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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?
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thanks a lot for this extremely valuable comment¨
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Can somebody assist me with the intranasal inhalation protocol(detailed or standardized).
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It is essential to use anesthesia and neuromuscular blocking agent before intranasal administration of dust in mice. However, you should have approved protocol from your Institutional Animal Care Committee to do the experiment. In the protocol, you should have provided details on anesthetics etc to be followed.
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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.
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there is publications about Dogs; Chest X-ray shows generalized bronchial and/or interstitial changes. The cytology of the bronchoalveolar lavage may reveal excessive amounts of mucus, hyperplasia of epithelial cells, neutrophil or macrophagic infiltration.
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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?
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Hi,
you need to compare the disease versus control samples when doing the statistical test. I didn't fully get if the problem is that you lack the information of which samples belongs to which category or it is a coding problem. As for the former, usually datasets have a metadata file in which the sample names you find in the gene expression table are present, and the treatment information is included. If it is a coding problem, you can index the sample names to divide the data into Asthmatic, Healthy and COPD.
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Hi
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 ?
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Certainly not.
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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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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
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Many ELISA kits are available to measure the level of HIF-alpha (eg, https://www.abcam.com/HIF-1-alpha-Transcription-Factor-Assay-Kit-ab133104.html; https://www.raybiotech.com/human-hif-1alpha-transcription-factor-activity-assay/; https://www.cellbiolabs.com/hif-1-alpha-sandwich-elisa, etc) Need to have ELISA capability and consider in what fluid you are measuring HIF (eg, bronchial supernatant from washings vs CSF fluid OR is it a in vitro system).
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Dear all,
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?
thank you
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Respected Scholars,
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
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I am also searching for COPD HRCT image datasets. Does anyone know the link? Kindly share it?
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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!
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FRESH EVENTS SUGGEST MORE LIKE THIS
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Thrombosis and coagulopathies are common features of sever COVID_19 and COPD patients demonstrate abnormal remodeling processes following lung injury, so one can expect significantly abnormal tissue remodeling following SARS_CoV_2 infection. ,so the risk of pulmonary embolism increased in COPD patients.
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Emphysema is categorised as COPD as you know. Can immunotherapy resolve or reduce its symptoms and severity?
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Please take a look at this useful link.
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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?
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It might not be a good idea to introduce more microbiota into the lung, as they are one cause for inflammation. How about using the cellular homeostasis maintenance function of autophagy/xenophagy to control the microbiota population in lungs, repair the dysfunctional epithelial cells, and decrease the overall inflammation level in the lungs:
Autophagy can e triggered by nutritional deficient stress like starvation.
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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
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Dear doctor Hayes,
Let me intruduce myself: Jan van Egmond, PhD, (E-mail: Jan.vanEgmond.kf@gmail.com) retired clinical physicist at the Radboud University in Nijmegen, the Netherlands. I worked in our animal lab in Nijmegen for several years on the lung damage caused by artificial ventilation (positive pressure ventilation). Several publications can be found about the subject from our group. And you will find my name also on several publications. But there was always a discrapency in our view on the cause of the damage. The whole group accepted the common view that damage is caused by overstretching of the alveoli. I always made clear in the group that there must be another cause; the stretching bij a PPV TV of 500 ml is negligible to the stretching of the alveoli of a marathon runner with a tidal volume of several liters. There must be another cause, and I think it is easily found in the literature about artificial ventilation. Before 1952 there was in fact only one accepted way to ventilate a patient artificially: the iron lung. It is interesting to see a picture of a tremendous hall in Copenhagen with many iron lungs with poilio patients. But if you look carefully at the picture you see a few normal beds in the corner of the hall. At those beds several patients were saved by artificial ventilation with positive pressure by students that were willing to ventilate the patients with a balloon for a period of two hours, and then be shifted for another student. This succes of PPV was the start of its development, and in fact the development of the intensive care unit.
