Bibliografie tematiche / APC MIN

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Letteratura scientifica selezionata sul tema "APC MIN"

Autore: Grafiati
Pubblicato: 10 dicembre 2022
Ultima modifica: 29 gennaio 2023

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Articoli di riviste sul tema "APC MIN"

1

Bhandaru, Madhuri, Daniela S. Kempe, Anand Rotte, Rexhep Rexhepaj, Dietmar Kuhl e Florian Lang. "Hyperaldosteronism, hypervolemia, and increased blood pressure in mice expressing defective APC". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 297, n. 3 (settembre 2009): R571—R575. http://dx.doi.org/10.1152/ajpregu.00070.2009.

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Abstract (sommario):
Adenomatous polyposis coli (APC) fosters degradation of β-catenin, a multifunctional protein upregulating the serum- and glucocorticoid-inducible kinase (SGK1). SGK1 regulates a wide variety of renal transport processes. The present study explored the possibility that APC influences renal function. To this end, metabolic cage experiments were performed in mice carrying a loss-of-function mutation in the APC gene ( apc Min/+), their wild-type littermates ( apc+/+), and apc Min/+ mice lacking functional SGK1 ( apc Min/+ /sgk1−/−). As a result, mean body weight, food intake, fluid intake, salt appetite, urinary flow, as well as plasma Na+ and K+ concentrations were similar in apc Min/+ mice, apc+/+ mice, and apc Min/+ /sgk1−/− mice. Glomerular filtration rate and absolute renal Na+ excretion were decreased, and fractional urinary K+ excretion was enhanced in apc Min/+ mice. The antinatriuresis, but not the hypofiltration and kaliuresis was partially reversed by additional lack of SGK1. Plasma corticosterone and aldosterone concentrations were significantly enhanced in apc Min/+ mice. While the plasma corticosterone concentration was similar in apc+/+ mice and apc Min/+ /sgk1−/− mice, plasma aldosterone was even higher in apc Min/+ /sgk1−/− mice than in apc Min/+ mice. The hyperaldosteronism of apc Min/+ mice was paralleled by significantly elevated plasma volume and blood pressure. The experiments reveal an influence of defective APC on adrenal hormone release and renal function, effects partially but not completely explained by APC dependence of SGK1 expression.
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2

Swietlicki, Elzbieta A., Shashi Bala, Jianyun Lu, Anisa Shaker, Gowri Kularatna, Marc S. Levin e Deborah C. Rubin. "Epimorphin deletion inhibits polyposis in the Apcmin/+ mouse model of colon carcinogenesis via decreased myofibroblast HGF secretion". American Journal of Physiology-Gastrointestinal and Liver Physiology 305, n. 8 (15 ottobre 2013): G564—G572. http://dx.doi.org/10.1152/ajpgi.00486.2012.

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Abstract (sommario):
Interactions between the epithelium and surrounding mesenchyme/stroma play an important role in normal gut morphogenesis, the epithelial response to injury, and epithelial carcinogenesis. The tumor microenvironment, composed of stromal cells including myofibroblasts and immune cells, regulates tumor growth and the cancer stem cell niche. Deletion of epimorphin (Epim), a syntaxin family member expressed in myofibroblasts and macrophages, results in partial protection from colitis and from inflammation-induced colon cancer in mice. We sought to determine whether epimorphin deletion protects from polyposis in the Apc min/+ mouse model of intestinal carcinogenesis. Epim− /− mice were crossed to Apc min/+ mice; Apc min/+ and Apc min/+ /Epim− /− mice were killed at 3 mo of age. Polyp numbers and sizes were quantified in small intestine and colon, and gene expression analyses for pathways relevant to epithelial carcinogenesis were performed. Primary myofibroblast cultures were isolated, and expression and secretion of selected growth factors from Apc min/+ and Apc min/+ /Epim− /− myofibroblasts were examined by ELISA. Small bowel polyposis was significantly inhibited in Apc min/+ /Epim− /− compared with Apc min/+ mice. Apc min/+ /Epim− /− compared with Apc min/+ polyps and adjacent uninvolved intestinal mucosa had increased transforming growth factor-β (TGF-β) expression and signaling with increased P-Smad2/3 expression. Myofibroblasts isolated from Apc min/+ /Epim− /− vs. Apc min/+ mice had markedly decreased hepatocyte growth factor (HGF) expression and secretion. We concluded that Epim deletion inhibits polyposis in Apc min/+ mice, associated with increased mucosal TGF-β signaling and decreased myofibroblast HGF expression and secretion. Our data suggest that Epim deletion reduces tumorigenicity of the stromal microenvironment.
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3

Lin, Songbai, Sei-Jung Lee, Hyunsuk Shim, Jerold Chun e C. Chris Yun. "The absence of LPA receptor 2 reduces the tumorigenesis by ApcMin mutation in the intestine". American Journal of Physiology-Gastrointestinal and Liver Physiology 299, n. 5 (novembre 2010): G1128—G1138. http://dx.doi.org/10.1152/ajpgi.00321.2010.

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Abstract (sommario):
Lysophosphatidic acid (LPA) is a lipid mediator that mediates several effects that promote cancer progress. The LPA receptor type 2 (LPA2) expression is often elevated in several types of cancers, including colorectal cancer (CRC). In this study, we investigated the role of LPA2 in the development of intestinal adenomas by comparing Apc Min/+ mice with Apc Min/+ /Lpar2 −/− mice. There were 50% fewer intestinal adenomas in Apc Min/+ /Lpar2 −/− mice than Apc Min/+ mice. Smaller-size adenomas (<1 mm) were found at higher frequencies in Apc Min/+ /Lpar2 −/− mice compared with Apc Min/+ mice at the two age groups examined. The expression level of LPA2 correlated with increased size of intestinal adenomas. Reduced tumor multiplicity and size in Apc Min/+ /Lpar2 −/− mice correlated with decreased proliferation of intestinal epithelial cells. Apc Min/+ /Lpar2 −/− mice showed an increased level of apoptosis, suggesting that LPA2-mediated signaling stimulates intestinal tumor development and progress by regulating both cell proliferation and survival. In addition, the expression levels of Krüpple-like factor 5 (KLF5), β-catenin, cyclin D1, c-Myc, and hypoxia-inducible factor-1α (HIF-1α) were significantly altered in Apc Min/+ /Lpar2 −/− mice compared with Apc Min/+ mice. In vitro studies using HCT116 cells showed that LPA induced cyclin D1, c-Myc, and HIF-1α expression, which was attenuated by knockdown of LPA2. In summary, intestinal tumor initiated by Apc mutations is altered by LPA2-mediated signaling, which regulates tumor growth and survival by altering multiple targets.
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Hutson, Anne M., Christina A. Sam, Yuko Mori-Akiyama e Preethi H. Gunaratne. "MicroRNAs Dysregulation in APC(MIN/+) Mouse Adenomas". Gastroenterology 140, n. 5 (maggio 2011): S—191. http://dx.doi.org/10.1016/s0016-5085(11)60771-3.

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5

Kevin, Leo G., Peter Katz, Amadou K. S. Camara, Enis Novalija, Matthias L. Riess e David F. Stowe. "Anesthetic Preconditioning". Anesthesiology 99, n. 2 (1 agosto 2003): 385–91. http://dx.doi.org/10.1097/00000542-200308000-00020.

