Science topic
Inflammation - Science topic
A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function.
Questions related to Inflammation
Hay dolor inflamación , toma medicamentos para el dolor y la inflamación desde hace casi un mes
"Evidence is accumulating that in general, RNS {reactive nitrogen species}drive inflammation and cancers associated with inflammation." (Hofseth 2008)
"Nitric oxide production is increased in patients with inflammatory myositis." (Wanchu, Khullar 1999).
Can someone help me understand the reasons for the increased production of nitric oxide in patients with inflammatory myopathies?
A patient with desminopathy (mutation Thr341Pro DES in a heterozygous state) with the progression of the disease has a decrease in taste and smell, immunosuppression, and an increase in IgA in the blood.
Oddly enough, but all this is characteristic of infections, including viral ones. For example, it is known that if the hepatitis C virus is not treated, then death will occur in 20 years.
In the identified case of late onset desminopathy, muscle weakness manifests itself at the age of 30, and death occurs 20 years after the onset of the disease.
Could the desmin mutation in myofibrillar myopathy be caused by an infection?
Perhaps the infection contributes to the progression of desminopathy?
Numerous studies have used the hRBC membrane stability assay to evaluate the anti-inflammatory activity of a certain compound or extract. I have also read that the membrane of lysosome and erythrocytes are comparable in terms of stability. Upon further reading, I think that there might also be a lot of differences between their membranes, especially the number and composition of the membrane lipids and proteins. These differences may reduce the reliability of the assay.
Is the hRBC membrane stabilization assay more of a screening method for anti-inflammatory activity? And are there studies that have intricately discussed and compared lysosome and erythrocytes membranes to support the validity of hRBC assay for measuring anti-inflammatory activity?
I have tried to prepare it, but couldn't get the crystals. This is the method that I refer to:
"4 g uric acid (Sigma) was dissolved and heated in 800mL H2O with NaOH (9mL/0.5 N), adjusted to pH 8.9 at 60C, cooled overnight in a cold room, washed and dried."
Instead of getting crystals, I found that my solution become very hazy and formed precipitate.
Can anyone please give me a suggestion or further information about preparing MSU crystals?
Thank you in advance.
What is the immunological test through which we determine the activation of microglia cells?

I would like to buildup a small active research group including a comprhensive subspecialities in Clinical Biochemistry, Molecular Biology, Internal medicine, statisticians to be shared in writing research articles, review, chapters and books. Who see him a suitable he can comment here with his email or whatsapp no to communicate later.
Does anyone know a protocol to induce inflammation in transwell Caco-2 cells? I'm having difficulty finding a strong and consistent model for that.
After 21 days of Caco-2 monolayer differentiation in transwell plates, my idea is to induce inflammation using LPS (1 microgram/mL) on the basolateral side. Studies however, present different ways of doing this: (a) by applying LPS to both sides (apical, basolateral) or (b) by applying LPS to only one of the sides (apical or basolateral). Also, many dosages are used by studies, varying from ng to micrograms.
Therefore, I'm very confused regarding which dosage of LPS to use and the compartment (apical, basolateral) of choice. If anyone has done this successfully, please let me know.
Thank you so much,
Greeting everyone,
Recently, our lab want to create an in vitro inflammatory cell model by recombinant TNF-a on either 3T3-L1 or HL-1 (cardiomyocytes). I read several articles and many methods showed they used serum-free medium when they added rTNF-a to the cell. However, I can not find any evidences that show FBS would influence the function of TNF-a in the cell. I think cells will under a starvation condition further trigger more stress signals and influence the result. Does anyone knows why those protocols remove FBS when they add TNF-a into the cell?
Thank you for your patience and response.
Best regards,
A patient with desminopathy survived Covid-19 six months ago without pneumonia, but with a temporary loss of smell and taste. After Covid-19, we note an accelerated progression of desminopathy, penetration accelerates, new muscles are quickly involved in the pathological process, muscle mass decreases, and heart function worsens. Perhaps the infection or its consequences are somehow connected with the mechanism of progression of desminopathy?
Hello,
The high-end journals Nature and Cell not only publish top-quality research but also very catchy schematic figures, for instance, those on infection
One thing that I have noticed is that these figures have remarkably the same style. I imagine that, if each team produced its own schematic image, the style would have been different. It look like, instead, there is a single person drawing these schematics.
The question I have is:
- does Cell (or Nature) have stardards for the production of schematic figures?
In other words:
1. does Cell have a publication team that produces the figures based on the drafts given by the authors?
