Prevalence and causes of blindness and visual impairment in Muyuka: a rural health district in South West Province, Cameroon.

AIM: To estimate the prevalence and causes of blindness and visual impairment in the population aged 40 years and over in Muyuka, a rural district in the South West Province of Cameroon. METHODS: A multistage cluster random sampling methodology was used to select 20 clusters of 100 people each. In each cluster households were randomly selected and all eligible people had their visual acuity (VA) measured by an ophthalmic nurse. Those with VA <6/18 were examined by an ophthalmologist. RESULTS: 1787 people were examined (response rate 89.3%). The prevalence of binocular blindness was 1.6% (95% CI: 0.8% to 2.4%), 2.2% (1.% to 3.1%) for binocular severe visual impairment, and 6.4% (5.0% to 7.8%) for binocular visual impairment. Cataract was the main cause of blindness (62.1%), severe visual impairment (65.0%), and visual impairment (40.0%). Refractive error was an important cause of severe visual impairment (15.0%) and visual impairment (22.5%). The cataract surgical coverage for people was 55% at the <3/60 level and 33% at the <6/60 level. 64.3% of eyes operated for cataract had poor visual outcome (presenting VA<6/60). CONCLUSIONS: Strategies should be developed to make cataract services affordable and accessible to the population in the rural areas. There is an urgent need to improve the outcome of cataract surgery. Refractive error services should be provided at the community level

Magnetic dipole moments in single and coupled split-ring resonators

We examine the role of magnetic dipoles in single and coupled pairs of metallic split-ring resonators by numerically computing their magnitude and examining their relative contributions to the scattering cross section. We demonstrate that magnetic dipoles can strongly influence the scattering cross section along particular directions. It is also found that the magnetic dipole parallel to the incident magnetic field and/or high-order multipoles may play a significant role in the linear response of coupled split-ring resonators.Comment: 7 pages, 3 figures, 1 tabl

Cataract prevalence, cataract surgical coverage and barriers to uptake of cataract surgical services in Pakistan: the Pakistan National Blindness and Visual Impairment Survey.

AIM: To estimate the prevalence of visual impairment and blindness caused by cataract, the prevalence of aphakia/pseudophakia, cataract surgical coverage (CSC) and to identify barriers to the uptake of cataract services among adults aged >or=30 years in Pakistan. METHODS: Probability proportional-to-size procedures were used to select a nationally representative sample of adults. Each subject underwent interview, visual acuity measurement, autorefraction, biometry and ophthalmic examination. Those that saw <6/12 in either eye underwent a more intensive examination procedure including corrected visual acuity, slit lamp and dilated fundus examination. CSC was calculated for different levels of visual loss by person and by eye. Individuals with <6/60 in the better eye as a result of cataract were interviewed regarding barriers. RESULTS: 16 507 Adults were examined (95.5% response rate). The crude prevalence of blindness (presenting <3/60 in the better eye) caused by bilateral cataract was 1.75% (95% CI 1.55%, 1.96%). 1317 Participants (633 men; 684 women) had undergone cataract surgery in one or both eyes, giving a crude prevalence of 8.0% (95% CI 7.6%, 8.4%). The CSC (persons) at <3/60, <6/60 and <6/18 were 77.1%, 69.3% and 43.7%, respectively. The CSC (eyes) at <3/60, <6/60 and <6/18 were 61.4%, 52.2% and 40.7%, respectively. Cost of surgery (76.1%) was the main barrier to surgery. CONCLUSION: Approximately 570 000 adults are estimated to be blind (<3/60) as a result of cataract in Pakistan, and 3,560000 eyes have a visual acuity of <6/60 because of cataract. Overall, the national surgical coverage is good but underserved populations have been identified

Lesion topography and microscopic white matter tract damage contribute to cognitive impairment in symptomatic carotid artery disease

