Relevant bibliographies by topics / APC

Academic literature on the topic 'APC'

Author: Grafiati
Published: 4 June 2021
Last updated: 25 May 2024

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Journal articles on the topic "APC"

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Yorio, Jeffrey Thomas, Patricia S. Fox, Richard Wayne Joseph, Roland Bassett, and Michael A. Davies. "Assessment of absolute lymphocyte count (ALC) as a predictor of progression-free survival (PFS) and overall response rate (ORR) in metastatic melanoma (MM) patients (pts) treated with high-dose interleukin-2 (HD IL-2)." Journal of Clinical Oncology 31, no. 15_suppl (May 20, 2013): 9096. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.9096.

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9096 Background: HD IL-2 is an approved immunotherapy that can achieve durable cures in MM pts. Due to toxicity and low ORR, identification of predictors of clinical benefit would enhance pt selection and outcomes with HD IL-2. Recent research identified a positive correlation for ALC ≥ 1000 (either at baseline or at dose 3) with OS among MM pts treated with the immunotherapy agent ipilimumab. We tested the hypothesis that ALC (≥ 1000) or other hematological parameters correlates with clinical benefit from HD IL2. Methods: Results of hematologic testing in patients (n=98) treated with HD IL2 at MD Anderson Cancer Center were collected, including absolute levels of neutrophils (ANC), lymphocytes (ALC), monocytes (AMC), eosinophils (AEC), and platelets (APC) at baseline, after cycle 1 (C1), and after cycle 2 (C2) of HD IL-2; changes in each parameter for each interval were also calculated. Hematologic values were assessed as categorical (for ALC, ≥ 1000 Yes/No; other parameters, above upper limit of normal [ULN] Yes/No) and continuous variables. Associations between these parameters and PFS and ORR were analyzed. Results: ALC was≥ 1000 in 75 pts (76%) at baseline, in 81 (83%) after C1, and in 80 of 86 pts (93%) after completion of C2 of HD IL-2. PFS was not significantly associated with ALC ≥ 1000 at baseline (HR 0.69, p=0.13), after C1 (HR 1.32, p=0.33), or after C2 (HR 1.01, p=0.98). ALC ≥ 1000 at each timepoint was not significantly associated with ORR or OS. There was no significant difference in the change in ALC with HD IL2 treatment among responders versus non-responders. Among baseline hematological factors, APC > ULN was significantly associated with PFS (p=0.001), but it was rare (2/98 patients). Exploratory analyses identified significantly shorter PFS for patients with baseline APC > 300 (11%, HR 2.75, p=0.002). Analysis of hematologic factors as continuous values identified significant associations with PFS for AMC (HR 2.42, p=0.03) and AEC (HR 1.73, p=0.009) after C2. Conclusions: ALC ≥ 1000 did not correlate with PFS, ORR, or OS with HD IL-2 therapy in this cohort of metastatic melanoma pts.
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Alali, Muayad, Cassandra Prather, Lara A. Danziger-Isakov, Michelle L. Kussin, Malak Khalifeh, Nashwan Al Othman, and Allison H. Bartlett. "Absolute Monocyte Count as Early and Safe Marker for Antibiotic Cessation in Febrile Neutropenia Without Etiology in Pediatric Oncology Patients." Journal of Pediatric Hematology/Oncology 45, no. 6 (June 26, 2023): e702-e709. http://dx.doi.org/10.1097/mph.0000000000002696.

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Background: There is no practice standard regarding antibiotic duration in children with cancer and unexplained febrile neutropenia (FN). We hypothesized that absolute monocyte count (AMC) and absolute phagocyte count (APC= ANC + AMC + bands) are more sensitive, earlier, and safe markers of antibiotic cessation compared with absolute neutrophil count (ANC). Methods: A retrospective review of FN episodes (FNEs) in pediatric oncology patients was conducted between 2009 and 2016. Included patients were afebrile for 24 hours and without an identified infectious source at antibiotic cessation. Primary endpoints, including recurrent fever, readmission, bloodstream infection, microbiologically documented infection, and adverse outcomes, were assessed 10 days after antibiotic cessation and compared among different bone marrow recovery parameters (ANC, AMC, APC). Secondary endpoints included length of FN stay, antibiotic-free days, and cost. Results: Three hundred ninety-one FNEs in 235 patients were included. Three groups were compared based on ANC (cells/μL) at the time of antibiotic cessation: < 200 in 102 (26%), 200 to 500 in 111 (28%), and >500 in 178 (46%). No statistically significant differences in primary endpoints were identified among the 3 ANC groups; however, a trend toward unfavorable outcomes in the ANC ≤200 cells/μL group compared with the ANC >200 cells/μL was observed. Primary endpoints based on AMC >100 cells/μL at the time of antibiotic cessation showed statistically significant favorable outcomes compared AMC ≤100 cells/μL (80%, 88%, 90%, 89%, and 93% risk reduction in recurrent fever, readmission, new bloodstream infection, new microbiologically documented infection, and adverse events, respectively). Similar favorable results were seen when APC >300 cells/μL was used as a threshold for antibiotic cessation. The median length of stay for FN if discharged when AMC >100 cells/μL was 3 days shorter and associated with fewer unfavorable outcomes, thus resulting in fewer hospital days, fewer antibiotic days, and decreased cost. Conclusion: Our results suggest that AMC >100 cells/μL (regardless of ANC) or APC >300 cells/μL may be safe thresholds for empiric antibiotic cessation and result in reduced unfavorable clinical outcomes within 10 days postdischarge, reduced antibiotic days of therapy and reduced health care costs. Further prospective studies are needed to validate AMC as an accurate surrogate marker for antibiotic cessation in FNEs in children with cancer.
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Alali, Muayad. "#32 Pediatric Febrile Neutropenia with Low Risk of Systemic Infection: When Is It Safe to Stop Antibiotics?" Journal of the Pediatric Infectious Diseases Society 11, Supplement_1 (June 14, 2022): S1—S2. http://dx.doi.org/10.1093/jpids/piac041.003.

