Yes / Extensive research has demonstrated the potential effectiveness of curcumin against various diseases, including asthma and cancers. However, few studies have used liquid-based vehicles in the preparation of curcumin formulations. Therefore, the current study proposed the use of nanoemulsion and microsuspension formulations to prepare nebulised curcuminoid for lung delivery. Furthermore, this work expressed a new approach to understanding the aerosol performance of nanoparticles compared to microsuspension formulations. The genotoxicity of the formulations was also assessed. Curcuminoid nanoemulsion formulations were prepared in three concentrations (100, 250 and 500 µg/ml) using limonene and oleic acid as oil phases, while microsuspension solutions were prepared by suspending curcuminoid particles in isotonic solution (saline solution) of 0.02% Tween 80. The average fine particle fraction (FPF) and mass median aerodynamic diameter (MMAD) of the nebulised microsuspension formulations ranged from 26% and 7.1 µm to 40% and 5.7 µm, for 1000 µg/ml and 100 µg/ml respectively. In a comparison of the low and high drug concentrations of the nebulised nanoemulsion, the average FPF and MMAD of the nebulised nanoemulsion formulations prepared with limonene oil ranged from 50% and 4.6 µm to 45% and 5.6 µm, respectively; whereas the FPF and MMAD of the nebulised nanoemulsion prepared with oleic acid oil ranged from 46% and 4.9 µm to 44% and 5.6 µm, respectively. The aerosol performance of the microsuspension formulations were concentration dependent, while the nanoemulsion formulations did not appear to be dependent on the curcuminoids concentration. The performance and genotoxicity results of the formulations suggest the suitability of these preparations for further inhalation studies in animals.

Yes / Mycobacterium kansasii is an opportunistic pathogen and one of the most commonly encountered species in individuals with lung disease. We here report the complete genome sequence of 12 clinical isolates of M. kansasii from patients with pulmonary disease in Brazil. / CNPq (scholarships 207422/2014-1, 500769/2014-1, 311554/2013-0; grants 407624/2012-0, 459100/2014-9).

Lung cancer is the leading cause of cancer-related deaths worldwide. One of the most common genetic aberrations in lung cancer patients is Kirsten rat sarcoma viral oncogene homolog (KRAS). The KRAS protein is a Ras superfamily GTPase that switches between an active GTP-bound form and an inactive GDP-bound form. The consequence of KRAS mutations results in constitutively active downstream pathways involved in uncontrolled cell proliferation and survival. Fortunately, there has been a recent development of KRASG12C inhibitors that directly target mutant KRAS, thereby arresting its proliferative effects. A recently FDA-approved KRASG12C inhibitor for the treatment of non-small cell lung cancer, Sotorasib (AMG 510), has been shown to produce insubstantial clinical response rates and a short duration of response. Similar to other targeted therapies, the limitations of this treatment are primarily due to the emergence of drug resistance. Drug resistance has been studied extensively regarding other anticancer treatments; however, the underlying molecular mechanisms remain poorly characterized. Our investigation begins by establishing and analyzing a subpopulation of cancer cells that evolve and mediate drug resistance, known as drug-tolerant persister cells (DTPCs), in KRASG12C mutant cells using AMG 510. First, we observed the reactivation of a pro-proliferative kinase, ERK, in AMG 510 DTPCs. Additionally, whole transcriptomics analysis, RT-qPCR, and immunofluorescent staining demonstrated significant upregulation of AQP4 in AMG 510 DTPCs compared to drug sensitive cells (DSCs). Aquaporin 4 (AQP4) is a water-selective transmembrane protein that regulates fluid homeostasis in many organ systems, including the lungs, and is involved in intracellular calcium signaling. We aim to explore the connections between AQP4, ERK, and calcium signaling in promoting drug tolerance to AMG 510. The insights gained from this research could lead to improved targeted therapies and clinical outcomes by identifying AQP4 as a resistance-driving biomarker.

