Thursday, October 4, 2018

SCIREQ Blog has moved!


Thank you for following the SCIREQ Blog. 


We moved our Blog to a new portal and invite you to continue reading our posts and stay informed about:

         »        Events & User Group Meetings
         »        Products Developments
         »        Recent Publications
         »        and news from the pulmonary community.



Follow this link to visit SCIREQ Blog!

Happy Reading!

Your SCIREQ Team 

Monday, July 23, 2018

FASEB’s Lung Epithelium in Health and Diseases conference



SCIREQ is proud to sponsor FASEB’s Lung Epithelium in Health and Diseases conference which will take place from July 29th to August 3rd, 2018 in St. Bonaventure, NY. The scientific research conference will bring together leading scientists and junior researchers to discuss the latest findings in the field of lung epithelium biology. 

The conference program touches on various respiratory ailments, disease models and novel research techniques, including:

  • Mucociliary transport in cystic fibrosis (Michael Welsh, University of Iowa)
  • Lung development and regeneration (Jeffrey Whitsett, Cincinnati Children’s; Bernard Thébaud, University of Ottawa)
  • Neuroendocrine Hyperplasia of Infancy (Lisa Young, Vanderbilt University)
  • Disease modelling with organoid culture systems and cryopreserved human lung slices  (Xingbin Ai, Brigham & Women’s Hospital; Barry Stripp, Cedars-Sinai)
  • Genetics and Genomics of Lung Diseases (Steve Rowe , U.of Alabama; David Schwartz, U.of Colorado)
  • And many other topics

Links:
Program: https://secure.faseb.org/src-programs/11508.pdf  
Conference website: http://faseb.org/src/micro/Site/Lung/Home.aspx 

We look forward to talks, poster sessions and new collaboration opportunities that will emerge from the FASEB event.

Thursday, July 5, 2018

Bronchopulmonary Dysplasia (BPD) after 50 years – BPD Symposium at Stanford

A momentous symposium was held at Stanford university last year to commemorate the 50th anniversary since the original description of Bronchopulmonary Dysplasia (BPD) was first articulated1 by Dr. William Northway and him team in 1967. 

This symposium, which was attended by several leaders in the field, was held as a platform where researchers could come together and highlight the progress that has been made to date, along with discuss future perspectives. 

The event was divided into 5 sessions with keynote presentations provided by speakers who have made noteworthy contributions in the field of BPD. We are proud to say that amongst such speakers were Dr. Bernard Thébaud, Dr. Rory Morty and Dr. Rob Tepper, who gave very informed and thought provoking lectures during the symposium, are active users of our SCIREQ systems!

We would like to extend our Thank You to all investigators who constantly strive towards making new strides in this field of preclinical pediatric research.

Learn more about how SCIREQ’s solutions can be implemented into your research needs or how our instruments are being utilized to study Bronchopulmonary Dysplasia



1Northway et. al. Pulmonary Disease Following Respirator Therapy of Hyaline-Membrane Disease — Bronchopulmonary Dysplasia, N Engl J Med 1967; 276:357-368


Friday, June 22, 2018

IDEAL OR ACTUAL BODY WEIGHT OF THE OBESE SUBJECT?

When working with obese mice, what weight should be used when performing flexiVent measurements?



This question is quite an important one for two reasons. First, there is a substantial difference in weight between the obese subjects vs. the lean control group. For instance, obese mice can weigh 50g or more, while their age-matched control group can typically weigh 30g. While there is this significant difference in the weight between both groups, there may not be a large difference in the actual size of the subjects’ lungs.

Second, when working with the flexiVent system, the body weight of the subject is used to scale the amplitude of volume-controlled ventilation patterns and perturbations, such as the Snapshot-150 or the Quick Prime-3. In obese animals, the increase in body weight is not proportional to the subject’s lung size, so sending in a larger volume can have adverse effects on the subject’s lungs.



A recent study performed by Dr. Guivarchis et al.1, highlights the harmful effects of ventilating obese subjects with a tidal volume based on actual weight vs ideal weight using the flexiVent system. In this study, the effects of two hours of mechanical ventilation in a diet-induced obese mice model, with tidal volume calculated on either the actual body weight or the ideal body weight (based on the mean weight of control mice) were demonstrated. Their findings indicate that in comparison to lean control subjects, mechanically ventilating obese subjects with a tidal volume based on actual body weight is harmful.

They observed a noticeable variation in lung mechanics and associated lung inflammation in obese mice ventilated with a tidal volume based on actual body weight. In contrast, obese mice ventilated with a tidal volume calculated using the ideal body weight had lung mechanics and inflammation parameters close to the lean control group.

Therefore, when studies involve the assessment of obese mice, SCIREQ recommends entering the average weight of the lean control group rather than using the actual weight of the obese subjects.


1Guivarch et al. Pulmonary Effects of Adjusting Tidal Volume to Actual or Ideal Body Weight in Ventilated Obese Mice. Sci Rep. 2018 Apr 24;8(1):6439. doi: 10.1038/s41598-018-24615-5.

Monday, June 11, 2018

To open or close the lungs – that is the question!

Although often necessary, mechanical ventilation of small animals during pulmonary measurements can lead to both acute and chronic damage to their lungs, also known as ventilator-induced lung injury (VILI). The injury happens as a result of the frequent opening and closing of alveolar air sacs. Nevertheless, the two most common, and greatly contrasting methods, to study respiratory diseases include open lung- and closed lung-approaches. This has led to many pulmonary researchers conducting experiments with the goal of determining which approach is the least harmful and the best possible way to minimize VILI.

TO OPEN THE LUNGS?

Open-chest models are often used to study ARDS and acute myocardial ischemia and reperfusion. These models allow for investigating cardiac physiology, morphological changes of the lungs, as well as the evaluation of therapeutic interventions. This procedure allows for invasive lung function measurements and tissue harvesting for further experimentation, but must be performed under deep anesthesia. Since opening the chest causes the lungs to collapse, the animals must be mechanically ventilated throughout the process.

The flexiVent has often been used in open-chest experiments, as the system allows for ventilation of the subject with a user-defined positive end-expiratory pressure (PEEP), which can be set to prevent airway collapse. Further, it can facilitate the complete recruitment of the lungs, using the Deep Inflation perturbation, before measurements can be taken.


TO CLOSE THE LUNGS?

Recent experimental evidence suggests that high PEEP does not necessarily reduce lung injury but instead, may lead to the contrary. Higher PEEP results in overstretching the alveolar sacs and potential development of edema, among other cardiopulmonary impairment. Moreover, a recent article by Dr. Patricia Rocco and team1, points out that most publications comparing high PEEP with no PEEP, do so with a combination of low tidal volume and high tidal volume, respectively. Thus, there is no clear indication as to what exactly led to the observed outcomes – high PEEP or low tidal volume.

Dr. Rocco goes on to recommend “in order to minimize VILI, we should consider moving away from the classical concept of ‘open up the lungs and keep them open’ towards ‘close down the lungs and keep them closed’”. Fortunately, the flexiVent can be adapted to different experimental conditions, and can provide detailed pulmonary measurements even as research trends change.


1Pelosi, P. et al. 2018. Close down the lungs and keep them resting to minimize ventilator-induced lung injury. Critical Care 22 (1):72.

Monday, May 14, 2018

Must see posters at ATS!

ATS is just around the corner and we hope to see you in San Diego!

We are looking forward to learning more about respiratory research, especially these interesting flexiVent poster sessions:

During our annual breakfast event at ATS on Monday, May 21st, Dr. Otmar Schmid (Helmholtz Zentrum, Germany) will discuss his “off-label” use of the flexiVent for the delivery of inhaled compounds. By optimizing the ventilation profiles and nebulizer settings, Dr. Schmid and Dr. Annette Robichaud obtained significant improvements in aerosol deposition rates, as well as homogenous deposition profiles.

The technique developed by Dr.Schmid could be useful in studies for optimized inhaled drug delivery using the flexiVent. If you are interested, please feel free to join us by registering here.

We would love to learn more about your research and discuss some tailored solutions. Find us at Booth #1535 in Exhibit Hall D.

Exhibit Hours

Sunday, May 20       10:30 am – 3:30 pm
Monday, May 21      10:30 am – 3:30 pm
Tuesday, May 22      10:30 am – 3:30 pm








Monday, April 16, 2018

Cardiopulmonary Solutions by emka & SCIREQ

emka & SCIREQ offer a unique perspective into the preclinical study of heart and lung diseases, allowing for novel insights into cardiopulmonary diseases such as heart failure, arrhythmia, COPD, pulmonary hypertension and more.

Will you be attending the Experimental Biology meeting in San Diego next week? If so, visit booth #1624 to learn more about our range of cardiopulmonary solutions, including:

Model Development with the inExpose:
  • In vivo disease models that mimic complex pathophysiological mechanisms of cardiopulmonary diseases using the inExpose, an automated platform for reproducible inhalation exposure (1,2)
  • Smoke-induced alterations in cardiac and respiratory function through cigarette or e-cigarette exposure (3,4)
  • Effective drug intervention for both preclinical subjects and cell culture exposures through aerosols (5,6).
 Respiratory Mechanics Measurements with the flexiVent:
  • Studying the underlying pathophysiology of cardiopulmonary diseases by measuring the structure and function of the lung, along with quantifying the effects of pulmonary hypertension and decreased vascularization with the flexiVent (7,8,9).
  • Pressure-volume manoeuvres, forced expired volume and other endpoints of clinical translational value performed by the flexiVent (10,11).

High-throughput Screening Using Whole Body Plethysmography
  • Whole Body Plethysmography can be an easy tool for screening subjects quickly for preliminary respiratory data with the option of delivering inhaled therapeutics (12,13,14).
  • Easy integration with simultaneous cardio and neuro recordings: electroencephalogram (EEG), electrocardiogram (ECG) & electromyogram (EMG).

Wireless Biopotential Monitoring using Implantable Telemetry
  • Monitoring physiological data from conscious freely moving rodents and large animals using easyTEL implantable telemetry systems. Different models are available to meet your study needs and provide monitoring of ECG, EEG, blood pressure, breathing rate, temperature and acceleration from 3-axis accelerometer (activity).

Exhibit Hours - Booth 1624
Sunday, April 22nd 9:00am – 4pm
Monday, April 23rd 9:00am – 4pm
Tuesday, April 24th 9:00am – 4pm


Click here to set-up a meeting to learn more about our solutions for cardiopulmonary studies.

References

1) Weist, E.F., et al. (2017). Omega-3 Polyunsaturated Fatty Acids Protect Against Cigarette Smoke-Induced Oxidative Stress and vascular Dysfunction. Toxicological Sciences, 156(1): 300-310
2) Tewari et al. (2011). Identification of differentially expressed proteins in blood plasma of control and cigarette smoke-exposed mice by 2-D DIGE/MS. Proteomics, 11: 2051, 2011.
3) Olfert, M. et al. (2018). Chronic exposure to electronic cigarette results in impaired cardiovascular function in mice. J of Applied Physiology, 124(3): 573-582
4) Alasmari F, Crotty Alexander LE, Nelson JA, et al. (2017). Effects of Chronic Inhalation of Electronic Cigarettes Containing Nicotine on Glial Glutamate Transporters and α-7 Nicotinic Acetylcholine Receptor in Female CD-1 Mice. Vol 77. Elsevier Inc
5) Patolla et al. (2010). Formulation, characterization and pulmonary deposition of nebulized celecoxib encapsulated nanostructured lipid carriers. J Control Release. 144: 233-241
6) De Santis, et al. (2014). Pharmaceutical composition of oxidised avidin suitable for inhalation - De Santis. U.S. patent application 14/236,445
7) Alsaid, H., et al. (2011). Serial MRI characterization of the functional and morphological changes in mouse lung in response to cardiac remodeling following myocardial infarction. Magnetic Resonance in Medicine, 67(1): 191-200
8) Dayeh, N.R et al. (2017). Echocardiographic validation of pulmonary hypertension due to heart failure with reduced ejection fraction in mice. Scientific Reports, 1363
9) Karmouty-Quintana, H., et al. 2012. The A2B Adenosine Receptor Modulates Pulmonary Hypertension Associated With Interstitial Lung Disease. The FASEB Journal, 26(6): 2546-2557
10) Devos, F.C et al. (2017). Forced expiration measurements in mouse models of obstructive and restrictive lung diseases. Respiratory Research, 18(123)
11) Vanoirbeek, J. (2016). Forced Expiratory Volume (FEV) Measurements in Mouse Models of Lung Disease. American Journal of Respiratory and Critical Care Medicine, 193, A5957
12) Olea et al. (2011). Effects of cigarette smoke and chronic hypoxia on airways remodelling and resistance. Clinical Significance, 15; 179(2-3): 305-313
13) Ramnath et al. (2014). Extracellular matrix defects in aneurysmal fibulin-4 mice predispose to lung emphysema. PLOS One, 9(9): 106054
14) Zhuang, P., et al. (2016). cAMP-PKA-CaMKII signalling pathway is involved in aggravated cardiotoxicity during Fuzi and Beimu Combination Treatment of Experimental Pulmonary Hypertension. Scientific Reports, 6, 34903