Overview

Turmeric (Curcuma longa) has been used for 4,000 years to treat a variety of conditions. Studies show that turmeric may help fight infections andsome cancers, reduce inflammation, and treat digestive problems.

Many studies have taken place in test tubes and animals. Turmeric may not work as well in humans. Some studies have used an injectable form of curcumin, the active substance in turmeric, and not all studies agree. Finally, some of the studies show conflicting evidence.

Turmeric is widely used in cooking and gives Indian curry its flavor and yellow color. It is also used in mustard and to color butter and cheese. Turmeric has been used in both Ayurvedic and Chinese medicine as an anti-inflammatory, to treat digestive and liver problems, skin diseases, and wounds.

Curcumin is also a powerful antioxidant. Antioxidants scavenge molecules in the body known as free radicals, which damage cell membranes, tamper with DNA, and even cause cell death. Antioxidants can fight free radicals and may reduce or even help prevent some of the damage they cause.

In addition, curcumin lowers the levels of two enzymes in the body that cause inflammation. It also stops platelets from clumping together to form blood clots.

Research suggests that turmeric may be helpful for the following conditions:

Indigestion or Dyspepsia

Curcumin stimulates the gallbladder to produce bile, which some people think may help improve digestion. The German Commission E, which determines which herbs can be safely prescribed in Germany, has approved turmeric for digestive problems. And one double-blind, placebo-controlled study found that turmeric reduced symptoms of bloating and gas in people suffering from indigestion.

Ulcerative colitis

Turmeric may help people with ulcerative colitis stay in remission. Ulcerative colitis is a chronic disease of the digestive tract where symptoms tend to come and go. In one double-blind, placebo-controlled study, people whose ulcerative colitis was in remission took either curcumin or placebo, along with conventional medical treatment, for 6 months. Those who took curcumin had a significantly lower relapse rate than those who took placebo.

Stomach Ulcers

Turmeric does not seem to help treat stomach ulcers. In fact, there is some evidence that it may increase stomach acid, making existing ulcers worse. (See "Precautions" section.)

Osteoarthritis

Because ofturmeric's ability to reduce inflammation, researchers have wondered ifit may help relieve osteoarthritis pain. One study found that people using an Ayurvedic formula of herbs and minerals with turmeric, winter cherry (Withinia somnifera), boswellia (Boswellia serrata), and zinc had less pain and disability. But it's impossible to know whether turmeric, one of the other supplements, or all of them together, was responsible for the effects.

Heart Disease

Early studies suggested that turmeric may help prevent atherosclerosis, the buildup of plaque that can block arteries and lead to heart attack or stroke. In animal studies, an extract of turmeric lowered cholesterol levels and kept LDL (bad) cholesterol from building up in blood vessels. Because it stops platelets from clumping together, turmeric may also prevent blood clots from building up along the walls of arteries. But a double-blind, placebo-controlled study found that taking curcumin, the active ingredient in turmeric, at a dose of up to 4 g per day did not improve cholesterol levels.

Cancer

There has been a great deal of research on turmeric's anti-cancer properties, but results are still very preliminary. Evidence from test tube and animal studies suggests that curcumin may help prevent or treat several types of cancers, including prostate, breast, skin, and colon cancer. Tumeric's preventive effects may relate to its antioxidant properties, which protect cells from damage. More research is needed. Cancer should be treated with conventional medications. Don't use alternative therapies alone to treat cancer. If you choose to use complementary therapies along with your cancer treatment, make sure you tell all your doctors.

Bacterial and Viral Infections

Test tube and animal studies suggest turmeric may kill bacteria and viruses, but researchers don't know whether it would work in people.

Uveitis

A preliminary study suggests curcumin may help treat uveitis, an inflammation of the eye's iris. Preliminary research suggests that curcumin may be as effective as corticosteroids, the type of medication usually prescribed. More research is needed.

Neurodegenerative Conditions

Tumeric's powerful antioxidant, anti-inflammatory, and circulatory effects may help prevent and treat neurodegenerative diseases, including Alzheimer disease, Parkinson disease, multiple sclerosis, and other conditions.

A relative of ginger, turmeric is a perennial plant that grows 5 to 6 feet high in the tropical regions of Southern Asia, with trumpet-shaped, dull yellow flowers. Its roots are bulbs that also produce rhizomes, which then produce stems and roots for new plants. Turmeric is fragrant and has a bitter, somewhat sharp taste. Although it grows in many tropical locations, the majority of turmeric is grown in India, where it is used as a main ingredient in curry.

The roots, or rhizomes and bulbs, are used in medicine and food. They are generally boiled and then dried, turning into the familiar yellow powder. Curcumin, the active ingredient, has antioxidant properties. Other substances in this herb have antioxidant properties as well.

Turmeric is available in the following forms:

Bromelain increases the absorption and anti-inflammatory effects of curcumin, so it is often combined with turmeric products.

Pediatric

Turmeric supplements haven't been studied in children, so there is no recommended dose.

Adult

The following doses are recommended for adults:

The use of herbs is a time-honored approach to strengthening the body and treating disease. However, herbs can trigger side effects and may interact with other herbs, supplements, or medications. For these reasons, you should take herbs with care, under the supervision of a health care provider.

Turmeric in food is considered safe.

Turmeric and curcumin supplements are considered safe when taken at the recommended doses. However, taking large amounts of turmeric for long periods of time may cause stomach upset and, in extreme cases, ulcers. People who have gallstones or obstruction of the bile passages should talk to their doctor before taking turmeric.

If you have diabetes, talk to your doctor before taking turmeric supplements. Turmeric may lower blood sugar levels. When combined with medications for diabetes, turmeric could cause hypoglycemia (low blood sugar).

Although it is safe to eat foods with turmeric, pregnant and breastfeeding women should not take turmeric supplements.

Because turmeric may act like a blood thinner, you should stop taking it at least 2 weeks before surgery. Tell your doctor and surgeon that you have been taking turmeric.

If you are being treated with any of the following medications, you should not use turmeric or curcumin in medicinal forms without first talking to your health care provider.

Blood-thinning medications -- Turmeric may strengthen the effects of these drugs, raising the risk of bleeding. Blood thinners include warfarin (Coumadin), clopidogrel (Plavix), and aspirin, among others.

Drugs that reduce stomach acid -- Turmeric may interfere with the action of these drugs, increasing the production of stomach acid:

Diabetes Medications -- Turmeric may strengthen the effects of these drugs, increasing the risk of hypoglycemia (low blood sugar).

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Curcuma longa

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Surgeon performs bone marrow harvest

The terms "Hodgkin's Disease," "Hodgkin's Lymphoma," and "Hodgkin Lymphoma" are used interchangeably throughout this site.

Bone Marrow Transplants (BMT) and Peripheral Blood Stem Cell Transplants (PBSCT) are emerging as mainstream treatment for many cancers, including Hodgkin's Disease and Medium/High grade aggressive)Non-Hodgkin's lymphoma.

BMTs have been used to treat lymphoma for more than 10 years, but until recently they were used mostly within clinical trials. Now BMTs are being used in conjunction with high doses of chemotherapy as a mainstream treatment.

When high doses of chemotherapy are planned, which can destroy the patients bone marrow, physicians will typically remove marrow from the patients bone before treatment and freeze it. After chemotherapy, the marrow is thawed and injected into a vein to replace destroyed marrow. This type of transplant is called an autologous transplant. If the transplanted marrow is from another person, it is called an allogeneic transplant.

In PBSCTs, another type of autologous transplant, the patient's blood is passed through a machine that removes the stem cells the immature cells from which all blood cells develop. This procedure is called apheresis and usually takes three or four hours over one or more days. After treatment to kill any cancer cells, the stem cells are frozen until they are transplanted back to the patient. Studies have shown that PBSCTs result in shorter hospital stays and are safer and more cost effective than BMTs.

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Bone Marrow and Stem Cell Transplants Lymphoma Info

Recommendation and review posted by sam

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Genetic Engineering, the process of extracting DNA (deoxyribonucleic acid, which makes up the genes of all living things) from one organism and combining it with the DNA of another organism, thus introducing new hereditary traits into the recipient organism. The nature and characteristics of every living creature is determined by the special combinations of genes carried by its cells. The slightest alteration in these combinations can bring about significant changes in an organism and also its progeny. The science of devising techniques of modifying or controlling genes and genetic combinations is referred to as genetic engineering. It was practiced in one form or another in the past by farmers and agriculturists trying to create economically viable species of plants and animals through various breeding techniques Genetic engineering, as a science, was developed in the mid-1970's primarily to create new strains of microorganisms that produce certain chemicals useful in manufacturing or as drugs. Genetic engineering is now also applied to improving plants and creating transgenic animals (animals containing foreign genetic material).

Some persons oppose genetic engineering on religious, ethical, or social grounds. Among the religious questions is whether humans have the right to transfer traits from one organism to another. A social concern is the possibility of creating harmful organisms that, if accidentally released into the environment, could cause epidemics.The creation of human clones, for example, is facing serious opposition especially on moral grounds. Organizations, such as the National Institutes of Health (NIH), are seeking to control the harmful effects of genetic engineering by imposing guidelines and safety measures for genetic experimentation. Treatment of hereditary defects through gene transplantation and controlled interchange of genes between specified species was approved in 1985 and 1987 respectively by the NIH and the National Academy of Sciences. The USDA has framed regulations for the genetic alteration of plants by plant breeders.

The U.S. Supreme Court ruled in 1980 that genetically engineered microorganisms could be patented. In 1988 the U.S. Patent and Trademark Office issued its first patent for a higher form of life, a transgenic mouse that is highly susceptible to certain cancers that appear frequently in humans. This mouse is used in cancer research.

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Genetic Engineering - HowStuffWorks

Recommendation and review posted by Bethany Smith

Genetic tests have been developed for thousands of diseases. Most tests look at single genes and are used to diagnose rare genetic disorders, such as Fragile X Syndrome and Duchenne Muscular Dystrophy. In addition, some genetic tests look at rare inherited mutations of otherwise protective genes, such as BRCA1 and BRCA2, which are responsible for some hereditary breast and ovarian cancers. However, a growing number of tests are being developed to look at multiple genes that may increase or decrease a persons risk of common diseases, such as cancer or diabetes. Such tests and other applications of genomic technologies have the potential to help prevent common disease and improve the health of individuals and populations. For example, predictive gene tests may be used to help determine the risk of developing common diseases, and pharmacogenetic tests may be used to help identify genetic variations that can influence a persons response to medicines. There is much we still need to learn about how effective these new tests are, and the best way to use them to improve health. Learn more.

Despite the many scientific advances in genetics, researchers have only identified a small fraction of the genetic component of most diseases. Therefore, genetic tests for many diseases are developed on the basis of limited scientific information and may not yet provide valid or useful results to individuals who are tested. However, many genetic tests are being marketed prematurely to the public through the Internet, TV, and other media. This may lead to the misuse of these tests and the potential for physical or psychological harms to the public. At the same time, valid and useful tests, such as those for hereditary breast and ovarian cancer or for Lynch syndrome, a form of hereditary colorectal cancer, are not widely used, in part because of limited research on how to get useful tests implemented into practice across U.S. communities. Individuals can learn more about specific genetic tests by visiting the Web sites listed below or by talking with their doctor.

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In 2008, the former Secretary's Advisory Committee on Genetics, Health and Society of the U.S. Department of Health and Human Services released a report identifying gaps in the regulation, oversight, and usefulness of genetic testing. They expressed the need for timely, reliable information that health care providers, payers, public health practitioners, policy makers, and consumers could use to make more informed decisions about the appropriate use of these tests in clinical and public health practice.

To begin addressing this need for reliable information, CDCs Office of Public Health Genomics (OPHG) established the Evaluation of Genomic Applications in Practice and Prevention (EGAPP) Initiative project to systematically evaluate genetic tests and other applications of genomic technology that are in transition from research to clinical and public health practice. Since 2005, the independent EGAPP Working Group has released nine recommendations on the validity and utility of specific genetic tests.

The U.S. Preventive Services Task Force (USPSTF) has also released recommendations on specific genetic tests used in selected clinical scenarios involving breast cancer, colorectal cancer, and hemochromatosis.

In addition the Genetic Test Registry was developed by NCBI. The article "The NIH genetic testing registry: a new, centralized database of genetic tests to enable access to comprehensive information and improve transparency" in the journal Nucleic Acids Research describes in detail this database.

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Also see the genetic testing and genetic counseling sections of CDCs Office of Public Health Genomics resource guide.

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Excerpt from:
Genomics |Genetic Testing

Recommendation and review posted by Bethany Smith

Genetic testing is the process of using medical tests to look for changes (mutations) in a persons genes or chromosomes. Hundreds of different genetic tests are used today, and more are being developed.

Genetic testing can be used in different situations. The type of testing most often used to check for cancer risk is called predictive gene testing. Its used to look for gene mutations that might put a person at risk of getting a disease. Its usually done in families with a history that suggests theres a disease that may be inherited. An example is testing for changes in the BRCA1 and BRCA2 genes (known breast cancer genes) in a woman whose mother and sister had breast cancer.

Genetic testing is also used for other reasons:

All of these forms of genetic testing, including predictive gene testing, look for gene changes that are passed from one generation to the next and are found in every cell in the body. Except for the newborn screening tests, they are used mainly for people with certain types of disease that seem to run in their families. They are not needed by most people.

