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Article ; Online: Light-driven eco-evolutionary dynamics in a synthetic replicator system.

Liu, Kai / Blokhuis, Alex / van Ewijk, Chris / Kiani, Armin / Wu, Juntian / Roos, Wouter H / Otto, Sijbren

2023 Volume 16, Issue 1, Page(s) 79–88

Abstract: Darwinian evolution involves the inheritance and selection of variations in reproducing entities. Selection can be based on, among others, interactions with the environment. Conversely, the replicating entities can also affect their environment ... ...

Abstract	Darwinian evolution involves the inheritance and selection of variations in reproducing entities. Selection can be based on, among others, interactions with the environment. Conversely, the replicating entities can also affect their environment generating a reciprocal feedback on evolutionary dynamics. The onset of such eco-evolutionary dynamics marks a stepping stone in the transition from chemistry to biology. Yet the bottom-up creation of a molecular system that exhibits eco-evolutionary dynamics has remained elusive. Here we describe the onset of such dynamics in a minimal system containing two synthetic self-replicators. The replicators are capable of binding and activating a co-factor, enabling them to change the oxidation state of their environment through photoredox catalysis. The replicator distribution adapts to this change and, depending on light intensity, one or the other replicator becomes dominant. This study shows how behaviour analogous to eco-evolutionary dynamics-which until now has been restricted to biology-can be created using an artificial minimal replicator system.
MeSH term(s)	Light ; Catalysis
Language	English
Publishing date	2023-08-31
Publishing country	England
Document type	Journal Article
ZDB-ID	2464596-5
ISSN	1755-4349 ; 1755-4330
ISSN (online)	1755-4349
ISSN	1755-4330
DOI	10.1038/s41557-023-01301-2
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Article ; Online: Measurement of C1-Inhibitor function alone is sufficient for diagnosis of hereditary angioedema.

Kiani-Alikhan, Sorena / Walker, Elizabeth / Hickey, Alaco / Grigoriadou, Sofia / Buckland, Matt / Scott, Chris

Journal of clinical pathology

2021 Volume 75, Issue 11, Page(s) 787–788

Abstract: The World Allergy Organisiation/European Academy of Allergy and Clinical Immunology (WAO/EAACI) 2017/2018 guidelines recommend measuring complement4 levels, followed by C1-inhibitor level and function for diagnosis of hereditary angioedema (HAE). We ... ...

Abstract	The World Allergy Organisiation/European Academy of Allergy and Clinical Immunology (WAO/EAACI) 2017/2018 guidelines recommend measuring complement4 levels, followed by C1-inhibitor level and function for diagnosis of hereditary angioedema (HAE). We analysed 6 months' worth of data generated in our laboratory which is a specialist regional immunology service and also provides laboratory service for the Barts Health immunology department, which is a GA2LEN/HAEi-Angioedema Centre of Excellence and Reference (ACARE) and hence, investigates a large number of patients for HAE. We found that an efficient and sensitive approach for laboratory diagnosis of HAE is to only test the C1-inhibitor function. This approach had a sensitivity of 100% and reduced the cost of laboratory investigations for HAE diagnosis by 45%.
MeSH term(s)	Humans ; Angioedemas, Hereditary/diagnosis ; Complement C1 Inhibitor Protein/genetics ; Angioedema/diagnosis ; Clinical Laboratory Techniques
Chemical Substances	Complement C1 Inhibitor Protein
Language	English
Publishing date	2021-10-07
Publishing country	England
Document type	Journal Article
ZDB-ID	80261-x
ISSN	1472-4146 ; 0021-9746
ISSN (online)	1472-4146
ISSN	0021-9746
DOI	10.1136/jclinpath-2021-207538
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Book ; Online: Sepsis World Model

Kiani, Amirhossein / Wang, Chris / Xu, Angela

A MIMIC-based OpenAI Gym "World Model" Simulator for Sepsis Treatment

2019

Abstract: Sepsis is a life-threatening condition caused by the body's response to an infection. In order to treat patients with sepsis, physicians must control varying dosages of various antibiotics, fluids, and vasopressors based on a large number of variables in ...

