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  1. Article ; Online: Chronic Kidney Disease and Dietary Measures to Improve Outcomes.

    Akchurin, Oleh M

    Pediatric clinics of North America

    2018  Volume 66, Issue 1, Page(s) 247–267

    Abstract: Chronic kidney disease is an ongoing deterioration of renal function that often progresses to end-stage renal disease. Management goals in children include slowing disease progression, prevention and treatment of complications, and optimizing growth, ... ...

    Abstract Chronic kidney disease is an ongoing deterioration of renal function that often progresses to end-stage renal disease. Management goals in children include slowing disease progression, prevention and treatment of complications, and optimizing growth, development, and quality of life. Nutritional management is critically important to achieve these goals. Control of blood pressure, proteinuria, and metabolic acidosis with dietary and pharmacologic measures may slow progression of chronic kidney disease. Although significant progress in management has been made, further research is required to resolve many outstanding controversies. We review recent developments in pediatric chronic kidney disease, focusing on dietary measures to improve outcomes.
    MeSH term(s) Child ; Diagnosis, Differential ; Disease Progression ; Humans ; Kidney Function Tests ; Quality of Life ; Renal Insufficiency, Chronic/diagnosis ; Renal Insufficiency, Chronic/diet therapy ; Renal Insufficiency, Chronic/etiology
    Language English
    Publishing date 2018-11-16
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 215711-1
    ISSN 1557-8240 ; 0031-3955
    ISSN (online) 1557-8240
    ISSN 0031-3955
    DOI 10.1016/j.pcl.2018.09.007
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Skeletal muscle single fiber force production declines early in juvenile male mice with chronic kidney disease.

    Momb, Brent A / Patino, Edwin / Akchurin, Oleh M / Miller, Mark S

    Physiological reports

    2023  Volume 11, Issue 7, Page(s) e15651

    Abstract: Children with chronic kidney disease (CKD) frequently exhibit delayed physical development and reduced physical performance, presumably due to skeletal muscle dysfunction. However, the cellular and molecular basis of skeletal muscle impairment in ... ...

    Abstract Children with chronic kidney disease (CKD) frequently exhibit delayed physical development and reduced physical performance, presumably due to skeletal muscle dysfunction. However, the cellular and molecular basis of skeletal muscle impairment in juvenile CKD remains poorly understood. Cellular (single fiber) and molecular (myosin-actin interactions and myofilament properties) function was examined ex vivo in slow (soleus) and fast (extensor digitorum longus) contracting muscles of juvenile male (6 weeks old) CKD and control mice. CKD was induced by 0.2% adenine diet for 3 weeks starting at 3 weeks of age. Specific tension (maximal isometric force divided by cross-sectional area) was reduced in larger myosin heavy chain (MHC) I and IIA fibers and in all IIB fibers in juvenile male mice with CKD due to fewer strongly bound myosin-actin cross-bridges. Fiber cross-sectional area in juvenile CKD mice was unchanged in MHC I and IIB fibers and increased in MHC IIA fibers, compared to controls. CKD slowed cross-bridge kinetics (slower rate of myosin force production and longer myosin attachment time, t
    MeSH term(s) Male ; Mice ; Animals ; Actins/metabolism ; Muscle Fibers, Skeletal/metabolism ; Muscle, Skeletal/metabolism ; Muscle Contraction/physiology ; Myosins/metabolism ; Myosin Heavy Chains/metabolism ; Renal Insufficiency, Chronic/metabolism
    Chemical Substances Actins ; Myosins (EC 3.6.4.1) ; Myosin Heavy Chains (EC 3.6.4.1)
    Language English
    Publishing date 2023-04-05
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 2724325-4
    ISSN 2051-817X ; 2051-817X
    ISSN (online) 2051-817X
    ISSN 2051-817X
    DOI 10.14814/phy2.15651
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Are we ready to reliably assess transition readiness?

