Biomedical subjects
Publications and source records attributed to J R Abbott.
A life-size nylon model of a traumatized mandible was produced from CT scan data by the process of laser sintering. The model was used for pre-operative planning and for production of surgical aids in order to facilitate the restoration of a large bony defect. Vascularized iliac crest bone was harvested, titanium implants placed and the bone then grafted to the mandible.
Goats which have recovered from acute Anaplasma ovis infection remain seropositive, although infected erythrocytes cannot be detected by microscopic examination. Persistence of A. ovis 17 to 21 months following experimental infection was demonstrated by PCR detection of the msp-5 gene. Quantitative analysis of persistent rickettsemia over time showed that all levels were below the limit of microscopic detection and ranged from a low of 10(2) organisms/ml to peaks of 10(6) organisms/ml. Two patterns of persistent rickettsemia were observed: the first was characterized by cyclic fluctuations at 6- to 9-week intervals, similar to the pattern described for A. marginale-infected cattle, while in the second pattern, repetitive cycles did not occur and the rickettsemia levels were relatively constant. The msp-2 and msp-3 multigene families, which provide the genetic capacity for outer membrane protein antigenic variation during persistent A. marginale rickettsemia, were identified in the A. ovis genome by Southern blot analysis, and expression of an MSP-2 homologue was confirmed by using immunoblots.
omega-GVIA conotoxin has been used to mark presynaptic N-type voltage sensitive calcium channels (VSCC). Litzinger et al. used omega-conotoxin binding to describe a critical period of neurodevelopment in Swiss Webster mice between postnatal days (PND) 11 and 14, which appears to be important to the initiation of proper final development of the central nervous system. In this study, we compare how three different omega-conotoxins (i.e. GVIA from Conus geographus, MVIIA from Conus magus, and RVIA from Conus radiatus) mark N-type VSCC during this critical period in Swiss Webster mouse cortex. 125I-GVIA was bound to Swiss Webster mouse cortex synaptosomal membrane fractions at postnatal days 8 and 14. 125I-GVIA binding displacement curves were obtained by incubating membranes with increasing concentrations of unlabeled GVIA, MVIIA, and RVIA. Displacement curves and IC50 were calculated for each of these three omega-conotoxins, and then compared. At PND 14, GVIA, MVIIA and RVIA were able to displace greater than 95% of 125I-GVIA binding. At PND 8, however, MVIIA was only able to displace 83% of 125I-GVIA binding, and RVIA was only able to block 84%. The IC50 does not appear to change significantly during this period of development for any of the omega-conotoxins. The inability of MVIIA and RVIA to completely block 125I-GVIA binding in pre-critical period Swiss Webster cortex denotes an alteration in the composition of N-type VSCC binding sites. With this data, we have suggested the presence of subtypes of the N-type VSCC in the cortex of pre-critical period Swiss Webster mouse.
The voltage-sensitive calcium channel probe 125I-omega-GVIA conotoxin has been shown to be a developmental marker in whole brain preparations of Swiss Webster mice. The present study looks more carefully at regional dissections of the mouse brain (cerebrum, cerebellum, and brain stem) at postnatal day 8 and postnatal day 16. 125I-omega-GVIA conotoxin binding, thought to be presynaptic, showed a dramatic increase between postnatal days 8 and 16 in the cerebral cortex, a decrease in the cerebellum, and no change in the brain stem. The dramatic cerebral cortex increases indicated by these binding data correspond to a critical period between postnatal day 11 and postnatal day 14 in Swiss Webster mice; during this critical period, dendrites exhibit rapid outgrowth, sensory modalities come on line, electroencephalographic patterns mature, and the cortex reaches adult proportions. This period parallels a similar initiation of electrical maturation in the 28- to 32-week neonatal human brain. We conclude from these data that the unusual clinical presentation of neonatal seizures is not just the result of immature myelin formation. It includes incomplete synapse formation linking the cortex to the brain stem.
Voltage sensitive calcium channel (VSCC) probes 125I-omega-GVIA Conotoxin (omega-GVIA), (+)-[5-methyl-3H]-PN200-110 (3H-PN200), and 3H-Nimodipine were bound to developing Swiss Webster mouse whole brain from postnatal days 3 to 24. 125I-omega-GVIA binding, thought to be presynaptic, showed a 50% increase between days 11 and 14. 3H-dihydropyridine binding, thought to be postsynaptic, showed spike patterns when measured developmentally. 3H-PN200 binding showed a > 150% increase between days 11 and 15. 3H-Nimodipine binding showed a > 100% increase between days 11 and 14. Depolarization-induced 45Ca fluxes also increased between days 8 and 16 by > 500%. The dramatic increases indicated by these binding data correspond to a critical period described by Himwich (Int. Rev. Neurobiol. 4, 117, 1962) between postnatal days 11 and 14 in Swiss Webster mice; during this critical period, dendrites exhibit rapid outgrowth, sensory modalities come on line, EEG patterns mature, and the cortex reaches adult proportions. We conclude from these data that the increase in VSCC activity parallels a critical period in the development of the central nervous system in Swiss Webster mice.
The length of the root of the mandibular canine tooth has been considered by many authors as being a source of weakness in the mandible. It has also been suggested that a direct blow or a bending force around this tooth can result in traumatic injury. We advance a theory that implicates the maxillary canine tooth as directly contributing to the mandibular canine region fracture pattern.
