StemCell Therapy

Lymph nodes are small, bean-shaped masses of tissue that are located in clusters throughout the body, including in the armpit. Lymph nodes play a crucial role in helping to fight infection; they filter and trap bacteria, viruses, and other unwanted substances in the body, so that special white blood cells (called lymphocytes) can then destroy them.

When treating cancer, doctors sometimes choose to remove and biopsy nearby lymph nodes to learn whether any of the nodes contain cancer cells. This information helps determine whether the cancer has spread to other parts of the body, a process known as staging. This information also helps the health care team decide on an appropriate and tailored treatment plan.

As with any surgical procedure, there might be side effects. You may sustain some degree of nerve damage during the procedure, resulting in tingling, numbness, or weakness in your arm. These neuropathy symptoms can be mild or more severe, depending on the extent of nerve involvement. You may experience swelling in the arm due to a build-up of lymph fluid that is no longer draining effectively through the remaining lymph nodes; this condition is called lymphedema. You may experience a temporary inflammation of blood vessels in your armpit as well as a higher potential for blood clotting and infection at the biopsy site.

If your health care team has recommended this procedure for you, it is likely because they feel that the benefits outweigh any of these potential risks. Nevertheless, it is always a good idea to have a frank discussion with your surgeon about possible side effects and any preventive measures you can take to lower your risk of experiencing them.

We offer resources about lymphedema and neuropathy.

For more information about lymphedema, please visit The National Lymphedema Network.

To learn more about lymph node removal surgery, please visit The National Cancer Institute.

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Neuropathy, Cancer, Information, Resources | CancerCare

by Waden E. Emery III MD FAAN, Neuromuscular NeurologistBoard Certified in Neurology, Asst Clinical Professor in NeurologyMiller School of Medicine University of Miami

Your nervous system consists of two primary systems, the Peripheral Nervous System and the Central Nervous System.

The Central Nervous System is made up of the brain and spinal cord.

The Peripheral Nervous System is the largest nervous system of the human body running throughoutyour entire body except foryour brain andyour spinal cord, and is separated into two distinct systems, the Somatic Nervous System and the Autonomic Nervous System.

Autonomic Neuropathy is a Peripheral Neuropathy. That is to say every person that has Autonomic Neuropathy has Peripheral Neuropathy, but everyone that has Peripheral Neuropathymay or maynot have Autonomic Neuropathy.

Peripheral Neuropathyusually affects the hands and feet, causing weakness, numbness, tingling and pain. It can also result in trouble with balance and walking, as well as in problems with grasping items, such as a coffee cup or salt shaker. Peripheral Neuropathys course is variable; it can come and go, slowly progressing over many years, or it can become severe and debilitating. However, if diagnosed early, Peripheral Neuropathy can often be controlled.

Human Nerve Cell

Neuropathy is a result of damage to the nerves most often found in the Peripheral Nervous Systemthat controlsthe motor, sensory, or autonomic nerves required to transmit voluntary and involuntary messages to the brain. Neuropathy can affect or damage the axon (actual nerve), and/or the myelin (covering of the nerves which assists in the transmission signals). Neuropathy can alsoaffect or damage the small and/or large fiber nerves. Small Fiber Neuropathy can now be diagnosed with a simple skin biopsy.

Living with Autonomic Neuropathy In looking at the various components of the autonomic nervous system which can be affected by autonomic neuropathy, these authorities note that it can and does affect the urinary, the cardiac (heart beat), digestive, pulmonary (breathing) systems, it also affects the bodys ability to regulate temperature, tearing, sexual functions, blood pressure, saliva production, swallowing among other body systems that function automaticallyREAD MORE

Small Fiber Neuropathy So many neuropathy patients have heard these words from very qualified neurologists and health professionals. Your EMG and Nerve Conduct Studies are normal. You do not have neuropathy not so quick. Dr. Norman Latov of Cornell University states that the EMG and Nerve Conduct Studies only measure damage toREAD MORE

Diabetic Neuropathy According to the experts, diabetic neuropathy is the most common cause of about 50% of all neuropathies. Dr. Todd Levine recently participated in a Facebook chat on the subject of Understanding Pre-Diabetes, Diabetes, and Diabetic Neuropathy. Some doctors deny the existence of neuropathy from pre-diabetes but see the following two references: 1. Norman Latov, MDREAD MORE

Celiac Disease and Neuropathy Dr. Howard Sanders published an article on The Link Between Celiac Disease and Neuropathy and was featured on The Neuropathy Associations website before they closed on Dec 31, 2014 and brings attention to the need for some patients presenting with neuropathy and the symptoms of Celiac Disease to be tested. Howard. W. Sander, M.D. is aREAD MORE

Medication Induced Neuropathy Peter D. Donofrio, M.D. is professor of Neurology and director of the Neuromuscular Division of the Department of Neurology at Vanderbilt University Medical Center. He is director of Neuropathy Center at Vanderbilt. To read his excellent article on Medication Induced Neuropathy and insights on the LIMITS of the blood-brain barrier a concept which was often misused byREAD MORE

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What is Neuropathy? | Neuropathy Support Network

Peripheral neuropathy (PN) is damage to or disease affecting nerves, which may impair sensation, movement, gland or organ function, or other aspects of health, depending on the type of nerve affected. Common causes include toxic exposure such as Agent Orange, systemic diseases (such as diabetes or leprosy), hyperglycemia-induced glycation,[1][2][3] vitamin deficiency, medication (e.g., chemotherapy, or commonly prescribed antibiotics including metronidazole and the fluoroquinolone class of antibiotics (Ciprofloxacin, Levaquin, Avelox etc.)), traumatic injury, including ischemia, radiation therapy, excessive alcohol consumption, immune system disease, coeliac disease, or viral infection. It can also be genetic (present from birth) or idiopathic (no known cause).[4][5][6] In conventional medical usage, the word neuropathy (neuro-, "nervous system" and -pathy, "disease of")[7] without modifier usually means peripheral neuropathy.

Neuropathy affecting just one nerve is called "mononeuropathy" and neuropathy involving nerves in roughly the same areas on both sides of the body is called "symmetrical polyneuropathy" or simply "polyneuropathy". When two or more (typically just a few, but sometimes many) separate nerves in disparate areas of the body are affected it is called "mononeuritis multiplex", "multifocal mononeuropathy", or "multiple mononeuropathy".[4][5][6]

Peripheral neuropathy may be chronic (a long-term condition where symptoms begin subtly and progress slowly) or acute (sudden onset, rapid progress, and slow resolution). Acute neuropathies demand urgent diagnosis. Motor nerves (that control muscles), sensory nerves, or autonomic nerves (that control automatic functions such as heart rate, body temperature, and breathing) may be affected. More than one type of nerve may be affected at the same time. Peripheral neuropathies may be classified according to the type of nerve predominantly involved, or by the underlying cause.[4][5][6]

Neuropathy may cause painful cramps, fasciculations (fine muscle twitching), muscle loss, bone degeneration, and changes in the skin, hair, and nails. Additionally, motor neuropathy may cause impaired balance and coordination or, most commonly, muscle weakness; sensory neuropathy may cause numbness to touch and vibration, reduced position sense causing poorer coordination and balance, reduced sensitivity to temperature change and pain, spontaneous tingling or burning pain, or skin allodynia (severe pain from normally nonpainful stimuli, such as light touch); and autonomic neuropathy may produce diverse symptoms, depending on the affected glands and organs, but common symptoms are poor bladder control, abnormal blood pressure or heart rate, and reduced ability to sweat normally.[4][5][6]

Peripheral neuropathy may be classified according to the number and distribution of nerves affected (mononeuropathy, mononeuritis multiplex, or polyneuropathy), the type of nerve fiber predominantly affected (motor, sensory, autonomic), or the process affecting the nerves; e.g., inflammation (neuritis), compression (compression neuropathy), chemotherapy (chemotherapy-induced peripheral neuropathy).

Mononeuropathy is a type of neuropathy that only affects a single nerve.[8] Diagnostically, it is important to distinguish it from polyneuropathy because when a single nerve is affected, it is more likely to be due to localized trauma or infection.

The most common cause of mononeuropathy is physical compression of the nerve, known as compression neuropathy. Carpal tunnel syndrome and axillary nerve palsy are examples. Direct injury to a nerve, interruption of its blood supply resulting in (ischemia), or inflammation also may cause mononeuropathy.

"Polyneuropathy" is a pattern of nerve damage that is quite different from mononeuropathy, often more serious and affecting more areas of the body. The term "peripheral neuropathy" sometimes is used loosely to refer to polyneuropathy. In cases of polyneuropathy, many nerve cells in various parts of the body are affected, without regard to the nerve through which they pass; not all nerve cells are affected in any particular case. In distal axonopathy, one common pattern is that the cell bodies of neurons remain intact, but the axons are affected in proportion to their length; the longest axons are the most affected. Diabetic neuropathy is the most common cause of this pattern. In demyelinating polyneuropathies, the myelin sheath around axons is damaged, which affects the ability of the axons to conduct electrical impulses. The third and least common pattern affects the cell bodies of neurons directly. This usually picks out either the motor neurons (known as motor neuron disease) or the sensory neurons (known as sensory neuronopathy or dorsal root ganglionopathy).

The effect of this is to cause symptoms in more than one part of the body, often symmetrically on left and right sides. As for any neuropathy, the chief symptoms include motor symptoms such as weakness or clumsiness of movement; and sensory symptoms such as unusual or unpleasant sensations such as tingling or burning; reduced ability to feel sensations such as texture or temperature, and impaired balance when standing or walking. In many polyneuropathies, these symptoms occur first and most severely in the feet. Autonomic symptoms also may occur, such as dizziness on standing up, erectile dysfunction, and difficulty controlling urination.

Polyneuropathies usually are caused by processes that affect the body as a whole. Diabetes and impaired glucose tolerance are the most common causes. Hyperglycemia-induced formation of advanced glycation end products (AGEs) is related to diabetic neuropathy.[9] Other causes relate to the particular type of polyneuropathy, and there are many different causes of each type, including inflammatory diseases such as Lyme disease, vitamin deficiencies, blood disorders, and toxins (including alcohol and certain prescribed drugs).

Most types of polyneuropathy progress fairly slowly, over months or years, but rapidly progressive polyneuropathy also occurs. It is important to recognize that at one time it was thought that many of the cases of small fiber peripheral neuropathy with typical symptoms of tingling, pain, and loss of sensation in the feet and hands were due to glucose intolerance before a diagnosis of diabetes or pre-diabetes. However, in August 2015, the Mayo Clinic published a scientific study in the Journal of the Neurological Sciences showing "no significant increase in...symptoms...in the prediabetes group", and stated that "A search for alternate neuropathy causes is needed in patients with prediabetes." [10]

The treatment of polyneuropathies is aimed firstly at eliminating or controlling the cause, secondly at maintaining muscle strength and physical function, and thirdly at controlling symptoms such as neuropathic pain.

Mononeuritis multiplex, occasionally termed polyneuritis multiplex, is simultaneous or sequential involvement of individual noncontiguous nerve trunks,[11] either partially or completely, evolving over days to years and typically presenting with acute or subacute loss of sensory and motor function of individual nerves. The pattern of involvement is asymmetric, however, as the disease progresses, deficit(s) becomes more confluent and symmetrical, making it difficult to differentiate from polyneuropathy.[12] Therefore, attention to the pattern of early symptoms is important.

Mononeuritis multiplex also may cause pain, which is characterized as deep, aching pain that is worse at night and frequently in the lower back, hip, or leg. In people with diabetes mellitus, mononeuritis multiplex typically is encountered as acute, unilateral, and severe thigh pain followed by anterior muscle weakness and loss of knee reflex.[medical citation needed]

Electrodiagnostic medicine studies will show multifocal sensory motor axonal neuropathy.

It is caused by, or associated with, several medical conditions:

Autonomic neuropathy is a form of polyneuropathy that affects the non-voluntary, non-sensory nervous system (i.e., the autonomic nervous system), affecting mostly the internal organs such as the bladder muscles, the cardiovascular system, the digestive tract, and the genital organs. These nerves are not under a person's conscious control and function automatically. Autonomic nerve fibers form large collections in the thorax, abdomen, and pelvis outside the spinal cord. They have connections with the spinal cord and ultimately the brain, however. Most commonly autonomic neuropathy is seen in persons with long-standing diabetes mellitus type 1 and 2. In mostbut not allcases, autonomic neuropathy occurs alongside other forms of neuropathy, such as sensory neuropathy.

Autonomic neuropathy is one cause of malfunction of the autonomic nervous system, but not the only one; some conditions affecting the brain or spinal cord also may cause autonomic dysfunction, such as multiple system atrophy, and therefore, may cause similar symptoms to autonomic neuropathy.

