Science topic

Liver Diseases - Science topic

Pathological processes of the LIVER.
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If you agree with the new name , you can add your name to the authorship of this statement by filling the simple survey below.
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Yes
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Why edema in nephrotic syndrome is periorbital ? If its due to protien loss then there is protien loss in chronic liver disease too but there is no periorbital edema then what is the underlying pathophysiology of periorbital edema in nephrotic syndrome
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The hypoalbuminemia leeds to fluid retention everyhere including the periorbitary area
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Can we combine alcoholic and non-alcoholic liver disease into a single fatty liver risk scoring system?
If no, why?
If yes, what will be the potential of such research and implications.?
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I am looking for potential collaboration in research about clinical nutrition of patients with liver disease
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Please have look on our(Eminent Biosciences (EMBS)) collaborations.. and let me know if interested to associate with us
Our recent publications In collaborations with industries and academia in India and world wide.
EMBS publication In association with Universidad Tecnológica Metropolitana, Santiago, Chile. Publication Link: https://pubmed.ncbi.nlm.nih.gov/33397265/
EMBS publication In association with Moscow State University , Russia. Publication Link: https://pubmed.ncbi.nlm.nih.gov/32967475/
EMBS publication In association with Icahn Institute of Genomics and Multiscale Biology,, Mount Sinai Health System, Manhattan, NY, USA. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/29199918
EMBS publication In association with University of Missouri, St. Louis, MO, USA. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/30457050
EMBS publication In association with Virginia Commonwealth University, Richmond, Virginia, USA. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/27852211
EMBS publication In association with ICMR- NIN(National Institute of Nutrition), Hyderabad Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/23030611
EMBS publication In association with University of Minnesota Duluth, Duluth MN 55811 USA. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/27852211
EMBS publication In association with University of Yaounde I, PO Box 812, Yaoundé, Cameroon. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/30950335
EMBS publication In association with Federal University of Paraíba, João Pessoa, PB, Brazil. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/30693065
Eminent Biosciences(EMBS) and University of Yaoundé I, Yaoundé, Cameroon. Publication Link: https://pubmed.ncbi.nlm.nih.gov/31210847/
Eminent Biosciences(EMBS) and University of the Basque Country UPV/EHU, 48080, Leioa, Spain. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/27852204
Eminent Biosciences(EMBS) and King Saud University, Riyadh, Saudi Arabia. Publication Link: http://www.eurekaselect.com/135585
Eminent Biosciences(EMBS) and NIPER , Hyderabad, India. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/29053759
Eminent Biosciences(EMBS) and Alagappa University, Tamil Nadu, India. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/30950335
Eminent Biosciences(EMBS) and Jawaharlal Nehru Technological University, Hyderabad , India. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/28472910
Eminent Biosciences(EMBS) and C.S.I.R – CRISAT, Karaikudi, Tamil Nadu, India. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/30237676
Eminent Biosciences(EMBS) and Karpagam academy of higher education, Eachinary, Coimbatore , Tamil Nadu, India. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/30237672
Eminent Biosciences(EMBS) and Ballets Olaeta Kalea, 4, 48014 Bilbao, Bizkaia, Spain. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/29199918
Eminent Biosciences(EMBS) and Hospital for Genetic Diseases, Osmania University, Hyderabad - 500 016, Telangana, India. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/28472910
Eminent Biosciences(EMBS) and School of Ocean Science and Technology, Kerala University of Fisheries and Ocean Studies, Panangad-682 506, Cochin, India. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/27964704
Eminent Biosciences(EMBS) and CODEWEL Nireekshana-ACET, Hyderabad, Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/26770024
Eminent Biosciences(EMBS) and Bharathiyar University, Coimbatore-641046, Tamilnadu, India. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/27919211
Eminent Biosciences(EMBS) and LPU University, Phagwara, Punjab, India. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/31030499
Eminent Biosciences(EMBS) and Department of Bioinformatics, Kerala University, Kerala. Publication Link: http://www.eurekaselect.com/135585
Eminent Biosciences(EMBS) and Gandhi Medical College and Osmania Medical College, Hyderabad 500 038, India. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/27450915
Eminent Biosciences(EMBS) and National College (Affiliated to Bharathidasan University), Tiruchirapalli, 620 001 Tamil Nadu, India. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/27266485
Eminent Biosciences(EMBS) and University of Calicut - 673635, Kerala, India. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/23030611
Eminent Biosciences(EMBS) and NIPER, Hyderabad, India. ) Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/29053759
Eminent Biosciences(EMBS) and King George's Medical University, (Erstwhile C.S.M. Medical University), Lucknow-226 003, India. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/25579575
Eminent Biosciences(EMBS) and School of Chemical & Biotechnology, SASTRA University, Thanjavur, India Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/25579569
Eminent Biosciences(EMBS) and Safi center for scientific research, Malappuram, Kerala, India. Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/30237672
Eminent Biosciences(EMBS) and Dept of Genetics, Osmania University, Hyderabad Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/25248957
EMBS publication In association with Institute of Genetics and Hospital for Genetic Diseases, Osmania University, Hyderabad Publication Link: https://www.ncbi.nlm.nih.gov/pubmed/26229292
Sincerely,
Dr. Anuraj Nayarisseri
Principal Scientist & Director,
Eminent Biosciences.
Mob :+91 97522 95342
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I am working on qPCR of cDNA from liver in various states of health and disease, and our housekeeping genes show a fair amount of variation between disease states and other groupings. Which housekeeping genes do you use for liver research?
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We have come across hundreds of amoebic liver abscess cases here in northern Sri Lanka. We treat all of them with metronidazole and sometimes with percutaneous aspiration. All of them recover. But we don't have any laboratory tests to confirm amoebiasis objectively.
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Anti gal nac plus gal nac antigen before treatment is simple best combination
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In a DCLD patient who is on diuretics, the recommendation in a patient with ascites and AKI is to stop diuretics and start albumin. But when the diuretics should be restarted remains a dilemma, because these patients are commonly prone to recurrent AKI.