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Abstract (sommario):
Background Anesthetic preconditioning (APC) is protective for several aspects of cardiac function and structure, including left ventricular pressure, coronary flow, and infarction. APC may be protective, however, only if the duration of ischemia is within a certain, as yet undefined range. Brief ischemia causes minimal injury, and APC would be expected to provide little benefit. Conversely, very prolonged ischemia would ultimately cause serious injury with or without APC. Previous investigations used a constant ischemic time as the independent variable to assess ischemia-induced changes in dependent functional and structural variables. The purpose of the study was to define the critical limits of efficacy of APC by varying ischemic time. Methods Guinea pig hearts (Langendorff preparation; n = 96) underwent pretreatment with sevoflurane (APC) or no treatment (control), before global ischemia and 120 min reperfusion. Ischemia durations were 20, 25, 30, 35, 40, and 45 min. Results At 120 min reperfusion, developed (systolic-diastolic) left ventricular pressure was increased by APC compared with control for ischemia durations of 25-40 min. Infarction was decreased by APC for ischemia durations of 25-40 min, but not 20 or 45 min. APC improved coronary flow and vasodilator responses for all ischemia durations longer than 25 min, and decreased ventricular fibrillation on reperfusion for ischemia durations longer than 30 min. Conclusions Although APC protects against vascular dysfunction and dysrhythmias after prolonged ischemia, protection against contractile dysfunction and infarction in this model is restricted to a range of ischemia durations of 25-40 min. These results suggest that APC may be effective in a subset of patients who have cardiac ischemia of intermediate duration.
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6

McCully, James D., Yoshiya Toyoda, Masahisa Uematsu, Robert D. Stewart e Sidney Levitsky. "Adenosine-enhanced ischemic preconditioning: adenosine receptor involvement during ischemia and reperfusion". American Journal of Physiology-Heart and Circulatory Physiology 280, n. 2 (1 febbraio 2001): H591—H602. http://dx.doi.org/10.1152/ajpheart.2001.280.2.h591.

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Abstract (sommario):
Adenosine-enhanced ischemic preconditioning (APC) extends the cardioprotection of ischemic preconditioning (IPC) by both significantly decreasing myocardial infarct size and significantly enhancing postischemic functional recovery. In this study, the role of adenosine receptors during ischemia-reperfusion was determined. Rabbit hearts ( n = 92) were used for Langendorff perfusion. Control hearts were perfused for 180 min, global ischemia hearts received 30-min ischemia and 120-min reperfusion, and IPC hearts received 5-min ischemia and 5-min reperfusion before ischemia. APC hearts received a bolus injection of adenosine coincident with IPC. Adenosine receptor (A1, A2, and A3) antagonists were used with APC before ischemia and/or during reperfusion. GR-69019X (A1/A3) and MRS-1191/MRS-1220 (A3) significantly increased infarct size in APC hearts when administered before ischemia and significantly decreased functional recovery when administered during both ischemia and reperfusion ( P < 0.05 vs. APC). DPCPX (A1) administered either before ischemia and/or during reperfusion had no effect on APC cardioprotection. APC-enhanced infarct size reduction is modulated by adenosine receptors primarily during ischemia, whereas APC-enhanced postischemic functional recovery is modulated by adenosine receptors during both ischemia and reperfusion.
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7

Novalija, Enis, Leo G. Kevin, Janis T. Eells, Michele M. Henry e David F. Stowe. "Anesthetic Preconditioning Improves Adenosine Triphosphate Synthesis and Reduces Reactive Oxygen Species Formation in Mitochondria after Ischemia by a Redox Dependent Mechanism". Anesthesiology 98, n. 5 (1 maggio 2003): 1155–63. http://dx.doi.org/10.1097/00000542-200305000-00018.

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Background Mitochondrial changes that characterize the heart after anesthetic preconditioning (APC) or the mechanisms by which mitochondrial triggering factors lead to protection are unknown. This study hypothesized that generation of reactive oxygen species (ROS) during APC is required to initiate the mitochondrial protective effects, and that APC leads to improved mitochondrial electron transport chain function and cardiac function during reperfusion. Methods Isolated guinea pig hearts were subject to 30 min ischemia and 120 min reperfusion. Prior to ischemia hearts were either untreated (I/R), or treated with sevoflurane (APC), in the presence or absence of the ROS scavenger tiron (TIR), or the superoxide dismutase mimetic MnTBAP (TBAP). Intracellular ROS were measured by spectrofluorometry using the fluorescent probe dihydroethidium (DHE). In another series of experiments, using the same protocol, hearts were reperfused for only 5 min and removed for measurement of adenosine triphosphate (ATP) synthesis by luciferin-luciferase luminometry and ROS generation by dichlorohydro-fluorescein (DCF) fluorescence in isolated mitochondria. Results The APC improved cardiac function and reduced infarction. Tiron or MnTBAP abrogated the protection afforded by APC. Mitochondrial ATP synthesis was decreased by 70 +/- 3% after IR alone, by only 7 +/- 3% after APC, by 69 +/- 2% after APC+TIR, and by 71 +/- 3% after APC + TBAP. Mitochondrial ROS formation (DCF) increased by 48 +/- 3% after IR alone, by 0 +/- 2% after APC, by 43 +/- 4% after APC + TIR, and by 46 +/- 3% after APC + TBAP. ROS generation (DHE) was increased in I/R group at 5 and 120 min reperfusion. This was attenuated by APC but this protective effect was abrogated in APC + TIR and APC + TBAP groups. Conclusions The results indicate that ROS are central both in triggering and mediating APC, and that the mitochondrion is the target for these changes.
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Riess, Matthias L., Amadou K. S. Camara, Qun Chen, Enis Novalija, Samhita S. Rhodes e David F. Stowe. "Altered NADH and improved function by anesthetic and ischemic preconditioning in guinea pig intact hearts". American Journal of Physiology-Heart and Circulatory Physiology 283, n. 1 (1 luglio 2002): H53—H60. http://dx.doi.org/10.1152/ajpheart.01057.2001.

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Abstract (sommario):
NADH increases during ischemia because O2 shortage limits NADH oxidation at the electron transport chain. Ischemic (IPC) and anesthetic preconditioning (APC) attenuate cardiac reperfusion injury. We examined whether IPC and APC similarly alter NADH, i.e., mitochondrial metabolism. NADH fluorescence was measured at the left ventricular wall of 40 Langendorff-prepared guinea pig hearts. IPC was achieved by two 5-min periods of ischemia and APC by exposure to 0.5 or 1.3 mM sevoflurane for 15 min, each ending 30 min before 30 min of global ischemia. During ischemia, NADH initially increased in nonpreconditioned control hearts and then gradually declined below baseline levels. This increase in NADH was lower after APC but not after IPC. The subsequent decline was slower after IPC and APC. On reperfusion, NADH was less decreased after IPC or APC, mechanical and metabolic functions were improved, and infarct size was lower compared with controls. Our results indicate that IPC and APC cause distinctive changes in mitochondrial metabolism during ischemia and thus lead to improved function and tissue viability on reperfusion.
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Riess, Matthias L., Enis Novalija, Amadou K. S. Camara, Janis T. Eells, Qun Chen e David F. Stowe. "Preconditioning with Sevoflurane Reduces Changes in Nicotinamide Adenine Dinucleotide during Ischemia–Reperfusion in Isolated Hearts". Anesthesiology 98, n. 2 (1 febbraio 2003): 387–95. http://dx.doi.org/10.1097/00000542-200302000-00019.

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Abstract (sommario):
Background Ischemia causes an imbalance in mitochondrial metabolism and accumulation of nicotinamide adenine dinucleotide (NADH). We showed that anesthetic preconditioning (APC), like ischemic preconditioning, improved mitochondrial NADH energy balance during ischemia and improved function and reduced infarct size on reperfusion. Opening adenosine triphosphate-sensitive potassium (K(atp)) channels may be involved in triggering APC. The authors tested if effects of APC on NADH concentrations before, during, and after ischemia are reversible by 5-hydroxydecanoate (5-HD), a putative mitochondrial K channel blocker. Methods Nicotinamide adenine dinucleotide fluorescence was measured in 60 guinea pig Langendorff-prepared hearts assigned into five groups: (1) no treatment before ischemia; (2) APC by exposure to 1.3 mm sevoflurane for 15 min; (3) 200 microm 5-HD from 5 min before to 15 min after sevoflurane exposure; (4) 35 min 5-HD alone; and (5) no treatment and no ischemia. Sevoflurane was washed out for 30 min, and 5-HD for 15 min, before 30-min ischemia and 120-min reperfusion. Results Nicotinamide adenine dinucleotide was reversibly increased during sevoflurane exposure before ischemia, and the increase and rate of decline in NADH during ischemia were reduced after APC. 5-HD abolished these changes in NADH. On reperfusion, function was improved and infarct size reduced after APC compared with other groups. Conclusion Anesthetic preconditioning was evidenced by improved mitochondrial bioenergetics as assessed from NADH concentrations during ischemia and by attenuated reperfusion injury. Reversal of APC by bracketing sevoflurane exposure with 5-HD suggests that APC is triggered by mitochondrial K channel opening or, alternatively, by attenuated mitochondrial respiration without direct involvement of mitochondrial K channel opening.
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Kohno, Masataka, Michiko Momoi, Myat Lin Oo, Ji-Hye Paik, Yong-Moon Lee, Krishnan Venkataraman, Youxi Ai et al. "Intracellular Role for Sphingosine Kinase 1 in Intestinal Adenoma Cell Proliferation". Molecular and Cellular Biology 26, n. 19 (1 ottobre 2006): 7211–23. http://dx.doi.org/10.1128/mcb.02341-05.