Cancer-related genetic tests are most commonly done as predictive genetic tests. They may be used:

Sometimes after a person has been diagnosed with cancer, the doctor will order tests to look for gene changes in a sample of the cancer cells. These tests can give information on a persons outlook (prognosis) and can sometimes help tell whether certain types of treatment might be useful.

These types of tests look for gene changes only in the cancer cells that are taken from the patient. These tests are not the same as the tests used to find out about inherited cancer risk.

This document does not cover gene testing done on cancer cells. For more about this kind of testing and its use in cancer treatment, see our information on specific types of cancer.

The rest of this document focuses on predictive genetic testing for inherited mutations as they relate to cancer.

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What is genetic testing? - American Cancer Society

Recommendation and review posted by Bethany Smith

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Genetic engineering news, articles and information:

Recommendation and review posted by Bethany Smith

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GENE THERAPY:

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Caveat:

Medicine is an ever-changing science. As new research and clinical experience broaden our knowledge, changes in treatment and drug therapy are required. I have checked with sources believed to be reliable in their efforts to provide information that is complete and generally in accord with the standards accepted at the time of publishing this article. However, in view of the possibility of human error or changes in medical sciences, I do not assure that the information contained herein is in every respect accurate or complete, and I disclaim all responsibility for any errors or omissions or for the results obtained from use of the information contained in this work. Readers are encouraged to confirm the information contained herein with other sources. I have taken some information from articles that were published few years ago. The facts and conclusions presented may have since changed and may no longer be accurate. Questions about personal health should always be referred to a physician or other health care professional.

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Prologue:

BLASPHEMY! some cried when the concept of gene therapy first surfaced. For them tinkering with the genetic constitution of human beings was equivalent to playing God, and this they perceived as being sacrilegious! On the other side was the scientific community, abuzz with excitement at the prospect of being able to wipe certain genetic disorders in humans entirely from the human gene pool. Although the term gene therapy was first introduced during the 1980s, the controversy about the rationality of this line of treatment still rages on. In the center of the debate lie the gene therapy pros and cons that derive opinions from religious, ethical and undoubtedly, political domains. The concept of genes as carriers of phenotypic information was introduced in the early 19th century by Gregor Mendel, who later demonstrated the properties of genetic inheritance in peas. Over the next 100 years, many significant discoveries lead to the conclusions that genes encode proteins and reside on chromosomes, which are composed of DNA. These findings culminated in the central dogma of molecular biology, that proteins are translated from RNA, which is transcribed from DNA. James Watson was quoted as saying we used to think that our fate was in our stars, but now we know, in large measures, our fate is in our genes. Genes, the functional unit of heredity, are specific sequences bases that encode instructions to make proteins. Although genes get a lot of attentions, it is the proteins that perform most life functions. When genes are altered, encoded proteins are unable to carry out their normal functions, resulting in genetic disorders. Gene therapy is a novel therapeutic branch of modern medicine. Its emergence is a direct consequence of the revolution heralded by the introduction of recombinant DNA methodology in the 1970s. Gene therapy is still highly experimental, but has the potential to become an important treatment regimen. In principle, it allows the transfer of genetic information into patient tissues and organs. Consequently, diseased genes can be eliminated or their normal functions rescued. Furthermore, the procedure allows the addition of new functions to cells, such as the production of immune system mediator proteins that help to combat cancer and other diseases. Most scientists believe the potential for gene therapy is the most exciting application of DNA science, yet undertaken.

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Note:

Please read my other articles Stem cell therapy and human cloning, Cell death and Genetically modified before reading this article.

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The rapid pace of technological advances has profound implications for medical applications far beyond their traditional roles to prevent, treat, and cure disease. Cloning, genetic engineering, gene therapy, human-computer interfaces, nanotechnology, and designer drugs have the potential to modify inherited predispositions to disease, select desired characteristics in embryos, augment normal human performance, replace failing tissues, and substantially prolong life span. As gene therapy is uprising in the field of medicine, scientists believe that after 20 years, this will be the last cure of every genetic disease. Genes may ultimately be used as medicine and given as simple intravenous injection of gene transfer vehicle that will seek our target cells for stable, site-specific chromosomal integration and subsequent gene expression. And now that a draft of the human genome map is complete, research is focusing on the function of each gene and the role of the faulty gene play in disease. Gene therapy will ultimately play Copernican part and will change our lives forever.

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Gene therapy, the experimental therapy as on today:

Gene therapy is an experimental technique that uses genes to treat or prevent diseases. Genes are specific sequences of bases that encode instructions on how to make proteins. When genes are altered so that the encoded proteins are unable to carry out their normal functions, genetic disorders can result. Gene therapy is used for correcting defective genes responsible for disease development. Researchers may use one of several approaches for correcting faulty genes. Although gene therapy is a promising treatment which helps successfully treat and prevent various diseases including inherited disorders, some types of cancer, and certain viral infections, it is still at experimental stage. Gene therapy is presently only being tested for the treatment of diseases that have no other cures. Currently, the only way for you to receive gene therapy is to participate in a clinical trial. Clinical trials are research studies that help doctors determine whether a gene therapy approach is safe for people. They also help doctors understand the effects of gene therapy on the body. Your specific procedure will depend on the disease you have and the type of gene therapy being used.

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Introduction to gene therapy:

Gene therapy is a clinical strategy involving gene transfer with therapeutic purposes. It is based on the concept that an exogenous gene (transgene) is able to modify the biology and phenotype of target cells, tissues and organs. Initially designed to definitely correct monogenic disorders, such as cystic fibrosis, severe combined immunodeficiency or muscular dystrophy, gene therapy has evolved into a promising therapeutic modality for a diverse array of diseases. Targets are expanding and currently include not only genetic, but also many acquired diseases, such as cancer, tissue degeneration or infectious diseases. Depending on the duration planned for the treatment, type and location of target cells, and whether they undergo division or are quiescent, different vectors may be used, involving nonviral methods, non-integrating viral vectors or integrating viral vectors. The first gene therapy clinical trial was carried out in 1989, in patients with advanced melanoma, using tumor-infiltrating lymphocytes modified by retroviral transduction. In the early nineties, a clinical trial with children with severe combined immunodeficiency (SCID) was also performed, by retrovirus transfer of adenosine deaminase gene to lymphocytes isolated from these patients. Since then, more than 5,000 patients have been treated in more than 1,000 clinical protocols all over the world. Despite the initial enthusiasm, however, the efficacy of gene therapy in clinical trials has not been as high as expected; a situation further complicated by ethical and safety concerns. Further studies are being developed to solve these limitations.

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Historical development of gene therapy:

Chronology of development of gene therapy technology:

1970s, 1980s and earlier:

In 1972 Friedmann and Roblin authored a paper in Science titled Gene therapy for human genetic disease? Rogers (1970) was cited for proposing that exogenous good DNA be used to replace the defective DNA in those who suffer from genetic defects. However, these authors concluded that it was premature to begin gene therapy studies in humans because of lack of basic knowledge of genetic regulation and of genetic diseases, and for ethical reasons. They did, however, propose that studies in cell cultures and in animal models aimed at development of gene therapies be undertaken. Such studiesas well as abortive gene therapy studies in humanshad already begun as of 1972. In the 1970s and 1980s, researchers applied such technologies as recombinant DNA and development of viral vectors for transfer of genes to cells and animals to the study and development of gene therapies.

1990s:

The first approved gene therapy case in the United States took place on 14 September 1990, at the National Institute of Health, under the direction of Professor William French Anderson. It was performed on a four year old girl named Ashanti DeSilva. It was a treatment for a genetic defect that left her with ADA-SCID, a severe immune system deficiency. The effects were only temporary, but successful. New gene therapy approach repairs errors in messenger RNA derived from defective genes. This technique has the potential to treat the blood disorder thalassaemia, cystic fibrosis, and some cancers. Researchers at Case Western Reserve University and Copernicus Therapeutics are able to create tiny liposomes 25 nanometers across that can carry therapeutic DNA through pores in the nuclear membrane. Sickle-cell disease is successfully treated in mice. The mice which have essentially the same defect that causes sickle cell disease in humans through the use a viral vector, were made to express the production of fetal hemoglobin (HbF), which normally ceases to be produced by an individual shortly after birth. In humans, the use of hydroxyurea to stimulate the production of HbF has long been shown to temporarily alleviate the symptoms of sickle cell disease. The researchers demonstrated this method of gene therapy to be a more permanent means to increase the production of the therapeutic HbF. In 1992 Doctor Claudio Bordignon working at the Vita-Salute San Raffaele University, Milan, Italy performed the first procedure of gene therapy using hematopoietic stem cells as vectors to deliver genes intended to correct hereditary diseases. In 2002 this work led to the publication of the first successful gene therapy treatment for adenosine deaminase-deficiency (SCID). The success of a multi-center trial for treating children with SCID (severe combined immune deficiency or bubble boy disease) held from 2000 and 2002 was questioned when two of the ten children treated at the trials Paris center developed a leukemia-like condition. Clinical trials were halted temporarily in 2002, but resumed after regulatory review of the protocol in the United States, the United Kingdom, France, Italy, and Germany. In 1993 Andrew Gobea was born with severe combined immunodeficiency (SCID). Genetic screening before birth showed that he had SCID. Blood was removed from Andrews placenta and umbilical cord immediately after birth, containing stem cells. The allele that codes for ADA was obtained and was inserted into a retrovirus. Retroviruses and stem cells were mixed, after which the viruses entered and inserted the gene into the stem cells chromosomes. Stem cells containing the working ADA gene were injected into Andrews blood system via a vein. Injections of the ADA enzyme were also given weekly. For four years T cells (white blood cells), produced by stem cells, made ADA enzymes using the ADA gene. After four years more treatment was needed. The 1999 death of Jesse Gelsinger in a gene therapy clinical trial resulted in a significant setback to gene therapy research in the United States. Jesse Gelsinger had ornithine transcarbamylase deficiency. In a clinical trial at the University of Pennsylvania, he was injected with an adenoviral vector carrying a corrected gene to test the safety of use of this procedure. He suffered a massive immune response triggered by the use of the viral vector, and died four days later. As a result, the U.S. FDA suspended several clinical trials pending the re-evaluation of ethical and procedural practices in the field.

2003:

In 2003 a University of California, Los Angeles research team inserted genes into the brain using liposomes coated in a polymer called polyethylene glycol. The transfer of genes into the brain is a significant achievement because viral vectors are too big to get across the bloodbrain barrier. This method has potential for treating Parkinsons disease. RNA interference or gene silencing may be a new way to treat Huntingtons disease. Short pieces of double-stranded RNA (short, interfering RNAs or siRNAs) are used by cells to degrade RNA of a particular sequence. If a siRNA is designed to match the RNA copied from a faulty gene, then the abnormal protein product of that gene will not be produced.

2006:

In March 2006 an international group of scientists announced the successful use of gene therapy to treat two adult patients for X-linked chronic granulomatous disease, a disease which affects myeloid cells and which gives a defective immune system. The study, published in Nature Medicine, is believed to be the first to show that gene therapy can cure diseases of the myeloid system. In May 2006 a team of scientists led by Dr. Luigi Naldini and Dr. Brian Brown from the San Raffaele Telethon Institute for Gene Therapy (HSR-TIGET) in Milan, Italy reported a breakthrough for gene therapy in which they developed a way to prevent the immune system from rejecting a newly delivered gene. Similar to organ transplantation, gene therapy has been plagued by the problem of immune rejection. So far, delivery of the normal gene has been difficult because the immune system recognizes the new gene as foreign and rejects the cells carrying it. To overcome this problem, the HSR-TIGET group utilized a newly uncovered network of genes regulated by molecules known as microRNAs. Dr. Naldinis group reasoned that they could use this natural function of microRNA to selectively turn off the identity of their therapeutic gene in cells of the immune system and prevent the gene from being found and destroyed. The researchers injected mice with the gene containing an immune-cell microRNA target sequence, and the mice did not reject the gene, as previously occurred when vectors without the microRNA target sequence were used. This work will have important implications for the treatment of hemophilia and other genetic diseases by gene therapy. In August 2006, scientists at the National Institutes of Health (Bethesda, Maryland) successfully treated metastatic melanoma in two patients using killer T cells genetically retargeted to attack the cancer cells. This study constitutes one of the first demonstrations that gene therapy can be effective in treating cancer. In November 2006 Preston Nix from the University of Pennsylvania School of Medicine reported on VRX496, a gene-based immunotherapy for the treatment of human immunodeficiency virus (HIV) that uses a lentiviral vector for delivery of an antisense gene against the HIV envelope. In the Phase I trial enrolling five subjects with chronic HIV infection who had failed to respond to at least two antiretroviral regimens, a single intravenous infusion of autologous CD4 T cells genetically modified with VRX496 was safe and well tolerated. All patients had stable or decreased viral load; four of the five patients had stable or increased CD4 T cell counts. In addition, all five patients had stable or increased immune response to HIV antigens and other pathogens. This was the first evaluation of a lentiviral vector administered in U.S. Food and Drug Administration-approved human clinical trials for any disease. Data from an ongoing Phase I/II clinical trial were presented at CROI 2009.

2007:

On 1 May 2007 Moorfields Eye Hospital and University College Londons Institute of Ophthalmology announced the worlds first gene therapy trial for inherited retinal disease. The first operation was carried out on a 23 year-old British male, Robert Johnson, in early 2007. Lebers congenital amaurosis is an inherited blinding disease caused by mutations in the RPE65 gene. The results of a small clinical trial in children were published in New England Journal of Medicine in April 2008. They researched the safety of the subretinal delivery of recombinant adeno-associated virus (AAV) carrying RPE65 gene, and found it yielded positive results, with patients having modest increase in vision, and, perhaps more importantly, no apparent side-effects.