The signs and symptoms of autonomic neuropathy include the following:

Neuritis is a general term for inflammation of a nerve[21] or the general inflammation of the peripheral nervous system. Symptoms depend on the nerves involved, but may include pain, paresthesia (pins-and-needles), paresis (weakness), hypoesthesia (numbness), anesthesia, paralysis, wasting, and disappearance of the reflexes.

Causes of neuritis include:

Types of neuritis include:

Those with diseases or dysfunctions of their nerves may present with problems in any of the normal nerve functions. Symptoms vary depending on the types of nerve fiber involved.[citation needed]In terms of sensory function, symptoms commonly include loss of function ("negative") symptoms, including numbness, tremor, impairment of balance, and gait abnormality.[24] Gain of function (positive) symptoms include tingling, pain, itching, crawling, and pins-and-needles. Motor symptoms include loss of function ("negative") symptoms of weakness, tiredness, muscle atrophy, and gait abnormalities; and gain of function ("positive") symptoms of cramps, and muscle twitch (fasciculations).[25]

In the most common form, length-dependent peripheral neuropathy, pain and parasthesia appears symmetrically and generally at the terminals of the longest nerves, which are in the lower legs and feet. Sensory symptoms generally develop before motor symptoms such as weakness. Length-dependent peripheral neuropathy symptoms make a slow ascent of leg, while symptoms may never appear in the upper limbs; if they do, it will be around the time that leg symptoms reach the knee.[26] When the nerves of the autonomic nervous system are affected, symptoms may include constipation, dry mouth, difficulty urinating, and dizziness when standing.[25]

The causes are grouped broadly as follows:

Peripheral neuropathy may first be considered when an individual reports symptoms of numbness, tingling, and pain in feet. After ruling out a lesion in the central nervous system as a cause, diagnosis may be made on the basis of symptoms, laboratory and additional testing, clinical history, and a detailed examination.

During physical examination, specifically a neurological examination, those with generalized peripheral neuropathies most commonly have distal sensory or motor and sensory loss, although those with a pathology (problem) of the nerves may be perfectly normal; may show proximal weakness, as in some inflammatory neuropathies, such as GuillainBarr syndrome; or may show focal sensory disturbance or weakness, such as in mononeuropathies. Classically, ankle jerk reflex is absent in peripheral neuropathy.

A physical examination will involve testing the deep ankle reflex as well as examining the feet for any ulceration. For large fiber neuropathy, an exam will usually show an abnormally decreased sensation to vibration, which is tested with a 128-Hz tuning fork, and decreased sensation of light touch when touched by a nylon monofilament.[26]

Diagnostic tests include electromyography (EMG) and nerve conduction studies (NCSs), which assess large myelinated nerve fibers.[26] Testing for small-fiber peripheral neuropathies often relates to the autonomic nervous system function of small thinly- and unmyelinated fibers. These tests include a sweat test and a tilt table test. Diagnosis of small fiber involvement in peripheral neuropathy may also involve a skin biopsy in which a 3mm-thick section of skin is removed from the calf by a punch biopsy, and is used to measure the skin intraepidermal nerve fiber density (IENFD), the density of nerves in the outer layer of the skin.[24] Reduced density of the small nerves in the epidermis supports a diagnosis of small-fiber peripheral neuropathy.

Laboratory tests include blood tests for vitamin B-12 levels, a complete blood count, measurement of thyroid stimulating hormone levels, a comprehensive metabolic panel screening for diabetes and pre-diabetes, and a serum immunofixation test, which tests for antibodies in the blood.[25]

The treatment of peripheral neuropathy varies based on the cause of the condition, and treating the underlying condition can aid in the management of neuropathy. When peripheral neuropathy results from diabetes mellitus or prediabetes, blood sugar management is key to treatment. In prediabetes in particular, strict blood sugar control can significantly alter the course of neuropathy.[24] In peripheral neuropathy that stems from immune-mediated diseases, the underlying condition is treated with intravenous immunoglobulin or steroids. When peripheral neuropathy results from vitamin deficiencies or other disorders, those are treated as well.[24]

A range of medications that act on the central nervous system has been found to be useful in managing neuropathic pain. Commonly used treatments include tricyclic antidepressants (such as nortriptyline or amitriptyline), the serotonin-norepinephrine reuptake inhibitor (SNRI) medication duloxetine, and antiepileptic therapies such as gabapentin, pregabalin, or sodium valproate. Few studies have examined whether nonsteroidal anti-inflammatory drugs are effective in treating peripheral neuropathy.[38]

Symptomatic relief for the pain of peripheral neuropathy may be obtained by application of topical capsaicin. Capsaicin is the factor that causes heat in chili peppers. The evidence suggesting that capsaicin applied to the skin reduces pain for peripheral neuropathy is of moderate to low quality and should be interpreted carefully before using this treatment option.[39] Local anesthesia often is used to counteract the initial discomfort of the capsaicin. Some current research in animal models has shown that depleting neurotrophin-3 may oppose the demyelination present in some peripheral neuropathies by increasing myelin formation.[40]

Evidence supports the use of cannabinoids for some forms of neuropathic pain.[41]

Transcutaneous electrical nerve stimulation therapy may be effective and safe in the treatment of diabetic peripheral neuropathy. A recent review of three trials involving 78 patients found some improvement in pain scores after 4 and 6, but not 12 weeks of treatment and an overall improvement in neuropathic symptoms at 12 weeks.[42] Another review of four trials found significant improvement in pain and overall symptoms, with 38% of patients in one trial becoming asymptomatic. The treatment remains effective even after prolonged use, but symptoms return to baseline within a month of cessation of treatment.[43]

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Peripheral neuropathy - Wikipedia

Overview

Peripheral neuropathy, a result of damage to your peripheral nerves, often causes weakness, numbness and pain, usually in your hands and feet. It can also affect other areas of your body.

Your peripheral nervous system sends information from your brain and spinal cord (central nervous system) to the rest of your body. Peripheral neuropathy can result from traumatic injuries, infections, metabolic problems, inherited causes and exposure to toxins. One of the most common causes is diabetes mellitus.

People with peripheral neuropathy generally describe the pain as stabbing, burning or tingling. In many cases, symptoms improve, especially if caused by a treatable condition. Medications can reduce the pain of peripheral neuropathy.

Peripheral neuropathy care at Mayo Clinic

Every nerve in your peripheral system has a specific function, so symptoms depend on the type of nerves affected. Nerves are classified into:

Signs and symptoms of peripheral neuropathy might include:

If autonomic nerves are affected, signs and symptoms might include:

Peripheral neuropathy can affect one nerve (mononeuropathy), two or more nerves in different areas (multiple mononeuropathy) or many nerves (polyneuropathy). Carpal tunnel syndrome is an example of mononeuropathy. Most people with peripheral neuropathy have polyneuropathy.

Seek medical care right away if you notice unusual tingling, weakness or pain in your hands or feet. Early diagnosis and treatment offer the best chance for controlling your symptoms and preventing further damage to your peripheral nerves.

Not a single disease, peripheral neuropathy is nerve damage caused by a number of conditions. Causes of neuropathies include:

In a number of cases, no cause can be identified (idiopathic).

Peripheral neuropathy risk factors include:

Complications of peripheral neuropathy can include:

The best way to prevent peripheral neuropathy is to manage medical conditions that put you at risk, such as diabetes, alcoholism or rheumatoid arthritis.

For example:

Aug. 09, 2017

See more here:

Peripheral neuropathy - Symptoms and causes - Mayo Clinic

This post was last updated on 9/10/2018.

Burning fingertips, sensations of walking on glass, and sleepless nights. Living with neuropathic pain is no way to live at all.

Yet thousands of people like you and me have to deal with, largely unpredictable, bursts of pain.

Youre not alone if you feel like your whole life is governed by pain. This post will give a brief overview of the prevalence of this class of pain as well as the causes before going into the evidence indicating the cannabinoid CBD can be effective in treating neuropathic pain of all kinds and causes.

After that, well talk about how to use CBD oil for neuropathic pain, as well as other product options (including which products to pick and where to get them). But first lets get a lay of the land.

Chronic pain has become an epidemic, especially as the Boomer generation approaches old age. For example, in Europe, chronic pain effects 1 in 4 elderly people.3

In Australia, this epidemic is of massive proportions, extending to over half of the elderly population, and as high as 80% of patients in nursing homes.4

In the US, responses to an ABC News poll indicate that as many as 38 million adults in the US deal with chronic pain on a daily basis, and as many as 12 million US citizens have used cannabis to help alleviate this pain.

To this point, the available medications for attempting to treat this pain are limited to anti-steroidals, opiates, and anti-depressants all hardcore drugs with harsh side effects of their own, and limited effectiveness. Its almost as though the patient is trading a half-cure for being put on even more drugs to deal with the debilitating side effects. My opinion here, but this system seems broken.

Peripheral neuropathy has many causes. At its core, it is nerve damage due to either chronic inflammation in the body or sudden trauma. Inflammation is your bodys natural response triggered by incoming stimuli that is perceived to be a threat to your body.

Neuropathy symptoms can arise due to inflammation related to:

These are just a few of many potential causes of neuropathy, albeit the most statistically common.

An oromucosal spray named Sativex was approved back in 2005 by the Canadian government for use in treating neuropathy.5 While Sativex itself is a brand name and must be obtained with a prescription, the important thing to note is that it is essentially just a combination of THC and CBD, cannabidiol, not much different than just using a full spectrum hemp extract in combination with THC.

Lets be real: it literally is just a full spectrum cannabis extract, extracted with ethanol, packaged up and branded by GW Pharmaceuticals. This is something you could buy yourself.

Sativex (THC + CBD) was found in multiple clinical trials to be extremely effective in controlling neuropathy pain in MS patients, as well as arthritis. It was later approved by the United States FDA in 2006 for trials to control cancer related neuropathy.

Historically, and quite ironically, Western understanding of the biological underpinnings of the pain system in the body was originally glimpsed through the lens of studying the plants cannabis, opium poppies, willow bark, and chile peppers. Out of the study of these plants and the naturally effective medicine inherent in them pharmaceutical companies formulated synthetic, highly addictive, drugs such as morphine, codeine, oxycontin.

Due to lack of commercial feasibility and patentability, pharmaceutical companies before the early 2000s hadnt made any endocannabinoid drug-derivatives.6Cannabinoids, however, are very well known for their analgesic effect in controlling pain in humans.7 Ask any anesthesiologist and they will agree, activation of the CB1 receptor (cannabinoid receptor 1) will lead to almost immediate alleviation of pain and inflammation.8 This pain reduction can be seen in fibromyalgia patients when treated with cannabis910 and even in cases of intestinal pain with IBS.

Cannabinoids like CBD have been shown to alleviate this pain by also activating glycine receptors.11

This study found some really convincing evidence for this neuropathic pain control in rats.12 According to the researchers,

The non-psychoactive compound, cannabidiol, or CBD, is the only component present at a high level in the extract able to bind to this receptor: thus cannabidiol was the compound responsible for the antinociceptive behavior observed.

A recent review by Dr. Igor Grant, director of the Center for Medicinal Cannabis Research at the University of California compared the effectiveness of cannabis against tricyclic antidepressants, gabapentin, anticonvulsants, and selective serotonin reuptake inhibitors. Cannabis was more effective than all except tricyclics at reducing neuropathy. 11

Cannabis as a treatment of neuropathic painis one of the topics with the most substantive collection of studies in the medical literature behind it.12This study also goes through the effective cannabinoids for neuropathic pain.12 And now, according to some researchers, cannabinoids hold the most potential for providing relief for thousands of sufferers, since nearly all pharmaceutical treatments fall short and have lead researchers to conclude that pharma treatment options for neuropathic pain have limited efficacy and use is fraught with dose dependent adverse effects.2

Due to Western medicines inability to formulate an effective treatment for neuropathy, many neuropathy sufferers are understandably turning tocannabis, namely hemps cannabidiol, as an alternative for pain management.

For a detailed guide about treating neuropathy with CBD, the kinds if neuropathy you may be experiencing, and recommended products shown to work against neuropathy for readers in the past, see our Neuropathy page.

In conclusion, CBD oil looks really promising for nerve painand neuropathy patients. CBD is probably good alternative treatment for neuropathic pain. CBD may have the ability to lower pain which is linked to its potent effect as an antioxidant and ability to lower inflammation significantly, and quickly. In fact, when put head to head against the other well-known antioxidants alpha-tocopherol(Vitamin E) and ascorbate (Vitamin C), cannabidiol beat out both of them in effectiveness with regards to lowering glutamate toxicity in neurons.1

What have you got to lose? This also comes after a careful analysis of the clinical trials of Sativex, which just appears to be a full spectrum cannabis extract similar to the ones found on this page, in combination with THC.

