513 resultados para AIRWAYS ICPs
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In - Commuter Airlines: Their Changing Role – an essay by J. A. F. Nicholls, Transportation Coordinator, Department of Marketing and Environment, College of Business Administration, Florida International University, Nicholls initially observes: “The great majority of airline passenger miles flown in the United States are between large conurbations. People living in metropolitan areas may be quite unaware of commuter airlines and their role in our transportation system. These airlines are, however, communications lifelines for dwellers in small - and not so small - towns and rural areas. More germanely, commuter airlines have also developed a pivotal role vis-a-vis the major carriers in this country. The author discusses the antecedents of the commuter Airlines, their current role, and future prospects.” Huh; conurbations? Definition: [n.] a large urban area created when neighboring towns spread into and merge with each other In providing a brief history on the subject of commuter airlines, Nicholls states: “…there had been a sort of commuter airline as far back as 1926 when, for example, the Florida Airways Corporation provided flights between Jacksonville and Atlanta, Colonial Air Lines between New York and Boston, and Ford Air Transport from Detroit to Cleveland.” “The passage of the Civil Aeronautics Act in 1938 was pivotal in encouraging and developing a passenger orientation by the airlines…” Nicholls informs you. Nicholls provides for the importance of this act by saying: “The CAA was empowered to act “in the public interest and in accordance with the public convenience and necessity.” Only the CAA itself could determine what constituted the “public convenience and necessity.” Nobody, however, could provide air transportation for public purposes without a Certificate of Public Convenience and Necessity, dispensed by the CAA.” The author wants you to know that this all happens in the age of airline regulation; that is to say, pre de-regulation i.e. 1978. Airlines could not and did not act on their own behalf; their actions were governed by the regulating agency, that being the Civil Aeronautics Board [CAB], who administered the conditions set forth by the CAA. “In 1944 the CAB introduced a new category of service called feeder airlines to provide local service-short-haul, low density-for smaller communities. These carriers soon became known as air taxis since they operated as common carriers, without a regular schedule,” says Nicholls in describing the evolution of the service. In 1969 the CAB officially designated these small air carriers as commuter airlines. They were, and are subject to passenger limits and freight/weight restrictions. Nicholls continues by defining how air carriers are labeled and categorized post 1978; in the age of de-regulation.
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In his essay - Toward a Better Understanding of the Evolution of Hotel Development: A Discussion of Product-Specific Lodging Demand - by John A. Carnella, Consultant, Laventhol & Horwath, cpas, New York, Carnella initially describes his piece by stating: “The diversified hotel product in the united states lodging market has Resulted in latent room-night demand, or supply-driven demand resulting from the introduction of a lodging product which caters to a specific set of hotel patrons. The subject has become significant as the lodging market has moved toward segmentation with regard to guest room offerings. The author proposes that latent demand is a tangible, measurable phenomenon best understood in light of the history of the guest room product from its infancy to its present state.” The article opens with an ephemeral depiction of hotel development in the United States, both pre’ and post World War II. To put it succinctly, the author wants you to know that the advent of the inter-state highway system changed the complexion of the hotel industry in the U.S. “Two essential ingredients were necessary for the next phase of hotel development in this country. First was the establishment of the magnificently intricate infrastructure which facilitated motor vehicle transportation in and around the then 48 states of the nation,” says Carnella. “The second event…was the introduction of affordable highway travel. Carnella goes on to say that the next – big thing – in hotel evolution was the introduction of affordable air travel. “With the airways filled with potential lodging guests, developers moved next to erect a new genre of hotel, the airport hotel,” Carnella advances his picture. Growth progressed with the arrival of the suburban hotel concept, which wasn’t fueled by developments in transportation, but by changes in people’s living habits, i.e. suburban affiliations as opposed to urban and city population aggregates. The author explores the distinctions between full-service and limited service lodging operations. “The market of interest with consideration to the extended-stay facility is one dominated by corporate office parks,” Carnella proceeds. These evolutional states speak to latent demand, and even further to segmentation of the market. “Latent demand… is a product-generated phenomenon in which the number of potential hotel guests increases as the direct result of the introduction of a new lodging facility,” Carnella brings his unique insight to the table with regard to the specialization process. The demand is already there; just waiting to be tapped. In closing, “…there must be a consideration of the unique attributes of a lodging facility relative to its ability to attract guests to a subject market, just as there must be an examination of the property's ability to draw guests from within the subject market,” Carnella proposes.
