Relevant bibliographies by topics / Invasive phenotypes

Academic literature on the topic 'Invasive phenotypes'

Author: Grafiati
Published: 4 June 2021
Last updated: 20 February 2023

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Journal articles on the topic "Invasive phenotypes"

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Mareel, Marc M., Frans M. Van Roy, and Patrick De Baetselier. "The invasive phenotypes." Cancer and Metastasis Reviews 9, no. 1 (July 1990): 45–62. http://dx.doi.org/10.1007/bf00047588.

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Golmohammadi, Rahim, Mohammad Reza Mohajeri, Alireza Mosavi Jarrahi, Ali Reza Moslem, Akbar Pejhan, and Ali Gohari. "Histopathologic Characteristics of Invasive and Non-invasive Ductal Tumors have Relationship with Different Phenotypes of ER / PR Receptors in Breast Cancer Patients." Asian Pacific Journal of Cancer Biology 6, no. 3 (July 9, 2021): 181–85. http://dx.doi.org/10.31557/apjcb.2021.6.3.181-185.

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Objective: Contradictory reports have been published regarding the expression levels of the hormone receptors of estrogen and progesterone (ER / PR) and theirclinical importance in diagnosis of breast cancer. The aim of this study was to evaluate the relationship between pathological features of invasive and non-invasive ductal tumors by different ER / PR phenotypes. Methods: This descriptive-analytical study was performed on 74 specimens of breast cancer referred to Isfahan Hospitals for diagnosis between 2015 - 2018. After fixation of the specimens in formalin, tissue passage, cross section and H / E staining, the specimens were divided into two groups: non- invasive and Invasive ductal Carcinoma. After removing of mask, expression of different ER / PR phenotypes was performed using primary monoclonal antibody and immunohistochemically methods. Results: From 74 malignant specimens, 61 (82.4%) were in the category of invasive ductal tumors and 13 cases (17.6%) were in the category of non-invasive ductal tumors. Out of 73 patients with positive ER or PR phenotype 47 samples (63.5%) had ER + / PR +phenotypes, 6 samples had (8.1%) ER+ / PR –phenotype, 20 samples (27%) had ER- / PR + phenotype and only one sample (1.4%) had the ER- / PR- phenotype and was in the category of invasive ductal tumors. There was not detected ER- / PR- phenotype expression in non-invasive ductal tumor. Further analysis showed that there were not significant difference between ER / PR phenotype and tumor stage (p =0.36) or with tumor Grade (P=0.38), high age of menopause or post menopause (P> 0.05). Conclusion: Our data shows that expression of ER- / PR- phenotype only was detected in invasive ductal tumor. It is thought that the tumor type maybe affects the expression of different types of ER / PR hormone receptor phenotypes in breast cancer patients.
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Mukhopadhyay, Utpal K., Patrick Mooney, Lilly Jia, Robert Eves, Leda Raptis, and Alan S. Mak. "Doubles Game: Src-Stat3 versus p53-PTEN in Cellular Migration and Invasion." Molecular and Cellular Biology 30, no. 21 (August 23, 2010): 4980–95. http://dx.doi.org/10.1128/mcb.00004-10.

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ABSTRACT We have recently shown that Src induces the formation of podosomes and cell invasion by suppressing endogenous p53, while enhanced p53 strongly represses the Src-induced invasive phenotype. However, the mechanism by which Src and p53 play antagonistic roles in cell invasion is unknown. Here we show that the Stat3 oncogene is a required downstream effector of Src in inducing podosome structures and related invasive phenotypes. Stat3 promotes Src phenotypes through the suppression of p53 and the p53-inducible protein caldesmon, a known podosome antagonist. In contrast, enhanced p53 attenuates Stat3 function and Src-induced podosome formation by upregulating the tumor suppressor PTEN. PTEN, through the inactivation of Src/Stat3 function, also stabilizes the podosome-antagonizing p53/caldesmon axis, thereby further enhancing the anti-invasive potential of the cell. Furthermore, the protein phosphatase activity of PTEN plays a major role in the negative regulation of the Src/Stat3 pathway and represses podosome formation. Our data suggest that cellular invasiveness is dependent on the balance between two opposing forces: the proinvasive oncogenes Src-Stat3 and the anti-invasive tumor suppressors p53-PTEN.
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Zhang, Luna, Anqun Chen, Yanjiao Li, Duohui Li, Shiping Cheng, Liping Cheng, and Yinzhan Liu. "Differences in Phenotypic Plasticity between Invasive and Native Plants Responding to Three Environmental Factors." Life 12, no. 12 (November 25, 2022): 1970. http://dx.doi.org/10.3390/life12121970.

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The phenotypic plasticity hypothesis suggests that exotic plants may have greater phenotypic plasticity than native plants. However, whether phenotypic changes vary according to different environmental factors has not been well studied. We conducted a multi-species greenhouse experiment to study the responses of six different phenotypic traits, namely height, leaf number, specific leaf area, total biomass, root mass fraction, and leaf mass fraction, of native and invasive species to nutrients, water, and light. Each treatment was divided into two levels: high and low. In the nutrient addition experiment, only the leaf mass fraction and root mass fraction of the plants supported the phenotypic plasticity hypothesis. Then, none of the six traits supported the phenotypic plasticity hypothesis in the water or light treatment experiments. The results show that, for different environmental factors and phenotypes, the phenotypic plasticity hypothesis of plant invasion is inconsistent. When using the phenotypic plasticity hypothesis to explain plant invasion, variations in environmental factors and phenotypes should be considered.
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Pershing, Nicole L., Aurélie Kapusta, Shannon Nielsen, Hillary Crandall, E. Kent Korgenski, Carrie L. Byington, Krow Ampofo, and Anne J. Blaschke. "#64: An odyssey Beyond the Capsule: Genetic Determinants of Pediatric Invasive Streptococcus pneumoniae Empyema." Journal of the Pediatric Infectious Diseases Society 10, Supplement_1 (March 1, 2021): S7. http://dx.doi.org/10.1093/jpids/piaa170.021.

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Abstract Background Streptococcus pneumoniae is among the most common causes of invasive bacterial infections in children, including pneumonia, bacteremia, and meningitis. Over 90 different serotypes (ST) of pneumococcus exist, with enrichment of some ST within specific invasive phenotypes. Other than capsular genes, molecular determinants of particular invasive phenotypes remain largely unknown. Although vaccination targeting especially invasive ST capsular antigens has successfully decreased the incidence of invasive pneumococcal disease (IPD), new ST have emerged, suggesting methods to target other aspects of pneumococcal invasiveness are needed. Methods Pneumococcal isolates from IPD were collected from children presenting to Primary Children’s Hospital from 1996–2018. All viable isolates underwent next-generation sequencing (Illumina), quality control filtering for contamination and low coverage, de novo genome assembly with SPADES, and annotation with PROKKA. Clinical phenotypes were manually validated with physician chart review. Isolates were serotyped via Quelling and in silico using SeroBA. ROARY was used for pan-genome assembly, and SCOARY for microbial genome-wide association studies. RAxML was used for phylogenetic analysis. Results A total of 354 viable pneumococcal isolates were available for genomic analysis including a spectrum of invasive phenotypes: pneumonia (n = 138, of which 54 were complicated by empyema), CNS infection (n = 50), SSTI/bone infections (n = 42), and isolated bacteremia (n = 68). Thirteen samples were censored for poor coverage or genetic contamination. Invasive isolates spanned 37 capsular ST. The pneumococcal pan-genome comprised 6462 genes, of which only 23% were shared by at least 99% of samples. Phylogenetic relatedness resulted in clustering of some ST (e.g., ST1, ST3), whereas others (eg ST19A) were more broadly distributed. Empyema and meningitis phenotypes were distributed across the phylogenetic tree, but enriched in distinct clusters that crossed ST clusters. Genes involved in empyemagenic pneumococcal capsule production, and those implicated in sensing of preferred sugars or non-preferred sugar metabolism were statistically correlated with the empyema phenotype. Conclusion There is marked genetic diversity among invasive pneumococcal isolates, potentially contributing to the variability of disease phenotypes observed. Clustering of invasive phenotypes across ST suggests a genetic signature for invasive phenotypes other than capsule genes alone, further supported by enrichment of specific genes associated with alternative sugar metabolism in empyema isolates. Critical determinants of invasive phenotypes will inform future efforts at disease prevention and treatment.
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Bultemeier, Brett W., Mike D. Netherland, Jason A. Ferrell, and William T. Haller. "Differential Herbicide Response among Three Phenotypes ofCabomba caroliniana." Invasive Plant Science and Management 2, no. 4 (October 2009): 352–59. http://dx.doi.org/10.1614/ipsm-09-035.1.

