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Multiple Sclerosis, Causes, Tests, Diagnosis & Treatment

August 20th, 2015

Multiple sclerosis is an autoimmune disorder in which the bodys immune system attacks the protective sheath (myelin) that insulates your nerves and helps mediate the transmission of nerve impulses. As a result, the electrical impulses that travel along the nerves decelerates, which slows down the communication between your brain and rest of the body. Furthermore, nerve damage also occurs. Symptoms of multiple sclerosis may vary with the extent of nerve damage and the type of nerves affected.

As multiple sclerosis progresses, a person may begin to lose the ability to see, walk, write or speak. According to the National Multiple Sclerosis Society, multiple sclerosis is the leading cause (with the exception of physical trauma) of neurological disability beginning in early to mid-adulthood (most people are diagnosed between the ages of 20 and 50), with 200 people being diagnosed with multiple sclerosis every week.

Overall, multiple sclerosis affects an estimated 400,000 Americans and is significantly more common amongst women. Currently there is no cure for multiple sclerosis. However, treatments can help treat attacks, modify the course of the disease and treat symptoms.

Symptoms of multiple sclerosis vary between individuals and can change as the disease progresses. Episodes can last for days, weeks, or months. These episodes alternate with periods of reduced or no symptoms (remissions). Multiple sclerosis symptoms include:

The exact cause of multiple sclerosis is currently unknown. It is generally accepted that multiple sclerosis is an autoimmune disorder. Scientists believe that a host of factors may contribute to the onset of multiple sclerosis including, exposure to environmental toxins, genetics, and childhood exposure to certain viruses or bacteria.

The following factors may increase your risk of developing multiple sclerosis:

In order to make a diagnosis of multiple sclerosis, your doctor must definitively conclude all of the following:

There is currently no cure for multiple sclerosis. Treatment regimens typically focus on managing symptoms and attacks of multiple sclerosis.

Multiple sclerosis treatment regimens include:

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Multiple Sclerosis, Causes, Tests, Diagnosis & Treatment

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Multiple Sclerosis News Topix

August 20th, 2015

multiple sclerosis (MS) | pathology | Britannica.com

August 20th, 2015

Multiple sclerosis(MS),also called disseminated sclerosis, a progressive disease of the central nervous system characterized by the destruction of the myelin sheath surrounding the nerve fibres of the brain, spinal cord, and optic nerves. As a result, the transmission of nerve impulses becomes impaired, particularly in pathways involved with vision, sensation, and movement.

MS has a worldwide distribution but is five times more common in temperate regions than in tropical regions. The disease primarily occurs in individuals between the ages of 20 and 40, and women are affected by the disease more often than men.

There are four major types of MS: relapsing-remitting (RRMS), secondary-progressive (SPMS), primary-progressive (PPMS), and progressive-relapsing (PRMS). About 8085 percent of patients are diagnosed initially with RRMS. In this form of the disease, onset is usually gradual, and there are alternating intervals of symptom exacerbation and complete symptom remission. In many patients with RRMS, symptoms may worsen gradually during subsequent recurrences and eventually may no longer disappear during remissions. When this occurs, the patients diagnosis changes from RRMS to SPMS. About 1015 percent of patients have PPMS, which is characterized by steady disease progression from the time of onset, without relapse-remission cycles. PRMS is a rare form of the disease, occurring in less than 5 percent of MS patients. This type is distinguished from other forms of MS by its steady worsening of symptoms from the time of onset, in which intermittent flare-ups become increasingly severe. There are no periods of complete symptom remission in PRMS.

In most forms of the disease, initial symptoms include numbness or tingling in the extremities or on the side of the face, muscle weakness, dizziness, unsteady gait, and visual disturbances such as blurred or double vision and partial blindness. The intensity of these early symptoms subsides in most individuals for months or even years. But in progressive forms of MS, remissions usually become shorter as the disease advances. New signs and symptoms may appear, including abnormal reflexes, difficulty in coordinating and controlling movement, bladder dysfunction, and neuropsychological problems such as depression, memory loss, and emotional instability. Eventually the impairment of motor control can develop into complete paralysis. Despite disease progression, most people with MS have a normal life expectancy.

The cause of MS remains unclear, but in many cases there is evidence of a genetic component. In fact, nearly five dozen different genetic variations have been associated with increased risk for the disease. Variations occurring in a cluster of genes that make up the major histocompatibility complex (MHC; also called human leukocyte antigen, or HLA, system), which regulates immune function, appear to have the most significant effect on risk. Some of these variations appear to be associated with environmental factors that precipitate the onset of disease. For example, the risk of MS in northern Europeans who carry a particular MHC variant is exacerbated by vitamin D deficiency, which weakens immune function.

Vitamin D deficiency as a factor in the development of MS has been further implicated by the identification of rare loss-of-function variations in a gene known as CYP27B1 that result in reduced vitamin D levels in the body. The inheritance of one copy (from one parent) of the mutated gene is sufficient to produce MS (inheritance of two copies, one from each parent, causes vitamin D-dependent rickets I, or pseudo-vitamin D-deficiency rickets). Thus, in those people who carry variations associated with or intensified by vitamin D deficiency, vitamin D supplementation may confer some degree of protection against MS.

There are also variations in other genes that have been identified and associated with MS, including several occurring in genes that encode proteins for signaling molecules known as interleukin receptors. These receptors are expressed on the cell membranes of B and T lymphocytes and play an important role in regulating lymphocyte development. Some variations in interleukin receptor genes are associated with autoimmune diseases, such as type 1 diabetes and Graves disease. There is much evidence suggesting that MS results from an autoimmune reaction in which a malfunctioning immune system produces T cells that react with and damage the bodys own cells, specifically the myelin sheath of nerve fibres. The trigger for this autoimmune reaction is not known, but it is suspected to be related to genetic factors, with the interaction of variations in multiple genes, rather than a single gene, being a likely cause. Some scientists believe these changes in immune function could also be the result of exposure to a virus.

There is no cure for MS, but a number of medications, such as corticosteroids, are used to alleviate symptoms. In addition, there are a handful of disease-modifying agents available for MS. These agents can reduce the frequency of relapses and generally slow the progress of the disease. Immunotherapy with different forms of interferon beta, a protein the body normally produces to modulate immune response, is used to reduce the severity and frequency of the exacerbation periods of the disease. Natalizumab (Tysabri), a monoclonal antibody (an antibody clone derived from a single immune cell), is also effective for controlling the severity and frequency of relapses. Natalizumab attaches to molecules on the cell membrane of lymphocytes, preventing them from entering the central nervous system and attacking nerve cells. Another monoclonal antibody, called Alemtuzumab (Campath), which is used to treat chronic lymphocytic leukemia, also binds to the cell membrane of lymphocytes but works by stimulating antibody-mediated destruction of the cells. In clinical trials in patients with early-stage RRMS, this agent not only stopped progression of the disease but also facilitated the restoration of nerve function in some patients. Other disease-modifying agents used to treat MS include glatiramer acetate (Copaxone) and the immunosuppressant drug mitoxantrone (Novantrone).

Another treatment for MS that has been explored in clinical trials is a form of stem cell therapy called autologous (self) hematopoietic stem cell transplant. This therapy has been tested only in patients who have not responded to conventional treatment regimens and therefore elect to undergo immunosuppressive therapy to destroy lymphocytes that have acquired autoimmune characteristics. Prior to the administration of immunosuppressive drugs, hematopoietic stem cells are harvested from the patients blood or bone marrow. These cells are then frozen and stored for later reinfusion into the patient following immunosuppressive therapy. Because hematopoietic stem cells have the potential to develop into normally functioning lymphocytes, transplant provides the patients immune system with an opportunity to recover normal activity. This treatment has proved successful in stopping or delaying disease progression in some patients, and, in rare cases, it has even led to the repair of neurological damage. However, significant risks are associated with stem cell therapy, including increased susceptibility to infection and possibility of transplant failure or relapse of disease.

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multiple sclerosis (MS) | pathology | Britannica.com

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Multiple Sclerosis – Lab Tests Online

August 20th, 2015

Multiple sclerosis (MS) is a disease that affects the . It causes and the destruction of . Myelin surrounds nerve fibers and acts like insulation on a wire, preventing "short-circuits" that divert a nerve signal from having its desired effects. The "demyelination" process interferes with nerve impulse transmission, affects muscular control, and causes a variety of sensory, motor, and psychological symptoms. Damage to the myelin usually resolves with time and symptoms subside, but repeated attacks can lead to a continual process of demyelination and remyelination, which produces nerve fiber scarring and progressive disability.

The cause of MS is unknown. It is thought to be an autoimmune process triggered by a , environmental factors, and/or a genetic predisposition. Typically, MS first appears and is diagnosed when individuals are between 20 and 50 years of age, although it can occur in young children. It affects women more frequently than men, is more common in Northern European Caucasians than other ethnic groups, and is seen in greater numbers in people who live in temperate climates than warm ones. According to the National Multiple Sclerosis Society, MS affects about 2.1 million people worldwide. It is estimated that about 250,000 to 350,000 people in the U.S. have MS, according to the National Institute on Neurological Disorders and Stroke. The risk of developing this disease is estimated to be about 1 in 750 in the general population. In families with an affected member, the risk rises to 1 in 40, and it is about 1 in 4 for the identical twin of an affected person, strengthening the notion of a genetic component to the cause.

There is no single test that can conclusively diagnose MS. Instead, health practitioners look for a combination of factors to determine if a patient has MS. The factors are described in a document called the "McDonald Criteria," named for the doctor who chaired the 2001 panel of experts charged with establisheding criteria for an accurate diagnosis. The document is updated regularly as new research improves our understanding of the disease. Physicians will consult a patient's medical history and a variety of clinical and laboratory tests to aid in their diagnosis. In applying the criteria for diagnosing MS, a health practitioner must:

Once diagnosed, an individual may be classified as having one of several types of MS, based on signs and symptoms, frequency of relapses, rate of disease progression, and the number of areas that are damaged in the CNS:

Because MS can attack any area of the , the and of MS are many and varied. They are associated with what the nerves in the affected area(s) are responsible for controlling. Symptoms of MS may come and go, and their duration may last from days to months. Some of these include:

According to the National Multiple Sclerosis Society, about 85% of those with multiple sclerosis initially have relapsing-remitting MS. They experience periodic attacks or relapses followed by healing and symptom remission. Later in the course of the disease, about half develop secondary-progressive MS. Their symptoms and disabilities worsen as they continue to have relapses but do not fully recover. About 10% of people with MS have a progressive form of the disease. They grow gradually worse without experiencing remissions.

Although there is no single test or set of tests that can establish a diagnosis of multiple sclerosis (MS), there are three tests that are generally considered useful:

Laboratory tests There are no laboratory tests that are completely specific for multiple sclerosis, but several laboratory tests are helpful in diagnosing or excluding this disease as the cause of a person's signs and symptoms. The most useful tests look for evidence of production within the central nervous system.

IgG index = [IgG (CSF) / IgG (serum)] / [Albumin (CSF) /Albumin (serum)]

An elevated IgG index indicates increased production of IgG within the central nervous system. It is found in about 90% of MS cases.

Health practitioners may also test for diseases that can cause symptoms similar to MS to determine if they may be responsible for a patient's illness. Examples include:

Non-laboratory tests

In addition to the standard MRI, there are a variety of specialized techniques that may be performed, such as functional MRI, magnetic resonance spectroscopy, and diffusion-tensor MRI. The National Multiple Sclerosis Society (NMSS) web site has more information on the use of MRI in MS.

Two other types of evoked potentials may be used, though less commonly. Brain stem auditory evoked potentials (BAEP) is a test that helps detect lesions in the brainstem causing delays in the transmission of sounds. Somatosensory evoked potentials (SSEP) is a test that applies a brief electrical stimulus to the wrist or ankle. It detects disruptions in the pathways from the arms and legs to the brain at very specific points of the central nervous system.

There is no cure for multiple sclerosis, but a variety of treatments are available that can reduce the frequency and severity of relapses.

The goals of MS treatment are to slow the progression of the disease, relieve symptoms, and minimize the effects of acute attacks. Health practitioners may prescribe corticosteroids for short periods of time to help reduce the severity of relapses as well as other medications to address specific symptoms, such as beta interferon, copolymer I, natalizumab and fingolimod, the first oral therapy approved by the U.S. Food and Drug Administration for treatment and management of MS symptoms. Fatigue and depression sometimes associated with MS may be treated with appropriate antidepressants or steroidal drugs. For more on specific medications that may be prescribed, see the Treatments page on the National MS Society web site.

MS does not significantly decrease the lifespan of those who have it, but it can frequently and intermittently affect quality of life. People with MS usually work with a team of professionals who help support and monitor their condition and address their changing needs. Current MS research is directed toward understanding the cause of MS in hopes of developing better drugs to treat, if not cure or prevent the disease.

On This Site Tests: CSF Analysis, Protein Electrophoresis Conditions: Autoimmune Disorders, Sarcoidosis, Vasculitis, Lyme Disease, Systemic Lupus Erythematosus

Elsewhere On The Web Multiple Sclerosis Foundation The National Multiple Sclerosis Society (NMSS) National Institute of Neurological Diseases and Stroke: MS Information Page Multiple Sclerosis Association of America Multiple Sclerosis Discovery Forum

Article Sources

NOTE: This article is based on research that utilizes the sources cited here as well as the collective experience of the Lab Tests Online Editorial Review Board. This article is periodically reviewed by the Editorial Board and may be updated as a result of the review. Any new sources cited will be added to the list and distinguished from the original sources used.

Sources Used in Current Review

(2011) National Multiple Sclerosis Society. Treatments. Available online at http://www.nationalmssociety.org/about-multiple-sclerosis/what-we-know-about-ms/treatments/medications/interferon-beta-1b/index.aspx through http://www.nationalmssociety.org. Accessed April 2013.

(2011) National Multiple Sclerosis Society. Diagnosing MS. Available online at http://www.nationalmssociety.org/about-multiple-sclerosis/what-we-know-about-ms/diagnosing-ms/index.aspx throughhttp://www.nationalmssociety.org.Accessed April 2013.

(2011) National Multiple Sclerosis Society. Diagnosis Criteria. PDF available for download at http://www.nationalmssociety.org/ms-clinical-care-network/clinical-resources-and-tools/core-curriculum/diagnosing-multiple-sclerosis/diagnostic-criteria/index.aspx through http://www.nationalmssociety.org. Accessed April 2013.

(August 14, 2012) National Institute on Neurologic Disorders and Stroke. Multiple Sclerosis. Available online at http://www.ninds.nih.gov/disorders/multiple_sclerosis/multiple_sclerosis.htm through http://www.ninds.nih.gov. Accessed April 2013.

