Rational and Objectives-Volumetric high-resolution scans can be acquired of the lungs with multi-detector CT (MDCT). Such scans have potential to facilitate useful visualization, characterization, and quantification of the extent of diffuse lung diseases, such as Usual Interstitial Pneumonitis or Idiopathic Pulmonary Fibrosis (UIP/IPF). There is a need to objectify, standardize and improve the accuracy and repeatability of pulmonary disease characterization and quantification from such scans. This paper presents a novel texture analysis approach toward classification and quantification of various pathologies present in lungs with UIP/IPF. The approach integrates a texture matching method with histogram feature analysis.

We have demonstrated that our novel method is computationally efficient and produces results comparable to expert radiologic judgment. It is effective in the classification of normal versus abnormal tissue and performs as well as the experts in distinguishing among typical pathologies present in lungs with UIP/IPF. The continuing development of quantitative metrics will improve quantification of disease and provide objective measures of disease progression.

Use of dynamic z-axis collimation reduces dose in helical CT by minimizing overscanning. Percentage dose reductions are larger for shorter scan lengths and greater pitch values.

In airway smooth muscle (ASM) cells, excitation-contraction coupling is accomplished via a cascade of events that connect an elevation of cytosolic Ca concentration ([Ca]) with cross-bridge attachment and ATP-consuming mechanical work. Excitation-energy coupling is mediated by linkage of the elevation of [Ca] to an increase in mitochondrial Ca concentration, which in turn stimulates ATP production. Proximity of mitochondria to the sarcoplasmic reticulum (SR) and plasma membrane is thought to be an important mechanism to facilitate mitochondrial Ca uptake. In this regard, mitochondrial movement in ASM cells may be key in establishing proximity. Mitochondria also move where ATP or Ca buffering is needed. Mitochondrial movement is mediated through interactions with the Miro-Milton molecular complex, which couples mitochondria to kinesin motors at microtubules. We examined mitochondrial movement in human ASM cells and hypothesized that, at basal [Ca] levels, mitochondrial movement is necessary to establish proximity of mitochondria to the SR and that, during the transient increase in [Ca] induced by agonist stimulation, mitochondrial movement is reduced, thereby promoting transient mitochondrial Ca uptake. We further hypothesized that airway inflammation disrupts basal mitochondrial movement via a reduction in Miro and Milton expression, thereby disrupting the ability of mitochondria to establish proximity to the SR and, thus, reducing transient mitochondrial Ca uptake during agonist activation. The reduced proximity of mitochondria to the SR may affect establishment of transient "hot spots" of higher [Ca] at the sites of SR Ca release that are necessary for mitochondrial Ca uptake via the mitochondrial Ca uniporter.