2,772 research outputs found
Senescence and pre-malignancy: How do tumors progress?
Cellular senescence is a tumor suppressor response that has been observed both in vitro and in vivo, and features of senescence have been documented in various human premalignant lesions, including melanoma, colon and lung adenoma, prostatic intraepithelial neoplasia, and others. The fact that a subset of these lesions eventually progress to malignant invasive tumors suggests that premalignant cells can either bypass or escape the senescent response. Much work has been done to understand the mechanisms underlying such progression, but it remains unclear whether tumors progress by evasion of senescence induction, or by disruption of senescence maintenance, or whether both mechanisms can occur in human cancer development. This review presents the current evidence for mechanisms of senescence evasion and reversion, and discusses what has been learnt about this process using in vitro and in vivo experimental systems. As we learn more about the key signaling effectors of senescence, the hope is that appropriate targets will be identified for preservation and-or re-induction of senescence in human tumors. Such knowledge may also find application in better estimation of risks of cancer progression in individual premalignant lesions, which will lead to more accurate allocation of appropriate treatment options for such patients. © 2011 Elsevier Ltd.Acosta JC, 2008, CELL, V133, P1006, DOI 10.1016-j.cell.2008.03.038; Bartkova J, 2006, NATURE, V444, P633, DOI 10.1038-nature05268; Beausejour CM, 2003, EMBO J, V22, P4212, DOI 10.1093-emboj-cdg417; Berman HK, 2010, CANCER PREV RES, V3, P579, DOI 10.1158-1940-6207.CAPR-10-0073; Bihani T, 2004, CELL CYCLE, V3, P1201; Braig M, 2005, NATURE, V436, P660, DOI 10.1038-nature03841; BRASH DE, 1991, P NATL ACAD SCI USA, V88, P10124, DOI 10.1073-pnas.88.22.10124; BURCH HB, 1995, ENDOCRIN METAB CLIN, V24, P663; Busuttil RA, 2006, DNA REPAIR, V5, P52, DOI 10.1016-j.dnarep.2005.07.006; BUTTRAM VC, 1981, FERTIL STERIL, V36, P433; Campisi J, 2007, NAT REV MOL CELL BIO, V8, P729, DOI 10.1038-nrm2233; Campisi J, 2005, CELL, V120, P513, DOI 10.1016-j.cell.2005.02.003; Cappell M S, 2007, Minerva Gastroenterol Dietol, V53, P351; Chakrabarti J, 2004, BRIT J CANCER, V91, P954, DOI 10.1038-sj.bjc.6602059; Chang BD, 1999, CANCER RES, V59, P3761; Chen ZB, 2005, NATURE, V436, P725, DOI 10.1038-nature03918; Collado M, 2005, NATURE, V436, P642, DOI 10.1038-436642a; Collins LC, 2005, CANCER-AM CANCER SOC, V103, P1778, DOI 10.1002-cncr.20979; Coppe JP, 2008, PLOS BIOL, V6, P2853, DOI 10.1371-journal.pbio.0060301; Courtois-Cox S, 2006, CANCER CELL, V10, P459, DOI 10.1016-j.ccr.2006.10.003; Cristofalo VJ, 2005, EXP GERONTOL, V40, P836, DOI 10.1016-j.exger.2005.08.005; Dankort D, 2007, GENE DEV, V21, P379, DOI 10.1101-gad.1516407; Denchi EL, 2005, MOL CELL BIOL, V25, P2660, DOI 10.1128-MCB.25.7.2660-2672.2005; Dhomen N, 2009, CANCER CELL, V15, P294, DOI 10.1016-j.ccr.2009.02.022; Dickinson SI, 2010, CANCER CONTROL, V17, P214; di Fagagna FD, 2008, NAT REV CANCER, V8, P512, DOI 10.1038-nrc2440; Di Micco R, 2006, NATURE, V444, P638, DOI 10.1038-nature05327; Di Micco R, 2011, NAT CELL