- Joanna Morrell added an answer:34How to get rid of non-specific signals in the staining of immunofluorescent microscopy?We are trying to stain mouse lungs in an allergic asthma model for immunofluorescent microscopy. We are blocking the tissue with unlabeled mouse and goat IgGs, 2% BSA, avidin, and biotin. Nevertheless, we still get a strong non-specific signal mainly from the branchial epithelium filled with mucus. I would appreciate any suggestions on how we could get rid of these non-specific signals.
- Silvia Josefina Venero Fernández added an answer:4How can I explore the psychological factors which might have an impact on asthma symptoms what would be the appropriate qualitative study design?
please let me know and give reference to my objective.
I suggestion use the Beck anxiety and depression but you should consider other factors characteristic of their populationFollowing
- Ishag Adam added an answer:1Do premature infants have a better Apgar's score if their asthmatic mothers get ICS?
If asthmatic mother get inhaled corticosteroids has fewer or no attacs, better oxygienisation. But the absorbed fraction has effect on her baby. We treat pregnant asthmatic women with budesonide based on safety dates. Has this fraction lungselectivity in embryos too? Can it facilitat the maturation of airways? Have somebody dates? Are there any differents between budesonide, cycloserin, BDP and fluticasone -P/F ?
Unfortunately asthma itself during pregnancy has many effects on the mother and unborn baby. These can not be dissected from the effects of its treatment and we can hardly say it is due to the treatment of AsthmaFollowing
- Mitch Gersh added an answer:2Why is it important to understand the differences between diagnoses (i.e., COPD, CHF, ARDS, asthma) when determining appropriate ventilator settings?
I'm interested in the potential adverse effects when inappropriate settings are made and the challenges clinicians face when making the right choice. Also, how might these decisions change given the particular patient demographic (i.e., neonate, pediatric, adult, geriatric)?
These questions relate to research I am doing for an article I'm writing for RT: For Decision Makers in Respiratory Care.
There are a couple of things to remember. First, it has been shown that it is not only the ARDS patients but all ventilated patients should be ventilated at a volume of 6ml/kg to prevent barotrauma along with ARDS or multisystem failure.. Second, it is not only the pulmonary disease that affects how you manage a ventilator. You could be more limited in adding PEEP when a patient is septic, you are more limited on the rate when someone has Asthma or severe bronchospasm and have to accept or even use permissive hypercapnia as a plan. There is no absolute perfect way to ventilator all patients based on age or disease process because there is usually more than one process going on. The art of ventilation is titrating and adjusting to the individual patient. Managing for a pH, not a PaCO2 maintain adequate oxygenation but not hyperoxygenating and making sure the patient is in sync with the ventilator. This requires close observation of the patient and adjusting the ventilator settings to the patient. These concepts apply to all patients from newborn to geriatric across all types of disease processes.Following
- Majid Mirsadraee added an answer:10What is your opinion about using antihistamines in asthma?Drugs such as Loratadine or Zaditen.
Low effect high sedation good action in limited subjectsFollowing
- Randall C Johnson added an answer:1Synaptotagmin-13 differentiated expressed in asthma (in 2 different datasets), is it biologically consistent?
I get 2 geo dataset of RNA expression (http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE43696 and other), same platform same use, and both bronchial epithelial cells, and classes (control, mild moderate asthma, and severe asthma).
The aim of all of this was to classify as best as i could with supervised methods. Without FSS (feature subset selection), we got bad results. But, when we reduced both datasets we get AUC > 0.75 as overall. So, this filter is consistent and the sondes(genes) we get are important.
It is true (and biologically consistent) because we get genes like CPA3, WNK4, SCGB1A1.. Although, we find genes like TDRD5 (spermiogenesis), C12orf39 (agoraphobia), PLAC4 (placenta-especific), and syt13.
What could you say about this? Are they just some random genes? Or it could be logical to find those things?
If you want more information about the procedure i have a document about it.
Thanks in advance.
That sounds interesting. A meta analysis including additional data sets would be helpful to reduce the likelihood of false positive associations. Gene-gene and gene-environment interactions are complicated enough that it seems one can always find a plausible mechanism or pathway for just about any gene. Sometimes you find something unexpected (and exciting) that pans out, but often they don't.Following
- Closed account added an answer:3Role of magnesium sulfate in acute exacerbation of bronchial asthma and chronic obstructive airway disease: What is the difference and efficacy?
Which randomised-controlled trial (RCT) and study have been done to explain this?
Dear Dr Bikash, Thank you for the thorough explanation with evidence-based supports.Following
- Jamal AlKhateeb added an answer:8Can anyone recommend literature for Asthma and mental health?
My background is in mental health, however I am new to the study of asthma. What are the key conversations regarding the interaction of these two elements should I get myself up to speed on?
