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Статті в журналах з теми "Intracellular spread"
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Minton, Kirsty. "Intracellular tunnels spread disease." Nature Reviews Molecular Cell Biology 17, no. 10 (September 1, 2016): 609. http://dx.doi.org/10.1038/nrm.2016.124.
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Pieper, Rembert, C. R. Fisher, Moo-Jin Suh, S. T. Huang, P. Parmar, and S. M. Payne. "Analysis of the Proteome of Intracellular Shigella flexneri Reveals Pathways Important for Intracellular Growth." Infection and Immunity 81, no. 12 (October 7, 2013): 4635–48. http://dx.doi.org/10.1128/iai.00975-13.
Повний текст джерелаАнотація:
ABSTRACTGlobal proteomic analysis was performed withShigella flexneristrain 2457T in association with three distinct growth environments:S. flexnerigrowing in broth (in vitro),S. flexnerigrowing within epithelial cell cytoplasm (intracellular), andS. flexnerithat were cultured with, but did not invade, Henle cells (extracellular). Compared toin vitroand extracellular bacteria, intracellular bacteria had increased levels of proteins required for invasion and cell-to-cell spread, including Ipa, Mxi, and Ics proteins. Changes in metabolic pathways in response to the intracellular environment also were evident. There was an increase in glycogen biosynthesis enzymes, altered expression of sugar transporters, and a reduced amount of the carbon storage regulator CsrA. Mixed acid fermentation enzymes were highly expressed intracellularly, while tricarboxylic acid (TCA) cycle oxidoreductive enzymes and most electron transport chain proteins, except CydAB, were markedly decreased. This suggested that fermentation and the CydAB system primarily sustain energy generation intracellularly. Elevated levels of PntAB, which is responsible for NADPH regeneration, suggested a shortage of reducing factors for ATP synthesis. These metabolic changes likely reflect changes in available carbon sources, oxygen levels, and iron availability. Intracellular bacteria showed strong evidence of iron starvation. Iron acquisition systems (Iut, Sit, FhuA, and Feo) and the iron starvation, stress-associated Fe-S cluster assembly (Suf) protein were markedly increased in abundance. Mutational analysis confirmed that the mixed-acid fermentation pathway was required for wild-type intracellular growth and spread ofS. flexneri. Thus, iron stress and changes in carbon metabolism may be key factors in theS. flexneritransition from the extra- to the intracellular milieu.
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Keegan, Richard M., Lillian R. Talbot, Yung-Heng Chang, Michael J. Metzger, and Josh Dubnau. "Intercellular viral spread and intracellular transposition of Drosophila gypsy." PLOS Genetics 17, no. 4 (April 22, 2021): e1009535. http://dx.doi.org/10.1371/journal.pgen.1009535.
Повний текст джерелаАнотація:
It has become increasingly clear that retrotransposons (RTEs) are more widely expressed in somatic tissues than previously appreciated. RTE expression has been implicated in a myriad of biological processes ranging from normal development and aging, to age related diseases such as cancer and neurodegeneration. Long Terminal Repeat (LTR)-RTEs are evolutionary ancestors to, and share many features with, exogenous retroviruses. In fact, many organisms contain endogenous retroviruses (ERVs) derived from exogenous retroviruses that integrated into the germ line. These ERVs are inherited in Mendelian fashion like RTEs, and some retain the ability to transmit between cells like viruses, while others develop the ability to act as RTEs. The process of evolutionary transition between LTR-RTE and retroviruses is thought to involve multiple steps by which the element loses or gains the ability to transmit copies between cells versus the ability to replicate intracellularly. But, typically, these two modes of transmission are incompatible because they require assembly in different sub-cellular compartments. Like murine IAP/IAP-E elements, the gypsy family of retroelements in arthropods appear to sit along this evolutionary transition. Indeed, there is some evidence that gypsy may exhibit retroviral properties. Given that gypsy elements have been found to actively mobilize in neurons and glial cells during normal aging and in models of neurodegeneration, this raises the question of whether gypsy replication in somatic cells occurs via intracellular retrotransposition, intercellular viral spread, or some combination of the two. These modes of replication in somatic tissues would have quite different biological implications. Here, we demonstrate that Drosophila gypsy is capable of both cell-associated and cell-free viral transmission between cultured S2 cells of somatic origin. Further, we demonstrate that the ability of gypsy to move between cells is dependent upon a functional copy of its viral envelope protein. This argues that the gypsy element has transitioned from an RTE into a functional endogenous retrovirus with the acquisition of its envelope gene. On the other hand, we also find that intracellular retrotransposition of the same genomic copy of gypsy can occur in the absence of the Env protein. Thus, gypsy exhibits both intracellular retrotransposition and intercellular viral transmission as modes of replicating its genome.
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Weddle, Erin, and Hervé Agaisse. "Principles of intracellular bacterial pathogen spread from cell to cell." PLOS Pathogens 14, no. 12 (December 13, 2018): e1007380. http://dx.doi.org/10.1371/journal.ppat.1007380.
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Ireton, Keith. "Molecular mechanisms of cell–cell spread of intracellular bacterial pathogens." Open Biology 3, no. 7 (July 2013): 130079. http://dx.doi.org/10.1098/rsob.130079.
