Science topic

Asthma - Science topic

Asthma is 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).
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I'm trying to calculate the sample size I should have to study gene expression of IL-4 in asthmatic patients so I need a paper that is close to my work.
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You can use this study if you still do not calculate the sample size:
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As known, licorice root is used for the treatment of peptic ulcers, asthma, pharyngitis, malaria, abdominal pain, insomnia and infections.what is the reason of this diversity?
I need a good reference for that.
Best Regards
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Licorice is used to treat dermatitis, liver swelling, mouth sores, and a variety of other ailments, but there is no scientific evidence to back up most of these claims.
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I would like to ask about your experience in reporting spirometry results.
In the reports from spirometry examinations we usually see the flow-volume and volume-time curves obtained from the best maneuvers. What criteria for displaying best flow-volume or volume-time curves are recommended?
I think, we have few options:
1. Select curve with the largest FVC
2. Select curve with the largest sum of FEV1 and FVC
3. Select curve with the largest FEV1
Of course the curve should be correctly performed (according to ATS/ERS standards).
In the example below the results of PRE/POST examinations are displayed, but unfortunately there are no information about selection criteria of the curves from PRE and POST maneuvers.
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Repeated spirometry and repeated attempts is to achieve 3 acceptable FEV1s and FVC and choose the highest FVC in restricted disease and highest FEV1 in obstructive disease , this will give a good information
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Asthma is a chronic, obstructive disease;
In asthma we have hypersecretion of mucos ;the main component of mucos is mucin ; the main airway mucins are muc 5ac and muc 5b that are released from goblet cell and submucosal glands ,respectively.
Asthma characterized by some changes, like: thickening of the lamina reticularis, epithelial shedding, subepithelial fibrosis, inflammatory cell infiltration, goblet cell hyperplasia, myofibroblast proliferation, smooth muscle hyperplasia and hypertrophy, and neovascularization of the airway wall
According to the findings ; increased amount of the muc5ac and decreased amount of muc5b is observed.
Goblet cell hyperplasia can cause more expression of muc5 ac but there is no evidence for the reason of decreased amounts of muc5b .I'm looking toward this decreasing reasons.
I will be thankful if you share your ideas with me .
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يمكنك مراجعة اهل الاختصاص
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Antihistamines block the actions of histamine and also have effects on inflammation which is independent of histamine-H(1)-receptor antagonism. Many physicians prescribe antihistamines for asthma patients. However, recent studies have shown that controlling allergic rhinitis with antihistamines has a small, indirect effect in improving asthma symptoms.
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No, antihistamines do not improve bronhial asthma. Some benefits could be present in rhinitis, asociated to asthma.
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Lately there has been an animated discussion on the adjustments GINA 2020 made to asthma pharmacotherapy and further changes that were made recently in GINA 2021: bottomline: we should try to avoid at all cost SABA only use.
Two treatment tracks are proposed, Track 1 and Track 2, the former being the preferred one. In 12+yo patients with asthma GINA 2021 suggests to fuse Step 1 and 2, leaving for both groups only rescue ICS-FORM, without maintenance as preferred therapy (Track 1), with rescue SABA + ICS as alternative Step 1 and ICS maintenance and SABA rescue as alternative Step 2.
Patients with symptoms once a month or less and no risk-factors for exacerbations would be candidates to start in Step 1.
DISCUSSION QUESTION: should we get rid of Step 1 all together, and only leave it as a possible step-down from Step 2 once patients are fully controlled?
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Taxometric analysis is commonly done for psychiatric diagnosis to assess discrete categories vs dimension or dimensions + categories. But has it been done for medical diagnoses with similar characteristics. The best example I can think of is hypertension (HTN). I have attached a graphic file looking at the most recent systolic BP recommendation and the distribution of blood pressures in the population. I also searched available literature for taxometric analysis of hypertension and could find nothing.
Is it possible that all polygenic, quantitative rather than qualitative disorders (HTN, asthma, diabetes, etc) produce the same results as psychiatric disorders in general? (I have found one study of metabolic syndrome.)
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I can mention one study with taxometric analysis in parastic disease:
Anshu Malhotra et al. Taxometric analysis of helminths of marine fishes 1.Pedunculacetabulum spinatum n. Sp., from chlorinemus mandetta and wenyonia rhincodonti n. Sp., from Rhincondon typus. Journal of parastic diseases, 2011:35(2):222_9.
DOI. 10.1007./s12639_011_0049_0
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Hi
I am doing a research where we need to use a graph for patients to score themselves and i want to do it online. It is very similar to Peak Flow Graph for asthma
Is there a free website to do that ?
Thnaks
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Plz try above site.
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Also, is it possible to run any kind of regression analysis using two different year's data for 2 different variables? for example: co2 emission data for 2019 and asthma prevalence data for 2018.
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Hello Muhammad,
Sure, you could do this sort of thing. I think that your case for a causal relationship would be better served by using, say, 2018 data for CO2 emission, and 2019 data for asthma prevalence, however.
The question is, what is the smallest level at which you could collect reliable data for both variables? At the country level, a state level, a district/township/municipality level? The higher the level of aggregation, the greater the likelihood that observed relationships would not mirror very well what you would find if you had the luxury of tracking the two variables at the individual person level. Sociologists refer to this phenomenon as the ecological fallacy.
Good luck with your work.
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I am developing model of asthma in mice using HDM. I was asked this question in order to submit the a protocol for developing a disease in animals. Searching in the literature, I can not find any evidence of symptoms of asthma appeared on mice after house dust mite administration. Is that True?
Thank you.
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Hi, sure they do.