2. alternatively, do the authors produce their own schematics following certain rules?
3. if 2, what are these rules?
4. are there ready-made vectorial files with the elements of these schematic figures (such as cells, molecules etc)?
Thank you
I have been trying to do immunofluorescent labeling of IL-13 in mice brains (on animals injected with LPS to simulate inflammation) without much success. I am currently using 35 micron thick slices prepared by cryostat, the brains have been flushed with saline and fixed with 4% PFA. I've tried a lot of different techniques such as antigen retrieval, using TSA amplification, etc., as well as changed a lot of variables such as varying length of blocking, primary antibody incubation, etc. If anyone has had success staining for IL-13 or any other inflammatory cytokines such as IL-6 in mice brain, could you share what methods you used? Thank you!
We recently conducted a research in my lab that used varying doses of i.p LPS injection with the aim of inducing intestinal inflammation and immune disorder. Doses of 1, 1, and 2mg/kg BW of LPS was i.p. injected at 17, 19 and 21 days old to broiler chickens accordingly. However, upon analyses, there is no effect of LPS on any of the immune parameters tested in the plasma and tissues. We detected the plasma LPS concentration using ELISA kits and there is no significant differences between the LPS treated and untreated group.
Please is there any scientific reason for this? The LPS was recently purchased and stored under accurate conditions prior to use.
In a patient with hereditary desminopathy (mutation Thr341Pro DES in the heterozygous state) over the past three years, an increase in the blood uric acid level up to 440-480 µmol / l was established by 1.5 times (the norm is 428.4 µmol / l). With the progression of the disease, the level has risen and is above normal. It is known that uric acid is an antioxidant. Is it necessary to reduce the level of uric acid?
The patient has no problems with the joints.
So many researches have proved the effects of chronic inflammation or oxidative stress on human health, but no systematic discussion about the relationship between both. From what we can know now, the inflammatory process can induce oxidative stress, in return, the oxidative stress can also induce inflammation. Is it possible to decide who comes first? Or it is a new chicken-and-egg problem?
In many animal pain models, FCA (Freud's Complete Adjuvant) and carrageenan are injected (in the paw for instance) to induce an experimental immune response and then, assess inflammatory induced hyperalgesia. While carrageenan-induced hyperalgesia lasts a few days, FCA-induced hyperalgesia can last up to weeks using the same species and the same mode of administration.
What are the molecular mechanisms that drives such differences, knowing that CFA and carrageenan are different in nature (heat killed Mycobacterium tuberculosis and polysaccharide extracted from red seaweeds) ?
Hi everyone,
Do you have any experience in preparing sample dilutions to measure the concentrations of inflammatory cytokines (TNFα, TGFβ, MCP-1, IL-1α, IL-1β, IL-6, and so forth) for an ELISA when it comes to any rat brain tissue, especially hippocampus. I'd prefer not to perform a pretest, and waste any well-strips beforehand. Based on your experience from different labs, what would be the expected protein concentration ranges of these cytokines in a supernatant saved from tissue homogenate prepared from a healthy rat (Sprague Dawley) brain tissue (hippocampus)?
Kind regards,
I induced ACh and SFb with TNFa and INFg for 96 hour. On the cell viability assay, I saw an increase in number of the cells in comparison with control condition. I read papers reporting that cell proliferation should be inhibited. Thus, reducing cell number. Any explanation for this?
Hi!
I become quite curious about mitochondrial behaviours in tissue.
How does mitochondria affect intercellular communication (both cytokine, small molecule, and mechano-signalling?
How is the mitochondrial influence in intercellular communication in the microenvironment of inflammation, stem-cell differentiation, tumor and neuro conduction of excitation?
How is the signalling pathway behind (both transcriptomic/proteomic and metabonomic)?
Are there some most nonnegligible/core article in this topic?
Thank you!
I have tried with no success various UV-B stresses but I did not find an increase in beta galactosidase.
I was wondering if euthanizing mice by carbon dioxide inhalation would cause activation of NF-kB inflammatory response?
Hello
Recently, I am curious to know about mechanisms of endometriosis and signaling pathways.
I have a question about the difference between signaling pathways in benign tumors and malignant tumors.
Since I studied, I noticed that the signaling pathway involved in benign and cancerous cells is similar, like MAPK signaling, Wnt Signaling, Apoptosis, Cell adhesion and angiogenesis.
So, what is the difference between endometriosis and ovary cancer in terms of pathway ?
Thank you in advance.