    Akchurin, Oleh M

    Pediatric transplantation

    2015  Volume 19, Issue 8, Page(s) 807–809

    MeSH term(s) Humans ; Surveys and Questionnaires ; Transition to Adult Care
    Language English
    Publishing date 2015-12
    Publishing country Denmark
    Document type Comment ; Editorial
    ZDB-ID 1390284-2
    ISSN 1399-3046 ; 1397-3142
    ISSN (online) 1399-3046
    ISSN 1397-3142
    DOI 10.1111/petr.12524
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    Zs.A 4947: Show issues Location:
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  4. Article ; Online: Iron Supplementation Improves Skeletal Muscle Contractile Properties in Mice with CKD.

    Momb, Brent A / Patino, Edwin / Akchurin, Oleh M / Miller, Mark S

    Kidney360

    2022  Volume 3, Issue 5, Page(s) 843–858

    Abstract: Background: Patients with chronic kidney disease (CKD) frequently have compromised physical performance, which increases their mortality; however, their skeletal muscle dysfunction has not been characterized at the single-fiber and molecular levels. ... ...

    Abstract Background: Patients with chronic kidney disease (CKD) frequently have compromised physical performance, which increases their mortality; however, their skeletal muscle dysfunction has not been characterized at the single-fiber and molecular levels. Notably, interventions to mitigate CKD myopathy are scarce.
    Methods: The effect of CKD in the absence and presence of iron supplementation on the contractile function of individual skeletal muscle fibers from the soleus and extensor digitorum longus muscles was evaluated in 16-week-old mice. CKD was induced by the adenine diet, and iron supplementation was by weekly iron dextran injections.
    Results: Maximally activated and fatigued fiber force production was decreased 24%-52% in untreated CKD, independent of size, by reducing strongly bound myosin/actin cross-bridges and/or decreasing myofilament stiffness in myosin heavy chain (MHC) I, IIA, and IIB fibers. Additionally, myosin/actin interactions in untreated CKD were slower for MHC I and IIA fibers and unchanged or faster in MHC IIB fibers. Iron supplementation improved anemia and did not change overall muscle mass in CKD mice. Iron supplementation ameliorated CKD-induced myopathy by increasing strongly bound cross-bridges, leading to improved specific tension, and/or returning the rate of myosin/actin interactions toward or equivalent to control values in MHC IIA and IIB fibers.
    Conclusions: Skeletal muscle force production was significantly reduced in untreated CKD, independent of fiber size, indicating that compromised physical function in patients is not solely due to muscle mass loss. Iron supplementation improved multiple aspects of CKD-induced myopathy, suggesting that timely correction of iron imbalance may aid in ameliorating contractile deficits in CKD patients.
    MeSH term(s) Actins/metabolism ; Adenine/metabolism ; Animals ; Dextrans/metabolism ; Dietary Supplements ; Iron/metabolism ; Mice ; Muscle, Skeletal/metabolism ; Myosin Heavy Chains/metabolism ; Myosins/metabolism ; Renal Insufficiency, Chronic/drug therapy
    Chemical Substances Actins ; Dextrans ; Iron (E1UOL152H7) ; Myosin Heavy Chains (EC 3.6.4.1) ; Myosins (EC 3.6.4.1) ; Adenine (JAC85A2161)
    Language English
    Publishing date 2022-03-25
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 2641-7650
    ISSN (online) 2641-7650
    DOI 10.34067/KID.0004412021
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  5. Article ; Online: Update on inflammation in chronic kidney disease.

    Akchurin, Oleh M / Kaskel, Frederick

    Blood purification

    2015  Volume 39, Issue 1-3, Page(s) 84–92

    Abstract: Background: Despite recent advances in chronic kidney disease (CKD) and end-stage renal disease (ESRD) management, morbidity and mortality in this population remain exceptionally high. Persistent, low-grade inflammation has been recognized as an ... ...

