The evolution of rock friction is more sensitive to slip than elapsed time, even at near-zero slip rates.

Nearly all frictional interfaces strengthen as the logarithm of time when sliding at ultra-low speeds. Observations of also logarithmic-in-time growth of interfacial contact area under such conditions have led to constitutive models that assume that this frictional strengthening results from purely time-dependent, and slip-insensitive, contact-area growth. The main laboratory support for such strengthening has traditionally been derived from increases in friction during "load-point hold" experiments, wherein a sliding interface is allowed to gradually self-relax down to subnanometric slip rates. In contrast, following step decreases in the shear loading rate, friction is widely reported to increase over a characteristic slip scale, independent of the magnitude of the slip-rate decrease-a signature of slip-dependent strengthening. To investigate this apparent contradiction, we subjected granite samples to a series of step decreases in shear rate of up to 3.5 orders of magnitude and load-point holds of up to 10,000 s, such that both protocols accessed the phenomenological regime traditionally inferred to demonstrate time-dependent frictional strengthening. When modeling the resultant data, which probe interfacial slip rates ranging from 3 .[Formula: see text]. to less than [Formula: see text], we found that constitutive models where low slip-rate friction evolution mimics log-time contact-area growth require parameters that differ by orders of magnitude across the different experiments. In contrast, an alternative constitutive model, in which friction evolves only with interfacial slip, fits most of the data well with nearly identical parameters. This leads to the surprising conclusion that frictional strengthening is dominantly slip-dependent, even at subnanometric slip rates.

Sustained eruptions on Enceladus explained by turbulent dissipation in tiger stripes.

Spacecraft observations suggest that the plumes of Saturn's moon Enceladus draw water from a subsurface ocean, but the sustainability of conduits linking ocean and surface is not understood. Observations show eruptions from "tiger stripe" fissures that are sustained (although tidally modulated) throughout each orbit, and since the 2005 discovery of the plumes. Peak plume flux lags peak tidal extension by ∼1 rad, suggestive of resonance. Here, we show that a model of the tiger stripes as tidally flexed slots that puncture the ice shell can simultaneously explain the persistence of the eruptions through the tidal cycle, the phase lag, and the total power output of the tiger stripe terrain, while suggesting that eruptions are maintained over geological timescales. The delay associated with flushing and refilling of O(1)-m-wide slots with ocean water causes erupted flux to lag tidal forcing and helps to buttress slots against closure, while tidally pumped in-slot flow leads to heating and mechanical disruption that staves off slot freezeout. Much narrower and much wider slots cannot be sustained. In the presence of long-lived slots, the 10(6)-y average power output of the tiger stripes is buffered by a feedback between ice melt-back and subsidence to O(10(10)) W, which is similar to observed power output, suggesting long-term stability. Turbulent dissipation makes testable predictions for the final flybys of Enceladus by Cassini Our model shows how open connections to an ocean can be reconciled with, and sustain, long-lived eruptions. Turbulent dissipation in long-lived slots helps maintain the ocean against freezing, maintains access by future Enceladus missions to ocean materials, and is plausibly the major energy source for tiger stripe activity.

Depolarization-induced release of amino acids from the vestibular nuclear complex.

There is evidence from immunohistochemistry, quantitative microchemistry, and pharmacology for several amino acids as neurotransmitters in the vestibular nuclear complex (VNC), including glutamate, γ-aminobutyrate (GABA), and glycine. However, evidence from measurements of release has been limited. The purpose of this study was to measure depolarization-stimulated calcium-dependent release of amino acids from the VNC in brain slices. Coronal slices containing predominantly the VNC were prepared from rats and perfused with artificial cerebrospinal fluid (ACSF) in an interface chamber. Fluid was collected from the chamber just downstream from the VNC using a microsiphon. Depolarization was induced by 50 mM potassium in either control calcium and magnesium concentrations or reduced calcium and elevated magnesium. Amino acid concentrations in effluent fluid were measured by high performance liquid chromatography. Glutamate release increased fivefold during depolarization in control calcium concentration and twofold in low calcium/high magnesium. These same ratios were 6 and 1.5 for GABA, 2 and 1.3 for glycine, and 2 and 1.5 for aspartate. Differences between release in control and low calcium/high magnesium ACSF were statistically significant for glutamate, GABA, and glycine. Glutamine release decreased during and after depolarization, and taurine release slowly increased. No evidence for calcium-dependent release was found for serine, glutamine, alanine, threonine, arginine, taurine, or tyrosine. Our results support glutamate and GABA as major neurotransmitters in the VNC. They also support glycine as a neurotransmitter and some function for taurine.