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ABSTRACT Sphingosine kinase (Sphk) enzymes are important in intracellular sphingolipid metabolism as well as in the biosynthesis of sphingosine 1-phosphate (S1P), an extracellular lipid mediator. Here, we show that Sphk1 is expressed and is required for small intestinal tumor cell proliferation in Apc Min/+ mice. Adenoma size but not incidence was dramatically reduced in Apc Min/+ Sphk −/ − mice. Concomitantly, epithelial cell proliferation in the polyps was significantly attenuated, suggesting that Sphk1 regulates adenoma progression. Although the S1P receptors (S1P1R, S1P2R, and S1P3R) are expressed, polyp incidence or size was unaltered in Apc Min/+ S1p2r −/ −, Apc Min/+ S1p3r −/ −, and Apc Min/+ S1p1r +/ − bigenic mice. These data suggest that extracellular S1P signaling via its receptors is not involved in adenoma cell proliferation. Interestingly, tissue sphingosine content was elevated in the adenomas of Apc Min/ + Sphk1 −/ − mice, whereas S1P levels were not significantly altered. Concomitantly, epithelial cell proliferation and the expression of the G1/S cell cycle regulator CDK4 and c-myc were diminished in the polyps of Apc Min/ + Sphk1 −/ − mice. In rat intestinal epithelial (RIE) cells in vitro, Sphk1 overexpression enhanced cell cycle traverse at the G1/S boundary. In addition, RIE cells treated with sphingosine but not C6-ceramide exhibited reduced cell proliferation, reduced retinoblastoma protein phosphorylation, and cyclin-dependent kinase 4 (Cdk4) expression. Our findings suggest that Sphk1 plays a critical role in intestinal tumor cell proliferation and that inhibitors of Sphk1 may be useful in the control of intestinal cancer.
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Più fonti

Tesi sul tema "APC MIN"

1

Degg, Natalie Lindsay. "Modification of adenoma multiplicity in irradiated Apc(Min) mice by chromosome 16 segments from BALB/c". Thesis, University of Bristol, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.419212.

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2

Wong, Wing Yan. "Proteomics analysis of anti-cancer effects of gynostemma pentaphyllum saponins in Apc min/+ colorectal cancer mouse model". HKBU Institutional Repository, 2012. https://repository.hkbu.edu.hk/etd_ra/1421.

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3

Urbanska, Aleksandra. "A novel microencapsulated probiotic yogurt formulation for oral delivery in the suppression of intestinal tumorigenesis in «Apc»Min mice". Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=32612.

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Abstract (sommario):
There is a direct relationship between the development of colon cancer and exogenous factors, such as diet. The immunomodulatory effect of probiotic bacteria has been postulated earlier; however, due to low clinical efficacy and associated limitations they have not been devised as cancer theraphy and preventative procedures. One of the main obstacles is the efficient delivery of live bacterial cells to targeted sites. The work contained in this dissertation aims to develop and evaluate a yogurt based formulation containing microencapsulated live probiotic bacterial cells for use in colon cancer prevention and theraphy. Alginate – poly-L-lysine – alginate (APA) and alginate-chitosan (AC) microcapsule systems have been optimized, prepared and characterized. Survival of Lactobacillus acidophilus cells and mechanical stability of the microcapsules were evaluated in various pH conditions in presence of yogurt and simulated gastrointestinal fluids. The physical properties of the microcapsules were investigated using a computer controlled dynamic simulated human gastrointestinal (GI) model. Results show that the APA microcapsule system was more robust, had higher retention capacity, preserved better bacterial viability and had greater resistance to GI environment. The ApcMin mouse was used to investigate the potential of a microencapsulated probiotic yogurt formulation for clinical efficacy and safety. As ApcMin mice are genetically predisposed to spontaneously develop multiple intestinal and colonic adenomas, they provide a practical and genetically relevant model system for cancer prevention studies. Using various biomarkers such as interleukin - 1β, interleukin - 6, i
Le cancer colorectal est l'une des malignités les plus répandues dans le monde occidental. La majorité des cancers colorectaux sont soit localement ou régionalement invasifs au moment du diagnostic, limitant les options de traitements et réduisant les taux de survies. Plusieurs études épidémiologiques et laboratoires suggèrent une relation entre le développent du cancer du colon et des facteurs exogènes, tel que le régime alimentaire. L'effet immunomodulateur des bactéries probiotiques a été postulé; cependant, en raison de l'efficacité clinique réduite et d'autres limitations qui y sont associées, elles n'ont pas été conçues comme une thérapie préventive du cancer. L'un des plus grands obstacles reste l'administration efficace des bactéries vivantes aux organes ciblés. Le travail décrit dans cette dissertation vise à développer et à évaluer une formulation à base de yogourt contenant des cellules bactériennes probiotiques vivantes pour l'atténuation de l'inflammation gastro-intestinale qui cause le développement du cancer du colon, par la conduite d'études in vitro et in vivo. Des systèmes microcapsules Alginate – poly-L-lysine – alginate (APA) et alginate-chitosan (AC) ont été optimisés, préparés et caractérisés. La survie de cellules Lactobacillus acidophilus et la stabilité mécanique des microcapsules ont été évaluées sous diverses conditions de pH et en présence de yogourt et de fluides gastro-intestinales simulées. Les propriétés physiques des microcapsules ont été investiguées en utilisant un model gastro-intestinale (GI) humain dynamique, simulé et contrôlé par ordinateur. Les résultats démontren
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Forest, Virginie. "Interactions cellules épithéliales coliques / lymphocytes intra-épithéliaux dans le contexte de la mutation Min du gène Apc : influence d'un glucide indigestible butyrogène". Nantes, 2002. http://www.theses.fr/2002NANT27VS.

