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[Title] Activated protein C attenuates leukocyte elastase-induced lung injury in mice.

The purpose of the current study was to (1) examine the relationship between LE-induced lung injury and specific markers of inflammation and cytokine/chemokine, and to (2) determine the potential of activated protein C (APC), a potent immunomodulator, to block the inflammatory response to LE.

Total cells, total protein, and neutrophils were increased and peaked at 16 h in bronchial alveolar lavage fluid.

Administration of LE up-regulated the synthesis of proinflammatory cytokines, IL-1beta and IL-6, chemokines, keratinocyte-derived chemokine, and macrophage inflammatory protein 2 in bronchial alveolar lavage fluid, and their peaks were at 6 h.

Furthermore, the mice were treated with APC at 0.2, 2.0, and 10 mg/kg (i.v.) after instillation of LE.

Therapeutic treatment of APC at 2.0 and 10 mg/kg significantly attenuated the increases in all these parameters.

Lung histology revealed that, in addition to inflammation, alveolar hemorrhage and alveolar wall destruction induced by LE were also attenuated by APC.

Finally, the expression of tissue plasminogen activator and plasminogen activator inhibitor in whole lung of mice exposed to LE, detected by means of reverse-transcriptase-polymerase chain reaction, were not influenced by the treatment with APC.

These data demonstrate that intratracheal administration of LE to mice causes a transient inflammatory response, and APC can play a protective role against LE-induced lung injury.

[MeSH-major] Inflammation Mediators / therapeutic use. Leukocyte Elastase / toxicity. Lung Diseases / chemically induced. Lung Diseases / pathology. Protein C / metabolism. Protein C / therapeutic use

[MeSH-minor] Animals. Enzyme Activation / physiology. Female. Fibrinolysis. Intubation, Intratracheal. Mice. Mice, Inbred C57BL. Neutrophil Activation / physiology. Neutrophil Infiltration / physiology. Neutrophils / pathology. Pulmonary Alveoli / drug effects. Pulmonary Alveoli / metabolism. Pulmonary Alveoli / pathology

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(PMID = 18628688.001).

[ISSN] 1073-2322

[Journal-full-title] Shock (Augusta, Ga.)

[ISO-abbreviation] Shock

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Inflammation Mediators; 0 / Protein C; EC 3.4.21.37 / Leukocyte Elastase

   

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[Title] Chromosomal and methylation alterations in sporadic and familial adenomatous polyposis-related duodenal carcinomas.

Primary carcinomas of the small intestine are rare and the mechanism of their pathogenesis is poorly understood.

Patients with familial adenomatous polyposis (FAP) have a high risk of developing duodenal carcinomas.

Therefore, five FAP-related duodenal carcinomas were characterized for chromosomal and methylation alterations, which were compared to those observed in sporadic duodenal carcinomas.

Comparative genomic hybridization (CGH) and methylation-specific multiplex ligation-dependent probe amplification (MS-MLPA) was performed in 10 primary sporadic and five primary FAP-related duodenal carcinomas.

In the FAP-related carcinomas, frequent gains were observed on chromosomes 8, 17 and 19, whereas in sporadic carcinomas they occurred on chromosomes 8, 12, 13 and 20.

In 60% of the sporadic carcinomas, gains in the regions of chromosome 12 were observed which were absent in the FAP-related carcinomas (P=0.04).

Hypermethylation was observed in the immunoglobulin superfamily genes member 4 (IGSF4), TIMP metallopeptidase inhibitor 3 (TIMP3), Estrogen receptor 1 (ESR1), adenomatous polyposis coli (APC), H-cadherin (CDH13) and paired box gene 6 (PAX6) genes.

Hypermethylation of PAX6 was only observed in FAP-related carcinomas (3/5) and not in sporadic carcinomas (P=0.02).

In conclusion, in contrast to sporadic duodenal carcinomas, gains on chromosome 12 were not observed in duodenal carcinomas of patients with FAP.

Identification of the genes in these regions of chromosome 12 could lead to a better understanding of the carcinogenesis pathways leading to sporadic and FAP-related duodenal carcinomas.

Furthermore, hypermethylation seems to be a general feature of both FAP-related duodenal carcinomas as well as sporadic duodenal carcinomas with the exception of the PAX6 gene, which is methylated only in FAP-related carcinomas.

[MeSH-major] Adenocarcinoma / genetics. Adenomatous Polyposis Coli / genetics. Chromosome Aberrations. DNA Methylation. Duodenal Neoplasms / genetics

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(PMID = 17873900.001).

[ISSN] 0893-3952

[Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc

[ISO-abbreviation] Mod. Pathol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

   

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[Title] Expression of beta-catenin and its mechanism of delocalization in intestinal-type early gastric cancer based on mucin expression.

The biological characteristics of intestinal-type early gastric cancers (ICs) differ based on mucin phenotypes.

There was increased cytoplasmic and nuclear beta-catenin expression (delocalization) in ICs with a predominant intestinal mucin phenotype (ICIP; 46.3% [25/54 cases]) compared to ICs with a predominant gastric mucin phenotype (ICGP; 20% [11/55 cases]).

There were no beta-catenin or APC mutations in ICs.

APC promoter hypermethylation was present in 49 of 105 (46.7%) cases of ICs.

There was a significant relationship between APC promoter hypermethylation and beta-catenin delocalization in ICs, especially in ICIPs.

There was no relationship between beta-catenin delocalization and APC gene loss of heterozygosity in ICs.

In conclusion, we showed that beta-catenin delocalization was more evident in ICIPs, and APC promoter hypermethylation might play a role in delocalization of beta-catenin, especially in ICIPs.

[MeSH-minor] Adult. Aged. Alleles. Base Sequence. Cell Nucleus / metabolism. DNA Methylation. DNA Mutational Analysis. DNA, Neoplasm / genetics. DNA, Neoplasm / isolation & purification. Female. Gastrectomy. Gastric Mucosa / metabolism. Gastric Mucosa / pathology. Genes, APC. Humans. Immunohistochemistry. Loss of Heterozygosity. Male. Middle Aged. Molecular Sequence Data. Mutation. Polymerase Chain Reaction. Polymorphism, Restriction Fragment Length. Polymorphism, Single-Stranded Conformational. Promoter Regions, Genetic. Retrospective Studies. Sequence Analysis, DNA. Time Factors

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(PMID = 19475529.001).

[ISSN] 1699-5848

[Journal-full-title] Histology and histopathology

[ISO-abbreviation] Histol. Histopathol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Spain

[Chemical-registry-number] 0 / CTNNB1 protein, human; 0 / DNA, Neoplasm; 0 / Mucins; 0 / beta Catenin

   

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[Title] Regulation of stromal cell cyclooxygenase-2 in the ApcMin/+ mouse model of intestinal tumorigenesis.

Cyclooxygenase-2 (Cox-2) is expressed predominantly by stromal cells in intestinal adenomas from the Apc(Min/+) mouse model of familial adenomatous polyposis.

We investigated the mechanistic basis of stromal cell Cox-2 expression in Apc(Min/+) mouse adenomas, as well as Cox-2 expression and activity in histologically normal (HN) Apc(Min/+) mouse intestine, in order to gain further insights into regulation of Cox-2 as a potential chemoprevention target.

Upregulation of Cox-2 in intestinal tumours is not an intrinsic feature of Apc(Min/+) macrophages as bone marrow-derived Apc(Min/+) macrophages did not exhibit an abnormality in Cox-2 expression or activity.

Intestinal permeability to lactulose or mannitol was similar in Apc(Min/+) mice and wild-type littermates, implying that macrophage activation by luminal antigen is unlikely to explain stromal cell Cox-2 induction.

Moreover, stromal cells exhibited differential expression of Cox-2 and inducible nitric oxide synthase, suggesting 'alternative' (M2) rather than 'classical' (M1) macrophage activation.

SMNCs from HN Apc(Min/+) intestinal mucosa exhibited similar levels of Cox-2 mRNA and protein, but produced more Cox-2-derived PGE(2) than wild-type cells at 70 days of age.

There was an age-dependent decline in PGE(2) synthesis by Apc(Min/+) SMNCs, despite tumour progression.

These data suggest that other Cox-2-independent factors also control PGE(2) levels during Apc(Min/+) mouse intestinal tumorigenesis.

[MeSH-major] Adenoma / genetics. Adenomatous Polyposis Coli Protein / genetics. Cyclooxygenase 2 / biosynthesis. Intestinal Neoplasms / genetics

[MeSH-minor] Animals. Cell Transformation, Neoplastic. Chemoprevention. Dinoprostone / biosynthesis. Disease Models, Animal. Flow Cytometry. Gene Expression Regulation. Macrophages. Mice. Mice, Inbred C57BL. Permeability. Stromal Cells / enzymology

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(PMID = 16219637.001).

[ISSN] 0143-3334

[Journal-full-title] Carcinogenesis

[ISO-abbreviation] Carcinogenesis

[Language] eng

[Grant] United Kingdom / Medical Research Council / / G116/146

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; EC 1.14.99.1 / Cyclooxygenase 2; K7Q1JQR04M / Dinoprostone

   

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[Title] Detection of epithelial apoptosis in pelvic ileal pouches for ulcerative colitis and familial adenomatous polyposis.

