Science topic

Ulcer - Science topic

Ulcer is a lesion on the surface of the skin or a mucous surface, produced by the sloughing of inflammatory necrotic tissue.
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In case of diabetes, there were several evidence of prolonged inflammation due to interruption of m1 to m2 macrophage polarization. So if anyone want to promote wound healing in case of diabetic ulcer how to target M1 macrophage and induce its polarization towards M2, which proteins need to be targeted ?
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Good evening,
As far as I know, ESWT extracorporeal shock waves can improve wound healing, especially in diabetics. The ISMST (a learned society on ESWT) could provide you with more detailed information on this subject. ESWT are known to act on macrophages.
Kind regards.
Grégory VIEQUE
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Endoform™ Antimicrobial is indicated for the management of acute and chronic wounds including partial- and full-thickness wounds, pressure ulcers, venous ulcers, diabetic ulcers, chronic vascular ulcers, tunneled/undermined wounds, surgical wounds (donor sites, grafts, post-Mohs surgery, post-laser surgery, podiatric and wound dehiscence), traumatic wounds (abrasions, lacerations, second-degree burns and skin tears) and draining wounds.
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The endoform is a type of advanced wound care product, specifically a natural extracellular matrix (ECM) scaffold derived from ovine (sheep) sources. It is used to support wound healing by providing a structure that mimics the natural human ECM, which plays a critical role in tissue repair and regeneration. Here are some key applications and benefits of using Endoform in wound care:
Applications of Endoform
  1. Chronic WoundsDiabetic Ulcers: Endoform can be used to treat diabetic foot ulcers by promoting the growth of new tissue and aiding in the wound closure process. Venous Leg Ulcers: It helps in the management of venous leg ulcers by supporting the natural healing process and reducing the risk of infection.
  2. Acute WoundsSurgical Wounds: Endoform can be applied to surgical wounds to enhance healing and reduce the likelihood of complications such as infections. Traumatic Wounds: For wounds caused by trauma, Endoform can provide structural support and facilitate faster healing.
  3. BurnsPartial-Thickness Burns: Endoform is beneficial in treating partial-thickness burns by providing a scaffold for cell migration and tissue regeneration.
  4. Pressure UlcersBedsores: In patients with pressure ulcers, particularly those who are bedridden or immobile, Endoform helps in reducing the wound size and promoting healing.
  5. Infected WoundsBiofilm Management: Endoform can disrupt biofilms and reduce bacterial load in infected wounds, thus supporting the healing process.
Benefits of Using Endoform
  1. Mimics Natural ECMStructural Support: Endoform provides a structure similar to the body’s own ECM, which supports cell attachment, migration, and proliferation. Bioactivity: It contains natural bioactive components that can help modulate inflammation and promote healing.
  2. VersatilityMultiple Wound Types: Suitable for a wide range of wound types, including chronic, acute, and infected wounds. Different Stages of Healing: Can be used at various stages of the wound healing process.
  3. Ease of UseApplication: Endoform is easy to apply and can conform to the wound bed, ensuring good contact with the wound surface. Hydration: It maintains a moist wound environment, which is critical for optimal healing.
  4. Reduces Healing TimeAccelerated Healing: By providing the necessary support and bioactive signals, Endoform can accelerate the wound healing process. Reduced Complications: Helps in reducing the risk of wound-related complications such as infections and chronic non-healing states.
  5. Patient ComfortMinimized Pain: Application of Endoform is generally well-tolerated by patients, and it can help in minimizing wound pain.
Mechanism of Action
  1. Scaffold for Cell MigrationEndoform provides a physical scaffold that cells can attach to and migrate through, facilitating the formation of new tissue.
  2. Modulation of InflammationThe bioactive components within Endoform can help modulate the inflammatory response, reducing chronic inflammation that can impede healing.
  3. Promotion of AngiogenesisEndoform supports the formation of new blood vessels, which is crucial for delivering nutrients and oxygen to the healing tissue.
  4. Support for Collagen DepositionIt promotes the deposition of new collagen, a key component of the extracellular matrix that provides strength and structure to the new tissue.
