Comparison of postnatal lung growth and development between C3H/HeJ and C57BL/6J mice

2006 ◽  
Vol 100 (5) ◽  
pp. 1577-1583 ◽  
Author(s):  
Shawn E. Soutiere ◽  
Wayne Mitzner

Previous work by our group has demonstrated substantial differences in lung volume and morphometric parameters between inbred mice. Specifically, adult C3H/HeJ (C3) have a 50% larger lung volume and 30% greater mean linear intercept than C57BL/6J (B6) mice. Although much of lung development occurs postnatally in rodents, it is uncertain at what age the differences between these strains become manifest. In this study, we performed quasi-static pressure-volume curves and morphometric analysis on neonatal mice. Lungs from anesthetized mice were degassed in vivo using absorption of 100% O2. Pressure-volume curves were then recorded in situ. The lungs were then fixed by instillation of Zenker’s solution at a constant transpulmonary pressure. The left lung from each animal was used for morphometric determination of mean air space chord length ( Lma). We found that the lung volume of C3 mice was substantially greater than that of B6 mice at all ages. In contrast, there was no difference in Lma (62.7 μm in C3 and 58.5 μm in B6) of 3-day-old mice. With increasing age (8 days), there was a progressive decrease in the Lma of both strains, with the magnitude of the decrease in B6 Lma mice exceeding that of C3. C3 lung volume remained 50% larger. The combination of parenchymal architectural similarity with lung air volume differences and different rates of alveolar septation support the hypothesis that lung volume and alveolar dimensions are independently regulated.

RSC Advances ◽  
2016 ◽  
Vol 6 (110) ◽  
pp. 108635-108644 ◽  
Author(s):  
Xian-En Zhao ◽  
Yongrui He ◽  
Ping Yan ◽  
Na Wei ◽  
Renjun Wang ◽  
...  

In situ UA-DDLLME coupled with UHPLC-MS/MS has been developed for simultaneous determination of neurotransmitters and baicalein from Parkinson's disease rats.


1976 ◽  
Vol 41 (4) ◽  
pp. 581-589 ◽  
Author(s):  
H. L. Hahn ◽  
P. D. Graf ◽  
J. A. Nadel

In 18 open-chest dogs we obtained pressure-diameter (P-D) curves from tantalum bronchograms and pressure-volume (P-V) curves by plethysmography. After vagotomy most of the decrease in diameter with decreasing transpulmonary pressure (Ptp) occured below 10 cmH2O and there was no P-D hysteresis. Smaller airways narrowed more with decreasing Ptp than larger ones. Bronchodilators did not increase diameters after vagotomy (P less than 0.2). With vagi intact, diameters were smaller at all Ptp (P less than 0.01) and exhibited hysteresis, but the lung P-V curve was unchanged. Vagal stimulation narrowed airways further at all Ptp and hysteresis was marked. Smaller airways narrowed more with vagal stimulation than larger ones. Vagal stimulation did not change the deflation limb of the P-V curve but decreased inflation volumes slightly at all Ptp (P less than 0.01). We conclude that in vivo toneis vagal and that it affects the physical properties of airways, but not oflungs, making the airways remarkably independent from lung parenchyma.


Parasitology ◽  
2000 ◽  
Vol 120 (6) ◽  
pp. 547-551 ◽  
Author(s):  
O. BILLKER ◽  
A. J. MILLER ◽  
R. E. SINDEN

Malarial gametocytes circulate in the peripheral blood of the vertebrate host as developmentally arrested intra-erythrocytic cells, which only resume development into gametes when ingested into the bloodmeal of the female mosquito vector. The ensuing development encompasses sexual reproduction and mediates parasite transmission to the insect. In vitro the induction of gametogenesis requires a drop in temperature and either a pH increase from physiological blood pH (ca pH 7·4) to about pH 8·0, or the presence of a gametocyte-activating factor recently identified as xanthurenic acid (XA). However, it is unclear whether either the pH increase or XA act as natural triggers in the mosquito bloodmeal. We here use pH-sensitive microelectrodes to determine bloodmeal pH in intact mosquitoes. Measurements taken in the first 30 min after ingestion, when malarial gametogenesis is induced in vivo, revealed small pH increases from 7·40 (mouse blood) to 7·52 in Aedes aegypti and to 7·58 in Anophěles stephensi. However, bloodmeal pH was clearly suboptimal if compared to values required to induce gametogenesis in vitro. Xanthurenic acid is shown to extend the pH-range of exflagellation in vitro in a dose-dependent manner to values that we have observed in the bloodmeal, suggesting that in vivo malarial gametogenesis could be further regulated by both these factors.


1972 ◽  
Vol 6 (3) ◽  
pp. 279-286 ◽  
Author(s):  
M. L. Constantin
Keyword(s):  

Inbred mice of strains CBA/T6T6, A, C57BL/10Sn and B10.LP were found to be infested in ascending order of severity by Myocoptes musculinus or Myobia musculi mites. All of the 4 insecticidal preparations applied to 5-month-old mice killed the adult stages of Myocoptes musculinus within 2-6 hours, but only 1 was active against Myobia musculi. This latter was 100% active in vitro at 0.5%, but 1% was required in vivo. At 3% it killed 2 of 20 mice, but at 1% it did not interfere with insemination and reproduction, neither did it damage newborn young.


PLoS ONE ◽  
2021 ◽  
Vol 16 (7) ◽  
pp. e0246270
Author(s):  
Pratyusha Mandal ◽  
John D. Lyons ◽  
Eileen M. Burd ◽  
Michael Koval ◽  
Edward S. Mocarski ◽  
...  

During infectious disease, pathogen load drives inflammation and immune response that together contribute to tissue injury often resulting in organ dysfunction. Pulmonary failure in SARS-CoV2-infected hospitalized COVID-19 patients is one such prominent example. Intervention strategies require characterization of the host-pathogen interaction by accurately assessing all of the above-mentioned disease parameters. To study infection in intact mammals, mice are often used as essential genetic models. Due to humane concerns, there is a constant unmet demand to develop studies that reduce the number of mice utilized while generating objective data. Here, we describe an integrated method of evaluating lung inflammation in mice infected with Pseudomonas aeruginosa or murine gammaherpesvirus (MHV)-68. This method conserves animal resources while permitting evaluation of disease mechanisms in both infection settings. Lungs from a single euthanized mouse were used for two purposes-biological assays to determine inflammation and infection load, as well as histology to evaluate tissue architecture. For this concurrent assessment of multiple parameters from a single euthanized mouse, we limit in-situ formalin fixation to the right lung of the cadaver. The unfixed left lung is collected immediately and divided into several segments for biological assays including determination of pathogen titer, assessment of infection-driven cytokine levels and appearance of cell death markers. In situ fixed right lung was then processed for histological determination of tissue injury and confirmation of infection-driven cell death patterns. This method reduces overall animal use and minimizes inter-animal variability that results from sacrificing different animals for different types of assays. The technique can be applied to any lung disease study in mice or other mammals.


2019 ◽  
Author(s):  
Dimos Goundaroulis ◽  
Erez Lieberman Aiden ◽  
Andrzej Stasiak

Knots in the human genome would greatly impact diverse cellular processes ranging from transcription to gene regulation. To date, it has not been possible to directly examine the genome in vivo for the presence of knots. Recently, methods for serial fluorescent in situ hybridization have made it possible to measure the 3d position of dozens of consecutive genomic loci, in vivo. However, the determination of whether genomic trajectories are knotted remains challenging, because small errors in the localization of a single locus can transform an unknotted trajectory into a highly-knotted trajectory, and vice versa. Here, we use stochastic closure analysis to determine whether a genomic trajectory is knotted in the setting of experimental noise. We analyse 4727 deposited genomic trajectories of a 2Mb long chromatin interval from chromosome 21. For 243 of these trajectories, their knottedness could be reliably determined despite the possibility of localization errors. Strikingly, in each of these 243 cases, the trajectory was unknotted. We note a potential source of bias, insofar as knotted contours may be more difficult to reliably resolve. Nevertheless, our data is consistent with a model where, at the scales probed, the human genome is often free of knots.


1990 ◽  
Vol 69 (5) ◽  
pp. 1702-1708 ◽  
Author(s):  
S. S. Margulies ◽  
G. A. Farkas ◽  
J. R. Rodarte

The performance of the diaphragm is influenced by its in situ length relative to its optimal force-generating length (Lo). Lead markers were sutured to the abdominal surface of the diaphragm along bundles of the left ventral, middle, and dorsal regions of the costal diaphragm and the left crural diaphragm of six beagle dogs. After 2-3 wk postoperative recovery, the dogs were anesthetized, paralyzed, and scanned prone and supine in the Dynamic Spatial Reconstructor (DSR) at a total lung capacity (TLC), functional residual capacity (FRC), and residual volume (RV). The location of each marker was digitized from the reconstructed DSR images, and in situ lengths were determined. After an overdose of anesthetic had been administered to the dogs, each marked diaphragm bundle was removed, mounted in a 37 degrees C in vitro chamber, and adjusted to Lo (maximum tetanic force). The operating length of the diaphragm, or in situ length expressed as percent Lo, varied from region to region at the lung volumes studied; variability was least at RV and increased with increasing lung volume. At FRC, all regions of the diaphragm was shorter in the prone posture compared with the supine, but there was no clear gravity-dependent vertical gradient of in situ length in either posture. Because in vitro length-tension characteristics were similar for all diaphragm regions, regional in vivo length differences indicate that the diaphragm's potential to generate maximal force is nonuniform.


1985 ◽  
Vol 59 (1) ◽  
pp. 205-210 ◽  
Author(s):  
T. A. Standaert ◽  
W. A. LaFramboise ◽  
R. E. Tuck ◽  
D. E. Woodrum

This report describes the design of an apparatus and the procedures used to serially measure the total lung capacity and the functional residual capacity of small animals utilizing the N2-washout technique. The calibration data indicate that the technique is accurate to within 1 ml and has a variance of less than 5%. The in vivo lung volume measurements of rats were validated by comparing them with values obtained with a water-displacement technique; the means were within 0.3 ml. Examples of the precision and changes in lung volume of animals during studies are included to demonstrate the reliability and usefulness of the technique.


1996 ◽  
Vol 80 (3) ◽  
pp. 742-746 ◽  
Author(s):  
S. Suzuki ◽  
T. Akahori ◽  
N. Miyazawa ◽  
M. Numata ◽  
T. Okubo ◽  
...  

It is unknown how the in vivo alveolar surface area-to-volume ratio (S/V) changes in low-pressure pulmonary edema. Here, the S/V is the area of the air-tissue interface per unit total volume (air plus tissue). We hypothesized that in oleic acid (OA)-induced edema inactivation of the pulmonary surfactant may increase surface tension and decrease the S/V at any given lung volume. OA (0.04 mg/kg) was intravenously injected into dogs. We measured the in vivo S/V (equivalent to the inverse of optical mean free path by light-scattering stereology and the pressure-volume (PV) curve 60-90 min after OA administration. OA administration decreased the lung volume at each transpulmonary pressure and increased the wet-to-dry weight ratio. The S/V decreased after OA administration (optical mean free path increased). The air-filled PV curves shifted downward after OA, but the saline-filled PV curves after OA administration did not differ significantly from control saline-filled curves. The difference in transpulmonary pressure between air- and saline-filled PV curves (an index of the magnitude of surface tension) was increased in OA-induced pulmonary edema. This study suggests that in OA-induced pulmonary edema the alveolar surface tension increases and the S/V decreases, presumably due to inactivation of surfactant by serum leakage to alveoli.


2004 ◽  
Vol 96 (5) ◽  
pp. 1658-1664 ◽  
Author(s):  
Shawn E. Soutiere ◽  
Wayne Mitzner

Maximal lung volume or total lung capacity in experimental animals is dependent on the pressure to which the lungs are inflated. Although 25-30 cmH2O are nominally used for such inflations, mouse pressure-volume (P-V) curves show little flattening on inflation to those pressures. In the present study, we examined P-V relations and mean alveolar chord length in three strains (C3H/HeJ, A/J, and C57BL/6J) at multiple inflation pressures. Mice were anesthetized, and their lungs were degassed in vivo by absorption of 100% O2. P-V curves were then recorded in situ with increasing peak inflation pressure in 10-cmH2O increments up to 90 cmH2O. Lungs were quickly frozen at specific pressures for morphometric analysis. The inflation limbs never showed the appearance of a plateau, with lung volume increasing 40-60% as inflation pressure was increased from 30 to 60 cmH2O. In contrast, parallel flat deflation limbs were always observed, regardless of the inflation pressure, indicating that the presence of a flat deflation curve cannot be used to justify measurement of total lung capacity in mice. Alveolar size increased monotonically with increasing pressure in all strains, and there was no evidence of irreversible lung damage from these inflations to high pressures. These results suggest that the mouse lung never reaches a maximal volume, even up to nonphysiological pressures >80 cmH2O.


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