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
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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!
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Thanks Irena,
Do you think or have you experienced labelling soluble interleukins, that they diffuse in the intercellular space i.e. extracellular matrix? Or do you usually find them mainly within cells?
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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
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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.
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I guess the best timing was missed.
In my first LPS experiment, I stayed in the lab overnight to monitor the LPS response and got the first-handand dynamic data. The acute inflammation response comes very quickly, 3-6h for mice, and 1h for some cells. Just a reference.
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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.
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The change in the level of uric acid and biochemical parameters in a patient with an identified case of desminopathy is presented in the article https://www.researchgate.net/publication/357311034_CHANGE_IN_REDOX_STATUS_AND_BIOCHEMICAL_PARAMETERS_IN_PATIENT_WITH_DESMINOPATHY_T341P_SEVERAL_YEARS_AFTER_DISEASE_SYMPTOMS_ONSET
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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?
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Oxidative stress is mainly due to inflammatory mediators such as ROS, RNS free radicals produced by inflammatory cells such as macrophages and neutrophils activates NF-KB a key transcription factor involved in the process leads to tissue damage, cell aging, DNA damage, and cell death.
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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) ?
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Simon Bruce Perrin Again, most experiments on animals can be considered "torture", depending on your point of view. Does fear conditioning not cause pain, stress, and fear in animals?
Pain models like FCA have very little effect on the animals' well-being as measured by weight, grooming, socialization etc. In fact, usually you cannot distinguish between pain model animals and sham controls based on these well-being indices. You get much stronger effects on these indices when using other common paradigms such as repeated exposure to non-painful stressors (e.g., forced swim test).
We have ethics committees to deal with these issues, and fortunately we do not rely on one high-horsed person's opinion. Now please stop harassing research students in pain labs and clear the stage for people who might actually have helpful answers to their valid and interesting scientific questions. Good day
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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,
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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?
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There is an explanation. ACh can both increase and inhibit cell proliferation depending on the concentration.
See my publications and monographs.
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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!
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You can refer to this article
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I have tried with no success various UV-B stresses but I did not find an increase in beta galactosidase.
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Hi Anthony L, Yes: we often used the DNA-damaging drug etoposide to induce senescence. Soluble in DMSO. 10 uM was often ok, though the best concentration can vary with the cell type -- it gets toxic at higher concentrations (because extensive DNA damage is toxic). It was added to recently plated cells for 48 h, then removed, and the cells were left for 5 days to develop the senescent characteristics -- although this may also vary with cell type. So for a new cell type you might want to try lower and higher concentrations, and different timings. We published this method (used as a positive control) in Cairney CJ et al. 2017, PLoS Genetics. (See Supplementary File 2.)
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I was wondering if euthanizing mice by carbon dioxide inhalation would cause activation of NF-kB inflammatory response?
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I wouldn't call it euthanasia because CO2 is toxic and kills by acidification of the blood and lung inflammation. Euthanasia should not interfere with the animal's metabolism or be painful.
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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?
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Dear Massimo Zipoli, thank you very much for your reply! As you know, desmin is expressed in all types of muscle cells (skeletal, smooth, cardiac muscles, diaphragm), as well as in tumor cells.
In this family with desminopathy, we identified a large number of cancers (n = 6): bladder (2 cases in men), prostate, skin, uterus, rectum (article in the appendix). For example, it is known that dysfunction and pathological changes in the smooth muscles of the bladder are associated with the overexpression of desmin.
Thus, the likelihood of infecting cells with the mutation is quite high.
Article
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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
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It would be better to compare benign and malignant conditions in the same organ/tissue: endometriosis vs endometrial cancer, for example, instead of uterus compared with ovary tissue.
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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.
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Before collecting serum from mice post infection, you need to optimize the time, for which you need to do an experiment with a group of animals by infecting these and taking blood at different time points. Extract RNA from the blood and do real PCR for any inflammation cytokines gene. So that you may reach to a conclusion about time points to sacrifice mice.
Attaching a paper in which they sacrificed mice at 4 day.
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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.
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If your cells have been passaged too many times or if they are infected with Mycoplasma, they may not respond to TLR -- and hence LPS -- stimulation. You may also want to try a different batch of LPS.