    Abstract Background: Despite recent advances in chronic kidney disease (CKD) and end-stage renal disease (ESRD) management, morbidity and mortality in this population remain exceptionally high. Persistent, low-grade inflammation has been recognized as an important component of CKD, playing a unique role in its pathophysiology and being accountable in part for cardiovascular and all-cause mortality, as well as contributing to the development of protein-energy wasting.
    Summary: The variety of factors contribute to chronic inflammatory status in CKD, including increased production and decreased clearance of pro-inflammatory cytokines, oxidative stress and acidosis, chronic and recurrent infections, including those related to dialysis access, altered metabolism of adipose tissue, and intestinal dysbiosis. Inflammation directly correlates with the glomerular filtration rate (GFR) in CKD and culminates in dialysis patients, where extracorporeal factors, such as impurities in dialysis water, microbiological quality of the dialysate, and bioincompatible factors in the dialysis circuit play an additional role. Genetic and epigenetic influences contributing to inflammatory activation in CKD are currently being intensively investigated. A number of interventions have been proposed to target inflammation in CKD, including lifestyle modifications, pharmacological agents, and optimization of dialysis. Importantly, some of these therapies have been recently tested in randomized controlled trials.
    Key messages: Chronic inflammation should be regarded as a common comorbid condition in CKD and especially in dialysis patients. A number of interventions have been proven to be safe and effective in well-designed clinical studies. This includes such inexpensive approaches as modification of physical activity and dietary supplementation. Further investigations are needed to evaluate the effects of these interventions on hard outcomes, as well as to better understand the role of inflammation in selected CKD populations (e.g., in children).
    MeSH term(s) Acidosis/complications ; Acidosis/mortality ; Acidosis/pathology ; Acidosis/therapy ; Anti-Inflammatory Agents/therapeutic use ; Cardiovascular Diseases/complications ; Cardiovascular Diseases/mortality ; Cardiovascular Diseases/pathology ; Cardiovascular Diseases/therapy ; Cytokines/biosynthesis ; Dietary Supplements ; Exercise ; Glomerular Filtration Rate ; Humans ; Inflammation/complications ; Inflammation/mortality ; Inflammation/pathology ; Inflammation/therapy ; Kidney Failure, Chronic/complications ; Kidney Failure, Chronic/mortality ; Kidney Failure, Chronic/pathology ; Kidney Failure, Chronic/therapy ; Oxidative Stress ; Randomized Controlled Trials as Topic ; Renal Dialysis ; Survival Analysis ; Wasting Syndrome/complications ; Wasting Syndrome/mortality ; Wasting Syndrome/pathology ; Wasting Syndrome/therapy
    Chemical Substances Anti-Inflammatory Agents ; Cytokines
    Language English
    Publishing date 2015
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 605548-5
    ISSN 1421-9735 ; 0253-5068
    ISSN (online) 1421-9735
    ISSN 0253-5068
    DOI 10.1159/000368940
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    Zs.A 1872: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  6. Article ; Online: Late steroid resistance in childhood nephrotic syndrome: do we now know more than 40 years ago?

    Akchurin, Oleh M / Kaskel, Frederick J

    Pediatric nephrology (Berlin, Germany)

    2013  Volume 28, Issue 8, Page(s) 1157–1160

    Abstract: The formation of steroid resistance in children with nephrotic syndrome (NS) who were initially steroid responsive was described decades ago but has not been studied in sufficient depth. Except for the International Study of Kidney Disease in Children, ... ...