I am researching this topic currently. PubMed, ScienceDirect, ERIC, and SpringerLink provide a comprehensive list of studies related to bronchial asthma and mental health (psychosocial aspects). Good luck.Following
- Bizaya Malla asked a question:OpenIs KL-6 produced in lung bronchial epithelial cells ?
I am curious to know if KL-6 protein production is diminished in asthma and COPD. I found literatures suggesting that KL-6 is primarily produced by ALVEOLAR epithelial cells type II, but could not find literatures showing if KL-6 is also produced by brochial epithelial cells. Would be glad to know primary cell culture from bronchial biopsies for expression of KL-6.
- Pal Bela Szecsi added an answer:21Does a person whose Total IgE test is positive i.e., concentration of IgE is above the normal level, go for a repeat test in the same year?
Also, do we have separate kits for reagents, conjugate and calibrators for Allergen Specific IgE or the complete thing comes in one kit?
The short answer is NO.
Total IgE have limited clinical use and even levels of allergen specific IgE do not reflect clinical symptoms.
So measure total IgE seldom, and certainly not repeatedly.Following
- Oscar L. Sierra added an answer:1Does anyone have treated A549 cell with IL-13 to induce periostin release?
In many papers it is mentioned that IL-13 can induce periostin release from airway epithelial cells. But I did not find about the A549 cell. Is there any information regarding the release of periostin from A549 cell after IL-13 treatment?
The best approach is to have at least two types of cell cultures: 1-regular submerged cells attached to plastic or collagen coated multiwell plates and treat with a known dose of IL-13 and harvest cells at different times for RNA and Western blot. 2-Differentiate cells in air-liquid interfase cultures and do a likewise treatment. If IL-13 does not stimulate periostin mRNA synthesis or protein accumulation then it's unlikely that you'll figure out the proper conditions.Following
- Marlina Lovett added an answer:12When do you use Theophylline in pediatric patients?
Theophylline in pediatric patients
I have seen Aminophylline used for very sick bronchospastic patients. The times in which I have seen it used, are patients that are either intubated or on high BiPAP settings with a large amount of bronchodilators already being used (continuous albuterol, magnesium, atrovent, IV steroids, +/- ketamine). But, when it is used, levels are followed quite frequently.Following
- Sailesh Palikhe added an answer:4Does anyone have any idea about cytokines that can induce periostin release?
I want know whether there are cytokines besides IL-13, that can induce periostin from airway epithelial cells.
Thank you all for your answers.
I was looking for cytokines other than IL-13 and IL-4.
I will try with TNFα and IL-17 to induce periostin release from airway epithelial cells.
- Michael Rostagno-Lasky added an answer:14In a metacholine challenge test - I have observed that some patients overcome the challenge test, while some don't - why is it so?
What is the ratio of negative positive patients passing the induced asthma test even though asthma is duly induced during the test and reversed if proven detrimental?
Bronchospasm exists on a continuum. Asymptomatic patients (on days of testing) may pass an MCT on one occasion and fail on another (20% decline in FEV-1). Some patients who test + on MCT will decline asthma medications stating (to the effect) that their breathing does not improve, and their breathing is fine as is. Patients on the lower end of normal for FVC will be affected clinically far more by any given degree of bronchospasm than those at the high end (the variability in my experience is that FVC varies from 70 - 169% of predicted, in the absence of any detectable pulmonary pathology (~10,000 patients). A patient whose FVC was 140% of predicted, & an FEV-1 decline of 35% during MCT, had notable expiratory wheezing, and declared that he felt fine, and had routinely run up many flights of stairs feeling exactly this way in his capacity as a firefighter. He reacted as expected to albuterol. I'd expect that had his FVC been 80% of predicted, his clinical appearance and subjective experience during MCT would have been more severe. Physical exhaustion as the MCT proceeds can bias the test, while remaining repeatable. Some patients show a sharp decline in FEV-1 on the first FVC, & a considerable increase on trials 2 and 3. If trials 2 & 3 are used, being repeatable, and trial 1 is discarded, it may miss those patients who rapidly improve post methacholine exposure. Never under estimate biochemical diversity. Clinically, choosing whether to treat using only MCT results, may not be optimal for all patients.Following
- Rhonda Vosmus added an answer:4What percent of asthma in the US is considered moderately persistent, utilizing NHLBI Guidelines?
I am looking for percent of each severity class (per NHLBI Guidelines) generally seen in Primary care.
- MOHAMMAD Nabavi added an answer:9Do you consider Bronchial asthma and Hay fever are atopy associations or a collective term for a group of diseases?
The word ‘atopy’ was introduced by Coca in 1923 as a convenient collective term for a group of diseases, chief among which are asthma and hay fever, which occur spontaneously in individuals who have a family history of susceptibility.
allergic rhino-sino-tonsilo-adeno-bronchitis is the correct name of these two condition. in fact you can not manage asthma without considering underlying allergic inflammation of the upper airways and vice verca. Hence the unified airway theory or principle is the correct terminology.Following
- Amy C. Paulson added an answer:5How could we generate an asthma warning system through monitoring environmental factors?
Asthma is a serious issue. Early warnings for asthmatic are very important. In many countries pollen count or its covering area, pollutants, dust are monitored, but there is a need for combined efforts to minimize the triggers.
We definitely see seasonal variations and geographical variations in asthma exacerbations. Where I am located is one of the worst places for people who have asthma to live. It's a combination of factors - long, warm wet growing season; pollen and mold rich environment; and, significant pollution from industry, ports and traffic corridors. You might take a look at this - I believe they used a modeling approach to determine which areas are the "worst" when multiple factors are considered together.
- George Christoff added an answer:5Who knows about ongoing studies of vitamin D as a possible adjunct to standard therapy in paediatric asthma?
I have published recently about the association between asthma exacerbation and hours of sunlight exposure in UK children. I am interested in undertaking a large study of vitamin D versus placebo to see whether this reduces asthma admissions. Obviously I am aware of the Majak study but does anyone know what active research is going on?
This could be of some help as well: http://www.waojournal.org/content/7/1/27Following
- George Christoff added an answer:5How useful are asthma action plans for pediatric asthma patients?
I am looking into the compliance rate of asthma action plans in the pediatric patient population. How useful are they. Are there results from focus groups regarding asthma action plans?
Asthma action plans are the corner stone of modern asthma management. So their usefulness is beyond question. On the other hand it depends to a great extend on patients' compliance. A prerequisite for a high compliance with an asthma action plan is it being tailored to the specific characteristics of the patient group. If you need further information on asthma action plans in different focus groups I suggest you try a search in the medical databases available.Following
- Emanuele Cauda added an answer:3Who should I contact if I wanted a "bronchodilator inhaler" charged with solid spherical microparticles?
I need to find a company/facility that is interested in loading a drug inhaler cartridge (something generally used for asthmatic people) with monodisperse microsize particles. These are solid spheres in the range of 1-10 um. I want a cheap and quick way to create an aerosol using this inhaler for the testing of samplers. Any suggestion and contacts are very welcome.
Thanks for the suggestion. I searched hard-shell capsules and they might be good for my application. I need to discover though if each capsule can be used only once. If so, this could be problematic considering the cost of the microsphere and the fact I would need few micrograms in the each capsule.
I am very familiar with cascade impactors and I don't think is what I need for this idea.ThanksFollowing
- Isra Dmour added an answer:2Any guidelines on dosing with a MDI(metered dose inhaler)in a BE study?
Any ideas on minimizing inconsistency of dose delivery with MDI's in bio studies. Eg contamination, statics and ?inspirational flow rate? Is this at all necessary?
I think you may benifit from this:
Guideline on the Requirements for clinical documentation for Orally Inhaled products (OIP) Including the Requirements for demonstration of therapeutic equivalence between two inhaled products for use in the treatment of ASTHMA and Chronic Obstructive Pulmonary disease (COPD) in Adults and For use in the treatment of Asthma in children and adolescents CPMP/EWP/4151/00Rev1, 22 January 2009 European Commission, Brussels, ENTR/CT 3, Detailed guidance on the collection, verification and presentation of adverse reaction reports arising from clinical trials on medicinal products for human use, Revision 2, April 2006
ot this :
Guideline On The Investigation Of Bioequivalence. Committee For Medicinal Products For Human Use (Chmp), European Medicines Agency (ema), Doc. Ref.: CPMP/EWP/QWP/1401/98 Rev. 1/ Corr, London, 20 January 2010.
Available at: http://www.ema.europa.eu/docs/en_GB/document_library/Scientific_guideline/2010/01/WC500070039.pdfFollowing
- John D Blakey added an answer:2What is the best humanized monoclonal antibody used to treat lung inflammation in asthma disease?
Monoclonal antibody therapy for asthma disease.
Because asthma is a syndrome rather than a specific disease, there are no "best" treatments. As we've previously seen with medications such as LABAs, ICS, and montelukast what is "best" depends on the processes underlying the asthma and the outcome measured. From the landmark FACET study to recent papers (e.g. Flood-Page then Haldar) investigating Mepolizumab, the effectiveness of a medication depends on patient selection and endpoints measured (airflow measures vs exacerbations). As more antibodies are brought to market, what's best will also be influenced by ease of administration and shelf-life, and by cost.
