Science topic

Peritonitis - Science topic

INFLAMMATION of the PERITONEUM lining the ABDOMINAL CAVITY as the result of infectious, autoimmune, or chemical processes. Primary peritonitis is due to infection of the PERITONEAL CAVITY via hematogenous or lymphatic spread and without intra-abdominal source. Secondary peritonitis arises from the ABDOMINAL CAVITY itself through RUPTURE or ABSCESS of intra-abdominal organs.
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A very Emergency case, The Mother of my best friend, the results of her MRI said that she had nodular peritoneal thickening that suggested peritoneal serosal carcinoma, and ovarian cancer, also she has ascites, what is the source of ascites in case of high CA-125? We are suggesting a surgery to remove the ovarian, peritoneal biopsy and taking different samples to histology laboratory for culture and characterization, Any Informations would be helpful and well Appreciated, Many Thanks
Ali
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I am NOT a doctor but as compter science professional, little more AI provided detail:
In cases where there is nodular peritoneal thickening, ovarian cancer, and ascites, the source of ascites can be the result of various factors, including the presence of cancer cells in the peritoneal cavity.
CA-125 is a tumor marker that is often elevated in cases of ovarian cancer, although it can also be elevated in other conditions. The presence of high CA-125 levels, along with the imaging findings of nodular peritoneal thickening, suggests the possibility of peritoneal serosal carcinoma, which is a type of cancer that affects the lining of the abdominal cavity (peritoneum). Ovarian cancer can sometimes spread to the peritoneum, leading to peritoneal serosal carcinoma.
Ascites refers to the accumulation of fluid in the abdominal cavity. In the context of ovarian cancer, ascites can occur due to several reasons, including:
1. Peritoneal involvement: Cancer cells can spread to the peritoneum, leading to inflammation and the production of fluid.
2. Impaired lymphatic drainage: The presence of cancer can disrupt the normal flow of lymphatic fluid, leading to its accumulation in the abdomen.
3. Liver involvement: Advanced ovarian cancer can involve the liver, leading to impaired liver function and fluid accumulation.
Surgery, as you mentioned, is often a crucial component of the treatment plan for ovarian cancer. The specific surgical procedures performed can vary depending on the individual case, but they may include removal of the ovaries (oophorectomy), peritoneal biopsy, and collection of various samples for histological examination. These procedures aim to obtain a definitive diagnosis, determine the extent of the disease, and guide further treatment decisions.
Please consult qualified healthcare professionals who can provide personalized advice and guidance based on the specific details of your best friend's mother's case. They will be able to provide the most accurate information and help determine the most appropriate course of action.
Hope it helps
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With regard to patients suffering form spontaneous bacterial peritonitis, it seems counterintuitive that those patients tend to NEVER have anerobes as the causative agents despite the common leakage theory that should allow anerobes (that fill the gut) to leak whenever the opportunity is present? Is the leakage theory a sloppy theory? Do we need to tinker it a little bit? Should we adapt a new theory?! Or, should we go playing more in our labs hoping to uncover the real etiology and decipher this anerobes enigma?
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The main bacteria causing spontaneous bacterial peritonitis (SBP) are Escherichia coli and Streptococcus viridans) and not Pneumococci
Usually, 75% of spontaneous bacterial peritonitis is caused by infections by aerobic gram-negative organisms (50% of these being Escherichia coli). The remainder has been due to aerobic gram-positive organisms (mainly Viridans group streptococci).
Anaerobic organisms are rare because of the high oxygen tension of the ascitic fluid. A single organism is noted in 92% of cases, and 8% of cases are polymicrobial.
For details, please have a look at this Medscape article link under Pathophysiology and Etiology:
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I am trying to establish an ovarian cancer preclinical model through peritoneal injection into C57BL/6 mice.
The parental ID8 p53-/- cell line was modified through lentiviral infection in order to express OVA peptide and GFP-luciferase. We injected 5·10e^6 cells per mice.
In day 40 after injection we did not get any tumor in any of the mice.
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Couple things.... the ID8 cells you generated are expressing 3+ new proteins, each on their own can potentially slow tumor growth by increasing the immunogenicity of the tumor (especially for OVA). Knowing this, you should have included a set of mice with the parental ID8 p53 -/- along side as a positive control.
