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Article ; Online: Dynamic Navigation for Dental Implant Placement.

Pinter, Gabor Tamas / Decker, Roland / Szenasi, Gabor / Barabas, Peter / Huszar, Tamas

Journal of visualized experiments : JoVE

2022 , Issue 187

Abstract: In modern implantology, the application of surgical navigation systems is becoming increasingly important. In addition to static surgical navigation methods, a guide-independent dynamic navigation implant placement procedure is becoming more widespread. ... ...

Abstract	In modern implantology, the application of surgical navigation systems is becoming increasingly important. In addition to static surgical navigation methods, a guide-independent dynamic navigation implant placement procedure is becoming more widespread. The procedure is based on computer-guided dental implant placement utilizing optical control. This work aims to demonstrate the technical steps of a new dynamic computer-aided implant surgery (DCAIS) system (design, calibration, surgery) and check the accuracy of the results. Based on cone-beam computed tomography (CBCT) scans, the exact positions of implants are determined with dedicated software. The first step of the operation is the calibration of the navigation system, which can be performed in two ways: 1) based on CBCT images taken with a marker or 2) based on CBCT images without markers. Implants are inserted with the aid of real-time navigation according to the preoperative plans. The accuracy of the interventions can be evaluated based on postoperative CBCT images. The preoperative images containing the planned positions of the implants and postoperative CBCT images were compared based on the angulation (degree), platform, and apical deviation (mm) of the implants. To evaluate the data, we calculated the standard deviation (SD), mean, and standard error of the mean (SEM) of deviations within planned and performed implant positions. Differences between the two calibration methods were compared based on this data. Based on the interventions performed so far, the use of DCAIS allows for high-precision implant placement. A calibration system that does not require labeled CBCT recording allows for surgical intervention with similar accuracy as a system that uses labeling. The accuracy of the intervention can be improved by training.
MeSH term(s)	Computer-Aided Design ; Computers ; Cone-Beam Computed Tomography ; Dental Implants ; Imaging, Three-Dimensional ; Software ; Surgery, Computer-Assisted/methods
Chemical Substances	Dental Implants
Language	English
Publishing date	2022-09-13
Publishing country	United States
Document type	Journal Article ; Video-Audio Media
ZDB-ID	2259946-0
ISSN	1940-087X ; 1940-087X
ISSN (online)	1940-087X
ISSN	1940-087X
DOI	10.3791/63400
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Article ; Online: Cherubism in three siblings.

Jákob, Noémi / Pintér, Gábor Tamás / Kotmayer, Lili / Nagy, Péter / Bödör, Csaba / Barabás, Péter / Bécser, Janka / Szabó, György / Bogdán, Sándor

Orvosi hetilap

2022 Volume 163, Issue 11, Page(s) 446–452

Abstract: Összefoglaló. A cherubismus ritka, autoszomális dominánsan öröklődő megbetegedés. A fibroossealis elváltozások csoportjába tartozik. Jellemzője az állcsontok szimmetrikus duzzanata, a típusos radiológiai elváltozások és az SH3BP2-gén mutációja. ... ...