Changes of amino acid concentrations in the rat vestibular nuclei after midline lesions.

Changes in concentrations of amino acids, especially GABA, glutamate, and aspartate, occur in vestibular nuclei after removal of cerebellar and labyrinth inputs. Here, we examined the effects of transecting midline-crossing connections between the two vestibular nuclear complexes, which especially include commissural connections. Three rats were euthanized at each of 2, 7, and 30 days after a midline cut at the level of the vestibular nuclei. Two sham-lesioned rats were prepared for surgery but no cut made. Samples of superior (SuVN), dorsal and ventral lateral (LVNd and LVNv), dorsal and ventral medial (MVNd and MVNv), and spinal vestibular nuclei (SpVN) were microdissected from freeze-dried coronal sections and assayed for amino acid concentrations. Reductions of GABA concentration occurred by 2 days and continued through 30 days after surgery in most regions. Glutamate and aspartate concentrations decreased by 2 days in LVN and MVN, then glutamate showed some recovery by 30 days. Glutamine and taurine concentrations increased in almost all regions. Glycine concentration decreased in MVN and LVNv. Our results support association of GABA, glutamate, aspartate, and to some extent glycine, with vestibular crossed connections. Comparisons to our previous studies suggest some complex lesion effects, especially in LVNd.

Comparison of gamma-aminobutyrate receptors in the medial vestibular nucleus of control and Scn8a mutant mice.

The Purkinje cells of the cerebellum provide inhibitory input to vestibular nucleus neurons, with gamma-aminobutyrate (GABA) as neurotransmitter. Using extracellular recordings and bath application of agonists and antagonists, we compared GABA receptors in the medial vestibular nucleus of brain slices from Scn8a mutant mice of med(J) type, in which there is greatly reduced spontaneous and evoked activity of Purkinje cells, to those in slices from control mice. Muscimol, an agonist at GABA(A) receptors, produced a larger reduction of firing rate in neurons of mutant mice than in neurons of control mice, whereas there was no difference for baclofen, an agonist at GABA(B) receptors. In most cases tested, the effects of muscimol and baclofen remained similar when synaptic transmission was blocked, suggesting that the effects were predominantly directly upon GABA receptors of the neurons being recorded from. The up-regulation of GABA(A) receptors was similar in magnitude to that previously found for rats with bilateral transection of the inferior cerebellar peduncle. It may relate in both cases to reduced Purkinje cell input to medial vestibular nucleus neurons. The lack of effect on GABA(B) receptors suggests that the changes found with peduncle transection may have resulted from something more than reduced Purkinje cell activity, such as reduced concentrations of GABA, or that reduction of Purkinje cell activity in Scn8a mutant mice was insufficient to affect GABA(B) receptors. Other possible explanations of the results cannot be excluded since the Scn8a mutation affects other neuron types besides Purkinje cells.

Changes of amino acid concentrations in the rat vestibular nuclei after inferior cerebellar peduncle transection.

Although there is a close relationship between the vestibular nuclear complex (VNC) and the cerebellum, little is known about the contribution of cerebellar inputs to amino acid neurotransmission in the VNC. Microdissection of freeze-dried brain sections and high-performance liquid chromatography (HPLC) were combined to measure changes of amino acid concentrations within the VNC of rats following transection of the cerebellovestibular connections in the inferior cerebellar peduncle. Distributions of 12 amino acids within the VNC at 2, 4, 7, and 30 days after surgery were compared with those for control and sham-lesioned rats. Concentrations of gamma-aminobutyric acid (GABA) decreased by 2 days after unilateral peduncle transection in nearly all VNC regions on the lesioned side and to lesser extents on the unlesioned side and showed partial recovery up to 30 days postsurgery. Asymmetries between the two sides of the VNC were maintained through 30 days. Glutamate concentrations were reduced bilaterally in virtually all regions of the VNC by 2 days and showed complete recovery in most VNC regions by 30 days. Glutamine concentrations increased, starting 2 days after surgery, especially on the lesioned side, so that there was asymmetry generally opposite that of glutamate. Concentrations of taurine, aspartate, and glycine also underwent partially reversible changes after peduncle transection. The results suggest that GABA and glutamate are prominent neurotransmitters in bilateral projections from the cerebellum to the VNC and that amino acid metabolism in the VNC is strongly influenced by its cerebellar connections.

Effects of unilateral vestibular ganglionectomy on glutaminase activity in the vestibular nerve root and vestibular nuclear complex of the rat.

The metabolism of glutamate, the most likely neurotransmitter of vestibular ganglion cells, includes synthesis from glutamine by the enzyme glutaminase. We used microdissection combined with a fluorometric assay to measure glutaminase activity in the vestibular nerve root and nuclei of rats with unilateral vestibular ganglionectomy. Glutaminase activity in the lesioned-side vestibular nerve root decreased by 62% at 4 days after ganglionectomy and remained at similar values through 30 days. No change occurred in the contralateral vestibular nerve root. Glutaminase activity changes in the vestibular nuclei were lesser in magnitude and more complex, including contralateral increases as well as ipsilateral decreases. At 4 days after ganglionectomy, glutaminase activity was 10-20% lower in individual lesioned-side nuclei compared with their contralateral counterparts. By 14 and 30 days after ganglionectomy, there were no statistically significant differences between the nuclei on the two sides. This transient asymmetry of glutaminase activities in the vestibular nuclei contrasts with the sustained asymmetry in the vestibular nerve root and suggests that intrinsic, commissural, or descending pathways are involved in the recovery of chemical symmetry. This recovery resembles our previous finding for glutamate concentrations in the vestibular nuclei and may partially underlie central vestibular compensation after peripheral lesions.

The impact of osteoporosis on patients with maxillofacial trauma.

BACKGROUND: Although maxillofacial injuries in the elderly population frequently result from falls and motor vehicle crashes, the association between osteoporosis and fractures of the maxillofacial region remains poorly defined. OBJECTIVE: To evaluate the relationship between osteoporosis and maxillofacial trauma in the elderly. DESIGN, SETTING, AND MAIN OUTCOME MEASURES: A retrospective review of 59 patients 60 years or older treated for maxillofacial fractures at a trauma center between 1989 and 2000 was performed. The severity of osteoporosis was graded by evaluating the radiographic appearance of the vertebral bodies of each trauma patient using the Saville index. The number of maxillofacial fractures and the severity of osteoporosis in each patient was assessed to determine whether an association between osteoporosis and maxillofacial trauma exists. RESULTS: Of the 59 patients evaluated, 51% were injured by falls and 46% were involved in motor vehicle crashes. Seventy-three percent of the patients had multiple facial fractures. As the severity of osteoporosis worsened, patients were more likely to sustain a greater number of maxillofacial fractures (P=.01). The mechanism of injury had no impact on the relationship between osteoporosis and the number of fractures. CONCLUSIONS: Osteoporosis is an independent risk factor for the development of maxillofacial fractures. Since more than half of these patients are injured by falls, safety measures must be instituted to prevent fall-related maxillofacial injuries in the home and the community.

The assessment and management of the dizzy patient.

A significant number of individuals are affected by symptoms of dizziness. It is the most common complaint among patients over 75 years of age. A large number of these patients seek counsel from their physicians. It is imperative for the evaluating physician to obtain a thorough history and perform a complete physical exam. The proper diagnostic studies must also be obtained to confirm or rule out particular diagnoses. The physician should never assume that the dizziness is the result of normal aging prior to ruling out pathologic conditions.

