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Longitudinal correlation of biomarkers of cardiac injury, inflammation, and coagulation to outcome in hospitalized COVID-19 patients.
Li C, Jiang J, Wang F, Zhou N, Veronese G, Moslehi JJ, Ammirati E, Wang DW
(2020) J Mol Cell Cardiol 147: 74-87
MeSH Terms: Aged, Betacoronavirus, Biomarkers, Blood Coagulation, COVID-19, Coronavirus Infections, Critical Illness, Cytokines, Female, Heart Injuries, Humans, Inflammation, Longitudinal Studies, Male, Middle Aged, Pandemics, Pneumonia, Viral, Prognosis, Retrospective Studies, SARS-CoV-2, Troponin I
Show Abstract · Added September 29, 2020
BACKGROUND - Cardiac injury, as measured by troponin elevation, has been reported among hospitalized coronavirus disease 2019 (COVID-19) patients and portends a poor prognosis. However, how the dynamics of troponin elevation interplay with inflammation and coagulation biomarkers over time is unknown. We assessed longitudinal follow-up of cardiac injury, inflammation and coagulation markers in relation to disease severity and outcome.
METHODS - We retrospectively assessed 2068 patients with laboratory-confirmed COVID-19 between January 29 and April 1, 2020 at Tongji Hospital in Wuhan, China. We defined cardiac injury as an increase in high sensitivity cardiac troponin-I (hs-cTnI) above the 99th of the upper reference limit. We explored the dynamics of elevation in hs-cTnI and the relationship with inflammation (interleukin [IL]-6, IL-8, IL-10, IL-2 receptor, tumor necrosis factor-α, C-reactive protein) and coagulation (d-dimer, fibrinogen, international normalized ratio) markers in non-critically ill versus critically ill patients longitudinally and further correlated these markers to survivors and non-survivors.
RESULTS - Median age was 63 years (first to third quartile 51-70 years), 51.4% of whom were women. When compared to non-critically ill patients (N = 1592, 77.0%), critically ill (defined as requiring mechanical ventilation, in shock or multiorgan failure) patients (N = 476, 23.0%), had more frequent cardiac injury on admission (30.3% vs. 2.3%, p < 0.001), with increased mortality during hospitalization (38.4% vs. 0%, p < 0.001). Among critically ill patients, non-survivors (N = 183) had a continuous increase in hs-cTnI levels during hospitalization, while survivors (N = 293) showed a decrease in hs-cTnI level between day 4 and 7 after admission. Specifically, cardiac injury is an independent marker of mortality among critically ill patients at admission, day 4-7 and 8-14. Consistent positive correlations between hs-cTnI and interleukin (IL)-6 on admission (r = 0.59), day 4-7 (r = 0.66) and day 8-14 (r = 0.61; all p < 0.001) and d-dimer (at the same timepoints r = 0.54; 0.65; 0.61, all p < 0.001) were observed. A similar behavior was observed between hs-cTnI and most of other biomarkers of inflammation and coagulation.
CONCLUSIONS - Cardiac injury commonly occurs in critically ill COVID-19 patients, with increased levels of hs-cTnI beyond day 3 since admission portending a poor prognosis. A consistent positive correlation of hs-cTnI with IL-6 and d-dimer at several timepoints along hospitalization could suggest nonspecific cytokine-mediated cardiotoxicity.
Copyright © 2020. Published by Elsevier Ltd.
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21 MeSH Terms
Mortality and Pre-Hospitalization use of Renin-Angiotensin System Inhibitors in Hypertensive COVID-19 Patients.
Chen C, Wang F, Chen P, Jiang J, Cui G, Zhou N, Moroni F, Moslehi JJ, Ammirati E, Wang DW
(2020) J Am Heart Assoc 9: e017736
MeSH Terms: Adult, Aged, Angiotensin Receptor Antagonists, Angiotensin-Converting Enzyme Inhibitors, Antihypertensive Agents, COVID-19, China, Coronavirus Infections, Female, Hospital Mortality, Humans, Hypertension, Male, Middle Aged, Pandemics, Patient Admission, Pneumonia, Viral, Prognosis, Protective Factors, Renin-Angiotensin System, Retrospective Studies, Risk Assessment, Risk Factors
Show Abstract · Added September 29, 2020
Background There has been significant controversy regarding the effects of pre-hospitalization use of renin-angiotensin system (RAS) inhibitors on the prognosis of hypertensive COVID-19 patients. Methods and Results We retrospectively assessed 2,297 hospitalized COVID-19 patients at Tongji Hospital in Wuhan, China, from January 10 to March 30, 2020; and identified 1,182 patients with known hypertension on pre-hospitalization therapy. We compared the baseline characteristics and in-hospital mortality between hypertensive patients taking RAS inhibitors (N=355) versus non-RAS inhibitors (N=827). Of the 1,182 hypertensive patients (median age 68 years, 49.1% male), 12/355 (3.4%) patients died in the RAS inhibitors group vs. 95/827 (11.5%) patients in the non-RAS inhibitors group (p<0.0001). Adjusted hazard ratio for mortality was 0.28 (95% CI 0.15-0.52, p<0.0001) at 45 days in the RAS inhibitors group compared with non-RAS inhibitors group. Similar findings were observed when patients taking angiotensin receptor blockers (N=289) or angiotensin converting enzyme inhibitors (N=66) were separately compared with non-RAS inhibitors group. The RAS inhibitors group compared with non-RAS inhibitors group had lower levels of C-reactive protein (median 13.5 vs. 24.4 pg/mL; p=0.007) and interleukin-6 (median 6.0 vs. 8.5 pg/mL; p=0.026) on admission. The protective effect of RAS inhibitors on mortality was confirmed in a meta-analysis of published data when our data were added to previous studies (odd ratio 0.44, 95% CI 0.29-0.65, p<0.0001). Conclusions In a large single center retrospective analysis we observed a protective effect of pre-hospitalization use of RAS inhibitors on mortality in hypertensive COVID-19 patients; which might be associated with reduced inflammatory response.