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Abstract (sommario):
L'incidence des cancers colorectaux est très élevée en France. La mise en place d'un micro-environnement favorable à l'intégrité de l'épithélium colique par la nutrition est une stratégie de prévention. Des fructo-oligosaccharides à chaînes courtes (ccFOS) (fibres prébiotiques et butyrogènes) réduisent spécifiquement dans le côlon l'incidence des tumeurs dans un modèle génétique murin de cancérogenèse intestinale (mutation du gène Apc: Adenomatous Polyposis Coli). La fonctionnalité du système immunitaire local est indispensable à cet effet. Le mécanisme de cette action serait lié à la production de butyrate par fermentation des ccFOS et à l'action immunostimulatrice de la flore. Le butyrate régule l'expression de gènes susceptibles d'interférer avec les processus d'homéostasie cellulaire (prolifération, apoptose, interactions lympho-épithéliales) et tissulaire (migration). Pour étudier l'interférence des ccFOS avec le processus de cancérisation nous avons établi des lignées de cellules épithéliales coliques porteuses ou non de la mutation Min du gène Apc. Les capacités migratoires des cellules Apc +/Min sont diminuées, mais restaurées par le butyrate avec une réorganisation du cytosquelette d'actine. Les cellules Apc +/Min sont plus sensibles à l'apoptose et à l'arrêt du cycle cellulaire en G1 induis par le butyrate. In vivo, les ccFOS modulent l'expression des ARNm de l'IL-15 dans la muqueuse colique et celle du RaIL-15 à la surface des lymphocytes intra-épithéliaux (LIE). La cytokine IL-15 régule de nombreuses fonctions lymphocytaires (prolifération, cytotoxicité, survie). Des cocultures ont montré une augmentation de l'expression de ICAM dans le contexte cumulé Apc +/Min et des interactions avec les LIE. Cette molécule a des fonctions immunologiques et de remodelage tissulaire. Ce travail a permis de dégager des pistes sur les mécanismes (stimulation du système immunitaire local, régulation de l'homéostasie cellulaire et tissulaire) et des marqueurs et/ou effecteurs biologiques (ICAM-1, RTNFa, IL-15, RaIL-15) des effets des ccFOS sur la cancérogenèse colique et peuvent rendre compte des effets préventifs observés dans le modèle Min. Ces résultats peuvent mieux définir, documenter et cibler les actions en prévention primaire des cancers colorectaux
Colorectal cancer is one of the most common cancers in France. A beneficial micro-environment provided by the nutrition could participate in the maintenance of the colic epithelial integrity and as such, act as a possible strategy in the prevention of colon cancer. Short-chain fructo-oligosaccharides (sc-FOS) (prebiotic and butyrogenic fiber) decrease specifically the incidence of tumors in a mouse genetic model of intestinal carcinogenesis (mutation of Apc gene: Adenomatous Polyposis Coli). A local, functional immune system is required in this effect. The mechanism of this action could be linked to butyric production by fermentation of scFOS and to the immuno-stimulation property of the flora. Butyrate regulates gene expression and could interfere with cell homeostasis (proliferation, apoptosis, lympho-epithelial interaction) and tissue homeostasis (motility). To study the interference of scFOS with cancerogenesis process, we have established colic epithelial cell lines containing the wild type or mutated Apc gene. The motility of Apc +/Min cells are decreased, however the presence of butyrate can restore the rate of motility in these cells probably through a reorganization of the actin cytosekeleton. The Apc +/Min cells are more susceptible to apoptosis and to cell cycle arrest (in G1) with butyrate. In vivo, scFOS, modulates the mRNA expression of IL-15 in colic mucosa as well as surface expression of IL-15Ra in intra-epithelial lymphocytes (IEL). IL-15 regulate multiple lymphocyte functions (proliferation, cytotoxicity, survival). In our cellular model, we have established a co-culture system which shows an increase expression of ICAM-1 specifically in the presence of the Apc gene mutation and an interaction between epithelial cells and IEL. This molecule have immunological functions and acts in tissue remodelling processes. This research has opened up interesting possible pathways implicated in the mechanisms of action of scFOS on colorectal carcinogenesis in Min mouse (stimulation of local immune system, regulation of cellular and tissular homeostasis), and biological markers and/or effectors (ICAM-1,RTNFa, IL-15, IL-15Ra). This could open up into a new strategy in colorectal cancer primary prevention
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5

Behrends, Thomas [Verfasser], Lutz [Akademischer Betreuer] Schomburg, Werner [Akademischer Betreuer] Kloas e Petra [Akademischer Betreuer] Seemann. "Zur Interaktion von Genotyp und Ernährung bei Darmkrebs : Selen- und Selenoprotein P-abhängige Tumorigenese im Apc min/+ -Mausmodell / Thomas Behrends. Gutachter: Lutz Schomburg ; Werner Kloas ; Petra Seemann". Berlin : Humboldt Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2013. http://d-nb.info/1030313652/34.

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6

Bellocq-Goncalves, Delphine. "Etude sur modèle murin de la bioactivation métabolique des amines aromatiques hétérocycliques par les cellules épithéliales coliques mutées ou non sur le gène Adenomatous polyposis coli (Apc)". Toulouse 3, 2008. http://www.theses.fr/2008TOU30049.

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Les amines aromatiques hétérocycliques (AAHs) sont formées après cuisson des aliments : viandes rouges et poissons. Ces composés mutagènes et cancérigènes sont impliqués dans la carcinogenèse colorectale mais le rôle des cellules intestinales dans la bioactivation des AAHs n'est pas clairement établi. Une mutation du gène Adenomatous polyposis coli (Apc) apparaît précocement dans les cancers coliques. Les cellules coliques Apc+/+ et ApcMultiple intestinal neoplasia (Min)/+ constituent un modèle pertinent pour l'étude de la promotion tumorale. Les études qui sont présentées ont permis d'étudier les capacités de bioactivation métabolique de ces cellules vis-à-vis de 3 AAHs, PhIP, MeIQx et IQ. En condition d'induction par le 2,3,7,8-tétrachlorodibenzo-p-dioxine (TCDD), les cellules ApcMin/+ produisent des taux plus élevés de métabolites réactifs. Eu égard à la cancérogénicité des AHHs en lien avec la formation d'adduits à l'ADN, ces cellules mutées sont rendues " métaboliquement compétentes ". Par RT-qPCR, nous avons montré qu'après induction par le TCDD les cellules ApcMin/+ présentent des niveaux d'expression des gènes CYP1A1, CYP1A2 et CYP1B1 plus élevés que les cellules Apc+/+. Ainsi, in situ, la bioactivation des AAHs peut être à l'origine de nouvelles mutations. Après transfection des cellules Apc par la forme humaine du CYP1A2, les niveaux d'ARNm, de protéines et les activités enzymatiques mesurées sont plus importants dans les cellules ApcMin/+. Ces résultats indiquent que le gène Apc est impliqué dans la régulation de l'expression des cytochromes P450 (CYPs). Un lien existerait entre le récepteur Ah, principal acteur de la régulation des CYPs de la famille 1, et Apc, acteur de la voie de signalisation Wnt/ß-caténine. Les CYPs impliqués dans la bioactivation des AAHs pourraient, en lien avec une perturbation de l'homéostasie cellulaire liée à une mutation du gène Apc, être un facteur majeur de la promotion des cancers colorectaux, voire de leur initiation
Heterocyclic aromatic amines (HAA) are formed in cooked red meat and fish and are considered as potent promoting dietary factors of colon carcinogenesis. Role of intestine cells in HAA bioactivation is not yet fully explained. Loss of function of the Adenomatous polyposis coli (APC) gene product is an early and frequent event in human colorectal carcinogenesis. Normal (Apc+/+) and premalignant (ApcMultiple intestinal neoplasia (Min)/+) mouse colonic epithelial cells allow to study carcinogenesis promotion, but were not characterized for bioactivation of HAA. The overall goal of this work was to characterize the metabolic bioactivation potential towards three HAA, i. E. PhIP, MeIQx and IQ in these colonic cell lines. ApcMin/+ cells when induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) produce significantly higher amount of HAA reactive metabolites than Apc+/+ cells. Parallel RT-qPCR experiments demonstrate that induction by TCDD has prevailing effects in gene expression of CYP1A1, CYP1A2 and CYP1B1 in ApcMin/+ cells. So, a more important metabolic HAA bioactivation potential measured in ApcMin/+ cells can be linked to a higher probability to generate in situ new mutations. After transfection of Apc+/+ and ApcMin/+ cells with human CYP1A2 gene, we have shown that mRNA and protein levels, and also a CYP1A2-related activity were increased in mutated cells. These results indicate that mutation of Apc gene leads to a co-ordinated dysregulation of CYPs expression in mouse colon epithelial cells. A possible link between the aryl hydrocarbon receptor, a main actor in the regulation of CYP1 family expression, with the Apc gene, a main actor of the Wnt/ß-catenin pathway may exist. This disrupted expression of CYP1 members in connection with the mutation of Apc may be of great importance in colorectal carcinogenesis
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Mtotywa, Matolwandile Mzuvukile. "Productivity measurement and its relationship to quality in a South African Minting Company". Thesis, University of South Africa, 2007. http://hdl.handle.net/10500/51.

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The aim of this study was to investigate a productivity measurement at the South African Minting Company and evaluate the relationship between productivity and quality. Special emphasis was given to profit-linked total factor model as the tool for measurement. This was encouraged by their ability to separate productivity, profitability and price recovery. Three models were selected and evaluated. These models American Productivity Center (APC) Model, “Profitability = productivity + price recovery” (PPP) model and multi-factor productivity measurement model (MFPMM). APC model was selected as the suitable model because of its simplicity, easy to set up, its ability to produce both financial and non financial data, and allow for route cause analysis with expert system, and more insight for the manager with Microsoft Excels’ What if analysis “Goal seek”. APC model was set up for four periods, from 1 April 2004 to 30 September 2007. The overall profitability results of the circulation coins profit center show an overall positive contribution. There was a break-even of the price recovery for 2006 financial year (period 2). In 2007 financial year (period 3), there was a negative contribution, and this improved to almost break-even in the six month period during this 2008 financial year (period 4). This means there was much more inflation on input resources and the recovery was not fully realised in the price of goods sold. Individual input costs show that the negative price recovery is culminating from material, labour and energy costs contributions. There is a plausible explanation for material and labour, but not for energy. The metal volatility is the underlying cause of the price variation. Labour variation was a company strategy to adjust employee to higher percentiles. Productivity was always positive with the highest contribution in the current financial year (period 4). This means that the profitability at SA Mint has been driven by productivity in the past two financial years. iv Survey of the questionnaire shows average scores for productivity and quality. It is noteworthy, that the lowest mean score for productivity is for the statement “Products are produced in error-free process”. This is a productivity quality measure. In addition, the same variable shows r2 value of 0.42. A conclusion is that even though productivity and quality are highly correlated and show a highly positive relationship, there is a concern on quality in the company. A link can be made that low price recovery becomes more difficult when the quality is not always good. Defective product is a cost, because the product does not reach the customer and if the product is reworked it is still a cost, though low, but more importantly it decreases the available capacity. This study was successful in setting up APC model and producing data that is worthy to the company and academic world. Finally, this study was successful in its quest to establish the relationship between productivity and quality.
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Malmkvist, Hampus. "Developing an API wrapper with usability in mind". Thesis, Linköpings universitet, Interaktiva och kognitiva system, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-93637.

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When you are creating new software today, more often than not you will use API’s. Users choosing between different API’s would probably look at functionality but also accessibility and ease of use. It would therefore seem motivated for API providers to create usable and accessible API’s.This thesis is about the things that make an API more usable, and then those things are used in practice to increase the usability of CloudMe’s API. CloudMe’s core API is documented to increase usability and a wrapper for the API is developed to allow people more ways to use CloudMe’s service. The APIwrapper is created in Java and was developed thoroughly with regards to usability.
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Sabo, Silvio. "Hur man kan användaGoogle Maps API:er för att beräkna och analysera restidskvoter". Thesis, Linnéuniversitetet, Institutionen för datavetenskap och medieteknik (DM), 2018. http://urn.kb.se/resolve?urn=urn:nbn:se:lnu:diva-75140.

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Denna rapport avhandlar ett arbete inom ämnet datavetenskap och handlarom utvecklingen av ett system för att studera restidkvoten för sträckor somtrafikeras av Västtrafik, som är en av Sveriges största regionalakollektivtrafikmyndigheter. Restidskvoten anges som förhållandet mellanrestiden med kollektivtrafik och att resa med personbil ([restidkollektivtrafik] / [restid biltrafik]). Med detta som grund har ett system föratt inhämta data om restider med hjälp av Google Maps Directions API samtberäkna restidskvoter och annan metadata utifrån denna insamlade dataskapats. Systemet används till att göra dagliga körningar och lagrar inhämtaddata i en databas hos Västtrafik. Till systemet finns också en dashboard somkan användas för att göra sökningar i databasen som byggts upp och på såsätt hämta, visualisera och analysera önskad data. Restidsdata förkollektivtrafik som erhållits från Google har i stickprov jämförts medrestidsdata från Västtrafik och även om det fanns några avvikelser så stämdede väl överens. Därav dras slutsatsen att data från Google går att använda tillatt beräkna och analysera restidskvoter.
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Hu, Xingdong. "Sheng cun fan shi li xing yu chuan tong : Yuan Ming Qing shi qi nan fang min zu fa lü bian qian yan jiu /". Beijing : Zhongguo she hui ke xue chu ban she, 2005. http://catalog.hathitrust.org/api/volumes/oclc/68159992.html.

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Libri sul tema "APC MIN"

1

Xie, Liuyi. Nong min wen xue ABC. [Beijing: Beijing zhong xian tuo fang ke ji fa zhan you xian gong si, 2012.

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B, Holland I., a cura di. ABC proteins: From bacteria to man. Amsterdam: Academic Press, 2003.

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3

Wong, Y. Joel, e Stephen R. Wester, a cura di. APA handbook of men and masculinities. Washington: American Psychological Association, 2016. http://dx.doi.org/10.1037/14594-000.

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Illich, Ivan. ABC: The alphabetization of the popular mind. New York: Vintage Books, 1989.

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Illich, Ivan. ABC: The alphabetization of the popular mind. San Francisco: North Point Press, 1988.

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Illich, Ivan. ABC: The alphabetization of the popular mind. Harmondsworth: Penguin, 1989.

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7

APL 2003 (2003 San Diego, Calif.). APL 2003 "Stretching the Mind": San Diego, CA, June 11, 2003-June 14, 2003. New York: ACM Press, 2003.

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Jun dui zheng zhi gong zuo ABC. Beijing: Guo fang da xue chu ban she, 2005.

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9

Mootz, Andreas. Visuelle Erfassung des Werkstoffübergangs beim MIG/MAG-Impulslichtbogenschweissen. München: Hanser, 1991.

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Mein erster Kinder-Brockhaus: [ein buntes Bilder-Abc]. 8a ed. Gütersloh: Brockhaus, 2012.

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Capitoli di libri sul tema "APC MIN"

1

Nalbantoglu, ILKe, Valerie Blanc e Nicholas O. Davidson. "Characterization of Colorectal Cancer Development in Apc min/+ Mice". In Methods in Molecular Biology, 309–27. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3603-8_27.

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Whelan, Jay, Melissa B. Hansen Petrik, Michael F. McEntee e Mark G. Obukowicz. "Dietary Epa Reduces Tumor Load in Apc Min/+ Mice by Altering Arachidonic Acid Metabolism, But Conjugated Linoleic Acid, Gamma- And Alpha-Linolenic Acids Have No Effect". In Advances in Experimental Medicine and Biology, 579–84. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-0193-0_88.

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Benavent, Enrique, Ángel Corberán, Isaac Plana e José María Sanchis. "Chapter 11: Arc Routing Problems with Min-Max Objectives". In Arc Routing, 255–80. Philadelphia, PA: Society for Industrial and Applied Mathematics, 2015. http://dx.doi.org/10.1137/1.9781611973679.ch11.

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Hering, Ekbert, e Ulrich Mühleisen. "ABC-Analyse". In Marketing mit dem PC, 1–17. Wiesbaden: Vieweg+Teubner Verlag, 1987. http://dx.doi.org/10.1007/978-3-322-85897-9_1.

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Thieme, Kurt H. "Mind Mapping". In Das ABC des Selbstmanagements, 66–69. Wiesbaden: Gabler Verlag, 1995. http://dx.doi.org/10.1007/978-3-322-91142-1_15.

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Iwamoto, Derek Kenji, e Aylin Kaya. "Asian American men." In APA handbook of men and masculinities., 285–97. Washington: American Psychological Association, 2016. http://dx.doi.org/10.1037/14594-013.

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Ojeda, Lizette, e Kurt C. Organista. "Latino American men." In APA handbook of men and masculinities., 299–318. Washington: American Psychological Association, 2016. http://dx.doi.org/10.1037/14594-014.

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Strokoff, Johanna, Tyler C. Halford e Jesse Owen. "Men and psychotherapy." In APA handbook of men and masculinities., 753–74. Washington: American Psychological Association, 2016. http://dx.doi.org/10.1037/14594-034.

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Nguyen, Thanh Tu. "Motorcycles in a Long-Term Perspective: Case of Ho Chi Minh City". In AUC 2019, 219–29. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-5608-1_18.

