1 40 23 Hyperlink A link, or reference, to another resource on the Internet. URL https://doi.org/10.3390/antiox11050888 Dublin Core The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/. Title A name given to the resource Ocular Hypertension Results in Hypoxia within Glia and Neurons throughout the Visual Projection Creator An entity primarily responsible for making the resource Assraa Hassan Jassim Nana Yaa Nsiah Denise M Inman Date A point or period of time associated with an event in the lifecycle of the resource 2022 Description An account of the resource The magnitude and duration of hypoxia after ocular hypertension (OHT) has been a matter of debate due to the lack of tools to accurately report hypoxia. In this study, we established a topography of hypoxia in the visual pathway by inducing OHT in mice that express a fusion protein comprised of the oxygen-dependent degradation (ODD) domain of HIF-1α and a tamoxifen-inducible Cre recombinase (CreERT2) driven by a ubiquitous CAG promoter. After tamoxifen administration, tdTomato expression would be driven in cells that contain stabilized HIF-1α. Intraocular pressure (IOP) and visual evoked potential (VEP) were measured after OHT at 3, 14, and 28 days (d) to evaluate hypoxia induction. Immunolabeling of hypoxic cell types in the retina and optic nerve (ON) was performed, as well as retinal ganglion cell (RGC) and axon number quantification at each time point (6 h, 3 d, 14 d, 28 d). IOP elevation and VEP decrease were detected 3 d after OHT, which preceded RGC soma and axon loss at 14 and 28 d after OHT. Hypoxia was detected primarily in Müller glia in the retina, and microglia and astrocytes in the ON and optic nerve head (ONH). Hypoxia-induced factor (HIF-α) regulates the expression of glucose transporters 1 and 3 (GLUT1, 3) to support neuronal metabolic demand. Significant increases in GLUT1 and 3 proteins were observed in the retina and ON after OHT. Interestingly, neurons and endothelial cells within the superior colliculus in the brain also experienced hypoxia after OHT as determined by tdTomato expression. The highest intensity labeling for hypoxia was detected in the ONH. Initiation of OHT resulted in significant hypoxia that did not immediately resolve, with low-level hypoxia apparent out to 14 and 28 d, suggesting that continued hypoxia contributes to glaucoma progression. Restricted hypoxia in retinal neurons after OHT suggests a hypoxia management role for glia. Source A related resource from which the described resource is derived Antioxidants (Basel) . 2022 Apr 29;11(5):888. doi: 10.3390/antiox11050888. Language A language of the resource English 2022 Astrocytes Glaucoma hypoxia Microglia Müller glia Retinal Ganglion Cells Dublin Core The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/. Title A name given to the resource Articles Published in 2021 Creator An entity primarily responsible for making the resource Shelley Harrell Publisher An entity responsible for making the resource available Shelley Harrell Date A point or period of time associated with an event in the lifecycle of the resource 2021 Description An account of the resource Items published in 2021 Text A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text. URL Address <table width="91" style="border-collapse:collapse;width:68pt;"><colgroup><col width="91" style="width:68pt;" /></colgroup><tbody><tr style="height:15pt;"><td width="91" height="20" class="xl18" style="width:68pt;height:15pt;"><a href="http://doi.org/10.1089/ars.2020.8180">http://doi.org/10.1089/ars.2020.8180</a></td> </tr></tbody></table> NEOMED College NEOMED College of Medicine NEOMED Department Department of Pharmaceutical Sciences Update Year & Number Jan to Aug list 2021 Dublin Core The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/. Title A name given to the resource Oxidative Stress and Hypoxia Modify Mitochondrial Homeostasis During Glaucoma. Creator An entity primarily responsible for making the resource Jassim AH; Fan Y; Pappenhagen N; Nsiah NY; Inman DM Publisher An entity responsible for making the resource available Antioxidants & Redox Signaling Date A point or period of time associated with an event in the lifecycle of the resource 2021 2021-04-29 Description An account of the resource Aims: Cellular response to hypoxia can include transition from respiration to glycolysis via upregulation of glycolytic enzymes and transporters, as well as mitophagy induction to eliminate surplus mitochondria. Our purpose was to evaluate the impact of hypoxia-inducible factor-1α (HIF-1α) stabilization on mitochondrial homeostasis and oxidative stress in a chronic model of glaucoma. Results: Retina and optic nerve (ON) were evaluated from young and aged DBA/2J (D2) glaucoma model mice and the control strain, the DBA/2-Gpnmb+. Hypoxic retinal ganglion cells (RGCs) were observed in young and aged D2 retina, with a significant increase in HIF-1α protein in the aged D2 retina. Reactive oxygen species observed in young D2 retina and ON were followed by significant decreases in antioxidant capacity in aged D2 retina and ON. HIF-1α targets such as neuron-specific glucose transporter-3 and lactate dehydrogenase were decreased or unchanged, respectively, in aged D2 retina despite an increased hypoxia response in RGCs. Mitochondrial mass was decreased in aged D2 retina concomitant with decreased mitochondrially encoded electron transport chain transcripts despite a stable nuclear-encoded TFAM (mitochondrial transcription factor), suggesting a breakdown in the nuclear-mitochondrial communication. Decreased mitophagy-associated proteins p62 and Rheb were observed in aged D2 retina, although p62 was significantly increased in the aged D2 ON. Innovation and Conclusion: The increased reactive oxygen species concomitant with HIF-1α upregulation despite reduced glucose transporters, mis-match of nuclear- and mitochondrial-encoded transcripts, and signs of reduced mitophagy suggest that retinas from D2 mice with chronic intraocular pressure elevation transition to pseudohypoxia without consistent metabolic reprogramming before significant RGC loss Identifier An unambiguous reference to the resource within a given context <table width="91" style="border-collapse:collapse;width:68pt;"><colgroup><col width="91" style="width:68pt;" /></colgroup><tbody><tr style="height:15pt;"><td width="91" height="20" class="xl18" style="width:68pt;height:15pt;"><a href="http://doi.org/10.1089/ars.2020.8180">http://doi.org/10.1089/ars.2020.8180</a></td> </tr></tbody></table> Format The file format, physical medium, or dimensions of the resource Journal Article 2021 Glaucoma glycolysis HIF-1α hypoxia Oxidative Stress PGC-1α Text A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text. URL Address <a href="https://doi.org/10.3389/fcell.2021.636321">https://doi.org/10.3389/fcell.2021.636321</a> NEOMED College NEOMED College of Medicine NEOMED Department Department of Pharmaceutical Sciences Update Year & Number jan to aug 2021 list Dublin Core The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/. Title A name given to the resource Absence of cytochrome P450-1b1 increases susceptibility of pressure-induced axonopathy in the murine retinal projection. Creator An entity primarily responsible for making the resource Amirmokhtari N; Foresi BD; Dewan SS; Bouhenni RA; Smith MA Publisher An entity responsible for making the resource available Frontiers In Cell And Developmental Biology Date A point or period of time associated with an event in the lifecycle of the resource 2021 2021-03-05 Description An account of the resource Adult mixed sex Cyp1b1–/– [129S6.129 × 1(B6)-Cyp1b1TM1Gonz/Mmnc] mice were obtained from the Mutant Mouse Resource and Research Center (MMRRC) at JAX (Jackson Laboratories) and genotyped before experimentation to confirm the transgene. These mice have a targeted mutation caused by a disrupted coding sequence associated with exon three of the Cyp1b1 gene. Age-matched 129S6.129 × 1(B6) mice were used as wildtype controls (Buters et al., 1999; Libby et al., 2003). Mice were maintained in the Comparative Medicine Unit at Northeast Ohio Medical University on a 12-hour light/dark cycle with standard rodent chow available ad libitum. All experimental procedures were approved by the Northeast Ohio Medical University Institutional Animal Care and Use Committee and conducted in accordance with the Guide for Care and Use of Laboratory Animals published by the National Institutes of Health. Subject The topic of the resource Glaucoma is a group of heterogeneous neuro-ophthalmologic conditions that impair vision through the functional disruption and eventual degeneration of retinal ganglion cells (RGCs), the neuronal substrates responsible for eye-brain communication (Davis et al., 2016; Quigley and Broman, 2006). Glaucoma is most often attributed to the aging adult (Davis et al., 2016; Tham et al., 2014), however, befalls pediatric and adolescent populations (Kaur et al., 2011), thereby placing it in a unique group of neurodegenerative conditions that afflict populations on both ends of the lifespan. Identifier An unambiguous reference to the resource within a given context <a href="%20https%3A//doi.org/10.3389/fcell.2021.636321">doi.org/10.3389/fcell.2021.636321</a> Rights Information about rights held in and over the resource 2021 Amirmokhtari, Foresi, Dewan, Bouhenni and Smith. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. Format The file format, physical medium, or dimensions of the resource Journal Article 2021 axonal transport disruption Glaucoma microbead occlusion model nodes of Ranvier Retinal ganglion cell Text A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text. URL Address <a href="http://doi.org/10.1089/ars.2020.8180" target="_blank" rel="noreferrer noopener">http://doi.org/10.1089/ars.2020.8180</a> ISSN 1557-7716 Search for Full-text Locate full-text within NEOMED Library's e-journal collections <a href="http://neomed.idm.oclc.org/login?url=http://doi.org/10.1089/ars.2020.8180" target="_blank" rel="noreferrer noopener">NEOMED Full-text Holding (if available) - Proxy DOI: 10.1089/ars.2020.8180</a> <p>Users with a NEOMED Library login can search for full-text journal articles at the following url: <a href="https://libraryguides.neomed.edu/home">https://libraryguides.neomed.edu/home</a></p> Update Year & Number May 2021 List NEOMED College NEOMED College of Pharmacy NEOMED Department Department of Pharmaceutical Sciences NEOMED Student Publications Dublin Core The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/. Title A name given to the resource Oxidative Stress and Hypoxia Modify Mitochondrial Homeostasis During Glaucoma. Publisher An entity responsible for making the resource available Antioxidants & Redox Signaling Date A point or period of time associated with an event in the lifecycle of the resource 2021 2021-04-29 Subject The topic of the resource glaucoma; oxidative stress; hypoxia; glycolysis; HIF-1α; PGC-1α Creator An entity primarily responsible for making the resource Jassim AH; Fan Y; Pappenhagen N; Nsiah NY; Inman DM Description An account of the resource Aims: Cellular response to hypoxia can include transition from respiration to glycolysis via upregulation of glycolytic enzymes and transporters, as well as mitophagy induction to eliminate surplus mitochondria. Our purpose was to evaluate the impact of hypoxia-inducible factor-1α (HIF-1α) stabilization on mitochondrial homeostasis and oxidative stress in a chronic model of glaucoma. Results: Retina and optic nerve (ON) were evaluated from young and aged DBA/2J (D2) glaucoma model mice and the control strain, the DBA/2- Gpnmb + . Hypoxic retinal ganglion cells (RGCs) were observed in young and aged D2 retina, with a significant increase in HIF-1α protein in the aged D2 retina. Reactive oxygen species observed in young D2 retina and ON were followed by significant decreases in antioxidant capacity in aged D2 retina and ON. HIF-1α targets such as neuron-specific glucose transporter-3 and lactate dehydrogenase were decreased or unchanged, respectively, in aged D2 retina despite an increased hypoxia response in RGCs. Mitochondrial mass was decreased in aged D2 retina concomitant with decreased mitochondrially encoded electron transport chain transcripts despite a stable nuclear-encoded TFAM (mitochondrial transcription factor), suggesting a breakdown in the nuclear-mitochondrial communication. Decreased mitophagy-associated proteins p62 and Rheb were observed in aged D2 retina, although p62 was significantly increased in the aged D2 ON. Innovation and Conclusion: The increased reactive oxygen species concomitant with HIF-1α upregulation despite reduced glucose transporters, mis-match of nuclear- and mitochondrial-encoded transcripts, and signs of reduced mitophagy suggest that retinas from D2 mice with chronic intraocular pressure elevation transition to pseudohypoxia without consistent metabolic reprogramming before significant RGC loss. Identifier An unambiguous reference to the resource within a given context <a href="http://doi.org/10.1089/ars.2020.8180" target="_blank" rel="noreferrer noopener">10.1089/ars.2020.8180</a> Rights Information about rights held in and over the resource Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s). Format The file format, physical medium, or dimensions of the resource journalArticle 2021 Antioxidants & redox signaling Department of Pharmaceutical Sciences Fan Y Glaucoma glycolysis HIF-1α hypoxia Inman DM Jassim AH journalArticle May 2021 List NEOMED College of Pharmacy Student NEOMED Student Publications Nsiah NY Oxidative Stress Pappenhagen N PGC-1α Text A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text. URL Address <a href="http://doi.org/10.3389/fcell.2021.636321" target="_blank" rel="noreferrer noopener">http://doi.org/10.3389/fcell.2021.636321</a> Pages 636321 Volume 9 ISSN 2296-634X Search for Full-text Locate full-text within NEOMED Library's e-journal collections <a href="http://neomed.idm.oclc.org/login?url=http://doi.org/10.3389/fcell.2021.636321" target="_blank" rel="noreferrer noopener">NEOMED Full-text Holding (if available) - Proxy DOI: 10.3389/fcell.2021.636321</a> <p>Users with a NEOMED Library login can search for full-text journal articles at the following url: <a href="https://libraryguides.neomed.edu/home">https://libraryguides.neomed.edu/home</a></p> Update Year & Number April 2021 List NEOMED College NEOMED College of Pharmacy NEOMED College of Graduate Studies NEOMED Department Department of Pharmaceutical Sciences NEOMED Student Publications Dublin Core The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/. Title A name given to the resource Absence of cytochrome P450-1b1 increases susceptibility of pressure-induced axonopathy in the murine retinal projection. Publisher An entity responsible for making the resource available Frontiers In Cell And Developmental Biology Date A point or period of time associated with an event in the lifecycle of the resource 2021 1905-7 Subject The topic of the resource axonal transport disruption; glaucoma; microbead occlusion model; nodes of Ranvier; retinal ganglion cell Creator An entity primarily responsible for making the resource Amirmokhtari N; Foresi BD; Dewan SS; Bouhenni RA; Smith MA Description An account of the resource Mutations in the cytochrome P450-1B1 (Cyp1b1) gene is a common genetic predisposition associated with various human glaucomas, most prominently in primary congenital glaucoma (PCG). The role of Cyp1b1 in the eye is largely unknown, however, its absence appears to drive the maldevelopment of anterior eye structures responsible for aqueous fluid drainage in murine models. Nevertheless, vision loss in glaucoma ultimately results from the structural and functional loss of retinal ganglion cells (RGCs). Cyp1b1's influence in the development and support of retinal ganglion cell structure and function under normal conditions or during stress, such as elevated ocular pressure; the most common risk factor in glaucoma, remains grossly unknown. Thus, to determine the role of Cyp1b1 in normal retinal projection development we first assessed the strucutrual integrity of RGCs in the retina, optic nerve, and superior colliculus in un-manipulated (naïve) Cyp1b1-knockout (Cyp1b1(-/-)) mice. In addition, in a separate cohort of Cyp1b1(-/-) and wildtype mice, we elevated and maintained intraocular pressure (IOP) at glaucomatous levels for 5-weeks, after which we compared RGC density, node of Ranvier morphology, and axonal transport between the genotypes. Our results demonstrate that naïve Cyp1b1(-/-) mice develop an anatomically intact retinal projection absent of overt glaucomatous pathology. Following pressure elevation, Cyp1b1(-/-) accelerated degradation of axonal transport from the retina to the superior colliculus and altered morphology of the nodes of Ranvier and adjacent paranodes in the optic nerves. Together this data suggests the absence Cyp1b1 expression alone is insufficient to drive murine glaucomatous pathology, however, may increase the vulnerability of retinal axons to disease relevant elevations in IOP. Identifier An unambiguous reference to the resource within a given context <a href="http://doi.org/10.3389/fcell.2021.636321" target="_blank" rel="noreferrer noopener">10.3389/fcell.2021.636321</a> Rights Information about rights held in and over the resource Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s). Format The file format, physical medium, or dimensions of the resource journalArticle 2021 Amirmokhtari N April 2021 List axonal transport disruption Bouhenni RA Department of Pharmaceutical Sciences Dewan SS Foresi BD Frontiers In Cell And Developmental Biology Glaucoma journalArticle microbead occlusion model NEOMED College of Graduate Studies Student NEOMED College of Pharmacy NEOMED Student Publications nodes of Ranvier Retinal ganglion cell Smith MA Text A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text. URL Address <a href="http://doi.org/10.1016/j.nbd.2020.105146" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.nbd.2020.105146</a> Rights Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s). Pages 105146 Volume 147 ISSN 1095-953X 0969-9961 Search for Full-text Locate full-text within NEOMED Library's e-journal collections <a href="http://neomed.idm.oclc.org/login?url=http://doi.org/10.1016/j.nbd.2020.105146" target="_blank" rel="noreferrer noopener">NEOMED Full-text Holding (if available) - Proxy DOI: 10.1016/j.nbd.2020.105146</a> <p>Users with a NEOMED Library login can search for full-text journal articles at the following url: <a href="https://libraryguides.neomed.edu/home">https://libraryguides.neomed.edu/home</a></p> Update Year & Number October 2020 List NEOMED College NEOMED College of Graduate Studies Student NEOMED Department NEOMED Student Publications Dublin Core The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/. Title A name given to the resource Retinal ganglion cell loss and gliosis in the retinofugal projection following intravitreal exposure to amyloid-beta. Publisher An entity responsible for making the resource available Neurobiology of Disease Date A point or period of time associated with an event in the lifecycle of the resource 2020 2020-10-26 Subject The topic of the resource Inflammation; Glaucoma; Alzheimer's disease; Retina; Superior colliculus; Amyloid-beta; CD36; Cluster of differentiation 36 Creator An entity primarily responsible for making the resource Simons ES;Smith M A;Dengler-Crish C M;Crish SD Description An account of the resource Pathological accumulations of amyloid-beta (Aβ) peptide are found in retina early in Alzheimer's disease, yet its effects on retinal neuronal structure remain unknown. To investigate this, we injected fibrillized Aβ(1-42) protein into the eye of adult C57BL/6 J mice and analyzed the retina, optic nerve (ON), and the superior colliculus (SC), the primary retinal target in mice. We found that retinal Aβ exposure stimulated microglial activation and retinal ganglion cell (RGC) loss as early as 1-week post-injection. Pathology was not limited to the retina, but propagated into other areas of the central nervous system. Microgliosis spread throughout the retinal projection (retina, ON, and SC), with multiplex protein quantitation demonstrating an increase