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Abstract Background There are no standard practices about antibiotics duration in unexplained stable febrile neutropenia (FN). Absolute neutrophile count (ANC) recovery has been used clinically to represent bone marrow recovery (BMR) but data about safe ANC threshold for antibiotic cessation (AC) and discharge is still unknown. Other markers should be considered. We hypothesized that absolute monocyte count (AMC), and absolute phagocyte count (APC= ANC + AMC+ bands) are more sensitive, and an earlier safe marker of AC compared with ANC Method A retrospective review was performed for FN episodes (FNEs) at a single institution (2009 and 2016) in pediatric oncology patients. Eligible FNEs who were a febrile for 24 hours and had no documented infectious source identified at AC and did not receive chemotherapy 10 days following AC. Ten-day post-AC primary end points (recurrent fever, readmission, blood stream infection BSI, microbiology documented infection MDI, and adverse outcomes) were assessed and compared among different BMR parameters (ANC vs AMC vs APC). Secondary end point compares length of stay, antibiotics free days and cost-effectiveness among different BMR markers. Results Eligible FNEs were 391 at time of AC in 235 patients. Three groups were compared based on ANC (cells/μL) at the time of AC : &lt; 200 in 102 (26%), 200-500 in 111 (28%), and &gt;500 /uL in 178 (46%) with an overall ten-day recurrent fever rate 7.4% (29/391). No significant differences in primary end point outcomes rates were identified among 3 ANC groups (11.7%,, 6.3% and 5.6% respectively, P=0.06) and readmission (10%,4.5%, 4%, respectively; P=0.05)(Table 1), however, there is a trend toward unfavorable outcomes in ANC&lt; 200 group compared with ANC&gt;200. In subset analysis in group of ANC&gt;200, favorable outcomes in (ANC&gt;200 with AMC&gt;100) than in the (ANC&gt;200 with AMC&lt;100) group. There was significant risk reduction in primary end points (75% in recurrent fever, 85% readmission, 87% in BSI, 88% in MDI and 87% in adverse events in (ANC&gt;200 with AMC&gt;100) compared with (ANC&gt;200 with AMC&lt;100/uL) group. More importantly, primary end points based on AMC&gt;100 /uL as BMR for AC, regardless ANC values, showed significant favorable outcomes compared AMC&lt;100 /uL. There is 80%, 88, 90%, 89%, and 93% risk reduction in end points recurrent fever, readmission BSI, MDI, and adverse outcomes respectively. Similar favorable results were seen when APC&gt;300 used as threshold for AC (Table 2, 3). Median of length of stay of FN was 3 days shorter using AMC &gt;100/uL for BMR compared with any threshold of ANC (P&lt; 0.01) and decrease overall FN cost stay (P&lt; 0.01). Conclusion Our results suggest that AMC &gt; 100 /uL regardless of ANC/uL, or APC&gt; 300 or ANC&gt;200 with AMC&gt;100/uL all are a safe thresholds for empiric AC. Further prospective studies are needed to validate AMC as accurate surrogate for AC in FN children with cancer.
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Fearnhead, N. S. "The ABC of APC." Human Molecular Genetics 10, no. 7 (April 1, 2001): 721–33. http://dx.doi.org/10.1093/hmg/10.7.721.

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Booth, JL, ES Duggan, VI Patel, J. Metcalf, M. Langer, KM Coggeshall, and A. Braun. "ID: 106: ALVEOLAR ESCAPE BY BACILLUS ANTHRACIS SPORES DOES NOT REQUIRE A CARRIER CELL AND IS NOT ALTERED BY LETHAL TOXIN." Journal of Investigative Medicine 64, no. 4 (March 22, 2016): 960.2–961. http://dx.doi.org/10.1136/jim-2016-000120.101.

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RationaleThe lung is the entry site for Bacillus anthracis in inhalation anthrax, the most deadly form of the disease. B. anthracis spores must escape from the alveolus, pass to the regional lymph nodes, germinate and enter the circulatory system as vegetative bacteria to cause systemic disease. Of the resident lung cells, three have been reported to take up B. anthracis spores: the antigen presenting cells (APC) alveolar macrophages and dendritic cells, and alveolar epithelial cells (AEC). Also, B. anthracis produces the exotoxins lethal factor and protective antigen (PA) which combine to form lethal toxin (LT), a metalloproteinase important in pathogenicity. The roles of carrier cells and the effects of B. anthracis toxins in escape of spores from the alveolus are unclear, especially in humans.MethodsWe employed a human lung organ culture model and a human A549 alveolar epithelial cell culture model, along with fluorescent confocal imaging to quantitate spore partitioning between APC and AEC, and the effects of B. anthracis LT and PA on this process. Cell types were distinguished by positive staining for HLA-DR (APC) and cytokeratin (AEC).ResultsWe found that spores progressed through the lung slice over time, and that spore movement was not dependent on cell internalization. Both free and cell-associated spores moved through slices between 2 and 48 hrs of incubation. However, partitioning of spores between AEC, APC, and the extracellular space did not significantly change over this time. After 2 hrs, 4.7% of spores were in APC; 13.8% in AEC; and 81.5% were not cell-associated. By 48 hrs, 2.9% were in APC; 12.7% were in AEC; and 84.4% were not cell-associated. Spores also internalized in a non-uniform manner, with more variable spore internalization into AEC than into APC. At all incubation times, the majority of cell-associated spores were in AEC, not in APC. PA and LT did not affect transit of the spores through the lung tissue or the distribution of spores into AEC and APC. In A549 cells, spore internalization increased significantly after 24 hrs incubation. However, there was no statistically consistent effects of PA or LT on spore internalization in A549 cells.ConclusionsOverall, our results support a “Jailbreak”-like model of spore escape from the alveolus that involves transient passage of spores, although this occurs through intact AEC. However, subsequent transport of spores by APC from the lung to the lymph nodes may occur.
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Bell, Stephen A. J. "ANPC member profile for APC." Australasian Plant Conservation: journal of the Australian Network for Plant Conservation 29, no. 1 (August 2020): 38–39. http://dx.doi.org/10.5962/p.373844.

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Chang, Joanne T., Jihyoun Jeon, Hutcha Sriplung, Seesai Yeesoonsang, Surichai Bilheem, Laura Rozek, Imjai Chitapanarux, et al. "Temporal Trends and Geographic Patterns of Lung Cancer Incidence by Histology in Thailand, 1990 to 2014." Journal of Global Oncology, no. 4 (December 2018): JGO.18.00013. http://dx.doi.org/10.1200/jgo.18.00013.