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When normal s.cratinine
Normal creatinine clearance
When developing any urgent need for diuretic
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Hola
I'm working on a project that deals with clinical named entity recognition, relation extraction etc. I'm currently using Scispacy library for NER work. However, I'm searching for a open source package for relation extraction from clinical notes (Eg. In the following sentence "Dementia due to Alzheimer disease." I except a model that should recognize the relationship that its not just dementia and its is dementia due to Alzheimer.)
Spending sometime on reading articles and surfing google
I found the following packages:
1. SemRep
2. BioBERT
3. Clincal BioBERT
etc.
from the articles, I also got to know that clincal BioBERT to be the suitable model. However, when I tried running the model from transformer library I just found the following output
Code
from transformers import AutoModelForTokenClassification, AutoTokenizer, pipeline
model =  AutoModelForTokenClassification.from_pretrained("emilyalsentzer/Bio_Discharge_Summary_BERT")
tokenizer = AutoTokenizer.from_pretrained("emilyalsentzer/Bio_Discharge_Summary_BERT")
nlp = pipeline('ner', model=model, tokenizer=tokenizer)
text = "Dementia due to Alzheimers disease. Kidney failure due to liver disease."
nlp(text)
Out put:
[{'entity': 'LABEL_1', 'index': 1, 'score': 0.562394917011261, 'word': 'dementia'}, {'entity': 'LABEL_0', 'index': 2, 'score': 0.5325632691383362, 'word': 'due'}, {'entity': 'LABEL_1', 'index': 3, 'score': 0.5473843812942505, 'word': 'to'}, {'entity': 'LABEL_1', 'index': 4, 'score': 0.5070908069610596, 'word': 'alzheimer'}, {'entity': 'LABEL_0', 'index': 5, 'score': 0.5742462873458862, 'word': '##s'}, {'entity': 'LABEL_1', 'index': 6, 'score': 0.5498184561729431, 'word': 'disease'}, {'entity': 'LABEL_1', 'index': 7, 'score': 0.5163406133651733, 'word': '.'}, {'entity': 'LABEL_1', 'index': 8, 'score': 0.5038259625434875, 'word': 'kidney'}, {'entity': 'LABEL_1', 'index': 9, 'score': 0.5872519612312317, 'word': 'failure'}, {'entity': 'LABEL_0', 'index': 10, 'score': 0.523786723613739, 'word': 'due'}, {'entity': 'LABEL_1', 'index': 11, 'score': 0.5193214416503906, 'word': 'to'}, {'entity': 'LABEL_1', 'index': 12, 'score': 0.5457456707954407, 'word': 'liver'}, {'entity': 'LABEL_1', 'index': 13, 'score': 0.5755748748779297, 'word': 'disease'}, {'entity': 'LABEL_1', 'index': 14, 'score': 0.5418881177902222, 'word': '.'}]
From the above output, I except labels such as disease, organ etc. However, the model labeled the entity as 'LABEL_1' or 'LABEL_0'.
How do I use the clinical BioBERT to extract relations. Please advice.
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I am working on liver disease classification using Machine learning. I would like to know is there any public dataset available for liver disease patients data which includes both liver functional test results and liver image of same patient.
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Hello mates,
I would like to learn what is the median HBsAg value (as well as the range) in treatment-näive CHB patients. Please also show me the paper or guidance (AASLD, EASL, APASL, etc.)
I have found some documents, all of which tell the HBsAg level in patients treated or with advanced liver diseases (e.g. fibrosis, cirrhosis).
Thank you very much!
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Hi Bingqian
I would suggest you refer to these articles.
Best
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I want to research on liver disease patients behaviours and habits in shiraz city. How can I calculate sample size accurately?
Thanks
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Thanks for your consideration.
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we are doing a meta-analysis (liver disease related ) and have progressed satisfactorily. Now we wish to publish our protocol. Can any one suggest few journals where we can publish it
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1.BMJ open
2.Systematic review (BioMed)
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I need to know what precautions need to be taken for using CCl4 in the mouse model of inducing liver fibrosis. I plan to inject the CCl4 intraperitonealy. The biosafety comittee has questions as to the toxicity of the CCl4 to laboratory and animal care staff.
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Ibrahim El Sayed - I think it is usually important to study the effect on two models rather than one, so that you show that the effects are not related to CCl4 effect, but the pathological changes in the liver.
Complications could be development of ascites, gastritis, bleeding, cirrhosis or cholestasis occur or animal death.
The model in mice is not identical to human liver fibrosis/cirrhosis. See this publication for example. CCl4 is toxic and you have to follow toxicological lab regulations.
BMC Gastroenterol. 2010 Jul 9;10:79. doi: 10.1186/1471-230X-10-79.
Mouse model of carbon tetrachloride induced liver fibrosis: Histopathological changes and expression of CD133 and epidermal growth factor.
Fujii T1, Fuchs BC, Yamada S, Lauwers GY, Kulu Y, Goodwin JM, Lanuti M, Tanabe KK.
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Dear Colleagues:
the first table of the article describes the differences between cirrhotic and non cirrhotic hepatocellular carcinomas and notes that when the first is caused by alcoholic or viral insults to the organ, the later is, among other causes, derived of metabolic alterations. This statement, I consider should be revised because it has been widely studied the association of non-alcoholic fat liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) as cirrhosis causatives and their close link to metabolic origins.
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Metabolic syndrome is a constellation of problems including obesity, dyslipidemia, diabetes, and insulin resistance These diseases are associated with both increased risk for, and worsened outcomes of many types of cancer. In the liver, inflammatory and angiogenic changes due to underlying insulin resistance and fatty liver disease will likely lead to increased numbers of patients with HCC in the near future. Much work needs to be done to define more clearly the risks for development of HCC in those with underlying metabolic syndrome, the best methods of screening those at risk, and ultimately, the best treatments targeting the underlying mechanisms of pathogenesis.
