To see the other types of publications on this topic, follow the link: The Invasion of Normandy.
Journal articles on the topic 'The Invasion of Normandy'
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the top 50 journal articles for your research on the topic 'The Invasion of Normandy.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.
1
Liscum, Mannie. "Allied Deception Operations and the Invasion of Normandy." Global War Studies 8, no. 1 (June 1, 2011): 153–56. http://dx.doi.org/10.5893/19498489.08.01.10.
Full text
2
Vassie, John, and Byung Ho Choi. "Simulation of Normandy Invasion on 6th of June, 1944." Journal of Coastal Research 85 (May 2018): 1071–75. http://dx.doi.org/10.2112/si85-215.1.
Full text
3
Hamburger, Kenneth. "Book Review: E-Boat Alert: Defending the Normandy Invasion Fleet." War in History 6, no. 3 (July 1999): 375–77. http://dx.doi.org/10.1177/096834459900600316.
Full text
4
Stamp, Gavin. "High Victorian Gothic and the Architecture of Normandy." Journal of the Society of Architectural Historians 62, no. 2 (June 1, 2003): 194–211. http://dx.doi.org/10.2307/3592477.
Full textAbstract:
High Victorian Gothic in England was an exotic style, and the importance of Italian Gothic precedents in its development has long been recognized, as has the interest in thirteenth-century French Gothic in the 1850s. What has received much less attention is the influence of the medieval buildings of Normandy. In this article, I examine the historical and cultural connections between England and Normandy, which were stimulated by the Napoleonic Wars and the threat of invasion, and were further encouraged by the ease of crossing the English Channel. Seeking the origins of English Gothic and Romanesque architecture, antiquaries and artists explored Normandy in the decades after Waterloo, anticipating the interest of architects. Whether the results of travel or study of a growing number of publications on the medieval architecture of Normandy, numerous midcentury buildings show intimate acquaintance with thirteenth-century churches in Normandy-old village churches with saddleback towers or distinctive spires, which, paradoxically, resemble High Victorian designs in their rugged austerity.
5
Harvey, John H., Shelly K. Stein, and Paul K. Scott. "Fifty Years of Grief: Accounts and Reported Psychological Reactions of Normandy Invasion Veterans." Journal of Narrative and Life History 5, no. 4 (January 1, 1995): 315–32. http://dx.doi.org/10.1075/jnlh.5.4.02fif.
Full textAbstract:
Abstract From Normandy combat veterans, we obtained narrative evidence on the experiences of loss and grief associated with their involvement in the invasion in France, June 6, 1944. Twelve veterans were interviewed in person in Nor-mandy at the time of the 1994 reunion, and 31 were subsequently interviewed by telephone. We present veterans' reports of battle experiences on D-Day and how they believe those experiences were manifest in psychological reactions over the last 50 years. Our analysis of these reports is framed by a theoretical conception that emphasizes the value of developing and communicating story-like constructions, which we refer to as accounts, as a constructive way of psychologically coping with severe stressors and loss over time. Most of the veterans reported lifelong grieving associated with their losses at Normandy. This grief recurred for most on anniversary dates and when thinking of war and death in general. For some, it was manifest in compelling, regular thoughts about the loss of their friends and their firsthand experiences of loss during the D-Day fighting. Many veterans also reported years of depression associated with their war experience. Some indicated that they kept their stories and feelings mostly private over the half century, and only now, around the time of the commemoration, did they open up. Veterans who indicated that they coped best with their trauma over time emphasized the healing power of working on and telling their stories to close others. (Grief Work, Social and Clinical Psy-chology) "These are the fathers we never knew, the uncles we never met, the friends who never returned, the heroes we can never repay."-President Bill Clinton speak-ing at the American cemetery near Omaha Beach, Normandy, France, June 6, 1994. "I don't think there's a day that goes by that I don't think and grieve about it. When you think about it, you think it was just yesterday. It's so clear in my mind. I'll never forget."-Normandy combat veteran, age 74, reflecting on his experience during the D-Day invasion.
6
Gimblett, Richard H. "Book Review: Gators of Neptune: Naval Amphibious Planning for the Normandy Invasion." International Journal of Maritime History 19, no. 1 (June 2007): 449–50. http://dx.doi.org/10.1177/084387140701900185.
Full text
7
Lewis, Adrian R. "The Americans at D-Day: The American Experience at the Normandy Invasion (review)." Journal of Military History 69, no. 3 (2005): 878–79. http://dx.doi.org/10.1353/jmh.2005.0168.
Full text
8
Laudicina, Matthew. "Book Review: D-Day: The Essential Reference Guide." Reference & User Services Quarterly 58, no. 1 (October 10, 2018): 62. http://dx.doi.org/10.5860/rusq.58.1.6852.
Full textAbstract:
The Normandy Landings, commonly referred to as D-Day, was a pivotal moment in the course of the Second World War. This successful invasion of the northwestern beaches of France marked the beginning of the Allied liberation of the western front, and would ultimately lead to the defeat of Nazi Germany. D-Day: The Essential Reference Guide successfully provides quality reference information on this major historical event.
9
Everett, M. E., C. J. Pierce, N. Save, R. R. Warden, D. B. Dickson, R. A. Burt, and J. C. Bradford. "Geophysical investigation of the June 6, 1944 D-Day invasion site at Pointe du Hoc, Normandy, France." Near Surface Geophysics 4, no. 5 (December 1, 2005): 289–304. http://dx.doi.org/10.3997/1873-0604.2005052.
Full text
10
Schofield, John. "D-Day sites in England: an assessment." Antiquity 75, no. 287 (March 2001): 77–83. http://dx.doi.org/10.1017/s0003598x00052753.
Full textAbstract:
Between midnight on 6 June (D-Day) and 30 June 1944, over 850,000 men landed on the invasion beachheads of Normandy, together with nearly 150,000 vehicles and 570,000 tons ofsupplies. Assembled in camps and transit areas over the preceding months, this force was dispatched from a string of sites along Britain's coastline between East Anglia and South Wales (Dobinson 1996: 2). The article reviews those sites in England involved in this embarkation. English Heritage's Monuments Protection Programme (MPP) aims to identify surviving sites and recommend appropriate protection for them.
11
BULLEY, MICHAEL. "Intellectual franglais." English Today 21, no. 1 (January 2005): 56–57. http://dx.doi.org/10.1017/s0266078405001124.
Full textAbstract:
Some adjectival links across the Channel. Of the countless delights and complexities to be discovered in the relationships among the Indo-European languages, particularly fascinating are the connections between English and French. The two languages start together in proto-Indo-European (if there ever was such a thing), diverge into the Germanic and Latinate branches of the family, come together (north of the channel only) with the merging of French and English after the invasion of William of Normandy in 1066, and have been glued together even more by the influence of the classical languages, particularly Latin, in and after the Renaissance.
12
Benbow, Tim. "The contribution of Royal Navy aircraft carriers and the Fleet Air Arm to Operation ‘Overlord’, 1944." War in History 26, no. 2 (September 18, 2017): 265–86. http://dx.doi.org/10.1177/0968344517702417.
Full textAbstract:
This article examines the utility of naval aviation, specifically the contribution of the British naval air arm to Operation Overlord. It argues that while there were practical reasons for carriers not being present directly off the Normandy beaches, British naval aviation supported the invasion both directly (from ashore, and from carriers operating at a distance) and indirectly, over a long period. It was also performing a range of other roles in several theatres. Navies and naval aviation contribute to campaigns in a way that is different to land-based forces; understanding this requires a bigger map and a longer timeline.
13
Hansford, R. F. "The Development of Shipborne Navigational Radar." Journal of Navigation 50, no. 3 (September 1997): 390–99. http://dx.doi.org/10.1017/s0373463300019019.
Full textAbstract:
This paper was first published in the Journal in 1947 (Vol. 1, p. 118). Sections 1 and 2 are summarized in order to save space. Sections 3, 4 and 5 are reprinted with only a little abridgment. The paper is followed by comment from the original author.The original paper gave a comprehensive account of the development of navigational radar in the United Kingdom from the beginning of World War II up to the time of writing.The use that was made of the very early radars was mentioned and the improvements brought about by the introduction of the PPI (Plan Position Indicator) and centimetric radar were described. An account was given of how radar assisted the Normandy landings, and of the techniques employed including the use of radar predictions of the Normandy coastline (produced in great secrecy) which were optically superimposed on the PPI. Also shown on the predictions were the planned approach tracks to the shore. An example of one of these predictions compared with the post-invasion radar photograph is shown in Fig. 1. This superimposition of geographical information on the PPI was to become of great significance in later years.
