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AUGUST 2003 NO. 18
In this issue Tony Haas, our current President, writes his last letter from the President's desk. Tony will have served the maximum of four years as President in September and at our Annual General Meeting to be held in the Foundation of the Blind premises at 121 Adelaide Road in Wellington, he hands over to a newly elected President.
There is much more eye research being undertaken in New Zealand these days and we feature some of this in the Research section of this issue. Some of it is researching various aspects of Cataracts, a common occurrence in many of our members. Some of it is helping to detect diabetic retinopathy in Auckland, particularly in Maori and Pacific islanders, preventing them from going blind with this condition as well as having diabetes, which is a life changing disorder in itself. Wellington Optometrists also have a diabetic screening programme in Lower Hutt to do the same thing. It is one of Retina's goals to prevent blindness in New Zealand wherever it is possible and the Society has been concentrating on this aspect for the past year. Our Pacific Blindness Prevention Initiative has put our Society firmly on the map.
At its teleconference meeting on 18th August the Committee appointed Dr Rachel Barnes to be a member of the Retina Scientific & Medical Advisory Board (SMAB). Her talents as a New Zealander trained in ophthalmology in this country who has had further research experience overseas are very welcome. She writes her first report for the society after her attendance at the ARVO International Conference held in May at Fort Lauderdale, U.S.A.
We start a new series called Your Questions Answered in this issue. I hope you will take advantage of this generous offer from our Scientific & Medical Advisory Board to answer your questions, by sending me all the questions that you wish you knew the answer to, about your or your family's retinal condition, so that all who read this newsletter may benefit from the experts' answers.
With this newsletter are copies of two Retina NZ brochures - an updated version of our Society pamphlet in larger print and a new release "Coping Strategies" - Coping with some sight loss or a degenerative retinal eye condition.
June Ombler, Editor,
207 Forbury Road, St Clair, Dunedin.
Phone: (03) 455 8813 Email: firstname.lastname@example.org
FAREWELL FROM THE OUTGOING RETINA NZ PRESIDENT's DESK
The contribution of new talent in Retina New Zealand's team to the launch of the Save our Sight campaign at Parliament shows what the society can do.
Kaye Newton, a nominee to succeed me as President on Sept 20, was able to present the society and some of its partners to an influential audience of Parliamentarians, Ministry of Health and other officials, non government organizations, media and others united in their interest in the Save our Sight message.
Behind the scenes, the fact that the event was being held and that Associate Minister of Health and Minister for Disability Issues Ruth Dyson was going to speak, efforts were being made to remove the blockages facing the Pacific Peoples Blindness & Diabetes Initiative. The setting provided the circuit breaker, and talks between the initiative and government officials were got back on track.
The formal SOS launch, and the preparatory work delegated to Retina Wellington branch's established and new members, deepened the partnership with the leadership of such agencies as the NZ Association of Optometrists, RNZFB, Save Sight Society, Diabetes New Zealand. It opened channels to others ranging from opposition health spokespeople to Grey Power. They, and other relationships, are valuable assets for Retina New Zealand to work with if it is to address met and unmet needs amongst people with threats to the back of the eye.
The successful Parliamentary launch showed how Retina's capability can be expanded by bringing in new, older and younger talent, as has happened in Wellington with Allan Jones in the chair, and a committee that now includes Denise Keay, a Retina but non RNZFB member, who added her public policy skills to the mix that made the event. These people were not active in Retina a year ago, and they are not the only new talent around who have or who can make a difference if given roles to perform.
The return to Retina New Zealand activities of Lynn Keogh in Dunedin, as Chairperson of Retina Otago/Southland, is another sign that a new generation is stepping into the society's leadership. The southern society has significant responsibilities to Retina with its delegated responsibility for the consumer perspective on the research programme - a part of Retina's work unfunded by RNZFB, and potentially able to attract many resources (financial and other) that can give people cause for hope.
