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Article ; Online: Successful Removal of a Fractured Self-expanding Metallic Airway Stent Via Flexible Bronchoscopy: A Case Report.

Williams, Sarah / Halverson, Quinn M / Patterson, Dalton T / Styrvoky, Kim / Ochoa, Cristhiaan D

Journal of bronchology & interventional pulmonology

2022 Volume 29, Issue 3, Page(s) e43–e46

MeSH term(s)	Airway Obstruction/etiology ; Airway Obstruction/surgery ; Bronchial Diseases/complications ; Bronchoscopy/adverse effects ; Device Removal/adverse effects ; Humans ; Stents/adverse effects
Language	English
Publishing date	2022-06-22
Publishing country	United States
Document type	Case Reports ; Letter
ZDB-ID	2478320-1
ISSN	1948-8270 ; 1944-6586
ISSN (online)	1948-8270
ISSN	1944-6586
DOI	10.1097/LBR.0000000000000775
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Zs.A 4027: Show issues

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Article ; Online: ROS signaling and ER stress in cardiovascular disease.

Ochoa, Cristhiaan D / Wu, Ru Feng / Terada, Lance S

Molecular aspects of medicine

2018 Volume 63, Page(s) 18–29

Abstract: The endoplasmic reticulum (ER) produces the vast majority of all proteins secreted into the extracellular space, including hormones and cytokines, as well as cell surface receptors and other proteins which interact with the environment. Accordingly, this ...

Abstract	The endoplasmic reticulum (ER) produces the vast majority of all proteins secreted into the extracellular space, including hormones and cytokines, as well as cell surface receptors and other proteins which interact with the environment. Accordingly, this organelle controls essentially all vital links to a cell's external milieu, responding to systemic metabolic, inflammatory, endocrine, and mechanical stimuli. The central role the ER plays in meeting protein synthetic and quality control requirements in the face of such demands is matched by an extensive and versatile ER stress response signaling network. ROS mediate several critical aspects of this response. Nox4, an ER resident capable of producing ROS, acts as a proximal signaling intermediate to transduce ER stress-related conditions to the unfolded protein response, a homeostatic corrective mechanism. However, chronic ER stress caused by unrelenting internal or external demands produces a secondary rise in ROS, generally resulting in cell death. Sorting out the involvement of ROS at different levels of the ER stress response in specific cell types is key to understanding the molecular basis for chronic diseases such as atherosclerosis, hypertension, and diabetes. Here, we provide an overview of ER stress signaling with an emphasis on the role of ROS.
MeSH term(s)	Animals ; Autophagy ; Biomarkers ; Cardiovascular Diseases/etiology ; Cardiovascular Diseases/metabolism ; Endoplasmic Reticulum/metabolism ; Endoplasmic Reticulum Stress ; Humans ; Reactive Oxygen Species/metabolism ; Signal Transduction ; Unfolded Protein Response
Chemical Substances	Biomarkers ; Reactive Oxygen Species
Language	English
Publishing date	2018-03-22
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	197640-0
ISSN	1872-9452 ; 0098-2997
ISSN (online)	1872-9452
ISSN	0098-2997
DOI	10.1016/j.mam.2018.03.002
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Article: Bronchoscopic management of a primary endobronchial salivary epithelial-myoepithelial carcinoma: A case report.

Patterson, Dalton T / Halverson, Quinn / Williams, Sarah / Bishop, Justin A / Ochoa, Cristhiaan D / Styrvoky, Kim

Respiratory medicine case reports

2020 Volume 30, Page(s) 101083

Abstract: Here, we discussed a 55 y/o African man who recently immigrated from Nigeria to the United States and who presented to Parkland Memorial Hospital with a productive, intermittent cough of one year duration. The cough was associated with shortness of ... ...

