The prevalence of ocular diseases in primary and junior high school students on Orchid Island

AbstractObjectiveTo assess the prevalence of refractive error and ocular diseases in primary and junior high school students on Orchid Island.Materials and MethodsThis is a cross-sectional study of all students in the primary and junior high schools on Orchid Island conducted within 1 week in 2008. Each student received a visual acuity examination without correction with the Landolt-C chart. An experienced ophthalmologist performed associated assessments through retinoscopy, slit lamp, and fundoscopy.ResultsOf the 403 student residents, 260 were primary school students (139 boys and 121 girls) and 143 were junior high school students (74 boys and 69 girls). Visual acuity in two eyes was < 0.1, in 14 eyes was between 0.1 and 0.3, in 34 eyes was between 0.4 and 0.7, in 225 eyes was between 0.8 and 1.0, and in 531 eyes was between 1.2 and 2.0. Myopia was found in 21 students (21/403, 5.21%; 9 primary school students and 12 junior high school students). Four students (4/403, 0.99%) had amblyopia, of whom two had anisometropia (unilateral high hyperopia), one had high astigmatism in both eyes, and the other had unilateral esotropia. Lens dislocation was found in one student (0.25%) with Marfan syndrome. Retinal vasculitis and optic atrophy were found in one student (0.25%) with systemic lupus erythematosus.ConclusionBecause it is a small, isolated island, Orchid Island still has a unique traditional culture and life style. Therefore the prevalence of myopia in primary school and junior high school students on Orchid Island is low, and 94% of all the students had uncorrected visual acuity above 0.8

CTX-M and Plasmid-mediated AmpC-Producing Enterobacteriaceae, Singapore

10.3201/eid1006.030726Emerging Infectious Diseases1061172-117

Use of Ceftriaxone in Treating Cognitive and Neuronal Deficits Associated With Dementia With Lewy Bodies

Dementia with Lewy bodies (DLB) is caused by accumulation of Lewy bodies, destruction of mitochondria, and excess of glutamate in synapses, which eventually leads to excitotoxicity, neurodegeneration, and cognitive impairments. Ceftriaxone (CEF) reduces excitotoxicity by increasing glutamate transporter 1 expression and glutamate reuptake. We investigated whether CEF can prevent cognitive decline and neurological deficits and increase neurogenesis in DLB rats. Male Wistar rats infused with viral vector containing human alpha-synuclein (α-syn) gene, SNCA, in the lateral ventricle were used as a rat model of DLB. CEF (100 mg/kg/day, i.p.) was injected in these rats for 27 days. The active avoidance test and object recognition test was performed. Finally, the brains of all the rats were immunohistochemically stained to measure α-syn, neuronal density, and newborn cells in the hippocampus and substantia nigra. The results revealed that DLB rats had learning and object recognition impairments and exhibited cell loss in the nigrostriatal dopaminergic system, and hippocampal CA1, and dentate gyrus (DG). Additionally, DLB rats had fewer newborn cells in the DG and substantia nigra pars reticulata and more α-syn immune-positive cells in the DG. Treatment with CEF improved cognitive function, reduced cell loss, and increased the number of newborn cells in the brain. To our knowledge, this is the first study showing that CEF prevents loss of neurogenesis in the brain of DLB rats. CEF may therefore has clinical potential for treating DLB

Chromobacterium violaceum infection: A clinical review of an important but neglected infection

Background: Increasing reported cases with Chrombacterium violaceum infection has been noticed in recent decades. It is noteworthy for its difficult-to-treat entity characterized by a high frequency of sepsis, easily distantant metastasis, multidrug-resistance, and frequent relapse, and high mortality rate. Methods: The English-language literature was reviewed from 1952 through December 2009 by an electronic view via the PubMed and Medline databases and manual searches. Results: One hundred and six patients with Chrombacterium violaceum infection from the literature were studied. The four leading clinical manifestations reviewed in the published literature, in the order of frequency, were fever (100%), sepsis (82%), skin lesions (67.9%), and abdominal pain (31.1%). Localized abscess was found in 52 patients (49%) and liver was the mostly common involved organ. Fifty-six patients (53%) were dead. Almost all of the penicillin, ampicillin, and first and second-generation cephalosporins exhibited totally resistant to Chrombacterium violaceum. The most important risk factors in mortality in 61 patients with Chrombacterium violaceum bacteremia were at a young age (p = 0.0789), presence of localized abscess (p = 0.030), shorter clinical course (p < 0.001), and inappropriate antimicrobial treatment (p < 0.001). Seven patients (6.6%) experienced of relapse or reinfection, with a median interval of 135 days (range, 4 to 1095 days). Conclusions: A high index of suspicion for Chromobacterium violaceum infection is required along with prompt diagnosis, optimal antimicrobial therapy, and adequate therapeutic duration for a successful therapy

Retinoic Acid Protects and Rescues the Development of Zebrafish Embryonic Retinal Photoreceptor Cells from Exposure to Paclobutrazol

Paclobutrazol (PBZ) is a widely used fungicide that shows toxicity to aquatic embryos, probably through rain-wash. Here, we specifically focus on its toxic effect on eye development in zebrafish, as well as the role of retinoic acid (RA), a metabolite of vitamin A that controls proliferation and differentiation of retinal photoreceptor cells, in this toxicity. Embryos were exposed to PBZ with or without RA from 2 to 72 h post-fertilization (hpf), and PBZ-treated embryos (2–72 hpf) were exposed to RA for additional hours until 120 hpf. Eye size and histology were examined. Expression levels of gnat1 (rod photoreceptor marker), gnat2 (cone photoreceptor marker), aldehyde dehydrogenases (encoding key enzymes for RA synthesis), and phospho-histone H3 (an M-phase marker) in the eyes of control and treated embryos were examined. PBZ exposure dramatically reduces photoreceptor proliferation, thus resulting in a thinning of the photoreceptor cell layer and leading to a small eye. Co-treatment of PBZ with RA, or post-treatment of PBZ-treated embryos with RA, partially rescues photoreceptor cells, revealed by expression levels of marker proteins and by retinal cell proliferation. PBZ has strong embryonic toxicity to retinal photoreceptors, probably via suppressing the production of RA, with effects including impaired retinal cell division