Abstract	Sepsis is a life-threatening condition caused by the body's response to an infection. In order to treat patients with sepsis, physicians must control varying dosages of various antibiotics, fluids, and vasopressors based on a large number of variables in an emergency setting. In this project we employ a "world model" methodology to create a simulator that aims to predict the next state of a patient given a current state and treatment action. In doing so, we hope our simulator learns from a latent and less noisy representation of the EHR data. Using historical sepsis patient records from the MIMIC dataset, our method creates an OpenAI Gym simulator that leverages a Variational Auto-Encoder and a Mixture Density Network combined with a RNN (MDN-RNN) to model the trajectory of any sepsis patient in the hospital. To reduce the effects of noise, we sample from a generated distribution of next steps during simulation and have the option of introducing uncertainty into our simulator by controlling the "temperature" variable. It is worth noting that we do not have access to the ground truth for the best policy because we can only evaluate learned policies by real-world experimentation or expert feedback. Instead, we aim to study our simulator model's performance by evaluating the similarity between our environment's rollouts with the real EHR data and assessing its viability for learning a realistic policy for sepsis treatment using Deep Q-Learning. Comment: This project was done as a class project for CS221 at Stanford University
Keywords	Computer Science - Machine Learning ; Statistics - Machine Learning
Subject code	006
Publishing date	2019-12-15
Publishing country	us
Document type	Book ; Online
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Article ; Online: Quantification of human C1 esterase inhibitor protein using an automated turbidimetric immunoassay.

Tange, Clare E / Kaur, Amrit / Verma, Nisha / Hickey, Alaco / Grigoriadou, Sofia / Scott, Chris / Kiani, Sorena / Steven, Rachael / Ponsford, Mark / El-Shanawany, Tariq / Jolles, Stephen / Harding, Stephen / Parker, Antony R

Journal of clinical laboratory analysis

2018 Volume 33, Issue 1, Page(s) e22627

Abstract: Background: Impaired levels or function of C1 inhibitor (C1-INH) results in angioedema due to increased bradykinin. It is important to distinguish between angioedema related to C1-INH deficiency and that caused by other mechanisms, as treatment options ... ...

Abstract	Background: Impaired levels or function of C1 inhibitor (C1-INH) results in angioedema due to increased bradykinin. It is important to distinguish between angioedema related to C1-INH deficiency and that caused by other mechanisms, as treatment options are different. In hereditary (HAE) and acquired (AAE) angioedema, C1-INH concentration is measured to aid patient diagnosis. Here, we describe an automated turbidimetric assay to measure C1-INH concentration on the Optilite Methods: Linearity, precision, and interference were established over a range of C1-INH concentrations. The 95th percentile reference interval was generated from 120 healthy adult donors. To compare the Optilite C1-INH assay with a predicate assay used in a clinical laboratory, samples sent for C1-INH investigation were used. The predicate results were provided to allow comparison. Results: The Optilite C1-INH assay was linear across the measuring range at the standard sample dilution. Intra and interassay variability was <6%. The 95th percentile adult reference interval for the assay was 0.21-0.38 g/L. There was a strong correlation between the Optilite concentrations and those generated with the predicate assay (R Conclusion: The Optilite assay allows the automated and precise quantification of C1-INH concentrations in patient samples. It could therefore be used as a tool to aid the investigation of patients with angioedema.
MeSH term(s)	Adult ; Aged ; Aged, 80 and over ; Angioedema/blood ; Angioedema/diagnosis ; Automation, Laboratory ; Complement C1 Inhibitor Protein/analysis ; Female ; Humans ; Immunoturbidimetry/methods ; Limit of Detection ; Linear Models ; Male ; Middle Aged ; Reproducibility of Results ; Young Adult
Chemical Substances	Complement C1 Inhibitor Protein
Language	English
Publishing date	2018-07-29
Publishing country	United States
Document type	Journal Article
ZDB-ID	645095-7
ISSN	1098-2825 ; 0887-8013
ISSN (online)	1098-2825
ISSN	0887-8013
DOI	10.1002/jcla.22627
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Article: Overexpression of elastin fragments in infarcted myocardium attenuates scar expansion and heart dysfunction.

Mizuno, Tomohiro / Mickle, Donald A G / Kiani, Chris G / Li, Ren-Ke

American journal of physiology. Heart and circulatory physiology

2005 Volume 288, Issue 6, Page(s) H2819–27

Abstract: Ventricular dilation after myocardial infarction can cause heart failure. Increasing strength and elasticity in the infarct region might prevent ventricular dilation. Because elastin provides strength, extensibility, and resilience to tissues and ... ...

