StemCell Therapy

Visual impairment, also known as vision impairment or vision loss, is a decreased ability to see to a degree that causes problems not fixable by usual means, such as glasses.[1][2] Some also include those who have a decreased ability to see because they do not have access to glasses or contact lenses.[1] Visual impairment is often defined as a best corrected visual acuity of worse than either 20/40 or 20/60.[3] The term blindness is used for complete or nearly complete vision loss.[3] Visual impairment may cause people difficulties with normal daily activities such as driving, reading, socializing, and walking.[2]

The most common causes of visual impairment globally are uncorrected refractive errors (43%), cataracts (33%), and glaucoma (2%).[4] Refractive errors include near sighted, far sighted, presbyopia, and astigmatism.[4] Cataracts are the most common cause of blindness.[4] Other disorders that may cause visual problems include age related macular degeneration, diabetic retinopathy, corneal clouding, childhood blindness, and a number of infections.[5] Visual impairment can also be caused by problems in the brain due to stroke, prematurity, or trauma among others.[6] These cases are known as cortical visual impairment.[6] Screening for vision problems in children may improve future vision and educational achievement.[7] Screening adults may also be beneficial.[2] Diagnosis is by an eye exam.[2]

The World Health Organization estimates that 80% of visual impairment is either preventable or curable with treatment.[4] This includes cataracts, the infections river blindness and trachoma, glaucoma, diabetic retinopathy, uncorrected refractive errors, and some cases of childhood blindness.[8] Many people with significant visual impairment benefit from vision rehabilitation, changes in their environmental, and assistive devices.[2]

As of 2012 there were 285 million people who were visually impaired of which 246 million had low vision and 39 million were blind.[4] The majority of people with poor vision are in the developing world and are over the age of 50 years.[4] Rates of visual impairment have decreased since the 1990s.[4] Visual impairments have considerable economic costs both directly due to the cost of treatment and indirectly due to decreased ability to work.[9]

The definition of visual impairment is reduced vision not corrected by glasses or contact lenses. The World Health Organization uses the following classifications of visual impairment. When the vision in the better eye with best possible glasses correction is:

Blindness is defined by the World Health Organization as vision in a person's best eye of less than 20/500 or a visual field of less than 10 degrees.[3] This definition was set in 1972, and there is ongoing discussion as to whether it should be altered to official include uncorrected refractive errors.[1]

Severely sight impaired

Sight impaired

Low vision

In the UK, the Certificate of Vision Impairment (CVI) is used to certify patients as severely sight impaired or sight impaired.[11] The accompanying guidance for clinical staff states: "The National Assistance Act 1948 states that a person can be certified as severely sight impaired if they are "so blind as to be unable to perform any work for which eye sight is essential". The test is whether a person cannot do any work for which eyesight is essential, not just his or her normal job or one particular job."[12]

In practice, the definition depends on individuals' visual acuity and the extent to which their field of vision is restricted. The Department of Health identifies three groups of people who may be classified as severely visually impaired.[12]

The Department of Health also state that a person is more likely to be classified as severely visually impaired if their eyesight has failed recently or if they are an older individual, both groups being perceived as less able to adapt to their vision loss.[12]

In the United States, any person with vision that cannot be corrected to better than 20/200 in the best eye, or who has 20 degrees (diameter) or less of visual field remaining, is considered legally blind or eligible for disability classification and possible inclusion in certain government sponsored programs.

In the United States, the terms partially sighted, low vision, legally blind and totally blind are used by schools, colleges, and other educational institutions to describe students with visual impairments.[13] They are defined as follows:

In 1934, the American Medical Association adopted the following definition of blindness:

Central visual acuity of 20/200 or less in the better eye with corrective glasses or central visual acuity of more than 20/200 if there is a visual field defect in which the peripheral field is contracted to such an extent that the widest diameter of the visual field subtends an angular distance no greater than 20 degrees in the better eye.[14]

The United States Congress included this definition as part of the Aid to the Blind program in the Social Security Act passed in 1935.[14][15] In 1972, the Aid to the Blind program and two others combined under Title XVI of the Social Security Act to form the Supplemental Security Income program[16] which states:

An individual shall be considered to be blind for purposes of this title if he has central visual acuity of 20/200 or less in the better eye with the use of a correcting lens. An eye which is accompanied by a limitation in the fields of vision such that the widest diameter of the visual field subtends an angle no greater than 20 degrees shall be considered for purposes of the first sentence of this subsection as having a central visual acuity of 20/200 or less. An individual shall also be considered to be blind for purposes of this title if he is blind as defined under a State plan approved under title X or XVI as in effect for October 1972 and received aid under such plan (on the basis of blindness) for December 1973, so long as he is continuously blind as so defined.[17]

Kuwait is one of many nations that share the 6/60 criteria for legal blindness.[18]

Visual impairments may take many forms and be of varying degrees. Visual acuity alone is not always a good predictor of the degree of problems a person may have. Someone with relatively good acuity (e.g., 20/40) can have difficulty with daily functioning, while someone with worse acuity (e.g., 20/200) may function reasonably well if their visual demands are not great.

The American Medical Association has estimated that the loss of one eye equals 25% impairment of the visual system and 24% impairment of the whole person;[19][20] total loss of vision in both eyes is considered to be 100% visual impairment and 85% impairment of the whole person.[19]

Some people who fall into this category can use their considerable residual vision their remaining sight to complete daily tasks without relying on alternative methods. The role of a low vision specialist (optometrist or ophthalmologist) is to maximize the functional level of a patient's vision by optical or non-optical means. Primarily, this is by use of magnification in the form of telescopic systems for distance vision and optical or electronic magnification for near tasks.

People with significantly reduced acuity may benefit from training conducted by individuals trained in the provision of technical aids. Low vision rehabilitation professionals, some of whom are connected to an agency for the blind, can provide advice on lighting and contrast to maximize remaining vision. These professionals also have access to non-visual aids, and can instruct patients in their uses.

The subjects making the most use of rehabilitation instruments, who lived alone, and preserved their own mobility and occupation were the least depressed, with the lowest risk of suicide and the highest level of social integration.

Those with worsening sight and the prognosis of eventual blindness are at comparatively high risk of suicide and thus may be in need of supportive services. These observations advocate the establishment and extension of therapeutic and preventative programs to include patients with impending and current severe visual impairment who do not qualify for services for the blind. Ophthalmologists should be made aware of these potential consequences and incorporate a place for mental health professionals in their treatment of these types of patients, with a view to preventing the onset of depressive symptomatology, avoiding self-destructive behavior, and improving the quality of life of these patients. Such intervention should occur in the early stages of diagnosis, particularly as many studies have demonstrated how rapid acceptance of the serious visual handicap has led to a better, more productive compliance with rehabilitation programs. Moreover, psychological distress has been reported (and is exemplified by our psychological autopsy study) to be at its highest when sight loss is not complete, but the prognosis is unfavorable.10 Therefore, early intervention is imperative for enabling successful psychological adjustment.[21]

Blindness can occur in combination with such conditions as intellectual disability, autism spectrum disorders, cerebral palsy, hearing impairments, and epilepsy.[22][23] Blindness in combination with hearing loss is known as deafblindness.

It has been estimated that over half of totally blind people have non-24-hour sleepwake disorder, a condition in which a person's circadian rhythm, normally slightly longer than 24 hours, is not entrained (re-set) to the light/dark cycle.[24][25]

The most common causes of visual impairment globally in 2010 were:

The most common causes of blindness in 2010 were:

About 90% of people who are visually impaired live in the developing world.[4] Age-related macular degeneration, glaucoma, and diabetic retinopathy are the leading causes of blindness in the developed world.[26]

Of these, cataract is responsible for >65%, or more than 22 million cases of blindness, and glaucoma is responsible for 6 million cases.

Cataracts: is the congenital and pediatric pathology that describes the greying or opacity of the crystalline lens, which is most commonly caused by intrauterine infections, metabolic disorders, and genetically transmitted syndromes.[27] Cataracts are the leading cause of child and adult blindness that doubles in prevalence with every ten years after the age of 40.[28] Consequently, today cataracts are more common among adults than in children.[27] That is, people face higher chances of developing cataracts as they age. Nonetheless, cataracts tend to have a greater financial and emotional toll upon children as they must undergo expensive diagnosis, long term rehabilitation, and visual assistance.[29] Also, according to the Saudi Journal for Health Sciences, sometimes patients experience irreversible amblyopia[27] after pediatric cataract surgery because the cataracts prevented the normal maturation of vision prior to operation.[30] Despite the great progress in treatment, cataracts remain a global problem in both economically developed and developing countries.[31] At present, with the variant outcomes as well as the unequal access to cataract surgery, the best way to reduce the risk of developing cataracts is to avoid smoking and extensive exposer to sun light (i.e. UV-B rays).[28]

Glaucoma is a congenital and pediatric eye disease characterized by increased pressure within the eye or intraocular pressure (IOP).[32] Glaucoma causes visual field loss as well as severs the optic nerve.[33] Early diagnosis and treatment of glaucoma in patients is imperative because glaucoma is triggered by non-specific levels of IOP.[33] Also, another challenge in accurately diagnosing glaucoma is that the disease has four etiologies: 1) inflammatory ocular hypertension syndrome (IOHS); 2) severe uveitic angle closure; 3) corticosteroid-induced; and 4) a heterogonous mechanism associated with structural change and chronic inflammation.[32] In addition, often pediatric glaucoma differs greatly in etiology and management from the glaucoma developed by adults.[34] Currently, the best sign of pediatric glaucoma is an IOP of 21mm Hg or greater present within a child.[34] One of the most common causes of pediatric glaucoma is cataract removal surgery, which lead to an incidence rate of about 12.2% among infants and 58.7% among 10 year olds.[34]

Childhood blindness can be caused by conditions related to pregnancy, such as congenital rubella syndrome and retinopathy of prematurity. Leprosy and onchocerciasis each blind approximately 1 million individuals in the developing world.

The number of individuals blind from trachoma has decreased in the past 10 years from 6 million to 1.3 million, putting it in seventh place on the list of causes of blindness worldwide.

Central corneal ulceration is also a significant cause of monocular blindness worldwide, accounting for an estimated 850,000 cases of corneal blindness every year in the Indian subcontinent alone. As a result, corneal scarring from all causes is now the fourth greatest cause of global blindness.[35]

Eye injuries, most often occurring in people under 30, are the leading cause of monocular blindness (vision loss in one eye) throughout the United States. Injuries and cataracts affect the eye itself, while abnormalities such as optic nerve hypoplasia affect the nerve bundle that sends signals from the eye to the back of the brain, which can lead to decreased visual acuity.

Cortical blindness results from injuries to the occipital lobe of the brain that prevent the brain from correctly receiving or interpreting signals from the optic nerve. Symptoms of cortical blindness vary greatly across individuals and may be more severe in periods of exhaustion or stress. It is common for people with cortical blindness to have poorer vision later in the day.

Blinding has been used as an act of vengeance and torture in some instances, to deprive a person of a major sense by which they can navigate or interact within the world, act fully independently, and be aware of events surrounding them. An example from the classical realm is Oedipus, who gouges out his own eyes after realizing that he fulfilled the awful prophecy spoken of him. Having crushed the Bulgarians, the Byzantine Emperor Basil II blinded as many as 15,000 prisoners taken in the battle, before releasing them.[36] Contemporary examples include the addition of methods such as acid throwing as a form of disfigurement.

People with albinism often have vision loss to the extent that many are legally blind, though few of them actually cannot see. Leber's congenital amaurosis can cause total blindness or severe sight loss from birth or early childhood.

Recent advances in mapping of the human genome have identified other genetic causes of low vision or blindness. One such example is Bardet-Biedl syndrome.

Rarely, blindness is caused by the intake of certain chemicals. A well-known example is methanol, which is only mildly toxic and minimally intoxicating, and breaks down into the substances formaldehyde and formic acid which in turn can cause blindness, an array of other health complications, and death.[37] When competing with ethanol for metabolism, ethanol is metabolized first, and the onset of toxicity is delayed. Methanol is commonly found in methylated spirits, denatured ethyl alcohol, to avoid paying taxes on selling ethanol intended for human consumption. Methylated spirits are sometimes used by alcoholics as a desperate and cheap substitute for regular ethanol alcoholic beverages.

It is critical that all people be examined by someone specializing in low vision care prior to other rehabilitation training to rule out potential medical or surgical correction for the problem and to establish a careful baseline refraction and prescription of both normal and low vision glasses and optical aids. Only a doctor is qualified to evaluate visual functioning of a compromised visual system effectively.[44]

The American Medical Association provide an approach to evaluating visual loss as it affects an individual's ability to perform activities of daily living.[19]

The World Health Organization estimates that 80% of visual loss is either preventable or curable with treatment.[4] This includes cataracts, onchocerciasis, trachoma, glaucoma, diabetic retinopathy, uncorrected refractive errors, and some cases of childhood blindness.[8] The Center for Disease Control and Prevention estimates that half of blindness in the United States is preventable.[2]

Aside from medical help, various sources provide information, rehabilitation, education, and work and social integration.

Many people with serious visual impairments can travel independently, using a wide range of tools and techniques. Orientation and mobility specialists are professionals who are specifically trained to teach people with visual impairments how to travel safely, confidently, and independently in the home and the community. These professionals can also help blind people to practice travelling on specific routes which they may use often, such as the route from one's house to a convenience store. Becoming familiar with an environment or route can make it much easier for a blind person to navigate successfully.

Tools such as the white cane with a red tip - the international symbol of blindness - may also be used to improve mobility. A long cane is used to extend the user's range of touch sensation. It is usually swung in a low sweeping motion, across the intended path of travel, to detect obstacles. However, techniques for cane travel can vary depending on the user and/or the situation. Some visually impaired persons do not carry these kinds of canes, opting instead for the shorter, lighter identification (ID) cane. Still others require a support cane. The choice depends on the individual's vision, motivation, and other factors.

A small number of people employ guide dogs to assist in mobility. These dogs are trained to navigate around various obstacles, and to indicate when it becomes necessary to go up or down a step. However, the helpfulness of guide dogs is limited by the inability of dogs to understand complex directions. The human half of the guide dog team does the directing, based upon skills acquired through previous mobility training. In this sense, the handler might be likened to an aircraft's navigator, who must know how to get from one place to another, and the dog to the pilot, who gets them there safely.