BACKGROUND: Ileal pouch-anal anastomosis (IPAA) is the surgical procedure of choice for patients with refractory ulcerative colitis (UC) and for familial adenomatous polyposis (FAP) with many rectal polyps.

Pouchitis is one of the more frequent complications after IPAA in UC patients; however, it is rare in FAP.

OBJECTIVE: Evaluate pro-apoptotic activity in endoscopically and histological normal mucosa of the ileal pouch in patients with UC and FAP.

METHODS: Eighteen patients (nine with UC and nine with FAP) with J pouch after total rectocolectomy were studied.

The specimens were snap-frozen and the expressions of Bax and Bcl-2 were determined by immunoblot of protein extracts and by immunohistochemistry analysis.

FADD, Caspase-8, APAF-1 and Caspase-9 were evaluated by immunoprecipitation and immunoblot.

RESULTS: Patients with UC had significantly higher protein levels of Bax and APAF-1, Caspase-9 than patients with FAP, but were similar to controls.

Immunohistochemistry for Bax showed less intensity of immunoreactions in FAP than in UC and Controls.

CONCLUSION: Patients with FAP present lower levels of pro-apoptotic proteins in all methods applied, even in the absence of clinical and endoscopic pouchitis and dysplasia in the histological analysis.

However, FAP patients had low pro-apoptotic activity in the mucosa, and it could explain the tendency to low cell turn over and presence of adenomas in this syndrome.

[MeSH-major] Adenomatous Polyposis Coli / surgery. Apoptosis / physiology. Colitis, Ulcerative / surgery. Colonic Pouches / pathology. Intestinal Mucosa / pathology

[MeSH-minor] Animals. Apoptosis Regulatory Proteins / metabolism. Apoptotic Protease-Activating Factor 1 / metabolism. Caspase 8 / metabolism. Caspase 9 / metabolism. Humans. Ileum / anatomy & histology. Ileum / pathology. Proto-Oncogene Proteins c-bcl-2 / metabolism. bcl-2-Associated X Protein / metabolism

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(PMID = 20113505.001).

[ISSN] 1479-5876

[Journal-full-title] Journal of translational medicine

[ISO-abbreviation] J Transl Med

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / APAF1 protein, human; 0 / Apoptosis Regulatory Proteins; 0 / Apoptotic Protease-Activating Factor 1; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-2-Associated X Protein; EC 3.4.22.- / Caspase 8; EC 3.4.22.- / Caspase 9

[Other-IDs] NLM/ PMC2843649

   

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[Title] An important role of Tyk2 in APC function of dendritic cells for priming CD8+ T cells producing IFN-gamma.

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(PMID = 17048270.001).

[ISSN] 0014-2980

[Journal-full-title] European journal of immunology

[ISO-abbreviation] Eur. J. Immunol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Germany

[Chemical-registry-number] 0 / Antigens, Bacterial; 0 / Cytokines; 0 / HLA-A Antigens; 0 / HLA-B Antigens; 0 / OVA-8; 0 / Peptide Fragments; 82115-62-6 / Interferon-gamma; 9006-59-1 / Ovalbumin; EC 2.7.10.2 / TYK2 Kinase; EC 2.7.10.2 / Tyk2 protein, mouse

   

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[Title] Microtubule-bundling activity of APC is stimulated by interaction with PSD-95.

Adenomatous polyposis coli (APC) tumor suppressor protein binds to microtubules, leading to microtubule bundling and stabilization.

The protein also interacts with postsynaptic density (PSD)-95, a major scaffolding protein in neurons.

Here, we analyzed the effects of PSD-95 on the microtubule-bundling activity of APC.

The coexpression of APC and PSD-95 in COS-7 cells enhanced microtubule-bundle formation compared with the expression of APC alone.

A mutant APC variant that does not associate with PSD-95 did not enhance microtubule bundling, despite coexpression with PSD-95.

Immunoelectron microscopy showed that the APC-PSD-95 complex sometimes colocalized on microtubules in processes of cultured neurons.

These results suggest that the microtubule-bundling activity of APC is regulated by its interaction with PSD-95, which might modulate microtubule architecture and dynamics in neurons.

[MeSH-major] Adenomatous Polyposis Coli Protein / physiology. Microtubules / metabolism. Nerve Tissue Proteins / physiology

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(PMID = 16701944.001).

[ISSN] 0304-3940

[Journal-full-title] Neuroscience letters

[ISO-abbreviation] Neurosci. Lett.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Ireland

[Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein; 0 / Nerve Tissue Proteins; 0 / postsynaptic density proteins

   

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[Title] Colorectal carcinomas in MUTYH-associated polyposis display histopathological similarities to microsatellite unstable carcinomas.

BACKGROUND: MUTYH-associated polyposis (MAP) is a recessively inherited disorder which predisposes biallelic carriers for a high risk of polyposis and colorectal carcinoma (CRC).

Since about one third of the biallelic MAP patients in population based CRC series has no adenomas, this study aimed to identify specific clinicopathological characteristics of MAP CRCs and compare these with reported data on sporadic and Lynch CRCs.

METHODS: From 44 MAP patients who developed > or = 1 CRCs, 42 of 58 tumours were analyzed histologically and 35 immunohistochemically for p53 and beta-catenin.

KRAS2, the mutation cluster region (MCR) of APC, p53, and SMAD4 were analyzed for somatic mutations.

RESULTS: MAP CRCs frequently localized to the proximal colon (69%, 40/58), were mucinous in 21% (9/42), and had a conspicuous Crohn's like infiltrate reaction in 33% (13/40); all of these parameters occurred at a higher rate than reported for sporadic CRCs.

Tumour infiltrating lymphocytes (TILs) were also highly prevalent in MAP CRCs.

Somatic APC MCR mutations occurred in 14% (5/36) while 64% (23/36) had KRAS2 mutations (22/23 c.34G>T).

CONCLUSION: MAP CRCs show some similarities to micro-satellite unstable cancers, with a preferential proximal location, a high rate of mucinous histotype and increased presence of TILs.

These features should direct the practicing pathologist towards a MAP aetiology of CRC as an alternative for a mismatch repair deficient cause.

High frequent G>T transversions in APC and KRAS2 (mutated in early tumour development) but not in P53 and SMAD4 (implicated in tumour progression) might indicate a predominant MUTYH effect in early carcinogenesis.

[MeSH-major] Adenomatous Polyposis Coli / genetics. Adenomatous Polyposis Coli / pathology. Colorectal Neoplasms / genetics. Colorectal Neoplasms / pathology. DNA Glycosylases / genetics. Microsatellite Instability

[MeSH-minor] Adult. Aged. Alleles. Cohort Studies. Female. Genetic Predisposition to Disease. Humans. Immunohistochemistry. Lymphocytes, Tumor-Infiltrating / immunology. Male. Middle Aged. Mutation. Tissue Array Analysis

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(PMID = 19527492.001).

[ISSN] 1471-2407

[Journal-full-title] BMC cancer

[ISO-abbreviation] BMC Cancer

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] EC 3.2.2.- / DNA Glycosylases; EC 3.2.2.- / mutY adenine glycosylase

[Other-IDs] NLM/ PMC2706846

   

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The present study characterized more precisely which pathways and cellular events of the allergic response are amplified by DEP in view of the maturation/activation/function of antigen-presenting cells (APC) and the antigen-specific Th response.

We evaluated the effects of DEP on the phenotype and function of bone marrow-derived dendritic cells (BMDC) in vitro and on the expression pattern of APC-related molecules in the murine lung in the presence or absence of antigen in vivo.

In addition, an in vivo experiment showed that repetitive pulmonary exposure to DEP plus antigen (OVA) increased the numbers of MHC class II+cells and those expressing CD11c, DEC205 (DC markers), CD80, CD86 (co-stimulatory molecules), F4/80 (a macrophage marker), and CD19 (a B-cell differentiation antigen) in the lung as compared to that of others (vehicle, DEP, or OVA).

In conclusion, enhancement of allergic responses by DEP can be explained via two novel mechanisms, i.e., enhancement effects on APC including DC and on antigen-specific Th response, which culminate in the promotion of local and systemic dysregulated Th immunity.

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(PMID = 19064938.001).

[ISSN] 1535-3702

[Journal-full-title] Experimental biology and medicine (Maywood, N.J.)

[ISO-abbreviation] Exp. Biol. Med. (Maywood)

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Antigens; 0 / Epitopes; 0 / Histocompatibility Antigens Class II; 0 / Immunoglobulins; 0 / Particulate Matter; 0 / Vehicle Emissions; 9006-59-1 / Ovalbumin

   

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METHODS: Two multiplex polymerase chain reaction (PCR) assays were developed to detect the 16SrDNA, collagenase (prtC) and fimbria (fimA) genes of P. gingivalis and the 16SrDNA, leukotoxin (lktA) and fimbria-associated protein (fap) genes of A. actinomycetemcomitans in 60 sulcus samples from 30 periodontal healthy subjects and in 122 subgingival plaque samples from 61 patients with CP.