BIOL, V13, P292, DOI 10.1038-ncb2170; DIMRI GP, 1995, P NATL ACAD SCI USA, V92, P9363, DOI 10.1073-pnas.92.20.9363; Dirac AMG, 2003, J BIOL CHEM, V278, P11731, DOI 10.1074-jbc.C300023200; Farrell WE, 1998, ANN MED, V30, P192, DOI 10.3109-07853899808999403; Feldser DM, 2007, CANCER CELL, V11, P461, DOI 10.1016-j.ccr.2007.02.026; Ferbeyre G, 2000, GENE DEV, V14, P2015; Fonseca R, 1997, ANN INTERN MED, V127, P1013; Gauthier ML, 2007, CANCER CELL, V12, P479, DOI 10.1016-j.ccr.2007.10.017; Gire V, 1998, MOL CELL BIOL, V18, P1611; Goldman R, 2003, J NUTR, V133, p965S; Gosselin K, 2009, CANCER RES, V69, P7917, DOI 10.1158-0008-5472.CAN-08-2510; Gray-Schopfer VC, 2006, BRIT J CANCER, V95, P496, DOI 10.1038-sj.bjc.6603283; Ha L, 2007, P NATL ACAD SCI USA, V104, P10968, DOI 10.1073-pnas.0611638104; Haggman MJ, 1997, J UROLOGY, V158, P12, DOI 10.1097-00005392-199707000-00004; Hanahan D, 2000, CELL, V100, P57, DOI 10.1016-S0092-8674(00)81683-9; Hartmann LC, 2005, NEW ENGL J MED, V353, P229, DOI 10.1056-NEJMoa044383; Jasperson KW, 2010, GASTROENTEROLOGY, V138, P2044, DOI 10.1053-j.gastro.2010.01.054; Kennedy AL, 2010, CELL DIV, V5, DOI 10.1186-1747-1028-5-16; Kortlever RM, 2006, NAT CELL BIOL, V8, P877, DOI 10.1038-ncb1448; Kosar M, 2011, CELL CYCLE, V10, P457, DOI 10.4161-cc.10.3.14707; Krtolica A, 2001, P NATL ACAD SCI USA, V98, P12072, DOI 10.1073-pnas.211053698; Kuilman T, 2010, GENE DEV, V24, P2463, DOI 10.1101-gad.1971610; Kuilman T, 2008, CELL, V133, P1019, DOI 10.1016-j.cell.2008.03.039; Lee Erica H, 2010, Plast Reconstr Surg, V125, p188e, DOI 10.1097-PRS.0b013e3181d6e89a; Levy A, 2003, FRONT NEUROENDOCRIN, V24, P94, DOI 10.1016-S0091-3022(03)00012-8; Lukasova E, 2005, J LEUKOCYTE BIOL, V77, P100, DOI 10.1189-jlb.0704388; Majumder PK, 2008, CANCER CELL, V14, P146, DOI 10.1016-j.ccr.2008.06.002; Mallette FA, 2007, J BIOL CHEM, V282, P34938, DOI 10.1074-jbc.M707074200; Mallette FA, 2007, CELL CYCLE, V6, P1831; Michaloglou C, 2005, NATURE, V436, P720, DOI 10.1038-nature03890; Moiseeva O, 2006, MOL BIOL CELL, V17, P1583, DOI 10.1091-mbc.E05-09-0858; Mooi WJ, 2006, NEW ENGL J MED, V355, P1037, DOI 10.1056-NEJMra062285; Nardella C, 2008, GENE DEV, V22, P2172, DOI 10.1101-gad.1699608; Narita M, 2003, CELL, V113, P703, DOI 10.1016-S0092-8674(03)00401-X; Narita M, 2006, CELL, V126, P503, DOI 10.1016-j.cell.2006.05.052; PAGE DL, 1994, WORLD J SURG, V18, P32; Park YS, 2008, ANN SURG ONCOL, V15, P1968, DOI 10.1245-s10434-008-9927-9; Roberson RS, 2005, CANCER RES, V65, P2795, DOI 10.1158-0008-5472.CAN-04-1270; Rodier F, 2009, NAT CELL BIOL, V11, P973, DOI 10.1038-ncb1909; Saab R, 2010, THESCIENTIFICWORLDJO, V10, P727, DOI 10.1100-tsw.2010.68; Saab R, 2009, CANCER RES, V69, P440, DOI 10.1158-0008-5472.CAN-08-1892; Sabah M, 2007, APPL IMMUNOHISTO M M, V15, P64, DOI 10.1097-01.pai.0000201809.43554.ed; Sage J, 2003, NATURE, V424, P223, DOI 10.1038-nature01764; Sarkisian CJ, 2007, NAT CELL BIOL, V9, P493, DOI 10.1038-ncb1567; Schmitt CA, 2007, BBA-REV CANCER, V1775, P5, DOI 10.1016-j.bbcan.2006.08.005; Schmitt CA, 2002, CELL, V109, P335, DOI 10.1016-S0092-8674(02)00734-1; Serrano M, 2001, CURR OPIN CELL BIOL, V13, P748, DOI 10.1016-S0955-0674(00)00278-7; Shamma A, 2009, CANCER CELL, V15, P255, DOI 