If you failed to see tumors in your positive control group, you either didn't inject as many cells as you thought (i.e. counting errors, substantial cell death) or you were working with a different cell line.
The original parental ID8 cell line grows very slowly (8-10 weeks), and the ID8-OVA cells are sooooo much slower (12-15).
Check these papers out.
The original ID8 p53-/- paper
Walton, J. et al. CRISPR/Cas9-Mediated Trp53 and Brca2 Knockout to Generate Improved Murine Models of Ovarian High-Grade Serous Carcinoma. Cancer Res 76, 6118–6129 (2016).
ID8-Luc2
Baert, T. et al. The dark side of ID8-Luc2: pitfalls for luciferase tagged murine models for ovarian cancer. J Immunother Cancer 3, 57 (2015).
ID8-GFP
Lee, W. et al. Neutrophils facilitate ovarian cancer premetastatic niche formation in the omentum. J Exp Med 216, 176–194 (2018).
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Hello!
My SR with meta-analysis will be looking at risk-reducing salpingo oophorectomy on ovarian/peritoneal/falloptian tube cancer risks, as well as risk-reduction mastectomy on breast cancer risks in BRCA2+ carriers.
For the inclusion criteria, am I allowed to include people who previously had breast cancer in my search for the ovarian cancer risk-reducing salpingo-oophorectomy data and people who never had breast cancer before for the breast cancer mastectomy data?
Meaning, am I allowed to have two types of inclusion criteria in one SR as I have two study types being analyzed, or must it only contain people with/without breast cancer? The unifying factor is that all participants are BRCA2+ carriers and are women.
I hope this makes sense!!
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Before trying to give a tentative answer, I would like to ask: What is your research question / are your research questions? And a bit nitpicky: Allowed by who?
My impression is that you have two quite distinct research questions:
- What is the effect on ovarian cancer of salpingo-oophorectomy in women who are BRCA2+ and have a history of breast cancer?
- What is the effect on breast cancer of mastectomy in women who are BRCA2+ without a history of breast cancer?
I expect that you will find no trials that address both questions at the same time, and even if they do, they will very likely report on the two questions separately.
Whether you say that you do one SLR or two does not seem to matter substantially, therefore I would say: call it what you think is best.
Doing one or two meta-analyses of course does make a substantial difference. I see no reason why you would want to put both those questions into one meta-analysis but maybe you do. E.g. is there any provider interested in the result of that one meta-analysis? (I can’t imagine that any patient has that interest, if only because no-one patient can have both a history of breast cancer and not have that.)
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I'm pretty sure they are mostly macrophages since after a 2 hour incubation in M199 they are stuck with pseudopodia. My slides just aren't pretty enough for me. I'm using Fisherbrand Wight-Giemsa Stain on rabbit cells from a peritoneal wash (days after drawing monocytes to the location with a peritoneal proteose peptone injection). But my concern is that at some point my counts are off because I can't distinguish between macrophages and other large multi-nucleated cells.
My method:
20uL of 10^6 Trypan blue visualized cells are spread, dried using a Bunsen burner, and then fixed with Methanol for 60s.
Slide is flooded with 1mL Wright-Giemsa Stain and incubated 2 minutes.
Add 1.5mL 1X PBS at pH 7. Gently tipped to mix, for 1 minute.
Stands for 2min.
Rinsed well with De-Ionized water.
Dried and visualized at 400X.
Does it have to air dry rather than use a flame?
I am just having a hard time with the outer membranes. Should I use a different method?
Any help is appreciated!
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This is a common problem if the stain used is old, or not mixed properly if using after a long time. I would suggest, you use a fresh bottle of stain (if using ready-made) or just make a new stock. We prepare Giemsa stain and when used after 4-6 months, we usually don't get good staining.
Give it a shot.