Abstract	Here, we discussed a 55 y/o African man who recently immigrated from Nigeria to the United States and who presented to Parkland Memorial Hospital with a productive, intermittent cough of one year duration. The cough was associated with shortness of breath and chest pain. Cough was not associated with voice hoarseness, hemoptysis, melanoptysis, and wheezing. He had a computed tomography (CT) scan of the chest that showed a 1.9 cm mass in the right main stem bronchus with ipsilateral right lower lobe consolidation and bronchiectasis. The patient was seen by pulmonology who recommended bronchoscopy for diagnosis and possible intervention. Bronchoscopy showed a 90% obstructing mass in the proximal right mainstem bronchus and bronchus intermedius. The mass was large and endobronchial, circumferential, exophytic, and polypoid. The decision was made to undergo bronchoscopic tumor ablation using electrocautery snare, argon plasma coagulation (APC), suction, and forceps. The tumor was successful ablated. Microscopic examination revealed eosinophilic ducts tightly coupled with a surrounding layer of clear cell myoepithelial cells and the diagnosis of epithelial-myoepithelial carcinoma (EMC) of the lung was made. The patient was discharged from the hospital with scheduled outpatient visits for monitoring of the carcinoma by pulmonology and thoracic surgery. Unfortunately, he was lost to follow up.
Language	English
Publishing date	2020-05-07
Publishing country	England
Document type	Case Reports
ZDB-ID	2666110-X
ISSN	2213-0071
ISSN	2213-0071
DOI	10.1016/j.rmcr.2020.101083
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Article ; Online: Studies on the cell biology of interendothelial cell gaps.

Ochoa, Cristhiaan D / Stevens, Troy

American journal of physiology. Lung cellular and molecular physiology

2011 Volume 302, Issue 3, Page(s) L275–86

Abstract: Pain, redness, heat, and swelling are hallmarks of inflammation that were recognized as early as the first century AD. Despite these early observations, the mechanisms responsible for swelling, in particular, remained an enigma for nearly two millennia. ... ...

Abstract	Pain, redness, heat, and swelling are hallmarks of inflammation that were recognized as early as the first century AD. Despite these early observations, the mechanisms responsible for swelling, in particular, remained an enigma for nearly two millennia. Only in the past century have scientists and physicians gained an appreciation for the role that vascular endothelium plays in controlling the exudation that is responsible for swelling. One of these mechanisms is the formation of transient gaps between adjacent endothelial cell borders. Inflammatory mediators act on endothelium to reorganize the cytoskeleton, decrease the strength of proteins that connect cells together, and induce transient gaps between endothelial cells. These gaps form a paracellular route responsible for exudation. The discovery that interendothelial cell gaps are causally linked to exudation began in the 1960s and was accompanied by significant controversy. Today, the role of gap formation in tissue edema is accepted by many, and significant scientific effort is dedicated toward developing therapeutic strategies that will prevent or reverse the endothelial cell gaps that are present during the course of inflammatory illness. Given the importance of this field in endothelial cell biology and inflammatory disease, this focused review catalogs key historical advances that contributed to our modern-day understanding of the cell biology of interendothelial gap formation.
MeSH term(s)	Animals ; Cell Biology ; Cytoskeleton/metabolism ; Edema/metabolism ; Endothelium/metabolism ; Endothelium/pathology ; Endothelium/ultrastructure ; Extracellular Matrix/metabolism ; Humans ; Inflammation/metabolism ; Lung/metabolism ; Lung/pathology ; Permeability ; Venules/pathology
Language	English
Publishing date	2011-09-30
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	1013184-x
ISSN	1522-1504 ; 1040-0605
ISSN (online)	1522-1504
ISSN	1040-0605
DOI	10.1152/ajplung.00215.2011.
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Article ; Online: RasGRF Couples Nox4-Dependent Endoplasmic Reticulum Signaling to Ras.

Wu, Ru Feng / Liao, Chengxu / Hatoum, Hadi / Fu, Guosheng / Ochoa, Cristhiaan D / Terada, Lance S

Arteriosclerosis, thrombosis, and vascular biology

2017 Volume 37, Issue 1, Page(s) 98–107

Abstract: Objectives: In response to endoplasmic reticulum (ER) stress, endothelial cells initiate corrective pathways such as the unfolded protein response. Recent studies suggest that reactive oxygen species produced on the ER may participate in homeostatic ... ...