Yes / Lung cancer remains a major cause of preventable death and early diagnosis is critical to improving survival chances. The chest X-ray (CXR) remains the most common initial investigation, but clinical pathways need to support timely diagnosis through, where necessary, escalation of abnormal findings to ensure priority reporting and early CT scan. This single-centre study included a retrospective evaluation of a rapid lung cancer CXR pathway in its first year of operation (May 2018-April 2019). The pathway was initially designed for primary care referrals but could also be used for any CXR demonstrating abnormal findings. A parallel cross-sectional survey of radiographers explored their understanding, adherence and concerns regarding their role in the pathway operation. Primary care referrals on the rapid diagnostic pathway were low (n = 51/21,980; 0.2%), with 11 (21.6%) requiring a CT scan. A further 333 primary care CXR were escalated by the examining radiographer, with 100 (30.0%) undergoing a CT scan. Overall, 64 of the CT scans (57.7%) were abnormal or demonstrated suspicious findings warranting further investigation. There were 39 confirmed primary lung carcinomas, most with advanced disease. Survey responses showed that most radiographers were familiar with the pathway but some expressed concerns regarding their responsibilities and limited knowledge of CXR pathologies. This baseline evaluation of the rapid lung cancer pathway demonstrated poor referral rates from primary care and identified the need for improved engagement. Radiographer escalation of abnormal findings is an effective adjunct but underlines the need for appropriate awareness, training, and ongoing support. Engagement of the multiprofessional team is critical in new pathway implementation. Rapid diagnostic pathways can enable early diagnosis and the radiographer has a key role to play in their success.

Thesis (MScPhysio)--Stellenbosch University, 2015. / ENGLISH ABSTRACT: Background: Pulmonary tuberculosis (PTB) remains a major concern worldwide. Although PTB is curable, both the disease and its treatment may have considerable medical, social and psychological consequences which may result in a decreased quality of life and functioning. Characterization of the functional capabilities of PTB patients post-treatment and the impact of PTB on their quality of life may identify a need for more holistic management of PTB treatment that extends beyond microbiological cure. Methods: Firstly, an in-depth scoping review was conducted using the following key words: Pulmonary tuberculosis (MESH term) and Health related quality of life (HRQoL), Pulmonary tuberculosis (MESH term) and Spirometry and Pulmonary tuberculosis (MESH term) and Six minute walk test or 6MWT to review the current literature reporting on the HRQoL, lung function measurements and exercise capacity of a PTB population (Chapter 2). Secondly, a cross-sectional, quantitative, descriptive study was conducted. The study setting included five primary health care facilities (PHCF) in the Breede Valley sub-district of the Cape Winelands East District, Western Cape, South Africa. Adult patients diagnosed with PTB, 18 years and older and who were successfully managed through the Cape Winelands District Health Care system were considered for the study if they had least two negative sputum sample results and had completed at least five months of anti-tuberculosis treatment. Post treatment bronchodilator lung function tests, health related quality of life using the BOLD core questionnaire and six minute walk test distance (6MWD) was measured. Findings: The comprehensive broad search of the literature yielded a total of 2446 articles. A total of 2422 articles were excluded since the title; abstract or full text article did not conform to the review question or were eliminated as duplicates across databases. Twenty-seven articles divided amongst the three subsections i.e. PTB and HRQoL (n=13), PTB and Spirometry (n=9) and PTB and exercise capacity (n=6), were included in the review. In the cross-sectional study, 328 names were obtained from the TB registers of the five included PHCF of which 45 patients were included in the study (56% male; mean age, 39.88±10.20 years). The majority of patients (n= 206; 63%) were not contactable, and could not be recruited. Approximately half the total sample, (n=23; 52%) presented with normal lung function while n=11 (25%) presented with a restrictive pattern, n=9 (21%) presented with an obstructive pattern and only n=1 (2%) presented with a mixed pattern (defined as FEV1<80% predicted, FVC<80% predicted and FEV1/FVC<0.7). The mean six minute walk distance (6MWD) was 294.5m±122.7m. Respondents scored poorly