No abstract

The average dimensions (diameter, length, and volume) of the airways in the mammalian bronchial tree, long thought to be exponential functions of the generation number, are shown to be power laws in generation number modulated by a harmonic variation. These data are satisfactorily described by means of a functional scaling relation--renormalization group property--between successive generations for the average variable of interest. This type of scaling may provide a mechanism for the morphogenesis of complex but highly stable structures.

Background & Aims-Achalasia esophagus is characterized by loss of peristalsis and incomplete esophago-gastric junction (EGJ) relaxation. We studied mechanisms of esophageal emptying in patients with achalasia using simultaneous high-resolution manometery (HRM), multiple intraluminal impedance (MII), and high frequency intra-luminal ultrasound (HFIUS) image recordings.

The present study reports the development and characterization of a murine model of right ventricular dysfunction following graded constriction in the pulmonary artery via microsurgical approaches. To analyze in vivo ventricular function, a technique of x-ray contrast microangiography was developed to allow the quantitative analysis of ventricular volumes and of ejection fraction in normal and pressure-overloaded right ventricle. Severe, chronic pulmonary arterial banding for 14 days resulted in right ventricular dilatation and dysfunction, associated with right atrial enlargement, and angiographic evidence of tricuspid regurgitation. These effects were dependent on the extent of hemodynamic overload, since more moderate pulmonary arterial constriction resulted in hypertrophy with maintenance of right ventricular function. With severe pulmonary artery constriction, the murine right ventricle displays a failing heart phenotype including chamber dilation with reduced function that resembles right ventricular dysfunction in man during chronic pulmonary arterial hypertension. Northern and immunoblot analyses demonstrate a marked down-regulation of phospholamban mRNA and its corresponding protein with both levels of constriction, while a less pronounced but significant depression of sarcoplasmic reticulum Ca2+-ATPase protein was observed with severe overload, suggesting that this pattern is an early genetic marker of ventricular dysfunction. By coupling mouse genetics with this murine model and the ability to assess cardiac function in vivo, one should be able to test the role of the down-regulation of phospholamban and other defred alterations in the cardiac muscle gene program in the onset of the failing heart phenotype.Cardiac muscle failure is one of the most important problems in cardiovascular medicine. Although the physiology of the failing heart has been the subject of intense scientific inquiry, relatively little is known regarding the signaling pathways within cardiac muscle cells which mediate the progression from compensatory hypertrophy to cardiac muscle dysfunction. Although ventricular chamber dilation with reduced myocardial shortening and contractile velocity (1), as well as abnormal Ca2+ handling, appear to be hallmarks of the end-stage failing human heart (2), the molecular pathways which lead to these distinct phenotypes are unclear. One of the difficulties has been the paucity of animal model systems for analysis of the effects of the manipulation of a set of genes on cardiac function in the intact animal.Utilizing recent advances in microsurgical approaches to create a graded constriction in the pulmonary artery (PA), we have developed and characterized a murine model of right ventricle (RV) hypertrophy and failure. In addition, a technique for digitized microangiography was developed to allow the quantitative analysis of in vivo cardiac function, ventricular volumes, and ejection fraction in normal and pressureoverloaded murine myocardium. Severe, chronic pulmonary arterial banding for ...

In patients with EO, there is selective dysfunction of the longitudinal muscle contraction during peristalsis. It is proposed that the longitudinal muscle dysfunction in EO may contribute to dysphagia.

Objective Anal sphincter complex consists of anatomically overlapping internal anal sphincter (IAS), external anal sphincter (EAS) & puborectalis muscle (PRM). We determined the functional morphology of anal sphincter muscles using high definition manometery (HDAM), 3D-ultrasound (US) and Magnetic resonance (MR) imaging. Patients We studied 15 nulliparous women. Interventions HDAM probe equipped with 256 pressure transducers was used to measure the anal canal pressures at rest and squeeze. Lengths of IAS, PRM and EAS were determined from the 3D-US images and superimposed on the HDAM plots. Movements of anorectal angle with squeeze were determined from the dynamic MR images. Results HDAM plots reveal that anal canal pressures are highly asymmetric in the axial and circumferential direction. Anal canal length determined by the 3D-US images is slightly smaller than measured by HDAM. The EAS (1.9 ± 0.5 cm long) and PRM (1.7 ± 0.4 cm long) surround distal and proximal parts of the anal canal respectively. With voluntary contraction, anal canal pressures increase in the proximal (PRM) and distal (EAS zone) parts of anal canal. Posterior peak pressure in the anal canal moves cranially in relationship to the anterior peak pressure, with squeeze. Similar to the movement of peak posterior pressure, MR images show cranial movement of anorectal angle with squeeze. Conclusion Our study proves that the PRM is responsible for the closure of the cranial part of anal canal. HDAM, in addition to measuring constrictor function can also record the elevator function of levator ani/pelvic floor muscles.

Electrical activation of the ventricles via the His-Purkinje system is represented on the body surface by a waveform with a broad range of frequency components. We speculate that this process is mediated by current flow through a fractal-like conduction network and therefore that the broadband spectrum of the depolarization waveform should be scaled as a power-law distribution. The prediction is confirmed by Fourier analysis of electrocardiographic data from healthy men. This observation suggests a new dynamical link between nonlinear (fractal) structure and nonlinear function in a stable physiologic system.

The current understanding is that longitudinal muscle contraction begins before and outlasts circular muscle contraction during esophageal peristalsis in normal subjects. The goal of our study was to reassess the relationship between the contractility of two muscle layers using novel ways to look at the muscle contraction. We studied normal subjects using synchronized high-frequency ultrasound imaging and manometry. Swallow-induced peristalsis was recorded at 5 and 10 cm above the lower esophageal sphincter (LES). Ultrasound (US) images were analyzed for muscle cross-sectional area (CSA) and circularity index of the esophagus during various phases of esophageal contraction. A plot of the M mode US image, muscle CSA, and esophageal circularity index was developed to assess the temporal correlation between various parameters. The muscle CSA wave began before and lasted longer than the contraction pressure wave at both 5 and 10 cm above the LES. M mode US images revealed that the onset of muscle CSA wave was temporally aligned with the onset of lumen collapse. The peak muscle CSA occurred in close proximity with the peak pressure wave. The esophagus started to become more circular (decrease in circularity index) with the onset of the muscle CSA wave. The circularity index and muscle CSA returned to the baseline at approximately the same time. In conclusion, the onset of lumen collapse and return of circularity index of the esophagus are likely to be the true markers of the onset and end of circular muscle contraction. Circular and longitudinal muscle layers of the esophagus contract in a precise synchronous fashion during peristalsis in normal subjects.