Pub Date : 2018-06-27DOI: 10.19080/jojo.2018.06.555699
Ferdinand Rapthap
{"title":"Normative Data of Macular Thickness and Retinal Nerve Fiber Layer Thickness (RNFL) With Axial Length and CCT by SLO OCT/Lenstar on Tribal People","authors":"Ferdinand Rapthap","doi":"10.19080/jojo.2018.06.555699","DOIUrl":"https://doi.org/10.19080/jojo.2018.06.555699","url":null,"abstract":"","PeriodicalId":91023,"journal":{"name":"JOJ ophthalmology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43623948","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2018-05-30DOI: 10.19080/jojo.2018.06.555696
Frings A
Purpose: To identify and evaluate the 100 most frequently cited articles containing uveitis research Methods: Utilizing Databases, specifically of the Institute for Scientific Information, we recognized all issued articles relevant to the topic of uveitis research. All articles containing uveitis research, a publication date ranging from 1900 to September 2016, and had been cited at least 100 times, were included. The top 100 of that list matching the criteria from the above were then further analyzed. Results: Out of the 100 most-cited articles the most cited one in uveitis research with 923 citations was entitled Standardization of uveitis nomenclature for reporting clinical data. A result of the First International Workshop (Jabs et al.) . Citations ranged from 106 to 923 and the two main focus areas were clinical and basic research articles. The leading countries of origin were the U.S. followed by the United Kingdom. Most articles represented Level-III evidence, followed by Level IIb and IV. Conclusions: Our present study demonstrates that the majority (n= 54) of the top ranked articles were published in six of the top ranked journals. Four of these journals originated in the U.S. and one each of these originated in the Netherlands and the U.K. Younger case studies had higher citation rate (in 2015) as older studies. The biggest portion of articles represented Level -III clinical outcome studies implicating that even smaller case series or cohort studies could gain attention.
{"title":"The Top Hundred Papers of Uveitis Research. A Bibliometric Analysis","authors":"Frings A","doi":"10.19080/jojo.2018.06.555696","DOIUrl":"https://doi.org/10.19080/jojo.2018.06.555696","url":null,"abstract":"Purpose: To identify and evaluate the 100 most frequently cited articles containing uveitis research Methods: Utilizing Databases, specifically of the Institute for Scientific Information, we recognized all issued articles relevant to the topic of uveitis research. All articles containing uveitis research, a publication date ranging from 1900 to September 2016, and had been cited at least 100 times, were included. The top 100 of that list matching the criteria from the above were then further analyzed. Results: Out of the 100 most-cited articles the most cited one in uveitis research with 923 citations was entitled Standardization of uveitis nomenclature for reporting clinical data. A result of the First International Workshop (Jabs et al.) . Citations ranged from 106 to 923 and the two main focus areas were clinical and basic research articles. The leading countries of origin were the U.S. followed by the United Kingdom. Most articles represented Level-III evidence, followed by Level IIb and IV. Conclusions: Our present study demonstrates that the majority (n= 54) of the top ranked articles were published in six of the top ranked journals. Four of these journals originated in the U.S. and one each of these originated in the Netherlands and the U.K. Younger case studies had higher citation rate (in 2015) as older studies. The biggest portion of articles represented Level -III clinical outcome studies implicating that even smaller case series or cohort studies could gain attention.","PeriodicalId":91023,"journal":{"name":"JOJ ophthalmology","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68375466","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2018-05-30DOI: 10.19080/jojo.2018.06.555697
Carmen M. Cusack
{"title":"Spectacles: Sight and Education","authors":"Carmen M. Cusack","doi":"10.19080/jojo.2018.06.555697","DOIUrl":"https://doi.org/10.19080/jojo.2018.06.555697","url":null,"abstract":"","PeriodicalId":91023,"journal":{"name":"JOJ ophthalmology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2018-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49543491","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-12-11DOI: 10.19080/jojo.2017.05.555673
Levy N, Paz T, Leiba H, Hadas B, Parness R
Long-chain 3-hydroxyacyl-CoA dehydrogenase (LCHAD) deficiency is an autosomal recessive disorder of mitochondrial fatty acid beta oxidation, associated with hypoketotic hypoglycemia, hepatic steatosis, rhabdomyolysis, cardiomyopathy, polyneuropathy and retinal changes. We present the course of retinal findings in a case of a 6-year-old girl with LCHAD deficiency diagnosed at birth, and hence early treated and followed. Our patient had annual eye exams from the age of 1 year. Clinical examinations, ocular coherence tomography (OCT) and electroretinogram (ERG) findings during follow up are presented. At the age of 3 years, after systemic deteriorations, nyctalopia appeared with pigmentary retinopathy changes in both eyes. ERG was subnormal while Infra-red reflectance imaging with OCT displayed more advanced stage of the disease. Progressive chorioretinopathy with visual impairment was observed along the follow up on clinical exams, as well as on repeated OCTs and ERGs.