on all sub-domains of the SF-12v2 except vitality. Role emotional and role physical scored lowest with mean scores of 28.1 and 35.27 respectively, while vitality scored the highest with 52.78. Stellenbosch University https://scholar.sun.ac.za 4 | P a g e Conclusion The findings of this thesis suggest that even after microbiological cure, PTB patients may suffer from a decreased quality of life, impaired lung function and a decreased exercise capacity. Specific challenges to data collection in a rural region were identified; which included patient recruitment, field testing of exercise capacity (6MWD), and the generalizabilty of standardized questionnaires in rural regions. The findings of this pilot study serves to inform the planning of a larger observational study, in the rural Cape Winelands of the Western Cape, South Africa. / AFRIKAANSE OPSOMMING: Agtergrond Pulmonêre tuberkulose (PTB) wek wêreldwyd steeds groot kommer. Hoewel dit geneeslik is, kan die siekte sowel as die behandeling daarvan beduidende mediese, maatskaplike en sielkundige gevolge hê, wat lewensgehalte en funksionering kan knou. Die tipering van PTB-pasiënte se funksionele vermoëns ná behandeling sowel as die impak van PTB op hul lewensgehalte kan dalk dui op ’n behoefte aan die meer holistiese bestuur van PTB-behandeling, wat méér as blote mikrobiologiese genesing insluit. Metodes Eerstens is ’n diepgaande bestekstudie aan die hand van die volgende trefwoorde onderneem: pulmonêre tuberkulose (MeSH-term) en gesondheidsverwante lewensgehalte (HRQoL), pulmonêre tuberkulose (MeSH-term) en spirometrie, en pulmonêre tuberkulose (MeSH-term) en die ses minute lange stapafstandtoets (6MWT). Na aanleiding daarvan is die huidige literatuur oor die HRQoL, longfunksiemetings en oefenvermoë van ’n PTB-populasie bestudeer (hoofstuk 2). Tweedens is ’n kwantitatiewe, beskrywende deursneestudie onderneem. Die studie-omgewing het bestaan uit vyf fasiliteite vir primêre gesondheidsorg in die Breedevallei-subdistrik van die streek Kaapse Wynland-Oos, Wes-Kaap, Suid-Afrika. Volwasse pasiënte van 18 jaar en ouer wat met PTB gediagnoseer is en suksesvol deur die distriksgesondheidsorgstelsel van die Kaapse Wynland-streek bestuur word, is vir die studie oorweeg indien minstens twee van die pasiënt se sputummonsters TB-negatiewe resultate opgelewer het en die persoon reeds minstens vyf maande vir tuberkulose behandel is. Studiemetings het ingesluit brongodilator-longfunksietoetse ná behandeling, gesondheidsverwante beoordelings van lewensgehalte met behulp van die BOLD-vraelys, en die aflegging van ’n ses minute lange stapafstandtoets (6MWT). Bevindinge Die omvattende breë soektog van die literatuur het 'n totaal van 2446 artikels opgelewer. 'n Totaal van 2422 artikels is uitgesluit, aangesien die titel; abstrakte of volledige teks artikel het nie voldoen aan die navorsings vraag, of is uitgeskakel as duplikate oor databasisse. Sewe en twintig artikels verdeel tussen die drie onderafdelings, naamlik PTB en HRQoL (n = 13), PTB en Spirometrie (n = 9) en PTB en oefening kapasiteit (n = 6), is ingesluit in die oorsig. In die deursneestudie is 328 name uit die TB-registers van die vyf ondersoekpersele bekom. Altesaam 45 pasiënte (56% mans; gemiddelde ouderdom 39.88±10.20 jaar) is by die studie ingesluit. Die oorgrote meerderheid pasiënte (n = 206; 63%) kon nie bereik word nie, en dus ook nie gewerf word nie. Ongeveer die helfte van die algehele steekproef (n = 23; 52%) se longfunksie was normaal; n = 11 (25%) het ’n restriktiewe patroon getoon; n = 9 (21%) ’n obstruktiewe patroon, en slegs n = 1 (2%) ’n gemengde patroon (wat omskryf word as ’n FEV1-voorspellingswaarde van <80%, ’n FVC-voorspellingswaarde van <80%, en FEV1/FVC van <0.7). Die gemiddelde afstand wat in die ses minute lange staptoets afgelê is (6MWD), was 294,5 m±122,7 m. Respondente behaal swak Stellenbosch University https://scholar.sun.ac.za 6 | P a g e op al die sub-domein van die SF-12v2 behalwe vitaliteit. Rol emosionele en rol fisiese behaal laagste met die gemiddelde tellings van 28.1 en 35,27 onderskeidelik, terwyl vitaliteit behaal die hoogste met 52,78. Gevolgtrekking Die bevindinge van hierdie tesis gee te kenne dat PTB-pasiënte selfs ná mikrobiologiese genesing dalk swakker lewensgehalte, verswakte longfunksie en ’n afname in oefenvermoë ondervind. Bepaalde uitdagings vir data-insameling in ’n landelike omgewing is uitgewys, onder meer pasiëntewerwing, veldtoetsing van oefenvermoë (6MWD) en die veralgemeenbaarheid van gestandaardiseerde vraelyste in landelike gebiede. Die bevindinge van hierdie proefstudie kan gebruik word om die beplanning van ’n groter waarnemingstudie in die landelike Kaapse Wynland-streek in die Wes-Kaap, Suid-Afrika, te rig.

