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What Is Spinal Cord Trauma? – Spinal Cord Injury …

Injury to the spinal cord is a medical emergency that may result in severe and permanent disability. The spinal cordwhich along with the brain comprises the central nervous systemis a bundle of nerve cells that travels almost the entire length of the spine, connecting the brain to the nerves in the rest of the body.

The vertebrae, the small bones that make up the spine, form a bony tunnel that surrounds the cord and protects it from injury. However, if a blow is severe enough, or if the bones are weakened by disease, the spinal cord is vulnerable to damage.

Destroyed nerve cells cannot regenerate; injury to the spinal cord may thus result in permanent paralysis of the legs (paraplegia) or, in the case of a neck injury, the arms, torso and legs (quadriplegia). About half of the cases of spinal cord injury involve the neck.

However, partial or complete recovery may be expected in cases when neurons in the spinal cord have been traumatized but not completely destroyed. Outcome thus depends upon both the severity and the specific location of the injury. Damage to the spinal cord will affect nerves at the level of the injury and below.

Source:

Johns Hopkins Symptoms and Remedies: The Complete Home Medical Reference

Simeon Margolis, M.D., Ph.D., Medical Editor

Prepared by the Editors of The Johns Hopkins Medical Letter: Health After 50

Updated by Remedy Health Media

Publication Review By: the Editorial Staff at HealthCommunities.com

Published: 24 Aug 2011

Last Modified: 22 Jul 2015

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What Is Spinal Cord Trauma? - Spinal Cord Injury ...

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12,500 Approximate number of new spinal cord injury cases in the U.S. each year.

276,000 Estimated number of people in the U.S. living with spinal cord injury in 2014.

$4,724,181 Estimated total lifetime medical costs for someone who suffered the most severe type of SCI injury at age 25.

$2,596,329 The estimated total lifetime medical costs for someone who suffered the most severe type of SCI injury at age 50.

30 Percentage of SCI injuries caused by vehicle crashes, the leading cause of SCI crashes since 2010.

11 Average number of days in acute care treatment centers for people who suffered SCI.

36 Average number of days in rehabilitation for SCI injury patients.

42 Average age of injury for people with SCI in the U.S.

80 Percentage of people with SCI who are male.

23 The disproportionate percentage of SCI injuries that occur among black people, who only make up 12 percent of the general population.

Source: National SCI Statistical Center

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Spinal Cord Injury Rehabilitation | BrainAndSpinalCord.org

Treatment for spinal cord injuries can be divided into to two stages: acute and rehabilitation. The acute phase begins at the time of injury, and lasts until the person is stabilized. The rehabilitation phase begins as soon as the person has stabilized and is ready to begin working toward his or her independence.

During the acute phase, it is very important that the person receive prompt medical care. The faster the person accesses treatment, the better his or her chances are at having the least amount of impairment possible. In most cases, like in the all too common suv rollover, the injured person will be sent to the closest hospital or center equipped to deal with spinal cord injuries.

The first few days of the acute stage are accompanied by spinal shock, in which the persons reflexes dont work. During this stage, its very difficult to determine an exact prognosis, as some function beyond what is currently being seen may occur later. At this stage other complications from the accident or injury will also be present, such as brain injury, broken bones, or bruising.

Once the acute phase is over and the person has been stabilized, he or she enters the rehabilitation stage of treatment. Treatment during this phase has the goal of returning as much function as possible to the person. Because all spinal cord injuries are different, a unique plan designed to help the person function and succeed in everyday life is designed. The plan often includes:

In most cases, rehabilitation occurs at an approved and accredited spinal cord injury treatment center.

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Spinal Cord Injury – Spinal Cord Injury – Paralysis Resource …

Spinal cord injury involves damage to the nerves within the spinal canal; most SCIs are caused by trauma to the vertebral column, thereby affecting the spinal cord's ability to send and receive messages from the brain to the body's systems that control sensory, motor and autonomic function below the level of injury.

The spinal cord and the brain together make up the central nervous system (CNS). The spinal cord coordinates the body's movement and sensation.

The spinal cord includes neurons and long nerve fibers called axons. Axons in the spinal cord carry signals downward from the brain (along descending pathways) and upward toward the brain (along ascending pathways). Many axons in these pathways are covered by sheaths of an insulating substance called myelin, which gives them a whitish appearance; therefore, the region in which they lie is called "white matter."

The nerve cells themselves, with their tree-like branches called dendrites that receive signals from other nerve cells, make up "gray matter." This gray matter lies in a butterfly-shaped region in the center of the spinal cord.

Like the brain, the spinal cord is enclosed in three membranes (meninges): the pia mater, the innermost layer; the arachnoid, a delicate middle layer; and the dura mater, which is a tougher outer layer.

The spinal cord is organized into segments along its length. Nerves from each segment connect to specific regions of the body. The segments in the neck, or cervical region, referred to as C1 through C8, control signals to the neck, arms, and hands.

Those in the thoracic or upper back region (T1 through T12) relay signals to the torso and some parts of the arms. Those in the lumbar or mid-back region just below the ribs (L1 through L5) control signals to the hips and legs.

Finally, the sacral segments (S1 through S5) lie just below the lumbar segments in the mid-back and control signals to the groin, toes, and some parts of the legs. The effects of spinal cord injury at different segments along the spine reflect this organization.

Several types of cells carry out spinal cord functions. Large motor neurons have long axons that control skeletal muscles in the neck, torso, and limbs. Sensory neurons called dorsal root ganglion cells, whose axons form the nerves that carry information from the body into the spinal cord, are found immediately outside the spinal cord. Spinal interneurons, which lie completely within the spinal cord, help integrate sensory information and generate coordinated signals that control muscles.

Glia, or supporting cells, far outnumber neurons in the brain and spinal cord and perform many essential functions. One type of glial cell, the oligodendrocyte, creates the myelin sheaths that insulate axons and improve the speed and reliability of nerve signal transmission. Other glia enclose the spinal cord like the rim and spokes of a wheel, providing compartments for the ascending and descending nerve fiber tracts.

Astrocytes, large star-shaped glial cells, regulate the composition of the fluids that surround nerve cells. Some of these cells also form scar tissue after injury. Smaller cells called microglia also become activated in response to injury and help clean up waste products. All of these glial cells produce substances that support neuron survival and influence axon growth. However, these cells may also impede recovery following injury.

After injury, nerve cells, or neurons, of the peripheral nervous system (PNS), which carry signals to the limbs, torso, and other parts of the body, are able to repair themselves. Injured nerves in the CNS, however, are not able to regenerate.

Nerve cells of the brain and spinal cord respond to trauma and damage differently than most other cells of the body, including those in the PNS. The brain and spinal cord are confined within bony cavities that protect them, but this also renders them vulnerable to compression damage caused by swelling or forceful injury. Cells of the CNS have a very high rate of metabolism and rely upon blood glucose for energy these cells require a full blood supply for healthy functioning. CNS cells are particularly vulnerable to reductions in blood flow (ischemia).

Other unique features of the CNS are the "blood-brain-barrier" and the "blood-spinal-cord barrier." These barriers, formed by cells lining blood vessels in the CNS, protect nerve cells by restricting entry of potentially harmful substances and cells of the immune system. Trauma may compromise these barriers, perhaps contributing to further damage in the brain and spinal cord. The blood-spinal-cord barrier also prevents entry of some potentially therapeutic drugs.

Finally, in the brain and spinal cord, the glia and the extracellular matrix (the material that surrounds cells) differ from those in peripheral nerves. Each of these differences between the PNS and CNS contributes to their different responses to injury.

Complete vs. Incomplete What is the difference between a "complete injury" and a "incomplete injury?" Persons with an incomplete injury have some spared sensory or motor function below the level of injury the spinal cord was not totally damaged or disrupted. In a complete injury, nerve damage obstructs every signal coming from the brain to the body parts below the injury.

While there's almost always hope of recovering function after a spinal cord injury, it is generally true that people with incomplete injuries have a better chance of getting some return.

In a large study of all new spinal cord injuries in Colorado, reported by Craig Hospital, only one in seven of those who were completely paralyzed immediately after injury got a significant amount of movement back. But, of those who still had some movement in their legs immediately after injury, three out of four got significantly better.

About 2/3 of those with neck injuries who can feel the sharpness of a pin-stick in their legs eventually get enough muscle strength to be able to walk. Of those with neck injuries who can only feel light touch, about 1 in 8 may eventually walk.

The sooner muscles start working again, the better the chances are of additional recovery. But when muscles come back later - after the first several weeks - they are more likely to be in the arms than in the legs.

As long as there is some improvement and additional muscles recovering function, the chances are better that more improvement is possible.

The longer there is no improvement, the lower the odds it will start to happen on its own.

Statistics Approximately 1,275,000 people in the United States have sustained traumatic spinal cord injuries. Males account for 61 percent of all SCIs and females 39 percent.

For more statistics about spinal cord injury and paralysis read: One Degree of Separation -- Paralysis and Spinal Cord Injury in the United States.

Research and cures Currently, there is no cure for spinal cord injuries. However, ongoing research to test surgical and drug therapies is progressing rapidly. Injury progression prevention drug treatments, decompression surgery, nerve cell transplantation, nerve regeneration, and complex drug therapies are all being examined as a means to overcome the effects of spinal cord injury.

Source: American Association of Neurological Surgeons, Craig Hospital, Christopher and Dana ReeveFoundation, The National Institute of Neurological Disorders and Stroke

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spinal cord injury – The New York Times

Back to TopCauses

The spinal cord contains the nerves that carry messages between your brain and body. The cord passes through your neck and back.

Spinal cord trauma can be caused by injuries to the spine, such as:

A minor injury can damage the spinal cord if the spine is weakened, such as from rheumatoid arthritis or osteoporosis. Injury can also occur if the spinal canal protecting the spinal cord has become too narrow (spinal stenosis) due to the normal aging process.

Direct injury, such as bruises, can occur to the spinal cord if the bones or disks have been weakened. Fragments of bone (such as from broken vertebrae, which are the spine bones) or fragments of metal (such as from a traffic accident or gunshot) can damage the spinal cord.

Direct damage can occur if the spinal cord is pulled, pressed sideways, or compressed. This may occur if the head, neck, or backis twisted abnormally during an accident or intense chiropractic manipulation.

Bleeding, fluid buildup, and swelling can occur inside or outside the spinal cord (but within the spinal canal). Thebuildup of blood or fluid canpress onthe spinal cord and damage it.

Most spinal cord trauma happens to young, healthy individuals. Men ages 15to 35 are mostoften affected. The death rate tends to be higher in young children with spinal injuries.

