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Article ; Online: Pharmacological Management of Cardiac Arrhythmias in the Fetal and Neonatal Periods: A Scientific Statement From the American Heart Association: Endorsed by the Pediatric & Congenital Electrophysiology Society (PACES).

Batra, Anjan S / Silka, Michael J / Borquez, Alejandro / Cuneo, Bettina / Dechert, Brynn / Jaeggi, Edgar / Kannankeril, Prince J / Tabulov, Christine / Tisdale, James E / Wolfe, Diana

Circulation

2024 Volume 149, Issue 10, Page(s) e937–e952

Abstract: Disorders of the cardiac rhythm may occur in both the fetus and neonate. Because of the immature myocardium, the hemodynamic consequences of either bradyarrhythmias or tachyarrhythmias may be far more significant than in mature physiological states. ... ...

Abstract	Disorders of the cardiac rhythm may occur in both the fetus and neonate. Because of the immature myocardium, the hemodynamic consequences of either bradyarrhythmias or tachyarrhythmias may be far more significant than in mature physiological states. Treatment options are limited in the fetus and neonate because of limited vascular access, patient size, and the significant risk/benefit ratio of any intervention. In addition, exposure of the fetus or neonate to either persistent arrhythmias or antiarrhythmic medications may have yet-to-be-determined long-term developmental consequences. This scientific statement discusses the mechanism of arrhythmias, pharmacological treatment options, and distinct aspects of pharmacokinetics for the fetus and neonate. From the available current data, subjects of apparent consistency/consensus are presented, as well as future directions for research in terms of aspects of care for which evidence has not been established.
MeSH term(s)	Infant, Newborn ; United States ; Child ; Humans ; American Heart Association ; Arrhythmias, Cardiac/diagnosis ; Arrhythmias, Cardiac/drug therapy ; Tachycardia ; Fetus ; Electrophysiology
Language	English
Publishing date	2024-02-05
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	80099-5
ISSN	1524-4539 ; 0009-7322 ; 0069-4193 ; 0065-8499
ISSN (online)	1524-4539
ISSN	0009-7322 ; 0069-4193 ; 0065-8499
DOI	10.1161/CIR.0000000000001206
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Article ; Online: CPSF3 inhibition blocks pancreatic cancer cell proliferation through disruption of core histone mRNA processing.

Alahmari, Abdulrahman A / Chaubey, Aditi H / Jonnakuti, Venkata S / Tisdale, Arwen A / Schwarz, Carla D / Cornwell, Abigail C / Maraszek, Kathryn E / Paterson, Emily J / Kim, Minsuh / Venkat, Swati / Gomez, Eduardo Cortes / Wang, Jianmin / Gurova, Katerina V / Yalamanchili, Hari Krishna / Feigin, Michael E

RNA (New York, N.Y.)

2024 Volume 30, Issue 3, Page(s) 281–297

Abstract: Pancreatic ductal adenocarcinoma (PDAC) is a lethal disease with limited effective treatment options, potentiating the importance of uncovering novel drug targets. Here, we target cleavage and polyadenylation specificity factor 3 (CPSF3), the 3' ... ...

Abstract	Pancreatic ductal adenocarcinoma (PDAC) is a lethal disease with limited effective treatment options, potentiating the importance of uncovering novel drug targets. Here, we target cleavage and polyadenylation specificity factor 3 (CPSF3), the 3' endonuclease that catalyzes mRNA cleavage during polyadenylation and histone mRNA processing. We find that
MeSH term(s)	Humans ; Cell Line, Tumor ; Cell Proliferation ; Gene Expression Regulation, Neoplastic ; Histones/genetics ; Pancreatic Neoplasms/drug therapy ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/metabolism ; Polyadenylation ; RNA, Messenger/genetics ; RNA, Messenger/metabolism
Chemical Substances	Histones ; RNA, Messenger ; CPSF3 protein, human
Language	English
Publishing date	2024-02-16
Publishing country	United States
Document type	Journal Article
ZDB-ID	1241540-6
ISSN	1469-9001 ; 1355-8382
ISSN (online)	1469-9001
ISSN	1355-8382
DOI	10.1261/rna.079931.123
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Zs.A 4777: Show issues

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Article ; Online: Reversing cachexia.