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Metagenomics is the culture-independent study of genetic material obtained directly from environmental samples. It has become a realistic approach to understanding microbial communities thanks to advances in high-throughput DNA sequencing technologies over the past decade. Current research has shown that different sites of the human body house varied bacterial communities. There is a strong correlation between an individual’s microbial community profile at a given site and disease. Metagenomics is being applied more often as a means of comparing microbial profiles in biomedical studies. The analysis of the data collected using metagenomics can be quite challenging and there exist a plethora of tools for interpreting the results. An automatic analytical workflow for metagenomic analyses has been implemented and tested using synthetic datasets of varying quality. It is able to accurately classify bacteria by taxa and correctly estimate the richness and diversity of each set. The workflow was then applied to the study of the airways microbiome in Chronic Obstructive Pulmonary Disease (COPD). COPD is a progressive lung disease resulting in narrowing of the airways and restricted airflow. Despite being the third leading cause of death in the United States, little is known about the differences in the lung microbial community profiles of healthy individuals and COPD patients. Bronchoalveolar lavage (BAL) samples were collected from COPD patients, active or ex-smokers, and never smokers and sequenced by 454 pyrosequencing. A total of 56 individuals were recruited for the study. Substantial colonization of the lungs was found in all subjects and differentially abundant genera in each group were identified. These discoveries are promising and may further our understanding of how the structure of the lung microbiome is modified as COPD progresses. It is also anticipated that the results will eventually lead to improved treatments for COPD.
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The lungs are vital organs whose airways are lined with a continuous layer of epithelial cells. Epithelial cells in the distal most part of the lung, the alveolar space, are specialized to facilitate gas exchange. Proximal to the alveoli is the airway epithelium, which provides an essential barrier and is the first line of defense against inhaled toxicants, pollutants, and pathogens. Although the postnatal lung is a quiescent organ, it has an inherent ability to regenerate in response to injury. Proper balance between maintaining quiescence and undergoing repair is crucial, with imbalances in these processes leading to fibrosis or tumor development. Stem and progenitor cells are central to maintaining balance, given that they proliferate and renew both themselves and the various differentiated cells of the lung. However, the precise mechanisms regulating quiescence and repair in the lungs are largely unknown. In this dissertation, ionizing radiation is used as a physiologically relevant injury model to better understand the repair process of the airway epithelium. We use in vitro and in vivo mouse models to study the response of a secretory progenitor, the club cell, to various doses and qualities of ionizing radiation. Exposure to radiation found in space environments and in some types of radiotherapy caused clonal expansion of club cells specifically in the most distal branches of the airway epithelium, indicating that the progenitors residing in the terminal bronchioles are radiosensitive. This clonal expansion is due to an increase in p53-dependent apoptosis, senescence, and mitotic defects. Through the course of this work, we discovered that p53 is not only involved in radiation response, but is also a novel regulator of airway epithelial homeostasis. p53 acts in a gene dose-dependent manner to regulate the composition of airway epithelium by maintaining quiescence and regulating differentiation of club progenitor cells in the steady-state lung. The work presented in this dissertation represents an advance in our understanding of the molecular mechanisms underlying maintenance of airway epithelial progenitor cells as well as their repair following ionizing radiation exposure.