There are several examples of new talent in the wings in Auckland that the society needs to enable it to provide effective service in the northern population centre. Camille Guy's journalism can help inform people who are best reached by mass media. The Tongan Health Society, Akamarama and individual Tongan and Samoan leaders Retina works with in the Pacific initiative could assist and be assisted by Retina New Zealand if it wants to help population groups at risk.
The capability in and behind Christchurch based Kaye Newton is partly over to the executive and members to mobilize for the thrust forward by the incoming leadership.
The new talent I have singled out in my farewell newsletter as President are, I suspect, the tip of the iceberg of talent in Retina's membership.
One of my great failures in four year's of President was my failure to connect with many of the members outside channels like this column. So my farewell message now is to urge you to make yourself known to the branch leadership in your area, put your toe in the water, and get and gain the privilege of helping yourselves and others.
I have gained a lot as an individual from my time in the society - the essence was that I learnt what peers and experts thought possible and not. I was able to measure my own performance against others, learn about ideas to help me cope, and apply them.
The best technique I learned was to use the information technology more - I will. It liberates me when I thought I was going to keep losing access to information - which for a humble wordsmith, is a threat. The computer, with software and power tailored to my needs, is my opportunity. Now I want to use the gift of time to upgrade my IT skills.
I wish you all the best, as I retire into Retina's background, ready to refocus my attention.
Anthony Haas, 12 August 2003
REPORT ON RETINA INTERNATIONAL SCIENTIFIC AND MEDICAL ADVISORY BOARD MEETING HELD IN FORT LAUDERDALE, MIAMI IN MAY 2003
From Dr Rachel Barnes, Auckland Ophthalmologist who attended on behalf of Retina NZ
In May of this year I was privileged to attend the annual Retina International Scientific and Medical Advisory Board meeting at ARVO. It was a great experience to share a table with so many of the world's leading researchers in the retinal field. The discussions were very broad in scope and covered many different areas of research. I would like to take the opportunity to share a couple of presentations that I found particularly interesting.
One highlight of the meeting was Matt La Vail's update on the current state of research into medical treatments for retinitis pigmentosa. There are numerous different types of agents being investigated, and he pointed out a useful synergy with glaucoma research in the potential for agents that protect and restore nerve function to play a beneficial role in both diseases.
One agent that has been investigated in a randomised controlled trial is
Docosahexaenoic Acid (DHA) - a type of omega 3 fatty acid. Hoffman and colleagues reported their findings at ARVO this year of their 4 year study of males with X-linked retinitis pigmentosa who received either 400 mg of DHA daily or placebo. They found that there was a beneficial effect on electro-physiological measures of retinal function with slower deterioration in the treated group. However, there was no significant effect on visual field or acuity. While the authors rightly point out that further research is needed to establish effective dosages and beneficial effects in retinitis pigmentosa, it would seem very reasonable in the meantime to eat a diet rich in omega 3 fatty acids, especially as biological safety concerns and adverse events associated with their intake are negligible. Good sources of omega 3 fatty acids are oily fish such as salmon and tuna, and flax seed oil.
Another presentation that I found very interesting was Raymond Lund's talk on Schwann cell transplantation. Schwann cells are supporting cells in the peripheral nervous system, and are not normally found within the eye. However, it is known that they produce a number of growth factors that have been shown to be useful in cell culture and animal model experiments in preserving photoreceptor function. The idea is that by transplanting these cells into the eye, an ongoing source of growth factors will be produced and may therefore benefit visual function. So far early results in rat and mice models of retinitis pigmentosa have been very encouraging, although there does seem to be a gradual loss of the effect. A group in China has performed a Schwann cell transplant on a human volunteer with retinitis pigmentosa. The very early electro-physiological results in this patient have been somewhat disappointing, but it will be very interesting to see what progress the patient makes over time.
OBESITY MAY WORSEN EYE DISEASE COMMON IN OLD AGE
By Linda Carroll, New York (Reuters Health), 9 June 2003
Obesity may increase the risk that the eye disease macular degeneration will worsen, a new study shows. But physical activity may reduce the risk, according to the study published in the Archives of Ophthalmology.
Age-related macular degeneration is a condition in which the macula, a spot at the center of the retina, degrades with time. As the macula deteriorates, it becomes increasingly difficult for people with the condition to focus on objects directly in front of them. Peripheral vision is generally unaffected.
Approximately 30 percent of people who are 75 years or older have some degree of macular degeneration. Most have a mild form, however.
No one knows exactly why the macula begins to degenerate, but some risk factors have been identified, according to the study's lead author, Dr Johanna M. Seddon, an associate professor at the Harvard Medical School and director of the epidemiology unit at the Massachusetts Eye and Ear Infirmary, both in Boston.
These factors include cigarette smoking, high levels of dietary fat and low levels of antioxidants, Seddon said in an interview with Reuters Health. Studies have shown that antioxidant vitamin and mineral supplements can reduce the risk of disease progression and vision loss, Seddon said.
Scientists suspect that a possible cause for the disease could be compromised blood flow to the retina, according to Seddon. For this reason, Seddon and her colleagues wanted to look at some of the factors that are also linked with the artery disease atherosclerosis.
For the new study, researchers followed 261 patients who were at least 60 and had signs of mild age-related macular degeneration. Often patients with mild disease have no obvious symptoms, Seddon said. But a doctor can see signs of deterioration in the retina.
The patients were followed for an average of 4.6 years. The patients' height, weight and blood pressure were measured annually. The patients performed waist and hip measurements themselves.
Ultimately, the researchers determined that overweight and obese participants were more than twice as likely to have their macular degeneration worsen to the advanced form of the disease during the course of the study than those who were thinner. A larger waist-to-hip ratio was also associated with an increased risk of disease progression.
But patients who exercised vigorously at least three times a week had a 25 percent reduction in the risk that their disease would worsen.
Seddon suggests that anyone in their mid 50s with a family history of macular degeneration have their eyes tested for this condition.
SOURCE: Archives of Ophthalmology 2003;121:785-792.
AUCKLAND CATARACT STUDY GOING STRONG
Press release from the University of Auckland's Faculty of Medical and Health Science, 26 June 2003
Auckland's elderly are providing clues to some of the secrets of the world's most common cause of blindness - cataracts.
Professor Charles McGhee, the Chair of Ophthalmology at The University of Auckland's Faculty of Medical and Health Science, leads a team studying cataracts in the Auckland metropolitan area. The research began in 1999 with a study based in the Rodney district, since then the project has evolved and led to a variety of spin-off projects.
"Cataracts are not only a common cause of blindness, but are thought to indirectly shorten people's lives through a reduced quality of life and the risks of visual impairment."
"Cataracts are a huge problem throughout the world, and although New Zealand has representative numbers of people with the condition, the cases do seem to be more severe. This is partly connected to the high rate of diabetes in New Zealand, particularly amongst Maori and Pacific Island people, which leads to earlier diabetic cataracts."
Professor McGhee, who is also the Clinical Director in Ophthalmology for Auckland Healthcare, says New Zealand has a high rate of hard nuclear cataracts, the most severe form of cataracts, which are generally less common in developed countries.
"When I worked in Scotland I'd probably see one such advanced hard cataract a month, whereas here I see three or four a week. Partly this is because in the UK and the USA people present with their cataract at a much earlier stage," he says.
The Auckland Cataract Study started in 1999 and follows 500 people from the Auckland region. The research has highlighted the link between diabetes and cataracts and shown that some people are more likely to have the condition than others. Women are generally more susceptible because of longer lives, as are diabetics and Maori and Pacific Island people.
The subjects also had a high level of other diseases: "More than half of those in the study had high blood pressure, or diabetes, or they'd had a stroke in the past. But this is partly a manifestation of their age, as the mean age of the participants was 77," he says.
Initially the participants had been on waiting lists for a cataract operation for up to three years - something Professor McGhee and his team quickly turned around.