(Updated April 2013) Luzzio C. Multiple Sclerosis. Medscape Reference. Available online at http://emedicine.medscape.com/article/1146199-overview through http://emedicine.medscape.com. Accessed April 2013.

Sources Used in Previous Reviews

Thomas, Clayton L., Editor (1997). Taber's Cyclopedic Medical Dictionary. F.A. Davis Company, Philadelphia, PA [18th Edition].

Pagana, Kathleen D. & Pagana, Timothy J. (2001). Mosby's Diagnostic and Laboratory Test Reference 5th Edition: Mosby, Inc., Saint Louis, MO.

Espay, A. (2002 May 6, Updated). Multiple sclerosis [20 paragraphs]. MedlinePlus Medical Encyclopedia [On-line information]. Available online at http://www.nlm.nih.gov/medlineplus/ency/article/000737.htm.

(2003 August 12). About MS What Is Multiple Sclerosis? National Multiple Sclerosis Society [On-line information]. Available online at http://www.nationalmssociety.org/What%20is%20MS.asp through http://www.nationalmssociety.org.

(2001 July 1, Reviewed). NINDS Multiple Sclerosis Information Page. NINDS [On-line information]. Available online at http://www.ninds.nih.gov/health_and_medical/disorders/multiple_sclerosis.htm through http://www.ninds.nih.gov.

Mayo Clinic Staff (2004 May 7). Multiple sclerosis. MayoClinic.com [On-line information]. Available online at http://www.mayoclinic.com/invoke.cfm?id=DS00188 through http://www.mayoclinic.com.

Kiriakopoulos, E. (2003 August 10, Updated). CSF oligoclonal banding. MedlinePlus Medical Encyclopedia [On-line information]. Available online at http://www.nlm.nih.gov/medlineplus/ency/article/003631.htm.

( 1995-2004). Multiple Sclerosis and Related Diseases, Introduction. The Merck Manual Second Home Edition [On-line information]. Available online at http://www.mult-sclerosis.org/oligoclonalbanding.html through http://www.mult-sclerosis.org.

Holland, N. (2003 December). Overview of Multiple Sclerosis. MSNursing, NMSS [On-line information]. Available online at http://www.nationalmssociety.org/ms_nursing/overview.asp through http://www.nationalmssociety.org.

(2002 Updated). Multiple Sclerosis: Hope Through Research. NINDS [On-line information]. Available online at http://www.ninds.nih.gov/health_and_medical/pubs/multiple_sclerosis.htm through http://www.ninds.nih.gov.

( 2004). Immunoglobulin G, CSF Index and Immunoglobulin G/Albumin Ratio, CSF. ARUPs Guide to Clinical Laboratory Testing [On-line information]. Available online at http://www.aruplab.com/guides/clt/tests/clt_al9b.jsp through http://www.aruplab.com.

( 2004). Oligoclonal Banding and Multiple Sclerosis Panel. ARUPs Guide to Clinical Laboratory Testing [On-line information]. Available online at http://www.aruplab.com/guides/clt/tests/clt_112b.jsp#1143660 through http://www.aruplab.com.

( 2004). Myelin Basic Protein. ARUPs Guide to Clinical Laboratory Testing [On-line information]. Available online at http://www.aruplab.com/guides/clt/tests/clt_a94b.jsp#1142392 through http://www.aruplab.com.

(Updated 2008 December). Multiple Sclerosis: Hope Through Research. NINDS, National Institute of Health. Available online at http://www.ninds.nih.gov/disorders/multiple_sclerosis/detail_multiple_sclerosis.htm through http://www.ninds.nig.gov. Accessed March 2009.

Minden, S.and Frankel, D. (Updated May 2008). PLAINTALK: A Booklet about MS for Families. National Multiple Sclerosis Society. [On-line information]. Available online at http://www.nationalmssociety.org/multimedia-library/brochures/managing-major-changes/index.aspx through http://www.nationalmssociety.org. Accessed March 2009.

Dangond, F. (Updated 2008 July 3). Multiple Sclerosis. Emedicine.com. [On-line information]. Available online at http://emedicine.medscape.com/article/1146199-overview through http://www.emedcine.medscape.com. Accessed March 2009.

Brian R. Apatoff, B. (Revised August 2007). Multiple Sclerosis. Merck Manual for Healthcare Professionals. [On-line information]. Available online at http://www.merck.com/mmpe/sec16/ch222/ch222b.html?qt=MS&alt=sh through http://www.merck.com. Accessed March 2009.

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Multiple Sclerosis - Lab Tests Online

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Multiple sclerosis | University of Maryland Medical Center

August 20th, 2015

Introduction

Multiple sclerosis (MS) is an unpredictable disease of the nervous system that disrupts communication between the brain and other parts of the body. Its effects can range from relatively mild in most cases to somewhat disabling to devastating. The symptoms may mysteriously occur and then disappear. In the worst cases, a person with MS may be unable to:

During an MS "flare", inflammation occurs in areas of the white matter (pale colored nerve tissue) of the central nervous system in random patches called plaques. This is followed by destruction of myelin, the fatty covering that protects nerve cell fibers in the brain and spinal cord. Myelin allows for the smooth, high-speed transmission of electrochemical messages between the brain, the spinal cord, and the rest of the body. When myelin is damaged, it may block or slow neurological transmission of messages, resulting in diminished or lost function.

Symptoms of MS include:

The cause of MS is unknown. Scientists think the disease isan autoimmune condition influenced by genetic and environmental factors. Other theories include a childhood virus that primes the immune system for an attack against myelin in early adulthood.

People with the following conditions or characteristics are at risk for developing MS:

If you have symptoms associated with MS, you should see your health care provider. Your provider will:

The primary goal of treatment is to reduce the severity of attacks using certain medications and to extend the individual's physical functioning for as long as possible.

Your health care provider may prescribe the following medications, (or a combination of the following medications):

Surgery may help treat severe and disabling tremors and reduce severe spasms.

A comprehensive treatment plan for MS may include a range of complementary and alternative medical therapies (CAM). Always work with a knowledgeable provider when seeking CAM therapies for the treatment of MS. Some CAM therapies may interfere with conventional treatments. Inform all of your providers about any CAM therapies you are considering.

These nutritional tips may help reduce symptoms:

You may address nutritional deficiencies with the following supplements:

Herbs are one way to strengthen and tone the body's systems. As with any therapy, you should speak with your provider before starting treatment. You may use herbs as dried extracts (capsules, powders, and teas), glycerites (glycerine extracts), or tinctures (alcohol extracts). Unless otherwise indicated, make teas with 1 tsp. herb per cup of hot water. Steep covered 5 to 10 minutes for leaf or flowers, and 10 to 20 minutes for roots. Drink 2 to 4 cups per day. You may use tinctures alone or in combination as noted.

Although few studies have examined the effectiveness of specific homeopathic therapies, professional homeopaths may consider the following remedies for the treatment of gastritis symptoms (nausea and vomiting) based on their knowledge and experience. Before prescribing a remedy, homeopaths take into account your constitutional type, includes your physical, emotional, and psychological makeup. An experienced homeopath assesses all of these factors when determining the most appropriate treatment for you individually. Combination remedies may be used for fatigue, spasm, and to help rid the body of impurities. Remedies include:

About 70% of people experience attacks and remissions, and about half of these undergo a chronic, progressive worsening after about 10 years. 10 to 15% of people experience a chronic, progressive, worsening of the disease from the initial onset, and 15 to 20% of people have a relatively mild course of the disease. Most people with MS live for 30 years or more with the disease, many still working and mobile, though bladder, bowel and sexual dysfunction are common among this population. People who have MS are at a higher risk than the general population of:

MS is also associated with increased risk of some cancers, including urinary organs and brain tumors.

People with MS will need lifelong monitoring, especially during flare-ups.

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Multiple sclerosis | University of Maryland Medical Center

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Medical Xpress – multiple sclerosis

August 20th, 2015

Team finds early inflammatory response paralyzes T cells

In a discovery that is likely to rewrite immunology text books, researchers at UC Davis have found that early exposure to inflammatory cytokines, such as interleukin 2, can "paralyze" CD4 T cells, immune components that help ...

Kessler Foundation's Lauren Strober, PhD, explores the association of secondary fatigue and sleep disturbances in multiple sclerosis (MS). "Fatigue in multiple sclerosis: a look at the role of poor sleep" was published in ...

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Both the doctors who treat multiple sclerosis and the people who experience it agree that the disease is highly unpredictable.

They are tiny magic bullets that are quietly shaping the lives of millions of patients around the world. Produced in the lab, invisible to the naked eye, relatively few people are aware of these molecules' existence or where ...

It takes a surprisingly small cluster of brain cells deep within the cerebellum to learn how to serve a tennis ball, or line up a hockey shot. Researchers at McGill University led by Kathleen Cullen from the Department of ...

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Cancer drug maker Celgene said it will buy Receptos for $7.32 billion in cash, gaining a drug Receptos is studying as a treatment for multiple sclerosis and ulcerative colitis.

People living with multiple sclerosis have the dice loaded against them when it comes to their decision-making ability as their neurological disease progresses, according to a new study from the University of Alberta's Faculty ...

Multiple sclerosis (abbreviated to MS, known as disseminated sclerosis or encephalomyelitis disseminata) is an inflammatory disease in which the fatty myelin sheaths around the axons of the brain and spinal cord are damaged, leading to demyelination and scarring as well as a broad spectrum of signs and symptoms. Disease onset usually occurs in young adults, and it is more common in women. It has a prevalence that ranges between 2 and 150 per 100,000. MS was first described in 1868 by Jean-Martin Charcot.

MS affects the ability of nerve cells in the brain and spinal cord to communicate with each other effectively. Nerve cells communicate by sending electrical signals called action potentials down long fibers called axons, which are contained within an insulating substance called myelin. In MS, the body's own immune system attacks and damages the myelin. When myelin is lost, the axons can no longer effectively conduct signals. The name multiple sclerosis refers to scars (sclerosesbetter known as plaques or lesions) particularly in the white matter of the brain and spinal cord, which is mainly composed of myelin. Although much is known about the mechanisms involved in the disease process, the cause remains unknown. Theories include genetics or infections. Different environmental risk factors have also been found.

Almost any neurological symptom can appear with the disease, and often progresses to physical and cognitive disability. MS takes several forms, with new symptoms occurring either in discrete attacks (relapsing forms) or slowly accumulating over time (progressive forms). Between attacks, symptoms may go away completely, but permanent neurological problems often occur, especially as the disease advances.

There is no known cure for multiple sclerosis. Treatments attempt to return function after an attack, prevent new attacks, and prevent disability. MS medications can have adverse effects or be poorly tolerated, and many patients pursue alternative treatments, despite the lack of supporting scientific study. The prognosis is difficult to predict; it depends on the subtype of the disease, the individual patient's disease characteristics, the initial symptoms and the degree of disability the person experiences as time advances. Life expectancy of people with MS is 5 to 10 years lower than that of the unaffected population.

This text uses material from Wikipedia licensed under CC BY-SA

Tracking mobile phone data is often associated with privacy issues, but these vast datasets could be the key to understanding how infectious diseases are spread seasonally, according to a study published in the Proceedings ...

Some people find it difficult to make decisions. In a new study, neuroeconomists from the University of Zurich now reveal that the intensity of the communication between different regions of the brain dictates whether we ...

An international team of scientists headed by biologists at UC San Diego has discovered that an important class of stem cells known as human "induced pluripotent stem cells," or iPSCs, which are derived from an individual's ...

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Medical Xpress - multiple sclerosis

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Multiple sclerosis – Genetics Home Reference

August 20th, 2015

Reviewed April 2013

Multiple sclerosis is a condition characterized by areas of damage (lesions) on the brain and spinal cord. These lesions are associated with destruction of the covering that protects nerves and promotes the efficient transmission of nerve impulses (the myelin sheath) and damage to nerve cells. Multiple sclerosis is considered an autoimmune disorder; autoimmune disorders occur when the immune system malfunctions and attacks the body's own tissues and organs, in this case tissues of the nervous system.

Multiple sclerosis usually begins in early adulthood, between ages 20 and 40. The symptoms vary widely, and affected individuals can experience one or more effects of nervous system damage. Multiple sclerosis often causes sensory disturbances in the limbs, including a prickling or tingling sensation (paresthesia), numbness, pain, and itching. Some people experience Lhermitte sign, which is an electrical shock-like sensation that runs down the back and into the limbs. This sensation usually occurs when the head is bent forward. Problems with muscle control are common in people with multiple sclerosis. Affected individuals may have tremors, muscle stiffness (spasticity), exaggerated reflexes (hyperreflexia), weakness or partial paralysis of the muscles of the limbs, difficulty walking, or poor bladder control. Multiple sclerosis is also associated with vision problems, such as blurred or double vision or partial or complete vision loss. Infections that cause fever can make the symptoms worse.

There are several forms of multiple sclerosis: relapsing-remitting MS, secondary progressive MS, primary progressive MS, and progressive relapsing MS. The most common is the relapsing-remitting form, which affects approximately 80 percent of people with multiple sclerosis. Individuals with this form of the condition have periods during which they experience symptoms, called clinical attacks, followed by periods without any symptoms (remission). The triggers of clinical attacks and remissions are unknown. After about 10 years, relapsing-remitting MS usually develops into another form of the disorder called secondary progressive MS. In this form, there are no remissions, and symptoms of the condition continually worsen.

Primary progressive MS is the next most common form, affecting approximately 10 to 20 percent of people with multiple sclerosis. This form is characterized by constant symptoms that worsen over time, with no clinical attacks or remissions. Primary progressive MS typically begins later than the other forms, around age 40.

Progressive relapsing MS is a rare form of multiple sclerosis that initially appears like primary progressive MS, with constant symptoms. However, people with progressive relapsing MS also experience clinical attacks of more severe symptoms.

An estimated 1.1 to 2.5 million people worldwide have multiple sclerosis. Although the reason is unclear, this condition is more common in regions that are farther away from the equator. In Canada, parts of the northern United States, western and northern Europe, Russia, and southeastern Australia, the condition affects approximately 1 in 2,000 to 2,400 people. It is less common closer to the equator, such as in Asia, sub-Saharan Africa, and parts of South America, where about 1 in 20,000 people are affected. For unknown reasons, most forms of multiple sclerosis affect women twice as often as men; however, women and men are equally affected by primary progressive MS.

Although the cause of multiple sclerosis is unknown, variations in dozens of genes are thought to be involved in multiple sclerosis risk. Changes in the HLA-DRB1 gene are the strongest genetic risk factors for developing multiple sclerosis. Other factors associated with an increased risk of developing multiple sclerosis include changes in the IL7R gene and environmental factors, such as exposure to the Epstein-Barr virus, low levels of vitamin D, and smoking.

