchyme ingrowth may continuously serve as a partly convincing but incomplete embryologic model to explain membranous duodenal atresia. Tandler’s theory has some weak points regarding the epithelial-mesenchymal interaction, the predisposition of the post-ampullary region, the association of duodenal atresia with other malformations and trisomy 21, and familial occurrence. Shrinkage artifacts, misinterpretation of a three-dimensional problem investigated with a two-dimensional tool (light microscope), animal studies, and the lack of apoptosis call the real existence of a solid stage in early duodenal embryology into question. Conclusion: More sophisticated morphologic, genetic and molecular-biological investigations revealed new insights regarding endoderm to mesoderm signaling as an important key to the pathogenesis of duodenal atresia.
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