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See the article here:

CBD and Neuropathy: Almost Magical Pain Relief Benefits

If you were on the ground in Vietnam the VA law now presumes you were exposed to Agent Orange/Toxic Herbicides, the VA law now recognizes that Agent Orange or Toxic Herbicidescause Chronic Peripheral Neuropathy (or any diagnosis related to PN) so you DO NOT HAVE TO PROVE this by VA law. The one trick the VA and IOM put in the new law is the requirement of EARLY ONSET and this is a bogus requirement. See more below on how to challenge this part of the law.

Here is how to work an application or appeal and the references that you should use in the appeal:

First, you will find all that you need to know in the Vietnam Veterans of America (VVA) bookletto submit an Agent Orange / Toxic Herbicidesclaim for yourself, or for surviving family members of deceased Vietnam veterans, or for biological children of Vietnam veterans born with certain birth defects (listed in the booklet), or for incarcerated Vietnam veterans and information on other benefits available to Vietnam veterans with Agent Orange or toxic herbicides related illnesses.

To print a copy of theVVAbooklet click on this title: The VVA Self Help Guideto Service Connected Disability Compensation for Exposure to Agent Orange: For Veterans and Their Families. Then in the RIGHT column, click on the booklet and print!

Next, we highly recommend that you find a Service Officer from the VVA. Enter youre STATE in the SEARCH form and it will list those for your entire State. Then select the one that is nearest to you.

Effective immediately in 2015there is a new way to file a claimaccording to the VA. Click on the link to see this information.

Direct Basis: If your illness is not listed in the VA list of presumptive illnesses, the law permits the veteran to establish proof of a direct connection between exposure to Agent Orange or Toxic Herbicides, symptoms of a chronic neuropathy, diagnosis and medical history by establishment of reasonable doubt and the principle of high probability, without early on-set.

This process just requires more documentation of the medical tests, diagnosis, and statements that all other causes of your illness have been ruled out and it is more likely than not due to exposure to toxic herbicides used during the Vietnam War. In our guidance on Chronic Peripheral Neuropathy, there are cases listed where this was accomplished to which you can refer and see the decision that was made and why.

In this process of a direct basis,the information on Affidavits andLegal Casesfor AO and Peripheral Neuropathy, prior to the rule of presumptioncould be helpful and you may find these in this booklet by clicking on the link.

FACTS ON AGENT ORANGE AND THE VA RECOGNITION OF CHRONIC PERIPHERAL NEUROPATHY.

For decades the VA with support from the Institute of Medicine denied that there could be chronic neuropathy from agent orange exposure. Then in 2010 after years of false claims the IOM acknowledge that they were wrong and the VA now recognizes Chronic PN from Agent Orange if you were on the ground in Vietnam with one catch which I will discuss below and how to defeat the VA on early onset.

Peripheral Neuropathy is now listed as presumptive to AO exposure see the ruling:

If your neuropathy is secondary to a VA recognized disease then you do not have to deal with the early onset requirement in VA law. Examples would be diabetes (Prediabetes is a recognized cause of neuropathy), cancer, treatments for cancer and so forth which the VA recognizes as due to Agent Orange exposure.These are common recognized conditions that cause chronic neuropathy. You can quote or refer to Dr. Norman Latovs book to show this as the case if needed. Norman Latov MD, PhD, Peripheral Neuropathy: When the Numbness, Weakness, and Pain Wont Stop, 2007 AAN Press

If the above is not the case, I would submit an appeal with the following statement in response to any legal claimby the VA.

NOTE: When you submit a statement to the VA it is wise to do so using the following statement at the end by your signature and then have it notarized:

I declare (or certify, verify, or state) under penalty of perjury that the foregoing is true and correct. Executed on (date). (Signature)

Peripheral Neuropathy is presumptively related to exposure to Agent Orange or toxic herbicides and no proof of this relationship as a cause is required by the current VA law. This is especially true when medicine is not able to establish another cause for the Neuropathy and often terms it idiopathic or of unknown cause. The VA law does require the early onset at 10% disabling levels within 1 year after exposure. However, please be advised that following the war the medical establishment did not have the clinical knowledge to diagnose, treat or even knowledge to recognize the symptoms of Peripheral Neuropathy in the 1960s, 70s let alone at the 10% disabling level. The symptoms were often misdiagnosed as symptoms of other medical issues or worse dismissed. Often medical personnel would report these symptoms as of no consequence while even failing to record them under the circumstances of the battlefield. Add to this the veterans desire to do nothing but return home, ignoring the symptoms.Little research was available regarding the effects of Agent Orange on veterans during their service. Furthermore, it is now know that the component of arsenic in Agent Blue used extensively during the Vietnam War following long term exposure will cause a delayed onset of a progressive chronic sensorimotor axonal polyneuropathy and therefore rules out any need for the early onset in the law since nothing has ever been evaluated given long term exposure to arsenic and the other compounds in the various components of Agent Orange. The following references support this statement.

Use the following references in YOUR APPEAL to support the above statement regarding early on-set.

1.No books for patient help to even recognize the symptoms of Peripheral Neuropathy, were available to the veterans until 2007: See: Norman Latov MD, PhD, Peripheral Neuropathy: When the Numbness, Weakness, and Pain Wont Stop, 2007 AAN Press AND the book reveals the difficulty in diagnosis in the years during and following the Vietnam War. Books on Peripheral Neuropathy

2.In 2012, Neurology struggles to diagnose Peripheral Neuropathy even in 2015: SEE: How to Diagnose Peripheral Neuropathy? No Simple Answers by Mark Moran, Neurology Today, March 15, 2012.

3. In 2001, Toxic Neuropathies were often dismissed by the principle that once removed from the toxin; the neuropathy resolved and did not become chronic! In 2010 the Institute of Medicine and the VA law recognized Agent Orange related toxic neuropathy years after exposure and this conclusion followed years of denial by the IOM and the VA. See: Peripheral Neuropathy: A Practical Approach to Diagnosis and Management by Dr. Didier Cross, M.D., Editor, 2001 and Chapter 21, page 387, Identification and Diagnosis of Toxic Polyneuropathies Dr. Alan Berger.

4. Thomas H. Brannagan, MD, Director, Neuropathy Center of Excellence, Columbia University, as quoted in the DVD production Coping with Chronic Neuropathy, 2010, (Lecture by LTC Eugene B Richardson, USA (Ret) who went for four decades before diagnosis and treatment with chronic neuropathy that has left him VA recognized 100% disabled due to Agent Orange exposure and Peripheral Neuropathy and a link to hisstory is listedin a following paragraph: One Mans Journey with Neuropathy) by the Network for Neuropathy Support, Inc., dba Neuropathy Support Network. For years medicine did not have the tools to diagnose or treat Neuropathy and the patient was left on their own Note: Today this DVD is endorsed by leading Neuromuscular Neurologists in the field of Peripheral Neuropathy, Psychiatrists, Psychologists, Nurses, Dermatologists, Retired General Officers, other senior officers of the U.S. Army and other medical professionals as well as by patients worldwide who are just now beginning to grasp the clinical aspects of Peripheral Neuropathy.

5. In December 2002, in the Neurology 59 (Supplement 6), Norman Latov, MD, PhD, et el, published a document regarding the difficulties in the diagnosis and treatment of immune-mediated neuropathies, titled Advances in the diagnosis and treatment of CIDP and related immune-mediated neuropathies.

6. The Journal of the Peripheral Nervous System the official Journal of the Peripheral Nerve Society, Volume 17, Supplement 2, May 2012, editor David R. Cornblath of John Hopkins University School of Medicine, Baltimore, MD, in the various scientific articles notes not only the current research that is being done, but the lack of the medical establishments ability to diagnose and treat many of the chronic neuropathies even in 2012 let alone in 1960 and 1970. Dr. Thomas H. Brannagan III of Columbia University, College of Physicians and Surgeons, New York, NY, states in the opening article, Many patients are not aware of their diagnosis, are not given the diagnosis or (are) treated, or the diagnosis is delayed and this is in 2012! Currently, the only treatments available for neuropathy are aimed at treating the underlying medical conditions that cause the neuropathy or treating symptoms such as pain. Neither treats the actual nerve fiber dysfunction or fiber loss or helps nerve fibers regenerate.Continued research into the underlying mechanisms of neuropathyare needed to address this unmet medical need among patients with neuropathy and again this is the science in 2012 not 1960 and 1970 when no tools existed to diagnose the patients neuropathy let alone clinical knowledge to recognize the many symptoms of neuropathy following exposure to Agent Orange.

7. Louis Weimer, MD, recorded on DVD, A lecture on Autonomic Neuropathy Under Recognized Syndrome, January 17, 2001

8. In the Textbook of Peripheral Neuropathy by Peter D. Donofrio, M.D., published by DEMOS Medical, 2012 (numerous other authors contributing to the work) (Professor of Neurology, Chief of the Neuromuscular Section, Vanderbilt University Medical Center, Nashville, TN), notes that acute arsenic exposure is associated with sensorimotor axonal polyneuropathy see pages 89-91 in the text article Occupational, Biologic, and Environmental Toxic Neuropathies by James W Albers, M.D. PhD, Emeritus Professor of Neurology, University of Michigan Health System, Ann Arbor, Michigan, for full description of symptoms and treatments. Arsenic in what was called Agent Blue was used to destroy the food supplies throughout Vietnam from 1962 to 1971. The use of arsenic was not condemned for use by the FDA until 2011 when a peer-evaluated study was completed and 89 forms of arsenic out of 102 compounds were removed from the market because they convert from organic to inorganic arsenic. Bottom line, arsenic is a heavy metal, like lead, and all heavy metals are dangerous and carcinogenic causing Chronic Peripheral Neuropathy along with other damage to the human body. To read the dangers and damages done by arsenic in Agent Blue along with the many warnings that were ignored by those responsible, see the article Agent Blue by Loana Hoyman in the May/June 2015 issue, Volume 35. No. 3, of the Vietnam Veterans of America publication.

9. Arsenic in the Environment: Blue by Loana Hoylman published in VVA Veteran (Vietnam Veterans of America) July/August 2015 Vol 35, No. 4 notes that the World Health Organization said in 2012 that Arsenic contaminated water is the greatest threat to health in the world reporting that Arsenic is a known neurotoxin. Arsenic was the main component in Agent Blue used in Vietnam. The use of Arsenic in agricultural use was banned in 1980 with more stringent ban confirmed in 2014 when evidence of environmental poisoning was confirmed. While we are all exposed to Arsenic, Vietnam Veterans for a year or more were exposed to Agent Blue and are at the highest risk for the cumulative effects of Arsenic from food and water. The problem with arsenic is that it stays in the (human) system. It accumulates in the body as one consumes contaminated food and comes in contact with a contaminated environment especially if exposure is over a long period of time such as was true for the veteran of Vietnam.

10. In 2003 FOCAL PERIPHERAL NEUROPATHIES by Geraint Fuller: See J Neurol Neurosurg Psychiatry 2003;74:ii20-ii24 doi:10.1136/jnnp.74.suppl_2.ii20 Dr GN Fuller, Department of Neurology, Gloucester Royal Hospital, Great Western Road, Gloucester GL1 3NN, UK; geraint@Fullerg.demon.co.uk focal peripheral neuropathiesFocal peripheral neuropathies are not at the fashionable end of the neurological street. However they are important, as they are very common, sometimes disabling, and often treatable. They can also be a source of confusion when they occur in patients with other neurological diseases. The management of focal peripheral neuropathies is based on certain general principles with a relatively limited backing from clinical trials. These principles relate to understanding the:

11. VA: Presumptive Service Connection and Disability Compensation, November 18, 2014 7-5700 R41405. This Congressional Service Report shows clearly the serious problems of historical fact in the early onset rule in VA law specifically for Peripheral Neuropathy.This requirement is a bogus requirement that stands in the face of facts, not the least of which is that the medical establishment, during the years of and following the Vietnam War, could not recognize the symptoms of peripheral neuropathy let alone at the 10% disabling level as required by VA law since 2010. This document shows clearly that there was no medical basis to make a determination as to early onset retroactive to the period of the Vietnam War, as to making any sound conclusions, establishing standards, diagnostic codes, disability determinations or for establishing an absolute mandatory time specific criteria for symptoms or a diagnosis for Peripheral Neuropathy, due to exposure to Agent Orange/Agent Blue and other toxins in the decade of and for many years following the Vietnam War.

12. Include these statements witha copy of the document One Mans Journey with Neuropathy showing by clear examplethe bogus nature of the early onset requirement.

In 2013 the VA began recognizing that exposure to Agent Orange (AO) causes Chronic Peripheral Neuropathy. However the Institute of Medicine (IOM)added a requirement of early on-set to connect the condition with AO exposure. Yet during the decades of the Vietnam War and after,even to the current year, clinical diagnosis and recognition of the symptoms of PN are just now being recognizedand diagnosis and treatmentremain difficult.