The HLA-DRB1 gene belongs to a family of genes called the human leukocyte antigen (HLA) complex. The HLA complex helps the immune system distinguish the body's own proteins from proteins made by foreign invaders (such as viruses and bacteria). Each HLA gene has many different normal variations, allowing each person's immune system to react to a wide range of foreign proteins. Variations in several HLA genes have been associated with increased multiple sclerosis risk, but one particular variant of the HLA-DRB1 gene, called HLA-DRB1*15:01, is the most strongly linked genetic factor.

The IL7R gene provides instructions for making one piece of two different receptor proteins: the interleukin 7 (IL-7) receptor and the thymic stromal lymphopoietin (TSLP) receptor. Both receptors are embedded in the cell membrane of immune cells. These receptors stimulate signaling pathways that induce the growth and division (proliferation) and survival of immune cells. The genetic variation involved in multiple sclerosis leads to production of an IL-7 receptor that is not embedded in the cell membrane but is instead found inside the cell. It is unknown if this variation affects the TSLP receptor.

Because the HLA-DRB1 and IL-7R genes are involved in the immune system, changes in either might be related to the autoimmune response that damages the myelin sheath and nerve cells and leads to the signs and symptoms of multiple sclerosis. However, it is unclear exactly what role variations in either gene plays in development of the condition.

Read more about the HLA-DRB1 and IL7R genes.

See a list of genes associated with multiple sclerosis.

The inheritance pattern of multiple sclerosis is unknown, although the condition does appear to be passed down through generations in families. The risk of developing multiple sclerosis is higher for siblings or children of a person with the condition than for the general population.

These resources address the diagnosis or management of multiple sclerosis and may include treatment providers.

You might also find information on the diagnosis or management of multiple sclerosis in Educational resources and Patient support.

General information about the diagnosis and management of genetic conditions is available in the Handbook.

To locate a healthcare provider, see How can I find a genetics professional in my area? in the Handbook.

You may find the following resources about multiple sclerosis helpful. These materials are written for the general public.

You may also be interested in these resources, which are designed for healthcare professionals and researchers.

For more information about naming genetic conditions, see the Genetics Home Reference Condition Naming Guidelines and How are genetic conditions and genes named? in the Handbook.

The Handbook provides basic information about genetics in clear language.

These links provide additional genetics resources that may be useful.

The resources on this site should not be used as a substitute for professional medical care or advice. Users seeking information about a personal genetic disease, syndrome, or condition should consult with a qualified healthcare professional. See How can I find a genetics professional in my area? in the Handbook.

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Multiple sclerosis - Genetics Home Reference

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Multiple Sclerosis Symptoms, Diagnosis, Treatments and …

August 20th, 2015

Multiple Sclerosis: Introduction

Multiple sclerosis is a progressive autoimmune disease and the most common neurological disease diagnosed in young adults. Multiple sclerosis commonly called MS, attacks the central nervous system and can cause significant nerve damage. The progression and severity of the disease varies greatly between individuals and it can result in a wide variety of effects, from mild to severe and disabling. These include muscle weakness, loss of balance, inability to walk, and paralysis.

The causes of multiple sclerosis are not well understood. Researchers believe that the body's immune system begins to attack its own nervous system, specifically the myelin, a fatty material that covers and insulates the nerve cells in the central nervous system. Healthy myelin is vital to the normal, rapid movement of electrical impulses through the nerve pathways.

In multiple sclerosis, patches of myelin in the brain and spinal cord become inflamed, swell, and develop lesions. Myelin and nerve cells become damaged, which wreck havoc with the normal transmission of electrical impulses.

It is believed that this process may be triggered by a combination of genetic factors and environmental elements, such as exposure to a virus or some infections.

Symptoms of multiple sclerosis can vary greatly between individuals. In the early stages of the disease, symptoms come and go, and people with multiple sclerosis can experience periods of remission, in which symptoms disappear and periods of relapse, in which symptoms reappear. Symptoms may worsen during relapses and complications can include seizures, changes in mentation, muscle spasms, and depression.

Symptoms generally first appear between the ages of 20 and 40 years. Most often, the first symptom is visual changes. Other symptoms may include dizziness, muscle weakness, incoordination, balance problems, fatigue, trembling, abnormal sensations in the extremities, and cognitive impairment, and paralysis. For more information on symptoms, refer to symptoms of multiple sclerosis.

Testing for multiple sclerosis is an involved process because there is no single test that will specifically diagnose the condition. In addition, a definitive diagnosis of multiple sclerosis may often be delayed because early symptoms are often mild, vague, disappear for periods of time, and/or may mimic other conditions. Multiple tests are needed to rule out other conditions that can be confused with multiple sclerosis or that have similar symptoms affecting the nervous system. These include some viral infections, lupus, lime disease, and vitamin deficiencies. For more information on misdiagnosis, refer to misdiagnosis of multiple sclerosis.

A diagnosis of multiple sclerosis is generally made by a neurologist and is made based on the compilation of a thorough neurological history and physical, blood tests, a lumbar puncture, and an MRI, which may show the brain and spinal cord damage and lesions characteristic of multiple sclerosis.

There is no cure for multiple sclerosis, but the disease can be managed and symptoms controlled to various degrees of success with a variety of medications, such as interferons, copolymer, novantrone, natalizumab, corticosteroids, and muscle relaxers. Other therapies include physical therapy, avoiding heat, regular exercise, eating a healthy well-balanced diet and maintaining an optimal weight. Equipment, such as walkers, canes, and braces may also be needed to help maintain independence. For more information on treatment, refer to treatment of multiple sclerosis. ...more

Multiple Sclerosis: Multiple sclerosis is a nerve or spinal cord disease that causes random damage to parts of the nervous system. The result is a diverse range of possible symptoms depending on which parts of the cord are damaged, and how often the inflammation reoccurs. Typical symptoms are any kind of tingling, numbness, burning sensations, "pins-and-needles" or other types of sensory changes in various parts of the body; also possible are vision changes (see a full list of symptoms).

Prognosis of multiple sclerosis is highly variable. Some people have very minor problems, whereas others can end up in a wheelchair, lose vision, or other nasty complications. It just depends which part of the spinal cord or nervous system is attacked. Some people have what is called a "single sclerosis" where there is only one incident of a sclerosis (lesion) on the spinal cord, and this may or may not progress to "multiple" sclerosis.

The cause of multiple sclerosis is an autoimmune disease, which means that the immune system is somehow triggered to mount an attack against its own good cells - in this case the cells that surround nerves. ...more

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Multiple Sclerosis

August 20th, 2015

What Is Multiple Sclerosis? Multiple sclerosis is a disease of the central nervous system (brain and spinal cord) that usually first appears between the ages of 20 and 40, and affects women twice as often as men. Also known as MS, multiple sclerosis is the leading cause of disability among young adults.

An unpredictable disease of the central nervous system, multiple sclerosis can range from being relatively benign to somewhat disabling to devastating as communication between the brain and other parts of the body is disrupted.

Although multiple sclerosis was first diagnosed in 1849, the earliest known description of a person with possible MS dates back to fourteenth-century Holland.

There are four patterns of multiple sclerosis. The more common pattern is an episode of symptoms that lasts for days or weeks followed by a period of no symptoms for weeks or months. This type of multiple sclerosis is called relapsing-remitting MS.

A less common pattern of multiple sclerosis is a steady worsening of symptoms from the first sign of illness. This is called primary-progressive MS.

The two other main forms of multiple sclerosis include secondary-progressive and progressive-relapsing.

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Multiple Sclerosis

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Are People Born Gay? Genetics and Homosexuality

August 20th, 2015

Introduction

There is a common belief among liberals that people are born either gay or straight. Conservatives tend to believe that sexual orientation is actually sexual preference, which is chosen by the individual. This page represents a review of the scientific literature on the basis for homosexual orientation.

Are people born gay or straight? Much of the current media sources assume the question is a solved scientific problem with all the evidence pointing toward a biological (probably genetic) basis for a homosexual orientation. Contrary to this perception, the question has been poorly studied (or studied poorly), although there is some evidence on both sides of question. In addition, many of the initial studies, which were highly touted by the media as "proof" for a biological basis for homosexuality, have been contradicted by later, more thorough studies. This evidence falls into four basic categories:

Until a few years ago, sexual orientation used to be called sexual preference. Obviously, the two terms denote significant differences in the the manner by which sexuality develops. A preference is something that is chosen, whereas orientation is merely something that defines us. The differences are potentially important regarding how the law applies to those who are gay. If homosexuality is not chosen, but actually is a biologically-determined characteristic over which we have no choice, then laws should not treat gays and straights differently, since homosexuality would be equivalent to one's race, over which we have no control.

Since sexual attraction begins in the brain, researchers first examined the question of sexual orientation by comparing the anatomy of brains from males and females. These studies showed that male and female brains showed sexual dimorphism in the pre-optic area of the hypothalamus, where males demonstrated a greater than two-fold difference in cell number and size compared to females.1 A second study found that two of four Interstitial Nuclei of the Anterior Hypothalamus (INAH) were at least twice as large in males as females.2 Since the INAH was involved in sexual dimorphism, it was hypothesized by Simon LeVay that there might be differences in this region in heterosexual vs. homosexual men. Postmortem examination of the brains of AIDS patients vs. control male subjects (presumed to be heterosexual) showed that the presumably heterosexual men exhibited INAH3 that were twice the size of both females and presumably homosexual men who had died of AIDS.3 The study has been criticized for its uncertainty of sexual orientation of the subjects, and potential complications caused by the AIDS virus (which does infect the human brain), and also by lowered testosterone levels found in AIDS patients. A popularized Newsweek cover story, "Is This Child Gay?"4 characterized LeVay as a "champion for the genetic side," even though the study involved no genetic data at all.

A subsequent study by Byne, et al. examined the question of INAH3 size on the basis of sex, sexual orientation, and HIV status.5 The study found large differences in INAH3 volume on the basis of sex (with the male INAH3 being larger than the female INAH3). However, the volume of IHAH3 was decreased in male heterosexual men who had contracted AIDS (0.108 mm3 compared with 0.123 mm3 in male controls). There was no statistically significant difference between IHAH3 sizes of male heterosexuals vs. male homosexuals who had contracted AIDS (0.108 mm3 and 0.096 mm3, respectively). The study also found that there were no differences in the number of neurons in the INAH3 based upon sexual orientation, although researchers found significant differences between males and females, as in other studies.5 It was obvious from this study that LeVay's study was fatally flawed due to the AIDS complication, and that there were no differences in the INAH3 based upon sexual orientation.

The role of the hypothalamus in sexual orientation was further studied by Swaab, et al. Other researchers had hypothesized that differentiation of the hypothalamus occurred before birth. However, Swaab's study showed that the sexually dimorphic nucleus (SDN) of more than 100 subjects decreased in volume and cell number in the females only 2-4 years postnatal. This finding complicated the findings of the brain studies, since not only chemical and hormonal factors, but also social factors, might have influenced this process.6

A study by Allen and Gorski examined the anterior commissure of the brain, finding that females and homosexual males exhibited a larger size than heterosexual males.7 However, later studies using larger sample sizes found no such differences.8

Complicating the issue of brain differences between homosexuals and heterosexuals is the problem that sexual experiences themselves can affect brain structure.9 So, the question will always be whether homosexual practice changes the brain or whether the brain results in homosexual practice.

Since sexual differentiation occurs within the womb, as a result of hormonal influences, it has been hypothesized that homosexuality may result from a differential hormone balance in the wombs of those who eventually exhibit a homosexual orientation. Since hormonal levels within the womb are not available, proxies for hormonal influences have been used to examine the question of how hormonal influences might impact sexual orientation. These proxies include differences in skeletal size and shape, including the ratio of the long bones of the arms and legs relative to arm span or stature and the hand bones of adults (the ratio of the length of the various phalanges).

Studies have shown that ratios of digit length are predictors of several hormones, including testosterone, luteinizing hormone and estrogen.10 In women, the index finger (2D, second digit) is almost the same length as the fourth digit (4D). However, in men, the index finger is usually shorter than the fourth. It has been shown that this greater 2D:4D ratio in females is established in two-year-olds. It has been hypothesized that the sex difference in the 2D:4D ratio reflects the prenatal influence of androgen on males. A study by Williams, et al. showed that the 2D:4D ratio of homosexual men was not significantly different from that of heterosexual men for either hand.11 However, homosexual women displayed significantly smaller 2D:4D ratios compared with heterosexual women (see figure to right). It has been hypothesized that women exposed to more androgens in the womb tend to express a homosexual orientation. However, since these hormone levels were never measured, one is left with the proxy of finger lengths as a substitute. Studies have found that the more older brothers a boy has, the more likely he is to develop a homosexual orientation.12 This study also found that homosexual men had a greater than expected proportion of brothers among their older siblings (229 brothers: 163 sisters) compared with the general population (106 males: 100 females). Males who had two or more older brothers were found to have lower 2D:4D ratios,11 suggesting that they had experienced increased androgens in the womb. Why increased androgens would predispose both males and females to be homosexual was not explained in the study.

Another study examined the length of long bones in the arms, legs and hands. Both homosexual males and heterosexual females had less long bone growth in the arms, legs and hands, than heterosexual males or homosexual females.13 Accordingly, the researchers hypothesized that male homosexuals had less androgen exposure during development than male heterosexuals, while female homosexuals had greater steroid exposure during development than their heterosexual counterparts. Of course, with regard to male homosexuality, this study directly contradicted the presumed results of the Williams study above, which "showed" that males with multiple older brothers (who tended to be homosexual) experienced increased androgen exposure.

A study of one homosexual vs. two heterosexual male triplets found that the homosexual triplets scored more on the female side of the Masculinity-Femininity scale of the Minnesota Multiphasic Personality Inventory,14 suggesting a possible hormonal influence (decreased androgens) involved in male homosexual orientation.

All of the studies reporting possible hormonal influence on homosexuality suffer from the lack of any real evidence that hormones actually play any role in sexual orientation. The fact that contradictory studies report increased11,15 vs. decreased13-14 androgens as a basis for homosexuality doesn't provoke confidence that the proxies are really true. Obviously, a study that documented real hormone levels, as opposed to proxies, would probably provide more definitive data.

Studies involving a rare hormonal imbalance, congenital adrenal hyperplasia (CAH), caused by defective 21-hydroxylase enzyme, suggest that hormonal abnormalities can influence sexual orientation. CAH results in increased production of male hormones during development. In males, increased androgens has little effect. However, female fetuses that develop in this environment develop ambiguous external genitalia, which complicates subsequent development. In utero treatment with dexamethasone reduces the androgen imbalance, resulting in an individual who is genetically and phenotypically female. However, dexamethasone treatment also results in reduced homosexual orientation among treated females,16 suggesting that some homosexuality may result from hormonal influences during development. Homosexual rights groups have suggested that dexamethasone treatment not be given, because it reduces homosexual orientation in females affected by CAH.

The observation that familial factors influence the prevalence of homosexuality led to a the initiation of number of twin studies, which are a proxy for the presence of possible genetic factors. Most of these early studies suffered from methodological flaws. Kallmann sampled subjects from correctional and psychiatric institutionsnot exactly representative "normal" populations.17 Bailey et al. published a number of studies in the early 1990's, examining familial factors involved in both male and female homosexuality. These studies suffered from the manner in which subjects were recruited, since the investigators advertised in openly gay publications, resulting in skewed populations.18 Later studies by the same group did not suffer from this selection bias, and found the heritability of homosexuality in Australia was up to 50 and 60% in females but only 30% in males.19

A study by Kendler et al. in 2000 examined 1,588 twins selected by a random survey of 50,000 households in the United States.20 The study found 3% of the population consisted of non-heterosexuals (homosexuals and bisexuals) and a genetic concordance rate of 32%, somewhat lower than than found in the Australian studies. The study lost statistical significance when twins were broken down into male and female pairs, because of the low rate (3%) of non-heterosexuals in the general U.S. population.

A Finnish twin study reported the "potential for homosexual response," not just overt homosexual behavior, as having a genetic component.21

On a twist on homosexual twin studies, an Australian research group examined the question of whether homophobia was the result of nature or nurture.22 Surprisingly, both familial/environmental and genetic factors seemed to play a role as to whether or not a person was homophobic. Even more surprising, a separate research group in the U.S. confirmed these results (also adding that attitudes towards abortion were also partly genetic).23 Now, even homophobes can claim that they were born that way!

Twin studies suffer from the problem of trying to distinguish between environmental and genetic factors, since twins tend to live within the same family unit. A study examining the effect of birth order on homosexual preference concluded, "The lack of relationship between the strength of the effect and degree of homosexual feelings in the men and women suggests the influence of birth order on homosexual feelings was not due to a biological, but a social process in the subjects studied."12 So, although the twin studies suggest a possible genetic component for homosexual orientation, the results are certainly not definitive.

An examination of family pedigrees revealed that gay men had more homosexual male relatives through maternal than through paternal lineages, suggesting a linkage to the X chromosome. Dean Hamer24 found such an association at region Xq28. If male sexual orientation was influenced by a gene on Xq28, then gay brothers should share more than 50% of their alleles at this region, whereas their heterosexual brothers should share less than 50% of their alleles. In the absence of such an association, then both types of brothers should display 50% allele sharing. An analysis of 40 pairs of gay brothers and found that they shared 82% of their alleles in the Xq28 region, which was much greater than the 50% allele sharing that would be expected by chance.25 However, a follow-up study by the same research group, using 32 pairs of gay brothers and found only 67% allele sharing, which was much closer to the 50% expected by chance.26 Attempts by Rice et al. to repeat the Hamer study resulted in only 46% allele sharing, insignificantly different from chance, contradicting the Hamer results.27 At the same time, an unpublished study by Alan Sanders (University of Chicago) corroborated the Rice results.28 Ultimately, no gene or gene product from the Xq28 region was ever identified that affected sexual orientation. When Jonathan Marks (an evolutionary biologist) asked Hamer what percentage of homosexuality he thought his results explained, his answer was that he thought it explained 5% of male homosexuality. Marks' response was, "There is no science other than behavioral genetics in which you can leave 97.5% of a phenomenon unexplained and get headlines."29

A study of 13,000 New Zealand adults (age 16+) examined sexual orientation as a function of childhood history.30 The study found a 3-fold higher prevalence of childhood abuse for those who subsequently engaged in same sex sexual activity. However, childhood abuse was not a major factor in homosexuality, since only 15% of homosexuals had experienced abuse as children (compared with 5% among heterosexuals).30 So, it would appear from this population that only a small percentage of homosexuality (~10%) might be explained by early childhood abusive experiences.

If homosexual orientation were completely genetic, one would expect that it would not change over the course of one's life. For females, sexual preference does seem to change over time. A 5-year study of lesbians found that over a quarter of these women relinquished their lesbian/bisexual identities during this period: half reclaimed heterosexual identities and half gave up all identity labels.31 In a survey of young minority women (16-23 years of age), half of the participants changed their sexual identities more than once during the two-year survey period.32 In another study of subjects who were recruited from organizations that serve lesbian/gay/bisexual youths (ages 14 to 21 years) in New York City, the percentage that changed from a lesbian/gay/bisexual orientation to a heterosexual orientation was 5% over the period of just 12 months (the length of the survey).33 Other studies have confirmed that sexual orientation is not fixed in all individuals, but can change over time, especially in women.34 A recent example of an orientation change occurred with The Advocate's "Person of the Year" for 2005. Kerry Pacer was the youngest gay advocate, chosen for her initiation of a "gay-straight alliance" at White County High School in Cleveland, Georgia. However, four years later, she is raising her one year old daughter, along with the baby's father.35 Another former lesbian, British comedienne Jackie Clune, spent 12 years in lesbian relationships before marrying a man and producing 4 children.36 Michael Glatze came out at age 20 and went on to be a leader in the homosexual rights movement. At age 30, he came out in the opposite direction, saying, "In my experience, "coming out" from under the influence of the homosexual mindset was the most liberating, beautiful and astonishing thing I've ever experienced in my entire life."37 A 2011 study of Christian gays who wanted to change their sexual orientation found that 23% of the subjects reported a successful "conversion" to heterosexual orientation and functioning, while an additional 30% reported stable behavioral chastity with substantive dis-identification with homosexual orientation.38 However, 20% of the subjects reported giving up on the process and fully embraced a gay identity, while another 27% fell in between the two extremes.38 Obviously, for at least some individuals, being gay or straight is something they can choose.

The question of nature vs. nurture can also be seen by examining children of homosexual vs. heterosexual parents. If homosexuality were purely biological, one would expect that parenting would not influence it. Paul Cameron published a study in 2006 that claimed that the children of homosexual parents expressed a homosexual orientation much more frequently than the general population.39 Although claims of bias were made against the study, another study by Walter Schuum in 2010 confirmed Cameron's results by statistically examining the results of 10 other studies that addressed the question.40 In total, 262 children raised by homosexual parents were included in the analysis. The results showed that 16-57% of such children adopted a homosexual lifestyle. The results were even more striking in daughters of lesbian mothers, 33% to 57% of whom became lesbians themselves. Since homosexuals makeup only ~5% of the population, it is clear that parenting does influence sexual orientation.

It always amazes me when people say that they were born gay. Looking back on my own experience, I would never say that I was "born straight." I really didn't have any interest in females until about the seventh grade. Before that time, they weren't really interesting, since they weren't interested in sports or riding bikes or anything else I liked to do.

I am not a huge fan of Neo Darwinian evolution. Nevertheless, there is some clear evidence that natural selection (and sexual selection) does act upon populations and has acted on our own species to produce racial differences.41 Natural selection postulates that those genetic mutations that favor survival and reproduction will be selected, whereas those that compromise survival and reproduction will be eliminated. Obviously, a gene or series of genes that produce non-reproducing individuals (i.e., those who express pure homosexual behavior) will be rapidly eliminated from any population. So, it would be expected that any "gay gene" would be efficiently removed from a population. However, it is possible that a gene favoring male homosexuality could "hide" within the human genome if it were located on the X-chromosome, where it could be carried by reproducing females, and not be subject to negative selection by non-reproducing males. In order to survive, the gene(s) would be expected to be associated with higher reproductive capacity in women who carry it (compensating for the generation of non-reproducing males). I can't imagine a genetic scenario in which female homosexuality would ever persist within a population.

Within the last decade, genetic analysis of heritable traits has taken a huge step forward with the advent of DNA microarray technology. Using this technology, it is possible to scan large lengths of the human genome (even an entire genome wide scanGWAS) for numerous individuals, at quite reasonable costs. This DNA microarray technology has led to the discovery of genes that are associated with complex diseases, such as Crohn's Disease, which is the topic of my research. If homosexuality truly has a genetic component, DNA microarray studies would not only definitively prove the point, but would identify specific gene(s) or loci that might be associated with those who express a homosexual orientation. The first attempt to do genome wide scans on homosexual males was done by Mustanski et al. in 2005.42 The results suggested possible linkage near microsatellite D7S798 on chromosome 7q36. However, an attempt to repeat the finding (along with ~6000 well-defined SNPs spread comparatively evenly across the human genome) failed to find any significant SNPs.43 However, a third study using Chinese subjects found a weak association at the SHH rs9333613 polymorphism of 7q36.44 A more general study, examining mate choice among different populations, found no genetic link, prompting the investigators to speculate that such choices were "culturally driven."45 The largest genome wide scan was conducted by 23andMe. 7887 unrelated men and 5570 unrelated women of European ancestry were analyzed by GWAS. Although unpublished, the data was presented at the American Society of Human Genetics annual meeting in San Francisco, showing that there were no loci associated with sexual orientation, including Xq28 on the X chromosome.46 So, the preliminary studies on possible genetic causes of homosexual orientation tends to rule out any dramatic genetic component to sexual orientation.

Why are people gay? The question of how homosexual orientation originates has been the subject of much press, with the general impression being promoted that homosexuality is largely a matter of genes, rather than environmental factors. However, if one examines the scientific literature, one finds that it's not quite as clear as the news bytes would suggest. The early studies that reported differences in the brains of homosexuals were complicated by HIV infection and were not substantiated by larger, better controlled studies. Numerous studies reported that possible hormonal differences affected homosexual orientation. However, these studies were often directly contradictory, and never actually measured any hormone levels, but just used proxies for hormonal influences, without direct evidence that the proxies were actually indicative of true hormone levels or imbalances. Twin studies showed that there likely are genetic influences for homosexuality, although similar studies have shown some genetic influences for homophobia and even opposition to abortion. Early childhood abuse has been associated with homosexuality, but, at most, only explains about 10% of those who express a homosexual orientation. The fact that sexual orientation is not constant for many individuals, but can change over time suggests that at least part of sexual orientation is actually sexual preference. Attempts to find a "gay gene" have never identified any gene or gene product that is actually associated with homosexual orientation, with studies failing to confirm early suggestions of linkage of homosexuality to region Xq28 on the X chromosome. The question of genetic influences on sexual orientation has been recently examined using DNA microarray technology, although, the results have largely failed to pinpoint any specific genes as a factor in sexual orientation.

La Gentica y la Homosexualidad: Nace la gente, homosexual?

http://www.godandscience.org/evolution/genetics_of_homosexuality.html Last updated November 25, 2013

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Are People Born Gay? Genetics and Homosexuality

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Researchers create lab-grown brain using human skin cells …

August 20th, 2015

Published August 19, 2015

This image of the lab-grown brain is labeled to show identifiable structures: the cerebral hemisphere, the optic stalk and the cephalic flexure, a bend in the mid-brain region, all characteristic of the human fetal brain.(The Ohio State University)

Researchers at The Ohio State University were able to create a nearly complete human brain that matches the brain maturity of a 5-week-old fetus by using adult human skin cells.

The brain organoid is about the size of a pencil eraser and has an identifiable structure containing 99 percent of the genes present in the human fetal brain, according to a news release. Scientists say its the most complete human brain model yet developed.

It not only looks like the developing brain, its diverse cell types express nearly all genes like a brain, Rene Anand, a professor of biological chemistry and pharmacology at Ohio State, said in a news release. Weve struggled for a long time trying to solve complex brain disease problems that cause tremendous pain and suffering. The power of this brain model bodes very well for human health because it gives us better and more relevant options to test and develop therapeutics other than rodents.

Anand, who began his quest four years ago, studies the association between nicotinic receptors and central nervous system disorders. Hes hopeful that the lab-grown brain will provide ethical and more rapid and accurate testing of experimental drugs before the clinical trial stage.

In central nervous system diseases, this will enable studies of either underlying genetic susceptibility or purely environmental influences, or a combination, Anand said in the news release. Genomic science infers there are up to 600 genes that give rise to autism, but we are stuck there. Mathematical correlations and statistical methods are insufficient to in themselves identify causation. You need an experimental system you need a human brain.

Anand and his team built the model system in 15 weeks, using techniques to convert adult skin cells into pluripotent cells, which are immature cells that can be programmed to become any tissue in the body. They worked to differentiate pluripotent stem cells into cells that are designed to become neural tissue, according to the news release.

While the model lacks a vascular system, it does contain a spinal cord, all major regions of the brain, multiple cell types, signaling circuitry and a retina, according to the news release.

Anand reported on his research at the 2015 Military Health System Research Symposium.

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ETHICAL Stem Cells Grow Human Brain | National Review Online

August 20th, 2015

This is an achievement: Scientists have used skin cells to build a rudimentary human brain. (These were induced pluripotent stem cells.) From The Guardian story:

Though not conscious the miniature brain, which resembles that of a five-week-old foetus, could potentially be useful for scientists who want to study the progression of developmental diseases. It could also be used to test drugs for conditions such as Alzheimers and Parkinsons, since the regions they affect are in place during an early stage of brain development.

The brain, which is about the size of a pencil eraser, is engineered from adult human skin cells and is the most complete human brain model yet developed, claimed Rene Anand of Ohio State University, Columbus, who presented the work today at the Military Health System Research Symposium in Fort Lauderdale, Florida.

May it be so.

Lets analyze what this breakthrough could portend:

1. No need for unethical human cloning to derive cells for use in research and drug testing.

2. No need for fetal farming for experimentation and organ transplants.

3. No need for Planned Parenthood dismemberments of fetuses killed in a less crunchy way in abortion.

Remember when embryonic stem cells were OUR ONLY HOPE?

And that those of us who said that particular meme wasnt true were anti science? Pshaw.

#applause

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ETHICAL Stem Cells Grow Human Brain | National Review Online

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What is Knee Osteoarthritis? | Arthritis-Health

August 19th, 2015

Gradual onset of knee pain, stiffness and swelling are typical symptoms of knee osteoarthritis. Arthritis of the knee comes in several forms. Osteoarthritis is by far the most common form, followed by some forms of inflammatory arthritis, such as rheumatoid arthritis and gout.

While there are many similarities in the symptoms and treatments of knee pain from various types of arthritis, this article focuses on osteoarthritis.

Osteoarthritis involves two primary processes:

Article continues below

This degenerative process can lead to abnormal joint function, pain and stiffness. The osteoarthritic process is gradual, with symptoms that may come and go and eventually worsen over a number of years. One of the primary symptoms of persons with knee osteoarthritis is pain. This pain may follow a pattern, for example:

There are several risk factors that make one more likely to develop the condition. The primary risk factors are advanced age (over age 45), prior knee injury, and excess weight.

This article provides an in-depth review of the symptoms, causes and risk factors, diagnostic process, and surgical and nonsurgical treatments for osteoarthritis of the knee.

