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Carbon Monoxide Rapidly Impairs Alveolar Fluid Clearance by Inhibiting Epithelial Sodium Channels
(2009)
Carbon monoxide (CO) is currently being evaluated as a therapeutic modality in the treatment of patients with acute lung injury and acute respiratory distress syndrome. No study has assessed the effects of CO on transepithelial ion transport and alveolar fluid reabsorption, two key aspects of alveolocapillary barrier function that are perturbed in acute lung injury/acute respiratory distress syndrome. Both CO gas (250 ppm) and CO donated by the CO donor, CO-releasing molecule (CORM)-3 (100 mu M in epithelial lining fluid), applied to healthy, isolated, ventilated, and perfused rabbit lungs, significantly blocked Na-22(+) clearance from the alveolar compartment, and blocked alveolar fluid reabsorption after fluid challenge. Apical application of two CO donors, CORM-3 or CORM-A1 (100 mu M), irreversibly inhibited amiloride-sensitive short-circuit currents in H441 human bronchiolar epithelial cells and primary rat alveolar type II cells by up to 40%. Using a nystatin permabilization approach, the CO effect was localized to amiloride-sensitive channels on the apical surface. This effect was abolished by hemoglobin, a scavenger of CO, and was not observed when inactive forms of CO donors were employed. The effects of CO were not blocked by 8-bromoguanosine-3',5'-cyclic guanosine monophosphate, soluble guanylate cyclase inhibitors (methylene blue and 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one), or inhibitors of trafficking events (phalloidin oleate, MG-132, and brefeldin A), but the amiloride affinity of H441 cells was reduced after CO exposure. These data indicate that CO rapidly inhibits sodium absorption across the airway epithelium by cyclic guanosine monophosphate-and trafficking-independent mechanisms, which may rely on critical histidine residues in amiloride-sensitive channels or associated regulatory proteins on the apical surface of lung epithelial cells.
Mechanical properties and microstructure of heavy aluminum bonding wires for power applications
(2009)
The invention relates to compounds that include peptide and peptidomimetics that inhibit estrogen receptor dependent cell proliferation. The compounds of the invention are useful for treating cell proliferative disorders or physiological conditions characterized by undesirable or unwanted estrogen induced cell proliferation, including breast cancer.
Kompendium Q-M-A
(2009)
The nutrient element calcium
(2009)
Trust and Social Capital: Revisiting an Offshoring Failure Story of a Small German Software Company
(2009)
We have designed an inexpensive intelligent pedestrian counting system. The pedestrian counting system consists of several counters that can be connected together in a distributed fashion and communicate over the wireless channel. The motion pattern is recorded using a set of passive infrared (PIR) sensors. Each counter has one wireless sensor node that processes the PIR sensor data and transmits it to a base station. Then echo state network, a special kind of recurrent neural network, is used to predict the pedestrian count from the input pattern. The evaluation of the performance of such networks in a novel kind of application is one focus of this work. The counter gave a performance of 80.4% which is better than the commercially available low-priced pedestrian counters. The article reports the experiments we did for analyzing the counterperformance and lists the strengths and limitations of the current implementation. It will also report the preliminary test results obtained by substituting the PIR sensors with low-cost active IR distance sensors which can improve the counter performance further.
3D-Imaging
(2009)
Physiology and behavior have historically been treated as separate subjects in the study of Drosophila. The latter is mentioned mainly in the context of neurobiology, while the former has been considered to take in studies of metabolism, cell biology and anatomy, among others. Of late, the line distinguishing physiology and behavior has become thinner, and this is exceptionally apparent in recent studies of nutrient signaling and of the regulation of feeding. This review represents a brief examination of the nexus between these intersecting fields of research in Drosophila. Other recently published reviews serve as complements to this one.
In den vergangenen zehn Jahren haben sich die Suchmaschinen und insbesondere Google zu einem unverzichtbaren Bestandteil des Internets entwickelt. Parallel dazu hat die Anzahl von kommerziellen Websites zugenommen. Suchmaschinenmarketing bietet Unternehmen die Möglichkeit, Kunden nahezu ohne Streuverluste anzusprechen und somit Absatzziele optimal zu realisieren.