Risk factors include:

Older people with weakenedbones (from osteoporosis) or persons with other medical problems (such as stroke) that make them more likely to fallmay also have spinal cord injury.

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CDC – Publications – Injuries – Spinal Cord – HRQOL

Injuries Spinal Cord

Brotherton SS, Krause JS, Nietert PJ. A pilot study of factors associated with falls in individuals with incomplete spinal cord injury. J Spinal Cord Med. 2007;30(3):243-250. abstract html

Krause JS, Broderick LE, Saladin LK, Broyles J. Racial disparities in health outcomes after spinal cord injury: mediating effects of education and income. J Spinal Cord Med 2006;29(1):1725. abstract

LaVela SL, Weaver FM, Goldstein B, Chen K, Miskevics S, Rajan S, Gater DR. Diabetes mellitus in individuals with spinal cord injury or disorder. J Spinal Cord Med 2006;29(4):387395. abstract

Lavela SL, Weaver FM, Smith B, Chen K. Disease prevalence and use of preventive services: comparison of female veterans in general and those with spinal cord injuries and disorders. J Womens Health 2006;15(3):301311. abstract

Krause JS, Broderick L. Outcomes after spinal cord injury: comparisons as a function of gender and race and ethnicity. Arch Phys Med Rehabil 2004;85(3):355362. abstract

Houlihan BV, Drainoni ML, Warner G, Nesathurai S, Wierbicky J, Williams S. The impact of Internet access for people with spinal cord injuries: a descriptive analysis of a pilot study. Disabil Rehabil 2003;25(8):422431. abstract

Krause JS, Coker JL, Charlifue S, Whiteneck GG. Health outcomes among American Indians with spinal cord injury. Arch Phys Med Rehabil 2000;81(7):9241. abstract

Andresen EM, Fouts BS, Romeis JC, Brownson CA. Performance of health-related quality of life instruments in a spinal cord injured population. Archives of Physical Medicine and Rehabilitation 1999;80:877884. abstract

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CDC - Publications - Injuries - Spinal Cord - HRQOL

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Spinal Cord Injury: Treatments and Rehabilitation Symptoms …

What are the causes of spinal cord injury?

The most common cause of spinal cord injury is trauma. Nearly half of the injuries are caused by motor vehicle accidents. Other types of trauma include:

Spinal cord injury can also be caused by compression of the cord by a tumor, infection, or inflammation. Some patients have a smaller than normal spinal canal (called spinal stenosis) and are at a higher risk of injury to the spinal cord.

All tissues in your body including the spinal cord require a good blood supply to deliver oxygen and other nutrients. Failure of this blood supply to the spinal cord can cause spinal cord injury. This can be caused by an aneurysm (ballooning of a blood vessel), compression of a blood vessel or a prolonged drop in blood pressure.

The symptoms of spinal cord injury depend on where the spinal cord is injured and whether or not the injury is complete or incomplete. In incomplete injuries, patients have some remaining function of their bodies below the level of injury, while in complete injuries they have no function below the level of injury.

Injuries to the spinal cord can cause weakness or complete loss of muscle function and loss of sensation in the body below the level of injury, loss of control of the bowels and bladder, and loss of normal sexual function. Spinal cord injuries in the upper neck can cause difficulty breathing and may require the use of a breathing machine, or ventilator.

Medically Reviewed by a Doctor on 6/4/2015

Spinal Cord Injury - Causes Question: What was the cause of your spinal cord injury?

Spinal Cord Injury - Symptoms Question: What were the symptoms associated with your spinal cord injury?

Spinal Cord Injury - Treatment Question: What was the treatment for your spinal cord injury?

Spinal Cord Injury - Prognosis Question: hat is your spinal cord injury prognosis?

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Spinal Cord Injury Center – Treatments, Research …

A spinal cord injury (SCI) involves damage to the spinal cord and nerve roots. Car accidents, falls, violent acts, and non-traumatic disorders can injure the spinal cord. SCI temporarily or permanently stops or alters the ability of the brain to communicate with other parts of the body.

Paralysis is a common outcome (temporary or permanent). However, spinal cord injury involves much more than damage to the spinal cord. After the primary injury, a cascade of secondary events can occur, such as inflammation, that can amplify the effects of the injury. Those secondary events can also cause pain or other symptoms. Currently, there is intense research interest in this secondary response to injury.

The National Spinal Cord Injury Statistical Center reported approximately 12,000 new cases of SCI occur each year in the United States. However, since incident studies have not been conducted since the 1990s, it is not known if this number has changed.1

Facts about Spinal Cord Injury

The severity of a spinal cord injury depends on where the spinal cord is damaged and if the injury is complete or incomplete.

Complete SCI

Incomplete SCI

There are different types of incomplete spinal cord injury. Included are: anterior cord syndrome, central cord syndrome, and Brown-Squard syndrome.

Anterior Cord Syndrome The anterior spinal cord is the front section. Symptoms may be caused when this part of the cord is compressed by a bone fragment or when there is insufficient blood supply. Symptoms include functional (motor skills) and sensory loss (i.e., light touch, pinprick) below the injury level.2

Central Cord Syndrome The central spinal cord is the middle area. These nerve fibers are large and exchange information between the spinal cord and the cerebral cortex (gray matter in the brain). The cerebral cortex is important to personality, interpreting sensation (feeling), and movement (motor function). The central spinal cord is important for hand and arm function, such as fine motor control (e.g., writing), although the lower body can be affected (e.g., loss of bladder control), too.

Brown-Squard Syndrome This syndrome affects one-half of the spinal cord, either the left or right side. If the right-hand side of the spinal cord is injured, symptoms affect the right side of the body (and if the left-hand side of the spinal cord is injured, the left side of the body is affected). It is characterized by partial loss of function or impaired function.

Spinal Levels and Areas Possibly Affected by SCI

A note about interpreting the table: Remember that a complete SCI affects all spinal cord function below the injury. For example, a thoracic injury may start at the torso and arms level, but it will also affect the low back, pelvis, groin, tailbone, legs, and toes.

Updated on: 08/28/14

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Spinal Cord Injuries | Quadriplegic | Stem Cells | Stem Cell …

After 26 years in a wheel chair William Orr is walking. Granted it is with the assistance of a walker, but he is walking. Orr is walking to get his mail, he is walking to rehab from his parked car and he is planning on walking into his 35th high school reunion. The 52-year-old Aurora man has been a quadriplegic for half his life, since a car hit him while he was riding his bike back in 1986. He suffered a C6-C7 incomplete spinal cord injury and has used a wheel chair since.In August of 2010, Orr underwent what many believe is a first of its kind stem cell procedure in Naples, Florida, using bone marrow from his hip that doctors believe has regenerated damaged cells in his spinal cord. He had such a good response that a second treatment was performed in July 2012. Subsequently, Orr has gained both motor and sensory improvement, as well as having the majority of his muscle spasms dissipate.

There is a remarkable difference. The results for Mr. Orr and others in the treatment group are truly remarkable and have exceeded our expectations said Michael Calcaterra for Intercellular Sciences. Frankly, this is an area that regeneration was thought not to be possible.

I feel like a new person, said Orr. And its only going to get better. He hopes to someday be walking without the walker. Doctors believe that if his quadriceps strength continues to improve as well as his foot lift, then its a real possibility. In the meantime, hes relishing every new sensation, big or small. Its this amazing work ethic and attitude along with the stem cells, his doctor insists, that will help get this man back on his feet again.

UPDATE:

In July 2013, Mr. Orr took his first independent steps in 27 years as his spinal regeneration continues.

About Adult Stem Cells

Stem cells reside in adult bone marrow and fat, as well as other tissues and organs of the body. These cells have a natural ability to repair damaged tissue, however in people with degenerative diseases they are not released and directed enough to fully repair damaged tissue. Adult stem cells can be extracted from many areas of the body, including the bone marrow, fat, and peripheral blood. Since the stem cells come from the patient there is no possibility for rejection or tumor formation, also there is none of the moral issues involving embryonic cells. Stem cells isolated from the bone marrow or fat have the ability to become different cell types (i.e. nerve cells, liver cells, heart cells, and cartilage cells). Studies have also shown that these cells are capable of homing to and repairing damaged tissue. Studies have shown that these stem cells secrete proteins and peptides that stimulate healing of damaged tissue, including heart muscle and spinal cord. Animal studies have shown stem cells to be reparative in spinal cord injury.

About the Procedure

Spinal cord injury patients are treated utilizing stem cells from their own bodies. The procedure involves obtaining 480ml of bone marrow aspirate from the hip bone, this is done under anesthesia so the patient is completely comfortable. The sample is then put through a process that first activates and then concentrates the stem cells. The stem cells are then delivered to the area of spinal injury utilizing a novel method of intra-arterial injection in a vascular angiography suite. This is an outpatient procedure and minimally invasive. The patient is discharged later that day.

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Spinal Cord Injury – Rehabilitation Institute of Chicago

As you leave the acute-care hospital, you have to make a very important decision... This is the time to choose RIC.

For spinal cord injury recovery, you need the nations #1 rehabilitation hospital* At the Rehabilitation Institute of Chicago (RIC), wecombine science and care, to Advance Human Ability.

As a nationally recognized leader, the Rehabilitation Institute of Chicago Spinal Cord Injury Rehabilitation Program offers a comprehensive rehabilitative approach to help you maximize your recovery potential and equip you with tools to succeed when you leave.

Thousands of patients choose RIC from across the country and around the world. RIC has been ranked the No. 1 Rehabilitation Hospital in the country for more than two decades by U.S. News & World Report. Each year more than 50,000 patients travel to RIC from around the globe to advance their abilities.

And, as the Midwest Regional Spinal Cord Injury Model System Centera federal designation from the National Institute on Disability and Rehabilitation Research RIC delivers the most innovative care.

RIC offers one of the only national programs that can treat patients at all levels of spinal cord injury: Ventilator dependent Diaphragmatic pacing Complete tetraplegia Complete paraplegia Incomplete injuries

Mark Stephan, who fractured his C2 and C3 vertebrae in a bicycle accident that paralyzed him from the neck down.

After intensive inpatient rehabilitation at RIC, he walked out one month later on his own two feet.

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Causes of Spinal Cord Injury (SCI) – Causes of spinal cord …

The most common causes of spinal cord injury is a broken neck or back neck (causing damage to the bones of the spine that surround the spinal cord). This often results in damage to the nerves of the spinal cord inside the spinal column. This is known as traumatic injury. Traumatic spinal cord injury may be caused by:

Road traffic accidents, domestic and work-related accidents, sports injuries, self-harm, assault or complications following surgery e.g., corrective surgery for spinal deformity e.g. scoliosis.

