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Hi everyone,
I struggle to find a single-cell or bulk-sequencing dataset showing the transcriptomic effects of a medical treatment (i.e. COX1 or 2 -inhibition) in patients of inflammatory diseases. My plan is to search for the correlation of the treatment with several genes connected to my project.
I am not a bio-informatician and therefore I depend so far on visualization tools like ( https://immunogenomics.io/ampsle). Most of these tools unfortunately only show cell-specific expression patterns, but no effect of any treatment. I know, analysis tools like https://www.immport.org/home exist - however they don't help without the right dataset.
I already searched through https://singlecell.broadinstitute.org/ or https://www.ebi.ac.uk/gxa/sc/home, but again - I didn't find any dataset with COX-inhibitors. Maybe they include the information which patient got such a treatment, but I don't know how to access that.
Can anyone help me to find/get access to such a dataset?
I hope the solution is not too obvious and I waste your time.
Thank you in advance and cheers,
Peter
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well explained. other tics on those datasets databases, are quality and relevance of each data. When published, data should thereby be clean...I hope.
fred
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inflammation NF KB 
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Nice Contribution Rikard G Fred
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Why do steroid injections help to relieve pain?
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Vitamin D3 is not a vitamin at all, it is actually a POWERFUL  seco-steroid hormone that is involved in bone and joint and tissue remodeling, as well as immune system modulation. It alters the expression of 2,000+ of your genes. If you are low in Vitamin D3, your immune system will be out of focus  and may accidentally attack good tissues (autoimmune disease) or ignore bad actors or defective cells  (infections from bacteria, fungi or viruses,  and cancer cells). Now you might not know this but when tissues need to be repaired in your body, quite often there is a lot of destruction and then rebuilding going on. And the repair mechanisms in your body  borrow many of the components  of your immune system to tear down tissue that needs to be remodeled (macrophages for example). Having low levels of Vitamin D3  can lead to an impaired healing process in addition to immune system problems. This impaired healing process is what causes plantar fasciitis to become a chronic ailment that can last  for many years , even decades. There  are various self reports of people who have cured their plantar fasciitis  simply, quickly, and for a cost of next to nothing by simply  boosting their Vitamin D3 levels including myself.
To make the heel spurs disappear
First Set of Required Nutrients:
  • Vitamin A: Non-Synthetic/Not plant based. Cod liver oil is best option.
  • Vitamin D: Sunshine exposure ideal. If that is not available, Cod Liver Oil is needed every day.
  • Vitamin K2 (MK7): Required for vitamin A and D to function properly.
  • Boron: Mineral that regulates calcium transport on cell membranes. Required for strong bones.
  • Second Set of Required Nutrients:
  • Calcium: Eat Chard/Kale/Dark leafy greens/sardines/anchovies. If you do not eat these, you need to supplement calcium with a raw, whole food based source of calcium.
  • Magnesium: Required for strong bones. Most important mineral for bones beside calcium.
  • Trace Minerals Concentrate: Bones require various minerals. Bestway to have these minerals is with trace mineral concentrates. These trace minerals would be available in your food, but factory farming on depleted soil make trace minerals nearly impossible to obtain from food. Trace mineral research has the best source.
Other deficient nutrients that adding will help foot pain:
Vitamin B-1 Deficiency
Scientists discovered vitamin B-1, or thiamine, first. Along with the other B vitamins, it's water-soluble, meaning it isn't stored by your body and is excreted with your urine. You need vitamin B-1 to help digest carbohydrates, use fats and proteins, manufacture red blood cells and assist the proper functioning of your immune and nervous systems. Alcoholics and the elderly are prone to deficiency of vitamin B-1, resulting in beriberi, a disease causing weakness, fatigue, an enlarged heart and confusion. It also causes edema, burning, tingling and stabbing pain in your feet and lower legs.
Vitamin B-12 Deficiency
Vitamin B-12 has the most complex chemical structure of all the B vitamins and the only one that contains the metal cobalt, according to Oregon State University. Vitamin B-12 is an integral part of DNA and enzyme synthesis, nervous system functions and red blood cell production. Unlike the other B vitamins, vitamin B-12 is stored in your liver. Deficiency of vitamin B-12 is prevalent in the Vegetarians and elderly and sometimes results in a condition called pernicious anemia. The symptoms of a vitamin B-12 deficiency include poor appetite, sore tongue, memory loss and dementia, along with difficulty walking and painful tingling sensations and numbness in your feet.
