Science topic

Gastrointestinal Diseases - Science topic

Diseases in any segment of the GASTROINTESTINAL TRACT from ESOPHAGUS to RECTUM.
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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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Is best to prevention also to treatment.
The best test option for screening of CRC is FIT test and consecutively colonoscopy.
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A case of three males who presented strong precordial pain, in supine and prone position during night, with GERD and hiatal hernia type I ascertained by gastroscopy, treated by single manoeuvre, is described.
Methods
Manoeuvre consist in laying down patient in supine position, legs straight down and hands by his sides, using a pillow to lift up the head. Done that, subject should actively arches spine (at least 7-8 cm from the couch at level T12-L2), taking hyperlodosis position, without lifting sacral region, upper thoracic sections or any other segments from the couch.
Case Report
Three males complaining of stabbing precordial chest pain (mean ± standard deviation age, 24.6 ± 2.88 years; range, 20–28 years) have been treated between November 2016 and August 2017. Subjects have not suffered of any cardiac problem, normal EKG, pressure 80-120 mmhg, BMI 21.93 ± 2.49. While hiatal hernia type I and reflux disorders had been ascertained by gastroscopy in two of them, in the same year and three years before respectively. Patients, stated to have suffered in the previous two weeks of strong precordial pain, in supine and prone position during night, not accompanied by burning retrosternal discomfort. Subjects also declared have not taken medication for GERD, or any other type of drugs and were symptomatic during the visit.
They were instructed to holding aforesaid position for 10 seconds at least, performing 3 time or more (with pause of 30 seconds between each prove), until symptoms vanish. The manoeuvre was applied in each patients and complete precordial pain resolution was obtained in all attempts. Indeed, despite pain comes back after manoeuvre ends and patients laying down supine, three, four repetitions of aforesaid manoeuvre spaced with intervals of 30 seconds were able to lead a complete and sustained resolution of symptoms, all night long.
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Agreed with Mansoor Zafar very interesting read!
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Do diaphragmatic breathing and speech therapy actually help? How often did you require multidisciplinary team approach?
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Rumination syndrome is a condition in which people repeatedly and unintentionally regurgitate undigested or partially digested food. It affects mainly infants, young children, and people with cognitive disabilities/depression.
Clinically, we need to rule out gastroparesis/bulimia in adults patient that vomit after taking food. I would say it's rare in adults...
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Hello! Do you know any marketed and standardised or registered product derived from plants and used as anti-diarrhoeal or anti-infective in the gastrointestinal diseases in ruminants? Like for e.g. allicin, berberine, or may be purified fractions of some extracts, essential oils, oleoresins, etc., but it must be really standardised or registered in the EU, USA, Canada, Japan or somewhere and it must NOT be polyherbal formulation. Please help me if you know any such products. Thank you,
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Dear fellow researchers,
Does anyone hold any useful information (or possibly a reasonable estimate) on the incidence rates (by age groups, if possible) of lactose intolerance and/or lactase deficiency in US?
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Please see the following RG link and PDF attachment.
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Hi all,
I am wondering if you can comment on statistical interpretation of dysbiotic microbiome. For example, we treated a system with antimicrobials and now community is changed. Initial community is inhibited and new community took over the system. Now the question is, how can we say that this change is dysbiosis? Is there any statistical criteria established? Or its just qualitative interpretation? I assume that diversity and richness analysis may be used for this purpose but again what would be cutoff for such a purpose?
Thanks and looking forward to to your opinions...
Best,
Arslan
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Meta-genomics study will be the ideal method, For statistical analysis you should take care of environmental, food and other conditions of the replicates, with precise experimental planning, replications and treatments.
I hope it will help you in your study
Thank you
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Good evening.
I´m searching for references related with the effect of Amprolium on the sporulating activity of Eimeria spp. oocysts.
Thank you.
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Thank you Mr. Hiba for your share and recommendation. Regards.
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There are some formula for estimating nares to lower esophageal sphincter distance in infants based on height. I'm looking for some data in adults to estimate such distance based on gender and height. What is important for me is the upper margin of the LES as we need to place a probe 5 cm above LES.
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Hi Sedat, Tnx. I saw this before but this study was aimed for placing intra-gastric tube. We aim for placing a probe 5 cm above the LES so location of the upper margin of the LES is important for us.
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With this test could be possible obtain a complete precordial pain resolution (GERD related) in a few seconds. Manoeuvre is completely painless. However how does it work is partially uncleared, and it can be applied only in symptomatic subjects.