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AbstractCabomba is a submersed aquatic plant native to the southeastern United States that is commonly sold worldwide through the aquarium trade. While infrequently managed in its native range, cabomba has recently been reported as invasive and tolerant to management efforts in the northern areas of the United States and in other countries. Invasive populations of cabomba are characterized by a phenotype that is bright green. In contrast, cabomba native to the southeastern United States is characterized by a red phenotype, while plants sold through the aquarium trade have intermediate characteristics of both the green and red phenotypes. The response of the three cabomba phenotypes to selected herbicides was evaluated by measuring photosynthetic response over the course of a static 144-hr exposure. Plants were exposed to the maximum recommended use-rates of 2,4-D, carfentrazone, copper, diquat, endothall (amine and dipotasium salt formulation), flumioxazin, quinclorac, triclopyr, and a combination of diquat and copper. A submersed plant species known to be sensitive to each of these herbicides was also included to compare photosynthetic response of the cabomba to a susceptible plant. The photosynthetic response of the red and green phenotypes differed following exposure to carfentrazone, diquat, 2,4-D, triclopyr, and flumioxazin. Diquat, diquat plus copper, endothall (amine salt), and flumioxazin were the only products that resulted in a greater than 50% reduction of photosynthesis in all three phenotypes of cabomba. A second experiment was conducted where all three phenotypes of cabomba were exposed to these four herbicides for 24 hr, and photosynthesis was evaluated. Following the 24-hr exposure, results further documented distinct response differences between the green and red phenotypes, with the green phenotype demonstrating a reduced sensitivity to the herbicides evaluated. Results demonstrate clear phenotypic differences in response to herbicide treatments and lack of susceptibility of cabomba to most herbicides.
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Gajic, Ina, Natasa Opavski, Vera Mijac, and L. Ranin. "Macrolide-resistant phenotypes of invasive streptococcus pneumoniae isolates in Serbia." Archives of Biological Sciences 64, no. 4 (2012): 1377–82. http://dx.doi.org/10.2298/abs1204377g.

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Macrolide resistance in Streptococcus pneumoniae has emerged as an important worldwide problem over the past decade. The aim of this study was to investigate macrolide-resistant phenotypes and the antimicrobial susceptibility patterns of invasive pneumococci in Serbia. A total of 68 invasive pneumococcal strains, collected from 2009 to 2011, were sent from regional laboratories to the National Reference Laboratory. Susceptibility testing was performed using the VITEK2 system and phenotypes were determined by triple-test. Overall penicillin and erythromycin nonsusceptibility rates were 26% and 43%, respectively. Resistance rates were higher in children than in adults. Co-resistance to penicillin and erythromycin was detected in 18% strains. Resistance rates to the third generation of cephalosporins, TMP-SXT and tetracycline were 16%, 37% and 29%, respectively. All isolates were fully susceptible to vancomycin, linezolid, fluoroquinolones, telithromycin and rifampicin. Twenty-two isolates (79%) an expressed macrolide-lincosamide-streptogramin B (MLSB) resistance phenotype and M phenotype was found in 21% of macrolide resistant strains.
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ANDERSEN, J., L. BERTHELSEN, B. BECH JENSEN, and I. LIND. "Dynamics of the meningococcal carrier state and characteristics of the carrier strains: a longitudinal study within three cohorts of military recruits." Epidemiology and Infection 121, no. 1 (August 1998): 85–94. http://dx.doi.org/10.1017/s0950268898008930.

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Three cohorts of Danish male military recruits (n=1069) were studied for pharyngeal meningococcal carriage during 3 months at different seasons: 39–47% of entrants were meningococcal carriers and the carriage rate remained constant over time and season. However, individual changes in the carrier state occurred frequently, and after 3 months 34% had changed carrier state on one or more occasions. Initially, a loss of carriage predominated; on the other hand almost 20% of non-carriers had acquisition of meningococci within the first month. The serological phenotypes of the 670 carrier strains were compared with those of 261 invasive strains recovered concurrently from patients with meningococcal disease country-wide. Both carrier strains and invasive strains were phenotypically heterogeneous. Almost 60% of the invasive strains belonged to three phenotypes: B[ratio ]15[ratio ]P1.7, 16, C[ratio ]2a[ratio ]P1.2, 5 and C[ratio ]2b[ratio ]P1.2, 5. In contrast, these phenotypes only amounted to 3·2% of the carrier strains, among which no phenotype was found with a prevalence above 4·9%. However, 30% of the carrier strains had serological phenotypes identical to those of 80% of the invasive strains. Our results indicated that the transmission rate of potential pathogenic carrier strains did not differ from that of other carrier strains.
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Gajić, Ina, Miloš Marković, Dušan Kekić, Sunčica Popović, Vera Mijač, Lazar Ranin, and Nataša Opavski. "Serotypes and antimicrobial susceptibility of invasive 'Streptococcus pneumoniae' isolated in Serbia in 2012-2013." Medicinska istrazivanja 50, no. 2 (2016): 49–53. http://dx.doi.org/10.5937/medist1602049g.

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The aim of this study was to: determine susceptibility patterns of invasive Streptococcus pneumoniae to antimicrobial agents, evaluate macrolide resistance phenotypes and genotypes and identify capsular serotypes among invasive isolates of S. pneumoniae circulating in Serbia. The total of 85 invasive pneumococcal strains, collected during 2012 and 2013, were sent from regional laboratories to the National Reference Laboratory. Susceptibility testing was performed by disk diffusion and E test, while phenotypes and genotypes of macrolide resistant strains were determined by double-test and PCR, respectively. Serotyping was performed by Quelling reaction. The overall penicillin and erythromycin non-susceptibility rates were 14.12% and 28.23%, respectively. Resistance rates were significantly higher in children than in adults and (p<0,01). Co-resistance to penicillin and erythromycin was detected in 7.06% strains. Resistance rates to tetracycline and chloramphenicol were 29.41% and 15.29%, respectively. The rate of multi resistance was 27.06%. cMLS phenotype was detected in 62.5% of all macrolide resistant isolates, while 37.5% expressed M phenotype. All 15 isolates with cMLS phenotype harbored ermB gene and all M isolates harbored mefA. The most common resistant serotypes were 3, 9A and 23F. This study revealed that penicillin and macrolide resistance among invasive pneumococcal isolates is high. Obtained results emphasize the need for continuous monitoring of invasive pneumococcal disease in Serbia.
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Nicotra, Adrienne B., and Amy Davidson. "Adaptive phenotypic plasticity and plant water use." Functional Plant Biology 37, no. 2 (2010): 117. http://dx.doi.org/10.1071/fp09139.

