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Article ; Online: Duration of SARS-CoV-2 mRNA vaccine persistence and factors associated with cardiac involvement in recently vaccinated patients.

Krauson, Aram J / Casimero, Faye Victoria C / Siddiquee, Zakir / Stone, James R

NPJ vaccines

2023 Volume 8, Issue 1, Page(s) 141

Abstract: At the start of the COVID-19 pandemic, the BNT162b2 (BioNTech-Pfizer) and mRNA-1273 (Moderna) mRNA vaccines were expediently designed and mass produced. Both vaccines produce the full-length SARS-CoV-2 spike protein for gain of immunity and have greatly ... ...

Abstract	At the start of the COVID-19 pandemic, the BNT162b2 (BioNTech-Pfizer) and mRNA-1273 (Moderna) mRNA vaccines were expediently designed and mass produced. Both vaccines produce the full-length SARS-CoV-2 spike protein for gain of immunity and have greatly reduced mortality and morbidity from SARS-CoV-2 infection. The distribution and duration of SARS-CoV-2 mRNA vaccine persistence in human tissues is unclear. Here, we developed specific RT-qPCR-based assays to detect each mRNA vaccine and screened lymph nodes, liver, spleen, and myocardium from recently vaccinated deceased patients. Vaccine was detected in the axillary lymph nodes in the majority of patients dying within 30 days of vaccination, but not in patients dying more than 30 days from vaccination. Vaccine was not detected in the mediastinal lymph nodes, spleen, or liver. Vaccine was detected in the myocardium in a subset of patients vaccinated within 30 days of death. Cardiac ventricles in which vaccine was detected had healing myocardial injury at the time of vaccination and had more myocardial macrophages than the cardiac ventricles in which vaccine was not detected. These results suggest that SARS-CoV-2 mRNA vaccines routinely persist up to 30 days from vaccination and can be detected in the heart.
Language	English
Publishing date	2023-09-27
Publishing country	England
Document type	Journal Article
ISSN	2059-0105
ISSN (online)	2059-0105
DOI	10.1038/s41541-023-00742-7
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Article ; Online: An elevated IgG4 response in chronic infectious aortitis is associated with aortic atherosclerosis.

Siddiquee, Zakir / Smith, R Neal / Stone, James R

Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc

2015 Volume 28, Issue 11, Page(s) 1428–1434

Abstract: Recently, it was shown that infectious bacterial aortitis can stimulate an elevated IgG4⁺ plasma cell response in the vessel wall, which could mimic IgG4 aortitis/periaortitis. However, the factors that are associated with an elevated IgG4⁺ plasma cell ... ...

