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PubMedDate not supplied

In vitro biomechanical and histological assessment of pilot hole diameter for positive-profile external skeletal fixation pins in canine tibiae.

This study was conducted to evaluate the effect of pilot hole (PH) diameter (0, 1.5, 2.0, 2.7, 3.1, 3.3, 3.5, and 3.7 mm) on the biomechanical and microstructural performance of positive-profile threaded external skeletal fixation pins (3.18 mm inner diameter, 3.97 mm outer diameter) using cadaveric canine tibiae. Eight pins per pilot hole diameter (four pins per bone) were used to assess differences in end-insertional torque and pin pull-out strength. Histological evaluation of eight bicortical pin tracts per pilot hole diameter was accomplished using computer-interfaced videomicroscopy on specimens processed using a bulk-staining technique. Compared with no predrill, use of 2.7 mm PH increased end-insertional torque and pull-out strength by 25% and 13.5%, respectively. No significant differences were observed in biomechanical variables for the PH diameter range of 2.0 to 3.1 mm. Compared with no predrill, use of a 3.1 mm PH increased thread area by 18%. Microfracturing around the threads decreased as PH diameter increased. Damage to the interface at the entry and exit sites of both near and far cortices also decreased as PH diameter increased. It was concluded that predrilling a PH whose diameter approximates, but does not exceed the inner diameter of the positive profile pin will not only improve initial pin stability compared with no predrilling, but it will also reduce microstructural damage that may lead to excessive bone resorption and premature pin loosening.

Animals↗

PubMed1985

The limbic system and the localisation of herpes simplex encephalitis.

The selective destruction of temporal and frontal lobe structures by herpes simplex encephalitis has been explained as a consequence of the proximity of those regions to the point of entry of the virus in the encephalon, through olfactory pathways or meningeal branches of the trigeminal nerves. An alternative hypothesis is presented: that the encephalitis is due to a special affinity of the herpes simplex Type 1 virus for the limbic cortices, that is, that distinctive neuroanatomical, neurochemical and neuroimmunological properties of those cortices permit the virus to manifest its destructive behaviour, regardless of the route of entry to the CNS, possibly during altered immunological states. The study of the neurochemical and neuroimmunological properties of the limbic cortices may be a useful approach to the enigma of why and when herpes simplex Type 1 causes encephalitis.

Animals↗

PubMed1992

Biocompatibility and ingrowth of Trevira prostheses following replacement of the cruciate ligaments.

Five of 97 cruciate ligament prostheses (5.15 per cent) implanted for an average of 3 years (8-53 months) in 70 patients with acute chronic cruciate ligament instability were removed due to failure after a mean of 9 (3-15) months. Investigation of the explanted polyethylene terephthalate (PET)-grafts by scanning electron and light microscopy showed not bony but fibrous tissue ingrowth in all parts of the prostheses. The extent of local host response in the interface region differed with the intensity of mechanical strain at the three parts of the prostheses (intra-articular, bone tunnel, cortical). Inflammatory cells and foreign body giant cells were abundant close to the rupture sites at the intra-articular entries of the bone tunnels and scarce at the intra-articular part of the prostheses and at the cortical anchoring. Evaluation of the reasons for early prostheses failure indicates that (1) non-ideal placement of bone tunnels and (2) inadequate strain were responsible for reoccurring instability and rupture after prosthetic cruciate ligament replacement.

Anterior Cruciate Ligament↗

PubMed1992

Ouabain-induced cell swelling in rabbit connecting tubule: evidence for thiazide-sensitive Na(+)-Cl- cotransport.

Mechanisms of Na+ entry across the luminal membrane of the rabbit connecting tubule (CNT) and cortical collecting duct (CCD) were investigated in vitro by analyzing factors that block the ouabain-induced tubular swelling. In the CNT and CCD, cell swelling caused by 100 microM ouabain added to the bath was completely blocked by luminal Na+ removal, suggesting that the main factor inducing cell swelling is Na+ entry through the luminal membrane. Trichlormethiazide (100 microM) and amiloride (10 microM) inhibited the swelling in CNT when applied in combination to the lumen, but not when given separately. The swelling was also inhibited by Cl- omission from the lumen in the presence of amiloride. By contrast, no effect was noted when furosemide (100 microM), 4-acetamide-4'-isothiocyanatostilben-2,2'-disulfonic acid (1 mM) or 5-(N-ethyl-N-isopropyl)amiloride (100 microM) was added to the lumen in the presence of amiloride, indicating the absence of any influence of the Na(+)-K(+)-2Cl- cotransporter and the parallel Na+/H+, Cl-/HCO3- exchanger. The cell swelling in the CCD was blocked by luminal addition of amiloride alone with no effect from trichlormethiazide. In CNT, when the ouabain-induced cell swelling was prevented by both diuretics, addition of parathyroid hormone (PTH, 3 nM) to the bath induced cell swelling, suggesting that another Na+ entry pathway is newly generated by PTH. These results demonstrate that ouabain-induced cell swelling depends on Na+ entry across the luminal membrane. In the CNT, the pathways include an amiloride-sensitive Na+ channel, thiazide-sensitive Na(+)-Cl- cotransport and a PTH-stimulated Na+ pathway, whereas the CCD has only the amiloride-sensitive Na+ channel.

Amiloride↗

PubMed2000

Two pathways control chromaffin cell cortical F-actin dynamics during exocytosis.

Neurosecretory cells including chromaffin cells possess a mesh of filamentous actin underneath the plasma membrane. We have proposed that the F-actin network acts as a barrier to the secretory vesicles blocking their access to exocytotic sites at the plasma membrane. Disassembly of cortical F-actin in chromaffin cells in response to stimulation is thought to allow the free movement of secretory vesicles to exocytotic sites. Moreover, experiments by us using morphometric analysis of resting and stimulated chromaffin cells together with membrane capacitance measurements have shown that cortical F-actin controls the traffic of vesicles from the vesicle reserve compartment to the release-ready vesicle compartment. The dynamics of the cortical F-actin is controlled by two pathways: A) stimulation-induced Ca(2+) entry and scinderin activation; and B) protein kinase C (PKC) activation and MARCKS (myristoylated alanine-rich C kinase substrate) phosphorylation. When chromaffin cells are stimulated through nicotinic receptors, cortical F-actin disassembly is mainly through the intervention of pathway A, since in the presence of PKC inhibitors, F-actin disassembly in response to cholinergic stimulation is only blocked by 20%. Pathway A involves the activation of scinderin by Ca(2+) with a consequent F-actin severing. Pathway B is fully activated by phorbol esters and in this case PKC blockers inhibit by 100% the disruption of cortical F-actin. This pathway operates through MARCKS. A peptide with amino acid sequence corresponding to the phosphorylation site domain of MARCKS, which also corresponds to its actin binding site, blocks PMA potentiation of Ca(2+)-induced catecholamine release. The results suggest that under physiological conditions (i.e., nicotinic receptor stimulation) pathway A is the principal mechanism for the control of cortical F-actin dynamic changes.

Actins↗

PubMedDate not supplied

[Relationship between evoked potential parameters and perception].

Somatosensory EPs and reaction time were recorded simultaneously in 7-8 years old children when they solved perceptual tasks with 4 levels of complexity. The obtained data confirm the studies, suggesting the lack of connection between perceptual processes and amplitude-temporal parameters of early and late EP components in the projection cortical area. The method of recording summary evoked activity, while allowing to determine the degree of involvement of nervous elements or structures in the response to sensory signals, does not reveal spatial-temporary patterns of impulse activity in the cortical and cortical-subcortical-cortical loops providing for perception. The idea that dynamics of EP parameters produced by multiple sensory signals reflects the process of entry into memory and read out of stored information may be efficient for the understanding of mechanisms underlying higher cortical functions.

Child↗

PubMed2001

Microtubule organization in root cells of Medicago truncatula during development of an arbuscular mycorrhizal symbiosis with Glomus versiforme.

The colonization of plants by arbuscular mycorrhizal fungi has been shown to induce changes in cytoplasmic organization and morphology of root cells. Because of their role in a variety of cellular functions in plants, it is likely that microtubules are involved either in the signaling events leading to the establishment of the symbiosis or in changes in host cell morphology and cytoplasmic architecture. Recent studies of the arbuscular mycorrhizal symbiosis have shown that root cortical cells reorganize their microtubules upon colonization. These studies, however, have focused primarily on the cells containing hyphal coils or arbuscules and did not include descriptions of microtubule changes in adjacent cells. To probe further into the potential role of the microtubule cytoskeleton in the establishment of arbuscular mycorrhizal symbiosis, we examined the three-dimensional arrangement of microtubules in roots of the model legume Medicago truncatula colonized by the arbuscular mycorrhizal fungus Glomus versiforme by indirect immunofluorescence and confocal microscopy. Our data show extensive remodeling of the microtubule cytoskeleton from the early stages of arbuscule development until arbuscule collapse and senescence. While confirming some of the microtubule patterns shown in other mycorrhizal systems, our results also reveal that cortical cells adjacent to those containing arbuscules or adjacent to intercellular hyphae reorganize their microtubules. This indicates that the cortical cells initiate the modification of their cytoskeleton prior to entry of the fungus and is consistent with signal exchange between the symbionts prior to fungal penetration of the cells.

Cell Wall↗

PubMed2001

Cortical granule exocytosis in Bufo arenarum oocytes matured in vitro.

Denuded Bufo arenarum oocytes matured in vitro by progesterone treatment exhibited abnormal segmentation due to the penetration of more than one sperm. These oocytes were able to respond to activation stimuli and exhibited the external signs characteristic of activation. However, the prevention of polyspermy was not effective in these oocytes, which exhibited numerous sperm in their cytoplasm. The aim of this work was to analyse the cortical reaction in polyspermic Bufo arenarum oocytes matured in vitro. The result indicate that the cortical reaction of these oocytes seems to occur with a chronological sequence similar to that described for ovoposited oocytes of this species. In addition, when, 1 min after pricking, cortical granule exocytosis occurred, the oocytes became refractory to sperm entry, suggesting that they are able to establish a slow block to polyspermy.

Animals↗

PubMed2001

Interaction of the novel anticonvulsant, BIA 2-093, with voltage-gated sodium channels: comparison with carbamazepine.

PURPOSE: BIA 2-093 [(S)-(-)-10-acetoxy-10,11-dihydro-5H-dibenz/b,f/azepine-5-carboxamide] is endowed with an anticonvulsant potency similar to that of carbamazepine (CBZ), but produces less cognitive and motor impairment. This study evaluated whether voltage-gated sodium channels (VGSCs) are a primary locus for the action of BIA 2-093. METHODS: We used the whole-cell voltage-clamp technique in the mouse neuroblastoma cell line N1E-115 to investigate the effects of BIA 2-093 and CBZ on VGSCs, displacement of [3H]-batrachotoxinin A 20-alpha-benzoate ([3H]-BTX), and [3H]-saxitoxin to define their relative potency to bind to rat brain sodium channels, and inhibition of uptake of 22Na by rat brain cortical synaptosomes stimulated by veratridine as a measure of sodium entry. RESULTS: The inhibitory potencies of BIA 2-093 and CBZ increased as the holding potential was made less negative (-100, -90, -80, and -70 mV) with median inhibitory concentration (IC50) values (in microM) of, respectively, 4,337, 618, 238, and 139 for BIA 2-093, and 1,506, 594, 194, and 101 for CBZ. BIA 2-093 displayed a similar potency in displacing [3H]-BTX (IC50 values, 222 vs. 361 microM; p > 0.05) and inhibiting the uptake of 22Na (IC50 values, 36 vs. 138 microM; p > 0.05). Both drugs failed to displace [3H]-saxitoxin in concentrations up to 300 microM. CONCLUSIONS: BIA 2-093, like CBZ, inhibits sodium currents in a voltage-dependent way by an interaction predominantly with the inactivated state of the channel and interacts with neurotoxin receptor site 2, but not with receptor site 1. BIA 2-093 displayed a potency blocking VGSCs similar to that of CBZ.

Animals↗

PubMed2003

Determinants of renal microvascular response to ACh: afferent and efferent arteriolar actions of EDHF.

The renal microvascular actions of ACh were investigated using the in vitro perfused hydronephrotic rat kidney. ACh reversed ANG II-induced vasoconstriction in the afferent and efferent arteriole by 106 +/- 2 and 75 +/- 5%, respectively. Inhibition of nitric oxide synthase [NOS; 100 micromol/l N(G)-nitro-L-arginine methyl ester (L-NAME)] and cyclooxygenase (COX; 10 micromol/l ibuprofen) prevented the sustained response of the afferent arteriole but did not reduce the magnitude of the initial dilation (97 +/- 7%). However, NOS/COX inhibition abolished the response of the efferent arteriole. The underlying mechanisms mediating this endothelium-derived hyperpolarizing factor (EDHF)-like response were characterized using K channel blockers. Ba (100 micromol/l), tetraethylammonium (1 mmol/l), and ouabain (3 mmol/l) had no effect, arguing against a role of an inward rectifier K channel, large-conductance Ca-activated K channel, or Na,K-ATPase. Charybdotoxin (10 nmol/l) and apamin (1.0micromol/l) attenuated the response when administered alone (63 +/- 7% and 37 +/- 5%, respectively) and abolished the response when coadministered (0.1 +/- 1.0%). These findings indicate that, as in other vascular beds, the renal EDHF-like response to ACh involves K channels that are sensitive to a combination of apamin and charybdotoxin. Our finding that EDHF modulates preglomerular, but not postglomerular, tone is consistent with the evolving concept that vasomotor mechanisms in cortical efferent arterioles do not involve voltage-gated Ca entry.

4-Aminopyridine↗

PubMed2000

Spindle-like thalamocortical synchronization in a rat brain slice preparation.

We obtained rat brain slices (550-650 microm) that contained part of the frontoparietal cortex along with a portion of the thalamic ventrobasal complex (VB) and of the reticular nucleus (RTN). Maintained reciprocal thalamocortical connectivity was demonstrated by VB stimulation, which elicited orthodromic and antidromic responses in the cortex, along with re-entry of thalamocortical firing originating in VB neurons excited by cortical output activity. In addition, orthodromic responses were recorded in VB and RTN following stimuli delivered in the cortex. Spontaneous and stimulus-induced coherent rhythmic oscillations (duration = 0.4-3.5 s; frequency = 9-16 Hz) occurred in cortex, VB, and RTN during application of medium containing low concentrations of the K(+) channel blocker 4-aminopyridine (0.5-1 microM). This activity, which resembled electroencephalograph (EEG) spindles recorded in vivo, disappeared in both cortex and thalamus during application of the excitatory amino acid receptor antagonist kynurenic acid in VB (n = 6). By contrast, cortical application of kynurenic acid (n = 4) abolished spindle-like oscillations at this site, but not those recorded in VB, where their frequency was higher than under control conditions. Our findings demonstrate the preservation of reciprocally interconnected cortical and thalamic neuron networks that generate thalamocortical spindle-like oscillations in an in vitro rat brain slice. As shown in intact animals, these oscillations originate in the thalamus where they are presumably caused by interactions between RTN and VB neurons. We propose that this preparation may help to analyze thalamocortical synchronization and to understand the physiopathogenesis of absence attacks.

4-Aminopyridine↗

PubMed1987

Bioelectric responses of sea urchin eggs inseminated with oyster spermatozoa: a sperm evoked potential without egg activation.

Multiple oyster spermatozoa can enter sea urchin eggs with or often without fertilization membrane formation (Osanai and Kyozuka, 1982). In the present work, electrical responses of sea urchin (Temnopleurus hardwicki) eggs inseminated with oyster (Crassostrea gigas) sperm were examined and correlated to the failure of monospermy and egg activation. With diluted sperm, a transient depolarization of the membrane with a constant pattern appeared repeatedly and discretely, and the depolarizations (sperm evoked potentials, SEPs) were not associated with fertilization membrane elevation. With dense sperm, the SEPs occurred consecutively, and sometimes an assembled consecutive depolarization was followed by an activation potential associated with cortical granule discharge. When the membrane potential was artificially held at positive levels, the frequency of SEPs was strongly suppressed but not completely blocked. The present results indicate that an individual heterologous spermatozoon neither produces a depolarization sufficient to block additional sperm entry, nor stimulates egg activation, and that simultaneous entries of multiple heterologous spermatozoa, as possibly reflected by the assembled consecutive depolarizations, induce cortical granule discharge and egg activation.

Animals↗

PubMed1985

Cortical granule exocytosis in sea urchin eggs is inhibited by drugs that alter intracellular calcium stores.

In sea urchin eggs fertilization is accompanied by cortical granule exocytosis, a secretory event thought to be initiated by release of intracellularly sequestered calcium. We have examined the effect of two drugs on this process: chlortetracycline (CTC), a known chelator of intracellular calcium, and 8-(N,N-diethylamino)octyl-3,4,5-trimethoxybenzoate (TMB-8), an antagonist of intracellular calcium release in both skeletal and smooth muscle. Preincubation of eggs for 10 min with either CTC or TMB-8 blocked sperm entry, inhibited the burst of 45Ca2+ efflux normally seen postinsemination, and prevented fertilization envelope elevation. Half-maximal inhibition occurred with 200 microM CTC and 60 microM TMB-8. Electron microscopy confirmed that cortical granule exocytosis had been blocked, although inhibition was not due to a direct effect on exocytosis. CTC and TMB-8 had no effect on Ca2+-stimulated granule fusion in isolated egg cortices. Rather, these drugs block the early events in egg activation: sperm incorporation and triggering of exocytosis. These two effects appear to be independent since addition of either drug just before insemination permits sperm entry but inhibits calcium release and cortical granule exocytosis.

Animals↗

PubMed2003

Neuroprotective effects of a new synthetic peptide, CMX-9236, in in vitro and in vivo models of cerebral ischemia.

NGF (nerve growth factor) and BDNF (brain-derived neurotrophic factor) are protein molecules (MW 26 and 13.6 kDa, respectively) that are neuroprotective in the middle cerebral artery occlusion (MCAO) rat stroke model. Their mechanism of action involves the activation of transcription factor AP-1 that turns on neuronal growth genes. In our ongoing studies we are designing short peptides that mimic some of the properties of full-length neurotrophic factors. We have synthesized a neuroprotective 14-amino acid peptide (CMX-9236) with an N-terminal docosahexaenoic acid (DHA). DHA enhances entry through the blood-brain barrier. Using primary rat brain cortical cultures and a fluorescent assay we found that CMX-9236 can counteract the excitotoxic effects of glutamate or kainate, reversing the intracellular accumulation of Ca(2+) to normal levels. Administration (i.v.) of CMX-9236 post initiation of ischemia reduced the lesion volumes from 178+/-50 to 117+/-55 mm(3) in the temporary rat MCAO model (90 min), and from 216+/-58 to 127+/-57 mm(3) in the permanent (24 h) model for stroke, corresponding to 34+/-28% (P=0.01) and 41+/-19% (P=0.038) reductions of the infarct volumes. Neurological behavior scores showed 57 and 47% improvements for treated temporary and permanent models, respectively. Dose-response studies indicated a 60-fold activation of AP-1 transcription factor in cells treated with 100 ng/ml of the peptide. These studies illustrate that a small peptide can function as a neuroprotective agent and an activator of a beneficial signal transduction pathway.

Animals↗

PubMed1986

Mandibular osteomyelitis caused by Actinomyces Israelii. Report of a case.

An unusual case of cervicofacial actinomycosis with cortical osteomyelitis of the ascending ramus is presented. The portal of entry of the infection was most probably by an extra oral route. The authors have emphasized the importance of repeated smear examinations, cultures, and sensitivity tests to rule out actinomycosis in such cervicofacial infections. The difficulties encountered in the isolation of A. Israelii are discussed.

Actinomyces↗

PubMed2000

Glycine triggers an intracellular calcium influx in oligodendrocyte progenitor cells which is mediated by the activation of both the ionotropic glycine receptor and Na+-dependent transporters.

Using fluo-3 calcium imaging, we demonstrate that glycine induces an increase in intracellular calcium concentration ([Ca2+]i) in cortical oligodendrocyte progenitor (OP) cells. This effect results from a calcium entry through voltage-gated calcium channels (VGCC), as it is observed only in OP cells expressing such channels, and it is abolished either by removal of calcium from the extracellular medium or by application of an L-type VGCC blocker. Glycine-triggered Ca2+ influx in OP cells actually results from an initial depolarization that is the consequence of the activation of both the ionotropic glycine receptor (GlyR) and Na+-dependent transporters, most probably the glycine transporters 1 (GLYT1) and/or 2 (GLYT2) which are colocalized in these cells. Through this GlyR- and transporter-mediated effect on OP intrcellular calcium concentration [Ca2+]i, glycine released by neurons may, as well as other neurotransmitters, serve as a signal between neurons and OP during development.