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The emergence of new techniques in plant science, including molecular and phenomic tools, presents a novel opportunity to re-evaluate the way we examine the phenotype. Our increasing capacity for phenotyping means that not only can we consider increasing numbers of species or varieties, but also that we can effectively quantify the phenotypes of these different genotypes under a range of environmental conditions. The phenotypic plasticity of a given genotype, or the range of phenotypes, that can be expressed dependent upon environment becomes something we can feasibly assess. Of particular importance is phenotypic variation that increases fitness or survival – adaptive phenotypic plasticity. Here, we examine the case of adaptive phenotypic plasticity in plant water use traits and consider how taking an ecological and evolutionary perspective on plasticity in these traits might have relevance for agriculture, horticulture and the management of native and invasive plant species in an era of rapid climate change.
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Dissertations / Theses on the topic "Invasive phenotypes"

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Bloomfield, Kelly Louise, and n/a. "Investigation of the Role of Thioredoxin in the Invasive Phenotype and its Interaction with the Transcription Factor Sp1." Griffith University. School of Biomolecular and Biomedical Science, 2003. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20031021.120018.

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Thioredoxin is a small ubiquitous oxido-reductase found in all species. The highly conserved active site, which facilitates thioredoxins redox activity, contains two redox active cysteine residues. Thioredoxin has numerous protein substrates to which it donates H+ ions and it can also function as a free radical scavenger. Through these activities thioredoxin is able to influence the redox state of not only its protein targets, but also the entire cellular environment. Thioredoxin has been implicated in many biological functions, and one mechanism by which it influences these functions is through interactions with a number of transcription factors including NF-kappa-B and p53. Thioredoxin also has numerous extracellular biological roles. It has been shown that thioredoxin is actively secreted from a number of normal and transformed cell lines including fibroblasts and activated B and T cells. This study investigates the role of thioredoxin in embryonic implantation and cancer cell metastasis, two physiological functions which rely on the same basic processes. Thioredoxin expression has previously been shown to be increased in many cancers. However it has not yet been established whether this increase is a causative or a side effect of the cancerous phenotype. Similarly thioredoxin expression has previously been shown to be increased during different phases of the oestrus cycle and pregnancy. This thesis describes the role of thioredoxin in embryonic implantation using a marmoset model. A thioredoxin cDNA was isolated and subsequently sequenced. Preliminary antibody experiments indicated that the anti human thioredoxin monoclonal antibodies available in our laboratory would recognise marmoset thioredoxin. Subsequently immunocytochemistry using anti human thioredoxin antibodies was carried out on sectioned marmoset uterus and embryonic tissue. The results indicated that thioredoxin is expressed by cells at the embryonic-maternal interface of early implantation sites. Further studies demonstrated that thioredoxin is also expressed and secreted by cultured blastocysts in vitro. This thesis also describes the role of thioredoxin in cancer cell metastasis. Results of this study indicate that thioredoxin is actively involved in facilitating the invasive phenotype of breast cancer cells. The two cell lines utilised were MCF-7, a well differentiated, relatively non-invasive breast cancer cell line; and MDA-MB-231, a poorly differentiated, highly invasive breast cancer cell line. The cell lines were transfected with thioredoxin sense, antisense and 1SS (encodes thioredoxin with both active cysteine residues mutated to serine residues and is thus redox inactive) constructs. The results demonstrate that when endogenous thioredoxin levels are increased, i.e. transfected with a sense thioredoxin construct, the invasive breast cancer cell line MDA-MB-231 becomes more invasive, conversely when endogenous levels are decreased, i.e. transfected with antisense or 1SS constructs, the invasive capacity of these cells decreases. However, when the endogenous level of thioredoxin was manipulated in the relatively non-invasive cell line MCF-7 very little effect was observed. Results also indicate that thioredoxin has the ability to act as a chemoattractant for actively invading breast cancer cells. Both of these functions appear to be dependent on thioredoxin's redox activity. Additional studies described in this thesis have shown that thioredoxin is involved in the regulation of Sp1 in vitro. Sp1 is a transcription factor known to regulate the transcription of a number of genes whose products are intimately involved in the invasive phenotype. The results in this study suggest that Sp1 DNA binding is regulated by thioredoxin such that when reduced by the enzyme its binding to DNA is facilitated. Results also indicate that Sp1 may regulate the transcription of thioredoxin by binding to Sp1 sites within the thioredoxin promoter.
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Bloomfield, Kelly Louise. "Investigation of the Role of Thioredoxin in the Invasive Phenotype and its Interaction with the Transcription Factor Sp1." Thesis, Griffith University, 2003. http://hdl.handle.net/10072/366170.

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Thioredoxin is a small ubiquitous oxido-reductase found in all species. The highly conserved active site, which facilitates thioredoxins redox activity, contains two redox active cysteine residues. Thioredoxin has numerous protein substrates to which it donates H+ ions and it can also function as a free radical scavenger. Through these activities thioredoxin is able to influence the redox state of not only its protein targets, but also the entire cellular environment. Thioredoxin has been implicated in many biological functions, and one mechanism by which it influences these functions is through interactions with a number of transcription factors including NF-_B and p53. Thioredoxin also has numerous extracellular biological roles. It has been shown that thioredoxin is actively secreted from a number of normal and transformed cell lines including fibroblasts and activated B and T cells. This study investigates the role of thioredoxin in embryonic implantation and cancer cell metastasis, two physiological functions which rely on the same basic processes. Thioredoxin expression has previously been shown to be increased in many cancers. However it has not yet been established whether this increase is a causative or a side effect of the cancerous phenotype. Similarly thioredoxin expression has previously been shown to be increased during different phases of the oestrus cycle and pregnancy. This thesis describes the role of thioredoxin in embryonic implantation using a marmoset model. A thioredoxin cDNA was isolated and subsequently sequenced. Preliminary antibody experiments indicated that the anti human thioredoxin monoclonal antibodies available in our laboratory would recognise marmoset thioredoxin. Subsequently immunocytochemistry using anti human thioredoxin antibodies was carried out on sectioned marmoset uterus and embryonic tissue. The results indicated that thioredoxin is expressed by cells at the embryonic-maternal interface of early implantation sites. Further studies demonstrated that thioredoxin is also expressed and secreted by cultured blastocysts in vitro. This thesis also describes the role of thioredoxin in cancer cell metastasis. Results of this study indicate that thioredoxin is actively involved in facilitating the invasive phenotype of breast cancer cells. The two cell lines utilised were MCF-7, a well differentiated, relatively non-invasive breast cancer cell line; and MDA-MB-231, a poorly differentiated, highly invasive breast cancer cell line. The cell lines were transfected with thioredoxin sense, antisense and 1SS (encodes thioredoxin with both active cysteine residues mutated to serine residues and is thus redox inactive) constructs. The results demonstrate that when endogenous thioredoxin levels are increased, i.e. transfected with a sense thioredoxin construct, the invasive breast cancer cell line MDA-MB-231 becomes more invasive, conversely when endogenous levels are decreased, i.e. transfected with antisense or 1SS constructs, the invasive capacity of these cells decreases. However, when the endogenous level of thioredoxin was manipulated in the relatively non-invasive cell line MCF-7 very little effect was observed. Results also indicate that thioredoxin has the ability to act as a chemoattractant for actively invading breast cancer cells. Both of these functions appear to be dependent on thioredoxin's redox activity. Additional studies described in this thesis have shown that thioredoxin is involved in the regulation of Sp1 in vitro. Sp1 is a transcription factor known to regulate the transcription of a number of genes whose products are intimately involved in the invasive phenotype. The results in this study suggest that Sp1 DNA binding is regulated by thioredoxin such that when reduced by the enzyme its binding to DNA is facilitated. Results also indicate that Sp1 may regulate the transcription of thioredoxin by binding to Sp1 sites within the thioredoxin promoter.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Biomolecular and Biomedical Sciences
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Kelley, Amanda. "The Effect of Temperature on Phenotypes of the Invasive European Green Crab: Physiologic Mechanisms that Facilitate Invasion Success." PDXScholar, 2013. https://pdxscholar.library.pdx.edu/open_access_etds/1004.

