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13. The SIRE2 Toolkit.

Author

Adams, J. H., Robinson, Z. D., Nonnast, J. H., Fisher, J. H., Hope, D. M., Lane, Z. B., Reed, R. A., Fisher, J. Z., Warren, K. M., and Sierawski, B. D.

Subjects
IONIZING radiation, EARTH system science, MAGNETIC fields, ACQUISITION of data, ELECTRONICS
Abstract

The Space Ionizing Radiation Environment and Effects (SIRE2) toolkit has been developed to update and extend the tools used by the space and radiation effects community. It includes new environment models, the capability to examine how the environment changes along satellite and other trajectories and batch processing capabilities for both environments and radiation effects on electronics. An overview of the capabilities in the SIRE2 Toolkit is provided, and examples of applying SIRE2 to satellite orbits and arbitrary trajectories are given. Key Points: The calculation options include legacy models, the latest models, and batch calculations of space radiation environments and radiation effectsThe tools allow space radiation environment calculations on segments of orbits and on arbitrary spacecraft trajectoriesSIRE2 provides a new probabilistic model for solar energetic particle peak flux [ABSTRACT FROM AUTHOR]

Published
2020
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14. X-ray transport and radiation response assessment (XTRRA) experiments at the National Ignition Facility

Author

Fournier, K. B., primary, Brown, C. G., additional, Yeoman, M. F., additional, Fisher, J. H., additional, Seiler, S. W., additional, Hinshelwood, D., additional, Compton, S., additional, Holdener, F. R., additional, Kemp, G. E., additional, Newlander, C. D., additional, Gilliam, R. P., additional, Froula, N., additional, Lilly, M., additional, Davis, J. F., additional, Lerch, MAJ. A., additional, and Blue, B. E., additional

Published
2016
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19. Multi-keV x-ray source development experiments on the National Ignition Facility

Author

Fournier, K. B., primary, May, M. J., additional, Colvin, J. D., additional, Kane, J. O., additional, Schneider, M., additional, Dewald, E., additional, Thomas, C. A., additional, Compton, S., additional, Marrs, R. E., additional, Moody, J., additional, Bond, E., additional, Michel, P., additional, Fisher, J. H., additional, Newlander, C. D., additional, and Davis, J. F., additional

Published
2010
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34. Surfactant protein-D regulates surfactant phospholipid homeostasis in vivo.

Author

Korfhagen, T R, Sheftelyevich, V, Burhans, M S, Bruno, M D, Ross, G F, Wert, S E, Stahlman, M T, Jobe, A H, Ikegami, M, Whitsett, J A, and Fisher, J H

Abstract

Surfactant protein D (SP-D) is a 43-kDa member of the collectin family of collagenous lectin domain-containing proteins that is expressed in epithelial cells of the lung. The SP-D gene was targeted by homologous recombination in embryonic stem cells that were used to produce SP-D (+/-) and SP-D (-/-) mice. Both SP-D (-/-) and SP-D (+/-) mice survived normally in the perinatal and postnatal periods. Whereas no abnormalities were observed in SP-D (+/-) mice, alveolar and tissue phosphatidylcholine pool sizes were markedly increased in SP-D (-/-) mice. Increased numbers of large foamy alveolar macrophages and enlarged alveoli were also observed in SP-D (-/-) mice. Phospholipid composition was unaltered in SP-D (-/-) mice, but surfactant morphology was abnormal, consisting of dense phospholipid membranous arrays with decreased tubular myelin. The pulmonary lipoidosis in the SP-D (-/-) mice was not associated with accumulation of surfactant proteins B or C, or their mRNAs, distinguishing the disorder from alveolar proteinosis syndromes. Surfactant protein A mRNA was reduced and, SP-A protein appeared to be reduced in SP-D (-/-) compared with wild type mice. Targeting of the mouse SP-D gene caused accumulation of surfactant lipid and altered phospholipid structures, demonstrating a previously unsuspected role for SP-D in surfactant lipid homeostasis in vivo.

Published
1998

37. PULMONIC INTERSTITIAL AND MEDIASTINAL EMPHYSEMA: REPORT OF A FATAL CASE IN WHICH THE EMPHYSEMA OCCURRED IN A CHILD AS A RESULT OF THE ASPIRATION OF PEANUT FRAGMENTS

Author

FISHER, J. H. and MACKLIN, C. C.