Spontaneous activity in rat vestibular nuclei in brain slices and effects of acetylcholine agonists and antagonists.

Extracellular recording was used to investigate spontaneously active neurons in all four major nuclei of the rat vestibular nuclear complex (VNC) in brainstem slices. The density of spontaneously active neurons was highest in the medial vestibular nucleus (MVN), slightly lower in the superior (SuVN) and spinal (SpVN) nuclei, and lowest in the lateral vestibular nucleus (LVN). We compared the effects of acetylcholine agonists and antagonists on spontaneously discharging neurons in MVN, SuVN, and SpVN with those in the nearby dorsal cochlear nucleus (DCN). The proportion of neurons responding to carbachol was greatest in DCN and smallest in SpVN. Unlike in DCN, some neurons in MVN, SuVN, and SpVN showed decreased firing during carbachol or muscarine. Magnitudes of responses to carbachol and muscarine were closely correlated (P<0.01). MVN neurons possessed nicotinic as well as muscarinic receptors. Activation of either type was unaffected by blocking synaptic transmission. The IC(50) values for the muscarinic subtype-preferential antagonists were compared, and tropicamide, preferential for M(4), was the most potent. Our results suggest that: (1) the relative numbers of spontaneously active neurons in rat VNC differ among nuclei; (2) acetylcholine agonists elicit changes in mean firing rates of neurons in MVN, SuVN and SpVN, but fewer neurons respond, and responses are smaller than in DCN; (3) both muscarinic and nicotinic acetylcholine receptors are present on MVN neurons, but muscarinic receptors may be more prominent.

Remodeling of synaptic connections in the deafferented vestibular nuclear complex.

To determine if synaptic remodeling in the vestibular nuclear complex (VNC) may be involved in vestibular compensation, expressions of growth-associated protein-43 (GAP-43) and synaptosome-associated protein of 25 kDa (SNAP-25) were examined by immunoblotting and immunocytochemistry after unilateral vestibular ganglionectomy (UVG) in rats. GAP-43 expression increased bilaterally in the VNC after UVG, but more rapidly on the lesioned side, and remained high through 60 days. It was mainly associated with boutons at all survival times but was also present in some axonal processes and, at 7 days after UVG, in some somata. SNAP-25 expression also increased bilaterally, more rapidly on the lesioned side, but decreased bilaterally after peaking at 14 days. Its distribution in the VNC resembled that of GAP-43 but was more completely localized to boutons. Comparisons were made with auditory centers of the same rats, since the lesion also deafferented that system. Our results combined with those of previous studies suggest that degeneration of the vestibular nerve fibers is required for increased expression of GAP-43 in the VNC. The results suggest that axonal sprouting and synaptogenesis are involved in synaptic remodeling bilaterally in the rat VNC after UVG.

Plasticity of gamma-aminobutyrate receptors in the medial vestibular nucleus of rat after inferior cerebellar peduncle transection.

Extracellular single unit recordings were made from regularly discharging medial vestibular nucleus neurons in brain slices from control rats and from rats surviving 7 days after bilateral transection of the inferior cerebellar peduncle. Decreases in firing rate during perfusion with the gamma-aminobutyric acid (GABA) agonists, muscimol (GABA(A)) and baclofen (GABA(B)), were greater in lesioned rats than in control rats. For the grouped data, the half-maximally-effective concentrations of muscimol and baclofen were 3.2 microM, as compared with 19.6 microM for control, and 0.8 microM, as compared with 2.7 microM for control, respectively. The antagonists bicuculline (GABA(A)) and 2-OH-saclofen (GABA(B)) only minimally affected the spontaneous firing rates of neurons in lesioned rats, significantly less than in control rats. The data suggest that the decreases of endogenous GABA levels in the medial vestibular nucleus after inferior cerebellar peduncle transection are accompanied by up-regulation of GABA(A) and, to a lesser extent, GABA(B) receptors.