Sorry not to answer your question definitively, but I'd be surprised if anyone did. In a few years time we should have a better handle on who should have mepo, who lebrikizumab, etcFollowing
- Daniel Laskowski added an answer:4What is the best method for induction of bronchial asthma in mice?
There are many different methods for induction of bronchial asthma using mice as animal model particularly by OVA albumin. Can you suggest other ways to get good results?
- Joanna Szram added an answer:2What has a higher potential to cause asthma - glycol ethers or organic quaternary ammonium compounds?
Both glycol ethers and organic quaternary ammonium compounds are increasingly associated with causing asthma among workers handling chemicals which contain either or both of the compounds.
However, little information other than their intrinsic characteristics of being airway irritants is available.
How comparable can these two groups of compounds be?
Organic quaternary ammonium compounds are a known, reported low molecular mass asthmagen. There is a wealth of information available on this topic in the published literature; also the University of Manchester have worked with chemists to create an Asthma Hazard Program; headed up by Professor Raymond Agius.
glycol ether is to my understanding a VOC and so is irritant/exacerbatory of pre-existing airway hyper-reactivity. the potential for irritant induced asthma , aside from an acute, normall one off, high dose exposure is still debated. again, lots of literature out there.Following
- Michael E Wechsler added an answer:9Can anyone suggest whether increasing ICS dose or adding LABA to ICS works best for Asthmatic patients?
In asthmatic children whose symptoms are uncontrolled on standard doses of inhaled corticosteroids (ICS), guidelines recommend to either increase the ICS dose or to add further controller medication, e.g. a long acting beta-agonist (LABA)
Is it important to follow the stepwise approach in treating Adults and children with asthma which almost all international guidelines recommend, or is it ok to change it around if you see that it works best!
In addition, In Bahrain, in the primary health care setting precisly, physicians tend to 'skip' starting with mono therapy (ICS) and start directly with combination Tx like seretide Diskus, patients find it easier to use and they get better on so many levels,, so is that ok?
There is no perfect answer to this question for all subjects.
Different studies have shown that addition of either of these agents, or even an anticholinergic therapy such as tiotropium, can be effective as add-on therapy.
One strategy is to try to identify predictive biomarkers, such as exhaled NO, or blood or sputum eosinophils. For many of these patients who have increased levels of these,, increasing the dose of inhaled corticosteroids is often beneficial.
In the acute setting, when a patient is poorly controlled, I try to get them under better control and i often do both, increase the dose of the inhaled corticosteroid AND add a long acting beta agonist. Once well controlled, I will step them down sequentially.Following
- Eskandar Ahdab added an answer:11I want to ask about pattern of asthma prevalence in children age groups whether there is any pathophysiology of disease describing different prevalence?ISAAC studies have commonly used age groups of 6-7 years and 13-14 years for describing the burden, why were other age groups not taken into account ? Is there any scientific justification for that? Some studies have also used age groups of 3-7 years, 8-14 years and 15-17 years to find out the difference in prevalence using ISAAC questionnaire as study tool. Are they justified in that by choosing these age groups and if yes, what could be the possible explanation of that in we look at course of disease whether there is increasing trend as the age increases (3-7 years) and there is the dip in between years (8-14 years) and then again rise in the trend (15-17 years)?thank you Kathy and BenjaminFollowing
- Ayodeji Osunkentan added an answer:3What is the current best evidence in the treatment of asthma in adults older than 60 years?If possible, provide a recent systematic review in pdf
- Prasad D.K. Dhulipala added an answer:2Does anyone know a protocol for isolation and culture of airway smooth muscle cells from the trachea of mice?I have prepared a mouse model of asthma. I need ASM cells to do some in-vitro experiments. Can somebody tell me a nice user friendly protocol please?
Please contact Yangxio Wang at Albany medical college or Dr. Micheal Kotlikoff at Cornell Univ.Following
- Israel Amirav added an answer:4Are there articles about Zileuton as inhalable formulation?
Did anybody read or know any reference/ research work about Zileuton as DPI or MDI formulation !?
In addition to my previous answer- Invion company work with 3M Drug Delivery Systems to develop inhaled formulations of zafirlukast to be delivered using 3M’s MDI technology.
- Khaled Saad added an answer:4What are the new data in GINA guidelines in pediatric asthma?GINA guidelines in pediatric asthma.
Thanks José Angelo RizzoFollowing
A form of bronchial disorder with three distinct components: airway hyper-responsiveness (RESPIRATORY HYPERSENSITIVITY), airway INFLAMMATION, and intermittent AIRWAY OBSTRUCTION. It is characterized by spasmodic contraction of airway smooth muscle, WHEEZING, and dyspnea (DYSPNEA, PAROXYSMAL).