Browse
Submit Data
Databases
API
Help

Dataset Information

16 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Atypical posterior pole retinitis.

ABSTRACT: Purpose:Necrotizing retinopathy is an uncommon, devastating, potentially blinding condition, which can be seen in both immunocompetent and immunocompromised patients. The purpose of this case is to report a new subset of necrotizing viral retinopathy. Observation:A 34-year old lady presented to our outpatient department with sudden diminution of vision in both eyes following a brief history of viral fever with vesicular rashes. Fundus examination showed areas of necrotizing retinitis in posterior pole involving macula with scattered superficial retinal hemorrhages, cotton-wool spots in both the eyes. She was treated with intravenous acyclovir and oral valacyclovir. Conclusion and importance:Our case may represent a new subset of necrotizing viral retinopathy, which may intermediate the clinical pictures of acute retinal necrosis and progressive outer retinal necrosis.

SUBMITTER: Dutta Majumder P

PROVIDER: S-EPMC6582377 | biostudies-literature | 2019 Sep

REPOSITORIES: biostudies-literature

ACCESS DATA

Json Xml

Publications

Atypical posterior pole retinitis.

Dutta Majumder Parthopratim P Mistry Saurabh S Luthra Saurabh S Shrutanjoy M Das Sekar Varsha V Rishi Ekta E Biswas Jyotirmay J

American journal of ophthalmology case reports 20190613

<h4>Purpose</h4>Necrotizing retinopathy is an uncommon, devastating, potentially blinding condition, which can be seen in both immunocompetent and immunocompromised patients. The purpose of this case is to report a new subset of necrotizing viral retinopathy.<h4>Observation</h4>A 34-year old lady presented to our outpatient department with sudden diminution of vision in both eyes following a brief history of viral fever with vesicular rashes. Fundus examination showed areas of necrotizing retini ...[more]

PMID: 31245654

Similar Datasets

Submacular Parasite Masquerading as Posterior Pole Granuloma.

Project description:Parasites enter the eye through hematogenous spread. The interaction with host immune system may result in its destruction but not without collateral damage to the vital retinal structures. Currently, the accepted treatment for ocular parasitosis is surgical removal or direct laser photocoagulation. A 24-year-old Indian woman presented with abrupt painless loss of vision to 5/300. A large yellow-white lesion centered at macula was observed with associated retinal and subretinal hemorrhage and neurosensory retinal detachment. A parasite was seen protruding at the center of the lesion. Fluorescein angiography demonstrated disc leakage and vessel wall staining. Ultrasonography demonstrated a highly reflective subretinal lesion with aftershadowing. Serological test was positive for anti-cysticercus (IgM) antibody. Treatment with prednisolone and albendazole resulted in resolution of the lesion within 2 months with improvement of visual acuity to 20/400. A noncystic form of subretinal cysticercosis is likely with suggestive B-scan ultrasonography and serological investigations.

| S-EPMC4477082 | biostudies-literature

Guinea pig myopia model ocular posterior pole

Project description:Proteomic analyses of the ocular posterior pole tissues at 6 weeks after induction of form-deprived myopia and lens-induced myopia models in guinea pigs.

2022-11-01 | PXD037872 |

Mutations in FLVCR1 cause posterior column ataxia and retinitis pigmentosa.

Project description:The study of inherited retinal diseases has advanced our knowledge of the cellular and molecular mechanisms involved in sensory neural signaling. Dysfunction of two specific sensory modalities, vision and proprioception, characterizes the phenotype of the rare, autosomal-recessive disorder posterior column ataxia and retinitis pigmentosa (PCARP). Using targeted DNA capture and high-throughput sequencing, we analyzed the entire 4.2 Mb candidate sequence on chromosome 1q32 to find the gene mutated in PCARP in a single family. Employing comprehensive bioinformatic analysis and filtering, we identified a single-nucleotide coding variant in the feline leukemia virus subgroup C cellular receptor 1 (FLVCR1), a gene encoding a heme-transporter protein. Sanger sequencing confirmed the FLVCR1 mutation in this family and identified different homozygous missense mutations located within the protein's transmembrane channel segment in two other unrelated families with PCARP. To determine whether the selective pathologic features of PCARP correlated with FLVCR1 expression, we examined wild-type mouse Flvcr1 mRNA levels in the posterior column of the spinal cord and the retina via quantitative real-time reverse-transcriptase PCR. The Flvcr1 mRNA levels were most abundant in the retina, followed by the posterior column of the spinal cord and other brain regions. These results suggest that aberrant FLVCR1 causes a selective degeneration of a subpopulation of neurons in the retina and the posterior columns of the spinal cord via dysregulation of heme or iron homeostasis. This finding broadens the molecular basis of sensory neural signaling to include common mechanisms that involve proprioception and vision.

| S-EPMC2978959 | biostudies-literature

Barentsz is essential for the posterior localization of oskar mRNA and colocalizes with it to the posterior pole.

Project description:The localization of Oskar at the posterior pole of the Drosophila oocyte induces the assembly of the pole plasm and therefore defines where the abdomen and germ cells form in the embryo. This localization is achieved by the targeting of oskar mRNA to the posterior and the localized activation of its translation. oskar mRNA seems likely to be actively transported along microtubules, since its localization requires both an intact microtubule cytoskeleton and the plus end-directed motor kinesin I, but nothing is known about how the RNA is coupled to the motor. Here, we describe barentsz, a novel gene required for the localization of oskar mRNA. In contrast to all other mutations that disrupt this process, barentsz-null mutants completely block the posterior localization of oskar mRNA without affecting bicoid and gurken mRNA localization, the organization of the microtubules, or subsequent steps in pole plasm assembly. Surprisingly, most mutant embryos still form an abdomen, indicating that oskar mRNA localization is partially redundant with the translational control. Barentsz protein colocalizes to the posterior with oskar mRNA, and this localization is oskar mRNA dependent. Thus, Barentsz is essential for the posterior localization of oskar mRNA and behaves as a specific component of the oskar RNA transport complex.

| S-EPMC2196428 | biostudies-literature

Quick-freeze/deep-etch electron microscopy visualization of the mouse posterior pole.

Project description:The mouse is one of the most commonly used mammalian systems to study human diseases. In particular it has been an invaluable tool to model a multitude of ocular pathologies affecting the posterior pole. The aim of this study was to create a comprehensive map of the ultrastructure of the mouse posterior pole using the quick-freeze/deep-etch method (QFDE). QFDE can produce detailed three-dimensional images of tissue structure and macromolecular moieties, without many of the artifacts introduced by structure-altering post-processing methods necessary to perform conventional transmission electron microscopy (cTEM). A total of 18 eyes from aged C57BL6/J mice were enucleated and the posterior poles were processed, either intact or with the retinal pigment epithelium (RPE) cell layer removed, for imaging by either QFDE or cTEM. QFDE images were correlated with cTEM cross-sections and en face images through the outer retina. Nicely preserved outer retinal architecture was observed with both methods, however, QFDE provided excellent high magnification imaging, with greater detail, of the apical, central, and basal planes of the RPE. Furthermore, key landmarks within Bruch's membrane, choriocapillaris, choroid and sclera were characterized and identified. In this study we developed methods for preparing the outer retina of the mouse for evaluation with QFDE and provide a map of the ultrastructure and cellular composition of the outer posterior pole. This technique should be applicable for morphological evaluation of mouse models, in which detailed visualization of subtle ocular structural changes is needed or in cases where post-processing methods introduce unacceptable artifacts.

| S-EPMC5836515 | biostudies-literature

Ocular posterior pole pathological modifications related to complicated pregnancy. A review.

Project description:Ocular posterior pole modification are a pathological manifestation in complicated pregnancies, especially when pregnancy induced hypertension is present (PIH), as well as in preeclampsia (PE) or eclampsia. Nonetheless, as the pregnancy evolves, the possibility for an aggravated evolution with HELLP syndrome, disseminated intravascular coagulation, and idiopathic thrombocytopenic purpura may have an ocular manifestation that, mainly, implies a loss of visual field or acuity, that, left unattended, may constitute a permanent impairment. Pregestational conditions like pituitary adenoma or genetic pedigree for complement factor H gene (1q31.1) single nucleotide mutations could lead to central serous chorioretinopathy or retinal detachment with severe, ischemic, central cilioretinal artery or vein occlusion and optic nerve atrophy. Furthermore, although subtle in many cases, any new visual symptoms during pregnancy should constitute an alarming factor for obstetrical reevaluation and ophthalmological approach in order to preserve the mother's quality of life.

| S-EPMC5710026 | biostudies-other

Behavioral consequences of selective damage to frontal pole and posterior cingulate cortices.

