Friday, September 30, 2016

Organizer Eye pain seeing spots


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Importance Of Massage Seattle Provides




The process of kneading body muscles is importance since freshen and makes someone feel lively. People may wish to free from stress by visiting institutions that offer these services. This will help lower the level of stress that leads to weird decisions such a committing suicide. Doctors have recommended that it is proper to go for massage Seattle offers since it makes someone relax and therefore forgetting past oppressions.

One can opt for the process as the experience is very beneficial. One feels gentle and relaxed. Just like some people like going to party as a way of unwinding, others like going for a rubdown. There are some who are so into it such that it is part of their weekly or monthly cost in their budget.

Apart from being a stress remover, kneading is also responsible for pain healing and consolation. In case one has been hit on a certain part of the body, he or she can resort to this as a way of relieving the pain. It thus relieves many types of muscle pains. This is not forgetting the emotional pain. Thus, this is a cure to most of the situations that one faces in life and are unpleasant, one can try this one out.

If you become used to body muscles treatment the instances of invasion by disease lowers. The body regains the power to heal itself even without administration of drugs. Natural healing is important since administration of some drugs may form an addictive state such that if you do not take certain drugs for a specified period you are likely to experience health problems. The cost of medication may also be high and therefore this process will help cut off these expenses.

This practice of muscle treatment is important to athletes since it helps recover faster and reduce the pain an athlete acquired due muscle stretching during the race. The process of running is usually tough and will imply stretching of body muscle that will then later contract leading to pain. An athlete therefore has to make regular visit to institutions that treats body muscles in order to keep the body fit.

Pregnant women should frequently have muscle treatment to make it easy to deliver safely. There process involves muscle stretching and contraction in order to be able to pull without strains. This will increase the chances of giving birth safely therefore avoiding surgeries. The process of surgery is usually matters of speculations since the chances of survival are not certain.

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It is right to always visit one place for the rubdown. This is because the expert gets used to you and thus is aware of the way you like it. It is common for one to prefer a member from the opposite sex to do it on him or her. However you like it, it is important to practice massage Seattle provides.




About the Author:
By Kathryn Neal





Thursday, September 29, 2016

AMD Update 6 An Overview of New Treatments for Dry AMD


Those of you who have been following this space know that I have been reporting on new drug and device treatments for wet age-related macular degeneration for the past several years. I haven’t paid much attention to the treatments under development for the dry form, basically because most are drug-related, and my knowledge of how drugs work is limited. However, I recently read an excellent overview of the new drugs that are being developed for dry AMD, written by Dr. Philip Rosenfeld (the father of Avastin for use in AMD) and John Legarreta, a medical student at State University of New York at Buffalo, which presents a clear picture of current developments in this important field.

I have previously written about the potential for the use of lasers to treat dry AMD by Iridex, but that attempt did not prove successful. I have also written about the Ellex 2RT (retinal regeneration) program that might hold potential in the early intervention in dry AMD. Links to both of these writeups are shown at the end of this posting.

With about 80% to 90% of newly diagnosed AMD cases being of the dry variety, and with no effective treatment currently in use, it is important to track the developmental work underway in this area. This review appeared in the November 2009 issue of Retinal Physician, and with the permission of the magazines publishers, here is the complete writeup:

Preclinical and Phase 1 Drugs in Development for Dry AMD: An Overview

Retinal Physician, November 2009

Philip J. Rosenfeld, MD, PhD ● John Legaretta, BFA

Philip J. Rosenfeld, MD, PhD, is professor of ophthalmology at the Bascom Palmer Eye Institute at the University of Miami Miller School of Medicine in Florida. He receives significant research support from Potentia and Alexion, and he has a minimal advisory relationship with Potentia. John Legarreta, BFA, is a medical student at the School of Medicine and Biomedical Sciences, State University of New York at Buffalo. He has no financial interest in any products mentioned in this article. Dr. Rosenfeld can be reached at prosenfeld@med.miami.edu.


The vast majority of AMD patients have the nonexudative or dry form of the disease, characterized by a constellation of clinical features, including drusen, disturbances of the retinal pigment epithelium (pigment clumping and/or dropout), and geographic atrophy (GA) of the macula. As defined by the Age-Related Eye Disease Study (AREDS), the severity of AMD can be classified into three categories: early, intermediate, and advanced.

[Editors Note: For a breakdown on the number of people in the three categories noted above in both dry and wet AMD in 2007, as estimated by Market Scope, please see the link to the table shown at the end of this posting.]

While drusen alone, particularly those of smaller size, do not seem to be associated with vision loss, at least one large druse measuring 125 μm in diameter is sufficient for the diagnosis of intermediate AMD. Dry AMD may remain static or progress slowly to produce a greater number and distribution of drusen with areas of GA. The increase in size or area of drusen or pigment abnormalities (focal hyper- or hypopigmentation of the retinal pigment epithelium [RPE]) predicts the likelihood of developing vision-threatening lesions in AMD, which include central GA and neovascularization, the advanced forms of AMD.(1)

CURRENT TREATMENT OPTIONS FOR DRY AMD

Antiangiogenic therapies have been developed to treat wet AMD. While drugs such as ranibizumab (Lucentis, Genentech) and bevacizumab (Avastin, Genentech) have revolutionized the care of patients with neovascular AMD, under the best of circumstances, treatment converts the neovascular form of AMD back to dry AMD. There is no evidence to suggest that these antiangiogenic drugs have any beneficial effect on the underlying degenerative process known as dry AMD. Currently, there is no proven drug treatment for dry AMD; however, the cessation of smoking and treatments based on nutritional recommendations and supplements can slow disease progression. Nutrient-based treatments for AMD were evaluated in the AREDS trial.(2)

TARGETING THE CAUSE OF AMD

The overall goal of treatment for dry AMD is to target the underlying cause of the disease and halt, or at least slow, the loss of vision. This approach has been hampered by two major issues. First, there are no reliable in vitro systems for testing the efficacy of any drug for dry AMD, and second, no true animal model exists for AMD. A well-developed macula is only found in primates and birds, and while numerous attempts have been made to develop nonprimate models for AMD, and these models highlight various pathological features of human AMD, none of these animal models truly replicates the disease process seen in humans. The only model that may be useful for potential drug testing is the naturally occurring monkey colonies that have been found to develop drusen.(3)

The second issue that has hampered drug development is the uncertainty surrounding the best molecular pathway to target for the treatment of dry AMD. However, several different strategies have evolved. These strategies have targeted three major therapeutic areas of investigation: preservation of photoreceptors and the RPE (neuroprotection), prevention of oxidative damage, and suppression of inflammation. Each strategy is supported by varying degrees of scientific evidence and will have to await validation based on clinical trial outcomes.