in endogenously produced Aβ in the ON and SC corresponding to the injected retinas. Surprisingly, this pathology spread to the opposite side, with unilateral Aβ eye injections driving increased Aβ levels, neuroinflammation, and RGC death in the opposite, un-injected retinal projection. As Aβ-mediated microglial activation has been shown to propagate Aβ pathology, we also investigated the role of the Aβ-binding microglial scavenger receptor CD36 in this pathology. Transgenic mice lacking the CD36 receptor were resistant to Aβ-induced inflammation and RGC death up to 2 weeks following exposure. These results indicate that Aβ pathology drives regional neuropathology in the retina and does not remain isolated to the affected eye, but spreads throughout the nervous system. Further, CD36 may serve as a promising target to prevent Aβ-mediated inflammatory damage. Identifier An unambiguous reference to the resource within a given context <a href="http://doi.org/10.1016/j.nbd.2020.105146" target="_blank" rel="noreferrer noopener">10.1016/j.nbd.2020.105146</a> Format The file format, physical medium, or dimensions of the resource journalArticle 2020 Alzheimer's disease amyloid-beta CD36 Cluster of differentiation 36 Crish SD Dengler-Crish C M Glaucoma Inflammation journalArticle NEOMED College of Graduate Studies Student NEOMED Student Publications Neurobiology of disease October 2020 List retina Simons ES Smith M A superior colliculus Text A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text. URL Address <a href="http://doi.org/10.1007/s10439-020-02608-8" target="_blank" rel="noreferrer noopener">http://doi.org/10.1007/s10439-020-02608-8</a> ISSN 1573-9686 Search for Full-text Locate full-text within NEOMED Library's e-journal collections <a href="http://neomed.idm.oclc.org/login?url=http://doi.org/10.1007/s10439-020-02608-8" target="_blank" rel="noreferrer noopener">NEOMED Full-text Holding (if available) - Proxy DOI: 10.1007/s10439-020-02608-8</a> <p>Users with a NEOMED Library login can search for full-text journal articles at the following url: <a href="https://libraryguides.neomed.edu/home">https://libraryguides.neomed.edu/home</a></p> Update Year & Number September 2020 List NEOMED College NEOMED College of Medicine Student NEOMED Department NEOMED Student Publications Dublin Core The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/. Title A name given to the resource Transcorneal electrical stimulation reduces neurodegenerative process in a mouse model of glaucoma. Publisher An entity responsible for making the resource available Annals Of Biomedical Engineering Date A point or period of time associated with an event in the lifecycle of the resource 2020 2020-09-24 Subject The topic of the resource Glaucoma; Optic nerve; BDNF; Retina; p75NTR; Transcorneal electrical stimulation Creator An entity primarily responsible for making the resource Jassim, AH;Cavanaugh M;Shah JS;Willits R;Inman DM Description An account of the resource Glaucoma is a neurodegenerative disease in which the retinal ganglion cell axons of the optic nerve degenerate concomitant with synaptic changes in the retina, leading finally to death of the retinal ganglion cells (RGCs). Electrical stimulation has been used to improve neural regeneration in a variety of systems, including in diseases of the retina. Therefore, the focus of this study was to investigate whether transcorneal electrical stimulation (TES) in the DBA2/J mouse model of glaucoma could improve retinal or optic nerve pathology and serve as a minimally invasive treatment option. Mice (10 months-old) received 21 sessions of TES over 8 weeks, after which we evaluated RGC number, axon number, and anterograde axonal transport using histology and immunohistochemistry. To gain insight into the mechanism of proposed protection, we also evaluated inflammation by quantifying CD3 + T-cells and Iba1 + microglia; perturbations in metabolism were shown via the ratio pAMPK to AMPK, and changes in trophic support were tested using protein capillary electrophoresis. We found that TES resulted in RGC axon protection, a reduction in inflammatory cells and their activation, improved energy homeostasis, and a reduction of the cell death-associated p75NTR. Collectively, the data indicated that TES maintained axons, decreased inflammation, and increased trophic factor support, in the form of receptor presence and energy homeostasis, suggesting that electrical stimulation impacts several facets of the neurodegenerative process in glaucoma. Identifier An unambiguous reference to the resource within a given context <a href="http://doi.org/10.1007/s10439-020-02608-8" target="_blank" rel="noreferrer noopener">10.1007/s10439-020-02608-8</a> Rights Information about rights held in and over the resource Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s). Format The file format, physical medium, or dimensions of the resource journalArticle 2020 Annals Of Biomedical Engineering BDNF Cavanaugh M Glaucoma Hassan JA Inman DM journalArticle NEOMED College of Medicine Student NEOMED Student Publications optic nerve p75NTR retina September 2020 List Shah JS Transcorneal electrical stimulation Willits R Text A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text. URL Address <a href="http://doi.org/10.1016/j.exer.2020.108257" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.exer.2020.108257</a> Pages 108257 Volume 201 ISSN 1096-0007 Search for Full-text Locate full-text within NEOMED Library's e-journal collections <a href="http://neomed.idm.oclc.org/login?url=http://doi.org/10.1016/j.exer.2020.108257" target="_blank" rel="noreferrer noopener">NEOMED Full-text Holding (if available) - Proxy DOI: 10.1016/j.exer.2020.108257</a> <p>Users with a NEOMED Library login can search for full-text journal articles at the following url: <a href="https://libraryguides.neomed.edu/home">https://libraryguides.neomed.edu/home</a></p> Update Year & Number September 2020 List NEOMED College NEOMED College of Medicine Student NEOMED College of Medicine NEOMED Department NEOMED Student Publications Department of Integrative Medical Sciences Dublin Core The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/. Title A name given to the resource The role of TRPV4 channels in ocular function and pathologies. Publisher An entity responsible for making the resource available Experimental Eye Research Date A point or period of time associated with an event in the lifecycle of the resource 2020 2020-09-29 Subject The topic of the resource Glaucoma; TRPV4; Angiogenesis; Retina; Calcium channel; Cornea; Diabetic retinopathy; Lens; Osmolarity Creator An entity primarily responsible for making the resource Guarino BD;Paruchuri S;Thodeti CK Description An account of the resource Transient potential receptor vanilloid 4 (TRPV4) is an ion channel responsible for sensing osmotic and mechanical signals, which in turn regulates calcium signaling across cell membranes. TRPV4 is widely expressed throughout the body, and plays an important role in normal physiological function, as well as different pathologies, however, its role in the eye is not well known. In the eye, TRPV4 is expressed in various tissues, such as the retina, corneal epithelium, ciliary body, and the lens. In this review, we provide an overview on TRPV4 structure, activation, mutations, and summarize the current knowledge of TRPV4 function and signaling mechanisms in various locations throughout the eye, as well as its role in ocular diseases, such as glaucoma and diabetic retinopathy. Based on the available data, we highlight the therapeutic potential of TRPV4 as well as the shortcomings of current research. Finally, we provide future perspectives on the implications of targeting TRPV4 to treat various ocular pathologies. (Copyright © 2020 Elsevier Ltd. All rights reserved.) Identifier An unambiguous reference to the resource within a given context <a href="http://doi.org/10.1016/j.exer.2020.108257" target="_blank" rel="noreferrer noopener">10.1016/j.exer.2020.108257</a> Rights Information about rights held in and over the resource Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s). Format The file format, physical medium, or dimensions of the resource journalArticle 2020 angiogenesis calcium channel Cornea Department of Integrative Medical Sciences diabetic retinopathy Experimental eye research Glaucoma Guarino BD journalArticle Lens NEOMED College of Medicine NEOMED College of Medicine Student NEOMED Student Publications Osmolarity Paruchuri S retina September 2020 List Thodeti CK TRPV4 Text A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text. URL Address <a href="http://doi.org/10.1016/j.nbd.2020.104944" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.nbd.2020.104944</a> Pages 104944 Volume 141 ISSN 1095-953X 0969-9961 Search for Full-text Locate full-text within NEOMED Library's e-journal collections <a href="http://neomed.idm.oclc.org/login?url=http://doi.org/10.1016/j.nbd.2020.104944" target="_blank" rel="noreferrer noopener">NEOMED Full-text Holding (if available) - Proxy DOI: 10.1016/j.nbd.2020.104944</a> <p>Users with a NEOMED Library login can search for full-text journal articles at the following url: <a href="https://libraryguides.neomed.edu/home">https://libraryguides.neomed.edu/home</a></p> Update Year & Number June 2020 Update II NEOMED College NEOMED College of Pharmacy NEOMED Department NEOMED Student Publications Department of Pharmaceutical Sciences Dublin Core The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/. Title A name given to the resource MCT2 overexpression rescues metabolic vulnerability and protects retinal ganglion cells in two models of glaucoma. Publisher An entity responsible for making the resource available Neurobiology of disease Date A point or period of time associated with an event in the lifecycle of the resource 2020 2020-05-15 Subject The topic of the resource Glaucoma; Metabolism; Monocarboxylate transporter; Ocular hypertension; Retinal ganglion cell Creator An entity primarily responsible for making the resource Harun-Or-Rashid Mohammad; Pappenhagen Nathaniel; Zubricky Ryan; Coughlin Lucy; Jassim Assraa Hassan; Inman