Histamine - Science topic

I'm working with THP1 macrophages and I want to stimulate the H1 receptors with histamine. What is the best time to achieve the best stimulation effect?. I'm not sure about that. I have read different works and most of them indicate 24-hour stimulation.

Most of the acute rhinitis are due to allergic and non allergic ( infective ) causes e.g, influenza virus, rhinovirus etc. What ever the causes of rhinitis, main features are due to the action of chemical mediators released from mast cells or lymphocytes. In this sense histamine has very short time ( half life 20 minutes) role in comparative to other chemical mediators causing rhinitis. So, antihistamine has little role to abate the symptoms. Rather NSAIDs have some role over paracetamol and antihistamines.

But single dose of prednisolone has best action to abate the symptoms promptly with in 10 to 12 hours. We have treated recently 14 cases of acute rhinitis with single dose of 40mg along with famotidine 40mg 12 hourly. About more than 90% symptoms abated with a single dose of prednisolone. Fifty percent of the patients required another dose of prednisolone after 24 hours.

I try to synthesize N1-benzylhistamine

by meaning i need reaction happen at N1 of histamine not at primary NH2 group

Nowhere in my education and training do I remember anyone suggesting antihistamines for neuropathic pain. I've used Neurontin, Lyrica, anti-depressants, desensitization, mirror therapy, Lidocaine patches, capsaicin..... But antihistamines just never occurred to me.

Until, that is, I was desperate for pain relief from my shingles. In a moment of burning, somewhat itchy desperation, I grabbed the Benadryl cream I kept on hand for occasional skin reactions. It worked--not just on the bit of itchiness, but the whole spectrum of my shingles pain--the skin ripping off, stabbing, bone-breaking pain.

Fast forward a couple of weeks and I'm looking to relieve some sinus drainage and I try Xyzal. Even better! I can't believe the relief I'm experiencing from these two medications.

So, I went to PubMed. There's a little bit here and there, but not a real focus on the role of histamine in neuropathy. While my experience is anecdotal, the significant reductions in pain immediately following 2 different routes and classes of antihistamines suggests a possible histamine component to neuropathic pain.

Are any clinicians recommending or prescribing antihistamines for their nerve pain patients? Is this something to add to our armamentarium of treatments?

I have performed docking of Human Histamine receptor H1 (PDB - 3RZE) with ligands such as Propofol and Eugenol. After completing docking process, I want to conclude final results and obtain the best docked conformation. What parameters and steps should I consider for this?

I am a functional medicine physician utilizing a protocol for depression and all mood disorders that looks at key markers that reflect neurotransmitter activity. Based on extensive research, as many as 95% of persons with mood disorders are experiencing one or more of 5 major biotypes; these nutrient conditions are highly responsive to proper supplementation. Markers tell us about nutrient status, oxidative stress and methylation. Methylation with respect to SERT and DERT is highly useful as it impacts levels of serotonin and dopamine activity. Overmethylators are high in these nuerotransmitters. Undermethylators are low. This is because their reuptake enzymes are either over or under active.

I am looking for a reliable antibody against histamine and was wondering if anyone has any experience?

Anti-histaminergic (H1 antagonists) drugs could be prescribed at low doses for their sedative effects. Nevertheless, some reviews and articles reported a decrease of sedative effect that can occur as soon as 10 days. What could explain that antagonists H1 do not longer lead to sedation after fews days ?

I would like to know if there is any possibility to apply the capillary colum CP Sil 88 for food safety analysis?

I realise that it is a CG column for FAME analysis but I would like to investigate if someone knows hat it is possible to apply it for pesticides, contaminants, histamine, or in the food safety field

Thanks in advance

What should be the wavelenght range ? If anyone have reference please suggest me.

I need to to pulse some primary T cells with an enzyme that has bacterial lipopolysaccharides (LPS) as a substrate. The enzyme is generated by Antigen presenting cells and secreted to target LPS in order to neutralise it, since LPS can induce an immune response. If I purchase this recombinant enzyme tagged with Histamine and purified from E.coli, will it be active when introduced to cells in culture at 37 degrees Celcius?

I am investigating products of mast cell degranulation and see if there is any correlation  link between the release of Histamine and Beta-hexasominidse.

i am going to use histamine as skin prick test in cattle but I am unable to find the dose rate of histamine in cattle. I could only find it in humans. 

I am going to study the effect of a mast cell stabilizer on histamine content in rat kidney tissue. What are the methods used for this purpose .. chemical methods, colorimetric ,ELIZA , .... etc. Many thanks

Hossam Mohamed

National Organization for drug control and Research

I want to determine the drug effect in inhibiting human bronchial smooth muscle contraction induced with histamine. Currently, I tried it with

1. 0.5 X 10^6 cell per well in 24 well plate with 2 mg/ml collagen gel

    - histamine concentration : 10 - 100 uM

2. 0.2 X 10^6 cell per well in 24 well plate with 1.5 mg/ml collagen gel

    - histamine concentration : 10 - 100 uM

Both conditions did not work. The induced group showed no difference with the normal control group.

And, for the 2 mg/ml collagen gel, the spindle shape of the cell did not look normal as compared to the 1.5 mg/ml collagen gel.

Any recommendations to improve my assay?

Thanks.

Best regards,

Hui Min

(PhD student)

I have work histamine decarboxylase gene (Hdc) from histamine forming bcateria, my primer was amplified the particular regions but i will get primer diamer in agarose gel... how to avoid the primer diamer in agarose gel?

