Comparison of Two Different In Vivo Models and an In Vitro Model for Caloric Determination of Four Novel Fiber Ingredients

2013 ◽  
Vol 61 (50) ◽  
pp. 12374-12379 ◽  
Author(s):  
Sarah Cervantes-Pahm ◽  
Brenda K. Knapp ◽  
Beob G. Kim ◽  
Yanhong Liu ◽  
Carl M. Parsons ◽  
...  
Keyword(s):  
In Vitro Model ◽  
In Vivo Models ◽  
Vitro Model

In vivo determination of surface tension in the horse trachea and in vitro model studies

1997 ◽  
Vol 109 (1) ◽  
pp. 81-93 ◽  
Author(s):  
V Im Hof ◽  
P Gehr ◽  
V Gerber ◽  
M.M Lee ◽  
S Schürch
Keyword(s):  
Surface Tension ◽  
In Vitro Model ◽  
Model Studies ◽  
Vitro Model

scholarly journals Heat-Shock Proteins Gene Expression in Peripheral Blood Mononuclear Cells as an Indicator of Heat Stress in Beef Calves

Animals ◽  
2020 ◽  
Vol 10 (5) ◽  
pp. 895 ◽  
Author(s):  
Won-Seob Kim ◽  
Jalil Ghassemi Nejad ◽  
Sang-Gun Roh ◽  
Hong-Gu Lee
Keyword(s):  
Gene Expression ◽  
In Vitro Model ◽  
Hsp70 Gene ◽  
In Vivo Models ◽  
Blood Samples ◽  
Beef Calves ◽  
In Vivo Experiment ◽  
Vitro Model

This study was conducted to investigate the effect of HS on HSPs gene expression in bovine PBMCs of beef calves in in vitro and in vivo models. In the in vitro experiment, blood samples were collected from the jugular vein of five beef calves (age: 174.2 ± 5.20 days, BW: 145.2 ± 5.21 kg). In the in vivo experiment, sixteen Korean native male beef calves (age: 169.6 ± 4.60 days, BW: 136.9 ± 6.23 kg) were exposed to ambient temperature for seven days (22 to 24 °C, relative humidity 60%; temperature–humidity index (THI) = 68 to 70) and subsequently to the temperature and humidity corresponding to the target THI level for 21 days (HS). For PBMC isolation, blood samples were collected every three days. In the in vitro model, the cell viability was significantly decreased in HS groups compared with the control group (p = 0.015). The expression of HSP70 (p = 0.022), HSP90 (p = 0.003) and HSPB1 (p = 0.026) genes was increased in the HS group in in vitro model. In the in vivo experiment, the HSP70 gene expression was increased after sudden exposure to HS conditions (severe THI levels; THI = 88 to 90), whereas HSP90 and HSPB1 showed no differences among the THI groups (p > 0.05). However, in the severe THI group, the HSP70 gene expression returned to normal range after six days of continuous HS. In conclusion, the HSP70 gene plays a pivotal role in protecting cells from damage and is sensitive to HS in immune cells compared with other HSP genes in in vitro and in vivo models. In addition, the in vivo models suggest that calves exhibit active physiological mechanisms of adaptation to HS after six days of continuous exposure by regulating the HSP70 gene expression.

Nitric oxide donors attenuate increase in pressure drop across membrane oxygenators

Perfusion ◽  
1999 ◽  
Vol 14 (5) ◽  
pp. 331-336 ◽  
Author(s):  
F De Somer ◽  
L Foubert ◽  
E Schacht ◽  
G Van Nooten
Keyword(s):  
Nitric Oxide ◽  
Pressure Drop ◽  
In Vitro Model ◽  
Membrane Oxygenator ◽  
In Vivo Models ◽  
Initial Resistance ◽  
Membrane Oxygenators ◽  
Vitro Model

We have evaluated the effect of nitric oxide (NO) on the pressure drop across a membrane oxygenator in one in vitro model and two in vivo models (using four dogs and five pigs). In all the experiments sodium nitroprusside (SNP) was used as a NO source, whereas gaseous NO was only used in the in vitro model. The drugs were given when the pressure drop or resistance across the device increased to at least twice the baseline values. In the in vitro model, both SNP and gaseous NO decreased the pressure drop to 75% of its peak value after 10 min and to 67% after 20 min. In the dog model, resistance decreased from 390 to 153 mmHg/l/min after 5 min and to 85 mmHg/l/min after 20 min for a baseline value of 75 mmHg/l/min. The initial resistance across the membrane oxygenator in the pig model increased from 6.6 ± 1.3 to 74 ± 38 mmHg/l/min. An infusion of 10 μg/kg/min SNP reduced the resistance to 16 ± 5 mmHg/l/min.

scholarly journals Generation of human chambered cardiac organoids from pluripotent stem cells for improved modelling of cardiovascular diseases

2021 ◽  
Author(s):  
Beatrice Xuan Ho ◽  
Jeremy Pang ◽  
Qian Hua Phua ◽  
Lee Chuen Liew ◽  
Boon Min Poh ◽  
...  
Keyword(s):  
Cardiovascular Diseases ◽  
Pluripotent Stem Cells ◽  
In Vitro Model ◽  
Cell Type ◽  
In Vivo Models ◽  
Cell Type Composition ◽  
Type Composition ◽  
Vitro Model

Recent progress on murine and human cardiac organoids have provided understanding to the developmental processes of the heart. However, there is still an unfulfilled need for improved modelling of cardiovascular diseases using human cardiac organoids. Herein, we report successful generation of intrinsically formed human chambered cardiac organoids (CCO) and highlight its utility in modelling disease. Single cell transcriptomic profiling of CCOs showed appropriate cardiovascular cell type composition exhibiting improved maturation. Functionally, CCOs recapitulated clinical cardiac hypertrophy by exhibiting thickened chamber walls, reduced ejection fractions, increased myofibrillar disarray and tachycardia. Therefore, CCOs improve current capabilities of disease modelling as an in vitro model bridging the gap to in vivo models, with the ability to assess functional parameters that previously can only be achieved in animal systems.

scholarly journals Statins Reduce Lipopolysaccharide-Induced Cytokine and Inflammatory Mediator Release in an In Vitro Model of Microglial-Like Cells

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
A. J. McFarland ◽  
A. K. Davey ◽  
S. Anoopkumar-Dukie
Keyword(s):  
In Vitro Model ◽  
No Production ◽  
In Vivo Models ◽  
Cellular Models ◽  
Reductase Inhibitors ◽  
Inflammatory Conditions ◽  
Vitro Model ◽  
Coa Reductase

The anti-inflammatory effects of statins (HMG-CoA reductase inhibitors) within the cardiovascular system are well-established; however, their neuroinflammatory potential is unclear. It is currently unknown whether statins’ neurological effects are lipid-dependent or due to pleiotropic mechanisms. Therefore, the assumption that all statin compounds will have the same effect within the central nervous system is potentially inappropriate, with no studies to date having compared all statins in a single model. Thus, the aim of this study was to compare the effects of the six statins (atorvastatin, fluvastatin, pitavastatin, pravastatin, rosuvastatin, and simvastatin) within a single in vitro model of neuroinflammation. To achieve this, PMA-differentiated THP-1 cells were used as surrogate microglial cells, and LPS was used to induce inflammatory conditions. Here, we show that pretreatment with all statins was able to significantly reduce LPS-induced interleukin (IL)-1βand tumour necrosis factor (TNF)-αrelease, as well as decrease LPS-induced prostaglandin E2 (PGE2). Similarly, global reactive oxygen species (ROS) and nitric oxide (NO) production were decreased following pretreatment with all statins. Based on these findings, it is suggested that more complex cellular models should be considered to further compare individual statin compounds, including translation into in vivo models of acute and/or chronic neuroinflammation.

scholarly journals Generation of a Novel In Vitro Model to Study Endothelial Dysfunction from Atherothrombotic Specimens

2021 ◽  
Author(s):  
Susan Gallogly ◽  
Takeshi Fujisawa ◽  
John D. Hung ◽  
Mairi Brittan ◽  
Elizabeth M. Skinner ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Dysfunction ◽  
In Vitro Model ◽  
Umbilical Vein ◽  
Coronary Syndrome ◽  
Coronary Endothelial Cells ◽  
Vitro Model ◽  
Umbilical Vein Endothelial Cells

Abstract Purpose Endothelial dysfunction is central to the pathogenesis of acute coronary syndrome. The study of diseased endothelium is very challenging due to inherent difficulties in isolating endothelial cells from the coronary vascular bed. We sought to isolate and characterise coronary endothelial cells from patients undergoing thrombectomy for myocardial infarction to develop a patient-specific in vitro model of endothelial dysfunction. Methods In a prospective cohort study, 49 patients underwent percutaneous coronary intervention with thrombus aspiration. Specimens were cultured, and coronary endothelial outgrowth (CEO) cells were isolated. CEO cells, endothelial cells isolated from peripheral blood, explanted coronary arteries, and umbilical veins were phenotyped and assessed functionally in vitro and in vivo. Results CEO cells were obtained from 27/37 (73%) atherothrombotic specimens and gave rise to cells with cobblestone morphology expressing CD146 (94 ± 6%), CD31 (87 ± 14%), and von Willebrand factor (100 ± 1%). Proliferation of CEO cells was impaired compared to both coronary artery and umbilical vein endothelial cells (population doubling time, 2.5 ± 1.0 versus 1.6 ± 0.3 and 1.2 ± 0.3 days, respectively). Cell migration was also reduced compared to umbilical vein endothelial cells (29 ± 20% versus 85±19%). Importantly, unlike control endothelial cells, dysfunctional CEO cells did not incorporate into new vessels or promote angiogenesis in vivo. Conclusions CEO cells can be reliably isolated and cultured from thrombectomy specimens in patients with acute coronary syndrome. Compared to controls, patient-derived coronary endothelial cells had impaired capacity to proliferate, migrate, and contribute to angiogenesis. CEO cells could be used to identify novel therapeutic targets to enhance endothelial function and prevent acute coronary syndromes.

scholarly journals 3D Environment Is Required In Vitro to Demonstrate Altered Bone Metabolism Characteristic for Type 2 Diabetics

2021 ◽  
Vol 22 (6) ◽  
pp. 2925
Author(s):  
Victor Häussling ◽  
Romina H Aspera-Werz ◽  
Helen Rinderknecht ◽  
Fabian Springer ◽  
Christian Arnscheidt ◽  
...  
Keyword(s):  
Bone Metabolism ◽  
In Vitro Model ◽  
Bone Diseases ◽  
3D Environment ◽  
Type 2 Diabetics ◽  
Mineralized Matrix ◽  
Vitro Model

A large British study, with almost 3000 patients, identified diabetes as main risk factor for delayed and nonunion fracture healing, the treatment of which causes large costs for the health system. In the past years, much progress has been made to treat common complications in diabetics. However, there is still a lack of advanced strategies to treat diabetic bone diseases. To develop such therapeutic strategies, mechanisms leading to massive bone alterations in diabetics have to be well understood. We herein describe an in vitro model displaying bone metabolism frequently observed in diabetics. The model is based on osteoblastic SaOS-2 cells, which in direct coculture, stimulate THP-1 cells to form osteoclasts. While in conventional 2D cocultures formation of mineralized matrix is decreased under pre-/diabetic conditions, formation of mineralized matrix is increased in 3D cocultures. Furthermore, we demonstrate a matrix stability of the 3D carrier that is decreased under pre-/diabetic conditions, resembling the in vivo situation in type 2 diabetics. In summary, our results show that a 3D environment is required in this in vitro model to mimic alterations in bone metabolism characteristic for pre-/diabetes. The ability to measure both osteoblast and osteoclast function, and their effect on mineralization and stability of the 3D carrier offers the possibility to use this model also for other purposes, e.g., drug screenings.

scholarly journals Exposure of ichnovirus particles to digitonin leads to enhanced infectivity and induces fusion from without in an in vitro model system

2007 ◽  
Vol 88 (11) ◽  
pp. 2977-2984 ◽  
Author(s):  
Don Stoltz ◽  
Renée Lapointe ◽  
Andrea Makkay ◽  
Michel Cusson
Keyword(s):  
Outer Membrane ◽  
In Vitro Model ◽  
Model System ◽  
Host Cells ◽  
Fusion Event ◽  
Susceptible Host ◽  
In Vitro Model System ◽  
Vitro Model

Unlike most viruses, the mature ichnovirus particle possesses two unit membrane envelopes. Following loss of the outer membrane in vivo, nucleocapsids are believed to gain entry into the cytosol via a membrane fusion event involving the inner membrane and the plasma membrane of susceptible host cells; accordingly, experimentally induced damage to the outer membrane might be expected to increase infectivity. Here, in an attempt to develop an in vitro model system for studying ichnovirus infection, we show that digitonin-induced disruption of the virion outer membrane not only increases infectivity, but also uncovers an activity not previously associated with any polydnavirus: fusion from without.

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