10.1016-j.ccr.2009.03.001; Shay JW, 2004, ONCOGENE, V23, P2919, DOI 10.1038-sj.onc.1207518; Skomedal H, 1999, GYNECOL ONCOL, V73, P223, DOI 10.1006-gyno.1999.5346; Soucek L, 2008, NATURE, V455, P679, DOI 10.1038-nature07260; STEIN GH, 1985, J CELL PHYSIOL, V122, P343, DOI 10.1002-jcp.1041220303; Sun PQ, 2007, CELL, V128, P295, DOI 10.1016-j.cell.2006.11.050; Takahashi A, 2006, NAT CELL BIOL, V8, P1291, DOI 10.1038-ncb1491; Tateishi U, 2003, RADIOGRAPHICS, V23, P1477, DOI 10.1148-rg.236015526; te Poele RH, 2002, CANCER RES, V62, P1876; Untergasser G, 2003, EXP GERONTOL, V38, P1179, DOI 10.1016-j.exger.2003.08.008; Ventura A, 2007, NATURE, V445, P661, DOI 10.1038-nature05541; Vijg J, 2005, ANN NY ACAD SCI, V1055, P35, DOI 10.1196-annals.1323.007; Wajapeyee N, 2008, CELL, V132, P363, DOI 10.1016-j.cell.2007.12.032; Wu CH, 2007, P NATL ACAD SCI USA, V104, P13028, DOI 10.1073-pnas.0701953104; Xu M, 2008, MOL CELL BIOL, V28, P1713, DOI 10.1128-MCB.01360-07; Xue W, 2007, NATURE, V445, P656, DOI 10.1038-nature05529; Young AP, 2008, NAT CELL BIOL, V10, P361, DOI 10.1038-ncb1699; Zhang RG, 2005, DEV CELL, V8, P19, DOI 10.1016-j.devcel.2004.10.019; Zhang ZH, 2006, MODERN PATHOL, V19, P1339, DOI 10.1038-modpathol.3800655; Zheng Y, 2009, OMICS, V13, P301, DOI 10.1089-omi.2009.001410111
Communicating with terminal patients: Lessons from wit and students
[No abstract available]Deloney LA, 2003, TEACH LEARN MED, V15, P247, DOI 10.1207-S15328015TLM1504_06; Ellershaw J, 2003, BRIT MED J, V326, P30, DOI 10.1136-bmj.326.7379.30; Garg A, 1997, CAN MED ASSOC J, V156, P1159; Kirk P, 2004, BRIT MED J, V328, P1343, DOI 10.1136-bmj.38103.423576.55; Lloyd-Williams M, 2003, BRIT MED J, V327, P221, DOI 10.1136-bmj.327.7408.221-b; Saab BR, 2005, FAM MED, V37, P9032
Continuous improvement at Saab Aerosystems
The today’s high tech society with demands for new innovations and a cost effective work puts the companies to the test with many and complicated demands. To be a part of the evolution the companies have to establish good quality together with high profit. The global environment demands that companies work in line with total quality management and continuous improvements are a part of that. Saab has for a long time had one dominating product and one customer. The demands for continuous improvements has there for not been as notified as for today due to the monopoly situation. Along with new customers and new products, more and highly set demands for innovation and creativity becomes a reality to meet. The purpose of this thesis is to give suggestions to a work process which Saab Aerosystems can follow to increase the continuous improvements within the company. The author has interviewed employees at Saab Aerosystems for the purpose to get more knowledge about the work for improvements of today and what the visions are for future work. Interviews were also performed at two companies with no connection to Saab Aerosystems. The purpose was to investigate how the improvement work is managed and performed to if possible bring ideas to the work process. Based on the theoretical frame of reference and the interviews a work process was established on how Saab Aerosystems will have a well