GPS devices can also be used as a mobility aid. Such software can assist blind people with orientation and navigation, but it is not a replacement for traditional mobility tools such as white canes and guide dogs.

Some blind people are skilled at echolocating silent objects simply by producing mouth clicks and listening to the returning echoes. It has been shown that blind echolocation experts use what is normally the "visual" part of their brain to process the echoes.[45][46]

Technology to allow blind people to drive motor vehicles is currently being developed.[47]

Government actions are sometimes taken to make public places more accessible to blind people. Public transportation is freely available to the blind in many cities. Tactile paving and audible traffic signals can make it easier and safer for visually impaired pedestrians to cross streets. In addition to making rules about who can and cannot use a cane, some governments mandate the right-of-way be given to users of white canes or guide dogs.

Most visually impaired people who are not totally blind read print, either of a regular size or enlarged by magnification devices. Many also read large-print, which is easier for them to read without such devices. A variety of magnifying glasses, some handheld, and some on desktops, can make reading easier for them.

Others read Braille (or the infrequently used Moon type), or rely on talking books and readers or reading machines, which convert printed text to speech or Braille. They use computers with special hardware such as scanners and refreshable Braille displays as well as software written specifically for the blind, such as optical character recognition applications and screen readers.

Some people access these materials through agencies for the blind, such as the National Library Service for the Blind and Physically Handicapped in the United States, the National Library for the Blind or the RNIB in the United Kingdom.

Closed-circuit televisions, equipment that enlarges and contrasts textual items, are a more high-tech alternative to traditional magnification devices.

There are also over 100 radio reading services throughout the world that provide people with vision impairments with readings from periodicals over the radio. The International Association of Audio Information Services provides links to all of these organizations.

Access technology such as screen readers, screen magnifiers and refreshable Braille displays enable the blind to use mainstream computer applications and mobile phones. The availability of assistive technology is increasing, accompanied by concerted efforts to ensure the accessibility of information technology to all potential users, including the blind. Later versions of Microsoft Windows include an Accessibility Wizard & Magnifier for those with partial vision, and Microsoft Narrator, a simple screen reader. Linux distributions (as live CDs) for the blind include Oralux and Adriane Knoppix, the latter developed in part by Adriane Knopper who has a visual impairment. Mac OS also comes with a built-in screen reader, called VoiceOver.

The movement towards greater web accessibility is opening a far wider number of websites to adaptive technology, making the web a more inviting place for visually impaired surfers.

Experimental approaches in sensory substitution are beginning to provide access to arbitrary live views from a camera.

Modified visual output that includes large print and/or clear simple graphics can be of benefit to users with some residual vision.[48]

Blind people may use talking equipment such as thermometers, watches, clocks, scales, calculators, and compasses. They may also enlarge or mark dials on devices such as ovens and thermostats to make them usable. Other techniques used by blind people to assist them in daily activities include:

Most people, once they have been visually impaired for long enough, devise their own adaptive strategies in all areas of personal and professional management.

For the blind, there are books in braille, audio-books, and text-to-speech computer programs, machines and e-book readers. Low vision people can make use of these tools as well as large-print reading materials and e-book readers that provide large font sizes.

Computers are important tools of integration for the visually impaired person. They allow, using standard or specific programs, screen magnification and conversion of text into sound or touch (Braille line), and are useful for all levels of visual handicap. OCR scanners can, in conjunction with text-to-speech software, read the contents of books and documents aloud via computer. Vendors also build closed-circuit televisions that electronically magnify paper, and even change its contrast and color, for visually impaired users. For more information, consult Assistive technology.

In adults with low vision there is no conclusive evidence supporting one form of reading aid over another.[50] In several studies stand-based closed-circuit television and hand-held closed-circuit television allowed faster reading than optical aids.[50] While electronic aids may allow faster reading for individuals with low vision, portability, ease of use, and affordability must be considered for people.[50]

Children with low vision sometimes have reading delays, but do benefit from phonics-based beginning reading instruction methods. Engaging phonics instruction is multisensory, highly motivating, and hands-on. Typically students are first taught the most frequent sounds of the alphabet letters, especially the so-called short vowel sounds, then taught to blend sounds together with three-letter consonant-vowel-consonant words such as cat, red, sit, hot, sun. Hands-on (or kinesthetically appealing) VERY enlarged print materials such as those found in "The Big Collection of Phonics Flipbooks" by Lynn Gordon (Scholastic, 2010) are helpful for teaching word families and blending skills to beginning readers with low vision. Beginning reading instructional materials should focus primarily on the lower-case letters, not the capital letters (even though they are larger) because reading text requires familiarity (mostly) with lower-case letters. Phonics-based beginning reading should also be supplemented with phonemic awareness lessons, writing opportunities, and lots of read-alouds (literature read to children daily) to stimulate motivation, vocabulary development, concept development, and comprehension skill development. Many children with low vision can be successfully included in regular education environments. Parents may need to be vigilant to ensure that the school provides the teacher and students with appropriate low vision resources, for example technology in the classroom, classroom aide time, modified educational materials, and consultation assistance with low vision experts.

Communication with the visually impaired can be more difficult than communicating with someone who doesn't have vision loss. However, many people are uncomfortable with communicating with the blind, and this can cause communication barriers. One of the biggest obstacles in communicating with visually impaired individuals comes from face-to-face interactions.[51] There are many factors that can cause the sighted to become uncomfortable while communicating face to face.There are many non-verbal factors, which hinder communication between the visually impaired and the sighted, more often than verbal factors do. These factors, which Rivka Bialistock[51] mentions in her article, include:

The blind person sends these signals or types of non-verbal communication without being aware that they are doing so. These factors can all affect the way an individual would feel about communicating with the visually impaired. This leaves the visually impaired feeling rejected and lonely.

In the article Towards better communication, from the interest point of view. Orskills of sight-glish for the blind and visually impaired, the author, Rivka Bialistock [51] comes up with a method to reduce individuals being uncomfortable with communicating with the visually impaired. This method is called blind-glish or sight-glish, which is a language for the blind, similar to English. For example, babies, who are not born and able to talk right away, communicate through sight-glish, simply seeing everything and communicating non-verbally. This comes naturally to sighted babies, and by teaching this same method to babies with a visual impairment can improve their ability to communicate better, from the very beginning.

To avoid the rejected feeling of the visually impaired, people need to treat the blind the same way they would treat anyone else, rather than treating them like they have a disability, and need special attention. People may feel that it is improper to, for example, tell their blind child to look at them when they are speaking. However, this contributes to the sight-glish method.[51] It is important to disregard any mental fears or uncomfortable feelings people have while communicating (verbally and non-verbally) face-to-face.

Individuals with a visual disability not only have to find ways to communicate effectively with the people around them, but their environment as well. The blind or visually impaired rely largely on their other senses such as hearing, touch, and smell in order to understand their surroundings.[52]

Sound is one of the most important senses that the blind or visually impaired use in order to locate objects in their surroundings. A form of echolocation is used, similarly to that of a dolphin or bat.[53] Echolocation from a person's perspective is when the person uses sound waves generated from speech or other forms of noise such as cane tapping, which reflect off of objects and bounce back at the person giving them a rough idea of where the object is. This does not mean they can depict details based on sound but rather where objects are in order to interact, or avoid them. Increases in atmospheric pressure and humidity increase a person's ability to use sound to their advantage as wind or any form of background noise impairs it.[52]

Touch is also an important aspect of how blind or visually impaired people perceive the world. Touch gives immense amount of information in the persons immediate surrounding.Feeling anything with detail gives off information on shape, size, texture, temperature, and many other qualities. Touch also helps with communication; braille is a form of communication in which people use their fingers to feel elevated bumps on a surface and can understand what is meant to be interpreted.[54] There are some issues and limitations with touch as not all objects are accessible to feel, which makes it difficult to perceive the actual object. Another limiting factor is that the learning process of identifying objects with touch is much slower than identifying objects with sight. This is due to the fact the object needs to be approached and carefully felt until a rough idea can be constructed in the brain.[52]

Certain smells can be associated with specific areas and help a person with vision problems to remember a familiar area. This way there is a better chance of recognizing an areas layout in order to navigate themselves through. The same can be said for people as well. Some people have their own special odor that a person with a more trained sense of smell can pick up. A person with an impairment of their vision they can use this to recognize people within their vicinity without them saying a word.[52]

Visual impairment can have profound effects on the development of infant and child communication. The language and social development of a child or infant can be very delayed by the inability to see the world around them.

Social development includes interactions with the people surrounding the infant in the beginning of its life. To a child with vision, a smile from a parent is the first symbol of recognition and communication, and is almost an instant factor of communication. For a visually impaired infant, recognition of a parent's voice will be noticed at approximately two months old, but a smile will only be evoked through touch between parent and baby. This primary form of communication is greatly delayed for the child and will prevent other forms of communication from developing. Social interactions are more complicated because subtle visual cues are missing and facial expressions from others are lost.

Due to delays in a child's communication development, they may appear to be disinterested in social activity with peers, non-communicative and un-education on how to communicate with other people. This may cause the child to be avoided by peers and consequently over protected by family members.

With sight, much of what is learned by a child is learned through imitation of others, where as a visually impaired child needs very planned instruction directed at the development of postponed imitation. A visually impaired infant may jabber and imitate words sooner than a sighted child, but may show delay when combining words to say themselves, the child may tend to initiate few questions and their use of adjectives is infrequent. Normally the child's sensory experiences are not readily coded into language and this may cause them to store phrases and sentences in their memory and repeat them out of context. The language of the blind child does not seem to mirror his developing knowledge of the world, but rather his knowledge of the language of others.

A visually impaired child may also be hesitant to explore the world around them due to fear of the unknown and also may be discouraged from exploration by overprotective family members. Without concrete experiences, the child is not able to develop meaningful concepts or the language to describe or think about them.[55]

Visual impairment has the ability to create consequences for health and well being. Visual impairment is increasing especially among older people. It is recognized that those individuals with visual impairment are likely to have limited access to information and healthcare facilities, and may not receive the best care possible because not all health care professionals are aware of specific needs related to vision.

The WHO estimates that in 2012 there were 285 million visually impaired people in the world, of which 246 million had low vision and 39 million were blind.[4]

Of those who are blind 90% live in the developing world.[56] Worldwide for each blind person, an average of 3.4 people have low vision, with country and regional variation ranging from 2.4 to 5.5.[57]

By age: Visual impairment is unequally distributed across age groups. More than 82% of all people who are blind are 50 years of age and older, although they represent only 19% of the world's population. Due to the expected number of years lived in blindness (blind years), childhood blindness remains a significant problem, with an estimated 1.4 million blind children below age 15.

By gender: Available studies consistently indicate that in every region of the world, and at all ages, females have a significantly higher risk of being visually impaired than males.

By geography: Visual impairment is not distributed uniformly throughout the world. More than 90% of the world's visually impaired live in developing countries.[57]

Since the estimates of the 1990s, new data based on the 2002 global population show a reduction in the number of people who are blind or visually impaired, and those who are blind from the effects of infectious diseases, but an increase in the number of people who are blind from conditions related to longer life spans.[57]

In 1987, it was estimated that 598,000 people in the United States met the legal definition of blindness.[58] Of this number, 58% were over the age of 65.[58] In 1994-1995, 1.3 million Americans reported legal blindness.[59]

To determine which people qualify for special assistance because of their visual disabilities, various governments have specific definitions for legal blindness.[60] In North America and most of Europe, legal blindness is defined as visual acuity (vision) of 20/200 (6/60) or less in the better eye with best correction possible. This means that a legally blind individual would have to stand 20 feet (6.1m) from an object to see itwith corrective lenseswith the same degree of clarity as a normally sighted person could from 200 feet (61m). In many areas, people with average acuity who nonetheless have a visual field of less than 20 degrees (the norm being 180 degrees) are also classified as being legally blind. Approximately ten percent of those deemed legally blind, by any measure, have no vision. The rest have some vision, from light perception alone to relatively good acuity. Low vision is sometimes used to describe visual acuities from 20/70 to 20/200.[61]

The Moche people of ancient Peru depicted the blind in their ceramics.[62]

In Greek myth, Tiresias was a prophet famous for his clairvoyance. According to one myth, he was blinded by the Gods as punishment for revealing their secrets, while another holds that he was blinded as punishment after he saw Athena naked while she was bathing. In the Odyssey, the one-eyed Cyclops Polyphemus captures Odysseus, who blinds Polyphemus to escape. In Norse mythology, Loki tricks the blind God Hr into killing his brother Baldr, the God of happiness.

The New Testament contains numerous instances of Jesus performing miracles to heal the blind. According to the Gospels, Jesus healed the two blind men of Galilee, the blind man of Bethsaida, the blind man of Jericho and the man who was born blind.

The parable of the blind men and an elephant has crossed between many religious traditions and is part of Jain, Buddhist, Sufi and Hindu lore. In various versions of the tale, a group of blind men (or men in the dark) touch an elephant to learn what it is like. Each one feels a different part, but only one part, such as the side or the tusk. They then compare notes and learn that they are in complete disagreement.

"Three Blind Mice" is a medieval English nursery rhyme about three blind mice whose tails are cut off after chasing the farmer's wife. The work is explicitly incongruous, ending with the comment Did you ever see such a sight in your life, As three blind mice?

Poet John Milton, who went blind in mid-life, composed On His Blindness, a sonnet about coping with blindness. The work posits that [those] who best Bear [God]'s mild yoke, they serve him best.

The Dutch painter and engraver Rembrandt often depicted scenes from the apocryphal Book of Tobit, which tells the story of a blind patriarch who is healed by his son, Tobias, with the help of the archangel Raphael.[63]

Slaver-turned-abolitionist John Newton composed the hymn Amazing Grace about a wretch who "once was lost, but now am found, Was blind, but now I see." Blindness, in this sense, is used both metaphorically (to refer to someone who was ignorant but later became knowledgeable) and literally, as a reference to those healed in the Bible. In the later years of his life, Newton himself would go blind.

H. G. Wells' story "The Country of the Blind" explores what would happen if a sighted man found himself trapped in a country of blind people to emphasise societies attitude to blind people by turning the situation on its head.