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liver disease in pregnancy
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Naser,
I’m not sure if this question is “settled”. When I performed a considerable amount OB anesthesia, my department standard supported Epidural anesthesia for labor (In this case). Although, if the patient was nearing 8cm dilation, a SAB (1ml 0.25% bupivacaine and 20 mcg fentanyl) would usually get the patient to delivery. Today we have an option to place bilateral erector spinae catheters, which should provide adequate comfort during the early stages of labor. Although I do not participate in OB anesthesia on a regular basis.
Regards,
Christopher
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I learned recently, that autophagy may have a protective role against the development of a number of neurodegenerative diseases. As I am working on liver diseases, with mice deficient for some autophagy receptors, i had like to know which section of the liver and the brain are suitable for histological examination.
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Mireille Kameni you are very welcom!
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LDQOL - Liver disease quality of life questionnaire use in India
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I don´t know that, but you must contact with the Indian Association for the Study of liver diseases to get the needed information
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I wish to study the prevalence of different types of hepatitis visiting our hospital. That is - what is the prevalence of viral or drug or hypoxic hepatitis.
Second objective will be to see the prognosis of hepatitis in those people who already have a liver disease. That is, I wish to compare group A (with pre existing liver disease) & Group B ( no pre-existing liver disease) and see the prognosis of hepatitis in both these groups.
Doubt 1. What will be the study design? Cross Sectional?
Doubt 2. I plan to enrol every patient admitted with hepatitis. What type of sampling method can I call this?
Doubt 3. How do I decide the sample size required? Unable to find an old relevant study.
Doubt 4. Do I need to set the power of this study?
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This will be a hospital based [as opposed to community based] study. The first part of study will be cross sectional and will be reported as frequency [%] of different type of hepatitis. The second part will be longitudinal as the outcome is measured after treatment so needs follow up. The outcome may be reported as mortality, length of hospital stay etc. If all patients are included there is no need of sampling and consecutive cases may be included.
Normally sample size and power of a study needs to be calculated if one is measuring the outcome of a specific intervention [drug, devices etc] to lay emphasis on the significance of outcome [poorer or better] but in the case suggested since only standard care is given, it is best to report the outcome with univariate statistics e.g. % mortality in both groups may be compared by chi square test, difference in length of hospital stay by students "t" test.
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Normally we do ultrasound to confirm etiology of pancreatitis. Can we avoid doing one and exclude gallstones as cause of pancreatitis just on the basis of LFT's?
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According to recent studies
weight-for-age percentile is a significant independent predictor of gallstone pancreatitis in children. while Amylase, AST, or ethnicity were not found to be significant predictors of gallstone pancreatitis.
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Can someone help me about that technical details???
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Hi, I don't have any detailed protocol myself but being at your placr I would rather consider use of the combination of palmitate and oleate. Moreover, If you would like to mimic the steatosis in vitro, I would suggest using primary Heps or HepaRG cells (hepatocyte-like cells) cause HepG2 in the end are hepatoma (cancer) cells
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Excessive fat accumulation within hepaocytes seems pathological. Can it be a cause of cirrhosis or chronic liver disease?
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The pathogenesis of how the accumulated hepatic fat causes liver damage is a complicated issue.
According to “ 2 or multiple hits hypothesis”, the accumulated hepatic fat in some people causes injury to liver cells (nonalcoholic steatohepatitis or NASH) through direct lipotoxicity from free fatty acids (FFAs), oxidative stress, mitochondrial dysfunction, gut microbiota/LPS, activation of fibrogenesis, etc.
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Beta carotene is said to be used with caution in those with some form of liver / renal impairment, but when I checked the metabolism of beta carotene, there is a portion which is converted into retinol (Vitamin A) which is contraindicated for any one with liver disease. So, is there something missing? Reference of the image attached "
Herb, Nutrient, and Drug Interactions"
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Vitamin A deficiency is widespread in many societies and it is associated with night blindness and infectious morbidity. Although beta-carotene or vitamin A supplementation did not appear to affect risk of maternal or infant mortality, weekly supplementation or food fortification is still an important public health goal
Beta-carotene is an important source of vitamin A for humans and it is recommended that people should consume 6mg per day when the intake of preformed vitamin A is low. Beta-carotene levels aresignificantly lower in individuals with increased obesity and body mass index, including children.
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spices you should be incorporating into your diet on a regular basis
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there are number of spices but turmeric tops the list for anti cancer properties
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Which agent is the best for occasional use for someone who has NAFLD ? and why ?
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I believe ibuprofen is best because its metabolism in the liver, not affected by NAFLD because their metabolism pathway occur by number of CYP isoforms for example S-IBU is predominantly via CYP2C9 whereas R-IBU is more via CYP2C8. A number of other CYPs are capable of metabolism at high concentrations of IBU: CYP3A4, CYP2C8, CYP2C19, CYP2D6, CYP2E1, and CYP2B6 for 2-hydroxylation and CYP2C19 for 3-hydroxylation. In addition it less drug - drug and drug - disease interaction than aspirin. While acetaminophen is hepatotoxic and not preferred here. Aspirin to be used for headache should be taken at high dose (300-500)mg or more and it has wide range of adverse effects and drug-drug or disease interaction.
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I have read studies that showed benefit for those who have NAFLD, and ingest Curcumin but Unfortunately the COMMUNITY HERBAL MONOGRAPH ON CURCUMA LONGA L., RHIZOMA which is adopted by the Committee on Herbal Medicinal Products lists Liver disease to be a contraindication for Turmeric consumption, and when I sent them, they said that NAFLD is included in the "liver disease" category? So is it contraindicated for NAFLD patients or not ?
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The best reference for the assessment is The National Toxicology Program, Technical Report number 427-
TOXICOLOGY AND CARCINOGENESIS
STUDIES OF TURMERIC OLEORESIN
I would encourage you to carefully read the whole report. Definitely chronic use of this substance is associate with several pathological changes affecting the liver and the gastrointestinal system plus other organs. We cannot assume that chronic intake of Turmeric Oleoresin is safe. I attach a copy of the report.
