Science topic

Gastric Ulcer - Science topic

A peptic ulcer is a defect in the lining of the stomach or the first part of the small intestine, an area called the duodenum. A peptic ulcer in the stomach is called a gastric ulcer.
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Could anyone help to find the method for stomach ulcer induction in rats according to Shay et al. or published work on it more in detail?
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Aspirin
indomethacin
alcohol
pylorus ligation
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Helicobacter pylori inhabit the gastrointestinal tract, one person’s poison may be another’s cure. Helicobacter pylori, the bacterium that causes gastric ulcers and stomach cancer in some people, may actually protect against cancer of the esophagus. So, What about your experience in the paradoxical effect of Helicobacter pylori infection? and why their resistance to treatment was increased?
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I have no experience in this field, but i think the following article will be helpful
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please provide me with following article.
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Moxifloxacin-based triple therapy is a safe and well-tolerated option in anti-H. pylori therapy. In second-line treatment, the combination of a PPI, moxifloxacin, and metronidazole or tinidazole is a valid option, especially in countries where bismuth salts are unavailable. In first-line therapy, a moxifloxacin-based triple therapy cannot generally be recommended. However, under specific circumstances, this combination might be considered as an individual first-line treatment option. Thus, in a population with low primary quinolone resistance and high primary clarithromycin resistance, a PPI triple therapy with moxifloxacin and metronidazole or tinidazole could be a valuable alternative
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Curling in 1842 was the first to describe detail that, Acute gastroduodenal erotions and Gastric ulcers can be associated to burning injuries nomely "Curling's ulceration".
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I thank all for the scientific experience contribution.
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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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In our first experiment we got the average value of 800 µg of alcian blue/ gram of wet stomach in normal control group (when we read at 580 nm in absorbance reader) but in the second experiment with different set of animals at same wavelength and in the same instrument we got the average value of 60 µg of alcian blue /gram of wet stomach for normal control group.
What is the reason for this difference?
Is this normal (experiment to experiment based) observation? Or abnormal observation because of some other reasons?
Is there any specific range for gastric mucosa content in Wistar rats?
Your help is greatly appreciated.
Thanks and regards
Eshvendar reddy
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why not do an Alcian Blue staining of longitutinally sectioned stomach? remember the rat stomach has the fundus actually covered with squamous epipthelium with no goblet cells.  if you took too much of this part it may explain the differences.
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Aspirin and numerous NSAIDs, including acetaminophen and those inhibiting selectively COX-2, are amongst the most commonly consumed drugs on the planet. Aspirin at doses less than 100 mg per day or greater than 1 gm per day have equivalent effects on platelet COX-1 derived TxA2. They both suppress it completely. However, increasing daily doses of aspirin increasingly inhibit PGI2 coincidentally with this effect, which suggest that the cardioprotective efficacy of aspirin may be progressively attenuated as the dose is increased. Similarly, locally formed, COX-1 derived PGE2 and PGI2 are protective of gastroduodenal epithelial integrity and platelet COX-1 derived TxA2 contributes to hemostatic competence. Disruption of these pathways by NSAIDs (even those which selective for inhibition of COX-2) resulted in serious gastrointestinal events. That may reflect their impact on gastroduodenal epithelial COX-2 dependent prostanoids that accelerate ulcer healing. As we still poorly understand inter-individual differences in anti-inflammatory efficacy amongst the reversibly acting NSAIDs, the hard evidence how to address the above question is in short supply.
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In continuation to above,  the gastropathy can be avoided by use of low dose of aspirin topically, avoiding oral route. A transdermal preparation avoids hepatic portal circulation where a large fraction is presystemically deacetylated. Added  advantage would be further  reduction in dose. We need to research and develop such a transdermal aspirin preparation
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None
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You could search a database using the link below.
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I'm working on anti-ulcer and ulcer-healing effects of fruit peels extracts on stress-induced gastric ulcers. In order to test the gastroprotective effect of the extracts how many days should I feed the extracts to rats before subjecting it to procedure of inducing ulcer?
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It ill also depend on the method of producing stress ulcers.  I would try a single oral dose.
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please how can can i induce stomach ulcer orally in rabbits and also using biochemical markers to diagnose the ulcer in the rabbits.
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One should distinguish the chronic ulcer and the multiple acute ulcers and erosions of the stomach depending on what you need to obtain. The aforementioned ways will cause rather the latter alterations. For the former to produce, I would recommend the Okabe acetic model. It is reliable, cheep, and may give longlasting ulcer with recurrences.
For reference:
Okabe S. & Amagase K. An overview of acetic acid ulcer models. The history and state of the art of peptic ulcer research. Biol. Pharm. Bull., 2005; 28(8): 1321-41.
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Which is more ulcerogenic to the stomach: aspirin or clopidogryl?
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The association between H. pylori and gastric cancer may be explained by two possible mechanisms: one is based on a carcinogenesis-promoting effect of H. pylori itself and the other is based on the establishment of a carcinogenic environment due to long-term infection with H. pylori. In the second case, although H. pylori may have no carcinogenesis-promoting effect itself, infection causes inflammation of the gastric mucosa and chronic infection causes mucosal atrophy, resulting in intestinal metaplasia. These latter changes are considered precursors of gastric cancer.
A peptic ulcer is a break in the inner lining of the esophagus, stomach, or duodenum. A peptic ulcer of the stomach is called a gastric ulcer; of the duodenum, a duodenal ulcer; and of the esophagus, an esophageal ulcer. Peptic ulcers occur when the lining of these organs is corroded by the acidic digestive (peptic) juices which are secreted by the cells of the stomach. A peptic ulcer differs from an erosion because it extends deeper into the lining of the esophagus, stomach, or duodenum and excites more of an inflammatory reaction from the tissues that are eroded.
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30 year old who under went an attempted lap chole converted to open,also underwent a diagnostic Lap 8months ago,presented with complaints of abdominal pain,feels full with small quantity ,no vomitings and no significant  loss of weight.She was hospitalised twice after surgery for pain and was treated conservatively as per her hospital records.OGD in their hospital showed a gastric ulcer and a repeat was said to have the ulcer healed.Clinical exam is normal except Right subcoastal incision and multiple Lap port scars.OGD in our hospital showed the above suspected diagnosis and technically difficult to extract.CECT report is awaited.
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If a foreign body is present without doubt, it should be extracted if the surgical risk is not prohibitive. Open abdominal exploration seems the best approach. Once you have diagnosed it, you have to inform the patient about what happened and what you are intending to do to help her. Failure to do so is potentially dangerous to her and to yourself.
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I gone through many papers that they calculated the ulcer index in the stomach of a rat model. They gave some score depending on the ulcer's color and size. I don't understand how to give the score and how to calculate the UI. Kindly let me about this or suggest any other method to calculate the UI.
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Ulcer index
The number of ulcers was counted by using the magnifying glass. Severity scores: normal coloration as 0, red coloration 0.5, spot ulcer 1.0, hemorrhagic stress 1.5, deep ulcer 2.0 and perforations as 3.0.
Ulcer index = (UN + US+ UP) x 10 rais to power -1
UN = Average of number of ulcer per animal
US = Average of severity score
UP = Percentage of animal with ulcer
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I am working with gastric ulcers and I need a culture of Helicobacter Pylori. Does anyone have any idea where I can get a culture in and around India?
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You can contact to any well known hospital in your close vicinity. The doctors who do biopsy for ulcer patient they can provide you the sample on request or on some other conditions.