For decades with the symptoms of chronic neuropathy clearly recorded in LTC Richardsons medical records, the VA denied all of this information for six years. The VA reviewers did this out of ignorance of both the symptoms of PN and the difficulty of diagnosis by noting that the symptoms, while clearly in his medical records, by blaming the symptoms on other medical conditions.

Then after his Neuromuscular Neurologist submitted the facts from his service medical records, the VA reviewers lied four times about the clear statements in his medical records stating that these facts were not in his medical records.

Over six years later the VA is still delaying his request for a hearing on these issues, so that his claim is retroactive to his first submission of his original application and the fact that all the information in regards to these issues are included in his original submission.

(Attach a copy of this career officers story (One Mans Journey with Neuropathy) to your submission as it shows the bogus nature of the early onset requirement.)

The experience of LTC Eugene B Richardson, USA (Retired) with currently 100% VA disability due to Chronic Neuropathy after service in Vietnam in 1967-68 is told in this story and shows the lack of medical science and limits of medicine in general to recognize the symptoms of neuropathy and to diagnose neuropathy, let alone at the 10% level of disability.

Helpful Doctors Statement: A statement from a doctor to the effect that given that chronic peripheral neuropathy is now recognized as presumptive to exposure to Agent Orange or toxic herbicides by the VA and given that all other causes of the patients neuropathy have been ruled out by testing, it is likely greater than a 50% probability that the patients peripheral neuropathy is more likely than not due to exposure to Agent Orange and toxic herbicides.

10. Board of Veterans Appeals cases:

Make reference to these legal cases where limited information was used to prove the veterans cases on a DIRECT basis before the VA changed the law to recognize Chronic Peripheral Neuropathy:a. Citation Nr. 0606156 03/03/06 Docket No. 04-19 301 On Appeal from the Department of Veterans Affairs Regional Office in Phoenix, Arizona

b. Citation Nr. 0802669 01/24/08 Docket No. 97-33 277 On Appeal from the Department of Veterans Affairs Regional Office in Atlanta, Georgia

c. Citation Nr. 0306225 04/01/03 Docket No. 97-18 169 On Appeal from the Department of Veterans Affairs Regional Office in Milwaukee, Wisconsin

d. Citation Nr. 0821251 06/27/08 Docket No. 05-17 482 On Appeal from the Department of Veterans Affairs Regional Office in Nashville, Tennessee

APPENDEX

COPIES OF SUCCESSFUL LEGAL CASES (Symptoms developed after the one year presumptive period)

1. Case from Phoenix, Arizona

Citation Nr: 0606156 Decision Date: 03/03/06 Archive Date: 03/14/06

(DOCKET NO. 04-19 301) DATE On appeal from the Department of Veterans Affairs Regional Office in Phoenix, Arizona

THE ISSUES

1. Entitlement to service connection for peripheral neuropathy of both lower extremities, claimed as nerve damage to the legs and feet and also as circulatory damage to the feet as due to Agent Orange.

2. Entitlement to service connection for skin cancer, claimed as spots on the face, arms, and hands that tingle and also as nerve damage.

REPRESENTATION

Veteran represented by: Arizona Veterans Service Commission

WITNESS AT HEARING ON APPEAL

Veteran ATTORNEY FOR THE BOARD

J.W. Kim, Associate Counsel

INTRODUCTION

The veteran served on active duty from March 1963 to March 1966, including service in the Republic of Vietnam.

These matters come before the Board of Veterans Appeals (Board) on appeal of rating decisions by the Department of Veterans Affairs (VA) Regional Office (RO) in Phoenix, Arizona. In a January 2003 rating decision, the RO denied service connection for peripheral neuropathy of the left and right lower extremities. In a December 2003 rating decision, the RO continued the prior denials of service connection for peripheral neuropathy and denied service connection for skin cancer, claimed as spots on the face, arms, and hands that tingle and also as nerve damage. The veteran timely perfected an appeal of these determinations to the Board. In September 2005, the veteran testified before the undersigned Veterans Law Judge at a Board hearing at the RO.

The issue of service connection for skin cancer, claimed as spots on the face, arms, and hands that tingle and also as nerve damage, is addressed in the REMAND portion of the decision below and is REMANDED to the RO via the Appeals Management Center (AMC), in Washington, DC.

FINDINGS OF FACT

Resolving all reasonable doubt in favor of the veteran, peripheral neuropathy of both lower extremities is related to service, specifically to exposure to Agent Orange.

CONCLUSION OF LAW

Peripheral neuropathy of both lower extremities was incurred in active service. 38 U.S.C.A. 1101, 1110, 1112, 1113,1116, 5107 (West 2002); 38 C.F.R. 3.102, 3.303, 3.307,3.309 (2005).

REASONS AND BASES FOR FINDINGS AND CONCLUSION

Initially, the Board finds that the agency of original jurisdiction has substantially satisfied the duties to notify and assist, as required by the Veterans Claims Assistance Act of 2000. 38 U.S.C.A. 5100, 5102, 5103, 5103A, 5107, 5126 (West 2002 & Supp. 2005); 38 C.F.R. 3.102, 3.156(a), 3.159 and 3.326(a) (2005).

To the extent that there may be any deficiency of notice or assistance, there is no prejudice to the veteran in proceeding with this case given the favorable nature of the Boards decision. Service connection may be granted for disability resulting from disease or injury incurred in or aggravated by service. 38 U.S.C.A. 1110 (West 2002); 38 C.F.R. 3.303(a) (2005).

Service connection may also be awarded for a chronic condition when: (1) a chronic disease manifests itself and is identified as such in service (or within the presumptive period under 38 C.F.R. 3.307) and the veteran presently has the same condition; or (2) a chronic disease manifests itself during service (or within the presumptive period) but is not identified until later and there is a showing of continuity of symptomatology after discharge. 38 C.F.R. 3.303(b) (2005); see 38 C.F.R. 3.307, 3.309 (2005).

A veteran who, during active military, naval, or air service, served in the Republic of Vietnam during the Vietnam era, and has a disease listed at 38 C.F.R. 3.309(e), shall be presumed to have been exposed during such service to an herbicide agent, unless there is affirmative evidence to establish that the veteran was not exposed to any such agent during that service. 38 C.F.R. 3.307(a)(6)(iii).

If a veteran was exposed to an herbicide agent during active military, naval, or air service, the following diseases shall be service connected if the requirements of 38 C.F.R. 3.307(a)(6)(iii) are met, even though there is no record of such disease during service, provided further that the rebuttable presumption provisions of 38 C.F.R. 3.307(d) are also satisfied: Chloracne or other acne form disease consistent with Chloracne; Type II Diabetes; Hodgkins disease; multiple myeloma; non-Hodgkins lymphoma; acute and sub-acute peripheral neuropathy; porphyria cutanea tarda; prostate cancer; respiratory cancers (cancer of the lung, bronchus, larynx or trachea); and soft-tissue sarcoma (other than osteosarcoma, chondrosarcoma, Kaposis sarcoma, or mesothelioma). 38 C.F.R. 3.309(e); 66 Fed. Reg. 23,166, 23,168-69 (May 8, 2001)

The term acute and sub-acute peripheral neuropathy means transient peripheral neuropathy that appears within weeks or months of exposure to an herbicide agent and resolves within two years of the date of onset. Note 2, 38 C.F.R. 3.309(e).

The veteran contends, in essence, that he has peripheral neuropathy of both lower extremities due to exposure to Agent Orange during service. He asserts that symptoms developed in approximately 1970 and that they have gradually become worse, but that he did not seek treatment until April 2002.

The record shows that the veteran served in the Republic of Vietnam during the Vietnam era. Thus, exposure to Agent Orange is presumed. 38 C.F.R. 3.307(a)(6)(iii). Initially, the Board notes that only acute and sub-acute peripheral neuropathy are recognized by VA as diseases associated with exposure to Agent Orange. 38 C.F.R. 3.309(e).

In this regard, the record shows that the veteran does not have acute or sub-acute peripheral neuropathy as defined by VA regulations. The fact that the veteran is not entitled to the foregoing regulatory presumption of service connection does not preclude an evaluation as to whether he is entitled to service connection on a direct basis or entitled to presumptive service connection for a chronic disease. See Combee v. Brown, 34 F.3d 1039 (Fed. Cir. 1994).

After review, the Board notes a December 2002 VA neurological disorders examination report and a July 2003 letter from Dr. Durham, the veterans private treating physician.

The VA examination report reflects the examiners difficulty in determining the etiology of the veterans peripheral neuropathy. The examiner stated that there is no clear cut evidence that exposure to herbicides caused the veterans peripheral neuropathy and acknowledged the discomfort of defining the veterans disorder as a neuropathy of unknown etiology. The examiner explained that unfortunately many peripheral neuropathies are of unknown etiology and to arbitrarily assign one to a caustic agent does not seem to be the best medical decision.

Dr. Durham begins his letter by noting that he has taken several comprehensive histories from the veteran and can find no other type of exposures either personal or industrial that could potentially account for the veterans neuropathy. He also noted reviewing the veterans VA medical records, including the above examination report, his own medical records, VAs Guide on Agent Orange Claims, and the veterans rating decision. Dr. Durham acknowledged that the veterans claim was denied because he did not complain of symptoms within the very short time period cited by VA after exposure to herbicides. He stated that it is clearly documented in the medical literature that neuropathy can be latent for a period of up to decades, and a denial based on short term exposure and short term initiation of acute complaints seems to be somewhat arbitrary. He opined that, given that the veteran does not have any evidence of any of the other major problems with which neuropathy is often associated, there is at least a 51 percent probability that the veterans neuropathy may be directly linked to exposure to dioxin/Agent Orange.

The Board acknowledges that the veterans claims file was not made available to Dr. Durham. The Board observes that review of the claims file is only required where necessary to ensure a fully informed examination or to provide an adequate basis for the examiners findings and conclusions. See VAOPGCPREC 20-95; 61 Fed. Reg. 10,064 (1996).

In this case, the Board finds that resort to the veterans claims file was not necessary because the veteran provided an accurate account of his medical history, thus ensuring a fully informed examination. In this regard, the Board observes that the veterans account as related to Dr. Durham essentially reflected the evidence of record at that time.

Further, Dr. Durham did review several pertinent documents, including the VA examination report. Given the above, and resolving all reasonable doubt in favor of the veteran, the Board finds that the veterans peripheral neuropathy of both lower extremities is due to his exposure to Agent Orange during service.

ORDER

Service connection for peripheral neuropathy of both lower extremities is granted.

2. Case from Atlanta, Georgia.

Citation Nr: 0802669

Decision Date: 01/24/08 Archive Date: 01/30/08

(DOCKET NO. 97-33 277 ) DATE On appeal from the Department of Veterans Affairs Regional Office in Atlanta, Georgia

THE ISSUE

Entitlement to service connection for peripheral neuropathy, to include on a direct basis and as secondary

to Agent Orange Exposure.

REPRESENTATION

Appellant represented by: Georgia Department of Veterans Services

WITNESSES AT HEARING ON APPEAL

Appellant and his spouse

ATTORNEY FOR THE BOARD

Tzu Wang, Associate Counsel

INTRODUCTION

The veteran served on active duty from July 1948 to August 1969. He served in the Republic of Vietnam from September 4,1967 to September 4, 1968.

This matter initially came before the Board of Veterans Appeals (Board) from a January 1997 rating decision of the Department of Veterans Affairs (VA) Regional Office (RO) in Atlanta, Georgia. In January 1998, the appellant and his spouse testified at the RO before a Decision Review Officer; a copy of the transcript has been associated with the claims file.

Subsequently, in December 1998 and August 2003, the Board remanded this case to the RO for further evidentiary development. In September 2007, the Board referred this case to the VAs Veterans Health Administration (VHA) for a medical opinion. The specialists opinion, dated October 18,2007, has been associated with the claims folder and, as required by law and regulation, the Board provided the appellant and his representative copies of this opinion and afforded them time to respond with additional evidence or argument. 38 C.F.R. 20.903(a) (2007). The case is now before the Board for further appellate consideration.

FINDING OF FACT

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Guidelines for Veterans Agent Orange and Peripheral ...

The physicians and the medical team at Five Stones Healing Arts & Wellness Center strive to achieve optimal health and wellness by focusing on what matters most: helping patients to achieve the essential balance of healing and lifestyle in mind, body, and spirit.

Located in Leesburg, Virginia, this practice centers on the Five Stones of optimal health: Healthful Eating, Balanced Movement, Integrative and Functional Medicine, Mindful Stress Management, and Interconnected Living.