14
Watarai, Masahisa, Yoichi Kamata, Shunji Kozaki, and Chihiro Sasakawa. "rho, a Small GTP-Binding Protein, Is Essential for Shigella Invasion of Epithelial Cells." Journal of Experimental Medicine 185, no. 2 (January 20, 1997): 281–92. http://dx.doi.org/10.1084/jem.185.2.281.
Full textAbstract:
Shigella, the causative agents of bacillary dysentery, are capable of invading mammalian cells that are not normally phagocytic. Uptake of bacteria by the mammalian cells is directed by bacterial factors named IpaB, IpaC, and IpaD invasins, in which Ipa invasins secreted into the bacterial environment can interact with α5β1 integrin. We report here that Shigella invasion of epithelial cells requires rho activity, a ras-related GTP-binding protein. The invasive capacity of Shigella flexneri for Chinese hamster ovary (CHO) cells and other epithelial cells were greatly reduced when treated with Clostridium botulinum exoenzyme C3 transferase. Conversely, uptake of bacteria by CHO cells was promoted upon microinjection of an activated rho variant, Val14RhoA. Attachment of S. flexneri to CHO cells can elicit tyrosine phosphorylation of pp125FAK and paxillin, localized accumulation of F-actin, vinculin, and talin, and activation of protein kinase C, which were all blocked by the treatment with C3 transferase. Our results indicate that cellular signal transduction regulated by rho is essential for Shigella invasion of epithelial cells.
15
Hotary, Kevin B., Ikuo Yana, Farideh Sabeh, Xiao-Yan Li, Kenn Holmbeck, Henning Birkedal-Hansen, Edward D. Allen, Nobuaki Hiraoka, and Stephen J. Weiss. "Matrix Metalloproteinases (MMPs) Regulate Fibrin-invasive Activity via MT1-MMP–dependent and –independent Processes." Journal of Experimental Medicine 195, no. 3 (January 28, 2002): 295–308. http://dx.doi.org/10.1084/jem.20010815.
Full textAbstract:
Cross-linked fibrin is deposited in tissues surrounding wounds, inflammatory sites, or tumors and serves not only as a supporting substratum for trafficking cells, but also as a structural barrier to invasion. While the plasminogen activator-plasminogen axis provides cells with a powerful fibrinolytic system, plasminogen-deleted animals use alternate proteolytic processes that allow fibrin invasion to proceed normally. Using fibroblasts recovered from wild-type or gene-deleted mice, invasion of three-dimensional fibrin gels proceeded in a matrix metalloproteinase (MMP)-dependent fashion. Consistent with earlier studies supporting a singular role for the membrane-anchored MMP, MT1-MMP, in fibrin-invasive events, fibroblasts from MT1-MMP–null mice displayed an early defect in invasion. However, MT1-MMP–deleted fibroblasts circumvented this early deficiency and exhibited compensatory fibrin-invasive activity. The MT1-MMP–independent process was sensitive to MMP inhibitors that target membrane-anchored MMPs, and further studies identified MT2-MMP and MT3-MMP, but not MT4-MMP, as alternate pro-invasive factors. Given the widespread distribution of MT1-, 2-, and 3-MMP in normal and neoplastic cells, these data identify a subset of membrane-anchored MMPs that operate in an autonomous fashion to drive fibrin-invasive activity.
16
Dauvin, Jean-Claude. "Asian Shore Crabs Hemigrapsus spp. (Crustacea: Brachyura: Grapsoidea) continue their invasion around the Cotentin Peninsula, Normandy, France: Status of the Hemigrapsus population in 2009." Aquatic Invasions 4, no. 4 (December 2009): 605–11. http://dx.doi.org/10.3391/ai.2009.4.4.6.
Full text
17
Filler, Scott G., and Donald C. Sheppard. "Fungal Invasion of Normally Non-Phagocytic Host Cells." PLoS Pathogens 2, no. 12 (2006): e129. http://dx.doi.org/10.1371/journal.ppat.0020129.
Full text
18
Wills, Henry. "Archaeological aspects of D-Day: Operation Overlord." Antiquity 68, no. 261 (December 1994): 843–45. http://dx.doi.org/10.1017/s0003598x00047554.
Full textAbstract:
The September Editorial (68: 477–9) noticed how the Normandy invasions of D-Day 1944 are, and are not, archaeologically visible. The author of the pioneering book on the pillbox defences of Britain in the Second World War explains what little there is surviving in southern England. Static defences, we see, leave traces in a way a mobile attack does not.
19
Ziober, Barry L., Sol S. Silverman, and Randall H. Kramer. "Adhesive Mechanisms Regulating Invasion and Metastasis in Oral Cancer." Critical Reviews in Oral Biology & Medicine 12, no. 6 (November 2001): 499–510. http://dx.doi.org/10.1177/10454411010120060401.
Full textAbstract:
It is the relentless invasion and growth into surrounding tissue that characterize oral squamous cell carcinoma. Metastasis is perhaps the most challenging and important aspect of cancer progression, in that it generally signifies limited survival and ineffective therapy. Inherent in metastasis is invasion, the process by which cells infiltrate into adjacent tissues, degrading basement membranes and extracellular matrix and disrupting tissue architecture and sometimes organ function. The factors that regulate these processes are complex and likely involve loss of the controls that are normally in place in physiologic tissue modeling. Adhesion receptors and their ligands are important in modulating not only invasion of oral squamous cell carcinoma cells but also their survival and proliferation. Normal oral mucosal epithelial cells use integrins to maintain their anchorage to the basement membrane, whereas the formation of stratifying cell layers depends on the formation of intercellular adhesions mediated by cadherins. The process of squamous cell carcinoma invasion and dissemination requires active cell migration through the extracellular matrix with the simultaneous remodeling of intercellular adhesions. Integrins are clearly important in the invasive process, whereas intercellular adhesion receptors restrain invasion and promote a more differentiated phenotype.
20
Sabet, Amr G. E. "Cobra II." American Journal of Islam and Society 25, no. 2 (April 1, 2008): 110–13. http://dx.doi.org/10.35632/ajis.v25i2.1474.
Full textAbstract:
This book deals with the April 2003 American invasion and occupation ofIraq. Its title comes from the code name of the military operation designedto drive toward Baghdad. The code name, in turn, was inspired by GeneralGeorge Patton’s 1944 military operation Cobra, during which the Allied forces broke out from Normandy to liberate France – hence Cobra II.Written in a journalistic and investigative style, it chronicles the developmentsand events leading to the Bush administration’s decision to attackIraq. Described as a war of “choice” rather than of “necessity” (p. xxxi), itswiftly defeated the Iraqi army and toppled Saddam Hussein’s regime.However, it was a failure insofar as it generated a virulent insurgencythat the occupyingAmerican army could not suppress. This insurgency wasan unexpected by-product of the program of “transformation” espoused byformer Secretary of Defense Donald Rumsfeld. As part of President GeorgeW. Bush’s vision of overhauling theAmerican military, this programbecamea sort of “official ideology” (p. 8) and response to two main concerns: (1)the long time (six months) it took to plan and amassAmerican forces duringthe lead-up to the 1992 GulfWar that had reversed Iraq’s invasion of Kuwait(this length of time was considered to fall short of credible “superpower”projection), and (2) the American military’s ability to fight two major warssimultaneously, which came to be known as the “two-war doctrine” (pp. 5and 9). The problem with the second consideration was that it required largeground forces to implement the doctrine, at a time when the foreseen transformationsought to trim American forces in favor of high-tech space andprecision weapons ...
21
Persson, Anders. "Right for the Wrong Reason?: A New Look at the 6 June 1944 D-Day Forecast by a Neutral Swede." Bulletin of the American Meteorological Society 101, no. 7 (July 1, 2020): E993—E1006. http://dx.doi.org/10.1175/bams-d-18-0311.1.