Tisdale, Michael J

Cell

2010 Volume 142, Issue 4, Page(s) 511–512

Abstract: Muscle atrophy (cachexia) in cancer patients is a life-threatening condition for which therapeutic options are limited. Zhou et al. (2010) now identify a new target for treating cachexia, the activin type-2 receptor (ActRIIB). In several mouse models of ... ...

Abstract	Muscle atrophy (cachexia) in cancer patients is a life-threatening condition for which therapeutic options are limited. Zhou et al. (2010) now identify a new target for treating cachexia, the activin type-2 receptor (ActRIIB). In several mouse models of cachexia, the authors reversed wasting of skeletal and cardiac muscle and increased life span by blocking ActRIIB with a decoy receptor.
Language	English
Publishing date	2010-08-20
Publishing country	United States
Document type	Comment ; Journal Article
ZDB-ID	187009-9
ISSN	1097-4172 ; 0092-8674
ISSN (online)	1097-4172
ISSN	0092-8674
DOI	10.1016/j.cell.2010.08.004
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Zs.A 1167: 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)
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Article ; Online: Are tumoral factors responsible for host tissue wasting in cancer cachexia?

Tisdale, Michael J

Future oncology (London, England)

2010 Volume 6, Issue 4, Page(s) 503–513

Abstract: Both cytokines and tumor factors have been implicated in tissue loss in cancer cachexia. Loss of adipose tissue is most likely due to the tumor (and host) factor zinc-alpha2-glycoprotein because of its direct lipolytic effect, ability to sensitize ... ...

Abstract	Both cytokines and tumor factors have been implicated in tissue loss in cancer cachexia. Loss of adipose tissue is most likely due to the tumor (and host) factor zinc-alpha2-glycoprotein because of its direct lipolytic effect, ability to sensitize adipocytes to lipolytic stimuli and increased expression in cachexia. TNF-alpha and the tumor factor proteolysis-inducing factor are the major contenders for skeletal muscle atrophy; both increase protein degradation through the ubiquitin-proteasome pathway and depress protein synthesis through phosphorylation of eukaryotic initiation factor 2 alpha. However, while most studies report proteolysis-inducing factor levels to correlate with the appearance of cachexia, there is some disagreement regarding a correlation between serum levels of TNF-alpha and weight loss. Furthermore, only antagonists to proteolysis inducing factor prevent muscle loss in cancer patients, suggesting that tumor factors are the most important.
MeSH term(s)	Cachexia/complications ; Cachexia/physiopathology ; Cytokines/genetics ; Cytokines/physiology ; Humans ; Neoplasms/complications ; Neoplasms/genetics ; Neoplasms/physiopathology ; Tumor Necrosis Factors/metabolism
Chemical Substances	Cytokines ; Tumor Necrosis Factors
Language	English
Publishing date	2010-04
Publishing country	England
Document type	Journal Article
ZDB-ID	2184533-5
ISSN	1744-8301 ; 1479-6694
ISSN (online)	1744-8301
ISSN	1479-6694
DOI	10.2217/fon.10.20
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Article ; Online: Cancer cachexia.

Tisdale, Michael J

Current opinion in gastroenterology

2010 Volume 26, Issue 2, Page(s) 146–151

Abstract: Purpose of review: Although cachexia has a major effect on both the morbidity and mortality of cancer patients, information on the mechanisms responsible for this condition is limited. This review summarizes recent data in this area.: Recent findings!# ...