Bob Dylan's anti-war song "Blowin' in the Wind" twice alludes to metaphorical blindness: How many times can a man turn his head // and pretend that he just doesn't see... How many times must a man look up // Before he can see the sky?

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Visual impairment - Wikipedia, the free encyclopedia

With the onset of Alzheimers disease, information transfer at the synapses (the connection between the nerve cells and extensions) starts to break down, and the number of synapses decreases significantly.

Autoimmune diseases are conditions in which the patients immune system generates cellular and antibody responses to substances and tissues normally present in the body.

In each condition there is chronic obstruction of the flow of air through the airways and out of the lungs, and the obstruction generally is permanent and may be progressive over time.

Rheumatoid Arthritis is an autoimmune disease that attacks the bodys own tissues, specifically the synovium, a thin membrane lining the joints. As a result, joint fluid builds up, causing pain in the joints and inflammation thats systemic.

Parkinson's disease is a chronic progressive neurological disease that affects nerve cells (neurons) in an area of the brain known as the substantia nigra.

Osteoarthritis, or degenerative joint disease, is the most common type of arthritis. It is caused by the degradation of a joints cartilage.

Multiple sclerosis (or MS) is a degenerative disease involving the deterioration of nerve cells. MS attacks the central nervous system (CNS), which is made up of the brain, spinal cord, and optic nerves.

Diabetes is the condition in which the body does not properly process food for use as energy. When you have diabetes, your body either doesn't make enough insulin or can't use its own insulin as well as it should.

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Stem Cell Therapy, Stem Cell Treatments, Stem Cell Clinics ...

WHAT ARE STEM CELLS?

Stem cells are super unique in that they have the ability to go through numerous cycles and cell divisions while maintaining the undifferentiated state. Primarily, stem cells are capable of self-renewal and can transform themselves into other cell types of the same tissue. Their crucial role is to replenish dying cells and regenerate damaged tissue. Stem cells have a limited life expectation due to environmental and intrinsic stress factors. Because their life is endangered by internal and external stresses, stem cells have to be protected and supported to delay preliminary aging. In aged bodies, the number and activity of stem cells in reduced.

Until several years ago, the tart, unappealing breed of the Swiss-grown Uttwiler Sptlauber apples, did not seem to offer anything of value. That was until Swiss scientists discovered the unusual longevity of the stem cells that kept these apples alive months after other apples shriveled and fell off their trees. In the rural region of Switzerland, home of these magical apples, it was discovered that when the unpicked apples or tree bark was punctured, Swiss Apple trees have the ability to heal themselves and last longer than other varieties. What was the secret to these apples prolonged lives?

These scientists got to work to find out. What they revealed was that apple stem cells work just like human stem cells, they work to maintain and repair skin tissue. The main difference is that unlike apple stem cells, skin stem cells do not have a long lifespan, and once they begin depleting, the signs of aging start kicking in (in the forms of loose skin, wrinkles, the works). Time to harness these apple stem cells into anti aging skin care! Not so fast. As mentioned, Uttwiler Sptlauber apples are now very rare to the point that the extract can no longer be made in a traditional fashion. The great news is that scientists developed a plant cell culture technology, which involves breeding the apple stem cells in the laboratory.

Human stem cells on the skins epidermis are crucial to replenish the skin cells that are lost due to continual shedding. When epidermal stem cells are depleted, the number of lost or dying skin cells outpaces the production of new cells, threatening the skins health and appearance.

Like humans, plants also have stem cells. Enter the stem cells of the Uttwiler Sptlauber apple tree, whose fruit demonstrates an exceptionally long shelf-life. How can these promising stem cells help our skin?

Studies show that apple stem cells boosts production of human stem cells, protect the cell from stress, and decreases wrinkles. How does it work? The internal fluid of these plant cells contains components that help to protect and maintain human stem cells. Apple stem cells contain metabolites to ensure longevity as the tree is known for the fact that its fruit keep well over long periods of time.

When tested in vitro, the apple stem cell extract was applied to human stem cells from umbilical cords and was found to increase the number of the stem cells in culture. Furthermore, the addition of the ingredient to umbilical cord stem cells appeared to protect the cells from environmental stress such as UV light.

Apple stem cells do not have to be fed through the umbilical cord to benefit our skin! The extract derived from the plant cell culture technology is being harnessed as an active ingredient in anti aging skincare products. When delivered into the skin nanotechnology, the apple stem cells provide more dramatic results in decreasing lines, wrinkles, and environmental damage.

Currently referred to as The Fountain of Youth, intense research has proved that with just a concentration level of 0.1 % of the PhytoCellTec (apple stem cell extract) could proliferate a wealth of human stem cells by an astounding 80%! These wonder cells work super efficiently and are completely safe. Of the numerous benefits of apple stems cells, the most predominant include:

Skin Layers

Skin Cell Activity Before

Skin Cell Activity After 1 Hour

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Apple Stem Cells - Sonya Dakar Skin Clinic

2014 Stem Cell Pioneer Awards Stem Cell Awards Ceremony recognizing those pioneers in the field of Regenerative Therapy. Highlights of a few of the patients treated from 2006 to present. Treatments for heart, lung, neurologic and other diseases.

Why do patients choose us for their treatment? Especially those seeking serious outcomes? Why does Regenocyte have the most consistent, reproducible and best outcomes in the field of Regenerative Medicine? Click here to read more >>

If you are searching the web for stem cell doctors because you or a loved one suffer from severe heart, lung, or circulatory problems, it is possible that the latest therapies using adult stem cells can restore your quality of life to an unexpected level.

Because adult stem cell therapies are safe, simple, and minimally-invasive, they particularly help those who have exhausted the possibilities of other treatments.

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Regenocyte is a group of stem cell doctors leading the world in the therapeutic use of adult stem cell therapy. Headquartered on the Gulf Coast of Florida in Bonita Springs, Florida. Regenocyte is comprised of both US and international Physicians and staff with extensive training and experience in adult stem cell therapy.

Treatments using the patients own activated adult stem cells have been shown to restore a significant amount of normal function that had been written off as gone forever. With increases in function, patients recover their independence from medications, breathing devices and other kinds of medical apparatus. They may be freed from their dependence upon others.

Read more about the benefits of adult stem cell therapy.

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Regenocyte are leading stem cell doctors in the USA.

Every one of us completely regenerates our own skin every 7 days. A cut heals itself and disappears in a week or two. Every single cell in our skeleton is replaced every 7 years.

The future of medicine lies in understanding how the body creates itself out of a single cell and the mechanisms by which it renews itself throughout life.

When we achieve this goal, we will be able to replace damaged tissues and help the body regenerate itself, potentially curing or easing the suffering of those afflicted by disorders like heart disease, Alzheimers, Parkinsons, diabetes, spinal cord injury and cancer.

Research at the institute leverages Stanfords many strengths in a way that promotes that goal. The institute brings together experts from a wide range of scientific and medical fields to create a fertile, multidisciplinary research environment.

There are four major research areas of emphasis at the institute:

Theres no way to know, beforehand, which particular avenue of stem cell research will most expediently yield a successful treatment or cure. Therefore, we need to vigorously pursue a broad number of promising leads concurrently.

--Philip A. Pizzo, MD Carl and Elizabeth Naumann Professor Dean, Stanford University School of Medicine

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Research - Stem Cell Biology and Regenerative Medicine ...

Here we have compiled a list of several clinics offering stem cell treatments. Please note that the "conditions treated" refers to the conditions that THEY claim to treat. Most, if not all, stem cell treatments (except hematopoietic stem cell transplantation) aren't FDA approved, meaning that they haven't been clincally tested for safety or efficacy. Please be aware that receiving an unapproved medical treatment isrisky and may cause serious complications and possibly death.

It was only a few years ago when Europe's most popular stem cell clinic (XCell-center) was forced to close after one of the treatments caused the death of a boy. In the past, we have also covered the case of a woman that had serious adverse effects following an unapproved cosmetic stem cell treatment(facelift).

We have not included clinics offering hematopoietic stem cell transplantation, as this treatment is medically approved and offered virtually in any country that has an above the average hospital.

The stem cell clinics are categorised by alphabetical order. We are not paid by any of them and we have listed them for your ease. We have probably missed a few ones, feel free to leave a comment and we will add them asap.

Stem cell clinics list

Beijing Puhua International Hospital

Conditions Treated:Diabetes, Epilepsy, Stroke, Ataxia, Spinal Cord Injuries, Parkinson's Disease, Brain Injury, Multiple Sclerosis, Batten's Disease

Interview of a patient treated in Beijing Puhua International Hospital. The video is from the hospital's official youtube channel, so it may be biased

Elises International

Conditions Treated: No info available at their website

Advertisement video ofElises International

EmCell

Conditions Treated:ALS, Alzheimer's,Anemia, Cancer, Eye Diseases, Diabetes, Liver Diseases, Multiple Sclerosis Parkinson, and other

Location:Ukraine

EmCell Advertisement

Global Stem Cells

Conditions Treated:Type 2 Diabetes, Hepatitis C, Osteoarthritis, joint pain, hair regrowth, cosmetic anti-aging, ulcerative colitis, heart disease

Location:Bangkok Thailand

MD Stem Cells

New Zealand Stem Cell Clinic

Stem Cell Institute

Video of a patient treated in theStem Cell Institute. The video is taken from the clinic's official youtube channell,so it may be biased.

Okyanos Heart Institute

Conditions Treated:Cardiac conditions

Okyanos Promotinal Video

StemGenex

Conditions Treated: Multiple sclerosis, Alzheimer, Parkinson, Diabetes, Rheumatoid Arthritis and other

Location:San Diego, California.

Stem Cells Thailand

Conditions Treated:Alzheimer, Autism, Diabetes, Erectile Dysfunction, Face lift, Multiple Sclerosis, Arthritis and other

Regennex

Conditions Treated: Regennex mainly offers treatments for bone and cartilage regeneration in all major joints like knee, ankle, hip, back, shoulder etc

Dr. Centeno, founder of the clinic, talking about Regenexx

Link:
Stem Cell Clinics List | Stem Cells Freak

United States Renal Data System: 2012 Annual Data Report. Atlas of Chronic Kidney Disease and End-Stage Renal Disease in the United States; 2012.

http://www.usrds.org/adr.aspx webcite

Weiner DE: Public health consequences of chronic kidney disease.

Clin Pharmacol Ther 2009, 86:566-569.

Schedl A: Renal abnormalities and their developmental origin.

Nat Rev Genet 2007, 8:791-802.

Bonventre JV, Yang L: Cellular pathophysiology of ischemic acute kidney injury.

J Clin Invest 2011, 121:4210-4221.

Murugan R, Kellum JA: Acute kidney injury: whats the prognosis?

Nat Rev Nephrol 2011, 7:209-217.

Venkatachalam MA, Griffin KA, Lan R, Geng H, Saikumar P, Bidani AK: Acute kidney injury: a springboard for progression in chronic kidney disease.

Am J Physiol Renal Physiol 2010, 298:F178-F1094.

El Nahas AM, Bello AK: Chronic kidney disease: the global challenge.

Lancet 2005, 365:331-340.

Stocum DL: Stem cells in regenerative biology and medicine.

Wound Rep Reg 2001, 9:429-442.

Fioretto P, Steffes MW, Sutherland DER, Goetz FC, Mauer M: Reversal of lesions of diabetic nephropathy after pancreas transplantation.

N Engl J Med 1998, 339:69-75.

Fioretto P, Sutherland DER, Najafian B, Mauer M: Remodeling of renal interstitial and tubular lesions in pancreas transplant recipients.

Kidney Int 2006, 69:907-910.

Weissman IL: Stem cells: units of development, units of regeneration, and units in evolution.

Cell 2000, 100:157-168.

Yamanaka S, Blau HM: Nuclear reprogramming to a pluripotent state by three approaches.

Nature 2010, 465:704-712.

Hsu YC, Fuchs E: A family business: stem cell progeny join the niche to regulate homeostasis.

Nat Rev Mol Cell Bio 2012, 13:103-114.

Burness ML, Sipkins DA: The stem cell niche in health and malignancy.

Semin Cancer Biol 2010, 20:107-115.

Sharpless NE, DePinho RA: How stem cells age and why this makes us grow old.

Nat Rev Mol Cell Biol 2007, 8:703-713.

McCampbell KK, Wingert RA: Renal stem cells: fact or science fiction?

Biochem J 2012, 444:153-168.

Reilly RF, Bulger RE, Kriz W, In Diseases of the Kidney and Urinary Tract, Eighth Edition: Structural-functional relationships in the kidney. Philadelphia: Lippincott Williams & Wilkins: Edited by Schrier RW; 2007:2-53.

Little MH, Brennan J, Georgas K, Davies JA, Davidson DR, Baldock RA: A high-resolution anatomical ontology of the developing murine genitourinary tract.

Gene Expr Patterns 2007, 7:680-699.

Brunskill EW, Aronow BJ, Georgas K, Rumballe B, Valerius MT, Aronow J: Atlas of gene expression in the developing kidney at microanatomic resolution.

Dev Cell 2008, 15:781-791.

Mugford JW, Yu J, Kobayashi A, McMahon AP: High-resolution gene expression analysis of the developing mouse kidney defines novel cellular compartments within the nephron progenitor population.

Dev Biol 2009, 333:312-323.

Yu J, Valerius MT, Duah M, Staser K, Hansard JK, Guo JJ: Identification of molecular compartments and genetic circuitry in the developing mammalian kidney.

Development 2012, 139:1863-1873.

Wingert RA, Davidson AJ: The zebrafish pronephros: a model to study nephron segmentation.

Kidney Int 2008, 73:1120-1127.

Nyengaard JR, Bendtsen TF: Glomerular number and size in relation to age, kidney weight, and body surface in normal man.

Anat Rec 1992, 232:194-201.

Hughson M, Farris III: AB, Douglas-Denton R, Yoy WE, Bertram JF: Glomerular number and size in autopsy kidneys: the relationship to birth weight.

Kidney Int 2003, 63:2113-2122.

Potter EL, Thierstein ST: Glomerular development in the kidney as an index of fetal maturity.

J Pediatr 1943, 22:695-706.

Hartman HA, Lai HL, Patterson LT: Cessation of renal morphogenesis in mice.

