Month: August 2013

A recent article in The Journal of the American Medical
Association reports that when preschool children in villages
in Ethiopia took the antibiotic azithromycin twice per year instead of
once per year, the number of children with eye infections caused by the
contagious eye disease trachoma was significantly reduced. The study
was conducted by Muluken Melese of Orbis International, Addis Ababa,
Ethiopia and colleagues.

Trachoma is the an infectious eye disease that is the leading cause of
the world’s preventable blindness. It is caused by the a chlamydia
bacterium.

Trachoma is common in poor, dry areas like rural sub-Saharan Africa,
but it has been eradicated from Western Europe and the United
States. “The World Health Organization has launched a program
to control trachoma, relying in large part on annual repeated mass
azithromycin administrations. Program administrators anticipate that
the treatments will reduce the prevalence of the ocular strains of
chlamydia that cause trachoma to a level low enough that resulting
blindness will be no longer be a major public health concern. However,
local elimination of ocular chlamydia may be obtainable,” according to
the authors of the study..

The elimination of trachoma is possible, according to some mathematical
models. However, it may require recurrent treatment in areas where
people are at a greater risk of becoming infected. It is regarded that
elimination is a particularly important goal – if antibotics are
discontinued and communities lose some their immunity, there is a
concern that infection may return.

The researchers focused on the Gurage Zone in Ethiopia – 16 rural
villages with a high prevalence of trachoma. They analyzed the results
of azithromycin given once and twice per year to all residents age 1
year or older from March 2003 to April 2005. About 91% of the 16,403
eligible individuals received their scheduled treatment.

One major result of the study showed a 6-fold decrease in infections of
preschool children from eight villages who received two annual
treatments compared to one, from 42.6% to 6.8% by 24 months. When the
treatment was administered four times in the other eight villages,
infections were reduced in preschool children by a factor of 35, from
31.6% to 0.9% by 24 months.

The researchers report that at 24 months, 0.9 percent of children were
infected in the biannually treated villages compared to 6.8 percent of
children in the annually treated villages – a significant difference.
At 24 months, 75% of preschool children did not show any infection
after receiving biannual treatment compared to 12.5% of the residents
receiving annual treatments. There was also an association between
having no infection identified at 24 months and being in the biannual
treatment group.

“Biannual coverage of a large portion of the community may be necessary
to eliminate infection from a severely affected community or at least
to do so in a timely manner. Although programs may be reluctant to
devote their scarce resources to more frequent treatment, this may be
more cost-effective in the long term. Local elimination of the ocular
strains of chlamydia from villages is a feasible goal but may require
biannual distributions in hyperendemic areas. The results of this study
confirm models that suggest treatments will need to be given for more
than the 2 years to predictably achieve elimination in more than 95
percent of villages. Whether elimination from a larger area is possible
will depend on the frequency of community-to-community
transmission,” conclude the researchers.

An editorial by David Mabey and Anthony W. Solomon of the London School
of Hygiene & Tropical Medicine, London maintains that the
research performed by Melese and colleagues is valuable for the
treatment of trachoma.

They write:

“Treating entire regions twice yearly could help ensure that gains made
from frequent antibiotic use are not eroded by reintroduction of
infection from outside the treated area but will significantly increase
the cost of antibiotics and of their distribution. Finally, studies to
examine whether more frequent azithromycin use will result in the
emergence of macrolide-resistant strains of C. trachomatis or other
important pathogens are urgently required, for such an outcome would
more than offset any gain derived from biannual treatment. In the
meantime, the findings of Melese et al represent an important
contribution to understanding how blinding trachoma can be reduced and
hopefully eliminated.”

Comparison of Annual and Biannual Mass Antibiotic
Administration for Elimination of Infectious Trachoma
Muluken Melese, Wondu Alemayehu, Takele Lakew, Elizabeth Yi, Jenafir
House, Jaya D. Chidambaram, Zhaoxia Zhou, Vicky
Cevallos, Kathryn Ray, Kevin Cyrus Hong, Travis C. Porco,
Isabella Phan, Ali Zaidi, Bruce D. Gaynor, John P. Whitcher, Thomas M.
Lietman
JAMA. (2008). Vol. 299 No. 7: pp. 778-784
Click
Here to View Abstract

Mass Antibiotic Administration for Eradication of Ocular
Chlamydia trachomatis
David Mabey and Anthony W. Solomon
JAMA. (2008). Vol. 299 No. 7: pp. 819-820
Click
Here to View Abstract

: Peter M Crosta

University of Kentucky ophthalmology researcher Dr. Jayakrishna Ambati has once again received a national honor for his research in the field of age-related macular degeneration (AMD). Ambati was recently granted a prestigious 2006 Lew R. Wasserman Award by Research to Prevent Blindness (RPB), the world’s leading voluntary organization supporting eye research.

The RPB Wasserman Award is given annually to scientists and physicians conducting ophthalmologic research at major medical institutions. Recipients are selected by their peers.

The award not only comes with a great amount of recognition and respect from peers, but also a $55,000 grant to UK.

“The grant money from this award will be used to hire additional staff, as well as to further my research in macular degeneration,” said Ambati. “This award is very exciting personally, but it also means great things for the University of Kentucky. The money will support our mission of solving the puzzle of macular degeneration.”

AMD, a progressive deterioration of the retina, is the leading cause of legal blindness in the United States. “Dr. Ambati has helped to build a first class research group in Age Related Macular Degeneration here at UK,” said Dr. Andrew Pearson, Chair, UK College of Medicine Department of Ophthalmology and Visual Sciences. “His accomplishments have resulted not only in this prestigious award from RPB but also in substantial grant support and the publication of his findings in superb medical journals such as Nature Medicine, the Journal of Clinical Investigation and the Proceedings of the National Academy of Sciences.

“It feels very rewarding to know that I am highly respected enough among my peers for them to award me this honor. Even though I am receiving the credit, I would really like to thank my group of researchers. They are an immensely talented group of people,” said Ambati.

Ambati received his bachelor’s from The Johns Hopkins University and completed medical school at the State University of New York. Following a residency in ophthalmology at the University of Rochester, he completed clinical and research fellowships in medical and surgical diseases of the retina and vitreous at the Massachusetts Eye and Ear Infirmary of Harvard Medical School. Ambati is a UK College of Medicine associate professor and Vice Chair of the Department of Ophthalmology and Visual Sciences.

“Dr. Ambati is focused on dissecting the underlying mechanism responsible for AMD with a goal of using this knowledge to develop treatment strategies to prevent the onset of significant visual loss,” said Pearson.

“With the aging of baby boomers, AMD promises to become an even more common cause for vision loss. We can only hope that with generous support like this from RPB and the continued dedication of Dr. Ambati that we are able to find the solution soon.”

In striving to become a Top 20 public research institution, the University of Kentucky is a catalyst for a new Commonwealth – a Kentucky that is healthier, better educated, and positioned to compete in a global and changing economy. For more information about UK’s efforts to become a Top 20 university, please go to uky.edu/OPBPA/Top20.html

Contact: Allison Elliott
University of Kentucky

Ethambutol, a vital component of multidrug regimens for Mycobacterium avium complex (MAC) lung disease, can cause ocular toxicity if taken on a daily basis, according to a study in the second issue for July 2005 of the American Thoracic Society’s peer-reviewed journal. Writing in the American Journal of Respiratory and Critical Care Medicine, the researchers recommended monthly visual acuity and color discrimination testing for patients taking doses of the drug greater than 15 to 20 milligrams per kilogram of body weight, those who receive the medication for longer than 2 months, and patients with renal insufficiency since the compound is cleared by the kidneys.

According to the investigators, the central fibers of the optic nerve are most commonly affected. The drug can cause blurred vision, decreased visual acuity, central blind or dark spots in the visual field, and often loss of the ability to detect green and sometimes red.

They point out, however, that ethambutol is a critical component of routine therapy for MAC disease which accounts for most mycobacterial infections other than tuberculosis in humans. MAC disease bacteria usually affect the lung, but may involve the lymph nodes, bones, joints, and skin. These bacteria are highly resistant to most antibiotics, but the infections they cause are not contagious. MAC infection in the lung usually develops slowly; the first symptoms generally involve coughing and spitting up mucus.

In this study, 229 patients with MAC lung disease received 16 months of multidrug therapy that included ethambutol. Patients on daily therapy received ethambutol at 25-mg/kg doses for the first 2 months, and then 15 mg/kg doses for the remainder of therapy. Patients on three-day-a-week therapy (Monday, Wednesday, and Friday) received a 25 mg/kg dose each day.

Of the 229 patients, 50 were known to have preexisting ocular disease.

The authors said that while on ethambutol, 97 patients consulted an ophthalmologist and 24, or 10 percent, stopped taking the drug temporarily. Eight of the 139 patients on daily therapy were diagnosed with ocular toxicity caused by the drug.

After they discontinued the drug, all patients with ocular disease caused by ethambutol returned to the same visual status they had prior to the start of the study.

The research article appears in the second issue for July 2005 of the American Thoracic Society’s peer-reviewed American Journal of Respiratory and Critical Care Medicine.

For the complete text of these articles, please see the American Thoracic Society Online Web Site at atsjournals. For either contact information or to request a complimentary journalist subscription to ATS journals online, or if you would like to add your name to the Society’s twice monthly journal news e-mail list, contact Cathy Carlomagno at 212-315-6442, or at ccarlomagnothoracic.

Cathy Carlomagno
ccarlomagnothoracic
212-315-6442
American Thoracic Society
American Thoracic Society Journal news tips for July 2005 (second issue)
www.thoracic

The team of Dr. Robert Koenekoop which includes Dr. Irma Lopez from the Research Institute of the MUHC at the Montreal Children’s Hospital played a crucial role in the international collaboration that led to the discovery of a new gene that causes Leber congenital amaurosis (LCA) and retinitis pigmentosa (RP), two devastating forms of childhood blindness.

This finding of this new gene, called SPATA7, is remarkable because it identifies a new retinal metabolic disease pathway that may be crucial for many patients. It also opens a new avenue for a potential genetic therapy. Gene therapy targeting different genes has recently proved successful for the same disease in human subjects. The study will be published on March 5th, 2009 in the American Journal of Human Genetics.

New cell mechanism at play

Researchers have now identified a total of fifteen genes involved in LCA, but SPATA7 is the first gene with a mutation that disrupts the protein transport between two important compartments of the cell: the endoplasmic reticulum and the Golgi apparatus. All proteins in every cell have to pass through this transport pathway; thus SPATA7 plays a major role and its mutation may affect many aspects of vision.

“Until now we were not aware that this cellular mechanism played a role in LCA or any other eye disease. This is a very important step that opens up a number of new research avenues, particularly in our understanding of the specific cellular processes involved in blindness. This finding also increases the number of potential therapeutic targets and therefore the chances of finding a treatment. We are extremely motivated by all of these new possibilities,” explained Dr. Koenekoop.

First step towards gene therapy

“This is an incredible discovery that gives great hope to LCA patients and their families, that gene based therapies can and will be developed to restore sight,” said Sharon Colle, President and CEO of The Foundation Fighting Blindness, the leading private charity for vision research. “We are proud to fund such important discoveries involving prominent Canadian researchers and institutions.”

A careful assessment of patients with some specific genetic types of LCA also demonstrated that their retinal cells (specifically the rod and cone photoreceptors), although not functional for vision, were still present and in relatively good condition. This critical observation will allow researchers to continue on the path towards gene therapies. Therapies targeting different genes for the same disease have already shown success in the United Kingdom and in the US, meaning that LCA patients can now enjoy hope for the future.

A new and innovative technology

SPATA7 was identified using an innovative technology developed in the different laboratories involved in this international collaboration. “We started this protocol about two years ago, and it has already helped us to identify four new genes associated with LCA and RP before we discovered SPATA7,” explained Dr Koenekoop.

The technique is based on DNA-chips and involves three steps: first the genetic material of the patient is screened to find mutations in 14 specific LCA and RP genes. The LCA and RP patients that are negative for this detailed screen are then subjected to a second DNA chip, this one to identify significant stretches of homozygosity in SNP markers. SNPs are single nucleotide repeats, which are natural variations in the human genome. These homozygous regions may contain new genes and are carefully probed based on functional information and then subjected to sequencing. “This method is indeed both very powerful and very promising for the future,” said Dr. Koenekoop.

Notes:

Funding

The Canadian component of this project was funded by The Foundation Fighting Blindness Canada (FFB) and by the Fonds de la recherche en sant?� du Qu?�bec (FRSQ).

Dr. Robert Koenekoop

Dr. Robert Koenekoop is the Director of the Division of Pediatric Ophthalmology and the McGill Ocular Genetics Laboratory at the Montreal Children’s Hospital of the MUHC. He is a researcher in medical genetics and genomics with the Research Institute at the Montreal Children’s Hospital of the MUHC. Dr. Koenekoop is also an Associate Professor in Human Genetics and Ophthalmology in the Faculty of Medicine at McGill University.

Partners

This project is a collaboration between the laboratory of Dr. Robert Koenekoop at the Research Institute of the MUHC at the Montreal Children’s Hospital; the laboratory of Dr. Rui Chen, Texas Children’s Hospital, Baylor College of Medicine, Houston; and the laboratory of Dr. Anneke den Hollander, the Nijmegen Centre for Molecular Life Sciences, Radboud University Nijmegen, in The Netherlands. The DNA chips were developed in collaboration with Dr. Rando Allikmets of Columbia University.

The original article and a short audio document can be found here.

The Research Institute of the McGill University Health Centre (RI MUHC) is a world-renowned biomedical and health-care hospital research centre. Located in Montreal, Quebec, the institute is the research arm of the MUHC, the university health center affiliated with the Faculty of Medicine at McGill University. The institute supports over 600 researchers, nearly 1200 graduate and post-doctoral students and operates more than 300 laboratories devoted to a broad spectrum of fundamental and clinical research. The Research Institute operates at the forefront of knowledge, innovation and technology and is inextricably linked to the clinical programs of the MUHC, ensuring that patients benefit directly from the latest research-based knowledge.

The Research Institute of the MUHC is supported in part by the Fonds de la recherche en sant?� du Qu?�bec.

For further details visit: muhc/research.

The Montreal Children’s Hospital (MCH) is the pediatric teaching hospital of the McGill University Health Centre and is affiliated with McGill University. The MCH is a leader in providing a broad spectrum of highly specialized care to newborns, children, and adolescents from across Quebec. Our areas of medical expertise include programs in brain development/behaviour, cardiovascular sciences, critical care, medical genetics and oncology, tertiary medical and surgical services, and trauma care. Fully bilingual, the hospital also promotes multiculturalism and serves an increasingly diverse community in more than 50 languages. The Montreal Children’s Hospital sets itself apart with its team approach to innovative patient care. Our health professionals and staff are dedicated to ensuring children and their families receive exceptional health care in a friendly and supportive environment.

Source:
Isabelle Kling
McGill University Health Centre

People suffering from a severe retinal disease will sooner or later lose
their eyesight considerably, or even become completely blind. Those
affected, family members, researchers and doctors hope that this fate
might be avoided one day by a better understanding of the reasons for
this disease. Coordinated by the geneticist Ronald Roepman from
Nijemegen, an important step has now been made in this direction by an
international research team with the participation of the GSF – National
Research Center for Environment and Health: they identified a further
gene for the inherited retinal disease Leber Congenital Amaurosis (LCA)
and discovered first evidences of how it functions. This represents new
opportunities for gene therapy, which especially for LCA, is considered
as very promising since the disease is caused by a single mutation.
LCA causes blindness very early on – often shortly after or within a few
months of birth. The disease can be caused through a single mutation in
different genes; with the newly discovered LCA5 gene, ten
disease-causing genes had been identified so far which are responsible
for approx. 60 % of all LCA diseases. “All these deficiencies lead in
the end to the same symptoms, however, in order to treat the disease
efficiently with the individual patient, it is important to know which
gene mutation occurred in the specific case and what it causes”,
underlines Dr. Marius Ueffing (GSF Institute for Human Genetics), who
leads the project at GSF.

The LCA5 gene encodes the lebercilin, a so far unknown protein. Through
proteomic methods, Ueffing’s team could demonstrate that lebercilin
specifically interacts with other proteins which play a role in the
protein transport in the cells. Thus the scientists concluded that
lebercilin is relevant for the protein transport within the optical
cell: as shown by electro-microscopic pictures, within the optical cell
described as the photoreceptor, lebercilin binds the most to the
so-called cilium, the connection point between the interior and exterior
segments of the photoreceptor. Through this “molecular transport belt”,
the optical crimson must be also transported into the exterior segment
of the optical cell. The light reception takes place exactly here. If
the lebercilin synthesis is disturbed, the already used optical crimson
in the exterior segment cannot be replaced anymore and the eyesight is
lost, according to the researchers’ hypothesis.

Very similar transport processes also play a role in other body parts,
e.g. in the kidneys. Lebercilin is part of a complex network of proteins
which controls ciliary transport processes, or directly take part in
them. Disruptions in the cooperation of such molecular networks at the
protein interaction level often build the molecular basis of diseases.
In the case of ciliary diseases (ciliopathies), the restricted
functionalities of cilium cause deafness, blindness or even severe
syndrome diseases. LCA is therefore a good model which also enables to
gain more knowledge over other difficultly treatable diseases in the
long term.

LCA itself is so far incurable. However, patients and doctors set their
hopes high on gene therapy: since each type of LCA is caused by the
mutation of a single gene, the affected persons could be helped by
exchanging this gene. Such a LCA gene therapy has been already
successfully implemented for dogs who naturally suffer from LCA: the
treated dogs regained their permanent eyesight due to this therapy. A
clinical study of twelve human patients is currently being carried out
at a large-scale London hospital with encouraging results. If these
findings prove to be withstandable, there will also be gene therapy
available for LCA5 gene deficiencies in five to ten years time, says
Ueffing. “The affected persons urge for a faster procedure” underlines
Ueffing, “but researchers and doctors assume a big responsibility
concerning the development and implementation of gene therapies.
Therefore, very high safety standards must be set in this field.”

Mutations in LCA5, encoding the ciliary protein lebercilin, cause Leber congenital amaurosis
Anneke I den Hollander, Robert K Koenekoop, Moin D Mohamed, Heleen H
Arts, Karsten Boldt, Katherine V Towns, Tina Sedmak, Monika Beer,
Kerstin Nagel-Wolfrum, Martin McKibbin, Sharola Dharmaraj, Irma Lopez,
Lenka Ivings, Grange A Williams, Kelly Springell, C Geoff Woods, Hussain
Jafri, Yasmin Rashid, Tim M Strom, Bert van der Zwaag, Ilse Gosens,
Ferry F J Kersten, Erwin van Wijk, Joris A Veltman, Marijke N Zonneveld,
Sylvia E C van Beersum, Irene H Maumenee, Uwe Wolfrum, Michael E
Cheetham, Marius Ueffing, Frans P M Cremers, Chris F Inglehearn & Ronald
Roepman;
Nature Genetics Jul; 39(7) 2007:889-95; Nature Genetics advance online publication Published online: 3 June 2007; doi:10.1038/ng2066

GSF – National Research Center for Environment and Health
gsf.de

Johnson & Johnson Vision Care, Inc., today announced that its ACUVUE® ADVANCE™ with HYDRACLEAR™, ACUVUE® ADVANCE™ for ASTIGMATISM, and ACUVUE® OASYS™ with HYDRACLEAR™ PLUS Brand Contact Lenses are the first contact lenses to receive the World Council of Optometry’s (WCO) Global Seal of Acceptance for Ultraviolet Absorbing Contact Lenses. The announcement was made at the annual meeting of the American Optometric Association in Boston.

“In awarding the Global Seal of Acceptance, the World Council of Optometry Global Commission on Ophthalmic Standards (WCO GCOS), which provides independent evaluation of ophthalmic related products, has determined that the ACUVUE® ADVANCE™ and ACUVUE® OASYS™ brands meet established, recognized and accepted standards that are adopted by the WCO GCOS,” said WCO President Robert Chappell. “These include published standards of International Standards Organization (ISO) and American National Standards Institute (ANSI).”

The ISO and ANSI standards classify UV-blocking contact lenses into two groups based on the lens’ absorptive capacity at its minimum thickness. Class 2 UV-blockers must absorb at least 70 percent of UVA and more than 95 percent of UVB radiation. Class 1 UV-blockers must absorb a minimum of 90 percent UVA and at least 99 percent UVB radiation. Only products that meet these standards may claim to be UV blocking. All three lenses previously received the American Optometric Association (AOA) Seal of Acceptance for Ultraviolet Absorbers/Blockers.

“Not all contact lens lines offer UV protection, and, of those that do, not all provide similar absorption levels,” explains Cristina Schnider, OD, Director, Medical Affairs, VISTAKON®, Division of Johnson & Johnson Vision Care Inc. “All ACUVUE® Brand Contact Lenses offer effective UV-blocking, and among contact lens brands, ACUVUE® ADVANCE™, ACUVUE® ADVANCE™ for ASTIGMATISM, and ACUVUE® OASYS™ with more than 90 percent of UVA rays and 99 percent of UVB rays blocked*??�are the only lenses to achieve Class I UV blocking status.”

Experts say the effects of UV radiation are cumulative and can do irreversible harm to all structures of the eye and surrounding tissue that are left unprotected or under-protected. Certain conditions, such as age-related cataract, may not manifest for years at which point the damage is already done and it is too late to reverse the effects of the sun. “That’s why it is important to get maximum protection beginning in childhood,” advises Dr. Schnider. “The most complete measure of UV protection can be achieved with a combination of UV-absorbing sunglasses, a wide-brimmed hat, and UV-blocking contact lenses.”

Because they cover the entire cornea and limbus, UV-blocking contact lenses offer an added level of protection when worn with UV blocking sunglasses. While many sunglasses block UV rays that enter through the lenses, most do not prevent unfiltered rays from reaching the eyes through the sides, as well as the top, and/or bottom of the glasses. Due to their inability to block these peripheral rays, some sunglasses block as little as 50 percent of all UV radiation from reaching the eyes.

“It is just as important to block these peripheral UV rays,” warns Dr. Schnider. “UV-blocking contact lenses provide added protection by effectively blocking sunlight that may enter the cornea from the top, bottom, or sides of the glasses.” Although UV-blocking contact lenses provide important added protection for patients, they should not be viewed as a stand-alone solution. Contact lenses should always be worn in conjunction with high-quality UV-blocking sunglasses and a wide-brimmed hat for maximum UV protection for the eyes.

ACUVUE® ADVANCE™ Brand Contact Lenses with HYDRACLEAR™, ACUVUE® ADVANCE™ for ASTIGMATISM and ACUVUE® OASYS™ Brand Contact Lenses with HYDRACLEAR™ PLUS are indicated for daily wear vision correction. ACUVUE® OASYS™ may also be worn for up to six consecutive nights/seven days of extended wear as recommended by an eye care professional.

Contact lenses should not be worn for longer periods than recommended by an eye care professional. As with all contact lenses, eye problems, including corneal ulcers, can develop. Some wearers may also experience mild irritation, itching or discomfort. Lenses should not be worn if the wearer has an eye infection or experiences eye discomfort, excessive tearing, vision changes, redness or other eye problems. If these conditions occur, the wearer should contact their eye care professional. Consult the patient information guide available from your doctor for complete information.

About The World Council of Optometry

WCO is an international organization dedicated to the enhancement and development of eye and vision care worldwide. Representing over 200,000 optometrists from 75 member organizations in 41 countries, WCO serves as a forum for optometric organizations to respond to public health needs and opportunities around the world. The WCO is a member of the International Agency for the Prevention of Blindness and maintains official relations with the World Health Organization.

Johnson & Johnson Vision Care Inc.

The VISTAKON division of Johnson & Johnson Vision Care, Inc., specializes in disposable contact lenses which it markets under such brand names as ACUVUE®, ACUVUE® ADVANCE™ with HYDRACLEAR™, ACUVUE® ADVANCE™ for ASTIGMATISM, ACUVUE® OASYS™ with HYDRACLEAR™ PLUS, ACUVUE® and ACUVUE® 2; 1-DAY ACUVUE®; ACUVUE® BIFOCAL; ACUVUE® TORIC and ACUVUE® 2 COLOURS™.

ACUVUE®, ACUVUE® ADVANCE™, HYDRACLEAR™, ACUVUE® OASYS™, ACUVUE® 2 COLOURS™, and VISTAKON® are trademarks of Johnson & Johnson Vision Care, Inc.

??� Helps protect against transmission of harmful UV radiation to the cornea and into the eye.

WARNING: UV-absorbing contact lenses are NOT substitutes for protective UV-absorbing eyewear such as UV-absorbing goggles or sunglasses because they do not completely cover the eye and surrounding area. You should continue to use UV-absorbing eyewear as directed. NOTE: Long term exposure to UV radiation is one of the risk factors associated with cataracts. Exposure is based on a number of factors such as environmental conditions (altitude, geography, cloud cover) and personal factors (extent and nature of outdoor activities). UV-Blocking contact lenses help provide protection against harmful UV radiation. However, clinical studies have not been done to demonstrate that wearing UV-Blocking contact lenses reduces the risk of developing cataracts or other eye disorders. Consult your eye care practitioner for more information.

Johnson & Johnson Vision Care Inc
jnj/home.htm

As physicians our goal is to provide the best quality of life for our patients. Data shows that nearly 95 percent of LASIK patients are satisfied with their outcomes-the highest for almost any surgical procedure. However, we do know that a very small percentage, less than 2 percent, will have complications that impact their quality of life. By examining LASIK’s impact on the patient quality of life and identifying the factors that may influence patient satisfaction, the FDA study can help us understand how we can extend patient satisfaction even further. The participation of the Department of Defense will be a tremendous benefit for the study, because of the Department’s considerable experience with LASIK. The Academy stands ready to assist the FDA in the development of the study.

The Academy offers a free resource for consumers who are thinking about whether to have LASIK. “Is Lasik For Me?: A Patient’s Guide to Refractive Surgery” offers objective and balanced information about refractive surgery, as well as links to other documents that patients may find useful. The fifteen-page guide is produced by the Academy, the International Society of Refractive Surgery (ISRS) and Ophthalmic Mutual Insurance Company. “Is LASIK for Me?” is available here.