However, your observation may be not reliable (they rub their noses, and feel irritated). The most objective measurement of the in vivo lung function is performed by whole-body plethysmography. You measure the airway reactivity (as fold increase of enhanced pause (Penh) values for the increasing concentration of methacholine relative to baseline. Please refer to the manuscript, as attached
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People with asthma may worry whether their asthma may put them at risk for getting coronavirus (COVID-19). It can be confusing because both asthma and coronavirus share symptoms of cough and shortness of breath. What are the clear guidelines in such cases?
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Asthma patients (in most of the cases) already had previous history of symptoms suggestive of asthma and are mostly aware of their specific aural or predisposing factors with likely family history and no exposure or contact with someone with flu like symptoms. One might find it difficult to differentiate the type of respiratory distress as a sign. However, I don't expect to see fever, anosmia, headache or throat pain in a clear cut asthmatic case.
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Dear all -
I'm trying to understand if it might be an idea to treat Asthma by using small molecules produced by bacterial microbiomes. I read that several small molecules such as Ac, Propionate and others can help treating Asthma in mice - any further studies in humans?? Are there any phase 1-3 clinical trial studies on that?
Thank you and have a nice day
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Acetate or propionate don't have any direct role in treatment of any disease and in this case Asthma. These can be used as a supplement as they can help the gut microflora, or pH balance, however, they do not have any other effect/property which could directly be involved in the treatment.
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By extracting the clinical terms from the prescription which basically depends on the symptoms of Asthma diseases and apply the machine learning algorithm for prediction of diseases
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CVA is more likely to get early in the morning and in winter. Bronchial asthma may aggravate at night. Some psychological diseases worsen on fullmoon days. Why is that?
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Yes. Thank dear Victoria Blinkhorn. Your information is useful.
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anti IL-5 therapy for asthma
do it can plays a role in treatment of the acute phase of patients with COVID19 who suffers from asthma ?
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Seems to be effective one in asthmatic patients.
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Eucalyptus leaf contains chemicals that might help control blood sugar. It also contains chemicals that might have activity against bacteria and fungi. Eucalyptus oil contains chemicals that might help pain and inflammation. It might also block chemicals that cause asthma. - 0.4% to 0.6% eucalyptus extract can improve bad breath in some people.
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This question relates to possible protection from COVID-19 by IgA antibody in the lungs.
I live in Japan where many people suffer from hay fever (allergic rhinitis), the season of which now is coming to an end.
People with allergic rhinitis have enhanced type 2 immunity ("Th2 immunity"), including elevated levels of cytokine IL-5 ( ), so are expected to have a stronger IgA response.
The immune system protects against SARS-CoV-2 with antibodies, amongst which IgA in the lung lumen should be non-inflammatory, as well as with cytotoxic responses that may induce a strong inflammation followed by ARDS (acute respiratory distress syndrome). So a stronger reliance on the IgA arm of the immune system upon SARS-CoV-2 infection probably reduces the risk of ARDS(-induced death).
So far, compared to other countries, Japan hasn't been hit very hard by COVID-19, and I wonder whether that may in part be explained by many people having an immune system with "type 2 polarization" caused by the hay fever. If so, that non-specific protection may soon wane if the hay fever season is finished.
To my frustration, I can't find that much information about luminal IgA in the lungs relevant to the above. If anyone can elaborate, I would be grateful.
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Allergies - a kind of Antigen - Antibody reaction ( Hypersensitivity Reaction ) - Increases the body defence mechanism .
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Covid 19 is new to us , well it has some common symptoms as asthma. Would you please elaborate how awareness can play a significant role to reduce impact on both disease?
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The invent of the vaccine of COVID-19 seems to remain after the virus is infected by a large audience. It is understood that the strongest resistance against COVID-19 will be realized by loading vitamin C.
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If you know a good journal about the keywords mentioned above and the following features, please let me know. regards
1) isi - scopus or pubmed indexed
2) low impact factor
3) high acceptance rate to some extent
4)accepting systematic reviews
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Parsa - it depends what you mean by low impact factor. As you are investigating behaviour and tobacco consumption - then it is a good idea to target 'health education' journals i.e. Health Education, Health Education Journal, Health Education Research - as well as health pomotion i.e. Health Promotion International, Global Health Promotion etc.
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Entire world is witnessing deaths due to corona virus. But the mortality rate due other diseases like Cancer, Tuberculosis, Hepatitis, Maleria, Diabetes, Asthma, etc is still higher than the mortality rate due to the present corona virus, even after having established treatment against such diseases.
I would be thankful if someone throws light on this.
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Because more media and health care attention is being paing to Coronavirus disease COVID-19 pandemic.
Reality is that up to 500,000 deaths occur due to seasonal influenza every-year (1) despite availability of a vaccine. Over 17 million deaths occur every year due to Ischemic heart disease (2).
Out of sight, out of mind!
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Hello , i did an rflp to detect a snp for asthma and I have case and control group what is the best way to do a statistical analysis in excel to determine whether it is related to disease , my data are in nominal form
Is there a step by step guide to tell me what to do ... thank you
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Hello Joseph Shenekji Joseph,
You can do these manually in Excel but online tools are available too For eg. "SNP_tools" is an MS Excel add-in for analysis of genotype data.
You can follow these steps:
1. Determination of Allelic and Genotype frequencies for cases and controls.
2. Hardy-Weinberg equilibrium check by chi-square test
3. Association with the disease using the chi-square test.
4. Normality check by Shapiro-Wilk test
5. Compare the demographic variables like age by t-test (parametric) or Mann Whitney test (no-parametric) between cases and controls
6. If you have a clinical variable such as disease severity to correlate go for Pearson (parametric) or Spearman (non-parametric) correlation test.
I generally do this kind of analysis in SPSS, a software where you can perform statistical analysis after uploading the dataset. Softwares like R, MedCalc and GraphPad Prism are also there. R is an open-source application. You might also like to consult a biostatistician at your university who will scrutinize the properties of your dataset and tell you what tests fit best.
