Publications by authors named "Shane Carr"

8 Publications

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Otolaryngology Residency Program Rankings and Social Media Usage: A Longitudinal Analysis.

Laryngoscope 2021 May 17. Epub 2021 May 17.

Department of Otolaryngology-Head and Neck Surgery, Vanderbilt University Medical Center, Nashville, Tennessee, U.S.A.

Objective: Social media is a powerful networking tool among health care organizations. This study determines correlations between program reputation and social media activity and popularity, specifically among otolaryngology residency programs.

Methods: Accredited programs, excluding military and osteopathic, in the United States were included. Activity and popularity on Facebook, Twitter, and Instagram were assessed during the same 7-month period from 2016 to 2020. Doximity Residency reputation scores (dividing programs into quartiles) and US News & World Report (comparing programs affiliated with top hospitals versus those with unranked hospitals) were utilized to compare differences based on reputation.

Results: Of 104 programs, 91 (88%) had social media accounts. Instagram and Twitter were more commonly used than Facebook, with 78 (75%), 49 (47%), and 42 (40%) accounts, respectively. The cumulative use of all three platforms grew yearly, while Twitter (R  = 0.9863) and Instagram (R  = 0.9955) presence increased exponentially. Doximity's top quartile programs had more Facebook (P = .020), Twitter (P < .001), and Instagram (P = .102) accounts. First-quartile programs also adopted each platform months before fourth-quartile programs. Stratified by US News & World Report, ranked programs had more social media accounts, with 24 (53%) on Facebook (P = .028), 32 (71%) on Twitter (P < .001), and 37 (82%) on Instagram (P = .155). Programs with higher reputations were more active and exhibited increased likes and followers over time.

Conclusion: Social media use among otolaryngology programs has grown exponentially, with Instagram and Twitter becoming the dominant platforms. Higher ranked programs are more active on social media, have more followers, and adopt social media earlier.

Level Of Evidence: Level 4 Laryngoscope, 2021.
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http://dx.doi.org/10.1002/lary.29621DOI Listing
May 2021

Halofuginone, a Promising Drug for Treatment of Pulmonary Hypertension.

Br J Pharmacol 2021 Mar 10. Epub 2021 Mar 10.

Section of Physiology, Division of Pulmonary, Critical Care and Sleep Medicine.

Background And Purpose: Halofuginone (HF) is a febrifugine derivative originally isolated from Chinese traditional herb Chang Shan that exhibits anti-hypertrophic, anti-fibrotic and anti-proliferative effects. We sought to investigate whether HF induced pulmonary vasodilation and attenuates chronic hypoxia induced pulmonary hypertension (HPH).

Experimental Approach: Patch-clamp experiments were conducted to examine the activity of voltage dependent Ca channels (VDCC) in pulmonary artery smooth muscle cells (PASMC). Digital fluorescence microscopy was used to measure intracellular Ca concentration in PASMC. Isolated perfused and ventilated mouse lungs were used to measure pulmonary artery pressure (PAP). Mice exposed to hypoxia (10% O ) for 4 weeks was used as model of HPH for in vivo experiments.

Key Results: HF increased voltage-gated K (Kv) currents in PASMC and K currents through KCNA5 channels in HEK cells transfected with KCNA5 gene. HF (0.03-1μM) inhibited receptor-operated Ca entry (ROCE) in HEK cells transfected with calcium-sensing receptor gene and attenuated store-operated (SOCE) Ca entry in PASMC. Acute (3-5min) intrapulmonary application of HF significantly and reversibly inhibited alveolar hypoxia-induced pulmonary vasoconstriction in dose-dependent manner (0.1-10μM). Intraperitoneal administration of HF (0.3mg/kg, for 2 weeks) partially reversed the established PH in mice.

Conclusion And Implications: HF is a potent pulmonary vasodilator by activating Kv channels and blocking voltage-gated, receptor-operated and store-operated Ca channels in PASMC. The therapeutic effect of HF on experimental PH is probably due to combination of its vasodilative effect via inhibition of E-C coupling and anti-proliferative effect via inhibition of the PI3K/AKT/mTOR signaling pathway.
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http://dx.doi.org/10.1111/bph.15442DOI Listing
March 2021

Endothelial platelet-derived growth factor-mediated activation of smooth muscle platelet-derived growth factor receptors in pulmonary arterial hypertension.

Pulm Circ 2020 Jul-Sep;10(3):2045894020948470. Epub 2020 Sep 10.