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Purpose Lung cancer is one of the most common cancers worldwide and in Thailand. We characterize and forecast region-specific patterns of lung cancer incidence by histology and sex. Methods We analyzed lung cancer incidence trends in Thailand by histology (adenocarcinoma [AdC]; squamous cell carcinoma [SCC]; and large-cell, small-cell, and other carcinomas) from 1990 to 2014 in four cancer registries in three regions (north, Chiang Mai Province and Lampang Province; northeast: Khon Kaen Province; south: Songkhla Province). Annual percent change (APC) was calculated to quantify the incidence rate trends using joinpoint regression. Age-period-cohort models were used to examine the temporal trends of AdC and SCC by age, calendar year, and birth cohort. We projected the incidence of AdC and SCC up to 2030 using three independent approaches: joinpoint, age-period-cohort, and Nordpred models. Results AdC incidence significantly increased from 1990 to 2012 in Chiang Mai males (APC, 1.3%), Songkhla males from 2004 to 2014 (APC, 2.5%), Songkhla females from 1990 to 2014 (APC, 5.9%), and Khon Kaen females from 2005 to 2014 (APC, 3.1%). Conversely, SCC incidence significantly decreased from 1990 to 2012 in Chiang Mai males and females (APC, −1.2% and −4.8%, respectively), Lampang males and females from 1993 to 2014 (APC, −5.4% and −5.2%, respectively), and Songkhla females from 1990 to 2014 (APC, −2.1%). In general, trends of AdC and SCC correlated more with birth cohort than with calendar year. Three projection models suggested that incidence rates of AdC in Songkhla may continue to increase until 2030. Conclusion Temporal trends of lung cancer by histology varied among regions in Thailand. Reduction of lung cancer incidence in Thailand likely will require prevention strategies tailored to each specific region.
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Abboud, Yazan, Madison Fraser, Imran Qureshi, and Kaveh Hajifathalian. "Early-Onset Colorectal Cancer: Are Neuroendocrine Tumors or Adenocarcinomas the Culprit? Analysis of the Largest U.S. Cancer Incidence Database, 2001–2020." Journal of Clinical Medicine 13, no. 4 (February 15, 2024): 1098. http://dx.doi.org/10.3390/jcm13041098.

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(1) Background: While prior data showed an increasing incidence of colorectal cancer (CRC) in young adults, the contribution of adenocarcinoma (ADC) and neuroendocrine tumors (NETs) to this trend is not well studied. Therefore, we conducted a comparative analysis of the incidence rates and time trends of colorectal ADC and NETs in young adults (aged 24–54) using the United States Cancer Statistics (USCS) database. (2) Methods: Age-adjusted CRC incidence rates between 2001 and 2020 were calculated and categorized by sex, histopathology, and stage at diagnosis. Annual percentage change (APC) and average APC (AAPC) were computed via joinpoint regression utilizing weighted Bayesian information criteria to generate the simplest trend. Pairwise comparative analysis of ADC and NETs was conducted using tests of identicalness and parallelism. (3) Results: In this study, 514,875 patients were diagnosed with early-onset-CRC between 2001 and 2020 (54.8% men). While CRC incidence was significantly increased, including both ADC (448,670 patients) and NETs (36,205 patients), a significantly greater increase was seen for NETs (AAPC = 2.65) compared to ADC (AAPC = 0.91), with AAPC difference = 1.73 (p = 0.01) and non-identical non-parallel trends (p-values < 0.001). This was most notable in males (AAPC difference = 1.81, p = 0.03) and for early-stage tumors (AAPC difference = 3.56, p < 0.001). (4) Conclusions: Our study, covering ~98% of the U.S. population provides the first comparative analysis of early-onset CRC histopathological subtypes, showing that the rate of increase of NETs in young adults is much greater than that of ADC. Given that patients with NETs with malignant behavior can experience significant mortality, our findings are importance, highlighting the rapidly increasing NET incidence in young adults and encouraging early screening that can improve outcomes.
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Omar, Mohd Shah Fazly, Syirah Nazirah Mohd Tajuddin, Sabariah Md Noor, and Zainina Seman. "Full Blood Count Parameters in COVID-19 Patients With Disease Severity, Patient Outcome and Vaccination Status." LAB MEDICINE AND RESEARCH IN PATHOLOGY 19, s16 (December 16, 2023): 16–23. http://dx.doi.org/10.47836/mjmhs.19.s16.4.

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Introduction: A link between full blood count (FBC) parameters with the severity and prognosis of individuals with coronavirus disease 2019 (COVID-19) infection is shown. We aim to identify changes in FBC parameters depending on patients’ characteristics, the severity of the disease and vaccination status. Methods: A cross-sectional retrospective laboratory study is done on 208 respondents who were selected from February 2021 to December 2022 in the Pathology Department of the Tuanku Ja’afar Hospital in Negeri Sembilan. All patients are confirmed COVID-19 positive by real-time reverse transcriptase-polymerase chain reaction (RT-PCR) of pharyngeal and nasal swab specimens. Patients are further classified based on their COVID clinical stages, severity, vaccination status and outcome. The statistical data are analysed using IBM SPSS version 27. Results: Severe patients have significantly lower absolute lymphocyte count (ALC), absolute monocyte count (AMC), absolute eosinophil count (AEC) and absolute basophil count (ABC) but higher mean platelet volume (MPV), absolute neutrophil count (ANC), neutrophil to lymphocyte ratio (NLR) and immature granulocytes (IG) compared to non-severe patients (p < 0.05). Similar findings are seen among non-survivors (p < 0.05). Fully vaccinated patients have significantly lower NLR and MPV but higher ALC, AMC, AEC and ABC than unvaccinated or partially vaccinated patients (p < 0.05). Conclusion: Selected FBC parameters of COVID-19 patients (platelets, ANC, NLR, MPV, ALC, AMC, AEC, and ABC) are significantly different depending on patients’ severity, outcome and vaccination status. These results might give a clear insight for clinicians to anticipate the severity and outcome of patients based on the patient’s FBC parameters.
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Ormiston, Cameron K., Wayne R. Lawrence, Saanie Sulley, Meredith S. Shiels, Emily A. Haozous, Catherine M. Pichardo, Erica S. Stephens, et al. "Trends in Adolescent Suicide by Method in the US, 1999-2020." JAMA Network Open 7, no. 3 (March 29, 2024): e244427. http://dx.doi.org/10.1001/jamanetworkopen.2024.4427.