The knee is a flexible, weight-bearing joint especially prone to wear-and-tear and therefore likely to be affected by osteoarthritis. According to the Centers for Disease Control and Prevention (CDC), nearly half of Americans may experience the symptoms of knee osteoarthritis at some point during their lives, and it is a leading cause of disability in people over age 50.1

An arthritic knee has thinned, damaged or missing cartilage in the joint. The damaged cartilage is not in and of itself a source of pain or other symptoms. Instead, the damaged or missing cartilage causes friction between bones and other knee problems, which in turn cause knee pain and related symptoms.

Other than some sort of trauma or acute injury, the most common source of pain in the knee joint is arthritis, usually osteoarthritis. Inflammatory arthritis, such as rheumatoid arthritis or gout, are less common.

In an osteoarthritic knee, the articular cartilage is thinned, damaged or entirely worn away. When the knee cartilage has deteriorated in such a manner, the following process ensues:

It is important to note that cartilage does not contain nerves, so damaged cartilage is not the primary source of pain in knee osteoarthritis. Likewise, bone spurs are a normal sign of aging and the presence of bone spurs alone are not a cause for concern. However, the friction between bones and other resulting abnormalities in the knee can cause discomfort and pain.

Chronic knee discomfort and/or minor pain may warrant evaluation, since an appropriate treatment program can encourage healthy joint function and minimize or halt the progression of symptoms. As a general rule, if the osteoarthritis is diagnosed and treated early in the disease process, health care professionals believe that the outcome will be better for the patient in terms of less pain and fewer complications.

References:

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What is Knee Osteoarthritis? | Arthritis-Health

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Symptoms of Knee osteoarthritis – RightDiagnosis.com

August 19th, 2015

Symptoms of Knee osteoarthritis

The list of signs and symptoms mentioned in various sources for Knee osteoarthritis includes the 16 symptoms listed below:

Research symptoms & diagnosis of Knee osteoarthritis:

Review the available symptom checkers for these symptoms of Knee osteoarthritis:

Review the available Assessment Questionnaires for the symptoms of Knee osteoarthritis:

Do I have Knee osteoarthritis?

Diseases that may be commonly undiagnosed in related medical areas:

Home medical tests related to Knee osteoarthritis:

Research all specialists including ratings, affiliations, and sanctions.

More information about symptoms of Knee osteoarthritis and related conditions:

Click on any of the symptoms below to see a full list of other causes including diseases, medical conditions, toxins, drug interactions, or drug side effect causes of that symptom.

Onset of Knee osteoarthritis: Symptoms usually start after the age of 45 but can occur in younger people.

These general reference articles may be of interest in relation to medical signs and symptoms of disease in general:

Full list of premium articles on symptoms and diagnosis

The symptom information on this page attempts to provide a list of some possible signs and symptoms of Knee osteoarthritis. This signs and symptoms information for Knee osteoarthritis has been gathered from various sources, may not be fully accurate, and may not be the full list of Knee osteoarthritis signs or Knee osteoarthritis symptoms. Furthermore, signs and symptoms of Knee osteoarthritis may vary on an individual basis for each patient. Only your doctor can provide adequate diagnosis of any signs or symptoms and whether they are indeed Knee osteoarthritis symptoms.

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About Knee Osteoarthritis – Causes, Symptoms & Diagnosis …

August 19th, 2015

Indication

Synvisc-One (hylan G-F 20) is indicated for the treatment of pain in osteoarthritis (OA) of the knee in patients who have failed to respond adequately to conservative non-pharmacologic therapy and simple analgesics, e.g., acetaminophen.

Before trying Synvisc-One, tell your doctor if you have had an allergic reaction, such as swelling of the face, tongue or throat, respiratory difficulty, rash, itching or hives to SYNVISC or any hyaluronan-based products. Allergic reactions, some which can be potentially severe, have been reported during the use of Synvisc-One. Should not be used in patients with an infected knee joint, skin disease or infection around the area where the injection will be given, and should be used with caution when there is swelling of the legs due to problems with venous stasis or lymphatic drainage.

Synvisc-One is only for injection into the knee, performed by a doctor or other qualified health care professional. Synvisc-One has not been tested to show pain relief in joints other than the knee. Tell your doctor if you are allergic to products from birds such as feathers, eggs or poultry or if your leg is swollen or infected.

Synvisc-One has not been tested in children (21years old), pregnant women or women who are nursing. You should tell your doctor if you think you are pregnant or if you are nursing a child.

Talk to your doctor before resuming strenuous weight-bearing activities after treatment.

The side effects sometimes seen after Synvisc-One include (<2% each): pain, swelling, heat, redness, and/or fluid build-up in or around the knee. Tell your doctor if you experience any side effects after treatment with Synvisc-One.

View the Complete Prescribing Information for Synvisc-One

SYNVISC (hylan G-F 20) is used to relieve knee pain due to osteoarthritis (OA). It is for patients who do not get enough relief from simple painkillers such as acetaminophen, or from exercise and physical therapy.

Before trying SYNVISC, tell your doctor if you have had an allergic reaction, such as swelling of the face, tongue or throat, respiratory difficulty, rash, itching or hives to SYNVISC or any hyaluronan-based products. Serious allergic reactions have been reported. Should not be used in patients with an infected knee joint, skin disease or infection around the area where the injection will be given, or circulatory problems in the legs.

SYNVISC is only for injection into the knee, performed by a doctor or other qualified health care professional. SYNVISC has not been tested to show pain relief in joints other than the knee. Tell your doctor if you are allergic to products from birds - such as feathers, eggs or poultry - or if your leg is swollen or infected.

SYNVISC has not been tested in children (21years old), pregnant women or women who are nursing. You should tell your doctor if you think you are pregnant or if you are nursing a child. Talk to your doctor before resuming strenuous weight-bearing activities after treatment.

The side effects sometimes seen after SYNVISC include pain, swelling, heat, redness, and/or fluid buildup in or around the knee. These reactions were generally mild and did not last long, but in rare occasions these side effects were more severe. The most commonly occurring adverse events outside of the injected knee were rash, fever, nausea, and headache.

View the Complete Prescribing Information for SYNVISC

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History of biotechnology – Wikipedia, the free encyclopedia

August 18th, 2015

Biotechnology is the application of scientific and engineering principles to the processing of materials by biological agents to provide goods and services.[1] From its inception, biotechnology has maintained a close relationship with society. Although now most often associated with the development of drugs, historically biotechnology has been principally associated with food, addressing such issues as malnutrition and famine. The history of biotechnology begins with zymotechnology, which commenced with a focus on brewing techniques for beer. By World War I, however, zymotechnology would expand to tackle larger industrial issues, and the potential of industrial fermentation gave rise to biotechnology. However, both the single-cell protein and gasohol projects failed to progress due to varying issues including public resistance, a changing economic scene, and shifts in political power.

Yet the formation of a new field, genetic engineering, would soon bring biotechnology to the forefront of science in society, and the intimate relationship between the scientific community, the public, and the government would ensue. These debates gained exposure in 1975 at the Asilomar Conference, where Joshua Lederberg was the most outspoken supporter for this emerging field in biotechnology. By as early as 1978, with the synthesis of synthetic human insulin, Lederberg's claims would prove valid, and the biotechnology industry grew rapidly. Each new scientific advance became a media event designed to capture public support, and by the 1980s, biotechnology grew into a promising real industry. In 1988, only five proteins from genetically engineered cells had been approved as drugs by the United States Food and Drug Administration (FDA), but this number would skyrocket to over 125 by the end of the 1990s.

The field of genetic engineering remains a heated topic of discussion in today's society with the advent of gene therapy, stem cell research, cloning, and genetically modified food. While it seems only natural nowadays to link pharmaceutical drugs as solutions to health and societal problems, this relationship of biotechnology serving social needs began centuries ago.

Biotechnology arose from the field of zymotechnology or zymurgy, which began as a search for a better understanding of industrial fermentation, particularly beer. Beer was an important industrial, and not just social, commodity. In late 19th century Germany, brewing contributed as much to the gross national product as steel, and taxes on alcohol proved to be significant sources of revenue to the government.[2] In the 1860s, institutes and remunerative consultancies were dedicated to the technology of brewing. The most famous was the private Carlsberg Institute, founded in 1875, which employed Emil Christian Hansen, who pioneered the pure yeast process for the reliable production of consistent beer. Less well known were private consultancies that advised the brewing industry. One of these, the Zymotechnic Institute, was established in Chicago by the German-born chemist John Ewald Siebel.

The heyday and expansion of zymotechnology came in World War I in response to industrial needs to support the war. Max Delbrck grew yeast on an immense scale during the war to meet 60 percent of Germany's animal feed needs.[3] Compounds of another fermentation product, lactic acid, made up for a lack of hydraulic fluid, glycerol. On the Allied side the Russian chemist Chaim Weizmann used starch to eliminate Britain's shortage of acetone, a key raw material in explosives, by fermenting maize to acetone. The industrial potential of fermentation was outgrowing its traditional home in brewing, and "zymotechnology" soon gave way to "biotechnology."

With food shortages spreading and resources fading, some dreamed of a new industrial solution. The Hungarian Kroly Ereky coined the word "biotechnology" in Hungary during 1919 to describe a technology based on converting raw materials into a more useful product. He built a slaughterhouse for a thousand pigs and also a fattening farm with space for 50,000 pigs, raising over 100,000 pigs a year. The enterprise was enormous, becoming one of the largest and most profitable meat and fat operations in the world. In a book entitled Biotechnologie, Ereky further developed a theme that would be reiterated through the 20th century: biotechnology could provide solutions to societal crises, such as food and energy shortages. For Ereky, the term "biotechnologie" indicated the process by which raw materials could be biologically upgraded into socially useful products.[4]

This catchword spread quickly after the First World War, as "biotechnology" entered German dictionaries and was taken up abroad by business-hungry private consultancies as far away as the United States. In Chicago, for example, the coming of prohibition at the end of World War I encouraged biological industries to create opportunities for new fermentation products, in particular a market for nonalcoholic drinks. Emil Siebel, the son of the founder of the Zymotechnic Institute, broke away from his father's company to establish his own called the "Bureau of Biotechnology," which specifically offered expertise in fermented nonalcoholic drinks.[5]

The belief that the needs of an industrial society could be met by fermenting agricultural waste was an important ingredient of the "chemurgic movement."[6] Fermentation-based processes generated products of ever-growing utility. In the 1940s, penicillin was the most dramatic. While it was discovered in England, it was produced industrially in the U.S. using a deep fermentation process originally developed in Peoria, Illinois. The enormous profits and the public expectations penicillin engendered caused a radical shift in the standing of the pharmaceutical industry. Doctors used the phrase "miracle drug", and the historian of its wartime use, David Adams, has suggested that to the public penicillin represented the perfect health that went together with the car and the dream house of wartime American advertising.[7] In the 1950s, steroids were synthesized using fermentation technology. In particular, cortisone promised the same revolutionary ability to change medicine as penicillin had.

Even greater expectations of biotechnology were raised during the 1960s by a process that grew single-cell protein. When the so-called protein gap threatened world hunger, producing food locally by growing it from waste seemed to offer a solution. It was the possibilities of growing microorganisms on oil that captured the imagination of scientists, policy makers, and commerce.[8] Major companies such as British Petroleum (BP) staked their futures on it. In 1962, BP built a pilot plant at Cap de Lavera in Southern France to publicize its product, Toprina.[9] Initial research work at Lavera was done by Alfred Champagnat,[10] In 1963, construction started on BP's second pilot plant at Grangemouth Oil Refinery in Britain.[10]

As there was no well-accepted term to describe the new foods, in 1966 the term "single-cell protein" (SCP) was coined at MIT to provide an acceptable and exciting new title, avoiding the unpleasant connotations of microbial or bacterial.[9]

The "food from oil" idea became quite popular by the 1970s, when facilities for growing yeast fed by n-paraffins were built in a number of countries. The Soviets were particularly enthusiastic, opening large "BVK" (belkovo-vitaminny kontsentrat, i.e., "protein-vitamin concentrate") plants next to their oil refineries in Kstovo (1973) [11][12][13] and Kirishi (1974).[14]

By the late 1970s, however, the cultural climate had completely changed, as the growth in SCP interest had taken place against a shifting economic and cultural scene (136). First, the price of oil rose catastrophically in 1974, so that its cost per barrel was five times greater than it had been two years earlier. Second, despite continuing hunger around the world, anticipated demand also began to shift from humans to animals. The program had begun with the vision of growing food for Third World people, yet the product was instead launched as an animal food for the developed world. The rapidly rising demand for animal feed made that market appear economically more attractive. The ultimate downfall of the SCP project, however, came from public resistance.[15]

This was particularly vocal in Japan, where production came closest to fruition. For all their enthusiasm for innovation and traditional interest in microbiologically produced foods, the Japanese were the first to ban the production of single-cell proteins. The Japanese ultimately were unable to separate the idea of their new "natural" foods from the far from natural connotation of oil.[15] These arguments were made against a background of suspicion of heavy industry in which anxiety over minute traces of petroleum was expressed. Thus, public resistance to an unnatural product led to the end of the SCP project as an attempt to solve world hunger.

Also, in 1989 in the USSR, the public environmental concerns made the government decide to close down (or convert to different technologies) all 8 paraffin-fed-yeast plants that the Soviet Ministry of Microbiological Industry had by that time.[14]

In the late 1970s, biotechnology offered another possible solution to a societal crisis. The escalation in the price of oil in 1974 increased the cost of the Western world's energy tenfold.[16] In response, the U.S. government promoted the production of gasohol, gasoline with 10 percent alcohol added, as an answer to the energy crisis.[7] In 1979, when the Soviet Union sent troops to Afghanistan, the Carter administration cut off its supplies to agricultural produce in retaliation, creating a surplus of agriculture in the U.S. As a result, fermenting the agricultural surpluses to synthesize fuel seemed to be an economical solution to the shortage of oil threatened by the Iran-Iraq war. Before the new direction could be taken, however, the political wind changed again: the Reagan administration came to power in January 1981 and, with the declining oil prices of the 1980s, ended support for the gasohol industry before it was born.[17]

Biotechnology seemed to be the solution for major social problems, including world hunger and energy crises. In the 1960s, radical measures would be needed to meet world starvation, and biotechnology seemed to provide an answer. However, the solutions proved to be too expensive and socially unacceptable, and solving world hunger through SCP food was dismissed. In the 1970s, the food crisis was succeeded by the energy crisis, and here too, biotechnology seemed to provide an answer. But once again, costs proved prohibitive as oil prices slumped in the 1980s. Thus, in practice, the implications of biotechnology were not fully realized in these situations. But this would soon change with the rise of genetic engineering.