But after this change of strategy, publications started about atelectasis, and the development of PPV is since characterized by the struggle against atelectasis (PEEP, small TV, intermittent large TV, etc). I think that a great issue in the development has been the idea that there is no difference between negative and positive pressure (Comroe 1902). But this is a big mistake! Comroe is right in two situations: in a rigid tube the flow is determined by the pressure difference, so sucking at one site, is equivalent to blowing with the same pressure difference at the other. And the second point: a balloon has a size determined by the pressure difference between inside and outside. The volume of the balloon will not change if you add an atmosphere at both sides.
But look at the registration of a flow-volume curve in the lung-function lab. Forced expiration takes much longer than forced inspiration, although the pressure difference (in vs outside), so the driving force of the flow, is much larger during expiration than during inspiration. So there is difference in flow. And we know why: airways are no rigid tubes, so during expiration the thorax pressure is high and the tubes are compressed and resistance is high. During normal ventilation one first creates low pressure in the thorax, the airways become wide, the resistance is low, and the flow is high and reaches the deeper parts of the lungs easily. But during PPV the pressure in the thorax remains high and we press air into the lungs. And, moreover, each volume we press into the lung raises the thorax pressure. And the deeper parts of the lungs are not easily reached. Resulting in atelectasis. That is why the standard manual in anesthesiology tells the doctor to ask the patient to take a few deep sighs to solve the atelectasis. So for the anesthesiologist, PPV gives almost no trouble, procedures are relatively short, and lungs are most of the time healthy. But the effect of high resistance during inspiration of PPV increases with time (ICU) but also with a damaged lung that looses compliance.
So especially with damaged non-compliable lungs NPV will offer advantages. And for COVID-19 (also lost compliance) I see these advantages:
1. no intubation
2. no paralysis, no narcosis
3. much less interaction with the circulation
4. better oxygenation
See also Grasso et al. Am J Respir Crit Care Med. 2008 Feb 15;177(4):412-8.
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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.
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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!
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Dear Dr Ligen Yu ,
Natural non-aggressive way to prevent serious COVID-19 would be to sustain healthy life-style; to justify body weight, blood pressure, blood glucose and lipid, and especially visceral fat, before cytokine storm develops, I believe.
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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?
Thanks!
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Note that your data seems to be paired (you have data from the same patients, before and after their first visit.
I don't think that Prism can do this, and I don't have SPSS.But I can tell you that it is quite simple to do in R (www.r-project.org):
If "exacerbations" is a numerical vector with the observed numbers of exacerbations, "time" is a factor with levels before/after, and "patient" is a factor with patient IDs (in a paired design each ID will occur twice), you can fit an appropriate negative binomial model with:
model <- MASS::glm.nb(exacerbations ~ patient + time)
The coefficients and confidence intervals are obtained with
coef(model)
confint(model)
You can make an analysis of deviance with
anova(model)
You get the likelihood ratio test with
drop1(model, scope = "time", test = "LRT")
and a summary with a coefficients table with
summary(model)
(note that the tests here are Wald tests).
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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.
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Dear Helen,
I share here Dr Glize's work about aphasia. I hope you could find data your are looking for.
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Please colleagues
Can you help me in getting a recent published references state how the occurrence of COPD (chronic obstructive pulmonary disease) differ according to gender?
Regards;
Hussein Abid
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I think that women are more than men for exposure to COPD.
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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?
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Yes. Change in ECF pH is a feature of acidosis. However it is best to utilise arterial blood samples in analyzing blood gases and pH
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i am looking for articles on end of life COPD care for a assignment as a district nurse specilaist role
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start with google search then go to Medline or cinhal
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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.
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The first question that I think should come to mind is: why does the predicted risk change between T and T+1? This might be due to factors that have nothing to do with a true shift in risk, such as measurement error variations and circadian rhythm. Obviously, a shift due to these factors isn't relevant to the patient, it's noise.