    Abstract The formation of steroid resistance in children with nephrotic syndrome (NS) who were initially steroid responsive was described decades ago but has not been studied in sufficient depth. Except for the International Study of Kidney Disease in Children, conducted more than three decades ago, when only cyclophosphamide was available as a second-line agent in steroid-resistant NS, only a handful of small studies have addressed the problem of late steroid resistance (LSR) over the past 40 years. Epidemiology and risk factors for the formation of LSR and differences in outcomes when compared with initial steroid resistance still remain unknown. While multiple second-line treatment choices (calcineurin inhibitors, mycophenolate mofetil, rituximab) exist today, therapeutic approaches to the patients with LSR remain empirical, as no evidence-based data have become available. In the current issue of Pediatric Nephrology, Straatmann et al. report retrospective data on the treatment outcomes for 29 pediatric NS patients with LSR from eight participating centers of the Midwest Pediatric Research Consortium. The authors describe a current pattern of second-line agents used in their cohort and show that the majority of patients (66 %) achieved complete or partial remission after a period of observation for 85 ± 47 months. The authors also describe the data on renal histology. While these data represent an important step forward in our understanding of LSR, further work is needed before firm clinical recommendations can be made. Large-scale prospective studies are required to answer important questions about the epidemiology, genetics and outcomes in late steroid-resistant NS, explore the role of medication adherence and develop evidence-based practice guidelines.
    MeSH term(s) Female ; Humans ; Immunosuppressive Agents/therapeutic use ; Kidney/drug effects ; Male ; Nephrotic Syndrome/congenital ; Nephrotic Syndrome/drug therapy
    Chemical Substances Immunosuppressive Agents
    Language English
    Publishing date 2013-05-25
    Publishing country Germany
    Document type Editorial ; Comment
    ZDB-ID 631932-4
    ISSN 1432-198X ; 0931-041X
    ISSN (online) 1432-198X
    ISSN 0931-041X
    DOI 10.1007/s00467-013-2509-5
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    Zs.A 2196: Show issues Location:
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  7. Article ; Online: Urine-based multi-omic comparative analysis of COVID-19 and bacterial sepsis-induced ARDS.

    Batra, Richa / Uni, Rie / Akchurin, Oleh M / Alvarez-Mulett, Sergio / Gómez-Escobar, Luis G / Patino, Edwin / Hoffman, Katherine L / Simmons, Will / Whalen, William / Chetnik, Kelsey / Buyukozkan, Mustafa / Benedetti, Elisa / Suhre, Karsten / Schenck, Edward / Cho, Soo Jung / Choi, Augustine M K / Schmidt, Frank / Choi, Mary E / Krumsiek, Jan

    Molecular medicine (Cambridge, Mass.)

    2023  Volume 29, Issue 1, Page(s) 13

    Abstract: Background: Acute respiratory distress syndrome (ARDS), a life-threatening condition during critical illness, is a common complication of COVID-19. It can originate from various disease etiologies, including severe infections, major injury, or ... ...

    Abstract Background: Acute respiratory distress syndrome (ARDS), a life-threatening condition during critical illness, is a common complication of COVID-19. It can originate from various disease etiologies, including severe infections, major injury, or inhalation of irritants. ARDS poses substantial clinical challenges due to a lack of etiology-specific therapies, multisystem involvement, and heterogeneous, poor patient outcomes. A molecular comparison of ARDS groups holds the potential to reveal common and distinct mechanisms underlying ARDS pathogenesis.
    Methods: We performed a comparative analysis of urine-based metabolomics and proteomics profiles from COVID-19 ARDS patients (n = 42) and bacterial sepsis-induced ARDS patients (n = 17). To this end, we used two different approaches, first we compared the molecular omics profiles between ARDS groups, and second, we correlated clinical manifestations within each group with the omics profiles.
    Results: The comparison of the two ARDS etiologies identified 150 metabolites and 70 proteins that were differentially abundant between the two groups. Based on these findings, we interrogated the interplay of cell adhesion/extracellular matrix molecules, inflammation, and mitochondrial dysfunction in ARDS pathogenesis through a multi-omic network approach. Moreover, we identified a proteomic signature associated with mortality in COVID-19 ARDS patients, which contained several proteins that had previously been implicated in clinical manifestations frequently linked with ARDS pathogenesis.
    Conclusion: In summary, our results provide evidence for significant molecular differences in ARDS patients from different etiologies and a potential synergy of extracellular matrix molecules, inflammation, and mitochondrial dysfunction in ARDS pathogenesis. The proteomic mortality signature should be further investigated in future studies to develop prediction models for COVID-19 patient outcomes.
    MeSH term(s) Humans ; COVID-19/complications ; Proteomics ; Multiomics ; Respiratory Distress Syndrome/etiology ; Sepsis/complications ; Inflammation
    Language English
    Publishing date 2023-01-26
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 1283676-x
    ISSN 1528-3658 ; 1076-1551
    ISSN (online) 1528-3658
    ISSN 1076-1551
    DOI 10.1186/s10020-023-00609-6
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    Zs.A 4456: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  8. Article ; Online: Update on Inflammation in Chronic Kidney Disease

    Akchurin, Oleh M. / Kaskel, Frederick

    Blood Purification

    2015  Volume 39, Issue 1-3, Page(s) 84–92

    Abstract: Background: Despite recent advances in chronic kidney disease (CKD) and end-stage renal disease (ESRD) management, morbidity and mortality in this population remain exceptionally high. Persistent, low-grade inflammation has been recognized as an ... ...

