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Article ; Online: Magnetic-Assisted Capsule Endoscopy in Children With Crohn Disease: Feasibility and Impact on Gastric Transit Time.

Di Nardo, Giovanni / Micheli, Federica / Cozzi, Denis A / Mercantini, Paolo / Parisi, Pasquale / Baccini, Flavia / Mennini, Maurizio / Raucci, Umberto / Marasco, Giovanni

Journal of pediatric gastroenterology and nutrition

2023 Volume 76, Issue 5, Page(s) 646–651

Abstract: Objectives: Standard capsule endoscopy (CE) is ineffective for upper gastrointestinal (GI) tract examination because it does not allow operator-controlled navigation of the capsule. Magnetically assisted capsule endoscopy (MACE) may offer a solution to ... ...

Abstract	Objectives: Standard capsule endoscopy (CE) is ineffective for upper gastrointestinal (GI) tract examination because it does not allow operator-controlled navigation of the capsule. Magnetically assisted capsule endoscopy (MACE) may offer a solution to these problems. This pilot study is aimed to evaluate the feasibility of MACE system in pediatric Crohn disease (CD) and if magnetic steering could enhance capsule gastric emptying when compared with standard CE. Methods: Pediatric CD patients already studied by standard small bowel CE were enrolled. All participants swallowed a magnetically assisted CE and an external magnetic field navigator was used to guide the capsule through the upper GI tract. Maneuverability, completeness of the MACE examination, differences in the esophageal transit time (ETT), gastric transit time (GTT), and pyloric transit time (PTT) between standard CE and MACE were assessed. Results: Ten patients [mean age 11.4 years (range 6-15); 60% male] were enrolled. Maneuverability was defined as good and fair in 60% and 40% of participants, respectively. Completeness of MACE examination was 95%, 65%, and 92.5% in the esophagus, proximal, and distal stomach, respectively. Transpyloric passage of the capsule under magnetic control was successfully performed in 80% of patients. Magnetic intervention significantly increased ETT ( P < 0.001) and reduced GTT and PTT ( P = 0.002). No significant adverse events occurred. Conclusions: MACE is a safe and feasible technique in children. Magnetic steering enhances capsule gastric emptying and facilitates capsule transpyloric passage when compared with standard CE.
MeSH term(s)	Humans ; Male ; Child ; Adolescent ; Female ; Capsule Endoscopy/methods ; Crohn Disease/diagnosis ; Feasibility Studies ; Pilot Projects ; Stomach ; Gastrointestinal Transit ; Magnetic Phenomena
Language	English
Publishing date	2023-02-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	603201-1
ISSN	1536-4801 ; 0277-2116
ISSN (online)	1536-4801
ISSN	0277-2116
DOI	10.1097/MPG.0000000000003733
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Article ; Online: Galectin-9 Regulates Monosodium Urate Crystal-Induced Gouty Inflammation Through the Modulation of Treg/Th17 Ratio.

Mansour, Adel Abo / Raucci, Federica / Saviano, Anella / Tull, Samantha / Maione, Francesco / Iqbal, Asif Jilani

Frontiers in immunology

2021 Volume 12, Page(s) 762016

Abstract: Gout is caused by depositing monosodium urate (MSU) crystals within the articular area. The infiltration of neutrophils and monocytes drives the initial inflammatory response followed by lymphocytes. Interestingly, emerging evidence supports the view ... ...

Abstract	Gout is caused by depositing monosodium urate (MSU) crystals within the articular area. The infiltration of neutrophils and monocytes drives the initial inflammatory response followed by lymphocytes. Interestingly, emerging evidence supports the view that
MeSH term(s)	Animals ; Ankle Joint/immunology ; Anti-Inflammatory Agents/therapeutic use ; Arthritis, Gouty/drug therapy ; Arthritis, Gouty/immunology ; Cells, Cultured ; Cytokines/immunology ; Galectins/therapeutic use ; Humans ; Male ; Mice ; T-Lymphocytes, Regulatory/drug effects ; T-Lymphocytes, Regulatory/immunology ; Uric Acid
Chemical Substances	Anti-Inflammatory Agents ; Cytokines ; Galectins ; Uric Acid (268B43MJ25)
Language	English
Publishing date	2021-10-28
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2021.762016
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Article ; Online: MicroRNA-34a: the bad guy in age-related vascular diseases

Raucci, Angela / Macrì, Federica / Castiglione, Stefania / Badi, Ileana / Vinci, Maria Cristina / Zuccolo, Estella

Cell. Mol. Life Sci.. 2021 Dec., v. 78, no. 23 p.7355-7378

2021

Abstract: The age-related vasculature alteration is the prominent risk factor for vascular diseases (VD), namely, atherosclerosis, abdominal aortic aneurysm, vascular calcification (VC) and pulmonary arterial hypertension (PAH). The chronic sterile low-grade ... ...

Abstract	The age-related vasculature alteration is the prominent risk factor for vascular diseases (VD), namely, atherosclerosis, abdominal aortic aneurysm, vascular calcification (VC) and pulmonary arterial hypertension (PAH). The chronic sterile low-grade inflammation state, alias inflammaging, characterizes elderly people and participates in VD development. MicroRNA34-a (miR-34a) is emerging as an important mediator of inflammaging and VD. miR-34a increases with aging in vessels and induces senescence and the acquisition of the senescence-associated secretory phenotype (SASP) in vascular smooth muscle (VSMCs) and endothelial (ECs) cells. Similarly, other VD risk factors, including dyslipidemia, hyperglycemia and hypertension, modify miR-34a expression to promote vascular senescence and inflammation. miR-34a upregulation causes endothelial dysfunction by affecting ECs nitric oxide bioavailability, adhesion molecules expression and inflammatory cells recruitment. miR-34a-induced senescence facilitates VSMCs osteoblastic switch and VC development in hyperphosphatemia conditions. Conversely, atherogenic and hypoxic stimuli downregulate miR-34a levels and promote VSMCs proliferation and migration during atherosclerosis and PAH. MiR34a genetic ablation or miR-34a inhibition by anti-miR-34a molecules in different experimental models of VD reduce vascular inflammation, senescence and apoptosis through sirtuin 1 Notch1, and B-cell lymphoma 2 modulation. Notably, pleiotropic drugs, like statins, liraglutide and metformin, affect miR-34a expression. Finally, human studies report that miR-34a levels associate to atherosclerosis and diabetes and correlate with inflammatory factors during aging. Herein, we comprehensively review the current knowledge about miR-34a-dependent molecular and cellular mechanisms activated by VD risk factors and highlight the diagnostic and therapeutic potential of modulating its expression in order to reduce inflammaging and VD burn and extend healthy lifespan.
Keywords	B-cell lymphoma ; adhesion ; aneurysm ; apoptosis ; atherosclerosis ; bioavailability ; calcification ; diabetes ; elderly ; humans ; hyperglycemia ; hyperlipidemia ; hypertension ; inflammation ; longevity ; metformin ; nitric oxide ; people ; phenotype ; pulmonary artery ; risk factors ; sirtuins ; smooth muscle ; therapeutics
Language	English
Dates of publication	2021-12
Size	p. 7355-7378.
Publishing place	Springer International Publishing
Document type	Article ; Online
Note	Review
ZDB-ID	1358415-7
ISSN	1420-9071 ; 1420-682X
ISSN (online)	1420-9071
ISSN	1420-682X
DOI	10.1007/s00018-021-03979-4
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: MicroRNA-34a: the bad guy in age-related vascular diseases.

Raucci, Angela / Macrì, Federica / Castiglione, Stefania / Badi, Ileana / Vinci, Maria Cristina / Zuccolo, Estella

Cellular and molecular life sciences : CMLS

2021 Volume 78, Issue 23, Page(s) 7355–7378

Abstract	The age-related vasculature alteration is the prominent risk factor for vascular diseases (VD), namely, atherosclerosis, abdominal aortic aneurysm, vascular calcification (VC) and pulmonary arterial hypertension (PAH). The chronic sterile low-grade inflammation state, alias inflammaging, characterizes elderly people and participates in VD development. MicroRNA34-a (miR-34a) is emerging as an important mediator of inflammaging and VD. miR-34a increases with aging in vessels and induces senescence and the acquisition of the senescence-associated secretory phenotype (SASP) in vascular smooth muscle (VSMCs) and endothelial (ECs) cells. Similarly, other VD risk factors, including dyslipidemia, hyperglycemia and hypertension, modify miR-34a expression to promote vascular senescence and inflammation. miR-34a upregulation causes endothelial dysfunction by affecting ECs nitric oxide bioavailability, adhesion molecules expression and inflammatory cells recruitment. miR-34a-induced senescence facilitates VSMCs osteoblastic switch and VC development in hyperphosphatemia conditions. Conversely, atherogenic and hypoxic stimuli downregulate miR-34a levels and promote VSMCs proliferation and migration during atherosclerosis and PAH. MiR34a genetic ablation or miR-34a inhibition by anti-miR-34a molecules in different experimental models of VD reduce vascular inflammation, senescence and apoptosis through sirtuin 1 Notch1, and B-cell lymphoma 2 modulation. Notably, pleiotropic drugs, like statins, liraglutide and metformin, affect miR-34a expression. Finally, human studies report that miR-34a levels associate to atherosclerosis and diabetes and correlate with inflammatory factors during aging. Herein, we comprehensively review the current knowledge about miR-34a-dependent molecular and cellular mechanisms activated by VD risk factors and highlight the diagnostic and therapeutic potential of modulating its expression in order to reduce inflammaging and VD burn and extend healthy lifespan.
MeSH term(s)	Aortic Aneurysm, Abdominal/genetics ; Aortic Aneurysm, Abdominal/pathology ; Atherosclerosis/genetics ; Atherosclerosis/pathology ; Cardiovascular Diseases/genetics ; Cardiovascular Diseases/pathology ; Cardiovascular System/pathology ; Cellular Senescence/physiology ; Endothelial Cells/metabolism ; Humans ; Inflammation/genetics ; Inflammation/pathology ; MicroRNAs/genetics ; Muscle, Smooth, Vascular/pathology ; Pulmonary Arterial Hypertension/genetics ; Pulmonary Arterial Hypertension/pathology ; Vascular Calcification/genetics ; Vascular Calcification/pathology
Chemical Substances	MIRN34 microRNA, human ; MicroRNAs
Language	English
Publishing date	2021-10-26
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	1358415-7
ISSN	1420-9071 ; 1420-682X
ISSN (online)	1420-9071
ISSN	1420-682X
DOI	10.1007/s00018-021-03979-4
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Effects of RAGE Deletion on the Cardiac Transcriptome during Aging.

Scavello, Francesco / Piacentini, Luca / Castiglione, Stefania / Zeni, Filippo / Macrì, Federica / Casaburo, Manuel / Vinci, Maria Cristina / Colombo, Gualtiero I / Raucci, Angela

International journal of molecular sciences

2022 Volume 23, Issue 19

Abstract: Cardiac aging is characterized by increased cardiomyocyte hypertrophy, myocardial stiffness, and fibrosis, which enhance cardiovascular risk. The receptor for advanced glycation end-products (RAGE) is involved in several age-related diseases. RAGE ... ...

Abstract	Cardiac aging is characterized by increased cardiomyocyte hypertrophy, myocardial stiffness, and fibrosis, which enhance cardiovascular risk. The receptor for advanced glycation end-products (RAGE) is involved in several age-related diseases. RAGE knockout (
MeSH term(s)	Aging/genetics ; Aging/metabolism ; Animals ; Fatty Acids ; Female ; Fibrosis ; Glycation End Products, Advanced/genetics ; Glycation End Products, Advanced/metabolism ; Interferon-beta/genetics ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Receptor for Advanced Glycation End Products/genetics ; Receptor for Advanced Glycation End Products/metabolism ; Transcriptome ; Triglycerides
Chemical Substances	Fatty Acids ; Glycation End Products, Advanced ; Receptor for Advanced Glycation End Products ; Triglycerides ; Interferon-beta (77238-31-4)
Language	English
Publishing date	2022-09-22
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms231911130
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Article ; Online: The functional link between microsomal prostaglandin E synthase-1 (mPGES-1) and peroxisome proliferator-activated receptor γ (PPARγ) in the onset of inflammation.

Maione, Francesco / Casillo, Gian Marco / Raucci, Federica / Iqbal, Asif J / Mascolo, Nicola

Pharmacological research

2020 Volume 157, Page(s) 104807

Abstract: Many years have elapsed since the discovery of anti-inflammatories as effective therapeutics for the treatment of inflammatory-related diseases, but we are still uncovering their various mechanisms of action. Recent biochemical and pharmacological ... ...

Abstract	Many years have elapsed since the discovery of anti-inflammatories as effective therapeutics for the treatment of inflammatory-related diseases, but we are still uncovering their various mechanisms of action. Recent biochemical and pharmacological studies have shown that in different tissues and cell types lipid mediators from thearachidonic acid cascade, play a crucial role in the initiation and resolution of inflammation by shifting from pro-inflammatory prostaglandin (PG)E
MeSH term(s)	Animals ; Anti-Inflammatory Agents/therapeutic use ; Humans ; Inflammation/drug therapy ; Inflammation/enzymology ; Inflammation/immunology ; Inflammation Mediators/metabolism ; PPAR gamma/metabolism ; Prostaglandin-E Synthases/metabolism ; Signal Transduction/drug effects
Chemical Substances	Anti-Inflammatory Agents ; Inflammation Mediators ; PPAR gamma ; PPARG protein, human ; PTGES protein, human (EC 5.3.99.3) ; Prostaglandin-E Synthases (EC 5.3.99.3)
Language	English
Publishing date	2020-04-22
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1003347-6
ISSN	1096-1186 ; 0031-6989 ; 1043-6618
ISSN (online)	1096-1186
ISSN	0031-6989 ; 1043-6618
DOI	10.1016/j.phrs.2020.104807
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Article ; Conference proceedings: N-Acylethanolamine acid amidase (NAAA) inhibition rescues intestinal fibrosis through IL-23 pathway

Nanì, MariaFrancesca / Lucariello, Giuseppe / Pagano, Ester / Cattaneo, Fabio / Cicia, Donatella / Raucci, Federica / Tropeano, FrancescaPaola / Petrosino, Stefania / Cicco, PaolaDe / Borrelli, Francesca / Izzo, AngeloA. / Romano, Barbara

Zeitschrift für Gastroenterologie

2023 Volume 61, Issue 03

Event/congress	50. Jahrestagung der Gesellschaft für Gastroenterologie in Bayern e.V., Erlangen, 2023-04-21
Language	German
Publishing date	2023-03-01
Publisher	Georg Thieme Verlag
Publishing place	Stuttgart ; New York
Document type	Article ; Conference proceedings
ZDB-ID	201387-3
ISSN	1439-7803 ; 0044-2771 ; 0172-8504
ISSN (online)	1439-7803
ISSN	0044-2771 ; 0172-8504
DOI	10.1055/s-0043-1764100
Database	Thieme publisher's database

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Zs.A 111: 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 ; Conference proceedings: N-Acylethanolamine acid amidase (NAAA) inhibition rescues intestinal fibrosis through IL-23 pathway

Zeitschrift für Gastroenterologie

2023 Volume 61, Issue 03

Event/congress	50. Jahrestagung der Gesellschaft für Gastroenterologie in Bayern e.V., Erlangen, 2023-04-21
Language	German
Publishing date	2023-03-01
Publisher	Georg Thieme Verlag
Publishing place	Stuttgart ; New York
Document type	Article ; Conference proceedings
ZDB-ID	201387-3
ISSN	1439-7803 ; 0044-2771 ; 0172-8504
ISSN (online)	1439-7803
ISSN	0044-2771 ; 0172-8504
DOI	10.1055/s-0043-1764094
Database	Thieme publisher's database

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Zs.A 111: 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: Interleukin-17A (IL-17A): A silent amplifier of COVID-19.

Maione, Francesco / Casillo, Gian Marco / Raucci, Federica / Salvatore, Cristian / Ambrosini, Giovanna / Costa, Luisa / Scarpa, Raffaele / Caso, Francesco / Bucci, Mariarosaria

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

2021 Volume 142, Page(s) 111980

Abstract: One of the hallmarks of COVID-19 is the cytokine storm that provokes primarily pneumonia followed by systemic inflammation. Emerging evidence has identified a potential link between elevated interleukin-17A (IL-17A) levels and disease severity and ... ...

Abstract	One of the hallmarks of COVID-19 is the cytokine storm that provokes primarily pneumonia followed by systemic inflammation. Emerging evidence has identified a potential link between elevated interleukin-17A (IL-17A) levels and disease severity and progression. Considering that per se, IL-17A can activate several inflammatory pathways, it is plausible to hypothesize an involvement of this cytokine in COVID-19 clinical outcomes. Thus, IL-17A could represent a marker of disease progression and/or a target to develop therapeutic strategies. This hypothesis paper aims to propose this "unique" cytokine as a silent amplifier of the COVID-19 immune response and (potentially) related therapy.
MeSH term(s)	Biomarkers/blood ; COVID-19/diagnosis ; COVID-19/drug therapy ; COVID-19/immunology ; Cytokine Release Syndrome/etiology ; Cytokine Release Syndrome/immunology ; Disease Progression ; Drug Discovery ; Humans ; Inflammation Mediators/metabolism ; Interleukin-17/blood ; Interleukin-17/immunology ; Severity of Illness Index
Chemical Substances	Biomarkers ; Inflammation Mediators ; Interleukin-17
Language	English
Publishing date	2021-07-29
Publishing country	France
Document type	Journal Article
ZDB-ID	392415-4
ISSN	1950-6007 ; 0753-3322 ; 0300-0893
ISSN (online)	1950-6007
ISSN	0753-3322 ; 0300-0893
DOI	10.1016/j.biopha.2021.111980
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Article ; Online: High Phosphate-Induced JAK-STAT Signalling Sustains Vascular Smooth Muscle Cell Inflammation and Limits Calcification.

Macrì, Federica / Vigorito, Ilaria / Castiglione, Stefania / Faggiano, Stefano / Casaburo, Manuel / Fanotti, Nadia / Piacentini, Luca / Vigetti, Davide / Vinci, Maria Cristina / Raucci, Angela

Biomolecules

2023 Volume 14, Issue 1

Abstract: Vascular calcification (VC) is an age-related complication characterised by calcium-phosphate deposition in the arterial wall driven by the osteogenic transformation of vascular smooth muscle cells (VSMCs). The JAK-STAT pathway is an emerging target in ... ...

Abstract	Vascular calcification (VC) is an age-related complication characterised by calcium-phosphate deposition in the arterial wall driven by the osteogenic transformation of vascular smooth muscle cells (VSMCs). The JAK-STAT pathway is an emerging target in inflammation. Considering the relationship between VC and inflammation, we investigated the role of JAK-STAT signalling during VSMC calcification. Human aortic smooth muscle cells (HASMCs) were cultured in high-inorganic phosphate (Pi) medium for up to 7 days; calcium deposition was determined via Alizarin staining and colorimetric assay. Inflammatory factor secretion was evaluated via ELISA and JAK-STAT members' activation using Western blot or immunohistochemistry on HASMCs or calcified aortas of Vitamin D-treated C57BL6/J mice, respectively. The JAK-STAT pathway was blocked by JAK Inhibitor I and Von Kossa staining was used for calcium deposits in murine aortic rings. During Pi-induced calcification, HASMCs released IL-6, IL-8, and MCP-1 and activated JAK1-JAK3 proteins and STAT1. Phospho-STAT1 was detected in murine calcified aortas. Blocking of the JAK-STAT cascade reduced HASMC proliferation and pro-inflammatory factor expression and release while increasing calcium deposition and osteogenic transcription factor RUNX2 expression. Consistently, JAK-STAT pathway inhibition exacerbates mouse aortic ring calcification ex vivo. Intriguingly, our results suggest an alternative link between VSMC inflammation and VC.
MeSH term(s)	Humans ; Animals ; Mice ; Muscle, Smooth, Vascular ; Calcium ; Janus Kinases ; STAT Transcription Factors ; Signal Transduction ; Vascular Calcification/chemically induced ; Inflammation
Chemical Substances	Calcium (SY7Q814VUP) ; Janus Kinases (EC 2.7.10.2) ; STAT Transcription Factors
Language	English
Publishing date	2023-12-24
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2701262-1
ISSN	2218-273X ; 2218-273X
ISSN (online)	2218-273X
ISSN	2218-273X
DOI	10.3390/biom14010029
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