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Invasion physiology is an emerging field that endeavors to understand the influence of physiological traits on the establishment of non-native species in novel environments. The invasive European green crab,Carcinus maenas, is one of the world's most successful aquatic invaders, and is currently distributed across temperate marine ecosystems globally. The work presented here explored the thermal physiology of this species, and has highlighted several physiological traits that have likely influenced establishment success. Intraspecific comparisons of crabs sampled from the northern and southern edges of their recipient, or invaded range on the west coast of North America have identified both organismal and cellular physiological difference with respect to upper and lower thermal tolerances. Crabs sampled from British Columbia, Canada (BC) had a significantly lower mean upper thermal tolerance threshold and heat shock protein synthesis, Hsp70, compared to their warm acclimated conspecifics sampled from California (CA). These differential physiologic responses may be rooted in the disparate natural thermal habitats that each population occupies within their respective environments. The ability of this species to extend its current range limits was also investigated. Range expansion to the south has been limited, and is likely restricted by this species lack of adaptation to warmer temperatures. Because range expansion has been chiefly northward, characterizing this species' response to cold stress can identify whether colder temperatures poleward may limit further range expansion. Cold tolerance capacity was determined in the laboratory, and crabs sampled from Vancouver Island, British Columbia were able to withstand the over-wintering thermal regime that occurs in Sitka, Alaska, a site that is currently beyond the range limits of this species. Furthermore, intraspecific assessments found that the cold acclimated BC population exposed to cold shock significantly down regulated protein levels of cyclin D1, cell cycle modulator. Distinct differences in carapace width (CW) were detected along the thermal gradient present in the green crabs' range. This variation in body size was utilized to the test the temperature size rule hypothesis for ectotherms. Simply stated, the temperature size rule is the tendency for ectotherms to develop slower but mature to a larger body sizes at cooler temperatures. The results supported this hypothesis as crabs sampled from the warm portion of the range were found to be smaller than crabs sampled from the colder portion of the range. This pattern was detected along the native range as well. Differences in body size have the potential to influence the scope of invasion; larger individuals are generally more fecund and longer lived, which can increase both the intensity and frequency of larval dispersal that could further propel range expansion. The physiologic properties that the green crab possesses which may influence invasion success were examined using peer-reviewed literature with the aim of determining if these physiological traits confer invasion success across taxa. This analysis tested four hypotheses: 1) Broad geographic temperature tolerances (thermal width) confer a higher upper thermal tolerance threshold when comparing invasive and native species. 2) The upper thermal extreme experienced in nature is correlated with upper thermal tolerance threshold. 3) Protein chaperone expression, a cellular mechanism underlying thermal tolerance threshold, is greater in invasive organisms than in native ones. 4) Acclimation to higher temperatures can promote a greater range of thermal tolerance for invasives compared to natives. These preliminary results generally support the four stated hypotheses, and provide a solid foundation for further studies to explore and identify physiologic traits that facilitate invasion success. Overall, these studies investigated the thermal physiology ofCarcinus maenasfrom an invasive metapopulation and have brought about significant advances in our understanding of what physiologic traits correlate to invasion success in this species. In addition, the data presented here can aid resource managers in identifying habitats, based on thermal tolerance measurements that fit the criteria for invasion. Understanding how invasive organisms vary with respect to thermal tolerance can aid our understanding the patterns and processes of species invasions.
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Dooley, Nora P. "The proliferative and invasive phenotypes of malignant gliomas, regulation by protein kinase C (PKC)." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape10/PQDD_0025/NQ50149.pdf.

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Dooley, Nora P. "The proliferative & invasive phenotypes of malignant gliomas : regulation by protein kinase C (PKC)." Thesis, McGill University, 1998. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=35694.

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The malignant phenotype, by definition, is composed of two facets, consisting of the tumor's ability to proliferate as well as its ability to invade the surrounding normal tissue. We propose that in malignant gliomas the protein kinase C (PKC) family of enzymes, which has been shown to be overexpressed in these tumours, plays a pivotal role in both their proliferative and invasive capacity. In the first genes of experiments where the expression of the alpha isoform of PKC was significantly decreased following antisense oligonucleotide treatment, we were able to report the novel finding that this inhibition not only inhibits glioma proliferation in a dose-dependent manner but that this inhibition of growth was the consequence of programmed cell death (1). In the second focus of this thesis, we addressed the postulate that the high PKC activity present in glioblastoma cells may also contribute to the invasive nature of this tumor by modulating the expression of proteolytic enzymes, the matrix metalloproteinases, (MMPs). In contrast to previous studies implicating MMP-9, our data demonstrated that MMP-2 was the metalloproteinase most closely associated with glioma invasion. Furthermore, we were also able to report that the regulation of MMP-2, and thus glioma invasion, could be modulated by PKC (2). In summary, this work presents evidence to support a role for PKC in both the proliferative and invasive phenotypes which characterize malignant gliomas. The translational nature of this research is readily illustrated by the emergence of clinical trials in which PKC and MMPs constitute the principal chemotherapeutic targets.
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Crespo, Lessmann Astrid. "Identificación del fenotipo inflamatorio del asma mediante métodos no invasivos." Doctoral thesis, Universitat Autònoma de Barcelona, 2016. http://hdl.handle.net/10803/394036.

