Science topic

Inflammatory Bowel Disease - Science topic

In medicine, inflammatory bowel disease (IBD) is a group of inflammatory conditions of the colon and small intestine. The major types of IBD are Crohn's disease and ulcerative colitis.
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In our traditional medicine some plants are used to cure Gastrointestinal disease. do some one know about some plants or phytochemical to cure IBD?
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Many synthetic drugs are currently in use to treat IBD such as 5-aminosalicylic acid corticosteroids. However, they all have some drawbacks as long-term use result in many complications. These problems encourage us to look out for alternative medicine. Numerous in vitro and in vivo experiments showed that the plant-derived secondary metabolites including phenolic compounds, glucosinolates, alkaloids, terpenoids, oligosaccharides, and quinones could reduce permeability, ameliorate-related dysfunctions with promising results. In addition, many of them could modulate enzymatic activity, suppress the inflammatory transcriptional factors, ease oxidative stress, and reduce pro-inflammatory cytokines secretion.
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Hello!
I am currently searching for a suitable agent to mimic IBD-like inflammatory condition in HT29 cells. I have found publications where researchers used DSS, TNBS etc. However, I am still in search of some articles about IFN gamma. In some papers, IFN gamma was used to disrupt intestinal barrier function but they did not mention if the condition was similar to IBD or not. I would like suggestions, protocol or related papers on whether I can use IFN gamma to induce IBD or not.
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Zaim Gashi thank you very much sir for the insight.
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Hi all, I wounld like to know how do you collect the stools from TNBS colitis mice. I found it's hard for C57BL/6 and Balb/c to discharge feces after 2.5%(wt/vol) TNBS enema. 50% mice refuse to discharge their feces. Some mice can only excrete a little brown liquid. I collect their stools by placing them to the empty box with some white tissues and I post a image below about my stool collecting setups. Besides, the body weight of those mice decline rapidly after enema ,therefore I guess the mice may refuse to eat after enema, and which cause it lost weight and have no stools to discharge. But, the stool is important in TNBS colits scoring system. Could anyone please help me on that?
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I would like you to refer to the article below. It may be helpful.
Highlight:
After the colitis induction the animals develop several manifestations of acute colitis. Those include inconsistent stool formation and occult or even bloody diarrhea. Intracolonic administration of TNBS/ethanol to rats induces a severe illness characterized by bloody diarrhea and a dramatic loss of body weight during the first week. Then the body weight increases but diarrhea still persists for about two weeks. Introduction of TNBS, for example, led to significant weight loss (mean 10% loss in body weight) and development of liquid bloody stools in all exposed animals, whereas control (saline) animals remained healthy and gained weight (mean 30% gain over 12 days). Body weight loss is caused in part by the marked effects of TNBS itself on the gut (diarrhea and perhaps reduced fluid absorption additionally), but systemic inflammatory response may also play a role. Further non-specific signs that point to a general deterioration include piloerection of fur and decreased movements of the animals. The onset and severity of the aforementioned symptoms is variable and depends on the specific animal species, strain and the dosing of ethanol and TNBS that are administered. The significance of assessing those symptoms is reflected by the development of multiple scores that quantify acute intestinal inflammation.
Best,
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I am trying all the protocol to extract the clean phospholipase A2 from the inflammatory bowel disease patient's stool samples. All the time I am heading to the dead-end.
I have tried Chroloform-methanol extraction and then used the BCA assay to detect the concentration of the proteins. Then that sample used in gel electrophoresis to see the protein bands and could not see any protein bands. Can anyone help what went wrong, please?
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Wolfgang Schechinger Thank you for your answer.
Yes, I for the protein nice layer but don't know what happened the after steps because I couldn't see any proteins bands in the gel.
Of course, searching the " detection of PLA2 in stool" was my 1st thing.
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Hi every one.
I'm looking for any one who has successfully isolated and grown F.prausnitzii
This year is our first step in our move towards targeted treatment of Inflammatory Bowel Disease in Children.
If you would like to discuss bacterial isolation from stool, share successful methods or ask more questions for your own work I would love to hear from you.
Our first hurdle is finding a replacement for Rumen fluid in our culture methods for isolation.
Any Ideas?
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Hi, I was just wondering if you ever came up with anything regarding the rumen fluid. I am trying to use it in media for bacterial culture and I am having a hard time filtering mine. Any suggestions?
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Before starting, I apologize in advance in case any obvious link eluded me.
By the way, I've recently compared anti-s IgG levels in two people and I couldn’t help but notice a curious fact: IgG levels detected in a young female person with IBD a year after the infection were three times higher (despite treatment with azathioprine) than those detected in another woman who received her second Pfizer vaccine shot.
I’m undoubtedly aware that this comparison isn’t statistically significant nor sufficiently accurate, but I was wondering whether there might be other similar data suggesting a possible explanation.
Thanks in advance to everybody who will indulge my curiosity.
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Hello Sara
IBD is a result of a defective immune system. IBD patients have significantly elevated serum levels of IgG and IgM.
Azathioprine is an immunosuppressant that decreases synthesis of IgG and IgM. But it does not have any effect on serum immunoglobulin concentrations. So even if the production of immunoglobulins
show a decrease there is no significant decrease in the serum immunoglobulin levels when treated with azathioprine.
You can refer to the research article given below for more information.
J Clin Invest. 1972
Best Wishes.
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Hello,
I am trying to differentiate HT-29 cell line using Methotrexate (MTX). I came across an old article that suggested treating cells for 3 months in order to reach their confluence state, leading for mucus secretion.
I was wondering if anyone here could suggest a protocol for differentiating the cells with MTX, so they could be more morphologically similar to goblet cells and secret mucus.
Thank you
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I am also having the same problem. Its great honor if you could share with me.
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Hello everyone! I am researching the molecular mechanisms which drive depression in the context of gut microbiota. From what I know, depression's pathogenesis primarily relies on Tryptophan metabolism. On one hand, the pathway is perturbed to the kynurenic pathway which leads to the formation of kynurenic metabolites (KYNA, QA, XA, etc). These kynurenic metabolites exert neurotoxic effects which ultimately drive depression phenotypes. They are also able to affect the enteric nervous system, the gut millieu, and immune system which contribute to depression.
On the other hand, Tryptophan metabolism can also be driven towards serotonin synthesis. Inflammatory bowel disease and its likes (Crohn's disease, colitis) have been shown to have increased serotonin (evidenced by increased TPH expression) and decreased SERT expression. Serotonin has been shown to be pro-inflammatory and this supports the inflammatory theory of depression.
