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Academic literature on the topic 'Muc expression'

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Published: 11 March 2023

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Journal articles on the topic "Muc expression"

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Kuznetsov, O. E., V. M. Tsyrkunov, and S. Sh Kerimova. "Mucin expression in liver cancer." Doklady of the National Academy of Sciences of Belarus 67, no. 1 (March 4, 2023): 59–65. http://dx.doi.org/10.29235/1561-8323-2023-67-1-59-65.

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Increasing incidence, difficulties in early diagnosis, and a high mortality rate in liver cancer (LC) determine the relevance of studying the mechanisms of its development. The aim of the work is to evaluate the expression of high molecular weight glycoproteins MUC-1, MUC-13 in liver cancer. The object of study is LC tissue samples of 65 patients from the archives and 34 blood serum samples from patients with morphologically confirmed LC. The age of subjects was 26– 97 years. The level of antibodies to MUC-1 and MUC-13 was studied by ELISA. The reference value ranges of MUC-1 (0.250 ± 0.10 ng/ml) and MUC-13 (0.321 ± 0.13 ng/ml) in the blood serum of healthy individuals were established. The concentration of antibodies to MUC-1 and MUC-13 in the blood serum in RP was significantly higher than that in practically healthy individuals. The concentration of MUC-1 and MUC-13 in the LC tumor tissue was higher than that in the blood serum of apparently healthy individuals and LC patients. With a confirmed LC diagnosis, the level of antibodies to MUC-1 in the blood serum, which exceeds 0.373 ng/ml, and the level of antibodies to MUC-13, which is more than 0.939 ng/ml, may indicate a high risk of a tumor process.
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Colecchia, Maurizio, Salvatore Lo Vullo, Patrizia Giannatempo, Daniele Raggi, Federica Perrone, Nicola Nicolai, Mario Catanzaro, et al. "Frequent expression of androgen receptor (AR) on tumor cells of muscle-invasive (MIUC) and metastatic urothelial carcinoma (mUC): Insights for clinical research." Journal of Clinical Oncology 35, no. 15_suppl (May 20, 2017): e16019-e16019. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.e16019.

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e16019 Background: Advanced UC treatment is being revolutionized by immunotherapy (IT). However, < 30% of patients (pts) will benefit from IT, and additional therapeutic targets are needed. Findings from analyses supporting an investigator-led, AR-based clinical research program are presented. Methods: From 09/2015, we collected the archival tissue blocks from pts who have been treated or consulted at our center and received platinum-based chemotherapy (CT) for MIUC or mUC. Immunohistochemistry (IHC) was performed on 3µm slides using mouse anti-human AR monoclonal Ab (Dako, clone AR441). ≥1% cutoff for AR+ IHC of tumor cells (TC) was used. AR-expressing pts were further stratified as follows: 1-5%, 5-25%, and 25-100%. Univariable (UVA) and multivariable (MVA) Cox models for overall survival (OS) were fitted, the latter adjusted for clinical stage (MIUC vs mUC), presence of visceral metastases, platinum CT type. OS was calculated from the date of first administration of CT. Exploratory PD-L1 co-expression, by TC or stroma (SP142 Ab, 1% cutoff), was analyzed in all pts. Results: 105 pts (46 MIUC and 59 mUC) had their tumor stained. 80 (76.2%) had bladder primary tumor, 85 (80.9%) had pure UC. 59 received cisplatin and 46 carboplatin. Overall, 37 pts (35.2%) had AR-expressing TC, 17 (16.2%) with ≥25% expression. Cox models were built on 93 pts with follow-up duration of ≥6 months. AR-expressing was equally distributed between MIUC and mUC pts (44.4% and 55.6%). On UVA, AR expression was not associated with OS, neither dichotomizing AR+/AR- pts (p = 0.477) nor after accounting for AR-positivity strata (p = 0.845). The same results were confirmed on MVA (p = 0.505 and p = 0.875). In AR+ vs. AR- pts, PD-L1 was equally expressed in the stroma (67.5 vs 57.9%) but less expressed by TC (39.4% vs 52%). Conclusions: AR is frequently expressed on TC of pts with MIUC and mUC, and AR expression does not seem to be associated with OS in these pts. AR pathway is worthy of clinical studies to synergistically act with anti-PD-L1 therapy. AR sequencing and FISH analysis in positive pts is ongoing, and a clinical program of a named-basis administration of antiandrogen therapy has started at our center.
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Shet, Tanuja, Sucheta Valsangar, and Suhas Dhende. "Secretory Carcinoma of Breast: Pattern of MUC 2/MUC 4/MUC 6 Expression." Breast Journal 19, no. 2 (January 11, 2013): 222–24. http://dx.doi.org/10.1111/tbj.12085.

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Jiang, Zhipeng, Huashe Wang, Liang Li, Zehui Hou, Wei Liu, Taicheng Zhou, Yingru Li, and Shuang Chen. "Analysis of TGCA data reveals genetic and epigenetic changes and biological function of MUC family genes in colorectal cancer." Future Oncology 15, no. 35 (December 2019): 4031–43. http://dx.doi.org/10.2217/fon-2019-0363.

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Aim: Few studies focused on functions and regulatory networks of MUC family members in colorectal cancer based on comprehensive analysis of online database. Materials & methods: Copy number variation, methylation, pathway analysis and drug influence on MUC expression were analyzed based on The Cancer Genome Atlas and GTEx database. Results: Copy number variation analysis showed MUC heterozygous amplification and heterozygous deletion predominate. Methylation of MUC17, MUC12 and MUC4 were found related to gene expression. Function of MUC family genes mainly affects pathways such as apoptosis, cell cycle, DNA damage and EMT pathways. PLX4720, dabrafenib, gefitinib, afatinib and austocystin D can alter the expression of MUC gene. Conclusion: The genetic and epigenetic changes of MUC are related to the level of MUC expression in colorectal cancer.
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Treon, Steven P., Joseph A. Mollick, Mitsuyoshi Urashima, Gerrard Teoh, Dharminder Chauhan, Atsushi Ogata, Noopur Raje, et al. "Muc-1 Core Protein Is Expressed on Multiple Myeloma Cells and Is Induced by Dexamethasone." Blood 93, no. 4 (February 15, 1999): 1287–98. http://dx.doi.org/10.1182/blood.v93.4.1287.

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Abstract Monoclonal antibodies (MoAbs) that selectively identify Muc-1 core protein (MoAbs DF3-P, VU-4H5) determinants were used to identify the Muc-1 glycoform present on 7 multiple myeloma (MM) cell lines, 5 MM patient plasma cells, 12 MM patient B cells, as well as 32 non-MM cell lines and normal hematopoietic cells. Flow cytometry studies demonstrated that all MM cell lines, MM patient plasma cells, and MM patient B cells expressed Muc-1 core protein epitopes. Circulating B cells from 4 normal donors also expressed Muc-1 core protein. In contrast, Muc-1 core protein was absent on 28 of 32 non-MM neoplastic cell lines, 17 of which expressed Muc-1. Splenic and tonsillar B cells, CD34+ stem cells, resting T cells, and bone marrow plasma cells obtained from normal donors both lacked Muc-1 glycoforms. We next studied the effects of estrogen, progesterone, and glucocorticoid receptor agonists and antagonists on Muc-1 expression, because consensus sequences for the response elements of these steroids are present on the Muc-1 gene promoter. These studies showed that dexamethasone (Dex) induced Muc-1 expression on MM cell lines, as determined by both flow cytometry and Western blot analyses. Dex also induced upregulation of Muc-1 on prostate and ovarian cancer cell lines. Time and dose-response studies demonstrated that Dex induced maximal cell surface Muc-1 expression by 24 hours at concentrations of 10−8 mol/L. Dex induced Muc-1 upregulation could be blocked with a 10-fold excess of the glucocorticoid receptor antagonist RU486, confirming that Dex was acting via the glucocorticoid receptor. No changes in Muc-1 expression were observed on MM cells treated with estrogen and progesterone receptor agonists and antagonists or with RU486. These studies provide the framework for targeting Muc-1 core protein in vaccination and serotherapy trials in MM. In addition, the finding that Muc-1 expression on MM cells can be augmented by Dex at pharmacologically achievable levels suggests their potential utility in enhancing treatments targeting Muc-1 in MM.
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Treon, Steven P., Joseph A. Mollick, Mitsuyoshi Urashima, Gerrard Teoh, Dharminder Chauhan, Atsushi Ogata, Noopur Raje, et al. "Muc-1 Core Protein Is Expressed on Multiple Myeloma Cells and Is Induced by Dexamethasone." Blood 93, no. 4 (February 15, 1999): 1287–98. http://dx.doi.org/10.1182/blood.v93.4.1287.404k14_1287_1298.