SCI can also be caused by so-called non-traumatic cord injury. Examples include:

Infection of the spinal nerve cells (bacterial and viral), cysts or tumours pressing on the spinal cord, interruption of the blood supply to the spinal cord (causing cord damage), congenital medical conditions (i.e. present since birth) that affect the structure of the spinal column e.g., spina bifida. Resultant Disability from these causes of spinal cord injury Quadriplegia, incomplete 31.2% - Paraplegia, complete 28.2% - Paraplegia, incomplete 23.1% - Quadriplegia, complete 17.5%

Facts and Figures from these causes of spinal cord injury Traumatic injuries account for the largest percentage of SCIs. Road traffic accidents account for the largest cause of spinal cord injuries worldwide.

In the USA violence accounts for the next largest cause of spinal cord injuries with which result primarily from gunshot wounds. This category has steadily risen over the last years there while motor vehicle crashes and sport related injuries have declined.

Falls and sporting activities make up the smallest group of causes of spinal cord injuries in the USA, However, within the sporting activity category, diving accidents cause the overwhelming majority of all spinal cord injuries that are sports related.

In the UK 2-3 people every day become paralysed as a result of spinal cord injury. That is 700+ each year adding to the 40,000 living here that are already paralysed. The figures for incomplete injuries may indeed be much higher because they don't take account of those people who have been treated by general hospitals instead of a specialist spinal injuries unit. Today advances in medical knowledge and patient management at the scene of an injury mean a lot more people will survive an SCI.

Our statistics are very similar to the USA (see chart) Road traffic accidents are still the biggest cause of traumatic cord injuries. SCI from gun crime although more prevalent today than ever is far lower than the American figure.

Since 1988, 45% of all injuries have been complete, 55% incomplete. Complete injuries result in total loss of sensation and function below the injury level. Incomplete injuries result in partial loss. "Complete" does not necessarily mean the cord has been severed. Each of the above categories can occur in paraplegia and quadriplegia.

Except for the incomplete-Preserved motor (functional), no more than 0.9% fully recover, although all can improve from the initial diagnosis. Overall, slightly more than 1/2 of all injuries result in quadriplegia. However, the proportion of quadriplegics increase markedly after age 45, comprising 2/3 of all injuries after age 60 and 87% of all injuries after age 75. 92% of all sports injuries result in quadriplegia.

Most people with neurologically complete lesions above C-3 die before receiving medical treatment. Those who survive are usually dependent on mechanical respirators to breathe.

50% of all cases have other injuries associated with the spinal cord injury.

A breakdown of the causes of sporting related spinal cord injuries worldwide reveals the following:

Diving 66.0% - Rugby & American Football 6.1% - Winter Sports 6.1% - Surfing 3.1% - Trampoline 2.6% - Wrestling 2.3% - Gymnastics 2.2% - Horseback Riding 2.0% - Other 9.6%

Tetraplegia - Paraplegia - Complete SCI - Incomplete SCI - Treatment - Complications - Causes of SCI - My Injury

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Spinal Cord Injury – Medical Disability Guidelines

ICD-9-CM: 952.00 - Spinal Cord Injury, without Evidence of Spinal Bone Injury; C1-C4 Level with Unspecified Spinal Cord Injury 952.01 - Spinal Cord Injury, without Evidence of Spinal Bone Injury; C1-C4 Level with Complete Lesion of Spinal Cord 952.02 - Spinal Cord Injury, Cervical Spine with Anterior Cord Syndrome 952.03 - Spinal Cord Injury, without Evidence of Spinal Bone Injury; C1-C4 level with Central Cord Syndrome 952.04 - Spinal Cord Injury, without Evidence of Spinal Bone Injury; C1-C4 level with Other Specified Spinal Cord Injury 952.05 - Spinal Cord Injury, without Evidence of Spinal Bone Injury; C5-C7 level with Unspecified Spinal Cord Injury 952.06 - Spinal Cord Injury, without Evidence of Spinal Bone Injury; C5-C7 level with Complete Lesion Of Spinal Cord 952.07 - Spinal Cord Injury, without Evidence of Spinal Bone Injury; C5-C7 level with Anterior Cord Syndrome 952.08 - Spinal Cord Injury, without Evidence of Spinal Bone Injury; C5-C7 level with Central Cord Syndrome 952.09 - Spinal Cord Injury, without Evidence of Spinal Bone Injury;C5-C7 level with Other Specified Spinal Cord Injury 952.10 - Thoracic Spinal Cord Injury without Evidence of Spinal Bone Injury; T1-T6 Level with Unspecified Spinal Cord Injury 952.11 - Thoracic Spinal Cord Injury without Evidence of Spinal Bone Injury; T1-T6 Level with Complete Lesion of Spinal Cord 952.12 - Thoracic Spinal Cord Injury without Evidence of Spinal Bone Injury; T1-T6 Level with Anterior Cord Syndrome 952.13 - Thoracic Spinal Cord Injury without Evidence of Spinal Bone Injury; T1-T6 Level with Central Cord Syndrome 952.14 - Thoracic Spinal Cord Injury without Evidence of Spinal Bone Injury; T1-T6 Level with Other Specified Spinal Cord Injury 952.15 - Thoracic Spinal Cord Injury without Evidence of Spinal Bone Injury; T7-T12 Level with Unspecified Spinal Cord Injury 952.16 - Thoracic Spinal Cord Injury without Evidence of Spinal Bone Injury; T7-T12 Level with Complete Lesion of Spinal Cord 952.17 - Thoracic Spinal Cord Injury without Evidence of Spinal Bone Injury; T7-T12 Level with Anterior Cord Syndrome 952.18 - Thoracic Spinal Cord Injury without Evidence of Spinal Bone Injury; T7-T12 Level with Central Cord Syndrome 952.19 - Thoracic Spinal Cord Injury without Evidence of Spinal Bone Injury; T7-T12 Level with Other Specified Spinal Cord Injury 952.2 - Lumbar Spinal Cord Injury without Evidence of Spinal Bone Injury 952.3 - Sacral Spinal Cord Injury without Evidence of Spinal Bone Injury 952.8 - Spinal Cord Injury without Evidence of Spinal Bone Injury, Multiple Sites 952.9 - Spinal Cord Injury, Unspecified

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Spinal Cord Injury Network – Spinal Cord Injury

My name is Andy and my cycling accident and Spinal Cord Injury in 1994 radically changed my life. Breaking my neck took a second to do but my resulting disability (spinal cord injury) will last my lifetime. Hopefully this website will assist others in understanding the nature of spinal cord injury (SCI).

If you, a family member or a friend have recently suffered a Spinal Cord Injury then although a 'normal' life may seem impossible now, let me assure you with time and knowledge things can and will get better. Spinal Cord Injury take many forms. There is tetraplegia (called quadriplegia or quadraplegia in USA), paraplegia and there are complete or incomplete lesions too. The most severe complete Spinal Cord Injury (high neck) will result in complete body paralysis and require a ventilator to breathe. The most incomplete Spinal Cord Injury may be able to walk virtually normally again but still suffer impaired continence bodily functions as a result of the cord lesion.

Every Spinal Cord Injury and the resulting disability is unique as are the people who have suffered them. If you are SCI yourself, a relative, friend, health professional or just someone seeking further information about life with a spinal cord injury you are ALL welcome here at the Spinal Injury Network. There's a lot of useful information about spinal cord injury on this site and an active community on the Message Boards too.

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Spinal Cord Injury Levels & Classification

Wise Young, Ph.D., M.D. W. M. Keck Center for Collaborative Neuroscience Rutgers University, Piscataway, NJ

When people are injured, they are often told that they have an injury at a given spinal cord level and are given a qualifier indicating the severity of injury, i.e. "complete" or "incomplete". They may also be told that they are classified according to the American Spinal Injury Association (ASIA) Classification, as a ASIA A, B, C, or D. They may also be told that they have a bony fracture or involvement of one or more spinal segments or vertebral levels. What most people do not know is doctors are frequently confused about the definition of spinal cord injury levels, the definition of complete and incomplete injury, and the classification of spinal cord injury. In the early 1990's, when I co-chaired the committee that helped define the currently accepted ASIA Classification, there was no single definition of level, completeness of injury, or classification. In this article, I will briefly address the issue of spinal cord injury levels, the definition of "complete" spinal cord injury, and the ASIA Classification approach towards spinal cord injury.

The spinal cord is situated within the spine. The spine consists of a series of vertebral segments. The spinal cord itself has "neurological" segmental levels which are defined by the spinal roots that enter and exist the spinal column between each of the vertebral segments. As shown in the figure the spinal cord segmental levels do not necessarily correspond to the bony segments. The vertebral levels are indicated on the left side while the cord segmental levels are listed for the cervical (red), thoracic (green), lumbar (blue), and sacral (yellow) cord.

Vertebral segments. There are 7 cervical (neck), 12 thoracic (chest), 5 lumbar (back), and 5 sacral (tail) vertebrae. The thoracic vertebrae are defined by The spinal cord segments are not necessarily situated at the same vertebral levels. For example, while the C1 cord is located at the C1 vertebra, the C8 cord is situated at the C7 vertebra. While the T1 cord is situated at the T1 vertebra, the T12 cord is situated at the T8 vertebra. The lumbar cord is situated between T9 and T11 vertebrae. The sacral cord is situated between the T12 to L2 vertebrae.

Spinal Roots. The spinal roots for C1 exit the spinal column at the atlanto-occiput junction. The spinal roots for C2 exit the spinal column at the atlanto-axis. The C3 roots exit between C2 and C3. The C8 root exits between C7 and C8. The first thoracic root or T1 exits the spinal cord between T1 and T2 vertebral bodies. The T12 root exits the spinal cord between T1 and L1. The L1 root exits the spinal cord between L1 and L2 bodies. The L5 root exits the cord between L1 and S1 bodies.

The Cervical Cord. The first and second cervical segments are special because this is what holds the head. The lower back of the head is called the Occiput. The first cervical vertebra, upon which the head is perched is sometimes called Atlas, after the Greek mythological figure who held up earth. The second cervical vertebra is sometimes called the Axis, upon which Atlas pivots. The interface between the occiput and the atlas is therefore called the atlanto-occiput junction. The interface between the first and second vertebra is called the atlanto-axis junction. The C3 cord contains the phrenic nucleus. The cervical cord innervates the deltoids (C4), biceps (C4-5), wrist extensors (C6), triceps (C7), wrist extensors (C8), and hand muscles (C8-T1).