RESULTS: The 16SrDNA, prtC and fimA genes of P. gingivalis were detected in 92.6%, 85.2% and 80.3% of the subgingival plaque samples respectively, while the 16SrDNA, lktA and fap genes of A. actinomycetemcomitans were in 84.4%, 75.4% and 50.0% respectively.

Nucleotide sequence analysis showed 98.62%~100% homology of the PCR products in these genes with the reported sequences. P. gingivalis strains with prtC+/fimA+ and A. actinomycetemcomitans with lktA+ were predominant in deep pockets (>6 mm) or in sites with attachment loss > or =5 mm than in shallow pockets (3~4 mm) or in sites with attachment loss < or =2 mm (P<0.05). P. gingivalis strains with prtC+/fimA+ also showed higher frequency in gingival index (GI)=3 than in GI=1 group (P<0.05).

CONCLUSION: Infection of P. gingivalis with prtC+/fimA+ and A. actinomycetemcomitans with lktA+ correlates with periodontal destruction of CP in Chinese.

Nonetheless P. gingivalis fimA, prtC genes and A. actinomycetemcomitans lktA gene are closely associated with periodontal destruction, while A. actinomycetemcomitans fap gene is not.

[MeSH-minor] Adult. Aged. China / epidemiology. Chronic Disease. Female. Humans. Male. Middle Aged. Prevalence. Risk Assessment / methods. Risk Factors. Species Specificity. Statistics as Topic

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(PMID = 17266188.001).

[ISSN] 1673-1581

[Journal-full-title] Journal of Zhejiang University. Science. B

[ISO-abbreviation] J Zhejiang Univ Sci B

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] China

[Other-IDs] NLM/ PMC1791058

   

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[Title] Identification of candidate cooperative genes of the Apc mutation in transformation of the colon epithelial cell by retroviral insertional mutagenesis.

The mutation of Apc is an important early genetic event in colon carcinogenesis.

To identify cooperative genes for the Apc(Min) mutation the authors carried out retroviral insertional mutagenesis (RIM) using Min mouse-derived IMCE colon epithelial cells.

Anchorage-independent transformed colonies were induced by retroviral infection only in IMCE cells, while no transformation was found in young adult mouse colon (YAMC) cells that are normal for Apc.

These data suggest the importance of cytoskeletal function in Apc-related tumor development and the usefulness of RIM in non-hematopoietic tissues, providing new insight into the early stage of colon carcinogenesis.

[MeSH-major] Cell Transformation, Neoplastic / genetics. Colon / pathology. Genes, APC. Mutagenesis, Insertional. Mutation. Retroviridae / genetics

[MeSH-minor] Animals. Cell Line. Dyneins / genetics. Epithelial Cells / pathology. Membrane Proteins / genetics. Mice. Microtubules / metabolism. Neoplasm Proteins / genetics. Up-Regulation

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(PMID = 18294281.001).

[ISSN] 1349-7006

[Journal-full-title] Cancer science

[ISO-abbreviation] Cancer Sci.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Ahnak protein, mouse; 0 / Membrane Proteins; 0 / Neoplasm Proteins; EC 3.6.4.2 / Dnah3 protein, mouse; EC 3.6.4.2 / Dyneins

   

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While several lines of evidence suggest that mutations in adenomatous polyposis coli (APC) may promote chromosome instability, at least in colon cancer, the underlying mechanisms remain unclear.

Here, we turn our attention to GSK-3 - a protein kinase, which in concert with APC, targets beta-catenin for proteolysis - and ask whether GSK-3 is required for accurate chromosome segregation.

Analysis of synchronised HeLa cells shows that GSK-3 inhibitors do not prevent G1/S progression or cell division.

CONCLUSION: Thus, not only do our observations indicate a role for GSK-3 in accurate chromosome segregation, but they also raise the possibility that, if used as therapeutic agents, GSK-3 inhibitors may induce unwanted side effects by inducing chromosome instability.

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(PMID = 17697341.001).

[ISSN] 1471-2121

[Journal-full-title] BMC cell biology

[ISO-abbreviation] BMC Cell Biol.

[Language] ENG

[Grant] United Kingdom / Wellcome Trust / /

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Protein Kinase Inhibitors; 0 / beta Catenin; EC 2.7.11.1 / glycogen synthase kinase 3 beta; EC 2.7.11.26 / Glycogen Synthase Kinase 3

[Other-IDs] NLM/ PMC1976608

   

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[Title] Cross-species comparison of human and mouse intestinal polyps reveals conserved mechanisms in adenomatous polyposis coli (APC)-driven tumorigenesis.

The majority of sporadic colorectal cancers are triggered by mutations in the adenomatous polyposis coli (APC) tumor suppressor gene, leading to the constitutive activation of the Wnt/beta-catenin signaling pathway and formation of adenomas.

Despite this common genetic basis, colorectal cancers are very heterogeneous in their degree of differentiation, growth rate, and malignancy potential.

Here, we applied a cross-species comparison of expression profiles of intestinal polyps derived from hereditary colorectal cancer patients carrying APC germline mutations and from mice carrying a targeted inactivating mutation in the mouse homologue Apc.

This comparative approach resulted in the establishment of a conserved signature of 166 genes that were differentially expressed between adenomas and normal intestinal mucosa in both species.

Functional analyses of the conserved genes revealed a general increase in cell proliferation and the activation of the Wnt/beta-catenin signaling pathway.

Moreover, the conserved signature was able to resolve expression profiles from hereditary polyposis patients carrying APC germline mutations from those with bi-allelic inactivation of the MYH gene, supporting the usefulness of such comparisons to discriminate among patients with distinct genetic defects.

[MeSH-major] Adenomatous Polyposis Coli / metabolism. Adenomatous Polyposis Coli Protein / metabolism. Cell Transformation, Neoplastic / metabolism. Colorectal Neoplasms / pathology. Intestinal Polyps / metabolism

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(PMID = 18403596.001).

[ISSN] 1525-2191

[Journal-full-title] The American journal of pathology

[ISO-abbreviation] Am. J. Pathol.

[Language] eng

[Grant] United Kingdom / Medical Research Council / / G0301154

[Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Adenomatous Polyposis Coli Protein

[Other-IDs] NLM/ PMC2329845

   

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[Title] Molecular insights into mammalian end-binding protein heterodimerization.

Microtubule plus-end tracking proteins (+TIPs) are involved in many microtubule-based processes.

End binding (EB) proteins constitute a highly conserved family of +TIPs.

Here we used a combination of methods to investigate the dimerization properties of the three human EB proteins EB1, EB2, and EB3.

Based on Förster resonance energy transfer, we demonstrate that the C-terminal dimerization domains of EBs (EBc) can readily exchange their chains in solution.

We further document that EB1c and EB3c preferentially form heterodimers, whereas EB2c does not participate significantly in the formation of heterotypic complexes.

Fluorescence spectroscopy and nuclear magnetic resonance studies in the presence of the cytoskeleton-associated protein-glycine-rich domains of either CLIP-170 or p150(glued) or of a fragment derived from the adenomatous polyposis coli tumor suppressor protein show that chain exchange of EBc domains can be controlled by binding partners.

Extension of these studies of the EBc domains to full-length EBs demonstrate that heterodimer formation between EB1 and EB3, but not between EB2 and the other two EBs, occurs both in vitro and in cells as revealed by live cell imaging.

[MeSH-major] Microtubule-Associated Proteins / metabolism. Models, Molecular. Protein Multimerization / physiology

[MeSH-minor] Animals. CHO Cells. Cell Line. Cricetinae. Cricetulus. Humans. Kinetics. Magnetic Resonance Spectroscopy. Neoplasm Proteins / chemistry. Neoplasm Proteins / genetics. Neoplasm Proteins / metabolism. Protein Structure, Quaternary. Protein Structure, Tertiary. Recombinant Proteins / chemistry. Recombinant Proteins / genetics. Recombinant Proteins / metabolism. Spectrometry, Fluorescence

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(PMID = 20008324.001).

[ISSN] 1083-351X

[Journal-full-title] The Journal of biological chemistry

[ISO-abbreviation] J. Biol. Chem.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / MAPRE1 protein, human; 0 / MAPRE3 protein, human; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / Recombinant Proteins; 144198-36-7 / dynactin; 148349-95-5 / cytoplasmic linker protein 170

[Other-IDs] NLM/ PMC2820806

   

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A causal link for COX-2 in epithelial tumorigenesis was shown in genetically manipulated animal models of colon and breast carcinoma.

COX enzymes are targets for cancer prevention as shown by the observation that nonselective COX and selective COX-2 inhibitors have been reported to effectively prevent experimental colon cancer and can regress colorectal polyps in patients with familial adenomatous polyposis.

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(PMID = 16688727.001).