functioning continuous improvement process.Dagens högteknologiska samhälle med ständiga krav på nya innovationer och kostnadseffektivt arbete ställer stora krav på företag. För att följa med i utvecklingen måste företagen upprätta en god kvalitet i samband med hög lönsamhet. Den globala konkurrensen kräver att företagen arbetar med offensiv kvalitetsutveckling och som en del av det ingår ständiga förbättringar. Saab har länge haft en dominerande produkt och en kund. På grund av monopolsituation har kraven på att ständigt förbättras ej uppmärksammats på ett lika tydligt sätt som för dagens situation. I samband med nya kunder och nya produkter ställs högre krav på innovation och kreativitet att ständigt förbättras. Saab Aerosystems arbetar idag med ett verksamhetsutvecklingsprojekt som inkluderar ett antal delprojekt. Syftet med examensarbetet är att ta fram en handlingsplan för hur Saab Aerosystems ska få igång en självgående ändamålsenlig ständig förbättringsverksamhet. Författaren har intervjuat anställda på Saab Aerosystems för att få en bredare kunskap kring förbättringsverksamheten idag samt hur visionerna för hur framtida förbättringsarbete ska se ut och vidareutvecklas. Intervjuer utfördes även på två externa företag för att undersöka hur deras förbättringsarbete ter sig och för att om möjligt inhämta idéer till handlingsplanen. Utifrån den teoretiska referensramen och de interna och externa interjvuerna upprättades en handlingsplan för hur Saab Aerosystems ska få igång en ständig förbättringsverksamhet
Resultados perinatais de transfusões intra-uterinas realizadas por doença hemolítica perinatal na maternidade Carmela Dutra - Florianópolis
Trabalho de Conclusão de Curso - Universidade Federal de Santa Catarina. Curso de Medicina. Departamento de Tocoginecologia
Developing scenarios to assess sunflower and soybean yield under different sowing dates and water regimes in the Bekaa valley (Lebanon): Simulations with Aquacrop
In a semi-arid environment, the main challenge for crop production is water
limitation in space and in time. Considered as appropriate tools, models are used to
evaluate the effects of water deficit on crop productivity for better irrigation
planning and sustainable yield. The AquaCrop model was tested using data
collected during a 4-year experiment on soybean (Glycine max L. Merril) and
sunflower (Helianthus annuus L.) in the Bekaa Valley of Lebanon. The model was
found to accurately simulate final crop biomass, yield and cumulative
evapotranspiration: in fact the Wilmot index of agreement (IoA) values were
0.97, 0.96 and 0.96, respectively, for soybean and 0.93, 0.95 and 0.93, respectively,
for sunflower, while the relative RMSE was 0.04, 0.05 and 0.02, respectively,
for soybean and 0.04, 0.06 and 0.04, respectively, for sunflower. The analysis of
irrigation scenarios showed that the early planting of sunflower could demonstrate
a greater efficiency than late sowing. In addition, applying three irrigations, of
100 mm each, prior to flowering, at mid flowering stage and at the beginning of
seed formation could lead to highest yields (ranging between 4.51 and 2.34 t ha-1)
and crop water productivity (CWP) (ranging between 1.5 and 0.78 kg m-3).