Abstract	Objectives: In response to endoplasmic reticulum (ER) stress, endothelial cells initiate corrective pathways such as the unfolded protein response. Recent studies suggest that reactive oxygen species produced on the ER may participate in homeostatic signaling through Ras in response to ER stress. We sought to identify mechanisms responsible for this focal signaling pathway. Approach and results: In endothelial cells, we found that ER stress induced by tunicamycin activates the NADPH (nicotinamide adenine dinucleotide phosphate) oxidase Nox4 focally on the ER surface but not on the plasma membrane. Ras activation is also restricted to the ER, occurs downstream of Nox4, and is required for activation of the unfolded protein response. In contrast, treatment with the growth factor VEGF (vascular endothelial growth factor) results in Ras activation and reactive oxygen species production confined instead to the plasma membrane and not to the ER, demonstrating local coupling of reactive oxygen species and Ras signals. We further identify the calcium-responsive, ER-resident guanyl exchange factors RasGRF1 and RasGRF2 as novel upstream mediators linking Nox4 with Ras activation in response to ER stress. Oxidation of the sarcoendoplasmic reticulum calcium ATPase and increases in cytosolic calcium caused by ER stress are blocked by Nox4 knockdown, and reduction in cytosolic free calcium prevents both Ras activation and the unfolded protein response. Conclusions: ER stress triggers a localized signaling module on the ER surface involving Nox4-dependent calcium mobilization, which directs local Ras activation through ER-associated, calcium-responsive RasGRF.
MeSH term(s)	Calcium Signaling/drug effects ; Cells, Cultured ; Endoplasmic Reticulum/drug effects ; Endoplasmic Reticulum/enzymology ; Endoplasmic Reticulum Stress/drug effects ; Human Umbilical Vein Endothelial Cells/drug effects ; Human Umbilical Vein Endothelial Cells/enzymology ; NADPH Oxidase 4 ; NADPH Oxidases/genetics ; NADPH Oxidases/metabolism ; Proto-Oncogene Proteins p21(ras)/genetics ; Proto-Oncogene Proteins p21(ras)/metabolism ; RNA Interference ; Reactive Oxygen Species/metabolism ; Sarcoplasmic Reticulum Calcium-Transporting ATPases/metabolism ; Transfection ; Tunicamycin/pharmacology ; Unfolded Protein Response ; Vascular Endothelial Growth Factor A/pharmacology ; ras Guanine Nucleotide Exchange Factors/genetics ; ras Guanine Nucleotide Exchange Factors/metabolism ; ras-GRF1/genetics ; ras-GRF1/metabolism
Chemical Substances	KRAS protein, human ; RASGRF1 protein, human ; RASGRF2 protein, human ; Reactive Oxygen Species ; Vascular Endothelial Growth Factor A ; ras Guanine Nucleotide Exchange Factors ; ras-GRF1 ; Tunicamycin (11089-65-9) ; NADPH Oxidase 4 (EC 1.6.3.-) ; NADPH Oxidases (EC 1.6.3.-) ; NOX4 protein, human (EC 1.6.3.-) ; Sarcoplasmic Reticulum Calcium-Transporting ATPases (EC 3.6.3.8) ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2)
Language	English
Publishing date	2017-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	1221433-4
ISSN	1524-4636 ; 1079-5642
ISSN (online)	1524-4636
ISSN	1079-5642
DOI	10.1161/ATVBAHA.116.307922
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Zs.A 1705: Show issues

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Article ; Online: Clinician Variation in Ordering and Completion of Low-Dose Computed Tomography for Lung Cancer Screening in a Safety-Net Medical System.

Gerber, David E / Hamann, Heidi A / Dorsey, Olivia / Ahn, Chul / Phillips, Jessica L / Santini, Noel O / Browning, Travis / Ochoa, Cristhiaan D / Adesina, Joyce / Natchimuthu, Vijaya Subbu / Steen, Eric / Majeed, Harris / Gonugunta, Amrit / Lee, Simon J Craddock

Clinical lung cancer

2020 Volume 22, Issue 4, Page(s) e612–e620

Abstract: Background: Less than 5% of eligible individuals in the United States undergo lung cancer screening. Variation in clinicians' participation in lung cancer screening has not been determined.: Patients and methods: We studied medical providers who ... ...