[ISSN] 0899-1987

[Journal-full-title] Molecular carcinogenesis

[ISO-abbreviation] Mol. Carcinog.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Cyclooxygenase Inhibitors; 0 / Prostaglandins; EC 1.14.99.1 / Cyclooxygenase 2

[Number-of-references] 53

   

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[Title] Fibroblast growth factor 9 has oncogenic activity and is a downstream target of Wnt signaling in ovarian endometrioid adenocarcinomas.

Roughly 40% of ovarian endometrioid adenocarcinomas (OEA) have constitutive activation of Wnt signaling as a result of oncogenic mutations in the beta-catenin protein or inactivating mutations in key negative regulators of beta-catenin, such as the adenomatous polyposis coli and Axin tumor suppressor proteins.

Using microarray and quantitative PCR-based approaches, we found that fibroblast growth factor (FGF9) expression was increased >6-fold in primary OEAs with Wnt/beta-catenin pathway defects compared with OEAs lacking such defects.

[MeSH-major] Carcinoma, Endometrioid / genetics. Fibroblast Growth Factor 9 / genetics. Ovarian Neoplasms / genetics. Wnt1 Protein / metabolism

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(PMID = 16452189.001).

[ISSN] 0008-5472

[Journal-full-title] Cancer research

[ISO-abbreviation] Cancer Res.

[Language] eng

[Grant] United States / PHS HHS / / NIH P30 46952; United States / NCI NIH HHS / CA / R01 CA 85463; United States / NCI NIH HHS / CA / R01 CA 94172; United States / NCI NIH HHS / CA / U19 CA 84953

[Publication-type] Journal Article; Research Support, N.I.H., Extramural

[Publication-country] United States

[Chemical-registry-number] 0 / FGF9 protein, human; 0 / Fibroblast Growth Factor 9; 0 / RNA, Messenger; 0 / Wnt1 Protein; 0 / beta Catenin

   

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[Title] Not-so-pseudo a substrate: Acm1-mediated inhibition of the APC.

In a recent issue of Molecular Cell, Enquist-Newman et al. (2008) demonstrate that Acm1 is ubiquitinated by APC(Cdc20).

By contrast, the high-affinity interaction between Acm1 and APC(Cdh1) renders it a poor substrate, but a specific inhibitor, of the APC(Cdh1) complex.

[MeSH-major] Repressor Proteins / metabolism. Saccharomyces cerevisiae / metabolism. Saccharomyces cerevisiae Proteins / metabolism. Ubiquitin-Protein Ligase Complexes / antagonists & inhibitors. Ubiquitin-Protein Ligase Complexes / metabolism

[MeSH-minor] Anaphase-Promoting Complex-Cyclosome. Cdc20 Proteins. Cdh1 Proteins. Cell Cycle Proteins / metabolism. Mitosis. Substrate Specificity. Ubiquitination

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[CommentOn] Mol Cell. 2008 May 23;30(4):437-46 [18498748.001]

(PMID = 18538651.001).

[ISSN] 1097-4164

[Journal-full-title] Molecular cell

[ISO-abbreviation] Mol. Cell

[Language] eng

[Publication-type] Comment; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Acm1 protein, S cerevisiae; 0 / CDC20 protein, S cerevisiae; 0 / CDH1 protein, S cerevisiae; 0 / Cdc20 Proteins; 0 / Cdh1 Proteins; 0 / Cell Cycle Proteins; 0 / Repressor Proteins; 0 / Saccharomyces cerevisiae Proteins; EC 6.3.2.19 / Anaphase-Promoting Complex-Cyclosome; EC 6.3.2.19 / Ubiquitin-Protein Ligase Complexes

   

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High level of nutrients and water activity, direct contact with soil, and lack of thermal procedures during primary processing make fresh produce a potential food safety hazard.

Aerobic plate counts (APC) of dilutions were determined.

Statistical analysis (least significant difference-based analysis of variance) showed that there were no significant (P > 0.05) differences in APC among control, water at 25 degrees C, and 5% acetic acid at 25 degrees C.

Thermal treatments with water at 95 degrees C, and 5% acetic acid at 95 degrees C, were both significantly (P < 0.05) more effective in APC reduction than were nonthermal treatments, but were not significantly different from each other.

Results indicated that a thermal water immersion intervention in primary processing of fresh melons can result in a 3-log reduction of natural microflora surface contamination, but 5% acetic acid will not significantly augment this reduction.

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(PMID = 20501053.001).

[ISSN] 0362-028X

[Journal-full-title] Journal of food protection

[ISO-abbreviation] J. Food Prot.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Anti-Infective Agents, Local; Q40Q9N063P / Acetic Acid

   

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This recognition results in the formation of a so-called immune synapse (IS) at the T-cell/APC interface, which is crucial for T-cell activation.

Dynamic analysis of T-cell/APC interaction by AFM revealed that in the presence of antigen interaction forces increased from 1 to 2 nN at early time-points to a maximum of approximately 14 nN after 30 min and decreased again after 60 min.

BIRT377 almost completely abolish the interaction forces, emphasizing the importance of LFA-1/ICAM-1-interactions for firm T-cell/APC adhesion.

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[ErratumIn] Proc Natl Acad Sci U S A. 2010 Feb 2;107(5):2373

(PMID = 19822763.001).

[ISSN] 1091-6490

[Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America

[ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.

[Language] ENG

[Grant] United States / NEI NIH HHS / EY / PN2 EY016586

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / BIRT 377; 0 / Imidazolidines; 0 / Lymphocyte Function-Associated Antigen-1; 0 / Peptide Fragments; 126547-89-5 / Intercellular Adhesion Molecule-1; EC 3.2.1.- / hen egg lysozyme; EC 3.2.1.17 / Muramidase

[Other-IDs] NLM/ PMC2764924

   

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We investigated whether the circadian clock modulated core molecular processes necessary for memory formation in vivo by analyzing circadian regulation of basal and LTS-induced levels of phosphorylated mitogen-activated protein kinase (P-MAPK) and Aplysia CCAAT/enhancer binding protein (ApC/EBP).

In contrast, the circadian clock regulated basal levels of ApC/EBP protein with peak levels at night, antiphase to the rhythm in LTS.

Importantly, LTS training during the (subjective) day produced greater increases in P-MAPK and ApC/EBP than training at night.

Thus, circadian modulation of LTS occurs, at least in part, by suppressing changes in key proteins at night.

Rescue of long-term memory formation at night required both facilitation of MAPK and transcription in conjunction with LTS training, confirming that the circadian clock at night actively suppresses MAPK activation and transcription involved in memory formation.

The circadian clock appears to modulate LTS at multiple levels.

Together, our studies suggest that the circadian clock modulates LTS at multiple steps and locations during the formation of long-term memory.

[MeSH-minor] Animals. CCAAT-Enhancer-Binding Proteins / metabolism. Electric Stimulation / methods. Enzyme Activation / physiology. Ganglia, Invertebrate / enzymology. Hemolymph / metabolism. Mitogen-Activated Protein Kinases / metabolism. Phosphorylation. Serotonin / metabolism

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(PMID = 16928854.001).

[ISSN] 1529-2401

[Journal-full-title] The Journal of neuroscience : the official journal of the Society for Neuroscience

[ISO-abbreviation] J. Neurosci.

[Language] eng

[Grant] United States / NINDS NIH HHS / NS / NS050589

[Publication-type] Journal Article; Research Support, N.I.H., Extramural

[Publication-country] United States

[Chemical-registry-number] 0 / CCAAT-Enhancer-Binding Proteins; 333DO1RDJY / Serotonin; EC 2.7.11.24 / Mitogen-Activated Protein Kinases

   

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[Title] Cardiovascular protective role for activated protein C during endotoxemia in rats.

OBJECTIVE: We examined whether activated protein C (APC) treatment improves cardiovascular inflammation and dysfunction in endotoxemic rats.

INTERVENTIONS: Internal carotid artery and external jugular vein were catheterized under sterile conditions in rats.

Instrumented rats infused or not with APC (240 microg/kg per hour) were challenged with E. coli endotoxin (10 mg/kg).

MEASUREMENTS AND RESULTS: Endotoxin administration induced systemic hypotension, depression of myocardial systolic performance and reduction in capillary density of the small intestine muscularis layer.

Plasma levels of nitrite/nitrate, tumor necrosis factor alpha and macrophage migration inhibitory factor, mesentery venule leukocyte-endothelium interactions, heart and small intestine myeloperoxidase activities were increased in endotoxin-treated rats.

APC largely prevented endotoxin-induced cardiovascular dysfunction with improved systemic hemodynamics, functional capillary density, and myocardial contractile performance.

Beneficial cardiovascular effects of APC were associated with attenuation of entotoxin-induced inflammatory response in terms of plasma levels of nitrite/nitrate, tumor necrosis factor alpha, macrophage migration inhibitory factor, and endothelial cell-leukocyte activation.

CONCLUSION: APC reduces systemic and tissue inflammation and preserves cardiovascular function during experimental endotoxemia.