Check out the following:
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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.
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In fact, It's better to do the whole experiments on immortalized cell line at first. We usually do the experiments on RAW264.7 and iBMDM, and later on primary BMDM. It's convenient to use cell line to grope the phenotype and the protocol.
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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?
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Probably affect facial nerve and glossopharyngeal nerve in the pons and medulla oblongata?
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"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.
"Chronic inflammation can result from the following:
  1. 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.
  2. 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.
  3. 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).
  4. 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.
  5. 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?
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Bogdan Socea Thanks for sharing - I agree!
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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.
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Hello, you may consider consulting this and other papers:
Since TLR4, and capase-1 pathways are present, HL-60 should respond to LPS, though the strength of which may vary according to differentiation status.
THP-1 for example (as a model of differentiated macrophages), can be "optimally" differentiated with very low dose of PMA (5 ng/mL; ) before LPS challenge and other manipulations. The doses and duration of PMA affect differentiation outcomes. I can imagine some similar scenarios for HL-60. A good way to go about it, may be first find some "optimal" conditions for differentiating the cells, based on methodolgy papers.
If in fact, your differentiation method is new and improved (with strong reproducibility), you can actually compare the expression profiles changes before and after (IL-6, IL-1beta, NF-kB activation, iNOS, MPO, etc.). That itself could be a worthwhile way to establish a model.
Good luck!
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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?
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I agree with Japneet Kaur. The problem in the cilia of olfactory sensory neurons. The myofibrilar myopathy is a genetic disease that associated with the primary ciliary dyskinesia. The primary ciliary dyskinesia resulted in defective cilia and olfactory receptors.
Attached, please find the article describing both myofibrilar myopathy and primary ciliary dyskinesia.
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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
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tahnks
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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?
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In 8579 cases from 30 provinces out of Wuhan, “the median age of cases was 44 years (33-56)... “ though “schools in China were closed for most of the epidemic because of the 2020 Chinese New Year holidays” https://www.thelancet.com/pdfs/journals/laninf/PIIS1473-3099(20)30230-9.pdf
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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
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Hey Hamed,
in general lysis of a cell (not only from a macrophage) releases cytoplasmic components that normally do not occur extracellulary. These "out-of-place" components are called DAMPs (Danger-associated molecular patterns) and include a broad spectrum of molecule classes (e.g. ATP, actin, Histones, heat shock proteins and many more).
A lot of cells can detect these components that are not foreign (like bacteria, fungi, viruses) but still are not a good sign, because they mean that somewhere cells are damaged. It depends on the DAMP and the cell, which detects the DAMP, if an inflammation is triggered. The topic is quite complex but there are good reviews.
For example you can have a look at these two for starters:
All the best,
Marc
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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).
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Dear Yosvany Castillo! Thank you very much for your answer. Over the past 2 years in this patient with desminopathy (Thr341Pro DES mutation in the heterozygous state), the C4 level of the complement component decreased to 0.36 g/l without taking medications.
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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?
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LPS binds to TLR on macrophages, stimulates phosphorylation cascade to produce inflammasome, which lead to maturation of IL-1b.
You can use LPS alone in consentration 100 ng/ml up to 1 ug/ml, or use in combination with IFN-g 50 ng/ml + LPS 20 ng/ml.
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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?
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The toothpaste may affect gut microbiota balance of the digestive tract thus affecting natural PH levels. The triclosan is proving s extremely aggressive. https://stm.sciencemag.org/content/10/443/eaan4116
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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.
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Dear Prof. Gheita sir,
Thank you for your very informative response. Hope you would like to response to other related problems in future.
Thank you!
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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!
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Dear Alana,
I hope this is helpful.
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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?
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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,
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You can use the adipose tissue directly to determine inflammation levels (via qRT-PCR) or collect blood at sacrifice and run an ELISA on that. I am not sure why you did not see any difference in weight gain in the animals. Which diets did you use, mouse strain, and ages? Were you able to visually detect a weight gain difference between the mice? Is it possible that you ran your statistical test incorrectly?
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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?
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Depending on the length of your experiment location on the plate can influence activation of PBMC. Wells along the edge of a 96 well plate, and the corner wells in particular (where people often put controls) can evaporate more quickly than other wells on the plate, this can lead to stress which can activate the PBMC. If your stimulation is more than a couple of days it is worth filling the outer wells with PBS or DI water. You can also just vary the location of your negative control well to see if that changes anything.
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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.
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informative discussion.
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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.
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Why are you using LPS isolated from different bacteria?
Even LPS isolated from different stains of E.coli will have differences in activation/stimulation of immunity.
You can buy LPS from E.coli O111;B4 from Sigma too.
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Hi everybody.
I want to make inflammation cell model. I am thinking use mononuclear cells. How can I create inflammation cell model.
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So first demonstrate a blocked pivot and swing endothelia (indicating chronic inflammatory sway) and then with the drug implementation, a persistent return of the dance indicating inflammatory elimination.
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If inflammation plays a part in the cause of psychiatric disorders--what might be causing the inflammation to begin with?
& 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
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Dennis Mazur thanks for sharing. I agree that the field of immunology is complex, and I'm confident as we ask more questions and do more research, we will find more answers. Some will take longer than others.
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What causes Abacterial prostatits?
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There is no direct evidence for pathophysiology. I guess sexual behaviours and std pathogens like ureoplasma and mycoplasms etc should be investigated.
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Why testis less prone for inflammation ?
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Dear Sagar, blood-testis barrier occlude the entrance of microorganisms into seminiferous tubules, so that inflammation doesn't occur there.
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I found a lymph node-like granule under the thymus. Is it a lymph node of MLN?
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Here is a diagram of murine lymph nodes. Also an article that explains a method of locating them for the first time. Good luck!
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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.
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The short answer is penetrance variability and phenotypic variability. but in your case there is no phenotypic variability as both the proband and his father had the same phenotype. however, the differences between the cases is likely due to penetrance variability. to do into details about these factors will be too long. thanks.
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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.
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Dear Muneeb and Anne, many thanks for your answers and recommendations.
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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.
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I am not very relative, but to the best of my knowledge IL-10 is the best antidote, similarly HemeOxygenase 1 can also be considered.
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Do all pathogens increase the ESR, or do some increase it far less than others, or not at all?
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Hi Sourav, Suspected as much. Probably any sub-acute infection such as CMV, etc.
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Dear Professor and colleagues:
inflammation and cell proliferation induced via activation of nFKappaB leading to an increase in the transcription of pro-inflammatory cytokines (IL-1β, TNF-α, and IL-6...)
in case of abnormal metabolism, cancer cells need inflammation to growth and to form a new blood vessels "neoangiogenesis" which will supply cancer cells by nutrients and oxygen... thus, to the spread of tumors to other organs which we call "Metastasis".
In the other hand, Sugar supports this mechanism, but how? I mean what are the specific signaling pathways that lead to increasing Glucose metabolism during aerobic glycosis (Warburg effect)!!!??
Could anybody help me to know what are the most signaling pathways involved in the metabolic pathways...
Thank you very much for you valuable answers,
Sincerely,
Fouzia
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GSK3beta is negatively downregulated signalling moleculue. That means, when GSK3beta is phosphorylated at serine 9 in presence of signals like Akt/PI3K/PKA/Wnt , they participate in metabolic syndromes.
As you have mention' GSK3beta induces inflammation and cell proliferation via activation of nFKappaB leading to an increase in the transcription of pro-inflammatory cytokines (IL-1β, TNF-α, and IL-6) '
''it means all these sequences are happening when GSK-3beta is unhpshorylatd/activated, so we need to phosphorylate/deactivate GSK-3beta in order to avchive anti-inflamatory effects which is prequisite in metabolic syndrome. Additionally GSK-3beta has shown to mitigate insulin resistance, which again confirm that inactivation/phophorylation of GSK-3beta is prerquisite for acting against metabolic syndrome.
GSK-3beta act by phosphorylation/deactivation of GSK-3beta at ser9 domain.
in brief, Akt/PI3K/PKA/Wnt and as mentioned by John Patrick Alao, mTOR pathways should be considered
You may refer to : Song WJ, Song EA, Jung MS, Choi SH, Baik HH, Jin BK, Kim JH, Chung SH. Phosphorylation and Inactivation of GSK3β by Dual-Specificity Tyrosine (Y)-Phosphorylation-Regulated Kinase 1A (Dyrk1A). Journal of Biological Chemistry. 2014 Dec 4:jbc-M114.
regards,
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Inflammation and reactive oxygen species (ROS) production after central nervous system injury. What about the cancer?