CLINICAL TRIAL ENDPOINTS IN DRY AMD

The most obvious study endpoint for dry AMD therapies would be the preservation of visual acuity; however, studies using visual acuity as an endpoint will take many years to complete. To decrease the time required to show a benefit from a drug, surrogate endpoints have been developed that might indicate a positive outcome without waiting the years required to show visual acuity benefit.

One surrogate endpoint is the prevention of disease progression from dry to wet AMD. This endpoint was first used in the study investigating anecortave acetate (Retaane, Alcon) for the treatment of dry AMD. While the drug failed to prevent progression of dry to wet AMD, the study demonstrated the feasibility of this study design. Another strategy is to assume that a treatment for dry AMD might also affect the underlying stimulus for neovascularization in wet AMD. If true, then a potential endpoint might be to demonstrate that a drug for dry AMD is able to decrease the need for retreatment with antiangiogenic therapy in wet AMD or improve the visual acuity outcome. This study design has not been tested.

A feature of dry AMD that could serve as a surrogate endpoint is the area of drusen in the macula. While drusen area as measured by fundus photography has already been explored as an endpoint in the failed laser-to-drusen trials, (4-6) the change in drusen volume in response to pharmacotherapy is a novel clinical trial endpoint that has not been explored previously. Spectral-domain optical coherence tomography has the potential to reliably and reproducibly identify drusen in the macula and provide truly automated volume quantification. The most likely surrogate clinical trial endpoint, based on a symposium held in Washington, DC, and sponsored by the National Eye Institute and the Food and Drug Administration, is an endpoint that assesses a drug’s effects on the growth of GA, since GA is a feature of dry AMD that directly causes loss of photoreceptors and the RPE. (7)

DRUGS TO PROMOTE SURVIVAL OF PHOTORECEPTORS AND THE RPE

No matter what the underlying cause of AMD, drugs that can preserve viable photoreceptors and maintain the RPE should preserve vision. One strategy to promote survival of photoreceptors and the RPE is to protect cells against ischemia and improve the choroidal circulation in patients with dry AMD. Two studies are currently using this strategy. In Europe, an ongoing multicenter, randomized, placebo-controlled study is investigating the use of an offlabel, generic drug known as trimetazidine (Vastarel MR, 35 mg tablet), a drug currently used for the treatment of angina pectoris. Trimetazidine improves myocardial glucose utilization by stopping fatty acid metabolism, and it is considered to have cytoprotective effects in ischemic conditions. Other uses for this drug include the treatment of vertigo, tinnitus, and vision loss and visual field loss due to vascular causes. The primary goal of this study is to slow the conversion of dry AMD to wet AMD.

Another drug being investigated for its vasodilatory effect is Alprostadil, also known as prostaglandin E1 (PGE1). The presumed rationale is based on the belief that improved circulation would slow the progression of AMD. This multicenter, randomized, placebo-controlled study is ongoing in Europe.

Another strategy to preserve the macular function is to prevent apoptosis by using neuroprotective agents. Ciliary neurotrophic factor (CNTF), a potent neuroprotective agent, has been shown to inhibit photoreceptor apoptosis in an animal model of retinal degeneration (8) and is being investigated as a treatment for dry AMD. Using encapsulated cell technology that permits CNTF-producing transfected cells to be implanted into the vitreous cavity, Neurotech Pharmaceuticals (Lincoln, RI) has developed a sustained-release platform that produces CNTF for a year or longer. The phase 2 study is completed and data analysis is currently under way. Other neuroprotective agents currently under investigation for dry AMD include a brimonidine tartrate intravitreal implant (Allergan, Irvine, CA) and topical tandospirone (Alcon, Fort Worth, TX).

Yet another strategy is to interfere with the normal visual cycle and preserve vision by decreasing the accumulation of toxic metabolites, such as lipofuscin and the retinal fluorophore A2E. This strategy is being pursued by Sirion Therapeutics (Tampa, FL) with the use of fenretinide - N-(4-hydroxyphenyl) retinamide - for the treatment of dry AMD. Fenretinide binds retinol-binding protein in the circulation and prevents uptake of retinol by the RPE, thus downregulating photoreceptor metabolism. The phase 2 study investigating fenretinide for the treatment of GA is fully enrolled and in its second year of follow-up.

Downregulation of photoreceptor activity is also being investigated using the drug ACU-4429 (Acucela, Bothell, WA). ACU-4429 is a small nonretinoid molecule that functions as a modulator of the isomerase (RPE65) required for the conversion of all transretinol to 11-cis-retinal in the RPE. By modulating isomerization, ACU-4429 slows the visual cycle in rod photoreceptors and decreases the accumulation of A2E. The ongoing phase 1 study has shown so far that the drug is safe and well tolerated in healthy volunteers. A phase 2 study for treatment of dry AMD is currently being planned.

A novel strategy for the preservation of photoreceptors and the RPE borrows a therapeutic strategy used for the treatment of Alzheimer's disease. An antibody against amyloid ß has completed a phase 1 study as an intravenous treatment for GA in AMD patients. This antibody, known as RN6G (Pfizer, New York, NY), was shown to decrease the amount of amyloid ß in the eye from a mouse model of AMD when given as a systemic therapy.(9) A phase 2 study is currently under way.

The therapies under investigation that seek to preserve photoreceptors and the RPE are summarized in Table 1.


(Note: I have reproduced the tables included with the article. By clicking on the tables they will open in a new window or tab in a larger more readable size. Or, go to the original online writeup for a clearer view of the table contents.)