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Monoclonal antibodies (MoAbs) that selectively identify Muc-1 core protein (MoAbs DF3-P, VU-4H5) determinants were used to identify the Muc-1 glycoform present on 7 multiple myeloma (MM) cell lines, 5 MM patient plasma cells, 12 MM patient B cells, as well as 32 non-MM cell lines and normal hematopoietic cells. Flow cytometry studies demonstrated that all MM cell lines, MM patient plasma cells, and MM patient B cells expressed Muc-1 core protein epitopes. Circulating B cells from 4 normal donors also expressed Muc-1 core protein. In contrast, Muc-1 core protein was absent on 28 of 32 non-MM neoplastic cell lines, 17 of which expressed Muc-1. Splenic and tonsillar B cells, CD34+ stem cells, resting T cells, and bone marrow plasma cells obtained from normal donors both lacked Muc-1 glycoforms. We next studied the effects of estrogen, progesterone, and glucocorticoid receptor agonists and antagonists on Muc-1 expression, because consensus sequences for the response elements of these steroids are present on the Muc-1 gene promoter. These studies showed that dexamethasone (Dex) induced Muc-1 expression on MM cell lines, as determined by both flow cytometry and Western blot analyses. Dex also induced upregulation of Muc-1 on prostate and ovarian cancer cell lines. Time and dose-response studies demonstrated that Dex induced maximal cell surface Muc-1 expression by 24 hours at concentrations of 10−8 mol/L. Dex induced Muc-1 upregulation could be blocked with a 10-fold excess of the glucocorticoid receptor antagonist RU486, confirming that Dex was acting via the glucocorticoid receptor. No changes in Muc-1 expression were observed on MM cells treated with estrogen and progesterone receptor agonists and antagonists or with RU486. These studies provide the framework for targeting Muc-1 core protein in vaccination and serotherapy trials in MM. In addition, the finding that Muc-1 expression on MM cells can be augmented by Dex at pharmacologically achievable levels suggests their potential utility in enhancing treatments targeting Muc-1 in MM.
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Braga, V. M., L. F. Pemberton, T. Duhig, and S. J. Gendler. "Spatial and temporal expression of an epithelial mucin, Muc-1, during mouse development." Development 115, no. 2 (June 1, 1992): 427–37. http://dx.doi.org/10.1242/dev.115.2.427.

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The Muc-1 mucin is found as a transmembrane protein in the apical surface of glandular epithelia. To provide insight into possible functions, we have assessed the timing of expression and the distribution of the Muc-1 protein during mouse embryogenesis using three different techniques: RT-PCR, northern blots and immunohistochemistry. Our results indicate that Muc-1 expression correlates with epithelial differentiation in stomach, pancreas, lung, trachea, kidney and salivary glands. Once started, Muc-1 synthesis continually increases with time, mainly due to epithelial area growth. Our data suggest that expression of the Muc-1 gene is under spatial and temporal control during organogenesis. Although Muc-1 is present in different organs, its expression is not induced systemically, but according to the particular onset of epithelial polarization and branching morphogenesis of each individual organ. It is of particular interest that Muc-1 protein can be detected lining the apical surfaces of the developing lumens when the epithelium of these organs is still undergoing folding and branching, and glandular activity has not yet started. We speculate that Muc-1 may participate in epithelial sheet differentiation/lumen formation during early development of the organs known to express it. This speculation is based on: (1) the detection of Muc-1 expression early during organogenesis, (2) the defined apical localization in different epithelia, (3) the decrease in cell-cell interactions when Muc-1 protein is highly expressed and (4) the possible interaction of its cytoplasmic tail with the actin cytoskeleton. However, it remains to be established using in vitro systems, whether the temporal and local expression of the Muc-1 gene coincident with the morphogenetic events described here is relevant for the process.
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Braga, V. M., and S. J. Gendler. "Modulation of Muc-1 mucin expression in the mouse uterus during the estrus cycle, early pregnancy and placentation." Journal of Cell Science 105, no. 2 (June 1, 1993): 397–405. http://dx.doi.org/10.1242/jcs.105.2.397.

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The Muc-1 protein is an integral membrane protein that is expressed apically by simple secretory epithelia in many different organs. We present in this paper a study on Muc-1 protein expression in the mouse uterus during early pregnancy, placentation and the estrus cycle. Muc-1 immunopositive reaction is found in the decidua by day 8 of pregnancy onwards. The observed pattern was unusual, since Muc-1 protein was present in spherical cytoplasmic granules in granular metrial gland cells. Both the intracellular pattern of expression and the lymphoid origin of these cells were striking results. Muc-1 is thought to be an epithelial differentiation marker, and this is the first report of its expression by non-epithelial cells. Our results on Muc-1 expression in the uterus of cycling mice showed that higher levels of Muc-1 mRNA and protein correlate with higher levels of plasma estrogen in the estrus and proestrus phases. However, in ovariectomized mice without hormone replacement, the endometrium expressed high levels of this protein. These levels could not be substantially changed by estrogen, although progesterone reduced the levels of Muc-1 protein associated with the epithelium. These data together with the normal expression in the cycling mice suggest that progesterone might repress Muc-1 expression during the metestrus and diestrus phases. In cycling mice, when plasma progesterone is at its nadir and the estrogen level is elevated in estrus and proestrus phases, Muc-1 concentration would increase to its basal level, not because of estrogen stimulation, but due to lack of progesterone repression.(ABSTRACT TRUNCATED AT 250 WORDS)
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Brugger, Wolfram, Hans-Jörg Bühring, Frank Grünebach, Wichard Vogel, Sepp Kaul, Robert Müller, Tim H. Brümmendorf, et al. "Expression of MUC-1 Epitopes on Normal Bone Marrow: Implications for the Detection of Micrometastatic Tumor Cells." Journal of Clinical Oncology 17, no. 5 (May 1999): 1535. http://dx.doi.org/10.1200/jco.1999.17.5.1535.