Impression:-
Endoform is a versatile and effective wound care product that leverages the principles of extracellular matrix biology to support and enhance the natural wound healing process. Its applications in chronic, acute, and infected wounds make it a valuable tool for clinicians in promoting faster and more efficient wound healing, thereby improving patient outcomes several times
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Despite many attempts I am still unable to find the original version of this paper and would appreciate if anyone can locate it for us:
Baker PG, Haig G (1981) Metronidazole in the treatment of chronic pressure sores and ulcers: a comparison with standard treatment in general practice. Practitioner 225(1354): 569–73
We would reapply appreciate some assistance with this
Best wishes
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Really? Crazy! Did they tell you why? I googled a little, and it's in the Cochrane Library, Cochrane Central Registry of Controlled Trials.
I'm a medical historian, and my intrepid interlibrary loan staff never failed to unearth articles for me, even articles over a century old.
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I have implanted a tumoral cell line subcutaneously in nude mice.
After intratumoral gene therapy treatment, a subgroup of mice develops ulcerated tumors.
Any idea how to avoid this?.
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Ulceration may occur when tumors develop subcutaneously. The cause could be in situation where large tumors develop on the ventral surface and are subjected to constant abrasion, or sometimes these ulcerations could be caused due to the cell's origin type. There are cell lines that are predisposed to ulcerate.
I would suggest you change the initial tumor cell dose. Inject reduced cell number, and if ulceration is characteristic of the tumor line, you should try to complete the experiment in the latent period before ulceration.
Best.
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For Eye Ulcer prediction we need image dataset, kindly share where to get those.
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I want to test if having a previous ulcer (Yes/No question) influences a diabetic patients level of knowledge (questionnaire- scale data) and practice of footcare (questionnaire-scale data). What statistical test should I use?
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You should use Mann-Whitney test to explore the presence of significant differences between the two groups (yes/not ulcer history). Then, after categorizing the population into two groups on the basis of the median value of the scales of those who have not had the ulcer (or other threshold based on the indexes of the scales used), you could perform a logistic regression to predict the condition of "having a score higher than the median value (or other threshold)” based on the independent variable presence / absence of ulcer history (in this way the estimates could also be corrected by other covariates).
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1- Surgical excision followed by diet, biofeedback, APC and Sucralfate
or
2- Endoscopic debulking followed by diet, biofeedback, APC and Sucralfate?
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In adults, a quarter of SRUS may appear as polypoid lesions. Rectal prolapse can be seem in about 1/5 of SRUS in adults.
Topical sucralfate, salicylate, corticosteroids, mesalazine have been reported to be effective. Surgery is considered only for patients not responsive to conservative measures and biofeedback.
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I have a set of experiments trying to stop the activity or expansion of the rot produced with these bacteria
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I think that the types of microorganisms to be of great importance in predicting wound healing and infection. Although appropriate systemic antibiotics are essential for the treatment of deteriorating, in addition to controlling the growing conditions
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A 58 years old male reports to you with a fissure like ulcer on the elevated part of lingual ridge from the past 2 months. he further tells two episodes of whitish flakes coming out from the fissure. his medical records show that he is under medication for multiple myeloma for the past 8 months.
what is your likely diagnosis and how would you manage the case?
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Hi Bikash
The plaques could be amyloid (secondary to myeloma) deposits. You may want to biopsy them. If the suspicion is confirmed, ideally the patient should have a SAP scan. As to treatment, the choice would be a velcade based combination. (eg VCD).
Best wishes
Siva
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We have measured over time the weight loss, disease symptoms (weight loss; stool consistency, rectal prolapse, rectal bleeding; spine curvature) and colon histological changes (leukocyte infiltration, goblet cell depletion, epithelial hyperplasia, crypt size, and submucosal inflammation and ulceration) after H&E staining in 2% DSS treated 8–12-week-old C57bl6/j mouse. Colon histological changes have been studied at day 8, the point of higher weight loss before weight recovery (DSS for 5 days+3 days of water).
We have compared a control group versus our group of study (Study-group).
After independently repeating the experiments several times, we have consistently observed:
-no differences in weight loss overtime between groups
-statistically significant REDUCTION of disease symptoms in the study group
-but significant INCREASE in colon histological damage in the study group (particularly in leukocyte infiltration, goblet cell depletion, crypt damage and ulcerations).
It is well stablished the correlation between disease symptoms and colon histological damage, but we have not observed this effect this time.
Could you help me to explain this discrepancy?
What could be the mechanisms related to these two different effects?