Abstract	Background: Less than 5% of eligible individuals in the United States undergo lung cancer screening. Variation in clinicians' participation in lung cancer screening has not been determined. Patients and methods: We studied medical providers who ordered ≥ 1 low-dose computed tomography (LDCT) for lung cancer screening from February 2017 through February 2019 in an integrated safety-net healthcare system. We analyzed associations between provider characteristics and LDCT orders and completion using chi-square, Fisher exact, and Student t tests, as well as ANOVA and multinomial logistic regression. Results: Among an estimated 194 adult primary care physicians, 144 (74%) ordered at least 1 LDCT, as did 39 specialists. These 183 medical providers ordered 1594 LDCT (median, 4; interquartile range, 2-9). In univariate and multivariate models, family practice providers (P < .001) and providers aged ≥ 50 years (P = .03) ordered more LDCT than did other clinicians. Across providers, the median proportion of ordered LDCT that were completed was 67%. The total or preceding number of LDCT ordered by a clinician was not associated with the likelihood of LDCT completion. Conclusion: In an integrated safety-net healthcare system, most adult primary care providers order LDCT. The number of LDCT ordered varies widely among clinicians, and a substantial proportion of ordered LDCT are not completed.
MeSH term(s)	Adult ; Early Detection of Cancer/methods ; Female ; Humans ; Lung Neoplasms/diagnostic imaging ; Male ; Mass Screening/methods ; Middle Aged ; Safety-net Providers ; Tomography, X-Ray Computed/methods
Language	English
Publishing date	2020-12-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2145146-1
ISSN	1938-0690 ; 1525-7304
ISSN (online)	1938-0690
ISSN	1525-7304
DOI	10.1016/j.cllc.2020.12.001
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Zs.MO 440: Show issues

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Article ; Online: Tracking the Nonenrolled: Lung Cancer Screening Patterns Among Individuals not Accrued to a Clinical Trial.

Gerber, David E / Hamann, Heidi A / Chavez, Claudia / Dorsey, Olivia / Santini, Noel O / Browning, Travis / Ochoa, Cristhiaan D / Adesina, Joyce / Natchimuthu, Vijaya Subbu / Steen, Eric / Zhu, Hong / Lee, Simon J Craddock

Clinical lung cancer

2020 Volume 21, Issue 4, Page(s) 326–332

Abstract: Introduction: For lung cancer screening, the available data are often derived from patients enrolled prospectively in clinical trials. We, therefore, investigated lung cancer screening patterns among individuals eligible for, but not enrolled in, a ... ...

Abstract	Introduction: For lung cancer screening, the available data are often derived from patients enrolled prospectively in clinical trials. We, therefore, investigated lung cancer screening patterns among individuals eligible for, but not enrolled in, a screening trial. Patients and methods: From February 2017 through February 2019, we enrolled subjects in a trial examining telephone-based navigation during low-dose computed tomography (LDCT) for lung cancer screening. We identified patients for whom LDCT was ordered and who were approached, but not enrolled, in the trial. We categorized nonenrollment as the patient had declined or could not be reached. We compared the characteristics and LDCT completion rates among these groups and the enrolled population using the 2-sample t test and χ Results: Of 900 individuals approached for participation (mean age, 62 years; 45% women, 53% black), 447 were enrolled in the screening clinical trial. No significant demographic differences were found between the enrolled and nonenrolled cohorts. Of the 453 individuals not enrolled, 251 (55%) had declined participation and 202 (45%) could not be reached, despite up to 6 attempts. LDCT completion was significantly associated with enrollment status: 81% of enrolled individuals, 73% of individuals who declined participation, and 49% of those who could not be reached (P < .001). Conclusions: In the present single-center study, demographic factors did not predict for participation in a lung cancer screening trial. Lung cancer screening adherence rates were substantially lower for those not enrolled in a screening trial, especially for those who could not be contacted. These findings may inform the broader implementation of screening programs.
MeSH term(s)	Clinical Trials as Topic ; Early Detection of Cancer/standards ; Female ; Follow-Up Studies ; Humans ; Lung Neoplasms/diagnosis ; Lung Neoplasms/diagnostic imaging ; Male ; Middle Aged ; Patient Selection ; Practice Guidelines as Topic/standards ; Prognosis ; Prospective Studies ; Risk Factors ; Tomography, X-Ray Computed/methods
Language	English
Publishing date	2020-02-26
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2145146-1
ISSN	1938-0690 ; 1525-7304
ISSN (online)	1938-0690
ISSN	1525-7304
DOI	10.1016/j.cllc.2020.02.010
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Zs.MO 440: Show issues

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Article ; Online: Thrombospondin-1, endothelium and systemic vascular tone.

Ochoa, Cristhiaan D / Fouty, Brian W / Hales, Charles A

Future cardiology

2011 Volume 7, Issue 2, Page(s) 169–172

Abstract: Evaluation of: Bauer EM, Qin Y, Miller TW et al.: Thrombospondin-1 supports blood pressure by limiting eNOS activation and endothelial dependent vasorelaxation. Cardiovasc. Res. 88, 471-481 (2010). Several lines of evidence, both in vivo and ex vivo, ... ...

Abstract	Evaluation of: Bauer EM, Qin Y, Miller TW et al.: Thrombospondin-1 supports blood pressure by limiting eNOS activation and endothelial dependent vasorelaxation. Cardiovasc. Res. 88, 471-481 (2010). Several lines of evidence, both in vivo and ex vivo, suggest that thrombospondin-1 (TSP-1) is important in maintaining systemic vascular tone. Recently published papers demonstrate that TSP-1 can inhibit vascular smooth muscle relaxation by interfering with the interaction between nitric oxide (NO) and soluble guanylyl cyclase, providing a possible mechanism of action to explain this observation. While these in vitro experiments in vascular smooth muscle cells were provocative, it is not clear how such a large protein circulating in the plasma could cross the intact endothelial basal membrane and regulate NO/cGMP signaling in smooth muscle in vivo. This raised the question of whether TSP-1 could modulate NO/cGMP signaling through another mechanism. Herein, we evaluate a recently published paper by Bauer and colleagues that examined whether TSP-1 could exert vasoactive effects without directly accessing the vascular smooth muscle. In their studies they found that TSP-1 could inhibit the NO/cGMP signaling pathway through an alternate mechanism: inhibiting the activation of endothelial NO synthase (eNOS), and therefore NO production in endothelial cells. These findings, combined with previous results from these investigators, suggest that TSP-1 can blunt NO/cGMP signaling through two different mechanisms: inhibiting NO production in endothelial cells by preventing the agonist-induced influx of Ca(2+) required to activate endothelial NO synthase and blunting the ability of endothelial-derived NO to activate soluble guanylyl cyclase in vascular smooth muscle cells. The importance of these two pathways in supporting systemic and pulmonary vascular tone in health and disease is unclear.
Language	English
Publishing date	2011-03
Publishing country	England
Document type	Comment ; Journal Article
ZDB-ID	2274267-0
ISSN	1744-8298 ; 1479-6678
ISSN (online)	1744-8298
ISSN	1479-6678
DOI	10.2217/fca.11.7
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Article ; Online: New developments in lung endothelial heterogeneity: Von Willebrand factor, P-selectin, and the Weibel-Palade body.

Ochoa, Cristhiaan D / Wu, Songwei / Stevens, Troy

Seminars in thrombosis and hemostasis

2010 Volume 36, Issue 3, Page(s) 301–308

Abstract: Quiescent pulmonary endothelium establishes an antithrombotic, anti-inflammatory surface that promotes blood flow. However, the endothelium rapidly responds to injury and inflammation by promoting thrombosis and enabling the directed transmigration of ... ...

Abstract	Quiescent pulmonary endothelium establishes an antithrombotic, anti-inflammatory surface that promotes blood flow. However, the endothelium rapidly responds to injury and inflammation by promoting thrombosis and enabling the directed transmigration of inflammatory cells, such as neutrophils, into the alveolar airspace. Although the endothelial cell signals responsible for establishing a prothrombotic surface are distinct from those responsible for recognizing circulating neutrophils, these processes are highly interrelated. Von Willebrand factor (VWF)-stimulated secretion plays an important role in thrombus formation, and P-selectin surface expression plays a key role in neutrophil binding necessary for transmigration. Both VWF and P-selectin are located within Weibel-Palade bodies in pulmonary arteries and arterioles, yet Weibel-Palade bodies are absent in capillaries. Despite the absence of the Weibel-Palade bodies, pulmonary capillaries express both VWF and P-selectin. The physiological and pathophysiological significance of these observations is unclear. In this review, we address some anatomical and physiological features that distinguish pulmonary artery, capillary, and vein endothelium. In addition, we review our current understanding regarding the stimulated secretion of VWF and P-selectin in pulmonary artery and capillary endothelium. This information is considered in the context of vasculitis and pneumonia, two pathophysiological processes to which the stimulated secretion of VWF and P-selectin contribute.
MeSH term(s)	Endothelium, Vascular/chemistry ; Endothelium, Vascular/physiology ; Humans ; Lung/blood supply ; P-Selectin/physiology ; Phenotype ; Pneumonia/etiology ; Vasculitis/etiology ; Weibel-Palade Bodies/chemistry ; von Willebrand Factor/physiology
Chemical Substances	P-Selectin ; von Willebrand Factor
Language	English
Publishing date	2010-05-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	196901-8
ISSN	1098-9064 ; 0094-6176
ISSN (online)	1098-9064
ISSN	0094-6176
DOI	10.1055/s-0030-1253452
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Article ; Online: Cold exposure reveals two populations of microtubules in pulmonary endothelia.

Ochoa, Cristhiaan D / Stevens, Troy / Balczon, Ron

American journal of physiology. Lung cellular and molecular physiology

2010 Volume 300, Issue 1, Page(s) L132–8

Abstract: Microtubules are composed of α-tubulin and β-tubulin dimers. Microtubules yield tubulin dimers when exposed to cold, which reassemble spontaneously to form microtubule fibers at 37°C. However, mammalian neurons, glial cells, and fibroblasts have cold- ... ...

Abstract	Microtubules are composed of α-tubulin and β-tubulin dimers. Microtubules yield tubulin dimers when exposed to cold, which reassemble spontaneously to form microtubule fibers at 37°C. However, mammalian neurons, glial cells, and fibroblasts have cold-stable microtubules. While studying the microtubule toxicity mechanisms of the exotoxin Y from Pseudomonas aeruginosa in pulmonary microvascular endothelial cells, we observed that some endothelial microtubules were very difficult to disassemble in the cold. As a consequence, we designed studies to test the hypothesis that microvascular endothelium has a population of cold-stable microtubules. Pulmonary microvascular endothelial cells and HeLa cells (control) were grown under regular cell culture conditions, followed by exposure to an ice-cold water bath and a microtubule extraction protocol. Polymerized microtubules were detected by immunofluorescence confocal microscopy and Western blot analyses. After cold exposure, immunofluorescence revealed that the majority of HeLa cell microtubules disassembled, whereas a smaller population of endothelial cell microtubules disassembled. Immunoblot analyses showed that microvascular endothelial cells express the microtubule cold-stabilizing protein N-STOP (neuronal stable tubule-only polypeptides), and that N-STOP binds to endothelial microtubules after cold exposure, but not if microtubules are disassembled with nocodazole before cold exposure. Hence, pulmonary endothelia have a population of cold-stable microtubules.
MeSH term(s)	Cells, Cultured ; Cold Temperature ; Endothelium/cytology ; Endothelium/physiology ; HeLa Cells/cytology ; HeLa Cells/physiology ; Humans ; Lung/cytology ; Lung/physiology ; Microcirculation/physiology ; Microtubules/physiology ; Neurons/physiology ; Pulmonary Circulation/physiology ; Tubulin/physiology
Chemical Substances	Tubulin
Language	English
Publishing date	2010-10-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1013184-x
ISSN	1522-1504 ; 1040-0605
ISSN (online)	1522-1504
ISSN	1040-0605
DOI	10.1152/ajplung.00185.2010
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