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PURPOSE: The expression of the carcinoma-associated mucin MUC-1 is thought to be restricted to epithelial cells and is used for micrometastatic tumor cell detection in patients with solid tumors, including those with breast cancer. Little is known, however, about the expression of MUC-1 epitopes in normal hematopoietic cells. MATERIALS AND METHODS: MUC-1 expression was analyzed by flow cytometry and immunocytology on bone marrow (BM) mononuclear cells and purified CD34+ cells from healthy volunteers, using different anti-MUC-1–specific monoclonal antibodies. In addition, Western blotting of MUC-1 proteins was performed. RESULTS: Surprisingly, 2% to 10% of normal human BM mononuclear cells expressed MUC-1, as defined by the anti–MUC-1 antibodies BM-2 (2E11), BM-7, 12H12, MAM-6, and HMFG-1. In contrast, two antibodies recognizing the BM-8 and the HMFG-2 epitopes of MUC-1 were not detected. MUC-1+ cells from normal BM consisted primarily of erythroblasts and normoblasts. In agreement with this, normal CD34+ cells cultured in vitro to differentiate into the erythroid lineage showed a strong MUC-1 expression on day 7 proerythroblasts. Western blotting of these cells confirmed that the reactive species is the known high molecular weight MUC-1 protein. CONCLUSION: Our data demonstrate that some MUC-1 epitopes are expressed on normal BM cells and particularly on cells of the erythroid lineage. Hence the application of anti–MUC-1 antibodies for disseminated tumor cell detection in BM or peripheral blood progenitor cells may provide false-positive results, and only carefully evaluated anti–MUC-1 antibodies (eg, HMFG-2) might be selected. Furthermore, MUC-1–targeted immunotherapy in cancer patients might be hampered by the suppression of erythropoiesis.
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Schmitt, Fernando C., Mónica B. Pereira, and Celso A. Reis. "MUC 5 expression in breast carcinomas." Human Pathology 30, no. 10 (October 1999): 1270–71. http://dx.doi.org/10.1016/s0046-8177(99)90052-7.

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Dissertations / Theses on the topic "Muc expression"

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BORTESI, Laura. "Muc expression and their prognostic value in cholangiocarcinoma." Doctoral thesis, Università degli Studi di Verona, 2009. http://hdl.handle.net/11562/337443.

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Il colangiocarcinoma (CC) è un tumore composto da cellule che ricordano quelle dei dotti biliari e rappresenta il secondo tumore epatico come incidenza dopo l’epatocarcinoma, costituendo il 5-10% delle neoplasie primitive epatiche. A livello mondiale il colangiocarcinoma rende conto del 3% di tutti i carcinomi del tratto gastroenterico. Numerosi studi hanno messo in evidenza il fatto che i tassi di incidenza e mortalità per il colangiocarcinoma intraepatico (IHCC) stanno aumentando, mentre quelli per il colangiocarcinoma extraepatico (EHCC) stanno globalmente diminuendo. Ad oggi l’unica terapia potenzialmente curativa è quella chirurgica e questi pazienti hanno una prognosi infausta con una sopravvivenza di pochi mesi. Al momento una delle ragioni per cui questo tumore si presenta tardivamente è la mancanza di un marcatore diagnostico sensibile e specifico che permetta una diagnosi precoce. Lo scopo del nostro lavoro era trovare un marcatore sensibile e specifico, dosabile nel siero dei pazienti che si correli con il tipo tumorale e con le dimensioni del tumore in quanto la sopravvivenza è del 70-80% per quei pazienti con tumori piccoli scoperti incidentalmente in corso di trapianto per colangite sclerosante primitiva. Le Mucine sono glicoproteine altamente glicosilate con un ruolo protettivo nelle cellule, servendo in parte da barriera per la superficie delle cellule epiteliali e per le cellule tumorali. Boonla C et al. recentemente hanno dimostrato che la mucina MUC5AC è presente in concentrazioni significative nel siero dei pazienti con CC. In un lavoro recente, MUC5AC correlava significativamente con l’invasione perineurale e uno stadio avanzato di malattia. Ci sono pochi studi sulla espressione delle mucine, in particolare il tipo gastrico e la loro relazione con la morfologia e la prognosi dei colangiocarcinomi. Abbiamo analizzato mediante immunoistochimica tutti i nostri casi per MUC1, MUC2, MUC6 e MUC5AC. I risultati più significativi sono stati con MUC5AC. Recentemente il Liver Cancer Study Group of Japan ha suddiviso IHCC in tre tipi morfologici: mass-forming (MF), periductal infiltrating (PI) e intraductal growth (IG). Il tipo MF è caratterizzato dalla presenza di una massa tondeggiante a margini distinti all’interno del parenchima epatico, il tipo PI è caratterizzato da una infiltrazione tumorale lungo i dotti biliari,che occasionalmente interessa i vasi e/o il parenchima epatico, il tipo IG da una crescita papillare e/o granulare all’interno del lume dei dotti. Il tipo PI è correlato ad una maggiore incidenza di invasioni perineurali, metastasi linfonodali e recidive extraepatiche rispetto al tipo MF. La sopravvivenza a 5 anni dei pazienti con tumori IG o MF è significativamente migliore di quelli con tumori MF più PI o solo PI. C’è sempre più evidenza che i colangiocarcinomi intraepatici debbano essere suddivisi in periferici e periilari su base eziopatogenetica, di comportamento biologico e caratteristiche cliniche. I CC periilari probabilmente derivano dall’epitelio di rivestimento dei rami principali dei dotti epatici di destra e sinistra e dalle ghiandole peribiliari che li circondano e istologicamente sono adenocarcinomi con caratteristiche dei tipi ilari e extraepatici. I CC periferici presumibilmente originano dai piccoli dotti biliari, duttuli e canali di Hering. Probabilmente sono coinvolte nella tumorigenesi le cellule progenitrici epatiche. Distinguere però tumori periilari da ilari è spesso difficile soprattutto in casi avanzati. Nel nostro studio insieme con i chirurghi proponiamo una classificazione di questo tipo: periferici per colangiocarcinomi che si sviluppano nel parenchima epatico, periilari per tumori localizzati nel fegato ma che interessano l’ilo e per i tumori di Klatskin e extraepatici per tumori del tratto biliare distale. Questa classificazione correla bene con la morfologia. La maggior parte (30/35) CC periferici sono di tipo MF con solo 5 casi MF+PI. I tumori periilari e gli extraepatici sono principalmente PI o MF+PI rispecchiando un differente pattern di crescita tra le due forme. Al di là di un diverso pattern di crescita c’è anche una differenza statisticamente significativa rispetto alla espressione di MUC5AC. 30 dei 35 casi (85,7%) di CC periferico erano MUC5AC negativi. 26 di 39 (66,6%) CC periilari erano MUC5AC positivi, con intensità variabile ma positivi. 13 casi erano negativi, di questi in 8 c’erano alcune cellule positive anche se non sufficienti a raggiungere il cut-off del 5%, non sappiamo se sia di qualche significato ma è diverso dalla negatività completa che si vede nei MF. Nel nostro studio MUC5AC sembra essere un buon marcatore immunoistochimico che può distinguere colangiocarcinomi periferici da periilari, che correla bene con la morfologia e ha anche un significato prognostico. Questo marcatore può essere misurato nel siero e può essere usato nel pannello dei marcatori tumorali da utilizzare nei colangiocarcinomi che può essere utile anche nel followup.
Cholangiocarcinoma (CC) is a malignant tumour composed of cells resembling those of the bile ducts and the second most common primary hepatic tumor after hepatocellular carcinoma, comprising 5-10% of primary liver neoplasms. Worldwide, cholangiocarcinoma accounts for 3% of all gastrointestinal cancers. Several studies have shown that the incidence and mortality rates of intrahepatic CC (IHCC) are rising, and those of extrahepatic cholangiocarcinoma (EHCC) are declining worldwide. To date, radical surgery is the only therapy offering a potential cure for CC patients, whose prognosis is generally poor with survival limited to few months. At present, the lack of a sensitive and specific early diagnostic marker is one of the reasons why CC has a fairly late presentation. Our aim was to find out a sensitive and specific marker which could be detected in patient serum and be correlated with tumor type and tumor burden since the potential survival benefit from early detection is shown by 70-80% survival for patients with early cholangiocarcinoma that was discovered incidentally on transplantation for primary sclerosing cholangitis. Mucins are heavily glycosylated glycoproteins and play a protective role in cells, in part serving as a barrier to the epithelial surface and to tumor cells. Boonla C. et al. recently showed that MUC5AC mucin is present in significant concentrations in serum from patients with CC. In a recent report, MUC5AC significantly correlated with neural invasion and advanced CC stage. Only a few studies have been carried out about mucins expression, in particular the gastric type and their relationship with CC morphology and prognosis. We stained all tissue for MUC1, MUC2, MUC6 and MUC5AC. The only interesting results were with MUC5AC. Recently the Liver Cancer Study Group of Japan divided IHCC into three morphological types: mass-forming (MF), periductal infiltrating (PI) and intraductal growth (IG). MF type is characterized by the presence of a spherical mass with a distinct border in the liver parenchyma, PI type presents tumor infiltration along the bile duct, occasionally involving the surrounding blood vessels and/or hepatic parenchyma, IG is characterized by papillary and/or granular growth into the bile duct lumen. PI type of CC present a significantly higher frequency of perineural invasion, lymph node metastasis and extrahepatic recurrence than MF type. The 5-year survival rates of patients with IG tumors or MF tumors is significantly better than those of patients with MF plus PI tumors or PI type alone. There is increasing evidence that intrahepatic cholangiocarcinoma should be divided in peripheral CC and perihilar CC based on etiopathogenesis, biological behaviour and clinical features. Perihilar CC may evolve from the lining epithelia of the major branches of the right and left hepatic bile duct and also from peribiliary glands around them and histologically is an adenocarcinoma resembling many of the features of hilar or extrahepatic CC. Peripheral CC presumably develop from small bile duct, ductules or canals of Hering. Hepatic progenitor cell may be involved in the tumorigenesis of peripheral CC. Distinguishing perihilar from hilar CC is often difficult, especially in advanced cases. In this study together with the surgeons we propose a different classification: peripheral CC for tumors that growth inside the liver parenchima, perihilar for tumors located in the liver but involving the hilum and for Klatskin tumors and extrahepatic for tumors of the distal biliary tract. This classification correlates well with morphology. Most (30/35) peripheral CC are of the MF type with only 5 cases MF+PI. Perihilar CC and EHCC are mostly PI or MF+PI reflecting a different growth pattern between the two. Beside a different growth pattern there is a statistical difference between the tumor types when comparing MUC5AC expression. 30 out of 35 (85,7%) peripheral CC were MUC5AC negative. 26 out of 39 (66,6%) perihilar CC were MUC5AC positive with different intensities but positive. 13 cases were negative. Of these 13 cases in 8 cases there were same positive cells but not enough to reach 5% of the total (our cut-off value), we don’t know if this positivity is of any significance, but it is something different compared to the true negativity that we see in MF. In our study MUC5AC seems to be a good immunohistochemical marker that can distinguish peripheral from perihilar CC, that correlates well with morphology and has a prognostic significance as well. This marker can be measured in the serum and can be used in the panel of tumor markers to search for in CC and could be useful in the follow-up.
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Bedei, Ivonne. "Untersuchung zur MUC-18-Expression des metastasierenden malignen Melanoms mittels der RT-PCR-Methode." Ulm : Universität Ulm, Medizinische Fakultät, 2001. http://www.bsz-bw.de/cgi-bin/xvms.cgi?SWB9818607.