Full textAbstract:
Abstract There are at least three popular perceptions surrounding the weather forecast for the D-day landing in Normandy, 6 June 1994: 1) that the Allied weather forecasters predicted a crucial break or “window of opportunity” in the unsettled weather prevailing at the time; 2) that the German meteorologists, lacking observations from the North Atlantic, failed to see this break coming and thus the invasion took the Wehrmacht by surprise; and 3) that the American forecasters, guided by a skillful analog system, predicted the favorable conditions several days ahead but got no support from their pessimistic British colleagues. This article will present evidence taken mostly from hitherto rather neglected sources of information, transcripts of the telephone discussions between the Allied forecasters and archived German weather analyses. They show that 1) the synoptic development for the invasion was not particularly well predicted and, if there was a break in the weather, it occurred for reasons other than those predicted; 2) the German forecasters were fairly well informed about the large-scale synoptic situation over most of the North Atlantic, probably thanks to decoded American analyses; and 3) from the viewpoint of a “neutral Swede,” the impression is that the American analog method might not have performed as splendidly as its adherents have claimed, but also not as badly as its critics have alleged. Finally, the D-day forecast, the discussions among the forecasters, and their briefings with the Allied command are interesting not only from a historical perspective, but also as an early and well-documented example of decision-making under meteorological uncertainty.
22
Nitsche-Schmitz, Patric, Manfred Rohde, and Gursharan Chhatwal. "Invasion mechanisms of Gram-positive pathogenic cocci." Thrombosis and Haemostasis 98, no. 09 (2007): 488–96. http://dx.doi.org/10.1160/th07-03-0179.
Full textAbstract:
SummaryGram-positive cocci are important human pathogens. Streptococci and staphylococci in particular are a major threat to human health,since they cause a variety of serious invasive infections. Their invasion into normally sterile sites of the host depends on elaborated bacterial mechanisms that involve adhesion to the host tissue, its degradation, internalisation by host cells, and passage through epithelia and endothelia. Interactions of bacterial surface proteins with proteins of the host’s extracellular matrix as well as with cell surface receptors are crucial factors in these processes, and some of the key mechanisms are similar in many pathogenic Gram-positive cocci.Therapies that interfere with these mechanisms may become efficient alternatives to today’s antibiotic treatments.
23
Hazan, Rachel B., Greg R. Phillips, Rui Fang Qiao, Larry Norton, and Stuart A. Aaronson. "Exogenous Expression of N-Cadherin in Breast Cancer Cells Induces Cell Migration, Invasion, and Metastasis." Journal of Cell Biology 148, no. 4 (February 21, 2000): 779–90. http://dx.doi.org/10.1083/jcb.148.4.779.
Full textAbstract:
E- and N-cadherin are calcium-dependent cell adhesion molecules that mediate cell–cell adhesion and also modulate cell migration and tumor invasiveness. The loss of E-cadherin–mediated adhesion has been shown to play an important role in the transition of epithelial tumors from a benign to an invasive state. However, recent evidence indicates that another member of the cadherin family, N-cadherin, is expressed in highly invasive tumor cell lines that lacked E-cadherin expression. These findings have raised the possibility that N-cadherin contributes to the invasive phenotype. To determine whether N-cadherin promotes invasion and metastasis, we transfected a weakly metastatic and E-cadherin–expressing breast cancer cell line, MCF-7, with N-cadherin and analyzed the effects on cell migration, invasion, and metastasis. Transfected cells expressed both E- and N-cadherin and exhibited homotypic cell adhesion from both molecules. In vitro, N-cadherin–expressing cells migrated more efficiently, showed an increased invasion of Matrigel, and adhered more efficiently to monolayers of endothelial cells. All cells produced low levels of the matrix metalloproteinase MMP-9, which was dramatically upregulated by treatment with FGF-2 only in N-cadherin–expressing cells. Migration and invasion of Matrigel were also greatly enhanced by this treatment. When injected into the mammary fat pad of nude mice, N-cadherin–expressing cells, but not control MCF-7 cells, metastasized widely to the liver, pancreas, salivary gland, omentum, lung, lymph nodes, and lumbar spinal muscle. The expression of both E- and N-cadherin was maintained both in the primary tumors and metastatic lesions. These results demonstrate that N-cadherin promotes motility, invasion, and metastasis even in the presence of the normally suppressive E-cadherin. The increase in MMP-9 production by N-cadherin–expressing cells in response to a growth factor may endow them with a greater ability to penetrate matrix protein barriers, while the increase in their adherence to endothelium may improve their ability to enter and exit the vasculature, two properties that may be responsible for metastasis of N-cadherin–expressing cells.
24
Gorby, Gary L., Edward N. Robinson Jr., Lee R. Barley, Christopher M. Clemens, and Zell A. McGee. "Microbial invasion: a covert activity?" Canadian Journal of Microbiology 34, no. 4 (April 1, 1988): 507–12. http://dx.doi.org/10.1139/m88-087.
Full textAbstract:
In contrast to nonpathogenic microorganisms that exist happily in biofilms on various organic and inorganic surfaces, many pathogenic microbes have the additional ability to invade host tissues by inducing their own endocytosis and transport across normally protective barriers. This phenomenon, designated " parasite-directed endocytosis," has been observed with a variety of surfaces (intestinal, genital, nasopharyngeal, and tracheal epithelium) as well as in endothelial cells. The mechanisms involved in invasion may involve a single factor as described for some species of Yersinia, or may require multiple factors as observed in Shigellae. For the majority of pathogens, the molecular mechanisms of invasion are not well understood (e.g., Neisseria gonorrhoeae). Because parasite-directed endocytosis is reminiscent of receptor-mediated endocytosis, it is quite possible that some pathogens engage in biologic mimicry by producing a molecule that resembles a natural host ligand, for which there is a host cell receptor. Such a masquerade may allow some microbes to enter the host's inner sanctum covertly in a manner analogous to the Trojan horse, rather than overtly by destroying the mucosa and entering host tissues directly. Whereas this hypothesis is speculative at present, bacteria that produce molecules resembling insulin, calmodulin, and chorionic gonadotropin have been described.
25
Apolo, Andrea Borghese, Young H. Lee, Fabiola Cecchi, Piyush K. Agarwal, Howard L. Parnes, Kattie Khadar, Amelia Summerell, et al. "Preclinical and correlative studies of cabozantinib (XL184) in urothelial cancer (UC)." Journal of Clinical Oncology 31, no. 15_suppl (May 20, 2013): 4543. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.4543.
Full textAbstract:
4543 Background: Mounting evidence supports Met as a therapeutic target in urothelial cancer (UC). Activated Met can promote angiogenesis and tumor growth by upregulating VEGF and may play a role in UC pathogenesis. Cabozantinib inhibits VEGFR2 and Met pathways. In this study, we assessed shed Met (sMet) levels in the urine and serum of UC patients (pts) and cabozantinib’s effects on HGF-driven UC cell growth and invasion. Methods: sMet levels in serum and urine samples from 31 pts with UC (23 metastatic, 8 muscle-invasive) were correlated with stage, presence of visceral metastases and urinary source. The effects of cabozantinib on 4 human UC-derived cell lines were studied in vitro. Intact RT4, TCC-SUP, T24M2 and T24M3 cells at 80% confluence were serum deprived 16 h, then left untreated or treated with hepatocyte growth factor (HGF) and/or cabozantinib prior to analysis of Met, phospho- (p)Met, pAkt, Akt, pMAPK and MAPK by immunoassay or immunoblotting. Cabozantinib effects on basal and HGF-induced UC cell invasion, proliferation and soft agar growth were measured. Results: Median serum Met levels were modestly higher in pts with metastatic versus muscle-invasive disease. Urinary Met levels were clearly higher in pts with visceral metastasis (P=0.0111) and in urine from ileal conduits and neobladders compared to normally voided urine, regardless of stage (P=0.0489). Met content in UC cell lines was low in RT4 and higher in T24M2, T24M3 and TCC-SUP. Basal pMet content was universally low, increased significantly by HGF and this was reversed by cabozantinib. HGF-driven increases in pAkt/Akt and pMAPK/MAPK in all 4 cell lines were reversed by cabozantinib, as were HGF-enhanced UC cell invasion, proliferation and anchorage independent growth. Conclusions: Median urinary sMet is significantly higher in pts with visceral metastasis and in specimens from ileal conduits and neobladders relative to normally voided urine. UC cell Met content in culture increased with disease grade; HGF stimulated activation of Met and known effectors, and enhanced invasion, growth rate and anchorage-independent growth; cabozantinib effectively reversed these HGF-driven effects. These data support evaluation of cabozantinib in pts with metastatic UC.