"In a joint initiative, we assessed patients and performed 500 cataract operations between the university and hospital ophthalmology departments and got the waiting list down to under six months. A spin-off from that was being able to involve patients in ongoing research into the causes of cataract and the outcomes of contemporary no stitch small incision surgery," he says.
The participants have been closely followed post operation and it was found that 98.5 percent of patients had significant visual improvement post operation. They also reported a significantly improved quality of life.
The team is now looking to extend the study to further define factors that predispose people to cataracts.
"We are using the lens tissue that is routinely removed to look at the nature of the cataract so that we can work out the genetic protein, or structure of the cataract. That could theoretically help us to develop a medicinal or drug cure rather than a surgical operation for cataracts in the future," Professor McGhee says.
The team is also examining the intra-ocular lenses (implants) which replace the cataract to enable the person to see. Professor McGhee says it is important to discover whether implants can be improved to minimise aberrations.
"The human eye has evolved over millions of years to try and minimise distortions and we are replacing that with a man-made acrylic lens which will obviously have its own minor optical distortions."
"The Auckland study, which is the largest of its kind ever undertaken in New Zealand, is providing us with some excellent data for trying to come up with more effective ways of treating cataracts," Professor McGhee says.
Six senior clinical and laboratory researchers continue to be involved in the Auckland Cataract Study at The University of Auckland.
FIRST DRUG THERAPY FOR RP's TO ENTER HUMAN SAFETY STUDIES
From the U.S. Foundation Fighting Blindness, 26 July 2003
The Foundation Fighting Blindness recently learned that the U.S. Food and Drug Administration (FDA) approved an application from the biotechnology company Neurotech, to begin a phase 1 human clinical trial to test the safety of a delivery device containing a drug to treat patients with end-stage RP.
Clinical testing is scheduled to begin in the fall of 2003.
This safety study represents the first clinical trial of a drug therapy for RP.
One of the major challenges to treatment of retinal disease has been the ability to deliver therapeutic drugs directly to the retina. Neurottech, based in France and Rhode Island, developed Encapsulated Cell Technology (ECT), which enables controlled, continuous, long term delivery of a drug called ciliary neurotrophic factor (CNTF) in patients with end-stage RP.
The Foundation Fighting Blindness (FFB) was an early supporter of the use of this technology for retinal diseases.
Dr Gerald Chader, Chief Scientific Officer of FFB said, "Today's announcement is one we've all been anxiously awaiting. CNTF and several other drug therapies have shown promise in a wide variety of animal models with RP. However, none of these drugs can pass through the blood/retina barrier, making traditional drug delivery with systemic injections or pills ineffective. Neurotech's implantable ECT device may have at last broken through this previously formidable barrier."
The ECT device is a testament to The Foundation's perseverance in advancing retinal disease therapies. The ECT device was originally developed for use in treating Lou Gehrig's disease and cancer. It was during these studies that FFB realized that the ECT might be adaptable to treat diseases of the retina. FFB encouraged Neurotech to test the device with CNTF in RP animal models. Through FFB's innovative Medical Therapy Program, which reaches out to industry to encourage and foster vision research, FFB provided funding to support these important tests.
ECT consists of a very small capsule containing retinal pigment epithelial cells (RPE) that have been genetically modified to produce CNTF. The capsule has very small pores that allow oxygen and nutrients to diffuse in to sustain the RPE cells and also allow CNTF to diffuse out. The tiny pores prevent the modified RPE cells from escaping and protect the cells from the body's immune system.
CNTF was chosen for its potent ability to delay the death of retinal photoreceptor cells in animal studies.
Because CNTF has not been tested in patients before, the first phase of this clinical trial will test the drug and the ECT device in 10 pre-selected patients with end-stage RP. In this way, the safety of the treatment can be evaluated without risk to existing vision. If all goes well in this phase I safety study, a phase II trial would then test the ability of the treatment to preserve vision in sighted RP patients. The timing of future trials is not yet known, and at this time patients are not being selected for future trials.
ECT and other emerging drug delivery devices could open the door for several survival factors that, like CNTF, have shown promise in treating the entire spectrum of retinal degenerative diseases. We hope to soon see other drug therapies join CNTF in clinical trials. There's still more work ahead, but The Foundation's efforts are clearly bearing fruit.
EYE RESEARCH BENEFITS FROM PHOTOGRAPHY SKILLS
From Auckland District Health Board Newsletter Nova, August 2003
Photographers from Auckland DHB's Department of Medical Photography and Graphic Design have gained certification to provide diagnostic images for two externally-funded international drug research trials addressing blindness.
Diabetic Retinopathy trial
Diabetes is the leading cause of blindness in New Zealand. That is because diabetes damages blood vessels of the Retina (back of the eye) - termed Diabetic Retinopathy - leading to haemorrhages/oedema within the eye that may result in loss of vision. The DIRECT programme is an international multi-centre trial of the drug Candesartan, which is primarily a blood pressure reducing agent. Candesartan may prevent the formation of abnormal blood vessels. If these abnormal vessels can be detected at an early stage, loss of sight can be prevented. Previous studies have demonstrated that there appears to be a beneficial effect on diabetic retinopathy outcome with drugs that work in the same way as Candesartan. This trial aims to prove whether that benefit is conclusive.
Auckland DHB is involved with this trial through its Diabetes Service and its director Dr Paul Drury is principal investigator.
In the study, patients' degree of diabetic retinopathy is determined by strictly standardised retinal photographs during the trial period of three to four years.
Auckland medical photographers Alex Fraser, Janine Ford and Sarah Harper have been accredited by the Retinopathy Grading Centre at Hammersmith Hospital in the UK to take the retinal photographs whose evaluation will determine the study outcome.
Trial to treat age-related macular degeneration
A research study for pharmaceutical company ALCON involves the use of a new drug, called Anecortave Acetate, to treat Age-related Macular Degeneration (ARMD). This condition is one of the leading causes of blindness in older people, resulting in total loss of central vision.
Alex Fraser has been certified by the Digital Angiography Reading Centre (DARC) in New york for this study and Janine Ford's certification is expected to follow shortly. They are required to provide two kinds of dye-injected photographs: fluorescein angiography (FA) and indocyanine green (ICG). The high-quality, standardised imaging in these studies provides the information that is needed in order to treat macular degeneration with one of a number of new options.
Angiograms from Auckland are transmitted to DARC in New York over a special internet link within hours of the procedure being performed. Within two days the results of the angiograms are faxed back to ophthalmologists at Auckland Hospital.
Auckland Ophthalmology is the largest eye unit in New Zealand and is closely associated with the Department of Ophthalmology in the University of Auckland and its research programmes.
YOUR QUESTIONS ANSWERED
The following letter, received from one of our members, starts a new series. It was referred to our Scientific & Medical Advisory Board (SMAB) for comment and we print below a very informative article in reply to her query. The SMAB have generously offered to answer a member's question in each forthcoming newsletter. The question must be a general and not personal one, so that we can all benefit from the experts' answers. So please send your question to the Editor, June Ombler, 207 Forbury Road, St Clair Dunedin or email it to email@example.com who will refer it to Retina's SMAB to answer. If you do not wish your name to be recorded, send a nom de plume. I need your real name and address as well but this will not be printed. EDITOR.
As an extreme myope I was very interested in the profile of Peer Support Co-ordinator Elizabeth East (and her experience with severe myopia) in the August 2002 newsletter.
Since joining Retina in 2000 I have met members with a variety of retinal conditions as a result of severe myopia. I also know several people who (like me) have had retinal detachments and are pleased to hear that an organisation like Retina exists. When I had my first spontaneous detachment at age 32, I did know that very short-sighted people were at risk, but had thought the risk did not present until late middle-age. A registrar at Wellington Hospital said, "Well, short-sighted people often have ropey retinas - we don't really know why, and spontaneous detachments can occur in younger people too." (At that stage the eye in which I had the detachment required about 15 or 16 dioptres of correction, and was my better eye.) One theory I heard around that time is that retinas are closely related to brain tissue, brain tissue isn't elastic in the way most body tissue is, and the elongated eye of the extreme myope stretches the retina so much that it tears; once torn detachment is inevitable. This sounds logical to me, but whether it was valid then and is still now (over 20 years and more detachments later), I don't know.
Myopia is a common condition, but many people do not realise that while most myopes' degree of short-sight stops increasing post-adolescence, a much smaller percentage continue to experience ongoing increase through their twenties and even into their thirties. Though short sight is hereditary, extreme myopes can feel like freaks within their own (moderately short-sighted) families. I've also heard that extreme myopes may be at higher than average risk of MD, glaucoma, cataracts, etc. And cataract operations can pose particular problems for extreme myopes anyway because of the recognised risk (to anyone undergoing cataract removal) of a retinal detachment as a result of surgery.
"Why do some peoples' eyes simply keep on elongating and do themselves serious damage?"
RETINAL DETACHMENT IN MYOPIA
Sarah Welch, MBChB and Andrea Vincent MB ChB, FRANZCO
Department of Ophthalmology, Auckland Hospital
Myopia is the medical term for what is commonly called short-sightedness. If someone is myopic their eyes do not focus clearly for distance vision although they may be able to see well close up. Myopia can be corrected with spectacles or contact lenses or, in some cases, laser refractive surgery. Myopia is usually classified by the strength of spectacles required to correct it, measured in dioptres. Myopic eyes requiring 6 dioptres or more of correction are classified as highly myopic or severely myopic.
In New Zealand about a quarter of the population are myopic but most have mild or moderate myopia and do not have severe myopia. Much research exists into the cause of myopia, and like many diseases of the eye, myopia is likely a result of interacting genetic, environmental and epigenetic traits. The fact that myopia tends to run in familiae and is more common in certain ethnic groups strongly suggests a genetic cause. As yet, no single gene has been identified as causing myopia, but up to four loci are identified. Recently, linkage was demonstrated to the long arm of chromosome 17 in an autosomal dominant pedigree with high myopia. Linkage has also been established to loci on chromosome 18p, 12q, and 7q. There has been research suggesting prolonged close work as a child or a teenager, (for example reading or studying), may induce myopia to some extent, but this is not proven. A recent study also suggested night-lights for children caused myopia, but no further evidence has substantiated this.
Myopia is sometimes associated with some other eye diseases, particularly the connective tissue disorders. This group of diseases including Marfans syndrome, Ehlers-Danlos and Sticklers syndrome, are characterised by weakness of connective tissues, specifically collagen and fibrillin. These proteins are significant structural components of the ocular tissues. Mutations in the genes encoding these proteins account for the defective strength and altered properties of the tissue. These diseases provide us with the greatest clues and understanding of pathologic myopia. As yet, there is no proven method for stopping the progression of myopia.
Most myopes have no problems with their eyes, apart from requiring distance correction. However those with extreme myopia may develop other problems, with increasing frequency and severity as the axial length increases. In severe myopia the whole eyeball is elongated (increased axial length). All layers of the eye may be stretched and thinned in high axial myopia including the outer wall, the sclera, as well as the retina. Because of this, in high myopia, there is a greater risk of retinal detachments than in the normal length eye. As mentioned, evidence from the connective tissue group of disorders suggests a structural weakness in the tissues of the eye, which allows the pathologically myopic eye to stretch and thin with time.
A retinal detachment occurs in high myopia when there is a break in the thinned, stretched retina. Fluid gets in under the retina, and it peels off the inside of the eye like wallpaper off a wall. No treatment is currently available to prevent this thinning, however, it is important to be aware of the symptoms of retinal detachment. The three main symptoms are: an increase of floaters or black spots in the vision of one eye, a curtain obscuring the vision in one eye, or bright flashing lights in the vision of one eye. These may occur independently or sequentially, and if they do, an ophthalmologist or optometrist should be consulted urgently. Early repair of retinal detachments frequently has a good visual outcome, but left untreated, retinal detachments can be blinding.