Deficiency of Biotin
Although it's classified in the B vitamin family, AltMD states biotin is actually a coenzyme that works along with the B vitamins. You get biotin through your diet. You need biotin for the synthesis of fatty acids, to build protein from amino acids and obtain energy from the breakdown of carbohydrates. It also helps maintain the health of your nerves, skin, hair and nails. Biotin deficiency causes fatigue, grayish skin color, skin rashes and problems with digestion. It also causes your skin to become painfully sensitive to touch with tingling in your feet and hands.
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Hujoel used US diabetic data (NHANES III, 1988-94) to show that persons with gingivitis had a 57% increased risk of retinal haemorrhage
Innate immunity has been suggested to play an important role in chronic inflammatory disease. In periodontitis, pathogens induce a local inflammatory response and activate innate immunity through activation of Toll-like receptors (TLRs) . This activation leads to the production of pro-inflammatory cytokines and the recruitment of phagocytes and lymphocytes into the inflammatory zone). Meanwhile, in the retinal immune system, the retinal pigment epithelium (RPE) cells play a pivotal role in immune responses, and they express TLRs and are a rich source of cytokines, chemokines and growth factors. The complement system is a pivotal actor in the innate immune system. Its activation through the classical, alternative, or lectin pathway produces several complement fragments (C3a, C5a, and C4a) that are frequently observed in the host response in ocular disorders and periodontitis .
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Yes, it can be transmitted to the body throughout the body if it is systemic . He fully agreed with Dr. Ahmed Sami best regard .
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Gluten sensitive enteropathy, also known as celiac disease, is an autoimmune inflammatory disease affecting the small intestine, so I think it is organ specific autoimmune disease; however, the clinical features are diverse. I searched in internet to know if it is organ specific or non-organ specific disease but I could not find an answer.
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Very clear the answer. It is a Systemic Autoimmune Disease because can be affected several organs simultaneously or later in the evolution.
It is the only systemic autoimmune disease whose etiology is very well defined only by the gluten
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We isolated it from rectal tissue of a patient having a chronic intestinal inflammatory disease.
we failed to obtain a mycelium form. The colonies are white and  the culture are actidione-sensitive. 
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Bonjour
si je peux me permettre d'écrire en langue française (puisque vs êtes affilié à une université marocaine)....Il semble que vous avez une forme fongique levuroidale, ou peut être une levure, certains mycotaxons comme Aureobasidium et Monilinia présentent cette allure, mais je crois que tu peux soit refaire les prélèvements pour distinguer les hyphes, sinon il est possible d'obtenir (éventuellement) une forme filamenteuse d'un champignon si par exemple vous le mettez sous conditions expérimentales particulières comme un déficit en Calcium, un milieu hyperchargé en Mg, une qualité photonique particulière (UV), ou thermiques particulières des stérols.......etc
Enfin, reste les techniques moléculaires pour identifier avec précision ce mycotaxon
Bon courage
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As an osteopath, I often come into contact with chronic pain, which is more and more due to a drowning inflammation.
In addition to manual techniques for optimizing blood flow, innervation and mobility, advice is given about nutrition and possible supplementation.
All too often, patients (especially in professional sports) with chronic inflammation have long taken NSAIDs. However, this is increasingly questioned by scientists.
Medication management obviously does not belong to the treatment strategy of an osteopath. Nevertheless, I often get questions from patients themselves what they should do with this.
What do you recommend? What products/supplements do you work with? What advice do you give?
References:
 
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Dear Bart De Swaef,
I am a chronic OA patient since 8 years...it affected my quality of life (could not  walk fast, run)...but never resorted to taking any medications....still successfully able to manage the problems...i followed a simple yet an effective practice...i was an overweight earlier....started doing a regular mild exercises (mostly stretches, squats and mild weight bearing exercises as well) and reduced my weight by 5-7 kg....regular exercise improved my immune status as well (earlier i had chronic bouts of common cold, allergic rhinitis, but frequency of illness are very less now)...changed my food habits....more protein, more fibers and less carbohydrates....my fat intake is as usual as earlier...no more pain... now I walk fast, run... we should not arrest the normal protective role of inflammation by taking medicines....inflammation is very essential for our own survival...I am not a medical practitioner to recommend a treatment strategy, but got a lot of benefits from simply changing my lifestyle and diet...