Bronchopulmonary dysplasia (BPD) is a chronic neonatal lung injury (CNLI) affecting infants of < 32 weeks gestation, which has a significant associated morbidity and mortality. The hallmarks of BPD as seen in the current era are arrested alveologenesis and parenchymal thickening. Those most severely affected may develop pulmonary hypertension which worsens the prognosis. No effective preventive therapy exists. Generation of damaging reactive oxygen species is implicated in its development. The more recently recognized reactive nitrogen species may also contribute to this disease. Thus, there is considerable interest in preventive antioxidant therapies, but results to date have not been promising. Newborn rats, exposed to 60% O2 for 14 days, develop a parenchymal injury and pulmonary hypertension that resembles the morphological features of human BPD. Previous studies have shown that following exposure to 60% O2, a pulmonary influx of neutrophils is followed by that of macrophages. Inhibiting the influx of neutrophils prevents the generation of reactive oxygen species, while simultaneously enhancing postnatal lung growth. Other interventions have shown that development of pulmonary hypertension is dependent upon increases in both 8-isoprostane and its downstream regulator of vascular tone, endothelin-1. Gentler ventilation strategies, incorporated to minimize induction of stretch-mediated pro-inflammatory cytokines, have shown benefits of permissive hypercapnia in adult lung injury. Multicentre clinical trials of permissive hypercapnia in neonates have not shown benefit. Therapeutic hypercapnia has been demonstrated to have a protective effect of PaCO2 in both acute studies of ventilator-induced and ischemia-reperfusion injuries in animal models. In the studies reported herein, therapeutic hypercapnia was found to completely protect against CNLI and attenuate 60% O2-induced macrophage-derived protein nitration. The likely nitrating agent was macrophage-derived peroxynitrite. The critical role of peroxynitrite, in the development of chronic neonatal lung injury in this model, was confirmed using a peroxynitrite decomposition catalyst. This protected against the impairments of alveolarization and of pulmonary vascularization induced by 60% O2. These results suggest a more significant role for reactive nitrogen species than previously recognized. Finally, preliminary evidence is presented supporting a role for neutrophil-derived elastase in initiating the macrophage influx in the lungs, required for peroxynitrite generation, during 60% O2-mediated injury.

While realistic in vitro testing of dry powder inhalers (DPIs) can be used to establish in vitro–in vivo correlations (IVIVCs) and predict in vivo lung doses, the aerodynamic particle size distributions (APSDs) of those doses and their regional lung deposition remains unclear. Four studies were designed to improve testing centered on the behavior of Novolizer®. Different oropharyngeal geometries were assessed by testing different mouth-throat (MT) models across a realistic range of inhalation profiles (IPs) with Salbulin® Novolizer®. Small and large Virginia Commonwealth University (VCU) and Oropharyngeal Consortium (OPC) models produced similar ranges for total lung dose in vitro (TLDin vitro), while results for medium models differed significantly. While either group may be selected to represent variations in oropharyngeal geometry, OPC models were more difficult to use, indicating that VCU models were preferable. To facilitate simulation of human IPs through DPIs, inhalation profile data from a VCU clinical trial were analyzed. Equations were developed to represent the range of flow rate vs. time curves for use with DPIs of known airflow resistance. A new method was developed to couple testing using VCU MT models and simulated IPs with cascade impaction to assess the APSDs of TLDin vitro for Budelin® Novolizer®. This method produced IVIVCs for Budelin’s total lung dose, TLD, and was sufficiently precise to distinguish between values of TLDin vitro and their APSDs, resulting from tests using appropriately selected MT models and IPs. For example, for slow inhalation, TLD values were comparable in vivo and in vitro; TLDin vitro ranged from 12.2±2.9 to 66.8±1.7 mcg aerosolized budesonide while APSDs in vitro had mass median aerodynamic diameters of 3.26±0.27 and 2.17±0.03 µm, respectively. To explore the clinical importance of these variations, a published computational fluid dynamic (CFD) model was modified and coupled to accept the output of realistic in vitro tests as initial conditions at the tracheal inlet. While simplified aerosol size metrics and flow conditions used to shorten CFD simulations produced small differences in theoretical predictions of regional lung deposition, the results broadly agreed with the literature and were generally consistent with the median values reported clinically for Budelin.