The Thoracic Cord. The thoracic vertebral segments are defined by those that have a rib. These vertebral segments are also very special because they form the back wall of the pulmonary cavity and the ribs. The spinal roots form the intercostal (between the ribs) nerves that run on the bottom side of the ribs and these nerves control the intercostal muscles and associated dermatomes.

The Lumbosacral Cord. The lumbosacral vertebra form the remainder of the segments below the vertebrae of the thorax. The lumbosacral spinal cord, however, starts at about T9 and continues only to L2. It contains most of the segments that innervate the hip and legs, as well as the buttocks and anal regions.

The Cauda Equina. In human, the spinal cord ends at L2 vertebral level. The tip of the spinal cord is called the conus. Below the conus, there is a spray of spinal roots that is frequently called the cauda equina or horse's tail. Injuries to T12 and L1 vertebra damage the lumbar cord. Injuries to L2 frequently damage the conus. Injuries below L2 usually involve the cauda equina and represent injuries to spinal roots rather than the spinal cord proper.

In summary, spinal vertebral and spinal cord segmental levels are not necessarily the same. In the upper spinal cord, the first two cervical cord segments roughly match the first two cervical vertebral levels. However, the C3 through C8 segments of the spinal cords are situated between C3 through C7 bony vertebral levels. Likewise, in the thoracic spinal cord, the first two thoracic cord segments roughly match first two thoracic vertebral levels. However, T3 through T12 cord segments are situated between T3 to T8. The lumbar cord segments are situated at the T9 through T11 levels while the sacral segments are situated from T12 to L1. The tip of the spinal cord or conus is situated at L2 vertebral level. Below L2, there is only spinal roots, called the cauda equina.

A dermatome is a patch of skin that is innervated by a given spinal cord level. Figure 2 is taken from the ASIA classification manual, obtainable from the ASIA web site. Each dermatome has a specific point recommended for testing and shown in the figure. After injury, the dermatomes can expand or contract, depending on plasticity of the spinal cord.

C2 to C4. The C2 dermatome covers the occiput and the top part of the neck. C3 covers the lower part of the neck to the clavicle (the horizontal bone that goes to the shoulder. C4 covers the area just below the clavicle.

C5 to T1. These dermatomes are all situated in the arms. C5 covers the lateral arm at and above the elbow. C6 covers the forearm and the radial (thumb) side of the hand. C7 is the middle finger, C8 is the lateral aspects of the hand, and T1 covers the medial side of the forearm.

T2 to T12. The thoracic covers the axillary and chest region. T3 to T12 covers the chest and back to the hip girdle. The nipples are situated in the middle of T4. T10 is situated at the umbilicus. T12 ends just above the hip girdle.

L1 to L5. The cutaneous dermatome representating the hip girdle and groin area is innervated by L1 spinal cord. L2 and 3 cover the front part of the thighs. L4 and L5 cover medial and lateral aspects of the lower leg.

S1 to S5. S1 covers the heel and the middle back of the leg. S2 covers the back of the thighs. S3 cover the medial side of the buttocks and S4-5 covers the perineal region. S5 is of course the lowest dermatome and represents the skin immediately at and adjacent to the anus.

Ten muscle groups represent the motor innervation by the cervical and lumbosacral spinal cord. The ASIA system does not include the abdominal muscles (i.e. T10-11) because the thoracic levels are much easier to determine from sensory levels. It also excludes certain muscles (e.g. hamstrings) because the segmental levels that innervate them are already represented by other muscles.

Arm and hand muscles. C5 represents the elbow flexors (biceps), C6 the wrist extensors, C7 the elbow extensors (triceps), C8 the finger flexors, and T1 the little finger abductor (outward movement of the pinky finger).

Leg and foot muscles. The leg muscles represent the lumbar segments, i.e. L2 are the hip flexors (psoas), L3 the knee extensors (quadriceps), L4 the ankle dorsiflexors (anterior tibialis), L5 the long toe extensors (hallucis longus), S1 the ankle plantar flexors (gastrocnemius).

The anal sphincter is innervated by the S4-5 cord and represents the end of the spinal cord. The anal sphincter is a critical part of the spinal cord injury examination. If the person has any voluntary anal contraction, regardless of any other finding, that person is by definition a motor incomplete injury.

It is important to note that the muscle groups specified in the ASIA classifications represent a gross over simplication of the situation. Almost every muscle received innervation from two or more segments.

In summary, the spinal cord segment serve specific motor and sensory regions of the body. The sensory regions are called dermatomes with each segment of the spinal cord innervating a particularly area of skin. The distribution of these dermatomes are relatively straightforward except on the limbs. In the arms, the cervical dermatomes C5 to T1 are arrayed from proximal radial (C5) to distal (C6-8) and proximal medial (T1). In the legs, the L1 to L5 dermatomes cover the front of the leg from proximal to distal while the sacral dermatomes cover the back of the leg.

Differences between neurological and rehabilitation definitions of spinal cord injury levels. Doctors use two different definitions for spinal cord injury levels. Given the same neurological examination and findings, neurologists and physiatrists may not assign the same spinal cord injury level. In general, neurologists define the level of injury as the first spinal segmental level that shows abnormal neurological loss. Thus, for example, if a person has loss of biceps, the motor level of the injury is often said to be C4. In contrast, physiatrists or rehabilitation doctors tend to define level of injury as the lowest spinal segmental level that is normal. Thus, if a patient has normal C3 sensations and absent C4 sensation, a physiatrist would say the sensory level is C3 whereas a neurologist or neurosurgeon would call it a C4 injury level. Most orthopedic surgeons tend to refer to the bony level of injury as the level of injury.

EXAMPLE. The most common cervical spinal injuries involve C4 or C5. Take, for example, a person who has had a burst fracture of the C5 vertebral body. A burst fracture usually indicates severe trauma to vertebral body that typically injures the C6 spinal cord situated at the C5 vertebrae and also the C4 spinal roots that exits the spinal column between the C4 and C5 vertebra. Such an injury should cause a loss of sensations in C4 dermatome and weak deltoids (C4) due to injury to the C4 roots. Due to edema (swelling of the spinal cord), the biceps (C5) may be initially weak but should recover. The wrist extensors (C6), however, should remain weak and sensation at and below C6 should be severely compromised. A neurosurgeon or neurologist examining the above patient usually would conclude that there is a burst fracture at C5 from the x-rays, an initial sensory level at C4 (the first abnormal sensory dermatome) and the partial loss of deltoids and biceps would imply a motor level at C4 (the highest abnormal muscle level). Over time, as the patient recovers the C4 roots and the C5 spinal cord, both the sensory level and motor level should end up at C6. Such recovery is often attributed to "root" recovery. On the other hand, a physiatrist would conclude that the patient initially has a C3 sensory level, a C4 motor level, and a C5 vertebral injury level. If the patient recovers the C4 root and the C5 cord, the physiatrist would conclude that both the sensory and motor levels are C5.

Discrepant lower thoracic vertebral and cord levels. The spinal vertebral and cord segmental levels become increasingly discrepant further down the spinal column. For example, a T8 vertebral injury will result in a T12 spinal cord or neurological level. A T11 vertebral injury, in fact, will result in a L5 lumbar spinal cord level. Most patients and even many doctors do not understand how discrepant the vertebral and spinal cord levels can get in the lower spinal cord.

EXAMPLE. The most common thoracic spinal cord injury involves T11 and T12. A patient with a T11 vertebral injury may have or recover sensations in the L1 through L4 dermatomes which include the front of the leg down to the mid-shin level. In addition, such a patient should recover hip extensors, knee extensors, and even ankle dorsiflexion. However, the sacral functions, including bowel and bladder and many of the flexor functions of the leg may be absent or weak. As in the case of cervical and thoracic spinal cord injury, it is important to assess both sensory and motor function.

Conus and Cauda Equina Injuries. Injuries to the spinal column at L2 or lower will damage the tip of the spinal cord, called the conus, or the spray of spinal roots that are descending to the appropriate spinal vertebral levels to exit the spinal canal or the caudal equina. Please note that the spinal roots for L2 through S5 all descend in the cauda equina and injury to these roots would disrupt sensory and motor fibers from these segments. Strictly speaking, the spinal roots are part of the peripheral nervous system as opposed to the spinal cord. Peripheral nerves are supposed to be able to regenerate to some extent. However, the spinal roots are different from peripheral nerves in two respects. First, the neurons from which sensory axons emanate are situated in the dorsal root ganglia (DRG) which are located just outside the spinal column. One branch of the DRG goes into the spinal cord (called the central branch) and the other is the peripheral branch.

Thus, a spinal root injury is damaging the central branch of the sensory nerve whereas peripheral nerve injury usually damages the peripheral branch. The sensory axon must grow back into the spinal cord in order to restore function and they generally will not do so because of axonal growth inhibitors in the spinal cord and particular at the so-called PNS-CNS junction at the dorsal root entry zone. Second, the cauda equina contains the ventral roots of the spinal cord, through which the motor axons of the spinal cord pass to innervate muscles. If the injury to the ventral root is close to the motoneurons that sent the axons, the injury may damage the motoneuron itself. Both of these factors significantly reduce the likelihood of neurological recovery in a cauda equina injury compared to a peripheral nerve injury.

Most clinicians commonly describe injuries as "complete" or "incomplete".

Traditionally, "complete" spinal cord injury means having no voluntary motor or conscious sensory function below the injury site. However, this definition is often difficult to apply. The following three example illustrate the weaknesses and ambiguity of the traditional definition. The ASIA committee considered these questions when it formulated the classification system for spinal cord injury in 1992.

Most clinicians would regard a person as complete if the person has any level below which no function is present. The ASIA Committee decided to take this criterion to its logical limit, i.e. if the person has any spinal level below which there is no neurological function, that person would be classified as a "complete" injury. This translates into a simple definition of "complete" spinal cord injury: a person is a "complete" if they do not have motor and sensory function in the anal and perineal region representing the lowest sacral cord (S4-S5).

The decision to make the absence and presence of function at S4-5 the definition for "complete" injury not only resolved the problem of the zone of partial preservation but lateral preservation of function but it also resolved the issue of recovery of function. As it turns out, very few patients who have loss of S4/5 function recovered such function spontaneously. As shown in figure 3 below, while this simplifies the criterion for assessing whether an injury is "complete", the ASIA classification committee decided that both motor and sensory levels should be expressed on each side separately, as well as the zone of partial preservation.

In the end, the whole issue of "complete" versus "incomplete" injury may be a moot issue. The absence of motor and sensory function below the injury site does not necessarily mean that there are no axons that cross the injury site. Many clinicians equate a "complete" spinal cord injury with the lack of axons crossing the injury site. However, much animal and clinical data suggest that an animal or person with no function below the injury site can recover some function when the spinal cord is reperfused (in the case of an arteriovenous malformation causing ischemia to the cord), decompressed (in the case of a spinal cord that is chronically compressed), or treated with a drug such as 4-aminopyridine. The labeling of a person as being "complete" or "incomplete", in my opinion, should not be used to deny a person hope or therapy.