Severely myopic eyes may also be affected by other changes to the stretched and thinned retina. Occasionally the retina, or its underlying membranes, may break because of extreme thinning. As a result there can be bleeding on the retina, long term scarring, or the formation of new blood vessels, all of which can affect vision. It is recommended that high myopes, (over 6 dioptres), have an annual dilated retinal examination by an optometrist or ophthalmologist. These eye professionals should also be consulted if any alteration in the vision is noticed.
SETTING THE SIGHTS ON BETTER EYE CARE
From Health and Disability News, Issue 4, July 2003
A man already blind in his left eye owes the sight in the right eye to a new free retinal screening set up for diabetics in Greater Wellington and the Wairarapa. If he had not had the problem detected and immediately treated, doctors believe he could have been totally blind within weeks.
This man is one of 4,000 people screened in the first year of the new screening programme developed by the Wellington Independent Practitioners Association (WIPA) with the New Zealand Association of Optometrists. In a New Zealand first, optometrists provide screening in the Wellington, Hutt Valley and Wairarapa District Health Boards' areas.
All people known to have diabetes are referred for screening. An optometrist takes a photograph of the person's eyes and within minutes they can sit at a computer with the optometrist and be shown a photograph of the back of their eye. They can then discuss the condition of their eye and what needs to be done to maintain their sight.
Many people have been referred on to hospital eye clinics for treatment, with others placed on a recall system to ensure they are screened again in time to pick up any deterioration in their retina.
Blindness in people with diabetes can occur suddenly with no warning. Diabetic changes can be well advanced before vision is affected, and treatment is often not an option at this stage. This simple test can prevent irreversible damage and loss of sight.
THE PARROT VOICE MATE
I came across the following message on an email list and as it sounded so useful for people with low vision or no vision, or even people who are not yet registered as legally blind, I thought I would check whether the Foundation of the Blind stocked it. They do and after the following email message which details some of its good features, a summary of the Foundation's listing of the Parrot Voice Mate in its catalogue follows.
If this seems rather expensive, how about suggesting to your family that they give you some money towards it instead of a Christmas or birthday present. EDITOR.
"One of the most useful devices I own is something called A Voice Mate. It is several things in one. It is a digital (tapeless) note-taker that allows me to record up to 40 minutes of messages and play them back anytime, anywhere. I use it for everything - grocery lists, airline/bus schedules, messages, directions - you name it.
The Voice Mate also has a built-in telephone book that allows me to speak someone's name, and it gives me that person's telephone number back in my own voice. It then produces the touch-tones necessary so that the phone number can be automatically dialled for you right through your telephone's handset. The Voice Mate also contains an Appointment Scheduler, allowing you to schedule appointments weeks, months or even years in advance. It really lets you keep track of things.
It also has a Talking Calculator built-in, allowing you to do various arithmetic functions, including percents. It has memories as well.
The unit's Control Panel allows you to customize various features, including the speed at which it speaks and the loudness of the unit's voice.
What's really unique about the Voice Mate is that it utilizes Voice Recognition (VR) technology. You speak the name (in the phone book) or the appointment (in the scheduler) and it jumps right to and returns the information you're looking for - in your own, natural voice."
George Cassel, U.K.
TR0119 Parrot Voicemate - Third Generation, now running on version 3.6
Latest Parrot model as at March 2003. Voice input - Voice output - Voice search. Every key, every function and every option is spoken. A compact (5.3in x 2.7in x 0.6in) and lightweight (5.25 ounces) voice interactive unit that allows the use of its many functions through voice commands and responses. It offers a telephone directory, address book, voice notepad, meeting planner, musical and talking alarm clock, talking calculator and facility for a PC interface by adding the option Parrot Datalink for storing data and updating software via the internet. Earphone included. Has 40 minutes of recording memory. Uses 4 AAA batteries (included). Price for members $468.45, for non members $624.60.
TR0039 Parrot Datalink
Comes with a serial cable and software so that you can back up your information onto a computer and update the Parrot's software via the internet. For use with the Parrot Voicemate third generation only. Price for members $102.60, for non members $136.80.
