Summary1 Data from elevations ranging from mixed hardwood-conifer forest at 600 m to subalpine Abies balsamea forest at 1120 m indicate that canopy gaps are not static but expand over time due to mortality of trees at the gap margin and coalescence of gaps. Gap expansion is more frequent than gap initiation. Ultimately such disturbance patches may become more extensive than is normally considered as typical of gap-phase disturbance, but the processes of development are the same. 2 Disturbance agents involved in gap initiation tend to differ from those involved in gap expansion. Spruce beetle, dwarf mistletoe and most root diseases predominate as agents of gap initiation, while windthrow/windsnap, chronic wind stress and Armillaria root disease are important agents of gap expansion. 3 Concepts of equilibrium gap-phase dynamics and a shifting-mosaic steady state do not fully account for the dynamics of these spruce-fir forests. A spruce beetle outbreak in the late 1970s/early 1980s killed most of a cohort of dominant, emergent Picea rubens . This epidemic initiated a long-term cycle of disturbance and release that is likely to be repeated in many years when a new cohort of P. rubens becomes sufficiently large to sustain another major bark beetle outbreak. 4 Episodic disturbance agents affect long-lived, dominant species at infrequent but regular intervals (up to hundreds of years) and operate at the landscape level. Gap-phase cycles appear to be nested within the long-term cycle. Over the long term, episodic disturbance drives such 'nested bicycle' dynamics. 5 Spatial and temporal distribution of disturbance results not only from stochastic events such as storms, but also from host specificity of agents of disturbance, their tendency to attack certain age classes of trees, local and regional contagion, and susceptibility of trees at the edge of disturbance patches.

Background Vagus nerve stimulation therapy (VNS) has been used for chronic heart failure (CHF), and is believed to improve imbalance of autonomic control by increasing parasympathetic activity. Although it is known that there is neural communication between the VN and the cervical sympathetic trunk, there are few data regarding the quantity and/or distribution of the sympathetic components within the VN. Objective To examine the sympathetic component within human VN and correlate these with the presence of cardiac and neurologic diseases. Methods We performed immunohistochemistry on 31 human cervical and thoracic VNs (total 104 VNs) from autopsies and we reviewed the patients’ records. We correlated the quantity of sympathetic nerve fibers within the VNs with cardiovascular and neurologic disease states. Results All 104 VNs contain TH positive (sympathetic) nerve fibers; the mean TH positive areas were 5.47% in right cervical, 3.97% in left cervical, 5.11% in right thoracic, and 4.20% in left thoracic VN. The distribution of TH positive nerve fibers varied from case to case: central, peripheral, or scattered throughout nerve bundles. No statistically significant differences in nerve morphology were seen between diseases in which VNS is considered effective (depression and CHF), and other cardiovascular diseases, or neurodegenerative disease. Conclusion Human VNs contain sympathetic nerve fibers. The sympathetic component within the VN could play a role in physiologic effects reported with VNS. The recognition of sympathetic nerve fibers in the VNs may lead to better understanding of the therapeutic mechanisms of VNS.

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Correlation of MUC4 expression with clinical outcomes may establish MUC4 as a potential molecular prognostic marker for these tumors.