Повний текст джерелаАнотація:
Several bacterial pathogens, including Listeria monocytogenes , Shigella flexneri and Rickettsia spp., have evolved mechanisms to actively spread within human tissues. Spreading is initiated by the pathogen-induced recruitment of host filamentous (F)-actin. F-actin forms a tail behind the microbe, propelling it through the cytoplasm. The motile pathogen then encounters the host plasma membrane, forming a bacterium-containing protrusion that is engulfed by an adjacent cell. Over the past two decades, much progress has been made in elucidating mechanisms of F-actin tail formation. Listeria and Shigella produce tails of branched actin filaments by subverting the host Arp2/3 complex. By contrast, Rickettsia forms tails with linear actin filaments through a bacterial mimic of eukaryotic formins. Compared with F-actin tail formation, mechanisms controlling bacterial protrusions are less well understood. However, recent findings have highlighted the importance of pathogen manipulation of host cell–cell junctions in spread. Listeria produces a soluble protein that enhances bacterial protrusions by perturbing tight junctions. Shigella protrusions are engulfed through a clathrin-mediated pathway at ‘tricellular junctions’—specialized membrane regions at the intersection of three epithelial cells. This review summarizes key past findings in pathogen spread, and focuses on recent developments in actin-based motility and the formation and internalization of bacterial protrusions.
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Roos, Tomas T., Megg G. Garcia, Isak Martinsson, Rana Mabrouk, Bodil Israelsson, Tomas Deierborg, Asgeir Kobro-Flatmoen, Heikki Tanila та Gunnar K. Gouras. "Neuronal spreading and plaque induction of intracellular Aβ and its disruption of Aβ homeostasis". Acta Neuropathologica 142, № 4 (16 липня 2021): 669–87. http://dx.doi.org/10.1007/s00401-021-02345-9.
Повний текст джерелаАнотація:
AbstractThe amyloid-beta peptide (Aβ) is thought to have prion-like properties promoting its spread throughout the brain in Alzheimer’s disease (AD). However, the cellular mechanism(s) of this spread remains unclear. Here, we show an important role of intracellular Aβ in its prion-like spread. We demonstrate that an intracellular source of Aβ can induce amyloid plaques in vivo via hippocampal injection. We show that hippocampal injection of mouse AD brain homogenate not only induces plaques, but also damages interneurons and affects intracellular Aβ levels in synaptically connected brain areas, paralleling cellular changes seen in AD. Furthermore, in a primary neuron AD model, exposure of picomolar amounts of brain-derived Aβ leads to an apparent redistribution of Aβ from soma to processes and dystrophic neurites. We also observe that such neuritic dystrophies associate with plaque formation in AD-transgenic mice. Finally, using cellular models, we propose a mechanism for how intracellular accumulation of Aβ disturbs homeostatic control of Aβ levels and can contribute to the up to 10,000-fold increase of Aβ in the AD brain. Our data indicate an essential role for intracellular prion-like Aβ and its synaptic spread in the pathogenesis of AD.
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Meyer, Diane Hutchins, John E. Rose, Joan E. Lippmann, and Paula M. Fives-Taylor. "Microtubules Are Associated with Intracellular Movement and Spread of the Periodontopathogen Actinobacillus actinomycetemcomitans." Infection and Immunity 67, no. 12 (December 1, 1999): 6518–25. http://dx.doi.org/10.1128/iai.67.12.6518-6525.1999.
Повний текст джерелаАнотація:
ABSTRACT Actinobacillus actinomycetemcomitans SUNY 465, the invasion prototype strain, enters epithelial cells by an actin-dependent mechanism, escapes from the host cell vacuole, and spreads intracellularly and to adjacent epithelial cells via intercellular protrusions. Internalized organisms also egress from host cells into the assay medium via protrusions that are associated with just a single epithelial cell. Here we demonstrate that agents which inhibit microtubule polymerization (e.g., colchicine) and those which stabilize polymerized microtubules (e.g., taxol) both increase markedly the number of intracellular A. actinomycetemcomitansorganisms. Furthermore, both colchicine and taxol prevented the egression of A. actinomycetemcomitans from host cells into the assay medium. Immunofluorescence microscopy revealed that protrusions that mediate the bacterial spread contain microtubules.A. actinomycetemcomitans SUNY 465 and 652, strains that are both invasive and egressive, interacted specifically with the plus ends (growing ends) of the filaments of microtubule asters in a KB cell extract. By contrast, neither A. actinomycetemcomitans 523, a strain that is invasive but not egressive, nor Haemophilus aphrophilus, a noninvasive oral bacterium with characteristics similar to those of A. actinomycetemcomitans, bound to microtubules. Together these data suggest that microtubules function in the spread and movement of A. actinomycetemcomitans and provide the first evidence that host cell dispersion of an invasive bacterium may involve the usurption of host cell microtubules.
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Reeves, Stephanie A., Alfredo G. Torres, and Shelley M. Payne. "TonB Is Required for Intracellular Growth and Virulence of Shigella dysenteriae." Infection and Immunity 68, no. 11 (November 1, 2000): 6329–36. http://dx.doi.org/10.1128/iai.68.11.6329-6336.2000.
Повний текст джерелаАнотація:
ABSTRACT To assess the importance of TonB-dependent iron transport systems to growth of Shigella in vivo, a tonB mutant ofShigella dysenteriae was isolated and tested in cultured cells. The tonB mutant invaded epithelial cells, but did not form plaques in confluent monolayers of Henle cells, indicating an inability of this mutant to spread from cell to cell. The rate of intracellular multiplication of the tonB mutant was reduced significantly compared to that of the wild type. The loss of virulence in the tonB mutant was not due to loss of either Shu or Ent, the TonB-dependent systems which allow for transport of heme and ferrienterobactin, respectively. A shuA mutant lacking the outer membrane receptor for heme, an entB mutant defective in enterobactin synthesis, and a shuA entB double mutant each were able to invade cultured cells, multiply intracellularly, and form wild-type plaques. The ability of S. dysenteriae to access iron during intracellular growth was assessed by flow cytometric analysis of an iron- and Fur-regulated shuA-gfp reporter construct. Low levels of green fluorescent protein expression in the intracellular environment were observed in all strains, indicating that iron is available to intracellular bacteria, even in the absence of TonB-dependent iron transport. The failure of the tonBmutant to grow well in an iron-replete intracellular environment suggests that TonB plays a role in addition to heme- and siderophore-mediated iron acquisition in vivo, and this function is required for the intracellular growth and intercellular spread ofS. dysenteriae.