Purpose: To investigate associations between neuroimaging markers of cerebrovascular disease, including lesion topography and extent and severity of strategic and global cerebral tissue injury, and cognition in carotid artery disease (CAD). Materials and Methods: All participants gave written informed consent to undergo brain magnetic resonance imaging and the Addenbrooke’s Cognitive Examination–Revised. One hundred eight patients with symptomatic CAD but no dementia were included, and a score less than 82 represented cognitive impairment. Group comparison and interrelations between global cognitive and fluency performance, lesion topography, and ultrastructural damage were assessed with voxel-based statistics. Associations between cognition, medial temporal lobe atrophy (MTA), lesion volumes, and global white matter ultrastructural damage indexed as increased mean diffusivity were tested with regression analysis by controlling for age. Diagnostic accuracy of imaging markers selected from a multivariate prediction model was tested with receiver operating characteristic analysis. Results: Cognitively impaired patients (n = 53 [49.1%], classified as having probable vascular cognitive disorder) were older than nonimpaired patients (P = .027) and had more frequent MTA (P<.001), more cortical infarctions (P = .016), and larger volumes of acute (P = .028) and chronic (P = .009) subcortical ischemic lesions. Lesion volumes did not correlate with global cognitive performance (lacunar infarctions, P = .060; acute lesions, P = .088; chronic subcortical ischemic lesions, P = .085). In contrast, cognitive performance correlated with presence of chronic ischemic lesions within the interhemispheric tracts and thalamic radiation (P< .05, false discovery rate corrected). Skeleton mean diffusivity showed the closest correlation with cognition (R2 = 0.311, P< .001) and promising diagnostic accuracy for vascular cognitive disorder (area under the curve, 0.82 [95% confidence interval: 0.75, 0.90]). Findings were confirmed in subjects with a low risk of preclinical Alzheimer disease indexed by the absence of MTA (n = 85). Conclusion: Subcortical white matter ischemic lesion locations and severity of ultrastructural tract damage contribute to cognitive impairment in symptomatic CAD, which suggests that subcortical disconnection within large-scale cognitive neural networks is a key mechanism of vascular cognitive disorder

Therapeutic Alliance and Involuntary Commitment of a Minor

Children are legally entitled to be present throughout the commitment hearing for continued hospitalization. The effect of this process on the therapeutic alliance between the child and the psychiatrist warrants examination. A case study of a 14 year-old boy who participated in the court proceedings is presented. The outcome of the hearing resulted in a disruption of the therapeutic alliance. Alter natives to current commitment procedures for minors are discussed

Antagonists of the Receptor-G Protein Interface Block Gi-coupled Signal Transduction

The carboxyl terminus of heterotrimeric G protein alpha subunits plays an important role in receptor interaction. We demonstrate that peptides corresponding to the last 11 residues of Galphai1/2 or Galphao1 impair agonist binding to A1 adenosine receptors, whereas Galphas or Galphat peptides have no effect. Previously, by using a combinatorial library we identified a series of Galphat peptide analogs that bind rhodopsin with high affinity (Martin, E. L., Rens-Domiano, S., Schatz, P. J., and Hamm, H. E. (1996) J. Biol. Chem. 271, 361-366). Native Galphai1/2 peptide as well as several analogs were tested for their ability to modulate agonist binding or antagonist-agonist competition using cells overexpressing human A1 adenosine receptors. Three peptide analogs decreased the Ki, suggesting that they disrupt the high affinity receptor-G protein interaction and stabilize an intermediate affinity state. To study the ability of the peptides to compete with endogenous Galphai proteins and block signal transduction in a native setting, we measured activation of G protein-coupled K+ channels through A1 adenosine or gamma-aminobutyric acid, type B, receptors in hippocampal CA1 pyramidal neurons. Native Galphai1/2, peptide, and certain analog peptides inhibited receptor-mediated K+ channel gating, dependent on which receptor was activated. This differential perturbation of receptor-G protein interaction suggests that receptors that act on the same G protein can be selectively disrupted