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  1. Article ; Online: Mentoring from the diverse lens of epidemiologists reveals a dynamic and mutually rewarding relationship.

    Forman, M R / Wright, J L / Waring, S C / Liese, A D

    Annals of epidemiology

    2021  Volume 60, Page(s) 28–30

    MeSH term(s) Career Choice ; Epidemiologists ; Humans ; Mentoring ; Mentors
    Language English
    Publishing date 2021-05-03
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1074355-8
    ISSN 1873-2585 ; 1047-2797
    ISSN (online) 1873-2585
    ISSN 1047-2797
    DOI 10.1016/j.annepidem.2021.04.013
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  2. Article: Vestibular anus; report of a case.

    WRIGHT, J L

    The Journal of obstetrics and gynaecology of the British Empire

    2008  Volume 54, Issue 6, Page(s) 824

    MeSH term(s) Anal Canal/abnormalities ; Ear, Inner ; Humans ; Vestibule, Labyrinth
    Language English
    Publishing date 2008-09-05
    Publishing country England
    Document type Journal Article
    ZDB-ID 3091-0
    ISSN 0307-1871
    ISSN 0307-1871
    DOI 10.1111/j.1471-0528.1947.tb10768.x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Book: An outline of Kikaonde grammar

    Wright, J. L

    2007  

    Author's details J. L. Wright
    Keywords Kaonde language/Grammar ; Zambia
    Language English
    Size viii, 45 S, 23 cm
    Publisher Bookworld Publ. and UNZA Press
    Publishing place Lusaka, Zambia
    Document type Book
    ISBN 9789982240499 ; 9982240498
    Database Former special subject collection: coastal and deep sea fishing

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  4. Article: Unconstitutional or impossible: the irreconcilable gap between managed care and due process in Medicaid and Medicare.

    Wright, J L

    The Journal of contemporary health law and policy

    2001  Volume 17, Issue 1, Page(s) 135–180

    MeSH term(s) Conflict of Interest/economics ; Conflict of Interest/legislation & jurisprudence ; Decision Making ; Humans ; Insurance Coverage/legislation & jurisprudence ; Managed Care Programs/economics ; Managed Care Programs/legislation & jurisprudence ; Managed Care Programs/standards ; Medicaid/legislation & jurisprudence ; Medicaid/standards ; Medicare/legislation & jurisprudence ; Medicare/standards ; Patient Advocacy/legislation & jurisprudence ; Refusal to Treat/legislation & jurisprudence ; Reimbursement, Incentive/legislation & jurisprudence ; United States
    Language English
    Publishing date 2001-02-07
    Publishing country United States
    Document type Journal Article ; Legal Case
    ZDB-ID 228325-6
    ISSN 0882-1046
    ISSN 0882-1046
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: Old stone face.

    Wright, J L

    The Journal of family practice

    2001  Volume 50, Issue 1, Page(s) 89–90

    MeSH term(s) Humans ; Interpersonal Relations ; Professional-Family Relations ; Resuscitation Orders
    Language English
    Publishing date 2001-01
    Publishing country United States
    Document type Journal Article
    ZDB-ID 197883-4
    ISSN 0094-3509
    ISSN 0094-3509
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: Diseases of the small airways.

    Wright, J L

    Lung

    2001  Volume 179, Issue 6, Page(s) 375–396

    Abstract: The respiratory tree is involved in a wide range of pathological conditions. The consequences of these processes vary from negligible to severe airflow obstruction with resultant hypoxia and respiratory failure. Although almost all of the processes ... ...