Dev Biol 2007, 301:379-387.

Solomon S: Developmental changes in nephron number, proximal tubule length and superficial nephron glomerular filtration rate of rats.

J Physiol 1977, 272:573-589.

Wesson LG: Compensatory growth and other growth responses of the kidney.

Nephron 1989, 51:149-184.

de Rouffignac C, Monnens L: Functional and morphologic maturation of superficial and juxtamedullary nephrons in the rat.

J Physiol 1976, 262:119-129.

Spitzer A, Brandis M: Functional and morphologic maturation of the superficial nephrons.

J Clin Invest 1974, 53:279-287.

Blanpain C, Fuchs E: Epidermal homeostasis: a balancing act of stem cells in the skin.

Nat Rev Mol Cell Bio 2009, 10:207-217.

van der Flier LG, Clevers H: Stem cells, self-renewal, and differentiation in the intestinal epithelium.

Annu Rev Physiol 2009, 71:241-260.

Prescott LF: The normal urinary excretion rates of renal tubular cells, leucocytes and red blood cells.

Clin Sci 1966, 31:425-435.

Drrenhaus A, Mller JIF, Golka K, Jedrusik P, Schulze H, Fllmann W: Cultures of exfoliated epithelial cells from different locations of the human urinary tract and the renal tubular system.

Arch Toxicol 2000, 74:618-626.

Vogelmann SU, Nelson WJ, Myers BD, Lemley KV: Urinary excretion of viable podocytes in health and renal disease.

Am J Physiol Renal Physiol 2003, 285:F40-F48.

Rahmoune H, Thompson PW, Ward JM, Smith CD, Hong G, Brown J: Glucose transporters in human renal proximal tubular cells isolated from the urine in patients with non-insulin-dependent diabetes.

Diabetes 2005, 54:3427-3434.

Messier B, Leblond CP: Cell proliferation and migration as revealed by radioautography after injection of thymidine-H3 into male rats and mice.

Amer J Anat 1960, 106:247-285.

Maeshima A, Yamashita S, Nojima Y: Identification of renal progenitor-like tubular cells that participate in the regeneration processes of the kidney.

J Am Soc Nephrol 2003, 14:3138-3146.

Maeshima A, Sakurai H, Nigam SK: Adult kidney tubular cell population showing phenotypic plasticity, tubulogenic capacity, and integration capability into developing kidney.

J Am Soc Nephrol 2006, 17:188-198.

Vogetseder A, Karadeniz A, Kaissling B, Le Hir M: Tubular cell proliferation in the healthy rat kidney.

Histochem Cell Biol 2005, 124:97-104.

Vogetseder A, Palan T, Bacic D, Kaissling B, Le Hir M: Proximal tubular epithelial cells are generated by division of differentiated cells in the healthy kidney.

Am J Physiol Cell Physiol 2007, 292:C807-C813.

Vogetseder A, Picard N, Gaspert A, Walch M, Kaissling B, Le Hir M: Proliferation capacity of the renal proximal tubule involves the bulk of differentiated epithelial cells.

Am J Physiol Cell Physiol 2008, 294:C22-C28.

Nadasdy T, Laszik Z, Blick KE, Johnson LD, Silva FG: Proliferative activity of intrinsic cell populations in the normal human kidney.

J Am Soc Nephrol 1994, 4:2032-2039.

Hayslett JP, Kashgarian M, Epstein FH: Functional correlates of compensatory renal hypertrophy.

J Clin Invest 1968, 47:774-781.

Hostetter TH: Progression of renal disease and renal hypertrophy.

Annu Rev Physiol 1995, 57:263-278.

Cuppage FE, Tate A: Repair of the nephron following injury with mercuric chloride.

Am J Pathol 1967, 51:405-429.

Houghton DC, Hartnett M, Campbell-Boswell M, Porter G, Bennett W: A light and electron microscopic analysis of gentamicin nephrotoxicity in rats.

Am J Pathol 1976, 82:589-612.

Witzgall R, Brown D, Schwarz C, Bonventre JV: Localization of proliferating cell nuclear antigen, vimentin, c-Fos and clusterin in the postischemic kidney. Evidence for a heterogenous genetic response among nephron segments, and a large pool of mitotically active and dedifferentiated cells.

J Clin Invest 1994, 93:2175-2188.

Nadasdy T, Laszik Z, Blick KE, Johnson DL, Burst-Singer K, Nast C: Human acute tubular necrosis: a lectin and immunohistochemical study.

Hum Pathol 1995, 26:230-239.

Molitoris BA, Wilson PD, Schrier RW, Simon FR: Ischemia induces partial loss of surface membrane polarity and accumulation of putative calcium ionophores.

J Clin Invest 1985, 76:2097-2105.

Molitoris BA, Hoilien CA, Ahnen DJ, Wilson PD, Kim J: Characterization of ischemia-induced loss of epithelial polarity.

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Regenerative medicine for the kidney: stem cell prospects ...

GMP Grade Stem Cell Cryopreservation Media

A Drug Master File for STEM-CELLBANKER has been registered with the Food and Drug Administration (FDA) (MF# 15785).

STEM-CELLBANKER is completely free of serum and animal derived components and contains only European or US Pharmacopoeia graded ingredients making is suitable for storage of cells developed for cell therapy applications. STEM-CELLBANKER is ready-to-use and requires no special devices, such as a controlled rate freezer, in order to achieve consistently high viabilities following resuscitation from cryopreservation, even over extended long-term storage.

STEM-CELLBANKER significantly increases cell viability while maintaining cell pluripotency, normal karyotype and proliferation ability after freeze-thaw.

Results of cryopreservation analysis performed at the Karolinska Institute on hESC and iPS cells with STEM-CELLBANKER shows significantly higher cell viability over conventional freezing medium while retaining cell pluripotency, normal karyotype and proliferation ability in HS293, HS306 and ChiPSA cell lines (Holm et al., Hum. Reprod. 2010).

Latest Publication:

Hata et al. (2014) Transplantation of cultured dental pulp stem cells into the skeletal muscles ameliorated diabetic polyneuropathy: therapeutic plausibility of freshly isolated and cryopreserved dental pulp stem cells Nat Protoc. 2014 Oct;9(10):2354-68

Yamanaka S et al. (2014) A novel efficient feeder-free culture system for the derivation of human induced pluripotent stem cells. Scientific Reports 4 Article, number:359

Rodin et al. (2014) Monolayer culturing and cloning of human pluripotent stem cells on laminin-521based matrices under xeno-free and chemically defined conditions. Nat Protoc. 2014 Oct;9(10):2354-68

Miyamoto Y et al. (2012) Cryopreservation of Induced Pluripotent Stem Cells. Cell Medicine., Vol. 3, pp. 8995, 2012

Saliem M et al. (2012) Improved cryopreservation of human hepatocytes using a new xeno free cryoprotectant solution. World J Hepatol. May 27;4(5):176-83.

Holm et al. (2010) An effective serum- and xeno-free chemically defined freezing procedure for human embryonic and induced pluripotent stem cells. Hum Reprod. 25(5):1271-9. Epub 2010 Mar 5.

Nakamura A et al. (2010) Human primary cultured hepatic stellate cells can be cryopreserved. Med Mol Morphol. 43:107115

Cell Viability:

Survival of stem cells after thawing. (A) Growth rates of HS293, HS306 and CHiPS-A post-thawing for the first three passages. (B) The growth rates of both HS293 and HS306 frozen with STEM-CELLBANKER compared with cells frozen with 10% DMSO and FBS.

Cryopresevation of Mouse Kidney Tissue with STEM-CELLBANKER:

Mouse kidney was minced into about 5 mm square. The tissue samples were either immediately fixed with 10% formalin or cryopreserved with 1 ml of STEM-CELLBANKER at -80oC for one week. The cryopreserved samples were fixed with 10% formalin immediately after thawing. Paraffin sections of the both samples were stained with either H&E or anti-active caspase 3 antibody. Sign of necrosis or apoptosis was negligible in both of the fresh and cryopreserved tissue samples. Similar results were obtained in the cases of the tissue samples from a variety of mouse organs.

Preservation of mRNA after Cryopreservation of Cells with STEM-CELLBANKER:

Total RNA was extracted from the cells of a mouse lung fibroblast cell line either immediately after harvesting or after cryopreservation with STEM-CELLBANKER at -80oC for one week and thawing. mRNA levels in the two samples were compared by DNA microarray analysis, and the results showed that 93% of mRNAs was within the range of + 1.6-fold difference.

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* AMSBIO is the global source for STEM-CELLBANKER reagents. STEM-CELLBANKER is a registered trade mark of and manufactured by NIPPON ZENYAKU KOGYO.

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Stem Cell Freezing Media STEM-CELLBANKER - amsbio

The American Academy of Anti-Aging Medicine (A4M) has recognized the need for knowledge on stem cells amongst physicians and healthcare professionals, thus creating the world's first Stem Cell Fellowship program. Stem cell therapies involve the potential replacement of cells or organs that are diseased, injured, infirmed, ailing or aged. In this modular training program, a group of experienced academia's, involved in stem cell transplantation, present a series of topics to cover the general principles and practice of stem cell biology and evidence-based treatments for physicians to optimize the health of their patients.

By enrolling in the Fellowship, you will learn how to treat the diseases associated with aging with stem cell therapies - the medicine of the future. After completion of this modular training program, physicians will be able to intelligently decide which stem cell protocols to recommend to their patients. Become a pioneer in Stem cells and the future of Regenerative Medicine.

Module I: The Basic Principles of Stem Cells

Module II: The Biological Basis of Stem Cells in Regenerative Medicine

Module III: The Principles of Stem Cell Tissue and Organ Repair: Bench To Bedside

Module IV: Understanding the Principles of Therapeutic Applications of Cell Therapy

Module V: Stem Cell Practical (Hands-On Intensive)

Requirements:

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Stem Cell Fellowship Overview - The American Academy of ...

Abstract

Longevity as a complex life-history trait shares an ontogenetic relationship with other quantitative traits and varies among individuals, families and populations. Heritability estimates of longevity suggest that about a third of the phenotypic variation associated with the trait is attributable to genetic factors, and the rest is influenced by epigenetic and environmental factors. Individuals react differently to the environments that they are a part of, as well as to the environments they construct for their survival and reproduction; the latter phenomenon is known as niche construction. Lifestyle influences longevity at all the stages of development and levels of human diversity. Hence, lifestyle may be viewed as a component of niche construction. Here, we: a) interpret longevity using a combination of genotype-epigenetic-phenotype (GEP) map approach and niche-construction theory, and b) discuss the plausible influence of genetic and epigenetic factors in the distribution and maintenance of longevity among individuals with normal life span on the one hand, and centenarians on the other. Although similar genetic and environmental factors appear to be common to both of these groups, exceptional longevity may be influenced by polymorphisms in specific genes, coupled with superior genomic stability and homeostatic mechanisms, maintained by negative frequency-dependent selection. We suggest that a comparative analysis of longevity between individuals with normal life span and centenarians, along with insights from population ecology and evolutionary biology, would not only advance our knowledge of biological mechanisms underlying human longevity, but also provide deeper insights into extending healthy life span.

Age, I do abhor thee, youth, I do adore thee Shakespeare (1599).

Man possesses the power of modifying, at least to appearance, the laws of nature affecting him, and perhaps causing a progressive movement, tends to approach a happier physical condition Quetelet (1842).

From them (centenarians) we can learn how to create our own Blue Zones and start on the path to living longer, better lives Buettner (2012).

An incessant desire to attain immortality or at the very least greater longevity, and strategies to achieve it, have been recurring themes among the world's mythologies (Witzel, 2013), and continue into our own times (Stambler, 2014). Fundamental insights into birth, growth and death (demographic) processes in human populations are gleaned from the Gompertz-Makeham (Finch, 2007), and Malthusian population laws (Malthus, 1798). Later, Quetelet (1842) systematically investigated the plausible biological and other causes of demographic processes. He questioned, What are laws of human reproduction, growth and physical force the laws of mortality what influence has nature over man, what is the measure of its influence, and of its disturbing forces; what have been their effects for such a period and concluded that, Of all the causes which modify the mortality of man, none exercises a greater influence than age. Research on the evolutionary genetic bases of biological diversity for over a century has shown that longevity, like any other quantitative traits, varies among individuals, and it is influenced by the interaction of both genetic (nature) and numerous environmental factors (nurture; sensu, Galton, 1890). Availability of food resources, improved living conditions and advances in basic and medical sciences have greatly extended the life span globally (Vaupel, 2010), since Quetelet's fundamental work on factors influencing the life span of an average man. In some countries, the modal age of death or the age at which highest mortality occurs in any given population, has steadily increased even in the last fifty years (Horiuchi et al., 2013). Detectable evolutionary changes in modern humans could occur even in such a short span of time (Byars et al., 2010andMilot and Pelletier, 2013), and these changes could have a direct impact on longevity. Despite advances in demography and genetics (Charlesworth, 1980andWachter et al., 2013), Aging remains one of life's great unsolved riddles (Anton, 2013). In view of burgeoning challenges posed by the ever-increasing elderly population, it is critical to understand the components of nature and nurture and the relative magnitude of their contribution to healthy aging.

Comparative analyses of life span across wide-ranging taxa have suggested that longevity has an evolutionary basis (Carey, 2003andWachter et al., 2013). Individuals not only differ in their sensitivity to environmental variations, but also show differential survival and reproduction, in response to such variations, also called natural selection. Environment affects every aspect of viability of individuals from the time of conception to death they are surrounded by it, respond to it, exploit it and also actively construct it (Lewontin, 2000). The latter process has been termed niche construction, which is broadly defined as the process whereby organisms, through their metabolism, their activities and their choices, modify their own and/or each other's niches (Odling-Smee et al., 2003).