Abstract	Recently, it was shown that infectious bacterial aortitis can stimulate an elevated IgG4⁺ plasma cell response in the vessel wall, which could mimic IgG4 aortitis/periaortitis. However, the factors that are associated with an elevated IgG4⁺ plasma cell response in infectious aortitis are unclear. To ascertain these factors, 17 cases of infectious aortitis and 6 cases of non-infectious severe abdominal aortic atherosclerosis were assessed for the magnitude of IgG4⁺ plasma cell response. The degree of IgG4⁺ plasma cell infiltration was determined by immunohistochemistry. Infectious cases were subcharacterized as chronic (>3 weeks duration) or acute (<3 weeks duration) based on the duration of symptoms, and as involving either the ascending aorta or the distal aorta, ie, the descending thoracic and/or abdominal aorta. There was a 5-16-fold greater degree of IgG4⁺ plasma cell infiltration in the chronic distal infectious aortitis group compared with the other three infectious aortitis groups (P ≤ 0.0007), and compared with non-infectious severe abdominal aortic atherosclerosis (P<0.0008). This resulted in a greater IgG4/IgG ratio in the chronic distal infectious aortitis group compared with the acute ascending and acute distal infectious aortitis groups (P<0.03). The degree of IgG4⁺ plasma cell infiltration in chronic distal infectious aortitis overlaps with that seen in the aortitis and periaortitis of IgG4-related disease. In the chronic infectious aortitis cases, the degree of IgG4⁺ plasma cell infiltration was more intense in patients with moderate to severe aortic atherosclerosis compared with those patients with less aortic atherosclerosis (P=0.007). These findings indicate that an elevated IgG4⁺ plasma cell response occurs in the descending thoracic and abdominal aorta in the setting of chronic bacterial infectious aortitis and pre-existing atherosclerosis. This inflammatory response to chronic infection in atherosclerosis-laden aortas may have implications for the development of IgG4-rich inflammatory atherosclerotic aortic aneurysms.
MeSH term(s)	Aged ; Aorta/pathology ; Aortitis/etiology ; Aortitis/immunology ; Atherosclerosis/complications ; Atherosclerosis/immunology ; Bacterial Infections/complications ; Bacterial Infections/immunology ; Chronic Disease ; Female ; Humans ; Immunoglobulin G/immunology ; Immunohistochemistry ; Male ; Middle Aged ; Plasma Cells/pathology
Chemical Substances	Immunoglobulin G
Language	English
Publishing date	2015-09-04
Publishing country	United States
Document type	Journal Article
ZDB-ID	645073-8
ISSN	1530-0285 ; 0893-3952
ISSN (online)	1530-0285
ISSN	0893-3952
DOI	10.1038/modpathol.2015.105
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Article ; Online: Dense IgG4 plasma cell infiltrates associated with chronic infectious aortitis: implications for the diagnosis of IgG4-related disease.

Siddiquee, Zakir / Zane, Nicholas A / Smith, R Neal / Stone, James R

Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology

2012 Volume 21, Issue 6, Page(s) 470–475

Abstract: Background: IgG4-related aortitis is a newly recognized form of noninfectious aortitis that occurs as part of the spectrum of a systemic disease referred to as IgG4-related disease. IgG4-related aortitis is distinguished from giant cell aortitis and ... ...

Abstract	Background: IgG4-related aortitis is a newly recognized form of noninfectious aortitis that occurs as part of the spectrum of a systemic disease referred to as IgG4-related disease. IgG4-related aortitis is distinguished from giant cell aortitis and Takayasu aortitis in part by the presence of increased numbers of IgG4-expressing plasma cells. Chronic infectious aortitis can also display lymphoplasmacytic infiltrates, but the degree of IgG4 expression in these cases has not been specifically evaluated. Methods: Two cases of chronic active infectious abdominal aortitis were prospectively identified. Both were due to gram-positive bacteria, and at least one of the cases was due to chronic active Staphylococcus aureus infection. The degree of IgG4 plasma cell infiltration was assessed by immunohistochemistry. Results: Both cases of chronic infectious aortitis focally displayed high levels of IgG4-expressing plasma cells, greater than 50% of the IgG-expressing plasma cells, and greater than 50 IgG4-expressing plasma cells per high-power field. Conclusions: Focal dense IgG4 plasma cell infiltrates can be seen in association with chronic infectious aortitis due to gram-positive bacteria, including Staphylococcus aureus. This observation supports the proposal that chronic Staphylococcus aureus infection may stimulate a Th2-mediated elevation in IgG4. The pathologic diagnosis of IgG4-related aortitis should not be based solely on the presence of increased IgG4 plasma cell counts from immunohistochemistry, but requires consideration of the overall pathology, including careful exclusion of infectious aortitis.
MeSH term(s)	Aged ; Aged, 80 and over ; Aorta, Abdominal/immunology ; Aorta, Abdominal/microbiology ; Aorta, Abdominal/pathology ; Aortitis/diagnosis ; Aortitis/immunology ; Aortitis/microbiology ; Bacterial Infections/diagnosis ; Bacterial Infections/immunology ; Chronic Disease ; Fatal Outcome ; Female ; Gram-Positive Bacteria/isolation & purification ; Humans ; Immune System Diseases/diagnosis ; Immune System Diseases/immunology ; Immune System Diseases/microbiology ; Immunoglobulin G/metabolism ; Lymphocyte Count ; Male ; Plasma Cells/immunology ; Plasma Cells/pathology ; Prospective Studies
Chemical Substances	Immunoglobulin G
Language	English
Publishing date	2012-11
Publishing country	United States
Document type	Case Reports ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1134600-0
ISSN	1879-1336 ; 1054-8807
ISSN (online)	1879-1336
ISSN	1054-8807
DOI	10.1016/j.carpath.2012.02.001
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Article ; Online: Altered vascular activation due to deficiency of the NADPH oxidase component p22phox.