Denise M Description An account of the resource Improving cellular access to energy substrates is one strategy to overcome observed declines in energy production and utilization in the aged and pathologic central nervous system. Monocarboxylate transporters (MCTs), the movers of lactate, pyruvate, and ketone bodies into or out of a cell, are significantly decreased in the DBA/2 J mouse model of glaucoma. In order to confirm MCT decreases are disease-associated, we decreased MCT2 in the retinas of MCT2(fl/+) mice using an injection of AAV2-cre, observing significant decline in ATP production and visual evoked potential. Restoring MCT2 levels in retinal ganglion cells (RGCs) via intraocular injection of AAV2-GFP-MCT2 in two models of glaucoma, the DBA/2 J (D2), and a magnetic bead model of ocular hypertension (OHT), preserved RGCs and their function. Viral-mediated overexpression of MCT2 increased RGC density and axon number, reduced energy imbalance, and increased mitochondrial function as measured by cytochrome c oxidase and succinate dehydrogenase activity in both models of glaucoma. Ocular hypertensive mice injected with AAV2:MCT2 had significantly greater P1 amplitude as measured by pattern electroretinogram than mice with OHT alone. These findings indicate overexpression of MCT2 improves energy homeostasis in the glaucomatous visual system, suggesting that expanding energy input options for cells is a viable option to combat neurodegeneration. Identifier An unambiguous reference to the resource within a given context <a href="http://doi.org/10.1016/j.nbd.2020.104944" target="_blank" rel="noreferrer noopener">10.1016/j.nbd.2020.104944</a> Rights Information about rights held in and over the resource Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s). Format The file format, physical medium, or dimensions of the resource journalArticle 2020 Coughlin Lucy Department of Pharmaceutical Sciences Glaucoma Harun-Or-Rashid Mohammad Inman Denise M Jassim Assraa Hassan journalArticle June 2020 Update II Metabolism Monocarboxylate transporter NEOMED College of Pharmacy Student NEOMED Student Publications Neurobiology of disease Ocular Hypertension Pappenhagen Nathaniel Retinal ganglion cell Zubricky Ryan Text A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text. URL Address <a href="http://doi.org/10.1016/j.survophthal.2019.12.003" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.survophthal.2019.12.003</a> Rights Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s). ISSN 1879-3304 Search for Full-text Locate full-text within NEOMED Library's e-journal collections <a href="http://ezproxy.neomed.idm.oclc.org/login?url=http://doi.org/10.1016/j.survophthal.2019.12.003" target="_blank" rel="noreferrer noopener">NEOMED Full-text Holding (if available) - Proxy DOI: 10.1016/j.survophthal.2019.12.003</a> <p>Users with a NEOMED Library login can search for full-text journal articles at the following url: <a href="https://libraryguides.neomed.edu/home">https://libraryguides.neomed.edu/home</a></p> Update Year & Number January 2020 Update NEOMED College NEOMED College of Medicine NEOMED Department NEOMED Student Publications Dublin Core The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/. Title A name given to the resource Current Management of Uveitis-associated Ocular Hypertension and Glaucoma Publisher An entity responsible for making the resource available Survey of Ophthalmology Date A point or period of time associated with an event in the lifecycle of the resource 2019 2019-12-06 Subject The topic of the resource corticosteroid; glaucoma; glaucoma surgery; intraocular pressure management; ocular hypertension; uveitis Creator An entity primarily responsible for making the resource Kesav Natasha; Palestine Alan G; Kahook Malik Y; Pantcheva Mina B Description An account of the resource Glaucoma secondary to ocular inflammation is potentially blinding and requires aggressive multifaceted management. The pathogenesis is related to the intraocular pressure (IOP) elevation secondary to compromised aqueous humor outflow by inflammatory cells, chemical mediators released into the aqueous, and to the uveitic therapy itself (corticosteroid induced). The management of uveitic glaucoma (UG) needs a careful combination between anti-inflammatory therapy and appropriate IOP-lowering drugs to prevent worsening of condition and long-term visual loss. While there have been novel medications that have emerged in the management of glaucoma and uveitis, around 30% of UG eyes do not respond to maximal medical therapy and require surgical intervention. Studied procedures include laser therapy, filtration surgery, and glaucoma drainage devices, as well as recent surgical techniques for intraocular pressure control such as minimally invasive glaucoma surgery and angle-based procedures. We review and update the medical and surgical management of UG. Identifier An unambiguous reference to the resource within a given context <a href="http://doi.org/10.1016/j.survophthal.2019.12.003" target="_blank" rel="noreferrer noopener">10.1016/j.survophthal.2019.12.003</a> PMID: 31816329 Format The file format, physical medium, or dimensions of the resource Journal Article 2019 corticosteroid Glaucoma glaucoma surgery intraocular pressure management January 2020 Update Journal Article Kahook Malik Y Kesav Natasha NEOMED College of Medicine Student NEOMED Student Publications Ocular Hypertension Palestine Alan G Pantcheva Mina B Survey of Ophthalmology uveitis Text A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text. URL Address <a href="http://doi.org/10.1167/iovs.15-17885" target="_blank" rel="noreferrer noopener">http://doi.org/10.1167/iovs.15-17885</a> Rights Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s). Pages 8215-8227 Issue 13 Volume 56 Search for Full-text Locate full-text within NEOMED Library's e-journal collections <p>Users with a NEOMED Library login can search for full-text journal articles at the following url: <a href="https://libraryguides.neomed.edu/home">https://libraryguides.neomed.edu/home</a></p> Dublin Core The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/. Title A name given to the resource Decreased Energy Capacity And Increased Autophagic Activity In Optic Nerve Axons With Defective Anterograde Transport Publisher An entity responsible for making the resource available Investigative Ophthalmology & Visual Science Date A point or period of time associated with an event in the lifecycle of the resource 2015 2015-12 Subject The topic of the resource anterograde transport; autophagy; cholera; cholera-toxin; degeneration; dying back process; endoplasmic-reticulum; glaucoma; microscopy; Mitochondria; mitophagy; mouse model; Ophthalmology; optic neuropathy; stress; toxin-B Creator An entity primarily responsible for making the resource Kleesattel D; Crish S D; Inman D M Description An account of the resource PURPOSE. Autophagy is a critical process, compromised in neurodegenerative disease, by which terminally differentiated cells like neurons manage cytoskeletal and organelle turnover. How autophagy relates to associated neurodegenerative pathologies remain unclear. We examined autophagy in optic neuropathy by investigating cytoskeletal degradation, mitochondria, and autophagic vesicles in the DBA2/J mouse model of glaucoma exhibiting differing levels of axon transport functionality. METHODS. DBA/2J and DBA/2J(wt-gpnmb) control mice 11 to 14 months of age were injected with cholera toxin-B (CTB) to assay anterograde axonal transport. Axonal mitochondria and autophagic vesicles were analyzed with respect to transport integrity in proximal and distal optic nerve using serial block face scanning electron microscopy (3D EM). RESULTS. Several indices varied significantly between the DBA/2J and DBA/2Jwt-gpnmb mice, including mitochondrial volume, average number of autophagic vesicles per axon, and mitochondrial cristae. However, there were no differences in mitochondrial cristae for axons with functional versus dysfunctional CTB transport, suggesting that mitochondrial dysfunction precedes overt transport blockade. Anterograde transport failure was accompanied by a dissociation of the relationship between mitochondrial and axon volumes. Autophagic vesicle profiles were significantly increased in optic nerve with transport deficit, consistent with greater autophagic activity. Mitochondria within autophagosomes, indicative of mitophagy, were observed in both proximal and distal axons. CONCLUSIONS. Loss of anterograde transport in DBA/2J optic nerve is concomitant with diminished mitochondrial volume, increased cytoskeletal breakdown and autophagic activity, and accumulation of autophagic profiles, including signs of mitophagy, in proximal optic nerve. Axons with transport deficit are metabolically underserved, though not necessarily from mitophagy. Identifier An unambiguous reference to the resource within a given context <a href="http://doi.org/10.1167/iovs.15-17885" target="_blank" rel="noreferrer noopener">10.1167/iovs.15-17885</a> Format The file format, physical medium, or dimensions of the resource Journal Article or Conference Abstract Publication 2015 anterograde transport Autophagy Cholera cholera-toxin Crish S D degeneration Department of Pharmaceutical Sciences dying back process endoplasmic-reticulum Glaucoma Inman D M Investigative ophthalmology & visual science Journal Article or Conference Abstract Publication Kleesattel D Microscopy Mitochondria mitophagy Mouse model NEOMED College of Pharmacy Ophthalmology optic neuropathy Stress toxin-B Text A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text. URL Address <a href="http://doi.org/10.1007/s10534-014-9790-z" target="_blank" rel="noreferrer noopener">http://doi.org/10.1007/s10534-014-9790-z</a> Rights Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s). Pages 1291-1301 Issue 6 Volume 27 Search for Full-text Locate full-text within NEOMED Library's e-journal collections <p>Users with a NEOMED Library login can search for full-text journal articles at the following url: <a href="https://libraryguides.neomed.edu/home">https://libraryguides.neomed.edu/home</a></p> Dublin