Title translation	A cherubismus előfordulása három testvérben.
Abstract	Összefoglaló. A cherubismus ritka, autoszomális dominánsan öröklődő megbetegedés. A fibroossealis elváltozások csoportjába tartozik. Jellemzője az állcsontok szimmetrikus duzzanata, a típusos radiológiai elváltozások és az SH3BP2-gén mutációja. Szövettanilag nem különül el az óriássejtes granulomától. A csontelváltozások és a fibroticus szövet felszaporodása pubertás előtt kezdődik, ezután stagnálás vagy visszafejlődés következik be. A magyar orvosi irodalomban a szerzők elsőként tárgyalják három testvér kórtörténete alapján a cherubismust. A diagnózist a hasonló klinikai tünetek, a típusos kórlefolyás, a szinte azonos radiológiai kép, a szövettan és a genetikai elváltozások biztosítják. A testvérek és az anya csíravonalában kimutatott azonos mutáció akkor is megfelel egy dominánsan öröklődő szindrómának (például cherubismusnak), ha a betegség az anyában klinikailag nem manifesztálódott, de genetikailag igen. A szerzők összefoglalják a kórkép kezelési lehetőségeit: a sebészi (excochleatio, ,,decountouring", esetleg reszekció) és a gyógyszeres (biszfoszfonát, kalcitonin, szteroid stb.) terápiát. Egyezik a véleményük azokéval, akik azon az állásponton vannak, hogy a beavatkozásokkal várni kell, és meg kell figyelni a betegeket a várható regresszió miatt. Saját eseteikben csak a növekvő tumorrész excochleatióját végezték, főleg kozmetikai okok és a szövettan biztosítása érdekében. Orv Hetil. 2022; 163(11): 446-452. Summary. Cherubism is a rare autosomal, dominant bone disorder, characterised by symmetrical expansion of the jaws along the typical radiological and genetic (SH3BP2 mutation) features. It belongs to the heterogenous group of fibro-osseous lesions. Its histology is the same as that of giant-cell granuloma. The bone lesions and fibrous tissue expansion increase before puberty and regress thereafter. For the first time in Hungarian medical literature, the authors discuss the condition of cherubism in the case of three siblings. The diagnosis of these three siblings is supported by the clinical, radiological, microscopic and genetic data. In all three, the bone lesions and fibrous tissue expansion increased before puberty and stabilized thereafter. The radiological results and the molecular findings were nearly identical. The identical mutation shown in the germ lines of the three siblings and the mother correspond to a dominantly inherited syndrome (e.g., cherubism) even if the condition did not manifest in the mother. The authors summarize the treatment options of the disease: surgical (excochleation, decountouring, in rare case resection) and drug (bisphosphonate, calcitonin, steroid, etc.) therapy. They agree with those who are of the opinion that interventions should wait and the patients should be observed ("wait and see") for the expected regression. In their own cases, only excochleation of the growing tumor was performed, mainly for cosmetic reasons and to secure the tissue. Orv Hetil. 2022; 163(11): 446-452.
MeSH term(s)	Adaptor Proteins, Signal Transducing/genetics ; Adaptor Proteins, Signal Transducing/metabolism ; Cherubism/diagnosis ; Cherubism/genetics ; Cherubism/pathology ; Humans ; Mutation ; Siblings
Chemical Substances	Adaptor Proteins, Signal Transducing ; SH3BP2 protein, human
Language	Hungarian
Publishing date	2022-03-13
Publishing country	Hungary
Document type	Case Reports ; Journal Article
ZDB-ID	123879-6
ISSN	1788-6120 ; 0030-6002
ISSN (online)	1788-6120
ISSN	0030-6002
DOI	10.1556/650.2022.32309
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Article ; Online: A trans-kingdom T6SS effector induces the fragmentation of the mitochondrial network and activates innate immune receptor NLRX1 to promote infection.

Sá-Pessoa, Joana / López-Montesino, Sara / Przybyszewska, Kornelia / Rodríguez-Escudero, Isabel / Marshall, Helina / Ova, Adelia / Schroeder, Gunnar N / Barabas, Peter / Molina, María / Curtis, Tim / Cid, Víctor J / Bengoechea, José A

Nature communications

2023 Volume 14, Issue 1, Page(s) 871

Abstract: Bacteria can inhibit the growth of other bacteria by injecting effectors using a type VI secretion system (T6SS). T6SS effectors can also be injected into eukaryotic cells to facilitate bacterial survival, often by targeting the cytoskeleton. Here, we ... ...

Abstract	Bacteria can inhibit the growth of other bacteria by injecting effectors using a type VI secretion system (T6SS). T6SS effectors can also be injected into eukaryotic cells to facilitate bacterial survival, often by targeting the cytoskeleton. Here, we show that the trans-kingdom antimicrobial T6SS effector VgrG4 from Klebsiella pneumoniae triggers the fragmentation of the mitochondrial network. VgrG4 colocalizes with the endoplasmic reticulum (ER) protein mitofusin 2. VgrG4 induces the transfer of Ca
MeSH term(s)	Cullin Proteins/metabolism ; NF-KappaB Inhibitor alpha ; NF-kappa B/metabolism ; Reactive Oxygen Species/metabolism ; Immunity, Innate
Chemical Substances	Cullin Proteins ; NF-KappaB Inhibitor alpha (139874-52-5) ; NF-kappa B ; Reactive Oxygen Species
Language	English
Publishing date	2023-02-16
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-36629-3
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Article: The Role of Lipoxidation in the Pathogenesis of Diabetic Retinopathy.

