Evidence of Tissue Invasion in Chicks by Euhaplorchis californiensis Martin, 1950, (Trematoda: Heterophyidae)

1954 ◽  
Vol 40 (3) ◽  
pp. 316
Author(s):  
Lois W. Wong
Author(s):  
Azadi A. ◽  
Khazaei M. ◽  
Ashrafi H.

Cancer, an uncontrollable growth of cells, is among the leading causes of mortality and morbidity throughout the world. Malignant neoplasms are difficult to treat diseases because of their single in kind characteristics such as tissue invasion, metastasis, evading reticuloendothelial system (RES) and so forth. In recent decade polymeric nanoparticulate systems has gained special attention in drug delivery and targeting among all biocompatible nanoforms. Among these systems, chitosan-based hydrogel nanoparticles have been wildly utilized for drug delivery purposes. The usage of chitosan nanogels in cancer therapy significantly improved in recent years. The various cancers were the target of chitosan nanogels. Also, modification of other delivery systems with chitosan were much reported. The aim of this study is the review and update of the recent studies on chitosan nanogels applications in cancer therapy by focus on cancer based classification.


2005 ◽  
Vol 15 (11) ◽  
pp. 1667-1683 ◽  
Author(s):  
MIROSŁAW LACHOWICZ

In this paper two new mathematical models are proposed that correspond to a macroscopic model of tissue invasion of solid tumours, in terms of a system of reaction-diffusion-chemotaxis equations. The first model is defined at the micro-scale level of a large number of interacting individual entities, and is in terms of a linear (Markov) equation. The second model refers to the meso-scale level of description of test-entities and is given in terms of a bilinear Boltzmann-type equation. Mathematical relationships among these three possible descriptions are formulated. Explicit error estimates are given.


2012 ◽  
Vol 94 (5) ◽  
pp. 456-464 ◽  
Author(s):  
Emily Mavin ◽  
Shaheda S. Ahmed ◽  
Graeme O’Boyle ◽  
Brie Turner ◽  
Stephen Douglass ◽  
...  

2009 ◽  
Vol 185 (1) ◽  
pp. 11-19 ◽  
Author(s):  
Farideh Sabeh ◽  
Ryoko Shimizu-Hirota ◽  
Stephen J. Weiss

Tissue invasion during metastasis requires cancer cells to negotiate a stromal environment dominated by cross-linked networks of type I collagen. Although cancer cells are known to use proteinases to sever collagen networks and thus ease their passage through these barriers, migration across extracellular matrices has also been reported to occur by protease-independent mechanisms, whereby cells squeeze through collagen-lined pores by adopting an ameboid phenotype. We investigate these alternate models of motility here and demonstrate that cancer cells have an absolute requirement for the membrane-anchored metalloproteinase MT1-MMP for invasion, and that protease-independent mechanisms of cell migration are only plausible when the collagen network is devoid of the covalent cross-links that characterize normal tissues.


Author(s):  
Richard A. Seidu ◽  
Min Wu ◽  
Zhaoliang Su ◽  
Huaxi Xu

Gliomas represent 60% of primary intracranial brain tumors and 80% of all malignant types, with highest morbidity and mortality worldwide. Although glioma has been extensively studied, the molecular mechanisms underlying its pathology remain poorly understood. Clarification of the molecular mechanisms involved in their development and/or treatment resistance is highly required. High mobility group box 1 protein (HMGB1) is a nuclear protein that can also act as an extracellular trigger of inflammation, proliferation and migration, through receptor for advanced glycation end products and toll like receptors in a number of cancers including gliomas. It is known that excessive release of HMGB1 in cancer leads to unlimited replicative potential, ability to develop blood vessels (angiogenesis), evasion of programmed cell death (apoptosis), self-sufficiency in growth signals, insensitivity to inhibitors of growth, inflammation, tissue invasion and metastasis. In this review we explore the mechanisms by which HMGB1 regulates apoptosis and autophagy in glioma. We also looked at how HMGB1 mediates glioma regression and promotes angiogenesis as well as possible signaling pathways with an attempt to provide potential therapeutic targets for the treatment of glioma.


1983 ◽  
Vol 13 (3) ◽  
pp. 359-364 ◽  
Author(s):  
M. Nicole ◽  
D. Nandris ◽  
J.-P. Geiger

Using an artificial inoculation technique, a kinetic infection study of Heveabrasiliensis (Willd. ex Adr. de Juss) Mull. Arg. by Rigidoporuslignosus (Kl.) Imazeki has shown the existence of a three-stage infection process: (i) a particularly fast contamination stage. After 15 days of exposure, all plants showed rhizomorphs to be present on taproots; (ii) the spread of epiphytic mycelium all over taproots is associated with numerous punctual penetrations allowing tissue invasion and infection. Beginning at the apex, a rot develops and progresses upward; in less than 3 months, it affects nearly 40% of the invaded plants' taproot. In response to this, the host develops reaction mechanisms which become evident at the cellular level and on the entire plant; and (iii) at this time, a state of equilibrium is reached between the host and the parasite which is shown through a stagnant disease progress. The efficiency of the various host reactions observed in the plants is discussed. [Journal translation]


Microbiology ◽  
2009 ◽  
Vol 155 (1) ◽  
pp. 198-209 ◽  
Author(s):  
Scott W. Bearden ◽  
Christopher Sexton ◽  
Joshua Pare ◽  
Janet M. Fowler ◽  
Cindy G. Arvidson ◽  
...  

It is established that Yersinia pestis, the causative agent of bubonic plague, recently evolved from enteropathogenic Yersinia pseudotuberculosis by undergoing chromosomal degeneration while acquiring two unique plasmids that facilitate tissue invasion (pPCP) and dissemination by fleabite (pMT). Thereafter, plague bacilli spread from central Asia to sylvatic foci throughout the world. These epidemic isolates exhibit a broad host range including man as opposed to enzootic (pestoides) variants that remain in ancient reservoirs where infection is limited to muroid rodents. Cells of Y. pseudotuberculosis are known to express glucose-6-phosphate dehydrogenase (Zwf) and aspartase (AspA); these activities are not detectable in epidemic Y. pestis due to missense mutations (substitution of proline for serine at amino position 155 of Zwf and leucine for valine at position 363 of AspA). In this study, functional Zwf was found in pestoides strains E, F and G but not seven other enzootic isolates; enzymic activity was associated with retention of serine at amino acid position 155. Essentially, full AspA activity occurred in pestoides isolates where valine (pestoides A, B, C and D) or serine (pestoides E, F, G and I) occupied position 363. Reduced activity occurred in strains Angola and A16, which contained phenylalanine at this position. The k cat but not K m of purified AspA from strain Angola was significantly reduced. In this context, aspA of the recently described attenuated enzootic microtus biovar encodes active valine at position 363, further indicating that functional AspA is a biomarker for avirulence of Y. pestis in man.


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