- published: 22 Mar 2012
- views: 20564
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Air date: Wednesday, March 21, 2012, 3:00:00 PM
Time displayed is Eastern Time, Washington DC Local
Category: Wednesday Afternoon Lectures
Description: The Greek myth of the giant Prometheus stealing fire from the Olympian gods and giving it to humans, and the gods' "Trojan horse" gift to Prometheus of the beautiful but incorrigibly curious Pandora neatly symbolizes the symbiotic origin of mitochondrial DNA (mtDNA) and its role in human health and pathology (including aging).
I will review our relatively recent awareness of mtDNA and our even more recent discovery of its important role in human pathology. The first two pathogenic mutations in mtDNA were reported in 1988: 24 years later, over 200 point mutations and innumerable deletions have been associated with an extraordinary variety of human disorders, most of them multisystemic ("mitochondrial encephalomyopathies") but some tissue-specific (for example, mitochondrial myopathies). After a brief reminder of the unique rules of mitochondrial genetics, I will propose a genetic classification of the mitochondrial disorders and provide examples of different mtDNA-related diseases. As a myologist by training, I feel obliged to stress the importance of the muscle biopsy in our diagnostic approach to mitochondrial diseases. As mtDNA mutations are so common, it is important to recognize which are pathogenic and which are neutral polymorphisms. I will, therefore, review and provide examples of the "canonical" criteria of mtDNA pathogenicity, including heteroplasmy, single fiber PCR, and the cybrid technology.
In 2000, I wrote a review titled "Mutations in mtDNA: are we scraping the bottom of the barrel?" (Brain Pathology 2000:10:431-441). I will proceed to show that we are far from scratching the bottom of the barrel. We are still debating the frequency of mtDNA-related disorders; novel mutations or novel clinical phenotypes are still being reported at a brisk pace; the role of homoplasmic pathogenic mutations is not yet fully understood; similarly, the modulating role of mtDNA haplotypes is still being described; and -- importantly -- the pathogenic mechanism of mtDNA mutations is not yet understood (in other words, we still do not understand why MELAS differs from MERRF when both syndromes are due to mutations in mtDNA tRNA genes). It has been aptly said that mtDNA is the slave of nuclear DNA (nDNA), in that, in the course of the millennia, mtDNA has lost most of its original autonomy and now depends heavily on nuclear DNA for its basic functions, including replication and maintenance. Thus, besides disorders (reviewed above) due to "primary" mtDNA mutations, there are many disorders due to mutations in nuclear genes controlling mtDNA replication (mtDNA depletion syndromes), mtDNA maintenance (multiple mtDNA deletions syndromes) or mtDNA translation. These "indirect hits" (defects of intergenomic communication) are transmitted as mendelian traits but have genetic features that overlap with mitochondrial genetics. Thanks to new generation mitoexome sequencing, the neat subdivision between mtDNA depletion and multiple mtDNA syndromes is crumbling, as mutations in the same genes (usually involved with the homeostasis of the mitochondrial nucleotide pool) can impair either mtDNA replication or maintenance (or both).
In a provocative article, the late Anita Harding wondered whether normal aging wasn't the most common mitochondrial disease of them all. There is considerable evidence that this is true and largely due to spontaneous accumulations of mtDNA deletions in postmitotic tissues.
Finally, although I don't have the time to review therapeutic strategies, I will consider a potentially preventive approach to mtDNA-related diseases, namely cytoplasmic transfer. Although successful in primates and 2in preliminary experiments with defective human oocytes, this therapeutic modality requires careful ethical screening.
The NIH Wednesday Afternoon Lecture Series includes weekly scientific talks by some of the top researchers in the biomedical sciences worldwide.
For more information, visit:
The NIH Director's Wednesday Afternoon Lecture Series
Author: Dr. Salvatore DiMauro, Columbia University Medical Center
Runtime: 01:04:37
Permanent link: http://videocast.nih.gov/launch.asp?17182
http://www.stomponstep1.com/folate-b12-deficiency-megaloblastic-anemia-hypersegmented/
Vitamin B9 (Folate/Folic Acid) is very important for 1 carbon chemical reactions (AKA methylation) during the creation of DNA. These functions are particularly important in tissues that undergo frequent cellular division (like hematopoietic cells) and during periods of rapid cellular division (such as infancy and pregnancy). Folate is found naturally in leafy vegetables and Folium is the Latin word for leaf. Today many grains are also fortified with Folate. With so many items having Folate added a deficiency from decreased intake of Folate is not very common. Usually a deficiency is caused by an increased demand for folate through pregnancy or hemolytic anemias such as Sickle Cell Disease. Folate deficiencies in pregnant women are linked with the occurrence of Neural Tube Defects in the fetus. A deficiency can also be caused by drugs that inhibit the pathways that Folate is involved in such as Trimethoprim (antibiotic) and Methotrexate (Chemotherapy).
A Folate deficiency primarily causes anemia (decreased red blood cells). Anemias can present with a wide range of symptoms including weakness, fatigue, pale skin and shortness of breath. Folate Deficiency causes a specific type of Anemia called Macrocytic/Megaloblstic Anemia where the size (Mean Corpuscular Volume) of the red blood cells increased. This is because as the creation of DNA is inhibited the cell cycle in the hematopoietic cells is stalled. Cellular division is stopped but the cell continues to grow resulting in a smaller number of cells which are larger than normal cells. Patients with this type of anemia also often present with Hypersegmented Neutrophils on a blood smear, which is a neutrophil with 5 or more "segments" in the nucleus.
You are also going to see an elevation of Homocysteine levels in Folate Deficiency. This is because B12 needs to receive a methyl group from Folate so it can pass it on to Homocysteine to create Methionine. Less Folate means B12 doesn't have a methyl group to pass on and Homocysteine builds up. Unlike B12 deficiencies, Folate deficiency does not result in a buildup of Methylmalonic Acid or neurological symptoms.
Vitamin B12 (Cobalamin) is a vitamin, like Folate, that is important for 1 carbon chemical reactions. B12 is found in many animal products and Vegans are at the highest risk of deficiency. B12 taken in through the diet is bound to proteins. Stomach acid and digestive enzymes must first separate B12 from the proteins. If there is a deficiency of stomach acid due to disease or medication (like proton pump inhibitors or antacids) it can cause decreased absorption and B12 deficiency. Once it is no longer protein bound, B12 binds Intrinsic Factor which is released by the Parietal Cells in the stomach. Intrinsic Factor then chaperones the B12 to the terminal ileum where it is absorbed. Pernicious Anemia is the autoimmune destruction of parietal cells which leads to less Intrinsic Factor production. Less intrinsic factor means less B12 absorption and B12 deficiency. Damage to the terminal ileum, such as in Crohn's Disease, can also inhibit B12 absorption.
Folate and B12 work closely together handing off methyl groups to each other. It is sort of like a game of hot potato. Folate doesn't "want" the methyl group so it passes it on to B12. B12 doesn't "want" it either so it passes it off to methionine. In effect, B12 helps recycle methyltetrahydrofolate back into tetrohydrofolate which can be used to create DNA. This means that a deficiency of B12 can cause a deficiency of Folate as less Folate is being recycled into its "active" form. Therefore, B12 deficiency present very similarly to Folate deficiency. You get Macrocytic/Megaloblastic Anemia with Hypersegmented Neutrophils and increased Homocysteine levels.
If you mistakenly diagnose Folate Deficiency when it is really B12 Deficiency the patient will get better with Folate supplementation, but permanent neurological damage will be done overtime.
Odd chain fatty acids are broken down to eventually give Methylmalonyl CoA. B12 is a cofactor in the process that converts methylmalonyl CoA into Succinyl CoA which can then be used in the TCA cycle to generate energy. If there is not enough B12 this reaction is slowed and Methylmalonic Acid builds up. This Methylmalonic Acid build up is toxic to neurons and leads to demyelination in the posterior and lateral columns of the spinal cord. This is called Subacute Combined Degeneration and presents with peripheral numbness/tingling, spasticity, and loss of vibration and proprioception.
- published: 14 Jun 2014
- views: 27227
Most often, the leukemia cells in this phase act like of acute myeloid (aml), but they 4 nov 2014 leukaemia is often described as or chronic. Jan 2007 the natural history of chronic myeloid leukemia (cml) progresses from a relatively blast crisis is fundamentally different than phase in many aspects. This is when the leukaemia transforms into an acute (usually myeloid leukaemia) cml divided three different phases chronic, accelerated, or blastic. When it comes to the symptoms, aml or acute myeloid leukemia first being chronic phase that stage when cancer is readily most patients quickly notice symptoms associated with disease. In the accelerated phase, you have more obvious symptoms. Go through a series of maturing stages ('precursor' or blast cells) before forming into (in contrast, in acute myeloid leukaemia (aml) the abnormal cells that are 22 feb 2016 treatment options for chronic leukemia based on (for definitions different response types, see how do you know if getting higher and symptoms appearing becoming more severe. Difference between aml and cml what are the differences cml? . Between myeloblasts and myelocytes in their stage of development contain chronic myelogenous leukemia (cml) is known as a leukemia, also spelled leukaemia, group cancers that usually begin the bone marrow result high numbers abnormal white blood cells. Chronic myelomonocytic leukaemia (cmml) foundation. What are the differences between leukemia and lymphoma cibmtr. Aml is the most common type of acute leukaemia in adults. Chronic myeloid leukaemia (cml)cml)treating chronic leukemia by phase. Cml and types of chronic leukaemia staging for myeloid (cml) leukemia cml phases the biology blast crisis hematology ash education program. This page is about the different stages of chronic myeloid leukaemia. Difference between aml and cml. There are other sections on acute myeloid leukaemia, lymphoblastic 13 nov 2014 there 3 stages in cml, chronic, accelerated and blast phase. Difference between
2 jan 2011 aml vs cml is better known medically as acute myeloid leukemia. Mds is a group of diseases that affects, to greater or lesser extent, the production cmml different chronic myeloid leukaemia (cml). Later stage stem cell differentiation. Some may present with an enlarged spleen, fatigue, or other symptoms that might not be readily recognized as extreme learn about the overview and differences in 4 primary types of leukemia (aml, cml, all, between four main have to do discuss treatment options oncology information specialist, who is available 24 7 at (800) 615 3055, chat us 3 dec 2015 blood bone marrow you classify cml from aml then go for no this stage, before 10 feb 2002 chronic myelogenous a disease which patients too many mature white cells. National cml types of leukemia 4 primary any advice on the difference between & aml? Researchgate. Both aml and cml 13 aug 1999 in chronic leukemia, the blood forming cells eventually mature, or differentiate there are over a dozen different types of but four occur most frequently. Leukaemia and lymphoma what's the difference? Acute leukemia difference? Healthline. These white blood cells are not fully developed and called blasts or leukemia. Go through a series of maturing stages ('precursor' or blast cells) before forming into (in contrast, in acute myeloid leukaemia (aml) the abnormal cells that are chronic (cml) is cancer blood this because outlook (prognosis) and treatments vary for different types. Chronic myeloid leukaemia (cml) is a cancer of blood forming cells in the this because outlook (prognosis) and treatments vary for different types. Causes g2 m delay, the stage is set to accumulate dna damage without or oncogenes, especially those found in acute myeloid leukemia cells might be dividing too quickly surviving chronic leukaemia (cml). Chronic myelogenous leukemia) become aml oncolink. Approximately 20 Difference between aml and cml what are the differences cml? . Leukemia aml, cml, all and cll rn. Symptoms may include bleeding and bruising problems, feeling tired, fever, however, about 90. Leukemia types, acute myelogenous leukemia (aml), chronic wikipedia. Cml or chronic myelogenous leukemia is a slow growing form of affecting the myeloid cells in marrow. Some people with chronic phase leukemia have symptoms when they are acute lymphoblastic for about 25. The symptoms of blood and lymphatic cancers can be very non specific occur in will determined by the stage lymphoma, addition to a number 8 jul 2016 common signs acute leukemia are chronic myeloid (cml) may also associated with gene your outlook depend on age, overall health, leukemiaaml, or 26 percent 66. Aml or acute myelogenous leukemia is a disease in which patients have too many immature white blood cells their bone marrow that are not capable of maturing properly treatment, and describe the characteristics, symptoms, diagnosis, treatment f
- published: 23 Nov 2016
- views: 192
NEW DELHI: India on Thursday test-fired for the first time its nuclear capable most-ambitious strategic missile, the over 5,000-km range Agni-V, in a bid to join the super exclusive ICBM (intercontinental ballistic missile) club that counts just US, Russia,China, France and UK as its members.
The solid-fuelled Agni-V, which will bring the whole of China as well as other regions under its strike envelope, was tested from Wheeler Island off the Odisha coast at 8.07 am.
''We have met all our mission objectives,'' said a jubilant DRD0 chief controller of missiles, Avinash Chander.
DRD0 chief V K Saraswat, in turn, said India had emerged as a major missile power with Thursday's test.
The nuclear-capable, three-stage Agni-V, about 50-tonne in weight and 17.5-metre tall, will become fully operational by 2014-2015 after "four to five repeatable tests" and user trials.
India could have gone for a higher strike range but believes the solid-fuelled Agni-V is "more than adequate'' to meet current threat perceptions and security concerns. The missile can, after all, even hit the northernmost parts of China.
India, of course, cannot match China in terms of its vast nuclear and missile arsenals. But missiles like Agni-V and the 3,500-km Agni-IV, tested last November, will certainly add teeth to its credible minimum nuclear deterrence posture.
With a canister-launch system to impart higher road mobility, the missile will give the armed forces much greater operational flexibility than the earlier-generation of Agni missiles.
"The accuracy levels of Agni-V and Agni-IV, with their better guidance and navigation systems, are far higher than Agni-I (700-km), Agni-II (2,000-km) and Agni-III (3,000-km),'' said the source.
The Agni missiles will get deadlier once MIRV (multiple independently targetable re-entry vehicles) payloads for them are developed. An MIRV payload on a missile carries several nuclear warheads, which can be programmed to hit different targets. A flurry of such missiles can hence completely overwhelm BMD (ballistic missile defence) systems.
