[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 100 of about 11569
1. Zhong Q, Roychowdhury V, Boykin P, Nirenberg S: Non-Poisson Fluctuation Statistics In Neuronal Inter-Spike Intervals (ISI): Hurst parameter Estimates of Mouse Retinal Ganglion Signals. Conf Proc IEEE Eng Med Biol Soc; 2005;2:2095-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Non-Poisson Fluctuation Statistics In Neuronal Inter-Spike Intervals (ISI): Hurst parameter Estimates of Mouse Retinal Ganglion Signals.
  • There is considerable recent interest in both (i) modelling the retinal ganglion cells, so that the models can generate output that approximates the actual response of the retina (such models will help design retinal prosthetics); and (ii) understanding how relevant information is encoded in the spike patterns generated by the ganglion cells (these neuronal codes will help understand how the brain analyzes visual scenes).
  • The widespread use of the Poisson model is partly for the sake of convenience, and partly due to the fact that those claiming on fractal nature of ISI are contradictory: In [1] a long-range dependency (i.e., Hurst parameter [2], H > 0.5) is claimed in cat's retina, and in [3] an H < 0.5 and a long-range anti-correlation are claimed for paddlefish electroreceptors.

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17282641.001).
  • [ISSN] 1557-170X
  • [Journal-full-title] Conference proceedings : ... Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE Engineering in Medicine and Biology Society. Annual Conference
  • [ISO-abbreviation] Conf Proc IEEE Eng Med Biol Soc
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


2. Villar-Cheda B, Abalo XM, Anadón R, Rodicio MC: Calbindin and calretinin immunoreactivity in the retina of adult and larval sea lamprey. Brain Res; 2006 Jan 12;1068(1):118-30
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Calbindin and calretinin immunoreactivity in the retina of adult and larval sea lamprey.
  • The presence of calretinin and calbindin immunoreactivity is studied in the retina of larval and adult lamprey and their respective distributions are compared.
  • Calretinin distribution is also studied in the retina of transforming stages.
  • In the adult retina large and small bipolar cells, with respectively stratified or diffuse axons, the inner row of horizontal cells and ganglion cells and/or some amacrine cells were labeled with anti-calretinin antibody.
  • In the differentiated central retina of larval lampreys, numerous calretinin immunoreactive bipolar and ganglion cells were observed, while, in the lateral retina, only ganglion cells were labeled, accordingly with the lack of differentiation of other neural cell types.
  • CR-ir bipolar cells appeared in the retina by the stage 5 of transformation, i.e. about the time when differentiation of photoreceptors occurs.
  • The comparison of the distribution of calretinin and calbindin between adult and larval central retina of lampreys shows striking differences that could be related to the different functionality of eyes in these two stages of the life cycle of lampreys.
  • In addition, this is the first report on the presence of calcium-binding proteins in the larval and transforming lamprey retina, on the presence of calretinin- and calbindin-immunoreactive horizontal cells in adult lamprey retinas and on the differential stratification of bipolar cell terminals.
  • [MeSH-major] Lampreys / physiology. Larva / physiology. Retina / growth & development. Retina / metabolism. S100 Calcium Binding Protein G / metabolism
  • [MeSH-minor] Animals. Blotting, Western. Calbindin 2. Calbindins. Image Processing, Computer-Assisted. Immunohistochemistry. Retinal Ganglion Cells / drug effects. Retinal Ganglion Cells / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16368080.001).
  • [ISSN] 0006-8993
  • [Journal-full-title] Brain research
  • [ISO-abbreviation] Brain Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Calbindin 2; 0 / Calbindins; 0 / S100 Calcium Binding Protein G
  •  go-up   go-down


3. Zhang L, Tang S, Huang B, Chen X, Lai Y: [The retinoid acid injected into sub retinal space couldn't reverse the retinal degeneration of mouse]. Yan Ke Xue Bao; 2005 Jun;21(2):116-8, 131
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [The retinoid acid injected into sub retinal space couldn't reverse the retinal degeneration of mouse].
  • PURPOSE: To study the prevention of retinoid acid (RA) to the retinal degeneration when being injected into sub retinal space.
  • METHODS: 10(-3) mol/L RA and phosphate buffered saline (PBS) were injected into the sub retinal space of 8 retinal degeneration (rd) mice respectively.
  • CONCLUSIONS: The degeneration of retina couldn't be stopped and the degenerated retina couldn't be restored to normal through the injection RA into the sub retinal space of rd mouse.

  • Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17165343.001).
  • [ISSN] 1000-4432
  • [Journal-full-title] Yan ke xue bao = Eye science
  • [ISO-abbreviation] Yan Ke Xue Bao
  • [Language] CHI
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 5688UTC01R / Tretinoin
  •  go-up   go-down


Advertisement
4. Nakajima E, David LL, Bystrom C, Shearer TR, Azuma M: Calpain-specific proteolysis in primate retina: Contribution of calpains in cell death. Invest Ophthalmol Vis Sci; 2006 Dec;47(12):5469-75
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Calpain-specific proteolysis in primate retina: Contribution of calpains in cell death.
  • PURPOSE: One of the leading causes of blindness is retinal damage caused by the high intraocular pressure (IOP) in glaucoma.
  • Previous studies in rats have suggested that the proteolytic enzyme calpain (EC 3.4.22.17) is involved in retinal cell death during ischemia and in acute high IOP.
  • Ubiquitous, calcium-activated calpain-1 and -2 from monkey retina are highly homologous to rat calpains, although expression patterns in variants of tissue-specific calpain-3 are different between monkey and rodent retinas.
  • Thus, the purpose of the present study was to investigate the involvement of calpain-induced proteolysis in retinal cell death in primates.
  • Endogenous tissue calpains were also directly activated in monkey and human retinal soluble proteins by incubating with 2.5 mM calcium.
  • The resultant proteolysis of monkey retinal proteins was assessed by 2D electrophoresis (2-DE).
  • RESULTS: In hypoxic retina, leakage of lactate dehydrogenase (LDH) from retinas into the medium increased, indicating cell death.
  • In retinal soluble proteins incubated with calcium, a total of 15 spots from 2-DE of retinal soluble proteins were identified by mass spectrometry.
  • [MeSH-major] Anoxia / enzymology. Calpain / metabolism. Retina / enzymology

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CALCIUM, ELEMENTAL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17122138.001).
  • [ISSN] 0146-0404
  • [Journal-full-title] Investigative ophthalmology & visual science
  • [ISO-abbreviation] Invest. Ophthalmol. Vis. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] EC 3.4.22.- / Calpain; SY7Q814VUP / Calcium
  •  go-up   go-down


5. Goldmann T, Rebibo-Sabbah A, Overlack N, Nudelman I, Belakhov V, Baasov T, Ben-Yosef T, Wolfrum U, Nagel-Wolfrum K: Beneficial read-through of a USH1C nonsense mutation by designed aminoglycoside NB30 in the retina. Invest Ophthalmol Vis Sci; 2010 Dec;51(12):6671-80
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Beneficial read-through of a USH1C nonsense mutation by designed aminoglycoside NB30 in the retina.
  • Here, we investigated the capability of the novel synthetic aminoglycoside NB30 for the translational read-through of the USH1C-p.R31X nonsense mutation as a retinal therapy option.
  • METHODS: Read-through of p.R31X by three commercial, clinically applied aminoglycosides and the synthetic derivative NB30 was validated in vitro, in cell culture, and in retinal explants.
  • Biocompatibility of aminoglycosides was determined in retinal explants by TUNEL assays.
  • In addition, gentamicin, paromomycin, and NB30 induced read-through of p.R31X in mouse retinal explants.
  • [MeSH-major] Adaptor Proteins, Signal Transducing / genetics. Aminoglycosides / pharmacology. Codon, Nonsense / drug effects. Retina / drug effects

  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20671281.001).
  • [ISSN] 1552-5783
  • [Journal-full-title] Investigative ophthalmology & visual science
  • [ISO-abbreviation] Invest. Ophthalmol. Vis. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Aminoglycosides; 0 / Codon, Nonsense; 0 / Gentamicins; 0 / USH1C protein, human; 61JJC8N5ZK / Paromomycin
  •  go-up   go-down


6. Wei W, Elstrott J, Feller MB: Two-photon targeted recording of GFP-expressing neurons for light responses and live-cell imaging in the mouse retina. Nat Protoc; 2010 Jul;5(7):1347-52
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Two-photon targeted recording of GFP-expressing neurons for light responses and live-cell imaging in the mouse retina.
  • Cell type-specific green fluorescent protein (GFP) expression in the retina has been achieved in an expanding repertoire of transgenic mouse lines, which are valuable tools for dissecting the retinal circuitry.
  • This protocol offers fast and sensitive detection of GFP while preserving the light sensitivity of the retina, and can be used to obtain light responses and the detailed morphology of a GFP-expressing cell.
  • Targeting of a GFP-expressing neuron takes less than 3 min, and the retina preparation remains light sensitive and suitable for recording for at least 8 h.
  • This protocol can also be applied to study retinal neurons labeled with other two photon-excitable fluorophores.
  • It is assumed that potential users of this protocol will have a basic understanding of retinal physiology and patch-clamp recording, which are not described in detail here.

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20595962.001).
  • [ISSN] 1750-2799
  • [Journal-full-title] Nature protocols
  • [ISO-abbreviation] Nat Protoc
  • [Language] ENG
  • [Grant] United States / NEI NIH HHS / EY / R01 EY013528; United States / NEI NIH HHS / EY / R01 EY019498; United States / NEI NIH HHS / EY / R01EY013528; United States / NEI NIH HHS / EY / R01EY019498
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 147336-22-9 / Green Fluorescent Proteins
  • [Other-IDs] NLM/ NIHMS654461; NLM/ PMC4303237
  •  go-up   go-down


7. Shu X, Zeng Z, Gautier P, Lennon A, Gakovic M, Patton EE, Wright AF: Zebrafish Rpgr is required for normal retinal development and plays a role in dynein-based retrograde transport processes. Hum Mol Genet; 2010 Feb 15;19(4):657-70
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Zebrafish Rpgr is required for normal retinal development and plays a role in dynein-based retrograde transport processes.
  • Mutations in the human RPGR gene cause one of the most common and severe forms of inherited retinal dystrophy, but the function of its protein product remains unclear.
  • These defects are consistent with a ciliary function and were rescued by human RPGR but not by RPGR mutants causing retinal dystrophy.
  • Unlike mammals, RPGR knockdown in zebrafish resulted in both abnormal development and increased cell death in the dysplastic retina.
  • Developmental abnormalities in the eye included lamination defects, failure to develop photoreceptor outer segments and a small eye phenotype, associated with increased cell death throughout the retina.
  • ZFRPGR2 is therefore necessary both for the normal differentiation and lamination of the retina and to prevent apoptotic retinal cell death, which may relate to its proposed role in dynein-based retrograde transport processes.
  • [MeSH-major] Dyneins / metabolism. Eye Proteins / metabolism. Retina / growth & development. Retinal Diseases / metabolism. Zebrafish / growth & development. Zebrafish Proteins / metabolism

  • MedlinePlus Health Information. consumer health - Retinal Disorders.
  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
  • SciCrunch. OMIM: Data: Gene Annotation .
  • ZFIN. ZFIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19955120.001).
  • [ISSN] 1460-2083
  • [Journal-full-title] Human molecular genetics
  • [ISO-abbreviation] Hum. Mol. Genet.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G120/875; United Kingdom / Medical Research Council / / MC/ PC/ U127585840; United Kingdom / Medical Research Council / / MC/ U127584475; United Kingdom / Medical Research Council / / MC/ U127585840
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Eye Proteins; 0 / RPGR protein, zebrafish; 0 / Zebrafish Proteins; EC 3.6.4.2 / Dyneins
  •  go-up   go-down


8. Firth SI, Feller MB: Dissociated GABAergic retinal interneurons exhibit spontaneous increases in intracellular calcium. Vis Neurosci; 2006 Sep-Oct;23(5):807-14
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dissociated GABAergic retinal interneurons exhibit spontaneous increases in intracellular calcium.
  • Early in development, before the retina is responsive to light, neurons exhibit spontaneous activity.
  • Networks comprised of spontaneously active starburst cells initiate correlated bursts of action potentials that propagate across the developing retina with a periodicity on the order minutes.
  • To determine whether other retinal interneurons have similar "pacemaking" properties, we have utilized cultures of dissociated neurons from the rat retina.
  • Whole cell voltage clamp recordings in the absence of antagonists for fast neurotransmitters revealed that after 7 days in culture, individual retinal neurons receive bursts of GABA-A receptor mediated synaptic input with a periodicity similar to that measured in spontaneously active GABAergic neurons.
  • Together, these findings indicate that spiking GABAergic interneurons can function as pacemakers in the developing retina.
  • [MeSH-major] Calcium / metabolism. Extracellular Fluid / metabolism. Interneurons / metabolism. Retina / cytology. gamma-Aminobutyric Acid / metabolism

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. PICROTOXIN .
  • Hazardous Substances Data Bank. TETRODOTOXIN .
  • Hazardous Substances Data Bank. CALCIUM, ELEMENTAL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17020635.001).
  • [ISSN] 0952-5238
  • [Journal-full-title] Visual neuroscience
  • [ISO-abbreviation] Vis. Neurosci.
  • [Language] eng
  • [Grant] United States / NEI NIH HHS / EY / EY016417; United States / NEI NIH HHS / EY / EY13528
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anesthetics, Local; 0 / Chelating Agents; 0 / Excitatory Amino Acid Antagonists; 0 / GABA Antagonists; 0 / Pyridazines; 104104-50-9 / gabazine; 124-87-8 / Picrotoxin; 139890-68-9 / 1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester; 4368-28-9 / Tetrodotoxin; 526U7A2651 / Egtazic Acid; 56-12-2 / gamma-Aminobutyric Acid; 6OTE87SCCW / 6-Cyano-7-nitroquinoxaline-2,3-dione; 76726-92-6 / 2-Amino-5-phosphonovalerate; SY7Q814VUP / Calcium
  •  go-up   go-down


9. Chiu K, Lam TT, Ying Li WW, Caprioli J, Kwong Kwong JM: Calpain and N-methyl-d-aspartate (NMDA)-induced excitotoxicity in rat retinas. Brain Res; 2005 Jun 7;1046(1-2):207-15
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The purpose of present study was to examine the involvement of mu- and m-calpain in NMDA-induced excitotoxicity in the adult rat retina.
  • TdT-mediated biotin-dUTP nick end labeling (TUNEL) positive cells in the inner retina co-localized with moderate or intense mu-calpain immunoreactivity.
  • Simultaneous injection of 2 nmol of a calpain inhibitor (calpain inhibitor II) significantly reduced the number of TUNEL-positive cells in the inner retina at 18 h after NMDA injection and preserved RGC-like cells counted at 7 days after injection.
  • The results of this study showed that mu-calpain may be involved in mediating NMDA-induced excitotoxicity in the rat retina and calpain inhibitors may play a therapeutic role in NMDA related disease.
  • [MeSH-major] Apoptosis / physiology. Calpain / metabolism. Neurons / enzymology. Retina / enzymology. Retinal Diseases / enzymology

  • MedlinePlus Health Information. consumer health - Retinal Disorders.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15878434.001).
  • [ISSN] 0006-8993
  • [Journal-full-title] Brain research
  • [ISO-abbreviation] Brain Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Isoenzymes; 0 / Neurotoxins; 6384-92-5 / N-Methylaspartate; EC 3.4.22.- / Calpain; EC 3.4.22.- / m-calpain; EC 3.4.22.- / mu-calpain
  •  go-up   go-down


10. Song Y, Gong YY, Xie ZG, Li CH, Gu Q, Wu XW: Edaravone (MCI-186), a free radical scavenger, attenuates retinal ischemia/reperfusion injury in rats. Acta Pharmacol Sin; 2008 Jul;29(7):823-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Edaravone (MCI-186), a free radical scavenger, attenuates retinal ischemia/reperfusion injury in rats.
  • AIM: To investigate the effect of edaravone (MCI-186), a free radical scavenger, against ischemia/reperfusion (I/R) injury in the rat retina.
  • METHODS: Retinal ischemia was induced in male Sprague-Dawley rats by elevating intraocular pressure to 110 mmHg for 60 min.
  • The levels of malondialdehyde (MDA) and superoxide dismutase (SOD) in the retinal tissues were determined on d 1 after I/R injury.
  • The apoptosis of retinal neurons was detected on d 1 after I/R injury by terminal deoxynucleotidyl transferase-mediated digoxigenin-dUTP nick-end labeling staining.
  • RESULTS: Edaravone lowered MDA levels, raised SOD activity, and attenuated I/R-induced apoptosis of retinal neurons within the inner nuclear, ganglion cell, and outer nuclear layers of the rat retina.
  • CONCLUSION: Edaravone can protect the retina from I/R injury in rats through reducing oxidative stress and inhibiting apoptosis of retinal neurons, which suggests that edaravone might be a potential choice for the treatment of I/R-induced eye disorders.
  • [MeSH-major] Antipyrine / analogs & derivatives. Free Radical Scavengers / pharmacology. Reperfusion Injury / prevention & control. Retinal Diseases / prevention & control

  • MedlinePlus Health Information. consumer health - Retinal Disorders.
  • Hazardous Substances Data Bank. MALONALDEHYDE .
  • Hazardous Substances Data Bank. 3-METHYL-1-PHENYL-2-PYRAZOLIN-5-ONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18565280.001).
  • [ISSN] 1745-7254
  • [Journal-full-title] Acta pharmacologica Sinica
  • [ISO-abbreviation] Acta Pharmacol. Sin.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Free Radical Scavengers; 4Y8F71G49Q / Malondialdehyde; EC 1.15.1.1 / Superoxide Dismutase; S798V6YJRP / phenylmethylpyrazolone; T3CHA1B51H / Antipyrine
  •  go-up   go-down


11. Cashman SM, McCullough L, Kumar-Singh R: Improved retinal transduction in vivo and photoreceptor-specific transgene expression using adenovirus vectors with modified penton base. Mol Ther; 2007 Sep;15(9):1640-6
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Improved retinal transduction in vivo and photoreceptor-specific transgene expression using adenovirus vectors with modified penton base.
  • Adenovirus (Ad) vectors can be injected into human ocular tissues without producing adverse events and are therefore a promising means of gene transfer to the retina.
  • However, when administered subretinally, Ad vectors primarily transduce the retinal pigment epithelium (RPE), whereas the majority of mutant gene products that cause photoreceptor (PR) degeneration are expressed exclusively in the PR cells.
  • We compared expression levels from CMV and chicken beta actin (CBA) promoters in neural retina and found that CBA has a 173-fold greater potency than CMV.
  • We also investigated the nature of the Ad-RPE interaction in murine retina and determined that the RGD domain in Ad penton plays a key role in RPE tropism.
  • Deletion of the RGD domain coupled with use of the CBA promoter permitted transgene expression in neural retina approximately 667 times more efficiently than with Ad5 vectors.
  • [MeSH-major] Adenoviridae / genetics. Genetic Vectors / genetics. Photoreceptor Cells / metabolism. Retina / metabolism

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17505470.001).
  • [ISSN] 1525-0016
  • [Journal-full-title] Molecular therapy : the journal of the American Society of Gene Therapy
  • [ISO-abbreviation] Mol. Ther.
  • [Language] eng
  • [Grant] United States / NEI NIH HHS / EY / EY013887; United States / NEI NIH HHS / EY / EY014991
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Actins; 147336-22-9 / Green Fluorescent Proteins; 9009-81-8 / Rhodopsin
  •  go-up   go-down


12. Takechi M, Kawamura S: Temporal and spatial changes in the expression pattern of multiple red and green subtype opsin genes during zebrafish development. J Exp Biol; 2005 Apr;208(Pt 7):1337-45
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Occurrence of opsin subtypes by gene duplication is characteristic of fish but little is known whether the subtypes are expressed differently in the retina, either spatially or temporally.
  • Here we show by in situ hybridization the dynamic expression patterns of the opsin subtypes in the zebrafish retina.
  • In the adult retina, LWS-2 was expressed in the central to dorsal area and LWS-1 in the ventral and peripheral areas.
  • The expression started with the shortest wavelength subtype RH2-1 followed by the longer wavelength ones, and in the adult retina, the shorter wavelength subtypes (RH2-1 and RH2-2) were expressed in the central to dorsal area and longer wavelength subtypes (RH2-3 and RH2-4) in the ventral and peripheral areas.
  • [MeSH-major] Gene Expression Regulation, Developmental. Retina / metabolism. Rod Opsins / metabolism. Zebrafish / embryology. Zebrafish / metabolism

  • ZFIN. ZFIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15781894.001).
  • [ISSN] 0022-0949
  • [Journal-full-title] The Journal of experimental biology
  • [ISO-abbreviation] J. Exp. Biol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Rod Opsins
  •  go-up   go-down


13. Ganesan P, He S, Xu H: Analysis of retinal circulation using an image-based network model of retinal vasculature. Microvasc Res; 2010 Jul;80(1):99-109
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Analysis of retinal circulation using an image-based network model of retinal vasculature.
  • This paper presents the results of a circulation analysis using an image based network model of a murine retinal vasculature, which closely represents the 3D vascular distribution of the retina.
  • The uneven distribution of the red blood cells at vascular network bifurcations (i.e., plasma skimming effect), the microvascular diameter effect (i.e., Fahraeus-Lindqvist effect) and the role of endothelium surface layer (i.e., in vivo viscosity) were considered in determining the viscosity of the blood in the retinal vessel segments.
  • The analysis shows that the distribution of the blood hematocrit (H(D)) in the retinal network is very non-uniform, with lower values at the pre-equator region (near the optic disc) and higher values in the equator region of the retina.
  • WSS is greater in smaller vessels located near the optic disc than that in the mainstream retinal vessels.
  • The results presented can be directly useful to ophthalmologists and researchers working with retinal vasculature.
  • [MeSH-major] Models, Anatomic. Models, Biological. Regional Blood Flow / physiology. Retinal Vessels / anatomy & histology. Retinal Vessels / physiology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20156460.001).
  • [ISSN] 1095-9319
  • [Journal-full-title] Microvascular research
  • [ISO-abbreviation] Microvasc. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


14. Cox JA, Kucenas S, Voigt MM: Molecular characterization and embryonic expression of the family of N-methyl-D-aspartate receptor subunit genes in the zebrafish. Dev Dyn; 2005 Nov;234(3):756-66
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Molecular characterization and embryonic expression of the family of N-methyl-D-aspartate receptor subunit genes in the zebrafish.
  • The NR2 subunits show less identity, differing most at the N- and C-termini.
  • NR1.1 is found in brain, retina, and spinal cord at 24 hours postfertilization (hpf).
  • NR2 developmental gene expression varies: both paralogs of the NR2A are expressed at 48 hpf in the retina, only one paralog of the NR2B is expressed at low levels in the heart at 48 hpf.
  • Both paralogs of the NR2D are expressed: 2D.1 is in the forebrain, retina, and spinal cord at 24 hpf, whereas the 2D.2 is only found in the retina.

  • COS Scholar Universe. author profiles.
  • ZFIN. ZFIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Developmental Dynamics 234:756-766, 2005. (c) 2005 Wiley-Liss, Inc.
  • (PMID = 16123982.001).
  • [ISSN] 1058-8388
  • [Journal-full-title] Developmental dynamics : an official publication of the American Association of Anatomists
  • [ISO-abbreviation] Dev. Dyn.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Complementary; 0 / Protein Subunits; 0 / Receptors, N-Methyl-D-Aspartate
  •  go-up   go-down


15. Whitlock NA, Agarwal N, Ma JX, Crosson CE: Hsp27 upregulation by HIF-1 signaling offers protection against retinal ischemia in rats. Invest Ophthalmol Vis Sci; 2005 Mar;46(3):1092-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Hsp27 upregulation by HIF-1 signaling offers protection against retinal ischemia in rats.
  • PURPOSE: Previous work from the authors' laboratory has shown that Hsp27 is specifically upregulated after retinal ischemic preconditioning (IPC), and this upregulation acts as a key cytoprotective factor in preventing retinal ischemic damage.
  • In vitro results were then applied to an in vivo model of retinal ischemia to determine whether CoCl(2) upregulates rHsp27 and protects the retina from ischemic injury.
  • RESULTS: CoCl(2) upregulated Hsp27 in cultured retinal neurons.
  • Furthermore, CoCl(2) upregulated Hsp27 in the rat retina and protected the rat retina from ischemic injury.
  • [MeSH-major] DNA-Binding Proteins / metabolism. Heat-Shock Proteins / metabolism. Neoplasm Proteins / metabolism. Nuclear Proteins / metabolism. Reperfusion Injury / prevention & control. Retinal Diseases / prevention & control. Retinal Vessels / metabolism. Signal Transduction. Transcription Factors / metabolism
  • [MeSH-minor] Animals. Base Sequence. Blotting, Western. Cell Line, Transformed. Cobalt / pharmacology. Cytoprotection. Electroretinography. Female. Fluorescent Antibody Technique, Indirect. HSP27 Heat-Shock Proteins. Hypoxia-Inducible Factor 1. Hypoxia-Inducible Factor 1, alpha Subunit. Ischemic Preconditioning. Molecular Sequence Data. Rats. Rats, Inbred BN. Retinal Ganglion Cells / drug effects. Retinal Ganglion Cells / metabolism. Up-Regulation

  • MedlinePlus Health Information. consumer health - Retinal Disorders.
  • Hazardous Substances Data Bank. COBALT, ELEMENTAL .
  • Hazardous Substances Data Bank. COBALTOUS CHLORIDE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15728570.001).
  • [ISSN] 0146-0404
  • [Journal-full-title] Investigative ophthalmology & visual science
  • [ISO-abbreviation] Invest. Ophthalmol. Vis. Sci.
  • [Language] eng
  • [Grant] United States / NEI NIH HHS / EY / EY014793; United States / NEI NIH HHS / EY / EY09741
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / HSP27 Heat-Shock Proteins; 0 / Heat-Shock Proteins; 0 / Hif1a protein, rat; 0 / Hspb1 protein, rat; 0 / Hypoxia-Inducible Factor 1; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Neoplasm Proteins; 0 / Nuclear Proteins; 0 / Transcription Factors; 3G0H8C9362 / Cobalt; EVS87XF13W / cobaltous chloride
  •  go-up   go-down


16. Park CH, Kim YS, Kim YH, Choi MY, Yoo JM, Kang SS, Choi WS, Cho GJ: Calcineurin mediates AKT dephosphorylation in the ischemic rat retina. Brain Res; 2008 Oct 9;1234:148-57
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Calcineurin mediates AKT dephosphorylation in the ischemic rat retina.
  • We examined the interdependence between CaN and Akt/protein kinase B (PKB) in the rat retina after transient ischemia.
  • These results indicate that CaN cleavage negatively regulates Akt phosphorylation and is involved in retinal cell apoptosis after transient ischemia.
  • [MeSH-major] Calcineurin / physiology. Ischemia / metabolism. Ischemia / pathology. Oncogene Protein v-akt / metabolism. Retinal Vessels / metabolism. Retinal Vessels / pathology

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18703031.001).
  • [ISSN] 0006-8993
  • [Journal-full-title] Brain research
  • [ISO-abbreviation] Brain Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / bcl-Associated Death Protein; EC 2.7.11.1 / Oncogene Protein v-akt; EC 3.1.3.16 / Calcineurin; WM0HAQ4WNM / Tacrolimus
  •  go-up   go-down


17. Vakrou C, Whitaker D, McGraw PV, McKeefry D: Functional evidence for cone-specific connectivity in the human retina. J Physiol; 2005 Jul 1;566(Pt 1):93-102
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Functional evidence for cone-specific connectivity in the human retina.
  • Two competing theories, the cone-selective hypothesis and the random-wiring hypothesis, are currently equivocal to the architecture of the primate retina.