Even if it is a true shift in risk I doubt it is generally helpful to dichotomize into "relevant" vs "not relevant" predicted risk shift. The only setting where I can imagine a relevant vs not relevant shift categorization might be relevant is when the risk makes a shift passing a treatment threshold. To be useful (and regardless of whether it is a true risk shift or due to measurement error), such a clinically relevant treatment threshold should already exist and be used, which in my experience remains rare.
This idea of relevant shifts in risk categories relates to reclassification tables, see for instance here:
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cor pulmonale is quite common in copd . but it is diagnosed quite late.We want to manage at the earlist.HOW?
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EVERY COPD PATIENT WHO COMES WITH AN EXACERBATION SHOULD MANDATORILY HAVE AN ECHO
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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.
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clarify when or not high flow nasal cannulae may be proposed as a valid alternative choise for hypercapnic acute respiratory failure COPD patients and when could be better to swich to non-invasive mechanical ventilation ?
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Thanks for your comment, Michael McPeck
Yes, you have pointed out an important advantage/possibility of HFNC.
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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"?
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Adnan Wshah You can do it, and not only that, it is highly desirable to expand theoretical frameworks. The only caution is to validate the addition through some scientific process such as Delphi.
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 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
 
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I am now working on similar topic.
Have you solved automatic detection for CAP arousal?
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Does the patient's underlying illness, does the negative pressure of suction need to change?
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hi there,
is it about secondary pneumothorax? i really think the question needs to be more clear.
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Hi.
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?
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Thanks Ahsan, I am specially interested in Amyotrophic Lateral Sclerosis, Multiple System Atrophy and Progressive Supranuclear Palsy. Also ME/CFS. I have mapped in great detail 100s of residences in relation to environmental sources of EMFs (MHz and GHz). Very high levels of Reactive Oxygen Species are generated as the body is in fact an electro-chemical construct as acts as a pick-up antenna for RF signals. We are about to have our third paper published in neurological literature.
Best wishes Anne Silk
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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!
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You should use sheep.
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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.
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Maybe prevention is the best in these cases. Pregnant women need more intensive behavioral and pharmacological support to stop smoking, be aware of the consequences for their children. This part of the prevention we are forgetting, the woman who smokes every time is more prevalent, as well as pregnant women who smoke, it seems that they have a lack of information about the harmful effects of tobacco on the fetus.
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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?
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Dear Shovan,
I suggest to take a look at the WHO Global health Estimates 2000-2015 http://www.who.int/healthinfo/global_burden_disease/estimates/en/
where you can find:
  1. Cause specific mortality at global, region and country levels from 2000 to 2015: http://www.who.int/healthinfo/global_burden_disease/estimates/en/index1.html
  2. Disease burden 2000-2015 with estimates of DALY, YLL and YLD http://www.who.int/healthinfo/global_burden_disease/estimates/en/index2.html
I also suggest to take a look at the Mortality and global health estimates page in the WHO Global Health Observatory: http://www.who.int/gho/mortality_burden_disease/en/
I hope this helps
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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?
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Hi. Thanks. I think so, too. But why not? It is a essential problem by classification in COPD phenotyp and by treatment(see mepolizumab) eosinophilic severe asthma. Best regards Paula
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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 .
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One must be selective in the post-surgical population with COPD. Although the morbidity and mortality is increased when a surgical patient is re-intubated, a thoughtful assessment of pathophysiology must be made. Residual muscle weakness associated with neuromuscular blockers, narcosis or residual anesthetic gases will exasperate COPD symptoms and may be best resolved with a short course of mechanical ventilation. I have had anecdotal experience of patients receiving NIV when tracheal intubation would have prevented significant gastric distention.
Regards,
Christopher
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a- Smoking cessation
b- Long term supplemental Oxygen Therapy ( LTOT )
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Dear, Smoking cessation will have the highest decreasing mortality rate.