Clinicians have long used a clinical scale to grade severity of neurological loss. First devised at Stokes Manville before World War II and popularized by Frankel in the 1970's, the original scoring approach segregated patients into five categories, i.e. no function (A), sensory only (B), some sensory and motor preservation (C), useful motor function (D), and normal (E).

The ASIA Impairment Scale is follows the Frankel scale but differs from the older scale in several important respects. First, instead of no function below the injury level, ASIA A is defined as a person with no motor or sensory function preserved in the sacral segments S4-S5. This definition is clear and unambiguous. ASIA B is essentially identical to Frankel B but adds the requirement of preserved sacral S4-S5 function. It should be noted that ASIA A and B classification depend entirely on a single observation, i.e. the preservation of motor and sensory function of S4-5.

The ASIA scale also added quantitive criteria for C and D. The original Frankel scale asked clinicians to evaluate the usefulness of lower limb function. This not only introduced a subjective element to the scale but ignored arm and hand function in patients with cervical spinal cord injury. To get around this problem, ASIA stipulated that a patient would be an ASIA C if more than half of the muscles evaluated had a grade of less than 3/5. If not, the person was assigned to ASIA D.

ASIA E is of interest because it implies that somebody can have spinal cord injury without having any neurological deficits at least detectable on a neurological examination of this type. Also, the ASIA motor and sensory scoring may not be sensitive to subtle weakness, presence of spasticity, pain, and certain forms of dyesthesia that could be a result of spinal cord injury. Note that such a person would be categorized as an ASIA E.

These changes in the ASIA scale significantly improved the reliability and consistency of the classification. Although it was more logical, the new definition of "complete" injury does not necessarily mean that it better reflects injury severity. For example, is there any situation where a person could be an ASIA B and better off the ASIA C or even ASIA D?

The new ASIA A categorization turns out to be more predictive of prognosis than the previous definition where the presence of function several segments below the injury site but the absence of function below a given level could be interpreted as an "incomplete" spinal cord injury.

The ASIA committee also classified incomplete spinal cord injuries into five types. A central cord syndrome is associated with greater loss of upper limb function compared to the lower limbs. The Brown-Sequard syndrome results from a hemisection lesion of the spinal cord. Anterior cord syndrome occurs when the injury affects the anterior spinal tracts, including the vestibulospnal tract. Conus medullaris and cauda equina syndromes occur with damage to the conus or spinal roots of the cord.

Much confusion surrounds the terminology associated with spinal cord injury levels, severity, and classification. The American Spinal Injury Association tried to sort some of these issues and standardize the language that is used to describe spinal cord injury. The ASIA Spinal Cord Injury Classification approach has now been adopted by almost every major organization associated with spinal cord injury. This has resulted in more consistent terminology being used to /describe the findings in spinal cord injury around the world.

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Spinal Cord Injury Levels & Classification

Recommendation and review posted by sam

Genome Medicine

Medicine in the post-genomic era

Genome Medicine publishes peer-reviewed research articles, new methods, software tools, reviews and comment articles in all areas of medicine studied from a post-genomic perspective. Areas covered include, but are not limited to, disease genomics (including genome-wide association studies and sequencing-based studies), disease epigenomics, pathogen and microbiome genomics, immunogenomics, translational genomics, pharmacogenomics and personalized medicine, proteomics and metabolomics in medicine, systems medicine, and ethical, legal and social issues.

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DNA-PK inhibition boosts Cas9-mediated HDR

Transient pharmacological inhibition of DNA-PKcs can stimulate homology-directed repair following Cas9-mediated induction of a double strand break, and is expected to reduce the downstream workload.

Genomics of epilepsy

Candace Myers and Heather Mefford review how advances in genomic technologies have aided variant discovery, leading to a rapid increase in our understanding of epilepsy genetics.

CpG sites associated with atopy

Thirteen novel epigenetic loci associated with atopy and high IgE were found that could serve 55 as candidate loci; of these, four were within genes with known roles in the immune response.

Longitudinal 'omic profiles

A pilot study quantifying gene expression and methylation profile consistency over a year shows high longitudinal consistency, with individually extreme transcript abundance in a small number of genes which may be useful for explaining medical conditions or guiding personalized health decisions.

Ovarian cancer landscape

Exome sequencing of mucinous ovarian carcinoma tumors reveals multiple mutational targets, suggesting tumors arise through many routes, and shows this group of tumors is distinct from other subtypes.

NGS-guided cancer therapy

Jeffrey Gagan and Eliezer Van Allen review how next-generation sequencing can be incorporated into standard oncology clinical practice and provide guidance on the potential and limitations of sequencing.

ClinLabGeneticist

A platform for managing clinical exome sequencing data that includes data entry, distribution of work assignments, variant evaluation and review, selection of variants for validation, report generation.

Semantic workflow for clinical omics

A clinical omics analysis pipeline using the Workflow Instance Generation and Specialization (WINGS) semantic workflow platform demonstrates transparency, reproducibility and analytical validity.

Stephen McMahon and colleagues review treatments for pain relief, which are often inadequate, and discuss how understanding of the genomic and epigenomic mechanisms might lead to improved drugs.

View more review articles

Errors in RNA-Seq quantification affect genes of relevance to human disease

Robert C and Watson M

Genome Biology 2015, 16:177

Exploiting single-molecule transcript sequencing for eukaryotic gene prediction

Minoche AE, Dohm JC, Schneider J, Holtgrwe D, Viehver P, Montfort M, Rosleff Srensen T, Weisshaar B et al.

Genome Biology 2015, 16:184

Analysis methods for studying the 3D architecture of the genome

Ay F and Noble WS

Genome Biology 2015, 16:183

Graded gene expression changes determine phenotype severity in mouse models of CRX-associated retinopathies

Ruzycki PA, Tran NM, Kefalov VJ, Kolesnikov AV and Chen S

Genome Biology 2015, 16:171

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Genome Medicine

Recommendation and review posted by Bethany Smith

Dimerix Bioscience

Developing and Commercialising Drug Therapies

Dimerix Bioscience is a public unlisted clinical stage drug discovery and development company, and a wholly owned subsidiary of Sun Biomedical Limited (ASX:SBN Sun Biomedical Home Page). Based in Melbourne, Dimerixs lead clinical program is a Phase 2 study in Chronic Kidney Disease, DMX-200. This study has repurposing of existing molecules at its core, and upon successful results from this study, Dimerix intends to pursue the pathway of registration of a product for an orphan indication. The study has been initiated at the Austin Hospital under the supervision of Professor Power, and is currently recruiting patients.

The therapeutic rationale for DMX-200 was developed from Dimerixs core patented technology, known as Receptor Heteromer Investigation Technology (Receptor HIT) which can be used to elucidate receptor interactions. Applying this technology to receptors such as G-protein coupled receptors (GPCRs), Dimerix is able to identify differences in signaling behavior when receptors interact as heteromers, as expected in vivo, compared with the traditional analysis of single target receptors in isolation. In recent years Dimerix has been approached by several top 10 Pharmaceutical companies, and has assisted these with their drug discovery programs by applying the HIT technology and in house knowledge. These studies have assisted in validating Dimerixs in vitro approach as a rationale for pursuing in vivo therapeutic studies.

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Dimerix Bioscience

Recommendation and review posted by sam

Multiple Sclerosis Pictures: MS Brain Lesions, Symptoms …

What Is Multiple Sclerosis (MS)?

MS is a chronic disease that damages the nerves in the spinal cord and brain, as well as the optic nerves. Sclerosis means scarring, and people with MS develop multiple areas of scar tissue in response to the nerve damage. Depending on where the damage occurs, symptoms may include problems with muscle control, balance, vision, or speech.

Nerve damage can cause:

These symptoms may lead to frequent tripping or difficulty walking.

More than half of people with MS experience a vision problem called optic neuritis. This inflammation of the optic nerve may cause blurred vision, loss of color vision, eye pain, or blindness, usually in one eye. The problem is usually temporary and tends to improve within a few weeks. In many cases, vision problems are the first sign of MS.

Although less common than vision problems, some people with MS develop slurred speech. This happens when MS damages the nerves that carry speech signals from the brain. Some people also have trouble swallowing.

MS can take a toll on mental sharpness. Some people may find it takes longer to solve problems. Others may have mild memory loss or trouble concentrating. Most people with MS also experience some loss of bladder control, because signals between the brain and bladder are interrupted. Finally, fatigue is a common problem. You may feel tired even after a good night's sleep.

Confusion, slurred speech, and muscle weakness can be symptoms of MS, but they can also be signs of a stroke. Anyone who suddenly has trouble speaking or moving his or her limbs should be taken to the ER immediately. Treating a stroke within the first few hours provides the best odds of a successful recovery.

In people with MS, the body's own immune system attacks the tissue surrounding the nerve fibers in the brain, spinal cord, and optic nerves. This covering is made of a fatty substance called myelin. It insulates the nerves and helps them send electrical signals that control movement, speech, and other functions. When myelin is destroyed, scar tissue forms, and nerve messages are not transmitted properly.

The roots of MS remain mysterious, but doctors see some surprising trends. It's most common in regions far from the equator, including Scandinavia and other parts of Northern Europe. These areas get less sunlight, so some researchers believe that vitamin D (the "sunshine vitamin") may be involved. Research suggests a possible link between vitamin D deficiency and autoimmune disorders, but studies are ongoing. Genetics appear to play a role, as well.

MS is at least twice as common in women as it is in men. While it can strike people of any race, Caucasians appear to be most at risk. The chances of developing the condition are highest between ages 20 and 50.

Tests are often used, along with a medical history and neurological exam, to diagnose MS and rule out other causes of symptoms. More than 90% of people with MS have scar tissue that shows up on an MRI scan. A spinal tap can check for abnormalities in the fluid that bathes the brain and spinal cord. Tests to look at electrical activity of nerves can also help with diagnosis. Lab tests can help rule out other autoimmune conditions or infections such as HIV or Lyme disease.

MS is different in every person. Doctors usually see four forms:

Relapsing-remitting: Symptoms flare during acute attacks, then improve nearly completely or "remit." This is the most common form of MS.

Primary-progressive: MS slowly but steadily worsens.

Secondary-progressive: Begins as relapsing-remitting type, then becomes progressive.

Progressive-relapsing: The underlying disease steadily worsens. The patient has acute relapses, which may or may not remit. This is the least common form of MS.