Do you know any reference in the literature explaining this potential contradictory results?
Attending to our results, do you think that our study group is suffering from less or increased IBD?
For the interest of the IBD in patients, is it more important to reduce the symptomatology or improve the tissue damage? How could we study these two points in our model? Any recommendation?
Thank you
Sincerely
Jose Maria
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I forget to mention that our study group also showed a large colon lengh, a symptom of reduced colitis.
In summary, our study group showed the same weigh loss, less disease symptoms and increased colon lengh but worse colon histology.
Than you
Sincerely
Jose Maria
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Most of the dissolution tests use 900 mL of medium. How was this volume defined? Is there any correlation with the volume of gastric fluid in humans?
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The volume of dissolution medium to be used is defined considering "sink condition." The solubility of the drug substance is quantitatively determined in several dissolution media within the physiological pH range at 37 °C. Using this value, the volume of dissolution medium necessary to obtain a saturated solution of the highest dose of the product to be marketed is calculated. Sink condition is considered as at least 3 times this volume. Some companies work with 5 times or 10 times this value. There are some instances where the dissolution test is more discriminative if sink condition is not followed. The volume of dissolution medium has no relationship with the volume of gastric fluids in humans. According to information available in the literature, a realistic volume to simulate the total fluid available in the stomach in the fasted state is in the range of 250-300 mL.
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Antacids to Gastrities or Gastric / Duodonal ulser - Please share your feelings .
Sincerely Yours ,
Jaydip Datta
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Interested
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Recently, we have injected s.c. B16F10 tumor cells in BL/6 mice. At around 12-15th day some animals showed ulcerations in tumors , with a big hole in the middle (it looks like a volcano). We have also observed this problem in MC38 and EG7 tumors. This did not happen to us so often until now. Any suggestion or personal experience that helps us to resolve this issue will be really appreciated. Thanks in advance.
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Try decreasing the number injected vital cells
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in fact i want to understand why some ophthalmonyiasis cases acompiend with ulcer
i also want to know what are the expected bacterial species are responsible for this type of ulcers
if there any research can save me
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Ophthalmomyiasis is actually infestation of eyes with larvae of house flies that is maggots in eye. Usually occurs either implantation of hatching egg in eye or long standing open wounds in eye such as cancers of eyes. On these open wounds the fly gives it larvae which eats up the decaying tissues. while eye ulcers usually refers to the corneal ulcer caused following trauma or otherwise by microbes bacteria, fungi and viruses.Lid ulceration can occur in lid cancers on which fly lay larvae developing in maggots that can be called ophthamomyiasis.
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We are conducting a meta-analysis that includes primary studies which compare different support surfaces for the prevention of pression ulcers. We have come across a cross-over trial and we are not quite sure of how to introduce data into Revman. We are thinking of adding up results from both periods and making the study similar to a parallel trial but we don´t know if this approach is correct.
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I have already evaluated the forest plot. Now I want to swap the data that means i want to exchange the control and experimental group. When I swap the Group label 1 and 2, why the data in the table is not swapping automatically? Can anyone tell me how to do it?
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Ulcer is more in the northern part of Nigeria. Which plant source have the potential to cure or kill the ulcer bacteria?
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The problem is one of stress and possibly poor nutritional intake leading to reduced immunological response to the bacteria. Without a knowledge of what plants you have available that have a bacteraicidical effect (without other adverse effect) all I can recommend is garlic. This has a well documented antibiotic effect when taken raw. I cannot recommend a dose as the plant varies in efficacy.
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I am working on prevalence of microbial agents associated with chronic non-healing ulcer.
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Sorry no idea.
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On your web pages there is an article by Telichowska KS with bibliographic data of the Integrative Molecular Medicine (IMM) journal (Telichowska KS (2019) Wound coverage by linen dressing accelerate ulcer healing. Volume 6: 1-3. Integr Mol Med, 2019 doi: 10.15761/IMM.1000371)). Unfortunately, there is no such article on the IMM's page. The article was withdrawn a few months ago from OAtext publisher pageges, remove it from your pages.
Jan Szopa, professor of biochemistry University of Wroclaw
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Yes you can if you is the only author or all authors do the same procedures: 1-Select the withdrawm manuscript from your puplication list 2- Click in the square icon (placed in the right of share rectangle) 3- Select remove 4- Select Permanently delete the publication page from ResearchGate
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The formulation is meant to give a prolonged release locally and is meant to be coated over an implant to provide pain relief caused due to the same.