26
Apolo, Andrea Borghese, Young H. Lee, Fabiola Cecchi, Piyush K. Agarwal, Howard L. Parnes, Kattie Khadar, Amelia Summerell, et al. "Preclinical and correlative studies of cabozantinib (XL184) in urothelial cancer (UC)." Journal of Clinical Oncology 31, no. 6_suppl (February 20, 2013): 314. http://dx.doi.org/10.1200/jco.2013.31.6_suppl.314.
Full textAbstract:
314 Background: Mounting evidence supports Met as a target in urothelial cancer (UC). Activated Met can promote angiogenesis and tumor growth by upregulating VEGF and may play a role in UC pathogenesis. Cabozantinib inhibits both VEGFR2 and Met pathways. In this study, we assessed shed Met (sMet) levels in the urine and serum of UC patients (pts) and cabozantinib’s effects on HGF-driven UC cell growth and invasion. Methods: sMet levels in serum and urine samples from 31 pts with UC (23 metastatic, 8 muscle-invasive) were correlated with stage, presence of visceral metastases and urinary source. The effects of cabozantinib on 4 human UC-derived cell lines were studied in vitro. Intact RT4, TCC-SUP, T24M2 and T24M3 cells at 80% confluence were serum deprived 16 h, then left untreated or treated with hepatocyte growth factor (HGF) and/or cabozantinib prior to analysis of Met, phospho- (p)Met, pAkt, Akt, pMAPK and MAPK by immunoassay or immunoblotting. Cabozantinib effects on basal and HGF-induced UC cell invasion, proliferation and soft agar growth were measured. Results: Median serum Met levels were modestly higher in pts with metastatic versus muscle-invasive disease. Urinary Met levels were clearly higher in pts with visceral metastasis (p=0.0111) and in urine from ileal conduits and neobladders compared to normally voided urine, regardless of stage (p=0.0489). Met content in UC cell lines was low in RT4 and higher in T24M2, T24M3 and TCC-SUP. Basal pMet content was universally low, increased significantly by HGF and this was reversed by cabozantinib. HGF-driven increases in pAkt/Akt and pMAPK/MAPK in all 4 cell lines were reversed by cabozantinib, as were HGF-enhanced UC cell invasion, proliferation and anchorage independent growth. Conclusions: Median urinary sMet is significantly higher in pts with visceral metastasis and in specimens from ileal conduits and neobladders relative to normally voided urine. UC cell Met content in culture increased with disease grade; HGF stimulated activation of Met and known effectors, and enhanced invasion, growth rate and anchorage-independent growth; cabozantinib effectively reversed these HGF-driven effects. These data support evaluation of cabozantinib in pts with metastatic UC.
27
Edwards, Andrew M., Tracy J. Grossman, and Joel D. Rudney. "Fusobacterium nucleatum Transports Noninvasive Streptococcus cristatus into Human Epithelial Cells." Infection and Immunity 74, no. 1 (January 2006): 654–62. http://dx.doi.org/10.1128/iai.74.1.654-662.2006.
Full textAbstract:
ABSTRACT Analysis of human buccal epithelial cells frequently reveals an intracellular polymicrobial consortium of bacteria. Although several oral bacteria have been demonstrated to invade cultured epithelial cells, several others appear unable to internalize. We hypothesized that normally noninvasive bacteria may gain entry into epithelial cells via adhesion to invasive bacteria. Fusobacterium nucleatum is capable of binding to and invading oral epithelial cells. By contrast, Streptococcus cristatus binds weakly to host cells and is not internalized. F. nucleatum and S. cristatus coaggregate strongly via an arginine-sensitive interaction. Coincubation of KB or TERT-2 epithelial cells with equal numbers of F. nucleatum and S. cristatus bacteria led to significantly increased numbers of adherent and internalized streptococci. F. nucleatum also promoted invasion of KB cells by other oral streptococci and Actinomyces naeslundii. Dissection of fusobacterial or streptococcal adhesive interactions by using sugars, amino acids, or antibodies demonstrated that this phenomenon is due to direct attachment of S. cristatus to adherent and invading F. nucleatum. Inhibition of F. nucleatum host cell attachment and invasion with galactose, or fusobacterial-streptococcal coaggregation by the arginine homologue l-canavanine, abrogated the increased S. cristatus adhesion to, and invasion of, host cells. In addition, polyclonal antibodies to F. nucleatum, which inhibited fusobacterial attachment to both KB cells and S. cristatus, significantly decreased invasion by both species. Similar decreases were obtained when epithelial cells were pretreated with cytochalasin D, staurosporine, or cycloheximide. These studies indicate that F. nucleatum may facilitate the colonization of epithelial cells by bacteria unable to adhere or invade directly.
28
Everson, Carol A., and Linda A. Toth. "Systemic bacterial invasion induced by sleep deprivation." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 278, no. 4 (April 1, 2000): R905—R916. http://dx.doi.org/10.1152/ajpregu.2000.278.4.r905.
Full textAbstract:
Profound sleep disruption in humans is generally believed to cause health impairments. Through comparative research, specific physical effects and underlying mechanisms altered by sleep deprivation are being elucidated. Studies of sleep-deprived animals previously have shown a progressive, chronic negative energy balance and gradual deterioration of health, which culminate in fatal bloodstream infection without an infectious focus. The present study investigated the conditions antecedent to advanced morbidity in sleep-deprived rats by determining the time course and distribution of live microorganisms in body tissues that are normally sterile. The tissues cultured for microbial growth included the blood, four major organs, six regional lymph nodes, the intestine, and the skin. The principal finding was early infection of the mesenteric lymph nodes by bacteria presumably translocated from the intestine and bacterial migration to and transient infection of extraintestinal sites. Presence of pathogenic microorganisms and their toxins in tissues constitutes a septic burden and chronic antigenic challenge for the host. Bacterial translocation and pathogenic sequelae provide mechanisms by which sleep deprivation appears to adversely affect health.
29
Ryder, Paul. "Strategy and Semiosis: Insights from Operation Fortitude." southern semiotic review 2021 i, no. 14 (July 14, 2021): 37–50. http://dx.doi.org/10.33234/ssr.14.3.
Full textAbstract:
The European summer of 1944 saw what is arguably the greatest deception wrought through deliberate miscommunication. Operation Fortitude focussed on convincing the Nazis that the invasion of Europe would come not at Normandy but further north at the Pas-de-Calais. Seeing the enemy almost completely wrong-footed, Fortitude remains the most devastating deception in the history of warfare. It is also a campaign that teaches us a great deal about the internal dynamics and semiotics of strategy more generally. Accordingly, I propose that Operation Fortitude speaks profoundly to the principle of polysemy and to the related idea that, in competitive fields, strategic design may see to it that we are deceived into misreading tactics in relation to their informing concepts. Directly related to the above, the paper proposes that, since it is always founded upon a more or less difficult-to-fathom conceptual core, all strategy inevitably deceives—and that the question of deception is merely a matter of degree. Further to the above, I also argue that Operation Fortitude teaches us that, at its heart, good strategy seldom depends upon a singular concept but upon several cooperating abstractions. The paper’s final substantive point is that Operation Fortitude reminds us that in order to think productively about strategy, it pays to bear in mind the following military principle: at its most effective, strategy is a unique and exquisitely synergistic coupling of objectives, concepts, and (dehabitualised) tactics.
30
Wilson, Rebecca L., Jessica Elthon, Steven Clegg, and Bradley D. Jones. "Salmonella enterica Serovars Gallinarum and Pullorum Expressing Salmonella enterica Serovar Typhimurium Type 1 Fimbriae Exhibit Increased Invasiveness for Mammalian Cells." Infection and Immunity 68, no. 8 (August 1, 2000): 4782–85. http://dx.doi.org/10.1128/iai.68.8.4782-4785.2000.