I am interested in the progression of events that link histamine producing foods to poor gut health, leaky gut, under methylation, pyroleia, sleep disorders, tinnitus and the skin itching. Then how a person can crave the very foods that are bad for them and appear to need less sleep eventually leading to mental health issues.....

histamine, ELISA/EIA, supernatants

I don't understand why the standard curve is decreasing as a function of histamine concentration instead of increasing.

Could somebody help me to figure it out?

while in vitro antihistaminic activity muscles get tired  and does not give contraction with histamine solution 

I  was wondering if there is a general consensus as to which marker is more accurate and/or suitable at reflecting mast cell degranulation in vitro? I've read that beta hex is more accurate and histamine tends to be more inconsitently measured/detectable (more inconsistent results).

Looking forward to some experts' comments!

Thanks much

Upon carrying out CV studies of Serotonin and Histamine (separately) it appears the oxidation half reaction is irreversible with the successive peak values dropping significantly. Which reaction mechanism does these two reactions correspond to which conforms with this observation? 

It was observed that the allergic patients have 1350 % elevated level of IgE in systemic circulation as compared to healthy individuals. What would be the numerous symptoms observe during this situation. How to control allergies like urticaria/itching under such condition. Which one is the best class of drug to control it i.e. Immune suppressant like Azathioprine or Antihistaminics or Others class of drugs? 

Need to test on tears (small fluid sample)

We have data for pure histamine. Our prototype is detecting tuna meat which contains histamine. There is a possibility that the data collected in our prototype has noise or other parameters are being detected aside from histamine. We want somehow to filter those collected data and match these data to our pure histamine data. 

any algorithms that may help to extract those data? 

There have been few tests that I have seen done, and the processes are out of date and quite extensive. I was hoping there may be an easier process (if you know a way to do it, please provide as much detail as possible) so that I may perform the experiment at my university for my senior project. Thank you.

I use sodium tetraborate buffer. It never dissolves easily in water (10.0 mM, adjusted to pH 10.0 by 10.0 mM & 1.0 mM NaOH). It still look hazy. It is to be added to (OPA, Methanol and 2-Mercaptoethanol)

When u extract histamine in fish and analyse by UPLC, u find lot of orher peaks other than histamine. Could someone list lhe other metabolites and is there a way of identifying it.

I will use to react with 1,3,5-Benzenetricarbonyl trichloride.

I am validating the histamine content of tuna fish through the use if FTIR Spectrometer. However, I can't find any procedure to do extraction for spectrometer. I hope you can help me with this. Thanks.

We are informed that MIT used a modified single-walled carbon nanotube to detect chemical produced by spoiled meat. However, the detection of chemical is through vapor/gas. We are trying to use this concept in different sample which is for solid matter like spoiled meat. 

I'm doing beta hexosamidase to check for the release of histamine from my cells. However, the colour of  the supernatant samples develops only after a few days. What could be the reasons? Could it be the passage number of my RBL cells? 

I am trying to activate T cells by stimulating WBC with TNF-alpha and/or histamine. I hope to detect an activation status of CD3 cells detectable by CD69 over-expression (as a model of inflammatory activation). Do anyone share a protocol to stimulate WBC with TNF-alpha/histamine in order to observe this activation?

I want to understand how carageenan causes inflammation. Carageenan induced paw edema is a standard method to get the idea of anti inflammatory of different products. But I am not able to understand how inflammation is caused by carageenan. Which pathways get activated and what other factors which are involved. I want to understand the process of carageenan induced edema with time.

As it is closely related species, in the spoilage fishes u find close retention times

Ka1 and Ka2 of Histamine molecule 

As histamine is a non florescent compound, can we detect it without derivatization with UV detector. If possible, at what wavelength do we have to detect.

Hi, I am looking for the dosage of this agonist methylhistaprodifen and dimethylhistaprodifen in mice in mg/kg. I haven't yet found any dosage in other species as well. Has anyone worked with this specific agonist?

We need to know how to determine the levels of histamine in serum and in mammary cancer in an animal model. Can it be made using frozen samples? What is the best technique?

I was wondering if anyone more experienced than me would be able to help me with my RT-qPCR data analysis.

Experimental background: I am looking at the effect of histamine and hyperoxia on the expression of 3 genes in healthy term placenta. I have five biological groups; uncultured placenta (control), 20% oxygen, 20% oxygen with histamine, 8% oxygen and 8% oxygen with histamine. I have an n of 3 for each group and ran each sample in duplicate. I have done one gene thus far. I have normalised my ddCt values according to a method by Willhelms et al. (http://www.ncbi.nlm.nih.gov/pubmed/18485881) as placenta is heterogeneous and I wanted to take into account variation within each treatment group. This has been fine and I have produced a graph showing my fold changes relative to the control and calculated 95% CIs. This shows that all my explants significantly increase the expression of the gene compared to control.

Main question: what should I be doing to determine whether there is any difference in gene expression between my groups? Should I be using the fold change data (so effectively looking at whether one group increases gene expression compared to the control more than the other), or should I be analysing actual gene expression between each group (dCt)? The problem with the second one is that I end up with non-normalised values and I am not sure how to normalise them (I rigidly followed the method in Willhelms' paper with an attached spreadsheet with formulae!). The paper suggested using Mann-Whitney to compare two fold change groups. But is this the best way to show changes in gene expression?

Any advice would be greatly appreciated.

I'm going to use the RBL-2H3 cell line for my in vitro study involving the inhibitory activity of honey bee product on mast cell degranulation. I just want to know if there is anyone who has experience dealing with this type of cell? Is it easy/difficult to handle? I would be glad if someone can share their precious experiences working with this cell.

Recently histamine-3 receptor was discovered but its physiological role is unknown. Is there any report related to this concern?