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  1. Article ; Online: Peripheral Blood Omics and Other Multiplex-based Systems in Pulmonary and Critical Care Medicine.

    Balnis, Joseph / Lauria, Eitel J M / Yucel, Recai / Singer, Harold A / Alisch, Reid S / Jaitovich, Ariel

    American journal of respiratory cell and molecular biology

    2023  Volume 69, Issue 4, Page(s) 383–390

    Abstract: Over the last years, the use of peripheral blood-derived big datasets in combination with machine learning technology has accelerated the understanding, prediction, and management of pulmonary and critical care conditions. The goal of this article is to ... ...

    Abstract Over the last years, the use of peripheral blood-derived big datasets in combination with machine learning technology has accelerated the understanding, prediction, and management of pulmonary and critical care conditions. The goal of this article is to provide readers with an introduction to the methods and applications of blood omics and other multiplex-based technologies in the pulmonary and critical care medicine setting to better appreciate the current literature in the field. To accomplish that, we provide essential concepts needed to rationalize this approach and introduce readers to the types of molecules that can be obtained from the circulating blood to generate big datasets; elaborate on the differences between bulk, sorted, and single-cell approaches; and the basic analytical pipelines required for clinical interpretation. Examples of peripheral blood-derived big datasets used in recent literature are presented, and limitations of that technology are highlighted to qualify both the current and future value of these methodologies.
    MeSH term(s) Humans ; Machine Learning ; Critical Care ; Forecasting
    Language English
    Publishing date 2023-06-28
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 1025960-0
    ISSN 1535-4989 ; 1044-1549
    ISSN (online) 1535-4989
    ISSN 1044-1549
    DOI 10.1165/rcmb.2023-0153PS
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 2851: Show issues Location:
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  2. Article ; Online: AMP-Activated Protein Kinase (AMPK) at the Crossroads Between CO

    Balnis, Joseph / Korponay, Tanner C / Jaitovich, Ariel

    International journal of molecular sciences

    2020  Volume 21, Issue 3

    Abstract: Skeletal muscle dysfunction is a major comorbidity in chronic obstructive pulmonary disease (COPD) and other pulmonary conditions. Chronic ... ...

    Abstract Skeletal muscle dysfunction is a major comorbidity in chronic obstructive pulmonary disease (COPD) and other pulmonary conditions. Chronic CO
    MeSH term(s) AMP-Activated Protein Kinases/metabolism ; Animals ; Carbon Dioxide/metabolism ; Comorbidity ; Humans ; Hypercapnia/metabolism ; Muscle, Skeletal/metabolism ; Muscular Atrophy/metabolism ; Pulmonary Disease, Chronic Obstructive/metabolism ; Ribosomes/metabolism
    Chemical Substances Carbon Dioxide (142M471B3J) ; AMP-Activated Protein Kinases (EC 2.7.11.31)
    Language English
    Publishing date 2020-01-31
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms21030955
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Whole-Genome Methylation Sequencing Reveals that COVID-19-induced Epigenetic Dysregulation Remains 1 Year after Hospital Discharge.

    Balnis, Joseph / Madrid, Andy / Hogan, Kirk J / Drake, Lisa A / Adhikari, Anish / Vancavage, Rachel / Singer, Harold A / Alisch, Reid S / Jaitovich, Ariel

    American journal of respiratory cell and molecular biology

    2023  Volume 68, Issue 5, Page(s) 594–597

    MeSH term(s) Humans ; COVID-19 ; Whole Genome Sequencing ; DNA Methylation ; Epigenesis, Genetic ; Hospitals
    Language English
    Publishing date 2023-04-27
    Publishing country United States
    Document type Letter ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1025960-0
    ISSN 1535-4989 ; 1044-1549
    ISSN (online) 1535-4989
    ISSN 1044-1549
    DOI 10.1165/rcmb.2022-0433LE
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2851: Show issues Location:
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  4. Article: Hypercapnia-Driven Skeletal Muscle Dysfunction in an Animal Model of Pulmonary Emphysema Suggests a Complex Phenotype.

    Balnis, Joseph / Lee, Chun Geun / Elias, Jack A / Jaitovich, Ariel

    Frontiers in physiology

    2020  Volume 11, Page(s) 600290

    Abstract: Patients with chronic pulmonary conditions such as chronic obstructive pulmonary disease (COPD) often develop skeletal muscle dysfunction, which is strongly and independently associated with poor outcomes including higher mortality. Some of these ... ...

