Prevalence and causes of vision loss in sub-Saharan Africa in 2015: magnitude, temporal trends and projections

Background This study aimed to assess the prevalence and causes of vision loss in sub-Saharan Africa (SSA) in 2015, compared with prior years, and to estimate expected values for 2020. Methods A systematic review and meta-analysis assessed the prevalence of blindness (presenting distance visual acuity <3/60 in the better eye), moderate and severe vision impairment (MSVI; presenting distance visual acuity <6/18 but ≥3/60) and mild vision impairment (MVI; presenting distance visual acuity <6/12 and ≥6/18), and also near vision impairment (<N6 or N8 in the presence of ≥6/12 best-corrected distance visual acuity) in SSA for 1990, 2010, 2015 and 2020. In SSA, age-standardised prevalence of blindness, MSVI and MVI in 2015 were 1.03% (80% uncertainty interval (UI) 0.39–1.81), 3.64% (80% UI 1.71–5.94) and 2.94% (80% UI 1.05–5.34), respectively, for male and 1.08% (80% UI 0.40–1.93), 3.84% (80% UI 1.72–6.37) and 3.06% (80% UI 1.07–5.61) for females, constituting a significant decrease since 2010 for both genders. There were an estimated 4.28 million blind individuals and 17.36 million individuals with MSVI; 101.08 million individuals were estimated to have near vision loss due to presbyopia. Cataract was the most common cause of blindness (40.1%), whereas undercorrected refractive error (URE) (48.5%) was the most common cause of MSVI. Sub-Saharan West Africa had the highest proportion of blindness compared with the other SSA subregions. Conclusions Cataract and URE, two of the major causes of blindness and vision impairment, are reversible with treatment and thus promising targets to alleviate vision impairment in SSA

Alternative splicing and differential subcellular localization of the rat FGF antisense gene product

<p>Abstract</p> <p>Background</p> <p>GFG/NUDT is a nudix hydrolase originally identified as the product of the fibroblast growth factor-2 antisense (FGF-AS) gene. While the FGF-AS RNA has been implicated as an antisense regulator of FGF-2 expression, the expression and function of the encoded GFG protein is largely unknown. Alternative splicing of the primary FGF-AS mRNA transcript predicts multiple GFG isoforms in many species including rat. In the present study we focused on elucidating the expression and subcellular distribution of alternatively spliced rat GFG isoforms.</p> <p>Results</p> <p>RT-PCR and immunohistochemistry revealed tissue-specific GFG mRNA isoform expression and subcellular distribution of GFG immunoreactivity in cytoplasm and nuclei of a wide range of normal rat tissues. FGF-2 and GFG immunoreactivity were co-localized in some, but not all, tissues examined. Computational analysis identified a mitochondrial targeting sequence (MTS) in the N-terminus of three previously described rGFG isoforms. Confocal laser scanning microscopy and subcellular fractionation analysis revealed that all rGFG isoforms bearing the MTS were specifically targeted to mitochondria whereas isoforms and deletion mutants lacking the MTS were localized in the cytoplasm and nucleus. Mutation and deletion analysis confirmed that the predicted MTS was necessary and sufficient for mitochondrial compartmentalization.</p> <p>Conclusion</p> <p>Previous findings strongly support a role for the FGF antisense RNA as a regulator of FGF2 expression. The present study demonstrates that the antisense RNA itself is translated, and that protein isoforms resulting form alternative RNA splicing are sorted to different subcellular compartments. FGF-2 and its antisense protein are co-expressed in many tissues and in some cases in the same cells. The strong conservation of sequence and genomic organization across animal species suggests important functional significance to the physical association of these transcript pairs.</p

Prevalence and causes of vision loss in East Asia in 2015: magnitude, temporal trends and projections