{"title":"Long Term Ophthalmic Follow Up in LCHAD Deficiency","authors":"Levy N, Paz T, Leiba H, Hadas B, Parness R","doi":"10.19080/jojo.2017.05.555673","DOIUrl":"https://doi.org/10.19080/jojo.2017.05.555673","url":null,"abstract":"Long-chain 3-hydroxyacyl-CoA dehydrogenase (LCHAD) deficiency is an autosomal recessive disorder of mitochondrial fatty acid beta oxidation, associated with hypoketotic hypoglycemia, hepatic steatosis, rhabdomyolysis, cardiomyopathy, polyneuropathy and retinal changes. We present the course of retinal findings in a case of a 6-year-old girl with LCHAD deficiency diagnosed at birth, and hence early treated and followed. Our patient had annual eye exams from the age of 1 year. Clinical examinations, ocular coherence tomography (OCT) and electroretinogram (ERG) findings during follow up are presented. At the age of 3 years, after systemic deteriorations, nyctalopia appeared with pigmentary retinopathy changes in both eyes. ERG was subnormal while Infra-red reflectance imaging with OCT displayed more advanced stage of the disease. Progressive chorioretinopathy with visual impairment was observed along the follow up on clinical exams, as well as on repeated OCTs and ERGs.","PeriodicalId":91023,"journal":{"name":"JOJ ophthalmology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46973423","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-01-01Epub Date: 2017-09-15DOI: 10.19080/jojo.2017.04.555643
Lalit P Singh, Takhellambam S Devi, Thangal Yumnamcha
Mitochondria are responsible for bioenergetics, metabolism and apoptosis signals in health and disease. The retina being a part of the central nervous system consumes large amounts of glucose and oxygen to generate ATP via the mitochondrial oxidative phosphorylation for its phototransduction and visual function. During ATP generation, electrons leak from the mitochondrial electron transport chain, which is captured by molecular oxygen to produce reactive oxygen species (ROS). These mtROS damage mitochondrial proteins, mtDNA, and membrane lipids and release them in the cytosol. Mitochondrial components are recognized as danger-associated molecular patterns (DAMPS) by cytosolic pattern recognition receptors such as NOD-like receptors, NLRP3 inflammasomes. They process pro-caspase-1 to active caspase-1, which cleaves pro-inflammatory IL-1β o mature IL-1β causing inflammation and cell death by pyroptosis. To counter the damaging action of mtROS and inflammasomes in fully differentiated cells in the retina, the removal of the damaged and dysfunctional mitochondria by a double-membrane autophagic process via lysosomal degradation called mitophagy is critical for mitochondrial homeostasis and cell survival. Nonetheless, under chronic diseases including diabetic retinopathy (DR), mitophagy dysregulation and NLRP3 inflammasome activation exist, which cause premature cell death and disease progression. Recently, the thioredoxin-interacting protein TXNIP, which is strongly induced by diabetes and inhibits anti-oxidant function of thioredoxin, has been implicated in mitochondrial dysfunction, mitophagic dysregulation and NLRP3 inflammasome activation in DR. Therefore, TXNIP silencing or pharmacological inhibition may normalize mitophagic flux and NLRP3 inflammasome activation, which will prevent or slow down the progression of DR.
{"title":"The Role of Txnip in Mitophagy Dysregulation and Inflammasome Activation in Diabetic Retinopathy: A New Perspective.","authors":"Lalit P Singh, Takhellambam S Devi, Thangal Yumnamcha","doi":"10.19080/jojo.2017.04.555643","DOIUrl":"https://doi.org/10.19080/jojo.2017.04.555643","url":null,"abstract":"<p><p>Mitochondria are responsible for bioenergetics, metabolism and apoptosis signals in health and disease. The retina being a part of the central nervous system consumes large amounts of glucose and oxygen to generate ATP via the mitochondrial oxidative phosphorylation for its phototransduction and visual function. During ATP generation, electrons leak from the mitochondrial electron transport chain, which is captured by molecular oxygen to produce reactive oxygen species (ROS). These mtROS damage mitochondrial proteins, mtDNA, and membrane lipids and release them in the cytosol. Mitochondrial components are recognized as danger-associated molecular patterns (DAMPS) by cytosolic pattern recognition receptors such as NOD-like receptors, NLRP3 inflammasomes. They process pro-caspase-1 to active caspase-1, which cleaves pro-inflammatory IL-1β o mature IL-1β causing inflammation and cell death by pyroptosis. To counter the damaging action of mtROS and inflammasomes in fully differentiated cells in the retina, the removal of the damaged and dysfunctional mitochondria by a double-membrane autophagic process via lysosomal degradation called mitophagy is critical for mitochondrial homeostasis and cell survival. Nonetheless, under chronic diseases including diabetic retinopathy (DR), mitophagy dysregulation and NLRP3 inflammasome activation exist, which cause premature cell death and disease progression. Recently, the thioredoxin-interacting protein TXNIP, which is strongly induced by diabetes and inhibits anti-oxidant function of thioredoxin, has been implicated in mitochondrial dysfunction, mitophagic dysregulation and NLRP3 inflammasome activation in DR. Therefore, TXNIP silencing or pharmacological inhibition may normalize mitophagic flux and NLRP3 inflammasome activation, which will prevent or slow down the progression of DR.</p>","PeriodicalId":91023,"journal":{"name":"JOJ ophthalmology","volume":"4 4","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/10/89/nihms907209.PMC5786434.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35773735","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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