2008:

In May 2008, two more groups, one at the University of Florida and another at the University of Pennsylvania, reported positive results in independent clinical trials using gene therapy to treat Lebers congenital amaurosis. In all three clinical trials, patients recovered functional vision without apparent side-effects. These studies, which used adeno-associated virus, have spawned a number of new studies investigating gene therapy for human retinal disease.

2009:

In September 2009, the journal Nature reported that researchers at the University of Washington and University of Florida were able to give trichromatic vision to squirrel monkeys using gene therapy, a hopeful precursor to a treatment for color blindness in humans. In November 2009, the journal Science reported that researchers succeeded at halting a fatal genetic disorder called adrenoleukodystrophy in two children using a lentivirus vector to deliver a functioning version of ABCD1, the gene that is mutated in the disorder.

2010:

A paper by Komromy et al. published in April 2010, deals with gene therapy for a form of achromatopsia in dogs. Achromatopsia, or complete color blindness, is presented as an ideal model to develop gene therapy directed to cone photoreceptors. Cone function and day vision have been restored for at least 33 months in two young dogs with achromatopsia. However, the therapy was less efficient for older dogs. In September 2010, it was announced that an 18 year old male patient in France with beta-thalassemia major had been successfully treated with gene therapy. Beta-thalassemia major is an inherited blood disease in which beta haemoglobin is missing and patients are dependent on regular lifelong blood transfusions. A team directed by Dr. Phillipe Leboulch (of the University of Paris, Bluebird Bio and Harvard Medical School) used a lentiviral vector to transduce the human -globin gene into purified blood and marrow cells obtained from the patient in June 2007. The patients haemoglobin levels were stable at 9 to 10 g/dL, about a third of the hemoglobin contained the form introduced by the viral vector and blood transfusions had not been needed. Further clinical trials were planned. Bone marrow transplants are the only cure for thalassemia but 75% of patients are unable to find a matching bone marrow donor.

2011:

In 2007 and 2008, a man being treated by Gero Htter was cured of HIV by repeated Hematopoietic stem cell transplantation with double-delta-32 mutation which disables the CCR5 receptor; this cure was not completely accepted by the medical community until 2011. This cure required complete ablation of existing bone marrow which is very debilitating. In August 2011, two of three subjects of a pilot study were confirmed to have been cured from chronic lymphocytic leukemia (CLL). The study carried out by the researchers at the University of Pennsylvania used genetically modified T cells to attack cells that expressed the CD19 protein to fight the disease. In 2013, the researchers announced that 26 of 59 patients had achieved complete remission and the original patient had remained tumor-free. Human HGF plasmid DNA therapy of cardiomyocytes is being examined as a potential treatment for coronary artery disease as well as treatment for the damage that occurs to the heart after myocardial infarction.

2012:

The FDA approves clinical trials of the use of gene therapy on thalassemia major patients in the US. Researchers at Memorial Sloan Kettering Cancer Center in New York begin to recruit 10 participants for the study in July 2012. The study is expected to end in 2014. In July 2012, the European Medicines Agency recommended approval of a gene therapy treatment for the first time in either Europe or the United States. The treatment, called Alipogene tiparvovec (Glybera), compensates for lipoprotein lipase deficiency (LPLD), which can cause severe pancreatitis. People with LPLD cannot break down fat, and must manage their disease with a restricted diet. However, dietary management is difficult, and a high proportion of patients suffer life-threatening pancreatitis. The recommendation was endorsed by the European Commission in November 2012 and commercial rollout is expected in late 2013. In December 2012, it was reported that 10 of 13 patients with multiple myeloma were in remission or very close to it three months after being injected with a treatment involving genetically engineered T cells to target proteins NY-ESO-1 and LAGE-1 which exist only on cancerous myeloma cells.

2013:

In March 2013, Researchers at the Memorial Sloan-Kettering Cancer Center in New York, reported that three of five subjects who had acute lymphocytic leukemia (ALL) had been in remission for five months to two years after being treated with genetically modified T cells which attacked cells with CD19 genes on their surface, i.e. all B-cells, cancerous or not. The researchers believed that the patients immune systems would make normal T-cells and B-cells after a couple of months however they were given bone marrow to make sure. One patient had relapsed and died and one had died of a blood clot unrelated to the disease. Following encouraging Phase 1 trials, in April 2013, researchers in the UK and the US announced they were starting Phase 2 clinical trials (called CUPID2 and SERCA-LVAD) on 250 patients at several hospitals in the US and Europe to use gene therapy to combat heart disease. These trials were designed to increase the levels of SERCA2a protein in the heart muscles and improve the function of these muscles. The FDA granted this a Breakthrough Therapy Designation which would speed up the trial and approval process in the USA. In July 2013 the Italian San Raffaele Telethon Institute for Gene Therapy (HSR-TIGET) reported that six children with two severe hereditary diseases had been treated with a partially deactivated lentivirus to replace a faulty gene and after 732 months the results were promising. Three of the children had metachromatic leukodystrophy which causes children to lose cognitive and motor skills. The other children had Wiskott-Aldrich syndrome which leaves them to open to infection, autoimmune diseases and cancer due to a faulty immune system. In October 2013, the Great Ormond Street Hospital, London reported that two children born with adenosine deaminase severe combined immunodeficiency disease (ADA-SCID) had been treated with genetically engineered stem cells 18 months previously and their immune systems were showing signs of full recovery. Another three children treated since then were also making good progress. ADA-SCID children have no functioning immune system and are sometimes known as bubble children. In October 2013, Amit Nathswani of the Royal Free London NHS Foundation Trust in London reported that they had treated six people with haemophilia in early 2011 using genetically engineered adeno-associated virus. Over two years later all six were still producing blood plasma clotting factor.

2014:

In January 2014, researchers at the University of Oxford reported that six people suffering from choroideremia had been treated with a genetically engineered adeno-associated virus with a copy of a gene REP1. Over a six month to two year period all had improved their sight. Choroideremia is an inherited genetic eye disease for which in the past there has been no treatment and patients eventually go blind. In March 2014 researchers at the University of Pennsylvania reported that 12 patients with HIV had been treated since 2009 in a trial with a genetically engineered virus with a rare mutation known to protect against HIV (CCR5 deficiency). Results were promising.

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The three main issues for the coming decade will be public perceptions, scale-up and manufacturing, and commercial considerations. Focusing on single-gene applications, which tend to be rarer diseases, will produce successful results sooner than the current focus on the commoner, yet more complex, cancer and heart diseases.

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What is Gene?

A gene is an important unit of hereditary information. It provides the code for living organisms traits, characteristics, function, and physical development. Each person has around 25,000 genes that are located on 46 chromosomes. Gene is a segment of DNA found on chromosome that codes for a particular protein. It acts as a blue print for making enzymes and other proteins for every biochemical reaction and structure of body.

What is allele?

Alleles are two or more alternative forms of a gene that can occupy a specific locus (location) on a chromosome.

What is DNA?

Deoxyribonucleic acid (DNA) is a nucleic acid that contains the genetic information used in the development and function of all known living organisms. The main role of DNA is the long-term storage of information. DNA is often compared to a set of blueprints or a recipe or code, since it contains the instructions needed to construct other components of cells, such as proteins. The DNA segments that carry this genetic information are called genes.

What are Chromosomes?

A chromosome is a singular piece of DNA, which contains many genes. Chromosomes also contain DNA-bound proteins, which serve to package the DNA and control its functions. Chromosomes are found inside the nucleus of cells.

What are Proteins?

Proteins are large organic compounds made of amino acids. They are involved in many processes within cells. Proteins act as building blocks, or function as enzymes and are important in communication among cells.

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What are plasmids?

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Plasmid is any extrachromosomal heritable determinant. Plasmids are fragments of double-stranded DNA that can replicate independently of chromosomal DNA, and usually carry genes. Although they can be found in Bacteria, Archaea and Eukaryotes, they play the most significant biological role in bacteria where they can be passed from one bacterium to another by horizontal gene transfer, usually providing a context-dependent selective advantage, such as antibiotic resistance.

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In the center of every cell in your body is a region called the nucleus. The nucleus contains your DNA which is the genetic code you inherited from each of your parents. The DNA is ribbon-like in structure, but normally exists in a condensed form called chromosomes. You have 46 chromosomes (23 from each parent), which are in turn comprised of thousands of genes. These genes encode instructions on how to make proteins. Proteins make up the majority of a cells structure and perform most life functions. Genes tell cells how to work, control our growth and development, and determine what we look like and how our bodies work. They also play a role in the repair of damaged cells and tissues. Each person has more than 25,000 genes, which are made up of DNA. You have 2 copies of every gene, 1 inherited from your mother and 1 from your father.

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DNA or deoxyribonucleic acid is the very long molecule that encodes the genetic information. A gene is a stretch of DNA required to make a functional product such as part or all of a protein. People have about 25,000 genes. During gene therapy, DNA that codes for specific genes is delivered to individual cells in the body.

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The Human Genome:

The human genome is the entire genetic code that resides in every cell in your body (with the exception of red blood cells). The genome is divided into 23 chromosome pairs. During reproduction, two copies of the chromosomes (one from each parent) are passed onto the offspring. While most chromosomes are identical for males and females, the exceptions are the sex chromosomes (known as the X and Y chromosomes). Each chromosome contains thousands of individual genes. These genes can be further divided into sequences called exons and introns, which are in turn made up of even shorter sequences called codons. And finally, the codons are made up of base pairs, combinations of four bases: adenine, cytosine, thymine, and guanine. Or A, C, T, and G for short. The human genome is vast, containing an estimated 3.2 billion base pairs. To put that in perspective, if the genome was a book, it would be hundreds of thousands of pages long. Thats enough room for a dozen copies of the entire Encyclopaedia Britannica, and all of it fits inside a microscopic cell.

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Our genes help make us unique. Inherited from our parents, they go far in determining our physical traits like eye color and the color and texture of our hair. They also determine things like whether babies will be male or female, the amount of oxygen blood can carry, and the likelihood of getting certain diseases. Scientists believe that every human has about 25,000 genes per cell. A mutation, or change, in any one of these genes can result in a disease, physical disability, or shortened life span. These mutations can be passed from one generation to another, inherited just like a mothers curly hair or a fathers brown eyes. Mutations also can occur spontaneously in some cases, without having been passed on by a parent. With gene therapy, the treatment or elimination of inherited diseases or physical conditions due to these mutations could become a reality. Gene therapy involves the manipulation of genes to fight or prevent diseases. Put simply, it introduces a good gene into a person who has a disease caused by a bad gene. Variations on genes are known as alleles. Because of changes in the genetic code caused by mutations, there are often more than one type of gene in the gene pool. For example, there is a specific gene to determine a persons blood type. Therefore, a person with blood type A will have a different version of that gene than a person with blood type B. Some genes work in tandem with each other.

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Genes to protein:

Chromosomes contain long chains of DNA built with repeating subunits known as nucleotides. That means a single gene is a finite stretch of DNA with a specific sequence of nucleotides. Those nucleotides act as a blueprint for a specific protein, which gets assembled in a cell using a multistep process.

1. The first step, known as transcription, begins when a DNA molecule unzips and serves as a template to create a single strand of complementary messenger RNA.

2. The messenger RNA then travels out of the nucleus and into the cytoplasm, where it attaches to a structure called the ribosome.

3. There, the genetic code stored in the messenger RNA, which itself reflects the code in the DNA, determines a precise sequence of amino acids. This step is known as translation, and it results in a long chain of amino acids a protein.

Proteins are the workhorses of cells. They help build the physical infrastructure, but they also control and regulate important metabolic pathways. If a gene malfunctions if, say, its sequence of nucleotides gets scrambled then its corresponding protein wont be made or wont be made correctly. Biologists call this a mutation, and mutations can lead to all sorts of problems, such as cancer and phenylketonuria. Gene therapy tries to restore or replace a defective gene, bringing back a cells ability to make a missing protein.

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Length measurements of DNA/RNA:

The following abbreviations are commonly used to describe the length of a DNA/RNA molecule:

bp = base pair(s) one bp corresponds to approximately 3.4 (340 pm) of length along the strand, or to roughly 618 or 643 daltons for DNA and RNA respectively.

kb (= kbp) = kilo base pairs = 1,000 bp

Mb = mega base pairs = 1,000,000 bp

Gb = giga base pairs = 1,000,000,000 bp.

For case of single-stranded DNA/RNA units of nucleotides are used, abbreviated nt (or knt, Mnt, Gnt), as they are not paired.

Note:

Please do not confuse these terms with computer data units.

kb in molecular biology is kilobase pairs = 1000 base pairs

kb in computer data is kilobytes = 1000 bytes

_

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Dr Rajiv Desai Blog Archive GENE THERAPY

Recommendation and review posted by Bethany Smith

Every year, more than 10,000 people in the U.S. sustain a spinal cord injury (SCI). An SCI changes a persons life in an instant, creating new challenges for everyday life. Paralyzed Veterans of America membership offers resources and benefits to meet the needs of veterans who have sustained these injuries.

Explore our resources below about spinal cord injury, andtalk to us if you need help understanding and selecting treatment options.