While these explanations do not completely contradict each other and that they may simultaneously contribute to depression, an "irony" still exist that one says a perturbation towards kynurenine while the other is towards serotonin. Either way, Tryptophan is consumed and surely leads towards an increased bias to one pathway (ie. increased serotogenic or increased kynurenic). Hence, do you know of any articles which settle this apparent contradiction? Or perhaps there is something I incorrectly understand?
Thank you!
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Simon N Young thank you for your response.
1. Yes, they cannot cross the BBB but kynurenine and tryptophan can. Trp can be converted by microglia and astrocytes using IDO to kynurenine. From thereon, they can be metabolized into these acids. Is this not a mechanism which kynurenine metabolites exert negative effects on the brain?
2. Thank you for this. I , too, am more familiar with the low serotonin associated with depression. I just asked about high serotonin and IBS because it conflicts this explanation. Perhaps inflammation and other factors caused by IBS influence increased depression incidence found in patients.
And yes, MDD is indeed multifactorial. I am interested in how gut microbiota possibly exert influence in the etiology of depression via Trp metabolism.
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I am investigating the genetic diversity of a few species over geographic distance via IBD. I have my input file in txt format, however, I have troubles specifying populations.
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Thank you so much Jose Alberto Lopez-Aleman for this input. I will surely try those. I was using IBD application. Thanks, again.
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Dearest colleagues,
I am writing a proposal for a project concerning IBD research and substitution according to the 3R principle. Therefore I would like to know the actual numbers of animals (mouse, rat, etc.) used for TNBS, DNBS and DSS induded colitis in the years 2017-2019.
I tried the official announcments (e.g. European statistic report on the use of animals), but I only find general information ( e.g. # animals in gastrointestinal research).
Do you have a suggestion how to easily address that matter in short time?
I started now by looking at each publication of each year and manually collecting the numbers, however this is really time consuming. Maybe there is a automated approach.
I am looking forward to any suggestion, thank you very much in advance.
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Hi,
I think now a days you need to define the sample number of your experiment. whether you submitting a grant or article, you need to follow it at several places. The best way is to calculate by itself by using various software's which you can find in the recent literature of papers submitted to Nature, Cell publications by going to star methods.
Another method is to go through various studies which related to your experiment design and deduce the common number of animals they have used.
you need to take into consideration various parameters while defining your sample size, like the type of your study, quality of your animal facility, mortality of species etc.
I hope it is somewhat useful to you!
Hamid
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Can cox inhibitors be use in the treatment for inflammatory bowel disease like ulcerative colitis
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What's the prognosis of UC and crohn's disease in patients with coagulation problems and what are best way of management
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For patients with GI issues with the large intestine (IBS, spastic colon, ulcerative colitis), I have seen a pattern that foods with carageenan and xanathan gum, both polysaccharides used as emulsifiers, worsen GI issues and pain. However, the supplement Inulin seems to helpful for patients. Is there something about the molecular structure of carageenan and xanathan gum that results in more harm than other polysaccharides? Are carageenan and xanathan gum more prone to causing oxidative damage in the large intestine?
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Inulin is fermented by bacteria that normalize the colon and is considered a prebiotic. Prebiotics may improve gastrointestinal health as well as potentially enhance calcium absorption. Inulin is classified as a prebiotic because of its ability to stimulate the growth of beneficial bacteria such as Bifidobacteria
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please , anyone send me the articles on Bcl-2, Bax, and other apoptosis-associated proteins, focused on inflammatory bowel diseases.
thanks advanced
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Becker, C., Watson, A. J., & Neurath, M. F. (2013). Complex roles of caspases in the pathogenesis of inflammatory bowel disease. Gastroenterology, 144(2), 283-293.
This is the ResearchGate link:
(see under paragraph: 'The Intrinsic Apoptosis Pathway'
Peppelenbosch, M. P., & Van Deventer, S. J. H. (2004). T cell apoptosis and inflammatory bowel disease. Gut, 53(11), 1556-1558.
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Are there any specific recommendations for management of bisacodyl abuse? Is the approach of stopping bisacodyl immediately ( or tapering it down) + adding lactulose throughout ? Are there any guidelines regarding dosing/regimens/period of tapering bisacodyl and adding lactulose?
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@ Ayman Tawbe
PLEASE CHECK IT
https://toxnet.nlm.nih.gov › cgi-bin › sis › search
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How would I go about investigating state of the intestinal epithelium of someone with IBD and colon cancer?what would I observe f I use immunostaining
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With inmunochemical studies about the lymphocytes subtipes and several interleukines perhaps
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I am looking to profile the microbiome from stool samples collected from 17 Ulcerative colitis paitents by qPCR. eventually we plan to do 16s sequencing, but it is taking a long time to get samples and I have a student that needs a manageable project.
Does anyone have a good reference or protocol for a panel of qPCR primers that I could use to look at the relative abundance of major groups associated with IBD or energy metabolism?
Also, if I was to do absolute quantification where could I buy positive control DNA to match for each primer set?
Thank You!
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For the primers you can look the paper, actually i did long time ago and few species, please look this paper. ' Real-Time Analysis of Mucosal Flora in Patients with Inflammatory Bowel Disease in India. J. Clin. Microbiol. 2010'.
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Hi all,
I would like to know how do you optimize colitis model in mice/rats. It is known that females are more resistant than males itself but I have some issues on ulceration between male animals too. What is the best amount of TNBS and the ratio of TNBS/Ethanol in practice?
Thanks in advance
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Dear collegue
we have tried to test different models of colitis and made the conclusion that DSS colitis is the most easy, cheap and pathogenesis - related model.
But if you decided to use TNBS, you should be sure that all mice (or rats) have the similar microbiome. They should be SPF and parazites -free too. In our practice the presence of the ectromelia virus meets much more often than we think and it induce a very heavy colitis with the total death of the group. I recommend tp pay the attention to this side of the process
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In a recent experimentation where we tested an agent's effect on the oxidative stress status on mice (inflammatory model of IBD), we found that livers and colons present a similar response plot.
In the aim to dig deeper, we tried to test our agent on mitochondrial swelling (in vitro). We were surprised to find that low doses induced a significant decrease in Liver mitochondrial activity compared to colons, which were not affected.
any speculation regarding this phenomena is deeply appreciated.
PS: The agent used has a metalloid characteristics.
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What are the differences between liver and colon mitochondria may be the first question to answer? Some inflammatory products influence some pathways but not others due to their multiple, or single targetted effects.
Logic, not current expertise.
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Patient was diagnosed with acute refractory Ulcerative Colitis 4 years ago. Medications have not helped and thus patient is looking to alternative treatments. Patient reported, upon taking 3 grams of pharmaceutical grade Glycine supplement, number of daily bowel movements immediately reduced from 8 to 2 and bleeding reduced significantly. Has anyone else seen of or heard of such an impact with Glycine? What could be the therapeutic mechanism?
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Glycine prevent colitis by inhibiting induction of inflammatory cytokines and chemokines. It is postulated that glycine may be useful for the treatment of inflammatory bowel diseases as an immunomodulating nutrient.
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Can anybody suugest some primary cells or cell lines for IBD/Cronh's diseases? What is the common protocol to induce inflammation in the healthy cells in vitro? Is there any diseased/transgenic cell lines?
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Hi
Cannot see how you could replicate what happens in colonic epithelium in IBD using cells lines. Maintaining normal human colonic epithelial cells in culture is very difficult, and doing the same with inflamed cells from IBD patients likely to be even harder. The dextran sulphate model of acute colitis in rats produces the same histological features and ion transporter/channel abnormalities as seen in human ulcerative colitis. Hope that helps.
Regards
Professor Geoffrey Sandle
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Is the number of neutrophils and monocytes in "normal" blood high enough to make the fecal calprotectin test become positive even in the case of a non-inflammatory source of bleeding (e.g., bleeding from hemorrhoids)?
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Thank you, Kamran. This reference helps a lot.
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Interleukin 17 (IL-17) is a class of closely related molecules known to be increased in the human body by exposure to Fluoride by ingestion from water and food, or metabolism of Fluorocarbon anaesthetics and propellants. IL-17 causes Autoimmune Diseases including Psoriasis, Rheumatoid Arthritis, Asthma, Lupus, Multiple Sclerosis, Inflammatory Bowel Disease, Transplant rejection, and destruction of Liver and Heart Cells. IL-17 is also implicated in Skin Cancer.
Other Interleukins are known to be elevated by Fluoride, leading to attacks on other critical cellular and organ systems. Australia's National Health and Medical Research Council actively suppresses this Interleukin science while promoting Water Fluoridation using industrial waste. Can the science community influence this behaviour?
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Dear Michael after reading your answer i did look up to the internet and started reaading bout flouride in water.
I am now able to get some insight about the big problem the humans are facing.
Lets hope that the council for water management will take up the issue in a more seroius manner.
It also has made a difference to my understnading of the disease patterns of autoimmunity.
Thank you for the insights.
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There are many kinds of IBD models.If I wanna do some research about UC ,which model should I use(to push a drug into clinical research)
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Thanks for your answers.
Now I'm trying TNBS model on rat,but there is a problem that rat's distal colon is easily wounded during clysis and rat died of ileus. Could you give me some suggestions to solve the problem?@ Maria Zizzo
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Is there any study out there where the genetic risk for IBD has been addressed in the context of a certain microbiota composition, say enterotype, or according to presence/absence of indicator species or metabolic pathways?
We have recently published that for colitis induced by T cells transferred into Rag-deficient recipients, the expression of T-bet by the T cells matters only in the context of a certain microbiota. In one type of recipients, T-bet was critical for disease and T-bet-deficient T cells were unable to induce inflammation whereas in another set of recipients T-bet-deficient T cells induced inflammation just as potently as WT T cells did.
Has anything comparable been shown for humans, e.g. that gene XYZ confers an increased risk for IBD only in the context of a Genus abc-dominated microbiota. Or the other way around, say some kind of dysbiosis predisposes an individual for IBD only in combination with a certain genetic risk factor?
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genetic risk for IBD and microbiota or entero*
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Is laparoscopy the gold standard for inflammatory bowel diseases, such as ulcerative colitis and Crohn's disease?
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No , laparoscopy is not the gold standard but endoscopy is.
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thank you
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thank you for your response .
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ECCO 2014
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thank you so much. and I have read the guideline of 2014 ECCO ,which said "when there is latent TB and active IBD,anti-TNF should be at least 3 weeks after starting  
chemotherapy".we now had a patient who is in active IBD,but had a history of TB 5years ago which had been totally cured. so the question is where did you get the contents of "isoniazid 600 mg/day during 6 month. I am looking forward to your answer.
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Chronic PD therapy
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Inflammatory bowel disease is not a contraindication to PD unless the patient has had multiple complicated bowel surgeries. However, patients with IBD are prone to adhesions due to either peritoneal inflammation or bowel surgeries. With this in mind, laparoscopic PD catheter insertion (which allows for direct visualization and adhesiolysis if necessary) would be the preferred catheter insertion method. The impact of IBD on the peritoneal membrane is unknown, but the majority of patients would likely achieve adequate clearance and UF.
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The pathogenesis of celiac disease involves interplay of genetic, host microbiome and environmental factors like IBD. These include dynamic changes and exposure times starting from neonatal period. Recently there is rise in incidence of both celiac disease and IBD in India. Can anybody say whether this is result of similar changes in microbiome and environmental factors like diet, use of antibiotics?
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These papers that may be of interest to you. The rise of obesity and the use of anti-biotics and proton-pump inhibitors have greatly reduced the diversity of the microbiome. The use of emulsifiers in the food supply compromises the gut barrier. 
  1. Mar Rodríguez M, Pérez D, Javier Chaves F, et al. Obesity changes the human gut mycobiome. Scientific Reports. 2015;5:14600. doi:10.1038/srep14600.
  1. Corouge M, Loridant S, Fradin C, et al. Humoral Immunity Links Candida albicans Infection and Celiac Disease. Naglik JR, ed. PLoS ONE. 2015;10(3):e0121776. doi:10.1371/journal.pone.0121776.
  1. Serena G, Yan S, Camhi S, et al. Proinflammatory cytokine interferon-gamma and microbiome-derived metabolites dictate epigenetic switch between forkhead box protein 3 isoforms in coeliac disease. Clinical and experimental immunology. 2017:n/a-n/a. Manuscript available from author on ResearchGate.
  2. Lerner A, Matthias T. Changes in intestinal tight junction permeability associated with industrial food additives explain the rising incidence of autoimmune disease. Autoimmunity reviews. 2015;14(6):479-489. http://www.sciencedirect.com/science/article/pii/S1568997215000245
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I have been looking more closely at the reduction of defensin 5 alpha reported by Wu et al in the ALS mouse model as to me, the leaky gut is the first notable symptom for ALS and it occurs ahead of neurological symptoms.  My self selecting question about whether or not people had gut issues ahead of ALS found that 60% of respondents said they had gut issues ahead, and for years by some of them.  So, given that the lack of defensin 5 alpha is causing a shift away from butyrate forming microbiota to a more harmful one and a reduced protection from intestinal barrier which causes a huge range of other problems, figuring out how to help the body make defensin 5 alpha seems like a good strategy for fighting back.
So, what can help the body make defensin 5 alpha?  Anyone have any sources for doing that?
Wu, Shaoping, et al. "Leaky intestine and impaired microbiome in an amyotrophic lateral sclerosis mouse model." Physiological reports 3.4 (2015): e12356.