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Drevets, Douglas A., Todd A. Jelinek, and Nancy E. Freitag. "Listeria monocytogenes-Infected Phagocytes Can Initiate Central Nervous System Infection in Mice." Infection and Immunity 69, no. 3 (March 1, 2001): 1344–50. http://dx.doi.org/10.1128/iai.69.3.1344-1350.2001.
Повний текст джерелаАнотація:
ABSTRACT Listeria monocytogenes-infected phagocytes are present in the bloodstream of experimentally infected mice, but whether they play a role in central nervous system (CNS) invasion is unclear. To test whether bacteria within infected leukocytes could establish CNS infection, experimentally infected mice were treated with gentamicin delivered by surgically implanted osmotic pumps. Bacterial inhibitory titers in serum and plasma ranged from 1:16 to 1:256, and essentially all viable bacteria in the bloodstream of treated mice were leukocyte associated. Nevertheless, CNS infection developed in gentamicin-treated animals infected intraperitoneally or by gastric lavage, suggesting that intracellular bacteria could be responsible for neuroinvasion. This was supported by data showing that 43.5% of bacteria found with blood leukocytes were intracellular and some colocalized with F-actin, indicating productive intracellular parasitism. Experiments using an L. monocytogenes strain containing a chromosomal actA-gfpuv-plcB transcriptional fusion showed that blood leukocytes were associated with intracellular and extracellularly bound green fluorescent protein-expressing (GFP+) bacteria. Treatment with gentamicin decreased the numbers of extracellularly bound GFP+ bacteria significantly but did not affect the numbers of intracellular GFP+ bacteria, suggesting that the latter were the result of intercellular spread of GFP+ bacteria to leukocytes. These data demonstrate that infected leukocytes and the intracellularL. monocytogenes harbored within them play key roles in neuroinvasion. Moreover, they suggest that phagocytes recruited to infected organs such as the liver or spleen are themselves parasitized by intercellular spread of L. monocytogenes and then reenter the bloodstream and contribute to the systemic dissemination of bacteria.
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Zeldovich, Varvara B., Jennifer R. Robbins, Mirhan Kapidzic, Peter Lauer, and Anna I. Bakardjiev. "Invasive Extravillous Trophoblasts Restrict Intracellular Growth and Spread of Listeria monocytogenes." PLoS Pathogens 7, no. 3 (March 3, 2011): e1002005. http://dx.doi.org/10.1371/journal.ppat.1002005.
Повний текст джерелаДисертації з теми "Intracellular spread"
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Olofsson, Jenny. "Amoebae as Hosts and Vectors for Spread of Campylobacter jejuni." Doctoral thesis, Uppsala universitet, Institutionen för medicinska vetenskaper, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-255804.
Повний текст джерелаАнотація:
Campylobacter jejuni is the leading bacterial cause of gastrointestinal diarrheal disease in humans worldwide. This zoonotic pathogen has a complex epidemiology due to its presence in many different host organisms. The overall aim of this thesis was to explore the role of amoebae of the genus Acanthamoeba as an intermediate host and vector for survival and dissemination of C. jejuni. Earlier studies have shown that C. jejuni can enter, survive and replicate within Acanthamoebae spp. In this thesis, I have shown that C. jejuni actively invades Acanthamoeba polyphaga. Once inside, C. jejuni could survive within the amoebae by avoiding localization to degradative lysosomes. We also found that A. polyphaga could protect C. jejuni in acid environments with pH levels far below the range in which the bacterium normally survives. Furthermore, low pH triggered C. jejuni motility and invasion of A. polyphaga. In an applied study I found that A. polyphaga also could increase the survival of C. jejuni in milk and juice both at room temperature and at +4ºC, but not during heating to recommended pasteurization temperatures. In the last study we found that forty environmental C. jejuni isolates with low bacterial concentrations could be successfully enriched using the Acanthamoeba-Campylobacter coculture (ACC) method. Molecular genetic analysis using multilocus sequence typing (MLST) and sequencing of the flaA gene, showed no genetic changes during coculture. The results of this thesis have increased our knowledge on the mechanisms behind C. jejuni invasion and intracellular survival in amoebae of the genus Acanthamoeba. By protecting C. jejuni from acid environments, Acanthamoebae could serve as important reservoirs for C. jejuni e.g. during acid sanitation of chicken stables and possibly as vectors during passage through the stomach of host animals. Furthermore, Acanthamoeba spp. could serve as a vehicle and reservoir introducing and protecting C. jejuni in beverages such as milk and juice. Validation of the ACC method suggests that it is robust and could be used even in outbreak investigations where genetic fingerprints are compared between isolates. In conclusion, Acanthamoeba spp. are good candidates for being natural hosts and vectors of C. jejuni.
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Doyle, Matthew Thomas. "Polarity and secretion of Shigella flexneri IcsA: a classical autotransporter." Thesis, 2015. http://hdl.handle.net/2440/98693.