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Women undergoing risk reducing bilateral salpingo-oophorectomy especially if they are BRCA1 or BRCA2 pathogenic variant carriers are warned of a residual risk of primary peritoneal cancer. A meta-analysis of studies showed only a 79% reduction in risk of ovarian type cancer after BSO in BRCA1 and BRCA2 carriers. Meaning for a BRCA1 carrier there could still be a 10% risk of primary peritoneal cancer with a high likely mortality rate. Having been involved in referring women to a gynaecological service that undertakes very careful surgery with bagging of the tubes and ovaries we have only now seen our first primary peritoneal cancer after more than 38 years of operations on nearly 600 carriers. Given that it is now thought that the great majority of high grade serous ovarian cancers originate from fimbrial precursor cells rather than for instance ovarian rest cells we feel that if careful surgery is undertaken early enough before the main risk period that this risk reduction is likely to be >95% rather than only 79%. This means a residual risk of only around 2% for BRCA1 and 1% for BRCA2. Do fellow clinicians agree?
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Risk of peritoneal cancer after risk reducing SO in BRCA mutation carries depends on timing and technique of surgery ranging from 1to 10%.Counselling and patient selection is important.
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I am studying phagocytosis/efferocytosis in vivo and have been using the peritoneum as a source of cells, but have a very low yield of dendritic cells. I also have a lot of CD19+ B-cells that take up 50-60% of the peritoneal exudate cells.
What would be the best tissue site for studying dendritic cell phagocytosis in vivo so that I can get a good yield.
Most protocols that use the peritoneum focus on macrophages.
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Skin would be best source IMHO, but harvesting might be challenging. DC make up <1% of circulating PBMC in blood, that's why we draw blood for the monocytes first
Good Luck
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In a stab or gunshot wound, is peritoneal violation alone (without any intra-abd. organ injuries) an indication for laparotomy? Previously I was under the impression that any time a non-sterile object is introduced into the peritoneum, it WILL get infected and cause peritonitis, and so you had to wash out the abdomen. However, it seems some stab wounds can be managed conservatively, even if it enters the peritoneum. So what is the general principle here?
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As a General Surgeon, residing in a crisis ridden environment,
I have personally managed several cases of penetrating abdominal wound- Non-operatively. For such patients early; prompt and repeated assessment is mandatory with - CT scan, Focused Assessment with Sonography in Trauma (FAST)- Abdominal and Plain radiograph of the abdomen which showed non-peritoneal or very minimal peritoneal transversations- otherwise adjudged as minimal peritoneal contamination.
The Key to such NON-OPERATIVE CARE is based on 1) patient is hemodynamically stable, 2) Vital Signs like Temp.; Pulse rate and Respiratory rate and BP and other clinical parameters remain normal and stable over and above 72 hours of care.
The decision to embark on OPERATIVE CARE including Laparoscopy (Diagnostic & Therapeutic) or Emergency Laparotomy is hinged on deteriorating overall parameters regarded as Severe Peritoneal contamination== Generalized or Localized Peritonitis as the case may be.
Thanks for the nice question
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by lavage peritoneal, could i get macrophages in high purity? and how many macrophages can i get by this procedure?
Please share your experience that may helpful to my experiment. Thanks.
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You are welcome :)
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Cause : Usage of Asbestos as insulator . Effect : Mesothelioma cancer ; Lung / peritoneal /larynx and ovary (8) cancer .
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Naser Ahmed Mahmoud Elsawy
Thank you , this is very helpful
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Thanks in advance
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Im not sure what you need the cells for, but I have only heard of peritoneal lavage on dead mice. I would think that it could be done on a live mouse (it is no more invasive than abdominal surgery) but it depends on your ethics committee.
If you are after a serial source of infiltrating monocytes/macrophages, measuring chemoattractants or infection, you could consider the 'air pouch' model where a subcutaneous space on the back is inflated with air and exudate can be washed and collected serially.
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Hi!
Can anyone suggest a protocol for intracellular staining of peritoneal mast cells for cytokine detection by flow cytometry?
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I wish to know if peritoneal injection of MSU in mice is proper study model for gout? Most common are air pouch model or ankle inflammation. Is peritoneal based gout model are clinically relevant?.
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Thank you Flavio....
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Hi!
In our lab, we are currently having a lot of trouble with extracting RNA from rat peritoneal mast cells. Mast cells were isolated from rat peritoneum and a method of Chomczynski was used to extract the RNA. We have obtained yields of 0.8 ug/uL RNA (from 0.5x106mast cells); A260/280 ~ 1,99. But in qRT-PCR we obtained unsatisfactory results.
Thanks a lot.
Elzbieta
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Dear Elżbieta Kozłowska,
Can you describe your problems with PCr in more detailes? It is likely that the problems are not related to the isolation of RNA, but to subsequent stages.