The team at Five Stones Healing Arts & Wellness Center provide comprehensive medical care, including diagnosis, treatment, health assessments, screenings and lab work, and referrals. They offer an extensive collection of effective programs, classes, and services tailored to each patient.

Functional medicine is an integral part of the practices mission. The Five Stones medical team aims to identify and treat the causes of illnesses and conditions both chronic and acute by addressing lifestyle, genetic, environmental, and physiological factors that can lead to chronic disease and complex ailments.

This medical center treats patients of all ages, including men, women, and children. They specialize in the treatment of chronic and complex conditions, stress management, healthy weight-loss, healthy aging, cancer recovery, food allergies, and more.

Merging an array of therapies including integrative, functional, and holistic the board-certified practitioners at this practice offer a unique approach to health care. They offer a range of treatments, such as botanical medicines, nutritional supplements, pharmaceutical drugs, nutrition and detoxification programs, therapeutic bodywork, energy healing, and bio-identical hormone therapy.

Visit Five Stones Healing Arts & Wellness Center, serving patients in the Leesburg, Northern Virginia, and greater Washington, DC, area. New patients are welcome.

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Veterinary medicine, also called veterinary science, medical specialty concerned with the prevention, control, diagnosis, and treatment of diseases affecting the health of domestic and wild animals and with the prevention of transmission of animal diseases to people. Veterinarians ensure a safe food supply for people by monitoring and maintaining the health of food-producing animals.

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animal disease

The branch of medicine called veterinary medicine deals with the study, prevention, and treatment of diseases not only in domesticated animals but also in wild animals and in animals used in scientific research. The prevention, control, and eradication of diseases of economically important animals are agricultural concerns. Programs for the

Persons serving as doctors to animals have existed since the earliest recorded times, and veterinary practice was already established as a specialty as early as 2000 bce in Babylonia and Egypt. The ancient Greeks had a class of physicians who were called horse-doctors, and the Latin term for the specialty, veterinarius (pertaining to beast of burden), came to denote the field in modern times. Today veterinarians serve worldwide in private and corporate clinical practice, academic programs, private industry, government service, public health, and military services. They often are supported in their work by other veterinary medicine professionals, such as veterinary nurses and veterinary technicians.

Veterinary medicine has made many important contributions to animal and human health. Included are dramatic reductions in animal sources of human exposure to tuberculosis and brucellosis. Safe and effective vaccines have been developed for prevention of many companion (pet) animal diseasese.g., canine distemper and feline distemper (panleukopenia). The vaccine developed for control of Mareks disease in chickens was the first anticancer vaccine. Veterinarians developed surgical techniques, such as hip-joint replacement and organ transplants, that were later applied successfully to people.

A major challenge to veterinary medicine is adequately attending to the diversity of animal species. Veterinarians address the health needs of domestic animals, including cats, dogs, chickens, horses, cows, sheep, pigs, and goats; wildlife; zoo animals; pet birds; and ornamental fish. The sizes of animals that are treated vary from newborn hamsters to adult elephants, as do their economic values, which range from the undefinable value of pet animal companionship to the high monetary value of a winning racehorse. Medicating this variety of tame and wild animals requires special knowledge and skills.

On the basis of recognition by the World Health Organization (WHO) or the government of a country, there are about 450 veterinary degree programs worldwide. The level of veterinary training varies greatly among the various countries, and only about one-third of these programs designate the degree awarded as a doctors degree. Professional training of veterinarians is commonly divided into two phases. The first, or basic science, phase consists of classroom study and laboratory work in the preclinical sciences, including the fields of anatomy, physiology, pathology, pharmacology, toxicology, nutrition, microbiology, and public health. The second phase focuses on the clinical sciences and includes classroom study of infectious and noninfectious diseases, diagnostic and clinical pathology, obstetrics, radiology, anesthesiology, surgery, and practice management and hands-on clinical experience in the colleges veterinary teaching hospital. The clinical experience gives students the opportunity to treat sick animals, perform surgery, and communicate with animal owners. Student activities in the clinical setting are conducted under the supervision of graduate veterinarians on the faculty. Several important opportunities for additional training are available to graduate veterinarians. Internship (one-year) and residency (two-to-five-year) programs enable veterinarians to gain clinical proficiency in one or two medical specialties. Graduate veterinarians can also pursue advanced degree programs. Usually the field of advanced study is medically oriented, but some seek advanced degrees in areas such as business.

Most clinical-practice veterinarians treat only companion animals and usually within the practices clinic, or animal hospital. A small proportion treat only food-producing animals or horses, most often by traveling to the location of the animal in a vehicle equipped for veterinary services in the field. Most of the remainder in clinical practice are in mixed practices, which deal with both small animals and large domestic animals such as cattle or horses. Some small-animal practices offer services for special species such as ornamental fish, caged birds, and reptiles. Some practices may limit work to a specific medical area such as surgery, dentistry, dermatology, or ophthalmology. Corporate-owned animal hospitals have increased in number and are often combined with a retail outlet for pet supplies.

Veterinarians in academia administer the basic and clinical science programs of veterinary colleges. In addition, they conduct basic and clinical research, the latter of which may involve application of new instrumentation technologies for diagnosis and treatment of animal diseases. Included are echocardiography, laser lithotripsy, endoscopy, nuclear scintigraphy, ultrasonography, computed tomography (CT) scans, and magnetic resonance imaging (MRI; see nuclear magnetic resonance).

Veterinary medicine intersects with private industry in such areas as marketing of animal-health products, monitoring of animal health in large commercial animal-production programs, and biomedical research. Veterinary specialists in industry work in the fields of toxicology, laboratory animal medicine, pathology, molecular biology, and genetic engineering. Pharmaceutical companies employ veterinarians in the development, safety testing, and clinical evaluation of drugs, chemicals, and biological products such as antibiotics and vaccines for animals and people.

National and local governments employ veterinarians in those agencies charged with public health, protection of the environment, agricultural research, food and drug safety, food-animal inspection, the health of imported animals, and the humane treatment of animals. Veterinarians working in public-health programs, for example, evaluate the safety of food-processing plants, restaurants, and water supplies. They also monitor and help control animal and human disease outbreaks. The increased threat of bioterrorism has given veterinarians vital roles in the protection of the food supply for animals and people and in early detection of use of zoonotic organisms as weapons. Veterinarians also work in aerospace; e.g., they have been scientific advisers on animal use in the U.S. space program and have been members of U.S. space shuttle crews. Veterinarians in military service perform biomedical research, care for military dogs, and protect troops through food-inspection and communicable-disease monitoring-and-control programs.

See also animal disease.

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Your eyes are your windows to the world. Healthy eyes and vision make it possible for you to see and enjoy the world around you. When you think of what it takes to keep your body healthy, things like nutrition and exercise probably come to mind. But what does it take to have healthy vision? What does it mean to have healthy eyes?

Take a look at the anatomy of the eye.

Healthy eyes are eyes that see clearly and have no visible irritation or disease.

But even though you think you are seeing your best and your eyes don't have any noticeable symptoms of disease, they may not be as healthy as they could be. The human brain is amazingly good at covering up slight vision problems. For example, your brain might compensate for a slight vision problem in your right eye by making you use your left eye more.

This is the reason why having an eye exam is so important, especially for young children who may not even know the difference in having blurry or clear vision.

When an eye doctor looks into your eyes, he or she can determine if you are seeing your best, and if your eyes are free of disease that could cause vision loss over time. During an eye exam, an eye doctor performs several simple tests to determine if the major parts of your eyes are working together correctly and efficiently enough to assure you are seeing your world with the best possible vision.

Taking good care of your eyes will help keep them healthy and help to maintain good vision through the years. As you age, your eyes and vision will change. It is important to receive professional eye care, including dilated eye exams, to diagnose eye disease early enough to prevent vision loss.

Taking care of your eyes also includes protecting your eyes from UV rays and eating healthy foods. A diet rich in lutein and omega-3s helps protect against eye disease.

Of course, your family history will also determine your eye health in some ways. Having a family history of eye disease puts you at higher risk for developing the disease. Make sure your eye doctor is aware of your complete medical history.

Scheduling an annual eye exam is one of the most important steps you can take in protecting your eyes and vision. Vision is one of our most precious senses, yet vision and eye care is often neglected. The eyes provide hints about our overall health, as the dilated pupil can reveal the presence of undiagnosed problems throughout the body. An eye doctor can detect eye problems at their earliest stages, giving you time to be treated before major damage occurs to your eyesight. Regular eye exams also give your eye doctor a chance to help you correct or adapt to vision changes as you age.

During a comprehensive eye exam, your eye doctor will perform several different tests and procedures to check your vision as well as the overall health of your eyes. A comprehensive eye examination takes about an hour and should consist of most of the following parts:

If your eye doctor discovers a problem with your eyes or vision, you will be informed immediately. In cases of small vision problems or simple eye infections, your eye doctor will most likely treat the problem the same day. If a larger problem is discovered, however, you will probably be re-appointed for further testing another day.

Being diagnosed with an eye disease can be very stressful and disturbing. Although it may be difficult, do all you can to understand more about the disease. Learning how to manage the disease and how to cope with vision loss that may occur can help relieve your fears.

The amount of vision loss you suffer will vary depending on your diagnosis. No matter what diagnosis you receive, you can find ways to take charge of your vision and eye health. Never be afraid to ask for help from others and remember to stay positive. Know that challenges may arise, but you will be able to tackle them if you are prepared.

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Eye Health - Conditions, Treatment, and More

Dr. Hufnagel's Biography Dr. Hufnagel is a cornea-trained, board-certified ophthalmologist. He is a graduate of UCLA, Yale and Johns Hopkins Universities. Dr. Hufnagel has been recognized as a VISX STAR, an award granted only to the leading excimer laser surgeons in the United States. Dr. Hufnagel has participated in an FDA-sponsored investigation for LASIK surgery. His pioneering involvement with excimer lasers dates back to 1987 with published studies on the pathological aspects of laser surgery applied to the cornea. To date, he has performed several thousand laser vision correction procedures and tailors all surgeries to each patient’s individual needs. He is an instructor in IntraLASE™ bladeless LASIK surgical technique and actively teaches LASIK to other surgeons. After getting to know Dr. Marc Werner, we thought you might want to meet Dr. Thierry Hufnagel. If you still have questions for Dr. Hufnagel, like his opinions on the iFS laser or what his Ben and Jerry’s ice cream flavor would be, let us know in the comments below. Where are you originally from? I hail from Paris (France, not Texas!) What is your favorite memory from your years at Johns Hopkins? My fondest memory about Hopkins? People were referred there from all over the world for advice and treatment. I once examined this very famous Chicago lawyer who came in for cataract surgery. He was referred to me by my mentor, Dr. Walter Stark. After the lawyer came in for surgery, I told Dr. Stark that I thought he shouldn’t operate on the patient. I didn’t think that patient had a cataract! After further testing, we found that the patient’s visual loss was actually from a brain tumor, not a cataract. From that day on, they all thought I was pretty smart…very funny! How many years have you been practicing laser surgery? I opened my first LASIK center in New York City at the Trump Tower in 1995 called Insight Vision. What made you pick ophthalmology, particularly LASIK, as a specialty? When you ask patients about LASIK, most of them will tell you it’s the best thing they ever did! Not getting married, not having children, but having LASIK done! Lots of people see their need for glasses or contacts as a serious disability. Providing people with the gift of sight is very rewarding. My first rotation in medical school was in a hospice with end-of-life cancer patients. I couldn’t do anything to help except pushing the morphine. I felt pretty useless. I looked for the field where I thought I could be the most helpful. Obstetrics and bringing babies to life or ophthalmology and providing the gift of sight were the two options I looked into. Then by chance, I landed in the eye business, not the maternity ward! Where do you teach LASIK to other surgeons? We do all of the teaching in our office where we have a state-of-the-art facility. Your favorite thing about New York? Melting pot, for sure.

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Ophthalmologists near South Plainfield, NJ - Eye Surgeon

There is considerable excitement about the use of stem cells for cardiovascular disease. Stem cells are unspecialized cells with the unique property to self-renew or make copies of themselves and to differentiate into specialized cells. The goal of stem cell therapy is to enhance the body's natural process of regeneration. There are a considerable number of stem cells currently under investigation for patients with heart attacks, angina, heart failure, and peripheral arterial disease. We have made considerable progress but have many questions left to answer.

Timothy Henry, MD, FACC, is Chief of Cardiology at Cedars Sinai Heart Institute in Los Angeles, California. Dr. Henry earned his bachelor's degree at the University of North Dakota, graduated from medical school at University of California, San Francisco, in 1982, and was chief medicine resident from 1982--1986 at University of Colorado Health Sciences Center. He completed his training as a cardiology fellow, chief cardiology fellow, and interventional cardiology fellow at University of Minnesota in 1991. His research interests include interventional cardiology, acute myocardial infarction and novel therapies, including stem cell and gene therapy, for patients who are not candidates for standard revascularization techniques.