- published: 19 Apr 2012
- views: 55286
catch a fire, Fire it up
Corrupt stirring it up
It's buring hot, drifing
Hitting every slot
With a drop kick ,
It's toxic
Trouble, like your girl in a mosh pit
I've lost it
And that the only way that we rock shit
Banging heads and ripping threads
If i wasn't rocking shows
I'd be better of dead
With a one two
One word can destroy your whole crew
And that's toxic
[CHORUS]
Toxic, loud and abnoxious
Crazy Town's toxic
With that, rock your block Shit
Toxic, popping more lip
We love to talk shit
Rocking you block with that
stright out the block shit
Toxic
A budda, blastic
Blacklisted. twisted of faith
My vocal's fatal
As naughty v block concotions
Rock youe cradel
I thought I wait 'til The timeing was right
To inginte
Cause people like me
we only come out at night
I rock the main line
And party with fine bitches
Which is a dirty job
But somebody's got to do it
So, who the crew with?
More has than vivid
Lyrics explicit
So fuck the crities
We leave them hanging
like INXS.
[CHORUS]
Toxic threasholds of
Colomibian gold
You can't roll how we roll
We possess you soul
And push the panic
Is it godly or satanic?
Toxic or organic?
Manic minds refind or frantic
Just the way we planned it
See. we be stomping around The planet
And we stand alone
We inflitrate your chromosomes
No clone
Our DNA has got a strain
Of it's own And it's Toxic
- published: 31 May 2008
- views: 450857
Therapy of lymphoma inspired by functional and structural genomics
Air date: Wednesday, February 1, 2017, 3:00:00 PM
Category: WALS - Wednesday Afternoon Lectures
Runtime: 01:06:46
Description: Wednesday Afternoon Lecture Series
Dr. Staudt's laboratory uses genomic technologies to discover molecular subtypes of cancer and develop therapies that target oncogenic regulatory pathways in each subtype. This endeavor is now commonly known as precision medicine and is the direct fruit of the Human Genome Project.
The Staudt laboratory has designed the "Lymphochip," a custom DNA microarray that profiles gene expression in normal lymphocytes as well as in malignant lymphomas and leukemias. His laboratory defined two dominant molecular subtypes of the most common form of non-Hodgkin lymphoma–diffuse large B-cell lymphoma (DLBCL)—and showed that they arise from distinct stages of normal B-cell differentiation, utilize different oncogenic mechanisms, and respond differently to therapy. These subtypes, termed activated B-cell-like (ABC) and germinal center B-cell-like (GCB), are now recognized as distinct diseases. The laboratory has used functional genomics methods (RNAi and CRISPR-Cas9 screens) and structural genomics methods (e.g. cancer gene resequencing) to identify essential regulatory pathways that drive the malignant proliferation and survival of these lymphomas, thereby identifying potential therapeutic targets. For ABC DLBCL, the Staudt laboratory defined a “chronic active” form of B-cell receptor (BCR) signaling that activates the pro-survival NF-kB pathway. Over one fifth of ABC DLBCLs have mutations affecting the CD79B or CD79A subunits of the BCR, which augment BCR signaling. To attack chronic active BCR signaling therapeutically, the Staudt laboratory initiated clinical trials in relapsed/refractory DLBCL of ibrutinib, a drug used to treat B-cell cancers. Ibrutinib is an irreversible and highly selective inhibitor of the BTK, a key kinase that is required for BCR-dependent NF-kB activation. Monotherapy with ibrutinib induced a high rate of complete and partial responses in ABC DLBCL, while GCB DLBCL tumors rarely responded. When the tumors were genomically analyzed, the scientists found that patients with mutations in the BCR together with mutations in the signaling adapter MYD88 had the highest response rate. This clinical observation led Dr. Staudt's laboratory to delineate molecular mechanisms by which MYD88 augments BCR-dependent NF-kB activation. Based on this knowledge, Dr. Staudt has recently conducted clinical studies in primary central nervous system lymphoma, an aggressive cancer with an ABC gene expression profile and very frequent mutations in the BCR and MYD88. For his lecture, Dr. Staudt will present encouraging responses to ibrutinib alone and in combination with chemotherapy in patients with relapsed and refractory disease.
About the G. Burroughs Mider lecture:
Established in 1968 in honor of the first NIH director of laboratories and clinics, this lecture is part of the Wednesday Afternoon Lecture Series. It is presented by an NIH intramural scientist in recognition of and appreciation for his or her outstanding contributions to biomedical research.
For more information go to https://oir.nih.gov/wals/2016-2017/therapy-lymphoma-inspired-functional-structural-genomics
Author: Louis M. Staudt, M.D., Ph.D., Director, Center for Cancer Genomics, National Cancer Institute, NIH
Permanent link: https://videocast.nih.gov/launch.asp?21110
- published: 02 Feb 2017
- views: 74
For more information, log on to-
http://shomusbiology.weebly.com/
Download the study materials here-
http://shomusbiology.weebly.com/bio-materials.html
Source: Dr. Lopamudra Roy
This video will help you to understand what is leukemia & Lymphoma.
Leukemia (American English) or leukaemia (British English) is a type of cancer of the blood or bone marrow characterized by an abnormal increase of immature white blood cells called "blasts". Leukemia is a broad term covering a spectrum of diseases. In turn, it is part of the even broader group of diseases affecting the blood, bone marrow, and lymphoid system, which are all known as hematological neoplasms.
Leukemia is a treatable disease. Most treatments involve chemotherapy, medical radiation therapy, hormone treatments, or bone marrow transplant. The rate of cure depends on the type of leukemia as well as the age of the patient. Children are more likely to be permanently cured than adults. Even when a complete cure is unlikely, most people with a chronic leukemia and many people with an acute leukemia can be successfully treated for years. Sometimes, leukemia is the effect of another cancer, known as blastic leukemia, which usually involves the same treatment, although usually unsuccessful.
Leukemia can affect people at any age. In 2000 approximately 256,000 children and adults around the world had developed some form of leukemia, and 209,000 have died from it.[1] About 90% of all leukemias are diagnosed in adults.
Lymphoma is a type of blood cancer that occurs when B or T lymphocytes,[1] the white blood cells that form a part of the immune system and help protect the body from infection and disease, divide faster than normal cells or live longer than they are supposed to. Lymphoma may develop in the lymph nodes, spleen, bone marrow, blood or other organs[2] and eventually they form a tumor.[1]
Typically, lymphoma presents as a solid tumor of lymphoid cells. Treatment might involve chemotherapy and in some cases radiotherapy and/or bone marrow transplantation, and lymphomas can be curable depending on the histology, type, and stage of the disease.[3] These malignant cells often originate in lymph nodes, presenting as an enlargement of the node (a tumor). It can also affect other organs in which case it is referred to as extranodal lymphoma. Extranodal sites include the skin, brain, bowels and bone. Lymphomas are closely related to lymphoid leukemias, which also originate in lymphocytes but typically involve only circulating blood and the bone marrow (where blood cells are generated in a process termed haematopoesis) and do not usually form static tumors.[3] There are many types of lymphomas, and in turn, lymphomas are a part of the broad group of diseases called hematological neoplasms.
- published: 03 Dec 2013
- views: 4926
Armed gunmen stormed into Bacha Khan University in Charsadda, early morning where two blasts were heard amid heavy firing, Express News reported. “Armed men stormed into the university premises early this morning,” Sardheri police officials told The Express Tribune, adding that two explosions were heard inside the building. Officials added that two guards were injured at the gate. Meanwhile, extensive firing continues in the area and heavy contingents of elite force have been deployed.
पाकिस्तान में पेशावर के नज़दीक बच्चा खान यूनिवर्सिटी पर आतंकी हमला हुआ है | दो बम धमको के बाद गोलियां चलने की आवाज़ सुनाई दे रही है | अब तक किसी के हताहत होने की खबर नहीं है |
- published: 20 Jan 2016
- views: 105507
DNA
Deoxyribonucleic acid (
i/diˈɒksiˌraɪboʊnjʊˌkliːɪk, -ˌkleɪɪk/;DNA) is a molecule that carries most of the genetic instructions used in the development, functioning and reproduction of all known living organisms and many viruses. DNA is a nucleic acid; alongside proteins and carbohydrates, nucleic acids compose the three major macromolecules essential for all known forms of life. Most DNA molecules consist of two biopolymer strands coiled around each other to form a double helix. The two DNA strands are known as polynucleotides since they are composed of simpler units called nucleotides. Each nucleotide is composed of a nitrogen-containing nucleobase—either cytosine (C), guanine (G), adenine (A), or thymine (T)—as well as a monosaccharide sugar called deoxyribose and a phosphate group. The nucleotides are joined to one another in a chain by covalent bonds between the sugar of one nucleotide and the phosphate of the next, resulting in an alternating sugar-phosphate backbone. According to base pairing rules (A with T, and C with G), hydrogen bonds bind the nitrogenous bases of the two separate polynucleotide strands to make double-stranded DNA. The total amount of related DNA base pairs on Earth is estimated at 5.0 x 1037, and weighs 50 billion tonnes. In comparison, the total mass of the biosphere has been estimated to be as much as 4 TtC (trillion tons of carbon).
This page contains text from Wikipedia, the Free Encyclopedia -
https://wn.com/DNA
This article is licensed under the Creative Commons Attribution-ShareAlike 3.0 Unported License, which means that you can copy and modify it as long as the entire work (including additions) remains under this license.
This article is licensed under the Creative Commons Attribution-ShareAlike 3.0 Unported License, which means that you can copy and modify it as long as the entire work (including additions) remains under this license.
Precursor cell
In cytology, a precursor cell, also called a blast cell or simply blast, is a type of partially differentiated, usually unipotent cell that has lost most or all of the stem cell multipotency.
Usually a precursor cell is a stem cell which has the capacity to differentiate into only one cell types. Sometimes precursor cell is used as an alternative term for unipotent stem cells.
A blastoma is a type of cancer created by malignancies of precursor cells.
In embryology, precursor cells are a group of cells that differentiate later into one organ.
Cytological types
References
Precursor cell – Britannica Online Encyclopedia
External links
This page contains text from Wikipedia, the Free Encyclopedia -
https://wn.com/Precursor_cell
This article is licensed under the Creative Commons Attribution-ShareAlike 3.0 Unported License, which means that you can copy and modify it as long as the entire work (including additions) remains under this license.
This article is licensed under the Creative Commons Attribution-ShareAlike 3.0 Unported License, which means that you can copy and modify it as long as the entire work (including additions) remains under this license.
B12
B12 most often refers to:
B12 or B-12 may also refer to:
Biology
Entertainment
Transportation
This page contains text from Wikipedia, the Free Encyclopedia -
https://wn.com/B12
This article is licensed under the Creative Commons Attribution-ShareAlike 3.0 Unported License, which means that you can copy and modify it as long as the entire work (including additions) remains under this license.
This article is licensed under the Creative Commons Attribution-ShareAlike 3.0 Unported License, which means that you can copy and modify it as long as the entire work (including additions) remains under this license.
Folic acid
Folic acid or folate is a B vitamin. It is also referred to as vitamin M,vitamin B9,vitamin Bc (or folacin), pteroyl-L-glutamic acid, and pteroyl-L-glutamate.
Food supplement manufacturers often use the term folate for something different from "pure" folic acid: in chemistry, folate refers to the deprotonated ion, and folic acid to the neutral molecule—which both coexist in water. The International Union of Pure and Applied Chemistry and the International Union of Biochemistry and Molecular Biology state that folate and folic acid are the preferred synonyms for pteroylglutamate and pteroylglutamic acid, respectively.
Folate indicates a collection of "folates" that is not chemically well-characterized, including other members of the family of pteroylglutamates, or mixtures of them, having various levels of reduction of the pteridine ring, one-carbon substitutions and different numbers of glutamate residues.
Folic acid is synthetically produced, and used in fortified foods and supplements on the theory that it is converted into folate. However, folic acid is a synthetic oxidized form, not significantly found in fresh natural foods. To be used it must be converted to tetrahydrofolate (tetrahydrofolic acid) by dihydrofolate reductase (DHFR). Increasing evidence suggests that this process may be slow in humans.
This page contains text from Wikipedia, the Free Encyclopedia -
https://wn.com/Folic_acid
This article is licensed under the Creative Commons Attribution-ShareAlike 3.0 Unported License, which means that you can copy and modify it as long as the entire work (including additions) remains under this license.
This article is licensed under the Creative Commons Attribution-ShareAlike 3.0 Unported License, which means that you can copy and modify it as long as the entire work (including additions) remains under this license.
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64:37Mitochondrail DNA: Prometheus' Gift or Pandora's Box?
Mitochondrail DNA: Prometheus' Gift or Pandora's Box?Mitochondrail DNA: Prometheus' Gift or Pandora's Box?
Air date: Wednesday, March 21, 2012, 3:00:00 PM Time displayed is Eastern Time, Washington DC Local Category: Wednesday Afternoon Lectures Description: The Greek myth of the giant Prometheus stealing fire from the Olympian gods and giving it to humans, and the gods' "Trojan horse" gift to Prometheus of the beautiful but incorrigibly curious Pandora neatly symbolizes the symbiotic origin of mitochondrial DNA (mtDNA) and its role in human health and pathology (including aging). I will review our relatively recent awareness of mtDNA and our even more recent discovery of its important role in human pathology. The first two pathogenic mutations in mtDNA were reported in 1988: 24 years later, over 200 point mutations and innumerable deletions have been associated with an extraordinary variety of human disorders, most of them multisystemic ("mitochondrial encephalomyopathies") but some tissue-specific (for example, mitochondrial myopathies). After a brief reminder of the unique rules of mitochondrial genetics, I will propose a genetic classification of the mitochondrial disorders and provide examples of different mtDNA-related diseases. As a myologist by training, I feel obliged to stress the importance of the muscle biopsy in our diagnostic approach to mitochondrial diseases. As mtDNA mutations are so common, it is important to recognize which are pathogenic and which are neutral polymorphisms. I will, therefore, review and provide examples of the "canonical" criteria of mtDNA pathogenicity, including heteroplasmy, single fiber PCR, and the cybrid technology. In 2000, I wrote a review titled "Mutations in mtDNA: are we scraping the bottom of the barrel?" (Brain Pathology 2000:10:431-441). I will proceed to show that we are far from scratching the bottom of the barrel. We are still debating the frequency of mtDNA-related disorders; novel mutations or novel clinical phenotypes are still being reported at a brisk pace; the role of homoplasmic pathogenic mutations is not yet fully understood; similarly, the modulating role of mtDNA haplotypes is still being described; and -- importantly -- the pathogenic mechanism of mtDNA mutations is not yet understood (in other words, we still do not understand why MELAS differs from MERRF when both syndromes are due to mutations in mtDNA tRNA genes). It has been aptly said that mtDNA is the slave of nuclear DNA (nDNA), in that, in the course of the millennia, mtDNA has lost most of its original autonomy and now depends heavily on nuclear DNA for its basic functions, including replication and maintenance. Thus, besides disorders (reviewed above) due to "primary" mtDNA mutations, there are many disorders due to mutations in nuclear genes controlling mtDNA replication (mtDNA depletion syndromes), mtDNA maintenance (multiple mtDNA deletions syndromes) or mtDNA translation. These "indirect hits" (defects of intergenomic communication) are transmitted as mendelian traits but have genetic features that overlap with mitochondrial genetics. Thanks to new generation mitoexome sequencing, the neat subdivision between mtDNA depletion and multiple mtDNA syndromes is crumbling, as mutations in the same genes (usually involved with the homeostasis of the mitochondrial nucleotide pool) can impair either mtDNA replication or maintenance (or both). In a provocative article, the late Anita Harding wondered whether normal aging wasn't the most common mitochondrial disease of them all. There is considerable evidence that this is true and largely due to spontaneous accumulations of mtDNA deletions in postmitotic tissues. Finally, although I don't have the time to review therapeutic strategies, I will consider a potentially preventive approach to mtDNA-related diseases, namely cytoplasmic transfer. Although successful in primates and 2in preliminary experiments with defective human oocytes, this therapeutic modality requires careful ethical screening. The NIH Wednesday Afternoon Lecture Series includes weekly scientific talks by some of the top researchers in the biomedical sciences worldwide. For more information, visit: The NIH Director's Wednesday Afternoon Lecture Series Author: Dr. Salvatore DiMauro, Columbia University Medical Center Runtime: 01:04:37 Permanent link: http://videocast.nih.gov/launch.asp?17182 -
7:53Bio Tonic - Blasting Plastic
Bio Tonic - Blasting Plastic -
13:14Folate & B12 Deficiency, Megaloblastic Anemia Hypersegmented Macrocytic Methylmalonic
Folate & B12 Deficiency, Megaloblastic Anemia Hypersegmented Macrocytic MethylmalonicFolate & B12 Deficiency, Megaloblastic Anemia Hypersegmented Macrocytic Methylmalonic
http://www.stomponstep1.com/folate-b12-deficiency-megaloblastic-anemia-hypersegmented/ Vitamin B9 (Folate/Folic Acid) is very important for 1 carbon chemical reactions (AKA methylation) during the creation of DNA. These functions are particularly important in tissues that undergo frequent cellular division (like hematopoietic cells) and during periods of rapid cellular division (such as infancy and pregnancy). Folate is found naturally in leafy vegetables and Folium is the Latin word for leaf. Today many grains are also fortified with Folate. With so many items having Folate added a deficiency from decreased intake of Folate is not very common. Usually a deficiency is caused by an increased demand for folate through pregnancy or hemolytic anemias such as Sickle Cell Disease. Folate deficiencies in pregnant women are linked with the occurrence of Neural Tube Defects in the fetus. A deficiency can also be caused by drugs that inhibit the pathways that Folate is involved in such as Trimethoprim (antibiotic) and Methotrexate (Chemotherapy). A Folate deficiency primarily causes anemia (decreased red blood cells). Anemias can present with a wide range of symptoms including weakness, fatigue, pale skin and shortness of breath. Folate Deficiency causes a specific type of Anemia called Macrocytic/Megaloblstic Anemia where the size (Mean Corpuscular Volume) of the red blood cells increased. This is because as the creation of DNA is inhibited the cell cycle in the hematopoietic cells is stalled. Cellular division is stopped but the cell continues to grow resulting in a smaller number of cells which are larger than normal cells. Patients with this type of anemia also often present with Hypersegmented Neutrophils on a blood smear, which is a neutrophil with 5 or more "segments" in the nucleus. You are also going to see an elevation of Homocysteine levels in Folate Deficiency. This is because B12 needs to receive a methyl group from Folate so it can pass it on to Homocysteine to create Methionine. Less Folate means B12 doesn't have a methyl group to pass on and Homocysteine builds up. Unlike B12 deficiencies, Folate deficiency does not result in a buildup of Methylmalonic Acid or neurological symptoms. Vitamin B12 (Cobalamin) is a vitamin, like Folate, that is important for 1 carbon chemical reactions. B12 is found in many animal products and Vegans are at the highest risk of deficiency. B12 taken in through the diet is bound to proteins. Stomach acid and digestive enzymes must first separate B12 from the proteins. If there is a deficiency of stomach acid due to disease or medication (like proton pump inhibitors or antacids) it can cause decreased absorption and B12 deficiency. Once it is no longer protein bound, B12 binds Intrinsic Factor which is released by the Parietal Cells in the stomach. Intrinsic Factor then chaperones the B12 to the terminal ileum where it is absorbed. Pernicious Anemia is the autoimmune destruction of parietal cells which leads to less Intrinsic Factor production. Less intrinsic factor means less B12 absorption and B12 deficiency. Damage to the terminal ileum, such as in Crohn's Disease, can also inhibit B12 absorption. Folate and B12 work closely together handing off methyl groups to each other. It is sort of like a game of hot potato. Folate doesn't "want" the methyl group so it passes it on to B12. B12 doesn't "want" it either so it passes it off to methionine. In effect, B12 helps recycle methyltetrahydrofolate back into tetrohydrofolate which can be used to create DNA. This means that a deficiency of B12 can cause a deficiency of Folate as less Folate is being recycled into its "active" form. Therefore, B12 deficiency present very similarly to Folate deficiency. You get Macrocytic/Megaloblastic Anemia with Hypersegmented Neutrophils and increased Homocysteine levels. If you mistakenly diagnose Folate Deficiency when it is really B12 Deficiency the patient will get better with Folate supplementation, but permanent neurological damage will be done overtime. Odd chain fatty acids are broken down to eventually give Methylmalonyl CoA. B12 is a cofactor in the process that converts methylmalonyl CoA into Succinyl CoA which can then be used in the TCA cycle to generate energy. If there is not enough B12 this reaction is slowed and Methylmalonic Acid builds up. This Methylmalonic Acid build up is toxic to neurons and leads to demyelination in the posterior and lateral columns of the spinal cord. This is called Subacute Combined Degeneration and presents with peripheral numbness/tingling, spasticity, and loss of vibration and proprioception. -
1:37AML Vs CML - Stages, Symptoms Differences of AML and CML
AML Vs CML - Stages, Symptoms Differences of AML and CMLAML Vs CML - Stages, Symptoms Differences of AML and CML
Most often, the leukemia cells in this phase act like of acute myeloid (aml), but they 4 nov 2014 leukaemia is often described as or chronic. Jan 2007 the natural history of chronic myeloid leukemia (cml) progresses from a relatively blast crisis is fundamentally different than phase in many aspects. This is when the leukaemia transforms into an acute (usually myeloid leukaemia) cml divided three different phases chronic, accelerated, or blastic. When it comes to the symptoms, aml or acute myeloid leukemia first being chronic phase that stage when cancer is readily most patients quickly notice symptoms associated with disease. In the accelerated phase, you have more obvious symptoms. Go through a series of maturing stages ('precursor' or blast cells) before forming into (in contrast, in acute myeloid leukaemia (aml) the abnormal cells that are 22 feb 2016 treatment options for chronic leukemia based on (for definitions different response types, see how do you know if getting higher and symptoms appearing becoming more severe. Difference between aml and cml what are the differences cml? . Between myeloblasts and myelocytes in their stage of development contain chronic myelogenous leukemia (cml) is known as a leukemia, also spelled leukaemia, group cancers that usually begin the bone marrow result high numbers abnormal white blood cells. Chronic myelomonocytic leukaemia (cmml) foundation. What are the differences between leukemia and lymphoma cibmtr. Aml is the most common type of acute leukaemia in adults. Chronic myeloid leukaemia (cml)cml)treating chronic leukemia by phase. Cml and types of chronic leukaemia staging for myeloid (cml) leukemia cml phases the biology blast crisis hematology ash education program. This page is about the different stages of chronic myeloid leukaemia. Difference between aml and cml. There are other sections on acute myeloid leukaemia, lymphoblastic 13 nov 2014 there 3 stages in cml, chronic, accelerated and blast phase. Difference between 2 jan 2011 aml vs cml is better known medically as acute myeloid leukemia. Mds is a group of diseases that affects, to greater or lesser extent, the production cmml different chronic myeloid leukaemia (cml). Later stage stem cell differentiation. Some may present with an enlarged spleen, fatigue, or other symptoms that might not be readily recognized as extreme learn about the overview and differences in 4 primary types of leukemia (aml, cml, all, between four main have to do discuss treatment options oncology information specialist, who is available 24 7 at (800) 615 3055, chat us 3 dec 2015 blood bone marrow you classify cml from aml then go for no this stage, before 10 feb 2002 chronic myelogenous a disease which patients too many mature white cells. National cml types of leukemia 4 primary any advice on the difference between & aml? Researchgate. Both aml and cml 13 aug 1999 in chronic leukemia, the blood forming cells eventually mature, or differentiate there are over a dozen different types of but four occur most frequently. Leukaemia and lymphoma what's the difference? Acute leukemia difference? Healthline. These white blood cells are not fully developed and called blasts or leukemia. Go through a series of maturing stages ('precursor' or blast cells) before forming into (in contrast, in acute myeloid leukaemia (aml) the abnormal cells that are chronic (cml) is cancer blood this because outlook (prognosis) and treatments vary for different types. Chronic myeloid leukaemia (cml) is a cancer of blood forming cells in the this because outlook (prognosis) and treatments vary for different types. Causes g2 m delay, the stage is set to accumulate dna damage without or oncogenes, especially those found in acute myeloid leukemia cells might be dividing too quickly surviving chronic leukaemia (cml). Chronic myelogenous leukemia) become aml oncolink. Approximately 20 Difference between aml and cml what are the differences cml? . Leukemia aml, cml, all and cll rn. Symptoms may include bleeding and bruising problems, feeling tired, fever, however, about 90. Leukemia types, acute myelogenous leukemia (aml), chronic wikipedia. Cml or chronic myelogenous leukemia is a slow growing form of affecting the myeloid cells in marrow. Some people with chronic phase leukemia have symptoms when they are acute lymphoblastic for about 25. The symptoms of blood and lymphatic cancers can be very non specific occur in will determined by the stage lymphoma, addition to a number 8 jul 2016 common signs acute leukemia are chronic myeloid (cml) may also associated with gene your outlook depend on age, overall health, leukemiaaml, or 26 percent 66. Aml or acute myelogenous leukemia is a disease in which patients have too many immature white blood cells their bone marrow that are not capable of maturing properly treatment, and describe the characteristics, symptoms, diagnosis, treatment f -
4:33India successfully test fires Agni 5 ICBM 5000KM missile
India successfully test fires Agni 5 ICBM 5000KM missileIndia successfully test fires Agni 5 ICBM 5000KM missile
NEW DELHI: India on Thursday test-fired for the first time its nuclear capable most-ambitious strategic missile, the over 5,000-km range Agni-V, in a bid to join the super exclusive ICBM (intercontinental ballistic missile) club that counts just US, Russia,China, France and UK as its members. The solid-fuelled Agni-V, which will bring the whole of China as well as other regions under its strike envelope, was tested from Wheeler Island off the Odisha coast at 8.07 am. ''We have met all our mission objectives,'' said a jubilant DRD0 chief controller of missiles, Avinash Chander. DRD0 chief V K Saraswat, in turn, said India had emerged as a major missile power with Thursday's test. The nuclear-capable, three-stage Agni-V, about 50-tonne in weight and 17.5-metre tall, will become fully operational by 2014-2015 after "four to five repeatable tests" and user trials. India could have gone for a higher strike range but believes the solid-fuelled Agni-V is "more than adequate'' to meet current threat perceptions and security concerns. The missile can, after all, even hit the northernmost parts of China. India, of course, cannot match China in terms of its vast nuclear and missile arsenals. But missiles like Agni-V and the 3,500-km Agni-IV, tested last November, will certainly add teeth to its credible minimum nuclear deterrence posture. With a canister-launch system to impart higher road mobility, the missile will give the armed forces much greater operational flexibility than the earlier-generation of Agni missiles. "The accuracy levels of Agni-V and Agni-IV, with their better guidance and navigation systems, are far higher than Agni-I (700-km), Agni-II (2,000-km) and Agni-III (3,000-km),'' said the source. The Agni missiles will get deadlier once MIRV (multiple independently targetable re-entry vehicles) payloads for them are developed. An MIRV payload on a missile carries several nuclear warheads, which can be programmed to hit different targets. A flurry of such missiles can hence completely overwhelm BMD (ballistic missile defence) systems. -
2:59Crazy Town- Toxic
Crazy Town- ToxicCrazy Town- Toxic
catch a fire, Fire it up Corrupt stirring it up It's buring hot, drifing Hitting every slot With a drop kick , It's toxic Trouble, like your girl in a mosh pit I've lost it And that the only way that we rock shit Banging heads and ripping threads If i wasn't rocking shows I'd be better of dead With a one two One word can destroy your whole crew And that's toxic [CHORUS] Toxic, loud and abnoxious Crazy Town's toxic With that, rock your block Shit Toxic, popping more lip We love to talk shit Rocking you block with that stright out the block shit Toxic A budda, blastic Blacklisted. twisted of faith My vocal's fatal As naughty v block concotions Rock youe cradel I thought I wait 'til The timeing was right To inginte Cause people like me we only come out at night I rock the main line And party with fine bitches Which is a dirty job But somebody's got to do it So, who the crew with? More has than vivid Lyrics explicit So fuck the crities We leave them hanging like INXS. [CHORUS] Toxic threasholds of Colomibian gold You can't roll how we roll We possess you soul And push the panic Is it godly or satanic? Toxic or organic? Manic minds refind or frantic Just the way we planned it See. we be stomping around The planet And we stand alone We inflitrate your chromosomes No clone Our DNA has got a strain Of it's own And it's Toxic -
66:46Therapy of lymphoma inspired by functional and structural genomics
Therapy of lymphoma inspired by functional and structural genomicsTherapy of lymphoma inspired by functional and structural genomics
Therapy of lymphoma inspired by functional and structural genomics Air date: Wednesday, February 1, 2017, 3:00:00 PM Category: WALS - Wednesday Afternoon Lectures Runtime: 01:06:46 Description: Wednesday Afternoon Lecture Series Dr. Staudt's laboratory uses genomic technologies to discover molecular subtypes of cancer and develop therapies that target oncogenic regulatory pathways in each subtype. This endeavor is now commonly known as precision medicine and is the direct fruit of the Human Genome Project. The Staudt laboratory has designed the "Lymphochip," a custom DNA microarray that profiles gene expression in normal lymphocytes as well as in malignant lymphomas and leukemias. His laboratory defined two dominant molecular subtypes of the most common form of non-Hodgkin lymphoma–diffuse large B-cell lymphoma (DLBCL)—and showed that they arise from distinct stages of normal B-cell differentiation, utilize different oncogenic mechanisms, and respond differently to therapy. These subtypes, termed activated B-cell-like (ABC) and germinal center B-cell-like (GCB), are now recognized as distinct diseases. The laboratory has used functional genomics methods (RNAi and CRISPR-Cas9 screens) and structural genomics methods (e.g. cancer gene resequencing) to identify essential regulatory pathways that drive the malignant proliferation and survival of these lymphomas, thereby identifying potential therapeutic targets. For ABC DLBCL, the Staudt laboratory defined a “chronic active” form of B-cell receptor (BCR) signaling that activates the pro-survival NF-kB pathway. Over one fifth of ABC DLBCLs have mutations affecting the CD79B or CD79A subunits of the BCR, which augment BCR signaling. To attack chronic active BCR signaling therapeutically, the Staudt laboratory initiated clinical trials in relapsed/refractory DLBCL of ibrutinib, a drug used to treat B-cell cancers. Ibrutinib is an irreversible and highly selective inhibitor of the BTK, a key kinase that is required for BCR-dependent NF-kB activation. Monotherapy with ibrutinib induced a high rate of complete and partial responses in ABC DLBCL, while GCB DLBCL tumors rarely responded. When the tumors were genomically analyzed, the scientists found that patients with mutations in the BCR together with mutations in the signaling adapter MYD88 had the highest response rate. This clinical observation led Dr. Staudt's laboratory to delineate molecular mechanisms by which MYD88 augments BCR-dependent NF-kB activation. Based on this knowledge, Dr. Staudt has recently conducted clinical studies in primary central nervous system lymphoma, an aggressive cancer with an ABC gene expression profile and very frequent mutations in the BCR and MYD88. For his lecture, Dr. Staudt will present encouraging responses to ibrutinib alone and in combination with chemotherapy in patients with relapsed and refractory disease. About the G. Burroughs Mider lecture: Established in 1968 in honor of the first NIH director of laboratories and clinics, this lecture is part of the Wednesday Afternoon Lecture Series. It is presented by an NIH intramural scientist in recognition of and appreciation for his or her outstanding contributions to biomedical research. For more information go to https://oir.nih.gov/wals/2016-2017/therapy-lymphoma-inspired-functional-structural-genomics Author: Louis M. Staudt, M.D., Ph.D., Director, Center for Cancer Genomics, National Cancer Institute, NIH Permanent link: https://videocast.nih.gov/launch.asp?21110 -
6:16Leukemia and lymphoma
Leukemia and lymphomaLeukemia and lymphoma
For more information, log on to- http://shomusbiology.weebly.com/ Download the study materials here- http://shomusbiology.weebly.com/bio-materials.html Source: Dr. Lopamudra Roy This video will help you to understand what is leukemia & Lymphoma. Leukemia (American English) or leukaemia (British English) is a type of cancer of the blood or bone marrow characterized by an abnormal increase of immature white blood cells called "blasts". Leukemia is a broad term covering a spectrum of diseases. In turn, it is part of the even broader group of diseases affecting the blood, bone marrow, and lymphoid system, which are all known as hematological neoplasms. Leukemia is a treatable disease. Most treatments involve chemotherapy, medical radiation therapy, hormone treatments, or bone marrow transplant. The rate of cure depends on the type of leukemia as well as the age of the patient. Children are more likely to be permanently cured than adults. Even when a complete cure is unlikely, most people with a chronic leukemia and many people with an acute leukemia can be successfully treated for years. Sometimes, leukemia is the effect of another cancer, known as blastic leukemia, which usually involves the same treatment, although usually unsuccessful. Leukemia can affect people at any age. In 2000 approximately 256,000 children and adults around the world had developed some form of leukemia, and 209,000 have died from it.[1] About 90% of all leukemias are diagnosed in adults. Lymphoma is a type of blood cancer that occurs when B or T lymphocytes,[1] the white blood cells that form a part of the immune system and help protect the body from infection and disease, divide faster than normal cells or live longer than they are supposed to. Lymphoma may develop in the lymph nodes, spleen, bone marrow, blood or other organs[2] and eventually they form a tumor.[1] Typically, lymphoma presents as a solid tumor of lymphoid cells. Treatment might involve chemotherapy and in some cases radiotherapy and/or bone marrow transplantation, and lymphomas can be curable depending on the histology, type, and stage of the disease.[3] These malignant cells often originate in lymph nodes, presenting as an enlargement of the node (a tumor). It can also affect other organs in which case it is referred to as extranodal lymphoma. Extranodal sites include the skin, brain, bowels and bone. Lymphomas are closely related to lymphoid leukemias, which also originate in lymphocytes but typically involve only circulating blood and the bone marrow (where blood cells are generated in a process termed haematopoesis) and do not usually form static tumors.[3] There are many types of lymphomas, and in turn, lymphomas are a part of the broad group of diseases called hematological neoplasms. -
5:21Garage band '' blastic sounds'' by djchecko
Garage band '' blastic sounds'' by djcheckoGarage band '' blastic sounds'' by djchecko
song created by djchecko. ''loops'' -
0:41Bacha Khan University terror attack in Pakistan's Charsadda , 20 killed
Bacha Khan University terror attack in Pakistan's Charsadda , 20 killedBacha Khan University terror attack in Pakistan's Charsadda , 20 killed
Armed gunmen stormed into Bacha Khan University in Charsadda, early morning where two blasts were heard amid heavy firing, Express News reported. “Armed men stormed into the university premises early this morning,” Sardheri police officials told The Express Tribune, adding that two explosions were heard inside the building. Officials added that two guards were injured at the gate. Meanwhile, extensive firing continues in the area and heavy contingents of elite force have been deployed. पाकिस्तान में पेशावर के नज़दीक बच्चा खान यूनिवर्सिटी पर आतंकी हमला हुआ है | दो बम धमको के बाद गोलियां चलने की आवाज़ सुनाई दे रही है | अब तक किसी के हताहत होने की खबर नहीं है |
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Mitochondrail DNA: Prometheus' Gift or Pandora's Box?
Air date: Wednesday, March 21, 2012, 3:00:00 PM Time displayed is Eastern Time, Washington DC Local Category: Wednesday Afternoon Lectures Description: The Greek myth of the giant Prometheus stealing fire from the Olympian gods and giving it to humans, and the gods' "Trojan horse" gift to Prometheus of the beautiful but incorrigibly curious Pandora neatly symbolizes the symbiotic origin of mitochondrial DNA (mtDNA) and its role in human health and pathology (including aging). I will review our relatively recent awareness of mtDNA and our even more recent discovery of its important role in human pathology. The first two pathogenic mutations in mtDNA were reported in 1988: 24 years later, over 200 point mutations and innumerable deletions have been associated with an extraor...
published: 22 Mar 2012 -
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Folate & B12 Deficiency, Megaloblastic Anemia Hypersegmented Macrocytic Methylmalonic
http://www.stomponstep1.com/folate-b12-deficiency-megaloblastic-anemia-hypersegmented/ Vitamin B9 (Folate/Folic Acid) is very important for 1 carbon chemical reactions (AKA methylation) during the creation of DNA. These functions are particularly important in tissues that undergo frequent cellular division (like hematopoietic cells) and during periods of rapid cellular division (such as infancy and pregnancy). Folate is found naturally in leafy vegetables and Folium is the Latin word for leaf. Today many grains are also fortified with Folate. With so many items having Folate added a deficiency from decreased intake of Folate is not very common. Usually a deficiency is caused by an increased demand for folate through pregnancy or hemolytic anemias such as Sickle Cell Disease. Folate defici...
published: 14 Jun 2014 -
AML Vs CML - Stages, Symptoms Differences of AML and CML
Most often, the leukemia cells in this phase act like of acute myeloid (aml), but they 4 nov 2014 leukaemia is often described as or chronic. Jan 2007 the natural history of chronic myeloid leukemia (cml) progresses from a relatively blast crisis is fundamentally different than phase in many aspects. This is when the leukaemia transforms into an acute (usually myeloid leukaemia) cml divided three different phases chronic, accelerated, or blastic. When it comes to the symptoms, aml or acute myeloid leukemia first being chronic phase that stage when cancer is readily most patients quickly notice symptoms associated with disease. In the accelerated phase, you have more obvious symptoms. Go through a series of maturing stages ('precursor' or blast cells) before forming into (in contrast, in ac...
published: 23 Nov 2016 -
India successfully test fires Agni 5 ICBM 5000KM missile
NEW DELHI: India on Thursday test-fired for the first time its nuclear capable most-ambitious strategic missile, the over 5,000-km range Agni-V, in a bid to join the super exclusive ICBM (intercontinental ballistic missile) club that counts just US, Russia,China, France and UK as its members. The solid-fuelled Agni-V, which will bring the whole of China as well as other regions under its strike envelope, was tested from Wheeler Island off the Odisha coast at 8.07 am. ''We have met all our mission objectives,'' said a jubilant DRD0 chief controller of missiles, Avinash Chander. DRD0 chief V K Saraswat, in turn, said India had emerged as a major missile power with Thursday's test. The nuclear-capable, three-stage Agni-V, about 50-tonne in weight and 17.5-metre tall, will become fully ope...
published: 19 Apr 2012 -
Crazy Town- Toxic
catch a fire, Fire it up Corrupt stirring it up It's buring hot, drifing Hitting every slot With a drop kick , It's toxic Trouble, like your girl in a mosh pit I've lost it And that the only way that we rock shit Banging heads and ripping threads If i wasn't rocking shows I'd be better of dead With a one two One word can destroy your whole crew And that's toxic [CHORUS] Toxic, loud and abnoxious Crazy Town's toxic With that, rock your block Shit Toxic, popping more lip We love to talk shit Rocking you block with that stright out the block shit Toxic A budda, blastic Blacklisted. twisted of faith My vocal's fatal As naughty v block concotions Rock youe cradel I thought I wait 'til The timeing was right To inginte Cause people like me we only come ...
published: 31 May 2008 -
Therapy of lymphoma inspired by functional and structural genomics
Therapy of lymphoma inspired by functional and structural genomics Air date: Wednesday, February 1, 2017, 3:00:00 PM Category: WALS - Wednesday Afternoon Lectures Runtime: 01:06:46 Description: Wednesday Afternoon Lecture Series Dr. Staudt's laboratory uses genomic technologies to discover molecular subtypes of cancer and develop therapies that target oncogenic regulatory pathways in each subtype. This endeavor is now commonly known as precision medicine and is the direct fruit of the Human Genome Project. The Staudt laboratory has designed the "Lymphochip," a custom DNA microarray that profiles gene expression in normal lymphocytes as well as in malignant lymphomas and leukemias. His laboratory defined two dominant molecular subtypes of the most common form of non-Hodgkin ly...
published: 02 Feb 2017 -
Leukemia and lymphoma
For more information, log on to- http://shomusbiology.weebly.com/ Download the study materials here- http://shomusbiology.weebly.com/bio-materials.html Source: Dr. Lopamudra Roy This video will help you to understand what is leukemia & Lymphoma. Leukemia (American English) or leukaemia (British English) is a type of cancer of the blood or bone marrow characterized by an abnormal increase of immature white blood cells called "blasts". Leukemia is a broad term covering a spectrum of diseases. In turn, it is part of the even broader group of diseases affecting the blood, bone marrow, and lymphoid system, which are all known as hematological neoplasms. Leukemia is a treatable disease. Most treatments involve chemotherapy, medical radiation therapy, hormone treatments, or bone marrow transplan...
published: 03 Dec 2013 -
Garage band '' blastic sounds'' by djchecko
song created by djchecko. ''loops''
published: 30 May 2011 -
Bacha Khan University terror attack in Pakistan's Charsadda , 20 killed
Armed gunmen stormed into Bacha Khan University in Charsadda, early morning where two blasts were heard amid heavy firing, Express News reported. “Armed men stormed into the university premises early this morning,” Sardheri police officials told The Express Tribune, adding that two explosions were heard inside the building. Officials added that two guards were injured at the gate. Meanwhile, extensive firing continues in the area and heavy contingents of elite force have been deployed. पाकिस्तान में पेशावर के नज़दीक बच्चा खान यूनिवर्सिटी पर आतंकी हमला हुआ है | दो बम धमको के बाद गोलियां चलने की आवाज़ सुनाई दे रही है | अब तक किसी के हताहत होने की खबर नहीं है |
published: 20 Jan 2016
Mitochondrail DNA: Prometheus' Gift or Pandora's Box?
- Order: Reorder
- Duration: 64:37
- Updated: 22 Mar 2012
- views: 20564
Air date: Wednesday, March 21, 2012, 3:00:00 PM
Time displayed is Eastern Time, Washington DC Local
Category: Wednesday Afternoon Lectures
Descript...
Air date: Wednesday, March 21, 2012, 3:00:00 PM
Time displayed is Eastern Time, Washington DC Local
Category: Wednesday Afternoon Lectures
Description: The Greek myth of the giant Prometheus stealing fire from the Olympian gods and giving it to humans, and the gods' "Trojan horse" gift to Prometheus of the beautiful but incorrigibly curious Pandora neatly symbolizes the symbiotic origin of mitochondrial DNA (mtDNA) and its role in human health and pathology (including aging).
I will review our relatively recent awareness of mtDNA and our even more recent discovery of its important role in human pathology. The first two pathogenic mutations in mtDNA were reported in 1988: 24 years later, over 200 point mutations and innumerable deletions have been associated with an extraordinary variety of human disorders, most of them multisystemic ("mitochondrial encephalomyopathies") but some tissue-specific (for example, mitochondrial myopathies). After a brief reminder of the unique rules of mitochondrial genetics, I will propose a genetic classification of the mitochondrial disorders and provide examples of different mtDNA-related diseases. As a myologist by training, I feel obliged to stress the importance of the muscle biopsy in our diagnostic approach to mitochondrial diseases. As mtDNA mutations are so common, it is important to recognize which are pathogenic and which are neutral polymorphisms. I will, therefore, review and provide examples of the "canonical" criteria of mtDNA pathogenicity, including heteroplasmy, single fiber PCR, and the cybrid technology.
In 2000, I wrote a review titled "Mutations in mtDNA: are we scraping the bottom of the barrel?" (Brain Pathology 2000:10:431-441). I will proceed to show that we are far from scratching the bottom of the barrel. We are still debating the frequency of mtDNA-related disorders; novel mutations or novel clinical phenotypes are still being reported at a brisk pace; the role of homoplasmic pathogenic mutations is not yet fully understood; similarly, the modulating role of mtDNA haplotypes is still being described; and -- importantly -- the pathogenic mechanism of mtDNA mutations is not yet understood (in other words, we still do not understand why MELAS differs from MERRF when both syndromes are due to mutations in mtDNA tRNA genes). It has been aptly said that mtDNA is the slave of nuclear DNA (nDNA), in that, in the course of the millennia, mtDNA has lost most of its original autonomy and now depends heavily on nuclear DNA for its basic functions, including replication and maintenance. Thus, besides disorders (reviewed above) due to "primary" mtDNA mutations, there are many disorders due to mutations in nuclear genes controlling mtDNA replication (mtDNA depletion syndromes), mtDNA maintenance (multiple mtDNA deletions syndromes) or mtDNA translation. These "indirect hits" (defects of intergenomic communication) are transmitted as mendelian traits but have genetic features that overlap with mitochondrial genetics. Thanks to new generation mitoexome sequencing, the neat subdivision between mtDNA depletion and multiple mtDNA syndromes is crumbling, as mutations in the same genes (usually involved with the homeostasis of the mitochondrial nucleotide pool) can impair either mtDNA replication or maintenance (or both).
In a provocative article, the late Anita Harding wondered whether normal aging wasn't the most common mitochondrial disease of them all. There is considerable evidence that this is true and largely due to spontaneous accumulations of mtDNA deletions in postmitotic tissues.
Finally, although I don't have the time to review therapeutic strategies, I will consider a potentially preventive approach to mtDNA-related diseases, namely cytoplasmic transfer. Although successful in primates and 2in preliminary experiments with defective human oocytes, this therapeutic modality requires careful ethical screening.
The NIH Wednesday Afternoon Lecture Series includes weekly scientific talks by some of the top researchers in the biomedical sciences worldwide.
For more information, visit:
The NIH Director's Wednesday Afternoon Lecture Series
Author: Dr. Salvatore DiMauro, Columbia University Medical Center
Runtime: 01:04:37
Permanent link: http://videocast.nih.gov/launch.asp?17182
https://wn.com/Mitochondrail_Dna_Prometheus'_Gift_Or_Pandora's_Box
Air date: Wednesday, March 21, 2012, 3:00:00 PM
Time displayed is Eastern Time, Washington DC Local
Category: Wednesday Afternoon Lectures
Description: The Greek myth of the giant Prometheus stealing fire from the Olympian gods and giving it to humans, and the gods' "Trojan horse" gift to Prometheus of the beautiful but incorrigibly curious Pandora neatly symbolizes the symbiotic origin of mitochondrial DNA (mtDNA) and its role in human health and pathology (including aging).
I will review our relatively recent awareness of mtDNA and our even more recent discovery of its important role in human pathology. The first two pathogenic mutations in mtDNA were reported in 1988: 24 years later, over 200 point mutations and innumerable deletions have been associated with an extraordinary variety of human disorders, most of them multisystemic ("mitochondrial encephalomyopathies") but some tissue-specific (for example, mitochondrial myopathies). After a brief reminder of the unique rules of mitochondrial genetics, I will propose a genetic classification of the mitochondrial disorders and provide examples of different mtDNA-related diseases. As a myologist by training, I feel obliged to stress the importance of the muscle biopsy in our diagnostic approach to mitochondrial diseases. As mtDNA mutations are so common, it is important to recognize which are pathogenic and which are neutral polymorphisms. I will, therefore, review and provide examples of the "canonical" criteria of mtDNA pathogenicity, including heteroplasmy, single fiber PCR, and the cybrid technology.
In 2000, I wrote a review titled "Mutations in mtDNA: are we scraping the bottom of the barrel?" (Brain Pathology 2000:10:431-441). I will proceed to show that we are far from scratching the bottom of the barrel. We are still debating the frequency of mtDNA-related disorders; novel mutations or novel clinical phenotypes are still being reported at a brisk pace; the role of homoplasmic pathogenic mutations is not yet fully understood; similarly, the modulating role of mtDNA haplotypes is still being described; and -- importantly -- the pathogenic mechanism of mtDNA mutations is not yet understood (in other words, we still do not understand why MELAS differs from MERRF when both syndromes are due to mutations in mtDNA tRNA genes). It has been aptly said that mtDNA is the slave of nuclear DNA (nDNA), in that, in the course of the millennia, mtDNA has lost most of its original autonomy and now depends heavily on nuclear DNA for its basic functions, including replication and maintenance. Thus, besides disorders (reviewed above) due to "primary" mtDNA mutations, there are many disorders due to mutations in nuclear genes controlling mtDNA replication (mtDNA depletion syndromes), mtDNA maintenance (multiple mtDNA deletions syndromes) or mtDNA translation. These "indirect hits" (defects of intergenomic communication) are transmitted as mendelian traits but have genetic features that overlap with mitochondrial genetics. Thanks to new generation mitoexome sequencing, the neat subdivision between mtDNA depletion and multiple mtDNA syndromes is crumbling, as mutations in the same genes (usually involved with the homeostasis of the mitochondrial nucleotide pool) can impair either mtDNA replication or maintenance (or both).
In a provocative article, the late Anita Harding wondered whether normal aging wasn't the most common mitochondrial disease of them all. There is considerable evidence that this is true and largely due to spontaneous accumulations of mtDNA deletions in postmitotic tissues.
Finally, although I don't have the time to review therapeutic strategies, I will consider a potentially preventive approach to mtDNA-related diseases, namely cytoplasmic transfer. Although successful in primates and 2in preliminary experiments with defective human oocytes, this therapeutic modality requires careful ethical screening.
The NIH Wednesday Afternoon Lecture Series includes weekly scientific talks by some of the top researchers in the biomedical sciences worldwide.
For more information, visit:
The NIH Director's Wednesday Afternoon Lecture Series
Author: Dr. Salvatore DiMauro, Columbia University Medical Center
Runtime: 01:04:37
Permanent link: http://videocast.nih.gov/launch.asp?17182
- published: 22 Mar 2012
- views: 20564
Bio Tonic - Blasting Plastic
- Order: Reorder
- Duration: 7:53
- Updated: 15 Sep 2012
- views: 10052
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Bio-Tonic -- Divina
Psy-Trance
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Folate & B12 Deficiency, Megaloblastic Anemia Hypersegmented Macrocytic Methylmalonic
- Order: Reorder
- Duration: 13:14
- Updated: 14 Jun 2014
- views: 27227
http://www.stomponstep1.com/folate-b12-deficiency-megaloblastic-anemia-hypersegmented/
Vitamin B9 (Folate/Folic Acid) is very important for 1 carbon chemical r...
http://www.stomponstep1.com/folate-b12-deficiency-megaloblastic-anemia-hypersegmented/
Vitamin B9 (Folate/Folic Acid) is very important for 1 carbon chemical reactions (AKA methylation) during the creation of DNA. These functions are particularly important in tissues that undergo frequent cellular division (like hematopoietic cells) and during periods of rapid cellular division (such as infancy and pregnancy). Folate is found naturally in leafy vegetables and Folium is the Latin word for leaf. Today many grains are also fortified with Folate. With so many items having Folate added a deficiency from decreased intake of Folate is not very common. Usually a deficiency is caused by an increased demand for folate through pregnancy or hemolytic anemias such as Sickle Cell Disease. Folate deficiencies in pregnant women are linked with the occurrence of Neural Tube Defects in the fetus. A deficiency can also be caused by drugs that inhibit the pathways that Folate is involved in such as Trimethoprim (antibiotic) and Methotrexate (Chemotherapy).
A Folate deficiency primarily causes anemia (decreased red blood cells). Anemias can present with a wide range of symptoms including weakness, fatigue, pale skin and shortness of breath. Folate Deficiency causes a specific type of Anemia called Macrocytic/Megaloblstic Anemia where the size (Mean Corpuscular Volume) of the red blood cells increased. This is because as the creation of DNA is inhibited the cell cycle in the hematopoietic cells is stalled. Cellular division is stopped but the cell continues to grow resulting in a smaller number of cells which are larger than normal cells. Patients with this type of anemia also often present with Hypersegmented Neutrophils on a blood smear, which is a neutrophil with 5 or more "segments" in the nucleus.
You are also going to see an elevation of Homocysteine levels in Folate Deficiency. This is because B12 needs to receive a methyl group from Folate so it can pass it on to Homocysteine to create Methionine. Less Folate means B12 doesn't have a methyl group to pass on and Homocysteine builds up. Unlike B12 deficiencies, Folate deficiency does not result in a buildup of Methylmalonic Acid or neurological symptoms.
Vitamin B12 (Cobalamin) is a vitamin, like Folate, that is important for 1 carbon chemical reactions. B12 is found in many animal products and Vegans are at the highest risk of deficiency. B12 taken in through the diet is bound to proteins. Stomach acid and digestive enzymes must first separate B12 from the proteins. If there is a deficiency of stomach acid due to disease or medication (like proton pump inhibitors or antacids) it can cause decreased absorption and B12 deficiency. Once it is no longer protein bound, B12 binds Intrinsic Factor which is released by the Parietal Cells in the stomach. Intrinsic Factor then chaperones the B12 to the terminal ileum where it is absorbed. Pernicious Anemia is the autoimmune destruction of parietal cells which leads to less Intrinsic Factor production. Less intrinsic factor means less B12 absorption and B12 deficiency. Damage to the terminal ileum, such as in Crohn's Disease, can also inhibit B12 absorption.
Folate and B12 work closely together handing off methyl groups to each other. It is sort of like a game of hot potato. Folate doesn't "want" the methyl group so it passes it on to B12. B12 doesn't "want" it either so it passes it off to methionine. In effect, B12 helps recycle methyltetrahydrofolate back into tetrohydrofolate which can be used to create DNA. This means that a deficiency of B12 can cause a deficiency of Folate as less Folate is being recycled into its "active" form. Therefore, B12 deficiency present very similarly to Folate deficiency. You get Macrocytic/Megaloblastic Anemia with Hypersegmented Neutrophils and increased Homocysteine levels.
If you mistakenly diagnose Folate Deficiency when it is really B12 Deficiency the patient will get better with Folate supplementation, but permanent neurological damage will be done overtime.
Odd chain fatty acids are broken down to eventually give Methylmalonyl CoA. B12 is a cofactor in the process that converts methylmalonyl CoA into Succinyl CoA which can then be used in the TCA cycle to generate energy. If there is not enough B12 this reaction is slowed and Methylmalonic Acid builds up. This Methylmalonic Acid build up is toxic to neurons and leads to demyelination in the posterior and lateral columns of the spinal cord. This is called Subacute Combined Degeneration and presents with peripheral numbness/tingling, spasticity, and loss of vibration and proprioception.
https://wn.com/Folate_B12_Deficiency,_Megaloblastic_Anemia_Hypersegmented_Macrocytic_Methylmalonic
http://www.stomponstep1.com/folate-b12-deficiency-megaloblastic-anemia-hypersegmented/
Vitamin B9 (Folate/Folic Acid) is very important for 1 carbon chemical reactions (AKA methylation) during the creation of DNA. These functions are particularly important in tissues that undergo frequent cellular division (like hematopoietic cells) and during periods of rapid cellular division (such as infancy and pregnancy). Folate is found naturally in leafy vegetables and Folium is the Latin word for leaf. Today many grains are also fortified with Folate. With so many items having Folate added a deficiency from decreased intake of Folate is not very common. Usually a deficiency is caused by an increased demand for folate through pregnancy or hemolytic anemias such as Sickle Cell Disease. Folate deficiencies in pregnant women are linked with the occurrence of Neural Tube Defects in the fetus. A deficiency can also be caused by drugs that inhibit the pathways that Folate is involved in such as Trimethoprim (antibiotic) and Methotrexate (Chemotherapy).
A Folate deficiency primarily causes anemia (decreased red blood cells). Anemias can present with a wide range of symptoms including weakness, fatigue, pale skin and shortness of breath. Folate Deficiency causes a specific type of Anemia called Macrocytic/Megaloblstic Anemia where the size (Mean Corpuscular Volume) of the red blood cells increased. This is because as the creation of DNA is inhibited the cell cycle in the hematopoietic cells is stalled. Cellular division is stopped but the cell continues to grow resulting in a smaller number of cells which are larger than normal cells. Patients with this type of anemia also often present with Hypersegmented Neutrophils on a blood smear, which is a neutrophil with 5 or more "segments" in the nucleus.
You are also going to see an elevation of Homocysteine levels in Folate Deficiency. This is because B12 needs to receive a methyl group from Folate so it can pass it on to Homocysteine to create Methionine. Less Folate means B12 doesn't have a methyl group to pass on and Homocysteine builds up. Unlike B12 deficiencies, Folate deficiency does not result in a buildup of Methylmalonic Acid or neurological symptoms.
Vitamin B12 (Cobalamin) is a vitamin, like Folate, that is important for 1 carbon chemical reactions. B12 is found in many animal products and Vegans are at the highest risk of deficiency. B12 taken in through the diet is bound to proteins. Stomach acid and digestive enzymes must first separate B12 from the proteins. If there is a deficiency of stomach acid due to disease or medication (like proton pump inhibitors or antacids) it can cause decreased absorption and B12 deficiency. Once it is no longer protein bound, B12 binds Intrinsic Factor which is released by the Parietal Cells in the stomach. Intrinsic Factor then chaperones the B12 to the terminal ileum where it is absorbed. Pernicious Anemia is the autoimmune destruction of parietal cells which leads to less Intrinsic Factor production. Less intrinsic factor means less B12 absorption and B12 deficiency. Damage to the terminal ileum, such as in Crohn's Disease, can also inhibit B12 absorption.
Folate and B12 work closely together handing off methyl groups to each other. It is sort of like a game of hot potato. Folate doesn't "want" the methyl group so it passes it on to B12. B12 doesn't "want" it either so it passes it off to methionine. In effect, B12 helps recycle methyltetrahydrofolate back into tetrohydrofolate which can be used to create DNA. This means that a deficiency of B12 can cause a deficiency of Folate as less Folate is being recycled into its "active" form. Therefore, B12 deficiency present very similarly to Folate deficiency. You get Macrocytic/Megaloblastic Anemia with Hypersegmented Neutrophils and increased Homocysteine levels.
If you mistakenly diagnose Folate Deficiency when it is really B12 Deficiency the patient will get better with Folate supplementation, but permanent neurological damage will be done overtime.
Odd chain fatty acids are broken down to eventually give Methylmalonyl CoA. B12 is a cofactor in the process that converts methylmalonyl CoA into Succinyl CoA which can then be used in the TCA cycle to generate energy. If there is not enough B12 this reaction is slowed and Methylmalonic Acid builds up. This Methylmalonic Acid build up is toxic to neurons and leads to demyelination in the posterior and lateral columns of the spinal cord. This is called Subacute Combined Degeneration and presents with peripheral numbness/tingling, spasticity, and loss of vibration and proprioception.
- published: 14 Jun 2014
- views: 27227
AML Vs CML - Stages, Symptoms Differences of AML and CML
- Order: Reorder
- Duration: 1:37
- Updated: 23 Nov 2016
- views: 192
Most often, the leukemia cells in this phase act like of acute myeloid (aml), but they 4 nov 2014 leukaemia is often described as or chronic. Jan 2007 the natur...
Most often, the leukemia cells in this phase act like of acute myeloid (aml), but they 4 nov 2014 leukaemia is often described as or chronic. Jan 2007 the natural history of chronic myeloid leukemia (cml) progresses from a relatively blast crisis is fundamentally different than phase in many aspects. This is when the leukaemia transforms into an acute (usually myeloid leukaemia) cml divided three different phases chronic, accelerated, or blastic. When it comes to the symptoms, aml or acute myeloid leukemia first being chronic phase that stage when cancer is readily most patients quickly notice symptoms associated with disease. In the accelerated phase, you have more obvious symptoms. Go through a series of maturing stages ('precursor' or blast cells) before forming into (in contrast, in acute myeloid leukaemia (aml) the abnormal cells that are 22 feb 2016 treatment options for chronic leukemia based on (for definitions different response types, see how do you know if getting higher and symptoms appearing becoming more severe. Difference between aml and cml what are the differences cml? . Between myeloblasts and myelocytes in their stage of development contain chronic myelogenous leukemia (cml) is known as a leukemia, also spelled leukaemia, group cancers that usually begin the bone marrow result high numbers abnormal white blood cells. Chronic myelomonocytic leukaemia (cmml) foundation. What are the differences between leukemia and lymphoma cibmtr. Aml is the most common type of acute leukaemia in adults. Chronic myeloid leukaemia (cml)cml)treating chronic leukemia by phase. Cml and types of chronic leukaemia staging for myeloid (cml) leukemia cml phases the biology blast crisis hematology ash education program. This page is about the different stages of chronic myeloid leukaemia. Difference between aml and cml. There are other sections on acute myeloid leukaemia, lymphoblastic 13 nov 2014 there 3 stages in cml, chronic, accelerated and blast phase. Difference between
2 jan 2011 aml vs cml is better known medically as acute myeloid leukemia. Mds is a group of diseases that affects, to greater or lesser extent, the production cmml different chronic myeloid leukaemia (cml). Later stage stem cell differentiation. Some may present with an enlarged spleen, fatigue, or other symptoms that might not be readily recognized as extreme learn about the overview and differences in 4 primary types of leukemia (aml, cml, all, between four main have to do discuss treatment options oncology information specialist, who is available 24 7 at (800) 615 3055, chat us 3 dec 2015 blood bone marrow you classify cml from aml then go for no this stage, before 10 feb 2002 chronic myelogenous a disease which patients too many mature white cells. National cml types of leukemia 4 primary any advice on the difference between & aml? Researchgate. Both aml and cml 13 aug 1999 in chronic leukemia, the blood forming cells eventually mature, or differentiate there are over a dozen different types of but four occur most frequently. Leukaemia and lymphoma what's the difference? Acute leukemia difference? Healthline. These white blood cells are not fully developed and called blasts or leukemia. Go through a series of maturing stages ('precursor' or blast cells) before forming into (in contrast, in acute myeloid leukaemia (aml) the abnormal cells that are chronic (cml) is cancer blood this because outlook (prognosis) and treatments vary for different types. Chronic myeloid leukaemia (cml) is a cancer of blood forming cells in the this because outlook (prognosis) and treatments vary for different types. Causes g2 m delay, the stage is set to accumulate dna damage without or oncogenes, especially those found in acute myeloid leukemia cells might be dividing too quickly surviving chronic leukaemia (cml). Chronic myelogenous leukemia) become aml oncolink. Approximately 20 Difference between aml and cml what are the differences cml? . Leukemia aml, cml, all and cll rn. Symptoms may include bleeding and bruising problems, feeling tired, fever, however, about 90. Leukemia types, acute myelogenous leukemia (aml), chronic wikipedia. Cml or chronic myelogenous leukemia is a slow growing form of affecting the myeloid cells in marrow. Some people with chronic phase leukemia have symptoms when they are acute lymphoblastic for about 25. The symptoms of blood and lymphatic cancers can be very non specific occur in will determined by the stage lymphoma, addition to a number 8 jul 2016 common signs acute leukemia are chronic myeloid (cml) may also associated with gene your outlook depend on age, overall health, leukemiaaml, or 26 percent 66. Aml or acute myelogenous leukemia is a disease in which patients have too many immature white blood cells their bone marrow that are not capable of maturing properly treatment, and describe the characteristics, symptoms, diagnosis, treatment f
https://wn.com/Aml_Vs_Cml_Stages,_Symptoms_Differences_Of_Aml_And_Cml
Most often, the leukemia cells in this phase act like of acute myeloid (aml), but they 4 nov 2014 leukaemia is often described as or chronic. Jan 2007 the natural history of chronic myeloid leukemia (cml) progresses from a relatively blast crisis is fundamentally different than phase in many aspects. This is when the leukaemia transforms into an acute (usually myeloid leukaemia) cml divided three different phases chronic, accelerated, or blastic. When it comes to the symptoms, aml or acute myeloid leukemia first being chronic phase that stage when cancer is readily most patients quickly notice symptoms associated with disease. In the accelerated phase, you have more obvious symptoms. Go through a series of maturing stages ('precursor' or blast cells) before forming into (in contrast, in acute myeloid leukaemia (aml) the abnormal cells that are 22 feb 2016 treatment options for chronic leukemia based on (for definitions different response types, see how do you know if getting higher and symptoms appearing becoming more severe. Difference between aml and cml what are the differences cml? . Between myeloblasts and myelocytes in their stage of development contain chronic myelogenous leukemia (cml) is known as a leukemia, also spelled leukaemia, group cancers that usually begin the bone marrow result high numbers abnormal white blood cells. Chronic myelomonocytic leukaemia (cmml) foundation. What are the differences between leukemia and lymphoma cibmtr. Aml is the most common type of acute leukaemia in adults. Chronic myeloid leukaemia (cml)cml)treating chronic leukemia by phase. Cml and types of chronic leukaemia staging for myeloid (cml) leukemia cml phases the biology blast crisis hematology ash education program. This page is about the different stages of chronic myeloid leukaemia. Difference between aml and cml. There are other sections on acute myeloid leukaemia, lymphoblastic 13 nov 2014 there 3 stages in cml, chronic, accelerated and blast phase. Difference between
2 jan 2011 aml vs cml is better known medically as acute myeloid leukemia. Mds is a group of diseases that affects, to greater or lesser extent, the production cmml different chronic myeloid leukaemia (cml). Later stage stem cell differentiation. Some may present with an enlarged spleen, fatigue, or other symptoms that might not be readily recognized as extreme learn about the overview and differences in 4 primary types of leukemia (aml, cml, all, between four main have to do discuss treatment options oncology information specialist, who is available 24 7 at (800) 615 3055, chat us 3 dec 2015 blood bone marrow you classify cml from aml then go for no this stage, before 10 feb 2002 chronic myelogenous a disease which patients too many mature white cells. National cml types of leukemia 4 primary any advice on the difference between & aml? Researchgate. Both aml and cml 13 aug 1999 in chronic leukemia, the blood forming cells eventually mature, or differentiate there are over a dozen different types of but four occur most frequently. Leukaemia and lymphoma what's the difference? Acute leukemia difference? Healthline. These white blood cells are not fully developed and called blasts or leukemia. Go through a series of maturing stages ('precursor' or blast cells) before forming into (in contrast, in acute myeloid leukaemia (aml) the abnormal cells that are chronic (cml) is cancer blood this because outlook (prognosis) and treatments vary for different types. Chronic myeloid leukaemia (cml) is a cancer of blood forming cells in the this because outlook (prognosis) and treatments vary for different types. Causes g2 m delay, the stage is set to accumulate dna damage without or oncogenes, especially those found in acute myeloid leukemia cells might be dividing too quickly surviving chronic leukaemia (cml). Chronic myelogenous leukemia) become aml oncolink. Approximately 20 Difference between aml and cml what are the differences cml? . Leukemia aml, cml, all and cll rn. Symptoms may include bleeding and bruising problems, feeling tired, fever, however, about 90. Leukemia types, acute myelogenous leukemia (aml), chronic wikipedia. Cml or chronic myelogenous leukemia is a slow growing form of affecting the myeloid cells in marrow. Some people with chronic phase leukemia have symptoms when they are acute lymphoblastic for about 25. The symptoms of blood and lymphatic cancers can be very non specific occur in will determined by the stage lymphoma, addition to a number 8 jul 2016 common signs acute leukemia are chronic myeloid (cml) may also associated with gene your outlook depend on age, overall health, leukemiaaml, or 26 percent 66. Aml or acute myelogenous leukemia is a disease in which patients have too many immature white blood cells their bone marrow that are not capable of maturing properly treatment, and describe the characteristics, symptoms, diagnosis, treatment f
- published: 23 Nov 2016
- views: 192
India successfully test fires Agni 5 ICBM 5000KM missile
- Order: Reorder
- Duration: 4:33
- Updated: 19 Apr 2012
- views: 55286
NEW DELHI: India on Thursday test-fired for the first time its nuclear capable most-ambitious strategic missile, the over 5,000-km range Agni-V, in a bid to joi...
NEW DELHI: India on Thursday test-fired for the first time its nuclear capable most-ambitious strategic missile, the over 5,000-km range Agni-V, in a bid to join the super exclusive ICBM (intercontinental ballistic missile) club that counts just US, Russia,China, France and UK as its members.
The solid-fuelled Agni-V, which will bring the whole of China as well as other regions under its strike envelope, was tested from Wheeler Island off the Odisha coast at 8.07 am.
''We have met all our mission objectives,'' said a jubilant DRD0 chief controller of missiles, Avinash Chander.
DRD0 chief V K Saraswat, in turn, said India had emerged as a major missile power with Thursday's test.
The nuclear-capable, three-stage Agni-V, about 50-tonne in weight and 17.5-metre tall, will become fully operational by 2014-2015 after "four to five repeatable tests" and user trials.
India could have gone for a higher strike range but believes the solid-fuelled Agni-V is "more than adequate'' to meet current threat perceptions and security concerns. The missile can, after all, even hit the northernmost parts of China.
India, of course, cannot match China in terms of its vast nuclear and missile arsenals. But missiles like Agni-V and the 3,500-km Agni-IV, tested last November, will certainly add teeth to its credible minimum nuclear deterrence posture.
With a canister-launch system to impart higher road mobility, the missile will give the armed forces much greater operational flexibility than the earlier-generation of Agni missiles.
"The accuracy levels of Agni-V and Agni-IV, with their better guidance and navigation systems, are far higher than Agni-I (700-km), Agni-II (2,000-km) and Agni-III (3,000-km),'' said the source.
The Agni missiles will get deadlier once MIRV (multiple independently targetable re-entry vehicles) payloads for them are developed. An MIRV payload on a missile carries several nuclear warheads, which can be programmed to hit different targets. A flurry of such missiles can hence completely overwhelm BMD (ballistic missile defence) systems.
https://wn.com/India_Successfully_Test_Fires_Agni_5_Icbm_5000Km_Missile
NEW DELHI: India on Thursday test-fired for the first time its nuclear capable most-ambitious strategic missile, the over 5,000-km range Agni-V, in a bid to join the super exclusive ICBM (intercontinental ballistic missile) club that counts just US, Russia,China, France and UK as its members.
The solid-fuelled Agni-V, which will bring the whole of China as well as other regions under its strike envelope, was tested from Wheeler Island off the Odisha coast at 8.07 am.
''We have met all our mission objectives,'' said a jubilant DRD0 chief controller of missiles, Avinash Chander.
DRD0 chief V K Saraswat, in turn, said India had emerged as a major missile power with Thursday's test.
The nuclear-capable, three-stage Agni-V, about 50-tonne in weight and 17.5-metre tall, will become fully operational by 2014-2015 after "four to five repeatable tests" and user trials.
India could have gone for a higher strike range but believes the solid-fuelled Agni-V is "more than adequate'' to meet current threat perceptions and security concerns. The missile can, after all, even hit the northernmost parts of China.
India, of course, cannot match China in terms of its vast nuclear and missile arsenals. But missiles like Agni-V and the 3,500-km Agni-IV, tested last November, will certainly add teeth to its credible minimum nuclear deterrence posture.
With a canister-launch system to impart higher road mobility, the missile will give the armed forces much greater operational flexibility than the earlier-generation of Agni missiles.
"The accuracy levels of Agni-V and Agni-IV, with their better guidance and navigation systems, are far higher than Agni-I (700-km), Agni-II (2,000-km) and Agni-III (3,000-km),'' said the source.
The Agni missiles will get deadlier once MIRV (multiple independently targetable re-entry vehicles) payloads for them are developed. An MIRV payload on a missile carries several nuclear warheads, which can be programmed to hit different targets. A flurry of such missiles can hence completely overwhelm BMD (ballistic missile defence) systems.
- published: 19 Apr 2012
- views: 55286
Crazy Town- Toxic
- Order: Reorder
- Duration: 2:59
- Updated: 31 May 2008
- views: 450857
catch a fire, Fire it up
Corrupt stirring it up
It's buring hot, drifing
Hitting every slot
With a drop kick ,
It's toxic
Trouble, like your girl in ...
catch a fire, Fire it up
Corrupt stirring it up
It's buring hot, drifing
Hitting every slot
With a drop kick ,
It's toxic
Trouble, like your girl in a mosh pit
I've lost it
And that the only way that we rock shit
Banging heads and ripping threads
If i wasn't rocking shows
I'd be better of dead
With a one two
One word can destroy your whole crew
And that's toxic
[CHORUS]
Toxic, loud and abnoxious
Crazy Town's toxic
With that, rock your block Shit
Toxic, popping more lip
We love to talk shit
Rocking you block with that
stright out the block shit
Toxic
A budda, blastic
Blacklisted. twisted of faith
My vocal's fatal
As naughty v block concotions
Rock youe cradel
I thought I wait 'til The timeing was right
To inginte
Cause people like me
we only come out at night
I rock the main line
And party with fine bitches
Which is a dirty job
But somebody's got to do it
So, who the crew with?
More has than vivid
Lyrics explicit
So fuck the crities
We leave them hanging
like INXS.
[CHORUS]
Toxic threasholds of
Colomibian gold
You can't roll how we roll
We possess you soul
And push the panic
Is it godly or satanic?
Toxic or organic?
Manic minds refind or frantic
Just the way we planned it
See. we be stomping around The planet
And we stand alone
We inflitrate your chromosomes
No clone
Our DNA has got a strain
Of it's own And it's Toxic
https://wn.com/Crazy_Town_Toxic
catch a fire, Fire it up
Corrupt stirring it up
It's buring hot, drifing
Hitting every slot
With a drop kick ,
It's toxic
Trouble, like your girl in a mosh pit
I've lost it
And that the only way that we rock shit
Banging heads and ripping threads
If i wasn't rocking shows
I'd be better of dead
With a one two
One word can destroy your whole crew
And that's toxic
[CHORUS]
Toxic, loud and abnoxious
Crazy Town's toxic
With that, rock your block Shit
Toxic, popping more lip
We love to talk shit
Rocking you block with that
stright out the block shit
Toxic
A budda, blastic
Blacklisted. twisted of faith
My vocal's fatal
As naughty v block concotions
Rock youe cradel
I thought I wait 'til The timeing was right
To inginte
Cause people like me
we only come out at night
I rock the main line
And party with fine bitches
Which is a dirty job
But somebody's got to do it
So, who the crew with?
More has than vivid
Lyrics explicit
So fuck the crities
We leave them hanging
like INXS.
[CHORUS]
Toxic threasholds of
Colomibian gold
You can't roll how we roll
We possess you soul
And push the panic
Is it godly or satanic?
Toxic or organic?
Manic minds refind or frantic
Just the way we planned it
See. we be stomping around The planet
And we stand alone
We inflitrate your chromosomes
No clone
Our DNA has got a strain
Of it's own And it's Toxic
- published: 31 May 2008
- views: 450857
Therapy of lymphoma inspired by functional and structural genomics
- Order: Reorder
- Duration: 66:46
- Updated: 02 Feb 2017
- views: 74
Therapy of lymphoma inspired by functional and structural genomics
Air date: Wednesday, February 1, 2017, 3:00:00 PM
Category: WALS - Wednesday Afternoon Lec...
Therapy of lymphoma inspired by functional and structural genomics
Air date: Wednesday, February 1, 2017, 3:00:00 PM
Category: WALS - Wednesday Afternoon Lectures
Runtime: 01:06:46
Description: Wednesday Afternoon Lecture Series
Dr. Staudt's laboratory uses genomic technologies to discover molecular subtypes of cancer and develop therapies that target oncogenic regulatory pathways in each subtype. This endeavor is now commonly known as precision medicine and is the direct fruit of the Human Genome Project.
The Staudt laboratory has designed the "Lymphochip," a custom DNA microarray that profiles gene expression in normal lymphocytes as well as in malignant lymphomas and leukemias. His laboratory defined two dominant molecular subtypes of the most common form of non-Hodgkin lymphoma–diffuse large B-cell lymphoma (DLBCL)—and showed that they arise from distinct stages of normal B-cell differentiation, utilize different oncogenic mechanisms, and respond differently to therapy. These subtypes, termed activated B-cell-like (ABC) and germinal center B-cell-like (GCB), are now recognized as distinct diseases. The laboratory has used functional genomics methods (RNAi and CRISPR-Cas9 screens) and structural genomics methods (e.g. cancer gene resequencing) to identify essential regulatory pathways that drive the malignant proliferation and survival of these lymphomas, thereby identifying potential therapeutic targets. For ABC DLBCL, the Staudt laboratory defined a “chronic active” form of B-cell receptor (BCR) signaling that activates the pro-survival NF-kB pathway. Over one fifth of ABC DLBCLs have mutations affecting the CD79B or CD79A subunits of the BCR, which augment BCR signaling. To attack chronic active BCR signaling therapeutically, the Staudt laboratory initiated clinical trials in relapsed/refractory DLBCL of ibrutinib, a drug used to treat B-cell cancers. Ibrutinib is an irreversible and highly selective inhibitor of the BTK, a key kinase that is required for BCR-dependent NF-kB activation. Monotherapy with ibrutinib induced a high rate of complete and partial responses in ABC DLBCL, while GCB DLBCL tumors rarely responded. When the tumors were genomically analyzed, the scientists found that patients with mutations in the BCR together with mutations in the signaling adapter MYD88 had the highest response rate. This clinical observation led Dr. Staudt's laboratory to delineate molecular mechanisms by which MYD88 augments BCR-dependent NF-kB activation. Based on this knowledge, Dr. Staudt has recently conducted clinical studies in primary central nervous system lymphoma, an aggressive cancer with an ABC gene expression profile and very frequent mutations in the BCR and MYD88. For his lecture, Dr. Staudt will present encouraging responses to ibrutinib alone and in combination with chemotherapy in patients with relapsed and refractory disease.
About the G. Burroughs Mider lecture:
Established in 1968 in honor of the first NIH director of laboratories and clinics, this lecture is part of the Wednesday Afternoon Lecture Series. It is presented by an NIH intramural scientist in recognition of and appreciation for his or her outstanding contributions to biomedical research.
For more information go to https://oir.nih.gov/wals/2016-2017/therapy-lymphoma-inspired-functional-structural-genomics
Author: Louis M. Staudt, M.D., Ph.D., Director, Center for Cancer Genomics, National Cancer Institute, NIH
Permanent link: https://videocast.nih.gov/launch.asp?21110
https://wn.com/Therapy_Of_Lymphoma_Inspired_By_Functional_And_Structural_Genomics
Therapy of lymphoma inspired by functional and structural genomics
Air date: Wednesday, February 1, 2017, 3:00:00 PM
Category: WALS - Wednesday Afternoon Lectures
Runtime: 01:06:46
Description: Wednesday Afternoon Lecture Series
Dr. Staudt's laboratory uses genomic technologies to discover molecular subtypes of cancer and develop therapies that target oncogenic regulatory pathways in each subtype. This endeavor is now commonly known as precision medicine and is the direct fruit of the Human Genome Project.
The Staudt laboratory has designed the "Lymphochip," a custom DNA microarray that profiles gene expression in normal lymphocytes as well as in malignant lymphomas and leukemias. His laboratory defined two dominant molecular subtypes of the most common form of non-Hodgkin lymphoma–diffuse large B-cell lymphoma (DLBCL)—and showed that they arise from distinct stages of normal B-cell differentiation, utilize different oncogenic mechanisms, and respond differently to therapy. These subtypes, termed activated B-cell-like (ABC) and germinal center B-cell-like (GCB), are now recognized as distinct diseases. The laboratory has used functional genomics methods (RNAi and CRISPR-Cas9 screens) and structural genomics methods (e.g. cancer gene resequencing) to identify essential regulatory pathways that drive the malignant proliferation and survival of these lymphomas, thereby identifying potential therapeutic targets. For ABC DLBCL, the Staudt laboratory defined a “chronic active” form of B-cell receptor (BCR) signaling that activates the pro-survival NF-kB pathway. Over one fifth of ABC DLBCLs have mutations affecting the CD79B or CD79A subunits of the BCR, which augment BCR signaling. To attack chronic active BCR signaling therapeutically, the Staudt laboratory initiated clinical trials in relapsed/refractory DLBCL of ibrutinib, a drug used to treat B-cell cancers. Ibrutinib is an irreversible and highly selective inhibitor of the BTK, a key kinase that is required for BCR-dependent NF-kB activation. Monotherapy with ibrutinib induced a high rate of complete and partial responses in ABC DLBCL, while GCB DLBCL tumors rarely responded. When the tumors were genomically analyzed, the scientists found that patients with mutations in the BCR together with mutations in the signaling adapter MYD88 had the highest response rate. This clinical observation led Dr. Staudt's laboratory to delineate molecular mechanisms by which MYD88 augments BCR-dependent NF-kB activation. Based on this knowledge, Dr. Staudt has recently conducted clinical studies in primary central nervous system lymphoma, an aggressive cancer with an ABC gene expression profile and very frequent mutations in the BCR and MYD88. For his lecture, Dr. Staudt will present encouraging responses to ibrutinib alone and in combination with chemotherapy in patients with relapsed and refractory disease.
About the G. Burroughs Mider lecture:
Established in 1968 in honor of the first NIH director of laboratories and clinics, this lecture is part of the Wednesday Afternoon Lecture Series. It is presented by an NIH intramural scientist in recognition of and appreciation for his or her outstanding contributions to biomedical research.
For more information go to https://oir.nih.gov/wals/2016-2017/therapy-lymphoma-inspired-functional-structural-genomics
Author: Louis M. Staudt, M.D., Ph.D., Director, Center for Cancer Genomics, National Cancer Institute, NIH
Permanent link: https://videocast.nih.gov/launch.asp?21110
- published: 02 Feb 2017
- views: 74
Leukemia and lymphoma
- Order: Reorder
- Duration: 6:16
- Updated: 03 Dec 2013
- views: 4926
For more information, log on to-
http://shomusbiology.weebly.com/
Download the study materials here-
http://shomusbiology.weebly.com/bio-materials.html
Source: ...
For more information, log on to-
http://shomusbiology.weebly.com/
Download the study materials here-
http://shomusbiology.weebly.com/bio-materials.html
Source: Dr. Lopamudra Roy
This video will help you to understand what is leukemia & Lymphoma.
Leukemia (American English) or leukaemia (British English) is a type of cancer of the blood or bone marrow characterized by an abnormal increase of immature white blood cells called "blasts". Leukemia is a broad term covering a spectrum of diseases. In turn, it is part of the even broader group of diseases affecting the blood, bone marrow, and lymphoid system, which are all known as hematological neoplasms.
Leukemia is a treatable disease. Most treatments involve chemotherapy, medical radiation therapy, hormone treatments, or bone marrow transplant. The rate of cure depends on the type of leukemia as well as the age of the patient. Children are more likely to be permanently cured than adults. Even when a complete cure is unlikely, most people with a chronic leukemia and many people with an acute leukemia can be successfully treated for years. Sometimes, leukemia is the effect of another cancer, known as blastic leukemia, which usually involves the same treatment, although usually unsuccessful.
Leukemia can affect people at any age. In 2000 approximately 256,000 children and adults around the world had developed some form of leukemia, and 209,000 have died from it.[1] About 90% of all leukemias are diagnosed in adults.
Lymphoma is a type of blood cancer that occurs when B or T lymphocytes,[1] the white blood cells that form a part of the immune system and help protect the body from infection and disease, divide faster than normal cells or live longer than they are supposed to. Lymphoma may develop in the lymph nodes, spleen, bone marrow, blood or other organs[2] and eventually they form a tumor.[1]
Typically, lymphoma presents as a solid tumor of lymphoid cells. Treatment might involve chemotherapy and in some cases radiotherapy and/or bone marrow transplantation, and lymphomas can be curable depending on the histology, type, and stage of the disease.[3] These malignant cells often originate in lymph nodes, presenting as an enlargement of the node (a tumor). It can also affect other organs in which case it is referred to as extranodal lymphoma. Extranodal sites include the skin, brain, bowels and bone. Lymphomas are closely related to lymphoid leukemias, which also originate in lymphocytes but typically involve only circulating blood and the bone marrow (where blood cells are generated in a process termed haematopoesis) and do not usually form static tumors.[3] There are many types of lymphomas, and in turn, lymphomas are a part of the broad group of diseases called hematological neoplasms.
https://wn.com/Leukemia_And_Lymphoma
For more information, log on to-
http://shomusbiology.weebly.com/
Download the study materials here-
http://shomusbiology.weebly.com/bio-materials.html
Source: Dr. Lopamudra Roy
This video will help you to understand what is leukemia & Lymphoma.
Leukemia (American English) or leukaemia (British English) is a type of cancer of the blood or bone marrow characterized by an abnormal increase of immature white blood cells called "blasts". Leukemia is a broad term covering a spectrum of diseases. In turn, it is part of the even broader group of diseases affecting the blood, bone marrow, and lymphoid system, which are all known as hematological neoplasms.
Leukemia is a treatable disease. Most treatments involve chemotherapy, medical radiation therapy, hormone treatments, or bone marrow transplant. The rate of cure depends on the type of leukemia as well as the age of the patient. Children are more likely to be permanently cured than adults. Even when a complete cure is unlikely, most people with a chronic leukemia and many people with an acute leukemia can be successfully treated for years. Sometimes, leukemia is the effect of another cancer, known as blastic leukemia, which usually involves the same treatment, although usually unsuccessful.
Leukemia can affect people at any age. In 2000 approximately 256,000 children and adults around the world had developed some form of leukemia, and 209,000 have died from it.[1] About 90% of all leukemias are diagnosed in adults.
Lymphoma is a type of blood cancer that occurs when B or T lymphocytes,[1] the white blood cells that form a part of the immune system and help protect the body from infection and disease, divide faster than normal cells or live longer than they are supposed to. Lymphoma may develop in the lymph nodes, spleen, bone marrow, blood or other organs[2] and eventually they form a tumor.[1]
Typically, lymphoma presents as a solid tumor of lymphoid cells. Treatment might involve chemotherapy and in some cases radiotherapy and/or bone marrow transplantation, and lymphomas can be curable depending on the histology, type, and stage of the disease.[3] These malignant cells often originate in lymph nodes, presenting as an enlargement of the node (a tumor). It can also affect other organs in which case it is referred to as extranodal lymphoma. Extranodal sites include the skin, brain, bowels and bone. Lymphomas are closely related to lymphoid leukemias, which also originate in lymphocytes but typically involve only circulating blood and the bone marrow (where blood cells are generated in a process termed haematopoesis) and do not usually form static tumors.[3] There are many types of lymphomas, and in turn, lymphomas are a part of the broad group of diseases called hematological neoplasms.
- published: 03 Dec 2013
- views: 4926
Garage band '' blastic sounds'' by djchecko
- Order: Reorder
- Duration: 5:21
- Updated: 30 May 2011
- views: 81
song created by djchecko. ''loops''
song created by djchecko. ''loops''
https://wn.com/Garage_Band_''_Blastic_Sounds''_By_Djchecko
song created by djchecko. ''loops''
- published: 30 May 2011
- views: 81
Bacha Khan University terror attack in Pakistan's Charsadda , 20 killed
- Order: Reorder
- Duration: 0:41
- Updated: 20 Jan 2016
- views: 105507
Armed gunmen stormed into Bacha Khan University in Charsadda, early morning where two blasts were heard amid heavy firing, Express News reported. “Armed men sto...
Armed gunmen stormed into Bacha Khan University in Charsadda, early morning where two blasts were heard amid heavy firing, Express News reported. “Armed men stormed into the university premises early this morning,” Sardheri police officials told The Express Tribune, adding that two explosions were heard inside the building. Officials added that two guards were injured at the gate. Meanwhile, extensive firing continues in the area and heavy contingents of elite force have been deployed.
पाकिस्तान में पेशावर के नज़दीक बच्चा खान यूनिवर्सिटी पर आतंकी हमला हुआ है | दो बम धमको के बाद गोलियां चलने की आवाज़ सुनाई दे रही है | अब तक किसी के हताहत होने की खबर नहीं है |
https://wn.com/Bacha_Khan_University_Terror_Attack_In_Pakistan's_Charsadda_,_20_Killed
Armed gunmen stormed into Bacha Khan University in Charsadda, early morning where two blasts were heard amid heavy firing, Express News reported. “Armed men stormed into the university premises early this morning,” Sardheri police officials told The Express Tribune, adding that two explosions were heard inside the building. Officials added that two guards were injured at the gate. Meanwhile, extensive firing continues in the area and heavy contingents of elite force have been deployed.
पाकिस्तान में पेशावर के नज़दीक बच्चा खान यूनिवर्सिटी पर आतंकी हमला हुआ है | दो बम धमको के बाद गोलियां चलने की आवाज़ सुनाई दे रही है | अब तक किसी के हताहत होने की खबर नहीं है |
- published: 20 Jan 2016
- views: 105507
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64:37
Mitochondrail DNA: Prometheus' Gift or Pandora's Box?
Air date: Wednesday, March 21, 2012, 3:00:00 PM
Time displayed is Eastern Time, Washingt...
published: 22 Mar 2012
Mitochondrail DNA: Prometheus' Gift or Pandora's Box?
Mitochondrail DNA: Prometheus' Gift or Pandora's Box?
- Report rights infringement
- published: 22 Mar 2012
- views: 20564
7:53
Bio Tonic - Blasting Plastic
Humaan Design´s Page For More Music
LIKE (Y)
https://www.facebook.com/humaandessigns
Bio...
published: 15 Sep 2012
Bio Tonic - Blasting Plastic
Bio Tonic - Blasting Plastic
- Report rights infringement
- published: 15 Sep 2012
- views: 10052
13:14
Folate & B12 Deficiency, Megaloblastic Anemia Hypersegmented Macrocytic Methylmalonic
http://www.stomponstep1.com/folate-b12-deficiency-megaloblastic-anemia-hypersegmented/
Vi...
published: 14 Jun 2014
Folate & B12 Deficiency, Megaloblastic Anemia Hypersegmented Macrocytic Methylmalonic
Folate & B12 Deficiency, Megaloblastic Anemia Hypersegmented Macrocytic Methylmalonic
- Report rights infringement
- published: 14 Jun 2014
- views: 27227
1:37
AML Vs CML - Stages, Symptoms Differences of AML and CML
Most often, the leukemia cells in this phase act like of acute myeloid (aml), but they 4 n...
published: 23 Nov 2016
AML Vs CML - Stages, Symptoms Differences of AML and CML
AML Vs CML - Stages, Symptoms Differences of AML and CML
- Report rights infringement
- published: 23 Nov 2016
- views: 192
4:33
India successfully test fires Agni 5 ICBM 5000KM missile
NEW DELHI: India on Thursday test-fired for the first time its nuclear capable most-ambiti...
published: 19 Apr 2012
India successfully test fires Agni 5 ICBM 5000KM missile
India successfully test fires Agni 5 ICBM 5000KM missile
- Report rights infringement
- published: 19 Apr 2012
- views: 55286
2:59
Crazy Town- Toxic
catch a fire, Fire it up
Corrupt stirring it up
It's buring hot, drifing
Hitting ever...
published: 31 May 2008
Crazy Town- Toxic
Crazy Town- Toxic
- Report rights infringement
- published: 31 May 2008
- views: 450857
66:46
Therapy of lymphoma inspired by functional and structural genomics
Therapy of lymphoma inspired by functional and structural genomics
Air date: Wednesday, ...
published: 02 Feb 2017
Therapy of lymphoma inspired by functional and structural genomics
Therapy of lymphoma inspired by functional and structural genomics
- Report rights infringement
- published: 02 Feb 2017
- views: 74
6:16
Leukemia and lymphoma
For more information, log on to-
http://shomusbiology.weebly.com/
Download the study mater...
published: 03 Dec 2013
Leukemia and lymphoma
Leukemia and lymphoma
- Report rights infringement
- published: 03 Dec 2013
- views: 4926
5:21
Garage band '' blastic sounds'' by djchecko
song created by djchecko. ''loops''
published: 30 May 2011
Garage band '' blastic sounds'' by djchecko
Garage band '' blastic sounds'' by djchecko
- Report rights infringement
- published: 30 May 2011
- views: 81
0:41
Bacha Khan University terror attack in Pakistan's Charsadda , 20 killed
Armed gunmen stormed into Bacha Khan University in Charsadda, early morning where two blas...
published: 20 Jan 2016
Bacha Khan University terror attack in Pakistan's Charsadda , 20 killed
Bacha Khan University terror attack in Pakistan's Charsadda , 20 killed
- Report rights infringement
- published: 20 Jan 2016
- views: 105507
Mitochondrail DNA: Prometheus' Gift or Pandora's B...
Bio Tonic - Blasting Plastic...
Folate & B12 Deficiency, Megaloblastic Anemia Hype...
AML Vs CML - Stages, Symptoms Differences of AML ...
India successfully test fires Agni 5 ICBM 5000KM m...
Crazy Town- Toxic...
Therapy of lymphoma inspired by functional and str...
Leukemia and lymphoma...
Garage band '' blastic sounds'' by djchecko...
Bacha Khan University terror attack in Pakistan's ...
See more photos of blastic dna
-
Lyrics list:lyrics
-
Plastic Town, Luckie Strike
Plastic Town
Lyrics written by Bubba.
No one knows, no one sees
The rhymes and what they mean
Sour lies, and shrouded town
As shallow as this soggy ground
Smog covered truth, light rail trains
Cellophane people and what they say
Eyes that lie, lips that sting
There's gotta be someway out for me
(chorus-)
There's gotta be someway someway
There's gotta be someway out for me
They can't see me
Only what they want from me
The truth is here
But it's not what they want to see
(chorus)
Maybe one day we could find a way
To wash this dirty old town away
And all it's plastic people
Could roll down the river into the bay
Then I'll run
And sing I'm free
We're victims here
If we stay the dream will end
Dead ends
And dead friends
There's gotta be someway out for me
back
In the Age Of Trump And Liberal Fascism, Who’s The Real Brownshirts?
Edit WorldNews.com 10 Feb 2017
Article by WN.com Correspondent Dallas DarlingSince reality first exists in the mind and nowhere else, in the Age of Trump and Liberal Fascism some warn it’s become more difficult to tell who the real Brownshirts are ... De-Legitimizing the State and Leaders through Common Crime. Nazi fascism indeed depended on rebel rousers ... They also won the “streets,” and the imagination of the German people ... The message was clear ... 2 Snyder, Dr. Louis L ... ....
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Donald Trump just lost, bigly
Edit The Independent 10 Feb 2017
President Trump has been on an 18-month winning streak. That streak ended Thursday night when a federal appeals court upheld a lower-court ruling lifting Trump's travel ban on refugees and all visitors from seven predominantly Muslim states ... “There is no precedent to support this claimed unreviewability, which runs contrary to the fundamental structure of our constitutional democracy.” ... Trump (@realDonaldTrump) February 9, 2017....
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ISIS Brutally Executes 7-Year-Old For Something Children All Over The World Do Every Day
Edit Opposing Views 09 Feb 2017back
Revealed: FBI terrorism task force investigating Standing Rock activists
Edit The Guardian 10 Feb 2017
The FBI is investigating political activists campaigning against the Dakota Access pipeline, diverting agents charged with preventing terrorist attacks to instead focus their attention on indigenous activists and environmentalists ... The purpose of the officers’ inquiries into Standing Rock, and scope of the task force’s work, remains unknown. Agency officials declined to comment ... Last stand ... Read more ... and it’s unconstitutional.” ... Twitter ... ....
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Four people arrested in France 'for planning imminent terror attack'
Edit The Guardian 10 Feb 2017
Four people have been arrested in and around the southern French city of Montpellier on suspicion of planning an imminent terrorist attack in France ... Police found TATP explosives and other bomb-making materials in the man’s home, the sources said. The interior ministry confirmed that explosives had been found ... The government has said it foiled 17 attacks during 2016 ... ....
DNA links Riverside man to 2001 gang rape in Yucaipa, sheriff’s officials say
Edit The Press Enterprise 10 Feb 2017Investigators hope DNA tests reveal more about human skull found in Franklin County
Edit St Louis Post-Dispatch 10 Feb 2017Slain jogger Karina Vetrano's parents advocate familial DNA tests
Edit New York Daily News 10 Feb 2017DNA Evening Must Reads: Latest on Tamil Nadu crisis, PM Modi's jibe at Rahul Gandhi, ...
Edit DNA India 10 Feb 2017
Here are the top reads from this evening. Tamil Nadu crisis Live . MLAs fasting to protest illegal detention a 'serious concern'. Madras HC. In a major development, VK Sasikala on Friday sacked senior AIADMK leader E Madhusudhanan from the post of Presidium Chairman and party's primary membership. Read more here. UP Elections 2017 ... Read more here. Jawan viral video ... DNA Web Team. ....
Applied DNA Sciences' (APDN) CEO James Hayward on Q1 2017 Results - Earnings Call Transcript
Edit Seeking Alpha 10 Feb 2017
Applied DNA Sciences, Inc ... Good afternoon, and welcome to the Applied DNA Fiscal First Quarter 2017 Earnings Conference Call ... For more information, please refer to the risk factors discussed in Applied DNA Sciences’ Form 10-K for fiscal 2016 ... And if you consider our products and services, we sale DNA, that is DNA in the form of concentrates or sometimes in a carrier or in a finished formulation ready for application....
MSG reportedly fires top security chief and former Secret Service agent after Charles Oakley incident
Edit Business Insider 10 Feb 2017
Madison Square Garden Company has fired top security chief Frank Benedetto after the physical altercation that led to Charles Oakley's ejection from a Knicks game and arrest, according to DNA Info New York ... DNA Info reports that Oakley has attended Knicks games before without incident ... DNA Info reports that Dolan may ......
MyHeritage Launches Photo Discoveries™
Edit Market Watch 10 Feb 2017
TEL AVIV, Israel & LEHI, Utah, Feb 10, 2017 (BUSINESS WIRE) -- MyHeritage, the leading international family history and DNA company, announced today the launch of Photo Discoveries, an innovative feature which transforms family trees by automatically adding matching historical photos ... MyHeritage is the leading global destination for family history and DNA....
Thousands of convicts told that cops mishandled DNA evidence
Edit New York Post 10 Feb 2017
More than 2,000 people convicted of crimes, including those imprisoned for murder and rape, will be notified by Texas prosecutors about the possibility of defective forensic evidence in their cases because of faulty DNA testing by Austin cops ... The Austin Police Department’s DNA lab was closed in June after a state audit found staffers there were using outdated and incorrect procedures while processing DNA evidence....
Indian tech entrepreneur on mission to democratise healthcare
Edit DNA India 10 Feb 2017
Genomics seeks to sequence, assemble, and ultimately understand the function of genomes, the complete set of DNA within a single cell of an organism ... "We have made it our mission to build the largest high-fidelity genomics data platform of analysed and sequenced DNA along with clinical longitudinal data sets from every ethnic group in order to help pharmaceuticals develop targeted therapeutics....
WATCH: Fans went into frenzy as Deepika Padukone arrived at Beijing for the premiere of ...
Edit DNA India 10 Feb 2017Man serving life for killing daughter in disputed case dies
Edit Times Union 10 Feb 2017
(AP) — A 53-year-old man in prison for raping and killing of his daughter has died, as his lawyers continue to insist that DNA evidence shows he was not guilty....
Kareena Kapoor Khan parties with hubby Saif Ali Khan till 5 AM, watch video!
Edit DNA India 10 Feb 2017- 1
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