DRUGS TO PREVENT INJURY FROM OXIDATIVE STRESS AND MICRONUTRIENT DEPLETION

In AMD, oxidative stress and the depletion of essential micronutrients are considered to be driving forces in disease progression. This disease paradigm assumes that AMD is caused by a lifelong exposure to free radicals - a byproduct of high oxygen consumption in the neural retina and RPE - combined with exposure to environmental toxins, such as those derived from smoking, in conjunction with inadequate levels of naturally occurring antioxidants. These exposures and deficits result in the accumulation of cellular debris - particularly oxidized lipids, which promote inflammation and may be directly toxic to the macular tissues - resulting in the clinical manifestations known as AMD. This paradigm is supported by epidemiologic studies showing that diets rich in antioxidants decrease the risk of AMD, while smoking was associated with an increased risk of AMD.(10)

Support for this nutrient-based paradigm was provided by the AREDS trial. This multicenter, NEI-sponsored study evaluated the effect of pharmacological doses of zinc and/or a formulation containing nutrients with antioxidant properties (vitamin C, vitamin E, and beta-carotene) on the rate of progression to advanced AMD and on visual acuity. The use of these vitamins and micronutrients reduced the risk of developing advanced AMD by about 25%.(2) The overall risk of moderate vision loss was reduced by 19% at five years. The theory of oxidative damage as a cause for AMD has also been supported by the findings that individuals have an increased risk of developing AMD if they carry a specific genetic polymorphism in mitochondrial DNA (A4917G), an organelle important for oxidative metabolism, and in nuclear DNA within the 5'-upstream region of a genetic locus important for DNA repair (ERCC6). DNA damage can be caused by oxidative stress.(11,12)

The AREDS2 trial, now under way, is designed to evaluate the effect of dietary xanthophylls (lutein/zeaxanthin) and/or omega-3 long-chain polyunsaturated fatty acids (LCPUFA), known as docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), on the progression to advanced AMD (www.areds2.org). These micronutrients are believed to function not only as antioxidants, but also as anti-inflammatory and antiangiogenic agents, according to epidemiologic and laboratory studies. In addition, AREDS2 will investigate the effects of eliminating betacarotene and the effects of reducing zinc in the original AREDS on the development and progression of AMD.

A topical antioxidant called OT-551 (Othera Pharmaceuticals, Exton, PA) was being explored as a treatment for dry AMD. OT-551 (4-cyclopropanoyloxy- 1-hydroxy-2,2,6,6-tetramethylpiperidine HCl) is a small lipophilic molecule that readily penetrates the cornea. OT-551 is converted by ocular esterases to TEMPOL-H (TP-H), the active metabolite that is a potent free-radical scavenger that does not penetrate the cornea. In animal studies, topical therapy has resulted in excellent ocular bioavailability, with significant levels of TP-H achieved in the retina.

The drug OT-551 was shown to possess antiinflammatory and antiangiogenic properties, as well as antioxidant properties. OT-551 was also shown to protect against oxidative damage in vitro, protect against light damage in vivo,(13) suppress photoreceptor cell death in animal models, and block angiogenesis stimulated by growth factors. Based on these preclinical data, OT-551 was being investigated as a therapy for GA in AMD. This two-year, phase 2 trial, known as the OMEGA (OT-551 Multicenter Evaluation of Geographic Atrophy) study, was stopped after 18 months, due to an apparent lack of efficacy in preventing the enlargement rate of GA in AMD.

The therapies under investigation that seek to prevent injury from oxidative stress and micronutrient depletion are summarized in Table 2.


DRUGS TO SUPPRESS INFLAMMATION

Genetic association studies using different populations have shown that inflammation appears to be the driving force behind AMD.(14) In 2005, four groups identified a genetic polymorphism in complement factor H (CFH), which was associated with an increased risk of developing AMD.(15-18) The documented risk-conferring single-nucleotide polymorphism (SNP) was a thymine (T) to cytosine (C) substitution at nucleotide 1277 in exon 9, which results in a tyrosine-to-histidine change at amino acid position 402 (Y402H) of the CFH protein.

Since complement is a system of serum proteins that comprise an important arm of the innate immune system, association studies have definitively linked AMD to the immune system. Also, two independent studies reported the association of the complement factor 3 gene with AMD, (19,20) as well as the complement factor B/component 2 gene.(21) An association between the complement factor 1 gene and AMD has been reported too.(22) Less robust associations have been reported between AMD and SERPING1, which regulates the first component of complement (C1), (23) and between AMD and C7 and mannose binding lectin 2 (MBL2) loci.(24) Protective alleles associated with the complement pathway have also been reported. Two of the five CFH-related genes (CFHR1-5), which lie within the regulators of complement activation (RCA) locus on chromosome 1q32, known as CFHR1 and CFHR3, are considered to be protective against AMD.(25)

These genetic association studies would imply that inhibition of complement activation would be a reasonable strategy for the treatment of AMD. However, after a lifetime of complement-mediated damage, such a strategy might have no effect on disease progression later in life. One drug being investigated is POT-4 (Potentia Pharmaceuticals, Louisville, KY), a cyclic peptide comprised of 13 amino acids, that is derived from compstatin. POT-4 binds reversibly to complement component 3 (C3) and prevents its proteolytic activation to C3a and C3b and the subsequent release of all downstream anaphylatoxins, as well as the formation of terminal membrane attack complex. As a C3 inhibitor, POT-4 inhibits all three major pathways of complement activation. POT-4 has unique slow-release properties due to the formation of an intravitreal gel at higher doses, which should permit less frequent intravitreal injections to achieve prolonged complement inhibition.

The phase 1 dose-escalation study, known as Assessment of Safety of Intravitreal POT-4 Therapy for Patients with Neovascular AMD (ASaP), was performed on patients with advanced neovascular lesions with the intention to pursue POT-4 as a treatment for dry AMD. To date, POT-4 appears safe up to a dose of 1.05 mg, with evidence of efficacy at the higher doses.