    Abstract Patients with chronic pulmonary conditions such as chronic obstructive pulmonary disease (COPD) often develop skeletal muscle dysfunction, which is strongly and independently associated with poor outcomes including higher mortality. Some of these patients also develop chronic CO
    Language English
    Publishing date 2020-10-29
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2564217-0
    ISSN 1664-042X
    ISSN 1664-042X
    DOI 10.3389/fphys.2020.600290
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  5. Article ; Online: AMP-Activated Protein Kinase (AMPK) at the Crossroads Between CO 2 Retention and Skeletal Muscle Dysfunction in Chronic Obstructive Pulmonary Disease (COPD)

    Joseph Balnis / Tanner C. Korponay / Ariel Jaitovich

    International Journal of Molecular Sciences, Vol 21, Iss 3, p

    2020  Volume 955

    Abstract: Skeletal muscle dysfunction is a major comorbidity in chronic obstructive pulmonary disease (COPD) and other pulmonary conditions. Chronic CO 2 retention, or hypercapnia, also occur in some of these patients. Both muscle dysfunction and hypercapnia ... ...

    Abstract Skeletal muscle dysfunction is a major comorbidity in chronic obstructive pulmonary disease (COPD) and other pulmonary conditions. Chronic CO 2 retention, or hypercapnia, also occur in some of these patients. Both muscle dysfunction and hypercapnia associate with higher mortality in these populations. Over the last years, we have established a mechanistic link between hypercapnia and skeletal muscle dysfunction, which is regulated by AMPK and causes depressed anabolism via reduced ribosomal biogenesis and accelerated catabolism via proteasomal degradation. In this review, we discuss the main findings linking AMPK with hypercapnic pulmonary disease both in the lungs and skeletal muscles, and also outline potential avenues for future research in the area based on knowledge gaps and opportunities to expand mechanistic research with translational implications.
    Keywords ampk ; protein anabolism ; protein catabolism ; copd ; muscle atrophy ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Subject code 610
    Language English
    Publishing date 2020-01-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  6. Article ; Online: Persistent blood DNA methylation changes one year after SARS-CoV-2 infection.

    Balnis, Joseph / Madrid, Andy / Hogan, Kirk J / Drake, Lisa A / Adhikari, Anish / Vancavage, Rachel / Singer, Harold A / Alisch, Reid S / Jaitovich, Ariel

    Clinical epigenetics

    2022  Volume 14, Issue 1, Page(s) 94

    Abstract: We recently reported the COVID-19-induced circulating leukocytes DNA methylation profile. Here, we hypothesized that some of these genes would persist differentially methylated after disease resolution. Fifteen participants previously hospitalized for ... ...

    Abstract We recently reported the COVID-19-induced circulating leukocytes DNA methylation profile. Here, we hypothesized that some of these genes would persist differentially methylated after disease resolution. Fifteen participants previously hospitalized for SARS-CoV-2 infection were epityped one year after discharge. Of the 1505 acute illness-induced differentially methylated regions (DMRs) previously identified, we found 71 regions with persisted differentially methylated, with an average of 7 serial CpG positions per DMR. Sixty-four DMRs persisted hypermethylated, and 7 DMR persisted hypomethylated. These data are the first reported evidence that DNA methylation changes in circulating leukocytes endure long after recovery from acute illness.
    MeSH term(s) Acute Disease ; COVID-19/genetics ; CpG Islands ; DNA Methylation ; Humans ; SARS-CoV-2
    Language English
    Publishing date 2022-07-23
    Publishing country Germany
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2553921-8
    ISSN 1868-7083 ; 1868-7075
    ISSN (online) 1868-7083
    ISSN 1868-7075
    DOI 10.1186/s13148-022-01313-8
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article: A role for cytoglobin in regulating intracellular hydrogen peroxide and redox signals in the vasculature.

    Mathai, Clinton / Jourd'heuil, Frances / Pham, Le Gia Cat / Gilliard, Kurrim / Balnis, Joseph / Jen, Annie / Overmyer, Katherine A / Coon, Joshua J / Jaitovich, Ariel / Boivin, Benoit / Jourd'heuil, David

    bioRxiv : the preprint server for biology

    2023  

    Abstract: The oxidant hydrogen peroxide serves as a signaling molecule that alters many aspects of cardiovascular functions. Recent studies suggest that cytoglobin - a hemoglobin expressed in the vasculature - may promote electron transfer reactions with proposed ... ...

