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The IMP increased from 4.7 (SD = 1.8) mmHg at baseline to 48.6 (SD = 7.1) mmHg when the model of elevated IMP was applied.
This study was designed to investigate the oesophageal seal of the novel supralaryngeal airway device, I-Gel™ (I-Gel), in comparison with two of the laryngeal mask airways, Classic™ (cLMA) and ProSeal™ (pLMA), in a model of elevated oesophageal pressure.
Therefore, the purpose of the present study was to investigate the amplitude of pulse-synchronous IMP oscillations relation to the absolute IMP with a high-end fiber-optic pressure measurement system in an experimental model of elevated IMP (simulated compartment syndrome) in the human leg.
Therefore, the TG CaMKIIδC mouse can be regarded as a model of elevated CaMKII activity, but also as a pathophysiological relevant model of non-ischemic HF.
We chose both a mouse genetic model and a rat pharmacological model of elevated Vmax in order to increase the likelihood of observing reproducible effects by minimizing potential flaws/changes in a single model, such as developmental alterations in the genetic model, off-target modifications in the pharmacological model, or species effects that could be driving the observed changes.
Quantification of these internal ONH changes is beyond the scope of the current report, but these images suggest the possibility of using this technique to monitor and better understand the physical consequences of cellular responses to elevated IOP, particularly at the site of initial injury, that we have observed in our chronic model of elevated IOP [ 31, 42].
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The application of a pneumoperitoneum served as a model for elevated IAP.
The amplitude of the pulse-synchronous IMP oscillations increases with increasing absolute level of IMP during a model of abnormally elevated IMP in the human leg.
Mean intramuscular pressure (IMP) and standard deviation during a model of abnormally elevated IMP that was induced by venous obstruction of a casted leg.
In a rabbit model of GERD, elevated IL-6 expression correlated with induction of several tight junction-related proteins (Claudin-1, Occludin, JAM-1, ZO-1) [ 57] and altered the motogenic activity of smooth muscle cells [ 58].
Using the first transgenic animal model to elevate circulating levels of IGF-I to those comparable to women at increased risk of breast cancer, we showed that moderately high levels of systemic IGF-I have no effect on pubertal mammary gland development, initiating mammary tumorigenesis or promoting ErbB2 driven mammary carcinogenesis.
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Justyna Jupowicz-Kozak
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