    Abstract Background: Despite recent advances in chronic kidney disease (CKD) and end-stage renal disease (ESRD) management, morbidity and mortality in this population remain exceptionally high. Persistent, low-grade inflammation has been recognized as an important component of CKD, playing a unique role in its pathophysiology and being accountable in part for cardiovascular and all-cause mortality, as well as contributing to the development of protein-energy wasting. Summary: The variety of factors contribute to chronic inflammatory status in CKD, including increased production and decreased clearance of pro-inflammatory cytokines, oxidative stress and acidosis, chronic and recurrent infections, including those related to dialysis access, altered metabolism of adipose tissue, and intestinal dysbiosis. Inflammation directly correlates with the glomerular filtration rate (GFR) in CKD and culminates in dialysis patients, where extracorporeal factors, such as impurities in dialysis water, microbiological quality of the dialysate, and bioincompatible factors in the dialysis circuit play an additional role. Genetic and epigenetic influences contributing to inflammatory activation in CKD are currently being intensively investigated. A number of interventions have been proposed to target inflammation in CKD, including lifestyle modifications, pharmacological agents, and optimization of dialysis. Importantly, some of these therapies have been recently tested in randomized controlled trials. Key Messages: Chronic inflammation should be regarded as a common comorbid condition in CKD and especially in dialysis patients. A number of interventions have been proven to be safe and effective in well-designed clinical studies. This includes such inexpensive approaches as modification of physical activity and dietary supplementation. Further investigations are needed to evaluate the effects of these interventions on hard outcomes, as well as to better understand the role of inflammation in selected CKD populations (e.g., in children).© 2015 S. Karger AG, Basel
    Keywords Inflammation ; Cytokines ; Chronic kidney disease ; 
End-stage renal disease ; Dialysis ; Malnutrition ; 
Protein-energy wasting
    Language English
    Publisher S. Karger AG
    Publishing place Basel
    Publishing country Switzerland
    Document type Article ; Online
    ZDB-ID 605548-5
    ISSN 1421-9735 ; 0253-5068 ; 0253-5068
    ISSN (online) 1421-9735
    ISSN 0253-5068
    DOI 10.1159/000368940
    Database Karger publisher's database

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1872: Show issues Location:
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    ab Jg. 2022: Lesesaal (EG)

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  9. Article: Urine-based multi-omic comparative analysis of COVID-19 and bacterial sepsis-induced ARDS.

    Batra, Richa / Uni, Rie / Akchurin, Oleh M / Alvarez-Mulett, Sergio / Gómez-Escobar, Luis G / Patino, Edwin / Hoffman, Katherine L / Simmons, Will / Chetnik, Kelsey / Buyukozkan, Mustafa / Benedetti, Elisa / Suhre, Karsten / Schenck, Edward / Cho, Soo Jung / Choi, Augustine M K / Schmidt, Frank / Choi, Mary E / Krumsiek, Jan

    medRxiv : the preprint server for health sciences

    2022  

    Abstract: Acute respiratory distress syndrome (ARDS), a life-threatening condition during critical illness, is a common complication of COVID-19. It can originate from various disease etiologies, including severe infections, major injury, or inhalation of ... ...