Kimiya
I'm working on establishing an murine infection model of the Prototheca algae. Not much is known about the dynamics of the infection, nor the induced immune response. I'd like to use the LEGENDplex Mouse Inflammation panel to measure levels of the cytokines in serum of sacrificed mice, previously infected with the algae via either three routes (intraperitoneal, intramammary and subcutaneously). However, I'm not sure what would be the best time point of collecting the serum, sufficient for infection to develop and to observe the change in cytokine levels.
Hi everybody,
I am working with a RAW 264.7 cell line to test the mRNA expression of the proinflammatory cytokines. Right now, I'm having some problems, hoping to get some useful advice.
RAW 264.7 cell line was cultured in RPMI medium supplemented with 10% FBS (no antibiotics). Culture conditions 37oC and 5% CO2.
I inoculated with a density of 8x10 ^ 5 cells / well ( 6-well plate). After 24 hours of incubation with the above conditions, I treated the cells with 1 ug/ml concentration of LPS. After 24 hours, the culture medium was measured for the NO value (Griess assay, NaNO2 calibration curve); however, the NO value was very low (below 5 uM) (no difference between the LPS-treated sample and the control)
Observed under the microscope, the RAW cell morphology (cultured after 24 hours) (as shown in the picture) was like the cells under stress.
I think that this cell line has been altered after many passes, so LPS does not inflame it.
I am just wondering whether different labs prepare immortalized bone marrow derived macrophages (BMDM) in their labs. I have experience of preparing primary BMDM from mice femur, but have no idea about immortalized BMDM. I would be grateful if somebody could answer my question.
Over the past three years, a patient with hereditary desminopathy (Thr341Pro DES mutation in the heterozygous state) has an uneven decrease in muscle strength in the hands. In the right hand, the decrease in muscular strength in the last three years is 2.1 times, and in the left one - 1.5 times. In a weaker limb, the disease progresses faster. A similar pattern is observed in the legs. The father of the patient had the same changes.
A patient with hereditary desminopathy (mutation Thr341Pro DES in a heterozygous state) with disease progression has a significant decrease in taste. How can this fact be explained?
"In chronic inflammation, IL-6 has a detrimental role that favours mononuclear cell accumulation at the site of injury, through continuous MCP-1 secretion, angioproliferation and anti-apoptotic functions on T cells [30]. This may increase serum levels of IL-6 and provide the basis for the amplification step of chronic inflammatory proliferation."
Interleukin-6 is released by monocytes and macrophages in response to other inflammatory cytokines which include interleukin-11, and tumor necrosis factor (TNF)-beta.
Chapter Chronic Inflammation
"Chronic inflammation can result from the following:
- Failure of eliminating the agent causing an acute inflammation such as infectious organisms including Mycobacterium tuberculosis, protozoa, fungi, and other parasites that can resist host defenses and remain in the tissue for an extended period.
- Exposure to a low level of a particular irritant or foreign materials that cannot be eliminated by enzymatic breakdown or phagocytosis in the body including substances or industrial chemical that can be inhaled over a long period, for example, silica dust.
- An autoimmune disorder in which the immune system is sensitized to the normal component of the body and attacks healthy tissue giving rise to diseases such as rheumatoid arthritis, systemic lupus erythematosus (SLE).
- Recurrent episodes of acute inflammation. However, in some cases, chronic inflammation is an independent response and not a sequel to acute inflammation for example diseases such as tuberculosis and rheumatoid arthritis.
- Inflammatory and biochemical inducers are causing oxidative stress and mitochondrial dysfunction such as increased production of free radical molecules, advanced glycation end products (AGEs), uric acid (urate) crystals, oxidized lipoproteins, homocysteine, and others."
Cytokine Panel (ARUP):
Interleukin 2 Receptor (CD25) Soluble
Interleukin 12
Interferon gamma
Interleukin 4
Interleukin 5
Interleukin 10
Interleukin 13
Interleukin 1 beta
Interleukin 6
Interleukin 8
Tumor Necrosis Factor - alpha
Interleukin 2
Interleukin 17
Question:
If CRC patients had a hair sample analyzed for fungal cultures, what fungi would be found?
I'm replacing primary neutrophils with the neutrophil-like cell line HL-60 for immunological studies.
Do HL-60 cells, differentiated towards the granulocyte phenotype with retinoic acid or DMSO, secrete inflammatory mediators such as interleukins in response to LPS?
I'm unfamiliar with their expression of TLR4/MD2/CD14.
