10 research outputs found

    It’s Never Too Early or Too Late—End the Epidemic of Alzheimer’s by Preventing or Reversing Causation From Pre-birth to Death

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    The path to sporadic Alzheimer’s is a tragic journey beginning prior to birth and ending in the most dreaded disease of society. Along the disease path are a myriad of clues that portend AD, many of which are complaints of seemingly unrelated conditions from chronic migraines, mood disorders, eye diseases, metabolic syndromes, periodontal diseases, hormonal and autoimmune diseases. Properly treating, not just managing, these diseases, prior to onset of dementia, may significantly reduce dementia incidences. Current high levels of health complaints reflect a state of generalized poor health and compromised immunity. During the mid-Victorian era, people were long-lived yet healthy, suffering from chronic diseases at one tenth the rate of peoples today. It’s our poor health, at any age that increases susceptibility to chronic diseases and Alzheimer’s. Infection is involved in many cases of Alzheimer’s and other neurodegenerative diseases but is also implicated in many chronic conditions. Scientists looking for causation recognize that Alzheimer’ is multifactorial and systemic—not “brain only.” To slow, stop and reverse the AD epidemic, identification and reversal of causal factors must occur across the entire life spectrum of humans. This approach simply gives consideration to enhancing immune status of our bodies and brain, and controlling inflammation and infection, throughout the entire age spectrum. Infection is a causal factor, but the root cause is multi-factorial and immune health related. Pasteur stated it best when acknowledging the work of Bernard in 19th Century France, “The seed is nothing, the soil is everything.

    Posterior vitreous detachment following panretinal laser photocoagulation

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    A total of 30 eyes of 19 patients with type I diabetes, varying severity of retinopathy, and no posterior vitreous detachment (PVD) were studied clinically, and vitreous examination was performed by preset lens biomicroscopy. Follow-up was 4.0-7.5 years. A total of 15 eyes underwent panretinal laser photocoagulation (PRP) and 15 eyes were left untreated. The incidence of PVD was 8 of 15 (53%) after PRP and 1 of 15 (7%) in untreated eyes (P\u3c0.02). Minimal vitreous hemorrhage occurred in 4 of 7 treated eyes (57%) that did not develop PVD and in only 2 of 8 (25%) that did. In treated eyes with no history of vitreous hemorrhage, the incidence of PVD was 6/9 (67%); in treated eyes with minimal vitreous hemorrhage at any time, it was 2/6 (33%). In treated eyes, the presence of Diabetic Retinopathy Study (DRS) high-risk characteristics was equally frequent in eyes that developed PVD as in those that did not. These data suggest that PVD occurs following PRP, independent of the severity of diabetic retinopathy or prior vitreous hemorrhage. © 1990 Springer-Verlag

    Branch Vein Occlusion

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    Three hundred sixty-six cases of branch vein occlusion entered within the multicenter Branch Vein Occlusion Randomized Clinical Trial have been reviewed. Four cases that developed retinal neovascularization outside of the retinal area involved with the occlusion have been documented by photography and fluorescein angiography

    黄斑疾患 黄斑疾患に対する新しい検査法―診断と治療への応用―

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    黄斑疾患に対する新しい検査法に関し,診断と治療への応用に力点をおいて述べた.黄斑部の形態検査として,網膜厚と網膜の微細構造をretinal thickness analyzer,Heidelberg retina tomograph,optical coherence tomographyの3機種を用いて検討した.又,scanning laser ophthalmoscopeを用い,黄斑部における硝子体と網膜表層から深層迄の観察が可能なことを示した.黄斑部の機能検査としては,脈絡膜血流量,黄斑周囲の網膜血流量,中心窩脈絡毛細管板の血流量の測定を行った.黄斑浮腫の発症に血液網膜柵の障害が関与しているかを検討する為には,differential fluorophotometryを新しく開発した.治療法については,黄斑部光凝固法,黄斑変性に対する新しい治療法(光線力学療法),硝子体手術シミュレーションシステムについて述べ
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