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Underground hardrock mining can be very energy intensive and in large part this can be attributed to the power consumption of underground ventilation systems. In general, the power consumed by a mine’s ventilation system and its overall scale are closely related to the amount of diesel power in operation. This is because diesel exhaust is a major source of underground air pollution, including diesel particulate matter (DPM), NO2 and heat, and because regulations tie air volumes to diesel engines. Furthermore, assuming the size of airways remains constant, the power consumption of the main system increases exponentially with the volume of air supplied to the mine. Therefore large diesel fleets lead to increased energy consumption and can also necessitate large capital expenditures on ventilation infrastructure in order to manage power requirements. Meeting ventilation requirements for equipment in a heading can result in a similar scenario with the biggest pieces leading to higher energy consumption and potentially necessitating larger ventilation tubing and taller drifts. Depending on the climate where the mine is located, large volumes of air can have a third impact on ventilation costs if heating or cooling the air is necessary. Annual heating and cooling costs, as well as the cost of the associated infrastructure, are directly related to the volume of air sent underground. This thesis considers electric mining equipment as a means for reducing the intensity and cost of energy consumption at underground, hardrock mines. Potentially, electric equipment could greatly reduce the volume of air needed to ventilate an entire mine as well as individual headings because they do not emit many of the contaminants found in diesel exhaust and because regulations do not connect air volumes to electric motors. Because of the exponential relationship between power consumption and air volumes, this could greatly reduce the amount of power required for mine ventilation as well as the capital cost of ventilation infrastructure. As heating and cooling costs are also directly linked to air volumes, the cost and energy intensity of heating and cooling the air would also be significantly reduced. A further incentive is that powering equipment from the grid is substantially cheaper than fuelling them with diesel and can also produce far fewer GHGs. Therefore, by eliminating diesel from the underground workers will enjoy safer working conditions and operators and society at large will gain from a smaller impact on the environment. Despite their significant potential, in order to produce a credible economic assessment of electric mining equipment their impact on underground systems must be understood and considered in their evaluation. Accordingly, a good deal of this thesis reviews technical considerations related to the use of electric mining equipment, especially ones that impact the economics of their implementation. The goal of this thesis will then be to present the economic potential of implementing the equipment, as well as to outline the key inputs which are necessary to support an evaluation and to provide a model and an approach which can be used by others if the relevant information is available and acceptable assumptions can be made.
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In today’s technology-driven marketplace, the adoption and management of corporate and customer-facing Social Networking Sites (SNs) is often viewed as a key success factor for Travel Industry (TI) organisations. Knowledge management and the sharing of expertise and experiences through communication between internal and external stakeholders via social networks is an activity which TI organisations are aiming to exploit in order to improve the open sharing, retrieval, organisation and leveraging of knowledge. Through a study of currently-available literature relating to social networking adoption within the TI and a case study analysis of corporate social networking practices at three multi-national TI organisations (British Airways, Thomas Cook and Marriott Hotels), it may be observed that correlations exist between the development of social networking and the processes TI organisations now use to manage knowledge. We explore how these companies are currently utilizing SNs to improve knowledge management practices inside and outside of their organisational boundaries. From our analysis, lessons may emerge as to how TI companies are gaining competitive advantage through the use of social networking; a proposed strategy is identified to determine how TI organisations may make best use of social networks.
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The choice of model used to study human respiratory syncytial virus (RSV) infection is extremely important. RSV is a human pathogen that is exquisitely adapted to infection of human hosts. Rodent models, such as mice and cotton rats, are semi-permissive to RSV infection and do not faithfully reproduce hallmarks of RSV disease in humans. Furthermore, immortalized airway-derived cell lines, such as HEp-2, BEAS-2B, and A549 cells, are poorly representative of the complexity of the respiratory epithelium. The development of a well-differentiated primary pediatric airway epithelial cell models (WD-PAECs) allows us to simulate several hallmarks of RSV infection of infant airways. They therefore represent important additions to RSV pathogenesis modeling in human-relevant tissues. The following protocols describe how to culture and differentiate both bronchial and nasal primary pediatric airway epithelial cells and how to use these cultures to study RSV cytopathogenesis.
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RATIONALE: As more preterm infants recover from severe bronchopulmonary dysplasia (BPD), it is critical to understand the clinical consequences of this condition on the lung health of adult survivors.
OBJECTIVES: To assess structural and functional lung parameters in young adult BPD survivors and preterm and term controls Methods: Young adult survivors of BPD (mean age 24) underwent spirometry, lung volumes, transfer factor, lung clearance index and fractional exhaled nitric oxide measurements together with high-resolution chest tomographic (CT) imaging and cardiopulmonary exercise testing.