Wang, He / Albadawi, Hassan / Siddiquee, Zakir / Stone, Jillian M / Panchenko, Mikhail P / Watkins, Michael T / Stone, James R

Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology

2013 Volume 23, Issue 1, Page(s) 35–42

Abstract: Background: Reactive oxygen species generated by nicotinamide adenine dinucleotide phosphate (NADPH) oxidase play important roles in vascular activation. The p22(phox) subunit is necessary for the activity of NADPH oxidase complexes utilizing Nox1, Nox2, ...

Abstract	Background: Reactive oxygen species generated by nicotinamide adenine dinucleotide phosphate (NADPH) oxidase play important roles in vascular activation. The p22(phox) subunit is necessary for the activity of NADPH oxidase complexes utilizing Nox1, Nox2, Nox3, and Nox4 catalytic subunits. Methods: We assessed p22(phox)-deficient mice and human tissue for altered vascular activation. Results: Mice deficient in p22(phox) were smaller than their wild-type littermates but showed no alteration in basal blood pressure. The wild-type littermates were relatively resistant to forming intimal hyperplasia following carotid ligation, and the intimal hyperplasia that developed was not altered by p22(phox) deficiency. However, at the site of carotid artery ligation, the p22(phox)-deficient mice showed significantly less vascular elastic fiber loss compared with their wild-type littermates. This preservation of elastic fibers was associated with a reduced matrix metallopeptidase (MMP) 12/tissue inhibitor of metalloproteinase (TIMP) 1 expression ratio. A similar decrease in the relative MMP12/TIMP1 expression ratio occurred in human coronary artery smooth muscle cells upon knockdown of the hydrogen peroxide responsive kinase CK1αLS. In the ligated carotid arteries, the p22(phox)-deficient mice showed reduced expression of heterogeneous nuclear ribonucleoprotein C (hnRNP-C), suggesting reduced activity of CK1αLS. In a lung biopsy from a human patient with p22(phox) deficiency, there was also reduced vascular hnRNP-C expression. Conclusions: These findings indicate that NADPH oxidase complexes modulate aspects of vascular activation including vascular elastic fiber loss, the MMP12/TIMP1 expression ratio, and the expression of hnRNP-C. Furthermore, these findings suggest that the effects of NADPH oxidase on vascular activation are mediated in part by protein kinase CK1αLS.
MeSH term(s)	Animals ; Carotid Artery Injuries/enzymology ; Carotid Artery Injuries/pathology ; Carotid Artery, Common/enzymology ; Carotid Artery, Common/pathology ; Case-Control Studies ; Casein Kinase Ialpha/genetics ; Casein Kinase Ialpha/metabolism ; Cells, Cultured ; Coronary Vessels/enzymology ; Coronary Vessels/pathology ; Cytochrome b Group/deficiency ; Cytochrome b Group/genetics ; Elastic Tissue/enzymology ; Elastic Tissue/pathology ; Female ; Granulomatous Disease, Chronic/enzymology ; Granulomatous Disease, Chronic/genetics ; Granulomatous Disease, Chronic/pathology ; Heterogeneous-Nuclear Ribonucleoprotein Group C/metabolism ; Humans ; Hyperplasia ; Infant ; Male ; Matrix Metalloproteinase 12/metabolism ; Mice ; Mice, Knockout ; Muscle, Smooth, Vascular/enzymology ; Muscle, Smooth, Vascular/pathology ; NADPH Oxidases/deficiency ; NADPH Oxidases/genetics ; Neointima ; RNA Interference ; Reactive Oxygen Species/metabolism ; Tissue Inhibitor of Metalloproteinase-1/metabolism ; Transfection
Chemical Substances	Cytochrome b Group ; Heterogeneous-Nuclear Ribonucleoprotein Group C ; Reactive Oxygen Species ; TIMP1 protein, human ; Timp1 protein, mouse ; Tissue Inhibitor of Metalloproteinase-1 ; NADPH Oxidases (EC 1.6.3.-) ; Cyba protein, mouse (EC 1.6.3.1) ; Casein Kinase Ialpha (EC 2.7.11.1) ; MMP12 protein, human (EC 3.4.24.65) ; Matrix Metalloproteinase 12 (EC 3.4.24.65)
Language	English
Publishing date	2013-09-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1134600-0
ISSN	1879-1336 ; 1054-8807
ISSN (online)	1879-1336
ISSN	1054-8807
DOI	10.1016/j.carpath.2013.08.003
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Article ; Online: Direct Pharmacological Inhibition of β-Catenin by RNA Interference in Tumors of Diverse Origin.