Повний текст джерелаАнотація:
The classical autotransporter IcsA is an essential virulence factor for the enteropathogen Shigella flexneri as it provides adherence properties and allows intra- and intercellular spreading in the colonic mucosa. IcsA is an outer membrane surface protein that specifically hijacks host-cell actin recruiting and polymerising complexes allowing actin polymerisation as a form of actin-based motility (ABM). Importantly, since IcsA is localised specifically at one end of the bacterium (the pole), the resulting ABM is unidirectional which is a requirement for efficient S. flexneri dissemination. However, the molecular mechanisms that generate IcsA polarity remain poorly understood. Furthermore, IcsA is a member of the autotransporter family of secreted virulence factors (Type Va). Although many steps in the autotransporter pathway have been elucidated, it is still poorly understood how these diverse proteins are efficiently translocated to the bacterial cell surface. As such, this thesis investigates the two arms of IcsA biogenesis: (1) polar targeting and (2) autotransport. Regarding IcsA polarity, it was identified here that the IcsA-specific outer membrane protease IcsP localises to the septa of dividing S. flexneri and to the opposing pole relative IcsA. The concentration of IcsP was higher at the septum than the pole showing a life cycle dependent distribution of IcsP. This provides the basis of a model where IcsP is important during division of S. flexneri for setting up (and the continued maintenance of) IcsA polarity by the proteolysis of misdirected IcsA. Further, multiple previous reports have suggested that the S. flexneri lipopolysaccharide O-antigen surface structure can influence IcsA polarity by augmenting membrane fluidity or by asymmetric masking of IcsA surface exposure. These notions were tested here resulting in data that clearly refutes these models and agues simply that IcsA exposure is masked symmetrically over the bacterial cell surface. Finally, IcsA itself contains polar targeting (PT) regions that direct it to the pole by an, as yet, unclear mechanism. Examination of these regions revealed that the central PT (cPT) is most important in polarity augmentation and contains critical polarity targeting function residues. Regarding IcsA autotransport, a highly conserved but uncharacterised autotransporter motif was scrutinized for potential biogenesis functions and was designated in this work as the passenger-associated transport repeat (PATR). It was found that the PATR plays a critical role in the efficient secretion of IcsA to the cell surface. Strikingly, bioinformatics analyses revealed that the PATR delineates an important separate autotransporter sub-type with unique functions, composition, and architecture.Thesis (Ph.D.) (Research by Publication) -- University of Adelaide, School of Biological Sciences, 2015.
Книги з теми "Intracellular spread"
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Cummings, Jeffrey L., and Jagan A. Pillai. Neurodegenerative Diseases. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190233563.003.0001.
Повний текст джерелаАнотація:
Neurodegenerative diseases (NDDs) are growing in frequency and represent a major threat to public health. Advances in scientific progress have made it clear that NDDs share many underlying processes, including shared intracellular mechanisms such as protein misfolding and aggregation, cell-to-cell prion-like spread, growth factor signaling abnormalities, RNA and DNA disturbances, glial cell changes, and neuronal loss. Transmitter deficits are shared across many types of disorders. Means of studying NDDs with human iPS cells and transgenic models are similar. The progression of NDDs through asymptomatic, prodromal, and manifest stages is shared across disorders. Clinical features of NDDs, including cognitive impairment, disease progression, age-related effects, terminal stages, neuropsychiatric manifestations, and functional disorders and disability, have many common elements. Clinical trials, biomarkers, brain imaging, and regulatory aspects of NDD can share information across NDDs. Disease-modifying and transmitter-based therapeutic interventions, clinical trials, and regulatory approaches to treatments for NDDs are also similar.
Частини книг з теми "Intracellular spread"
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Marrie, T. J. "Coxiella burnetii infections (Q fever)." In Oxford Textbook of Medicine, 923–26. Oxford University Press, 2010. http://dx.doi.org/10.1093/med/9780199204854.003.070641_update_003.
Повний текст джерелаАнотація:
Q fever is a zoonosis caused by Coxiella burnetii, an intracellular Gram-negative spore-forming bacterium, the common animal reservoirs of which are cattle, sheep, and goats, although in a large outbreak in the Netherlands it appears that rats, Rattus norvegicus and R. rattus, may have played a role in the spread of the condition. ...
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Jannet Ruiz-Pérez, Nancy, Jaime Sánchez-Navarrete, and Julia D. Toscano-Garibay. "Natural Products for Salmonellosis: Last Decade Research." In Salmonella - a Challenge From Farm to Fork [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.96207.
Повний текст джерелаАнотація:
Salmonellosis is a disease of great relevance in terms of public health given the economic and social impact that causes both in developing and highly industrialized countries. Due to its transmission mechanism, it affects hundreds or thousands of people every year and is considered an acute disease of worldwide distribution. Causative agent of salmonellosis is salmonella specie which are small gram-negative bacilli and facultative intracellular pathogen of the Enterobacteriaceae family. Multidrug resistance is reported more frequently in strains of salmonella, raising the necessity of new strategies to combat its spread and to treat the disease. Natural products (NPs) derived from traditional medicine knowledge have become an important resource to this end. In this chapter, we present a summary of information published from 2010 to 2020, as a sample of the potentiality of NPs as agents for Salmonellosis. This search was not exhaustive, rather, we aim to obtain a random sample of information using the simplest terms on the matter of natural products for salmonellosis, hopefully, as a reference source for interested researchers.
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Y. Liu, Alvin, Tatjana Crnogorac-Jurcevic, James J. Lai, and Hung-Ming Lam. "Antibody Therapy Targeting Cancer-Specific Cell Surface Antigen AGR2." In Advances in Precision Medicine Oncology. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.96492.