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Opt Soc Am. 1977 Feb;67(2):202-7 [839300.001]
  • [Cites] Science. 1986 Apr 11;232(4747):193-202 [2937147.001]
  • [Cites] Vision Res. 1986;26(1):23-32 [3716212.001]
  • [Cites] J Opt Soc Am A. 1987 Aug;4(8):1568-78 [3625338.001]
  • [Cites] J Opt Soc Am A. 1987 Aug;4(8):1579-82 [3625339.001]
  • [Cites] J Opt Soc Am A. 1987 Aug;4(8):1583-93 [3625340.001]
  • [Cites] Nature. 1989 Oct 19;341(6243):643-6 [2797190.001]
  • [Cites] J Opt Soc Am A. 1989 Nov;6(11):1784-93 [2585175.001]
  • [Cites] J Neurosci. 1990 Feb;10(2):649-69 [2303866.001]
  • [Cites] Physiol Rev. 1991 Apr;71(2):447-80 [2006220.001]
  • [Cites] Vision Res. 1991;31(1):119-30 [2006545.001]
  • [Cites] J Opt Soc Am A. 1991 Feb;8(2):404-14 [2007915.001]
  • [Cites] J Comp Neurol. 1991 Oct 22;312(4):610-24 [1722224.001]
  • [Cites] J Physiol. 1991 Oct;442:47-64 [1798037.001]
  • [Cites] Nature. 1992 Apr 23;356(6371):716-8 [1570016.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Oct 15;89(20):9666-70 [1409680.001]
  • [Cites] Vision Res. 1992 Oct;32(10):1913-30 [1287988.001]
  • [Cites] Vision Res. 1993 May;33(8):1053-65 [8506645.001]
  • [Cites] J Neurosci. 1993 Dec;13(12):5334-55 [8254378.001]
  • [Cites] Vision Res. 1993 Dec;33(18):2773-88 [8296472.001]
  • [Cites] Nature. 1994 Feb 24;367(6465):731-5 [8107868.001]
  • [Cites] Nature. 1994 Sep 1;371(6492):70-2 [8072528.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Jan 23;93(2):582-8 [8570599.001]
  • [Cites] Vision Res. 1996 Jul;36(13):1995-2000 [8759439.001]
  • [Cites] J Opt Soc Am A Opt Image Sci Vis. 1997 Jan;14(1):1-12 [8988615.001]
  • [Cites] Vis Neurosci. 1998 Jan-Feb;15(1):161-75 [9456515.001]
  • [Cites] J Neurosci. 1998 May 1;18(9):3373-85 [9547245.001]
  • [Cites] Prog Retin Eye Res. 1999 Nov;18(6):737-63 [10530750.001]
  • [Cites] J Physiol. 1961 Dec;159:203-21 [13883391.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Apr 25;97(9):4997-5002 [10781111.001]
  • [Cites] Vision Res. 2000;40(14):1801-11 [10837827.001]
  • [Cites] Annu Rev Neurosci. 2000;23:743-75 [10845080.001]
  • [Cites] Nat Neurosci. 2001 Apr;4(4):409-16 [11276232.001]
  • [Cites] J Neurosci. 2001 Apr 15;21(8):2768-83 [11306629.001]
  • [Cites] Nature. 2001 Apr 19;410(6831):933-6 [11309618.001]
  • [Cites] J Neurosci. 2002 Jul 15;22(14):6158-75 [12122075.001]
  • [Cites] Vis Neurosci. 2002 Jan-Feb;19(1):109-18 [12180855.001]
  • [Cites] Nature. 2003 Dec 11;426(6967):668-71 [14668866.001]
  • [Cites] Vis Neurosci. 2003 Sep-Oct;20(5):511-21 [14977330.001]
  • [Cites] J Opt Soc Am. 1966 Jul;56(7):966-77 [4959282.001]
  • [Cites] J Neurophysiol. 1966 Nov;29(6):1115-56 [4961644.001]
  • [Cites] Exp Brain Res. 1974;21(5):447-454 [4442497.001]
  • [Cites] Nature. 1978 Jan 5;271(5640):54-6 [625324.001]
  • [Cites] Vision Res. 1981;21(9):1341-56 [6976039.001]
  • [Cites] Annu Rev Psychol. 1982;33:41-85 [6977310.001]
  • [Cites] Vision Res. 1982;22(9):1123-31 [7147723.001]
  • [Cites] Vision Res. 1983;23(1):1-11 [6868374.001]
  • [Cites] Vision Res. 1983;23(5):529-40 [6880050.001]
  • [Cites] Vision Res. 1984;24(8):789-800 [6474836.001]
  • [Cites] J Physiol. 1984 Dec;357:241-65 [6512691.001]
  • [Cites] J Physiol. 1985 Feb;359:381-400 [3999044.001]
  • [Cites] Nature. 1977 Apr 7;266(5602):554-6 [859622.001]
  • (PMID = 15845585.001).
  • [ISSN] 0022-3751
  • [Journal-full-title] The Journal of physiology
  • [ISO-abbreviation] J. Physiol. (Lond.)
  • [Language] ENG
  • [Grant] United Kingdom / Wellcome Trust / /
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC1464730
  •  go-up   go-down


18. Lukasiewicz PD: Synaptic mechanisms that shape visual signaling at the inner retina. Prog Brain Res; 2005;147:205-18
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Synaptic mechanisms that shape visual signaling at the inner retina.
  • The retina is a layered structure that processes information in two stages.
  • [MeSH-major] Retina / physiology. Signal Transduction / physiology. Synapses / physiology. Visual Pathways / physiology

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15581708.001).
  • [ISSN] 0079-6123
  • [Journal-full-title] Progress in brain research
  • [ISO-abbreviation] Prog. Brain Res.
  • [Language] eng
  • [Grant] United States / NEI NIH HHS / EY / EY02687; United States / NEI NIH HHS / EY / EY08922
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] Netherlands
  • [Number-of-references] 93
  •  go-up   go-down


19. Reed BT, Sullivan SJ, Tsai G, Coyle JT, Esguerra M, Miller RF: The glycine transporter GlyT1 controls N-methyl-D-aspartic acid receptor coagonist occupancy in the mouse retina. Eur J Neurosci; 2009 Dec;30(12):2308-17
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The glycine transporter GlyT1 controls N-methyl-D-aspartic acid receptor coagonist occupancy in the mouse retina.
  • We examined the role of GlyT1, the high-affinity glycine transporter, in the mouse retina with an emphasis on the role of glycine as a coagonist of N-methyl-D-aspartic acid (NMDA) receptors.
  • Capillary electrophoresis was used to separate and quantitatively measure glycine release from isolated retina preparations; pharmacologically blocking GlyT1 with N-[3-([1,1-biphenyl]-4-yloxy)-3-(4-fluorophenyl)propyl]-N-methylglycine in the WT retina generated a significantly larger accumulation of glycine into the bathing environment when compared with the GlyT1(-/+) retinas.
  • These observations are discussed in view of contemporary issues about NMDA receptor coagonist function in the vertebrate retina and the role of glycine vs. D-serine as the endogenous coagonist.

  • Hazardous Substances Data Bank. GLYCINE .
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Exp Eye Res. 2007 Jan;84(1):191-9 [17094966.001]
  • [Cites] J Biol Chem. 2006 May 19;281(20):14151-62 [16551623.001]
  • [Cites] J Neurosci. 2009 Feb 4;29(5):1469-79 [19193893.001]
  • [Cites] J Neurochem. 1999 Nov;73(5):2184-94 [10537079.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Nov 9;96(23):13409-14 [10557334.001]
  • [Cites] J Neurosci Methods. 1999 Nov 15;93(2):169-75 [10634502.001]
  • [Cites] J Comp Neurol. 2000 Apr 24;420(1):98-112 [10745222.001]
  • [Cites] Prog Brain Res. 2001;131:712-8 [11420983.001]
  • [Cites] Br J Pharmacol. 2001 Dec;134(7):1429-36 [11724748.001]
  • [Cites] Brain Res. 2002 Mar 8;929(2):202-9 [11864625.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 May 27;100(11):6789-94 [12750462.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Jun 1;101(22):8485-90 [15159536.001]
  • [Cites] Cold Spring Harb Symp Quant Biol. 1965;30:393-402 [4956618.001]
  • [Cites] Z Zellforsch Mikrosk Anat. 1969;100(1):60-82 [5354186.001]
  • [Cites] J Neurophysiol. 1970 May;33(3):405-20 [5439344.001]
  • [Cites] Science. 1977 Nov 18;198(4318):748-50 [910159.001]
  • [Cites] J Neurochem. 1981 Oct;37(4):867-77 [7320727.001]
  • [Cites] J Neurosci. 1983 Aug;3(8):1701-11 [6135763.001]
  • [Cites] Nature. 1987 Feb 5-11;325(6104):529-31 [2433595.001]
  • [Cites] Science. 1988 Aug 12;241(4867):835-7 [2841759.001]
  • [Cites] J Comp Neurol. 1990 Jan 8;291(2):281-304 [2298935.001]
  • [Cites] Prog Neurobiol. 1990;35(1):53-74 [1699248.001]
  • [Cites] FEBS Lett. 1992 Jan 13;296(1):33-6 [1730289.001]
  • [Cites] Neuron. 1992 May;8(5):927-35 [1534013.001]
  • [Cites] Mol Pharmacol. 1992 May;41(5):923-30 [1375318.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Aug 1;89(15):7189-93 [1353889.001]
  • [Cites] J Physiol. 1992 Apr;449:589-606 [1355793.001]
  • [Cites] J Neurochem. 1993 Feb;60(2):783-6 [8419554.001]
  • [Cites] Neuron. 1993 Oct;11(4):725-38 [8104431.001]
  • [Cites] J Neurochem. 1995 Jul;65(1):454-8 [7790891.001]
  • [Cites] Invest Ophthalmol Vis Sci. 1996 Jul;37(8):1618-24 [8675405.001]
  • [Cites] Ann N Y Acad Sci. 1993 Dec 20;707:136-52 [9137549.001]
  • [Cites] J Neurosci. 1997 Jun 15;17(12):4580-90 [9169519.001]
  • [Cites] J Neurochem. 1998 Jun;70(6):2628-36 [9603230.001]
  • [Cites] Vis Neurosci. 1998 Mar-Apr;15(2):219-29 [9605524.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Dec 22;95(26):15730-4 [9861038.001]
  • [Cites] Vis Neurosci. 1999 Mar-Apr;16(2):231-9 [10367958.001]
  • [Cites] Cereb Cortex. 2005 Apr;15(4):448-59 [15749988.001]
  • [Cites] J Physiol. 2005 Mar 15;563(Pt 3):777-93 [15661817.001]
  • [Cites] Neurosci Lett. 2005 Sep 2;385(1):58-63 [15950382.001]
  • [Cites] Neurosci Lett. 2005 Oct 21;387(2):75-9 [16084022.001]
  • [Cites] Glia. 2006 Mar;53(4):401-11 [16342169.001]
  • [Cites] J Neurophysiol. 2007 Jul;98(1):122-30 [17507508.001]
  • (PMID = 20092573.001).
  • [ISSN] 1460-9568
  • [Journal-full-title] The European journal of neuroscience
  • [ISO-abbreviation] Eur. J. Neurosci.
  • [Language] ENG
  • [Grant] United States / NEI NIH HHS / EY / EY003014-31; United States / NEI NIH HHS / EY / R01 EY003014; United States / NEI NIH HHS / EY / R01 EY003014-31
  • [Publication-type] Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Glycine Plasma Membrane Transport Proteins; 0 / NR1 NMDA receptor; 0 / NR2A NMDA receptor; 0 / NR2B NMDA receptor; 0 / Receptors, N-Methyl-D-Aspartate; 0 / Slc6a9 protein, mouse; 6384-92-5 / N-Methylaspartate; TE7660XO1C / Glycine
  • [Other-IDs] NLM/ NIHMS221454; NLM/ PMC2910544
  •  go-up   go-down


20. Martin PM, Dun Y, Mysona B, Ananth S, Roon P, Smith SB, Ganapathy V: Expression of the sodium-coupled monocarboxylate transporters SMCT1 (SLC5A8) and SMCT2 (SLC5A12) in retina. Invest Ophthalmol Vis Sci; 2007 Jul;48(7):3356-63
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of the sodium-coupled monocarboxylate transporters SMCT1 (SLC5A8) and SMCT2 (SLC5A12) in retina.
  • PURPOSE: Monocarboxylates are primary energy substrates in the retina.
  • Expression of SMCT1 and SMCT2 has been studied in several tissues; however, little is known about their expression in retina.
  • In the present study, the authors asked whether SMCT1 and SMCT2 are also expressed in retina and, if so, in which particular retinal cell types.
  • METHODS: SMCT1 and SMCT2 expression was analyzed in intact mouse retina and cultured retinal cells (ganglion, Müller, RPE) by RT-PCR, in situ hybridization, and immunofluorescence.
  • SMCT2 mRNA and protein were detected only in neural retina, with a pattern of protein localization consistent with labeling of Müller cells.
  • CONCLUSIONS: These data provide the first evidence for the expression of SMCT1 and SMCT2 in the retina and for the cell-type specific distribution of these transporters within the retina.
  • These studies suggest that SMCT1 and SMCT2 play a differential role in monocarboxylate transport in the retina in a cell type-specific manner.
  • [MeSH-major] Cation Transport Proteins / metabolism. Connective Tissue Cells / metabolism. Monocarboxylic Acid Transporters / metabolism. Pigment Epithelium of Eye / metabolism. Retina / metabolism. Retinal Ganglion Cells / metabolism

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17591909.001).
  • [ISSN] 0146-0404
  • [Journal-full-title] Investigative ophthalmology & visual science
  • [ISO-abbreviation] Invest. Ophthalmol. Vis. Sci.
  • [Language] eng
  • [Grant] United States / NEI NIH HHS / EY / R01 EY012830
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cation Transport Proteins; 0 / Monocarboxylic Acid Transporters; 0 / RNA, Messenger; 0 / Slc5a12 protein, mouse; 0 / Slc5a8 protein, mouse
  •  go-up   go-down


21. Wang H, Lau BW, Yau SY, Li SY, Leung N, Wang NL, Tang SW, Lee TM, So KF: Roles of paroxetine and corticosterone on adult mammalian ciliary body cell proliferation. Chin Med J (Engl); 2010 May 20;123(10):1305-10
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: The neurogenesis in retina of adult mammals is generally abolished, and this renders the retina lack of regenerative capacity.
  • CONCLUSIONS: The results illustrate that proliferation of retinal progenitor cells situated in ciliary body are subjected to regulation by selective serotonin reuptake inhibitors (SSRI) and corticosteroid, which is similar to our previous findings in neurogenic regions in central nervous system (CNS).
  • This provides information for future investigation of retinal stem cell biology and potential treatment of retinal degenerative diseases.

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. PAROXETINE HYDROCHLORIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20529586.001).
  • [ISSN] 0366-6999
  • [Journal-full-title] Chinese medical journal
  • [ISO-abbreviation] Chin. Med. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 41VRH5220H / Paroxetine; W980KJ009P / Corticosterone
  •  go-up   go-down


22. Alvaro AR, Rosmaninho-Salgado J, Ambrósio AF, Cavadas C: Neuropeptide Y inhibits [Ca2+]i changes in rat retinal neurons through NPY Y1, Y4, and Y5 receptors. J Neurochem; 2009 Jun;109(5):1508-15
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Neuropeptide Y inhibits [Ca2+]i changes in rat retinal neurons through NPY Y1, Y4, and Y5 receptors.
  • Neuropeptide Y (NPY) and NPY receptors are widely distributed in the CNS, including the retina, but the role of NPY in the retina is largely unknown.
  • The aim of this study was to investigate whether NPY modulates intracellular calcium concentration ([Ca(2+)](i)) changes in retinal neurons and identify the NPY receptors involved.
  • In conclusion, NPY inhibits KCl-evoked [Ca(2+)](i) increase in retinal neurons through the activation of NPY Y(1), Y(4), and Y(5) receptors.
  • This effect may be viewed as a potential neuroprotective mechanism of NPY against retinal neurodegeneration.
  • [MeSH-major] Calcium / metabolism. Neural Inhibition / drug effects. Neurons / drug effects. Neuropeptide Y / pharmacology. Receptors, Neuropeptide Y / physiology. Retina / cytology

  • Hazardous Substances Data Bank. CALCIUM, ELEMENTAL .
  • Hazardous Substances Data Bank. POTASSIUM CHLORIDE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19344373.001).
  • [ISSN] 1471-4159
  • [Journal-full-title] Journal of neurochemistry
  • [ISO-abbreviation] J. Neurochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Neuropeptide Y; 0 / Receptors, Neuropeptide Y; 0 / neuropeptide Y-Y1 receptor; 0 / neuropeptide Y4 receptor; 0 / neuropeptide Y5 receptor; 660YQ98I10 / Potassium Chloride; SY7Q814VUP / Calcium
  •  go-up   go-down


23. Schmidt TM, Kofuji P: Functional and morphological differences among intrinsically photosensitive retinal ganglion cells. J Neurosci; 2009 Jan 14;29(2):476-82
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Functional and morphological differences among intrinsically photosensitive retinal ganglion cells.
  • A subset of ganglion cells in the mammalian retina express the photopigment melanopsin and are intrinsically photosensitive (ipRGCs).
  • Morphological studies have confirmed the existence of at least three distinct subpopulations of ipRGCs, but studies of the physiology of ipRGCs at the single cell level have focused mainly on M1 cells, the dendrites of which stratify solely in sublamina a (OFF sublamina) of the retinal inner plexiform layer (IPL).
  • The goal of the current study was to compare the morphology, intrinsic light response, and intrinsic membrane properties of M1 and M2 cells in the mouse retina.

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CALCIUM, ELEMENTAL .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Physiol. 2002 Feb 1;538(Pt 3):787-802 [11826165.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Sep 16;105(37):14181-6 [18779590.001]
  • [Cites] Science. 2002 Feb 8;295(5557):1070-3 [11834835.001]
  • [Cites] Curr Biol. 2003 Aug 5;13(15):1290-8 [12906788.001]
  • [Cites] Nature. 2005 Feb 17;433(7027):749-54 [15716953.001]
  • [Cites] Neuron. 2005 Dec 22;48(6):987-99 [16364902.001]
  • [Cites] Neuroscience. 2006 Jun 19;140(1):123-36 [16626866.001]
  • [Cites] J Comp Neurol. 2006 Jul 20;497(3):326-49 [16736474.001]
  • [Cites] Curr Biol. 2007 Jun 5;17(11):981-8 [17524644.001]
  • [Cites] J Physiol. 2007 Jul 1;582(Pt 1):279-96 [17510182.001]
  • [Cites] Eur J Neurosci. 2008 Apr;27(7):1763-70 [18371076.001]
  • [Cites] Nature. 2008 May 1;453(7191):102-5 [18432195.001]
  • [Cites] PLoS One. 2008;3(6):e2451 [18545654.001]
  • [Cites] J Neurophysiol. 2008 Jul;100(1):371-84 [18480363.001]
  • [Cites] Science. 2002 Feb 8;295(5557):1065-70 [11834834.001]
  • (PMID = 19144848.001).
  • [ISSN] 1529-2401
  • [Journal-full-title] The Journal of neuroscience : the official journal of the Society for Neuroscience
  • [ISO-abbreviation] J. Neurosci.
  • [Language] ENG
  • [Grant] United States / NEI NIH HHS / EY / R01 EY012949-09; United States / NEI NIH HHS / EY / R01 EY012949; United States / NEI NIH HHS / EY / EY012949-09; United States / NEI NIH HHS / EY / R21 EY018885-01; United States / NEI NIH HHS / EY / R01EY012949; United States / NEI NIH HHS / EY / T32EY0707133; United States / NEI NIH HHS / EY / EY018885-01; United States / NEI NIH HHS / EY / R21-EY018885; United States / NEI NIH HHS / EY / R21 EY018885
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Rod Opsins; 0 / enhanced green fluorescent protein; 0 / melanopsin; 147336-22-9 / Green Fluorescent Proteins; EC 2.3.1.6 / Choline O-Acetyltransferase; SY7Q814VUP / Calcium
  • [Other-IDs] NLM/ NIHMS87384; NLM/ PMC2752349
  •  go-up   go-down


24. Yaji N, Yamato M, Yang J, Okano T, Hori S: Transplantation of tissue-engineered retinal pigment epithelial cell sheets in a rabbit model. Biomaterials; 2009 Feb;30(5):797-803
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Transplantation of tissue-engineered retinal pigment epithelial cell sheets in a rabbit model.
  • The retinal pigment epithelium (RPE) plays an important role in maintaining a healthy neural retina.
  • We conclude that tissue-engineered RPE cell sheets harvested from temperature-responsive culture dishes can be effectively transplanted beneath the neural retina.
  • [MeSH-major] Cell Transplantation / methods. Pigment Epithelium of Eye / cytology. Retina / cytology. Tissue Engineering / methods

  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19036433.001).
  • [ISSN] 1878-5905
  • [Journal-full-title] Biomaterials
  • [ISO-abbreviation] Biomaterials
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  •  go-up   go-down


25. Peters S, Tatar O, Spitzer MS, Szurman P, Aisenbrey S, Lüke M, Adam A, Yoeruek E, Grisanti S: Analysis of the neuronal marker protein gene product 9.5 in internal limiting membranes after indocyanine-green assisted peeling. Retina; 2009 Feb;29(2):243-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Indocyanine green-assisted internal limiting membrane (ILM) peeling was suspected to disrupt the innermost layer of the neural retina.
  • RESULTS: A selective expression of protein gene product 9.5 was found in neuronal fibers of the retina and optic nerve of donor eyes.
  • CONCLUSION: Focal expression of protein gene product 9.5 in only 1 of 10 surgical ILM specimens argues against a general indocyanine green-related disruption of the innermost retinal layers.
  • [MeSH-major] Basement Membrane / metabolism. Biomarkers / metabolism. Coloring Agents. Indocyanine Green. Retinal Perforations / metabolism. Ubiquitin Thiolesterase / metabolism
  • [MeSH-minor] Eye Banks. Humans. Nerve Fibers / metabolism. Neurons / metabolism. Ophthalmologic Surgical Procedures. Optic Nerve / metabolism. Retinal Ganglion Cells / metabolism. Tissue Donors. Vitrectomy

  • Hazardous Substances Data Bank. INDOCYANINE GREEN .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18827736.001).
  • [ISSN] 1539-2864
  • [Journal-full-title] Retina (Philadelphia, Pa.)
  • [ISO-abbreviation] Retina (Philadelphia, Pa.)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Coloring Agents; EC 3.1.2.15 / UCHL1 protein, human; EC 3.1.2.15 / Ubiquitin Thiolesterase; IX6J1063HV / Indocyanine Green
  •  go-up   go-down


26. Chao HM, Chen YH, Liu JH, Lee SM, Lee FL, Chang Y, Yeh PH, Pan WH, Chi CW, Liu TY, Lui WY, Ho LT, Kuo CD, Lin DE, Chan CC, Yang DM, Lin AM, Chao FP: Iron-generated hydroxyl radicals kill retinal cells in vivo: effect of ferulic acid. Hum Exp Toxicol; 2008 Apr;27(4):327-39
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Iron-generated hydroxyl radicals kill retinal cells in vivo: effect of ferulic acid.
  • Obvious disorganization including loss of photoreceptor outer segments and cholinergic amacrines together with a wide-spreading ferric distribution across the retina was present, which were related to the eletro-retinographic and pathologic dysfunctions.
  • Thus, siderosis stimulates oxidative stress, and possibly, subsequent excitotoxicity, and calcium influx, which explains why the retina is impaired electro-physiologically and pathologically.
  • [MeSH-major] Coumaric Acids / therapeutic use. Ferrous Compounds / toxicity. Iron / toxicity. Retina / drug effects. Retinal Diseases / prevention & control. Siderosis / drug therapy

  • MedlinePlus Health Information. consumer health - Iron.
  • MedlinePlus Health Information. consumer health - Retinal Disorders.
  • Hazardous Substances Data Bank. FERULIC ACID .
  • Hazardous Substances Data Bank. IRON, ELEMENTAL .
  • Hazardous Substances Data Bank. CALCIUM, ELEMENTAL .
  • Hazardous Substances Data Bank. FERROUS SULFATE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18684804.001).
  • [ISSN] 0960-3271
  • [Journal-full-title] Human & experimental toxicology
  • [ISO-abbreviation] Hum Exp Toxicol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Coumaric Acids; 0 / Ferrous Compounds; 0 / Glutamates; 3352-57-6 / Hydroxyl Radical; 39R4TAN1VT / ferrous sulfate; AVM951ZWST / ferulic acid; E1UOL152H7 / Iron; EC 1.15.1.1 / Superoxide Dismutase; SY7Q814VUP / Calcium
  •  go-up   go-down


27. Benyelles N, Soubrane G: [Age-related macular degeneration]. Rev Prat; 2006 Jun 15;56(11):1194-201
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Transliterated title] La dégénérescence maculaire liée à l'âge.
  • It is a spectrum of related diseases that have in common the progressive decline of vision as a consequence of dysfunction of the central retina and its underlying supporting elements, principally the retinal pigment epithelium and choroid in older adults.
  • [MeSH-major] Macular Degeneration / diagnosis. Macular Degeneration / therapy

  • Genetic Alliance. consumer health - Macular Degeneration.
  • MedlinePlus Health Information. consumer health - Macular Degeneration.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16903520.001).
  • [ISSN] 0035-2640
  • [Journal-full-title] La Revue du praticien
  • [ISO-abbreviation] Rev Prat
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Number-of-references] 19
  •  go-up   go-down


28. Guo C, Hirano AA, Stella SL Jr, Bitzer M, Brecha NC: Guinea pig horizontal cells express GABA, the GABA-synthesizing enzyme GAD 65, and the GABA vesicular transporter. J Comp Neurol; 2010 May 15;518(10):1647-69
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Gamma-aminobutyric acid (GABA) is likely expressed in horizontal cells of all species, although conflicting physiological findings have led to considerable controversy regarding its role as a transmitter in the outer retina.
  • This study has evaluated key components of the GABA system in the outer retina of guinea pig, an emerging retinal model system.
  • Furthermore, immunostaining of retinal whole mounts and acutely dissociated retinas showed GAD(65) and VGAT immunoreactivity in both A-type and B-type horizontal cells.
  • These studies demonstrate the presence of GABA, GAD(65), and VGAT in horizontal cells of the guinea pig retina, and support the idea that GABA is synthesized from GAD(65), taken up into synaptic vesicles by VGAT, and likely released by a vesicular mechanism from horizontal cells.
  • [MeSH-major] Glutamate Decarboxylase / metabolism. Isoenzymes / metabolism. Retinal Horizontal Cells / enzymology. Retinal Horizontal Cells / physiology. Vesicular Inhibitory Amino Acid Transport Proteins / metabolism. gamma-Aminobutyric Acid / metabolism