Departments of Medicine and Physiology, The University of Arizona, Tucson, USA.

Platelet-derived growth factor is one of the major growth factors found in human and mammalian serum and tissues. Abnormal activation of platelet-derived growth factor signaling pathway through platelet-derived growth factor receptors may contribute to the development and progression of pulmonary vascular remodeling and obliterative vascular lesions in patients with pulmonary arterial hypertension. In this study, we examined the expression of platelet-derived growth factor receptor isoforms in pulmonary arterial smooth muscle and pulmonary arterial endothelial cells and investigated whether platelet-derived growth factor secreted from pulmonary arterial smooth muscle cell or pulmonary arterial endothelial cell promotes pulmonary arterial smooth muscle cell proliferation. Our results showed that the protein expression of platelet-derived growth factor receptor α and platelet-derived growth factor receptor β in pulmonary arterial smooth muscle cell was upregulated in patients with idiopathic pulmonary arterial hypertension compared to normal subjects. Platelet-derived growth factor activated platelet-derived growth factor receptor α and platelet-derived growth factor receptor β in pulmonary arterial smooth muscle cell, as determined by phosphorylation of platelet-derived growth factor receptor α and platelet-derived growth factor receptor β. The platelet-derived growth factor-mediated activation of platelet-derived growth factor receptor α/platelet-derived growth factor receptor β was enhanced in idiopathic pulmonary arterial hypertension-pulmonary arterial smooth muscle cell compared to normal cells. Expression level of platelet-derived growth factor-AA and platelet-derived growth factor-BB was greater in the conditioned media collected from idiopathic pulmonary arterial hypertension-pulmonary arterial endothelial cell than from normal pulmonary arterial endothelial cell. Furthermore, incubation of idiopathic pulmonary arterial hypertension-pulmonary arterial smooth muscle cell with conditioned culture media from normal pulmonary arterial endothelial cell induced more platelet-derived growth factor receptor α activation than in normal pulmonary arterial smooth muscle cell. Accordingly, the conditioned media from idiopathic pulmonary arterial hypertension-pulmonary arterial endothelial cell resulted in more pulmonary arterial smooth muscle cell proliferation than the media from normal pulmonary arterial endothelial cell. These data indicate that (a) the expression and activity of platelet-derived growth factor receptor are increased in idiopathic pulmonary arterial hypertension-pulmonary arterial smooth muscle cell compared to normal pulmonary arterial smooth muscle cell, and (b) pulmonary arterial endothelial cell from idiopathic pulmonary arterial hypertension patients secretes higher level of platelet-derived growth factor than pulmonary arterial endothelial cell from normal subjects. The enhanced secretion (and production) of platelet-derived growth factor from idiopathic pulmonary arterial hypertension-pulmonary arterial endothelial cell and upregulated platelet-derived growth factor receptor expression (and function) in idiopathic pulmonary arterial hypertension-pulmonary arterial smooth muscle cell may contribute to enhancing platelet-derived growth factor/platelet-derived growth factor receptor-associated pulmonary vascular remodeling in pulmonary arterial hypertension.
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http://dx.doi.org/10.1177/2045894020948470DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7707860PMC
September 2020

Determining the Effect of External Stressors and Cognitive Distraction on Microsurgical Skills and Performance.

Front Surg 2019 22;6:77. Epub 2020 Jan 22.

Department of Plastic and Reconstructive Surgery, Galway University Hospital, Galway, Ireland.

Microsurgery is an essential element of Plastic Surgery practice. There is a paucity of studies assessing the impact of stress and cognitive distraction on technical microsurgical performance. The ability to complete cognitive and technical skills in parallel has not been assessed in a microsurgical setting. To test the hypothesis that cognitive distraction and external stressors negatively affect microsurgical performance in a high fidelity simulation setting. Fourteen surgeons across all levels of training undertook 2 microsurgical skills sessions, 1 month apart. Session one established baseline microsurgical skill. In session two, skills were assessed with the introduction of realistic operative room cognitive distractions (ORDIs). Outcome measures were efficiency and accuracy, measured by Time to Completion (TTC) and Anastomosis Lapse Index (ALI), respectively. Fourteen participants (6 novices, 5 plastic surgery specialist trainees and 3 consultants) completed both microsurgical skills sessions. In total, 28-microvascular anastomosis were analyzed. Mean baseline TTC for the group was 20.36 min. With cognitive distraction and external stress mean TTC decreased to 17.87 min. Mean baseline ALI score for the group was 3.32 errors per anastomosis. The introduction of cognitive distraction and external stress increased the mean to 4.86 errors per anastomosis. Total errors per anastomosis increased from 91 errors at baseline to 137 errors with cognitive distraction and external stress. Under stress, participants were more efficient but had reduced anastomotic accuracy. Under stress, surgeons were more efficient, this translated into faster completion of a microsurgical anastomosis. Efficiency, however, came at the expense of accuracy.
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http://dx.doi.org/10.3389/fsurg.2019.00077DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6987403PMC
January 2020