Dihydropyrimidine dehydrogenase (DPD) deficiency is an infrequently described autosomal recessive disorder of the pyrimidine degradation pathway and can lead to mental and motor retardation and convulsions. DPD deficiency is also known to cause a potentially lethal toxicity following administration of the antineoplastic agent 5-fluorouracil. In an ongoing study of 72 DPD deficient patients, we analysed the molecular background of 5 patients in more detail in whom initial sequence analysis did not reveal pathogenic mutations. In three patients, a 13.8 kb deletion of exon 12 was found and in one patient a 122 kb deletion of exon 14–16 of DPYD. In the fifth patient, a c.299_302delTCAT mutation in exon 4 was found and also loss of heterozygosity of the entire DPD gene. Further analysis demonstrated a de novo deletion of approximately 14 Mb of chromosome 1p13.3–1p21.3, which includes DPYD. Haploinsufficiency of NTNG1, LPPR4, GPSM2, COL11A1 and VAV3 might have contributed to the severe psychomotor retardation and unusual craniofacial features in this patient. Our study showed for the first time the presence of genomic deletions affecting DPYD in 7% (5/72) of all DPD deficient patients. Therefore, screening of DPD deficient patients for genomic deletions should be considered.
Mitochondrial neurogastrointestinal encephalomyopathy is an autosomal recessive disorder in which a nuclear mutation of the thymidine phosphorylase gene leads to mitochondrial genomic dysfunction. Herein, we report a 29-year-old Iranian man with abdominal pain, diarrhea, hearing loss, ophthalmoplegia, sensorimotor axonal neuropathy, and elevated muscle enzymes. Magnetic resonance imaging showed leukoencephalopathic changes. Metabolite analysis revealed a very high thymidine concentration in the patient's urine consistent with the diagnosis of mitochondrial neurogastrointestinal encephalomyopathy.
Several publications suggest a potential association between the administration of Gadolinium-based contrast agents (GBCAs) and the onset of a rare but serious disease, Nephrogenic Systemic Fibrosis (NSF). The aim of this study was to determine the elimination time-course of Gadolinium (Gd) from skin tissue after application of GBCAs in rats. Seven different marketed GBCAs were injected on five consecutive days at a dose of 2.5 mmol/kg bodyweight into the tail vein of Han-Wistar rats and the Gd concentrations were determined by Inductively Coupled Plasma Mass Spectrometry (ICP-MS) in skin biopsies taken at various time-points up to a year after the last injection. Most of the administered Gd was eliminated from the skin within a time-period of about 2 months. However, the repeated administration of linear GBCAs resulted in long-term retention of a small portion of the administered Gd in the skin tissue of rats, with substantially higher values observed in animals treated with non-ionic linear agents than in those that received ionic linear GBCAs. Following treatment with macrocyclic GBCAs, Gd values in the skin were in the same range as observed in the controls from day 24 post-injection onwards. In summary, we observed a correlation between the complex stability of GBCAs and the amount of residual Gd in the skin up to a year after application of GBCAs.
The Olig3 gene encodes a bHLH factor that is expressed in the ventricular zone of the dorsal alar plate of the hindbrain. We found that the Olig3(+) progenitor domain encompassed subdomains that co-expressed Math1, Ngn1, Mash1 and Ptf1a. Olig3(+) cells give rise to neuronal types in the dorsal alar plate that we denote as class A neurons. We used genetic lineage tracing to demonstrate that class A neurons contribute to the nucleus of the solitary tract and to precerebellar nuclei. The fate of class A neurons was not correctly determined in Olig3 mutant mice. As a consequence, the nucleus of the solitary tract did not form, and precerebellar nuclei, such as the inferior olivary nucleus, were absent or small. At the expense of class A neurons, ectopic Lbx1(+) neurons appeared in the alar plate in Olig3 mutant mice. By contrast, electroporation of an Olig3 expression vector in the chick hindbrain suppressed the emergence of Lbx1(+) neurons. Climbing fiber neurons of the inferior olivary nucleus express Foxd3 and require Olig3 as well as Ptf1a for the determination of their fate. We observed that electroporation of Olig3 and Ptf1a expression vectors, but not either alone, induced Foxd3. We therefore propose that Olig3 can cooperate with Ptf1a to determine the fate of climbing fiber neurons of the inferior olivary nucleus.