Ganesh, Shanthi / Koser, Martin L / Cyr, Wendy A / Chopda, Girish R / Tao, Junyan / Shui, Xue / Ying, Bo / Chen, Dongyu / Pandya, Purva / Chipumuro, Edmond / Siddiquee, Zakir / Craig, Kevin / Lai, Chengjung / Dudek, Henryk / Monga, Satdarshan P / Wang, Weimin / Brown, Bob D / Abrams, Marc T

Molecular cancer therapeutics

2016 Volume 15, Issue 9, Page(s) 2143–2154

Abstract: The Wnt/β-catenin pathway is among the most frequently altered signaling networks in human cancers. Despite decades of preclinical and clinical research, efficient therapeutic targeting of Wnt/β-catenin has been elusive. RNA interference (RNAi) ... ...

Abstract	The Wnt/β-catenin pathway is among the most frequently altered signaling networks in human cancers. Despite decades of preclinical and clinical research, efficient therapeutic targeting of Wnt/β-catenin has been elusive. RNA interference (RNAi) technology silences genes at the mRNA level and therefore can be applied to previously undruggable targets. Lipid nanoparticles (LNP) represent an elegant solution for the delivery of RNAi-triggering oligonucleotides to disease-relevant tissues, but have been mostly restricted to applications in the liver. In this study, we systematically tuned the composition of a prototype LNP to enable tumor-selective delivery of a Dicer-substrate siRNA (DsiRNA) targeting CTNNB1, the gene encoding β-catenin. This formulation, termed EnCore-R, demonstrated pharmacodynamic activity in subcutaneous human tumor xenografts, orthotopic patient-derived xenograft (PDX) tumors, disseminated hematopoietic tumors, genetically induced primary liver tumors, metastatic colorectal tumors, and murine metastatic melanoma. DsiRNA delivery was homogeneous in tumor sections, selective over normal liver and independent of apolipoprotein-E binding. Significant tumor growth inhibition was achieved in Wnt-dependent colorectal and hepatocellular carcinoma models, but not in Wnt-independent tumors. Finally, no evidence of accelerated blood clearance or sustained liver transaminase elevation was observed after repeated dosing in nonhuman primates. These data support further investigation to gain mechanistic insight, optimize dose regimens, and identify efficacious combinations with standard-of-care therapeutics. Mol Cancer Ther; 15(9); 2143-54. ©2016 AACR.
MeSH term(s)	Animals ; Apolipoproteins E/chemistry ; Apolipoproteins E/metabolism ; Carcinoma, Hepatocellular/genetics ; Carcinoma, Hepatocellular/metabolism ; Cell Line, Tumor ; Disease Models, Animal ; Gene Expression Regulation, Neoplastic ; Gene Silencing ; Humans ; Lipids/chemistry ; Liver Neoplasms/genetics ; Liver Neoplasms/metabolism ; Male ; Melanoma, Experimental ; Mice ; Nanoparticles/chemistry ; Neoplasm Metastasis ; Neoplasms/genetics ; Neoplasms/metabolism ; RNA Interference ; RNA, Small Interfering/administration & dosage ; RNA, Small Interfering/chemistry ; RNA, Small Interfering/genetics ; Structure-Activity Relationship ; Wnt Signaling Pathway ; Xenograft Model Antitumor Assays ; beta Catenin/genetics ; beta Catenin/metabolism ; ras Proteins/genetics ; ras Proteins/metabolism
Chemical Substances	Apolipoproteins E ; Lipids ; RNA, Small Interfering ; beta Catenin ; ras Proteins (EC 3.6.5.2)
Language	English
Publishing date	2016-07-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2063563-1
ISSN	1538-8514 ; 1535-7163
ISSN (online)	1538-8514
ISSN	1535-7163
DOI	10.1158/1535-7163.MCT-16-0309
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Zs.A 5750: Show issues