Dr. Henry has published over 250 manuscripts and book chapters and has served on the Research Committee for the Minnesota Affiliate of the AHA and the Emergency Care Committee for the ACC; he currently serves on the Advisory Committee for the AHA Mission: Lifeline Program, the AHA Acute Cardiac Care Committee of the Council on Clinical Cardiology and on the ACC Interventional Subcommittee. He has served as national principal investigator of multiple large, multicenter trials in acute coronary syndromes, myocardial infarction and angiogenesis including several ongoing cardiovascular stem cell trials including RENEW, ALLSTAR and ATHENA. He is also principal investigator for 1 of 7 NIH Clinical Cardiovascular Stem Cell Centers. He is a fellow at ACC and SCAI and a member of Alpha Omega Alpha and the AHA Council on Clinical Cardiology.

In the spirit of ideas worth spreading, TEDx is a program of local, self-organized events that bring people together to share a TED-like experience. At a TEDx event, TEDTalks video and live speakers combine to spark deep discussion and connection in a small group. These local, self-organized events are branded TEDx, where x = independently organized TED event. The TED Conference provides general guidance for the TEDx program, but individual TEDx events are self-organized.* (*Subject to certain rules and regulations)

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Stem cell therapy -- beyond the headlines: Timothy Henry ...

The arthritis in Maureen Munsies ankles was so intense until barely a year ago, she literally had to crawl on hands and knees to get upstairs.

The pain, she recalls now, took my breath away, and played havoc with the avid hikers favourite pastime.

In desperation, Munsie turned to a Toronto-area clinic that provides a treatment many experts consider still experimental, unproven and of questionable safety.

The 63-year-old says the stem cells she received at Regenervate Medical Injection Therapy 18 months ago were transformational, all but eliminating the debilitating soreness and even allowing her to hike Argentinas Patagonia mountains two months ago.

For me its been a life saver, Munsie says. Ive been able to do it all again I dont have any of that pain, at all.

Canadians drawn to the healing promise of stem cells have for years travelled outside the country to such places as Mexico, China or Arizona, taking part in a dubious form of medical tourism.

But Regenervate is one of a handful of clinics in Canada that have begun offering injections of stem cells, satisfying growing demand but raising questions about whether a medical idea with huge potential is ready for routine patient care.

Especially when those patients can pay thousands of dollars for the service.

Clinics in Ontario and Alberta are treating arthritis, joint injuries, disc problems and even skin conditions with stem cells typically taken from patients fat tissue or bone marrow.

The underlying idea is compelling: stem cells can differentiate or transform into many other types of cell, a unique quality that evidence suggests allows them to grow or regenerate tissue damaged by disease or injury.

Researchers including hundreds in Canada alone are examining stem-cell treatments for everything from ailing hearts to severed spinal cords.

With few exceptions, however, the concept is still being studied in the lab or in human trials; virtually none of the treatments have been definitively proven effective by science or approved by regulators like Health Canada.

The fact that Canadian clinics are now offering stem-cell treatments commercially is concerning on a number of levels, not least because of safety issues, says Ubaka Ogbogu, a health law professor at the University of Alberta.

Three U.S. women were blinded after receiving stem-cell injections in their eyes, while other American patients have developed bony masses or tumours at injection sites, Ogbogu said.

Stem cells have to be controlled to act exactly the way you want them to act, and thats why the research takes time, he said. It is simply wrong for these clinics to take a proof of concept and run with it.

Ogbogu says Health Canada must crack down on the burgeoning industry but says the regulator has so far been conspicuous by its inaction.

Other experts say the procedures provided here typically for joint pain are likely relatively safe, but still warn that care must be taken that the stem cells do not develop into the wrong type of tissue, or at the wrong place.

Alberta Health Services convened a workshop on the issue late last year, concluding there is an urgent need to develop a certification system for cell preparation and delivery to avoid spontaneous transformation of (stem cells) into unwanted tissue.

But one of the pioneers of the service in Canada says theres no empirical evidence that such growths can develop, and suggests the treatments only real risk as with any invasive procedure is infection.

Meanwhile, patients at Regenervate have enjoyed impressive outcomes after paying fees from $750 to $3,900, says Dr. Douglas Stoddard, the clinics medical director.

About 80 per cent report less pain, stiffness and weakness within a few months of getting their stem-cell injection, he said. His treatments efficacy, though, has not been tested in a randomized controlled trial, the gold-standard scientific study which would compare the injections to a sham or other treatment and identify any placebo effect.

I believe medical progress is not just limited to the laboratory and randomized double-blind trials, Stoddard said. A lot of progress starts in the clinic, dealing with patients You see something works, you see something has merit, and then its usually the scientists that seem to catch up later.

The Orthopedic Sport Institute in Collingwood, Ont., the Central Alberta Pain and Rehabilitation Institute and Cleveland Clinic in Toronto all advertise similar stem-cell treatments for orthopedic problems.

Edmontons Regen Clinic says it plans to start doing so this fall.

Ottawas Innovo says it also treats a range of back conditions with injections between the vertebrae, and uses stem cells to alleviate nerve damage.

Orthopedic Sport says its doctor focuses on FDA and Health Canada approved stem-cell injection therapy for patient care.

In fact, no treatment of the sort the clinics here provide has ever been authorized.

Health Canada says the vast majority of stem-cell therapies would constitute a drug and therefore need to be authorized after a clinical trial or new drug submission.

A number of stem-cell trials are underway, but only one treatment Prochymal has been approved, said department spokesman Eric Morrissette. Designed to combat graft-versus-host disease where bone marrow transplants for treating cancer essentially attack the patients body its unlike any of the services the stem-cell providers here offer.

But as the U.S. Food and Drug Administration aggressively pursues the hundreds of clinics in America, Health Canada says only that its committed to addressing complaints it receives.

It will take action based on the risk posed to the general public, said Morrissette, who encouraged people to pass on to the department information about possible non-compliant products.

Stoddard said the injections his clinics provide are made up of minimally manipulated tissue from patients own bodies and any attempt to crack down would be regulation for the sake of regulation.

But academic experts remain skeptical about the effectiveness of the treatments.

Scientific evidence suggests the injections may help alleviate joint pain temporarily, but probably just because of anti-inflammatory secretions from the cells not regeneration, said Dr. David Hart, an orthopedic surgery professor at the University of Calgary who headed the Alberta workshop.

Theres a need for understanding whats going on here and theres a need for regulation, he said.

Most of the clinics say they use a centrifuge to concentrate the stem cells after removing them from patients fat tissue or bone marrow. But its unclear if the clinics even know how many cells they are eventually injecting into patients, says Jeff Biernaskie, a stem-cell scientist at the University of Calgary.

Munsie, on the other hand, has no doubts about the value of her own treatment, even with a $3,000 price tag.

The procedure from extraction of fat tissue in her behind to the injection of cells into her ankles took barely over an hour.

Within three months, the retired massage therapist from north of Toronto says she could walk her dogs again. Last week, she was hiking near Banff.

Im a real believer in it, and the possibility of stem cells, says Munsie. I just think Wow, if we can heal with our own body, its pretty amazing.

(The story was modified July 6 to clarify lack of clinical-trial evidence for Regenervate procedures.)

tblackwell@nationalpost.com

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Canadian clinics begin offering stem-cell treatments ...

Guatemala City has the largest Medical District of all of Central America, a city within the city, dedicated almost exclusely to private medical providers. Besides the many private clinics and laboratories, the medical district consists of 5 large private hospitals and a top notch radiotherapy center, equipped with the most up to date technology.

Those private hospitals cater to the Guatemalan middle class, as well to the Americans and Europeans residing in Guatemala. The following medical specialties are taken care of in Guatemala-Citys medical district: cardiology, orthopedics, gynecology, obstetrics, bariatric and gastric surgery, organ transplant, pediatry, oncology. The choice of your hospital depends in large extent of which hospital your Specialist MD is affiliated with.

Specialist Doctors are often affiliated with more than one hospital within the medical district. A remarkable unknown fact is that the percentage of nocosomial infection rate in Guatemala Citys private hospitals is lower than the infection rate in most American hospitals. The ratio of nurse/patient is 1 to 3. Anyone who has been a patient in one of Guatemala Citys hospitals can testify about the quality of care and the warm attention given by Doctors and medical staff.

Read our testimonials

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Hospitals in Guatemala | Medical Tourism Guatemala

Achondroplasia is a form of short-limbed dwarfism. The word achondroplasia literally means "without cartilage formation." Cartilage is a tough but flexible tissue that makes up much of the skeleton during early development. However, in achondroplasia the problem is not in forming cartilage but in converting it to bone (a process called ossification), particularly in the long bones of the arms and legs. Achondroplasia is similar to another skeletal disorder called hypochondroplasia, but the features of achondroplasia tend to be more severe.

All people with achondroplasia have short stature. The average height of an adult male with achondroplasia is 131 centimeters (4 feet, 4 inches), and the average height for adult females is 124 centimeters (4 feet, 1 inch). Characteristic features of achondroplasia include an average-size trunk, short arms and legs with particularly short upper arms and thighs, limited range of motion at the elbows, and an enlarged head () with a . Fingers are typically short and the ring finger and middle finger may diverge, giving the hand a three-pronged () appearance. People with achondroplasia are generally of normal intelligence.

Health problems commonly associated with achondroplasia include episodes in which breathing slows or stops for short periods (apnea), obesity, and recurrent ear infections. In childhood, individuals with the condition usually develop a pronounced and permanent sway of the lower back () and bowed legs. Some affected people also develop abnormal front-to-back curvature of the spine () and back pain. A potentially serious complication of achondroplasia is , which is a narrowing of the spinal canal that can pinch (compress) the upper part of the spinal cord. Spinal stenosis is associated with pain, tingling, and weakness in the legs that can cause difficulty with walking. Another uncommon but serious complication of achondroplasia is hydrocephalus, which is a buildup of fluid in the brain in affected children that can lead to increased head size and related brain abnormalities.

Link:
Achondroplasia - Genetics Home Reference - NIH

Stem Cell Therapy for Autoimmune Diseases

Today, new treatments and advances in research are giving new hope to people affected by Autoimmune Diseases. StemGenexStem Cell Research Centre provides stem cell therapy for Autoimmune Diseases to help those with unmet clinical needs achieve optimum health and better quality of life.

Stem cell therapy for Autoimmune Diseases is being studied for efficacy in improving the complications in patients through the use of their own stem cells.These autoimmune disorder treatments may help patients who dont respond to typical drug treatment, want to reduce their reliance on medication, or are looking to try stem cell therapy before starting drug treatment.

To learn more about becoming a patient and receiving treatment for autoimmune diseases through the use of stem cells at StemGenex, please contact one of our Patient Advocates at (800) 609-7795. Below are some frequently asked questions aboutstem cell therapy for Autoimmune Diseases.

The bodys immune system is a complex network of special cells and organs that defends the body from germs and other foreign invaders. In order for the immune system to function properly, it needs the ability to tell the difference between what's you and what's foreign. When the immune system cannot, it attacks normal cells by mistake. The result of these misguided attacks is what is known as autoimmune disease.

Millions of people suffer from over eighty different types of known autoimmune diseases. Common autoimmune diseases include:

Stem cells that come from your adipose (fat) tissue have distinct functional properties including immunomodulatory and anti-inflammatory functional properties which have the capability of repairing and regenerating damaged tissue associated with disease and injury.

Upholding the highest levels of ethical conduct, safety and efficacy is our primary focus. Five clinical stem cell studies for Parkinson's Disease, Multiple Sclerosis, Osteoarthritis, Rheumatoid Arthritis and Chronic Obstructive Pulmonary Disease (COPD) are registered through the National Institutes of Health (NIH) at http://www.clinicaltrials.gov/stemgenex. Each clinical study is reviewed and approved by an independent Institutional Review Board (IRB) to ensure proper oversight and protocols are being followed.

Stem cells are the basic building blocks of human tissue and have the ability to repair, rebuild, and rejuvenate tissues in the body. When a disease or injury strikes, stem cells respond to specific signals and set about to facilitate the healing process by differentiating into specialized cells required for the bodys repair.

There are four known types of stem cells which include:

StemGenex provides autologous adult stem cells (from fat tissue) where the stem cells come from the person receiving treatment.

StemGenex provides autologous adult adipose-derived stem cells (from fat tissue) where the stem cells come from the person receiving treatment.

We tap into our bodys stem cell reserve daily to repair and replace damaged or diseased tissue. When the bodys reserve is limited and as it becomes depleted, the regenerative power of our body decreases and we succumb to disease and injury.

Three sources of stem cells from a patients body are used clinically which include adipose tissue (fat), bone marrow and peripheral blood.