Abstract	Ventricular dilation after myocardial infarction can cause heart failure. Increasing strength and elasticity in the infarct region might prevent ventricular dilation. Because elastin provides strength, extensibility, and resilience to tissues and maintains tissue architecture, we studied the effect of elastin expression in the infarct on scar expansion and heart function. COS-7 cells transfected with a plasmid with an elastin gene fragment or a vector were seeded into a Gelfoam mesh and cultured. Mechanical stretch test (n = 5/group) showed that the elastin mesh was more elastic (P < 0.05) and tensile (P < 0.05) than the vector mesh. In an in vivo study in rats, 6 days after left anterior descending coronary artery ligation, COS-7 cells (Cell group, n = 7) or COS-7 cells with elastin gene (Elastin group, n = 9) or vector (Vector group, n = 9) were transplanted into the infarct; infarcted rats served as controls (n = 7). Over 8 wk the Cell group did not demonstrate effects on scar expansion and deterioration of heart function vs. controls. In contrast, infarct expansion was smaller and heart function was better maintained in the Elastin group vs. the Vector group (P < 0.05). At 8 wk after cell transplantation Langendorff data showed that the Elastin group had greater (P < 0.01) developed pressure and a smaller left ventricular volume than the Vector group. Western blot and histology showed accumulated elastin in the Elastin group infarct. Changing the extracellular matrix composition of a myocardial infarct by increasing elastin fragment content attenuated scar expansion, ventricular dilation, and onset of heart dysfunction.
MeSH term(s)	Animals ; Aorta ; Base Sequence ; COS Cells ; Chlorocebus aethiops ; Cicatrix/prevention & control ; DNA Primers ; Elastin/genetics ; Extracellular Matrix/metabolism ; Genetic Vectors ; Heart/physiology ; Heart/physiopathology ; Myocardial Infarction/metabolism ; Peptide Fragments/genetics ; Rats ; Recombinant Proteins/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Transfection
Chemical Substances	DNA Primers ; Peptide Fragments ; Recombinant Proteins ; Elastin (9007-58-3)
Language	English
Publishing date	2005-01-28
Publishing country	United States
Document type	Journal Article ; 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.00862.2004
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Article ; Online: Elastin stabilizes an infarct and preserves ventricular function.

Mizuno, Tomohiro / Yau, Terrence M / Weisel, Richard D / Kiani, Chris G / Li, Ren-Ke

Circulation

2005 Volume 112, Issue 9 Suppl, Page(s) I81–8

Abstract: Background: After a myocardial infarction, the injured region becomes fibrotic and the myocardial scar may expand if the ventricular wall lacks elasticity. Cardiac dilatation may precipitate the vicious cycle of progressive heart failure. The present ... ...

Abstract	Background: After a myocardial infarction, the injured region becomes fibrotic and the myocardial scar may expand if the ventricular wall lacks elasticity. Cardiac dilatation may precipitate the vicious cycle of progressive heart failure. The present study evaluated the functional benefits of increasing elastin within a myocardial scar using cell based gene therapy. Methods and results: A myocardial infarction was generated by ligation of the left anterior descending artery in rats. Six days later, 2 x 10(6) syngeneic rat endothelial cells transfected with the rat elastin gene (elastin group, n=14) or an empty plasmid (control group, n=14) were transplanted into the infarct scar. Cardiac function, left ventricular (LV) volume, and infarct size were monitored over 3 months by echocardiography, Langendorff measurements, and planimetry. Elastin deposition was evaluated in the cells and in the infarct region by Western blot assay and by histological examination. Recombinant elastin was found in the scar in the elastin group but not the control group during the 3 months after cell transplantation. Histological assessment demonstrated organized elastic fibers within the infarct region. LV volume and infarct size were significantly smaller (P<0.05) in the elastin group than in the control group. Cardiac function evaluated by echocardiography and during Langendorff perfusion was significantly better (P<0.05) in the elastin group than in the control group. Conclusions: Expressing recombinant elastin within the myocardial scar reduced scar expansion and prevented LV enlargement after a myocardial infarction. Altering matrix remodeling after an infarct preserved the LV function for at least 3 months.
MeSH term(s)	Animals ; Cells, Cultured/metabolism ; Cells, Cultured/transplantation ; Cicatrix/metabolism ; Cicatrix/pathology ; Drug Evaluation, Preclinical ; Elastin/genetics ; Elastin/physiology ; Endothelial Cells/metabolism ; Endothelial Cells/transplantation ; Extracellular Matrix/ultrastructure ; Genetic Therapy ; Heart Failure/etiology ; Heart Failure/prevention & control ; Hypertrophy, Left Ventricular/etiology ; Hypertrophy, Left Ventricular/prevention & control ; Male ; Myocardial Infarction/complications ; Myocardial Infarction/diagnostic imaging ; Myocardial Infarction/pathology ; Myocardial Infarction/physiopathology ; Myocardial Infarction/therapy ; Myocardium/chemistry ; Myocardium/pathology ; Random Allocation ; Rats ; Rats, Inbred Lew ; Recombinant Fusion Proteins/analysis ; Recombinant Fusion Proteins/biosynthesis ; Recombinant Fusion Proteins/physiology ; Single-Blind Method ; Transfection ; Ultrasonography ; Ventricular Function, Left/physiology ; Ventricular Remodeling
Chemical Substances	Recombinant Fusion Proteins ; Elastin (9007-58-3)
Language	English
Publishing date	2005-08-30
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
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	10.1161/01.CIRCULATIONAHA.105.523795
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Article: Quantitative analysis of survival of transplanted smooth muscle cells with real-time polymerase chain reaction.

Yasuda, Tamotsu / Weisel, Richard D / Kiani, Chris / Mickle, Donald A G / Maganti, Manjula / Li, Ren-Ke

The Journal of thoracic and cardiovascular surgery

2005 Volume 129, Issue 4, Page(s) 904–911

Abstract: Background: Cell transplantation improves heart function after myocardial infarction. This study investigated the survival of implanted cells in normal and infarcted myocardium.: Methods: Male rat aortic smooth muscle cells were cultured. For the in ... ...

Abstract	Background: Cell transplantation improves heart function after myocardial infarction. This study investigated the survival of implanted cells in normal and infarcted myocardium. Methods: Male rat aortic smooth muscle cells were cultured. For the in vitro study, male smooth muscle cells mixed with female smooth muscle cells or male smooth muscle cells injected into a piece of female rat myocardium were used to evaluate the accuracy of quantitative real-time polymerase chain reaction to measure Y chromosomes. For the in vivo study, 2 million live or dead male smooth muscle cells were injected into normal or infarcted female myocardium. At 1 hour and 1 and 4 weeks after transplantation, hearts, lungs, and kidneys were harvested for measurement of Y chromosomes. Results: In vitro, the accuracy of polymerase chain reaction measurement was excellent in cultured cells (r2 = 0.996) and the myocardium (r2 = 0.786). In vivo, 1 hour after 2 x 10(6) cell implantation, live cell numbers decreased to 1.0 +/- 0.2 x 10 6 and 1.1 +/- 0.3 x 10(6) , and dead cell numbers decreased to 0.9 +/- 0.2 x 10(6) and 0.8 +/- 0.2 x 10(6) in the normal and infarcted myocardium, respectively (P < .01 for all groups). Lungs and kidneys contained 8.5% and 1.5% of the implanted cells, but no cells were detected at 1 week. At 1 week, no dead smooth muscle cells were detected in the normal or infarcted myocardium. The numbers of live cells at 1 and 4 weeks were 0.48 +/- 0.06 x 10(6) and 0.27 +/- 0.07 x 10(6) in normal myocardium and 0.29 +/- 0.08 x 10(6) and 0.18 +/- 0.05 x 10(6) in infarcted myocardium. Conclusions: One hour after implantation, only 50% of smooth muscle cells remained in the implanted area. Some implanted cells deposited in other tissue. Implanted cell survival progressively decreased during the 4-week study.
MeSH term(s)	Animals ; Antimetabolites ; Brain/pathology ; Bromodeoxyuridine ; Cell Death ; Cell Survival ; Cells, Cultured ; DNA/genetics ; Female ; Graft Survival ; Kidney/pathology ; Lung/pathology ; Male ; Muscle, Smooth, Vascular/cytology ; Myocardial Infarction/surgery ; Myocardium/pathology ; Myocytes, Smooth Muscle/transplantation ; Polymerase Chain Reaction ; Rats ; Rats, Inbred Lew ; Time Factors ; Y Chromosome/genetics
Chemical Substances	Antimetabolites ; DNA (9007-49-2) ; Bromodeoxyuridine (G34N38R2N1)
Language	English
Publishing date	2005-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3104-5
ISSN	1097-685X ; 0022-5223
ISSN (online)	1097-685X
ISSN	0022-5223
DOI	10.1016/j.jtcvs.2004.06.027
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Article: Structure and function of aggrecan.