Another complement inhibitor under investigation is eculizumab (Soliris, Alexion Pharmaceuticals), a humanized monoclonal antibody derived from a murine antihuman C5 antibody. Eculizumab specifically binds the terminal complement protein C5, thereby inhibiting its cleavage to C5a and C5b during complement activation. The strategic blockade of the complement cascade at C5 prevents the release of the downstream anaphylatoxin C5a and prevents the formation of the cytolytic membrane attack complex.

Eculizumab is FDA-approved for the intravenous treatment of another complement-mediated disease known as paroxysmal nocturnal hemoglobinuria. At the Bascom Palmer Eye Institute, we are performing a phase 2 investigation with eculizumab for the treatment of patients with dry AMD, known as the COMPLement Inhibition with Eculizumab for the Treatment of Non-Exudative Age-Related Macular Degeneration (COMPLETE) Study. Patients with GA or high-risk drusen are being randomized 2:1 to receive intravenous infusions of eculizumab or placebo.

Ophthotech's ARC-1905 (Princeton, NJ), an anti-C5 aptamer, is another complement inhibitor being tested in AMD. ARC-1905 is being administered by intravitreal injection. The phase 1 dose-escalation study was performed in combination with ranibizumab therapy for the treatment of wet AMD. Genentech/Roche are developing an anti-Complement Factor D antibody Fab (FCFD4514S), which is in a phase 2 trial. Another phase 1 study using ARC1905 for dry AMD is currently under way.

Another complement inhibitor in preclinical studies is JPE1375 (Jerini Ophthalmic, New York, NY), a small, peptidomimetic molecular antagonist against the C5a receptor, which prevents binding of C5a, thus inhibiting the biological activity of C5a. Additional complement inhibitors are being pursued in preclinical studies by several companies, but details are not yet available.

More generalized immune suppression for the treatment of dry AMD is being pursued with the use of subcutaneous glatiramer acetate (Copaxone, Teva Pharmaceuticals, Kfar- Saba, Israel), intravitreal sustained-release fluocinolone acetonide (Iluvien implant, Alimera Sciences, Alpharetta, GA), and subcutaneous sirolimus (rapamycin), a macrolide fungicide with immunosuppressive properties.

The therapies under investigation that seek to suppress inflammation are summarized in Table 3.


SUMMARY

Several different strategies are being investigated, but it will take years before we know if any of them are successful. While we await positive outcomes, these clinical trials will produce a wealth of natural history data on the progression of dry AMD and provide us with extensive experience using several different imaging modalities to track disease progression. With this experience, our clinical trial designs will improve over time and the appropriate clinical trial endpoints should become obvious. With all the drugs in development, there is a good chance that a treatment breakthrough should occur within the next decade. RP

REFERENCES

1. Ferris FL, Davis MD, Clemons TE, et al. A simplified severity scale for agerelated macular degeneration: AREDS Report No. 18. Arch Ophthalmol. 2005;123:1570-1574.
2. A randomized, placebo-controlled, clinical trial of high-dose supplementation with vitamins C and E, beta carotene, and zinc for age-related macular degeneration and vision loss: AREDS report no. 8. Arch Ophthalmol. 2001;119:1417-1436.
3. Kaidzu S, Tanito M, Ohira A, et al. Immunohistochemical analysis of aldehydemodified proteins in drusen in cynomolgus monkeys (Macaca fascicularis). Exp Eye Res. 2008;86:856-859.
4. Laser treatment in patients with bilateral large drusen: the complications of age-related macular degeneration prevention trial. Ophthalmology. 2006;113:1974-1986.
5. Friberg TR, Musch DC, Lim JI, et al. Prophylactic treatment of age-related macular degeneration report number 1: 810-nanometer laser to eyes with drusen. Unilaterally eligible patients. Ophthalmology. 2006;113:622 e1.
6. Owens SL, Bunce C, Brannon AJ, et al. Prophylactic laser treatment hastens choroidal neovascularization in unilateral age-related maculopathy: final results of the drusen laser study. Am J Ophthalmol. 2006;141:276-281.
7. Csaky KG, Richman EA, Ferris FL 3rd. Report from the NEI/FDA Ophthalmic Clinical Trial Design and Endpoints Symposium. Invest Ophthalmol Vis Sci. 2008;49:479-489.
8. Tao W, Wen R, Goddard MB, et al. Encapsulated cell-based delivery of CNTF reduces photoreceptor degeneration in animal models of retinitis pigmentosa. Invest Ophthalmol Vis Sci. 2002;43:3292-3298.
9. Ding JD, Lin J, Mace BE, et al. Targeting age-related macular degeneration with Alzheimer's disease based immunotherapies: anti-amyloid-beta antibody attenuates pathologies in an age-related macular degeneration mouse model. Vision Res. 2008;48:339-345.
10. Risk factors associated with age-related macular degeneration. A case-control study in the age-related eye disease study: Age-Related Eye Disease Study Report Number 3. Ophthalmology. 2000;107:2224-2232.
11. Canter JA, Olson LM, Spencer K, et al. Mitochondrial DNA polymorphism A4917G is independently associated with age-related macular degeneration. PLoS One. 2008;3:e2091.
12. Tuo J, Ning B, Bojanowski CM, et al. Synergic effect of polymorphisms in ERCC6 5' flanking region and complement factor H on age-related macular degeneration predisposition. Proc Natl Acad Sci U S A. 2006;103:9256-9261.
13. Tanito M, Li F, Elliott MH, et al. Protective effect of TEMPOL derivatives against light-induced retinal damage in rats. Invest Ophthalmol Vis Sci. 2007;48:1900-1905.
14. Patel M, Chan CC. Immunopathological aspects of age-related macular degeneration. Semin Immunopathol. 2008;30:97-110.
15. Edwards AO, Ritter R, 3rd, Abel KJ, et al. Complement factor H polymorphism and age-related macular degeneration. Science. 2005;308:421-424.
16. Hageman GS, Anderson DH, Johnson LV, et al. A common haplotype in the complement regulatory gene factor H (HF1/CFH) predisposes individuals to age-related macular degeneration. Proc Natl Acad Sci U S A. 2005;102:7227-7232.
17. Haines JL, Hauser MA, Schmidt S, et al. Complement factor H variant increases the risk of age-related macular degeneration. Science. 2005;308:419-421.
18. Klein RJ, Zeiss C, Chew EY, et al. Complement factor H polymorphism in agerelated macular degeneration. Science. 2005;308:385-389.
19. Maller JB, Fagerness JA, Reynolds RC, et al. Variation in complement factor 3 is associated with risk of age-related macular degeneration. Nat Genet. 2007;39:1200-1201.
20. Yates JR, Sepp T, Matharu BK, et al. Complement C3 variant and the risk of age-related macular degeneration. N Engl J Med. 2007;357:553-561.
21. Gold B, Merriam JE, Zernant J, et al. Variation in factor B (BF) and complement component 2 (C2) genes is associated with age-related macular degeneration. Nat Genet. 2006;38:458-462.
22. Fagerness JA, Maller JB, Neale BM, et al. Variation near complement factor I is associated with risk of advanced AMD. Eur J Hum Genet. 2009;17;100-104.
23. Ennis S, Jomary C, Mullins R, et al. Association between the SERPING1 gene and age-related macular degeneration: a two-stage case-control study. Lancet. 2008;372:1828-1834.
24. Dinu V, Miller PL, Zhao H. Evidence for association between multiple complement pathway genes and AMD. Genet Epidemiol. 2007;31:224-237.
25. Hughes AE, Orr N, Esfandiary H, et al. A common CFH haplotype, with deletion of CFHR1 and CFHR3, is associated with lower risk of age-related macular degeneration. Nat Genet. 2006;38:1173-1177.