Повний текст джерелаАнотація:
For anterior gradient 2 (AGR2), normal cells express the intracellular form iAGR2 localized to the endoplasmic reticulum while cancer cells express the extracellular form eAGR2 localized on the cell surface and secreted. Antibodies targeting eAGR2+ cancer cells for eradication will spare normal cells. Two AGR2 monoclonal antibodies, P1G4 and P3A5, were shown to recognize specifically eAGR2+ pancreatic tumors implanted in mice. In addition, P1G4 showed enhancement in drug inhibition of tumor growth. Human:mouse chimeric antibodies of IgG1, IgG2, IgG4 were generated for both antibodies. These human IgG were shown to lyse eAGR2+ prostate cancer cells in vitro with human serum. AGR2 has an important function in distal spread of cancer cells, and is highly expressed in prostate, pancreatic, bladder metastases. Therefore, immunotherapy based on AGR2 antibody-mediated ADCC and CDC is highly promising. Cancer specificity of eAGR2 predicts possibly minimal collateral damage to healthy tissues and organs. Moreover, AGR2 therapy, once fully developed and approved, can be used to treat other solid tumors since AGR2 is an adenocarcinoma antigen found in many common malignancies.
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Atkinson, Martin E. "The central nervous system." In Anatomy for Dental Students. Oxford University Press, 2013. http://dx.doi.org/10.1093/oso/9780199234462.003.0009.
Повний текст джерелаАнотація:
The nervous system is an integrating system which acts rapidly by transmitting signals as electrical impulses over often considerable distances to coordinate bodily activities. The brain and spinal cord make up the central nervous system (CNS); incoming information travels in ascending (sensory) tracts that link the spinal cord to the brain and outgoing information passes down descending (motor) tracts linking the brain to the spinal cord. The CNS integrates responses to incoming information and sends the information to effector tissues (usually striated or smooth muscles or glands). Incoming and outgoing information is carried to and from the periphery to the CNS via 12 pairs of cranial nerves connected to the brain and 31 pairs of spinal nerves connected to the spinal cord; they constitute the peripheral nervous system (PNS). Sensory (afferent) information from the external environment is obtained through the organs of special sense in the eyes, ears, nose and tongue, and skin and mucosa lining bodily cavities: we are aware of these stimuli. Information from internal sources is equally important and vital for maintaining homeostasis, but we are usually Neurons are the basic cellular units of the nervous system. As the principal function of the nervous system is conduction of electrical signals over considerable distances, neurons are highly specialized for this f unction. Neurons have: • A specific shape with long cellular extensions; • Highly specialized membranes to control ionic movements to allow electrical activity to spread along the cellular extensions; • A very specialized internal transport system to distribute cellular metabolites along the processes. The general shape of neurons is shown in Figure 3.1. Note first of all, the relatively large cell body near the top of the picture; this contains the nucleus and the intracellular organelles necessary for synthetic functions so is similar to any other cell. What make neurons special are the long processes that emanate from the cell body. Dendrites are short multiple processes that branch extensively from and transmit impulses towards the cell body. Compare the dendrites in Figure 3.1 with the other process, the axon, which transmits impulses away from the cell body.
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Hassan Flaih, Mohammed. "Geographical Distribution of Cutaneous Leishmaniasis and Pathogenesis." In Leishmaniasis - General Aspects of a Stigmatized Disease. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.101841.
Повний текст джерелаАнотація:
Leishmaniasis is still considered to be a global health problem, which spreads in most countries in the world. Leishmania is an intracellular obligate protistan parasite that causes different clinical symptoms in infected humans and other animals. There are clinically different types of the disease including: visceral, cutaneous or muco-cutaneous leishmaniasis. Approximately, two million new infections occurring annually; 0.7 to 1.2 million cases are recorded with cutaneous leishmaniasis and 200,000–400,000 cases return for visceral leishmaniasis. However, Cutaneous leishmaniasis considers one of uncontrolled wobbling endemic diseases, especially in Iraq, which occurs at the skin to cause a dermal lesion. Usually, the lesion is spontaneously healed to leave a colorless depressed scar and permanent immunity.
Тези доповідей конференцій з теми "Intracellular spread"
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Chen, Yi-Chun, Huei-Jyuan Pan, Li-Wei Chu, Chung-Shi Yang, and Chau-Hwang Lee. "An image processing algorithm to tackle noisy point spread functions in 3D intracellular particle tracking." In 2011 International Quantum Electronics Conference (IQEC) and Conference on Lasers and Electro-Optics (CLEO) Pacific Rim. IEEE, 2011. http://dx.doi.org/10.1109/iqec-cleo.2011.6193844.
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Sarvestani, Alireza. "A Theoretical Analysis for the Effect of Substrate Elasticity on Cellular Adhesion." In ASME 2010 First Global Congress on NanoEngineering for Medicine and Biology. ASMEDC, 2010. http://dx.doi.org/10.1115/nemb2010-13311.
Повний текст джерелаАнотація:
Cell behavior is mediated by variety of physiochemical properties of extracellular matrix (ECM). Material composition, surface chemistry, roughness, and distribution pattern of cell adhesive proteins are among the ECM properties which are known to modulate various cellular physiological functions. Mechanical stiffness of ECM in particular is found to be a major regulator for multiple aspects of cellular function. Experiments show that cells in general, exhibit an apparent adhesion preference for stiffer substrates with a larger projected spread area with increasing the substrate stiffness. In addition, it seems that the effect of substrates elasticity is strongly coupled with adhesivity of the substrate; on relatively stiff substrates the spread area of the cells exhibits strong biphasic dependence to the changes in ligand density, whereas on soft substrates their limited spreading is much less sensitive to the density of surface ligands. This study aims to propose a theoretical basis for the interplay between substrate elasticity and cellular adhesion, using an equilibrium thermodynamic model. Within this framework, the equilibrium contact area is assumed to ensure minimization of the free energy contributed by interfacial adhesive and repulsive interactions between the membrane and substrate as well as the deformation of cell and substrate. Hence, this thermodynamic model overlooks the contribution of intracellular signaling or actively regulated cytoskeleton and assumes that cell adhesion is solely a result of the balance between the membrane-substrate repulsive potentials, stored elastic energy, binding enthalpy, and mixing entropy of mobile receptors. The predictions of this purely mechanistic model for cell adhesion qualitatively follow the experimental results featuring the variation of cell spread area on compliant bio-adhesive substrates. This suggests that the mechanistic pathways inherent to membrane-substrate interactions may be equally important as intracellular signaling pathways to mediate the cellular adhesion.
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Ay, Emrah, and Nizami Duran. "Resistance of SARS CoV-2 to Seawater." In The 9th International Conference on Advanced Materials and Systems. INCDTP - Leather and Footwear Research Institute (ICPI), Bucharest, Romania, 2022. http://dx.doi.org/10.24264/icams-2022.iii.2.
Повний текст джерелаАнотація:
SARS CoV-2, which is the cause of Covid-19 disease, has become the only and most important agenda of the world due to its mortality and morbidity that globally affects the whole world. The virus has profoundly affected life all over the world. The lifestyles of people have changed due to the virus. This study is planned to understand how important sea water is in SARS-CoV-2 transmission. The study aimed to determine whether there is a risk of sea water in SARS-CoV-2 transmission. The effectiveness of seawater on SARS CoV-2 viability has been investigated in different dilutions of seawater in different time periods. Experiments were carried out in three different titrations of SARS CoV-2 in Vero cell lines. Viral replication has been investigated by detecting morphological changes occurring in cells, cell viability, and the RT-PCR method. Seawater has been found to be highly potent inhibitory on SARS CoV-2 about time and dose. Especially within 300 seconds, seawater has been found to inhibit viral replication up to 1/32 dilution. These results show that viral transmission through seawater is quite difficult for people swimming in the sea during the pandemic. Seawater-mediated spread of SARS-CoV-2 is out of the question. However, these results should not be interpreted as the prophylactic activity of saline against viruses, which are obligate intracellular parasites.
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Baker, Brendon M., Colin K. Choi, Britta Trappmann, and Christopher S. Chen. "Engineered Fibrillar Extracellular Matrices for the Study of Directed Cell Migration." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80943.
Повний текст джерелаАнотація:
The biology of cell adhesion and migration has traditionally been studied on 2D glass or plastic surfaces. While such studies have shed light on the molecular mechanisms governing these processes [1], current knowledge is limited by the dissimilarity between the flat surfaces conventionally employed and the topographically complex extracellular matrix (ECM) cells routinely navigate within the body. On ECM-coated flat surfaces, cells are presented with an unlimited expanse of adhesive ligand and can spread and migrate freely. Conversely, the availability of ligand in vivo is generally restricted to ECM structures, forcing cells to form adhesions in prescribed locations distributed through 3D space depending on the geometry and organization of the surrounding matrix [2]. These physical constraints on cell adhesion likely have profound consequences on intracellular signaling and resulting migration, and calls into question whether the mechanisms and modes of cell motility observed on flat substrates are truly reflective of the in vivo scenario [3]. The topographies of ECMs found in vivo are varied but largely fibrillar, ranging from the tightly crosslinked fibers that form the sheet-like basement membrane, to the structure of fibrin-rich clots and collagenous connective tissues. Collagen comprises approximately 25% of the human body by mass, and as such, purified collagen has served as a popular setting for the study of cell migration within a fibrillar context for many decades [4]. However, a major limitation to the use of these gels is the inability to orthogonally dictate key structural features that impact cell behavior. For example, in contrast to the large range of fiber diameters found in vivo within connective tissue resulting from hierarchical collagen assembly and multiple types of collagens [3], collagen gels are limited to fibril diameters of ∼500nm. Furthermore, recreating the structural anisotropy common to connective tissues in collagen gels is technically challenging [5]. Thus, there remains a significant need for engineered fibrillar materials that afford precise and independent control of architectural and mechanical features for application in cell biology. In this work, we develop two approaches to fabricating fibrillar ECMs in order to study cell adhesion and migration in vitro.
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"Impact of Heparan Sulphate Binding Domain of Chemokine CCL21 to Migration of Breast Cancer Cells." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0132.