Core The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/. Title A name given to the resource Abnormal Metal Levels In The Primary Visual Pathway Of The Dba/2j Mouse Model Of Glaucoma Publisher An entity responsible for making the resource available Biometals Date A point or period of time associated with an event in the lifecycle of the resource 2014 2014-12 Subject The topic of the resource alzheimers-disease; amyloid-beta; aqueous-humor; Biochemistry & Molecular Biology; ganglion-cell degeneration; gene-expression; Glaucoma; ICP-MS; iron; microarray analysis; neurodegeneration; neurodegeneration; Retina; Retina; Superior colliculus; synapse Creator An entity primarily responsible for making the resource DeToma A S; Dengler-Crish C M; Deb A; Braymer J J; Penner-Hahn J E; Van der Schyf C J; Lim M H; Crish S D Identifier An unambiguous reference to the resource within a given context <a href="http://doi.org/10.1007/s10534-014-9790-z" target="_blank" rel="noreferrer noopener">10.1007/s10534-014-9790-z</a> Format The file format, physical medium, or dimensions of the resource Journal Article or Conference Abstract Publication 2014 alzheimers-disease amyloid-beta aqueous-humor Biochemistry & Molecular Biology Biometals Braymer J J Crish S D Deb A Dengler-Crish C M Department of Pharmaceutical Sciences DeToma A S ganglion-cell degeneration gene-expression Glaucoma ICP-MS iron Lim M H Microarray Analysis NEOMED College of Pharmacy Neurodegeneration Penner-Hahn J E retina superior colliculus synapse Van der Schyf C J Text A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text. URL Address <a href="http://doi.org/10.1016/j.nbd.2013.07.001" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.nbd.2013.07.001</a> Rights Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s). Pages 26-37 Volume 59 Search for Full-text Locate full-text within NEOMED Library's e-journal collections <p>Users with a NEOMED Library login can search for full-text journal articles at the following url: <a href="https://libraryguides.neomed.edu/home">https://libraryguides.neomed.edu/home</a></p> Dublin Core The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/. Title A name given to the resource Proximal inhibition of p38 MAPK stress signaling prevents distal axonopathy Publisher An entity responsible for making the resource available Neurobiology of Disease Date A point or period of time associated with an event in the lifecycle of the resource 2013 2013-11 Subject The topic of the resource Glaucoma; Neurodegeneration; Neurosciences & Neurology; death; amyotrophic-lateral-sclerosis; mouse model; ocular hypertension; activated protein-kinase; up-regulation; alzheimers-disease brain; Axonopathy; experimental glaucoma; ganglion-cell neurons; Heat shock protein; p38 MAPK; rat retina; Retinal ganglion cell Creator An entity primarily responsible for making the resource Dapper J D; Crish S D; Pang I H; Calkins D J Description An account of the resource The p38 mitogen-activated protein kinase (MAPK) isoforms are phosphorylated by a variety of stress stimuli in neurodegenerative disease and act as upstream activators of myriad pathogenic processes. Thus, p38 MAPK inhibitors are of growing interest as possible therapeutic interventions. Axonal dysfunction is an early component of most neurodegenerative disorders, including the most prevalent optic neuropathy, glaucoma. Sensitivity to intraocular pressure at an early stage disrupts anterograde transport along retinal ganglion cell (RGC) axons to projection targets in the brain with subsequent degeneration of the axons themselves; RGC body loss is much later. Here we show that elevated ocular pressure in rats increases p38 MAPK activation in retina, especially in RGC bodies. Topical eye-drop application of a potent and selective inhibitor of the p38 MAPK catalytic domain (Ro3206145) prevented both the degradation of anterograde transport to the brain and degeneration of axons in the optic nerve. Ro3206145 reduced in the retina phosphorylation of tau and heat-shock protein 27, both down-stream targets of p38 IVIAPK activation implicated in glaucoma, as well as expression of two inflammatory responses. We also observed increased p38 MAPK activation in mouse models. Thus, inhibition of p38 MAPK signaling in the retina may represent a therapeutic target for preventing early pathogenesis in optic neuropathies. (C) 2013 Elsevier Inc. All rights reserved. Identifier An unambiguous reference to the resource within a given context <a href="http://doi.org/10.1016/j.nbd.2013.07.001" target="_blank" rel="noreferrer noopener">10.1016/j.nbd.2013.07.001</a> Format The file format, physical medium, or dimensions of the resource Journal Article or Conference Abstract Publication 2013 activated protein-kinase alzheimers-disease brain amyotrophic-lateral-sclerosis Axonopathy Calkins D J Crish S D Dapper J D Death Department of Pharmaceutical Sciences experimental glaucoma ganglion-cell neurons Glaucoma Heat shock protein Journal Article or Conference Abstract Publication Mouse model NEOMED College of Pharmacy Neurobiology of disease Neurodegeneration Neurosciences & Neurology Ocular Hypertension p38 MAPK Pang I H rat retina Retinal ganglion cell Up-Regulation Text A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text. URL Address n/a Rights Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s). Pages 1880-1892 Issue 204 Volume 16 Search for Full-text Locate full-text within NEOMED Library's e-journal collections <p>Users with a NEOMED Library login can search for full-text journal articles at the following url: <a href="https://libraryguides.neomed.edu/home">https://libraryguides.neomed.edu/home</a></p> Dublin Core The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/. Title A name given to the resource Suppression of transforming growth factor-beta effects in rabbit subconjunctival fibroblasts by activin receptor-like kinase 5 inhibitor Publisher An entity responsible for making the resource available Molecular Vision Date A point or period of time associated with an event in the lifecycle of the resource 2010 2010-09 Subject The topic of the resource anti-scarring agent; Biochemistry & Molecular Biology; choroidal; extracellular-matrix; fibrosis; glaucoma; identification; in-vivo; mitomycin-c; neovascularization; Ophthalmology; Surgery; tgf-beta Creator An entity primarily responsible for making the resource Sapitro J; Dunmire J J; Scott S E; Sutariya V; Geldenhuys W J; Hewit M; Yue Byjt; Nakamura H Description An account of the resource Purpose: Transforming growth factor-beta (TGF-beta) activity has been implicated in subconjunctival scarring in eyes following glaucoma filtration surgery (GFS). The purpose of this study is to determine whether an inhibitor for activin receptor-like kinase (ALK) 5 (also known as TGF-beta receptor type I) could suppress TGF-beta activity and thereby promote filtering bleb survival after GFS in a rabbit model. Methods: An ALK-5 inhibitor, SB-505124, was used. A docking study was performed to investigate the interaction between the inhibitor and the receptor. Immunofluorescence for connective tissue growth factor (CTGF) and alpha-smooth muscle actin (alpha-SMA) was performed in cultured rabbit subconjunctival fibroblasts. Immunoblotting for phosphorylated Smad2 (pSmad2), CTGF, and alpha-SMA was also performed. In an in vivo rabbit GFS model, SB-505124 was delivered in a lactose tablet during surgery. Eyes were examined by slit-lamp and intraocular pressure (IOP) was measured until the time of bleb failure or up to 28 days after surgery. Tissue sections on day 5 after surgery were histologically evaluated after staining with hematoxylin and eosin. The sections were also immunostained for CTGF and alpha-SMA. In addition, cell outgrowth from dissected subconjunctival tissues placed in a cell culture flask with media was investigated. Results: The docking study indicated hydrogen bond interactions between SB-505124 and amino acids His-283 and Ser-280 ALK-5. Suppression of pSmad2, CTGF, and alpha-SMA by SB-505124 was observed in cultured fibroblasts. Filtering blebs in the GFS with SB-505124 group were maintained for more than 10 days, and the period of bleb survival was significantly longer than that in controls. IOP levels after surgery seemed to be related to bleb survival. Histologically, subconjunctival cell infiltration and scarring at the surgical site in the GFS with SB-505124 and mitomycin C (MMC) groups were much subsided compared to controls. Suppression of CTGF and alpha-SMA by SB-505124 was also observed by immunofluorescence. Cell outgrowth from explants dissected from eyes to which SB-505124 was applied during GFS was robust while outgrowth was poor from those treated with MMC. Conclusions: The ALK-5 inhibitor SB-505124 was efficacious both in vitro and in vivo in suppressing the TGF-beta action. The inhibitor may provide a novel therapy for preventing ocular inflammation and scarring. Identifier An unambiguous reference to the resource within a given context n/a Format The file format, physical medium, or dimensions of the resource Journal Article 2010 anti-scarring agent Biochemistry & Molecular Biology choroidal Dunmire J J extracellular-matrix Fibrosis Geldenhuys W J Glaucoma Hewit M identification in-vivo Journal Article mitomycin-c Molecular Vision Nakamura H Neovascularization Ophthalmology Sapitro J Scott S E Surgery Sutariya V tgf-beta Yue Byjt Text A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text. URL Address <a href="http://doi.org/10.1186/s12974-015-0399-0" target="_blank" rel="noreferrer noopener">http://doi.org/10.1186/s12974-015-0399-0</a> Rights Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s). Pages 13-13 Volume 12 Search for Full-text Locate full-text within NEOMED Library's e-journal collections <p>Users with a NEOMED Library login can search for full-text journal articles at the following url: <a href="https://libraryguides.neomed.edu/home">https://libraryguides.neomed.edu/home</a></p> Dublin Core The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/. Title A name given to the resource Early pro-inflammatory cytokine elevations