Manoeuvre has been conceived, and tested on subject, 23 years old, BMI: 19,48, pressure: 80-120 mmhg, normal EKG, without any cardiac problem and with hiatal hernia type I ascertained by gastroscopy. Presenting, strong precordial pain in supine and prone position during night, not accompanied by burning retrosternal discomfort. The subject does not take medication for GERD, or any other type of drugs.
It was performed 3 time every session (with pause of 30'' between each prove) and for 5 consecutive days on symptomatic subject. 
Therefore, I'm looking for researches who have possibility to provide data, in order to verify this hypothesis.
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Since I had the opportunity to test the manoeuvre on two other subjects I provided to collect data on a single specific project. If you are interested you may found out more here https://www.researchgate.net/project/New-single-manoeuvre-leading-GERD-precordial-chest-pain-resolution-in-few-seconds-small-case-series
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We can work together on drug delivery systems to the gastrointestinal tract.
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Dear Ahmad Sira and Kaushal Deep Singh 
We are working on methodology.
Our aim is to develop a new oral drug that can be used in gastrointestinal bleeding patients coming to our emergency department.
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I am looking for clinical studies or drug trials related to children (age 0 to 6 preferably) that looked at children with varying GI issues, fistula, GERD symptoms, ulcers, etc that might have looked at child behavior. ADHD just seemed an easy search term, but it doesn't have to be limited to ADHD spectrum diagnoses.
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"Are you aware of any that considered congenital defects though?"
I expect the 1946 study, and subsequent UK Cohort studies, did.   But surely fistulas are too rare to have any bearing on population levels of ADHD?  Also, I doubt the relevance of any medical cause of ADHD or developmental disorder acting after the first year of life.
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Anismus (synonyms: spastic pelvic floor syndrome, sphincter dyssynergia, pelvic floor dyssynergia, dyssynergic defecation, paradoxal puborectal contraction) is a malfunction of the external anal sphincter and puborectalis muscle during defecation. It occurs in children and adults, sometimes from birth.
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Child anusmus which means spastic contractions of the external anal sphincter can be due to organic, functional or psychological causes. Organic causes are causes of painful defecation. These include abrasions in the skin around the anus, and irritations of the anal skin like in Oxyuriraius (Pin-worm infestation). Also, infection of the anal skin e.g. fungal infection.
Anal fissure and anal fistula are important painful lesions which may lead to anusmus.
Lacerations in the anal sphincters (internal anal sphincter IAS, and external anal sphincter EAS) can lead painful conditions and subsequently anusmus.
Functional conditions like changes in the bowel habits e.g. constipation &/or diarrhea.
Psychological conditions as in conditions of fecal incontinence, leads, fear of embarrassment will lead to anusmus.     
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Specifically pertaining to colorectal and pancreatic cancer alongside other gastrointestinal malignancies, I was wondering what the experience has been in terms of data dictionaries, statistical support, size of databases and completeness of data. 
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A good source for cancer database research, including gastrointestinal malignancies, is the The Surveillance, Epidemiology, and End Results (SEER) database. It is maintained by the National Cancer Institute. 
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Currently, I’m working with model of gastric ulcer induced by EtOH or NSAIDs (diclofenac). I use ImageJ software for macroscopic scoring to compare the ulcer area.  Unfortunately, I couldn’t find any reliable system for microscopic scoring.
Could you recommend any scoring system to use in microphotographs (H&E staining) obtained from mice stomachs?
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Thank you Dr Hosseini for useful articles. 
Finally, I have decided to use method described by Shimoyama et al. in article:
Shimoyama, A.T., Santin, J.R., Machado, I.D. et al. Naunyn-Schmiedeberg's Arch Pharmacol (2013) 386: 5. doi:10.1007/s00210-012-0807-2, wich description you can find below.
Histological analysis:
After macroscopic analysis, a small portion of each stomach was fixed in 4 % formalin solution, dehydrated through increasing grades of alcohol, and embedded in paraffin. Five-micrometer sections were made using a microtome, and stained with hematoxylin-eosin solution. Tissue preparations were observed and microphotographed under a light Axioplan 2 Zeiss microscope. Leukocyte infiltration was assessed microscopically (×100), with counts being made in ten fields per specimen.
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Samples are mouse plasma, from GI illness models (so mostly G neg bacteraemias expected); samples were collected in EDTA for other things, but want to check relative bacterial load if possible. ~200microl sample available. Absolute quantitation or speciation is not required, so something like endotoxin assays would be ok, but I understand most dont work on plasma.