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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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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.
thank you
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It makes perfect sense to me sir to extubate to HFNC. It is much less invasive and with the ability to give 100% FIO2 and up to 40 or 50 Liters, depending on your facilities policy, it is a very good substitute for the bipap. If you habe been weaning to PS/peep ventilation only prior to extubation, then aren’t you essentially already in bipap mode? If you are weaning to PS on the vent then extubating, are you not just repeating the same ventilation mode twice by going to bipap thus wasting your time, supply, and adding to patient costs? It just seems pointless to do so if you have weaned from vent In that mode. HFNC is able to generate the cpap effect and the patient is much more comfortable with it vs the bipap. With it having the capability to be giving 100% FIO2 and tons of flow. It seems like the logical next step to em and one I always prefer. Thank you for all your researc!
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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.
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My email is gerondlake-bakaar@centura.org . Feel free to get in touch
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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?
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No fewer than the Graces, No more than the Muses.
Seriously, between 3 and 9 ( or 10 ) should suffice.
You might find the following of value:
Research in Nursing & Health, 2006, 29, 489–497
The Content Validity Index: Are You Sure You Know What’s
Being Reported? Critique and Recommendations
Denise F. Polit, 1,2* Cheryl Tatano Beck3**
You can find it on RG
Good luck
Chris
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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.
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Thanks @ Catia Cilloniz
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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 :)
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You ask an important question with far ranging implications and complex solutions.
I think the best framework to use in approaching this question is a model developed for  the US Institute Medicine. In practical terms, it recommends four categories of care (Wellness Basics, Restorative Therapies, Symptom Relief, Over-care avoidance - these are not the names they use, but are ones that are much easier to grasp).
I think the best way to answer your question is to  restate it, "what is the best way to optimize physical health in each of the four categories of care, for someone with severe mental illness?". I think the restatement is important, because the answers in each category are different. Typically, activity is required in all categories at the same time. In addition, these approaches are best deployed within the context of a recovery model of evolutionary improvement and ever-increasing self-determination.
I'll assert the highest level answer in all four categories.
Wellness Basics. These include 1) Housing & Security, 2) Diet & Digestion, 3) Exercise & Sleep, 4) Calm Awareness, 5) Effective Self-Management, 6) Purpose & Meaning, 7) Social & Outer Engagement, 8) Belief, Hope & Self-Transcendence. There are hundreds of RCTs that support that doing the right things in these areas directly support both mental and physical health. For instance, housing is the absolute first thing that one must do to support the physical wellness of someone with severe mental illness. Without it, their life nearly always remains in shambles. Approaches to wellness in this category are normal disciplines of wellness for everyone and are fairly well understood, though not always within reach. The challenge here is that these approaches often requires self-determination and lifestyle changes, things that can be extremely hard for people with severe mental illness. But, the good news here is that most of these things do not require medical intervention and can often, with a little creativity, be found without huge expense.
Restorative Therapies. These are mental health interventions targeted at suspected root causes of mental health symptoms, divided into two groups: Biomedical and Psychosocial. The Biomedical ones are directly tied to both physical health and mental health. Things like Nutrient therapy, Pathogen therapy, Endocrine therapy, Food Allergy Therapy, detoxification therapy, etc. are all therapeutic responses to physical issues that are well-known to potentially cause mental health symptoms. Approaches to wellness in this category are squarely within the medical discipline. It demands - though it is rare in conventional psychiatry today - robust biomedical testing. This testing is one of the cornerstones of integrative psychiatry, which is producing recovery rates substantially higher than those from drug therapy alone (the best evidence of this is through extensive open-label trials with Nutrient Therapy). Dr. Michael First, editor of the DSM-5 laments that current psychiatry often jumps to symptom-based diagnoses and all but avoids step three of the differential diagnosis process (the step that looks for underlying causative issues).
Symptom Relief. Effort here is to relieve residual mental health symptoms that the first two categories don't address. Psychotropics are by far the most common option here, but there are others with a smaller, but non-trivial evidence base: herbs, very small current electro-stimulation devices (like tDCS, tACS, CES, etc.), sensory therapy, etc. This area is predominantly tangential to the issue of physical health, with one exception. Symptom relief to some degree is often a mandatory first step to achieve stabilization. It is only after some measure of stabilization that we can even begin to consider improving physical health through approaches in the first two categories of care.