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Thank you for your answers...
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This question is aimed to refer good quality and authentic reference book/text book publication for proper understanding of diagnosis and management of the various non healing ulcers including diabetic ulcers, venous ulcers, arterial ulcers, infected ulcers, cellulitic ulcers, trophic and tropical ulcers, burns management etc.
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Start here:
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Aphthous Ulcer is common during stressful condition. As reactivation of  HSV is always associated with decreased immunity due to any cause. Decreased immunity is most common during prolong stress and so we can imply aphthous ulcer to reactivation of HSV. Recurrence of stress is common and  so recurrence of  aphthous ulcer also common. This recurrence can be prevented by levamisole for many years.
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Hi. Mostly aphthous ulcers, can be a result of stress, certain vitamin deficiency, hormonal fluctuations and even unintended mouth injuries.
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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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Recently, I implanted breast MDA-MB-231 tumor cells in NSG mice. Surprisingly, some mice showed ulceration in their tumors at tumor size around 200-300 mm3 much below the humane endpoint. I never observed such problem with other tumor xenografts I did in the past such as small cell lung cancer H146 and ALL MOLT-4 xenografts. Although I used CB-17 SCID mice for those studies. I am wondering whether this is common with this cell line or mice strain or the combination of both? Any suggestions or personal experience will be appreciated.
Thanks
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Aggressive cell lines like MDA-MB-231 can also lead to ulceration by invading into dermis and secreting MMP's. Interaction of inflammatory site with the NK and monocytes in the NSG will lead to ulceration.
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There are so many diseases in the world such as cancer, HIV AIDS, ulcer and many more. How did they come into the world?
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Dear Obed
thanks for your question.
in this paper you can find good answers to your question:
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clinically how can an ulcer be differentiated as Decubitus Ulcer or Diabetic Ulcer ??
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Further research by continuous bedside observation (considered the gold standard) and by adequately qualified major research teams are still important for understanding the peculiarities of pressure-related injuries in pediatrics. Who are the institutions and people interested in the subject, to work together?
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I am interested - currently working at Ambo University - referal hospital.
A small unit is functioning at pediatric ward . We have to see the feasibility of study to do here .
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a gentleman with isr has prolapse of colon after isr, while a feels a whitehead procedure in 2 phases may be good, has anyone any experience on this
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You've misunderstood - we all perform ISR/ ULARs etc. And all of us who do are aware of the possibility of prolapse. The issue is having the facilities available to diagnose and know-how to manage the complication which technically, we have created.
Are you saying you have an ano-rectal physiology lab? If so, then those figures should help you make a decision as to whether surgery is indicated or not. The abstract above doesn't answer the query
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Many Institutions in Africa lack skilled experience physicians for endoscopy ,especially enteric endoscopy, WE HAVE so much suspected Ulcer patients in North-East Nigeria ,this may be the same for some Muslim dominated countries,does any one know ,where doctors from poor resource setting can attend cheap hand-on training courses for Endoscopy,enteroscopy and Ultrasound courses?.
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Have a look on it..
Note: I am not attached to any of the above courses. I just came across about this piece of information and thought it might be useful to you
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To detect does cow's milk treat the ulcer caused by giving aspirin to rats
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Hi
I agree with A.R. A. Al-Aqaby
regards
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I need clinical randomised trials from 2010 until now
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Apart from the Clinical trial Registries of various individual countries, Cochrane evidence/library could also help.
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Has anyone has experience in PRP Dressing
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I have used in a few cases and the results were promising, Various studies prove the efficacy of PRP by the kits but a proper protocol is yet to be formulated
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Are there any problems in using the dextrose 20% solution for injection orally if no oral dosage form is available in the country? 
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Yes, it can be used orally for managing hypoglycemia in conscious diabetic patients with intact swallowing function. Just make certain that patients take in plenty of water, because the dextrose will also cause the body to lose more water through urination. Monitor for signs of dehydration.
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I am trying to grow B16F10 melanoma cell line in RAG-/- mice, the process used to work perfectly but now I have some problems with the tumor, it looks ulcerated and doesn't grow the same way !! I have genotyped my RAG mice and they don't express any CD4, CD8 or B cells. I will check mycoplasma contamination but would like to know if there are any other things I should look for !! Thanks in advance 
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you are welcome
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We have a case where a 13 years old female mixed dog with insulinoma underwent surgery to remove a well-encapsulated insulinoma. After the surgery it was treated with toceranib fosfat (Palladia). Before the surgery this dog had hipoclucemic crysis and after the surgery those still appears more frequently than before. So we want to know if those attacks are real hypoglycemic crisis or are related with hipokalemia so how the serum potassium behaves? Greetings.
  
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Thank you for your answers. We looked for metastases but they must be microscopic or not large enough to be seen on ultrasound. The dose of Toceranib is 75 mg each 48 hours resting the weekends. We have realized that the problem is that one of the cornerstones of treatment, corticosteroids, were not being taken because of osteoarthritis, our patient was taking NSAIDs and stopped taking them due side effects. 
 
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For a long period of Blastocystis infection there are some small ulcers found at end of ileum.
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A 5 years old child with  erythromelalgia and presented with severe bilateral feet pain resistant tol all of the following combination treatment: gabapentin, amitryptilin, prednisolon, Sandimmune, Local lidoocain. tramadol , NSAIDs, and aspirin. How to treat her? what we can do for her? 
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To my experience erythromelalgia is a vasodilating condition, an analogous to vascular algodystrophy. Primary treatment should focus on identifying and avoiding the triggering factor, which is most commonly the exposure to different and extreme temperatures or repetitive microtrauma. Elevating the extremities above the level of the body softens the symptoms and this can confirm if the condition is erythromelalgia or not.
Medications are rarely helpful. The use of analgesics and NSAIDS may help to subside symptoms but time is needed far from the triggering factor in order someone to be cured.
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A patient took 4500 mg acetaminophen in 3 days span along with the following drugs prescribed by a homeopath practitioner- Arsenic, Calcium Sulphide and Bryum album (dipped in alcohol). He developed Fulminant Hepatic Failure SGPT rocketed from 1158 U/L to 3796 U/L overnight. No virus detected. Can acetaminophen do such damage at so low dose?
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complex interaction between paracetamol and alcohol intak
the acute administration of ethanol inhibits the potentially toxic oxidative metabolism of paracetamol and protects against liver damage. This protection decreased when the concentration of ethanol decreased.the critical period is that the time between ethanol and paracetamol intak
while chronic alcoholism, microsomal enzyme induced with increased toxic metabolic activation of paracetamol and enhanced hepatotoxicity.  elevation of SGOT/SGPT ratio may be 5 times greater than normal
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who can give me a aricle about application of skin tissue engineering for treatment of diabetic ulcer?
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Medscape education guide may answer your question.
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doxycycline is long acting tetracycline which mostly used for treatment of acne vulgaris
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Primarily, doxycycline is excreted in bile to feces, and part of doxycycline is inactivated in the liver and 40 % of it is excreted by kidneys in urine, while the majority of first-generation tetracyclines are not metabolized Instead, they are most often eliminated by renal excretion.
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I need an article which deals about small rupture (lesions) of the aorta due to atheroma. Can these cause ulceration as well as small lesions?
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Maybe this is helpful:
Wada H, Sakata N, Tashiro T.Clinicopathological study on penetrating atherosclerotic ulcers and aortic dissection: distinct pattern of development of initial event. Heart Vessels. 2016 Nov;31(11):1855-1861. Epub 2016 Feb 18.
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Good day, all.
I tried using filter paper soaked in 99.5% acetic acid and applied it for 40 seconds, but it doesn't work. Out of 6 rats, only one developed ulcer. This method is based on a paper. Could anyone suggest a better method? 
Thank you in advance :D
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Buccal mucosal lesions can be induced by local injection of 50 μl of 99.7% acetic acid into the buccal mucosa.See:Therapeutic effect of rebamipide in a modified acetic acid-induced buccal mucosal ulcer model link.springer.com/article/10.1163/156856002321544864
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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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Specifically I think of children on (1) NSAIDS, (2) systemic steroids, and (3) in critically ill children (i.e., stress ulcer prophylaxis)? What medications are recommended and which doses should be used? Does the start of a prophylaxis depend on (1) planned duration of the NSAIDs/steroid treatement (or do you start prophylaxis in any case?), (2) the dosages of NSAIDs/steroids applied, (3) the type of NSAIDS used, and (4) the presence of certain risk factors (like in adults)? However, if there are no widely acknowledged recommendations (I am afraid this is the case) how do you handle this problem in your hospital/department?