Project description:Frontal pole cortex (FPC) and posterior cingulate cortex (PCC) have close neuroanatomical connections, and imaging studies have shown coactivation or codeactivation of these brain regions during performance of certain tasks. However, they are among the least well-understood regions of the primate brain. One reason for this is that the consequences of selective bilateral lesions to either structure have not previously been studied in any primate species. We studied the effects of circumscribed bilateral lesions to FPC or PCC on monkeys' ability to perform an analog of Wisconsin Card Sorting Test (WCST) and related tasks. In contrast to lesions in other prefrontal regions, neither posttraining FPC nor PCC lesions impaired animals' abilities to follow the rule switches that frequently occurred within the WCST task. However, FPC lesions were not without effect, because they augmented the ability of animals to adjust cognitive control after experiencing high levels of conflict (whereas PCC lesions did not have any effect). In addition, FPC-lesioned monkeys were more successful than controls or PCC-lesioned animals at remembering the relevant rule across experimentally imposed distractions involving either an intervening secondary task or a surprising delivery of free reward. Although prefrontal cortex posterior to FPC is specialized for mediating efficient goal-directed behavior to maximally exploit reward opportunities from ongoing tasks, our data led us to suggest that FPC is, instead, specialized for disengaging executive control from the current task and redistributing it to novel sources of reward to explore new opportunities/goals.

| S-EPMC4517212 | biostudies-other

Biogenesis of the posterior pole is mediated by the exosome/microvesicle protein-sorting pathway.

Project description:Biogenesis of the posterior pole is critical to directed cell migration and other polarity-dependent processes. We show here that proteins are targeted to the posterior pole on the basis of higher order oligomerization and plasma membrane binding, the same elements that target proteins to exosomes/microvesicles (EMVs), HIV, and other retrovirus particles. We also demonstrate that the polarization of the EMV protein-sorting pathway can occur in morphologically non-polarized cells, defines the site of uropod formation, is induced by increased expression of EMV cargo proteins, and is evolutionarily conserved between humans and the protozoan Dictyostelium discoideum. Based on these results, we propose a mechanism of posterior pole biogenesis in which elevated levels of EMV cargoes (i) polarize the EMV protein-sorting pathway, (ii) generate a nascent posterior pole, and (iii) prime cells for signal-induced biogenesis of a uropod. This model also offers a mechanistic explanation for the polarized budding of EMVs and retroviruses, including HIV.

| S-EPMC3243529 | biostudies-literature

'Ab interno' intravitreal suturing of a large traumatic scleral perforation at the posterior pole.

Project description: Not available

| S-EPMC2095494 | biostudies-literature

A splice-site variant in FLVCR1 produces retinitis pigmentosa without posterior column ataxia.

Project description:FLVCR1 (feline leukemia virus subgroup c receptor 1) is a transmembrane protein involved in the trafficking of intracellular heme. Homozygous variants in FLVCR1 have been described in association with a clinical syndrome of posterior column ataxia with retinitis pigmentosa (PCARP). Here, we describe a patient with non-syndromic retinitis pigmentosa homozygous for a splice-site variant in FLVCR1 (c.1092 + 5G>A) without evidence of posterior column ataxia or cerebellar degeneration. We suggest an association between intronic splice-site variants in FLVCR1 and the absence of posterior column degeneration and suggest a hypothesis to explain this observation. Should this association be proven, it would provide valuable prognostic information for patients. Retinal degeneration appears to be the sole clinical manifestation of this FLVCR1 variant; gene therapy approaches using an adeno-associated viral vector with sub-retinal delivery may therefore represent a therapeutic approach to halting retinal degeneration in this patient group.

| S-EPMC5841564 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data