Over-care avoidance. This is a huge challenge in psychiatry today. Ill-advised polypharmacy and off-label prescribing, prescribing at dosages over recommended levels, over prescribing of psychotropics to vulnerable populations (the elderly, veterans, foster children...) and probably the most detrimental - antipsychotic polypharmacy - have been known to substantially impact physical health negatively. These are well understood by the APA and they have campaigns to reel-in some of these, especially antipsychotic polypharmacy. This has a huge implication on physical health. Outcomes from overcare are stark: significantly increased chances of death and a far ranging list of serious side effects.
So, how do we ensure the physical health of people with severe mental illness? 1) Focus outside of the medical discipline on the most out-of-balance wellness basics to establish new healthier lifestyle choices, 2) through robust biomedical testing, search for and address any physical issues found that are commonly known to cause mental health issues, 3) do enough symptom relief to reach a measure of stability so that a focus on physical health can be begun, 4) be ever vigilant to avoid over-care and seek "minimal effective dosages", starting dosages small and ramping slowly, 5) deliver these wellness approaches within the context of a recovery model that maximizes self-determination and recognizes that recovery is an iterative, evolutionary process where setbacks are common.
To deliver the above in a coordinated way is extremely difficult today and, to be done well, requires a holistic approach to patient care. I think to make substantive progress, we need to adopt something similar to this 4-categories of care model and train case workers on its fundamentals and how they can help individuals map into available services in each area.
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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...
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In the Netherlands we have widely implemented the term Lung Attack about 3 years ago (in a campaign from the Dutch Lung Foundation) and has landed quite well (until then there was not an widely accepted alternative to the complex term 'exacerbation'). It somehow emphasizes the severity of these events in terms of it's impact on mortality (which is worse compared to cardiac failure/hear attack), accelerated lung function decline and quality of life. Another advantage is that it underlines the acuteness of these events. 
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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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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. 
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Hi there
here at my lab we are conducting a study in dogs evaluating the effect of CPAP in the laringeal function in dogs under general anesthesia. It is a clinical study. The CPAP is applyed by the helmet. Maybe we can share some info
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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 
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Dear Rokib,
The following references and link describe the use of cigarette smoke to induce COPD (chronic obstructive pulmonary disease):
Stevenson C. S., Birrell M. A. Moving towards a new generation of animal models for asthma and COPD with improved clinical relevance. Pharmacol. Ther. 2011;130:93–105. [PubMed]
Vlahos R., Bozinovski S., Gualano R. C., Ernst M., Anderson G. P. Modelling COPD in mice. Pulm. Pharmacol. Ther. 2006;19:12–17. [PubMed]
Stevenson C. S., Belvisi M. G. Preclinical animal models of asthma and chronic obstructive pulmonary disease. Expert Rev. Respir. Med. 2008;2:631–643. [PubMed]
Churg A., Cosio M., Wright J. L. Mechanisms of cigarette smoke-induced COPD: insights from animal models. Am. J. Physiol. Lung Cell. Mol. Physiol. 2008;294:L612–L631. [PubMed]
Wright J. L., Cosio M., Churg A. Animal models of chronic obstructive pulmonary disease. Am. J. Physiol. Lung Cell. Mol. Physiol. 2008;295:L1–L15. [PMC free article] [PubMed]
Wright J. L., Churg A. Animal models of cigarette smoke-induced chronic obstructive pulmonary disease. Expert Rev. Respir. Med. 2010;4:723–734. [PubMed]
Hoping this will be helpful,
Rafik
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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. 
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Such patients often remain asymptomatic even on long follow up.
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Properioceptive  Neurofacilitation in COPD 
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I share the Irena Paiuk response 
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What S aureus strain would be best for inducing pneumonia in mice?
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I am not sure SA or indeed any organism can "induce" pneumonia.  I think pneumonia is caused by damage to the lungs, as noted by Bhoj, producing protected niches which certain opportunistic organisms are able to exploit, causing more damage and illness.
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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.
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Hm.
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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.
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This is a good question.   There is no safe non-invasive protocol for testing 'emphysema' (static compliance, lung volume subdivisions) in mice.   Respiratory pattern has not been well-described in elastase or transgene induced emphysema in mice.   We use repeated orotracheal intubation (without tracheostomy) to obtain static lung compliance and lung volume subdivisions.  The mice were repeatedly tested and recovered well.  The key is to use a proper catheter for orotracheal intubation and a lot of practice to get this to work.   As well, we developed a method for measuring specific airway resistance (sRaw = Raw * FRC) that should demonstrate increased sRaw after elastase injury or similar emphysema in mice (see Lofgren et al 2006) which is totally non-invasive and permits longitudinal study.    Finally, Wayne Mintzer's group from Johh Hopkins published a paper showing that using gas chromatography one can get measures of single breath DLco (DFCO in their paper, Fallica et al 2011) that would work to quantify diffusion limitation in murine emphysema.  Hope this helps to think about it. 
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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?
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Hi Vaideesh, 
There is not an specific way to measure the mean linear intercept, you should adapt and use your "custom" mask to evaluate. I can explain shortly what I did.
a) Load your image
b) Duplicate it (as backup)
c) Make your duplicate image Binary (Process - Binary - Make Binary)
d) Skeletonize the image ( Plugins - Skeleton - Skeletonize 2d-3d)
e) Multiply Images (Use your custom grid and multiply with the Skeletonized Image)
f) Count the intercepts (Analyze - Analyze Particles)
Remember to set the scale in order to know the distance.
For me it's the simpliest way and it only takes 2 minutes to get results!!!
Best
Juanjo
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role of echocardiogram in managing patients with COPD
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In a patient admitted with dyspnea due to COPD , it is essential to exclude LV dysfunction . As smoking is the cause of COPD & can also cause CAD . an urgent echo would help , in deciding whether LV dysfunction is playing a role in the symptom , In addition to the RV changes of Cor Pulmonale of COPD . The addition of diuretics gives immediate relief to cardiac failure in COPD . The message is that in every patient with COPD , LV dysfunction should not be missed .
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Management of pulmonary amyloidosis in Sjogren's syndrome.
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What's the type of pulmonary amyloidosis, AA or light chain? If it is a localized light chain amyloidosis, without symptoms and functional impairment of the lung, maybe follow-up is the choice. 
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I am doing a summary on a group exercise on COPD and I would like to drive home a point.
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unfashionable but important
smoking can kill slowly as well
disability for years and getting worse
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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...
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I suggest to read this article: N Engl J Med 2012;366:1968-77. I know that it is frustrating but as MD, we should avoid to harm our patients. Best regards, G
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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? 
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Bronchoscopy will not show pathological findings always in bronchial tree TB. Even broncos optic biopsy is pos in about 60 to 85% cases. Modern CT scan may be of some diagnostic use.  In these cases the diagnostic dilemma may lead to confusion and uncertainty in starting ATT. The choice is left to the specialist, based on clinical acumen and the available epidemiological links, ATT is advocated. If available culture of the biopsy will help in confirmation of diagnosis. 
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i want to know the correlation of oxidants/radicals and the inactivation of the alpha 1 proteinase inhibitor and the consequensis of this action...
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ROMs can definitely oxidize a-1PI, but this has to be highly localized.
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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)?
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I don't think you can call it COPD if it's in vitro. Sure you can expose cells to cigarette smoke extract, but that's really just a model of smoke exposure. 
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We sometimes experienced that influenza vaccination may cause exacerbation in some patients with COPD. Are there any publications about that and experience?
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No!
Another fear mongering for anti-vaccine activists
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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
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I am wondering, in particular, what kind of previous diseases you are referring to.
I would not hesitate, in general, to use MTX in the sarcoid patient you describe.  
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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?
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Dear Shakila,
Currently, I am working on the 'Rehabilitation, Sport and Active lifestyle' (ReSpAct) study. This is a multicenter, longitudinal cohort study in The Netherlands that evaluates a physical activity and sport stimulation program. The program aims to stimulate an active lifestyle in persons with a physical disability and/or chronic disease subsequent to the rehabilitation period.
Also patients with COPD have the opportunity to participate in the program when receiving treatment in a hospital or rehabilitation center that offers the program. An important part of the program consists of tailored counseling based on motivational interviewing (MI). These counseling sessions are offered by a 'Sports Counseling Center' within the hospital of rehab center.
Patients receive one face-to-face conversation and four telephone counseling calls by a counselor. During patient contact, the counselor makes use of MI. With the different conversations, patients are supported and guided in maintaining an active lifestyle in the home environment. The stages of change serve as the basis of the conversations and help the counselor to guide patients in their process of physical activity behavioural change. 
The first publication on the ReSpAct study can be found here:
We are currently working on an article with a more detailed description of the program.
Other interesting publications on a similar physical activity and sports stimulation program based on tailored counseling are:
van der Ploeg HP, Streppel KR, van der Beek AJ, et al. Successfully improving physical activity behavior after rehabilitation. Am J Health Promot. 2007;21(3):153-59.
van der Ploeg HP, Streppel KR, van der Beek AJ, et al. Underlying mechanisms of improving physical activity behavior after rehabilitation. Int J Behav Med. 2008;15(2):101-08.
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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?
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The person who might be able to help you is Dr. Jerrold Abraham, University of Syracuse Medical Center. He did some work a few years back on heavy metal disease. I recall that he followed patients with "odd" exposures. He is a pathologist. Perhaps an analysis of your Pt's lung parenchyma (Bx) might help to resolve agent or agents involved. Good luck. AML 
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What patient population would be appropriate for this particular drug?
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It has been approved by the European MA. We still can not use it in Spain. In my opinion it will be appropriate for COPD patients with moderate to very severe obstruction (GOLD grade II to IV) without frequent exacerbations and without characteristics of ACOS (Asthma-COPD syndrome overlap). 
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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.
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Hi All
Thanks-it's been a while since I logged in! I ended up combining cells from 3 wells and had enough RNA in the end.  
Best wishes
Brendan 
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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?
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Dr Mamuda
I’ve known about some very interesting experiences with sustainable sanitation in Haiti, after the 2010 earthquake. (see SuSan Lessons Learned, v11, 12.08.2012 - AK & TF.docx)
In countries with low sanitation coverage, the improvement of sanitation coverage the prodution of biogas for cooking and lighting purposes are welcome. Even sometimes in addition to this lack of access to toilets, urban centres have dilapidated rainwater drainage systems which often flood and spread waterborne diseases, including cholera. With this figure, my answer is yes this could be the future for developing countries.
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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.
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Dear Mike
Please a recent article that uses murine alveolar type I cell line.
J Gen Virol. 2014 Feb;95(Pt 2):350-62. doi: 10.1099/vir.0.058438-0. Epub 2013 Nov 16.
Characterization of innate responses to influenza virus infection in a novel lung type I epithelial cell model.
Rosenberger CM1, Podyminogin RL, Askovich PS, Navarro G, Kaiser SM, Sanders CJ, McClaren JL, Tam VC, Dash P, Noonan JG, Jones BG, Surman SL, Peschon JJ, Diercks AH, Hurwitz JL, Doherty PC, Thomas PG, Aderem A.
Author information
1Seattle Biomedical Research Institute, 307 Westlake Avenue North, Suite 500, Seattle, WA 98109, USA.
Abstract
Type I alveolar epithelial cells are a replicative niche for influenza in vivo, yet their response to infection is not fully understood. To better characterize their cellular responses, we have created an immortalized murine lung epithelial type I cell line (LET1). These cells support spreading influenza virus infection in the absence of exogenous protease and thus permit simultaneous analysis of viral replication dynamics and host cell responses. LET1 cells can be productively infected with human, swine and mouse-adapted strains of influenza virus and exhibit expression of an antiviral transcriptional programme and robust cytokine secretion. We characterized influenza virus replication dynamics and host responses of lung type I epithelial cells and identified the capacity of epithelial cell-derived type I IFN to regulate specific modules of antiviral effectors to establish an effective antiviral state. Together, our results indicate that the type I epithelial cell can play a major role in restricting influenza virus infection without contribution from the haematopoietic compartmen
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Ultra long acting beta 2 agonist.