When a person sustains an SCI, the communication between the brain and other parts of the body is disrupted, and messages no longer flow past the damaged area. The extent of the communication breakdown is dependent on both the severity and location of the injury. The human spinal cord is a bundle of nerve cells and fibers approximately 17 inches long that extends from the brain to the lower back. The spinal cord carries messages from the brain to all parts of the body and receives incoming messages from the body as well.

The nerves that lie only within the spinal cord itself are called upper motor neurons (UMNs). These run only between the brain and the spinal nerves. The spinal nerves branch out from the spinal cord into the tissues of the body. Spinal nerves are also called lower motor neurons (LMNs). In movement, the brain sends messages through the spinal cord (UMNs) to the spinal nerves (LMNs). The LMNs then carry these messages to the muscles to coordinate complicated movements such as walking. In this way, the brain can influence movement.

Most spinal injuries damage both UMNs and LMNs. A complete injury cuts or squeezes all the UMNs running down the spinal cord. In a UMN injury, control by the brain no longer exists because messages from the brain cant get through the point of injury. The LMNs act by themselves, causing reflexes without limit. One example is spasticity. Spasticity is the uncontrolled movement of the arms or legs. LMN injuries are a different story. This kind of injury is found, for the most part, at the lower tip of the spinal cord, or the cauda equina.

Spasticity is not found in LMN injuries as it is in UMN injuries, because muscles governed by these LMNs tend to shrink or atrophy. Stated simply, a UMN injury is one where the UMN pathway is broken, and the LMNs below the injury are intact and spasticity is noted. An LMN injury, usually at the cauda equina, abolishes nerve contact with muscles controlled below the injury and no spasticity develops.

There are many causes of these injuries, which can be traumatic or non-traumatic. Traumatic injuries include injuries sustained in military service, auto accidents, falls, sports injuries,or violence. Non-traumatic injuries may be caused by arthritis, cancer, infections, or disk degeneration of the spine.

Spinal cord injuries can occur at any level of the spinal cord, and the level of the injury will dictate which bodily functions are altered or lost. Damage to the spinal cord can cause changes in movement, feeling, bladder control, or other bodily functions. How many changes there are depends on where the spinal cord was injured and how severely the spinal cord was injured.

Immediately after a spinal cord injury, the spinal cord stops doing its job for a period of time called spinal shock. The return of reflexes below the level of injury marks the end of spinal shock. At this time, a doctor can determine if the injury is complete or incomplete. If the injury is incomplete, some feelings and movement may come back.

Rehabilitation begins immediately. The individual will be instructed in strengthening exercises, new styles of movement, and the use of special equipment. If additional recovery of feeling or movement does not occur, a rehabilitation team will help the individual to develop new goals.

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Spinal Cord Injury Information - Paralyzed Veterans of America

Recommendation and review posted by sam

Contents Spinal Cord Injury Overview

A spinal cord injury (SCI) is caused by damage or trauma to the spinal cord that results in a loss or impaired function causing reduced mobility or sensation.

Common causes of damage to the spinal cord are:

The spinal cord does not have to be severed in order for a loss of function to occur. In most people with SCI the spinal cord is intact, but the cellular damage resulting from compression or inflammation results in the loss of function. An SCI is very different from back injuries such as ruptured disks, spinal stenosis or pinched nerves. The later involves musculoskeletal and peripheral nerve changes where as a spinal cord injury involves damage to the central nervous system.

It is possible for a person to "break their back or neck" yet not sustain a spinal cord injury as long as only the bones (the vertebrae) around the spinal cord are damaged, but the spinal cord is not affected. In such cases the person may not experience paralysis after the affected vertebrae are stabilised. Fractured vertebrae and dislocated vertebrae can be stabilised using surgical management such as traction, vertebral fusion, fixation using titanium plates or rods and for less severe fractures of the vertebra bed rest.

The spinal cord is the major bundle of tightly compacted nerves contained within the vertebral column that carry nerve impulses to and from the brain throughout the body. The brain and the spinal cord constitute the central nervous system. Motor and sensory nerves outside the central nervous system constitute the peripheral nervous system, and another system of nerves that control involuntary functions such as blood pressure and temperature regulation are the sympathetic and parasympathetic nervous systems.

The spinal cord is about 18 inches in length and extends from the base of the brain vertically downwards through the middle of the spinal column to around the waist. The pathways that are situated within the spinal cord are called upper motor neurons (UMN's). Their function is to carry messages back and forth from the brain along spinal tracts within the spinal cord responsible for specific functions. The spinal nerves that branch out from the spinal cord to parts of the body are peripheral nerves called lower motor neurons (LMN's). These spinal nerves exit and enter between each vertebra and communicate with specific areas of the body. The sensory portions of the LMN carry messages about sensation from the skin and muscles such as pain, temperature, joint position and information from organs to the spinal cord and upwards via ascending spinal tracts to the brain. The motor portions of the LMN receive messages from the brain via descending tracts in the spinal cord to initiate actions such as muscle movement, gland functions and certain internal organ commands.

The spinal cord is surrounded by a hollow column of bones called vertebrae. These bones constitute the spinal column (back bones and neck bones). Generally the higher in the spinal column the spinal cord injury occurs, the more physical impairment a person will experience resulting in an increased level of paralysis. The vertebra are named according to their location. The seven vertebrae in the neck are called the cervical vertebrae. The top vertebra is called C1 or atlas vertebra and connects the top of the spinal column to the skull. The bottom cervical vertebra is called C7. Cervical SCI's usually result in loss of function in the arms and legs resulting in tetraplegia which is also referred to as quadriplegia. The next twelve vertebra are called the thoracic vertebra, T1-T12. The first thoracic vertebra T1 is the vertebra where the top rib attaches. There are 5 lumbar vertebrae, one fused sacral vertebra and one fused coccygeal vertebra.

So to recap, the five sections of the vertebral column are:

An injury to the spinal cord segments contained within the cervical spinal vertebrae C1-C7 usually result in paralysis of all four limbs to some degree resulting in tetraplegia (quadriplegia). Injuries in the thoracic region usually affect the chest and the legs and result in paraplegia. The vertebra in the lower back between the thoracic vertebra where the ribs attach and the pelvis are the lumbar vertebra. The sacral vertebra run from the pelvis to the end of the spinal column. Injuries to the five lumbar vertebra (L1 thru L5) and similarly to the five sacral vertebra (S1 thru S5) generally result in varying loss of function in the hips, legs, bladder, bowel and sexual function.

The spinal cord ends between L1-L2 where a mass of spinal nerves continue downwards inside the lumbar (L2-L5) and sacral (S1-S2) vertebrae. This mass of spinal nerves is referred to as the cauda equina and damage to these nerve roots is referred to as cauda equina syndrome.

The effects of SCI depend on the type of injury and the level of the injury. SCI can be divided into two types of injury: complete and incomplete. A complete injury results in no function below the level of neurological injury: no sensation and no voluntary movement. Both sides of the body are equally affected. An incomplete injury results in some preserved function below the level of neurological injury. A person with an incomplete injury may be able to move one limb more than another, may be able to feel parts of the body that cannot be moved, or may have more function on one side of the body than the other.

Types of incomplete spinal cord injury are:

With the recent advances in medical intervention and treatment of acute SCI, incomplete injuries are becoming more common. The most frequent spinal cord injury neurological classifications at time of discharge (2014) from a spinal injury centre is incomplete tetraplegia (31.6%), followed by incomplete paraplegia (18.6%), complete paraplegia (24.6%) and complete tetraplegia (19.3%). It is estimated that less than 1% of individuals diagnosed with a spinal cord injury experienced a complete neurological recovery at the time of hospital discharge. Over the last 20 years, the incidence of individuals with incomplete tetraplegia has increased whilst complete paraplegia and complete tetraplegia have decreased.

The level of injury is very helpful in predicting what parts of the body might be affected by paralysis resulting in loss of function. Remember that in incomplete injuries there can be a wide variation in the prognoses.

Cervical (neck) injuries usually result in Quadriplegia/Tetraplegia. Injuries to the spinal cord segments above the C4 level (C1,C2, C3) may result in the need of breathing aids such as mechanical ventilators or diaphragm pacemakers. Diaphragm pacemaker devices may be required to stimulate the phrenic nerve to initiate a persons breathing due to weak innervation of the diaphragm. C5 injuries often result in shoulder (deltoid) and biceps control, but no control of the wrist or hand. C6 injuries generally yield wrist control (wrist extensors), but no finger hand function. Individuals with C7-T1 injuries can straighten their arms (triceps) but still may have dexterity problems with the hand and fingers.

It is interesting to note that in the cervical area of the spine the nerve roots exit the spinal column above the vertebra, except for C7 where a pair of nerve roots also exit both above and below the vertebra. This is why there are seven cervical vertebrae but eight pairs of cervical nerve roots, C1-C8. From T1 downwards all spinal nerves then exit the spinal column below the vertebrae.

Injuries at the thoracic level and below result in paraplegia, with the hands not affected. At T1 to T8 whilst there is good control of the hands, trunk control may vary as the result of lack of abdominal muscle control. Lower thoracic injuries (T9 to T12) allow good truck control and good abdominal muscle control. Sitting balance is very good. Lumbar and sacral injuries yield decreasing control of the hip flexors and legs.

To reference the spinal segments discussed above, the 5 spinal segments are:

Sources

The above information has been written with reference from the following sources: https://www.nscisc.uab.edu/ Sekhon, Lali H.S.; Fehlings, Michael G. (2001). "Epidemiology, Demographics, and Pathophysiology of Acute Spinal Cord Injury". Spine 26 (24 Suppl): S212. doi:10.1097/00007632-200112151-00002. PMID11805601. Alexander Vaccaro; Michael Fehlings (2010). Spine and Spinal Cord Trauma: Evidence-Based Management. Thieme Publishers. ISBN9781604062229. Retrieved 2012-05-06.

Updated: May 2014

Showing the difference between spinal cord injury levels and the difference between tetraplegia (quadriplegia) and paraplegia. Note that there are seven cervical vertebrae, but eight pairs of cervical nerve roots due to how nerve roots exit the cervical vertebrae.

Any medical treatments or therapies discussed on this website should be reviewed by a medical professional before being acted upon.

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What is a Spinal Cord Injury? - Apparelyzed

Recommendation and review posted by sam

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Life Extension - Products on Sale, Coupons, Reviews, Free ...

Recommendation and review posted by Bethany Smith

The following is a guest post by Amber Larsen of Massage and Health by Amber Kim:

My body, my face, my features will never be repeated. How I look is not going to mimic the girl next to me in the gym. My body shape will not be the same as another female that I may be slightly jealous of because shes thinner than me. My ass is going to be bigger and there is nothing I can do about it.

My genetics did it.

It's amazing - on average, most women will have about thirteen negative thoughts about their appearance per day. If you break it down, it means that every waking hour we think negatively about ourselves. I cant lie; I know I have done the same. My ass is too big, my abs stick out, my latissimus dorsi is getting a bit too big because my bras are cutting into my skin (CrossFit did it).

According to cognitive behavioral psychology, the self-hate is called withdrawal emotions. These emotions make us want to withdraw from situations or things that are linked to the emotions that are causing us to feel this way. Essentially, you can say you can be withdrawing from yourself. This can cause us to either make drastic decisions, such as not to eat, or do things that can do us harm, or do the opposite - not take care of ourselves because we ask whats the use? I hope in writing this it can shed some light as to why you body looks the way it does, and how to embrace that you are unique and to work with your genetics.

What exactly is genetics? Genetics is a wide domain, but in short it is the study of heredity, more specifically the characteristics we inherit from our parents. Our appearance, abilities, susceptibility to disease, and even life span is influenced by heredity. That is just skimming the surface of genetics, but an overall view is that your body shape and your abilities in the gym are inherited from your parents. So what does that say about my personal body? My lower half will always be bigger because it is inherited from my father side. My upper body will always be a wee bit smaller because its inherited from my mothers side. The bottom line is, ladies, I will never weigh 110 pounds. Its not in my genetics, and you know what? Im okay with that.

Many times the media portrays an ideal size for a woman, but you know what? For a healthy woman who eats correctly and exercises on a regular basis there is no ideal size. The reason is because genetically we are all different. There is nothing wrong with a woman who has a leaner, thinner body, because she may be genetically predisposed to having a leaner frame. There is also nothing wrong with a woman who tends to be stronger looking with a larger frame for the same reason. Both body images are different, but both are ideal based on each individual womans inherited genetics.

Is your view on your body slowly changing?

So take a good look at my body (yes this is more difficult for me then you think). This photo is from 2012 and this is me at 140 pounds. If you see, my body is a bit stocky, bulky, and (since I am 53) technically overweight. By the way, you can see some of my cellulite and, yes, I did throw away my scale! My abs stick out and so does my ass.

You can see my body is made up of mostly fast-twitch muscle fibers, or type II muscle fibers. My muscles are different in that they contain a higher number of glycolytic enzymes, which means my muscles do very well anaerobically. Also, my body can be viewed as a bit of a subtype of fast twitch muscles in that I am efficient in strength movements and halfway decent at aerobic movements (not the best though). My body is adaptable with endurance training, but it will not be my strongest area of fitness. Bottom line, the body you see is genetically predisposed to strength work.

Now, a slow-twitch body will not look exactly like this. A slow-twitch body will be leaner because the muscle fibers tend to be longer. These muscles contain larger amounts of mitochondria and higher concentrations of myoglobin than my own body. Again, slow twitch muscle tissue is an inherited trait.