    Abstract The respiratory tree is involved in a wide range of pathological conditions. The consequences of these processes vary from negligible to severe airflow obstruction with resultant hypoxia and respiratory failure. Although almost all of the processes described herein are associated with activation of cytokines, ecosanoids, or peptide hormones, detailed descriptions of these interactions are beyond the scope of this article.
    MeSH term(s) Acute Disease ; Air Pollutants/adverse effects ; Airway Obstruction/physiopathology ; Asthma/physiopathology ; Bronchi/physiopathology ; Bronchial Diseases/diagnosis ; Bronchial Diseases/etiology ; Bronchial Diseases/physiopathology ; Bronchiectasis/diagnosis ; Bronchiectasis/etiology ; Bronchiectasis/physiopathology ; Bronchiolitis/microbiology ; Bronchiolitis/physiopathology ; Humans ; Respiratory System/anatomy & histology ; Smoking/physiopathology
    Chemical Substances Air Pollutants
    Language English
    Publishing date 2001
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 6165-7
    ISSN 1432-1750 ; 0341-2040
    ISSN (online) 1432-1750
    ISSN 0341-2040
    DOI 10.1007/s004080000074
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article: The importance of ultramicroscopic emphysema in cigarette smoke-induced lung disease.

    Wright, J L

    Lung

    2001  Volume 179, Issue 2, Page(s) 71–81

    Abstract: To determine the role of the alveolar pores in cigarette smoke-induced lung disease, we examined the alveolar pores of guinea pigs exposed to cigarette smoke for 12 months, and compared these data to those obtained from sham-smoked animals, correlating ... ...

    Abstract To determine the role of the alveolar pores in cigarette smoke-induced lung disease, we examined the alveolar pores of guinea pigs exposed to cigarette smoke for 12 months, and compared these data to those obtained from sham-smoked animals, correlating the data with airspace size and lung function. We found that the smoke-exposed animals had a larger mean number of pores per alveolus (p < 0.001), and the distributions of pore size and shape were significantly shifted to indicate a larger and more irregular pore configuration (p < 0.001, 01 respectively). In the smoke exposed group, there was a significant correlation of pore number with total lung capacity (TLC) (0.68 p < 0.05), RV (0.70, p < 0.05), and FEV(0.1)/FVC(-0.77, p < 0.02). No correlations were identified between pore size or shape and the lung function tests. We conclude that cigarette smoke exposure produces an increase in the number of alveolar pores, a process which we believe represents ultramicroscopic emphysema. These alterations appear to precede any increase in airspace size, and may help to explain abnormal lung function in cigarette smokers without macroscopic emphysema or small airway disease. This is the first study to clearly document an increased number of alveolar pores, with a significant number of either/or large and irregular pores, after chronic smoke exposure, but in the absence of gross emphysema.
    MeSH term(s) Animals ; Female ; Forced Expiratory Volume ; Guinea Pigs ; Microscopy, Electron, Scanning ; Pulmonary Alveoli/ultrastructure ; Pulmonary Emphysema/etiology ; Pulmonary Emphysema/pathology ; Pulmonary Emphysema/physiopathology ; Residual Volume ; Tobacco Smoke Pollution/adverse effects ; Total Lung Capacity ; Vital Capacity
    Chemical Substances Tobacco Smoke Pollution
    Language English
    Publishing date 2001
    Publishing country United States
    Document type Journal Article
    ZDB-ID 6165-7
    ISSN 1432-1750 ; 0341-2040
    ISSN (online) 1432-1750
    ISSN 0341-2040
    DOI 10.1007/s004080000048
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article: Short-term exposure to cigarette smoke induces endothelial dysfunction in small intrapulmonary arteries: analysis using guinea pig precision cut lung slices.

    Wright, J L / Churg, A

    Journal of applied physiology (Bethesda, Md. : 1985)

    2008  Volume 104, Issue 5, Page(s) 1462–1469

    Abstract: The pathogenesis of cigarette smoke-induced pulmonary hypertension is not understood. We have previously shown that smoke rapidly and persistently, but discoordinately, upregulates gene expression of mediators that control vasoconstriction, ... ...