Best wishes,
@
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Recent data is suggesting that steroids might increase the shedding of COVID 19 comes from treating hospitalized patients with systemic steroids just for the viral illness. The use of steroids for treating other diseases (like asthma) was not studied.
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Absolutely should be given just because they reduce interstitial inflammation as a part of COVID 19 pathogenicity.
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There are several papers addressing asthma management self-efficacy (confidence) among nurses specifically, and other health care providers generally. However, trying to get in contact with them to obtain theses validated tools but could not get a response.
"Developing a scale to measure self-efficacy on asthma teaching for health care providers"
"Asthma management efficacy of school nurses in Taiwan"
These are some of those papers. Can anyone assist me to obtain the tool? and getting in contact with those authors
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That was really really helpful Garry McDonald
I appreciate that
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I want to know if anyone knows some statistical simulation model that relates tobacco with childhood asthma. Recently we had ​​a publication, but found very little information.
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Please also see the following PDF attachments.
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I am looking for studies which estimated the number of new asthma cases in children (i.e. asthma onset) that can be attributed to traffic-related air pollution or traffic emissions. I only managed to find 2 by Laura Perez - below FYI. Did I miss any and is anyone aware of such studies (peer reviewed or not)?
Chronic burden of near-roadway traffic pollution in 10 European cities (APHEKOM network)
Global goods movement and the local burden of childhood asthma in southern California
Many thanks in advance,
Haneen. 
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Sorry, I dont know, so I should follow the colleagues responses to obtain more informations.
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Metaanalysis of prospective epidemiologic studies.
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Kindly see the following RG links and PDF attachments.
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It would be nice to discuss with you.
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Dear Samuel,
I am definitely interested in exploring fungal diagnostics in resource-limited settings, as I am from such a country. Additionally, fungal asthma has not been explored in my country, Namibia.Therefore, I would like to be part of this study.
You can contact me on the following email address: cdunaiski@nust.na
Thank you for the opportunity. I look forward to this collaboration.
Kind regards,
Cara Mia Dunaiski
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I found different LPS from E. Coli with different serotypes. Is there any difference between O111:B4 serotype and O55:B5?
I would appreciate if someone could provide me with a good protocol of inducing asthma in mice using LPS.
Thanks
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Unfortunately I haven't had any experience in this but absolutely different serotypes active immune system,s pathways in different way so seek for pathways and check with your goals.
Regards.
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classification of bronchial asthma in Saudi arabia
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The asthma affects more than 2 million people in Saudi Arabia, and majority of them have uncontrolled asthma with their quality of life adversely being impacted. The reasons for prevalence of asthma in Saudi Arabia include change in lifestyle, socioeconomic status, dietary habits and allergens, dust, tobacco smoke, sandstorms, and industrial and vehicular pollutants. Please take a look at the following RG links for more details.
Thanks!
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Lab investigations showed raised serum IgG, positive ASMA, positive anti delta and E virus antibody
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If the patient has antibodies against HEV and HDV, it is reasonable to assume that he has been infected with these virus. If he had also been infected with HBV, one would expect antibodies against this virus. Raised IgG indicates an ongoing infection, but not with what. AFAIK, it is usual to determine circulating virus antigen and nucleic acid to ascertain how active the infection is. In addition, liver enzymes can be determined in serum, to measure liver damage. Whether a liver biopsy is indicated, only an experienced internist can tell.
Could be an example for Hickam's dictum: "Patients can have as many diseases as they darn well please".
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9-year-old child has asthma, he tried short acting B2- agonists PRN, and combination of long acting B2-agonists/ICS but no improvement. The only LTRA available (singulair) is not covered, any recommendations rather than systemic corticosteroid to be next step?
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Hello, Inhaled corticosteroid as the initial maintenance therapy, ideally started within 2 years of symptom onset, is highly effective in both children and adults and across various degrees of asthma severity. If asthma is not controlled, the choice of subsequent add-on therapies differs between children and adults.
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Greeting
Any one can recommend an asthma knowldge questionnaire that can be used to assess the knowldge level of school nurses?
There is a validated one (AKQ). I do not have it in hand. If some one can send it I would appreciate
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We've successfully used the Newcastle Asthma Knowledge Questionnaire in a research context for parents of children with asthma
1. What are 3 main symptoms of asthma?
2. One in ten children will have asthma at some time during their childhood.
3. Children with asthma have abnormally sensitive air passages in their lung.
4. If one child in a family has asthma then all of his/her brothers and sisters are likely to have asthma as well.
5. Most children with asthma have an increase in mucus when they drink cow’s milk.
6. Write down everything that you know may trigger an asthma attack.
7. During an attack of asthma the wheeze may be due to muscles tightening in the wall of the air passages in the lungs.
8. During an attack of asthma, wheeze may due to swelling in the lining of the air passage in the lung.
9. Asthma damages the heart.
10. Write down two treatments (drugs) for asthma that are commonly used on a daily basis.
11. Which asthma treatments (drugs) are useful during an asthma attack?
12. Antibiotics are an important part of treatment for most children with asthma.
13. Most children with asthma should not consume dairy products.
14. Allergy shots cure asthma.
15. If a person dies from an asthma attack, this usually means that the final attack must have begun so quickly that there was no time to start any
treatment.
16. People with asthma usually have ‘nervous problems’.
17. Asthma is infectious (i.e. you can catch it from another person).
18. Inhaled medications for asthma (e.g. Ventolin inhalers) have fewer side effects than tablets or syrups.
19. Short courses of oral steroids (such as prednisolone) usually cause significant side effects.
20. Some asthma treatments (such as Ventolin) damage the heart.
21. A five year old child has an asthma attack and takes two puffs from a Ventolín® inhaler (a metered-dose inhaler). After five minutes there is no improvement. Give some reasons why this may have happened.