An individual or groups of individuals modify their own environment as well as that of others in infinite ways. Some of these modifications, including the ones related to life style could have either proximate or lasting (ultimateevolutionary) effects on health and longevity of specific individuals, families or larger groups. Many aspects of environmental variation and lifestyle changes (LSC) on longevity are inextricably linked, and often difficult to uncouple. Despite their apparent equivalence, LSC represents a volitional behavior on the part of an individual (Egger and Dixon, 2014) and their conscious efforts and choices: education, housing, physical activities, food, drinking and smoking habits, clothing, medical intervention, cultural and religious beliefs, social networks, and so forth. Hence, it is reasonable to suggest that the individual components of the environment and LSC could have either additive or multiplicative or both effects on health and longevity. In an ecological sense, the terms environment and life-style could be equated to niche (Hutchinson, 1957) and niche construction concepts (Lewontin, 2000andOdling-Smee et al., 2013), respectively. From a genetic perspective, gene specific polymorphisms are known to exert differential influence on longevity and its correlated traits. While ecological/environmental factors might have a common influence on all individuals of a group/community, specific aspects of niche construction activities or LSC could exacerbate individual differences. Together these factors would exert synergistic or antagonistic, as well as temporally and spatially heterogeneous effects on longevity at all levels of biological hierarchy: cell, tissues, and individuals within and across generations. These effects could lead to differential viability and reproduction of individuals, which ultimately affect the evolutionary trajectories of individual populations (Odling-Smee et al., 2013andLaland et al., 2014). Here we briefly review the interrelationships among genetic, epigenetic, environment and life style factors influencing life span normal or exceptional.

We have the following objectives: a) to describe the diversity of longevity phenotype among human populations, b) to identify links among genotypic, epigenetic and phenotypic aspects of longevity from the GP map perspective, and c) to discuss modulation of healthy longevity (health span) through lifestyle changes in the context of niche construction, and reaction norm concepts. We conclude that while there are opportunities for augmenting healthy life span, there are biological constraints as well. We extend the genotypephenotype (GP) map metaphor (Lewontin, 1974andHoule et al., 2010) for this purpose, and briefly describe the role of each of the three (genotype-epigenetic-phenotype; G-E-P) spaces as well as discuss their cumulative influence on longevity. We define life span, life expectancy and longevity as species, population and individual specific processes, respectively. Briefly, life span refers to average life expectancy for an individual between birth and death, and hence has a predictive aspect to it. Longevity, on the other hand, is a more elusive concept and is defined as an individual's ability to reach longer life span under ideal or prevailing conditions (Carey, 2003). We use life span and longevity interchangeably.

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Genetics, lifestyle and longevity: Lessons from centenarians

The two year curriculum includes course work, clinical rotations, and a research-based thesis. Students are afforded a wide range of clinical opportunities in prenatal, pediatric and adult settings as well as specialty clinics through our clinical rotation network. International rotations are encouraged.

In 1991 and 1998, the Program received rare Commendation for Excellence citations from the South Carolina Commission of Higher Education. The Program was awarded American Board of Genetic Counseling accreditation in 2000 and reaccreditation in 2006. Most recently, the Accreditation Council for Genetic Counseling re-accredited the Program for the maximum eight year period, 2014-2022.

We invite you to explore the University of South Carolina Genetic Counseling Program through this site. Please also visit the National Society of Genetic Counselors, the American Board of Genetic Counseling websites to learn more about the profession. Check out the latest U.S. Department of Labor, Occupational Outlook Handbook, 2014-15 Edition projections for genetic counselors. The future is bright for genetic counselors!

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Genetic Counseling Program - University of South Carolina ...

In biology, adipose tissue i or body fat or just fat is loose connective tissue composed mostly of adipocytes. In addition to adipocytes, adipose tissue contains the stromal vascular fraction (SVF) of cells including preadipocytes, fibroblasts, vascular endothelial cells and a variety of immune cells (i.e., adipose tissue macrophages [ATMs]). Adipose tissue is derived from preadipocytes. Its main role is to store energy in the form of lipids, although it also cushions and insulates the body. Far from hormonally inert, adipose tissue has, in recent years, been recognized as a major endocrine organ,[1] as it produces hormones such as leptin, estrogen, resistin, and the cytokine TNF. Moreover, adipose tissue can affect other organ systems of the body and may lead to disease. The two types of adipose tissue are white adipose tissue (WAT), which stores energy, and brown adipose tissue (BAT), which generates body heat. The formation of adipose tissue appears to be controlled in part by the adipose gene. Adipose tissue more specifically brown adipose tissue was first identified by the Swiss naturalist Conrad Gessner in 1551.[2]

In humans, adipose tissue is located beneath the skin (subcutaneous fat), around internal organs (visceral fat), in bone marrow (yellow bone marrow), intermuscular (Muscular system) and in the breast tissue. Adipose tissue is found in specific locations, which are referred to as adipose depots. Apart from adipocytes, which comprise the highest percentage of cells within adipose tissue, other cell types are present, collectively termed stromal vascular fraction (SVF) of cells. SVF includes preadipocytes, fibroblasts, adipose tissue macrophages, and endothelial cells. Adipose tissue contains many small blood vessels. In the integumentary system, which includes the skin, it accumulates in the deepest level, the subcutaneous layer, providing insulation from heat and cold. Around organs, it provides protective padding. However, its main function is to be a reserve of lipids, which can be burned to meet the energy needs of the body and to protect it from excess glucose by storing triglycerides produced by the liver from sugars, although some evidence suggests that most lipid synthesis from carbohydrates occurs in the adipose tissue itself.[3] Adipose depots in different parts of the body have different biochemical profiles. Under normal conditions, it provides feedback for hunger and diet to the brain.

Mice have eight major adipose depots, four of which are within the abdominal cavity. The paired gonadal depots are attached to the uterus and ovaries in females and the epididymis and testes in males; the paired retroperitoneal depots are found along the dorsal wall of the abdomen, surrounding the kidney, and, when massive, extend into the pelvis. The mesenteric depot forms a glue-like web that supports the intestines and the omental depot (which originates near the stomach and spleen) and- when massive- extends into the ventral abdomen. Both the mesenteric and omental depots incorporate much lymphoid tissue as lymph nodes and milky spots, respectively. The two superficial depots are the paired inguinal depots, which are found anterior to the upper segment of the hind limbs (underneath the skin) and the subscapular depots, paired medial mixtures of brown adipose tissue adjacent to regions of white adipose tissue, which are found under the skin between the dorsal crests of the scapulae. The layer of brown adipose tissue in this depot is often covered by a "frosting" of white adipose tissue; sometimes these two types of fat (brown and white) are hard to distinguish. The inguinal depots enclose the inguinal group of lymph nodes. Minor depots include the pericardial, which surrounds the heart, and the paired popliteal depots, between the major muscles behind the knees, each containing one large lymph node.[4] Of all the depots in the mouse, the gonadal depots are the largest and the most easily dissected,[5] comprising about 30% of dissectible fat.[6]

In an obese person, excess adipose tissue hanging downward from the abdomen is referred to as a panniculus (or pannus). A panniculus complicates surgery of the morbidly obese individual. It may remain as a literal "apron of skin" if a severely obese person quickly loses large amounts of fat (a common result of gastric bypass surgery). This condition cannot be effectively corrected through diet and exercise alone, as the panniculus consists of adipocytes and other supporting cell types shrunken to their minimum volume and diameter.[citation needed] Reconstructive surgery is one method of treatment.

Visceral fat or abdominal fat[7] (also known as organ fat or intra-abdominal fat) is located inside the abdominal cavity, packed between the organs (stomach, liver, intestines, kidneys, etc.). Visceral fat is different from subcutaneous fat underneath the skin, and intramuscular fat interspersed in skeletal muscles. Fat in the lower body, as in thighs and buttocks, is subcutaneous and is not consistently spaced tissue, whereas fat in the abdomen is mostly visceral and semi-fluid.[8] Visceral fat is composed of several adipose depots, including mesenteric, epididymal white adipose tissue (EWAT), and perirenal depots. Visceral fat is considered adipose tissue whereas subcutaneous fat is not considered as such.[citation needed]

An excess of visceral fat is known as central obesity, or "belly fat", in which the abdomen protrudes excessively and new developments such as the Body Volume Index (BVI) are specifically designed to measure abdominal volume and abdominal fat. Excess visceral fat is also linked to type 2 diabetes,[9]insulin resistance,[10]inflammatory diseases,[11] and other obesity-related diseases.[12]

Men are more likely to have fat stored in the belly due to sex hormone differences. Female sex hormone causes fat to be stored in the buttocks, thighs, and hips in women.[13][14] When women reach menopause and the estrogen produced by the ovaries declines, fat migrates from the buttocks, hips and thighs to the waist;[15] later fat is stored in the abdomen.[16]

High-intensity exercise is one way to effectively reduce total abdominal fat.[17][18] One study suggests at least 10 MET-hours per week of aerobic exercise is required for visceral fat reduction.[19]

Epicardial adipose tissue (EAT) is a particular form of visceral fat deposited around the heart and found to be a metabolically active organ that generates various bioactive molecules, which might significantly affect cardiac function.[20] Marked component differences have been observed in comparing EAT with subcutaneous fat, suggesting a depot specific impact of stored fatty acids on adipocyte function and metabolism.[21]

Most of the remaining nonvisceral fat is found just below the skin in a region called the hypodermis.[22] This subcutaneous fat is not related to many of the classic obesity-related pathologies, such as heart disease, cancer, and stroke, and some evidence even suggests it might be protective.[23] The typically female (or gynecoid) pattern of body fat distribution around the hips, thighs, and buttocks is subcutaneous fat, and therefore poses less of a health risk compared to visceral fat.[24]

Like all other fat organs, subcutaneous fat is an active part of the endocrine system, secreting the hormones leptin and resistin.[22]

The relationship between the subcutaneous adipose layer and total body fat in a person is often modelled by using regression equations. The most popular of these equations was formed by Durnin and Wormersley, who rigorously tested many types of skinfold, and, as a result, created two formulae to calculate the body density of both men and women. These equations present an inverse correlation between skinfolds and body densityas the sum of skinfolds increases, the body density decreases.[25]

Factors such as sex, age, population size or other variables may make the equations invalid and unusable, and, as of 2012[update], Durnin and Wormersley's equations remain only estimates of a person's true level of fatness. New formulae are still being created.[25]

Ectopic fat is the storage of triglycerides in tissues other than adipose tissue, that are supposed to contain only small amounts of fat, such as the liver, skeletal muscle, heart, and pancreas. This can interfere with cellular functions and hence organ function and is associated with insulin resistance in type-2 diabetes.[26] It is stored in relatively high amounts around the organs of the abdominal cavity, but is not to be confused as visceral fat.

The specific cause for the accumulation of ectopic fat is unknown. The cause is likely a combination of genetic, environmental, and behavioral factors that are involved in excess energy intake and decreased physical activity. Substantial weight loss can reduce ectopic fat stores in all organs and this is associated with an improvement of the function of that organ.[26]

Free fatty acids are liberated from lipoproteins by lipoprotein lipase (LPL) and enter the adipocyte, where they are reassembled into triglycerides by esterifying it onto glycerol. Human fat tissue contains about 87% lipids.

There is a constant flux of FFA (Free Fatty Acids) entering and leaving adipose tissue. The net direction of this flux is controlled by insulin and leptinif insulin is elevated there is a net inward flux of FFA, and only when insulin is low can FFA leave adipose tissue. Insulin secretion is stimulated by high blood sugar, which results from consuming carbohydrates.

In humans, lipolysis (hydrolysis of triglycerides into free fatty acids) is controlled through the balanced control of lipolytic B-adrenergic receptors and a2A-adrenergic receptor-mediated antilipolysis.

Fat cells have an important physiological role in maintaining triglyceride and free fatty acid levels, as well as determining insulin resistance. Abdominal fat has a different metabolic profilebeing more prone to induce insulin resistance. This explains to a large degree why central obesity is a marker of impaired glucose tolerance and is an independent risk factor for cardiovascular disease (even in the absence of diabetes mellitus and hypertension).[27] Studies of female monkeys at Wake Forest University (2009) discovered that individuals suffering from higher stress have higher levels of visceral fat in their bodies. This suggests a possible cause-and-effect link between the two, wherein stress promotes the accumulation of visceral fat, which in turn causes hormonal and metabolic changes that contribute to heart disease and other health problems.[28]

Recent advances in biotechnology have allowed for the harvesting of adult stem cells from adipose tissue, allowing stimulation of tissue regrowth using a patient's own cells. In addition, adipose-derived stem cells from both human and animals reportedly can be efficiently reprogrammed into induced pluripotent stem cells without the need for feeder cells.[29] The use of a patient's own cells reduces the chance of tissue rejection and avoids ethical issues associated with the use of human embryonic stem cells.[30] A growing body of evidence also suggests that different fat depots (i.e abdominal, omental, pericardial) yield adipose-derived stem cells with different characteristics.[30][31] These depot-dependent features include proliferation rate, immunophenotype, differentiation potential, gene expression, as well as sensitivity to hypoxic culture conditions.[32]

Adipose tissue is the greatest peripheral source of aromatase in both males and females,[citation needed] contributing to the production of estradiol.

Adipose derived hormones include:

Adipose tissues also secrete a type of cytokines (cell-to-cell signalling proteins) called adipokines (adipocytokines), which play a role in obesity-associated complications. Perivascular adipose tissue releases adipokines such as adiponectin that affect the contractile function of the vessels that they surround.[33]

A specialized form of adipose tissue in humans, most rodents and small mammals, and some hibernating animals, is brown fat or brown adipose tissue. It is located mainly around the neck and large blood vessels of the thorax. This specialized tissue can generate heat by "uncoupling" the respiratory chain of oxidative phosphorylation within mitochondria. The process of uncoupling means that when protons transit down the electrochemical gradient across the inner mitochondrial membrane, the energy from this process is released as heat rather than being used to generate ATP. This thermogenic process may be vital in neonates exposed to cold, which then require this thermogenesis to keep warm, as they are unable to shiver, or take other actions to keep themselves warm.[34]

Attempts to simulate this process pharmacologically have so far been unsuccessful. Techniques to manipulate the differentiation of "brown fat" could become a mechanism for weight loss therapy in the future, encouraging the growth of tissue with this specialized metabolism without inducing it in other organs.