    Abstract The pathogenesis of cigarette smoke-induced pulmonary hypertension is not understood. We have previously shown that smoke rapidly and persistently, but discoordinately, upregulates gene expression of mediators that control vasoconstriction, vasoproliferation, and vasorelaxation in small intrapulmonary arteries. To investigate the possibility that smoke also induces endothelial dysfunction, a finding common to other forms of pulmonary hypertension, we exposed guinea pigs to smoke or air (control) daily for 2 wk and then prepared precision-cut lung slices. After exposure to endothelin-1, a vasoconstrictor, intra-acinar arteries in lung slices derived from smoke-exposed animals constricted more rapidly (greater constriction at a given concentration of endothelin) than did vessels from air-exposed animals. To examine relaxation responses, arteries were constricted with the vasoconstrictor U-46619 and then relaxed with progressively increasing doses of acetylcholine. Vessels from smokers had a delayed response to acetylcholine compared with vessels from controls. The NO synthase inhibitor N(G)-nitro-L-arginine methyl ester reduced relaxation in both control and smoke-exposed arteries, whereas the NO donor sodium nitroprusside increased relaxation of the smoke-exposed arteries, confirming that endothelial dysfunction with decreased effective NO production is present. These findings show that precision cut lung slices can be used to examine the physiological effects of cigarette smoke on intra-acinar pulmonary arteries and indicate that even relatively short-term exposure to smoke produces endothelial dysfunction with a resulting tendency to earlier constriction and later relaxation in cigarette smokers. These changes may be important in the development of pulmonary hypertension.
    MeSH term(s) 15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid/pharmacology ; Acetylcholine/pharmacology ; Animals ; Arteries/pathology ; Dose-Response Relationship, Drug ; Endothelin-1/pharmacology ; Endothelium, Vascular/drug effects ; Enzyme Inhibitors/pharmacology ; Female ; Guinea Pigs ; Lung/pathology ; Muscle Contraction/drug effects ; NG-Nitroarginine Methyl Ester/pharmacology ; Nitric Oxide Synthase Type III/antagonists & inhibitors ; Nitroprusside/pharmacology ; Organ Culture Techniques ; Pulmonary Circulation/drug effects ; Pulmonary Circulation/physiology ; Smoke/adverse effects ; Nicotiana ; Vascular Diseases/chemically induced ; Vascular Diseases/pathology ; Vasoconstrictor Agents/pharmacology ; Vasodilation/drug effects ; Vasodilation/physiology ; Vasodilator Agents/pharmacology
    Chemical Substances Endothelin-1 ; Enzyme Inhibitors ; Smoke ; Vasoconstrictor Agents ; Vasodilator Agents ; Nitroprusside (169D1260KM) ; 15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid (76898-47-0) ; Nitric Oxide Synthase Type III (EC 1.14.13.39) ; Acetylcholine (N9YNS0M02X) ; NG-Nitroarginine Methyl Ester (V55S2QJN2X)
    Language English
    Publishing date 2008-03-20
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 219139-8
    ISSN 1522-1601 ; 8750-7587 ; 0021-8987 ; 0161-7567
    ISSN (online) 1522-1601
    ISSN 8750-7587 ; 0021-8987 ; 0161-7567
    DOI 10.1152/japplphysiol.00520.2007
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Pulmonary hypertension and vascular oxidative damage in cigarette smoke exposed eNOS(-/-) mice and human smokers.

    Wright, J L / Zhou, S / Churg, A

    Inhalation toxicology

    2012  Volume 24, Issue 11, Page(s) 732–740

    Abstract: Context: Cigarette smoke is known to be associated with pulmonary hypertension in humans and in animal models. Although the etiology of pulmonary hypertension in smokers is not understood, recent work has suggested a role for inducible nitric oxide ... ...

    Abstract Context: Cigarette smoke is known to be associated with pulmonary hypertension in humans and in animal models. Although the etiology of pulmonary hypertension in smokers is not understood, recent work has suggested a role for inducible nitric oxide synthase (iNOS) in inducing oxidative stress.
    Objective and methods: To further evaluate this question, we assessed eNOS-/- mice exposed to air or cigarette smoke for the presence of pulmonary hypertension and examined vascular remodeling and expression of nitrotyrosine, a marker of reactive nitrogen species-induced oxidative damage, using immunohistochemistry. To ascertain whether oxidants may play a role in humans, we also examined lung tissue from nonsmokers, and patients with chronic obstructive pulmonary disease (COPD) with and without pulmonary hypertension.
    Results: We found that eNOS(-/-) mice developed increased pulmonary arterial pressure after six months cigarette smoke exposure, and this was associated with vascular remodeling and increased vascular nitrotyrosine staining. iNOS gene expression was decreased in the pulmonary arteries of the smoke exposed animals, and no protein was detectable by immunohistochemistry. In humans, vascular nitrotyrosine staining intensity was increased in smokers with COPD compared to nonsmokers, and further increased in smokers with combined COPD and pulmonary hypertension.
    Conclusions: We conclude that cigarette smoke-induced pulmonary hypertension is associated with evidence of oxidative vascular damage by reactive nitrogen species, but that iNOS does not appear to be the major contributor to such damage. Most likely the source of reactive nitrogen species is the cigarette smoke itself.
    MeSH term(s) Animals ; Biomarkers ; Humans ; Hypertension, Pulmonary/chemically induced ; Lung/blood supply ; Mice ; Mice, Knockout ; Nitric Oxide Synthase Type II/genetics ; Nitric Oxide Synthase Type II/metabolism ; Nitric Oxide Synthase Type III/genetics ; Nitric Oxide Synthase Type III/metabolism ; Oxidative Stress/drug effects ; Smoking/adverse effects ; Tyrosine/analogs & derivatives ; Tyrosine/metabolism
    Chemical Substances Biomarkers ; 3-nitrotyrosine (3604-79-3) ; Tyrosine (42HK56048U) ; Nitric Oxide Synthase Type II (EC 1.14.13.39) ; Nitric Oxide Synthase Type III (EC 1.14.13.39)
    Language English
    Publishing date 2012-09
    Publishing country England
    Document type Journal Article
    ZDB-ID 1038809-6
    ISSN 1091-7691 ; 0895-8378
    ISSN (online) 1091-7691
    ISSN 0895-8378
    DOI 10.3109/08958378.2012.715698
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Series "matrix metalloproteinases in lung health and disease": Matrix metalloproteinases in COPD.

    Churg, A / Zhou, S / Wright, J L

    The European respiratory journal

    2012  Volume 39, Issue 1, Page(s) 197–209

    Abstract: There is considerable evidence that matrix metalloproteinases (MMPs) are up- and/or downregulated in chronic obstructive pulmonary disease (COPD), particularly in emphysema, in which they probably participate in proteolytic attack on the alveolar wall ... ...

    Abstract There is considerable evidence that matrix metalloproteinases (MMPs) are up- and/or downregulated in chronic obstructive pulmonary disease (COPD), particularly in emphysema, in which they probably participate in proteolytic attack on the alveolar wall matrix. Recent data suggest that MMPs also have major roles in driving inflammation or shutting it down, as well as modifying the release of fibrogenic growth factors, processes that are important in the genesis of the various lesions of COPD. In cigarette smoke-induced animal models of emphysema, MMP-12 appears to play a consistent and important role, whereas the data for other MMPs are difficult to interpret. In human lungs, evidence for a role for MMPs is more tenuous and there are numerous contradictions in the literature. Little is known about the effects of MMPs in small airway remodelling, smoke-induced pulmonary hypertension and chronic bronchitis, but MMP-12 participates in experimental small airway modelling. To date, the accumulated data suggest that selective inhibition of MMP-12 might be a viable therapy for emphysema and small airway remodelling, but subtle differences in the functions of MMP-12 in animals and humans mandate caution with this approach. Whether inhibition of other MMPs might be useful is unclear.
    MeSH term(s) Animals ; Bronchitis/enzymology ; Collagen/metabolism ; Emphysema/metabolism ; Humans ; Hypertension, Pulmonary/enzymology ; Inflammation ; Matrix Metalloproteinases/metabolism ; Mice ; Mice, Inbred C57BL ; Models, Biological ; Pulmonary Disease, Chronic Obstructive/enzymology ; Pulmonary Disease, Chronic Obstructive/physiopathology ; Smoking ; Treatment Outcome
    Chemical Substances Collagen (9007-34-5) ; Matrix Metalloproteinases (EC 3.4.24.-)
    Language English
    Publishing date 2012-01
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 639359-7
    ISSN 1399-3003 ; 0903-1936
    ISSN (online) 1399-3003
    ISSN 0903-1936
    DOI 10.1183/09031936.00121611
    Database MEDical Literature Analysis and Retrieval System OnLINE

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