Augustine, Josy / Troendle, Evan P / Barabas, Peter / McAleese, Corey A / Friedel, Thomas / Stitt, Alan W / Curtis, Tim M

Frontiers in endocrinology

2021 Volume 11, Page(s) 621938

Abstract: Lipids can undergo modification as a result of interaction with reactive oxygen species (ROS). For example, lipid peroxidation results in the production of a wide variety of highly reactive aldehyde species which can drive a range of disease-relevant ... ...

Abstract	Lipids can undergo modification as a result of interaction with reactive oxygen species (ROS). For example, lipid peroxidation results in the production of a wide variety of highly reactive aldehyde species which can drive a range of disease-relevant responses in cells and tissues. Such lipid aldehydes react with nucleophilic groups on macromolecules including phospholipids, nucleic acids, and proteins which, in turn, leads to the formation of reversible or irreversible adducts known as advanced lipoxidation end products (ALEs). In the setting of diabetes, lipid peroxidation and ALE formation has been implicated in the pathogenesis of macro- and microvascular complications. As the most common diabetic complication, retinopathy is one of the leading causes of vision loss and blindness worldwide. Herein, we discuss diabetic retinopathy (DR) as a disease entity and review the current knowledge and experimental data supporting a role for lipid peroxidation and ALE formation in the onset and development of this condition. Potential therapeutic approaches to prevent lipid peroxidation and lipoxidation reactions in the diabetic retina are also considered, including the use of antioxidants, lipid aldehyde scavenging agents and pharmacological and gene therapy approaches for boosting endogenous aldehyde detoxification systems. It is concluded that further research in this area could lead to new strategies to halt the progression of DR before irreversible retinal damage and sight-threatening complications occur.
MeSH term(s)	Animals ; Antioxidants/administration & dosage ; Diabetic Retinopathy/drug therapy ; Diabetic Retinopathy/metabolism ; Diabetic Retinopathy/pathology ; Free Radical Scavengers/administration & dosage ; Glycation End Products, Advanced/metabolism ; Humans ; Lipid Peroxidation/drug effects ; Lipid Peroxidation/physiology ; Oxidative Stress/drug effects ; Oxidative Stress/physiology
Chemical Substances	Antioxidants ; Free Radical Scavengers ; Glycation End Products, Advanced
Language	English
Publishing date	2021-02-18
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2592084-4
ISSN	1664-2392
ISSN	1664-2392
DOI	10.3389/fendo.2020.621938
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Article ; Online: COMP-Ang1: Therapeutic potential of an engineered Angiopoietin-1 variant.

Wallace, Robert G / Rochfort, Keith D / Barabas, Peter / Curtis, Timothy M / Uehara, Hironori / Ambati, Balamurali K / Cummins, Philip M

Vascular pharmacology

2021 Volume 141, Page(s) 106919

Abstract: The Angiopoietin-1/2 system is an opportune target for therapeutic intervention in a wide range of vascular pathologies, particularly through its association with endothelium. The complex multi-domain structure of native human Angiopoietin-1 has hindered ...

