Questions related to Inflammatory Diseases
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,
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 .
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.
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?
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?
Currently theorising the mechanism of atopic dermatitis and how calcium signalling can be related to this skin inflammatory disease.
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.
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.
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?
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?
- 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.
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. .
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?
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.
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.
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.
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
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?
Whether a drug proven to be effective in human RAFLS model can be directly taken to clinical trials?
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?
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.
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?
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.
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.
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.
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.
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.
Can anyone recommend chemotherapeutic agents or a good reference comparing efficacy at local injection?