Performed by Board Certified Physicians, dormant stem cells are extracted from the patients adipose tissue (fat) through a minimally invasive mini-liposuction procedure with little to no downtime.

During the liposuction procedure, a small area (typically the abdomen) is numbed with an anesthetic and patients receive mild to moderate sedation. Next, the extracted dormant stem cells are isolated from the fat and activated, and then comfortably infused back into the patient intravenously (IV) and via other directly targeted methods of administration. The out-patient procedure takes approximately four to five hours.

StemGenex provides multiple administration methods for patients with Autoimmune Diseases to best target the disease related conditions and symptoms which include:

Since each condition and patient are unique, there is no guarantee of what results will be achieved or how quickly they may be observed. According to patient feedback, some patients report results in one to three months, however, it may take as long as six to nine months. Individuals interested in stem cell therapy are urged to consult with their physician before choosing investigational autologous adipose-derived stem cell therapy as a treatment option.

In order to determine if you are a good candidate for adult stem cell treatment, you will need to complete a medical history form which will be provided by your StemGenex Patient Advocate. Once you complete and submit your medical history form, our medical team will review your records and determine if you are a qualified candidate for adult stem cell therapy.

StemGenex team members are here to help assist and guide you through the patient process.

Patients travel to StemGenex located in Del Mar, California located in San Diego County for stem cell treatment from all over the United States, Canada and around the globe. Treatment will consist of one visit lasting a total of three days. The therapy is minimally invasive and there is little to no down time. Majority of patients fly home the day after treatment.

The side effects of the mini-liposuction procedure are minimal and may include but are not limited to: minor swelling, bruising and redness at the procedure site, minor fever, headache, or nausea. However, these side effects typically last no longer than 24 hours and are experienced mostly by people with sensitivity to mild anesthesia. No long-term negative side effects or risks have been reported.

The side effects of adipose-derived stem cell therapy are minimal and may include but are not limited to: infection, minor bleeding at the treatment sites and localized pain. However, these side effects typically last no longer than 24 hours. No long-term negative side effects or risks have been reported.

StemGenex provides adult stem cell treatment with mesenchymal stem cells which come from the person receiving treatment. Embryonic stem cells are typically associated with ethical and political controversies.

The FDA is currently in the process of defining a regulatory path for cellular therapies. A Scientific Workshop and Public Hearing Draft Guidances Relating to the Regulation of Human Cells, Tissues or Cellular or Tissue-Based Products was held in September 2016 at the National Institutes of Health (NIH) in Bethesda, MD. Currently, stem cell treatment is not FDA approved.

In March 2016, bipartisan legislation, the REGROW Act was introduced to the Senate and House of Representatives to develop and advance stem cell therapies.

Stem cell treatment is not covered by health insurance at this time. The cost for standard preoperative labs are included. Additional specific labs may be requested at the patients expense.

With over 80 different types of Autoimmune Diseases and hundreds of symptoms, some of the most common symptoms include:

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Autoimmune Disorder Treatment - Stem Cell Therapy, Stem ...

Stem cell therapies have great potential to cure currently untreatable diseases and to even extend lifespans. Due to their differentiating qualities, they have been used for novel regenerative protocols. Ongoing progress towards the clinical use of dental pulp stem cells has recently expanded the possibilities for clinical applications based on pulp and periodontal tissue regeneration. Dental stem cells are a kind of mesenchymal cell that reside within the dental pulp and are classified as postnatal stem cell populations.

At present, there are two approved clinical trials and one clinical trial protocol related to dental stem cells that have not yet started recruiting. Nevertheless, these trials are still in an early phase that are testing the feasibility of the stem cells and the tolerance of the stem cell implantation, but have not applied the cells on patients for accruing diseases.

One trial in China is using stem cells from human exfoliated deciduous teeth (SHED) as the main target for investigation. Investigators from China are aiming to explore and clarify if autologous (cells or tissues obtained from the same individual) SHED stem cell transplantation can efficiently regenerate pulp (the center part of a tooth) and periodontal (connective tissue known as gum) tissue in immature permanent teeth and necrotic pulp of teeth in humans.

Millions of teeth are accidentally and forcibly detached each year, especially causing losses of immature permanent teeth in children. This clinical trial is starting to recruit patients with immature permanent teeth and pulp necrosis. SHED will be used as the cell source for regenerating pulp and periodontal tissue in immature teeth.

One of the main limitations in bone regeneration is lack of vascularization of newly sharp tissue. A new trial starting in France is aiming to use the dental stem cells of a simple and non-invasive tissue source such as dental pulp to develop a brand new pre-vascularized tissue-engineered bone construct. The dental pulp stem cells were isolated from the dental tissue of patients wisdom teeth and then used to assess their endothelial and osteoblastic differentiation to obtain pre-vascularized tissue engineered bone construct. Furthermore, one commercial differentiation medium is also used to evaluate its effect on the cell differentiation and production of a prevascularized bone construct.

TOOTH (The Open study Of dental pulp stem cell Therapy in Humans), a clinical trial protocol, is an open study, phase 1, single-blind clinical trial being conducted by Australian researchers. The protocol is investigating the use of dental pulp stem cell therapy for stroke survivors with chronic disability, with the aims of determining the maximum tolerable dose of the cell therapy, and the safety and feasibility for patients with chronic stroke.

Taken together with those trials, on going or just a start, the regenerating methods are still emphasized on the early phase clinical study of improving human diseases. Although clinical trials using dental pulp stem cells for treating human diseases are not very common, preclinical research has broadened the extent of potential clinical applications. Dental stem cells can differentiate into several cell types, such as neurons, adipocytes, and chondrocytes. From that, their therapeutic potential has been identified for various conditions, including neurological disorders, angiogenesis and vasculogenesis, liver disease, diabetes mellitus, and for regenerative ocular therapy, bone tissue engineering, and, of course, therapeutic applications in dentistry such as regenerative endodontic therapy, dentin regeneration, regenerative periodontal therapy, and bioengineered teeth.

Stem cell therapies have been a hot topic of research for years, but progress toward clinical trials for applications to humans has been slow due to ethical concerns and source obtained for transplantation. Dental pulp stem cells could resolve both these issues, by using human exfoliated deciduous teeth instead of invasive source such as embryonic stem cells. Pending successful completion of ongoing clinical trials, we can hope to see further work towards applying regenerative therapies based on dental stem cells for other organs, ultimately generating novel therapies to cure currently untreatable diseases.

Please note: PreScouter provides secondary research and is not associated with the experiments or getting volunteers for clinical trials.

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Tina is a dedicated, enthusiastic and innovative Pre-Clinical Researcher and Medical Writer who has a strong academic background encompassing a PhD in Clinical Science, a Masters in General Physiology and a Bachelors in Clinical Psychology. She has always been passionate about delivering exciting medical information. Tina is a technically-proficient researcher with exposure to multiple fields including urology, reproductive health, immunology, endocrinology and rheumatology gained across healthcare, clinical trials and pharmaceutical organizations. She joined PreScouter as a Global Scholar recently. Besides her medical research, she also starts up a commercial business with her favorite thing FOOD.

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A review of dental stem cells where are we now in ...

My Family Health Portrait (MFHP) has a new home

Starting September 6, 2018, My Family Health Portrait has a new home, the CDC Public Health Genomics Knowledge Base (PHGKB). CDC's Office of Public Health Genomics developed PHGKB as a suite of searchable databases, tools and resources to facilitate translation and implementation of genomics in clinical and public health programs.

NHGRI researchers used whole genome sequence data to pinpoint the single origin of the sickle cell mutation to the "wet" period of the Sahara 7,300 years ago. The mutation causes blood hemoglobin to be crescent shaped, reducing its ability to carry oxygen. Charles N. Rotimi, Ph.D., study co-author and NHGRI senior investigator, said the finding overturns previous theories that the mutation arose in multiple locations. This will help clinicians redefine sickle cell subgroups and treat patients more effectively, said lead author Daniel Shriner, Ph.D. Read more in the March 8 American Journal of Human Genetics.

On November 21, 2017,experts from NHGRI's Social and Behavioral Research Branch (SBRB) turned to a Reddit "Ask Me Anything" (AMA) to answer questions about their work on family health history. AMA hosts were Laura Koehly, Ph.D., SBRB chief, Chris Marcum, Ph.D., a staff scientist, and Jielu Lin, Ph.D., a post-doctoral fellow. The team answered questions from how to change behaviors after learning disease risk through family health history, to understanding risk when family health history is unknown. Here, we recap the event.

Precision medicine is a revolutionary approach to healthcare that takes into account individual differences in lifestyle, environment - and especially our genomes. However, a recent paper suggested that some people are being left behind. NHGRI recently published a perspective that lays out the challenges to achieving diversity in genomics research and what we are doing to help.Check out the newNature Review Geneticspublication that appeared online (ahead of print) on November 20.

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Health - National Human Genome Research Institute (NHGRI)

Necrosis (from the Greek "death, the stage of dying, the act of killing" from "dead") is a form of cell injury which results in the premature death of cells in living tissue by autolysis.[1]

Necrosis is caused by factors external to the cell or tissue, such as infection, toxins, or trauma which result in the unregulated digestion of cell components.

In contrast, apoptosis is a naturally occurring programmed and targeted cause of cellular death.

While apoptosis often provides beneficial effects to the organism, necrosis is almost always detrimental and can be fatal.[2]

Cellular death due to necrosis does not follow the apoptotic signal transduction pathway, but rather various receptors are activated, and result in the loss of cell membrane integrity and an uncontrolled release of products of cell death into the extracellular space.[1]

This initiates in the surrounding tissue an inflammatory response which attracts leukocytes and nearby phagocytes which eliminate the dead cells by phagocytosis. However, microbial damaging substances released by leukocytes would create collateral damage to surrounding tissues.[3] This excess collateral damage inhibits the healing process. Thus, untreated necrosis results in a build-up of decomposing dead tissue and cell debris at or near the site of the cell death. A classic example is gangrene. For this reason, it is often necessary to remove necrotic tissue surgically, a procedure known as debridement.

Structural signs that indicate irreversible cell injury and the progression of necrosis include dense clumping and progressive disruption of genetic material, and disruption to membranes of cells and organelles.[4]

There are six distinctive morphological patterns of necrosis:[5]

Necrosis may occur due to external or internal factors.

External factors may involve mechanical trauma (physical damage to the body which causes cellular breakdown), damage to blood vessels (which may disrupt blood supply to associated tissue), and ischemia.[11] Thermal effects (extremely high or low temperature) can result in necrosis due to the disruption of cells.

In frostbite, crystals form, increasing the pressure of remaining tissue and fluid causing the cells to burst.[11] Under extreme conditions tissues and cells die through an unregulated process of destruction of membranes and cytosol.[12]

Internal factors causing necrosis include: trophoneurotic disorders; injury and paralysis of nerve cells. Pancreatic enzymes (lipases) are the major cause of fat necrosis.[11]

Necrosis can be activated by components of the immune system, such as the complement system; bacterial toxins; activated natural killer cells; and peritoneal macrophages.[1] Pathogen-induced necrosis programs in cells with immunological barriers (intestinal mucosa) may alleviate invasion of pathogens through surfaces affected by inflammation.[1] Toxins and pathogens may cause necrosis; toxins such as snake venoms may inhibit enzymes and cause cell death.[11] Necrotic wounds have also resulted from the stings of Vespa mandarinia.[13]

Pathological conditions are characterized by inadequate secretion of cytokines. Nitric oxide (NO) and reactive oxygen species (ROS) are also accompanied by intense necrotic death of cells.[11] A classic example of a necrotic condition is ischemia which leads to a drastic depletion of oxygen, glucose, and other trophic factors and induces massive necrotic death of endothelial cells and non-proliferating cells of surrounding tissues (neurons, cardiomyocytes, renal cells, etc.).[1] Recent cytological data indicates that necrotic death occurs not only during pathological events but it is also a component of some physiological process.[11]

Activation-induced death of primary T-lymphocytes and other important constituents of the immune response are caspase-independent and necrotic by morphology; hence, current researchers have demonstrated that the occurrence of necrotic cell death can not only occur during pathological processes but also during normal processes such as tissue renewal, embryogenesis, and immune response.[11]

Until recently, necrosis was thought to be an unregulated process.[14] There are two broad pathways in which necrosis may occur in an organism.[14]

The first of these two pathways initially involves oncosis, where swelling of the cells occur.[14] The cell then proceeds to blebbing, and this is followed by pyknosis, in which nuclear shrinkage transpires.[14] In the final step of this pathway the nucleus is dissolved into the cytoplasm, which is referred to as karyolysis.[14]

The second pathway is a secondary form of necrosis that is shown to occur after apoptosis and budding.[14] Cellular changes of necrosis occur in this secondary form of apoptosis, where the nucleus breaks into fragments, which is known as karyorrhexis.[14]

The nucleus changes in necrosis, and characteristics of this change are determined by manner in which its DNA breaks down:

Plasma alterations are also seen in necrosis. Plasma membranes appear discontinuous when viewed with an electron microscope. This discontinuous membrane is caused by cell blebbing and the loss of microvilli.[5]

There are many causes of necrosis, and as such treatment is based upon how the necrosis came about. Treatment of necrosis typically involves two distinct processes: Usually, the underlying cause of the necrosis must be treated before the dead tissue itself can be dealt with.