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Spångberg Zepezauer, Anna Karin. "Mein Wissens-ABC zum Thema Jahresabschlussanalyse". In Steuerlehre und Bilanzierung für das Bachelor-Studium, 289. Wiesbaden: Springer Fachmedien Wiesbaden, 2017. http://dx.doi.org/10.1007/978-3-658-04326-1_23.

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Atti di convegni sul tema "APC MIN"

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Fredenburgh, J. C., D. Collen e M. E. Nesheim. "Enhancement by Activated Protein C of tPA-induced Lysis in a Cell-free System". In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644379.

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The profibrinolytic activity of human activated protein C (APC) was studied in a cell-free system using human plasma. Normal and Ba+* citrate adsorbed human plasmas were dialyzed against 150mM NaCl, 20mM Hepes, pH 7.4 and diluted to an A280 of 16. Reactions were initiated by the addition of aliquots of plasma to cuvettes containing human melanoma tPA and human thrombin at final concentrations of 1 and 30nM, respectively. The effects of Ca+* and varying concentrations of APC on clotlysis times were examined by monitoring turbidity at 600nM while maintaining the temperature at 37°C. The lysis time, defined as the midpoint of turbidity change, was 128 min for normal plasma containing 10 mM Ca+* and showed progressive and saturable shortening to about 90 min at > 50nM APC. In the absence of Ca+*, lysis time was 55 min for normal plasma and did not shorten in response to APC. With Ba+* citrate adsorbed plasma, the lysis time was 82 min in the presence of 10mM Ca+*, and shortened to 42 min without Ca+*. APC had no effect on lysis time in Ba+* adsorbed plasma either with or without Ca+*. Both bovine and human APC were equally potent. Electrophoresis in DodSO4 and autoradiography of plasma samples containing 125I-labelled plasminogen indicated enhanced rates of plasminogen activation in the presence of APC. These data indicate that APC decreases lysis time in vitro at the level of plasminogen activation. This effect is dependent on Ca+* and may involve additional vitamin K-dependent protein ( s).
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Tumlinson, Alexandre R., Jennifer K. Barton, James McNally, Angelika Unterhuber, Boris Hermann, Harald Sattmann e Wolfgang Drexler. "Imaging APC/Min(+/−) colon cancer model mice with ultrahigh resolution endoscopic FD-OCT at 800nm". In Frontiers in Optics. Washington, D.C.: OSA, 2005. http://dx.doi.org/10.1364/fio.2005.fmc1.

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Wojtal, Daria, Roopali Chaudhary, Kyster K. Nanan, Simona Morone e Juliet M. Daniel. "Abstract 1302: Effect of intestinal-specific Kaiso overexpression on the APC MIN/+ mouse colon cancer model". In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-1302.

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Geiger, M., M. J. Heeb, B. Binder e J. H. Griffin. "FUNCTIONAL CHARACTERIZATION OF PROTEIN C INHIBITORS (PCI) FROM PLASMA AND URINE". In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643815.

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Immunoblotting studies showed that human plasma and urine contain components that form heparin-dependent complexes with activated protein C (APC) and urokinase (UPA) and that the presence of either active enzyme decreases complex formation by the other (Geiger et al. 1986, Circ. 74:11-234). To investigate whether these findings are due to competition of APC and UPA for one or more heparin-dependent inhibitors, a functional assay for PCI was developed to study the time course of inhibition of protein C (PC) in purified or crude systems in the presence or absence of stimulating or interfering substances. Microtiter plates coated with monoclonal anti-protein C antibodies were incubated with diluted plasma supplemented with 125I-pc. After activation of bound PC with Protac C, the wells were washed and then incubated with samples containing PCI in the presence or absence of heparin for varying times. The remaining amidolytic activity on the substrate S-2366 was determined as Δ A405/time/cpm bound. Using plasma as a source of PCI, APC inhibition followed pseudo first order kinetics and a linear relation between the pseudo first order rate constant, k, and plasma concentration was observed from 6% to 40% plasma with k = 0.012/min at 20% plasma. A dose dependent increase in k was observed in the presence of heparin, with half maximal stimulation at 2 to 4 U/ml and maximal stimulation (k = 0.05/min at 20% plasma at heparin concentration > 10 U/ml. Urinary PCI was partially purified vising heparin Sepharose chromatography from which it coeluted at 0.35 M NaCl with UPA inhibitory activity. Partially purified urinary PCI inhibited APC and UPA, and competitions similar to those obtained with plasma PCI were observed. The effect of UPA on the inhibition of APC by PCI in plasminogen-depleted plasma and by urinary PCI was studied. In both systems, UPA caused a significant decrease in the inhibition of APC in the absence or presence of heparin. These results and our previous immunobloting data demonstrate competition of APC and UPA for common heparin-dependent PCIs in plasma and urine.
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Joost, S., A. Koedam, Joost C. M. Meijers, Jan J. Sixma e Bonno N. Bouma. "VON WILLEBRAND FACTOR PROTECTS FACTOR VIII FROM INACTIVATION BY ACTIVATED PROTEIN C AND PROTEIN S". In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643618.

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Activated protein C (APC) inactivated the cofactors factor V (FV) and factor VIII (FVIII). In the case of FV, this reaction and the respective roles of Ca2+ , phospholipids and protein S have been well documented. We investigated the role of protein S and von Willebrand factor (VWF) on the inactivation of FVIII.Purified human factor VIII (3 units/ml) was incubated with protein C (0.2 μg/ml) in the presence of 8 μg/ml phospholipid, 5 mM CaCl, and 1 unit/ml hirudin. Factor VIII coagulant activity decreased with a pseudo first-order rate constant of 0.09 min . The reaction rate increased linearly with the concentration of prot^ig S in the incubation mixture. 12I-FVIII was incubated under the same conditions. SDS-polyacrylamide gel electrophoresis showed cleavage products of Mr 43 and 22 kDa. High Mr bands (FVIII-heavy chain) ranging fromMr 108 to208 kDa disappeared while the Mr 80 kDa FVIII-lightchain remained unchanged. The degradationpattern was not changed by addition of protein S.The FVIII-VWF complex was reconstitutedby mixing the two components (±2 units VWF/units FVIII) and lowering the calcium concentration to 2 mM. The inactivation of the FVIII-VWF complex by APC proceeded at a 15- to 20-fold slower rate as compared to the isolated FVIII, indicating a protection of FVIII by VWF. Protein S exhibited no cofactor activity on the inactivation of FVIII-VWF by APC. The protective effect of VWF was lost completely after activation of the FVIII-VWF complexwith thrombin (0.05 units/ml).When FVIII (0.1 units/ml) was added toplasma of a patient with severe von Willebrand's disease, 96% of its activitywas lost in 20 min after the addition of APC. All of the FVIII activity was retained when haemophilic plasma was used. Mixing experiments showed that one unit ofVWF unit FVIII is needed to fully protec FVIII against APC. These results may explain the observed lability of FVIII in von Willebrand's disease patients.
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Chang, Wen-Chi L., Christina M. Ferrara, Harry S. Cooper, Stacy L. Mosier, Esther Kaunga, Clinton J. Grubbs, Ronald A. Lubet e Margie Lee Clapper. "Abstract LB-457: Effect of naproxen and NO-naproxen on intestinal neoplasia in the Apc +/Min-FCCC mouse model". In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-lb-457.

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de Four, N. J., R. M. Bertina e F. Havgrkate. "STIMULATION OF FIBRINOLYSIS BY ACTIVATED PROTEIN C (APC)". In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642961.

