LIVIVO - Search results -

Search results

Result 1 - 10 of total 116

Search options

Article ; Online: Organ Crosstalk Contributes to Muscle Wasting in Chronic Kidney Disease.

Wang, Xiaonan H / Price, S Russ

2023 Volume 43, Issue 2, Page(s) 151409

Abstract: Muscle wasting (ie, atrophy) is a serious consequence of chronic kidney disease (CKD) that reduces muscle strength and function. It reduces the quality of life for CKD patients and increases the risks of comorbidities and mortality. Current treatment ... ...

Abstract	Muscle wasting (ie, atrophy) is a serious consequence of chronic kidney disease (CKD) that reduces muscle strength and function. It reduces the quality of life for CKD patients and increases the risks of comorbidities and mortality. Current treatment strategies to prevent or reverse skeletal muscle loss are limited owing to the broad and systemic nature of the initiating signals and the multifaceted catabolic mechanisms that accelerate muscle protein degradation and impair protein synthesis and repair pathways. Recent evidence has shown how organs such as muscle, adipose, and kidney communicate with each other through interorgan exchange of proteins and RNAs during CKD. This crosstalk changes cell functions in the recipient organs and represents an added dimension in the complex processes that are responsible for muscle atrophy in CKD. This complexity creates challenges for the development of effective therapies to ameliorate muscle wasting and weakness in patients with CKD.
MeSH term(s)	Humans ; Quality of Life ; Muscular Atrophy/etiology ; Muscular Atrophy/metabolism ; Muscular Atrophy/pathology ; Renal Insufficiency, Chronic/metabolism ; Muscle, Skeletal/metabolism ; Muscle, Skeletal/pathology ; Proteolysis
Language	English
Publishing date	2023-08-22
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	604652-6
ISSN	1558-4488 ; 0270-9295
ISSN (online)	1558-4488
ISSN	0270-9295
DOI	10.1016/j.semnephrol.2023.151409
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Se 784: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Going micro in CKD-related cachexia.

Wang, Xiaonan H / Price, S Russ

Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association

2020 Volume 35, Issue 9, Page(s) 1462–1464

MeSH term(s)	Cachexia/etiology ; Humans ; MicroRNAs ; Muscle, Skeletal ; Muscular Atrophy ; Renal Insufficiency, Chronic/complications
Chemical Substances	MicroRNAs
Language	English
Publishing date	2020-02-14
Publishing country	England
Document type	Editorial ; Comment
ZDB-ID	90594-x
ISSN	1460-2385 ; 0931-0509
ISSN (online)	1460-2385
ISSN	0931-0509
DOI	10.1093/ndt/gfaa025
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 2198: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 329: Show issues

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: A New Dimension to the Mechanisms Causing Muscle Loss in CKD.

Price, S Russ / Bailey, James L

Journal of the American Society of Nephrology : JASN

2020 Volume 31, Issue 11, Page(s) 2495–2496

MeSH term(s)	Humans ; Muscle Proteins ; Muscle, Skeletal ; Renal Insufficiency, Chronic/etiology
Chemical Substances	Muscle Proteins
Language	English
Publishing date	2020-10-09
Publishing country	United States
Document type	Editorial ; Comment
ZDB-ID	1085942-1
ISSN	1533-3450 ; 1046-6673
ISSN (online)	1533-3450
ISSN	1046-6673
DOI	10.1681/ASN.2020091341
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 3344: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Muscle Atrophy in CKD: A Historical Perspective of Advancements in Its Understanding.

Price, S Russ / Mitch, William E / Garibotto, Giacomo

Journal of renal nutrition : the official journal of the Council on Renal Nutrition of the National Kidney Foundation

2022 Volume 33, Issue 6S, Page(s) S88–S92

Abstract: Objective: This perspective reviews the seminal clinical and experimental observations that led to today's current mechanistic model of muscle protein loss (wasting) in patients with chronic kidney disease (CKD).: Results and conclusion: Early ... ...