  • COS Scholar Universe. author profiles.
  • SciCrunch. The Antibody Registry: Reagent: Antibodies .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2009 Wiley-Liss, Inc.
  • [Cites] Cell Tissue Res. 1994 May;276(2):295-307 [8020065.001]
  • [Cites] Vision Res. 1994 May;34(10):1235-46 [8023433.001]
  • [Cites] Vis Neurosci. 1994 May-Jun;11(3):501-17 [8038125.001]
  • [Cites] J Comp Neurol. 1994 Jul 22;345(4):602-11 [7962703.001]
  • [Cites] Prog Brain Res. 1994;102:261-73 [7800817.001]
  • [Cites] Brain Res Mol Brain Res. 1994 Oct;26(1-2):47-54 [7854065.001]
  • [Cites] J Comp Neurol. 1995 Jan 16;351(3):374-84 [7706548.001]
  • [Cites] J Neurosci Methods. 1995 Feb;56(2):115-23 [7752677.001]
  • [Cites] J Comp Neurol. 1995 Mar 20;353(4):553-71 [7759615.001]
  • [Cites] J Neurosci. 1996 Jul 15;16(14):4479-90 [8699258.001]
  • [Cites] Brain Res Mol Brain Res. 1995 Nov;33(2):319-25 [8750892.001]
  • [Cites] Brain Res Mol Brain Res. 1995 Oct;33(1):7-21 [8774941.001]
  • [Cites] J Neurosci. 1996 Oct 1;16(19):6255-64 [8815906.001]
  • [Cites] J Comp Neurol. 1996 Feb 26;366(1):15-33 [8866843.001]
  • [Cites] J Comp Neurol. 1996 Nov 11;375(2):212-24 [8915826.001]
  • [Cites] Annu Rev Neurosci. 1997;20:125-56 [9056710.001]
  • [Cites] Brain Res Brain Res Rev. 2004 Jul;45(3):196-212 [15210304.001]
  • [Cites] Neuroscience. 2004;128(3):519-30 [15381281.001]
  • [Cites] J Neurophysiol. 2004 Nov;92(5):2789-801 [15240758.001]
  • [Cites] Science. 1966 Sep 30;153(3744):1639-41 [5917075.001]
  • [Cites] Proc R Soc Lond B Biol Sci. 1966 Nov 15;166(1002):80-111 [4382694.001]
  • [Cites] Brain Res. 1971 Dec 10;35(1):1-15 [5134225.001]
  • [Cites] Nat New Biol. 1972 Feb 16;235(59):217-8 [4334931.001]
  • [Cites] Exp Eye Res. 1974 Nov;19(5):435-47 [4154209.001]
  • [Cites] Proc R Soc Lond B Biol Sci. 1974 Jul 30;186(1085):317-31 [4154444.001]
  • [Cites] Vision Res. 1975 Mar;15(3):459-61 [166509.001]
  • [Cites] Exp Eye Res. 1978 Mar;26(3):275-89 [639880.001]
  • [Cites] Brain Res. 1980 Oct 20;199(2):401-14 [7417791.001]
  • [Cites] J Comp Neurol. 1981 Mar 20;197(1):113-27 [7014659.001]
  • [Cites] Exp Eye Res. 1981 Apr;32(4):445-50 [7238629.001]
  • [Cites] Brain Res. 1982 Feb 4;233(1):211-5 [6120741.001]
  • [Cites] J Physiol. 1982 Feb;323:211-27 [6808119.001]
  • [Cites] J Neural Transm. 1982;54(1-2):1-18 [6286870.001]
  • [Cites] Exp Eye Res. 1982 Dec;35(6):573-84 [7151891.001]
  • [Cites] Exp Eye Res. 1983 Feb;36(2):215-29 [6825739.001]
  • [Cites] Brain Res. 1983 Mar 14;263(1):63-75 [6132667.001]
  • [Cites] Vision Res. 1983;23(4):399-411 [6880038.001]
  • [Cites] Brain Res. 1983 Jul 4;270(2):273-83 [6136312.001]
  • [Cites] J Comp Neurol. 1983 Jun 20;217(2):167-75 [6886050.001]
  • [Cites] Brain Res. 1984 Mar 26;296(1):75-86 [6370374.001]
  • [Cites] J Neurosci. 1984 Dec;4(12):2948-55 [6502214.001]
  • [Cites] Brain Res. 1985 Oct 7;344(2):286-95 [2994837.001]
  • [Cites] Cell Tissue Res. 1986;243(1):117-23 [3510739.001]
  • [Cites] Brain Res. 1986 Feb 12;365(1):70-7 [3947987.001]
  • [Cites] Invest Ophthalmol Vis Sci. 1986 May;27(5):674-8 [3700017.001]
  • [Cites] Vision Res. 1986;26(1):33-44 [3012877.001]
  • [Cites] Exp Eye Res. 1986 Jun;42(6):631-44 [3487464.001]
  • [Cites] J Physiol. 1986 Apr;373:443-61 [3746679.001]
  • [Cites] Proc Natl Acad Sci U S A. 1986 Nov;83(22):8808-12 [2430303.001]
  • [Cites] Histochemistry. 1987;86(5):485-90 [3294761.001]
  • [Cites] Neurosci Lett. 1987 Jun 26;77(3):255-60 [3302765.001]
  • [Cites] Vision Res. 1987;27(1):23-30 [3303678.001]
  • [Cites] Science. 1987 Oct 16;238(4825):350-5 [2443977.001]
  • [Cites] J Comp Neurol. 1988 Feb 8;268(2):281-97 [3360989.001]
  • [Cites] J Neurosci. 1988 Jun;8(6):2123-30 [3385490.001]
  • [Cites] J Comp Neurol. 1989 Jan 1;279(1):43-54 [2913060.001]
  • [Cites] J Comp Neurol. 1989 Jan 1;279(1):55-67 [2913061.001]
  • [Cites] Invest Ophthalmol Vis Sci. 1989 Apr;30(4):652-9 [2649448.001]
  • [Cites] J Chem Neuroanat. 1988 Jul-Aug;1(4):177-94 [3267345.001]
  • [Cites] J Comp Neurol. 1989 Oct 22;288(4):593-600 [2808751.001]
  • [Cites] J Comp Neurol. 1989 Oct 22;288(4):691-7 [2530250.001]
  • [Cites] Neuroscience. 1990;35(2):375-475 [2199841.001]
  • [Cites] J Comp Neurol. 1990 Jul 22;297(4):509-24 [2384611.001]
  • [Cites] Science. 1990 Sep 14;249(4974):1303-6 [1975955.001]
  • [Cites] Vis Neurosci. 1989;2(5):425-35 [2487080.001]
  • [Cites] J Comp Neurol. 1990 Dec 8;302(2):417-24 [2289978.001]
  • [Cites] Neuron. 1991 Jul;7(1):91-100 [2069816.001]
  • [Cites] J Neurosci. 1992 Apr;12(4):1394-408 [1556600.001]
  • [Cites] J Comp Neurol. 1992 Jun 15;320(3):394-7 [1377202.001]
  • [Cites] Neuron. 1992 Aug;9(2):337-48 [1497897.001]
  • [Cites] J Biol Chem. 1992 Sep 5;267(25):17491-3 [1517200.001]
  • [Cites] J Biol Chem. 1992 Oct 15;267(29):21098-104 [1400419.001]
  • [Cites] J Neurosci Methods. 1993 Jun;48(1-2):51-63 [8104259.001]
  • [Cites] Neuron. 1993 Sep;11(3):401-7 [8104430.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Nov 1;90(21):10081-5 [7694280.001]
  • [Cites] Neurosci Lett. 1993 Nov 26;163(1):71-3 [8295736.001]
  • [Cites] J Neurosci. 1994 Mar;14(3 Pt 2):1834-55 [8126575.001]
  • [Cites] Arch Pathol Lab Med. 1994 Jun;118(6):633-9 [8204010.001]
  • [Cites] Annu Rev Neurosci. 1994;17:569-602 [7516126.001]
  • [Cites] Vis Neurosci. 1994 Jan-Feb;11(1):135-42 [8011576.001]
  • [Cites] Exp Eye Res. 2005 Jan;80(1):9-21 [15652521.001]
  • [Cites] Neuroscience. 2005;132(1):103-13 [15780470.001]
  • [Cites] J Neurosci. 2005 Apr 20;25(16):4108-17 [15843613.001]
  • [Cites] J Comp Neurol. 2005 Jul 18;488(1):70-81 [15912504.001]
  • [Cites] Vision Res. 2005 Sep;45(20):2659-67 [15923018.001]
  • [Cites] Vis Neurosci. 2005 May-Jun;22(3):263-74 [16079002.001]
  • [Cites] Vis Neurosci. 2005 May-Jun;22(3):317-24 [16079007.001]
  • [Cites] J Comp Neurol. 2005 Dec 12;493(2):274-90 [16255028.001]
  • [Cites] J Comp Neurol. 2006 Feb 1;494(4):651-62 [16374803.001]
  • [Cites] Neuron. 2006 Jan 5;49(1):81-94 [16387641.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2006 Apr;47(4):1682-90 [16565409.001]
  • [Cites] Mol Biol Cell. 2006 Apr;17(4):1652-63 [16452635.001]
  • [Cites] J Comp Neurol. 2006 Jun 10;496(5):698-705 [16615127.001]
  • [Cites] Exp Brain Res. 2006 Jul;172(3):322-30 [16501965.001]
  • [Cites] Neurosignals. 2006-2007;15(1):13-25 [16825800.001]
  • [Cites] BMC Neurosci. 2006;7:54 [16839421.001]
  • [Cites] J Comp Neurol. 2006 Nov 1;499(1):132-43 [16958091.001]
  • [Cites] Brain Res Bull. 2006 Dec 11;71(1-3):219-23 [17113949.001]
  • [Cites] J Comp Neurol. 2007 Jan 10;500(2):222-38 [17111372.001]
  • [Cites] J Comp Neurol. 2007 Feb 1;500(4):734-45 [17154255.001]
  • [Cites] Vis Neurosci. 2006 Nov-Dec;23(6):931-9 [17266785.001]
  • [Cites] J Membr Biol. 2006;213(2):89-100 [17417704.001]
  • [Cites] J Physiol. 2007 Jun 1;581(Pt 2):529-41 [17331999.001]
  • [Cites] Mol Psychiatry. 2007 Jul;12(7):612-3 [17592481.001]
  • [Cites] Vis Neurosci. 2007 Jul-Aug;24(4):489-502 [17640443.001]
  • [Cites] Neuron. 2007 Dec 6;56(5):851-65 [18054861.001]
  • [Cites] J Neurosci. 2008 Jan 9;28(2):456-64 [18184788.001]
  • [Cites] J Neurosci. 2008 May 7;28(19):4878-87 [18463241.001]
  • [Cites] J Neurosci. 2008 May 28;28(22):5691-5 [18509030.001]
  • [Cites] Genesis. 2008 Jul;46(7):357-67 [18615733.001]
  • [Cites] J Comp Neurol. 2008 Oct 10;510(5):525-38 [18680202.001]
  • [Cites] J Comp Neurol. 2009 Jan 1;512(1):6-26 [18975268.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2009 May;50(5):2417-26 [19117938.001]
  • [Cites] J Physiol. 2009 May 15;587(Pt 10):2353-64 [19332495.001]
  • [Cites] Exp Eye Res. 2009 Jun;88(6):1100-6 [19450446.001]
  • [Cites] J Neurosci. 2000 Jul 1;20(13):4904-11 [10864948.001]
  • [Cites] J Comp Neurol. 2000 Aug 14;424(1):1-23 [10888735.001]
  • [Cites] Neuron. 2000 Jul;27(1):85-95 [10939333.001]
  • [Cites] J Neurosci. 2000 Sep 15;20(18):6789-96 [10995822.001]
  • [Cites] J Physiol. 2001 Jul 15;534(Pt. 2):489-500 [11454966.001]
  • [Cites] Neurosci Lett. 2001 Sep 14;310(2-3):161-4 [11585592.001]
  • [Cites] J Neurosci. 2001 Nov 1;21(21):8636-47 [11606651.001]
  • [Cites] Brain Res. 2001 Nov 23;919(2):242-9 [11701136.001]
  • [Cites] Neuroscience. 2001;107(1):127-42 [11744253.001]
  • [Cites] Neuron. 2001 Dec 20;32(6):1107-17 [11754841.001]
  • [Cites] J Comp Neurol. 2002 Apr 8;445(3):227-37 [11920703.001]
  • [Cites] J Comp Neurol. 2002 Jul 15;449(1):76-87 [12115694.001]
  • [Cites] Glia. 2002 Sep;39(3):217-28 [12203388.001]
  • [Cites] Physiol Rev. 2002 Oct;82(4):875-91 [12270946.001]
  • [Cites] J Comp Neurol. 2002 Dec 9;454(2):168-76 [12412141.001]
  • [Cites] J Physiol. 2002 Nov 15;545(Pt 1):183-98 [12433959.001]
  • [Cites] J Neurosci. 2003 Jan 15;23(2):518-29 [12533612.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2003 Feb;44(2):856-65 [12556422.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Apr 1;100(7):4293-8 [12634427.001]
  • [Cites] J Neurophysiol. 2003 Sep;90(3):1363-74 [12966170.001]
  • [Cites] J Neurosci. 2003 Oct 29;23(30):9924-8 [14586022.001]
  • [Cites] Eur J Pharmacol. 2003 Oct 31;479(1-3):127-37 [14612144.001]
  • [Cites] J Neurosci. 2003 Nov 12;23(32):10249-57 [14614083.001]
  • [Cites] J Gen Physiol. 2003 Dec;122(6):657-71 [14610018.001]
  • [Cites] J Gen Physiol. 2003 Dec;122(6):653-6 [14610023.001]
  • [Cites] Pflugers Arch. 2004 Feb;447(5):519-31 [12719981.001]
  • [Cites] Pflugers Arch. 2004 Feb;447(5):756-9 [12750892.001]
  • [Cites] Diabetologia. 2004 Feb;47(2):221-4 [14676944.001]
  • [Cites] J Neurosci. 2004 Apr 14;24(15):3736-45 [15084653.001]
  • [Cites] Vision Res. 1996 Dec;36(24):3987-95 [9068851.001]
  • [Cites] Biochemistry. 1997 Mar 25;36(12):3535-42 [9132004.001]
  • [Cites] J Comp Neurol. 1997 Apr 21;380(4):449-71 [9087525.001]
  • [Cites] J Comp Neurol. 1997 Apr 21;380(4):520-32 [9087530.001]
  • [Cites] Nature. 1997 Oct 23;389(6653):870-6 [9349821.001]
  • [Cites] FEBS Lett. 1997 Nov 10;417(2):177-83 [9395291.001]
  • [Cites] J Comp Neurol. 1998 Jun 22;396(1):51-63 [9623887.001]
  • [Cites] Vision Res. 1998 May;38(10):1411-30 [9667008.001]
  • [Cites] Vis Neurosci. 1998 Jul-Aug;15(4):743-53 [9682875.001]
  • [Cites] Invest Ophthalmol Vis Sci. 1998 Aug;39(9):1685-93 [9699558.001]
  • [Cites] J Physiol. 1998 Nov 15;513 ( Pt 1):33-42 [9782157.001]
  • [Cites] J Neurosci. 1998 Dec 1;18(23):9733-50 [9822734.001]
  • [Cites] J Cell Sci. 1999 Mar;112 ( Pt 6):811-23 [10036231.001]
  • [Cites] Acta Ophthalmol Scand. 1999 Jun;77(3):255-60 [10406141.001]
  • [Cites] Int J Dev Neurosci. 1999 Jun;17(3):201-13 [10452364.001]
  • [Cites] Adv Neurol. 1999;79:189-201 [10514814.001]
  • (PMID = 20235161.001).
  • [ISSN] 1096-9861
  • [Journal-full-title] The Journal of comparative neurology
  • [ISO-abbreviation] J. Comp. Neurol.
  • [Language] eng
  • [Grant] United States / NEI NIH HHS / EY / R01 EY015573; United States / NEI NIH HHS / EY / R56 EY004067; United States / NEI NIH HHS / EY / R56 EY004067-29; United States / NEI NIH HHS / EY / EY 15573
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Calbindins; 0 / Isoenzymes; 0 / S100 Calcium Binding Protein G; 0 / Vesicular Inhibitory Amino Acid Transport Proteins; 0 / vesicular GABA transporter; 56-12-2 / gamma-Aminobutyric Acid; EC 4.1.1.15 / Glutamate Decarboxylase
  • [Other-IDs] NLM/ NIHMS500201; NLM/ PMC3736838
  •  go-up   go-down


29. Berkowitz BA, Roberts R, Oleske DA, Chang M, Schafer S, Bissig D, Gradianu M: Quantitative mapping of ion channel regulation by visual cycle activity in rodent photoreceptors in vivo. Invest Ophthalmol Vis Sci; 2009 Apr;50(4):1880-5
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • PURPOSE: To test the hypothesis that the extent of outer retina uptake of manganese, measured noninvasively with manganese-enhanced MRI (MEMRI), is a quantitative biomarker of photoreceptor ion channel regulation by visual cycle activity.
  • METHODS: Four groups of animals were studied: control rats adapted to three different background light intensities, dark-adapted control mice systemically pretreated with retinylamine, and dark-adapted mice with a nonsense mutation in exon 3 of the RPE65 gene (RPE65(rd12)) with and without systemic 11-cis-retinal pretreatment.
  • Central retinal thickness and intraretinal ion channel regulation were measured from the MEMRI data.
  • RESULT: No differences (P>0.05) in retinal thickness were noted within any arm of this study.
  • In rats, manganese uptake was inversely proportional to the background light intensity in the outer retina but not in the inner retina.
  • Specific inhibition at the level of RPE65 activity, either acutely with retinylamine or chronically in RPE65(rd12) mice, similarly reduced (P<0.05) outer retinal manganese uptake compared with that in control mice.
  • In RPE65(rd12) mice, outer retinal manganese uptake returned to normal (P>0.05) after 11-cis retinal treatment.
  • Inner retinal uptake was supernormal (P<0.05) in retinylamine-treated mice but normal in untreated or 11-cis treated RPE65(rd12) mice.
  • CONCLUSIONS: The present data support measuring the extent of manganese uptake in the outer retina as an analytic noninvasive metric of visual cycle regulation of photoreceptor ion channel activity in vivo.

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. MANGANESE, ELEMENTAL .
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Invest Ophthalmol Vis Sci. 2001 Nov;42(12):2964-9 [11687543.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2008 Nov;49(11):5083-8 [18552381.001]
  • [Cites] J Biol Chem. 2002 Oct 25;277(43):40491-8 [12176991.001]
  • [Cites] FEBS Lett. 2003 Sep 11;551(1-3):128-32 [12965217.001]
  • [Cites] Exp Eye Res. 2003 Nov;77(5):627-38 [14550405.001]
  • [Cites] J Physiol. 2003 Nov 1;552(Pt 3):763-76 [12949220.001]
  • [Cites] Invest Ophthalmol. 1976 Jan;15(1):64-70 [1245384.001]
  • [Cites] Invest Ophthalmol Vis Sci. 1978 Jun;17(6):489-98 [659071.001]
  • [Cites] Magn Reson Med. 1993 Jul;30(1):18-27 [8371670.001]
  • [Cites] Invest Ophthalmol Vis Sci. 1994 Jan;35(1):9-32 [7507907.001]
  • [Cites] Invest Ophthalmol Vis Sci. 1996 Sep;37(10):2089-98 [8814148.001]
  • [Cites] Nat Genet. 1997 Oct;17(2):139-41 [9326927.001]
  • [Cites] NMR Biomed. 2004 Dec;17(8):532-43 [15617052.001]
  • [Cites] Mol Vis. 2005 Feb 28;11:152-62 [15765048.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jun 7;102(23):8162-7 [15917330.001]
  • [Cites] Nat Neurosci. 2005 Jul;8(7):961-8 [15924136.001]
  • [Cites] Bioessays. 2006 Apr;28(4):344-54 [16547945.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2006 Jun;47(6):2668-74 [16723485.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Jul 5;103(27):10432-7 [16788070.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2006 Aug;47(8):3579-85 [16877432.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Nov 14;103(46):17525-30 [17088544.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2007 Aug;48(8):3796-804 [17652754.001]
  • [Cites] Mol Vis. 2007;13:1701-10 [17960108.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2008 Jul;49(7):3178-84 [18362105.001]
  • [Cites] Prog Retin Eye Res. 2008 Jul;27(4):391-419 [18632300.001]
  • [Cites] Vis Neurosci. 2002 Jan-Feb;19(1):61-70 [12180860.001]
  • (PMID = 19060264.001).
  • [ISSN] 1552-5783
  • [Journal-full-title] Investigative ophthalmology & visual science
  • [ISO-abbreviation] Invest. Ophthalmol. Vis. Sci.
  • [Language] ENG
  • [Grant] United States / NEI NIH HHS / EY / EY018109-02; United States / NEI NIH HHS / EY / R21 EY018109; United States / NEI NIH HHS / EY / EY018109; United States / NEI NIH HHS / EY / R21 EY018109-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Carrier Proteins; 0 / Diterpenes; 0 / Eye Proteins; 0 / Ion Channels; 42Z2K6ZL8P / Manganese; 43219-27-8 / retinylamine; EC 3.1.1.64 / retinoid isomerohydrolase; EC 5.2.- / cis-trans-Isomerases
  • [Other-IDs] NLM/ NIHMS109112; NLM/ PMC2696261
  •  go-up   go-down


30. Okuno T, Oku H, Sugasawa J, Hamamura HW, Nakamura K, Ikeda T: [The ocular features in a father and a son with central areolar choroidal dystrophy]. Nippon Ganka Gakkai Zasshi; 2008 Aug;112(8):688-94
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Optical coherence tomography (OCT) at the chorioretinal atrophy areas showed thinning of retinal thickness with a disappearance of a line corresponding to the outer segment of the photoreceptor cells, but thickening of a line of the retinal pigment epithelium.
  • His OCT also showed findings similar to those of case 1, but the retina was thinner than in case 1 in the chorioretinal atrophy area.
  • DISCUSSION: The rest of the retina outside the chorioretinal atrophy area in these CACD patients also seemed to be damaged because both the ERG and EOG showed damage.
  • These two cases revealed that a CACD patient could maintain relatively good visual acuity, even though the chorioretinal atrophy had involved the foveal area, and also indications were that retinal functions had been damaged.

  • Genetic Alliance. consumer health - Choroidal Dystrophy Central Areolar.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18767495.001).
  • [ISSN] 0029-0203
  • [Journal-full-title] Nippon Ganka Gakkai zasshi
  • [ISO-abbreviation] Nippon Ganka Gakkai Zasshi
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  •  go-up   go-down


31. Lai H, Zeng H, Zhang C, Wang L, Tso MO, Lai S: Toxic effect of methamphetamine on the retina of CD1 mice. Curr Eye Res; 2009 Sep;34(9):785-90
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Toxic effect of methamphetamine on the retina of CD1 mice.
  • PURPOSE: To investigate whether systemic administration of methamphetamine (METH) induces retinal damage in CD1 mice.
  • Immunostaining of glial fibrillary acidic protein (GFAP), S-100 for astrocytes and Muller cells, CD11b for microglia, and tyrosine hydroxylase (TH) and TUNEL labeling for apoptotic cell death were performed on the retinal sections on day 1 and day 7 post-exposure.
  • The results suggest that METH has a neurotoxic effect on CD1 mouse retina.

  • MedlinePlus Health Information. consumer health - Methamphetamine.
  • MedlinePlus Health Information. consumer health - Retinal Disorders.
  • Hazardous Substances Data Bank. d-METHAMPHETAMINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Pharmacol Exp Ther. 1994 Aug;270(2):752-60 [8071868.001]
  • [Cites] Brain Res Dev Brain Res. 1993 Apr 16;72(2):325-8 [8097974.001]
  • [Cites] Brain Res. 1998 Sep 21;806(1):1-7 [9739098.001]
  • [Cites] Birth Defects Res A Clin Mol Teratol. 2005 Jun;73(6):455-60 [15880787.001]
  • [Cites] Prog Neurobiol. 2005 Apr;75(6):406-33 [15955613.001]
  • [Cites] Brain Res. 2005 Jul 19;1050(1-2):190-8 [15987631.001]
  • [Cites] Brain Res. 2005 Jul 12;1049(2):171-81 [16043139.001]
  • [Cites] BMJ. 2005 Sep 3;331(7515):476 [16141155.001]
  • [Cites] Ann N Y Acad Sci. 2006 Aug;1074:590-603 [17105955.001]
  • [Cites] Ann N Y Acad Sci. 2006 Aug;1074:604-19 [17105956.001]
  • [Cites] Int J Neurosci. 2007 Jan;117(1):1-9 [17365096.001]
  • [Cites] Doc Ophthalmol. 2008 Nov;117(3):245-55 [18563464.001]
  • [Cites] Brain Res. 2000 Apr 28;863(1-2):106-11 [10773198.001]
  • [Cites] Brain Res Brain Res Rev. 2001 Aug;36(1):1-22 [11516769.001]
  • [Cites] Brain Res Mol Brain Res. 2001 Sep 10;93(1):64-9 [11532339.001]
  • [Cites] Ann N Y Acad Sci. 2002 Jun;965:522-8 [12105127.001]
  • [Cites] J Chem Neuroanat. 2002 Jul;24(2):95-107 [12191726.001]
  • [Cites] Neurosci Lett. 2003 Nov 27;352(1):13-6 [14615038.001]
  • [Cites] Int Rev Cytol. 2003;230:263-90 [14692684.001]
  • [Cites] Brain Res Dev Brain Res. 2003 Dec 30;147(1-2):153-62 [14741760.001]
  • [Cites] Doc Ophthalmol. 2004 Jan;108(1):17-40 [15104164.001]
  • [Cites] Neurosci Lett. 2004 Sep 9;367(3):349-54 [15337264.001]
  • [Cites] J Pharmacol Exp Ther. 2004 Oct;311(1):1-7 [15163680.001]
  • [Cites] Neurochem Int. 2004 Dec;45(8):1133-41 [15380623.001]
  • [Cites] Exp Eye Res. 1979 Jan;28(1):63-9 [376324.001]
  • [Cites] Eur J Pharmacol. 1980 Aug 29;66(2-3):201-5 [6108224.001]
  • [Cites] J Neurocytol. 1990 Jun;19(3):338-42 [1975269.001]
  • [Cites] J Neurosci. 1995 Feb;15(2):1308-17 [7869099.001]
  • (PMID = 19839872.001).
  • [ISSN] 1460-2202
  • [Journal-full-title] Current eye research
  • [ISO-abbreviation] Curr. Eye Res.
  • [Language] ENG
  • [Grant] United States / NIDA NIH HHS / DA / R01 DA012777; United States / NIDA NIH HHS / DA / DA012777-10; United States / NIDA NIH HHS / DA / R01 DA015020-01A1; United States / NIDA NIH HHS / DA / DA-15020; United States / NIDA NIH HHS / DA / R01 DA015020; United States / NIDA NIH HHS / DA / R01 DA012777-10; United States / NIDA NIH HHS / DA / DA015020-01A1
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD11b; 0 / Dopamine Agents; 0 / Glial Fibrillary Acidic Protein; 0 / S100 Proteins; 44RAL3456C / Methamphetamine; EC 1.14.16.2 / Tyrosine 3-Monooxygenase
  • [Other-IDs] NLM/ NIHMS141581; NLM/ PMC2765663
  •  go-up   go-down


32. Townsend KA, Wollstein G, Danks D, Sung KR, Ishikawa H, Kagemann L, Gabriele ML, Schuman JS: Heidelberg Retina Tomograph 3 machine learning classifiers for glaucoma detection. Br J Ophthalmol; 2008 Jun;92(6):814-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Heidelberg Retina Tomograph 3 machine learning classifiers for glaucoma detection.
  • AIMS: To assess performance of classifiers trained on Heidelberg Retina Tomograph 3 (HRT3) parameters for discriminating between healthy and glaucomatous eyes.

  • Genetic Alliance. consumer health - Glaucoma.
  • MedlinePlus Health Information. consumer health - Glaucoma.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Invest Ophthalmol Vis Sci. 2006 Aug;47(8):3374-80 [16877405.001]
  • [Cites] J Glaucoma. 2006 Aug;15(4):299-305 [16865006.001]
  • [Cites] Ophthalmology. 2007 Mar;114(3):466-71 [17141321.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2007 Jun;48(6):2653-60 [17525196.001]
  • [Cites] Ophthalmology. 2007 Nov;114(11):1981-7 [17445899.001]
  • [Cites] Br J Ophthalmol. 1999 Jun;83(6):664-9 [10340972.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2000 Jun;41(7):1730-42 [10845593.001]
  • [Cites] Am J Ophthalmol. 2001 Jul;132(1):57-62 [11438054.001]
  • [Cites] Arch Ophthalmol. 2001 Jul;119(7):985-93 [11448320.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2002 Nov;43(11):3444-54 [12407155.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2004 Sep;45(9):3144-51 [15326133.001]
  • [Cites] Arch Ophthalmol. 1977 Dec;95(12):2149-56 [588106.001]
  • [Cites] Biometrics. 1988 Sep;44(3):837-45 [3203132.001]
  • [Cites] Arch Ophthalmol. 1991 Jan;109(1):77-83 [1987954.001]
  • [Cites] Ophthalmology. 1992 Jan;99(1):19-28 [1741133.001]
  • [Cites] Ophthalmology. 1998 Aug;105(8):1557-63 [9709774.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2005 Nov;46(11):4121-9 [16249489.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2005 Nov;46(11):4147-52 [16249492.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2006 Dec;47(12):5348-55 [17122123.001]
  • (PMID = 18523087.001).
  • [ISSN] 1468-2079
  • [Journal-full-title] The British journal of ophthalmology
  • [ISO-abbreviation] Br J Ophthalmol
  • [Language] ENG
  • [Grant] United States / NEI NIH HHS / EY / R01 EY013178-08; United States / NEI NIH HHS / EY / EY013178-08; United States / NEI NIH HHS / EY / R01-EY013178; United States / NEI NIH HHS / EY / P30 EY008098-20; United States / NEI NIH HHS / EY / R01 EY013178; United States / NEI NIH HHS / EY / P30-EY008098; United States / NEI NIH HHS / EY / P30 EY008098
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ NIHMS84279; NLM/ PMC2916743
  •  go-up   go-down


33. Youn HY, Chou BR, Cullen AP, Sivak JG: Effects of 400 nm, 420 nm, and 435.8 nm radiations on cultured human retinal pigment epithelial cells. J Photochem Photobiol B; 2009 Apr 2;95(1):64-70
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effects of 400 nm, 420 nm, and 435.8 nm radiations on cultured human retinal pigment epithelial cells.
  • The present study demonstrates narrowband short-wavelengths radiation- (400, 420, and 435.8 nm) induced cellular damage of cultured human retinal pigment epithelial cells using in vitro biological assays to determine wavelengths that are responsible for photochemical lesions of the retina.
  • This work involved the exposure of retinal pigment epithelial (RPE) cells (ARPE-19) to narrowband light of three different wavelengths (400, 420, and 435.8 nm) using a xenon arc lamp and interference filters.
  • [MeSH-major] Epithelial Cells / radiation effects. Light. Pigment Epithelium of Eye / radiation effects. Retinal Pigments / radiation effects

  • COS Scholar Universe. author profiles.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19201202.001).
  • [ISSN] 1873-2682
  • [Journal-full-title] Journal of photochemistry and photobiology. B, Biology
  • [ISO-abbreviation] J. Photochem. Photobiol. B, Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Retinal Pigments
  •  go-up   go-down


34. Wurm A, Pannicke T, Iandiev I, Bühner E, Pietsch UC, Reichenbach A, Wiedemann P, Uhlmann S, Bringmann A: Changes in membrane conductance play a pathogenic role in osmotic glial cell swelling in detached retinas. Am J Pathol; 2006 Dec;169(6):1990-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Detachment of the neural retina from the pigment epithelium may be associated with tissue edema; however, the mechanisms of fluid accumulation are not understood.
  • Because retinal detachment is usually not accompanied by vascular leakage, we investigated whether the osmotic swelling characteristics of retinal glial (Müller) cells are changed after experimental detachment of the porcine retina.
  • Osmotic stress, induced by application of a hypotonic bath solution to retinal slices, caused swelling of Müller cell bodies in 7-day-detached retinas, but no swelling was inducible in slices of control retinas.
  • Müller cell somata in slices of retinal areas that surround local detachment in situ also showed osmotic swelling, albeit at a smaller amplitude.
  • The amplitude of osmotic Müller cell swelling correlated with the decrease in the K+ conductance, suggesting a causal relationship between both gliotic alterations.
  • We propose that a dysregulation of the ion and water transport through Müller cells may impair the fluid absorption from the retinal tissue, resulting in chronic fluid accumulation after detachment.
  • This knowledge may lead to a better understanding of the mechanisms involved in retinal degeneration after detachment.
  • [MeSH-major] Cell Membrane / physiology. Neuroglia / physiology. Retinal Detachment / metabolism

  • MedlinePlus Health Information. consumer health - Retinal Detachment.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Invest Ophthalmol Vis Sci. 2001 Apr;42(5):1072-9 [11274088.001]
  • [Cites] J Neurosci. 2000 Aug 1;20(15):5733-40 [10908613.001]
  • [Cites] Graefes Arch Clin Exp Ophthalmol. 2002 Feb;240(2):85-9 [11931084.001]
  • [Cites] J Neurocytol. 2001 May;30(5):379-90 [11951049.001]
  • [Cites] Ophthalmology. 2002 May;109(5):920-7 [11986098.001]
  • [Cites] Surv Ophthalmol. 2002 Aug;47 Suppl 1:S203-18 [12204717.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2002 Nov;43(11):3555-66 [12407168.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2002 Nov;43(11):3567-74 [12407169.001]
  • [Cites] Exp Eye Res. 2003 Mar;76(3):333-42 [12573662.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2003 Sep;44(9):4026-34 [12939325.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2003 Sep;44(9):4114-22 [12939335.001]
  • [Cites] Semin Ophthalmol. 2003 Jun;18(2):67-73 [14566625.001]
  • [Cites] Glia. 2004 Jan 1;45(1):59-66 [14648546.001]
  • [Cites] Mol Cell Neurosci. 2004 Aug;26(4):493-502 [15276152.001]
  • [Cites] Am J Ophthalmol. 1968 Sep;66(3):396-410 [4970986.001]
  • [Cites] Bibl Ophthalmol. 1969;79:80-90 [4981416.001]
  • [Cites] Invest Ophthalmol Vis Sci. 1986 Feb;27(2):168-83 [3943943.001]
  • [Cites] Science. 1987 Aug 21;237(4817):896-8 [3616619.001]
  • [Cites] Nippon Ganka Gakkai Zasshi. 1989 Oct;93(10):1002-8 [2603845.001]
  • [Cites] Invest Ophthalmol Vis Sci. 1991 May;32(6):1739-48 [2032796.001]
  • [Cites] Nippon Ganka Gakkai Zasshi. 1992 Feb;96(2):259-64 [1558024.001]
  • [Cites] J Neurosci. 1993 Aug;13(8):3333-45 [8340811.001]
  • [Cites] Arch Ophthalmol. 1994 Jan;112(1):117-22 [8285878.001]
  • [Cites] Am J Ophthalmol. 1994 Sep 15;118(3):368-76 [7916177.001]
  • [Cites] J Cereb Blood Flow Metab. 1994 Nov;14(6):1030-9 [7929645.001]
  • [Cites] Invest Ophthalmol Vis Sci. 1995 May;36(6):990-6 [7730033.001]
  • [Cites] Trends Neurosci. 1996 Aug;19(8):307-12 [8843598.001]
  • [Cites] J Neurosci. 1997 Apr 1;17(7):2324-37 [9065493.001]
  • [Cites] Invest Ophthalmol Vis Sci. 1998 Feb;39(2):424-34 [9478003.001]
  • [Cites] Invest Ophthalmol Vis Sci. 1998 Aug;39(9):1694-702 [9699559.001]
  • [Cites] Pharmacol Rev. 1998 Sep;50(3):413-92 [9755289.001]
  • [Cites] Glia. 1999 Mar;26(1):47-54 [10088671.001]
  • [Cites] Am J Ophthalmol. 1999 Aug;128(2):155-64 [10458170.001]
  • [Cites] Am J Ophthalmol. 1999 Aug;128(2):165-72 [10458171.001]
  • [Cites] Ophthalmic Res. 2004 Sep-Oct;36(5):241-9 [15583429.001]
  • [Cites] Klin Oczna. 2004;106(4-5):581-4 [15646473.001]
  • [Cites] Prog Retin Eye Res. 2005 May;24(3):395-431 [15708835.001]
  • [Cites] J Pharmacol Exp Ther. 2005 Dec;315(3):1036-45 [16144977.001]
  • [Cites] Diabetes. 2006 Mar;55(3):633-9 [16505225.001]
  • [Cites] J Neurosci Res. 2006 Mar;83(4):538-50 [16435394.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2006 May;47(5):2161-71 [16639028.001]
  • [Cites] J Comp Neurol. 2002 Oct 28;452(4):392-9 [12355421.001]
  • [Cites] Am J Ophthalmol. 2000 Feb;129(2):186-90 [10682971.001]
  • [Cites] Doc Ophthalmol. 1999;97(3-4):239-49 [10896337.001]
  • [Cites] Doc Ophthalmol. 1999;97(3-4):297-309 [10896343.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2001 May;42(6):1363-9 [11328752.001]
  • (PMID = 17148663.001).
  • [ISSN] 0002-9440
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hypotonic Solutions; 0 / Potassium Channels, Inwardly Rectifying; 0 / Purines; W60KTZ3IZY / purine
  • [Other-IDs] NLM/ PMC1780250
  •  go-up   go-down


35. Hilbe MM, Soldati GG, Zlinszky KK, Wunderlin SS, Ehrensperger FF: Immunohistochemical study of PrP(Sc) distribution in neural and extraneural tissues of two cats with feline spongiform encephalopathy. BMC Vet Res; 2009;5:11
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Two domestic shorthair cats presenting with progressive hind-limb ataxia and increased aggressiveness were necropsied and a post mortem diagnosis of Feline Spongiform Encephalopathy (FSE) was made.
  • In addition, a diffuse glial reaction involving astrocytes and microglia and intraneuronal vacuolation in a few neurons in the brain stem was present.Heavy PrPSc immunostaining was detected in brain, retina, optic nerve, pars nervosa of the pituitary gland, trigeminal ganglia and small amounts in the myenteric plexus of the small intestine (duodenum, jejunum) and slightly in the medulla of the adrenal gland.
  • The pattern of abnormal PrP in the retina corresponded to that found in a captive cheetah with FSE, in sheep with scrapie and was similar to nvCJD in humans.