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In 1960 Mammen and Seegers reported the discovery of a new protein (autoprothrombin II-A, APC) with both anticoagulant and profibrinolytic activity. They found that APC accelerated clot lysis in vitro and proposed that this was due to a reduction of plasmin - inhibitory activity. Many years later Comp et al (J Clin Inv 68: 1221) reported that the infusion of APC into dogs resulted in an increase in circulating plasminogen activator activity. This observation stimulated more extensive studies of the profibrinolytic effects of APC.In our laboratories we have studied the effect of human APC on clot lysis both in whole blood (human) and in a system of purified human proteins. In these systems 125I-labelled fibrinogen was incorporated in a clot formed after the addition of Jombin (complete clot formation within 5 min) and the subsequent lysis of this clot was followed by measuring the release of I-labelled fibrin degradation products (FDP) into the supernatant. Human t-PA was added to the system to achieve complete lysis of the clot within a few hours.When APC was added to citrated whole blood before clot formation, it was found to accelerate clot lysis in a dose dependent way. This effeg| was specific for APC and dependent on an intact active site, on the presence of protein S (the protein cofactor of APC) and Ca . The presence of APC did not influence the composition of the FDP formed, as analysed by means of SDS-polyacry-1 amide gel electroforesis, and its effect was found to be independent of the presence or absence of a.-antiplasmin.Subsequently we developped a clot lysis system using the purified human proteins of the fibrinolytic system: fibrinogen, FXIII, t-PA, PAI-1 (from human endothelial cells), glu-plasminogen and a -antiplasmin. In this system clot lysis was dependent on the concentrations of plasminogen, -antiplasmin, t-PA and PAI-1, but independent on the thrombin concentration and the presence or absence of phospholipids (purified from human brain). In the absence of PAI-1, no effect of APC on clot lysis was observed. However, in the presence of PAI-1, APC accelerated clot lysis. This effect was independent of the presence or absence of phospholipids and/or protein S and could be explained by the observation that APC can form a complex with PAI-1 (~ 95 kd) and under certain conditions even can convert active PAI-1 (~ 46 kd) into an inactive degradation product (~ 42 kd). However, complex formation is relatively slow anti high PAI-1 concentrations are needed to observe the reaction. The addition of protein S or phospholipids in the presence of Ca did not stimulate complex formation. Therefore, it seems highly unlikely that neutralization of PAI-1 by APC is responsible for the profibrinolytic effect of APC in the whole blood clot lysis.A completely different explanation for the profibrinolytic effect of APC was suggested by the observation that the addition of blood-platelets to the system of purified fibrinolytic components introduced a dependence of the clot lysis rate on the thrombin concentration (decrease in clot lysis at increasing thrombin concentration). This finding opened the possibility that APC stimulated fibrinolysis by reducing the effective thrombin concentration. Subsequent experiments using the whole blood clot lysis system revealed that in the presence of anti-FX antibodies clot lysis was no longer accelerated by APC, while the actual rate of clot lysis depended on the concentration of thrombin added.We like to propose, that in a blood clot lysis system APC most likely accelerates fibrinolysis by reducing the effective thrombin concentration; if at all, neutralization of PAI-1 may play only a minor role.
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Chang, Wen-Chi L., Esther Kaunga, Harry S. Cooper, Lisa Vanderveer, Jing Peng, Yongchao Zhang, Chen S. Suen e Margie L. Clapper. "Abstract 2806: Effect of ED-71, an analogue of Vitamin D3, on intestinal neoplasia in the Apc+/Min-FCCC mouse model". In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-2806.

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Vanderveer, Lisa, Suresh Paramasivam, Kara Williams, Harry Cooper, Karthik Devarajan, Suraj Peri, Yan Zhou et al. "Abstract 182: Differential response of epithelial cells from colorectal adenomas and adjacent nonneoplastic colonic mucosa to aspirin and atorvastatin in Apc+/Min-FCCCmice." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-182.

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Suzuki, Koji, Yoshihiro Deyashiki, Junji Nishioka, Kazunori Toma e Shuji Yamamoto. "THE INHIBITOR OF ACTIVATED PROTEIN C: STRUCTURE AND FUNCTION". In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642963.

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In the final step of protein C pathway, activated protein C (APC) is neutralized with a plasma inhibitor, termed protein C inhibitor (PCI). PCI was first described by Marlar and Griffin (1980) and then isolated from human plasma as a homogeneous form and characterized by the authors (1983). PCI is a single chain glycoprotein with M 57,000 and a plasma concentration of 5 ug/ml. Analysis of a cDNA nucleotide sequence has clarified that a precursor of human PCI consists of a mature protein of 387 amino acid residues (M 43,759) and a signal peptide of 19 amino acid residues. Only one cysteine residue is present in the entire protein as in α1antitrypsin (α1AT) and α1antichymotrypsin (α1ACT). Three Asn-X-Ser/Thr sequences and two Ser/Thr-X-X-Pro sequences are present as potential attachment sites of carbohydrate chains. Based on the amino acid sequence of the carboxyl-terminal peptide released from the inhibitor by APC digestion, the reactive site peptide bond of PCI was found to be Arg(354)-Ser(355). It is similar to the reactive sites of the other serine protease inhibitors which are located to their carboxyl-terminal Arg(393)-Ser (394), Met(358)-Ser(359) and Leu(358)-Ser(359) in antithrombin III, α1AT and α1ACT, respectively. The alignment of the amino acid sequence of PCI with heparin cofactor II, α1plasmin inhibitor, ovalbumin, angiotensinogen and the above noted plasma inhibitors showed that PCI is a member of serine protease inhibitor superfamily. PCI inhibits APC noncompetitively in a 1:1 stoichiometry and forms a covalent acyl-bond with a Ser residue in the active center of APC. The half life of APC in plasma approximately 30 min, which is rather slow compared with the other protease inhibitors. However, optimal concentrations of heparin, dextran sulfate and its derivatives potentiate the rate of inhibition 30-60 fold. PCI has Ki of 10-8m for APC, and can inhibit thrombin, Factor Xa, urokinase and tissue plasminogen activator as well in the presence of heparin or dextran sulfate, though the Ki for these enzymes is slightly higher. During the complex formation with APC, PCI is cleaved by the complexed APC to form a modified form with M 54,000. PCI is synthesized in several hepatoma cell lines and decreased in plasma of patients with liver cirrhosis. It is also decreased in patients with DIC or those during cardiopulmonary bypass in parallel with the decrease in protein C, suggesting that PCI participates in regulation of the protein C pathway in intravascular coagulation. Recently, we have obtained the recombinant PCI from COS-1 cells which were transfected with expression vector pSV2 containing the cDNA of PCI. The recombinant PCI had the same Mr and specific activity as the protein purified from plasma. It also had an affinity for heparin and dextran sulfate. Moreover, we have predicted a three dimentional structure of the proteolytically modified PCI with computer graphics based on its amino acid sequence homology with the modified α1AT whose structure had been elucidated with X-ray crystallography. All potential carbohydrate attachment sites were estimated to exist on the surface of the protein. Succesively we have constructed the interaction model between the intact PCI predicted from the modified form and the active center of APC which was simulated from that of trypsin. From the model, it was observed that the amino-group of Arg (354, PI site) of PCI could strongly interact with the carboxy1-group of Asp (88, SI site) of the heavy chain of APC at the base of the active center pocket of the enzyme.
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Rapporti di organizzazioni sul tema "APC MIN"

1

Gutierrez, Julian Monge. Mini-App Resilience Using Different Levels of Precision. Office of Scientific and Technical Information (OSTI), luglio 2019. http://dx.doi.org/10.2172/1545748.

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Ferenbaugh, Charles R. PENNANT: An Unstructured Mesh Mini-App for Advanced Architecture Research. Office of Scientific and Technical Information (OSTI), maggio 2013. http://dx.doi.org/10.2172/1079561.

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3

Reynolds, A., e T. Palmer. Introduction to an MCGIDI Mini-App and Performance Comparisons with XSBench. Office of Scientific and Technical Information (OSTI), giugno 2022. http://dx.doi.org/10.2172/1874857.

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CALS TEST NETWORK WRIGHT-PATTERSON AFB OH. Technical IGES Evaluation Using: SA-ALC/TIMCE Data, MIL-D-28OOA (IGES). Fort Belvoir, VA: Defense Technical Information Center, maggio 1993. http://dx.doi.org/10.21236/ada312282.

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5

CALS TEST NETWORK WRIGHT-PATTERSON AFB OH. Technical Raster Transfer Using: AlliedSignal Technical Services' Data Supporting: SA-ALC/TILDM's EDCARS System, MIL-STD-1840A, MIL-D-28002A (Raster). Fort Belvoir, VA: Defense Technical Information Center, settembre 1994. http://dx.doi.org/10.21236/ada306832.

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6

CALS TEST NETWORK WRIGHT-PATTERSON AFB OH. Technical Publication Transfer Test Using: OC-ALC/TISDTPP ATOS, MIL-D-28000 (IGES), MIL-M-28001A (SGML). Quick Short Test Report. Fort Belvoir, VA: Defense Technical Information Center, maggio 1992. http://dx.doi.org/10.21236/ada313228.

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7

Nantung, Tommy E., Jusang Lee, John E. Haddock, M. Reza Pouranian, Dario Batioja Alvarez, Jongmyung Jeon, Boonam Shin e Peter J. Becker. Structural Evaluation of Full-Depth Flexible Pavement Using APT. Purdue University, 2021. http://dx.doi.org/10.5703/1288284317319.

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The fundamentals of rutting behavior for thin full-depth flexible pavements (i.e., asphalt thickness less than 12 inches) are investigated in this study. The scope incorporates an experimental study using full-scale Accelerated Pavement Tests (APTs) to monitor the evolution of each pavement structural layer's transverse profiles. The findings were then employed to verify the local rutting model coefficients used in the current pavement design method, the Mechanistic-Empirical Pavement Design Guide (MEPDG). Four APT sections were constructed using two thin typical pavement structures (seven-and ten-inches thick) and two types of surface course material (dense-graded and SMA). A mid-depth rut monitoring and automated laser profile systems were designed to reconstruct the transverse profiles at each pavement layer interface throughout the process of accelerated pavement deterioration that is produced during the APT. The contributions of each pavement structural layer to rutting and the evolution of layer deformation were derived. This study found that the permanent deformation within full-depth asphalt concrete significantly depends upon the pavement thickness. However, once the pavement reaches sufficient thickness (more than 12.5 inches), increasing the thickness does not significantly affect the permanent deformation. Additionally, for thin full-depth asphalt pavements with a dense-graded Hot Mix Asphalt (HMA) surface course, most pavement rutting is caused by the deformation of the asphalt concrete, with about half the rutting amount observed within the top four inches of the pavement layers. However, for thin full-depth asphalt pavements with an SMA surface course, most pavement rutting comes from the closet sublayer to the surface, i.e., the intermediate layer. The accuracy of the MEPDG’s prediction models for thin full-depth asphalt pavement was evaluated using some statistical parameters, including bias, the sum of squared error, and the standard error of estimates between the predicted and actual measurements. Based on the statistical analysis (at the 95% confidence level), no significant difference was found between the version 2.3-predicted and measured rutting of total asphalt concrete layer and subgrade for thick and thin pavements.
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8

Pilemalm, Sofie. Hur expanderar vi konceptet civila insatspersoner: Att hantera organisatoriska och IT-relaterade hinder. Linköping University Electronic Press, giugno 2022. http://dx.doi.org/10.3384/9789179294083.

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För mer än tio år sedan startade kommunal räddningstjänst det första initiativet där civila engagerades som första insatspersoner – Förstärkt Medmänniska i Medelpad. Sedan dess har konceptet – civila insatspersoner (CIP) spridit sig till ett tjugotal räddningstjänster, i glesbygd och på landsbygd men även till urbana miljöer genom ett initiativ taget av Södertörns Brandsvarsförbund. Både de räddningstjänster som tillämpar konceptet och myndigheter som Myndigheten för samhällsskydd och beredskap (MSB) och SOS Alarm är överens om nyttan CIP tillför genom att förkorta responstider, rädda liv och egendom. Trots detta har konceptet inte fått den spridning man hoppats på. Vi vet att hindren är både organisatoriska och specifikt relaterade till utlarmning med hjälp av existerande IT-stöd, appar eller SMS-listor. I den här studien utforskar vi dessa hinder vidare. Vi ger också ett antal förslag på hur de identifierade hindren kan hanteras. Detta genom att genomföra en kvalitativ intervjustudie där vi jämför och kontrasterar perspektiv från myndigheter, räddningstjänst, kommersiella app-utvecklare och de civila insatspersonerna själva (slutanvändare). Vi beskriver både organisatoriska och IT-relaterade hinder och hur de hänger samman. De centrala organisatoriska hindren handlar dels om konkreta utmaningar där det inte finns någon budget eller tid allokerad för att arbeta med CIP-konceptet där det finns viss ovana av förändringsarbete. De handlar också om kulturellt motstånd, det vill säga upplevd konkurrens från CIP vilket gör att initiativen kan sakna stöd både från ledningsnivå i räddningstjänster och från brandmän på operativ nivå. Legala aspekter är också centralt där det för närvarande existerar olika tolkningar av lagstiftning runt ansvar för arbetsmiljö. När det gäller IT-stöden är vissa hinder rent tekniska och relaterar till svårigheter med att få till en korrekt geofencing och att utveckla appar som ska fungera – inte bara på en enhet utan på olika mobila lösningar som ägs av privatpersoner (Iphone, Android i olika versioner). Andra hinder hänger ihop med organisatoriska frågor och konkurrens på den privata marknaden. Exempelvis har SOS Alarm en dubbel roll som privat och statlig aktör och har en app och ett application programming interface (API) under utveckling. De kommersiella leverantörerna kan inte leverera till samma låga kostnad som SOS Alarm och kommer inte åt vissa funktioner (till exempel att dra tillbaka resurser om en situation eskalerar till något farligt). Samtidigt var SOS Alarms app vid tiden för studien inte färdig. Detta sätter räddningstjänsterna i en olycklig situation utvecklingsmässigt och de får fortsätta förlita sig på de SMS-listor som egentligen endast var tänkt som en initial lösning. Vi föreslår ett antal åtgärder för att adressera hindren där de viktigaste är att MSB tar en koordinerande roll, och upprättandet av samverkansgrupper bestående av representanter för samtliga aktörer som ska vara med och driva konceptet, inklusive civila insatspersoner, kommunal räddningstjänst, SOS Alarm, socialtjänst, försäkringsbolag och fastighetsägare. Vi argumenterar också för hur man kan nyttja existerande kunskapsnätverk för CIP mer effektivt erfarenhetsutbyte. När det gäller ett gemensamt API är ett släppande av detta centralt för att utlarmning ska fungera, konceptet expandera – och överleva över tid. Här föreslår vi expertgrupper med representanter för myndigheter, systemutvecklare, app-leverantörer, SOS Alarm och inte minst slutanvändare. Vi ser också att tiden är mogen för dynamisk resursallokering, det vill säga att när CIP:ar blir fler måste det bli möjligt att larma ut på kompetens och specialisering (till exempel för att undvika larmtrötthet i storstadsområden) men att övriga hinder måste adresseras först. Vidare i ett teoretiskt perspektiv diskuterar vi våra resultat i termer av ”digitalized co-production” (digitaliserad samproduktion). Co-production är ett sätt att involvera samhällsmedborgare i tjänsteutveckling i offentlig sektor där expansion och nya former möjliggörs av ökad digitalisering. Här tar vi ett delvis annat perspektiv där vi i stället tittar på när digitalisering och IT blir hinder för samproduktionen. Vi argumenterar också för att CIP är en helt ny, framväxande hybridform av co-production som behöver starkare styrning än traditionell co-production. Här kan vår studie bidra till successiv ackumulering av kunskap.
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Petrova, Atanaska, Tsvetelina Borisova, Yana Feodorova, Irina Stanimirova, Tsonka Miteva-Katrandzhieva, Michael Petrov e Marianna Murdjeva. Analysis of OprD Receptor in Carbapenem Resistant Clinical Isolates Pseudomonas aeruginosa and Interplay between the Expression of Main Efflux Pumps and Intrinsic AmpC. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, dicembre 2018. http://dx.doi.org/10.7546/crabs.2018.12.15.

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10

CALS TEST NETWORK WRIGHT-PATTERSON AFB OH. Technical Raster Transfer Using: Grumman Aerospace Corp. Data Supporting: SA/ALC-TIRA's F15 DST Program, MIL-R-28OO2A (Raster) Quick Short Test Report. Fort Belvoir, VA: Defense Technical Information Center, maggio 1994. http://dx.doi.org/10.21236/ada312331.

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