Traumatic loss of large portions of the maxilla remains uncommon. Reconstruction demands careful attention to both the anatomy of the primary deformity as well as the associated secondary changes if there is to be acceptable restoration of facial aesthetics and function. In concert with rebuilding the missing maxilla, reconstruction may frequently involve repositioning the apparently undisturbed mandible.
Explore the source record for details and available documents.
The technique of monocortical non-compression miniplate fixation of mandibular angle fractures is reviewed. A study of our first 50 patients treated using this technique reveals that consistent reduction and stabilization of these mandibular fractures can be achieved without the requirement for intermaxillary fixation. Such results were produced with minimal postoperative morbidity.
The microstructures of (beta + gamma) silver-tin alloys are especially influenced by both homogenization temperature and subsequent heat treatment. When the alloy is cooled from homogenization temperatures above approximately 200 degrees C, lenticular regions of the ordered orthorhombic gamma phase precipitate from within the disordered h.c.p. beta phase on three structurally equivalent planes, (1210), (1120), and (2110), to form a Widmanstatten structure. When the duplex alloys were homogenized at temperatures below approximately 200 degrees C, where the beta/(beta + gamma) phase boundary is vertical, these structures were not observed.
Electron diffraction evidence confirming the ordered orthorhombic crystal structure of the gamma phase of the silver-tin system has been obtained, and it has been established by optical metallography that an alloy with a composition corresponding to the dental amalgam alloy formula Ag3Sn (i.e., 26.85 wt % Sn) lies outside the single gamma phase field and in the duplex (gamma + Sn) phase field adjacent to it. Studies of the mechanism of the hardening reaction of single crystals of homogeneous gamma phase alloys with mercury were carried out using both scanning and transmission electron microscopy. Mercury attack occurred preferentially along well-defined planes in the single crystals. Using electron channeling and trace analysis techniques these planes of preferential attack were found to be [010] and [011], and from transmission electron microscopy of thin foils these were shown to be slip bands and deformation twins, respectively. In bicrystals of gamma phase material, preferential attack also occurred along grain boundaries. Similar preferential mercury attack, leading to the development of deep planar intrusions into the gamma phase material, was observed in an experimental dental amalgam prepared from a lathe-cut homogeneous gamma phase amalgam alloy. It is believed that the presence of such features would have important implications for the clinical performance of dental amalgam.
Vibratory polishing is shown to be a method for preparing amalgam specimens for microscopic examination of grain structure without chemical etches. The paper describes the optimum parameters for six amalgams and 14 abrasives under varying loads and polishing times.
To examine the quantitative change in the gamma 2 phase, specimens of three conventional, four dispersed-phase and two ternary amalgams were prepared. A higher energy amalgamator caused more gamma 2 phase to be formed in conventional amalgam and less in the dispersed-phase material. With storage at 37 degrees C this gamma 2 phase decreased quantitatively in dispersed-phase amalgams over one week but not in conventional amalgams. The selective etch system of gamma 2 did not disclose this phase in the ternary amalgams.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The objective of the investigation was to examine the reactions of mercury with silver-tin alloys with compositions spanning the phase fields beta, (beta + gamma), gamma, and (gamma + Sn). The experimental methods employed include the application of light microscopy, scanning electron microscopy, and electron probe microanalysis. These techniques were used to investigate the mechanisms of reaction and to identify the nature and morphology of the reaction products formed on bulk specimens of the alloys. The progress and characteristics of the reactions that occur during hardening of amalgams prepared from powders of these alloys were monitored using a high-sensitivity dilatometer. These results were correlated with direct observations on the development of the microstructures. The reaction of mercury with the beta-phase alloy occurred rapidly and resulted in a very marked and rapid expansion during the initial stages of hardening. gamma-Phase alloys, on the other hand, reacted more slowly and contracted markedly during hardening. The behavior of amalgams made from alloys with compositions lying between these two extremes appeared to be explicable in terms of the characteristics of the separate phases from which they were constituted.
Aberrant synapse formation has been implicated in development and propagation of epileptic potential. Litzinger et al. (1993a) showed that omega-GVIA conotoxin may be used as a marker for synapse formation in nonepileptic mice. We conducted omega-GVIA binding in synaptosomal preparations from epileptic DBA/2J mice at different developmental ages. Binding in DBA/2J mice was compared with omega-GVIA binding in synaptosomal preparations from nonepileptic C57/B1, Swiss Webster, and AJ mice. Striking differences between these strains of mice are evident in the developmental sequence and pattern of N-type voltage-sensitive calcium channels (VSCC). In contrast to nonepileptic mice, the DBA/2J mice show a slow increase in omega-GVIA binding between postnatal days 2 and 8. This increase corresponds to onset of susceptibility to seizure in this strain. In addition to the difference in developmental sequence, DBA/2J mice have fewer binding sites for omega-GVIA throughout development, suggesting changes in channel structure or number. These data show that in DBA/2J mice development of the VSCC in brain is different from that in nonepileptic mice. This difference in development in presynaptic membranes responsible for neurotransmitter release may represent a change in synaptic activity that plays a role in epileptogenesis.