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La tesis doctoral que presento es el resultado del trabajo realizado en el Servicio de Neumología del Hospital de la Santa Creu i Sant Pau de Barcelona y del Institut de Recerca Biomèdica de Sant Pau (IIB Sant Pau), siguiendo las normativas de la Universitat Autònoma de Barcelona para su presentación como compendio de publicaciones. El estudio de la inflamación bronquial en el asma, se ha convertido en una herramienta valiosa para el diagnóstico, control y predicción de respuestas terapéuticas. En los últimos años ha aumentado el interés en los métodos que permitan evaluar de una forma no invasiva la inflamación de la vía aérea. Entre los métodos no invasivos descritos usados en la práctica clínica para evaluar la inflamación de la vía aérea figuran: el recuento de células inflamatorias en el esputo inducido y la fracción exhalada de óxido nítrico (FeNO). La temperatura del aire exhalado y la nariz electrónica se plantean como nuevas herramientas de medición de la inflamación bronquial y del control del asma. La línea de investigación desarrollada tuvo como objetivo fundamental mejorar los conocimientos sobre los fenotipos inflamatorios del asma a través de métodos no invasivos. Está basada en tres proyectos. El primero, es un proyecto clínico cuyos resultados muestran que existen un alto porcentaje de pacientes con disociación entre los resultados de la FeNO y de los eosinófilos en el esputo inducido y que cursan con características clínicas e inflamatorias diferenciales. Los otros dos proyectos permiten conocer la utilidad en el asma de dos nuevos métodos no invasivos como lo son, la temperatura del aire exhalado (TAE) y el reconocimiento de patrones de compuestos orgánicos volátiles mediante la “nariz electrónica”. Estos trabajos aportaron como resultados principales que en el caso de la TAE, no parece que éste sea un método que proporcione una información clínica útil puesto que no se encontró ninguna correlación entre este método y el grado de control del asma, la gravedad de la enfermedad, la obstrucción bronquial, o la inflamación bronquial. Por otro lado, los resultados del tercer estudio sí que fueron alentadores, puesto que de manera significativa, el uso de la nariz electrónica en un entorno clínico habitual permitió discriminar con fiabilidad los diferentes fenotipos inflamatorios bronquiales en pacientes con asma. Así pues, los resultados de esta tesis sirven como fundamento del estudio y aplicabilidad de diversos métodos no invasivos en el asma.
This doctoral thesis is the result of the work done in the Service of Respiratory Medicine of the Hospital de la Santa Creu i Sant Pau in Barcelona and the Institute of Biomedical Research of Sant Pau (IIB Sant Pau), following the regulations of the Universitat Autònoma de Barcelona. The study of bronchial inflammation in asthma has become a valuable tool for its diagnosis, monitoring and prediction of therapeutic responses. In recent years, there has been an increased interest in methods of noninvasive evaluation of the airway inflammation. The described non-invasive methods used in the clinical practice to assess airway inflammation include the inflammatory cell counts in induced sputum and the fractional exhaled nitric oxide (FeNO). The exhaled breath temperature and the electronic nose device are considered to be new tools for measuring airway inflammation and control of asthma. The line of the developed research had as a main goal to improve the knowledge of inflammatory phenotypes of asthma through non-invasive methods. It is based on three projects. The first (1) is a clinical project that shows a high percentage of patients with dissociation between the results of the FeNO and eosinophils in induced sputum, presenting clinical and inflammatory differential characteristics. The other two projects provide an insight into the utility of two non-invasive diagnostic methods: 2) the exhaled breath temperature (EBT) and 3) the recognition of the patterns formed by organic volatile compounds using the electronic nose device. The second study does not support the usefulness of the EBT plateau, because no correlation was found between EBT and control of asthma, severity of disease, bronchial obstruction or bronchial inflammation. Furthermore, the results of the third study were encouraging since the using of an e-nose device in a regular clinical setting can reliably discriminate different inflammatory asthma phenotypes among patients with persistent asthma. Thus, the results of this thesis disclosed the applicability of various non-invasive methods performed in routine clinical practice.
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Rice, Kelly C. "Regulation of the colonization and invasive phenotypes by protease activity in Staphylococcus aureus, analysis of fibronectin-binding protein (FNBP) and V8 protease as paradigms of this concept." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/NQ63692.pdf.

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Okoro, Chinyere Kyna. "Invasive Salmonella typhimurium : linking phenotype to genotype." Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.607714.

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Thorn, Christopher Charles. "The molecular characteristics of the invasive phenotype in colorectal cancer." Thesis, University of Leeds, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.493284.

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The infiltrative growth pattern in colorectal cancer has been demonstrated to confer a poor prognosis particularly in early stage disease. The phenotype demonstrates histological features of aggression and with reference to the contrasting pushing phenotype provides an in vivo model for invasive behaviour which has hitherto not been exploited in the context of molecular biology.
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Frevola, Danielle Marie Frevola. "Can Surrounding Land Use Promote Phenotypic Plasticity and Invasion Success in Wetland Plants Through Variable Nutrient Regimes?" The Ohio State University, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=osu1531230832080876.

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Books on the topic "Invasive phenotypes"

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Rice, Kelly C. regulation of the colonization and invasive phenotypes by protease activity in staphylococcus aureus: Analysis of fibronectin-binding protein (FNBP) and V8 protease as paradigms of this concept. 2001.

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Ritchie, James, Darren Green, Constantina Chrysochou, and Philip A. Kalra. Renal artery stenosis. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0215.

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In fibromuscular disease (FMD), renal artery occlusion seems to be rare. Balloon angioplasty appears moderately successful in the medium term in controlling hypertension, at least in younger patients. In more complicated circumstances, medical therapy may be preferred. Similar approaches have been used in Takayasu disease but with less information about lasting outcomes.In atherosclerotic renal disease, the risk of renal artery occlusion and loss of renal function seems higher, but so are the complications of invasive management. Randomized clinical studies have not shown better blood pressure control or renal outcomes between medical therapy and percutaneous revascularization. As a consequence, modern management of atherosclerotic renovascular disease is primarily pharmacological, with interventional techniques reserved for selected presentations such as rapidly declining therapy, acute occlusion, or characteristic ‘flash’ pulmonary oedema.Whilst this approach is widely accepted, long-term outcome data are scant and there is ongoing research interest into specific disease phenotypes, refined interventional techniques, and novel treatment strategies aimed at preserving the renal microcirculation.
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McGrath, Joanne C. A comparison of phenotypic plasticity in lythrum salicaria l., an invasive hydrophyte, and lythrum alatum pursh., its noninvasive congener: A thesis in Biology. 1995.

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Singhi, Pratibha, Karthi Nallasamy, and Sunit Singhi. Fungal Infections of the Central Nervous System. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0162.

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Fungal infections of the central nervous system are important because of their increasing incidence and the growing population of at-risk individuals. CNS spread is usually hematogenous but rarely can be due to direct invasion from adjacent structures. Morphology of the infecting fungus may predict the regions affected and the lesion phenotype. Meningitis and mass lesions are the most frequent. This chapter reviews the current understanding of the neuropathogenesis of fungal infections with mention of histopathological and imaging correlations. Important aspects of management are also discussed. Diagnosis requires strong clinical suspicion. Treatment is often multimodal with prolonged drug therapy, surgery, and supportive care.
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Geri, Guillaume, and Jean-Paul Mira. Host–pathogen interactions in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0306.

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Infection by a pathogenic micro-organism triggers a coordinated activation of both innate and adaptive immune responses. The innate immune response quickly triggers an antimicrobial response that will initiate development of a pathogen-specific, long-lasting adaptive immune response. Accurate recognition of microbial-associated molecular patterns by pattern-recognition receptors (PRRs) is the cornerstone of this immediate response. Most studied PRRs are Toll-like receptors (TLRs) and their kinase signalling cascades that activate nuclear transcription factors, and induce gene expression and cytokine production. Deficiencies or genetic variability in these different signalling pathways may lead to recurrent pyogenic infections and severe invasive diseases. After initial contact between the host and pathogen, numerous factors mediate the inflammatory response, as pro-inflammatory cytokines and chemokines. Apart from host genetic variability, pathogen diversity also influences the phenotypic features of various infectious diseases. Genomic analysis may assist in the development of targeted therapies or new therapeutic strategies based on both patient and microorganism genotype.
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Machado, Pedro M. Inclusion body myositis. Edited by Hector Chinoy and Robert Cooper. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198754121.003.0011.

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Sporadic inclusion body myositis (IBM) is an acquired muscle disorder associated with ageing, for which there is no effective treatment. It is characterized by a typical early clinical phenotype with (often asymmetric) weakness of the knee extensors and finger flexors, potential involvement of pharyngeal and upper-oesophageal muscles (which may contribute to malnutrition and aspiration), and progressive and slow deterioration, which may lead to severe disability and loss of quality of life. Muscle biopsy shows chronic myopathic features, lymphocytic infiltration with invasion of non-necrotic fibres, rimmed vacuoles, mitochondrial changes, and pathological accumulation of proteins in the muscle tissue. It remains uncertain whether IBM is primarily an immune-mediated inflammatory myopathy or a degenerative myopathy with an associated inflammatory component. This chapter will describe the clinical features, natural history, investigations, current pathogenic concepts, outcome measures, and therapeutic approaches in IBM. Despite recent clues, in many respects IBM remains an unsolved mystery.
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Bass, Cristina, Barbara Bauce, and Gaetano Thiene. Arrhythmogenic right ventricular cardiomyopathy: diagnosis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0360.