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Comp Pathol. 2001 Jul;125(1):48-57 [11437516.001]
  • [Cites] Schweiz Arch Tierheilkd. 2002 Oct;144(10):550-7 [12442705.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2003 Jan;44(1):342-6 [12506094.001]
  • [Cites] Vet Rec. 2003 Mar 29;152(13):387-92 [12696704.001]
  • [Cites] Histochem Cell Biol. 2003 May;119(5):415-22 [12783238.001]
  • [Cites] Vet Rec. 1990 Dec 15;127(24):586-8 [2075687.001]
  • [Cites] Vet Rec. 1991 Sep 14;129(11):233-6 [1957458.001]
  • [Cites] Vet Rec. 1992 Oct 3;131(14):307-10 [1279883.001]
  • [Cites] Aust Vet J. 1992 Jul;69(7):171 [1445084.001]
  • [Cites] Vet Rec. 1992 Nov 7;131(19):431-4 [1455592.001]
  • [Cites] Vet Rec. 1994 Apr 23;134(17):449 [8048218.001]
  • [Cites] Vet Rec. 1995 Apr 29;136(17):444 [7631481.001]
  • [Cites] Nature. 1996 Oct 24;383(6602):685-90 [8878476.001]
  • [Cites] Vet Rec. 1997 Sep 13;141(11):270-1 [9316242.001]
  • [Cites] Nature. 1997 Oct 2;389(6650):498-501 [9333239.001]
  • [Cites] Lancet. 1998 Oct 3;352(9134):1116-7 [9798590.001]
  • [Cites] J Virol. 1999 Nov;73(11):9386-92 [10516047.001]
  • [Cites] Brain Res. 2006 Sep 7;1108(1):188-94 [16836987.001]
  • [Cites] Vet Pathol. 2006 Sep;43(5):733-9 [16966452.001]
  • [Cites] PLoS One. 2007;2(9):e859 [17848990.001]
  • [Cites] J Comp Pathol. 2008 Jan;138(1):12-22 [18061608.001]
  • [Cites] J Pathol. 2008 Jun;215(2):126-34 [18381605.001]
  • [Cites] Emerg Infect Dis. 2008 Sep;14(9):1406-12 [18760007.001]
  • [Cites] Vet Rec. 2001 Apr 7;148(14):437-41 [11338713.001]
  • [CommentIn] BMC Vet Res. 2010;6:41 [20684771.001]
  • (PMID = 19335885.001).
  • [ISSN] 1746-6148
  • [Journal-full-title] BMC veterinary research
  • [ISO-abbreviation] BMC Vet. Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / PrPSc Proteins
  • [Other-IDs] NLM/ PMC2673214
  •  go-up   go-down


36. Yao Y, Jiang L, Wang ZJ, Zhang MN: Scleral buckling procedures for longstanding or chronic rhegmatogenous retinal detachment with subretinal proliferation. Ophthalmology; 2006 May;113(5):821-5
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Scleral buckling procedures for longstanding or chronic rhegmatogenous retinal detachment with subretinal proliferation.
  • OBJECTIVE: To investigate longstanding or chronic retinal detachments (RDs) with subretinal strands and their clinical features and therapeutic effects using conventional retinal surgery.
  • MAIN OUTCOME MEASURES: Visual acuity (VA) and postoperative anatomic retinal reattachment at the final follow-up visit between 3 and 24 months (mean, 6.9).
  • Longstanding or chronic RD with subretinal proliferation had subretinal proliferative strands (i.e., a shallow RD) and a smooth atrophic detached retina, not a thickened retina.
  • [MeSH-major] Retinal Detachment / surgery. Scleral Buckling / methods. Vitreoretinopathy, Proliferative / surgery

  • MedlinePlus Health Information. consumer health - Retinal Detachment.
  • Hazardous Substances Data Bank. SULFUR HEXAFLUORIDE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Ophthalmology. 2007 Aug;114(8):1591-2; author reply 1592 [17678707.001]
  • (PMID = 16650678.001).
  • [ISSN] 1549-4713
  • [Journal-full-title] Ophthalmology
  • [ISO-abbreviation] Ophthalmology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] WS7LR3I1D6 / Sulfur Hexafluoride
  •  go-up   go-down


37. Yang SS, McDonald HR, Everett AI, Johnson RN, Jumper JM, Fu AD: Retinal damage caused by air-fluid exchange during pars plana vitrectomy. Retina; 2006 Mar;26(3):334-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Retinal damage caused by air-fluid exchange during pars plana vitrectomy.
  • PURPOSE: To report two cases of retinal damage associated with air infusion during pars plana vitrectomy.
  • METHODS: The authors reviewed the course of two patients who had retinal damage during par plana vitrectomy and air-fluid exchange for the treatment of macular hole and optic pit-related macular detachment, respectively.
  • RESULTS: As a result of high air infusion flow during air-fluid exchange, retinal damage was created in the area contralateral to the infusion port.
  • This area subsequently developed into a large retinal break associated with retinal detachment.
  • In the second case, retinal whitening was noted intraoperatively.
  • CONCLUSIONS: High infusion flow during air-fluid exchange in eyes undergoing vitrectomy surgery may result in significant retinal damage.
  • This pressure-induced trauma initially causes retinal whitening that may be seen intraoperatively or during the early postoperative period.
  • The region of damaged retina may develop a retinal break and detachment or a corresponding visual field defect.
  • [MeSH-major] Air. Eye Injuries / etiology. Intraoperative Complications. Retina / injuries. Retinal Diseases / etiology. Vitrectomy / adverse effects

  • MedlinePlus Health Information. consumer health - Eye Injuries.
  • MedlinePlus Health Information. consumer health - Retinal Disorders.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16508435.001).
  • [ISSN] 0275-004X
  • [Journal-full-title] Retina (Philadelphia, Pa.)
  • [ISO-abbreviation] Retina (Philadelphia, Pa.)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


38. de Crecchio G, Alfieri MC, Cennamo G, Forte R: Congenital macular macrovessels. Graefes Arch Clin Exp Ophthalmol; 2006 Sep;244(9):1183-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: From the records of patients with vascular anomalies seen at the Retina Department of the University Federico II in Naples from 1980 to 2005, we reviewed all cases presenting an abnormal, large, retinal vessel crossing the macular region.
  • In one case late, mild, intraretinal staining along the anomalous vessel indicated retinal oedema.
  • [MeSH-major] Retinal Diseases / etiology. Retinal Vein / abnormalities
  • [MeSH-minor] Adolescent. Aged. Child, Preschool. Eye Abnormalities / diagnosis. Eye Abnormalities / etiology. Fluorescein Angiography. Humans. Male. Ophthalmoscopy. Visual Acuity

  • MedlinePlus Health Information. consumer health - Retinal Disorders.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Ophthalmologica. 1986;193(3):143-5 [3561945.001]
  • [Cites] Br Med Bull. 1970 May;26(2):103-6 [4911762.001]
  • [Cites] AMA Arch Ophthalmol. 1956 Jan;55(1):119-22 [13275183.001]
  • [Cites] Am J Ophthalmol. 1973 Feb;75(2):224-41 [4697179.001]
  • [Cites] Arch Ophthalmol. 1982 Sep;100(9):1430-6 [7115168.001]
  • [Cites] Arch Ophthalmol. 2000 Jan;118(1):146-7 [10636437.001]
  • (PMID = 16453126.001).
  • [ISSN] 0721-832X
  • [Journal-full-title] Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie
  • [ISO-abbreviation] Graefes Arch. Clin. Exp. Ophthalmol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Germany
  •  go-up   go-down


39. Rucci M, Casile A: Fixational instability and natural image statistics: implications for early visual representations. Network; 2005 Jun-Sep;16(2-3):121-38
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • It is known that stimuli tend to fade when they are stabilized on the retina for several seconds.
  • However, it is unclear whether the physiological motion of the retinal image serves a visual purpose during the brief periods of natural visual fixation.
  • This study examines the impact of fixational instability on the statistics of the visual input to the retina and on the structure of neural activity in the early visual system.
  • We show that fixational instability introduces a component in the retinal input signals that, in the presence of natural images, lacks spatial correlations.

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16411492.001).
  • [ISSN] 0954-898X
  • [Journal-full-title] Network (Bristol, England)
  • [ISO-abbreviation] Network
  • [Language] eng
  • [Grant] United States / NEI NIH HHS / EY / EY15732-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  •  go-up   go-down


40. Framme C, Walter A, Prahs P, Regler R, Theisen-Kunde D, Alt C, Brinkmann R: Structural changes of the retina after conventional laser photocoagulation and selective retina treatment (SRT) in spectral domain OCT. Curr Eye Res; 2009 Jul;34(7):568-79
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Structural changes of the retina after conventional laser photocoagulation and selective retina treatment (SRT) in spectral domain OCT.
  • BACKGROUND: Spectral domain optical coherence tomography (SD-OCT) in patients can deliver retinal cross-sectional images with high resolution.
  • This may allow the evaluation of the extent of damage to the retinal pigment epithelium (RPE) and the neurosensory retina after laser treatment.
  • This article aims to investigate the value of SD-OCT in comparing laser lesions produced by conventional laser photocoagulation and selective retina treatment (SRT).
  • MATERIAL AND METHODS: In a retrospective study, conventional retinal laser (CRL) lesions and SRT laser lesions were evaluated with SD-OCT.
  • CRL lesions were applied with an ophthalmoscopically slightly grayish-white appearance (Nd:YAG laser at 532-nm wavelength; power 100-200 mW; retinal spot diameter 100 microm; pulse duration 100 ms).
  • SRT lesions were applied with a Nd:YLF (527 nm; pulse duration 200 ns [30 pulses at 100 Hz]; energy 100-200 microJ/pulse; retinal spot diameter 200 microm) and were visible only angiographically.
  • In contrast, the neural retina appeared unaffected after SRT.
  • RPE atrophy appeared subsequently only in CRL lesions, whereas the neurosensory retina appeared unaffected following SRT.
  • These results suggest the selective effect of SRT in humans without causing adverse effects to the neurosensory retina.
  • [MeSH-major] Laser Coagulation / adverse effects. Lasers, Solid-State / adverse effects. Postoperative Complications. Retina / pathology. Retinal Diseases / diagnosis. Retinal Diseases / surgery. Tomography, Optical Coherence
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Atrophy. Humans. Middle Aged. Retinal Pigment Epithelium / pathology. Retrospective Studies


41. Zangerl B, Lindauer SJ, Acland GM, Aguirre GD: Identification of genetic variation and haplotype structure of the canine ABCA4 gene for retinal disease association studies. Mol Genet Genomics; 2010 Oct;284(4):243-50
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of genetic variation and haplotype structure of the canine ABCA4 gene for retinal disease association studies.
  • Over 200 mutations in the retina specific member of the ATP-binding cassette transporter superfamily (ABCA4) have been associated with a diverse group of human retinal diseases.
  • As orthologous genes are commonly mutated in canine models of human blinding disorders, canine ABCA4 appears to be an ideal candidate gene to identify and study sequence changes in dogs affected by various forms of inherited retinal degeneration.
  • [MeSH-major] ATP-Binding Cassette Transporters / genetics. Polymorphism, Single Nucleotide. Retinal Diseases / genetics
  • [MeSH-minor] Amino Acid Substitution. Animals. Dog Diseases / genetics. Dogs / genetics. Female. Genetic Variation. Humans. Male. Models, Animal. Mutation. Retinal Degeneration / genetics. Retinal Degeneration / veterinary. Species Specificity

  • MedlinePlus Health Information. consumer health - Retinal Disorders.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Bioinformatics. 2005 Jan 1;21(1):131-4 [15333454.001]
  • [Cites] Graefes Arch Clin Exp Ophthalmol. 2005 Feb;243(2):90-100 [15614537.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2007 May;48(5):1959-67 [17460247.001]
  • [Cites] Am J Hum Genet. 2002 Dec;71(6):1480-2 [12515255.001]
  • [Cites] Nat Genet. 1997 Sep;17(1):15-6 [9288089.001]
  • [Cites] Trans Am Ophthalmol Soc. 2003;101:437-84 [14971589.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2002 Jun;43(6):1980-5 [12037008.001]
  • [Cites] Science. 2004 May 21;304(5674):1160-4 [15155949.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2005 Dec;46(12):4739-46 [16303974.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 May 1;90(9):3968-72 [8387203.001]
  • [Cites] Science. 1997 Sep 19;277(5333):1805-7 [9295268.001]
  • [Cites] Hum Mol Genet. 1998 Mar;7(3):355-62 [9466990.001]
  • [Cites] Pflugers Arch. 2007 Feb;453(5):581-9 [16586097.001]
  • [Cites] J Bioenerg Biomembr. 2001 Dec;33(6):523-30 [11804194.001]
  • [Cites] Mol Vis. 2004 Mar 29;10:223-32 [15064680.001]
  • [Cites] BMC Vet Res. 2008;4:23 [18593457.001]
  • [Cites] Hum Mol Genet. 2001 Nov 1;10(23):2671-8 [11726554.001]
  • [Cites] Biochim Biophys Acta. 2009 Jul;1791(7):573-83 [19230850.001]
  • [Cites] J Negat Results Biomed. 2006;5:19 [17134500.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2008 Feb;49(2):772-80 [18235027.001]
  • [Cites] Nature. 2010 Apr 8;464(7290):898-902 [20237475.001]
  • [Cites] Arch Ophthalmol. 2007 Feb;125(2):205-12 [17296896.001]
  • [Cites] PLoS One. 2007;2(12):e1324 [18091995.001]
  • [Cites] Cell. 1999 Jul 9;98(1):13-23 [10412977.001]
  • [Cites] Genomics. 2006 Nov;88(5):551-63 [16938425.001]
  • [Cites] Evol Bioinform Online. 2007 Feb 23;1:47-50 [19325852.001]
  • [Cites] J Biol Chem. 1999 Mar 19;274(12):8269-81 [10075733.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Apr 15;100(8):4742-7 [12671074.001]
  • [Cites] Mamm Genome. 2009 Feb;20(2):109-23 [19130129.001]
  • [Cites] Genomics. 2006 Sep;88(3):293-301 [16806805.001]
  • [Cites] Nat Genet. 2000 Oct;26(2):242-6 [11017087.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2008 Sep;49(9):3821-9 [18515570.001]
  • [Cites] Nature. 2005 Dec 8;438(7069):803-19 [16341006.001]
  • [Cites] Science. 2007 Apr 13;316(5822):222-34 [17431167.001]
  • [Cites] Eur J Hum Genet. 2008 Jul;16(7):812-9 [18285826.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2001 May;42(6):1179-89 [11328725.001]
  • [Cites] Hum Mol Genet. 2009 Mar 1;18(5):931-41 [19074458.001]
  • (PMID = 20661590.001).
  • [ISSN] 1617-4623
  • [Journal-full-title] Molecular genetics and genomics : MGG
  • [ISO-abbreviation] Mol. Genet. Genomics
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / R24 GM082910-04; United States / NIGMS NIH HHS / GM / R24 GM082910; United States / NEI NIH HHS / EY / R01 EY006855; United States / NEI NIH HHS / EY / P30 EY-001583; United States / NEI NIH HHS / EY / R01 EY017549-01A1; United States / NEI NIH HHS / EY / EY-06855; United States / PHS HHS / / 017549; United States / NEI NIH HHS / EY / P30 EY001583; United States / NEI NIH HHS / EY / R01 EY017549; United States / NEI NIH HHS / EY / R01 EY006855-25
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / ABCA4 protein, human; 0 / ATP-Binding Cassette Transporters
  • [Other-IDs] NLM/ NIHMS240990; NLM/ PMC2954605
  •  go-up   go-down


42. Hagigit T, Abdulrazik M, Orucov F, Valamanesh F, Hagedorn M, Lambert G, Behar-Cohen F, Benita S: Topical and intravitreous administration of cationic nanoemulsions to deliver antisense oligonucleotides directed towards VEGF KDR receptors to the eye. J Control Release; 2010 Aug 3;145(3):297-305
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Our results showed that below 10 microl/ml, a 2.5% mid-chain triglycerides cationic DOTAP nanoemulsion was non-toxic on HUVEC and retinal cells.
  • The kinetic results of fluorescent ODN (Hex) distribution in DOTAP nanoemulsion following intravitreal injection in the rat showed that the nanoemulsion penetrates all retinal cells.
  • Pharmacokinetic and ocular tissue distribution of radioactive ODN following intravitreal injection in rabbits showed that the DOTAP nanoemulsion apparently enhanced the intraretinal penetration of the ODNs up to the inner nuclear layer (INL) and might yield potential therapeutic levels of ODN in the retina over 72 h post injection.
  • [MeSH-minor] Administration, Topical. Animals. Cations / chemistry. Cell Line. Cell Line, Tumor. Cell Survival. Humans. Male. Rabbits. Rats. Rats, Inbred Lew. Thionucleotides / administration & dosage

  • MedlinePlus Health Information. consumer health - Eye Care.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright (c) 2010 Elsevier B.V. All rights reserved.
  • [ErratumIn] J Control Release. 2011 Jun 10;152(2):325. Lambert, Martin [corrected to Hagedorn, Martin]
  • (PMID = 20420865.001).
  • [ISSN] 1873-4995
  • [Journal-full-title] Journal of controlled release : official journal of the Controlled Release Society
  • [ISO-abbreviation] J Control Release
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Cations; 0 / Emulsions; 0 / Oligonucleotides, Antisense; 0 / Thionucleotides; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2
  •  go-up   go-down


43. Schulmeister K, Husinsky J, Seiser B, Edthofer F, Fekete B, Farmer L, Lund DJ: Ex vivo and computer model study on retinal thermal laser-induced damage in the visible wavelength range. J Biomed Opt; 2008 Sep-Oct;13(5):054038
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ex vivo and computer model study on retinal thermal laser-induced damage in the visible wavelength range.
  • Excised bovine eyes are used as models for threshold determination of 532-nm laser-induced thermal damage of the retina in the pulse duration regime of 100 micros to 2 s for varying laser spot size diameters.
  • A previously unknown variation of the spot size dependence is seen for different pulse durations, which allows for a more complete understanding of the retinal thermal damage.
  • We conclude that the damage mechanism at threshold detected at 24 and 1 h for the nonhuman primate model is retinal pigment epithelium (RPE) cell damage and not thermal coagulation of the sensory retina.
  • This work validates the bovine ex vivo and computer models for prediction of thresholds of thermally induced damage in the time domain of 10 micros to 2 s, which provides the basis for safety analysis of more complicated retinal exposure scenarios such as repetitive pulses, nonconstant retinal irradiance profiles, and scanned exposure.
  • [MeSH-major] Eye Burns / etiology. Eye Burns / pathology. Lasers / adverse effects. Models, Biological. Radiation Injuries / etiology. Radiation Injuries / pathology. Retina / injuries. Retina / pathology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19021418.001).
  • [ISSN] 1083-3668
  • [Journal-full-title] Journal of biomedical optics
  • [ISO-abbreviation] J Biomed Opt
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


44. Strauss RW, Kampik A, Neubauer AS: [Topographic, 3D and Quantitative analysis of autofluorescence in dry, age-related macular degeneration]. Klin Monbl Augenheilkd; 2007 Dec;224(12):927-31
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Transliterated title] Topografische, 3D- und quantitative Darstellung der Autofluoreszenz bei trockener altersabhängiger Makuladegeneration.
  • OBJECTIVE: Autofluorescence of the retina allows one to quantify and follow the extent and progression of dry, age-related macular degeneration (ARMD) changes.
  • METHODS: In a consecutive series of 15 patients with mild dry AMD and 15 patients without retinal pathologies, one 30 degrees autofluorescence image was obtained with the Heidelberg retina angiograph (HRA).
  • [MeSH-major] Fluorescein Angiography. Image Processing, Computer-Assisted. Imaging, Three-Dimensional. Macular Degeneration / pathology. Retina / pathology

  • Genetic Alliance. consumer health - Macular Degeneration.
  • MedlinePlus Health Information. consumer health - Macular Degeneration.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18260056.001).
  • [ISSN] 0023-2165
  • [Journal-full-title] Klinische Monatsblätter für Augenheilkunde
  • [ISO-abbreviation] Klin Monbl Augenheilkd
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
  •  go-up   go-down


45. Baye LM, Link BA: The disarrayed mutation results in cell cycle and neurogenesis defects during retinal development in zebrafish. BMC Dev Biol; 2007 Apr 05;7:28
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The disarrayed mutation results in cell cycle and neurogenesis defects during retinal development in zebrafish.
  • BACKGROUND: The vertebrate retina is derived from proliferative neuroepithelial cells of the optic cup.
  • During retinal development, cell proliferation and the processes of cell cycle exit and neurogenesis are coordinated in neuroepithelial progenitor cells.
  • However the specific mechanisms and exact relationships of cell cycle regulation and neurogenesis in the vertebrate retina remain largely unknown.
  • RESULTS: We have isolated and characterized a zebrafish mutant, disarrayed (drya64), which exhibits retinal defects in cell cycle regulation and neurogenesis.
  • Although retinogenesis is delayed, mutant retinal cells eventually differentiate to all major cell types.
  • Examination of the disarrayed mitotic cycle using BrdU and direct imaging techniques revealed that retinal neuroepithelial cells have an extended cell cycle period and reduced rate of cell cycle exit and neurogenesis, despite the fact that neurogenesis initiates at the appropriate time of development.
  • CONCLUSION: The disarrayed mutant shows defects in both cell cycle regulation and neurogenesis and provides insights into the coordinated regulation of these processes during retinal development.

  • COS Scholar Universe. author profiles.
  • SciCrunch. ZFIN: Data: Gene Expression .
  • ZFIN. ZFIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Dev Neurosci. 2000;22(1-2):44-55 [10657697.001]
  • [Cites] Dev Biol. 2000 Nov 15;227(2):279-93 [11071755.001]
  • [Cites] Nat Rev Neurosci. 2001 Feb;2(2):109-18 [11252990.001]
  • [Cites] Dev Biol. 2001 May 15;233(2):329-46 [11336499.001]
  • [Cites] Neuron. 2001 Jun;30(3):725-36 [11430806.001]
  • [Cites] Development. 2001 Jul;128(13):2497-508 [11493566.001]
  • [Cites] Cell Tissue Res. 2001 Nov;306(2):199-207 [11702231.001]
  • [Cites] Dev Genes Evol. 2001 Dec;211(12):603-10 [11819118.001]
  • [Cites] Development. 2002 May;129(10):2435-46 [11973275.001]
  • [Cites] Results Probl Cell Differ. 2002;39:1-25 [12353465.001]
  • [Cites] Curr Opin Neurobiol. 2003 Feb;13(1):26-33 [12593979.001]
  • [Cites] Development. 2003 Jun;130(11):2479-94 [12702661.001]
  • [Cites] Nat Genet. 2003 May;34(1):53-8 [12692551.001]
  • [Cites] Development. 2003 Aug;130(15):3427-36 [12810590.001]
  • [Cites] Cell Cycle. 2003 Jul-Aug;2(4):350-7 [12851489.001]
  • [Cites] Neuron. 2003 Oct 9;40(2):199-208 [14556704.001]
  • [Cites] Dev Biol. 2003 Dec 1;264(1):240-54 [14623245.001]
  • [Cites] Genes Dev. 2006 Nov 1;20(21):3036-48 [17079690.001]
  • [Cites] J Cell Sci. 2003 Dec 15;116(Pt 24):4947-55 [14625388.001]
  • [Cites] Brain Res. 1985 Aug;353(2):229-39 [4041905.001]
  • [Cites] Nature. 1987 Jul 9-15;328(6126):131-6 [3600789.001]
  • [Cites] Science. 1988 Mar 4;239(4844):1142-5 [2449732.001]
  • [Cites] J Neurocytol. 1989 Jun;18(3):311-8 [2746304.001]
  • [Cites] Neuron. 1988 Mar;1(1):15-26 [3272153.001]
  • [Cites] Nature. 1990 Dec 20-27;348(6303):728-30 [2259382.001]
  • [Cites] J Neurosci. 1995 Sep;15(9):6046-57 [7666188.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Jan 23;93(2):589-95 [8570600.001]
  • [Cites] Dev Dyn. 1995 Jul;203(3):253-310 [8589427.001]
  • [Cites] Dev Dyn. 1996 Mar;205(3):293-307 [8850565.001]
  • [Cites] Curr Opin Genet Dev. 1997 Oct;7(5):651-8 [9388782.001]
  • [Cites] Neuron. 1997 Nov;19(5):981-94 [9390513.001]
  • [Cites] Trends Genet. 1998 Sep;14(9):358-63 [9769731.001]
  • [Cites] Development. 1998 Dec;125(23):4821-33 [9806930.001]
  • [Cites] Dev Biol. 1999 Mar 15;207(2):309-21 [10068465.001]
  • [Cites] Methods Cell Biol. 2004;77:505-19 [15602929.001]
  • [Cites] Dev Biol. 2005 Apr 15;280(2):467-81 [15882586.001]
  • [Cites] Development. 2005 Jun;132(11):2573-85 [15857917.001]
  • [Cites] Science. 2005 Jun 24;308(5730):1927-30 [15976303.001]
  • [Cites] J Neurosci. 2005 Jul 13;25(28):6533-8 [16014714.001]
  • [Cites] Neuron. 2005 Aug 4;47(3):353-64 [16055060.001]
  • [Cites] Genetics. 2005 Aug;170(4):1827-37 [15937129.001]
  • [Cites] J Cell Biol. 2005 Dec 19;171(6):991-9 [16365165.001]
  • [Cites] Brain Res. 2006 May 9;1088(1):57-67 [16650835.001]
  • [Cites] Trends Neurosci. 2006 Oct;29(10):563-70 [16920202.001]
  • [Cites] Development. 2000 May;127(10):2177-88 [10769241.001]
  • [Cites] Bioessays. 2000 Aug;22(8):685-8 [10918298.001]
  • [Cites] Neuron. 2000 Aug;27(2):251-63 [10985346.001]
  • [Cites] Dev Dyn. 2000 Nov;219(3):391-401 [11066095.001]
  • [Cites] Curr Opin Neurobiol. 2001 Feb;11(1):66-73 [11179874.001]
  • (PMID = 17411431.001).
  • [ISSN] 1471-213X
  • [Journal-full-title] BMC developmental biology
  • [ISO-abbreviation] BMC Dev. Biol.
  • [Language] ENG
  • [Grant] United States / NEI NIH HHS / EY / R01 EY014167; United States / NEI NIH HHS / EY / T32 EY014536; United States / NEI NIH HHS / EY / 5T32EY014536; United States / NEI NIH HHS / EY / R01EY01467
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Genetic Markers
  • [Other-IDs] NLM/ PMC1854893
  •  go-up   go-down


46. Umino Y, Everhart D, Solessio E, Cusato K, Pan JC, Nguyen TH, Brown ET, Hafler R, Frio BA, Knox BE, Engbretson GA, Haeri M, Cui L, Glenn AS, Charron MJ, Barlow RB: Hypoglycemia leads to age-related loss of vision. Proc Natl Acad Sci U S A; 2006 Dec 19;103(51):19541-5
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The retina is among the most metabolically active tissues in the body, requiring a constant supply of blood glucose to sustain function.
  • Metabolic stress from moderate hypoglycemia led to late-onset loss of retinal function in Gcgr(-/-) mice, loss of visual acuity, and eventual death of retinal cells.
  • Retinal function measured by the electroretinogram b-wave threshold declined >100-fold from age 9 to 13 months, whereas decreases in photoreceptor function measured by the ERG a-wave were delayed by 3 months.
  • At 10 months of age Gcgr(-/-) mice began to lose visual acuity and exhibit changes in retinal anatomy, including an increase in cell death that was initially more pronounced in the inner retina.
  • Decreases in retinal function and visual acuity correlated directly with the degree of hypoglycemia.
  • Linkage between low blood glucose and loss of vision in mice may highlight the importance for glycemic control in diabetics and retinal diseases related to metabolic stress as macular degeneration.
  • [MeSH-major] Apoptosis / physiology. Hypoglycemia / complications. Receptors, Glucagon / genetics. Retina / pathology. Vision Disorders / etiology

  • MedlinePlus Health Information. consumer health - Hypoglycemia.
  • MedlinePlus Health Information. consumer health - Vision Impairment and Blindness.
  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nature. 1990 Jan 25;343(6256):364-6 [2137202.001]
  • [Cites] Diabetes. 1989 Mar;38(3):285-90 [2645186.001]
  • [Cites] J Neurosci. 1992 Mar;12(3):840-53 [1312136.001]
  • [Cites] Invest Ophthalmol Vis Sci. 1992 Sep;33(10):2798-808 [1526729.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Nov 7;92(23):10545-9 [7479837.001]
  • [Cites] Eur J Ophthalmol. 1996 Jan-Mar;6(1):81-6 [8744856.001]
  • [Cites] Brain. 1996 Aug;119 ( Pt 4):1277-87 [8813290.001]
  • [Cites] Am J Ophthalmol. 1960 Nov;50:875-89 [13724151.001]
  • [Cites] J Neurophysiol. 1963 Jul;26:617-34 [14012566.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2004 Dec;45(12):4611-6 [15557474.001]
  • [Cites] Vis Neurosci. 2005 Sep-Oct;22(5):615-8 [16332272.001]
  • [Cites] Adv Exp Med Biol. 2006;572:169-72 [17249571.001]
  • [Cites] Optom Vis Sci. 2001 Jun;78(6):425-30 [11444632.001]
  • [Cites] Arch Ophthalmol. 2001 Oct;119(10):1417-36 [11594942.001]
  • [Cites] Vis Neurosci. 2001 Nov-Dec;18(6):983-93 [12020089.001]
  • [Cites] Nature. 2002 Sep 26;419(6905):367-74 [12353028.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Feb 4;100(3):1438-43 [12552113.001]
  • [Cites] J Neurosci. 2003 Jul 2;23(13):5723-31 [12843276.001]
  • [Cites] Vis Neurosci. 2003 Mar-Apr;20(2):211-20 [12916741.001]
  • [Cites] Nature. 2003 Aug 21;424(6951):952-6 [12931191.001]
  • [Cites] Annu Rev Neurosci. 2003;26:657-700 [14527271.001]
  • [Cites] Nat Med. 2003 Nov;9(11):1390-7 [14566334.001]
  • [Cites] N Engl J Med. 2004 May 27;350(22):2272-9 [15163777.001]
  • [Cites] Adv Exp Med Biol. 2003;533:259-67 [15180272.001]
  • [Cites] Exp Eye Res. 2004 Sep;79(3):321-9 [15336494.001]
  • [Cites] J Comp Neurol. 1980 Nov 1;194(1):193-207 [7440795.001]
  • [Cites] J Gen Physiol. 1981 Jun;77(6):667-92 [6267165.001]
  • [Cites] J Clin Invest. 1991 Sep;88(3):934-42 [1885778.001]
  • (PMID = 17159157.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Publication-type] Comparative Study; 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.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Blood Glucose; 0 / Receptors, Glucagon
  • [Other-IDs] NLM/ PMC1697832
  •  go-up   go-down


47. Helmlinger D, Hardy S, Abou-Sleymane G, Eberlin A, Bowman AB, Gansmüller A, Picaud S, Zoghbi HY, Trottier Y, Tora L, Devys D: Glutamine-expanded ataxin-7 alters TFTC/STAGA recruitment and chromatin structure leading to photoreceptor dysfunction. PLoS Biol; 2006 Mar;4(3):e67
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Spinocerebellar ataxia type 7 (SCA7) is one of several inherited neurodegenerative disorders caused by a polyglutamine (polyQ) expansion, but it is the only one in which the retina is affected.
  • In conclusion, we describe here a set of events accounting for SCA7 pathogenesis in the retina, in which polyQ-expanded ATXN7 deregulated TFTC/STAGA recruitment to a subset of genes specifically expressed in rod photoreceptors, leading to chromatin alterations and consequent progressive loss of rod photoreceptor function.
  • [MeSH-minor] Animals. Ataxin-7. Cell Nucleus / metabolism. Chromatin Assembly and Disassembly / genetics. Down-Regulation / genetics. Mice. Mice, Inbred C57BL. Mice, Transgenic. Microscopy, Immunoelectron. Peptides / pharmacology. Promoter Regions, Genetic / genetics. Protein Binding. RNA, Messenger / genetics. Retinal Rod Photoreceptor Cells / cytology. Retinal Rod Photoreceptor Cells / drug effects. Retinal Rod Photoreceptor Cells / metabolism. Retinal Rod Photoreceptor Cells / ultrastructure. Transcription, Genetic / genetics

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. Glutamine .
  • Jackson Laboratory JAX®Mice Database. culture/stock collections - B6.129S7-Atxn7<tm1Hzo>/J (subscription/membership/fee required).
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • antibodies-online. View related products from antibodies-online.com (subscription/membership/fee required).
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nat Genet. 2001 Dec;29(4):447-52 [11694879.001]
  • [Cites] J Neurosci. 1998 Nov 1;18(21):8936-46 [9786999.001]
  • [Cites] Cell. 2002 May 31;109(5):551-62 [12062099.001]
  • [Cites] Hum Mol Genet. 2002 Aug 15;11(17):1927-37 [12165555.001]
  • [Cites] J Biol Chem. 2002 Sep 6;277(36):32875-82 [12107188.001]
  • [Cites] Plant Mol Biol. 2002 Dec;50(6):925-47 [12516863.001]
  • [Cites] EMBO Rep. 2003 Jan;4(1):18-23 [12524514.001]
  • [Cites] Neuron. 2003 Feb 6;37(3):383-401 [12575948.001]
  • [Cites] Trends Genet. 2003 May;19(5):233-8 [12711212.001]
  • [Cites] Nat Genet. 2003 May;34(1):42-51 [12692553.001]
  • [Cites] Trends Genet. 2003 Jun;19(6):321-9 [12801725.001]
  • [Cites] Hum Mol Genet. 2004 Jan 1;13(1):53-67 [14613968.001]
  • [Cites] Eur J Hum Genet. 2004 Jan;12(1):2-15 [14571264.001]
  • [Cites] J Neurosci. 2004 Feb 25;24(8):1881-7 [14985428.001]
  • [Cites] Mol Cell. 2004 Feb 27;13(4):573-85 [14992726.001]
  • [Cites] Cell. 2004 Mar 5;116(5):683-98 [15006351.001]
  • [Cites] Nat Genet. 2004 Apr;36(4):351-60 [14991054.001]
  • [Cites] Cell. 2004 May 14;117(4):427-39 [15137937.001]
  • [Cites] Curr Opin Cell Biol. 2004 Jun;16(3):285-92 [15145353.001]
  • [Cites] Hum Mol Genet. 2004 Jun 15;13(12):1257-65 [15115762.001]
  • [Cites] Genes Dev. 2004 Sep 1;18(17):2147-60 [15342492.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Oct 19;101(42):15106-11 [15477594.001]
  • [Cites] J Comp Neurol. 1979 Nov 15;188(2):245-62 [500858.001]
  • [Cites] J Cell Sci Suppl. 1993;17:189-95 [8144697.001]
  • [Cites] J Biol Chem. 1999 Feb 26;274(9):5895-900 [10026213.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Apr 27;96(9):4814-9 [10220376.001]
  • [Cites] J Biol Chem. 1999 Jun 25;274(26):18285-9 [10373431.001]
  • [Cites] Mol Cell Biol. 2005 Feb;25(3):958-68 [15657424.001]
  • [Cites] Hum Mol Genet. 2005 Mar 1;14(5):679-91 [15661755.001]
  • [Cites] Nat Genet. 2005 May;37(5):526-31 [15806102.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jun 14;102(24):8472-7 [15932940.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jun 14;102(24):8478-82 [15932941.001]
  • [Cites] Hum Mol Genet. 2006 Mar 1;15(5):691-703 [16434483.001]
  • [Cites] Biochem Soc Symp. 2006;(73):155-63 [16626296.001]
  • [Cites] J Biol Chem. 2002 Mar 8;277(10):7989-95 [11773077.001]
  • [Cites] Brain. 1994 Jun;117 ( Pt 3):445-60 [8032856.001]
  • [Cites] J Biol Chem. 1996 Feb 2;271(5):2667-75 [8576239.001]
  • [Cites] Development. 1997 Jun;124(12):2345-54 [9199361.001]
  • [Cites] Genes Dev. 1997 Jul 1;11(13):1640-50 [9224714.001]
  • [Cites] Hum Mol Genet. 2000 Apr 12;9(6):909-16 [10767314.001]
  • [Cites] Hum Mol Genet. 2000 May 22;9(9):1259-71 [10814708.001]
  • [Cites] J Biol Chem. 2000 Sep 22;275(38):29794-9 [10887186.001]
  • [Cites] J Neurosci. 2000 Oct 1;20(19):7317-24 [11007889.001]
  • [Cites] Hum Mol Genet. 2000 Oct 12;9(17):2491-506 [11030754.001]
  • [Cites] Nat Rev Mol Cell Biol. 2000 Nov;1(2):137-43 [11253366.001]
  • [Cites] EMBO J. 2001 Jun 15;20(12):3187-96 [11406595.001]
  • [Cites] Hum Mol Genet. 2001 Aug 1;10(16):1619-26 [11487564.001]
  • [Cites] Science. 2001 Aug 10;293(5532):1133-6 [11498590.001]
  • [Cites] Br J Ophthalmol. 2001 Oct;85(10):1244-7 [11567972.001]
  • [Cites] Neuron. 2001 Sep 27;31(6):913-27 [11580893.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Nov 6;98(23):13201-6 [11687606.001]
  • [Cites] Nat Genet. 1997 Sep;17(1):65-70 [9288099.001]
  • [Cites] Neuron. 1997 Nov;19(5):1017-30 [9390516.001]
  • [Cites] Cell. 1997 Nov 14;91(4):531-41 [9390562.001]
  • [Cites] Cell. 1998 Jul 10;94(1):45-53 [9674426.001]
  • [Cites] J Biol Chem. 1998 Sep 11;273(37):23781-5 [9726987.001]
  • [CommentIn] PLoS Biol. 2006 Mar;4(3):e70 [20076538.001]
  • (PMID = 16494529.001).
  • [ISSN] 1545-7885
  • [Journal-full-title] PLoS biology
  • [ISO-abbreviation] PLoS Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ataxin-7; 0 / Atxn7 protein, mouse; 0 / DNA-Binding Proteins; 0 / Nerve Tissue Proteins; 0 / Peptides; 0 / RNA, Messenger; 0RH81L854J / Glutamine; 26700-71-0 / polyglutamine
  • [Other-IDs] NLM/ PMC1382020
  •  go-up   go-down


48. Ozdemir H, Karacorlu M, Karacorlu S: Serous macular detachment in central retinal vein occlusion. Retina; 2005 Jul-Aug;25(5):561-3
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Serous macular detachment in central retinal vein occlusion.
  • PURPOSE: To describe serous macular detachment in patients with central retinal vein occlusion (CRVO) by using optical coherence tomography (OCT).
  • In all cases, the increased thickness of the retina was related primarily to the hyporeflective intraretinal cavities.
  • A serous macular detachment composed of retinal elevation over a nonreflective cavity with minimal shadowing of the underlying tissues was seen in 18 eyes (81.8%).
  • [MeSH-major] Retinal Detachment / etiology. Retinal Vein Occlusion / complications
  • [MeSH-minor] Aged. Blood. Exudates and Transudates. Female. Fluorescein Angiography. Humans. Macular Edema / diagnosis. Macular Edema / etiology. Male. Middle Aged. Tomography, Optical Coherence. Visual Acuity

  • MedlinePlus Health Information. consumer health - Retinal Detachment.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16077350.001).
  • [ISSN] 0275-004X
  • [Journal-full-title] Retina (Philadelphia, Pa.)
  • [ISO-abbreviation] Retina (Philadelphia, Pa.)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


49. Butler JM, Guthrie SM, Koc M, Afzal A, Caballero S, Brooks HL, Mames RN, Segal MS, Grant MB, Scott EW: SDF-1 is both necessary and sufficient to promote proliferative retinopathy. J Clin Invest; 2005 Jan;115(1):86-93
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • It is caused by oxygen starvation in the retina inducing aberrant formation of blood vessels that destroy retinal architecture.
  • SDF-1 induces human retinal endothelial cells to increase expression of VCAM-1, a receptor for very late antigen-4 found on many hematopoietic progenitors, and reduce tight cellular junctions by reducing occludin expression.
  • Intravitreal injection of blocking antibodies to SDF-1 prevented retinal neovascularization in our murine model, even in the presence of exogenous VEGF.

  • MedlinePlus Health Information. consumer health - Diabetic Eye Problems.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. TRIAMCINOLONE .
  • SciCrunch. OMIM: Data: Gene Annotation .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Arch Ophthalmol. 2003 Jan;121(1):57-61 [12523885.001]
  • [Cites] Blood. 2005 Mar 1;105(5):1916-22 [15546953.001]
  • [Cites] Cloning Stem Cells. 2002;4(4):339-51 [12626097.001]
  • [Cites] Circulation. 2003 Mar 11;107(9):1322-8 [12628955.001]
  • [Cites] Glia. 2003 Apr 15;42(2):139-48 [12655598.001]
  • [Cites] Cell Prolif. 2003 Apr;36(2):75-86 [12680875.001]
  • [Cites] Leuk Lymphoma. 2003 Apr;44(4):575-82 [12769333.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2003 Nov;44(11):4908-13 [14578416.001]
  • [Cites] Blood. 2004 Jul 15;104(2):565-71 [15054039.001]
  • [Cites] Nat Med. 2004 Aug;10(8):858-64 [15235597.001]
  • [Cites] Proc Natl Acad Sci U S A. 1974 May;71(5):1906-9 [4209883.001]
  • [Cites] Am J Ophthalmol. 1976 Apr;81(4):383-96 [944535.001]
  • [Cites] Am J Ophthalmol. 1980 Dec;90(6):810-6 [7446668.001]
  • [Cites] Am J Ophthalmol. 1981 Jun;91(6):785-8 [7246702.001]
  • [Cites] Invest Ophthalmol Vis Sci. 1991 Jan;32(1):53-64 [1702773.001]
  • [Cites] J Mol Biol. 1999 Nov 5;293(4):865-81 [10543973.001]
  • [Cites] Thromb Res. 2000 Sep 15;99(6):587-94 [10974345.001]
  • [Cites] Stem Cells. 2001;19(5):453-66 [11553854.001]
  • [Cites] Blood. 2002 Apr 15;99(8):2703-11 [11929756.001]
  • [Cites] Ophthalmology. 2002 May;109(5):920-7 [11986098.001]
  • [Cites] J Exp Med. 2002 May 6;195(9):1145-54 [11994419.001]
  • [Cites] Gene Ther. 2002 May;9(10):631-41 [12032709.001]
  • [Cites] Nat Med. 2002 Jun;8(6):607-12 [12042812.001]
  • [Cites] Nat Med. 2002 Sep;8(9):1004-10 [12145646.001]
  • [Cites] Br J Ophthalmol. 2003 Jan;87(1):24-7 [12488256.001]
  • [Cites] Blood. 2004 Jan 1;103(1):133-5 [12969964.001]
  • [Cites] Arch Ophthalmol. 1992 Aug;110(8):1155-9 [1497531.001]
  • [Cites] Acta Ophthalmol (Copenh). 1992 Dec;70(6):814-9 [1488893.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Nov 7;92(23):10457-61 [7479819.001]
  • [Cites] Invest Ophthalmol Vis Sci. 1997 Aug;38(9):1653-66 [9286254.001]
  • [Cites] J Biol Chem. 1998 Aug 7;273(32):20556-67 [9685413.001]
  • [Cites] FASEB J. 1999 Jan;13(1):9-22 [9872925.001]
  • [Cites] Am J Pathol. 1999 Apr;154(4):1125-35 [10233851.001]
  • [Cites] Prog Retin Eye Res. 2003 Jan;22(1):1-29 [12597922.001]
  • (PMID = 15630447.001).
  • [ISSN] 0021-9738
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL70738; United States / NEI NIH HHS / EY / EY12601; United States / NIAMS NIH HHS / AR / T32 AR007603; United States / NEI NIH HHS / EY / R01 EY012601; United States / NHLBI NIH HHS / HL / HL70813; United States / NIAMS NIH HHS / AR / T32AR07603; United States / NHLBI NIH HHS / HL / R01 HL070738; United States / NHLBI NIH HHS / HL / R21 HL070813
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Antibodies; 0 / CXCL12 protein, human; 0 / Chemokine CXCL12; 0 / Chemokines, CXC; 0 / Cxcl12 protein, mouse; 1ZK20VI6TY / Triamcinolone
  • [Other-IDs] NLM/ PMC539202
  •  go-up   go-down


50. Clark SJ, Perveen R, Hakobyan S, Morgan BP, Sim RB, Bishop PN, Day AJ: Impaired binding of the age-related macular degeneration-associated complement factor H 402H allotype to Bruch's membrane in human retina. J Biol Chem; 2010 Sep 24;285(39):30192-202
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Impaired binding of the age-related macular degeneration-associated complement factor H 402H allotype to Bruch's membrane in human retina.
  • Age-related macular degeneration (AMD) is the predominant cause of blindness in the industrialized world where destruction of the macula, i.e. the central region of the retina, results in loss of vision.
  • AMD is preceded by the formation of deposits in the macula, which accumulate between the Bruch's membrane and the retinal pigment epithelium (RPE).
  • These deposits are associated with complement-mediated inflammation and perturb retinal function.
  • [MeSH-major] Bruch Membrane / metabolism. Complement Activation. Heparitin Sulfate / metabolism. Macular Degeneration / metabolism. Retinal Pigment Epithelium / metabolism

  • Genetic Alliance. consumer health - Macular Degeneration.
  • MedlinePlus Health Information. consumer health - Macular Degeneration.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • SciCrunch. OMIM: Data: Gene Annotation .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Carbohydr Res. 1994 Mar 4;255:1-26 [8181000.001]
  • [Cites] J Biol Chem. 1991 Sep 5;266(25):16847-53 [1832158.001]
  • [Cites] J Immunol. 1998 Apr 1;160(7):3342-8 [9531293.001]
  • [Cites] Science. 2005 Apr 15;308(5720):419-21 [15761120.001]
  • [Cites] Science. 2005 Apr 15;308(5720):421-4 [15761121.001]
  • [Cites] Science. 2005 Apr 15;308(5720):385-9 [15761122.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 May 17;102(20):7227-32 [15870199.001]
  • [Cites] Clin Exp Immunol. 2006 May;144(2):342-52 [16634809.001]
  • [Cites] J Biol Chem. 2006 Jun 16;281(24):16512-20 [16533809.001]
  • [Cites] J Biol Chem. 2006 Aug 25;281(34):24713-20 [16787919.001]
  • [Cites] J Immunol. 2006 Nov 1;177(9):6308-16 [17056561.001]
  • [Cites] J Immunol. 2007 Mar 15;178(6):3831-6 [17339482.001]
  • [Cites] J Biol Chem. 2007 Apr 13;282(15):10894-900 [17293598.001]
  • [Cites] J Exp Med. 2007 Jun 11;204(6):1249-56 [17517971.001]
  • [Cites] J Exp Med. 2007 Oct 1;204(10):2277-83 [17893204.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2008 May;49(5):1763-70 [18263814.001]
  • [Cites] J Biol Chem. 2008 Nov 7;283(45):30451-60 [18786923.001]
  • [Cites] Mol Microbiol. 2008 Nov;70(3):583-94 [18627465.001]
  • [Cites] Adv Exp Med Biol. 2008;632:117-42 [19025119.001]
  • [Cites] Lancet. 2008 Nov 22;372(9652):1835-45 [19027484.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Mar 17;106(11):4366-71 [19255449.001]
  • [Cites] Nature. 2009 Apr 16;458(7240):890-3 [19225461.001]
  • [Cites] Glycobiology. 2009 Dec;19(12):1537-46 [19729381.001]
  • [Cites] Prog Retin Eye Res. 2010 Mar;29(2):95-112 [19961953.001]
  • [Cites] Biochem Soc Trans. 2010 Oct;38(5):1342-8 [20863311.001]
  • [Cites] Thromb Haemost. 2000 Dec;84(6):1052-6 [11154113.001]
  • [Cites] Prog Retin Eye Res. 2001 Nov;20(6):705-32 [11587915.001]
  • [Cites] J Biol Chem. 2002 Jan 25;277(4):2444-53 [11714710.001]
  • [Cites] Annu Rev Biochem. 2002;71:435-71 [12045103.001]
  • [Cites] Eur J Immunol. 2003 Apr;33(4):962-9 [12672062.001]
  • [Cites] Anal Biochem. 2004 Jul 1;330(1):123-9 [15183770.001]
  • [Cites] J Exp Med. 1979 Nov 1;150(5):1202-15 [501288.001]
  • [Cites] Biosci Rep. 1983 Dec;3(12):1119-31 [6199050.001]
  • [Cites] Immunogenetics. 1988;27(3):211-4 [2962936.001]
  • [Cites] Biochem J. 1988 Jan 15;249(2):593-602 [2963625.001]
  • [Cites] Anal Biochem. 1989 Nov 1;182(2):319-26 [2610349.001]
  • [Cites] Proc Natl Acad Sci U S A. 1990 May;87(10):3982-6 [1692629.001]
  • [Cites] Exp Eye Res. 1990 Oct;51(4):451-62 [2120081.001]
  • [Cites] J Immunol. 1996 Dec 15;157(12):5422-7 [8955190.001]
  • (PMID = 20660596.001).
  • [ISSN] 1083-351X
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0900538; United Kingdom / Medical Research Council / / G0900592
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / complement factor H, human; 80295-65-4 / Complement Factor H; 9050-30-0 / Heparitin Sulfate
  • [Other-IDs] NLM/ PMC2943316
  •  go-up   go-down


51. Maggesissi RS, Gardino PF, Guimarães-Souza EM, Paes-de-Carvalho R, Silva RB, Calaza KC: Modulation of GABA release by nitric oxide in the chick retina: different effects of nitric oxide depending on the cell population. Vision Res; 2009 Oct;49(20):2494-502
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Modulation of GABA release by nitric oxide in the chick retina: different effects of nitric oxide depending on the cell population.
  • gamma-Aminobutyric acid (GABA) is considered to be the most important inhibitory neurotransmitter in the central nervous system, including the retina.
  • It has been shown that nitric oxide (NO) can influence the physiology of all retinal neuronal types, by mechanisms including modulation of GABA release.
  • However, until now, there have been no data concerning the effects on endogenous GABA release of NO produced by cells in the intact retina.
  • In the present study, we have investigated how NO production induced by drugs influences the release of endogenous GABA in cells of the intact retina of mature chicken.
  • [MeSH-major] Chickens / metabolism. Nitric Oxide / physiology. Retina / metabolism. gamma-Aminobutyric Acid / metabolism
  • [MeSH-minor] Amacrine Cells / metabolism. Animals. Arginine / pharmacology. N-Methylaspartate / pharmacology. Nitric Oxide Synthase Type I / physiology. Retinal Ganglion Cells / drug effects. Retinal Ganglion Cells / metabolism. Tissue Culture Techniques. Tissue Fixation / methods

  • Hazardous Substances Data Bank. NITRIC OXIDE .
  • Hazardous Substances Data Bank. (L)-ARGININE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19666044.001).
  • [ISSN] 1878-5646
  • [Journal-full-title] Vision research
  • [ISO-abbreviation] Vision Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 31C4KY9ESH / Nitric Oxide; 56-12-2 / gamma-Aminobutyric Acid; 6384-92-5 / N-Methylaspartate; 94ZLA3W45F / Arginine; EC 1.14.13.39 / Nitric Oxide Synthase Type I
  •  go-up   go-down


52. Pointer MA, Cheng CH, Bowmaker JK, Parry JW, Soto N, Jeffery G, Cowing JA, Hunt DM: Adaptations to an extreme environment: retinal organisation and spectral properties of photoreceptors in Antarctic notothenioid fish. J Exp Biol; 2005 Jun;208(Pt 12):2363-76
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adaptations to an extreme environment: retinal organisation and spectral properties of photoreceptors in Antarctic notothenioid fish.
  • The identity and spectral location of maximal absorbance of the SWS1 and Rh2 pigments was confirmed by in vitro expression of the recombinant opsins followed by regeneration with 11-cis retinal.
  • Expression of the Rh2 opsin is localised to double cone receptors in both the central and peripheral retina, whereas SWS2 opsin expression is present only in the peripheral retina.
  • SWS1 cones could not be identified by either microspectrophotometry or in situ hybridisation, presumably reflecting their low number and/or uneven distribution across the retina.
  • A study of photoreceptor organisation in the retina of two species, the shallower dwelling Trematomus hansoni and the deeper dwelling Dissostichus mawsoni, identified a square mosaic in the former, and a row mosaic in the latter species; the row mosaic in Dissostichus mawsoni with less tightly packed cone photoreceptors allows for a higher rod photoreceptor density.
  • [MeSH-major] Adaptation, Biological. Darkness. Perciformes / physiology. Photoreceptor Cells, Vertebrate / metabolism. Phylogeny. Retinal Pigments / metabolism

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15939776.001).
  • [ISSN] 0022-0949
  • [Journal-full-title] The Journal of experimental biology
  • [ISO-abbreviation] J. Exp. Biol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / DNA Primers; 0 / Retinal Pigments
  •  go-up   go-down


53. Trenholm S, Baldridge WH: The effect of aminosulfonate buffers on the light responses and intracellular pH of goldfish retinal horizontal cells. J Neurochem; 2010 Oct;115(1):102-11
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The effect of aminosulfonate buffers on the light responses and intracellular pH of goldfish retinal horizontal cells.
  • Retinal horizontal cell feedback acts as a gain control at the first synapse in the visual system and generates center-surround receptive fields in the outer retina.
  • Intracellular recording from horizontal cells in isolated goldfish retina revealed that rollback was blocked only by aminosulfonates with an acid dissociation constant suited for buffering at the pH (7.5) of the Ringer's solution.
  • [MeSH-major] Goldfish / physiology. Retinal Horizontal Cells / drug effects. Retinal Horizontal Cells / radiation effects. Sulfonic Acids / pharmacology

  • Hazardous Substances Data Bank. GLUTAMIC ACID HYDROCHLORIDE .
  • Hazardous Substances Data Bank. SULFAMIC ACID .
  • Hazardous Substances Data Bank. AMMONIUM SULFAMATE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] © 2010 The Authors. Journal Compilation © 2010 International Society for Neurochemistry.
  • (PMID = 20633206.001).
  • [ISSN] 1471-4159
  • [Journal-full-title] Journal of neurochemistry
  • [ISO-abbreviation] J. Neurochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Buffers; 0 / Fluoresceins; 0 / Fluorescent Dyes; 0 / Sulfonic Acids; 3KX376GY7L / Glutamic Acid; 85138-49-4 / 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein; 9NFU33906Q / sulfamic acid; RWW266YE9I / HEPES; SIV03811UC / Kainic Acid
  •  go-up   go-down


54. Esche M, Hirrlinger PG, Rillich K, Yafai Y, Pannicke T, Reichenbach A, Weick M: Signalling of sphingosine-1-phosphate in Müller glial cells via the S1P/EDG-family of G-protein-coupled receptors. Neurosci Lett; 2010 Aug 16;480(2):101-5
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Proliferation and migration of retinal Müller glial cells are involved in pathological events such as proliferative vitreoretinopathy and proliferative diabetic retinopathy.
  • Here we show that cultured Müller cells from the guinea pig retina respond to application of S1P with an increase in the intracellular calcium content in a concentration-dependent manner (EC(50) 11nM).
  • Thus, the data indicate that Müller cells might be involved in S1P signalling in the retina.
  • [MeSH-major] Lysophospholipids / physiology. Neuroglia / metabolism. Receptors, Lysosphingolipid / physiology. Retina / physiology. Sphingosine / analogs & derivatives

  • Hazardous Substances Data Bank. CALCIUM, ELEMENTAL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2010 Elsevier Ireland Ltd. All rights reserved.
  • (PMID = 20540988.001).
  • [ISSN] 1872-7972
  • [Journal-full-title] Neuroscience letters
  • [ISO-abbreviation] Neurosci. Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Estrenes; 0 / Lysophospholipids; 0 / Pyrrolidinones; 0 / Receptors, Lysosphingolipid; 112648-68-7 / 1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione; 26993-30-6 / sphingosine 1-phosphate; EC 3.1.4.- / Type C Phospholipases; NGZ37HRE42 / Sphingosine; SY7Q814VUP / Calcium
  •  go-up   go-down


55. Mäthger LM, Roberts SB, Hanlon RT: Evidence for distributed light sensing in the skin of cuttlefish, Sepia officinalis. Biol Lett; 2010 Oct 23;6(5):600-3
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The amino acid sequence of the opsin polypeptide that these transcripts would produce was identical in retina and fin tissue samples, but the ventral skin opsin transcripts differed by a single amino acid.
  • Since the opsin in the fin is identical to that of the retina (λmax=492 nm), and the ventral transcripts are also unlikely to be spectrally different, colour discrimination by the skin opsins is unlikely.

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Pigment Cell Res. 2001 Oct;14(5):312-9 [11601652.001]
  • [Cites] Biol Rev Camb Philos Soc. 1963 May;38(2):204-40 [4385905.001]
  • [Cites] Am Zool. 1969 May;9(2):429-42 [5362276.001]
  • [Cites] Nature. 1975 Jan 31;253(5490):370-2 [1110782.001]
  • [Cites] J Exp Biol. 1998 Aug;201(Pt 15):2299-306 [9662500.001]
  • [Cites] Nature. 1958 Nov 8;182(4645):1288-90 [13600294.001]
  • [Cites] J Exp Biol. 2010 Jan 15;213(2):249-55 [20038658.001]
  • [Cites] Vision Res. 2006 May;46(11):1746-53 [16376404.001]
  • [Cites] J Exp Biol. 2006 May;209(Pt 10):1944-55 [16651559.001]
  • [Cites] Zoolog Sci. 2006 Sep;23(9):815-9 [17043404.001]
  • [Cites] J R Soc Interface. 2009 Apr 6;6 Suppl 2:S149-63 [19091688.001]
  • [Cites] Exp Dermatol. 2009 Jun;18(6):567-70 [19493002.001]
  • [Cites] Pigment Cell Res. 2005 Oct;18(5):360-9 [16162176.001]
  • (PMID = 20392722.001).
  • [ISSN] 1744-957X
  • [Journal-full-title] Biology letters
  • [ISO-abbreviation] Biol. Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Opsins; 63231-63-0 / RNA
  • [Other-IDs] NLM/ PMC2936158
  •  go-up   go-down


56. Otto JM, Kromeier M, Bach M, Kommerell G: Microstrabismus: Fixation point scotoma, a perimetric artefact. Vision Res; 2009 Mar;49(5):575-81
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • On the retina of the strabismic eye, the stereotarget was imaged at one of seven locations, between 2 degrees nasally and 2 degrees temporally, whereas on the retina of the non-strabismic eye, the stereotarget was imaged always in the centre.

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19200806.001).
  • [ISSN] 1878-5646
  • [Journal-full-title] Vision research
  • [ISO-abbreviation] Vision Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  •  go-up   go-down


57. Messmer EM, Zapp DM, Mackert MJ, Thiel M, Kampik A: In vivo confocal microscopy of filtering blebs after trabeculectomy. Arch Ophthalmol; 2006 Aug;124(8):1095-103
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHOD: In vivo confocal microscopy using the Heidelberg Retina Tomograph/Rostock Cornea Module (Heidelberg Engineering, Heidelberg, Germany) was performed in 53 filtering blebs in 45 patients 6 days to 30 years postoperatively.
  • CONCLUSIONS: In vivo confocal microscopy using the Heidelberg Retina Tomograph/Rostock Cornea Module permits diagnostic imaging of filtering blebs and differentiation between good and insufficient bleb function.

  • MedlinePlus Health Information. consumer health - Glaucoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16908811.001).
  • [ISSN] 0003-9950
  • [Journal-full-title] Archives of ophthalmology (Chicago, Ill. : 1960)
  • [ISO-abbreviation] Arch. Ophthalmol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


58. Hall MO, Obin MS, Heeb MJ, Burgess BL, Abrams TA: Both protein S and Gas6 stimulate outer segment phagocytosis by cultured rat retinal pigment epithelial cells. Exp Eye Res; 2005 Nov;81(5):581-91
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Both protein S and Gas6 stimulate outer segment phagocytosis by cultured rat retinal pigment epithelial cells.
  • Survival of the retina requires the daily phagocytosis of photoreceptor outer segments (OS) by the overlying retinal pigment epithelium (RPE).
  • The existence of redundant ligands for Mer-dependent OS phagocytosis underscores the critical role of this process in the maintenance of retinal function.

  • COS Scholar Universe. author profiles.
  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15949798.001).
  • [ISSN] 0014-4835
  • [Journal-full-title] Experimental eye research
  • [ISO-abbreviation] Exp. Eye Res.
  • [Language] eng
  • [Grant] United States / NEI NIH HHS / EY / EY 013956; United States / NEI NIH HHS / EY / EY 13078; United States / NEI NIH HHS / EY / EY00331; United States / NEI NIH HHS / EY / EY11705; United States / NHLBI NIH HHS / HL / HL 70002
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Intercellular Signaling Peptides and Proteins; 0 / Protein S; 0 / Proto-Oncogene Proteins; 0 / growth arrest-specific protein 6; EC 2.7.10.1 / Mertk protein, rat; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases
  •  go-up   go-down


59. Sinha D, Hose S, Zhang C, Neal R, Ghosh M, O'Brien TP, Sundin O, Goldberg MF, Robison WG Jr, Russell P, Lo WK, Samuel Zigler J Jr: A spontaneous mutation affects programmed cell death during development of the rat eye. Exp Eye Res; 2005 Mar;80(3):323-35
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Homozygous Nuc1 rats are fully viable and have microphthalmia, retinal abnormalities and disruption of lens structure shortly before birth.
  • Homozygous retinas are thicker than normal, and TUNEL labeling indicates roughly half the number of apoptotic cells compared to a wild-type retina.
  • The transient layer of Chievitz persists in adult Nuc1 retina, indicative of delayed development.
  • [MeSH-minor] Animals. Cell Nucleus / ultrastructure. Electrophoresis, Polyacrylamide Gel / methods. Eye Proteins / analysis. Heterozygote. In Situ Nick-End Labeling / methods. Lens, Crystalline / cytology. Lens, Crystalline / growth & development. Lens, Crystalline / ultrastructure. Microscopy, Electron / methods. Mutation / genetics. Mutation / physiology. Phenotype. Rats. Rats, Sprague-Dawley. Retina / cytology. Retina / growth & development

  • MedlinePlus Health Information. consumer health - Eye Care.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15721615.001).
  • [ISSN] 0014-4835
  • [Journal-full-title] Experimental eye research
  • [ISO-abbreviation] Exp. Eye Res.
  • [Language] eng
  • [Grant] United States / NEI NIH HHS / EY / EY05314
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Eye Proteins
  •  go-up   go-down


60. Yokoi T, Yokoi T, Kobayashi Y, Nishina S, Azuma N: Risk factors for recurrent fibrovascular proliferation in aggressive posterior retinopathy of prematurity after early vitreous surgery. Am J Ophthalmol; 2010 Jul;150(1):10-15.e1
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Eyes with stage 4A or 4B disease in which fibrovascular tissue was not attached to the vitreous base were included; those in which fibrovascular tissue was attached extensively to vitreous base or those without dense photocoagulation to the nonvascularized retina were excluded.
  • Data on gender, gestational age, birth weight, Apgar score, intubation duration, severe systemic complications, preoperative ROP stage, zone, fibrovascular tissue and vitreous base adhesion, clock hours of fibrovascular tissue, postmenstrual age at the initial application of dense photocoagulation, dense photocoagulation to both vascularized and nonvascularized retina, postmenstrual age at vitrectomy, and intraoperative hemorrhage were collected and analyzed.
  • Both univariate and multivariate analysis indicated application of dense photocoagulation to both the vascularized and nonvascularized retina was a significant factor in the decreased recurrence of fibrovascular tissue (P = .002 and P = .008, respectively).
  • CONCLUSIONS: Application of preoperative dense photocoagulation to vascularized and nonvascularized retina may be important for lowering the recurrence of fibrovascular tissue in eyes with AP ROP.
  • [MeSH-major] Postoperative Complications. Retinal Vessels / pathology. Retinopathy of Prematurity / surgery. Vitrectomy. Vitreous Body / surgery

  • MedlinePlus Health Information. consumer health - After Surgery.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20609704.001).
  • [ISSN] 1879-1891
  • [Journal-full-title] American journal of ophthalmology
  • [ISO-abbreviation] Am. J. Ophthalmol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


61. Shields CL, Benevides R, Materin MA, Shields JA: Optical coherence tomography of retinal astrocytic hamartoma in 15 cases. Ophthalmology; 2006 Sep;113(9):1553-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Optical coherence tomography of retinal astrocytic hamartoma in 15 cases.
  • OBJECTIVE: To describe the features of retinal astrocytic hamartoma using optical coherence tomography (OCT).
  • PARTICIPANTS: Fifteen consecutive eyes from 14 patients with retinal astrocytic hamartoma.
  • MAIN OUTCOME MEASURES: Optical coherence tomography characteristics of the tumor.
  • By ophthalmoscopy, the mean basal diameter of the tumor was 3.6 mm.
  • By OCT, the tumor showed hyperreflectivity at its surface, internal retinal disorganization, and a gradual gently sloping transition from a normal retina into a tumorous retina in all 15 cases (100%).
  • By OCT, the retinal disorganization was limited to the inner retina in 3 (20%), outer retina in 0 (0%), full retina in 5 (33%), and inner retina with no view of deeper layers due to shadowing in 7 (47%).
  • On OCT, there was mild retinal traction on the surface of the tumor in 4 (27%), discrete internal moth-eaten optically empty spaces representing intralesional calcification or intratumoral cavities in 10 (67%), and optical shadowing posterior to the tumor in 14 (93%).
  • Other retinal findings on OCT included shallow elevation of the adjacent retina in 2 (13%), adjacent retinal edema in 4 (27%), and macular edema in 3 (20%).
  • CONCLUSIONS: Retinal astrocytic hamartoma shows characteristic features on OCT, including a gradual transition from a normal retina into an optically hyperreflective mass with retinal disorganization, characteristic moth-eaten spaces, and posterior shadowing.
  • [MeSH-major] Astrocytes / pathology. Hamartoma / pathology. Retinal Diseases / pathology. Tomography, Optical Coherence / methods

  • MedlinePlus Health Information. consumer health - Retinal Disorders.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16949441.001).
  • [ISSN] 1549-4713
  • [Journal-full-title] Ophthalmology
  • [ISO-abbreviation] Ophthalmology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


62. Zhang XM, Li Liu DT, Chiang SW, Choy KW, Pang CP, Lam DS, Yam GH: Immunopanning purification and long-term culture of human retinal ganglion cells. Mol Vis; 2010;16:2867-72
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunopanning purification and long-term culture of human retinal ganglion cells.
  • PURPOSE: To establish a robust method to isolate primary retinal ganglion cells (RGCs) from human fetal retina for long-term culture while maintaining neuronal morphology and marker protein expression.
  • [MeSH-major] Cell Culture Techniques / methods. Cell Separation / methods. Retinal Ganglion Cells / cytology. Retinal Ganglion Cells / immunology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Development. 2000 Aug;127(15):3237-47 [10887080.001]
  • [Cites] J Neurosci Methods. 2010 Oct 15;192(2):233-9 [20691729.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2001 Apr;42(5):1096-106 [11274091.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2002 Dec;43(12):3735-43 [12454045.001]
  • [Cites] Proc Natl Acad Sci U S A. 1979 Jan;76(1):514-7 [284369.001]
  • [Cites] Science. 1984 Apr 20;224(4646):303-6 [6143400.001]
  • [Cites] Neuroscience. 1984 Apr;11(4):847-55 [6146113.001]
  • [Cites] Exp Brain Res. 1988;73(2):393-401 [3265109.001]
  • [Cites] Neuron. 1988 Nov;1(9):791-803 [2908449.001]
  • [Cites] Neuroscience. 1994 Jan;58(2):399-409 [8152546.001]
  • [Cites] Neuron. 1995 Oct;15(4):805-19 [7576630.001]
  • [Cites] Br J Ophthalmol. 1996 May;80(5):389-93 [8695555.001]
  • [Cites] J Glaucoma. 1997 Feb;6(1):37-43 [9075079.001]
  • [Cites] Arch Ophthalmol. 1965 May;73:724-45 [14281994.001]
  • [Cites] Curr Opin Ophthalmol. 2005 Apr;16(2):84-8 [15744137.001]
  • [Cites] Mol Vis. 2005;11:208-15 [15788999.001]
  • [Cites] J Glaucoma. 2005 Aug;14(4):305-7 [15990613.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2005 Aug;46(8):2983-91 [16043875.001]
  • [Cites] J Neurosci. 2005 Dec 14;25(50):11595-604 [16354917.001]
  • [Cites] Prog Retin Eye Res. 2007 Jul;26(4):379-97 [17482863.001]
  • [Cites] Mol Vis. 2009;15:920-6 [19421410.001]
  • [Cites] Ophthalmic Res. 2009;42(1):29-35 [19478538.001]
  • [Cites] Mol Vis. 2010;16:246-51 [20161817.001]
  • [Cites] Brain Res Mol Brain Res. 2001 Jan 31;86(1-2):1-12 [11165366.001]
  • (PMID = 21203402.001).
  • [ISSN] 1090-0535
  • [Journal-full-title] Molecular vision
  • [ISO-abbreviation] Mol. Vis.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers
  • [Other-IDs] NLM/ PMC3012647
  •  go-up   go-down


63. Huang SP, Palla S, Ruzycki P, Varma RA, Harter T, Reddy GB, Petrash JM: Aldo-keto reductases in the eye. J Ophthalmol; 2010;2010:521204
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Using quantitative reverse transcriptase-PCR and immunohistochemical staining, we observed expression of both AKR genes in cornea, iris, ciliary body, lens, and retina.
  • Expression of AKR1B1 was the highest in lens and retina, whereas AKR1B10 was the highest in cornea.

  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Pharmacol Res. 2007 Jun;55(6):498-510 [17574431.001]
  • [Cites] Curr Opin Ophthalmol. 1999 Dec;10(6):483-9 [10662255.001]
  • [Cites] Diabetes. 2005 Jun;54(6):1615-25 [15919781.001]
  • [Cites] Biochim Biophys Acta. 1998 Aug 20;1399(2-3):198-202 [9765596.001]
  • [Cites] J Biol Chem. 1998 May 8;273(19):11429-35 [9565553.001]
  • [Cites] Diabetes Care. 1998 Jan;21(1):143-56 [9538986.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Mar 28;92(7):2780-4 [7708723.001]
  • [Cites] J Biol Chem. 1993 Dec 5;268(34):25687-93 [8245005.001]
  • [Cites] Diabetes Metab Rev. 1988 Jun;4(4):323-37 [3134179.001]
  • [Cites] Diabetes. 1988 Dec;37(12):1658-64 [3142801.001]
  • [Cites] Diabetes. 1984 Jun;33(6):562-6 [6427040.001]
  • [Cites] Invest Ophthalmol Vis Sci. 1979 Mar;18(3):237-41 [106020.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2004 Nov;45(11):4083-90 [15505059.001]
  • [Cites] FASEB J. 2004 Sep;18(12):1450-2 [15231732.001]
  • [Cites] Biochem J. 2003 Aug 1;373(Pt 3):973-9 [12732097.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2006 May;47(5):2036-44 [16639013.001]
  • (PMID = 20628518.001).
  • [ISSN] 2090-0058
  • [Journal-full-title] Journal of ophthalmology
  • [ISO-abbreviation] J Ophthalmol
  • [Language] ENG
  • [Grant] United States / NEI NIH HHS / EY / P30 EY002687; United States / NEI NIH HHS / EY / R01 EY005856
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2902055
  •  go-up   go-down


64. Nagata T, Koyanagi M, Tsukamoto H, Terakita A: Identification and characterization of a protostome homologue of peropsin from a jumping spider. J Comp Physiol A Neuroethol Sens Neural Behav Physiol; 2010 Jan;196(1):51-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Peropsin, a member of the opsin family, has characteristics of two functionally distinct opsin-groups, that is, amino acid residues conserved among opsins for light-sensing and a retinal-photoisomerase-like molecular property.
  • In addition, the spider peropsin was localized to non-visual cells in the retina, and fluorescence from reduced retinal chromophore was also observed in the region where peropsin was localized.

  • MedlinePlus Health Information. consumer health - Eye Care.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Vision Res. 1995 Apr;35(8):1011-7 [7762157.001]
  • [Cites] Cell Tissue Res. 1983;233(2):335-45 [6616571.001]
  • [Cites] Biochemistry. 1996 Feb 27;35(8):2625-9 [8611566.001]
  • [Cites] Photochem Photobiol. 2008 Jul-Aug;84(4):1024-30 [18513236.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Oct 7;105(40):15576-80 [18832159.001]
  • [Cites] Nature. 1968 Aug 3;219(5153):450-4 [5668423.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Sep 2;94(18):9893-8 [9275222.001]
  • [Cites] J Biol Chem. 1999 Mar 5;274(10):6085-90 [10037690.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 May 3;102(18):6303-8 [15851682.001]
  • [Cites] Nat Genet. 2001 Jul;28(3):256-60 [11431696.001]
  • [Cites] Nucleic Acids Res. 2002 Jul 15;30(14):3059-66 [12136088.001]
  • [Cites] Nat Struct Mol Biol. 2004 Mar;11(3):284-9 [14981504.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Apr 27;101(17):6687-91 [15096614.001]
  • [Cites] J Mol Evol. 2008 Feb;66(2):130-7 [18217181.001]
  • [Cites] FEBS Lett. 2002 Nov 20;531(3):525-8 [12435605.001]
  • [Cites] J Neurochem. 2008 May;105(3):883-90 [18088357.001]
  • [Cites] Curr Biol. 2005 Jun 7;15(11):1065-9 [15936279.001]
  • [Cites] Vision Res. 1989;29(6):639-52 [2626821.001]
  • [Cites] FEBS Lett. 1998 Nov 13;439(1-2):66-70 [9849879.001]
  • [Cites] Genome Biol. 2005;6(3):213 [15774036.001]
  • [Cites] Nature. 1967 May 6;214(5088):573-5 [6036171.001]
  • (PMID = 19960196.001).
  • [ISSN] 1432-1351
  • [Journal-full-title] Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology
  • [ISO-abbreviation] J. Comp. Physiol. A Neuroethol. Sens. Neural. Behav. Physiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Rrh protein, mouse; 9009-81-8 / Rhodopsin
  •  go-up   go-down


65. de Wit GC, Franssen L, Coppens JE, van den Berg TJ: Simulating the straylight effects of cataracts. J Cataract Refract Surg; 2006 Feb;32(2):294-300
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • PURPOSE: To study the additional straylight falling on the retina (retinal straylight) caused by cataract and find commercially available filters to simulate the cataract straylight effects.
  • METHODS: The retinal straylight addition of cataract was derived from straylight parameter data in the literature.
  • [MeSH-major] Cataract / complications. Glare. Retina / radiation effects. Scattering, Radiation

  • Genetic Alliance. consumer health - Cataracts.
  • MedlinePlus Health Information. consumer health - Cataract.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16565008.001).
  • [ISSN] 0886-3350
  • [Journal-full-title] Journal of cataract and refractive surgery
  • [ISO-abbreviation] J Cataract Refract Surg
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


66. Mora RC, Bonilha VL, Shin BC, Hu J, Cohen-Gould L, Bok D, Rodriguez-Boulan E: Bipolar assembly of caveolae in retinal pigment epithelium. Am J Physiol Cell Physiol; 2006 Mar;290(3):C832-43
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bipolar assembly of caveolae in retinal pigment epithelium.
  • We examined the expression and distribution of caveolae and caveolins in retinal pigment epithelium (RPE), which plays key roles in retinal support, visual cycle, and acts as the main barrier between blood and retina.

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16251472.001).
  • [ISSN] 0363-6143
  • [Journal-full-title] American journal of physiology. Cell physiology
  • [ISO-abbreviation] Am. J. Physiol., Cell Physiol.
  • [Language] ENG
  • [Grant] United States / NEI NIH HHS / EY / R01 EY008538; United States / NEI NIH HHS / EY / EY-00331; United States / NEI NIH HHS / EY / EY-00444; United States / NEI NIH HHS / EY / EY-8538
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Caveolin 1; 0 / Caveolin 2
  •  go-up   go-down


67. Sundin OH, Leppert GS, Silva ED, Yang JM, Dharmaraj S, Maumenee IH, Santos LC, Parsa CF, Traboulsi EI, Broman KW, Dibernardo C, Sunness JS, Toy J, Weinberg EM: Extreme hyperopia is the result of null mutations in MFRP, which encodes a Frizzled-related protein. Proc Natl Acad Sci U S A; 2005 Jul 5;102(27):9553-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Nanophthalmos is a rare disorder of eye development characterized by extreme hyperopia (farsightedness), with refractive error in the range of +8.00 to +25.00 diopters.
  • Because the cornea and lens are normal in size and shape, hyperopia occurs because insufficient growth along the visual axis places these lensing components too close to the retina.
  • Nanophthalmic eyes show considerable thickening of both the choroidal vascular bed and scleral coat, which provide nutritive and structural support for the retina.
  • This gene is not critical for retinal function, as patients entirely lacking MFRP can still have good refraction-corrected vision, produce clinically normal electro-retinograms, and show only modest anomalies in the dark adaptation of photoreceptors.

  • MedlinePlus Health Information. consumer health - Eye Care.
  • COS Scholar Universe. author profiles.
  • SciCrunch. OMIM: Data: Gene Annotation .
  • SciCrunch. Clinical Genomic Database: Data: Gene Annotation .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nat Genet. 2000 Jul;25(3):289-93 [10888875.001]
  • [Cites] Am J Hum Genet. 1998 Sep;63(3):861-9 [9718341.001]
  • [Cites] Nat Rev Genet. 2001 Mar;2(3):165-74 [11256068.001]
  • [Cites] Genet Epidemiol. 2001 Apr;20(3):307-15 [11255240.001]
  • [Cites] Biochem Biophys Res Commun. 2001 Mar 23;282(1):116-23 [11263980.001]
  • [Cites] Cell. 2001 Nov 16;107(4):513-23 [11719191.001]
  • [Cites] Vision Res. 2002 Feb;42(4):517-25 [11853768.001]
  • [Cites] Hum Mol Genet. 2002 Aug 1;11(16):1879-86 [12140190.001]
  • [Cites] Nat Genet. 2002 Oct;32(2):326-30 [12172548.001]
  • [Cites] J Cell Sci. 2003 Jul 1;116(Pt 13):2627-34 [12775774.001]
  • [Cites] Hum Mol Genet. 2003 Oct 15;12(20):2657-67 [12944416.001]
  • [Cites] Vision Res. 2004 Mar;44(7):643-53 [14751549.001]
  • [Cites] Cell. 2004 Mar 19;116(6):883-95 [15035989.001]
  • [Cites] Prog Retin Eye Res. 2004 May;23(3):307-80 [15177205.001]
  • [Cites] J Biol Chem. 2004 Aug 13;279(33):34464-71 [15192093.001]
  • [Cites] Neuron. 2004 Aug 19;43(4):447-68 [15312645.001]
  • [Cites] Vision Res. 2004;44(21):2445-56 [15358080.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2004 Oct;45(10):3683-9 [15452077.001]
  • [Cites] Am J Hum Genet. 1974 Sep;26(5):588-97 [4422075.001]
  • [Cites] Am J Ophthalmol. 1976 Mar;81(3):300-6 [1258954.001]
  • [Cites] Trans Ophthalmol Soc U K. 1979 Jul;99(2):272-83 [298427.001]
  • [Cites] Ophthalmology. 1986 Apr;93(4):534-41 [3703530.001]
  • [Cites] Arch Ophthalmol. 1987 Mar;105(3):366-71 [3827713.001]
  • [Cites] Graefes Arch Clin Exp Ophthalmol. 1994 Sep;232(9):545-52 [7959094.001]
  • [Cites] Hum Mol Genet. 1995 Oct;4(10):1837-44 [8595404.001]
  • [Cites] J Biol Chem. 1996 Feb 23;271(8):4468-76 [8626800.001]
  • [Cites] Bioessays. 1996 Jun;18(6):439-42 [8787532.001]
  • [Cites] Nature. 1996 Jul 18;382(6588):225-30 [8717036.001]
  • [Cites] Acta Ophthalmol Scand. 1997 Jun;75(3):325-8 [9253989.001]
  • [Cites] Br J Ophthalmol. 1998 Mar;82(3):276-9 [9602624.001]
  • [Cites] Am J Hum Genet. 1998 Nov;63(5):1411-8 [9792868.001]
  • [Cites] Nat Genet. 1999 Jun;22(2):188-91 [10369264.001]
  • [Cites] Optom Vis Sci. 2004 Oct;81(10):762-8 [15557850.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2000 Sep;41(10):3149-57 [10967077.001]
  • (PMID = 15976030.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NEI NIH HHS / EY / R01 EY013610; United States / NEI NIH HHS / EY / EY013610; United States / NEI NIH HHS / EY / EY10813
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / MFRP protein, human; 0 / Membrane Proteins
  • [Other-IDs] NLM/ PMC1172243
  •  go-up   go-down


68. Ye JH, Goo YS: Comparison of voltage parameters for the stimulation of normal and degenerate retina. Conf Proc IEEE Eng Med Biol Soc; 2007;2007:5783-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Comparison of voltage parameters for the stimulation of normal and degenerate retina.
  • Retinal prosthesis is regarded as a promising method for restoring vision for the blind with retinal diseases such as retinitis pigmentosa (RP) and age related macular degeneration (ARMD).
  • Among the several prerequisites for retinal prosthesis to succeed, one of the most important is the optimization of electrical stimuli applied through the prosthesis.
  • Since the electrical characteristics of diseased retina are expected to be different with those of normal retina, we investigated different voltage parameters to stimulate normal and degenerate retina.
  • The retinal degeneration model (rd/rd mouse) was compared against control mice.
  • The distribution patterns of evoked responses appeared only on a site distant from the stimulation electrode on the rd/rd retina.
  • Conversely, in normal retina, evenly distributed response patterns were observed.
  • Since the charge intensity tends to decrease with the distance from stimulation electrode, the uneven patterns from the rd/rd mouse retina suggest that lower charge is required to evoke a response from rd/rd retina.
  • [MeSH-major] Electric Stimulation / methods. Evoked Potentials, Visual. Retina / physiopathology. Retinal Degeneration / physiopathology. Retinal Ganglion Cells

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18003327.001).
  • [ISSN] 1557-170X
  • [Journal-full-title] Conference proceedings : ... Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE Engineering in Medicine and Biology Society. Annual Conference
  • [ISO-abbreviation] Conf Proc IEEE Eng Med Biol Soc
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


69. Takase H, Yu CR, Liu X, Fujimoto C, Gery I, Egwuagu CE: Induction of suppressors of cytokine signaling (SOCS) in the retina during experimental autoimmune uveitis (EAU): potential neuroprotective role of SOCS proteins. J Neuroimmunol; 2005 Nov;168(1-2):118-27
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Induction of suppressors of cytokine signaling (SOCS) in the retina during experimental autoimmune uveitis (EAU): potential neuroprotective role of SOCS proteins.
  • We show here that SOCS expression in retina is temporarily correlated with progression of experimental autoimmune uveitis (EAU), an organ-specific autoimmune disease that serves as model of human uveitis.
  • Surprisingly, SOCS5 is constitutively expressed in retina.
  • [MeSH-major] Cytokines / metabolism. Neuroprotective Agents / therapeutic use. Retina / drug effects. Signal Transduction / physiology. Suppressor of Cytokine Signaling Proteins / therapeutic use. Uveitis / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16154209.001).
  • [ISSN] 0165-5728
  • [Journal-full-title] Journal of neuroimmunology
  • [ISO-abbreviation] J. Neuroimmunol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, CD4; 0 / Cytokines; 0 / Neuroprotective Agents; 0 / RNA, Messenger; 0 / Retinol-Binding Proteins; 0 / Suppressor of Cytokine Signaling Proteins; 0 / interphotoreceptor retinoid binding protein, rat
  •  go-up   go-down


70. Nickerson PE, Emsley JG, Myers T, Clarke DB: Proliferation and expression of progenitor and mature retinal phenotypes in the adult mammalian ciliary body after retinal ganglion cell injury. Invest Ophthalmol Vis Sci; 2007 Nov;48(11):5266-75
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Proliferation and expression of progenitor and mature retinal phenotypes in the adult mammalian ciliary body after retinal ganglion cell injury.
  • PURPOSE: Despite the identification of a small population of cells residing in the ciliary body (CB) of the adult mammalian eye that have the capacity to generate retina-like cells in vitro, their activity in vivo remains quiescent.
  • The authors sought to identify whether the predictable and time-dependent death of retinal ganglion cells (RGCs) results in activation of progenitor-like cells within the CB.
  • Finally, recoverin, the expression of which is normally restricted to photoreceptors and bipolar cells of the retina, is upregulated in the CB in a manner that is independent of proliferation.
  • CONCLUSIONS: Together, these results suggest that progenitorlike cells of the CB respond to cues associated with the loss of a single retinal cell type and that a subpopulation of those cells may differentiate into a cell that bears phenotypic resemblance to those seen in the retina.
  • [MeSH-major] Cell Proliferation. Ciliary Body / cytology. Retina / cytology. Retinal Ganglion Cells / pathology. Stem Cells / cytology

  • MedlinePlus Health Information. consumer health - Stem Cells.
  • COS Scholar Universe. author profiles.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17962482.001).
  • [ISSN] 0146-0404
  • [Journal-full-title] Investigative ophthalmology & visual science
  • [ISO-abbreviation] Invest. Ophthalmol. Vis. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Homeodomain Proteins; 0 / Intermediate Filament Proteins; 0 / Nerve Tissue Proteins; 0 / Nes protein, mouse; 0 / Nestin; 0 / Rcvrn protein, mouse; 0 / Transcription Factors; 0 / Vsx2 protein, mouse; 135844-11-0 / Recoverin
  •  go-up   go-down


71. Arora A, McKay GJ, Simpson DA: Prediction and verification of miRNA expression in human and rat retinas. Invest Ophthalmol Vis Sci; 2007 Sep;48(9):3962-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Little is known about their role in the retina.
  • The purpose of this study was to establish the retinal expression of those miRNAs predicted to target genes involved in vision.
  • METHODS: miRNAs potentially targeting important "retinal" genes, as defined by expression pattern and implication in disease, were predicted using a published algorithm (TargetScan; Envisioneering Medical Technologies, St. Louis, MO).
  • The presence of candidate miRNAs in human and rat retinal RNA was assessed by RT-PCR. cDNA levels for each miRNA were determined by quantitative PCR.
  • RESULTS: Sixty-seven miRNAs were predicted to target one or more of the 320 retinal genes listed herein.
  • All 11 candidate miRNAs tested were expressed in the retina, including miR-7, miR-124, miR135a, and miR135b.
  • CONCLUSIONS: Many miRNAs likely to regulate genes important for retinal function are present in the retina.
  • Conservation of miRNA retinal expression patterns from rats to humans supports evidence from other tissues that disruption of miRNAs is a likely cause of a range of visual abnormalities.
  • [MeSH-major] Alcohol Oxidoreductases / genetics. Gene Expression Regulation. IMP Dehydrogenase / genetics. MicroRNAs / genetics. Retina / metabolism

  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17724173.001).
  • [ISSN] 0146-0404
  • [Journal-full-title] Investigative ophthalmology & visual science
  • [ISO-abbreviation] Invest. Ophthalmol. Vis. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 3' Untranslated Regions; 0 / MicroRNAs; EC 1.1.- / Alcohol Oxidoreductases; EC 1.1.1.- / trans-retinol dehydrogenase; EC 1.1.1.205 / IMP Dehydrogenase; EC 1.1.1.205 / IMPDH1 protein, human
  •  go-up   go-down


72. Ogilvie JM, Ohlemiller KK, Shah GN, Ulmasov B, Becker TA, Waheed A, Hennig AK, Lukasiewicz PD, Sly WS: Carbonic anhydrase XIV deficiency produces a functional defect in the retinal light response. Proc Natl Acad Sci U S A; 2007 May 15;104(20):8514-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Carbonic anhydrase XIV deficiency produces a functional defect in the retinal light response.
  • CA IV immunostaining is limited to the choriocapillaris overlying the retina, whereas CA XIV is expressed within the retina in Müller glial cells and retinal pigment epithelium.
  • Reductions in the dark-adapted response were not progressive between 2 and 10 months, and no differences in retinal morphology were observed between wild-type and CA XIV-null mice.
  • However, CA IV/CA XIV double mutants showed a greater deficit in light response than the CA XIV-null retina.
  • Our results indicate that CA XIV, which regulates extracellular pH and pCO(2), plays an important part in producing a normal retinal light response.

  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Invest Ophthalmol Vis Sci. 1994 Apr;35(5):2577-84 [8163345.001]
  • [Cites] Nature. 1990 Jan 25;343(6256):364-6 [2137202.001]
  • [Cites] Invest Ophthalmol Vis Sci. 1995 May;36(6):1019-26 [7730011.001]
  • [Cites] Annu Rev Biochem. 1995;64:375-401 [7574487.001]
  • [Cites] J Neurosci. 1996 Jan;16(1):159-68 [8613782.001]
  • [Cites] Prog Neurobiol. 1996 Feb;48(2):73-103 [8737439.001]
  • [Cites] Am J Hum Genet. 1998 Nov;63(5):1307-15 [9792858.001]
  • [Cites] Invest Ophthalmol Vis Sci. 1998 Nov;39(12):2443-9 [9804152.001]
  • [Cites] Nat Genet. 1999 Apr;21(4):355-6 [10192380.001]
  • [Cites] Nat Genet. 1999 Jul;22(3):248-54 [10391211.001]
  • [Cites] Nat Genet. 1999 Jul;22(3):255-9 [10391212.001]
  • [Cites] J Med Genet. 1999 Sep;36(9):691-3 [10507726.001]
  • [Cites] Hum Mol Genet. 2005 Jan 15;14(2):255-65 [15563508.001]
  • [Cites] J Neurosci. 2005 Apr 20;25(16):4108-17 [15843613.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 May 31;102(22):8030-5 [15901897.001]
  • [Cites] Exp Eye Res. 2005 Oct;81(4):492-500 [16126196.001]
  • [Cites] Biochem J. 2005 Nov 15;392(Pt 1):83-92 [16083424.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Nov 15;102(46):16771-6 [16260723.001]
  • [Cites] Glia. 2006 Feb;53(3):241-7 [16265666.001]
  • [Cites] Retina. 2006 Oct;26(8):922-7 [17031294.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Nov 1;90(21):10081-5 [7694280.001]
  • [Cites] Glia. 2000 Aug;31(2):125-30 [10878599.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Feb 13;98(4):1918-23 [11172051.001]
  • [Cites] Hum Mol Genet. 2001 Jul 15;10(15):1555-62 [11468273.001]
  • [Cites] Mol Cell. 2001 Aug;8(2):375-81 [11545739.001]
  • [Cites] Hum Mol Genet. 2002 Jan 1;11(1):87-92 [11773002.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2003 May;44(5):2260-6 [12714669.001]
  • [Cites] Vis Neurosci. 2003 Mar-Apr;20(2):211-20 [12916741.001]
  • [Cites] Physiol Rev. 2003 Oct;83(4):1183-221 [14506304.001]
  • [Cites] Int Rev Cytol. 2003;230:263-90 [14692684.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Apr 27;101(17):6617-22 [15090652.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2004 Aug;45(8):2767-77 [15277503.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Aug 17;101(33):12300-5 [15295099.001]
  • [Cites] Invest Ophthalmol Vis Sci. 1982 Nov;23(5):678-83 [6813284.001]
  • [Cites] Invest Ophthalmol Vis Sci. 1983 Jan;24(1):37-46 [6826313.001]
  • [Cites] J Physiol. 1984 Feb;347:85-110 [6608584.001]
  • [Cites] Vision Res. 1984;24(3):275-80 [6426165.001]
  • [Cites] Ann N Y Acad Sci. 1984;429:430-46 [6430181.001]
  • [Cites] Am J Ophthalmol. 1985 Apr 15;99(4):396-9 [3920916.001]
  • [Cites] Invest Ophthalmol Vis Sci. 1990 Sep;31(9):1914-8 [2211037.001]
  • [Cites] Proc Natl Acad Sci U S A. 1991 Apr 1;88(7):2716-20 [1901414.001]
  • [Cites] Nature. 1991 Dec 12;354(6353):478-80 [1749427.001]
  • [Cites] Nature. 1991 Dec 12;354(6353):480-3 [1684223.001]
  • [Cites] Exp Eye Res. 1992 May;54(5):685-97 [1623953.001]
  • [Cites] Exp Eye Res. 1992 May;54(5):711-8 [1623955.001]
  • [Cites] Graefes Arch Clin Exp Ophthalmol. 1993 May;231(5):254-6 [8319913.001]
  • [Cites] Exp Eye Res. 1986 Jun;42(6):585-93 [3720873.001]
  • [Cites] Bioessays. 1989 Jun;10(6):186-92 [2500929.001]
  • [Cites] Invest Ophthalmol Vis Sci. 1994 Oct;35(11):3957-61 [7928195.001]
  • (PMID = 17485676.001).
  • [ISSN] 0027-8424
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NEI NIH HHS / EY / EY08922; United States / NEI NIH HHS / EY / P30 EY002687; United States / NIDCD NIH HHS / DC / P30 DC004665; United States / NIGMS NIH HHS / GM / R01 GM034182-22; United States / NIGMS NIH HHS / GM / GM34182; United States / NIDDK NIH HHS / DK / R01 DK040163; United States / NIDDK NIH HHS / DK / DK40163; United States / NEI NIH HHS / EY / EY02687; United States / NIGMS NIH HHS / GM / R01 GM034182; United States / NEI NIH HHS / EY / R03 EY015113; United States / NIDDK NIH HHS / DK / DK040163-19; United States / NIDDK NIH HHS / DK / R01 DK040163-19; United States / NEI NIH HHS / EY / R01 EY008922; United States / NEI NIH HHS / EY / EY015113; United States / NIGMS NIH HHS / GM / GM034182-22
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] EC 4.2.1.- / Carbonic Anhydrase IV; EC 4.2.1.1 / Carbonic Anhydrases; EC 4.2.1.1 / carbonic anhydrase XIV
  • [Other-IDs] NLM/ PMC1895981
  •  go-up   go-down


73. Liu X, Wang W, Wang AR, Ning Q, Luo XP: [Pathogenesis of retinal neovascularization in a rat model of oxygen fluctuations-induced retinopathy]. Zhonghua Er Ke Za Zhi; 2007 Jan;45(1):7-13
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Pathogenesis of retinal neovascularization in a rat model of oxygen fluctuations-induced retinopathy].
  • The authors developed a rat model of retinal neovascularization by repeated fluctuations of inhaled oxygen between hypoxia and hyperoxia to investigate the mechanism of the development of retinal neovascularization, the regulation of vascular endothelial growth factor (VEGF) and KDR/Flk-1 (VEGFR-2) expression.
  • The status of retinal vasculature on day 4 after oxygen exposure was also observed.
  • The retinas were dissected and stained by using a histochemical method for detecting adenosine diphosphatase (ADPase) activity, digital images of the retinas were captured and the peripheral avascular retina were measured.
  • HE staining on methacrylate sections of eyes was used for counting the number of nuclei extending from retinal area into vitreous to identify extraretinal neovascularization.
  • (1) The animal model was successfully established: the avascular areas of retina of 18-day-old rats were larger than those of the control group and the numbers of nuclei extending from retinal area into vitreous in exposed group were significantly higher compared to the control (P < 0.05). (2) The expression of VEGF and Flk-1 on the 14(th) day in the oxygen group was significantly stronger than that of the control group (P < 0.05).
  • In the oxygen group, VEGF and Flk-1 expression was the strongest in the retina on the 18(th) day, the result had significant difference as compared with the 14(th) and 25(th) day (P < 0.05), and they were also stronger than that of the control group (P < 0.05).
  • CONCLUSION: Fluctuation in oxygen is associated with the development of retinal neovascularization in the retinopathy.
  • Increased expressions of VEGF and Flk-1 in the oxgen fluctuations-induced neovascularized retina suggested that VEGF and Flk-1 might play a critical role in the pathogenesis of ROP.
  • The results also indicated the positive feedback in the pathogenesis of ROP that the synergistic interaction of VEGF and Flk-1 in the retinal vascular proliferation.
  • [MeSH-major] Disease Models, Animal. Oxygen / adverse effects. Retinal Neovascularization / pathology. Retinopathy of Prematurity / pathology

  • Hazardous Substances Data Bank. OXYGEN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17349140.001).
  • [ISSN] 0578-1310
  • [Journal-full-title] Zhonghua er ke za zhi = Chinese journal of pediatrics
  • [ISO-abbreviation] Zhonghua Er Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Vascular Endothelial Growth Factor A; 0 / vascular endothelial growth factor A, rat; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2; S88TT14065 / Oxygen
  •  go-up   go-down


74. Lukáts A, Szabó A, Röhlich P, Vígh B, Szél A: Photopigment coexpression in mammals: comparative and developmental aspects. Histol Histopathol; 2005 04;20(2):551-74
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Whereas in the upper retinal field the ratio of short wave to middle-to-long wave cones falls in the usual range (1:10), in the ventral retinal field M/L-pigment expression is completely missing.
  • In other species without retinal division, dual cones appear during development, suggesting that M/L-cones develop from S-cones.
  • In the comparative part of this report the retinal cone distribution of eight rodent species is reported.
  • In two species dual cones appear in adult specimens without retinal division, and dual elements either occupy the dorsal peripheral retina, or make up the entire cone population.
  • This is the first observation proving that all cones of a retina are of dual nature.
  • In the developmental part, the retinal maturation of other species is examined to test the hypothesis of transitory coexpression.
  • In these species S-pigment expression precedes that of the M/L-pigment, but dual cones are either identified in a small number or they are completely missing from the developing retina.
  • [MeSH-major] Mammals / growth & development. Mammals / metabolism. Retinal Cone Photoreceptor Cells / growth & development. Retinal Cone Photoreceptor Cells / metabolism. Retinal Pigments / metabolism
  • [MeSH-minor] Animals. Humans. Immunohistochemistry. Mice. Photoreceptor Cells, Vertebrate / metabolism. Primates. Rabbits. Retina / anatomy & histology. Retina / growth & development. Retina / metabolism. Rodentia. Species Specificity. Tupaiidae

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15736061.001).
  • [ISSN] 0213-3911
  • [Journal-full-title] Histology and histopathology
  • [ISO-abbreviation] Histol. Histopathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Retinal Pigments
  • [Number-of-references] 132
  •  go-up   go-down


75. Stella SL Jr, Hu WD, Vila A, Brecha NC: Adenosine inhibits voltage-dependent Ca2+ influx in cone photoreceptor terminals of the tiger salamander retina. J Neurosci Res; 2007 Apr;85(5):1126-37
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adenosine inhibits voltage-dependent Ca2+ influx in cone photoreceptor terminals of the tiger salamander retina.
  • To assess the impact of adenosine on Ca(2+) influx though voltage-gated Ca(2+) channels in cone terminals, whole-cell perforated-patch clamp recording and Ca(2+) imaging with fluo-4 were used on isolated cones and salamander retinal slices.

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. GLUTAMIC ACID HYDROCHLORIDE .
  • Hazardous Substances Data Bank. Adenosine .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • [Cites] J Gen Physiol. 1996 May;107(5):621-30 [8740375.001]
  • [Cites] Pharmacol Rev. 2001 Dec;53(4):527-52 [11734617.001]
  • [Cites] J Neurophysiol. 2002 Jan;87(1):351-60 [11784755.001]
  • [Cites] J Neurochem. 2002 May;81(3):550-6 [12065663.001]
  • [Cites] An Acad Bras Cienc. 2002 Sep;74(3):437-51 [12378312.001]
  • [Cites] J Neurosci. 2003 Mar 1;23(5):1659-66 [12629170.001]
  • [Cites] J Physiol. 2003 Mar 15;547(Pt 3):761-74 [12562925.001]
  • [Cites] J Neurophysiol. 2003 Jul;90(1):165-74 [12843308.001]
  • [Cites] J Neurophysiol. 2003 Sep;90(3):1747-53 [12724369.001]
  • [Cites] J Neurosci. 2003 Nov 19;23(33):10475-86 [14627631.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2004 Oct;45(10):3740-8 [15452085.001]
  • [Cites] J Physiol. 1978 Jul;280:449-70 [211229.001]
  • [Cites] Brain Res. 1986 Nov 19;398(1):106-12 [3801882.001]
  • [Cites] Proc Natl Acad Sci U S A. 1987 Jun;84(11):3906-10 [3473489.001]
  • [Cites] J Neurosci Methods. 1987 Jun;20(2):139-49 [3037200.001]
  • [Cites] J Gen Physiol. 1989 Oct;94(4):719-43 [2482325.001]
  • [Cites] J Neurochem. 1990 Feb;54(2):648-55 [2299359.001]
  • [Cites] J Neurochem. 1990 Nov;55(5):1603-11 [2213012.001]
  • [Cites] Vis Neurosci. 1989;2(2):109-16 [2487641.001]
  • [Cites] J Neurosci Methods. 1991 Mar;37(1):15-26 [2072734.001]
  • [Cites] Cell Mol Neurobiol. 1991 Oct;11(5):463-84 [1683815.001]
  • [Cites] J Neurochem. 1992 May;58(5):1699-705 [1560227.001]
  • [Cites] Neuron. 1993 Feb;10(2):327-34 [8382501.001]
  • [Cites] J Neurosci. 1993 Aug;13(8):3533-48 [8340818.001]
  • [Cites] Nature. 1993 Sep 16;365(6443):256-8 [8396730.001]
  • [Cites] J Pharmacol Exp Ther. 1994 Feb;268(2):537-45 [8113965.001]
  • [Cites] Neuron. 1994 May;12(5):1139-48 [8185949.001]
  • [Cites] J Neurosci. 1994 Aug;14(8):5131-46 [8046473.001]
  • [Cites] Vis Neurosci. 1997 Mar-Apr;14(2):207-12 [9147473.001]
  • [Cites] J Neurophysiol. 1997 Apr;77(4):2175-90 [9114264.001]
  • [Cites] Exp Eye Res. 1997 Nov;65(5):595-602 [9367639.001]
  • [Cites] J Pharmacol Exp Ther. 1998 May;285(2):568-72 [9580599.001]
  • [Cites] Exp Eye Res. 1997 Dec;65(6):771-9 [9441700.001]
  • [Cites] Pharmacol Rev. 1998 Sep;50(3):413-92 [9755289.001]
  • [Cites] Vis Neurosci. 1998 Nov-Dec;15(6):1175-87 [9839981.001]
  • [Cites] Invest Ophthalmol Vis Sci. 1999 May;40(6):1200-16 [10235554.001]
  • [Cites] J Neurochem. 1999 Jun;72(6):2345-55 [10349843.001]
  • [Cites] Vision Res. 1999 Jul;39(15):2519-35 [10396621.001]
  • [Cites] J Neurosci. 1999 Sep 1;19(17):7249-61 [10460231.001]
  • [Cites] J Neurosci. 2005 Jan 5;25(1):215-22 [15634784.001]
  • [Cites] Neuron. 2005 Apr 21;46(2):275-83 [15848805.001]
  • [Cites] Neuron. 2005 Jun 2;46(5):731-44 [15924860.001]
  • [Cites] J Neurosci. 2005 Jun 8;25(23):5502-10 [15944378.001]
  • [Cites] J Neurophysiol. 1999 Dec;82(6):2947-55 [10601431.001]
  • [Cites] Neuron. 1999 Dec;24(4):809-17 [10624945.001]
  • [Cites] Curr Opin Neurobiol. 2000 Jun;10(3):321-7 [10851173.001]
  • [Cites] J Physiol. 2000 Jul 1;526 Pt 1:143-55 [10878107.001]
  • [Cites] Eur J Neurosci. 2000 Oct;12(10):3537-48 [11029623.001]
  • [Cites] J Comp Neurol. 2001 Mar 19;431(4):424-36 [11223812.001]
  • [Cites] Annu Rev Neurosci. 2001;24:31-55 [11283304.001]
  • [Cites] Curr Opin Neurobiol. 2001 Oct;11(5):544-9 [11595486.001]
  • [Cites] J Comp Neurol. 2001 Oct 15;439(2):224-34 [11596050.001]
  • (PMID = 17304584.001).
  • [ISSN] 0360-4012
  • [Journal-full-title] Journal of neuroscience research
  • [ISO-abbreviation] J. Neurosci. Res.
  • [Language] ENG
  • [Grant] United States / NEI NIH HHS / EY / R01 EY004067; United States / NEI NIH HHS / EY / R01 EY015573; United States / NIDDK NIH HHS / DK / P30 DK041301; United States / NEI NIH HHS / EY / EY 15573; United States / NEI NIH HHS / EY / EY 04067; United States / NEI NIH HHS / EY / R56 EY004067; United States / NIDDK NIH HHS / DK / DK 41301
  • [Publication-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.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Calcium Channels; 0 / Cytoskeletal Proteins; 0 / Fluorescent Dyes; 0 / Neuropeptides; 0 / PCLO protein, human; 0 / Vesicle-Associated Membrane Protein 1; 3KX376GY7L / Glutamic Acid; K72T3FS567 / Adenosine
  • [Other-IDs] NLM/ NIHMS501544; NLM/ PMC3737423
  •  go-up   go-down


76. Beszédesová N, Budinská E, Skorkovská S: [Functional integrity of neural retina in 2. type diabetics]. Cesk Slov Oftalmol; 2009 Jul;65(4):124-30
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Functional integrity of neural retina in 2. type diabetics].
  • The purpose of this prospective longitudinal study was to investigate early defects in functional integrity of neural retina in 2. type diabetic patients without or with mild diabetic retinopathy (DR) since there is an evidence of early functional changes in neural retina before occurrence of clinical manifestation of DR.
  • In conclusion, it was not proved in this study that CS test is suitable for the screening for DR or early functional defects in neural retina before clinical manifestation of DR.
  • Early diagnosis of DM and good compensation of diabetes, blood pressure and serum lipids level can postpone the onset of DR as well as the visual functions impairments.

  • MedlinePlus Health Information. consumer health - Diabetes Type 2.
  • MedlinePlus Health Information. consumer health - Diabetic Eye Problems.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19750829.001).
  • [ISSN] 1211-9059
  • [Journal-full-title] Ceská a slovenská oftalmologie : casopis Ceské oftalmologické spolecnosti a Slovenské oftalmologické spolecnosti
  • [ISO-abbreviation] Cesk Slov Oftalmol
  • [Language] slo
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Czech Republic
  • [Chemical-registry-number] 0 / Hemoglobin A, Glycosylated
  •  go-up   go-down


77. Ribelayga C, Mangel SC: Identification of a circadian clock-controlled neural pathway in the rabbit retina. PLoS One; 2010;5(6):e11020
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of a circadian clock-controlled neural pathway in the rabbit retina.
  • BACKGROUND: Although the circadian clock in the mammalian retina regulates many physiological processes in the retina, it is not known whether and how the clock controls the neuronal pathways involved in visual processing.
  • Because A-type horizontal cells make synaptic contact exclusively with cones, these observations indicate that the circadian clock in the mammalian retina substantially increases rod input to A-type horizontal cells at night by enhancing rod-cone coupling.
  • CONCLUSIONS/SIGNIFICANCE: Considered together, these results identify the rod-cone gap junction as a key site in mammals through which the retinal clock, using dopamine activation of D(2) receptors, controls signal flow in the day and night from rods into the cone system.
  • [MeSH-major] Circadian Rhythm. Neurons / physiology. Retina / physiology. Visual Pathways

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Comp Neurol. 1982 Jul 1;208(3):288-303 [6288777.001]
  • [Cites] J Neurosci. 2009 Dec 2;29(48):15178-86 [19955370.001]
  • [Cites] J Neurosci. 1986 Dec;6(12):3505-17 [3794785.001]
  • [Cites] J Comp Neurol. 1989 Nov 22;289(4):537-53 [2592596.001]
  • [Cites] J Neurocytol. 1990 Oct;19(5):731-6 [1706416.001]
  • [Cites] J Neurosci. 1992 Mar;12(3):840-53 [1312136.001]
  • [Cites] Vis Neurosci. 1994 May-Jun;11(3):549-60 [7518689.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Nov 7;92(23):10658-62 [7479860.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 May 14;93(10):4655-60 [8643459.001]
  • [Cites] Vis Neurosci. 1995 Nov-Dec;12(6):1151-75 [8962834.001]
  • [Cites] Physiol Rev. 1998 Jan;78(1):189-225 [9457173.001]
  • [Cites] Annu Rev Physiol. 2005;67:491-514 [15709967.001]
  • [Cites] J Neurophysiol. 2005 Mar;93(3):1476-85 [15525810.001]
  • [Cites] Prog Retin Eye Res. 2005 Jul;24(4):433-56 [15845344.001]
  • [Cites] J Neurosci. 2005 Nov 30;25(48):11201-9 [16319320.001]
  • [Cites] Curr Biol. 2006 Feb 21;16(4):389-95 [16488873.001]
  • [Cites] Eur J Neurosci. 2007 Jun;25(11):3195-216 [17552989.001]
  • [Cites] Neuron. 2008 Aug 14;59(3):462-74 [18701071.001]
  • [Cites] Neuron. 2008 Sep 11;59(5):790-801 [18786362.001]
  • [Cites] Brain Res Brain Res Rev. 2000 Apr;32(1):121-9 [10751661.001]
  • [Cites] Prog Retin Eye Res. 2000 Jul;19(4):385-419 [10785616.001]
  • [Cites] Vis Neurosci. 2000 Jul-Aug;17(4):509-28 [11016572.001]
  • [Cites] Prog Retin Eye Res. 2001 May;20(3):351-84 [11286897.001]
  • [Cites] J Neurosci. 2001 Apr 15;21(8):2897-902 [11306641.001]
  • [Cites] Prog Brain Res. 2001;131:419-36 [11420960.001]
  • [Cites] Prog Brain Res. 2001;131:487-503 [11420965.001]
  • [Cites] Prog Brain Res. 2001;131:505-18 [11420966.001]
  • [Cites] J Physiol. 2002 Nov 1;544(Pt 3):801-16 [12411525.001]
  • [Cites] Neuron. 2002 Nov 14;36(4):703-12 [12441058.001]
  • [Cites] Curr Biol. 2002 Nov 19;12(22):1900-7 [12445382.001]
  • [Cites] J Comp Neurol. 2003 Dec 8;467(2):243-53 [14595771.001]
  • [Cites] J Physiol. 2004 Jan 15;554(Pt 2):467-82 [14565990.001]
  • [Cites] J Biol Rhythms. 2004 Apr;19(2):91-102 [15038849.001]
  • [Cites] Doc Ophthalmol. 2004 Jan;108(1):17-40 [15104164.001]
  • [Cites] Annu Rev Neurosci. 2004;27:393-418 [15217338.001]
  • [Cites] J Physiol. 2004 Aug 1;558(Pt 3):897-912 [15181169.001]
  • [Cites] J Opt Soc Am. 1964 Dec;54(12):1451-9 [5868597.001]
  • [Cites] Vision Res. 1969 Nov;9(11):1331-44 [5358838.001]
  • [Cites] Proc Natl Acad Sci U S A. 1973 Jun;70(6):1677-81 [4198274.001]
  • [Cites] J Comp Neurol. 1975 Feb 15;159(4):473-502 [1092733.001]
  • [Cites] J Comp Neurol. 1977 Mar 1;172(1):109-35 [838876.001]
  • [Cites] J Comp Neurol. 1999 Mar 1;405(1):75-87 [10022197.001]
  • [Cites] Vision Res. 1999 May;39(9):1611-30 [10343855.001]
  • [Cites] Nat Neurosci. 2005 Jan;8(1):61-6 [15580271.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Sep 16;105(37):14181-6 [18779590.001]
  • [Cites] Eur J Neurosci. 2009 Feb;29(4):761-7 [19200071.001]
  • [Cites] Vision Res. 1983;23(11):1221-7 [6659372.001]
  • (PMID = 20548772.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Grant] United States / NEI NIH HHS / EY / R01 EY005102; United States / NEI NIH HHS / EY / R01 EY018640
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2883549
  •  go-up   go-down


78. Reichman S, Kalathur RK, Lambard S, Aït-Ali N, Yang Y, Lardenois A, Ripp R, Poch O, Zack DJ, Sahel JA, Léveillard T: The homeobox gene CHX10/VSX2 regulates RdCVF promoter activity in the inner retina. Hum Mol Genet; 2010 Jan 15;19(2):250-61
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The homeobox gene CHX10/VSX2 regulates RdCVF promoter activity in the inner retina.
  • Rod-derived Cone Viability Factor (RdCVF) is a trophic factor with therapeutic potential for the treatment of retinitis pigmentosa, a retinal disease that commonly results in blindness.
  • Since CHX10/VSX2 is expressed predominantly in the inner retina, this finding motivated us to demonstrate that RdCVF is expressed in the inner as well as the outer retina.
  • Interestingly, the loss of rods in the rd1 mouse, a model of retinitis pigmentosa, is associated with decreased expression of RdCVF by inner retinal cells as well as by rods.
  • Based upon these results, we propose an alternative therapeutic strategy aimed at recapitulating RdCVF expression in the inner retina, where cell loss is not significant, to prevent secondary cone death and central vision loss in patients suffering from retinitis pigmentosa.