In a patient with hereditary desminopathy (Thr341Pro DES mutation in a heterozygous state) with disease progression, a significant decrease in olfaction is noted. How can this fact be explained?
Yesterday (27.4.20), I become aware of this in the UK, but have not very much information about it.
These links may be of help:
Exclusive: National alert as ‘coronavirus-related condition may be emerging in children’
COVID-19: Alert Over Multisystem Hyperinflammatory State in Children
Is this only found in England and does anyone know any more about the syndrome? It involves gastrointestinal symptoms (causing abdominal pain) and cardiac inflammation.
Thank you,
Mary Wilson
Vagal activity has been shown to reduce inflammatory activity ( )and modulate immune responses. In COVID-19 infections young patients usually experience mild symptoms, whereas in some elder patients fatal interstitial pneumonias are observed.
Vagal activity, as seen from respiratory modulation of heart rate, is strong in childhood and dimishes with aging .
Is there any observation, that vagal activity might protect against too strong immune reaction as suspected in pneumonia?
Would it make sense to strengthen vagal activity as a preventive measure in the population before the big wave of infection arrives?
I just wonder whether lysis of macrophages due to chemical compounds/toxins could trigger inflammation or not. If yes, what is the route and signalling pathway? May you please provide some valid references?
Much appreciated,
Hamed
Within three years, a patient with a desminopathy (Thr341Pro DES mutation) was found to have a 17% increase in the level of C4 complement components to 0.41 g / l (Norm 0.1-0.4 g / l).
I have seen several papers showing that LPS stimulation alone induces mature IL1b release from macrophages. Can anybody explain the release of matured IL1b in LPS alone stimulation condition and LPS+ATP stimulation condition have similar mechanism?
Does LPS stimulation alone induce inflammasome activation in macrophage?
A patient with hereditary desminopathy (Thr341Pro DES mutation in a heterozygous state) was recommended to refuse toothpaste. He continued to brush his teeth twice a day with a toothbrush with only water. As a result, within one month we noted a significant increase in strength and muscle mass in this patient. The patient did not take any medications during this period. After 30 days, the muscle condition returned to its original level. How can this positive effect be explained?
Hi colleagues
Actually I am confused about the activation of CCR2.
1. I would like to know that does CCR2 need to be activated for the binding of MCP-1; for example, integrins in leukocytes are needed to be activated to be bound with the adhesion molecules of the endothelium?
2. If not, then can MCP-1 stimulates monocytes to express CCR2 in higher extent?
What do you think regarding this?
Would you like to share your idea?
Thanks you.
I am currently writing an essay regarding the effects of inflammation in the development of hypertension and just don't seem to be understanding it. If anyone could help me understand this, it would be such a great help!
It is shown that heparin can decrease the level of inflammatory bio-markers and improve patient's condition. However, the mechanism underlying its anti-inflammatory effect is not well-understood. Can anyone please explain what could the possible mechanism be?
Objective: Inflammation of adipocyte induced by high fat diet.
MY problem:
After being fed with the High fat and Low Fat diets for about 10 weeks, the body weight between groups is not significant (p>0.05). I don't have any idea "what happen!".
1. I would like to know that is it possible to make sure that the model have got adipocyte inflammation by using blood sample?
2. If the ans of 1. is yes, I would like to know how to do?
3. If the ans of 1. is no, could you please give me some suggestion "how to make sure that this model already got local inflammation?"
4. From my case study, is it possible that no weight gain but inflammation induced by HFD?
Thank you for your kindness and your time to read and reply.
Thank you for every comment and recommend.
Best regard,
I am treated PBMCs with various compound to observe cytokine expression using ELISA, however, I am getting high expression in my untreated control cells as compared to my media-only control. I am using frozen PBMCs which are thawed, washed and rested over night in RPMI at 37C and 5% humidity. The cells are treated for 24 hours in the same conditions then cell culture supernatants are collected and run in the ELISA. Are the certain conditions are stresses that may induce cytokine expression in untreated cells?
A patient with hereditary desminopathy (a mutation of Thr341Pro DES in a heterozygous state) with the progression of the disease has been established for a long-term healing of skin tissue when it is damaged, compared with a healthy person. The blood sugar level of a patient with desminopathy is normal.