Abstract	The Angiopoietin-1/2 system is an opportune target for therapeutic intervention in a wide range of vascular pathologies, particularly through its association with endothelium. The complex multi-domain structure of native human Angiopoietin-1 has hindered its widespread applicability as a therapeutic agent, prompting the search for alternative approaches to mimicking the Ang1:Tie2 signalling axis; a system with highly complex patterns of regulation involving multiple structurally similar molecules. An engineered variant, Cartilage Oligomeric Matrix Protein - Angiopoietin-1 (COMP-Ang1), has been demonstrated to overcome the limitations of the native molecule and activate the Tie2 pathway with several fold greater potency than Ang1, both in vitro and in vivo. The therapeutic efficacy of COMP-Ang1, at both the vascular and systemic levels, is evident from multiple studies. Beneficial impacts on skeletal muscle regeneration, wound healing and angiogenesis have been reported alongside renoprotective, anti-hypertensive and anti-inflammatory effects. COMP-Ang1 has also demonstrated synergy with other compounds to heighten bone repair, has been leveraged for potential use as a co-therapeutic for enhanced targeted cancer treatment, and has received considerable attention as an anti-leakage agent for microvascular diseases like diabetic retinopathy. This review examines the vascular Angiopoietin:Tie2 signalling mechanism, evaluates the potential therapeutic merits of engineered COMP-Ang1 in both vascular and systemic contexts, and addresses the inherent translational challenges in moving this potential therapeutic from bench-to-bedside.
MeSH term(s)	Angiopoietin-1/genetics ; Angiopoietin-1/therapeutic use ; Cartilage Oligomeric Matrix Protein/genetics ; Humans ; Protein Engineering ; Receptor, TIE-2/genetics ; Receptor, TIE-2/metabolism ; Signal Transduction ; Wound Healing
Chemical Substances	Angiopoietin-1 ; Cartilage Oligomeric Matrix Protein ; Receptor, TIE-2 (EC 2.7.10.1)
Language	English
Publishing date	2021-09-25
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2082846-9
ISSN	1879-3649 ; 1537-1891 ; 1879-3649
ISSN (online)	1879-3649 ; 1537-1891
ISSN	1879-3649
DOI	10.1016/j.vph.2021.106919
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Article: Ion channels and myogenic activity in retinal arterioles.

Barabas, Peter / Augustine, Josy / Fernández, José A / McGeown, J Graham / McGahon, Mary K / Curtis, Tim M

Current topics in membranes

2020 Volume 85, Page(s) 187–226

Abstract: Retinal pressure autoregulation is an important mechanism that protects the retina by stabilizing retinal blood flow during changes in arterial or intraocular pressure. Similar to other vascular beds, retinal pressure autoregulation is thought to be ... ...

Abstract	Retinal pressure autoregulation is an important mechanism that protects the retina by stabilizing retinal blood flow during changes in arterial or intraocular pressure. Similar to other vascular beds, retinal pressure autoregulation is thought to be mediated largely through the myogenic response of small arteries and arterioles which constrict when transmural pressure increases or dilate when it decreases. Over recent years, we and others have investigated the signaling pathways underlying the myogenic response in retinal arterioles, with particular emphasis on the involvement of different ion channels expressed in the smooth muscle layer of these vessels. Here, we review and extend previous work on the expression and spatial distribution of the plasma membrane and sarcoplasmic reticulum ion channels present in retinal vascular smooth muscle cells (VSMCs) and discuss their contribution to pressure-induced myogenic tone in retinal arterioles. This includes new data demonstrating that several key players and modulators of the myogenic response show distinctively heterogeneous expression along the length of the retinal arteriolar network, suggesting differences in myogenic signaling between larger and smaller pre-capillary arterioles. Our immunohistochemical investigations have also highlighted the presence of actin-containing microstructures called myobridges that connect the retinal VSMCs to one another. Although further work is still needed, studies to date investigating myogenic mechanisms in the retina have contributed to a better understanding of how blood flow is regulated in this tissue. They also provide a basis to direct future research into retinal diseases where blood flow changes contribute to the pathology.
MeSH term(s)	Animals ; Arterioles/metabolism ; Arterioles/physiology ; Biomechanical Phenomena ; Homeostasis ; Humans ; Ion Channels/metabolism ; Muscle Development ; Retina/physiology
Chemical Substances	Ion Channels
Language	English
Publishing date	2020-02-26
Publishing country	United States
Document type	Journal Article ; Review
ISSN	1063-5823
ISSN	1063-5823
DOI	10.1016/bs.ctm.2020.01.008
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Article ; Online: Single-cell transcriptomic profiling provides insights into retinal endothelial barrier properties.