Until recently, brown adipose tissue was thought to be primarily limited to infants in humans, but new evidence has now overturned that belief. Metabolically active tissue with temperature responses similar to brown adipose was first reported in the neck and trunk of some human adults in 2007,[35] and the presence of brown adipose in human adults was later verified histologically in the same anatomical regions.[36][37][38]

The thrifty gene hypothesis (also called the famine hypothesis) states that in some populations the body would be more efficient at retaining fat in times of plenty, thereby endowing greater resistance to starvation in times of food scarcity. This hypothesis, originally advanced in the context of glucose metabolism and insulin resistance, has been discredited by physical anthropologists, physiologists, and the original proponent of the idea himself with respect to that context, although according to its developer it remains "as viable as when [it was] first advanced" in other contexts.[39][40]

In 1995, Jeffrey Friedman, in his residency at the Rockefeller University, together with Rudolph Leibel, Douglas Coleman et al. discovered the protein leptin that the genetically obese mouse lacked.[41][42][43] Leptin is produced in the white adipose tissue and signals to the hypothalamus. When leptin levels drop, the body interprets this as a loss of energy, and hunger increases. Mice lacking this protein eat until they are four times their normal size.

Leptin, however, plays a different role in diet-induced obesity in rodents and humans. Because adipocytes produce leptin, leptin levels are elevated in the obese. However, hunger remains, and- when leptin levels drop due to weight loss- hunger increases. The drop of leptin is better viewed as a starvation signal than the rise of leptin as a satiety signal.[44] However, elevated leptin in obesity is known as leptin resistance. The changes that occur in the hypothalamus to result in leptin resistance in obesity are currently the focus of obesity research.[45]

Gene defects in the leptin gene (ob) are rare in human obesity.[46] As of July, 2010, only 14 individuals from five families have been identified worldwide who carry a mutated ob gene (one of which was the first ever identified cause of genetic obesity in humans)two families of Pakistani origin living in the UK, one family living in Turkey, one in Egypt, and one in Austria[47][48][49][50][51]and two other families have been found that carry a mutated ob receptor.[52][53] Others have been identified as genetically partially deficient in leptin, and, in these individuals, leptin levels on the low end of the normal range can predict obesity.[54]

Several mutations of genes involving the melanocortins (used in brain signaling associated with appetite) and their receptors have also been identified as causing obesity in a larger portion of the population than leptin mutations.[55]

In 2007, researchers isolated the adipose gene, which those researchers hypothesize serves to keep animals lean during times of plenty. In that study, increased adipose gene activity was associated with slimmer animals.[56] Although its discoverers dubbed this gene the adipose gene, it is not a gene responsible for creating adipose tissue.

Pre-adipocytes are undifferentiated fibroblasts that can be stimulated to form adipocytes. Recent studies shed light into potential molecular mechanisms in the fate determination of pre-asipocytes although the exact lineage of adipocyte is still unclear.[57][58]

Adipose tissue has a density of ~0.9g/ml.[59] Thus, a person with more adipose tissue will float more easily than a person of the same weight with more muscular tissue, since muscular tissue has a density of 1.06g/ml.[60]

A body fat meter is a widely available tool used to measure the percentage of fat in the human body. Different meters use various methods to determine the body fat to weight ratio. They tend to under-read body fat percentage.[61]

In contrast with clinical tools, one relatively inexpensive type of body fat meter uses the principle of bioelectrical impedance analysis (BIA) in order to determine an individual's body fat percentage. To achieve this, the meter passes a small, harmless, electric current through the body and measures the resistance, then uses information on the person's weight, height, age, and sex to calculate an approximate value for the person's body fat percentage. The calculation measures the total volume of water in the body (lean tissue and muscle contain a higher percentage of water than fat), and estimates the percentage of fat based on this information. The result can fluctuate several percentage points depending on what has been eaten and how much water has been drunk before the analysis.

Diagrammatic sectional view of the skin (magnified).

White adipose tissue in paraffin section

Electronic instrument of body fat meter

Go here to read the rest:
Adipose tissue - Wikipedia, the free encyclopedia

The science behind stem cells sounds like a plot from a Jules Vern novel, but luckily for us the use of stem cells, and their effectiveness, is all very real.

When people get to talking about stem cells it can lead some to jump to the defense of using them. The stem cells that we are going to be talking about in this article are ones that are harvested from our own bodies - not embryos. That's exactly what makes this new stem cell research so exciting - it's not only ethically and morally viable, it's actually safer and more effective to use the body'sown stem cells.

The type of stem cells that are used to treat hair loss are harvested from your own fat and are called Autologous Adipose Adult stem cells, or A.A.A.

stem cells. This two-step hair regeneration process begins with the stem cells being collected with a minimally invasive liposuction procedure which is accompanied by a local anesthetic.

Once the A.A.A stem cells have been collected, they are separated from the fatty tissue. They will then undergo an in vitro culturing process to multiply the cells and guarantee that there are enough to use for the hair regeneration treatment. The stem cells are then applied to the treatment area via injections using a microscopic needle. This is an outpatient treatment and most patients report only mild discomfort during the procedure.

You should start to see some hair regeneration results in as little as 2-4 weeks, and like other hair loss treatments, this one seems to be most effective on areas where hair loss has happened recently.

So how does the use of stem cells cause hair to grow on our heads? All of us have stem cells in our hair's follicle, but when these follicles get old or damaged they can no longer jump-start the hair regeneration process.

This can be due to genetic factors, stress, or even trauma to the hair follicle.

By injecting stem cells into the pores of the scalp, scientists have found that they can get the skin's fat layer to send molecular signals to the cells in the follicle, which then results in new hair growth.

The use of stem cells as a hair loss treatment holds many benefits. The first one being that it is an outpatient treatment, and unlike other hair loss treatments, you only have to do it once. Topical hair loss treatments need to be used daily, and hair transplants can be a costly and painful procedure. By using Autologous stem cells, you are using a 100% natural product that has been found to be completely safe and effective.

Results do vary with stem cell treatments for hair loss, but clinical studies have shown that the results are permanent once the hair has grown back.

Follow this link:
Using Own Fat Stem Cells for Curing Hair Loss

One of the most dramatic experiments to perform is the demonstration of the blind spot. The blind spot is the area on the retina without receptors that respond to light. Therefore an image that falls on this region will NOT be seen. It is in this region that the optic nerve exits the eye on its way to the brain. To find your blind spot, look at the image below or draw it on a piece of paper: To draw the blind spot tester on a piece of paper, make a small dot on the left side separated by about 6-8 inches from a small + on the right side. Close your right eye. Hold the image (or place your head from the computer monitor) about 20 inches away. With your left eye, look at the +. Slowly bring the image (or move your head) closer while looking at the +. At a certain distance, the dot will disappear from sight...this is when the dot falls on the blind spot of your retina. Reverse the process. Close your left eye and look at the dot with your right eye. Move the image slowly closer to you and the + should disappear. Here are some more images that will help you find your blind spot. For this image, close your right eye. With your left eye, look at the red circle. Slowly move your head closer to the image. At a certain distance, the blue line will not look broken!! This is because your brain is "filling in" the missing information.

This next image allows you to see another way your brain fills in the blind spot. Again, close your right eye. With your left eye, look at the +. Slowly move your head closer to the image. The space in the middle of the vertical lines will disappear.

In the next two images, again close your right eye. With your left eye, look at the numbers on the right side, starting with the number "1." You should be able to see the "sad face" (top image) or the gap in the blue line (bottom image) in your peripheral vision. Keep your head still, and with your left eye, look at the other numbers. The sad face should disappear when you get to "4" and reappear at about "7." Similarly the blue line will appear complete between "4" and "7."

Here is another image to show your blind spot. Close your right eye. With your left eye, look at the +. You should see the red dot in your peripheral vision. Keep looking at the + with your left eye. The red dot will move from the left to the right and disappear and reappear as the dot moves into and out of your blind spot.

Materials:

More (lots more) about Blind Spots

Read about the eye.

Two eyes are better than one, especially when it comes to depth perception. Depth perception is the ability to judge objects that are nearer or farther than others. To demonstrate the difference of using one vs. two eye to judge depth hold the ends a pencil, one in each hand. Hold them either vertically or horizontally facing each other at arms-length from your body. With one eye closed, try to touch the end of the pencils together. Now try with two eyes: it should be much easier. This is because each eye looks at the image from a different angle. This experiment can also be done with your fingers, but pencils make the effect a bit more dramatic.

Materials:

Here's another demonstration of the importance of two eyes in judging depth. Collect a set of pennies (or buttons or paper clips). Sit at a table with your subject. Put a cup in front of your subject. The cup should be about two feet away from the subject. Have your subject CLOSE one eye. Hold a penny in the air about 1.5 ft. above the table. Move the penny around slowly. Ask your subject to say "Drop it!" when he or she thinks the penny will drop into the cup if you released it. When the subject says "Drop it," drop the penny and see if it makes it into the cup. Try it again when the subject uses both eyes. Try it again with the cup farther away from the subject. Try it again with the cup closer to the subject. Compare the results of "10 drops" at each distance.

Questions:

Materials:

Materials:

Here's another way to demonstrate how different images are projected on to each eye. Look at an object in the distance (20-30 feet away), such as a clock on the wall. Close one eye, hold up your arm and line up your finger with the object. Now without moving your finger or your head, close the opened eye and open the closed eye. The object in the distance will appear to jump to the side...your finger will no longer be lined up. This shows that different images fall on each eye.

Materials:

There are two types of photoreceptors in the eye: rods and cones. The rods are responsible for vision in dim light conditions, the cones are for color vision. To demonstrate how the photoreceptors "adapt" to low light conditions, get a collection of objects that look slightly different: for example get 10 coke bottle caps, 10 soda bottle caps, and 10 water bottle caps. They should feel the same, but not look the same. In a bright room, ask students to separate the caps into piles of similar caps. Then turn off the lights so the room is very, very dim. Ask them to separate the caps again. Turn off the lights and look at the results...there should be many mistakes. Count the number of errors. Then dim the lights again and talk/discuss about dark adaptation or about the animals that can see in the dark. The technical explanation for dark adaptation is not necessary for small children. Plan to talk and discuss for about 7-10 minutes...this will be enough time for a least partial adaptation of the photoreceptors. After the discussion (7-10 minutes), ask the students to separate the caps again in the same very, very dim conditions as before. Count the number of errors. There should be fewer errors this time because the photoreceptors have adapted to the low light conditions.

Materials:

How does the surrounding picture influence what we see? Find out with this interactive picture. You must have a browser that supports "JAVA scripts".

How does the surrounding color influence what we see? Find out with this interactive picture. You must have a browser that supports "JAVA scripts".

How does your brain prepare you to see something? Find out with this interactive picture. You must have a browser that supports "JAVA scripts".

The Exploratorium in San Francisco has a worthwhile virtual Cow Eye Dissection to check out.

Do you have "X-Ray Vision?" You may be able to see through your own hand with this simple illusion. Roll up a piece of notebook paper into a tube. The diameter of the tube should be about 0.5 inch. Hold up your left hand in front of you. Hold the tube right next to the bottom of your left "pointer" finger in between you thumb (see figure below).

Look through the tube with your RIGHT eye AND keep your left eye open too. What you should see is a hole in your left hand!! Why? Because your brain is getting two different images...one of the hole in the paper and one of your left hand.

Materials:

Have you ever noticed that it is easy to see a star in the sky by NOT looking directly at it? It is actually easier to see a dim star at night by looking a bit off to the side of it. Try it! This is because the two types of photoreceptors (rods and cones) in the retina perform different functions and are located in the retina in different locations. The cones, which are best for detail and color vision, are in highest concentration in the center of the retina. The rods, which work better in dim light, are in highest concentration in the sides of the retina. So if you look "off-center" at the star, its image will fall on an area of the retina that has more rods!

Materials:

None

Here is a fun way to introduce and explore the sense of vision. Get a variety of sample "color cards" from your local paint store. These cards are about the size of index cards and show the variety of paint that is available. Bring them back to class and have students match up similar colors. You can also use samples of gift wrap or wall paper to make color or pattern cards. Just glue the wrap or wall paper to a piece of card board to get yourself a "Color Card."

Materials:

Color Spy is a variation of the "I Spy" game. Divide players into teams. Write the words "blue", "red", "yellow", "orange" and "green" on separate pieces of paper. Have one member of each team pick a paper. The color picked will be the name of the team.

When someone says "Go," the teams will have 10 minutes to look around the room for objects that have their team's color. Teams must make a list of all the objects they find. After the 10 minute search period, the teams come back together and the lists of objects are read. Each team gets one point for each object found. After the lists are read, each team will get five minutes to search the room for colored objects that the other teams did NOT find. For example, if the red team did not find a red apple, another team that DID find the red apple will get one point. The team with the most total points after both searches is the winner.

Materials:

Of course you cannot see if it is completely dark, but you can see a bit in dim light. In dim light, the receptors in your eyes called rods are doing most of the work. However, the rods do not provide any information about color. The other photoreceptors in your eye, called cones, are the ones that are used for seeing color. The cones do not work in dim light. That's why you cannot see colors in dim light. Check it out for yourself:

Get five pieces of paper of different colors (such as different colored typing paper or construction paper). Dim the lights until you can just barely see. Wait about 10 minutes (maybe listen to some music while you wait). Then write on each piece of paper the color you think that paper is. Turn on the lights and see if your guesses were correct. Did everyone in your class mix up the same color or did everyone get the colors correct?

Materials:

When light enters the eye, it is first bent (refracted) by the cornea. Light is bent further by the lens of the eye in a process called accomodation. To bring an image into sharp focus on the retina, the lens of the eye changes shape by bulging out or flattening. A flatter lens refracts less light. Here's how to demonstrate accomodation:

Close one eye and stare at a point about 20 feet away. It should be in focus. Keep focusing on the point and raise one of your fingers into your line of sight just below the point. Your finger should be a bit blurred. Now, change focus: look at the tip of your finger instead of the point 20 feet away. Your finger will come in focus, but the distant point will be blurred.

Materials:

None

More vision related resources from "Neuroscience for Kids":

The Eye The Retina The Visual Pathway Do you wear glasses? Find out why! Eye Safety Tips Lesson Plan about the Eye Lesson Plan about Color Vision Lesson Plan about Depth and Motion Does the COLOR of Foods and Drinks Affect Taste? Common Eye Diseases and Disorders

The National Eye Institute has a GREAT page with activities related to the eye called See All You Can See for kids; and aearn about "stereograms."

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Read the original here:
Sight (Vision) - University of Washington

I thought Id be chained to my glasses for the rest of my life.