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Thank you for your answers. However, my question did not refer to the general use of PPI or H2 blockers in children.  In contrast, I wanted to know your practice regarding the ulcer-prophylactic application of PPI, H2 blockers and sucralfate in children on steroids or NSAIDs.
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a man in age 50 with end stage of prostate cancer
there are Lesions like 1 stage bedsores on the back of his hip area
i want to know more about the new methods of the treatments
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In sexually transmitted infections, it is important to differentiate a painful ulcer from a painless one. This is because painless ulcers are seen in the chancre of primary syphilis while painful tender ones are seen in Herpes and though rare, in chancroid (H. ducreyi).
I can guess that it must be due to peripheral nerves, but how does this happen?
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Perhaps some pathogens would invade peripheral nerve fibers during the pathogenesis as their skin lesions developed. So we know the existence of neurosyphillis and postherpetic neuralgia.
Some pathogens might numb nerve fibers, others might fire them.
The pathogens also might release some chemical substance into the periphery in the early phase.
Possible mechanisms include cytokines, inflammatory mediators, inhibitory neurotransmitters or anything.
You just asked a great question. It is a fundamental issue.
You could take down some samples of peripheral nerve fibers closely near the skin lesions to do pathology (even electric microscopy). To see what happened?
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In my literature review, I have so far found only one case study of an ulcerating malignant wounds / lesions being successfully healed using proper wound bed preparation and the TIME paradigm. Hardly any available literature indicates these types of wounds can be healed; they are usually managed with conventional methods of topical agents, debriding, dressings, and pain management if radiation treatment, chemotherapy or surgery are not deemed suitable or have been ineffective.
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In this case, you can read this article
Fungating breast cancer and other malignant wounds: epidemiology, assessment and management. Sok Yuen Beha, Leong Chai Leowb. 137-144
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I am working upon naproxen as an an anti- inflammatory and analgesic agent
However naproxen is reported as gastrointestinal ulcer causing drug. How
ulceration can be controlled while using naproxen as an active ingredient?. 
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Dear Gul,
Alternatively, persons that have GI ulcer are given COX-2 selective nonsteroidal anti-inflammatory drugs (NSAID) such as celecoxib as a replacement to NSAIDs such as naproxen since they do not negatively affect the GI.
For more on this class of drugs, please use the following link:
Hoping this along with my first answer will fully cover the answer to your question.
Rafik
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One my surgical colleagues has a referred a patient to me who has suffered chronic ulcerative lesions in her perineal area for several years and has undergone multiple surgical procedures. Specimens from the affected perianal area have yielded a variety of microorganisms over the past three years and as a result she has received multiple courses of antibiotics but with little or no effect.
Given her prolonged history of recurrent skin and soft tissue infection, the chronic course of the illness and her poor response to antibiotics, I believe that this may be a case of Pyoderma gangrenosum.
Many thanks in anticipation for your advice and helpful comments
Kind regards
Dr Sayed S Bukahri FRCPath
Consultant in Infection
University Hospitals of Leicester NHS Trust
UK
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May be topical use of Betadine 10% will be useful and also Bactroban 1% crem
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Pressure ulcer is a potential total or partially immobilized patients problem being caused by different factors influencing its formation.
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My experience confirm that zeolite cures injuries, ulcers and other 
issues
Roque -Malherbe 
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What is the genetic influence of necrosis in diabetic ulcers?
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Thanks for the reference. 
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How do you handle growth delay data from mice that develop ulceration over their SC tumors following rapid growth rate; include data until exclusion or totally exclude data? 
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Dear Anders,
I do not think that you can exclude any tumor from your statistical analyses, even if they are ulcerating.
WHich type of model are you using?
How big are the tumors when you are ending the experiment?
When do you see the first appearance of ulceration?
Best regards
Robert
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52 yrman presented with dysphagia of 6months and acid peptic symtoms for 3years. Now he drinks a glass of water to swallow solid food. He has lost 4 kgs of weight. Upper GI endoscopy showed ulcerative leision at the GE jn ,biopsy adenocarcinoma. CECT showed tumour at the GEjn extending in to the fundus of stomach,small perigastric glands at ge jn are present.
