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Purpose: Lung function is typically characterized by spirometer measurements, which do not offer spatially specific information. Imaging during exhalation provides spatial information but is challenging due to large movement over a short time. The purpose of this work is to provide a solution to lung imaging during forced expiration using accelerated magnetic resonance imaging. The method uses radial golden angle stack-of-stars gradient echo acquisition and compressed sensing reconstruction. Methods: A technique for dynamic three-dimensional imaging of the lungs from highly undersampled data is developed and tested on six subjects. This method takes advantage of image sparsity, both spatially and temporally, including the use of reference frames called bookends. Sparsity, with respect to total variation, and residual from the bookends, enables reconstruction from an extremely limited amount of data. Results: Dynamic three-dimensional images can be captured at sub-150 ms temporal resolution, using only three (or less) acquired radial lines per slice per timepoint. The images have a spatial resolution of 4.6 x 4.6 x 10 mm. Lung volume calculations based on image segmentation are compared to those from simultaneously acquired spirometer measurements. Conclusion: Dynamic lung imaging during forced expiration is made possible by compressed sensing accelerated dynamic three-dimensional radial magnetic resonance imaging. (C) 2015 Wiley Periodicals, Inc.

The American alligator (Alligator mississippiensis) is an aquatic diving reptile with a periodic breathing pattern. Previous work has identified pulmonary stretch receptors (PSR), both rapidly- and slowly-adapting, and intrapulmonary chemoreceptors (IPCs) that modulate breathing patterns in alligators. The purpose of the present study was to identify the effects of prolonged lung inflation and deflation (simulated dives) on PSR and/or IPC firing characteristics in the alligator. The effects of airway pressure, hypercapnia, and hypoxia on dynamic and static responses of pulmonary stretch receptors (PSR) were studied in juvenile alligators (mean mass = 246 g) at 24°C. Receptor activity appeared to be a mixture of slowly-adapting PSRs (SARs) and rapidly-adapting PSRs (RARs) with varying thresholds and degrees of adaptation, but no CO2 sensitivity. Dives were simulated in order to character receptor activity before, during, and after prolonged periods of lung inflation and deflation. Some stretch receptors showed a change in dynamic response, exhibiting inhibition for several breaths after 1 min of lung inflation, but were unaffected by prolonged deflation. For SAR, the post-dive inhibition was inhibited by CO2 and hypoxia alone. These airway stretch receptors may be involved in recovery of breathing patterns and lung volume during pre- and post-diving behavior and apneic periods in diving reptiles. These results suggest that inhibition of PSR firing following prolonged inflation may promote post-dive ventilation in alligators.

Pulmonary arterial hypertension (PAH) is a disease of the lung vessels that causes severe effects on the right ventricle of the heart; ultimately, most patients with severe PAH die as a result of right heart failure. However, little is known about the causes of right heart failure. Here, we describe a pattern of gene expression that differs between the normal rat left ventricle (LV) and right ventricle (RV). These genes are known to be involved in the development of the heart as well as adaptations to the heart during stress. This gene expression pattern is used as a baseline to describe changes in gene expression the occur in the RV as a result of adaptive hypertrophy, stimulated by chronic hypoxia, or right ventricular failure (RVF), caused by administration of Su5416 and hypoxia. The genes differing between RVF and hypertrophy encode glycolytic enzymes, mitochondrial electron transport chain complexes, cell-growth promoting proteins, and angiogenic capillary maintenance proteins. Additionally, we show that RVF is associated with an increase in the serum cytokine production of IL-1 beta, IL-10, TNF-alpha, and VEGF. Finally, we show that treatment with the beta-adrenergic receptor blocker carvedilol partially changed the gene expression pattern seen with RVF. The most profound effects were on the genes encoding glycolytic enzymes and mitochondrial electron transport chain complexes. Together, these results show that the normal LV and RV have a distinct pattern of expression and that the failing RV is characterized by changes in cell growth, angiogenesis, and energy utilization. Treatment with carvedilol can partially reverse these gene expression changes in the failing RV.