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After a special treatment of mice with chronic liver disease, I see a significant increase of monocyte-derived macrophages in the liver along with increased fibrosis and compensatory proliferation.
I stained liver section for Cl.Casp3 (Apoptosis) and observe that these monocytes (besides hepatocytes) are also apoptotic.
Can anyone give me hints why these monocytes undergo apoptosis inside the liver? Don't they support the inflammatory milieu?
Thanks!!
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Thank you both for your answers!
@wy Do you have an publication for me indicating the life-span of monocytes in mice?
@SS Normally we perform FACS analysis, gating LY6C+/CD11b+/F4/80+ cells as monocyte-derived macrophages. I did not yet check for lysosomal structures or endocytic vacuoles.
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What is the positive?
High coffee intake reduced all-cause mortality from cancer, circulatory disorders, and digestive and respiratory diseases. Controversy remains, however, regarding the relationship of coffee and benefit for liver disease.
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Yes, it is. There are many papers that favors this suggestion, indeed
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I found high levels of cytokine and expression of CD Markers role in damge of liver .if there is any cause that progress the chronic liver disease?
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Thank you Dr . I worked research about cytokine relation with pathogenesis of HCV
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When worms migrate from the liver to their site of reproduction, S. haematobium worms usually end up in vessels in urogenital organs whereas S. mansoni, japonicum etc. usually ends up in gastroinstestinal vessels. What is the most plausible theory for this ability to migrate to one organ but not another?
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beyond to evolution 
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Concentration of protease inhibitor (cystatin) increases with progression of liver diseases like liver fibrosis and carcinoma..then why dont these inhibitors inhibit viral proteases and HCV replication??If they do,then how disease progresses....
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According to literature, Cystatins from different sources are currently in use against viral diseases including Hepatitis C. if they actually inhibit viral replication then why their concentration enhanced with disease progression, why they dont stop virus in that case...its only because of virus evolution?? 
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Is it effective for the detection of fatty liver (mainly for mild degree)?
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42 year male, case of Hepatitis C (genotype 3) with very high viral load, was treated with Sofosbuvir 400 mg OD with Ribavirin 800 mg, tolerated well with rapid viral response rate. After 12 wks of therapy, he has started c/o severe weakness, and his baseline blood parameters showed Hb of 5.6 gm/dl amd TC of 5000/cmm with normal DLC. Other parameters are normal. Now, whether to stop Ribavirin or simply reduce the dose? Is there any role of Erythropoitein? If yes, at what dose?
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Kindly look at the attached link.
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Thanks in advance for your replies.
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Osmotic fragility depends upon surface to volume ratio. In different diseased condition, they differ a lot. Kindly follow the attached links for little more information.
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citaloperam is the best subject for  susceptible liver pateints? what is the liver toxicity risks?
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it's not the best, only one of the "cleanest" SSRI's, meaning it has very little effect on other than serotonin receptors. It is quite mild and I am not aware of "toxic effect" on the liver, certainly not when given in therapeutic doses and not anymore than other SSRi's and antidepressants. Citalopram is cleared by the liver which might affect its pharmacokinetics but its therapeutic window is wide and for additional info refer to the attached link. In sum, the risk is small
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I am working with mice liver injury model where I need to monitor serum ALT and AST levels. Here I have got a problem that I could not proceed with serum seperation of my blood samples (kept in serum vials) and left them at 20degree C without serum seperation for atleast 28hrs. All I want to ask is that what kind of effects will it have upon the results? If the results of ALT and AST levels will be reliable? I can not repeat the test as it was a lonng process so suggest me some troubleshoots as well.
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Simple question and good answers, which are useful for daily research.  
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(A case) A 68-year male with maintenance dialysis presented appetite loss and general fatigue. Ultrasonography revealed a 10cm sized tumor at the segment S7 in the liver, suggesting HCC. Retention of ascites was evident. Serum HBs-antigen and serum HCV-antibody regularly checked showed negative results. However, three months prior, serum HBs-antigen was positive. This time when HCC was discovered, serum HBs-antigen was found to be negative. Further laboratory analysis revealed positive results of serum HBs-antibody, HBc-antibody, HBe-antibody, and negative results of serum HBe-antigen and IgM HBc-antibody. HBV-DNA was not detected. Tumor markers, AFP and PIVKA-II, were remarkably elevated. In this patient, he has no history of vaccination. He has never been investigated for serum HBc-antibody and HBs-antibody.  
I suppose that HCC in this patient originates in occult HBV and the necessity in estimating serum HBc-antibody and HBs-antibody even if serum HBs-antigen is negative.
Do you agree to my idea that HCC in this patient derived from occult HCC?
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Do you have more images of the tumor? The location of the tumor seems favorable for laparoscopic liver resection. It may be in segment 6 rather than 7. We are doing laparoscopic resection even in Child B patients with good results. Laparoscopy itself decrease systemic inflammatory response that is responsible for postoperative complications in cirrhotic patients.
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The diagnosis of eosinophilic esophagitis (EoE) is based on consensus reccommendations published in 2007. Nevertheless non uniformity in diagnostic defintion and non adherence to consensus recomendations continue to  be  observed even in recent publications.It leads to a definition problem of EoE since it is known that esophageal eosinophilia may be caused also by GERD,PP- responsive EE and extraesophageal systemic diseases. What is your stratgy for assuring a diagnosis of EoE in suspected patients?
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I agree at all with your new sugestión of curse. Thank you for your coment
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Recently, I met a patient with HCC recurrence, who received liver resection just 5 months ago, and followed with twice TACE treatment.
The primary single tumor is small, just 2cm diameter. APF is higher than 2000.
This is not the first time I met the patient like this. According to my experience, I feel that the recurrence is more easily detected in small HCC than big HCC. I searched many papers, but without relevant evidence.
Does someone have the idea about this issue?
Thanks for you answer in advance! 
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There is a known proverb that says that "Surgery is Prince, selection of cases is Queen and Biology is King" You can find your answer looking at this proverb.
However, in my opinion the most important fact is that when you have a large HCC and you proceed with surgery it means that it has not spread to other organs, not spread to lymphnodes and usually is a single tumor with no satellite lesions. This is your favorable biology right in front of you telling you that you can go with the operation and it may no recur. All other large tumors are not referred to you because the bad biology has already surfaced.
On the other hand, when you have a small tumor you have no idea if the biology is favorable or not because there was no enough time for the tumor to show distance metastases or lymphnodes and we expect cure in those cases and we are frequently deceived. In this context you are going to operate more small tumors with uncertain biology and whenever you face a really mean biology, it will strike back with full force like your case mentioned above.
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It is found that vitamin C supplement helps in reducing MDA level in liver disease patient. Further studies suggest that zinc level is reduced in liver patient. So what will be the relation between MDA and Zinc?
Again we know that NO is a lipid peroxidation products. If NO (Nitric oxide) is also increase in liver patient then what will be the relation between zinc and NO?
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Best regards,
Kívia
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The major risk of overconsumption of a high fibre diet will lead to excessive intake of phytosterols that lead to neurodegeneration. Diets that are high in fibre in the developing world may also contain toxic xenobiotics that may lead to insulin resistance, NAFLD cardiovascular disease and brain damage.
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 What we see in the US is very poor and very low fiber diet. NAFLD and NASH, obesity and even cardiovascular disease tend to associate rather with obesity, high fat and low fiber diet. I would not change my clinical recommendation of healthy fiber intake in the US unless I would find compelling studies done in industrialized countries showing a detrimental effect of fiber intake. At this point as far as I am aware a plant based diet containing at least 20-25 grams of fiber per day is the healthiest for most people in the industrialized world.
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I am especially asking for the methods which will show the presence of liver function enzymes (ALP, ALT etc.) by colour change.
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Sayad,
Sorry for such a long post but it is a complex answer.  I hope this is what you need.
ALP reagent is used to measure alkaline phosphatase activity by a kinetic rate method using a 2-amino-2-methyl-1-propanol (AMP) buffer. In the reaction, alkaline phosphatase catalyzes the hydrolysis of the colorless organic phosphate ester substrate, p-nitrophenylphosphate, to the yellow colored product, p-nitrophenol, and phosphate. This reaction occurs at an alkaline pH of 10.3.  The ratio used is one part sample to 50 parts reagent. The system monitors the change in absorbance at 410 nanometers. This change in absorbance is directly proportional to the activity of ALP in the sample and is used by the System to calculate and express ALP activity.
The AST reagent is used to measure aspartate aminotransferase activity by an enzymatic rate method.1,2 In the assay reaction, the AST catalyzes the reversible transamination of L-aspartate and α-ketoglutarate to oxaloacetate and L-glutamate. The oxaloacetate is then reduced to malate in the presence of malate dehydrogenase (MDH) with the concurrent oxidation of β-Nicotinamide Adenine Dinucleotide (reduced form) (NADH) to β-Nicotinamide Adenine Dinucleotide (NAD). The ratio used is one part sample to 11 parts reagent. The system monitors the rate of change in absorbance at 340 nanometers over a fixed-time interval. This rate of change in absorbance is directly proportional to the activity of AST in the sample and is used by the SYNCHRON® System(s) to calculate and express the AST activity.
The AST reagent is used to measure aspartate aminotransferase activity by an enzymatic rate method.1,2 In the assay reaction, the AST catalyzes the reversible transamination of L-aspartate and α-ketoglutarate to oxaloacetate and L-glutamate. The oxaloacetate is then reduced to malate in the presence of malate dehydrogenase (MDH) with the concurrent oxidation of β-Nicotinamide Adenine Dinucleotide (reduced form) (NADH) to β-Nicotinamide Adenine Dinucleotide (NAD).  The ratio used is one part sample to 11 parts reagent. The system monitors the rate of change in absorbance at 340 nanometers over a fixed-time interval. This rate of change in absorbance is directly proportional to the activity of AST in the sample and is used by the SYNCHRON® System(s) to calculate and express the AST activity.
LD reagent is used to measure lactate dehydrogenase activity by an enzymatic rate method.2,3 In the reaction, LD catalyzes the reversible oxidation of L-lactate to pyruvate with the concurrent reduction of β-nicotinamide adenine dinucleotide (NAD) to reduced β-nicotinamide adenine dinucleotide (NADH). The ratio used is one part sample to 20 parts reagent. The system monitors the change in absorbance at 340 nanometers. This change in absorbance is directly proportional to the activity of lactate dehydrogenase in the sample and is used by the System to calculate and express the lactate dehydrogenase activity.
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I have MRI images, and I am working in medical diagnosis using computer classifications
I need the features data set of each disease to use it in learning the ANN
The required dataset of images consists of the infected image and another image with a colored line around the lesion.
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 Dear Dr Ali,
Thank you very much for your response. The paper you sent is very helpful for understanding Acute and chronic liver disease.
Unfortunately, I need some real images
I am working in computer science. Trying to find out an automatic method for liver diseases classification
The required dataset of images consists of the infected image and another image with a colored line around the lesion
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Liver section of a Sculpin 
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x 400
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We did for the first time the CCl4 liver inflammatory model in mice. Note that we did not start with phenobarbital previous to CCl4 protocol and we gave intraperitoneally 2ml/Kg (2:5 v/v CCl4 in mineral oil) that we planned to do twice a week. After the first injection the animal facility people told us that the mice suffered (abdominal pain and that they walked abnormally) and the next day the disconfort seemed less but there is still some appaerence of pain, although they have to admit much less. The animal facility people want to do something about it, before the next injection this Friday. Put analgesia.
Can someone tell us if this pain is normal in mice? Do you think that it is possible that our solution was corrupted somehow?
Finally is it OK to add a pain killer to the mice in this model? As many should give liver inflamation by themselves we are reluctant to accept this change? if yes which one is suggested for this type of experiments?
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Hi, I was giving ip injections of CCL4 to C57Bl6 mice and also saw that after injection they showed signs of abdominal pain and disconfort that lasted 24h and often they lost weight during that period (a sign of disconfort). 
I hope I helped you
Marta
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Specifically I am interested in effects of that flavonoid on heart, liver and skin associated conditions. Thanks in advance.
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Dr Yaroslav,
Although hundred of papers were released about quercetin that described quercetin  as a typical antioxidant flavonoid  but these studies  still  surround querceitn mainly in one circle '' a possible protective agents from heart disease''. some trials used quercertin in controlling liver cancer cataract and so on. 
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any guidelines for refractory ascites?
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Dear All,
I am studying the mechanism of a protein localized in the mitochondria of liver in a mice knocked out for my specific protein. The liver has increased lipid droplets in aged mice. Also my protein was previously shown to involve in positive lipid metabolism. In this context, to understand its mechanism followed by other experiments, I hypothesize that B Oxidation could be increased in those mice. However, I am not sure if it fit with the observation that those mice also develop fatty liver upon aging? 
Is it possible and making sense. Or my reasoning is wrong?
Any suggestion, criticism will be really helpful
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It depends of the equilibrium of three liver metabolic processes: De Novo lipid synthesis, VLDL formation and export and fatty acid oxidation. Even with increased fatty acid oxidation, an excess of DNL and a reduction in VLDL export can produce fatty liver.
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This is a young female patient post SLEEVE gastrectomy, presented with massive PE, her baseline INR was 1.9 "mostly nutritional", she was started on therapeutic LMWH and warfarin, second day her INR jumped to 4, what is the right action.
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Answering directly your question, I don't think it was the best decision to stop enoxaparin only after one day, but now that it's done the best solution is to manage the dose of warfarin to achive optimum INR.    
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Instead of using commercial Avidin Biotin Complex, is there any conventional method/recipe to quench endogenous biotin in liver sections? 
Would be delighted to know!
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Dear Nasir,
There are a lot of recipes and commercially available quenchers of biotin. It is a big issue particularly in liver and lymph nodes, as you already see the issue yourself. According to my experience none can do the job sufficiently, e.g. to "mask" completely the endogenous biotin. You can get certain signal to noise ratios for sure but almost never as good as expected. On top you introduce additional steps in the procedure, which makes it more complicated and, therefore, prone to more errors in the end.
I would rather suggest that you switch to avidin-biotin free system, rather than using quenching of the endogenous biotin.
Cheers,
Ivan
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We developed an ELISA array for the detection of autoimmune liver disease related antibodies in our experiment. the identified results from ELISA array for M2, SP100, GP210, RO-52 positive sera are agreement with the results from EUROIMMUN KITS, but  the results for LC-1 are obviously different. Many "positive" sera identified by ELISA array could not be identified by EUROIMMUN KITS. Beside a possible cause of different antigen used, any other possibility?
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Keep in mind autoimmune liver diseases may have high titers of anti-albumin IgG. A sensitve assay can detect them, Is your solid matrix coated with hu or Bovine albumin/
is your buffer contain albumin? Check all and revalidate.
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Fetuin-A is a gycoprotein secreted by the liver and released in high concentrations. It plays a role as a physiological inhibitor of insulin receptor  tyrosine kinase associated with insulin resistance. It has been associated with metabolic syndrome and atherosclerosis . Many authors suggest that fetuin-A may be an independent risk factor for type 2 diabetes and marker of diabetes complications.
Nevertheless the value of fetuin-A as an independent predictor of diabetes in chronic liver diseases has not been evaluated. Is it possible that fetuin-A is involved in genesis of diabetes and induction of bad outcome in patients with liver cirrhosis?
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Yes, this may happen if patients with metabolic syndrome and hepatic steatosis time and poor control of their metabolism, reaching developing DM2, and simultaneously continue to hepatic steatosis hepatitis and eventually cirrhosis without intervention another etiologic agent as would be the case in other patients who have concomitant chronic active viral hepatitis (B or C) or liver damage by alcohol.
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Any articles/literature in support of the same?
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Dear all,
Is their any datasets for NAFLD which includes non-invasive attributes like liver function tests, symptoms, risk factors, chemical ,markers etc.
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Hello, greetings.
I was wondering about possible outcomes of estrogen hormones supplementation in light of fatty liver disease in women with PCOS. 
As PCOS and nonalcoholic fatty liver disease share some possible common pathophisiological tracts, i.e. insulin resistance, the prevalence of fatty liver disease in this group of patients is propably underestimated. 
I was wondering about possible data on  influence of estrogens supplementation (which lasts for many years in this group of patients) on course of NAFLD or even it's progression/regression? 
I found a little data on this problem (see link below), or maybe I am not searching for it sufficiently well. This article concludes that estrogens may have possible hepato-protective action.
On the other hand, I've had always in my mind, that chronic liver disease remains a contrindication for estrogen-based contraception.
Maybe you have some thoughts on this topic.
Regards!
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Hello,
Below are three papers. One is on the presentation of NAFLD and PCOS. The second (one that will answer your question about hepatoprotective effects of estrogen in NAFLD/PCOS) is more helpful to your specific question. It states that there are hepatoprotective benefits to estrogen supplementation in patients with PCOS and NAFLD. 
Finally, the third is a paper on the benefits of estrogen in patients with chronic liver disease and hep. B infection.
Let me know if these fail to fully answer the question to your satisfaction. I am happy to keep looking for more materials.
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After a hysteroscopy D & C operation, a female was found to be infected by UTI proteus mirabilis. In the middle of clindamycin treatment (not the tested "Sensitive" antibiotic), specifically 2 days later, she was infected with enterococcus faecalis. Following this, hereunder was found -
1. The liver enzyme ALT was raised three times, ALP by two times, GGT by two times
2. A HPB ultrasound found that the patient (obese) has no "remarkable symptom" as the bowel gases clouded the pancreas, liver and gall bladder a.k.a. the radiographer cannot "see" anything but bowel gases
3. The patient was tested negative for all hepatitis (isn't increased liver enzyme is all about hepatitis illnesses?) 
4. A week later, a re-run of the test indicated the same result, could it be that fatty liver is the most likely diagnosis? If so, what is / are the next treatment?
5. How dangerous is the fatty liver considering the likely infiltration could be in the premise of 40% of the obese patient?
Thanks and regards - Mariam
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The elevation of the liver enzymes is not specific for viral hepatitis only .Many factors can cause elevation of sgot &sgpt just as introperative hypotension can cause ischemic hepatitis , effect of anesthesia, sepsis induced cholestasis, autoimmune markers must be done.PCR HCV&HBV must be done to exclude acute hepatitis.
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How often you meet false negative results at the relatively low but pathological levels of PMN in ascitic fluid (for example, polymorphonuclear cell count <500 cells/mm3)?
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 I think manual cell counter is a best method. I was see sometimes strong difference betwen this 2 methods and in my experience normally the manual method y more consistent with the others clinical and laboratories parameters
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There is a clear reduced dose for paracetamol for stable cirrhotic, but for acute compromisation of liver function such severe acute hepatitis or post agressive liver resection no clear data about a safe adjusted  antipyretic drug use according to liver function. Can monitoring paracetamol level prevent its hepatotoxicity in such citation?
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High fever is distinctly rare among hepatitis.
First, consider angiocholitis, then drug-induced hepatitis, the alcoholic.
Finally, is fever's treatment necessary in addition to cause's treatment?
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Have you seen other location of this sign?
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It is a very interesting question, Zmicer. Actually, spider angiomas also called as telangiectasias, are not specific to liver cirrhosis or portal hypertension. Nevertheless, they are frequent (not exclusive) in liver cirrhosis and located on skin and mucosa of superior vena cava territory. It is certain that hyper estrogenic theory of genesis is the most mentioned, however it has never been proved. We can see them all the long of GI tract from mouth to rectum without relation to liver cirrhosis, neither plasma estrogen high levels nor portal hypertension. In these locations they are frequent cause of bleeding and risk factors are genetics, advanced age and renal insufficiency.
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hello every one, can any one ANNOTATE these sections ?? with best histopathological diagnosis ?
I have some notes but i want the best annotations, Because i am new in this disciplinary !
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The slides 1,2 and 6 have reference center lobular vein. The cords of hepatocytes have radial configuration normal. The variant is the 2 having less glycogen hepatocytes and discreet cloudy degeneration, and obliterating the sinusoids. The slide 3 and 5 are referenced to a portal space with minimal chronic inflammatory changes. These slides show totally nonspecific minor changes. The slide 4 seems to me he has hepatocyte proliferation with clutter of cords, no appreciation of sinusoids and there binucleaciones, this seems an adenoma. The cuts seem rodent (rat or mouse).
To integrate these findings should be known treatment received by animals.
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How much of aflatoxins in the daily diet can be caused liver cancer when we say they have hepatocarcinogenicity effects in human? 
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Hello,
If you are doing a risk assessment, the following publication from 2010, came up with a BMDL10 (bench mark dose associated with a 10% increase in liver cancer in Fisher rats, at the lower 10 percentile confidence interval) for aflatoxin B1 of 250 ng/kg bw/day.  The work was part of a broader effort to illustrate the application of the margin of exposure (MOE) risk assessment approach to genotoxic/carcinogenic substances in foods.  For aflatoxin B1, they found that human dietary exposures were about 100 to 600 fold lower than the BMDL10 (MoE range of 100 to 600).  Assuming a simple linear mathematical relationship, that would work out to a theoretical cancer risk level of about 1-in-1000 to 1-in-6000.  So that would be 1 theoretical additional liver cancer from the diet attributable to aflatoxin in 1000 to 6000 exposed "individuals".  However, as pointed out by the previous responder, extrapolation from animal data to humans can introduce a lot of uncertainty.
Citations are below.
Benford et al., Application of the margin of exposure (MoE) approach to substances in food that are genotoxic and carcinogenic: example: aflatoxin B1 (AFB1). Food Chem Toxicol. 2010 Jan;48 Suppl 1:S34-41. doi: 10.1016/j.fct.2009.10.037. Review. PubMed PMID: 20113853.
Benford et al., Application of the Margin of Exposure (MOE) approach to substances in food that are genotoxic and carcinogenic. Food Chem Toxicol. 2010 Jan;48 Suppl 1:S2-24. doi: 10.1016/j.fct.2009.11.003. Review. PubMed PMID: 20113851.
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I am working with some Hepatic Stellate Cells (HSCs), but I need some more information on culture maintenance, materials for optimal growth, etc. I have read several papers, but I was wondering if anyone knew of a book that provided a good overview for culturing hepatic tissues.
Thanks for the help.
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Dear Joseph, if you are talking about primary human HSC then I recommend Sancho-Bru P et all J Hepatol. 2005 Aug;43(2):272-82. We have also experience with LX2 cells. If this could help, feel free to contact me.
Good luck!
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The distinction between HRS and ATN can be clinically uncertain (if biopsy is under risk).
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Dear Adrian and Dear Zmicer
Adrian, I agree with your last comment.  Then, one can conclude that HRS is a prerenal, non responding to vascular volume expanders and non renal parenchimal condition,  exclusive of cirrhotic patients ,occurring spontaneously or secondary to a precipitating factor. Right?
It leads to answer  Zmicer´s question :Type 1 hepatorenal syndrome (HRS) does not  lead to acute tubular necrosis (ATN) in the absence of other insult.
Best regards both
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Does anybody have any information about clinical trials of Vitamin E in cirrhosis (of the kind not related to alcohol abuse)? There are reports in the literature of its use in CCl4 induced cirrhosis in animals. Also, does anybody know about the pathophysiology and prognostic significance of functional heart murmurs in the same kind of liver disease?
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Dear Dr.Strebel,
I agree with what you have pointed out. With reference to the  discussion, I have mentioned that there is no role of the drugs in cirrhosis. The other point is that NASH by itself is not a fully curable disease and hence both UDCA and Vitamin E are given for short time periods [may 6m - 1 year] for normalisation of liver enzymes if found elevated. There is no question of giving both drugs for years together. At least I have found it extremely useful in my patients. 
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Internal Medicine, Gastroenterology, Hepatology
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A chronic liver disease may be argued only by the combination of different investigations including laboratory test able to indicate cytolysis (transaminases), cholestatsis (gammaGT, bilirubin, alkaline phosphatase), parenchimal function (albumin, prothrombin, cholinesterase, cholesterol, ammonium), immunological (immunoglobulin, protein elechtrophoresis, autoantibodies), viral (HBV, HCV), metabolic (ferritin, ceruloplasmin) and morphological (mainly transabdominal ultrasonography with information about volume, echoes reflection homogenicity, portal vein and biliary tract dilation, splenomegaly, ascites prsence/absence).
On these bases, a single pathognomonic stigmata does not exist.
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Since oral metronidazole is absorbed directly into the portal circulation, theoretically it will concentrate more in liver and hence a question arise about the dosage. 
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Dear Thirunavukarasu,
even as a gastroenterologist and herpetologist I never lost an active thought about the topic you raised. Yet, as it has stringent rationale endorsed by pharmacokinetics, I realised my laziness. Of course I was aware that you can treat any C. diff. colitis with intravenous Metronidazole, as it is mostly excreted by the hepatic/biliary route without metabolism/inactivation. In contrast, for Vancomycin the intravenous route will never work to treat C. diff colitis... However, back to your question, as the Metronidazole takes the 'straight' binary route (with some entero-biliary recirculation), it not only accumulates in the liver but also in the gut. Maybe this is an explanation, why the dosage needed to treat intestinal as well as hepatic amoebiasis does not differ.
All the best, Bruno
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We know that R0 resection is clearly desirable in preventing local recurrences, but in the setting of large resections, e.g. extended or trisegmentectomy, with potential R1 resection due to positive margins, has anyone had experience with IORT to supplement margins?  The use of IORT in rectal cancer and breast cancer have been demonstrated, but little reports for primary intrahepatic cholangiocarcinoma or HCC.  
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Maybe a  better question to ask is: do you use Stereotactic body radiotherapy (SBRT) aka Cyberknife, for treatment of any liver tumors?  There has been a wealth of experience from Asia that SBRT is as effective and less toxicity than TACE or RFA.
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Most patients with NASH are clinically detected by the combination of metabolic sdr, hepatic steatosis on radiology and elevated ALT levels. However, it is known that some patients with NASH have normal ALT levels. Does the NAFLD score work among these patients too in the decision whether or not to perform a liver biopsy?
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In USA general population 30% of individuals may have liver steatosis. Most of them have clinically-non-relevant simple steatosis. Nevertheless  5% have inflammation and fibrosis, a condition known as NASH. The presence of fibrosis is associated with high rate of liver related complications and mortality. So the necessity for detecting fibrosis in patients with liver steatosis is clear. Liver biopsy is the gold standard test for diagnosis of fibrosis.  The NAFD fibrosis score was proposed for clinical use in 2007 by Angulo et al. It is composed of six parameters: age, BMI, fasting blood glucose, serum platelets count, plasma albumin and plasma AST/ALT ratio. It is a non invasive and easy available tool for estimating fibrosis in patients with NAFLD. It can be calculated on line on:http://nafldscore.com/ .
When NAFLD score results is -1.5 there is a very low probability of fibrosis (Negative predictive value is 93%). Medium values -1.6 to 0.67 have moderate probabilities while 0.67 or higher values have a PPV of 90%.
This score has been validated in diverse publications in NAFLD patients in order to estimate prognosis of liver complications and death. It does not replace liver biopsy but it may be useful for optimizing the use of this procedure. Particularly for avoiding unnecesary biopsies.
For answering your question if a NAFLD patient with normal enzymes has NAFLD score inferior to -1.5, liver biopsy should not be performed. If it is 0.67 or higher,  liver biopsy is guaranteed.  Values from -1.5 to 0.67 make us monitoring the patient and repeat NAFD score every 6 months.   
 Treeprasertsuk S et al World J Gastroenterol 2013; 19: 1219-1229
Angulo P  et al HEPATOLOGY 2007;45: 846-854
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We need a more efficient protocol for the induction of colorectal cancer liver metastases in athymic nude mice since we are not doing satisfactory with our current one.
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Thanks all!
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In a recently prospective study (CANONIC) it has been shown that the patients without a prior history of acute decompensation, acute-on-chronic liver failure was characterized by higher mortality compared with acute-on-chronic liver failure in patients with a prior history of acute decompensation.
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I thank all for the responses.
I think, that rapid deterioration or “critically ill cirrhotic” could be regarded as acute decompensation and as acute-on-chronic liver failure (ACLF).
ACLF is potentially reversible, but acute decompensation could also be potentially reversible condition. ACLF usually results following a precipitating event (bacterial infection, GI bleeding, HBV etc.), and the AD develops because of the same events.
It is important to know, why one patient is tolerant to accelerating events, but others are not.
Excellent research CANONIC has given us the tool for stratification of risk for critically ill cirrhotic (CLIF-SOFA score).
Identification of risk defines early specific treatments and intensive management.
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I would like to improve the detection of fatty liver disease using these routine images.
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I also recommend you the following article:
Targeted Hepatic Sonography During Clinic Visits for Detection of Fatty Liver in Overweight Children: A Pilot Study JUM April 2013 32:637-643
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Calcium deficiency in Chronic liver disease
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Cirrhosis is itself a state of malnutrition. Studies have shown decreased bone mineral density. Hence calcium and Vitamin D supplementation is needed.
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Can anybody help me with identification of the organisms in the liver and intestine of turtles? We suspect Entamoeba and/or Balantidium.
Few photos of the organisms in the sections, stained with HE and PAS are in the attached photos. The organs, staining and the maginification are listed in the file names.
Thank your very much for your help!
Tanja
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Thank you very muck for your answers.
The turtles are Leopard tortoise (Geochelone pardalis).
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