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Siewert type III
1. Laparoscopy
2. Jejunostomy temporary
3. Neoadjuvant treatment radio and chemotherapy
4. If advance disease total gastrectomy with distal esophagectomy transhiatal lympn nodes removal
5. If no advance disease 2 stage Yvor Lewis abdominal and thoracic approach
6. Paleative treatment if peritoneal disease
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Chronic mouth ulcers are common with type2 DM will not allow to continue low carbohydrate diets .
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Greetings from Muller Family!
Thanks for reply.!can you inform me concentration of peroxide?It is literally burning!we tried at first with this but after stopping within months soreness comes back !
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what is the effect of collagen on diabetic ulcers?
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Collagen-containing wound dressings have been used in the treatment of diabetes-related foot ulcers (DFU). Collagen components, such as fibroblast and keratinocytes, are a major part of skin development. Collagen may be harvested from a variety of sources including living and nonliving bovine, porcine, and equine skin. Once harvested (via a proprietary process), a native collagen bioscaffold matrix is created that stabilizes the vascular and cellar components, which become incorporated into the wound bed.1 Preliminary findings suggest that collagen-containing wound dressings may have several advantageous features. Cullen et al2 reported the findings from the testing of an oxygenized regenerated cellulose (ORC)/collagen dressing. After use of the ORC/collagen dressing, researchers analyzed wound fluid and found a significant decrease in collagenase-like activity; gelatinase, matrix metalloproteinase (MMP)-2, and MMP-9 levels; and increased scavenged free radicals and binding of growth factors.For more please at the following link, its free paper.
Regards
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can we use from collagen in wound dressing for faster wound healing?
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I think it's better for cells migration and proliferation. 
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How can one detect diabetic ulcers and eliminate it at an early stage?
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Dear Dr. Khandare,
I think it is better localize your question in diabetic foot as the most common ulcer in diabetes.
Regards,
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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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Unfortunately, many people still depend on Aspirin as a rapid analgesic for many chronic diseases for a long time, their stomach is subjected to ulcer, and recently some researches recommend Aspirin for cardiac patients although many selective COX inhibitors are discovered, that's made me ask why these researches ignore the other risks for Aspirin.
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Dear Mohamed Aoued
Personally I take acetylsalicylic acid 100 mg for over 4 years. This is an antiplatelet agent. I read a lot of studies have been performed on patients with cardiovascular disease. It Seems that gives excellent results.
Syncerely
FADEL  
 
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I am intersted in viewing the latest research on device related pressure ulcers.  Particulary how to prevent PrUs under trachs, BIPAPS, vent tubes and nasal canulas. I am not finding anything new since Joyce Black's published work in 2010.
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There are at least 2 devices that seem promising"
- MOViNSESE by  kinematix
-Compliant cocept
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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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There a many causes of colonic ulcers in tropical countries.
History of 2 weeks fever with pain upper abdomen without any bowel symptoms.
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Solitary caecal (better paravalvular) ulcer is well known.
In metropolitan France, it is usually idiopathic,sometimes to slow-release NSAID tablets rarely and  due to Behçet's disease.
It is very frequently asymptomatic and, when idiopathic, disappears within 2 months.
When NSAID induced, cicatrization occurs with 1 month after withdrawal.
In the my case of Behçet's, it has disappeard within 2 weeks after starting amiodarone for arrythmia, in parrallel with aphtous buccal ulcers.
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We have run across a tumor cell line with a high-incidence of ulceration formation (leading to early euthanization in tumor-growth experiments). During a conversation with another group the idea of using Matrigel during injections was suggested as a means of preventing this.
Does anyone have any relevant experience with this solution (Subcutaneous injections)?
Alternatively does anyone have suggestions for reducing incidences of tumor ulcerations?
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Don't think so - Matrigel is primarily used to avoid dissemination upon injection - I think that the matrix is cleared and replaced by a proper matrix quire rapidly. Ulceration is more tumor-dependent I am afraid. It may be worsenen by the localization as well. Breast cancer (e.g., Mammary fat pad models) tend to ulcerate more frequently/rapidly since the tumor is more likely to be in contact with the ground when the mouse moved and frictions may increase the phenomenon.  When s.s.c. grafting on the flank or on the back, the same model (MDA231 for instance) showed fewer ulceration. It may depend on the tumor size as well - normally small tumors are less likely to ulcerate, based upon my own experience.  Reducing the number of cells to be injected could be a solution (we gave up the "1 million cells ssc" paradigm in my unit and start with 80-150 000 cells; works fine). I hope this helps?