Many thanks in advance!
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This is an important question I need the answer
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As entitled, I seek for antibodies for IHC staining of mast cells in inflamed mouse colon. However, it cannot be antibody targeting chymases or tryptases.
Can someone recommend a perfect antigen of mast cells to be stained?
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CD117 (c-Kit) lack the specificity. 
Did you ever use clone AA1 of Mast Cell Tryptase? THis mouse monoclonal antibody requires Mouse-on-Mouse Kit, but the IHC result tends to be nice both in human and mouse samples.
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Hi everyone, I was wondering if I could please receive some feedback with something? 
I am currently investigating what genes are being up regulated/down regulated in pigs suffering from a disease. We have collected bone tissue samples from healthy and diseased pigs across 3 age groups, extracted them for RNA, converted to cDNA and use qPCR to measure gene expression.
We are using the Pfafll method to calculate fold changes in our genes, and therefore require a calibrator on the 96-well plate. I was told by my supervisory team to pool my cDNA, from healthy and diseased pigs from all 3 age groups, and use this as the calibrator. Just to be clear; I made cDNA from bone RNA from all of my samples; and then cDNA was pooled and aliquoted to serve as a calibrator.
In my particular case, looking for changes in gene expression in diseased animals, would it make sense to have had only control samples pooled to form the calibrator and then calculate fold changes in diseased animals? My supervisor told me to pool everything, including diseased animals, so the calibrator effectively makes a standard curve and every individual sample can be calculated by referring back to this calibrator. However because the calibrator was a pooled sample from everything, does this mean that the expression values that I have obtained from my samples are not relative to anything? Therefore we would not know if the values for individual samples are relative to control or diseased? It would be great to hear your feedback on this, and whether this data can still be used. 
Also, would this data still be valid if, for example, I average the normalized expression values from my controls; and then show the fold changes in expression for disease animals relative to the average of my controls?
I look forward to hearing your thoughts on this, many thanks in advance!    
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 Dear Andre,
You are right. but, our gene of interest have been expressed in both controls and affected cases. in your opinion, in this status, can I use each control as a calibrator against his/her diseased state? if yes. please tell me what is the most suitable statistical test to analysis of difference among groups?
thank you
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Could anyone can provide a list of parasitic and viral agents which cause gastro intestinal manifestations and list of inexpensive detection modalities available for the same.
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refer to a chapter in any Gastroenterology textbook on gi infections
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I came across data from Osteopathy but missing evidence based data from Physical Therapy. All about Diagnosis/Red Flags, Prevention and treatment is welcome. Thank you!
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patients with perienal descent
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In most of the cases, the  obstructed defecation syndrome (ODS) is mainly treated  conservative  (fiber diet, laxatives, biofeedback). Reading the literature, it’s found that  nearly 20% of the patients need surgical approach. Only in selective cases surgical procedures are indicated: rectal prolapse excision, rectocele and/or enterocele repair, partial myotomy of the puborectalis muscle. The stapled transanal rectal resection (STARR) may lead to severe complications , such as stenosis.  As gastroenterologist, I consider, as the first line of treatment, the conservative approach and then the surgical procedures. in agreement with the proctologists surgeons. All this, after careful consideration with defeco-Rmn.
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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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Isolated studies have proven superiority of this combination over plain aspirin in reducing gastric disturbances. The FDC of low dose aspirin and glycine is approved in India. However, data on its efficacy, safety and comparison with enteric coated aspirin is sparse.
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Dear Neel,
I have read this report and found it to be a good start to open a discussion on this new issue:
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Glycine virtually eliminates adverse GI effects of aspirin
Postby haidut » Tue Aug 05, 2014 6:39 pm
I posted a study earlier on co-administration of glycine improving the absorption of aspirin. It looks like it also prevents the negative GI symptoms of aspirin intake in some people. The ratio needed is 2:1 in favor of aspirin, which means that if you are taking 1g of aspirin, you need to take 500mg of glycine with it. I have tried it myself, and it not only removed whatever minor GI symptoms aspirin was giving me, but it also removed the insomnia effect that high doses of aspirin had for me when taken before bed. Last night I took 2g of aspirin with 1g of glycine and had the best sleep in months, without waking up even once. Previously, 2g of aspirin before bed would keep me sweating and awake for hours.
"...To determine the tolerability of a glycine (Gly)-containing acetylsalicylic acid (ASA) preparation (Gly-ASA), investigators selected 1135 patients already receiving longterm antiplatelet therapy for a noninterventional trial of Gly-ASA 50 to 300 mg daily. After an average treatment period of 42.6 days, tolerability rating scores and the frequency of 5 gastrointestinal (GI) complaints were compared with those reported for any previous treatment, including plain ASA. After treatment with Gly-ASA, the mean percentage of patients without GI complaints increased more than 2-fold, from 28.2% to 60.6%. Furthermore, the mean percentage of patients reporting any GI symptoms as "always" present decreased from 8.5% to 0.5%. Gly-ASA tolerability was rated "excellent" or "good" by 98% of the patients. "
"...The relative solubility and rate of dissolution of aspirin in water and glycine solution have been measured. A technique involving a mathematical examination of the front profile of chromatograms has been used to study the extent of the adsorption of glycine from aqueous solution on aspirin.Aspirin is more soluble and more rapidly dissolved in glycine solution than water, and glycine is found to adsorb, in significant amounts, on aspirin crystals. The findings are discussed in an attempt to explain, in physico-chemical terms, differences in taste and adhesion to the oral mucosa that are discernible when aspirin tablets compounded with or without glycine are savoured."
Looks like some countries even sell a packaged combo already:
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Re: Glycine virtually eliminates adverse GI effects of aspir
Postby SQu » Wed Aug 06, 2014 4:05 am
Thanks for great info! I love aspirin. I've been taking a non prescription cold remedy in the evenings which you add hot water to and drink. It's 800 mg aspirin, 50 mg caffeine, 45 mg ascorbic acid, 2.6 mg menthol and 4254 mg sucrose. I've been adding extra sugar and fructose, and 2 tablespoons gelatin to it just because it's an easy way to get gelatin. At 35% glycine if 2 tbs is 30g that's a bit over 10g of glycine .
According to this it looks like a teaspoon of gelatin would be plenty at about 1.7g but do you think taking more gelatin earlier in the evening might help with later doses of aspirin? I often take aspirin at night when I wake up. It's one of those things that sometimes helps me get back to sleep and stay asleep, but not always. Actually everything I do is like that. It's the staying asleep that's the issue.
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Re: Glycine virtually eliminates adverse GI effects of aspir
Postby haidut » Wed Aug 06, 2014 11:46 am
sueq wrote:Thanks for great info! I love aspirin. I've been taking a non prescription cold remedy in the evenings which you add hot water to and drink. It's 800 mg aspirin, 50 mg caffeine, 45 mg ascorbic acid, 2.6 mg menthol and 4254 mg sucrose. I've been adding extra sugar and fructose, and 2 tablespoons gelatin to it just because it's an easy way to get gelatin. At 35% glycine if 2 tbs is 30g that's a bit over 10g of glycine .
According to this it looks like a teaspoon of gelatin would be plenty at about 1.7g but do you think taking more gelatin earlier in the evening might help with later doses of aspirin? I often take aspirin at night when I wake up. It's one of those things that sometimes helps me get back to sleep and stay asleep, but not always. Actually everything I do is like that. It's the staying asleep that's the issue.
There is a well-done, widely-cited, human study showing 3g glycine at bedtime pretty much eliminated sleep problems.
If you take aspirin before bed I'd definitely up my glycine/gelatin intake as well to get even better sleep and protect the stomach from aspirin. I posted another study showing glycine exerts most of its actions at "surprisingly" low doses of 500mg-1,000mg a day. So, your 30g of gelatin is plenty I think.
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Re: Glycine virtually eliminates adverse GI effects of aspir
Postby SQu » Wed Aug 06, 2014 12:22 pm
Ok, going to have it just before bed then. Thanks!
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Re: Glycine virtually eliminates adverse GI effects of aspir
Postby Suikerbuik » Wed Aug 06, 2014 1:14 pm
At the end of the week when you're tired and your sleeping is affected aspirin really helps you sleep like a baby, at least for me. Also the energy is increased, hands warm up immediately - like 5mcg T3 thyroid hormone can do.
However after I have been using it for about 3 days, 500-2000 mg/day tried different doses. I really become fatigued, also feel like it stresses the kidneys (uric acid probably - I've been tested slightly above refenrence for uric acid a few years ago without any aspirin).
Thyroid hormone doesn't introduce any of these issues. I still suspect there's more, maybe something with the antibody response and endotoxin exposure like J. mentioned. I only tried aspirin max. 5 days, but tried this a few times over again but I keep experiencing the same. I am also not convinced that aspirin really is something that's required, so I keep it with thyroid.