Full textAbstract:
ABSTRACT Salmonella enterica serovars Gallinarum and Pullorum are S. enterica biotypes that exhibit host specificity for poultry and aquatic birds and are not normally capable of causing disease in mammalian hosts. During their evolution toward host restriction serovars Gallinarum and Pullorum lost their ability to mediate mannose-sensitive hemagglutination (MSHA), a phenotype correlated with adherence to certain cell types. Because adherence is an essential requirement for invasion of cells by bacterial pathogens, we examined whether MHSA type 1 fimbriae would increase the ability of serovars Pullorum and Gallinarum to invade normally restrictive cells. Serovars Gallinarum and Pullorum expressing S. entericaserovar Typhimurium strain LT2 type 1 fimbriae exhibited a 10- to 20-fold increased ability to adhere to and a 20- to 60-fold increased invasion efficiency of the human epithelial HEp-2 cell line. Invasion was accompanied by extensive ruffling of the membranes of the HEp-2 cells. In a murine ligated ileal loop model, a 32% increase in the number of M-cell ruffles was seen when serovar Gallinarum expressed serovar Typhimurium type 1 fimbriae.
31
Dauvin, Jean-Claude. "Establishment of the invasive Asian shore crab Hemigrapsus sanguineus (De Haan, 1835) (Crustacea: Brachyura: Grapsoidea) from the Cotentin Peninsular, Normandy, France." Aquatic Invasions 4, no. 3 (September 2009): 467–72. http://dx.doi.org/10.3391/ai.2009.4.3.4.
Full text
32
Chen, Xi, and Carol A. Kumamoto. "A conserved G protein (Drg1p) plays a role in regulation of invasive filamentation in Candida albicans." Microbiology 152, no. 12 (December 1, 2006): 3691–700. http://dx.doi.org/10.1099/mic.0.29246-0.
Full textAbstract:
During infection, the opportunistic fungal pathogen Candida albicans grows invasively into the tissues of its host, forming filaments that penetrate the host tissue. To search for genes that are important for invasive filamentation, a screen for mutants that were defective in invasion of agar medium was conducted. A mutant carrying an insertion mutation in the locus of a gene, termed here DRG1, was identified. DRG1 encodes a highly conserved cytoplasmic G protein, with orthologues in the genomes of organisms from humans to yeast and archaea. C. albicans strains lacking Drg1p were defective in producing filaments that penetrated agar media, but produced filaments normally under other conditions, such as during liquid growth. When inoculated intravenously into mice, the drg1 null mutant caused delayed lethality accompanied by delayed invasive growth in the kidneys of the host, in comparison with those of the wild-type strain. These results implicate Drg1p in the control of invasive filamentation in the laboratory, and in the progression of invasive disease in the host.
33
Habyarimana, Fabien, Matthew C. Swearingen, Glenn M. Young, Stephanie Seveau, and Brian M. M. Ahmer. "Yersinia enterocolitica Inhibits Salmonella enterica Serovar Typhimurium and Listeria monocytogenes Cellular Uptake." Infection and Immunity 82, no. 1 (October 14, 2013): 174–83. http://dx.doi.org/10.1128/iai.00984-13.
Full textAbstract:
ABSTRACTYersinia enterocoliticabiovar 1B employs two type three secretion systems (T3SS), Ysa and Ysc, which inject effector proteins into macrophages to prevent phagocytosis. Conversely,Salmonella entericaserovar Typhimurium uses a T3SS encoded bySalmonellapathogenicity island 1 (SPI1) to actively invade cells that are normally nonphagocytic and a second T3SS encoded by SPI2 to survive within macrophages. Given the distinctly different outcomes that occur with regard to host cell uptake ofS. Typhimurium andY. enterocolitica, we investigated how each pathogen influences the internalization outcome of the other.Y. enterocoliticareducesS. Typhimurium invasion of HeLa and Caco-2 cells to a level similar to that observed using anS. Typhimurium SPI1 mutant alone. However,Y. enterocoliticahad no effect onS. Typhimurium uptake by J774.1 or RAW264.7 macrophage-like cells.Y. enterocoliticawas also able to inhibit the invasion of epithelial and macrophage-like cells byListeria monocytogenes.Y. enterocoliticamutants lacking either the Ysa or Ysc T3SS were partially defective, while double mutants were completely defective, in blockingS. Typhimurium uptake by epithelial cells.S. Typhimurium encodes a LuxR homolog, SdiA, which detectsN-acylhomoserine lactones (AHLs) produced byY. enterocoliticaand upregulates the expression of an invasin (Rck) and a putative T3SS effector (SrgE). Two different methods of constitutively activating theS. Typhimurium SdiA regulon failed to reverse the uptake blockade imposed byY. enterocolitica.
34
Mueller, Kimberly J., and Nancy E. Freitag. "Pleiotropic Enhancement of Bacterial Pathogenesis Resulting from the Constitutive Activation of the Listeria monocytogenes Regulatory Factor PrfA." Infection and Immunity 73, no. 4 (April 2005): 1917–26. http://dx.doi.org/10.1128/iai.73.4.1917-1926.2005.
Full textAbstract:
ABSTRACT Listeria monocytogenes is a facultative intracellular bacterial pathogen that causes serious disease in immunocompromised individuals, pregnant women, and neonates. Bacterial virulence is mediated by the expression of specific gene products that facilitate entry into host cells and enable bacterial replication; the majority of these gene products are regulated by a transcriptional activator known as PrfA. L. monocytogenes strains containing prfA E77K or prfA G155S mutations exhibit increased expression of virulence genes in broth culture and are hypervirulent in mice. To define the scope of the influences of the prfA E77K and prfA G155S mutations on L. monocytogenes pathogenesis, multiple aspects of bacterial invasion and intracellular growth were examined. Enhanced bacterial invasion of host epithelial cells was dependent on the expression of a number of surface proteins previously associated with invasion, including InlA, InlB, and ActA. In addition to these surface proteins, increased production of the hly-encoded secreted hemolysin listeriolysin O (LLO) was also found to significantly enhance bacterial invasion into epithelial cell lines for both prfA mutant strains. Although prfA E77K and prfA G155S strains were similar in their invasive phenotypes, the infection of epithelial cells with prfA E77K strains resulted in host cell plasma membrane damage, whereas prfA G155S strains did not alter plasma membrane integrity. Bacterial infection of human epithelial cells, in which the production of LLO is not required for bacterial entry into the cytosol, indicated that prfA E77K cytotoxic effects were mediated via LLO. Both prfA E77K and prfA G155S strains were more efficient than wild-type bacteria in gaining access to the host cell cytosol and in initiating the polymerization of host cell actin, and both were capable of mediating LLO-independent lysis of host cell vacuoles in cell lines for which L. monocytogenes vacuole disruption normally requires LLO activity. These experiments illuminate the diverse facets of L. monocytogenes pathogenesis that are significantly enhanced by the constitutive activation of PrfA via prfA mutations and underscore the critical role of this protein in promoting L. monocytogenes virulence.
35
Jusino, Shirley, Srikumar P. Chellappan, and Harold I. Saavedra. "Role of E2F3 and shugoshin I in epithelial-to-mesenchymal transition and cell invasion in breast cancer." Journal of Clinical Oncology 38, no. 15_suppl (May 20, 2020): e13100-e13100. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.e13100.