Watson, Mark I / Barabas, Peter / McGahon, Mary / McMahon, Megan / Fuchs, Marc A / Curtis, Tim M / Simpson, David A

Molecular vision

2020 Volume 26, Page(s) 766–779

Abstract: Purpose: To better characterize retinal endothelial barrier properties through analysis of individual transcriptomes of primary bovine retinal microvascular endothelial cells (RMECs).: Methods: Individual RMECs were captured on the Fluidigm C1 system, ...

Abstract	Purpose: To better characterize retinal endothelial barrier properties through analysis of individual transcriptomes of primary bovine retinal microvascular endothelial cells (RMECs). Methods: Individual RMECs were captured on the Fluidigm C1 system, cDNA libraries were prepared using a Nextera XT kit, and sequencing was performed on a NextSeq system (Illumina). Data analysis was performed using R packages Scater, SC3, and Seurat, and the browser application Automated Single-cell Analysis Pipeline (ASAP). Alternative splicing events in single cells were quantified with Outrigger. Cytoscape was used for network analyses. Results: Application of a single-cell RNA sequencing (scRNA-seq) analysis workflow showed that RMECs form a relatively homogeneous population in culture, with the main differences related to proliferation status. Expression of markers from along the arteriovenous tree suggested that most cells originated from capillaries. Average gene expression levels across all cells were used to develop an in silico model of the inner blood-retina barrier incorporating junctional proteins not previously reported within the retinal vasculature. Correlation of barrier gene expression among individual cells revealed a subgroup of genes highly correlated with PECAM-1 at the center of the correlation network. Numerous alternative splicing events involving exons within microvascular barrier genes were observed, and in many cases, individual cells expressed one isoform exclusively. Conclusions: We optimized a workflow for single-cell transcriptomics in primary RMECs. The results provide fundamental insights into the genes involved in formation of the retinal-microvascular barrier.
MeSH term(s)	Alternative Splicing/genetics ; Animals ; Biomarkers/metabolism ; Blood-Retinal Barrier/metabolism ; Cattle ; Computer Simulation ; Endothelial Cells/metabolism ; Gene Expression Profiling ; Models, Biological ; Reproducibility of Results ; Single-Cell Analysis
Chemical Substances	Biomarkers
Language	English
Publishing date	2020-11-27
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2017540-1
ISSN	1090-0535 ; 1090-0535
ISSN (online)	1090-0535
ISSN	1090-0535
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Article ; Online: VEGF-B Is an Autocrine Gliotrophic Factor for Müller Cells under Pathologic Conditions.

Llorián-Salvador, María / Barabas, Peter / Byrne, Eimear M / Lechner, Judith / Augustine, Josy / Curtis, Timothy M / Chen, Mei / Xu, Heping

Investigative ophthalmology & visual science

2020 Volume 61, Issue 11, Page(s) 35

Abstract: Purpose: Müller glia are important in retinal health and disease and are a major source of retinal VEGF-A. Of the different VEGF family members, the role of VEGF-A in retinal health and disease has been studied extensively. The potential contribution of ...