Even after the initial cause of the necrosis has been halted, the necrotic tissue will remain in the body. The body's immune response to apoptosis, which involves the automatic breaking down and recycling of cellular material, is not triggered by necrotic cell death due to the apoptotic pathway being disabled.[20]

If calcium is deficient, pectin cannot be synthesized, and therefore the cell walls cannot be bonded and thus an impediment of the meristems. This will lead to necrosis of stem and root tips and leaf edges.[21] For example, necrosis of tissue can occur in Arabidopsis thaliana due to plant pathogens.

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Necrosis - Wikipedia

Genetics of aging is generally concerned with life extension associated with genetic alterations, rather than with accelerated aging diseases leading to reduction in lifespan.

The first mutation found to increase longevity in an animal was the age-1 gene in Caenorhabditis elegans. Michael Klass discovered that lifespan of C.elegans could be altered by mutations, but Klass believed that the effect was due to reduced food consumption (calorie restriction).[1] Thomas Johnson later showed that life extension of up to 65% was due to the mutation itself rather than due to calorie restriction,[2] and he named the gene age-1 in the expectation that other genes that control aging would be found. The age-1 gene encodes the catalytic subunit of class-I phosphatidylinositol 3-kinase(PI3K).

A decade after Johnson's discovery daf-2, one of the two genes that are essential for dauer larva formation,[3] was shown by Cynthia Kenyon to double C.elegans lifespan.[4] Kenyon showed that the daf-2 mutants, which would form dauers above 25C (298K; 77F) would bypass the dauer state below 20C (293K; 68F) with a doubling of lifespan.[4] Prior to Kenyon's study it was commonly believed that lifespan could only be increased at the cost of a loss of reproductive capacity, but Kenyon's nematodes maintained youthful reproductive capacity as well as extended youth in general. Subsequent genetic modification (PI3K-null mutation) to C.elegans was shown to extend maximum life span tenfold.[5][6]

Genetic modifications in other species have not achieved as great a lifespan extension as have been seen for C.elegans. Drosophila melanogaster lifespan has been doubled.[7] Genetic mutations in mice can increase maximum lifespan to 1.5times normal, and up to 1.7times normal when combined with calorie restriction.[8]

In yeast, NAD+-dependent histone deacetylase Sir2 is required for genomic silencing at three loci: the yeast mating loci, the telomeres and the ribosomal DNA (rDNA). In some species of yeast, replicative aging may be partially caused by homologous recombination between rDNA repeats; excision of rDNA repeats results in the formation of extrachromosomal rDNA circles (ERCs). These ERCs replicate and preferentially segregate to the mother cell during cell division, and are believed to result in cellular senescence by titrating away (competing for) essential nuclear factors. ERCs have not been observed in other species (nor even all strains of the same yeast species) of yeast (which also display replicative senescence), and ERCs are not believed to contribute to aging in higher organisms such as humans (they have not been shown to accumulate in mammals in a similar manner to yeast). Extrachromosomal circular DNA (eccDNA) has been found in worms, flies, and humans. The origin and role of eccDNA in aging, if any, is unknown.

Despite the lack of a connection between circular DNA and aging in higher organisms, extra copies of Sir2 are capable of extending the lifespan of both worms and flies (though, in flies, this finding has not been replicated by other investigators, and the activator of Sir2 resveratrol does not reproducibly increase lifespan in either species.[9]) Whether the Sir2 homologues in higher organisms have any role in lifespan is unclear, but the human SIRT1 protein has been demonstrated to deacetylate p53, Ku70, and the forkhead family of transcription factors. SIRT1 can also regulate acetylates such as CBP/p300, and has been shown to deacetylate specific histone residues.

RAS1 and RAS2 also affect aging in yeast and have a human homologue. RAS2 overexpression has been shown to extend lifespan in yeast.

Other genes regulate aging in yeast by increasing the resistance to oxidative stress. Superoxide dismutase, a protein that protects against the effects of mitochondrial free radicals, can extend yeast lifespan in stationary phase when overexpressed.

In higher organisms, aging is likely to be regulated in part through the insulin/IGF-1 pathway. Mutations that affect insulin-like signaling in worms, flies, and the growth hormone/IGF1 axis in mice are associated with extended lifespan. In yeast, Sir2 activity is regulated by the nicotinamidase PNC1. PNC1 is transcriptionally upregulated under stressful conditions such as caloric restriction, heat shock, and osmotic shock. By converting nicotinamide to niacin, nicotinamide is removed, inhibiting the activity of Sir2. A nicotinamidase found in humans, known as PBEF, may serve a similar function, and a secreted form of PBEF known as visfatin may help to regulate serum insulin levels. It is not known, however, whether these mechanisms also exist in humans, since there are obvious differences in biology between humans and model organisms.

Sir2 activity has been shown to increase under calorie restriction. Due to the lack of available glucose in the cells, more NAD+ is available and can activate Sir2. Resveratrol, a stilbenoid found in the skin of red grapes, was reported to extend the lifespan of yeast, worms, and flies (the lifespan extension in flies and worms have proved to be irreproducible by independent investigators[9]). It has been shown to activate Sir2 and therefore mimics the effects of calorie restriction, if one accepts that caloric restriction is indeed dependent on Sir2.

According to the GenAge database of aging-related genes, there are over 1800 genes altering lifespan in model organisms: 838 in the soil roundworm (Caenorhabditis elegans), 883 in the bakers' yeast (Saccharomyces cerevisiae), 170 in the fruit fly (Drosophila melanogaster) and 126 in the mouse (Mus musculus).[10]

The following is a list of genes connected to longevity through research [10] on model organisms:

Ned Sharpless and collaborators demonstrated the first in vivo link between p16-expression and lifespan.[11] They found reduced p16 expression in some tissues of mice with mutations that extend lifespan, as well as in mice that had their lifespan extended by food restriction. Jan van Deursen and Darren Baker in collaboration with Andre Terzic at the Mayo Clinic in Rochester, Minn., provided the first in vivo evidence for a causal link between cellular senescence and aging by preventing the accumulation of senescent cells in BubR1 progeroid mice.[12] In the absence of senescent cells, the mices tissues showed a major improvement in the usual burden of age-related disorders. They did not develop cataracts, avoided the usual wasting of muscle with age. They retained the fat layers in the skin that usually thin out with age and, in people, cause wrinkling. A second study led by Jan van Deursen in collaboration with a team of collaborators at the Mayo Clinic and Groningen University, provided the first direct in vivo evidence that cellular senescence causes signs of aging by eliminating senescent cells from progeroid mice by introducing a drug-inducible suicide gene and then treating the mice with the drug to kill senescent cells selectively, as opposed to decreasing whole body p16.[13] Another Mayo study led by James Kirkland in collaboration with Scripps and other groups demonstrated that senolytics, drugs that target senescent cells, enhance cardiac function and improve vascular reactivity in old mice, alleviate gait disturbance caused by radiation in mice, and delay frailty, neurological dysfunction, and osteoporosis in progeroid mice. Discovery of senolytic drugs was based on a hypothesis-driven approach: the investigators leveraged the observation that senescent cells are resistant to apoptosis to discover that pro-survival pathways are up-regulated in these cells. They demonstrated that these survival pathways are the "Achilles heel" of senescent cells using RNA interference approaches, including Bcl-2-, AKT-, p21-, and tyrosine kinase-related pathways. They then used drugs known to target the identified pathways and showed these drugs kill senescent cells by apoptosis in culture and decrease senescent cell burden in multiple tissues in vivo. Importantly, these drugs had long term effects after a single dose, consistent with removal of senescent cells, rather than a temporary effect requiring continued presence of the drugs. This was the first study to show that clearing senescent cells enhances function in chronologically aged mice.[14]

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Genetics of aging - Wikipedia

As you start to learn about stem cells, one of the most common questions tohave is, What types of stem cells exist?There is not an agreed-upon number of stem cell types, because one can classify stem cells either by differentiation potential(what they can turn into) or by origin (from where they are sourced).This post is dedicated to explaining the five types of stem cells, based on differentiation potential.

The five different types of stem cells discussed in this article are:

All stem cells that exist can be classified into one of five groups based on their differentiation potential. Each of these stem cell types is explored in greater detail below.

The Rise of Direct Cell Reprogramming | BioInformant https://t.co/q0vwT6CffR#allogeneic #totipotent #pluripotent #multipotent #autologous pic.twitter.com/ycoDP8mYa6

Todd C Bertsch (@todd_bertsch) February 19, 2018

These stem cells are the most powerful that exist.

They can differentiate into embryonic, as well as extra-embryonic tissues, such as chorion, yolk sac, amnion, and the allantois. In humans and other placental animals, these tissues form the placenta.

The most important characteristic of a totipotent cell is that it can generate a fully-functional, living organism.

The best-known example of a totipotent cell is a fertilized egg (formed when a sperm and egg unite to form a zygote).

It is at or around four days post-fertilization that these cells begin to specialize into pluripotent cells, which as described below, are flexible cell types but cannot produce an entire organism.

Theyre aliveeee!! Turned our human pluripotent stem cells into beating cardio!!! ::happy tears::Next up crispR KO fun #stemcellscientist #WomenInScience #futureBIOhacker pic.twitter.com/GVg4pb9Xri

Kristin Pagel (@DeeDeeTroit84) March 31, 2018

The next most powerful type of stem cell is the pluripotent stem cell.

The importance of this cell type is that it can self-renew and differentiate into any of the three germ layers, which are: ectoderm, endoderm, and mesoderm. These three germ layers further differentiate to form all tissues and organs within a human being.

There are several known types of pluripotent stem cells.

Among the natural pluripotent stem cells, embryonic stem cells are the best example.However, a type of human-made pluripotent stem cell also exists, which is the induced pluripotent stem cell (iPS cell).

iPS cells were first produced from mouse cells in 2006 and human cells in 2007, and are tissue-specific cells that can be reprogrammed to become functionally similar to embryonic stem cells.

Because of their powerful ability to differentiate in a wide diversity of tissues and their non-controversial nature, induced pluripotent stem cells are well-suited for use in cellular therapy and regenerative medicine.

Did you know that bone marrow contains multipotent stem cells that give rise to all the cells of the blood? pic.twitter.com/NcYJsdPJXi

caremotto (@caremotto) January 17, 2018

Multipotent stem cells are a middle-range type of stem cell, in that they can self-renew and differentiate into a specific range of cell types.

An excellent example of this cell type is the mesenchymal stem cell (MSC).

Mesenchymal stem cells can differentiate into osteoblasts (a type of bone cell), myocytes (muscle cells), adipocytes (fat cells), and chondrocytes (cartilage cells).

These cells types are fairly diverse in their characteristics, which is why mesenchymal stem cells are classified as multipotent stem cells.

The next type of stem cells, oligopotent cells, are similar to the prior category (multipotent stem cells), but they become further restricted in their capacity to differentiate.

While these cells can self-renew and differentiate, they can only do so to a limited extent. They can only do so into closely related cell types.

An excellent example of this cell type is the hematopoietic stem cell (HSC).

HSCs are cells derived from mesoderm that can differentiate into other blood cells. Specifically, HSCs are oligopotent stem cells that can differentiate into both myeloid and lymphoid cells.

Myeloid cells includebasophils, dendritic cells, eosinophils, erythrocytes, macrophages, megakaryocytes, monocytes, neutrophils, and platelets, while lymphoid cells include B cells, T cells, and natural kills cells.

Finally, we have the unipotent stem cells, which are the least potent and most limited type of stem cell.

An example of this stem cell type would be muscle stem cells.

While muscle stem cells can self-renew and differentiate, they can only do so into a single cell type. They are unidirectional in their differentiation capacity.

The purpose of these stem cellcategories is to assess thefunctional capacity of stem cells based on their differentiation potential.

Importantly, each category has different stem cell research applications, medical applications, and drug development applications.

Watch this video and learn about the 5 types of stem cells:

In your opinion, which of the following types of stem cells have the best potential to form any tissue type? Mention them in the comments section below.

To learn more, view:Stem Cell Fact Sheet Types of Stem Cells and their Use in Medicine

Do You Know The 5 Types Of Stem Cells?

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Do You Know the 5 Types of Stem Cells? | BioInformant