MEASUREMENTS AND MAIN RESULTS: 25 adult BPD survivors, (mean ± SD gestational age 26.8 ± 2.3 weeks; birth weight 866 ± 255 g), 24 adult prematurely born non-BPD controls (gestational age 30.6 ± 1.9 weeks; birth weight 1234 ± 207 g) and 25 adult term birth control subjects (gestational age 38.5 ± 0.9 weeks; and birth weight 3569 ± 2979 g) were studied. BPD subjects were more likely to be wakened by cough (OR 9.7, 95% CI: 1.8 to 52.6), p<0.01), wheeze and breathlessness (OR 12.2, 95%CI: 1.3 to 112), p<0.05) than term controls after adjusting for sex and current smoking. Preterm subjects had greater airways obstruction than term subjects. BPD subjects had significantly lower values for FEV1 and FEF25-75 (% predicted and z scores) than term controls (both p<0.001). Although non-BPD subjects also had lower spirometric values than term controls, none of the differences reached statistical significance. More BPD subjects (25%) had fixed airflow obstruction than non-BPD (12.5%) and term (0%) subjects (p=0.004). Both BPD and non-BPD subjects had significantly greater impairment in gas transfer (KCO % predicted) than term subjects (both p<0.05). Eighteen (37%) preterm participants were classified as small for gestational age (birth weight < 10th percentile for gestational age). These subjects had significantly greater impairment in FEV1 (% predicted and z scores) than those born appropriate for gestational age. BPD survivors had significantly more severe radiographic structural lung impairment than non-BPD subjects. Both preterm groups had impaired exercise capacity compared to term controls. There was a trend for greater limitation and leg discomfort in BPD survivors.
CONCLUSIONS: Adult preterm birth survivors, especially those who developed BPD, continue to experience respiratory symptoms and exhibit clinically important levels of pulmonary impairment.
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Cystic Fibrosis (CF) lung disease is characterised by a chronic and exaggerated inflammation in the airways. Despite recent developments to therapeutically overcome the underlying functional defect in CFTR (cystic fibrosis transmembrane conductance regulator), there is still an unmet need to also normalise the inflammatory response. The prolonged and heightened inflammatory response in CF is in part mediated by a lack of intrinsic downregulation of the pro-inflammatory NF-kB pathway. We have previously identified reduced expression of the NF-kB down-regulator A20 in CF as a key target to normalise the inflammatory response. Here we have used publically available gene array expression data together with sscMap (statistically significant connections’map)to successfully predict drugs already licensed for the use in humans to induce A20 mRNA and protein expression and thereby reduce inflammation. The effect of the predicted drugs on A20 and NFkB (p65) expression (mRNA) as well as pro-inflammatory cytokine release (IL-8) in the presence and absence of bacterial LPS was shown in bronchial epithelial cells lines (16HBE14o-, CFBE41o-) and in primary nasal epithelial cells (PNECs) from patients with CF (Phe508del homozygous) and non-CF controls. Additionally, the specificity of the drug action on A20 was confirmed using cell lines with TNFAIP3 (A20) knockdown (siRNA). We also show that the A20 inducing effect of ikarugamycin and quercetin is lower in CF derived airway epithelial cells than in non-CF cells.
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Severe asthma represents a major unmet clinical need. Eosinophilic inflammation persists in the airways of many patients with uncontrolled asthma, despite high-dose inhaled corticosteroid therapy. Suppressors of cytokine signalling (SOCS) are a family of molecules involved in the regulation of cytokine signalling via inhibition of the Janus kinase-signal transducers and activators of transcription pathway. We examined SOCS expression in the airways of asthma patients and investigated whether this is associated with persistent eosinophilia.
Healthy controls, mild/moderate asthmatics and severe asthmatics were studied. Whole genome expression profiling, quantitative PCR and immunohistochemical analysis were used to examine expression of SOCS1, SOCS2 and SOCS3 in bronchial biopsies. Bronchial epithelial cells were utilised to examine the role of SOCS1 in regulating interleukin (IL)-13 signalling in vitro.
SOCS1 gene expression was significantly lower in the airways of severe asthmatics compared with mild/moderate asthmatics, and was inversely associated with airway eosinophilia and other measures of T-helper type 2 (Th2) inflammation. Immunohistochemistry demonstrated SOCS1 was predominantly localised to the bronchial epithelium. SOCS1 overexpression inhibited IL-13-mediated chemokine ligand (CCL) 26 (eotaxin-3) mRNA expression in bronchial epithelial cells.
Severe asthma patients with persistent airway eosinophilia and Th2 inflammation have reduced airway epithelial SOCS1 expression. SOCS1 inhibits epithelial IL-13 signalling, supporting its key role in regulating Th2-driven eosinophilia in severe asthma.
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PURPOSE OF REVIEW: Anaerobic bacteria are not only normal commensals, but are also considered opportunistic pathogens and have been identified as persistent members of the lower airway community in people with cystic fibrosis of all ages and stages of disease. Currently, the role of anaerobic bacteria in cystic fibrosis lower airway disease is not well understood. Therefore, this review describes the recent studies relating to the potential pathophysiological role(s) of anaerobes within the cystic fibrosis lungs.
RECENT FINDINGS: The most frequently identified anaerobic bacteria in the lower airways are common to both cystic fibrosis and healthy lungs. Studies have shown that in cystic fibrosis, the relative abundance of anaerobes fluctuates in the lower airways with reduced lung function and increased inflammation associated with a decreased anaerobic load. However, anaerobes found within the lower airways also produce virulence factors, may cause a host inflammatory response and interact synergistically with recognized pathogens.
SUMMARY: Anaerobic bacteria are potentially members of the airway microbiota in health but could also contribute to the pathogenesis of lower airway disease in cystic fibrosis via both direct and indirect mechanisms. A personalized treatment strategy that maintains a normal microbial community may be possible in the future.
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BACKGROUND: Asthma and rhinitis have a complex etiology, depending on multiple genetic and environmental risk factors. An increasing number of susceptibility genes are currently being identified, but the majority of reported associations have not been consistently replicated across populations of different genetic backgrounds. PURPOSE: To evaluate whether polymorphisms of IL4R (rs1805015), IL13 (rs20541), IL17A (rs2275913) and GSTP1 (rs1695) genes are associated with rhinitis and/or asthma in adults of Portuguese ancestry. METHODS: 192 unrelated healthy individuals and 232 patients, 83 with rhinitis and 149 with asthma, were studied. All polymorphisms were detected by real time polymerase chain reaction (PCR) using TaqMan assays. RESULTS: Comparing to controls, significant association with asthma was observed for GSTP1 rs1695 AA genotype (odds ratio (OR) - 1.96; 95% CI - 1.18 to 3.25; p=0.010). The association sustains for allergic asthma (OR - 2.17; 95% CI - 1.23 to 3.80; p=0.007). IL13 rs20541 GG genotype was associated with less susceptibility to asthma (OR - 0.55, 95% CI - 0.33 to 0.94, p=0.028). Among patients, IL17A rs2275913 AA genotype was less associated with asthma than with rhinitis (OR - 0.20; 95% CI of 0.07 to 0.56; p=0.002). A similar association was found for IL13 rs20541 GG genotype (OR - 0.48; 95% CI of 0.25 to 0.93; p=0.031). There were no significant differences in the distribution of allelic and genotypic frequencies between patients and controls for the IL4R polymorphism' analyzed. CONCLUSION: These results support the existence of a significant association between GSTP1 rs1695 and IL13 rs20541 SNPs, with susceptibility to asthma, in the population studied. Different genotype profiles of IL17A and IL13 genes seem to influence the clinical pattern of disease expression mainly confined to the upper airways, as rhinitis, or including the lower airways, as asthma.
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The cytokine hormone leptin is a key signalling molecule in many pathways that control physiological functions. Although leptin demonstrates structural conservation in mammals, there is evidence of positive selection in primates, lagomorphs and chiropterans. We previously reported that the leptin genes of the grey and harbour seals (phocids) have significantly diverged from other mammals. Therefore we further investigated the diversification of leptin in phocids, other marine mammals and terrestrial taxa by sequencing the leptin genes of representative species. Phylogenetic reconstruction revealed that leptin diversification was pronounced within the phocid seals with a high dN/dS ratio of 2.8, indicating positive selection. We found significant evidence of positive selection along the branch leading to the phocids, within the phocid clade, but not over the dataset as a whole. Structural predictions indicate that the individual residues under selection are away from the leptin receptor (LEPR) binding site. Predictions of the surface electrostatic potential indicate that phocid seal leptin is notably different to other mammalian leptins, including the otariids. Cloning the grey seal leptin binding domain of LEPR confirmed that this was structurally conserved. These data, viewed in toto, support a hypothesis that phocid leptin divergence is unlikely to have arisen by random mutation. Based upon these phylogenetic and structural assessments, and considering the comparative physiology and varying life histories among species, we postulate that the unique phocid diving behaviour has produced this selection pressure. The Phocidae includes some of the deepest diving species, yet have the least modified lung structure to cope with pressure and volume changes experienced at depth. Therefore, greater surfactant production is required to facilitate rapid lung re-inflation upon surfacing, while maintaining patent airways. We suggest that this additional surfactant requirement is met by the leptin pulmonary surfactant production pathway which normally appears only to function in the mammalian foetus.
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Recent advances in the massively parallel computational abilities of graphical processing units (GPUs) have increased their use for general purpose computation, as companies look to take advantage of big data processing techniques. This has given rise to the potential for malicious software targeting GPUs, which is of interest to forensic investigators examining the operation of software. The ability to carry out reverse-engineering of software is of great importance within the security and forensics elds, particularly when investigating malicious software or carrying out forensic analysis following a successful security breach. Due to the complexity of the Nvidia CUDA (Compute Uni ed Device Architecture) framework, it is not clear how best to approach the reverse engineering of a piece of CUDA software. We carry out a review of the di erent binary output formats which may be encountered from the CUDA compiler, and their implications on reverse engineering. We then demonstrate the process of carrying out disassembly of an example CUDA application, to establish the various techniques available to forensic investigators carrying out black-box disassembly and reverse engineering of CUDA binaries. We show that the Nvidia compiler, using default settings, leaks useful information. Finally, we demonstrate techniques to better protect intellectual property in CUDA algorithm implementations from reverse engineering.
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A síndrome da apneia e hipopneia obstrutiva do sono (SAHOS) é uma patologia que atinge cerca de 4% da população adulta, é uma doença crónica, progressiva, com alta morbilidade e mortalidade. A apneia do sono e o ronco têm despertado a atenção da área da saúde devido às inúmeras comorbilidades associadas. Esta síndrome é caracterizada por obstrução parcial ou total das vias aéreas superiores durante o sono e manifesta-se como uma redução (hipopneia) ou cessação (apneia) do fluxo aéreo. A queixa habitual dos pacientes além dos problemas sociais como ronco e a hipersonolência diurna, são a preocupação com outros quadros que esta patologia pode desencadear, como insuficiência cardíaca e hipertensão pulmonar. O tratamento da apneia obstrutiva do sono é multidisciplinar e indispensável, podendo ser realizado de diversas formas, tanto conservadoras como cirúrgicas, dependendo de inúmeros fatores como a gravidade da doença, as alterações anatómicas das vias aéreas superiores, idade e condições sistémicas do paciente. Os aparelhos intra orais têm sido usados durante anos, no tratamento da SAHOS como controle da obstrução das vias aéreas superiores. A terapia com aparelhos intraorais é simples e reversível. O sucesso do tratamento com aparelhos intra orais para o ronco e SAHOS leve e moderada é comprovado pela grande maioria dos estudos. A facilidade de uso, manutenção e conforto quando comparados a outros tratamentos faz com que os aparelhos intrabucais sejam considerados de fácil aceitação pelos pacientes. Através de uma revisão de literatura discutiu-se o uso de aparelhos intrabucais para o tratamento dessa patologia, destacando a eficácia e as limitações dessa terapia, os principais sintomas clínicos, os principais efeitos colaterais oclusais, o grau de colaboração e o índice de satisfação dos pacientes. Foi possível concluir que aparelhos intrabucais de avanço mandibular estão amplamente indicados para o tratamento do ronco e da SAHOS como terapia principal, ou alternativa naqueles pacientes que não podem suportar a terapia da pressão positiva das vias aéreas e que para o sucesso do tratamento é fundamental uma equipe multidisciplinar, incluindo um Médico Dentista e a colaboração do paciente.