Повний текст джерелаАнотація:
Lymph node metastasis constitutes a key event in breast cancer progression. Chemokines are small proteins, which can promote metastatic spread by inducing cancer cell migration and invasion. Chemokine function is dependant upon their binding to both cell surface heparan sulphate (HS) molecules and to their specific receptor. Our group has demonstrated a significant increase in chemokine receptor CCR7 expression in cancerous breast epithelia compared to healthy controls. This study is designed to test the hypothesis that a non-HS binding forms of chemokine CCL21 can disrupt the normal response to CCL21, therefore reducing the metastasis of CCR7-expressing cancer cells. Truncated CCL21 chemokine (Δ98- 134 c-terminal basic extension), was synthesised to investigate a possible linkage between chemokine binding capacity and cell activation. Wild type (WT) and mutant-CCL21 were tested for their ability to stimulate a dose-dependent increase in intracellular-free calcium in peripheral blood mononuclear cell (PBMC) and breast cancer epithelial cells MDA-MB-231. Mutant-CCL21 at concentrations 5 and 10nM showed potential to mobilise Ca2+ at levels similar to that produced by WT-CCl21. A series of experiments was performed to determine how deletion of the HS-binding site altered the ability of CCL21 to stimulate chemotaxis within a concentration gradient generated by free solute diffusion. PBMC stimulated to migrate by wild-type CCL21 was not significantly different from that stimulated by mutant (P> 0.05). Similar results were observed in assays using MDA-MB-231 cells. A further series of experiments was performed to compare the potential of WT and mutant-CCL21 to stimulate the migration of cells across endothelium. In contrast to results for trans-filter migration, it was found that the non HSbinding mutant stimulated no increased in transendothelial cell migration above the background at each of the tested concentrations, 10, 30 and 50 nM respectively (P>0.05). However, WT-CCL21 stimulated significant increased PBMC migration at each of the tested concentration (all P <0.001). Furthermore, the effect of heparin on chemotactic properties of WT and mutant- CCL21 was examined. Interestingly, heparin (250 µg/ml) completely inhibit the chemotaxis mediated by WT-CCL21 (5nM) (P < 0.001), whereas it did not inhibit the chemotaxis at concentrations 100, 250 & 500 µg/ml in response to mutant CCL21 (5nM) (P > 0.05). Similar assay will be performed using MDA-MB-231 cells. Work is ongoing to characterise the biophysical properties of mutant-CCL21 and determine its potential role for a therapeutic blockade of the migration of breast cancer cells in-vivo. Our primarily data showed that mutant CCL21 in xenograft brain tumor models showed substantial inhibition of tumour growth. Our results indicate that truncated CCL21 chemokine might be a potential preventive biofactor for human breast cancer metastasis by targeting chemokine receptor genes.
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"Arbitrary Power Waveforms Measurement for Electrosurgical Unit Analyzers." In NCSL International Workshop & Symposium. NCSL International, 2018. http://dx.doi.org/10.51843/wsproceedings.2018.44.
Повний текст джерелаАнотація:
The Standards and Calibration Laboratory (SCL) in Hong Kong has developed a measurement system for the testing of electrosurgical unit (ESU) analyzers. ESUs are medical device widely used by surgeons and medical practitioners in surgical operations and in outpatient procedures. ESUs generate high frequency signals usually in the range of 200 kHz to 500 kHz with power up to 300 W to heat up tissues by induced intracellular oscillation of ionized molecules. By precisely controlling the power and duty cycle of the output waveform, various electrosurgical procedures including cut, coagulate, desiccate, fulgurate or spray of tissues can be performed. Routine performance check of ESUs is commonly conducted by ESU analyzers, which is a high frequency electronic load designed to measure the output parameters of various ESU modes. In this paper a method developed for the testing of ESU analyzers at the SCL is presented. By utilizing high speed digital sampling system, high frequency arbitrary power waveforms measurement function of ESU analyzers can be tested by simultaneous measurement of voltage and current components.
Звіти організацій з теми "Intracellular spread"
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Epel, Bernard, and Roger Beachy. Mechanisms of intra- and intercellular targeting and movement of tobacco mosaic virus. United States Department of Agriculture, November 2005. http://dx.doi.org/10.32747/2005.7695874.bard.
Повний текст джерелаАнотація:
To cause disease, plant viruses must replicate and spread locally and systemically within the host. Cell-to-cell virus spread is mediated by virus-encoded movement proteins (MPs), which modify the structure and function of plasmodesmata (Pd), trans-wall co-axial membranous tunnels that interconnect the cytoplasm of neighboring cells. Tobacco mosaic virus (TMV) employ a single MP for cell- cell spread and for which CP is not required. The PIs, Beachy (USA) and Epel (Israel) and co-workers, developed new tools and approaches for study of the mechanism of spread of TMV that lead to a partial identification and molecular characterization of the cellular machinery involved in the trafficking process. Original research objectives: Based on our data and those of others, we proposed a working model of plant viral spread. Our model stated that MPᵀᴹⱽ, an integral ER membrane protein with its C-terminus exposed to the cytoplasm (Reichel and Beachy, 1998), alters the Pd SEL, causes the Pd cytoplasmic annulus to dilate (Wolf et al., 1989), allowing ER to glide through Pd and that this gliding is cytoskeleton mediated. The model claimed that in absence of MP, the ER in Pd (the desmotubule) is stationary, i.e. does not move through the Pd. Based on this model we designed a series of experiments to test the following questions: -Does MP potentiate ER movement through the Pd? - In the presence of MP, is there communication between adjacent cells via ER lumen? -Does MP potentiate the movement of cytoskeletal elements cell to cell? -Is MP required for cell-to-cell movement of ER membranes between cells in sink tissue? -Is the binding in situ of MP to RNA specific to vRNA sequences or is it nonspecific as measured in vitro? And if specific: -What sequences of RNA are involved in binding to MP? And finally, what host proteins are associated with MP during intracellular targeting to various subcellular targets and what if any post-translational modifications occur to MP, other than phosphorylation (Kawakami et al., 1999)? Major conclusions, solutions