The origins of biotechnology culminated with the birth of genetic engineering. There were two key events that have come to be seen as scientific breakthroughs beginning the era that would unite genetics with biotechnology. One was the 1953 discovery of the structure of DNA, by Watson and Crick, and the other was the 1973 discovery by Cohen and Boyer of a recombinant DNA technique by which a section of DNA was cut from the plasmid of an E. coli bacterium and transferred into the DNA of another.[18] This approach could, in principle, enable bacteria to adopt the genes and produce proteins of other organisms, including humans. Popularly referred to as "genetic engineering," it came to be defined as the basis of new biotechnology.

Genetic engineering proved to be a topic that thrust biotechnology into the public scene, and the interaction between scientists, politicians, and the public defined the work that was accomplished in this area. Technical developments during this time were revolutionary and at times frightening. In December 1967, the first heart transplant by Christian Barnard reminded the public that the physical identity of a person was becoming increasingly problematic. While poetic imagination had always seen the heart at the center of the soul, now there was the prospect of individuals being defined by other people's hearts.[19] During the same month, Arthur Kornberg announced that he had managed to biochemically replicate a viral gene. "Life had been synthesized," said the head of the National Institutes of Health.[19] Genetic engineering was now on the scientific agenda, as it was becoming possible to identify genetic characteristics with diseases such as beta thalassemia and sickle-cell anemia.

Responses to scientific achievements were colored by cultural skepticism. Scientists and their expertise were looked upon with suspicion. In 1968, an immensely popular work, The Biological Time Bomb, was written by the British journalist Gordon Rattray Taylor. The author's preface saw Kornberg's discovery of replicating a viral gene as a route to lethal doomsday bugs. The publisher's blurb for the book warned that within ten years, "You may marry a semi-artificial man or womanchoose your children's sextune out painchange your memoriesand live to be 150 if the scientific revolution doesnt destroy us first."[20] The book ended with a chapter called "The Future If Any." While it is rare for current science to be represented in the movies, in this period of "Star Trek", science fiction and science fact seemed to be converging. "Cloning" became a popular word in the media. Woody Allen satirized the cloning of a person from a nose in his 1973 movie Sleeper, and cloning Adolf Hitler from surviving cells was the theme of the 1976 novel by Ira Levin, The Boys from Brazil.[21]

In response to these public concerns, scientists, industry, and governments increasingly linked the power of recombinant DNA to the immensely practical functions that biotechnology promised. One of the key scientific figures that attempted to highlight the promising aspects of genetic engineering was Joshua Lederberg, a Stanford professor and Nobel laureate. While in the 1960s "genetic engineering" described eugenics and work involving the manipulation of the human genome, Lederberg stressed research that would involve microbes instead.[22] Lederberg emphasized the importance of focusing on curing living people. Lederberg's 1963 paper, "Biological Future of Man" suggested that, while molecular biology might one day make it possible to change the human genotype, "what we have overlooked is euphenics, the engineering of human development."[23] Lederberg constructed the word "euphenics" to emphasize changing the phenotype after conception rather than the genotype which would affect future generations.

With the discovery of recombinant DNA by Cohen and Boyer in 1973, the idea that genetic engineering would have major human and societal consequences was born. In July 1974, a group of eminent molecular biologists headed by Paul Berg wrote to Science suggesting that the consequences of this work were so potentially destructive that there should be a pause until its implications had been thought through.[24] This suggestion was explored at a meeting in February 1975 at California's Monterey Peninsula, forever immortalized by the location, Asilomar. Its historic outcome was an unprecedented call for a halt in research until it could be regulated in such a way that the public need not be anxious, and it led to a 16-month moratorium until National Institutes of Health (NIH) guidelines were established.

Joshua Lederberg was the leading exception in emphasizing, as he had for years, the potential benefits. At Asilomar, in an atmosphere favoring control and regulation, he circulated a paper countering the pessimism and fears of misuses with the benefits conferred by successful use. He described "an early chance for a technology of untold importance for diagnostic and therapeutic medicine: the ready production of an unlimited variety of human proteins. Analogous applications may be foreseen in fermentation process for cheaply manufacturing essential nutrients, and in the improvement of microbes for the production of antibiotics and of special industrial chemicals."[25] In June 1976, the 16-month moratorium on research expired with the Director's Advisory Committee (DAC) publication of the NIH guidelines of good practice. They defined the risks of certain kinds of experiments and the appropriate physical conditions for their pursuit, as well as a list of things too dangerous to perform at all. Moreover, modified organisms were not to be tested outside the confines of a laboratory or allowed into the environment.[18]

Atypical as Lederberg was at Asilomar, his optimistic vision of genetic engineering would soon lead to the development of the biotechnology industry. Over the next two years, as public concern over the dangers of recombinant DNA research grew, so too did interest in its technical and practical applications. Curing genetic diseases remained in the realms of science fiction, but it appeared that producing human simple proteins could be good business. Insulin, one of the smaller, best characterized and understood proteins, had been used in treating type 1 diabetes for a half century. It had been extracted from animals in a chemically slightly different form from the human product. Yet, if one could produce synthetic human insulin, one could meet an existing demand with a product whose approval would be relatively easy to obtain from regulators. In the period 1975 to 1977, synthetic "human" insulin represented the aspirations for new products that could be made with the new biotechnology. Microbial production of synthetic human insulin was finally announced in September 1978 and was produced by a startup company, Genentech.,[26] although that company did not commercialize the product themselves, instead, it licensed the production method to Eli Lilly and Company. 1978 also saw the first application for a patent on a gene, the gene which produces human growth hormone, by the University of California, thus introducing the legal principle that genes could be patented. Since that filing, almost 20% of the more than 20,000 genes in the human DNA have been patented.[27]

The radical shift in the connotation of "genetic engineering" from an emphasis on the inherited characteristics of people to the commercial production of proteins and therapeutic drugs was nurtured by Joshua Lederberg. His broad concerns since the 1960s had been stimulated by enthusiasm for science and its potential medical benefits. Countering calls for strict regulation, he expressed a vision of potential utility. Against a belief that new techniques would entail unmentionable and uncontrollable consequences for humanity and the environment, a growing consensus on the economic value of recombinant DNA emerged.

With ancestral roots in industrial microbiology that date back centuries, the new biotechnology industry grew rapidly beginning in the mid-1970s. Each new scientific advance became a media event designed to capture investment confidence and public support.[28] Although market expectations and social benefits of new products were frequently overstated, many people were prepared to see genetic engineering as the next great advance in technological progress. By the 1980s, biotechnology characterized a nascent real industry, providing titles for emerging trade organizations such as the Biotechnology Industry Organization (BIO).

The main focus of attention after insulin were the potential profit makers in the pharmaceutical industry: human growth hormone and what promised to be a miraculous cure for viral diseases, interferon. Cancer was a central target in the 1970s because increasingly the disease was linked to viruses.[29] By 1980, a new company, Biogen, had produced interferon through recombinant DNA. The emergence of interferon and the possibility of curing cancer raised money in the community for research and increased the enthusiasm of an otherwise uncertain and tentative society. Moreover, to the 1970s plight of cancer was added AIDS in the 1980s, offering an enormous potential market for a successful therapy, and more immediately, a market for diagnostic tests based on monoclonal antibodies.[30] By 1988, only five proteins from genetically engineered cells had been approved as drugs by the United States Food and Drug Administration (FDA): synthetic insulin, human growth hormone, hepatitis B vaccine, alpha-interferon, and tissue plasminogen activator (TPa), for lysis of blood clots. By the end of the 1990s, however, 125 more genetically engineered drugs would be approved.[30]

Genetic engineering also reached the agricultural front as well. There was tremendous progress since the market introduction of the genetically engineered Flavr Savr tomato in 1994.[31] Ernst and Young reported that in 1998, 30% of the U.S. soybean crop was expected to be from genetically engineered seeds. In 1998, about 30% of the US cotton and corn crops were also expected to be products of genetic engineering.[31]

Genetic engineering in biotechnology stimulated hopes for both therapeutic proteins, drugs and biological organisms themselves, such as seeds, pesticides, engineered yeasts, and modified human cells for treating genetic diseases. From the perspective of its commercial promoters, scientific breakthroughs, industrial commitment, and official support were finally coming together, and biotechnology became a normal part of business. No longer were the proponents for the economic and technological significance of biotechnology the iconoclasts.[32] Their message had finally become accepted and incorporated into the policies of governments and industry.

According to Burrill and Company, an industry investment bank, over $350 billion has been invested in biotech since the emergence of the industry, and global revenues rose from $23 billion in 2000 to more than $50 billion in 2005. The greatest growth has been in Latin America but all regions of the world have shown strong growth trends. By 2007 and into 2008, though, a downturn in the fortunes of biotech emerged, at least in the United Kingdom, as the result of declining investment in the face of failure of biotech pipelines to deliver and a consequent downturn in return on investment.[33]

There has been little innovation in the traditional pharmaceutical industry over the past decade and biopharmaceuticals are now achieving the fastest rates of growth against this background, particularly in breast cancer treatment. Biopharmaceuticals typically treat sub-sets of the total population with a disease whereas traditional drugs are developed to treat the population as a whole. However, one of the great difficulties with traditional drugs are the toxic side effects the incidence of which can be unpredictable in individual patients.

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What are the potential uses of human stem cells and the …

August 17th, 2015

There are many ways in which human stem cells can be used in research and the clinic. Studies of human embryonic stem cells will yield information about the complex events that occur during human development. A primary goal of this work is to identify how undifferentiated stem cells become the differentiated cells that form the tissues and organs. Scientists know that turning genes on and off is central to this process. Some of the most serious medical conditions, such as cancer and birth defects, are due to abnormal cell division and differentiation. A more complete understanding of the genetic and molecular controls of these processes may yield information about how such diseases arise and suggest new strategies for therapy. Predictably controlling cell proliferation and differentiation requires additional basic research on the molecular and genetic signals that regulate cell division and specialization. While recent developments with iPS cells suggest some of the specific factors that may be involved, techniques must be devised to introduce these factors safely into the cells and control the processes that are induced by these factors.

Human stem cells are currently being used to test new drugs. New medications are tested for safety on differentiated cells generated from human pluripotent cell lines. Other kinds of cell lines have a long history of being used in this way. Cancer cell lines, for example, are used to screen potential anti-tumor drugs. The availability of pluripotent stem cells would allow drug testing in a wider range of cell types. However, to screen drugs effectively, the conditions must be identical when comparing different drugs. Therefore, scientists must be able to precisely control the differentiation of stem cells into the specific cell type on which drugs will be tested. For some cell types and tissues, current knowledge of the signals controlling differentiation falls short of being able to mimic these conditions precisely to generate pure populations of differentiated cells for each drug being tested.

Perhaps the most important potential application of human stem cells is the generation of cells and tissues that could be used for cell-based therapies. Today, donated organs and tissues are often used to replace ailing or destroyed tissue, but the need for transplantable tissues and organs far outweighs the available supply. Stem cells, directed to differentiate into specific cell types, offer the possibility of a renewable source of replacement cells and tissues to treat diseases including maculardegeneration, spinal cord injury, stroke, burns, heart disease, diabetes, osteoarthritis, and rheumatoid arthritis.

Figure 3. Strategies to repair heart muscle with adult stem cells. Click here for larger image.

2008 Terese Winslow

For example, it may become possible to generate healthy heart muscle cells in the laboratory and then transplant those cells into patients with chronic heart disease. Preliminary research in mice and other animals indicates that bone marrow stromal cells, transplanted into a damaged heart, can have beneficial effects. Whether these cells can generate heart muscle cells or stimulate the growth of new blood vessels that repopulate the heart tissue, or help via some other mechanism is actively under investigation. For example, injected cells may accomplish repair by secreting growth factors, rather than actually incorporating into the heart. Promising results from animal studies have served as the basis for a small number of exploratory studies in humans (for discussion, see call-out box, "Can Stem Cells Mend a Broken Heart?"). Other recent studies in cell culture systems indicate that it may be possible to direct the differentiation of embryonic stem cells or adult bone marrow cells into heart muscle cells (Figure 3).

Cardiovascular disease (CVD), which includes hypertension, coronary heart disease, stroke, and congestive heart failure, has ranked as the number one cause of death in the United States every year since 1900 except 1918, when the nation struggled with an influenza epidemic. Nearly 2,600 Americans die of CVD each day, roughly one person every 34 seconds. Given the aging of the population and the relatively dramatic recent increases in the prevalence of cardiovascular risk factors such as obesity and type 2 diabetes, CVD will be a significant health concern well into the 21st century.

Cardiovascular disease can deprive heart tissue of oxygen, thereby killing cardiac muscle cells (cardiomyocytes). This loss triggers a cascade of detrimental events, including formation of scar tissue, an overload of blood flow and pressure capacity, the overstretching of viable cardiac cells attempting to sustain cardiac output, leading to heart failure, and eventual death. Restoring damaged heart muscle tissue, through repair or regeneration, is therefore a potentially new strategy to treat heart failure.

The use of embryonic and adult-derived stem cells for cardiac repair is an active area of research. A number of stem cell types, including embryonic stem (ES) cells, cardiac stem cells that naturally reside within the heart, myoblasts (muscle stem cells), adult bone marrow-derived cells including mesenchymal cells (bone marrow-derived cells that give rise to tissues such as muscle, bone, tendons, ligaments, and adipose tissue), endothelial progenitor cells (cells that give rise to the endothelium, the interior lining of blood vessels), and umbilical cord blood cells, have been investigated as possible sources for regenerating damaged heart tissue. All have been explored in mouse or rat models, and some have been tested in larger animal models, such as pigs.

A few small studies have also been carried out in humans, usually in patients who are undergoing open-heart surgery. Several of these have demonstrated that stem cells that are injected into the circulation or directly into the injured heart tissue appear to improve cardiac function and/or induce the formation of new capillaries. The mechanism for this repair remains controversial, and the stem cells likely regenerate heart tissue through several pathways. However, the stem cell populations that have been tested in these experiments vary widely, as do the conditions of their purification and application. Although much more research is needed to assess the safety and improve the efficacy of this approach, these preliminary clinical experiments show how stem cells may one day be used to repair damaged heart tissue, thereby reducing the burden of cardiovascular disease.

In people who suffer from type1 diabetes, the cells of the pancreas that normally produce insulin are destroyed by the patient's own immune system. New studies indicate that it may be possible to direct the differentiation of human embryonic stem cells in cell culture to form insulin-producing cells that eventually could be used in transplantation therapy for persons with diabetes.

To realize the promise of novel cell-based therapies for such pervasive and debilitating diseases, scientists must be able to manipulate stem cells so that they possess the necessary characteristics for successful differentiation, transplantation, and engraftment. The following is a list of steps in successful cell-based treatments that scientists will have to learn to control to bring such treatments to the clinic. To be useful for transplant purposes, stem cells must be reproducibly made to:

Also, to avoid the problem of immune rejection, scientists are experimenting with different research strategies to generate tissues that will not be rejected.