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Arrhythmogenic cardiomyopathy is a heart muscle disease clinically characterized by life-threatening ventricular arrhythmias and pathologically by an acquired and progressive dystrophy of the ventricular myocardium with fibrofatty replacement. The clinical manifestations of arrhythmogenic cardiomyopathy vary according to the ‘phenotypic’ stage of the underlying disease process. Since there is no ‘gold standard’ to reach the diagnosis of arrhythmogenic cardiomyopathy, multiple categories of diagnostic information have been combined. Different diagnostic categories include right ventricular morphofunctional abnormalities (by echocardiography and/or angiography and/or cardiovascular magnetic resonance imaging), histopathological features on endomyocardial biopsy, electrocardiogram, arrhythmias, and family history, including genetics. The diagnostic criteria were revised in 2010 to improve diagnostic sensitivity, but with the important prerequisite of maintaining diagnostic specificity. Quantitative parameters have been put forward and abnormalities are defined based on the comparison with normal subject data. A definite diagnosis of arrhythmogenic cardiomyopathy is achieved when two major, or one major and two minor, or four minor criteria from different categories are met. The main differential diagnoses are idiopathic right ventricular outflow tract tachycardia, myocarditis, sarcoidosis, dilated cardiomyopathy, right ventricular infarction, congenital heart diseases with right ventricular overload, and athlete’s heart. Among diagnostic tools, contrast-enhanced cardiovascular magnetic resonance is playing a major role in detecting subepicardial-midmural left ventricular free wall involvement, even preceding morphofunctional abnormalities. Moreover, electroanatomical mapping is an invasive tool able to detect early right ventricular free wall involvement in terms of low-voltage areas. Both techniques are increasingly used in the diagnostic work-up although are not yet part of diagnostic criteria.
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Book chapters on the topic "Invasive phenotypes"

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DeLosh, René M., and Robert H. Shoemaker. "Evaluation of Real-Time In Vitro Invasive Phenotypes." In Methods in Molecular Biology, 165–80. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1350-4_12.

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Thorn, Christopher C., Deborah Williams, and Thomas C. Freeman. "Oligonucleotide Microarray Expression Profiling of Contrasting Invasive Phenotypes in Colorectal Cancer." In Methods in Molecular Biology, 203–21. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-163-5_17.

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Vinchure, Omkar, and Ritu Kulshreshtha. "MicroRNA Regulation of Invasive Phenotype of Glioblastoma." In MicroRNA, 173–200. Boca Raton : Taylor & Francis, 2018. | “A CRC title, part of the Taylor & Francis imprint, a member of the Taylor & Francis Group, the academic division of T&F Informa plc.”: CRC Press, 2018. http://dx.doi.org/10.1201/b22195-9.

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Lande, Russell. "EVOLUTION OF PHENOTYPIC PLASTICITY IN COLONIZING SPECIES." In Invasion Genetics, 165–74. Chichester, UK: John Wiley & Sons, Ltd, 2016. http://dx.doi.org/10.1002/9781119072799.ch9.

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MacMillan, Connor D., Ann F. Chambers, and Alan B. Tuck. "Progression of Early Breast Cancer to an Invasive Phenotype." In Breast Cancer Metastasis and Drug Resistance, 143–59. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-5647-6_8.

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Blows, Mark W., and Katrina McGuigan. "THE DISTRIBUTION OF GENETIC VARIANCE ACROSS PHENOTYPIC SPACE AND THE RESPONSE TO SELECTION." In Invasion Genetics, 187–205. Chichester, UK: John Wiley & Sons, Ltd, 2016. http://dx.doi.org/10.1002/9781119072799.ch11.

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Wang, Haizhen, and Xiangwei Wu. "Detection and Enumeration of Circulating Tumor Cells with Invasive Phenotype." In Advances in Experimental Medicine and Biology, 133–41. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-55947-6_7.

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Bei, Amy Kristine, and Manoj T. Duraisingh. "Measuring Plasmodium falciparum Erythrocyte Invasion Phenotypes Using Flow Cytometry." In Malaria Vaccines, 167–86. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2815-6_14.

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Pierleoni, Paola, Alberto Belli, Roberto Concetti, Lorenzo Palma, Federica Pinti, Sara Raggiunto, Simone Valenti, and Andrea Monteriù. "A Non-invasive Method for Biological Age Estimation Using Frailty Phenotype Assessment." In Lecture Notes in Electrical Engineering, 81–94. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-05921-7_7.

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James, John F. "Invasion of tissue culture cells by Neisseria gonorrhoeae colony phenotype variants." In Gonococci and Meningococci, 703–9. Dordrecht: Springer Netherlands, 1988. http://dx.doi.org/10.1007/978-94-009-1383-7_110.

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Conference papers on the topic "Invasive phenotypes"

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Yoon, Hong-Jun, Arvind Ramanathan, Folami Alamudun, and Georgia Tourassi. "Deep radiogenomics for predicting clinical phenotypes in invasive breast cancer." In Fourteenth International Workshop on Breast Imaging, edited by Elizabeth A. Krupinski. SPIE, 2018. http://dx.doi.org/10.1117/12.2318508.

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Harrandah, Amani, Sasanka S. Chukkapalli, Ann Progulske-Fox, William Dunn, Kesavalu Lakshmyya, and Edward K. Chan. "Abstract 5139:F. nucleatuminduces invasive phenotypes in oral cancer cells in vitro." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-5139.

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Zhang, Guihua, and Lynne Marie Postovit. "Abstract 5204: Nodal regulates invasive phenotypes in extravillous and choriocarcinoma trophoblast cells." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-5204.

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Williams, KE, NLP Barnes, K. Cheema, N. Dimopoulos, NJ Bundred, and G. Landberg. "Abstract PD04-06: Molecular Phenotypes of DCIS predict Invasive and DCIS recurrence." In Abstracts: Thirty-Fifth Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 4‐8, 2012; San Antonio, TX. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/0008-5472.sabcs12-pd04-06.

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Hanna, Matthew G., Anne Grabenstetter, Dara S. Ross, and Lee K. Tan. "Abstract P5-02-09: The prevalence of invasive lobular carcinomas with unconventional immunohistochemical phenotypes." In Abstracts: 2019 San Antonio Breast Cancer Symposium; December 10-14, 2019; San Antonio, Texas. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.sabcs19-p5-02-09.

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Antonov, Vladimir, and Galina Ignatova. "Non-invasive sanitation of a bronchial tree with different phenotypes of chronic obstructive pulmonary disease." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa4235.

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Wilson, Mike R., Jake J. Reske, and Ronald L. Chandler. "Abstract PO048: Inhibition of P300 histone acetyltransferase activity rescues invasive phenotypes of ARID1A-deficient endometrial epithelium." In Abstracts: AACR Virtual Special Conference: Endometrial Cancer: New Biology Driving Research and Treatment; November 9-10, 2020. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1557-3265.endomet20-po048.

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Kolmert, Johan, Cristina Gomez, Diane Lefaudeux, Bertrand DeMeulder, Anna James, Charles Auffray, Craig Wheelock, and Sven-Erik Dahlen. "Non-invasive urinary lipid mediator excretion profiles identify sub-phenotypes of asthma in the U-BIOPRED study." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.oa4954.

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Shaker, Hudhaifah, Nigel J. Bundred, Harith Albadry, Sarah L. Nicholson, Susan Pritchard, Karin Jirström, Goran Landberg, and Cliona C. Kirwan. "Abstract P6-08-30: The thrombin clotting pathway is upregulated in the stroma of pre-invasive breast cancer and further upregulated in aggressive invasive breast cancer phenotypes." In Thirty-Seventh Annual CTRC-AACR San Antonio Breast Cancer Symposium; December 9-13, 2014; San Antonio, TX. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.sabcs14-p6-08-30.

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Ghosh, Arnab, Sandipto Sarkar, Sonia Ghosh, Priyanka Ray, Mohi Quadir, Sushanta K. Banerjee, and Snigdha Banerjee. "Abstract 1234: Zoledronic acid-induced suppression of invasive phenotypes of pancreatic cancer cells is mediated through downregulation of CYR61/CCN1." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-1234.

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Reports on the topic "Invasive phenotypes"

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Kelley, Amanda. The Effect of Temperature on Phenotypes of the Invasive European Green Crab: Physiologic Mechanisms that Facilitate Invasion Success. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.1004.

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Corscadden, Louise, and Anjali Singh. Grip Strength Test In Rodents. ConductScience, January 2023. http://dx.doi.org/10.55157/cs2023109.

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The grip strength test is one of the most commonly applied tests in animal laboratories to measure neuromuscular functions or disorders. It was first developed in the 1970s. Today a wide range of techniques are available to study muscle strength in rodents. These methods are categorized into two categories:[2] Invasive method: In situ and in vitro measurements of muscle force are invasive methods. Non-invasive method: This method only includes in vivo measurement tests to analyze muscle force such as treadmill tests, wire hang tests, swimming endurance, vertical pole test, and grip strength tests. The most convenient technique of all tests is the grip strength test. It’s most convenient and causes less stress to animals. The grip test has been widely used in order to investigate the phenotypes of transgenic mice with neuromuscular disease and evaluate potential compounds involved in the motor functioning of organisms. The tests have been serving the purpose for 30 years either alone or in combination with other tests.
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Watson, Peter. Identification of Markers of the Invasive Phenotype in Human Breast Cancer (96 Cancer). Fort Belvoir, VA: Defense Technical Information Center, October 1999. http://dx.doi.org/10.21236/ada382826.

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Hunter, Martha S., and Einat Zchori-Fein. Rickettsia in the whitefly Bemisia tabaci: Phenotypic variants and fitness effects. United States Department of Agriculture, September 2014. http://dx.doi.org/10.32747/2014.7594394.bard.

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The sweet potato whitefly, Bemisia tabaci (Hemiptera: Aleyrodidae) is a major pest of vegetables, field crops, and ornamentals worldwide. This species harbors a diverse assembly of facultative, “secondary” bacterial symbionts, the roles of which are largely unknown. We documented a spectacular sweep of one of these, Rickettsia, in the Southwestern United States in the B biotype (=MEAM1) of B. tabaci, from 1% to 97% over 6 years, as well as a dramatic fitness benefit associated with it in Arizona but not in Israel. Because it is critical to understand the circumstances in which a symbiont invasion can cause such a large change in pest life history, the following objectives were set: 1) Determine the frequency of Rickettsia in B. tabaci in cotton across the United States and Israel. 2) Characterize Rickettsia and B. tabaci genotypes in order to test the hypothesis that genetic variation in either partner is responsible for differences in phenotypes seen in the two countries. 3) Determine the comparative fitness effects of Rickettsia phenotypes in B. tabaci in Israel and the United States. For Obj. 1, a survey of B. tabaci B samples revealed the distribution of Rickettsia across the cotton-growing regions of 13 sites from Israel and 22 sites from the USA. Across the USA, Rickettsia frequencies were heterogeneous among regions, but were generally at frequencies higher than 75% and close to fixation in some areas, whereas in Israel the infection rates were lower and declining. The distinct outcomes of Rickettsia infection in these two countries conform to previouslyreported phenotypic differences. Intermediate frequencies in some areas in both countries may indicate a cost to infection in certain environments or that the frequencies are in flux. This suggests underlying geographic differences in the interactions between bacterial symbionts and the pest. Obj. 2, Sequences of several Rickettsia genes in both locations, including a hypervariableintergenic spacer gene, suggested that the Rickettsia genotype is identical in both countries. Experiments in the US showed that differences in whitefly nuclear genotype had a strong influence on Rickettsia phenotype. Obj. 3. Experiments designed to test for possible horizontal transmission of Rickettsia, showed that these bacteria are transferred from B. tabaci to a plant, moved inside the phloem, and could be acquired by other whiteflies. Plants can serve as a reservoir for horizontal transmission of Rickettsia, a mechanism that may explain the occurrence of phylogenetically-similarsymbionts among unrelated phytophagous insect species. This plant-mediated transmission route may also exist in other insect-symbiont systems, and since symbionts may play a critical role in the ecology and evolution of their hosts, serve as an immediate and powerful tool for accelerated evolution. However, no such horizontal transmission of Rickettsia could be detected in the USA, underlining the difference between the interaction in both countries, or between B. tabaci and the banded wing whitefly on cotton in the USA (Trialeurodes sp. nr. abutiloneus) and the omnivorous bug Nesidiocoristenuis. Additionally, a series of experiments excluded the possibility that Rickettsia is frequently transmitted between B. tabaci and its parasitoid wasps Eretmocerusmundus and Encarsiapergandiella. Lastly, ecological studies on Rickettsia effects on free flight of whiteflies showed no significant influence of symbiont infection on flight. In contrast, a field study of the effects of Rickettsia on whitefly performance on caged cotton in the USA showed strong fitness benefits of infection, and rapid increases in Rickettsia frequency in competition population cages. This result confirmed the benefits to whiteflies of Rickettsia infection in a field setting.
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Horwitz, Benjamin A., and Barbara Gillian Turgeon. Fungal Iron Acquisition, Oxidative Stress and Virulence in the Cochliobolus-maize Interaction. United States Department of Agriculture, March 2012. http://dx.doi.org/10.32747/2012.7709885.bard.

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Our project focused on genes for high affinity iron acquisition in Cochliobolus heterostrophus, a necrotrophic pathogen of maize, and their intertwined relationship to oxidative stress status and virulence of the fungus on the host. An intriguing question was why mutants lacking the nonribosomal peptide synthetase (NRPS) gene (NPS6) responsible for synthesis of the extracellular siderophore, coprogen, are sensitive to oxidative stress. Our overall objective was to understand the mechanistic connection between iron stress and oxidative stress as related to virulence of a plant pathogen to its host. The first objective was to examine the interface where small molecule peptide and reactive oxygen species (ROS) mechanisms overlap. The second objective was to determine if the molecular explanation for common function is common signal transduction pathways. These pathways, built around sensor kinases, response regulators, and transcription factors may link sequestering of iron, production of antioxidants, resistance to oxidative stress, and virulence. We tested these hypotheses by genetic manipulation of the pathogen, virulence assays on the host plant, and by following the expression of key fungal genes. An addition to the original program, made in the first year, was to develop, for fungi, a genetically encoded indicator of redox state based on the commercially available Gfp-based probe pHyper, designed for animal cell biology. We implemented several tools including a genetically encoded indicator of redox state, a procedure to grow iron-depleted plants, and constructed a number of new mutants in regulatory genes. Lack of the major Fe acquisition pathways results in an almost completely avirulent phenotype, showing how critical Fe acquisition is for the pathogen to cause disease. Mutants in conserved signaling pathways have normal ability to regulate NPS6 in response to Fe levels, as do mutants in Lae1 and Vel1, two master regulators of gene expression. Vel1 mutants are sensitive to oxidative stress, and the reason may be underexpression of a catalase gene. In nps6 mutants, CAT3 is also underexpressed, perhaps explaining the sensitivity to oxidative stress. We constructed a deletion mutant for the Fe sensor-regulator SreA and found that it is required for down regulation of NPS6 under Fe-replete conditions. Lack of SreA, though, did not make the fungus over-sensitive to ROS, though the mutant had a slow growth rate. This suggests that overproduction of siderophore under Fe-replete conditions is not very damaging. On the other hand, increasing Fe levels protected nps6 mutants from inhibition by ROS, implying that Fe-catalyzed Fenton reactions are not the main factor in its sensitivity to ROS. We have made some progress in understanding why siderophore mutants are sensitive to oxidative stress, and in doing so, defined some novel regulatory relationships. Catalase genes, which are not directly related to siderophore biosynthesis, are underexpressed in nps6 mutants, suggesting that the siderophore product (with or without bound Fe) may act as a signal. Siderophores, therefore, could be a target for intervention in the field, either by supplying an incorrect signal or blocking a signal normally provided during infection. We already know that nps6 mutants cause smaller lesions and have difficulty establishing invasive growth in the host. Lae1 and Vel1 are the first factors shown to regulate both super virulence conferred by T-toxin, and basic pathogenicity, due to unknown factors. The mutants are also altered in oxidative stress responses, key to success in the infection court, asexual and sexual development, essential for fungal dissemination in the field, aerial hyphal growth, and pigment biosynthesis, essential for survival in the field. Mutants in genes encoding NADPH oxidase (Nox) are compromised in development and virulence. Indeed the triple mutant, which should lack all Nox activity, was nearly avirulent. Again, gene expression experiments provided us with initial evidence that superoxide produced by the fungus may be most important as a signal. Blocking oxidant production by the pathogen may be a way to protect the plant host, in interactions with necrotrophs such as C. heterostrophus which seem to thrive in an oxidant environment.
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Ficht, Thomas, Gary Splitter, Menachem Banai, and Menachem Davidson. Characterization of B. Melinensis REV 1 Attenuated Mutants. United States Department of Agriculture, December 2000. http://dx.doi.org/10.32747/2000.7580667.bard.

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Brucella Mutagenesis (TAMU) The working hypothesis for this study was that survival of Brucella vaccines was directly related to their persistence in the host. This premise is based on previously published work detailing the survival of the currently employed vaccine strains S19 and Rev 1. The approach employed signature-tagged mutagenesis to construct mutants interrupted in individual genes, and the mouse model to identify mutants with attenuated virulence/survival. Intracellular survival in macrophages is the key to both reproductive disease in ruminants and reticuloendothelial disease observed in most other species. Therefore, the mouse model permitted selection of mutants of reduced intracellular survival that would limit their ability to cause reproductive disease in ruminants. Several classes of mutants were expected. Colonization/invasion requires gene products that enhance host-agent interaction or increase resistance to antibacterial activity in macrophages. The establishment of chronic infection requires gene products necessary for intracellular bacterial growth. Maintenance of chronic infection requires gene products that sustain a low-level metabolism during periods characterized little or no growth (1, 2). Of these mutants, the latter group was of greatest interest with regard to our originally stated premise. However, the results obtained do not necessarily support a simplistic model of vaccine efficacy, i.e., long-survival of vaccine strains provides better immunity. Our conclusion can only be that optimal vaccines will only be developed with a thorough understanding of host agent interaction, and will be preferable to the use of fortuitous isolates of unknown genetic background. Each mutant could be distinguished from among a group of mutants by PCR amplification of the signature tag (5). This approach permitted infection of mice with pools of different mutants (including the parental wild-type as a control) and identified 40 mutants with apparently defective survival characteristics that were tentatively assigned to three distinct classes or groups. Group I (n=13) contained organisms that exhibited reduced survival at two weeks post-infection. Organisms in this group were recovered at normal levels by eight weeks and were not studied further, since they may persist in the host. Group II (n=11) contained organisms that were reduced by 2 weeks post infection and remained at reduced levels at eight weeks post-infection. Group III (n=16) contained mutants that were normal at two weeks, but recovered at reduced levels at eight weeks. A subset of these mutants (n= 15) was confirmed to be attenuated in mixed infections (1:1) with the parental wild-type. One of these mutants was eliminated from consideration due to a reduced growth rate in vitro that may account for its apparent growth defect in the mouse model. Although the original plan involved construction of the mutant bank in B. melitensis Rev 1 the low transformability of this strain, prevented accumulation of the necessary number of mutants. In addition, the probability that Rev 1 already carries one genetic defect increases the likelihood that a second defect will severely compromise the survival of this organism. Once key genes have been identified, it is relatively easy to prepare the appropriate genetic constructs (knockouts) lacking these genes in B. melitensis Rev 1 or any other genetic background. The construction of "designer" vaccines is expected to improve immune protection resulting from minor sequence variation corresponding to geographically distinct isolates or to design vaccines for use in specific hosts. A.2 Mouse Model of Brucella Infection (UWISC) Interferon regulatory factor-1-deficient (IRF-1-/- mice have diverse immunodeficient phenotypes that are necessary for conferring proper immune protection to intracellular bacterial infection, such as a 90% reduction of CD8+ T cells, functionally impaired NK cells, as well as a deficiency in iNOS and IL-12p40 induction. Interestingly, IRF-1-/- mice infected with diverse Brucella abortus strains reacted differently in a death and survival manner depending on the dose of injection and the level of virulence. Notably, 50% of IRF-1-/- mice intraperitoneally infected with a sublethal dose in C57BL/6 mice, i.e., 5 x 105 CFU of virulent S2308 or the attenuated vaccine S19, died at 10 and 20 days post-infection, respectively. Interestingly, the same dose of RB51, an attenuated new vaccine strain, did not induce the death of IRF-1-/- mice for the 4 weeks of infection. IRF-1-/- mice infected with four more other genetically manipulated S2308 mutants at 5 x 105 CFU also reacted in a death or survival manner depending on the level of virulence. Splenic CFU from C57BL/6 mice infected with 5 x 105 CFU of S2308, S19, or RB51, as well as four different S2308 mutants supports the finding that reduced virulence correlates with survival Of IRF-1-/- mice. Therefore, these results suggest that IRF-1 regulation of multi-gene transcription plays a crucial role in controlling B. abortus infection, and IRF-1 mice could be used as an animal model to determine the degree of B. abortus virulence by examining death or survival. A3 Diagnostic Tests for Detection of B. melitensis Rev 1 (Kimron) In this project we developed an effective PCR tool that can distinguish between Rev1 field isolates and B. melitensis virulent field strains. This has allowed, for the first time, to monitor epidemiological outbreaks of Rev1 infection in vaccinated flocks and to clearly demonstrate horizontal transfer of the strain from vaccinated ewes to unvaccinated ones. Moreover, two human isolates were characterized as Rev1 isolates implying the risk of use of improperly controlled lots of the vaccine in the national campaign. Since atypical B. melitensis biotype 1 strains have been characterized in Israel, the PCR technique has unequivocally demonstrated that strain Rev1 has not diverted into a virulent mutant. In addition, we could demonstrate that very likely a new prototype biotype 1 strain has evolved in the Middle East compared to the classical strain 16M. All the Israeli field strains have been shown to differ from strain 16M in the PstI digestion profile of the omp2a gene sequence suggesting that the local strains were possibly developed as a separate branch of B. melitensis. Should this be confirmed these data suggest that the Rev1 vaccine may not be an optimal vaccine strain for the Israeli flocks as it shares the same omp2 PstI digestion profile as strain 16M.
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