Best regards,
Maxim
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a patient in septic shock on high vasopressors due to secondary peritonitis(?diverticular rupture) ,cannot be mobilized to CAT scan as surgeons requested
the ultrasound showed fluid with floating debris and sediment
can the drainage of the peritoneal cavity help to stabilize the patient even temporarily?
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Are abdominal carcinoid carcinomas having peritoneal mets sensitive to chemotherapy agents used intraoperatively? Is cytoreduction surgery of peritoneal mets in carcinoid carcinomas complicated by potential for initiating neuroendocrine syndrome?
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My pleasure
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PD chronic therapy
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The changing of the titanium adaptor should always be performed with strict aseptic technique. However, since the titanium adaptor can be difficult to remove, it is always a concern that the PD nurse could accidentally contaminate the distal end of the PD catheter or the new titanium connector, thus putting the PD patient at risk for peritonitis from touch contamination.
In general, unless the titanium adaptor for some reason is obviously soiled, we would not recommend changing the adaptor routinely with each episode of peritonitis.
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Hello,
We test the effect of different substances on the immune cells of the peritoneum. After activation we sort them and we now want to run a gene expression array.
The problem is that after they are activated cells of course start to migrate. This is especially problematic for the macrophages (they migrate super fast).
SO...
1. How do I block the migration of the macrophages?
2. How do I block migration of the B1a cells?
Your response would be very very very much appreciated!
Cheers!
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1) The most important rule: all operations with viable macrophages should be performed on ice using icy solutions. 
2)To prevent migration, the activating stimulus needs to remain in the peritoneum during activation. So, you will need activating substance in high molecular weight not allowing absorption in peritoneum or this substance in immobilized form on any particles, beads or erythrocytes.
3) If the activation requires short time, you can use i.p. injection of activating substance and, then, after cervical dislocation to inject i.p. cold (icy) PBS (5-10 ml per 1 mouse). After subsequent shaking of inflated peritoneum during 1 min you can aspirate  peritoneal lavage containing macrophages. Cold PBS will prevent migration of macrophages and losses due to their adhesion to the walls of vessels.
Sorry, I have no idea what to do with B1a cells.
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Lambeck et al., (2007) detected that the median concentration of serum IL-7 in healthy patients is 2.9pg/ml. They have also detected that the median concentration of serum IL-7 in ovarian cancer patients is 5.3 pg/ml.
While Xie et al., (2004) have estimated that the median serum level of IL-7 in ovarian cancer patients is 32.49 pg/ml, and the median peritoneal level of IL-7 (mainly by tumor cells) in ovarian cancer patients is 17.39 pg/ml.
I need both the shedding rate and shedding fraction for IL-7, can I get them from its level (conc.) in the serum or the peritoneal fluid? 
Trinder et al., (1999) have estimated that the production rate for IL-7 in renal cancer cell lines is ranging from 3.9 to 15.1 pg/ml/10^(6) cells/day. Can I benefit from this information in estimating the production rate for IL-7 in ovarian cancer?
Thanks in advance.
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Sorry. No idea.
I am a clinician.
Regards
Bernardo Rapoport
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I wanted to stain for B-1 Cells in mouse peritoneal cryo samples. I dont know which antibodies should i use for the classification , B220 and CD5 are one which i thought i could use? Does anyone knows the sure/ correct method for the labelling of B1 cells in IHC..
Thank you
seeking your kind assistance...
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CD5 is a good marker for identifying B1 cells, but cannot be used on its own because it will label T-cells as well.
I haven't tried this myself, but I would recommend a combination of CD5 and a B-cell-specific transcription factor, e.g., Pax5. This should work in immunohistochemistry because it combines a membrane antigen (CD5) with a nuclear antigen and discrimination of signals should not be a problem.
Good luck
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Distinguishing between peritoneal and other (liver, lung, brain and bone) metastases for metastatic stomach adenocarcinomas can be important in directing chemotherapy. Was there a way to distinguish peritoneal metastases from the other metastatic sites using SEER data before 2010?
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Dear Dr. Morgan,
Sorry I can not answer your questions, because I do not work in this area of research.
DANIZA MARÍA IVANOVIC MARINCOVICH
Profesora Titular
Universidad de Chile. INTA.