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Article: Transcriptional analysis of doxorubicin-induced cardiotoxicity.

Yi, Xiaoming / Bekeredjian, Raffi / DeFilippis, Nicholas J / Siddiquee, Zakir / Fernandez, Eduardo / Shohet, Ralph V

American journal of physiology. Heart and circulatory physiology

2005 Volume 290, Issue 3, Page(s) H1098–102

Abstract: Doxorubicin is an effective chemotherapeutic agent against a broad range of tumors. However, a threshold dose of doxorubicin causes an unacceptably high incidence of heart failure and limits its clinical utility. We have established two models of ... ...

Abstract	Doxorubicin is an effective chemotherapeutic agent against a broad range of tumors. However, a threshold dose of doxorubicin causes an unacceptably high incidence of heart failure and limits its clinical utility. We have established two models of doxorubicin cardiotoxicity in mice: 1) in an acute model, mice are treated with 15 mg/kg of doxorubicin once; and 2) in a chronic model, they receive 3 mg/kg weekly for 12 wk. Using echocardiography, we have monitored left ventricular function during treatment in the chronic model and seen the expected development of dilated cardiomyopathy. Treated mice showed histological abnormalities similar to those seen in patients with doxorubicin cardiomyopathy. To investigate transcriptional regulation in these models, we used a muscle-specific cDNA microarray. We have identified genes that respond to doxorubicin exposure in both models and confirmed these results using real-time PCR. In the acute model, a set of genes is regulated early and rapidly returns to baseline levels, consistent with the half-life of doxorubicin. In the chronic model, which mimics the clinical situation much more closely, we identified dysregulated genes that implicate specific mechanisms of cardiac toxicity. These include STARS, a hypertrophy-responsive gene; SNF1-kinase, a potential modulator of ATP levels; and AXUD1, a downstream target of the proapoptotic regulator AXIN1.
MeSH term(s)	Animals ; Cardiomyopathy, Dilated/chemically induced ; Cardiomyopathy, Dilated/metabolism ; Cardiomyopathy, Dilated/pathology ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Doxorubicin/administration & dosage ; Doxorubicin/toxicity ; Heart/drug effects ; Male ; Mice ; Mice, Inbred C57BL ; Myocardium/metabolism ; Transcription Factors/metabolism ; Ventricular Dysfunction, Left/chemically induced ; Ventricular Dysfunction, Left/metabolism ; Ventricular Dysfunction, Left/pathology
Chemical Substances	Transcription Factors ; Doxorubicin (80168379AG)
Language	English
Publishing date	2005-10-21
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	603838-4
ISSN	1522-1539 ; 0363-6135
ISSN (online)	1522-1539
ISSN	0363-6135
DOI	10.1152/ajpheart.00832.2005
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Article: MAP3K11/GDF15 axis is a critical driver of cancer cachexia.