Ghosh, Dipankar, et al. "Paneth cell trypsin is the processing enzyme for human defensin-5." Nature immunology 3.6 (2002): 583-590.
Wang, Wei, et al. "Effect of bifidobacterium on defensin-5 expression in intestinal injury of preweaning rats." World journal of gastroenterology: WJG 21.9 (2015): 2638.
Hetz, Claudio, et al. "XBP-1 deficiency in the nervous system protects against amyotrophic lateral sclerosis by increasing autophagy." Genes & development 23.19 (2009): 2294-2306.  (my note - helps the paneth cells, I think)
Courth, Lioba F., et al. "Crohn's disease-derived monocytes fail to induce Paneth cell defensins." Proceedings of the National Academy of Sciences 112.45 (2015): 14000-14005.
Kaser, Arthur, et al. "XBP1 links ER stress to intestinal inflammation and confers genetic risk for human inflammatory bowel disease." Cell 134.5 (2008): 743-756.
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I have trouble inducing T cell transfer colitis in mice. I have been strugling for many years and tried several troubleshooting without any luck. It doesn't seem mice are responding to transferred T cells. Here are my protocol.
Recipient: BALB/c Rag1 KO mouse 8-10wk
Donor: BALB/c Foxp3-eGFP, WT and gene KO I crossed.
I am trying to match gender between recipient and donor.
T cell sorting: CD4+ GFP- CD25- CD45RBhi CD44low
We don't have sorting facility, so I have to take 1 hour travel to nearby university.
injection: 4 x 10^5 sorted T cell via retro orbital sinus injection in 200ul PBS
The problem is that I cannot see weight loss in WT-transferred recipients in next 5-6 weeks. Threre are sometimes visible loss in one or two mice, but I need to see clear weight loss in all WTmice so that I cen tell whether KO of a gene makes any difference.
I tried several troubleshooting such as,
Changing fluorescent Abs: It turned out I was using depleting clones. I switched to non-depleting ones.
Raising recipients in non-SPF condition: colitis is dependent on gut microbiota so I breed Rag1 KO in non-SPF condition. I also use non-autoclaved water and non-irradiated chow.
T cell viability: since FACS facility is far, I keep cells on ice and count viable cells with trypan blue right before the injection. Also I coat harvesting tube for sorting with FBS as I heard that it helps with cell viability.
It would be a great help if somebody can tell what I am doing wrong. Thanks.
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Dear Douglas,
Thanks for your input. Yes there is concern that my mice might not be "dirty" enough. That is why I started breeding in non-SPF condition. Also I am considering having them co-housing with a hamster or something. I heard that co-housing Rag1 KO with inflammasome-defective mice in SPF condition also helps, but I dont have those strains.
Dear Akshat,
Thanks for your input. It is routine dose for inducing colitis. I heard more than that would actually inhibit colitis but don't know why exactly.
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β casomorphin-7, a bioactive peptide present in A1 milk can increase the production of gastric and intestinal mucin. It is hypothesised that the production of such mucin may protect the intestinal endothelium in inflammatory bowel disease.
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The article by Woodford is useful, I already had this one. The side effects of BCM7 seem to be serious and would require a RCT to ascertain the safe doses for patients with asthma and those without.
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Hello
We want to estimate gut inflammation and oxidative stress. For certain reasons, we can't use gut tissue in human disease model. Can we use stool samples to estimate inflammation cytokines and oxidative stress? Alternatively, I read somewhere that there are few cytokines, which are only associated with gut inflammation and can act as indicator of gut inflammation only. They can be studied in plasma. Are there existing similar oxidative stress indicator for gut as well?
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HI Dear 
it is suitably to use liver biopsy to used them in IHC. the best marker is 8-OHDG. Also you can check them using ELISA kits but the collection and preservation time of serum must be not more than 6 hours.
BR
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Hi colleagues,
  Here I did microarrary analysis of the mice colon mucosa, the results shwed that Immunoglobulin heavy chain (gamma polypeptide) and immunoglobulin kappa joining 1 expression increased 11 fold in gene KO mice, so here I want to ask, this  Immunoglobulin heavy chain (gamma polypeptide) is IgA or IgG? how to explain this increased fold change.
Thanks!
Xin
53.5 588.9 3.46 11.02 0.1139 " Mus musculus mRNA for immunoglobulin gamma-2a heavy chain, complete cds, anti-malathion monoclonal antibody MLT2-23. " AB097847 Ighg Immunoglobulin heavy chain (gamma polypeptide) 12 F2|12 380794.
237.4 1011.4 2.09 4.26 0.1544 " Mus musculus cDNA clone MGC:36290 IMAGE:4224032, complete cds. " BC027418 Igkj1 immunoglobulin kappa joining 1 6 C|6 30.0 cM 110759
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Hi Jakob,
  Thanks for your message.
  Do you know why IgG2a specifically increased in intestine of KO mice, I mean which bacteria or  antigen can specifically stimulate the epithelial cell and then further stimulate the B cells to secrete the IgG2a? 
Xin
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Hi,
I have some question about Peyer's patches in mice ileum:
1. What is the number of Peyer's patches in mice ileum?
2. What is the length of ileum? 10 cm?
3. I want to compare the size of Peyer's patches between WT and KO mice, do I need to measure all the Peyer's patches in mice ileum, and then compare the average size between WT and KO? 
Thanks!
Xin
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Dear Xin,
The statistical problem you are stating , and I interpreted as, you need to compare two groups based on the some quantitative variable. Try applying the Binomial test of proportion to check the statistical difference. If you find the sample size is large enough then you can think of applying Z-test too.
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i need help for solution of this case really?what is the best treatment with a case of 45 years old male patient with 1.5*2 cm large superfacial oral ulcers affecting unilateral buccal mucosa and lateral tongue surfaces with burrning pain with a history of recurrence every 3 months for 2 years peroid.The patient took topical and systemic steroids with out benefit, systemically he had drugs for colitis for the past 7months??
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The best treatment  for recurrent multiple oral ulcers undoubtedly is the gluten-free diet, followed strictly and for the whole life, because most of these patients are celiacs and they don´t know it
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I am trying to treat the 21 days differentiated Caco2 monolayer with LPS at the concentration of 5µg/ml.
During the differentiate stage (21 days), I feed the cells with DMEM 10%FBS, 1% NEAA, 1% Glutamax, 2.5% HEPES, 4.5g/L D-Glucose and 110mg/L sodium pyruvate.
After that, I use the HBSS media with 2.5% HEPES for LPS treating.
I add the LPS with HBSS media to the apical side of the trans well at the total of 450µl, and 750µl HBSS media alone in the basolateral side.