Abstract

Although interstitial emphysema of the lungs and mediastinum ha,s been known for a long time, there has recently been a revival of interest in it. Many of the papers on that condition, however, have dealt with its occurrence among adults and with instances in which it promptly cleared up. We here describe the condition as it occurred in a young child in whom it rapidly progressed to a fatal ending and in whom the initial cause was the impaction of peanut fragments in the right main bronchus. REPORT OF CASE J. B., a white girl of 22 months, previously healthy, was admitted to the Children's Hospital on Nov. 23, 1937. Three days before, on November 20, while chewing a mouthful of peanuts, she took a sudden deep breath and aspirated a number of the fragments. She immediately choked, coughed and became blue. She continued to have coughing spells and on

Published
1940
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42. The gene encoding the hydrophobic surfactant protein SP-C is located on 8p and identifies an EcoRI RFLP

Author

Fisher, J H, Emrie, P A, Drabkin, H A, Kushnik, T, Gerber, M, Hofmann, T, and Jones, C

Subjects
Polymorphism, Genetic, Proteolipids, Chromosome Mapping, Pulmonary Surfactants, DNA, Hybrid Cells, Chromosome Banding, Deoxyribonuclease EcoRI, Cricetinae, Karyotyping, Animals, Humans, Polymorphism, Restriction Fragment Length, Research Article, Chromosomes, Human, Pair 8
Abstract

Pulmonary surfactant is composed primarily of phospholipids but also contains three known surfactant-specific proteins. These proteins are important in determining the physical properties of pulmonary surfactant--including its ability to adsorb to an air-liquid interface and its structure--but also appear to influence surfactant metabolism. We have previously assigned two surfactant proteins, SP-A (a 28-36-kDa glycoprotein) and SP-B (an 18-kDa hydrophobic protein), to the short arm of chromosome 10 and to chromosome 2, respectively. We now report that the gene encoding the 5-8 kDa hydrophobic surfactant protein SP-C is located on the short arm of chromosome 8. A cDNA clone encoding the entire protein recognizes a useful EcoRI restriction-site-length polymorphism. Evaluation of congenital syndromes manifesting autosomal abnormalities does not further elucidate the functional role of this protein in promoting normal respiratory physiology.

Published
1988

43. B. PYOCYANEUS SEPTICÆMIA *

Author

Fisher, J. H., Ross, C. C., Lewis, J. A., Geddes, J. H., Brien, F. S., Busby, E. D., Kennedy, F. S., and Duffy, J. L.

Subjects
Bacteria, Sepsis, Humans, Case Reports
Published
1950

46. BREAST ABSCESS IN INFANT *

Author

Meissner, G. F. and Fisher, J. H.

Subjects
Breast Diseases, Sepsis, Staphylococcus, Humans, Infant, Case Reports, Breast, Staphylococcal Infections, Child, Infections, Abscess
Published
1947

47. An Investigation of Abnormal Uterine Bleeding *

Author

Fisher, J. H. and Smith, Ivan H.

Subjects
Uterine Neoplasms, Uterus, Short Communications, Humans, Female, Hemorrhage, Uterine Hemorrhage, Genital Diseases, Female
Published
1957

48. Primary Amyloidosis *

Author

Fisher, J. H. and Thompson, R. B.

Subjects
Humans, Immunoglobulin Light-chain Amyloidosis, Case Reports, Amyloidosis, Neoplasms, Plasma Cell, Aged
Published
1958

50. Baseline characteristics and comorbidities in the CAnadian REgistry for Pulmonary Fibrosis

Author

Fisher, J. H, Kolb, M., Algamdi, M., Morisset, J., Johannson, K. A, Shapera, S., Wilcox, P., To, T., Sadatsafavi, M., Manganas, H., Khalil, N., Hambly, N., Halayko, A. J, Gershon, A. S, Fell, C. D, Cox, G., and Ryerson, C. J

Subjects
body regions, respiratory system, behavioral disciplines and activities, respiratory tract diseases, 3. Good health
Abstract

Background: The CAnadian REgistry for Pulmonary Fibrosis (CARE-PF) is a multi-center, prospective registry designed to study the natural history of fibrotic interstitial lung disease (ILD) in adults. The aim of this cross-sectional sub-study was to describe the baseline characteristics, risk factors, and comorbidities of patients enrolled in CARE-PF to date. Methods: Patients completed study questionnaires and clinical measurements at enrollment and each follow-up visit. Environmental exposures were assessed by patient self-report and comorbidities by the Charlson Comorbidity Index (CCI). Baseline characteristics, exposures, and comorbidities were described for the overall study population and for incident cases, and were compared across ILD subtypes. Results: The full cohort included 1285 patients with ILD (961 incident cases (74.8%)). Diagnoses included connective tissue disease-associated ILD (33.3%), idiopathic pulmonary fibrosis (IPF) (24.7%), unclassifiable ILD (22.3%), chronic hypersensitivity pneumonitis (HP) (7.5%), sarcoidosis (3.2%), non-IPF idiopathic interstitial pneumonias (3.0%, including idiopathic nonspecific interstitial pneumonia (NSIP) in 0.9%), and other ILDs (6.0%). Patient-reported exposures were most frequent amongst chronic HP, but common across all ILD subtypes. The CCI was ≤2 in 81% of patients, with a narrow distribution and range of values. Conclusions: CTD-ILD, IPF, and unclassifiable ILD made up 80% of ILD diagnoses at ILD referral centers in Canada, while idiopathic NSIP was rare when adhering to recommended diagnostic criteria. CCI had a very narrow distribution across our cohort suggesting it may be a poor discriminator in assessing the impact of comorbidities on patients with ILD.

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