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ImportanceAdolescent suicide in the US is a major public health problem, yet temporal trends in suicide methods by demographics are understudied.ObjectiveTo examine national trends in suicide mortality by method (firearm, poisoning, hanging and asphyxiation, and all other means) from 1999 to 2020 by demographic characteristics.Design, Setting, and ParticipantsThis serial cross-sectional study used national death certificate data of adolescent (aged 10-19 years) suicide decedents compiled by the National Center for Health Statistics from January 1, 1999, to December 31, 2020. Data analysis was performed from April 1, 2023, to July 9, 2023.ExposuresAge, sex, and race and ethnicity.Main Outcomes and MeasuresTrends in age-standardized mortality rates and average annual percent change (AAPC) in rates were estimated by age, sex, and race and ethnicity for each suicide method.ResultsThis study assessed data from 47 217 adolescent suicide decedents. From 1999 to 2020, suicide by firearm (AAPC, 1.0; 95% CI, 0.1-1.9), poisoning (AAPC, 2.7; 95% CI, 1.0-4.4), hanging and asphyxiation (AAPC, 2.4; 95% CI, 0.2-4.6), and other means (AAPC, 2.9; 95% CI, 1.2-4.6) increased. Rapidly increasing rates were observed among female adolescents for poisoning (AAPC, 4.5; 95% CI, 2.3-6.7) and hanging and asphyxiation (AAPC, 5.9; 95% CI, 5.0-6.8) suicides. From 2007 to 2020, firearm suicides sharply increased among female (annual percent change [APC], 7.8; 95% CI, 6.0-9.5) and male (APC, 5.3; 95% CI, 4.3-6.3) adolescents. Firearm suicide rates increased among Black adolescents from 2012 to 2020 (APC, 14.5; 95% CI, 9.7-19.5), Asian and Pacific Islander adolescents from 2008 to 2020 (APC, 12.0; 95% CI, 9.7-14.5), American Indian and Alaska Native adolescents from 2014 to 2020 (APC, 10.6; 95% CI, 2.6-19.3), and Hispanic or Latino adolescents from 2011 to 2020 (APC, 10.2; 95% CI, 6.3-13.8). During the study period, Black adolescents had the highest average increase in hanging and asphyxiation suicides (AAPC, 4.2; 95% CI, 3.2-5.2). From 2011 to 2020, poisoning suicide deaths increased (APC, 12.6; 95% CI, 8.5-16.7) among female adolescents.Conclusions and RelevanceSuicide rates increased across all methods from 1999 to 2020. Differences were noted by sex, age, and race and ethnicity. Increasing suicide rates among racial and ethnic minoritized youth are especially concerning, and effective prevention strategies are urgently needed.
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Dissertations / Theses on the topic "APC"

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Cuddihy, Jane. "The non-Wnt functions of APC : unravelling the link between APC and apoptosis." Thesis, University of Dundee, 2016. https://discovery.dundee.ac.uk/en/studentTheses/bfb0d6ce-149b-4152-a591-943d61e2c714.

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Colorectal cancer (CRC) is the second most common cause of cancer-related death in the UK and Western world. More than 90% of sporadic CRCs harbour mutations in the multi-functional tumour suppressor gene Adenomatous polyposis coli (Apc). The most commonly studied function of APC is its role as a scaffold for the β-catenin destruction complex involved in Wnt signalling. However, APC binds many other proteins. For example, it directly binds to and stabilises microtubules and actin. These non-Wnt related functions of APC are poorly understood. My PhD examines non-Wnt functions of APC. To this end, I created degron-tagged APC in DT40 cells that allowed for the rapid, conditional degradation of endogenous APC. The aim was to identify the immediate effects on cellular processes. Then, to identify the contribution of different APC domains by measuring the ability to rescue any defects when reintroducing fragments of APC. However, creation of these degron-tagged Apc knock-in cell lines resulted in hypomorphic phenotypes and auxin-associated off-target effects. Nonetheless, I compared the response of APChigh, APClow, and APCminimal cells to DNA damaging agents and Taxol® but found no significant differences. Subsequently, I focused on the relationship between APC and apoptosis. Previous observations suggested that deficiency in Apc rendered cells less sensitive to low doses of Taxol®. However, Apc deficient cells were more readily killed when Taxol® was combined with the Bcl-2 inhibitor, ABT-737. One possible explanation is the increase in Bcl-2 protein upon Apc depletion. However, I found that ABT-737, Taxol® and Apc depletion each cause activation of the unfolded protein response. This suggests that these treatments elicit a stress response that can stimulate apoptosis. Moreover, the same treatments also cause changes in mitochondria. Importantly, all of these effects do not require an increase in the β-catenin protein. Together, my data reveal novel links between APC and apoptosis that could be exploited clinically.
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Rauh, Nadine. "Regulation des APC/C Inhibitors ERP1." Diss., lmu, 2006. http://nbn-resolving.de/urn:nbn:de:bvb:19-52598.

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McCaffery, Dennis. "The role of Apc in medulloblastoma." Thesis, University of Edinburgh, 2008. http://hdl.handle.net/1842/2693.