Abstract	Purpose of review: Although cachexia has a major effect on both the morbidity and mortality of cancer patients, information on the mechanisms responsible for this condition is limited. This review summarizes recent data in this area. Recent findings: Cachexia is defined as loss of muscle, with or without fat, frequently associated with anorexia, inflammation and insulin resistance. Loss of adipose mass is due to an increased lipolysis through an increased expression of hormone-sensitive lipase. Adipose tissue does not contribute to the inflammatory response. There is an increased phosphorylation of both protein kinase R (PKR) and eukaryotic initiation factor 2 on the alpha-subunit in skeletal muscle of cachectic cancer patients, which would lead to muscle atrophy through a depression in protein synthesis and an increase in degradation. Mice lacking the ubiquitin ligase MuRF1 are less susceptible to muscle wasting under amino acid deprivation. Expression of MuRF1 and atrogin-1 is increased by oxidative stress, whereas nitric oxide may protect against muscle atrophy. Levels of interleukin (IL)-6 correlate with cachexia and death due to an increase in tumour burden. Ghrelin analogues and melanocortin receptor antagonists increase food intake and may have a role in the treatment of cachexia. Summary: These findings provide impetus for the development of new therapeutic agents.
MeSH term(s)	Adipose Tissue/metabolism ; Animals ; Anorexia/mortality ; Anorexia/physiopathology ; Anorexia/therapy ; Cachexia/etiology ; Cachexia/mortality ; Cachexia/physiopathology ; Cachexia/therapy ; Disease Models, Animal ; Disease Progression ; Humans ; Mice ; Muscular Atrophy/metabolism ; Muscular Atrophy/physiopathology ; Neoplasms/complications ; Neoplasms/mortality ; Neoplasms/physiopathology ; Neuropeptides/therapeutic use ; Prognosis ; Risk Assessment ; Survival Analysis ; Weight Loss
Chemical Substances	Neuropeptides
Language	English
Publishing date	2010-03
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	632571-3
ISSN	1531-7056 ; 0267-1379
ISSN (online)	1531-7056
ISSN	0267-1379
DOI	10.1097/MOG.0b013e3283347e77
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Zs.A 2072: Show issues

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Article: Mechanisms of cancer cachexia.

Tisdale, Michael J

Physiological reviews

2009 Volume 89, Issue 2, Page(s) 381–410

Abstract: Up to 50% of cancer patients suffer from a progressive atrophy of adipose tissue and skeletal muscle, called cachexia, resulting in weight loss, a reduced quality of life, and a shortened survival time. Anorexia often accompanies cachexia, but appears ... ...

Abstract	Up to 50% of cancer patients suffer from a progressive atrophy of adipose tissue and skeletal muscle, called cachexia, resulting in weight loss, a reduced quality of life, and a shortened survival time. Anorexia often accompanies cachexia, but appears not to be responsible for the tissue loss, particularly lean body mass. An increased resting energy expenditure is seen, possibly arising from an increased thermogenesis in skeletal muscle due to an increased expression of uncoupling protein, and increased operation of the Cori cycle. Loss of adipose tissue is due to an increased lipolysis by tumor or host products. Loss of skeletal muscle in cachexia results from a depression in protein synthesis combined with an increase in protein degradation. The increase in protein degradation may include both increased activity of the ubiquitin-proteasome pathway and lysosomes. The decrease in protein synthesis is due to a reduced level of the initiation factor 4F, decreased elongation, and decreased binding of methionyl-tRNA to the 40S ribosomal subunit through increased phosphorylation of eIF2 on the alpha-subunit by activation of the dsRNA-dependent protein kinase, which also increases expression of the ubiquitin-proteasome pathway through activation of NFkappaB. Tumor factors such as proteolysis-inducing factor and host factors such as tumor necrosis factor-alpha, angiotensin II, and glucocorticoids can all induce muscle atrophy. Knowledge of the mechanisms of tissue destruction in cachexia should improve methods of treatment.
MeSH term(s)	Adipose Tissue/metabolism ; Adipose Tissue/pathology ; Atrophy ; Cachexia/drug therapy ; Cachexia/physiopathology ; Energy Metabolism/physiology ; Humans ; Muscle, Skeletal/metabolism ; Muscle, Skeletal/pathology ; Neoplasms/physiopathology
Language	English
Publishing date	2009-04
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	209902-0
ISSN	1522-1210 ; 0031-9333
ISSN (online)	1522-1210
ISSN	0031-9333
DOI	10.1152/physrev.00016.2008
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Article ; Online: Zinc-alpha2-glycoprotein in cachexia and obesity.