After 24hrs, the LPS did not show any effect on the TEER of the monolayer, but the cells is dying at this time due the serum free media HBSS.
Normally LPS take long time to have some effect (More than 48hrs I think) but I cannot change the media in the middle of experiment.
Should I wait more for the LPS to take effect or I should change it back to the growth media (DMEM) ? Because if the monolayer is damaged, it's definitely affect the TEER value.
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You could try treating with serum-free LPS media for a few hours, then replacing with fresh LPS-free media.
A greater concern is that Caco-2 cells have been reported to be unresponsive to LPS treatment (lack of TLR4 expression):
Inflammatory parameters in Caco-2 cells: Effect of stimuli nature, concentration, combination and cell differentiation.
Responsiveness of intestinal epithelial cell lines to lipopolysaccharide is correlated with Toll-like receptor 4 but not Toll-like receptor 2 or CD14 expression.
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Colon ulcer, inflammatory bowel disease. 
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Oxazolone can also be used (Schiechl et al 2011; Gerlach et al 2014)
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Many trials were done for treatment of many diseases using stem cell therapy including chronic inflammatory bowel diseases 
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Overall, mixed results have been reported regarding the efficacy of haematopoyetic and mesenchymal stem cells in refractory luminal Crohn's disease in phase I/II trials.
Concerning perianal fistulae secondary to Crohn's disease, results have been in general optimistics and several reports suggest an improved healing in patients subject to stem cell therapy (Dis Colon Rectum 2009, 52:79; J Colorectal Dis 2013, 28:313; Int J Colorectal Dis. 2013;28:313; Gastroenterology. 2015;149:918)
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Great thanks for answering my question.I,am really very grateful to you for the wonderful and reaching out your Scientific answers.
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I am looking for a panel of immune cell subtypes that in your opinion are fundamenatl to understand the possible immune imbalance in the intestine and mesenteric lymph node of DSS-induced colitis mice.
Which markers for which cells?
Thank you
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Dear Giuseppe,
I would suggest you to have a look to this paper: http://www.hindawi.com/journals/bmri/2012/718617/
I found it quite helpful when I wrote the animal protocol for the DSS-induced colitis in mice. Hope this will help you!
Cheers,
Alessia
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I am planning to do in vivo neutralization of IL-6 cytokine in DSS-induced colitis mouse model. I am wondering if anyone has used anti IL-6 monoclonal antibody to do that in a colitis model before. The majority of papers out there are using anti IL-6R monoclonal antibody and mainly in adoptive T-cell transfer models. I found one paper that used anti IL-6 antibody to neutralize the cytokine itself (link below) in a mouse model of DSS-induced intestinal inflammation and wanted to know if other groups have used that clone to neutralize IL-6 in vivo?
Link to the paper of IL-6 neutralization in DSS-induced colitis mouse model:
Thanks in advance!
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You can have a look in this review. They have nicely explained different targets in colitis with references. 
Nat Rev Immunol. 2014 May;14(5):329-42. doi: 10.1038/nri3661. Epub 2014 Apr 22.
Cytokines in inflammatory bowel disease.
Neurath MF1.
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I am looking for a colleague to share experience and advice.
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In case of suspicion Crohn , we prefer, the first one, US study of the last ileal loop (SICUS). The RMN secondarily . If your service does not have a sonographer delicate, resonanc, with the study of the loops, is indicated .
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I am debating with pharmacology colleagues whether ampicillin and amoxicillin, which possess an NH2 group and, the latter, also an OH group more than penicillin G are more hydrophilic or more lipophilic than penicillin G. I always explain to students that aminopenicillins are more hydrophilic, and, therefore, pass more easily through Gram negative bacteria LPS, via the porins. My colleagues instead think that amoxicillin and ampicillin are more lipophilic and diffuse better through lipids of Gram negative lipid outer layer. Who is right?
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You are right. Ampicillin and amoxicillin are more polar / hydrophilic than benzylpenicillin ( Pen G) because of the presence of a polar group (NH2) in the amide side chain  and (OH) in amoxicillin at para position. It is therefore because of this hydrophilic property  that makes them to have high affinity to the Gram negative cell wall.  hence these two compounds are indicated for both Gram (+) and (-) infection while Pen G is useful only for Gram (+) infection.
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I want to test the implications of a potentially pro inflammatory substance provided through diet, that affects the epithelium integrity, on developing chronic inflammation of the GI tract, I need a mouse model that develops inflammatory phenotype once the epithelium is disrupted. I'd like to know if anyone has experienced using this model? Are there any other mouse models that are more suitable?
Thank you 
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Thank you for responding
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Chronic diarrhea (started at 4 months of age - anamnesis); colonoscopy shows non-specific aspect - friability of the mucosa, hyperemia, edematous in the recto-sigmoid area, other segments are not explored!).
Rectal mucosa shows no architectural disturbance, no pathologic inflammation, no other significant pathologic changes but evident pseudomelanosis coli.
Thanky you!
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Hello, Dr. Nylund, you are right, thank you. It was my first opinion, also, but the child is hospitalized since last month and NBT test is in favor of CGD. Other tests are in work now (DHR?) and I wait  a call from the clinician...
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Would like to know anyone involved in studying epigenetic changes in inflammatory bowel disease. 
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 The following three reviews may useful for you
1..Loddo I, Romano C.Inflammatory Bowel Disease: Genetics, Epigenetics, and Pathogenesis. Front Immunol. 2015 Nov 2;6:551. eCollection 2015. Review. Free article
2. Beaudet AL. Epigenetics and complex human disease: is there a role in IBD? J Pediatr Gastroenterol Nutr. 2008 Apr;46 Suppl 1:E2. doi: 10.1097/01.mpg.0000313815.73649.37. Review. No abstract available.
3. Jenke AC, Zilbauer M. Epigenetics in inflammatory bowel disease. Curr Opin Gastroenterol. 2012 Nov;28(6):577-84. doi: 10.1097/MOG.0b013e328357336b. Review.
Further you can do a search in pubmed  enter the following terms in following  in your search box and search
inflammatory bowel disease AND epigenetics[TW]
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Interferon Gamma Release Assay is a test done to detect Interferon-gamma release by lymphocytes sensitised to mycobacterium tuberculosis. Its a test often done to detect latent TB. Crohn's disease is an IBD, in which Interferon-gamma plays an important role. So since this cytokine is common to both, is it possible to have a false postive IGRA in a patient with active Crohn's disease? Especially in countries like India, where almost everyone has been either vaccinated (with BCG), or exposed to the tubercle bacillus at some point of time; but not everybody develops the disease.
Please do give your inputs, with any references if possible.
Thanks in advance !
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Hello, IGRA are not sensitive enough, they provide good specificity for the accurate diagnosis of intestinal tuberculosis, which may be helpful in the differential diagnosis of intestinal tuberculosis from Crohn’s disease.
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What is the most promising marker for IBD?
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I would say NO "most promising" lab marker for IBD till now.
We need multiple approaches to make the diagnosis of IBD, even to differentiate the other diagnosis such as tuberculosis, esp in developing countries.
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IL-22  was suggested to play a protective role in the pathogenesis of IBD. For example, IL-22 induces the expression of mucus-associated molecules and the restitution of mucus-producing goblet cells, hence probably enhancing the innate defence mechanisms. however, Previous studies demonstrated that either the expression of IL-22 or the numbers of IL-22+ cells was higher in IBD patients as well as the murine models of colitis. these findings seems to be paradoxical. That is why? thank you!
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I'm looking for a significative dosage to evaluate intestinal permeability in chronic disease but not in inflammatory bowel diseases 
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Dear Morgane, 
here is a review of :
Current methodologies used for evaluation of intestinal permeability and absorption
Praveen V Balimane, Saeho Chong, Richard A Morrison
Journal of Pharmacological and Toxicological Methods
Volume 44, Issue 1, July–August 2000, Pages 301–312
Current Directions in Drug Discovery:A Review of Modern Techniques
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GERD induced injury to esophageal mucosa, can we detect mucosal derangement non-invasively by stool analysis  
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Serum Pepsinogen has been proposed as a marker of injury in GORD, but with non satisfactory results (Serum gastrin and pepsinogens do not correlate with the different grades of severity of gastro-oesophageal reflux disease: a matched case-control study. Aliment Pharmacol Ther, 2008). Instead, measurement of pepsinogen in the salivary secretion (Peptest (R)) has yielded better results.
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I was trying to do the TNBS model in C57BL/6 mouse. I was following the paper
Wirtz S, Neufert C, Weigmann B, et al. Chemically induced mouse models of intestinal inflammation[J]. Nature protocols, 2007, 2(3): 541-546.
However, I found out drug reflex is a big problem which made the result very inconsistent. Wondering anyone has experience on this. 
I heard some people suggest fast mouse for 24h. But I found the colon lumen still have poop after this. When the stool is in the colon, the drug can't distribute evenly in the colon.
Some suggest wash the colon with saline before TNBS induction, if this is helpful, I'd like to know more details.
Or, any other suggestions?
Thx. 
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We have done oxazolone which similarly uses rectal administration.  We do not fast the mice.  If you fast them, they will eat their bedding and poop anyway. We perform the enemas under isoflurane anesthesia. We are typically able to massage out (using pressure on the abdomen) several pellets of stool. We also keep the mice inverted for 2 minutes after administration and then they are still for a while after recovering from anesthesia.  We try to do the enemas first thing in the morning as the mice are more active at night than during the day. 
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I want to know that which passage of CaCO-2 can i use as IBD model and method for its differentiation?
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IBD is a complex disease, rather than using a single cell line, I'd suggest to use at least a co-colture model as proposed in Leonard 2010 (http://www.ncbi.nlm.nih.gov/pubmed/20809575)
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BDP and budesonide are locally acting steroid drugs with very low systemic availability and toxicity. Commercially used in the treatment of colitis. Most reasearchers used budesonide for colon delivery, Please comments
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Thanks Michal.
Its very useful review paper. i will study it, However i m still searching any recent reported colinic delivery system loaded with BDP in the therapy of IBD, which i could not find.
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A 19 year old who was operated for Heirshprung's disease (Ileoanl anstamosis) 2years ago elsewhere presented with subacute small bowel obstruction. Abdomen is distended and small bowel loops are seen. It is not tender. Digital rectal examination is normal. CT scan showed distended small bowel loops up to the anus and Anus is collapsed.
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I quite agree with Dr. Prasanna's circumstance of moment, to maintain a conservative treatment to ensure daily evacuation of stool and occasional enema, "Primum Non Nocere".
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My current protocol suggests mice aged 8-12 weeks infected on day 0 with a single 5exp9 dose of Citrobacter rodentium. I have tried a few variations of this based on literature searches (younger mice etc) and failed to induce colitis each time. Prior to infection I have check the viability of the bacteria using a luminescent imager and post infection plated dilutions of the innouculum to confirm the dose. I am happy that my gavage is reaching the GI tract and plating of faecal pellet suspensions seems to confirm bacterial attachment and shedding. Any suggestions?
Thanks
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Thanks James. I have tried using younger mice to no avail and in each trial I have used mice that fit into the weight category you specify. 
The strain was made by a colleague so I will go back and make sure it is as it should be, thank you very much for your suggestions.
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I would like to do a TNBS experiment in mice on 129SvEv background. Are these mice susceptible to the TNBS ? what dose do you typically use for the enema and do you sensitize the mice a week before that ? 
Finally, did anyone try to induce TNBS colitis in Rag2-/- mice a couple of weeks after transfer of CD4 cells. Does this work ? 
Thank you, appreciate your help !
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I thought you planned something like that, and I guess it would work. May depend on the genetic background of the Rag2-/- mice: are they also 129SvEv? I think these experiments were done in the early days of adoptive transfer colitis in Powrie's lab.
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I am going to evaluate the effect of Herbal medicine extract and Probiotic in TNBS-induced mice colitis by modulating the gut microbiota structure .In order to find out the most influenced or changed species by high-throughput sequencing. The fecal sample is important .
I tend to A plan. Because the drug and probiotic have Sufficient time to adjust the mice gut mirobiota before TNBS administration.But I confused about the collecting time point . Most colitis gut microbiome study just have two time point like B Plan ,before and after treatment . In A plan.it has three time point.From day -21to day 0, it is easy to find the microbiota change in nnormal circumstances.but under the environment of TNBS, should I compared day-21,day3 or day-21,day3?
If I choose the B plan,I wonder whether the short-term treatment of in the acute colitis models might have a significant change in the microbial distribution. So,Can anyone give me some suggestions?
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thank you very much.but at day3,it is very hard to collect the fecal sample because of the TNBS administration.The cecum content may be more avaliable.but in that way.the microbiome is signficantly different to the day -14 and day0(natural excrement ).I am looking forward for your advices!
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Smart phone application in the NHS for measuring self reported symptoms of inflammatory bowel disease.
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Hi,
 If you want to measure the impact of a mobile health web application, then you have to conduct a research on it and find out the impact percentage from it.
Mobile health is used in the following:
1) To access and controlled sharing of health data and information
2) The health and lifestyle tracking
3) The management of chronic disease and outcomes
4) to share the decision making
5) The social networks and learning health systems
6) The management of behavioral healthcare.