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Medulloblastomas represent the most frequent malignant brain tumour in children, and are thought to develop in the posterior fossa of the cerebellum. Some patients with medulloblastomas have a deficiency in the tumour suppressor gene Apc (Turcot’s syndrome). Although the majority of medulloblastomas arise sporadically, people with Apc mutations are 92 times more likely to develop medulloblastomas. Apc encodes a very large protein known to function as a regulator of the Wnt signalling pathway. Activation of the canonical Wnt pathway leads to the stabilisation of beta-catenin. In response to Wnt signals, beta-catenin translocates to the nucleus where it interacts with the LEF/TCF family of transcription factors to activate transcription of target genes such as c-myc and cyclinD1. Mutations of Apc that cause an increase in beta-catenin are found to be tumourgenic, whereas other mutations are not. Therefore it is thought that the main tumour suppression function of Apc is in its ability to destabilise and hence reduce cytoplasmic beta-catenin. The central hypothesis of this thesis is that the loss of Apc can lead to the development of medulloblastoma. Work from other groups has reported activation of Wnt signalling in a proportion of primary medulloblastomas. We undertook a study to assess this by using the cre-loxP recombination system to mutate Apc in a temporal and spatial manner. This approach is necessary as Apc has many functions in development and Apc mutant mice (Apcmin) do not develop past embryonic day 6.5 (E6.5). To date, there are no known cre-strains available to mutate Apc specifically in the cerebellum at early postnatal stages, so we combined the creloxP method with an avian retrovirus mediated method for tissue specific gene delivery (RCAS/tv-a system), in an attempt to create a strain of mice which carried the genotype Ntv-a +;ApcLoxP/LoxP. This would allow us to infect an RCAS-cre virus directly into the hindbrain at postnatal day 4 (P4). However subsequent genotyping of these animals showed that none carried the desired genotype of Ntv-a +;ApcLoxP/LoxP, making it impossible for both copies of Apc to be mutated in a mouse most likely because both the Ntv-a and Apc transgenes were located on the same chromosome. Consistent with this, out of a total of 265 mice none were found to have the Ntv-a +;ApcLoxP/LoxP genotype. We then adopted an alternative method for mutating Apc by infecting ApcLoxP/LoxP mice directly with an AdCre virus. PCR analysis showed that Apc was mutated, however the AdCre virus did not infect cells of the cerebellum, and instead only infected the choroid plexus. In these animals, 7 of 94 (7%) developed hydrocephalus indicating that losing Apc in the choroid plexus may promote hydrocephalus. Finally, to address the role of Apc in normal hindbrain development, we crossed our ApcLoxP/LoxP mice to an En1cre strain which caused mutation in Apc from E8.5 in the midhindbrain region. The resulting En1cre+;ApcLoxP/LoxP mutants displayed hydrocephalus in all ventricles and an in-growth of mesenchyme tissue at the mid-hindbrain border, closely associated with a tumour-like area of cells showing activated Wnt signalling. No mice were found to live past E18.5. In conclusion, the role of Apc in medulloblastoma remains unclear. Future studies could use a different technique to mutate Apc such as crossing ApcLoxP/LoxP mice to the new nestin-creER strain and inducting cre with administration of tamoxifen.
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Menéndez, Vilà Mireia. "Variants del gen APC i càncer colorectal." Doctoral thesis, Universitat de Barcelona, 2007. http://hdl.handle.net/10803/1885.

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Les mutacions germinals d'elevada penetrància del gen APC que originen una proteïna truncada són les responsables de la majoria de casos de poliposi, mentre que les variants missense, que canvien un aminoàcid de la proteïna, es detecten en una minoria dels casos. S'han identificat diverses variants missense en el gen APC, però el seu potencial patogènic és encara motiu de controvèrsia, el què limita la utilitat de la seva detecció en el consell genètic. L'estudi de la presència de les variants en la població control i en les diferents poblacions de càncer colorectal (CCR) esporàdic i hereditari, juntament amb la realització d'anàlisis funcionals, podrien ajudar a conèixer l'impacte de les variants del gen APC en el desenvolupament del CCR. El nostre objectiu és determinar el significat funcional de les variants identificades en el gen APC en pacients afectes de poliposi adenomatosa familiar en relació al risc de desenvolupar CCR tant esporàdic com hereditari.

L'anàlisi molecular de la regió codificant del gen APC realitzat en 138 famílies amb poliposi adenomatosa familiar clàssica (n= 98) i poliposi adenomatosa familiar atenuada (n= 40) ha permès la identificació de deu variants missense del gen APC: G101E, K957N, N1026S, L1129S, I1307K, E1317Q, D1822V, A2274V, G2502S i P2681L. En el nostre estudi s'han caracteritzat amb diferent profunditat set d'aquestes deu variants: G101E, N1026S, L1129S, D1822V, A2274V, G2502S i P2681L. La variant APC G101E, identificada en una família de poliposi clàssica, no s'associa a la malaltia ni sembla tenir cap funció modificadora del fenotip de poliposi. L'efecte biològic de les variants APC A2274V i APC P2681L, identificades en dues famílies de poliposi, és encara desconegut. La variant APC G2502S és un polimorfisme que no sembla tenir rellevància clínica. La variant APC L1129S, identificada en dues famílies de poliposi, no altera la interacció de la proteïna APC 4x15 amb la beta-catenina. La variant APC D1822V és un polimorfisme que incrementa el risc de desenvolupar CCR en pacients amb història prèvia d'adenomes i no s'associa amb la història familiar de CCR. La variant APC N1026S, que està present de forma exclusiva en una família de poliposi adenomatosa familiar atenuada, disminueix la unió d'APC amb beta-catenina i activa moderadament la transcripció mitjançada pel complex beta-catenina/Tcf-4. Aquests resultats indiquen que la variant APC N1026S és patogènica i és la mutació responsable del desenvolupament de la poliposi atenuada a la família on es va identificar.
La caracterització funcional de les variants del gen APC és de gran importància per conèixer la seva contribució en el desenvolupament de la poliposi i facilitar l'assessorament genètic.
Truncating germline mutations in the APC gene are responsible for the majority of Familial Adenomatous Polyposis (FAP) cases, while in a minority of cases missense mutations, leading to single amino acid changes, are detected. Germline missense variants in the APC gene have been reported although their contribution to FAP is controversial, limiting their use in genetic counseling. The aim of this thesis is to determine the functional relevance of the variants identified in the APC gene in FAP patients in order to establish its pathogenicity.

The molecular analysis of the APC gene was performed in 138 classical (n= 98) and attenuated (n= 40) FAP families and allowed the identification of ten missense variants. In this thesis, seven out of these ten APC variants have been characterised: G101E, N1026S, L1129S, D1822V, A2274V, G2502S and P2681L. The APC G101E variant, identified in a classical FAP family, is not associated with the disease. The biological effect of APC A2274V and APC P2681L variants, identified in two FAP families, remains unknown. The APC G2502S variant is a polymorphism without clinical relevance. The APC L1129S variant, identified in two FAP families, does not modify the interaction of the APC 4x15 protein with beta-catenin. The APC D1822V variant is a polymorphism associated with an increased risk of adenoma transformation and does not associate with family history of colorectal cancer. The APC N1026S variant, identified for the first time in an attenuated FAP family, diminishes beta-catenin binding to APC and moderately activates beta-catenin/Tcf-4-mediated transcription. These findings strongly support a pathogenic role of the APC N1026S variant in the AFAP phenotype.
In summary, functional characterization of APC variants is crucial to elucidate their contribution to FAP and improve genetic counseling.
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Ivaniutsin, Uladzislau. "The role of Apc in cortical development." Thesis, University of Edinburgh, 2008. http://hdl.handle.net/1842/29174.