To summarize, stem cells offer exciting promise for future therapies, but significant technical hurdles remain that will only be overcome through years of intensive research.

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Hypopituitarism Symptoms and Treatment | Hormone Health …

August 17th, 2015

What is hypopituitarism?

Hypopituitarism (also called pituitary insufficiency) is a rare condition in which your pituitary gland doesnt make enough of certain hormones. Your body cant work properly when important glands, such as your thyroid gland and adrenal gland, dont get the hormones they need from your pituitary gland.

The pituitary gland is a pea-sized gland found at the base of your brain. It is called the master gland because it affects the action of many other important glands that produce their own hormones. The pituitary gland affects almost all parts of your body.

Hypopituitarism can develop very slowly, over several months or even over several years.

Hypopituitarism can be caused by

Sometimes, the cause is unknown.

Symptoms can include one or more of the following:

Your doctor will check your hormone levels with blood tests. You may have other tests, such as an MRI of your pituitary gland, to help find the cause of your hypopituitarism.

Treatment usually includes taking the hormones youre missing, sometimes for life. Your doctor also will teach you how to take extra cortisone (a hormone) when you are sick or under stress. If a tumor is causing your hypopituitarism, you might need surgery to remove it and/or possibly radiation treatment. If needed, you can take medicine for infertility.

You will need to get regular check-ups. Its wise to wear medical identification, such as a bracelet or pendant, which provides information about your condition in case of an emergency.

You can expect a normal life span, as long as you regularly take the medications recommended by your doctor.

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Heart Stem Cell Therapy | University of Utah Health Care

August 16th, 2015

Keeping in tradition with the Us commitment to advance the fields of medicine and surgery, our physicians are focusing on regenerative medicine as the next frontier in treating cardiovascular disease. Researchers within the Cardiovascular Center estimate cell therapy will be FDA-approved within three years. The goal of this therapy is to give cells back to the heart in order for it to grow stronger, work harder, and function more like a younger heart. Currently, studies include the potentiality of injecting cardiac repair cells into patients hearts to improve function.

This is the first trial of its kind in the United States, providing heart patients who have limited or no other options with a viable treatment. Using some of the best imaging technology, researchers have been able to see improvements in patients within six months after injecting their own cells directly into the left ventricle of the heart during minimally invasive surgery.

To contact us, please use the contact number provided.

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Stem cell and skin care. | Esthetics Association Florida

August 15th, 2015

It is astonishing how the cosmetic industry uses medical discoveries and put these formulas into skin cream jars.

In 2009 the American company Voss laboratories was the first that introduced stem cell active ingredients into a cosmetic product. Due to the fact that the company didnt reveal their secret ingredients, it created a worldwide rumor that the company might be using human stem cells.

The world started to question if this would be ethical and safe.

Coming from the medical stand point: with human stem cells you can actually build and rebuild human organs but also carcinogenic cell. For that reason it created great concerns.

Now days many trendsetting companies producing stem cell creams and serums that dont use human stem cells

Stem cells are a class of undifferentiated cells that are able to differentiate into specialized cell types

Adult or somatic stem cells exist throughout the body after embryonic development and are found inside of different types of tissue. These stem cells have been found in tissues such as the brain, bone marrow, blood, blood vessels, skeletal muscles, liver, and the Skin ( basal layer and fat layer) . They remain in a quiescent or non-dividing state for years until activated by disease or tissue injury.

Adult stem cells can divide ( copy) or self-renew indefinitely, enabling them to generate a range of cell types from the originating organ or even regenerates the entire original organ.

Plant Stem Cells benefits human skin.

Stem cells from a rare red grape variety provide the basis for Israel based company On-Macabim latest skin care ingredient.

This variety is one of the few red grapes that have red flesh and juice the majority have red skin but white flesh and juice which is due to the high quantity of anthocyanins in the fruit.

The anthocyanins, also present in the flesh, leading to higher antioxidant levels overall.

The technology was developed last year and allows to extract stem cells from the plant which can then be formulated into a cosmetic ingredient to help protect the stem cells in human skin.

To harvest the stem cells the company first induces a wound in the plant which causes the surrounding cells to dedifferentiate (turn back into stem cells) and form a wound healing tissue called a callus.

Once the wound has healed these cells can differentiate again and build new tissue

According to On-macabim, these plant stem cells contain components and epigenetic factors that can protect human skin stem cells form UV radiation, inflammation, oxidative stress, neutralize free radicals and reverse the effects of photoaging.

Stem cells are found in the epidermal layer of the skin and are involved in skin growth and regeneration. If they are harmed by UV radiation,

their power to regenerate will be jeopardized.

Grape stem cells have the ability to promote healthy skin proliferation.

Grape Stem Cells Counteract Negative

Effects of UV Radiation on

Skin Stem Cells

In an in-vitro study, skin stem cells were treated with and without

the Grape Stem Cells.

Some were exposed to UVA+UVB-light; others were unexposed.

CFE was determined in each case.

Results confirmed that cells treated with the Grape Stem Cells increased

the CFE of the skin stem cells. A 58% decrease in CFE was observed

when skin stem cells were exposed to UV radiation (control).

However, the presence of the Grape Stem Cells counteracted the negative effect of UV radiation on the cells as the CFE remained at the same level when exposed to the UV radiation.

Therefore, the Grape Stem Cells protect skin stem cells against UV stress.

Benefits of the Grape Stem Cell products

Regenerative, repair and rejuvenating properties

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Vaccines: About/Terms/Glossary

August 15th, 2015

A

Acellular vaccine: Listen [MP3] A vaccine containing partial cellular material as opposed to complete cells.

Acquired Immune Deficiency Syndrome (AIDS): A medical condition where the immune system cannot function properly and protect the body from disease. As a result, the body cannot defend itself against infections (like pneumonia). AIDS is caused by the Human Immunodeficiency Virus (HIV). This virus is spread through direct contact with the blood and body fluids of an infected individual. High risk activities include unprotected sexual intercourse and intravenous drug use (sharing needles). There is no cure for AIDS, however, research efforts are on-going to develop a vaccine.

Active immunity: The production of antibodies against a specific disease by the immune system. Active immunity can be acquired in two ways, either by contracting the disease or through vaccination. Active immunity is usually permanent, meaning an individual is protected from the disease for the duration of their lives.

Acute: Listen [MP3] A short-term, intense health effect.

Adjuvant: Listen [MP3] A substance (e.g. aluminum salt) that is added during production to increase the body's immune response to a vaccine.

Adverse events: Undesirable experiences occurring after immunization that may or may not be related to the vaccine.

Advisory Committee on Immunization Practices (ACIP): A panel of 10 experts who make recommendations on the use of vaccines in the United States. The panel is advised on current issues by representatives from the Centers for Disease Control and Prevention, Food and Drug Administration, National Institutes of Health, American Academy of Pediatrics, American Academy of Family Physicians, American Medical Association and others. The recommendations of the ACIP guide immunization practice at the federal, state and local level.

Allergy: A condition in which the body has an exaggerated response to a substance (e.g. food or drug). Also known as hypersensitivity.

Anaphylaxis: Listen [MP3] An immediate and severe allergic reaction to a substance (e.g. food or drugs). Symptoms of anaphylaxis include breathing difficulties, loss of consciousness and a drop in blood pressure. This condition can be fatal and requires immediate medical attention.

Anthrax: Listen [MP3] An acute infectious disease caused by the spore-forming bacterium Bacillus anthracis. Anthrax most commonly occurs in hoofed mammals and can also infect humans.

Antibiotic: Listen [MP3] A substance that fights bacteria.

Antibody: Listen [MP3] A protein found in the blood that is produced in response to foreign substances (e.g. bacteria or viruses) invading the body. Antibodies protect the body from disease by binding to these organisms and destroying them.

Antigens: Listen [MP3] Foreign substances (e.g. bacteria or viruses) in the body that are capable of causing disease. The presence of antigens in the body triggers an immune response, usually the production of antibodies.

Antitoxin: Listen [MP3] Antibodies capable of destroying toxins generated by microorganisms including viruses and bacteria.

Antiviral: Literally "against-virus" -- any medicine capable of destroying or weakening a virus.

Arthralgia: Listen [MP3] Joint pain.

Arthritis: A medical condition characterized by inflammation of the joints which results in pain and difficulty moving.

Association: The degree to which the occurrence of two variables or events is linked. Association describes a situation where the likelihood of one event occurring depends on the presence of another event or variable. However, an association between two variables does not necessarily imply a cause and effect relationship. The term association and relationship are often used interchangeably. See causal and temporal association.

Asthma: A chronic medical condition where the bronchial tubes (in the lungs) become easily irritated. This leads to constriction of the airways resulting in wheezing, coughing, difficulty breathing and production of thick mucus. The cause of asthma is not yet known but environmental triggers, drugs, food allergies, exercise, infection and stress have all been implicated.

Asymptomatic infection: Listen [MP3] The presence of an infection without symptoms. Also known as inapparent or subclinical infection.

Attenuated vaccine: Listen [MP3] A vaccine in which live virus is weakened through chemical or physical processes in order to produce an immune response without causing the severe effects of the disease. Attenuated vaccines currently licensed in the United States include measles, mumps, rubella, polio, yellow fever and varicella. Also known as a live vaccine.

Autism: A chronic developmental disorder usually diagnosed between 18 and 30 months of age. Symptoms include problems with social interaction and communication as well as repetitive interests and activities. At this time, the cause of autism is not known although many experts believe it to be a genetically based disorder that occurs before birth.

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B cells: Small white blood cells that help the body defend itself against infection. These cells are produced in bone marrow and develop into plasma cells which produce antibodies. Also known as B lymphocytes.

Bacteria: Tiny one-celled organisms present throughout the environment that require a microscope to be seen. While not all bacteria are harmful, some cause disease. Examples of bacterial disease include diphtheria, pertussis, tetanus, Haemophilus influenzae, and pneumococcal.

Bias: Flaws in the collection, analysis or interpretation of research data that lead to incorrect conclusions.

Biological plausibility: A causal association (or relationship between two factors) is consistent with existing medical knowledge.

Bone marrow: Soft tissue located within bones that produce all blood cells, including the ones that fight infection.

Booster shots: Additional doses of a vaccine needed periodically to "boost" the immune system. For example, the tetanus and diphtheria (Td) vaccine which is recommended for adults every ten years.

Brachial neuritis: Listen [MP3] Inflammation of nerves in the arm causing muscle weakness and pain.

Breakthrough infection: Development of a disease despite a person's having responded to a vaccine.

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Causal association: Listen [MP3] The presence or absence of a variable (e.g. smoking) is responsible for an increase or decrease in another variable (e.g. cancer). A change in exposure leads to a change in the outcome of interest.

Chickenpox: See Varicella.

Chronic health condition: A health related state that lasts for a long period of time (e.g. cancer, asthma).

Combination vaccine: Two or more vaccines administered in a single dose in order to reduce the number of shots given. For example, the MMR (measles, mumps, rubella) vaccine.

Communicable: That which can be transmitted from one person or animal to another. Also known as infectious.

Crohn's disease: Listen [MP3] A chronic medical condition characterized by inflammation of the bowel. Symptoms include abdominal pain, diarrhea, fever, loss of appetite and weight loss. The cause of Crohn's disease is not yet known, but genetic, dietary and infectious factors may play a part.

Community immunity: A situation in which a sufficient proportion of a population is immune to an infectious disease (through vaccination and/or prior illness) to make its spread from person to person unlikely. Even individuals not vaccinated (such as newborns and those with chronic illnesses) are offered some protection because the disease has little opportunity to spread within the community. Also known as herd immunity.

Conjugate vaccine: Listen [MP3] The joining together of two compounds (usually a protein and polysaccharide) to increase a vaccine's effectiveness.

Conjunctivitis: Listen [MP3] Inflammation of the mucous membranes surrounding the eye causing the area to become red and irritated. The membranes may be irritated because of exposure to heat, cold or chemicals. This condition is also caused by viruses, bacteria or allergies.

Contraindication: Listen [MP3] A condition in a recipient which is likely to result in a life-threatening problem if a vaccine were given.

Convulsion: See Seizure.

Crib or Cot Death: See Sudden Infant Death Syndrome (SIDS).

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Deltoid: Listen [MP3] A muscle in the upper arm where shots are usually given.

Demyelinating disorders: Listen [MP3] A medical condition where the myelin sheath is damaged. The myelin sheath surrounds nerves and is responsible for the transmission of impulses to the brain. Damage to the myelin sheath results in muscle weakness, poor coordination and possible paralysis. Examples of demyelinating disorders include Multiple Sclerosis (MS), optic neuritis, transverse neuritis and Guillain-Barre Syndrome (GBS).

Diabetes: A chronic health condition where the body is unable to produce insulin and properly breakdown sugar (glucose) in the blood. Symptoms include hunger, thirst, excessive urination, dehydration and weight loss. The treatment of diabetes requires daily insulin injections, proper nutrition and regular exercise. Complications can include heart disease, stroke, neuropathy, poor circulation leading to loss of limbs, hearing impairment, vision problems and death.

Diphtheria: Listen [MP3] A bacterial disease marked by the formation of a false membrane, especially in the throat, which can cause death.

Disease: Sickness, illness or loss of health.

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Efficacy rate: Listen [MP3] A measure used to describe how good a vaccine is at preventing disease.

Encephalitis: Listen [MP3] Inflammation of the brain caused by a virus. Encephalitis can result in permanent brain damage or death.

Encephalopathy: Listen [MP3] A general term describing brain dysfunction. Examples include encephalitis, meningitis, seizures and head trauma.

Epidemic: Listen [MP3] The occurrence of disease within a specific geographical area or population that is in excess of what is normally expected.

Endemic: Listen [MP3] The continual, low-level presence of disease in a community

Erythema Multiforme: Listen [MP3] A medical condition characterized by inflammation of the skin or mucous membranes (including the mouth, throat and eyes). Erthema Multiforme has been reported following infection. Symptoms persist anywhere from 2 days to 4 weeks and include skin lesions, blisters, itching, fatigue, joint pain and fever.

Etiology: Listen [MP3] The cause of.

Exposure: Contact with infectious agents (bacteria or viruses) in a manner that promotes transmission and increases the likelihood of disease.

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Febrile: Listen [MP3] Relating to fever; feverish.

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Guillain-Barre Syndrome (GBS): Listen [MP3] A rare neurological disease characterized by loss of reflexes and temporary paralysis. Symptoms include weakness, numbness, tingling and increased sensitivity that spreads over the body. Muscle paralysis starts in the feet and legs and moves upwards to the arms and hands. Sometimes paralysis can result in the respiratory muscles causing breathing difficulties. Symptoms usually appear over the course of one day and may continue to progress for 3 or 4 days up to 3 or 4 weeks. Recovery begins within 2-4 weeks after the progression stops. While most patients recover, approximately 15%-20% experience persistent symptoms. GBS is fatal in 5% of cases.