Full textAbstract:
e13100 Background: Triple-negative breast cancer (TNBC) is the most aggressive and poorly prognostic breast cancer subtype, yet there are currently no biological therapies against this subtype. Our laboratory is finding the sources of novel biological targets in TNBC by studying the E2F transcription factors, which are essential for cellular proliferation and maintenance of genomic stability. While the deregulated Rb/E2F pathway signals the epithelial-to-mesenchymal transition (EMT), the underlining mechanism of how E2Fs drive EMT in TNBC remains unknown. We recently published that the E2F transcriptional activators (E2Fs) are overexpressed in the vast majority of TNBC and that their overexpression upregulates mitotic kinases such as TTK, which we have shown to induce EMT and invasion in TNBC cells. We also demonstrated that the E2Fs maintain genomic integrity in part through Shugoshin I (SGO1), which normally controls chromosome cohesion; however, the role of SGO1 in EMT in breast cancer is unknown. Our hypothesis is that E2F3 and SGO1 are highly expressed in TNBC and that their overexpression modulates EMT genes, thus promoting cell invasion. Methods: To test our hypothesis, we conducted siRNA transfection to knockdown E2F3 and SGO1 in MDA-MB-231 and Hs578t, which are TNBC cells. After 48 hours, we evaluated mRNA levels of EMT-related genes after E2F3 or SGO1 depletion using RT-PCR analysis. We also evaluated the effects of SGO1 depletion in protein localization by immunofluorescence. Furthermore, we evaluated the invasive behavior of MDA-MB-231 and Hs578t cells after SGO1 depletion using a Boyden Chamber Assay. Results: Our results demonstrate that E2F3 and SGO1 depletion decrease MMP3 mRNA levels. Moreover, E2F3 and SGO1 depletion restore E-cadherin expression and localization. Furthermore, E2F3 and SGO1 depletion significantly reduce cell invasion in MDA-MB-231 and Hs578t cells. Conclusions: Our results suggest that SGO1 is a promising drug target for breast cancer metastasis since EMT and invasion are essential early steps in breast cancer metastasis and E2F3 is presently undruggable.
36
Rangachari, K., AR Dluzewski, RJ Wilson, and WB Gratzer. "Cytoplasmic factor required for entry of malaria parasites into RBCs." Blood 70, no. 1 (July 1, 1987): 77–82. http://dx.doi.org/10.1182/blood.v70.1.77.77.
Full textAbstract:
Abstract Resealed ghosts of human RBCs, containing diluted cytosol, are susceptible to invasion by Plasmodium falciparum. If ATP is present, a dilution of up to about 30-fold, corresponding to an intracellular hemoglobin concentration of approximately 10 mg/mL, can be tolerated without total loss of susceptibility to invasion. Up to a dilution of about one-half this, the parasites also develop normally. When the cytosol is diluted by more than the critical amount, invasion of the resulting resealed ghosts falls off abruptly. If the diluent buffer is replaced by extraneous concentrated hemolysate, an indefinite dilution is possible without loss of invasion. There is thus an intracellular constituent, which must be present at a concentration above some critical level if the parasite is to enter the cell. The factor in question is not dialyzable. It is largely inactivated when the hemolysate is kept for approximately 1 day in the cold or for approximately 20 minutes at 45 degrees C. The inability of a heat- treated hemolysate to support invasion is not due to the generation of inhibitory products, because such a solution can be used as a diluent of a fresh hemolysate without inhibition of invasion. When the inactivated hemolysate is present as a major component, however, the parasites fail to develop to the trophozoite stage. The invasion-linked factor remains in the strongly adsorbed nonheme fraction when a batchwise separation from hemoglobin on an anion exchanger is made and is thus probably acidic in character; the adsorbed fraction, recovered from the ion-exchanger, substantially restores capacity for invasion when sealed into ghosts. Its activity is destroyed by treatment with trypsin. The adsorbed fraction contains many proteins. When fractionated on a gel filtration column by fast liquid chromatography, active material eluted at a volume corresponding to a mol wt for a globular protein in the region of 10,000. A component of apparent subunit mol wt of 13,000 was observed in sodium dodecyl sulfate- polyacrylamide gel electrophoresis (SDS-PAGE) of this eluate fraction.
37
Rangachari, K., AR Dluzewski, RJ Wilson, and WB Gratzer. "Cytoplasmic factor required for entry of malaria parasites into RBCs." Blood 70, no. 1 (July 1, 1987): 77–82. http://dx.doi.org/10.1182/blood.v70.1.77.bloodjournal70177.
Full textAbstract:
Resealed ghosts of human RBCs, containing diluted cytosol, are susceptible to invasion by Plasmodium falciparum. If ATP is present, a dilution of up to about 30-fold, corresponding to an intracellular hemoglobin concentration of approximately 10 mg/mL, can be tolerated without total loss of susceptibility to invasion. Up to a dilution of about one-half this, the parasites also develop normally. When the cytosol is diluted by more than the critical amount, invasion of the resulting resealed ghosts falls off abruptly. If the diluent buffer is replaced by extraneous concentrated hemolysate, an indefinite dilution is possible without loss of invasion. There is thus an intracellular constituent, which must be present at a concentration above some critical level if the parasite is to enter the cell. The factor in question is not dialyzable. It is largely inactivated when the hemolysate is kept for approximately 1 day in the cold or for approximately 20 minutes at 45 degrees C. The inability of a heat- treated hemolysate to support invasion is not due to the generation of inhibitory products, because such a solution can be used as a diluent of a fresh hemolysate without inhibition of invasion. When the inactivated hemolysate is present as a major component, however, the parasites fail to develop to the trophozoite stage. The invasion-linked factor remains in the strongly adsorbed nonheme fraction when a batchwise separation from hemoglobin on an anion exchanger is made and is thus probably acidic in character; the adsorbed fraction, recovered from the ion-exchanger, substantially restores capacity for invasion when sealed into ghosts. Its activity is destroyed by treatment with trypsin. The adsorbed fraction contains many proteins. When fractionated on a gel filtration column by fast liquid chromatography, active material eluted at a volume corresponding to a mol wt for a globular protein in the region of 10,000. A component of apparent subunit mol wt of 13,000 was observed in sodium dodecyl sulfate- polyacrylamide gel electrophoresis (SDS-PAGE) of this eluate fraction.
38
Mendrygal, Kiprian E., and Juan E. González. "Environmental Regulation of Exopolysaccharide Production in Sinorhizobium meliloti." Journal of Bacteriology 182, no. 3 (February 1, 2000): 599–606. http://dx.doi.org/10.1128/jb.182.3.599-606.2000.
Full textAbstract:
ABSTRACT Exopolysaccharide production by Sinorhizobium melilotiis required for invasion of root nodules on alfalfa and successful establishment of a nitrogen-fixing symbiosis between the two partners.S. meliloti wild-type strain Rm1021 requires production of either succinoglycan, a polymer of repeating octasaccharide subunits, or EPS II, an exopolysaccharide of repeating dimer subunits. The reason for the production of two functional exopolysaccharides is not clear. Earlier reports suggested that low-phosphate conditions stimulate the production of EPS II in Rm1021. We found that phosphate concentrations determine which exopolysaccharide is produced by S. meliloti. The low-phosphate conditions normally found in the soil (1 to 10 μM) stimulate EPS II production, while the high-phosphate conditions inside the nodule (20 to 100 mM) block EPS II synthesis and induce the production of succinoglycan. Interestingly, the EPS II produced by S. meliloti in low-phosphate conditions does not allow the invasion of alfalfa nodules. We propose that this invasion phenotype is due to the lack of the active molecular weight fraction of EPS II required for nodule invasion. An analysis of the function of PhoB in this differential exopolysaccharide production is presented.
39
Webster, Paul. "Early Events During Invasion of J774 Cells by Listeria Monocytogenes." Microscopy and Microanalysis 7, S2 (August 2001): 628–29. http://dx.doi.org/10.1017/s1431927600029214.
Full textAbstract:
The gram positive bacillus, Listeria monocytogenesis a contaminant of the food we eat and although it is a common pathogen in farm animals L. monocytogenesdoes not normally infect humans. However, immunocompromised individuals, infants and the elderly are susceptible to infection. The bacteria, taken into membrane bound phagosomes, use a thiol-activated cytolysin listeriolysin O to disrupt the membrane (LLO) and gain access to the cell cytoplasm. Subsequent actin polymerizations on the bacterial surface induce motility in the cell and long cytoplasmic protrusions at the cell surface that spread bacteria to neighboring cells.L. monocytogenesenters cells by phagocytosis. By using short infection times of 5 min or less, it was possible to examine early interactions between J774 cells and L. monocytogenes.This study shows that during the early stages of internalization the bacteria are able to modify the protein composition of the forming phagosome membrane.
40
Jung, Shin, Cameron Ackerley, Stacey Ivanchuk, Soma Mondal, Laurence E. Becker, and James T. Rutka. "Tracking the invasiveness of human astrocytoma cells by using green fluorescent protein in an organotypical brain slice model." Journal of Neurosurgery 94, no. 1 (January 2001): 80–89. http://dx.doi.org/10.3171/jns.2001.94.1.0080.
Full textAbstract:
Object. Although it is known that malignant astrocytomas infiltrate diffusely into regions of normal brain, it is frequently difficult to identify unequivocally the solitary, invading astrocytoma cell in histopathological preparations or experimental astrocytoma models. The authors describe an experimental system that facilitates the tracking of astrocytoma cells by using nonneoplastic cerebral tissue as the substrate for invasion. Methods. Cerebral tissue was cut into 1-mm-thick slices and cultured in the upper chamber of a Transwell culture dish on top of a polyester membrane (0.4-mm pore size) that was bathed in medium supplied by the lower chamber. Two astrocytoma cell lines, U-87 MG (U87) and U343 MG-A (U343), were selected because of their differing basal cell motilities in monolayer cultures. The astrocytoma cells were stably transfected with vectors that expressed green fluorescent protein (GFP), either alone or as a fusion protein with the receptor for hyaluronic acid—mediated motility (RHAMM) in either sense or antisense orientations. Stably transfected clones that had high levels of GFP expression were selected using the direct visualization provided by fluorescence microscopy and fluorescence-activated cell-sorter analysis. The GFP-expressing astrocytoma cell clones were implanted into the center of the brain slice and the degree of astrocytoma invasion into brain tissue was measured at different time points by using the optical sectioning provided by the confocal laser microscope. The authors observed that GFP-expressing astrocytoma cells could be readily tracked and followed in this model system. Individual astrocytoma cells that exhibited green fluorescence could be readily identified following their migration through the brain slices. The GFP-labeled U87 astrocytoma cells migrated farther into the brain slice than the U343 astrocytoma cells. The RHAMM-transfected GFP-labeled astrocytoma cells also infiltrated farther than the GFP-labeled astrocytoma cells themselves. The expression of antisense RHAMM virtually abrogated the invasion of the brain slices by both astrocytoma cell lines. Conclusions. The authors believe that this organotypical culture system may be of considerable utility in studying the process of astrocytoma invasion, not only because it provides a better representation of the extracellular matrix molecules normally encountered by invading astrocytoma cells, but also because the GFP tag enables tracking of highly migratory and invasive astrocytoma cells under direct vision.
41
Bahrami, Hassan, Reza Rezaee, Delair Nazhat, and Jakov Ostojic. "Evaluation of damage mechanisms and skin factor in tight gas reservoirs." APPEA Journal 51, no. 1 (2011): 639. http://dx.doi.org/10.1071/aj10045.
Full textAbstract:
Tight gas reservoirs normally have production problems due to very low matrix permeability and significant damage during well drilling, completion, stimulation and production. Therefore, they may not flow gas at optimum rates without advanced production improvement techniques. The main damage mechanisms and the factors that have significant influence on total skin factor in tight gas reservoirs include: mechanical damage to formation rock; plugging of natural fractures by mud solid particle invasion; relative permeability reduction around wellbore as a result of filtrate invasion; liquid leak-off into the formation during fracturing operations; water blocking; skin due to wellbore breakouts; and the damage associated with perforation. Drilling and fracturing fluids invasion mostly occurs through natural fractures and may also lead to serious permeability reduction in the rock matrix that surrounds the natural or hydraulic fractures. This study represents an evaluation of different damage mechanisms in tight gas formations, and examines the factors that can have significant influence on total skin factor and well productivity. Reservoir simulation was carried out based on a typical West Australian tight gas reservoir to understand how well productivity is affected by each of the damage mechanisms, such as natural fracture plugging, mud filtrate invasion, water blocking and perforation. Furthermore, some damage prevention and productivity improvement techniques are proposed, which can help improve well productivity in tight gas reservoirs.
42
Zhao, Lianjun, Qing Lv, Qiuping Xv, Jie Shao, Shu Su, Fanyan Meng, Jia Wei, et al. "Ginsenoside Rg3 to regulate the EMT induced by TGF-in gastric cancer." Journal of Clinical Oncology 35, no. 15_suppl (May 20, 2017): e23200-e23200. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.e23200.
Full textAbstract:
e23200 Background: To discuss the regulate effect of Ginsenoside Rg3 during the TGF-β1 induced EMT in human gastric cancer SNU-601 cell line. Methods: In the first part of our experiment, ninety-nine patients who were diagnosed as gastric cancer were admitted to this study eventually. The Luminex® xMAP technology was used to measure the plasma levels of TGF-β1. In the second part, human gastric cancer SNU-601 cell line were cultured normally. Inverted microscope was used to observe morphological changes. The cell relative growth rate of proliferation was analyzed by MTT assay. Wound-healing assay and transwell invasion assay were carried out to predict the capacity of Ginsenoside Rg3 in inhibiting migration and invasion. Western Blot was performed to analyze the influence of Ginsenoside Rg3 and TGF-β1 on the protein expression of E-cadherin and Vimentin. Results: The plasma cytokine levels of TGF-β1 were associated with vessel invasion, peritoneal involvement, TNM stage, T stage, N stage in gastric cancer patients. In Vitro Study, TGF-β1 stimulated epithelial-mesenchymal transition in SNU-601 cell lines. Ginsenoside Rg3 inhibited the TGF-β1 induced morphological changes, cell proliferation increase, cell migration and cell invasion. Ginsenoside Rg3 markedly increased expression of the epithelial marker E-cadherin, and repressed the upregulation and expression of the mesenchymal marker Vimentin during the TGF-β1 induced EMT in SNU-601 cell line. Conclusions: The plasma cytokine levels of TGF-β1 were associated with vessel invasion, peritoneal involvement, tumor stage in gastric cancer patients. TGF-β1 stimulated biological malignant behavior through EMT in gastric cancer. Ginsenoside Rg3 could inhibit the EMT induced by TGF-β1 in SNU-601 cell lines.
43
Schiffman, Carl. "Normandy." Missouri Review 16, no. 2 (1993): 7–19. http://dx.doi.org/10.1353/mis.1993.0026.
Full text
44
Sabry, J. H., T. P. O'Connor, L. Evans, A. Toroian-Raymond, M. Kirschner, and D. Bentley. "Microtubule behavior during guidance of pioneer neuron growth cones in situ." Journal of Cell Biology 115, no. 2 (October 15, 1991): 381–95. http://dx.doi.org/10.1083/jcb.115.2.381.
Full textAbstract:
The growth of an axon toward its target results from the reorganization of the cytoskeleton in response to environmental guidance cues. Recently developed imaging technology makes it possible to address the effect of such cues on the neural cytoskeleton directly. Although high resolution studies can be carried out on neurons in vitro, these circumstances do not recreate the complexity of the natural environment. We report here on the arrangement and dynamics of microtubules in live neurons pathfinding in response to natural guidance cues in situ using the embryonic grasshopper limb fillet preparation. A rich microtubule network was present within the body of the growth cone and normally extended into the distal growth cone margin. Complex microtubule loops often formed transiently within the growth cone. Branches both with and without microtubules were regularly observed. Microtubules did not extend into filopodia. During growth cone steering events in response to identified guidance cues, microtubule behaviour could be monitored. In turns towards guidepost cells, microtubules selectively invaded branches derived from filopodia that had contacted the guidepost cell. At limb segment boundaries, microtubules displayed a variety of behaviors, including selective branch invasion, and also invasion of multiple branches followed by selective retention in branches oriented in the correct direction. Microtubule invasion of multiple branches also was seen in growth cones migrating on intrasegmental epithelium. Both selective invasion and selective retention generate asymmetrical microtubule arrangements within the growth cone, and may play a key role in growth cone steering events.
45
Lyczak, Jeffrey B. "Commensal Bacteria Increase Invasion of Intestinal Epithelium by Salmonella enterica Serovar Typhi." Infection and Immunity 71, no. 11 (November 2003): 6610–14. http://dx.doi.org/10.1128/iai.71.11.6610-6614.2003.