Abstract	Purpose: Müller glia are important in retinal health and disease and are a major source of retinal VEGF-A. Of the different VEGF family members, the role of VEGF-A in retinal health and disease has been studied extensively. The potential contribution of other VEGF family members to retinal pathophysiology, however, remains poorly defined. This study aimed to understand the role of VEGF-B in Müller cell pathophysiology. Methods: The expression of different VEGFs and their receptors in human MIO-M1 and mouse QMMuC-1 Müller cell lines and primary murine Müller cells was examined by RT-PCR, ELISA, and Western blot. The effect of recombinant VEGF-B or VEGF-B neutralization on Müller cell viability and survival under normal, hypoxic, and oxidative (4-hydroxynonenal [4-HNE]) conditions was evaluated by Alamar Blue, Yo-Pro uptake, and immunocytochemistry. The expression of glial fibrillary acidic protein, aquaporin-4, inward rectifying K+ channel subtype 4.1, glutamine synthetase, and transient receptor potential vanilloid 4 under different treatment conditions was examined by RT-PCR, immunocytochemistry, and Western blot. Transient receptor potential vanilloid 4 channel activity was assessed using a Fura-2-based calcium assay. Results: VEGF-B was expressed in Müller cells at the highest levels compared with other members of the VEGF family. VEGF-B neutralization did not affect Müller cell viability or functionality under normal conditions, but enhanced hypoxia- or 4-HNE-induced Müller cell death and decreased inward rectifying K+ channel subtype 4.1 and aquaporin-4 expression. Recombinant VEGF-B restored Müller cell glutamine synthetase expression under hypoxic conditions and protected Müller cells from 4-HNE-induced damage by normalizing transient receptor potential vanilloid 4 channel expression and activity. Conclusions: Autocrine production of VEGF-B protects Müller cells under pathologic conditions.
MeSH term(s)	Animals ; Cells, Cultured ; Enzyme-Linked Immunosorbent Assay ; Ependymoglial Cells/metabolism ; Ependymoglial Cells/pathology ; Glial Fibrillary Acidic Protein/metabolism ; Humans ; Immunohistochemistry ; Mice ; Vascular Endothelial Growth Factor B/metabolism
Chemical Substances	Glial Fibrillary Acidic Protein ; Vascular Endothelial Growth Factor B
Language	English
Publishing date	2020-09-18
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	391794-0
ISSN	1552-5783 ; 0146-0404
ISSN (online)	1552-5783
ISSN	0146-0404
DOI	10.1167/iovs.61.11.35
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Article: Mouse Models of Stargardt 3 Dominant Macular Degeneration.

Barabas, Peter / Gorusupudi, Aruna / Bernstein, Paul S / Krizaj, David

Advances in experimental medicine and biology

2016 Volume 854, Page(s) 137–143

Abstract: Stargardt type 3 macular degeneration is dependent on a dominant defect in a single gene, ELOVL4 (elongase of very long chain fatty acids 4). The encoded enzyme, ELOVL4, is required for the synthesis of very long chain polyunsaturated fatty acids (VLC- ... ...

Abstract	Stargardt type 3 macular degeneration is dependent on a dominant defect in a single gene, ELOVL4 (elongase of very long chain fatty acids 4). The encoded enzyme, ELOVL4, is required for the synthesis of very long chain polyunsaturated fatty acids (VLC-PUFAs), a rare class of > C24 lipids. In vitro expression studies suggest that mutated ELOVL4(STGD3) proteins fold improperly, resulting in ER stress and formation of cytosolic aggresomes of wild type and mutant ELOVL4. Although a number of mouse models have been developed to determine whether photoreceptor cell loss in STGD3 results from depletion of VLC-PUFAs, aggresome-dependent cell stress or a combination of these two factors, none of these models adequately recapitulates the disease phenotype in humans. Thus, the precise molecular mechanism by which ELOVL4 mutation causes photoreceptor degeneration in mice and in human patients remains to be characterized. This mini review compares and evaluates current STGD3 mouse models and determines what conclusions can be drawn from past work.
MeSH term(s)	Animals ; Disease Models, Animal ; Eye Proteins/genetics ; Fatty Acids, Unsaturated/biosynthesis ; Humans ; Macular Degeneration/congenital ; Macular Degeneration/genetics ; Macular Degeneration/metabolism ; Membrane Proteins/genetics ; Mice, Knockout ; Mice, Transgenic ; Mutation
Chemical Substances	Elovl4 protein, mouse ; Eye Proteins ; Fatty Acids, Unsaturated ; Membrane Proteins
Language	English
Publishing date	2016
Publishing country	United States
Document type	Journal Article
ISSN	2214-8019 ; 0065-2598
ISSN (online)	2214-8019
ISSN	0065-2598
DOI	10.1007/978-3-319-17121-0_19
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Article ; Online: COMP-Ang1 Stabilizes Hyperglycemic Disruption of Blood-Retinal Barrier Phenotype in Human Retinal Microvascular Endothelial Cells.