Kiani, Chris / Chen, Liwen / Wu, Yao Jiong / Yee, Albert J / Yang, Burton B

Cell research

2002 Volume 12, Issue 1, Page(s) 19–32

Abstract: Aggrecan is the major proteoglycan in the articular cartilage. This molecule is important in the proper functioning of articular cartilage because it provides a hydrated gel structure (via its interaction with hyaluronan and link protein) that endows the ...

Abstract	Aggrecan is the major proteoglycan in the articular cartilage. This molecule is important in the proper functioning of articular cartilage because it provides a hydrated gel structure (via its interaction with hyaluronan and link protein) that endows the cartilage with load-bearing properties. It is also crucial in chondroskeletal morphogenesis during development. Aggrecan is a multimodular molecule expressed by chondrocytes. Its core protein is composed of three globular domains (G1, G2, and G3) and a large extended region (CS) between G2 and G3 for glycosaminoglycan chain attachment. G1 comprises the amino terminus of the core protein. This domain has the same structural motif as link protein. Functionally, the G1 domain interacts with hyaluronan acid and link protein, forming stable ternary complexes in the extracellular matrix. G2 is homologous to the tandem repeats of G1 and of link protein and is involved in product processing. G3 makes up the carboxyl terminus of the core protein. It enhances glycosaminoglycan modification and product secretion. Aggrecan plays an important role in mediating chondrocyte-chondrocyte and chondrocyte-matrix interactions through its ability to bind hyaluronan.
MeSH term(s)	Aggrecans ; Amino Acid Motifs ; Amino Acid Sequence ; Animals ; Binding Sites ; Cartilage, Articular/chemistry ; Cartilage, Articular/metabolism ; Chondrocytes/metabolism ; Extracellular Matrix/chemistry ; Extracellular Matrix/metabolism ; Extracellular Matrix Proteins ; Glycosaminoglycans/metabolism ; Humans ; Hyaluronic Acid/metabolism ; Lectins, C-Type ; Models, Biological ; Protein Structure, Tertiary ; Proteins/chemistry ; Proteoglycans/chemistry ; Proteoglycans/metabolism ; Structure-Activity Relationship ; Tandem Repeat Sequences
Chemical Substances	Aggrecans ; Extracellular Matrix Proteins ; Glycosaminoglycans ; Lectins, C-Type ; Proteins ; Proteoglycans ; link protein ; Hyaluronic Acid (9004-61-9)
Language	English
Publishing date	2002-03
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1319303-x
ISSN	1748-7838 ; 1001-0602
ISSN (online)	1748-7838
ISSN	1001-0602
DOI	10.1038/sj.cr.7290106
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Article ; Online: Dopamine receptor 1 neurons in the dorsal striatum regulate food anticipatory circadian activity rhythms in mice.

Gallardo, Christian M / Darvas, Martin / Oviatt, Mia / Chang, Chris H / Michalik, Mateusz / Huddy, Timothy F / Meyer, Emily E / Shuster, Scott A / Aguayo, Antonio / Hill, Elizabeth M / Kiani, Karun / Ikpeazu, Jonathan / Martinez, Johan S / Purpura, Mari / Smit, Andrea N / Patton, Danica F / Mistlberger, Ralph E / Palmiter, Richard D / Steele, Andrew D

eLife

2014 Volume 3, Page(s) e03781

Abstract: Daily rhythms of food anticipatory activity (FAA) are regulated independently of the suprachiasmatic nucleus, which mediates entrainment of rhythms to light, but the neural circuits that establish FAA remain elusive. In this study, we show that mice ... ...