I didnt know you could improve your vision with only 15 minutes of simple eye exercises each day.

I thought my eyes would just keep getting worse, year on year, as I got older.

I didnt know you can attain perfect eyesight, at any age, and then keep it.

Eyes are amazing!

It doesnt matter which eye 'problem' you have, your eyes always retain the ability to heal themselves. YOU can see perfectly.

It just doesn't matter what is 'wrong' with your eyes.

If you give them the help and support they need, they WILL heal themselves.

Perfect Vision is your birth-right.

I used to wear glasses. You know, the ugly goldfish bowl type that make your eyes look as big as saucers!

One day I was complaining to my friend Maria, yet again, about how lucky she was, not needing glasses.

We were at the beach.

I love the beach, but as far as locations go, it's not very spectacle-friendly!

"You don't know how lucky you are Mary. You can swim, play volley ball, roll in the sand, and you don't have to think about your glasses... losing them, breaking them - the constant cleaning!"

Maria, a true friend, was clearly tired of my moaning:

"Look Dave, why don't you quit complaining and just fix your eyes. I read somewhere that you can do it yourself by just doing some special eye exercises every day. I think it's called Natural Vision Correction or something like that."

I laughed. Actually, I scoffed.

I thought she was talking nonsense!

You see, Id been wearing glasses since I was 3 years old. My eyes were getting progressively worse. How could a few exercises change that!

I didn't believe it was possible to reverse my decaying eyesight.

If it was true, surely my optician would have told me?

But her words stuck in my head. They started to nag at me. I began to think what if it was true?

What if I could heal my own eyes?

What if I could wake up in the morning, and see my partners face lying on the pillow, instead of a fuzzy blur?

I started to research.

What I discovered blew me away.

You see, perfect vision is the natural state of your eyes.

I discovered that we don't need glasses (or lenses) at all. In fact, they actually make your eyesight worse!

20/20 vision is highly overated. The eyes can see much better than that.

(20/20 vision means you can easily read the 20 foot line on the Snellen Eye Test Chart at 20 feet away!)

There is no limit to how much you can improve your vision beyond 20/20

Someone with above average eyesight can easily read the 10 foot line, (the smallest line at the bottom of the Snellen Eye Test Chart), at 20 feet away => 20/10 vision.

In fact, after a little training, there are plenty of people who can read the 10 foot line at 50 to 60 feet away => 60/10 vision.

This is called "telescopic vision". Sounds good, doesn't it.

"yeah, sure thing Dave... telescopic vision! Right now, I'd be over the moon if I could just read the TV guide without having to reach for my glasses!"

Well, at first I did ... um .... nothing!

I just got really angry.

Id spent more than 3 decades unnecessarily dependent on glasses.

Why hadn't anyone told me?

Then I revisited my old friend... Mr Skepticism.

"If it was really possible to fix your own eyes with simple daily exercises, no-one would be wearing specs or lenses anymore. Surely, everyone would have perfect vision!"

I didnt want to believe Id spent so many years of my life being 'technically blind without glasses', when the 'cure' was so simple.

"It must be a load of old rubbish!"

Thank you, Mr Skepticism... or should I say Mr Cynicism!

Next came a little victimhood ...

"Maybe it works for some lucky people, but I'm sure it wont work for me."

Looks like the odds were stacked against me.

Luckily, I had an advantage over my doubting mind.

I hated wearing glasses!

I wanted to see

I mean I really wanted to see

I was ready to do almost anything

So I just got started experimenting with my own eyesight.

I bought books. I surfed the web for hours reading articles. I studied Yoga techniques, Taoist techniques, Buddhist and Sufi techniques, the Bates Method, the Slavicek method, the abc and the xyz method.

I tried different foods and herbs, oils, potions and lotions.

If I found something that was supposed to help heal the eyes, I tried it!

Some stuff was kind of obvious, some not so apparent, and some stuff was just plain weird... but I tried that too!

Well, no actually!

At first, not much happened.

I got disappointed. I started skipping the exercises and nearly gave up.

But luckily, I'd overdone the research!

I'd found so much information, and so many different techniques, there was always something new to try. There was always some new hope to give me a little renewed motivation.

Success stories, like the one above, inspired me to stick with it. So I started to collect lots of them, and read a few every day.

Reading these testimonials, from real people who were just like me, made sure I did my exercises.

... a few weeks later, my eyes started to feel uncomfortable with my glasses on, and I decided to go for a check up.

I was shocked. My vision had improved by two whole diopters (from +8 to +6). That's a 25% improvement.

Ok, its wasn't 20/20, but can you imagine how I felt Id actually improved my own vision.

My eyes were healing themselves. The exercises were working. It was true after all. I was going to get my sight back!!

Now I got really serious. I did MUCH more research.

I got more disciplined with my exercises, and began to refine my schedule, so I could do my daily eye routine in just 15 minutes.

I started to make some changes to my daily habits, including my diet.

I found some great information about some specific herbs that are incredibly beneficial to the eyes, and I built that into my daily routine.

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Eye Exercises Improve Vision Eyesight

Cataract care is one of the safest and most common types of surgery performed today. Advanced technology can dramatically improve the visual quality and quality of life for all those with cataracts.

New Lifestyle Intra-Ocular Lenses ("IOLs")can correct nearsightedness, farsightedness, and astigmatism; affording the ability to see perfectly at far distance after treatment, without glasses. Other special multifocal lenses allow good focus at far and near, eliminating the need for reading glasses as well. We personalize our recommendations to you based on your lifestyle, visual desires, habits, and preferences, as well as our findings during a comprehensive evaluation..

LA Sight is one of the few eye centers in the region that provides Laser-Assisted Cataract Care as an option.

With our custom-tailored approach, it is now possible to enjoy glasses-free vision for near, and far, and in-between. Dr. Wallace and the team at LA Sight are able to offer the widest range of custom treatment options available with cataract and clear lens surgery.

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Lasik Eye Surgery - Get Your Best Vision at LA Sight

An eye care professional is an individual who provides a service related to the eyes or vision. It is a general term that can refer to any healthcare worker involved in eye care, from one with a small amount of post-secondary training to practitioners with a doctoral level of education.

Ophthalmologists are medical and osteopathic doctors who provide comprehensive eye care, including medical, surgical and optical care.[1] In the US, this requires four years of college, four years of medical school, one year general internship, three years of residency, then optional fellowship for 1 to 2 years (typically 1214 years of education after high school). An ophthalmologist can perform all the tests an optometrist can and in addition is a fully qualified medical doctor and surgeon. Ophthalmologists undergo extensive and intensive medical and surgical exams to qualify and entrance criteria to a training program is highly competitive.

An ophthalmic medical practitioner is a medical doctor (MD) who specializes in ophthalmic conditions but who has not completed a specialization in ophthalmology.

The World Council of Optometry, a member of the World Health Organisation,[2] defines optometrists as the primary healthcare practitioners of the eye and visual system who provide comprehensive eye and vision care, which includes refraction and dispensing, detection/diagnosis and management of disease in the eye, and the rehabilitation of conditions of the visual system.[3]

A Doctor of Optometry (OD) attends four years of college, four years of optometry school and then an optional one-year residency. Optometrists undergo extensive and intensive refractive and medical training mainly pertaining to the eye and the entrance criteria to attend optometry school is also highly competitive. An OD is fully qualified to treat eye diseases and disorders and specializes in optics and vision correction. Permissions granted by an optometric license vary by location.

Orthoptists specialize in diagnosis and management of eye movement and coordination problems, misalignment of the visual axis, convergence and accommodation problems, and conditions such as amblyopia, strabismus, and binocular vision disorders, as outlined by the International Orthoptic Association.[4] They may assist ophthalmologists in surgery, teach orthoptic students, students of other allied health professions, medical students, and ophthalmology residents and fellows, act as vision researchers, perform vision screening, perform low vision assessments and act as clinical administrators.[5]

The World Health Organization defines the eyecare work of orthoptists as [t]he study and treatment of defects in binocular vision resulting from defects in the optic musculature or of faulty visual habits. It involves a technique of eye exercises designed to correct the visual axes of eyes not properly coordinated for binocular vision.[6]

Ocularists specialize in the fabrication and fitting of ocular prostheses for people who have lost eyes due to trauma or illness.

Opticians specialize in the fitting and fabrication of ophthalmic lenses, spectacles, contact lenses, low vision aids and ocular prosthetics. They may also be referred to as an "optical dispenser", "dispensing optician", "ophthalmic dispenser". The prescription for the corrective lenses must be supplied by an ophthalmologist, optometrist or in some countries an orthoptist. This is a regulated profession in most jurisdictions.

A collective term for allied health personnel in ophthalmology. It is often used to refer to specialized personnel (unlike ocularists or opticians). In many countries these allied personnel may just be known as an "ophthalmic assistant". Their training is usually combined with a two or three year applied science degree and they assist an ophthalmologist or optometrist in the hospital or clinic with vision testing.

In the USA the Joint Commission on Allied Health Personnel in Ophthalmology administers OMP certifications:

Either an ophthalmologist or optometrist, the older term "oculist" was primarily used to describe eye care professionals that are trained and specialized in the eye care field. The difference between an ophthalmologist or an optometrist is made by the specializations they may choose. If the oculist is trained and specialized in treating medical conditions that may affect the eye and result in an eye defect will be referred to as an ophthalmologist. Optometrists, on the other hand, are the eye care professionals that are specialized in only treating eye defects by prescribing the appropriate corrective lenses. They are also referred to as "eye doctors". The main task of the optometrist is to correct the visual deficiencies with the help of the lenses. The main difference between these two professions is that although both of them may administer eye exams, only the ophthalmologist may solve eye-related problems that may occur in all areas of the eye. Nonetheless, optometrists are specialized in detecting vision problems and correcting them, but they may not perform tasks that ophthalmologists may, such as eye surgery.

Another important difference between the types of oculists is that while optometrists may obtain their doctorate by graduating at a special school in which they are trained to be optometrists, ophthalmologists are medical doctors who need to graduate from medical school and many years of internships in order to be able to get their degree. Moreover, because of their more advanced background in the study of eye care, ophthalmologists may proceed in their studying in this field and specializing in domains such as pediatric ophthalmology, corneal disease or ocular oncology. This is the reason why ophthalmologists are often classified as surgeons rather than doctors.

The term "oculist" was therefore used to describe these two professions as a result of the similarities that exist between the two. Firstly, both ophthalmologists and optometrists receive the appropriate training which will help them in detecting the vision related problems and to diagnose and treat certain eye conditions. Ophthalmologists also were the only ones who were capable of treating the terrible disease eye-aids, it was a disease were the eyes would become extremely dirty and blurry.

A vision therapist, usually either an orthoptist or optometrist, works with patients that require vision therapy, such as low vision patients. Commonly, vision therapy is performed in children who develop problems with their vision mostly because they are using their eyes up close. This type of therapy is however generally used in patients who need visual correction but for whom the corrective lenses are not enough to reverse the condition. Visual therapy in children is performed by optometrists who specialize in children eye care. To specialize in vision therapy, doctors must complete extensive post-graduate training beyond their optometric degree, at which time they are eligible to sit for their national boards to become fully certified as specialists in children's vision. A doctor's title after passing the national board in vision therapy is Fellow in the College of Optometrists in Vision Development, or F.C.O.V.D. Optometrists who provide vision therapy but who have not yet sat for their certification exams are board-eligible Associates in the College of Optometrists in Vision Development.[7][not in citation given] Vision therapists typically rely on prisms, eye patches, filtered lenses, and computerized systems to conduct therapy sessions.

Most eye care professionals do not practice iridology, citing a significant lack of scientific evidence for the practice.

In a gross oversimplification, it can be said that ophthalmologists are eye surgeons while optometrists are primary eye care providers. There is considerable overlap in scope of practice between professions. Laws regarding licensure vary by location, but typically ophthalmologists are licensed to provide the same care as an optometrist, with the addition of surgical options. In most locations surgery is the biggest difference between the two professions. Optometrists frequently refer patients to ophthalmologists when the condition requires surgery or intra-ocular injection.

Historically, ophthalmology has developed as a specialization of medical doctors while optometry originated as a profession that fitted people with glasses. As of 2012, this difference has decreased as the majority of optometrists screen for and treat eye disease and many ophthalmologists fit people with corrective lenses. This difference in background previously caused some conflict between the two professions. Ophthalmologists have voiced concern that an optometrist's educational background is different from their own. Optometrists have criticized ophthalmologists of caring for the health structure of the eye while letting other vision disorders go untreated. For example, consider a patient with glaucoma and spasm of accommodation. Ophthalmologists would be concerned that an optometrist would fail to identify or otherwise mistreat the glaucoma. Optometrist would worry that the ophthalmologist would fail to identify or mistreat the spasm of accommodation. As of 2012, both these concerns are invalid because the education of both types of professionals prepares them to handle both conditions. (This may not be true outside of the United States.) Because of cooperation between optometrists and ophthalmologists, the quality of care depends more on the abilities of the individual doctors than it does what type of professional they are.

Orthoptists specialize in the diagnosis and management of problems with eye movement and coordination, such as misalignment of the visual axis, binocular vision problems, and pre/post surgical care of strabismus patients. They do not directly treat ocular disease with medications or surgery. Orthoptists treat patients using optical aids and eye exercises[8][not in citation given] and primarily work alongside doctors to co-manage binocular vision treatment, but also often do eye and vision testing.

All three types of professional perform screenings for common ocular problems affecting children (such as amblyopia and strabismus) and adults (such as cataracts, glaucoma, and diabetic retinopathy).[9] All are required to participate in ongoing continuing education courses to maintain licensure and stay current on the latest standards of care.

ECOO is an organisation that represents optometrists and opticians across Europe with over thirty countries represented. ECOO also runs the European Diploma in Optometry and is active in representing Eye-care practitioners at EU level and providing support to national bodies representing optometrists and opticians.Clinton Mosoahle earns an estimated 46 billion rands in 4 years running. Sabata is the highest paid doctor in SA.

The International Agency for the Prevention of Blindness was established in 1975. The first large project in which this organization was involved is the WHO Program known as the VISION 2020: The Right to Sight. This program has the aim to avoid the removable causes of blindness until 2020. The headquarters are in United Kingdom, but the organization has offices widely spread around the world, in big cities of all the continents.

