Composite bone models are increasingly used in orthopaedic biomechanics research and surgical education—applications that traditionally relied on cadavers. Cadaver bones are suboptimal for myriad reasons, including issues of cost, availability, preservation, and inconsistency between specimens. Further, cadaver samples disproportionately represent the elderly, whose bone quality may not be representative of the greater orthopaedic population. The current fourth-generation composite bone models provide an accurate reproduction of the biomechanical properties of human bone when placed under bending, axial, and torsional loads. The combination of glass fiber and epoxy resin components into a single phase has enabled manufacturing by injection molding. The high anatomic fidelity of the cadaver-based molds and negligible shrinkage properties of the epoxy resin results in a process that allows for excellent definition of anatomic detail in the cortical wall and optimized consistency of features between models. Recent biomechanical studies of composites have validated their use as a suitable substitute for cadaver specimens.

Chronic alcohol intake is associated with widespread disruptions in sleep and circadian rhythms in both human alcoholics and in experimental animals. Recent studies have demonstrated that chronic and acute ethanol treatments alter fundamental properties of the circadian pacemaker—including free-running period and responsiveness to photic and nonphotic phase-shifting stimuli—in rats and hamsters. In the present work, the authors extend these observations to the C57BL/6J mouse, an inbred strain characterized by very high levels of voluntary ethanol intake and by reliable and stable free-running circadian activity rhythms. Mice were housed individually in running-wheel cages under conditions of either voluntary or forced ethanol intake, whereas controls were maintained on plain water. Forced ethanol intake significantly attenuated photic phase delays (but not phase advances) and shortened free-running period in constant darkness, but voluntary ethanol intake failed to affect either of these parameters. Thus, high levels of chronic ethanol intake, beyond those normally achieved under voluntary drinking conditions, are required to alter fundamental circadian pacemaker properties in C57BL/6J mice. These observations may be related to the relative ethanol insensitivity displayed by this strain in several other phenotypic domains, including ethanol-induced sedation, ataxia, and withdrawal. Additional experiments will investigate chronobiological sensitivity to ethanol in a range of inbred strains showing diverse ethanol-related phenotypes.

Several studies have mapped brain regions associated with acute dyspnea perception. However, the time-course of brain activity during sustained dyspnea is unknown. Our objective was to determine the time-course of neural activity when dyspnea is sustained. Eight healthy subjects underwent brain blood oxygen level dependent functional magnetic imaging (BOLD-fMRI) during mechanical ventilation with constant mild hypercapnia (~45 mmHg). Subjects rated dyspnea (air hunger) via visual analog scale (VAS). Tidal volume (VT) was alternated every 90 seconds between high VT (0.96±0.23 L) that provided respiratory comfort (12±6% full scale) and low VT (0.48±0.08 L) which evoked air hunger (56±11% full scale). BOLD signal was extracted from a priori brain regions and combined with VAS data to determine air hunger related neural time-course. Air hunger onset was associated with BOLD signal increases that followed two distinct temporal profiles within sub-regions of the anterior insula, anterior cingulate and prefrontal cortices (cortico-limbic circuitry): (1) fast, BOLD signal peak <30 seconds and (2) slow, BOLD signal peak >40 seconds. BOLD signal during air hunger offset followed fast and slow temporal profiles symmetrical, but inverse (signal decreases) to the time-courses of air hunger onset. We conclude that differential cortico-limbic circuit elements have unique contributions to dyspnea sensation over time. We suggest that previously unidentified sub-regions are responsible for either the acute awareness or maintenance of dyspnea. These data enhance interpretation of previous studies and inform hypotheses for future dyspnea research.

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