For further information contact David Cole, Equipment Services, RNZFB, on
Freephone 0800 24 33 33, press option 4.
ASSET TESTING REMOVED
From DPA Bites, April/May 2003
Asset testing of older people in long-term residential care will be progressively removed as from 1 July 2005, Disability Issues Minister Ruth Dyson, who is also Associate Health Minister has announced.
From 1 July 2005, single people and couples with both partners in care will be able to keep up to $150,000 in assets (including both property and savings) before their assets are used to contribute to the cost of their care, up from $15,000 and $30,000 respectively.
The Minister said the decision was in line with the government's 1999 election promise and was based on human rights considerations. "It is unfair that people aged 65 and over are required to use up their assets to contribute to the cost of their care, whereas younger people are not."
The policy is expected to cost $103 million in 2005/2006, rising to $163 million in 2010/11 and $345 million in 2020/21. About 31,000 people, or 7 per cent of people aged 65 and over, are currently in long-term residential care. The new policy will apply to all new admissions and to people already in care who are not currently eligible for a residential care subsidy.
NOTICE FOR AUCKLAND BRANCH MEMBERS:
Although some Auckland Retina members are active in the national organization, we do not function as an Auckland regional group. This is partly because Auckland is so large. And travel so time consuming. Since some members use computers and have access to email, it would be possible to link up with each other that way. Would any Aucklanders interested in doing that please contact Camille Guy at firstname.lastname@example.org
REMINDER ABOUT THIS YEAR'S NATIONAL ANNUAL GENERAL MEETING:
This year's Retina NZ Inc. National Annual General Meeting, hosted by Wellington Branch, will be held at the premises of the Royal NZ Foundation of the Blind, 121 Adelaide Road, Newtown, Wellington on Saturday 20th September 2003. The rooms will be open at 10.00 am with morning tea available.
The day will begin at 11.00 am with Camille Guy speaking about "Computing Services for the Sight Impaired - What is available and How to access it", followed by a speaker from the Adaptive Technology Unit of the RNZFB.
During lunch provided by Wellington Branch there will be displays from relevant trade organisations.
At 1.30 pm, Russ Finnerty, National President of Diabetes NZ will open the afternoon session by talking about "Goals for the Partnership between Retina NZ and Diabetes NZ", followed by afternoon tea.
At 3.00 pm the National Annual General Meeting begins, presided over by retiring President Anthony Haas.
Then at 6.00 pm there will be a dinner at the Island Bay Cafe to which all members, their families and friends are cordially invited. The cost is $22.00 per head for three courses or $12.00 for Soup and Dessert.
Please fill in and return relevant forms, already posted to you, by 13th September to Sue Emirali, 56 Moana Road, Plimmerton or by phoning her at (04) 233 8364. For further information phone Janet Palmer on (04) 4767 329 and leave a message, or email her at email@example.com
This is a great chance to socialize and meet fellow members. Wellington Branch and the Executive Committee look forward to hosting you, your families and interested friends.
DO YOU NEED HELP OR ADVICE?
The Retina NZ Peer Support Scheme is a free and confidential service, operating nationwide. To make contact, telephone 0800 243 33 33, press 1 for General enquiries and then ask the call centre operator to put you in touch with a Peer Supporter in your area.
Ring any of the following freephone numbers if you want to speak to a geneticist or genetic counsellor about your own particular diagnosis of RP, Macular Degeneration or other retinal degenerative disorders.
Auckland Genetic Hotline
(Ask for Dr Andrea Vincent) 0800 476 123
Wellington Genetic Hotline 0508 364 436
Christchurch Genetic Hotline 0508 364 436
(South Island callers ask for Dr Caroline Lintott)
P.O. Box 27-177,
Phone: (04) 380 2160
Fax: (04) 389 5254.
Website address: www.retina.org.nz
CLOSING DATE FOR RECEIPT OF ARTICLES FOR THE NEXT ISSUE IS FRIDAY 7 November 2003.