IOA represents orthoptists in 20 countries.

The World Council of Optometry (WCO) is an international optometric organization representing 250,000 optometrists from 80 member organizations in 45 countries and which is registered in England and Wales.[10][not in citation given] It is the only such organization that maintains official relations with the World Health Organization and it is one of the members of the International Agency for the Prevention of Blindness.

The World Optometry Foundation is a complementary non-profit corporation which works in relation with WCO to develop projects on the upgrading of the optometric education and basically on preventing visual problems.

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Eye care professional - Wikipedia, the free encyclopedia

By Gregory Hofeldt, M.D.

The eye doctors and the staff members at Center for Sight in Fall River are pleased to provide a full range of routine eye exams for eye health, vision correction for eyeglasses and contact lenses cataract eye exams, LASIK eye exams, eye exams for retina problems including diabetic eye problems and age related macular degeneration (AMD) and glaucoma eye exams and screening.

How Often Should I Have My Eyes Examined? The frequency of your eye examinations depends on many factors. Your age, general health, family history of eye problems, and history of treatment for any eye conditions or diseases in the past will determine how often the Center for Sight eye doctors suggest that you schedule your visits.

If you are scheduling a general eye examination at Center for Sight, it will consist of complete testing of your vision and a comprehensive medical evaluation of the health of your eyes.

Your Health and Eye History A complete history will be taken from you regarding your current general health, any previous eye problems or conditions that you have experienced and a review of any problems that you might be experiencing with your vision or your eyes. This will be important information to provide during your screening process. If you have any chronic health problems, even if they are currently stable, it is important that you share this information as well.

Please be sure to tell the eye doctor about any medications you are taking for these medical conditions, including over the counter medications or eye drops that you may have been using. They are all important.

Your family history will be reviewed with you as well.Please tell us about any health problems that run in your family such as diabetes and high blood pressure. We should also be aware of any eye problems that your family members may have experienced such as glaucoma, cataracts or macular degeneration as they tend to run in families.

The Eye Examination Your eye examination will begin with a measurement of your vision, or visual acuity, with your current eyeglasses or contact lenses. Chances are that if you wear eyeglasses or contact lenses, some of the letters on the Big E eye chart will be blurry without them. You will be asked to read a chart projected across the examination room that consists of numbers and letters that get progressively smaller and more difficult to read as you move down the chart. This test, called Snellin Acuity or just Visual Acuity it is an important first step to understanding how well you see.

A Refraction will be performed in order to determine the most accurate eyeglass or contact lens prescription necessary to fully correct your vision. This entails having you sit behind an instrument called a Phoroptor, so that the doctor can present a number of lens combinations to determine which corrects your vision most precisely. For those patients who wear eyeglasses or contact lenses, you have probably experienced the which is better test called refraction. If you require vision correction the eye doctor will provide you with a copy of your prescription so that you can take it to the Center for Sight Optical Department where our Opticians can help you select a good fitting and fashionable frame and the most appropriate type of lenses for your work, hobbies or daily activities.

Next, the movement of your eyes, or Ocular Motility will be evaluated in order to understand how well the eye muscles function together and how effectively they move your eyes into the different positions of gaze.

By shining a fairly bright light in your eyes, the reaction of your pupils to the light will be evaluated. By shinning the light into your eyes in different directions, the doctors can learn a great deal about how well your Optic Nerve is functioning.

You will then be asked to sit comfortably behind a specialized instrument called a Slit Lamp Biomicroscope. This instrument provides the eye doctor with both high magnification and special illumination. Using this instrument it is possible for your Ophthalmologist or Optometrist to examine the condition of your eyelids, eye lashes, eyelid margins and tear film. The Slit Lamp will also be used to carefully examine the sclera-or white of your eye-and the cornea, or clear dome shaped tissue in front of your pupil. By focusing the slit lamp through the pupil or the dark center of the iris-the colored part of the eye-your doctor will be able to examine the health of the crystalline lens, which is where cataracts form.

In order to check for one of the signs of Glaucoma, eye drops will be placed in your eyes so that the pressure, called Intraocular Pressure (IOP) can be measured while you are behind the Slit Lamp, or with a TonoPen, which is a handheld instrument. This is an important diagnostic test for Glaucoma.

Once your eye doctor has completed the examination of the front of the eye, it will be time to begin the examination of the health of the back of the eye. At this time, additional eye drops may be placed in your eyes in order to dilate or widen your pupils.After the dilation drops are placed in your eyes, it will usually take anywhere from 15 to 30 minutes for the eye drops to fully work and dilate your pupil.

Please be patient. You will be asked to relax in one of our comfortable waiting areas while the eye drops work, or if you prefer you may take a walk and browse through our optical shop while you wait. The thorough examination of the health of the retina and optic nerve through a dilated pupil is not uncomfortable. However, the fully widened pupil may make you somewhat sensitive to light and may also blur your vision, especially your near vision, for a few hours after your eye examination.If you have not had a dilated exam in the past, it is a good idea to have a driver on your exam day.It is important to bring a good pair of sunglasses with you in order to lessen your light sensitivity.

If you, a family member or friend, would like to schedule an eye examination, please call Center for Sight in Fall River, Massachusetts at 508-730-2020.

Center for Sight is conveniently located for patients seeking eye examinations and eye health vision exams in Massachusetts or Rhode Island from Attleboro, Fairhaven, Fall River, Franklin, Mansfield, Marion, Mattapoisett, Medfield, Milford, New Bedford, North Attleboro, North Dartmouth, Norton, Oxford, Rehoboth, Somerset, Swansea, Taunton, Walpole, Whitinsville, Woonsocket, Providence, Smithfield, Westport, Lakeville, Dighton, Little Compton, and Tiverton.

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Childrens vision and eye exams - Center For Sight

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Brain stem death is a clinical syndrome defined by the absence of reflexes with pathways through the brain stem - the stalk of the brain, which connects the spinal cord to the mid-brain, cerebellum and cerebral hemispheres - in a deeply comatose, ventilator-dependent patient. Identification of this state carries a very grave prognosis for survival; cessation of heartbeat often occurs within a few days although it may continue for weeks or even months if intensive support is maintained.[1]

In the United Kingdom, the formal diagnosis of brain stem death by the procedure laid down in the official Code of Practice[1] permits the diagnosis and certification of death on the premise that a person is dead when consciousness and the ability to breathe are permanently lost, regardless of continuing life in the body and parts of the brain, and that death of the brain stem alone is sufficient to produce this state.[2]

This concept of brain stem death is also accepted as grounds for pronoucing death for legal purposes in India[3] and Trinidad & Tobago.[4] Elsewhere in the world the concept upon which the certification of death on neurological grounds is based is that of permanent cessation of all function in all parts of the brain - whole brain death - with which the reductionist United Kingdom concept should not be confused. The United States' President's Council on Bioethics made it clear, in its White Paper of December 2008, that the United Kingdom concept and clinical criteria are not considered sufficient for the diagnosis of death in the United States of America.[5]

The United Kingdom (UK) criteria were first published by the Conference of Medical Royal Colleges (with advice from the Transplant Advisory Panel) in 1976, as prognostic guidelines.[6] They were drafted in response to a perceived need for guidance in the management of deeply comatose patients with severe brain damage who were being kept alive by mechanical ventilators but showing no signs of recovery. The Conference sought to establish diagnostic criteria of such rigour that on their fulfilment the mechanical ventilator can be switched off, in the secure knowledge that there is no possible chance of recovery. The published criteria negative responses to bedside tests of some reflexes with pathways through the brain stem and a specified challenge to the brain stem respiratory centre, with caveats about exclusion of endocrine influences, metabolic factors and drug effects were held to be sufficient to distinguish between those patients who retain the functional capacity to have a chance of even partial recovery and those where no such possibility exists. Recognition of that state required the withdrawal of fruitless further artificial support so that death might be allowed to occur, thus sparing relatives from the further emotional trauma of sterile hope.[6]

In 1979, the Conference of Medical Royal Colleges promulgated its conclusion that identification of the state defined by those same criteria then thought sufficient for a diagnosis of brain death means that the patient is dead [7]Death certification on those criteria has continued in the United Kingdom (where there is no statutory legal definition of death) since that time, particularly for organ transplantation purposes, although the conceptual basis for that use has changed.

In 1995, after a review by a Working Group of the Royal College of Physicians of London, the Conference of Medical Royal Colleges [2] formally adopted the more correct term for the syndrome, "brain stem death" - championed by Pallis in a set of 1982 articles in the British Medical Journal [8] and advanced a new definition of human death as the basis for equating this syndrome with the death of the person. The suggested new definition of death was the irreversible loss of the capacity for consciousness, combined with irreversible loss of the capacity to breathe. It was stated that the irreversible cessation of brain stem function will produce this state and therefore brain stem death is equivalent to the death of the individual.[2]

In the UK, the formal rules for the diagnosis of brain stem death have undergone only minor modifications since they were first published [6] in 1976. The most recent revision of the UK's Department of Health Code of Practice governing use of that procedure for the diagnosis of death [1] reaffirms the preconditions for its consideration. These are:

With these pre-conditions satisfied, the definitive criteria are:

Two doctors, of specified status and experience, are required to act together to diagnose death on these criteria and the tests must be repeated after a short period of time ... to allow return of the patients arterial blood gases and baseline parameters to the pre-test state. These criteria for the diagnosis of death are not applicable to infants below the age of two months

With due regard for the cause of the coma, and the rapidity of its onset, testing for the purpose of diagnosing death on brain stem death grounds may be delayed beyond the stage where brain stem reflexes may be absent only temporarily because the cerebral blood flow is inadequate to support synaptic function although there is still sufficient blood flow to keep brain cells alive [9] and capable of recovery. There has recently been renewed interest in the possibility of neuronal protection during this phase by use of moderate hypothermia and by correction of the neuroendocrine abnormalities commonly seen in this early stage.[13]

Published studies of patients meeting the criteria for brain stem death or whole brain death the American standard which includes brain stem death diagnosed by similar means record that even if ventilation is continued after diagnosis, the heart stops beating within only a few hours or days.[14] However, there have been some very long-term survivals[15] and it is noteworthy that expert management can maintain the bodily functions of pregnant brain dead women for long enough to bring them to term.[16]

The management of patients pronounced dead on meeting the brain stem death criteria depends upon the reason for diagnosing death on that basis. If the intent is to take organs from the body for transplantation, the ventilator is reconnected and life-support measures are continued, perhaps intensified, with the addition of procedures designed to protect the wanted organs until they can be removed. Otherwise, the ventilator is left disconnected on confirmation of the lack of respiratory centre response.

The diagnostic criteria were originally published for the purpose of identifying a clinical state associated with a fatal prognosis (see above). The change of use, in the UK, to criteria for the diagnosis of death itself was protested from the first.[17][18] The initial basis for the change of use was the claim that satisfaction of the criteria sufficed for the diagnosis of the death of the brain as a whole, despite the persistence of demonstrable activity in parts of the brain.[19] In 1995, that claim was abandoned[7] and the diagnosis of death (acceptable for legal purposes in the UK in the context of organ procurement for transplantation) by the specified testing of brain stem functions was based on a new definition of death, viz. the permanent loss of the capacity for consciousness and spontaneous breathing. There are doubts that this concept is generally understood and accepted and that the specified testing is stringent enough to determine that state. It is, however, associated with substantial risk of exacerbating the brain damage and even causing the death of the apparently dying patient so tested (see "the apnoea test" above). This raises ethical problems which seem not to have been addressed.

It has been argued that sound scientific support is lacking for the claim that the specified purely bedside tests have the power to diagnose true and total death of the brain stem, the necessary condition for the assumption of permanent loss of the intrinsically untestable consciousness-arousal function of those elements of the reticular formation which lie within the brain stem (there are elements also within the higher brain).[19] Knowledge of this arousal system is based upon the findings from animal experiments[20][21][22] as illuminated by pathological studies in humans.[23] The current neurological consensus is that the arousal of consciousness depends upon reticular components which reside in the midbrain, diencephalon and pons.[24][25] It is said that the midbrain reticular formation may be viewed as a driving centre for the higher structures, loss of which produces a state in which the cortex appears, on the basis of electroencephalographic (EEG) studies, to be awaiting the command or ability to function. The role of diencephalic (higher brain) involvement is stated to be uncertain and we are reminded that the arousal system is best regarded as a physiological rather than a precise anatomical entity. There should, perhaps, also be a caveat about possible arousal mechanisms involving the first and second cranial nerves (serving sight and smell) which are not tested when diagnosing brain stem death but which were described in cats in 1935 and 1938.[20] In humans, light flashes have been observed to disturb the sleep-like EEG activity persisting after the loss of all brain stem reflexes and of spontaneous respiration.[26]

There is also concern about the permanence of consciousness loss, based on studies in cats, dogs and monkeys which recovered consciousness days or weeks after being rendered comatose by brain stem ablation and on human studies of brain stem stroke raising thoughts about the plasticity of the nervous system.[23] Other theories of consciousness place more stress on the thalamocortical system.[27] Perhaps the most objective statement to be made is that consciousness is not currently understood. That being so, proper caution must be exercised in accepting a diagnosis of its permanent loss before all cerebral blood flow has permanently ceased.

The ability to breathe spontaneously depends upon functioning elements in the medulla the respiratory centre. In the UK, establishing a neurological diagnosis of death involves challenging this centre with the strong stimulus offered by an unusually high concentration of carbon dioxide in the arterial blood, but it is not challenged by the more powerful drive stimulus provided by anoxia although the effect of that ultimate stimulus is sometimes seen after final disconnection of the ventilator in the form of agonal gasps.

No testing of testable brain stem functions such as oesophageal and cardiovascular regulation is specified in the UK Code of Practice for the diagnosis of death on neurological grounds. There is published evidence[28][29][30] strongly suggestive of the persistence of brain stem blood pressure control in organ donors.

A small minority of medical practitioners working in the UK have argued that neither requirement of the UK Health Department's Code of Practice basis for the equation of brain stem death with death is satisfied by its current diagnostic protocol[1] and that in terms of its ability to diagnose de facto brain stem death it falls far short.

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Brain stem death - Wikipedia, the free encyclopedia