Happy weekend!
Regards
Selvam
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I would like to discuss this model of EAE induced with rMBP is anyone has used it? 
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I am examining some signaling pathway’s effect on Extinction of cocaine-induced CPP. However, even for the control group, after induction of CPP, I cannot induce extinction of CPP beautifully using repeated re-test method. Do u guys have any good method to induce extinction of cocaine-induced CPP?
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Dear Xinjian,
Though you have not been specific on your research population (human/animal) or how you model your CPP ( Three-compartment chamber (or 2 or 4), and how are they defined; do you have a "forced answer"), I suggest reading the following chapter: https://www.ncbi.nlm.nih.gov/books/NBK5229/
Please pay attention to section 4.6.2. Psychostimulants, as it might have some suggestions on why you fail to get  excitation effect.
Hope this helps.
Success!
Jelena
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Currently theorising the mechanism of atopic dermatitis and how calcium signalling can be related to this skin inflammatory disease.
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Dear Dr. Jun-Wei
Look PDF attached may be related  your question
Good luck
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In human the pathogenesis of colitis is very complex process. Researchers use many reagents like acetic acid, TNBS, DSS, croton oil etc., to induce colitis in rats which showed different mechanisms of induction of colitis in rats. Hence, I request the researchers to give suggestions and share some publications about the limitations of different experimental models of colitis. I also request to suggest the preferred model to induce colitis in rats so that its pathogenesis is most similar to that of human.  
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This review article may be useful:
Animal models of intestinal fibrosis: new tools for the understanding of pathogenesis and therapy of human disease. Rieder et al. 2012. Am J Physiol Gastrointest Liver Physiol.
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Hi, 
We're setting up a study looking at a group of auto-immune/inflammatory/rheumatic diseases that affect women during their reproductive years, and affect the musculoskeletal system (e.g. Rheumatoid Arthritis, Lupus, vasculitis). 
I'm wondering what we could call this group of diseases when communicating with patients and the public so that it's clear what we mean? If we describe this as 'arthritis' for example, would women with Lupus or vasculitis identify with this group? Or would auto-immune diseases that affect the joints and muscles make sense?
I'm hoping to talk to some patients about this later in the week, but it would be great to have some ideas to take to them. Any advice from clinicians and researchers working in this area on terminology that we might use would be very welcome.
Thanks,
Rhiannon  
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I agree with Hans that you will muddle your clinical waters if you include conditions such as fibromyalgia, chronic fatigue, etc.  The more specific the group you look at, the fewer outliers.  The best of luck.
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Is rituximab useful in patients with myastenia gravis with and without rheumatic inflammatory diseases or HCV infection ?
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Biribidobiribbu'  
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Are there any instances where immune-based (inflammatory) diseases progress more rapidly in women than men?
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Sure. For example, progression of rheumatoid arthritis  has been shown to often be more rapid in women than women. See: 
Best wishes!
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We are looking at DAMP in its role as mediator of inflammatory cytokines in muscle tissue. What is your preferred method for determining DAMP level?
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I hope that following information will be helpful.
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I'm trying to make contact dermatitis model with FITC/aDBP.
General protocol of model use 20ul 0.5% FITC in vehicle (acetone : DBP = 1:1) per one ear. 
The amount FITC in 0.5% of 20ul vehicle is 0.1mg. It's too small amount to measure. 
So, I was wondering it is possible to make FITC stock (for example mix with acetone first and store, and before apply to ear mix with DBP) 
If anyone who made this FITC/aDBP model, could you give me some advice for me? 
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I have not worked with FITC model. But generally for each mice you require 40 ul (20ul to each ear) and 40*6=240 ul for each group. Considering you have 3 groups you need 240*3=720 ul. If you consider dead volume and wastage, at least 1 ml you need to prepare per study. So you can easily weigh 5 mg and dissolve in 1 ml of vehicle.
Hope it is useful
Nagaraj
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  • i'd like to start work on carrageenan induced paw edema i have been selected paw edema so could any one suggest a best treatment period for analysing protective effect of selected compound on paw edwma.
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Usually Carraggeenan paw oedema lasts for about 24 hours with a maximal at about 6 hours., depending on the protocol/concentration used... The compound you select and it's treatment regime rely heavily on the pharmacokinetics and dynamics of the compound, and the route of administration. a compound if given  s.c or i.p is best given about 30 min prior to the carrageenan, but if it has a short halflife high clearance, then you may need to redose. If you give it orally, it depends on the Tmax, and when it is highest in plasma... usually give it some time prior to the carrageenan admin (i.e. 30min-2 hr prior)... but again, if it is rapidly cleared then it may seem in effective.... If given I.v it can be given sometime during the oedema, but that said it may not be effective anyway as it depends on the PK/PD properties. The carrageenan oedema can be very non-specific and many compounds can be ineffective in this model if they target specific pathways. Does this help?
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The patient is 17 years old girl. Apart from being obese, there was no previous health problems. In April 2015 she underwent tetanus and diphtheria vaccination.
Suddenly, 17 AUG 2015, she mentioned intermittent scotomas. After the next 3 days, she had blurred vision and visual field defect (central blurred spot) in the right eye. Next, transient scotomas appeared in the left eye. Over next 4 days visual acuity decreased to inability to read.
Since the beginning of the symptoms she was seen by several ophthalmologists, who finally diagnosed: APMPPE.
Solu - Medrol (1000 mg/day) for five days (since 27 AUG 2015) was given, then methylprednisolon orally 48 mg a day is being continued. Slight improvement of visual acuity in the left eye was occured.
Toxoplasmosis, Toxocarosis, Lyme disease, Syphilis, CMV, EBV, HIV, HCV were excluded.
Chest X - ray image and brain MRI (without angio -) was normal .
Basic biochemical tests were normal, apart from urinary tract infection, which was succesfully treated.
ANA – screen, anty PR-3 (c-ANCA),  anty MPO (p-ANCA), serum protein electrophoresis, IgA, IgM, IgG – the results were within normal limits. Monoclonal protein and onconeural antibodies were absent. .            
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Does anyone remembered to withdraw the Caffeine from her diet?
In time: which is APMPPE?
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To improve data and reduce variability i would like to move away from outbred strain (Sprague Dawley) and use inbred rats. But it is nearly impossibly to work out which strain to use from the available ones: Lewis, Long Evans, Fischer, Kyoto and many more. I know, for example, that Lewis rats are used for some neuroimmunology (EAE model) but this is different to our model (effect of systemic LPS on the brain) and therefore might not be directly relevant. Do people have any experience with this type of work and inbred rats?
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Dear Diana,
As mentioned above i recommend the dark agouti rats. They are an invred strain that are great for reliable EAE research as immunisation with IFA and recombinant MOG is sufficient, you dont require further addition of pertussis or other complete adjuvants. 
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Paradoxically, high doses of Immunoglobulin G from pooled human sera have been used intravenously for treatment of some chronic inflammatory diseases (Newburger JW et al. N Engl J Med 3 15:341, 1986; Ronda N et al. Vox Sang 64:65, 1993), presumably based on its complement attenuating properties (Lutz HU et al. Blood 88:184, 1996; Lutz HU et al. Blood 103:465, 2004). Band 3 modifications likely to occur during RBC ageing enhance membrane affinity for normally circulating antiband 3 antibodies and bring about limited complement activation (Arese P et al. Cell Physiol Biochem 16:133, 2005). I wonder if autologous IgG is at a high enough concentration in normal serum that it may attenuate complement activity in spite of potential amplification of the immune senescence response during erythrocyte ageing. I would greatly appreciate comments on the subject.
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Yes,I am agree with Dr.Csaba.
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Does anyone have any information on the use of Pentosan polysulfate in Psoriatic arthritis.
I am aware of the research of Pentosan in O.A and R.A.
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Many thanks!
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I am conducting an experiment where I would like to detect inflammatory mouse proteins and measure its concentration in SDS. Does anyone have experience on this issue? The method based in flow citometry is efficient for protein measures? Thanks.
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I have used the Mouse Inflammation Kit, that contents reagents for capture and detection of IL-6, IL-10, IFN-γ, TNF, and IL-12p70. Which tissue you will use to quantitate the proteins?