Lerner, Lorena / Tao, Julie / Liu, Qing / Nicoletti, Richard / Feng, Bin / Krieger, Brian / Mazsa, Elizabeth / Siddiquee, Zakir / Wang, Ruoji / Huang, Lucia / Shen, Luhua / Lin, Jie / Vigano, Antonio / Chiu, M Isabel / Weng, Zhigang / Winston, William / Weiler, Solly / Gyuris, Jeno

Journal of cachexia, sarcopenia and muscle

2015 Volume 7, Issue 4, Page(s) 467–482

Abstract: Background: Cancer associated cachexia affects the majority of cancer patients during the course of the disease and thought to be directly responsible for about a quarter of all cancer deaths. Current evidence suggests that a pro-inflammatory state may ... ...

Abstract	Background: Cancer associated cachexia affects the majority of cancer patients during the course of the disease and thought to be directly responsible for about a quarter of all cancer deaths. Current evidence suggests that a pro-inflammatory state may be associated with this syndrome although the molecular mechanisms responsible for the development of cachexia are poorly understood. The purpose of this work was the identification of key drivers of cancer cachexia that could provide a potential point of intervention for the treatment and/or prevention of this syndrome. Methods: Genetically engineered and xenograft tumour models were used to dissect the molecular mechanisms driving cancer cachexia. Cytokine profiling from the plasma of cachectic and non-cachectic cancer patients and mouse models was utilized to correlate circulating cytokine levels with the cachexia phenotype. Results: Utilizing engineered tumour models we identified MAP3K11/GDF15 pathway activation as a potent inducer of cancer cachexia. Increased expression and high circulating levels of GDF15 acted as a key mediator of this process. In animal models, tumour-produced GDF15 was sufficient to trigger the cachexia phenotype. Elevated GDF15 circulating levels correlated with the onset and progression of cachexia in animal models and in patients with cancer. Inhibition of GDF15 biological activity with a specific antibody reversed body weight loss and restored muscle and fat tissue mass in several cachectic animal models regardless of their complex secreted cytokine profile. Conclusions: The combination of correlative observations, gain of function, and loss of function experiments validated GDF15 as a key driver of cancer cachexia and as a potential therapeutic target for the treatment and/or prevention of this syndrome.
Language	English
Publishing date	2015-10-29
Publishing country	Germany
Document type	Journal Article
ZDB-ID	2586864-0
ISSN	2190-6009 ; 2190-5991
ISSN (online)	2190-6009
ISSN	2190-5991
DOI	10.1002/jcsm.12077
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Article: Mice with cardiomyocyte-specific disruption of the endothelin-1 gene are resistant to hyperthyroid cardiac hypertrophy.

Shohet, Ralph V / Kisanuki, Yaz Y / Zhao, Xiao-Song / Siddiquee, Zakir / Franco, Fatima / Yanagisawa, Masashi

Proceedings of the National Academy of Sciences of the United States of America

2004 Volume 101, Issue 7, Page(s) 2088–2093

Abstract: Endothelin 1 (ET-1), a potent vasoconstrictor peptide expressed by endothelium, is also produced in the heart in response to a variety of stresses. It induces hypertrophy in cultured cardiac myocytes but only at concentrations far greater than those ... ...