A lesão pulmonar aguda é caracterizada por inflamação pulmonar podendo ser induzida diretamente (LPD), por inalação de lipopolissacarídeo (LPS), ou indiretamente (LPI), por mediadores inflamatórios liberados por órgãos distantes após lesão de isquemia e reperfusão (IR). A Bradicinina, mediador inflamatório, pode agir em dois receptores, um constitutivo (B2R), e um induzido por citocinas inflamatórias (B1R). Neste trabalho verificamos o papel do B1R em modelos de LPD e LPI. Em camundongos C57bl/6, a LPD foi induzida por tratamento intra-nasal com LPS, e a LPI foi induzida por 45 minutos de IR renal. Observamos alterações pulmonares em ambos os modelos de lesão 24 horas após o insulto, como aumento de infiltrado celular, hiperreatividade pulmonar à metacolina, aumento de permeabilidade vascular, e citocinas pró-inflamatórias. Bloqueamos o B1R com antagonista e vimos que a lesão pulmonar foi diminuída em ambos os modelos de lesão. Assim, sugerimos que o B1R contribui tanto para a LPD, induzida por LPS, quanto para a LPI, induzida por IR renal. / The acute lung injury (ALI) is characterized by lung inflammation and can be induced directly by lipopolysaccharides inhalation, or indirectly, by systemic inflammatory mediators released from distant organs after and ischemia and reperfusion injury (IRI). Bradykinin, an inflammatory mediator, can act in two different receptors; one is constitutive (B2R), whereas the other is induced by inflammatory cytokines (B1R). We aimed to study the role of B1R in models of direct and indirect ALI. Direct ALI was induced by LPS instillation in C57bl/6 mice, while indirect ALI was induced by 45 minutes of renal IRI. In both injuries, 24 hours after insult, animals presented an increase in cellular infiltration, vascular permeability, hyperreactivity to methacholine, and an up-regulation of pro-inflammatory cytokines in lungs. We blocked the B1R using antagonist and observed that the lung injury was attenuated in both injury models. Thus, we suggest that B1R has an important role in the development of both, direct ALI, induced by LPS, and indirect ALI induced by renal IRI.

INTRODUÇÃO: O transplante pulmonar é terapia reconhecida de tratamento de doenças terminais pulmonares. Os pulmões, entretanto, são muito susceptíveis às transformações hormonais e hidroeletrolíticas ocorridas no doador após a morte encefálica. As baixas taxas de aproveitamento dos pulmões alavancam pesquisas e meios de utilizar pulmões considerados nãoideais. Um desses modelos é o recondicionamento pulmonar ex-vivo concebido por Steen, no qual se utiliza uma solução hiperosmolar (Steen Solution®) para avaliação e melhora dos pulmões doados. Consideramos que o desenvolvimento de uma solução de recondicionamento pulmonar produzida no Brasil seria conveniente aos serviços de transplante e aos pacientes. Foram comparadas a solução de recondicionamento Steen Solution® e uma solução de fabricação nacional em modelo de ex vivo de pulmões humanos não aceitos para transplante, através da avaliação da mecânica ventilatória, hemodinâmica, trocas gasosas e histologia. MÉTODOS: Foram utilizados 16 pulmões de doadores em morte encefálica, considerados inadequados para o transplante pulmonar. Os pulmões foram submetidos à captação habitual e acondicionados sob isquemia fria por 10 horas. Após este período, os pulmões foram designados, por sorteio, para reperfusão com a solução padrão (Steen solution®) ou a solução nacional por 1h em modelo ex vivo. A lesão pulmonar foi estudada através de parâmetros gasométricos, resistência pulmonar e complacência pulmonar. Foram medidos os pesos em três tempos e relação peso úmido/peso seco após a reperfusão para avaliação de