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Enhanced Expression of Catalase in Mitochondria Modulates NF-κB-Dependent Lung Inflammation through Alteration of Metabolic Activity in Macrophages.
Han W, Fessel JP, Sherrill T, Kocurek EG, Yull FE, Blackwell TS
(2020) J Immunol 205: 1125-1134
MeSH Terms: Animals, Bone Marrow, Catalase, Lung, Macrophages, Mice, Mice, Inbred C57BL, Mice, Transgenic, Mitochondria, NAD, NF-kappa B, Pneumonia, Reactive Oxygen Species, Signal Transduction
Show Abstract · Added July 28, 2020
NF-κB is a reduction-oxidation-sensitive transcription factor that plays a key role in regulating the immune response. In these studies, we intended to investigate the role of mitochondrial-derived reactive oxygen species in regulating NF-κB activation by studying transgenic mice that overexpress mitochondrial-targeted human catalase (mCAT). We treated wild-type (WT) and mCAT mice with intratracheal instillation of LPS and found that mCAT mice had exaggerated NF-κB activation in the lungs, increased neutrophilic alveolitis, and greater lung inflammation/injury compared with WT mice. Additional studies using bone marrow chimeras revealed that this hyperinflammatory phenotype was mediated by immune/inflammatory cells. Mechanistic studies using bone marrow-derived macrophages (BMDMs) showed that LPS treatment induced a sustained increase in NF-κB activation and expression of NF-κB-dependent inflammatory mediators in mCAT BMDMs compared with WT BMDMs. Further investigations showed that cytoplasmic, but not mitochondrial, hydrogen peroxide levels were reduced in LPS-treated mCAT BMDMs. However, mCAT macrophages exhibited increased glycolytic and oxidative metabolism, coupled with increased ATP production and an increased intracellular NADH/NAD ratio compared with BMDMs from WT mice. Treatment of BMDMs with lactate increased the intracellular NADH/NAD ratio and upregulated NF-κB activation after LPS treatment, whereas treatment with a potent inhibitor of the mitochondrial pyruvate carrier (UK5099) decreased the NADH/NAD ratio and reduced NF-κB activation. Taken together, these findings point to an increased availability of reducing equivalents in the form of NADH as an important mechanism by which metabolic activity modulates inflammatory signaling through the NF-κB pathway.
Copyright © 2020 by The American Association of Immunologists, Inc.
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14 MeSH Terms
Tissue Is the Issue, Even During a Pandemic.
Shah KS, Moslehi JJ, Fang JC
(2020) Circulation 142: 423-425
MeSH Terms: Autopsy, COVID-19, Humans, Pneumonia, Risk, Tissue and Organ Procurement
Added September 29, 2020
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COVID-19 and Asian American Pacific Islanders.
Hu JR, Wang M, Lu F
(2020) J Gen Intern Med 35: 2763-2764
MeSH Terms: Asian Americans, Betacoronavirus, COVID-19, Coronavirus Infections, Humans, Oceanic Ancestry Group, Pandemics, Pneumonia, Viral, Racism, SARS-CoV-2
Added August 13, 2020
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COVID-19 and immune checkpoint inhibitors: initial considerations.