BACKGROUND
Neuronal migration is a crucial process that allows neurons to reach their correct target location to allow the nervous system to function properly. AP-2alpha is a transcription factor essential for neural crest cell migration and its mutation results in apoptosis within this cell population, as demonstrated by genetic models.
RESULTS
We down-modulated AP-2alpha expression in GN-11 neurons by RNA interference and observe reduced neuron migration following the activation of a specific genetic programme including the Adhesion Related Kinase (Axl) gene. We prove that Axl is able to coordinate migration per se and by ChIP and promoter analysis we observe that its transcription is directly driven by AP-2alpha via the binding to one or more functional AP-2alpha binding sites present in its regulatory region. Analysis of migration in AP-2alpha null mouse embryo fibroblasts also reveals an essential role for AP-2alpha in cell movement via the activation of a distinct genetic programme.
CONCLUSION
We show that AP-2alpha plays an essential role in cell movement via the activation of cell-specific genetic programmes. Moreover, we demonstrate that the AP-2alpha regulated gene Axl is an essential player in GN-11 neuron migration.
Background: Migration of mature and immature leukocytes in response to chemokines is not only essential during inflammation and host defense, but also during development of the hematopoietic system. Many molecules implicated in migratory polarity show uniform cellular distribution under non-activated conditions, but acquire a polarized localization upon exposure to migratory cues.
Methodology/Principal Findings: Here, we present evidence that raft-associated endocytic proteins (flotillins) are preassembled in lymphoid, myeloid and primitive hematopoietic cells and accumulate in the uropod during migration. Furthermore, flotillins display a polarized distribution during immunological synapse formation. Employing the membrane lipid-order sensitive probe Laurdan, we show that flotillin accumulation in the immunological synapse is concomittant with membrane ordering in these regions.
Conclusions: Together with the observation that flotillin polarization does not occur in other polarized cell types such as polarized epithelial cells, our results suggest a specific role for flotillins in hematopoietic cell polarization. Based on our results, we propose that in hematopoietic cells, flotillins provide intrinsic cues that govern segregation of certain microdomain-associated molecules during immune cell polarization.
Quereinsteiger und Neulinge der Vermittlung von Informationskompetenz werden grundlegend auf der Basis der vielfältigen praktischen Erfahrungen des Multiplikatorennetzwerks der AG Informationskompetenz NRW über strategische Konzepte, unterschiedliche Schulungsangebote für verschiedene Zielgruppen, Methodik und Didaktik von Schulungsveranstaltungen, Organisation und Infrastruktur sowie Evaluation und Qualitätsmanagement informiert.
Die traditionelle Managementtheorie fußt auf der Annahme, dass ein Unternehmen das Ergebnis bewusster, zweckrationaler Planung und Gestaltung ist und dass die Handlungen innerhalb der Strukturen eines Unternehmens ebenfalls zweckrational geleitet sind – oder dass sie dies zumindest sein sollten. Die meisten Modelle, die aus diesem traditionellen Grundverständnis hervorgegangen sind, folgen einer idealtypischen präskriptiven Grundlogik: Um ein Unternehmen erfolgreich in die Zukunft zu führen, beginnt man mit der Definition der unternehmerischen Ziele, analysiert das Unternehmen und seine Umwelt, entwirft und bewertet strategische Optionen, wählt eine dieser Optionen zur Umsetzung aus, strukturiert mit Hilfe von Maßnahmenplänen, Budgets und Zeitplänen den Umsetzungsprozess, kontrolliert den Fortschritt und die erzielten Ergebnisse und greift bei negativen Abweichungen vom angestrebten Soll gegebenenfalls korrigierend ein. Strategien sind in diesem Verständnis das explizit formulierbare Resultat eines aktiven, zielgerichteten, bewussten und rationalen Denkvorganges. Die Verantwortung für ihre Formulierung liegt in den Händen des Topmanagements. Es fällt die entsprechenden Entscheidungen und kontrolliert ihre Implementierung.