Abstract	Endothelin 1 (ET-1), a potent vasoconstrictor peptide expressed by endothelium, is also produced in the heart in response to a variety of stresses. It induces hypertrophy in cultured cardiac myocytes but only at concentrations far greater than those found in plasma. We tested whether ET-1 generated by cardiac myocytes in vivo is a local signal for cardiac hypertrophy. To avoid the perinatal lethality seen in systemic ET-1-null mice, we used the Cre/loxP system to generate mice with cardiac myocyte-specific disruption of the ET-1 gene. We used the alpha-myosin heavy chain promoter to drive expression of Cre and were able to obtain 75% reduction in ET-1 mRNA in cardiac myocytes isolated from these mice at baseline and after stimulation, in vivo, for 24 h with tri-iodothyronine (T3). Necropsy measurements of cardiac mass indexed for body weight showed a 57% reduction in cardiac hypertrophy in response to 16 days of exogenous T3 in mice homozygous for the disrupted ET-1 allele compared to siblings with an intact ET-1 gene. Moreover, in vivo MRI showed only a 3% increase in left ventricular mass indexed for body weight in mice with the disrupted allele after 3 weeks of T3 treatment versus a 27% increase in mice with an intact ET-1 gene. A reduced hypertrophic response was confirmed by planimetry of cardiac myocytes. We conclude that ET-1, produced locally by cardiac myocytes, and acting in a paracrine/autocrine manner, is an important signal for myocardial hypertrophy that facilitates the response to thyroid hormone.
MeSH term(s)	Aging ; Alleles ; Animals ; Cardiomegaly/chemically induced ; Cardiomegaly/genetics ; Endothelin-1/deficiency ; Endothelin-1/genetics ; Female ; Gene Deletion ; Genetic Predisposition to Disease/genetics ; Hyperthyroidism/genetics ; Integrases/genetics ; Integrases/metabolism ; Male ; Mice ; Mice, Knockout ; Myocytes, Cardiac/drug effects ; Myocytes, Cardiac/metabolism ; Organ Specificity ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Recombination, Genetic ; Triiodothyronine/pharmacology ; Viral Proteins/genetics ; Viral Proteins/metabolism
Chemical Substances	Endothelin-1 ; RNA, Messenger ; Viral Proteins ; Triiodothyronine (06LU7C9H1V) ; Cre recombinase (EC 2.7.7.-) ; Integrases (EC 2.7.7.-)
Language	English
Publishing date	2004-02-17
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.0307159101
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Article ; Online: Protein kinase CK1alphaLS promotes vascular cell proliferation and intimal hyperplasia.

Panchenko, Mikhail P / Siddiquee, Zakir / Dombkowski, David M / Alekseyev, Yuriy O / Lenburg, Marc E / Walker, Jennifer D / Macgillivray, Thomas E / Preffer, Frederic I / Stone, James R

The American journal of pathology

2010 Volume 177, Issue 3, Page(s) 1562–1572

Abstract: Protein kinase CK1alpha regulates several fundamental cellular processes including proliferation and differentiation. Up to four forms of this kinase are expressed in vertebrates resulting from alternative splicing of exons; these exons encode either the ...

Abstract	Protein kinase CK1alpha regulates several fundamental cellular processes including proliferation and differentiation. Up to four forms of this kinase are expressed in vertebrates resulting from alternative splicing of exons; these exons encode either the L-insert located within the catalytic domain or the S-insert located at the C terminus of the protein. Whereas the L-insert is known to target the kinase to the nucleus, the functional significance of nuclear CK1alphaLS has been unclear. Here we demonstrate that selective L-insert-targeted short hairpin small interfering RNA-mediated knockdown of CK1alphaLS in human vascular endothelial cells and vascular smooth muscle cells impairs proliferation and abolishes hydrogen peroxide-stimulated proliferation of vascular smooth muscle cells, with the cells accumulating in G(0)/G(1). In addition, selective knockdown of CK1alphaLS in cultured human arteries inhibits vascular activation, preventing smooth muscle cell proliferation, intimal hyperplasia, and proteoglycan deposition. Knockdown of CK1alphaLS results in the harmonious down-regulation of its target substrate heterogeneous nuclear ribonucleoprotein C and results in the altered expression or alternative splicing of key genes involved in cellular activation including CXCR4, MMP3, CSF2, and SMURF1. Our results indicate that the nuclear form of CK1alpha in humans, CK1alphaLS, plays a critical role in vascular cell proliferation, cellular activation, and hydrogen peroxide-mediated mitogenic signal transduction.
MeSH term(s)	Adult ; Aged ; Aged, 80 and over ; Blotting, Western ; Casein Kinase Ialpha/metabolism ; Cell Count ; Cell Proliferation ; Cells, Cultured ; Endothelial Cells/metabolism ; Endothelial Cells/pathology ; Endothelium, Vascular/metabolism ; Endothelium, Vascular/pathology ; Female ; Flow Cytometry ; Humans ; Hyperplasia/metabolism ; Hyperplasia/pathology ; Male ; Middle Aged ; Muscle, Smooth, Vascular/metabolism ; Muscle, Smooth, Vascular/pathology ; Myocytes, Smooth Muscle/metabolism ; Myocytes, Smooth Muscle/pathology ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction/physiology ; Thoracic Arteries/metabolism ; Thoracic Arteries/pathology ; Tunica Intima/metabolism ; Tunica Intima/pathology
Chemical Substances	Casein Kinase Ialpha (EC 2.7.11.1)
Language	English
Publishing date	2010-08-09
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2943-9
ISSN	1525-2191 ; 0002-9440
ISSN (online)	1525-2191
ISSN	0002-9440
DOI	10.2353/ajpath.2010.100327
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Article ; Online: Pediatric-type nodal follicular lymphoma: an indolent clonal proliferation in children and adults with high proliferation index and no BCL2 rearrangement.

