give me a tutorial on the aetiology, pathology ,clinical feature andclassification  of hepatosplenomegaly?
84849
Have you tried www.nlm.nih.gov/medlineplus/ency/article/003275.htm?
909893
check here for extensive info:\n\n\nhttp://rarediseases.org/search/rdbdetail_abstract.html?disname=Angelman%20Syndrome
421640
Here's one on evolutionary genetics.http://evolution.genetics.washington.edu/pgbook/pgbook.html  Most of the others I'm finding require a charge.  There is a wealth of genetics info on-line.  \n\nNot knowing what level you're studying at it's hard to say, but this http://gslc.genetics.utah.edu/units/disorders/index.cfm is pretty comprehensive and easy to navigate.
811214
I had the same problem, but before I tell u my story, did you test him against all the Hepatitis strands (A,B &C) if u did and negative then let me tell u my story, could apply to him.\n\nI spent months doing tests and I visited around 6 different doctors trying to find out what was wrong with my liver. Of course, I took the tests over and over again in different labs because liver tests are often not very accurate so I had to make sure.\n\nAnyways, to cut a long story short I discovered that I had no physical disease but I had a hereditary problem called "fatty liver syndrome" this bascially means that my liver accumulates fats more than normal people. There is no cure, what you can do is cut down on fatty food like cheese, burgers, milk, pizza etc and lose weight. In other words switch to healthy food, this is not easy of course, but it is a must to avoid damage to the liver. \n\nTalk to your doctor about fatty liver syndrome and check with his parents to see if they had a similar condition, better yet have them tested because it is hereiditary.\n\nGood luck.
250838
Good God man you are on the net, you have more information than you know what to do with right at your finger tips. Go to Yahoo's main page and type genetics into the search bar.
504817
Cell_line_name IMR-90 \nAccession_number ECACC 85020204  \nBrief_description Human Caucasian fetal lung fibroblast  \nDescription Human Caucasian fetal lung fibroblast  \nDepositor Dr P Jacobs, NIBSC, London, UK  \nBibliographic_reference Science 1977;196:60  \nMorphology Fibroblast  \nCulture_conditions EMEM (EBSS) + 2mM Glutamine + 1% Non Essential Amino Acids (NEAA) + 10% Fetal Bovine Serum (FBS). Split confluent cultures 1:3 to 1:6 i.e. seeding at 2-3x10,000 cells/cm2 using 0.25% trypsin or trypsin/EDTA; 5% CO2; 37C.  \nViruses See Properties  \nProperties Applications: Virus studies  \nRelease_conditions No restrictions. Patent: None Specified By Depositor  \nHazard CX  \nPassage_number 14  \nKaryotype 2n = 46, diploid  \nComments Derived from lung tissue of a 16 week old female Caucasian foetus. The cells have a virus susceptibility similar to WI-38 and MRC-5. The cells have a finite lifespan.  \nResearch_council_deposit No  \nPrice_code B  \n\nCell_line_name AV3  \nAccession_number ECACC 88102402  \nBrief_description Human amnion, HeLa characteristics  \nDescription Human amnion, HeLa characteristics  \nDepositor Obtained from ATCC, USA  \nBibliographic_reference Nature 1976;259:211  \nMorphology Epithelial  \nCulture_conditions EMEM + 2mM Glutamine + 10% Fetal Bovine Serum (FBS). Split confluent cultures 1:2 to 1:4 i.e. seeding at 2-5x100,000 cells/cm2 using 0.25% trypsin; 5% CO2; 37C.  \nViruses See Properties  \nProperties Applications: Virus studies: poliovirus 1  \nRelease_conditions No restrictions. Patent: None Specified By Depositor  \nHazard CX  \nPassage_number 276  \nKaryotype 2n = 46  \nComments This cell line was derived from normal human amnion and shown to be contaminated with HeLa cells. They are mainly used for virus studies (susceptible to poliovirus 1). HeLa marker chromosomes and type A G6PD have been detected. This cell line was found to have a HeLa profile by DNA fingerprinting.  \nResearch_council_deposit No  \nPrice_code C
841642
http://www.natap.org/2005/HCV/122105_01.htm  try this link it may help you
937680
http://www.herbalprovider.com/liver-cirrhosis.html?src=ggl&w=liver-cirrhosis&gclid=CND96LyJqogCFSdJYwodwUjjhw#cirrhosis
372921
http://faculty.clintoncc.suny.edu/faculty/Michael.Gregory/files/Bio%20101/Bio%20101%20Lectures/DNA/dna.htm
436433
Phone up the Royal college of Surgeons: there are some overseas exams these days. However there is a HIGH failure rate in these. You are advised to go on the official MRCS courses...where I will teach you!!!\nBrush up your anatomy and physiology.\nFor the viva there is a good book by David Lowe on the Pathology.\nGood Luck
591537
http://www.liverdoctor.com/Section4/fattyliver.asp
429386
Amegakaryocytic Thrombocytopenia (Amega)\n\nThese patients have bruising during the first year of life, due decreased production of platelets by the bone marrow (platelets are the cells which help the blood to clot). The physical appearance is otherwise normal. The gene for Amega has been identified. It is called "MPL." Males and females are affected equally.\n\n   1. What are the major findings on physical examination?\n         1. Bruises, bleeding, – tiny spots of bleeding into the skin ("petechiae")\n\n   2. What is the age at diagnosis?\n         1. From birth to 9 years\n         2. The diagnosis is usually made by 1 month of age\n\n   3. What is the pattern of bone marrow failure?\n         1. The bone marrow problems typically start with a low platelet count\n         2. Patients may eventually develop aplastic anemia when all 3 types of cells (red cells, white cells and platelets) are abnormally low because the bone marrow is not producing them.\n\n   4. What specific kinds of cancer develop?\n         1. Leukemia (cancer of the blood and bone marrow)\n\n   5. How is Amega specifically diagnosed?\n         1. Characteristic medical history\n         2. Mutation analysis (genetic testing)\n               1. Laboratories can now identify the genetic "error" (mutation) in some patients, which occurs in the gene called "MPL"\n               2. The disease occurs only if a person has two abnormal (mutant) genes. The inheritance is therefore thought to be of the autosomal recessive type
348317
that is very interesting and usefull information and  would normally concern me if i had not already had a test done in the recent months due to elevated liver enzymes, i also had a blood transfusion at birth . before 1979 . thanks
386097
Unfortunately, my friend, like with HCV, there is no standardized or commercial method available for HBV genotyping at the moment.\n\nthese websites may help : http://jcm.asm.org/cgi/content/full/41/12/5473\n\nhttp://www.biology-online.org/biology-forum/post-11699.html&highlight=\n\nhttp://www.aegis.com/news/pr/2001/PR011243.html\n\nyou can make your own mind up about which is most reliable.
903086
Too many to list and explain here, without copying and pasting  --and why should I do all your uni work for you? ;-)\n\nI will recommend a couple of good text books through.  Well worth a purchase or just get them on loan from your library...\n\nAlberts et al, Molecular Biology of the Cell\nStryer, Biochemistry\n\nIt's been since I bought mine.  Think I got editions 2 & 7 back in 1996 and I know both have been updated a couple of times since.  These are still a GREAT basic resourse for this sort of question.
462778
Absent or defective splenic function is associated with a high risk of fulminant bacterial infections and a high mortality rate. Asplenia and splenic hypoplasia are terms used to indicate complete or partial lack of splenic function. Loss of splenic function usually occurs as a result of surgical removal or autosplenectomy, ie, infarction in patients with hemoglobinopathies. Congenital splenic anomalies are usually accompanied by abnormalities in other organ systems, especially cardiac abnormalities, but they may occur in isolation. Polysplenia, ie, bilateral left-sidedness, is also frequently associated with congenital cardiac anomalies. \n\nPatients with polysplenia have multiple spleens, and their splenic function is usually normal. Isolated asplenia or hyposplenia is often diagnosed only after the patient has had a serious, fulminant, and often fatal infection. These conditions are extremely difficult to diagnose in the absence of other indicators. Morphologic anomalies of peripheral blood erythrocytes, such as Howell-Jolly (HJ) bodies, may be the only evidence of the presence of a nonfunctional spleen .\nWorldwide, most patients with asplenia or hyposplenia have an underlying hemoglobinopathy such as sickle cell disease.\nIsolated asplenia and polysplenia are commonly associated with significant abnormalities involving other organ systems.\nAn awareness of these associations and syndromes may help in screening the patient for splenic dysfunction.\nThe most important clinical indication for the evaluation of splenic function is the presence of complex congenital heart disease. Patients should be evaluated for splenic dysfunction if any of the following are present:\nRecurrent infection or sepsis, especially with encapsulated organisms\nFamily history of asplenia or polysplenia\nCyanotic congenital heart disease or complex cardiac malformations\nEvidence of visceral heterotaxy or other associated malformations\nBilateral trilobed or bilobed lungs on chest radiographs\nIn contrast, the presentation of patients with isolated congenital absence or hypoplasia of the spleen may be less dramatic.\nChildren with these conditions may present to the primary caretaker with fever or overwhelming sepsis, or they may even be moribund.\nAssociated cardiovascular, pulmonary, gastrointestinal, or genitourinary abnormalities may not be present to alert the physician to their underlying immunocompromised state.\nFeatures such as thrombocytosis, HJ bodies in red cells, and recurrent episodes of invasive infections with encapsulated organisms may be helpful in identifying individuals with isolated absence or hypoplasia of the spleen. The absence of these features, however, does not exclude splenic malfunction, although it may make the diagnosis more difficult.
509034
www.dnaftb.org\nhttp://www.dnai.org/\n\nHope u like my answer