and achievements. A new quantitative tool was developed to measure the "coefficient of conductivity" of Pd to cytoplasmic soluble proteins. Employing this tool, we measured changes in Pd conductivity in epidermal cells of sink and source leaves of wild-type and transgenic Nicotiana benthamiana (N. benthamiana) plants expressing MPᵀᴹⱽ incubated both in dark and light and at 16 and 25 ᵒC (Liarzi and Epel, 2005 (appendix 1). To test our model we measured the effect of the presence of MP on cell-to-cell spread of a cytoplasmic fluorescent probe, of two ER intrinsic membrane protein-probes and two ER lumen protein-probes fused to GFP. The effect of a mutant virus that is incapable of cell-to-cell spread on the spread of these probes was also determined. Our data shows that MP reduces SEL for cytoplasmic molecules, dilates the desmotubule allowing cell-cell diffusion of proteins via the desmotubule lumen and reduces the rate of spread of the ER membrane probes. Replicase was shown to enhance cell-cell spread. The data are not in support of the proposed model and have led us to propose a new model for virus cell-cell spread: this model proposes that MP, an integral ER membrane protein, forms a MP:vRNAER complex and that this ER-membrane complex diffuses in the lipid milieu of the ER into the desmotubule (the ER within the Pd), and spreads cell to cell by simple diffusion in the ER/desmotubule membrane; the driving force for spread is the chemical potential gradient between an infected cell and contingent non-infected neighbors. Our data also suggests that the virus replicase has a function in altering the Pd conductivity. Transgenic plant lines that express the MP gene of the Cg tobamovirus fused to YFP under the control the ecdysone receptor and methoxyfenocide ligand were generated by the Beachy group and the expression pattern and the timing and targeting patterns were determined. A vector expressing this MPs was also developed for use by the Epel lab . The transgenic lines are being used to identify and isolate host genes that are required for cell-to-cell movement of TMV/tobamoviruses. This line is now being grown and to be employed in proteomic studies which will commence November 2005. T-DNA insertion mutagenesis is being developed to identify and isolate host genes required for cell-to-cell movement of TMV.
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Splitter, Gary, and Menachem Banai. Microarray Analysis of Brucella melitensis Pathogenesis. United States Department of Agriculture, 2006. http://dx.doi.org/10.32747/2006.7709884.bard.
Повний текст джерелаАнотація:
Original Objectives 1. To determine the Brucella genes that lead to chronic macrophage infection. 2. To identify Brucella genes that contribute to infection. 3. To confirm the importance of Brucella genes in macrophages and placental cells by mutational analysis. Background Brucella spp. is a Gram-negative facultative intracellular bacterium that infects ruminants causing abortion or birth of severely debilitated animals. Brucellosis continues in Israel, caused by B. melitensis despite an intensive eradication campaign. Problems with the Rev1 vaccine emphasize the need for a greater understanding of Brucella pathogenesis that could improve vaccine designs. Virulent Brucella has developed a successful strategy for survival in its host and transmission to other hosts. To invade the host, virulent Brucella establishes an intracellular niche within macrophages avoiding macrophage killing, ensuring its long-term survival. Then, to exit the host, Brucella uses placenta where it replicates to high numbers resulting in abortion. Also, Brucella traffics to the mammary gland where it is secreted in milk. Missing from our understanding of brucellosis is the surprisingly lillie basic information detailing the mechanisms that permit bacterial persistence in infected macrophages (chronic infection) and dissemination to other animals from infected placental cells and milk (acute infection). Microarray analysis is a powerful approach to determine global gene expression in bacteria. The close genomic similarities of Brucella species and our recent comparative genomic studies of Brucella species using our B. melitensis microarray, suqqests that the data obtained from studying B. melitensis 16M would enable understanding the pathogenicity of other Brucella organisms, particularly the diverse B. melitensis variants that confound Brucella eradication in Israel. Conclusions Results from our BARD studies have identified previously unknown mechanisms of Brucella melitensis pathogenesis- i.e., response to blue light, quorum sensing, second messenger signaling by cyclic di-GMP, the importance of genomic island 2 for lipopolysaccharide in the outer bacterial membrane, and the role of a TIR domain containing protein that mimics a host intracellular signaling molecule. Each one of these pathogenic mechanisms offers major steps in our understanding of Brucella pathogenesis. Strikingly, our molecular results have correlated well to the pathognomonic profile of the disease. We have shown that infected cattle do not elicit antibodies to the organisms at the onset of infection, in correlation to the stealth pathogenesis shown by a molecular approach. Moreover, our field studies have shown that Brucella exploit this time frame to transmit in nature by synchronizing their life cycle to the gestation cycle of their host succumbing to abortion in the last trimester of pregnancy that spreads massive numbers of organisms in the environment. Knowing the bacterial mechanisms that contribute to the virulence of Brucella in its host has initiated the agricultural opportunities for developing new vaccines and diagnostic assays as well as improving control and eradication campaigns based on herd management and linking diagnosis to the pregnancy status of the animals. Scientific and Agricultural Implications Our BARD funded studies have revealed important Brucella virulence mechanisms of pathogenesis. Our publication in Science has identified a highly novel concept where Brucella utilizes blue light to increase its virulence similar to some plant bacterial pathogens. Further, our studies have revealed bacterial second messengers that regulate virulence, quorum sensing mechanisms permitting bacteria to evaluate their environment, and a genomic island that controls synthesis of its lipopolysaccharide surface. Discussions are ongoing with a vaccine company for application of this genomic island knowledge in a Brucella vaccine by the U.S. lab. Also, our new technology of bioengineering bioluminescent Brucella has resulted in a spin-off application for diagnosis of Brucella infected animals by the Israeli lab by prioritizing bacterial diagnosis over serological diagnosis.