Mon projet porte d'une part sur le rôle de la voie TGF-b/Alk1 dans l’hypertension artérielle (HTAP) humaine et expérimentale. Le but est d’évaluer in vitro (i) l’expression du TGF-b et de ses récepteurs ALK1/Endogline dans les cellules endothéliales d’artères pulmonaires (CE-AP) de patients atteints d’HTAP idiopathique (HTAPi), (ii) les conséquence de l’activation de la voie TGF-b/ALK1 des CE-AP dans la synthèse de facteurs capables d’induire la prolifération des cellules musculaires lisses d’artères pulmonaires (CML-AP), (iii) identifier par une analyse protéomique différentielle la nature de ses facteurs paracrines, (iv) évaluer chez la souris la conséquence de la déficience en Endogline, co-récepteur de ALK1 sur le développement de l’hypertension artérielle pulmonaire. / My project relates to the role of the TGF-b/Alk1 pathway in human and experimental pulmobnary arterial hypertension (PAH). The goal is to evaluate in vitro (I) the expression of TGF-b and its receptors ALK1/Endoglin in pulmonary arterial endothelial (P-EC) of patients reached of idiopathic PAH (iPAH), (II) the consequence of the activation of the TGF-b/ALK1 pathway on the P-EC in the synthesis of factors able to induce the proliferation of the pulmonary arterial smooth muscle cell (PA-SMC), (III) to identify by a differential proteomic analysis the nature of its factors paracrines, (iv) to evaluate in the mouse the consequence of deficiency in Endoglin (co-receptor of ALK1) on the development of PAH.

ABSTRACT Introduction Circulating levels, and the ex vivo production, of the chemokines CCL3, CCL4, CCL5, CXCL8 and CXCL12 (known to play an important role in the pathogenesis of either human immunodeficiency virus type 1 (HIV-1) or tuberculosis (TB)) were examined in the context of both single infections with HIV-1 or Mycobacterium tuberculosis (Mtb) and coinfection with both organisms. We hypothesised that CCL3L1 gene copy number (known to affect CCL3 production, associated with susceptibility to and disease progression of HIV-1) would be associated with mother-to-child transmission (MTCT) of HIV-1, and that the IL8-251T→A single nucleotide polymorphism (SNP) (associated with enhanced CXCL8 production and susceptibility to TB in African Americans) would be highly represented in the South African Black population. Methods Samples used included (i) plasma, DNA samples and cell culture supernatants from control, HIV-1, TB and HIV-1/TB groups, (ii) DNA samples from mothers and their infants (grouped as HIV-1 exposed-uninfected, infected in utero, or infected intrapartum), and (iii) DNA samples from a populationbased study cohort. Chemokines were quantified by enzyme-linked immunosorbent assay (ELISA), CCL3L1 gene copy numbers were determined by real-time polymerase chain reaction (PCR), and a real-time PCR method was developed for identification of the IL8-251T→A SNP. DNA sequencing was used for confirmation. Results We found reduced ex vivo chemokine production in response to phytohaemagglutinin (PHA) together with increased plasma levels of chemokines in HIV-1 and TB patients. In contrast to that seen in Caucasians (median CCL3L1 copy number of 2), in Black individuals (median CCL3L1 copy number of 5) circulating levels of CCL3 did not correlate with CCL3L1 gene copy number; in addition, a high proportion of Black individuals were found to have CCL3L1 copy numbers below their population-specific median. Using MTCT as a model for studying HIV-1 transmission, infants who became infected with HIV-1 had significantly reduced CCL3L1 gene copy numbers. IL8-251A allele frequencies were found to be 0.41 for Caucasian groups, and 0.85 for Black groups; due to study limitations, the possible association of IL8-251T→A with TB susceptibility could not be addressed. Discussion The increased plasma levels of chemokines seen in HIV-1 and TB, likely due to chronic immune activation in vivo, may result in T cell anergy which in turn might be the cause of reduced PHA-stimulated ex vivo chemokine production. Our results suggest that Black South Africans may be at particularly high risk for acquiring HIV-1 (at least with respect to CCL3L1 gene copy number), and further imply the presence of other genetic polymorphisms which may influence plasma CCL3 levels. In addition, the high IL8-251A allele frequency (if indeed associated with TB in South African populations) in Black individuals suggests a greater risk for infection with Mtb. It will be important, in larger studies, to gain a more in-depth understanding of the relationships between host genotype and chemokine production phenotype, and to relate these measures to infection outcomes. Conclusions Together, these results highlight the importance of gaining an understanding of the effects of host genotype on the development of innate and acquired immunity to HIV-1 and TB, which will be key in the design of efficient therapies and prevention strategies.