Research suggests that the disease may be more active during the summer months. Heat and high humidity may also temporarily worsen symptoms. Very cold temperatures and sudden changes in temperature may aggravate symptoms, as well.

While there is no cure for MS, there are "disease-modifying drugs" that can reduce the frequency and severity of MS attacks. Use can result in less damage to the brain and spinal cord over time, slowing the progression of disability. When an attack does occur, high-dose corticosteroids can help cut it short. Many drugs are also available to manage troubling MS symptoms, such as muscle spasms, incontinence, and pain.

About half of people with MS develop some form of pain, either as a result of a short circuit in the nervous system or because of muscle spasms or strain. Doctors may prescribe antidepressants and anticonvulsant medications to ease nerve pain. Pain medicines and anti-spasm drugs may also be used. Muscle pain often responds well to massage and physical therapy. Be sure to discuss the options with your doctor if you find yourself in pain.

If MS affects balance, coordination, or muscle strength, you can learn to compensate. Physical therapy can help strengthen muscles, combat stiffness, and get around more easily. Occupational therapy can help retain coordination in your hands for dressing and writing. And if you're having trouble speaking or swallowing, a speech therapist can help.

Many nontraditional therapies for MS have not been well studied. Some people say acupuncture relieves symptoms such as muscle spasms and pain, but research to confirm its value isn't conclusive. Others have reported benefits from injections of bee venom, but a rigorous study, lasting 24 weeks, showed no improvements in disability, fatigue, or the number of MS attacks. It's important to inform your doctor about any supplements, special diets, or other therapies you want to try.

Doctors generally agree that its safe for women with MS to get pregnant. Research suggests no increased risk of complications during pregnancy. In fact, many women have fewer MS symptoms during pregnancy. High levels of hormones and proteins may suppress the immune system, reducing the odds of a new attack. It's best to talk with your doctors before pregnancy, as certain MS drugs should not be used while pregnant or nursing.In the early months after delivery, the odds for a relapse can rise.

The vast majority of people with MS are able to continue walking, though many benefit from some type of assistive device. Orthotic shoe inserts or leg braces can help increase stability. When one leg is stronger than the other, a cane can help. People with significant problems with their legs may need to use a walker. And a wheelchair or scooter may be best for those who are very unsteady or tire easily.

Making a few changes around the home can help you manage daily activities on your own. Install grab bars inside and outside the shower or tub. Use a non-slip mat. Add an elevated seat and safety rails to the toilet. Lower one of your kitchen counters so you can reach it from a sitting position. And get rid of any throw rugs, which are a tripping hazard.

Exercise can ease stiffness, fatigue, and other symptoms of MS. But overdoing it could make things worse. It's best to start slowly. Try exercising for 10 minutes at a time, then gradually working your way up to a longer session. Before you begin, check with your doctor about what type of activity and level of intensity would be most appropriate. A few possibilities include water aerobics, swimming, tai chi, and yoga.

Most people with MS live a normal or near-normal lifespan. While the condition may make it more difficult to get around or complete certain tasks, it doesn't always lead to severe disability. Thanks to effective medications, rehab therapies, and assistive devices, many people with MS remain active, stay in their jobs, and continue to enjoy their families and favorite activities.

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Multiple Sclerosis Pictures: MS Brain Lesions, Symptoms ...

Recommendation and review posted by simmons

Cell culture – Wikipedia, the free encyclopedia

Cell culture is the process by which cells are grown under controlled conditions, generally outside of their natural environment. In practice, the term "cell culture" now refers to the culturing of cells derived from multicellular eukaryotes, especially animal cells, in contrast with other types of culture that also grow cells, such as plant tissue culture, fungal culture, and microbiological culture (of microbes). The historical development and methods of cell culture are closely interrelated to those of tissue culture and organ culture. Viral culture is also related, with cells as hosts for the viruses.

The laboratory technique of maintaining live cell lines (a population of cells descended from a single cell and containing the same genetic makeup) separated from their original tissue source became more robust in the middle 20th century.[1][2]

The 19th-century English physiologist Sydney Ringer developed salt solutions containing the chlorides of sodium, potassium, calcium and magnesium suitable for maintaining the beating of an isolated animal heart outside of the body.[3] In 1885, Wilhelm Roux removed a portion of the medullary plate of an embryonic chicken and maintained it in a warm saline solution for several days, establishing the principle of tissue culture.[4]Ross Granville Harrison, working at Johns Hopkins Medical School and then at Yale University, published results of his experiments from 1907 to 1910, establishing the methodology of tissue culture.[5]

Cell culture techniques were advanced significantly in the 1940s and 1950s to support research in virology. Growing viruses in cell cultures allowed preparation of purified viruses for the manufacture of vaccines. The injectable polio vaccine developed by Jonas Salk was one of the first products mass-produced using cell culture techniques. This vaccine was made possible by the cell culture research of John Franklin Enders, Thomas Huckle Weller, and Frederick Chapman Robbins, who were awarded a Nobel Prize for their discovery of a method of growing the virus in monkey kidney cell cultures.

Cells can be isolated from tissues for ex vivo culture in several ways. Cells can be easily purified from blood; however, only the white cells are capable of growth in culture. Mononuclear cells can be released from soft tissues by enzymatic digestion with enzymes such as collagenase, trypsin, or pronase, which break down the extracellular matrix. Alternatively, pieces of tissue can be placed in growth media, and the cells that grow out are available for culture. This method is known as explant culture.

Cells that are cultured directly from a subject are known as primary cells. With the exception of some derived from tumors, most primary cell cultures have limited lifespan.

An established or immortalized cell line has acquired the ability to proliferate indefinitely either through random mutation or deliberate modification, such as artificial expression of the telomerase gene. Numerous cell lines are well established as representative of particular cell types.

For the majority of isolated primary cells, they undergo the process of senescence and stop dividing after a certain number of population doublings while generally retaining their viability (described as the Hayflick limit).

Cells are grown and maintained at an appropriate temperature and gas mixture (typically, 37C, 5% CO2 for mammalian cells) in a cell incubator. Culture conditions vary widely for each cell type, and variation of conditions for a particular cell type can result in different phenotypes.

Aside from temperature and gas mixture, the most commonly varied factor in culture systems is the cell growth medium. Recipes for growth media can vary in pH, glucose concentration, growth factors, and the presence of other nutrients. The growth factors used to supplement media are often derived from the serum of animal blood, such as fetal bovine serum (FBS), bovine calf serum, equine serum, and porcine serum. One complication of these blood-derived ingredients is the potential for contamination of the culture with viruses or prions, particularly in medical biotechnology applications. Current practice is to minimize or eliminate the use of these ingredients wherever possible and use human platelet lysate (hPL). This eliminates the worry of cross-species contamination when using FBS with human cells. hPL has emerged as a safe and reliable alternative as a direct replacement for FBS or other animal serum. In addition, chemically defined media can be used to eliminate any serum trace (human or animal), but this cannot always be accomplished with different cell types. Alternative strategies involve sourcing the animal blood from countries with minimum BSE/TSE risk, such as The United States, Australia and New Zealand,[6] and using purified nutrient concentrates derived from serum in place of whole animal serum for cell culture.[7]

Plating density (number of cells per volume of culture medium) plays a critical role for some cell types. For example, a lower plating density makes granulosa cells exhibit estrogen production, while a higher plating density makes them appear as progesterone-producing theca lutein cells.[8]

Cells can be grown either in suspension or adherent cultures. Some cells naturally live in suspension, without being attached to a surface, such as cells that exist in the bloodstream. There are also cell lines that have been modified to be able to survive in suspension cultures so they can be grown to a higher density than adherent conditions would allow. Adherent cells require a surface, such as tissue culture plastic or microcarrier, which may be coated with extracellular matrix (such as collagen and laminin) components to increase adhesion properties and provide other signals needed for growth and differentiation. Most cells derived from solid tissues are adherent. Another type of adherent culture is organotypic culture, which involves growing cells in a three-dimensional (3-D) environment as opposed to two-dimensional culture dishes. This 3D culture system is biochemically and physiologically more similar to in vivo tissue, but is technically challenging to maintain because of many factors (e.g. diffusion).

Cell line cross-contamination can be a problem for scientists working with cultured cells.[9] Studies suggest anywhere from 1520% of the time, cells used in experiments have been misidentified or contaminated with another cell line.[10][11][12] Problems with cell line cross-contamination have even been detected in lines from the NCI-60 panel, which are used routinely for drug-screening studies.[13][14] Major cell line repositories, including the American Type Culture Collection (ATCC), the European Collection of Cell Cultures (ECACC) and the German Collection of Microorganisms and Cell Cultures (DSMZ), have received cell line submissions from researchers that were misidentified by them.[13][15] Such contamination poses a problem for the quality of research produced using cell culture lines, and the major repositories are now authenticating all cell line submissions.[16] ATCC uses short tandem repeat (STR) DNA fingerprinting to authenticate its cell lines.[17]

To address this problem of cell line cross-contamination, researchers are encouraged to authenticate their cell lines at an early passage to establish the identity of the cell line. Authentication should be repeated before freezing cell line stocks, every two months during active culturing and before any publication of research data generated using the cell lines. Many methods are used to identify cell lines, including isoenzyme analysis, human lymphocyte antigen (HLA) typing, chromosomal analysis, karyotyping, morphology and STR analysis.[17]

One significant cell-line cross contaminant is the immortal HeLa cell line.

As cells generally continue to divide in culture, they generally grow to fill the available area or volume. This can generate several issues:

Among the common manipulations carried out on culture cells are media changes, passaging cells, and transfecting cells. These are generally performed using tissue culture methods that rely on aseptic technique. Aseptic technique aims to avoid contamination with bacteria, yeast, or other cell lines. Manipulations are typically carried out in a biosafety hood or laminar flow cabinet to exclude contaminating micro-organisms. Antibiotics (e.g. penicillin and streptomycin) and antifungals (e.g.amphotericin B) can also be added to the growth media.

As cells undergo metabolic processes, acid is produced and the pH decreases. Often, a pH indicator is added to the medium to measure nutrient depletion.

In the case of adherent cultures, the media can be removed directly by aspiration, and then is replaced. Media changes in non-adherent cultures involve centrifuging the culture and resuspending the cells in fresh media.

Passaging (also known as subculture or splitting cells) involves transferring a small number of cells into a new vessel. Cells can be cultured for a longer time if they are split regularly, as it avoids the senescence associated with prolonged high cell density. Suspension cultures are easily passaged with a small amount of culture containing a few cells diluted in a larger volume of fresh media. For adherent cultures, cells first need to be detached; this is commonly done with a mixture of trypsin-EDTA; however, other enzyme mixes are now available for this purpose. A small number of detached cells can then be used to seed a new culture. Some cell cultures, such as RAW cells are mechanically scraped from the surface of their vessel with rubber scrapers.

Another common method for manipulating cells involves the introduction of foreign DNA by transfection. This is often performed to cause cells to express a protein of interest. More recently, the transfection of RNAi constructs have been realized as a convenient mechanism for suppressing the expression of a particular gene/protein. DNA can also be inserted into cells using viruses, in methods referred to as transduction, infection or transformation. Viruses, as parasitic agents, are well suited to introducing DNA into cells, as this is a part of their normal course of reproduction.

Cell lines that originate with humans have been somewhat controversial in bioethics, as they may outlive their parent organism and later be used in the discovery of lucrative medical treatments. In the pioneering decision in this area, the Supreme Court of California held in Moore v. Regents of the University of California that human patients have no property rights in cell lines derived from organs removed with their consent.[19]

It is possible to fuse normal cells with an immortalised cell line. This method is used to produce monoclonal antibodies. In brief, lymphocytes isolated from the spleen (or possibly blood) of an immunised animal are combined with an immortal myeloma cell line (B cell lineage) to produce a hybridoma which has the antibody specificity of the primary lymphocyte and the immortality of the myeloma. Selective growth medium (HA or HAT) is used to select against unfused myeloma cells; primary lymphoctyes die quickly in culture and only the fused cells survive. These are screened for production of the required antibody, generally in pools to start with and then after single cloning.

A cell strain is derived either from a primary culture or a cell line by the selection or cloning of cells having specific properties or characteristics which must be defined. Cell strains are cells that have been adapted to culture but, unlike cell lines, have a finite division potential. Non-immortalized cells stop dividing after 40 to 60 population doublings[20] and, after this, they lose their ability to proliferate (a genetically determined event known as senescence).[21]

Mass culture of animal cell lines is fundamental to the manufacture of viral vaccines and other products of biotechnology.

Biological products produced by recombinant DNA (rDNA) technology in animal cell cultures include enzymes, synthetic hormones, immunobiologicals (monoclonal antibodies, interleukins, lymphokines), and anticancer agents. Although many simpler proteins can be produced using rDNA in bacterial cultures, more complex proteins that are glycosylated (carbohydrate-modified) currently must be made in animal cells. An important example of such a complex protein is the hormone erythropoietin. The cost of growing mammalian cell cultures is high, so research is underway to produce such complex proteins in insect cells or in higher plants, use of single embryonic cell and somatic embryos as a source for direct gene transfer via particle bombardment, transit gene expression and confocal microscopy observation is one of its applications. It also offers to confirm single cell origin of somatic embryos and the asymmetry of the first cell division, which starts the process.

Research in tissue engineering, stem cells and molecular biology primarily involves cultures of cells on flat plastic dishes. This technique is known as two-dimensional (2D) cell culture, and was first developed by Wilhelm Roux who, in 1885, removed a portion of the medullary plate of an embryonic chicken and maintained it in warm saline for several days on a flat glass plate. From the advance of polymer technology arose today's standard plastic dish for 2D cell culture, commonly known as the Petri dish. Julius Richard Petri, a German bacteriologist, is generally credited with this invention while working as an assistant to Robert Koch. Various researchers today also utilize culturing laboratory flasks, conicals, and even disposable bags like those used in single-use bioreactors.

Aside from Petri dishes, scientists have long been growing cells within biologically derived matrices such as collagen or fibrin, and more recently, on synthetic hydrogels such as polyacrylamide or PEG. They do this in order to elicit phenotypes that are not expressed on conventionally rigid substrates. There is growing interest in controlling matrix stiffness,[22] a concept that has led to discoveries in fields such as:

Cell culture in three dimensions has been touted as "Biology's New Dimension".[37] Nevertheless, the practice of cell culture remains based on varying combinations of single or multiple cell structures in 2D.[38] That being said, there is an increase in use of 3D cell cultures in research areas including drug discovery, cancer biology, regenerative medicine and basic life science research.[39] There are a variety of platforms used to facilitate the growth of three-dimensional cellular structures such as nanoparticle facilitated magnetic levitation,[40] gel matrices scaffolds, and hanging drop plates.[41]

3D Cell Culturing by Magnetic Levitation method (MLM) is the application of growing 3D tissue by inducing cells treated with magnetic nanoparticle assemblies in spatially varying magnetic fields using neodymium magnetic drivers and promoting cell to cell interactions by levitating the cells up to the air/liquid interface of a standard petri dish. The magnetic nanoparticle assemblies consist of magnetic iron oxide nanoparticles, gold nanoparticles, and the polymer polylysine. 3D cell culturing is scalable, with the capability for culturing 500 cells to millions of cells or from single dish to high-throughput low volume systems.

Cell culture is a fundamental component of tissue culture and tissue engineering, as it establishes the basics of growing and maintaining cells in vitro. The major application of human cell culture is in stem cell industry, where mesenchymal stem cells can be cultured and cryopreserved for future use. Tissue engineering potentially offers dramatic improvements in low cost medical care for hundreds of thousands of patients annually.

Vaccines for polio, measles, mumps, rubella, and chickenpox are currently made in cell cultures. Due to the H5N1 pandemic threat, research into using cell culture for influenza vaccines is being funded by the United States government. Novel ideas in the field include recombinant DNA-based vaccines, such as one made using human adenovirus (a common cold virus) as a vector,[42][43] and novel adjuvants.[44]

Plant cell cultures are typically grown as cell suspension cultures in a liquid medium or as callus cultures on a solid medium. The culturing of undifferentiated plant cells and calli requires the proper balance of the plant growth hormones auxin and cytokinin.

Cells derived from Drosophila melanogaster (most prominently, Schneider 2 cells) can be used for experiments which may be hard to do on live flies or larvae, such as biochemical studies or studies using siRNA. Cell lines derived from the army worm Spodoptera frugiperda, including Sf9 and Sf21, and from the cabbage looper Trichoplusia ni, High Five cells, are commonly used for expression of recombinant proteins using baculovirus.

For bacteria and yeasts, small quantities of cells are usually grown on a solid support that contains nutrients embedded in it, usually a gel such as agar, while large-scale cultures are grown with the cells suspended in a nutrient broth.

The culture of viruses requires the culture of cells of mammalian, plant, fungal or bacterial origin as hosts for the growth and replication of the virus. Whole wild type viruses, recombinant viruses or viral products may be generated in cell types other than their natural hosts under the right conditions. Depending on the species of the virus, infection and viral replication may result in host cell lysis and formation of a viral plaque.

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Human Gene Therapy

Editor-in-Chief: Terence R. Flotte, MD Deputy Editor, Europe: Thierry VandenDriessche, PhD Deputy Editor, U.S.: Barry J. Byrne, MD, PhD Human Gene Therapy Editor: Guangping Gao, PhD Methods Editor: Hildegard Bning, PhD Clinical Development Editor: James M. Wilson, MD, PhD

Latest Impact Factor* is 3.755 *2014 Journal Citation Reports published by Thomson Reuters, 2015

Human Gene Therapy is the premier, multidisciplinary journal covering all aspects of gene therapy. The Journal publishes in-depth coverage of DNA, RNA, and cell therapies by delivering the latest breakthroughs in research and technologies. Human Gene Therapy provides a central forum for scientific and clinical information, including ethical, legal, regulatory, social, and commercial issues, which enables the advancement and progress of therapeutic procedures leading to improved patient outcomes, and ultimately, to curing diseases.

The Journal is divided into three parts. Human Gene Therapy, the flagship, is published 12 times per year. HGT Methods, a bimonthly journal, focuses on the applications of gene therapy to product testing and development. HGT Clinical Development, a quarterly journal, serves as a venue for publishing data relevant to the regulatory review and commercial development of cell and gene therapy products.

Human Gene Therapy was voted one of the most influential journals in Biology and Medicine over the last 100 years by the Biomedical & Life Sciences Division of the Special Libraries Association.

Human Gene Therapy, HGT Methods, and HGT Clinical Development are under the editorial leadership of Editor-in-Chief Terence R. Flotte, MD, University of Massachusetts Medical School; Deput Editor Europe Thierry VandenDriessche, PhD, Free University of Brussels (VUB); Deputy Editor U.S. Barry J. Byrne, MD, PhD,Powell Gene Therapy Center, University of Florida, College of Medicine; Human Gene Therapy Editor Guangping Gao, PhD, University of Massachusetts Medical School; Methods Editor Hildegard Bning, PhD, University of Cologne; Clinical Development Editor James M. Wilson, MD, PhD,University of Pennsylvania School of Medicine, Gene Therapy Program; and other leading investigators. View the entire editorial board.

Audience: Geneticists, medical geneticists, molecular biologists, virologists, experimental researchers, and experimental medicine specialists, among others.

Human Gene Therapy and HGT Methods provide Instant Online publication 72 hours after acceptance

The views, opinions, findings, conclusions and recommendations set forth in any Journal article are solely those of the authors of those articles and do not necessarily reflect the views, policy or position of the Journal, its Publisher, its editorial staff or any affiliated Societies and should not be attributed to any of them.

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Human Gene Therapy

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Gene Therapy for Diseases | ASGCT – American Society of Gene …

Gene Therapy for Diseases

Gene Therapy has made important medical advances in less than two decades. Within this short time span, it has moved from the conceptual stage to technology development and laboratory research to clinical translational trials for a variety of deadly diseases. Among the most notable advancements are the following:

Severe Combined Immune Deficiency (ADA-SCID) ADA-SCID is also known as the bubble boy disease. Affected children are born without an effective immune system and will succumb to infections outside of the bubble without bone marrow transplantation from matched donors. A landmark study representing a first case of gene therapy "cure," or at least a long-term correction, for patients with deadly genetic disorder was conducted by investigators in Italy. The therapeutic gene called ADA was introduced into the bone marrow cells of such patients in the laboratory, followed by transplantation of the genetically corrected cells back to the same patients. The immune system was reconstituted in all six treated patients without noticeable side effects, who now live normal lives with their families without the need for further treatment.

Chronic Granulomatus Disorder (CGD) CGD is a genetic disease in the immune system that leads to the patients' inability to fight off bacterial and fungal infections that can be fatal. Using similar technologies as in the ADA-SCID trial, investigators in Germany treated two patients with this disease, whose reconstituted immune systems have since been able to provide them with full protection against microbial infections for at least two years.