Sunflower yields were low (0.42 t ha-1 to 0.37 t ha-1) and unreliable when one
single irrigation was performed only at the beginning of seed formation, while
highest values (ranging between 1.97 and 1.74 t ha-1) were obtained when it was
done prior to flowering. The highest yields and crop water productivity for soybean
were obtained when the crop was sown in April and by applying three irrigations, of 100 mm each, at full bloom, at seed enlargement and at mature seeds. Soybean
yield values ranged between 3.16 and 2.01 t ha-1, while CWP values varied from
1.05 to 0.67 kg m-3. However, irrigating at seed enlargement and mature seeds, as
well as applying only one irrigation of 100 mm at any growth stage, could lead to
very low yields and CWP
Clinical update on K-Ras targeted therapy in gastrointestinal cancers
KRAS mutations are common in pancreatic and colorectal cancers and are associated with lack of response to anti-epidermal growth factor receptor therapy. Ras is an established therapeutic target that has long eluded efforts to develop specific inhibitors, while targeting downstream signaling pathways has proven largely ineffective, highlighting a need for rational combination strategies to overcome resistance. Recently, renewed interest in directly targeting Ras has led to the development of several small-molecule inhibitors that bind directly to K-Ras or its effector proteins, downregulation of K-Ras expression using therapeutic antisense oligonucleotides or siRNAs, and targeting scaffold proteins such as kinase suppressor of Ras. Indirect approaches to inhibiting K-Ras include combining inhibitors of the mitogen-activated protein kinase pathway with novel targeted agents. Immunotherapy in early studies has also shown clinical promise. This review summarizes the current evidence for each of these approaches
Cellular Senescence: Many Roads, One Final Destination
Cellular senescence is a tumor-suppressor mechanism that has been shown to occur in response to multiple signals, including oncogenic stress, DNA damage, oxidative stress, telomere shortening, and other tumor-promoting insults. Over the past decade, much has been uncovered regarding the phenotype of this tumor-suppressor response and the underlying pathways necessary for its establishment. However, we have also learned that the intricate details of signaling pathways underlying senescence as a tumor-suppressor response are very much context dependent. In addition, cross-talk among pathways, and negative and positive feedback loops, all complicate our understanding of this process. This short review attempts to summarize what is known to date regarding senescence in tumor suppression, both in vitro and in vivo. Further insights into pathways necessary for senescence will hopefully identify appropriate targets for interventions to not only induce senescence as a treatment of cancerous lesions, but also to maintain this state in premalignant lesions in an effort to prevent progression to cancer
Software Requirements Division - An Interview Study at Saab AB, Electronic Defence Systems
Software requirements are a crucial part of software development.
They are also part of the main reason why
projects fail. The previous research in the area of software
requirements has not been focused on the division of software
requirements. This paper presents an interview study
with such a focus. Five people working at Saab AB, Electronic
Defence Systems, Operations G oteborg (Saab EDS)
were interviewed about software requirements division and
how they conduct such divisions at Saab EDS. The respondents
answers were summarized and analysed. The analysis
showed that Saab EDS divide software requirements into
four levels; customer, system, subsystem and lower level.
The software requirements division are conducted through
group discussions. The basis of the division of software requirements
is indicated to be based upon expert knowledge
and that the software requirements division decisions are
people dependent. The improvement that Saab EDS can
proceed with, suggested by the paper author, is to take "software
requirements division decision"-notes to be able to keep
track of the reasoning behind the software requirements division
decision
The Nordic Model and Structural Change: Lessons from the Collapse of Saab Automobile AB
The case of Saab and Trollhättan shows one way that societies can harness the productive side of creative destruction while mitigating the harm it causes
Hipertensão arterial na gestação: avaliação dos resultados maternos e perinatais na maternidade Carmela Dutra de 2002 a 2009.
Trabalho de Conclusão de Curso - Universidade Federal de Santa Catarina. Curso de Medicina. Departamento de Tocoginecologia
- …