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This thesis is devoted to examining the role of Apc protein in the development of the mouse telencephalon. As Apc-/- embryos die at gastrulation, a conditional knock-out approach was used to examine Apc’s role in cortical development. Mutant mice with conditional (flowed) alleles of Apc were crossed to a strain in which Cre expression is driven by the Emx1 promoter (Emx1Cre), allowing specific deletion of Apc in the dorsal telencephalon. The current work presents a detailed description and possible explanations of Apc’s functions in the developing cerebral cortex. Conditional knock-out of Apc in the cortex led to severe developmental defects in this region, showing that Apc is required for normal development of the cerebral cortex. The deletion of Apc leads to over-activation of the canonical Wnt pathway and disregulation of PCP Wnt pathway. I examined the expression of regional markers in the residual dorsal telencephalon in conditional Apc mutant embryos. Expression of Foxg1 is lost, showing that the mutant dorsal telencephalon loses telencephalic identify from E12.5. My data show that Apc is important for proper patterning of the cortex probably mostly by antagonizing the canonical Wnt pathway. Measurement of cell-cycle times revealed that in the absence of Apc, S-phase and cell cycle length remains similar to controls. Deletion of Apc in the dorsal telencephalon leads to defects in maintenance of the size of the progenitor pool and regulation of apoptosis. The conditional Apc deletion has a pleiotropic effect on cortical development. Developmental defects found include disregulation of Wnt signalling, loss of cell polarity, adhesion defects, cell identify defects, and disregulation of apoptosis. Assignment of these defects to particular functions of Apc is not completely clear yet.
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Naughton, Catherine. "Analysing Apc function in the mammary gland." Thesis, University of Edinburgh, 2003. http://hdl.handle.net/1842/23133.

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Tickenbrock, Lara. "Das Tumorsuppressor-Protein APC strukturelle und biochemische Aspekte /." [S.l.] : [s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=966017064.

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Cullingworth, J. "Tumour suppression mediated through DPC4, P53 and APC." Thesis, University of Edinburgh, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.649002.

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Mutations in the tumour suppressor genes SMAD4 (or DPC4, deleted in pancreatic cancer locus 4), APC (adenomatous polyposis coli) and p53 have been implicated in pancreatic cancer in humans. This thesis firstly documents the in vivo effects of mutations in these genes singly and in combination through spontaneous and carcinogen-induced murine models of pancreatic tumourigenesis. Second, it examines the in vitro effects of TGF-β signalling, of which Smad4 is the central mediator, on murine primary cultured pancreatic acinar cells. Previously p53-/- ApcMin/+ mice have been shown to develop pancreatic tumours. To examine the effect of Smad4 heterozygous mutation on the development of these tumours, Smad4+/- mutation was introduced into p53-/- and p53-/- ApcMin/+ mice. No pancreatic phenotype was found in p53-/-Smad4+/- animals. p53-/- ApcMin/+ Smad4+/- animals did not exhibit promotion of tumourigenesis in any tissue compared to the p53-/-ApcMin/+ mice. Immunohistochemical studies revealed loss of Smad4 protein within the majority of the lesions arising in p53-/-ApcMin/+Smad4+/- animals. Furthermore microdissection and mutational analysis revealed LOH for Apc and Smad4. Treatment of wild-type (WT) Smad4+/-, ApcMin/+ or ApcMin/+ Smad4+/- mice with N-Nitroso-N-Methyl Urea (NMU) resulted in abnormal foci in pancreatic acinar cells characterised by β-catenin stabilisation. Previously these foci have been shown to be the precursors of pancreatic neoplasia. Interestingly, only NMU-treated ApcMin/+Smad4+/- mice exhibit a significant increase in abnormal pancreas, which was found to be due to increased number of abnormal foci rather than increased focus size. A range of foci sizes were analysed, but only smaller abnormal foci were characterised by morphological nuclear atypia. These studies suggest functional co-operation between TGF-β and Wnt signalling pathways in the suppression of pancreatic tumourigenesis in the mouse.
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Segditsas, Stefania. "Mechanisms of intestinal tumorigenesis resulting from APC mutations." Thesis, University College London (University of London), 2008. http://discovery.ucl.ac.uk/15923/.

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Colorectal cancer typically arises through the sequential accumulation of mutations in different genes. Mutations in the adenomatous polyposis coli (APC) gene are thought to be the initiating step in this sequence of events and are found in the majority of early colorectal tumours. Investigation of these lesions has revealed that selection of 'optimal' combinations of mutations at the APC locus is in place, but the roles of such selected combinations have never been clarified. In the work presented in this thesis, I have demonstrated that similar constraints on APC mutations are active in tumours from attenuated FAP (AFAP) patients and that given the sub-optimal location of the germline APC mutation in these patients, additional somatic mutations are often required, especially in patients with germline mutations in the alternatively spliced region of exon 9. I have also shown that APC promoter hypermethylation does not appear to play a fundamental role in the selection of optimal APC genotypes. I have shown that the optimum combinations of mutations at APC are those that allow retention of some APC activity with respect to β-catenin degradation and that this has effects on the resulting activation of the Wnt signalling pathway. Optimal combinations of APC mutations result in intermediate nuclear β-catenin levels, which surprisingly highly activate a selection of Wnt targets. In an attempt to identify novel Wnt targets that are important for tumorigenesis and could serve as therapeutic targets, I have validated results from a cross-species comparison that identified a set of genes showing consistent differential expression between early tumour samples carrying APC mutations and normal tissue. In addition, I have investigated the biological function of one such-identified molecule, the serum/glucocorticoid-regulated kinase (SGK1), and I have revealed its potential role as a key regulator of intestinal cell differentiation and apoptosis.
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Sporri, Roman Andreas. "Reciprocal control of T cell and APC activation." Thesis, University College London (University of London), 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.411991.

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Books on the topic "APC"

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Näthke, Inke S., and Brooke M. McCartney, eds. APC Proteins. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-1145-2.

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Näthke, Inke S. APC proteins. New York, N.Y: Springer Science+Business Media, 2009.

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S, Näthke Inke, and McCartney Brooke M, eds. APC proteins. New York, N.Y: Springer Science+Business Media, 2009.

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S, Näthke Inke, and McCartney Brooke M, eds. APC proteins. New York, N.Y: Springer Science+Business Media, 2009.

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S, Näthke Inke, and McCartney Brooke M, eds. APC proteins. New York, N.Y: Springer Science+Business Media, 2009.