Louissaint, Abner / Ackerman, Adam M / Dias-Santagata, Dora / Ferry, Judith A / Hochberg, Ephraim P / Huang, Mary S / Iafrate, A John / Lara, Daniel O / Pinkus, Geraldine S / Salaverria, Itziar / Siddiquee, Zakir / Siebert, Reiner / Weinstein, Howard J / Zukerberg, Lawrence R / Harris, Nancy Lee / Hasserjian, Robert P

Blood

2012 Volume 120, Issue 12, Page(s) 2395–2404

Abstract: Pediatric follicular lymphoma (PFL) is a variant of follicular lymphoma (FL) presenting as localized lymphadenopathy in children. Unlike conventional adult FL, PFL typically does not recur or progress. Clear diagnostic criteria for PFL are lacking, and ... ...

Abstract	Pediatric follicular lymphoma (PFL) is a variant of follicular lymphoma (FL) presenting as localized lymphadenopathy in children. Unlike conventional adult FL, PFL typically does not recur or progress. Clear diagnostic criteria for PFL are lacking, and it is uncertain whether this indolent lymphoma is defined by age or may occur in adults. We analyzed 27 FL in patients < 40 years of age and found that all 21 cases that lacked a BCL2 gene abnormality (BCL2-N; P < .0001) and had > 30% Ki67 fraction (high proliferation index, HPI; P = .0007) were stage I and did not progress or recur; in comparison, all 6 cases with BCL2 rearrangement and/or PI < 30% were stage III/IV, and 5 of 6 recurred or progressed. In a separate cohort of 58 adult FL (≥ 18 years of age), all 13 BCL2-N/HPI cases were stage I, and none progressed or relapsed, whereas 11 of 15 stage I cases with BCL2 gene abnormality and/or LPI relapsed or progressed (P = .0001). The adult and pediatric BCL2-N/HPI FL cases had similar morphologic features. Our results confirm the highly indolent behavior of PFL and suggest that these are characterized by HPI and absence of BCL2 gene abnormality. PFL-like cases also occur in adults and are associated with indolent behavior in this patient population.
MeSH term(s)	Adolescent ; Adult ; Aged ; Aged, 80 and over ; Cell Proliferation ; Child ; Child, Preschool ; Cohort Studies ; Disease Progression ; Female ; Gene Rearrangement/genetics ; Humans ; Immunophenotyping ; In Situ Hybridization, Fluorescence ; Infant ; Infant, Newborn ; Ki-67 Antigen/metabolism ; Lymph Nodes/pathology ; Lymphoma, Follicular/genetics ; Lymphoma, Follicular/mortality ; Lymphoma, Follicular/pathology ; Male ; Middle Aged ; Neoplasm Recurrence, Local/genetics ; Neoplasm Recurrence, Local/mortality ; Neoplasm Recurrence, Local/pathology ; Prognosis ; Proto-Oncogene Proteins c-bcl-2/genetics ; Survival Rate ; Young Adult
Chemical Substances	Ki-67 Antigen ; Proto-Oncogene Proteins c-bcl-2
Language	English
Publishing date	2012-07-31
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood-2012-05-429514
Database	MEDical Literature Analysis and Retrieval System OnLINE

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