Full textAbstract:
ABSTRACT The intestinal microflora consists of a heterogeneous population of microorganisms and has many effects on the health status of its human host. Here, it is shown that the products of certain strains of bacteria normally present in the intestinal microflora are able to trigger redistribution of the cystic fibrosis transmembrane conductance regulator (CFTR) protein in epithelial cells. CFTR is used by Salmonella enterica serovar Typhi as a receptor on epithelial cells which mediate the translocation of this microorganism to the gastric submucosa. Serovar Typhi-epithelial cell adhesion and CFTR-dependent invasion by serovar Typhi of epithelial cells were increased following commensal-mediated CFTR redistribution. These data suggest that commensal microorganisms present in the intestinal lumen can affect the efficiency of serovar Typhi invasion of the intestinal submucosa. This could be a key factor influencing host susceptibility to typhoid fever.
46
Ojalvo, Laureen S., and Jeffrey W. Pollard. "The Expression Signatures of Mammary Tumor Associated Macrophages." Blood 110, no. 11 (November 16, 2007): 3850. http://dx.doi.org/10.1182/blood.v110.11.3850.3850.
Full textAbstract:
Abstract It is well established that an increased density of tumor-associated macrophages (TAMs) correlates with poor prognosis in many types of solid tumors. This evidence is particularly strong for breast cancers. A causal relationship between TAMs and poor prognosis was suggested by experiments whereby a genetic depletion of macrophages in a mouse model of breast cancer caused by the mammary restricted expression of the Polyoma Middle T oncoprotein (PyMT) slowed tumor progression and inhibited metastasis. Subsequent studies in these primary mammary tumors showed that TAMs directly or indirectly promote tumor angiogenesis as well as tumor cell migration, invasion and intravasion. TAMs are also thought to affect the inflammatory context of the tumor microenvironment by suppressing adaptive immune responses that would normally reject the growing tumor. The varied tasks ascribed to TAMs suggested that the tumor microenvironment educates different population of macrophages to perform specific tasks. In this study, we isolated TAMs from the PyMT primary tumors in order to evaluate their gene expression signatures compared to a resident splenic population in order to define specific tumor associated functions. To perform these studies mice that express enhanced green fluorescent protein (eGFP) from the colony stimulating factor 1 receptor (CSF-1R) mononuclear phagocytic restricted promoter were crossed to the PyMT animals to generate offspring with eGFP+ TAMs. Animals were injected with dye-conjugated dextran two hours prior to sacrifice in order to identify phagocytic cells, a characteristic of macrophages. We have established that these eGFP+/dextran+ cells are F4/80+ and define the TAM population. EGFP+/dextran+ TAMs were isolated using flow cytometry from late-stage tumors and splenic macrophages were sorted from non-tumor bearing animals using an identical protocol. These two populations were analyzed on gene expression oligoarrays to better elucidate specific mediators of TAM pathogenicity. We have identified approximately 100 genes whose transcript abundance are up or down regulated in the TAM population including genes mediating angiogenesis, adhesion and inflammation. Furthermore, genes previously described to define the tumor associated suppressor macrophage (MIF-1, MIP1α and TGFβ, high; IL-18, low) were similarly regulated amongst the three biological repeats. To further define individual TAM populations, we used an in vivo invasion assay to isolate a subset of TAMs that promote carcinoma cell motility in vivo. This assay involves the collection of invasive tumor cells and co-migrating invasive TAMs into EGF-containing microneedles placed directly into the primary tumor of an MMTV-PyMT animal. Previously, this assay was used to describe a paracrine loop in which carcinoma cells secrete CSF-1 that binds CSF-1R on TAMs leading to TAM secretion of epidermal growth factor (EGF) that binds the EGF receptor on carcinoma cells and stimulate their motility. Disrupting this paracrine loop is known to block the invasion of both cell types. Invasive TAMs isolated via this assay and separated from invasive carcinoma cells using CD11b magnetic beads were compared by gene expression arrays to TAMs sorted by flow cytometry (F4/80+/dextran+). The transcript abundance of about 200 genes were differentially regulated between these two populations. Together, these two studies illustrate key genes expressed in TAMs that may regulate tumor progression and furthermore, define a specific sub-population of TAMs that directly promotes tumor cell migration and invasion.
47
Caceci, T., T. Toth, R. H. Pyle, P. B. Siegel, and D. Ochs. "Stimulation of non-opsonic phagocytosis in avian respiratory phagocytes." Proceedings, annual meeting, Electron Microscopy Society of America 46 (1988): 140–41. http://dx.doi.org/10.1017/s042482010010278x.
Full textAbstract:
Avian respiratory disease costs the U. S. poultry industry millions of dollars per year in lost production. The avian respiratory system, while similar in many ways, differs from that of mammals anatomically, physiologically, and in its response to invasion by infectious agents. One of the least understood components is the variety of cell types collectively referred to as avian respiratory phagocytes (ARP), the first line of defense against invasion. The resident ARP population is normally very low, but numbers increase in response to certain stimuli. We undertook a study to quantify the extent of ARP influx and the degree of increase in phagocytic activity in response to the presence of non-pathogenic Pasteurella multocida. Chickens were stimulated by intratracheal inoculation of P. multocida, and the ARP's collected by lavage of the lungs and air sacs. Control birds were inoculated with vehicle carrying no P. multocida, and then lavaged.
48
Nishimura, Tamako, Shoko Ito, Hiroko Saito, Sylvain Hiver, Kenta Shigetomi, Junichi Ikenouchi, and Masatoshi Takeichi. "DAAM1 stabilizes epithelial junctions by restraining WAVE complex–dependent lateral membrane motility." Journal of Cell Biology 215, no. 4 (November 2, 2016): 559–73. http://dx.doi.org/10.1083/jcb.201603107.
Full textAbstract:
Epithelial junctions comprise two subdomains, the apical junctional complex (AJC) and the adjacent lateral membrane contacts (LCs), that span the majority of the junction. The AJC is lined with circumferential actin cables, whereas the LCs are associated with less-organized actin filaments whose roles are elusive. We found that DAAM1, a formin family actin regulator, accumulated at the LCs, and its depletion caused dispersion of actin filaments at these sites while hardly affecting circumferential actin cables. DAAM1 loss enhanced the motility of LC-forming membranes, leading to their invasion of neighboring cell layers, as well as disruption of polarized epithelial layers. We found that components of the WAVE complex and its downstream targets were required for the elevation of LC motility caused by DAAM1 loss. These findings suggest that the LC membranes are motile by nature because of the WAVE complex, but DAAM1-mediated actin regulation normally restrains this motility, thereby stabilizing epithelial architecture, and that DAAM1 loss evokes invasive abilities of epithelial cells.
49
Dmitry Laru. "NORMANDY NONFORMAT." Current Digest of the Russian Press, The 70, no. 014 (April 8, 2018): 14–15. http://dx.doi.org/10.21557/dsp.50971517.
Full text
50
Yau, Belinda, Nicholas Hunt, Andrew Mitchell, and Lay Too. "Blood‒Brain Barrier Pathology and CNS Outcomes in Streptococcus pneumoniae Meningitis." International Journal of Molecular Sciences 19, no. 11 (November 11, 2018): 3555. http://dx.doi.org/10.3390/ijms19113555.
Full textAbstract:
Streptococcus pneumoniae is a major meningitis-causing pathogen globally, bringing about significant morbidity and mortality, as well as long-term neurological sequelae in almost half of the survivors. Subsequent to nasopharyngeal colonisation and systemic invasion, translocation across the blood‒brain barrier (BBB) by S. pneumoniae is a crucial early step in the pathogenesis of meningitis. The BBB, which normally protects the central nervous system (CNS) from deleterious molecules within the circulation, becomes dysfunctional in S. pneumoniae invasion due to the effects of pneumococcal toxins and a heightened host inflammatory environment of cytokines, chemokines and reactive oxygen species intracranially. The bacteria‒host interplay within the CNS likely determines not only the degree of BBB pathological changes, but also host survival and the extent of neurological damage. This review explores the relationship between S. pneumoniae bacteria and the host inflammatory response, with an emphasis on the BBB and its roles in CNS protection, as well as both the acute and long-term pathogenesis of meningitis.