Source
American Academy of Ophthalmology

People who are blind from birth are able to detect tactile information faster than people with normal vision, according to a study in the Oct. 27 issue of The Journal of Neuroscience.

The brain requires a fraction of a second to register a sight, sound, or touch. In this study, a group of researchers led by Daniel Goldreich, PhD, of McMaster University explored whether people who have a special reliance on a particular sense – in the way blind people rely on touch – would process that sense faster.

“Our findings reveal that one way the brain adapts to the absence of vision is to accelerate the sense of touch,” Goldreich said. “The ability to quickly process non-visual information probably enhances the quality of life of blind individuals who rely to an extraordinary degree on the non-visual senses.”

The authors tested the tactile skills of 89 people with sight and 57 people with various levels of vision loss. The volunteers were asked to discern the movements of a small probe that was tapped against the tips of their index fingers. Both groups performed the same on simple tasks, such as distinguishing small taps versus stronger taps. But when a small tap was followed almost instantly by a larger and longer-lasting vibration, the vibration interfered with most participants’ ability to detect the tap – a phenomenon called masking. However, the 22 people who had been blind since birth performed better than both people with vision and people who had become blind later in life.

“We think interference happens because the brain has not yet completed the neural processing required to fully perceive the tap before the vibration arrives and disrupts it,” Goldreich said. “The more time between the tap and the vibration, the more formed the perception of the tap will be, and the less interference the vibration will cause.”

The authors measured the minimum amount of time needed for participants to perceive sensory input by varying the period between the tap and the vibration. They found that congenitally blind people required shorter periods than anyone else. Those same individuals also read Braille fastest. The authors note that each blind person’s perception time was approximately equal to the average time that person took to move a finger from one Braille character to the next as they read.

The findings suggest that early onset blindness leads to faster perception of touch. However, whether that advantage is due to the brain adapting to the absence of vision – a change called plasticity – or to a lifetime of practicing Braille is still unclear.

Richard Held, PhD, of Massachusetts Institute of Technology, an expert in the brain and visual development who was unaffiliated with the study, said the results suggest that a lack of visual experience changes how information acquired by touch is processed.

“The heightened skill of tactile integration seems to account for the remarkable speed of Braille-reading demonstrated by some congenitally blind individuals,” Held said. “This work constitutes a solid step forward in our understanding of the interaction between senses.”

The research was supported by the National Eye Institute and the Natural Sciences and Engineering Research Council in Canada.

Source:
Kat Snodgrass
Society for Neuroscience

University of New Hampshire professor Rick Cote has received $1.4 million from the National Institutes of Health (NIH) to continue research into the central enzyme that controls initial steps of vision and that, when defective, can result in retinitis pigmentosa, a leading inherited cause of blindness.

Retinitis pigmentosa, or RP, affects 1.5 million people worldwide. Typically, symptoms begin in childhood or early adulthood and progress from impairments in night vision to tunnel vision. The degree of vision loss varies, but in some cases RP leads to total blindness.

Cote, a professor of biochemistry and molecular biology who has received NIH funding through the National Eye Institute for 18 years, conducts fundamental research into visual signaling pathways in the photoreceptors of the retina. “Until you know how the retina functions normally, you’re not going to be able to understand how genetic or environmental defects in the visual pathway can cause vision loss or total blindness, or how to slow or prevent disease progression,” he says.

Normal functioning of the retina begins with light being absorbed by the photoreceptor cells, called rods and cones. Cones are responsible for color perception, daylight vision, and visual discrimination tasks like reading, while rods provide peripheral vision and vision in low light.

Central to rod and cone visual signaling is the phosphodiesterase (PDE) protein. This enzyme is activated by light and is directly responsible for the nerve impulse that signals the perception of light. “It’s therefore not surprising that this exquisitely light-sensitive enzyme can also cause retinal disease when its regulation or catalytic activity is impaired by a genetic mutation, as in certain forms of RP,” says Cote. Most of Cote’s research career has focused on better understanding how PDE functions. With such knowledge, he says, “we might someday be able to intervene therapeutically to prevent defects in PDE from causing retinal disease.”

Working with graduate and undergraduate students in his lab, along with three full-time research scientists, Cote uses a variety of molecular, biochemical, cell biological and pharmacological approaches to understand the structure of PDE and how it is regulated in darkness and in the light. This latest four-year NIH award will support several new directions in Cote’s research program. One project involves a collaboration with Tom Laue, professor of biochemistry and molecular biology, to use novel biophysical techniques to determine how small molecules and proteins bind to PDE and alter its structure and regulatory properties.

In another strand of his research, conducted in partnership with Karen Carleton, research associate professor with UNH’s Hubbard Center for Genome Studies, Cote is exploring the evolution of vertebrate rod and cone cells in the retina. By focusing on the evolution of the PDE protein, Cote and Carleton hope to better understand its functioning – and malfunctioning – in humans. “The basic plan for the human retina evolved at the time when vertebrates evolved from the invertebrates,” he says. In their preliminary work, Cote and Carleton have identified rod and cone photoreceptor PDE in species ranging from fish to humans, and their amino acid sequences are very similar.

Yet another line of work is to evaluate a newly discovered PDE binding protein (called GARP2) for its potential to turn off the PDE in rods during daytime – “rods are so light-sensitive that they can’t function in bright light,” Cote says – to conserve metabolic energy.

Cote is also exploring PDE’s sexier side: its relationship to Viagra and other drugs that treat erectile dysfunction. Of the 11 families of phosphodiesterases, the photoreceptor PDE – named PDE6 – is most closely related to PDE5, an enzyme abundant in smooth muscle tissue in our bodies.

Viagra and similar drugs (Levitra, Cialis) work by inhibiting PDE5, but most of these drugs also potently inhibit PDE6, causing temporary alterations in vision. A better understanding of the differences between PDE5 and 6 will result in creating drugs that selectively target PDE5 but do not affect PDE6 or the visual process. While Cote does not foresee an immediate role for these drugs in combating retinal diseases, PDE inhibitors have profound therapeutic potential in treating cardiovascular disease, asthma, diabetes, and cancer, making the development of PDE inhibitors with no adverse effects on vision very desirable.

After two decades of research on PDE, Cote remains fascinated with how rods and cones, and the proteins contained within these light-detecting cells, translate light into sight. “The activity of all these photoreceptor proteins – especially PDE – have to be coordinated on the millisecond time scale so we can see. It’s a miracle that it all works,” he says.

Rick Cote can be reached at rickteunh.edu or 603-862-2458. For more detailed information on Cote’s research, visit cote.unh.edu/.

Contact: Beth Potier

University of New Hampshire

View drug information on Cialis; Levitra; Viagra.

Standard Chartered’s Group Finance Director, Richard Meddings, has pledged to run The Standard Chartered Great City Race 2009 blindfolded to help raise funds for the race’s official community partner, Seeing is Believing (SiB). Today, organisers call for the other runners to start fundraising and help make a difference*.

Seeing is Believing is a charitable collaboration between Standard Chartered and the International Agency for Prevention of Blindness (IAPB) to help eradicate avoidable blindness. There are over 45 million blind people across the world and yet 80% of blindness is preventable or curable. The need to tackle this is acute – a child goes blind every minute and, tragically, 60% of children die within a year of going blind. As Chairman and long serving champion of SiB, Meddings has been raising thousands of pounds through fundraising, including auctioning the chance to guide him round the 5K race course.

The Standard Chartered Great City Race, now in its fifth year, takes place on Thursday 16 July through the closed off streets of London’s square mile. Companies are invited to enter teams of four or more runners with ??5 from every entry going directly to SiB. Standard Chartered has pledged to match pound for pound all funds raised for SiB, doubling the impact of all donations.

Richard Meddings commented, “The Standard Chartered Great City Race and Seeing is Believing form the perfect partnership to help raise the profile within the capital of this very worthy cause. 80% of cases of blindness are avoidable through prevention or cure so if runners raise additional sponsorship, we can make a real difference to tackling avoidable blindness. Standard Chartered will match all donations made through the race which will bring Seeing is Believing even closer to meeting its ambitious fundraising target to raise a further $20 million by the end of 2012.”

More than 90% of the world’s blind live in low and middle-income countries. With over half the world’s population now urban, the challenge of delivering eye-care services to swelling informal urban areas has grown considerably. Funds raised will go to the development of sustainable eye-care services in 20 less-advantaged urban areas in the developing world. These will provide poor and marginalised populations access to cataract surgery, preventative treatment, screening, and specialised medical interventions.

Now firmly established as the City’s premier corporate running challenge, this year’s race is on course to field the maximum 6,500 runners from teams representing all City business sectors. After last year’s sell-out success, City workers are advised to sign up as early as possible to avoid disappointment. Companies can go directly to the official race website at cityrace to enter their teams.

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City Race