Links:

Laser Treatments for AMD Show Promise; Ocular Surgery News, January 15, 2000.

Ellex 2RT Retina Regeneration Therapy: A First Report

AMD Cases in the U.S. by Type and Stage in 20007

Preclinical and Phase 1 Drugs in Development for Dry AMD: An Overview


CATARACT







CATARACT
Our eye is like a camera. A camera has a group of lenses to zoom and focus the image. The same job in human eye is done by a single structure called as “Lens”. This lens is placed behind the iris and helps in focusing and zooming the images.
This lens is a clear structure which is placed in a bag called as “Capsular bag” similar to a toffee being wrapped tightly by a plastic paper. But this capsular bag has no free ends.
In old age due to many bodily changes, this lens slowly starts losing its transparency. This opacification of lens is called as “Cataract”. Since cataract is a disorder of old age, every individual has to face it in old age. Cataracts commonly affect both eyes, but it is not uncommon for cataracts in one eye to advance more rapidly. Typical symptoms may include blurry vision, glare, difficulty with night vision, poor color vision, or frequent changes in eyeglass prescription.
There is no medical treatment for cataract. Surgery is the only treatment available. Cataract surgery is the most commonly performed surgery in the world. It has 98 percent success rate. With the advancements in surgical fields, now, a cataract surgery can be done without injection (needle prick), within a few minutes with Phaco. The patient can resume his duties on the same day of surgery.
Cataract surgery is performed to replace the opaque natural lens (cataract) with an artificial IOL. As said earlier, the lens is placed in capsular bag which has no free openings. To reach the lens, we need to make an opening in the surface of the bag. This is called capsulotomy. Through this opening, the lens is removed, leaving an empty bag. An artificial lens (IOL, IntraOcular Lens) is placed in this bag, which now starts doing the job of original lens. This bag is placed inside the eye ball (imagine the toffee being placed in a sealed box). To reach this we need to make an opening in the eyeball, which is called as “incision ”. Through this incision we reach the capsular bag, make an opening in the bag (capsulotomy), remove the lens and insert an IOL in the bag. Briefly, these are the steps of surgery. Since the structures of eye are very small, a microscope is used to magnify the image. Therefore it’s a microscopic surgery and requires utmost care and skill.
Surgical Techniques
There are many surgical techniques based on the different approaches in either of above mentioned steps. The incision can be placed on sclera or limbus or cornea. Corneal incision is the most preferred as it has least tissue manipulation. The size of incision can vary from a large 12 mm to less than 2 mm size. The lesser the size, the lesser the tissue manipulation and healing time and recovery time. A large incision may need stitches to close it. While smaller ones do not need stitches. Stitches should best be avoided as they cause redness, discomfort and watering. The removal of lens can be done manually which requires a large incision, or it can be done with Phaco with very small incision. Phaco is a technique where in a needle is passed into the lens, which dissolves the lens with ultrasound energy and sucks the lens. Phaco is the best and the most ideal technique of cataract surgery.
Anesthesia
The surgery is usually done under Local anesthesia (Peribulbar or Retrobulbar anesthesia) where an injection is given around the eye. Eye is massaged for the dispersion of injection. This injection has the risk of bleeding, optic nerve injury, globe injury etc. To prevent these complications, the latest preferred mode of anesthesia is Topical Anesthesia, where in ‘Eye drops’ are used instead of injection. It’s always advisable to find a surgeon who can operate without injection.
Intra Ocular Lens (IOL)
There are different types of IOLs available. Rigid IOLs need a large incision for insertion. Foldable IOL needs a small incision. Usually the IOL corrects only far distance. Patient requires glasses for reading. Multifocal IOL corrects both far and near vision which makes the patient less dependant on glasses. UV filter IOL s have the capacity to filter the ultraviolet rays which may be harmful to retina.
Role of anesthetist in cataract surgery:
Though the surgery is done under topical or peribulbar anesthesia, due to old age, there are risks of systemic complications like heart blocks, arrhythmias etc. An anesthetist will take care of such problems, if they arise. Therefore , Its advisable to undergo cataract surgery in a setup where an anesthetist is readily available.
Before the surgery, anesthetist examines the patient and advices him about medications. During surgery , he monitors for any untoward event and tackles it if arises.
Prior to operation:
Few important investigations like blood sugar, ECG etc. are done. Ocular tests like Eye pressure, Syringing are also done. Few tests are done to calculate the power of IOL that has to be placed. Pre anesthetic checkup is done for fitness.
Anesthetist’s orders need to be followed. On the day of surgery patient can have a head bath, as he would be asked not to have head bath for few weeks after surgery. You need to instill eyedrops on the morning of surgery as adviced. You need to change your clothes before being taken into the operation theatre.
During the operation:
Drops will be instilled to numb your eyes ( some surgeons may give an injection around the eye for the same purpose). You may be asked to follow some instructions like : “Staring at a light above”, ‘looking down’, ‘not to squeeze the lids’ etc.. You will be in full conscious , you may feel some sensation in the eye, but not the pain. The actual procedure lasts for about 20 to 30 minutes.
After the operation:
You will be shifted to recovery room, where you can have food after about 10 minutes. You will be asked to take few medications. You will be seen by the surgeon after couple of hours. Depending on the type of surgery done, the eye patch may be removed or will be kept for another day. You will be given the postoperative instructions ( a printed material would be given). You need to wear dark goggles in day time to protect the eye from sunlight and dust. At nights to protect from your own fingers , you should wear a eye shield. For about a month you have to instill eye drops as adviced. Usually two visits are required after the surgery, first after one week and next after a month. Glasses would be prescribed after one month of surgery. Till then, dark goggles should be used. You can resume your regular duties one day after the surgery if phaco is done.
What are potential complications of cataract surgery?
While cataract surgery is one of the safest procedures available with a high rate of success, rare complications can arise. The most common problems arising after surgery are persistent inflammation, changes in eye pressure, infection, or swelling of the retina at the back of the eye, and retinal detachment. If the capsular bag is injured, then the artificial lens may need to be placed in a different location. In very rare cases, the intraocular lens moves or does not function properly and may need to be repositioned, exchanged, or removed. All of these complications are extremely rare but can lead to significant visual loss if left untreated; thus, close follow-up is required after surgery.

