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For the past few months, I have been receiving strange review invitations from the famous "Susan Lee" at the HSPI Open Access Journal.
The most surprising aspect of these requests is that they all concern subjects far removed from my area of expertise (for example, one for a publication in the Journal of Forensic Science and Research and another in the Journal of Pulmonology and Respiratory Research). Moreover, the corresponding manuscripts were directly attached to the message ... I imagine a great manner to maintain the confidentiality.😕
Since my expertise lies more in organic chemistry, spectroscopy, and quantum calculations, you can imagine that I am not the right person to assess the quality of papers like "Risk Factors for Respiratory Diseases: A Comparison Between South Asia and Central Asia" or "Digital Forensics and Media Offenses – Investigating Synergy in the Cyber Age"...
Despite politely declining these invitations, I continue to receive requests from "Susan," which leads me to conclude that these journals are not serious.
Has anyone else had a similar experience, or am I the only lucky one here?
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thanks Rob for your prompt answer ... I assure you that Susan's email has been added to my list of unwanted senders ;).
Cordially
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Suppose I faced a series of very rare cases of pediatric patients, and I decided to conduct a study on the their parents to try to know the risk factors and psychological negative consequences on them because of their children got this rare infection. If i send them through WhatsApp a google form survey.
My question is what is the name of the method i used ?
is it “A case series design targeting the parents“ or is it “ retrospective study“
below what I already have written
“ A case series design was employed in the study. The design is often employed in the description of characteristics and outcomes among individuals who have a disease or exposure [8]. In this case, the focus was on parents whose children had been exposed to this rare infection “
8. Torres-Duque, C. A., Patino, C. M., & Ferreira, J. C. (2020). Case series: an essential study design to build knowledge and pose hypotheses for rare and new diseases. Jornal Brasileiro de Pneumologia, 46(4), e20200389. https://doi.org/10.36416/1806-3756/e20200389
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As per recent diagnostic criteria for the diagnosis of NTM, there is a chance of overdiagnosis of NTM, thereby enhancing the potential toxicities of the drugs. There is also a chance of undertreatment. How do you defend this column? What do you think?
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Hi, good day! Nontuberculous mycobacteria are a diverse group of mycobacterial species that causes different clinical infections in children and adults. According to Ingen (2013), 25 species have been strongly associated with NTM out of the 140 known NTM species in the literature/studies. Isolation of M. kansasii and M. malmoense from pulmonary specimens usually indicates disease, whereas Mycobacterium gordonae , M. simiae, or M. chelonae are said to be contaminants rather than causative agents of true disease. Mycobacterium avium complex (MAC), M. xenopi, and M. abscessus form an intermediate category between these two extremes (Ingen,2013). NTM species differ in their clinical relevance therefore, the need for correct species identification is very important. As per your question, to prevent the chance of overdiagnosis and undertreatment of NTM, it is crucial to identify the particular causative agent that caused the condition/illness as well as its clinical relevance. to make a firm diagnosis, a culture of the clinical specimens, and a histological examination of tissue biopsy specimens are needed. Diagnosing NTM disease is complex therefore a good communication between clinicians, radiologists, and microbiologists may help in optimizing the culture conditions in line with the particularities of the patients.
if you want to know more about the diagnosis of NMT, this article might help you:
Ingen, J. (2013). Diagnosis of Nontuberculous Mycobacterial Infections. Diagnosis of Nontuberculous Mycobacterial Infections. DOI:10.1055/s-0033-1333569
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I am currently looking for a journal/publisher in the field of pulmonology/cystic fibrosis with the option of rapid publication. I will be very grateful for the recommendations.
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This journal is rather rapid:
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I am looking for data related to breathing exercises that can be safely prescribed in case of spontaneous pneumothorax with / without bronchopleural fistula ; managed by inserting an intercostal drainage tube.
Can incentive spirometer be given to these patients ?
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I think that Expiratory exercise will increase the Transpleural pressure this will help to make the pressure at the point to prevent atelectasis
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The Well's score was designed to help predict the likelihood of PE by studying the PPV of PE of various clinical features in a population; obviously that population was not one in which COVID19 had become epidemic. For the next few months, while controlling the initial outbreak if the virus, can we still rely on the Well's score or has its validity been undermined by the fact we are now dealing with a very different population?
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No Well's score is unreliable in patients with Covid-19.R
Risk of thromboembolism in Covid-19 is high.
The Well's Score understabably does not consider this.
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This screenshot is from "Community Pharmacy Symptoms, Diagnosis, and Treatment". I wonder How Postnasal drip is experienced by Adults only as shown in the image, and Allergy which is the cause of PND is experienced by any age ? Shouldn't this be the other way around ? Because unless there is a PND, there would be no cough in this scenario ? And allergy is one of the causes of PND
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In adults main cause is DNS or Turbinate pathology
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Clot sustained in a accident, however patient doesn't has any sign or difficulties. Some physician suggest it may dissolve itself and other recommends a surgery. Please explain.
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thank u sir
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Hi,
I think the drug I've used expired (It was bought 3 years ago and stored at -20). Where should I purchase the drug? Also do mice in this model develop emphysema? 
Thank you in advance,
Ravit
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In my previous lab, we had tried to developed Bleomycin induced fibrosis model in Beas2b cell line as well in mice using Bleomycin sulfate from sigma. We were able to developed this in cell line, but we struggle in mice model. So we tried silica induced fibrosis model, which is an alternate of bleomycin.
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A 14 year old girl with Crohn's disease A1L3P, earlier received prednisone, azatioprin, infliximab (clinical improvement with 1 in 4 weeks scheme), relapsed in October. Recently she was switched to adalimumab (humira, 3 inj) with no significant improvement (3-4 liquid stools a day, oral cavity ulcers, elevated ESR and CRP). What would be advisable tactic to treat this patient?
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hello anastasia, there is no recipe for treatment refractory crohn´s disease in children. in my opinion you should act as follows: 1) rule out another disease (eg. CGD & other PID´s, primary vasculitis....) by all available means (upper & lower endoscopy with histology, blood tests etc). After ruling otu other diseasis you have several options (depending on disease location): a) vedolizumab (combine it with aza or MTX to reduce the probability of autoantibody formation) b) induction therapy with total EN (or corticosteroids) for 8-12 weeks plus MTX s.c. c) other medications off-label (eg thalidomide, ustekinumab, JAK inhibitors..) d) surgery.
good luck
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A - IM epinephrine
B - Endotracheal intubation.
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According to the severity of the case if the patient is severely hypoxic with delirium and impaired conscious save live with intubation followed by epinephrine if condition is hemodynamically stable give epinephrine and wait you may not need intubation
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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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What will be the best test in order to differentiate between Seminoma and Non Seminoma ?
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You may look the levels of tumor markets, if with elevated alphaphetoprotein, it does have a nonseminoma component; however gold standard for the diagnosis is pathology specimen result, so a biopsy should be done.
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I've seen lots of books and web sites say that normal ETCO2 is 35-45 mmHg.  But I can't seem to find any actual data on this.  Can anyone point me toward a a publication that shows the mean and standard deviation ETCO2 values in healthy subjects breathing normally?
The impetus for this question-- we're using the BIOPAC system and with a small sample of healthy subjects, we're seeing values of 3.5%-4.5% CO2 which translates to 27-34 mmHg (unless we're calculating it wrong).
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Hi David,
Agree with comments above, your values for baseline EtCO2 do seem a little low. I would like to point you in the direction of work by some of my colleagues' on normative physiological measurement data in a large cohort (n=119):
This demonstrated median EtCO2 values of 39.1(IQR 36.9–40.8) and mean 38.6 (SD 3.9). This is certainly inkeeping with studies using a basic nasal cannulae setup/face mask for TCD measurements.
However, be wary of the variation that exists between cannulae and facemasks as shown by some of my previous work:
Hope that helps,
Best wishes
Jatinder
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Endosonography: Do you routinely use combined EBUS-TBNA and EUS-B-FNA approach in staging lung cancer?
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no
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As we published in article The prospective register of acute decompensated heart failure: an experience of one center mean GFR on time of hospitalization was 63 ml/min, GFR below 60 ml was in 46% and increase up to 53% during hospital stay.
What do you think if it possible to use sorbents in those patients?
For examples - we use patiromer or similar sorbents in patients with hyperkaliemia...
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Little data known about sorbents in HF.
For example: Evaluation of Cross-Linked Polyelectrolyte (CLP) With Placebo in Heart Failure Subjects (STEPWISE).
"CLP-1001 has shown great promise in alleviating the negative impact of fluid overload in heart failure patients as demonstrated in our prior Phase 2a clinical trial. We look forward to reporting data from the STEPWISE trial later this year," said Detlef Albrecht, M.D., Sorbent's President and Chief Executive Officer. "I would like to thank our existing investors for their continued support. This new round of funding and the progress in our lead CLP program take us several steps closer to achieving our goal of bringing a new therapeutic option to advanced congestive heart failure patients."
I have little experience in clinical trials. Results published in N Engl J Med.
CONCLUSIONS
In patients with chronic kidney disease who were receiving RAAS inhibitors and who had hyperkalemia, patiromer treatment was associated with a decrease in serum potassium levels and, as compared with placebo, a reduction in the recurrence of hyperkalemia.
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which is best using MDIs or nebulizers?
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there are some studies on this, e.g. reference mentioned below 
Am J Perinatol. 2001 May;18(3):169-74.
A prospective controlled trial of albuterol aerosol delivered via metered dose inhaler-spacer device (MDI) versus jet nebulizer in ventilated preterm neonates.
Khalaf MN1, Hurley JF, Bhandari V.
Author information
 
Abstract
The objective of this study was to identify the most efficient and cost-effective nebulizer device for delivery of albuterol aerosol as a bronchodilator in ventilated preterm infants. Bronchodilators are frequently used as part of the therapeutic regimen of ventilatedpreterm infants. This can be delivered by different types of nebulizers like the Jet or metered dose inhaler (MDI) spacer device. Fifty-three premature infants being ventilated for RDS (24 to 34 weeks of gestation) were studied just prior to extubation. Twenty-four of them received standard doses of albuterol aerosol via Jet nebulizer and 29 via MDI-spacer. Heart rate, respiratory rate, oxygen saturation, lung compliance, and airway resistance were monitored prior and 15 minutes after albuterol delivery. There were significant changes in the parameters studied between pre- and postnebulizer treatment. In both groups, there was a significant improvement in lung function as evidenced by 13-24% decreased airway resistance (RAWE) and 3-7% increased lung compliance (CDYN). There was also a beneficial clinical response as demonstrated by increased oxygen saturations. These findings suggest that both MDI-spacer and Jet nebulizer are equally effective in delivering the albuterol aerosol to the lower respiratory tract. Since a small dose of albuterol delivered via the MDI-spacer improved lung function as effectively as a higher dose via the Jet nebulizer, the MDI-spacer would be the preferred mode of aerosol administration, especially because it takes only 2 minutes to deliver it. Furthermore, it was also cost-effective as one MDI-spacer treatment costs 2 cents, while a Jet treatment costs 10 cents in our neonatal intensive care unit (NICU).
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The indications for bronchoscopies -either rigide either flexible; diagnostic or interventional including diagnostic - largly differ from the paitents' age (0 month- to18 years) ,from the potential complication rate; and finally the bronchcopist's skill, knowledge and capability. Summerized the risk-benefit ratio.
There are geographic variation due to the economic situation of the certain country.
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dear doctor :
thanks a lot for such nice question again it is very hard to answer as there are very few indications in children 
I had do few cases for cystic fibrosis , TB survey  & foreign bodies removal 
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As we are not sputum for gram staining and gastric aspirate revealed less result we have to depend on indict evidence for starting ATT.
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Diagnosis of pulmonary TB in kids is predominantly clinical & microbiologic confirmation occurs very infrequently (~20-50%). Culture is the reference standard, but clearly not a gold standard. PCR, usually via Gene Xpert, is WHO recommended. But a negative culture or Xpert should not delay initiation of ATT. Lots of good review articles on the challenges on pediatric TB diagnosis. 
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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'm looking for a free and reliable software to assess the extent of lung emphysema and bronchiolar wall thickening on CT scans. Thank you!
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I am not aware of any free and reliable software on the market for assessing the extent of lung emphysema and bronchiolar wall thickening from CT scans. Most free CT scans software are not reliable. However, commercial CT analysis software are quite expensive.
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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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Similar to Hepatocellular carcinoma, radio frequency is an interventional solution.
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I am not expert.
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whats the role of corticosteroids in management of ARDS ?
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i assume that this relates to the aspect that - in the absence of shunting - all blood goes through the lung circulation, and consequently, this may act as a 'filter'
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We were not able to detect elevated EDP in mice using miller pressure catheter. But we see a clear increase in EDV in same mice using MRI scanning? What would be a possible explanation for this?  
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why
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i am going to use histamine as skin prick test in cattle but I am unable to find the dose rate of histamine in cattle. I could only find it in humans. 
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I have only worked in smaller animals like mice, guinea pig and rabbit for skin testing. The dose is determined on 1 mg/ml. Although the dose is an educational guess, I have not had problem with the dose I used.
I do not read the adequate dose of histamine is reported on cattle for skin testing. However, it is safe to start with 1mg/ml concentration of histamine. You may advance the dose starting from 1mg/ml steadily up to 5 mg/ml if you do not see a visible reaction at the lower dose after 15 min.
You must be careful how to apply skin test as it matters how deeply you inject histamine with needle. Subcutaneous injection should be the route to choose, and it would make the swelling size easier to measure. Also, make sure that you shave the hair off on the area where the skin test will be done, in order for you to mark the size of redness and wheal formation. Hope it helps.
Shih-Wen Huang,MD
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Since I need more no of images for detection
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Depends upon what information you want to collect and then put in the database.  I would start with that.  Do you want to just collect the images and save them for later analysis ?  What information do you want to collect from the images ?  Just the images themselves, like from a screen capture ?  The medical images for a medical imaging database, like from a PACS system.  Those images have other embedded information in them about the examination that usually isn't visible to the casual observer.
If you want to collect corresponding patient data and demographics, that is more complicated, but you can collect that.  You might even want to collect serial examinations for those studies for each patient.
I think you should start with a few things:
1.  Why are you collecting the data ?
2.  What data do you want to collect ?
3.  What are you going to do with the data once you have it ?
4.  How much data do you want to collect ?
5.  What are you trying to prove and what are the criteria for a proof.  Do you need to be 100% certain, or just within some level of certainty.
6.  What are going to do with the data once you have it ?  Is it just to prove a point, are the results going to have an impact upon what you are going to do next, that kind of thing.
Do you already have some images and data ?  I could probably help you with that if you are doing some sort of research project.
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I'm trying to determine if the reason bronchiolitis obliterans is not seen in smokers might have to do with obscuring of the specific pathology by a more generalized bronchiolitis 
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Diagnosis is your key. Agreed procedures for post-mortem pathology and the persistence of pathologists to diagnosis may not be standardized.
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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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So if there is any other site or any other way to design construct by itself by cloning the reporter but i don't know how to do it.
Thanks
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here I am sorry I can not help
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Hi ,I am trying to work on pepsin for antigen retrieval for formalin fixed paraffin embedded lung tissues.It did not work when I dissolved the lyophilized powder in 10mM HCl at ph 2.I want to know how to reconstitute it to have it working on my tissue.  Some protocols recommend usage of tris-HCl.Does anyone know how to reconstitute pepsin for IHC FFPE tissues for antigen retrieval
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Thanks all for the inputs! I got this product from Sigma/Roche and it doesn't say much about reconstitution.It just says working concentration is .05 mg/ml to 0.5 mg/ml.
@Ahmed -I did try dissolving in cold HCL and DDH2o with pH @ 2.2,it did not work effectively  on my tissues
One of the  protocols recommended adding some detergent to get optimum antigen retrieval .I made a diluent for pepsin .For 50 ml diluent , I added 49 ml of DH20 +0.5 ml of 12 N HCL +.05ML of Triton-x 100.I dissolved pepsin in the working concentration mentioned.It worked !
Thanks all.
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If treated, which agent is preferred agent? NOAC or vitamin K antagonist?
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I would not!
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One of my patients with COPD has got a dyspnoe, after inhalation of (heated?) grated ginger. His FEV1 decreased to 50%. Does anybody know the mechanism or other side effects of ginger in pulmonology?
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This is a tricky question. Ginger is believed to possess multiple effects among which strong antioxydant properties and in some studies inhalation of ginger essential oils in aromatherapy has shown positive effects on anticancer chemotherapy-induced emesis and nausea and bronchorelaxing properties in in-vivo models of experimental allergic asthma. So in principle the expected effect of ginger might not lead to pulmonary function deterioration unless the physico-chemical charateristics (and the amount!) of the material inhaled are such to determine a mechanical stress in the airways. Indeed it is known that coarse particles above a certain amount can cause "per sè" pulmonary function deterioration.
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Dear All,
I observed a 58 yo female patient in deep pain and was diagnosed as having a left-sided atypical chest pain. And she was sent for a chest X-Ray. It was found that she has a 1.0 cm x 0.8 cm lower left lung nodule. A repeat X-Ray is warranted but the result is still unknown.
My question is -
1. Could the atypical chest pain be the result of the lung nodule?
2. Her previous mammogram showed no abnormality, and she conducts her BSE monthly NOS. Could it be that there is some abnormality in the breast instead?
3. What could best explain her condition(s)?
Best regards - Mariam
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Dear Dr. Ahmad:
If the nodule was closely associated with the pleura then the chest pain can be explained.  If the nodule is close to the bronchioles, then there may be pain but more likely would produce a cough or hemoptysis.  Otherwise, if the nodule resides in the parenchyma of the lung there should not be any pain especially at the size you reported.
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Lungs are fixed by PFA and embeded in OCT and stored at -80oC. I am using the general protocol of abcam (http://www.abcam.com/protocols/immunostaining-paraffin-frozen-free-floating-protocol) to stain frozen sections of mice lungs and I get auto-fluorescence. 
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Yavuz,
Autofluorescence is always a problem with IF staining.  One of the things that can cause a great deal of autofluorescence is the fixing and permeabilizing agent used, but PFA is a good choice for this, as compared to methanol.  Another common cause of autofluorecence is the presence of RBCs in the sample.  Although this cannot be completely avoided, it can be reduced if you perfuse the animal with saline upon sacrifice before harvesting the tissue.  You can never remove all the RBCs, but perfusing does help. 
If you can't decrease the autofluorescence enough even with settings on your microscope/camera setup, then can you use IHC instead?  If you use adequate peroxide to quence the endogenous peroxidase activity (I use 3% peroxide in methanol--10x the concentration in the abcam protocol) then you can get very clear staining and be able to see the structure in the tissue. 
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Any specific way to analysis the trans pulmonary pressure
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My answer is limited to experience in measuring this in ambulatory humans in the upright position (measurement of lung compliance). I'm working on the premise that you are defining transpulmonary pressure as the difference between alveolar an pleural pressures.
Pleural pressures can be accurately estimated using an esophageal balloon catheter positioned in the lower 1/3 of the esophagus.  Alveolar pressures can be assumed to be equivalent to mouth pressures measured in the condition of no flow.
Our procedure was to position the catheter properly by having the subject swallow the balloon catheter while sipping water until the tip was approximately 50cm from the nares. We then attached the catheter to a pressure transducer and verified that a vigorous sniff produced a positive pressure deflection with respect to atmospheric pressure.  The balloon catheter is then pulled upward in small increments, checking the degree of negative deflection on sniff.  When consistent maximum negative pressure deflection is seen, the balloon catheter is likely to be positioned properly ( in the lower 1/3 of esophagus, with the entire balloon above the GE sphincter.
The then make an attachment to a pressure transducer that will reflect mouth pressure when the subject is breathing on a pneumotach (luerlok attachment just at the mouthpiece/filter) that has a shutter attached to it.  We have the subject inhale maximally and then passively exhale.  Our system will close the shutter briefly at pre-set volume or time intervals.  When the shutter is closed, the mouth pressure is assumed to be alveolar pressure. This is then plotted against exhaled volume to construct a pressure volume curve of the lung.
I hope this is helpful.
Best, Kevin
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Pulmonology, Chest Medicine, Thoracic Surgery ..
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we used it in PICU some years ago but not now  . the reason was that we had some complications with haemothorax. Now we perform early thoracocentesis and if we have a loculated empiema we perform thorachoscopy with excellent results and early discharge.
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Need a validated questionnaire to learn about physician satisfaction working with staff in our endoscopy department.
Also need a validated survey about staff satisfaction with their knowledge and skill levels for complex procedures
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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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There is little literature on this issue and practiced differ tremendously from one hospital to another. Some hospitals change the circuits Shen they are broken (.yes, some people are poor), most on a weekly basis, and some even after each patient. It is a very grey zone. and a permanent source of useless waste.
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Dear Teng Jing Ru, the afirmation of respiratory therapists of your institution is not entirely wrong. There isn't evidence to support the systematically circuit change. In my first answer I attach the guidelines of the American Association of Respiratory Care (AARC) with the recommendations of this.
Kind regards
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What are the DPLDs which increase lung volume rather than decreasing it?
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ILD with preserved or increased lung volumes 
lymphangioleiomyomatosis,
pulmonary Langerhans cell histiocytosis
some sarcoid patients
concomitant emphysema or asthma.if ILD develops in a patient with significant emphysema,
combined pulmonary fibrosis emphysema symdrome
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Prescription of high flow oxygen with subsequent increase of SpO2 above 92% without investigation of PaCO2 levels, has become a policy in many hospitals, especially in the ER. Is there any evidence supporting high FiO2 resulting in SpO2 higher than 92% in patients with hypercapnia? 
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Use of high flow of oxygen does not necessarily mean use of high FiO2, because they are two different parameters (L / min of gaseous mixture versus O2% in the gaseous mixture). In any case, I believe that the target of 88-92% of SO2 in hypercapnic patients should always be respected.
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pharmacology, pulmonology, veterinary,
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WOW!!!  What great responses !  I can add little or nothing except say that despite the chemical differences in the steroid molecules and delivery devises there is no one ICS that is best for every patient. All of these drugs have been studied extensively and all have their Pros and Cons --as well as a group in each camp who thinks A is better than B than C .
In reality there are little differences if one looks at the "average"(what ever that means) patient. I think the important thing here is to look at each individual response (INDIVIDUALIZE) and look for out for those who are different --greater susceptibly to adverse effects and less positive effects ( not all asthma patients respond to Corticosteroids--(something quite often forgotten).
Yes compliance is a major problem in asthma--and most other disorders-so once a day ICS may be important but COST is also important !!  $300 a month for an ICS ?? --and please don't say the patient does pay for it--The Public Always Pays
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In the case of spirometry, we measure flow, but in the case of FOT we measure resistance; This parameter (MEF 25-75) indicates development of small airways, i want to know if in FOT we have something similar. Thanks a lot!
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MEF 25-75 reduction alone, usually indicates peripheral airways obstruction. To my knowledge, in regard to FOT or IOS (impulse oscillometry), frequency dependence of resistance (i.e. fdr=R5-R20 in IOS and fdr=R4-R16 in FOT) expresses the peripheral respiratory system resistance. This is because high frequency oscillations (R20 for example) are impeded through their way via the large and medium calibre airways and never reach periphery. Low frequency resistance, on the other hand, expresses the total respiratory system resistance (both large and small airways). When an obstructive syndrome is concerned and other pathologies have been ruled out, fdr increase is a safe index of peripheral airways obstruction. Furthermore, it has been shown that fdr correlates significantly with reactance area (AX) measured only through impulse oscillometry, which is also a valuable index in such cases.
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Traditional lung rest strategies on respiratory ECMO seem to have little physiological or clinical trials justification. 
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Gothner M, Buchwald D, Schlebes A, Strauch JT, Schildhauer TA, Swol J.
Use of extracorporeal membrane oxygenation in combination with high-frequency oscillatory ventilation in post-traumatic ARDS. Acta Anaesthesiol Scand. 2013 Mar;57(3):391-4. doi: 10.1111/aas.12065. Epub 2013 Jan 8.
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Hi all
looking for information on on several zoonotic dz for an assignment. Ornithosis is one of them if anyone knows of an article relating to this infection in New Zealand I would be grateful.
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Dear Collegue!
As pulmonologist I see two type: an acut infection " atypical Pneumonia" and a chronic type: with X-ray exam shows signs of fibrosis. What is the concret problem? Sincerelly yours Paula
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In my opinion Methotrexate pathway doesn't lead to inhibition of Interferon gamma release but methotrexate potentially can cause immune-suppression through other pathways. Please advice.
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In South Africa, virtually all people should show a positive skin test - in our context, I would say no. 
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use of BIPAP on discharge in COPD or non COPd patient who never used it. Admission PCO2= high
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Hello Bikash Bhattari, 
I think, it depends if there is an acute or chronic situation; if acute respiratory failure then respiratory acidosis should be present and NIV should be start; if not, it is probable chronic respiratory failure, it,s better investigate the cause before starting non invasive ventilation if clinical situation allow it. Respiratory function test, rule out respiratory breathing disordered and obesity hypoventilation syndrome (most comon causes in my environment). If the patien is very symptomatic, with disnea, hipersomnia, be care  not use high oxygen flow, avoid respiratory depressant medication, and consider NIV then. If COPD is suspected or confirmed, depend on the previous situation, if multiple hospitalization with respiratory failure, or hypoventilation simptoms then you could consider NIV.
- Non Invasive ventilation in acute respiratory failure. Thorax 2002; 57:192-211
- Home mechanical ventilation. A Canadian Thoracic Society clinical practice guideline. Can Respir J 2011;18(4):197-215
- Gidelines for non invasive and invasive  mechanical ventilation for treatment of chronic respiratory failure. German Society for Pneumology. Pneumologie 2010; 64: 640–652
I hope I've been helpful. 
Regards, Raul Hidalgo
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I am interested whether SIT 910 and SIT 1729 follow certain pattern of transmissibility.
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Please refer to the following articles, not sure if this data exists for Europe or US:
JCM Accepted Manuscript Posted Online 11 February 2015
Mycobacterium tuberculosis lineage7 strains are associated with prolonged patient delay in pulmonary tuberculosis patients in Amhara Region, Ethiopia
Solomon A. Yimera,b,c,d, Gunnstein Norheimb, Amine Namouchia, Ephrem D. Zegeyea, Wibeke Kinanderb, Tone Tønjuma,e, Shiferaw Bekelef, Turid Mannsåkerb, Gunnar Bjuned, Abraham Aseffaf, Carol Holm-Hansenb
Recent genotyping studies of Mycobacterium tuberculosis (Mtb) in Ethiopia have reported the identification of a new phylogenetically distinct Mtb lineage, lineage 7. We therefore investigated the genetic diversity and association of specific Mtb lineages with sociodemographic and clinical parameters among pulmonary TB patients in the Amhara Region, Ethiopia. DNA was isolated from Mtb positive sputum specimens (n=240) and analyzed by PCR/24-locus MIRU-VNTR and spoligotyping. Bioinformatics analysis assigned the Mtb genotypes to global lineages, and associations between patient characteristics and genotype were evaluated using logistic regression analysis. The study revealed a high diversity of modern and pre-modern Mtb lineages among which approximately 25% were not previously reported. Among the Mtb strains (n=138) assigned to seven sub-groups, the largest cluster belonged to the lineage Central Asian (CAS) (n=60; 26.0%), the second largest to lineage 7 (n=36; 15.6%), and the third to Haarlem (n=35; 15.2%). Four sub-lineages were new in the MIRU-VNTRplus database, designated NW-ETH3, NW-ETH1, NW-ETH2, and NW43 ETH4 which included 24 (10.4%), 18 (7.8%), 8 (3.5%) and 5 (2.2%) isolates, respectively. Notably, patient delay was significantly longer among patients infected with lineage 7 strains (Mann-Whitney test p<0.008) compared to patients infected with CAS strains (AOR=4.7, 95% CI 1.6, 13.5). Lineage 7 strains also grew more slowly than other Mtb strains. Cases of Harlem infection (OR= 2.8 95% CI 1.2, 6.6) and NW-ETH3 (OR= 2.8 95% CI 1.0, 7.3) appeared in defined clusters. Intensified active case finding and contact tracing activities in the study region are needed to expedite diagnosis and treatment of TB.
APMIS. 2013 Sep;121(9):878-85. doi: 10.1111/apm.12046. Epub 2013 Jan 22.
Spoligotyping of Mycobacterium tuberculosis isolates among pulmonary tuberculosis patients in Amhara Region, Ethiopia.
Yimer SA1, Hailu E, Derese Y, Bjune GA, Holm-Hansen C.
Author information
1Norwegian Institute of Public Health, Oslo, Norway. yimsolo@yahoo.com
Abstract
The aim of this study was to characterize Mycobacterium tuberculosis isolates circulating in the Amhara Region of Ethiopia. Sputum samples were collected from new pulmonary tuberculosis (TB) patients in the Region. Genotyping of mycobacterial DNA was performed by spoligotyping and isolates were assigned to families using the SpolDB4 and the model-based program 'Spotclust'. A high level of diversity was found among the 237 isolates. Sixty-five different spoligopatterns were obtained. The T (30.8%), Central Asian (CAS; 21.1%) and U (17.7%) families were the predominant isolates comprising 69.6% of the total strains. Eighty-five per cent of the U lineage belonged to Spoligo-International-Type (SIT) 910 and SIT 1729. Only a few of these strains are included in SpolDB4 to date. Of the total strains, 41 (17.3%) were unique and have not been described in SpolDB4 to date. This study indicated that the TB epidemic in Amhara Region, Ethiopia, is characterized by the circulation of numerous M. tuberculosis strain families. The high proportion of SIT 910 and SIT 1729 strains may indicate an increase in the importance of these lineages in the transmission of TB in the study region.
© 2013 APMIS. Published by John Wiley & Sons Ltd.
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Observing a very frothy white layer on a bronchoalveolar fluid obtained with a very  good yield (155/200ml) prompted me to measure both the albumin and protein content of this fluid. The beer-like appearance reminded me of dissolving human albumin some years backi in a lab experiment. The concentrations obtained were very low (measured with the technique used for detection of microproteinuria...).
Protein 0.132 g/L and albumin 11.2mg/L. So far I have not found reference values for these findings.
Anyone aware of the normal range of protein and albumin content in BAL fluid?
Is the froth related to the yield rather than to an increased protein content?
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READ ABOUT THE UREA METHOD...
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We distributed the recent AAP guidelines for the management of bronchiolitis to our pediatric group but still find the inertia of routinely administering albuterol hard to reverse. What is the international experience?
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Here we experience the same problem. As we have no proper therapeutic measures to apply, we end up administering salbutamol (in our case) to almost all infants. However, we've been using saline in almost all cases, with apparent good results. 
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Inhaled NO has shown benefits as long term therapy for pulmonary arterial hypertension and other types of pulmonary hypertension. But the therapy also comes with some adverse effects (e.g., inflammation and oxidative damage to the lung) when used for a prolonged period of time. What recommendations would you make for weaning to ensure that the inhaled NO therapy is terminated safely?
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Can only address its use in PPHN. I will start NO at 20 PPM with 100% O2 then decrease FiO2 first as tolerated until 60%. After that I will decrease it down to 10 PPM if SpO2 is acceptable a few hours later down to 5 PPM. From 5PPM I will decrease by 1 PPM until NO is off then come back to wean FiO2. That is how I do it. To treat cor pulmonale in brochopulmonary dysplasia is different which is coordinate by our cardiologist.  
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In a resource poor setting, especially in our eastern part of India, thoracoscopes are not available in every centre so all we have to depend on is blind pleural biopsy or VATS under surgical guidance. So can we use a fibre-optic bronchoscope for medical thoracoscopy?
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NOW We  are having the conventional (rigid or semrigid) thoracoscopy in my department , I am doing the medical thoracoscopy in my ICU bedside  for critical patients , It works smoothly, good orientation and good biopsy but the wound is  bigger than before...
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Is Pseudomonas colonization a contraindication for BLVR with EBV if there is minimal secretions/sputum production?
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Dear Dr. Wrobel,
To my Experince, it is a Contraindication, I do not recommend because of the increased risk of Pneumonia. And it can be not tolerated for Gold-D COPD /Empysema patients.
Sputum Culture should be studied in all patients before the BLVR procedure.
Regards
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I want to start some in vitro exp. with bronchial tissue cell line, but I dont have som experience with this topic. Before I worked with fibroblast cell line, so I have some work skill with the culture and all work around. Please help me, the best with protocol. Thanks.
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Not my area of expertise. Sorry
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Which spirometer is good for research?
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I suggest MicroQuark, COSMED, Italy.
It is cheap,complies with ATS/ERS criteria and easy operate.
This spirometer needs to be attached to a PC or Laptop. There is another version with printer, it is a little bit more expensive. Please check at COSMED site.
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I plan to search prevalence of histoplasmosis in Yaoundé (Cameroon) where 12, 50% of cases have been detected in AIDS patients in recent study.
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histoplasmin is uavailable in Cameroon, so I need somebody to help me to buy it. Thanks
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We encountered a case of acute diffuse intravascular coagulation in a young women with progressive Stage IV NSCLC. There were no signs of infection of other complicating factors. Is it possible that the progessive tumour was the cause? We are aware of such situations in hematologic malignancies but unaware of it in solid tumours.
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Dear colleague,
We are all familiar with frequent and different stage of severity of lung cancer complications and some times, dismal ones. The more efficacious and more targeted treatment options we have the more frequent complications we are going to deal with. As part of the paraneoplastic syndrome in NSLC, the occurrence of the DIC is not excluded, and the clinicians must be aware of this really dismal complication of the different cell types of lung cancer. I recommend a very interesting paper regarding the incidence and the management of such cases. I hope it will be useful.
"Disseminated intravascular coagulation (DIC) and non-small cell lung cancer (NSCLC): report of a case and review of the literature.E Voulgaris, G Pentheroudakis, A Vassou, N Pavlidis Lung cancer.01/2009; 64(2):247-9. DOI:10.1016/j.lungcan.2008.10.027"
Warmest regards
Dr. Sotiriou Ioannis
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Is the term ALI is really obsolete after emergence of the new Berlin definition of ARDS ? Whats is the actual purpose of such a definition?
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I've recently read a great Editorial in British Journal of Anaesthesia. See Frohlich S et al (2013), BJA 111(5), 696-9. ARDS: progress unlikely with non-biological definition.
It certainly got me thinking!
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For measurement of Spray pattern and plume geometry of OINDP different Instruments like Sprayview, ADSA, Oxford laser are available. But if we compare the data or results every instrument having the different results for Same bottle or canister. Unlikely in content determination of same bottle or canister in HPLC of different make. Some automated actuators also have the same problem. Can any one help in this regard, how to solve the data variability issue if I am using two different make instrument. One for development purpose and another for in vitro studies. My development data and in vitro datas are different.
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Dear Biswajit, i agree with you, when we are doing same analysis with diffrent make of instrument (whether its HPLC or sprayview) it tends to differ from other make because of principle and applicability difference in make to make. Best way to eliminate the variation and establish authentisity is to keep one control or reference standard. When we are analysing same sample in diffrent make of HPLC we need to keep one standard along with sample as a reference and control. Similarly we can analyse a reference sample or calibration standard in sprayview also. I hope it may give you authentic results.
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Guidance, protocol for method development and validation of spray pattern, plume geometry and droplet size distribution of nasal spray, metered dose inhaler.
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I agree with Mr. Hossain. Also you can get it from some university where such kind of acedemic work is going on. Pls go through one of the article which shows Nasal formulation equivelency in diffrent kind of human nose pettern
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A 15 year old girl presented with exertional SOB for last 1 month which exacerbated for last 2 days. At OPD she was grade 4 Dyspneic with resting desaturation with cyanosis and following cxr. the patient had repeated sputum for AFB which were found to be negative. ELISA for HIV 1&2 was negative. the patient had dramatic response in improvement of SOB with pulsed methylprednisolone but deteriorated again after discontinuation. ABG was suggestive of PaO2/FiO2 less than 200 with increased D(A-a)O2. Patient partly denied mechanical ventilatory support.. as long as pt was on IV methylpred she remained stable but deteriorated just within 24 hr of its discontinuation. TLC normal, CRP raised, serum ANA negative, serum RA factor slightly raised. What may be the possibilities?
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When he was RMO in CNMC way back in 1997-98, I was his house staff. Convey my regards to him.
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Fixed airflow obstruction is a clinical subtype or phenotype of Difficult-to-treat Asthma. Is there any specific spirometry criteria on which we can tell of having fixed air-flow limitation in Asthma?
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Reversible airflow obstruction in Bronchial Asthma is defined as increase in FEV1 by > 200 ml & FEV1 > 12% post bronchodilator challenge . COPD is defined as post bronchodilator FEV1 / FVC < 0.7 which confirms that airflow obstruction is not fully reversible . If there is no post bronchodilator reversibility in bronchial asthma , it should be considered as fixed air flow obstruction . The main problem is that if spirometric findings of Bronchial Asthma is suggestive of COPD in elderly patients , it is difficult to diagnose the Asthma component ,unless the history of childhood wheeze , allergy , dry cough & non smoking is available
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Why oxygen therapy is not much of use in treating hypoxemia in OSA?
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This is because the problem in OSA is an obstruction in the upper ariway. If the upper airway is blocked, no gas can get to the lungs. If no gas can get through the upper airway, it doesn't matter how much oxygen is in that gas, the person will desaturate as they are effectively not breathing.
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Leukotriene inhibitors should only be used after acute attack has settled down.
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Normlly, I certainly do not use non-documenteddrugs. However in htis case it would be logic tl give Singulair despite the manufacturer has no documentation. It is an inhibitor. Most guidelines recommend epinephrine and some in addition steroids and antihistamines for treatment of anaphyaxis - despite there are no double blind trials. The pharmacology and biological actrivity of montelucast tells me it must be benificial for patients with severe asthma even though not documented. Waiting for documentation by Merk would not help patients. Non-Commercially supported trials will never come, since the impact is proably limited, but not risky.
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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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There are multiple minuses of classifying asthma on the basis of severity like the response to treatment, being on treatment and the like. Many bodies are now deviating from severity to control but severity is still used by many physicians as a 'habit' or as common parlance. Is it right?
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The consensus emerging from the discussion seems that we must assess severity when patients are first seen and subsequently assess only control. GINA has clearly done away with the severity. A study comparing management on the basis of severity and control could very much be on...to settle the issue conclusively.
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My brother has been admitted with massive left sided primary spontaneous pneumothorax which was properly managed by us with chest tube drainage with full expansion of underlying lung. We went for chemical pleurodesis in the form of povidone iodine but what I found is that there was 450 ml collection in the chest drain bag in the next 24 hours and which became nearly 15 ml in the next 24 hours. My question is how can we explain this 450 ml collection after pleurodesis indicated for primary spontaneous pneumothorax?
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In addition to pleural inflammation, chest drain is a foreign body that stimulates the production of pleural fluid
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Seeking information on Fat Embolism Syndrome
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Correction. It should be Pulmonary Thromboembolism rather than just Pulmonary Embolism.
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I have come across difficulties in dealing a case of an infant. Would you kindly give your valuable opinion?
A 7 month old infant presented to me with high grade fever with chill rigor for 1.5 months. Before presenting to us he has been seen and evaluated by many pediatricians. He had cough. He had received all the vaccines up to his age. Total count was elevated with neutrophilic predominance. His Chest X-ray revealed a large cavity in the left upper zone with a few infiltrations in the right lung. Sputum culture failed to reveal any organism. Sputum for AFB smear was negative so also the BACTEC culture. HRCT scan revealed a large cavity in the left upper zone. The infant had received many intravenous antibiotics including complete staph coverage with no clinical improvement. In this situation how will you approach to the case? Is TB yet a possibility though cavity is very rare in TB infancy? Will a course of ATD be helpful for the infant? What should be the next diagnostic work-up?
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it was a cavity not pneumatocele or something else. We did gastric lavage with pediatric ryle's tube and immediately send it for AFB smear and BACTEC culture. One thing you can't ignore a diagnosis of tuberculosis where though cavitary pulmonary tuberculosis is extremely rare in childhood. Being pulmonologist we were eager to exclude tb. Fluortesecent microscopic exmination of smear prepared from gastric aspirate showed AFB positive as scanty 11 as per new grading of sputum positivity under fluoresect microscope in RNTCP. We started ATD for this patient immediately and subsequently the BACTEC culture report showed growth of M. tb and follow up chest x-ray after 4 months of ATD showed almost complete radiological resolution as well as symptomatic improvement.
infant cavitary tb is an extremely rare entity though few support we got from the existing literature and in fact it is not so uncommon what we think. There are case series, articles on this in the literature. But in most of those cases they failed to demonstrate tubercle bacilli rather they diagnosed it on the basis of contact tracing, respones to treatment by ATD. But we demonstrated tubercle bacilli and one should know morning gastric aspirate is an usefull tool for pediatric age group who cannot expectorate properly.
Thank you.
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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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What is the role of diuretics in the management of ARDS?
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I agree with Fred's answer.Several studies in human have showed that using diuretics therapy and fluid restriction are beneficial in ARDS and Ali patients by reduction of the amount of EVLW. This approach is beneficial in clinical measures like lung compliance, gas exchange and length of time on the ventilator. However, the diuretic don’t reduce inflammation.
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A 13 year old boy in our institution presented with sudden onset dyspnea with cough. CXR revealed rt sided massive pneumothorax for which we put chest drain. The boy was improving then from 5 th day onwards the boy again had sudden onset SOB and repeat CXR revealed left sided pneumothorax. This time we put left sided chest drain and on follow up chest x-ray the air in the pleural space persists on both sides even after 7 days. We did a HRCT thorax which revealed bilateral multiple cystic lesions of varying size with some centrilobular nodules. On examination there was a newly appeared cervical lymph node on the right side excision biopsy report of which is pending?
In this scenario what are the possibilities of etiologies and what are the options left at our hand to reach an etiological diagnosis in our resource poor centre in east India?
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@ Arnab Maji: try European Journal of Internal Medicine (EJIM). The problem with case report is that it lets down the impact factor of any medical journal. And precisely that is the reason why most high impact journals do not accept case reports nowadays. Keep in touch with me through my e-mail getsamrat@yahoo.com as I will be in Kolkata from 20th July for a fortnight & am happy to sit down with you to discuss where this could go.....take care!
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should vitamins b given with ATT ???
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Pyridoxin has to be given with INH for peripheral neuropathy prophylaxis in all patients.
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Biomarkers are able to predict mortality in COPD patients. What are those biomarkers?
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May I recommend you the lecture of this paper: The role of systemic inflammatory biomarkers to predict mortality in chronic obstructive pulmonary disease
Emer Kelly, Caroline A Owen, Victor Pinto-Plata, and Bartolome R Celli
Expert Review of Respiratory Medicine, February 2013, Vol. 7, No. 1 , Pages 57-64
(doi: 10.1586/ers.12.82)
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Is there any proven efficacy of NIV in COPD with cor-pulmonale?
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To the best of my knowledge, there is no study showing long term effects of chronic NIV use in COPD patients. However, there is one study (open access) for the whole group of patients with chronic respiratory failure:
Thorax. 2001 Jul;56(7):524-8.
Long term effects of non-invasive mechanical ventilation on pulmonary haemodynamics in patients with chronic respiratory failure.
Schönhofer B, Barchfeld T, Wenzel M, Köhler D.
Schönhofer et al. could show that one year of NIV use in patients with restrictive thoracic disorders improved PA pressure and PVR. However, in COPD no changes were observed regarding pulmonary hemodynamics. It has to be mentioned that in this study the restrictive group had a higher PA pressure (32 mm Hg) than the COPD group (25 mm Hg) which may explain the lack in change.
The absence of prove does not mean the absence of an effect.
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How can we differentiate acute SLE pneumonitis from infectious pneumonia in a SLE patient if lavage fluid is negative for microbiology before starting methylprednisolone therapy?
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don't forget CRP, which in LES flair does not increase much; if it's infection, it will increase. But I think that BAL safely helps you to rule out infection (y compris tuberculosis).
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Sirtuitins (SIRT3) can cause differentiation in cells to perform different functions. Could they be used to induce stem cells to develop into different cells, for example retinal cells or keratinocytes?
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Dr Iqbal , you have to use 2 different approaches. 1) Over express SIRT3 and 2) silence SIRT3 by siRNA (transient knockdown) or shRNA(stable knockdown). In both the scenarios try inducing 4 different developmental programs 1) muscle program, 2) lipogenesis, 3) chondrogenesis and 4) Osteogenesis by the use of specific inducers. You can find these inducers published on pubmed. I think this will give you a convincing answer.
Choice of your cell line should be MSCs (mesenchymal stem cells) such as embryonic fibroblasts, they could be from any embryonic tissue.
I am proposing this approach witht the thought that it will give you a strong understanding of stemness that you can play with for experience sake.
Best,
RJ
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I breath in 20C air and the temp of my expiration is 37C (17C difference). Does it also mean if I breath in 10C air, the my expiration will be 27C?
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I think it is not so because the humidified expired air passes through the dead space and the temperature is also mixed with relatively cool air than the core temperature.
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what may be the causes of dyspnea in chronic arsenicosis? Can isolated pulmonary arterial hypertension be associated with and caused by chronic arsenicosis?
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we have had a patient of chronic arsenicosis. she had an unexplained dyspnea and found to have PAH on echocardiographic assessment with mean PASP is 65mmhg. We have excluded the lung, heart, thromboembolic and connective tissue diseases in the causation of PAH. Can it be due to chronic arsenic exposure itself? Any opinion will be of great help to me.
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Etoposide capsules in one study were administered for 5 days to a total dose of 800 mg/m2. A response rate of 70% and a median survival of 9.5 months was seen, result comparable with the efficacy of more toxic and complicated chemotherapy regimens. So can we rethink to give oral etoposide as a monotherapy in small cell lung cancer patients with poor performance status?
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I am totally agreed with you Dr Seyyed Mortaza Haggoo...but here i am givin stress on monotherapy with oral etoposide not all the platinum compounds...what is your idea about it and what is the indication ?
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Does anyone know about an open-source software that allows to measure lung volumes based on lung density?
Thank you for your help!
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Osirix (http://www.osirix-viewer.com) is able to do the job. Lung segmentation is straight forward with Osirix.
Drawback: It runs only under OsX.
General ROI Segmentation with Osirix:
Have a look at these plugins to make this task easier: