VC Levels Research Articles

Masseteric inflammation-induced Fos protein expression in the trigeminal interpolaris/caudalis transition zone: contribution of somatosensory–vagal–adrenal integration

The effects of vagotomy and adrenalectomy on the expression of Fos protein in brainstem neurons following the inflammation of masseter muscle were examined in order to differentiate the Fos activation related to nociceptive processing in contrast to that due to somatoautonomic processing. The inflammation was induced by a unilateral injection of complete Freund's adjuvant (CFA) into the masseter muscle under methohexital anesthesia after a small skin-cut (S-cut). After the CFA injection, Fos positive neurons were identified in bilateral spinal trigeminal nucleus (VSP), nucleus tractus solitarius (NTS), ventrolateral medulla (VLM) and inferior medial olivary nucleus (IOM). At the level of the trigeminal subnucleus interpolaris/caudalis (Vi/Vc) transition zone, there was a selective induction of Fos-like immunoreactivity (LI) in the VSP and NTS, when compared to control rats (anesthesia with or without S-cut). A major portion of the Fos-LI in the VSP at the level of the caudal Vc was apparently activated by S-cut. Bilateral adrenalectomy or a unilateral vagotomy resulted in a selective reduction of inflammation-induced Fos-LI in the VSP at the Vi/Vc transition zone ( P<0.05) and NTS ( P<0.05), but had less effect on Fos-LI in the caudal Vc. These results suggest that the inflammation of the masseter muscle, an injury of orofacial deep tissue, results in a widespread change in neuronal activity in the VSP and NTS that depends in part on the integrity of the adrenal cortex and vagus. Thus, in addition to somatotopically organized nociceptive responses, orofacial deep tissue injury also is coupled to somatovisceral and somatoautonomic processing that contribute to central neural activation.

Traffic management for an ATM switch with per-VC queuing: concept and implementation

The services to be supported by an asynchronous transfer mode (ATM)-based multiservice network differ significantly in terms of their traffic characteristics and required quality of service. During the last few years it has been broadly accepted that efficient use of transmission capacity is not possible unless these differences are reflected in the way the related traffic streams are handled within the ATM layer. To address this need, the ATM Forum and ITU-T have specified different real-time and non-real-time ATM-layer service categories. This article first discusses the requirements for traffic management in a switch supporting all these service categories from the service providers' and users' points of view. The first generation of ATM switches, typically equipped with small cell buffers, only satisfies the requirements for the real-time service categories (CBR, rt-VBR). Statistical multiplexing, if supported at all, is limited to connections with low peak cell rates. Larger cell buffers and new traffic control functions are required to support non-real-time service categories (nrt-VBR, ABR, UBR). A switch architecture which is scalable from small to large system sizes is presented. It provides the required buffering and additional functions for the non-real-time service categories with the aid of a statistical multiplexing unit (SMU), a module which can also be used as an optional addition to a conventional ATM switch. The focus is on the functional description of two novel yet key components of the SMU, namely the buffer management and cell scheduling functions. The buffer management function provides per-VC queuing and achieves an optimal utilization of the large cell buffer shared by connections of different service categories. The two-stage cell scheduling function supports traffic shaping on the VC and VP levels, and weighted fair queuing within groups of connections. The overall concept supports high link utilization, fairness, and throughput guarantees, and enables a migration from today's ATM networks to a fully integrated multiservice network. Finally, implementation aspects are discussed to show the feasibility of the concept for very high bit rates.

The crucial antioxidant action of schisandrin B in protecting against carbon tetrachloride hepatotoxicity in mice: A comparative study with butylated hydroxytoluene

A comparison between the effects of schisandrin B (Sch B) and butylated hydroxytoluene (BHT) treatments on hepatic antioxidant status was made to identify the critical antioxidant action of Sch B involved in hepatoprotection in mice. Whereas Sch B treatment (3 mmol/kg/day × 3, p.o.) increased the hepatic mitochondrial-reduced glutathione (GSH) level, BHT treatment at the same dosage regimen decreased it. However, both Sch B and BHT increased, albeit to a different extent, the activity of mitochondrial glutathione reductase. The differential effect of Sch B and BHT treatment on hepatic mitochondrial glutathione status became more apparent after carbon tetrachloride (CCl 4) challenge. Pretreatment with Sch B could sustain the hepatic mitochondrial GSH level in CCl 4-intoxicated mice and protect against CCl 4 hepatotoxicity. BHT pretreatment did not produce any protective effect on CCl 4-induced GSH depletion in mitochondrion and hepatocellular damage. Although both Sch B and BHT treatments increased hepatic ascorbic acid (VC) level in control animals, only Sch B pretreatment sustained a high hepatic VC level in CCl 4-intoxicated mice. Moreover, Sch B pretreatment prevented the CCl 4-induced decrease in the hepatic α-tocopherol (VE) level. However, Sch B inhibited NADPH oxidation in mouse liver microsomes incubated with CCl 4 in vitro, whereas BHT stimulated this oxidation. The ensemble of results suggests that the ability to sustain the hepatic mitochondrial GSH level and the hepatic VC and VE levels may represent the crucial antioxidant action of Sch B in protection against CCl 4 hepatotoxicity. The possible inhibition of CCl 4 metabolism by Sch B may also contribute to its hepatoprotective action.

Morphology of central terminations of intra-axonally stained, low-threshold mechanoreceptive primary afferent fibers from oral mucosa and periodontium in the rat

Horseradish peroxidase (HRP) was injected intra-axonally into functionally identified primary afferent fibers within the rat spinal trigeminal tract in order to study the morphology of their central terminations. They were physiologically determined to be large, myelinated afferent fibers from periodontium or oral mucosa by means of electrical and mechanical stimulation of their receptive fields. Twenty-eight axons that innervated the periodontium of incisors and 21 axons that innervated the oral mucosa were stained for distances of 2–5 mm from the injection sites at the levels of the main sensory nucleus (Vms), spinal trigeminal nucleus and rostral cervical spinal cord. The collaterals of these primary afferent fibers formed terminal arbors in the medial or dorsomedial part of the Vms, and the oral and interpolar spinal trigeminal nuclei (Vo and Vi). In the caudal spinal trigeminal nucleus (Vc), the collaterals of one half of the periodontium afferent fibers terminated mainly in lamina V at the rostral and middle levels of Vc. On the other hand, the collaterals of the other half of the periodontium afferent fibers terminated mainly in lamina IV at the rostral level of Vc, and rostrally these terminal areas shifted to the most medial part of Vi. The collaterals of mucosa afferent fibers terminated in lamina V at the rostral level of Vc, and these terminal areas shifted gradually to laminae III and IV as the parent axons traveled more caudally. These shifts were staggered rostrocaudally according to the rostrocaudal locations of the receptive fields. The density of collaterals of periodontium afferent fibers in Vi was significantly larger than that of mucosa afferent fibers. The average size of the varicosities of periodontium afferent fibers was significantly larger than those of mucosa afferent fibers in Vo, Vi and Vc. The average number of varicosities belonging to single collaterals of slowly-adapting periodontium afferent fibers in Vi were significantly larger than those in Vo. In Vi, the average number of varicosities of single collaterals of slowly-adapting periodontium afferent fibers were significantly larger than those of rapidly-adapting periodontium afferent fibers.

Biomechanics of the human chest, abdomen, and pelvis in lateral impact

Fourteen unembalmed cadavers were subjected to 44 blunt lateral impacts at velocities of approximately 4.5, 6.7, or 9.4 m/s with a 15 cm flat circular interface on a 23.4 kg pendulum accelerated to impact speed by a pneumatic impactor. Chest and abdominal injuries consisted primarily of rib fractures, with a few cases of lung or liver laceration in the highest severity impacts. There were two cases of pubic ramus fracture in the pelvic impacts. Logist analysis of the biomechanical responses and injury indicated that the maximum Viscous response had a slightly better correlation with injury than maximum compression for chest and abdominal impacts. A tolerance level of VC = 1.47 m/s for the chest and VC = 1.98 m/s for the abdomen were determined for a 25% probability of critical injury. Maximum compression was similarly set at C = 38% for the chest and at C = 44% for the abdomen. The experiments indicate that chest and abdominal injury may occur by a viscous mechanism during the rapid phase of body compression, and that the Viscous and compression responses are effective, complementary measures of injury risk in side impact. Although serious pelvic injury was infrequent, lateral public ramus fracture correlated with compression of the pelvis, not impact force or pelvic acceleration. Pelvic tolerance was set at 27% compression.