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Re: Glycine virtually eliminates adverse GI effects of aspir
Postby schultz » Wed Aug 06, 2014 1:42 pm
I've never heard of this before, but it is really interesting. Thank you for posting these.
Yesterday I stumbled upon an old Chris Masterjohn article in which he says...
"Muscle meats and eggs are very rich in methionine, which increases our need for homocysteine-neutralizing nutrients (vitamins B6, B12, folate, betaine, and choline), and also increases our need for the amino acid glycine..."
and...
"Glycine is depleted in the detoxification of excess methionine"
So would eating a lot of muscle meats - and very little gelatinous meats/gelatin - increase ones sensitivity (in a negative way) to aspirin?
I also wonder if this would also increase - or if glycine would decrease - gut sensitivity to other things such as gluten, dairy or other things that people claim to have issues with?
If the latter is true it would be kind of funny in a way because people who eat a specific paleo diet devoid of glycine would sort of make themselves intolerable to those things. This is speculation of course and I'm in no way trying to hate on the paleo community, just making conversation.
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Re: Glycine virtually eliminates adverse GI effects of aspirin
Postby Peata » Thu Jun 25, 2015 5:57 pm
Glycine definitely stops or prevents the GI effect of aspirin for me.
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Re: Glycine virtually eliminates adverse GI effects of aspirin
Postby Greg says » Tue Aug 11, 2015 4:10 pm
haidut wrote:I posted a study earlier on co-administration of glycine improving the absorption of aspirin. It looks like it also prevents the negative GI symptoms of aspirin intake in some people.
I have just been experimenting with 600mg of aspirin a day and immediately felt its positive effects. Warmth, happier, just more healthy. BUT… after a week I could feel the ringing in my ears, gassy, bubbly stomach, brain fog and fatigue and coughing up mucus.
Im now taking glycine hoping for this to pass.
What is the aspirin doing and what is the glycine doing to correct this?
RP says that the stomach will adapt to the aspirin but its a tough decision to carry on with it if its making one sicker. I really want to carry on with the aspirin.
I read haidut saying it depleted glycine but I take tons of glycine. 1 large tbsp a night. [which really helps sleep].
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Re: Glycine virtually eliminates adverse GI effects of aspirin
Postby haidut » Tue Aug 11, 2015 4:19 pm
Greg says wrote:haidut wrote:I posted a study earlier on co-administration of glycine improving the absorption of aspirin. It looks like it also prevents the negative GI symptoms of aspirin intake in some people.
I have just been experimenting with 600mg of aspirin a day and immediately felt its positive effects. Warmth, happier, just more healthy. BUT… after a week I could feel the ringing in my ears, gassy, bubbly stomach, brain fog and fatigue and coughing up mucus.
Im now taking glycine hoping for this to pass.
What is the aspirin doing and what is the glycine doing to correct this?
RP says that the stomach will adapt to the aspirin but its a tough decision to carry on with it if its making one sicker. I really want to carry on with the aspirin.
I read haidut saying it depleted glycine but I take tons of glycine. 1 large tbsp a night. [which really helps sleep].
One possible explanation is that aspirin irritates the gut in some people and Peat said the irritation manifests itself as ear ringing. Glycine is known gastro-protectant, so that could be it. In addition, aspirin depletes glycine since it conjugates with it and forms hippuric acid. That's how it is excreted from the body. So, taking extra aspirin may warrant getting extra glycine to compensate. I don't have specific info on how much aspirin will deplete how much glycine but the glycine:aspirin combo is commonly sold in 1:1 ratio in some European countries, so I guess you can take as much extra glycine as you are taking aspirin.
Drinking Alka-Seltzer, which is aspirin combined with baking soda and citric acid creates sodium acetylsalicylate and that has also been shown to completely eliminate stomach damage by aspirin. Or you can mix your own combo. The ratio is 1:3 aspirin:sodium_bicarbonate.
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Milky
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Glycine virtually eliminates adverse GI effects of aspirin
Postby Milky » Thu Aug 27, 2015 11:30 am
haidut,
What about this study comparing aspirin to aspirin+glycine preparations which mentions that, while those receiving aspirin with glycine did not complain of any side effects, intestinal damage/lesion scores were nearly identical to the non-glycine preparation? This seems to suggest a different cause or mechanism behind symptoms besides simply intestinal irritation/damage.
"In a randomized double-blind study the gastroduodenal tolerability of daily 500 mg acetylsalicylic acid (ASA, CAS 50-78-2) in combination with 250 mg glycine (CAS 56-40-6) (Godamed) and 500 mg ASA without addition of glycine were evaluated in 20 healthy volunteers giving upper GI-endoscopy. Both ASA-preparations have been taken over a period of 4 weeks. Endoscopic controls were performed at entry, and repeated after 7, 14 and 28 days of treatment. Both ASA-preparations induced comparable gastroduodenal damages during the whole test period: The lesions score of both groups on day 7, 14 and day 28 was almost identical. In contrast to plain ASA, where 9 of 10 volunteers reported gastrointestinal side effects, all subjects receiving ASA in combination with glycine did not complain from any dyspeptic symptoms, i.e. epigastric pain etc. "
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Glycine virtually eliminates adverse GI effects of aspirin
Postby haidut » Thu Aug 27, 2015 12:27 pm
Milky wrote:Source of the post haidut,
What about this study comparing aspirin to aspirin+glycine preparations which mentions that, while those receiving aspirin with glycine did not complain of any side effects, that intestinal damage/lesion scores were nearly identical to the non-glycine preparation? This seems to suggest a different cause or mechanism behind symptoms besides intestinal irritation/damage.
"In a randomized double-blind study the gastroduodenal tolerability of daily 500 mg acetylsalicylic acid (ASA, CAS 50-78-2) in combination with 250 mg glycine (CAS 56-40-6) (Godamed) and 500 mg ASA without addition of glycine were evaluated in 20 healthy volunteers giving upper GI-endoscopy. Both ASA-preparations have been taken over a period of 4 weeks. Endoscopic controls were performed at entry, and repeated after 7, 14 and 28 days of treatment. Both ASA-preparations induced comparable gastroduodenal damages during the whole test period: The lesions score of both groups on day 7, 14 and day 28 was almost identical. In contrast to plain ASA, where 9 of 10 volunteers reported gastrointestinal side effects, all subjects receiving ASA in combination with glycine did not complain from any dyspeptic symptoms, i.e. epigastric pain etc. "
Yeah, I have seen that study. Not sure what to make of it, as most people that start taking glycine with aspirin report reduction of GI symptoms. I guess if glycine does not work for you you can always try baking soda or caffeine.
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Milky
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Glycine virtually eliminates adverse GI effects of aspirin
Postby Milky » Thu Aug 27, 2015 12:33 pm
haidut wrote:Source of the post Yeah, I have seen that study. Not sure what to make of it, as most people that start taking glycine with aspirin report reduction of GI symptoms. I guess if glycine does not work for you you can always try baking soda or caffeine.
So far glycine works great...aspirin has always produced ringing/pressure in ears and an anxious/sweaty feeling every time I've tried it orally over the last few years (whole tabs, powder, dissolved in baking soda...doesn't matter), until recently when I tried it again with glycine. I've been taking whole 325mg tablets with nothing but positive benefits. It feels similar to taking ibuprofen in terms of anti-inflammatory effects. I'm just concerned about it still causing damage (as ibuprofen is also known to do), but not being aware of it...especially in the long-term.
My gut feeling is that if it feels good do it so that's what I'll continue to go by, but I'll update if I notice any further effects either way.
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Glycine virtually eliminates adverse GI effects of aspirin
Postby haidut » Thu Aug 27, 2015 1:09 pm
Milky wrote:Source of the posthaidut wrote:Source of the post Yeah, I have seen that study. Not sure what to make of it, as most people that start taking glycine with aspirin report reduction of GI symptoms. I guess if glycine does not work for you you can always try baking soda or caffeine.
So far glycine works great...aspirin has always produced ringing/pressure in ears and an anxious/sweaty feeling every time I've tried it orally over the last few years (whole tabs, powder, dissolved in baking soda...doesn't matter), until recently when I tried it again with glycine. I've been taking whole 325mg tablets with nothing but positive benefits. It feels similar to taking ibuprofen in terms of anti-inflammatory effects. I'm just concerned about it still causing damage (as ibuprofen is also known to do), but not being aware of it...especially in the long-term.
My gut feeling is that if it feels good do it so that's what I'll continue to go by, but I'll update if I notice any further effects either way.
I posted another thread showing that chronic intake of aspirin depletes glycine stores. Given that glycine is the primary inhibitory amino acid in the body, lower levels could explain the anxiety effects you are getting from aspirin. I think the combination of aspirin, glycine and caffeine should be good enough to block GI damage.
Hoping this will contribute positively to the understanding the benefits of using the indicated combination.
Rafik
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45 yrs male with a BMI of 50,Diabetic for 8years presented with severe malena for 3days.On admission his Hb was 8gr/dl bl sugar was 200mgs,dyslipedimia other Biochemical parameters were normal XRay chest, ECG, Echcardio were normal. Upper Gi endoscopy was normal, scope could not be negotiated in to the 3rd part.U/S scan howed only Fatty Liver. CECT with angio was done revealed lipomatous filling defects in the above mentioned areas. Pt was resuscitated with Blood transfusions and control of Bl sugar.But slow oozing continued even though pt became stable.
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This is an interesting and difficult problem.
Firstly, recurrence of bleeding implies treatment.
Secondly, medical treatment will, most probably, not be durably sufficient.
Thirdly, endoscopic localization of the lesion is compulsory. I would start with capsule to have a good over-view. In case of a clear-cut result, i.e. a bleeding and/or ulcerated lesion, its elective destruction seems to be the best way. Access to this lesion will probably be possible with a colonoscope which is largely available with numerous usable  devices. 
Fourthly, in case of an ulcerated lipoma, endoscopic treatment is not so easy. As a matter of fact, hot snaring is difficult (high impedance) and dangerous (thin wall). In case of an intermediate or pseudo-pedonculated shape (frequent because ulceration is, usually, the consequence of invaginations) and a normal elasticity under forceps, I would suggest to put a plastic snare, then cut a macro-biopsy with manual setting, high power, pure section, high manual tension on the wire by the endoscopist himself. The remaining of lipoma will be digested after necrosis of its base. If pathology is not perfectly benign (very improbable) : surgery.
In case of multiple lipoma, without certainty of bleeding location, I would treat the largest snarable by the same way and follow.
In the absence of any snarable, probably responsible lipoma, a surgical, sub-mucosal resection will probably be relatively easy, precisely because of the flatness of the lipoma.
Finally, if the problem fails to be solved, I would wait until a new bleeding and perform urgently endoscopy with colono or enteroscope with tatooing. Injection should be large  (1 ml, eliminate any air in the syringe) to allow dye to be visible on the peritoneal side.
Then, elective surgery will treat the responsible lipoma with resection-anastomosis if jejunal or en-coin resection if duodenal.
The probability of 2 lesions bleeding simultaneously is almost 0. In case of recurrence on another lipoma (improbable) the same algorithm can be applied.
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Since 1838 physicians have described it in London, England . The term was attributed to Dr. Gill who coined the term in 1858.  In physical diagnosis class in the 1950's in Manila, Philippines, we were advised that when an abdominal mass was felt, the differential diagnoses could include the Seven "F's": namely; Fat, Feces. Fetus, Flatus, Fluid, Fibroid. and "Phantom Tumor".  So, what is a phantom tumor? 
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Gossipium is latin for cotton. A "gossipiboma" refers to a  foregin body left inside  the abdomen after  laparotomy specifically a  cotton sponge but "recently"  used loosely for any foreign body inadvertently left inside the body cavity.
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Do you have any experiences with faecal microbiota transplant in patients with  megacolon due to C.difficile infection? We have already tried fidaxomycin (3 days), metronidazol, vancomycin for 2 weeks.
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I have used FMT to treat a single patient with toxic megacolon who refused surgery. We delivered the FMT via push enteroscope and the patient made a full recovery. Subtotal colectomy remains first line treatment usually however. Thecase is documented below.
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2 yr old with rectal biopsy confirmed Hirschsprung's dx. Had transanal Swenson's pull through. Intraop frozen section and Postop histopathology confirmed ganglion cells in pulled through margin. Patient had transient urinary retention that resolved in a few days. Started to have constipation after 2months of surgery. What are the management options available? Personal experiences will be appreciated.
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The distal stump below your 'colo-anal anastomosis' and/or the anal sphincters may still be aganglionic. Distal myotomy or SLIS (subcutaneous lateral internal sphinterotomy) may help. Remember to exclude dietary constipation which is on the increase in Nigerian children.
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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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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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I'm curious about how the incidence of disease in the gut might affect protein uptake. Has anyone looked into this yet?
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It depends, if the protein is easily digested (small intestine) then a negligible effect is observed. If the protein is structurally complex and needs to be digested by the microbiome in the large intestine, then it does. 
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Dear Colleagues
As you are aware, typhilitis is a form of enterocoloitis or neutropenic colitis, a significant necrotising process that develops in the gastrointestinal tract of patients with neutropenia.  It involves caecum and terminal ileum and often presents with fever, abdominal pain, diarrhoea, abdominal distension and rebound tenderness in the right lower quadrant.  I would appreciate your valued comments on optimal management of this condition.  Many thanks in anticipation for your contribution.