Tisdale, Michael J

Current opinion in supportive and palliative care

2009 Volume 3, Issue 4, Page(s) 288–293

Abstract: Purpose of review: Control of adipose mass is important in the treatment of both cachexia and obesity. This review focuses on a novel adipokine, zinc-alpha2-glycoprotein (ZAG), which plays an important role in the mobilization and utilization of stored ... ...

Abstract	Purpose of review: Control of adipose mass is important in the treatment of both cachexia and obesity. This review focuses on a novel adipokine, zinc-alpha2-glycoprotein (ZAG), which plays an important role in the mobilization and utilization of stored lipids. Recent findings: An increased lipolysis is responsible for the loss of adipose tissue in cachexia, through an increased lipolytic response to catecholamines, arising from an increased expression of hormone-sensitive lipase. In obesity, there is a decreased response of adipocytes to catecholamines and reduced expression of hormone-sensitive lipase. ZAG was identified as a lipolytic factor produced by certain cachexia-inducing tumours, and subsequently adipose tissue (both white and brown), the expression of which was found to increase in cachexia. In contrast, ZAG expression is low in obesity. ZAG not only increases lipolysis in white adipose tissue through the classical cyclic AMP pathway, but also stimulates an increase in expression of uncoupling protein-1 in brown adipose tissue, which would stimulate utilization of the release lipid to generate heat. Homozygous ZAG null mice show an increase in body weight, especially when fed a high-fat diet, whereas adipocytes from such animals show a resistance to lipolysis by catecholamines and agents that increase cyclic AMP levels. Summary: These results suggest that ZAG may play an important role in the regulation of adipose mass in obesity and cachexia.
MeSH term(s)	Adipose Tissue/physiology ; Biosynthetic Pathways/physiology ; Cachexia/etiology ; Cachexia/physiopathology ; Carrier Proteins/physiology ; Glycoproteins/physiology ; Humans ; Obesity/complications
Chemical Substances	AZGP1 protein, human ; Carrier Proteins ; Glycoproteins
Language	English
Publishing date	2009-12
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2633726-5
ISSN	1751-4266 ; 1751-4258
ISSN (online)	1751-4266
ISSN	1751-4258
DOI	10.1097/SPC.0b013e328331c897
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Article: Re: Wieland BM, et al. Is there a human homologue to the murine proteolysis-inducing factor?

Tisdale, Michael J

Clinical cancer research : an official journal of the American Association for Cancer Research

2008 Volume 14, Issue 7, Page(s) 2245; author reply 2245–6

MeSH term(s)	Animals ; Antibodies, Monoclonal ; Antibody Affinity ; Antibody Specificity ; Cross Reactions ; Humans ; Mice ; Proteoglycans/chemistry ; Proteoglycans/immunology ; Structural Homology, Protein
Chemical Substances	Antibodies, Monoclonal ; Proteoglycans ; proteolysis-inducing peptide
Language	English
Publishing date	2008-04-01
Publishing country	United States
Document type	Comment ; Letter
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-07-4769
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Article ; Online: Catabolic mediators of cancer cachexia.

Tisdale, Michael J

Current opinion in supportive and palliative care

2008 Volume 2, Issue 4, Page(s) 256–261

Abstract: Purpose of review: This review compares the catabolic actions of tumour necrosis factor-alpha (TNF-alpha) and proteolysis-inducing factor (PIF) and their involvement in human cancer cachexia.: Recent findings: TNF-alpha has a direct catabolic effect ... ...