Thesis (M.Med.(Paediatrics), Faculty of Health Sciences, University of the Witwatersrand, 2009 / Background In settings with a high burden of tuberculosis, children with unrecognised culture-confirmed pulmonary tuberculosis (PTB) may be discharged from hospital before mycobacterial culture results are available; in these cases clinical improvement may have been due to successful treatment of an intercurrent viral or bacterial co-infection. Aim To estimate the burden of tuberculosis in children who were enrolled in a double-blind, placebo-controlled pneumococcal conjugate vaccine (PCV) trial, and to probe for the presence of pneumococcal co-infection in trial participants who had a hospital-based diagnosis of PTB. Methods A retrospective case-finding strategy was adopted in order to define the tuberculosis case load amongst 39 836 children that had been enrolled in a PCV efficacy trial in Soweto, Gauteng Province. The trial follow-up period was 5.3 years. Children with a hospital-based diagnosis of tuberculosis were categorised by strength of evidence for the disease, HIV status and PCV vaccination status. Incidence rates and risk ratio assessments were conducted using standard statistical methods. Results Four-hundred and ninety-two episodes of tuberculosis arose amongst 425 of the 39 836 PCV Study participants. Tuberculosis incidence was 1067 per 100 000 children (95% Confidence Interval [CI], 968 – 1173), with the greatest burden observed amongst HIV-infected children (10 633 per 100 000 children [95% CI, 9411 – 11 969]; Risk Ratio [RR] 27.5 [95% CI, 22.6 – 33.5], P<0.001). The burden of PTB in the cohort was 982 cases per 100 000 children (95% CI, 887 – 1084): 9895 per 100 000 (95% CI, 8718 – 11 187) in the HIV-infected children and 352 per 100 000 (95% CI 294 – 417) in the HIV-uninfected children (RR 28.1; 95% CI, 22.9 – 34.6), P<0.001. PCV recipients exhibited a 44 percent (95% CI, 11 – 65), P=0.010, reduction in incident culture-confirmed PTB compared to placebo recipients; this apparent reduction was demonstrated chiefly in PCV-vaccinated HIV-infected children (RR 0.53; 95% CI, 0.31 – 0.90) compared to HIV-infected placebo recipients, P=0.017. Conclusions A high burden of tuberculosis is carried by children under 5.3 years in the study setting, with HIV-infected children bearing the brunt of the morbidity. Pneumococcal co-infections are common in the context of hospitalised PTB in the study setting.

A dissertation submitted to the Faculty of Medicine, University of the Witwatersrand, Johannesburg, in partial fulfillment of the requirements for the degree of Master of Medicine (Internal Medicine) Johannesburg 2001 / Introduction and Aim: The waxy outer cell wall of mycobacteria consists mainly of mycolic acids (MA). The unique immuno-stimulatory properties of MA via the CD 1-restricted antigen presentation pathway have been demonstrated in humans. Purification and isolation of M.tuberculosis (MTB) MA has allowed them to be applied as an antigen in an ELISA-based sero-diagnostic assay to detect specific antibodies in the sera of humans. The aim of the study was to measure the levels of antibody to MA in the sera of patients with culture proven pulmonary tuberculosis (PTB), and in control subjects without evidence of tuberculosis. / IT2018

O presente trabalho estuda alguns aspectos epidemiológicos da tuberculose pulmonar na Casa de Detenção de São Paulo, Brasil, durante o período de 1976 a 1980. São analisados dados relativos à prevalência e incidência da infecção tuberculosa, busca de casos pelo método bacteriológico e taxa de transmissibilidade da infecção. Os resultados mostram elevadas taxas de prevalência e incidência de infecção e de casos de tuberculose naquele Estabelecimento Penal, caracterizando população exposta a um alto risco de infecção e de adoecimento por tuberculose. / This paper presents some epidemiological aspects of pulmonary tuberculosis in a state prision of S.Paulo, Brazi1, from 1976 to 1980. Data concerning both the prevalence and incidence of tuberculosis infection, case finding by the bacteriological method and infectivity rate are analysed. Results show high rates of prevalence and incidence of infection as well as of active cases in that institution, characterizing this population as one being exposed to a high risk of infection and of developing tuberculosis.

by Ye Jian. / Abstract in English and Chinese. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1993. / Includes bibliographical references (leaves [140-147]). / ABSTRACT --- p.i / ACKNOWLEDGEMENTS --- p.v / LIST OF ABBREVIATIONS --- p.vi / TABLE OF CONTENTS / Chapter CHAPTER 1 --- Introduction / Chapter 1.1 --- What is the EBI technique --- p.1-1 / Chapter 1.2 --- Applications of the EBI technique --- p.1-2 / Chapter 1.3 --- The electrical impedance rheopneumography-an overview --- p.1-4 / Chapter 1.4 --- Goal of the work --- p.1-6 / Chapter 1.5 --- Main contributions of the work --- p.1-9 / Chapter 1.6 --- Organization of the thesis --- p.1-9 / Chapter CHAPTER 2 --- Principles of the EBI technique and physiological background of the rheopneumogram / Chapter 2.1 --- Tissue impedance and origins of impedance change --- p.2-1 / Chapter 2.1.1 --- Impedance of living organs --- p.2-1 / Chapter 2.1.2 --- Origins of impedance change --- p.2-2 / Chapter 2.2 --- The data acquisition system (DAS) --- p.2-3 / Chapter 2.2.1 --- Impedance detector --- p.2-3 / Chapter 2.2.2 --- Constant current source and safety consideration --- p.2-4 / Chapter 2.2.3 --- Computer interface --- p.2-5 / Chapter 2.3 --- Electrode systems --- p.2-6 / Chapter 2.3.1 --- Two-/four-electrode systems --- p.2-6 / Chapter 2.3.2 --- Geselowitz lead field theory --- p.2-6 / Chapter 2.3.3 --- Comparisons between the two-/four-electrode systems --- p.2-7 / Chapter 2.4 --- The human cardiovascular system --- p.2-8 / Chapter 2.4.1 --- System operation --- p.2-8 / Chapter 2.4.2 --- Pulmonary hemodynamics --- p.2-9 / Chapter 2.5 --- Physiological background of EIR waveform --- p.2-12 / Chapter 2.6 --- EIR wave morphology and pathological factors --- p.2-13 / Chapter 2.6.1 --- Variations in the a-wave --- p.2-13 / Chapter 2.6.2 --- Variations in the Z-wave --- p.2-14 / Chapter 2.6.3 --- Variations in the C-wave --- p.2-14 / Chapter CHAPTER 3 --- THE COMPOSITION OF IMPEDANCE SIGNAL / Chapter 3.1 --- Introduction --- p.3-1 / Chapter 3.1.1 --- Origins of the TIS --- p.3-1 / Chapter 3.1.2 --- EIR measurement and electrode position --- p.3-2 / Chapter 3.1.3 --- Optimal EIR measurement --- p.3-3 / Chapter 3.2 --- Current path in an inhomogeneous medium --- p.3-4 / Chapter 3.3 --- Numerical model --- p.3-5 / Chapter 3.3.1 --- 2D Model --- p.3-5 / Chapter 3.3.2 --- Tissue resistivity --- p.3-6 / Chapter 3.4 --- Calculation of the potential distribution --- p.3-7 / Chapter 3.5 --- Results --- p.3-9 / Chapter 3.5.1 --- Computer simulations --- p.3-9 / Chapter 3.5.2 --- Experimental results --- p.3-13 / Chapter 3.6 --- Discussions --- p.3-14 / Chapter 3.7 --- Conclusion --- p.3-16 / Chapter 3.8 --- Note on publications --- p.3-17 / Chapter CHAPTER 4 --- ON-LINE RESPIRATORY ARTEFACT REMOVAL VIA ADAPTIVE TECHNIQUE / Chapter 4.1 --- Introduction --- p.4-1 / Chapter 4.2 --- Analysis of the TIS --- p.4-3 / Chapter 4.3 --- Modified adaptive noise canceller --- p.4-7 / Chapter 4.3.1 --- Principle of the ANC method --- p.4-8 / Chapter 4.3.2 --- LMS algorithm --- p.4-8 / Chapter 4.3.3 --- MANC method --- p.4-9 / Chapter 4.3.4 --- Results --- p.4-10 / Chapter 4.4 --- Adaptive moving averager --- p.4-15 / Chapter 4.4.1 --- Modified moving averager --- p.4-15 / Chapter 4.4.2 --- Respiratory artefact elimination with adaptive MMA --- p.4-16 / Chapter 4.4.3 --- Performance of the adaptive MMA filter --- p.4-16 / Chapter 4.4.4 --- Results --- p.4-18 / Chapter 4.5 --- Adaptive FIR filter Design --- p.4-22 / Chapter 4.5.1 --- Introduction --- p.4-22 / Chapter 4.5.2 --- Adaptive FIR filter --- p.4-23 / Chapter 4.5.3 --- Results and discussions --- p.4-24 / Chapter 4.6 --- Simultaneously monitoring respiratory and pulmonary circulation- An application of TIS --- p.4-30 / Chapter 4.7 --- Comparisons of the proposed filter schemes --- p.4-33 / Chapter 4.7.1 --- Performance of the filters --- p.4-33 / Chapter 4.7.2 --- Computational complexity and reduced schemes --- p.4-34 / Chapter 4.8 --- Conclusions --- p.4-37 / Chapter 4.9 --- Notes on publications --- p.4-37 / Chapter CHAPTER 5 --- MODELING ANALYSIS OF THE RHEOPNEUMOGRAM / Chapter 5.1 --- Introduction --- p.5-1 / Chapter 5.2 --- Pulmonary circulation modeling --- p.5-2 / Chapter 5.3 --- Model deduction --- p.5-4 / Chapter 5.3.1 --- Pressure-flow in arteries and veins --- p.5-4 / Chapter 5.3.2 --- The two-chamber model and the EIR model --- p.5-5 / Chapter 5.4 --- Parameter estimation --- p.5-8 / Chapter 5.4.1 --- The fitting function and the parameter equations --- p.5-8 / Chapter 5.4.2 --- Curve fitting --- p.5-10 / Chapter 5.4.3 --- Solution of the parameter equations --- p.5-11 / Chapter 5.5 --- Study of the model parameter sensitivity --- p.5-12 / Chapter 5.6 --- Results --- p.5-13 / Chapter 5.7 --- Conclusion --- p.5-17 / Chapter 5.8 --- Notes on publications --- p.5-17 / Chapter CHAPTER 6 --- ANIMAL EXPERIMENTS AND CLINICAL OBSERVATIONS / Chapter 6.1 --- Introduction --- p.6-1 / Chapter 6.2 --- Animal experiments --- p.6-2 / Chapter 6.2.1 --- Methods --- p.6-2 / Chapter 6.2.2 --- Occlusion of the right pulmonary arterial blood flow --- p.6-3 / Chapter 6.2.3 --- Reflection waves in rheopneumogram --- p.6-4 / Chapter 6.3 --- Clinical observations --- p.6-4 / Chapter 6.3.1 --- Mitral valve stenosis --- p.6-5 / Chapter 6.3.2 --- Obstructive emphysema --- p.6-7 / Chapter 6.4 --- Conclusion remarks --- p.6-8 / Chapter 6.5 --- Notes on publications --- p.6-9 / Chapter CHAPTER 7 --- RECAPITULATION AND TOPICS FOR FUTURE INVESTIGATION / Chapter 7.1 --- Recapitulation --- p.7-1 / Chapter 7.2 --- Conclusions --- p.7-3 / Chapter 7.3 --- Topics for future investigation --- p.7-4 / Chapter 7.4 --- Applications of the EIR technique --- p.7-5 / REFERENCES / APPENDICES / Chapter A. --- A circuit diagram of the four-electrode system --- p.A-l / Chapter B. --- NISA/EMAG (A SOFTWARE PACKAGE OF FEM) --- p.A-2 / Chapter C. --- LMS algorithm --- p.A-3 / Chapter D. --- Curve fitting --- p.A-5 / Chapter E. --- List of publications --- p.A-8