BACKGROUND: To determine the prevalence and causes of blindness and vision impairment (VI) in East Asia in 2015 and to forecast the trend to 2020. METHODS: Through a systematic literature review and meta-analysis, we estimated prevalence of blindness (presenting visual acuity <3/60 in the better eye), moderate-to-severe vision impairment (MSVI; 3/60≤presenting visual acuity <6/18), mild vision impairment (mild VI: 6/18≤presenting visual acuity <6/12) and uncorrected presbyopia for 1990, 2010, 2015 and 2020. A total of 44 population-based studies were included. RESULTS: In 2015, age-standardised prevalence of blindness, MSVI, mild VI and uncorrected presbyopia was 0.37% (80% uncertainty interval (UI) 0.12%-0.68%), 3.06% (80% UI 1.35%-5.16%) and 2.65% (80% UI 0.92%-4.91%), 32.91% (80% UI 18.72%-48.47%), respectively, in East Asia. Cataract was the leading cause of blindness (43.6%), followed by uncorrected refractive error (12.9%), glaucoma, age-related macular degeneration, corneal diseases, trachoma and diabetic retinopathy (DR). The leading cause for MSVI was uncorrected refractive error, followed by cataract, age-related macular degeneration, glaucoma, corneal disease, trachoma and DR. The burden of VI due to uncorrected refractive error, cataracts, glaucoma and DR has continued to rise over the decades reported. CONCLUSIONS: Addressing the public healthcare barriers for cataract and uncorrected refractive error can help eliminate almost 57% of all blindness cases in this region. Therefore, public healthcare efforts should be focused on effective screening and effective patient education, with access to high-quality healthcare

The optic nerve head is the site of axonal transport disruption, axonal cytoskeleton damage and putative axonal regeneration failure in a rat model of glaucoma

The neurodegenerative disease glaucoma is characterised by the progressive death of retinal ganglion cells (RGCs) and structural damage to the optic nerve (ON). New insights have been gained into the pathogenesis of glaucoma through the use of rodent models; however, a coherent picture of the early pathology remains elusive. Here, we use a validated, experimentally induced rat glaucoma model to address fundamental issues relating to the spatio-temporal pattern of RGC injury. The earliest indication of RGC damage was accumulation of proteins, transported by orthograde fast axonal transport within axons in the optic nerve head (ONH), which occurred as soon as 8 h after induction of glaucoma and was maximal by 24 h. Axonal cytoskeletal abnormalities were first observed in the ONH at 24 h. In contrast to the ONH, no axonal cytoskeletal damage was detected in the entire myelinated ON and tract until 3 days, with progressively greater damage at later time points. Likewise, down-regulation of RGC-specific mRNAs, which are sensitive indicators of RGC viability, occurred subsequent to axonal changes at the ONH and later than in retinas subjected to NMDA-induced somatic excitotoxicity. After 1 week, surviving, but injured, RGCs had initiated a regenerative-like response, as delineated by Gap43 immunolabelling, in a response similar to that seen after ON crush. The data presented here provide robust support for the hypothesis that the ONH is the pivotal site of RGC injury following moderate elevation of IOP, with the resulting anterograde degeneration of axons and retrograde injury and death of somas

Internalisation Theory and outward direct investment by emerging market multinationals

The rise of multinational enterprises from emerging countries (EMNEs) poses an important test for theories of the multinational enterprise such as internalisation theory. It has been contended that new phenomena need new theory. This paper proposes that internalisation theory is appropriate to analyse EMNEs. This paper examines four approaches to EMNEs—international investment strategies, domestic market imperfections, international corporate networks and domestic institutions—and three case studies—Chinese outward FDI, Indian foreign acquisitions and investment in tax havens—to show the enduring relevance and predictive power of internalisation theory. This analysis encompasses many other approaches as special cases of internalisation theory. The use of internalisation theory to analyse EMNEs is to be commended, not only because of its theoretical inclusivity, but also because it has the ability to connect and to explain seemingly desperate phenomena

Lack of Effective Anti-Apoptotic Activities Restricts Growth of Parachlamydiaceae in Insect Cells

The fundamental role of programmed cell death in host defense is highlighted by the multitude of anti-apoptotic strategies evolved by various microbes, including the well-known obligate intracellular bacterial pathogens Chlamydia trachomatis and Chlamydia (Chlamydophila) pneumoniae. As inhibition of apoptosis is assumed to be essential for a successful infection of humans by these chlamydiae, we analyzed the anti-apoptotic capacity of close relatives that occur as symbionts of amoebae and might represent emerging pathogens. While Simkania negevensis was able to efficiently replicate within insect cells, which served as model for metazoan-derived host cells, the Parachlamydiaceae (Parachlamydia acanthamoebae and Protochlamydia amoebophila) displayed limited intracellular growth, yet these bacteria induced typical features of apoptotic cell death, including formation of apoptotic bodies, nuclear condensation, internucleosomal DNA fragmentation, and effector caspase activity. Induction of apoptosis was dependent on bacterial activity, but not bacterial de novo protein synthesis, and was detectable already at very early stages of infection. Experimental inhibition of host cell death greatly enhanced parachlamydial replication, suggesting that lack of potent anti-apoptotic activities in Parachlamydiaceae may represent an important factor compromising their ability to successfully infect non-protozoan hosts. These findings highlight the importance of the evolution of anti-apoptotic traits for the success of chlamydiae as pathogens of humans and animals

Ischemic Tolerance Protects the Rat Retina from Glaucomatous Damage

Glaucoma is a leading cause of acquired blindness which may involve an ischemic-like insult to retinal ganglion cells and optic nerve head. We investigated the effect of a weekly application of brief ischemia pulses (ischemic conditioning) on the rat retinal damage induced by experimental glaucoma. Glaucoma was induced by weekly injections of chondroitin sulfate (CS) in the rat eye anterior chamber. Retinal ischemia was induced by increasing intraocular pressure to 120 mmHg for 5 min; this maneuver started after 6 weekly injections of vehicle or CS and was weekly repeated in one eye, while the contralateral eye was submitted to a sham procedure. Glaucoma was evaluated in terms of: i) intraocular pressure (IOP), ii) retinal function (electroretinogram (ERG)), iii) visual pathway function (visual evoked potentials, (VEPs)) iv) histology of the retina and optic nerve head. Retinal thiobarbituric acid substances levels were assessed as an index of lipid peroxidation. Ischemic conditioning significantly preserved ERG, VEPs, as well as retinal and optic nerve head structure from glaucomatous damage, without changes in IOP. Moreover, ischemia pulses abrogated the increase in lipid peroxidation induced by experimental glaucoma. These results indicate that induction of ischemic tolerance could constitute a fertile avenue for the development of new therapeutic strategies in glaucoma treatment

A five-year retrospective study of the epidemiological characteristics and visual outcomes of patients hospitalized for ocular trauma in a Mediterranean area

<p>Abstract</p> <p>Background</p> <p>To determine the epidemiological characteristics and visual outcome of ocular trauma in southern Italy.</p> <p>Methods</p> <p>All cases of ocular trauma admitted to Department of Ophthalmology of Palermo University, Italy, from January 2001–December 2005 were retrospectively reviewed for open- or closed-globe injury (OGI or CGI). Data extracted included age, sex, residence, initial and final visual acuity (VA), cause and treatment of injury, hospitalization. The injuries were classified by Ocular Trauma Classification System (OTCS) and Birmingham Eye Trauma Terminology (BETT). We also referred to the Ocular Trauma Score (OTS) in evaluating the final visual outcome.</p> <p>Results</p> <p>Of the 298 eyes, there were 146 OGI and 152 CGI. Fifty eyes (16.8%) had an intraocular foreign body (IOFB). The annual incidence of eye injuries was 4.9 per 100,000. Most injuries occurred in men (84.6%, p < 0.0005), with an average age of 33.0 vs. 49.9 for women (p = 0.005). Cause of injury differed significantly by gender (p = 0.001) and urban vs. rural location (p = 0.009). The most frequent causes in men were outdoor activities related injuries (30.9%), work-related (25.4%), and sport-related (17.5%), and in women were home-related (52.2%) and outdoor activities related injuries (30.4%). In urban areas, road accidents were more frequent; in rural areas, work-related injuries were more frequent with a greater rate of IOFBs than in urban areas (p = 0.002).</p> <p>The incidence of OGI and CGI differed in work-related injuries (p < 0.0005), sport-related injuries (p < 0.0005), and assaults (p = 0.033). The final visual acuity was 20/40 (6/12) or better in 144 eyes (48.3%), 20/40–20/200 (6/12–6/60) in 90 eyes (30.2%), and <20/200 (6/60) or less in 46 eyes (15.5%). Eighteen eyes (6%) had a final acuity of no light perception. Of those eyes that presented with hand motion vision or better, 220 (86.6%) had a final vision of better than 20/200 (6/60). Initial visual acuity was found to be correlated with final visual acuity (Spearman's correlation coefficient = 0.658; p < 0.001). The likelihood of the final visual acuities in the OTS categories was correlated to that of the OTS study group in 12 of 14 cases (85.7%).</p> <p>Conclusion</p> <p>This analysis provides insight into the epidemiology of patients hospitalized for ocular trauma. The findings indicate that ocular trauma is a significant cause of visual loss in this population.</p