Kindly see the following links:
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The duration and depth of anesthesia is variable widely .A prolonged anesthesia may increase contact time of the TNBS solution with the colon. I did it by Ether ,but it is hard to control .So which is the ideally anesthesia ?intraperitoneal anesthesia or inhalation anesthesia? I know it may be Continuous Inhalation Anesthesia.because the anesthesia machine is not access to use for me.in addtion,if the mice can not be anesthesiaed ,how to avoid the mice quickly excrete the TNBS solution?
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* GUIDELINES - PREPARATION OF KETAMINE/XYLAZINE COCKTAIL FOR MICE
Use of a sterile injection vial is required (e.g. redtop blood collection tube; commercial injection vial)
Mixing instructions:Verify the concentration of your drugs prior to mixing
For a 10mL vial using ketamine 100 mg/mL and xylazine 100 mg/mL add:1.75mL ketamine (100 mg/mL)
0.25 mL xylazine (100 mg/mL)
8 mL saline or sterile water for injection
Use of the following template for a label is recommended:Mouse Anesthetic Mix: Ketamine/Xylazine
Dosage: 0.1 ml/ 20gm IP  
Delivers: 87.5 mg/kg Ketamine/12.5 mg/kg Xylazine
Concentration:  17.5 mg/mL Ketamine/2.5 mg/mL Xylazine
or 
Ketamine/Xylazine
The Ketamine/Xylazine combination is considered to be a very reliable anesthetic for mouse surgery. The recommended dose varies: It is 100-200 mg/kg body weight for Ketamine and 5-16 mg/kg body weight for Xylazine injected intraperitoneally. Although some labs use Ketamine at a dose of 35-50 mg/kg body weight, Ketamine at 50 mg/kg combined with 10 mg/kg Xylazine does not produce a consistent reliable level of immobilization or anes¬thesia in Syrian hamsters, and a dose of 150 mg/kg Ketamine combined with 10 mg/kg Xylazine has been suggested).
The most widely used dose of Ketamine/Xylazine for mouse surgery is 100 mg/kg and 10 mg/kg body weight, respectively (Flecknell 1993). Duration of the effect may be extended by increasing the proportion of Xylazine or by an additional dose of Ketamine.
Premedication with anticholinergic drugs such as atropine (0.02-0.05 mg/kg body weight) is often used to prevent bradycardia (slow heart rate) caused by Xylazine, and to control excessive bronchial and salivary secretions caused by Ketamine (Nowrouzian 1981; Magoon et al. 1988).
The recipe below provides an onset of 3-5 minutes with 30-40 minutes dura
tion of surgical anesthesia.
Ketamine (50 mg/ml) (Vetalar, Ketaset, Ketalar) 2 ml (100 mg)
Xylazine (20 mg/ml) (Rompun) 0.8 ml (16 mg)
Water (sterile) to 10 ml
Store at 4°C for a maximum of 2 weeks. Inject 0.1 ml per 10 grams of body weight (100 mg/kg Ketamine, 16 mg/kg Xylazine).
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the average weight of BALB/c mice  is about 20g, but in some groups the  weight is not homogeneous,for example the mini is 18g ,the max is 23g.in order to  reduce that disparity.Should I match the mice by body weight ? if I put the 18g or 23g around in each group? I wonder whether  it will have a influence on the colitis model ?
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Jun,
The randomization group is very important in vivo studies. Please do not put small mice or bigger mice into control group.
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i want to perform a genetic association study on inflammatory bowel disease, which is suggested to be not common in China. for example, i attempt to do four Single nucleotide polymorphisms in a special gene, what is the perfect ratio of the case to control? 1:1.5 or 1:2 ? i am really troubled. thanks.
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The "perfect" ratio depends on many factors. Usually it is driven by cost, since it is often easier and cheaper to obtain controls than cases. As the ratio deviates from 1:1 the incremental value per person in the more common group (sometimes one can get more cases than controls), decreases. This gives rise to the general rule of thumb that there is little benefit to be had for rations more extreme than 1:5. 
A very important consideration is that with extreme ratios one should guard against potential stratification; that is assembling a very large cohort from different sources can introduce interesting occult (hidden) stratification, which could generate spurious results.
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What is the consensus on the  morbidity, if any,  and treatments recommended.
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See : F.T.Tirol; Congenital Hyperrotated Colon, Abdominal Surgery, Winter/Spring, 2015; 11-17
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Treating refractory IBD a-UC with anti TNF alpha AB seems not to be the right answer for most of the developing countries specially in Latin American populations, due to the high pharmacoeconomic impact that this therapeutic strategy implied. Therefore, more pragmatical approach is needed and there is growing evidence that microbiota and some helminths (i.e. T.suis and/or N. americanus) help with down regulating the IL-17/IL-22 relationship.
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At UEGW last year and ECCO this year treatment results with TSO were presented for patients with Crohn's disease. It doesn't work. Several reasons, some of the authors blamed the inadequacy of the CDAI for such studies. Anti-TNF therapy is also heavily debated in my country and with again recent data that the rate of surgery might not decrease and surely the cost savings of fewer hospital admissions is offset by the cost of biologicals, maybe the answer is surgery!
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Hello everyone,
a colleague of mine was recently baffled when looking at liver tissue coming from IL10 knockout mice which spontaneously develop a chronic inflammatory bowel disease.
Can anyone with experience in histo(patho)logy tell me what the brighter structures in the attached picture are? Is this some kind of fibrosis or what are these cells?
Thank you alot in advance!
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I would like to consider the possibility of a necrotic granuloma and do a Acid-fast staining to rule-out a Mycobacterium infection and a GMS staining to explore for yeast and fungi. I would also suggest a staining for anti-mouse CD68 to study the presence of epithelioid macrophages which may look like the fibrosis described by some colleagues above.
When dealing with mice with IL10 deficiency, we need to remember that they show increased susceptibility to some infections and this should be a diagnosis to be included in the differential.
Regards.
Francisco G. La Rosa, MD
Pathologist - Associate Professor
University of Colorado Anschutz Campus
Department of Pathology
303-724-3782
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On mice colon mucosal mirobiome study, treat mice with DSS to induce colitis, then collect the mucosal microorganism to analyze mirobiome change, but colon has four different parts, so which part of colon I should use to collect the mucosal microorganism and can reflect the mirobiome change under colitis?
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I think it depends on your hypothesis. A better experiment may be a pilot where you look at various places throughout the colon, then for future experiments focus in on the area(s) where you saw the most DSS-induced change.  I know that isn't an ideal answer and it will take a lot more work, but I also see it as a potential reviewer question in the future once you try to publish. This would kill two birds with one stone, so to speak
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Through comparative proteome and immunohistochemistry, we found some molecules showed higher expression in IBS than the normal controls. Those molecules are very new for intestine or IBS, at first, we wish to understand their roles in IBS or functional gastrointestinal disorders based on the clinical data, then, to explore their basic mechanisms and the therapeutic potential with experiments.