Sullivan RJ, Johnson DB, Rini BI, Neilan TG, Lovly CM, Moslehi JJ, Reynolds KL
(2020) J Immunother Cancer 8:
MeSH Terms: Antineoplastic Agents, Immunological, COVID-19, Coronavirus Infections, Humans, Molecular Targeted Therapy, Neoplasms, Pandemics, Pneumonia, Viral, Programmed Cell Death 1 Receptor
Show Abstract · Added May 29, 2020
COVID-19 infections are characterized by inflammation of the lungs and other organs that ranges from mild and asymptomatic to fulminant and fatal. Patients who are immunocompromised and those with cardiopulmonary comorbidities appear to be particularly afflicted by this illness. During pandemic conditions, many aspects of cancer care have been impacted. One important clinical question is how to manage patients who need anticancer therapy, including immune checkpoint inhibitors (ICIs) during these conditions. Herein, we consider diagnostic and therapeutic implications of using ICI during this unprecedented period of COVID-19 infections. In particular, we consider the impact of ICI on COVID-19 severity, decisions surrounding continuing or interrupting therapy, diagnostic measures in patients with symptoms or manifestations potentially consistent with either COVID-19 or ICI toxicity, and resumption of therapy in infected patients. While more robust data are needed to guide clinicians on management of patients with cancer who may be affected by COVID-19, we hope this commentary provides useful insights for the clinical community.
© Author(s) (or their employer(s)) 2020. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.
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A primer on viral-associated olfactory loss in the era of COVID-19.
Soler ZM, Patel ZM, Turner JH, Holbrook EH
(2020) Int Forum Allergy Rhinol 10: 814-820
MeSH Terms: Betacoronavirus, COVID-19, Coronavirus Infections, Humans, Olfaction Disorders, Olfactory Perception, Pandemics, Pneumonia, Viral, SARS-CoV-2, Smell
Show Abstract · Added July 23, 2020
Early reports have suggested that smell loss may be an early symptom associated with the pandemic known as coronavirus disease 2019 (COVID-19). The possibility that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) might cause olfactory dysfunction is certainly plausible. Patients presenting to specialized smell clinics are commonly diagnosed with upper respiratory infection (URI)-associated olfactory loss and most are presumed to be viral related. In acute phases of infection, it is common to experience some smell loss as a result of nasal inflammation, mucosal edema, and obstruction of airflow into the olfactory cleft. In most cases, these episodes of smell loss are self-limiting and coincide with resolution of URI symptoms. However, in some cases the smell loss persists for months to years and this is presumed to occur through a more direct olfactory insult by the virus. It remains too early to know whether infection with SARS-CoV-2 causes persistent olfactory dysfunction. However, given the scale of this pandemic, if SARS-CoV-2 does cause chronic olfactory loss in even a small portion of those infected, then the overall population prevalence could be quite large. This review provides a brief, practical overview of viral-associated olfactory loss, realizing that evidence related to COVID-19 will likely not be clear for some time. Our goal is to highlight the existence and importance of this condition and provide information geared for both providers and patients. Practical suggestions regarding evaluation and treatment will be provided, realizing that there may be constraints on medical resources and the nature of this pandemic remains dynamic.
© 2020 ARS-AAOA, LLC.
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10 MeSH Terms
An autoimmune-based, paraneoplastic neurologic syndrome following checkpoint inhibition and concurrent radiotherapy for merkel cell carcinoma: case report.
Sherry AD, Bezzerides M, Khattab MH, Luo G, Ancell KK, Kirschner AN
(2020) Strahlenther Onkol 196: 664-670
MeSH Terms: Aged, Antibodies, Monoclonal, Humanized, Antineoplastic Agents, Immunological, Antineoplastic Combined Chemotherapy Protocols, Autoimmune Diseases of the Nervous System, Axilla, Carboplatin, Carcinoma, Merkel Cell, Combined Modality Therapy, Deglutition Disorders, Etoposide, Fatal Outcome, Fingers, Hallucinations, Humans, Lymphatic Metastasis, Male, Neuralgia, Palliative Care, Paraneoplastic Syndromes, Nervous System, Parenteral Nutrition, Total, Pneumonia, Aspiration, Positron Emission Tomography Computed Tomography, Radioimmunotherapy, Radiotherapy, High-Energy, Radiotherapy, Intensity-Modulated, Skin Neoplasms
Show Abstract · Added March 3, 2020
PURPOSE - Merkel cell carcinoma is highly sensitive to both radiation and immunotherapy. Moreover, concurrent radioimmunotherapy may capitalize on anti-tumor immune activity and improve Merkel cell treatment response, although an enhanced immune system may cross-react with native tissues and lead to significant sequelae.
METHODS - Here we present a case study of a patient with metastatic Merkel cell carcinoma treated with radiotherapy concurrent with pembrolizumab.
RESULTS - After radioimmunotherapy, the patient developed sensory neuropathy, visual hallucinations, and mixed motor neuron findings. Neurologic dysfunction progressed to profound gastrointestinal dysmotility necessitating parenteral nutrition and intubation with eventual expiration.