    Abstract The oxidant hydrogen peroxide serves as a signaling molecule that alters many aspects of cardiovascular functions. Recent studies suggest that cytoglobin - a hemoglobin expressed in the vasculature - may promote electron transfer reactions with proposed functions in hydrogen peroxide decomposition. Here, we determined the extent to which cytoglobin regulates intracellular hydrogen peroxide and established mechanisms. We found that cytoglobin decreased the hyperoxidation of peroxiredoxins and maintained the activity of peroxiredoxin 2 following challenge with exogenous hydrogen peroxide. Cytoglobin promoted a reduced intracellular environment and facilitated the reduction of the thiol-based hydrogen peroxide sensor Hyper7 after bolus addition of hydrogen peroxide. Cytoglobin also limited the inhibitory effect of hydrogen peroxide on glycolysis and reversed the oxidative inactivation of the glycolytic enzyme GAPDH. Our results indicate that cytoglobin in cells exists primarily as oxyferrous cytoglobin (CygbFe
    Language English
    Publishing date 2023-11-06
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.03.31.535146
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  8. Article ; Online: Decreased plasma cartilage acidic protein 1 in COVID-19.

    Johansson, Mats W / Balnis, Joseph / Muehlbauer, Laura K / Bukhman, Yury V / Stefely, Matthew S / Overmyer, Katherine A / Vancavage, Rachel / Tiwari, Anupama / Adhikari, Anish Raj / Feustel, Paul J / Schwartz, Bradford S / Coon, Joshua J / Stewart, Ron / Jaitovich, Ariel / Mosher, Deane F

    Physiological reports

    2023  Volume 11, Issue 17, Page(s) e15814

    Abstract: Cartilage acidic protein-1 (CRTAC1) is produced by several cell types, including Type 2 alveolar epithelial (T2AE) cells that are targeted by SARS-CoV2. Plasma CRTAC1 is known based on proteomic surveys to be low in patients with severe COVID-19. Using ... ...

    Abstract Cartilage acidic protein-1 (CRTAC1) is produced by several cell types, including Type 2 alveolar epithelial (T2AE) cells that are targeted by SARS-CoV2. Plasma CRTAC1 is known based on proteomic surveys to be low in patients with severe COVID-19. Using an ELISA, we found that patients treated for COVID-19 in an ICU almost uniformly had plasma concentrations of CRTAC1 below those of healthy controls. Magnitude of decrease in CRTAC1 distinguished COVID-19 from other causes of acute respiratory decompensation and correlated with established metrics of COVID-19 severity. CRTAC1 concentrations below those of controls were found in some patients a year after hospitalization with COVID-19, long COVID after less severe COVID-19, or chronic obstructive pulmonary disease. Decreases in CRTAC1 in severe COVID-19 correlated (r = 0.37, p = 0.0001) with decreases in CFP (properdin), which interacts with CRTAC1. Thus, decreases of CRTAC1 associated with severe COVID-19 may result from loss of production by T2AE cells or co-depletion with CFP. Determination of significance of and reasons behind decreased CRTAC1 concentration in a subset of patients with long COVID will require analysis of roles of preexisting lung disease, impact of prior acute COVID-19, age, and other confounding variables in a larger number of patients.
    MeSH term(s) Humans ; Calcium-Binding Proteins/blood ; COVID-19 ; Post-Acute COVID-19 Syndrome ; Proteomics ; RNA, Viral ; SARS-CoV-2
    Chemical Substances Calcium-Binding Proteins ; CRTAC1 protein, human ; RNA, Viral
    Language English
    Publishing date 2023-09-04
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2724325-4
    ISSN 2051-817X ; 2051-817X
    ISSN (online) 2051-817X
    ISSN 2051-817X
    DOI 10.14814/phy2.15814
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  9. Article ; Online: Deaccelerated Myogenesis and Autophagy in Genetically Induced Pulmonary Emphysema.

    Balnis, Joseph / Drake, Lisa A / Singer, Diane V / Vincent, Catherine E / Korponay, Tanner C / D'Armiento, Jeanine / Lee, Chun Geun / Elias, Jack A / Singer, Harold A / Jaitovich, Ariel

    American journal of respiratory cell and molecular biology

    2022  Volume 66, Issue 6, Page(s) 623–637

    Abstract: Patients with chronic obstructive pulmonary disease (COPD)-pulmonary emphysema often develop locomotor muscle dysfunction, which entails reduced muscle mass and force-generation capacity and is associated with worse outcomes, including higher mortality. ... ...