I am not super skinny (as you can see above), but its important to realize that each body is unique and has strengths and weaknesses. Each body is beautiful in its own right, and its important for all of you to embrace what makes you an individual. There is no ideal weight or look for any woman. Women look different based off of their genetic make up, and thats truly a beautiful thing. Just think - no one will ever look exactly like you. And you have automatically inherited strengths that will help you in your fitness goals.

Embrace the person you are. I know it can be difficult to stop the negative self talk that your body does not look like the skinny Victorias Secret model, but you know what? Maybe you were never meant to look that way based off of your genetic heredity. Maybe you were meant to look strong and maybe you were built for strength, which is beautiful. Even if you are a leaner person who wishes to look stronger, well you can, even with a leaner frame, and you can also embrace that your body allows you to work efficiently aerobically based on your genetic make-up.

The image you have of your body should be positive. No one can be you, and no one can look exactly like you because you are genetically different. There is so much beauty in that. Embrace the genetic make up that make your body unique to those around you. I hope you will not be afraid to wear that bikini this summer or to workout without a shirt on. Your body is beautiful because its uniquely you.

This is my body. I have learned to embrace the body that allows me to do amazing things. I hope you will do the same.

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The Female Form: Embrace Your Genetics and Find Beauty in ...

Recommendation and review posted by Bethany Smith

The Tahoma Clinic has a variety of programs for women who are interested in optimizing their health. The programs range from basic gynecological exams, menopausal support, gynecological conditions such as endometriosis and fibroids, to prevention against osteoporosis, Alzheimers, cardiovascular disease, and cancers. Each program is individualized to meet personal needs, as well as address your prior history and family history.

Our most popular program involves evaluation and use of Bio-identical natural hormone replacement therapy. The Tahoma Clinic offers the latest in Bio-identical natural hormone replacement therapy for women in a safe and effective manner. Dr. Jonathan Wright, MD originated the Triest blend of estrogens 25 years ago and is still leading the way today. Dr. Wright currently has two physicians on staff specializing in womens health, and has worked extensively with each of them in Bio-identical natural hormone replacement therapy.

Menopause is a natural process a womans body goes through as she ages. Many different approaches can be taken to help address this change. Diet and lifestyle are always at the core of the program. Vitamins, minerals, and other supplements as necessary are then added to support the foundation. Lastly, the Bio-identical hormones, which look exactly like the hormones you produce in your own body and originate from wild yam or soy, are formulated for you.

As we age, our hormone levels change. For example, as early as 30 years of age, our DHEA levels start declining. At the same time, our Cortisol starts to rise. This combination can result in weight gain, especially around the middle, increasing your risk of cardiovascular disease and insulin resistance. Other symptoms that occur with menopause include:

Each woman experiences these changes to varying degrees. There are many different approaches to managing your symptoms, and we will work with you to find the treatment that best supports your needs. To start, your hormone levels will be evaluated by a 24-hour urinalysis which allows for multiple metabolites to be measured accurately. Then, a physician will work with you to focus on methods to help you balance your hormones safely and effectively for your natural body composition.

Please , pleasecontact usto make an appointment with one of our doctors that specialize in womens health.

Learn more about the physicians at the Tahoma Clinic

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Bio-Identical Hormones & Women's Services at Dr. Wright's ...

Recommendation and review posted by Bethany Smith

Renal cell carcinoma (RCC, also known as hypernephroma, Grawitz tumor, renal adenocarcinoma) is a kidney cancer that originates in the lining of the proximal convoluted tubule, a part of the very small tubes in the kidney that transport waste molecules from the blood to the urine. RCC is the most common type of kidney cancer in adults, responsible for approximately 90-95% of cases.[1] Initial treatment is most commonly either partial or complete removal of the affected kidney(s) and remains the mainstay of curative treatment.[2] Where the cancer has not metastasised (spread to other organs) or burrowed deeper into the tissues of the kidney the 5-year survival rate is 65-90%,[3] but this is lowered considerably when the cancer has spread. It is relatively resistant to radiation therapy and chemotherapy, although some cases respond to targeted therapies such as sunitinib, temsirolimus, bevacizumab, interferon alfa and sorafenib which have improved the outlook for RCC.[4]

The body is remarkably good at hiding the symptoms and as a result people with RCC often have advanced disease by the time it is discovered.[5] The initial symptoms of RCC often include: blood in the urine (occurring in 40% of affected persons at the time they first seek medical attention), flank pain (40%), a mass in the abdomen or flank (25%), weight loss (33%), fever (20%), high blood pressure (20%), night sweats and generally feeling unwell.[1] RCC is also associated with a number of paraneoplastic syndromes (PNS) which are conditions caused by either the hormones produced by the tumour or by the body's attack on the tumour and are present in about 20% of those with RCC.[1] These syndromes most commonly affect tissues which have not been invaded by the cancer.[1] The most common PNSs seen in people with RCC are: anaemia (due to an underproduction of the hormone, erythropoietin), high blood calcium levels, polycythaemia (the opposite to anaemia, due to an overproduction of erythropoietin), thrombocytosis (too many platelets in the blood, leading to an increased tendency for blood clots and bleeds) and secondary amyloidosis.[6] When RCC metastasises it most commonly spreads to the lymph nodes, lungs, liver, adrenal glands, brain or bones.[6]

Historically, medical practitioners expected a person to present with three findings. This classic triad[7] is 1: haematuria, which is when there is blood present in the urine, 2: flank pain, which is pain on the side of the body between the hip and ribs, and 3: an abdominal mass, similar to bloating but larger. It is now known that this classic triad of symptoms only occurs in 10-15% of cases, and is usually indicative that the renal cell carcinoma (RCC) in an advanced stage.[7] Today, RCC is often asymptomatic (meaning little to no symptoms) and is generally detected incidentally when a person is being examined for other ailments.[8]

Other signs and symptom may include haematuria;[7] loin pain;[7] abdominal mass;[8]malaise, which is a general feeling of feeling unwell;[8] weight loss and/or loss of appetite;[9]anaemia resulting from depression of erythropoietin;[7]erythrocytosis (increased production of red blood cells) due to increased erythropoietin secretion;[7]varicocele, which is seen in males as an enlargement of the tissue at the testicle (more often the left testicle)[8]hypertension (high blood pressure) resulting from secretion of renin by the tumour;[10]hypercalcemia, which is elevation of calcium levels in the blood;[11] sleep disturbance or night sweats;[9] recurrent fevers;[9] and chronic fatigue.[12]

The greatest risk factors for RCC are lifestyle-related; smoking, obesity and hypertension (high blood pressure) have been estimated to account for up to 50% of cases.[13] Occupational exposure to some chemicals such as asbestos, cadmium, lead, chlorinated solvents, petrochemicals and PAH (polycyclic aromatic hydrocarbon) has been examined by multiple studies with inconclusive results.[14][15][16] Another suspected risk factor is the long term use of non-steroidal anti-inflammatory drugs (NSAIDS).[17]

Finally, studies have found that women who have had a hysterectomy are at more than double the risk of developing RCC than those who have not.[18] The reason for this remains unclear.

Hereditary factors have a minor impact on individual susceptibility with immediate relatives of people with RCC having a two to fourfold increased risk of developing the condition.[19] Other genetically linked conditions also increase the risk of RCC, including hereditary papillary renal carcinoma, hereditary leiomyomatosis, Birt-Hogg-Dube syndrome, hyperparathyroidism-jaw tumor syndrome, familial papillary thyroid carcinoma, von Hippel-Lindau disease[20] and sickle cell disease.[21]

The most significant disease affecting risk however is not genetically linked patients with acquired cystic disease of the kidney requiring dialysis are 30 times greater more likely than the general population to develop RCC.[22]

The tumour arises from the cells of the proximal renal tubular epithelium.[1] It is considered an adenocarcinoma.[6] There are two subtypes: sporadic (that is, non-hereditary) and hereditary.[1] Both such subtypes are associated with mutations in the short-arm of chromosome 3, with the implicated genes being either tumour suppressor genes (VHL and TSC) or oncogenes (like c-Met).[1]

The first steps taken to diagnose this condition are consideration of the signs and symptoms, and a medical history (the detailed medical review of past health state) to evaluate any risk factors. Based on the symptoms presented, a range of biochemical tests (using blood and/or urine samples) may also be considered as part of the screening process to provide sufficient quantitative analysis of any differences in electrolytes, renal and liver function, and blood clotting times.[21] Upon physical examination, palpation of the abdomen may reveal the presence of a mass or an organ enlargement.[23]

Although this disease lacks characterization in the early stages of tumor development, considerations based on diverse clinical manifestations, as well as resistance to radiation and chemotherapy are important. The main diagnostic tools for detecting renal cell carcinoma are ultrasound, computed tomography (CT) scanning and magnetic resonance imaging (MRI) of the kidneys.[24]

Renal cell carcinoma (RCC) is not a single entity, but rather a collection of different types of tumours, each derived from the various parts of the nephron (epithelium or renal tubules) and possessing distinct genetic characteristics, histological features, and, to some extent, clinical phenotypes.[21]

Clear Cell Renal Cell Carcinoma (CCRCC)

Array-based karyotyping can be used to identify characteristic chromosomal aberrations in renal tumors with challenging morphology.[28][29] Array-based karyotyping performs well on paraffin embedded tumours[30] and is amenable to routine clinical use. See also Virtual Karyotype for CLIA certified laboratories offering array-based karyotyping of solid tumours.

The 2004 World Health Organization (WHO) classification of genitourinary tumours recognizes over 40 subtypes of renal neoplasms. Since the publication of the latest iteration of the WHO classification in 2004, several novel renal tumour subtypes have been described:[31]

Laboratory tests are generally conducted when the patient presents with signs and symptoms that may be characteristic of kidney impairment. They are not primarily used to diagnose kidney cancer, due to its asymptomatic nature and are generally found incidentally during tests for other illnesses such as gallbladder disease.[33] In other words, these cancers are not detected usually because they do not cause pain or discomfort when they are discovered. Laboratory analysis can provide an assessment on the overall health of the patient and can provide information in determining the staging and degree of metastasis to other parts of the body (if a renal lesion has been identified) before treatment is given.

The presence of blood in urine is a common presumptive sign of renal cell carcinoma. The haemoglobin of the blood causes the urine to be rusty, brown or red in colour. Alternatively, urinalysis can test for sugar, protein and bacteria which can also serve as indicators for cancer. A complete blood cell count can also provide additional information regarding the severity and spreading of the cancer.[34]

The CBC provides a quantified measure of the different cells in the whole blood sample from the patient. Such cells examined for in this test include red blood cells (erythrocytes), white blood cells (leukocytes) and platelets (thrombocytes). A common sign of renal cell carcinoma is anaemia whereby the patient exhibits deficiency in red blood cells.[35] CBC tests are vital as a screening tool for examination the health of patient prior to surgery. Inconsistencies with platelet counts are also common amongst these cancer patients and further coagulation tests, including Erythrocyte Sedimentation Rate (ESR), Prothrombin Time (PT), Activated Partial Thromboplastin Time (APTT) should be considered.

Blood chemistry tests are conducted if renal cell carcinoma is suspected as cancer has the potential to elevate levels of particular chemicals in blood. For example, liver enzymes such as aspartate aminotransferase [AST] and alanine aminotransferase [ALT] are found to be at abnormally high levels.[36] The staging of the cancer can also be determined by abnormal elevated levels of calcium, which suggests that the cancer may have metastasised to the bones.[37] In this case, a doctor should be prompted for a CT scan. Blood chemistry tests also assess the overall function of the kidneys and can allow the doctor to decide upon further radiological tests.

The characteristic appearance of renal cell carcinoma (RCC) is a solid renal lesion which disturbs the renal contour. It will frequently have an irregular or lobulated margin and may be seen as a lump on the lower pelvic or abdomen region. Traditionally, 85 to 90% of solid renal masses will turn out to be RCC but cystic renal masses may also be due to RCC.[38] However, the advances of diagnostic modalities are able to incidentally diagnose a great proportion of patients with renal lesions that may appear to be small in size and of benign state. Ten percent of RCC will contain calcifications, and some contain macroscopic fat (likely due to invasion and encasement of the perirenal fat.[39] Deciding on the benign or malignant nature of the renal mass on the basis of its localized size is an issue as renal cell carcinoma may also be cystic. As there are several benign cystic renal lesions (simple renal cyst, haemorrhagic renal cyst, multilocular cystic nephroma, polycystic kidney disease), it may occasionally be difficult for the radiologist to differentiate a benign cystic lesion from a malignant one.[40] The Bosniak classification system for cystic renal lesions classifies them into groups that are benign and those that need surgical resection, based on specific imaging features.[41]

The main imaging tests performed in order to identify renal cell carcinoma are pelvic and abdominal CT scans, ultrasound tests of the kidneys (ultrasonography), MRI scans, intravenous pyelogram (IVP) or renal angiography.[42] Among these main diagnostic tests, other radiologic tests such as excretory urography, positron-emission tomography (PET) scanning, ultrasonography, arteriography, venography, and bone scanning can also be used to aid in the evaluation of staging renal masses and to differentiate non-malignant tumours from malignant tumours.

Contrast-enhanced Computed tomography (CT) scanning is a routinely used imaging procedure in determining the stage of the renal cell carcinoma in the abdominal and pelvic regions of the patient. CT scans have the potential to distinguish solid masses from cystic masses and may provide information on the localization, stage or spread of the cancer to other organs of the patient. Key parts of the human body which are examined for metastatic involvement of renal cell carcinoma may include the renal vein, lymph node and the involvement of the inferior vena cava.[43] According to a study conducted by Sauk et al., multidetector CT imaging characteristics have applications in diagnosing patients with clear renal cell carcinoma by depicting the differences of these cells at the cytogenic level.[44]

Ultrasonographic examination can be useful in evaluating questionable asymptomatic kidney tumours and cystic renal lesions if Computed Tomography imaging is inconclusive. This safe and non-invasive radiologic procedure uses high frequency sound waves to generate an interior image of the body on a computer monitor. The image generated by the ultrasound can help diagnose renal cell carcinoma based on the differences of sound reflections on the surface of organs and the abnormal tissue masses. Essentially, ultrasound tests can determine whether the composition of the kidney mass is mainly solid or filled with fluid.[42]

A Percutaneous biopsy can be performed by a radiologist using ultrasound or computed tomography to guide sampling of the tumour for the purpose of diagnosis by pathology. However this is not routinely performed because when the typical imaging features of renal cell carcinoma are present, the possibility of an incorrectly negative result together with the risk of a medical complication to the patient may make it unfavourable from a risk-benefit perspective.[11] However, biopsy tests for molecular analysis to distinguish benign from malignant renal tumours is of investigative interest.[11]

Magnetic Resonance Imaging (MRI) scans provide an image of the soft tissues in the body using radio waves and strong magnets. MRI can be used instead of CT if the patient exhibits an allergy to the contrast media administered for the test.[45][46] Sometimes prior to the MRI scan, an intravenous injection of a contrasting material called gadolinium is given to allow for a more detailed image. Patients on dialysis or those who have renal insufficiency should avoid this contrasting material as it may induce a rare, yet severe, side effect known as nephrogenic systemic fibrosis.[47] A bone scan or brain imaging is not routinely performed unless signs or symptoms suggest potential metastatic involvement of these areas. MRI scans should also be considered to evaluate tumour extension which has grown in major blood vessels, including the vena cava, in the abdomen. MRI can be used to observe the possible spread of cancer to the brain or spinal cord should the patient present symptoms that suggest this might be the case.

Intravenous pyelogram (IVP) is a useful procedure in detecting the presence of abnormal renal mass in the urinary tract. This procedure involves the injection of a contrasting dye into the arm of the patient. The dye travels from the blood stream and into the kidneys which in time, passes into the kidneys and bladder. This test is not necessary if a CT or MRI scan has been conducted.[48]

Renal angiography uses the same principle as IVP, as this type of X-ray also uses a contrasting dye. This radiologic test is important in diagnosing renal cell carcinoma as an aid for examining blood vessels in the kidneys. This diagnostic test relies on the contrasting agent which is injected in the renal artery to be absorbed by the cancerous cells.[49] The contrasting dye provides a clearer outline of abnormally-oriented blood vessels believed to be involved with the tumour. This is imperative for surgeons as it allows the patients blood vessels to be mapped prior to operation.[43]

The staging of renal cell carcinoma is the most important factor in predicting its prognosis.[50] Staging can follow the TNM staging system, where the size and extent of the tumour (T), involvement of lymph nodes (N) and metastases (M) are classified separately. Also, it can use overall stage grouping into stage I-IV, with the 1997 revision of AJCC described below:[50]

At diagnosis, 30% of renal cell carcinomas have spread to the ipsilateral renal vein, and 5-10% have continued into the inferior vena cava.[51]

The gross and microscopic appearance of renal cell carcinomas is highly variable. The renal cell carcinoma may present reddened areas where blood vessels have bled, and cysts containing watery fluids.[52] The body of the tumour shows large blood vessels that have walls composed of cancerous cells. Gross examination often shows a yellowish, multilobulated tumor in the renal cortex, which frequently contains zones of necrosis, haemorrhage and scarring. In a microscopic context, there are four major histologic subtypes of renal cell cancer: clear cell (conventional RCC, 75%), papillary (15%), chromophobic (5%), and collecting duct (2%). Sarcomatoid changes (morphology and patterns of IHC that mimic sarcoma, spindle cells) can be observed within any RCC subtype and are associated with more aggressive clinical course and worse prognosis. Under light microscopy, these tumour cells can exhibit papillae, tubules or nests, and are quite large, atypical, and polygonal.

Recent studies have brought attention to the close association of the type of cancerous cells to the aggressiveness of the condition. Some studies suggest that these cancerous cells accumulate glycogen and lipids, their cytoplasm appear "clear", the nuclei remain in the middle of the cells, and the cellular membrane is evident.[53] Some cells may be smaller, with eosinophilic cytoplasm, resembling normal tubular cells. The stroma is reduced, but well vascularised. The tumour compresses the surrounding parenchyma, producing a pseudocapsule.[54]

The most common cell type exhibited by renal cell carcinoma is the clear cell, which is named by the dissolving of the cells' high lipid content in the cytoplasm. The clear cells are thought to be the least likely to spread and usually respond more favourably to treatment. However, most of the tumours contain a mixture of cells. The most aggressive stage of renal cancer is believed to be the one in which the tumour is mixed, containing both clear and granular cells.[55]

The recommended histologic grading schema for RCC is the Fuhrman system (1982), which is an assessment based on the microscopic morphology of a neoplasm with haematoxylin and eosin (H&E staining). This system categorises renal cell carcinoma with grades 1, 2, 3, 4 based on nuclear characteristics. The details of the Fuhrman grading system for RCC are shown below:[56]

Nuclear grade is believed to be one of the most imperative prognostic factors in patients with renal cell carcinoma.[21] However, a study by Delahunt et al. (2007) has shown that the Fuhrman grading is ideal for clear cell carcinoma but may not be appropriate for chromophobe renal cell carcinomas and that the staging of cancer (accomplished by CT scan) is a more favourable predictor of the prognosis of this disease.[57] In relation to renal cancer staging, the Heidelberg classification system of renal tumours was introduced in 1976 as a means of more completely correlating the histopathological features with the identified genetic defects.[58]

The type of treatment depends on multiple factors and the individual, some of which include:[7][59]

Every form of treatment has both risks and benefits; a health care professional will provide the best options that suit the individual circumstances.

Active surveillance or "watchful waiting" is becoming more common as small renal masses or tumours are being detected and also within the older generation when surgery is not always suitable.[60] Active surveillance involves completing various diagnostic procedures, tests and imaging to monitor the progression of the RCC before embarking on a more high risk treatment option like surgery.[60] In the elderly, patients with co-morbidities, and in poor surgical candidates, this is especially useful.

Different procedures may be most appropriate, depending on circumstances.

Radical nephrectomy is the removal of the entire affected kidney including Gerota's fascia, the adrenal gland which is on the same side as the affected kidney, and the regional lymph nodes, all at the same time.[7] This method, although severe, is effective. But it is not always appropriate, as it is a major surgery that contains the risk of complication both during and after the surgery and can have a longer recovery time.[61] It is important to note that the other kidney must be fully functional, and this technique is most often used when there is a large tumour present in only one kidney.

Nephron-sparing partial nephrectomy is used when the tumor is small (less than 4cm in diameter) or when the patient has other medical concerns such as diabetes or hypertension.[7] The partial nephrectomy involves the removal of the affected tissue only, sparing the rest of the kidney, Gerota's fascia and the regional lymph nodes. This allows for more renal preservation as compared to the radical nephrectomy, and this can have positive long term health benefits.[62] Larger and more complex tumors can also be treated with partial nephrectomy by surgeons with a lot of kidney surgery experience.[63]

Laparoscopic nephrectomy uses laparoscopic surgery, with minimally invasive surgical techniques. Commonly referred to as key hole surgery, this surgery does not have the large incisions seen in a classically performed radical or partial nephrectomy, but still successfully removes either all or part of the kidney. Laparoscopic surgery is associated with shorter stays in the hospital and quicker recovery time but there are still risks associated with the surgical procedure.

Surgery for metastatic disease: If metastatic disease is present surgical treatment may still a viable option. Radical and partial nephrectomy can still occur, and in some cases if the metastasis is small this can also be surgically removed.[7] This depends on what stage of growth and how far the disease has spread.

Targeted ablative therapies are also known as percutaneous ablative therapies. Although the use of laparoscopic surgical techniques for complete nephrectomies has reduced some of the risks associated with surgery,[64] surgery of any sort in some cases will still not be feasible. For example, the elderly, people already suffering from severe renal dysfunction, or people who have several comorbidities, surgery of any sort is not warranted.[65] Instead there are targeted therapies which do not involve the removal of any organs or serious surgery. Rather, these therapies involve the ablation of the tumor or the affected area. Ablative treatments use imaging such as computed tomography (CT) or magnetic resonance imaging (MRI) to identify the location of the tumors, which ideally are smaller than 3.5cm and to guide the treatment. However there are some cases where ablation can be used on tumors that are larger.[65]

The two main types of ablation techniques that are used for renal cell carcinoma are radio frequency ablation and cryoablation.[65]

Radio frequency ablation uses an electrode probe which is inserted into the affected tissue, to send radio frequencies to the tissue to generate heat through the friction of water molecules. The heat destroys the tumor tissue.[7] Cell death will generally occur within minutes of being exposed to temperatures above 50C.

Cryoablation also involves the insertion of a probe into the affected area,[7] however, cold is used to kill the tumor instead of heat. The probe is cooled with chemical fluids which are very cold. The freezing temperatures cause the tumor cells to die by causing osmotic dehydration, which pulls the water out of the cell destroying the enzyme, organelles, cell membrane and freezing the cytoplasm.[65]

Immunotherapy is a method that activates the person's immune system and uses it to their own advantage. It was developed after observing that in some cases there was spontaneous regression.[66] That is, the renal cell carcinoma improved with no other therapies. Immunotherapy capitalises on this phenomenon and aims to build up a person's immune response to cancer cells.[66] Other medications target things such as growth factors that have been shown to promote the growth and spread of tumours.[67] They inhibit the growth factor in order to prevent tumours from forming.[68] There have been many different medications developed and most have only been approved in the last seven or so years.[69]

Some of the most recently developed treatments are listed below:[70]

Each of the treatments listed above is slightly different; some only work for a little while and others need to be used in conjunction with other therapies. There are also different side effects and risks associated with different forms of medication. As always, the advice of a health care professional should be sought if considering any of the therapies mentioned.

Chemotherapy and radiotherapy are not as successful in the case of RCC. RCC is resistant in most cases but there is about a 4-5% success rate sometimes, but this is often short lived with more tumours and growths developing later.[7]

Cancer vaccines are being developed but so far have been found to be effective for only certain forms of the RCC.[7] The vaccines are being designed to "prime" the immune system to provide tumour specific immunity.[66] They are still being developed but the present another treatment possibility.

Adjuvant therapy, which refers to therapy given after a primary surgery, has not been found to be beneficial in renal cell cancer.[72] Conversely, neoadjuvant therapy is administered before the intended primary or main treatment. In some cases neoadjuvant therapy has been shown to decrease the size and stage of the RCC to then allow it to be surgically removed.[68] This is a new form of treatment and the effectiveness of this approach is still being assessed in clinical trials.

Metastatic renal cell carcinoma (mRCC) is the spread of the primary renal cell carcinoma from the kidney to other organs. 25-30% of people have this metastatic spread by the time they are diagnosed with renal cell carcinoma.[73] This high proportion is explained by the fact that clinical signs are generally mild until the disease progresses to a more severe state.[74] The most common sites for metastasis are the lymph nodes, lung, bones, liver and brain.[8] How this spread affects the staging of the disease and hence prognosis is discussed in the Diagnosis and Prognosis section.

MRCC has a poor prognosis compared to other cancers although average survival times have increased in the last few years due to treatment advances. Average survival time in 2008 for the metastatic form of the disease was under a year[75] and by 2013 this improved to an average of 22 months.[76] Despite this improvement the 5 year survival rate for mRCC remains under 10%[77] and 20-25% of suffers remain unresponsive to all treatments and in these cases, the disease has a rapid progression.[76]

The available treatments for RCC discussed in the Treatment section are also relevant for the metastatic form of the disease. Options include interleukin-2 which is a standard therapy for advanced renal cell carcinoma.[72] In the past six years, seven new treatments have been approved specifically for mRCC (sunitinib, temsirolimus, bevacizumab, sorafenib, everolimus, pazopanib and axitinib).[4] These new treatments are based on the fact that renal cell carcinomas are very vascular tumors they contain a large number of blood vessels. The drugs aim to inhibit the growth of new blood vessels in the tumors, hence slowing growth and in some cases reducing the size of the tumors.[78] Side effects unfortunately are quite common with these treatments and include:[79]

Radiotherapy and chemotherapy are more commonly used in the metastatic form of RCC to target the secondary tumors in the bones, liver, brain and other organs. While not curative, these treatments do provide relief for suffers from symptoms associated with the spread of tumors.[76] Other potential treatments are still being developed, including tumor vaccines and small molecule inhibitors.[73]

The prognosis for renal cell carcinoma is largely influenced by a variety of factors, including tumour size, degree of invasion and metastasis, histologic type, and nuclear grade.[21] For metastatic renal cell carcinoma, factors which may present a poor prognosis include a low Karnofsky performance-status score (a standard way of measuring functional impairment in patients with cancer), a low haemoglobin level, a high level of serum lactate dehydrogenase, and a high corrected level of serum calcium.[80][81] For non-metastatic cases, the Leibovich scoring algorithm may be used to predict post-operative disease progression.[82]

Renal cell carcinoma is one of the cancers most strongly associated with paraneoplastic syndromes, most often due to ectopic hormone production by the tumour. The treatment for these complications of RCC is generally limited beyond treating the underlying cancer.

For those that have tumour recurrence after surgery, the prognosis is generally poor. Renal cell carcinoma does not generally respond to chemotherapy or radiation. Immunotherapy, which attempts to induce the body to attack the remaining cancer cells, has shown promise. Recent trials are testing newer agents, though the current complete remission rate with these approaches is still low, around 12-20% in most series. Most recently, treatment with tyrosine kinase inhibitors including nexavar, pazopanib, and rapamycin have shown promise in improving the prognosis for advanced RCC.[83]

The incidence of the disease varies according to geographic, demographic and, to a lesser extent, hereditary factors. There are some known risk factors, however the significance of other potential risk factors remains more controversial. The incidence of the cancer has been increasing in frequency worldwide at a rate of approximately 2-3% per decade[75] until the last few years where the number of new cases has stabilised.[14]

The incidence of RCC varies between sexes, ages, races and geographic location around the world. Men have a higher incidence than women (approximately 1.6:1)[72] and the vast majority are diagnosed after 65 years of age.[72] Asians reportedly have a significantly lower incidence of RCC than whites and while African countries have the lowest reported incidences, African Americans have the highest incidence of the population in the United States.[14] Developed countries have a higher incidence than developing countries, with the highest rates found in North America, Europe and Australia / New Zealand[84]

Daniel Sennert made the first reference suggesting a tumour arising in the kidney in his text Practicae Medicinae, first published in 1613.[85]

Miril published the earliest unequivocal case of renal carcinoma in 1810.[86] He described the case of Franoise Levelly, a 35 year old woman, who presented to Brest Civic Hospital on April 6, 1809, supposedly in the late stages of pregnancy.[85]

Koenig published the first classification of renal tumours based on macroscopic morphology in 1826. Koenig divided the tumors into scirrhous, steatomatous, fungoid and medullary forms.[87]

Following the classification of the tumour, researchers attempted to identify the tissue of origin for renal carcinoma.

The pathogenesis of renal epithelial tumours was debated for decades. The debate was initiated by Paul Grawitz when in 1883, he published his observations on the morphology of small, yellow renal tumours. Grawitz concluded that only alveolar tumours were of adrenal origin, whereas papillary tumours were derived from renal tissue.[85]

In 1893, Paul Sudeck challenged the theory postulated by Grawitz by publishing descriptions of renal tumours in which he identified atypical features within renal tubules and noted a gradation of these atypical features between the tubules and neighboring malignant tumour. In 1894, Otto Lubarsch, who supported the theory postulated by Grawitz coined the term hypernephroid tumor, which was amended tohypernephroma by Felix Victor Birch-Hirschfeld to describe these tumours.[88]

Vigorous criticism of Grawitz was provided by Oskar Stoerk in 1908, who considered the adrenal origin of renal tumours to be unproved. Despite the compelling arguments against the theory postulated by Grawitz, the term hypernephroma, with its associated adrenal connotation, persisted in the literature.[85]

Foot and Humphreys, and Foote et al. introduced the term Renal Celled Carcinoma to emphasize a renal tubular origin for these tumours. Their designation was slightly altered by Fetter to the now widely accepted term Renal Cell Carcinoma.[89]

Convincing evidence to settle the debate was offered by Oberling et al. in 1959 who studied the ultrastructure of clear cells from eight renal carcinomas. They found that the tumour cell cytoplasm contained numerous mitochondria and deposits of glycogen and fat. They identified cytoplasmic membranes inserted perpendicularly onto basement membrane with occasional cells containing microvilli along the free borders. They concluded that these features indicated that the tumours arose from the epithelial cells of the renal convoluted tubule, thus finally settling one of the most debated issues in tumour pathology.[85][90]

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Renal cell carcinoma - Wikipedia, the free encyclopedia

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Graduate Medical Education (GME): Medical Genetics

Maximilian Muenke, MD

Eligibility CriteriaCandidates with the MD degree must have completed an accredited U.S. residency training program and have a valid U.S. license. Previous training is usually in, but not limited to, Pediatrics, Internal Medicine or Obstetrics and Gynecology.

OverviewThe NIH has joined forces with training programs at the Children's National Medical Center, George Washington University School of Medicine and Washington Hospital Center. The combined training program in Medical Genetics is called the Metropolitan Washington, DC Medical Genetics Program. This is a program of three years duration for MDs seeking broad exposure to both clinical and research experience in human genetics.

The NIH sponsor of the program is National Human Genome Research Institute (NHGRI). Other participating institutes include the National Cancer Institute (NCI), the National Eye Institute (NEI), the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), the National Institute of Child Health and Human Development (NICHD), the National Institute on Deafness and Other Communication Disorders (NIDCD), the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), and the National Institute of Mental Health (NIMH). Metropolitan area participants include Children's National Medical Center (George Washington University), Walter Reed Army Medical Center, and the Department of Pediatrics, and the Department of Obstetrics and Gynecology at Washington Hospital Center. The individual disciplines in the program include clinical genetics, biochemical genetics, clinical cytogenetics, and clinical molecular genetics.

The primary goal of the training program is to provide highly motivated physicians with broad exposure to both clinical and research experiences in medical genetics. We train candidates to become effective, independent medical geneticists, prepared to deliver a high standard of clinical genetics services, and to perform state-of-the-art research in the area of genetic disease.

Structure of the Clinical Training Program

RotationsThis three year program involves eighteen months devoted to learning in clinical genetics followed by eighteen months of clinical or laboratory research.

Year 1Six months will be spent on rotation at the NIH. Service will include time spent on different outpatient genetics clinics, including Cancer Genetics and Endocrine Disorders and Genetic Ophthalmology; on the inpatient metabolic disease and endocrinology ward; on inpatient wards for individuals involved in gene therapy trials; and on the NIH Genetics Consultation Service.

Three months will be spent at Children's National Medical Center and will be concentrated on pediatric genetics. Fellows will participate in outpatient clinics, satellite and outreach clinics. They will perform consults on inpatients and patients with metabolic disorders and on the neonatal service. Fellows will be expected to participate in the relevant diagnostic laboratory studies on patients for whom they have provided clinical care.

One month will be spent at Walter Reed Army Medical Center and will concentrate on adult and pediatric clinical genetics. One month will be spent at Washington Hospital Center on rotations in prenatal genetics and genetic counseling.

Year 2 Fellows will spend one month each in clinical cytogenetics, biochemical genetics, and molecular diagnostic laboratories. The remaining three months will be devoted to elective clinical rotations on any of the rotations previously mentioned. The second six months will be spent on laboratory or clinical research. The fellow will spend at least a half-day per week in clinic at any one of the three participating institutions.

Year 3This year will be devoted to research, with at least a half day per week in clinic.

NIH Genetics Clinic (Required)Fellows see patients on a variety of research protocols. The Genetics Clinic also selectively accepts referrals of patients requiring diagnostic assessment and genetic counseling. Areas of interest and expertise include: chromosomal abnormalities, congenital anomalies and malformation syndromes, biochemical defects, bone and connective tissue disorders, neurological disease, eye disorders, and familial cancers.

Inpatient Consultation Service (Required)Fellows are available twenty-four hours daily to respond to requests for genetics consultation throughout the 325-bed hospital. Written consultation procedures call for a prompt preliminary evaluation, a written response within twenty-four hours, and a subsequent presentation to a senior staff geneticist, with an addendum to the consult, as needed. The consultant service fellow presents the most interesting cases from the wards during the Post-Clinic Patient Conference on Wednesday afternoons during which Fellows present interesting clinical cases for critical review. Once a month the fellow presents relevant articles for journal club.

Metropolitan Area Genetics Clinics

Other Clinical Opportunities: Specialty Clinics at NIHThe specialty clinics of NIH treat a large number of patients with genetic diseases. We have negotiated a supervised experience for some of the fellows at various clinics; to date, fellows have participated in the Cystic Fibrosis Clinic, the Lipid Clinic, and the Endocrine Clinic.

Lectures, Courses and SeminarsThe fellowship program includes many lectures, courses and seminars. Among them are a journal club and seminars in medical genetics during which invited speakers discuss research and clinical topics of current interest. In addition, the following four courses have been specifically developed to meet the needs of the fellows:

Trainees are encouraged to pursue other opportunities for continuing education such as clinical and basic science conferences, tutorial seminars, and postgraduate courses, which are plentiful on the NIH campus.

Structure of the Research Training ProgramFellows in the Medical Genetics Program pursue state-of-the-art research related to genetic disorders. Descriptions of the diverse interests of participating faculty are provided in this catalog. The aim of this program is to provide fellows with research experiences of the highest caliber and to prepare them for careers as independent clinicians and investigators in medical genetics.

Fellows entering the program are required to select a research supervisor which may be from among those involved on the Genetics Fellowship Faculty Program. It is not required that this selection be made before coming to NIH.

In addition to being involved in research, all fellows attend and participate in weekly research seminars, journal clubs and laboratory conferences, which are required elements of each fellow's individual research experience.

Program Faculty and Research Interests

Examples of Papers Authored by Program Faculty

Program GraduatesThe following is a partial list of graduates including their current positions:

Application Information

The NIH/Metropolitan Washington Medical Genetics Residency Program is accredited by the ACGME and the American Board of Medical Genetics. Upon successful completion of the three year program, residents are eligible for board certification in Clinical Genetics. During the third residency year, residents may elect to complete either (a) the requirements for one of the ABMG laboratory subspecialties, such as Clinical Molecular Genetics, Clinical Biochemical Genetics or Clinical Cytogenetics, or (b) a second one year residency program (e.g., Medical Biochemical Genetics).

Candidates should apply through ERAS, beginning July 1 of the year prior to their anticipated start date. Candidates with the MD or MD and PhD degree must have completed a U.S. residency in a clinically related field. Previous training is usually in, but not limited to, Pediatrics, Internal Medicine or Obstetrics and Gynecology. Four new positions are available each year. Interviews are held during August and September.

Electronic Application The quickest and easiest way to find out more about this training program or to apply for consideration is to do it electronically.

The NIH is dedicated to building a diverse community in its training and employment programs.

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Dr. Moroz and several members of his laboratory were recently featured in a story by Gainesvilles Our Town Magazine. The article follows the groundbreaking work done by the Moroz lab while at sea in their floating laboratory, a facility equipped with the latest in invertebrate sampling and genetic sequencing technology. Click here to read the

Please join us as Dr. Kate Mansfield from the University of Central Florida presents Tracking the sea turtle lost years for the Evenings at the Whitney public lecture series on Thursday, August 20th at 7 PM. Dr. Mansfield is a pioneer in satellite telemetry studies on wild sea turtles and will share her teams work

Whitney Lab undergraduate interns have been hard at work this summer helping out with our Marine Biology Summer Camp. Flagler College undergraduate internsMadison Skidmore and Cypres Ferran have been doing such a great job that they have caught the attention of the St. Augustine Record! Click here to read the full article!

Alexis Lanza, a Ph.D. student in the Seaver lab recently completed a journalism internship with the Society for Integrative and Comparative Biology (SICB). Lanza was 1 of 4 students who were awarded a learning opportunity on how to communicate a scientific topic to the general public. Her article detailed work by Dr. Sewall on the

The Sea Turtle release of Mahi earlier this month was a huge event! Over 200+ people attended the release includingstaff and volunteers from the Whitney Lab.Mahi, a juvenile green sea turtle, was rehabilitated by The Georgia Sea Turtle Center. After more than two years of intensive rehabilitation and care, the GSTC with local partners released

You may be thinking, wow, that little worm has such a complex nervous system with so many different nerve cells Yes indeed! In a recent paper entitled Nervous system development in lecithotrophic larval and juvenile stages of the annelid Capitella teleta published in the open access online journal Frontiers in Zoology on July 11,

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Whitney Laboratory for Marine Bioscience - St. Augustine, FL

Recommendation and review posted by sam

Biotechnology is the use of biological processes, organisms, or systems to manufacture products intended to improve the quality of human life. The earliest biotechnologists were farmers who developed improved species of plants and animals by cross pollenization or cross breeding. In recent years, biotechnology has expanded in sophistication, scope, and applicability.

The science of biotechnology can be broken down into subdisciplines called red, white, green, and blue. Red biotechnology involves medical processes such as getting organisms to produce new drugs, or using stem cells to regenerate damaged human tissues and perhaps re-grow entire organs. White (also called gray) biotechnology involves industrial processes such as the production of new chemicals or the development of new fuels for vehicles. Green biotechnology applies to agriculture and involves such processes as the development of pest-resistant grains or the accelerated evolution of disease-resistant animals. Blue biotechnology, rarely mentioned, encompasses processes in marine and aquatic environments, such as controlling the proliferation of noxious water-borne organisms.

Biotechnology, like other advanced technologies, has the potential for misuse. Concern about this has led to efforts by some groups to enact legislation restricting or banning certain processes or programs, such as human cloning and embryonic stem-cell research. There is also concern that if biotechnological processes are used by groups with nefarious intent, the end result could be biological warfare.

Also see nanotechnology and genetic engineering .

This was last updated in May 2007

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What is biotechnology? - Definition from WhatIs.com

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Amrita School of Biotechnology, with qualified faculty including several Ph. D.s recruited from academia and industry around the world, is perfectly poised to offer students an opportunity to develop expertise and succeed in building a career in the exciting areas of biotechnology and related fields. Our cutting-edge curricula with state-of-the-art facilities for teaching and research will provide a solid foundation in the biological sciences. With a vibrant academic environment and a unique approach to learning that involves thought-provoking discussions and constant interaction among students and faculty,...Read More

The School offers three postgraduate and two undergraduate programs in biotechnology, microbiology and bioinformatics as well as research programs.Read more

The Amrita School of Biotechnology offers programs of education at the undergraduate, postgraduate and research levels that bolsters core science concepts...Read more

The faculty, well-known and highly respected in their respective academic fraternities, is really what distinguishes School of Biotechnology. They are drawn from among the best minds in the world. This affords the school an extensive network of contacts which are instrumental in getting collaborative researches, live student projects and industry inputs so essential to quality biotechnology education. The faculty includes acclaimed scholars and award winning professors drawn from all life sciences disciplines. The eclectic blend of faculty, academicians, researchers, and professionals drawn from India and abroad...Read more

The Amrita School of Biotechnology in Amritapuri is also approved as a Centre of Relevance and Excellence [CORE] in Biomedical Technology under the Department of Science and Technology, Government of India, TIFAC Mission REACH programme. Read more

Over the years Amrita School of Biotechnology has developed working relationships with many of the best universities in the world. Strong collaboration with national and international organizations is the hallmark of all research carried out at Amrita School of Biotechnology and to this extent we have developed a broad range of international partnerships around the world. We, at Amrita, give tremendous significance to research and development of new products and technologies and with more than a hundred research projects aiming to benefit society...Read more

The School of Biotechnology is nestled in a serene campus located adjacent to the scenic backwaters of Kerala and the Arabian Sea. Despite the rigors of a life devoted to excellence in technology, creativity blossoms naturally and the spirit of selfless service adds fragrance to every event. The School has separate boarding and mess facilities for male and female students, faculties and researchers. An ever-updating library at the campus with a vast collection of qualitative publications help the student stay abreast with the current knowledge in academics and research domain. Medical assistance around the clock is available... Read more

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Biotechnology | Amrita Vishwa Vidyapeetham (Amrita University)

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Symptom Checker: Symptoms & Signs Index

Medical Author: Melissa Conrad Stppler, MD

Multiple sclerosis symptoms vary widely, and a description of "typical" symptoms is difficult. All the symptoms involve changes in neurologic functioning, but there are striking differences among patients in the type, severity, and frequency of these symptoms. Different disease patterns such as relapsing-remitting (RR), primary-progressive (PP), secondary-progressive (SP), and progressive-relapsing (PR) classify the condition according to the development and progression of symptoms over time. Relapsing-remitting (RR) multiple sclerosis is the most common type, in which symptoms (exacerbations of the condition) are followed by periods of time with reduced or no symptoms. These relatively symptom-free periods, known as remissions, can last for days or for many years.

Some cases of multiple sclerosis are so mild that the condition is difficult to diagnose. In other cases, there is a gradual decline in functioning through the years. In very rare cases, symptoms can be so severe and rapidly progressing as to be fatal within a short time (known as malignant or fulminant MS). Symptoms can be related to one body part or may involve multiple areas of the body. They may be of short duration or may persist for a long time. Some symptoms of multiple sclerosis are mild and cause inconvenience; others may be severe and debilitating.

Visual disturbances can be the first sign of MS. The vision changes can include blurred vision, distortions, or loss of vision in one eye. The vision symptoms can be accompanied by eye pain. Other symptoms can include tingling, numbness, prickling pain, or muscle spasms in the arms and legs that may occur at one or multiple sites. Weakness in the arm and leg muscles may occur, and this can sometimes affect balance and posture, causing clumsiness or lack of coordination. Other symptoms include fatigue, dizziness, difficulties with speech, tremors, heat intolerance, and loss of sensation. Sexual dysfunction and loss of bladder or bowel control can develop in more serious cases.

Mental changes can also occur as symptoms of multiple sclerosis. Memory loss, decreased ability to concentrate, attention deficits, an inability to perform sequential tasks, and changes in judgment have all been reported. Depression, mania, paranoia, and uncontrollable urges to laugh or weep are other symptoms that have been described.

Summary of Common MS Symptoms by MedicineNet Staff A review of our Patient Comments indicated that many people with multiple sclerosis (MS) have similar symptoms. Many patients said that they were in their 40s when their symptoms began. Optic neuritis was often the first MS symptom that people experienced. Initial symptoms also included numbness in the arms, feet, hands, and face, coupled with fatigue, dizziness, and difficulty walking. Several people also reported losing their balance and falling down, while others mentioned feeling a prickly heat sensation in their legs. Read on to learn more about MS symptoms in our Patient Comments.

Medically Reviewed by a Doctor on 4/8/2015

REFERENCE:

Luzzio, Christopher. "Multiple Sclerosis." Medscape.com. Nov. 24, 2014. <http://emedicine.medscape.com/article/1146199-overview>.

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Multiple Sclerosis (MS): Check Your Symptoms and Signs

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Overview of Multiple Sclerosis

Multiple sclerosis (MS) is an inflammatory, chronic, degenerative disorder that affects nerves in the brain and spinal cord. Myelin, the fatty substance that surrounds and insulates nerves and facilitates the conduction of nerve impulses is the initial target of inflammatory destruction in multiple sclerosis.

MS is characterized by intermittent damage to myelin, called demyelination. Demyelination causes scarring and hardening (sclerosis) of nerve tissue in the spinal cord, brain and optic nerves. Demyelination slows conduction of nerve impulses, which results in weakness, numbness, pain and vision loss.

Because different nerves are affected at different times, MS symptoms often worsen (exacerbate), improve, and develop in different areas of the body. Early symptoms of the disorder may include vision changes (e.g., blurred vision, blind spots), numbness, dizziness and muscle weakness.

MS can progress steadily or cause acute attacks (exacerbations) followed by partial or complete reduction in symptoms (remission). Most patients with the disease have a normal lifespan.

MS is the most common neurological cause of debilitation in young people. According to the National Institute of Neurological Disorders and Stroke, about 250,000 - 350,000 people in the United States have been diagnosed with multiple sclerosis. Worldwide, the incidence of MS is approximately 0.1 percent. Northern Europe, the northern United States, southern Australia, and New Zealand have the highest prevalence, with more than 30 cases per 100,000 people.

MS is more common in women and in Caucasians. The average age of onset is between 20 and 40, but the disorder may develop at any age. Children of parents with MS have a higher rate of incidence (30 - 50 percent).

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Multiple Sclerosis (MS) Overview - HealthCommunities.com

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A Close Look at MS Symptoms

Multiple sclerosis(MS) is a disease with unpredictable symptoms that can vary in intensity. While some people experience fatigue and numbness, severe cases of MS can cause paralysis, visionloss, and diminishedbrainfunction.

MS affects an estimated 2.3 million people worldwide. Womenare affected more than twice as often as men, according to the National MS Society. Family history is also a major risk factor.

MS is a progressive autoimmune disorder. That means the system designed to keep your body healthy mistakenly attacks parts of your body that are vital to everyday function. The protective covering of nerve cells are damaged, which leads to diminished function in the brain and spinal column.

The cause of MS largely remains a mystery, even though the disease was discovered in 1868. Researchers know the nerve damage is caused by inflammation, but the cause of the inflammation is still unknown.

The most common early signs of MS arevision problems, clinically called optic neuritis. Inflammation affects the optic nerve and disrupts central vision. This can lead toblurred visionin one or both eyes, double vision, or loss of contrast or vivid colors.

You may not notice the vision problems immediately, as degeneration of clear vision can be slow. Pain when you look up or to one side also can accompany vision loss.

MS affects nerves in the brain and spinal column (the bodys message center). This means it can send conflicting signals around the body. Sometimes, no signals are sent. This results in the most common symptom:numbness.

Tingling sensations and numbness are the most common warning signs of MS. Common sites of numbness include the face, arms, legs, and fingers.

Chronic pain and involuntary muscle spasms are also common with MS. One study, according to the National MS Society, showed that half of people with MS had either clinically significant pain or chronic pain.

Muscle stiffness or spasms (spasticity) are also common. They involve feelings of stiff muscles or joints as well as uncontrollable, painful jerking movements of extremities. The legs are most often affected, but back pain is also common.

Unexplainedfatigueand weaknessaffect about 80 percent of people in the early stages of MS.

Chronic fatigue occurs when nerves deteriorate in the spinal column. Usually, the fatigue appears suddenly and lasts for weeks before improving. The weakness is most noticeable in the legs at first.

Dizzinessand problems with coordination and balance can decrease the mobility of someone with MS. Your doctor may refer to these as problems with yourgait.People with MS often feel lightheaded, dizzy, or feel as if their surroundings are spinning (vertigo). This symptom often occurs when a person stands up.

Adysfunctional bladderis another symptom occurring in up to 80 percent of people with MS. This can include urinating frequently, strong urges to urinate, or inability to hold in urine.

Urinary-related symptoms are often manageable. Less often, people with MS experience constipation, diarrhea, or loss of bowel control.

Sexual arousalcan also be a problem for people with MS because it begins in the central nervous system where MS attacks.

About half of people with MS will develop some kind of issue with their cognitive function. This can include:

Depression and other emotional health problems are also common.

Major depressionis common among people with MS. The stresses of MS can also cause irritability, mood swings, and a condition calledpseudobulbar affect: bouts of uncontrollable crying and laughing.

Coping with MS symptoms, along with relationship or family issues, can make depression and other emotional disorders even more challenging.

Not everyone with MS will have the same symptoms. Different symptoms can manifest themselves during attacks. Along with the symptoms mentioned on the previous slides, MS can also cause:

MS often astounds doctors because of how much it can vary in both its severity and the ways that it affects people. Attacks can last a few weeks and then disappear. However, relapses can get progressively worse, more unpredictable, and come with different symptoms.

However, early detection may help prevent MS from progressing quickly.

MS isnt necessarily hereditary. However, you have a higher chance of developing the disease if you have a close relative with MS, according to theNational MS Society.

The general population only has a tenth of a percent chance of developing MS. But theNational MS Societyreports that number jumps to 2.5 to 5 percent if you have a sibling or parent with MS.

Heredity isnt the only factor in determining MS. An identical twin only has a 25 percent chance of developing MS if their twin has the disease. While genetics is certainly a risk factor, its not the only one.

A doctor most likely a neurologist will perform several tests to diagnose MS, including:

Doctors use these tests to look for damage to the central nervous system in two separate areas that occurred at least one month apart. These tests are also used to rule out other conditions.

MS is a challenging disorder, but researchers have discovered many treatments that can slow its progression.

The best defense against MS is seeing your doctor immediately after you experience the first warning signs. This is especially important if someone in your immediate family has the disorder, as its one of the key risk factors for MS.

Don't hesitate. It could make all the difference.

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13 Early Signs & Symptoms of Multiple Sclerosis

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Multiple Sclerosis (cont.) When to Seek Medical Care

The symptoms of multiple sclerosis are very variable and differ from patient to patient. They can also be confused with symptoms of many other conditions. A physician should be notified if you or someone you know has any of the signs and symptoms associated with multiple sclerosis. Also check with a doctor if you or someone you know has any signs or symptoms that may not be associated but that are of concern. The person may not have multiple sclerosis, but because of the nonspecific nature of this disease, it is best to let a qualified professional make that determination.

Several of the symptoms of multiple sclerosis may be severe enough to send the patient to a hospital's emergency department.

Diagnosing multiple sclerosis is difficult. The vague and nonspecific nature of this disease mimics many other diseases. Doctors combine history, physical exam, laboratory work, and sophisticated medical imaging techniques to arrive at a diagnosis.

Medically Reviewed by a Doctor on 3/12/2015

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Multiple Sclerosis Causes, Symptoms, Treatment - When to ...

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What is multiple sclerosis (MS)?

Multiple sclerosis is an autoimmune disease that affects the nervous system. Normally, antibodies produced by the immune system help protect the body against viruses, bacteria and other foreign substances. In people who have MS, the immune system destroys the substance that surrounds and protects your nerve cells the myelin sheath.

The job of the nervous system is to send electrical messages back and forth from the brain to different parts of the body. Normally, the brain quickly sends signals through the spinal cord and then through nerves that branch out to all organs and body parts. When myelin around nerves is damaged or destroyed, the nerves cant function properly to deliver these signals in the right way. This can cause symptoms throughout the body.

The most common form of MS is known as relapsing-remitting MS (RRMS). When people who have this kind of MS have flare-ups, the symptoms become noticeably worse. Then there is a period of recovery, when symptoms get better or disappear completely for some time. In RRMS, symptom flare-ups may be triggered by an infection, such as the flu. More than 50% of people who have RRMS develop the secondary progressive type in which there are relapses followed by a gradual worsening of the disease.

About 15% to 20% of people who have MS have a form known as primary-progressive MS (PPMS). In this kind of MS, the disease gets steadily worse, without any remissions. A fourth typeprogressive relapsing MSis rare, but the pattern follows a worsening of the disease with sudden, clear relapses.

Often MS is mild, but some people lose the ability to write, speak or walk.

This information was developed as part of an educational program made possible through support from AstraZeneca.

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Multiple Sclerosis | Overview

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