Rochfort, Keith D / Carroll, Lara S / Barabas, Peter / Curtis, Timothy M / Ambati, Balamurali K / Barron, Niall / Cummins, Philip M

Investigative ophthalmology & visual science

2019 Volume 60, Issue 10, Page(s) 3547–3555

Abstract: Purpose: Current treatments for diabetic retinopathy (DR) have considerable limitations, underpinning the need for new therapeutic options. In this article, the ability of an engineered angiopoietin-1 variant (COMP-Ang1) to ameliorate the injurious ... ...

Abstract	Purpose: Current treatments for diabetic retinopathy (DR) have considerable limitations, underpinning the need for new therapeutic options. In this article, the ability of an engineered angiopoietin-1 variant (COMP-Ang1) to ameliorate the injurious effects of hyperglycemia on barrier integrity in a human retinal microvascular endothelial cell (HRMvEC) model is comprehensively investigated. Methods: Confluent HRMvECs were treated (0-72 hours) with d-glucose (5 or 30 mM) in the absence and presence of COMP-Ang1 (10-200 ng/mL). l-glucose (30 mM) was used as osmotic control. Posttreatment, intact cell monolayers were monitored for permeability to FITC-dextran 40 kDa. Cells were also harvested for analysis of interendothelial junction targets by RT-qPCR and Western blotting. The impact of receptor tyrosine kinase Tie2 gene silencing on COMP-Ang1 efficacy was also evaluated. Results: Treatment with 30 mM d-glucose (but not l-glucose) demonstrated a time-dependent elevation in the mean rate of FITC-dextran diffusion across intact HRMvEC monolayers, in parallel with significant reductions in mRNA/protein levels of occludin, claudin-5, ZO-1, and VE-Cadherin. These effects were all attenuated by COMP-Ang1 in a concentration-dependent fashion, with 200 ng/mL recovering barrier function by ∼88%, and recovering reduced interendothelial junction protein levels by more than 50%. Finally, Tie2 knockdown by small interfering RNA silencing blocked the ability of COMP-Ang1 to mitigate against hyperglycemia-induced permeabilization of HRMvECs and depletion of junctional expression levels. Conclusions: In summary, this article presents a reproducible in vitro cell study that quantifies the concentration-dependent efficacy of COMP-Ang1 to mitigate the injurious effects of hyperglycemic challenge on HRMvEC barrier properties via Tie2-mediated signaling.
MeSH term(s)	Antigens, CD/genetics ; Blood-Retinal Barrier/physiology ; Blotting, Western ; Cadherins/genetics ; Capillary Permeability/drug effects ; Cells, Cultured ; Claudin-5/genetics ; Dextrans/metabolism ; Dose-Response Relationship, Drug ; Endothelial Cells/drug effects ; Endothelial Cells/metabolism ; Fluorescein-5-isothiocyanate/analogs & derivatives ; Fluorescein-5-isothiocyanate/metabolism ; Gene Silencing/physiology ; Glucose/pharmacology ; Humans ; Hyperglycemia/metabolism ; Hyperglycemia/prevention & control ; Occludin/genetics ; Phenotype ; RNA, Messenger/genetics ; Real-Time Polymerase Chain Reaction ; Receptor, TIE-2/genetics ; Recombinant Fusion Proteins/pharmacology ; Retinal Vessels/drug effects ; Retinal Vessels/metabolism
Chemical Substances	Antigens, CD ; CLDN5 protein, human ; COMP-Ang1 fusion protein ; Cadherins ; Claudin-5 ; Dextrans ; OCLN protein, human ; Occludin ; RNA, Messenger ; Recombinant Fusion Proteins ; cadherin 5 ; fluorescein isothiocyanate dextran ; Receptor, TIE-2 (EC 2.7.10.1) ; TEK protein, human (EC 2.7.10.1) ; Fluorescein-5-isothiocyanate (I223NX31W9) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2019-08-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	391794-0
ISSN	1552-5783 ; 0146-0404
ISSN (online)	1552-5783
ISSN	0146-0404
DOI	10.1167/iovs.19-27644
Database	MEDical Literature Analysis and Retrieval System OnLINE

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