Best, 
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Trying to find someone with expertise on treating this disease.
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Yes, i have experience in management of patients with Buruli ulcer
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These patients have increased risk of stress ulcers like any intensive patients but H2A have myelosupression potential and IPP increase risk of bacterial transposition from the gut. Antacids?
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We usually use IPP in critical period around transplantation, the risk of bacterial transposition could be decreased by appropriate food preparation.
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In the setting of prescribing anti-ulcer medication please comment on the following combinations :
1.Ranitidine with Omeprazole
2.Antacid with Ranitidine
3.Sucralfate with Omeprazole
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Poly phramcy. this trend was recently strated with pantoprazole and domperidone.magine wht could happen when a lay man uses this medication along with bowel stopper.
there must be some strong reason if two drugs of the same category are added.
triple drug Anti diabetics have laimed more lives.
waht if an heart patient ahs to use cardiac drugs with PPI.
Since antiacids are used most often without prescriptions it wuld be best not to combine two drugs.
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I am a psychology student and I am currently searching for the cause of ulcers. (gastric- peptic- or dudodenal) related to psychological or psychophysiological factors. I think that ulcers are not primarily caused by stress. Does anyone know good research regarding this topic?
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Ulcers pathogenesis is linked to first aphorisma of Swartz: No acid, no ulcer, successively modifed by Marshall into: No Helicobacter, no ulcer. These two apparent contradictions are easily reconcilable. Ulcer does not develop until there is a correct balance among aggressive intraluminal factors (expecially HCl and pepsin) and barrier function (epythelial turnover, mucosal levels of prostaglandins, neutral mucin production, microcirculation). Helicobacter pylori has the ability to induce a deregulation of these factors, but NSAIDs may do the same interacting with prostaglandins. And so uraemia or congestive gastropathy due to portal hypertension or diabetes by inducing delayed gastric emptying and altered micricirculation may alter the balance between protection and aggression to gastric mucosa. Stress could play a role through an alteration of rain-gut axis that at the moment is an interesting and promising field of investigation.
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Should I assess the GI damage of a 4-week period of NSAID use by endoscopy, histology or Visual Analogue Scale for dyspeptic symptoms? Which one would be the best choice to show the damage?
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Upper endoscopy cannot be proposed as a routinary investigation, it needs to be performed in the case of alarm symptoms (haematmesis, melena or ulcer-like acitve clinical signs, which occur simultaneously to NSAID administration). Moreover, it may investigate only gastro-duodenal injuries and not intestinal ones which are more frequent than estimated. A specific histological picture does not exist for NSAID damage, it may be useful to detect a simultaneous presence of Helicobacter pylori. Dyspeptic symptoms may be related to a lot of factors and are not specific. On the light of cost-benefit ratio, I think that a good approach could be the detection of the blood in the stools and fecal calprotectin baseline and in the course of treatment. Chenges in the results may indicate a potential iatrogen effect and stimulate further investigations in a limted sample of patients.
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Most of the research papers available are anti-ulcer activities of so and so drug. Is it a correct term for natural drugs, because mostly they are used for prevention of ulcer, not for treatment. I think instead of anti-ulcer, gastro-protective is the right term for such drugs.
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Gastro Protector - its natural, Like a Preventing Particularly to GIT.
Anti- Ulcer - denotes Preventing from Ulcerative Problem(common Ulceration Preventor).
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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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Corticosteroids like prednisolone are effective in controlling severe idiopathic oral ulcers. Their use though is not without side effects especially when prescribed in high doses and for long periods.
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Yes, Dear Najla. As a minimum, baseline laboratory tests are: Complete blood count with platelets, Liver function tests, serum creatinine, urine analysis. These must be repeated after a month, then every 2 months. One must also know if there is a history of hepatitis, and do a tuberculin test. In doubt, do get the full battery of viral tests for hepatitis B & C. Good luck. Usually azathioprine is very well tolerated if there are no infections.