If anyone have interest in this research please join us, especially, welcome the clinical researchers who can provide the samples and data of IBS patients.
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 i am really intersted as i am suffering from IBS
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Local factors contributing to the certain clinico-morphologic form of the acute calculous cholecystitis to develop remain obscure. What is your opinion, may some histological alterations including the pseudopylorization or the intestinal metaplasia take part in the pathogenesis of this disease being more prominent in the case comparing to the pattern of the mucosal lining in the chronic cholecystitis?
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Dr.Rodrigo,
Thank you for the reply!
May I ask as to have you any statistical data on the glandular metaplasia comparing the mucosal linings' alterations in the acute cholecystitis and in the chronic one?
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In a prospective study on patients with pelvic malignancies undergoing pelvic radiotherapy, we found an association between vitamin D deficiency and severity of radiation induced proctitis. This association was independent from age, gender, cancer type, and BMI. What could be the mechanisms behind this association?
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Hi 
there is a considerable body of work suggestion that vitamin D has anti-inflammatory effects in inflammatory bowel disease (IBD), particularly from animal models of IBD (Cantrona  and others).  The human translation is less clear at this point, but emerging evidence suggests that vitamin D supplementation may prevent relapse in RCTs in IBD.  As well as anti-inflammatory effects, newer mechanisms such as effects on autophagy, gut barrier functional and on microbiota have been suggested for vitamin D. 
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We are going to evaluate the immunomodulatory effects of vitamin D in an intestinal mucosal injury model. What are the Pros and Cons of measuring 1,25(OH)2D in contrast to 25(OH)D for this investigation?
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The immuno modulatory effect is  1,25OH2 related, so it would make sense to measure 1,25 OH2. However, measuring 1,25OH2 gives you the blood / plasma level, when you want to know also the tissue level.
The mechanism of immunomodulatory effect of 1,25OH is clearly presented in a paper of van Etten and Mathieu in J Steroid Biochem Mol Biol 2005.
Another point to take into account:  the level of 1,25OH2 is maintained in a narrow range even over a wide range of 25OH concentrations, including severe deficiency.
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Total number of genome regions known to be associated with inflammatory bowel disease is up to 99.
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the literature "Advances in IBD genetics" has suggested that there are more than 160 loci containing IBD susceptibility genes
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There is a 5 year old child who developed UC at 2 years and subsequently sclerosing cholangitis. Steroids / Immuran and Ramicade x 1 year are unable to induce remission. Is there a possibility of it being a IL10R involvement though he does not meet the criteria of being an EO/VEO UC? Has anyone faced a similar issue? 
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Thanks for the lead, shall do that. 
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In the literature it is either unclear or not mentioned what people do and if there is a consensus of how to do this.
From what I have seen, when you prime with LPS, you are in complete media but then you change media for without FBS before adding ATP. Is that correct?
My second question is: once you're done priming with LPS do you change media before pulsing with ATP (if you are using complete media all the way through)?
Thanks!
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Excellent question! It depends on what your method to assess the inflammasome is. If you are measuring IL1b or IL18 readout by ELISA or cell death by LDH then you can use complete medium for all steps. If, on the other hand, you are doing a Western Blot then it is generally recommended to use serum-free medium because detection of activated caspase-1 and processed IL1b and IL18 in the supernatant have to be concentrated (by your favorite method) and serum will overload your concentrated sample. I usually wash once with serum-free medium and then add serum-free medium with my stimulus.
Be aware, however, that some stimuli take many hours to take effect and serum starvation can cause off target responses. In these cases it is sometimes effective to use a very low concentration of serum (1% or less) simply to keep your cells alive. You might still run the risk of overloading the concentration process, so you will have to optimize it according to your protocol.
For ATP, since that's the example you used, you should be OK with serum-free conditions because the effect is quite fast (30-60 minutes for very robust response).
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I'm wondering if there's a specific serum marker of activated T cells.
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Thank you for your answer
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32years with nearly 5 years history of confirmed ulcerative colitis(pan colitis) who is on pentosa,mesalamine ,steroids and other supportive measures presented with daily rectal bleeding ,loss of weight of over 20kgs,feverish feeling but no fever.His quality of life is getting affected.Azathiaprine has not yet tried.Seeks a remedy for this.would you suggest pursuing medical management or Total colectomy with Ileo-Anal pouch?
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1. you need to stage his colitis - is it severe ? moderate? - staging is important to further management - clinical staging (Trulove Witts), endoscopic staging (Mayo or UCEIS).
2. if the patient has severe colitis, he needs hospitalization, iv steroids, enteral nutrition, sometimes antibiotics iv, if it fails after 3-5 days there is a seroous argument for colectomy or antiTNF or cyclosprin iv
3. if colitis is moderate there is room for azatioprine therapy since it takes weeks to months for this treatment to have an effect
4. important thing is to rule out other etiology of colitis - bacterial infection, parasites, CMV colitis, drugs, cancer .....
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Citrobacter rodentium were grown overnight in LB broth ,after  centrifugation ,the pellet were resuspended with PBS.BABL/C mice were inoculated by oral gavage (approximately 2X10^8 CFU).
But after one week ,the mice show no significant body weight loss,however, in some article the authors reported  that Cr-infected mice demonstrated significant weight loss by day2-day3 postinfection.So I would like to know whether the rapid loss of body weight is a overt clinical sign of  infection? and is 2X10^8 CFU enough to induced the colitis ?should I  increase the concentration?
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Yes there have been some reports of Balbc mice being resistant to Citrobacter infection.  You could increase the dose but the best way to determine if your mice are infected is to plate homogenized feces onto selective media plate to determine the shedding kinetics.  Also the microflora of the mouse colony in that particular mouse room could be very competitive with Citrobacter.
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Two studies up to now have shown an association between adenosine deaminase activity and disease activity in patients with Crohn’s disease and ulcerative colitis. We conducted a similar study in Crohn’s disease and in addition evaluated fecal calprotectin which is a known accurate disease activity marker for IBDs. But, we found no association between ADA activity and disease activity (evaluated by CDAI). Also no association was between ADA activity and FC, CRP, or ESR. But, ESR, CRP, and FC were all associated with disease activity.
What could be the reason for this difference between the study results?
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I am agreed with Prof.Enzo entirely in that it may become a novel investigation: to compare the ADA and FC levels in a certain group of patients with Crohn's disease.
Some attention may be paid as to the sources of ADA and FC to explain that discrepancy. What is your opinion, are they produced by the same or by the different cells?
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Fecal markers of intestinal inflammation.
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