22. During an asthma attack that is being treated at home, your child needs to use an inhaler with a space chamber (or mask) every two hours. He is getting better but after two hours he is having difficulty breathing. Since the child is not getting worse, it is OK to continue giving the treatment every two hours.
23. Write ways in which one can help prevent an asthma attack during exercise.
24. Children with asthma become addicted to their asthma drugs.
25. Swimming is the only suitable sport for asthmatics.
26. Parental smoking may make the child’s asthma worse.
27. With appropriate treatment most children with asthma should be able to lead a normal life with no restrictions on activity.
28. The best way to measure the severity of a child’s asthma is for the doctor to listen to the child’s chest.
29. Asthma is usually more of a problem at night than during the day.
30. Most children with asthma will have stunted growth.
31. Children with frequent asthma symptoms should take preventive drugs.
Example Answers
Coughing, wheezing, shortness of breath
True
True
False
False
Allergens, colds, and exercise
True
True
False
Two of: inhaled corticosteroids, chromones, montelukast, long-acting beta-2-adrenergic agonist combinations.
Two out of: short-acting beta- 2-adrenergic preparation, ipratropium bromide, oral corticosteroids, and oxygen
False
False
False
False
False
False
True
False
False
Two from: the medication has expired, inhaler is empty, poor technique, insufficient dosage
False
Two out of: warm-up exercises, short-action beta-2 agonists or chromones prior to exercising, managing asthma more carefully, breathing through the
nose, warm and humid environment.
False
False
True
True
False
True
False
True
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I have a result in my acute asthma mouse asthma model that is really confusing me. In our 2 groups of allergic mice, we see that one group has more severe asthma, as indicated by significantly increased eosinophil influx into the BAL and increased inflammation and goblet cells in the lung histology. However, when we measure cytokines in the BAL (with expectation of seeing increased IL-4, IL-5, IL-13 etc.), all cytokines in the severe asthma group are significantly decreased.
This has been replicated multiple times so I am quite sure of the data.
Our protocol sensitizes subcutaneously with OVA on day 0, 7 and 14, then allergy is induced by exposure to an OVA aerosol for 20 minutes per day on days 25, 26 and 27. Animals are sacrificed on day 28.
I would be really grateful if someone could offer some insight on this.
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When we challenged allergic ships that were sensitive to egg protein, the asthma attacks occurred in two patterns - one immediate, and one delayed like 20 min. later. The only measure we found that was consistent with the clinical findings was the early rise and the late rise of plasma thrombospondin (TSP), which was released from activated platelets. And, the platelet activation was induced by the interleukin and cytokine release. Perhaps you may look at the pattern of the onset of asthma attacks after allergen challenges.
Shih-Wen Huang, MD
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I want to check eosinophil level in the mice blood/serum, for my experiment, using ELISA kit. need your advice, Thank you !
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We have used EDN for serum and sputum samples and it should work in BAL as well. And I would assume other eosinophil marker such as EPX, ECP or MBP should work as well. In human tissue staining of eosinophils EPX works very well (see )
MPO activity is frequently used as surrogate for neutrophils. I'm not aware of a similar assay for EPX.
Having a quick look I would chose for EPX ELISA because companies of known quality provide such ELISAs e.g. https://www.lsbio.com/elisakits/mouse-eosinophil-peroxidase-epx-elisa-kit-sandwich-elisa-ls-f7707/7707?trid=247.
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I am doing a project on predictive analysis of asthma exacerbation. My analysis focus is on Lung function measures, like Peak Expiratory Flow.
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The International Study of Asthma and Allergies in Childhood (ISAAC) has data from 1994-2012 of bigger international study of asthma. The questionnaire included a question of asthma exacerbation.
From the " The ISAAC page data archive:
ISAAC datasets have now been deposited in an openly accessible data archive. Individual- and centre-level data and documentation from ISAAC Phases One, Two and Three are now accessible at the following webpage: http://discover.ukdataservice.ac.uk/catalogue?sn=8131.
This is the link of ISAAC: http://isaac.auckland.ac.nz/
You could try to obtain the data and good luck.
Best wishes from Castelló (Spain)
Alberto
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There is a paucity of data regarding the distribution of bronchial mucus thickness along the bronchial tree. Any reference would be warmly appreciated !
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Dear colleagues,
If it can help, please refer to our new article where we collected several references about this topic:
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I am reviewing Fluoride Death Data including the excess deaths attributable to Fluoride Toxicity, including but not limited to: Alzheimer’s, Anaesthetic Hyperthermia, Aortic Rupture, Asthma, Cancer, Cataract, Chronic Kidney Disease (including Pyelonephritis), Chronic Obstructive Pulmonary Disease, Crime (including Fluoride enhanced Plumbosolvency leading to elevated Blood Lead Levels), Diabetes, Fluoridation overdosing, Eclampsia, Foetal and Perinatal mortality, Gels, Rinses and Toothpastes, Hip Fracture, Liver Failure (including Fat Burner and Tea products), Stroke, Sudden Infant Death Syndrome, Suicide. I have already found many references but would like assistance in building a comprehensive bibliography.
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Fluoride is known to increase the incidence of bone fracture. Older adults have a 5- to 8-fold increased risk for all-cause mortality during the
first 3 months after hip fracture. We can therefore safely say Fluoride causes excess deaths via this mechanism.
See this interesting article with references.
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Interleukin 17 (IL-17) is a class of closely related molecules known to be increased in the human body by exposure to Fluoride by ingestion from water and food, or metabolism of Fluorocarbon anaesthetics and propellants. IL-17 causes Autoimmune Diseases including Psoriasis, Rheumatoid Arthritis, Asthma, Lupus, Multiple Sclerosis, Inflammatory Bowel Disease, Transplant rejection, and destruction of Liver and Heart Cells. IL-17 is also implicated in Skin Cancer.
Other Interleukins are known to be elevated by Fluoride, leading to attacks on other critical cellular and organ systems. Australia's National Health and Medical Research Council actively suppresses this Interleukin science while promoting Water Fluoridation using industrial waste. Can the science community influence this behaviour?
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Dear Michael after reading your answer i did look up to the internet and started reaading bout flouride in water.
I am now able to get some insight about the big problem the humans are facing.
Lets hope that the council for water management will take up the issue in a more seroius manner.
It also has made a difference to my understnading of the disease patterns of autoimmunity.
Thank you for the insights.
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Hi-
I would greatly appreciate advice on if my understanding of how to apply an odds ratio from a particular study to another similar situation. I am working on a project to build 'asthma-safe' (i.e. 'green') housing to reduce hospital utilization of asthmatic children.
A study compared the number of children who had visited the hospital due to asthma within the last year based on whether they lived in 'green' housing or 'conventional. They found an odds ratio of .24:
"The sample included 44 unique children with asthma, with 30 children participating in 2 visits (74 visits in total). The adult-reported children’s asthma exacerbations are detailed in Table 3. Children’s asthma exacerbations were also all lower in the green than the conventional homes. In models adjusted for season, children in green homes were less likely than those in conventional homes to experience asthma symptoms in the past month (OR = 0.34; 95% CI = 0.12, 1.00), an asthma attack (OR = 0.31; 95% CI = 0.11, 0.88), an asthma-related hospital visit (OR = 0.24; 95% CI = 0.06, 0.88), or missed school days in the past year (OR = 0.21; 95% CI = 0.06, 0.74)."
Colton, M. D., Laurent, J. G. C., MacNaughton, P., Kane, J., Bennett-Fripp, M., Spengler, J., & Adamkiewicz, G. (2015). Health benefits of green public housing: Associations with asthma morbidity and building-related symptoms. American journal of public health, 105(12), 2482-2489.
Is the below a fair interpretation/application?
  • An apartment building has 10 children with asthma.
  • On average, XX% (let’s say 50%) of children with asthma go to the hospital in a given year.
  • If the apartment building is green, then 12% of those children would be expected to go to the hospital (24% * 50%).
  • Of children who go to hospital for asthma, they go an average of XX times per year (let’s say 1.5).
  • So utilization reduction would be 7.5 hospital visits expected per year in control (10 * 50% * 1.5), and 1.8 hospital visits (10 *50% * 24% * 1.5) expected per year in treatment?
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If OR is less than 1.0 it means that analysed factor is protective to this disease and in contrast above that 1.0 is a risk factor.
Good luck !
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Give the name of genes polymorphisms (snps) in asthma
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Asthma is a complex disorder which has many genetic and environmental causes.
Numerous genomewide studies for screening gene polymorphisms in asthma have revealed some susceptibility loci; among them are regions 2q, 5q, 6p, 11q, 12q, and 13q.63 Several polymorphisms are associated with asthma risk in IL-10, RANTES, TGFB1, ADAM33, CCR5, TLR-10, IL-4, IL-13, IL-8, IL-18, TNF, TLR-4, VDR and others.
Ref: Zhang J, Pare PD, Sandford AJ. Recent advances in asthma genetics. Respir Res 2008; 9: 4.
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Hello all,
I have a doubt on Feature Selection. Actually, i am working on asthma patients dataset and I need to select the features that are actually making difference between the asthma patients and normal people. So, I have to do the feature selection and I am using filter techniques for feature selection. And, Finally, my doubt is how can we select the best k features from feature ranking. Can we use the grid search to know the k features???
Thanks in advance,
Dhanunjaya, Mitta
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You could do PCA anyway and see afterwards if there are specific features which closely belong to single PCs.
By the way: considering the big number of features you will have large redundancy and reduncdancy is likely to affect the filter for feature selection as well. I.e., apart from not knowing the number k to choose, i would not be sure if you can trust your list.
Greetings, Sebastian
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Studies on the prevalence of COPD in patients with HCV are also scant. In patients with chronic HCV infection, prevalence of COPD (17.6%) and bronchial asthma (14.7%) is significantly higher compared to that in patients with hepatitis B infection matched in age, gender and smoking status (COPD 5%, bronchial asthma 1.7%).[31,32,33]
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Hi Chandan,
That sounds unusual, it may be related to immune system activation by HCV and chronicity of the infection. The references listed may have some more information if you could tell us what they are?
BW
Tom
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Hi,
in many spirometer reports there are predictive curves at flow-volume plots (see figures attached to this question). I would like to draw similar predictive curves to the results that I analyzed based on predictive FEV1, FVC and PEF calculated using clinical data (age, weight, height, race, etc.).
My question is about the placement of the maximum flow point (PEF) in x-axis, so at the volume scale.
There are any recommendations for this point?
Should I choose a constant value? I read that the 'time to PEF' should be less than 150 ms, so maybe it would be a starting point to calculate volume where I should put predictive PEF value at the flow-volume plot.
Thanks for any suggestions!
Mateusz
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I would suggest you assemble a large population of flow volume plots , then do multiple linear or spline regressions on age ht sex etc for certain curve parameters, eg peak flow, time to return to zero flow, point of inflexion. Then construct a "predicted curve" for a person of certain age/ht/ sex etc do a spline fit using these calculated parameters.
the examples of predicted curves you give are only idealised.
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Forced inspiratory vital capacity (FIVC) and forced first-second inspiratory volume (FIVC) may be increased or descreased in obesity, asthma or both?
I could only find references about VIF1 in the performance evaluation of swimmers.
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J Clin Med Res. 2016;8(2):105-110
Influence of Body Composition on Lung Function and Respiratory Muscle Strength in Children With Obesity Dirceu Costa Juniora, Fabiana S. Peixoto-Souzab, Poliane N. Araujob, Marcela C. Barbalho-Moulinc, Viviane C. Alvesb, Evelim L. F. D. Gomesb, Dirceu Costa
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I'm trying to simulate an acute asthma exacerbation with an ASL5000 active servo lung, to model the particle distribution of salbutamol (albuterol) Metered Dose Inhaler vs salbutamol Dry Powder Inhaler. I am hoping to see which performs better at the reduced flow produced by patients at this time. 
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less than 60% predicted value with variability +/-  30%    (for both FEV and PIFR)
absolute volumes depend on body size (age/ht/sex)
.
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Immunotherapy is a good option to treat Allergy and Asthma. Does any centre give its training?
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In the US, any of the approved fellowship training programs for allergy, asthma and immunology should be able to help training the staffs who would like to learn the treatment with immunotherapy. If you are not the candidate of fellowship program, you may need to contact with program director to discuss your individual situation.
Shih-Wen Huang, MD
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Now we are trying to establish the house dust mite-induced airway inflammation in B6 mice. The most used brands of HDM extracts are Greer and Indoor laboratories.  I am wondering is there any agents of these company in Taiwan? And the HDM products are 10000 AU/ml or 30000 AU/ml? How to change the unit from AU/ml to ug?  
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The House Dust Mite (HDM)-induced asthma model in the mouse can be used to assess the in vivo efficacy of anti-asthma drug. The model features many similarities to human allergic asthma, including the presence of eosinophilic lung inflammation, release of inflammatory mediators, and cytokines primarily associated with TH2-type inflammation. In addition, total and differential cell counts of inflammatory cells in the lung can be performed in the bronchoalveolar lavage fluid at various time points to observe in time course of inflammation and evaluate the effects of compounds. Many studies in the past appeared to focus on acute allergen challenge procedures. It is recognized, however, that asthma is a chronic inflammatory disease resulting from continued or intermittent allergen exposure, usually via inhalation. HDM would be an excellent  allergen to develop chronic allergen exposure models in mice to study human disease of asthma..
Shih-Wen Huang, MD
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I am conducting a research focusing on the impact of maternal mental health in the childhood asthma control and I need to know which is the best test to be done in a Primary Care.
Thanks
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My pleasure. BJCP
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Clinical examination needs a stethoscope to listen wheeze . Just listening cough asking patient to cough or manually eliciting cough can we determine that?
How easily coughing is produced manually in a young child who cannot follow your request to cough?
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Thank you Dr Lam. You are correct sir. But your young patient who cannot follow your command what you will do for them clinically to detect wheeze which is audible in stethoscope?
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I theorize that intraorally adherent dental probiotics may improve dental health and overall health by eliminating morning breath.
Plenty of evidence exists supporting some efficacy of dental probiotics to reduce periodontal inflammation -- which is one of the portals of the oral/systemic link.
However, none of the research has been done on a dental probiotic that can last 8 hours intraorally.
I have observational evidence of periodontal improvement with an adherent dental probiotic lozenge.
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I'll send you three bottles  -- how's that?
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various sudies have commented on sarcoidosis,TB ,ild and lung cancer having supportive role if not diagnosticof flow cytometry of BAL fluid
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I think it has a role 
now I am start working on the role of protein profile in patients with UIP
waiting the results
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asthma factors, induced gene, risk factors, albumin effectiveness, respiratory system, immunological reactions.
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Dear ahmed
there are many factors that indicate to asthma induced by ovalbumin such as physiological factor ( through hematology) immuniological factor ( through cytokines) and histological factor, the following artical can help you
thank you for your question
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i am looking for asthma treatment
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beta agonists are used for 2 main reasons
inhaled for treatment of airway obstruction in asthma and COPD 
oral or intravenous as tocolytics, to decrease uterine contractions in preterm labours 
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comparison of antihistamines
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Dear Anju,
Try to google the topic with "fexofenadine in comparison to..." comparison between H1-blockers".
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How can I develop self-management education program for asthmatic Patient ?
Am in the process of developing a program on patient education for the nurses. The idea is for nurses to understand the impact education has on patient outcomes,knowledge ,attitude etc. Any ideas on how to structure the program and how to develop a frame work on structuring asthma patient
I hope someone assist me with my fully appreciated how I design the program for adult asthma patient .
My study Aim:
to develop and to test a patient-centred, culturally specific education programme on self-management of asthma in adults.
Thank you.
Dail
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Have a look at the Asthma UK website- there are loads of useful resources that we give out to our patients in our Asthma clinic. Including the ACT score, asthma management plans for individual patients. Good starting point.
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One of the most miserable symptoms of allergy is fatigue. Do allergens disturb electrolytes? 
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I think the question is a real one as most clinicians would be asked by the patients, especially during the allergy seasons. The gentlemen above both offered the reasonable answers.
My take are:
First, the active immunological reactions in the host that resulted in the release of whole host of mediators. Those interleukins or cytokines are known to cause fatigue, especially interferon, IL-1, IL-6 and TNF.
Second, the quality of sleep suffered. Patients might toss around whole night without getting proper rest. They could hardly got into the state of deep sleep that relieve most of fatigue.
Third, we could not rule out what the drugs, especially of anti-histamine or decongestant(s) that might disturb sleep as well as causing drowsiness while trying to stay awake.
SWH
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I am trying to extrapolate airway surface liquid concentrations from BAL concentrations. If anyone can help me with this with appropriate references?
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this is very important question even for me also. i insert 1.5 mL of PBS in a mice for BALF and i get average protein concentrion is 0.2 to 0.8 mg/mL. since in real time the total volume of surfactant of lungs would be less then 100 uL (cant say exactly) and we collect 1 to 1.5 mL total wash. so i am too waiting for answer of this question
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small airway disease was cosidered tobe initial stage of COPD so people were using these parameters. but nowadays it is almost abandoned. why?
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These measures are much less reproducible than FEV1 within individuals and also suffer from lack of  reliable "predicted" values for epidemiology. Hence their use has declined and FEV1 dominates.
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18 months old with Crohn disease, steroid dependent and with allergic reaction to Infliximab.
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I USED for 4 yrs old child
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By providing Vitamin D supplementation in poorly controlled asthmatics with a low Vit D serum level, would this help to prevent and control their asthma rather than initially increasing corticosteroids
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Several studies have been conducted on the association between asthma  and vitamin D levels.  Asthma is a multifactorial disorder of the airways and various genetic and environmental factors contribute to the disease pathogenesis. As far as vitamin D deficiency is concerned, studies have reported controversial outcomes. Dr. Stephanie Korn and colleagues were the first to correlate severity of asthma with vitamin D status. In this cross-sectional study conducted on 280 adult asthmatics and 40 healthy volunteers,  vitamin D levels were similar in asthmatics (25.6 ±11.8 ng/ml) and healthy subjects (26.2 ±16.8 ng/ml), (p = 0.778).  Vitamin D levels were the lowest in severe asthmatics (24.0 ± 11.8 ng/ml), p = 0.046 compared to intermittent, mild or moderate, controlled and uncontrolled group. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3648461/
Several studies correlate vitamin D levels with asthma severity and have published different outcomes. In another retrospective study conducted in Soudi Arabia on 194 children with asthma, no significant difference was found in good asthmatics (53.4 ± 24.2) and poorly controlled asthmatics (51.5 ± 25.3), p= 0.657. Vitamin D levels were reported to be lower in females (65.5%) than males (46.8), p= 0.019.
Chun-Tao Liu and colleagues have conducted a meta-analysis on supplementation of vitamin D alongwith asthma controllers and effect on clinical outcomes in patients with asthma. In this metaanalysis, 903 patients with asthma were included and 453 received vitamin D supplementation alongwith common asthma controllers. It was found that vitamin D supplementation could significantly increase serum 25-hydroxyvitamin D levels (z = 5.50, P < 0.001 and z = 6.16, P < 0.001), but there was no effect of vitamin D levels on asthma exacerbation, FeNO, lung function (FEV1%) and asthma symptoms (ACT).
Thus, to find out if there is any link between poorly controlled asthma and vitamin D, more clinical trial need to be conducted and the factors involved and the mechanisms of pathogenesis should be explored to understand the exact scenario.
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Hi,
I am looking for some studies focused on prediction of exacerbation in chronic pulmonary diseases (especially asthma and COPD) considering changes in respiratory parameters (measured by spirometed or peak flow meter), other features of patient's condition, external factor (pollution, allergy, temperature, humidity or pressure changes) etc. detected a few day before occuring exacerbation.
The example of the study that I am iterested in is:
where the predictors were PEF and FEV1 value obtained from daily measurements. 
Thank you for every suggestion.
Mateusz
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Increases in exhaled nitric oxide (FeNO), when measured daily, has been shown to predict moderate asthma exacerbations, as shown by van det Valk et al.
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In patient with asthma and atrial fibrillation, does bisoprolol or any cardio-selective beta blocker changes pulmonary function test?
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It is assumed that beta-1-antagonists have less effect on the pulmonary system. This is an experimental research  claim. Nonetheless,in real life and humans all 'beta1-selective' beta-blockers affect the pulmonary system. This is especially true in asthma, because it is an inherent characteristic of this disease that beta-receptors are different from those of patients with normal pulmonary function. In asthma the 'selectivity' is partially lost. However, it is uncommon that the effect is large and really clinically significant.
It is a common experience that patients with asthma and overlap syndrome are treated with inhaled beta-agonists and also receive oral beta-blockers. This is a pharmacologic  wrong choice.
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I am hoping to distribute a 10 minute Qualtrics survey to families of children dealing with a pediatric chronic illness (asthma, epilepsy, type 1 diabetes, juvenile RA....). Both children and parents answer some questions. The children must be between 8 and 17 and both parent and child must be able to read English. This is for my dissertation and I need about 100 more participants. Thank you!!
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In Morocco, you can contact 
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Dear all, 
I'm checking the effects of the combination between two compounds in an asthma mouse model. During metabolism, these two compounds shared some similar cytochromes, such as CYP2C9, CYP3A4. However, one compound is metabolized mainly by Cytochrome P4502C8 (CYP2C8), and the other one is an inhibitor of CYP2C8. 
So, we want to check if we use two compounds separately, at least 6 hours apart, is there any possible interaction between them? Can you give me any advice on that?
Thank you, 
Best regards, 
Tu Trinh
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Animal models are suboptimal for checking drug-interactions with regard to relevance in vivo in human (if this is your major interest). 
Sharing similar CYPs is normally not a problem when combining two drugs as long as effective concentrations are below saturating concentrations. Therapeutic concentrations are normally in the nmolar range. When combining two drugs that are both metabolized by the same enzyme, the enzyme is more active under combination. If one drug is an inhibitor and the other a substrate the interaction effect depends on the affinities of the compounds and the concentrations that are used. It would be helpful if you have information on Ki and Km on the compounds. Then you may suggest if there will be an interaction.
Best regards
Christoph 
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Desensitization is used for treating asthma,but evidences are controversial.
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The allergic specific immunotherapy is most effective treatment for IgE mediated diseases.It change the naturale course of disease.I work 16 years with SCIT andSLITH and I have very good resiltes.You can finfd it in my papers,
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In our proposed hypothesis (2005), the leading role in the development  attacks of breathlessness in patients with bronchial asthma given to hyperactivity of the bronchi. The specific immune response in the bronchi walls, realized for the destruction of tissue forms  fungi of the genus Paecilomyces and limit their proliferation in lung tissue.Eosinophils play an important role of effector cells  in the antibody-cell - mediated cytotoxicity (see appendix). 
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In my opinion eosinophil is a barrier breaker (independently to the fact if the effect is addressed to infectious/parasitic organism or to mucosal barrier like the bronchial one). Therefore, it develops hyperreactivity due to epithelial damage/denudation and local nerve irritation. In addition, the survival effect due to nerve growth factor (NGF) is insufficient because of low expression of respective receptors tyrosine kinase A (TrkA) in epithelial cells in bronchi. You can see the address: the www.novapublishers.com/catalog/product_info.php?products_id=31360&osCsid=dd67b6261b0c086c85e8f2108701869f
(Mingomataj et al. The magic eosinophil: a breaker of biological barriers. In: Eosinophils: Structure, Biological Properties and Role in Disease. Ed: Walsh GM. Novapublishers Inc.  2012, ISBN: 978-1-61122-270-8).
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What is the therapeutic index of salbutamol, or another drug that treats Asthma via inhaler? I need it to get an indication of the toxicity of the drugs used.
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Dear Josh,
A double-blind, randomized crossover study in 28 asthmatic patients assessed the relative therapeutic index for inhaled formoterol and salbutamol. Pre-drug administration FEV1 (mean 2.08 l) was 49–93% of predicted and reversibility 16–82% after inhalation of salbutamol. Patients inhaled single doses of formoterol (Oxis®) (4.5, 18 and 54 μg, delivered doses) via Turbuhaler, salbutamol (Ventolin>®) (200 and 1800 μg) via pressurized metered dose inhaler (pMDI) and placebo at intervals of 48 h or more. Individual maximum FEV1 and minimum S-K+ were calculated. Relative local (maximum FEV1) and systemic (minimum S-K+) dose potencies, and their ratio, the relative therapeutic index, were estimated using a non-linear mixed effect model. The drug effects were well tolerated and dose dependent. A log-linear approximation was used to describe the bronchodilatory effect, whereas a sigmoid approximation was more apt to describe the decrease in serum potassium concentration. A bivariate dose–response model based on these principles was fitted simultaneously to all data. The mean relative therapeutic index between formoterol 4.5–54 μg given via Turbuhaler and salbutamol 200–1800 μg given via pMDI was estimated to be 2.5 in favour of formoterol; this trend was not statistically significant.
To view the full publication, please use the following link:
Eur J Clin Pharmacol. 2002 Jul;58(4):S61-7.
Assessment of a relative therapeutic index between inhaled formoterol and salbuterol in asthma patients.
Rosenborg J1, Larsson P, Rott Z, Böcskei C, Poczi M, Juhász G.
Author information
 
Abstract
OBJECTIVE:
To quantify the relation between local and systemic magnitudes of effects of inhaled formoterol and salbutamol.
METHODS:
Twenty-eight stable asthmatic patients completed this double-blind, randomised crossover study. Pre-drug administration FEV1 (mean 2.08 L) was 49-93% of predicted and reversibility 16-82% after inhalation of salbutanmol. Patients inhaled three single doses of formoterol fumarate dihydrate (Oxis) (delivered doses of 4.5, 18 and 54 microg) via Turbuhaler, two single doses of salbutamol (200 and 1800 microg) via a pressurised metered dose inhaler (pMDI) and placebo at intervals of 48 h or more. Individual maximum FEV1 and minimum S-K+ were calculated. A classic sigmoid model of log-dose response was used to discriminate pharmacologically between formoterol and salbutamol. Relative local (maximum FEV1) and systemic (minimum S-KC) dose potencies, and their ratio, the relative therapeutic index, were estimated using an on-linear mixed effect model.
RESULTS:
The drug effects were well tolerated and dose dependent The bronchodilating effect was on a part of the dose response curve that could be well approximated by a log-linear function, the serum potassium suppressing effect sometimes was not (the lowest doses differed only marginally from placebo). Thus, a log-linear approximation was used to describe bronchodilation, whereas a sigmoid approximation was more apt to describe the decrease in serum potassium concentration. A bivariate dose-response model based on these principles was fitted simultaneously to all data. The mean relative therapeutic index was estimated to be 2.5 (95%confidence interval: 0.9-6.5).
CONCLUSIONS:
The mean relative therapeutic index between formoterol (Oxis) 4.5-54 microg given via Turbuhaler and salbutamol 200-1800 microg given via pMDI was estimated to 2.5 in favour of formoterol; this trend was not statistically significant.
Hoping this will be helpful,
Rafik
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Attached I send two documents in PDF with photographs of the sample, stained with MGG, another with Pap. Final magnification of 400x.
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these cells are the size of lymphocytes with very dense nuclei, I think  they could be apoptotic cells, perhaps due to therapy?
you can try confirm apoptotic cells by immunocytochemical detection of c-caspase 3?
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When do we need to use oral steroids to control an acute asthma in a type 2 diabetes patient?
What dose could we use?
Do we need to to use insulin at the same time if the diabetes isn't in control?
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If the crisis is moderate-severe you can't go around systemic CS, so use them but add shorts of rapid acting insulin according to glucose levels. Here a co-management with endocrinologist might be recommendable. concluding: asthmatic crisis in DM patient should be managed as any crisis, but adding rapid acting insulin according to needs (which can also be elevated due to infection ) 
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Asthma, ICS, MDI, Corticosteroid, Pulmonology  How many buffs of corticosteroid inhaler are needed to induce systemic side effect in asthmatic patient?
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Dear Collegeau!
What do you mean on"systemic side effect". I think one thing is the cortisol suppression and other things are the Cushing-syndrome, the osteoporosis or diabetes.  Sorry:The article is in Hungarian language, but you can use the references. Best regards
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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?
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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.
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please let me know and give reference to my objective.
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I suggestion use the Beck anxiety and depression but you should consider other factors characteristic of their population