Abstract	Daily rhythms of food anticipatory activity (FAA) are regulated independently of the suprachiasmatic nucleus, which mediates entrainment of rhythms to light, but the neural circuits that establish FAA remain elusive. In this study, we show that mice lacking the dopamine D1 receptor (D1R KO mice) manifest greatly reduced FAA, whereas mice lacking the dopamine D2 receptor have normal FAA. To determine where dopamine exerts its effect, we limited expression of dopamine signaling to the dorsal striatum of dopamine-deficient mice; these mice developed FAA. Within the dorsal striatum, the daily rhythm of clock gene period2 expression was markedly suppressed in D1R KO mice. Pharmacological activation of D1R at the same time daily was sufficient to establish anticipatory activity in wild-type mice. These results demonstrate that dopamine signaling to D1R-expressing neurons in the dorsal striatum plays an important role in manifestation of FAA, possibly by synchronizing circadian oscillators that modulate motivational processes and behavioral output.
MeSH term(s)	Animals ; Anticipation, Psychological ; Behavior, Animal ; Body Temperature ; Caloric Restriction ; Circadian Rhythm ; Cues ; Diet ; Dopamine/metabolism ; Fasting ; Feeding Behavior ; Handling, Psychological ; Mice, Knockout ; Neostriatum/metabolism ; Neurons/metabolism ; Period Circadian Proteins/genetics ; Period Circadian Proteins/metabolism ; Physical Conditioning, Animal ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Receptors, Dopamine D1/metabolism
Chemical Substances	Per2 protein, mouse ; Period Circadian Proteins ; RNA, Messenger ; Receptors, Dopamine D1 ; Dopamine (VTD58H1Z2X)
Language	English
Publishing date	2014-09-12
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.03781
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Article: Versican protects cells from oxidative stress-induced apoptosis.

Wu, Yaojiong / Wu, Jin / Lee, Daniel Y / Yee, Albert / Cao, Liu / Zhang, Yaou / Kiani, Chris / Yang, Burton B

Matrix biology : journal of the International Society for Matrix Biology

2005 Volume 24, Issue 1, Page(s) 3–13

Abstract: Oxidant injury plays a critical role in the degenerative changes that are characterized by a decline in parenchymal cell numbers and viability, and occur with aging and in the etiology of many diseases. The extracellular proteoglycan versican is widely ... ...

Abstract	Oxidant injury plays a critical role in the degenerative changes that are characterized by a decline in parenchymal cell numbers and viability, and occur with aging and in the etiology of many diseases. The extracellular proteoglycan versican is widely distributed in the extracellular matrix surrounding the cells. This study examines whether versican plays a role in protecting cells from free radical-induced apoptosis. Stable expression of versican or its C-terminal domain significantly decreased H(2)O(2)-induced cellular apoptosis. Cells in adherent monolayer were more resistant to H(2)O(2)-induced apoptosis than cells cultured in suspension. While vigorous trypsinization caused integrin cleavage and rendered the cells more susceptible to H(2)O(2)-induced damages, expression of versican or its C-terminal domain enhanced cell attachment and expression of beta1 integrin and fibronectin. Enhanced cell-matrix interaction by addition of manganese (MnCl(2)) to cultures also significantly diminished H(2)O(2)-induced apoptosis. The results suggest that versican plays an important role in reducing oxidant injury through an enhancement of cell-matrix interaction.
MeSH term(s)	Annexin A5/chemistry ; Apoptosis ; Astrocytoma/metabolism ; Blotting, Western ; Cell Adhesion ; Cell Line, Tumor ; Cell Proliferation ; Cell Separation ; Cell Survival ; Chlorides/pharmacology ; Chondroitin Sulfate Proteoglycans/chemistry ; Chondroitin Sulfate Proteoglycans/metabolism ; Dose-Response Relationship, Drug ; Fibronectins/chemistry ; Fibronectins/metabolism ; Flow Cytometry ; Free Radicals ; Glycosaminoglycans/chemistry ; Humans ; Hydrogen Peroxide/chemistry ; Hydrogen Peroxide/pharmacology ; Integrin beta1/metabolism ; Lectins, C-Type ; Manganese/chemistry ; Manganese Compounds/pharmacology ; Oxidants/chemistry ; Oxidative Stress ; Protein Binding ; Protein Structure, Tertiary ; Reactive Oxygen Species ; Transgenes ; Trypsin/pharmacology ; Versicans
Chemical Substances	Annexin A5 ; Chlorides ; Chondroitin Sulfate Proteoglycans ; Fibronectins ; Free Radicals ; Glycosaminoglycans ; Integrin beta1 ; Lectins, C-Type ; Manganese Compounds ; Oxidants ; Reactive Oxygen Species ; VCAN protein, human ; Versicans (126968-45-4) ; Manganese (42Z2K6ZL8P) ; Hydrogen Peroxide (BBX060AN9V) ; Trypsin (EC 3.4.21.4) ; manganese chloride (QQE170PANO)
Language	English
Publishing date	2005-02
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1183793-7
ISSN	1569-1802 ; 0945-053X
ISSN (online)	1569-1802
ISSN	0945-053X
DOI	10.1016/j.matbio.2004.11.007
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Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito