Database : MEDLINE
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[PMID]: 29524771
[Au] Autor:Devrukhakar PS; M SS; G S; R S
[Ad] Address:School of Advance Sciences, Vellore Institute of technology (VIT), Katpadi, Vellore, Tamil Nadu 632014, India.
[Ti] Title:Proposal of degradation pathway with toxicity prediction for hydrolytic and photolytic degradation products of timolol.
[So] Source:J Pharm Biomed Anal;154:7-15, 2018 Feb 28.
[Is] ISSN:1873-264X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Timolol (TIM) is a potent ß-adrenergic blocker, useful in treatment of ocular hypertension or open-angle glaucoma. Development and validation of stability indicating LCMS assay method for TIM was accomplished coherent with ICH guideline. Successful chromatographic separation of TIM with its four degradation products was attained by using gradient elution mode on reverse phase column using ammonium acetate buffer, pH 4.6 as mobile phase A and organic solvent as the mobile phase B. Chromatographic conditions were set such as 1.0 mL min flow rate, 20 µL injection volume, 30 °C column temperature and 320 nm detection wavelength. Four major degradation products obtained from hydrolysis and photolysis, were identified and characterized with the combination of liquid chromatography-electrospray ionization mass spectrometry (LC-ESI/MS/MS) and accurate mass measurements. Degradation pathways were identified based on a comparison of the fragmentation pattern of the [M+H] ions of TIM and its degradation products. The method validation was performed as per ICH guideline Q2 (R1).
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  2 / 60464 MEDLINE  
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[PMID]: 29524673
[Au] Autor:Raghunathan V; Benoit J; Kasetti R; Zode G; Salemi M; Phinney BS; Keller KE; Staverosky JA; Murphy CJ; Acott T; Vranka J
[Ad] Address:Department of Basic Sciences, University of Houston, Houston, TX, 77204, USA; The Ocular Surface Institute, University of Houston, Houston, TX, 77204, USA. Electronic address: vraghunathan@uh.edu.
[Ti] Title:Glaucomatous cell derived matrices differentially modulate non-glaucomatous trabecular meshwork cellular behavior.
[So] Source:Acta Biomater;, 2018 Mar 07.
[Is] ISSN:1878-7568
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Ocular hypertension is a causal risk-factor to developing glaucoma. This is associated with stiffening of the trabecular meshwork (TM), the primary site of resistance to aqueous-humor-outflow. The mechanisms underlying this stiffening or how pathologic extracellular matrix (ECM) affects cell function are poorly understood. It is recognized that mechanotransduction systems allow cells to sense and translate the intrinsic biophysical properties of ECM into intracellular signals to control gene transcription, protein expression, and cell behavior. Using an anterior segment perfusion model, we document that there are significantly more low flow regions that are much stiffer, and fewer high flow regions that are less stiff in glaucomatous TM (GTM) when compared to non-glaucomatous TMs (NTM). GTM tissue also has fewer cells overall when compared with NTM tissue. In order to study the role of pathologic ECM in glaucoma disease progression, we conducted studies using cell derived matrices (CDM). First, we characterized the mechanics, composition and organization of fibronectin in ECM deposited by GTM and NTM cells treated with glucocorticosteroids. Then, we determined that these GTM-derived ECM are able to induce stiffening of normal NTM cells, and alter their gene/protein expression to resemble that of a glaucomatous phenotype. Further, we demonstrate that GTM-derived ECM causes endoplasmic reticular stress in NTM. They also became resistant to being reorganized by these NTM cells. These phenomena were exacerbated by ECMs obtained from steroid treated glaucoma model groups. Collectively, our data demonstrates that CDMs represent a novel tool for the study of bidirectional interactions between TM cells and their immediate microenvironment. STATEMENT OF SIGNIFICANCE: Extracellular matrix (ECM) changes are prevalent in a number of diseases. The precise mechanisms by which changes in the ECM contribute to disease progression is unclear, primarily due to absence of appropriate models. Here, using glaucoma as a disease model, we document changes in cell derived matrix (CDM) and tissue mechanics that contribute to the pathology. Subsequently, we determine the effect that ECMs from diseased and healthy individuals have on healthy cell behaviors. Data emanating from this study demonstrate that CDMs are a potent tool for the study of cell-ECM interactions.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  3 / 60464 MEDLINE  
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[PMID]: 29516053
[Au] Autor:Manoiu MR; Amri JA; Èšicle A; Stan C
[Ad] Address:Department of Ophthalmology, Emergency District Hospital Cluj-Napoca, Romania.
[Ti] Title:Case report: bilateral optic nerve head drusen and glaucoma.
[So] Source:Rom J Ophthalmol;61(4):310-314, 2017 Oct-Dec.
[Is] ISSN:2457-4325
[Cp] Country of publication:Romania
[La] Language:eng
[Ab] Abstract:Optic nerve head drusen is an incidental finding in current ophthalmological practice. Although patients rarely display symptoms, structural, and functional defects, there are exceptional cases when clinical appearance can make it difficult to diagnose underlying or coexisting conditions, such as glaucoma. The following case report demonstrates how overlapping optic nerve pathologies can interfere in clinical judgement and therapeutic decision making in a young male patient, with relevant family history for both glaucoma and bilateral optic nerve head drusen.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Process

  4 / 60464 MEDLINE  
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[PMID]: 29516048
[Au] Autor:Strehaianu MV; Dascalescu D; Ionescu C; Burcel M; Potop V; Corbu C
[Ad] Address:Clinical Ophthalmology Emergency Hospital Bucharest, Romania.
[Ti] Title:The importance of ganglion cell complex investigation in myopic patients.
[So] Source:Rom J Ophthalmol;61(4):284-289, 2017 Oct-Dec.
[Is] ISSN:2457-4325
[Cp] Country of publication:Romania
[La] Language:eng
[Ab] Abstract:Glaucoma is an optic neuropathy that affects the ganglion cell complex in all its components: cell bodies, dendrites, and axons, the dendritic arbor being the first one damaged. This is the reason why the thickness of the ganglion cell and internal plexiform layers can be taken into account as an early predictor of the glaucomatous changes, along with the retinal nerve fiber layer (RNFL) thickness. However, due to disc tilting and peripapillary atrophy, the RNFL evaluation may be prone to errors in myopic patients. We presented the cases of two myopic patients, who, after a routine examination, were identified as glaucoma suspects. The Optical Coherence Tomography (OCT) scan revealed a nerve fiber loss which was not confirmed by the ganglion cell complex scan. Thereafter we manually adjusted the optic disc margins according to the patients' myopic changes and this time the retinal nerve fiber layer was also normal. We observed that the ganglion cell complex evaluation led to fewer errors than the retinal nerve fiber layer evaluation, particularly in front of a myopic patient. Nevertheless, various investigations should be considered in the attempt to issue a diagnosis of glaucoma.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Process

  5 / 60464 MEDLINE  
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[PMID]: 29516047
[Au] Autor:Zemba M; Danilova T; Pulbere L; Stamate AC
[Ad] Address:Department of Ophthalmology, "Dr. Carol Davila" Central University Military Emergency Hospital, Bucharest, Romania.
[Ti] Title:Uncommon form of normal-tension glaucoma.
[So] Source:Rom J Ophthalmol;61(4):275-283, 2017 Oct-Dec.
[Is] ISSN:2457-4325
[Cp] Country of publication:Romania
[La] Language:eng
[Ab] Abstract:Aim: To present diagnostic particularities, assessment of prognosis, and the need for treatment in a case of normal-tension glaucoma. Methods: - presentation of clinical changes and investigations supporting the diagnosis; - careful anamnesis that disclosed new elements, useful for the evaluation of the case. Results: after a two-year follow-up period, we can ascertain that the optic atrophy is non-progressive. Conclusions: the assessment of risk factors and a rigorous anamnesis were significant for the establishment of prognosis and need for treatment.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Process

  6 / 60464 MEDLINE  
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[PMID]: 29516042
[Au] Autor:Potop V; Corbu C
[Ad] Address:Clinical Ophthalmology Emergency Hospital Bucharest, Romania.
[Ti] Title:The role of clear lens extraction in angle closure glaucoma.
[So] Source:Rom J Ophthalmol;61(4):244-248, 2017 Oct-Dec.
[Is] ISSN:2457-4325
[Cp] Country of publication:Romania
[La] Language:eng
[Ab] Abstract:Clear lens extraction can be considered a therapeutic option in angle closure glaucoma (ACG). Even if it does not represent the first choice of treatment, it can be taken into consideration when the topical treatment does not control the intraocular pressure (IOP) and iridotomy does not have a positive effect on the angle closure, especially in appositional angle closure when biometry or ultrabiomicroscopy (UBM) show lens involvement. In angle closure glaucoma, clear lens extraction represents an etiological treatment that takes into account the role of the lens in the pathogenesis of the disease. If we ignore it and we choose a filtrating surgery as therapeutic option we can end up with complications such as prolonged athalamia, corneal damage and lens opacification that will eventually require cataract surgery, but performed late and with higher risks. Before performing a filtrating surgery in ACG, we should take an UBM. We also need to choose the best moment to perform surgery, after topical treatment and iridotomy have been tested, but before trabecular damage appears.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Process

  7 / 60464 MEDLINE  
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[PMID]: 29249729
[Au] Autor:Park S; Kim K; Kim Y; Seo K
[Ad] Address:Department of Veterinary Clinical Sciences, College of Veterinary Medicine and Research Institute for Veterinary Science, Seoul National University, 1 Gwanak-ro, Gwanak-gu, Seoul, 08826, Korea.
[Ti] Title:Bilateral anterior segment dysgenesis with the presumed Peters' anomaly in a cat.
[So] Source:J Vet Med Sci;80(2):297-301, 2018 Feb 20.
[Is] ISSN:1347-7439
[Cp] Country of publication:Japan
[La] Language:eng
[Ab] Abstract:A seven-month-old female domestic shorthaired cat was presented for buphthalmos in the right eye and corneal cloudiness in the left eye. Full ophthalmic examinations were performed for both eyes and enucleation was done for the right nonvisual eye. Congenital glaucoma caused by anterior segment dysgenesis was confirmed for the right eye. In the left eye, slit-lamp examination revealed focal corneal edema with several iris strands from iris collarette to the affected posterior corneal surfaces. Circular posterior corneal defect was suggested to be the cause of edema. Goniodysgenesis, additionally, was identified. Taken together, the diagnosis of Peters' anomaly which is a subtype of anterior segment dysgenesis was suggested in the left eye.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Process
[do] DOI:10.1292/jvms.17-0532

  8 / 60464 MEDLINE  
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[PMID]: 29523993
[Au] Autor:Edlinger FSM; Schrems-Hoesl LM; Mardin CY; Laemmer R; Kruse FE; Schrems WA
[Ad] Address:Department of Ophthalmology, University of Erlangen-Nuremberg, Schwabachanlage 6, 91054, Erlangen, Germany.
[Ti] Title:Structural changes of macular inner retinal layers in early normal-tension and high-tension glaucoma by spectral-domain optical coherence tomography.
[So] Source:Graefes Arch Clin Exp Ophthalmol;, 2018 Mar 09.
[Is] ISSN:1435-702X
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:PURPOSE: Assessment of the diagnostic ability of segmented macular inner retinal layer thickness and peripapillary retinal nerve fiber layer (pRNFL) measured by spectral-domain optical coherence tomography (SD-OCT) in patients with normal-tension (NT) and high-tension (HT) perimetric and preperimetric glaucoma. METHODS: The 212 participants included 45 healthy subjects, 55 patients with ocular hypertension, 56 patients with preperimetric glaucoma, and 56 patients with perimetric glaucoma. The preperimetric and perimetric groups were further subdivided into NT and HT groups. Sectoral and global thickness of macular retinal nerve fiber layer (mRNFL), ganglion cell layer (mGCL), inner plexiform layer (mIPL), ganglion cell complex (mGCC), and pRNFL were measured using SD-OCT (Spectralis, Heidelberg Engineering, Germany). Diagnostic performance was ascertained by sectoral and global comparison of the sensitivities at specificity ≥ 95%. RESULTS: For all layers, the largest thickness decrease was reported in the HT perimetric group. In all groups, the sensitivities of mGCL showed a comparable diagnostic value to pRNFL in order to distinguish between healthy subjects and glaucoma patients. In the perimetric group, mGCL (85.7%) exhibited higher sensitivities than mRNFL (78.6%) and mGCC (78.6%). Both mRNFL and pRNFL demonstrated equal diagnostic performance in the HT perimetric group (88.5 and 96.2%), in the NT groups, mRNFL was inferior to all other layers. CONCLUSION: The sensitivities of mGCL and mRNFL were comparable to the sensitivities of pRNFL. In clinical application, mGCL and mRNFL, with a focus on the temporal and inferior sectors, may provide a convincing supplementation to pRNFL. CLINICAL TRIAL REGISTRATION: Erlangen Glaucoma Registry www.clinicaltrials.gov ID: NCT00494923.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[Cl] Clinical Trial:ClinicalTrial
[St] Status:Publisher
[do] DOI:10.1007/s00417-018-3944-6

  9 / 60464 MEDLINE  
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[PMID]: 29486164
[Au] Autor:Nakashima KI; Iwao K; Inoue T; Haga A; Tsutsumi T; Mochita MI; Fujimoto T; Tanihara H
[Ad] Address:Department of Ophthalmology, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan.
[Ti] Title:Stimulation of the adenosine A3 receptor, not the A1 or A2 receptors, promote neurite outgrowth of retinal ganglion cells.
[So] Source:Exp Eye Res;170:160-168, 2018 Feb 24.
[Is] ISSN:1096-0007
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Among candidate neuroprotective agents, adenosine is thought to be a possible treatment for central nervous system disorders. Adenosine elicits biological effects through four G protein-coupled receptors (A , A , A , and A ). The A and A receptors stimulate adenylyl cyclase (AC) and increase cyclic adenosine monophosphate (cAMP) levels, whereas A and A receptors inhibit AC and decrease cAMP levels. Several studies have investigated the effects of adenosine receptors (AdoRs) in glaucoma, because modulation of A , A , or A receptor regulates intraocular pressure. In addition, AdoR-related phenomena may induce neuroprotective effects in retinal neurons. Notably, A , A , and A receptor agonists reportedly inhibit retinal ganglion cell (RGC) death in in vitro and in vivo glaucoma models. However, there is limited knowledge of the effects of AdoR activation on neurite outgrowth or the regeneration of RGCs. In this report, we described the role of an AdoR subtype in neurite outgrowth and RGC axonal regeneration. The distribution of AdoRs in the retina was evaluated by immunohistochemical analysis. Using primary cultured rat RGCs in vitro and an optic nerve crush model in vivo, neurite elongation was evaluated after stimulation by the following AdoR agonists: CHA, an A receptor agonist; CGS21680, an A receptor agonist; BAY60-6583, an A receptor agonist; and 2-Cl-IB-MECA, an A receptor agonist. To determine the mechanism of neurite promotion, the candidate molecules of signal transduction associated with the neurite elongation of AdoRs were evaluated by enzyme-linked immunosorbent assay (ELISA) and Western blot analysis, respectively. All four AdoRs (A , A , A , and A ) were present in the inner retinal layers. Among the agonists for AdoR, only 2-Cl-IB-MECA significantly promoted neurite outgrowth in primary cultured RGCs. Signaling pathway analyses showed that 2-Cl-IB-MECA caused upregulated phosphorylation of Akt in cultured RGCs. Additionally, LY294002, an inhibitor of Akt, suppressed the neurite-promoting effects of the A receptor agonist in RGCs. Moreover, 2-Cl-IB-MECA increased the number of regenerating axons in the optic nerve crush model. Taken together, these data indicate that activation of the A receptor, not the A or A receptors, promotes in vitro and in vivo neurite outgrowth during the regeneration of rat RGCs, which is caused by the activation of an Akt-dependent signaling pathway. Therefore, AdoR activation may be a promising candidate for the development of novel regenerative modalities for glaucoma and other optic neuropathies.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher

  10 / 60464 MEDLINE  
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[PMID]: 29475084
[Au] Autor:Katoli P; Godbole A; Romanowski MJ; Clark K; Meredith E; Saenz-Vash V; Wang YK; Lewicki N; Nguyen AA; Lynch JM
[Ad] Address:Ophthalmology, Novartis Institutes for BioMedical Research, Cambridge, MA 02139, USA.
[Ti] Title:Full-length myocilin protein is purified from mammalian cells as a dimer.
[So] Source:Protein Expr Purif;147:38-48, 2018 Feb 21.
[Is] ISSN:1096-0279
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Myocilin (MYOC) is a secreted protein found in human aqueous humor (AH) and mutations in the MYOC gene are the most common mutation observed in glaucoma patients. Human AH analyzed under non-reducing conditions suggests that MYOC is not normally found in a monomeric form, but rather is predominantly dimeric. Although MYOC was first reported almost 20 years ago, a technical challenge still faced by researchers is an inability to isolate full-length MYOC protein for experimental purposes. Herein we describe two methods by which to isolate sufficient quantities of human full-length MYOC protein from mammalian cells. One method involved identification of a cell line (HeLa S3) that would secrete full-length protein (15 mg/L) while the second method involved a purification approach from 293 cells requiring identification and modification of an internal MYOC cleavage site (Glu214/Leu215). MYOC protein yield from 293 cells was improved by mutation of two MYOC N-terminal cysteines (C47 and C61) to serines. Analytical size exclusion chromatography of our full-length MYOC protein purified from 293 cells indicated that it is predominantly dimeric and we propose a structure for the MYOC dimer. We hope that by providing methods to obtain MYOC protein, researchers will be able to utilize the protein to obtain new insights into MYOC biology. The ultimate goal of MYOC research is to better understand this target so we can help the patient that carries a MYOC mutation retain vision and maintain quality of life.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher


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