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Doyle, David. M113 APC in Vietnam. Carrollton, TX: Squadron/Signal Publications, 2009.

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Consultative Committee of Accountancy Bodies. Auditing Practices Committee., ed. APC: The first ten years. (London): Auditing Practices Committee of CCAB Limited, 1986.

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Pang, S. F. Recycling of scrap APC-2. Manchester: UMIST, 1992.

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Campaign, ed. The APC creative planning awards. London: Haymarket Campaign, 1994.

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ʻAbīd, Lakhḍar. Les collectivités locales en Algérie (APW-APC). 2nd ed. Alger: Office des publications universitaires, 1986.

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Book chapters on the topic "APC"

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Groden, Joanna Louise, William Hankey, and Kenechi Ebede. "APC." In Cancer Therapeutic Targets, 955–66. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4419-0717-2_58.

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Mehlhorn, Heinz. "APC." In Encyclopedia of Parasitology, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27769-6_234-2.

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Groden, Joanna Louise, William Hankey, and Kenechi Ebede. "APC." In Cancer Therapeutic Targets, 1–12. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4614-6613-0_58-3.

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Groden, Joanna Louise, William Hankey, and Kenechi Ebede. "APC." In Cancer Therapeutic Targets, 1–12. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6613-0_58-4.

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Mehlhorn, Heinz. "APC." In Encyclopedia of Parasitology, 175. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-43978-4_234.

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Biswas-Fiss, Esther E., Stephanie Affet, Malissa Ha, Takaya Satoh, Joe B. Blumer, Stephen M. Lanier, Ana Kasirer-Friede, et al. "APC." In Encyclopedia of Signaling Molecules, 128. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100065.

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Lemen, Jen. "APC." In How to Become a Chartered Surveyor, 45–89. London: Routledge, 2021. http://dx.doi.org/10.1201/9781003156673-4.

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Neufeld, Kristi L. "Nuclear APC." In Advances in Experimental Medicine and Biology, 13–29. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-1145-2_2.

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Pötzsch, B., and I. Witt. "APC-Resistenz." In Hämostaseologie, 355–59. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-662-07673-6_42.

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Scharnagl, Hubert, Winfried März, Markus Böhm, Thomas A. Luger, Federico Fracassi, Alessia Diana, Thomas Frieling, et al. "APC Resistance." In Encyclopedia of Molecular Mechanisms of Disease, 129. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_8490.

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Conference papers on the topic "APC"

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Singh, Pawandeep. "Collaborative APC Project Management." In International Petroleum Technology Conference. International Petroleum Technology Conference, 2014. http://dx.doi.org/10.2523/17266-ms.

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Singh, Pawandeep. "Collaborative APC Project Management." In International Petroleum Technology Conference. International Petroleum Technology Conference, 2014. http://dx.doi.org/10.2523/iptc-17266-ms.

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Faron, Kamyar, Mark Freeland, Ole Krogh, Sukesh Patel, and Gayathri Raghavendra. "Multivariable versus univariable APC." In Microlithography 2004, edited by Kenneth W. Tobin, Jr. SPIE, 2004. http://dx.doi.org/10.1117/12.536472.

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Ausschnitt, Christopher P., Brian Barker, William A. Muth, Marc Postiglione, and Thomas Walentosky. "Industrial strength lithography APC." In Advanced Microelectronic Manufacturing, edited by Matt Hankinson and Christopher P. Ausschnitt. SPIE, 2003. http://dx.doi.org/10.1117/12.485310.

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Singh, P. "Collaborative APC Project Management." In IPTC 2014: International Petroleum Technology Conference. European Association of Geoscientists & Engineers, 2014. http://dx.doi.org/10.3997/2214-4609-pdb.395.iptc-17266-ms.

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Yoneda, Minoru, Jun Nishizawa, Stoshi Ooyama, Souichi Amano, Kouichi Onodera, and Kunihisa Yano. "Keeping Advanced Process Control (APC) Performance and Maintenance and Improvement of APC System." In 2006 SICE-ICASE International Joint Conference. IEEE, 2006. http://dx.doi.org/10.1109/sice.2006.315506.

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Belyackova, Z. Yu. "Risks of APC products standardization." In SCIENTIFIC AND TECHNICAL SUPPORT EFFICIENCY AND QUALITY PRODUCTION OF AGRICULTURAL PRODUCTS. VNIIPP, 2019. http://dx.doi.org/10.30975/978-5-9909889-2-7-2019-1-1-32-35.

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Peiffer, Keith. "Acoustic Panel Ceilings: Origins." In 108th Annual Meeting Proceedings. ACSA Press, 2020. http://dx.doi.org/10.35483/acsa.am.108.3.

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Acoustical panel ceilings (APCs) are a mainstay in contemporary architecture. As a flexible, modular system of cross-T frames and solid panels suspended from the structure above, the APC provides the enclosure above many of the spaces we inhabit everyday: schools, offices, hospitals, and retail stores. It is a humble system, functional yet inexpensive, and it is everywhere. If “the secret ambition of design is to become invisible” as Bruce Mau asserts, then the APC has achieved this hallowed place within design as an assembly that performs effortlessly while often receding into the background, ubiquitous and taken for granted. Its current status as a background material, however, belies its revolutionary beginnings. Although certainly not limited to this lineage, the contemporary APC was birthed as an in¬novative materialization of the aspirations, conflicts, and contradictions within Modernism, and is particularly indebted to the slab-style office buildings of the 1950s. To establish this context this paper will explore Modernism’s interests in standardization and industrialization of building components, clear-span universal space, and the integration of new technology through the following precedents: Mies van der Rohe’s clear-span pavilions, architectural magazines, product adver¬tisements featuring renderings by Helmut Jacoby, and three 1950s high-rise office buildings. The confluence of these interests, explored in architectural practice, spurred more than a decade of focused development of the suspended ceiling in the 1950s, resulting in the Acoustical Fire Guard product that closely resembles the APC still installed broadly today. Although architectural history and theory has not often mentioned the APC specifically, we can trace broader disciplinary influences to their manifestation in the APC. My interest is not in arguing for a newer or better alternative ceiling system, but in placing the APC at the center of the story, synthesizing various theoretical, historical, and technical developments to return to its beginnings with fresh eyes.
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van der Meer, F. J. M., N. H. van Tilburg, I. K. van der Linden, E. Briét, and R. M. Bertina. "A SECOND INHIBITOR OF ACTIVATED PROTEIN C (APC)." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643817.