    Abstract Acute respiratory distress syndrome (ARDS), a life-threatening condition during critical illness, is a common complication of COVID-19. It can originate from various disease etiologies, including severe infections, major injury, or inhalation of irritants. ARDS poses substantial clinical challenges due to a lack of etiology-specific therapies, multisystem involvement, and heterogeneous, poor patient outcomes. A molecular comparison of ARDS groups holds the potential to reveal common and distinct mechanisms underlying ARDS pathogenesis. In this study, we performed a comparative analysis of urine-based metabolomics and proteomics profiles from COVID-19 ARDS patients (n = 42) and bacterial sepsis-induced ARDS patients (n = 17). The comparison of these ARDS etiologies identified 150 metabolites and 70 proteins that were differentially abundant between the two groups. Based on these findings, we interrogated the interplay of cell adhesion/extracellular matrix molecules, inflammation, and mitochondrial dysfunction in ARDS pathogenesis through a multi-omic network approach. Moreover, we identified a proteomic signature associated with mortality in COVID-19 ARDS patients, which contained several proteins that had previously been implicated in clinical manifestations frequently linked with ARDS pathogenesis. In summary, our results provide evidence for significant molecular differences in ARDS patients from different etiologies and a potential synergy of extracellular matrix molecules, inflammation, and mitochondrial dysfunction in ARDS pathogenesis. The proteomic mortality signature should be further investigated in future studies to develop prediction models for COVID-19 patient outcomes.
    Language English
    Publishing date 2022-08-10
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2022.08.10.22277939
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article: Update on Inflammation in Chronic Kidney Disease

    Akchurin, Oleh M. / Kaskel, Frederick

    Blood Purification

    2015  Volume 39, Issue 1-3, Page(s) 84–92

    Abstract: Background: Despite recent advances in chronic kidney disease (CKD) and end-stage renal disease (ESRD) management, morbidity and mortality in this population remain exceptionally high. Persistent, low-grade inflammation has been recognized as an ... ...

    Institution Weill Cornell College of Medicine, Department of Pediatrics, New York, N.Y. and Albert Einstein College of Medicine, Department of Pediatrics, Bronx, N.Y., USA
    Abstract Background: Despite recent advances in chronic kidney disease (CKD) and end-stage renal disease (ESRD) management, morbidity and mortality in this population remain exceptionally high. Persistent, low-grade inflammation has been recognized as an important component of CKD, playing a unique role in its pathophysiology and being accountable in part for cardiovascular and all-cause mortality, as well as contributing to the development of protein-energy wasting. Summary: The variety of factors contribute to chronic inflammatory status in CKD, including increased production and decreased clearance of pro-inflammatory cytokines, oxidative stress and acidosis, chronic and recurrent infections, including those related to dialysis access, altered metabolism of adipose tissue, and intestinal dysbiosis. Inflammation directly correlates with the glomerular filtration rate (GFR) in CKD and culminates in dialysis patients, where extracorporeal factors, such as impurities in dialysis water, microbiological quality of the dialysate, and bioincompatible factors in the dialysis circuit play an additional role. Genetic and epigenetic influences contributing to inflammatory activation in CKD are currently being intensively investigated. A number of interventions have been proposed to target inflammation in CKD, including lifestyle modifications, pharmacological agents, and optimization of dialysis. Importantly, some of these therapies have been recently tested in randomized controlled trials. Key Messages: Chronic inflammation should be regarded as a common comorbid condition in CKD and especially in dialysis patients. A number of interventions have been proven to be safe and effective in well-designed clinical studies. This includes such inexpensive approaches as modification of physical activity and dietary supplementation. Further investigations are needed to evaluate the effects of these interventions on hard outcomes, as well as to better understand the role of inflammation in selected CKD populations (e.g., in children).
    Keywords Inflammation ; Cytokines ; Chronic kidney disease ; End-stage renal disease ; Dialysis ; Malnutrition ; Protein-energy wasting
    Language English
    Publishing date 2015-01-20
    Publisher S. Karger AG
    Publishing place Basel, Switzerland
    Document type Article
    Note Review
    ZDB-ID 605548-5
    ISSN 1421-9735 ; 0253-5068
    ISSN (online) 1421-9735
    ISSN 0253-5068
    DOI 10.1159/000368940
    Database Karger publisher's database

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    In stock of ZB MED Cologne/Königswinter

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    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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