[MeSH-major] Cardiovascular System / drug effects. Endotoxemia. Protein C Inhibitor / pharmacology. Serine Proteinase Inhibitors / pharmacology

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(PMID = 16601957.001).

[ISSN] 0342-4642

[Journal-full-title] Intensive care medicine

[ISO-abbreviation] Intensive Care Med

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Protein C Inhibitor; 0 / Serine Proteinase Inhibitors

   

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To address this missing information, a total of 2,548 sponge samples from pelts, preevisceration carcasses, and postintervention carcasses were collected from multiple large commercial lamb processing plants to determine aerobic plate counts, the prevalences of Escherichia coli O157:H7, non-O157 Shiga toxin-producing E. coli (STEC), and Salmonella.

The prevalences of E. coli O157:H7 from the pelts, the preevisceration carcasses, and the postintervention carcasses were 12.8, 1.6, and 2.9%, respectively.

The average Salmonella prevalences were 14.4, 4.3, and 1.8% for pelts, preevisceration carcasses, and postintervention carcasses, respectively.

A small number of STEC serotypes associated with severe human illness were isolated from postintervention carcasses.

The results of this study establish a baseline for microbiological quality and prevalences of Salmonella, E. coli O157:H7, and STEC in U.S. lamb processing plants.

[MeSH-major] Escherichia coli / isolation & purification. Food Contamination / analysis. Food-Processing Industry / standards. Salmonella / isolation & purification. Sheep / microbiology

[MeSH-minor] Abattoirs. Animals. Colony Count, Microbial. Consumer Product Safety. Escherichia coli O157 / isolation & purification. Food Microbiology. Humans. Meat / microbiology. Prevalence. Serotyping. United States

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(PMID = 17803136.001).

[ISSN] 0362-028X

[Journal-full-title] Journal of food protection

[ISO-abbreviation] J. Food Prot.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

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[Title] APC, MYH, and the correlation genotype-phenotype in colorectal polyposis.

BACKGROUND: Familial adenomatous polyposis (FAP) has been divided into two entities: classical (CFAP) and attenuated (AFAP).

With the discovery of MYH associated polyposis (MAP) syndrome, the clinical differences have become unclear.

The aim of our study was to investigate patients with polyposis treated in our institution for a correlation between genotype and phenotype.

Four groups were identified: AFAP, CFAP, MAP, and no-mutation patients.

RESULTS: Patient breakdown was CFAP patients (n = 322/294), AFAP patients (n = 13/41), MYH patients (n = 17) and no-mut patients (n = 32).

Patients not tested for APC mutation (n = 131) were excluded.

Major differences were found for MYH patients: later age at diagnosis, more cancers, fewer polyps, and more located in the right part of the colon.

For phenotype/genotype correlation, patients aged more than 35 years at the time of colectomy and with fewer than 100 polyps had significantly more mutation found on MYH.

CONCLUSIONS: This two-way analysis did not show any correlation that might help to identify a subgroup of patients with APC mutation that may be considered attenuated.

It is more likely that the MAP syndrome is the real AFAP.

[MeSH-major] Adenomatous Polyposis Coli / genetics. DNA Glycosylases / genetics. Genes, APC

[MeSH-minor] Adolescent. Adult. Female. Genetic Predisposition to Disease. Genotype. Humans. Male. Middle Aged. Mutation. Phenotype. Syndrome. Young Adult

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(PMID = 19169759.001).

[ISSN] 1534-4681

[Journal-full-title] Annals of surgical oncology

[ISO-abbreviation] Ann. Surg. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] EC 3.2.2.- / DNA Glycosylases; EC 3.2.2.- / mutY adenine glycosylase

   

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[Title] Novel human pathological mutations. Gene symbol: APC. Disease: adenomatous polyposis coli.

[MeSH-major] Adenomatous Polyposis Coli / genetics. Genes, APC. INDEL Mutation

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(PMID = 19320041.001).

[ISSN] 1432-1203

[Journal-full-title] Human genetics

[ISO-abbreviation] Hum. Genet.

[Language] eng

[Databank-accession-numbers] GENBANK/ HX080001

[Publication-type] Case Reports; Journal Article

[Publication-country] Germany

[Chemical-registry-number] 0 / Codon; 0 / Codon, Nonsense

   

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Graft-versus-Host Disease (GvHD) is the most serious complication of allogeneic stem cell transplantation (SCT) and results from an activation of donor lymphocytes by recipient antigen-presenting cells (APCs).

For a long time, it has been postulated that the intestinal microflora and endotoxin exert a crucial step in this APC activation, as there is early and severe gastrointestinal damage induced by pretransplant conditioning.

With the detailed description of pathogen-associated molecular patterns and pathogen recognition receptors single nucleotide polymorphisms of TLRs and especially NOD2 have been identified as potential risk factors of GvHD and transplant related complications thus further supporting the crucial role of innate immunity in SCT, related complications.

Gastrointestinal decontamination and neutralization of endotoxin have been used to interfere with this early axis of activation with some success but more specific approaches of modulation of innate immunity are needed for further improvement of clinical outcome.

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(PMID = 21188220.001).

[ISSN] 2042-0099

[Journal-full-title] International journal of inflammation

[ISO-abbreviation] Int J Inflam

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Other-IDs] NLM/ PMC3003997

   

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This is achieved by the action of ubiquitin ligases (E3s), which remove both negative and positive regulators of the cell cycle.

Though our current understanding of the plant cell cycle has improved a lot these recent years, the identity of the E3s regulating it and their mode of action is still in its infancy.

Thus the anaphase promoting complex/cyclosome (APC/C) not only controls mitotic events, but is also important in post-mitotic cells for normal plant development and cell differentiation.

[MeSH-minor] Anaphase-Promoting Complex-Cyclosome. Models, Biological. Plant Growth Regulators / metabolism. Ubiquitin-Protein Ligase Complexes / genetics. Ubiquitin-Protein Ligase Complexes / metabolism. Ubiquitin-Protein Ligases / genetics. Ubiquitin-Protein Ligases / metabolism

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[Copyright] Copyright © 2010 Elsevier Ltd. All rights reserved.

(PMID = 20810305.001).

[ISSN] 1879-0356

[Journal-full-title] Current opinion in plant biology

[ISO-abbreviation] Curr. Opin. Plant Biol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review

[Publication-country] England

[Chemical-registry-number] 0 / Plant Growth Regulators; EC 6.3.2.19 / Anaphase-Promoting Complex-Cyclosome; EC 6.3.2.19 / Ubiquitin-Protein Ligase Complexes; EC 6.3.2.19 / Ubiquitin-Protein Ligases

   

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In turn, Tome-1 itself is targeted for degradation by APC in the G1 phase of the cell cycle.

[MeSH-major] Cell Cycle / genetics. Cell Cycle Proteins / genetics. Promoter Regions, Genetic / genetics

[MeSH-minor] 5' Flanking Region / genetics. Animals. Base Sequence. Cell Division. Down-Regulation / genetics. G2 Phase. Humans. Mice. Molecular Sequence Data. Mutation / genetics. NIH 3T3 Cells. Sequence Alignment. Transcriptional Activation / genetics

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(PMID = 15733861.001).

[ISSN] 0014-5793

[Journal-full-title] FEBS letters

[ISO-abbreviation] FEBS Lett.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Netherlands

[Chemical-registry-number] 0 / CDCA3 protein, human; 0 / Cell Cycle Proteins; 0 / Tome-1 protein, mouse

   

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OBJECTIVE: Debate exists as to the benefits of performing mucosectomy as part of pouch surgery for ulcerative colitis (UC) and familial adenomatous polyposis (FAP).

Potential reasons for functional problems were investigated, as were rates of 'cuffitis', dysplasia, polyposis and cancer in the ileal pouch and anal canal.

Meta-analysis suggested that nighttime seepage of stool and resting and squeeze pressure were worse after mucosectomy.

Mucosectomy does seem to confer benefit in terms of disease control but this benefit does not reach statistical significance.

Performing mucosectomy results in some clinical benefits in terms of lower rates of inflammation and dysplasia in the retained mucosa in UC patients and lower rates of cuff polyposis in FAP patients.

However, on the basis of available evidence mucosectomy is only indicated in those cases where the patient is at a high risk of disease in the retained rectal cuff.

[MeSH-major] Colonic Pouches / adverse effects. Intestinal Mucosa / surgery. Proctocolectomy, Restorative / adverse effects

[MeSH-minor] Adenocarcinoma / prevention & control. Adenomatous Polyposis Coli / surgery. Anastomosis, Surgical / adverse effects. Anastomosis, Surgical / methods. Anus Neoplasms / prevention & control. Arsenates. Colitis, Ulcerative / surgery. Humans. Ileal Neoplasms / prevention & control. Randomized Controlled Trials as Topic

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(PMID = 17504334.001).

[ISSN] 1462-8910

[Journal-full-title] Colorectal disease : the official journal of the Association of Coloproctology of Great Britain and Ireland

[ISO-abbreviation] Colorectal Dis

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] England

[Chemical-registry-number] 0 / Arsenates; N7CIZ75ZPN / arsenic acid

[Number-of-references] 70

   

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[Title] Active systemic lupus erythematosus is associated with failure of antigen-presenting cells to express programmed death ligand-1.

