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In the context pronephric development and embryonic blood flow, studies by Serluca et al. show that zebrafish mutants lacking blood flow as a result of cardiac defects fail to form a glomerular capillary tuft, indicating that while the phenotype is renal the underlying cause of the phenotype may be cardiac disruption [ 49].
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Although the pathogenesis of takot-subo syndrome has not yet been established, compelling literature supports the theory that acute cardiac sympathetic disruption accompanied with norepinephrine seethe and spillover are the mechanisms of tako-tsubo syndrome [ 72].
This type is the most common and potentially lethal injury, and may cause major tracheobronchial disruption, cardiac contusions, aortic and diaphragmatic rupture [3].
Cardiac arrhythmias are disruptions in the normal electrical activity of the heart.
Staining with the chamber-specific antibodies MF20 and S46 demonstrated that subtle delay or disruption of cardiac looping was associated with the earliest observed defects in cardiac function.
The lack of effect of microtubule disruption on cardiac contractility in adult myocytes, and the concentration-dependent modulation of the rate of contraction by the disruptor nocodazole in neonatal myocytes, support the existence of functionally distinct microtubule populations.
Cardiomyocytes treated with AdXKN for 48 hrs demonstrated reduction in the expression of myosin heavy chain, an indication of disruption in cardiac cell sarcomeric structure and function (Fig. 2D).
Evidence for a critical role of Smyd proteins during organ development was first shown by the constitutive knockout of Smyd1/m-Bop, resulting in early embryonic lethality due to disruption of cardiac differentiation and morphogenesis [14].
The KATP channel is important for cardiac function; indeed, genetic disruption of the pore-forming subunit that comprises cardiac KATP channels renders the knockout mice less tolerant to different types of stress, resulting in abnormal cytosolic calcium handling, susceptibility to developing acute cardiac failure, and sudden cardiac death [42], [43].
Accumulating evidence has also implicated a role of the obese gene product leptin, which regulates food intake and energy expenditure, in the regulation of cardiac function, while the disruption of which contributes to obesity-associated cardiac contractile and morphometric defects [15], [16].
Cardiac dyssynchrony, triggered by disruption in coordinated wall motion, contributes to organ failure and poor outcome.
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