in the DBA/2J mouse model of glaucoma Publisher An entity responsible for making the resource available Journal of Neuroinflammation Date A point or period of time associated with an event in the lifecycle of the resource 2015 2015-09 Subject The topic of the resource Aging; axonal-transport; axoplasmic-transport; Cytokines; fibroblast-growth-factor; gene-expression; glaucoma; Immunology; inflammation; Intraocular pressure; Intraocular pressure; necrosis-factor-alpha; neurodegeneration; Neurosciences & Neurology; ocular hypertension; optic-nerve head; retinal ganglion-cells; tnf-alpha Creator An entity primarily responsible for making the resource Wilson G N; Inman D M; Denger-Crish C M; Smith M A; Crish S D Description An account of the resource Background: Neuroinflammation-astrogliosis, microglial activation, and changes in cytokine signaling-is a prominent feature of neurodegenerative disorders. Glaucoma is a group of chronic neurodegenerative conditions that make up the leading cause of irreversible blindness worldwide. Neuroinflammation has been postulated to play a significant role in the pathogenesis and progression of glaucomatous neurodegeneration. Though much is known regarding inflammation in the eye in glaucoma, little is known about cytokine activity outside of the retina where pathologies develop early. Methods: We traced the primary visual projection from the eye to the superior colliculus (SC) in DBA/2J and DBA/2J. Gpnmb(+) (control) mice using the anterograde tracer cholera toxin-B (CTB) to assay axonal transport deficits. Forty-eight hours later, visual structures were microdissected from fresh tissue based on transport outcome. Using magnetic bead multiplexing assays, we measured levels of 20 cytokines in the retina, proximal and distal optic nerves, CTB-positive and negative SC subdivisions, cerebellum, and serum at different ages representing different stages of pathology. Results: Pro-and anti-inflammatory cytokine levels in mice often changed in the same direction based on strain, age, and tissue. Significant elevations in retinal pro-inflammatory cytokines were observed in young DBA/2J mice compared to controls, followed by an age-dependent decrease in the DBA/2J mice. Proximal optic nerve of young DBA/2J mice showed a 50 % or greater decrease in levels of certain cytokines compared to older DBA/2J cohorts and controls, while both proximal and distal optic nerve of DBA/2Js showed elevations in IL-1 beta at all ages compared to controls. Pro-inflammatory cytokine IL-6 levels varied in accordance with transport outcome in the SC: IL-6 was elevated 44-80 % in glaucomatous DBA/2J collicular regions deficient in anterograde transport from retinal ganglion cells (RGCs) compared to areas with intact transport. Conclusion: Dysregulation of cytokine signaling in the RGC projection of DBA/2J mice was evident early in distal retinal targets, well before intraocular pressure elevation or axonal degeneration begins. Identifier An unambiguous reference to the resource within a given context <a href="http://doi.org/10.1186/s12974-015-0399-0" target="_blank" rel="noreferrer noopener">10.1186/s12974-015-0399-0</a> Format The file format, physical medium, or dimensions of the resource Journal Article 2015 Aging axonal-transport axoplasmic-transport Crish S D Cytokines Denger-Crish C M Department of Pharmaceutical Sciences fibroblast-growth-factor gene-expression Glaucoma Immunology Inflammation Inman D M Intraocular Pressure Journal Article Journal of neuroinflammation necrosis-factor-alpha NEOMED College of Pharmacy Neurodegeneration Neurosciences & Neurology Ocular Hypertension optic-nerve head retinal ganglion-cells Smith M A TNF-alpha Wilson G N Text A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text. URL Address <a href="http://doi.org/10.1517/14656560903292649" target="_blank" rel="noreferrer noopener">http://doi.org/10.1517/14656560903292649</a> Rights Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s). Pages 2759-2768 Issue 16 Volume 10 Search for Full-text Locate full-text within NEOMED Library's e-journal collections <p>Users with a NEOMED Library login can search for full-text journal articles at the following url: <a href="https://libraryguides.neomed.edu/home">https://libraryguides.neomed.edu/home</a></p> Dublin Core The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/. Title A name given to the resource Bimatoprost - a review Publisher An entity responsible for making the resource available Expert Opinion on Pharmacotherapy Date A point or period of time associated with an event in the lifecycle of the resource 2009 2009-11 Subject The topic of the resource acid; aqueous-humor; bimatoprost; clinical-trial; cost-effectiveness; elevated intraocular-pressure; fixed combination; free; glaucoma; human eyes; Intraocular pressure; ocular hypertension; open-angle glaucoma; Pharmacology & Pharmacy; prostaglandin; prostaglandin-ethanolamides; prostamide; prostamides Creator An entity primarily responsible for making the resource Patil A J; Vajaranant T S; Edward D P Description An account of the resource Bimatoprost is a synthetic prostamide analog that is efficacious in the treatment of open-angle glaucoma, ocular hypertension and other forms of glaucoma. it reduces intraocular pressure (IOP) by increasing uveoscleral and trabecular outflow. When used as a 0.03% topical preparation once daily, it demonstrates sustained lowering of IOP of 7 - 8 mmHg over a 24-h period. The drug has been found to be more effective than timolol. In some studies it has shown greater ability to lower IOP when compared with other prostaglandin analogs; whereas in others all three clinically used prostaglandin analogs were found to be equally effective. it shows good IOP reduction when used in combination with other glaucoma medications. A common side effect includes mild conjunctival hyperemia, which is generally reversible. Other side effects include periorbital pigmentation, discomfort, ocular surface hyperemia and skin changes. Pharmacoeconomic data indicate that bimatoprost is cost effective in the treatment of open-angle glaucoma. Identifier An unambiguous reference to the resource within a given context <a href="http://doi.org/10.1517/14656560903292649" target="_blank" rel="noreferrer noopener">10.1517/14656560903292649</a> Format The file format, physical medium, or dimensions of the resource Journal Article 2009 acid aqueous-humor bimatoprost clinical-trial cost-effectiveness Edward D P elevated intraocular-pressure Expert Opinion on Pharmacotherapy fixed combination free Glaucoma human eyes Intraocular Pressure Journal Article Ocular Hypertension open-angle glaucoma Patil A J Pharmacology & Pharmacy prostaglandin prostaglandin-ethanolamides prostamide prostamides Vajaranant T S Text A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text. URL Address <a href="http://doi.org/10.1007/s12035-019-1576-4" target="_blank" rel="noreferrer noopener">http://doi.org/10.1007/s12035-019-1576-4</a> Rights Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s). Dublin Core The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/. Title A name given to the resource Higher Reliance on Glycolysis Limits Glycolytic Responsiveness in Degenerating Glaucomatous Optic Nerve. Publisher An entity responsible for making the resource available Molecular neurobiology Date A point or period of time associated with an event in the lifecycle of the resource 2019 2019-04 Subject The topic of the resource Glaucoma; Mitochondria; DBA/2J; Fluorocitrate; Optic nerve; Seahorse analyzer Creator An entity primarily responsible for making the resource Jassim Assraa Hassan; Coughlin Lucy; Harun-Or-Rashid Mohammad; Kang Patrick T; Chen Yeong-Renn; Inman Denise M Description An account of the resource Metabolic dysfunction accompanies neurodegenerative disease and aging. An important step for therapeutic development is a more sophisticated understanding of the source of metabolic dysfunction, as well as to distinguish disease-associated changes from aging effects. We examined mitochondrial function in ex vivo aging and glaucomatous optic nerve using a novel approach, the Seahorse Analyzer. Optic nerves (ON) from the DBA/2J mouse model of glaucoma and the DBA/2-Gpnmb(+) control strain were isolated, and oxygen consumption rate (OCR) and extracellular acidification rate (ECAR), the discharge of protons from lactate release or byproducts of substrate oxidation, were measured. The glial-specific aconitase inhibitor fluorocitrate was used to limit the contribution of glial mitochondria to OCR and ECAR. We observed significant decreases in maximal respiration, ATP production, and spare capacity with aging. In the presence of fluorocitrate, OCR was higher, with more ATP produced, in glaucoma compared to aged ON. However, glaucoma ON showed lower maximal respiration. In the presence of fluorocitrate and challenged with ATPase inhibition, glaucoma ON was incapable of further upregulation of glycolysis to compensate for the loss of oxidative phosphorylation. Inclusion of 2-deoxyglucose as a substrate during ATPase inhibition indicated a significantly higher proportion of ECAR was derived from TCA cycle substrate oxidation than glycolysis in glaucoma ON. These data indicate that glaucoma axons have limited ability to respond to increased energy demand given their lower maximal respiration and inability to upregulate glycolysis when challenged. The higher ATP output from axonal mitochondria in glaucoma optic nerve compensates for this lack of resiliency but is ultimately inadequate for continued function. Identifier An unambiguous reference to the resource within a given context <a href="http://doi.org/10.1007/s12035-019-1576-4" target="_blank" rel="noreferrer noopener">10.1007/s12035-019-1576-4</a> 2019 Chen Yeong-Renn Coughlin Lucy DBA/2J Department of Integrative Medical Sciences Department of Pharmaceutical Sciences Fluorocitrate Glaucoma Harun-Or-Rashid Mohammad Inman Denise M Jassim Assraa Hassan Kang Patrick T Mitochondria Molecular neurobiology NEOMED College of Medicine NEOMED College of Pharmacy optic nerve Seahorse analyzer Text A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text. URL Address <a href="http://doi.org/10.3389/fnins.2018.00769" target="_blank" rel="noreferrer noopener">http://doi.org/10.3389/fnins.2018.00769</a> Pages 769–769 Volume 12 Dublin Core The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/. Title A name given to the resource Editorial: Axonopathy in Neurodegenerative Disease. Publisher An entity responsible for making the resource available Frontiers in neuroscience Date A point or period of time associated with an event in the lifecycle of the resource 2018 1905-7 Subject The topic of the resource axon degeneration; chemotherapy induced neuropathy; glaucoma; mitochondrial dysfuncion; neuropathy Creator An entity primarily responsible for making the resource Burgess Robert W; Crish Samuel D Identifier An unambiguous reference to the resource within a given context <a href="http://doi.org/10.3389/fnins.2018.00769" target="_blank" rel="noreferrer noopener">10.3389/fnins.2018.00769</a> Rights Information about rights held in and over the resource Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s). 