Amino Acid Transport Systems, Neutral↗

PubMed2002

Functional CXCR4 receptor development parallels sensitivity to HIV-1 gp120 in cultured rat astroglial cells but not in cultured rat cortical neurons.

The alpha chemokine receptor CXCR4 is used as the major coreceptor for the cell entry of T-cell-tropic human immunodeficiency virus-1 (HIV-1) isolates. Activation of this coreceptor by its natural ligand SDF1alpha is associated with an intracellular Ca(2+) increase. Because the HIV-1 glycoprotein 120 (gp120) is shedded from the surface of HIV-1-infected cells and is regarded as an injurious molecule in the pathogenesis of HIV-1-associated encephalopathy (HIVE), we investigated the effects of gp120 on the intracellular Ca(2+) regulation of astrocytes and neurons. After 5 days in vitro (DIV), SDF1alpha (50 nM) elicited a pertussis toxin-sensitive intracellular Ca(2+) increase due to Ca(2+) release from internal stores that was reduced by a blocking monoclonal antibody against the CXCR4 receptor in astrocytes and neurons. Parallel with the development of the SDF1alpha response, cells became sensitive to direct application of gp120 (1.25 microg/ml), which, similarly to SDF1alpha, elicited a transient intracellular Ca(2+) increase. However, short-term incubation with gp120 for 60 to 120 min induced a reduction of glutamate- or ATP-evoked intracellular Ca(2+) responses only in astrocytes and not in neurons, although functional CXCR4 receptors were expressed in both cell types. Therefore, our data strongly suggest that the CXCR4 receptor-mediated intracellular signaling pathway of gp120 differs in astrocytes and neurons.

AIDS Dementia Complex↗

PubMed1992

Simulation of motion on the skin. V. Effect of stimulus temporal frequency on the representation of moving bar patterns in primary somatosensory cortex of monkeys.

1. To assess the mechanisms used by cortical neurons to sense motion across the skin, we applied pulsatile stimuli to a series of adjacent positions on the glabrous skin of the hand using a computer-controlled OPTACON stimulator. We describe responses of 129 single neurons in primary somatosensory cortex of alert monkeys to a horizontal bar pattern that was displaced proximally or distally in 1.2-mm steps at 10-, 20-, and 40-ms intervals (100, 50, and 25 Hz, respectively). These frequencies span the range in which apparent motion is transformed perceptually in humans from a smooth uninterrupted sweep into a series of distinct pulses that are resolved as separate events. The experiments are thus designed to decipher the neural correlates distinguishing continuous motion from discrete taps. 2. Cortical receptive fields mapped with moving bar patterns spanned 5-24 rows on the tactile array (16.2 +/- 5.4, mean +/- SD). Over 40% of the fields encompassed 18 or more rows (greater than or equal to 21.6 mm), allowing these neurons to integrate spatial information from an entire image displayed on the OPTACON. Cortical receptive fields are considerably larger than those of mechanoreceptors mapped with the same moving bar patterns (4.2 +/- 2.3 rows, mean +/- SD), reflecting convergent inputs in subcortical and cortical relays. Responses were either relatively uniform across the field or strongest at the initial point of entry, depending on the frequency of stimulation. A sharply defined field center was absent from most of the cells recorded in this study. 3. Temporal frequency of stimulation appears to be a major determinant of cortical firing patterns. Low-frequency stimuli are more effective in activating cortical neurons, producing more spikes per sweep and greater phase-locking to individual stimuli than do high frequencies. The total spike output of cortical neurons is proportional to the pulse interval over the range 10-40 ms, increasing linearly by an average of 5.9 spikes/10-ms increase in pulse period. Peak firing rates and modulation amplitude are also highest when pulses are presented at long intervals, falling significantly as the stimulation frequency rises. The reduction in firing at high pulse rates is apparently due to central mechanisms, as both rapidly adapting and Pacinian corpuscle afferents display nearly constant spike outputs and uniform sensitivity within the field when tested with identical bar patterns. Central networks thus behave as low-pass filters, reducing cortical responses to rapidly applied sequential stimuli.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