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Hi,
You could check this article
It seems that, after apoptosis, ROS can be mediated by caspases to promote a regeneration process.
Regards
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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?
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Eosinophils can only be cultured in the presence of apoptosis-delaying cytokines such as IL-3, IL-5, and GM-CSF. Otherwise they are prone to undergoing apoptosis within a day of culture. There are many papers in the literature that describe techniques to sustain them in culture. However, they are not dividing cells so you will not be able to proliferate them after isolation from human blood.
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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??
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I have not ever heard such a thing...
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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?
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I was thinking in vivo, in cytoplasm released mtdna is now reported to be a signaling moity and may cause inflammation. In that scenario, would dnases act. If at all mtdna was unprotected, would dnase act on it?
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I want to induce liver inflammation in wistar rat, i m looking for simple and quick induction protocol.
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You can use the hepatotoxic drugs like carbon tetrachloride. See the article.
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I received my materials so late and mouses are older than the protocols suggested for inducing of EAE in c57 mouse
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6-8 weeks
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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? 
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Dear Guadalupe,
Thank you so much for attaching this article. It is really interesting and helpful.
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I'm evaluating these factors.
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Reference range and short- and long-term biological variation of interleukin (IL)-6, IL-17A and tissue necrosis factor-alpha using high sensitivity assays.
Todd J, Simpson P, Estis J, Torres V, Wub AH.
Cytokine. 2013 Dec;64(3):660-5. doi: 10.1016/j.cyto.2013.09.018. Epub 2013 Oct 12.
Serum IL-1beta levels in health and disease: a population-based study. 'The InCHIANTI study'.
Di Iorio A, Ferrucci L, Sparvieri E, Cherubini A, Volpato S, Corsi A, Bonafè M, Franceschi C, Abate G, Paganelli R.
Cytokine. 2003 Jun 21;22(6):198-205
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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.
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Glucocorticoids including cortisol which is counter-regulatory to insulin stimulate gluconeogenesis. Glucocorticoids are inflammatory and stimulate reactive oxidative species(ROS) which further damage the system by down regulating the uncoupling inflammatory proteins (UPS) which would have stabilized the metabolic system by forcing glycolysis to suppress gluconeogenesis and force more insulin to be produced instead of cortisol, et al. Remember unregulated gluconeogenesis  causes increased glucose in the blood and reduced insulin sensitivity.
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I do not mean steroids, all we know steroids, I mean some really new drugs. 
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You may find few in the following article: Generally the natural products derived from Food  are safe and long lasting.
 I have worked on  Apigenin flavonoid which is a good alternate found in dried parsley leaves.
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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.
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Thank you all for your insightful comments. As suggested, I have collaborated with chemistry experts for the same.
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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
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Yes, I agree with the above assessment. In my hands, TNF and IFN-gamma are the most potent, possibly also involving MCP.
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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!
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Dear all,
I am facing a similar problem when thawing BV-2 microglia cell line and I would highly appreciate your help since the only BV-2 cells I have are the ones in culture and I bought them to ICLC. I would rather recover the ones I have now than buying a new vial, if possible.
Two days ago I thawed the only BV-2 microglia vial in RPMI media since it was frozen in that media. 24 hours later I realized that around 30% of the cells were not attached, then I centrifuged the supernatant and I seeded the cells in DMEM, RPMI and DMEM:F12. From the cells I collected from the supernatant, I realized that there are more attached cells in DMEM or DMEM:F12 compared to RPMI media condition. I am not sure if this may be due to the fact that RPMI is also used when cells are grown in suspension (and therefore those cells are viable), or which the cause might be. Is that normal to have cells in suspension in BV-2 cultures? Or should I be worried about? Can it be due to an inflammation?
I kept the attached cells in RPMI media and the vast majority of them are still attached.