Dear friends,
Recently, we use LPS to induce 24h-mouse spesis model to explore the effect of some drugs to splenic Treg expansion. However, sometimes we failed to induce sepsis and splenic Treg expansion after LPS i. p. injection. I asked some friends and they told me that the mice in USA and mice in China have different lethal dose of LPS injection. In addition, they encourage me to use LPS produced in China, which may be a misture instead of ultrapure LPS from sigma. I wonder why sometimes LPS failed to expand Tregs in mice? In addition, may I know the different between LPS from Sigma and beyotimes? May I know some details about LPS subtype and application in experiments.
Yours
Shuoyang Liu
LPS from sigma is:
L9764 Sigma-Aldrich Lipopolysaccharides (rough strains) from Salmonella enterica serotype minnesota Re 595 (Re mutant).
LPS from beyotime(China) is : lipopolysaccharide purified from E. coli O111:B4, which is specific for TLR4 activation or TLR2.
The mice are bought from other labs. The body weight is from 17g-19g. The mice from other labs and from our breeding sometimes are different in response to LPS induction.
Hi everybody.
I want to make inflammation cell model. I am thinking use mononuclear cells. How can I create inflammation cell model.
If inflammation plays a part in the cause of psychiatric disorders--what might be causing the inflammation to begin with?
Relevant studies:
& Pre-diagnosis and post-diagnosis use of common analgesics and ovarian cancer prognosis (NHS/NHSII): a cohort study. https://www.thelancet.com/journals/lanonc/article/PIIS1470-2045(18)30373-5/fulltext
I found a lymph node-like granule under the thymus. Is it a lymph node of MLN?
Over the past four years, in a patient with desminopathy (Thr341Pro DES mutation in the heterozygous state), the majority of antioxidant status indicators increased 1.2-2.0 times. Including glutathione in the blood increased 1.8 times to a value of 896 μmol / l (the norm of 500 - 1500 μmol / l), and the level of coenzyme Q10 in the blood increased 1.8 times to a value of 0.8 mg / l (norm 0,4 - 1,6 mg / l), vitamins E and C increased by 1.3 times, respectively, to 6.4 and 6.2 μg / ml.
In the literature there are conflicting data on their effect on the human body.
Over the past six months, a patient with hereditary desminopathy (Thr341Pro DES mutation in the heterozygous state) has a 1.6-fold increase in the level of the pro-inflammatory cytokine interleukin-6 to a value of 8.77 pg / ml (<7.00 pg / ml).
In addition, several parameters indicate the presence of inflammation: an increase in the number of immunity cells with markers CD25 +, CD95 +, HLA-DR + in the T-cell link; as well as an elevated level of C4 complement components.
The level of other cytokines Il-1β, Il-8, Il-10, TNF-α is normal.
At the same time, the immunoregulatory index fell below the norm and is 1.19.
Details are indicated in the questions of this project "myofibrillar myopathy".
Dear scientists, please, join the discussion on this issue, do not limit yourself to viewing only. Ask me additional questions, send messages to your personal mail. Ready to answer any questions and listen to wishes.
Do all pathogens increase the ESR, or do some increase it far less than others, or not at all?
Inflammation and reactive oxygen species (ROS) production after central nervous system injury. What about the cancer?

We tried the eosinophil isolation kit from Mitenyi (immunomag. depl.), but the cells seem to get activated (increase in FSC/SSC by flow), adhere to the culture dish and die...
How long can we expect the cells to survive under "optimal" conditions?
I want to write a review article about inflammation or MS, but I need a good corresponding author. How can a good corresponding author find??
Are there differences in nuclear and mitochondrial DNA digestion by DNases? I want to test if enzymes can digest mtDNA. If they do, then is it with similar propensity to nuclear or there may be preferences considering protein-DNA complexes vs naked DNA?
I want to induce liver inflammation in wistar rat, i m looking for simple and quick induction protocol.
I received my materials so late and mouses are older than the protocols suggested for inducing of EAE in c57 mouse
I wanted to test some sample against neuro-inflammation in-vivo. Is there any established animal model especially to test neuro-inflammation? If not available, is it possible to induce inflammation in brain with LPS?
I'm evaluating these factors.
What is the normal range of IL-6 in rat sera in ng/ml?
Thanks for consideration
Hi,
I would like to know if inflammation stimulates or inhibits gluconeogenesis. Inflammation is known to trigger insulin resistance, which should lead to an increased gluconeogenesis since insulin inhibits gluconeogenesis. However, some papers claim that inflammation decreases gluconeogenesis. Does someone have a good knowledge of this phenomenon and could help me ?
Thank you.
I do not mean steroids, all we know steroids, I mean some really new drugs.
I am planning to design and synthesis of novel small inhibitors/antagonist of TLRs.