OBJECTIVE: Antigen-presenting cells (APC) play critical roles in establishing and maintaining peripheral tolerance.

This is accomplished in part via expression of negative co-stimulatory molecules such as programmed death ligand-1 (PD-L1) on tolerogenic APC, such as immature myeloid dendritic cells (mDC).

Several studies have strongly linked dysfunction of APC, including mDC, to the pathogenesis of SLE.

The objective of this study was to determine whether APC expressed PD-L1 protein at normal levels during active lupus.

In contrast, both mDC and Mo from patients with active SLE failed to up-regulate PD-L1 over a 5 day time course, expressing this protein only during disease remissions.

CONCLUSIONS: These data are the first to link active lupus with reversibly decreased PD-L1 expression on professional APC, suggesting a novel mechanism for loss of peripheral tolerance in SLE.

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(PMID = 18650228.001).

[ISSN] 1462-0332

[Journal-full-title] Rheumatology (Oxford, England)

[ISO-abbreviation] Rheumatology (Oxford)

[Language] ENG

[Grant] United States / NCRR NIH HHS / RR / M01 RR000037; United States / NIAMS NIH HHS / AR / T32 AR007108; United States / NCRR NIH HHS / RR / M01-RR-00037

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD274; 0 / CD274 protein, human

[Other-IDs] NLM/ PMC2722808

   

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[Title] Effects of vandetanib on adenoma formation in a dextran sodium sulphate enhanced Apc(MIN/+) mouse model.

The Apc(MIN/+) mouse is a well-characterised model of intestinal tumourigenesis in which animals develop macroscopically detectable adenomas.

However, most of the adenomas are formed in the small intestine and resolution of events in the colon, the most relevant site for human disease, is limited.

Inducing colitis with dextran sodium sulphate (DSS) can selectively enhance the development of lesions in the colon.

We demonstrated that a DSS pre-treatment is well tolerated and effective at inducing colon adenomas in an Apc(MIN/+) mouse model.

We then investigated the effect of inhibiting vascular endothelial growth factor (VEGFR)- and epidermal growth factor receptor (EGFR)-dependent signalling pathways on the development of adenomas induced in DSS-pretreated (DSS/Apc(MIN/+)) or non-DSS-pretreated (Apc(MIN/+)) mice using vandetanib (ZD6474), a potent and selective inhibitor of VEGFR and EGFR tyrosine kinase activity.

Eight-week old Apc(MIN/+) mice were given either drinking water or 1.8% DSS and then vandetanib (ZD6474) (50 mg/kg/day) or vehicle by oral gavage for 28 days and sacrificed 24 h after the last dose and assessed for adenoma formation in the intestines.

DSS pre-treatment was well tolerated and significantly enhanced formation of adenomas in the colon of control Apc(MIN/+) mice.

Vandetanib treatment significantly reduced adenoma formation in the small intestine by 68% (P=0.001) and the colon by 77% (from 13.8 to 3.1, P=0.01) of DSS-pretreated Apc(MIN/+) mice.

In the Apc(MIN/+) group, vandetanib also reduced the mean number of adenomas in the small intestine by 76% (P<0.001) and in the colon by 60% (from 3.9 to 1.5, P=0.1).

DSS-pre-treatment increased the resolution of the model, allowing us to confirm statistically significant effects of vandetanib on the development and growth of colon adenomas in the Apc(MIN/+) mouse.

Moreover these preclinical data provide a rationale for studying the effects of vandetanib in early stages of intestinal cancer in the clinic.

[MeSH-major] Adenoma / prevention & control. Antineoplastic Agents / pharmacology. Colitis / chemically induced. Colonic Neoplasms / prevention & control. Dextran Sulfate. Genes, APC. Piperidines / pharmacology. Protein Kinase Inhibitors / pharmacology. Quinazolines / pharmacology

[MeSH-minor] Animals. Disease Models, Animal. Intestine, Small / drug effects. Intestine, Small / enzymology. Intestine, Small / pathology. Mice. Mice, Inbred C57BL. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Receptor, Epidermal Growth Factor / metabolism. Vascular Endothelial Growth Factor Receptor-2 / antagonists & inhibitors. Vascular Endothelial Growth Factor Receptor-2 / metabolism. beta Catenin / metabolism

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(PMID = 20811697.001).

[ISSN] 1791-2423

[Journal-full-title] International journal of oncology

[ISO-abbreviation] Int. J. Oncol.

[Language] eng

[Grant] United Kingdom / Cancer Research UK / /

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Greece

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CTNNB1 protein, mouse; 0 / N-(4-bromo-2-fluorophenyl)-6-methoxy-7-((1-methylpiperidin-4-yl)methoxy)quinazolin-4-amine; 0 / Piperidines; 0 / Protein Kinase Inhibitors; 0 / Quinazolines; 0 / beta Catenin; 9042-14-2 / Dextran Sulfate; EC 2.7.10.1 / EGFR protein, mouse; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2

   

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Pathways of the molecular pathogenesis of colorectal carcinoma have been extensively studied and molecular lesions during the development of the disease have been revealed.

High up in the list of colorectal cancer lesions are APC (adenomatous polyposis coli), K-ras, Smad4 (or DPC4-deleted in pancreatic cancer 4) and p53 genes.

The ubiquitin-proteasome system (UPS) is comprised of a multi-unit cellular protease system that regulates several dozens of cell proteins after their ligation with the protein ubiquitin.

Given that among these proteins are regulators of the cell cycle, apoptosis, angiogenesis, adhesion and cell signalling, this system plays a significant role in cell fate and carcinogenesis.

UPS inhibition has been found to be a pre-requisite for apoptosis and is already clinically exploited with the proteasome inhibitor bortezomib in multiple myeloma.

Inhibition of Cox-2 by aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs) has been found to inhibit proliferation of colorectal cancer cells and in epidemiologic studies has been shown to reduce colon polyp formation in genetically predisposed populations and in the general population.

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(PMID = 17488476.001).

[ISSN] 1582-1838

[Journal-full-title] Journal of cellular and molecular medicine

[ISO-abbreviation] J. Cell. Mol. Med.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] Romania

[Chemical-registry-number] 0 / Cyclooxygenase Inhibitors; 0 / Ubiquitin; EC 1.14.99.1 / Cyclooxygenase 2; EC 3.4.25.1 / Proteasome Endopeptidase Complex

[Number-of-references] 298

[Other-IDs] NLM/ PMC3822826

   

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[Title] [Expression of endothelial protein C receptor in tumor cell lines and It's significance].

AIM: To detect the role of activated protein C(APC) on proliferation of endothelial cell and investigate the expression of endothelial protein C receptor( EPCR) in variety of tumor cell lines.

METHODS: The effect of APC on endotheliocyte proliferation was determined by MTT colorimetry.

RESULTS: APC can increase the proliferation of EC significantly.

CONCLUSION: APC can stimulate the proliferation of endothelial cell.

High expression of EPCR in tumor cell lines provides a potential biological marker for malignancies.

[MeSH-minor] Cell Line, Tumor. Cell Proliferation. Humans. Interleukin-6 / metabolism. Interleukin-8 / metabolism. Protein C / metabolism

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(PMID = 20619102.001).

[ISSN] 1007-8738

[Journal-full-title] Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology

[ISO-abbreviation] Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi

[Language] chi

[Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] China

[Chemical-registry-number] 0 / Antigens, CD; 0 / Interleukin-6; 0 / Interleukin-8; 0 / PROCR protein, human; 0 / Protein C; 0 / Receptors, Cell Surface

   

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[Title] Cutting edge: IFN-gamma enables APC to promote memory Th17 and abate Th1 cell development.

However, Th1, Th17, and memory but not naive T cells are colocalized in an inflammatory environment.

We show that IFN-gamma stimulates B7-H1 expression on APC subsets and abates their Th1 polarization capacity in a B7-H1-dependent manner.

Interestingly, IFN-gamma triggers APCs to produce IL-1 and IL-23 and enables them to induce memory Th17 expansion via IL-1 and IL-23 in a B7-H1-independent manner.

We propose a novel dynamic between Th1 and Th17 in the course of inflammation as follows: Th1-mediated inflammation is attenuated by IFN-gamma-induced B7-H1 on APCs and is evolved toward Th17-mediated chronic inflammation by IFN-gamma-induced, APC-derived IL-1 and IL-23.

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(PMID = 18941172.001).

[ISSN] 1550-6606

[Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)

[ISO-abbreviation] J. Immunol.

[Language] eng

[Grant] United States / NCI NIH HHS / CA / CA099985; United States / NCI NIH HHS / CA / CA123088

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, CD274; 0 / CD274 protein, human; 0 / Growth Inhibitors; 0 / Interleukin-1; 0 / Interleukin-17; 0 / Interleukin-23; 82115-62-6 / Interferon-gamma

   

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[Title] Elevated Dnmt3a activity promotes polyposis in Apc(Min) mice by relaxing extracellular restraints on Wnt signaling.

Here we use knock-in transgenic mice to investigate the consequences of intestinal epithelium-specific overexpression of de novo Dnmt3a.

METHODS: A novel gene targeting strategy, based on the intestinal epithelium-specific, uniform expression of the A33 glycoprotein, is employed to restrict Dnmt3a overexpression in homozygous A33(Dnmt3a) mutant mice.

RESULTS: A33(Dnmt3a) mice infrequently develop spontaneous intestinal polyps.

However, when genetically challenged, tumor multiplicity in A33(Dnmt3a);Apc(Min) compound mice is 3-fold higher than in Apc(Min) mice.

Although we observe a requirement for spontaneous loss of heterozygosity of the adenomatous polyposis coli (Apc) gene to trigger tumorigenesis in Apc(Min) mice, lesions in A33(Dnmt3a);Apc(Min) mice frequently retain the wild-type Apc allele.

However, epithelia from normal mucosa and polyps of A33(Dnmt3a);Apc(Min) mice show hypermethylation-mediated transcriptional silencing of the Wnt antagonists Sfrp5, and to a lesser extent, Sfrp1 and increased nuclear beta-catenin alongside activation of the Wnt-target gene Axin2/Conductin.

Conversely, enforced Sfrp5 expression suppresses canonical Wnt-signaling more effectively in wild-type than in Apc(Min) cells.

CONCLUSIONS: Aberrant activation of the canonical Wnt pathway, either by mono-allelic Apc loss or transcriptional silencing of Sfrp5 is largely insufficient to promote polyposis, but epistatic interactions between these genetic and epigenetic events enables initiation and promotion of disease.

[MeSH-major] Adenomatous Polyposis Coli / metabolism. DNA (Cytosine-5-)-Methyltransferase / metabolism. Genes, APC. Intestinal Mucosa / metabolism. Signal Transduction. Wnt Proteins / metabolism

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(PMID = 19454286.001).

[ISSN] 1528-0012

[Journal-full-title] Gastroenterology

[ISO-abbreviation] Gastroenterology

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Gpa33 protein, mouse; 0 / Membrane Glycoproteins; 0 / Wnt Proteins; EC 2.1.1.37 / DNA (Cytosine-5-)-Methyltransferase; EC 2.1.1.37 / DNA methyltransferase 3A

   

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[Title] UbcH10 has a rate-limiting role in G1 phase but might not act in the spindle checkpoint or as part of an autonomous oscillator.

Ubiquitin-dependent proteolysis mediated by the anaphase-promoting complex/cyclosome (APC/C) ubiquitin ligase lies at the heart of the cell cycle.

The APC/C targets mitotic cyclins for destruction in mitosis and G1 phase and is then inactivated at S phase, thereby generating the alternating states of high and low cyclin-Cdk activity required for the alternation of mitosis and DNA replication.

Two key questions are how the APC/C is held in check by the spindle-assembly checkpoint to delay cells in mitosis in the presence of improperly attached chromosomes, and how the APC/C is inactivated once cells exit mitosis.

The ubiquitin-conjugating protein UbcH10 has been proposed to be crucial in the answers to both questions.

However, here we show that the behaviour of UbcH10 is inconsistent with both a crucial role in the spindle checkpoint and in inactivating the APC/C as part of an autonomous oscillator.

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(PMID = 18559889.001).

[ISSN] 0021-9533

[Journal-full-title] Journal of cell science

[ISO-abbreviation] J. Cell. Sci.

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Cyclin A; EC 6.3.2.19 / UBE2C protein, human; EC 6.3.2.19 / Ubiquitin-Conjugating Enzymes

   

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[Title] Diflunisal stabilizes familial amyloid polyneuropathy-associated transthyretin variant tetramers in serum against dissociation required for amyloidogenesis.

Transthyretin (TTR) tetramer dissociation, misfolding and misassembly are required for the process of amyloid fibril formation associated with familial amyloid polyneuropathy (FAP).

Here, we investigated the feasibility of using these molecules for the treatment of FAP utilizing serum samples from 37 FAP patients with 10 different mutations.

We demonstrated that the TTR heterotetramer structures in FAP patients serum are significantly less stable than that in normal subjects, indicating the instability of the variant TTR structure is a fundamental cause of TTR amyloidosis.

Trivalent chromium at levels obtained by oral supplementation did not stabilize TTR in a statistically significant fashion.

Importantly, diflunisal increased serum TTR stability in FAP patients beyond the level of normal controls.

[MeSH-major] Amyloid Neuropathies, Familial / metabolism. Amyloid beta-Peptides / biosynthesis. Amyloid beta-Peptides / genetics. Anti-Inflammatory Agents, Non-Steroidal / pharmacology. Diflunisal / pharmacology. Prealbumin / biosynthesis. Prealbumin / genetics

[MeSH-minor] Adult. Aged. Chromium / pharmacology. Female. Flufenamic Acid / pharmacology. Humans. Hydrogen-Ion Concentration. Iron / physiology. Male. Middle Aged. Mutation / physiology. Protein Denaturation

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(PMID = 17028027.001).

[ISSN] 0168-0102

[Journal-full-title] Neuroscience research

[ISO-abbreviation] Neurosci. Res.

[Language] eng

[Grant] United States / NIDDK NIH HHS / DK / DK046335

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] Ireland

[Chemical-registry-number] 0 / Amyloid beta-Peptides; 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Prealbumin; 0R0008Q3JB / Chromium; 60GCX7Y6BH / Flufenamic Acid; 7C546U4DEN / Diflunisal; E1UOL152H7 / Iron

   

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[Title] Mycobacterium avium ssp. paratuberculosis recombinant heat shock protein 70 interaction with different bovine antigen-presenting cells.

Abstract Heat shock proteins (Hsp) can deliver antigen into the major histocompatibility complex class I presentation pathway of antigen-presenting cells (APC), a process called cross priming, thus stimulating antigen-specific CD8+ T-cell reactions.

Hsp were shown to elicit proinflammatory responses in APC.

Both processes require interaction of Hsp with APC via specific receptors.

Characterized monocyte-derived macrophages, monocyte-derived dendritic cells (DC) and BoMac, an immortalized bovine macrophage cell line, were used to investigate the interaction of rHsp70 with different bovine APC.

Involvement of CD91 as a cellular receptor for rHsp70 was demonstrated; however, competition studies with immature DC demonstrated that other receptors exist on bovine APC.

[MeSH-major] Antigen-Presenting Cells / immunology. Bacterial Proteins / immunology. HSP70 Heat-Shock Proteins / immunology. Mycobacterium avium subsp. paratuberculosis / immunology

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(PMID = 15787741.001).

[ISSN] 0300-9475

[Journal-full-title] Scandinavian journal of immunology

[ISO-abbreviation] Scand. J. Immunol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Antigens, CD14; 0 / Bacterial Proteins; 0 / Bacterial Vaccines; 0 / HSP70 Heat-Shock Proteins; 0 / alpha-Macroglobulins

   

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[Title] A rapid and sensitive prenatal diagnosis of familial amyloidotic polyneuropathy ATTR Val30Met by mass spectrometry.

OBJECTIVE: To make a prenatal diagnosis of familial amyloidotic polyneuropathy (FAP) by mass spectrometry with the amniotic fluid.

METHODS: Amniotic-fluid samples of three non-FAP pregnant women and six amniotic-fluid samples of fetal mice whose mother was a heterozygotic FAP amyloidgenic transthyretin (ATTR) Val30Met gene carrier were collected.

CONCLUSION: Mass spectrometry analysis of the amniotic fluid might be a useful tool to make a prenatal diagnosis of FAP ATTR Val30Met.

[MeSH-major] Amyloid Neuropathies, Familial / diagnosis. Mass Spectrometry / methods. Prealbumin / analysis. Prenatal Diagnosis / methods

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(PMID = 19609897.001).

[ISSN] 1097-0223

[Journal-full-title] Prenatal diagnosis

[ISO-abbreviation] Prenat. Diagn.

[Language] eng

[Publication-type] Evaluation Studies; Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Antibodies; 0 / Prealbumin; AE28F7PNPL / Methionine; HG18B9YRS7 / Valine

   

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[Title] Achieving routine sub 30 minute door-to-balloon times in a high volume 24/7 primary angioplasty center with autonomous ambulance diagnosis and immediate catheter laboratory access.

Using autonomous ambulance diagnosis with open access to the myocardial infarction center catheter laboratory, we compared reperfusion times and clinical outcomes for the final 2 years of TL with the first 3 years of PPCI.

RESULTS: Comparison was made between TL (2002-2004, n = 185) and PPCI (2004-2007, n = 704); all times are medians in minutes (interquartile range): for TL, symptom to needle 153 (85-225), call to needle 58 (49-73), first professional contact (FPC) to needle 47 (39-63), door to needle 18 (12-30) (mortality: 7.6% at 30 days, 9.2% at 1 year); for interhospital transfer PPCI (n = 227), symptom to balloon 226 (175-350), call to balloon 135 (117-188), FPC to balloon 121 (102-166), first door-to-balloon 100 (80-142) (mortality: 7.0% at 30 days, 12.3% at 1 year); for direct-access PPCI (n = 477), symptom to balloon 142 (101-238), call to balloon 79 (70-93), FPC to balloon 69 (59-82), door to balloon 20 (16-29) (mortality: 4.6% at 30 days, 8.6% at 1 year).