Abstract	Objective: This perspective reviews the seminal clinical and experimental observations that led to today's current mechanistic model of muscle protein loss (wasting) in patients with chronic kidney disease (CKD). Results and conclusion: Early International Society of Renal Nutrition and Metabolism (ISRNM) meetings facilitated discussions and hypotheses about the causes of muscle wasting in CKD. It became widely recognized that wasting is common and correlated with increased risks of mortality and morbidity. Although anorexia and dietary restrictions contribute to muscle loss, several features of CKD-associated wasting cannot be explained by malnutrition alone. The protein catabolism-inducing actions of metabolic acidosis, inflammation, insulin resistance, endocrine disorders and uremic toxins were progressively identified. Continued research to understand the interactions of inflammation, anabolic resistance, mitochondrial dysfunction, exercise, and nutrition on muscle protein turnover in patients with CKD will hopefully accelerate discoveries and treatments to ameliorate muscle wasting as well as the progression of CKD.
MeSH term(s)	Humans ; Renal Insufficiency, Chronic ; Muscular Atrophy ; Cachexia ; Muscle Proteins ; Inflammation/complications
Chemical Substances	Muscle Proteins
Language	English
Publishing date	2022-09-29
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1080003-7
ISSN	1532-8503 ; 1051-2276
ISSN (online)	1532-8503
ISSN	1051-2276
DOI	10.1053/j.jrn.2022.09.009
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 3273: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Pathophysiological mechanisms leading to muscle loss in chronic kidney disease.

Wang, Xiaonan H / Mitch, William E / Price, S Russ

Nature reviews. Nephrology

2021 Volume 18, Issue 3, Page(s) 138–152

Abstract: Loss of muscle proteins is a deleterious consequence of chronic kidney disease (CKD) that causes a decrease in muscle strength and function, and can lead to a reduction in quality of life and increased risk of morbidity and mortality. The effectiveness ... ...

Abstract	Loss of muscle proteins is a deleterious consequence of chronic kidney disease (CKD) that causes a decrease in muscle strength and function, and can lead to a reduction in quality of life and increased risk of morbidity and mortality. The effectiveness of current treatment strategies in preventing or reversing muscle protein losses is limited. The limitations largely stem from the systemic nature of diseases such as CKD, which stimulate skeletal muscle protein degradation pathways while simultaneously activating mechanisms that impair muscle protein synthesis and repair. Stimuli that initiate muscle protein loss include metabolic acidosis, insulin and IGF1 resistance, changes in hormones, cytokines, inflammatory processes and decreased appetite. A growing body of evidence suggests that signalling molecules secreted from muscle can enter the circulation and subsequently interact with recipient organs, including the kidneys, while conversely, pathological events in the kidney can adversely influence protein metabolism in skeletal muscle, demonstrating the existence of crosstalk between kidney and muscle. Together, these signals, whether direct or indirect, induce changes in the levels of regulatory and effector proteins via alterations in mRNAs, microRNAs and chromatin epigenetic responses. Advances in our understanding of the signals and processes that mediate muscle loss in CKD and other muscle wasting conditions will support the future development of therapeutic strategies to reduce muscle loss.
MeSH term(s)	Humans ; MicroRNAs/metabolism ; Muscle, Skeletal/metabolism ; Muscle, Skeletal/pathology ; Muscular Atrophy ; Quality of Life ; Renal Insufficiency, Chronic/complications ; Renal Insufficiency, Chronic/metabolism
Chemical Substances	MicroRNAs
Language	English
Publishing date	2021-11-08
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2490366-8
ISSN	1759-507X ; 1759-5061
ISSN (online)	1759-507X
ISSN	1759-5061
DOI	10.1038/s41581-021-00498-0
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 6334: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.MG 107: Show issues

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article: Raising Awareness of Alzheimer's Disease and Dementia in Native Americans in North Carolina.

Welsh-Bohmer, Kathleen A / Byrd, Goldie Smith / Dewees, Rachel / Bozoki, Andrea C / Martin, Patrick M / Plassman, Brenda / Price, S Russ

North Carolina medical journal

2022 Volume 83, Issue 1, Page(s) 77–78

MeSH term(s)	Alzheimer Disease/epidemiology ; American Indians or Alaska Natives ; Humans ; North Carolina/epidemiology ; Risk Factors
Language	English
Publishing date	2022-01-03
Publishing country	United States
Document type	Letter
ZDB-ID	422795-5
ISSN	0029-2559
ISSN	0029-2559
DOI	10.18043/ncm.83.1.77
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.B 169: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Inverse treatment planning for an electronic brachytherapy system delivering anisotropic radiation therapy.

