Chronic Obstructive Pulmonary Disease - Science topic
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Questions related to Chronic Obstructive Pulmonary Disease
This is an urgent request triggered by an actual situation. After an incidental pneumonectomy, a woman now 72 years old, suffering from longstanding COPD combined with a restrictive lung disease du to secondary deformations of the thoracic cage, remains fully conscious and mentally undisturbed while intubated and under mechanical ventilation. She is neither prepared to nor intends to die. Apparently, her respiratory center is highly dysfunctional but does not appear to be completely knocked out.
Would it be possible.
a) to stimulate the respiratory center by narrowly balancing the hypoxia and hypercapnia tolerance with special ventilator settings?
b) to directly stimulate the respiratory center?
Hi everyone, is there anyone knows to notice that the animal got Chronic Obstructive Pulmonary Disease/Emphysema (COPD) without using Pulmonary Maneuver System such as Buxco, etc. Preferred the non-invasive examination.
I've done RNA-seq analysis on a dataset downloaded from GEO looking at immune gene expression in Asthmatic, COPD and normal epithelial lung cells. Trying to do a t-test for my statistical analysis, but I need to group my data into Asthmatic, Healthy and COPD samples/cells as it doesn't show up in R which samples belong to which group?
If a person has already been diagnosed with COPD
Why perform full spirometry on them ?
Surely if they have been diagnosed then a good history and a handheld spirometer will suffice for monitoring purposes.
Are there any articles re this ?
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.
So I'm helping my radiology doctor in his Ph.D program about COPD and cognitive impairement and one of the objective is to measure Hif alpha mesurement. Where we can buy them and what is the cost? Thank you very much
do you have any idea on How to define a cut off point for SGRQ for good and poor quality of life of COPD patients? SGRQ is measuring the quality of life in continuous vale. We can measure only the score , mean and SD. I need to make it categorical value by dividing them into good and poor quality of life. how can i do this in statistical basis?
My research centers on Indian patients with COPD (Chronic Obstructive Pulmonary Diseases), thus I really need help in getting the datasets at the earliest. Your suggestions and insights are highly appreciated.
Thank you in anticipation
Are you prescribing home high flow therapy to COPD patients? As the clinical benefits of HFT beyond the hospital environment become become increasingly studied, we'd like to hear about your experience. Take the survey now!
FMT is showing promising results in terms of treatment of recurrent gut infections. Could be used this approach (microbiota transplantation) for the management of chronic respiratory diseases with microbiological component such as COPD or CF?
Is there any research group that has tried to perform this procedure on the respiratory tree?
Negative pressure ventilator like the biphasic cuirass ventilator (BCV) are non-invasive without the side effects associated with BiPAP, intubation and trachiosomy. These modern day 'iron lungs' treat pnuemonia and COPD. BCVs have a simple design that is likely faster to manufacture too which is very desirable in light of high demand for ventilators
The COPD assessment test (CAT) is a commonly used disease-specific Patient-completed questionnaire assessing globally the impact of COPD (cough, sputum, dysnea, chest tighteness) on health status for evaluating functional impairment in patients with COPD. Is it applicable to COVID-19 patient or we should develop a new Patient Oriented Outcome Measure for the assessment of lung function for Pulmonary Rehabilitation of the COVID patients.
In the COVID-19 infection, the main issues are not brought by the virus itself, but by our bodies' excessive immunological response to the infected organs - the cytokine storm. This cytokine storm destroys all cells near the focus of infection and kills the respiratory system. So is there any natural non-aggressive way to prevent the cytokine storm from happening in the severe COVID-19 cases?
Thank you in advance for your valuable opinions!
I have a group of COPD patients who went to a specific clinic. I want to compare the number of exacerbations they had in the 6-months prior to and 6-months after attending their first clinic visit. The number of exacerbations has a negative binomial distribution.
Is it possible to do such an analysis on either Prism or SPSS?
Alternatively, will a Wilcoxon test suffice?
I'm wondering if there is any literature on prognostic pessimism (PP) within areas of aphasia, speech disorders, stroke treatment, or any other similar area. I've found literature on PP and psychological disorders and some physical diseases (COPD / asthma) but looking for presence of PP in speech disorders.
Do acid-base disorders affect extracellular fluid pH? Or are these changes only detectable in blood?
For respiratory acidosis specifically, can the abnormal pH changes only be detected in arterial blood? Or can capillary blood or even interstitial fluid be used?
This might be a stupid question but hear me out if you have time.
Prediction rules (a.k.a multi-component prediction scores/indices) give individual-level predicted risk of mortality within a certain time frame (typically 3 years in COPD, some are 10 years). However, if you measured a certain prediction rule several times at different time points in a single patient you would get several predictions. If a patient receives two measurements and changes from 10% to 20% predicted risk of mortality within 3-years then maybe more treatment can be introduced. For certain prediction rules (depending on the components used) a 10% to 20% change may indicate progression of the disease.
Question: Is there any study out there that defines a clinically relevant change in predicted mortality?
I know that sounds odd but I need a threshold without looking a p-values (multiple testing problems).
Problems with this question: Certainly, to the patient any increase is relevant. Importantly, the expense and side effects of certain treatments may make somewhat large increases more tolerable.
I am trying to observe epigenetic markers that may identify early stages of COPD or predict disease prognosis in patients with COPD, I'm not quite sure how to calculate the sample size I need as there will be no intervention, only observation. I already calculated based on COPD prevailence of 2% against general population and got a sample size of 385, is this correct? it does seem too large.
We are currently exploring the perspectives of people with COPD on an intervention to reduce sedentary behaviour using the Theoretical Domains Framework (TDF). The TDF (the second version of it which we are using) does not EXPLICITLY include the continuum of motivation although it provides the domains that represent the automatic and reflective motivation. Therefore, the "lack of motivation" and the "enjoyment of sitting" themes can be difficult to put under any of the 14 domains. Can i add a new domain to the TDF and call it "Motivation"?
I’ll describe what I postulate provides the explanation of the CAP microarousal episodes during sleep.The information has been
based entirely on the conclusions of documented studies. Admittedly, and inasmuch as each conclusion individually is not new information per se. nevertheless, by combining and preferentially sequencing them,
it becomes possible to arrange a set of contingent propositions which facilitates the creation of new awareness.
The concept can be tested non-invasively during Cycle 1 of descending NREM sleep in a perfectly healthy individual. Additionally, it would provide support for the statement that “ ...several lines of evidence
suggest that the pulmonary circulation both has minimal neural regulation and is unresponsive to
changes in sleep state. and is both significantly important and key to understanding that peripheral
mechanisms cannot be excluded”. @ http://jap.physiology.org/content/88/3/1084
I'm interested to get in contact with researchers in Montana that has an interest in epidemiological research in general, or pulmonary/cardiovascular research with an epidemiological approach. Have tried online searches/googling, but no success that way, so why not try here?
I want to perform experiments with animal model of mitochondrial dysfunction in lung. I have seen a variety of OXPHOS defect models for other organs (heart, skeletal muscle, liver, brain etc.) but have not been able to find any specific model for lung. I wonder whether these models also feasible to be induced for lung or if there is any strict model generated for lung. It is also possible to induce mitochondrial dysfunction by cigarette smoke, but we prefer to utilize KO model.
Thank you in advance!
As the incidence of COPD is rising in women we started to see pregnant COPD patients. I could not find a research examining the COPD patients with pregnancy. There are few case reports about emphysema and pregnancy. But I see very few suggestions on treatment in a pregnant women with COPD. Are we going to give medications as severe asthma? Is there a case series or published research which I could not figure out? Thank you in advance.
How can i calculate or obtain the baseline mortality for COPD, IHD etc? Is it provided by the WHO? I couldn't find when i searched through WHO website. Can i consider total mortality due to a disease as baseline mortality?
The COPD is freqent. Parasitic-infestatio is even more and causes blood-eosinophilia. How can be predictiv the count of eo on COPD exacerbatio-phenotyp without exclusion of the helminthiosis or other parasitic disease?
what is the best management in Acute exacerbation of COPD which is resistant to medical management :
A- CPAP ( Non invasive positve pressure ventilation )
B- Intubation and mechanical Ventilation .
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]
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!
As we normally extubate chf, copd home o2 dependent patients to bipap and then transition them to nasal cannula- does any one of you have experience extubating the patients to nasal cannula ?
As high flow nasal cannula also has a peep effect and might be useful.
I have been working on oxidative stress in alcohol abuse - laetely using RPR to determine free radical produsction. alas most has been on rats. However, we have been working eith the diagnostic potential of FR determination for progression in COPD.
I am validating a questionnaire that I developed which examines the levels of personal disaster preparedness in people with COPD. I am trying to determine what is the number of experts I need when I am examining the content validity of a questionnaire using the content validity index?
There are several case definitions for Acute respiratory infection and Acute Lower Respiratory infection that could be used for community based surveillance. Elderly surveillance requires specific definitions since they have unique symptoms and case presentation. The issue of ARI and ALRI in elderly further gets complicated because majority of them tend to have COPD in a country like India. Kindly suggest a suitable definition that could fit in for this special age group.
lung funcion in non smokers with copd like disease
lung funcion afther specific tratment
identifiing ethiopathogenic factor
Anecdotally, much of the healthcare provided to people living with severe mental illness focuses on their mental health, negating physical health concerns including chronic disease. The co-morbidity of metabolic diseases (diabetes) and COPD (smoking) is especially large in this cohort, but are generally not receiving Management Plans from their GP, or are not following up referrals.
How can we improve these outcomes?
I'd like to hear your thoughts and inputs :)
Co-morbidities in COPD patients can mimic the typical symptoms which define an exacerbation of COPD - what if the worsening dyspnea is due to congestive heart failure? Would systemic corticosteroids and antibiotics be the appropriate treatment? Obviously not...
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.
I am interested in knowing the variation of laryngeal movement at rest and as CPAP is applied. I will like to know the difference between laryngeal movement in normals vs COPD patients and normals vs sleep apnoea patients.
Can anyone let me know the exact process and tentative time to infect Bronchitis in mice model ? I need to test a sample against mice model for bronchitis and for that purpose I want to have some bronchitis infected mice model. Which is the best way to have bronchitis infected mice model?
I have found that COPD (chronic obstructive pulmonary disease) can be infected by cigarette smoke. But whats the process for cigarette smoke and how many time it will need in this process ? Any other / best process if you can suggest it will be a great help. Thanks
Evidence for agressive therapy of obstruction in HOCM patients is still lacking. But obstruction with a high gradient lasting for years has to be harmful. Thus, clinicians have to consider safety of interventional/surgical therapy and natural prognosis of HOCM.
What is the really target of the corticosteroids in exacerbation of COPD? If the airways: why isn't enough the large dose-nebulised CS? Only the sputum is the cause? All of sever exacerbation need systemat.CS? The high dose ICS absorb from lung, and a few amount can the receptors saturate.
I work with mice models of pulmonary emphysema and currently use whole body plethysmography for measuring respiratory patterns of the mice and would like to know if anyone can suggest a way of getting more robust data.
I've come across papers that have used manual horizontal and vertical lines to calculate the points of intersection. There are some papers that have used complex programs to get MLI and Destructive Index. But is there any simpler method to do this using ImageJ, to draw lines on the image and count the points of intersection?
65 years old lady with gradually pregressive dyspnea....HRCT s/o ILD, rest of the blood parameters are normal. She was started with IV methyl prednisolone followed by oral tablets along with N Acetyl cysteine...but, she is not responding with increasing dyspnea.....today we have added tab azathioprine. Any suggestion please...
I've seen an italian man, HIV+ on treatment, who had a history of fever, cough, thoracic pain, some episodes of hemoptysis (I saw one of them, a big one, so he is credible).
We performed a CT scan (infiltrate in the upper right lobe tree-in-bud like) and a bronchoscopy (normal, except for a sign of previous bleeding in correspondence of the CT lesion) with BAL.
What do you think about the diagnosis? Would you start an anti-TB therapy ex-juvantibus?
i want to know the correlation of oxidants/radicals and the inactivation of the alpha 1 proteinase inhibitor and the consequensis of this action...
Currently, different in vitro models of COPD are applied in primary studies. The main question is "what is the best and most simple and also most reliable way to mimic the COPD situation in human airway epithelium cell line?"especially, when we want to investigate the inflammatory mediators. What is the best cell line to work on (individual or co-culture system)?
We sometimes experienced that influenza vaccination may cause exacerbation in some patients with COPD. Are there any publications about that and experience?
The 3E study group don't recommand the use of methotrexate in patients who had a previous pulmonary disease.So, sometimes, methotrexate can be the only alternative to treat corticodependant pulmonary sarcoidosis or myositis with interstitial disease. I didn't find any paper about the safety of methotrexate use in thus situations. In another hand, what is the relationsheap between a previous pulmonary disease and the risk of interstitial lung disease which is an impredictible hypersensitivity phenomenon?
Thank you for your answers
People with chronic obstructive pulmonary disease have sedentary life style due to the clinical course of their disease.Although there is current update on physical activity measurement tool, has anyone have used motivational stratergies to improve physical activity in those patients?
We had recently a young patient (under forty), without alfa 1antitripsin deficiency, with quite severe emphysema. He had exposure to carborundum without any kind of protection for fifteen years, besides being a heavy smoker for twenty years. He had a positive TB skin test, but repeatedly negative cultures. He had also some lung fibrosis and nodules, that fulfilled all criteria for silicosis, but his lung function was compatible with pure obstructive disease, without response to broncodilators, low DLCO and hyperinflation. Do anybody else have such cases?
I plate 0.5 x 10^6 monocytes/ml per well on a 24 well cell culture plate. I use RPMI medium supplemented with 15% human serum and harvest after 8 days. I am getting a very low yield of RNA at 2-3 ng/ microlitre. Could this be because my cell numbers are too low? I am using an RNA extraction kit from Sigma.
During the recently concluded CAHRD Meeting held in Liverpool (UK), one of the issues discussed was the prospect of reducing domestic air pollution (from burning biomass) and its negative health consequences, which particularly affects women and children.
I frequently come across papers reporting the success of domestic and public pit latrines designed to double up as bio digesters to produce bio gas for cooking and lighting purposes.
My questions are: Could this be the way forward for developing countries? How feasible is it to be scaled up?
Does anyone have a hint how to get hands on murine alveolar epithelial cells of type I? Preferable a protocol for a primary cell isolation but also comments on potential cell line are very welcome.
ATS/ERS statement 2005 recommends performing body plethysmography after spirometry and before DLCO/TLCO. I wonder whether performing body plethysmography adds relevant information required for clinical decision making. Any thoughts?
I have studied a lot about oxidative stress in COPD and asthma and have heard a bit about its induction during environmental factors. For e.g. the heat of cold induces it. Actually, I don't know the molecular mechanism. Cancer cells have high oxidative stress too.
We have made an AVF in a patient with GOLD IV (D) COPD obtaining a substantial amelioration of hypoxemia, excercise capacity and SGRQ (therefor BODE Index). We call this "endogenous oxygen therapy". There are two protocols running, one in the US and the other in Germany that haven`t still published there results as far as I know.
Currently we are conducting a large IPD meta-analysis to identify effect modifiers of success of self-management in patients with chronic obstructive pulmonary disease (COPD) or congestive heart failure (CHF). Principal investigators of the selected trials are asked to share individual patient data in order to answer our research questions. We chose to establish collaborations and reward each research group with a single co-authorship. Administrative or data management costs are reimbursed. So essentially, no fixed per study / per patient financial incentive is given. What's your opinion? Are we rewarding these investigators adequately?