How should I begin? I have requested many private companies to provide samples but they could'nt provide as per their policies. So please help in this regard.
Hello...
I’m using inflammation induced keratinocyte culture media to re-induce inflammatory responses in RAW 264.7 macrophages. When I transfer the media from inflammation-induced keratinocytes to RAW 264.7 macrophages, it clearly induce inflammatory responses (NO production etc.). What I want to know is, which cytokine or signaling molecule (coming from keratinocyte culture media) is usually responsible for inducing inflammation in RAW cells.
Thank you
I am growing BV2 cells in two different countries from different original stocks but exactly the same medium type and recipe, and the same flasks. In one country the cells do as expected, within 24 hours they're adhering and looking perfectly perky. In the other country 24 hours doesn't seem to be enough for them to adhere, they take up to two or three days sometimes and even then will only adhere to PLO coated flasks, which I've never had to use with this line before. I have absolutely no idea what's going wrong with these cells since I appear to be doing exactly the same in both countries! My only thought is that they're from different stocks BUT I have seen the badly behaved ones grow previously...just not recently!
I plan to check the impact of exogenous cytokines in alteration of M1 or M2 phenotype using mouse macrophages. I'm not familiar with the mouse macrophage cell line. For this purpose, which cell line is suitable? I will determine phenotypes by flow (CD86, IA/IE; M1, MR; M2) and iNOS/Arginase-1 ratio by qPCR.
I need to stimulate B cells with CD40 ligand. Which kind of stimulation will be the most efficient: beads or antibody?
I want to deplete circulating monocytes in a recipient mouse, in order to repopulate with monocytes from a donor mouse. What is the best method for long-term depletion? I know clodronate liposomes are used to deplete both macrophages and monocytes, but monocytes reapper in circulation 18h post-injection. Anti-CCR2 is also used to deplete Ly6Chi inflammatory monocytes, but I am not sure of its efficacy and lasting effect.
Thank you all!
I have been trying to separate different cell populations from whole blood using polymorphprep, I have blood from the same subject taking over a time course (with inflammation induction after first sample). The first sample separates without issue but the red blood cells don't sediment properly in the follow up samples. Is this an issue with polymorphprep? Does anyone know if it is related to the inflammation or just a coincidence?
What could be the factors like ROS, different cytokines, platelet derived growth factors etc which can actually induce the hypersecretion of insulin or insulin-like growth factors in the blood?
I am giving dose of P2-peptide 100ul in each hind paw and couldn't get much high score in rat model. I am using female lewis rats. can anybody suggest me the possible ways to get high score of EAN disease in rats.?
Deleting the transcription factor Brg1 from Tregs impairs Treg function, resulting in lethal inflammation mimicking that in scurfy mice (EMBO, 2013). We have now found that restoring Brg1 expression in the dying adolescents (using a method we developed) rapidly resolves the inflammation and rescues the mice. Questions:
1) In the dying mice, CD4 cells in the peripheral blood are predominantly CD44hi CD62L lo (effector-like), but within a few weeks after restoring Brg1 expression, the CD4 cells become largely CD44low CD62L hi (naive). Apparently, the effector-like cells have been rapidly converted to naive cells. This is unprecedented? Worthwhile to follow up?
2) Any interesting issues you would like us to address using this system?
Happy Holidays!
Tian
Hi,
We are planing to do an airway inflammation model using Ovalbumin (OVA).
We are planing to sensitize OVA/Alum 4 times(d0 and d14), on d21, d28 and d35 we will them a special substance and OVA/alum again on d42 and 56.
We will make a challenge on d63 and take the BAL on d65.
We are planing to use 100ug for the sensitization and 25ug for that challenge.
I read quite a lot of papers and people like to use like 20ug for sensitization. Is our dose too high for that? What about giving them 25ug instead of 100ug for sensitization?
Thank you,
Dominic
I have infected the mice foot pad with Mycobacterium marinum and my goal is to monitor the footpad swelling using digital caliper and then check the footpad cfu after termination.
My question is where exactly on the footpad should we measure? as the swelling kind of starts in the mid footpad region and then spreads towards the tarsal joint and digits.
Has anyone done this kind of study? from which region of footpad do you measure the swelling or do you just average the total by measuring front, mid and back of the footpad?
In experimental colitis due to inflammation the levels of various cytokines increases. The literature reported the increase of these levels in both colon tissue and serum.
Dear researchers, please suggest me where the levels of these cytokines should be preferred to assess colitis.