Badali, Daniel S / Vainer, Yonatan / Ellenor, Christopher W / Mitchell, Christopher R / Fishman, Kalman / Soro, Nicolas / Price, Russ / Funk, Tobias

Physics in medicine and biology

2021 Volume 66, Issue 5, Page(s) 55004

Abstract: An inverse radiation treatment planning algorithm for Sensus Healthcare's ... ...

Abstract	An inverse radiation treatment planning algorithm for Sensus Healthcare's Sculptura
MeSH term(s)	Algorithms ; Anisotropy ; Brachytherapy ; Humans ; Male ; Prostatic Neoplasms/radiotherapy ; Radiotherapy Dosage ; Radiotherapy Planning, Computer-Assisted/methods
Language	English
Publishing date	2021-02-13
Publishing country	England
Document type	Journal Article
ZDB-ID	208857-5
ISSN	1361-6560 ; 0031-9155
ISSN (online)	1361-6560
ISSN	0031-9155
DOI	10.1088/1361-6560/abda9a
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 199: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Calcineurin: a poorly understood regulator of muscle mass.

Hudson, Matthew B / Price, S Russ

The international journal of biochemistry & cell biology

2013 Volume 45, Issue 10, Page(s) 2173–2178

Abstract: This review will discuss the existing literature that has examined the role of calcineurin (CnA) in the regulation of skeletal muscle mass in conditions associated with hypertrophic growth or atrophy. Muscle mass is determined by the balance between ... ...

Abstract	This review will discuss the existing literature that has examined the role of calcineurin (CnA) in the regulation of skeletal muscle mass in conditions associated with hypertrophic growth or atrophy. Muscle mass is determined by the balance between protein synthesis and degradation which is controlled by a number of intracellular signaling pathways, most notably the insulin/IGF/phosphatidylinositol 3-kinase (PI3K)/Akt system. Despite being activated by IGF-1 and having well-described functions in the determination of muscle fiber phenotypes, calcineurin (CnA), a Ca(2+)-activated serine/threonine phosphatase, and its downstream signaling partners have garnered little attention as a regulator of muscle mass. Compared to other signaling pathways, the relatively few studies that have examined the role of CnA in the regulation of muscle size have produced discordant results. The reasons for these differences is not obvious but may be due to the selective nature of the genetic models studied, fluctuations in the endogenous level of CnA activity in various muscles, and the variable use of CnA inhibitors to inhibit CnA signaling. Despite the inconsistent nature of the outcomes, there is sufficient direct and indirect evidence to conclude that CnA plays a role in the regulation of skeletal muscle mass. This article is part of a Directed Issue entitled: Molecular basis of muscle wasting.
MeSH term(s)	Animals ; Calcineurin/genetics ; Calcineurin/metabolism ; Humans ; Hypertrophy/metabolism ; Mice, Transgenic ; Muscle, Skeletal/metabolism ; Muscle, Skeletal/pathology ; Muscular Atrophy/metabolism ; Muscular Atrophy/pathology ; Phosphorylation ; Signal Transduction
Chemical Substances	Calcineurin (EC 3.1.3.16)
Language	English
Publishing date	2013-07-06
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	1228429-4
ISSN	1878-5875 ; 1357-2725
ISSN (online)	1878-5875
ISSN	1357-2725
DOI	10.1016/j.biocel.2013.06.029
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 431: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: The impact of senescence on muscle wasting in chronic kidney disease.

Huang, Ying / Wang, Bin / Hassounah, Faten / Price, S Russ / Klein, Janet / Mohamed, Tamer M A / Wang, Yanhua / Park, Jeanie / Cai, Hui / Zhang, Xuemei / Wang, Xiaonan H

Journal of cachexia, sarcopenia and muscle

2022 Volume 14, Issue 1, Page(s) 126–141

Abstract: Background: Muscle wasting is a common complication of chronic kidney disease (CKD) that is associated with higher mortality. Although the mechanisms of myofibre loss in CKD has been widely studied, the contribution of muscle precursor cell (MPC) ... ...