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Haemophilus influenzae type b (Hib): Listen [MP3] A bacterial infection that may result in severe respiratory infections, including pneumonia, and other diseases such as meningitis.

Hepatitis A: A minor viral disease, that usually does not persist in the blood; transmitted through ingestion of contaminated food or water.

Hepatitis B: A viral disease transmitted by infected blood or blood products, or through unprotected sex with someone who is infected.

Hepatitis C: is a liver disease caused by the Hepatitis C virus (HCV), which is found in the blood of persons who have the disease. HCV is spread by contact with the blood of an infected person.

Hepatitis D: is a defective virus that needs the hepatitis B virus to exist. Hepatitis D virus (HDV) is found in the blood of persons infected with the virus.

Hepatitis E: is a virus (HEV) transmitted in much the same way as hepatitis A virus. Hepatitis E, however, does not often occur in the United States.

Herd immunity: See Community immunity.

Herpes Zoster: A disease characterized by painful skin lesions that occur mainly on the trunk (back and stomach) of the body but which can also develop on the face and in the mouth. Complications include headache, vomiting, fever and meningitis. Recovery may take up to 5 weeks. Herpes Zoster is caused by the same virus that is responsible for chickenpox. Most people are exposed to this virus during childhood. After the primary infection (chickenpox), the virus becomes dormant, or inactivated. In some people the virus reactivates years, or even decades, later and causes herpes zoster. Also known as the shingles.

Hives: The eruption of red marks on the skin that are usually accompanied by itching. This condition can be caused by an allergy (e.g. to food or drugs), stress, infection or physical agents (e.g. heat or cold). Also known as uticaria.

Hypersensitivity: Listen [MP3] A condition in which the body has an exaggerated response to a substance (e.g. food or drug). Also known as an allergy.

Hyposensitivity: Listen [MP3] A condition in which the body has a weakened or delayed reaction to a substance.

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Immune globulin: Listen [MP3] A protein found in the blood that fights infection. Also known as gamma globulin.

Immune system: The complex system in the body responsible for fighting disease. Its primary function is to identify foreign substances in the body (bacteria, viruses, fungi or parasites) and develop a defense against them. This defense is known as the immune response. It involves production of protein molecules called antibodies to eliminate foreign organisms that invade the body.

Immunity: Protection against a disease. There are two types of immunity, passive and active. Immunity is indicated by the presence of antibodies in the blood and can usually be determined with a laboratory test. See active and passive immunity.

Immunization: Listen [MP3] The process by which a person or animal becomes protected against a disease. This term is often used interchangeably with vaccination or inoculation.

Immunosupression: Listen [MP3] When the immune system is unable to protect the body from disease. This condition can be caused by disease (like HIV infection or cancer) or by certain drugs (like those used in chemotherapy). Individuals whose immune systems are compromised should not receive live, attenuated vaccines.

Inactivated vaccine: Listen [MP3] A vaccine made from viruses and bacteria that have been killed through physical or chemical processes. These killed organisms cannot cause disease.

Inapparent infection: The presence of infection without symptoms. Also known as subclinical or asymptomatic infection.

Incidence: The number of new disease cases reported in a population over a certain period of time.

Incubation period: The time from contact with infectious agents (bacteria or viruses) to onset of disease.

Infectious: Capable of spreading disease. Also known as communicable.

Infectious agents: Organisms capable of spreading disease (e.g. bacteria or viruses).

Inflammation: Redness, swelling, heat and pain resulting from injury to tissue (parts of the body underneath the skin). Also known as swelling.

Inflammatory Bowel Disease (IBD): A general term for any disease characterized by inflammation of the bowel. Examples include colitis and Crohn's disease. Symptoms include abdominal pain, diarrhea, fever, loss of appetite and weight loss.

Influenza: A highly contagious viral infection characterized by sudden onset of fever, severe aches and pains, and inflammation of the mucous membrane.

Intussusception: Listen [MP3] A type of bowel blockage that happens when one portion of the bowel slides into the next, much like the pieces of a telescope; it is treated in a hospital and may require surgery.

Investigational vaccine: A vaccine that has been approved by the Food and Drug Administration (FDA) for use in clinical trials on humans. However, investigational vaccines are still in the testing and evaluation phase and are not licensed for use in the general public.

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Jaundice: Listen [MP3] Yellowing of the skin and eyes. This condition is often a symptom of hepatitis infection.

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Lesion: Listen [MP3] An abnormal change in the structure of an organ, due to injury or disease.

Live vaccine: A vaccine in which live virus is weakened (attenuated) through chemical or physical processes in order to produce an immune response without causing the severe effects of the disease. Attenuated vaccines currently licensed in the United States include measles, mumps, rubella, shingles (herpes zoster), varicella, and yellow fever. Also known as an attenuated vaccine.

Lupus: A disease characterized by inflammation of the connective tissue (which supports and connects all parts of the body). Chronic swelling of the connective tissue causes damage to the skin, joints, kidneys, nervous system and mucous membranes. The disease begins with fever, joint pain and fatigue. Additional symptoms continue to develop over the years including nausea, fatigue, weight loss, arthritis, headaches and epilepsy. Problems with heart, lung and kidney function may also result. This condition is diagnosed most frequently in young women but also occurs in children.

Lyme disease: A bacterial disease transmitted by infected ticks. Human beings may come into contact with infected ticks during outdoor activities (camping, hiking). Symptoms include fatigue, chills, fever, headache, joint and muscle pain, swollen lymph nodes and a skin rash (in a circular pattern). Long-term problems include arthritis, nervous system abnormalities, irregular heart rhythm and meningitis. Lyme disease can be treated with antibiotics. A vaccine was available from 1998 to 2002.

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CDC – Arthritis – Basics – Definition – Osteoarthritis

August 14th, 2015

Osteoarthritis (OA) is a disease of the entire joint involving the cartilage, joint lining, ligaments, and underlying bone. The breakdown of these tissues eventually leads to pain and joint stiffness. The joints most commonly affected are the knees, hips, and those in the hands and spine. The specific causes of OA are unknown, but are believed to be a result of both mechanical and molecular events in the affected joint. Disease onset is gradual and usually begins after the age of 40. There is currently no cure for OA. Treatment for OA focuses on relieving symptoms and improving function, and can include a combination of patient education, physical therapy, weight control, use of medications, and eventually total joint replacement.

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Arthritis – Wikipedia, the free encyclopedia

August 13th, 2015

Arthritis (from Greek arthro-, joint + -itis, inflammation; plural: arthritides) is a form of joint disorder that involves inflammation of one or more joints.[1][2] There are over 100 different forms of arthritis.[3][4] The most common form of arthritis is osteoarthritis (degenerative joint disease), a result of trauma to the joint, infection of the joint, or age. Other arthritis forms are rheumatoid arthritis, psoriatic arthritis, and related autoimmune diseases. Septic arthritis is caused by joint infection.

The major complaint by individuals who have arthritis is joint pain. Pain is often a constant and may be localized to the joint affected. The pain from arthritis is due to inflammation that occurs around the joint, damage to the joint from disease, daily wear and tear of joint, muscle strains caused by forceful movements against stiff painful joints and fatigue.

There are several diseases where joint pain is primary, and is considered the main feature. Generally when a person has "arthritis" it means that they have one of these diseases, which include:

Joint pain can also be a symptom of other diseases. In this case, the arthritis is considered to be secondary to the main disease; these include:

An undifferentiated arthritis is an arthritis that does not fit into well-known clinical disease categories, possibly being an early stage of a definite rheumatic disease.[5]

Pain, which can vary in severity, is a common symptom in virtually all types of arthritis. Other symptoms include swelling, joint stiffness and aching around the joint(s). Arthritic disorders like lupus and rheumatoid arthritis can affect other organs in the body, leading to a variety of symptoms.[7] Symptoms may include:

It is common in advanced arthritis for significant secondary changes to occur. For example, arthritic symptoms might make it difficult for a person to move around and/or exercise, which can lead to secondary effects, such as:

These changes, in addition to the primary symptoms, can have a huge impact on quality of life.

Arthritis is the most common cause of disability in the USA. More than 20 million individuals with arthritis have severe limitations in function on a daily basis.[8]Absenteeism and frequent visits to the physician are common in individuals who have arthritis. Arthritis can make it very difficult for individuals to be physically active and some become home bound.

It is estimated that the total cost of arthritis cases is close to $100 billion of which almost 50% is from lost earnings. Each year, arthritis results in nearly 1 million hospitalizations and close to 45 million outpatient visits to health care centers.[9]

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Psoriasis – Wikipedia

August 12th, 2015

Psoriasis (psoriasis vulgaris) is een chronische auto-immuunziekte, gekenmerkt door een versnelde deling (proliferatie) en verminderde rijping (differentiatie) van hoorncellen in de opperhuid. Omdat de cellen niet normaal uitrijpen is ook het afschilferen verstoord, waardoor lokaal sterke afschilfering van huidschubben op de aangedane plaatsen plaatsvindt. Hoewel psoriasis vooral tot uiting komt in de huid, is het niet primair een huidprobleem, maar een ontregeling van het immuunsysteem (auto-immuunziekte[1][2][3]).

Periodes van vermindering van de symptomen worden vaak afgewisseld met periodes waarin de ziekte verergert.[4] De aangedane huid van een psoriasispatint vernieuwt zich in 6 7 dagen; bij niet-patinten is dit 26 27 dagen. De structuur van de zich vernieuwende huidlagen wijkt echter belangrijk af van normaal.

Psoriasis is niet besmettelijk. Ongeveer 2% van de wereldbevolking heeft de aandoening, alleen bij Zuid-Amerikaanse Indianen is ze veel zeldzamer. De hoogste incidentie wordt gevonden in Scandinavi en Noord-Europa (3%). Vaak bestaat er bij personen met psoriasis een genetische aanleg voor het optreden van een versnelde huiddeling. Het onderzoek hiernaar richt zich vooral op loci op de chromosomen 17q, 4q, 1q, 6p21.3 en het Psors 1 gen.[5]

De naam psoriasis komt van het Griekse "psora", dat jeuk of huiduitslag betekent. De eerste duidelijke beschrijving van dit ziektebeeld dateert uit 1801.[6] Mannen en vrouwen worden even vaak door deze aandoening getroffen, en 75% van de patinten vertoont de eerste verschijnselen vr het 40e levensjaar.

Er zijn verschillende typen psoriasis, waarvan het meest voorkomende (psoriasis vulgaris, ook wel psoriasis en plaque genoemd) de 'gewone psoriasis' is. Kenmerkend voor de meeste vormen van psoriasis zijn witte huidschilfers op rode plekken huid. Deze plekken worden ook wel plaques genoemd. Ze vertonen de volgende vier eigenschappen:

Ongeveer 20 procent van de patinten vertoont het fenomeen van Koebner. Door aspecifieke irritatie van de huid, ontwikkelen zich plaques op plaatsen waar dat eerder nog niet het geval was, bijvoorbeeld op de plaats waar een schram heeft gezeten of een brandwondje.

Veranderingen aan de nagels treden ook vaak op. De nagels van de handen in 50 procent, en de teennagels in 35 procent van de gevallen. Drie soorten veranderingen kunnen optreden:

In ongeveer 15% van de gevallen, treden naast huidafwijkingen ook gewrichtsklachten op, en ontwikkelt zich een seronegatieve polyartritis.[5]

Andere vormen van psoriasis zijn:

Arthritis psoriatica, is een chronische ontsteking van de gewrichten. De symptomen lijken deels op die van reuma, maar zijn niet exact dezelfde, en meestal zijn de huid- en nagelafwijkingen zoals die zich bij psoriasis voordoen aanwezig. Men kan zich afvragen of de symptomen wel een en dezelfde onderliggende etiologie hebben. Er zijn aanwijzingen dat het zou gaan om een zich elders dan in de huid manifesterende psoriasis, maar er zijn ook aanwijzingen dat het hier om een bijzondere vorm van artritis gaat.[9]

See more here:
Psoriasis - Wikipedia

Recommendation and review posted by simmons

Enthusiasm for personalized medicine is premature …

August 9th, 2015

August 5, 2015

The increasing national focus on personalized or 'precision' medicine is misguided, distracting from broader investments to reduce health inequities and address the social factors that affect population health, two leading public health scholars argue in the New England Journal of Medicine.

"There is now broad consensus that health differences between groups and within groups are not driven by clinical care, but by social-structural factors that shape our lives," write Sandro Galea, MD, DrPH, dean of the Boston University School of Public Health, and Ronald Bayer, PhD, professor of Sociomedical Sciences and co-director of the Center for the History and Ethics of Public Health at Columbia University's Mailman School of Public Health. "Yet seemingly willfully blind to this evidence, the United States continues to spend its health dollars overwhelmingly on clinical care.

"It is therefore not surprising that even as we far outpace all other countries in spending on health, we have poorer health indicators than many countries, some of them far less wealthy than ours."

Bayer and Galea say that while investments in precision medicine may ultimately "open new vistas of science" and make contributions to "a narrow set of conditions that are primarily genetically determined," enthusiasm about the promise of this research is premature. Leaders of the National Institutes of Health (NIH) have praised President Barack Obama's recent initiative to devote $215 million to personalized medicine, an emerging practice of medicine that uses an individual's genetic profile to guide decisions in regard to the diagnosis and treatment of disease.

"Without minimizing the possible gains to clinical care from greater realization of precision medicine's promise, we worry that an unstinting focus on precision medicine by trusted spokespeople for health is a mistakeand a distraction from the goal of producing a healthier population," they write.

Arguing that clinical intervention will not remedy pressing health problems that arise from environmental conditions and inequities in income and resources, they cite a 2013 report by the National Research Council and the Institute of Medicine that found Americans fared worse in terms of heart disease, birth outcomes, life expectancy and other indicators than their counterparts in other high-income countries. The report concluded that "decades of research have documented that health is determined by far more than health care."

They call for greater public investments in "broad, cross-sectional efforts" to minimize the socioeconomic and racial disparities in the U.S. that contribute to poor health.

Bayer and Galea say the NIH's most recent Estimates of Funding for Various Research, Condition and Disease Categories report shows that total support for research areas including the words 'gene,' 'genome' or 'genetic' was about 50 percent higher than funding for areas including the word 'prevention.' And investment in public health infrastructure, including local health departments, lags substantially behind that of other high-income countries.

In explaining why they felt compelled to speak out, Galea and Bayer said they are wary that that specialized medicine will push larger public health initiatives aside.

Excerpt from:
Enthusiasm for personalized medicine is premature ...

Recommendation and review posted by sam