29 Jul 2011

Glycoconjugates as well as Membrane Carbohydrates


Tissue recognize one another due to the saccharides attached to cell areas.
They're present generally since oligosaccharides associated through covalent links to lipids and/or protein developing Glycoconjugates. The actual lipid or protein part is integrated into the cell membrane layer structure, using the saccharide part towards the external membrane surface.
Membrane carbohydrates (2-10% of the membranes) are on the extracellular surface bounded to lipids or proteins from the membrane, forming glycoconjugates that serve as docking sites in cell recognition, adhesion and receptor action. These types of sugars include primarily glucose, galactose, mannose, fucose, N-acetyl galactosamine and N-acetyl glucosamine.
The different types of Glycoconjugates include

Type of glycoconjugates
Sugar string + protein = glycoprotein
Sugar string + lipid = glycolipid
Extremely long sugar chains (glycosaminoglycan) + protein = proteoglycan


Proteoglycans
 In the Proteoglycans, the Glucosaminoglycan moety types the greater fraction of the molecule (tipically a proteoglycan consists of 95 % of carbohydrates) and is the main site of biological activity, supplying several binding sites. They're discovered mostly in the extracellular matrix. They are major components of connective cells.
Glycoproteins:
Membrane layer bound glycoproteins take part in a wide range of cellular phenomena, including cell recognition, cell surface area antigenicity, etc. In the glycoproteins, the majority of the molecule consist of proteins; they have one or more oligosaccharides mounted on the protein, and they are definitely branched and do not possess serial repeats, so they tend to be rich in information, developing highly specific sites for recognition and higher affinity binding through additional proteins
Glycolipids
tend to be membrane lipids where the hydrophilic head organizations tend to be oligosaccharides.

As in glycoproteins, glycolipids act as particular sites with regard to recognition by carbohydrate holding proteins. The actual four kinds of human RBC have different oligosaccharides (antigens) in their cell membranes. Blood groups depends on the gangliosides (a type of sphingolipid) in the surface of the RBC .

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Details On HIV | AIDS


 What is HIV?
"HIV" stands for Human Immunodeficiency Virus.
Many persons also refer to HIV as the "AIDS virus.”

How is the virus Transmitted?

HIV lives in blood and other body fluids that hold blood or white blood cells. People have gotten HIV throughout:
• Unprotected sexual interaction with an HIV-infected human being. This includes vaginal or anal interaction, and by word of mouth sex on a man or woman without a condom or other barrier. association while a woman is having her period, or during outbreaks of genital sores or lesions (caused by herpes and other sexually transmitted diseases) can increase the risk of HIV transmission.
• sharing drug injection equipment (needles and/or works); or being accidentally stuck by needles or sharp objects contaminated with infected blood.
• infected blood used in transfusions, and infected blood products used in the treatment of certain diseases and disorders (like hemophilia), before March 1985. (Since 1985, federally mandated screening of the blood supply has reduced the risk of transmission through this route to 1 in 255, 000.)
• pregnancy, childbirth, and/or breastfeeding, where the virus is passed from mother to child.
• transplanted organs from infected donors. (Routine screening of organ donors also began in 1985.)
HIV and AIDS are not transmitted through casual contact (that is, where no blood or body fluids are involved). HIV is what gets passed from person to person. People don't "catch AIDS"; they "become infected with HIV. "

How do you prevent infection with HIV?
HIV in sufficient amounts to cause infection exists in blood, semen, vaginal fluid, and breast milk. You can prevent infection with HIV by making sure that these fluids from an HIV-infected man or woman don't have a chance to enter your body. The best ways to be sure are to practice safer sex by using condoms and to refuse to share drug-injection equipment with anyone.
• Use a latex condom every time you have sex.

If you have vaginal or anal sex, use a latex condom. Use a condom or a dental dam (a square of latex) if you have oral sex. A condom will keep the virus, which can be found in semen or vaginal fluids, from getting into your body. Always use a latex condom; lambskin condoms don't protect you from HIV. Always use a water-based lubricant, such as K-Y Jelly or Foreplay. Oil-based lubricants, like vegetable oil, hand lotion, or petroleum jelly (Vaseline), can make the condom break. It is best to use a lubricant that does not contain the spermicide nonoxynol-9. Research shows that nonoxynol-9 does not protect against HIV, and in fact, may cause irritation that can make it easier for HIV to be transmitted. For more information on nonoxynol-9, see this factsheet, created by the Global Campaign for Microbicides(see“global-campaign.org/index.htm”). Also, remember that many kinds of sex won't put you at risk for HIV infection. Try massage, masturbation (with a partner or alone), foreplay, phone sex, or kissing.

• Always use a sterile syringe.
If you use a syringe or needle for any reason, the best way to protect yourself from contracting HIV is to ALWAYS use a sterile syringe and needle and to never share them with anyone. Remember that cookers and cotton can also have HIV in them, so do not share them with anyone either.

What does an "HIV-positive" test result mean?
A positive test result means your body has been infected by the human immunodeficiency virus - and that you are capable of transmitting it to others. The test did not look for the actual virus itself, but found evidence of it in your blood. There's no way to tell from this result who gave you the virus, how long you've had it, or when it will begin to affect your health. You may see or hear the results called "HIV-positive, " "HIV+, " "HIV-antibody positive, " or "seropositive for HIV. " These terms all mean the same thing. People who have been infected with the human immunodeficiency virus are said to have "HIV disease. " While the virus itself is not a disease, it progressively damages the body's immune system. This puts you at risk for developing illnesses you wouldn't otherwise get.
At this time, doctors don't know of any way to rid the body of HIV. There is no cure. Once you've been infected, you have it for life.

How does HIV harm the body?
Viruses tend to be specialists. They zero in on a few particular types of cells in the body and move in. The human immunodeficiency virus is best known for targeting the T cells of the immune system. However, it can also attack cells of the brain, nervous system, digestive system, lymphatic system, and other parts of the body.
The immune system is made up of specialized cells in the bloodstream that fight off invading germs to keep the body healthy. The "T" cells (also referred to as "T4,” "helper-T, " or "CD4" cells) are the brains of the operation. These white blood cells identify invaders and give orders to soldier-type cells, which then battle various bacteria, viruses, cancers, fungi, and parasites that can make a person sick.
Like all viruses, HIV is only concerned in one thing: Reproducing itself. Once it has attacked and moved into a T cell, it converts that cell into a miniature virus factory. Eventually there are so many new viruses in the cell that the T cell explodes, scattering the HIV back into the bloodstream. The virus then moves on to fresh T cells and repeats the process. Over time, HIV can destroy virtually all of an infected person's T cells in this manner.
With fewer and fewer "leaders" to rely on for warnings, the "soldier" cells become powerless. They can no longer recognize and fight off common organisms that would not present a problem to a healthy immune system. These organisms may be lying dormant in the body already, or may enter from outside. The immune system's weakness gives them the opportunity to wake up, multiply, and cause illness. Thus, we call these illnesses "opportunistic infections. " People with fully functioning immune systems are almost never troubled by these particular infections -- but those with damaged immune systems are highly vulnerable to them.

So what's the connection between HIV and AIDS?
When a person with an HIV-weakened immune system comes down with one or more of these rare opportunistic infections, or has a T cell count below 200 or 14%, that person may be diagnosed by a doctor as having AIDS. "AIDS" stands for "Acquired Immune Deficiency Syndrome. " The "syndrome" part means that AIDS is not a single disease but a collection of diseases. The Centers for Disease Control (CDC) has put together a list of 26 "AIDS-defining illnesses" in adults. Diagnosis of Aids in children involves a list of slightly different ailments.
AIDS can be thought of as the most severe form of HIV disease. HIV is the primary agent that leads to the development of AIDS.
Importantly, though, not all people with HIV have AIDS. In fact, statistics from 2000 report that only about 32% of the estimated one million people in the U. S. Now infected with HIV have progressed to that stage of the disease. It is not yet known whether everyone living with HIV will go on to develop AIDS, or if HIV is the only factor that causes it. AIDS is only a small part of the total HIV picture; many experts describe it as "the tip of the iceberg. "

How much time do i have before I get sick?
One of the most important determining factors in whether or not a person will get sick largely depends on how soon in the disease progression they seek medical care. But, everyone with HIV will have a different experience. Those who do not receive drug therapy will increase their chances of becoming ill. A few men and women won't have any HIV-related symptoms at all. They may only come down with an AIDS-defining illness years down the road when their T cells are almost gone -- if ever. Others will face a continuing series of non-life-threatening symptoms (rashes, fungal infections, diarrhea) as the virus gradually weakens their immune system.
Based on past experience, most people who test positive for HIV will likely fall somewhere in between these two illness extremes. They can expect to have a few symptoms here and there over a number of years before being diagnosed with "frank" (or "full-blown" or "classic") AIDS. Symptoms won't show up on any set schedule or in any particular order.
Experts now say the average length of time between infection with the virus and diagnosis of the first serious AIDS-related illness is 10-15 years. Though no one knows exactly why, a large percentage of women, infants, and the elderly seem to become ill sooner.
However, keep in mind that these "predictions" apply to the group of HIV-infected people as a whole. You as an individual may have a very different outlook. A lot can depend on your general state of health at the time you got the virus, how long you've had it -- and how aggressively you decide to fight it now. Only time will tell what your own experience will be.

What if I previously have AIDS?
If you've already been diagnosed with AIDS, you may be sick now, but that doesn't mean you'll stay sick. With proper treatment, opportunistic infections can clear up and you could feel fine again (although you will, medically speaking, still have AIDS). Average life expectancy for people with AIDS varies widely. There are people who have lived with the disease for 20 years or more.
The key thing to remember is, an HIV-positive test result or diagnosis of AIDS is not an automatic, immediate "death sentence. " There are drugs and other preventive measures you can take to help increase your chances for staying well. With good medical care and a positive mental attitude, you can "survive and thrive" for years to come.

Doesn't AIDS kill you?
While the virus itself does not cause death, the opportunistic infections it allows are often lethal. Without therapy, the HIV virus is nearly 100% fatal.
In the past several years, however, critical advances in knowledge, drugs, and treatment philosophies have had a great impact on the life expectancy of HIV-positive individuals. Today, hundreds of thousands of HIV-positive men and women live long and productive lives thanks to new therapy regimens. But it is important to note that there is no cure for HIV. HIV therapies can be expensive and difficult to take, often resulting in severe, and in some cases, debilitating side effects. Not everyone benefits from HIV therapy. While there remains hope for people living with HIV, it is critical for every person, HIV-positive or negative, to practice prevention. For more information on national treatment guidelines, please see this “aidsinfo.nih.gov/”.

What symptoms or illnesses must i be inspection out for?
As mentioned, the CDC has drawn up a specific list of AIDS-defining illnesses. Doctors use this list to make a diagnosis of Aids in their HIV-infected patients who become ill.
The most common AIDS-related illness is pneumocystis carinii pneumonia ("PCP, " for short). The first symptoms to look out for are a dry cough and unusual shortness of breath. The bad news about PCP is that it's one of the most deadly diseases you'll be likely to face. The good news is, it often can be prevented. Your doctor can prescribe medication to be used on a regular basis. This is known as "prophylactic treatment. "
Kaposi's sarcoma (or "KS") is a cancer-like illness that occurs mainly in gay men. Those who get it may notice pink, brown, or purplish spots or lesions on their skin, or in their nose or mouth. KS can also show up internally. The external lesions can often be successfully removed, and the disease is treatable with radiation and chemotherapy.
There are 24 other AIDS-defining illnesses and conditions on the CDC list. You can ask your doctor to tell you more about them. Only a licensed medical practitioner is qualified to make a diagnosis of AIDS.
In general, if you notice any of the following symptoms in an extreme, chronic, or unexplainable form, it may signal an HIV- or AIDS-related condition:
1.       Night sweats or fever
2.       Cough, shortness of breath, tightness or pressure in the chest
3.       Loss of appetite
4.       Fatigue
5.       Weight loss
6.       Diarrhea
7.       Pain or difficulty swallowing
8.       Headaches
9.       Confusion or forgetfulness
10.     Change in vision
11.     Swollen glands
12.     Sores or whitish patches in the mouth
13.     Specific women's health problems, such as pelvic inflammatory disease, chronic yeast infections, and cervical abnormalities
14.     Any new skin condition (rash, hives, lump, lesion, sore, spot, or growth).
The key words to remember here are "extreme, " "chronic" (meaning it won't go away), and "unexplainable. " Every symptom on the list could just as easily apply to some other condition that may have nothing to do with HIV or AIDS. A person with one or more of those symptoms could have a plain old touch of the flu, just like anyone else. Try to resist the temptation to panic at every little twinge or "blah" day; it doesn't necessarily mean you now have AIDS, or that the end is near. If there's any doubt in your mind, ask your doctor.

What if I'm significant or enclose children?
If you are a mother or about to become one, you may feel an additional burden in response to the news that you're HIV-positive. It's natural for your mind to race through terrible questions: Are my children infected? If they are, will i see them die? What will happen to them if i die first? What will they think of me? How can i forgive myself if they contracted HIV through me? Facing your own illness may seem easy next to the specter of watching your children suffer or die.
To ease your mind of these worries, you'll want to gather lots of information. If you're pregnant now, decide whether you want to proceed with the pregnancy. If the answer is yes, learn what steps can be taken to help protect your health and the baby's. Don't assume any child born to you will be HIV-positive. The chances of delivering a baby with HIV can be as low as 1 in 12 when preventive measures are taken. As a mother or mother-to-be, it's more important than ever to seek out early medical care.
Recent clinical trials have shown that AZT (an antiviral medication) can reduce the risk of HIV transmission from mother to child more than threefold when the drug is administered to the mother during the pregnancy and delivery, and to the newborn during the first six weeks of life. If you are pregnant, the opportunity to decrease the chance that your baby will develop HIV infection is an important consideration as you examine your options. However, the decision to undergo this treatment or any other is yours alone. Get as much information as you can, and follow the course of action you feel most comfortable with.

What is Nonoxynol-9 and can it prevent HIV?
Nonoxynol-9 (N-9) (“archive.aidschicago.org/prevention/n9education.php”) is a detergent found in products sold over the counter as contraceptive spermicides. Condoms with added "spermicide" contain N-9, a chemical additive that, in addition to killing sperm, can erode the internal surfaces of the body, causing irritation and urinary tract infections. This can increase the risk of HIV infection during both vaginal and anal sex.
“archive.aidschicago.org/prevention/n9education.php” for more information.

What are microbicides?
Microbicides are anti-HIV ingredients that could be added to gels, foams, and creams that would be used during vaginal and/or rectal intercourse to reduce the risk of HIV infection. Microbicides could be used with condoms or alone, in situations where individuals will not or cannot negotiate condom usage with their partner. In these situations, individuals need the ability to have protection against HIV without a partner's knowledge. Currently, almost 30 possible microbicides have been developed and are in the research pipeline, but additional funding is needed to ensure these important HIV prevention tools become available worldwide. For more info see “archive.aidschicago.org/prevention/microbicides.php”

Anything in addition I need to keep track of?
Once you get established with a doctor, you will undergo periodic tests to monitor the number of T cells remaining in your blood. This "T cell count" or "CD4 count" will give you and your doctor an idea of how fast and far your disease is progressing, and help you decide when to schedule various treatments.
As a rule, an adult with a healthy immune system would expect to have a T cell count between 800 and 1500. An HIV-infected person with a T cell count of 500 might want to think about starting combination therapy to slow down the virus. People with counts below 200 usually are advised to add preventive treatments for PCP and other infections. You and your doctor can discuss these and other treatments together and decide which ones are best for you to try.
Keep in mind that T cell counts are neither exact nor unchanging. Your T cells may go up and down over time in response to pregnancy, an illness, a new medication, or many other factors. Counts may also vary considerably from day to day or at different times of day. Not everyone experiences a steady downward decline. Ultimately, the approximate number of T cells you have at any given time is much less important than your general state of health. You may have 400 T cells and feel lousy, or 10 T cells and feel great. Try not to let an unexpected or disappointing test result shake you up too much.

Where can i get more information?
The best place to go for advice about living with HIV is your own doctor. However, if she or he is not an HIV specialist, you both may benefit from further reading or consultation. (Besides, no one person -- your doctor included -- can be expected to know everything. )#) There are many excellent information sources and publications available free or at low cost from around the country. Please review our links(“archive.aidschicago.org/links/index.php”) document for a listing of other online resources. You may also call the state of Illinois HIV/AIDS and STD Hotline at 1-800-AID-AIDS for more information on AIDS and for referrals to testing and other services.
The point is, no matter where you are, you needn't feel isolated. Today's technology allows people living in small towns and rural areas access to the same high-quality information and support available in large urban areas. Let the big city come to you!
See for more info “archive.aidschicago.org”.

28 Jul 2011

DNA difference repair address

Any mutational event that disrupts the superhelical structure of DNA carries with it the potential to compromise the genetic stability of a cell. Mismatch repair is a system for recognising and repairing the erroneous insertion, deletion and mis-incorporation of bases that can arise during DNA replication and recombination, as-well as repairing some forms of DNA damage. The fact that the damage detection and repair systems are as complex as the replication machinery itself highlights the importance evolution has attached to DNA fidelity.
Mismatched bases include a G/T or A/C pairing (see DNA repair). The damage is repaired by excising the wrongly incorporated base and replacing it with the correct nucleotide. Usually, this involves more than just the mismatched nucleotide itself, and can lead to the removal of significant tracts of DNA.
Mismatch repair
There are two types of mismatch repair; long patch and short patch. Long patch can repair all types of mismatches (although it is primarily replication associated) and can excise tracts up-to a few kilobases long. Short patch repair handles only specific mismatches caused by damage to the genome, and removes lengths of around 10 nucleotides. Successful mismatch repair requires the error-free execution of three events:
1. Detection of a single mismatch, of which there are eight kinds, in the newly synthesised DNA. 2. Determining which of the two base pairs is incorrect. 3. Correcting the error by excision repair.
Mismatch repair is strand-specific. During DNA synthesis only the newly synthesised (daughter) strand will include errors, and replacing a base in the parental strand would actually introduce an error. The mismatch repair machinery has a number of cues which distinguish the newly synthesised strand from the template (parental). In gram-negative bacteria transient hemimethylation distinguishes the strands (the parental is methylated and daughter is not). In other prokaryotes and eukaryotes the exact mechanism is not clear.
Mismatch repair proteins
Mismatch Repair is a highly conserved process from prokaryotes to eukaryotes. The first evidence for mismatch repair was obtained from S. Pneumoniae (the hexA and hexB genes). Subsequent work on E. Coli has identified a number of genes that, when mutationally inactivated, cause hypermutable strains. The gene products are therefore called the "Mut" proteins, and are the major active components of the mismatch repair system. Three of these proteins are essential in detecting the mismatch and directing repair machinery to it; MutS, MutH and MutL (MutS is a homologue of HexA and MutL of HexB).
MutS forms a dimer (MutS2) that recognises the mismatched base on the daughter strand and binds the mutated DNA. MutH binds at hemimethylated sites along the daughter DNA, but its action is latent, being activated only upon contact by a MutL dimer (MutL2) which binds the MutS-DNA complex and acts as a mediator between MutS2 and MutH, activating the latter. The DNA is looped out to search for the nearest d(GATC) methylation site nearest the mismatch, which could be up to 1kb away. Upon activation by the MutS-DNA complex, MutH nicks the daughter strand near the mismatch and recruits a UvrD helicase (DNA Helicase II) to separate the two strands with a specific 3' to 5' polarity. The entire MutSHL complex then slides along the DNA in the direction of the mismatch, liberating the strand to be excised as it goes. An exonuclease trails the complex and digests the ss-DNA tail. The exonuclease recruited is dependent on which side of the mismatch MutH incises the strand - 5’ or 3’. If the nick made by MutH is on the 5’ end of the mismatch, either RecJ or ExoVIII (both 5’ to 3’ exonucleases) is used. If however the nick is on the 3’ end of the mismatch, ExoI (a 3' to 5' enzyme) is used.
The entire process ends past the mismatch site - i. E. Both the site itself and its surrounding nucleotides are fully excised. The single-stranded gap created by the exonuclease can then be repaired by DNA Polymerase III (assisted by single-strand binding protein), which uses the other strand as a template, and finally sealed by DNA ligase. Dam methylase then rapidly methylates the daughter strand.
MutS
When bound, the MutS2 dimer bends the DNA helix and shields approximately 20 base pairs. It has weak ATPase activity, and binding of ATP leads to the formation of tertiary structures on the surface of the molecule. The crystalline structure of MutS reveals that it is exceptionally asymmetric, and while it's active conformation is a dimer, only one of the two halves interact with the mismatch site.
In Eukaryotes, MutS homologs form two major heterodimers: Msh2/Msh6 and Msh2/Msh3. The Msh2/Msh6 pathway is involved primarily in base substitution and small loop mismatch repair. The Msh2/Msh3 pathway is also involved in small loop repair, in addtion to large loop (~10 nucleotide loops) repair. However, Msh2/Msh3 does not repair base substitutions.
MutL
MutL also has weak ATPase activity (it uses ATP for purposes of movement). It forms a complex with MutS and MutH, increasing the MutS footprint on the DNA.
However, the processivity (the distance the enzyme can move along the DNA before dissociating) of UvrD is only ~40-50bp. Because the distance between the nick created by MutH and the mismatch can average ~600 bp, if there isn't another UvrD loaded the unwound section is then free to reanneal to its complementary strand, forcing the process to start over. However, when assisted by MutL, the rate of UvrD loading is greatly increased. While the processivity (and ATP utilisation) of the individual UvrD molecules remains the same, the total effect on the DNA is boosted considerably; the DNA has no chance to reanneal, as each UvrD unwinds 40-50 bp of DNA, dissociates, and then is immediately replaced by another UvrD, repeating the process. This exposes large sections of DNA to exonuclease digestion, allowing for quick excision(and later replacement) of the incorrect DNA.
Eukaryotes have MutL homologs designated Mlh1 and Pms1. They form a heterodimer which mimics MutL in E. Coli. The human homologue of prokaryotic MutL has three forms designated as MutLα, MutLβ and MutLγ. The MutLα complex is made of two subunits MLH1 and PMS2, the MutLβ heterodimer is made of MLH1 and PMS1, while MutLγ is made of MLH1 and MLH3. MutLα acts as the matchmaker or facilitator, coordinating events in mismatch repair. It has recently been shown to be a DNA endonuclease that introduces strand breaks in DNA upon activation by mismatch and other required proteins, MutSa and PCNA. These strand interruptions serve as entry points for an exonuclease activity that removes mismatched DNA. Roles played by MutLβ and MutLγ in mismatch repair are less well understood.
MutH
MutH is a very weak endonuclease that is activated once bound to MutL (which itself is bound to MutS). It nicks unmethylated DNA and the unmethylated strand of hemimethylated DNA but does not nick fully methylated DNA. It has been experimentally shown that mismatch repair is random if neither strand is methylated. These behaviours led to the proposal that MutH determines which strand contains the mismatch. MutH has no Eukaryotic homolog. It's endonuclease function is taken up by MutL homologs, which have some specialized 5'-3' exonuclease activity. The strand bias for removing mismatches from the newly synthesized daughter strand in eukaryotes may be provided by the free 3’ ends of Okazaki fragments in the new strand created during replication
Defects in mismatch repair
Mutations in the human homologues of the Mut proteins affect genomic stability, which can result in microsatellite instability (MI). MI is implicated in most human cancers. Specifically the overwhelming majority of hereditary nonpolyposis colorectal cancers (HNPCC) are attributed to mutations in the genes encoding the MutS and MutL homologues, which allows them to be classified as tumour suppressor genes. A subtype of HNPCC is known as Muir-Torre Syndrome (MTS) which is associated with skin tumors.

MALARIAL INFECTIVITY ANIMATRONICS

Malaria is a vector-borne infectious disease caused by protozoan parasites. It is widespread in tropical and subtropical regions, including parts of the Americas, Asia, and Africa. Each year, it causes disease in approximately 650 million people and kills between one and three million, most of them young children in Sub-Saharan Africa. Malaria is commonly-associated with poverty, but is also a cause of poverty and a major hindrance to economic development.
video

Malaria is one of the most common infectious diseases and an enormous public-health problem. The disease is caused by protozoan parasites of the genus Plasmodium. The most serious forms of the disease are caused by Plasmodium falciparum and Plasmodium vivax, but other related species (Plasmodium ovale, Plasmodium malariae, and sometimes Plasmodium knowlesi) can also infect humans. This group of human-pathogenic Plasmodium species is usually referred to as malaria parasites.
Malaria parasites are transmitted by female Anopheles mosquitoes. The parasites multiply within red blood cells, causing symptoms that include symptoms of anemia (light headedness, shortness of breath, tachycardia etc. ), as well as other general symptoms such as fever, chills, nausea, flu-like illness, and in severe cases, coma and death. Malaria transmission can be reduced by preventing mosquito bites with mosquito nets and insect repellents, or by mosquito control by spraying insecticides inside houses and draining standing water where mosquitoes lay their eggs.
Pathogenesis
Malaria in humans develops via two phases: An exoerythrocytic (hepatic) and an erythrocytic phase. When an infected mosquito pierces a person's skin to take a blood meal, sporozoites in the mosquito's saliva enter the bloodstream and migrate to the liver. Within 30 minutes of being introduced into the human host, they infect hepatocytes, multiplying asexually and asymptomatically for a period of 6-15 days. During this so-called dormant time in the liver, the sporozoites are often referred to as hypnozoites. Once in the liver these organisms differentiate to yield thousands of merozoites which, following rupture of their host cells, escape into the blood and infect red blood cells, thus beginning the erythrocytic stage of the life cycle. The parasite escapes from the liver undetected by wrapping itself in the cell membrane of the infected host liver cell.
Within the red blood cells the parasites multiply further, again asexually, periodically breaking out of their hosts to invade fresh red blood cells. Several such amplification cycles occur. Thus, classical descriptions of waves of fever arise from simultaneous waves of merozoites escaping and infecting red blood cells.
Some P. Vivax and P. Ovale sporozoites do not immediately develop into exoerythrocytic-phase merozoites, but instead produce hypnozoites that remain dormant for periods ranging from several months (6-12 months is typical) to as long as three years. After a period of dormancy, they reactivate and produce merozoites. Hypnozoites are responsible for long incubation and late relapses in these two species of malaria.
The parasite is relatively protected from attack by the body's immune system because for most of its human life cycle it resides within the liver and blood cells and is relatively invisible to immune surveillance. However, circulating infected blood cells are destroyed in the spleen. To avoid this fate, the P. Falciparum parasite displays adhesive proteins on the surface of the infected blood cells, causing the blood cells to stick to the walls of small blood vessels, thereby sequestering the parasite from passage through the general circulation and the spleen. This "stickiness" is the main factor giving rise to hemorrhagic complications of malaria. High endothelial venules (the smallest branches of the circulatory system) can be blocked by the attachment of masses of these infected red blood cells. The blockage of these vessels causes symptoms such as in placental and cerebral malaria. In cerebral malaria the sequestrated red blood cells can breach the blood brain barrier possibly leading to coma.
Although the red blood cell surface adhesive proteins (called PfEMP1, for Plasmodium falciparum erythrocyte membrane protein 1) are exposed to the immune system they do not serve as good immune targets because of their extreme diversity; there are at least 60 variations of the protein within a single parasite and perhaps limitless versions within parasite populations. Like a thief changing disguises or a spy with multiple passports, the parasite switches between a broad repertoire of PfEMP1 surface proteins, thus staying one step ahead of the pursuing immune system.
Some merozoites turn into male and female gametocytes. If a mosquito pierces the skin of an infected person, it potentially picks up gametocytes within the blood. Fertilization and sexual recombination of the parasite occurs in the mosquito's gut, thereby defining the mosquito as the definitive host of the disease. New sporozoites develop and travel to the mosquito's salivary gland, completing the cycle. Pregnant women are especially attractive to the mosquitoes, and malaria in pregnant women is an important cause of stillbirths, infant mortality and low birth weight

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Genetic system Lecture


Human getting genetics have a very perform (e. G. Transforming a substance or binding to a substance)Sets of functions when sequenced can produce pathways (e. G. Output of one transformation is the input to another) Sets of pathways, because they interact with other pathways, create a genetic network of interactions. The emergent properties of these networks constitute the “observables” when we study cells.

At one point, biological cells can be thought of as "partially-mixed bags" of biological chemicals -- for the purpose gene regulatory network, these chemicals are chiefly the mRNAs and proteins that arise from gene expression. These mRNA and proteins interact with each other with various degrees of specificity. Some diffuse around the cell. Others are bound to cell membranes, interacting with molecules in the environment. Still others pass through cell membranes and mediate long range signals to other cells in a multi-cellular organism. These substances in addition to their connections include a gene regulatory network. A normal gene regulatory system seems something similar to this:

The nodes of this network are proteins, their matching mRNAs, and protein/protein complexes. Nodes that are depicted as lying the length of vertical lines are associated with the cell/environment interfaces, while the other medication is free-floating and diffusible. Implied are genes, the DNA sequences that are copy out to the mRNAs that translate into proteins. Edges between nodes represent individual molecular reactions, the protein/protein and protein/mRNA interactions by which the items of 1 gene influence those of another. These interactions can be inductive (the arrowheads), with an increase in the concentration of one leading to an increase in the other, or inhibitory (the filled circles), with an increase in one leading to a decrease in the other. A series of edges indicates a chain of such dependences, with cycles corresponding to feedback loops. The network structure is an abstraction of the system's chemical dynamics, describing the manifold ways in which one substance affects all the others to which it is connected. In practice, such GRNs are inferred from the biological literature on a given system and represent a distillation of the collective knowledge about a set of related biochemical reactions.

Genes can be viewed as nodes this network, with input being proteins such as transcription factors, and outputs being the level of gene expression. The node itself can also be viewed as a function which can be obtained by combining basic functions upon the inputs (in the Boolean network described below these are Boolean functions or gates computed using the basic AND, OR and NOT gates in electronics). These functions have been interpreted as performing a kind of data running inside cell, which determines cellular behaviour. The basic drivers within cells are levels of some proteins, which determine both spatial (tissue related) and temporal (developmental stage) co-ordinates of the cell, as a kind of "cellular memory". The gene networks are only beginning to be understood, and it is a next step for biology to attempt to deduce the functions for each gene "node", to help in custom modeling rendering conduct of the cell (see systems biology).

Mathematical types of GRNs have been developed to allow predictions of the versions to become examined. The most typical modelling method entails using combined normal differential equations (ODEs). Several other promising modeling techniques have been used, including Boolean networks, Petri nets, Bayesian networks, graphical Gaussian models, Stochastic, and Process Calculi. Conversely, techniques have been proposed for generating models of GRNs that best explain a set of time series observations.

Want the rest of this article? Please visit HereHuman getting genetics have a very perform (e. G. Transforming a substance or binding to a substance)Sets of functions when sequenced can produce pathways (e. G. Output of one transformation is the input to another) Sets of pathways, because they interact with other pathways, create a genetic network of interactions. The emergent properties of these networks constitute the “observables” when we study cells.

At one point, biological cells can be thought of as "partially-mixed bags" of biological chemicals -- for the purpose gene regulatory network, these chemicals are chiefly the mRNAs and proteins that arise from gene expression. These mRNA and proteins interact with each other with various degrees of specificity. Some diffuse around the cell. Others are bound to cell membranes, interacting with molecules in the environment. Still others pass through cell membranes and mediate long range signals to other cells in a multi-cellular organism. These substances in addition to their connections include a gene regulatory network. A normal gene regulatory system seems something similar to this:

The nodes of this network are proteins, their matching mRNAs, and protein/protein complexes. Nodes that are depicted as lying the length of vertical lines are associated with the cell/environment interfaces, while the other medication is free-floating and diffusible. Implied are genes, the DNA sequences that are copy out to the mRNAs that translate into proteins. Edges between nodes represent individual molecular reactions, the protein/protein and protein/mRNA interactions by which the items of 1 gene influence those of another. These interactions can be inductive (the arrowheads), with an increase in the concentration of one leading to an increase in the other, or inhibitory (the filled circles), with an increase in one leading to a decrease in the other. A series of edges indicates a chain of such dependences, with cycles corresponding to feedback loops. The network structure is an abstraction of the system's chemical dynamics, describing the manifold ways in which one substance affects all the others to which it is connected. In practice, such GRNs are inferred from the biological literature on a given system and represent a distillation of the collective knowledge about a set of related biochemical reactions.

Genes can be viewed as nodes this network, with input being proteins such as transcription factors, and outputs being the level of gene expression. The node itself can also be viewed as a function which can be obtained by combining basic functions upon the inputs (in the Boolean network described below these are Boolean functions or gates computed using the basic AND, OR and NOT gates in electronics). These functions have been interpreted as performing a kind of data running inside cell, which determines cellular behaviour. The basic drivers within cells are levels of some proteins, which determine both spatial (tissue related) and temporal (developmental stage) co-ordinates of the cell, as a kind of "cellular memory". The gene networks are only beginning to be understood, and it is a next step for biology to attempt to deduce the functions for each gene "node", to help in custom modeling rendering conduct of the cell (see systems biology).

Mathematical types of GRNs have been developed to allow predictions of the versions to become examined. The most typical modelling method entails using combined normal differential equations (ODEs). Several other promising modeling techniques have been used, including Boolean networks, Petri nets, Bayesian networks, graphical Gaussian models, Stochastic, and Process Calculi. Conversely, techniques have been proposed for generating models of GRNs that best explain a set of time series observations.

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27 Jul 2011

RESULTS OF VARIOUS SCHEMES AND EXAMINATIONS





 Note: - HRDG - CSIR is not responsible for any inadvertent error that may have crept in the results being published on NET. The results published on the NET are for immediate information to the candidates.

Complement System Animation

The particular accentuate method can be a biochemical cascade which usually aids apparent pathogens coming from a great affected person. It really is a single area of the greater disease fighting capability.
The particular accentuate method is made up of variety of tiny protein within the particular blood vessels, which usually come together to be able to eliminate targeted tissues simply by disrupting the mark cell's plasma tissue layer. Above 20 protein and also necessary protein broken phrases make-up the particular accentuate method, which includes serum protein, serosal protein, and also mobile tissue layer receptors. These kinds of protein are usually synthesized mostly inside the liver organ, and so they are the cause of concerning 5% with the globulin portion regarding blood vessels serum.


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The particular accentuate method just isn't versatile and also will not modify throughout ones own life span; therefore that belongs to the inborn disease fighting capability. Nonetheless, it could be new and also delivered directly into actions from the adaptive disease fighting capability.
A few biochemical path ways switch on the particular accentuate method: the particular time-honored accentuate walkway, the alternative accentuate walkway, as well as the mannose-binding lectin walkway
Review
The particular a few path ways almost all create homologous versions with the protease C3-convertase. The particular time-honored accentuate walkway generally needs antibodies regarding initial (certain resistant reply), even though the different walkway may be stimulated simply by C3 hydrolysis or perhaps antigens minus the reputation regarding antibodies (non-specific resistant reply). Mannose-binding lectin walkway belongs to the non-specific resistant reply at the same time. C3-convertase cleaves and also stimulates aspect C3, producing C3a and also C3b and also creating any cascade regarding more cleavage and also initial activities. C3b binds for the surface area regarding pathogens ultimately causing better internalization simply by phagocytic tissues simply by opsonization. C5a can be an crucial chemotactic necessary protein, supporting get inflammatory tissues. Equally C3a and also C5a have got anaphylatoxin action (mast mobile degranulation, improved vascular permeability, clean muscle tissue contraction). C5b starts the particular tissue layer strike walkway, which usually brings about the particular tissue layer strike intricate (MAC PC), composed of C5b, C6, C7, C8, and also polymeric C9. [2] MAC PC could be the cytolytic endproduct with the accentuate cascade; that varieties any transmembrane route, that causes osmotic lysis with the targeted mobile. Kupffer tissues as well as other macrophage mobile sorts aid apparent complement-coated pathogens. Within the inborn disease fighting capability, components of the particular accentuate cascade are located in types prior to when vertebrates; of late inside the protostome horseshoe crab types, getting the particular beginnings with the method again further than once was considered.
Time-honored walkway
The particular time-honored walkway will be induced simply by initial with the C1-complex (which usually contains a single molecule C1q and also a couple of compounds C1r and also C1s), both simply by C1q's holding to be able to antibodies coming from lessons Meters and also Gary, complexed together with antigens, or perhaps simply by the holding C1q to be able to the surface of the pathogen. This kind of holding contributes to conformational adjustments inside C1q molecule, leading for the initial regarding a couple of C1r (serine protease) compounds. Chances are they cleave C1s (one more serine protease). The particular C1-complex today binds to be able to and also breaks C2 and also C4, creating C2a and also C4b. The particular inhibition regarding C1r and also C1s will be governed simply by C1-inhibitor. C4b and also C2a situation to make C3-convertase (C4b2a intricate: NB the particular 2a is in fact the more expensive fragment with the a couple of, despite standard nomenclature designating 'b' broken phrases because the greater). Creation regarding C3-convertase signs the conclusion with the Time-honored Walkway, yet cleavage regarding C3 simply by this kind of enzyme delivers us all to be able to the start of the alternative Walkway.
Choice walkway
The alternative walkway will be induced simply by C3 hydrolysis immediately on top of your pathogen. No count on any pathogen-binding necessary protein just like the some other path ways. [1] Inside the choice walkway, the particular necessary protein C3 will be stated in the particular liver organ, which is next cleaved directly into C3a and also C3b simply by digestive enzymes inside the blood vessels. If you have simply no pathogen inside the blood vessels, the particular C3a and also C3b necessary protein broken phrases will probably be deactivated. Nonetheless, if you have any neighborhood pathogen, a number of the C3b is likely to the particular plasma tissue layer with the pathogen. Next, it's going to situation to be able to aspect T. This kind of intricate will likely then become cleaved simply by aspect N directly into Ba as well as the choice walkway C3-convertase, Bb.
The particular C3bBb intricate, which can be "hooked" on the surface of the pathogen, will likely then behave like any "chain saw", catalyzing the particular hydrolysis regarding C3 inside the blood vessels directly into C3a and also C3b, which usually really outcomes how many C3bBb absolutely hooked on any pathogen.
Right after hydrolysis regarding C3, C3b things to get C3bBbC3b, which usually cleaves C5 directly into C5a and also C5b. C5a and also C3a are usually proven to result in mast mobile degranulation. C5b together with C6, C7, C8, and also C9 (C5b6789) intricate to make the particular tissue layer strike intricate, also referred to as MAC PC, which can be placed in to the mobile tissue layer, "punches any hole", and also starts tissues lysis.
Lectin walkway (MBL : MASP)
The particular lectin walkway will be homologous for the time-honored walkway, yet with all the opsonin, mannan-binding lectin (MBL) and also ficolins, as opposed to C1q. This kind of walkway will be stimulated simply by holding mannan-binding lectin to be able to mannose residues around the pathogen surface area, which usually stimulates the particular MBL-associated serine proteases, MASP-1, MASP-2, MASP-3, that may next separated C4 directly into C4a and also C4b and also C2 directly into C2a and also C2b. C4b and also C2a next situation with each other to make C3-convertase, such as the particular time-honored walkway. Ficolins are usually homologous to be able to MBL and also operate by means of MASP in the same way. Inside invertebrates lacking any adaptive disease fighting capability, ficolins are usually extended and also their particular holding specificities diversified to compensate regarding having less pathogen-specific reputation compounds.
Rules with the Accentuate Method
The particular accentuate method gets the prospective being really harming to be able to sponsor cells that means the initial has to be snugly governed. The particular accentuate method will be governed simply by accentuate handle protein, which can be current with a increased awareness inside the blood vessels plasma compared to the accentuate protein by themselves. Several accentuate handle protein exist around the filters regarding self-cells avoiding these coming from getting precise simply by accentuate. An example will be CD59, which usually suppresses C9 polymerisation through the creation with the tissue layer strike intricate.
Function inside condition
It really is considered the accentuate method may well may play a role in lots of conditions having an resistant aspect, for instance Barraquer-Simons Symptoms, asthma, lupus erythematosus, glomerulonephritis, different kinds of rheumatoid arthritis, autoimmune heart problems, numerous sclerosis, inflammatory colon condition, and also ischemia-reperfusion accidents. The particular accentuate method can be getting increasingly implicated inside conditions with the key stressed method for instance Alzheimer's condition, as well as other neurodegenerative ailments.
Insufficiencies with the airport terminal walkway predispose to be able to equally autoimmune condition and also attacks (specifically meningitis, as a result of function the C56789 intricate takes on inside assaulting Gram unfavorable bacterias).
Modulation simply by attacks
Latest study provides recommended the accentuate method will be inflated in the course of HIV/AIDS to help expand injury our bodies

Monoclonal antibodies


Monoclonal antibodies (mAb or even moAb) tend to be antibodies which are similar simply because they had been made by 1 kind of defense cellular and therefore are just about all imitations of the solitary mother or father cellular. Provided (nearly) any kind of material, you'll be able to produce monoclonal antibodies which particularly hole to that particular material; they are able to after that function in order to identify or even cleanse which material. It's turn out to be an essential device within biochemistry and biology, molecular the field of biology as well as medication. Whenever utilized because medicines
The thought of the "magic bullet" was initially suggested through John Ehrlich that at the start from the twentieth hundred years postulated when the substance might be created which selectively specific the disease-causing patient, a contaminant for your patient might be shipped combined with the broker associated with selectivity.
Within the 1970s the actual B-cell most cancers myeloma had been recognized, also it had been recognized these cancer B-cells just about all create a solitary kind of antibody (the paraprotein). It was accustomed to research the actual framework associated with antibodies, however it wasn't however feasible to create similar antibodies particular to some provided antigen.
The procedure associated with generating monoclonal antibodies referred to over had been created through Georges Köhler, César Milstein, as well as Niels Kaj Jerne within 1975; these people discussed the actual Nobel Reward within Physiology or even Medication within 1984 for that breakthrough. The important thing concept had been to utilize a type of myeloma tissue which experienced dropped their own capability to exude antibodies, think of a way to blend these types of tissue along with wholesome antibody generating B-cells, and then choose for that effectively fused tissue.
Within 1988 Greg Winter season as well as their group pioneered the actual processes to humanize monoclonal antibodies, getting rid of the actual responses that lots of monoclonal antibodies triggered in certain sufferers.
Hybridoma
Monoclonal antibodies could be manufactured in cellular lifestyle or even within reside creatures. If your international material (a good antigen) is actually shot right into a vertebrate like a computer mouse or perhaps a human being, a few of the defense bodies B-cells may become plasma tissue and begin to create antibodies which notice that antigen. Every B-cell creates just one type of antibody, however various B-cells may create structurally various antibodies which hole in order to various components ("epitopes") from the antigen. This particular organic combination of antibodies present in serum is called polyclonal antibodies.
To create monoclonal antibodies, the actual B-cells in the spleen or even lymph nodes tend to be taken off a good pet that's been questioned many times using the antigen associated with curiosity. These types of B-cells tend to be after that fused along with myeloma growth tissue that may develop forever within lifestyle (myeloma is really a B-cell most cancers or even more particularly the plasmacytoma) which possess dropped a chance to create antibodies. This particular blend is performed through producing the actual cellular walls much more permeable through polyethylene glycol (PEG), electroporation or even, associated with historic significance, an infection along with a few computer virus. The actual fused crossbreed tissue (known as hybridomas), becoming most cancers tissue, may grow quickly as well as forever. Considerable amounts associated with antibodies may consequently end up being created. The actual hybridomas tend to be adequately diluted to make sure clonality (just about all tissue within the lifestyle originate in the exact same solitary cellular) as well as developed. The actual antibodies in the various imitations tend to be after that examined for his or her capability to hole towards the antigen (for instance having a check for example ELISA or even Antigen Microarray Assay) or even immuno-dot mark, and also the the majority of delicate the first is selected. Once the hybridoma tissue tend to be shot within rodents (within the peritoneal hole, the actual stomach), these people create growths that contains a good antibody-rich liquid known as ascites liquid.
Within the over procedure, myeloma cellular outlines which have dropped their own capability to create their very own antibodies or even antibody string are utilized, in order to not really ruin the prospective antibody. In addition, just myeloma tissue which have dropped a particular enzyme known as hypoxanthine-guanine phosphoribosyltransferase (HGPRT) and for that reason can't develop below particular problems (at the. grams. within the existence of the choice moderate known as LOATH moderate) are utilized; these types of tissue tend to be preselected through possibly 8-azaguanine or even 6-thioguanine(8-azaguanine may be proven to create hard to rely on outcomes. (truck Diggelen et ing 1979)) press before the blend because tissue which hold the HGPRT is going to be wiped out through the 8-azaguanine. Throughout the blend procedure numerous tissue may blend: Myeloma cellular along with myeloma cellular, spleen cellular along with spleen cellular, spleen cellular along with myeloma cellular, and so on. The required fusions to make hybridomas tend to be in between a proper B-cell, that creates antibodies from the antigen associated with curiosity, along with a myeloma cellular. Within these types of fairly uncommon fusions, the actual wholesome W cellular can make the actual HGPRT enzyme which will permit the fused cellular in order to endure within LOATH moderate to ensure that just the actual effectively fused tissue may develop within lifestyle. The actual moderate should be overflowing throughout choice in order to favor hybridoma development. This is often accomplished through the coating associated with feeder tissue or even health supplement press for example briclone. Manufacturing within cellular lifestyle is generally favored since the ascites method is quite unpleasant towards the pet and when alternative methods can be found, might be regarded as dishonest.
Recombinant
The actual manufacturing associated with Recombinant monoclonal antibodies entails systems, known as repertoire cloning or even phage display/yeast show. Recombinant antibody architectural entails using infections or even candida to produce antibodies, instead of rodents. These types of methods depend on quick cloning associated with immunoglobulin gene sections to produce your local library associated with antibodies along with somewhat various amino acidity sequences that antibodies along with preferred specificities could be chosen. These types of methods may be used to improve: the actual specificity along with that antibodies identify antigens, their own balance in a variety of environment problems, their own healing effectiveness, as well as their own detectability within analysis programs. Fermentation chambers happen to be accustomed to create these types of antibodies on the big size.
Programs
As soon as monoclonal antibodies for any provided material happen to be created, these people may be used to identify the actual existence as well as volume of it, for example inside a Traditional western mark check (in order to identify the proteins on the membrane layer) or even a good immunofluorescence check (in order to identify the material inside a cellular). Also, they are very helpful within immunohistochemistry that identify antigen within set cells areas. Monoclonal antibodies may also be used in order to cleanse the material along with methods known as immunoprecipitation as well as appreciation chromatography.

25 Jul 2011

Mayo health centre eyes future trials recruitment with heath information exchange


Drug developers would love to be able to find qualified patients for their studies as easily as doing a Google search. While that might be a long way from becoming a reality, the Mayo Clinic has become one of the latest healthcare groups to embark on creating a new breed of electronic health data exchange that could someday be used to identify patients for clinical trials, InformationWeek reports.
Mayo is tackling one of the biggest bugaboos in sharing electronic patient data, a lack of interoperability among records systems. With plans to roll out its next-generation health information exchange (HIE) in southeast Minnesota, the health group is utilizing a range of technologies such as the government's CONNECT software and the same unstructured information management architecture as tech giant IBM's ($IBM) Watson supercomputer, according to the InformationWeek piece.
A key to Mayo's project is to normalize terms from different electronic medical records systems and build databases that can be used to gain insights into the health of patients whose data reside in disparate systems. This effort faces some similar challenges in terms of normalizing information from different records systems as the Partnership to Advance Clinical Electronic Research (PACeR), which is planning a pilot project in New York State that aims to aid in clinical research and in overcoming challenges of finding patients for clinical trials.

Mayo health centre Builds Next-Gen Health in sequence Exchange


Open-source natural language processing software will provide additional context so that clinicians and researchers can better use patient data from a variety of sources.

By Ken Terry InformationWeek
Using a Beacon grant provided by the Office of the National Coordinator of Health IT, the Mayo Clinic is building what may be the next generation of health information exchanges (HIE) with a group of healthcare providers in southeast Minnesota. In this real-world demonstration, Mayo will apply the computer tools it is developing through a federal SHARP grant to create new methods of mining electronic health record (EHR) data.
"We're building a patient data repository for southeast Minnesota that will execute on a lot of the promise and principles we're articulating in our SHARP grant," said Christopher Chute, MD, a Mayo Clinic epidemiologist and the principal investigator on Mayo's SHARP grant.
Mayo is using the government's CONNECT software to establish the HIE. The world-famous group practice also is working with the pioneering Indiana Health Information Exchange to build a data repository like the one in Indianapolis. "We'll use that to do population health management, aggregate outcomes analysis, and comparative effectiveness research pooled across healthcare encounters by different providers with the same patients," said Chute.
What's different about Mayo's approach is that it will use natural language processing to identify terms in disparate EHRs so that they can be mapped to a normative terminology such as SNOMED CT. This "semantic interoperability" will make it possible to create databases that transcend the differences between the vocabularies in different EHRs.
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In contrast, Chute said, alternative HIE approaches such as that found in Microsoft's Amalga product simply provide a way of viewing data in disparate systems. "The Amalga tool pays very little attention to data normalization," Chute said. "It basically provides common views of the information and facilitates broad-scale review across multiple patients."
The researchers are using Mayo's open-source natural language processing software within a framework established by the IBM Watson Center to provide additional context so that clinicians and researchers can better use patient data from a variety of sources. The Watson supercomputer, which made headlines when it beat human contestants at "Jeopardy," uses the same UIMA (unstructured information management architecture) framework.
So far, the Mayo scientists have applied their new tools to records of 30 patients with diabetes at Intermountain Healthcare and about 10,000 patients from the Mayo Clinic. These tests demonstrated their ability to run through the process from end to end, said Chute, but did not show whether they could normalize data from different EHRs. That's one of the goals of the Beacon demonstration project.
The three legs of the SHARP stool, Chute said, include automating aspects of terminology mapping to a standard lexicon and "syntactic normalization" of defective HL7 or Continuity of Care Document (CCD) messages. Put another way: The new system can repair ill-formed HL7 or CCD messages by analyzing the messages to determine what's wrong with the syntax of the message and correct it so that its content can be understood.
The third leg of the stool is natural language processing, which will be applied to clinical notes containing data that doesn't show up in administrative codes, lab results, or medication lists. Analyzing signs and symptoms, for instance, can make the categorization of diagnoses much more accurate, he said.
In the long run, Chute predicted, the tools Mayo is developing might be useful in clinical trials--for example, in identifying candidates for studies--and in triggering clinical decision support. Someday, he added, it might be possible to apply natural language processing to physician dictation, so that terms could go into discrete fields in an EHR. While much research must be done before that happens, he noted that the current mode of documentation in EHRs tends to slow doctors down.
"I think we'll end up with a hybrid of some structured data, augmented by a large amount of dictated or textual data. And I hope we can leverage the content of that textual data in a reliable and efficient way."
Mayo's SHARP tools and its natural language processing program are open source, noted Chute, and any developer can get a free license. Commercial applications may be based on these tools, but Mayo isn't looking to profit from them, he said.
"We're not a software company. We're not trying to make money off this environment, we're trying to help our patients."
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