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Bull's Eye

The bullseye or bull's eye has, since 1833,[1] been the name for the center of a target and, by extension, since 1857,[1] has been given to any throw, toss, or shot that hits the center.

bull's eye

In a further development, success in an endeavor in which there is such inherent difficulty that most people are far more likely to choose, do, or identify something that is either unfortunately only close to or dismissively far from the ideal or necessary thing to choose can be called "hitting the bull's eye."

The center of the target may have come to be called the bull's eye from the practice of English archers who, both to develop and to exhibit their skills, would attempt to shoot an arrow through the eye socket of a bull's skull.[2]

Chloroquine and hydroxychloroquine can cause toxic retinopathy due to their binding of melanin in the retinal pigmented epithelium (RPE) as well as direct toxicity to retinal ganglion cells. Early findings include mottling of the RPE and blunted foveal reflex. As the retinopathy progresses, a bull's-eye maculopathy develops, as seen in these photos. In addition to the bull's-eye maculopathy, patients can demonstrate paracentral scotomas on visual field testing and parafoveal outer retinal atrophy on OCT.

Purpose: To report a case of bull's eye maculopathy, a novel finding in a patient with iron overload secondary to hereditary hemochromatosis with a homozygous mutation of the HFE gene.

Observations: A 39-year-old man with recently diagnosed hereditary hemochromatosis undergoing treatment by serial phlebotomy presented with bilateral progressive blurry vision and recent onset of photopsias and headaches. Fundus examination revealed a symmetric bull's eye maculopathy with photoreceptor loss and retinal pigment epithelium transmission defects in the area of speckled hyper- and hypo-pigmentation by multimodal imaging. Full field and multifocal electroretinograms demonstrated generalized rod and cone dysfunction with some central preservation of waveforms. Further systemic work-up revealed low ceruloplasmin, mildly decreased serum copper and zinc levels, and low urinary copper. The patient underwent testing for inherited retinal dystrophies, but was not found to have any known pathogenic gene mutations. His ferritin levels normalized with serial phlebotomy and his retinopathy did not appear to progress over 6 months with normalization of his iron levels.

Conclusions and importance: We report a case of bull's eye maculopathy in a patient with hereditary hemochromatosis with no previous exposure to iron chelators and no known inherited retinal dystrophy. Ocular involvement in hereditary hemochromatosis is relatively rare. In this case, the patient's low serum ceruloplasmin is thought to have increased the amount of redox-active ferrous iron and potentiated retinal iron toxicity resulting in the observed retinopathy. To the authors' knowledge, this is a potentially novel ocular manifestation of hereditary hemochromatosis.

A rash is a common sign of Lyme disease. But it doesn't always happen. The rash is usually a single circle that slowly spreads from the site of the tick bite. It may become clear in the center and look like a target or bull's-eye. The rash often feels warm to the touch, But it's usually not painful or itchy.

The current size and shape of the Bull's Eye Room were created by the addition of the 35'-10.5" wide pediment in 1778. Paint analysis of the inside face of the door trim, however, indicates there was a room in this location dating to the raising of the roof at the end of the 1750s. The most prominent feature of this room is the large oval or "bull's eye" window, which is the focal point of the west pediment. Some of the shelves in this room are part of the original shelving in this space. The shelving confirms this room was a storage space, almost certainly the "China Closet upstairs" mentioned in the 1799 inventory.

Protein kinase C-θ (PKC-θ), a central kinase in T cell signaling, has attracted attention as the only PKC targeted to the center of the immunological synapse1,2,3. The selective roles of PKC-θ in specific disease-causing T cells have kept it at center stage4,5,6. However, how PKC-θ 'hits the bull's eye' and how its activity is maintained once there have remained unknown. Two papers in this issue of Nature Immunology focus on these fundamental aspects of PKC-θ regulation7,8. Kong et al. apply a classic chimeric protein approach to discover the targeting motif in PKC-θ that brings it to the T cell synapse7. Chuang et al. identify a previously unknown kinase for phosphorylation of the major activation loop site and demonstrate upregulation of this kinase in a subset of patients with lupus8. These studies tag some 'old friends' in T antigen cell receptor (TCR)-proximal signaling for PKC-θ recruitment and a 'bright new face' that keeps the kinase active. 041b061a72

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