Divergent changes of p53 in pulmonary arterial endothelial and smooth muscle cells involved in the development of pulmonary hypertension.

Am J Physiol Lung Cell Mol Physiol 2019 01 25;316(1):L216-L228. Epub 2018 Oct 25.

State Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangdong Key Laboratory of Vascular Disease, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University , Guangzhou , China.

The tumor-suppressive role of p53, a transcription factor that regulates the expression of many genes, has been linked to cell cycle arrest, apoptosis, and senescence. The noncanonical function or the pathogenic role of p53 has more recently been implicated in pulmonary vascular disease. We previously reported that rapid nuclear accumulation of hypoxia-inducible factor (HIF)-1α in pulmonary arterial smooth muscle cells (PASMCs) upregulates transient receptor potential channels and enhances Ca entry to increase cytosolic Ca concentration ([Ca]). Also, we observed differences in HIF-1α/2α expression in PASMCs and pulmonary arterial endothelial cells (PAECs). Here we report that p53 is increased in PAECs, but decreased in PASMCs, isolated from mice with hypoxia-induced pulmonary hypertension (PH) and rats with monocrotaline (MCT)-induced PH (MCT-PH). The increased p53 in PAECs from rats with MCT-PH is associated with an increased ratio of Bax/Bcl-2, while the decreased p53 in PASMCs is associated with an increased HIF-1α. Furthermore, p53 is downregulated in PASMCs isolated from patients with idiopathic pulmonary arterial hypertension compared with PASMCs from normal subjects. Overexpression of p53 in normal PASMCs inhibits store-operated Ca entry (SOCE) induced by passive depletion of intracellularly stored Ca in the sarcoplasmic reticulum, while downregulation of p53 enhances SOCE. These data indicate that differentially regulated expression of p53 and HIF-1α/2α in PASMCs and PAECs and the cross talk between p53 and HIF-1α/2α in PASMCs and PAECs may play an important role in the development of PH via, at least in part, induction of PAEC apoptosis and PASMC proliferation.
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http://dx.doi.org/10.1152/ajplung.00538.2017DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6383500PMC
January 2019

STIM2 (Stromal Interaction Molecule 2)-Mediated Increase in Resting Cytosolic Free Ca Concentration Stimulates PASMC Proliferation in Pulmonary Arterial Hypertension.

Hypertension 2018 03 22;71(3):518-529. Epub 2018 Jan 22.

From the Division of Translational and Regenerative Medicine, Department of Medicine (S.S., S.G.C., K.M.M., M.R., A. Babicheva, A. Balistrieri, R.J.A., J.W., A.M., J.X.-J.Y.) and Department of Physiology (A.M., J.X.-J.Y.), The University of Arizona College of Medicine, Tucson.

An increase in cytosolic free Ca concentration ([Ca]) in pulmonary artery smooth muscle cells (PASMCs) triggers pulmonary vasoconstriction and stimulates PASMC proliferation leading to vascular wall thickening. Here, we report that STIM2 (stromal interaction molecule 2), a Ca sensor in the sarcoplasmic reticulum membrane, is required for raising the resting [Ca] in PASMCs from patients with pulmonary arterial hypertension (PAH) and activating signaling cascades that stimulate PASMC proliferation and inhibit PASMC apoptosis. Downregulation of STIM2 in PAH-PASMCs reduces the resting [Ca], whereas overexpression of STIM2 in normal PASMCs increases the resting [Ca] The increased resting [Ca] in PAH-PASMCs is associated with enhanced phosphorylation (p) of CREB (cAMP response element-binding protein), STAT3 (signal transducer and activator of transcription 3), and AKT, increased NFAT (nuclear factor of activated T-cell) nuclear translocation, and elevated level of Ki67 (a marker of cell proliferation). Furthermore, the STIM2-associated increase in the resting [Ca] also upregulates the antiapoptotic protein Bcl-2 in PAH-PASMCs. Downregulation of STIM2 in PAH-PASMCs with siRNA (1) decreases the level of pCREB, pSTAT3, and pAKT and inhibits NFAT nuclear translocation, thereby attenuating proliferation, and (2) decreases Bcl-2, which leads to an increase of apoptosis. In summary, these data indicate that upregulated STIM2 in PAH-PASMCs, by raising the resting [Ca], contributes to enhancing PASMC proliferation by activating the CREB, STAT3, AKT, and NFAT signaling pathways and stimulating PASMC proliferation. The STIM2-associated increase in the resting [Ca] is also involved in upregulating Bcl-2 that makes PAH-PASMCs resistant to apoptosis, and thus plays an important role in sustained pulmonary vasoconstriction and excessive pulmonary vascular remodeling in patients with PAH.
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http://dx.doi.org/10.1161/HYPERTENSIONAHA.117.10503DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5955710PMC
March 2018