edema. A partir de biópsias seriadas era calculado um score de lesão tecidual e grau de apoptose. RESULTADOS: A capacidade de oxigenação foi de 498,00 ± 37,53 mmHg no grupo STEEN e 521,00 ± 55,43 mmHg no grupo SRNac (p = 0,348). A capacidade relativa de oxigenação calculada ao final do recondicionamento foi 501,37 ± 207,77 no grupo STEEN e 470,30 ± 232,41 no grupo SRNac (p=0,782). Os pesos dos pulmões nos três momentos de avaliação foram: início da isquemia: STEEN = 1.026 ± 451 g, SRNac = 745 ± 282 g (p = 0,180); fim da isquemia: STEEN = 998 ± 391 g, SRNac = 738 ± 316 g (p = 0,184); e fim da reperfusão: STEEN = 1.097 ± 526 g, SRNac = 743 ± 248 g (p = 0,163). A relação peso úmido/peso seco foi 3,63 ± 1,26 no grupo SRNac e 2,06 ± 0,28 no grupo STEEN (p = 0,009). A resistência vascular pulmonar foi 787,99 ± 367,23 dina.s.cm-5 no grupo STEEN e 1.026,81 ± 1.112,53 dina.s.cm-5 no grupo SRNac (p = 0,575). A complacência pulmonar média foi 46,75 ± 20,99 mL/cmH2O no grupo STEEN e 49,74 ± 26,11 cmH2O no grupo SRNac (p = 0,809). O Escore de Lesão Pulmonar foi: STEEN = 4,38 ± 1,51 e SRNac = 4,50 ± 1,77 (p = 0,881). O número de células apoptóticas foi: STEEN = 2,4 ± 2,0 cel/mm2 e SRNac = 4,8 ± 6,9 cel/mm2 (p = 0,361). CONCLUSÕES: Os pulmões reperfundidos com a solução de recondicionamento de fabricação nacional apresentaram características morfológicas e funcionais similares aos que foram reperfundidos com a solução STEEN®, apesar do maior edema encontrado no grupo da solução nacional / INTRODUCTION: Lung transplantation is routine treatment of end-stage lung diseases. The lungs, however, are very susceptible to hormonal and electrolyte changes occurred in the donor after brain death. The low recovery rates of the lungs leverage researches and ways to use lungs considered non-ideal. One such model is the lung ex vivo reconditioning designed by Steen, in which using a hyperosmolar solution (Steen Solution®) for evaluation and improvement of donor lungs. We believe that the development of a pulmonary reconditioning solution produced in Brazil would be convenient to transplantation service and patients. Were compared the standard Steen Solution® and a national manufacturing solution in ex vivo model with human lungs not accepted for transplant, through the evaluation of respiratory mechanics, hemodynamics, gas exchange and histology. METHODS: 16 brain-dead donors lungs, considered unsuitable for lung transplantation, were used. The lungs were harvest as usual, packed and stored in cold ischemia for 10 hours. After this period, the lungs were appointed by randomization to reperfusion with the standard solution (Steen Solution®) or national solution for 1 h in ex vivo model. Lung injury was accessed by blood gas parameters, lung resistance and lung compliance. The weights were measured in three times and the after reperfusion wet weight / dry weight ratio for evaluation of edema. The degree of apoptosis and tissue injury score was calculated from serial biopsies. RESULTS: The oxygenation capacity was 498.00 ± 37.53mmHg in STEEN group and 521.00 ± 55.43mmHg in SRNac group (p = 0.348). The relative oxygenation capacity calculated at the end of the reconditioning was 501.37 ± 207.77 in the STEEN group and 470.30 ± 232.41 in the SRNac group (p = 0.782). The weights of lungs in the three stages of evaluation were: onset of ischemia: STEEN = 1,026 ± 451g, SRNac = 745 ± 282g (p = 0.180); end of ischemia: STEEN = 998 ± 391g, SRNac = 738 ± 316g (p = 0.184); and the end of reperfusion: STEEN = 1,097 ± 526g, SRNac = 743 ± 248g (p = 0.163). The wet weight / dry weight ratio was 3.63 ± 1.26 in SRNac group and 2.06 ± 0.28 in STEEN group (p = 0.009). Pulmonary vascular resistance was 787.99 ± 367.23dina.s.cm-5 in STEEN group and 1026.81 ± 1112.53dina.s.cm-5 in SRNac group (p = 0.575). The Lung Injury Score was: STEEN = 4.38 ± 1.51 and SRNac = 4.50 ± 1.77 (p = 0.881). The number of apoptotic cells was: STEEN = 2.4 ± 2.0 cells / mm 2 and SRNac = 4.8 ± 6.9 cells / mm2 (p = 0.361). CONCLUSIONS: The lungs reperfused with national manufacturing reconditioning solution presented morphological and functional characteristics similar to those reperfused with STEEN® solution despite the greater edema found in the group of national solution

Yu, Kai Shing. / "November 2010." / Thesis (M.Phil.)--Chinese University of Hong Kong, 2011. / Includes bibliographical references (leaves 103-114). / Abstracts in English and Chinese. / Abstract --- p.2 / 中文摘要 --- p.6 / List of Contents --- p.9 / List of Table --- p.12 / Abbreviation --- p.13 / Acknowledgement --- p.14 / Chapter Chapter 1: --- Introduction --- p.15 / Chapter 1.1 --- Epidemiology of lung cancer --- p.15 / Chapter 1.2 --- Overview of significant prognostic factors for patients with NSCLC --- p.18 / Chapter 1.2.1 --- Tumor related factors --- p.19 / Chapter 1.2.2 --- Patient related factors --- p.21 / Chapter 1.3 --- Overview of significant prognostic factors for SCLC patients --- p.22 / Chapter Chapter 2: --- Literature Review --- p.25 / Chapter 2.1 --- Prevalence of co-morbidity among lung cancer patients --- p.25 / Chapter 2.2 --- Impact of co-morbidity on non small cell lung cancer patients --- p.28 / Chapter 2.3 --- Impact of co-morbidity on small cell lung cancer patients --- p.36 / Chapter 2.4 --- Summary of evidence from literature review --- p.40 / Chapter Chapter 3: --- Aim and Objectives --- p.42 / Chapter 3.1 --- General aim --- p.42 / Chapter 3.2 --- Specific objectives --- p.42 / Chapter 3.3 --- Main hypothesis --- p.42 / Chapter Chapter 4: --- Methodology --- p.43 / Chapter 4.1 --- Research design --- p.43 / Chapter 4.2 --- Study population --- p.43 / Chapter 4.3 --- Sample size estimation --- p.45 / Chapter 4.4 --- Data collection --- p.47 / Chapter 4.4.1 --- Demographic information --- p.47 / Chapter 4.4.2 --- Co-morbidity --- p.51 / Chapter 4.4.3 --- Adverse symptoms --- p.51 / Chapter 4.4.4 --- Disease characteristics --- p.52 / Chapter 4.4.5 --- Baseline laboratory findings --- p.53 / Chapter 4.4.6 --- Treatment data --- p.53 / Chapter 4.4.7 --- Follow up --- p.53 / Chapter 4.5 --- Statistical analyses --- p.54 / Chapter Chapter 5: --- Results --- p.56 / Chapter 5.1 --- Description of cohort --- p.56 / Chapter 5.2 --- Baseline characteristics --- p.58 / Chapter 5.3 --- Symptom presentation --- p.62 / Chapter 5.4 --- Histological characteristics --- p.64 / Chapter 5.5 --- Treatment characteristics --- p.67 / Chapter 5.6 --- Haematological characteristics of study population --- p.69 / Chapter 5.7 --- Prevalence of co-morbidity --- p.71 / Chapter 5.8 --- Overall survival --- p.74 / Chapter 5.8.1 --- Univariate and multivariate survival analysis for SCLC patients --- p.75 / Chapter 5.8.2 --- Univariate and multivariate survival analysis for NSCLC patients --- p.77 / Chapter 5.8.3 --- In-depth analyses for the Impact of co-morbidity on lung cancer survival --- p.79 / Chapter 5.8.4 --- Selected underlying causes of death --- p.84 / Chapter Chapter 6: --- Discussion --- p.85 / Chapter 6.1 --- Prognostic factors --- p.85 / Chapter 6.2 --- Prevalence of co-morbidity --- p.89 / Chapter 6.3 --- Impact of co-morbidity on lung cancer survival --- p.92 / Chapter 6.4 --- Strengths and limitations of this study --- p.97 / Chapter Chapter 7: --- Conclusions --- p.101 / Chapter Chapter 8: --- Implications and Recommendations for medial practice --- p.102 / References --- p.103