  • COS Scholar Universe. author profiles.
  • HAL archives ouvertes. Full text from .
  • SciCrunch. OMIM: Data: Gene Annotation .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Neuron. 1993 Oct;11(4):595-605 [8398150.001]
  • [Cites] Hum Mutat. 1993;2(4):249-55 [8401533.001]
  • [Cites] Science. 1994 Jun 10;264(5165):1604-8 [8202715.001]
  • [Cites] Neuron. 1994 Aug;13(2):377-93 [7914735.001]
  • [Cites] Invest Ophthalmol Vis Sci. 1995 Feb;36(2):263-75 [7843898.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Apr 11;92(8):3249-53 [7724547.001]
  • [Cites] Invest Ophthalmol Vis Sci. 1995 Oct;36(11):2186-92 [7558711.001]
  • [Cites] Nucleic Acids Res. 1996 Jan 1;24(1):238-41 [8594589.001]
  • [Cites] Nat Genet. 1996 Apr;12(4):376-84 [8630490.001]
  • [Cites] J Comput Biol. 1994 Fall;1(3):191-8 [8790464.001]
  • [Cites] J Biol Chem. 1996 Nov 22;271(47):29612-8 [8939891.001]
  • [Cites] Ophthalmic Res. 1997;29(5):290-7 [9323720.001]
  • [Cites] Cell. 1997 Nov 14;91(4):531-41 [9390562.001]
  • [Cites] Am J Hum Genet. 1998 Mar;62(3):503-8 [9497269.001]
  • [Cites] Exp Eye Res. 2008 Apr;86(4):541-2 [17582398.001]
  • [Cites] BMC Genomics. 2008;9:208 [18457592.001]
  • [Cites] Gen Physiol Biophys. 2008 Jun;27(2):71-84 [18645221.001]
  • [Cites] J Neurochem. 2009 Jan;108(1):285-94 [19012751.001]
  • [Cites] Mol Ther. 2009 May;17(5):787-95 [19277021.001]
  • [Cites] Mol Cell Proteomics. 2009 Jun;8(6):1206-18 [19279044.001]
  • [Cites] Nat Biotechnol. 1996 Dec;14(13):1675-80 [9634850.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Jul 7;95(14):8357-62 [9653191.001]
  • [Cites] J Neurosci. 1998 Dec 1;18(23):9662-72 [9822727.001]
  • [Cites] Mech Dev. 1999 May;83(1-2):183-6 [10381579.001]
  • [Cites] Hum Mol Genet. 2005 Apr 1;14(7):913-23 [15703187.001]
  • [Cites] Retina. 2005 Dec;25(8 Suppl):S47 [16374333.001]
  • [Cites] J Biol Chem. 2006 Jan 13;281(2):744-51 [16236706.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Mar 7;103(10):3896-901 [16505355.001]
  • [Cites] Methods Mol Biol. 2006;326:61-87 [16780194.001]
  • [Cites] Nucleic Acids Res. 2006 Jul 1;34(Web Server issue):W578-83 [16845074.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Jul 25;103(30):11300-5 [16849425.001]
  • [Cites] Antioxid Redox Signal. 2007 Jan;9(1):25-47 [17115886.001]
  • [Cites] Antioxid Redox Signal. 2007 Aug;9(8):1035-57 [17567240.001]
  • [Cites] BMC Mol Biol. 2007;8:74 [17764561.001]
  • [Cites] Bioinformatics. 2008 Jan 15;24(2):276-8 [18037684.001]
  • [Cites] Brain Res. 2008 Feb 4;1192:99-113 [17919464.001]
  • [Cites] Arch Ophthalmol. 2000 Jun;118(6):807-11 [10865319.001]
  • [Cites] Genomics. 2000 Jul 15;67(2):128-39 [10903837.001]
  • [Cites] Int J Dev Biol. 2000;44(6):627-36 [11061426.001]
  • [Cites] Development. 2001 Apr;128(8):1313-22 [11262232.001]
  • [Cites] Hum Mol Genet. 2001 Jul 15;10(15):1571-9 [11468275.001]
  • [Cites] Mech Dev. 2001 Dec;109(2):315-22 [11731243.001]
  • [Cites] EMBO J. 2002 Apr 15;21(8):1978-86 [11953317.001]
  • [Cites] J Biol Chem. 2002 Jul 19;277(29):25877-83 [11943774.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2002 Oct;43(10):3292-8 [12356837.001]
  • [Cites] Nucleic Acids Res. 2003 Jul 1;31(13):3576-9 [12824369.001]
  • [Cites] Antioxid Redox Signal. 2004 Feb;6(1):15-7 [14713332.001]
  • [Cites] Antioxid Redox Signal. 2004 Feb;6(1):53-61 [14713335.001]
  • [Cites] Biol Cell. 2004 May;96(4):261-9 [15145530.001]
  • [Cites] Mol Neurobiol. 2004 Jun;29(3):229-42 [15181236.001]
  • [Cites] Dev Biol. 2004 Jul 15;271(2):388-402 [15223342.001]
  • [Cites] Nat Genet. 2004 Jul;36(7):755-9 [15220920.001]
  • [Cites] Mol Med. 2004 Jan-Jun;10(1-6):12-8 [15502878.001]
  • [Cites] Biochemistry. 1974 Jun 4;13(12):2633-7 [4831907.001]
  • [Cites] Biochemistry. 1977 Oct 18;16(21):4743-51 [911786.001]
  • [Cites] Invest Ophthalmol Vis Sci. 1978 Jun;17(6):489-98 [659071.001]
  • [Cites] Trends Neurosci. 1989 Jul;12(7):252-5 [2475935.001]
  • [Cites] Exp Eye Res. 1990 Jan;50(1):79-88 [2307198.001]
  • [Cites] Biotechniques. 1990 Apr;8(4):398-403 [1692716.001]
  • [Cites] Nature. 1990 Oct 18;347(6294):677-80 [1977087.001]
  • [Cites] Proc Natl Acad Sci U S A. 1980 Oct;77(10):5794-8 [6777776.001]
  • [Cites] J Comp Neurol. 1990 Nov 15;301(3):433-42 [2262600.001]
  • [Cites] Exp Eye Res. 1992 Jun;54(6):853-60 [1381682.001]
  • [Cites] Nat Genet. 1992 Jun;1(3):209-13 [1303237.001]
  • [Cites] Nat Genet. 1993 Jun;4(2):130-4 [8394174.001]
  • (PMID = 19843539.001).
  • [ISSN] 1460-2083
  • [Journal-full-title] Human molecular genetics
  • [ISO-abbreviation] Hum. Mol. Genet.
  • [Language] ENG
  • [Grant] United States / NEI NIH HHS / EY / R01 EY009769; United States / NEI NIH HHS / EY / 5R01EY009769
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Eye Proteins; 0 / Homeodomain Proteins; 0 / NXNL1 protein, human; 0 / RdCVF protein, mouse; 0 / Transcription Factors; 0 / VSX2 protein, human; 0 / Vsx2 protein, mouse; 52500-60-4 / Thioredoxins
  • [Other-IDs] NLM/ HALMS465889; NLM/ PMC2796890
  •  go-up   go-down


79. Rojas J, Fernandez I, Pastor JC, Garcia-Gutierrez MT, Sanabria MR, Brion M, Coco RM, Ruiz-Moreno JM, Garcia-Arumi J, Elizalde J, Ruiz-Miguel M, Gallardo JM, Corrales RM, Carracedo A: A strong genetic association between the tumor necrosis factor locus and proliferative vitreoretinopathy: the retina 4 project. Ophthalmology; 2010 Dec;117(12):2417-2423.e1-2
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A strong genetic association between the tumor necrosis factor locus and proliferative vitreoretinopathy: the retina 4 project.
  • OBJECTIVE: To assess the genetic contribution to proliferative vitreoretinopathy (PVR) and report the strong association observed in the tumor necrosis factor (TNF) locus.
  • DESIGN: As a component of The Retina 4 Project, a case-controlled, candidate gene association study in the TNF locus was conducted.
  • PARTICIPANTS AND CONTROLS: Blood from 450 patients with (138 cases) and without (312 controls) post-rhegmatogenous retinal detachment (RD) PVR was genotyped to determine polymorphisms located in the TNFα gene.
  • If supported in extended studies, the rs2229094(T→C) may have significant implications regarding the genetic risk of the retinal repairing process.
  • [MeSH-major] Lymphotoxin-alpha / genetics. Polymorphism, Single Nucleotide. Tumor Necrosis Factor-alpha / genetics. Vitreoretinopathy, Proliferative / genetics
  • [MeSH-minor] Case-Control Studies. Gene Frequency. Genotype. Humans. Membrane Proteins / genetics. Natural Cytotoxicity Triggering Receptor 3 / genetics. Retinal Detachment / genetics

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright © 2010 American Academy of Ophthalmology. Published by Elsevier Inc. All rights reserved.
  • (PMID = 20663564.001).
  • [ISSN] 1549-4713
  • [Journal-full-title] Ophthalmology
  • [ISO-abbreviation] Ophthalmology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / LST1 protein, human; 0 / Lymphotoxin-alpha; 0 / Membrane Proteins; 0 / NCR3 protein, human; 0 / Natural Cytotoxicity Triggering Receptor 3; 0 / Tumor Necrosis Factor-alpha
  •  go-up   go-down


80. Clark AM, Yun S, Veien ES, Wu YY, Chow RL, Dorsky RI, Levine EM: Negative regulation of Vsx1 by its paralog Chx10/Vsx2 is conserved in the vertebrate retina. Brain Res; 2008 Feb 4;1192:99-113
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Negative regulation of Vsx1 by its paralog Chx10/Vsx2 is conserved in the vertebrate retina.
  • Both are expressed in the retina and have important but distinct roles in retinal development.
  • Mutations in Chx10/Vsx2 cause reduced retinal progenitor cell (RPC) proliferation and an absence of bipolar cells, while mutations in Vsx1 impair differentiation of cone bipolar cells.
  • Given their structural similarities and importance in retinal development, we sought to determine if a regulatory interaction exists between these genes and whether inactivation of both genes blocks initiation of retinal development.
  • In mice deficient for both Chx10/Vsx2 and Vsx1 and zebrafish embryos co-injected with chx10/Vsx2 and vsx1 morpholinos, the changes in embryonic retinal development and marker expression are similar in magnitude to embryos with Chx10/Vsx2 loss of function only.
  • Although Vsx1 mRNA is upregulated in Chx10/Vsx2 deficient RPCs, Vsx1 does not genetically compensate for loss of Chx10/Vsx2, demonstrating that Prd-L:CVC genes, although important, are not absolutely required to initiate retinal development.

  • MedlinePlus Health Information. consumer health - Stem Cells.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • SciCrunch. ZFIN: Data: Gene Expression .
  • ZFIN. ZFIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Development. 2004 Oct;131(20):5139-52 [15459106.001]
  • [Cites] Development. 2004 Nov;131(22):5539-50 [15496443.001]
  • [Cites] Anat Embryol (Berl). 1976 Dec 22;150(1):85-97 [827941.001]
  • [Cites] EMBO J. 1991 Dec;10(12):3609-19 [1718739.001]
  • [Cites] Development. 2000 May;127(9):1911-9 [10751179.001]
  • [Cites] Development. 2000 Aug;127(16):3581-91 [10903182.001]
  • [Cites] Development. 1995 May;121(5):1253-62 [7789259.001]
  • [Cites] Dev Dyn. 1995 Jul;203(3):253-310 [8589427.001]
  • [Cites] Nat Genet. 1996 Apr;12(4):376-84 [8630490.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Apr 1;94(7):3088-93 [9096350.001]
  • [Cites] Development. 1997 May;124(10):1985-97 [9169845.001]
  • [Cites] Invest Ophthalmol Vis Sci. 1997 Jun;38(7):1293-303 [9191592.001]
  • [Cites] Mech Dev. 1997 May;63(2):133-43 [9203137.001]
  • [Cites] J Comp Neurol. 1997 Nov 24;388(3):495-505 [9368856.001]
  • [Cites] Development. 1998 Mar;125(5):869-77 [9449669.001]
  • [Cites] Dev Genet. 1998;23(2):128-41 [9770270.001]
  • [Cites] Dev Genes Evol. 1999 Mar;209(3):186-97 [10079362.001]
  • [Cites] Mol Cell. 1999 Mar;3(3):297-307 [10198632.001]
  • [Cites] Nucleic Acids Res. 1993 Mar 11;21(5):1087-95 [8464695.001]
  • [Cites] Neuron. 1993 Oct;11(4):689-701 [7691107.001]
  • [Cites] Neuron. 1994 Aug;13(2):377-93 [7914735.001]
  • [Cites] J Comp Neurol. 1994 Oct 22;348(4):596-606 [7836564.001]
  • [Cites] J Neurobiol. 2000 Feb 5;42(2):232-47 [10640330.001]
  • [Cites] Mech Dev. 2000 Feb;90(2):293-7 [10640715.001]
  • [Cites] Hum Genet. 2004 Sep;115(4):302-9 [15257456.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Dec 7;101(49):17144-9 [15569927.001]
  • [Cites] Development. 2005 Jan;132(1):177-87 [15576400.001]
  • [Cites] Dev Biol. 2005 Feb 15;278(2):560-75 [15680370.001]
  • [Cites] Development. 2005 Mar;132(5):913-23 [15673568.001]
  • [Cites] J Biol Chem. 2005 Mar 18;280(11):10100-8 [15647262.001]
  • [Cites] Mol Cell Biol. 2005 Apr;25(7):2573-82 [15767664.001]
  • [Cites] Dev Biol. 2005 May 15;281(2):240-55 [15893976.001]
  • [Cites] Curr Opin Genet Dev. 2005 Jun;15(3):348-53 [15917212.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2006 Jan;47(1):48-54 [16384943.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2006 Jan;47(1):386-96 [16384989.001]
  • [Cites] J Biol Chem. 2006 Jan 13;281(2):744-51 [16236706.001]
  • [Cites] Eur J Neurosci. 2006 Jan;23(1):75-82 [16420417.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Mar 28;103(13):4988-93 [16547132.001]
  • [Cites] PLoS Biol. 2006 Sep;4(9):e272 [16903786.001]
  • [Cites] Dev Genes Evol. 2006 Dec;216(12):829-34 [17103185.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2006 Dec;47(12):5243-50 [17122109.001]
  • [Cites] Ophthalmology. 2004 Apr;111(4):828-36 [15051220.001]
  • [Cites] Genomics. 2000 Jul 15;67(2):128-39 [10903837.001]
  • [Cites] Results Probl Cell Differ. 2000;31:69-91 [10929402.001]
  • [Cites] Nat Genet. 2000 Aug;25(4):397-401 [10932181.001]
  • [Cites] Development. 2000 Nov;127(21):4599-609 [11023863.001]
  • [Cites] Int J Dev Biol. 2000;44(6):627-36 [11061426.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 May 8;98(10):5602-7 [11331779.001]
  • [Cites] Biochem Biophys Res Commun. 2001 Aug 10;286(1):133-40 [11485319.001]
  • [Cites] Development. 2001 Jun;128(11):1951-69 [11493519.001]
  • [Cites] Development. 2001 Oct;128(20):4035-44 [11641226.001]
  • [Cites] Annu Rev Cell Dev Biol. 2001;17:255-96 [11687490.001]
  • [Cites] Curr Opin Cell Biol. 2001 Dec;13(6):706-14 [11698186.001]
  • [Cites] Mech Dev. 2001 Dec;109(2):315-22 [11731243.001]
  • [Cites] Semin Cell Dev Biol. 2001 Dec;12(6):475-84 [11735383.001]
  • [Cites] Hum Mol Genet. 2002 May 1;11(9):1029-36 [11978762.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2002 Nov;43(11):3522-9 [12407164.001]
  • [Cites] Development. 2003 Feb;130(3):539-52 [12490560.001]
  • [Cites] J Comp Neurol. 2003 Jun 23;461(2):187-204 [12724837.001]
  • [Cites] Cell Cycle. 2003 Jul-Aug;2(4):350-7 [12851489.001]
  • [Cites] Development. 2003 Nov;130(21):5155-67 [12944429.001]
  • [Cites] Nat Rev Genet. 2003 Nov;4(11):876-88 [14634635.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2004 Feb;45(2):375-84 [14744875.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Feb 10;101(6):1754-9 [14745032.001]
  • [Cites] Semin Cell Dev Biol. 2004 Feb;15(1):63-74 [15036209.001]
  • [Cites] Curr Biol. 2004 Mar 23;14(6):530-6 [15043821.001]
  • [Cites] Dev Biol. 2004 Jul 15;271(2):388-402 [15223342.001]
  • [Cites] Dev Biol. 2004 Oct 15;274(2):295-307 [15385160.001]
  • (PMID = 17919464.001).
  • [ISSN] 0006-8993
  • [Journal-full-title] Brain research
  • [ISO-abbreviation] Brain Res.
  • [Language] ENG
  • [Grant] United States / NEI NIH HHS / EY / R01-EY0013760; United States / NEI NIH HHS / EY / R01 EY013760; United States / NEI NIH HHS / EY / EY013760-01A2; United States / NEI NIH HHS / EY / R01 EY013760-01A2; United States / NEI NIH HHS / EY / R01 EY013760-03; United States / NEI NIH HHS / EY / EY0014800; United States / NINDS NIH HHS / NS / R01-NS0053897; United States / NICHD NIH HHS / HD / T32 HD007491; United States / NEI NIH HHS / EY / EY013760-02; United States / NEI NIH HHS / EY / R01 EY013760-02; United States / NEI NIH HHS / EY / P30 EY014800; United States / NINDS NIH HHS / NS / R01 NS053897; United States / NEI NIH HHS / EY / R01 EY013760-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Eye Proteins; 0 / Homeodomain Proteins; 0 / RNA, Messenger; 0 / Repressor Proteins; 0 / Transcription Factors; 0 / Vsx1 protein, mouse; 0 / Vsx2 protein, mouse
  • [Other-IDs] NLM/ NIHMS40831; NLM/ PMC3315787
  •  go-up   go-down


81. Butterwick A, Vankov A, Huie P, Freyvert Y, Palanker D: Tissue damage by pulsed electrical stimulation. IEEE Trans Biomed Eng; 2007 Dec;54(12):2261-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Repeated pulsed electrical stimulation is used in a multitude of neural interfaces; damage resulting from such stimulation was studied as a function of pulse duration, electrode size, and number of pulses using a fluorescent assay on chick chorioallontoic membrane (CAM) in vivo and chick retina in vitro.
  • Data from the chick model were verified by repeating some measurements on porcine retina in-vitro.
  • Damage threshold decreased with the number of pulses, dropping by a factor of 14 on the CAM and 7 on the retina as the number of pulses increased from 1 to 50, and remained constant for a higher numbers of pulses.
  • The threshold current density for repeated exposure on the retina varied between 0.061 A/cm2 at 6 ms to 1.3 A/cm2 at 6 micros.
  • The highest ratio of the damage threshold to the stimulation threshold in retinal ganglion cells occurred at pulse durations near chronaxie-around 1.3 ms.
  • [MeSH-major] Chorioallantoic Membrane / physiopathology. Chorioallantoic Membrane / radiation effects. Electric Stimulation / adverse effects. Radiation Injuries / etiology. Radiation Injuries / physiopathology. Retina / injuries. Retina / physiopathology

  • COS Scholar Universe. author profiles.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18075042.001).
  • [ISSN] 0018-9294
  • [Journal-full-title] IEEE transactions on bio-medical engineering
  • [ISO-abbreviation] IEEE Trans Biomed Eng
  • [Language] eng
  • [Grant] United States / NEI NIH HHS / EY / 2R01 EY 012888
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  •  go-up   go-down


82. Muto A, Arai K, Watanabe S: Rab11-FIP4 is predominantly expressed in neural tissues and involved in proliferation as well as in differentiation during zebrafish retinal development. Dev Biol; 2006 Apr 1;292(1):90-102
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Rab11-FIP4 is predominantly expressed in neural tissues and involved in proliferation as well as in differentiation during zebrafish retinal development.
  • In the developing retina, zRab11-FIP4 was expressed in progenitors throughout the retina at early stages; and then, along with the differentiation, the expression became gradually restricted to the ganglion cell layer and ciliary marginal zone. zRab11-FIP4A knockdown embryos exhibited eye phenotypes similar to those of the shh mutant, such as a small eye with impaired cell proliferation and the delay in cell-cycle exit and differentiation of retinal progenitors.
  • The lack of induction of p57kip2 and enhanced expression of cyclin D1 were observed in the morphant retina.
  • Importantly, the delay in cell-cycle exit was rescued by ectopic expression of either p57Kip2 or dominant-negative PKA, suggesting that Rab11-FIP4A plays pivotal roles in retinal development by regulating Shh signaling and a mechanism acting in parallel with Shh signaling in the control of cell-cycle exit.
  • [MeSH-major] Carrier Proteins / biosynthesis. Cell Differentiation / physiology. Cell Proliferation. Nerve Tissue Proteins / biosynthesis. Retina / embryology. Zebrafish / embryology. Zebrafish Proteins / biosynthesis. rab GTP-Binding Proteins / biosynthesis

  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • SciCrunch. ZFIN: Data: Gene Expression .
  • ZFIN. ZFIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16457799.001).
  • [ISSN] 0012-1606
  • [Journal-full-title] Developmental biology
  • [ISO-abbreviation] Dev. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p57; 0 / Hedgehog Proteins; 0 / Nerve Tissue Proteins; 0 / Oligonucleotides, Antisense; 0 / Rab11-FIP4 protein, zebrafish; 0 / Trans-Activators; 0 / Zebrafish Proteins; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases; EC 3.6.1.- / rab GTP-Binding Proteins; EC 3.6.1.- / rab11 protein
  •  go-up   go-down


83. Wang F, Cui H, Su Y, Zhao SG, Teng Y: Expression change of PirB in mice retina after optic nerve injury. Mol Med Rep; 2010 May-Jun;3(3):405-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression change of PirB in mice retina after optic nerve injury.
  • The aim of this study was to observe the location of paired immunoglobulin-like receptor B (PirB) in the retina and to evaluate the expressive varieties of PirB in the retina of mice after optic nerve injury.
  • In situ hybridization was used to observe the location of PirB mRNA in the retina of mice.
  • Western blotting was used to analyze the levels of PirB protein in retina 7 days after optic nerve crush.
  • Expression of PirB was located in the retinal ganglion cells of mice.
  • The level of PirB protein increased significantly in the retina after optic nerve crush compared to the control group.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 21472254.001).
  • [ISSN] 1791-3004
  • [Journal-full-title] Molecular medicine reports
  • [ISO-abbreviation] Mol Med Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  •  go-up   go-down


84. Besseau L, Vuilleumier R, Sauzet S, Boeuf G, Falcón J: [Photoperiodic control of melatonin synthesis in fish pineal and retina]. J Soc Biol; 2007;201(1):13-20
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Photoperiodic control of melatonin synthesis in fish pineal and retina].
  • [Transliterated title] Contrôle photopériodique de la synthèse de mélatonine par la rétine et l'épiphyse de poisson.
  • In fish, melatonin is produced by the photoreceptor cells of the retina and pineal organ.
  • It is also synthesized by other retinal cell types of the inner nuclear and ganglion cell layers.
  • Some fish species escape the high-at-night rule in the retina, and the rhythm displays a high-at-day profile, intermediate situations being sometimes observed.
  • [MeSH-major] Melatonin / biosynthesis. Photoperiod. Pineal Gland / physiology. Retina / physiology

  • Hazardous Substances Data Bank. MELATONIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17762820.001).
  • [ISSN] 1295-0661
  • [Journal-full-title] Journal de la Société de biologie
  • [ISO-abbreviation] J. Soc. Biol.
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] EC 2.3.1.87 / Arylalkylamine N-Acetyltransferase; JL5DK93RCL / Melatonin
  •  go-up   go-down


85. von Leithner PL, Ciurtin C, Jeffery G: Microscopic mammalian retinal pigment epithelium lesions induce widespread proliferation with differences in magnitude between center and periphery. Mol Vis; 2010;16:570-81
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Microscopic mammalian retinal pigment epithelium lesions induce widespread proliferation with differences in magnitude between center and periphery.
  • PURPOSE: The vertebrate retina develops from the center to the periphery.
  • In amphibians and fish the retinal margin continues to proliferate throughout life, resulting in retinal expansion.
  • However, some mammalian peripheral retinal pigment epithelial (RPE) cells continue to divide, perhaps as a vestige of this mechanism.
  • Unexpectedly, single lesions also resulted in RPE cells proliferating across the entire retina.
  • All lesions repaired and formed apparently normal relations with the neural retina.
  • Further, all lesions have a marked impact on both local and distant RPE cells, demonstrating a pan retinal signaling mechanism triggering proliferation across the tissue plane.
  • The fact that repairing cells were hypopigmented is of interest because reduced pigment is associated with enhanced proliferative capacities in the developing neural retina.
  • [MeSH-major] Mammals / metabolism. Retinal Pigment Epithelium / pathology

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. BROMODEOXYURIDINE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Curr Eye Res. 1997 Jan;16(1):9-18 [9043818.001]
  • [Cites] Hybridoma. 2001 Feb;20(1):47-52 [11289227.001]
  • [Cites] Graefes Arch Clin Exp Ophthalmol. 2001 Feb;239(2):87-95 [11372550.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2002 Oct;43(10):3312-8 [12356840.001]
  • [Cites] Int J Biochem Cell Biol. 2004 Aug;36(8):1482-91 [15147727.001]
  • [Cites] Invest Ophthalmol Vis Sci. 2004 Sep;45(9):3291-301 [15326154.001]
  • [Cites] J Embryol Exp Morphol. 1971 Aug;26(1):67-79 [5565078.001]
  • [Cites] J Comp Neurol. 1972 Mar;144(3):373-80 [5027336.001]
  • [Cites] Am J Ophthalmol. 1973 Jun;75(6):957-72 [4196669.001]
  • [Cites] Dev Biol. 1974 May;38(1):30-40 [4856982.001]
  • [Cites] Arch Ophthalmol. 1986 Sep;104(9):1377-82 [2428346.001]
  • [Cites] Ophthalmology. 1986 Aug;93(8):1113-9 [3763161.001]
  • [Cites] Arch Ophthalmol. 1989 Feb;107(2):264-9 [2464985.001]
  • [Cites] Invest Ophthalmol Vis Sci. 1990 May;31(5):890-8 [2335451.001]
  • [Cites] J Exp Zool Suppl. 1990;5:167-80 [1982493.001]
  • [Cites] J Comp Neurol. 1991 Jul 1;309(1):86-114 [1894769.001]
  • [Cites] Anat Rec. 1997 Nov;249(3):380-8 [9372172.001]
  • [Cites] Cell Cycle. 2005 Sep;4(9):1286-93 [16082214.001]
  • [Cites] J Comp Neurol. 2006 May 20;496(3):369-81 [16566005.001]
  • [Cites] Mol Vis. 2006;12:1243-9 [17110907.001]
  • [Cites] Biochim Biophys Acta. 2007 Apr;1772(4):457-66 [17158035.001]
  • [Cites] J Comp Neurol. 2007 Jul 1;503(1):128-34 [17480016.001]
  • [Cites] Mol Vis. 2008;14:1784-91 [18843376.001]
  • [Cites] Cell Adh Migr. 2008 Oct-Dec;2(4):252-3 [19262153.001]
  • [Cites] Exp Eye Res. 2010 Feb;90(2):368-72 [19833124.001]
  • [Cites] J Cell Physiol. 2000 Mar;182(3):311-22 [10653597.001]
  • [Cites] Neuron. 2001 Apr;30(1):65-78 [11343645.001]
  • (PMID = 20360994.001).
  • [ISSN] 1090-0535
  • [Journal-full-title] Molecular vision
  • [ISO-abbreviation] Mol. Vis.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ki-67 Antigen; G34N38R2N1 / Bromodeoxyuridine
  • [Other-IDs] NLM/ PMC2847682
  •  go-up   go-down


86. Bai Y, Ma JX, Guo J, Wang J, Zhu M, Chen Y, Le YZ: Müller cell-derived VEGF is a significant contributor to retinal neovascularization. J Pathol; 2009 Dec;219(4):446-54
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Müller cell-derived VEGF is a significant contributor to retinal neovascularization.
  • We therefore generated conditional VEGF knockout mice with an inducible Cre/lox system and determined the significance of Müller cell-derived VEGF in retinal development and maintenance and ischaemia-induced neovascularizartion and vascular leakage.
  • Retinal development in the conditional VEGF knockout mice was analysed by examining retinal and choroidal vasculatures and retinal morphology and function.
  • Ischaemia-induced retinal neovascularization and vascular leakage in the conditional VEGF knockout mice were analysed with fluorescein angiography, quantification of proliferative neovascular cells, immunohistochemistry, and immunoblotting using an oxygen-induced retinopathy model.
  • Our results demonstrated that disruption of Müller cell-derived VEGF resulted in no apparent defects in retinal and choroidal vasculatures and retinal morphology and function, significant inhibition of the ischaemia-induced retinal neovascularization and vascular leakage, and attenuation of the ischaemia-induced breakdown of the blood-retina barrier.
  • These results suggest that the retinal Müller cell-derived VEGF is a major contributor to ischaemia-induced retinal vascular leakage and pre-retinal and intra-retinal neovascularization.
  • The observation that a significant, but not complete, reduction of VEGF in the retina does not cause detectable retinal degeneration suggests that appropriate doses of anti-VEGF agents may be important to the safe treatment of retinal vascular diseases.
  • [MeSH-major] Retinal Neovascularization / physiopathology. Retinal Neurons / metabolism. Vascular Endothelial Growth Factor A / physiology
  • [MeSH-minor] Animals. Capillary Permeability / physiology. Cells, Cultured. Eye Proteins / metabolism. Humans. Ischemia / complications. Ischemia / physiopathology. Membrane Proteins / metabolism. Mice. Mice, Knockout. Occludin. Retina / metabolism. Retina / pathology. Retinal Vessels / growth & development

  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19768732.001).
  • [ISSN] 1096-9896
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Grant] United States / NEI NIH HHS / EY / EY012231; United States / NEI NIH HHS / EY / EY015650,; United States / NCRR NIH HHS / RR / P20 RR024215; United States / NCRR NIH HHS / RR / P20 RR17703; United States / NEI NIH HHS / EY / P30 EY12190
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Eye Proteins; 0 / Membrane Proteins; 0 / OCLN protein, human; 0 / Occludin; 0 / Ocln protein, mouse; 0 / Vascular Endothelial Growth Factor A; 0 / vascular endothelial growth factor A, mouse
  •  go-up   go-down


87. Luhtala S, Vaajanen A, Oksala O, Valjakka J, Vapaatalo H: Activities of angiotensin-converting enzymes ACE1 and ACE2 and inhibition by bioactive peptides in porcine ocular tissues. J Ocul Pharmacol Ther; 2009 Feb;25(1):23-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Activities of ACE1 and ACE2 and their inhibition by bioactive tripeptides (Ile-Pro-Pro, Val-Pro-Pro, Leu-Pro-Pro) as well as by a standard ACE-inhibitor captopril were assayed in the vitreous body, the retina and the ciliary body using fluorometric detection methods.
  • ACE1 activity was markedly higher in the ciliary body (3.7 +/- 0.7 mU/mg protein) than in retina (0.2 +/- 0.02 mU/mg), whereas ACE2 activities in the ciliary body (0.2 +/- 0.02 mU/mg) and retina (0.2 +/- 0.01 mU/mg) were at the same level.
  • CONCLUSION: To our knowledge the present findings constitute the first evidence of ACE2 activity in the ciliary and vitreous bodies, in addition to previously described activity in the retina.
  • [MeSH-major] Angiotensin-Converting Enzyme Inhibitors / pharmacology. Ciliary Body / enzymology. Peptidyl-Dipeptidase A / metabolism. Retina / enzymology. Vitreous Body / enzymology

  • Hazardous Substances Data Bank. CAPTOPRIL .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • antibodies-online. View related products from antibodies-online.com (subscription/membership/fee required).
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19232015.001).
  • [ISSN] 1557-7732
  • [Journal-full-title] Journal of ocular pharmacology and therapeutics : the official journal of the Association for Ocular Pharmacology and Therapeutics
  • [ISO-abbreviation] J Ocul Pharmacol Ther
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiotensin-Converting Enzyme Inhibitors; 0 / Oligopeptides; 0 / isoleucyl-prolyl-proline; 0 / leucyl-prolyl-proline; 0 / valyl-prolyl-proline; 9G64RSX1XD / Captopril; EC 3.4.15.1 / Peptidyl-Dipeptidase A; EC 3.4.17.- / angiotensin converting enzyme 2
  •  go-up   go-down


88. Lopez VM, Decatur CL, Stamer WD, Lynch RM, McKay BS: L-DOPA is an endogenous ligand for OA1. PLoS Biol; 2008 Sep 30;6(9):e236
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The neurosensory retina, which is not pigmented, exhibits pathologic changes secondary to the loss of pigmentation in the retina pigment epithelium (RPE).
  • How the loss of pigmentation in the RPE causes developmental defects in the adjacent neurosensory retina has not been determined, but offers a unique opportunity to investigate the interactions between these two important tissues.
  • Taken together, our results illustrate an autocrine loop between OA1 and tyrosinase linked through L-DOPA, and this loop includes the secretion of at least one very potent retinal neurotrophic factor.
  • OA1 is a selective L-DOPA receptor whose downstream effects govern spatial patterning of the developing retina.
  • Our results suggest that the retinal consequences of albinism caused by changes in melanin synthetic machinery may be treated by L-DOPA supplementation.


89. Pérez-González LE, Lajara-Blesa JJ: [Trans-scleral sutureless vitrectomy with a 25-G system for rhegmatogenous retinal detachment treatment]. Arch Soc Esp Oftalmol; 2007 Jul;82(7):437-42
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Trans-scleral sutureless vitrectomy with a 25-G system for rhegmatogenous retinal detachment treatment].
  • [Transliterated title] Cirugía del desprendimiento de retina regmatógeno mediante vitrectomía transescleral sin sutura con sistema 25-G.
  • PURPOSE: The evaluation of the trans-scleral sutureless vitrectomy (TSV) efficiency using a 25G system as an alternative in rhegmatogenous retinal detachment (RRD) treatment.
  • Eight of the detachments were "macula-off" at the time of diagnosis.
  • The average follow-up time was 6.8 months, and the main complications were cataracts in 7 of 11 phakic eyes (63.6%) and a new retinal detachment in 4 eyes (18.2%).
  • [MeSH-major] Retinal Detachment / surgery. Retinal Perforations / surgery. Vitrectomy / instrumentation