Investigadora Responsable
Proyecto FONDECYT 1100431-1150524
Avda. El Líbano 5524
Casilla 138-11
Santiago, Chile.
Teléfono: (56) 2 9781459
FAX: (56) 2 2214030
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I want culture macrophage from peritoneal rat with alternative natural product than RPMI
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The question is not clear!
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Would this patient be at risk for peritonitis?
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To the suggestion of Craig Lum  i would add an advice to use presternal peritoneal catheter
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46year old woman who underwent open resection of Fundus for GIST 4years ago with recurrence at the site and two peritoneal nodules near the spleen.Ever since surgery she is being followed by a medical oncologist.Pet scan one year ago was normal.
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Thanks Andrey,
upper GI endoscopy is normal,pt has beensent to the oncologist to down grade the tumour prior to surgery
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36 years old male with advanced splenic flexure carcinoma with involvement of the anterior abdominal wall, stomach and small bowel. HPE revealed moderately differentiated (Greade 2 to 3) adenocarcinoma. pT4bN1bMx. Received 12 cycles of Folfurie with avastin. Now PET CT shows Hypermetabolic spots, one 1.4X1.6 cms at anastomotic site and another 1.4X1.5 at left hypochondrium region(Peritoneal deposits).
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I agree that histological confirmation of actual metastatic disease is warranted; this could be achieved either by percutaneous biopsy or laparoscopic exploration. Laparoscopy would have the added benefit of establishing the extent of peritoneal disease and the possibility of a complete or near-complete cytoreduction. Also, colonoscopy should be done to rule out any metachronous colon lesions.
If and when peritoneal metastases are confirmed and you are certain that the liver remains clean, I would recommend proceeding with CRS-HIPEC. The question of whether he would require any additional systemic chemotherapy after his CRS-HIPEC depends on the success of the procedure. Good luck!
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How often you meet false negative results at the relatively low but pathological levels of PMN in ascitic fluid (for example, polymorphonuclear cell count <500 cells/mm3)?
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 I think manual cell counter is a best method. I was see sometimes strong difference betwen this 2 methods and in my experience normally the manual method y more consistent with the others clinical and laboratories parameters
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Hi all, I'm trying to do immunofluorescence on smears from peritoneal fluid, and I get some autofluorescence from eosinophils mainly. Does anyone know any method or something to avoid it? I usually do the washes with PBS+ tween 20 0'5%+ 1% triton-X. What do you think about it? thank you very much in advance.
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OK Nikolas, thank you so much! I'll try with PFA fixation. I use acetone fixation because the smears are stored at -80ºC, and I've never used before other kind of fixation with these samples. Thank you again for all.
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Plz let me know about incidence(%) of osteomyelitis, Septic arthritis, Peritonitis through all ages in USA and EU.
I study a new vaccine for MRSA ..
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Dear Dr. Kang,
Your question is a very difficult one. You are asking about incidence ? of a variety of septic conditions (from osteomyelitis ... to peritonitis). These conditions belong to different specialties, and  you should have to look in the specialized literature on this topic in the different specialties.
But first of all, you should have to clarify whether you are looking for data about the "incidence" or "prevalence". These are different terms and the rates are also different. The incidence rate is measured for a certain period (i.e. one year) and is more variable, while the prevalence is more constant and is measured cross-sectionally for the whole population or for groups of population (age, gender, profession, etc.).
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I'm looking for a protocol for MGG staining protocol for BAL and peritoneal cells smears for the morphological assessment of the different cell populations.
Is it the same as the standard protocol used for blood smears?
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Get your BAL and peritoneal washings unfixed. Make cytospins and air dry the spins. Then try an ordinary MGG protocol. You can make adjustments to the staining in the washing procedure at the end, if necessary. You should filter your Giemsa solution often, to avoid staining particles to pollute and disturbe the cellular materiale.
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Thanks in advance....
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Hi Kathiravan,
this is not an easy task. If you want to convert the dose from oral to i.p. you need to have in mind a lot of things that happens with the compound that you are applying. I.P. route is convenient for liposolubile compounds but oral route is preferable for drug application in humans. To make my answer shorter: if you dont know the pharmacodynamics and pharmacokinetics of the compound for either of this way's of application it is hard to predict the exact dose that you need to apply. 
You can always give several similar doses and check their effects in animals.
all best
Nikola
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We are studying the IL-1b secretion by TG-elicited mouse peritoneal macrophages, but saw a big variation in the amount of IL-1b secretion after LPS and ATP stimulation. We normalize the cytokine amount to the BCA data, and saw the IL-1b level could range from 30pg to~350pg per ug of cellular protein. We usually flush the peritoneal cells at 72hr after TG ip injection and culture the exudate cells in medium, at 37C overnight to allow macrophages to adhere. The following day, we will wash the cells once with PBS to remove the floating cells and stimulate the adherent macrophages with LPS (4hrs) and ATP(30mins. ATP in small aliquot, no freeze-thaw). The harvested supernatant will then undergo a brief spin (~3000rpm, 5mins) and IL-1b is measured by ELISA (R&D kit for mature mouse IL-1b). We used both male and female mice. But is such big variation in IL-1b level normal?
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Difference in the rate of adherence might be crucial. I don't have an experience with Jackson lab mice. But animal facilities can be a huge problem and it is very difficult to deal with that. And TG should be sterile, of course. Microbiological control could be nice in this situation, but not always possible. Just try to do your best. And I would also check is it really good idea to use TG. We normally use it to address bactericidal activity of macrophages. Sometimes it is better to use naive residential peritoneal macrophages without stimulation (warm medium  is a trick).
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The peritoneal adhesions have been one of the major challenges for both the surgeons and the patients themselves. All treatment modalities ever suggested to solve the problem show low, if any, effectiveness. On the other hand, the serosal lining disappears on the posterior surfaces of the duodenum, pancreas, and the ascending and descending colon; the mesothelial 'processus vaginalis' in the spermatic cord vanishes as well during the embryonic development governing by some genes. So, one may expect that those very genes might become of use for the peritoneal adhesions to diminish or even to resolve completely.
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Well, I was seemingly wrong having this idea that the mesotheliocytes'  hyperproliferation might lead to the adhesions and peritoneal fibrosis development. Quite the contrary, the fibroblasts become activated and proliferate excessively after the disappearance of the mesothelial lining as the consequence of the deliterious necrosis and apoptosis of the cells have already occured and if the lining failed to restore in due time.
So, the idea has turned full circle and came again to that that has been known for long.
However, there have been some evidence that the mesotheliocytes, being the cells of the mesenchymal origin, and able themselves to differentiate into various mesenchymal cells including the fibroblasts, myocytes, etc., under conditions those are not understood completely [Rinkevich Y, et al. Identification and prospective isolation of a mesothelial precursor lineage giving rise to smooth muscle cells & fibroblasts for mammalian internal organs, and their vasculature. Nat Cell Biol. 2012 December ; 14(12): 1251–1260].
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I'm using REDCap for the first time and wanting to track peritonitis episodes in patients on peritoneal dialysis. These may happen multiple times per patient. There are no strictly defined visits (as there would be in a clinical trial) and there will be indefinite follow-up - I'm therefore using the traditional, and not the longitudinal, REDCap setup.
I'm thinking that I should have a new/different data entry form for each episode of peritonitis e.g. episode1, episode2, etc. This just feels very clumsy though so I would appreciate any other suggestions.
Thanks
Razeen
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Do a search for "adverse event" in the official REDCap forums (see link below), they have many workarounds there.
Instead of using a form for each episode of peritonitis, you could use one general adverse event form, add many adverse event variables (let's say 10), and use branching logic in order to hide the variables that aren't needed. You can always add more variables if needed.
Check out the REDCap shared library, you can find some useful templates for Adverse Events (there's even one with branching logic).
Hope this helps,
Hendrick.
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The fear is Peritonitits fronm cdiff translocation
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actually many systems prevent peritonitis and patient training should obtain this ; manual systems ( CAPD ) or automated systems ( nocturnal or daily peritoneal dialysis )  are used for different pts peritoneum characteristics however peritonitis prevention is always the goal
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I want to generate polyclonal sera in mice by injecting hybridomas in peritoneal cavity of mice. Could anybody recommend a simple protocol to isolate the cells from peritoneal cavity once again! 