Sayed S Bukhari MD FRCPath
Consultant in Infection
Midlands, UK
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Please review the following article
Crit Care Clin. 2001 Jul;17(3):531-70, vii-viii.
Infectious morbidity in critically ill patients with cancer.
Safdar A1, Armstrong D.
Author information
1Department of Medicine, Division of Infectious Diseases, University of South Carolina School of Medicine, Columbia, South Carolina, USA. safdar@richmed.medpark.sc.edu
Abstract
Infection frequently complicates the course of cancer treatment and often adversely affects the outcome. Patients have a greater tendency for acquiring infections caused by opportunistic microorganisms. Agents with low virulence potential may lead to invasive and often life-threatening infections because of altered host immune function. The immune dysfunction may be caused by the underlying malignancy, by antineoplastic chemotherapy, or by invasive procedures during supportive care.
PMID:
11525048
[PubMed - indexed for MEDLINE]
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I want to work on human cell lines(Gastro intestinal) to check for the activity against some group of bacteria??? please suggest me who can provide this service
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You can get secondary human cell line from Americal type cell collection(ATCC). Also  you can  procure from National centre for cell line (NCCS) Pune,India, but NCCS will not assure for absence of mycoplasma contamination in the culture.You visit NCCS web page for further details.
all the best
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Dear All,
I have a 60 year old male. He has had radical cystectomy, nephrectomy on the right and an urostoma constructed with an ileum conduit in his left lower abdomen. He was operated in 2/2014 due to a first recurrence of this parastomal hernia with a sublay-mesh. Then he developed a subcutaneous urinoma 2 days later and needed revisional surgery. the mesh needed to be removed, the hernia was closed with direct closure without a new mesh. After a few weeks he was developing a new parastomal hernia, as expected and presented in my outpatient clinic. 
He need repair of his parastomal hernia, because its painful and disturbs in daily life. 
The question is: which approach should we take? I think that direct approach from outside trying to fix the hernia with another mesh in sublay position will be difficult, because i'm expecting adhesions in the subfascial plane and large dissection will be needed. We decided for performing a transabdominal approach, with adhesiolysis and direct closure of the hernia including a IPOM mesh support (DynaMesh). 
Any suggestions? Henry.
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Just saw the patient 2 weeks post-OP.
He is doing well. Due to the inability to resect the complete hernia sac from inside, he developed a subcutaneous seroma. We will wait until it has resolved. beside that he is doing great and back to his normal life activity.
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Adrenomedullin (AM) seems to be linked to pancreatic adenocarcinoma (ADC) and new-onset diabetes (NOD). Does anyone have any experience in this field? We are trying to test serum AM levels and immunohistochemical AM staining in patients with pancreatic ADC. We need to share our experience.
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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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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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45 women suffering from irritable bowel syndrome which is refractory to conventional treatment
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Nausea is unlikely to be present in only IBS unless it is associated with functional dyspepsia or GERD. In such cases promotility agents like cinitapride might help in addition to acid suppressors. However remember that drug refractory IBS patients have major psychological disturbances ane feeling of nausea may be due to this also especially in women
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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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Nowdays, endoscopists face the economic pressure to increase the number of colonoscopies by decreasing procedure time. Are there evidence based recommendations about the time limits of the withdrawal time? During this phase careful inspection occurs.
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Dear Collegue,
according to my own opinion, the withdrawel time is important for beginners and for endoscopists with low experience. I performed nearly 60.000 colonoscopies, my ADR is 30% and I doubt, that a withdrawal time over 6 minutes leads to a hiegher detection rate in my praxctice.
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The identification of a definite point of obstruction, the ‘transition zone’, with dilated small bowel loops proximal to the site of obstruction and collapsed loops distally, is the most reliable CT criterion for diagnosing small bowel obstruction .
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I work with inflammatory bowel disease and I want to analyse TGF-beta activity/levels
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The first question is do you want total or just the active TGF. The best way I have found is by ELISA. Requires little sample and you get an answer within 8 hours. There is also a mink cell line that has been transformed with a TGF dependent luc promoter which has been widely published and is generally accepted. I still prefer the ELISA... its more costly but it is quantitative and discriminates between active and latent. using an acid incubation. Hope this helps
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These samples are obtained from patients suffering from gastrointestinal disease.
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PCR.......