Relevant bibliographies by topics / Cystic fibrosis Lungs Life (Biology) Biotechnology

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Academic literature on the topic 'Cystic fibrosis Lungs Life (Biology) Biotechnology'

Author: Grafiati
Published: 4 June 2021
Last updated: 12 February 2022

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Journal articles on the topic "Cystic fibrosis Lungs Life (Biology) Biotechnology"

1

Phillipson, Greg. "Cystic fibrosis and reproduction." Reproduction, Fertility and Development 10, no. 1 (1998): 113. http://dx.doi.org/10.1071/r98044.

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Cystic fibrosis (CF) is the most common autosomal recessive disease. CF and congenital bilateral absence of the vas deferens (CBAVD) share a genetic and embryological background. Since the 1960s, medical therapy to reduce the progressive obstructive lung disease and nutritional deficiencies has resulted in most CF patients reaching adulthood. With the improved life expectancy of CF patients, new issues in reproductive health and pregnancy management have arisen. Puberty is delayed, with menarche often occurring eighteen months later than the average. Almost all men with CF are azoospermic. In both CF and CBAVD, the vas deferens is absent and the seminal vesicles are often hypoplastic. Many women with CF are subfertile, and if pregnancy is achieved there is an observed increase in maternal morbidity and mortality. The understanding of the molecular basis of CF and CBAVD has evolved, with the identification of hundreds of CF gene mutations and discovery of an associated intron polymorphism of the CF gene. The concept of severe and mild mutations has been introduced to explain the severe and mild phenotype variations such as the pancreatic insufficient and pancreatic sufficient patient. This paper reviews the above issues to assist with the management of infertile couples with CF or CBAVD.
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2

Daniels, Jonathan B., Jessica Scoffield, Jessica L. Woolnough, and Laura Silo-Suh. "Impact of glycerol-3-phosphate dehydrogenase on virulence factor production byPseudomonas aeruginosa." Canadian Journal of Microbiology 60, no. 12 (December 2014): 857–63. http://dx.doi.org/10.1139/cjm-2014-0485.

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Pseudomonas aeruginosa establishes life-long chronic infections in the cystic fibrosis (CF) lung by utilizing various adaptation strategies. Some of these strategies include altering metabolic pathways to utilize readily available nutrients present in the host environment. The airway sputum contains various host-derived nutrients that can be utilized by P. aeruginosa, including phosphatidylcholine, a major component of lung surfactant. Pseudomonas aeruginosa can degrade phosphatidylcholine to glycerol and fatty acids to increase the availability of usable carbon sources in the CF lung. In this study, we show that some CF-adapted P. aeruginosa isolates utilize glycerol more efficiently as a carbon source than nonadapted isolates. Furthermore, a mutation in a gene required for glycerol utilization impacts the production of several virulence factors in both acute and chronic isolates of P. aeruginosa. Taken together, the results suggest that interference with this metabolic pathway may have potential therapeutic benefits.
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3

Lara-Reyna, Samuel, Jonathan Holbrook, Heledd H. Jarosz-Griffiths, Daniel Peckham, and Michael F. McDermott. "Dysregulated signalling pathways in innate immune cells with cystic fibrosis mutations." Cellular and Molecular Life Sciences 77, no. 22 (May 4, 2020): 4485–503. http://dx.doi.org/10.1007/s00018-020-03540-9.

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Abstract Cystic fibrosis (CF) is one of the most common life-limiting recessive genetic disorders in Caucasians, caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR). CF is a multi-organ disease that involves the lungs, pancreas, sweat glands, digestive and reproductive systems and several other tissues. This debilitating condition is associated with recurrent lower respiratory tract bacterial and viral infections, as well as inflammatory complications that may eventually lead to pulmonary failure. Immune cells play a crucial role in protecting the organs against opportunistic infections and also in the regulation of tissue homeostasis. Innate immune cells are generally affected by CFTR mutations in patients with CF, leading to dysregulation of several cellular signalling pathways that are in continuous use by these cells to elicit a proper immune response. There is substantial evidence to show that airway epithelial cells, neutrophils, monocytes and macrophages all contribute to the pathogenesis of CF, underlying the importance of the CFTR in innate immune responses. The goal of this review is to put into context the important role of the CFTR in different innate immune cells and how CFTR dysfunction contributes to the pathogenesis of CF, highlighting several signalling pathways that may be dysregulated in cells with CFTR mutations.
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4

Tomlin, Kerry L., Oisin P. Coll, and Howard Ceri. "Interspecies biofilms ofPseudomonas aeruginosaandBurkholderia cepacia." Canadian Journal of Microbiology 47, no. 10 (October 1, 2001): 949–54. http://dx.doi.org/10.1139/w01-095.

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The leading cause of morbidity and mortality in cystic fibrosis (CF) continues to be lung infections with Pseudomonas aeruginosa biofilms. Co-colonization of the lungs with P. aeruginosa and Burkholderia cepacia can result in more severe pulmonary disease than P. aeruginosa alone. The interactions between P. aeruginosa biofilms and B. cepacia are not yet understood; one possible association being that mixed species biofilm formation may be part of the interspecies relationship. Using the Calgary Biofilm Device (CBD), members of all genomovars of the B. cepacia complex were shown to form biofilms, including those isolated from CF lungs. Mixed species biofilm formation between CF isolates of P. aeruginosa and B. cepacia was readily achieved using the CBD. Oxidation–fermentation lactose agar was adapted as a differential agar to monitor mixed biofilm composition. Scanning electron micrographs of the biofilms demonstrated that both species readily integrated in close association in the biofilm structure. Pseudomonas aeruginosa laboratory strain PAO1, however, inhibited mixed biofilm formation of both CF isolates and environmental strains of the B. cepacia complex. Characterization of the soluble inhibitor suggested pyocyanin as the active compound.Key words: Burkholderia cepacia, Pseudomonas aeruginosa, mixed biofilms, cystic fibrosis, pyocyanin.
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Cardenas, Silvia, Mario Scuri, Lennie Samsell, Barbara Ducatman, Pablo Bejarano, Alexander Auais, Melissa Doud, Kalai Mathee, and Giovanni Piedimonte. "Neurotrophic and neuroimmune responses to early-life Pseudomonas aeruginosa infection in rat lungs." American Journal of Physiology-Lung Cellular and Molecular Physiology 299, no. 3 (September 2010): L334—L344. http://dx.doi.org/10.1152/ajplung.00017.2010.

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Early-life respiratory infection with Pseudomonas aeruginosa is common in children with cystic fibrosis or immune deficits. Although many of its clinical manifestations involve neural reflexes, little information is available on the peripheral nervous system of infected airways. This study sought to determine whether early-life infection triggers a neurogenic-mediated immunoinflammatory response, the mechanisms of this response, and its relationship with other immunoinflammatory pathways. Weanling and adult rats were inoculated with suspensions containing P. aeruginosa (PAO1) coated on alginate microspheres suspended in Tris-CaCl2 buffer. Five days after infection, rats were injected with capsaicin to stimulate nociceptive nerves in the airway mucosa, and microvascular permeability was measured using Evans blue as a tracer. PAO1 increased neurogenic inflammation in the extra- and intrapulmonary compartments of weanlings but not in adults. The mechanism involves selective overexpression of NGF, which is critical for the local increase in microvascular permeability and for the infiltration of polymorphonuclear leukocytes into infected lung parenchyma. These effects are mediated in part by induction of downstream inflammatory cytokines and chemokines, especially IL-1β, IL-18, and leptin. Our data suggest that neurogenic-mediated immunoinflammatory mechanisms play important roles in airway inflammation and hyperreactivity associated with P. aeruginosa when infection occurs early in life.
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6

Ajonuma, Louis Chukwuemeka, Lai Ling Tsang, Gui Hong Zhang, Connie Hau Yan Wong, Miu Ching Lau, Lok Sze Ho, Dewi Kenneth Rowlands, et al. "Estrogen-Induced Abnormally High Cystic Fibrosis Transmembrane Conductance Regulator Expression Results in Ovarian Hyperstimulation Syndrome." Molecular Endocrinology 19, no. 12 (December 1, 2005): 3038–44. http://dx.doi.org/10.1210/me.2005-0114.

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Abstract Ovarian hyperstimulation syndrome (OHSS) remains one of the most life-threatening and potentially fatal complications of assisted reproduction treatments, arising from excessive stimulation of the ovaries by exogenous gonadotropins administrated during in vitro fertilization procedures, which is characterized by massive fluid shift and accumulation in the peritoneal cavity and other organs, including the lungs and the reproductive tract. The pathogenesis of OHSS remains obscure, and no definitive treatments are currently available. Using RT-PCR, Western blot, and electrophysiological techniques we show that cystic fibrosis transmembrane conductance regulator (CFTR), a cAMP-activated chloride channel expressed in many epithelia, is involved in the pathogenesis of OHSS. Upon ovarian hyperstimulation, rats develop OHSS symptoms, with up-regulated CFTR expression and enhanced CFTR channel activity, which can also be mimicked by administration of estrogen, but not progesterone, alone in ovariectomized rats. Administration of progesterone that suppresses CFTR expression or antiserum against CFTR to OHSS animals results in alleviation of the symptoms. Furthermore, ovarian hyperstimulation does not induce detectable OHSS symptoms in CFTR mutant mice. These findings confirm a critical role of CFTR in the pathogenesis of OHSS and may provide grounds for better assisted reproduction treatment strategy to reduce the risk of OHSS and improve in vitro fertilization outcome.
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7

Lewenza, Shawn, Michelle B. Visser, and Pamela A. Sokol. "Interspecies communication betweenBurkholderia cepaciaandPseudomonas aeruginosa." Canadian Journal of Microbiology 48, no. 8 (August 1, 2002): 707–16. http://dx.doi.org/10.1139/w02-068.

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Burkholderia cepacia and Pseudomonas aeruginosa are opportunistic pathogens that commonly cause pulmonary infections in cystic fibrosis patients and occasionally co-infect patients' lungs. Both organisms possess quorum-sensing systems dependent on N-acyl homoserine lactone (N-acyl-HSL). Cross-feeding assays demonstrated that P. aeruginosa and B. cepacia were able to utilize heterologous N-acyl-HSL signaling molecules. The ability of quorum-sensing genes from one species to complement the respective quorum-sensing mutations in the heterologous species was also examined. These studies suggest that B. cepacia CepR can use N-acyl-HSLs synthesized by RhlI and LasI and that P. aeruginosa LasR and RhlR can use N-acyl-HSLs synthesized by CepI. It is possible that a mixed bacterial population of B. cepacia and P. aeruginosa can coordinately regulate some of their virulence factors and influence the progression of lung disease due to infection with these organisms.Key words: quorum sensing, Burkholderia cepacia, Pseudomonas aeruginosa, cystic fibrosis.
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8

Beaudoin, Trevor, Shawn D. Aaron, Tracy Giesbrecht-Lewis, Kathy Vandemheen, and Thien-Fah Mah. "Characterization of clonal strains of Pseudomonas aeruginosa isolated from cystic fibrosis patients in Ontario, Canada." Canadian Journal of Microbiology 56, no. 7 (July 2010): 548–57. http://dx.doi.org/10.1139/w10-043.

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Pseudomonas aeruginosa is an opportunistic pathogen that can form biofilms in the lungs and airways of cystic fibrosis (CF) patients, resulting in chronic endobronchial infection. Two clonal strains of P. aeruginosa, named type A and type B, have recently been identified and have been found to infect more than 20% of CF patients in Ontario, Canada. In this study, 4 type A and 4 type B isolates retrieved from 8 CF patients in Ontario, Canada, were characterized. All 8 isolates grew well in rich medium and formed biofilms in vitro. Antibiotic resistance profiles of bacteria grown in biofilms and planktonic culture were studied via minimal bactericidal concentration assays for tobramycin, gentamicin, and ciprofloxacin. Compared to laboratory strains of P. aeruginosa, all 8 isolates showed increased resistance to all antibiotics studied in both biofilm and planktonic assays. Gene expression analysis of mexX, representing the MexXY–OprM efflux pump, and mexA, representing MexAB–OprM, revealed that these genes were up-regulated in the 8 clinical isolates. These results suggest clonal type A and type B isolates of P. aeruginosa isolated from CF patients in Ontario, Canada, show a multidrug resistance pattern that can be partially explained as being due to the increased expression of common antibiotic efflux systems.
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9

Vincent, Antony T., Steve J. Charette, and Jean Barbeau. "Unexpected diversity in the mobilome of a Pseudomonas aeruginosa strain isolated from a dental unit waterline revealed by SMRT Sequencing." Genome 61, no. 5 (May 2018): 359–65. http://dx.doi.org/10.1139/gen-2017-0239.

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The Gram-negative bacterium Pseudomonas aeruginosa is found in several habitats, both natural and human-made, and is particularly known for its recurrent presence as a pathogen in the lungs of patients suffering from cystic fibrosis, a genetic disease. Given its clinical importance, several major studies have investigated the genomic adaptation of P. aeruginosa in lungs and its transition as acute infections become chronic. However, our knowledge about the diversity and adaptation of the P. aeruginosa genome to non-clinical environments is still fragmentary, in part due to the lack of accurate reference genomes of strains from the numerous environments colonized by the bacterium. Here, we used PacBio long-read technology to sequence the genome of PPF-1, a strain of P. aeruginosa isolated from a dental unit waterline. Generating this closed genome was an opportunity to investigate genomic features that are difficult to accurately study in a draft genome (contigs state). It was possible to shed light on putative genomic islands, some shared with other reference genomes, new prophages, and the complete content of insertion sequences. In addition, four different group II introns were also found, including two characterized here and not listed in the specialized group II intron database.
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10

Gilleland Jr., H. E. "Adaptive alterations in the outer membrane of gram-negative bacteria during human infection." Canadian Journal of Microbiology 34, no. 4 (April 1, 1988): 499–502. http://dx.doi.org/10.1139/m88-085.

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The outer membrane of gram-negative bacteria is a dynamic structure that is capable of altering its ultrastructure and chemistry in order to adapt to changes in its environment. In human infections, outer-membrane alterations are known to play a role in mediating serum resistance, iron uptake, adaptation by Pseudomonas aeruginosa to colonization of the lungs of cystic fibrosis patients, and adaptive resistance to the polymyxin and aminoglycoside antibiotics. This adaptive antibiotic resistance is due to alterations in the cation binding sites within the outer membrane so that these cationic antibiotics can no longer penetrate through the membrane effectively. Adaptive resistance is not stable but is maintained only in the continued presence of the antibiotic. Hence, the role that this type of resistance to cationic antibiotics plays in clinical treatment of human infections remains inadequately assessed.
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Dissertations / Theses on the topic "Cystic fibrosis Lungs Life (Biology) Biotechnology"

1

Maynard, Ronald J. "Risking the future : biomedicine and modernity in the lives of adults with cystic fibrosis /." Thesis, Connect to this title online; UW restricted, 2003. http://hdl.handle.net/1773/6402.

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