Regards
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A hybridoma by definition and by the way it is generated produces only one type of antibody, i.e. a monoclonal antibody. It is unclear from your question whether you want to inject one hybridoma or several. In the first case you get an ascites with a monoclonal antibody, in the second case a mixture of several monoclonal antibodies, which does not equate with a polyclonal serum. Polyclonal sera are often made by injecting the antigen into rabbits or goats, then collecting the serum from blood samples.
In any case, making ascites is considered painful to mice, and would need a very good justification why it is preferable way of producing antibodies over in vitro cultivation of your hybridoma(s).
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A lady, 29 years old, five years history of Crohn disease, quite moderate. No family history traced.
The patient referred to the gastroenterologic department on the 6th of May with a vague abdominal pain, subfebrile body temperature, and sulfosalicilates were prescribed 500 mg thrice a day. On the 8th of May, about 7.00 a.m. a bout of severe pain along the whole stomach. A surgeon on duty examination was performed, and the patient was transferred to the 1st department of Surgery at 7.15. A pneumoperitoneum under the diaphragm was recognized on the X-ray upright position. The lady was taken into operation room, and the midline incision was made. Approximately 2 L of the intestinal contents was revealed in the abdominal cavity. Futher examination discovered a loose inflammatory mass in the right iliac fossa, and a perforation of the mesenteric border of the ileum as less as 10 cm from the ileocaecal junction.
I have never met before a perforation into the free abdominal cavity due to the Crohn disease. What would be the best way to complete the operation? What medication would be the best choise for the patient?
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What have we for today:
The patient is walking along the ward, eats and drinks. There has been no high temperature for 4 days of the post-operatinal time. No vomit. A once-a day-stool.
As for the blood routine tests, they as follow:
Er - 1.87*10^12; Hb - 49 g/L; Ht-13.9%; Le - 9.1*10^9; n-16; s-64; l-12; M-8.
the general serum protein - 45.1 g/L; urea- 4.9 mmol/L; creatinine - 61 mcmol/L; glucose - 3.54 mmol/L; ALaT - 2.1; ASaT- 8.2; alpha-amylase- 189.3 IU/L; K+2.4; Na+139; protrombine index- 94%; fibrinogen - 3.9 g/L; bacterial growth from serum- sterile; osmolarity - 279 mmol/L; proseptine - 583 pg/ml;
From the abdominal cavity were detected growth of:
E.coli - up to 10^6 CFU/g
Ent.faecalis - up to 10^6 CFU/g
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Some say, a methylene blue test, but others say it may cause chemical peritonitis.
Is glucose measurement a reliable test?
What are some other diagnostic tests and how are they performed?
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Glucose measurement was OK for us for years, still is...
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Distention of the small intestine loops by liquid and gas content, along with contemporarily disappearance of the colon 'pneumatization', are characteristic for the severe secondary and for the tertiary peritonitis cases. One may suggest that either phenomena are developed due to, or connected, with dramatic changes of both the small and large intestines microflora quantity and quality.
However, I could find no data on this matter. I would be obliged for any help on the topic.
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Interesting question but to the best of my knowledge this has not been studied.
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I'm trying to identify the effect of different cytokines on the level of F4/80 expression in macrophages from the peritoneum that may be produced when sterile inflammation is induced. I understand I will be checking in isolation and in vivo, as it maybe different.
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I recomend you old paper: Ajuebor MN, Das AM, Virág L, Flower RJ, Szabó C, Perretti M. Role of resident peritoneal macrophages and mast cells in chemokine production and neutrophil migration in acute inflammation: evidence for an inhibitory loop involving endogenous IL-10J Immunol. 1999 Feb 1;162(3):1685-91.
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One of my 40 year old patients, since 6 months on PD has from the start a complete symptom free phenomenon of a pink bag every morning after the long dwell. He is completely syymptom free, has no secondary symptoms suspicious for malignancy and no weight loss. He has stable blood results including a normal Haemoglobin without EPO. Hardly any WBC, cultures all negative. The exit site looks great and there has been no peritonitis. Abdo US normal with normal catheter position. He is a high average transporter and ultrafiltrates well on low concentration standard dextrose bags.
I tend not to worry about it. Anybody here different opinion and any further explanations?
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is the patient male or female? A pink bag is very common in female young PD patients every 4 weeks. Another benign cause of pink dwell is the use of calcium channel blockers.