Biomechanics of injury in lateral impacts

Fourteen anesthetized swine were subjected to blunt lateral impact at velocities of 4.3, 6.7, or 8.2 m/s with a 15 cm flat pendulum weighing 23.4 kg accelerated to impact speed by a power-assisted pneumatic impactor. Injuries consisted of laceration of the liver and spleen resulting in severe hemoperitoneum and death by ventricular fibrillation and respiratory arrest in the highest severity impacts. Logist analysis of the biomechanical responses and serious or fatal injury indicated that the maximum Viscous response ( VC) had the best correlation with injury risk. A tolerance level of VC = 0.89 m/s was determined for a 25% probability of serious injury. In contrast, maximum chest compression did not correlate with injury. The experiments indicate that internal organ and soft tissue injury may occur by a Viscous mechanism during the rapid phase of compression of the body. The Viscous response is an effective measure of injury risk in side impacts.

The flash-evoked afterdischarge

(1) The flash-evoked afterdischarge has been analysed under various functional states along the visual pathway: optic tract (OT), lateral geniculate body (LG) and cortical areas 17 and 18 (VC). Experiments were mainly conducted in the unanaesthetized cat (encéphale isolé, cerveau isoléor immobilized with Flaxedil), but findings from anaesthetized preparations were also recorded in order to correlate data obtained in various experimental conditions. The use or non-use of anaesthetics and the different locations of the recording LG and VC electrodes may account for divergences in literature concerning the correlations between cortical and subcortical flash-evoked events, and the nature of the VC photic afterdischarge. (2) A differentiation between the early wave and the subsequent (post-primary) complex was attempted in the unanaesthetized cat. Similar dissociations could be found in experiments performed on vigil submammals and night-active monkeys. By changing the parameters of test flash stimulus and during background illumination parallel alterations of the initial ( a) VC wave and of the OT and LG responses occurred. This indicates the extracortical (retinal) origin of the early wave of the VC. On the other hand, central specific origin and cortical elaboration of the b-complex (after-discharge) are suggested by many experimental findings: (i) alterations induced by variation in parameters of the test flash and by steady retinal illumination, opposite in sign to those undergone by the early VC deflection and the OT and LG responses; enhancement of the b-complex by decreasing the flash intensity is though to result from diminution of inhibitory mechanisms set in motion by strong photic stimulation; (ii) potentiation by preceding LG or direct VC stimulation, without affecting the early wave; (iii) close time-relation between the b-complex recorded from the surface and unit discharges in the depth of the VC under the potentiating influence of steady light; (iv) simulation of naturally desynchronized photically elicited impulses by trains of high-frequency pulses applied to the central afferent pathway and inducing a multiple response in the VC, the late components of which resemble in reactivity the flash-evoked afterdischarge; (v) the pattern of the b-complex which, under the selective potentiation induced by steady light, strikingly resembles that of a centrally evoked response with fast spikes preceding the biphasic slow sequence; in a few, privileged experiments, close temporal relation could be found between such a b-wave and grouped unit discharges recorded from the lateral part of the LG; even in such a case, the most part of the b-complex seemed to be elaborated in the VC since decortication left unaltered the fast positive spikes while inducing disappearance of the subsequent slow sequence. (3) The mechanisms of the steady-light potentiating effect mediated by the specific pathway and mainly exerted at the VC level are discussed. (4) Some correlations between the photically evoked afterdischarge and perceptual integrative processes of the VC are suggested.