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The inactivation of APC in plasma, as measured with the chromogenic substrate S2366, follows, in the absence of heparin, pseudo-first order kinetics. The ti of about 20 minutes is independent of the APC concentration (31-500 nM) and increases linearly with the dilution of the plasma. These observations suggest that the concentration of the APC inhibitor in plasma is much higher than 500 nM, which is much higher than the concentration of 88 nM reported by Suzuki for the protein C inhibitor (PCI).In the presence of heparin (5 IU/ml) the inactivation of APC becomes biphasic. Fast inactivation with an apparent ti of 8 minutes is followed by slower inactivation with a ti of 20 minutes.Removal of PCI from the plasma with α-PCI antibodies (kindly provided by Dr. Suzuki) has no effect on APC inactivation in the absence of heparin. However, in this plasma APC inactivation could not be stimulated by addition of heparin (absence of fast phase of APC-inactivation). These data suggest the presence of two APC inhibitors in plasma: the heparin dependent PCI (PCI-I), earlier reported by Suzuki, and a sofar unknown heparin-independent inhibitor (PCI-II).Further experiments showed that this PC I-11 has a molecular weight of 60 kD and is different from the APC-binding protein reported by Kisiel. Using Heparin-Sepharose affinity chromatography we could separate PCI -II from both PCI-I and the APC binding protein. In this PC I-11 preparation APC inactivation was accompanied by the formation of an APC-PCI -11 complex of about 105 kD as demonstrated by immunoblotting with a-PC antibodies after SDS-PAGE. The identity of PCI-II is unknown; however, it is different from antithrombin III, heparin cofactor II, α1-antitrypsin and β2-antiplasmin.The demonstration of the presence of two APC inhibitors in plasma will require a re-evaluation of the current functional assays for the APC inhibitor.
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Novotny, Vaclav, Michal Kolovratnik, Monika Vitvarova, and Jana P. Jakobsen. "Analysis and Design of Novel Absorption Power Cycle Plants." In ASME 2016 10th International Conference on Energy Sustainability collocated with the ASME 2016 Power Conference and the ASME 2016 14th International Conference on Fuel Cell Science, Engineering and Technology. American Society of Mechanical Engineers, 2016. http://dx.doi.org/10.1115/es2016-59272.

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Absorption Power Cycles (APCs) provide an interesting field within power cycles. The multicomponent mixture with variable temperature across boiling is employed as a working fluid. This has a potential for decreasing exergy loss associated with heat transfer during phase change processes (boiling and condensation). Absorption process has also an effect of lowering exhaust pressure of a turbine. The APCs hold a potential for heat recovery applications at very low temperatures, where constant temperature of boiling and condensation largely limits performance and economic effectiveness of Organic Rankine cycles (ORCs). Theoretical calculations show superiority of APC over extensive range of considered ORC working fluid. The advantage of APC further increases when air cooled condenser needs to be used instead of wet cooling tower. With the same boundary conditions for all cycles the APC provides higher utilization efficiency and power output at source temperatures below approximately 120 °C, for temperatures as low as 60 °C the net power output can be surpassed even more than three times. The proposed APC employs aqueous solution of salts considered generally for absorption cooling (Lithium Bromide, Lithium Chloride, Calcium Chloride) as a working fluid. Unlike ammonia used in mixture with water in Kalina APC or often ORC working fluids, used salts are non-toxic, environmentally friendly and pure water in expander simplifies its design. After summary of theoretical research from thermodynamics point of view are discussed principles, aspects and issues for design of single components of the cycle. Results of sizing are presented on two examples with 100 °C heat source. First one is 20 kWe unit using hot air as a heat source and air cooled condenser, second one is 500 kWe unit with heat source being pressurized water and using wet cooling tower heat rejection. Results show possibility of building relatively efficient system for even small power output with turbine isentropic efficiency nearly 80 % for the 20 kWe unit, but relatively large heat exchangers.
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Reports on the topic "APC"

1

Xu, Xingchen, Zuan Peng, Jacob Rochester, and Mike Sumption. Recent Progress with APC $Nb_3Sn$ Conductors. Office of Scientific and Technical Information (OSTI), October 2018. http://dx.doi.org/10.2172/1508015.

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Abazajian, Kevork. CMB-S4 Decadal Survey APC White Paper. Office of Scientific and Technical Information (OSTI), July 2019. http://dx.doi.org/10.2172/1556957.

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Chu, Xuehao. Validating T-BEST Models with 100% APC Counts. Tampa, FL: University of South Florida, February 2007. http://dx.doi.org/10.5038/cutr-nctr-rr-2005-02.

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Jarrett, Christy R. A New APC-Like Gene Involved in Regulation of B-Catenin/LEF. Fort Belvoir, VA: Defense Technical Information Center, July 2001. http://dx.doi.org/10.21236/ada404820.

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Jarrett, Christy. A New APC-like Gene Involved in Regulation of B-catenin/LEF. Fort Belvoir, VA: Defense Technical Information Center, July 2000. http://dx.doi.org/10.21236/ada390791.

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Jarrett, Christy R. A New APC-Like Gene Involved in Regulation of Beta-Catenin/LEF Signaling. Fort Belvoir, VA: Defense Technical Information Center, July 2002. http://dx.doi.org/10.21236/ada409414.

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Ghosh, Sajal K. Do EBV Encoded Small RNAs Interfere with Tumor Suppressor APC in EBV Associated Breast Cancers. Fort Belvoir, VA: Defense Technical Information Center, August 2006. http://dx.doi.org/10.21236/ada462843.

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Trebaol, George O., and Randy L. Heckman. Intelligibility Performance of the LPC-10 and APC/SQ Speech Algorithms in a Fading Environment. Fort Belvoir, VA: Defense Technical Information Center, February 1985. http://dx.doi.org/10.21236/ada166102.

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Smith, Arfon M., and et al. Astro2020 APC White Paper: Elevating the Role of Software as a Product of the Research Enterprise. Office of Scientific and Technical Information (OSTI), July 2019. http://dx.doi.org/10.2172/1558442.

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Medof, M. E. Augmentation of Antitumor T-Cell Responses by Increasing APC T-Cell C5a/C3a-C5aR/C3aR Interactions. Fort Belvoir, VA: Defense Technical Information Center, March 2013. http://dx.doi.org/10.21236/ada585489.

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