With autonomous ambulance diagnosis and open access direct to the catheter laboratory, a median door-to-balloon time of <30 minutes day and night was achieved, and >95% of patients were reperfused within 1 hour.

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[ErratumIn] Am Heart J. 2010 Feb;159(2):330

(PMID = 19853705.001).

[ISSN] 1097-6744

[Journal-full-title] American heart journal

[ISO-abbreviation] Am. Heart J.

[Language] eng

[Publication-type] Comparative Study; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Fibrinolytic Agents

   

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We demonstrated that LAB induced strong TLR2-expressing APC responses in blood and spleen, HRV induced a TLR3 response in spleen, and TLR9 responses were induced by either HRV (in spleen) or LAB (in blood).

LAB and HRV have an additive effect on TLR2- and TLR9-expressing APC responses, consistent with the adjuvant effect of LAB.

LAB enhanced the IFN-gamma and IL-4 responses in serum, but it had a suppressive effect on the TLR3- and TLR9-expressing CD14- APC responses in spleen and the serum IFN-alpha response induced by HRV.

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(PMID = 19054578.001).

[ISSN] 0165-2427

[Journal-full-title] Veterinary immunology and immunopathology

[ISO-abbreviation] Vet. Immunol. Immunopathol.

[Language] ENG

[Grant] United States / NIAID NIH HHS / AI / R01 AI033561-11; United States / NIAID NIH HHS / AI / R01 AI033561; United States / NCCIH NIH HHS / AT / R21 AT002524-02; United States / NCCIH NIH HHS / AT / R21 AT002524; United States / NIAID NIH HHS / AI / AI033561-11; United States / NCCIH NIH HHS / AT / 1R21AT002524; United States / NIAID NIH HHS / AI / R01AI033561

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't

[Publication-country] Netherlands

[Chemical-registry-number] 0 / Cytokines; 0 / Toll-Like Receptors

[Other-IDs] NLM/ NIHMS89734; NLM/ PMC2653198

   

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Nowadays, patients with ulcerative colitis or familial adenomatous polyposis of the colon undergo proctocolectomy as the definitive treatment for their underlying disease.

This contribution describes the surgical indications and pathophysiological changes for the colon J-pouch and ileoanal reservoir.

In addition, explanations of the surgical techniques for both procedures are presented.

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(PMID = 18210064.001).

[ISSN] 1433-0563

[Journal-full-title] Der Urologe. Ausg. A

[ISO-abbreviation] Urologe A

[Language] ger

[Publication-type] English Abstract; Journal Article; Review

[Publication-country] Germany

[Number-of-references] 40

   

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[Title] Dietary anthocyanin-rich tart cherry extract inhibits intestinal tumorigenesis in APC(Min) mice fed suboptimal levels of sulindac.

A promising approach for cancer chemoprevention might be a combination therapy utilizing dietary phytochemicals and anticarcinogenic pharmaceuticals at a suboptimal dosage to minimize any potential adverse side effects.

Mice that were fed anthocyanin-rich extract (at any dose) in combination with sulindac had fewer tumors and a smaller total tumor burden (total tumor area per mouse) in the small intestine when compared to mice fed sulindac alone.

These results suggest that a dietary combination of tart cherry anthocyanins and sulindac is more protective against colon cancer than sulindac alone.

[MeSH-major] Anthocyanins / administration & dosage. Antineoplastic Agents / administration & dosage. Fruit / chemistry. Intestinal Neoplasms / prevention & control. Prunus / chemistry. Sulindac / administration & dosage

[MeSH-minor] Adenomatous Polyposis Coli / genetics. Animals. Diet. Female. Male. Mice. Mice, Inbred C57BL. Mice, Mutant Strains. Mutation. Plant Extracts / administration & dosage. Plant Extracts / chemistry

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(PMID = 17147414.001).

[ISSN] 0021-8561

[Journal-full-title] Journal of agricultural and food chemistry

[ISO-abbreviation] J. Agric. Food Chem.

[Language] eng

[Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.

[Publication-country] United States

[Chemical-registry-number] 0 / Anthocyanins; 0 / Antineoplastic Agents; 0 / Plant Extracts; 184SNS8VUH / Sulindac

   

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[Title] Immunization in familial amyloidotic polyneuropathy: counteracting deposition by immunization with a Y78F TTR mutant.

The mechanism of amyloid formation in familial amyloidotic polyneuropathy (FAP), a hereditary disorder associated with mutant transthyretin (TTR), is still unknown.

To test whether TTR deposition in FAP can be counteracted by antibodies for cryptic epitopes, we immunized with TTR Y78F, transgenic mice carrying the most common FAP-associated TTR mutant--V30M (transthyretin mutant with methionine replacing valine at position 30)--at selected ages that present normally with either nonfibrillar or TTR amyloid deposition.

Compared to age-matched control nonimmunized mice, Y78F-immunized mice had a significant reduction in TTR deposition usually found in this strain, in particular in stomach and intestine; by contrast, animals immunized with V30M did not show differences in deposition in comparison with nonimmunized mice.

Immunohistochemical analyses of tissues revealed that immunization with Y78F lead to infiltration by lymphocytes and macrophages at common deposition sites, but not in tissues such as liver, choroid plexus, and Langerhans islets, in which TTR is produced.

Therefore, TTR immunization with selected TTR mutants has potential application in immune therapy for FAP.

[MeSH-major] Amyloid Neuropathies, Familial / prevention & control. Mutation. Prealbumin / administration & dosage

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(PMID = 16357867.001).

[ISSN] 0023-6837

[Journal-full-title] Laboratory investigation; a journal of technical methods and pathology

[ISO-abbreviation] Lab. Invest.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Prealbumin

   

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These differences are not mediated by a different interaction with RhoGDIs.

[MeSH-major] Cell Movement. Neoplasm Invasiveness. Pancreatic Neoplasms / pathology. rho GTP-Binding Proteins / metabolism. rhoA GTP-Binding Protein / metabolism

[MeSH-minor] Cell Line, Tumor. Deep Brain Stimulation. Humans. Protein Isoforms / chemistry. Protein Isoforms / genetics. Protein Isoforms / metabolism. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. rap GTP-Binding Proteins / chemistry. rap GTP-Binding Proteins / genetics. rap GTP-Binding Proteins / metabolism

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(PMID = 19642867.001).

[ISSN] 1437-4315

[Journal-full-title] Biological chemistry

[ISO-abbreviation] Biol. Chem.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Germany

[Chemical-registry-number] 0 / Protein Isoforms; 0 / RHOC protein, human; 0 / RNA, Messenger; EC 3.6.5.2 / rap GTP-Binding Proteins; EC 3.6.5.2 / rho GTP-Binding Proteins; EC 3.6.5.2 / rhoA GTP-Binding Protein

   

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[Title] Activation of EDTA-resistant gelatinases in malignant human tumors.

Among the many proteases associated with human cancer, seprase or fibroblast activation protein alpha, a type II transmembrane glycoprotein, has two types of EDTA-resistant protease activities: dipeptidyl peptidase and a 170-kDa gelatinase activity.

To test if activation of gelatinases associated with seprase could be involved in malignant tumors, we used a mammalian expression system to generate a soluble recombinant seprase (r-seprase).

Proteins purified from experimental xenografts and malignant tumors using antibody- or lectin-affinity columns in the presence of 5 mmol/L EDTA were assayed for seprase activation in vivo.

Seprase expression and activation occur most prevalently in ovarian carcinoma but were also detected in four other malignant tumor types, including adenocarcinoma of the colon and stomach, invasive ductal carcinoma of the breast, and malignant melanoma.

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(PMID = 17047060.001).

[ISSN] 0008-5472

[Journal-full-title] Cancer research

[ISO-abbreviation] Cancer Res.

[Language] ENG

[Grant] United States / NCI NIH HHS / CA / R01 CA039077; United States / NIBIB NIH HHS / EB / R01EB002065; United States / NIBIB NIH HHS / EB / R01 EB002065; United States / NCRR NIH HHS / RR / M01 RR010710; United States / NCRR NIH HHS / RR / M01RR10710; United States / NCI NIH HHS / CA / R01CA0039077

[Publication-type] Journal Article; Research Support, N.I.H., Extramural

[Publication-country] United States

[Chemical-registry-number] 0 / Membrane Proteins; 0 / Recombinant Proteins; 9G34HU7RV0 / Edetic Acid; EC 3.4.14.- / Dipeptidyl-Peptidases and Tripeptidyl-Peptidases; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.- / fibroblast activation protein alpha; EC 3.4.24.- / Gelatinases

[Other-IDs] NLM/ NIHMS11890; NLM/ PMC1626657