Abstract	Background: Muscle wasting is a common complication of chronic kidney disease (CKD) that is associated with higher mortality. Although the mechanisms of myofibre loss in CKD has been widely studied, the contribution of muscle precursor cell (MPC) senescence remains poorly understood. Senescent MPCs no longer proliferate and can produce proinflammatory factors or cytokines. In this study, we tested the hypothesis that the senescence associated secretory phenotype (SASP) of MPCs contributes to CKD-induced muscle atrophy and weakness. Methods: CKD was induced in mice by 5/6th nephrectomy. Kidney function, muscle size, and function were measured, and markers of atrophy, inflammation, and senescence were evaluated using immunohistochemistry, immunoblots, or qPCR. To study the impact of senescence, a senolytics cocktail of dasatinib + quercetin (D&Q) was given orally to mice for 8 weeks. To investigate CKD-induced senescence at the cellular level, primary MPCs were incubated with serum from CKD or control subjects. The roles of specific proteins in MPC senescence were studied using adenoviral transduction, siRNA, and plasmid transfection. Results: In the hindlimb muscles of CKD mice, (i) the senescence biomarker SA-β-gal was sharply increased (~30-fold); (ii) the DNA damage response marker γ-H2AX was increased 1.9-fold; and (iii) the senescence pathway markers p21 and p16 Conclusions: Senescent MPCs are likely to contribute to the development of muscle wasting during CKD by producing inflammatory cytokines. Limiting senescence with senolytics ameliorated muscle wasting and improved muscle strength in vivo and restored cultured MPC functions. These results suggest potential new therapeutic targets to improve muscle health and function in CKD.
MeSH term(s)	Animals ; Mice ; Cyclin-Dependent Kinase Inhibitor p16/genetics ; Cyclin-Dependent Kinase Inhibitor p16/metabolism ; Senotherapeutics ; Renal Insufficiency, Chronic/complications ; Cytokines/metabolism ; Muscular Atrophy/etiology ; Muscles/metabolism ; RNA, Small Interfering
Chemical Substances	Cyclin-Dependent Kinase Inhibitor p16 ; Senotherapeutics ; Cytokines ; RNA, Small Interfering
Language	English
Publishing date	2022-11-09
Publishing country	Germany
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2586864-0
ISSN	2190-6009 ; 2190-5991
ISSN (online)	2190-6009
ISSN	2190-5991
DOI	10.1002/jcsm.13112
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Cyclooxygenase-2 in the kidney: good, BAD, or both?

Russ Price, S / Klein, Janet D

Kidney international

2011 Volume 80, Issue 9, Page(s) 905–907

Abstract: Hypertonic stress in the kidney inner medulla is common, yet inner medullary cells adapt to limit cell death. Küper et al. have identified a cell-survival response by which increased cyclooxygenase-2 (COX-2) stimulates a prostaglandin E(2) (PGE(2))/ ... ...

Abstract	Hypertonic stress in the kidney inner medulla is common, yet inner medullary cells adapt to limit cell death. Küper et al. have identified a cell-survival response by which increased cyclooxygenase-2 (COX-2) stimulates a prostaglandin E(2) (PGE(2))/protein kinase A (PKA)-mediated inactivation of the pro-apoptotic protein BAD. However, the PGE(2)/PKA pathway is not the only means to inactivate BAD and limit cell death. This Commentary shows a broader picture of this pathway to examine the kidney's BAD options.
MeSH term(s)	Animals ; Apoptosis ; Cyclooxygenase 2/metabolism ; Epithelial Cells/enzymology ; Kidney Medulla/enzymology ; bcl-Associated Death Protein/metabolism
Chemical Substances	Bad protein, mouse ; bcl-Associated Death Protein ; Ptgs2 protein, mouse (EC 1.14.99.-) ; Cyclooxygenase 2 (EC 1.14.99.1)
Language	English
Publishing date	2011-10-31
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Comment
ZDB-ID	120573-0
ISSN	1523-1755 ; 0085-2538
ISSN (online)	1523-1755
ISSN	0085-2538
DOI	10.1038/ki.2011.263
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 797: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

To top

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito