Lung nodule volumetry is used to diagnose the likelihood of malignancy in nodules detected during thoracic CT scans. These measurements are unreliable when the patient is subject to respiratory motion. We seek to understand the relationship between reconstructed images and the actual size of nodules subject to motion induced by quiet breathing. CT images of solid spheres of varying size and composition were acquired while travelling through a known path to approximate the motion of a pulmonary nodule during respiration. The measured size of the sphere’s image was found to increase non-linearly with speed. However, these relationships were dependent on the CT number of the sphere and the reconstruction filter used to generate the image. From these results we expect that for a specific CT number we can estimate the size of an object from a CT image if the speed of the object at the time of the scan is known.

Recently, we discovered patients with inherited adenosine deaminase (ADA) deficiency are predisposed to pulmonary alveolar proteinosis (PAP). PAP is characterized by the accumulation of surfactant in the alveoli. To overcome ethical issues and limited patient samples, animal models are often utilized. Here, I investigated the lung abnormalities in ADA deficient (ADA -/-) mice, which suffer from severe hypoxia, till their death at 3 weeks. I hypothesized that, similar to ADA-deficient patients, ADA -/- mice demonstrate evidence of PAP. Indeed, electron microscopy showed thickening of type I cells, accumulation of apoptotic foamy alveolar macrophages, cholesterol and lipoproteinaceous material that is periodic-acid Schiff (PAS) positive and diagnostic of PAP. Moreover, the pulmonary abnormalities were corrected with supplementation of ADA. In conclusion, we demonstrated evidence of PAP in ADA -/- mice for the first time and their suitability to study pathogenesis of PAP in ADA deficiency.

This investigator studied the right upper lobe of the lung in 16 autopsy cases with 11 different systemic and pulmonary pathologies. Four of the lungs were diagnosed as normal, six as emphysematous, and six had other recognizable pathology. Portions of each lung were fixed in Bouin's solution, embedded in paraffin, and sectioned at five microns. They were stained with the Periodic Acid Stain and observed under the phase contrast microscope. The alveolar-capillary basement membrane appeared blue under phase contrast in comparison to the surrounding tissue which was red. There was no statistical difference found in the alveolar-capillary basement membrane width of normal lung versus the emphysematous lung or the lung of a case with any other pulmonary pathology that was studied. The phase contrast microscope proved to be a valuable tool for studying the basement membrane in the lung.Ball State UniversityMuncie, IN 47306

The alveoli of mammalian lungs are covered in a thin lipid film referred to as pulmonary surfactant. The primary purpose of pulmonary surfactant is to reduce the surface tension of the air/liquid interface allowing breathing with minimal effort required. We investigated the effect of addition of cholesterol and amyloid-β peptide on structure and function of Bovine Lung Extract Surfactant (BLES) and model lipid films. In our first experiment, we have demonstrated the effect of amyloid-β and cholesterol on lipid films of DPPC, DPPC-DOPG and BLES. We saw that cholesterol inhibits multilayer formation in all monolayers. Amyloid-β increases multilayer formation in DPPC and DPPC-DOPG, but reduced multilayer formation in BLES. When cholesterol and amyloid-β is added to BLES, 1% amyloid-β is inconsequential, whereas 10% amyloid-β allows BLES to regain some of its surfactant function. In our second experiment, we observed that for bothanionic DOPG and cationic DOTAP films which are in the fluid phase, amyloid-β interacts with the bilayer much quicker than in zwitterionic DPPC which is in the gel phase. Approaching 24 hours, we see small fibrils form on the bilayer, but these fibrils are considerably smaller than those formed when amyloid-β is incubated in solution. For fluid phase bilayer membrane, disruption is also observed. We investigated the effect of addition of cholesterol and amyloid-β peptide on structure and function of Bovine Lung Extract Surfactant (pulmonary surfactant BLES) and model lipid films. In our first experiment, we have demonstrated the effect of amyloid-β and cholesterol on lipid films of DPPC, DPPC-DOPG and BLES. We saw that cholesterol inhibits multilayer formation in all monolayers. Amyloid-β increases multilayer formation in DPPC and DPPC-DOPG, but reduced multilayer formation in BLES. When cholesterol and amyloid-β is added to BLES, 1% amyloid-β is in consequential, whereas 10% amyloid-β allows BLES to regain some of its surfactant function. In our second experiment, we observed that in anionic DOPG films, amyloid-β inserts into the bilayer much quicker than in zwitterionic DPPC. Approaching 24 hours, we see small fibrils form in the bilayer, but these fibrils are considerably smaller than those formed when amyloid-β is incubated in solution.

The alveoli of mammalian lungs are covered in a thin lipid film referred to as pulmonary surfactant. The primary purpose of pulmonary surfactant is to reduce the surface tension of the air/liquid interface allowing breathing with minimal effort required. We investigated the effect of addition of cholesterol and amyloid-β peptide on structure and function of Bovine Lung Extract Surfactant (BLES) and model lipid films. In our first experiment, we have demonstrated the effect of amyloid-β and cholesterol on lipid films of DPPC, DPPC-DOPG and BLES. We saw that cholesterol inhibits multilayer formation in all monolayers. Amyloid-β increases multilayer formation in DPPC and DPPC-DOPG, but reduced multilayer formation in BLES. When cholesterol and amyloid-β is added to BLES, 1% amyloid-β is inconsequential, whereas 10% amyloid-β allows BLES to regain some of its surfactant function. In our second experiment, we observed that for bothanionic DOPG and cationic DOTAP films which are in the fluid phase, amyloid-β interacts with the bilayer much quicker than in zwitterionic DPPC which is in the gel phase. Approaching 24 hours, we see small fibrils form on the bilayer, but these fibrils are considerably smaller than those formed when amyloid-β is incubated in solution. For fluid phase bilayer membrane, disruption is also observed. We investigated the effect of addition of cholesterol and amyloid-β peptide on structure and function of Bovine Lung Extract Surfactant (pulmonary surfactant BLES) and model lipid films. In our first experiment, we have demonstrated the effect of amyloid-β and cholesterol on lipid films of DPPC, DPPC-DOPG and BLES. We saw that cholesterol inhibits multilayer formation in all monolayers. Amyloid-β increases multilayer formation in DPPC and DPPC-DOPG, but reduced multilayer formation in BLES. When cholesterol and amyloid-β is added to BLES, 1% amyloid-β is in consequential, whereas 10% amyloid-β allows BLES to regain some of its surfactant function. In our second experiment, we observed that in anionic DOPG films, amyloid-β inserts into the bilayer much quicker than in zwitterionic DPPC. Approaching 24 hours, we see small fibrils form in the bilayer, but these fibrils are considerably smaller than those formed when amyloid-β is incubated in solution.

Thesis (Ph. D.)--University of Hong Kong, 2001. / Includes bibliographical references (leaves 93-120).

Thesis--Ph. D., University of Hong Kong.

published_or_final_version / Medical Sciences / Master / Master of Medical Sciences

No description available.

ABSTRACT Asthma exemplifies a major medical concern and is a considerable cause of morbidity and mortality in Western society. Controversy still exists regarding the most effective mode and intensity of exercise training for asthmatics. Thus, the purpose of the study was to determine whether walking or jogging at 60% of age-predicted heart rate maximum can increase effort-dependent pulmonary function parameters in moderate, persistent asthmatics. Forty-four sedentary asthmatics were randomly assigned to either a non-exercising control (NE) group (n = 22) or an eight-week moderate-intensity aerobic exercise (AE) group (n = 22). Results indicated that the subjects in the AE training group significantly (p = 0.05) increased their forced vital capacity (FVC), forced expiratory volume in one second (FEV1), peak expiratory flow (PEF), maximal voluntary ventilation (MVV) and inspiratory vital capacity (IVC). The NE group did not exhibit any significant changes in any of the measured variables. Therefore, walking or jogging at 60% heart rate maximum for 30 minutes three times a week for eight weeks can effectively improve the effort-dependent pulmonary parameters in moderate, persistent asthmatics. This represents a strong argument to support the inclusion of this mode of aerobic training in the treatment of moderate, persistent asthma due to its effectiveness, inexpensiveness and lowrisk.