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Indacterol is clearly superior to salmeterol and other LABA's as monotherapy in clinical trials, and that's a promised fulfilled in clinical practice. The stumbling block is the fact that it is yet to be made available in combination with an ICS and (at least in the UK) there aren't any single agent ICS's licenced for use in COPD; and neither is there research evidence with such combinations. It's excellent therefore for the persistently short of breath non-exacerbator, or perhaps the milder exacerbator but it's tricky to fit into a reasonable treatment scheme for severe disease. (An exception; the reason to push the dose from 150 to 300 mcg is an improvement in dyspnoea in some trials with this; occasional for a highly symptomatic patient, that is one who is just horribly short of breath, I'll split the inhalers and try pushing the indacterol dose in case it helps. Sometimes it does, sometimes it doesn't)
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Using either absolute values or %predicted will not make a difference if you are studying a change in the same patient group. However, while comparing two groups I would prefer %predicted over absolute values. I also feel that both the approaches have their own flaws.
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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?
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Hello, bodyplethysmography gives you the best informations about airway resistance at rest and the degree of hyperinflation. We always perform bodyplethysmographie in our patients. Especially in emphysema, where FEV1 is always low you have informations about the variability of airway obstruction and hyperinflation in order to control the effect of your therapy. Best regards. Kurt Rasche
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The management overlaps so much.
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There are totally different diseases in terms of pathogenesis, inflammation, risk factors (i.e. for COPD smoking, for asthma atopy/AHR), lung function, reversibility, symptoms (chronic and progressively worsening in COPD vs sporadic in asthma), epidemiology etc etc. However, in a proportion around 10% there is a coexistence (overlap of the 2 diseases) and also there is a progression of asthmatic smokers to COPD. A big question unanswered yet, is whether asthma in COPD represents a COPD phenotype or a COPD comorbidity.
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Which of the following has the better correlation with dyspnea and quality of life in COPD? -
1. FEV1
2. RV/TLC
3. FVC
4. IC
Answer with reason and proper references.
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All of them have a certain value. Dyspnea in COPD has many dimensions (respiratory, cardiovascular, muscular, mental etc.). Among the respiratory you listed, the most valuable is the IC since it reflects hyperinflation. However, in static and not dynamic (exercise) conditions, hyperinflation is better represented by FRC or TGV if you prefer (in body plethysmograph). RV/TLC reflects gas trapping which is also assumed by FVC (since RV+VC=TLC). Gas trapping is a paragog of hyperinflation. FEV1, although the most widely used spirometric index, supports COPD diagnosis and classification, however it does not correlate with dyspnea.
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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.
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Here is another publication regarding the effects of oxidative stress on airway injury.
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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.
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Marcelo:
La evaluación se hizo al mes de realizada la FAV. Es importante decir que en comunicaciones previas, la evaluación se ha hecho a las 12 semanas y por lo tanto, podemos asumir que el efecto de la FAV puede ser progresivo en el tiempo y por lo tanto es posible que al reevaluar al paciente en un tiempo mas alejado el efecto positivo de la FAV será mayor. En efecto, hemos controlado recientemente al paciente (a los 6 meses post intervención) y su Pa02 actual es de 73 mm Hg (97% Sa02) no sintiéndose limitado en su capacidad de ejercicio.
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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?
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I think so. I gave my data for such an analysis and got named as an author on the paper (with the opportunity to contribute to the paper too) and received no financial reimbursement but I was happy with that. I was generally happy to contribute my data for the greater good.
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Biomarkers are able to predict mortality in COPD patients. What are those biomarkers?
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