2018 axon degeneration Burgess Robert W chemotherapy induced neuropathy Crish Samuel D Department of Pharmaceutical Sciences Frontiers in neuroscience Glaucoma mitochondrial dysfuncion NEOMED College of Pharmacy Neuropathy Text A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text. URL Address <a href="http://doi.org/10.3389/fnins.2016.00494" target="_blank" rel="noreferrer noopener">http://doi.org/10.3389/fnins.2016.00494</a> Pages 494–494 Volume 10 Dublin Core The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/. Title A name given to the resource Early Cytoskeletal Protein Modifications Precede Overt Structural Degeneration in the DBA/2J Mouse Model of Glaucoma. Publisher An entity responsible for making the resource available Frontiers in neuroscience Date A point or period of time associated with an event in the lifecycle of the resource 2016 1905-07 Subject The topic of the resource glaucoma; phosphorylation; amyloid-beta; axonal transport; cytoskeleton; neurofilament; spectrin; tau Creator An entity primarily responsible for making the resource Wilson Gina N; Smith Matthew A; Inman Denise M; Dengler-Crish Christine M; Crish Samuel D Description An account of the resource Axonal transport deficits precede structural loss in glaucoma and other neurodegenerations. Impairments in structural support, including modified cytoskeletal proteins, and microtubule-destabilizing elements, could be initiating factors in glaucoma pathogenesis. We investigated the time course of changes in protein levels and post-translational modifications in the DBA/2J mouse model of glaucoma. Using anterograde tract tracing of the retinal projection, we assessed major cytoskeletal and transported elements as a function of transport integrity in different stages of pathological progression. Using capillary-based electrophoresis, single- and multiplex immunosorbent assays, and immunofluorescence, we quantified hyperphosphorylated neurofilament-heavy chain, phosphorylated tau (ptau), calpain-mediated spectrin breakdown product (145/150 kDa), beta-tubulin, and amyloid-beta42 proteins based on age and transport outcome to the superior colliculus (SC; the main retinal target in mice). Phosphorylated neurofilament-heavy chain (pNF-H) was elevated within the optic nerve (ON) and SC of 8-10 month-old DBA/2J mice, but was not evident in the retina until 12-15 months, suggesting that cytoskeletal modifications first appear in the distal retinal projection. As expected, higher pNF-H levels in the SC and retina were correlated with axonal transport deficits. Elevations in hyperphosphorylated tau (ptau) occurred in ON and SC between 3 and 8 month of age while retinal ptau accumulations occurred at 12-15 months in DBA/2J mice. In vitro co-immunoprecipitation experiments suggested increased affinity of ptau for the retrograde motor complex protein dynactin. We observed a transport-related decrease of beta-tubulin in ON of 10-12 month-old DBA/2J mice, suggesting destabilized microtubule array. Elevations in calpain-mediated spectrin breakdown product were seen in ON and SC at the earliest age examined, well before axonal transport loss is evident. Finally, transport-independent elevations of amyloid-beta42, unlike pNF-H or ptau, occurred first in the retina of DBA/2J mice, and then progressed to SC. These data demonstrate distal-to-proximal progression of cytoskeletal modifications in the progression of glaucoma, with many of these changes occurring prior to complete loss of functional transport and axon degeneration. The earliest changes, such as elevated spectrin breakdown and amyloid-beta levels, may make retinal ganglion cells susceptible to future stressors. As such, targeting modification of the axonal cytoskeleton in glaucoma may provide unique opportunities to slow disease progression. Identifier An unambiguous reference to the resource within a given context <a href="http://doi.org/10.3389/fnins.2016.00494" target="_blank" rel="noreferrer noopener">10.3389/fnins.2016.00494</a> Rights Information about rights held in and over the resource Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s). 2016 amyloid-beta Axonal Transport Crish Samuel D cytoskeleton Dengler-Crish Christine M Department of Pharmaceutical Sciences Frontiers in neuroscience Glaucoma Inman Denise M NEOMED College of Pharmacy neurofilament Phosphorylation Smith Matthew A spectrin Tau Wilson Gina N Text A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text. URL Address <a href="http://doi.org/10.3389/fnins.2014.00290" target="_blank" rel="noreferrer noopener">http://doi.org/10.3389/fnins.2014.00290</a> Pages 290–290 Volume 8 Dublin Core The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/. Title A name given to the resource Anterograde transport blockade precedes deficits in retrograde transport in the visual projection of the DBA/2J mouse model of glaucoma. Publisher An entity responsible for making the resource available Frontiers in neuroscience Date A point or period of time associated with an event in the lifecycle of the resource 2014 1905-07 Subject The topic of the resource glaucoma; optic nerve; axonal transport; axonopathy; neurodegeneration; ocular; superior colliculi; vision disorders Creator An entity primarily responsible for making the resource Dengler-Crish Christine M; Smith Matthew A; Inman Denise M; Wilson Gina N; Young Jesse W; Crish Samuel D Description An account of the resource Axonal transport deficits have been reported as an early pathology in several neurodegenerative disorders, including glaucoma. However, the progression and mechanisms of these deficits are poorly understood. Previous work suggests that anterograde transport is affected earlier and to a larger degree than retrograde transport, yet this has never been examined directly in vivo. Using combined anterograde and retrograde tract tracing methods, we examined the time-course of anterograde and retrograde transport deficits in the retinofugal projection in pre-glaucomatous (3 month-old) and glaucomatous (9-13 month old) DBA/2J mice. DBA/2J-Gpnmb (+) mice were used as a control strain and were shown to have similar retinal ganglion cell densities as C57BL/6J control mice-a strain commonly investigated in the field of vision research. Using cholera toxin-B injections into the eye and FluoroGold injections into the superior colliculus (SC), we were able to measure anterograde and retrograde transport in the primary visual projection. In DBA/2J, anterograde transport from the retina to SC was decreased by 69% in the 9-10 month-old age group, while retrograde transport was only reduced by 23% from levels seen in pre-glaucomatous mice. Despite this minor reduction, retrograde transport remained largely intact in these glaucomatous age groups until 13-months of age. These findings indicate that axonal transport deficits occur in semi-functional axons that are still connected to their brain targets. Structural persistence as determined by presence of estrogen-related receptor beta label in the superficial SC was maintained beyond time-points where reductions in retrograde transport occurred, also supporting that transport deficits may be due to physiological or functional abnormalities as opposed to overt structural loss. Identifier An unambiguous reference to the resource within a given context <a href="http://doi.org/10.3389/fnins.2014.00290" target="_blank" rel="noreferrer noopener">10.3389/fnins.2014.00290</a> Rights Information about rights held in and over the resource Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s). 