Supervised exercise therapy in the management of peripheral arterial disease - an assessment of compliance.

Vasa 2017 May 30;46(3):219-222. Epub 2017 Jan 30.

1 Vascular Surgery, Beaumont Hospital, Dublin, Ireland.

Background: Supervised exercise therapy (SET) is an effective option in the management of peripheral arterial disease (PAD). Unfortunately, poor compliance remains prevalent. This study aimed to assess patient exercise compliance and to identify factors influencing symptomatic improvement and SET participation.

Patients And Methods: Data regarding attendance at SET for this cohort study were extracted from a prospectively maintained database of patients with claudication attending SET at Dublin City University. All patients had ankle brachial index confirmed PAD with associated intermittent claudication. Exercise performance and symptomatic data were gathered retrospectively using patient charts and interviews.

Results: Ninety-eight patients were referred for SET during the study period. The mean age was 69.2 (± 10.1) with 18 % being female. Median follow-up was 25.1 months (IQ range 17.0-31.6). Overall, the mean number of sessions attended per patient was 19.5. Exercise compliance was associated with a significant improvement in symptoms (p = 0.001). Other factors including anatomical level of claudication (P = 0.042) and educational level (p = 0.007) were found to affect the outcome of SET. Multivariate analysis revealed hypertension as a predictor of symptomatic outcome after SET (p = 0.045). Furthermore, ex-smokers (p = 0.021) and those previously diagnosed with hypercholesterolaemia (p = 0.020) or ischaemic heart disease (p = 0.029) had superior exercise compliance. Using linear regression, smoking history (p = 0.024) was identified as a predictor of compliance to SET.

Conclusions: Establishing exercise compliance remains challenging in the PAD cohort. Pre-exercise patient education and personalised exercise prescriptions may result in improvements in function and compliance.
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http://dx.doi.org/10.1024/0301-1526/a000612DOI Listing
May 2017

Anionic microemulsion-mediated low temperature synthesis of anisotropic silicalite-1 nanocrystals.

Langmuir 2005 Dec;21(25):12031-6

Department of Chemical Engineering, Texas A&M University, College Station, 77843-3122, USA.

The low-temperature (368 K) synthesis of silicalite-1 nanocrystals in anionic microemulsions is reported. In the presence of AOT/isooctane mixtures silicalite-1 nanocrystals can be formed that are coffin-shaped and approximately 100 x 40 x 200 nm in size. This is in contrast to samples made without the microemulsion under the same conditions where irregular spherical particles approximately 100 nm in diameter are formed. The current work shows that, in contrast to previous work in this area, the anionic microemulsions cannot stabilize colloidal silica due to the strong repulsive electrostatic forces between the anionic silicate species and the surfactant headgroup. The crystal morphology of the silicalite-1 obtained is also shown to be sensitive to the surfactant identity as syntheses using SDS/heptane/butanol mixtures lead to different morphologies. It is also possible to uncouple zeolite nucleation from growth in these systems. This was demonstrated by adding a solution containing 25 nm silicalite-1 nanocrystals to the AOT/isooctane mixture, which leads to large micron-sized spheres of silicalite-1 containing large mesopores. This report demonstrates that anionic microemulsions lead to fundamentally different crystal habits than the nonionic or cationic microemulsions investigated previously. The future outlook for the use of microemulsion-mediated zeolite growth is also discussed.
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http://dx.doi.org/10.1021/la052181uDOI Listing
December 2005
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