CONCLUSION - This case represents a unique autoimmune paraneoplastic neurologic syndrome, likely specific to neuroendocrine tumors and motivated by concurrent radioimmunotherapy. Recognition of the potential role of radioimmunotherapy may provide an advantage in anticipating these severe sequelae.
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27 MeSH Terms
β1 Integrin regulates adult lung alveolar epithelial cell inflammation.
Plosa EJ, Benjamin JT, Sucre JM, Gulleman PM, Gleaves LA, Han W, Kook S, Polosukhin VV, Haake SM, Guttentag SH, Young LR, Pozzi A, Blackwell TS, Zent R
(2020) JCI Insight 5:
MeSH Terms: Aging, Alveolar Epithelial Cells, Animals, Cell Adhesion, Chemokine CCL2, Chemokines, Disease Models, Animal, Epithelium, Integrin beta1, Lung, Macrophages, Mice, Mice, Inbred C57BL, Mice, Knockout, Pneumonia, Pulmonary Disease, Chronic Obstructive, Receptors, CCR2
Show Abstract · Added March 3, 2020
Integrins, the extracellular matrix receptors that facilitate cell adhesion and migration, are necessary for organ morphogenesis; however, their role in maintaining adult tissue homeostasis is poorly understood. To define the functional importance of β1 integrin in adult mouse lung, we deleted it after completion of development in type 2 alveolar epithelial cells (AECs). Aged β1 integrin-deficient mice exhibited chronic obstructive pulmonary disease-like (COPD-like) pathology characterized by emphysema, lymphoid aggregates, and increased macrophage infiltration. These histopathological abnormalities were preceded by β1 integrin-deficient AEC dysfunction such as excessive ROS production and upregulation of NF-κB-dependent chemokines, including CCL2. Genetic deletion of the CCL2 receptor, Ccr2, in mice with β1 integrin-deficient type 2 AECs impaired recruitment of monocyte-derived macrophages and resulted in accelerated inflammation and severe premature emphysematous destruction. The lungs exhibited reduced AEC efferocytosis and excessive numbers of inflamed type 2 AECs, demonstrating the requirement for recruited monocytes/macrophages in limiting lung injury and remodeling in the setting of a chronically inflamed epithelium. These studies support a critical role for β1 integrin in alveolar homeostasis in the adult lung.
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The Incidence of Laryngotracheal Stenosis in Neonates With a History of Ventilator-Associated Pneumonia.
Lowery AS, Gelbard A, Wootten C
(2020) Laryngoscope 130: 2252-2255
MeSH Terms: Bronchoalveolar Lavage, Bronchoalveolar Lavage Fluid, Case-Control Studies, Female, Humans, Incidence, Infant, Newborn, Intensive Care Units, Neonatal, Laryngostenosis, Male, Pneumonia, Ventilator-Associated, Retrospective Studies, Risk Factors, Tracheal Stenosis
Show Abstract · Added July 30, 2020
OBJECTIVES/HYPOTHESIS - Neonatal patients requiring prolonged intubation are susceptible to both infection and laryngotracheal stenosis (LTS). This study investigated the effect of ventilator-associated pneumonia (VAP) on the development of LTS in neonates.
STUDY DESIGN - Retrospective case-control study.
METHODS - The incidence of LTS in neonates with VAP was compared with the incidence of LTS in matched intubated controls without VAP. Patients were treated at a tertiary-care medical center from 2004 to 2014. Eligible patient records were assessed for the development of LTS. Demographics, medical comorbidities, infection characteristics, and treatment variables were compared using unpaired t test or χ test. Statistical significance was set a priori at P < .05.
RESULTS - When comparing the VAP patients with matched non-VAP controls, we found no significant differences in the incidence of LTS (VAP vs. non-VAP, 8.3% vs. 6.7%; P = .73). In subgroup analysis of the VAP cohort, LTS and non-LTS patients demonstrated similar VAP organisms on broncho-alveolar lavage (Klebsiella pneumoniae, Pseudomonas aeroginosa, Escherichia coli, methicillin-resistant Staphylococcus aureus, Streptococcus pneumoniae, and Enterobacter). Additionally, within the VAP cohort, LTS and non-LTS patients showed similar gestational age (LTS vs. non-LTS, 31.3 days vs. 28.1 days; P = .22), birth weight (LTS vs. non-LTS, 1.6 kg vs. 1.2 kg; P = .33), and similar intubation duration (LTS vs. non-LTS, 37.8 days vs. 27.5 days; P = .52).
CONCLUSIONS - In this neonatal cohort, VAP was not associated with an increased incidence of LTS. Given severity of the burden of LTS on the healthcare system, multi-institutional longitudinal investigation into contributing risk factors for neonatal LTS is warranted.
LEVEL OF EVIDENCE - NA Laryngoscope, 130:2252-2255, 2020.
© 2019 The American Laryngological, Rhinological and Otological Society, Inc.
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14 MeSH Terms