2014 Axonal Transport Axonopathy Crish Samuel D Dengler-Crish Christine M Department of Anatomy & Neurobiology Department of Pharmaceutical Sciences Frontiers in neuroscience Glaucoma Inman Denise M NEOMED College of Medicine NEOMED College of Pharmacy Neurodegeneration ocular optic nerve Smith Matthew A superior colliculi vision disorders Wilson Gina N Young Jesse W Text A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text. URL Address <a href="http://doi.org/10.1186/s12974-018-1346-7" target="_blank" rel="noreferrer noopener">http://doi.org/10.1186/s12974-018-1346-7</a> Pages 313–313 Issue 1 Volume 15 Dublin Core The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/. Title A name given to the resource Reduced AMPK activation and increased HCAR activation drive anti-inflammatory response and neuroprotection in glaucoma. Publisher An entity responsible for making the resource available Journal of neuroinflammation Date A point or period of time associated with an event in the lifecycle of the resource 2018 2018-11 Subject The topic of the resource AMP-activated protein kinase; AMP-Activated Protein Kinases/*metabolism; Animal; Animals; Biological; Calcium Binding Proteins – Metabolism; Calcium-Binding Proteins/metabolism; Cells – Drug Effects; Cells – Pathology; Diet; Disease Models; Eye Proteins/genetics; Female; G-Protein-Coupled – Metabolism; G-Protein-Coupled/*metabolism; Glaucoma; Glaucoma – Complications; Glaucoma – Pathology; Glaucoma/*complications/pathology; Impact of Events Scale; Inbred DBA; Inflammation – Etiology; Inflammation – Prevention and Control; Inflammation hydroxycarboxylic acid receptor; Inflammation/*etiology/*prevention & control; Ketogenic diet; Ketogenic/methods; Male; Membrane Glycoproteins; Membrane Glycoproteins/genetics; Mice; Microfilament Proteins – Metabolism; Microfilament Proteins/metabolism; Microglia/drug effects/pathology; Models; Mutation; Mutation/genetics; Neuroprotection/drug effects/*physiology; NLR Family; Optic Nerve – Pathology; Optic Nerve/pathology; Phosphotransferases – Metabolism; Proteins; Pyrin Domain-Containing 3 Protein/genetics/metabolism; Receptors; Retina – Drug Effects; Retina – Pathology; Retinal Ganglion Cells/drug effects/*pathology; Transgenic Creator An entity primarily responsible for making the resource Harun-Or-Rashid Mohammad; Inman Denise M Description An account of the resource BACKGROUND: Glaucoma is a chronic degenerative disease for which inflammation is considered to play a pivotal role in the pathogenesis and progression. In this study, we examined the impact of a ketogenic diet on the inflammation evident in glaucoma as a follow-up to a recent set of experiments in which we determined that a ketogenic diet protected retinal ganglion cell structure and function. METHODS: Both sexes of DBA/2J (D2) mice were placed on a ketogenic diet (keto) or standard rodent chow (untreated) for 8 weeks beginning at 9 months of age. DBA/2J-Gpnmb(+) (D2G) mice were also used as a non-pathological genetic control for the D2 mice. Retina and optic nerve (ON) tissues were micro-dissected and used for the analysis of microglia activation, expression of pro- and anti-inflammatory molecules, and lactate- or ketone-mediated anti-inflammatory signaling. Data were analyzed by immunohistochemistry, quantitative RT-PCR, ELISA, western blot, and capillary tube-based electrophoresis techniques. RESULTS: Microglia activation was observed in D2 retina and ON as documented by intense microglial-specific Iba1 immunolabeling of rounded-up and enlarged microglia. Ketogenic diet treatment reduced Iba1 expression and the activated microglial phenotype. We detected low energy-induced AMP-activated protein kinase (AMPK) phosphorylation in D2 retina and ON that triggered NF-kappaB p65 signaling through its nuclear translocation. NF-kappaB induced pro-inflammatory TNF-alpha, Identifier An unambiguous reference to the resource within a given context <a href="http://doi.org/10.1186/s12974-018-1346-7" target="_blank" rel="noreferrer noopener">10.1186/s12974-018-1346-7</a> Rights Information about rights held in and over the resource Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s). 2018 AMP-activated protein kinase AMP-Activated Protein Kinases/*metabolism Animal Animals Biological Calcium Binding Proteins – Metabolism Calcium-Binding Proteins/metabolism Cells – Drug Effects Cells – Pathology Department of Pharmaceutical Sciences Diet Disease Models Eye Proteins/genetics Female G-Protein-Coupled – Metabolism G-Protein-Coupled/*metabolism Glaucoma Glaucoma – Complications Glaucoma – Pathology Glaucoma/*complications/pathology Harun-Or-Rashid Mohammad Impact of Events Scale Inbred DBA Inflammation – Etiology Inflammation – Prevention and Control Inflammation hydroxycarboxylic acid receptor Inflammation/*etiology/*prevention & control Inman Denise M Journal of neuroinflammation Ketogenic diet Ketogenic/methods Male Membrane Glycoproteins Membrane Glycoproteins/genetics Mice Microfilament Proteins – Metabolism Microfilament Proteins/metabolism Microglia/drug effects/pathology Models Mutation Mutation/genetics NEOMED College of Pharmacy Neuroprotection/drug effects/*physiology NLR Family Optic Nerve – Pathology Optic Nerve/pathology Phosphotransferases – Metabolism Proteins Pyrin Domain-Containing 3 Protein/genetics/metabolism Receptors Retina – Drug Effects Retina – Pathology Retinal Ganglion Cells/drug effects/*pathology Transgenic Text A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text. URL Address <a href="http://doi.org/10.1080/00325481.1996.11946100" target="_blank" rel="noreferrer noopener">http://doi.org/10.1080/00325481.1996.11946100</a> Pages 107–10, 113–116 Issue 4 Volume 99 Dublin Core The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/. Title A name given to the resource Common eye disorders: six patients to refer. Publisher An entity responsible for making the resource available Postgraduate medicine Date A point or period of time associated with an event in the lifecycle of the resource 1996 1996-04 Subject The topic of the resource Adult; Aged; Angle-Closure/diagnosis/therapy; Corneal Ulcer/diagnosis/therapy; Eye Diseases/*diagnosis/*therapy; Female; Glaucoma; Humans; Iritis/diagnosis/therapy; Male; Referral and Consultation; Retinal Artery Occlusion/diagnosis/therapy; Retinal Detachment/diagnosis/therapy Creator An entity primarily responsible for making the resource Weinstock F J; Weinstock M B Description An account of the resource Thorough ocular history taking and physical examination are essential to establish a diagnosis in patients presenting with eye conditions. Some conditions require ophthalmologic referral to avoid serious complications and even vision loss. These include corneal ulcers, retinal detachment, iritis, glaucoma, retinal artery occlusion, and endophthalmitis. Because primary open-angle glaucoma can have an insidious onset and cause irreversible damage, funduscopic examination should be a part of every complete physical examination. Identifier An unambiguous reference to the resource within a given context <a href="http://doi.org/10.1080/00325481.1996.11946100" target="_blank" rel="noreferrer noopener">10.1080/00325481.1996.11946100</a> Rights Information about rights held in and over the resource Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s). 1996 Adult Aged Angle-Closure/diagnosis/therapy Corneal Ulcer/diagnosis/therapy Eye Diseases/*diagnosis/*therapy Female Glaucoma Humans Iritis/diagnosis/therapy Male Postgraduate medicine Referral and Consultation Retinal Artery Occlusion/diagnosis/therapy Retinal Detachment/diagnosis/therapy Weinstock F J Weinstock M B Text A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text. URL Address <a href="http://doi.org/10.1016/j.exer.2015.11.016" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.exer.2015.11.016</a> Pages 22–33 Volume 150 Dublin Core The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/. Title A name given to the resource Early astrocyte redistribution in the optic nerve precedes axonopathy in the DBA/2J mouse model of glaucoma. Publisher An entity responsible for making the resource available Experimental eye research Date A point or period of time associated with an event in the lifecycle of the resource 2016 2016-09 Subject The topic of the resource *Astrocyte; *Axonopathy; *Glaucoma; *Gliosis; *Neurodegeneration; *Retinal ganglion cell; Animal; Animals; Astrocytes/*pathology; Axons/pathology; Disease Models; Glaucoma; Imaging; Inbred DBA; Mice; Nerve Degeneration/etiology/*pathology; Open-Angle/*pathology; Optic Nerve Diseases/etiology/*pathology; Optic Nerve/*pathology; Photomicrography; Retinal Ganglion Cells/*pathology; Three-Dimensional; Time Factors Creator An entity primarily responsible for making the resource Cooper Melissa L; Crish Samuel D; Inman Denise M; Horner Philip J; Calkins David J Description An account of the resource Glaucoma challenges the survival of retinal ganglion cell axons in the optic nerve through processes dependent on both aging and ocular pressure. Relevant stressors likely include complex interplay between axons and astrocytes, both in the retina and optic nerve. In the DBA/2J mouse model of pigmentary glaucoma, early progression involves axonopathy characterized by loss of functional transport prior to outright degeneration. Here we describe novel features of early pathogenesis in the DBA/2J nerve. With age the cross-sectional area of the nerve increases; this is associated generally with diminished axon packing density and survival and increased glial coverage of the nerve. However, for nerves with the highest axon density, as the nerve expands mean cross-sectional axon area enlarges as well. This early expansion was marked by disorganized axoplasm and accumulation of hyperphosphorylated neurofilamants indicative of axonopathy. Axon expansion occurs without loss up to a critical threshold for size (about 0.45-0.50 mum(2)), above which additional expansion tightly correlates with frank loss of axons. As well, early axon expansion prior to degeneration is concurrent with decreased astrocyte ramification with redistribution of processes towards the nerve edge. As axons expand beyond the critical threshold for loss, glial area resumes an even distribution from the center to edge of the nerve. We also found that early axon expansion is accompanied by reduced numbers of mitochondria per unit area in the nerve. Finally, our data indicate that both IOP and nerve expansion are associated with axon enlargement and reduced axon density for aged nerves. Collectively, our data support the hypothesis that diminished bioenergetic resources in conjunction with early nerve and glial remodeling could be a primary inducer of progression of axon pathology in glaucoma. Identifier An unambiguous reference to the resource within a given context <a href="http://doi.org/10.1016/j.exer.2015.11.016" target="_blank" rel="noreferrer noopener">10.1016/j.exer.2015.11.016</a> Rights Information about rights held in and over the resource Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s). *Astrocyte *Axonopathy *Glaucoma *Gliosis *neurodegeneration *Retinal ganglion cell 2016 Animal Animals Astrocytes/*pathology Axons/pathology Calkins David J Cooper Melissa L Crish Samuel D Department of Pharmaceutical Sciences Disease Models Experimental eye research Glaucoma Horner Philip J Imaging Inbred DBA Inman Denise M Mice NEOMED College of Pharmacy Nerve Degeneration/etiology/*pathology Open-Angle/*pathology Optic Nerve Diseases/etiology/*pathology Optic Nerve/*pathology Photomicrography Retinal Ganglion Cells/*pathology Three-Dimensional Time Factors