Hemophilia Patients born with Hemophilia are not able to induce blood clots and suffer from external and internal bleeding that can be life threatening. In a clinical trial conducted in the United States , the therapeutic gene was introduced into the liver of patients, who then acquired the ability to have normal blood clotting time. The therapeutic effect however, was transient because the genetically corrected liver cells were recognized as foreign and rejected by the healthy immune system in the patients. This is the same problem faced by patients after organ transplantation, and curative outcome by gene therapy might be achievable with immune-suppression or alternative gene delivery strategies currently being tested in preclinical animal models of this disease.

Other genetic disorders After many years of laboratory and preclinical research in appropriate animal models of disease, a number of clinical trials will soon be launched for various genetic disorders that include congenital blindness, lysosomal storage disease and muscular dystrophy, among others.

Cancer Multiple gene therapy strategies have been developed to treat a wide variety of cancers, including suicide gene therapy, oncolytic virotherapy, anti-angiogenesis and therapeutic gene vaccines. Two-thirds of all gene therapy trials are for cancer and many of these are entering the advanced stage, including a Phase III trial of Ad.p53 for head and neck cancer and two different Phase III gene vaccine trials for prostate cancer and pancreas cancer. Additionally, numerous Phase I and Phase II clinical trials for cancers in the brain, skin, liver, colon, breast and kidney among others, are being conducted in academic medical centers and biotechnology companies, using novel technologies and therapeutics developed on-site.

Neurodegenerative Diseases Recent progress in gene therapy has allowed for novel treatments of neurodegenerative diseases such as Parkinson's Disease and Huntington's Disease, for which exciting treatment results have been obtained in appropriate animal models of the corresponding human diseases. Phase I clinical trials for these neurodegenerative disorders have been, or will soon be, launched.

Other acquired diseases The same gene therapeutic techniques have been applied to treat other acquired disorders such as viral infections (e.g. influenza, HIV, hepatitis), heart disease and diabetes, among others. Some of these have entered, or will soon be entering, into early phase clinical trials.

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Gene Therapy – Cancer Treatments – Moores Cancer Center, UC …

Gene therapy is an experimental treatment that involves inserting genetic material into your cells to give them a new function or restore a missing function, as cancer may be caused by damaged or missing genes, also known as gene mutations. Although gene therapy may be one way to overcome these changes and treat or prevent cancer, it is currently only available through clinical trials.

Cancer is caused by changes in our genes. Genes are inherited from our parents, and determine our traits and characteristics. They are made of biological molecules called deoxyribonucleic acid (DNA) and ribonucleic acid (RNA). DNA and RNA are responsible for making proteins, which have many functions, such as helping a cell to maintain its shape or controlling its growth and division. Changes or mutations in genes can affect the proteins and may sometimes lead to diseases, such as cancer.

Gene therapy is designed to modify cancer cells at the molecular level and replace a missing or bad gene with a healthy one. The new gene is delivered to the target cell via a vector, which is usually an inactive virus or liposome, a tiny fat bubble.

Gene therapy can be done in two ways: outside (ex vivo) or inside (in vivo) your body. Ex-vivo techniques involve taking some of the cancer cells out of your body, injecting them with good genes, and then putting them back into your body. The in-vivo process requires that good genes be put directly into a tumor, which may be difficult depending on its location or if the cancer has spread. Scientists generally use two types of cells in gene therapy the tumor cells themselves and immune system cells that attack the tumors.

Researchers from Moores Cancer Center at UC San Diego Health System are studying several gene therapy techniques for breast cancer, melanoma, leukemia and pancreatic cancer.

For example, they have been integrally involved in the development of Herceptin, a targeted therapy that is proving to be effective in curing localized human epidermal growth factor receptor-2 (HER2) breast cancer. HER2 controls how cells grow, divide and repair themselves.

Researchers have also been injecting a modified herpes virus into melanoma tumors, with the intention of improving the bodys immune defenses against the disease.

Gene therapy called TNFerade Biologic involves a DNA carrier containing the gene for tumor necrosis factor-alpha, an immune system protein with potent and well-documented anti-cancer effects. TNFerade is being studied in combination with radiation therapy for first-time treatment of inoperable pancreatic cancer.

TNFerade and the herpes strategies use gene therapy to enhance the killing effect of the primary mechanism radiation in TNFerade and viral induced cell lysis, or splitting, in the herpes virus.

When will gene therapy be available? Gene therapy is only available as a cancer treatment through clinical trials.

Are there any risks associated with gene therapy clinical trials? Yes. Viral vectors might infect healthy cells as well as cancer cells, a new gene might be inserted in the wrong location in the DNA, or the transferred genes could be overexpressed and produce too much of the missing protein, causing harm. All risks for any procedure should be discussed with your doctor.

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Articles about Gene Therapy – latimes

NEWS

October 24, 2012 | By Karen Kaplan, Los Angeles Times

Scientists have demonstrated a new type of gene therapy that would - in principle - allow mothers to avoid saddling their children with rare diseases that could result in heart problems, dementia, diabetes, deafness and other significant health issues. The disorders in question are all due to mutations in one of the 37 genes in our mitochondrial DNA. Mitochondria are structures within cells that convert the energy from food into a form that cells can use, according to this explainer from the NIH's National Library of Medicine.

HEALTH

September 13, 2012 | By Elaine Herscher

Genes make us who we are - in sickness and in health. We get our genetic makeup from our parents, of course, but in the future, we might be getting genes from our doctors too. Imagine your doctor promising to cure your cancer or heart disease by prescribing some new snippets of DNA. For some diseases, gene therapy is already a reality. In other cases, genetic cures are still years away. Despite many challenges and setbacks - including some that are surely yet to come - experts predict that gene therapy will eventually become a crucial and even common part of healthcare.

SCIENCE

August 15, 2012 | By Rosie Mestel, Los Angeles Times

Dog lovers may be interested in an article published this week in the New England Journal of Medicine: It highlights the discoveries scientists are making about diseases that various dog breeds are prone to -- and how those findings can benefit human health as well as that of canines. It's written by longtime dog genetics researcher Elaine Ostrander of the National Human Genome Research Institute. The discoveries are possible because of several things: First off, both the human genome and dog genomes have been sequenced.

SCIENCE

July 20, 2012 | By Thomas H. Maugh II, Los Angeles Times

The long-frustrated field of gene therapy is about to reach a major milestone: the first regulatory approval of a gene therapy treatment for disease in the West. The European Medicine Agency's Committee for Medicinal Products for Human Use said Friday that it is recommending approval of Glybera, a treatment for lipoprotein lipase deficiency manufactured by uniQure of Amsterdam. The European Commission generally follows the recommendations of the agency, and if it does so this time, the product could be available in all 27 members of the European Union by the end of the year.

SCIENCE

July 18, 2012 | By Jon Bardin, Los Angeles Times

We like to think of the Olympics as a level playing field - that's why doping is banned. But scientific research complicates this view: There are numerous genetic factors known to confer advantages in athletic contests, from mutations that increase the oxygen carrying capacity of blood to gene variants that confer an incredible increase in endurance, and these mutations appear to be especially common in Olympic athletes. In other words, we may want an egalitarian Olympic games, but it probably isn't in the cards.

NEWS

June 29, 2012 | By Jon Bardin, Los Angeles Times / For the Booster Shots blog

Can't kick cigarettes? A vaccine may one day help by preventing nicotine from reaching its target in the brain, according to research published this week. Most smoking therapies do a poor job of stopping the habit - 70% to 80% of smokers who use an approved drug therapy to quit relapse. Scientists say this is because the targets of existing therapies are imperfect, only slightly weakening nicotine's ability to find its target in the brain. So some scientists have been trying a different approach - creation of a vaccine.

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Articles about Gene Therapy - latimes

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Gene Therapy Technology Explanied

Virtually all cells in the human body contain genes, making them potential targets for gene therapy. However, these cells can be divided into two major categories: somatic cells (most cells of the body) or cells of the germline (eggs or sperm). In theory it is possible to transform either somatic cells or germ cells.

Gene therapy using germ line cells results in permanent changes that are passed down to subsequent generations. If done early in embryologic development, such as during preimplantation diagnosis and in vitro fertilization, the gene transfer could also occur in all cells of the developing embryo. The appeal of germ line gene therapy is its potential for offering a permanent therapeutic effect for all who inherit the target gene. Successful germ line therapies introduce the possibility of eliminating some diseases from a particular family, and ultimately from the population, forever. However, this also raises controversy. Some people view this type of therapy as unnatural, and liken it to "playing God." Others have concerns about the technical aspects. They worry that the genetic change propagated by germ line gene therapy may actually be deleterious and harmful, with the potential for unforeseen negative effects on future generations.

Somatic cells are nonreproductive. Somatic cell therapy is viewed as a more conservative, safer approach because it affects only the targeted cells in the patient, and is not passed on to future generations. In other words, the therapeutic effect ends with the individual who receives the therapy. However, this type of therapy presents unique problems of its own. Often the effects of somatic cell therapy are short-lived. Because the cells of most tissues ultimately die and are replaced by new cells, repeated treatments over the course of the individual's life span are required to maintain the therapeutic effect. Transporting the gene to the target cells or tissue is also problematic. Regardless of these difficulties, however, somatic cell gene therapy is appropriate and acceptable for many disorders, including cystic fibrosis, muscular dystrophy, cancer, and certain infectious diseases. Clinicians can even perform this therapy in utero, potentially correcting or treating a life-threatening disorder that may significantly impair a baby's health or development if not treated before birth.

In summary, the distinction is that the results of any somatic gene therapy are restricted to the actual patient and are not passed on to his or her children. All gene therapy to date on humans has been directed at somatic cells, whereas germline engineering in humans remains controversial and prohibited in for instance the European Union.

Somatic gene therapy can be broadly split into two categories:

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Gene Therapy Technology Explanied

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Personalized Medicine Conferences | Europe | Worldwide …

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Multiple sclerosis – MedlinePlus

Multiple sclerosis (MS) is a nervous system disease that affects your brain and spinal cord. It damages the myelin sheath, the material that surrounds and protects your nerve cells. This damage slows down or blocks messages between your brain and your body, leading to the symptoms of MS. They can include

No one knows what causes MS. It may be an autoimmune disease, which happens when your immune system attacks healthy cells in your body by mistake. Multiple sclerosis affects women more than men. It often begins between the ages of 20 and 40. Usually, the disease is mild, but some people lose the ability to write, speak, or walk.

There is no single test for MS. Doctors use a medical history, physical exam, neurological exam, MRI, and other tests to diagnose it. There is no cure for MS, but medicines may slow it down and help control symptoms. Physical and occupational therapy may also help.

NIH: National Institute of Neurological Disorders and Stroke

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Multiple sclerosis - MedlinePlus

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