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I have purchased a beta-amyloid (1-42) peptide in order to perform an active immunization in mice. In several papers, I have read that they dissolve the peptide in water., previous to emulsify with the adjuvant. However, the data sheet of the peptide indicates that the peptide is not soluble in water suggesting the use of NH4OH or DMSO to dissolve the peptide. I am worried about off target effects of these solvents in the mice
Could anybody indicate me what is the best way to dissolve the peptide??
Thank you in advance for your help
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Hi Fernando. This question has been the subject of several previous threads so you should start by searching the Q&A.  In addition to determining a good vehicle for injections, consider how different buffers alter aggregation and oligomerization of amyloid peptides.  DMSO can be used as a vehicle, but at low concentrations <2%.  The link below is a nice summary of handling amyloid peptides-
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Hello all !
I am investigating the role of mitochondria and/or mitochondrial biogenesis in inflammatory diseases.
I found the chemicals which protected against inflammatory diseases and induced mitochondrial biogenesis, respectively.
However, in this step, I would like to proof that this chemical played a protective role through mitochondrial biogensis in inflammatory diseases.
To do that, I think specific inhibitor and/or inducer for mitochondria and/or mitochondrial biogensis are required.
Is there any specific chemicals for this?
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So-Jin, could you please clarify what you mean by "inducing mitochondria"? You can make mitochondria work very hard by using known uncouplers (like DNP), but it won't make much of ATP.. That will also induce biogenesis - the cell will want to compensate for the lack of ATP production
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Whether a drug proven to be effective in human RAFLS model can be directly taken to clinical trials?
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you have two questions. Q1/ Why are RASLF used in anti-arthritic preclinical studies? Well, they provide a good model for synovial hyperplasia ( a hallmarlk of arthritis), in that we can directly monitor the effect of potential antiarthritc drugs against excessively growing fibroblasts that are taken directly for arthritic patients. Condrocytes (erosin of in arthritis another hallmark) can be tricky to culture. Many other cell types should also be studied (macrophages, osteoblasts/clasts) prior to any further in vitro claims of efficacy in arthritis. These will provide evidence of efficacy prior to moving the study to a higher organism with joints that can develop, and be treated for, arthritis (i.e. collagen or antigen-induced arthritis in rats or mice)
Q2/Whether s a drug can go directly for RASLF to clinical trial? in a word; No. You must always have evidence in a preclinical setting of efficacy and safety in a laboratory species with the arthritic disease AND in a normal healthy (phase 1-like preclinical) animal; such as rats, mice rabbits and even dogs. All global drug authorities (like FDA and EuMA) will demand enough preclinical evidence in a lab species, NOT just cells, prior to moving to hum an trials.
Hypothetical question to you; would you take a drug for your arthritis that has only ever been given to cells, shown non cytotoxic (therefore 'safe') and effective at, say, reducing fibroblast proliferation, and expect it to work for your condition??
I hope this helps! good luck
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Stop therapy or in which circunstances you will continue 
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Some investigators have suggested that TNF-α antagonists do not need to be discontinued if the patient has isolated induction of autoantibodies without any clinical manifestations of lupus (Ramos-Casals, Brito-Zeron etal. 2007; Kerbleski and Gottlieb 2009). In another study, 4 of 5 patients tolerated an alternative TNF inhibitor (adalimumabfor 3 patients, etanercept for 1) without recurrence of ATIL after discontinuation of infliximab (Wetter and Davis 2009).In any case, your position favors the security  in the present real world. We will see in the future. Thanks !
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With vaginal epithelium culture, I get fungal infection in spite of adding fungizone to the culture media. How can one get rid of the infection in both cases; mono-layer cell culture and 3D constructs with seeded vaginal epithelial cells?
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And, also
try adding  natamycin (blocking the ergosterol in fungal cell walls) that is aldo used for Foods.
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I'm working on Western blotting for an inflammatory disease and I'm having trouble finding a good loading control to use. I have previously tried beta actin, GAPDH, and alpha tubulin, but all appear to be too saturated. TBP was then tested but the variation between individual samples is too high. I'm thinking about trying ywhaz next. Anyone have any other suggestions? Thank you lots.
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Maybe you could use a lower amount of primary/secondary antibody? Maybe also lowering the exposition time? I've used actin most of the time without any problem, by exposing for just a few seconds the actin and longer periods for my proteins of interest.
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I would like to know why rheumatoid factors increases with age. And which molecular mechanism is implicated that this could happen.
Thanks!
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I discuss a mathematical model of a cellular mechanism for this in the attached paper. If the attachment does not link correctly, you can also find "Accounting for chance in the calculus of autoimmune disease" in my profile or at pubmed.
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I want to know what percent of total population is affected with RA?
If possible provide me the details through graphs, pie charts, or any statistical measures?
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I agree with the above. Overall, the prevalence of RA is about 0.5 to 1% worldwide, with some variation,
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Does neuroinflammation and neurodegeneration induced by continuous infusion (intracerebroventricular) of LPS occur in all CNS neurons or only in specific regions? The literature is rich in research about the hippocampus, but not on other regions. I have special interest in the hypothalamus.
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As you know LPS mediated inflammation is closely associated with nitric oxide production and up regulation of iNOS production at most sites all of which has considerable publications documenting LPS effect on inflammation. Other mediators also play a role. Systemic administration of LPS also produces change in the Nucleus Tractus Solitarii. There is a lot of literature supporting communication pathways between the immune system and brain. I have attached one for your consideration. You are treading on unknown territory as best I know and very interesting work, I look forward to hearing more.
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see above
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Please any body have a clue?
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Like the brain, there is a barrier between the cochlea and blood stream; however, there is emerging evidence showing that the cochlea is actively involved in immune reactions.
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One also has to keep in mind that the opinion about the status of the brain as immune-privileged organ is going to change. There is increasing evidence that even in the "normal" brain without any damage of the blood-brain-barrier some lymphocytes patrol the organ to search for pathogenic invaders. If this is prevented, e.g. by pharmacological blockade of the BBB by anti-VLA4-antibodies, lethal opportunistic infections of the brain were observed. Thus, even if the brain is definitively not to compare with other organs concerning the status of patrolling lymphocytes, the "immune privilege" is not absolute, but at least some basic immunological events are going on.
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In recent years there has been ample evidence demonstrating the critical role played by macrophages in chronic inflammatory diseases. While depletion of a particular subtype by antibody dependent method or by other marker dependent depletion, it may not be the best way to deal with this. If we could find a way to polarize or program by other means say harmless nutritional supplement or by a small molecule with a short life that could be tied to nanotechnology it may be of immense value.
I am wondering is there technology or technologies in progress that are addressing these issues at present? In case you are working on these lines, can you throw some insightful comments on this topic? I would greatly appreciate it.
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Here is another approach:
Bone marrow-derived alternatively activated macrophages reduce colitis without promoting fibrosis: participation of IL-10.
Leung G, Wang A, Fernando M, Phan VC, McKay DM.
Am J Physiol Gastrointest Liver Physiol. 2013 May 1;304(9):G781-92.
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A Windlass is the tightening of a rope or cable around a pivot point. The plantar fascia acts like a cable between the calcaneus and its distal insertion into the proximal phalanyx at the metatarsal phalangeal joints. When the toes are dorsiflexed (as in forefoot rocker), the heel and toes SHOULD become approximated, as the plantar fascia shortens from its winding around the metatarsal head, contributing to supination of the foot.
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Dear Jan Paul Wingerden. Thank you for sharing the articles and i will go through it .
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Normally it is chronic and only diagnosed after when patient suffer from severity symptoms. Therefore I want to know is there any method of its early detection.
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Current guidelines indicate that faecal calprotectin values > 150-200 could be a good indicator for endoscopy performance. Nevertheless, this investigation needs to be suggested by the symptoms of the patients. I do not think that a screening population for IBD may be a useful tool.
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http://www.nytimes.com/2013/02/12/science/testing-of-some-deadly-diseases-on-mice-mislead-report-says.html?hp&_r=0. Not a surprise to me. Burn outcomes with potential therapeutic modalities in mice and rats certainly have not predicted outcomes in humans, i.e. a series of clinical trials with anticoagulants based on rodent results failed in humans.
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Very important article to keep in mind when evaluating published material on inflammation, wound healing and burns in mice. However, mouse models are extremely useful for defining many genetic deficiencies in humans.
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Can anyone recommend chemotherapeutic agents or a good reference comparing efficacy at local injection?
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There is a difference between acute and chronic inflammation. Chronic inflammation is cancerogenic especially in people with damaged DNA repair mechanism. Acute inflammatory response, especially granulocytic component, has a important role in tumor regression (see on internet about Coley toxin and SR/CR mice)