Abstract	Purpose of review: This review compares the catabolic actions of tumour necrosis factor-alpha (TNF-alpha) and proteolysis-inducing factor (PIF) and their involvement in human cancer cachexia. Recent findings: TNF-alpha has a direct catabolic effect on skeletal muscle and adipose tissue, whereas PIF only has an effect on skeletal muscle. Both produce muscle atrophy through a depression of protein synthesis and an increase in protein degradation through the ubiquitin-proteasome proteolytic pathway, and this involves formation of reactive oxygen species leading to upregulation of the transcription factor nuclear factor-kappaB (NF-kappaB). TNF-alpha depresses protein synthesis through decreased phosphorylation of eukaryotic initiation factor-4E (eIF4E) binding protein (4E-BP1) leading to increased binding of eIF4E and a reduction in the active eIF4F complex, whereas with PIF depression of protein synthesis is due to an increased phosphorylation of eIF2 on the alpha-subunit. In general, serum levels of TNF-alpha do not correlate with weight loss in cancer patients and attempts to treat cachexia by interfering with TNF-alpha production, or action, have not been successful. Most studies show that PIF is detectable in the urine of cachectic cancer patients and its presence is indicative of weight loss. It is best to confirm that the band on Western blotting is PIF using both antibodies to the core peptide and the oligosaccharide chains. Summary: These results suggest that blocking the PIF receptor or signalling pathways in skeletal muscle might yield new types of agents for the treatment of cancer cachexia.
MeSH term(s)	Adipose Tissue/metabolism ; Cachexia/etiology ; Cachexia/metabolism ; Humans ; Muscle, Skeletal/metabolism ; Muscular Atrophy/etiology ; Muscular Atrophy/metabolism ; Neoplasms/complications ; Proteoglycans/metabolism ; Reactive Oxygen Species/metabolism ; Tumor Necrosis Factor-alpha/metabolism
Chemical Substances	Proteoglycans ; Reactive Oxygen Species ; Tumor Necrosis Factor-alpha ; proteolysis-inducing peptide
Language	English
Publishing date	2008-12-08
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2633726-5
ISSN	1751-4266 ; 1751-4258
ISSN (online)	1751-4266
ISSN	1751-4258
DOI	10.1097/spc.0b013e328319d7fa
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Article ; Online: Is there a common mechanism linking muscle wasting in various disease types?

Tisdale, Michael J

Current opinion in supportive and palliative care

2007 Volume 1, Issue 4, Page(s) 287–292

Abstract: Purpose of review: There have been a number of recent developments in our understanding of the cellular mechanisms leading to muscle atrophy, which are likely to be of major importance in the design of therapeutic agents.: Recent findings: Muscle ... ...

Abstract	Purpose of review: There have been a number of recent developments in our understanding of the cellular mechanisms leading to muscle atrophy, which are likely to be of major importance in the design of therapeutic agents. Recent findings: Muscle atrophy in a range of conditions is thought to be due to an increased expression of the ubiquitin-proteasome proteolytic pathway. The main transcription factors involved in muscle atrophy are nuclear factor-kappaB and the forkhead type transcription factors, as determined from experiments with transgenic mice. Catabolic agents such as cytokines, proteolysis-inducing factor and angiotensin II induce activation of nuclear factor-kappaB through an increase in reactive oxygen species, causing an increased gene expression of proteasome subunits and the ubiquitin ligase MuRF1. Glucocorticoids cause activation of forkhead type transcription factors possibly through an increase in expression of myostatin, which leads to an increased expression of the E3 ligase atrogin-1/MAFbx and cathepsin L. Forkhead type transcription factors is regulated by its state of phosphorylation induced by Akt, while activation of nuclear factor-kappaB requires reactive oxygen species and activation of the dsRNA-dependent protein kinase. Activation of dsRNA-dependent protein kinase also inhibits translational initiation of protein synthesis through phosphorylation of eukaryotic initiation factor 2 on the alpha-subunit. Summary: These results suggest a common mechanism leading to muscle atrophy, which has important implications in the clinical treatment of wasting diseases.
MeSH term(s)	Animals ; Humans ; Muscle, Skeletal/metabolism ; Muscle, Skeletal/pathology ; Muscular Atrophy/metabolism ; Muscular Atrophy/pathology ; NF-kappa B/metabolism ; Oxidative Stress/physiology ; Proteasome Endopeptidase Complex/metabolism ; Reactive Oxygen Species/metabolism ; Signal Transduction ; Ubiquitin/metabolism
Chemical Substances	NF-kappa B ; Reactive Oxygen Species ; Ubiquitin ; Proteasome Endopeptidase Complex (EC 3.4.25.1)
Language	English
Publishing date	2007-12
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2633726-5
ISSN	1751-4266 ; 1751-4258
ISSN (online)	1751-4266
ISSN	1751-4258
DOI	10.1097/SPC.0b013e3282f35238
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