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Brandenburg, Anna Klara. "Untersuchungen zur Expression der MUC1/Y und MUC/Z-Spleissvarianten des Tumorantigens MUC1 in Normalgeweben und Karzinomen des Magens sowie des ösophagogastrischen Überganges /." Köln, 2008. http://opac.nebis.ch/cgi-bin/showAbstract.pl?sys=000253343.

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Bedei, Ivonne [Verfasser]. "Untersuchung zur MUC-18-Expression des metastasierenden malignen Melanoms mittels der RT-PCR-Methode / Ivonne Bedei." Ulm : Universität Ulm. Medizinische Fakultät, 2002. http://d-nb.info/1015323618/34.

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Llupi, Matilda, and Rabije Qoku. "Expression of mucins in normal salivary glands and mucoepidermoid carcinoma of salivary glands." Thesis, Malmö högskola, Odontologiska fakulteten (OD), 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:mau:diva-19760.

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Mucoepidermoid carcinom (MEC) är en malign mucin-producerande tumör som förekommer i både stora och små spottkörtlar. Syftet med denna studie var att undersöka histologiskt uttryck av muciner (MUC1, MUC4, MUC5AC, MUC5B, MUC6) i MEC för att eventuellt hitta en korrelation mellan kvalitativt mucinuttryck och tumörgrad. Tolv låg- och fem höggradiga MEC och nio normala spottkörtlar intill tumörvävnad undersöktes med hjälp av immunohistokemi där proverna utvärderades med avseende på färgningsmönster och positivitet i specifika celltyper. Normala spottkörtelceller uttryckte främst cytoplasmatiskt mucin MUC5B. MUC1 och MUC4 uttrycktes i normala spottkörtelgångsceller i ungefär hälften av proverna medan MUC5AC uttryck var sällsynt i normala spottkörtlar. MEC:ar uttryckte MUC1, MUC4, MUC5AC och MUC5B. Den apikala delen av membranet i de bägarceller som omger cystiska hålrum visade den starkaste färgningen för MUC1 och MUC4. Uttryck av MUC4 i bägarceller minskade med ökad histologisk grad. Bägarcellers uttryck av MUC5B:s i låggradig MEC var mindre intensivt än uttrycket av MUC5AC i samma celler. Högre uttryck av MUC5B jämfört med MUC5AC noterades i höggradiga tumörer. Sammanfattningsvis uttrycker MEC olika mängd av muciner än normala spottkörtlar. MUC5AC:s uttryck i MEC verkar vara en metaplastisk funktion och MUC4 tycks relatera till tumörens differentieringsgrad. Förhållandet mellan MUC5AC och MUC5B uttryck skulle kunna vara ett användbart verktyg vid diagnostisering och prognosutvärdering av MEC.
Mucoepidermoid carcinomas (MECs) are malignant epithelial mucin-producing tumours encountered in both major and minor salivary glands. The aim of this study was to investigate the histological characteristics of the expression of mucins (MUC1, MUC4, MUC5AC, MUC5B, MUC6) in MECs in search for a possible correlation between qualitative mucin expression and tumour grade. Twelve low-grade, five high-grade MECs and nine normal salivary glands adjacent to tumour tissue were investigated for these mucins by immunohistochemistry. The samples were evaluated with respect to staining pattern and positivity of specific cell types. Normal acinar cells mainly expressed the cytoplasmic mucin MUC5B. MUC1 and MUC4 were expressed in normal ductal cells in approximately half of the samples whereas MUC5AC expression was rare in normal salivary glands. MECs expressed MUC1, MUC4, MUC5AC and MUC5B. The apical membrane of mucous cells lining the cystic cavities showed the strongest staining for MUC1 and MUC4. The expression of MUC4 in mucous cells decreased with increasing histological grade. Expression of salivary mucin MUC5B in mucous cells in low-grade MECs was less intense compared to the expression of MUC5AC in the same cells. In high-grade tumours, a higher expression of MUC5B compared to MUC5AC was noted. In conclusion, MECs express different mucin quantity compared to normal salivary glands. MUC5AC expression in salivary tumour tissue seems to be a metaplastic feature and MUC4 appears to be related to tumour differentiation grade. The relationship between MUC5AC and MUC5B expression could be a useful tool in the diagnosis and estimation of prognosis of MECs.
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Vogel, Teresa Maria [Verfasser]. "Die Expression von MHC Klasse I verwandten Genen (MIC) bei Psoriasis vulgaris / Teresa Maria Vogel." Kiel : Universitätsbibliothek Kiel, 2018. http://d-nb.info/1156264642/34.

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Carminati, Patricia de Oliveira. "Respostas celulares aos danos causados pelo antitumoral cisplatina em linhagens de fibroblastos humanos normais (MRC-5) e astrocítica (U343 MG-a)." Universidade de São Paulo, 2005. http://www.teses.usp.br/teses/disponiveis/17/17135/tde-21082007-103139/.

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Uma variedade de agentes antitumorais é capaz de induzir danos no material genético e estimular respostas como o bloqueio do ciclo celular, reparo do DNA ou apoptose. A resposta inicial das células é o bloqueio no ciclo em uma tentativa de reparar o dano, no entanto, se esse dano for muito extenso ou comprometer o metabolismo celular, uma cascata de sinalização aciona mecanismos alternativos que inibem a proliferação das células e acionam vias de morte. Os astrocitomas malignos são os tumores cerebrais mais comuns que afetam o sistema nervoso central, compreendendo mais de 60% dos tumores cerebrais primários. O tratamento padrão é a radioterapia seguida de quimioterapia, no entanto, o prognóstico para pacientes portadores desse tipo de câncer ainda continua desanimador. A cisplatina é um agente genotóxico largamente empregado no tratamento de gliomas, além de outros tipos de câncer. Essa droga liga-se ao DNA, formando aductos, os quais levam a um bloqueio na duplicação e na transcrição, podendo induzir apoptose nas células dependendo da extensão do dano. No presente trabalho foram avaliadas as respostas celulares ao tratamento com a cisplatina em linhagem de glioma (U343 MG-a) e em fibroblastos normais transformados por SV40 (MRC-5). Foram avaliadas as respostas em termos de sobrevivência celular, indução de apoptose e expressão gênica em larga escala pela técnica de micro-arranjos de cDNA, sendo esta última realizada somente para a linhagem U343. A cisplatina causou uma redução acentuada na sobrevivência das células MRC-5 (~1%) e U343 (< 1%) após cinco dias de tratamento (teste de sobrevivência celular) com concentrações que variavam de 12,5 a 300 ?M. O tratamento por 24 h com iguais concentrações de cisplatina reduziu a sobrevivência das linhagens em cerca de 20-80% (teste de citotoxicidade). Ambas as linhagens sofreram apoptose após o tratamento com diversas concentrações de cisplatina (12,5, 25 e 50 ?M). A linhagem U343 apresentou uma freqüência máxima de apoptose de 20,4% após o tratamento com 25 ?M de cisplatina por 72 h, enquanto a linhagem MRC-5 apresentou 11,0% de apoptose após 50 ?M de cisplatina por 48 h. Os dados de expressão gênica analisados pelo método de micro-aranjos de cDNA, obtidos 48 h após o tratamento das células U343 com 25 ?M de cisplatina, mostraram genes significativamente (p ?0,05) reprimidos relacionados principalmente com alterações no citoesqueleto (TBCD, RHOA, LIMK2 e MARK1), apoptose ou sobrevivência celular (BCL2-XL, ING1, RHOA, VDP, TIMP2, DYRK3 e NFKBIE), invasão celular ou metástase (LIMK2, TIMP2 e CALU), reparo de DNA (SMC1L1) e metabolismo celular (DYRK3, MARK1, TBCD, LIMK2, VDP e P4HB), entre outros processos. Esses dados apontam para um sério comprometimento da maquinaria celular como um todo após os danos induzidos pela cisplatina. Embora o mecanismo de apoptose justifique cerca de 20% da extensão de morte celular, conforme foi comprovado nos ensaios de apoptose (induzida por 25 ?M de cisplatina), a maior parte das células são eliminadas em conseqüência da ação da droga em vários níveis do metabolismo e manutenção da integridade celular, visto o elevado grau de citotoxicidade da cisplatina, demonstrado nos testes de sobrevivência.
A variety of antitumoral agents is capable of inducing DNA damage and eliciting cell cycle arrest, DNA repair or apoptotic responses. The initial response is a cell cycle arrest in an attempt to repair the DNA damage, but under conditions of extensive DNA lesions and high drug cytotoxicity, a signaling cascade triggers alternative mechanisms that inhibit cell proliferation and activate cell death pathways. Astrocytomas are the most common neoplasm of the central nervous system, comprising more than 60% of primary brain tumors. The standard treatment for theses tumors are radiotherapy followed by chemotherapy, however, the prognostic for these patients is still very discouraging. Cisplatin is an efficient DNA-damaging antitumor agent employed for the treatment of various human cancers, including gliomas. This drug binds to DNA, producing diverse types of adducts, which can block replication, transcription, and lead to apoptosis induction. In the present work, we analyzed cellular responses to treatments with the anticancer agent cisplatin in MRC-5 (normal human fibroblasts SV40 transformed) and U343 MG-a (glioma cell line). The responses were evaluated in terms of cell survival, apoptosis induction and profiles of gene expression by the cDNA microarrays method (only for U343 cell line). Cisplatin treatment resulted in a pronounced reduction in MRC-5 cell survival (~ 1%) and U343 (< 1%) after five days of treatment (cell survival test) with several concentrations of cisplatin, ranging from 12.5 to 300 ?M. Following 24h of treatment under similar cisplatin concentrations the survival was reduced at about 20-80% (cytotoxicity test). Both cell lines underwent apoptosis after treatment with different concentrations of cisplatin (12.5; 25 and 50 ?M), but U343 cells presented a maximal frequency of 20.4% apoptosis (25 ?M cisplatin treatment for 72h), while MRC-5 cells presented 11.0% (50 ?M cisplatin treatment for 48h). Analysis of gene expression performed for U343 cells treated with 25 ?M cisplatin for 48h showed several genes that were found significantly (p ? 0,05) down-regulated, most of them related with cytoskeleton alterations (TBCD, RHOA, LIMK2 and MARK1), apoptosis or cell survival (BCL2-XL, ING1, RHOA, VDP, TIMP2, DYRK3 and NFKBIE), cell invasion or metastasis (LIMK2, TIMP2 and CALU), DNA repair (SMC1L1), and cell metabolism (DYRK3, MARK1, TBCD, LIMK2, VDP and P4HB), among others. As a whole, these data demonstrate a serious commitment of the cell machinery after cisplatin-induced cellular damage. About 20% of the cell death corresponds to apoptosis, as was showed by the present assays. However, most of the cells are eliminated by the action of the drug in various levels of the metabolism and maintenance of cell integrity, due to the elevated degree of cisplatin citotoxicity, as demonstrated in cell survival tests.
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8

Berggren, Bremdal Karin. "Evolution of MHC Genes and MHC Gene Expression." Doctoral thesis, Uppsala universitet, Evolutionsbiologi, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-122011.

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Polymorphism in coding regions and regions controlling gene expression is the major determinant of adaptive differences in natural populations. Genes of the major histocompatibility complex (MHC) possess a high level of genetic variation, which is maintained by selection over long coalescence times. MHC genes encode antigen-presenting molecules in the adaptive immune system, which protects the host from infectious diseases. However, MHC molecules may also present self-peptides and for most autoimmune diseases there is a genetic factor associated with the MHC. MHC genes have been used to learn about the interplay of selection and historical population events. In domestic dogs and their progenitor, the wolf, I explored factors associated with domestication and breed formation and their influence not only on MHC coding regions but also on the haplotypic structure of the class II region. Polymorphism and strong selection was demonstrated in the proximal promoters of MHC genes in dogs and wolves. Hence, genetic variation associated with MHC gene expression may have at least equal importance for a well functioning immune system. Associations between promoter sequences and particular coding alleles suggested allele-specific expression patterns. SNP haplotypes of the MHC class II region revealed ancestral as well as convergent haplotypes, in which combinations of alleles are kept by selection. Interestingly, weaker allelic associations were found between different genes and between coding regions and promoters in dogs compared to wolves. Potentially, this could cause insufficient defense against infections and predispose dogs to autoimmune diseases. For example, I identified a site in the promoter region that showed a consistent difference between haplotypes conferring susceptibility and protection to diabetes in dogs, which should be investigated further. Furthermore, I investigated how selection and demographic changes associated with glacial and inter-glacial periods have affected MHC variation in European hedgehogs and extended the prevailing knowledge concerning their population history.
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Sandoval, Evandra Strazza Rodrigues. "Avaliação do efeito imunomodulador das células mesenquimais estromais humanas em linfócitos T infectados pelo HTLV-1." Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/60/60135/tde-18122014-163958/.

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As características das células estromais mesenquimais multipotentes (MSC) podem ser influenciadas em microambientes inflamatórios. No entanto, o comportamento das MSC frente às infecções virais e a exata contribuição da infecção para disfunção das MSC continuam a ser elucidadas. Neste trabalho, avaliamos o efeito imunossupressor de MSC em linfócitos T infectados pelo HTLV-1 e a susceptibilidade da MSC à infecção por este retrovírus. Os ensaios de co-cultivo utilizando MSC e linhagens de linfócitos infectados pelo HTLV-1 resultaram em diminuição na expressão do gene viral tax e do antígeno p19 do HTLV-1. A redução na expressão do gene tax e da proteína p19 foi relacionada com a maior secreção de IL-6 e aumento na expressão dos genes PGE2, IDO e VCAM-1. Para confirmar a influência da imunorregulação das MSC sobre linfócitos T infectados, comparamos a proliferação de linfócitos T isolados de indivíduos infectados pelo HTLV-1 e indivíduos controles cultivados na presença de MSC. Foi observado que as MSC inibem a linfoproliferação de forma similar em amostras controle e na infecção pelo HTLV-1; e este efeito foi mediado pela expressão de PGE2 e IDO. Além disso, a expressão do gene pol e da proteína p19 do HTLV-1 foi menor após o co-cultivo com MSC, indicando que a imunorregulação pelas MSC também atua nas células infectadas pelo HTLV-1. Em seguida, para investigar as alterações provocadas pelo HTLV-1 nas MSC, realizamos análises morfológicas e ultraestruturais em MSC expostas ao HTLV-1 in vitro. Os resultados revelaram que o HTLV-1 induziu o aparecimento de vesículas intracelulares e a expressão das moléculas de superfície VCAM-1, ICAM-1 e HLA-DR. Os níveis de VCAM-1 e HLA-DR também foram mais expressos em MSC cultivadas na presença de PBMC isoladas de indivíduos HAM/TSP. O HTLV-1 não alterou o processo de diferenciação das MSC em osteócitos e adipócitos. No entanto, o contato direto in vitro das MSC com células infectadas pelo HTLV-1 proporcionou uma eficiente infecção das MSC. As partículas virais isentas de células não foram capazes de causar a infecção em MSC. Por fim, para certificar a existência biológica de MSC infectadas pelo HTLV-1, avaliamos a medula óssea de seis indivíduos acometidos por esta infecção. Foi observado um infiltrado de linfócitos T CD4+ na medula óssea de indivíduos HTLV-1+ e a análise do DNA proviral revelou a presença do provírus integrado nessas células T CD4+. O número de unidades formadoras de colônia fibroblastóide (CFU-F) foi menor em indivíduos infectados pelo HTLV-1 quando comparado com o grupo controle. A expressão dos marcadores de superfície e o potencial de diferenciação in vitro em adipócitos e osteócitos foram similares nas MSC obtidas de indivíduos HTLV-1 e indivíduos controle. Foi demonstrada a presença do DNA proviral e da proteína p19 do HTLV-1 nas MSC isoladas de pacientes HTLV-1+. A comparação do perfil de expressão gênica global entre MSC isoladas de HAM/TSP e indivíduos assintomáticos para o HTLV-1 revelou que os genes da catepsina B e da proteína ribossomal L10 foram diferencialmente expressos. Em conclusão, este trabalho demonstra a importância das MSC na imunomodulação de linfócitos infectados pelo HTLV-1 e que a infecção pelo HTLV-1 altera características biológicas das MSC.
The characteristics of human multipotent mesenchymal stromal cells (MSC) can be influenced by the inflammatory microenvironment. However, the activity of the MSC against viral infections and the exact contribution of the infection to MSC dysfunction remain to be elucidated. We evaluated the immunosuppressive effect of MSC on HTLV-1 infected T lymphocytes and the susceptibility of MSC for this retroviral infection. Assays using co-culture of MSC and HTLV-1+ T lymphocyte lineages resulted in a decrease of tax gene expression and HTLV-1 p19 antigen. The reduction of the tax gene expression and the HTLV-1 p19 were associated with increased IL-6 secretion and higher PGE2, IDO and VCAM-1 gene expression. To confirm if MSC immunoregulation can influence the proliferation of HTLV-1 infected T lymphocytes, we compared the proliferation of HTLV-1+ individuals and healthy individuals cultured in the presence of MSC. It was observed that the lymphoproliferative inhibition by MSC in infected lymphocytes was similar to the control cells, and this effect was mediated by the expression of IDO and PGE2 genes. Furthermore, the pol gene and the HTLV-1 p19 protein were less expressed after co-culture assay with MSC, suggesting that the immunoregulation by MSC is effective in HTLV-1 infected T cells. In order to investigate the changes caused by HTLV-1 in MSC, we performed morphological and ultrastructural analysis of MSC exposed to HTLV-1 in vitro. The contact with HTLV-1 induced an increase of the intracellular vesicles, in addition the MSC cell surface molecules VCAM-1, ICAM-1 and HLA-DR were upregulated. The expression levels of VCAM-1 and HLA-DR molecules were increased in MSC cultured in the presence of PBMC isolated from HTLV-1 associated myelopathy/tropical spastic paraparesis (HAM/TSP) individuals. The MSC differentiation process into osteocytes and adipocytes was not impaired by HTLV-1. In addition, MSCs were efficiently infected by HTLV-1 in vitro due to the direct contact with the HTLV-1-infected cells. However, cell-free virus particles were not capable of causing productive infection. Finally, to ensure the biological function of MSC in HTLV-1 infected patients, we investigated bone marrow (BM) cells from HTLV-1 asymptomatic carriers (HAC) and HAM/TSP individuals. Initially, we observed an infiltration of CD4+ T-cell lymphocytes in BM from HTLV-1 infected individuals and the detection of provirus revealed HTLV-1 integration. The number of colonies of fibroblast progenitor cells (CFU-F) was lower in HTLV-1 infected individuals compared to control. HTLV-1 MSC isolated showed surface molecules expression and differentiation into adipogenic and osteogenic cells similar to control MSC. Proviral DNA and HTLV-1 p19 protein were detected in MSC from HTLV-1 patients. The comparison of global gene expression profiles between MSC isolated from HAM/TSP and HAC individuals revealed that cathepsin B and ribosomal protein L10 were differentially expressed. In conclusion, this study suggests the importance of MSC immunomodulation on HTLV-1 infected T lymphocytes and describe that HTLV-1 infects and alters the biological characteristics of MSC.
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Loh, Andrew Xiong Wan. "Cis-acting polymprophism of MIC game expression." Thesis, University College London (University of London), 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.497874.

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Books on the topic "Muc expression"

1

Hey, Neil Anthony. MUC1 expression in human endometrium. Manchester: University of Manchester, 1996.

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Urban, Robert G., and Roman M. Chicz. MHC Molecules: Expression, Assembly and Function. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4684-6462-7.

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1962-, Urban Robert G., and Chicz Roman M, eds. MHC molecules: Expression, assembly, and function. New York: Chapman & Hall, 1996.

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Eric, Blair G., Pringle Craig R, and Maudsley D. John, eds. Modulation of MHC antigen expression and disease. Cambridge: Cambridge University Press, 1995.

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Jaffe, Leah. Regulation of MHC Class I gene expression during mouse embryogenesis. [New York]: Columbia University, 1992.

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Tello, Carlos Alberto Barron. Transkription des Bakteriophagen Mu. Konstanz: Hartung-Gorre, 1986.

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Boeckh, Clemens. Expression der frühen Funktionen des mutagenen E.coli-Bakteriophagen Mu und ihre Wirkung auf die Wirtszellen. Konstanz: Hartung-Gorre, 1986.

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Winer, Shawn. Peptide dose, MHC affinity, and target self-antigen expression are critical for effective immunotherapy of nonobese diabetic mouse prediabetes. Ottawa: National Library of Canada, 2001.

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Cho, Chae-hyŏn. Chungganyŏp chulgi sep'o ŭi tonggyŏl pangbŏp kaebal mit yujŏnhakchŏk punsŏk e kwanhan yŏn'gu =: Development of cryopreservation and gene expression analysis in porcine mesenchyamal stem cell (MSC). [Seoul]: Nongch'on Chinhŭngch'ŏng, 2008.

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(filólogo), Brown Martin, ed. ¡No me des calabazas!: Equivalencias en inglés de expresiones cotidianas-- ¡y mucho más! ; Don't give me the cold shoulder! : literal (amusing) and colloquial (useful) translations of everyday expressions-- and so much more! [Madrid]: A. Arienza, 2010.

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Book chapters on the topic "Muc expression"

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Malik, Waqar. "Expressions." In Learn Swift on the Mac, 157–64. Berkeley, CA: Apress, 2015. http://dx.doi.org/10.1007/978-1-4842-0376-7_17.

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Malik, Waqar. "Expressions." In Learn Swift 2 on the Mac, 49–58. Berkeley, CA: Apress, 2015. http://dx.doi.org/10.1007/978-1-4842-1627-9_5.

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Malissen, B., and R. N. Germain. "Workshop Summary: Transfection of MHC Genes." In Regulation of Immune Gene Expression, 341–45. Totowa, NJ: Humana Press, 1986. http://dx.doi.org/10.1007/978-1-4612-5014-2_33.

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Chicz, Roman M., and Robert G. Urban. "Major Histocompatibility Antigens: An Introduction." In MHC Molecules: Expression, Assembly and Function, 1–8. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4684-6462-7_1.

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Parker, Kenneth C. "Epitope Prediction Algorithms for Class I MHC Molecules." In MHC Molecules: Expression, Assembly and Function, 163–80. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4684-6462-7_10.

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Jameson, Stephen C., and Kristin A. Hogquist. "Options for TCR Interactions: TCR Agonists, Antagonists and Partial Agonists." In MHC Molecules: Expression, Assembly and Function, 181–90. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4684-6462-7_11.

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Tsomides, Theodore J. "Role of Ligand Density in T Cell Reactions." In MHC Molecules: Expression, Assembly and Function, 191–206. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4684-6462-7_12.

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Vignali, Dario A. A. "Cooperative Recognition of MHC Class II:Peptide Complexes by the T Cell Receptor and CD4." In MHC Molecules: Expression, Assembly and Function, 207–28. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4684-6462-7_13.

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Colonna, Marco. "Receptors for MHC Class I Molecules in Human Natural Killer Cells." In MHC Molecules: Expression, Assembly and Function, 229–41. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4684-6462-7_14.

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Davenport, Miles P., and Adrian V. S. Hill. "The MHC in Host-Pathogen Evolution." In MHC Molecules: Expression, Assembly and Function, 243–60. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4684-6462-7_15.

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Conference papers on the topic "Muc expression"

1

Lee, Myung H. "Zernike decomposition of the thermal blooming-induced phase variation for a Gaussian beam." In OSA Annual Meeting. Washington, D.C.: Optica Publishing Group, 1990. http://dx.doi.org/10.1364/oam.1990.mu4.

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Thermal blooming is the critical phase-distortion degrading factor preventing a ground-based high-energy laser system from achieving a diffraction-limited irradiance profile at a distant target. Adaptive optical systems have been used to correct thermal-blooming-induced phase variation by applying the proper amount of each correcting mode (tilt, defocus, astigmatism, and coma) to the entire aperture. I have developed the analytical expression for these correcting modes,1 which are represented by Zernike polynomials for a uniform beam, and I have also explored the Zernike decomposition of phase variation for the Gaussian beam. In this paper, I present the analytic expression for the phase-variation decomposition for the Gaussian beam in the infinite and truncated cases. As a result, the expressions are reduced to error functions in terms of beam diameter, beam waist, and wind velocity. I compare these results with those of the uniform-beam case and obtain the steady-state limit, i.e., when the elapsed time is longer than the wind-clearing time.
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Uplinger, W. G. "Relative optical mass in a nonisothermal atmosphere." In OSA Annual Meeting. Washington, D.C.: Optica Publishing Group, 1988. http://dx.doi.org/10.1364/oam.1988.ww4.

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A closed-form expression is theoretically derived for the relative optical air mass as a function of zenith angle in an atmosphere with a temperature gradient. The effects of refraction are included, and the atmosphere is assumed to be in hydrostatic equilibrium. Due to the temperature gradient, the atmospheric density does not fall off exponentially with altitude but according to a power law. The radius of the earth is a factor in the expression; thus the relative air mass on other planets can also be calculated. The relative air mass is 1.0 for a vertical path and is around 40.0 for a horizontal path to space. A comparison is made to other expressions showing the effects of refraction and temperature at different altitudes in the atmosphere. Since refraction is much less at high altitudes in the atmosphere, the relative air mass is a definite function of altitude. The expressions presented here can be easily incorporated into computer programs. A similar expression can be derived for the equivalent pressure along an atmospheric path.
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Yarrison-Rice, Jan M., Gregory J. Salamo, William W. Clark, Edward J. Sharp, Gary L. Wood, and Ratnakar R. Neurgaonkar. "Measurements of photorefractive response times with low-irradiance picosecond and cw light sources." In OSA Annual Meeting. Washington, D.C.: Optica Publishing Group, 1991. http://dx.doi.org/10.1364/oam.1991.mu2.

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Following Valley’s work,1 the theoretical expression for the space-charge field’s (Esc) buildup is derived for both cw and picosecond-pulsed low-irradiance excitation, I ≫ Isat, where Isat is the intensity at which the number of excited charges saturates. The cw and picosecond-pulsed expressions for the time-dependent Esc both reduce to where m is the modulation index of the grating and τdi is the dielectric relaxation time. An explanation of how saturation affects the growth of the space-charge field for cw vs picosecond- pulsed excitation is presented. The differential equation for the space-charge field’s time dependence is solved numerically and compared to the quasi-cw result. Theoretically, saturation effects become noticeable for an input intensity of 10−3Isat. For 10 kW/cm2 peak intensity, 22.6-ps pulses, no evidence of saturation is observed experimentally for cerium-doped Sr0 6Ba04Nb2O6 (SBN). The rise times are com parable for pulsed and cw inputs of the same average intensity, over a range of average intensities. This provides a lower limit on the saturation intensity of 10 MW/cm2. An SPPC signal is observed in rhodium-doped SBN in the first 150 pulses (3.69-ps pulsewidth) of illumination yielding an early grating formation time of no longer than 554 ps.
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Li, Hanting, Mingzhe Sui, Zhaoqing Zhu, and Feng Zhao. "MMNet: Muscle Motion-Guided Network for Micro-Expression Recognition." In Thirty-First International Joint Conference on Artificial Intelligence {IJCAI-22}. California: International Joint Conferences on Artificial Intelligence Organization, 2022. http://dx.doi.org/10.24963/ijcai.2022/150.

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Facial micro-expressions (MEs) are involuntary facial motions revealing people’s real feelings and play an important role in the early intervention of mental illness, the national security, and many human-computer interaction systems. However, existing micro-expression datasets are limited and usually pose some challenges for training good classifiers. To model the subtle facial muscle motions, we propose a robust micro-expression recognition (MER) framework, namely muscle motion-guided network (MMNet). Specifically, a continuous attention (CA) block is introduced to focus on modeling local subtle muscle motion patterns with little identity information, which is different from most previous methods that directly extract features from complete video frames with much identity information. Besides, we design a position calibration (PC) module based on the vision transformer. By adding the position embeddings of the face generated by the PC module at the end of the two branches, the PC module can help to add position information to facial muscle motion-pattern features for the MER. Extensive experiments on three public micro-expression datasets demonstrate that our approach outperforms state-of-the-art methods by a large margin. Code is available at https://github.com/muse1998/MMNet.
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Ban, Kyeong-jin, Jong-chan Kim, and Eung-kon Kim. "An Object Expression System using Depth-maps." In 2011 IEEE/FTRA International Conference on Multimedia and Ubiquitous Engineering (MUE). IEEE, 2011. http://dx.doi.org/10.1109/mue.2011.18.

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Yano, Tomoki, Kouyou Otsu, and Tomoko Izumi. "Verification of the Effects of Personalized Evacuation Alerts using Behavioral or Location Information with the Sense of Urgency in a Disaster." In 13th International Conference on Applied Human Factors and Ergonomics (AHFE 2022). AHFE International, 2022. http://dx.doi.org/10.54941/ahfe1001701.

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Delayed evacuation from a huge disaster is one of the factors that increase human damage. It has been pointed out the difficulty in urging an early evacuation after a disaster because people tend to underestimate information that is inconvenient for them, which is called normalcy bias. The most effective way to urge evacuation is to contact each of the evacuees directly, such as calling them. That is, we consider that we should provide information to evacuees that makes them feel as if it is being said to them directly.In this study, we focus on disaster alert services which send disaster information to personal mobile devices (i.e., smartphones) and consider textual expressions of alert that generate a sense of urgency for disaster. Since people always carry their smartphones with them, we expect that personal expression of alert will be possible using the information available on their own smartphones. As for information obtained from a device, in this study, we focus on the location information acquired from GPS and the behavioral information of the user acquired from the accelerometer. We assume that if an alert with textual expression that seems to identify the individual user by using these information is provided, the user receives it will feel as if it is being said to him/her directly. As for the degree of identification of individuals, three degrees of expression are set for location and behavioral information, respectively. Concretely, for location information, 1. the first indicates that a river has flooded, and 2. the second one gives the name of flooded river, and 3. the last shows the distance from the flooded river to user’s current location. For behavioral information, 1. the first includes no information about user’s behavior, 2. the second indicates that the user is reading the alert message, and 3. the last points out how the user is operating the smartphone (e.g., a smartphone is in user’s hand or on user’s desk). We set nine patterns of alert expression by combining the expression based on location and behavioral information.To verify the effectiveness of the alert expressions, we conducted a comparative verification experiment for them. In this experiment, we had the collaborators perform the specified daily task alone in a dark room hearing rain. While the collaborators were performing the task, the one evacuation alert of the nine patterns was sent to them. After receiving the alert, the collaborators confirmed it and then answered the questionnaire. Each of the collaborators repeated this process five times. In the questionnaire, we asked questions about how much they felt a sense of urgency, and how much they thought the alert was directed at them and so on. As a result of this verification, we found that textual expression using location information tend to be more effective as they feel that the message is being said to them. We will describe the detailed experimental results in the camera ready manuscript.
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Westhoven, Martin, Tim van der Grinten, and Steffen Mueller. "Perceptions of a Help-Requesting Robot - Effects of Eye-Expressions, Colored Lights and Politeness of Speech." In MuC'19: Mensch-und-Computer. New York, NY, USA: ACM, 2019. http://dx.doi.org/10.1145/3340764.3340783.

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Xia, Fang, and Lv Hong. "Research on algorithm recognition based on characteristic expression." In 2011 International Conference on Mechatronic Science, Electric Engineering and Computer (MEC). IEEE, 2011. http://dx.doi.org/10.1109/mec.2011.6025995.

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Yang, Haisu, Rosalba Tamayo, Bruce Horten, Moacyr DaSilva, Maryann Gangi, Evelyn Vazquez, Daisy Joseph, Patricia Okamoto, and Thomas Scholl. "Abstract LB-274: Clinical significance of MUC1, MUC2 and CK17 expression patterns in the diagnosis of pancreatic carcinoma." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-lb-274.

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Miedler, J., F. Abdul-Karim, N. Wang, and J. Baar. "MUC1 expression in early-stage triple-negative breast cancer." In CTRC-AACR San Antonio Breast Cancer Symposium: 2008 Abstracts. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-3009.

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Reports on the topic "Muc expression"

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Carson, Daniel D. Mucin (MUC1) Expression and Function in Prostate Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, March 2004. http://dx.doi.org/10.21236/ada432401.

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Coticchia, Christine M., and Robert B. Dickson. Fas/FasL System in c-Myc Expressing Mammary Carcinoma Cells. Fort Belvoir, VA: Defense Technical Information Center, June 2002. http://dx.doi.org/10.21236/ada411302.

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Coticchia, Christine M., and Robert B. Dickson. Fas/FasL System in c-Myc Expressing Mammary Carcinoma Cells. Fort Belvoir, VA: Defense Technical Information Center, June 2003. http://dx.doi.org/10.21236/ada422986.

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Dickson, Robert B. Modulation of Cyclin Expression by C-MYC in Malignant and Nonmalignant Mammary Epithelial Cells. Fort Belvoir, VA: Defense Technical Information Center, September 1995. http://dx.doi.org/10.21236/ada302398.

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Popov, Todor M., Gergana S. Stancheva, Silva G. Giragosyan, Orlin V. Stoyanov, Sylvia E. Valcheva, Emil I. Tsenev, Radka P. Kaneva, and Diana P. Popova. Correlations between PKM2, HIF‑1α, c‑Myc and p53 mRNA Expression Levels in Laryngeal Carcinoma. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, May 2018. http://dx.doi.org/10.7546/crabs.2018.05.14.

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El Bejjani, Rachid M. Effect of MUC1 Expression on EGFR Endocytosis and Degradation in Human Breast Cancer Cell Lines. Fort Belvoir, VA: Defense Technical Information Center, April 2009. http://dx.doi.org/10.21236/ada504024.

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El Bejjani, Rachid M. Effect of MUC1 Expression on EGFR Endocytosis and Degradation in Human Breast Cancer Cell Lines. Fort Belvoir, VA: Defense Technical Information Center, April 2007. http://dx.doi.org/10.21236/ada470580.

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Lin, Charles. Understanding Selective Downregulation of c-Myc Expression through Inhibition of General Transcription Regulators in Multiple Myeloma. Fort Belvoir, VA: Defense Technical Information Center, June 2014. http://dx.doi.org/10.21236/ada605044.

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Lin, Charles. Understanding Selective Downregulation of c-Myc Expression through Inhibition of General Transcription Regulators in Multiple Myeloma. Fort Belvoir, VA: Defense Technical Information Center, June 2015. http://dx.doi.org/10.21236/ada620612.

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McGuffie, Eileen M., and Carlo V. Catapano. Development of Triplex-Forming Oligonucleotides to Inhibit Expression of the c-myc Oncogene in Breast Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, April 2003. http://dx.doi.org/10.21236/ada416148.

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