    Abstract Patients with chronic obstructive pulmonary disease (COPD)-pulmonary emphysema often develop locomotor muscle dysfunction, which entails reduced muscle mass and force-generation capacity and is associated with worse outcomes, including higher mortality. Myogenesis contributes to adult muscle integrity during injury-repair cycles. Injurious events crucially occur in the skeletal muscles of patients with COPD in the setting of exacerbations and infections, which lead to acute decompensations for limited periods of time, after which patients typically fail to recover the baseline status they had before the acute event. Autophagy, which is dysregulated in muscles from patients with COPD, is a key regulator of muscle stem-satellite- cells activation and myogenesis, yet very little research has so far mechanistically investigated the role of autophagy dysregulation in COPD muscles. Using a genetically inducible interleukin-13-driven pulmonary emphysema model leading to muscle dysfunction, and confirmed with a second genetic animal model, we found a significant myogenic dysfunction associated with the reduced proliferative capacity of satellite cells. Transplantation experiments followed by lineage tracing suggest that an intrinsic defect in satellite cells, and not in the COPD environment, plays a dominant role in the observed myogenic dysfunction. RNA sequencing analysis and direct observation of COPD mice satellite cells suggest dysregulated autophagy. Moreover, while autophagy flux experiments with bafilomycin demonstrated deacceleration of autophagosome turnover in COPD mice satellite cells, spermidine-induced autophagy stimulation leads to a higher replication rate and myogenesis in these animals. Our data suggest that pulmonary emphysema causes disrupted myogenesis, which could be improved with stimulation of autophagy and satellite cells activation, leading to an attenuated muscle dysfunction.
    MeSH term(s) Animals ; Autophagy ; Humans ; Mice ; Muscle Development ; Muscle, Skeletal ; Pulmonary Disease, Chronic Obstructive ; Pulmonary Emphysema/etiology
    Language English
    Publishing date 2022-03-14
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 1025960-0
    ISSN 1535-4989 ; 1044-1549
    ISSN (online) 1535-4989
    ISSN 1044-1549
    DOI 10.1165/rcmb.2021-0351OC
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  10. Article ; Online: Regulation of DNA damage and transcriptional output in the vasculature through a cytoglobin-HMGB2 axis.

    Mathai, Clinton / Jourd'heuil, Frances / Pham, Le Gia Cat / Gilliard, Kurrim / Howard, Dennis / Balnis, Joseph / Jaitovich, Ariel / Chittur, Sridar V / Rilley, Mark / Peredo-Wende, Ruben / Ammoura, Ibrahim / Shin, Sandra J / Barroso, Margarida / Barra, Jonathan / Shishkova, Evgenia / Coon, Joshua J / Lopez-Soler, Reynold I / Jourd'heuil, David

    Redox biology

    2023  Volume 65, Page(s) 102838

    Abstract: Identifying novel regulators of vascular smooth muscle cell function is necessary to further understand cardiovascular diseases. We previously identified cytoglobin, a hemoglobin homolog, with myogenic and cytoprotective roles in the vasculature. The ... ...

    Abstract Identifying novel regulators of vascular smooth muscle cell function is necessary to further understand cardiovascular diseases. We previously identified cytoglobin, a hemoglobin homolog, with myogenic and cytoprotective roles in the vasculature. The specific mechanism of action of cytoglobin is unclear but does not seem to be related to oxygen transport or storage like hemoglobin. Herein, transcriptomic profiling of injured carotid arteries in cytoglobin global knockout mice revealed that cytoglobin deletion accelerated the loss of contractile genes and increased DNA damage. Overall, we show that cytoglobin is actively translocated into the nucleus of vascular smooth muscle cells through a redox signal driven by NOX4. We demonstrate that nuclear cytoglobin heterodimerizes with the non-histone chromatin structural protein HMGB2. Our results are consistent with a previously unknown function by which a non-erythrocytic hemoglobin inhibits DNA damage and regulates gene programs in the vasculature by modulating the genome-wide binding of HMGB2.
    MeSH term(s) Animals ; Mice ; Cytoglobin/genetics ; DNA Damage ; Globins/genetics ; Globins/metabolism ; HMGB2 Protein/genetics ; HMGB2 Protein/metabolism ; Transcription Factors/genetics
    Chemical Substances Cytoglobin ; Globins (9004-22-2) ; HMGB2 Protein ; Transcription Factors ; Cygb protein, mouse
    Language English
    Publishing date 2023-08-09
    Publishing country Netherlands
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2701011-9
    ISSN 2213-2317 ; 2213-2317
    ISSN (online) 2213-2317
    ISSN 2213-2317
    DOI 10.1016/j.redox.2023.102838
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