My main concerned is the fact that the vast majority of my different plates (attached cells from the very beginning, supernatant maintained in DMEM, DMEM:F12 and RPMI) do not seem to have elongations. I would like to know if there is any way to recover these cells or if it takes some days for the cells to get those elongations. Do you think is worth doing adding primocin or plasmocin to the media so I could get rid of any potential micoplasma contamination that could avoid my cells to get protrusions?
Many thanks for your help!
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I need to stimulate B cells with CD40 ligand. Which kind of stimulation will be the most efficient: beads or antibody?
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No, we do not use HUVEC as feeder cells for B cell culture. I am not an B cell expert but I am sure there are some publications availabe about culture conditions. For the culture of isolated monocytes you must have M-CSF or GM-CSF in your medium.
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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!
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You could also use a LysM-DTR mouse.
Regarding neutrophil depletion, I would be careful with these Mab's ( you can also buy from Hölzl diagnostics, they have fast delivery and are already purified and of good quality). The drawback is, when I tried them myself in strong inflammatory conditions, in the end I had even more monocytes and neutrophils in the "depleted" group than in the non-depleted groups.
with long-term depletion you always run into the problem, that the animal will start to make auto-antibodies against the Mabs. With the DTR mouse you need to inject DT every few days, but at least there I never had a problem with auto-antibodies (I used timeframes of 6-8 weeks with injection 2x a week - but depending on your cell population of interest, you might need to give DT every 2-3 days). 
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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?
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Use ACK lysis buffer to lyse erythrocytes. Then isolate WBC according to demand by using polymorphoprep. 
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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? 
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OOOOOO...Dr. Alam............. What a great speech.......... Thanks for your comments, though........
If I am not wrong ResearchGate is a forum for scientific discussion and sharing......
And more over......... I know what is better for me.............So Please don't worry........... and Have fun.....
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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.? 
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Can you provide me with more detail as to the nature of your project? This will help me see if I can answer your question
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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
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Hi Simon and Ruan,
Happy New Year!
Thanks for your inputs! The arthritis and EAE experiments are indeed good ones although at this point we are focusing on the apparent conversion of effector cells to naive cells. The effector-like cells overproduce INFr when stimulated with Ion+PMA, suggesting they might be Th1 cells (EMBO, 2013). To test whether these cells can turn into naive cells, we are trying to adoptively transfer them into Brg KO mice and then restore Brg1 expression in the Tregs in the recipient mice to see if the transferred cells   can become naive cells.  BTW, following the restoration of Brg expression in Tregs, Tregs apparently proliferated, which should help resolve inflammation. 
Regarding Ruan's question, it seems Brg KO does not affect Treg development, number or stability (EMBO, 2013)
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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
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Dear, Dominic Schmidt
Firstly, you are welcome and secondly, up on my trivial experience, the answer will be yes. It is bad using such a high dose?. Because, that may emerge with sudden death (shock), or lead to anaphylaxis shock, cessation of respiratory due to completely bronchiospasm as well as, to immediate hypersensitivity .....ect. Sorry, that in final may lost all of your experiment animals. However, you can be use  a suitable dose of OVA ( accordance preparation) in 2 or 3 of different sites of sensitization at the same time, such as; inhalation (you must  be careful to avoidance inhales it ), I/P, I/M, I/N, I/O,S/C, and even as I/vag. Dear, Dominic. I, hope I help you, and as soon as possible I will send you the protocol (study design) for OVA sensitization in rabbits.
Best, Regard
NASEER ALMUKHTAR   
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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? 
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To get a true  measurement of inflammation, I  would suggest using plasma extravasation technique  using Evan's blue.  It is a more accurate measure of inflammation than microcaliper. The microcaliper puts pressure  on the tissue causing some of the inflammation (fluid) to displace during measurement. Using this method you would also get a total measurement of inflammation, regardless of placement of the device.  The protocol for this techniques can be  found here.
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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.
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question?
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No inflammatory cells, though vascularity is increased. I put my money on traumatic damage not necrosis. Check the margins for any inflammatory cells.
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HD patients
Nutritional and Inflammation Status
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Hello Toh Yoon,
thank you very much for your answer and orientation.Me and my team have already assessed about 3000 MHD, and We're currently trying to study the outcomes for the mortality over one year, so I'll sure be doing a ROC analysis and estimate the best cut-off value for our country's population, as you said.
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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.
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MSU crystals were prepared by first dissolving uric
acid (5 mg/ml) in 0.1 M borate buffer (pH 8.5), and, after passing through
a 0.45-mm filter, the supersaturated uric acid solution was left at room tem-
perature for 48 hours. The large crystals formed during the first 48 hours
were removed by centrifugation, and the supernatant uric acid solution
was incubated at room temperature for 5 more days to allow the formation
of fine crystals, which were harvested by centrifugation. After 2 washes
with absolute alcohol and 1 wash with acetone, the crystals were allowed
to air dry. Crystal size varied between 3 mm and 50 mm in length, with
48% of crystals less than 10 mm in length and a mean ± SD crystal size of
11.69 ± 6.6 mm. All reagents were prepared under pyrogen-free conditions.
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Do you have any idea why does this phenomenon happen?
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Dear Dr
Look PDF attached may help you
Good luck
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Does anybody publish work in stress and inflammation biomarkers (allostatic load measures, hsCRP, IL-6, MCP-1)? I am looking for a biological collaborator for my R grant in 'care for wife caregivers.'
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Thank. I will read your paper  more carefully when I am fully awake. 
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Hello everyone, 
I performed IP injection of mouse cancer cells (GL261, 75.000 cells) in C57bl/6 mice. However,  three weeks after, mice started to be moribund and necessitated to be sacrificed. Do you know if the presence of these cancer cells can induce an inflammation or any reaction that could provoke the decline of the mouse health? 
Thanks in advance !
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No we did not perform necropsy yet. But there is still some mice alive, maybe they will need to be sacrificed in the following days, I will pay attention to this area during the autopsy and sample tissue to have a look at immune cells by IHC 
Thank you! 
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β casomorphin-7, a bioactive peptide present in A1 milk can increase the production of gastric and intestinal mucin. It is hypothesised that the production of such mucin may protect the intestinal endothelium in inflammatory bowel disease.
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The article by Woodford is useful, I already had this one. The side effects of BCM7 seem to be serious and would require a RCT to ascertain the safe doses for patients with asthma and those without.
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I was recently working on the inflammatory factor expression variances between WT and knockout mice by inducing LPS. But I didn't get a convincible result by detecting several IFs. I was wondering if anyone knows the accurate relationship between the inflammatory response and the dose of LPS as well as the injection time. I will deeply appreciate your reply.
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Priya we use Working Conc 1µg/ml in our lab to induce inflammation in cell culture
(Keep LPS Stock Conc 1mg/ml@4degree)
Hope this helps
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I need to inhibit NF kappa B in a slowly growing human cell line isolated after KO of a gene. This will take 3-4 weeks. What is the less toxic inhibitor that I can use? I tried Bay 11-7082, but all treated cells died after 3-4 days, although control-treated cells survived. Thanks in advance!
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IkB-alpha super-repressor. But then toxicity depends on cell type irrespective of genetic or chemical inhibitors. In other words, it depends upon the extent to which the cells depend upon NF-kappa-B. However, you might get resistant cells over time, in both genetic and chemical inhibitor approaches.
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I'm currenly investigating the effects of the adipokines Leptin, Resistin and Visfatin on PBMCs, many papers report pro-inflammatory effects (mainly TNF-a and IL-6 secretion, although in low levels). In my experiments I see no secretion at all (ELISA) even at high doses, which makes me doubt bioactivity of the recombinant proteins. Does anyone know some good downstream targets I could use to test bioactivity e.g. by qPCR?
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You can check their expressions by qPCR
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It is widely known that bacterial infection, inflammation and oxidative stress are the known factors of liver sieve defenestration. However, the mechanisms involve LSECs defenestration associated with infection and inflammation are largely unknown. 
My question is how bacterial infection or inflammation leads to defenestration in the liver sieve
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Hey
Look for  this links PLZ
Padma V. Devarajan, ‎Sanyog Jain - 2014 - ‎Medical
damaged debris, bacterial and viral infections, endotoxins, etc. ... other growth factors (innate immune defense) and prevents liver inflammation [15]. ... together to form sieve plates permitting filtration, thereby allowing diffusion of many ... matrix leads to thickening of SEC causing defenestration of SEC followed by fibrosis.
Good luck