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Wednesday, September 28, 2016

Red spots on eye after lasik


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Important Considerations To Make When Searching For The Best Reiki Practitioner


By Beverly C. Ralph


Reiki is a well-embraced healing technique that originated from Japan. It works by the therapist using touch to channel energy into the patient and thus trigger the natural healing process of the body. This technique could be used to effectively enhance both physical and emotional well-being. Experts have proven the fact that it could also be used as an effective relaxation remedy that also assists in stress reduction. There are several common sense practices that could guide you in finding a reliable Reiki practitioner.

The entire practice is based on the notion of life force energy. Every living organism has energy that flows within it and around it. The higher the energy levels you have, the better your well-being and general happiness. When the patient is sick, stressed or anxious, the specialist would pass on his or her energy and assist them in finding relief.

There have been numerous controversies revolving around this practice. What is indisputable is that fact that it has miraculously worked for many. What scientists globally have affirmed is the fact that a simple feel good experience through touch could naturally and safely assist in not only healing but also rapid self-improvement. In the same spirit, Reiki has been successfully used to treat an array of illnesses and disorders.

In order for this practice to work for you, it will be of basic importance for you to find the right practitioner. You need someone who has been through training and understands the concepts of the practice in detail. The majorities of doctors who are serious about their practice will even take the step of finding membership in accredited groups of reiki doctors.

It is vital for you to consider the philosophies of practitioners who interest you. Keep in mind that you would be engaging in a practice that is based on touch and also on spiritual philosophies. Make sure that you are at ease with the values of the specialist you choose.

There is also an importance of doing a background check on potential practitioners. You have better chances of receiving a worthwhile service if you work with an expert who has extensively assisted patients with concerns just like yours. Most doctors in this field will engage in other practices such as acupuncture, massage and chiropractic care just to mention a few. It remains important to affirm that your specialist has a decent number of success cases.

Finding the right professional is important. Then again, it is crucial for the patient to maintain the right mentality. In practices that highly depend on self-healing, it takes not only a competent expert, but also an open minded patient for the right results to be achieved.




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Getting The Dream Shape With Zerona Therapy


By Harriett Crosby


Zerona therapy in long island is the latest and safest way to avoid excess fats into our body. Way back in the early years, liposuction had been the most used process by surgeons to eliminate excess body fats. Many people died because of this treatment because this can be very risky because of the way how it is to be done. But now, people prefer to have the lipolaser because it is safer and more effective than the suction which could damage tissues.

A lot of advantages are waiting once you consider this method for you. Getting the figure which is well sculpted is the most obvious outcome for having this. For few sessions, you can get the shape that you have been dreaming of. Advantages includes your health also. Since it lessens cholesterol build up, you can now avoid the possibilities of heart attack and other cholesterol related sickness.

Fat people could not avoid exhaustion because they can always feel the heaviness of there body. This is the reason why most of them are lazy, and because of this, they could no more use their energy which could weaken their metabolism. A weak metabolism could make someone very fat. With the zerona, you could feel the lightness and so you can use your energy. Then you will be having no problems for maintaining the body.

In order to survive in this world, you must have the high level of self esteem because this is where you will get your trust for yourself, your confidence and other emotional strengths. Being fat could make your self esteem low and a low self esteem could attract stress that can cause minor and major sicknesses like cancer or high fever.

Keeping yourself down have great side effects and one of these is eating too much. In this case, you will just make you case worst. Negativity could also help you attract problems that could lead to sickness. Physical aspect is very important in order to function very well, not unless if you are a person who does not care about everyone.

The best thing about this method is that it is not painful and the patient can do normal things what she used to do. Fats in this method will be crush to release triglycerides which is very important for muscle build up and for energy.

This is also the bad thing about it since it does not get the cells out, fats will just return if you will not use those energy made of triglycerides. Well, each session could cost you thousands and you should have the six session completed for better results. This might be very expensive for a middle clash but is less costly that the liposuction.

Though it is not painful, but since the cells were not removed, then you have to still do heavy exercises to maintain the shape. So thinking about the cost, it would be better to do the traditional way even if the results will take too much time. Balance diet still needs exercise. We all need to exercise and so no matter if you are already in shape or not you have to.

If you really need zerona therapy in long island, is not ideal for vanity. This is only recommended for those people which body is their capital like the models. If you are not one of them, then just be you.




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Tuesday, September 27, 2016

Looking for eye floaters cure but not sure of anything


Looking for eye floaters cure but not sure of anything? Here are the answers…

What are eye floaters?

These are small specks that the eye can see, if there is a change that takes place in the vitreous liquid in the eye, as a result of old age. These floaters will be seen when you rotate your eyes or when you blink them.

At first, when you notice these floaters, you will find that they are following the movements of your eyes. But later on you will see that these are starting to lag behind and they will also come to a halt, just a few seconds after your eyes stop moving.

Why you need eye floaters cure

These floaters are not to be taken lightly as they are very clearly visible when you will stare at the clear sky or at a white wall. People tend to confuse these floaters with light flashes, but these two are different.

Light flashes are actually taken as bright lights that happen to flash across the eyes. Mostly, people do not tend to pay notice to these eye floaters and they even go unnoticed as people do not find them to be troublesome. But the truth is that when they start to appear in excess, they must not be neglected and a doctor must be consulted.

What the doctor prescribes

Mostly, the doctor would prescribe antibiotics, to treat this problem. But, this kind of treatment is only prescribed, if the floaters have come about as a result of the white blood cells being present and causing an eye infection or eye-inflammation.

There are also various vitamins and many products that contain iodine, which is claimed to be a great cure for people suffering from these floaters. But of course, the effects of this are seen to vary from individual to individual.  Also, such results have not been proven clinically.

Other ways of getting rid of these floaters

Laser surgery is another method of treating these eye floaters. For this purpose, a laser that goes under the name of YAG is used. But, how effective this method of treatment is, is still left to be confirmed.

Vitrectomy is yet another surgical process that can be done to get rid of these floaters. But the truth is that surgery is not recommended to take care of this problem as even after surgery, the issue could come back. So, if you are looking for an eye floaters cure, the best thing for you to do would be to consult your doctor.

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How To Buy Colloidal Silver The Right Way


By Kristen Baird


Despite the huge efforts by our top medical researchers and physicians, there remains a part of this word of diseases that are yet to be discovered. The good news is, we now have modern modes of treatment that addresses a lot of the common illnesses we have today. There are those however that remains to be solved.

With the emergence of modern medication comes alternatives as well which can be proven and not by the public and experts. The question on how to buy colloidal silver Washington DC for instance, emerged out of the demand from people for the substance. Colloidal silver is said to have a variety of uses, but while users agree, experts has long dismissed the fact that it is indeed safe for everyone.

The fact that they are allowed to be sold in the market speaks of how valid they are. Still, the risk that they carry is big enough to discourage some who have serious health problems from taking them. If you are considering this as a good dietary supplement or as an antibiotic, then might as well look at the factors to think about prior to purchasing one.

Consult your doctor. First of all, you need to inform your doctor of any plans that involves taking in the substance. Your physician knows better about the stability of your present health and any attempt to take in more than your present medication can be harmful. Be sure to discuss the issue with him prior to buying anything.

Check the PPM. This is important to make sure that you are buying the substance that has a good concentration. Ideally, it should contain 10ppm and approximately 85 percent colloidal silver. Higher than this value is too strong and might create complications.

Ensure the purity of the substance. The most ideal pick is a solution that is clear. Dark colored ones indicate the presence of other substance like additives and stabilizers. The clearer the solution the better. While some of those added substance are claimed to be safe, they have other ingredients that can affect the natural effect of the product.

Size. A component that has the size of an atom is preferable than the bigger ones. This is due to the fact that smaller sized ones can easily get into the core of the viruses to destroy them ultimately. Compared to the bigger particles that may need the assistance of other chemicals to stick to the colloidal silver, smaller ones do not need to.

Credibility of the manufacturer. Just like how you buy a gadget, you do not want to have a product produced by an unknown brand. You feel more secured when you get it from a company that has a solid track of producing quality products. When buying colloidal silver, go for a shop or a store that is reputable and have been in business for long. Check the manufacturer as well. Go for the legal ones permitted to operate.

One thing you have to remember is that this is not the same to the medicines that doctors prescribe you. It can have similar effect to the health supplements that we have but generally, they are not considered as substitutes. Be mindful.




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Measurement and Dispensing of Progressive Lenses



Progressive addition lenses are made with the help of specially designed front surface curves. These changing surface curves cause the lens to gradually increase in plus power, beginning in the distance portion and ending in the near portion. These variable-powered progressive addition lenses should, according to design, permit clear vision at any given viewing distance merely by positioning the head and eyes.




PROGRESSIVE LENS CONSTRUCTION

Like a segmented multifocal, a progressive addition lens, or PAL, has certain distinct areas to the lens. But those areas in a progressive lens are not visible. The upper portion of the lens is basically the distance portion. The near portion of the lens, where the full near addition power is found, is down and inward. In between the distance and near portions is a progressive corridor where the power of the lens is gradually changing.

FRAME SELECTION

When choosing a frame for someone wearing a progressive addition lens, there must be enough room for the progressive zone and near portion. Because these areas are not visible like a bifocal segment is, they may be unintentionally cut off. This was a problem when progressive lenses were first introduced in the United States. At that particular time, many frames had narrow vertical dimensions. When progressive lenses were dispensed in these frames, much of the near portion was cut off. Since people could not see very well up close, dispensers falsely concluded that the lenses were no good. So frame selection is an important part of fitting progressives.

Here are some important points to keep in mind:

 1. The frame must have sufficient vertical depth. Each lens type has a manufacturer-recommended minimum fitting height. The recommendations of the lens manufacturer should be followed.  Standard minimum progressive addition lens fitting heights will vary, going down to a low of about 18 mm. If there is not enough vertical depth to allow the minimum fitting height, then either a different frame must be chosen, or a special short corridor lens that is designed for frames with a narrow vertical dimension should be used. Otherwise there will not be enough reading area left.

2. The frame must have sufficient lens area in the lower nasal portion where the near progressive optics are found. Sometime the frame has a large enough “B” dimension, but the shape is cut away nasally. Aviator shapes are an example of this type of frame.

3. The frame should have a short vertex distance. The closer the frame is to the eyes, the wider the field of view will be for both reading and distance vision.

4. The frame must be able to be adjusted for pantoscopic angle when facial structure will allow. A 10- to 12-degree angle is recommended. The intermediate and near fields of view are effectively wider when the progressive and near zones are closer to the eyes.

5. The frame must have sufficient face form. This also allows a wider viewing area through the progressive corridor.

CHOOSING THE RIGHT TYPE OF PROGRESSIVE

Most progressive lenses are made for general purpose wear since the majority of wearers only have one pair of glasses. Although general purpose progressives work for most people, here are some additional considerations:

1. What type of general purpose progressive is appropriate? It is possible to choose a certain type of general purpose progressive to fi t the needs of the wearer.

2. Does the wearer have a significant amount of cylinder power in the prescription? If so consider using a lens design that is atoric. Using such a design will reduce the amount of unwanted distortion that will otherwise be present in the periphery of the lens.

3. If the vertical “B” dimension of the frame is small, choose a short corridor progressive lens. A short corridor lens is still used for general purposes, but is meant for this type of frame.

4. Does this person use a computer a lot? Do they work in a small office environment where intermediate vision is important? If so they may need a near variable focus occupational progressive lens. This type of lens is made for closer viewing distances through the top of the lens and has both a wider intermediate progressive corridor and a wider near-viewing area. An occupational progressive lens should not be used as a person’s only pair of glasses, unless this person does not need a distance prescription and would otherwise only be wearing reading glasses. These lenses should be considered for a second pair of glasses.





MEASUREMENT AND ORDERING

A progressive addition lens has a rather narrow progressive corridor linking the distance and near portions of the lens. It is through this corridor that intermediate vision takes place. Unless the eye tracks down the exact center of this corridor, the lenses do not work very well. Therefore PD measurements must be taken for each eye individually and an exact vertical height specified for each eye.

To help make sure the progressive corridor is where it should be, the manufacture uses a fitting cross. The fitting cross is usually 4 mm above the start of the progressive corridor and is intended to be placed exactly in front of the wearer’s pupil center.

Standard Method for Taking Progressive Lens Fitting Measurements

1. Measure monocular distance PDs. The recommended method is to use a pupillometer.

2. Fit and fully adjust the actual frame to be worn. This includes pantoscopic tilt, frame height, vertex distance, face form, and nosepad alignment. Make certain the frame is straight on the face. If the temples are not adjusted, hold the frame in place while measuring so that it will not slip down the nose.

3. If the frame does not contain clear plastic lenses or the wearer’s old lenses, place clear (nonfrosted), transparent tape across the eyewire of the empty frame.

4. The dispenser is positioned with his or her eyes at the wearer’s eye level. With the wearer looking at the bridge of the fitter’s nose, the dispenser draws a horizontal line on the lens or tape. The line should go through the center of the pupil. This is done for both right and left eyes.

5. Place the frame on the manufacturer’s centration chart and move it left or right until the bridge is centered on the diagonally converging central alignment pattern. Then move the frame up or down until the marked horizontal pupil center lines are on the chart’s horizontal axis. Mark the previously measured PD for each eye as a vertical line that crosses the horizontal one.







6. For first one lens, then the other, read the fitting cross heights from the chart. Record these fitting cross heights and the monocular PDs on the order form and in the wearer’s record.






7. Check the size and shape of the frame on the lens picture portion of the centration chart. Do this by placing the frame on the lens blank circles of the centration chart so that the cross on the glazed lens overlaps the fitting cross on the picture.





8. Send the frame to the laboratory with the marks still on the lenses or tape.


DISPENSING PROGRESSIVES

Validation on the Patient

Once the prescription has proved to be correct, it is adjusted to fit the wearer. Normal frame fitting rules apply. In addition, to provide the maximum possible field of view, adjust the frame for:

1. A small vertex distance

2. Adequate face form

3. A maximum pantoscopic tilt that still looks appropriate for the wearer.

 With the visible markings still on the lenses, also check the following:

1. The fitting crosses should be in front of each pupil center. (Ensurance of the placement of the fitting crosses is especially important when the two eyes are not at an equal vertical height.)

2. The horizontal dashes on the lenses should be exactly horizontal and not tilted.

Removing the Visible Markings

The visible marks that are on a progressive addition lens when it comes back from the laboratory are non-water soluble. To remove them, use alcohol or an alcohol swab. Sometimes these marks can be stubborn. Some say that stubborn markings will come off easier if the lens is first heated in the hot air frame warmer. The alcohol may work better on the heated mark.

Instructing the Wearer at Dispensing

Adapting to progressive lenses can be made easier for a new wearer if the characteristics of the lenses are demonstrated at the time they are dispensed.

To demonstrate the full range of progressive lens versatility, hold a near-point chart at eye level at an intermediate distance. Instruct the wearer to look directly at the near-point card through the distance portion. Next ask the patient to tilt his or her head back until the letters on the card are clear. Gradually, bring the card closer to the eyes as the head is tilted still farther back, demonstrating the full range of viewing available.

TROUBLESHOOTING PROGRESSIVE PROBLEMS

Most problems encountered by progressive lens wearers are a direct result of basic fitting principles being ignored. Here are a few typical errors that should never occur, but do.

One monocular PD is correct; the other is wrong. This happens when the monocular PDs are done with a ruler or by marking the PD measurements on the lenses, and the fitter uses only one eye to measure both lenses.

The PD is given as a binocular PD, rather than as two monocular PDs.

Fitting cross height is measured for one eye, and the same measurement is written down for both eyes. Fitting cross heights must be individually measured for both eyes.


When a wearer does come back with a complaint, the most straightforward way to check for possible problems is to first put the progressive markings back on the lenses and see if they are correct in relation to where they should be when the prescription is worn. Often the problem will be obvious.




To verify distance power on a progressive addition lens, the lens must be positioned
with the arc around the lensmeter aperture as shown. This ensures that the power
reading will not be affected by the changing power in the progressive zone.







To verify prismatic effect, the lens is verified at the prism reference point (PRP)
located by the central dot directly below the fitting cross.







When both distance and near powers are low, the near power may be verified using the back vertex power as shown in the figure. In any case the near power must be read through the
near circle. The correct method, however, is to find the near add using front vertex powers.